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Albert Griffiths (1 January 1871 – 10 December 1927), better known as Young Griffo, was a World Featherweight boxing champion from 1890 to 1892, and according to many sources, one of the first boxing world champions in any class. Ring magazine founder Nat Fleischer rated Griffo as the eighth greatest featherweight of all time. He was inducted into the Ring Magazine Hall of Fame in 1954, the International Boxing Hall of Fame in 1991, and the Australian National Boxing Hall of Fame in 2003.During his career he defeated Abe Willis, champion Ike Weir, Horace Leeds, and Joe Harmon. He won bouts against champion Torpedo Billy Murphy a total of three times, twice in World Featherweight title matches. A prolific boxer of great opponents, after coming to America, he fought champions Solly Smith, "Kid" Lavigne, Joe Gans, Tommy Ryan, George Dixon, Frank Erne, and featherweight contender Joe Bernstein. He was recorded as fighting over two hundred professional fights in his career.
Griffo also put together the most consecutive bouts without defeat in recorded boxing history. As of May 2021, with the addition of Newspaper decisions, boxrec.com lists his record as initially starting off at 7–0–3 before he lost his first fight. After losing, he went on a four-year unbeaten streak of 79–1–38 before being defeated again 124 fights after his first loss.
Early life and titles
Albert Griffiths was born at Millers Point, Sydney, New South Wales, Australia on 1 January 1871. He took his ringname "Young Griffo" early in his career. Griffo turned pro in 1886, and until the age of 22, fought in his home land of Australia.
For four of his most successful years as a boxer, Harry Tuthill was his athletic trainer and Hugh Behan and Sam Tuckhorn were managers, but by his mid career Griffo went through a host of trainers and managers who tired of his drinking habits and unwillingness to train. He said in a 1902 interview with The Cincinnati Enquirer that Larry Foley of Sydney had acted as an important early boxing mentor, and indeed Griffo had trained at Foley's boxing school at Sydney's White Horse Hotel where several of the greatest champions had spent time, including triple weight class champion Bob Fitzsimmons.
Taking Australian Featherweight Championship
On 26 December 1889, he fought Nipper Peakes in Melbourne for the Australian Featherweight Championship winning in an eight-round points decision. He held the title for several years defending it against Abe Willis and George McKenzie in Sydney in 1890.
Taking World Featherweight Title vs. Billy Murphy, 1890
He first took the World Featherweight Title against Torpedo Billy Murphy on 2 September 1890 at the White Horse Hotel in Sydney in a fifteen-round decision. It was one of the first World Title matches ever held in Australia. At the time, the United States only recognized bouts that took place in North America, and so did not fully accept Griffo's claim to the World Title, but both Australia and Great Britain did. Subsequent to his death, the World Boxing Organization accepted Griffo's claim to the World Featherweight Title.
He defended the British and Australian version of the World Featherweight title against Paddy Moran on 4 November 1890 in a 13-round decision in Sydney. He defended the World Featherweight Title against George Powell on 12 March 1891 in a twenty-round disqualification in Sydney. Griffo defended the World Featherweight Title a third time against Torpedo Billy Murphy again in Sydney, Australia on 22 July 1891, winning in a 20-second round disqualification.In his final defense of the World Featherweight Title, he defeated Mick McCarthy on 22 March 1892 in Sydney in a fourth-round decision. He eventually vacated the title to fight at a higher weight.
He fought for the Australian Lightweight Title on 25 July 1892 against Jim Barron in Sydney, Australia in a 22-round bout that was declared a draw. The referee called the bout when both boxers appeared too battered and exhausted to continue. According to one source, an audience of 2,500 were present.
Boxing in the United States
In 1893, at the age of 22, he went to America. He boxed in the United States between November 1893 until his retirement from boxing in 1904 and remained there until his death in 1927. He arrived first in San Francisco and may have boxed a few bouts on the West Coast upon his arrival, but accounts differ. One of his first bouts in America was against "Young Scotty" in Chicago on 13 November 1893, where he was reputed to have challenged his opponent to hit him for several minutes while he bobbed his head and managed to avoid nearly every blow. At least one newspaper reported after his death that even in this early stage of his career, he had been pulled from a bar room before the fight with the skilled Black boxer, but his defensive skills in the bout were considered to have been extraordinary with Scotty unable to land a blow.
Bout with future World Featherweight Champion Solly Smith
On 3 January 1894, he fought future World Featherweight champion Solly Smith at the Tivoli Theatre in Chicago to a six-round draw. Smith, who had distinguished himself by the time he met Griffo, would take the World Featherweight Championship the following year.
On 23 January 1894, he fought an eight-round draw with John Van Heest in Chicago, making an impressive performance.
Match with Ike Weir, former world champion
On 17 March 1894, Griffo defeated Ike Weir at the Second Regiment Armory in Chicago. Griffo, as a lightweight, outweighed Weir considerably and dominated the bout, which was stopped by the police in the third round when Weir was down. Weir announced retirement after the bout but returned to the ring for a few more professional bouts and exhibitions. Although the bout officially was called a draw by the referee, Griffo knocked Weir down twice in the third round, with Weir taking a while to get to his feet. Many in the crowd were displeased with the official Draw decision. According to the Inter Ocean, as many as 5,000 were in attendance to watch "three of the fastest, fiercest and most brutal rounds ever fought in an American prize ring". Young Griffo made a veritable chopping block of Ike O'Neil Weir, the "Befast Spider". It is important to note that according to one source, Griffo may have outweighed Wier by as much as 30 lbs. during the bout, but discrepancies in the weights of opponents was more common in this era of boxing. Several newspaper accounts of the fight, written after Griffo's death, wrote that he had been drinking before the bout, but by most accounts he had the edge during most of the fighting, and Weir was a worthy opponent.On 27 August 1894, he lost to the famed seven-year undefeated World Lightweight Champion Jack McAuliffe in Brooklyn, New York, losing in a 10-round points decision. McAuliffe had lost his World Lightweight Championship only the year before. Griffo had lost few of his fights by referee decision before his bout with the legendary McAuliffe. Due to McAuliffe's extraordinary record as lightweight champion, he was considered one of Griffo's most skilled opponents.
Meeting three champions
Griffo fought an assortment of opponents who would at one time hold world championships.
Bouts with Lightweight contender "Kid" Lavigne
On 10 February 1894, he fought future World Lightweight Champion George "Kid" Lavigne for the first time in an eight-round draw in Chicago. On 12 October 1895, he fought Lavigne in a 20-round draw by points decision in Queens, New York. Lavigne would take the World Lightweight Championship only the following year.He subsequently fought an eight-round draw with the hard-hitting red head boxer Johnny Griffin at the Casino in Boston on 23 April 1894.
On 17 September 1894, he knocked out Eddie Loeber in only 2 minutes 36 seconds of the first round at the Seaside Athletic Club in Brooklyn. The Brooklyn Daily Eagle, wrote that the two men were very "poorly matched", and that it was a relief when the referee Dominick McAffrey stopped the bout. Hundreds of spectators struggled to shake hands with Griffo after the fight's conclusion.On 4 March 1895, he defeated Horace Leeds at the Seaside Athletic Club in Coney Island in a 12-round bout in front of a sizable crowd of 4000 spectators. One reporter believed Griffo to be over the 133 pound weight limit, and fighting at a weight of as much as 140. The fighting was fierce, and both men were described as being "badly pummeled" in a close bout that had the betting about even. He lost to Leeds on 7 August 1897, in a four-round newspaper decision in Atlantic City, New Jersey. During this period, he was managed by Hugh Behan, but Griffo had an assortment of trainers in his career.
Bouts with world champion George Dixon
On 28 October 1895, he fought the great Black Canadian champion George Dixon in a 10-round draw by points decision in Manhattan. Dixon had taken the World Featherweight Championship in 1891, and was one of the first recognized world champions. Griffo would fight Dixon two additional times in well attended matches. One source described their 20-round draw as a "battle that bristled throughout with glittering skill and generalship." On 19 January 1895, they would fight a 25-round draw in New York's Coney Island. His manager Hughey Behan had him jailed briefly before the Coney Island bout with Dixon so he could train in a sober state.
Arrests for assault and disorderly conduct
On 11 April 1896, he was arrested at a Casino he frequented in College Point, Long Island, on charges of assault against William Connors, a town trustee. He was discharged shortly after to attend a scheduled bout against boxer Charles McKeever. On 13 April, the day he would have faced trial on the assault charge, he lost the 20-round bout at the Empire Athletic Club with McKeever in Queens, New York, on a points decision of the referee. On 9 June 1896, he was arrested for driving intoxicated and disorderly conduct in Coney Island, New York, and was arraigned at the Coney Island Police Court. He was sentenced to twenty-five days in prison after pleading guilty. Around 20 November 1897, he was arrested for vagrancy in St. Louis, Missouri, but several nights drinking at a bar may have precipitated the arrest. He was not held for long and fought a bout the following month in California. On 28 September 1898, he was arrested in Chicago found running naked on State Street for a quarter mile. He reportedly assaulted the three officers who tried to arrest him. Another source states he had been drinking the night the incident occurred. On 14 January 1899, he was arrested and brought to Chicago's Harrison Street Police Station for struggling with a police officer to prevent the arrest of a Tom McGinty from the Clover Leaf Saloon, around 2:00 AM but released shortly after. He was sent to an insane asylum on 24 March 1899, after being judged insane in Chicago. He was arrested on suspicion of armed robbery against James H. Wilkerson on 9 September 1901, but only one source mentions this arrest. On 2 February 1902, he was discovered in the cold in a vacant lot near the Bridewell in Chicago, where he had been serving a sentence for disorderly conduct. It was feared he would lose his hands from frostbite. On 6 February 1902, he was sent back to an asylum. Around 25 February 1903, he was sent back to the Bridewell in Chicago for three months for "making trouble".
Three bouts with future Welterweight Champion Joe Gans
He fought the legendary World Light and Welterweight Champion Joe Gans three times, but never winning a bout. Griffo's 18 November 1895 bout with Gans in Gan's home of Baltimore, Maryland, appeared to some to be only an exhibition, with which many in the crowd were disappointed. A few even considered the bout a "fix", as Griffo told the audience, he had agreed not to "put out" Gans during the bout. Griffo considered his 15-round draw in Athens, Pennsylvania, at the Olympic Athletic Club on 21 September 1897 one of his best, as well as one of Gans' most skilled displays. Of his 10 July 1900 bout with Gans, an eighth-round loss by technical knockout at the Seaside Athletic Club, one source wrote, the referee stopped the bout one minute and 30 econds into the eighth round when "Griffo was so far gone that another punch from Gans would have put him out." Griffo was reported to have shown some of his early form, but was no match for the blows and conditioning of the "old master" Joe Gans, and was believed by one reporter to have had less stamina as the fight wound on. Griffo was down in both the first and seventh rounds, and he took off nearly a year from his boxing after this last fight with Gans.
Bouts with champions Frank Erne, and Billy Murphy
He met one time World Featherweight and Lightweight champion Frank Erne on 20 December 1895 in a four-round non-title fight that resulted in a draw in Buffalo, New York.He defeated Torpedo Billy Murphy in a non-title match ending in an eight-round points decision at the Casino in Boston on 7 May 1894. His 20-round draw bout with Jack Everhardt on 10 July 1896 in Buffalo, New York, was billed as a World 135 pound title. He had previously met Everhardt in a pre-arranged six-round draw in Brooklyn on 25 May, at which the crowd would have preferred a decision by the referee. He lost to World Welter and Middleweight Champion Tommy Ryan on 21 June 1897 in a non-title match in a third-round technical knockout in Brooklyn, New York.
Late boxing career
Serving time
On 15 August 1896, he was sentenced in Brooklyn to one year in prison for an assault on William Gottlieb the previous April. He did not box from August 1896 until June 1897.
Boxing after release
On 12 July 1897, he fought well known lightweight Owen Ziegler, in Philadelphia, Pennsylvania, in a six-round bout, which he won by newspaper decision. He considered Ziegler one of his more important opponents.He fought a close bout with Horace Leeds on 7 August 1897 in Atlantic City, New Jersey, in which The Philadelphia Inquirer felt Leeds had received more points.On 18 November 1897, Griffo was believed to have been drunk in a contest with Tom Tracey at the Colliseum in St. Louis. He rolled out of the boxing ring in the first round, and referee George Siler declared a No Contest. One source confirmed his story that he had been in a car accident before the fight which was the cause of his inability to complete the first round. The San Francisco Call wrote that Griffo's vehicle had been struck by a street car on the way to the bout, and that he had suffered a sprained shoulder as a result. He and two of his seconds were treated for injuries received as a result of the accident.He was defeated in an upset by Frank McConnell before three thousand spectators on 3 February 1898 in a 15-rounds points decision in San Francisco, California. McConnell only recently emerged from the amateur ranks, and had relatively little experience as a professional. Griffo showed great defensive skills in several rounds, but McConnell won the bout by taking the offensive throughout most of the fight.On 26 March 1898, he won a bout with the well known Black boxer, Young Peter Jackson in Red Bluff, California on a fourth-round disqualification. A few at ringside claimed that Jackson was actually Joe Gans, but this was found to be untrue.
Tragic bout with Bull McCarthy
On the evening of 27 April 1898, he fought Joseph Devitt, who gave the name of the boxer "Bull" McCarthy, in Sacramento, California. Griffo won the 20-round bout by knockout, but Devitt died the following evening of his injuries at Sister's Hospital. Devitt was diagnosed with a brain concussion, likely caused by a rain of blows to his head during the bout. Griffo was briefly taken into custody on charges of manslaughter as a result of the fight. The tragic result was a source of strong remorse for Griffo but it did not deter him from continuing his profession.
Late career decline
On 19 December 1901, he was advised to retire from boxing due to a "valvular affection of the heart that may bring death to him in the ring at any time." The diagnosis was made by a Dr. McGregor of the Olympic Athletic Club, and if accurate should have ended his boxing career.On 22 August 1902, he lost to three-time World Featherweight Title contender Joe Bernstein in Baltimore, Maryland in a 20-round points decision.He lost to lightweight boxer Joe Tipman in a fifth-round knockout on 29 September 1902 in Baltimore.In December 1902, after defeating Jack Bain in a ninth-round knockout in Baltimore, he took off at least a year from boxing before his fight with George Memsic around December 1903, also in Baltimore. In this stage of his career he was managed by Sam Tuckhorn, who was hoping to revive his career and convince the public of his fighting skills, but Griffo was nearing the end of his career.On 7 December 1903 in Peoria, Illinois, he defeated Jim Kenney in a four-round decision. Griffo showed great speed and cleverness according to the referee, Tom Dunn.One of his last well publicized bouts was a loss by first-round knockout against Tommy White on 10 February 1904 in Chicago, Illinois. He was already thirty-three at the time, and his age, drinking, and enormous number of previous fights had begun to tell on his speed and endurance in the ring. He was arrested in September 1909 in Chicago, as relatives from Australia had requested his arrest so as to help him obtain treatment for his drinking. Cyber Boxing Zone has him fighting two six-round, no-decision fights as late as 1911 with Welterweight champion William "Honey" Melody in September and Mike Leonard in May in New York, but these bouts were not confirmed by BoxRec and other boxers used the name Young Griffo. He served time at the Bridewell in Chicago, but was released around 28 November 1910, and returned to New York. He had plans to go on the vaudeville circuit with Charles Griffin, another boxer.In a tribute to Griffo, boxer Tommy Sullivan wrote in the 6 March 1916 Tacoma Daily News:
Not known as much of a puncher, but his skill was uncanny. He had wonderful head work, almost impenetrable defense, dazzling feints, and rapid two-handed methods of attack. The cleverest boxers and hardest punchers were made to look ridiculous when exchanging swats with him. He had a dislike of training and was deemed lazy. There were times he got drunk before a match [such as the Ike Weir and Tommy Tracy bouts].
Brief film career
He appeared as himself in the 1895 lost short Young Griffo vs. Battling Charles Barnett, which at least one source claims is the first film shown for profit. He appeared in at least two other films.
Apparently, two of his film roles were released near or after his death. Released in 1927, he had a minor role in Frank Capra's comedy Long Pants, and the following year in Harry Edwards' 1928 comedy The Best Man.
Tragic life after boxing
In March 1912, Griffo requested to be sent to the New York workhouse, partly a victim of alcoholism, which had affected him intermittently throughout his career. On 11 July 1912, he briefly was jailed for "almstaking" or begging. He had been arrested previously for begging.For the last 15 years of his life, he took donations and met friends at the entrance to New York's Rialto Theatre on Broadway and 42nd Street, becoming increasingly destitute by 1925. He spent some of his later years in asylums, and received a portion of his income from benefits staged by his friends. He had gained over 50 lbs. by the time of his death. He died in New York of heart disease, initially diagnosed as indigestion, on 7 December 1927 at age 56. He received medical aid too late after dragging himself into a hall from his small, rent-free room in a West side New York boarding house paid for by Jane F. Fish, an author of children's books. Many American newspapers ran stories on his life as a tragic tale of the effects of alcohol. He left no children nor were there any heirs that laid claim to his estate.Friends of his from the boxing and theatrical community provided for a burial. Several newspaper accounts after his death attributed his financial plight in part to his illiteracy as well as a poor understanding of numbers and currency, which made him an easy victim of unscrupulous handlers.He was laid to rest at Woodlawn Cemetery after a service at the Madison Avenue Baptist Church. Ring notables in attendance included Jack McAuliffe, Kid McPartland, Tommy Burns, James J. Corbett, and wealthy boxing promoter Tex Rickard, who provided funding for the burial plot and casket. Jane F. Fish also contributed to his funeral. Rickard was later repaid $500 of the $885 of funeral expenses he had donated out of a $3800 estate found to be attributed to Griffo after the funeral.
Professional boxing record
All information in this section is derived from BoxRec, unless otherwise stated.
Official record
All newspaper decisions are officially regarded as "no decision" bouts and are not counted in the win/loss/draw column.
Unofficial record
Record with the inclusion of newspaper decisions to the win/loss/draw column.
Boxing achievements
References
External links
Boxing record for Young Griffo from BoxRec (registration required)
Griffo: his life story and record / told by Jack Read (1926?)
Young Griffo: the will o'wisp of the roped square / Nat Fleischer (1928)
"Ring History of the Near-Champions: Young Griffo", National Police Gazette, New York: Richard K. Fox Publishing Co., CXX (23325): 7, 4 March 1922, retrieved 24 April 2013
Pictures held and digitised as part of the Arnold Thomas boxing collection by the National Library of Australia:
Albert Griffiths "Griffo", Feather Champion of the World, c1890
Albert Griffiths, 1893?
Albert Griffiths, c1927 "shortly before his death"
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Albert Griffiths (1 January 1871 – 10 December 1927), better known as Young Griffo, was a World Featherweight boxing champion from 1890 to 1892, and according to many sources, one of the first boxing world champions in any class. Ring magazine founder Nat Fleischer rated Griffo as the eighth greatest featherweight of all time. He was inducted into the Ring Magazine Hall of Fame in 1954, the International Boxing Hall of Fame in 1991, and the Australian National Boxing Hall of Fame in 2003.During his career he defeated Abe Willis, champion Ike Weir, Horace Leeds, and Joe Harmon. He won bouts against champion Torpedo Billy Murphy a total of three times, twice in World Featherweight title matches. A prolific boxer of great opponents, after coming to America, he fought champions Solly Smith, "Kid" Lavigne, Joe Gans, Tommy Ryan, George Dixon, Frank Erne, and featherweight contender Joe Bernstein. He was recorded as fighting over two hundred professional fights in his career.
Griffo also put together the most consecutive bouts without defeat in recorded boxing history. As of May 2021, with the addition of Newspaper decisions, boxrec.com lists his record as initially starting off at 7–0–3 before he lost his first fight. After losing, he went on a four-year unbeaten streak of 79–1–38 before being defeated again 124 fights after his first loss.
Early life and titles
Albert Griffiths was born at Millers Point, Sydney, New South Wales, Australia on 1 January 1871. He took his ringname "Young Griffo" early in his career. Griffo turned pro in 1886, and until the age of 22, fought in his home land of Australia.
For four of his most successful years as a boxer, Harry Tuthill was his athletic trainer and Hugh Behan and Sam Tuckhorn were managers, but by his mid career Griffo went through a host of trainers and managers who tired of his drinking habits and unwillingness to train. He said in a 1902 interview with The Cincinnati Enquirer that Larry Foley of Sydney had acted as an important early boxing mentor, and indeed Griffo had trained at Foley's boxing school at Sydney's White Horse Hotel where several of the greatest champions had spent time, including triple weight class champion Bob Fitzsimmons.
Taking Australian Featherweight Championship
On 26 December 1889, he fought Nipper Peakes in Melbourne for the Australian Featherweight Championship winning in an eight-round points decision. He held the title for several years defending it against Abe Willis and George McKenzie in Sydney in 1890.
Taking World Featherweight Title vs. Billy Murphy, 1890
He first took the World Featherweight Title against Torpedo Billy Murphy on 2 September 1890 at the White Horse Hotel in Sydney in a fifteen-round decision. It was one of the first World Title matches ever held in Australia. At the time, the United States only recognized bouts that took place in North America, and so did not fully accept Griffo's claim to the World Title, but both Australia and Great Britain did. Subsequent to his death, the World Boxing Organization accepted Griffo's claim to the World Featherweight Title.
He defended the British and Australian version of the World Featherweight title against Paddy Moran on 4 November 1890 in a 13-round decision in Sydney. He defended the World Featherweight Title against George Powell on 12 March 1891 in a twenty-round disqualification in Sydney. Griffo defended the World Featherweight Title a third time against Torpedo Billy Murphy again in Sydney, Australia on 22 July 1891, winning in a 20-second round disqualification.In his final defense of the World Featherweight Title, he defeated Mick McCarthy on 22 March 1892 in Sydney in a fourth-round decision. He eventually vacated the title to fight at a higher weight.
He fought for the Australian Lightweight Title on 25 July 1892 against Jim Barron in Sydney, Australia in a 22-round bout that was declared a draw. The referee called the bout when both boxers appeared too battered and exhausted to continue. According to one source, an audience of 2,500 were present.
Boxing in the United States
In 1893, at the age of 22, he went to America. He boxed in the United States between November 1893 until his retirement from boxing in 1904 and remained there until his death in 1927. He arrived first in San Francisco and may have boxed a few bouts on the West Coast upon his arrival, but accounts differ. One of his first bouts in America was against "Young Scotty" in Chicago on 13 November 1893, where he was reputed to have challenged his opponent to hit him for several minutes while he bobbed his head and managed to avoid nearly every blow. At least one newspaper reported after his death that even in this early stage of his career, he had been pulled from a bar room before the fight with the skilled Black boxer, but his defensive skills in the bout were considered to have been extraordinary with Scotty unable to land a blow.
Bout with future World Featherweight Champion Solly Smith
On 3 January 1894, he fought future World Featherweight champion Solly Smith at the Tivoli Theatre in Chicago to a six-round draw. Smith, who had distinguished himself by the time he met Griffo, would take the World Featherweight Championship the following year.
On 23 January 1894, he fought an eight-round draw with John Van Heest in Chicago, making an impressive performance.
Match with Ike Weir, former world champion
On 17 March 1894, Griffo defeated Ike Weir at the Second Regiment Armory in Chicago. Griffo, as a lightweight, outweighed Weir considerably and dominated the bout, which was stopped by the police in the third round when Weir was down. Weir announced retirement after the bout but returned to the ring for a few more professional bouts and exhibitions. Although the bout officially was called a draw by the referee, Griffo knocked Weir down twice in the third round, with Weir taking a while to get to his feet. Many in the crowd were displeased with the official Draw decision. According to the Inter Ocean, as many as 5,000 were in attendance to watch "three of the fastest, fiercest and most brutal rounds ever fought in an American prize ring". Young Griffo made a veritable chopping block of Ike O'Neil Weir, the "Befast Spider". It is important to note that according to one source, Griffo may have outweighed Wier by as much as 30 lbs. during the bout, but discrepancies in the weights of opponents was more common in this era of boxing. Several newspaper accounts of the fight, written after Griffo's death, wrote that he had been drinking before the bout, but by most accounts he had the edge during most of the fighting, and Weir was a worthy opponent.On 27 August 1894, he lost to the famed seven-year undefeated World Lightweight Champion Jack McAuliffe in Brooklyn, New York, losing in a 10-round points decision. McAuliffe had lost his World Lightweight Championship only the year before. Griffo had lost few of his fights by referee decision before his bout with the legendary McAuliffe. Due to McAuliffe's extraordinary record as lightweight champion, he was considered one of Griffo's most skilled opponents.
Meeting three champions
Griffo fought an assortment of opponents who would at one time hold world championships.
Bouts with Lightweight contender "Kid" Lavigne
On 10 February 1894, he fought future World Lightweight Champion George "Kid" Lavigne for the first time in an eight-round draw in Chicago. On 12 October 1895, he fought Lavigne in a 20-round draw by points decision in Queens, New York. Lavigne would take the World Lightweight Championship only the following year.He subsequently fought an eight-round draw with the hard-hitting red head boxer Johnny Griffin at the Casino in Boston on 23 April 1894.
On 17 September 1894, he knocked out Eddie Loeber in only 2 minutes 36 seconds of the first round at the Seaside Athletic Club in Brooklyn. The Brooklyn Daily Eagle, wrote that the two men were very "poorly matched", and that it was a relief when the referee Dominick McAffrey stopped the bout. Hundreds of spectators struggled to shake hands with Griffo after the fight's conclusion.On 4 March 1895, he defeated Horace Leeds at the Seaside Athletic Club in Coney Island in a 12-round bout in front of a sizable crowd of 4000 spectators. One reporter believed Griffo to be over the 133 pound weight limit, and fighting at a weight of as much as 140. The fighting was fierce, and both men were described as being "badly pummeled" in a close bout that had the betting about even. He lost to Leeds on 7 August 1897, in a four-round newspaper decision in Atlantic City, New Jersey. During this period, he was managed by Hugh Behan, but Griffo had an assortment of trainers in his career.
Bouts with world champion George Dixon
On 28 October 1895, he fought the great Black Canadian champion George Dixon in a 10-round draw by points decision in Manhattan. Dixon had taken the World Featherweight Championship in 1891, and was one of the first recognized world champions. Griffo would fight Dixon two additional times in well attended matches. One source described their 20-round draw as a "battle that bristled throughout with glittering skill and generalship." On 19 January 1895, they would fight a 25-round draw in New York's Coney Island. His manager Hughey Behan had him jailed briefly before the Coney Island bout with Dixon so he could train in a sober state.
Arrests for assault and disorderly conduct
On 11 April 1896, he was arrested at a Casino he frequented in College Point, Long Island, on charges of assault against William Connors, a town trustee. He was discharged shortly after to attend a scheduled bout against boxer Charles McKeever. On 13 April, the day he would have faced trial on the assault charge, he lost the 20-round bout at the Empire Athletic Club with McKeever in Queens, New York, on a points decision of the referee. On 9 June 1896, he was arrested for driving intoxicated and disorderly conduct in Coney Island, New York, and was arraigned at the Coney Island Police Court. He was sentenced to twenty-five days in prison after pleading guilty. Around 20 November 1897, he was arrested for vagrancy in St. Louis, Missouri, but several nights drinking at a bar may have precipitated the arrest. He was not held for long and fought a bout the following month in California. On 28 September 1898, he was arrested in Chicago found running naked on State Street for a quarter mile. He reportedly assaulted the three officers who tried to arrest him. Another source states he had been drinking the night the incident occurred. On 14 January 1899, he was arrested and brought to Chicago's Harrison Street Police Station for struggling with a police officer to prevent the arrest of a Tom McGinty from the Clover Leaf Saloon, around 2:00 AM but released shortly after. He was sent to an insane asylum on 24 March 1899, after being judged insane in Chicago. He was arrested on suspicion of armed robbery against James H. Wilkerson on 9 September 1901, but only one source mentions this arrest. On 2 February 1902, he was discovered in the cold in a vacant lot near the Bridewell in Chicago, where he had been serving a sentence for disorderly conduct. It was feared he would lose his hands from frostbite. On 6 February 1902, he was sent back to an asylum. Around 25 February 1903, he was sent back to the Bridewell in Chicago for three months for "making trouble".
Three bouts with future Welterweight Champion Joe Gans
He fought the legendary World Light and Welterweight Champion Joe Gans three times, but never winning a bout. Griffo's 18 November 1895 bout with Gans in Gan's home of Baltimore, Maryland, appeared to some to be only an exhibition, with which many in the crowd were disappointed. A few even considered the bout a "fix", as Griffo told the audience, he had agreed not to "put out" Gans during the bout. Griffo considered his 15-round draw in Athens, Pennsylvania, at the Olympic Athletic Club on 21 September 1897 one of his best, as well as one of Gans' most skilled displays. Of his 10 July 1900 bout with Gans, an eighth-round loss by technical knockout at the Seaside Athletic Club, one source wrote, the referee stopped the bout one minute and 30 econds into the eighth round when "Griffo was so far gone that another punch from Gans would have put him out." Griffo was reported to have shown some of his early form, but was no match for the blows and conditioning of the "old master" Joe Gans, and was believed by one reporter to have had less stamina as the fight wound on. Griffo was down in both the first and seventh rounds, and he took off nearly a year from his boxing after this last fight with Gans.
Bouts with champions Frank Erne, and Billy Murphy
He met one time World Featherweight and Lightweight champion Frank Erne on 20 December 1895 in a four-round non-title fight that resulted in a draw in Buffalo, New York.He defeated Torpedo Billy Murphy in a non-title match ending in an eight-round points decision at the Casino in Boston on 7 May 1894. His 20-round draw bout with Jack Everhardt on 10 July 1896 in Buffalo, New York, was billed as a World 135 pound title. He had previously met Everhardt in a pre-arranged six-round draw in Brooklyn on 25 May, at which the crowd would have preferred a decision by the referee. He lost to World Welter and Middleweight Champion Tommy Ryan on 21 June 1897 in a non-title match in a third-round technical knockout in Brooklyn, New York.
Late boxing career
Serving time
On 15 August 1896, he was sentenced in Brooklyn to one year in prison for an assault on William Gottlieb the previous April. He did not box from August 1896 until June 1897.
Boxing after release
On 12 July 1897, he fought well known lightweight Owen Ziegler, in Philadelphia, Pennsylvania, in a six-round bout, which he won by newspaper decision. He considered Ziegler one of his more important opponents.He fought a close bout with Horace Leeds on 7 August 1897 in Atlantic City, New Jersey, in which The Philadelphia Inquirer felt Leeds had received more points.On 18 November 1897, Griffo was believed to have been drunk in a contest with Tom Tracey at the Colliseum in St. Louis. He rolled out of the boxing ring in the first round, and referee George Siler declared a No Contest. One source confirmed his story that he had been in a car accident before the fight which was the cause of his inability to complete the first round. The San Francisco Call wrote that Griffo's vehicle had been struck by a street car on the way to the bout, and that he had suffered a sprained shoulder as a result. He and two of his seconds were treated for injuries received as a result of the accident.He was defeated in an upset by Frank McConnell before three thousand spectators on 3 February 1898 in a 15-rounds points decision in San Francisco, California. McConnell only recently emerged from the amateur ranks, and had relatively little experience as a professional. Griffo showed great defensive skills in several rounds, but McConnell won the bout by taking the offensive throughout most of the fight.On 26 March 1898, he won a bout with the well known Black boxer, Young Peter Jackson in Red Bluff, California on a fourth-round disqualification. A few at ringside claimed that Jackson was actually Joe Gans, but this was found to be untrue.
Tragic bout with Bull McCarthy
On the evening of 27 April 1898, he fought Joseph Devitt, who gave the name of the boxer "Bull" McCarthy, in Sacramento, California. Griffo won the 20-round bout by knockout, but Devitt died the following evening of his injuries at Sister's Hospital. Devitt was diagnosed with a brain concussion, likely caused by a rain of blows to his head during the bout. Griffo was briefly taken into custody on charges of manslaughter as a result of the fight. The tragic result was a source of strong remorse for Griffo but it did not deter him from continuing his profession.
Late career decline
On 19 December 1901, he was advised to retire from boxing due to a "valvular affection of the heart that may bring death to him in the ring at any time." The diagnosis was made by a Dr. McGregor of the Olympic Athletic Club, and if accurate should have ended his boxing career.On 22 August 1902, he lost to three-time World Featherweight Title contender Joe Bernstein in Baltimore, Maryland in a 20-round points decision.He lost to lightweight boxer Joe Tipman in a fifth-round knockout on 29 September 1902 in Baltimore.In December 1902, after defeating Jack Bain in a ninth-round knockout in Baltimore, he took off at least a year from boxing before his fight with George Memsic around December 1903, also in Baltimore. In this stage of his career he was managed by Sam Tuckhorn, who was hoping to revive his career and convince the public of his fighting skills, but Griffo was nearing the end of his career.On 7 December 1903 in Peoria, Illinois, he defeated Jim Kenney in a four-round decision. Griffo showed great speed and cleverness according to the referee, Tom Dunn.One of his last well publicized bouts was a loss by first-round knockout against Tommy White on 10 February 1904 in Chicago, Illinois. He was already thirty-three at the time, and his age, drinking, and enormous number of previous fights had begun to tell on his speed and endurance in the ring. He was arrested in September 1909 in Chicago, as relatives from Australia had requested his arrest so as to help him obtain treatment for his drinking. Cyber Boxing Zone has him fighting two six-round, no-decision fights as late as 1911 with Welterweight champion William "Honey" Melody in September and Mike Leonard in May in New York, but these bouts were not confirmed by BoxRec and other boxers used the name Young Griffo. He served time at the Bridewell in Chicago, but was released around 28 November 1910, and returned to New York. He had plans to go on the vaudeville circuit with Charles Griffin, another boxer.In a tribute to Griffo, boxer Tommy Sullivan wrote in the 6 March 1916 Tacoma Daily News:
Not known as much of a puncher, but his skill was uncanny. He had wonderful head work, almost impenetrable defense, dazzling feints, and rapid two-handed methods of attack. The cleverest boxers and hardest punchers were made to look ridiculous when exchanging swats with him. He had a dislike of training and was deemed lazy. There were times he got drunk before a match [such as the Ike Weir and Tommy Tracy bouts].
Brief film career
He appeared as himself in the 1895 lost short Young Griffo vs. Battling Charles Barnett, which at least one source claims is the first film shown for profit. He appeared in at least two other films.
Apparently, two of his film roles were released near or after his death. Released in 1927, he had a minor role in Frank Capra's comedy Long Pants, and the following year in Harry Edwards' 1928 comedy The Best Man.
Tragic life after boxing
In March 1912, Griffo requested to be sent to the New York workhouse, partly a victim of alcoholism, which had affected him intermittently throughout his career. On 11 July 1912, he briefly was jailed for "almstaking" or begging. He had been arrested previously for begging.For the last 15 years of his life, he took donations and met friends at the entrance to New York's Rialto Theatre on Broadway and 42nd Street, becoming increasingly destitute by 1925. He spent some of his later years in asylums, and received a portion of his income from benefits staged by his friends. He had gained over 50 lbs. by the time of his death. He died in New York of heart disease, initially diagnosed as indigestion, on 7 December 1927 at age 56. He received medical aid too late after dragging himself into a hall from his small, rent-free room in a West side New York boarding house paid for by Jane F. Fish, an author of children's books. Many American newspapers ran stories on his life as a tragic tale of the effects of alcohol. He left no children nor were there any heirs that laid claim to his estate.Friends of his from the boxing and theatrical community provided for a burial. Several newspaper accounts after his death attributed his financial plight in part to his illiteracy as well as a poor understanding of numbers and currency, which made him an easy victim of unscrupulous handlers.He was laid to rest at Woodlawn Cemetery after a service at the Madison Avenue Baptist Church. Ring notables in attendance included Jack McAuliffe, Kid McPartland, Tommy Burns, James J. Corbett, and wealthy boxing promoter Tex Rickard, who provided funding for the burial plot and casket. Jane F. Fish also contributed to his funeral. Rickard was later repaid $500 of the $885 of funeral expenses he had donated out of a $3800 estate found to be attributed to Griffo after the funeral.
Professional boxing record
All information in this section is derived from BoxRec, unless otherwise stated.
Official record
All newspaper decisions are officially regarded as "no decision" bouts and are not counted in the win/loss/draw column.
Unofficial record
Record with the inclusion of newspaper decisions to the win/loss/draw column.
Boxing achievements
References
External links
Boxing record for Young Griffo from BoxRec (registration required)
Griffo: his life story and record / told by Jack Read (1926?)
Young Griffo: the will o'wisp of the roped square / Nat Fleischer (1928)
"Ring History of the Near-Champions: Young Griffo", National Police Gazette, New York: Richard K. Fox Publishing Co., CXX (23325): 7, 4 March 1922, retrieved 24 April 2013
Pictures held and digitised as part of the Arnold Thomas boxing collection by the National Library of Australia:
Albert Griffiths "Griffo", Feather Champion of the World, c1890
Albert Griffiths, 1893?
Albert Griffiths, c1927 "shortly before his death"
|
sports discipline competed in
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{
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Alpendorf (German for alpine village) is a village and a part of the town St. Johann im Pongau. It is 55 km (34 mi) south of the Austrian city of Salzburg. It is at an altitude of 850 m (2,790 ft) above sea level.
It is 3 km (1.9 mi) away from the town centre of Sankt Johann im Pongau, a large town dominated by the Cathedral of Pongau.
The economy is largely dependent on tourism, particularly during the winter months when thousands of predominantly German, Danish and Dutch skiers visiting the village. The resort is popular with members of the British and American forces based in Germany. There are also a significant number of English and Welsh schools visiting the area.
Accommodation
The resort is largely made up of four- and five-star hotels with wellness areas and restaurants. More reasonably priced accommodation can be found in St Johann, where hotels run a free shuttle bus. There is also a free ski shuttle bus that runs throughout the season from St Johann to Alpendorf.
Skiing
Alpendorf serves as one of the gateways to the Salzburger Sportwelt, one of the five alliances that make up Ski Amadé, a network of resorts with over 870 slopes and 270 modern ski lifts.
The resort, as a result of its location in the Eastern Alps, has a good record for winter snow. There are lakes containing 30,000 cubic metres (1,100,000 cu ft) of fresh water, which is used by the snow cannon that cover 95% of the slopes.
Resort statistics
Altitude 850 m - 2188 m
Length of ski trails: 350 km
Cross-country trails: 220 km
Snow cannons: 150
Mountain restaurants: 80
Lift statistics
Button lifts: 1
T-Bars: 2
Chair lifts (4 to 8 seater): 35
Gondola lifts (6 to 16 seated and standing): 12
Aerial cable car: 1
People movements: 56,000 an hour
Slope statistics
Blue Slopes (least challenging): 119 km
Red Slopes (intermediate): 189 km
Black Slopes (difficult): 42 km
Famous residents
Hermann Maier (nearby village of Flachau)
Ralf Schumacher
External links
St Johann/Alpendorf Tourist Office
|
country
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Alpendorf (German for alpine village) is a village and a part of the town St. Johann im Pongau. It is 55 km (34 mi) south of the Austrian city of Salzburg. It is at an altitude of 850 m (2,790 ft) above sea level.
It is 3 km (1.9 mi) away from the town centre of Sankt Johann im Pongau, a large town dominated by the Cathedral of Pongau.
The economy is largely dependent on tourism, particularly during the winter months when thousands of predominantly German, Danish and Dutch skiers visiting the village. The resort is popular with members of the British and American forces based in Germany. There are also a significant number of English and Welsh schools visiting the area.
Accommodation
The resort is largely made up of four- and five-star hotels with wellness areas and restaurants. More reasonably priced accommodation can be found in St Johann, where hotels run a free shuttle bus. There is also a free ski shuttle bus that runs throughout the season from St Johann to Alpendorf.
Skiing
Alpendorf serves as one of the gateways to the Salzburger Sportwelt, one of the five alliances that make up Ski Amadé, a network of resorts with over 870 slopes and 270 modern ski lifts.
The resort, as a result of its location in the Eastern Alps, has a good record for winter snow. There are lakes containing 30,000 cubic metres (1,100,000 cu ft) of fresh water, which is used by the snow cannon that cover 95% of the slopes.
Resort statistics
Altitude 850 m - 2188 m
Length of ski trails: 350 km
Cross-country trails: 220 km
Snow cannons: 150
Mountain restaurants: 80
Lift statistics
Button lifts: 1
T-Bars: 2
Chair lifts (4 to 8 seater): 35
Gondola lifts (6 to 16 seated and standing): 12
Aerial cable car: 1
People movements: 56,000 an hour
Slope statistics
Blue Slopes (least challenging): 119 km
Red Slopes (intermediate): 189 km
Black Slopes (difficult): 42 km
Famous residents
Hermann Maier (nearby village of Flachau)
Ralf Schumacher
External links
St Johann/Alpendorf Tourist Office
|
located in the administrative territorial entity
|
{
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263
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|
Alpendorf (German for alpine village) is a village and a part of the town St. Johann im Pongau. It is 55 km (34 mi) south of the Austrian city of Salzburg. It is at an altitude of 850 m (2,790 ft) above sea level.
It is 3 km (1.9 mi) away from the town centre of Sankt Johann im Pongau, a large town dominated by the Cathedral of Pongau.
The economy is largely dependent on tourism, particularly during the winter months when thousands of predominantly German, Danish and Dutch skiers visiting the village. The resort is popular with members of the British and American forces based in Germany. There are also a significant number of English and Welsh schools visiting the area.
Accommodation
The resort is largely made up of four- and five-star hotels with wellness areas and restaurants. More reasonably priced accommodation can be found in St Johann, where hotels run a free shuttle bus. There is also a free ski shuttle bus that runs throughout the season from St Johann to Alpendorf.
Skiing
Alpendorf serves as one of the gateways to the Salzburger Sportwelt, one of the five alliances that make up Ski Amadé, a network of resorts with over 870 slopes and 270 modern ski lifts.
The resort, as a result of its location in the Eastern Alps, has a good record for winter snow. There are lakes containing 30,000 cubic metres (1,100,000 cu ft) of fresh water, which is used by the snow cannon that cover 95% of the slopes.
Resort statistics
Altitude 850 m - 2188 m
Length of ski trails: 350 km
Cross-country trails: 220 km
Snow cannons: 150
Mountain restaurants: 80
Lift statistics
Button lifts: 1
T-Bars: 2
Chair lifts (4 to 8 seater): 35
Gondola lifts (6 to 16 seated and standing): 12
Aerial cable car: 1
People movements: 56,000 an hour
Slope statistics
Blue Slopes (least challenging): 119 km
Red Slopes (intermediate): 189 km
Black Slopes (difficult): 42 km
Famous residents
Hermann Maier (nearby village of Flachau)
Ralf Schumacher
External links
St Johann/Alpendorf Tourist Office
|
Commons category
|
{
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0
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"text": [
"Alpendorf"
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|
Pentecost season, also known Pentecostide, as well as the time of Sundays after Pentecost or Sundays after Trinity, is a liturgical period, celebrated by some Christian churches, which immediately follows the Easter season. Although the start and end dates vary by liturgical tradition, the season typically begins on the day of Pentecost and continues throughout the rest of the liturgical year, ending just before the season of Advent. The liturgical color for this period is typically green or red.
Western Christianity
Roman Rite Catholicism
The Ordinary Form of the Roman Rite of the Catholic Church does not include a Pentecost season. Pentecost is considered the last day of the Easter season, and is followed by Ordinary Time.
Traditionalist Catholicism has an eight-day Octave of Pentecost, followed by Sundays after Pentecost that continue through to the end of the liturgical year.
The Catholic Church's Ordinariate Use for former Anglicans uses Trinity Sunday (the octave day of Pentecost) as the start of a liturgical period, with subsequent Sundays designated "Sundays after Trinity".
The various forms of the Roman Rite all use the color green for this period.
Moravianism
In the Moravian Church, the Pentecost season runs from the Feast of Pentecost itself to the Reign of Christ, the last Sunday of the liturgical year. Red is the liturgical color used for Pentecost Sunday; white is the liturgical color used for Trinity Sunday and Reign of Christ Sunday; green is the liturgical color used for the other Sundays of the Pentecost season.
Lutheranism
In the Lutheran Church–Missouri Synod, this period can be called "Season after Pentecost" or "Season of the Holy Trinity."
Anglicanism
The Book of Common Prayer refers to this period as the "Season after Pentecost."
Reformed
In the Reformed Churches, such as the Presbyterian Church (USA), the season is known as the "Time after Pentecost".The United Church of Christ, a Congregationalist denomination in the Reformed tradition, assigns the period of the liturgical calendar as "Time after Pentecost".
Methodism
Many Annual Conferences within the United Methodist Church observe Kingdomtide as a liturgical season spanning the latter portion of the period between Pentecost and the start of the Advent season.
Eastern Christianity
Byzantine Rite
The Byzantine Rite of Eastern Christianity uses the nomenclature of "Sundays after Pentecost."
West Syriac Rite
The Maronite Church, which uses the West Syriac Rite, celebrates a Pentecost season that extends until the Feast of the Exaltation of the Cross.
East Syriac Rite
The closest equivalent to a Pentecost season in the East Syriac Rite is the Season of Apostles, which begins with Pentecost and continues for seven weeks.
== References ==
|
instance of
|
{
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2170
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|
Kim Ki-su (born August 5, 1982) is a North Korean former football player.
Club statistics
References
External links
Kim Ki-su at J.League (archive) (in Japanese)
[1]
|
native language
|
{
"answer_start": [
43
],
"text": [
"Korean"
]
}
|
Kim Ki-su (born August 5, 1982) is a North Korean former football player.
Club statistics
References
External links
Kim Ki-su at J.League (archive) (in Japanese)
[1]
|
family name
|
{
"answer_start": [
0
],
"text": [
"Kim"
]
}
|
Kim Ki-su (born August 5, 1982) is a North Korean former football player.
Club statistics
References
External links
Kim Ki-su at J.League (archive) (in Japanese)
[1]
|
languages spoken, written or signed
|
{
"answer_start": [
43
],
"text": [
"Korean"
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}
|
Esdras Minville (November 7, 1896 in Grande-Vallée – December 9, 1975) was a Canadian writer, economist and sociologist. He served as the Dean of the Faculty of Social Sciences at the Université de Montréal, and was the first French-Canadian to serve as head of HEC Montréal. A staunch defender of Catholic social doctrine, Minville helped to found several co-operatives in the province.
He contributed to the Rowell-Sirois Commission, and chaired the Montreal Chamber of Commerce in 1947. His nationalist ideas resembled those of Victor Barbeau, François-Albert Angers and Lionel Groulx.
Published works
Invitation à l'étude, 1943
L'agriculture, 1943
Montréal économique, 1943
La forêt, 1944
L'homme d'affaires, 1944
Le citoyen canadien-français, 1946
Pêche et chasse, 1946
Les affaires: l'homme, les carrières, 1965
Awards
Honorary doctorate from the University of Ottawa
Honorary doctorate from the Université Laval
Honorary doctorate from the Université de Sherbrooke
Honorary doctorate from the Université de Montréal
Member of the Royal Society of Canada
1947 - Ludger-Duvernay Prize
1968 - Innis-Gérin Medal
External links
Canadian Encyclopedia
|
country of citizenship
|
{
"answer_start": [
1060
],
"text": [
"Canada"
]
}
|
Esdras Minville (November 7, 1896 in Grande-Vallée – December 9, 1975) was a Canadian writer, economist and sociologist. He served as the Dean of the Faculty of Social Sciences at the Université de Montréal, and was the first French-Canadian to serve as head of HEC Montréal. A staunch defender of Catholic social doctrine, Minville helped to found several co-operatives in the province.
He contributed to the Rowell-Sirois Commission, and chaired the Montreal Chamber of Commerce in 1947. His nationalist ideas resembled those of Victor Barbeau, François-Albert Angers and Lionel Groulx.
Published works
Invitation à l'étude, 1943
L'agriculture, 1943
Montréal économique, 1943
La forêt, 1944
L'homme d'affaires, 1944
Le citoyen canadien-français, 1946
Pêche et chasse, 1946
Les affaires: l'homme, les carrières, 1965
Awards
Honorary doctorate from the University of Ottawa
Honorary doctorate from the Université Laval
Honorary doctorate from the Université de Sherbrooke
Honorary doctorate from the Université de Montréal
Member of the Royal Society of Canada
1947 - Ludger-Duvernay Prize
1968 - Innis-Gérin Medal
External links
Canadian Encyclopedia
|
occupation
|
{
"answer_start": [
86
],
"text": [
"writer"
]
}
|
Esdras Minville (November 7, 1896 in Grande-Vallée – December 9, 1975) was a Canadian writer, economist and sociologist. He served as the Dean of the Faculty of Social Sciences at the Université de Montréal, and was the first French-Canadian to serve as head of HEC Montréal. A staunch defender of Catholic social doctrine, Minville helped to found several co-operatives in the province.
He contributed to the Rowell-Sirois Commission, and chaired the Montreal Chamber of Commerce in 1947. His nationalist ideas resembled those of Victor Barbeau, François-Albert Angers and Lionel Groulx.
Published works
Invitation à l'étude, 1943
L'agriculture, 1943
Montréal économique, 1943
La forêt, 1944
L'homme d'affaires, 1944
Le citoyen canadien-français, 1946
Pêche et chasse, 1946
Les affaires: l'homme, les carrières, 1965
Awards
Honorary doctorate from the University of Ottawa
Honorary doctorate from the Université Laval
Honorary doctorate from the Université de Sherbrooke
Honorary doctorate from the Université de Montréal
Member of the Royal Society of Canada
1947 - Ludger-Duvernay Prize
1968 - Innis-Gérin Medal
External links
Canadian Encyclopedia
|
award received
|
{
"answer_start": [
1103
],
"text": [
"Innis-Gérin Medal"
]
}
|
Esdras Minville (November 7, 1896 in Grande-Vallée – December 9, 1975) was a Canadian writer, economist and sociologist. He served as the Dean of the Faculty of Social Sciences at the Université de Montréal, and was the first French-Canadian to serve as head of HEC Montréal. A staunch defender of Catholic social doctrine, Minville helped to found several co-operatives in the province.
He contributed to the Rowell-Sirois Commission, and chaired the Montreal Chamber of Commerce in 1947. His nationalist ideas resembled those of Victor Barbeau, François-Albert Angers and Lionel Groulx.
Published works
Invitation à l'étude, 1943
L'agriculture, 1943
Montréal économique, 1943
La forêt, 1944
L'homme d'affaires, 1944
Le citoyen canadien-français, 1946
Pêche et chasse, 1946
Les affaires: l'homme, les carrières, 1965
Awards
Honorary doctorate from the University of Ottawa
Honorary doctorate from the Université Laval
Honorary doctorate from the Université de Sherbrooke
Honorary doctorate from the Université de Montréal
Member of the Royal Society of Canada
1947 - Ludger-Duvernay Prize
1968 - Innis-Gérin Medal
External links
Canadian Encyclopedia
|
Commons category
|
{
"answer_start": [
0
],
"text": [
"Esdras Minville"
]
}
|
Esdras Minville (November 7, 1896 in Grande-Vallée – December 9, 1975) was a Canadian writer, economist and sociologist. He served as the Dean of the Faculty of Social Sciences at the Université de Montréal, and was the first French-Canadian to serve as head of HEC Montréal. A staunch defender of Catholic social doctrine, Minville helped to found several co-operatives in the province.
He contributed to the Rowell-Sirois Commission, and chaired the Montreal Chamber of Commerce in 1947. His nationalist ideas resembled those of Victor Barbeau, François-Albert Angers and Lionel Groulx.
Published works
Invitation à l'étude, 1943
L'agriculture, 1943
Montréal économique, 1943
La forêt, 1944
L'homme d'affaires, 1944
Le citoyen canadien-français, 1946
Pêche et chasse, 1946
Les affaires: l'homme, les carrières, 1965
Awards
Honorary doctorate from the University of Ottawa
Honorary doctorate from the Université Laval
Honorary doctorate from the Université de Sherbrooke
Honorary doctorate from the Université de Montréal
Member of the Royal Society of Canada
1947 - Ludger-Duvernay Prize
1968 - Innis-Gérin Medal
External links
Canadian Encyclopedia
|
member of
|
{
"answer_start": [
1043
],
"text": [
"Royal Society of Canada"
]
}
|
Esdras Minville (November 7, 1896 in Grande-Vallée – December 9, 1975) was a Canadian writer, economist and sociologist. He served as the Dean of the Faculty of Social Sciences at the Université de Montréal, and was the first French-Canadian to serve as head of HEC Montréal. A staunch defender of Catholic social doctrine, Minville helped to found several co-operatives in the province.
He contributed to the Rowell-Sirois Commission, and chaired the Montreal Chamber of Commerce in 1947. His nationalist ideas resembled those of Victor Barbeau, François-Albert Angers and Lionel Groulx.
Published works
Invitation à l'étude, 1943
L'agriculture, 1943
Montréal économique, 1943
La forêt, 1944
L'homme d'affaires, 1944
Le citoyen canadien-français, 1946
Pêche et chasse, 1946
Les affaires: l'homme, les carrières, 1965
Awards
Honorary doctorate from the University of Ottawa
Honorary doctorate from the Université Laval
Honorary doctorate from the Université de Sherbrooke
Honorary doctorate from the Université de Montréal
Member of the Royal Society of Canada
1947 - Ludger-Duvernay Prize
1968 - Innis-Gérin Medal
External links
Canadian Encyclopedia
|
family name
|
{
"answer_start": [
7
],
"text": [
"Minville"
]
}
|
Esdras Minville (November 7, 1896 in Grande-Vallée – December 9, 1975) was a Canadian writer, economist and sociologist. He served as the Dean of the Faculty of Social Sciences at the Université de Montréal, and was the first French-Canadian to serve as head of HEC Montréal. A staunch defender of Catholic social doctrine, Minville helped to found several co-operatives in the province.
He contributed to the Rowell-Sirois Commission, and chaired the Montreal Chamber of Commerce in 1947. His nationalist ideas resembled those of Victor Barbeau, François-Albert Angers and Lionel Groulx.
Published works
Invitation à l'étude, 1943
L'agriculture, 1943
Montréal économique, 1943
La forêt, 1944
L'homme d'affaires, 1944
Le citoyen canadien-français, 1946
Pêche et chasse, 1946
Les affaires: l'homme, les carrières, 1965
Awards
Honorary doctorate from the University of Ottawa
Honorary doctorate from the Université Laval
Honorary doctorate from the Université de Sherbrooke
Honorary doctorate from the Université de Montréal
Member of the Royal Society of Canada
1947 - Ludger-Duvernay Prize
1968 - Innis-Gérin Medal
External links
Canadian Encyclopedia
|
given name
|
{
"answer_start": [
0
],
"text": [
"Esdras"
]
}
|
Esdras Minville (November 7, 1896 in Grande-Vallée – December 9, 1975) was a Canadian writer, economist and sociologist. He served as the Dean of the Faculty of Social Sciences at the Université de Montréal, and was the first French-Canadian to serve as head of HEC Montréal. A staunch defender of Catholic social doctrine, Minville helped to found several co-operatives in the province.
He contributed to the Rowell-Sirois Commission, and chaired the Montreal Chamber of Commerce in 1947. His nationalist ideas resembled those of Victor Barbeau, François-Albert Angers and Lionel Groulx.
Published works
Invitation à l'étude, 1943
L'agriculture, 1943
Montréal économique, 1943
La forêt, 1944
L'homme d'affaires, 1944
Le citoyen canadien-français, 1946
Pêche et chasse, 1946
Les affaires: l'homme, les carrières, 1965
Awards
Honorary doctorate from the University of Ottawa
Honorary doctorate from the Université Laval
Honorary doctorate from the Université de Sherbrooke
Honorary doctorate from the Université de Montréal
Member of the Royal Society of Canada
1947 - Ludger-Duvernay Prize
1968 - Innis-Gérin Medal
External links
Canadian Encyclopedia
|
languages spoken, written or signed
|
{
"answer_start": [
227
],
"text": [
"French"
]
}
|
Esdras Minville (November 7, 1896 in Grande-Vallée – December 9, 1975) was a Canadian writer, economist and sociologist. He served as the Dean of the Faculty of Social Sciences at the Université de Montréal, and was the first French-Canadian to serve as head of HEC Montréal. A staunch defender of Catholic social doctrine, Minville helped to found several co-operatives in the province.
He contributed to the Rowell-Sirois Commission, and chaired the Montreal Chamber of Commerce in 1947. His nationalist ideas resembled those of Victor Barbeau, François-Albert Angers and Lionel Groulx.
Published works
Invitation à l'étude, 1943
L'agriculture, 1943
Montréal économique, 1943
La forêt, 1944
L'homme d'affaires, 1944
Le citoyen canadien-français, 1946
Pêche et chasse, 1946
Les affaires: l'homme, les carrières, 1965
Awards
Honorary doctorate from the University of Ottawa
Honorary doctorate from the Université Laval
Honorary doctorate from the Université de Sherbrooke
Honorary doctorate from the Université de Montréal
Member of the Royal Society of Canada
1947 - Ludger-Duvernay Prize
1968 - Innis-Gérin Medal
External links
Canadian Encyclopedia
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writing language
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{
"answer_start": [
227
],
"text": [
"French"
]
}
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Andreas Holst Jensen (born 1 December 1994) is a Danish handball player for Montpellier Handball and the Danish national team.
Achievements
EHF Champions League
Runner-up: 2021
Danish Handball League
Winner: 2019, 2020, 2021
Runner-up: 2022
Danish Cup
Winner: 2018, 2021
Runner-up: 2020
Danish Super Cup
Winner: 2019, 2020, 2021
IHF Super Globe
Bronze medal: 2021
== References ==
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member of sports team
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{
"answer_start": [
76
],
"text": [
"Montpellier Handball"
]
}
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Andreas Holst Jensen (born 1 December 1994) is a Danish handball player for Montpellier Handball and the Danish national team.
Achievements
EHF Champions League
Runner-up: 2021
Danish Handball League
Winner: 2019, 2020, 2021
Runner-up: 2022
Danish Cup
Winner: 2018, 2021
Runner-up: 2020
Danish Super Cup
Winner: 2019, 2020, 2021
IHF Super Globe
Bronze medal: 2021
== References ==
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occupation
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{
"answer_start": [
56
],
"text": [
"handball player"
]
}
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Andreas Holst Jensen (born 1 December 1994) is a Danish handball player for Montpellier Handball and the Danish national team.
Achievements
EHF Champions League
Runner-up: 2021
Danish Handball League
Winner: 2019, 2020, 2021
Runner-up: 2022
Danish Cup
Winner: 2018, 2021
Runner-up: 2020
Danish Super Cup
Winner: 2019, 2020, 2021
IHF Super Globe
Bronze medal: 2021
== References ==
|
sport
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{
"answer_start": [
56
],
"text": [
"handball"
]
}
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Andreas Holst Jensen (born 1 December 1994) is a Danish handball player for Montpellier Handball and the Danish national team.
Achievements
EHF Champions League
Runner-up: 2021
Danish Handball League
Winner: 2019, 2020, 2021
Runner-up: 2022
Danish Cup
Winner: 2018, 2021
Runner-up: 2020
Danish Super Cup
Winner: 2019, 2020, 2021
IHF Super Globe
Bronze medal: 2021
== References ==
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family name
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{
"answer_start": [
14
],
"text": [
"Jensen"
]
}
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Andreas Holst Jensen (born 1 December 1994) is a Danish handball player for Montpellier Handball and the Danish national team.
Achievements
EHF Champions League
Runner-up: 2021
Danish Handball League
Winner: 2019, 2020, 2021
Runner-up: 2022
Danish Cup
Winner: 2018, 2021
Runner-up: 2020
Danish Super Cup
Winner: 2019, 2020, 2021
IHF Super Globe
Bronze medal: 2021
== References ==
|
given name
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{
"answer_start": [
0
],
"text": [
"Andreas"
]
}
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Habibul Islam Habib is a Bangladesh Nationalist Party politician and the former Member of Parliament of Satkhira-1.
Career
Habib was elected to parliament from Satkhira-1 as a Bangladesh Nationalist Party candidate in 2001. In 2015, he was charged with attacking a convoy of Prime Minister Sheikh Hasina in Satkhira in 2002.
== References ==
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country of citizenship
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{
"answer_start": [
25
],
"text": [
"Bangladesh"
]
}
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Diabetes, also known as diabetes mellitus, is a group of common endocrine diseases characterized by sustained high blood sugar levels. Diabetes is due to either the pancreas not producing enough insulin, or the cells of the body not responding properly to the insulin produced. Diabetes, if left untreated, leads to many health complications. Untreated or poorly treated diabetes accounts for approximately 1.5 million deaths per year.There is no widely accepted cure for most cases of diabetes. The most common treatment for type 1 diabetes is insulin replacement therapy (insulin injections). Anti-diabetic medications such as metformin and semaglutide, as well as lifestyle modifications, can be used to prevent or respond to type 2 diabetes. Gestational diabetes normally resolves shortly after delivery.
As of 2019, an estimated 463 million people had diabetes worldwide accounting for 8.8% of the adult population. Type 2 diabetes makes up about 90% of all diabetes cases. The prevalence of the disease continues to increase, most dramatically in low- and middle-income nations. Rates are similar in women and men, with diabetes being the 7th-leading cause of death globally. The global expenditure on diabetes-related healthcare is an estimated USD760 billion a year.
Signs and symptoms
The classic symptoms of untreated diabetes are unintended weight loss, polyuria (increased urination), polydipsia (increased thirst), and polyphagia (increased hunger). Symptoms may develop rapidly (weeks or months) in type 1 diabetes, while they usually develop much more slowly and may be subtle or absent in type 2 diabetes.Several other signs and symptoms can mark the onset of diabetes although they are not specific to the disease. In addition to the known symptoms listed above, they include blurred vision, headache, fatigue, slow healing of cuts, and itchy skin. Prolonged high blood glucose can cause glucose absorption in the lens of the eye, which leads to changes in its shape, resulting in vision changes. Long-term vision loss can also be caused by diabetic retinopathy. A number of skin rashes that can occur in diabetes are collectively known as diabetic dermadromes.
Diabetic emergencies
People with diabetes (usually but not exclusively in type 1 diabetes) may also experience diabetic ketoacidosis (DKA), a metabolic disturbance characterized by nausea, vomiting and abdominal pain, the smell of acetone on the breath, deep breathing known as Kussmaul breathing, and in severe cases a decreased level of consciousness. DKA requires emergency treatment in hospital. A rarer but more dangerous condition is hyperosmolar hyperglycemic state (HHS), which is more common in type 2 diabetes and is mainly the result of dehydration caused by high blood sugars.Treatment-related low blood sugar (hypoglycemia) is common in people with type 1 and also type 2 diabetes depending on the medication being used. Most cases are mild and are not considered medical emergencies. Effects can range from feelings of unease, sweating, trembling, and increased appetite in mild cases to more serious effects such as confusion, changes in behavior such as aggressiveness, seizures, unconsciousness, and rarely permanent brain damage or death in severe cases. Rapid breathing, sweating, and cold, pale skin are characteristic of low blood sugar but not definitive. Mild to moderate cases are self-treated by eating or drinking something high in rapidly absorbed carbohydrates. Severe cases can lead to unconsciousness and must be treated with intravenous glucose or injections with glucagon.
Complications
All forms of diabetes increase the risk of long-term complications. These typically develop after many years (10–20) but may be the first symptom in those who have otherwise not received a diagnosis before that time.The major long-term complications relate to damage to blood vessels. Diabetes doubles the risk of cardiovascular disease and about 75% of deaths in people with diabetes are due to coronary artery disease. Other macrovascular diseases include stroke, and peripheral artery disease. These complications are also a strong risk factor for severe COVID-19 illness.The primary complications of diabetes due to damage in small blood vessels include damage to the eyes, kidneys, and nerves. Damage to the eyes, known as diabetic retinopathy, is caused by damage to the blood vessels in the retina of the eye, and can result in gradual vision loss and eventual blindness. Diabetes also increases the risk of having glaucoma, cataracts, and other eye problems. It is recommended that people with diabetes visit an optometrist or ophthalmologist once a year. Damage to the kidneys, known as diabetic nephropathy, can lead to tissue scarring, urine protein loss, and eventually chronic kidney disease, sometimes requiring dialysis or kidney transplantation. Damage to the nerves of the body, known as diabetic neuropathy, is the most common complication of diabetes. The symptoms can include numbness, tingling, sudomotor dysfunction, pain, and altered pain sensation, which can lead to damage to the skin. Diabetes-related foot problems (such as diabetic foot ulcers) may occur, and can be difficult to treat, occasionally requiring amputation. Additionally, proximal diabetic neuropathy causes painful muscle atrophy and weakness.
There is a link between cognitive deficit and diabetes. Compared to those without diabetes, those with the disease have a 1.2 to 1.5-fold greater rate of decline in cognitive function. Having diabetes, especially when on insulin, increases the risk of falls in older people.
Causes
Diabetes mellitus is classified into six categories: type 1 diabetes, type 2 diabetes, hybrid forms of diabetes, hyperglycemia first detected during pregnancy, "unclassified diabetes", and "other specific types". "Hybrid forms of diabetes" include slowly evolving, immune-mediated diabetes of adults and ketosis-prone type 2 diabetes. "Hyperglycemia first detected during pregnancy" includes gestational diabetes mellitus and diabetes mellitus in pregnancy (type 1 or type 2 diabetes first diagnosed during pregnancy). The "other specific types" are a collection of a few dozen individual causes. Diabetes is a more variable disease than once thought and people may have combinations of forms.
Type 1
Type 1 diabetes is characterized by loss of the insulin-producing beta cells of the pancreatic islets, leading to insulin deficiency. This type can be further classified as immune-mediated or idiopathic. The majority of type 1 diabetes is of an immune-mediated nature, in which a T cell-mediated autoimmune attack leads to the loss of beta cells and thus insulin. It causes approximately 10% of diabetes mellitus cases in North America and Europe. Most affected people are otherwise healthy and of a healthy weight when onset occurs. Sensitivity and responsiveness to insulin are usually normal, especially in the early stages. Although it has been called "juvenile diabetes" due to the frequent onset in children, the majority of individuals living with type 1 diabetes are now adults."Brittle" diabetes, also known as unstable diabetes or labile diabetes, is a term that was traditionally used to describe the dramatic and recurrent swings in glucose levels, often occurring for no apparent reason in insulin-dependent diabetes. This term, however, has no biologic basis and should not be used. Still, type 1 diabetes can be accompanied by irregular and unpredictable high blood sugar levels, and the potential for diabetic ketoacidosis or serious low blood sugar levels. Other complications include an impaired counterregulatory response to low blood sugar, infection, gastroparesis (which leads to erratic absorption of dietary carbohydrates), and endocrinopathies (e.g., Addison's disease). These phenomena are believed to occur no more frequently than in 1% to 2% of persons with type 1 diabetes.
Type 1 diabetes is partly inherited, with multiple genes, including certain HLA genotypes, known to influence the risk of diabetes. In genetically susceptible people, the onset of diabetes can be triggered by one or more environmental factors, such as a viral infection or diet. Several viruses have been implicated, but to date there is no stringent evidence to support this hypothesis in humans.Type 1 diabetes can occur at any age, and a significant proportion is diagnosed during adulthood. Latent autoimmune diabetes of adults (LADA) is the diagnostic term applied when type 1 diabetes develops in adults; it has a slower onset than the same condition in children. Given this difference, some use the unofficial term "type 1.5 diabetes" for this condition. Adults with LADA are frequently initially misdiagnosed as having type 2 diabetes, based on age rather than a cause.
Type 2
Type 2 diabetes is characterized by insulin resistance, which may be combined with relatively reduced insulin secretion. The defective responsiveness of body tissues to insulin is believed to involve the insulin receptor. However, the specific defects are not known. Diabetes mellitus cases due to a known defect are classified separately. Type 2 diabetes is the most common type of diabetes mellitus accounting for 95% of diabetes. Many people with type 2 diabetes have evidence of prediabetes (impaired fasting glucose and/or impaired glucose tolerance) before meeting the criteria for type 2 diabetes. The progression of prediabetes to overt type 2 diabetes can be slowed or reversed by lifestyle changes or medications that improve insulin sensitivity or reduce the liver's glucose production.Type 2 diabetes is primarily due to lifestyle factors and genetics. A number of lifestyle factors are known to be important to the development of type 2 diabetes, including obesity (defined by a body mass index of greater than 30), lack of physical activity, poor diet, stress, and urbanization. Excess body fat is associated with 30% of cases in people of Chinese and Japanese descent, 60–80% of cases in those of European and African descent, and 100% of Pima Indians and Pacific Islanders. Even those who are not obese may have a high waist–hip ratio.Dietary factors such as sugar-sweetened drinks are associated with an increased risk. The type of fats in the diet is also important, with saturated fat and trans fats increasing the risk and polyunsaturated and monounsaturated fat decreasing the risk. Eating white rice excessively may increase the risk of diabetes, especially in Chinese and Japanese people. Lack of physical activity may increase the risk of diabetes in some people.Adverse childhood experiences, including abuse, neglect, and household difficulties, increase the likelihood of type 2 diabetes later in life by 32%, with neglect having the strongest effect.Antipsychotic medication side effects (specifically metabolic abnormalities, dyslipidemia and weight gain) and unhealthy lifestyles (including poor diet and decreased physical activity), are potential risk factors.
Gestational diabetes
Gestational diabetes resembles type 2 diabetes in several respects, involving a combination of relatively inadequate insulin secretion and responsiveness. It occurs in about 2–10% of all pregnancies and may improve or disappear after delivery. It is recommended that all pregnant women get tested starting around 24–28 weeks gestation. It is most often diagnosed in the second or third trimester because of the increase in insulin-antagonist hormone levels that occurs at this time. However, after pregnancy approximately 5–10% of women with gestational diabetes are found to have another form of diabetes, most commonly type 2. Gestational diabetes is fully treatable, but requires careful medical supervision throughout the pregnancy. Management may include dietary changes, blood glucose monitoring, and in some cases, insulin may be required.Though it may be transient, untreated gestational diabetes can damage the health of the fetus or mother. Risks to the baby include macrosomia (high birth weight), congenital heart and central nervous system abnormalities, and skeletal muscle malformations. Increased levels of insulin in a fetus's blood may inhibit fetal surfactant production and cause infant respiratory distress syndrome. A high blood bilirubin level may result from red blood cell destruction. In severe cases, perinatal death may occur, most commonly as a result of poor placental perfusion due to vascular impairment. Labor induction may be indicated with decreased placental function. A caesarean section may be performed if there is marked fetal distress or an increased risk of injury associated with macrosomia, such as shoulder dystocia.
Other types
Maturity onset diabetes of the young (MODY) is a rare autosomal dominant inherited form of diabetes, due to one of several single-gene mutations causing defects in insulin production. It is significantly less common than the three main types, constituting 1–2% of all cases. The name of this disease refers to early hypotheses as to its nature. Being due to a defective gene, this disease varies in age at presentation and in severity according to the specific gene defect; thus, there are at least 13 subtypes of MODY. People with MODY often can control it without using insulin.Some cases of diabetes are caused by the body's tissue receptors not responding to insulin (even when insulin levels are normal, which is what separates it from type 2 diabetes); this form is very uncommon. Genetic mutations (autosomal or mitochondrial) can lead to defects in beta cell function. Abnormal insulin action may also have been genetically determined in some cases. Any disease that causes extensive damage to the pancreas may lead to diabetes (for example, chronic pancreatitis and cystic fibrosis). Diseases associated with excessive secretion of insulin-antagonistic hormones can cause diabetes (which is typically resolved once the hormone excess is removed). Many drugs impair insulin secretion and some toxins damage pancreatic beta cells, whereas others increase insulin resistance (especially glucocorticoids which can provoke "steroid diabetes"). The ICD-10 (1992) diagnostic entity, malnutrition-related diabetes mellitus (ICD-10 code E12), was deprecated by the World Health Organization (WHO) when the current taxonomy was introduced in 1999.
Yet another form of diabetes that people may develop is double diabetes. This is when a type 1 diabetic becomes insulin resistant, the hallmark for type 2 diabetes or has a family history for type 2 diabetes. It was first discovered in 1990 or 1991.
The following is a list of disorders that may increase the risk of diabetes:
Pathophysiology
Insulin is the principal hormone that regulates the uptake of glucose from the blood into most cells of the body, especially liver, adipose tissue and muscle, except smooth muscle, in which insulin acts via the IGF-1. Therefore, deficiency of insulin or the insensitivity of its receptors play a central role in all forms of diabetes mellitus.The body obtains glucose from three main sources: the intestinal absorption of food; the breakdown of glycogen (glycogenolysis), the storage form of glucose found in the liver; and gluconeogenesis, the generation of glucose from non-carbohydrate substrates in the body. Insulin plays a critical role in regulating glucose levels in the body. Insulin can inhibit the breakdown of glycogen or the process of gluconeogenesis, it can stimulate the transport of glucose into fat and muscle cells, and it can stimulate the storage of glucose in the form of glycogen.Insulin is released into the blood by beta cells (β-cells), found in the islets of Langerhans in the pancreas, in response to rising levels of blood glucose, typically after eating. Insulin is used by about two-thirds of the body's cells to absorb glucose from the blood for use as fuel, for conversion to other needed molecules, or for storage. Lower glucose levels result in decreased insulin release from the beta cells and in the breakdown of glycogen to glucose. This process is mainly controlled by the hormone glucagon, which acts in the opposite manner to insulin.If the amount of insulin available is insufficient, or if cells respond poorly to the effects of insulin (insulin resistance), or if the insulin itself is defective, then glucose is not absorbed properly by the body cells that require it, and is not stored appropriately in the liver and muscles. The net effect is persistently high levels of blood glucose, poor protein synthesis, and other metabolic derangements, such as metabolic acidosis in cases of complete insulin deficiency.When glucose concentration in the blood remains high over time, the kidneys reach a threshold of reabsorption, and the body excretes glucose in the urine (glycosuria). This increases the osmotic pressure of the urine and inhibits reabsorption of water by the kidney, resulting in increased urine production (polyuria) and increased fluid loss. Lost blood volume is replaced osmotically from water in body cells and other body compartments, causing dehydration and increased thirst (polydipsia). In addition, intracellular glucose deficiency stimulates appetite leading to excessive food intake (polyphagia).
Diagnosis
Diabetes mellitus is diagnosed with a test for the glucose content in the blood, and is diagnosed by demonstrating any one of the following:
Fasting plasma glucose level ≥ 7.0 mmol/L (126 mg/dL). For this test, blood is taken after a period of fasting, i.e. in the morning before breakfast, after the patient had sufficient time to fast overnight.
Plasma glucose ≥ 11.1 mmol/L (200 mg/dL) two hours after a 75 gram oral glucose load as in a glucose tolerance test (OGTT)
Symptoms of high blood sugar and plasma glucose ≥ 11.1 mmol/L (200 mg/dL) either while fasting or not fasting
Glycated hemoglobin (HbA1C) ≥ 48 mmol/mol (≥ 6.5 DCCT %).A positive result, in the absence of unequivocal high blood sugar, should be confirmed by a repeat of any of the above methods on a different day. It is preferable to measure a fasting glucose level because of the ease of measurement and the considerable time commitment of formal glucose tolerance testing, which takes two hours to complete and offers no prognostic advantage over the fasting test. According to the current definition, two fasting glucose measurements at or above 7.0 mmol/L (126 mg/dL) is considered diagnostic for diabetes mellitus.
Per the WHO, people with fasting glucose levels from 6.1 to 6.9 mmol/L (110 to 125 mg/dL) are considered to have impaired fasting glucose. People with plasma glucose at or above 7.8 mmol/L (140 mg/dL), but not over 11.1 mmol/L (200 mg/dL), two hours after a 75 gram oral glucose load are considered to have impaired glucose tolerance. Of these two prediabetic states, the latter in particular is a major risk factor for progression to full-blown diabetes mellitus, as well as cardiovascular disease. The American Diabetes Association (ADA) since 2003 uses a slightly different range for impaired fasting glucose of 5.6 to 6.9 mmol/L (100 to 125 mg/dL).Glycated hemoglobin is better than fasting glucose for determining risks of cardiovascular disease and death from any cause.
Prevention
There is no known preventive measure for type 1 diabetes. Type 2 diabetes—which accounts for 85–90% of all cases worldwide—can often be prevented or delayed by maintaining a normal body weight, engaging in physical activity, and eating a healthy diet. Higher levels of physical activity (more than 90 minutes per day) reduce the risk of diabetes by 28%. Dietary changes known to be effective in helping to prevent diabetes include maintaining a diet rich in whole grains and fiber, and choosing good fats, such as the polyunsaturated fats found in nuts, vegetable oils, and fish. Limiting sugary beverages and eating less red meat and other sources of saturated fat can also help prevent diabetes. Tobacco smoking is also associated with an increased risk of diabetes and its complications, so smoking cessation can be an important preventive measure as well.The relationship between type 2 diabetes and the main modifiable risk factors (excess weight, unhealthy diet, physical inactivity and tobacco use) is similar in all regions of the world. There is growing evidence that the underlying determinants of diabetes are a reflection of the major forces driving social, economic and cultural change: globalization, urbanization, population aging, and the general health policy environment.
Management
Diabetes management concentrates on keeping blood sugar levels close to normal, without causing low blood sugar. This can usually be accomplished with dietary changes, exercise, weight loss, and use of appropriate medications (insulin, oral medications).Learning about the disease and actively participating in the treatment is important, since complications are far less common and less severe in people who have well-managed blood sugar levels. The goal of treatment is an A1C level below 5.7%. Attention is also paid to other health problems that may accelerate the negative effects of diabetes. These include smoking, high blood pressure, metabolic syndrome obesity, and lack of regular exercise. Specialized footwear is widely used to reduce the risk of diabetic foot ulcers by relieving the pressure on the foot. Foot examination for patients living with diabetes should be done annually which includes sensation testing, foot biomechanics, vascular integrity and foot structure.Concerning those with severe mental illness, the efficacy of type 2 diabetes self-management interventions is still poorly explored, with insufficient scientific evidence to show whether these interventions have similar results to those observed in the general population.
Lifestyle
People with diabetes can benefit from education about the disease and treatment, dietary changes, and exercise, with the goal of keeping both short-term and long-term blood glucose levels within acceptable bounds. In addition, given the associated higher risks of cardiovascular disease, lifestyle modifications are recommended to control blood pressure.Weight loss can prevent progression from prediabetes to diabetes type 2, decrease the risk of cardiovascular disease, or result in a partial remission in people with diabetes. No single dietary pattern is best for all people with diabetes. Healthy dietary patterns, such as the Mediterranean diet, low-carbohydrate diet, or DASH diet, are often recommended, although evidence does not support one over the others. According to the ADA, "reducing overall carbohydrate intake for individuals with diabetes has demonstrated the most evidence for improving glycemia", and for individuals with type 2 diabetes who cannot meet the glycemic targets or where reducing anti-glycemic medications is a priority, low or very-low carbohydrate diets are a viable approach. For overweight people with type 2 diabetes, any diet that achieves weight loss is effective.A 2020 Cochrane systematic review compared several non-nutritive sweeteners to sugar, placebo and a nutritive low-calorie sweetener (tagatose), but the results were unclear for effects on HbA1c, body weight and adverse events. The studies included were mainly of very low-certainty and did not report on health-related quality of life, diabetes complications, all-cause mortality or socioeconomic effects.
Medications
Glucose control
Most medications used to treat diabetes act by lowering blood sugar levels through different mechanisms. There is broad consensus that when people with diabetes maintain tight glucose control – keeping the glucose levels in their blood within normal ranges – they experience fewer complications, such as kidney problems or eye problems. There is however debate as to whether this is appropriate and cost effective for people later in life in whom the risk of hypoglycemia may be more significant.There are a number of different classes of anti-diabetic medications. Type 1 diabetes requires treatment with insulin, ideally using a "basal bolus" regimen that most closely matches normal insulin release: long-acting insulin for the basal rate and short-acting insulin with meals. Type 2 diabetes is generally treated with medication that is taken by mouth (e.g. metformin) although some eventually require injectable treatment with insulin or GLP-1 agonists.Metformin is generally recommended as a first-line treatment for type 2 diabetes, as there is good evidence that it decreases mortality. It works by decreasing the liver's production of glucose, and increasing the amount of glucose stored in peripheral tissue. Several other groups of drugs, mainly oral medication, may also decrease blood sugar in type 2 diabetes. These include agents that increase insulin release (sulfonylureas), agents that decrease absorption of sugar from the intestines (acarbose), agents that inhibit the enzyme dipeptidyl peptidase-4 (DPP-4) that inactivates incretins such as GLP-1 and GIP (sitagliptin), agents that make the body more sensitive to insulin (thiazolidinedione) and agents that increase the excretion of glucose in the urine (SGLT2 inhibitors). When insulin is used in type 2 diabetes, a long-acting formulation is usually added initially, while continuing oral medications.Some severe cases of type 2 diabetes may also be treated with insulin, which is increased gradually until glucose targets are reached.
Blood pressure lowering
Cardiovascular disease is a serious complication associated with diabetes, and many international guidelines recommend blood pressure treatment targets that are lower than 140/90 mmHg for people with diabetes. However, there is only limited evidence regarding what the lower targets should be. A 2016 systematic review found potential harm to treating to targets lower than 140 mmHg, and a subsequent systematic review in 2019 found no evidence of additional benefit from blood pressure lowering to between 130 – 140mmHg, although there was an increased risk of adverse events.2015 American Diabetes Association recommendations are that people with diabetes and albuminuria should receive an inhibitor of the renin-angiotensin system to reduce the risks of progression to end-stage renal disease, cardiovascular events, and death. There is some evidence that angiotensin converting enzyme inhibitors (ACEIs) are superior to other inhibitors of the renin-angiotensin system such as angiotensin receptor blockers (ARBs), or aliskiren in preventing cardiovascular disease. Although a more recent review found similar effects of ACEIs and ARBs on major cardiovascular and renal outcomes. There is no evidence that combining ACEIs and ARBs provides additional benefits.
Aspirin
The use of aspirin to prevent cardiovascular disease in diabetes is controversial. Aspirin is recommended by some in people at high risk of cardiovascular disease, however routine use of aspirin has not been found to improve outcomes in uncomplicated diabetes. 2015 American Diabetes Association recommendations for aspirin use (based on expert consensus or clinical experience) are that low-dose aspirin use is reasonable in adults with diabetes who are at intermediate risk of cardiovascular disease (10-year cardiovascular disease risk, 5–10%). National guidelines for England and Wales by the National Institute for Health and Care Excellence (NICE) recommend against the use of aspirin in people with type 1 or type 2 diabetes who do not have confirmed cardiovascular disease.
Surgery
Weight loss surgery in those with obesity and type 2 diabetes is often an effective measure. Many are able to maintain normal blood sugar levels with little or no medications following surgery and long-term mortality is decreased. There is, however, a short-term mortality risk of less than 1% from the surgery. The body mass index cutoffs for when surgery is appropriate are not yet clear. It is recommended that this option be considered in those who are unable to get both their weight and blood sugar under control.A pancreas transplant is occasionally considered for people with type 1 diabetes who have severe complications of their disease, including end stage kidney disease requiring kidney transplantation.
Self-management and support
In countries using a general practitioner system, such as the United Kingdom, care may take place mainly outside hospitals, with hospital-based specialist care used only in case of complications, difficult blood sugar control, or research projects. In other circumstances, general practitioners and specialists share care in a team approach. Home telehealth support can be an effective management technique.The use of technology to deliver educational programs for adults with type 2 diabetes includes computer-based self-management interventions to collect for tailored responses to facilitate self-management. There is no adequate evidence to support effects on cholesterol, blood pressure, behavioral change (such as physical activity levels and dietary), depression, weight and health-related quality of life, nor in other biological, cognitive or emotional outcomes.
Epidemiology
In 2017, 425 million people had diabetes worldwide, up from an estimated 382 million people in 2013 and from 108 million in 1980. Accounting for the shifting age structure of the global population, the prevalence of diabetes is 8.8% among adults, nearly double the rate of 4.7% in 1980. Type 2 makes up about 90% of the cases. Some data indicate rates are roughly equal in women and men, but male excess in diabetes has been found in many populations with higher type 2 incidence, possibly due to sex-related differences in insulin sensitivity, consequences of obesity and regional body fat deposition, and other contributing factors such as high blood pressure, tobacco smoking, and alcohol intake.The WHO estimates that diabetes resulted in 1.5 million deaths in 2012, making it the 8th leading cause of death. However another 2.2 million deaths worldwide were attributable to high blood glucose and the increased risks of cardiovascular disease and other associated complications (e.g. kidney failure), which often lead to premature death and are often listed as the underlying cause on death certificates rather than diabetes. For example, in 2017, the International Diabetes Federation (IDF) estimated that diabetes resulted in 4.0 million deaths worldwide, using modeling to estimate the total number of deaths that could be directly or indirectly attributed to diabetes.Diabetes occurs throughout the world but is more common (especially type 2) in more developed countries. The greatest increase in rates has however been seen in low- and middle-income countries, where more than 80% of diabetic deaths occur. The fastest prevalence increase is expected to occur in Asia and Africa, where most people with diabetes will probably live in 2030. The increase in rates in developing countries follows the trend of urbanization and lifestyle changes, including increasingly sedentary lifestyles, less physically demanding work and the global nutrition transition, marked by increased intake of foods that are high energy-dense but nutrient-poor (often high in sugar and saturated fats, sometimes referred to as the "Western-style" diet). The global number of diabetes cases might increase by 48% between 2017 and 2045.As of 2020, 38% of all US adults had prediabetes. Prediabetes is an early stage of diabetes.
History
Diabetes was one of the first diseases described, with an Egyptian manuscript from c. 1500 BCE mentioning "too great emptying of the urine." The Ebers papyrus includes a recommendation for a drink to take in such cases. The first described cases are believed to have been type 1 diabetes. Indian physicians around the same time identified the disease and classified it as madhumeha or "honey urine", noting the urine would attract ants.The term "diabetes" or "to pass through" was first used in 230 BCE by the Greek Apollonius of Memphis. The disease was considered rare during the time of the Roman empire, with Galen commenting he had only seen two cases during his career. This is possibly due to the diet and lifestyle of the ancients, or because the clinical symptoms were observed during the advanced stage of the disease. Galen named the disease "diarrhea of the urine" (diarrhea urinosa).The earliest surviving work with a detailed reference to diabetes is that of Aretaeus of Cappadocia (2nd or early 3rd century CE). He described the symptoms and the course of the disease, which he attributed to the moisture and coldness, reflecting the beliefs of the "Pneumatic School". He hypothesized a correlation between diabetes and other diseases, and he discussed differential diagnosis from the snakebite, which also provokes excessive thirst. His work remained unknown in the West until 1552, when the first Latin edition was published in Venice.Two types of diabetes were identified as separate conditions for the first time by the Indian physicians Sushruta and Charaka in 400–500 CE with one type being associated with youth and another type with being overweight. Effective treatment was not developed until the early part of the 20th century when Canadians Frederick Banting and Charles Herbert Best isolated and purified insulin in 1921 and 1922. This was followed by the development of the long-acting insulin NPH in the 1940s.
Etymology
The word diabetes ( or ) comes from Latin diabētēs, which in turn comes from Ancient Greek διαβήτης (diabētēs), which literally means "a passer through; a siphon". Ancient Greek physician Aretaeus of Cappadocia (fl. 1st century CE) used that word, with the intended meaning "excessive discharge of urine", as the name for the disease. Ultimately, the word comes from Greek διαβαίνειν (diabainein), meaning "to pass through", which is composed of δια- (dia-), meaning "through" and βαίνειν (bainein), meaning "to go". The word "diabetes" is first recorded in English, in the form diabete, in a medical text written around 1425.
The word mellitus ( or ) comes from the classical Latin word mellītus, meaning "mellite" (i.e. sweetened with honey; honey-sweet). The Latin word comes from mell-, which comes from mel, meaning "honey"; sweetness; pleasant thing, and the suffix -ītus, whose meaning is the same as that of the English suffix "-ite". It was Thomas Willis who in 1675 added "mellitus" to the word "diabetes" as a designation for the disease, when he noticed the urine of a person with diabetes had a sweet taste (glycosuria). This sweet taste had been noticed in urine by the ancient Greeks, Chinese, Egyptians, Indians, and Persians.
Society and culture
The 1989 "St. Vincent Declaration" was the result of international efforts to improve the care accorded to those with diabetes. Doing so is important not only in terms of quality of life and life expectancy but also economically – expenses due to diabetes have been shown to be a major drain on health – and productivity-related resources for healthcare systems and governments.
Several countries established more and less successful national diabetes programmes to improve treatment of the disease.People with diabetes who have neuropathic symptoms such as numbness or tingling in feet or hands are twice as likely to be unemployed as those without the symptoms.In 2010, diabetes-related emergency room (ER) visit rates in the United States were higher among people from the lowest income communities (526 per 10,000 population) than from the highest income communities (236 per 10,000 population). Approximately 9.4% of diabetes-related ER visits were for the uninsured.
Naming
The term "type 1 diabetes" has replaced several former terms, including childhood-onset diabetes, juvenile diabetes, and insulin-dependent diabetes mellitus. Likewise, the term "type 2 diabetes" has replaced several former terms, including adult-onset diabetes, obesity-related diabetes, and noninsulin-dependent diabetes mellitus. Beyond these two types, there is no agreed-upon standard nomenclature.Diabetes mellitus is also occasionally known as "sugar diabetes" to differentiate it from diabetes insipidus.
Other animals
Diabetes can occur in mammals or reptiles. Birds do not develop diabetes because of their unusually high tolerance for elevated blood glucose levels.In animals, diabetes is most commonly encountered in dogs and cats. Middle-aged animals are most commonly affected. Female dogs are twice as likely to be affected as males, while according to some sources, male cats are more prone than females. In both species, all breeds may be affected, but some small dog breeds are particularly likely to develop diabetes, such as Miniature Poodles.Feline diabetes is strikingly similar to human type 2 diabetes. The Burmese, Russian Blue, Abyssinian, and Norwegian Forest cat breeds are at higher risk than other breeds. Overweight cats are also at higher risk.The symptoms may relate to fluid loss and polyuria, but the course may also be insidious. Diabetic animals are more prone to infections. The long-term complications recognized in humans are much rarer in animals. The principles of treatment (weight loss, oral antidiabetics, subcutaneous insulin) and management of emergencies (e.g. ketoacidosis) are similar to those in humans.
References
External links
American Diabetes Association
IDF Diabetes Atlas
National Diabetes Education Program
ADA's Standards of Medical Care in Diabetes 2019
Polonsky KS (October 2012). "The past 200 years in diabetes". The New England Journal of Medicine. 367 (14): 1332–1340. doi:10.1056/NEJMra1110560. PMID 23034021. S2CID 9456681.
"Diabetes". MedlinePlus. U.S. National Library of Medicine.
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Diabetes, also known as diabetes mellitus, is a group of common endocrine diseases characterized by sustained high blood sugar levels. Diabetes is due to either the pancreas not producing enough insulin, or the cells of the body not responding properly to the insulin produced. Diabetes, if left untreated, leads to many health complications. Untreated or poorly treated diabetes accounts for approximately 1.5 million deaths per year.There is no widely accepted cure for most cases of diabetes. The most common treatment for type 1 diabetes is insulin replacement therapy (insulin injections). Anti-diabetic medications such as metformin and semaglutide, as well as lifestyle modifications, can be used to prevent or respond to type 2 diabetes. Gestational diabetes normally resolves shortly after delivery.
As of 2019, an estimated 463 million people had diabetes worldwide accounting for 8.8% of the adult population. Type 2 diabetes makes up about 90% of all diabetes cases. The prevalence of the disease continues to increase, most dramatically in low- and middle-income nations. Rates are similar in women and men, with diabetes being the 7th-leading cause of death globally. The global expenditure on diabetes-related healthcare is an estimated USD760 billion a year.
Signs and symptoms
The classic symptoms of untreated diabetes are unintended weight loss, polyuria (increased urination), polydipsia (increased thirst), and polyphagia (increased hunger). Symptoms may develop rapidly (weeks or months) in type 1 diabetes, while they usually develop much more slowly and may be subtle or absent in type 2 diabetes.Several other signs and symptoms can mark the onset of diabetes although they are not specific to the disease. In addition to the known symptoms listed above, they include blurred vision, headache, fatigue, slow healing of cuts, and itchy skin. Prolonged high blood glucose can cause glucose absorption in the lens of the eye, which leads to changes in its shape, resulting in vision changes. Long-term vision loss can also be caused by diabetic retinopathy. A number of skin rashes that can occur in diabetes are collectively known as diabetic dermadromes.
Diabetic emergencies
People with diabetes (usually but not exclusively in type 1 diabetes) may also experience diabetic ketoacidosis (DKA), a metabolic disturbance characterized by nausea, vomiting and abdominal pain, the smell of acetone on the breath, deep breathing known as Kussmaul breathing, and in severe cases a decreased level of consciousness. DKA requires emergency treatment in hospital. A rarer but more dangerous condition is hyperosmolar hyperglycemic state (HHS), which is more common in type 2 diabetes and is mainly the result of dehydration caused by high blood sugars.Treatment-related low blood sugar (hypoglycemia) is common in people with type 1 and also type 2 diabetes depending on the medication being used. Most cases are mild and are not considered medical emergencies. Effects can range from feelings of unease, sweating, trembling, and increased appetite in mild cases to more serious effects such as confusion, changes in behavior such as aggressiveness, seizures, unconsciousness, and rarely permanent brain damage or death in severe cases. Rapid breathing, sweating, and cold, pale skin are characteristic of low blood sugar but not definitive. Mild to moderate cases are self-treated by eating or drinking something high in rapidly absorbed carbohydrates. Severe cases can lead to unconsciousness and must be treated with intravenous glucose or injections with glucagon.
Complications
All forms of diabetes increase the risk of long-term complications. These typically develop after many years (10–20) but may be the first symptom in those who have otherwise not received a diagnosis before that time.The major long-term complications relate to damage to blood vessels. Diabetes doubles the risk of cardiovascular disease and about 75% of deaths in people with diabetes are due to coronary artery disease. Other macrovascular diseases include stroke, and peripheral artery disease. These complications are also a strong risk factor for severe COVID-19 illness.The primary complications of diabetes due to damage in small blood vessels include damage to the eyes, kidneys, and nerves. Damage to the eyes, known as diabetic retinopathy, is caused by damage to the blood vessels in the retina of the eye, and can result in gradual vision loss and eventual blindness. Diabetes also increases the risk of having glaucoma, cataracts, and other eye problems. It is recommended that people with diabetes visit an optometrist or ophthalmologist once a year. Damage to the kidneys, known as diabetic nephropathy, can lead to tissue scarring, urine protein loss, and eventually chronic kidney disease, sometimes requiring dialysis or kidney transplantation. Damage to the nerves of the body, known as diabetic neuropathy, is the most common complication of diabetes. The symptoms can include numbness, tingling, sudomotor dysfunction, pain, and altered pain sensation, which can lead to damage to the skin. Diabetes-related foot problems (such as diabetic foot ulcers) may occur, and can be difficult to treat, occasionally requiring amputation. Additionally, proximal diabetic neuropathy causes painful muscle atrophy and weakness.
There is a link between cognitive deficit and diabetes. Compared to those without diabetes, those with the disease have a 1.2 to 1.5-fold greater rate of decline in cognitive function. Having diabetes, especially when on insulin, increases the risk of falls in older people.
Causes
Diabetes mellitus is classified into six categories: type 1 diabetes, type 2 diabetes, hybrid forms of diabetes, hyperglycemia first detected during pregnancy, "unclassified diabetes", and "other specific types". "Hybrid forms of diabetes" include slowly evolving, immune-mediated diabetes of adults and ketosis-prone type 2 diabetes. "Hyperglycemia first detected during pregnancy" includes gestational diabetes mellitus and diabetes mellitus in pregnancy (type 1 or type 2 diabetes first diagnosed during pregnancy). The "other specific types" are a collection of a few dozen individual causes. Diabetes is a more variable disease than once thought and people may have combinations of forms.
Type 1
Type 1 diabetes is characterized by loss of the insulin-producing beta cells of the pancreatic islets, leading to insulin deficiency. This type can be further classified as immune-mediated or idiopathic. The majority of type 1 diabetes is of an immune-mediated nature, in which a T cell-mediated autoimmune attack leads to the loss of beta cells and thus insulin. It causes approximately 10% of diabetes mellitus cases in North America and Europe. Most affected people are otherwise healthy and of a healthy weight when onset occurs. Sensitivity and responsiveness to insulin are usually normal, especially in the early stages. Although it has been called "juvenile diabetes" due to the frequent onset in children, the majority of individuals living with type 1 diabetes are now adults."Brittle" diabetes, also known as unstable diabetes or labile diabetes, is a term that was traditionally used to describe the dramatic and recurrent swings in glucose levels, often occurring for no apparent reason in insulin-dependent diabetes. This term, however, has no biologic basis and should not be used. Still, type 1 diabetes can be accompanied by irregular and unpredictable high blood sugar levels, and the potential for diabetic ketoacidosis or serious low blood sugar levels. Other complications include an impaired counterregulatory response to low blood sugar, infection, gastroparesis (which leads to erratic absorption of dietary carbohydrates), and endocrinopathies (e.g., Addison's disease). These phenomena are believed to occur no more frequently than in 1% to 2% of persons with type 1 diabetes.
Type 1 diabetes is partly inherited, with multiple genes, including certain HLA genotypes, known to influence the risk of diabetes. In genetically susceptible people, the onset of diabetes can be triggered by one or more environmental factors, such as a viral infection or diet. Several viruses have been implicated, but to date there is no stringent evidence to support this hypothesis in humans.Type 1 diabetes can occur at any age, and a significant proportion is diagnosed during adulthood. Latent autoimmune diabetes of adults (LADA) is the diagnostic term applied when type 1 diabetes develops in adults; it has a slower onset than the same condition in children. Given this difference, some use the unofficial term "type 1.5 diabetes" for this condition. Adults with LADA are frequently initially misdiagnosed as having type 2 diabetes, based on age rather than a cause.
Type 2
Type 2 diabetes is characterized by insulin resistance, which may be combined with relatively reduced insulin secretion. The defective responsiveness of body tissues to insulin is believed to involve the insulin receptor. However, the specific defects are not known. Diabetes mellitus cases due to a known defect are classified separately. Type 2 diabetes is the most common type of diabetes mellitus accounting for 95% of diabetes. Many people with type 2 diabetes have evidence of prediabetes (impaired fasting glucose and/or impaired glucose tolerance) before meeting the criteria for type 2 diabetes. The progression of prediabetes to overt type 2 diabetes can be slowed or reversed by lifestyle changes or medications that improve insulin sensitivity or reduce the liver's glucose production.Type 2 diabetes is primarily due to lifestyle factors and genetics. A number of lifestyle factors are known to be important to the development of type 2 diabetes, including obesity (defined by a body mass index of greater than 30), lack of physical activity, poor diet, stress, and urbanization. Excess body fat is associated with 30% of cases in people of Chinese and Japanese descent, 60–80% of cases in those of European and African descent, and 100% of Pima Indians and Pacific Islanders. Even those who are not obese may have a high waist–hip ratio.Dietary factors such as sugar-sweetened drinks are associated with an increased risk. The type of fats in the diet is also important, with saturated fat and trans fats increasing the risk and polyunsaturated and monounsaturated fat decreasing the risk. Eating white rice excessively may increase the risk of diabetes, especially in Chinese and Japanese people. Lack of physical activity may increase the risk of diabetes in some people.Adverse childhood experiences, including abuse, neglect, and household difficulties, increase the likelihood of type 2 diabetes later in life by 32%, with neglect having the strongest effect.Antipsychotic medication side effects (specifically metabolic abnormalities, dyslipidemia and weight gain) and unhealthy lifestyles (including poor diet and decreased physical activity), are potential risk factors.
Gestational diabetes
Gestational diabetes resembles type 2 diabetes in several respects, involving a combination of relatively inadequate insulin secretion and responsiveness. It occurs in about 2–10% of all pregnancies and may improve or disappear after delivery. It is recommended that all pregnant women get tested starting around 24–28 weeks gestation. It is most often diagnosed in the second or third trimester because of the increase in insulin-antagonist hormone levels that occurs at this time. However, after pregnancy approximately 5–10% of women with gestational diabetes are found to have another form of diabetes, most commonly type 2. Gestational diabetes is fully treatable, but requires careful medical supervision throughout the pregnancy. Management may include dietary changes, blood glucose monitoring, and in some cases, insulin may be required.Though it may be transient, untreated gestational diabetes can damage the health of the fetus or mother. Risks to the baby include macrosomia (high birth weight), congenital heart and central nervous system abnormalities, and skeletal muscle malformations. Increased levels of insulin in a fetus's blood may inhibit fetal surfactant production and cause infant respiratory distress syndrome. A high blood bilirubin level may result from red blood cell destruction. In severe cases, perinatal death may occur, most commonly as a result of poor placental perfusion due to vascular impairment. Labor induction may be indicated with decreased placental function. A caesarean section may be performed if there is marked fetal distress or an increased risk of injury associated with macrosomia, such as shoulder dystocia.
Other types
Maturity onset diabetes of the young (MODY) is a rare autosomal dominant inherited form of diabetes, due to one of several single-gene mutations causing defects in insulin production. It is significantly less common than the three main types, constituting 1–2% of all cases. The name of this disease refers to early hypotheses as to its nature. Being due to a defective gene, this disease varies in age at presentation and in severity according to the specific gene defect; thus, there are at least 13 subtypes of MODY. People with MODY often can control it without using insulin.Some cases of diabetes are caused by the body's tissue receptors not responding to insulin (even when insulin levels are normal, which is what separates it from type 2 diabetes); this form is very uncommon. Genetic mutations (autosomal or mitochondrial) can lead to defects in beta cell function. Abnormal insulin action may also have been genetically determined in some cases. Any disease that causes extensive damage to the pancreas may lead to diabetes (for example, chronic pancreatitis and cystic fibrosis). Diseases associated with excessive secretion of insulin-antagonistic hormones can cause diabetes (which is typically resolved once the hormone excess is removed). Many drugs impair insulin secretion and some toxins damage pancreatic beta cells, whereas others increase insulin resistance (especially glucocorticoids which can provoke "steroid diabetes"). The ICD-10 (1992) diagnostic entity, malnutrition-related diabetes mellitus (ICD-10 code E12), was deprecated by the World Health Organization (WHO) when the current taxonomy was introduced in 1999.
Yet another form of diabetes that people may develop is double diabetes. This is when a type 1 diabetic becomes insulin resistant, the hallmark for type 2 diabetes or has a family history for type 2 diabetes. It was first discovered in 1990 or 1991.
The following is a list of disorders that may increase the risk of diabetes:
Pathophysiology
Insulin is the principal hormone that regulates the uptake of glucose from the blood into most cells of the body, especially liver, adipose tissue and muscle, except smooth muscle, in which insulin acts via the IGF-1. Therefore, deficiency of insulin or the insensitivity of its receptors play a central role in all forms of diabetes mellitus.The body obtains glucose from three main sources: the intestinal absorption of food; the breakdown of glycogen (glycogenolysis), the storage form of glucose found in the liver; and gluconeogenesis, the generation of glucose from non-carbohydrate substrates in the body. Insulin plays a critical role in regulating glucose levels in the body. Insulin can inhibit the breakdown of glycogen or the process of gluconeogenesis, it can stimulate the transport of glucose into fat and muscle cells, and it can stimulate the storage of glucose in the form of glycogen.Insulin is released into the blood by beta cells (β-cells), found in the islets of Langerhans in the pancreas, in response to rising levels of blood glucose, typically after eating. Insulin is used by about two-thirds of the body's cells to absorb glucose from the blood for use as fuel, for conversion to other needed molecules, or for storage. Lower glucose levels result in decreased insulin release from the beta cells and in the breakdown of glycogen to glucose. This process is mainly controlled by the hormone glucagon, which acts in the opposite manner to insulin.If the amount of insulin available is insufficient, or if cells respond poorly to the effects of insulin (insulin resistance), or if the insulin itself is defective, then glucose is not absorbed properly by the body cells that require it, and is not stored appropriately in the liver and muscles. The net effect is persistently high levels of blood glucose, poor protein synthesis, and other metabolic derangements, such as metabolic acidosis in cases of complete insulin deficiency.When glucose concentration in the blood remains high over time, the kidneys reach a threshold of reabsorption, and the body excretes glucose in the urine (glycosuria). This increases the osmotic pressure of the urine and inhibits reabsorption of water by the kidney, resulting in increased urine production (polyuria) and increased fluid loss. Lost blood volume is replaced osmotically from water in body cells and other body compartments, causing dehydration and increased thirst (polydipsia). In addition, intracellular glucose deficiency stimulates appetite leading to excessive food intake (polyphagia).
Diagnosis
Diabetes mellitus is diagnosed with a test for the glucose content in the blood, and is diagnosed by demonstrating any one of the following:
Fasting plasma glucose level ≥ 7.0 mmol/L (126 mg/dL). For this test, blood is taken after a period of fasting, i.e. in the morning before breakfast, after the patient had sufficient time to fast overnight.
Plasma glucose ≥ 11.1 mmol/L (200 mg/dL) two hours after a 75 gram oral glucose load as in a glucose tolerance test (OGTT)
Symptoms of high blood sugar and plasma glucose ≥ 11.1 mmol/L (200 mg/dL) either while fasting or not fasting
Glycated hemoglobin (HbA1C) ≥ 48 mmol/mol (≥ 6.5 DCCT %).A positive result, in the absence of unequivocal high blood sugar, should be confirmed by a repeat of any of the above methods on a different day. It is preferable to measure a fasting glucose level because of the ease of measurement and the considerable time commitment of formal glucose tolerance testing, which takes two hours to complete and offers no prognostic advantage over the fasting test. According to the current definition, two fasting glucose measurements at or above 7.0 mmol/L (126 mg/dL) is considered diagnostic for diabetes mellitus.
Per the WHO, people with fasting glucose levels from 6.1 to 6.9 mmol/L (110 to 125 mg/dL) are considered to have impaired fasting glucose. People with plasma glucose at or above 7.8 mmol/L (140 mg/dL), but not over 11.1 mmol/L (200 mg/dL), two hours after a 75 gram oral glucose load are considered to have impaired glucose tolerance. Of these two prediabetic states, the latter in particular is a major risk factor for progression to full-blown diabetes mellitus, as well as cardiovascular disease. The American Diabetes Association (ADA) since 2003 uses a slightly different range for impaired fasting glucose of 5.6 to 6.9 mmol/L (100 to 125 mg/dL).Glycated hemoglobin is better than fasting glucose for determining risks of cardiovascular disease and death from any cause.
Prevention
There is no known preventive measure for type 1 diabetes. Type 2 diabetes—which accounts for 85–90% of all cases worldwide—can often be prevented or delayed by maintaining a normal body weight, engaging in physical activity, and eating a healthy diet. Higher levels of physical activity (more than 90 minutes per day) reduce the risk of diabetes by 28%. Dietary changes known to be effective in helping to prevent diabetes include maintaining a diet rich in whole grains and fiber, and choosing good fats, such as the polyunsaturated fats found in nuts, vegetable oils, and fish. Limiting sugary beverages and eating less red meat and other sources of saturated fat can also help prevent diabetes. Tobacco smoking is also associated with an increased risk of diabetes and its complications, so smoking cessation can be an important preventive measure as well.The relationship between type 2 diabetes and the main modifiable risk factors (excess weight, unhealthy diet, physical inactivity and tobacco use) is similar in all regions of the world. There is growing evidence that the underlying determinants of diabetes are a reflection of the major forces driving social, economic and cultural change: globalization, urbanization, population aging, and the general health policy environment.
Management
Diabetes management concentrates on keeping blood sugar levels close to normal, without causing low blood sugar. This can usually be accomplished with dietary changes, exercise, weight loss, and use of appropriate medications (insulin, oral medications).Learning about the disease and actively participating in the treatment is important, since complications are far less common and less severe in people who have well-managed blood sugar levels. The goal of treatment is an A1C level below 5.7%. Attention is also paid to other health problems that may accelerate the negative effects of diabetes. These include smoking, high blood pressure, metabolic syndrome obesity, and lack of regular exercise. Specialized footwear is widely used to reduce the risk of diabetic foot ulcers by relieving the pressure on the foot. Foot examination for patients living with diabetes should be done annually which includes sensation testing, foot biomechanics, vascular integrity and foot structure.Concerning those with severe mental illness, the efficacy of type 2 diabetes self-management interventions is still poorly explored, with insufficient scientific evidence to show whether these interventions have similar results to those observed in the general population.
Lifestyle
People with diabetes can benefit from education about the disease and treatment, dietary changes, and exercise, with the goal of keeping both short-term and long-term blood glucose levels within acceptable bounds. In addition, given the associated higher risks of cardiovascular disease, lifestyle modifications are recommended to control blood pressure.Weight loss can prevent progression from prediabetes to diabetes type 2, decrease the risk of cardiovascular disease, or result in a partial remission in people with diabetes. No single dietary pattern is best for all people with diabetes. Healthy dietary patterns, such as the Mediterranean diet, low-carbohydrate diet, or DASH diet, are often recommended, although evidence does not support one over the others. According to the ADA, "reducing overall carbohydrate intake for individuals with diabetes has demonstrated the most evidence for improving glycemia", and for individuals with type 2 diabetes who cannot meet the glycemic targets or where reducing anti-glycemic medications is a priority, low or very-low carbohydrate diets are a viable approach. For overweight people with type 2 diabetes, any diet that achieves weight loss is effective.A 2020 Cochrane systematic review compared several non-nutritive sweeteners to sugar, placebo and a nutritive low-calorie sweetener (tagatose), but the results were unclear for effects on HbA1c, body weight and adverse events. The studies included were mainly of very low-certainty and did not report on health-related quality of life, diabetes complications, all-cause mortality or socioeconomic effects.
Medications
Glucose control
Most medications used to treat diabetes act by lowering blood sugar levels through different mechanisms. There is broad consensus that when people with diabetes maintain tight glucose control – keeping the glucose levels in their blood within normal ranges – they experience fewer complications, such as kidney problems or eye problems. There is however debate as to whether this is appropriate and cost effective for people later in life in whom the risk of hypoglycemia may be more significant.There are a number of different classes of anti-diabetic medications. Type 1 diabetes requires treatment with insulin, ideally using a "basal bolus" regimen that most closely matches normal insulin release: long-acting insulin for the basal rate and short-acting insulin with meals. Type 2 diabetes is generally treated with medication that is taken by mouth (e.g. metformin) although some eventually require injectable treatment with insulin or GLP-1 agonists.Metformin is generally recommended as a first-line treatment for type 2 diabetes, as there is good evidence that it decreases mortality. It works by decreasing the liver's production of glucose, and increasing the amount of glucose stored in peripheral tissue. Several other groups of drugs, mainly oral medication, may also decrease blood sugar in type 2 diabetes. These include agents that increase insulin release (sulfonylureas), agents that decrease absorption of sugar from the intestines (acarbose), agents that inhibit the enzyme dipeptidyl peptidase-4 (DPP-4) that inactivates incretins such as GLP-1 and GIP (sitagliptin), agents that make the body more sensitive to insulin (thiazolidinedione) and agents that increase the excretion of glucose in the urine (SGLT2 inhibitors). When insulin is used in type 2 diabetes, a long-acting formulation is usually added initially, while continuing oral medications.Some severe cases of type 2 diabetes may also be treated with insulin, which is increased gradually until glucose targets are reached.
Blood pressure lowering
Cardiovascular disease is a serious complication associated with diabetes, and many international guidelines recommend blood pressure treatment targets that are lower than 140/90 mmHg for people with diabetes. However, there is only limited evidence regarding what the lower targets should be. A 2016 systematic review found potential harm to treating to targets lower than 140 mmHg, and a subsequent systematic review in 2019 found no evidence of additional benefit from blood pressure lowering to between 130 – 140mmHg, although there was an increased risk of adverse events.2015 American Diabetes Association recommendations are that people with diabetes and albuminuria should receive an inhibitor of the renin-angiotensin system to reduce the risks of progression to end-stage renal disease, cardiovascular events, and death. There is some evidence that angiotensin converting enzyme inhibitors (ACEIs) are superior to other inhibitors of the renin-angiotensin system such as angiotensin receptor blockers (ARBs), or aliskiren in preventing cardiovascular disease. Although a more recent review found similar effects of ACEIs and ARBs on major cardiovascular and renal outcomes. There is no evidence that combining ACEIs and ARBs provides additional benefits.
Aspirin
The use of aspirin to prevent cardiovascular disease in diabetes is controversial. Aspirin is recommended by some in people at high risk of cardiovascular disease, however routine use of aspirin has not been found to improve outcomes in uncomplicated diabetes. 2015 American Diabetes Association recommendations for aspirin use (based on expert consensus or clinical experience) are that low-dose aspirin use is reasonable in adults with diabetes who are at intermediate risk of cardiovascular disease (10-year cardiovascular disease risk, 5–10%). National guidelines for England and Wales by the National Institute for Health and Care Excellence (NICE) recommend against the use of aspirin in people with type 1 or type 2 diabetes who do not have confirmed cardiovascular disease.
Surgery
Weight loss surgery in those with obesity and type 2 diabetes is often an effective measure. Many are able to maintain normal blood sugar levels with little or no medications following surgery and long-term mortality is decreased. There is, however, a short-term mortality risk of less than 1% from the surgery. The body mass index cutoffs for when surgery is appropriate are not yet clear. It is recommended that this option be considered in those who are unable to get both their weight and blood sugar under control.A pancreas transplant is occasionally considered for people with type 1 diabetes who have severe complications of their disease, including end stage kidney disease requiring kidney transplantation.
Self-management and support
In countries using a general practitioner system, such as the United Kingdom, care may take place mainly outside hospitals, with hospital-based specialist care used only in case of complications, difficult blood sugar control, or research projects. In other circumstances, general practitioners and specialists share care in a team approach. Home telehealth support can be an effective management technique.The use of technology to deliver educational programs for adults with type 2 diabetes includes computer-based self-management interventions to collect for tailored responses to facilitate self-management. There is no adequate evidence to support effects on cholesterol, blood pressure, behavioral change (such as physical activity levels and dietary), depression, weight and health-related quality of life, nor in other biological, cognitive or emotional outcomes.
Epidemiology
In 2017, 425 million people had diabetes worldwide, up from an estimated 382 million people in 2013 and from 108 million in 1980. Accounting for the shifting age structure of the global population, the prevalence of diabetes is 8.8% among adults, nearly double the rate of 4.7% in 1980. Type 2 makes up about 90% of the cases. Some data indicate rates are roughly equal in women and men, but male excess in diabetes has been found in many populations with higher type 2 incidence, possibly due to sex-related differences in insulin sensitivity, consequences of obesity and regional body fat deposition, and other contributing factors such as high blood pressure, tobacco smoking, and alcohol intake.The WHO estimates that diabetes resulted in 1.5 million deaths in 2012, making it the 8th leading cause of death. However another 2.2 million deaths worldwide were attributable to high blood glucose and the increased risks of cardiovascular disease and other associated complications (e.g. kidney failure), which often lead to premature death and are often listed as the underlying cause on death certificates rather than diabetes. For example, in 2017, the International Diabetes Federation (IDF) estimated that diabetes resulted in 4.0 million deaths worldwide, using modeling to estimate the total number of deaths that could be directly or indirectly attributed to diabetes.Diabetes occurs throughout the world but is more common (especially type 2) in more developed countries. The greatest increase in rates has however been seen in low- and middle-income countries, where more than 80% of diabetic deaths occur. The fastest prevalence increase is expected to occur in Asia and Africa, where most people with diabetes will probably live in 2030. The increase in rates in developing countries follows the trend of urbanization and lifestyle changes, including increasingly sedentary lifestyles, less physically demanding work and the global nutrition transition, marked by increased intake of foods that are high energy-dense but nutrient-poor (often high in sugar and saturated fats, sometimes referred to as the "Western-style" diet). The global number of diabetes cases might increase by 48% between 2017 and 2045.As of 2020, 38% of all US adults had prediabetes. Prediabetes is an early stage of diabetes.
History
Diabetes was one of the first diseases described, with an Egyptian manuscript from c. 1500 BCE mentioning "too great emptying of the urine." The Ebers papyrus includes a recommendation for a drink to take in such cases. The first described cases are believed to have been type 1 diabetes. Indian physicians around the same time identified the disease and classified it as madhumeha or "honey urine", noting the urine would attract ants.The term "diabetes" or "to pass through" was first used in 230 BCE by the Greek Apollonius of Memphis. The disease was considered rare during the time of the Roman empire, with Galen commenting he had only seen two cases during his career. This is possibly due to the diet and lifestyle of the ancients, or because the clinical symptoms were observed during the advanced stage of the disease. Galen named the disease "diarrhea of the urine" (diarrhea urinosa).The earliest surviving work with a detailed reference to diabetes is that of Aretaeus of Cappadocia (2nd or early 3rd century CE). He described the symptoms and the course of the disease, which he attributed to the moisture and coldness, reflecting the beliefs of the "Pneumatic School". He hypothesized a correlation between diabetes and other diseases, and he discussed differential diagnosis from the snakebite, which also provokes excessive thirst. His work remained unknown in the West until 1552, when the first Latin edition was published in Venice.Two types of diabetes were identified as separate conditions for the first time by the Indian physicians Sushruta and Charaka in 400–500 CE with one type being associated with youth and another type with being overweight. Effective treatment was not developed until the early part of the 20th century when Canadians Frederick Banting and Charles Herbert Best isolated and purified insulin in 1921 and 1922. This was followed by the development of the long-acting insulin NPH in the 1940s.
Etymology
The word diabetes ( or ) comes from Latin diabētēs, which in turn comes from Ancient Greek διαβήτης (diabētēs), which literally means "a passer through; a siphon". Ancient Greek physician Aretaeus of Cappadocia (fl. 1st century CE) used that word, with the intended meaning "excessive discharge of urine", as the name for the disease. Ultimately, the word comes from Greek διαβαίνειν (diabainein), meaning "to pass through", which is composed of δια- (dia-), meaning "through" and βαίνειν (bainein), meaning "to go". The word "diabetes" is first recorded in English, in the form diabete, in a medical text written around 1425.
The word mellitus ( or ) comes from the classical Latin word mellītus, meaning "mellite" (i.e. sweetened with honey; honey-sweet). The Latin word comes from mell-, which comes from mel, meaning "honey"; sweetness; pleasant thing, and the suffix -ītus, whose meaning is the same as that of the English suffix "-ite". It was Thomas Willis who in 1675 added "mellitus" to the word "diabetes" as a designation for the disease, when he noticed the urine of a person with diabetes had a sweet taste (glycosuria). This sweet taste had been noticed in urine by the ancient Greeks, Chinese, Egyptians, Indians, and Persians.
Society and culture
The 1989 "St. Vincent Declaration" was the result of international efforts to improve the care accorded to those with diabetes. Doing so is important not only in terms of quality of life and life expectancy but also economically – expenses due to diabetes have been shown to be a major drain on health – and productivity-related resources for healthcare systems and governments.
Several countries established more and less successful national diabetes programmes to improve treatment of the disease.People with diabetes who have neuropathic symptoms such as numbness or tingling in feet or hands are twice as likely to be unemployed as those without the symptoms.In 2010, diabetes-related emergency room (ER) visit rates in the United States were higher among people from the lowest income communities (526 per 10,000 population) than from the highest income communities (236 per 10,000 population). Approximately 9.4% of diabetes-related ER visits were for the uninsured.
Naming
The term "type 1 diabetes" has replaced several former terms, including childhood-onset diabetes, juvenile diabetes, and insulin-dependent diabetes mellitus. Likewise, the term "type 2 diabetes" has replaced several former terms, including adult-onset diabetes, obesity-related diabetes, and noninsulin-dependent diabetes mellitus. Beyond these two types, there is no agreed-upon standard nomenclature.Diabetes mellitus is also occasionally known as "sugar diabetes" to differentiate it from diabetes insipidus.
Other animals
Diabetes can occur in mammals or reptiles. Birds do not develop diabetes because of their unusually high tolerance for elevated blood glucose levels.In animals, diabetes is most commonly encountered in dogs and cats. Middle-aged animals are most commonly affected. Female dogs are twice as likely to be affected as males, while according to some sources, male cats are more prone than females. In both species, all breeds may be affected, but some small dog breeds are particularly likely to develop diabetes, such as Miniature Poodles.Feline diabetes is strikingly similar to human type 2 diabetes. The Burmese, Russian Blue, Abyssinian, and Norwegian Forest cat breeds are at higher risk than other breeds. Overweight cats are also at higher risk.The symptoms may relate to fluid loss and polyuria, but the course may also be insidious. Diabetic animals are more prone to infections. The long-term complications recognized in humans are much rarer in animals. The principles of treatment (weight loss, oral antidiabetics, subcutaneous insulin) and management of emergencies (e.g. ketoacidosis) are similar to those in humans.
References
External links
American Diabetes Association
IDF Diabetes Atlas
National Diabetes Education Program
ADA's Standards of Medical Care in Diabetes 2019
Polonsky KS (October 2012). "The past 200 years in diabetes". The New England Journal of Medicine. 367 (14): 1332–1340. doi:10.1056/NEJMra1110560. PMID 23034021. S2CID 9456681.
"Diabetes". MedlinePlus. U.S. National Library of Medicine.
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Diabetes, also known as diabetes mellitus, is a group of common endocrine diseases characterized by sustained high blood sugar levels. Diabetes is due to either the pancreas not producing enough insulin, or the cells of the body not responding properly to the insulin produced. Diabetes, if left untreated, leads to many health complications. Untreated or poorly treated diabetes accounts for approximately 1.5 million deaths per year.There is no widely accepted cure for most cases of diabetes. The most common treatment for type 1 diabetes is insulin replacement therapy (insulin injections). Anti-diabetic medications such as metformin and semaglutide, as well as lifestyle modifications, can be used to prevent or respond to type 2 diabetes. Gestational diabetes normally resolves shortly after delivery.
As of 2019, an estimated 463 million people had diabetes worldwide accounting for 8.8% of the adult population. Type 2 diabetes makes up about 90% of all diabetes cases. The prevalence of the disease continues to increase, most dramatically in low- and middle-income nations. Rates are similar in women and men, with diabetes being the 7th-leading cause of death globally. The global expenditure on diabetes-related healthcare is an estimated USD760 billion a year.
Signs and symptoms
The classic symptoms of untreated diabetes are unintended weight loss, polyuria (increased urination), polydipsia (increased thirst), and polyphagia (increased hunger). Symptoms may develop rapidly (weeks or months) in type 1 diabetes, while they usually develop much more slowly and may be subtle or absent in type 2 diabetes.Several other signs and symptoms can mark the onset of diabetes although they are not specific to the disease. In addition to the known symptoms listed above, they include blurred vision, headache, fatigue, slow healing of cuts, and itchy skin. Prolonged high blood glucose can cause glucose absorption in the lens of the eye, which leads to changes in its shape, resulting in vision changes. Long-term vision loss can also be caused by diabetic retinopathy. A number of skin rashes that can occur in diabetes are collectively known as diabetic dermadromes.
Diabetic emergencies
People with diabetes (usually but not exclusively in type 1 diabetes) may also experience diabetic ketoacidosis (DKA), a metabolic disturbance characterized by nausea, vomiting and abdominal pain, the smell of acetone on the breath, deep breathing known as Kussmaul breathing, and in severe cases a decreased level of consciousness. DKA requires emergency treatment in hospital. A rarer but more dangerous condition is hyperosmolar hyperglycemic state (HHS), which is more common in type 2 diabetes and is mainly the result of dehydration caused by high blood sugars.Treatment-related low blood sugar (hypoglycemia) is common in people with type 1 and also type 2 diabetes depending on the medication being used. Most cases are mild and are not considered medical emergencies. Effects can range from feelings of unease, sweating, trembling, and increased appetite in mild cases to more serious effects such as confusion, changes in behavior such as aggressiveness, seizures, unconsciousness, and rarely permanent brain damage or death in severe cases. Rapid breathing, sweating, and cold, pale skin are characteristic of low blood sugar but not definitive. Mild to moderate cases are self-treated by eating or drinking something high in rapidly absorbed carbohydrates. Severe cases can lead to unconsciousness and must be treated with intravenous glucose or injections with glucagon.
Complications
All forms of diabetes increase the risk of long-term complications. These typically develop after many years (10–20) but may be the first symptom in those who have otherwise not received a diagnosis before that time.The major long-term complications relate to damage to blood vessels. Diabetes doubles the risk of cardiovascular disease and about 75% of deaths in people with diabetes are due to coronary artery disease. Other macrovascular diseases include stroke, and peripheral artery disease. These complications are also a strong risk factor for severe COVID-19 illness.The primary complications of diabetes due to damage in small blood vessels include damage to the eyes, kidneys, and nerves. Damage to the eyes, known as diabetic retinopathy, is caused by damage to the blood vessels in the retina of the eye, and can result in gradual vision loss and eventual blindness. Diabetes also increases the risk of having glaucoma, cataracts, and other eye problems. It is recommended that people with diabetes visit an optometrist or ophthalmologist once a year. Damage to the kidneys, known as diabetic nephropathy, can lead to tissue scarring, urine protein loss, and eventually chronic kidney disease, sometimes requiring dialysis or kidney transplantation. Damage to the nerves of the body, known as diabetic neuropathy, is the most common complication of diabetes. The symptoms can include numbness, tingling, sudomotor dysfunction, pain, and altered pain sensation, which can lead to damage to the skin. Diabetes-related foot problems (such as diabetic foot ulcers) may occur, and can be difficult to treat, occasionally requiring amputation. Additionally, proximal diabetic neuropathy causes painful muscle atrophy and weakness.
There is a link between cognitive deficit and diabetes. Compared to those without diabetes, those with the disease have a 1.2 to 1.5-fold greater rate of decline in cognitive function. Having diabetes, especially when on insulin, increases the risk of falls in older people.
Causes
Diabetes mellitus is classified into six categories: type 1 diabetes, type 2 diabetes, hybrid forms of diabetes, hyperglycemia first detected during pregnancy, "unclassified diabetes", and "other specific types". "Hybrid forms of diabetes" include slowly evolving, immune-mediated diabetes of adults and ketosis-prone type 2 diabetes. "Hyperglycemia first detected during pregnancy" includes gestational diabetes mellitus and diabetes mellitus in pregnancy (type 1 or type 2 diabetes first diagnosed during pregnancy). The "other specific types" are a collection of a few dozen individual causes. Diabetes is a more variable disease than once thought and people may have combinations of forms.
Type 1
Type 1 diabetes is characterized by loss of the insulin-producing beta cells of the pancreatic islets, leading to insulin deficiency. This type can be further classified as immune-mediated or idiopathic. The majority of type 1 diabetes is of an immune-mediated nature, in which a T cell-mediated autoimmune attack leads to the loss of beta cells and thus insulin. It causes approximately 10% of diabetes mellitus cases in North America and Europe. Most affected people are otherwise healthy and of a healthy weight when onset occurs. Sensitivity and responsiveness to insulin are usually normal, especially in the early stages. Although it has been called "juvenile diabetes" due to the frequent onset in children, the majority of individuals living with type 1 diabetes are now adults."Brittle" diabetes, also known as unstable diabetes or labile diabetes, is a term that was traditionally used to describe the dramatic and recurrent swings in glucose levels, often occurring for no apparent reason in insulin-dependent diabetes. This term, however, has no biologic basis and should not be used. Still, type 1 diabetes can be accompanied by irregular and unpredictable high blood sugar levels, and the potential for diabetic ketoacidosis or serious low blood sugar levels. Other complications include an impaired counterregulatory response to low blood sugar, infection, gastroparesis (which leads to erratic absorption of dietary carbohydrates), and endocrinopathies (e.g., Addison's disease). These phenomena are believed to occur no more frequently than in 1% to 2% of persons with type 1 diabetes.
Type 1 diabetes is partly inherited, with multiple genes, including certain HLA genotypes, known to influence the risk of diabetes. In genetically susceptible people, the onset of diabetes can be triggered by one or more environmental factors, such as a viral infection or diet. Several viruses have been implicated, but to date there is no stringent evidence to support this hypothesis in humans.Type 1 diabetes can occur at any age, and a significant proportion is diagnosed during adulthood. Latent autoimmune diabetes of adults (LADA) is the diagnostic term applied when type 1 diabetes develops in adults; it has a slower onset than the same condition in children. Given this difference, some use the unofficial term "type 1.5 diabetes" for this condition. Adults with LADA are frequently initially misdiagnosed as having type 2 diabetes, based on age rather than a cause.
Type 2
Type 2 diabetes is characterized by insulin resistance, which may be combined with relatively reduced insulin secretion. The defective responsiveness of body tissues to insulin is believed to involve the insulin receptor. However, the specific defects are not known. Diabetes mellitus cases due to a known defect are classified separately. Type 2 diabetes is the most common type of diabetes mellitus accounting for 95% of diabetes. Many people with type 2 diabetes have evidence of prediabetes (impaired fasting glucose and/or impaired glucose tolerance) before meeting the criteria for type 2 diabetes. The progression of prediabetes to overt type 2 diabetes can be slowed or reversed by lifestyle changes or medications that improve insulin sensitivity or reduce the liver's glucose production.Type 2 diabetes is primarily due to lifestyle factors and genetics. A number of lifestyle factors are known to be important to the development of type 2 diabetes, including obesity (defined by a body mass index of greater than 30), lack of physical activity, poor diet, stress, and urbanization. Excess body fat is associated with 30% of cases in people of Chinese and Japanese descent, 60–80% of cases in those of European and African descent, and 100% of Pima Indians and Pacific Islanders. Even those who are not obese may have a high waist–hip ratio.Dietary factors such as sugar-sweetened drinks are associated with an increased risk. The type of fats in the diet is also important, with saturated fat and trans fats increasing the risk and polyunsaturated and monounsaturated fat decreasing the risk. Eating white rice excessively may increase the risk of diabetes, especially in Chinese and Japanese people. Lack of physical activity may increase the risk of diabetes in some people.Adverse childhood experiences, including abuse, neglect, and household difficulties, increase the likelihood of type 2 diabetes later in life by 32%, with neglect having the strongest effect.Antipsychotic medication side effects (specifically metabolic abnormalities, dyslipidemia and weight gain) and unhealthy lifestyles (including poor diet and decreased physical activity), are potential risk factors.
Gestational diabetes
Gestational diabetes resembles type 2 diabetes in several respects, involving a combination of relatively inadequate insulin secretion and responsiveness. It occurs in about 2–10% of all pregnancies and may improve or disappear after delivery. It is recommended that all pregnant women get tested starting around 24–28 weeks gestation. It is most often diagnosed in the second or third trimester because of the increase in insulin-antagonist hormone levels that occurs at this time. However, after pregnancy approximately 5–10% of women with gestational diabetes are found to have another form of diabetes, most commonly type 2. Gestational diabetes is fully treatable, but requires careful medical supervision throughout the pregnancy. Management may include dietary changes, blood glucose monitoring, and in some cases, insulin may be required.Though it may be transient, untreated gestational diabetes can damage the health of the fetus or mother. Risks to the baby include macrosomia (high birth weight), congenital heart and central nervous system abnormalities, and skeletal muscle malformations. Increased levels of insulin in a fetus's blood may inhibit fetal surfactant production and cause infant respiratory distress syndrome. A high blood bilirubin level may result from red blood cell destruction. In severe cases, perinatal death may occur, most commonly as a result of poor placental perfusion due to vascular impairment. Labor induction may be indicated with decreased placental function. A caesarean section may be performed if there is marked fetal distress or an increased risk of injury associated with macrosomia, such as shoulder dystocia.
Other types
Maturity onset diabetes of the young (MODY) is a rare autosomal dominant inherited form of diabetes, due to one of several single-gene mutations causing defects in insulin production. It is significantly less common than the three main types, constituting 1–2% of all cases. The name of this disease refers to early hypotheses as to its nature. Being due to a defective gene, this disease varies in age at presentation and in severity according to the specific gene defect; thus, there are at least 13 subtypes of MODY. People with MODY often can control it without using insulin.Some cases of diabetes are caused by the body's tissue receptors not responding to insulin (even when insulin levels are normal, which is what separates it from type 2 diabetes); this form is very uncommon. Genetic mutations (autosomal or mitochondrial) can lead to defects in beta cell function. Abnormal insulin action may also have been genetically determined in some cases. Any disease that causes extensive damage to the pancreas may lead to diabetes (for example, chronic pancreatitis and cystic fibrosis). Diseases associated with excessive secretion of insulin-antagonistic hormones can cause diabetes (which is typically resolved once the hormone excess is removed). Many drugs impair insulin secretion and some toxins damage pancreatic beta cells, whereas others increase insulin resistance (especially glucocorticoids which can provoke "steroid diabetes"). The ICD-10 (1992) diagnostic entity, malnutrition-related diabetes mellitus (ICD-10 code E12), was deprecated by the World Health Organization (WHO) when the current taxonomy was introduced in 1999.
Yet another form of diabetes that people may develop is double diabetes. This is when a type 1 diabetic becomes insulin resistant, the hallmark for type 2 diabetes or has a family history for type 2 diabetes. It was first discovered in 1990 or 1991.
The following is a list of disorders that may increase the risk of diabetes:
Pathophysiology
Insulin is the principal hormone that regulates the uptake of glucose from the blood into most cells of the body, especially liver, adipose tissue and muscle, except smooth muscle, in which insulin acts via the IGF-1. Therefore, deficiency of insulin or the insensitivity of its receptors play a central role in all forms of diabetes mellitus.The body obtains glucose from three main sources: the intestinal absorption of food; the breakdown of glycogen (glycogenolysis), the storage form of glucose found in the liver; and gluconeogenesis, the generation of glucose from non-carbohydrate substrates in the body. Insulin plays a critical role in regulating glucose levels in the body. Insulin can inhibit the breakdown of glycogen or the process of gluconeogenesis, it can stimulate the transport of glucose into fat and muscle cells, and it can stimulate the storage of glucose in the form of glycogen.Insulin is released into the blood by beta cells (β-cells), found in the islets of Langerhans in the pancreas, in response to rising levels of blood glucose, typically after eating. Insulin is used by about two-thirds of the body's cells to absorb glucose from the blood for use as fuel, for conversion to other needed molecules, or for storage. Lower glucose levels result in decreased insulin release from the beta cells and in the breakdown of glycogen to glucose. This process is mainly controlled by the hormone glucagon, which acts in the opposite manner to insulin.If the amount of insulin available is insufficient, or if cells respond poorly to the effects of insulin (insulin resistance), or if the insulin itself is defective, then glucose is not absorbed properly by the body cells that require it, and is not stored appropriately in the liver and muscles. The net effect is persistently high levels of blood glucose, poor protein synthesis, and other metabolic derangements, such as metabolic acidosis in cases of complete insulin deficiency.When glucose concentration in the blood remains high over time, the kidneys reach a threshold of reabsorption, and the body excretes glucose in the urine (glycosuria). This increases the osmotic pressure of the urine and inhibits reabsorption of water by the kidney, resulting in increased urine production (polyuria) and increased fluid loss. Lost blood volume is replaced osmotically from water in body cells and other body compartments, causing dehydration and increased thirst (polydipsia). In addition, intracellular glucose deficiency stimulates appetite leading to excessive food intake (polyphagia).
Diagnosis
Diabetes mellitus is diagnosed with a test for the glucose content in the blood, and is diagnosed by demonstrating any one of the following:
Fasting plasma glucose level ≥ 7.0 mmol/L (126 mg/dL). For this test, blood is taken after a period of fasting, i.e. in the morning before breakfast, after the patient had sufficient time to fast overnight.
Plasma glucose ≥ 11.1 mmol/L (200 mg/dL) two hours after a 75 gram oral glucose load as in a glucose tolerance test (OGTT)
Symptoms of high blood sugar and plasma glucose ≥ 11.1 mmol/L (200 mg/dL) either while fasting or not fasting
Glycated hemoglobin (HbA1C) ≥ 48 mmol/mol (≥ 6.5 DCCT %).A positive result, in the absence of unequivocal high blood sugar, should be confirmed by a repeat of any of the above methods on a different day. It is preferable to measure a fasting glucose level because of the ease of measurement and the considerable time commitment of formal glucose tolerance testing, which takes two hours to complete and offers no prognostic advantage over the fasting test. According to the current definition, two fasting glucose measurements at or above 7.0 mmol/L (126 mg/dL) is considered diagnostic for diabetes mellitus.
Per the WHO, people with fasting glucose levels from 6.1 to 6.9 mmol/L (110 to 125 mg/dL) are considered to have impaired fasting glucose. People with plasma glucose at or above 7.8 mmol/L (140 mg/dL), but not over 11.1 mmol/L (200 mg/dL), two hours after a 75 gram oral glucose load are considered to have impaired glucose tolerance. Of these two prediabetic states, the latter in particular is a major risk factor for progression to full-blown diabetes mellitus, as well as cardiovascular disease. The American Diabetes Association (ADA) since 2003 uses a slightly different range for impaired fasting glucose of 5.6 to 6.9 mmol/L (100 to 125 mg/dL).Glycated hemoglobin is better than fasting glucose for determining risks of cardiovascular disease and death from any cause.
Prevention
There is no known preventive measure for type 1 diabetes. Type 2 diabetes—which accounts for 85–90% of all cases worldwide—can often be prevented or delayed by maintaining a normal body weight, engaging in physical activity, and eating a healthy diet. Higher levels of physical activity (more than 90 minutes per day) reduce the risk of diabetes by 28%. Dietary changes known to be effective in helping to prevent diabetes include maintaining a diet rich in whole grains and fiber, and choosing good fats, such as the polyunsaturated fats found in nuts, vegetable oils, and fish. Limiting sugary beverages and eating less red meat and other sources of saturated fat can also help prevent diabetes. Tobacco smoking is also associated with an increased risk of diabetes and its complications, so smoking cessation can be an important preventive measure as well.The relationship between type 2 diabetes and the main modifiable risk factors (excess weight, unhealthy diet, physical inactivity and tobacco use) is similar in all regions of the world. There is growing evidence that the underlying determinants of diabetes are a reflection of the major forces driving social, economic and cultural change: globalization, urbanization, population aging, and the general health policy environment.
Management
Diabetes management concentrates on keeping blood sugar levels close to normal, without causing low blood sugar. This can usually be accomplished with dietary changes, exercise, weight loss, and use of appropriate medications (insulin, oral medications).Learning about the disease and actively participating in the treatment is important, since complications are far less common and less severe in people who have well-managed blood sugar levels. The goal of treatment is an A1C level below 5.7%. Attention is also paid to other health problems that may accelerate the negative effects of diabetes. These include smoking, high blood pressure, metabolic syndrome obesity, and lack of regular exercise. Specialized footwear is widely used to reduce the risk of diabetic foot ulcers by relieving the pressure on the foot. Foot examination for patients living with diabetes should be done annually which includes sensation testing, foot biomechanics, vascular integrity and foot structure.Concerning those with severe mental illness, the efficacy of type 2 diabetes self-management interventions is still poorly explored, with insufficient scientific evidence to show whether these interventions have similar results to those observed in the general population.
Lifestyle
People with diabetes can benefit from education about the disease and treatment, dietary changes, and exercise, with the goal of keeping both short-term and long-term blood glucose levels within acceptable bounds. In addition, given the associated higher risks of cardiovascular disease, lifestyle modifications are recommended to control blood pressure.Weight loss can prevent progression from prediabetes to diabetes type 2, decrease the risk of cardiovascular disease, or result in a partial remission in people with diabetes. No single dietary pattern is best for all people with diabetes. Healthy dietary patterns, such as the Mediterranean diet, low-carbohydrate diet, or DASH diet, are often recommended, although evidence does not support one over the others. According to the ADA, "reducing overall carbohydrate intake for individuals with diabetes has demonstrated the most evidence for improving glycemia", and for individuals with type 2 diabetes who cannot meet the glycemic targets or where reducing anti-glycemic medications is a priority, low or very-low carbohydrate diets are a viable approach. For overweight people with type 2 diabetes, any diet that achieves weight loss is effective.A 2020 Cochrane systematic review compared several non-nutritive sweeteners to sugar, placebo and a nutritive low-calorie sweetener (tagatose), but the results were unclear for effects on HbA1c, body weight and adverse events. The studies included were mainly of very low-certainty and did not report on health-related quality of life, diabetes complications, all-cause mortality or socioeconomic effects.
Medications
Glucose control
Most medications used to treat diabetes act by lowering blood sugar levels through different mechanisms. There is broad consensus that when people with diabetes maintain tight glucose control – keeping the glucose levels in their blood within normal ranges – they experience fewer complications, such as kidney problems or eye problems. There is however debate as to whether this is appropriate and cost effective for people later in life in whom the risk of hypoglycemia may be more significant.There are a number of different classes of anti-diabetic medications. Type 1 diabetes requires treatment with insulin, ideally using a "basal bolus" regimen that most closely matches normal insulin release: long-acting insulin for the basal rate and short-acting insulin with meals. Type 2 diabetes is generally treated with medication that is taken by mouth (e.g. metformin) although some eventually require injectable treatment with insulin or GLP-1 agonists.Metformin is generally recommended as a first-line treatment for type 2 diabetes, as there is good evidence that it decreases mortality. It works by decreasing the liver's production of glucose, and increasing the amount of glucose stored in peripheral tissue. Several other groups of drugs, mainly oral medication, may also decrease blood sugar in type 2 diabetes. These include agents that increase insulin release (sulfonylureas), agents that decrease absorption of sugar from the intestines (acarbose), agents that inhibit the enzyme dipeptidyl peptidase-4 (DPP-4) that inactivates incretins such as GLP-1 and GIP (sitagliptin), agents that make the body more sensitive to insulin (thiazolidinedione) and agents that increase the excretion of glucose in the urine (SGLT2 inhibitors). When insulin is used in type 2 diabetes, a long-acting formulation is usually added initially, while continuing oral medications.Some severe cases of type 2 diabetes may also be treated with insulin, which is increased gradually until glucose targets are reached.
Blood pressure lowering
Cardiovascular disease is a serious complication associated with diabetes, and many international guidelines recommend blood pressure treatment targets that are lower than 140/90 mmHg for people with diabetes. However, there is only limited evidence regarding what the lower targets should be. A 2016 systematic review found potential harm to treating to targets lower than 140 mmHg, and a subsequent systematic review in 2019 found no evidence of additional benefit from blood pressure lowering to between 130 – 140mmHg, although there was an increased risk of adverse events.2015 American Diabetes Association recommendations are that people with diabetes and albuminuria should receive an inhibitor of the renin-angiotensin system to reduce the risks of progression to end-stage renal disease, cardiovascular events, and death. There is some evidence that angiotensin converting enzyme inhibitors (ACEIs) are superior to other inhibitors of the renin-angiotensin system such as angiotensin receptor blockers (ARBs), or aliskiren in preventing cardiovascular disease. Although a more recent review found similar effects of ACEIs and ARBs on major cardiovascular and renal outcomes. There is no evidence that combining ACEIs and ARBs provides additional benefits.
Aspirin
The use of aspirin to prevent cardiovascular disease in diabetes is controversial. Aspirin is recommended by some in people at high risk of cardiovascular disease, however routine use of aspirin has not been found to improve outcomes in uncomplicated diabetes. 2015 American Diabetes Association recommendations for aspirin use (based on expert consensus or clinical experience) are that low-dose aspirin use is reasonable in adults with diabetes who are at intermediate risk of cardiovascular disease (10-year cardiovascular disease risk, 5–10%). National guidelines for England and Wales by the National Institute for Health and Care Excellence (NICE) recommend against the use of aspirin in people with type 1 or type 2 diabetes who do not have confirmed cardiovascular disease.
Surgery
Weight loss surgery in those with obesity and type 2 diabetes is often an effective measure. Many are able to maintain normal blood sugar levels with little or no medications following surgery and long-term mortality is decreased. There is, however, a short-term mortality risk of less than 1% from the surgery. The body mass index cutoffs for when surgery is appropriate are not yet clear. It is recommended that this option be considered in those who are unable to get both their weight and blood sugar under control.A pancreas transplant is occasionally considered for people with type 1 diabetes who have severe complications of their disease, including end stage kidney disease requiring kidney transplantation.
Self-management and support
In countries using a general practitioner system, such as the United Kingdom, care may take place mainly outside hospitals, with hospital-based specialist care used only in case of complications, difficult blood sugar control, or research projects. In other circumstances, general practitioners and specialists share care in a team approach. Home telehealth support can be an effective management technique.The use of technology to deliver educational programs for adults with type 2 diabetes includes computer-based self-management interventions to collect for tailored responses to facilitate self-management. There is no adequate evidence to support effects on cholesterol, blood pressure, behavioral change (such as physical activity levels and dietary), depression, weight and health-related quality of life, nor in other biological, cognitive or emotional outcomes.
Epidemiology
In 2017, 425 million people had diabetes worldwide, up from an estimated 382 million people in 2013 and from 108 million in 1980. Accounting for the shifting age structure of the global population, the prevalence of diabetes is 8.8% among adults, nearly double the rate of 4.7% in 1980. Type 2 makes up about 90% of the cases. Some data indicate rates are roughly equal in women and men, but male excess in diabetes has been found in many populations with higher type 2 incidence, possibly due to sex-related differences in insulin sensitivity, consequences of obesity and regional body fat deposition, and other contributing factors such as high blood pressure, tobacco smoking, and alcohol intake.The WHO estimates that diabetes resulted in 1.5 million deaths in 2012, making it the 8th leading cause of death. However another 2.2 million deaths worldwide were attributable to high blood glucose and the increased risks of cardiovascular disease and other associated complications (e.g. kidney failure), which often lead to premature death and are often listed as the underlying cause on death certificates rather than diabetes. For example, in 2017, the International Diabetes Federation (IDF) estimated that diabetes resulted in 4.0 million deaths worldwide, using modeling to estimate the total number of deaths that could be directly or indirectly attributed to diabetes.Diabetes occurs throughout the world but is more common (especially type 2) in more developed countries. The greatest increase in rates has however been seen in low- and middle-income countries, where more than 80% of diabetic deaths occur. The fastest prevalence increase is expected to occur in Asia and Africa, where most people with diabetes will probably live in 2030. The increase in rates in developing countries follows the trend of urbanization and lifestyle changes, including increasingly sedentary lifestyles, less physically demanding work and the global nutrition transition, marked by increased intake of foods that are high energy-dense but nutrient-poor (often high in sugar and saturated fats, sometimes referred to as the "Western-style" diet). The global number of diabetes cases might increase by 48% between 2017 and 2045.As of 2020, 38% of all US adults had prediabetes. Prediabetes is an early stage of diabetes.
History
Diabetes was one of the first diseases described, with an Egyptian manuscript from c. 1500 BCE mentioning "too great emptying of the urine." The Ebers papyrus includes a recommendation for a drink to take in such cases. The first described cases are believed to have been type 1 diabetes. Indian physicians around the same time identified the disease and classified it as madhumeha or "honey urine", noting the urine would attract ants.The term "diabetes" or "to pass through" was first used in 230 BCE by the Greek Apollonius of Memphis. The disease was considered rare during the time of the Roman empire, with Galen commenting he had only seen two cases during his career. This is possibly due to the diet and lifestyle of the ancients, or because the clinical symptoms were observed during the advanced stage of the disease. Galen named the disease "diarrhea of the urine" (diarrhea urinosa).The earliest surviving work with a detailed reference to diabetes is that of Aretaeus of Cappadocia (2nd or early 3rd century CE). He described the symptoms and the course of the disease, which he attributed to the moisture and coldness, reflecting the beliefs of the "Pneumatic School". He hypothesized a correlation between diabetes and other diseases, and he discussed differential diagnosis from the snakebite, which also provokes excessive thirst. His work remained unknown in the West until 1552, when the first Latin edition was published in Venice.Two types of diabetes were identified as separate conditions for the first time by the Indian physicians Sushruta and Charaka in 400–500 CE with one type being associated with youth and another type with being overweight. Effective treatment was not developed until the early part of the 20th century when Canadians Frederick Banting and Charles Herbert Best isolated and purified insulin in 1921 and 1922. This was followed by the development of the long-acting insulin NPH in the 1940s.
Etymology
The word diabetes ( or ) comes from Latin diabētēs, which in turn comes from Ancient Greek διαβήτης (diabētēs), which literally means "a passer through; a siphon". Ancient Greek physician Aretaeus of Cappadocia (fl. 1st century CE) used that word, with the intended meaning "excessive discharge of urine", as the name for the disease. Ultimately, the word comes from Greek διαβαίνειν (diabainein), meaning "to pass through", which is composed of δια- (dia-), meaning "through" and βαίνειν (bainein), meaning "to go". The word "diabetes" is first recorded in English, in the form diabete, in a medical text written around 1425.
The word mellitus ( or ) comes from the classical Latin word mellītus, meaning "mellite" (i.e. sweetened with honey; honey-sweet). The Latin word comes from mell-, which comes from mel, meaning "honey"; sweetness; pleasant thing, and the suffix -ītus, whose meaning is the same as that of the English suffix "-ite". It was Thomas Willis who in 1675 added "mellitus" to the word "diabetes" as a designation for the disease, when he noticed the urine of a person with diabetes had a sweet taste (glycosuria). This sweet taste had been noticed in urine by the ancient Greeks, Chinese, Egyptians, Indians, and Persians.
Society and culture
The 1989 "St. Vincent Declaration" was the result of international efforts to improve the care accorded to those with diabetes. Doing so is important not only in terms of quality of life and life expectancy but also economically – expenses due to diabetes have been shown to be a major drain on health – and productivity-related resources for healthcare systems and governments.
Several countries established more and less successful national diabetes programmes to improve treatment of the disease.People with diabetes who have neuropathic symptoms such as numbness or tingling in feet or hands are twice as likely to be unemployed as those without the symptoms.In 2010, diabetes-related emergency room (ER) visit rates in the United States were higher among people from the lowest income communities (526 per 10,000 population) than from the highest income communities (236 per 10,000 population). Approximately 9.4% of diabetes-related ER visits were for the uninsured.
Naming
The term "type 1 diabetes" has replaced several former terms, including childhood-onset diabetes, juvenile diabetes, and insulin-dependent diabetes mellitus. Likewise, the term "type 2 diabetes" has replaced several former terms, including adult-onset diabetes, obesity-related diabetes, and noninsulin-dependent diabetes mellitus. Beyond these two types, there is no agreed-upon standard nomenclature.Diabetes mellitus is also occasionally known as "sugar diabetes" to differentiate it from diabetes insipidus.
Other animals
Diabetes can occur in mammals or reptiles. Birds do not develop diabetes because of their unusually high tolerance for elevated blood glucose levels.In animals, diabetes is most commonly encountered in dogs and cats. Middle-aged animals are most commonly affected. Female dogs are twice as likely to be affected as males, while according to some sources, male cats are more prone than females. In both species, all breeds may be affected, but some small dog breeds are particularly likely to develop diabetes, such as Miniature Poodles.Feline diabetes is strikingly similar to human type 2 diabetes. The Burmese, Russian Blue, Abyssinian, and Norwegian Forest cat breeds are at higher risk than other breeds. Overweight cats are also at higher risk.The symptoms may relate to fluid loss and polyuria, but the course may also be insidious. Diabetic animals are more prone to infections. The long-term complications recognized in humans are much rarer in animals. The principles of treatment (weight loss, oral antidiabetics, subcutaneous insulin) and management of emergencies (e.g. ketoacidosis) are similar to those in humans.
References
External links
American Diabetes Association
IDF Diabetes Atlas
National Diabetes Education Program
ADA's Standards of Medical Care in Diabetes 2019
Polonsky KS (October 2012). "The past 200 years in diabetes". The New England Journal of Medicine. 367 (14): 1332–1340. doi:10.1056/NEJMra1110560. PMID 23034021. S2CID 9456681.
"Diabetes". MedlinePlus. U.S. National Library of Medicine.
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Diabetes, also known as diabetes mellitus, is a group of common endocrine diseases characterized by sustained high blood sugar levels. Diabetes is due to either the pancreas not producing enough insulin, or the cells of the body not responding properly to the insulin produced. Diabetes, if left untreated, leads to many health complications. Untreated or poorly treated diabetes accounts for approximately 1.5 million deaths per year.There is no widely accepted cure for most cases of diabetes. The most common treatment for type 1 diabetes is insulin replacement therapy (insulin injections). Anti-diabetic medications such as metformin and semaglutide, as well as lifestyle modifications, can be used to prevent or respond to type 2 diabetes. Gestational diabetes normally resolves shortly after delivery.
As of 2019, an estimated 463 million people had diabetes worldwide accounting for 8.8% of the adult population. Type 2 diabetes makes up about 90% of all diabetes cases. The prevalence of the disease continues to increase, most dramatically in low- and middle-income nations. Rates are similar in women and men, with diabetes being the 7th-leading cause of death globally. The global expenditure on diabetes-related healthcare is an estimated USD760 billion a year.
Signs and symptoms
The classic symptoms of untreated diabetes are unintended weight loss, polyuria (increased urination), polydipsia (increased thirst), and polyphagia (increased hunger). Symptoms may develop rapidly (weeks or months) in type 1 diabetes, while they usually develop much more slowly and may be subtle or absent in type 2 diabetes.Several other signs and symptoms can mark the onset of diabetes although they are not specific to the disease. In addition to the known symptoms listed above, they include blurred vision, headache, fatigue, slow healing of cuts, and itchy skin. Prolonged high blood glucose can cause glucose absorption in the lens of the eye, which leads to changes in its shape, resulting in vision changes. Long-term vision loss can also be caused by diabetic retinopathy. A number of skin rashes that can occur in diabetes are collectively known as diabetic dermadromes.
Diabetic emergencies
People with diabetes (usually but not exclusively in type 1 diabetes) may also experience diabetic ketoacidosis (DKA), a metabolic disturbance characterized by nausea, vomiting and abdominal pain, the smell of acetone on the breath, deep breathing known as Kussmaul breathing, and in severe cases a decreased level of consciousness. DKA requires emergency treatment in hospital. A rarer but more dangerous condition is hyperosmolar hyperglycemic state (HHS), which is more common in type 2 diabetes and is mainly the result of dehydration caused by high blood sugars.Treatment-related low blood sugar (hypoglycemia) is common in people with type 1 and also type 2 diabetes depending on the medication being used. Most cases are mild and are not considered medical emergencies. Effects can range from feelings of unease, sweating, trembling, and increased appetite in mild cases to more serious effects such as confusion, changes in behavior such as aggressiveness, seizures, unconsciousness, and rarely permanent brain damage or death in severe cases. Rapid breathing, sweating, and cold, pale skin are characteristic of low blood sugar but not definitive. Mild to moderate cases are self-treated by eating or drinking something high in rapidly absorbed carbohydrates. Severe cases can lead to unconsciousness and must be treated with intravenous glucose or injections with glucagon.
Complications
All forms of diabetes increase the risk of long-term complications. These typically develop after many years (10–20) but may be the first symptom in those who have otherwise not received a diagnosis before that time.The major long-term complications relate to damage to blood vessels. Diabetes doubles the risk of cardiovascular disease and about 75% of deaths in people with diabetes are due to coronary artery disease. Other macrovascular diseases include stroke, and peripheral artery disease. These complications are also a strong risk factor for severe COVID-19 illness.The primary complications of diabetes due to damage in small blood vessels include damage to the eyes, kidneys, and nerves. Damage to the eyes, known as diabetic retinopathy, is caused by damage to the blood vessels in the retina of the eye, and can result in gradual vision loss and eventual blindness. Diabetes also increases the risk of having glaucoma, cataracts, and other eye problems. It is recommended that people with diabetes visit an optometrist or ophthalmologist once a year. Damage to the kidneys, known as diabetic nephropathy, can lead to tissue scarring, urine protein loss, and eventually chronic kidney disease, sometimes requiring dialysis or kidney transplantation. Damage to the nerves of the body, known as diabetic neuropathy, is the most common complication of diabetes. The symptoms can include numbness, tingling, sudomotor dysfunction, pain, and altered pain sensation, which can lead to damage to the skin. Diabetes-related foot problems (such as diabetic foot ulcers) may occur, and can be difficult to treat, occasionally requiring amputation. Additionally, proximal diabetic neuropathy causes painful muscle atrophy and weakness.
There is a link between cognitive deficit and diabetes. Compared to those without diabetes, those with the disease have a 1.2 to 1.5-fold greater rate of decline in cognitive function. Having diabetes, especially when on insulin, increases the risk of falls in older people.
Causes
Diabetes mellitus is classified into six categories: type 1 diabetes, type 2 diabetes, hybrid forms of diabetes, hyperglycemia first detected during pregnancy, "unclassified diabetes", and "other specific types". "Hybrid forms of diabetes" include slowly evolving, immune-mediated diabetes of adults and ketosis-prone type 2 diabetes. "Hyperglycemia first detected during pregnancy" includes gestational diabetes mellitus and diabetes mellitus in pregnancy (type 1 or type 2 diabetes first diagnosed during pregnancy). The "other specific types" are a collection of a few dozen individual causes. Diabetes is a more variable disease than once thought and people may have combinations of forms.
Type 1
Type 1 diabetes is characterized by loss of the insulin-producing beta cells of the pancreatic islets, leading to insulin deficiency. This type can be further classified as immune-mediated or idiopathic. The majority of type 1 diabetes is of an immune-mediated nature, in which a T cell-mediated autoimmune attack leads to the loss of beta cells and thus insulin. It causes approximately 10% of diabetes mellitus cases in North America and Europe. Most affected people are otherwise healthy and of a healthy weight when onset occurs. Sensitivity and responsiveness to insulin are usually normal, especially in the early stages. Although it has been called "juvenile diabetes" due to the frequent onset in children, the majority of individuals living with type 1 diabetes are now adults."Brittle" diabetes, also known as unstable diabetes or labile diabetes, is a term that was traditionally used to describe the dramatic and recurrent swings in glucose levels, often occurring for no apparent reason in insulin-dependent diabetes. This term, however, has no biologic basis and should not be used. Still, type 1 diabetes can be accompanied by irregular and unpredictable high blood sugar levels, and the potential for diabetic ketoacidosis or serious low blood sugar levels. Other complications include an impaired counterregulatory response to low blood sugar, infection, gastroparesis (which leads to erratic absorption of dietary carbohydrates), and endocrinopathies (e.g., Addison's disease). These phenomena are believed to occur no more frequently than in 1% to 2% of persons with type 1 diabetes.
Type 1 diabetes is partly inherited, with multiple genes, including certain HLA genotypes, known to influence the risk of diabetes. In genetically susceptible people, the onset of diabetes can be triggered by one or more environmental factors, such as a viral infection or diet. Several viruses have been implicated, but to date there is no stringent evidence to support this hypothesis in humans.Type 1 diabetes can occur at any age, and a significant proportion is diagnosed during adulthood. Latent autoimmune diabetes of adults (LADA) is the diagnostic term applied when type 1 diabetes develops in adults; it has a slower onset than the same condition in children. Given this difference, some use the unofficial term "type 1.5 diabetes" for this condition. Adults with LADA are frequently initially misdiagnosed as having type 2 diabetes, based on age rather than a cause.
Type 2
Type 2 diabetes is characterized by insulin resistance, which may be combined with relatively reduced insulin secretion. The defective responsiveness of body tissues to insulin is believed to involve the insulin receptor. However, the specific defects are not known. Diabetes mellitus cases due to a known defect are classified separately. Type 2 diabetes is the most common type of diabetes mellitus accounting for 95% of diabetes. Many people with type 2 diabetes have evidence of prediabetes (impaired fasting glucose and/or impaired glucose tolerance) before meeting the criteria for type 2 diabetes. The progression of prediabetes to overt type 2 diabetes can be slowed or reversed by lifestyle changes or medications that improve insulin sensitivity or reduce the liver's glucose production.Type 2 diabetes is primarily due to lifestyle factors and genetics. A number of lifestyle factors are known to be important to the development of type 2 diabetes, including obesity (defined by a body mass index of greater than 30), lack of physical activity, poor diet, stress, and urbanization. Excess body fat is associated with 30% of cases in people of Chinese and Japanese descent, 60–80% of cases in those of European and African descent, and 100% of Pima Indians and Pacific Islanders. Even those who are not obese may have a high waist–hip ratio.Dietary factors such as sugar-sweetened drinks are associated with an increased risk. The type of fats in the diet is also important, with saturated fat and trans fats increasing the risk and polyunsaturated and monounsaturated fat decreasing the risk. Eating white rice excessively may increase the risk of diabetes, especially in Chinese and Japanese people. Lack of physical activity may increase the risk of diabetes in some people.Adverse childhood experiences, including abuse, neglect, and household difficulties, increase the likelihood of type 2 diabetes later in life by 32%, with neglect having the strongest effect.Antipsychotic medication side effects (specifically metabolic abnormalities, dyslipidemia and weight gain) and unhealthy lifestyles (including poor diet and decreased physical activity), are potential risk factors.
Gestational diabetes
Gestational diabetes resembles type 2 diabetes in several respects, involving a combination of relatively inadequate insulin secretion and responsiveness. It occurs in about 2–10% of all pregnancies and may improve or disappear after delivery. It is recommended that all pregnant women get tested starting around 24–28 weeks gestation. It is most often diagnosed in the second or third trimester because of the increase in insulin-antagonist hormone levels that occurs at this time. However, after pregnancy approximately 5–10% of women with gestational diabetes are found to have another form of diabetes, most commonly type 2. Gestational diabetes is fully treatable, but requires careful medical supervision throughout the pregnancy. Management may include dietary changes, blood glucose monitoring, and in some cases, insulin may be required.Though it may be transient, untreated gestational diabetes can damage the health of the fetus or mother. Risks to the baby include macrosomia (high birth weight), congenital heart and central nervous system abnormalities, and skeletal muscle malformations. Increased levels of insulin in a fetus's blood may inhibit fetal surfactant production and cause infant respiratory distress syndrome. A high blood bilirubin level may result from red blood cell destruction. In severe cases, perinatal death may occur, most commonly as a result of poor placental perfusion due to vascular impairment. Labor induction may be indicated with decreased placental function. A caesarean section may be performed if there is marked fetal distress or an increased risk of injury associated with macrosomia, such as shoulder dystocia.
Other types
Maturity onset diabetes of the young (MODY) is a rare autosomal dominant inherited form of diabetes, due to one of several single-gene mutations causing defects in insulin production. It is significantly less common than the three main types, constituting 1–2% of all cases. The name of this disease refers to early hypotheses as to its nature. Being due to a defective gene, this disease varies in age at presentation and in severity according to the specific gene defect; thus, there are at least 13 subtypes of MODY. People with MODY often can control it without using insulin.Some cases of diabetes are caused by the body's tissue receptors not responding to insulin (even when insulin levels are normal, which is what separates it from type 2 diabetes); this form is very uncommon. Genetic mutations (autosomal or mitochondrial) can lead to defects in beta cell function. Abnormal insulin action may also have been genetically determined in some cases. Any disease that causes extensive damage to the pancreas may lead to diabetes (for example, chronic pancreatitis and cystic fibrosis). Diseases associated with excessive secretion of insulin-antagonistic hormones can cause diabetes (which is typically resolved once the hormone excess is removed). Many drugs impair insulin secretion and some toxins damage pancreatic beta cells, whereas others increase insulin resistance (especially glucocorticoids which can provoke "steroid diabetes"). The ICD-10 (1992) diagnostic entity, malnutrition-related diabetes mellitus (ICD-10 code E12), was deprecated by the World Health Organization (WHO) when the current taxonomy was introduced in 1999.
Yet another form of diabetes that people may develop is double diabetes. This is when a type 1 diabetic becomes insulin resistant, the hallmark for type 2 diabetes or has a family history for type 2 diabetes. It was first discovered in 1990 or 1991.
The following is a list of disorders that may increase the risk of diabetes:
Pathophysiology
Insulin is the principal hormone that regulates the uptake of glucose from the blood into most cells of the body, especially liver, adipose tissue and muscle, except smooth muscle, in which insulin acts via the IGF-1. Therefore, deficiency of insulin or the insensitivity of its receptors play a central role in all forms of diabetes mellitus.The body obtains glucose from three main sources: the intestinal absorption of food; the breakdown of glycogen (glycogenolysis), the storage form of glucose found in the liver; and gluconeogenesis, the generation of glucose from non-carbohydrate substrates in the body. Insulin plays a critical role in regulating glucose levels in the body. Insulin can inhibit the breakdown of glycogen or the process of gluconeogenesis, it can stimulate the transport of glucose into fat and muscle cells, and it can stimulate the storage of glucose in the form of glycogen.Insulin is released into the blood by beta cells (β-cells), found in the islets of Langerhans in the pancreas, in response to rising levels of blood glucose, typically after eating. Insulin is used by about two-thirds of the body's cells to absorb glucose from the blood for use as fuel, for conversion to other needed molecules, or for storage. Lower glucose levels result in decreased insulin release from the beta cells and in the breakdown of glycogen to glucose. This process is mainly controlled by the hormone glucagon, which acts in the opposite manner to insulin.If the amount of insulin available is insufficient, or if cells respond poorly to the effects of insulin (insulin resistance), or if the insulin itself is defective, then glucose is not absorbed properly by the body cells that require it, and is not stored appropriately in the liver and muscles. The net effect is persistently high levels of blood glucose, poor protein synthesis, and other metabolic derangements, such as metabolic acidosis in cases of complete insulin deficiency.When glucose concentration in the blood remains high over time, the kidneys reach a threshold of reabsorption, and the body excretes glucose in the urine (glycosuria). This increases the osmotic pressure of the urine and inhibits reabsorption of water by the kidney, resulting in increased urine production (polyuria) and increased fluid loss. Lost blood volume is replaced osmotically from water in body cells and other body compartments, causing dehydration and increased thirst (polydipsia). In addition, intracellular glucose deficiency stimulates appetite leading to excessive food intake (polyphagia).
Diagnosis
Diabetes mellitus is diagnosed with a test for the glucose content in the blood, and is diagnosed by demonstrating any one of the following:
Fasting plasma glucose level ≥ 7.0 mmol/L (126 mg/dL). For this test, blood is taken after a period of fasting, i.e. in the morning before breakfast, after the patient had sufficient time to fast overnight.
Plasma glucose ≥ 11.1 mmol/L (200 mg/dL) two hours after a 75 gram oral glucose load as in a glucose tolerance test (OGTT)
Symptoms of high blood sugar and plasma glucose ≥ 11.1 mmol/L (200 mg/dL) either while fasting or not fasting
Glycated hemoglobin (HbA1C) ≥ 48 mmol/mol (≥ 6.5 DCCT %).A positive result, in the absence of unequivocal high blood sugar, should be confirmed by a repeat of any of the above methods on a different day. It is preferable to measure a fasting glucose level because of the ease of measurement and the considerable time commitment of formal glucose tolerance testing, which takes two hours to complete and offers no prognostic advantage over the fasting test. According to the current definition, two fasting glucose measurements at or above 7.0 mmol/L (126 mg/dL) is considered diagnostic for diabetes mellitus.
Per the WHO, people with fasting glucose levels from 6.1 to 6.9 mmol/L (110 to 125 mg/dL) are considered to have impaired fasting glucose. People with plasma glucose at or above 7.8 mmol/L (140 mg/dL), but not over 11.1 mmol/L (200 mg/dL), two hours after a 75 gram oral glucose load are considered to have impaired glucose tolerance. Of these two prediabetic states, the latter in particular is a major risk factor for progression to full-blown diabetes mellitus, as well as cardiovascular disease. The American Diabetes Association (ADA) since 2003 uses a slightly different range for impaired fasting glucose of 5.6 to 6.9 mmol/L (100 to 125 mg/dL).Glycated hemoglobin is better than fasting glucose for determining risks of cardiovascular disease and death from any cause.
Prevention
There is no known preventive measure for type 1 diabetes. Type 2 diabetes—which accounts for 85–90% of all cases worldwide—can often be prevented or delayed by maintaining a normal body weight, engaging in physical activity, and eating a healthy diet. Higher levels of physical activity (more than 90 minutes per day) reduce the risk of diabetes by 28%. Dietary changes known to be effective in helping to prevent diabetes include maintaining a diet rich in whole grains and fiber, and choosing good fats, such as the polyunsaturated fats found in nuts, vegetable oils, and fish. Limiting sugary beverages and eating less red meat and other sources of saturated fat can also help prevent diabetes. Tobacco smoking is also associated with an increased risk of diabetes and its complications, so smoking cessation can be an important preventive measure as well.The relationship between type 2 diabetes and the main modifiable risk factors (excess weight, unhealthy diet, physical inactivity and tobacco use) is similar in all regions of the world. There is growing evidence that the underlying determinants of diabetes are a reflection of the major forces driving social, economic and cultural change: globalization, urbanization, population aging, and the general health policy environment.
Management
Diabetes management concentrates on keeping blood sugar levels close to normal, without causing low blood sugar. This can usually be accomplished with dietary changes, exercise, weight loss, and use of appropriate medications (insulin, oral medications).Learning about the disease and actively participating in the treatment is important, since complications are far less common and less severe in people who have well-managed blood sugar levels. The goal of treatment is an A1C level below 5.7%. Attention is also paid to other health problems that may accelerate the negative effects of diabetes. These include smoking, high blood pressure, metabolic syndrome obesity, and lack of regular exercise. Specialized footwear is widely used to reduce the risk of diabetic foot ulcers by relieving the pressure on the foot. Foot examination for patients living with diabetes should be done annually which includes sensation testing, foot biomechanics, vascular integrity and foot structure.Concerning those with severe mental illness, the efficacy of type 2 diabetes self-management interventions is still poorly explored, with insufficient scientific evidence to show whether these interventions have similar results to those observed in the general population.
Lifestyle
People with diabetes can benefit from education about the disease and treatment, dietary changes, and exercise, with the goal of keeping both short-term and long-term blood glucose levels within acceptable bounds. In addition, given the associated higher risks of cardiovascular disease, lifestyle modifications are recommended to control blood pressure.Weight loss can prevent progression from prediabetes to diabetes type 2, decrease the risk of cardiovascular disease, or result in a partial remission in people with diabetes. No single dietary pattern is best for all people with diabetes. Healthy dietary patterns, such as the Mediterranean diet, low-carbohydrate diet, or DASH diet, are often recommended, although evidence does not support one over the others. According to the ADA, "reducing overall carbohydrate intake for individuals with diabetes has demonstrated the most evidence for improving glycemia", and for individuals with type 2 diabetes who cannot meet the glycemic targets or where reducing anti-glycemic medications is a priority, low or very-low carbohydrate diets are a viable approach. For overweight people with type 2 diabetes, any diet that achieves weight loss is effective.A 2020 Cochrane systematic review compared several non-nutritive sweeteners to sugar, placebo and a nutritive low-calorie sweetener (tagatose), but the results were unclear for effects on HbA1c, body weight and adverse events. The studies included were mainly of very low-certainty and did not report on health-related quality of life, diabetes complications, all-cause mortality or socioeconomic effects.
Medications
Glucose control
Most medications used to treat diabetes act by lowering blood sugar levels through different mechanisms. There is broad consensus that when people with diabetes maintain tight glucose control – keeping the glucose levels in their blood within normal ranges – they experience fewer complications, such as kidney problems or eye problems. There is however debate as to whether this is appropriate and cost effective for people later in life in whom the risk of hypoglycemia may be more significant.There are a number of different classes of anti-diabetic medications. Type 1 diabetes requires treatment with insulin, ideally using a "basal bolus" regimen that most closely matches normal insulin release: long-acting insulin for the basal rate and short-acting insulin with meals. Type 2 diabetes is generally treated with medication that is taken by mouth (e.g. metformin) although some eventually require injectable treatment with insulin or GLP-1 agonists.Metformin is generally recommended as a first-line treatment for type 2 diabetes, as there is good evidence that it decreases mortality. It works by decreasing the liver's production of glucose, and increasing the amount of glucose stored in peripheral tissue. Several other groups of drugs, mainly oral medication, may also decrease blood sugar in type 2 diabetes. These include agents that increase insulin release (sulfonylureas), agents that decrease absorption of sugar from the intestines (acarbose), agents that inhibit the enzyme dipeptidyl peptidase-4 (DPP-4) that inactivates incretins such as GLP-1 and GIP (sitagliptin), agents that make the body more sensitive to insulin (thiazolidinedione) and agents that increase the excretion of glucose in the urine (SGLT2 inhibitors). When insulin is used in type 2 diabetes, a long-acting formulation is usually added initially, while continuing oral medications.Some severe cases of type 2 diabetes may also be treated with insulin, which is increased gradually until glucose targets are reached.
Blood pressure lowering
Cardiovascular disease is a serious complication associated with diabetes, and many international guidelines recommend blood pressure treatment targets that are lower than 140/90 mmHg for people with diabetes. However, there is only limited evidence regarding what the lower targets should be. A 2016 systematic review found potential harm to treating to targets lower than 140 mmHg, and a subsequent systematic review in 2019 found no evidence of additional benefit from blood pressure lowering to between 130 – 140mmHg, although there was an increased risk of adverse events.2015 American Diabetes Association recommendations are that people with diabetes and albuminuria should receive an inhibitor of the renin-angiotensin system to reduce the risks of progression to end-stage renal disease, cardiovascular events, and death. There is some evidence that angiotensin converting enzyme inhibitors (ACEIs) are superior to other inhibitors of the renin-angiotensin system such as angiotensin receptor blockers (ARBs), or aliskiren in preventing cardiovascular disease. Although a more recent review found similar effects of ACEIs and ARBs on major cardiovascular and renal outcomes. There is no evidence that combining ACEIs and ARBs provides additional benefits.
Aspirin
The use of aspirin to prevent cardiovascular disease in diabetes is controversial. Aspirin is recommended by some in people at high risk of cardiovascular disease, however routine use of aspirin has not been found to improve outcomes in uncomplicated diabetes. 2015 American Diabetes Association recommendations for aspirin use (based on expert consensus or clinical experience) are that low-dose aspirin use is reasonable in adults with diabetes who are at intermediate risk of cardiovascular disease (10-year cardiovascular disease risk, 5–10%). National guidelines for England and Wales by the National Institute for Health and Care Excellence (NICE) recommend against the use of aspirin in people with type 1 or type 2 diabetes who do not have confirmed cardiovascular disease.
Surgery
Weight loss surgery in those with obesity and type 2 diabetes is often an effective measure. Many are able to maintain normal blood sugar levels with little or no medications following surgery and long-term mortality is decreased. There is, however, a short-term mortality risk of less than 1% from the surgery. The body mass index cutoffs for when surgery is appropriate are not yet clear. It is recommended that this option be considered in those who are unable to get both their weight and blood sugar under control.A pancreas transplant is occasionally considered for people with type 1 diabetes who have severe complications of their disease, including end stage kidney disease requiring kidney transplantation.
Self-management and support
In countries using a general practitioner system, such as the United Kingdom, care may take place mainly outside hospitals, with hospital-based specialist care used only in case of complications, difficult blood sugar control, or research projects. In other circumstances, general practitioners and specialists share care in a team approach. Home telehealth support can be an effective management technique.The use of technology to deliver educational programs for adults with type 2 diabetes includes computer-based self-management interventions to collect for tailored responses to facilitate self-management. There is no adequate evidence to support effects on cholesterol, blood pressure, behavioral change (such as physical activity levels and dietary), depression, weight and health-related quality of life, nor in other biological, cognitive or emotional outcomes.
Epidemiology
In 2017, 425 million people had diabetes worldwide, up from an estimated 382 million people in 2013 and from 108 million in 1980. Accounting for the shifting age structure of the global population, the prevalence of diabetes is 8.8% among adults, nearly double the rate of 4.7% in 1980. Type 2 makes up about 90% of the cases. Some data indicate rates are roughly equal in women and men, but male excess in diabetes has been found in many populations with higher type 2 incidence, possibly due to sex-related differences in insulin sensitivity, consequences of obesity and regional body fat deposition, and other contributing factors such as high blood pressure, tobacco smoking, and alcohol intake.The WHO estimates that diabetes resulted in 1.5 million deaths in 2012, making it the 8th leading cause of death. However another 2.2 million deaths worldwide were attributable to high blood glucose and the increased risks of cardiovascular disease and other associated complications (e.g. kidney failure), which often lead to premature death and are often listed as the underlying cause on death certificates rather than diabetes. For example, in 2017, the International Diabetes Federation (IDF) estimated that diabetes resulted in 4.0 million deaths worldwide, using modeling to estimate the total number of deaths that could be directly or indirectly attributed to diabetes.Diabetes occurs throughout the world but is more common (especially type 2) in more developed countries. The greatest increase in rates has however been seen in low- and middle-income countries, where more than 80% of diabetic deaths occur. The fastest prevalence increase is expected to occur in Asia and Africa, where most people with diabetes will probably live in 2030. The increase in rates in developing countries follows the trend of urbanization and lifestyle changes, including increasingly sedentary lifestyles, less physically demanding work and the global nutrition transition, marked by increased intake of foods that are high energy-dense but nutrient-poor (often high in sugar and saturated fats, sometimes referred to as the "Western-style" diet). The global number of diabetes cases might increase by 48% between 2017 and 2045.As of 2020, 38% of all US adults had prediabetes. Prediabetes is an early stage of diabetes.
History
Diabetes was one of the first diseases described, with an Egyptian manuscript from c. 1500 BCE mentioning "too great emptying of the urine." The Ebers papyrus includes a recommendation for a drink to take in such cases. The first described cases are believed to have been type 1 diabetes. Indian physicians around the same time identified the disease and classified it as madhumeha or "honey urine", noting the urine would attract ants.The term "diabetes" or "to pass through" was first used in 230 BCE by the Greek Apollonius of Memphis. The disease was considered rare during the time of the Roman empire, with Galen commenting he had only seen two cases during his career. This is possibly due to the diet and lifestyle of the ancients, or because the clinical symptoms were observed during the advanced stage of the disease. Galen named the disease "diarrhea of the urine" (diarrhea urinosa).The earliest surviving work with a detailed reference to diabetes is that of Aretaeus of Cappadocia (2nd or early 3rd century CE). He described the symptoms and the course of the disease, which he attributed to the moisture and coldness, reflecting the beliefs of the "Pneumatic School". He hypothesized a correlation between diabetes and other diseases, and he discussed differential diagnosis from the snakebite, which also provokes excessive thirst. His work remained unknown in the West until 1552, when the first Latin edition was published in Venice.Two types of diabetes were identified as separate conditions for the first time by the Indian physicians Sushruta and Charaka in 400–500 CE with one type being associated with youth and another type with being overweight. Effective treatment was not developed until the early part of the 20th century when Canadians Frederick Banting and Charles Herbert Best isolated and purified insulin in 1921 and 1922. This was followed by the development of the long-acting insulin NPH in the 1940s.
Etymology
The word diabetes ( or ) comes from Latin diabētēs, which in turn comes from Ancient Greek διαβήτης (diabētēs), which literally means "a passer through; a siphon". Ancient Greek physician Aretaeus of Cappadocia (fl. 1st century CE) used that word, with the intended meaning "excessive discharge of urine", as the name for the disease. Ultimately, the word comes from Greek διαβαίνειν (diabainein), meaning "to pass through", which is composed of δια- (dia-), meaning "through" and βαίνειν (bainein), meaning "to go". The word "diabetes" is first recorded in English, in the form diabete, in a medical text written around 1425.
The word mellitus ( or ) comes from the classical Latin word mellītus, meaning "mellite" (i.e. sweetened with honey; honey-sweet). The Latin word comes from mell-, which comes from mel, meaning "honey"; sweetness; pleasant thing, and the suffix -ītus, whose meaning is the same as that of the English suffix "-ite". It was Thomas Willis who in 1675 added "mellitus" to the word "diabetes" as a designation for the disease, when he noticed the urine of a person with diabetes had a sweet taste (glycosuria). This sweet taste had been noticed in urine by the ancient Greeks, Chinese, Egyptians, Indians, and Persians.
Society and culture
The 1989 "St. Vincent Declaration" was the result of international efforts to improve the care accorded to those with diabetes. Doing so is important not only in terms of quality of life and life expectancy but also economically – expenses due to diabetes have been shown to be a major drain on health – and productivity-related resources for healthcare systems and governments.
Several countries established more and less successful national diabetes programmes to improve treatment of the disease.People with diabetes who have neuropathic symptoms such as numbness or tingling in feet or hands are twice as likely to be unemployed as those without the symptoms.In 2010, diabetes-related emergency room (ER) visit rates in the United States were higher among people from the lowest income communities (526 per 10,000 population) than from the highest income communities (236 per 10,000 population). Approximately 9.4% of diabetes-related ER visits were for the uninsured.
Naming
The term "type 1 diabetes" has replaced several former terms, including childhood-onset diabetes, juvenile diabetes, and insulin-dependent diabetes mellitus. Likewise, the term "type 2 diabetes" has replaced several former terms, including adult-onset diabetes, obesity-related diabetes, and noninsulin-dependent diabetes mellitus. Beyond these two types, there is no agreed-upon standard nomenclature.Diabetes mellitus is also occasionally known as "sugar diabetes" to differentiate it from diabetes insipidus.
Other animals
Diabetes can occur in mammals or reptiles. Birds do not develop diabetes because of their unusually high tolerance for elevated blood glucose levels.In animals, diabetes is most commonly encountered in dogs and cats. Middle-aged animals are most commonly affected. Female dogs are twice as likely to be affected as males, while according to some sources, male cats are more prone than females. In both species, all breeds may be affected, but some small dog breeds are particularly likely to develop diabetes, such as Miniature Poodles.Feline diabetes is strikingly similar to human type 2 diabetes. The Burmese, Russian Blue, Abyssinian, and Norwegian Forest cat breeds are at higher risk than other breeds. Overweight cats are also at higher risk.The symptoms may relate to fluid loss and polyuria, but the course may also be insidious. Diabetic animals are more prone to infections. The long-term complications recognized in humans are much rarer in animals. The principles of treatment (weight loss, oral antidiabetics, subcutaneous insulin) and management of emergencies (e.g. ketoacidosis) are similar to those in humans.
References
External links
American Diabetes Association
IDF Diabetes Atlas
National Diabetes Education Program
ADA's Standards of Medical Care in Diabetes 2019
Polonsky KS (October 2012). "The past 200 years in diabetes". The New England Journal of Medicine. 367 (14): 1332–1340. doi:10.1056/NEJMra1110560. PMID 23034021. S2CID 9456681.
"Diabetes". MedlinePlus. U.S. National Library of Medicine.
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Diabetes, also known as diabetes mellitus, is a group of common endocrine diseases characterized by sustained high blood sugar levels. Diabetes is due to either the pancreas not producing enough insulin, or the cells of the body not responding properly to the insulin produced. Diabetes, if left untreated, leads to many health complications. Untreated or poorly treated diabetes accounts for approximately 1.5 million deaths per year.There is no widely accepted cure for most cases of diabetes. The most common treatment for type 1 diabetes is insulin replacement therapy (insulin injections). Anti-diabetic medications such as metformin and semaglutide, as well as lifestyle modifications, can be used to prevent or respond to type 2 diabetes. Gestational diabetes normally resolves shortly after delivery.
As of 2019, an estimated 463 million people had diabetes worldwide accounting for 8.8% of the adult population. Type 2 diabetes makes up about 90% of all diabetes cases. The prevalence of the disease continues to increase, most dramatically in low- and middle-income nations. Rates are similar in women and men, with diabetes being the 7th-leading cause of death globally. The global expenditure on diabetes-related healthcare is an estimated USD760 billion a year.
Signs and symptoms
The classic symptoms of untreated diabetes are unintended weight loss, polyuria (increased urination), polydipsia (increased thirst), and polyphagia (increased hunger). Symptoms may develop rapidly (weeks or months) in type 1 diabetes, while they usually develop much more slowly and may be subtle or absent in type 2 diabetes.Several other signs and symptoms can mark the onset of diabetes although they are not specific to the disease. In addition to the known symptoms listed above, they include blurred vision, headache, fatigue, slow healing of cuts, and itchy skin. Prolonged high blood glucose can cause glucose absorption in the lens of the eye, which leads to changes in its shape, resulting in vision changes. Long-term vision loss can also be caused by diabetic retinopathy. A number of skin rashes that can occur in diabetes are collectively known as diabetic dermadromes.
Diabetic emergencies
People with diabetes (usually but not exclusively in type 1 diabetes) may also experience diabetic ketoacidosis (DKA), a metabolic disturbance characterized by nausea, vomiting and abdominal pain, the smell of acetone on the breath, deep breathing known as Kussmaul breathing, and in severe cases a decreased level of consciousness. DKA requires emergency treatment in hospital. A rarer but more dangerous condition is hyperosmolar hyperglycemic state (HHS), which is more common in type 2 diabetes and is mainly the result of dehydration caused by high blood sugars.Treatment-related low blood sugar (hypoglycemia) is common in people with type 1 and also type 2 diabetes depending on the medication being used. Most cases are mild and are not considered medical emergencies. Effects can range from feelings of unease, sweating, trembling, and increased appetite in mild cases to more serious effects such as confusion, changes in behavior such as aggressiveness, seizures, unconsciousness, and rarely permanent brain damage or death in severe cases. Rapid breathing, sweating, and cold, pale skin are characteristic of low blood sugar but not definitive. Mild to moderate cases are self-treated by eating or drinking something high in rapidly absorbed carbohydrates. Severe cases can lead to unconsciousness and must be treated with intravenous glucose or injections with glucagon.
Complications
All forms of diabetes increase the risk of long-term complications. These typically develop after many years (10–20) but may be the first symptom in those who have otherwise not received a diagnosis before that time.The major long-term complications relate to damage to blood vessels. Diabetes doubles the risk of cardiovascular disease and about 75% of deaths in people with diabetes are due to coronary artery disease. Other macrovascular diseases include stroke, and peripheral artery disease. These complications are also a strong risk factor for severe COVID-19 illness.The primary complications of diabetes due to damage in small blood vessels include damage to the eyes, kidneys, and nerves. Damage to the eyes, known as diabetic retinopathy, is caused by damage to the blood vessels in the retina of the eye, and can result in gradual vision loss and eventual blindness. Diabetes also increases the risk of having glaucoma, cataracts, and other eye problems. It is recommended that people with diabetes visit an optometrist or ophthalmologist once a year. Damage to the kidneys, known as diabetic nephropathy, can lead to tissue scarring, urine protein loss, and eventually chronic kidney disease, sometimes requiring dialysis or kidney transplantation. Damage to the nerves of the body, known as diabetic neuropathy, is the most common complication of diabetes. The symptoms can include numbness, tingling, sudomotor dysfunction, pain, and altered pain sensation, which can lead to damage to the skin. Diabetes-related foot problems (such as diabetic foot ulcers) may occur, and can be difficult to treat, occasionally requiring amputation. Additionally, proximal diabetic neuropathy causes painful muscle atrophy and weakness.
There is a link between cognitive deficit and diabetes. Compared to those without diabetes, those with the disease have a 1.2 to 1.5-fold greater rate of decline in cognitive function. Having diabetes, especially when on insulin, increases the risk of falls in older people.
Causes
Diabetes mellitus is classified into six categories: type 1 diabetes, type 2 diabetes, hybrid forms of diabetes, hyperglycemia first detected during pregnancy, "unclassified diabetes", and "other specific types". "Hybrid forms of diabetes" include slowly evolving, immune-mediated diabetes of adults and ketosis-prone type 2 diabetes. "Hyperglycemia first detected during pregnancy" includes gestational diabetes mellitus and diabetes mellitus in pregnancy (type 1 or type 2 diabetes first diagnosed during pregnancy). The "other specific types" are a collection of a few dozen individual causes. Diabetes is a more variable disease than once thought and people may have combinations of forms.
Type 1
Type 1 diabetes is characterized by loss of the insulin-producing beta cells of the pancreatic islets, leading to insulin deficiency. This type can be further classified as immune-mediated or idiopathic. The majority of type 1 diabetes is of an immune-mediated nature, in which a T cell-mediated autoimmune attack leads to the loss of beta cells and thus insulin. It causes approximately 10% of diabetes mellitus cases in North America and Europe. Most affected people are otherwise healthy and of a healthy weight when onset occurs. Sensitivity and responsiveness to insulin are usually normal, especially in the early stages. Although it has been called "juvenile diabetes" due to the frequent onset in children, the majority of individuals living with type 1 diabetes are now adults."Brittle" diabetes, also known as unstable diabetes or labile diabetes, is a term that was traditionally used to describe the dramatic and recurrent swings in glucose levels, often occurring for no apparent reason in insulin-dependent diabetes. This term, however, has no biologic basis and should not be used. Still, type 1 diabetes can be accompanied by irregular and unpredictable high blood sugar levels, and the potential for diabetic ketoacidosis or serious low blood sugar levels. Other complications include an impaired counterregulatory response to low blood sugar, infection, gastroparesis (which leads to erratic absorption of dietary carbohydrates), and endocrinopathies (e.g., Addison's disease). These phenomena are believed to occur no more frequently than in 1% to 2% of persons with type 1 diabetes.
Type 1 diabetes is partly inherited, with multiple genes, including certain HLA genotypes, known to influence the risk of diabetes. In genetically susceptible people, the onset of diabetes can be triggered by one or more environmental factors, such as a viral infection or diet. Several viruses have been implicated, but to date there is no stringent evidence to support this hypothesis in humans.Type 1 diabetes can occur at any age, and a significant proportion is diagnosed during adulthood. Latent autoimmune diabetes of adults (LADA) is the diagnostic term applied when type 1 diabetes develops in adults; it has a slower onset than the same condition in children. Given this difference, some use the unofficial term "type 1.5 diabetes" for this condition. Adults with LADA are frequently initially misdiagnosed as having type 2 diabetes, based on age rather than a cause.
Type 2
Type 2 diabetes is characterized by insulin resistance, which may be combined with relatively reduced insulin secretion. The defective responsiveness of body tissues to insulin is believed to involve the insulin receptor. However, the specific defects are not known. Diabetes mellitus cases due to a known defect are classified separately. Type 2 diabetes is the most common type of diabetes mellitus accounting for 95% of diabetes. Many people with type 2 diabetes have evidence of prediabetes (impaired fasting glucose and/or impaired glucose tolerance) before meeting the criteria for type 2 diabetes. The progression of prediabetes to overt type 2 diabetes can be slowed or reversed by lifestyle changes or medications that improve insulin sensitivity or reduce the liver's glucose production.Type 2 diabetes is primarily due to lifestyle factors and genetics. A number of lifestyle factors are known to be important to the development of type 2 diabetes, including obesity (defined by a body mass index of greater than 30), lack of physical activity, poor diet, stress, and urbanization. Excess body fat is associated with 30% of cases in people of Chinese and Japanese descent, 60–80% of cases in those of European and African descent, and 100% of Pima Indians and Pacific Islanders. Even those who are not obese may have a high waist–hip ratio.Dietary factors such as sugar-sweetened drinks are associated with an increased risk. The type of fats in the diet is also important, with saturated fat and trans fats increasing the risk and polyunsaturated and monounsaturated fat decreasing the risk. Eating white rice excessively may increase the risk of diabetes, especially in Chinese and Japanese people. Lack of physical activity may increase the risk of diabetes in some people.Adverse childhood experiences, including abuse, neglect, and household difficulties, increase the likelihood of type 2 diabetes later in life by 32%, with neglect having the strongest effect.Antipsychotic medication side effects (specifically metabolic abnormalities, dyslipidemia and weight gain) and unhealthy lifestyles (including poor diet and decreased physical activity), are potential risk factors.
Gestational diabetes
Gestational diabetes resembles type 2 diabetes in several respects, involving a combination of relatively inadequate insulin secretion and responsiveness. It occurs in about 2–10% of all pregnancies and may improve or disappear after delivery. It is recommended that all pregnant women get tested starting around 24–28 weeks gestation. It is most often diagnosed in the second or third trimester because of the increase in insulin-antagonist hormone levels that occurs at this time. However, after pregnancy approximately 5–10% of women with gestational diabetes are found to have another form of diabetes, most commonly type 2. Gestational diabetes is fully treatable, but requires careful medical supervision throughout the pregnancy. Management may include dietary changes, blood glucose monitoring, and in some cases, insulin may be required.Though it may be transient, untreated gestational diabetes can damage the health of the fetus or mother. Risks to the baby include macrosomia (high birth weight), congenital heart and central nervous system abnormalities, and skeletal muscle malformations. Increased levels of insulin in a fetus's blood may inhibit fetal surfactant production and cause infant respiratory distress syndrome. A high blood bilirubin level may result from red blood cell destruction. In severe cases, perinatal death may occur, most commonly as a result of poor placental perfusion due to vascular impairment. Labor induction may be indicated with decreased placental function. A caesarean section may be performed if there is marked fetal distress or an increased risk of injury associated with macrosomia, such as shoulder dystocia.
Other types
Maturity onset diabetes of the young (MODY) is a rare autosomal dominant inherited form of diabetes, due to one of several single-gene mutations causing defects in insulin production. It is significantly less common than the three main types, constituting 1–2% of all cases. The name of this disease refers to early hypotheses as to its nature. Being due to a defective gene, this disease varies in age at presentation and in severity according to the specific gene defect; thus, there are at least 13 subtypes of MODY. People with MODY often can control it without using insulin.Some cases of diabetes are caused by the body's tissue receptors not responding to insulin (even when insulin levels are normal, which is what separates it from type 2 diabetes); this form is very uncommon. Genetic mutations (autosomal or mitochondrial) can lead to defects in beta cell function. Abnormal insulin action may also have been genetically determined in some cases. Any disease that causes extensive damage to the pancreas may lead to diabetes (for example, chronic pancreatitis and cystic fibrosis). Diseases associated with excessive secretion of insulin-antagonistic hormones can cause diabetes (which is typically resolved once the hormone excess is removed). Many drugs impair insulin secretion and some toxins damage pancreatic beta cells, whereas others increase insulin resistance (especially glucocorticoids which can provoke "steroid diabetes"). The ICD-10 (1992) diagnostic entity, malnutrition-related diabetes mellitus (ICD-10 code E12), was deprecated by the World Health Organization (WHO) when the current taxonomy was introduced in 1999.
Yet another form of diabetes that people may develop is double diabetes. This is when a type 1 diabetic becomes insulin resistant, the hallmark for type 2 diabetes or has a family history for type 2 diabetes. It was first discovered in 1990 or 1991.
The following is a list of disorders that may increase the risk of diabetes:
Pathophysiology
Insulin is the principal hormone that regulates the uptake of glucose from the blood into most cells of the body, especially liver, adipose tissue and muscle, except smooth muscle, in which insulin acts via the IGF-1. Therefore, deficiency of insulin or the insensitivity of its receptors play a central role in all forms of diabetes mellitus.The body obtains glucose from three main sources: the intestinal absorption of food; the breakdown of glycogen (glycogenolysis), the storage form of glucose found in the liver; and gluconeogenesis, the generation of glucose from non-carbohydrate substrates in the body. Insulin plays a critical role in regulating glucose levels in the body. Insulin can inhibit the breakdown of glycogen or the process of gluconeogenesis, it can stimulate the transport of glucose into fat and muscle cells, and it can stimulate the storage of glucose in the form of glycogen.Insulin is released into the blood by beta cells (β-cells), found in the islets of Langerhans in the pancreas, in response to rising levels of blood glucose, typically after eating. Insulin is used by about two-thirds of the body's cells to absorb glucose from the blood for use as fuel, for conversion to other needed molecules, or for storage. Lower glucose levels result in decreased insulin release from the beta cells and in the breakdown of glycogen to glucose. This process is mainly controlled by the hormone glucagon, which acts in the opposite manner to insulin.If the amount of insulin available is insufficient, or if cells respond poorly to the effects of insulin (insulin resistance), or if the insulin itself is defective, then glucose is not absorbed properly by the body cells that require it, and is not stored appropriately in the liver and muscles. The net effect is persistently high levels of blood glucose, poor protein synthesis, and other metabolic derangements, such as metabolic acidosis in cases of complete insulin deficiency.When glucose concentration in the blood remains high over time, the kidneys reach a threshold of reabsorption, and the body excretes glucose in the urine (glycosuria). This increases the osmotic pressure of the urine and inhibits reabsorption of water by the kidney, resulting in increased urine production (polyuria) and increased fluid loss. Lost blood volume is replaced osmotically from water in body cells and other body compartments, causing dehydration and increased thirst (polydipsia). In addition, intracellular glucose deficiency stimulates appetite leading to excessive food intake (polyphagia).
Diagnosis
Diabetes mellitus is diagnosed with a test for the glucose content in the blood, and is diagnosed by demonstrating any one of the following:
Fasting plasma glucose level ≥ 7.0 mmol/L (126 mg/dL). For this test, blood is taken after a period of fasting, i.e. in the morning before breakfast, after the patient had sufficient time to fast overnight.
Plasma glucose ≥ 11.1 mmol/L (200 mg/dL) two hours after a 75 gram oral glucose load as in a glucose tolerance test (OGTT)
Symptoms of high blood sugar and plasma glucose ≥ 11.1 mmol/L (200 mg/dL) either while fasting or not fasting
Glycated hemoglobin (HbA1C) ≥ 48 mmol/mol (≥ 6.5 DCCT %).A positive result, in the absence of unequivocal high blood sugar, should be confirmed by a repeat of any of the above methods on a different day. It is preferable to measure a fasting glucose level because of the ease of measurement and the considerable time commitment of formal glucose tolerance testing, which takes two hours to complete and offers no prognostic advantage over the fasting test. According to the current definition, two fasting glucose measurements at or above 7.0 mmol/L (126 mg/dL) is considered diagnostic for diabetes mellitus.
Per the WHO, people with fasting glucose levels from 6.1 to 6.9 mmol/L (110 to 125 mg/dL) are considered to have impaired fasting glucose. People with plasma glucose at or above 7.8 mmol/L (140 mg/dL), but not over 11.1 mmol/L (200 mg/dL), two hours after a 75 gram oral glucose load are considered to have impaired glucose tolerance. Of these two prediabetic states, the latter in particular is a major risk factor for progression to full-blown diabetes mellitus, as well as cardiovascular disease. The American Diabetes Association (ADA) since 2003 uses a slightly different range for impaired fasting glucose of 5.6 to 6.9 mmol/L (100 to 125 mg/dL).Glycated hemoglobin is better than fasting glucose for determining risks of cardiovascular disease and death from any cause.
Prevention
There is no known preventive measure for type 1 diabetes. Type 2 diabetes—which accounts for 85–90% of all cases worldwide—can often be prevented or delayed by maintaining a normal body weight, engaging in physical activity, and eating a healthy diet. Higher levels of physical activity (more than 90 minutes per day) reduce the risk of diabetes by 28%. Dietary changes known to be effective in helping to prevent diabetes include maintaining a diet rich in whole grains and fiber, and choosing good fats, such as the polyunsaturated fats found in nuts, vegetable oils, and fish. Limiting sugary beverages and eating less red meat and other sources of saturated fat can also help prevent diabetes. Tobacco smoking is also associated with an increased risk of diabetes and its complications, so smoking cessation can be an important preventive measure as well.The relationship between type 2 diabetes and the main modifiable risk factors (excess weight, unhealthy diet, physical inactivity and tobacco use) is similar in all regions of the world. There is growing evidence that the underlying determinants of diabetes are a reflection of the major forces driving social, economic and cultural change: globalization, urbanization, population aging, and the general health policy environment.
Management
Diabetes management concentrates on keeping blood sugar levels close to normal, without causing low blood sugar. This can usually be accomplished with dietary changes, exercise, weight loss, and use of appropriate medications (insulin, oral medications).Learning about the disease and actively participating in the treatment is important, since complications are far less common and less severe in people who have well-managed blood sugar levels. The goal of treatment is an A1C level below 5.7%. Attention is also paid to other health problems that may accelerate the negative effects of diabetes. These include smoking, high blood pressure, metabolic syndrome obesity, and lack of regular exercise. Specialized footwear is widely used to reduce the risk of diabetic foot ulcers by relieving the pressure on the foot. Foot examination for patients living with diabetes should be done annually which includes sensation testing, foot biomechanics, vascular integrity and foot structure.Concerning those with severe mental illness, the efficacy of type 2 diabetes self-management interventions is still poorly explored, with insufficient scientific evidence to show whether these interventions have similar results to those observed in the general population.
Lifestyle
People with diabetes can benefit from education about the disease and treatment, dietary changes, and exercise, with the goal of keeping both short-term and long-term blood glucose levels within acceptable bounds. In addition, given the associated higher risks of cardiovascular disease, lifestyle modifications are recommended to control blood pressure.Weight loss can prevent progression from prediabetes to diabetes type 2, decrease the risk of cardiovascular disease, or result in a partial remission in people with diabetes. No single dietary pattern is best for all people with diabetes. Healthy dietary patterns, such as the Mediterranean diet, low-carbohydrate diet, or DASH diet, are often recommended, although evidence does not support one over the others. According to the ADA, "reducing overall carbohydrate intake for individuals with diabetes has demonstrated the most evidence for improving glycemia", and for individuals with type 2 diabetes who cannot meet the glycemic targets or where reducing anti-glycemic medications is a priority, low or very-low carbohydrate diets are a viable approach. For overweight people with type 2 diabetes, any diet that achieves weight loss is effective.A 2020 Cochrane systematic review compared several non-nutritive sweeteners to sugar, placebo and a nutritive low-calorie sweetener (tagatose), but the results were unclear for effects on HbA1c, body weight and adverse events. The studies included were mainly of very low-certainty and did not report on health-related quality of life, diabetes complications, all-cause mortality or socioeconomic effects.
Medications
Glucose control
Most medications used to treat diabetes act by lowering blood sugar levels through different mechanisms. There is broad consensus that when people with diabetes maintain tight glucose control – keeping the glucose levels in their blood within normal ranges – they experience fewer complications, such as kidney problems or eye problems. There is however debate as to whether this is appropriate and cost effective for people later in life in whom the risk of hypoglycemia may be more significant.There are a number of different classes of anti-diabetic medications. Type 1 diabetes requires treatment with insulin, ideally using a "basal bolus" regimen that most closely matches normal insulin release: long-acting insulin for the basal rate and short-acting insulin with meals. Type 2 diabetes is generally treated with medication that is taken by mouth (e.g. metformin) although some eventually require injectable treatment with insulin or GLP-1 agonists.Metformin is generally recommended as a first-line treatment for type 2 diabetes, as there is good evidence that it decreases mortality. It works by decreasing the liver's production of glucose, and increasing the amount of glucose stored in peripheral tissue. Several other groups of drugs, mainly oral medication, may also decrease blood sugar in type 2 diabetes. These include agents that increase insulin release (sulfonylureas), agents that decrease absorption of sugar from the intestines (acarbose), agents that inhibit the enzyme dipeptidyl peptidase-4 (DPP-4) that inactivates incretins such as GLP-1 and GIP (sitagliptin), agents that make the body more sensitive to insulin (thiazolidinedione) and agents that increase the excretion of glucose in the urine (SGLT2 inhibitors). When insulin is used in type 2 diabetes, a long-acting formulation is usually added initially, while continuing oral medications.Some severe cases of type 2 diabetes may also be treated with insulin, which is increased gradually until glucose targets are reached.
Blood pressure lowering
Cardiovascular disease is a serious complication associated with diabetes, and many international guidelines recommend blood pressure treatment targets that are lower than 140/90 mmHg for people with diabetes. However, there is only limited evidence regarding what the lower targets should be. A 2016 systematic review found potential harm to treating to targets lower than 140 mmHg, and a subsequent systematic review in 2019 found no evidence of additional benefit from blood pressure lowering to between 130 – 140mmHg, although there was an increased risk of adverse events.2015 American Diabetes Association recommendations are that people with diabetes and albuminuria should receive an inhibitor of the renin-angiotensin system to reduce the risks of progression to end-stage renal disease, cardiovascular events, and death. There is some evidence that angiotensin converting enzyme inhibitors (ACEIs) are superior to other inhibitors of the renin-angiotensin system such as angiotensin receptor blockers (ARBs), or aliskiren in preventing cardiovascular disease. Although a more recent review found similar effects of ACEIs and ARBs on major cardiovascular and renal outcomes. There is no evidence that combining ACEIs and ARBs provides additional benefits.
Aspirin
The use of aspirin to prevent cardiovascular disease in diabetes is controversial. Aspirin is recommended by some in people at high risk of cardiovascular disease, however routine use of aspirin has not been found to improve outcomes in uncomplicated diabetes. 2015 American Diabetes Association recommendations for aspirin use (based on expert consensus or clinical experience) are that low-dose aspirin use is reasonable in adults with diabetes who are at intermediate risk of cardiovascular disease (10-year cardiovascular disease risk, 5–10%). National guidelines for England and Wales by the National Institute for Health and Care Excellence (NICE) recommend against the use of aspirin in people with type 1 or type 2 diabetes who do not have confirmed cardiovascular disease.
Surgery
Weight loss surgery in those with obesity and type 2 diabetes is often an effective measure. Many are able to maintain normal blood sugar levels with little or no medications following surgery and long-term mortality is decreased. There is, however, a short-term mortality risk of less than 1% from the surgery. The body mass index cutoffs for when surgery is appropriate are not yet clear. It is recommended that this option be considered in those who are unable to get both their weight and blood sugar under control.A pancreas transplant is occasionally considered for people with type 1 diabetes who have severe complications of their disease, including end stage kidney disease requiring kidney transplantation.
Self-management and support
In countries using a general practitioner system, such as the United Kingdom, care may take place mainly outside hospitals, with hospital-based specialist care used only in case of complications, difficult blood sugar control, or research projects. In other circumstances, general practitioners and specialists share care in a team approach. Home telehealth support can be an effective management technique.The use of technology to deliver educational programs for adults with type 2 diabetes includes computer-based self-management interventions to collect for tailored responses to facilitate self-management. There is no adequate evidence to support effects on cholesterol, blood pressure, behavioral change (such as physical activity levels and dietary), depression, weight and health-related quality of life, nor in other biological, cognitive or emotional outcomes.
Epidemiology
In 2017, 425 million people had diabetes worldwide, up from an estimated 382 million people in 2013 and from 108 million in 1980. Accounting for the shifting age structure of the global population, the prevalence of diabetes is 8.8% among adults, nearly double the rate of 4.7% in 1980. Type 2 makes up about 90% of the cases. Some data indicate rates are roughly equal in women and men, but male excess in diabetes has been found in many populations with higher type 2 incidence, possibly due to sex-related differences in insulin sensitivity, consequences of obesity and regional body fat deposition, and other contributing factors such as high blood pressure, tobacco smoking, and alcohol intake.The WHO estimates that diabetes resulted in 1.5 million deaths in 2012, making it the 8th leading cause of death. However another 2.2 million deaths worldwide were attributable to high blood glucose and the increased risks of cardiovascular disease and other associated complications (e.g. kidney failure), which often lead to premature death and are often listed as the underlying cause on death certificates rather than diabetes. For example, in 2017, the International Diabetes Federation (IDF) estimated that diabetes resulted in 4.0 million deaths worldwide, using modeling to estimate the total number of deaths that could be directly or indirectly attributed to diabetes.Diabetes occurs throughout the world but is more common (especially type 2) in more developed countries. The greatest increase in rates has however been seen in low- and middle-income countries, where more than 80% of diabetic deaths occur. The fastest prevalence increase is expected to occur in Asia and Africa, where most people with diabetes will probably live in 2030. The increase in rates in developing countries follows the trend of urbanization and lifestyle changes, including increasingly sedentary lifestyles, less physically demanding work and the global nutrition transition, marked by increased intake of foods that are high energy-dense but nutrient-poor (often high in sugar and saturated fats, sometimes referred to as the "Western-style" diet). The global number of diabetes cases might increase by 48% between 2017 and 2045.As of 2020, 38% of all US adults had prediabetes. Prediabetes is an early stage of diabetes.
History
Diabetes was one of the first diseases described, with an Egyptian manuscript from c. 1500 BCE mentioning "too great emptying of the urine." The Ebers papyrus includes a recommendation for a drink to take in such cases. The first described cases are believed to have been type 1 diabetes. Indian physicians around the same time identified the disease and classified it as madhumeha or "honey urine", noting the urine would attract ants.The term "diabetes" or "to pass through" was first used in 230 BCE by the Greek Apollonius of Memphis. The disease was considered rare during the time of the Roman empire, with Galen commenting he had only seen two cases during his career. This is possibly due to the diet and lifestyle of the ancients, or because the clinical symptoms were observed during the advanced stage of the disease. Galen named the disease "diarrhea of the urine" (diarrhea urinosa).The earliest surviving work with a detailed reference to diabetes is that of Aretaeus of Cappadocia (2nd or early 3rd century CE). He described the symptoms and the course of the disease, which he attributed to the moisture and coldness, reflecting the beliefs of the "Pneumatic School". He hypothesized a correlation between diabetes and other diseases, and he discussed differential diagnosis from the snakebite, which also provokes excessive thirst. His work remained unknown in the West until 1552, when the first Latin edition was published in Venice.Two types of diabetes were identified as separate conditions for the first time by the Indian physicians Sushruta and Charaka in 400–500 CE with one type being associated with youth and another type with being overweight. Effective treatment was not developed until the early part of the 20th century when Canadians Frederick Banting and Charles Herbert Best isolated and purified insulin in 1921 and 1922. This was followed by the development of the long-acting insulin NPH in the 1940s.
Etymology
The word diabetes ( or ) comes from Latin diabētēs, which in turn comes from Ancient Greek διαβήτης (diabētēs), which literally means "a passer through; a siphon". Ancient Greek physician Aretaeus of Cappadocia (fl. 1st century CE) used that word, with the intended meaning "excessive discharge of urine", as the name for the disease. Ultimately, the word comes from Greek διαβαίνειν (diabainein), meaning "to pass through", which is composed of δια- (dia-), meaning "through" and βαίνειν (bainein), meaning "to go". The word "diabetes" is first recorded in English, in the form diabete, in a medical text written around 1425.
The word mellitus ( or ) comes from the classical Latin word mellītus, meaning "mellite" (i.e. sweetened with honey; honey-sweet). The Latin word comes from mell-, which comes from mel, meaning "honey"; sweetness; pleasant thing, and the suffix -ītus, whose meaning is the same as that of the English suffix "-ite". It was Thomas Willis who in 1675 added "mellitus" to the word "diabetes" as a designation for the disease, when he noticed the urine of a person with diabetes had a sweet taste (glycosuria). This sweet taste had been noticed in urine by the ancient Greeks, Chinese, Egyptians, Indians, and Persians.
Society and culture
The 1989 "St. Vincent Declaration" was the result of international efforts to improve the care accorded to those with diabetes. Doing so is important not only in terms of quality of life and life expectancy but also economically – expenses due to diabetes have been shown to be a major drain on health – and productivity-related resources for healthcare systems and governments.
Several countries established more and less successful national diabetes programmes to improve treatment of the disease.People with diabetes who have neuropathic symptoms such as numbness or tingling in feet or hands are twice as likely to be unemployed as those without the symptoms.In 2010, diabetes-related emergency room (ER) visit rates in the United States were higher among people from the lowest income communities (526 per 10,000 population) than from the highest income communities (236 per 10,000 population). Approximately 9.4% of diabetes-related ER visits were for the uninsured.
Naming
The term "type 1 diabetes" has replaced several former terms, including childhood-onset diabetes, juvenile diabetes, and insulin-dependent diabetes mellitus. Likewise, the term "type 2 diabetes" has replaced several former terms, including adult-onset diabetes, obesity-related diabetes, and noninsulin-dependent diabetes mellitus. Beyond these two types, there is no agreed-upon standard nomenclature.Diabetes mellitus is also occasionally known as "sugar diabetes" to differentiate it from diabetes insipidus.
Other animals
Diabetes can occur in mammals or reptiles. Birds do not develop diabetes because of their unusually high tolerance for elevated blood glucose levels.In animals, diabetes is most commonly encountered in dogs and cats. Middle-aged animals are most commonly affected. Female dogs are twice as likely to be affected as males, while according to some sources, male cats are more prone than females. In both species, all breeds may be affected, but some small dog breeds are particularly likely to develop diabetes, such as Miniature Poodles.Feline diabetes is strikingly similar to human type 2 diabetes. The Burmese, Russian Blue, Abyssinian, and Norwegian Forest cat breeds are at higher risk than other breeds. Overweight cats are also at higher risk.The symptoms may relate to fluid loss and polyuria, but the course may also be insidious. Diabetic animals are more prone to infections. The long-term complications recognized in humans are much rarer in animals. The principles of treatment (weight loss, oral antidiabetics, subcutaneous insulin) and management of emergencies (e.g. ketoacidosis) are similar to those in humans.
References
External links
American Diabetes Association
IDF Diabetes Atlas
National Diabetes Education Program
ADA's Standards of Medical Care in Diabetes 2019
Polonsky KS (October 2012). "The past 200 years in diabetes". The New England Journal of Medicine. 367 (14): 1332–1340. doi:10.1056/NEJMra1110560. PMID 23034021. S2CID 9456681.
"Diabetes". MedlinePlus. U.S. National Library of Medicine.
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Diabetes, also known as diabetes mellitus, is a group of common endocrine diseases characterized by sustained high blood sugar levels. Diabetes is due to either the pancreas not producing enough insulin, or the cells of the body not responding properly to the insulin produced. Diabetes, if left untreated, leads to many health complications. Untreated or poorly treated diabetes accounts for approximately 1.5 million deaths per year.There is no widely accepted cure for most cases of diabetes. The most common treatment for type 1 diabetes is insulin replacement therapy (insulin injections). Anti-diabetic medications such as metformin and semaglutide, as well as lifestyle modifications, can be used to prevent or respond to type 2 diabetes. Gestational diabetes normally resolves shortly after delivery.
As of 2019, an estimated 463 million people had diabetes worldwide accounting for 8.8% of the adult population. Type 2 diabetes makes up about 90% of all diabetes cases. The prevalence of the disease continues to increase, most dramatically in low- and middle-income nations. Rates are similar in women and men, with diabetes being the 7th-leading cause of death globally. The global expenditure on diabetes-related healthcare is an estimated USD760 billion a year.
Signs and symptoms
The classic symptoms of untreated diabetes are unintended weight loss, polyuria (increased urination), polydipsia (increased thirst), and polyphagia (increased hunger). Symptoms may develop rapidly (weeks or months) in type 1 diabetes, while they usually develop much more slowly and may be subtle or absent in type 2 diabetes.Several other signs and symptoms can mark the onset of diabetes although they are not specific to the disease. In addition to the known symptoms listed above, they include blurred vision, headache, fatigue, slow healing of cuts, and itchy skin. Prolonged high blood glucose can cause glucose absorption in the lens of the eye, which leads to changes in its shape, resulting in vision changes. Long-term vision loss can also be caused by diabetic retinopathy. A number of skin rashes that can occur in diabetes are collectively known as diabetic dermadromes.
Diabetic emergencies
People with diabetes (usually but not exclusively in type 1 diabetes) may also experience diabetic ketoacidosis (DKA), a metabolic disturbance characterized by nausea, vomiting and abdominal pain, the smell of acetone on the breath, deep breathing known as Kussmaul breathing, and in severe cases a decreased level of consciousness. DKA requires emergency treatment in hospital. A rarer but more dangerous condition is hyperosmolar hyperglycemic state (HHS), which is more common in type 2 diabetes and is mainly the result of dehydration caused by high blood sugars.Treatment-related low blood sugar (hypoglycemia) is common in people with type 1 and also type 2 diabetes depending on the medication being used. Most cases are mild and are not considered medical emergencies. Effects can range from feelings of unease, sweating, trembling, and increased appetite in mild cases to more serious effects such as confusion, changes in behavior such as aggressiveness, seizures, unconsciousness, and rarely permanent brain damage or death in severe cases. Rapid breathing, sweating, and cold, pale skin are characteristic of low blood sugar but not definitive. Mild to moderate cases are self-treated by eating or drinking something high in rapidly absorbed carbohydrates. Severe cases can lead to unconsciousness and must be treated with intravenous glucose or injections with glucagon.
Complications
All forms of diabetes increase the risk of long-term complications. These typically develop after many years (10–20) but may be the first symptom in those who have otherwise not received a diagnosis before that time.The major long-term complications relate to damage to blood vessels. Diabetes doubles the risk of cardiovascular disease and about 75% of deaths in people with diabetes are due to coronary artery disease. Other macrovascular diseases include stroke, and peripheral artery disease. These complications are also a strong risk factor for severe COVID-19 illness.The primary complications of diabetes due to damage in small blood vessels include damage to the eyes, kidneys, and nerves. Damage to the eyes, known as diabetic retinopathy, is caused by damage to the blood vessels in the retina of the eye, and can result in gradual vision loss and eventual blindness. Diabetes also increases the risk of having glaucoma, cataracts, and other eye problems. It is recommended that people with diabetes visit an optometrist or ophthalmologist once a year. Damage to the kidneys, known as diabetic nephropathy, can lead to tissue scarring, urine protein loss, and eventually chronic kidney disease, sometimes requiring dialysis or kidney transplantation. Damage to the nerves of the body, known as diabetic neuropathy, is the most common complication of diabetes. The symptoms can include numbness, tingling, sudomotor dysfunction, pain, and altered pain sensation, which can lead to damage to the skin. Diabetes-related foot problems (such as diabetic foot ulcers) may occur, and can be difficult to treat, occasionally requiring amputation. Additionally, proximal diabetic neuropathy causes painful muscle atrophy and weakness.
There is a link between cognitive deficit and diabetes. Compared to those without diabetes, those with the disease have a 1.2 to 1.5-fold greater rate of decline in cognitive function. Having diabetes, especially when on insulin, increases the risk of falls in older people.
Causes
Diabetes mellitus is classified into six categories: type 1 diabetes, type 2 diabetes, hybrid forms of diabetes, hyperglycemia first detected during pregnancy, "unclassified diabetes", and "other specific types". "Hybrid forms of diabetes" include slowly evolving, immune-mediated diabetes of adults and ketosis-prone type 2 diabetes. "Hyperglycemia first detected during pregnancy" includes gestational diabetes mellitus and diabetes mellitus in pregnancy (type 1 or type 2 diabetes first diagnosed during pregnancy). The "other specific types" are a collection of a few dozen individual causes. Diabetes is a more variable disease than once thought and people may have combinations of forms.
Type 1
Type 1 diabetes is characterized by loss of the insulin-producing beta cells of the pancreatic islets, leading to insulin deficiency. This type can be further classified as immune-mediated or idiopathic. The majority of type 1 diabetes is of an immune-mediated nature, in which a T cell-mediated autoimmune attack leads to the loss of beta cells and thus insulin. It causes approximately 10% of diabetes mellitus cases in North America and Europe. Most affected people are otherwise healthy and of a healthy weight when onset occurs. Sensitivity and responsiveness to insulin are usually normal, especially in the early stages. Although it has been called "juvenile diabetes" due to the frequent onset in children, the majority of individuals living with type 1 diabetes are now adults."Brittle" diabetes, also known as unstable diabetes or labile diabetes, is a term that was traditionally used to describe the dramatic and recurrent swings in glucose levels, often occurring for no apparent reason in insulin-dependent diabetes. This term, however, has no biologic basis and should not be used. Still, type 1 diabetes can be accompanied by irregular and unpredictable high blood sugar levels, and the potential for diabetic ketoacidosis or serious low blood sugar levels. Other complications include an impaired counterregulatory response to low blood sugar, infection, gastroparesis (which leads to erratic absorption of dietary carbohydrates), and endocrinopathies (e.g., Addison's disease). These phenomena are believed to occur no more frequently than in 1% to 2% of persons with type 1 diabetes.
Type 1 diabetes is partly inherited, with multiple genes, including certain HLA genotypes, known to influence the risk of diabetes. In genetically susceptible people, the onset of diabetes can be triggered by one or more environmental factors, such as a viral infection or diet. Several viruses have been implicated, but to date there is no stringent evidence to support this hypothesis in humans.Type 1 diabetes can occur at any age, and a significant proportion is diagnosed during adulthood. Latent autoimmune diabetes of adults (LADA) is the diagnostic term applied when type 1 diabetes develops in adults; it has a slower onset than the same condition in children. Given this difference, some use the unofficial term "type 1.5 diabetes" for this condition. Adults with LADA are frequently initially misdiagnosed as having type 2 diabetes, based on age rather than a cause.
Type 2
Type 2 diabetes is characterized by insulin resistance, which may be combined with relatively reduced insulin secretion. The defective responsiveness of body tissues to insulin is believed to involve the insulin receptor. However, the specific defects are not known. Diabetes mellitus cases due to a known defect are classified separately. Type 2 diabetes is the most common type of diabetes mellitus accounting for 95% of diabetes. Many people with type 2 diabetes have evidence of prediabetes (impaired fasting glucose and/or impaired glucose tolerance) before meeting the criteria for type 2 diabetes. The progression of prediabetes to overt type 2 diabetes can be slowed or reversed by lifestyle changes or medications that improve insulin sensitivity or reduce the liver's glucose production.Type 2 diabetes is primarily due to lifestyle factors and genetics. A number of lifestyle factors are known to be important to the development of type 2 diabetes, including obesity (defined by a body mass index of greater than 30), lack of physical activity, poor diet, stress, and urbanization. Excess body fat is associated with 30% of cases in people of Chinese and Japanese descent, 60–80% of cases in those of European and African descent, and 100% of Pima Indians and Pacific Islanders. Even those who are not obese may have a high waist–hip ratio.Dietary factors such as sugar-sweetened drinks are associated with an increased risk. The type of fats in the diet is also important, with saturated fat and trans fats increasing the risk and polyunsaturated and monounsaturated fat decreasing the risk. Eating white rice excessively may increase the risk of diabetes, especially in Chinese and Japanese people. Lack of physical activity may increase the risk of diabetes in some people.Adverse childhood experiences, including abuse, neglect, and household difficulties, increase the likelihood of type 2 diabetes later in life by 32%, with neglect having the strongest effect.Antipsychotic medication side effects (specifically metabolic abnormalities, dyslipidemia and weight gain) and unhealthy lifestyles (including poor diet and decreased physical activity), are potential risk factors.
Gestational diabetes
Gestational diabetes resembles type 2 diabetes in several respects, involving a combination of relatively inadequate insulin secretion and responsiveness. It occurs in about 2–10% of all pregnancies and may improve or disappear after delivery. It is recommended that all pregnant women get tested starting around 24–28 weeks gestation. It is most often diagnosed in the second or third trimester because of the increase in insulin-antagonist hormone levels that occurs at this time. However, after pregnancy approximately 5–10% of women with gestational diabetes are found to have another form of diabetes, most commonly type 2. Gestational diabetes is fully treatable, but requires careful medical supervision throughout the pregnancy. Management may include dietary changes, blood glucose monitoring, and in some cases, insulin may be required.Though it may be transient, untreated gestational diabetes can damage the health of the fetus or mother. Risks to the baby include macrosomia (high birth weight), congenital heart and central nervous system abnormalities, and skeletal muscle malformations. Increased levels of insulin in a fetus's blood may inhibit fetal surfactant production and cause infant respiratory distress syndrome. A high blood bilirubin level may result from red blood cell destruction. In severe cases, perinatal death may occur, most commonly as a result of poor placental perfusion due to vascular impairment. Labor induction may be indicated with decreased placental function. A caesarean section may be performed if there is marked fetal distress or an increased risk of injury associated with macrosomia, such as shoulder dystocia.
Other types
Maturity onset diabetes of the young (MODY) is a rare autosomal dominant inherited form of diabetes, due to one of several single-gene mutations causing defects in insulin production. It is significantly less common than the three main types, constituting 1–2% of all cases. The name of this disease refers to early hypotheses as to its nature. Being due to a defective gene, this disease varies in age at presentation and in severity according to the specific gene defect; thus, there are at least 13 subtypes of MODY. People with MODY often can control it without using insulin.Some cases of diabetes are caused by the body's tissue receptors not responding to insulin (even when insulin levels are normal, which is what separates it from type 2 diabetes); this form is very uncommon. Genetic mutations (autosomal or mitochondrial) can lead to defects in beta cell function. Abnormal insulin action may also have been genetically determined in some cases. Any disease that causes extensive damage to the pancreas may lead to diabetes (for example, chronic pancreatitis and cystic fibrosis). Diseases associated with excessive secretion of insulin-antagonistic hormones can cause diabetes (which is typically resolved once the hormone excess is removed). Many drugs impair insulin secretion and some toxins damage pancreatic beta cells, whereas others increase insulin resistance (especially glucocorticoids which can provoke "steroid diabetes"). The ICD-10 (1992) diagnostic entity, malnutrition-related diabetes mellitus (ICD-10 code E12), was deprecated by the World Health Organization (WHO) when the current taxonomy was introduced in 1999.
Yet another form of diabetes that people may develop is double diabetes. This is when a type 1 diabetic becomes insulin resistant, the hallmark for type 2 diabetes or has a family history for type 2 diabetes. It was first discovered in 1990 or 1991.
The following is a list of disorders that may increase the risk of diabetes:
Pathophysiology
Insulin is the principal hormone that regulates the uptake of glucose from the blood into most cells of the body, especially liver, adipose tissue and muscle, except smooth muscle, in which insulin acts via the IGF-1. Therefore, deficiency of insulin or the insensitivity of its receptors play a central role in all forms of diabetes mellitus.The body obtains glucose from three main sources: the intestinal absorption of food; the breakdown of glycogen (glycogenolysis), the storage form of glucose found in the liver; and gluconeogenesis, the generation of glucose from non-carbohydrate substrates in the body. Insulin plays a critical role in regulating glucose levels in the body. Insulin can inhibit the breakdown of glycogen or the process of gluconeogenesis, it can stimulate the transport of glucose into fat and muscle cells, and it can stimulate the storage of glucose in the form of glycogen.Insulin is released into the blood by beta cells (β-cells), found in the islets of Langerhans in the pancreas, in response to rising levels of blood glucose, typically after eating. Insulin is used by about two-thirds of the body's cells to absorb glucose from the blood for use as fuel, for conversion to other needed molecules, or for storage. Lower glucose levels result in decreased insulin release from the beta cells and in the breakdown of glycogen to glucose. This process is mainly controlled by the hormone glucagon, which acts in the opposite manner to insulin.If the amount of insulin available is insufficient, or if cells respond poorly to the effects of insulin (insulin resistance), or if the insulin itself is defective, then glucose is not absorbed properly by the body cells that require it, and is not stored appropriately in the liver and muscles. The net effect is persistently high levels of blood glucose, poor protein synthesis, and other metabolic derangements, such as metabolic acidosis in cases of complete insulin deficiency.When glucose concentration in the blood remains high over time, the kidneys reach a threshold of reabsorption, and the body excretes glucose in the urine (glycosuria). This increases the osmotic pressure of the urine and inhibits reabsorption of water by the kidney, resulting in increased urine production (polyuria) and increased fluid loss. Lost blood volume is replaced osmotically from water in body cells and other body compartments, causing dehydration and increased thirst (polydipsia). In addition, intracellular glucose deficiency stimulates appetite leading to excessive food intake (polyphagia).
Diagnosis
Diabetes mellitus is diagnosed with a test for the glucose content in the blood, and is diagnosed by demonstrating any one of the following:
Fasting plasma glucose level ≥ 7.0 mmol/L (126 mg/dL). For this test, blood is taken after a period of fasting, i.e. in the morning before breakfast, after the patient had sufficient time to fast overnight.
Plasma glucose ≥ 11.1 mmol/L (200 mg/dL) two hours after a 75 gram oral glucose load as in a glucose tolerance test (OGTT)
Symptoms of high blood sugar and plasma glucose ≥ 11.1 mmol/L (200 mg/dL) either while fasting or not fasting
Glycated hemoglobin (HbA1C) ≥ 48 mmol/mol (≥ 6.5 DCCT %).A positive result, in the absence of unequivocal high blood sugar, should be confirmed by a repeat of any of the above methods on a different day. It is preferable to measure a fasting glucose level because of the ease of measurement and the considerable time commitment of formal glucose tolerance testing, which takes two hours to complete and offers no prognostic advantage over the fasting test. According to the current definition, two fasting glucose measurements at or above 7.0 mmol/L (126 mg/dL) is considered diagnostic for diabetes mellitus.
Per the WHO, people with fasting glucose levels from 6.1 to 6.9 mmol/L (110 to 125 mg/dL) are considered to have impaired fasting glucose. People with plasma glucose at or above 7.8 mmol/L (140 mg/dL), but not over 11.1 mmol/L (200 mg/dL), two hours after a 75 gram oral glucose load are considered to have impaired glucose tolerance. Of these two prediabetic states, the latter in particular is a major risk factor for progression to full-blown diabetes mellitus, as well as cardiovascular disease. The American Diabetes Association (ADA) since 2003 uses a slightly different range for impaired fasting glucose of 5.6 to 6.9 mmol/L (100 to 125 mg/dL).Glycated hemoglobin is better than fasting glucose for determining risks of cardiovascular disease and death from any cause.
Prevention
There is no known preventive measure for type 1 diabetes. Type 2 diabetes—which accounts for 85–90% of all cases worldwide—can often be prevented or delayed by maintaining a normal body weight, engaging in physical activity, and eating a healthy diet. Higher levels of physical activity (more than 90 minutes per day) reduce the risk of diabetes by 28%. Dietary changes known to be effective in helping to prevent diabetes include maintaining a diet rich in whole grains and fiber, and choosing good fats, such as the polyunsaturated fats found in nuts, vegetable oils, and fish. Limiting sugary beverages and eating less red meat and other sources of saturated fat can also help prevent diabetes. Tobacco smoking is also associated with an increased risk of diabetes and its complications, so smoking cessation can be an important preventive measure as well.The relationship between type 2 diabetes and the main modifiable risk factors (excess weight, unhealthy diet, physical inactivity and tobacco use) is similar in all regions of the world. There is growing evidence that the underlying determinants of diabetes are a reflection of the major forces driving social, economic and cultural change: globalization, urbanization, population aging, and the general health policy environment.
Management
Diabetes management concentrates on keeping blood sugar levels close to normal, without causing low blood sugar. This can usually be accomplished with dietary changes, exercise, weight loss, and use of appropriate medications (insulin, oral medications).Learning about the disease and actively participating in the treatment is important, since complications are far less common and less severe in people who have well-managed blood sugar levels. The goal of treatment is an A1C level below 5.7%. Attention is also paid to other health problems that may accelerate the negative effects of diabetes. These include smoking, high blood pressure, metabolic syndrome obesity, and lack of regular exercise. Specialized footwear is widely used to reduce the risk of diabetic foot ulcers by relieving the pressure on the foot. Foot examination for patients living with diabetes should be done annually which includes sensation testing, foot biomechanics, vascular integrity and foot structure.Concerning those with severe mental illness, the efficacy of type 2 diabetes self-management interventions is still poorly explored, with insufficient scientific evidence to show whether these interventions have similar results to those observed in the general population.
Lifestyle
People with diabetes can benefit from education about the disease and treatment, dietary changes, and exercise, with the goal of keeping both short-term and long-term blood glucose levels within acceptable bounds. In addition, given the associated higher risks of cardiovascular disease, lifestyle modifications are recommended to control blood pressure.Weight loss can prevent progression from prediabetes to diabetes type 2, decrease the risk of cardiovascular disease, or result in a partial remission in people with diabetes. No single dietary pattern is best for all people with diabetes. Healthy dietary patterns, such as the Mediterranean diet, low-carbohydrate diet, or DASH diet, are often recommended, although evidence does not support one over the others. According to the ADA, "reducing overall carbohydrate intake for individuals with diabetes has demonstrated the most evidence for improving glycemia", and for individuals with type 2 diabetes who cannot meet the glycemic targets or where reducing anti-glycemic medications is a priority, low or very-low carbohydrate diets are a viable approach. For overweight people with type 2 diabetes, any diet that achieves weight loss is effective.A 2020 Cochrane systematic review compared several non-nutritive sweeteners to sugar, placebo and a nutritive low-calorie sweetener (tagatose), but the results were unclear for effects on HbA1c, body weight and adverse events. The studies included were mainly of very low-certainty and did not report on health-related quality of life, diabetes complications, all-cause mortality or socioeconomic effects.
Medications
Glucose control
Most medications used to treat diabetes act by lowering blood sugar levels through different mechanisms. There is broad consensus that when people with diabetes maintain tight glucose control – keeping the glucose levels in their blood within normal ranges – they experience fewer complications, such as kidney problems or eye problems. There is however debate as to whether this is appropriate and cost effective for people later in life in whom the risk of hypoglycemia may be more significant.There are a number of different classes of anti-diabetic medications. Type 1 diabetes requires treatment with insulin, ideally using a "basal bolus" regimen that most closely matches normal insulin release: long-acting insulin for the basal rate and short-acting insulin with meals. Type 2 diabetes is generally treated with medication that is taken by mouth (e.g. metformin) although some eventually require injectable treatment with insulin or GLP-1 agonists.Metformin is generally recommended as a first-line treatment for type 2 diabetes, as there is good evidence that it decreases mortality. It works by decreasing the liver's production of glucose, and increasing the amount of glucose stored in peripheral tissue. Several other groups of drugs, mainly oral medication, may also decrease blood sugar in type 2 diabetes. These include agents that increase insulin release (sulfonylureas), agents that decrease absorption of sugar from the intestines (acarbose), agents that inhibit the enzyme dipeptidyl peptidase-4 (DPP-4) that inactivates incretins such as GLP-1 and GIP (sitagliptin), agents that make the body more sensitive to insulin (thiazolidinedione) and agents that increase the excretion of glucose in the urine (SGLT2 inhibitors). When insulin is used in type 2 diabetes, a long-acting formulation is usually added initially, while continuing oral medications.Some severe cases of type 2 diabetes may also be treated with insulin, which is increased gradually until glucose targets are reached.
Blood pressure lowering
Cardiovascular disease is a serious complication associated with diabetes, and many international guidelines recommend blood pressure treatment targets that are lower than 140/90 mmHg for people with diabetes. However, there is only limited evidence regarding what the lower targets should be. A 2016 systematic review found potential harm to treating to targets lower than 140 mmHg, and a subsequent systematic review in 2019 found no evidence of additional benefit from blood pressure lowering to between 130 – 140mmHg, although there was an increased risk of adverse events.2015 American Diabetes Association recommendations are that people with diabetes and albuminuria should receive an inhibitor of the renin-angiotensin system to reduce the risks of progression to end-stage renal disease, cardiovascular events, and death. There is some evidence that angiotensin converting enzyme inhibitors (ACEIs) are superior to other inhibitors of the renin-angiotensin system such as angiotensin receptor blockers (ARBs), or aliskiren in preventing cardiovascular disease. Although a more recent review found similar effects of ACEIs and ARBs on major cardiovascular and renal outcomes. There is no evidence that combining ACEIs and ARBs provides additional benefits.
Aspirin
The use of aspirin to prevent cardiovascular disease in diabetes is controversial. Aspirin is recommended by some in people at high risk of cardiovascular disease, however routine use of aspirin has not been found to improve outcomes in uncomplicated diabetes. 2015 American Diabetes Association recommendations for aspirin use (based on expert consensus or clinical experience) are that low-dose aspirin use is reasonable in adults with diabetes who are at intermediate risk of cardiovascular disease (10-year cardiovascular disease risk, 5–10%). National guidelines for England and Wales by the National Institute for Health and Care Excellence (NICE) recommend against the use of aspirin in people with type 1 or type 2 diabetes who do not have confirmed cardiovascular disease.
Surgery
Weight loss surgery in those with obesity and type 2 diabetes is often an effective measure. Many are able to maintain normal blood sugar levels with little or no medications following surgery and long-term mortality is decreased. There is, however, a short-term mortality risk of less than 1% from the surgery. The body mass index cutoffs for when surgery is appropriate are not yet clear. It is recommended that this option be considered in those who are unable to get both their weight and blood sugar under control.A pancreas transplant is occasionally considered for people with type 1 diabetes who have severe complications of their disease, including end stage kidney disease requiring kidney transplantation.
Self-management and support
In countries using a general practitioner system, such as the United Kingdom, care may take place mainly outside hospitals, with hospital-based specialist care used only in case of complications, difficult blood sugar control, or research projects. In other circumstances, general practitioners and specialists share care in a team approach. Home telehealth support can be an effective management technique.The use of technology to deliver educational programs for adults with type 2 diabetes includes computer-based self-management interventions to collect for tailored responses to facilitate self-management. There is no adequate evidence to support effects on cholesterol, blood pressure, behavioral change (such as physical activity levels and dietary), depression, weight and health-related quality of life, nor in other biological, cognitive or emotional outcomes.
Epidemiology
In 2017, 425 million people had diabetes worldwide, up from an estimated 382 million people in 2013 and from 108 million in 1980. Accounting for the shifting age structure of the global population, the prevalence of diabetes is 8.8% among adults, nearly double the rate of 4.7% in 1980. Type 2 makes up about 90% of the cases. Some data indicate rates are roughly equal in women and men, but male excess in diabetes has been found in many populations with higher type 2 incidence, possibly due to sex-related differences in insulin sensitivity, consequences of obesity and regional body fat deposition, and other contributing factors such as high blood pressure, tobacco smoking, and alcohol intake.The WHO estimates that diabetes resulted in 1.5 million deaths in 2012, making it the 8th leading cause of death. However another 2.2 million deaths worldwide were attributable to high blood glucose and the increased risks of cardiovascular disease and other associated complications (e.g. kidney failure), which often lead to premature death and are often listed as the underlying cause on death certificates rather than diabetes. For example, in 2017, the International Diabetes Federation (IDF) estimated that diabetes resulted in 4.0 million deaths worldwide, using modeling to estimate the total number of deaths that could be directly or indirectly attributed to diabetes.Diabetes occurs throughout the world but is more common (especially type 2) in more developed countries. The greatest increase in rates has however been seen in low- and middle-income countries, where more than 80% of diabetic deaths occur. The fastest prevalence increase is expected to occur in Asia and Africa, where most people with diabetes will probably live in 2030. The increase in rates in developing countries follows the trend of urbanization and lifestyle changes, including increasingly sedentary lifestyles, less physically demanding work and the global nutrition transition, marked by increased intake of foods that are high energy-dense but nutrient-poor (often high in sugar and saturated fats, sometimes referred to as the "Western-style" diet). The global number of diabetes cases might increase by 48% between 2017 and 2045.As of 2020, 38% of all US adults had prediabetes. Prediabetes is an early stage of diabetes.
History
Diabetes was one of the first diseases described, with an Egyptian manuscript from c. 1500 BCE mentioning "too great emptying of the urine." The Ebers papyrus includes a recommendation for a drink to take in such cases. The first described cases are believed to have been type 1 diabetes. Indian physicians around the same time identified the disease and classified it as madhumeha or "honey urine", noting the urine would attract ants.The term "diabetes" or "to pass through" was first used in 230 BCE by the Greek Apollonius of Memphis. The disease was considered rare during the time of the Roman empire, with Galen commenting he had only seen two cases during his career. This is possibly due to the diet and lifestyle of the ancients, or because the clinical symptoms were observed during the advanced stage of the disease. Galen named the disease "diarrhea of the urine" (diarrhea urinosa).The earliest surviving work with a detailed reference to diabetes is that of Aretaeus of Cappadocia (2nd or early 3rd century CE). He described the symptoms and the course of the disease, which he attributed to the moisture and coldness, reflecting the beliefs of the "Pneumatic School". He hypothesized a correlation between diabetes and other diseases, and he discussed differential diagnosis from the snakebite, which also provokes excessive thirst. His work remained unknown in the West until 1552, when the first Latin edition was published in Venice.Two types of diabetes were identified as separate conditions for the first time by the Indian physicians Sushruta and Charaka in 400–500 CE with one type being associated with youth and another type with being overweight. Effective treatment was not developed until the early part of the 20th century when Canadians Frederick Banting and Charles Herbert Best isolated and purified insulin in 1921 and 1922. This was followed by the development of the long-acting insulin NPH in the 1940s.
Etymology
The word diabetes ( or ) comes from Latin diabētēs, which in turn comes from Ancient Greek διαβήτης (diabētēs), which literally means "a passer through; a siphon". Ancient Greek physician Aretaeus of Cappadocia (fl. 1st century CE) used that word, with the intended meaning "excessive discharge of urine", as the name for the disease. Ultimately, the word comes from Greek διαβαίνειν (diabainein), meaning "to pass through", which is composed of δια- (dia-), meaning "through" and βαίνειν (bainein), meaning "to go". The word "diabetes" is first recorded in English, in the form diabete, in a medical text written around 1425.
The word mellitus ( or ) comes from the classical Latin word mellītus, meaning "mellite" (i.e. sweetened with honey; honey-sweet). The Latin word comes from mell-, which comes from mel, meaning "honey"; sweetness; pleasant thing, and the suffix -ītus, whose meaning is the same as that of the English suffix "-ite". It was Thomas Willis who in 1675 added "mellitus" to the word "diabetes" as a designation for the disease, when he noticed the urine of a person with diabetes had a sweet taste (glycosuria). This sweet taste had been noticed in urine by the ancient Greeks, Chinese, Egyptians, Indians, and Persians.
Society and culture
The 1989 "St. Vincent Declaration" was the result of international efforts to improve the care accorded to those with diabetes. Doing so is important not only in terms of quality of life and life expectancy but also economically – expenses due to diabetes have been shown to be a major drain on health – and productivity-related resources for healthcare systems and governments.
Several countries established more and less successful national diabetes programmes to improve treatment of the disease.People with diabetes who have neuropathic symptoms such as numbness or tingling in feet or hands are twice as likely to be unemployed as those without the symptoms.In 2010, diabetes-related emergency room (ER) visit rates in the United States were higher among people from the lowest income communities (526 per 10,000 population) than from the highest income communities (236 per 10,000 population). Approximately 9.4% of diabetes-related ER visits were for the uninsured.
Naming
The term "type 1 diabetes" has replaced several former terms, including childhood-onset diabetes, juvenile diabetes, and insulin-dependent diabetes mellitus. Likewise, the term "type 2 diabetes" has replaced several former terms, including adult-onset diabetes, obesity-related diabetes, and noninsulin-dependent diabetes mellitus. Beyond these two types, there is no agreed-upon standard nomenclature.Diabetes mellitus is also occasionally known as "sugar diabetes" to differentiate it from diabetes insipidus.
Other animals
Diabetes can occur in mammals or reptiles. Birds do not develop diabetes because of their unusually high tolerance for elevated blood glucose levels.In animals, diabetes is most commonly encountered in dogs and cats. Middle-aged animals are most commonly affected. Female dogs are twice as likely to be affected as males, while according to some sources, male cats are more prone than females. In both species, all breeds may be affected, but some small dog breeds are particularly likely to develop diabetes, such as Miniature Poodles.Feline diabetes is strikingly similar to human type 2 diabetes. The Burmese, Russian Blue, Abyssinian, and Norwegian Forest cat breeds are at higher risk than other breeds. Overweight cats are also at higher risk.The symptoms may relate to fluid loss and polyuria, but the course may also be insidious. Diabetic animals are more prone to infections. The long-term complications recognized in humans are much rarer in animals. The principles of treatment (weight loss, oral antidiabetics, subcutaneous insulin) and management of emergencies (e.g. ketoacidosis) are similar to those in humans.
References
External links
American Diabetes Association
IDF Diabetes Atlas
National Diabetes Education Program
ADA's Standards of Medical Care in Diabetes 2019
Polonsky KS (October 2012). "The past 200 years in diabetes". The New England Journal of Medicine. 367 (14): 1332–1340. doi:10.1056/NEJMra1110560. PMID 23034021. S2CID 9456681.
"Diabetes". MedlinePlus. U.S. National Library of Medicine.
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Diabetes, also known as diabetes mellitus, is a group of common endocrine diseases characterized by sustained high blood sugar levels. Diabetes is due to either the pancreas not producing enough insulin, or the cells of the body not responding properly to the insulin produced. Diabetes, if left untreated, leads to many health complications. Untreated or poorly treated diabetes accounts for approximately 1.5 million deaths per year.There is no widely accepted cure for most cases of diabetes. The most common treatment for type 1 diabetes is insulin replacement therapy (insulin injections). Anti-diabetic medications such as metformin and semaglutide, as well as lifestyle modifications, can be used to prevent or respond to type 2 diabetes. Gestational diabetes normally resolves shortly after delivery.
As of 2019, an estimated 463 million people had diabetes worldwide accounting for 8.8% of the adult population. Type 2 diabetes makes up about 90% of all diabetes cases. The prevalence of the disease continues to increase, most dramatically in low- and middle-income nations. Rates are similar in women and men, with diabetes being the 7th-leading cause of death globally. The global expenditure on diabetes-related healthcare is an estimated USD760 billion a year.
Signs and symptoms
The classic symptoms of untreated diabetes are unintended weight loss, polyuria (increased urination), polydipsia (increased thirst), and polyphagia (increased hunger). Symptoms may develop rapidly (weeks or months) in type 1 diabetes, while they usually develop much more slowly and may be subtle or absent in type 2 diabetes.Several other signs and symptoms can mark the onset of diabetes although they are not specific to the disease. In addition to the known symptoms listed above, they include blurred vision, headache, fatigue, slow healing of cuts, and itchy skin. Prolonged high blood glucose can cause glucose absorption in the lens of the eye, which leads to changes in its shape, resulting in vision changes. Long-term vision loss can also be caused by diabetic retinopathy. A number of skin rashes that can occur in diabetes are collectively known as diabetic dermadromes.
Diabetic emergencies
People with diabetes (usually but not exclusively in type 1 diabetes) may also experience diabetic ketoacidosis (DKA), a metabolic disturbance characterized by nausea, vomiting and abdominal pain, the smell of acetone on the breath, deep breathing known as Kussmaul breathing, and in severe cases a decreased level of consciousness. DKA requires emergency treatment in hospital. A rarer but more dangerous condition is hyperosmolar hyperglycemic state (HHS), which is more common in type 2 diabetes and is mainly the result of dehydration caused by high blood sugars.Treatment-related low blood sugar (hypoglycemia) is common in people with type 1 and also type 2 diabetes depending on the medication being used. Most cases are mild and are not considered medical emergencies. Effects can range from feelings of unease, sweating, trembling, and increased appetite in mild cases to more serious effects such as confusion, changes in behavior such as aggressiveness, seizures, unconsciousness, and rarely permanent brain damage or death in severe cases. Rapid breathing, sweating, and cold, pale skin are characteristic of low blood sugar but not definitive. Mild to moderate cases are self-treated by eating or drinking something high in rapidly absorbed carbohydrates. Severe cases can lead to unconsciousness and must be treated with intravenous glucose or injections with glucagon.
Complications
All forms of diabetes increase the risk of long-term complications. These typically develop after many years (10–20) but may be the first symptom in those who have otherwise not received a diagnosis before that time.The major long-term complications relate to damage to blood vessels. Diabetes doubles the risk of cardiovascular disease and about 75% of deaths in people with diabetes are due to coronary artery disease. Other macrovascular diseases include stroke, and peripheral artery disease. These complications are also a strong risk factor for severe COVID-19 illness.The primary complications of diabetes due to damage in small blood vessels include damage to the eyes, kidneys, and nerves. Damage to the eyes, known as diabetic retinopathy, is caused by damage to the blood vessels in the retina of the eye, and can result in gradual vision loss and eventual blindness. Diabetes also increases the risk of having glaucoma, cataracts, and other eye problems. It is recommended that people with diabetes visit an optometrist or ophthalmologist once a year. Damage to the kidneys, known as diabetic nephropathy, can lead to tissue scarring, urine protein loss, and eventually chronic kidney disease, sometimes requiring dialysis or kidney transplantation. Damage to the nerves of the body, known as diabetic neuropathy, is the most common complication of diabetes. The symptoms can include numbness, tingling, sudomotor dysfunction, pain, and altered pain sensation, which can lead to damage to the skin. Diabetes-related foot problems (such as diabetic foot ulcers) may occur, and can be difficult to treat, occasionally requiring amputation. Additionally, proximal diabetic neuropathy causes painful muscle atrophy and weakness.
There is a link between cognitive deficit and diabetes. Compared to those without diabetes, those with the disease have a 1.2 to 1.5-fold greater rate of decline in cognitive function. Having diabetes, especially when on insulin, increases the risk of falls in older people.
Causes
Diabetes mellitus is classified into six categories: type 1 diabetes, type 2 diabetes, hybrid forms of diabetes, hyperglycemia first detected during pregnancy, "unclassified diabetes", and "other specific types". "Hybrid forms of diabetes" include slowly evolving, immune-mediated diabetes of adults and ketosis-prone type 2 diabetes. "Hyperglycemia first detected during pregnancy" includes gestational diabetes mellitus and diabetes mellitus in pregnancy (type 1 or type 2 diabetes first diagnosed during pregnancy). The "other specific types" are a collection of a few dozen individual causes. Diabetes is a more variable disease than once thought and people may have combinations of forms.
Type 1
Type 1 diabetes is characterized by loss of the insulin-producing beta cells of the pancreatic islets, leading to insulin deficiency. This type can be further classified as immune-mediated or idiopathic. The majority of type 1 diabetes is of an immune-mediated nature, in which a T cell-mediated autoimmune attack leads to the loss of beta cells and thus insulin. It causes approximately 10% of diabetes mellitus cases in North America and Europe. Most affected people are otherwise healthy and of a healthy weight when onset occurs. Sensitivity and responsiveness to insulin are usually normal, especially in the early stages. Although it has been called "juvenile diabetes" due to the frequent onset in children, the majority of individuals living with type 1 diabetes are now adults."Brittle" diabetes, also known as unstable diabetes or labile diabetes, is a term that was traditionally used to describe the dramatic and recurrent swings in glucose levels, often occurring for no apparent reason in insulin-dependent diabetes. This term, however, has no biologic basis and should not be used. Still, type 1 diabetes can be accompanied by irregular and unpredictable high blood sugar levels, and the potential for diabetic ketoacidosis or serious low blood sugar levels. Other complications include an impaired counterregulatory response to low blood sugar, infection, gastroparesis (which leads to erratic absorption of dietary carbohydrates), and endocrinopathies (e.g., Addison's disease). These phenomena are believed to occur no more frequently than in 1% to 2% of persons with type 1 diabetes.
Type 1 diabetes is partly inherited, with multiple genes, including certain HLA genotypes, known to influence the risk of diabetes. In genetically susceptible people, the onset of diabetes can be triggered by one or more environmental factors, such as a viral infection or diet. Several viruses have been implicated, but to date there is no stringent evidence to support this hypothesis in humans.Type 1 diabetes can occur at any age, and a significant proportion is diagnosed during adulthood. Latent autoimmune diabetes of adults (LADA) is the diagnostic term applied when type 1 diabetes develops in adults; it has a slower onset than the same condition in children. Given this difference, some use the unofficial term "type 1.5 diabetes" for this condition. Adults with LADA are frequently initially misdiagnosed as having type 2 diabetes, based on age rather than a cause.
Type 2
Type 2 diabetes is characterized by insulin resistance, which may be combined with relatively reduced insulin secretion. The defective responsiveness of body tissues to insulin is believed to involve the insulin receptor. However, the specific defects are not known. Diabetes mellitus cases due to a known defect are classified separately. Type 2 diabetes is the most common type of diabetes mellitus accounting for 95% of diabetes. Many people with type 2 diabetes have evidence of prediabetes (impaired fasting glucose and/or impaired glucose tolerance) before meeting the criteria for type 2 diabetes. The progression of prediabetes to overt type 2 diabetes can be slowed or reversed by lifestyle changes or medications that improve insulin sensitivity or reduce the liver's glucose production.Type 2 diabetes is primarily due to lifestyle factors and genetics. A number of lifestyle factors are known to be important to the development of type 2 diabetes, including obesity (defined by a body mass index of greater than 30), lack of physical activity, poor diet, stress, and urbanization. Excess body fat is associated with 30% of cases in people of Chinese and Japanese descent, 60–80% of cases in those of European and African descent, and 100% of Pima Indians and Pacific Islanders. Even those who are not obese may have a high waist–hip ratio.Dietary factors such as sugar-sweetened drinks are associated with an increased risk. The type of fats in the diet is also important, with saturated fat and trans fats increasing the risk and polyunsaturated and monounsaturated fat decreasing the risk. Eating white rice excessively may increase the risk of diabetes, especially in Chinese and Japanese people. Lack of physical activity may increase the risk of diabetes in some people.Adverse childhood experiences, including abuse, neglect, and household difficulties, increase the likelihood of type 2 diabetes later in life by 32%, with neglect having the strongest effect.Antipsychotic medication side effects (specifically metabolic abnormalities, dyslipidemia and weight gain) and unhealthy lifestyles (including poor diet and decreased physical activity), are potential risk factors.
Gestational diabetes
Gestational diabetes resembles type 2 diabetes in several respects, involving a combination of relatively inadequate insulin secretion and responsiveness. It occurs in about 2–10% of all pregnancies and may improve or disappear after delivery. It is recommended that all pregnant women get tested starting around 24–28 weeks gestation. It is most often diagnosed in the second or third trimester because of the increase in insulin-antagonist hormone levels that occurs at this time. However, after pregnancy approximately 5–10% of women with gestational diabetes are found to have another form of diabetes, most commonly type 2. Gestational diabetes is fully treatable, but requires careful medical supervision throughout the pregnancy. Management may include dietary changes, blood glucose monitoring, and in some cases, insulin may be required.Though it may be transient, untreated gestational diabetes can damage the health of the fetus or mother. Risks to the baby include macrosomia (high birth weight), congenital heart and central nervous system abnormalities, and skeletal muscle malformations. Increased levels of insulin in a fetus's blood may inhibit fetal surfactant production and cause infant respiratory distress syndrome. A high blood bilirubin level may result from red blood cell destruction. In severe cases, perinatal death may occur, most commonly as a result of poor placental perfusion due to vascular impairment. Labor induction may be indicated with decreased placental function. A caesarean section may be performed if there is marked fetal distress or an increased risk of injury associated with macrosomia, such as shoulder dystocia.
Other types
Maturity onset diabetes of the young (MODY) is a rare autosomal dominant inherited form of diabetes, due to one of several single-gene mutations causing defects in insulin production. It is significantly less common than the three main types, constituting 1–2% of all cases. The name of this disease refers to early hypotheses as to its nature. Being due to a defective gene, this disease varies in age at presentation and in severity according to the specific gene defect; thus, there are at least 13 subtypes of MODY. People with MODY often can control it without using insulin.Some cases of diabetes are caused by the body's tissue receptors not responding to insulin (even when insulin levels are normal, which is what separates it from type 2 diabetes); this form is very uncommon. Genetic mutations (autosomal or mitochondrial) can lead to defects in beta cell function. Abnormal insulin action may also have been genetically determined in some cases. Any disease that causes extensive damage to the pancreas may lead to diabetes (for example, chronic pancreatitis and cystic fibrosis). Diseases associated with excessive secretion of insulin-antagonistic hormones can cause diabetes (which is typically resolved once the hormone excess is removed). Many drugs impair insulin secretion and some toxins damage pancreatic beta cells, whereas others increase insulin resistance (especially glucocorticoids which can provoke "steroid diabetes"). The ICD-10 (1992) diagnostic entity, malnutrition-related diabetes mellitus (ICD-10 code E12), was deprecated by the World Health Organization (WHO) when the current taxonomy was introduced in 1999.
Yet another form of diabetes that people may develop is double diabetes. This is when a type 1 diabetic becomes insulin resistant, the hallmark for type 2 diabetes or has a family history for type 2 diabetes. It was first discovered in 1990 or 1991.
The following is a list of disorders that may increase the risk of diabetes:
Pathophysiology
Insulin is the principal hormone that regulates the uptake of glucose from the blood into most cells of the body, especially liver, adipose tissue and muscle, except smooth muscle, in which insulin acts via the IGF-1. Therefore, deficiency of insulin or the insensitivity of its receptors play a central role in all forms of diabetes mellitus.The body obtains glucose from three main sources: the intestinal absorption of food; the breakdown of glycogen (glycogenolysis), the storage form of glucose found in the liver; and gluconeogenesis, the generation of glucose from non-carbohydrate substrates in the body. Insulin plays a critical role in regulating glucose levels in the body. Insulin can inhibit the breakdown of glycogen or the process of gluconeogenesis, it can stimulate the transport of glucose into fat and muscle cells, and it can stimulate the storage of glucose in the form of glycogen.Insulin is released into the blood by beta cells (β-cells), found in the islets of Langerhans in the pancreas, in response to rising levels of blood glucose, typically after eating. Insulin is used by about two-thirds of the body's cells to absorb glucose from the blood for use as fuel, for conversion to other needed molecules, or for storage. Lower glucose levels result in decreased insulin release from the beta cells and in the breakdown of glycogen to glucose. This process is mainly controlled by the hormone glucagon, which acts in the opposite manner to insulin.If the amount of insulin available is insufficient, or if cells respond poorly to the effects of insulin (insulin resistance), or if the insulin itself is defective, then glucose is not absorbed properly by the body cells that require it, and is not stored appropriately in the liver and muscles. The net effect is persistently high levels of blood glucose, poor protein synthesis, and other metabolic derangements, such as metabolic acidosis in cases of complete insulin deficiency.When glucose concentration in the blood remains high over time, the kidneys reach a threshold of reabsorption, and the body excretes glucose in the urine (glycosuria). This increases the osmotic pressure of the urine and inhibits reabsorption of water by the kidney, resulting in increased urine production (polyuria) and increased fluid loss. Lost blood volume is replaced osmotically from water in body cells and other body compartments, causing dehydration and increased thirst (polydipsia). In addition, intracellular glucose deficiency stimulates appetite leading to excessive food intake (polyphagia).
Diagnosis
Diabetes mellitus is diagnosed with a test for the glucose content in the blood, and is diagnosed by demonstrating any one of the following:
Fasting plasma glucose level ≥ 7.0 mmol/L (126 mg/dL). For this test, blood is taken after a period of fasting, i.e. in the morning before breakfast, after the patient had sufficient time to fast overnight.
Plasma glucose ≥ 11.1 mmol/L (200 mg/dL) two hours after a 75 gram oral glucose load as in a glucose tolerance test (OGTT)
Symptoms of high blood sugar and plasma glucose ≥ 11.1 mmol/L (200 mg/dL) either while fasting or not fasting
Glycated hemoglobin (HbA1C) ≥ 48 mmol/mol (≥ 6.5 DCCT %).A positive result, in the absence of unequivocal high blood sugar, should be confirmed by a repeat of any of the above methods on a different day. It is preferable to measure a fasting glucose level because of the ease of measurement and the considerable time commitment of formal glucose tolerance testing, which takes two hours to complete and offers no prognostic advantage over the fasting test. According to the current definition, two fasting glucose measurements at or above 7.0 mmol/L (126 mg/dL) is considered diagnostic for diabetes mellitus.
Per the WHO, people with fasting glucose levels from 6.1 to 6.9 mmol/L (110 to 125 mg/dL) are considered to have impaired fasting glucose. People with plasma glucose at or above 7.8 mmol/L (140 mg/dL), but not over 11.1 mmol/L (200 mg/dL), two hours after a 75 gram oral glucose load are considered to have impaired glucose tolerance. Of these two prediabetic states, the latter in particular is a major risk factor for progression to full-blown diabetes mellitus, as well as cardiovascular disease. The American Diabetes Association (ADA) since 2003 uses a slightly different range for impaired fasting glucose of 5.6 to 6.9 mmol/L (100 to 125 mg/dL).Glycated hemoglobin is better than fasting glucose for determining risks of cardiovascular disease and death from any cause.
Prevention
There is no known preventive measure for type 1 diabetes. Type 2 diabetes—which accounts for 85–90% of all cases worldwide—can often be prevented or delayed by maintaining a normal body weight, engaging in physical activity, and eating a healthy diet. Higher levels of physical activity (more than 90 minutes per day) reduce the risk of diabetes by 28%. Dietary changes known to be effective in helping to prevent diabetes include maintaining a diet rich in whole grains and fiber, and choosing good fats, such as the polyunsaturated fats found in nuts, vegetable oils, and fish. Limiting sugary beverages and eating less red meat and other sources of saturated fat can also help prevent diabetes. Tobacco smoking is also associated with an increased risk of diabetes and its complications, so smoking cessation can be an important preventive measure as well.The relationship between type 2 diabetes and the main modifiable risk factors (excess weight, unhealthy diet, physical inactivity and tobacco use) is similar in all regions of the world. There is growing evidence that the underlying determinants of diabetes are a reflection of the major forces driving social, economic and cultural change: globalization, urbanization, population aging, and the general health policy environment.
Management
Diabetes management concentrates on keeping blood sugar levels close to normal, without causing low blood sugar. This can usually be accomplished with dietary changes, exercise, weight loss, and use of appropriate medications (insulin, oral medications).Learning about the disease and actively participating in the treatment is important, since complications are far less common and less severe in people who have well-managed blood sugar levels. The goal of treatment is an A1C level below 5.7%. Attention is also paid to other health problems that may accelerate the negative effects of diabetes. These include smoking, high blood pressure, metabolic syndrome obesity, and lack of regular exercise. Specialized footwear is widely used to reduce the risk of diabetic foot ulcers by relieving the pressure on the foot. Foot examination for patients living with diabetes should be done annually which includes sensation testing, foot biomechanics, vascular integrity and foot structure.Concerning those with severe mental illness, the efficacy of type 2 diabetes self-management interventions is still poorly explored, with insufficient scientific evidence to show whether these interventions have similar results to those observed in the general population.
Lifestyle
People with diabetes can benefit from education about the disease and treatment, dietary changes, and exercise, with the goal of keeping both short-term and long-term blood glucose levels within acceptable bounds. In addition, given the associated higher risks of cardiovascular disease, lifestyle modifications are recommended to control blood pressure.Weight loss can prevent progression from prediabetes to diabetes type 2, decrease the risk of cardiovascular disease, or result in a partial remission in people with diabetes. No single dietary pattern is best for all people with diabetes. Healthy dietary patterns, such as the Mediterranean diet, low-carbohydrate diet, or DASH diet, are often recommended, although evidence does not support one over the others. According to the ADA, "reducing overall carbohydrate intake for individuals with diabetes has demonstrated the most evidence for improving glycemia", and for individuals with type 2 diabetes who cannot meet the glycemic targets or where reducing anti-glycemic medications is a priority, low or very-low carbohydrate diets are a viable approach. For overweight people with type 2 diabetes, any diet that achieves weight loss is effective.A 2020 Cochrane systematic review compared several non-nutritive sweeteners to sugar, placebo and a nutritive low-calorie sweetener (tagatose), but the results were unclear for effects on HbA1c, body weight and adverse events. The studies included were mainly of very low-certainty and did not report on health-related quality of life, diabetes complications, all-cause mortality or socioeconomic effects.
Medications
Glucose control
Most medications used to treat diabetes act by lowering blood sugar levels through different mechanisms. There is broad consensus that when people with diabetes maintain tight glucose control – keeping the glucose levels in their blood within normal ranges – they experience fewer complications, such as kidney problems or eye problems. There is however debate as to whether this is appropriate and cost effective for people later in life in whom the risk of hypoglycemia may be more significant.There are a number of different classes of anti-diabetic medications. Type 1 diabetes requires treatment with insulin, ideally using a "basal bolus" regimen that most closely matches normal insulin release: long-acting insulin for the basal rate and short-acting insulin with meals. Type 2 diabetes is generally treated with medication that is taken by mouth (e.g. metformin) although some eventually require injectable treatment with insulin or GLP-1 agonists.Metformin is generally recommended as a first-line treatment for type 2 diabetes, as there is good evidence that it decreases mortality. It works by decreasing the liver's production of glucose, and increasing the amount of glucose stored in peripheral tissue. Several other groups of drugs, mainly oral medication, may also decrease blood sugar in type 2 diabetes. These include agents that increase insulin release (sulfonylureas), agents that decrease absorption of sugar from the intestines (acarbose), agents that inhibit the enzyme dipeptidyl peptidase-4 (DPP-4) that inactivates incretins such as GLP-1 and GIP (sitagliptin), agents that make the body more sensitive to insulin (thiazolidinedione) and agents that increase the excretion of glucose in the urine (SGLT2 inhibitors). When insulin is used in type 2 diabetes, a long-acting formulation is usually added initially, while continuing oral medications.Some severe cases of type 2 diabetes may also be treated with insulin, which is increased gradually until glucose targets are reached.
Blood pressure lowering
Cardiovascular disease is a serious complication associated with diabetes, and many international guidelines recommend blood pressure treatment targets that are lower than 140/90 mmHg for people with diabetes. However, there is only limited evidence regarding what the lower targets should be. A 2016 systematic review found potential harm to treating to targets lower than 140 mmHg, and a subsequent systematic review in 2019 found no evidence of additional benefit from blood pressure lowering to between 130 – 140mmHg, although there was an increased risk of adverse events.2015 American Diabetes Association recommendations are that people with diabetes and albuminuria should receive an inhibitor of the renin-angiotensin system to reduce the risks of progression to end-stage renal disease, cardiovascular events, and death. There is some evidence that angiotensin converting enzyme inhibitors (ACEIs) are superior to other inhibitors of the renin-angiotensin system such as angiotensin receptor blockers (ARBs), or aliskiren in preventing cardiovascular disease. Although a more recent review found similar effects of ACEIs and ARBs on major cardiovascular and renal outcomes. There is no evidence that combining ACEIs and ARBs provides additional benefits.
Aspirin
The use of aspirin to prevent cardiovascular disease in diabetes is controversial. Aspirin is recommended by some in people at high risk of cardiovascular disease, however routine use of aspirin has not been found to improve outcomes in uncomplicated diabetes. 2015 American Diabetes Association recommendations for aspirin use (based on expert consensus or clinical experience) are that low-dose aspirin use is reasonable in adults with diabetes who are at intermediate risk of cardiovascular disease (10-year cardiovascular disease risk, 5–10%). National guidelines for England and Wales by the National Institute for Health and Care Excellence (NICE) recommend against the use of aspirin in people with type 1 or type 2 diabetes who do not have confirmed cardiovascular disease.
Surgery
Weight loss surgery in those with obesity and type 2 diabetes is often an effective measure. Many are able to maintain normal blood sugar levels with little or no medications following surgery and long-term mortality is decreased. There is, however, a short-term mortality risk of less than 1% from the surgery. The body mass index cutoffs for when surgery is appropriate are not yet clear. It is recommended that this option be considered in those who are unable to get both their weight and blood sugar under control.A pancreas transplant is occasionally considered for people with type 1 diabetes who have severe complications of their disease, including end stage kidney disease requiring kidney transplantation.
Self-management and support
In countries using a general practitioner system, such as the United Kingdom, care may take place mainly outside hospitals, with hospital-based specialist care used only in case of complications, difficult blood sugar control, or research projects. In other circumstances, general practitioners and specialists share care in a team approach. Home telehealth support can be an effective management technique.The use of technology to deliver educational programs for adults with type 2 diabetes includes computer-based self-management interventions to collect for tailored responses to facilitate self-management. There is no adequate evidence to support effects on cholesterol, blood pressure, behavioral change (such as physical activity levels and dietary), depression, weight and health-related quality of life, nor in other biological, cognitive or emotional outcomes.
Epidemiology
In 2017, 425 million people had diabetes worldwide, up from an estimated 382 million people in 2013 and from 108 million in 1980. Accounting for the shifting age structure of the global population, the prevalence of diabetes is 8.8% among adults, nearly double the rate of 4.7% in 1980. Type 2 makes up about 90% of the cases. Some data indicate rates are roughly equal in women and men, but male excess in diabetes has been found in many populations with higher type 2 incidence, possibly due to sex-related differences in insulin sensitivity, consequences of obesity and regional body fat deposition, and other contributing factors such as high blood pressure, tobacco smoking, and alcohol intake.The WHO estimates that diabetes resulted in 1.5 million deaths in 2012, making it the 8th leading cause of death. However another 2.2 million deaths worldwide were attributable to high blood glucose and the increased risks of cardiovascular disease and other associated complications (e.g. kidney failure), which often lead to premature death and are often listed as the underlying cause on death certificates rather than diabetes. For example, in 2017, the International Diabetes Federation (IDF) estimated that diabetes resulted in 4.0 million deaths worldwide, using modeling to estimate the total number of deaths that could be directly or indirectly attributed to diabetes.Diabetes occurs throughout the world but is more common (especially type 2) in more developed countries. The greatest increase in rates has however been seen in low- and middle-income countries, where more than 80% of diabetic deaths occur. The fastest prevalence increase is expected to occur in Asia and Africa, where most people with diabetes will probably live in 2030. The increase in rates in developing countries follows the trend of urbanization and lifestyle changes, including increasingly sedentary lifestyles, less physically demanding work and the global nutrition transition, marked by increased intake of foods that are high energy-dense but nutrient-poor (often high in sugar and saturated fats, sometimes referred to as the "Western-style" diet). The global number of diabetes cases might increase by 48% between 2017 and 2045.As of 2020, 38% of all US adults had prediabetes. Prediabetes is an early stage of diabetes.
History
Diabetes was one of the first diseases described, with an Egyptian manuscript from c. 1500 BCE mentioning "too great emptying of the urine." The Ebers papyrus includes a recommendation for a drink to take in such cases. The first described cases are believed to have been type 1 diabetes. Indian physicians around the same time identified the disease and classified it as madhumeha or "honey urine", noting the urine would attract ants.The term "diabetes" or "to pass through" was first used in 230 BCE by the Greek Apollonius of Memphis. The disease was considered rare during the time of the Roman empire, with Galen commenting he had only seen two cases during his career. This is possibly due to the diet and lifestyle of the ancients, or because the clinical symptoms were observed during the advanced stage of the disease. Galen named the disease "diarrhea of the urine" (diarrhea urinosa).The earliest surviving work with a detailed reference to diabetes is that of Aretaeus of Cappadocia (2nd or early 3rd century CE). He described the symptoms and the course of the disease, which he attributed to the moisture and coldness, reflecting the beliefs of the "Pneumatic School". He hypothesized a correlation between diabetes and other diseases, and he discussed differential diagnosis from the snakebite, which also provokes excessive thirst. His work remained unknown in the West until 1552, when the first Latin edition was published in Venice.Two types of diabetes were identified as separate conditions for the first time by the Indian physicians Sushruta and Charaka in 400–500 CE with one type being associated with youth and another type with being overweight. Effective treatment was not developed until the early part of the 20th century when Canadians Frederick Banting and Charles Herbert Best isolated and purified insulin in 1921 and 1922. This was followed by the development of the long-acting insulin NPH in the 1940s.
Etymology
The word diabetes ( or ) comes from Latin diabētēs, which in turn comes from Ancient Greek διαβήτης (diabētēs), which literally means "a passer through; a siphon". Ancient Greek physician Aretaeus of Cappadocia (fl. 1st century CE) used that word, with the intended meaning "excessive discharge of urine", as the name for the disease. Ultimately, the word comes from Greek διαβαίνειν (diabainein), meaning "to pass through", which is composed of δια- (dia-), meaning "through" and βαίνειν (bainein), meaning "to go". The word "diabetes" is first recorded in English, in the form diabete, in a medical text written around 1425.
The word mellitus ( or ) comes from the classical Latin word mellītus, meaning "mellite" (i.e. sweetened with honey; honey-sweet). The Latin word comes from mell-, which comes from mel, meaning "honey"; sweetness; pleasant thing, and the suffix -ītus, whose meaning is the same as that of the English suffix "-ite". It was Thomas Willis who in 1675 added "mellitus" to the word "diabetes" as a designation for the disease, when he noticed the urine of a person with diabetes had a sweet taste (glycosuria). This sweet taste had been noticed in urine by the ancient Greeks, Chinese, Egyptians, Indians, and Persians.
Society and culture
The 1989 "St. Vincent Declaration" was the result of international efforts to improve the care accorded to those with diabetes. Doing so is important not only in terms of quality of life and life expectancy but also economically – expenses due to diabetes have been shown to be a major drain on health – and productivity-related resources for healthcare systems and governments.
Several countries established more and less successful national diabetes programmes to improve treatment of the disease.People with diabetes who have neuropathic symptoms such as numbness or tingling in feet or hands are twice as likely to be unemployed as those without the symptoms.In 2010, diabetes-related emergency room (ER) visit rates in the United States were higher among people from the lowest income communities (526 per 10,000 population) than from the highest income communities (236 per 10,000 population). Approximately 9.4% of diabetes-related ER visits were for the uninsured.
Naming
The term "type 1 diabetes" has replaced several former terms, including childhood-onset diabetes, juvenile diabetes, and insulin-dependent diabetes mellitus. Likewise, the term "type 2 diabetes" has replaced several former terms, including adult-onset diabetes, obesity-related diabetes, and noninsulin-dependent diabetes mellitus. Beyond these two types, there is no agreed-upon standard nomenclature.Diabetes mellitus is also occasionally known as "sugar diabetes" to differentiate it from diabetes insipidus.
Other animals
Diabetes can occur in mammals or reptiles. Birds do not develop diabetes because of their unusually high tolerance for elevated blood glucose levels.In animals, diabetes is most commonly encountered in dogs and cats. Middle-aged animals are most commonly affected. Female dogs are twice as likely to be affected as males, while according to some sources, male cats are more prone than females. In both species, all breeds may be affected, but some small dog breeds are particularly likely to develop diabetes, such as Miniature Poodles.Feline diabetes is strikingly similar to human type 2 diabetes. The Burmese, Russian Blue, Abyssinian, and Norwegian Forest cat breeds are at higher risk than other breeds. Overweight cats are also at higher risk.The symptoms may relate to fluid loss and polyuria, but the course may also be insidious. Diabetic animals are more prone to infections. The long-term complications recognized in humans are much rarer in animals. The principles of treatment (weight loss, oral antidiabetics, subcutaneous insulin) and management of emergencies (e.g. ketoacidosis) are similar to those in humans.
References
External links
American Diabetes Association
IDF Diabetes Atlas
National Diabetes Education Program
ADA's Standards of Medical Care in Diabetes 2019
Polonsky KS (October 2012). "The past 200 years in diabetes". The New England Journal of Medicine. 367 (14): 1332–1340. doi:10.1056/NEJMra1110560. PMID 23034021. S2CID 9456681.
"Diabetes". MedlinePlus. U.S. National Library of Medicine.
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Diabetes, also known as diabetes mellitus, is a group of common endocrine diseases characterized by sustained high blood sugar levels. Diabetes is due to either the pancreas not producing enough insulin, or the cells of the body not responding properly to the insulin produced. Diabetes, if left untreated, leads to many health complications. Untreated or poorly treated diabetes accounts for approximately 1.5 million deaths per year.There is no widely accepted cure for most cases of diabetes. The most common treatment for type 1 diabetes is insulin replacement therapy (insulin injections). Anti-diabetic medications such as metformin and semaglutide, as well as lifestyle modifications, can be used to prevent or respond to type 2 diabetes. Gestational diabetes normally resolves shortly after delivery.
As of 2019, an estimated 463 million people had diabetes worldwide accounting for 8.8% of the adult population. Type 2 diabetes makes up about 90% of all diabetes cases. The prevalence of the disease continues to increase, most dramatically in low- and middle-income nations. Rates are similar in women and men, with diabetes being the 7th-leading cause of death globally. The global expenditure on diabetes-related healthcare is an estimated USD760 billion a year.
Signs and symptoms
The classic symptoms of untreated diabetes are unintended weight loss, polyuria (increased urination), polydipsia (increased thirst), and polyphagia (increased hunger). Symptoms may develop rapidly (weeks or months) in type 1 diabetes, while they usually develop much more slowly and may be subtle or absent in type 2 diabetes.Several other signs and symptoms can mark the onset of diabetes although they are not specific to the disease. In addition to the known symptoms listed above, they include blurred vision, headache, fatigue, slow healing of cuts, and itchy skin. Prolonged high blood glucose can cause glucose absorption in the lens of the eye, which leads to changes in its shape, resulting in vision changes. Long-term vision loss can also be caused by diabetic retinopathy. A number of skin rashes that can occur in diabetes are collectively known as diabetic dermadromes.
Diabetic emergencies
People with diabetes (usually but not exclusively in type 1 diabetes) may also experience diabetic ketoacidosis (DKA), a metabolic disturbance characterized by nausea, vomiting and abdominal pain, the smell of acetone on the breath, deep breathing known as Kussmaul breathing, and in severe cases a decreased level of consciousness. DKA requires emergency treatment in hospital. A rarer but more dangerous condition is hyperosmolar hyperglycemic state (HHS), which is more common in type 2 diabetes and is mainly the result of dehydration caused by high blood sugars.Treatment-related low blood sugar (hypoglycemia) is common in people with type 1 and also type 2 diabetes depending on the medication being used. Most cases are mild and are not considered medical emergencies. Effects can range from feelings of unease, sweating, trembling, and increased appetite in mild cases to more serious effects such as confusion, changes in behavior such as aggressiveness, seizures, unconsciousness, and rarely permanent brain damage or death in severe cases. Rapid breathing, sweating, and cold, pale skin are characteristic of low blood sugar but not definitive. Mild to moderate cases are self-treated by eating or drinking something high in rapidly absorbed carbohydrates. Severe cases can lead to unconsciousness and must be treated with intravenous glucose or injections with glucagon.
Complications
All forms of diabetes increase the risk of long-term complications. These typically develop after many years (10–20) but may be the first symptom in those who have otherwise not received a diagnosis before that time.The major long-term complications relate to damage to blood vessels. Diabetes doubles the risk of cardiovascular disease and about 75% of deaths in people with diabetes are due to coronary artery disease. Other macrovascular diseases include stroke, and peripheral artery disease. These complications are also a strong risk factor for severe COVID-19 illness.The primary complications of diabetes due to damage in small blood vessels include damage to the eyes, kidneys, and nerves. Damage to the eyes, known as diabetic retinopathy, is caused by damage to the blood vessels in the retina of the eye, and can result in gradual vision loss and eventual blindness. Diabetes also increases the risk of having glaucoma, cataracts, and other eye problems. It is recommended that people with diabetes visit an optometrist or ophthalmologist once a year. Damage to the kidneys, known as diabetic nephropathy, can lead to tissue scarring, urine protein loss, and eventually chronic kidney disease, sometimes requiring dialysis or kidney transplantation. Damage to the nerves of the body, known as diabetic neuropathy, is the most common complication of diabetes. The symptoms can include numbness, tingling, sudomotor dysfunction, pain, and altered pain sensation, which can lead to damage to the skin. Diabetes-related foot problems (such as diabetic foot ulcers) may occur, and can be difficult to treat, occasionally requiring amputation. Additionally, proximal diabetic neuropathy causes painful muscle atrophy and weakness.
There is a link between cognitive deficit and diabetes. Compared to those without diabetes, those with the disease have a 1.2 to 1.5-fold greater rate of decline in cognitive function. Having diabetes, especially when on insulin, increases the risk of falls in older people.
Causes
Diabetes mellitus is classified into six categories: type 1 diabetes, type 2 diabetes, hybrid forms of diabetes, hyperglycemia first detected during pregnancy, "unclassified diabetes", and "other specific types". "Hybrid forms of diabetes" include slowly evolving, immune-mediated diabetes of adults and ketosis-prone type 2 diabetes. "Hyperglycemia first detected during pregnancy" includes gestational diabetes mellitus and diabetes mellitus in pregnancy (type 1 or type 2 diabetes first diagnosed during pregnancy). The "other specific types" are a collection of a few dozen individual causes. Diabetes is a more variable disease than once thought and people may have combinations of forms.
Type 1
Type 1 diabetes is characterized by loss of the insulin-producing beta cells of the pancreatic islets, leading to insulin deficiency. This type can be further classified as immune-mediated or idiopathic. The majority of type 1 diabetes is of an immune-mediated nature, in which a T cell-mediated autoimmune attack leads to the loss of beta cells and thus insulin. It causes approximately 10% of diabetes mellitus cases in North America and Europe. Most affected people are otherwise healthy and of a healthy weight when onset occurs. Sensitivity and responsiveness to insulin are usually normal, especially in the early stages. Although it has been called "juvenile diabetes" due to the frequent onset in children, the majority of individuals living with type 1 diabetes are now adults."Brittle" diabetes, also known as unstable diabetes or labile diabetes, is a term that was traditionally used to describe the dramatic and recurrent swings in glucose levels, often occurring for no apparent reason in insulin-dependent diabetes. This term, however, has no biologic basis and should not be used. Still, type 1 diabetes can be accompanied by irregular and unpredictable high blood sugar levels, and the potential for diabetic ketoacidosis or serious low blood sugar levels. Other complications include an impaired counterregulatory response to low blood sugar, infection, gastroparesis (which leads to erratic absorption of dietary carbohydrates), and endocrinopathies (e.g., Addison's disease). These phenomena are believed to occur no more frequently than in 1% to 2% of persons with type 1 diabetes.
Type 1 diabetes is partly inherited, with multiple genes, including certain HLA genotypes, known to influence the risk of diabetes. In genetically susceptible people, the onset of diabetes can be triggered by one or more environmental factors, such as a viral infection or diet. Several viruses have been implicated, but to date there is no stringent evidence to support this hypothesis in humans.Type 1 diabetes can occur at any age, and a significant proportion is diagnosed during adulthood. Latent autoimmune diabetes of adults (LADA) is the diagnostic term applied when type 1 diabetes develops in adults; it has a slower onset than the same condition in children. Given this difference, some use the unofficial term "type 1.5 diabetes" for this condition. Adults with LADA are frequently initially misdiagnosed as having type 2 diabetes, based on age rather than a cause.
Type 2
Type 2 diabetes is characterized by insulin resistance, which may be combined with relatively reduced insulin secretion. The defective responsiveness of body tissues to insulin is believed to involve the insulin receptor. However, the specific defects are not known. Diabetes mellitus cases due to a known defect are classified separately. Type 2 diabetes is the most common type of diabetes mellitus accounting for 95% of diabetes. Many people with type 2 diabetes have evidence of prediabetes (impaired fasting glucose and/or impaired glucose tolerance) before meeting the criteria for type 2 diabetes. The progression of prediabetes to overt type 2 diabetes can be slowed or reversed by lifestyle changes or medications that improve insulin sensitivity or reduce the liver's glucose production.Type 2 diabetes is primarily due to lifestyle factors and genetics. A number of lifestyle factors are known to be important to the development of type 2 diabetes, including obesity (defined by a body mass index of greater than 30), lack of physical activity, poor diet, stress, and urbanization. Excess body fat is associated with 30% of cases in people of Chinese and Japanese descent, 60–80% of cases in those of European and African descent, and 100% of Pima Indians and Pacific Islanders. Even those who are not obese may have a high waist–hip ratio.Dietary factors such as sugar-sweetened drinks are associated with an increased risk. The type of fats in the diet is also important, with saturated fat and trans fats increasing the risk and polyunsaturated and monounsaturated fat decreasing the risk. Eating white rice excessively may increase the risk of diabetes, especially in Chinese and Japanese people. Lack of physical activity may increase the risk of diabetes in some people.Adverse childhood experiences, including abuse, neglect, and household difficulties, increase the likelihood of type 2 diabetes later in life by 32%, with neglect having the strongest effect.Antipsychotic medication side effects (specifically metabolic abnormalities, dyslipidemia and weight gain) and unhealthy lifestyles (including poor diet and decreased physical activity), are potential risk factors.
Gestational diabetes
Gestational diabetes resembles type 2 diabetes in several respects, involving a combination of relatively inadequate insulin secretion and responsiveness. It occurs in about 2–10% of all pregnancies and may improve or disappear after delivery. It is recommended that all pregnant women get tested starting around 24–28 weeks gestation. It is most often diagnosed in the second or third trimester because of the increase in insulin-antagonist hormone levels that occurs at this time. However, after pregnancy approximately 5–10% of women with gestational diabetes are found to have another form of diabetes, most commonly type 2. Gestational diabetes is fully treatable, but requires careful medical supervision throughout the pregnancy. Management may include dietary changes, blood glucose monitoring, and in some cases, insulin may be required.Though it may be transient, untreated gestational diabetes can damage the health of the fetus or mother. Risks to the baby include macrosomia (high birth weight), congenital heart and central nervous system abnormalities, and skeletal muscle malformations. Increased levels of insulin in a fetus's blood may inhibit fetal surfactant production and cause infant respiratory distress syndrome. A high blood bilirubin level may result from red blood cell destruction. In severe cases, perinatal death may occur, most commonly as a result of poor placental perfusion due to vascular impairment. Labor induction may be indicated with decreased placental function. A caesarean section may be performed if there is marked fetal distress or an increased risk of injury associated with macrosomia, such as shoulder dystocia.
Other types
Maturity onset diabetes of the young (MODY) is a rare autosomal dominant inherited form of diabetes, due to one of several single-gene mutations causing defects in insulin production. It is significantly less common than the three main types, constituting 1–2% of all cases. The name of this disease refers to early hypotheses as to its nature. Being due to a defective gene, this disease varies in age at presentation and in severity according to the specific gene defect; thus, there are at least 13 subtypes of MODY. People with MODY often can control it without using insulin.Some cases of diabetes are caused by the body's tissue receptors not responding to insulin (even when insulin levels are normal, which is what separates it from type 2 diabetes); this form is very uncommon. Genetic mutations (autosomal or mitochondrial) can lead to defects in beta cell function. Abnormal insulin action may also have been genetically determined in some cases. Any disease that causes extensive damage to the pancreas may lead to diabetes (for example, chronic pancreatitis and cystic fibrosis). Diseases associated with excessive secretion of insulin-antagonistic hormones can cause diabetes (which is typically resolved once the hormone excess is removed). Many drugs impair insulin secretion and some toxins damage pancreatic beta cells, whereas others increase insulin resistance (especially glucocorticoids which can provoke "steroid diabetes"). The ICD-10 (1992) diagnostic entity, malnutrition-related diabetes mellitus (ICD-10 code E12), was deprecated by the World Health Organization (WHO) when the current taxonomy was introduced in 1999.
Yet another form of diabetes that people may develop is double diabetes. This is when a type 1 diabetic becomes insulin resistant, the hallmark for type 2 diabetes or has a family history for type 2 diabetes. It was first discovered in 1990 or 1991.
The following is a list of disorders that may increase the risk of diabetes:
Pathophysiology
Insulin is the principal hormone that regulates the uptake of glucose from the blood into most cells of the body, especially liver, adipose tissue and muscle, except smooth muscle, in which insulin acts via the IGF-1. Therefore, deficiency of insulin or the insensitivity of its receptors play a central role in all forms of diabetes mellitus.The body obtains glucose from three main sources: the intestinal absorption of food; the breakdown of glycogen (glycogenolysis), the storage form of glucose found in the liver; and gluconeogenesis, the generation of glucose from non-carbohydrate substrates in the body. Insulin plays a critical role in regulating glucose levels in the body. Insulin can inhibit the breakdown of glycogen or the process of gluconeogenesis, it can stimulate the transport of glucose into fat and muscle cells, and it can stimulate the storage of glucose in the form of glycogen.Insulin is released into the blood by beta cells (β-cells), found in the islets of Langerhans in the pancreas, in response to rising levels of blood glucose, typically after eating. Insulin is used by about two-thirds of the body's cells to absorb glucose from the blood for use as fuel, for conversion to other needed molecules, or for storage. Lower glucose levels result in decreased insulin release from the beta cells and in the breakdown of glycogen to glucose. This process is mainly controlled by the hormone glucagon, which acts in the opposite manner to insulin.If the amount of insulin available is insufficient, or if cells respond poorly to the effects of insulin (insulin resistance), or if the insulin itself is defective, then glucose is not absorbed properly by the body cells that require it, and is not stored appropriately in the liver and muscles. The net effect is persistently high levels of blood glucose, poor protein synthesis, and other metabolic derangements, such as metabolic acidosis in cases of complete insulin deficiency.When glucose concentration in the blood remains high over time, the kidneys reach a threshold of reabsorption, and the body excretes glucose in the urine (glycosuria). This increases the osmotic pressure of the urine and inhibits reabsorption of water by the kidney, resulting in increased urine production (polyuria) and increased fluid loss. Lost blood volume is replaced osmotically from water in body cells and other body compartments, causing dehydration and increased thirst (polydipsia). In addition, intracellular glucose deficiency stimulates appetite leading to excessive food intake (polyphagia).
Diagnosis
Diabetes mellitus is diagnosed with a test for the glucose content in the blood, and is diagnosed by demonstrating any one of the following:
Fasting plasma glucose level ≥ 7.0 mmol/L (126 mg/dL). For this test, blood is taken after a period of fasting, i.e. in the morning before breakfast, after the patient had sufficient time to fast overnight.
Plasma glucose ≥ 11.1 mmol/L (200 mg/dL) two hours after a 75 gram oral glucose load as in a glucose tolerance test (OGTT)
Symptoms of high blood sugar and plasma glucose ≥ 11.1 mmol/L (200 mg/dL) either while fasting or not fasting
Glycated hemoglobin (HbA1C) ≥ 48 mmol/mol (≥ 6.5 DCCT %).A positive result, in the absence of unequivocal high blood sugar, should be confirmed by a repeat of any of the above methods on a different day. It is preferable to measure a fasting glucose level because of the ease of measurement and the considerable time commitment of formal glucose tolerance testing, which takes two hours to complete and offers no prognostic advantage over the fasting test. According to the current definition, two fasting glucose measurements at or above 7.0 mmol/L (126 mg/dL) is considered diagnostic for diabetes mellitus.
Per the WHO, people with fasting glucose levels from 6.1 to 6.9 mmol/L (110 to 125 mg/dL) are considered to have impaired fasting glucose. People with plasma glucose at or above 7.8 mmol/L (140 mg/dL), but not over 11.1 mmol/L (200 mg/dL), two hours after a 75 gram oral glucose load are considered to have impaired glucose tolerance. Of these two prediabetic states, the latter in particular is a major risk factor for progression to full-blown diabetes mellitus, as well as cardiovascular disease. The American Diabetes Association (ADA) since 2003 uses a slightly different range for impaired fasting glucose of 5.6 to 6.9 mmol/L (100 to 125 mg/dL).Glycated hemoglobin is better than fasting glucose for determining risks of cardiovascular disease and death from any cause.
Prevention
There is no known preventive measure for type 1 diabetes. Type 2 diabetes—which accounts for 85–90% of all cases worldwide—can often be prevented or delayed by maintaining a normal body weight, engaging in physical activity, and eating a healthy diet. Higher levels of physical activity (more than 90 minutes per day) reduce the risk of diabetes by 28%. Dietary changes known to be effective in helping to prevent diabetes include maintaining a diet rich in whole grains and fiber, and choosing good fats, such as the polyunsaturated fats found in nuts, vegetable oils, and fish. Limiting sugary beverages and eating less red meat and other sources of saturated fat can also help prevent diabetes. Tobacco smoking is also associated with an increased risk of diabetes and its complications, so smoking cessation can be an important preventive measure as well.The relationship between type 2 diabetes and the main modifiable risk factors (excess weight, unhealthy diet, physical inactivity and tobacco use) is similar in all regions of the world. There is growing evidence that the underlying determinants of diabetes are a reflection of the major forces driving social, economic and cultural change: globalization, urbanization, population aging, and the general health policy environment.
Management
Diabetes management concentrates on keeping blood sugar levels close to normal, without causing low blood sugar. This can usually be accomplished with dietary changes, exercise, weight loss, and use of appropriate medications (insulin, oral medications).Learning about the disease and actively participating in the treatment is important, since complications are far less common and less severe in people who have well-managed blood sugar levels. The goal of treatment is an A1C level below 5.7%. Attention is also paid to other health problems that may accelerate the negative effects of diabetes. These include smoking, high blood pressure, metabolic syndrome obesity, and lack of regular exercise. Specialized footwear is widely used to reduce the risk of diabetic foot ulcers by relieving the pressure on the foot. Foot examination for patients living with diabetes should be done annually which includes sensation testing, foot biomechanics, vascular integrity and foot structure.Concerning those with severe mental illness, the efficacy of type 2 diabetes self-management interventions is still poorly explored, with insufficient scientific evidence to show whether these interventions have similar results to those observed in the general population.
Lifestyle
People with diabetes can benefit from education about the disease and treatment, dietary changes, and exercise, with the goal of keeping both short-term and long-term blood glucose levels within acceptable bounds. In addition, given the associated higher risks of cardiovascular disease, lifestyle modifications are recommended to control blood pressure.Weight loss can prevent progression from prediabetes to diabetes type 2, decrease the risk of cardiovascular disease, or result in a partial remission in people with diabetes. No single dietary pattern is best for all people with diabetes. Healthy dietary patterns, such as the Mediterranean diet, low-carbohydrate diet, or DASH diet, are often recommended, although evidence does not support one over the others. According to the ADA, "reducing overall carbohydrate intake for individuals with diabetes has demonstrated the most evidence for improving glycemia", and for individuals with type 2 diabetes who cannot meet the glycemic targets or where reducing anti-glycemic medications is a priority, low or very-low carbohydrate diets are a viable approach. For overweight people with type 2 diabetes, any diet that achieves weight loss is effective.A 2020 Cochrane systematic review compared several non-nutritive sweeteners to sugar, placebo and a nutritive low-calorie sweetener (tagatose), but the results were unclear for effects on HbA1c, body weight and adverse events. The studies included were mainly of very low-certainty and did not report on health-related quality of life, diabetes complications, all-cause mortality or socioeconomic effects.
Medications
Glucose control
Most medications used to treat diabetes act by lowering blood sugar levels through different mechanisms. There is broad consensus that when people with diabetes maintain tight glucose control – keeping the glucose levels in their blood within normal ranges – they experience fewer complications, such as kidney problems or eye problems. There is however debate as to whether this is appropriate and cost effective for people later in life in whom the risk of hypoglycemia may be more significant.There are a number of different classes of anti-diabetic medications. Type 1 diabetes requires treatment with insulin, ideally using a "basal bolus" regimen that most closely matches normal insulin release: long-acting insulin for the basal rate and short-acting insulin with meals. Type 2 diabetes is generally treated with medication that is taken by mouth (e.g. metformin) although some eventually require injectable treatment with insulin or GLP-1 agonists.Metformin is generally recommended as a first-line treatment for type 2 diabetes, as there is good evidence that it decreases mortality. It works by decreasing the liver's production of glucose, and increasing the amount of glucose stored in peripheral tissue. Several other groups of drugs, mainly oral medication, may also decrease blood sugar in type 2 diabetes. These include agents that increase insulin release (sulfonylureas), agents that decrease absorption of sugar from the intestines (acarbose), agents that inhibit the enzyme dipeptidyl peptidase-4 (DPP-4) that inactivates incretins such as GLP-1 and GIP (sitagliptin), agents that make the body more sensitive to insulin (thiazolidinedione) and agents that increase the excretion of glucose in the urine (SGLT2 inhibitors). When insulin is used in type 2 diabetes, a long-acting formulation is usually added initially, while continuing oral medications.Some severe cases of type 2 diabetes may also be treated with insulin, which is increased gradually until glucose targets are reached.
Blood pressure lowering
Cardiovascular disease is a serious complication associated with diabetes, and many international guidelines recommend blood pressure treatment targets that are lower than 140/90 mmHg for people with diabetes. However, there is only limited evidence regarding what the lower targets should be. A 2016 systematic review found potential harm to treating to targets lower than 140 mmHg, and a subsequent systematic review in 2019 found no evidence of additional benefit from blood pressure lowering to between 130 – 140mmHg, although there was an increased risk of adverse events.2015 American Diabetes Association recommendations are that people with diabetes and albuminuria should receive an inhibitor of the renin-angiotensin system to reduce the risks of progression to end-stage renal disease, cardiovascular events, and death. There is some evidence that angiotensin converting enzyme inhibitors (ACEIs) are superior to other inhibitors of the renin-angiotensin system such as angiotensin receptor blockers (ARBs), or aliskiren in preventing cardiovascular disease. Although a more recent review found similar effects of ACEIs and ARBs on major cardiovascular and renal outcomes. There is no evidence that combining ACEIs and ARBs provides additional benefits.
Aspirin
The use of aspirin to prevent cardiovascular disease in diabetes is controversial. Aspirin is recommended by some in people at high risk of cardiovascular disease, however routine use of aspirin has not been found to improve outcomes in uncomplicated diabetes. 2015 American Diabetes Association recommendations for aspirin use (based on expert consensus or clinical experience) are that low-dose aspirin use is reasonable in adults with diabetes who are at intermediate risk of cardiovascular disease (10-year cardiovascular disease risk, 5–10%). National guidelines for England and Wales by the National Institute for Health and Care Excellence (NICE) recommend against the use of aspirin in people with type 1 or type 2 diabetes who do not have confirmed cardiovascular disease.
Surgery
Weight loss surgery in those with obesity and type 2 diabetes is often an effective measure. Many are able to maintain normal blood sugar levels with little or no medications following surgery and long-term mortality is decreased. There is, however, a short-term mortality risk of less than 1% from the surgery. The body mass index cutoffs for when surgery is appropriate are not yet clear. It is recommended that this option be considered in those who are unable to get both their weight and blood sugar under control.A pancreas transplant is occasionally considered for people with type 1 diabetes who have severe complications of their disease, including end stage kidney disease requiring kidney transplantation.
Self-management and support
In countries using a general practitioner system, such as the United Kingdom, care may take place mainly outside hospitals, with hospital-based specialist care used only in case of complications, difficult blood sugar control, or research projects. In other circumstances, general practitioners and specialists share care in a team approach. Home telehealth support can be an effective management technique.The use of technology to deliver educational programs for adults with type 2 diabetes includes computer-based self-management interventions to collect for tailored responses to facilitate self-management. There is no adequate evidence to support effects on cholesterol, blood pressure, behavioral change (such as physical activity levels and dietary), depression, weight and health-related quality of life, nor in other biological, cognitive or emotional outcomes.
Epidemiology
In 2017, 425 million people had diabetes worldwide, up from an estimated 382 million people in 2013 and from 108 million in 1980. Accounting for the shifting age structure of the global population, the prevalence of diabetes is 8.8% among adults, nearly double the rate of 4.7% in 1980. Type 2 makes up about 90% of the cases. Some data indicate rates are roughly equal in women and men, but male excess in diabetes has been found in many populations with higher type 2 incidence, possibly due to sex-related differences in insulin sensitivity, consequences of obesity and regional body fat deposition, and other contributing factors such as high blood pressure, tobacco smoking, and alcohol intake.The WHO estimates that diabetes resulted in 1.5 million deaths in 2012, making it the 8th leading cause of death. However another 2.2 million deaths worldwide were attributable to high blood glucose and the increased risks of cardiovascular disease and other associated complications (e.g. kidney failure), which often lead to premature death and are often listed as the underlying cause on death certificates rather than diabetes. For example, in 2017, the International Diabetes Federation (IDF) estimated that diabetes resulted in 4.0 million deaths worldwide, using modeling to estimate the total number of deaths that could be directly or indirectly attributed to diabetes.Diabetes occurs throughout the world but is more common (especially type 2) in more developed countries. The greatest increase in rates has however been seen in low- and middle-income countries, where more than 80% of diabetic deaths occur. The fastest prevalence increase is expected to occur in Asia and Africa, where most people with diabetes will probably live in 2030. The increase in rates in developing countries follows the trend of urbanization and lifestyle changes, including increasingly sedentary lifestyles, less physically demanding work and the global nutrition transition, marked by increased intake of foods that are high energy-dense but nutrient-poor (often high in sugar and saturated fats, sometimes referred to as the "Western-style" diet). The global number of diabetes cases might increase by 48% between 2017 and 2045.As of 2020, 38% of all US adults had prediabetes. Prediabetes is an early stage of diabetes.
History
Diabetes was one of the first diseases described, with an Egyptian manuscript from c. 1500 BCE mentioning "too great emptying of the urine." The Ebers papyrus includes a recommendation for a drink to take in such cases. The first described cases are believed to have been type 1 diabetes. Indian physicians around the same time identified the disease and classified it as madhumeha or "honey urine", noting the urine would attract ants.The term "diabetes" or "to pass through" was first used in 230 BCE by the Greek Apollonius of Memphis. The disease was considered rare during the time of the Roman empire, with Galen commenting he had only seen two cases during his career. This is possibly due to the diet and lifestyle of the ancients, or because the clinical symptoms were observed during the advanced stage of the disease. Galen named the disease "diarrhea of the urine" (diarrhea urinosa).The earliest surviving work with a detailed reference to diabetes is that of Aretaeus of Cappadocia (2nd or early 3rd century CE). He described the symptoms and the course of the disease, which he attributed to the moisture and coldness, reflecting the beliefs of the "Pneumatic School". He hypothesized a correlation between diabetes and other diseases, and he discussed differential diagnosis from the snakebite, which also provokes excessive thirst. His work remained unknown in the West until 1552, when the first Latin edition was published in Venice.Two types of diabetes were identified as separate conditions for the first time by the Indian physicians Sushruta and Charaka in 400–500 CE with one type being associated with youth and another type with being overweight. Effective treatment was not developed until the early part of the 20th century when Canadians Frederick Banting and Charles Herbert Best isolated and purified insulin in 1921 and 1922. This was followed by the development of the long-acting insulin NPH in the 1940s.
Etymology
The word diabetes ( or ) comes from Latin diabētēs, which in turn comes from Ancient Greek διαβήτης (diabētēs), which literally means "a passer through; a siphon". Ancient Greek physician Aretaeus of Cappadocia (fl. 1st century CE) used that word, with the intended meaning "excessive discharge of urine", as the name for the disease. Ultimately, the word comes from Greek διαβαίνειν (diabainein), meaning "to pass through", which is composed of δια- (dia-), meaning "through" and βαίνειν (bainein), meaning "to go". The word "diabetes" is first recorded in English, in the form diabete, in a medical text written around 1425.
The word mellitus ( or ) comes from the classical Latin word mellītus, meaning "mellite" (i.e. sweetened with honey; honey-sweet). The Latin word comes from mell-, which comes from mel, meaning "honey"; sweetness; pleasant thing, and the suffix -ītus, whose meaning is the same as that of the English suffix "-ite". It was Thomas Willis who in 1675 added "mellitus" to the word "diabetes" as a designation for the disease, when he noticed the urine of a person with diabetes had a sweet taste (glycosuria). This sweet taste had been noticed in urine by the ancient Greeks, Chinese, Egyptians, Indians, and Persians.
Society and culture
The 1989 "St. Vincent Declaration" was the result of international efforts to improve the care accorded to those with diabetes. Doing so is important not only in terms of quality of life and life expectancy but also economically – expenses due to diabetes have been shown to be a major drain on health – and productivity-related resources for healthcare systems and governments.
Several countries established more and less successful national diabetes programmes to improve treatment of the disease.People with diabetes who have neuropathic symptoms such as numbness or tingling in feet or hands are twice as likely to be unemployed as those without the symptoms.In 2010, diabetes-related emergency room (ER) visit rates in the United States were higher among people from the lowest income communities (526 per 10,000 population) than from the highest income communities (236 per 10,000 population). Approximately 9.4% of diabetes-related ER visits were for the uninsured.
Naming
The term "type 1 diabetes" has replaced several former terms, including childhood-onset diabetes, juvenile diabetes, and insulin-dependent diabetes mellitus. Likewise, the term "type 2 diabetes" has replaced several former terms, including adult-onset diabetes, obesity-related diabetes, and noninsulin-dependent diabetes mellitus. Beyond these two types, there is no agreed-upon standard nomenclature.Diabetes mellitus is also occasionally known as "sugar diabetes" to differentiate it from diabetes insipidus.
Other animals
Diabetes can occur in mammals or reptiles. Birds do not develop diabetes because of their unusually high tolerance for elevated blood glucose levels.In animals, diabetes is most commonly encountered in dogs and cats. Middle-aged animals are most commonly affected. Female dogs are twice as likely to be affected as males, while according to some sources, male cats are more prone than females. In both species, all breeds may be affected, but some small dog breeds are particularly likely to develop diabetes, such as Miniature Poodles.Feline diabetes is strikingly similar to human type 2 diabetes. The Burmese, Russian Blue, Abyssinian, and Norwegian Forest cat breeds are at higher risk than other breeds. Overweight cats are also at higher risk.The symptoms may relate to fluid loss and polyuria, but the course may also be insidious. Diabetic animals are more prone to infections. The long-term complications recognized in humans are much rarer in animals. The principles of treatment (weight loss, oral antidiabetics, subcutaneous insulin) and management of emergencies (e.g. ketoacidosis) are similar to those in humans.
References
External links
American Diabetes Association
IDF Diabetes Atlas
National Diabetes Education Program
ADA's Standards of Medical Care in Diabetes 2019
Polonsky KS (October 2012). "The past 200 years in diabetes". The New England Journal of Medicine. 367 (14): 1332–1340. doi:10.1056/NEJMra1110560. PMID 23034021. S2CID 9456681.
"Diabetes". MedlinePlus. U.S. National Library of Medicine.
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Diabetes, also known as diabetes mellitus, is a group of common endocrine diseases characterized by sustained high blood sugar levels. Diabetes is due to either the pancreas not producing enough insulin, or the cells of the body not responding properly to the insulin produced. Diabetes, if left untreated, leads to many health complications. Untreated or poorly treated diabetes accounts for approximately 1.5 million deaths per year.There is no widely accepted cure for most cases of diabetes. The most common treatment for type 1 diabetes is insulin replacement therapy (insulin injections). Anti-diabetic medications such as metformin and semaglutide, as well as lifestyle modifications, can be used to prevent or respond to type 2 diabetes. Gestational diabetes normally resolves shortly after delivery.
As of 2019, an estimated 463 million people had diabetes worldwide accounting for 8.8% of the adult population. Type 2 diabetes makes up about 90% of all diabetes cases. The prevalence of the disease continues to increase, most dramatically in low- and middle-income nations. Rates are similar in women and men, with diabetes being the 7th-leading cause of death globally. The global expenditure on diabetes-related healthcare is an estimated USD760 billion a year.
Signs and symptoms
The classic symptoms of untreated diabetes are unintended weight loss, polyuria (increased urination), polydipsia (increased thirst), and polyphagia (increased hunger). Symptoms may develop rapidly (weeks or months) in type 1 diabetes, while they usually develop much more slowly and may be subtle or absent in type 2 diabetes.Several other signs and symptoms can mark the onset of diabetes although they are not specific to the disease. In addition to the known symptoms listed above, they include blurred vision, headache, fatigue, slow healing of cuts, and itchy skin. Prolonged high blood glucose can cause glucose absorption in the lens of the eye, which leads to changes in its shape, resulting in vision changes. Long-term vision loss can also be caused by diabetic retinopathy. A number of skin rashes that can occur in diabetes are collectively known as diabetic dermadromes.
Diabetic emergencies
People with diabetes (usually but not exclusively in type 1 diabetes) may also experience diabetic ketoacidosis (DKA), a metabolic disturbance characterized by nausea, vomiting and abdominal pain, the smell of acetone on the breath, deep breathing known as Kussmaul breathing, and in severe cases a decreased level of consciousness. DKA requires emergency treatment in hospital. A rarer but more dangerous condition is hyperosmolar hyperglycemic state (HHS), which is more common in type 2 diabetes and is mainly the result of dehydration caused by high blood sugars.Treatment-related low blood sugar (hypoglycemia) is common in people with type 1 and also type 2 diabetes depending on the medication being used. Most cases are mild and are not considered medical emergencies. Effects can range from feelings of unease, sweating, trembling, and increased appetite in mild cases to more serious effects such as confusion, changes in behavior such as aggressiveness, seizures, unconsciousness, and rarely permanent brain damage or death in severe cases. Rapid breathing, sweating, and cold, pale skin are characteristic of low blood sugar but not definitive. Mild to moderate cases are self-treated by eating or drinking something high in rapidly absorbed carbohydrates. Severe cases can lead to unconsciousness and must be treated with intravenous glucose or injections with glucagon.
Complications
All forms of diabetes increase the risk of long-term complications. These typically develop after many years (10–20) but may be the first symptom in those who have otherwise not received a diagnosis before that time.The major long-term complications relate to damage to blood vessels. Diabetes doubles the risk of cardiovascular disease and about 75% of deaths in people with diabetes are due to coronary artery disease. Other macrovascular diseases include stroke, and peripheral artery disease. These complications are also a strong risk factor for severe COVID-19 illness.The primary complications of diabetes due to damage in small blood vessels include damage to the eyes, kidneys, and nerves. Damage to the eyes, known as diabetic retinopathy, is caused by damage to the blood vessels in the retina of the eye, and can result in gradual vision loss and eventual blindness. Diabetes also increases the risk of having glaucoma, cataracts, and other eye problems. It is recommended that people with diabetes visit an optometrist or ophthalmologist once a year. Damage to the kidneys, known as diabetic nephropathy, can lead to tissue scarring, urine protein loss, and eventually chronic kidney disease, sometimes requiring dialysis or kidney transplantation. Damage to the nerves of the body, known as diabetic neuropathy, is the most common complication of diabetes. The symptoms can include numbness, tingling, sudomotor dysfunction, pain, and altered pain sensation, which can lead to damage to the skin. Diabetes-related foot problems (such as diabetic foot ulcers) may occur, and can be difficult to treat, occasionally requiring amputation. Additionally, proximal diabetic neuropathy causes painful muscle atrophy and weakness.
There is a link between cognitive deficit and diabetes. Compared to those without diabetes, those with the disease have a 1.2 to 1.5-fold greater rate of decline in cognitive function. Having diabetes, especially when on insulin, increases the risk of falls in older people.
Causes
Diabetes mellitus is classified into six categories: type 1 diabetes, type 2 diabetes, hybrid forms of diabetes, hyperglycemia first detected during pregnancy, "unclassified diabetes", and "other specific types". "Hybrid forms of diabetes" include slowly evolving, immune-mediated diabetes of adults and ketosis-prone type 2 diabetes. "Hyperglycemia first detected during pregnancy" includes gestational diabetes mellitus and diabetes mellitus in pregnancy (type 1 or type 2 diabetes first diagnosed during pregnancy). The "other specific types" are a collection of a few dozen individual causes. Diabetes is a more variable disease than once thought and people may have combinations of forms.
Type 1
Type 1 diabetes is characterized by loss of the insulin-producing beta cells of the pancreatic islets, leading to insulin deficiency. This type can be further classified as immune-mediated or idiopathic. The majority of type 1 diabetes is of an immune-mediated nature, in which a T cell-mediated autoimmune attack leads to the loss of beta cells and thus insulin. It causes approximately 10% of diabetes mellitus cases in North America and Europe. Most affected people are otherwise healthy and of a healthy weight when onset occurs. Sensitivity and responsiveness to insulin are usually normal, especially in the early stages. Although it has been called "juvenile diabetes" due to the frequent onset in children, the majority of individuals living with type 1 diabetes are now adults."Brittle" diabetes, also known as unstable diabetes or labile diabetes, is a term that was traditionally used to describe the dramatic and recurrent swings in glucose levels, often occurring for no apparent reason in insulin-dependent diabetes. This term, however, has no biologic basis and should not be used. Still, type 1 diabetes can be accompanied by irregular and unpredictable high blood sugar levels, and the potential for diabetic ketoacidosis or serious low blood sugar levels. Other complications include an impaired counterregulatory response to low blood sugar, infection, gastroparesis (which leads to erratic absorption of dietary carbohydrates), and endocrinopathies (e.g., Addison's disease). These phenomena are believed to occur no more frequently than in 1% to 2% of persons with type 1 diabetes.
Type 1 diabetes is partly inherited, with multiple genes, including certain HLA genotypes, known to influence the risk of diabetes. In genetically susceptible people, the onset of diabetes can be triggered by one or more environmental factors, such as a viral infection or diet. Several viruses have been implicated, but to date there is no stringent evidence to support this hypothesis in humans.Type 1 diabetes can occur at any age, and a significant proportion is diagnosed during adulthood. Latent autoimmune diabetes of adults (LADA) is the diagnostic term applied when type 1 diabetes develops in adults; it has a slower onset than the same condition in children. Given this difference, some use the unofficial term "type 1.5 diabetes" for this condition. Adults with LADA are frequently initially misdiagnosed as having type 2 diabetes, based on age rather than a cause.
Type 2
Type 2 diabetes is characterized by insulin resistance, which may be combined with relatively reduced insulin secretion. The defective responsiveness of body tissues to insulin is believed to involve the insulin receptor. However, the specific defects are not known. Diabetes mellitus cases due to a known defect are classified separately. Type 2 diabetes is the most common type of diabetes mellitus accounting for 95% of diabetes. Many people with type 2 diabetes have evidence of prediabetes (impaired fasting glucose and/or impaired glucose tolerance) before meeting the criteria for type 2 diabetes. The progression of prediabetes to overt type 2 diabetes can be slowed or reversed by lifestyle changes or medications that improve insulin sensitivity or reduce the liver's glucose production.Type 2 diabetes is primarily due to lifestyle factors and genetics. A number of lifestyle factors are known to be important to the development of type 2 diabetes, including obesity (defined by a body mass index of greater than 30), lack of physical activity, poor diet, stress, and urbanization. Excess body fat is associated with 30% of cases in people of Chinese and Japanese descent, 60–80% of cases in those of European and African descent, and 100% of Pima Indians and Pacific Islanders. Even those who are not obese may have a high waist–hip ratio.Dietary factors such as sugar-sweetened drinks are associated with an increased risk. The type of fats in the diet is also important, with saturated fat and trans fats increasing the risk and polyunsaturated and monounsaturated fat decreasing the risk. Eating white rice excessively may increase the risk of diabetes, especially in Chinese and Japanese people. Lack of physical activity may increase the risk of diabetes in some people.Adverse childhood experiences, including abuse, neglect, and household difficulties, increase the likelihood of type 2 diabetes later in life by 32%, with neglect having the strongest effect.Antipsychotic medication side effects (specifically metabolic abnormalities, dyslipidemia and weight gain) and unhealthy lifestyles (including poor diet and decreased physical activity), are potential risk factors.
Gestational diabetes
Gestational diabetes resembles type 2 diabetes in several respects, involving a combination of relatively inadequate insulin secretion and responsiveness. It occurs in about 2–10% of all pregnancies and may improve or disappear after delivery. It is recommended that all pregnant women get tested starting around 24–28 weeks gestation. It is most often diagnosed in the second or third trimester because of the increase in insulin-antagonist hormone levels that occurs at this time. However, after pregnancy approximately 5–10% of women with gestational diabetes are found to have another form of diabetes, most commonly type 2. Gestational diabetes is fully treatable, but requires careful medical supervision throughout the pregnancy. Management may include dietary changes, blood glucose monitoring, and in some cases, insulin may be required.Though it may be transient, untreated gestational diabetes can damage the health of the fetus or mother. Risks to the baby include macrosomia (high birth weight), congenital heart and central nervous system abnormalities, and skeletal muscle malformations. Increased levels of insulin in a fetus's blood may inhibit fetal surfactant production and cause infant respiratory distress syndrome. A high blood bilirubin level may result from red blood cell destruction. In severe cases, perinatal death may occur, most commonly as a result of poor placental perfusion due to vascular impairment. Labor induction may be indicated with decreased placental function. A caesarean section may be performed if there is marked fetal distress or an increased risk of injury associated with macrosomia, such as shoulder dystocia.
Other types
Maturity onset diabetes of the young (MODY) is a rare autosomal dominant inherited form of diabetes, due to one of several single-gene mutations causing defects in insulin production. It is significantly less common than the three main types, constituting 1–2% of all cases. The name of this disease refers to early hypotheses as to its nature. Being due to a defective gene, this disease varies in age at presentation and in severity according to the specific gene defect; thus, there are at least 13 subtypes of MODY. People with MODY often can control it without using insulin.Some cases of diabetes are caused by the body's tissue receptors not responding to insulin (even when insulin levels are normal, which is what separates it from type 2 diabetes); this form is very uncommon. Genetic mutations (autosomal or mitochondrial) can lead to defects in beta cell function. Abnormal insulin action may also have been genetically determined in some cases. Any disease that causes extensive damage to the pancreas may lead to diabetes (for example, chronic pancreatitis and cystic fibrosis). Diseases associated with excessive secretion of insulin-antagonistic hormones can cause diabetes (which is typically resolved once the hormone excess is removed). Many drugs impair insulin secretion and some toxins damage pancreatic beta cells, whereas others increase insulin resistance (especially glucocorticoids which can provoke "steroid diabetes"). The ICD-10 (1992) diagnostic entity, malnutrition-related diabetes mellitus (ICD-10 code E12), was deprecated by the World Health Organization (WHO) when the current taxonomy was introduced in 1999.
Yet another form of diabetes that people may develop is double diabetes. This is when a type 1 diabetic becomes insulin resistant, the hallmark for type 2 diabetes or has a family history for type 2 diabetes. It was first discovered in 1990 or 1991.
The following is a list of disorders that may increase the risk of diabetes:
Pathophysiology
Insulin is the principal hormone that regulates the uptake of glucose from the blood into most cells of the body, especially liver, adipose tissue and muscle, except smooth muscle, in which insulin acts via the IGF-1. Therefore, deficiency of insulin or the insensitivity of its receptors play a central role in all forms of diabetes mellitus.The body obtains glucose from three main sources: the intestinal absorption of food; the breakdown of glycogen (glycogenolysis), the storage form of glucose found in the liver; and gluconeogenesis, the generation of glucose from non-carbohydrate substrates in the body. Insulin plays a critical role in regulating glucose levels in the body. Insulin can inhibit the breakdown of glycogen or the process of gluconeogenesis, it can stimulate the transport of glucose into fat and muscle cells, and it can stimulate the storage of glucose in the form of glycogen.Insulin is released into the blood by beta cells (β-cells), found in the islets of Langerhans in the pancreas, in response to rising levels of blood glucose, typically after eating. Insulin is used by about two-thirds of the body's cells to absorb glucose from the blood for use as fuel, for conversion to other needed molecules, or for storage. Lower glucose levels result in decreased insulin release from the beta cells and in the breakdown of glycogen to glucose. This process is mainly controlled by the hormone glucagon, which acts in the opposite manner to insulin.If the amount of insulin available is insufficient, or if cells respond poorly to the effects of insulin (insulin resistance), or if the insulin itself is defective, then glucose is not absorbed properly by the body cells that require it, and is not stored appropriately in the liver and muscles. The net effect is persistently high levels of blood glucose, poor protein synthesis, and other metabolic derangements, such as metabolic acidosis in cases of complete insulin deficiency.When glucose concentration in the blood remains high over time, the kidneys reach a threshold of reabsorption, and the body excretes glucose in the urine (glycosuria). This increases the osmotic pressure of the urine and inhibits reabsorption of water by the kidney, resulting in increased urine production (polyuria) and increased fluid loss. Lost blood volume is replaced osmotically from water in body cells and other body compartments, causing dehydration and increased thirst (polydipsia). In addition, intracellular glucose deficiency stimulates appetite leading to excessive food intake (polyphagia).
Diagnosis
Diabetes mellitus is diagnosed with a test for the glucose content in the blood, and is diagnosed by demonstrating any one of the following:
Fasting plasma glucose level ≥ 7.0 mmol/L (126 mg/dL). For this test, blood is taken after a period of fasting, i.e. in the morning before breakfast, after the patient had sufficient time to fast overnight.
Plasma glucose ≥ 11.1 mmol/L (200 mg/dL) two hours after a 75 gram oral glucose load as in a glucose tolerance test (OGTT)
Symptoms of high blood sugar and plasma glucose ≥ 11.1 mmol/L (200 mg/dL) either while fasting or not fasting
Glycated hemoglobin (HbA1C) ≥ 48 mmol/mol (≥ 6.5 DCCT %).A positive result, in the absence of unequivocal high blood sugar, should be confirmed by a repeat of any of the above methods on a different day. It is preferable to measure a fasting glucose level because of the ease of measurement and the considerable time commitment of formal glucose tolerance testing, which takes two hours to complete and offers no prognostic advantage over the fasting test. According to the current definition, two fasting glucose measurements at or above 7.0 mmol/L (126 mg/dL) is considered diagnostic for diabetes mellitus.
Per the WHO, people with fasting glucose levels from 6.1 to 6.9 mmol/L (110 to 125 mg/dL) are considered to have impaired fasting glucose. People with plasma glucose at or above 7.8 mmol/L (140 mg/dL), but not over 11.1 mmol/L (200 mg/dL), two hours after a 75 gram oral glucose load are considered to have impaired glucose tolerance. Of these two prediabetic states, the latter in particular is a major risk factor for progression to full-blown diabetes mellitus, as well as cardiovascular disease. The American Diabetes Association (ADA) since 2003 uses a slightly different range for impaired fasting glucose of 5.6 to 6.9 mmol/L (100 to 125 mg/dL).Glycated hemoglobin is better than fasting glucose for determining risks of cardiovascular disease and death from any cause.
Prevention
There is no known preventive measure for type 1 diabetes. Type 2 diabetes—which accounts for 85–90% of all cases worldwide—can often be prevented or delayed by maintaining a normal body weight, engaging in physical activity, and eating a healthy diet. Higher levels of physical activity (more than 90 minutes per day) reduce the risk of diabetes by 28%. Dietary changes known to be effective in helping to prevent diabetes include maintaining a diet rich in whole grains and fiber, and choosing good fats, such as the polyunsaturated fats found in nuts, vegetable oils, and fish. Limiting sugary beverages and eating less red meat and other sources of saturated fat can also help prevent diabetes. Tobacco smoking is also associated with an increased risk of diabetes and its complications, so smoking cessation can be an important preventive measure as well.The relationship between type 2 diabetes and the main modifiable risk factors (excess weight, unhealthy diet, physical inactivity and tobacco use) is similar in all regions of the world. There is growing evidence that the underlying determinants of diabetes are a reflection of the major forces driving social, economic and cultural change: globalization, urbanization, population aging, and the general health policy environment.
Management
Diabetes management concentrates on keeping blood sugar levels close to normal, without causing low blood sugar. This can usually be accomplished with dietary changes, exercise, weight loss, and use of appropriate medications (insulin, oral medications).Learning about the disease and actively participating in the treatment is important, since complications are far less common and less severe in people who have well-managed blood sugar levels. The goal of treatment is an A1C level below 5.7%. Attention is also paid to other health problems that may accelerate the negative effects of diabetes. These include smoking, high blood pressure, metabolic syndrome obesity, and lack of regular exercise. Specialized footwear is widely used to reduce the risk of diabetic foot ulcers by relieving the pressure on the foot. Foot examination for patients living with diabetes should be done annually which includes sensation testing, foot biomechanics, vascular integrity and foot structure.Concerning those with severe mental illness, the efficacy of type 2 diabetes self-management interventions is still poorly explored, with insufficient scientific evidence to show whether these interventions have similar results to those observed in the general population.
Lifestyle
People with diabetes can benefit from education about the disease and treatment, dietary changes, and exercise, with the goal of keeping both short-term and long-term blood glucose levels within acceptable bounds. In addition, given the associated higher risks of cardiovascular disease, lifestyle modifications are recommended to control blood pressure.Weight loss can prevent progression from prediabetes to diabetes type 2, decrease the risk of cardiovascular disease, or result in a partial remission in people with diabetes. No single dietary pattern is best for all people with diabetes. Healthy dietary patterns, such as the Mediterranean diet, low-carbohydrate diet, or DASH diet, are often recommended, although evidence does not support one over the others. According to the ADA, "reducing overall carbohydrate intake for individuals with diabetes has demonstrated the most evidence for improving glycemia", and for individuals with type 2 diabetes who cannot meet the glycemic targets or where reducing anti-glycemic medications is a priority, low or very-low carbohydrate diets are a viable approach. For overweight people with type 2 diabetes, any diet that achieves weight loss is effective.A 2020 Cochrane systematic review compared several non-nutritive sweeteners to sugar, placebo and a nutritive low-calorie sweetener (tagatose), but the results were unclear for effects on HbA1c, body weight and adverse events. The studies included were mainly of very low-certainty and did not report on health-related quality of life, diabetes complications, all-cause mortality or socioeconomic effects.
Medications
Glucose control
Most medications used to treat diabetes act by lowering blood sugar levels through different mechanisms. There is broad consensus that when people with diabetes maintain tight glucose control – keeping the glucose levels in their blood within normal ranges – they experience fewer complications, such as kidney problems or eye problems. There is however debate as to whether this is appropriate and cost effective for people later in life in whom the risk of hypoglycemia may be more significant.There are a number of different classes of anti-diabetic medications. Type 1 diabetes requires treatment with insulin, ideally using a "basal bolus" regimen that most closely matches normal insulin release: long-acting insulin for the basal rate and short-acting insulin with meals. Type 2 diabetes is generally treated with medication that is taken by mouth (e.g. metformin) although some eventually require injectable treatment with insulin or GLP-1 agonists.Metformin is generally recommended as a first-line treatment for type 2 diabetes, as there is good evidence that it decreases mortality. It works by decreasing the liver's production of glucose, and increasing the amount of glucose stored in peripheral tissue. Several other groups of drugs, mainly oral medication, may also decrease blood sugar in type 2 diabetes. These include agents that increase insulin release (sulfonylureas), agents that decrease absorption of sugar from the intestines (acarbose), agents that inhibit the enzyme dipeptidyl peptidase-4 (DPP-4) that inactivates incretins such as GLP-1 and GIP (sitagliptin), agents that make the body more sensitive to insulin (thiazolidinedione) and agents that increase the excretion of glucose in the urine (SGLT2 inhibitors). When insulin is used in type 2 diabetes, a long-acting formulation is usually added initially, while continuing oral medications.Some severe cases of type 2 diabetes may also be treated with insulin, which is increased gradually until glucose targets are reached.
Blood pressure lowering
Cardiovascular disease is a serious complication associated with diabetes, and many international guidelines recommend blood pressure treatment targets that are lower than 140/90 mmHg for people with diabetes. However, there is only limited evidence regarding what the lower targets should be. A 2016 systematic review found potential harm to treating to targets lower than 140 mmHg, and a subsequent systematic review in 2019 found no evidence of additional benefit from blood pressure lowering to between 130 – 140mmHg, although there was an increased risk of adverse events.2015 American Diabetes Association recommendations are that people with diabetes and albuminuria should receive an inhibitor of the renin-angiotensin system to reduce the risks of progression to end-stage renal disease, cardiovascular events, and death. There is some evidence that angiotensin converting enzyme inhibitors (ACEIs) are superior to other inhibitors of the renin-angiotensin system such as angiotensin receptor blockers (ARBs), or aliskiren in preventing cardiovascular disease. Although a more recent review found similar effects of ACEIs and ARBs on major cardiovascular and renal outcomes. There is no evidence that combining ACEIs and ARBs provides additional benefits.
Aspirin
The use of aspirin to prevent cardiovascular disease in diabetes is controversial. Aspirin is recommended by some in people at high risk of cardiovascular disease, however routine use of aspirin has not been found to improve outcomes in uncomplicated diabetes. 2015 American Diabetes Association recommendations for aspirin use (based on expert consensus or clinical experience) are that low-dose aspirin use is reasonable in adults with diabetes who are at intermediate risk of cardiovascular disease (10-year cardiovascular disease risk, 5–10%). National guidelines for England and Wales by the National Institute for Health and Care Excellence (NICE) recommend against the use of aspirin in people with type 1 or type 2 diabetes who do not have confirmed cardiovascular disease.
Surgery
Weight loss surgery in those with obesity and type 2 diabetes is often an effective measure. Many are able to maintain normal blood sugar levels with little or no medications following surgery and long-term mortality is decreased. There is, however, a short-term mortality risk of less than 1% from the surgery. The body mass index cutoffs for when surgery is appropriate are not yet clear. It is recommended that this option be considered in those who are unable to get both their weight and blood sugar under control.A pancreas transplant is occasionally considered for people with type 1 diabetes who have severe complications of their disease, including end stage kidney disease requiring kidney transplantation.
Self-management and support
In countries using a general practitioner system, such as the United Kingdom, care may take place mainly outside hospitals, with hospital-based specialist care used only in case of complications, difficult blood sugar control, or research projects. In other circumstances, general practitioners and specialists share care in a team approach. Home telehealth support can be an effective management technique.The use of technology to deliver educational programs for adults with type 2 diabetes includes computer-based self-management interventions to collect for tailored responses to facilitate self-management. There is no adequate evidence to support effects on cholesterol, blood pressure, behavioral change (such as physical activity levels and dietary), depression, weight and health-related quality of life, nor in other biological, cognitive or emotional outcomes.
Epidemiology
In 2017, 425 million people had diabetes worldwide, up from an estimated 382 million people in 2013 and from 108 million in 1980. Accounting for the shifting age structure of the global population, the prevalence of diabetes is 8.8% among adults, nearly double the rate of 4.7% in 1980. Type 2 makes up about 90% of the cases. Some data indicate rates are roughly equal in women and men, but male excess in diabetes has been found in many populations with higher type 2 incidence, possibly due to sex-related differences in insulin sensitivity, consequences of obesity and regional body fat deposition, and other contributing factors such as high blood pressure, tobacco smoking, and alcohol intake.The WHO estimates that diabetes resulted in 1.5 million deaths in 2012, making it the 8th leading cause of death. However another 2.2 million deaths worldwide were attributable to high blood glucose and the increased risks of cardiovascular disease and other associated complications (e.g. kidney failure), which often lead to premature death and are often listed as the underlying cause on death certificates rather than diabetes. For example, in 2017, the International Diabetes Federation (IDF) estimated that diabetes resulted in 4.0 million deaths worldwide, using modeling to estimate the total number of deaths that could be directly or indirectly attributed to diabetes.Diabetes occurs throughout the world but is more common (especially type 2) in more developed countries. The greatest increase in rates has however been seen in low- and middle-income countries, where more than 80% of diabetic deaths occur. The fastest prevalence increase is expected to occur in Asia and Africa, where most people with diabetes will probably live in 2030. The increase in rates in developing countries follows the trend of urbanization and lifestyle changes, including increasingly sedentary lifestyles, less physically demanding work and the global nutrition transition, marked by increased intake of foods that are high energy-dense but nutrient-poor (often high in sugar and saturated fats, sometimes referred to as the "Western-style" diet). The global number of diabetes cases might increase by 48% between 2017 and 2045.As of 2020, 38% of all US adults had prediabetes. Prediabetes is an early stage of diabetes.
History
Diabetes was one of the first diseases described, with an Egyptian manuscript from c. 1500 BCE mentioning "too great emptying of the urine." The Ebers papyrus includes a recommendation for a drink to take in such cases. The first described cases are believed to have been type 1 diabetes. Indian physicians around the same time identified the disease and classified it as madhumeha or "honey urine", noting the urine would attract ants.The term "diabetes" or "to pass through" was first used in 230 BCE by the Greek Apollonius of Memphis. The disease was considered rare during the time of the Roman empire, with Galen commenting he had only seen two cases during his career. This is possibly due to the diet and lifestyle of the ancients, or because the clinical symptoms were observed during the advanced stage of the disease. Galen named the disease "diarrhea of the urine" (diarrhea urinosa).The earliest surviving work with a detailed reference to diabetes is that of Aretaeus of Cappadocia (2nd or early 3rd century CE). He described the symptoms and the course of the disease, which he attributed to the moisture and coldness, reflecting the beliefs of the "Pneumatic School". He hypothesized a correlation between diabetes and other diseases, and he discussed differential diagnosis from the snakebite, which also provokes excessive thirst. His work remained unknown in the West until 1552, when the first Latin edition was published in Venice.Two types of diabetes were identified as separate conditions for the first time by the Indian physicians Sushruta and Charaka in 400–500 CE with one type being associated with youth and another type with being overweight. Effective treatment was not developed until the early part of the 20th century when Canadians Frederick Banting and Charles Herbert Best isolated and purified insulin in 1921 and 1922. This was followed by the development of the long-acting insulin NPH in the 1940s.
Etymology
The word diabetes ( or ) comes from Latin diabētēs, which in turn comes from Ancient Greek διαβήτης (diabētēs), which literally means "a passer through; a siphon". Ancient Greek physician Aretaeus of Cappadocia (fl. 1st century CE) used that word, with the intended meaning "excessive discharge of urine", as the name for the disease. Ultimately, the word comes from Greek διαβαίνειν (diabainein), meaning "to pass through", which is composed of δια- (dia-), meaning "through" and βαίνειν (bainein), meaning "to go". The word "diabetes" is first recorded in English, in the form diabete, in a medical text written around 1425.
The word mellitus ( or ) comes from the classical Latin word mellītus, meaning "mellite" (i.e. sweetened with honey; honey-sweet). The Latin word comes from mell-, which comes from mel, meaning "honey"; sweetness; pleasant thing, and the suffix -ītus, whose meaning is the same as that of the English suffix "-ite". It was Thomas Willis who in 1675 added "mellitus" to the word "diabetes" as a designation for the disease, when he noticed the urine of a person with diabetes had a sweet taste (glycosuria). This sweet taste had been noticed in urine by the ancient Greeks, Chinese, Egyptians, Indians, and Persians.
Society and culture
The 1989 "St. Vincent Declaration" was the result of international efforts to improve the care accorded to those with diabetes. Doing so is important not only in terms of quality of life and life expectancy but also economically – expenses due to diabetes have been shown to be a major drain on health – and productivity-related resources for healthcare systems and governments.
Several countries established more and less successful national diabetes programmes to improve treatment of the disease.People with diabetes who have neuropathic symptoms such as numbness or tingling in feet or hands are twice as likely to be unemployed as those without the symptoms.In 2010, diabetes-related emergency room (ER) visit rates in the United States were higher among people from the lowest income communities (526 per 10,000 population) than from the highest income communities (236 per 10,000 population). Approximately 9.4% of diabetes-related ER visits were for the uninsured.
Naming
The term "type 1 diabetes" has replaced several former terms, including childhood-onset diabetes, juvenile diabetes, and insulin-dependent diabetes mellitus. Likewise, the term "type 2 diabetes" has replaced several former terms, including adult-onset diabetes, obesity-related diabetes, and noninsulin-dependent diabetes mellitus. Beyond these two types, there is no agreed-upon standard nomenclature.Diabetes mellitus is also occasionally known as "sugar diabetes" to differentiate it from diabetes insipidus.
Other animals
Diabetes can occur in mammals or reptiles. Birds do not develop diabetes because of their unusually high tolerance for elevated blood glucose levels.In animals, diabetes is most commonly encountered in dogs and cats. Middle-aged animals are most commonly affected. Female dogs are twice as likely to be affected as males, while according to some sources, male cats are more prone than females. In both species, all breeds may be affected, but some small dog breeds are particularly likely to develop diabetes, such as Miniature Poodles.Feline diabetes is strikingly similar to human type 2 diabetes. The Burmese, Russian Blue, Abyssinian, and Norwegian Forest cat breeds are at higher risk than other breeds. Overweight cats are also at higher risk.The symptoms may relate to fluid loss and polyuria, but the course may also be insidious. Diabetic animals are more prone to infections. The long-term complications recognized in humans are much rarer in animals. The principles of treatment (weight loss, oral antidiabetics, subcutaneous insulin) and management of emergencies (e.g. ketoacidosis) are similar to those in humans.
References
External links
American Diabetes Association
IDF Diabetes Atlas
National Diabetes Education Program
ADA's Standards of Medical Care in Diabetes 2019
Polonsky KS (October 2012). "The past 200 years in diabetes". The New England Journal of Medicine. 367 (14): 1332–1340. doi:10.1056/NEJMra1110560. PMID 23034021. S2CID 9456681.
"Diabetes". MedlinePlus. U.S. National Library of Medicine.
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Diabetes, also known as diabetes mellitus, is a group of common endocrine diseases characterized by sustained high blood sugar levels. Diabetes is due to either the pancreas not producing enough insulin, or the cells of the body not responding properly to the insulin produced. Diabetes, if left untreated, leads to many health complications. Untreated or poorly treated diabetes accounts for approximately 1.5 million deaths per year.There is no widely accepted cure for most cases of diabetes. The most common treatment for type 1 diabetes is insulin replacement therapy (insulin injections). Anti-diabetic medications such as metformin and semaglutide, as well as lifestyle modifications, can be used to prevent or respond to type 2 diabetes. Gestational diabetes normally resolves shortly after delivery.
As of 2019, an estimated 463 million people had diabetes worldwide accounting for 8.8% of the adult population. Type 2 diabetes makes up about 90% of all diabetes cases. The prevalence of the disease continues to increase, most dramatically in low- and middle-income nations. Rates are similar in women and men, with diabetes being the 7th-leading cause of death globally. The global expenditure on diabetes-related healthcare is an estimated USD760 billion a year.
Signs and symptoms
The classic symptoms of untreated diabetes are unintended weight loss, polyuria (increased urination), polydipsia (increased thirst), and polyphagia (increased hunger). Symptoms may develop rapidly (weeks or months) in type 1 diabetes, while they usually develop much more slowly and may be subtle or absent in type 2 diabetes.Several other signs and symptoms can mark the onset of diabetes although they are not specific to the disease. In addition to the known symptoms listed above, they include blurred vision, headache, fatigue, slow healing of cuts, and itchy skin. Prolonged high blood glucose can cause glucose absorption in the lens of the eye, which leads to changes in its shape, resulting in vision changes. Long-term vision loss can also be caused by diabetic retinopathy. A number of skin rashes that can occur in diabetes are collectively known as diabetic dermadromes.
Diabetic emergencies
People with diabetes (usually but not exclusively in type 1 diabetes) may also experience diabetic ketoacidosis (DKA), a metabolic disturbance characterized by nausea, vomiting and abdominal pain, the smell of acetone on the breath, deep breathing known as Kussmaul breathing, and in severe cases a decreased level of consciousness. DKA requires emergency treatment in hospital. A rarer but more dangerous condition is hyperosmolar hyperglycemic state (HHS), which is more common in type 2 diabetes and is mainly the result of dehydration caused by high blood sugars.Treatment-related low blood sugar (hypoglycemia) is common in people with type 1 and also type 2 diabetes depending on the medication being used. Most cases are mild and are not considered medical emergencies. Effects can range from feelings of unease, sweating, trembling, and increased appetite in mild cases to more serious effects such as confusion, changes in behavior such as aggressiveness, seizures, unconsciousness, and rarely permanent brain damage or death in severe cases. Rapid breathing, sweating, and cold, pale skin are characteristic of low blood sugar but not definitive. Mild to moderate cases are self-treated by eating or drinking something high in rapidly absorbed carbohydrates. Severe cases can lead to unconsciousness and must be treated with intravenous glucose or injections with glucagon.
Complications
All forms of diabetes increase the risk of long-term complications. These typically develop after many years (10–20) but may be the first symptom in those who have otherwise not received a diagnosis before that time.The major long-term complications relate to damage to blood vessels. Diabetes doubles the risk of cardiovascular disease and about 75% of deaths in people with diabetes are due to coronary artery disease. Other macrovascular diseases include stroke, and peripheral artery disease. These complications are also a strong risk factor for severe COVID-19 illness.The primary complications of diabetes due to damage in small blood vessels include damage to the eyes, kidneys, and nerves. Damage to the eyes, known as diabetic retinopathy, is caused by damage to the blood vessels in the retina of the eye, and can result in gradual vision loss and eventual blindness. Diabetes also increases the risk of having glaucoma, cataracts, and other eye problems. It is recommended that people with diabetes visit an optometrist or ophthalmologist once a year. Damage to the kidneys, known as diabetic nephropathy, can lead to tissue scarring, urine protein loss, and eventually chronic kidney disease, sometimes requiring dialysis or kidney transplantation. Damage to the nerves of the body, known as diabetic neuropathy, is the most common complication of diabetes. The symptoms can include numbness, tingling, sudomotor dysfunction, pain, and altered pain sensation, which can lead to damage to the skin. Diabetes-related foot problems (such as diabetic foot ulcers) may occur, and can be difficult to treat, occasionally requiring amputation. Additionally, proximal diabetic neuropathy causes painful muscle atrophy and weakness.
There is a link between cognitive deficit and diabetes. Compared to those without diabetes, those with the disease have a 1.2 to 1.5-fold greater rate of decline in cognitive function. Having diabetes, especially when on insulin, increases the risk of falls in older people.
Causes
Diabetes mellitus is classified into six categories: type 1 diabetes, type 2 diabetes, hybrid forms of diabetes, hyperglycemia first detected during pregnancy, "unclassified diabetes", and "other specific types". "Hybrid forms of diabetes" include slowly evolving, immune-mediated diabetes of adults and ketosis-prone type 2 diabetes. "Hyperglycemia first detected during pregnancy" includes gestational diabetes mellitus and diabetes mellitus in pregnancy (type 1 or type 2 diabetes first diagnosed during pregnancy). The "other specific types" are a collection of a few dozen individual causes. Diabetes is a more variable disease than once thought and people may have combinations of forms.
Type 1
Type 1 diabetes is characterized by loss of the insulin-producing beta cells of the pancreatic islets, leading to insulin deficiency. This type can be further classified as immune-mediated or idiopathic. The majority of type 1 diabetes is of an immune-mediated nature, in which a T cell-mediated autoimmune attack leads to the loss of beta cells and thus insulin. It causes approximately 10% of diabetes mellitus cases in North America and Europe. Most affected people are otherwise healthy and of a healthy weight when onset occurs. Sensitivity and responsiveness to insulin are usually normal, especially in the early stages. Although it has been called "juvenile diabetes" due to the frequent onset in children, the majority of individuals living with type 1 diabetes are now adults."Brittle" diabetes, also known as unstable diabetes or labile diabetes, is a term that was traditionally used to describe the dramatic and recurrent swings in glucose levels, often occurring for no apparent reason in insulin-dependent diabetes. This term, however, has no biologic basis and should not be used. Still, type 1 diabetes can be accompanied by irregular and unpredictable high blood sugar levels, and the potential for diabetic ketoacidosis or serious low blood sugar levels. Other complications include an impaired counterregulatory response to low blood sugar, infection, gastroparesis (which leads to erratic absorption of dietary carbohydrates), and endocrinopathies (e.g., Addison's disease). These phenomena are believed to occur no more frequently than in 1% to 2% of persons with type 1 diabetes.
Type 1 diabetes is partly inherited, with multiple genes, including certain HLA genotypes, known to influence the risk of diabetes. In genetically susceptible people, the onset of diabetes can be triggered by one or more environmental factors, such as a viral infection or diet. Several viruses have been implicated, but to date there is no stringent evidence to support this hypothesis in humans.Type 1 diabetes can occur at any age, and a significant proportion is diagnosed during adulthood. Latent autoimmune diabetes of adults (LADA) is the diagnostic term applied when type 1 diabetes develops in adults; it has a slower onset than the same condition in children. Given this difference, some use the unofficial term "type 1.5 diabetes" for this condition. Adults with LADA are frequently initially misdiagnosed as having type 2 diabetes, based on age rather than a cause.
Type 2
Type 2 diabetes is characterized by insulin resistance, which may be combined with relatively reduced insulin secretion. The defective responsiveness of body tissues to insulin is believed to involve the insulin receptor. However, the specific defects are not known. Diabetes mellitus cases due to a known defect are classified separately. Type 2 diabetes is the most common type of diabetes mellitus accounting for 95% of diabetes. Many people with type 2 diabetes have evidence of prediabetes (impaired fasting glucose and/or impaired glucose tolerance) before meeting the criteria for type 2 diabetes. The progression of prediabetes to overt type 2 diabetes can be slowed or reversed by lifestyle changes or medications that improve insulin sensitivity or reduce the liver's glucose production.Type 2 diabetes is primarily due to lifestyle factors and genetics. A number of lifestyle factors are known to be important to the development of type 2 diabetes, including obesity (defined by a body mass index of greater than 30), lack of physical activity, poor diet, stress, and urbanization. Excess body fat is associated with 30% of cases in people of Chinese and Japanese descent, 60–80% of cases in those of European and African descent, and 100% of Pima Indians and Pacific Islanders. Even those who are not obese may have a high waist–hip ratio.Dietary factors such as sugar-sweetened drinks are associated with an increased risk. The type of fats in the diet is also important, with saturated fat and trans fats increasing the risk and polyunsaturated and monounsaturated fat decreasing the risk. Eating white rice excessively may increase the risk of diabetes, especially in Chinese and Japanese people. Lack of physical activity may increase the risk of diabetes in some people.Adverse childhood experiences, including abuse, neglect, and household difficulties, increase the likelihood of type 2 diabetes later in life by 32%, with neglect having the strongest effect.Antipsychotic medication side effects (specifically metabolic abnormalities, dyslipidemia and weight gain) and unhealthy lifestyles (including poor diet and decreased physical activity), are potential risk factors.
Gestational diabetes
Gestational diabetes resembles type 2 diabetes in several respects, involving a combination of relatively inadequate insulin secretion and responsiveness. It occurs in about 2–10% of all pregnancies and may improve or disappear after delivery. It is recommended that all pregnant women get tested starting around 24–28 weeks gestation. It is most often diagnosed in the second or third trimester because of the increase in insulin-antagonist hormone levels that occurs at this time. However, after pregnancy approximately 5–10% of women with gestational diabetes are found to have another form of diabetes, most commonly type 2. Gestational diabetes is fully treatable, but requires careful medical supervision throughout the pregnancy. Management may include dietary changes, blood glucose monitoring, and in some cases, insulin may be required.Though it may be transient, untreated gestational diabetes can damage the health of the fetus or mother. Risks to the baby include macrosomia (high birth weight), congenital heart and central nervous system abnormalities, and skeletal muscle malformations. Increased levels of insulin in a fetus's blood may inhibit fetal surfactant production and cause infant respiratory distress syndrome. A high blood bilirubin level may result from red blood cell destruction. In severe cases, perinatal death may occur, most commonly as a result of poor placental perfusion due to vascular impairment. Labor induction may be indicated with decreased placental function. A caesarean section may be performed if there is marked fetal distress or an increased risk of injury associated with macrosomia, such as shoulder dystocia.
Other types
Maturity onset diabetes of the young (MODY) is a rare autosomal dominant inherited form of diabetes, due to one of several single-gene mutations causing defects in insulin production. It is significantly less common than the three main types, constituting 1–2% of all cases. The name of this disease refers to early hypotheses as to its nature. Being due to a defective gene, this disease varies in age at presentation and in severity according to the specific gene defect; thus, there are at least 13 subtypes of MODY. People with MODY often can control it without using insulin.Some cases of diabetes are caused by the body's tissue receptors not responding to insulin (even when insulin levels are normal, which is what separates it from type 2 diabetes); this form is very uncommon. Genetic mutations (autosomal or mitochondrial) can lead to defects in beta cell function. Abnormal insulin action may also have been genetically determined in some cases. Any disease that causes extensive damage to the pancreas may lead to diabetes (for example, chronic pancreatitis and cystic fibrosis). Diseases associated with excessive secretion of insulin-antagonistic hormones can cause diabetes (which is typically resolved once the hormone excess is removed). Many drugs impair insulin secretion and some toxins damage pancreatic beta cells, whereas others increase insulin resistance (especially glucocorticoids which can provoke "steroid diabetes"). The ICD-10 (1992) diagnostic entity, malnutrition-related diabetes mellitus (ICD-10 code E12), was deprecated by the World Health Organization (WHO) when the current taxonomy was introduced in 1999.
Yet another form of diabetes that people may develop is double diabetes. This is when a type 1 diabetic becomes insulin resistant, the hallmark for type 2 diabetes or has a family history for type 2 diabetes. It was first discovered in 1990 or 1991.
The following is a list of disorders that may increase the risk of diabetes:
Pathophysiology
Insulin is the principal hormone that regulates the uptake of glucose from the blood into most cells of the body, especially liver, adipose tissue and muscle, except smooth muscle, in which insulin acts via the IGF-1. Therefore, deficiency of insulin or the insensitivity of its receptors play a central role in all forms of diabetes mellitus.The body obtains glucose from three main sources: the intestinal absorption of food; the breakdown of glycogen (glycogenolysis), the storage form of glucose found in the liver; and gluconeogenesis, the generation of glucose from non-carbohydrate substrates in the body. Insulin plays a critical role in regulating glucose levels in the body. Insulin can inhibit the breakdown of glycogen or the process of gluconeogenesis, it can stimulate the transport of glucose into fat and muscle cells, and it can stimulate the storage of glucose in the form of glycogen.Insulin is released into the blood by beta cells (β-cells), found in the islets of Langerhans in the pancreas, in response to rising levels of blood glucose, typically after eating. Insulin is used by about two-thirds of the body's cells to absorb glucose from the blood for use as fuel, for conversion to other needed molecules, or for storage. Lower glucose levels result in decreased insulin release from the beta cells and in the breakdown of glycogen to glucose. This process is mainly controlled by the hormone glucagon, which acts in the opposite manner to insulin.If the amount of insulin available is insufficient, or if cells respond poorly to the effects of insulin (insulin resistance), or if the insulin itself is defective, then glucose is not absorbed properly by the body cells that require it, and is not stored appropriately in the liver and muscles. The net effect is persistently high levels of blood glucose, poor protein synthesis, and other metabolic derangements, such as metabolic acidosis in cases of complete insulin deficiency.When glucose concentration in the blood remains high over time, the kidneys reach a threshold of reabsorption, and the body excretes glucose in the urine (glycosuria). This increases the osmotic pressure of the urine and inhibits reabsorption of water by the kidney, resulting in increased urine production (polyuria) and increased fluid loss. Lost blood volume is replaced osmotically from water in body cells and other body compartments, causing dehydration and increased thirst (polydipsia). In addition, intracellular glucose deficiency stimulates appetite leading to excessive food intake (polyphagia).
Diagnosis
Diabetes mellitus is diagnosed with a test for the glucose content in the blood, and is diagnosed by demonstrating any one of the following:
Fasting plasma glucose level ≥ 7.0 mmol/L (126 mg/dL). For this test, blood is taken after a period of fasting, i.e. in the morning before breakfast, after the patient had sufficient time to fast overnight.
Plasma glucose ≥ 11.1 mmol/L (200 mg/dL) two hours after a 75 gram oral glucose load as in a glucose tolerance test (OGTT)
Symptoms of high blood sugar and plasma glucose ≥ 11.1 mmol/L (200 mg/dL) either while fasting or not fasting
Glycated hemoglobin (HbA1C) ≥ 48 mmol/mol (≥ 6.5 DCCT %).A positive result, in the absence of unequivocal high blood sugar, should be confirmed by a repeat of any of the above methods on a different day. It is preferable to measure a fasting glucose level because of the ease of measurement and the considerable time commitment of formal glucose tolerance testing, which takes two hours to complete and offers no prognostic advantage over the fasting test. According to the current definition, two fasting glucose measurements at or above 7.0 mmol/L (126 mg/dL) is considered diagnostic for diabetes mellitus.
Per the WHO, people with fasting glucose levels from 6.1 to 6.9 mmol/L (110 to 125 mg/dL) are considered to have impaired fasting glucose. People with plasma glucose at or above 7.8 mmol/L (140 mg/dL), but not over 11.1 mmol/L (200 mg/dL), two hours after a 75 gram oral glucose load are considered to have impaired glucose tolerance. Of these two prediabetic states, the latter in particular is a major risk factor for progression to full-blown diabetes mellitus, as well as cardiovascular disease. The American Diabetes Association (ADA) since 2003 uses a slightly different range for impaired fasting glucose of 5.6 to 6.9 mmol/L (100 to 125 mg/dL).Glycated hemoglobin is better than fasting glucose for determining risks of cardiovascular disease and death from any cause.
Prevention
There is no known preventive measure for type 1 diabetes. Type 2 diabetes—which accounts for 85–90% of all cases worldwide—can often be prevented or delayed by maintaining a normal body weight, engaging in physical activity, and eating a healthy diet. Higher levels of physical activity (more than 90 minutes per day) reduce the risk of diabetes by 28%. Dietary changes known to be effective in helping to prevent diabetes include maintaining a diet rich in whole grains and fiber, and choosing good fats, such as the polyunsaturated fats found in nuts, vegetable oils, and fish. Limiting sugary beverages and eating less red meat and other sources of saturated fat can also help prevent diabetes. Tobacco smoking is also associated with an increased risk of diabetes and its complications, so smoking cessation can be an important preventive measure as well.The relationship between type 2 diabetes and the main modifiable risk factors (excess weight, unhealthy diet, physical inactivity and tobacco use) is similar in all regions of the world. There is growing evidence that the underlying determinants of diabetes are a reflection of the major forces driving social, economic and cultural change: globalization, urbanization, population aging, and the general health policy environment.
Management
Diabetes management concentrates on keeping blood sugar levels close to normal, without causing low blood sugar. This can usually be accomplished with dietary changes, exercise, weight loss, and use of appropriate medications (insulin, oral medications).Learning about the disease and actively participating in the treatment is important, since complications are far less common and less severe in people who have well-managed blood sugar levels. The goal of treatment is an A1C level below 5.7%. Attention is also paid to other health problems that may accelerate the negative effects of diabetes. These include smoking, high blood pressure, metabolic syndrome obesity, and lack of regular exercise. Specialized footwear is widely used to reduce the risk of diabetic foot ulcers by relieving the pressure on the foot. Foot examination for patients living with diabetes should be done annually which includes sensation testing, foot biomechanics, vascular integrity and foot structure.Concerning those with severe mental illness, the efficacy of type 2 diabetes self-management interventions is still poorly explored, with insufficient scientific evidence to show whether these interventions have similar results to those observed in the general population.
Lifestyle
People with diabetes can benefit from education about the disease and treatment, dietary changes, and exercise, with the goal of keeping both short-term and long-term blood glucose levels within acceptable bounds. In addition, given the associated higher risks of cardiovascular disease, lifestyle modifications are recommended to control blood pressure.Weight loss can prevent progression from prediabetes to diabetes type 2, decrease the risk of cardiovascular disease, or result in a partial remission in people with diabetes. No single dietary pattern is best for all people with diabetes. Healthy dietary patterns, such as the Mediterranean diet, low-carbohydrate diet, or DASH diet, are often recommended, although evidence does not support one over the others. According to the ADA, "reducing overall carbohydrate intake for individuals with diabetes has demonstrated the most evidence for improving glycemia", and for individuals with type 2 diabetes who cannot meet the glycemic targets or where reducing anti-glycemic medications is a priority, low or very-low carbohydrate diets are a viable approach. For overweight people with type 2 diabetes, any diet that achieves weight loss is effective.A 2020 Cochrane systematic review compared several non-nutritive sweeteners to sugar, placebo and a nutritive low-calorie sweetener (tagatose), but the results were unclear for effects on HbA1c, body weight and adverse events. The studies included were mainly of very low-certainty and did not report on health-related quality of life, diabetes complications, all-cause mortality or socioeconomic effects.
Medications
Glucose control
Most medications used to treat diabetes act by lowering blood sugar levels through different mechanisms. There is broad consensus that when people with diabetes maintain tight glucose control – keeping the glucose levels in their blood within normal ranges – they experience fewer complications, such as kidney problems or eye problems. There is however debate as to whether this is appropriate and cost effective for people later in life in whom the risk of hypoglycemia may be more significant.There are a number of different classes of anti-diabetic medications. Type 1 diabetes requires treatment with insulin, ideally using a "basal bolus" regimen that most closely matches normal insulin release: long-acting insulin for the basal rate and short-acting insulin with meals. Type 2 diabetes is generally treated with medication that is taken by mouth (e.g. metformin) although some eventually require injectable treatment with insulin or GLP-1 agonists.Metformin is generally recommended as a first-line treatment for type 2 diabetes, as there is good evidence that it decreases mortality. It works by decreasing the liver's production of glucose, and increasing the amount of glucose stored in peripheral tissue. Several other groups of drugs, mainly oral medication, may also decrease blood sugar in type 2 diabetes. These include agents that increase insulin release (sulfonylureas), agents that decrease absorption of sugar from the intestines (acarbose), agents that inhibit the enzyme dipeptidyl peptidase-4 (DPP-4) that inactivates incretins such as GLP-1 and GIP (sitagliptin), agents that make the body more sensitive to insulin (thiazolidinedione) and agents that increase the excretion of glucose in the urine (SGLT2 inhibitors). When insulin is used in type 2 diabetes, a long-acting formulation is usually added initially, while continuing oral medications.Some severe cases of type 2 diabetes may also be treated with insulin, which is increased gradually until glucose targets are reached.
Blood pressure lowering
Cardiovascular disease is a serious complication associated with diabetes, and many international guidelines recommend blood pressure treatment targets that are lower than 140/90 mmHg for people with diabetes. However, there is only limited evidence regarding what the lower targets should be. A 2016 systematic review found potential harm to treating to targets lower than 140 mmHg, and a subsequent systematic review in 2019 found no evidence of additional benefit from blood pressure lowering to between 130 – 140mmHg, although there was an increased risk of adverse events.2015 American Diabetes Association recommendations are that people with diabetes and albuminuria should receive an inhibitor of the renin-angiotensin system to reduce the risks of progression to end-stage renal disease, cardiovascular events, and death. There is some evidence that angiotensin converting enzyme inhibitors (ACEIs) are superior to other inhibitors of the renin-angiotensin system such as angiotensin receptor blockers (ARBs), or aliskiren in preventing cardiovascular disease. Although a more recent review found similar effects of ACEIs and ARBs on major cardiovascular and renal outcomes. There is no evidence that combining ACEIs and ARBs provides additional benefits.
Aspirin
The use of aspirin to prevent cardiovascular disease in diabetes is controversial. Aspirin is recommended by some in people at high risk of cardiovascular disease, however routine use of aspirin has not been found to improve outcomes in uncomplicated diabetes. 2015 American Diabetes Association recommendations for aspirin use (based on expert consensus or clinical experience) are that low-dose aspirin use is reasonable in adults with diabetes who are at intermediate risk of cardiovascular disease (10-year cardiovascular disease risk, 5–10%). National guidelines for England and Wales by the National Institute for Health and Care Excellence (NICE) recommend against the use of aspirin in people with type 1 or type 2 diabetes who do not have confirmed cardiovascular disease.
Surgery
Weight loss surgery in those with obesity and type 2 diabetes is often an effective measure. Many are able to maintain normal blood sugar levels with little or no medications following surgery and long-term mortality is decreased. There is, however, a short-term mortality risk of less than 1% from the surgery. The body mass index cutoffs for when surgery is appropriate are not yet clear. It is recommended that this option be considered in those who are unable to get both their weight and blood sugar under control.A pancreas transplant is occasionally considered for people with type 1 diabetes who have severe complications of their disease, including end stage kidney disease requiring kidney transplantation.
Self-management and support
In countries using a general practitioner system, such as the United Kingdom, care may take place mainly outside hospitals, with hospital-based specialist care used only in case of complications, difficult blood sugar control, or research projects. In other circumstances, general practitioners and specialists share care in a team approach. Home telehealth support can be an effective management technique.The use of technology to deliver educational programs for adults with type 2 diabetes includes computer-based self-management interventions to collect for tailored responses to facilitate self-management. There is no adequate evidence to support effects on cholesterol, blood pressure, behavioral change (such as physical activity levels and dietary), depression, weight and health-related quality of life, nor in other biological, cognitive or emotional outcomes.
Epidemiology
In 2017, 425 million people had diabetes worldwide, up from an estimated 382 million people in 2013 and from 108 million in 1980. Accounting for the shifting age structure of the global population, the prevalence of diabetes is 8.8% among adults, nearly double the rate of 4.7% in 1980. Type 2 makes up about 90% of the cases. Some data indicate rates are roughly equal in women and men, but male excess in diabetes has been found in many populations with higher type 2 incidence, possibly due to sex-related differences in insulin sensitivity, consequences of obesity and regional body fat deposition, and other contributing factors such as high blood pressure, tobacco smoking, and alcohol intake.The WHO estimates that diabetes resulted in 1.5 million deaths in 2012, making it the 8th leading cause of death. However another 2.2 million deaths worldwide were attributable to high blood glucose and the increased risks of cardiovascular disease and other associated complications (e.g. kidney failure), which often lead to premature death and are often listed as the underlying cause on death certificates rather than diabetes. For example, in 2017, the International Diabetes Federation (IDF) estimated that diabetes resulted in 4.0 million deaths worldwide, using modeling to estimate the total number of deaths that could be directly or indirectly attributed to diabetes.Diabetes occurs throughout the world but is more common (especially type 2) in more developed countries. The greatest increase in rates has however been seen in low- and middle-income countries, where more than 80% of diabetic deaths occur. The fastest prevalence increase is expected to occur in Asia and Africa, where most people with diabetes will probably live in 2030. The increase in rates in developing countries follows the trend of urbanization and lifestyle changes, including increasingly sedentary lifestyles, less physically demanding work and the global nutrition transition, marked by increased intake of foods that are high energy-dense but nutrient-poor (often high in sugar and saturated fats, sometimes referred to as the "Western-style" diet). The global number of diabetes cases might increase by 48% between 2017 and 2045.As of 2020, 38% of all US adults had prediabetes. Prediabetes is an early stage of diabetes.
History
Diabetes was one of the first diseases described, with an Egyptian manuscript from c. 1500 BCE mentioning "too great emptying of the urine." The Ebers papyrus includes a recommendation for a drink to take in such cases. The first described cases are believed to have been type 1 diabetes. Indian physicians around the same time identified the disease and classified it as madhumeha or "honey urine", noting the urine would attract ants.The term "diabetes" or "to pass through" was first used in 230 BCE by the Greek Apollonius of Memphis. The disease was considered rare during the time of the Roman empire, with Galen commenting he had only seen two cases during his career. This is possibly due to the diet and lifestyle of the ancients, or because the clinical symptoms were observed during the advanced stage of the disease. Galen named the disease "diarrhea of the urine" (diarrhea urinosa).The earliest surviving work with a detailed reference to diabetes is that of Aretaeus of Cappadocia (2nd or early 3rd century CE). He described the symptoms and the course of the disease, which he attributed to the moisture and coldness, reflecting the beliefs of the "Pneumatic School". He hypothesized a correlation between diabetes and other diseases, and he discussed differential diagnosis from the snakebite, which also provokes excessive thirst. His work remained unknown in the West until 1552, when the first Latin edition was published in Venice.Two types of diabetes were identified as separate conditions for the first time by the Indian physicians Sushruta and Charaka in 400–500 CE with one type being associated with youth and another type with being overweight. Effective treatment was not developed until the early part of the 20th century when Canadians Frederick Banting and Charles Herbert Best isolated and purified insulin in 1921 and 1922. This was followed by the development of the long-acting insulin NPH in the 1940s.
Etymology
The word diabetes ( or ) comes from Latin diabētēs, which in turn comes from Ancient Greek διαβήτης (diabētēs), which literally means "a passer through; a siphon". Ancient Greek physician Aretaeus of Cappadocia (fl. 1st century CE) used that word, with the intended meaning "excessive discharge of urine", as the name for the disease. Ultimately, the word comes from Greek διαβαίνειν (diabainein), meaning "to pass through", which is composed of δια- (dia-), meaning "through" and βαίνειν (bainein), meaning "to go". The word "diabetes" is first recorded in English, in the form diabete, in a medical text written around 1425.
The word mellitus ( or ) comes from the classical Latin word mellītus, meaning "mellite" (i.e. sweetened with honey; honey-sweet). The Latin word comes from mell-, which comes from mel, meaning "honey"; sweetness; pleasant thing, and the suffix -ītus, whose meaning is the same as that of the English suffix "-ite". It was Thomas Willis who in 1675 added "mellitus" to the word "diabetes" as a designation for the disease, when he noticed the urine of a person with diabetes had a sweet taste (glycosuria). This sweet taste had been noticed in urine by the ancient Greeks, Chinese, Egyptians, Indians, and Persians.
Society and culture
The 1989 "St. Vincent Declaration" was the result of international efforts to improve the care accorded to those with diabetes. Doing so is important not only in terms of quality of life and life expectancy but also economically – expenses due to diabetes have been shown to be a major drain on health – and productivity-related resources for healthcare systems and governments.
Several countries established more and less successful national diabetes programmes to improve treatment of the disease.People with diabetes who have neuropathic symptoms such as numbness or tingling in feet or hands are twice as likely to be unemployed as those without the symptoms.In 2010, diabetes-related emergency room (ER) visit rates in the United States were higher among people from the lowest income communities (526 per 10,000 population) than from the highest income communities (236 per 10,000 population). Approximately 9.4% of diabetes-related ER visits were for the uninsured.
Naming
The term "type 1 diabetes" has replaced several former terms, including childhood-onset diabetes, juvenile diabetes, and insulin-dependent diabetes mellitus. Likewise, the term "type 2 diabetes" has replaced several former terms, including adult-onset diabetes, obesity-related diabetes, and noninsulin-dependent diabetes mellitus. Beyond these two types, there is no agreed-upon standard nomenclature.Diabetes mellitus is also occasionally known as "sugar diabetes" to differentiate it from diabetes insipidus.
Other animals
Diabetes can occur in mammals or reptiles. Birds do not develop diabetes because of their unusually high tolerance for elevated blood glucose levels.In animals, diabetes is most commonly encountered in dogs and cats. Middle-aged animals are most commonly affected. Female dogs are twice as likely to be affected as males, while according to some sources, male cats are more prone than females. In both species, all breeds may be affected, but some small dog breeds are particularly likely to develop diabetes, such as Miniature Poodles.Feline diabetes is strikingly similar to human type 2 diabetes. The Burmese, Russian Blue, Abyssinian, and Norwegian Forest cat breeds are at higher risk than other breeds. Overweight cats are also at higher risk.The symptoms may relate to fluid loss and polyuria, but the course may also be insidious. Diabetic animals are more prone to infections. The long-term complications recognized in humans are much rarer in animals. The principles of treatment (weight loss, oral antidiabetics, subcutaneous insulin) and management of emergencies (e.g. ketoacidosis) are similar to those in humans.
References
External links
American Diabetes Association
IDF Diabetes Atlas
National Diabetes Education Program
ADA's Standards of Medical Care in Diabetes 2019
Polonsky KS (October 2012). "The past 200 years in diabetes". The New England Journal of Medicine. 367 (14): 1332–1340. doi:10.1056/NEJMra1110560. PMID 23034021. S2CID 9456681.
"Diabetes". MedlinePlus. U.S. National Library of Medicine.
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Diabetes, also known as diabetes mellitus, is a group of common endocrine diseases characterized by sustained high blood sugar levels. Diabetes is due to either the pancreas not producing enough insulin, or the cells of the body not responding properly to the insulin produced. Diabetes, if left untreated, leads to many health complications. Untreated or poorly treated diabetes accounts for approximately 1.5 million deaths per year.There is no widely accepted cure for most cases of diabetes. The most common treatment for type 1 diabetes is insulin replacement therapy (insulin injections). Anti-diabetic medications such as metformin and semaglutide, as well as lifestyle modifications, can be used to prevent or respond to type 2 diabetes. Gestational diabetes normally resolves shortly after delivery.
As of 2019, an estimated 463 million people had diabetes worldwide accounting for 8.8% of the adult population. Type 2 diabetes makes up about 90% of all diabetes cases. The prevalence of the disease continues to increase, most dramatically in low- and middle-income nations. Rates are similar in women and men, with diabetes being the 7th-leading cause of death globally. The global expenditure on diabetes-related healthcare is an estimated USD760 billion a year.
Signs and symptoms
The classic symptoms of untreated diabetes are unintended weight loss, polyuria (increased urination), polydipsia (increased thirst), and polyphagia (increased hunger). Symptoms may develop rapidly (weeks or months) in type 1 diabetes, while they usually develop much more slowly and may be subtle or absent in type 2 diabetes.Several other signs and symptoms can mark the onset of diabetes although they are not specific to the disease. In addition to the known symptoms listed above, they include blurred vision, headache, fatigue, slow healing of cuts, and itchy skin. Prolonged high blood glucose can cause glucose absorption in the lens of the eye, which leads to changes in its shape, resulting in vision changes. Long-term vision loss can also be caused by diabetic retinopathy. A number of skin rashes that can occur in diabetes are collectively known as diabetic dermadromes.
Diabetic emergencies
People with diabetes (usually but not exclusively in type 1 diabetes) may also experience diabetic ketoacidosis (DKA), a metabolic disturbance characterized by nausea, vomiting and abdominal pain, the smell of acetone on the breath, deep breathing known as Kussmaul breathing, and in severe cases a decreased level of consciousness. DKA requires emergency treatment in hospital. A rarer but more dangerous condition is hyperosmolar hyperglycemic state (HHS), which is more common in type 2 diabetes and is mainly the result of dehydration caused by high blood sugars.Treatment-related low blood sugar (hypoglycemia) is common in people with type 1 and also type 2 diabetes depending on the medication being used. Most cases are mild and are not considered medical emergencies. Effects can range from feelings of unease, sweating, trembling, and increased appetite in mild cases to more serious effects such as confusion, changes in behavior such as aggressiveness, seizures, unconsciousness, and rarely permanent brain damage or death in severe cases. Rapid breathing, sweating, and cold, pale skin are characteristic of low blood sugar but not definitive. Mild to moderate cases are self-treated by eating or drinking something high in rapidly absorbed carbohydrates. Severe cases can lead to unconsciousness and must be treated with intravenous glucose or injections with glucagon.
Complications
All forms of diabetes increase the risk of long-term complications. These typically develop after many years (10–20) but may be the first symptom in those who have otherwise not received a diagnosis before that time.The major long-term complications relate to damage to blood vessels. Diabetes doubles the risk of cardiovascular disease and about 75% of deaths in people with diabetes are due to coronary artery disease. Other macrovascular diseases include stroke, and peripheral artery disease. These complications are also a strong risk factor for severe COVID-19 illness.The primary complications of diabetes due to damage in small blood vessels include damage to the eyes, kidneys, and nerves. Damage to the eyes, known as diabetic retinopathy, is caused by damage to the blood vessels in the retina of the eye, and can result in gradual vision loss and eventual blindness. Diabetes also increases the risk of having glaucoma, cataracts, and other eye problems. It is recommended that people with diabetes visit an optometrist or ophthalmologist once a year. Damage to the kidneys, known as diabetic nephropathy, can lead to tissue scarring, urine protein loss, and eventually chronic kidney disease, sometimes requiring dialysis or kidney transplantation. Damage to the nerves of the body, known as diabetic neuropathy, is the most common complication of diabetes. The symptoms can include numbness, tingling, sudomotor dysfunction, pain, and altered pain sensation, which can lead to damage to the skin. Diabetes-related foot problems (such as diabetic foot ulcers) may occur, and can be difficult to treat, occasionally requiring amputation. Additionally, proximal diabetic neuropathy causes painful muscle atrophy and weakness.
There is a link between cognitive deficit and diabetes. Compared to those without diabetes, those with the disease have a 1.2 to 1.5-fold greater rate of decline in cognitive function. Having diabetes, especially when on insulin, increases the risk of falls in older people.
Causes
Diabetes mellitus is classified into six categories: type 1 diabetes, type 2 diabetes, hybrid forms of diabetes, hyperglycemia first detected during pregnancy, "unclassified diabetes", and "other specific types". "Hybrid forms of diabetes" include slowly evolving, immune-mediated diabetes of adults and ketosis-prone type 2 diabetes. "Hyperglycemia first detected during pregnancy" includes gestational diabetes mellitus and diabetes mellitus in pregnancy (type 1 or type 2 diabetes first diagnosed during pregnancy). The "other specific types" are a collection of a few dozen individual causes. Diabetes is a more variable disease than once thought and people may have combinations of forms.
Type 1
Type 1 diabetes is characterized by loss of the insulin-producing beta cells of the pancreatic islets, leading to insulin deficiency. This type can be further classified as immune-mediated or idiopathic. The majority of type 1 diabetes is of an immune-mediated nature, in which a T cell-mediated autoimmune attack leads to the loss of beta cells and thus insulin. It causes approximately 10% of diabetes mellitus cases in North America and Europe. Most affected people are otherwise healthy and of a healthy weight when onset occurs. Sensitivity and responsiveness to insulin are usually normal, especially in the early stages. Although it has been called "juvenile diabetes" due to the frequent onset in children, the majority of individuals living with type 1 diabetes are now adults."Brittle" diabetes, also known as unstable diabetes or labile diabetes, is a term that was traditionally used to describe the dramatic and recurrent swings in glucose levels, often occurring for no apparent reason in insulin-dependent diabetes. This term, however, has no biologic basis and should not be used. Still, type 1 diabetes can be accompanied by irregular and unpredictable high blood sugar levels, and the potential for diabetic ketoacidosis or serious low blood sugar levels. Other complications include an impaired counterregulatory response to low blood sugar, infection, gastroparesis (which leads to erratic absorption of dietary carbohydrates), and endocrinopathies (e.g., Addison's disease). These phenomena are believed to occur no more frequently than in 1% to 2% of persons with type 1 diabetes.
Type 1 diabetes is partly inherited, with multiple genes, including certain HLA genotypes, known to influence the risk of diabetes. In genetically susceptible people, the onset of diabetes can be triggered by one or more environmental factors, such as a viral infection or diet. Several viruses have been implicated, but to date there is no stringent evidence to support this hypothesis in humans.Type 1 diabetes can occur at any age, and a significant proportion is diagnosed during adulthood. Latent autoimmune diabetes of adults (LADA) is the diagnostic term applied when type 1 diabetes develops in adults; it has a slower onset than the same condition in children. Given this difference, some use the unofficial term "type 1.5 diabetes" for this condition. Adults with LADA are frequently initially misdiagnosed as having type 2 diabetes, based on age rather than a cause.
Type 2
Type 2 diabetes is characterized by insulin resistance, which may be combined with relatively reduced insulin secretion. The defective responsiveness of body tissues to insulin is believed to involve the insulin receptor. However, the specific defects are not known. Diabetes mellitus cases due to a known defect are classified separately. Type 2 diabetes is the most common type of diabetes mellitus accounting for 95% of diabetes. Many people with type 2 diabetes have evidence of prediabetes (impaired fasting glucose and/or impaired glucose tolerance) before meeting the criteria for type 2 diabetes. The progression of prediabetes to overt type 2 diabetes can be slowed or reversed by lifestyle changes or medications that improve insulin sensitivity or reduce the liver's glucose production.Type 2 diabetes is primarily due to lifestyle factors and genetics. A number of lifestyle factors are known to be important to the development of type 2 diabetes, including obesity (defined by a body mass index of greater than 30), lack of physical activity, poor diet, stress, and urbanization. Excess body fat is associated with 30% of cases in people of Chinese and Japanese descent, 60–80% of cases in those of European and African descent, and 100% of Pima Indians and Pacific Islanders. Even those who are not obese may have a high waist–hip ratio.Dietary factors such as sugar-sweetened drinks are associated with an increased risk. The type of fats in the diet is also important, with saturated fat and trans fats increasing the risk and polyunsaturated and monounsaturated fat decreasing the risk. Eating white rice excessively may increase the risk of diabetes, especially in Chinese and Japanese people. Lack of physical activity may increase the risk of diabetes in some people.Adverse childhood experiences, including abuse, neglect, and household difficulties, increase the likelihood of type 2 diabetes later in life by 32%, with neglect having the strongest effect.Antipsychotic medication side effects (specifically metabolic abnormalities, dyslipidemia and weight gain) and unhealthy lifestyles (including poor diet and decreased physical activity), are potential risk factors.
Gestational diabetes
Gestational diabetes resembles type 2 diabetes in several respects, involving a combination of relatively inadequate insulin secretion and responsiveness. It occurs in about 2–10% of all pregnancies and may improve or disappear after delivery. It is recommended that all pregnant women get tested starting around 24–28 weeks gestation. It is most often diagnosed in the second or third trimester because of the increase in insulin-antagonist hormone levels that occurs at this time. However, after pregnancy approximately 5–10% of women with gestational diabetes are found to have another form of diabetes, most commonly type 2. Gestational diabetes is fully treatable, but requires careful medical supervision throughout the pregnancy. Management may include dietary changes, blood glucose monitoring, and in some cases, insulin may be required.Though it may be transient, untreated gestational diabetes can damage the health of the fetus or mother. Risks to the baby include macrosomia (high birth weight), congenital heart and central nervous system abnormalities, and skeletal muscle malformations. Increased levels of insulin in a fetus's blood may inhibit fetal surfactant production and cause infant respiratory distress syndrome. A high blood bilirubin level may result from red blood cell destruction. In severe cases, perinatal death may occur, most commonly as a result of poor placental perfusion due to vascular impairment. Labor induction may be indicated with decreased placental function. A caesarean section may be performed if there is marked fetal distress or an increased risk of injury associated with macrosomia, such as shoulder dystocia.
Other types
Maturity onset diabetes of the young (MODY) is a rare autosomal dominant inherited form of diabetes, due to one of several single-gene mutations causing defects in insulin production. It is significantly less common than the three main types, constituting 1–2% of all cases. The name of this disease refers to early hypotheses as to its nature. Being due to a defective gene, this disease varies in age at presentation and in severity according to the specific gene defect; thus, there are at least 13 subtypes of MODY. People with MODY often can control it without using insulin.Some cases of diabetes are caused by the body's tissue receptors not responding to insulin (even when insulin levels are normal, which is what separates it from type 2 diabetes); this form is very uncommon. Genetic mutations (autosomal or mitochondrial) can lead to defects in beta cell function. Abnormal insulin action may also have been genetically determined in some cases. Any disease that causes extensive damage to the pancreas may lead to diabetes (for example, chronic pancreatitis and cystic fibrosis). Diseases associated with excessive secretion of insulin-antagonistic hormones can cause diabetes (which is typically resolved once the hormone excess is removed). Many drugs impair insulin secretion and some toxins damage pancreatic beta cells, whereas others increase insulin resistance (especially glucocorticoids which can provoke "steroid diabetes"). The ICD-10 (1992) diagnostic entity, malnutrition-related diabetes mellitus (ICD-10 code E12), was deprecated by the World Health Organization (WHO) when the current taxonomy was introduced in 1999.
Yet another form of diabetes that people may develop is double diabetes. This is when a type 1 diabetic becomes insulin resistant, the hallmark for type 2 diabetes or has a family history for type 2 diabetes. It was first discovered in 1990 or 1991.
The following is a list of disorders that may increase the risk of diabetes:
Pathophysiology
Insulin is the principal hormone that regulates the uptake of glucose from the blood into most cells of the body, especially liver, adipose tissue and muscle, except smooth muscle, in which insulin acts via the IGF-1. Therefore, deficiency of insulin or the insensitivity of its receptors play a central role in all forms of diabetes mellitus.The body obtains glucose from three main sources: the intestinal absorption of food; the breakdown of glycogen (glycogenolysis), the storage form of glucose found in the liver; and gluconeogenesis, the generation of glucose from non-carbohydrate substrates in the body. Insulin plays a critical role in regulating glucose levels in the body. Insulin can inhibit the breakdown of glycogen or the process of gluconeogenesis, it can stimulate the transport of glucose into fat and muscle cells, and it can stimulate the storage of glucose in the form of glycogen.Insulin is released into the blood by beta cells (β-cells), found in the islets of Langerhans in the pancreas, in response to rising levels of blood glucose, typically after eating. Insulin is used by about two-thirds of the body's cells to absorb glucose from the blood for use as fuel, for conversion to other needed molecules, or for storage. Lower glucose levels result in decreased insulin release from the beta cells and in the breakdown of glycogen to glucose. This process is mainly controlled by the hormone glucagon, which acts in the opposite manner to insulin.If the amount of insulin available is insufficient, or if cells respond poorly to the effects of insulin (insulin resistance), or if the insulin itself is defective, then glucose is not absorbed properly by the body cells that require it, and is not stored appropriately in the liver and muscles. The net effect is persistently high levels of blood glucose, poor protein synthesis, and other metabolic derangements, such as metabolic acidosis in cases of complete insulin deficiency.When glucose concentration in the blood remains high over time, the kidneys reach a threshold of reabsorption, and the body excretes glucose in the urine (glycosuria). This increases the osmotic pressure of the urine and inhibits reabsorption of water by the kidney, resulting in increased urine production (polyuria) and increased fluid loss. Lost blood volume is replaced osmotically from water in body cells and other body compartments, causing dehydration and increased thirst (polydipsia). In addition, intracellular glucose deficiency stimulates appetite leading to excessive food intake (polyphagia).
Diagnosis
Diabetes mellitus is diagnosed with a test for the glucose content in the blood, and is diagnosed by demonstrating any one of the following:
Fasting plasma glucose level ≥ 7.0 mmol/L (126 mg/dL). For this test, blood is taken after a period of fasting, i.e. in the morning before breakfast, after the patient had sufficient time to fast overnight.
Plasma glucose ≥ 11.1 mmol/L (200 mg/dL) two hours after a 75 gram oral glucose load as in a glucose tolerance test (OGTT)
Symptoms of high blood sugar and plasma glucose ≥ 11.1 mmol/L (200 mg/dL) either while fasting or not fasting
Glycated hemoglobin (HbA1C) ≥ 48 mmol/mol (≥ 6.5 DCCT %).A positive result, in the absence of unequivocal high blood sugar, should be confirmed by a repeat of any of the above methods on a different day. It is preferable to measure a fasting glucose level because of the ease of measurement and the considerable time commitment of formal glucose tolerance testing, which takes two hours to complete and offers no prognostic advantage over the fasting test. According to the current definition, two fasting glucose measurements at or above 7.0 mmol/L (126 mg/dL) is considered diagnostic for diabetes mellitus.
Per the WHO, people with fasting glucose levels from 6.1 to 6.9 mmol/L (110 to 125 mg/dL) are considered to have impaired fasting glucose. People with plasma glucose at or above 7.8 mmol/L (140 mg/dL), but not over 11.1 mmol/L (200 mg/dL), two hours after a 75 gram oral glucose load are considered to have impaired glucose tolerance. Of these two prediabetic states, the latter in particular is a major risk factor for progression to full-blown diabetes mellitus, as well as cardiovascular disease. The American Diabetes Association (ADA) since 2003 uses a slightly different range for impaired fasting glucose of 5.6 to 6.9 mmol/L (100 to 125 mg/dL).Glycated hemoglobin is better than fasting glucose for determining risks of cardiovascular disease and death from any cause.
Prevention
There is no known preventive measure for type 1 diabetes. Type 2 diabetes—which accounts for 85–90% of all cases worldwide—can often be prevented or delayed by maintaining a normal body weight, engaging in physical activity, and eating a healthy diet. Higher levels of physical activity (more than 90 minutes per day) reduce the risk of diabetes by 28%. Dietary changes known to be effective in helping to prevent diabetes include maintaining a diet rich in whole grains and fiber, and choosing good fats, such as the polyunsaturated fats found in nuts, vegetable oils, and fish. Limiting sugary beverages and eating less red meat and other sources of saturated fat can also help prevent diabetes. Tobacco smoking is also associated with an increased risk of diabetes and its complications, so smoking cessation can be an important preventive measure as well.The relationship between type 2 diabetes and the main modifiable risk factors (excess weight, unhealthy diet, physical inactivity and tobacco use) is similar in all regions of the world. There is growing evidence that the underlying determinants of diabetes are a reflection of the major forces driving social, economic and cultural change: globalization, urbanization, population aging, and the general health policy environment.
Management
Diabetes management concentrates on keeping blood sugar levels close to normal, without causing low blood sugar. This can usually be accomplished with dietary changes, exercise, weight loss, and use of appropriate medications (insulin, oral medications).Learning about the disease and actively participating in the treatment is important, since complications are far less common and less severe in people who have well-managed blood sugar levels. The goal of treatment is an A1C level below 5.7%. Attention is also paid to other health problems that may accelerate the negative effects of diabetes. These include smoking, high blood pressure, metabolic syndrome obesity, and lack of regular exercise. Specialized footwear is widely used to reduce the risk of diabetic foot ulcers by relieving the pressure on the foot. Foot examination for patients living with diabetes should be done annually which includes sensation testing, foot biomechanics, vascular integrity and foot structure.Concerning those with severe mental illness, the efficacy of type 2 diabetes self-management interventions is still poorly explored, with insufficient scientific evidence to show whether these interventions have similar results to those observed in the general population.
Lifestyle
People with diabetes can benefit from education about the disease and treatment, dietary changes, and exercise, with the goal of keeping both short-term and long-term blood glucose levels within acceptable bounds. In addition, given the associated higher risks of cardiovascular disease, lifestyle modifications are recommended to control blood pressure.Weight loss can prevent progression from prediabetes to diabetes type 2, decrease the risk of cardiovascular disease, or result in a partial remission in people with diabetes. No single dietary pattern is best for all people with diabetes. Healthy dietary patterns, such as the Mediterranean diet, low-carbohydrate diet, or DASH diet, are often recommended, although evidence does not support one over the others. According to the ADA, "reducing overall carbohydrate intake for individuals with diabetes has demonstrated the most evidence for improving glycemia", and for individuals with type 2 diabetes who cannot meet the glycemic targets or where reducing anti-glycemic medications is a priority, low or very-low carbohydrate diets are a viable approach. For overweight people with type 2 diabetes, any diet that achieves weight loss is effective.A 2020 Cochrane systematic review compared several non-nutritive sweeteners to sugar, placebo and a nutritive low-calorie sweetener (tagatose), but the results were unclear for effects on HbA1c, body weight and adverse events. The studies included were mainly of very low-certainty and did not report on health-related quality of life, diabetes complications, all-cause mortality or socioeconomic effects.
Medications
Glucose control
Most medications used to treat diabetes act by lowering blood sugar levels through different mechanisms. There is broad consensus that when people with diabetes maintain tight glucose control – keeping the glucose levels in their blood within normal ranges – they experience fewer complications, such as kidney problems or eye problems. There is however debate as to whether this is appropriate and cost effective for people later in life in whom the risk of hypoglycemia may be more significant.There are a number of different classes of anti-diabetic medications. Type 1 diabetes requires treatment with insulin, ideally using a "basal bolus" regimen that most closely matches normal insulin release: long-acting insulin for the basal rate and short-acting insulin with meals. Type 2 diabetes is generally treated with medication that is taken by mouth (e.g. metformin) although some eventually require injectable treatment with insulin or GLP-1 agonists.Metformin is generally recommended as a first-line treatment for type 2 diabetes, as there is good evidence that it decreases mortality. It works by decreasing the liver's production of glucose, and increasing the amount of glucose stored in peripheral tissue. Several other groups of drugs, mainly oral medication, may also decrease blood sugar in type 2 diabetes. These include agents that increase insulin release (sulfonylureas), agents that decrease absorption of sugar from the intestines (acarbose), agents that inhibit the enzyme dipeptidyl peptidase-4 (DPP-4) that inactivates incretins such as GLP-1 and GIP (sitagliptin), agents that make the body more sensitive to insulin (thiazolidinedione) and agents that increase the excretion of glucose in the urine (SGLT2 inhibitors). When insulin is used in type 2 diabetes, a long-acting formulation is usually added initially, while continuing oral medications.Some severe cases of type 2 diabetes may also be treated with insulin, which is increased gradually until glucose targets are reached.
Blood pressure lowering
Cardiovascular disease is a serious complication associated with diabetes, and many international guidelines recommend blood pressure treatment targets that are lower than 140/90 mmHg for people with diabetes. However, there is only limited evidence regarding what the lower targets should be. A 2016 systematic review found potential harm to treating to targets lower than 140 mmHg, and a subsequent systematic review in 2019 found no evidence of additional benefit from blood pressure lowering to between 130 – 140mmHg, although there was an increased risk of adverse events.2015 American Diabetes Association recommendations are that people with diabetes and albuminuria should receive an inhibitor of the renin-angiotensin system to reduce the risks of progression to end-stage renal disease, cardiovascular events, and death. There is some evidence that angiotensin converting enzyme inhibitors (ACEIs) are superior to other inhibitors of the renin-angiotensin system such as angiotensin receptor blockers (ARBs), or aliskiren in preventing cardiovascular disease. Although a more recent review found similar effects of ACEIs and ARBs on major cardiovascular and renal outcomes. There is no evidence that combining ACEIs and ARBs provides additional benefits.
Aspirin
The use of aspirin to prevent cardiovascular disease in diabetes is controversial. Aspirin is recommended by some in people at high risk of cardiovascular disease, however routine use of aspirin has not been found to improve outcomes in uncomplicated diabetes. 2015 American Diabetes Association recommendations for aspirin use (based on expert consensus or clinical experience) are that low-dose aspirin use is reasonable in adults with diabetes who are at intermediate risk of cardiovascular disease (10-year cardiovascular disease risk, 5–10%). National guidelines for England and Wales by the National Institute for Health and Care Excellence (NICE) recommend against the use of aspirin in people with type 1 or type 2 diabetes who do not have confirmed cardiovascular disease.
Surgery
Weight loss surgery in those with obesity and type 2 diabetes is often an effective measure. Many are able to maintain normal blood sugar levels with little or no medications following surgery and long-term mortality is decreased. There is, however, a short-term mortality risk of less than 1% from the surgery. The body mass index cutoffs for when surgery is appropriate are not yet clear. It is recommended that this option be considered in those who are unable to get both their weight and blood sugar under control.A pancreas transplant is occasionally considered for people with type 1 diabetes who have severe complications of their disease, including end stage kidney disease requiring kidney transplantation.
Self-management and support
In countries using a general practitioner system, such as the United Kingdom, care may take place mainly outside hospitals, with hospital-based specialist care used only in case of complications, difficult blood sugar control, or research projects. In other circumstances, general practitioners and specialists share care in a team approach. Home telehealth support can be an effective management technique.The use of technology to deliver educational programs for adults with type 2 diabetes includes computer-based self-management interventions to collect for tailored responses to facilitate self-management. There is no adequate evidence to support effects on cholesterol, blood pressure, behavioral change (such as physical activity levels and dietary), depression, weight and health-related quality of life, nor in other biological, cognitive or emotional outcomes.
Epidemiology
In 2017, 425 million people had diabetes worldwide, up from an estimated 382 million people in 2013 and from 108 million in 1980. Accounting for the shifting age structure of the global population, the prevalence of diabetes is 8.8% among adults, nearly double the rate of 4.7% in 1980. Type 2 makes up about 90% of the cases. Some data indicate rates are roughly equal in women and men, but male excess in diabetes has been found in many populations with higher type 2 incidence, possibly due to sex-related differences in insulin sensitivity, consequences of obesity and regional body fat deposition, and other contributing factors such as high blood pressure, tobacco smoking, and alcohol intake.The WHO estimates that diabetes resulted in 1.5 million deaths in 2012, making it the 8th leading cause of death. However another 2.2 million deaths worldwide were attributable to high blood glucose and the increased risks of cardiovascular disease and other associated complications (e.g. kidney failure), which often lead to premature death and are often listed as the underlying cause on death certificates rather than diabetes. For example, in 2017, the International Diabetes Federation (IDF) estimated that diabetes resulted in 4.0 million deaths worldwide, using modeling to estimate the total number of deaths that could be directly or indirectly attributed to diabetes.Diabetes occurs throughout the world but is more common (especially type 2) in more developed countries. The greatest increase in rates has however been seen in low- and middle-income countries, where more than 80% of diabetic deaths occur. The fastest prevalence increase is expected to occur in Asia and Africa, where most people with diabetes will probably live in 2030. The increase in rates in developing countries follows the trend of urbanization and lifestyle changes, including increasingly sedentary lifestyles, less physically demanding work and the global nutrition transition, marked by increased intake of foods that are high energy-dense but nutrient-poor (often high in sugar and saturated fats, sometimes referred to as the "Western-style" diet). The global number of diabetes cases might increase by 48% between 2017 and 2045.As of 2020, 38% of all US adults had prediabetes. Prediabetes is an early stage of diabetes.
History
Diabetes was one of the first diseases described, with an Egyptian manuscript from c. 1500 BCE mentioning "too great emptying of the urine." The Ebers papyrus includes a recommendation for a drink to take in such cases. The first described cases are believed to have been type 1 diabetes. Indian physicians around the same time identified the disease and classified it as madhumeha or "honey urine", noting the urine would attract ants.The term "diabetes" or "to pass through" was first used in 230 BCE by the Greek Apollonius of Memphis. The disease was considered rare during the time of the Roman empire, with Galen commenting he had only seen two cases during his career. This is possibly due to the diet and lifestyle of the ancients, or because the clinical symptoms were observed during the advanced stage of the disease. Galen named the disease "diarrhea of the urine" (diarrhea urinosa).The earliest surviving work with a detailed reference to diabetes is that of Aretaeus of Cappadocia (2nd or early 3rd century CE). He described the symptoms and the course of the disease, which he attributed to the moisture and coldness, reflecting the beliefs of the "Pneumatic School". He hypothesized a correlation between diabetes and other diseases, and he discussed differential diagnosis from the snakebite, which also provokes excessive thirst. His work remained unknown in the West until 1552, when the first Latin edition was published in Venice.Two types of diabetes were identified as separate conditions for the first time by the Indian physicians Sushruta and Charaka in 400–500 CE with one type being associated with youth and another type with being overweight. Effective treatment was not developed until the early part of the 20th century when Canadians Frederick Banting and Charles Herbert Best isolated and purified insulin in 1921 and 1922. This was followed by the development of the long-acting insulin NPH in the 1940s.
Etymology
The word diabetes ( or ) comes from Latin diabētēs, which in turn comes from Ancient Greek διαβήτης (diabētēs), which literally means "a passer through; a siphon". Ancient Greek physician Aretaeus of Cappadocia (fl. 1st century CE) used that word, with the intended meaning "excessive discharge of urine", as the name for the disease. Ultimately, the word comes from Greek διαβαίνειν (diabainein), meaning "to pass through", which is composed of δια- (dia-), meaning "through" and βαίνειν (bainein), meaning "to go". The word "diabetes" is first recorded in English, in the form diabete, in a medical text written around 1425.
The word mellitus ( or ) comes from the classical Latin word mellītus, meaning "mellite" (i.e. sweetened with honey; honey-sweet). The Latin word comes from mell-, which comes from mel, meaning "honey"; sweetness; pleasant thing, and the suffix -ītus, whose meaning is the same as that of the English suffix "-ite". It was Thomas Willis who in 1675 added "mellitus" to the word "diabetes" as a designation for the disease, when he noticed the urine of a person with diabetes had a sweet taste (glycosuria). This sweet taste had been noticed in urine by the ancient Greeks, Chinese, Egyptians, Indians, and Persians.
Society and culture
The 1989 "St. Vincent Declaration" was the result of international efforts to improve the care accorded to those with diabetes. Doing so is important not only in terms of quality of life and life expectancy but also economically – expenses due to diabetes have been shown to be a major drain on health – and productivity-related resources for healthcare systems and governments.
Several countries established more and less successful national diabetes programmes to improve treatment of the disease.People with diabetes who have neuropathic symptoms such as numbness or tingling in feet or hands are twice as likely to be unemployed as those without the symptoms.In 2010, diabetes-related emergency room (ER) visit rates in the United States were higher among people from the lowest income communities (526 per 10,000 population) than from the highest income communities (236 per 10,000 population). Approximately 9.4% of diabetes-related ER visits were for the uninsured.
Naming
The term "type 1 diabetes" has replaced several former terms, including childhood-onset diabetes, juvenile diabetes, and insulin-dependent diabetes mellitus. Likewise, the term "type 2 diabetes" has replaced several former terms, including adult-onset diabetes, obesity-related diabetes, and noninsulin-dependent diabetes mellitus. Beyond these two types, there is no agreed-upon standard nomenclature.Diabetes mellitus is also occasionally known as "sugar diabetes" to differentiate it from diabetes insipidus.
Other animals
Diabetes can occur in mammals or reptiles. Birds do not develop diabetes because of their unusually high tolerance for elevated blood glucose levels.In animals, diabetes is most commonly encountered in dogs and cats. Middle-aged animals are most commonly affected. Female dogs are twice as likely to be affected as males, while according to some sources, male cats are more prone than females. In both species, all breeds may be affected, but some small dog breeds are particularly likely to develop diabetes, such as Miniature Poodles.Feline diabetes is strikingly similar to human type 2 diabetes. The Burmese, Russian Blue, Abyssinian, and Norwegian Forest cat breeds are at higher risk than other breeds. Overweight cats are also at higher risk.The symptoms may relate to fluid loss and polyuria, but the course may also be insidious. Diabetic animals are more prone to infections. The long-term complications recognized in humans are much rarer in animals. The principles of treatment (weight loss, oral antidiabetics, subcutaneous insulin) and management of emergencies (e.g. ketoacidosis) are similar to those in humans.
References
External links
American Diabetes Association
IDF Diabetes Atlas
National Diabetes Education Program
ADA's Standards of Medical Care in Diabetes 2019
Polonsky KS (October 2012). "The past 200 years in diabetes". The New England Journal of Medicine. 367 (14): 1332–1340. doi:10.1056/NEJMra1110560. PMID 23034021. S2CID 9456681.
"Diabetes". MedlinePlus. U.S. National Library of Medicine.
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Edward William Staebler (December 26, 1872 – November 10, 1946) was a Michigan politician.
Early life
Edward W. Staebler was born in Lodi Township, Michigan to parents Michael and Katherine Rosina Staebler on December 26, 1872. Staebler was of German ancestry.
Career
Staebler was involved with an early automobile dealership in the city of Ann Arbor, Michigan. Staebler served as mayor of Ann Arbor from 1926 to 1931. Staebler was a Democrat. In 1932, Staebler ran unsuccessfully for the Michigan State House of Representatives representing Washtenaw County.
Personal life
Staebler married Magdalena Dold in 1895. Together, they had at least two children including U.S. Representative Neil Staebler.
Death
Staebler died on November 10, 1946. Staebler was interred at Forest Hill Cemetery in Ann Arbor.
== References ==
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place of birth
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Edward William Staebler (December 26, 1872 – November 10, 1946) was a Michigan politician.
Early life
Edward W. Staebler was born in Lodi Township, Michigan to parents Michael and Katherine Rosina Staebler on December 26, 1872. Staebler was of German ancestry.
Career
Staebler was involved with an early automobile dealership in the city of Ann Arbor, Michigan. Staebler served as mayor of Ann Arbor from 1926 to 1931. Staebler was a Democrat. In 1932, Staebler ran unsuccessfully for the Michigan State House of Representatives representing Washtenaw County.
Personal life
Staebler married Magdalena Dold in 1895. Together, they had at least two children including U.S. Representative Neil Staebler.
Death
Staebler died on November 10, 1946. Staebler was interred at Forest Hill Cemetery in Ann Arbor.
== References ==
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occupation
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Edward William Staebler (December 26, 1872 – November 10, 1946) was a Michigan politician.
Early life
Edward W. Staebler was born in Lodi Township, Michigan to parents Michael and Katherine Rosina Staebler on December 26, 1872. Staebler was of German ancestry.
Career
Staebler was involved with an early automobile dealership in the city of Ann Arbor, Michigan. Staebler served as mayor of Ann Arbor from 1926 to 1931. Staebler was a Democrat. In 1932, Staebler ran unsuccessfully for the Michigan State House of Representatives representing Washtenaw County.
Personal life
Staebler married Magdalena Dold in 1895. Together, they had at least two children including U.S. Representative Neil Staebler.
Death
Staebler died on November 10, 1946. Staebler was interred at Forest Hill Cemetery in Ann Arbor.
== References ==
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given name
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United Nations Security Council resolution 948, adopted on 15 October 1994, after recalling resolutions 841 (1993), 861 (1993), 862 (1993), 867 (1993), 873 (1993), 875 (1993), 905 (1994), 917 (1994), 933 (1994), 940 (1994) and 944 (1994), the Council welcomed the return of the legitimate President of Haiti Jean-Bertrand Aristide and lifted sanctions imposed on the country.The Council went on to welcome the process of implementing the Governors Island Agreement, the New York Pact, and the objectives of the United Nations with the convening of the Haitian National Parliament, expressing full support to all democratic institutions and leaders in the country and all states and organisations that had contributed to this outcome. The efforts of the multinational force established in Resolution 940 were also recognised.The United Nations Mission in Haiti (UNMIH) would replace the multinational force when a stable environment was established, supporting the efforts of the Secretary-General Boutros Boutros-Ghali to complete the composition of UNMIH. A new appointment of the Special Representative of the Secretary-General was welcomed, urging co-operation between the Secretaries-General of the United Nations and Organization of American States especially with regard to the return of the International Civilian Mission to Haiti.
Resolution 948 was adopted by 14 votes to none against, while Brazil abstained from the voting.
See also
History of Haiti
List of United Nations Security Council Resolutions 901 to 1000 (1994–1995)
Operation Uphold Democracy
References
External links
Works related to United Nations Security Council Resolution 948 at Wikisource
Text of the Resolution at undocs.org
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United Nations Security Council resolution 948, adopted on 15 October 1994, after recalling resolutions 841 (1993), 861 (1993), 862 (1993), 867 (1993), 873 (1993), 875 (1993), 905 (1994), 917 (1994), 933 (1994), 940 (1994) and 944 (1994), the Council welcomed the return of the legitimate President of Haiti Jean-Bertrand Aristide and lifted sanctions imposed on the country.The Council went on to welcome the process of implementing the Governors Island Agreement, the New York Pact, and the objectives of the United Nations with the convening of the Haitian National Parliament, expressing full support to all democratic institutions and leaders in the country and all states and organisations that had contributed to this outcome. The efforts of the multinational force established in Resolution 940 were also recognised.The United Nations Mission in Haiti (UNMIH) would replace the multinational force when a stable environment was established, supporting the efforts of the Secretary-General Boutros Boutros-Ghali to complete the composition of UNMIH. A new appointment of the Special Representative of the Secretary-General was welcomed, urging co-operation between the Secretaries-General of the United Nations and Organization of American States especially with regard to the return of the International Civilian Mission to Haiti.
Resolution 948 was adopted by 14 votes to none against, while Brazil abstained from the voting.
See also
History of Haiti
List of United Nations Security Council Resolutions 901 to 1000 (1994–1995)
Operation Uphold Democracy
References
External links
Works related to United Nations Security Council Resolution 948 at Wikisource
Text of the Resolution at undocs.org
|
legislated by
|
{
"answer_start": [
0
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"United Nations Security Council"
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United Nations Security Council resolution 948, adopted on 15 October 1994, after recalling resolutions 841 (1993), 861 (1993), 862 (1993), 867 (1993), 873 (1993), 875 (1993), 905 (1994), 917 (1994), 933 (1994), 940 (1994) and 944 (1994), the Council welcomed the return of the legitimate President of Haiti Jean-Bertrand Aristide and lifted sanctions imposed on the country.The Council went on to welcome the process of implementing the Governors Island Agreement, the New York Pact, and the objectives of the United Nations with the convening of the Haitian National Parliament, expressing full support to all democratic institutions and leaders in the country and all states and organisations that had contributed to this outcome. The efforts of the multinational force established in Resolution 940 were also recognised.The United Nations Mission in Haiti (UNMIH) would replace the multinational force when a stable environment was established, supporting the efforts of the Secretary-General Boutros Boutros-Ghali to complete the composition of UNMIH. A new appointment of the Special Representative of the Secretary-General was welcomed, urging co-operation between the Secretaries-General of the United Nations and Organization of American States especially with regard to the return of the International Civilian Mission to Haiti.
Resolution 948 was adopted by 14 votes to none against, while Brazil abstained from the voting.
See also
History of Haiti
List of United Nations Security Council Resolutions 901 to 1000 (1994–1995)
Operation Uphold Democracy
References
External links
Works related to United Nations Security Council Resolution 948 at Wikisource
Text of the Resolution at undocs.org
|
series ordinal
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{
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43
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"text": [
"948"
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Benjaminiomyces is a genus of fungi in the family Laboulbeniaceae. The genus contains four species.
References
External links
Benjaminiomyces at Index Fungorum
|
taxon rank
|
{
"answer_start": [
21
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"text": [
"genus"
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Benjaminiomyces is a genus of fungi in the family Laboulbeniaceae. The genus contains four species.
References
External links
Benjaminiomyces at Index Fungorum
|
parent taxon
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{
"answer_start": [
50
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"text": [
"Laboulbeniaceae"
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Benjaminiomyces is a genus of fungi in the family Laboulbeniaceae. The genus contains four species.
References
External links
Benjaminiomyces at Index Fungorum
|
taxon name
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{
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Rowland "Rowley" James (14 June 1885 – 4 July 1962) was an Australian politician and coalminer. He was a member of the House of Representatives from 1928 to 1958, representing the New South Wales seat of Hunter. He was a member of the Australian Labor Party (ALP), although during the 1930s he was associated with the breakaway Lang Labor faction.
Early life
James was born on 14 June 1885 in Lambton, New South Wales. He was the youngest of eleven children born to Welsh immigrant parents Mary Ann (née James) and Moses James. His father was a coal miner.James attended a local public school before beginning work as a coal miner in the Newcastle district. In 1912 he moved to Collie, Western Australia, where he was lodge secretary of the Collie River District Miners' Union of Workers. He returned to New South Wales in 1916 and was an officeholder in the Australasian Coal and Shale Employees' Federation, representing the northern district on the union's central council. In 1928 he sought to succeed Daniel Rees as general president of the federation, but withdrew to stand for parliament.
Politics
James was elected to the Australian House of Representatives for the Australian Labor Party in 1928, succeeding former Labor leader Matthew Charlton in the seat of Hunter. He was a critic of both the conservative government of Stanley Bruce and the Labor government of James Scullin for not prosecuting mine-owners during the protracted miner lock-out in northern New South Wales (1929–30), which led to accusations of inciting mob violence; Smith's Weekly published his record of convictions, including drunkenness and assaulting police.
A supporter of Jack Lang's proposal that New South Wales should not repay interest to British bond-holders in the height of the Great Depression, James joined Jack Beasley's Lang Labor Party, along with six other New South Wales MPs, who voted in opposition to defeat the Scullin government. At the ensuing elections, both Labor parties lost heavily but James easily retained his seat.
Re-admitted to the ALP in 1936, James was chairman of the parliamentary standing committee on public works from 1943, and led the Australian delegation to the first International Labour Organization coal-mining committee in London in 1945. He continued to be prominent in coal-mining affairs, and his support for Prime Minister Ben Chifley's stand on the 1949 coal strike prompted some to express a desire to expel him from the Miners' Federation.
A man who disliked convention, James was succeeded in the seat of Hunter in 1958 by ALP leader H. V. Evatt, who was in turn succeeded by James' son Bert. James died on 4 July 1962 in the Sydney suburb of Ashfield, and was survived by his wife, daughter and three of his five sons.
Personal life
James married Gladys Mary Davies in 1912, with whom he had a daughter and five sons. He died on 4 July 1962 in Ashfield, New South Wales, aged 77. Two of his sons predeceased him.James's son, William Thomas James, was a fitter on the NSW Railways, and was shot and killed by Roy Hindle at the South Maitland railway workshop on 20 November 1941. Hindle was acquitted of the charge of murder.
References
Fredman, L. E. (1996). "James, Rowland (Rowley) (1885-1962)". Australian Dictionary of Biography. National Centre of Biography, Australian National University. ISSN 1833-7538. Retrieved 25 August 2007.
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place of birth
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Rowland "Rowley" James (14 June 1885 – 4 July 1962) was an Australian politician and coalminer. He was a member of the House of Representatives from 1928 to 1958, representing the New South Wales seat of Hunter. He was a member of the Australian Labor Party (ALP), although during the 1930s he was associated with the breakaway Lang Labor faction.
Early life
James was born on 14 June 1885 in Lambton, New South Wales. He was the youngest of eleven children born to Welsh immigrant parents Mary Ann (née James) and Moses James. His father was a coal miner.James attended a local public school before beginning work as a coal miner in the Newcastle district. In 1912 he moved to Collie, Western Australia, where he was lodge secretary of the Collie River District Miners' Union of Workers. He returned to New South Wales in 1916 and was an officeholder in the Australasian Coal and Shale Employees' Federation, representing the northern district on the union's central council. In 1928 he sought to succeed Daniel Rees as general president of the federation, but withdrew to stand for parliament.
Politics
James was elected to the Australian House of Representatives for the Australian Labor Party in 1928, succeeding former Labor leader Matthew Charlton in the seat of Hunter. He was a critic of both the conservative government of Stanley Bruce and the Labor government of James Scullin for not prosecuting mine-owners during the protracted miner lock-out in northern New South Wales (1929–30), which led to accusations of inciting mob violence; Smith's Weekly published his record of convictions, including drunkenness and assaulting police.
A supporter of Jack Lang's proposal that New South Wales should not repay interest to British bond-holders in the height of the Great Depression, James joined Jack Beasley's Lang Labor Party, along with six other New South Wales MPs, who voted in opposition to defeat the Scullin government. At the ensuing elections, both Labor parties lost heavily but James easily retained his seat.
Re-admitted to the ALP in 1936, James was chairman of the parliamentary standing committee on public works from 1943, and led the Australian delegation to the first International Labour Organization coal-mining committee in London in 1945. He continued to be prominent in coal-mining affairs, and his support for Prime Minister Ben Chifley's stand on the 1949 coal strike prompted some to express a desire to expel him from the Miners' Federation.
A man who disliked convention, James was succeeded in the seat of Hunter in 1958 by ALP leader H. V. Evatt, who was in turn succeeded by James' son Bert. James died on 4 July 1962 in the Sydney suburb of Ashfield, and was survived by his wife, daughter and three of his five sons.
Personal life
James married Gladys Mary Davies in 1912, with whom he had a daughter and five sons. He died on 4 July 1962 in Ashfield, New South Wales, aged 77. Two of his sons predeceased him.James's son, William Thomas James, was a fitter on the NSW Railways, and was shot and killed by Roy Hindle at the South Maitland railway workshop on 20 November 1941. Hindle was acquitted of the charge of murder.
References
Fredman, L. E. (1996). "James, Rowland (Rowley) (1885-1962)". Australian Dictionary of Biography. National Centre of Biography, Australian National University. ISSN 1833-7538. Retrieved 25 August 2007.
|
place of death
|
{
"answer_start": [
2684
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"text": [
"Ashfield"
]
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|
Rowland "Rowley" James (14 June 1885 – 4 July 1962) was an Australian politician and coalminer. He was a member of the House of Representatives from 1928 to 1958, representing the New South Wales seat of Hunter. He was a member of the Australian Labor Party (ALP), although during the 1930s he was associated with the breakaway Lang Labor faction.
Early life
James was born on 14 June 1885 in Lambton, New South Wales. He was the youngest of eleven children born to Welsh immigrant parents Mary Ann (née James) and Moses James. His father was a coal miner.James attended a local public school before beginning work as a coal miner in the Newcastle district. In 1912 he moved to Collie, Western Australia, where he was lodge secretary of the Collie River District Miners' Union of Workers. He returned to New South Wales in 1916 and was an officeholder in the Australasian Coal and Shale Employees' Federation, representing the northern district on the union's central council. In 1928 he sought to succeed Daniel Rees as general president of the federation, but withdrew to stand for parliament.
Politics
James was elected to the Australian House of Representatives for the Australian Labor Party in 1928, succeeding former Labor leader Matthew Charlton in the seat of Hunter. He was a critic of both the conservative government of Stanley Bruce and the Labor government of James Scullin for not prosecuting mine-owners during the protracted miner lock-out in northern New South Wales (1929–30), which led to accusations of inciting mob violence; Smith's Weekly published his record of convictions, including drunkenness and assaulting police.
A supporter of Jack Lang's proposal that New South Wales should not repay interest to British bond-holders in the height of the Great Depression, James joined Jack Beasley's Lang Labor Party, along with six other New South Wales MPs, who voted in opposition to defeat the Scullin government. At the ensuing elections, both Labor parties lost heavily but James easily retained his seat.
Re-admitted to the ALP in 1936, James was chairman of the parliamentary standing committee on public works from 1943, and led the Australian delegation to the first International Labour Organization coal-mining committee in London in 1945. He continued to be prominent in coal-mining affairs, and his support for Prime Minister Ben Chifley's stand on the 1949 coal strike prompted some to express a desire to expel him from the Miners' Federation.
A man who disliked convention, James was succeeded in the seat of Hunter in 1958 by ALP leader H. V. Evatt, who was in turn succeeded by James' son Bert. James died on 4 July 1962 in the Sydney suburb of Ashfield, and was survived by his wife, daughter and three of his five sons.
Personal life
James married Gladys Mary Davies in 1912, with whom he had a daughter and five sons. He died on 4 July 1962 in Ashfield, New South Wales, aged 77. Two of his sons predeceased him.James's son, William Thomas James, was a fitter on the NSW Railways, and was shot and killed by Roy Hindle at the South Maitland railway workshop on 20 November 1941. Hindle was acquitted of the charge of murder.
References
Fredman, L. E. (1996). "James, Rowland (Rowley) (1885-1962)". Australian Dictionary of Biography. National Centre of Biography, Australian National University. ISSN 1833-7538. Retrieved 25 August 2007.
|
country of citizenship
|
{
"answer_start": [
59
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"text": [
"Australia"
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}
|
Rowland "Rowley" James (14 June 1885 – 4 July 1962) was an Australian politician and coalminer. He was a member of the House of Representatives from 1928 to 1958, representing the New South Wales seat of Hunter. He was a member of the Australian Labor Party (ALP), although during the 1930s he was associated with the breakaway Lang Labor faction.
Early life
James was born on 14 June 1885 in Lambton, New South Wales. He was the youngest of eleven children born to Welsh immigrant parents Mary Ann (née James) and Moses James. His father was a coal miner.James attended a local public school before beginning work as a coal miner in the Newcastle district. In 1912 he moved to Collie, Western Australia, where he was lodge secretary of the Collie River District Miners' Union of Workers. He returned to New South Wales in 1916 and was an officeholder in the Australasian Coal and Shale Employees' Federation, representing the northern district on the union's central council. In 1928 he sought to succeed Daniel Rees as general president of the federation, but withdrew to stand for parliament.
Politics
James was elected to the Australian House of Representatives for the Australian Labor Party in 1928, succeeding former Labor leader Matthew Charlton in the seat of Hunter. He was a critic of both the conservative government of Stanley Bruce and the Labor government of James Scullin for not prosecuting mine-owners during the protracted miner lock-out in northern New South Wales (1929–30), which led to accusations of inciting mob violence; Smith's Weekly published his record of convictions, including drunkenness and assaulting police.
A supporter of Jack Lang's proposal that New South Wales should not repay interest to British bond-holders in the height of the Great Depression, James joined Jack Beasley's Lang Labor Party, along with six other New South Wales MPs, who voted in opposition to defeat the Scullin government. At the ensuing elections, both Labor parties lost heavily but James easily retained his seat.
Re-admitted to the ALP in 1936, James was chairman of the parliamentary standing committee on public works from 1943, and led the Australian delegation to the first International Labour Organization coal-mining committee in London in 1945. He continued to be prominent in coal-mining affairs, and his support for Prime Minister Ben Chifley's stand on the 1949 coal strike prompted some to express a desire to expel him from the Miners' Federation.
A man who disliked convention, James was succeeded in the seat of Hunter in 1958 by ALP leader H. V. Evatt, who was in turn succeeded by James' son Bert. James died on 4 July 1962 in the Sydney suburb of Ashfield, and was survived by his wife, daughter and three of his five sons.
Personal life
James married Gladys Mary Davies in 1912, with whom he had a daughter and five sons. He died on 4 July 1962 in Ashfield, New South Wales, aged 77. Two of his sons predeceased him.James's son, William Thomas James, was a fitter on the NSW Railways, and was shot and killed by Roy Hindle at the South Maitland railway workshop on 20 November 1941. Hindle was acquitted of the charge of murder.
References
Fredman, L. E. (1996). "James, Rowland (Rowley) (1885-1962)". Australian Dictionary of Biography. National Centre of Biography, Australian National University. ISSN 1833-7538. Retrieved 25 August 2007.
|
member of political party
|
{
"answer_start": [
235
],
"text": [
"Australian Labor Party"
]
}
|
Rowland "Rowley" James (14 June 1885 – 4 July 1962) was an Australian politician and coalminer. He was a member of the House of Representatives from 1928 to 1958, representing the New South Wales seat of Hunter. He was a member of the Australian Labor Party (ALP), although during the 1930s he was associated with the breakaway Lang Labor faction.
Early life
James was born on 14 June 1885 in Lambton, New South Wales. He was the youngest of eleven children born to Welsh immigrant parents Mary Ann (née James) and Moses James. His father was a coal miner.James attended a local public school before beginning work as a coal miner in the Newcastle district. In 1912 he moved to Collie, Western Australia, where he was lodge secretary of the Collie River District Miners' Union of Workers. He returned to New South Wales in 1916 and was an officeholder in the Australasian Coal and Shale Employees' Federation, representing the northern district on the union's central council. In 1928 he sought to succeed Daniel Rees as general president of the federation, but withdrew to stand for parliament.
Politics
James was elected to the Australian House of Representatives for the Australian Labor Party in 1928, succeeding former Labor leader Matthew Charlton in the seat of Hunter. He was a critic of both the conservative government of Stanley Bruce and the Labor government of James Scullin for not prosecuting mine-owners during the protracted miner lock-out in northern New South Wales (1929–30), which led to accusations of inciting mob violence; Smith's Weekly published his record of convictions, including drunkenness and assaulting police.
A supporter of Jack Lang's proposal that New South Wales should not repay interest to British bond-holders in the height of the Great Depression, James joined Jack Beasley's Lang Labor Party, along with six other New South Wales MPs, who voted in opposition to defeat the Scullin government. At the ensuing elections, both Labor parties lost heavily but James easily retained his seat.
Re-admitted to the ALP in 1936, James was chairman of the parliamentary standing committee on public works from 1943, and led the Australian delegation to the first International Labour Organization coal-mining committee in London in 1945. He continued to be prominent in coal-mining affairs, and his support for Prime Minister Ben Chifley's stand on the 1949 coal strike prompted some to express a desire to expel him from the Miners' Federation.
A man who disliked convention, James was succeeded in the seat of Hunter in 1958 by ALP leader H. V. Evatt, who was in turn succeeded by James' son Bert. James died on 4 July 1962 in the Sydney suburb of Ashfield, and was survived by his wife, daughter and three of his five sons.
Personal life
James married Gladys Mary Davies in 1912, with whom he had a daughter and five sons. He died on 4 July 1962 in Ashfield, New South Wales, aged 77. Two of his sons predeceased him.James's son, William Thomas James, was a fitter on the NSW Railways, and was shot and killed by Roy Hindle at the South Maitland railway workshop on 20 November 1941. Hindle was acquitted of the charge of murder.
References
Fredman, L. E. (1996). "James, Rowland (Rowley) (1885-1962)". Australian Dictionary of Biography. National Centre of Biography, Australian National University. ISSN 1833-7538. Retrieved 25 August 2007.
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occupation
|
{
"answer_start": [
70
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"text": [
"politician"
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Rowland "Rowley" James (14 June 1885 – 4 July 1962) was an Australian politician and coalminer. He was a member of the House of Representatives from 1928 to 1958, representing the New South Wales seat of Hunter. He was a member of the Australian Labor Party (ALP), although during the 1930s he was associated with the breakaway Lang Labor faction.
Early life
James was born on 14 June 1885 in Lambton, New South Wales. He was the youngest of eleven children born to Welsh immigrant parents Mary Ann (née James) and Moses James. His father was a coal miner.James attended a local public school before beginning work as a coal miner in the Newcastle district. In 1912 he moved to Collie, Western Australia, where he was lodge secretary of the Collie River District Miners' Union of Workers. He returned to New South Wales in 1916 and was an officeholder in the Australasian Coal and Shale Employees' Federation, representing the northern district on the union's central council. In 1928 he sought to succeed Daniel Rees as general president of the federation, but withdrew to stand for parliament.
Politics
James was elected to the Australian House of Representatives for the Australian Labor Party in 1928, succeeding former Labor leader Matthew Charlton in the seat of Hunter. He was a critic of both the conservative government of Stanley Bruce and the Labor government of James Scullin for not prosecuting mine-owners during the protracted miner lock-out in northern New South Wales (1929–30), which led to accusations of inciting mob violence; Smith's Weekly published his record of convictions, including drunkenness and assaulting police.
A supporter of Jack Lang's proposal that New South Wales should not repay interest to British bond-holders in the height of the Great Depression, James joined Jack Beasley's Lang Labor Party, along with six other New South Wales MPs, who voted in opposition to defeat the Scullin government. At the ensuing elections, both Labor parties lost heavily but James easily retained his seat.
Re-admitted to the ALP in 1936, James was chairman of the parliamentary standing committee on public works from 1943, and led the Australian delegation to the first International Labour Organization coal-mining committee in London in 1945. He continued to be prominent in coal-mining affairs, and his support for Prime Minister Ben Chifley's stand on the 1949 coal strike prompted some to express a desire to expel him from the Miners' Federation.
A man who disliked convention, James was succeeded in the seat of Hunter in 1958 by ALP leader H. V. Evatt, who was in turn succeeded by James' son Bert. James died on 4 July 1962 in the Sydney suburb of Ashfield, and was survived by his wife, daughter and three of his five sons.
Personal life
James married Gladys Mary Davies in 1912, with whom he had a daughter and five sons. He died on 4 July 1962 in Ashfield, New South Wales, aged 77. Two of his sons predeceased him.James's son, William Thomas James, was a fitter on the NSW Railways, and was shot and killed by Roy Hindle at the South Maitland railway workshop on 20 November 1941. Hindle was acquitted of the charge of murder.
References
Fredman, L. E. (1996). "James, Rowland (Rowley) (1885-1962)". Australian Dictionary of Biography. National Centre of Biography, Australian National University. ISSN 1833-7538. Retrieved 25 August 2007.
|
family name
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{
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"text": [
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Rowland "Rowley" James (14 June 1885 – 4 July 1962) was an Australian politician and coalminer. He was a member of the House of Representatives from 1928 to 1958, representing the New South Wales seat of Hunter. He was a member of the Australian Labor Party (ALP), although during the 1930s he was associated with the breakaway Lang Labor faction.
Early life
James was born on 14 June 1885 in Lambton, New South Wales. He was the youngest of eleven children born to Welsh immigrant parents Mary Ann (née James) and Moses James. His father was a coal miner.James attended a local public school before beginning work as a coal miner in the Newcastle district. In 1912 he moved to Collie, Western Australia, where he was lodge secretary of the Collie River District Miners' Union of Workers. He returned to New South Wales in 1916 and was an officeholder in the Australasian Coal and Shale Employees' Federation, representing the northern district on the union's central council. In 1928 he sought to succeed Daniel Rees as general president of the federation, but withdrew to stand for parliament.
Politics
James was elected to the Australian House of Representatives for the Australian Labor Party in 1928, succeeding former Labor leader Matthew Charlton in the seat of Hunter. He was a critic of both the conservative government of Stanley Bruce and the Labor government of James Scullin for not prosecuting mine-owners during the protracted miner lock-out in northern New South Wales (1929–30), which led to accusations of inciting mob violence; Smith's Weekly published his record of convictions, including drunkenness and assaulting police.
A supporter of Jack Lang's proposal that New South Wales should not repay interest to British bond-holders in the height of the Great Depression, James joined Jack Beasley's Lang Labor Party, along with six other New South Wales MPs, who voted in opposition to defeat the Scullin government. At the ensuing elections, both Labor parties lost heavily but James easily retained his seat.
Re-admitted to the ALP in 1936, James was chairman of the parliamentary standing committee on public works from 1943, and led the Australian delegation to the first International Labour Organization coal-mining committee in London in 1945. He continued to be prominent in coal-mining affairs, and his support for Prime Minister Ben Chifley's stand on the 1949 coal strike prompted some to express a desire to expel him from the Miners' Federation.
A man who disliked convention, James was succeeded in the seat of Hunter in 1958 by ALP leader H. V. Evatt, who was in turn succeeded by James' son Bert. James died on 4 July 1962 in the Sydney suburb of Ashfield, and was survived by his wife, daughter and three of his five sons.
Personal life
James married Gladys Mary Davies in 1912, with whom he had a daughter and five sons. He died on 4 July 1962 in Ashfield, New South Wales, aged 77. Two of his sons predeceased him.James's son, William Thomas James, was a fitter on the NSW Railways, and was shot and killed by Roy Hindle at the South Maitland railway workshop on 20 November 1941. Hindle was acquitted of the charge of murder.
References
Fredman, L. E. (1996). "James, Rowland (Rowley) (1885-1962)". Australian Dictionary of Biography. National Centre of Biography, Australian National University. ISSN 1833-7538. Retrieved 25 August 2007.
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given name
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{
"answer_start": [
9
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"text": [
"Rowley"
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}
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A mezzanine (; or in Italian, a mezzanino) is an intermediate floor in a building which is partly open to the double-height ceilinged floor below, or which does not extend over the whole floorspace of the building, a loft with non-sloped walls. However, the term is often used loosely for the floor above the ground floor, especially where a very high-ceilinged original ground floor has been split horizontally into two floors.
Mezzanines may serve a wide variety of functions. Industrial mezzanines, such as those used in warehouses, may be temporary or semi-permanent structures.
In Royal Italian architecture, mezzanino also means a chamber created by partitioning that does not go up all the way to the arch vaulting or ceiling; these were historically common in Italy and France, for example in the palaces for the nobility at the Quirinal Palace.
Definition
A mezzanine is an intermediate floor (or floors) in a building which is open to the floor below. It is placed halfway (mezzo means 'half' in Italian) up the wall on a floor which has a ceiling at least twice as high as a floor with minimum height. A mezzanine does not count as one of the floors in a building, and generally does not count in determining maximum floorspace. The International Building Code permits a mezzanine to have as much as one-third of the floor space of the floor below. Local building codes may vary somewhat from this standard. A space may have more than one mezzanine, as long as the sum total of floor space of all the mezzanines is not greater than one-third the floor space of the complete floor below.Mezzanines help to make a high-ceilinged space feel more personal and less vast, and can create additional floor space. Mezzanines, however, may have lower-than-normal ceilings due to their location. The term "mezzanine" does not imply any particular function; mezzanines can be used for a wide array of purposes.Mezzanines are commonly used in modern architecture, which places a heavy emphasis on light and space.
Industrial mezzanines
In industrial settings, mezzanines may be installed (rather than built as part of the structure) in high-ceilinged spaces such as warehouses. These semi-permanent structures are usually free-standing, can be dismantled and relocated, and are sold commercially. Industrial mezzanine structures can be supported by structural steel columns and elements, or by racks or shelves. Depending on the span and the run of the mezzanine, different materials may be used for the mezzanine's deck like fibre cement boards. Some industrial mezzanines may also include enclosed, paneled office space on their upper levels. There are three basic types of industrial mezzanines: custom, standard or modular.
A structural engineer is sometimes hired to help determine whether the floor of the building can support a mezzanine (and how heavy the mezzanine may be), and to design the appropriate mezzanine.
Custom mezzanines
Custom Mezzanines are steel, raised industrial platform structures that are designed specifically to match the space and capacity needs of a given facility. It will, at a minimum, include a stairway for accessing the mezzanine. These structures typically are the strongest in terms of support capacity.
Standard mezzanines
Standard Mezzanines are steel, raised industrial platform structures that are completely self-supporting and are sold in pre-determined sizes and shapes. These off-the-shelf structures are usually strong (in terms of support capacity) and less expensive than custom mezzanines.
Modular mezzanines
Modular Mezzanines are a type of Industrial Mezzanine that can be assembled by bolting together standard-sized, self-supporting, independent raised platform structures.
Safety
Employees in material handling and manufacturing are often at risk of falls when they are on the job. Recent figures show approximately 20,000 serious injuries and nearly 100 fatalities a year in industrial facilities. Falls of people and objects from mezzanines are of particular concern.In many industrial operations, openings are cut into the guardrail on mezzanines and elevated work platforms to allow picking of palletized material to be loaded and unloaded, often with a fork truck, to upper levels. The Occupational Safety and Health Administration (OSHA) and International Building Council (IBC) have published regulations for fall protection and The American National Standards Institute (ANSI) has published standards for securing pallet drop areas to protect workers that work on elevated platforms and are exposed to openings.
In most cases, safety gates are used to secure these openings. OSHA requires openings 48 inches or taller to be secured with a fall protection system. Removable sections of railing or gates that swing or slide open would be used to open up the area and allow the transfer of material, and then close once the material is removed. However, current ANSI standards require dual-gate safety systems for fall protection.Dual-gate safety systems were created to secure these areas, allowing a barrier to be in place at all times, even while pallets are being loaded or removed. Dual-gate systems create a completely enclosed workstation providing protection for the worker during loading and off-loading operations. When the rear-side gate opens, the ledge gate automatically closes, ensuring there is always a gate between the operator and the ledge.
References
Bibliography
Aghayere, Abi O.; Vigil, Jason (2007). Structural Wood Design: A Practice-Oriented Approach. Hoboken, N.J.: John Wiley. ISBN 978-0-470-05678-3.
Allen, Edward; Iano, Joseph (2012). The Architect's Studio Companion: Rules of Thumb for Preliminary Design. Hoboken, N.J.: John Wiley & Sons. ISBN 978-0-470-64191-0.
Coates, Michael; Brooker, Graeme; Stone, Sally (2008). The Visual Dictionary of Interior Architecture and Design. Lausanne: AVA Academia. ISBN 9782940373802.
Drury, Jolyon; Falconer, Peter (2003). Buildings for Industrial Storage and Distribution. New York: Routledge. ISBN 0-7506-4819-8.
Guo, Qinghua (2010). The Mingqi Pottery Buildings of Han Dynasty China, 206 BC-AD 220: Architectural Representations and Represented Architecture. Portland, Ore.: Sussex Academic Press. ISBN 978-1-84519-321-8.
Habraken, N.J.; Teicher, Jonathan (1998). Structure of the Ordinary: Form and Control in the Built Environment. Cambridge, Massachusetts: MIT Press. ISBN 978-0-262-58195-0.
Harris, Cyril M. (1983). Illustrated Dictionary of Historic Architecture. New York: Dover Publications. ISBN 978-0-486-24444-0.
Materials Handling and Management Society (1993). The Professional Materials Handling Learning System: A Basic Reference Collection in Materials Handling. Volume 2. Charlotte, N.C.: Material Handling Education Foundation.
External links
Proper safeguarding for elevated work platforms (1:37 min. video)Video showing the main construction of an industrial mezzanine floor(2.46 min video)
|
title
|
{
"answer_start": [
429
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"text": [
"Mezzanine"
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A mezzanine (; or in Italian, a mezzanino) is an intermediate floor in a building which is partly open to the double-height ceilinged floor below, or which does not extend over the whole floorspace of the building, a loft with non-sloped walls. However, the term is often used loosely for the floor above the ground floor, especially where a very high-ceilinged original ground floor has been split horizontally into two floors.
Mezzanines may serve a wide variety of functions. Industrial mezzanines, such as those used in warehouses, may be temporary or semi-permanent structures.
In Royal Italian architecture, mezzanino also means a chamber created by partitioning that does not go up all the way to the arch vaulting or ceiling; these were historically common in Italy and France, for example in the palaces for the nobility at the Quirinal Palace.
Definition
A mezzanine is an intermediate floor (or floors) in a building which is open to the floor below. It is placed halfway (mezzo means 'half' in Italian) up the wall on a floor which has a ceiling at least twice as high as a floor with minimum height. A mezzanine does not count as one of the floors in a building, and generally does not count in determining maximum floorspace. The International Building Code permits a mezzanine to have as much as one-third of the floor space of the floor below. Local building codes may vary somewhat from this standard. A space may have more than one mezzanine, as long as the sum total of floor space of all the mezzanines is not greater than one-third the floor space of the complete floor below.Mezzanines help to make a high-ceilinged space feel more personal and less vast, and can create additional floor space. Mezzanines, however, may have lower-than-normal ceilings due to their location. The term "mezzanine" does not imply any particular function; mezzanines can be used for a wide array of purposes.Mezzanines are commonly used in modern architecture, which places a heavy emphasis on light and space.
Industrial mezzanines
In industrial settings, mezzanines may be installed (rather than built as part of the structure) in high-ceilinged spaces such as warehouses. These semi-permanent structures are usually free-standing, can be dismantled and relocated, and are sold commercially. Industrial mezzanine structures can be supported by structural steel columns and elements, or by racks or shelves. Depending on the span and the run of the mezzanine, different materials may be used for the mezzanine's deck like fibre cement boards. Some industrial mezzanines may also include enclosed, paneled office space on their upper levels. There are three basic types of industrial mezzanines: custom, standard or modular.
A structural engineer is sometimes hired to help determine whether the floor of the building can support a mezzanine (and how heavy the mezzanine may be), and to design the appropriate mezzanine.
Custom mezzanines
Custom Mezzanines are steel, raised industrial platform structures that are designed specifically to match the space and capacity needs of a given facility. It will, at a minimum, include a stairway for accessing the mezzanine. These structures typically are the strongest in terms of support capacity.
Standard mezzanines
Standard Mezzanines are steel, raised industrial platform structures that are completely self-supporting and are sold in pre-determined sizes and shapes. These off-the-shelf structures are usually strong (in terms of support capacity) and less expensive than custom mezzanines.
Modular mezzanines
Modular Mezzanines are a type of Industrial Mezzanine that can be assembled by bolting together standard-sized, self-supporting, independent raised platform structures.
Safety
Employees in material handling and manufacturing are often at risk of falls when they are on the job. Recent figures show approximately 20,000 serious injuries and nearly 100 fatalities a year in industrial facilities. Falls of people and objects from mezzanines are of particular concern.In many industrial operations, openings are cut into the guardrail on mezzanines and elevated work platforms to allow picking of palletized material to be loaded and unloaded, often with a fork truck, to upper levels. The Occupational Safety and Health Administration (OSHA) and International Building Council (IBC) have published regulations for fall protection and The American National Standards Institute (ANSI) has published standards for securing pallet drop areas to protect workers that work on elevated platforms and are exposed to openings.
In most cases, safety gates are used to secure these openings. OSHA requires openings 48 inches or taller to be secured with a fall protection system. Removable sections of railing or gates that swing or slide open would be used to open up the area and allow the transfer of material, and then close once the material is removed. However, current ANSI standards require dual-gate safety systems for fall protection.Dual-gate safety systems were created to secure these areas, allowing a barrier to be in place at all times, even while pallets are being loaded or removed. Dual-gate systems create a completely enclosed workstation providing protection for the worker during loading and off-loading operations. When the rear-side gate opens, the ledge gate automatically closes, ensuring there is always a gate between the operator and the ledge.
References
Bibliography
Aghayere, Abi O.; Vigil, Jason (2007). Structural Wood Design: A Practice-Oriented Approach. Hoboken, N.J.: John Wiley. ISBN 978-0-470-05678-3.
Allen, Edward; Iano, Joseph (2012). The Architect's Studio Companion: Rules of Thumb for Preliminary Design. Hoboken, N.J.: John Wiley & Sons. ISBN 978-0-470-64191-0.
Coates, Michael; Brooker, Graeme; Stone, Sally (2008). The Visual Dictionary of Interior Architecture and Design. Lausanne: AVA Academia. ISBN 9782940373802.
Drury, Jolyon; Falconer, Peter (2003). Buildings for Industrial Storage and Distribution. New York: Routledge. ISBN 0-7506-4819-8.
Guo, Qinghua (2010). The Mingqi Pottery Buildings of Han Dynasty China, 206 BC-AD 220: Architectural Representations and Represented Architecture. Portland, Ore.: Sussex Academic Press. ISBN 978-1-84519-321-8.
Habraken, N.J.; Teicher, Jonathan (1998). Structure of the Ordinary: Form and Control in the Built Environment. Cambridge, Massachusetts: MIT Press. ISBN 978-0-262-58195-0.
Harris, Cyril M. (1983). Illustrated Dictionary of Historic Architecture. New York: Dover Publications. ISBN 978-0-486-24444-0.
Materials Handling and Management Society (1993). The Professional Materials Handling Learning System: A Basic Reference Collection in Materials Handling. Volume 2. Charlotte, N.C.: Material Handling Education Foundation.
External links
Proper safeguarding for elevated work platforms (1:37 min. video)Video showing the main construction of an industrial mezzanine floor(2.46 min video)
|
main subject
|
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A mezzanine (; or in Italian, a mezzanino) is an intermediate floor in a building which is partly open to the double-height ceilinged floor below, or which does not extend over the whole floorspace of the building, a loft with non-sloped walls. However, the term is often used loosely for the floor above the ground floor, especially where a very high-ceilinged original ground floor has been split horizontally into two floors.
Mezzanines may serve a wide variety of functions. Industrial mezzanines, such as those used in warehouses, may be temporary or semi-permanent structures.
In Royal Italian architecture, mezzanino also means a chamber created by partitioning that does not go up all the way to the arch vaulting or ceiling; these were historically common in Italy and France, for example in the palaces for the nobility at the Quirinal Palace.
Definition
A mezzanine is an intermediate floor (or floors) in a building which is open to the floor below. It is placed halfway (mezzo means 'half' in Italian) up the wall on a floor which has a ceiling at least twice as high as a floor with minimum height. A mezzanine does not count as one of the floors in a building, and generally does not count in determining maximum floorspace. The International Building Code permits a mezzanine to have as much as one-third of the floor space of the floor below. Local building codes may vary somewhat from this standard. A space may have more than one mezzanine, as long as the sum total of floor space of all the mezzanines is not greater than one-third the floor space of the complete floor below.Mezzanines help to make a high-ceilinged space feel more personal and less vast, and can create additional floor space. Mezzanines, however, may have lower-than-normal ceilings due to their location. The term "mezzanine" does not imply any particular function; mezzanines can be used for a wide array of purposes.Mezzanines are commonly used in modern architecture, which places a heavy emphasis on light and space.
Industrial mezzanines
In industrial settings, mezzanines may be installed (rather than built as part of the structure) in high-ceilinged spaces such as warehouses. These semi-permanent structures are usually free-standing, can be dismantled and relocated, and are sold commercially. Industrial mezzanine structures can be supported by structural steel columns and elements, or by racks or shelves. Depending on the span and the run of the mezzanine, different materials may be used for the mezzanine's deck like fibre cement boards. Some industrial mezzanines may also include enclosed, paneled office space on their upper levels. There are three basic types of industrial mezzanines: custom, standard or modular.
A structural engineer is sometimes hired to help determine whether the floor of the building can support a mezzanine (and how heavy the mezzanine may be), and to design the appropriate mezzanine.
Custom mezzanines
Custom Mezzanines are steel, raised industrial platform structures that are designed specifically to match the space and capacity needs of a given facility. It will, at a minimum, include a stairway for accessing the mezzanine. These structures typically are the strongest in terms of support capacity.
Standard mezzanines
Standard Mezzanines are steel, raised industrial platform structures that are completely self-supporting and are sold in pre-determined sizes and shapes. These off-the-shelf structures are usually strong (in terms of support capacity) and less expensive than custom mezzanines.
Modular mezzanines
Modular Mezzanines are a type of Industrial Mezzanine that can be assembled by bolting together standard-sized, self-supporting, independent raised platform structures.
Safety
Employees in material handling and manufacturing are often at risk of falls when they are on the job. Recent figures show approximately 20,000 serious injuries and nearly 100 fatalities a year in industrial facilities. Falls of people and objects from mezzanines are of particular concern.In many industrial operations, openings are cut into the guardrail on mezzanines and elevated work platforms to allow picking of palletized material to be loaded and unloaded, often with a fork truck, to upper levels. The Occupational Safety and Health Administration (OSHA) and International Building Council (IBC) have published regulations for fall protection and The American National Standards Institute (ANSI) has published standards for securing pallet drop areas to protect workers that work on elevated platforms and are exposed to openings.
In most cases, safety gates are used to secure these openings. OSHA requires openings 48 inches or taller to be secured with a fall protection system. Removable sections of railing or gates that swing or slide open would be used to open up the area and allow the transfer of material, and then close once the material is removed. However, current ANSI standards require dual-gate safety systems for fall protection.Dual-gate safety systems were created to secure these areas, allowing a barrier to be in place at all times, even while pallets are being loaded or removed. Dual-gate systems create a completely enclosed workstation providing protection for the worker during loading and off-loading operations. When the rear-side gate opens, the ledge gate automatically closes, ensuring there is always a gate between the operator and the ledge.
References
Bibliography
Aghayere, Abi O.; Vigil, Jason (2007). Structural Wood Design: A Practice-Oriented Approach. Hoboken, N.J.: John Wiley. ISBN 978-0-470-05678-3.
Allen, Edward; Iano, Joseph (2012). The Architect's Studio Companion: Rules of Thumb for Preliminary Design. Hoboken, N.J.: John Wiley & Sons. ISBN 978-0-470-64191-0.
Coates, Michael; Brooker, Graeme; Stone, Sally (2008). The Visual Dictionary of Interior Architecture and Design. Lausanne: AVA Academia. ISBN 9782940373802.
Drury, Jolyon; Falconer, Peter (2003). Buildings for Industrial Storage and Distribution. New York: Routledge. ISBN 0-7506-4819-8.
Guo, Qinghua (2010). The Mingqi Pottery Buildings of Han Dynasty China, 206 BC-AD 220: Architectural Representations and Represented Architecture. Portland, Ore.: Sussex Academic Press. ISBN 978-1-84519-321-8.
Habraken, N.J.; Teicher, Jonathan (1998). Structure of the Ordinary: Form and Control in the Built Environment. Cambridge, Massachusetts: MIT Press. ISBN 978-0-262-58195-0.
Harris, Cyril M. (1983). Illustrated Dictionary of Historic Architecture. New York: Dover Publications. ISBN 978-0-486-24444-0.
Materials Handling and Management Society (1993). The Professional Materials Handling Learning System: A Basic Reference Collection in Materials Handling. Volume 2. Charlotte, N.C.: Material Handling Education Foundation.
External links
Proper safeguarding for elevated work platforms (1:37 min. video)Video showing the main construction of an industrial mezzanine floor(2.46 min video)
|
PyPI project
|
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Vítor Hugo Encarnação Freitas (born 3 March 1996), known as Vítor Barata, is a Portuguese professional footballer who plays as a central midfielder for Lebanese Premier League club Nejmeh.
Club career
Early in his football career, Barata underwent trials with Portuguese giants Benfica and Sporting CP, with whom he signed in August 2011 at the age of 14. He spent two years with the club, playing at youth level. On 5 November 2014, Barata made his professional debut with Marítimo B in a 2014–15 Segunda Liga match against União Madeira.In July 2019, Barata signed a two-year contract with Greek Super League 2 side Ergotelis.On 5 February 2022, Barata joined Polish III liga club Stal Stalowa Wola. He made his debut in a friendly against Polonia Bytom and scored one goal.On 6 July 2022, he returned to Greece to join Ágios Nikólaos.
References
External links
Vítor Barata at ForaDeJogo (archived)
Stats and profile at LPFP (in Portuguese)
Vítor Barata at Soccerway
|
native language
|
{
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79
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"text": [
"Portuguese"
]
}
|
Vítor Hugo Encarnação Freitas (born 3 March 1996), known as Vítor Barata, is a Portuguese professional footballer who plays as a central midfielder for Lebanese Premier League club Nejmeh.
Club career
Early in his football career, Barata underwent trials with Portuguese giants Benfica and Sporting CP, with whom he signed in August 2011 at the age of 14. He spent two years with the club, playing at youth level. On 5 November 2014, Barata made his professional debut with Marítimo B in a 2014–15 Segunda Liga match against União Madeira.In July 2019, Barata signed a two-year contract with Greek Super League 2 side Ergotelis.On 5 February 2022, Barata joined Polish III liga club Stal Stalowa Wola. He made his debut in a friendly against Polonia Bytom and scored one goal.On 6 July 2022, he returned to Greece to join Ágios Nikólaos.
References
External links
Vítor Barata at ForaDeJogo (archived)
Stats and profile at LPFP (in Portuguese)
Vítor Barata at Soccerway
|
position played on team / speciality
|
{
"answer_start": [
137
],
"text": [
"midfielder"
]
}
|
Vítor Hugo Encarnação Freitas (born 3 March 1996), known as Vítor Barata, is a Portuguese professional footballer who plays as a central midfielder for Lebanese Premier League club Nejmeh.
Club career
Early in his football career, Barata underwent trials with Portuguese giants Benfica and Sporting CP, with whom he signed in August 2011 at the age of 14. He spent two years with the club, playing at youth level. On 5 November 2014, Barata made his professional debut with Marítimo B in a 2014–15 Segunda Liga match against União Madeira.In July 2019, Barata signed a two-year contract with Greek Super League 2 side Ergotelis.On 5 February 2022, Barata joined Polish III liga club Stal Stalowa Wola. He made his debut in a friendly against Polonia Bytom and scored one goal.On 6 July 2022, he returned to Greece to join Ágios Nikólaos.
References
External links
Vítor Barata at ForaDeJogo (archived)
Stats and profile at LPFP (in Portuguese)
Vítor Barata at Soccerway
|
given name
|
{
"answer_start": [
0
],
"text": [
"Vítor"
]
}
|
Vítor Hugo Encarnação Freitas (born 3 March 1996), known as Vítor Barata, is a Portuguese professional footballer who plays as a central midfielder for Lebanese Premier League club Nejmeh.
Club career
Early in his football career, Barata underwent trials with Portuguese giants Benfica and Sporting CP, with whom he signed in August 2011 at the age of 14. He spent two years with the club, playing at youth level. On 5 November 2014, Barata made his professional debut with Marítimo B in a 2014–15 Segunda Liga match against União Madeira.In July 2019, Barata signed a two-year contract with Greek Super League 2 side Ergotelis.On 5 February 2022, Barata joined Polish III liga club Stal Stalowa Wola. He made his debut in a friendly against Polonia Bytom and scored one goal.On 6 July 2022, he returned to Greece to join Ágios Nikólaos.
References
External links
Vítor Barata at ForaDeJogo (archived)
Stats and profile at LPFP (in Portuguese)
Vítor Barata at Soccerway
|
languages spoken, written or signed
|
{
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79
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Velupillai Kumaraswamy (Tamil: வேலுப்பிள்ளை குமாரசுவாமி; 31 July 1919 – 10 March 1978) was a Ceylon Tamil lawyer, politician and Member of Parliament.
Early life and family
Kumaraswamy was born on 31 July 1919. He was the son of Velupillai, a proctor from Chavakachcheri in northern Ceylon. After school Kumaraswamy joined Ceylon Law College, qualifying as an advocate.
Kumaraswamy had a son (Vaheeswaran) and a daughter (Dushyanti).
Career
Whilst still studying law, Kumaraswamy stood as the All Ceylon Tamil Congress's (ACTC) candidate in Chavakachcheri at the 1947 parliamentary election. He won the election and entered Parliament. Kumaraswamy became a Parliamentary Secretary after the ACTC joined the United National Party dominated government in 1948.Kumaraswamy was re-elected at the 1952 parliamentary election. The ACTC left the UNP government in 1953 but Kumaraswamy chose to remain with the UNP. Kumaraswamy left the UNP in 1956 over the party's support of the Sinhala Only Act.Kumaraswamy stood for re-election in the constituency at the 1956 parliamentary election as an independent candidate but was defeated by the Illankai Tamil Arasu Kachchi (Federal Party) candidate V. N. Navaratnam. He was the ACTC's candidate in the constituency at the March 1960 and 1970 parliamentary elections but on each occasion was defeated by Navaratnam. He contested the 1977 parliamentary election as an independent candidate but was again defeated by Navaratnam.Kumaraswamy practised law in Colombo.
== References ==
|
member of political party
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"United National Party"
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Velupillai Kumaraswamy (Tamil: வேலுப்பிள்ளை குமாரசுவாமி; 31 July 1919 – 10 March 1978) was a Ceylon Tamil lawyer, politician and Member of Parliament.
Early life and family
Kumaraswamy was born on 31 July 1919. He was the son of Velupillai, a proctor from Chavakachcheri in northern Ceylon. After school Kumaraswamy joined Ceylon Law College, qualifying as an advocate.
Kumaraswamy had a son (Vaheeswaran) and a daughter (Dushyanti).
Career
Whilst still studying law, Kumaraswamy stood as the All Ceylon Tamil Congress's (ACTC) candidate in Chavakachcheri at the 1947 parliamentary election. He won the election and entered Parliament. Kumaraswamy became a Parliamentary Secretary after the ACTC joined the United National Party dominated government in 1948.Kumaraswamy was re-elected at the 1952 parliamentary election. The ACTC left the UNP government in 1953 but Kumaraswamy chose to remain with the UNP. Kumaraswamy left the UNP in 1956 over the party's support of the Sinhala Only Act.Kumaraswamy stood for re-election in the constituency at the 1956 parliamentary election as an independent candidate but was defeated by the Illankai Tamil Arasu Kachchi (Federal Party) candidate V. N. Navaratnam. He was the ACTC's candidate in the constituency at the March 1960 and 1970 parliamentary elections but on each occasion was defeated by Navaratnam. He contested the 1977 parliamentary election as an independent candidate but was again defeated by Navaratnam.Kumaraswamy practised law in Colombo.
== References ==
|
occupation
|
{
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114
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"politician"
]
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|
Velupillai Kumaraswamy (Tamil: வேலுப்பிள்ளை குமாரசுவாமி; 31 July 1919 – 10 March 1978) was a Ceylon Tamil lawyer, politician and Member of Parliament.
Early life and family
Kumaraswamy was born on 31 July 1919. He was the son of Velupillai, a proctor from Chavakachcheri in northern Ceylon. After school Kumaraswamy joined Ceylon Law College, qualifying as an advocate.
Kumaraswamy had a son (Vaheeswaran) and a daughter (Dushyanti).
Career
Whilst still studying law, Kumaraswamy stood as the All Ceylon Tamil Congress's (ACTC) candidate in Chavakachcheri at the 1947 parliamentary election. He won the election and entered Parliament. Kumaraswamy became a Parliamentary Secretary after the ACTC joined the United National Party dominated government in 1948.Kumaraswamy was re-elected at the 1952 parliamentary election. The ACTC left the UNP government in 1953 but Kumaraswamy chose to remain with the UNP. Kumaraswamy left the UNP in 1956 over the party's support of the Sinhala Only Act.Kumaraswamy stood for re-election in the constituency at the 1956 parliamentary election as an independent candidate but was defeated by the Illankai Tamil Arasu Kachchi (Federal Party) candidate V. N. Navaratnam. He was the ACTC's candidate in the constituency at the March 1960 and 1970 parliamentary elections but on each occasion was defeated by Navaratnam. He contested the 1977 parliamentary election as an independent candidate but was again defeated by Navaratnam.Kumaraswamy practised law in Colombo.
== References ==
|
given name
|
{
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"V."
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|
Geoff Travis (born 2 February 1952) is the founder of both Rough Trade Records and the Rough Trade chain of record shops. A former drama teacher and owner of a punk record shop, Travis founded the Rough Trade label in 1978.
Biography
Travis was born on 2 February 1952 in Stoke Newington, London, and was raised in Finchley. He is Jewish, his ancestors emigrated from Romania and Ukraine. Travis studied English at Churchill College, Cambridge. He worked as a drama teacher before opening the original Rough Trade record shop in Kensington Park Road, Notting Hill, London on 23 February 1976, setting up the record label two years later. He claimed that he chose the location because it was close to Powis Square, where Performance, one of his favourite films, was made. Travis was also instrumental in the foundation of the independent distribution network The Cartel. While Rough Trade was a key independent label, Travis also co-ran labels with major record companies, including Blanco y Negro in 1983 (with WEA) and Trade2 (with Island Records).Rough Trade was home to The Smiths, but by 1986, after three years on the label, the band were in dispute over finances. The song "Frankly, Mr. Shankly" from The Queen is Dead was reportedly a jibe at Travis.
The label was wound up in 1994 after briefly being revived in partnership with One Little Indian, but revived by Travis in 2001 with breakthrough acts The Strokes and The Libertines.Writer Douglas Wolk credited Travis as virtually defining "the British post-punk sound", and XFM viewed his impact on independent music as greater than anyone else's in the country.
Jamie Travis
Geoff Travis has a son called Jamie, who is one half of the post-rave pop duo Babeheaven with singer Nancy Andersen.
References
External links
Interview with Furious in Nov. 1996
Several interviews with Travis explaining his ideals are included in this 1979 TV documentary
|
place of birth
|
{
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273
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"Stoke Newington"
]
}
|
Geoff Travis (born 2 February 1952) is the founder of both Rough Trade Records and the Rough Trade chain of record shops. A former drama teacher and owner of a punk record shop, Travis founded the Rough Trade label in 1978.
Biography
Travis was born on 2 February 1952 in Stoke Newington, London, and was raised in Finchley. He is Jewish, his ancestors emigrated from Romania and Ukraine. Travis studied English at Churchill College, Cambridge. He worked as a drama teacher before opening the original Rough Trade record shop in Kensington Park Road, Notting Hill, London on 23 February 1976, setting up the record label two years later. He claimed that he chose the location because it was close to Powis Square, where Performance, one of his favourite films, was made. Travis was also instrumental in the foundation of the independent distribution network The Cartel. While Rough Trade was a key independent label, Travis also co-ran labels with major record companies, including Blanco y Negro in 1983 (with WEA) and Trade2 (with Island Records).Rough Trade was home to The Smiths, but by 1986, after three years on the label, the band were in dispute over finances. The song "Frankly, Mr. Shankly" from The Queen is Dead was reportedly a jibe at Travis.
The label was wound up in 1994 after briefly being revived in partnership with One Little Indian, but revived by Travis in 2001 with breakthrough acts The Strokes and The Libertines.Writer Douglas Wolk credited Travis as virtually defining "the British post-punk sound", and XFM viewed his impact on independent music as greater than anyone else's in the country.
Jamie Travis
Geoff Travis has a son called Jamie, who is one half of the post-rave pop duo Babeheaven with singer Nancy Andersen.
References
External links
Interview with Furious in Nov. 1996
Several interviews with Travis explaining his ideals are included in this 1979 TV documentary
|
educated at
|
{
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416
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"Churchill College"
]
}
|
Geoff Travis (born 2 February 1952) is the founder of both Rough Trade Records and the Rough Trade chain of record shops. A former drama teacher and owner of a punk record shop, Travis founded the Rough Trade label in 1978.
Biography
Travis was born on 2 February 1952 in Stoke Newington, London, and was raised in Finchley. He is Jewish, his ancestors emigrated from Romania and Ukraine. Travis studied English at Churchill College, Cambridge. He worked as a drama teacher before opening the original Rough Trade record shop in Kensington Park Road, Notting Hill, London on 23 February 1976, setting up the record label two years later. He claimed that he chose the location because it was close to Powis Square, where Performance, one of his favourite films, was made. Travis was also instrumental in the foundation of the independent distribution network The Cartel. While Rough Trade was a key independent label, Travis also co-ran labels with major record companies, including Blanco y Negro in 1983 (with WEA) and Trade2 (with Island Records).Rough Trade was home to The Smiths, but by 1986, after three years on the label, the band were in dispute over finances. The song "Frankly, Mr. Shankly" from The Queen is Dead was reportedly a jibe at Travis.
The label was wound up in 1994 after briefly being revived in partnership with One Little Indian, but revived by Travis in 2001 with breakthrough acts The Strokes and The Libertines.Writer Douglas Wolk credited Travis as virtually defining "the British post-punk sound", and XFM viewed his impact on independent music as greater than anyone else's in the country.
Jamie Travis
Geoff Travis has a son called Jamie, who is one half of the post-rave pop duo Babeheaven with singer Nancy Andersen.
References
External links
Interview with Furious in Nov. 1996
Several interviews with Travis explaining his ideals are included in this 1979 TV documentary
|
family name
|
{
"answer_start": [
6
],
"text": [
"Travis"
]
}
|
Geoff Travis (born 2 February 1952) is the founder of both Rough Trade Records and the Rough Trade chain of record shops. A former drama teacher and owner of a punk record shop, Travis founded the Rough Trade label in 1978.
Biography
Travis was born on 2 February 1952 in Stoke Newington, London, and was raised in Finchley. He is Jewish, his ancestors emigrated from Romania and Ukraine. Travis studied English at Churchill College, Cambridge. He worked as a drama teacher before opening the original Rough Trade record shop in Kensington Park Road, Notting Hill, London on 23 February 1976, setting up the record label two years later. He claimed that he chose the location because it was close to Powis Square, where Performance, one of his favourite films, was made. Travis was also instrumental in the foundation of the independent distribution network The Cartel. While Rough Trade was a key independent label, Travis also co-ran labels with major record companies, including Blanco y Negro in 1983 (with WEA) and Trade2 (with Island Records).Rough Trade was home to The Smiths, but by 1986, after three years on the label, the band were in dispute over finances. The song "Frankly, Mr. Shankly" from The Queen is Dead was reportedly a jibe at Travis.
The label was wound up in 1994 after briefly being revived in partnership with One Little Indian, but revived by Travis in 2001 with breakthrough acts The Strokes and The Libertines.Writer Douglas Wolk credited Travis as virtually defining "the British post-punk sound", and XFM viewed his impact on independent music as greater than anyone else's in the country.
Jamie Travis
Geoff Travis has a son called Jamie, who is one half of the post-rave pop duo Babeheaven with singer Nancy Andersen.
References
External links
Interview with Furious in Nov. 1996
Several interviews with Travis explaining his ideals are included in this 1979 TV documentary
|
given name
|
{
"answer_start": [
0
],
"text": [
"Geoff"
]
}
|
Geoff Travis (born 2 February 1952) is the founder of both Rough Trade Records and the Rough Trade chain of record shops. A former drama teacher and owner of a punk record shop, Travis founded the Rough Trade label in 1978.
Biography
Travis was born on 2 February 1952 in Stoke Newington, London, and was raised in Finchley. He is Jewish, his ancestors emigrated from Romania and Ukraine. Travis studied English at Churchill College, Cambridge. He worked as a drama teacher before opening the original Rough Trade record shop in Kensington Park Road, Notting Hill, London on 23 February 1976, setting up the record label two years later. He claimed that he chose the location because it was close to Powis Square, where Performance, one of his favourite films, was made. Travis was also instrumental in the foundation of the independent distribution network The Cartel. While Rough Trade was a key independent label, Travis also co-ran labels with major record companies, including Blanco y Negro in 1983 (with WEA) and Trade2 (with Island Records).Rough Trade was home to The Smiths, but by 1986, after three years on the label, the band were in dispute over finances. The song "Frankly, Mr. Shankly" from The Queen is Dead was reportedly a jibe at Travis.
The label was wound up in 1994 after briefly being revived in partnership with One Little Indian, but revived by Travis in 2001 with breakthrough acts The Strokes and The Libertines.Writer Douglas Wolk credited Travis as virtually defining "the British post-punk sound", and XFM viewed his impact on independent music as greater than anyone else's in the country.
Jamie Travis
Geoff Travis has a son called Jamie, who is one half of the post-rave pop duo Babeheaven with singer Nancy Andersen.
References
External links
Interview with Furious in Nov. 1996
Several interviews with Travis explaining his ideals are included in this 1979 TV documentary
|
languages spoken, written or signed
|
{
"answer_start": [
405
],
"text": [
"English"
]
}
|
The Ellicott City Granodiorite is a Silurian or Ordovician granitic pluton in Howard and Baltimore Counties, Maryland. It is described as a biotite granodiorite along the margin of the intrusion which grades into a quartz monzonite in its core. It intrudes through the Wissahickon Formation and the Baltimore Gabbro Complex.
In 1964, C. A. Hopson grouped the Ellicott City Granodiorite with the Guilford Quartz Monzonite and the Woodstock Quartz Monzonite as "Late-kinematic intrusive masses."In 1980, Crowley and Reinhardt of the Maryland Geological Survey remapped the Ellicott City Quadrangle and referred to this unit as the Ellicott City Granite, rather than granodiorite.
Description
Hopson reported the chemical composition (by %) of the Elicott City Granodiorite from two locations. H7-A is on River Road, 0.3 miles east of the Patapsco River Bridge, Ellicott City, and H18-1A is on U.S. Route 29, 200 yards south of U.S. Route 40.
Early quarrying
The 1898 account of Edward B. Mathews of the Maryland Geological Survey of the quarries at Ellicott City begins with a statement that there were two quarries; one on either side of the Patapsco River. The rock on the eastern, or Baltimore County, side is "a fine grained mass, with a decided foliation or gneissic structure," while the rock on the western, or Howard County side, is "more uniform and granitic." The text also refers to the figure of the polished slab on the left: "Here it also has a porphyritic structure in consequence of the development of large flesh-colored crystals of feldspar which are disseminated somewhat irregularly through the rock, as shown in (the figure)."
Mathews continued with a description of their historical importance:
The time of opening these quarries dates back probably into the last of the 18th century, but the details are entirely wanting. The beautiful appearance of some of the more uniformly porphyritic specimens early attracted attention, and in the earliest works which we have on this area, that by Dr. Hayden published in 1811, mention is made of these quarries. It is not certain whether the quarry on the Baltimore county side or the quarries of the Howard county side furnished the first material for Baltimore, but it is clearly evident from the character of the rock furnished for the Catholic Cathedral, that the gneiss was the more important rock at that time. Local tradition assigns the source of the stone sometimes to the Baltimore county side and sometimes to the Howard county side and the published information is equally conflicting and indefinite. When the Cathedral was constructed during the years 1806 to 1812 and subsequently from 1815 to 1821, the material was hauled from Ellicott City to Baltimore along the old Frederick road in huge wagons drawn by nine yoke of oxen. After furnishing the rock for this building, which must have been one of the most important stone structures in the United States at the time of its construction, the quarries evidently were worked only to meet local demands. In fact they have never since been of such relatively great importance. Dr. David Dale Owen, indeed, while studying the various building stones of Maryland at Cockeysville, Woodstock and Port Deposit, with the view of gaining all the information for the Smithsonian building, twice passed by these quarries and yet makes no mention of them. At the time of the Tenth Census the agent remarks that he "knows of no other place in the country where there are so many stone buildings in an area of the same size."
Mathews described recent (c. 1872-1898) operations at the quarries:
Of the quarries in operation at the present day those of Werner Bros, were opened as early as the beginning of the century. In 1872 Charles J. Werner reopened a quarry, which since his death in 1888 has been operated by his sons, who purchased in 1890 a second quarry, which had previously been opened by Robert Wilson. These quarries became of some importance in 1893, when one of them is spoken of as the principal Ellicott City quarry, although it is now producing little or no building stone except during the fall of the year when random rubble is quarried for local use. The output for the year 1896 did not aggregate over 200 perches. The most active quarry at the present is that operated by A. Weber. This quarry is situated on the Howard county side some distance below the station. The material has been furnished in recent years for some important buildings, as those of the Woman's College of Baltimore, but most of the material seems to be used for Belgian blocks, curbing and macadam.
Age
In 1973, M. W. Higgins reported a radiometric (Rb-Sr age) of 425 Ma, which placed the Ellicott City Granodiorite in the Silurian. In 1998, A. A. Drake revised the age to Ordovician based on the granodiorite's relationship with the Woodstock Quartz Monzonite.
See also
Guilford Quartz Monzonite
Oella Formation
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The Ellicott City Granodiorite is a Silurian or Ordovician granitic pluton in Howard and Baltimore Counties, Maryland. It is described as a biotite granodiorite along the margin of the intrusion which grades into a quartz monzonite in its core. It intrudes through the Wissahickon Formation and the Baltimore Gabbro Complex.
In 1964, C. A. Hopson grouped the Ellicott City Granodiorite with the Guilford Quartz Monzonite and the Woodstock Quartz Monzonite as "Late-kinematic intrusive masses."In 1980, Crowley and Reinhardt of the Maryland Geological Survey remapped the Ellicott City Quadrangle and referred to this unit as the Ellicott City Granite, rather than granodiorite.
Description
Hopson reported the chemical composition (by %) of the Elicott City Granodiorite from two locations. H7-A is on River Road, 0.3 miles east of the Patapsco River Bridge, Ellicott City, and H18-1A is on U.S. Route 29, 200 yards south of U.S. Route 40.
Early quarrying
The 1898 account of Edward B. Mathews of the Maryland Geological Survey of the quarries at Ellicott City begins with a statement that there were two quarries; one on either side of the Patapsco River. The rock on the eastern, or Baltimore County, side is "a fine grained mass, with a decided foliation or gneissic structure," while the rock on the western, or Howard County side, is "more uniform and granitic." The text also refers to the figure of the polished slab on the left: "Here it also has a porphyritic structure in consequence of the development of large flesh-colored crystals of feldspar which are disseminated somewhat irregularly through the rock, as shown in (the figure)."
Mathews continued with a description of their historical importance:
The time of opening these quarries dates back probably into the last of the 18th century, but the details are entirely wanting. The beautiful appearance of some of the more uniformly porphyritic specimens early attracted attention, and in the earliest works which we have on this area, that by Dr. Hayden published in 1811, mention is made of these quarries. It is not certain whether the quarry on the Baltimore county side or the quarries of the Howard county side furnished the first material for Baltimore, but it is clearly evident from the character of the rock furnished for the Catholic Cathedral, that the gneiss was the more important rock at that time. Local tradition assigns the source of the stone sometimes to the Baltimore county side and sometimes to the Howard county side and the published information is equally conflicting and indefinite. When the Cathedral was constructed during the years 1806 to 1812 and subsequently from 1815 to 1821, the material was hauled from Ellicott City to Baltimore along the old Frederick road in huge wagons drawn by nine yoke of oxen. After furnishing the rock for this building, which must have been one of the most important stone structures in the United States at the time of its construction, the quarries evidently were worked only to meet local demands. In fact they have never since been of such relatively great importance. Dr. David Dale Owen, indeed, while studying the various building stones of Maryland at Cockeysville, Woodstock and Port Deposit, with the view of gaining all the information for the Smithsonian building, twice passed by these quarries and yet makes no mention of them. At the time of the Tenth Census the agent remarks that he "knows of no other place in the country where there are so many stone buildings in an area of the same size."
Mathews described recent (c. 1872-1898) operations at the quarries:
Of the quarries in operation at the present day those of Werner Bros, were opened as early as the beginning of the century. In 1872 Charles J. Werner reopened a quarry, which since his death in 1888 has been operated by his sons, who purchased in 1890 a second quarry, which had previously been opened by Robert Wilson. These quarries became of some importance in 1893, when one of them is spoken of as the principal Ellicott City quarry, although it is now producing little or no building stone except during the fall of the year when random rubble is quarried for local use. The output for the year 1896 did not aggregate over 200 perches. The most active quarry at the present is that operated by A. Weber. This quarry is situated on the Howard county side some distance below the station. The material has been furnished in recent years for some important buildings, as those of the Woman's College of Baltimore, but most of the material seems to be used for Belgian blocks, curbing and macadam.
Age
In 1973, M. W. Higgins reported a radiometric (Rb-Sr age) of 425 Ma, which placed the Ellicott City Granodiorite in the Silurian. In 1998, A. A. Drake revised the age to Ordovician based on the granodiorite's relationship with the Woodstock Quartz Monzonite.
See also
Guilford Quartz Monzonite
Oella Formation
== References ==
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KWDC-LP is a Variety formatted broadcast radio station. The station is licensed to and serving Stockton in California. KWDC-LP is owned by San Joaquin Delta College and operated under their San Joaquin Delta Community College District licensee.
History
The station officially launched on at just before "the stroke of Noon" on January 1, 2015, but didn't officially get its License to Cover until April 6, 2015.On May 27, 2016, the station briefly signed off, though it did not file an application for special temporary authority with the Federal Communications Commission, after its founding instructor William Story retired. The student staff of KWDC-LP were to move to the Peace and Justice Network of San Joaquin Country-owned KXVS-LP to get their station on the air. Unfortunately, the station's website URL and slogan "The Voice of Stockton" were trademarked by the station's former general manager, who also redirected all of KWDC-LP's social media accounts to KXVS'. Eventually, KWDC-LP returned to the air on September 18, 2016. Subsequently, KXVS-LP went silent in late-September 2017 and its license was lost in late-September 2018.
References
External links
KWDC 93.5 Online
KWDC in the FCC FM station database
KWDC-LP on Radio-Locator
KWDC in Nielsen Audio's FM station database
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The Arauco Peninsula (Spanish: península de Arauco), is a peninsula in Southern Chile located in the homonymous Arauco Province. It projects northwest into the Pacific Ocean. The peninsula is located west of Cordillera de Nahuelbuta. Geologically it is a forearc high.
See also
Arauco Basin
Ranquil Formation
== References ==
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The 43rd (Wessex) Infantry Division was an infantry division of Britain's Territorial Army (TA). The division was first formed in 1908, as the Wessex Division. During the First World War, it was broken-up and never served as a complete formation. It was reformed in the TA in 1920, and then served in the campaign in North West Europe from June 1944 until May 1945, during the Second World War. The division suffered heavy casualties and gained an excellent reputation. After the Second World War, the division formed part of the postwar TA, and became the 43rd (Wessex) Division/District in 1961. It was finally disbanded in 1967.
Formation
The Territorial Force (TF) was formed on 1 April 1908 following the enactment of the Territorial and Reserve Forces Act 1907 (7 Edw.7, c.9) which combined and re-organised the old Volunteer Force, the Honourable Artillery Company and the Yeomanry. On formation, the TF contained 14 infantry divisions and 14 mounted yeomanry brigades. One of the divisions was the Wessex Division.The Wessex Division was formed in Southern Command from TF units in the south-western counties of Cornwall, Devon, Dorset, Hampshire, Somerset and Wiltshire. In peacetime, the divisional headquarters was at 19 Cathedral Close in Exeter.
Wessex Division Order of Battle 1908–1914Divisional HQ at Exeter
Hampshire Brigade at Southampton
4th Battalion, Hampshire Regiment at Winchester (joined 12th Indian Division and served in Mesopotamia)
5th Battalion, Hampshire Regiment at Southampton (served in Third Afghan War)
6th (Duke of Connaught's Own) Battalion, Hampshire Regiment at Portsmouth (joined 15th Indian Division and served in Mesopotamia)
7th Battalion, Hampshire Regiment at Bournemouth (served in Aden)South-Western Brigade at Taunton
4th Battalion, Somerset Light Infantry at Bath (joined 37th Indian Brigade and served in Mesopotamia)
5th Battalion, Somerset Light Infantry at Taunton (joined 75th Division and served in Palestine)
4th Battalion, Dorsetshire Regiment at Dorchester (joined 42nd Indian Brigade and served in Mesopotamia)
4th Battalion, Wiltshire Regiment at Trowbridge (joined 75th Division and served in Palestine)Devon & Cornwall Brigade at Exeter
4th Battalion, Devonshire Regiment at Exeter (joined 41st Indian Brigade and served in Mesopotamia)
5th (Prince of Wales's) Battalion, Devonshire Regiment at Plymouth (joined 75th Division and served in Palestine)
6th Battalion, Devonshire Regiment at Barnstaple (joined 36th Indian Brigade and served in Mesopotamia)
4th Battalion, Duke of Cornwall's Light Infantry at Truro (served in Aden, later with 75th Division in Palestine)Divisional Royal Artillery
I Wessex Brigade, Royal Field Artillery at Portsmouth (joined 3rd (Lahore) Division and served in Mesopotamia)
1st Hampshire Battery
2nd Hampshire Battery
3rd Hampshire Battery
1st Wessex Ammunition Column
II Wessex (Howitzer) Brigade, Royal Field Artillery at Ryde, Isle of Wight
4th Hampshire (Howitzer) Battery (served in Aden)
5th Hampshire (Howitzer) Battery (joined 6th (Poona) Division and served in Mesopotamia; captured at Kut)]
2nd Wessex Ammunition Column
III Wessex Brigade, Royal Field Artillery at Swindon (served in Third Afghan War)
6th Hampshire Battery
Dorsetshire Battery
Wiltshire Battery
3rd Wessex Ammunition Column
IV Wessex Brigade, Royal Field Artillery at Exeter
1st Devonshire Battery
2nd Devonshire Battery
3rd Devonshire Battery (served in Third Afghan War)
4th Wessex Ammunition Column
Wessex (Hampshire) Heavy Battery, Royal Garrison Artillery and Ammunition Column at Cosham (served on the Western Front)Wessex Divisional Engineers (joined 27th Division and served at Salonika)
1st Wessex Field Company at Bath (became 500th Field Company)
2nd Wessex Field Company at Weston-super-Mare (became 501st Field Company)
Wessex Divisional Telegraph Company ('Signal Company' from 1910) at ExeterDivisional Royal Army Medical Corps (joined 8th Division and served on the Western Front)
1st Wessex Field Ambulance at Exeter (became 24th Field Ambulance)
2nd Wessex Field Ambulance at Plymouth (became 25th Field Ambulance)
3rd Wessex Field Ambulance at Portsmouth (became 26th Field Ambulance)
Wessex Clearing Hospital at ExeterWessex Divisional Transport & Supply Column, Army Service Corps, at Exeter (joined 29th Division and served at Gallipoli)
Divisional Company at Andover (became 246 Company)
Devonshire and Cornwall Company at Plymouth (became 247 Company)
South Western Brigade Company at Bridgwater (became 248 Company)
Hampshire Brigade Company at Aldershot (became 249 Company)
First World War
On 29 July 1914, the Wessex Division was on Salisbury Plain carrying out its annual training camp when 'precautionary orders' were received, and next day the division took up emergency war stations in Somerset, Devon and Cornwall. The order to mobilise arrived on the evening of 4 August. Between 10 and 13 August the division concentrated on Salisbury Plain and began war training.On 24 September, at the special request of the Secretary of State for War, Earl Kitchener of Khartoum the Wessex Division accepted liability for service in British India to relieve the Regular Army units there for service on the Western Front. The division's infantry battalions (without their brigade headquarters) and artillery brigades embarked at Southampton on 8 October and were convoyed to Bombay, disembarking on 9 November. The engineers, medical units, transport, heavy battery and brigade ammunition columns also remained in the UK and joined formations composed of Regular units brought back from India and other imperial garrisons. Meanwhile, the battalions and batteries were immediately distributed to garrisons across India, reverting to peacetime service conditions, and the Wessex Division never saw service as a whole, though it was formally numbered the 43rd (1st Wessex) Division in 1915 and the brigades were designated 128th (Hampshire) Brigade, 129th (South Western) Brigade and 130th (Devon and Cornwall) Brigade.As soon as the Wessex Division had left for India, the home depots began raising 2nd Line units, distinguished from the 1st Line by a '2/' prefix. Recruitment and training of the 2nd Wessex Division proceeded so well that it was also sent to India in December 1914, and later received the notional title of 45th (2nd Wessex) Division.By early 1915 the need was growing for troops to be sent to various theatres of war, and the first drafts and formed units from the 1st Wessex Division began to go on active service, particularly to the Mesopotamian Front. By the end of the war only one battalion and five batteries remained in India, and most of these then participated in the Third Anglo-Afghan War.
Second World War
Mobilisation and training
43rd (Wessex) Division was reformed in 1920 and became part of the Territorial Army, which replaced the TF. In the period of international tension preceding the outbreak of the Second World War, the existing territorial divisions (known as the first-line) helped form new formations, known as the second-line. This process was known as duplicating. The division's duplicate was the 45th Infantry Division.
The TA was mobilised on the outbreak of war in September 1939 and the division began training in its home area. In May 1940 it was preparing to go overseas to join the British Expeditionary Force (BEF) in France, but the German invasion of the Low Countries on 10 May ended the 'Phoney War' before the division was ready. When the Battle of France was lost and the BEF was being evacuated from Dunkirk, 43rd (W) Division was one of the few reasonably well-equipped formations left in Home Forces to counter a German invasion of the United Kingdom. It formed part of the mobile GHQ Reserve disposed on the line from Northampton through North London to Aldershot, from which brigade groups could be despatched to any threatened area. During the period when invasion was most threatened, the division was stationed just north of London.By the end of 1940 the division was stationed under XII Corps in East Kent, where it remained for the next four years, first in defensive mode, later training intensively. It was later noted that its habitual training area round Stone Street, outside Folkestone, bore a marked resemblance to the Bocage countryside in Normandy where it would later fight.
In 1942, however, after the German invasion of the Soviet Union and the entrance of the United States into the war, the situation changed and the 43rd Division started training for offensive operations to return to mainland Europe. Throughout most of 1942, the division was part of XII Corps, serving alongside the 46th Infantry Division and 53rd (Welsh) Infantry Division. XII Corps was, at the time, commanded by Lieutenant-General Bernard Montgomery.In March 1942, the division also gained a new General Officer Commanding (GOC) in the form of Major-General Ivor Thomas. Thomas was a decorated officer who had served as a young battery commander in the Royal Artillery on the Western Front during the First World War where he was twice wounded and awarded the Military Cross and the Distinguished Service Order. He would command the 43rd Division until September 1945. Thomas was an effective but hard-driving commander, humourless and not universally liked, sometimes known as 'Butcher', or more jocularly by Lt-Gen Brian Horrocks and others as 'Von Thoma', after the German Lt-Gen Wilhelm Ritter von Thoma captured after the Battle of Alamein. (Horrocks also jokingly referred to Thomas's command as the 'Wicked Wyvern'). Critics of his training methods regarded 43rd (Wessex) Division as 'the most over-exercised in the Army'.
In June 1942, the 128th Infantry Brigade (consisting of three battalions of the Hampshire Regiment) was transferred to 46th Infantry Division. It was replaced first by 25th and later 34th Army Tank Brigade as part of an experiment with 'Mixed Divisions'. However the experiment was abandoned (deemed unsuitable for the type of terrain in North-western Europe) in late 1943 and the 34th Tank Brigade was replaced, in October 1943, by the 214th Independent Infantry Brigade, a Home Defence formation raised during the war that had been serving in Hampshire and Dorset District. After service in the Isle of Wight, 214th Brigade had received specialised training in combined operations under the Royal Marines at Inverary, and retained an individuality within the division. 214th Brigade would remain with the 43rd Division for the rest of the war.
Operation Overlord
XII Corps and 43rd (Wessex) Division were assigned to 21st Army Group for the Allied invasion of Normandy (Operation Overlord). They were follow-up formations, with 43rd (Wessex) Division scheduled to complete its landings 14 days after D Day (D +14, 20 June). However, shipping delays and a storm between 19 and 22 June delayed its arrival; the division finally concentrated round Bayeux on 24 June.HQ, A and C Squadrons of 43rd (Wessex) Reconnaissance Regiment were aboard the troopship Derrycunihy, which arrived off Sword Beach on the evening of 20 June. High seas and enemy shelling prevented unloading for three days and it was decided to move to Juno Beach for disembarkation. As the ship started engines it detonated an acoustic mine, splitting the ship in two, and the after part, packed with sleeping men of 43rd Recce Regiment, sank rapidly. Worse still, an ammunition lorry caught fire, and oil floating on the water was set alight. Landing craft and gunboats came alongside and picked up survivors, but the regiment lost 183 men, with another 120 evacuated wounded. Most of 43rd Recce Rgts's vehicles were landed from the beached fore part of the "Derrycunihy", and reinforcements were sent from England, but the regiment was not fully up to strength until the end of July 1944.
Operation Epsom
The division's first action, Operation Epsom starting on 26 June, involved following 15th (Scottish) Division's advance and then securing the captured objectives. However, this entailed some heavy fighting by 5th Battalion Duke of Cornwall's Light Infantry (DCLI) against a Panzer counter-attack at Cheux on 27 June. The supporting 17-pounder anti-tank guns were knocked out and the infantry had to stalk Panther tanks with their lighter 6-pounder anti-tank guns and hand-held PIATs. Other battalions mopped up the important objective of Manvieux. On 28 June 1st Battalion Worcestershire Regiment made an attack from Cheux against Mouen: they had to cross open cornfields, but had support from the whole divisional artillery and heavy mortars plus two medium artillery regiments. The infantry followed the Creeping barrage of smoke and High explosive shells and forced their way into the houses and gardens, using PIATs against those German tanks that had survived the barrage. On 29 June 129 Brigade advanced under fire to ford the River Odon and dug in, a German counter-attack against them in the evening being destroyed by the divisional artillery.
Hill 112
The division's first major offensive action of its own was Operation Jupiter, to take Hill 112, which had been briefly captured by British armour during 'Epsom' but had to be abandoned. The attack on 10 July was supported by all the divisional artillery and mortars, plus the artillery of 15th (Scottish) Division and 11th Armoured Division and 3rd and 8th Army Groups Royal Artillery (AGRAs). In the first phase 129th Brigade on the right, with all three battalions in line, and 130th Brigade on the left with one battalion, were to capture the hill and the road from it to Château de Fontaine. They were supported by Churchill tanks from 31st Tank Brigade. Then, while 129th Brigade formed a secure south-west flank, 130th Brigade and Churchill Crocodile flamethrowing tanks from 79th Armoured Division were to advance from Château de Fontaine to capture Eterville and Maltot and the high ground to the south-east. Finally, 214th Brigade in Kangaroo armoured personnel carriers accompanied by 4th Armoured Brigade was supposed to break through to the River Orne and seize bridgeheads.The massive barrage stunned but failed to suppress the defenders from 10th SS Panzer Division. When the Wessex infantry went forward they came under heavy fire and had to clear defenders from the dugouts and defensive positions of their outpost line on the forward slopes. 5th Battalion Dorsets and 9th Royal Tank Regiment, leading 130th Brigade against the farms on the lower ground, made quick progress, 7th Somerset Light Infantry passing through with the Churchills and Crocodiles to deal with Chateau de Fontaine. But 129th Brigade was slowed in its advance on Hill 112 itself, suffering heavy casualties on the open slopes, and then running into the recently-arrived Tiger I tanks of 102nd SS Heavy Panzer Battalion, which the Churchills and corps anti-tank guns of 86th (Devon) Anti-Tank Regiment, Royal Artillery, struggled to deal with. By mid-morning 129th Brigade only had a slender toehold on the edge of the plateau. Attempting to continue 130th Brigade's advance on Maltot, 7th Hampshires and 9th RTR came under crossfire from Hill 112, while some of the Tigers reached the village first. The leading Hampshire penetrated the village, leaving strongpoints to be mopped up later by the following Dorsets, but they were driven out by counter-attacks. 4th Dorsets, making a second attack, suffered heavy casualties. Two battalions of 214th Brigade had already been drawn into the fighting around Chateau de Fontaine, leaving 5th DCLI as the last uncommitted battalion. It attacked up the slopes of Hill 112, described as 'one of the most tragic acts of self-sacrifice in the entire North West European Campaign'. Launched at 20.30 towards 'The Orchard' on the crest of the hill, and supported by a squadron of 7th Royal Tank Regiment and all available guns, including the divisional light anti-aircraft guns, the attack reached the orchard, but could get no further. The infantry and anti-tank guns held off counter-attacks through the night from the newly-arrived 9th SS Panzer Division, and were reinforced in the morning by a company of 1st Worcesters and briefly by a squadron of Sherman tanks from the Royal Scots Greys. By mid-afternoon all the anti-tank guns on the hill had been knocked out, the tanks had to retire to the reverse slope, and the defence was almost over. The order was given to withdraw and 60 survivors of 5th DCLI were brought down. Both sides remained dug in on the slopes, with the hilltop left in No man's land. The division had to hold its positions under mortar fire for another 14 days, described by the commander of 214th Brigade as comparable only 'to the bombardment at Passchendaele'. This defence was followed by a final set-piece attack, Operation Express, in which 4th and 5th Wiltshires and 7th RTR succeeded in capturing Maltot on 22 July.
Overall, 43rd (Wessex) Division performed well in Normandy and was considered by many senior British officers to be one of the best divisions of the British Army during the war. For the rest of the war Bernard Montgomery, commanding all British and Canadian troops in the campaign, preferred to use formations such as 43rd (Wessex) and 15th (Scottish) to spearhead his assaults. This was mainly due to issues of morale because veteran formations such as the 7th Armoured and 51st (Highland), both of which had seen extensive service in North Africa and Italy (and fought poorly in Normandy, according to senior officers), were judged as tired and war-weary with morale being almost dangerously fragile. With formations that had spent years in the United Kingdom training such as the 43rd (Wessex), 15th (Scottish), 11th Armoured and 59th (Staffordshire) Divisions the problem of morale was less of an issue.
Mont Pinçon
After a short rest 43rd (Wessex) Division moved to XXX Corps to launch an attack towards the dominating height of Mont Pinçon as part of Operation Bluecoat. 8th Armoured Brigade was assigned to support the infantry. Starting at 08.00 on 30 July, the division was to force its way through enemy positions at Briquessard and advance through Cahagnes towards Ondefontaine. 130th Brigade led, reinforced by 4th Somerset Light Infantry and Sherman tanks of the Sherwood Rangers Yeomanry, followed by 214th Brigade and then 129th Brigade. Initial casualties were heavy, particularly from mines, and the advance achieved only 1,000 yards (910 m) on the first day. It took until the following morning to clear the mines and restart the advance with 214th Brigade and the tanks of 4th/7th Dragoon Guards. At 17.30 the brigade broke through, and 1st Worcesters riding on the tanks got beyond Cahagnes by nightfall. 7th Somerset Light Infantry cleared the village in the dark and, with the aid of the divisional artillery, fought off a counter-attack accompanied by heavy armour (probably Jagdpanthers) that had to be stalked with PIATs.The division fought its way forward during 1 August, then at 02.00 on 2 August 129th Brigade began its advance on Ondefontaine. It was a day of slow but steady progress against rifle and machine gun fire from commanding positions on the ridge in front, followed by another pre-dawn attack towards Ondefontaine, while 214th Brigade began working its way towards Mont Pinçon. 5th DCLI and B Squadron 4th/7th DG, supported by the divisional artillery and mortars, reached the top of the ridge and engaged enemy infantry and armour, while 1st Worcesters worked round the flank and took the crest. 43rd Recce Regiment (reformed after the Derrycunihy disaster) then went through to unhinge the Ondefontaine defences. The division was now facing east, with Mont Pinçon only 4 miles (6.4 km) away.
At 08.00 on 5 August, 4th Wiltshires moved out with B Squadron 13th/18th Royal Hussars, picking their way through the narrow lanes, while A Sqn took a parallel route carrying 5th Wiltshires. 4th Wiltshires found a bridge blown and went ahead without their tanks towards the strongly-held village of St Jean-le-Blanc, breaking up a counter-attack by calling down artillery fire. About 16.00 the battalion pioneers managed to bridge the stream and a Troop of B Sqn crossed, but withdrew to 'harbour' at dusk. Meanwhile, 5th Wiltshires got to the bridge over the Druance at the foot of Mont Pinçon but failed to capture it by the end of the day. Generals Ivor Thomas and Brian Horrocks (who had just taken command of XXX Corps) were anxious to push on, and had already cancelled Operation Blackwater, designed to reach the River Noireau, because it was too risky with Mont Pinçon still in enemy hands.A new attack was planned for 6 August, with 130th Brigade making a feint to the north, while 129th Brigade continued from the west. In the end, the dominating position fell to a surprise attack. 4th Somerset Light Infantry and the reduced 5th Wiltshires fought their way forward through sweltering weather all day. 5th Wiltshires secured the crossroads at La Variniere and 4th Wiltshires was due to pass through them, when at about 18.00 A Sqn 13th/18th Hussars managed to get two Troops up a steep track to the top of the hill. By 18.30, seven Shermans were on the summit, attempting to mount an all-round defence and calling for infantry support. A staff officer ran up to Lt-Gen Horrocks at XXX Corps HQ, shouting 'We've got it, sir!' As fog descended on the hill, the 4th Wiltshires and the rest of A and B Sqns of the Hussars picked their way up the almost undefended track, followed by 4th Somerset LI. By daybreak the summit was firmly held, despite heavy German bombardment, and 5th Wiltshires and C Sqn still held the crossroads below. 214th Brigade relieved the exhausted troops that morning.Having taken and then defended Mont Pinçon, 43rd (Wessex) Division participated in XXX Corps' advance. It crossed the Noireau on 15 August by a broken railway bridge and by wading, whereupon 204 Field Company RE set to work with a waterproofed bulldozer to build a tank ford and a trestle bridge named 'Genesis'. 553 Field Company and 207 Field Park Company then built the division's first Bailey bridge across the site of the railway bridge. The main opposition came from mortars and booby-trapped mines. Next morning 43rd Recce and the Sherwood Foresters were ready to continue the pursuit of the broken enemy, who were soon caught in the Falaise pocket.
Vernon Bridge
The breakout achieved, XXX Corps drove flat out for the River Seine (Operation Loopy), with 43rd (W) Division sent ahead to make an assault crossing at Vernon. For this operation it was assisted by the bridging specialists of 15th (Kent) GHQ Troops Royal Engineers, a medium artillery regiment and the Cromwell tanks of 15th/19th The King's Royal Hussars, the armoured reconnaissance regiment of 11th Armoured Division. US troops had already reached the west bank of the Seine, so the convoys of assault troops and bridging material moving eastwards had to be carefully coordinated to cross with US convoys repositioning to the south. The first convoy, Group One, consisted of nearly 1500 vehicles of 129th Brigade with its usual proportion of divisional artillery, engineers and support services, reinforced by 1st Worcesters. Some of the assault infantry rode in the DUKW amphibious trucks that were to carry them over the river. The group arrived at Vernon on the afternoon of 25 August, ready to begin the assault that evening against the defenders from 49th German Infantry Division.15th (Kent) GHQTRE was tasked with manning the DUKWs during the initial assault and then operating rafts until the first bridge could be laid. They also had storm boats in reserve but these had to be used in the first wave because launching points for DUKWs were hard to find. A 15-minute bombardment by the guns of 94th (Dorset Yeomanry) Field Regiment, 121st (West Riding) Medium Regiment (further back in Group Two) and C Sqn, 15th/19th Hussars, together with the heavy mortars of 8th Middlesex, was followed by a smoke barrage to cover the crossing at 19.00. On the right, 5th Wiltshires began crossing in eight storm boats manned by 15th (Kent) GHQTRE, but they grounded before reaching the far side, and were raked by machine gun fire. By the end of an hour only one boat remained. Only about a company had got across, and they were overrun during the night. Three of the four available DUKWs also grounded, the survivor ferrying across the rest of 5th Wiltshires in the dark. On the left, 4th Somerset LI got across in the storm boats relatively easily, but found that their bridgehead was on an island, and they were still cut off from the east bank, apart from a few men who scrambled over the wreckage of the railway bridge. 1st Worcesters failed to get over the broken road bridge into the village of Vernonnet, which was strongly held. In the dark 260th Field Company managed to bulldoze a slipway for the DUKWs, speeding up the crossing, and 129th Brigade got about a battalion and a half across in total, setting up a perimeter along the escarpment above the bridging site.The Wessex field companies now began work under fire on a Class 9 (9 tonne maximum load) Folding Boat Equipment (FBE) bridge while the infantry fought to expand the bridgehead and clear Vernonnet. The Worcesters got over the broken bridge, and light rafts began to get 6-pounder anti-tank guns and armoured cars of the recce regiment across, but work on the bridge was halted by heavy fire until 5th DCLI and 7th Somerset LI from newly-arrived 214th Brigade struggled across the broken road bridge into Vernonnet. By nightfall the bridgehead was reasonably secure, the FBE bridge named 'David' was complete and 15th (Kent) GHQTRE's rafting troops were arriving to get a tank ferry into operation before morning. 7th Army Troops Royal Engineers had also arrived to begin a Class 40 Bailey Bridge.Next morning (27 August) a squadron each of 15th/19th Hussars' Cromwells and 4th/7th DGs' Shermans were rafted across and held off an armoured counter-attack, the infantry and 43rd Recce cleared the banks and pushed through the forest until they were firmly established on the heights. By 28 August, 7th ATRE working under shellfire had built their Class 40 bridge, codenamed 'Goliath', and 11th Armoured was beginning to pour across to spearhead XXX Corps' advance. A second Class 40 named 'Saul' was built by 15th (Kent) GHQRE. After the Seine crossing, 43rd (Wessex) Division was 'grounded' while the rest of XXX Corps raced across northern France and Belgium. The division rested and received reinforcements (many of them experienced men drafted from the disbanded 59th (Staffordshire) Division).
Market Garden
When 43rd (Wessex) Division next moved, the war was now 250 miles (400 km) away. The first elements moved up to Brussels to protect headquarters and carry out engineering works, then the division concentrated at Diest to take part in Operation Market Garden, beginning on 17 September. In 'Garden', the ground part of the operation, XXX Corps was to link river crossings up to the Nederrijn at Arnhem via a 'carpet' of airborne troops. 43rd (Wessex) Division accompanied by 8th Armoured Bde was to follow Guards Armoured Division, carrying out assault crossings if any of the bridges were found to be destroyed, and guarding the 'corridor' to Arnhem. The advance up the only road ('Club Route') was slow but on 21 September 43rd (Wessex) Division caught up with the Guards at Nijmegen. Further progress was blocked by strong German forces, and 1st Airborne Division holding out at Arnhem was in a desperate plight. 43rd (Wessex) Division was ordered to pass through the Guards the following morning and make an all-out effort to reach the Nederrijn by a side road. The Germans were found to be dug in at Oosterhout and the countryside was so boggy that it was impossible to move vehicles off the road, making outflanking moves too slow. Despite the shortage of artillery ammunition coming up the precarious line of communication, the whole of the divisional artillery and heavy mortars were used, but it was evening before the division got through. 5th DCLI, supported by a squadron of 4th/7th DG, was ordered to make a dash over the last 10 miles (16 km) to get in touch with the Polish Parachute Brigade at Driel on the south bank of the Nederrijn. The journey took only 30 minutes, but the road behind the column was cut by German tanks that had to be hunted down and destroyed before support could be brought up. Attempts to launch DUKWs with supplies for 1st Airborne were unsuccessful.The whole of 23 September was taken up with getting support through to 5th DCLI and the Poles and in clearing the main road, though 43rd Recce Rgt was able to exploit westwards. During the night 5th Dorsets and the divisional engineers ferried a few hundred Poles across the Nederrijn in assault boats to reinforce 1st Airborne Division's shrinking perimeter. 4th Dorsets and the engineers made another assault crossing on the night of 24/25 September, suffering heavy casualties and getting few supplies across. By now 1st Airborne had been effectively destroyed, and the only course now was to evacuate the survivors. Their radios had been inoperable, and the only communication link had been through 64th (London) Medium Regiment, RA, attached to 43rd (Wessex) Division. Through this link the code word for the evacuation was passed, and during the night of 25/26 September a feint attack was made by 5th Wiltshires while around 2300 survivors of 1st Airborne and the Poles were ferried back to the south bank; few of 4th Dorsets made it back.The division was blamed by many airborne soldiers for its dilatory advance to the river, though the Corps commander, Lt-Gen Horrocks, defended the division, pointing out that it could not deploy any armoured vehicles (either 8th Armoured Bde or 43rd Recce Rgt's armoured cars and half-tracks) off the single road, nicknamed 'Hell's Highway', which was cut behind them on several occasions, and praising the division's hard fighting. Nevertheless, Maj-Gen Thomas replaced the commanding officer of 43rd Recce immediately after the battle.In the aftermath of Market Garden, 43rd (Wessex) Division was stationed on 'the Island' (between the Rivers Waal and Nederrijn). 43rd Recce Rgt, with 12th Battalion King's Royal Rifle Corps from 8th Armoured Bde under command, protected the division's open western flank. The concealed squadrons sent back reports, but were forbidden to engage the enemy in order to hide the extent of the position. However, on the night of 26/27 September a furious firefight broke out when the Germans crossed the river in strength and attempted to emplace anti-tank guns in 43rd Recce's hidden positions.The Germans launched a serious counter-attack from the east on 1 October, attacking 129th Bde strung out guarding the road from Nijmegen to the Nederrijn. 4th Somerset LI and 5th Wiltshires fought them off at Elst for 48 hours, the divisional artillery breaking up some of the attacks, and RAF medium bombers following up. Further north, 5th Dorsets beat off 116th Panzer Division and 7th Hampshires had to dislodge enemy troops who fortified themselves in some brick kilns, with the help of RAF Typhoons. On 5 October 43rd (Wessex) handed most of its positions over to the US 101st Airborne Division, leaving the anti-tank and mortar platoons and 5th DCLI, the divisional reserve, to help out. The attacks ended after one last attempt on 6 October. 43rd Wessex continued to hold the western part of the Island. The divisional historian records that "While the Division faced the monotony inseparable from static defence, the Reconnaissance Regiment fought a different type of war". This involved guarding the western end of the Island, cooperating with the Dutch Resistance and facilitating the escape across the river of British paratroops who had evaded capture.
Operation Clipper
43rd (Wessex) Division was then shifted east with XXX Corps to cooperate with the US Ninth Army by capturing the Geilenkirchen salient (Operation Clipper). XXX Corps had 43rd Wessex and 84th US Divisions under command for this attack, which entailed breaching the Siegfried Line defences and capturing a string of fortified villages. 84th US Division attacked on the morning of 18 November, supported by British specialist armour, and was through the line of pillboxes by midday. 214th Brigade then attacked on its left in the afternoon, led by 7th Somerset LI and tanks of 4th/7th DG, and took its first objective, the village of Neiderheide. But many of the tanks and most of the supply vehicles got bogged down while 1st Worcesters were threading their way through Gilrath to form up for the second phase towards Tripsrath. Without tanks, and the artillery having shifted to another target, 1st Worcesters struggled forward under shellfire and forced their way into the village at nightfall. The traffic jam of bogged vehicles disrupted the attacks by 5th Dorsets and 5th DCLI, but they got into Bauchem and Hocheide respectively, and patrols reached Geilenkirchen itself, which was surrounded. After driving off some counter-attacks by 15th Panzer Grenadier Division during the night, Geilenkirchen was captured after a stiff fight next day. But thereafter heavy rain turned the whole battlefield into mud while the infantry struggled to consolidate their positions under heavy shellfire from the Siegfried Line guns. One wood captured and grimly held first by 4th Dorsets and then 5th Dorsets for seven days became known as 'Dorset Wood'. On 22 November 5th DCLI suffered heavy casualties trying to take the high ground near Hoven to deny the enemy observation over the two Allied divisions. Overnight both sides shared the village of Hoven, before counter-attacks came in at dawn from 10th SS Panzer Division and 21st Panzer Division. Horrocks himself authorised the withdrawal of the DCLI before they were overwhelmed. Any further attempt to take Hoven was impossible due to the waterlogged state of the country, which then had to be defended in conditions resembling the worst of the Western Front in the First World War. Horrocks organised an ad hoc battalion from XXX Corps' service units to relieve Wessex infantry for rest. Planning was under way to renew the offensive when the Germans attacked in the Ardennes (the Battle of the Bulge) on 16 December.
Operation Blackcock
The division then later played a comparatively small part in the mainly American Battle of the Bulge, where it was placed on the River Meuse as a reserve. Once the German Ardennes Offensive had been halted, 43rd (Wessex) Division returned to the offensive in early 1945 in Operation Blackcock to reduce the Roer Triangle, though exploitation was prevented by bad weather.
Operation Veritable
The 43rd later played a large part in Operation Veritable attached to First Canadian Army, through the month-long fighting in the Reichswald to capture Kleve, roll up the Siegfried Line defences, cross the Goch escarpment and seize Xanten on the Rhine.
Across the Rhine
43rd (Wessex) Division was given a follow-up task in the assault crossing of the Rhine (Operation Plunder). Its leading brigade crossed the river on 25 March behind 51st (Highland) Division, which had carried the assault on the night of 23/24 March. It found itself in immediate combat, but had broken through by 29 March. During the subsequent pursuit, 43rd (Wessex) Division was given the task of opening 'Club Route' for XXX Corps. The division was divided into five battle groups for the first 25 miles (40 km) drive, incorporating units of 8th Armoured Brigade. The advance began on 30 March: German rearguards were either overcome or bypassed, and the Twente Canal was crossed, with troops of 129th Infantry Bde and 8th Armoured Bde liberating Lochem on 1–2 April. The pursuit continued through April and ended with the capture of Bremen and XXX Corps' drive into the Cuxhaven peninsula. Hostilities ended on 5 May after the German surrender at Lüneburg Heath.After a period as occupation forces in XXX Corps' district, 43rd (Wessex) Division's HQ and TA units were demobilised at the war's end. Throughout the North West Europe Campaign the 43rd (Wessex) Division, like so many other Allied divisions that fought from Normandy to Germany, had suffered very heavy casualties with the majority of them, 80% in some units, being suffered by the average Tommy in the infantry battalions. From June 1944 to May 1945 the 43rd (Wessex) Division, or the Yellow Devils or British SS Division as known by the Germans, had suffered well over 12,500 casualties, with almost 3,000 killed in action.
43rd (Wessex) Infantry Division Order of Battle 1939–1945128th Infantry Brigade (left 6 June 1942)
1/4th Battalion, Hampshire Regiment
2/4th Battalion, Hampshire Regiment
5th Battalion, Hampshire Regiment
128th Infantry Brigade Anti-Tank Company (formed 19 June 1940, disbanded 20 December 1941)129th Infantry Brigade
4th Battalion, Somerset Light Infantry
4th Battalion, Wiltshire Regiment
5th Battalion, Wiltshire Regiment
129th Infantry Brigade Anti-Tank Company (formed 14 May 1940, disbanded 20 December 1941)130th Infantry Brigade
7th Battalion, Hampshire Regiment
4th Battalion, Dorsetshire Regiment
5th Battalion, Dorsetshire Regiment
130th Infantry Brigade Anti-Tank Company (formed 17 May 1940, disbanded 20 December 1941)25th Tank Brigade (from 1 June 1942, left 2 September 1942)
51st (Leeds Rifles) Royal Tank Regiment
11th Royal Tank Regiment
142nd Regiment Royal Armoured Corps34th Tank Brigade (from 3 September 1942, left 10 September 1943)
North Irish Horse (left 3 September 1942)
147th Regiment Royal Armoured Corps
153rd Regiment Royal Armoured Corps
151st Regiment Royal Armoured Corps (from 3 September 1942)214th Infantry Brigade (from 5 September 1943)
7th Battalion, Somerset Light Infantry
5th Battalion, Duke of Cornwall's Light Infantry
9th Battalion, Somerset Light Infantry (left 30 September 1943)
1st Battalion, Worcestershire Regiment (from 30 September 1943)Divisional Troops
1/8th Battalion, Middlesex Regiment (joined as Machine Gun Battalion from 18 November 1941, redesignated 8th Battalion May 1942, left 1 October 1942, rejoined as Support Battalion 1 October 1943, again as MG Battalion 28 February 1944)
48th Battalion, Reconnaissance Corps (converted from 5th Battalion, Gloucestershire Regiment 20 November 1941, redesignated 43rd Battalion 1 January 1942, later 43rd Regiment 6 June 1942, finally 43rd (Wessex) Reconnaissance Regiment (The Gloucestershire Regiment), Royal Armoured Corps 1 January 1944)
94th (Queen's Own Dorset Yeomanry) Field Regiment, Royal Artillery
112th (Wessex) Field Regiment, Royal Artillery
141st (Queen's Own Dorset Yeomanry) Field Regiment, Royal Artillery (left 8 June 1942)
179th Field Regiment, Royal Artillery (from 9 June 1942)
59th (Duke of Connaught's Own) Anti-Tank Regiment, Royal Artillery
110th Light Anti-Aircraft Regiment, Royal Artillery (converted from 7th Battalion, Dorsetshire Regiment, joined 23 March 1941)
43rd (Wessex) Divisional Engineers204th (Wessex) Field Company, Royal Engineers
260th Field Company, Royal Engineers
553rd Field Company, Royal Engineers (from 13 January 1940)
207th (Wessex) Field Park Company, Royal Engineers
13th Bridging Platoon, Royal Engineers (from 1 October 1943)
43rd (Wessex) Divisional Signals, Royal Corps of Signals
Royal Army Service Corps
54, 504, 505, 506 Companies
Royal Army Medical Corps
129, 130, 213 Field Ambulances
14, 15, 38 Field Dressing Stations
38 Field Hygiene Section
Royal Army Ordnance Corps
43 Ordnance Field Park
306 Mobile Laundry and Bath Unit
Royal Electrical and Mechanical Engineers
129, 130, 214 Infantry Brigade Workshops
43 Wessex Division Provost Company, Royal Military Police
57 Field Security Section
Postal Unit
Postwar
The TA was reconstituted from 1 January 1947 and its units and formations including 43rd (Wessex) Infantry Division were reformed. However, the TA saw large numbers of amalgamations from 1950 onwards. In 1961 the division became a district headquarters as 43rd (Wessex) Division/District, and it was disbanded on the reduction of the TA into the Territorial and Army Volunteer Reserve on 1 April 1967, when many individual TA units lost their identities. The district headquarters itself formed the core of the structure for the creation of South West District under HQ UK Land Forces in 1972.
43rd (Wessex) Infantry Division Order of Battle 1947128 Infantry Brigade
4th Battalion, Royal Hampshire Regiment at Winchester
4th Battalion, Oxfordshire and Buckinghamshire Light Infantry at Oxford
4th/6th Battalion, Royal Berkshire Regiment at Reading129 Infantry Brigade
4th Battalion, Somerset Light Infantry at Bath
5th Battalion, Gloucestershire Regiment at Gloucester
4th Battalion, Wiltshire Regiment at Trowbridge130 (West Country) Infantry Brigade
4th Battalion, Devonshire Regiment at Exeter
5th (Prince of Wales's) Battalion, Devonshire Regiment at Plymouth
4th/5th Battalion, Duke of Cornwall's Light Infantry at Truro
4th Battalion, Dorsetshire Regiment at DorchesterRoyal Armoured Corps
Royal Wiltshire Yeomanry at SwindonRoyal Artillery
294 (Queen's Own Dorset Yeomanry) Field Regiment at Sherborne
296 (Royal Devon Yeomanry) Field Regiment at Exeter
387 (Queen's Own Oxfordshire Hussars) Field Regiment at Oxford
383 (Duke of Connaught's Royal Hampshire) Anti-Tank Regiment at Portsmouth
396 (Devon) Light Anti-Aircraft Regiment at Devonport
883 Locating Battery at BristolRoyal Engineers
110 Field Engineer Regiment204 Field Squadron
226 Field Squadron
260 Field Squadron
207 Field Park SquadronRoyal Corps of Signals
43rd (Wessex) Infantry Division Signal Regiment at Taunton 1 Squadron at Exeter
2 Squadron at Taunton
3 Squadron at Torquay, later BristolRoyal Army Service Corps
43 (Wessex) Infantry Divisional Column at Bristol504 Company at Swindon
505 Company at Didcot
506 Company at Plymouth
1567 Company at Plymouth
43 Ordnance Field Park, Royal Army Ordnance Corps
43 Divisional Royal Electrical and Mechanical Engineers
43 Divisional Royal Army Medical Corps
Commanders
The following officers commanded the division at various times:
Insignia
The banner of the kings of Wessex bore a golden Wyvern, a dragon with two eagle-like legs and the barbed tail of a snake. The 43rd (Wessex) Division adopted the golden wyvern on a blue square as its formation sign in 1935.
Memorials
The Hill 112 memorial was erected by the divisional engineers and later taken over by the Commonwealth War Graves Commission with an endowment from the Memorial Fund. The first memorial in England was at Castle Hill, Mere, in Wiltshire, acquired on a 199-year lease from the Duchy of Cornwall and entrusted to the Parish Council of Mere. Next the fund acquired Wynyard's Gap near Crewkerne, Somerset. Finally, Sir Richard Onslow (formerly of the Duke of Cornwall's Light Infantry) presented Rough Tor on Bodmin Moor to the National Trust as a memorial. The Roll of Honour is in the War Memorial Chapel in Salisbury Cathedral.A memorial stone stands at the end of a lane named 'Somerset' in Lochem, Netherlands, showing the Wessex Wyvern and listing 4th Bn Somerset Light Infantry, 4th Bn Wiltshire Regiment and units of 8th Armoured Bde who liberated Lochem on 1–2 April 1945. The horizontal inscription reads 'All the way from Normandy'.
See also
List of British divisions in World War I
List of British divisions in World War II
British Army Order of Battle (September 1939)
Notes
References
Bibliography
External links
Mark Conrad, The British Army, 1914 (archive site)
British Army units from 1945 on
Divisional insignia
The Long, Long Trail
Orders of Battle at Patriot Files
Graham Watson, The Territorial Army 1947
World War II Armed Forces
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The 43rd (Wessex) Infantry Division was an infantry division of Britain's Territorial Army (TA). The division was first formed in 1908, as the Wessex Division. During the First World War, it was broken-up and never served as a complete formation. It was reformed in the TA in 1920, and then served in the campaign in North West Europe from June 1944 until May 1945, during the Second World War. The division suffered heavy casualties and gained an excellent reputation. After the Second World War, the division formed part of the postwar TA, and became the 43rd (Wessex) Division/District in 1961. It was finally disbanded in 1967.
Formation
The Territorial Force (TF) was formed on 1 April 1908 following the enactment of the Territorial and Reserve Forces Act 1907 (7 Edw.7, c.9) which combined and re-organised the old Volunteer Force, the Honourable Artillery Company and the Yeomanry. On formation, the TF contained 14 infantry divisions and 14 mounted yeomanry brigades. One of the divisions was the Wessex Division.The Wessex Division was formed in Southern Command from TF units in the south-western counties of Cornwall, Devon, Dorset, Hampshire, Somerset and Wiltshire. In peacetime, the divisional headquarters was at 19 Cathedral Close in Exeter.
Wessex Division Order of Battle 1908–1914Divisional HQ at Exeter
Hampshire Brigade at Southampton
4th Battalion, Hampshire Regiment at Winchester (joined 12th Indian Division and served in Mesopotamia)
5th Battalion, Hampshire Regiment at Southampton (served in Third Afghan War)
6th (Duke of Connaught's Own) Battalion, Hampshire Regiment at Portsmouth (joined 15th Indian Division and served in Mesopotamia)
7th Battalion, Hampshire Regiment at Bournemouth (served in Aden)South-Western Brigade at Taunton
4th Battalion, Somerset Light Infantry at Bath (joined 37th Indian Brigade and served in Mesopotamia)
5th Battalion, Somerset Light Infantry at Taunton (joined 75th Division and served in Palestine)
4th Battalion, Dorsetshire Regiment at Dorchester (joined 42nd Indian Brigade and served in Mesopotamia)
4th Battalion, Wiltshire Regiment at Trowbridge (joined 75th Division and served in Palestine)Devon & Cornwall Brigade at Exeter
4th Battalion, Devonshire Regiment at Exeter (joined 41st Indian Brigade and served in Mesopotamia)
5th (Prince of Wales's) Battalion, Devonshire Regiment at Plymouth (joined 75th Division and served in Palestine)
6th Battalion, Devonshire Regiment at Barnstaple (joined 36th Indian Brigade and served in Mesopotamia)
4th Battalion, Duke of Cornwall's Light Infantry at Truro (served in Aden, later with 75th Division in Palestine)Divisional Royal Artillery
I Wessex Brigade, Royal Field Artillery at Portsmouth (joined 3rd (Lahore) Division and served in Mesopotamia)
1st Hampshire Battery
2nd Hampshire Battery
3rd Hampshire Battery
1st Wessex Ammunition Column
II Wessex (Howitzer) Brigade, Royal Field Artillery at Ryde, Isle of Wight
4th Hampshire (Howitzer) Battery (served in Aden)
5th Hampshire (Howitzer) Battery (joined 6th (Poona) Division and served in Mesopotamia; captured at Kut)]
2nd Wessex Ammunition Column
III Wessex Brigade, Royal Field Artillery at Swindon (served in Third Afghan War)
6th Hampshire Battery
Dorsetshire Battery
Wiltshire Battery
3rd Wessex Ammunition Column
IV Wessex Brigade, Royal Field Artillery at Exeter
1st Devonshire Battery
2nd Devonshire Battery
3rd Devonshire Battery (served in Third Afghan War)
4th Wessex Ammunition Column
Wessex (Hampshire) Heavy Battery, Royal Garrison Artillery and Ammunition Column at Cosham (served on the Western Front)Wessex Divisional Engineers (joined 27th Division and served at Salonika)
1st Wessex Field Company at Bath (became 500th Field Company)
2nd Wessex Field Company at Weston-super-Mare (became 501st Field Company)
Wessex Divisional Telegraph Company ('Signal Company' from 1910) at ExeterDivisional Royal Army Medical Corps (joined 8th Division and served on the Western Front)
1st Wessex Field Ambulance at Exeter (became 24th Field Ambulance)
2nd Wessex Field Ambulance at Plymouth (became 25th Field Ambulance)
3rd Wessex Field Ambulance at Portsmouth (became 26th Field Ambulance)
Wessex Clearing Hospital at ExeterWessex Divisional Transport & Supply Column, Army Service Corps, at Exeter (joined 29th Division and served at Gallipoli)
Divisional Company at Andover (became 246 Company)
Devonshire and Cornwall Company at Plymouth (became 247 Company)
South Western Brigade Company at Bridgwater (became 248 Company)
Hampshire Brigade Company at Aldershot (became 249 Company)
First World War
On 29 July 1914, the Wessex Division was on Salisbury Plain carrying out its annual training camp when 'precautionary orders' were received, and next day the division took up emergency war stations in Somerset, Devon and Cornwall. The order to mobilise arrived on the evening of 4 August. Between 10 and 13 August the division concentrated on Salisbury Plain and began war training.On 24 September, at the special request of the Secretary of State for War, Earl Kitchener of Khartoum the Wessex Division accepted liability for service in British India to relieve the Regular Army units there for service on the Western Front. The division's infantry battalions (without their brigade headquarters) and artillery brigades embarked at Southampton on 8 October and were convoyed to Bombay, disembarking on 9 November. The engineers, medical units, transport, heavy battery and brigade ammunition columns also remained in the UK and joined formations composed of Regular units brought back from India and other imperial garrisons. Meanwhile, the battalions and batteries were immediately distributed to garrisons across India, reverting to peacetime service conditions, and the Wessex Division never saw service as a whole, though it was formally numbered the 43rd (1st Wessex) Division in 1915 and the brigades were designated 128th (Hampshire) Brigade, 129th (South Western) Brigade and 130th (Devon and Cornwall) Brigade.As soon as the Wessex Division had left for India, the home depots began raising 2nd Line units, distinguished from the 1st Line by a '2/' prefix. Recruitment and training of the 2nd Wessex Division proceeded so well that it was also sent to India in December 1914, and later received the notional title of 45th (2nd Wessex) Division.By early 1915 the need was growing for troops to be sent to various theatres of war, and the first drafts and formed units from the 1st Wessex Division began to go on active service, particularly to the Mesopotamian Front. By the end of the war only one battalion and five batteries remained in India, and most of these then participated in the Third Anglo-Afghan War.
Second World War
Mobilisation and training
43rd (Wessex) Division was reformed in 1920 and became part of the Territorial Army, which replaced the TF. In the period of international tension preceding the outbreak of the Second World War, the existing territorial divisions (known as the first-line) helped form new formations, known as the second-line. This process was known as duplicating. The division's duplicate was the 45th Infantry Division.
The TA was mobilised on the outbreak of war in September 1939 and the division began training in its home area. In May 1940 it was preparing to go overseas to join the British Expeditionary Force (BEF) in France, but the German invasion of the Low Countries on 10 May ended the 'Phoney War' before the division was ready. When the Battle of France was lost and the BEF was being evacuated from Dunkirk, 43rd (W) Division was one of the few reasonably well-equipped formations left in Home Forces to counter a German invasion of the United Kingdom. It formed part of the mobile GHQ Reserve disposed on the line from Northampton through North London to Aldershot, from which brigade groups could be despatched to any threatened area. During the period when invasion was most threatened, the division was stationed just north of London.By the end of 1940 the division was stationed under XII Corps in East Kent, where it remained for the next four years, first in defensive mode, later training intensively. It was later noted that its habitual training area round Stone Street, outside Folkestone, bore a marked resemblance to the Bocage countryside in Normandy where it would later fight.
In 1942, however, after the German invasion of the Soviet Union and the entrance of the United States into the war, the situation changed and the 43rd Division started training for offensive operations to return to mainland Europe. Throughout most of 1942, the division was part of XII Corps, serving alongside the 46th Infantry Division and 53rd (Welsh) Infantry Division. XII Corps was, at the time, commanded by Lieutenant-General Bernard Montgomery.In March 1942, the division also gained a new General Officer Commanding (GOC) in the form of Major-General Ivor Thomas. Thomas was a decorated officer who had served as a young battery commander in the Royal Artillery on the Western Front during the First World War where he was twice wounded and awarded the Military Cross and the Distinguished Service Order. He would command the 43rd Division until September 1945. Thomas was an effective but hard-driving commander, humourless and not universally liked, sometimes known as 'Butcher', or more jocularly by Lt-Gen Brian Horrocks and others as 'Von Thoma', after the German Lt-Gen Wilhelm Ritter von Thoma captured after the Battle of Alamein. (Horrocks also jokingly referred to Thomas's command as the 'Wicked Wyvern'). Critics of his training methods regarded 43rd (Wessex) Division as 'the most over-exercised in the Army'.
In June 1942, the 128th Infantry Brigade (consisting of three battalions of the Hampshire Regiment) was transferred to 46th Infantry Division. It was replaced first by 25th and later 34th Army Tank Brigade as part of an experiment with 'Mixed Divisions'. However the experiment was abandoned (deemed unsuitable for the type of terrain in North-western Europe) in late 1943 and the 34th Tank Brigade was replaced, in October 1943, by the 214th Independent Infantry Brigade, a Home Defence formation raised during the war that had been serving in Hampshire and Dorset District. After service in the Isle of Wight, 214th Brigade had received specialised training in combined operations under the Royal Marines at Inverary, and retained an individuality within the division. 214th Brigade would remain with the 43rd Division for the rest of the war.
Operation Overlord
XII Corps and 43rd (Wessex) Division were assigned to 21st Army Group for the Allied invasion of Normandy (Operation Overlord). They were follow-up formations, with 43rd (Wessex) Division scheduled to complete its landings 14 days after D Day (D +14, 20 June). However, shipping delays and a storm between 19 and 22 June delayed its arrival; the division finally concentrated round Bayeux on 24 June.HQ, A and C Squadrons of 43rd (Wessex) Reconnaissance Regiment were aboard the troopship Derrycunihy, which arrived off Sword Beach on the evening of 20 June. High seas and enemy shelling prevented unloading for three days and it was decided to move to Juno Beach for disembarkation. As the ship started engines it detonated an acoustic mine, splitting the ship in two, and the after part, packed with sleeping men of 43rd Recce Regiment, sank rapidly. Worse still, an ammunition lorry caught fire, and oil floating on the water was set alight. Landing craft and gunboats came alongside and picked up survivors, but the regiment lost 183 men, with another 120 evacuated wounded. Most of 43rd Recce Rgts's vehicles were landed from the beached fore part of the "Derrycunihy", and reinforcements were sent from England, but the regiment was not fully up to strength until the end of July 1944.
Operation Epsom
The division's first action, Operation Epsom starting on 26 June, involved following 15th (Scottish) Division's advance and then securing the captured objectives. However, this entailed some heavy fighting by 5th Battalion Duke of Cornwall's Light Infantry (DCLI) against a Panzer counter-attack at Cheux on 27 June. The supporting 17-pounder anti-tank guns were knocked out and the infantry had to stalk Panther tanks with their lighter 6-pounder anti-tank guns and hand-held PIATs. Other battalions mopped up the important objective of Manvieux. On 28 June 1st Battalion Worcestershire Regiment made an attack from Cheux against Mouen: they had to cross open cornfields, but had support from the whole divisional artillery and heavy mortars plus two medium artillery regiments. The infantry followed the Creeping barrage of smoke and High explosive shells and forced their way into the houses and gardens, using PIATs against those German tanks that had survived the barrage. On 29 June 129 Brigade advanced under fire to ford the River Odon and dug in, a German counter-attack against them in the evening being destroyed by the divisional artillery.
Hill 112
The division's first major offensive action of its own was Operation Jupiter, to take Hill 112, which had been briefly captured by British armour during 'Epsom' but had to be abandoned. The attack on 10 July was supported by all the divisional artillery and mortars, plus the artillery of 15th (Scottish) Division and 11th Armoured Division and 3rd and 8th Army Groups Royal Artillery (AGRAs). In the first phase 129th Brigade on the right, with all three battalions in line, and 130th Brigade on the left with one battalion, were to capture the hill and the road from it to Château de Fontaine. They were supported by Churchill tanks from 31st Tank Brigade. Then, while 129th Brigade formed a secure south-west flank, 130th Brigade and Churchill Crocodile flamethrowing tanks from 79th Armoured Division were to advance from Château de Fontaine to capture Eterville and Maltot and the high ground to the south-east. Finally, 214th Brigade in Kangaroo armoured personnel carriers accompanied by 4th Armoured Brigade was supposed to break through to the River Orne and seize bridgeheads.The massive barrage stunned but failed to suppress the defenders from 10th SS Panzer Division. When the Wessex infantry went forward they came under heavy fire and had to clear defenders from the dugouts and defensive positions of their outpost line on the forward slopes. 5th Battalion Dorsets and 9th Royal Tank Regiment, leading 130th Brigade against the farms on the lower ground, made quick progress, 7th Somerset Light Infantry passing through with the Churchills and Crocodiles to deal with Chateau de Fontaine. But 129th Brigade was slowed in its advance on Hill 112 itself, suffering heavy casualties on the open slopes, and then running into the recently-arrived Tiger I tanks of 102nd SS Heavy Panzer Battalion, which the Churchills and corps anti-tank guns of 86th (Devon) Anti-Tank Regiment, Royal Artillery, struggled to deal with. By mid-morning 129th Brigade only had a slender toehold on the edge of the plateau. Attempting to continue 130th Brigade's advance on Maltot, 7th Hampshires and 9th RTR came under crossfire from Hill 112, while some of the Tigers reached the village first. The leading Hampshire penetrated the village, leaving strongpoints to be mopped up later by the following Dorsets, but they were driven out by counter-attacks. 4th Dorsets, making a second attack, suffered heavy casualties. Two battalions of 214th Brigade had already been drawn into the fighting around Chateau de Fontaine, leaving 5th DCLI as the last uncommitted battalion. It attacked up the slopes of Hill 112, described as 'one of the most tragic acts of self-sacrifice in the entire North West European Campaign'. Launched at 20.30 towards 'The Orchard' on the crest of the hill, and supported by a squadron of 7th Royal Tank Regiment and all available guns, including the divisional light anti-aircraft guns, the attack reached the orchard, but could get no further. The infantry and anti-tank guns held off counter-attacks through the night from the newly-arrived 9th SS Panzer Division, and were reinforced in the morning by a company of 1st Worcesters and briefly by a squadron of Sherman tanks from the Royal Scots Greys. By mid-afternoon all the anti-tank guns on the hill had been knocked out, the tanks had to retire to the reverse slope, and the defence was almost over. The order was given to withdraw and 60 survivors of 5th DCLI were brought down. Both sides remained dug in on the slopes, with the hilltop left in No man's land. The division had to hold its positions under mortar fire for another 14 days, described by the commander of 214th Brigade as comparable only 'to the bombardment at Passchendaele'. This defence was followed by a final set-piece attack, Operation Express, in which 4th and 5th Wiltshires and 7th RTR succeeded in capturing Maltot on 22 July.
Overall, 43rd (Wessex) Division performed well in Normandy and was considered by many senior British officers to be one of the best divisions of the British Army during the war. For the rest of the war Bernard Montgomery, commanding all British and Canadian troops in the campaign, preferred to use formations such as 43rd (Wessex) and 15th (Scottish) to spearhead his assaults. This was mainly due to issues of morale because veteran formations such as the 7th Armoured and 51st (Highland), both of which had seen extensive service in North Africa and Italy (and fought poorly in Normandy, according to senior officers), were judged as tired and war-weary with morale being almost dangerously fragile. With formations that had spent years in the United Kingdom training such as the 43rd (Wessex), 15th (Scottish), 11th Armoured and 59th (Staffordshire) Divisions the problem of morale was less of an issue.
Mont Pinçon
After a short rest 43rd (Wessex) Division moved to XXX Corps to launch an attack towards the dominating height of Mont Pinçon as part of Operation Bluecoat. 8th Armoured Brigade was assigned to support the infantry. Starting at 08.00 on 30 July, the division was to force its way through enemy positions at Briquessard and advance through Cahagnes towards Ondefontaine. 130th Brigade led, reinforced by 4th Somerset Light Infantry and Sherman tanks of the Sherwood Rangers Yeomanry, followed by 214th Brigade and then 129th Brigade. Initial casualties were heavy, particularly from mines, and the advance achieved only 1,000 yards (910 m) on the first day. It took until the following morning to clear the mines and restart the advance with 214th Brigade and the tanks of 4th/7th Dragoon Guards. At 17.30 the brigade broke through, and 1st Worcesters riding on the tanks got beyond Cahagnes by nightfall. 7th Somerset Light Infantry cleared the village in the dark and, with the aid of the divisional artillery, fought off a counter-attack accompanied by heavy armour (probably Jagdpanthers) that had to be stalked with PIATs.The division fought its way forward during 1 August, then at 02.00 on 2 August 129th Brigade began its advance on Ondefontaine. It was a day of slow but steady progress against rifle and machine gun fire from commanding positions on the ridge in front, followed by another pre-dawn attack towards Ondefontaine, while 214th Brigade began working its way towards Mont Pinçon. 5th DCLI and B Squadron 4th/7th DG, supported by the divisional artillery and mortars, reached the top of the ridge and engaged enemy infantry and armour, while 1st Worcesters worked round the flank and took the crest. 43rd Recce Regiment (reformed after the Derrycunihy disaster) then went through to unhinge the Ondefontaine defences. The division was now facing east, with Mont Pinçon only 4 miles (6.4 km) away.
At 08.00 on 5 August, 4th Wiltshires moved out with B Squadron 13th/18th Royal Hussars, picking their way through the narrow lanes, while A Sqn took a parallel route carrying 5th Wiltshires. 4th Wiltshires found a bridge blown and went ahead without their tanks towards the strongly-held village of St Jean-le-Blanc, breaking up a counter-attack by calling down artillery fire. About 16.00 the battalion pioneers managed to bridge the stream and a Troop of B Sqn crossed, but withdrew to 'harbour' at dusk. Meanwhile, 5th Wiltshires got to the bridge over the Druance at the foot of Mont Pinçon but failed to capture it by the end of the day. Generals Ivor Thomas and Brian Horrocks (who had just taken command of XXX Corps) were anxious to push on, and had already cancelled Operation Blackwater, designed to reach the River Noireau, because it was too risky with Mont Pinçon still in enemy hands.A new attack was planned for 6 August, with 130th Brigade making a feint to the north, while 129th Brigade continued from the west. In the end, the dominating position fell to a surprise attack. 4th Somerset Light Infantry and the reduced 5th Wiltshires fought their way forward through sweltering weather all day. 5th Wiltshires secured the crossroads at La Variniere and 4th Wiltshires was due to pass through them, when at about 18.00 A Sqn 13th/18th Hussars managed to get two Troops up a steep track to the top of the hill. By 18.30, seven Shermans were on the summit, attempting to mount an all-round defence and calling for infantry support. A staff officer ran up to Lt-Gen Horrocks at XXX Corps HQ, shouting 'We've got it, sir!' As fog descended on the hill, the 4th Wiltshires and the rest of A and B Sqns of the Hussars picked their way up the almost undefended track, followed by 4th Somerset LI. By daybreak the summit was firmly held, despite heavy German bombardment, and 5th Wiltshires and C Sqn still held the crossroads below. 214th Brigade relieved the exhausted troops that morning.Having taken and then defended Mont Pinçon, 43rd (Wessex) Division participated in XXX Corps' advance. It crossed the Noireau on 15 August by a broken railway bridge and by wading, whereupon 204 Field Company RE set to work with a waterproofed bulldozer to build a tank ford and a trestle bridge named 'Genesis'. 553 Field Company and 207 Field Park Company then built the division's first Bailey bridge across the site of the railway bridge. The main opposition came from mortars and booby-trapped mines. Next morning 43rd Recce and the Sherwood Foresters were ready to continue the pursuit of the broken enemy, who were soon caught in the Falaise pocket.
Vernon Bridge
The breakout achieved, XXX Corps drove flat out for the River Seine (Operation Loopy), with 43rd (W) Division sent ahead to make an assault crossing at Vernon. For this operation it was assisted by the bridging specialists of 15th (Kent) GHQ Troops Royal Engineers, a medium artillery regiment and the Cromwell tanks of 15th/19th The King's Royal Hussars, the armoured reconnaissance regiment of 11th Armoured Division. US troops had already reached the west bank of the Seine, so the convoys of assault troops and bridging material moving eastwards had to be carefully coordinated to cross with US convoys repositioning to the south. The first convoy, Group One, consisted of nearly 1500 vehicles of 129th Brigade with its usual proportion of divisional artillery, engineers and support services, reinforced by 1st Worcesters. Some of the assault infantry rode in the DUKW amphibious trucks that were to carry them over the river. The group arrived at Vernon on the afternoon of 25 August, ready to begin the assault that evening against the defenders from 49th German Infantry Division.15th (Kent) GHQTRE was tasked with manning the DUKWs during the initial assault and then operating rafts until the first bridge could be laid. They also had storm boats in reserve but these had to be used in the first wave because launching points for DUKWs were hard to find. A 15-minute bombardment by the guns of 94th (Dorset Yeomanry) Field Regiment, 121st (West Riding) Medium Regiment (further back in Group Two) and C Sqn, 15th/19th Hussars, together with the heavy mortars of 8th Middlesex, was followed by a smoke barrage to cover the crossing at 19.00. On the right, 5th Wiltshires began crossing in eight storm boats manned by 15th (Kent) GHQTRE, but they grounded before reaching the far side, and were raked by machine gun fire. By the end of an hour only one boat remained. Only about a company had got across, and they were overrun during the night. Three of the four available DUKWs also grounded, the survivor ferrying across the rest of 5th Wiltshires in the dark. On the left, 4th Somerset LI got across in the storm boats relatively easily, but found that their bridgehead was on an island, and they were still cut off from the east bank, apart from a few men who scrambled over the wreckage of the railway bridge. 1st Worcesters failed to get over the broken road bridge into the village of Vernonnet, which was strongly held. In the dark 260th Field Company managed to bulldoze a slipway for the DUKWs, speeding up the crossing, and 129th Brigade got about a battalion and a half across in total, setting up a perimeter along the escarpment above the bridging site.The Wessex field companies now began work under fire on a Class 9 (9 tonne maximum load) Folding Boat Equipment (FBE) bridge while the infantry fought to expand the bridgehead and clear Vernonnet. The Worcesters got over the broken bridge, and light rafts began to get 6-pounder anti-tank guns and armoured cars of the recce regiment across, but work on the bridge was halted by heavy fire until 5th DCLI and 7th Somerset LI from newly-arrived 214th Brigade struggled across the broken road bridge into Vernonnet. By nightfall the bridgehead was reasonably secure, the FBE bridge named 'David' was complete and 15th (Kent) GHQTRE's rafting troops were arriving to get a tank ferry into operation before morning. 7th Army Troops Royal Engineers had also arrived to begin a Class 40 Bailey Bridge.Next morning (27 August) a squadron each of 15th/19th Hussars' Cromwells and 4th/7th DGs' Shermans were rafted across and held off an armoured counter-attack, the infantry and 43rd Recce cleared the banks and pushed through the forest until they were firmly established on the heights. By 28 August, 7th ATRE working under shellfire had built their Class 40 bridge, codenamed 'Goliath', and 11th Armoured was beginning to pour across to spearhead XXX Corps' advance. A second Class 40 named 'Saul' was built by 15th (Kent) GHQRE. After the Seine crossing, 43rd (Wessex) Division was 'grounded' while the rest of XXX Corps raced across northern France and Belgium. The division rested and received reinforcements (many of them experienced men drafted from the disbanded 59th (Staffordshire) Division).
Market Garden
When 43rd (Wessex) Division next moved, the war was now 250 miles (400 km) away. The first elements moved up to Brussels to protect headquarters and carry out engineering works, then the division concentrated at Diest to take part in Operation Market Garden, beginning on 17 September. In 'Garden', the ground part of the operation, XXX Corps was to link river crossings up to the Nederrijn at Arnhem via a 'carpet' of airborne troops. 43rd (Wessex) Division accompanied by 8th Armoured Bde was to follow Guards Armoured Division, carrying out assault crossings if any of the bridges were found to be destroyed, and guarding the 'corridor' to Arnhem. The advance up the only road ('Club Route') was slow but on 21 September 43rd (Wessex) Division caught up with the Guards at Nijmegen. Further progress was blocked by strong German forces, and 1st Airborne Division holding out at Arnhem was in a desperate plight. 43rd (Wessex) Division was ordered to pass through the Guards the following morning and make an all-out effort to reach the Nederrijn by a side road. The Germans were found to be dug in at Oosterhout and the countryside was so boggy that it was impossible to move vehicles off the road, making outflanking moves too slow. Despite the shortage of artillery ammunition coming up the precarious line of communication, the whole of the divisional artillery and heavy mortars were used, but it was evening before the division got through. 5th DCLI, supported by a squadron of 4th/7th DG, was ordered to make a dash over the last 10 miles (16 km) to get in touch with the Polish Parachute Brigade at Driel on the south bank of the Nederrijn. The journey took only 30 minutes, but the road behind the column was cut by German tanks that had to be hunted down and destroyed before support could be brought up. Attempts to launch DUKWs with supplies for 1st Airborne were unsuccessful.The whole of 23 September was taken up with getting support through to 5th DCLI and the Poles and in clearing the main road, though 43rd Recce Rgt was able to exploit westwards. During the night 5th Dorsets and the divisional engineers ferried a few hundred Poles across the Nederrijn in assault boats to reinforce 1st Airborne Division's shrinking perimeter. 4th Dorsets and the engineers made another assault crossing on the night of 24/25 September, suffering heavy casualties and getting few supplies across. By now 1st Airborne had been effectively destroyed, and the only course now was to evacuate the survivors. Their radios had been inoperable, and the only communication link had been through 64th (London) Medium Regiment, RA, attached to 43rd (Wessex) Division. Through this link the code word for the evacuation was passed, and during the night of 25/26 September a feint attack was made by 5th Wiltshires while around 2300 survivors of 1st Airborne and the Poles were ferried back to the south bank; few of 4th Dorsets made it back.The division was blamed by many airborne soldiers for its dilatory advance to the river, though the Corps commander, Lt-Gen Horrocks, defended the division, pointing out that it could not deploy any armoured vehicles (either 8th Armoured Bde or 43rd Recce Rgt's armoured cars and half-tracks) off the single road, nicknamed 'Hell's Highway', which was cut behind them on several occasions, and praising the division's hard fighting. Nevertheless, Maj-Gen Thomas replaced the commanding officer of 43rd Recce immediately after the battle.In the aftermath of Market Garden, 43rd (Wessex) Division was stationed on 'the Island' (between the Rivers Waal and Nederrijn). 43rd Recce Rgt, with 12th Battalion King's Royal Rifle Corps from 8th Armoured Bde under command, protected the division's open western flank. The concealed squadrons sent back reports, but were forbidden to engage the enemy in order to hide the extent of the position. However, on the night of 26/27 September a furious firefight broke out when the Germans crossed the river in strength and attempted to emplace anti-tank guns in 43rd Recce's hidden positions.The Germans launched a serious counter-attack from the east on 1 October, attacking 129th Bde strung out guarding the road from Nijmegen to the Nederrijn. 4th Somerset LI and 5th Wiltshires fought them off at Elst for 48 hours, the divisional artillery breaking up some of the attacks, and RAF medium bombers following up. Further north, 5th Dorsets beat off 116th Panzer Division and 7th Hampshires had to dislodge enemy troops who fortified themselves in some brick kilns, with the help of RAF Typhoons. On 5 October 43rd (Wessex) handed most of its positions over to the US 101st Airborne Division, leaving the anti-tank and mortar platoons and 5th DCLI, the divisional reserve, to help out. The attacks ended after one last attempt on 6 October. 43rd Wessex continued to hold the western part of the Island. The divisional historian records that "While the Division faced the monotony inseparable from static defence, the Reconnaissance Regiment fought a different type of war". This involved guarding the western end of the Island, cooperating with the Dutch Resistance and facilitating the escape across the river of British paratroops who had evaded capture.
Operation Clipper
43rd (Wessex) Division was then shifted east with XXX Corps to cooperate with the US Ninth Army by capturing the Geilenkirchen salient (Operation Clipper). XXX Corps had 43rd Wessex and 84th US Divisions under command for this attack, which entailed breaching the Siegfried Line defences and capturing a string of fortified villages. 84th US Division attacked on the morning of 18 November, supported by British specialist armour, and was through the line of pillboxes by midday. 214th Brigade then attacked on its left in the afternoon, led by 7th Somerset LI and tanks of 4th/7th DG, and took its first objective, the village of Neiderheide. But many of the tanks and most of the supply vehicles got bogged down while 1st Worcesters were threading their way through Gilrath to form up for the second phase towards Tripsrath. Without tanks, and the artillery having shifted to another target, 1st Worcesters struggled forward under shellfire and forced their way into the village at nightfall. The traffic jam of bogged vehicles disrupted the attacks by 5th Dorsets and 5th DCLI, but they got into Bauchem and Hocheide respectively, and patrols reached Geilenkirchen itself, which was surrounded. After driving off some counter-attacks by 15th Panzer Grenadier Division during the night, Geilenkirchen was captured after a stiff fight next day. But thereafter heavy rain turned the whole battlefield into mud while the infantry struggled to consolidate their positions under heavy shellfire from the Siegfried Line guns. One wood captured and grimly held first by 4th Dorsets and then 5th Dorsets for seven days became known as 'Dorset Wood'. On 22 November 5th DCLI suffered heavy casualties trying to take the high ground near Hoven to deny the enemy observation over the two Allied divisions. Overnight both sides shared the village of Hoven, before counter-attacks came in at dawn from 10th SS Panzer Division and 21st Panzer Division. Horrocks himself authorised the withdrawal of the DCLI before they were overwhelmed. Any further attempt to take Hoven was impossible due to the waterlogged state of the country, which then had to be defended in conditions resembling the worst of the Western Front in the First World War. Horrocks organised an ad hoc battalion from XXX Corps' service units to relieve Wessex infantry for rest. Planning was under way to renew the offensive when the Germans attacked in the Ardennes (the Battle of the Bulge) on 16 December.
Operation Blackcock
The division then later played a comparatively small part in the mainly American Battle of the Bulge, where it was placed on the River Meuse as a reserve. Once the German Ardennes Offensive had been halted, 43rd (Wessex) Division returned to the offensive in early 1945 in Operation Blackcock to reduce the Roer Triangle, though exploitation was prevented by bad weather.
Operation Veritable
The 43rd later played a large part in Operation Veritable attached to First Canadian Army, through the month-long fighting in the Reichswald to capture Kleve, roll up the Siegfried Line defences, cross the Goch escarpment and seize Xanten on the Rhine.
Across the Rhine
43rd (Wessex) Division was given a follow-up task in the assault crossing of the Rhine (Operation Plunder). Its leading brigade crossed the river on 25 March behind 51st (Highland) Division, which had carried the assault on the night of 23/24 March. It found itself in immediate combat, but had broken through by 29 March. During the subsequent pursuit, 43rd (Wessex) Division was given the task of opening 'Club Route' for XXX Corps. The division was divided into five battle groups for the first 25 miles (40 km) drive, incorporating units of 8th Armoured Brigade. The advance began on 30 March: German rearguards were either overcome or bypassed, and the Twente Canal was crossed, with troops of 129th Infantry Bde and 8th Armoured Bde liberating Lochem on 1–2 April. The pursuit continued through April and ended with the capture of Bremen and XXX Corps' drive into the Cuxhaven peninsula. Hostilities ended on 5 May after the German surrender at Lüneburg Heath.After a period as occupation forces in XXX Corps' district, 43rd (Wessex) Division's HQ and TA units were demobilised at the war's end. Throughout the North West Europe Campaign the 43rd (Wessex) Division, like so many other Allied divisions that fought from Normandy to Germany, had suffered very heavy casualties with the majority of them, 80% in some units, being suffered by the average Tommy in the infantry battalions. From June 1944 to May 1945 the 43rd (Wessex) Division, or the Yellow Devils or British SS Division as known by the Germans, had suffered well over 12,500 casualties, with almost 3,000 killed in action.
43rd (Wessex) Infantry Division Order of Battle 1939–1945128th Infantry Brigade (left 6 June 1942)
1/4th Battalion, Hampshire Regiment
2/4th Battalion, Hampshire Regiment
5th Battalion, Hampshire Regiment
128th Infantry Brigade Anti-Tank Company (formed 19 June 1940, disbanded 20 December 1941)129th Infantry Brigade
4th Battalion, Somerset Light Infantry
4th Battalion, Wiltshire Regiment
5th Battalion, Wiltshire Regiment
129th Infantry Brigade Anti-Tank Company (formed 14 May 1940, disbanded 20 December 1941)130th Infantry Brigade
7th Battalion, Hampshire Regiment
4th Battalion, Dorsetshire Regiment
5th Battalion, Dorsetshire Regiment
130th Infantry Brigade Anti-Tank Company (formed 17 May 1940, disbanded 20 December 1941)25th Tank Brigade (from 1 June 1942, left 2 September 1942)
51st (Leeds Rifles) Royal Tank Regiment
11th Royal Tank Regiment
142nd Regiment Royal Armoured Corps34th Tank Brigade (from 3 September 1942, left 10 September 1943)
North Irish Horse (left 3 September 1942)
147th Regiment Royal Armoured Corps
153rd Regiment Royal Armoured Corps
151st Regiment Royal Armoured Corps (from 3 September 1942)214th Infantry Brigade (from 5 September 1943)
7th Battalion, Somerset Light Infantry
5th Battalion, Duke of Cornwall's Light Infantry
9th Battalion, Somerset Light Infantry (left 30 September 1943)
1st Battalion, Worcestershire Regiment (from 30 September 1943)Divisional Troops
1/8th Battalion, Middlesex Regiment (joined as Machine Gun Battalion from 18 November 1941, redesignated 8th Battalion May 1942, left 1 October 1942, rejoined as Support Battalion 1 October 1943, again as MG Battalion 28 February 1944)
48th Battalion, Reconnaissance Corps (converted from 5th Battalion, Gloucestershire Regiment 20 November 1941, redesignated 43rd Battalion 1 January 1942, later 43rd Regiment 6 June 1942, finally 43rd (Wessex) Reconnaissance Regiment (The Gloucestershire Regiment), Royal Armoured Corps 1 January 1944)
94th (Queen's Own Dorset Yeomanry) Field Regiment, Royal Artillery
112th (Wessex) Field Regiment, Royal Artillery
141st (Queen's Own Dorset Yeomanry) Field Regiment, Royal Artillery (left 8 June 1942)
179th Field Regiment, Royal Artillery (from 9 June 1942)
59th (Duke of Connaught's Own) Anti-Tank Regiment, Royal Artillery
110th Light Anti-Aircraft Regiment, Royal Artillery (converted from 7th Battalion, Dorsetshire Regiment, joined 23 March 1941)
43rd (Wessex) Divisional Engineers204th (Wessex) Field Company, Royal Engineers
260th Field Company, Royal Engineers
553rd Field Company, Royal Engineers (from 13 January 1940)
207th (Wessex) Field Park Company, Royal Engineers
13th Bridging Platoon, Royal Engineers (from 1 October 1943)
43rd (Wessex) Divisional Signals, Royal Corps of Signals
Royal Army Service Corps
54, 504, 505, 506 Companies
Royal Army Medical Corps
129, 130, 213 Field Ambulances
14, 15, 38 Field Dressing Stations
38 Field Hygiene Section
Royal Army Ordnance Corps
43 Ordnance Field Park
306 Mobile Laundry and Bath Unit
Royal Electrical and Mechanical Engineers
129, 130, 214 Infantry Brigade Workshops
43 Wessex Division Provost Company, Royal Military Police
57 Field Security Section
Postal Unit
Postwar
The TA was reconstituted from 1 January 1947 and its units and formations including 43rd (Wessex) Infantry Division were reformed. However, the TA saw large numbers of amalgamations from 1950 onwards. In 1961 the division became a district headquarters as 43rd (Wessex) Division/District, and it was disbanded on the reduction of the TA into the Territorial and Army Volunteer Reserve on 1 April 1967, when many individual TA units lost their identities. The district headquarters itself formed the core of the structure for the creation of South West District under HQ UK Land Forces in 1972.
43rd (Wessex) Infantry Division Order of Battle 1947128 Infantry Brigade
4th Battalion, Royal Hampshire Regiment at Winchester
4th Battalion, Oxfordshire and Buckinghamshire Light Infantry at Oxford
4th/6th Battalion, Royal Berkshire Regiment at Reading129 Infantry Brigade
4th Battalion, Somerset Light Infantry at Bath
5th Battalion, Gloucestershire Regiment at Gloucester
4th Battalion, Wiltshire Regiment at Trowbridge130 (West Country) Infantry Brigade
4th Battalion, Devonshire Regiment at Exeter
5th (Prince of Wales's) Battalion, Devonshire Regiment at Plymouth
4th/5th Battalion, Duke of Cornwall's Light Infantry at Truro
4th Battalion, Dorsetshire Regiment at DorchesterRoyal Armoured Corps
Royal Wiltshire Yeomanry at SwindonRoyal Artillery
294 (Queen's Own Dorset Yeomanry) Field Regiment at Sherborne
296 (Royal Devon Yeomanry) Field Regiment at Exeter
387 (Queen's Own Oxfordshire Hussars) Field Regiment at Oxford
383 (Duke of Connaught's Royal Hampshire) Anti-Tank Regiment at Portsmouth
396 (Devon) Light Anti-Aircraft Regiment at Devonport
883 Locating Battery at BristolRoyal Engineers
110 Field Engineer Regiment204 Field Squadron
226 Field Squadron
260 Field Squadron
207 Field Park SquadronRoyal Corps of Signals
43rd (Wessex) Infantry Division Signal Regiment at Taunton 1 Squadron at Exeter
2 Squadron at Taunton
3 Squadron at Torquay, later BristolRoyal Army Service Corps
43 (Wessex) Infantry Divisional Column at Bristol504 Company at Swindon
505 Company at Didcot
506 Company at Plymouth
1567 Company at Plymouth
43 Ordnance Field Park, Royal Army Ordnance Corps
43 Divisional Royal Electrical and Mechanical Engineers
43 Divisional Royal Army Medical Corps
Commanders
The following officers commanded the division at various times:
Insignia
The banner of the kings of Wessex bore a golden Wyvern, a dragon with two eagle-like legs and the barbed tail of a snake. The 43rd (Wessex) Division adopted the golden wyvern on a blue square as its formation sign in 1935.
Memorials
The Hill 112 memorial was erected by the divisional engineers and later taken over by the Commonwealth War Graves Commission with an endowment from the Memorial Fund. The first memorial in England was at Castle Hill, Mere, in Wiltshire, acquired on a 199-year lease from the Duchy of Cornwall and entrusted to the Parish Council of Mere. Next the fund acquired Wynyard's Gap near Crewkerne, Somerset. Finally, Sir Richard Onslow (formerly of the Duke of Cornwall's Light Infantry) presented Rough Tor on Bodmin Moor to the National Trust as a memorial. The Roll of Honour is in the War Memorial Chapel in Salisbury Cathedral.A memorial stone stands at the end of a lane named 'Somerset' in Lochem, Netherlands, showing the Wessex Wyvern and listing 4th Bn Somerset Light Infantry, 4th Bn Wiltshire Regiment and units of 8th Armoured Bde who liberated Lochem on 1–2 April 1945. The horizontal inscription reads 'All the way from Normandy'.
See also
List of British divisions in World War I
List of British divisions in World War II
British Army Order of Battle (September 1939)
Notes
References
Bibliography
External links
Mark Conrad, The British Army, 1914 (archive site)
British Army units from 1945 on
Divisional insignia
The Long, Long Trail
Orders of Battle at Patriot Files
Graham Watson, The Territorial Army 1947
World War II Armed Forces
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The 43rd (Wessex) Infantry Division was an infantry division of Britain's Territorial Army (TA). The division was first formed in 1908, as the Wessex Division. During the First World War, it was broken-up and never served as a complete formation. It was reformed in the TA in 1920, and then served in the campaign in North West Europe from June 1944 until May 1945, during the Second World War. The division suffered heavy casualties and gained an excellent reputation. After the Second World War, the division formed part of the postwar TA, and became the 43rd (Wessex) Division/District in 1961. It was finally disbanded in 1967.
Formation
The Territorial Force (TF) was formed on 1 April 1908 following the enactment of the Territorial and Reserve Forces Act 1907 (7 Edw.7, c.9) which combined and re-organised the old Volunteer Force, the Honourable Artillery Company and the Yeomanry. On formation, the TF contained 14 infantry divisions and 14 mounted yeomanry brigades. One of the divisions was the Wessex Division.The Wessex Division was formed in Southern Command from TF units in the south-western counties of Cornwall, Devon, Dorset, Hampshire, Somerset and Wiltshire. In peacetime, the divisional headquarters was at 19 Cathedral Close in Exeter.
Wessex Division Order of Battle 1908–1914Divisional HQ at Exeter
Hampshire Brigade at Southampton
4th Battalion, Hampshire Regiment at Winchester (joined 12th Indian Division and served in Mesopotamia)
5th Battalion, Hampshire Regiment at Southampton (served in Third Afghan War)
6th (Duke of Connaught's Own) Battalion, Hampshire Regiment at Portsmouth (joined 15th Indian Division and served in Mesopotamia)
7th Battalion, Hampshire Regiment at Bournemouth (served in Aden)South-Western Brigade at Taunton
4th Battalion, Somerset Light Infantry at Bath (joined 37th Indian Brigade and served in Mesopotamia)
5th Battalion, Somerset Light Infantry at Taunton (joined 75th Division and served in Palestine)
4th Battalion, Dorsetshire Regiment at Dorchester (joined 42nd Indian Brigade and served in Mesopotamia)
4th Battalion, Wiltshire Regiment at Trowbridge (joined 75th Division and served in Palestine)Devon & Cornwall Brigade at Exeter
4th Battalion, Devonshire Regiment at Exeter (joined 41st Indian Brigade and served in Mesopotamia)
5th (Prince of Wales's) Battalion, Devonshire Regiment at Plymouth (joined 75th Division and served in Palestine)
6th Battalion, Devonshire Regiment at Barnstaple (joined 36th Indian Brigade and served in Mesopotamia)
4th Battalion, Duke of Cornwall's Light Infantry at Truro (served in Aden, later with 75th Division in Palestine)Divisional Royal Artillery
I Wessex Brigade, Royal Field Artillery at Portsmouth (joined 3rd (Lahore) Division and served in Mesopotamia)
1st Hampshire Battery
2nd Hampshire Battery
3rd Hampshire Battery
1st Wessex Ammunition Column
II Wessex (Howitzer) Brigade, Royal Field Artillery at Ryde, Isle of Wight
4th Hampshire (Howitzer) Battery (served in Aden)
5th Hampshire (Howitzer) Battery (joined 6th (Poona) Division and served in Mesopotamia; captured at Kut)]
2nd Wessex Ammunition Column
III Wessex Brigade, Royal Field Artillery at Swindon (served in Third Afghan War)
6th Hampshire Battery
Dorsetshire Battery
Wiltshire Battery
3rd Wessex Ammunition Column
IV Wessex Brigade, Royal Field Artillery at Exeter
1st Devonshire Battery
2nd Devonshire Battery
3rd Devonshire Battery (served in Third Afghan War)
4th Wessex Ammunition Column
Wessex (Hampshire) Heavy Battery, Royal Garrison Artillery and Ammunition Column at Cosham (served on the Western Front)Wessex Divisional Engineers (joined 27th Division and served at Salonika)
1st Wessex Field Company at Bath (became 500th Field Company)
2nd Wessex Field Company at Weston-super-Mare (became 501st Field Company)
Wessex Divisional Telegraph Company ('Signal Company' from 1910) at ExeterDivisional Royal Army Medical Corps (joined 8th Division and served on the Western Front)
1st Wessex Field Ambulance at Exeter (became 24th Field Ambulance)
2nd Wessex Field Ambulance at Plymouth (became 25th Field Ambulance)
3rd Wessex Field Ambulance at Portsmouth (became 26th Field Ambulance)
Wessex Clearing Hospital at ExeterWessex Divisional Transport & Supply Column, Army Service Corps, at Exeter (joined 29th Division and served at Gallipoli)
Divisional Company at Andover (became 246 Company)
Devonshire and Cornwall Company at Plymouth (became 247 Company)
South Western Brigade Company at Bridgwater (became 248 Company)
Hampshire Brigade Company at Aldershot (became 249 Company)
First World War
On 29 July 1914, the Wessex Division was on Salisbury Plain carrying out its annual training camp when 'precautionary orders' were received, and next day the division took up emergency war stations in Somerset, Devon and Cornwall. The order to mobilise arrived on the evening of 4 August. Between 10 and 13 August the division concentrated on Salisbury Plain and began war training.On 24 September, at the special request of the Secretary of State for War, Earl Kitchener of Khartoum the Wessex Division accepted liability for service in British India to relieve the Regular Army units there for service on the Western Front. The division's infantry battalions (without their brigade headquarters) and artillery brigades embarked at Southampton on 8 October and were convoyed to Bombay, disembarking on 9 November. The engineers, medical units, transport, heavy battery and brigade ammunition columns also remained in the UK and joined formations composed of Regular units brought back from India and other imperial garrisons. Meanwhile, the battalions and batteries were immediately distributed to garrisons across India, reverting to peacetime service conditions, and the Wessex Division never saw service as a whole, though it was formally numbered the 43rd (1st Wessex) Division in 1915 and the brigades were designated 128th (Hampshire) Brigade, 129th (South Western) Brigade and 130th (Devon and Cornwall) Brigade.As soon as the Wessex Division had left for India, the home depots began raising 2nd Line units, distinguished from the 1st Line by a '2/' prefix. Recruitment and training of the 2nd Wessex Division proceeded so well that it was also sent to India in December 1914, and later received the notional title of 45th (2nd Wessex) Division.By early 1915 the need was growing for troops to be sent to various theatres of war, and the first drafts and formed units from the 1st Wessex Division began to go on active service, particularly to the Mesopotamian Front. By the end of the war only one battalion and five batteries remained in India, and most of these then participated in the Third Anglo-Afghan War.
Second World War
Mobilisation and training
43rd (Wessex) Division was reformed in 1920 and became part of the Territorial Army, which replaced the TF. In the period of international tension preceding the outbreak of the Second World War, the existing territorial divisions (known as the first-line) helped form new formations, known as the second-line. This process was known as duplicating. The division's duplicate was the 45th Infantry Division.
The TA was mobilised on the outbreak of war in September 1939 and the division began training in its home area. In May 1940 it was preparing to go overseas to join the British Expeditionary Force (BEF) in France, but the German invasion of the Low Countries on 10 May ended the 'Phoney War' before the division was ready. When the Battle of France was lost and the BEF was being evacuated from Dunkirk, 43rd (W) Division was one of the few reasonably well-equipped formations left in Home Forces to counter a German invasion of the United Kingdom. It formed part of the mobile GHQ Reserve disposed on the line from Northampton through North London to Aldershot, from which brigade groups could be despatched to any threatened area. During the period when invasion was most threatened, the division was stationed just north of London.By the end of 1940 the division was stationed under XII Corps in East Kent, where it remained for the next four years, first in defensive mode, later training intensively. It was later noted that its habitual training area round Stone Street, outside Folkestone, bore a marked resemblance to the Bocage countryside in Normandy where it would later fight.
In 1942, however, after the German invasion of the Soviet Union and the entrance of the United States into the war, the situation changed and the 43rd Division started training for offensive operations to return to mainland Europe. Throughout most of 1942, the division was part of XII Corps, serving alongside the 46th Infantry Division and 53rd (Welsh) Infantry Division. XII Corps was, at the time, commanded by Lieutenant-General Bernard Montgomery.In March 1942, the division also gained a new General Officer Commanding (GOC) in the form of Major-General Ivor Thomas. Thomas was a decorated officer who had served as a young battery commander in the Royal Artillery on the Western Front during the First World War where he was twice wounded and awarded the Military Cross and the Distinguished Service Order. He would command the 43rd Division until September 1945. Thomas was an effective but hard-driving commander, humourless and not universally liked, sometimes known as 'Butcher', or more jocularly by Lt-Gen Brian Horrocks and others as 'Von Thoma', after the German Lt-Gen Wilhelm Ritter von Thoma captured after the Battle of Alamein. (Horrocks also jokingly referred to Thomas's command as the 'Wicked Wyvern'). Critics of his training methods regarded 43rd (Wessex) Division as 'the most over-exercised in the Army'.
In June 1942, the 128th Infantry Brigade (consisting of three battalions of the Hampshire Regiment) was transferred to 46th Infantry Division. It was replaced first by 25th and later 34th Army Tank Brigade as part of an experiment with 'Mixed Divisions'. However the experiment was abandoned (deemed unsuitable for the type of terrain in North-western Europe) in late 1943 and the 34th Tank Brigade was replaced, in October 1943, by the 214th Independent Infantry Brigade, a Home Defence formation raised during the war that had been serving in Hampshire and Dorset District. After service in the Isle of Wight, 214th Brigade had received specialised training in combined operations under the Royal Marines at Inverary, and retained an individuality within the division. 214th Brigade would remain with the 43rd Division for the rest of the war.
Operation Overlord
XII Corps and 43rd (Wessex) Division were assigned to 21st Army Group for the Allied invasion of Normandy (Operation Overlord). They were follow-up formations, with 43rd (Wessex) Division scheduled to complete its landings 14 days after D Day (D +14, 20 June). However, shipping delays and a storm between 19 and 22 June delayed its arrival; the division finally concentrated round Bayeux on 24 June.HQ, A and C Squadrons of 43rd (Wessex) Reconnaissance Regiment were aboard the troopship Derrycunihy, which arrived off Sword Beach on the evening of 20 June. High seas and enemy shelling prevented unloading for three days and it was decided to move to Juno Beach for disembarkation. As the ship started engines it detonated an acoustic mine, splitting the ship in two, and the after part, packed with sleeping men of 43rd Recce Regiment, sank rapidly. Worse still, an ammunition lorry caught fire, and oil floating on the water was set alight. Landing craft and gunboats came alongside and picked up survivors, but the regiment lost 183 men, with another 120 evacuated wounded. Most of 43rd Recce Rgts's vehicles were landed from the beached fore part of the "Derrycunihy", and reinforcements were sent from England, but the regiment was not fully up to strength until the end of July 1944.
Operation Epsom
The division's first action, Operation Epsom starting on 26 June, involved following 15th (Scottish) Division's advance and then securing the captured objectives. However, this entailed some heavy fighting by 5th Battalion Duke of Cornwall's Light Infantry (DCLI) against a Panzer counter-attack at Cheux on 27 June. The supporting 17-pounder anti-tank guns were knocked out and the infantry had to stalk Panther tanks with their lighter 6-pounder anti-tank guns and hand-held PIATs. Other battalions mopped up the important objective of Manvieux. On 28 June 1st Battalion Worcestershire Regiment made an attack from Cheux against Mouen: they had to cross open cornfields, but had support from the whole divisional artillery and heavy mortars plus two medium artillery regiments. The infantry followed the Creeping barrage of smoke and High explosive shells and forced their way into the houses and gardens, using PIATs against those German tanks that had survived the barrage. On 29 June 129 Brigade advanced under fire to ford the River Odon and dug in, a German counter-attack against them in the evening being destroyed by the divisional artillery.
Hill 112
The division's first major offensive action of its own was Operation Jupiter, to take Hill 112, which had been briefly captured by British armour during 'Epsom' but had to be abandoned. The attack on 10 July was supported by all the divisional artillery and mortars, plus the artillery of 15th (Scottish) Division and 11th Armoured Division and 3rd and 8th Army Groups Royal Artillery (AGRAs). In the first phase 129th Brigade on the right, with all three battalions in line, and 130th Brigade on the left with one battalion, were to capture the hill and the road from it to Château de Fontaine. They were supported by Churchill tanks from 31st Tank Brigade. Then, while 129th Brigade formed a secure south-west flank, 130th Brigade and Churchill Crocodile flamethrowing tanks from 79th Armoured Division were to advance from Château de Fontaine to capture Eterville and Maltot and the high ground to the south-east. Finally, 214th Brigade in Kangaroo armoured personnel carriers accompanied by 4th Armoured Brigade was supposed to break through to the River Orne and seize bridgeheads.The massive barrage stunned but failed to suppress the defenders from 10th SS Panzer Division. When the Wessex infantry went forward they came under heavy fire and had to clear defenders from the dugouts and defensive positions of their outpost line on the forward slopes. 5th Battalion Dorsets and 9th Royal Tank Regiment, leading 130th Brigade against the farms on the lower ground, made quick progress, 7th Somerset Light Infantry passing through with the Churchills and Crocodiles to deal with Chateau de Fontaine. But 129th Brigade was slowed in its advance on Hill 112 itself, suffering heavy casualties on the open slopes, and then running into the recently-arrived Tiger I tanks of 102nd SS Heavy Panzer Battalion, which the Churchills and corps anti-tank guns of 86th (Devon) Anti-Tank Regiment, Royal Artillery, struggled to deal with. By mid-morning 129th Brigade only had a slender toehold on the edge of the plateau. Attempting to continue 130th Brigade's advance on Maltot, 7th Hampshires and 9th RTR came under crossfire from Hill 112, while some of the Tigers reached the village first. The leading Hampshire penetrated the village, leaving strongpoints to be mopped up later by the following Dorsets, but they were driven out by counter-attacks. 4th Dorsets, making a second attack, suffered heavy casualties. Two battalions of 214th Brigade had already been drawn into the fighting around Chateau de Fontaine, leaving 5th DCLI as the last uncommitted battalion. It attacked up the slopes of Hill 112, described as 'one of the most tragic acts of self-sacrifice in the entire North West European Campaign'. Launched at 20.30 towards 'The Orchard' on the crest of the hill, and supported by a squadron of 7th Royal Tank Regiment and all available guns, including the divisional light anti-aircraft guns, the attack reached the orchard, but could get no further. The infantry and anti-tank guns held off counter-attacks through the night from the newly-arrived 9th SS Panzer Division, and were reinforced in the morning by a company of 1st Worcesters and briefly by a squadron of Sherman tanks from the Royal Scots Greys. By mid-afternoon all the anti-tank guns on the hill had been knocked out, the tanks had to retire to the reverse slope, and the defence was almost over. The order was given to withdraw and 60 survivors of 5th DCLI were brought down. Both sides remained dug in on the slopes, with the hilltop left in No man's land. The division had to hold its positions under mortar fire for another 14 days, described by the commander of 214th Brigade as comparable only 'to the bombardment at Passchendaele'. This defence was followed by a final set-piece attack, Operation Express, in which 4th and 5th Wiltshires and 7th RTR succeeded in capturing Maltot on 22 July.
Overall, 43rd (Wessex) Division performed well in Normandy and was considered by many senior British officers to be one of the best divisions of the British Army during the war. For the rest of the war Bernard Montgomery, commanding all British and Canadian troops in the campaign, preferred to use formations such as 43rd (Wessex) and 15th (Scottish) to spearhead his assaults. This was mainly due to issues of morale because veteran formations such as the 7th Armoured and 51st (Highland), both of which had seen extensive service in North Africa and Italy (and fought poorly in Normandy, according to senior officers), were judged as tired and war-weary with morale being almost dangerously fragile. With formations that had spent years in the United Kingdom training such as the 43rd (Wessex), 15th (Scottish), 11th Armoured and 59th (Staffordshire) Divisions the problem of morale was less of an issue.
Mont Pinçon
After a short rest 43rd (Wessex) Division moved to XXX Corps to launch an attack towards the dominating height of Mont Pinçon as part of Operation Bluecoat. 8th Armoured Brigade was assigned to support the infantry. Starting at 08.00 on 30 July, the division was to force its way through enemy positions at Briquessard and advance through Cahagnes towards Ondefontaine. 130th Brigade led, reinforced by 4th Somerset Light Infantry and Sherman tanks of the Sherwood Rangers Yeomanry, followed by 214th Brigade and then 129th Brigade. Initial casualties were heavy, particularly from mines, and the advance achieved only 1,000 yards (910 m) on the first day. It took until the following morning to clear the mines and restart the advance with 214th Brigade and the tanks of 4th/7th Dragoon Guards. At 17.30 the brigade broke through, and 1st Worcesters riding on the tanks got beyond Cahagnes by nightfall. 7th Somerset Light Infantry cleared the village in the dark and, with the aid of the divisional artillery, fought off a counter-attack accompanied by heavy armour (probably Jagdpanthers) that had to be stalked with PIATs.The division fought its way forward during 1 August, then at 02.00 on 2 August 129th Brigade began its advance on Ondefontaine. It was a day of slow but steady progress against rifle and machine gun fire from commanding positions on the ridge in front, followed by another pre-dawn attack towards Ondefontaine, while 214th Brigade began working its way towards Mont Pinçon. 5th DCLI and B Squadron 4th/7th DG, supported by the divisional artillery and mortars, reached the top of the ridge and engaged enemy infantry and armour, while 1st Worcesters worked round the flank and took the crest. 43rd Recce Regiment (reformed after the Derrycunihy disaster) then went through to unhinge the Ondefontaine defences. The division was now facing east, with Mont Pinçon only 4 miles (6.4 km) away.
At 08.00 on 5 August, 4th Wiltshires moved out with B Squadron 13th/18th Royal Hussars, picking their way through the narrow lanes, while A Sqn took a parallel route carrying 5th Wiltshires. 4th Wiltshires found a bridge blown and went ahead without their tanks towards the strongly-held village of St Jean-le-Blanc, breaking up a counter-attack by calling down artillery fire. About 16.00 the battalion pioneers managed to bridge the stream and a Troop of B Sqn crossed, but withdrew to 'harbour' at dusk. Meanwhile, 5th Wiltshires got to the bridge over the Druance at the foot of Mont Pinçon but failed to capture it by the end of the day. Generals Ivor Thomas and Brian Horrocks (who had just taken command of XXX Corps) were anxious to push on, and had already cancelled Operation Blackwater, designed to reach the River Noireau, because it was too risky with Mont Pinçon still in enemy hands.A new attack was planned for 6 August, with 130th Brigade making a feint to the north, while 129th Brigade continued from the west. In the end, the dominating position fell to a surprise attack. 4th Somerset Light Infantry and the reduced 5th Wiltshires fought their way forward through sweltering weather all day. 5th Wiltshires secured the crossroads at La Variniere and 4th Wiltshires was due to pass through them, when at about 18.00 A Sqn 13th/18th Hussars managed to get two Troops up a steep track to the top of the hill. By 18.30, seven Shermans were on the summit, attempting to mount an all-round defence and calling for infantry support. A staff officer ran up to Lt-Gen Horrocks at XXX Corps HQ, shouting 'We've got it, sir!' As fog descended on the hill, the 4th Wiltshires and the rest of A and B Sqns of the Hussars picked their way up the almost undefended track, followed by 4th Somerset LI. By daybreak the summit was firmly held, despite heavy German bombardment, and 5th Wiltshires and C Sqn still held the crossroads below. 214th Brigade relieved the exhausted troops that morning.Having taken and then defended Mont Pinçon, 43rd (Wessex) Division participated in XXX Corps' advance. It crossed the Noireau on 15 August by a broken railway bridge and by wading, whereupon 204 Field Company RE set to work with a waterproofed bulldozer to build a tank ford and a trestle bridge named 'Genesis'. 553 Field Company and 207 Field Park Company then built the division's first Bailey bridge across the site of the railway bridge. The main opposition came from mortars and booby-trapped mines. Next morning 43rd Recce and the Sherwood Foresters were ready to continue the pursuit of the broken enemy, who were soon caught in the Falaise pocket.
Vernon Bridge
The breakout achieved, XXX Corps drove flat out for the River Seine (Operation Loopy), with 43rd (W) Division sent ahead to make an assault crossing at Vernon. For this operation it was assisted by the bridging specialists of 15th (Kent) GHQ Troops Royal Engineers, a medium artillery regiment and the Cromwell tanks of 15th/19th The King's Royal Hussars, the armoured reconnaissance regiment of 11th Armoured Division. US troops had already reached the west bank of the Seine, so the convoys of assault troops and bridging material moving eastwards had to be carefully coordinated to cross with US convoys repositioning to the south. The first convoy, Group One, consisted of nearly 1500 vehicles of 129th Brigade with its usual proportion of divisional artillery, engineers and support services, reinforced by 1st Worcesters. Some of the assault infantry rode in the DUKW amphibious trucks that were to carry them over the river. The group arrived at Vernon on the afternoon of 25 August, ready to begin the assault that evening against the defenders from 49th German Infantry Division.15th (Kent) GHQTRE was tasked with manning the DUKWs during the initial assault and then operating rafts until the first bridge could be laid. They also had storm boats in reserve but these had to be used in the first wave because launching points for DUKWs were hard to find. A 15-minute bombardment by the guns of 94th (Dorset Yeomanry) Field Regiment, 121st (West Riding) Medium Regiment (further back in Group Two) and C Sqn, 15th/19th Hussars, together with the heavy mortars of 8th Middlesex, was followed by a smoke barrage to cover the crossing at 19.00. On the right, 5th Wiltshires began crossing in eight storm boats manned by 15th (Kent) GHQTRE, but they grounded before reaching the far side, and were raked by machine gun fire. By the end of an hour only one boat remained. Only about a company had got across, and they were overrun during the night. Three of the four available DUKWs also grounded, the survivor ferrying across the rest of 5th Wiltshires in the dark. On the left, 4th Somerset LI got across in the storm boats relatively easily, but found that their bridgehead was on an island, and they were still cut off from the east bank, apart from a few men who scrambled over the wreckage of the railway bridge. 1st Worcesters failed to get over the broken road bridge into the village of Vernonnet, which was strongly held. In the dark 260th Field Company managed to bulldoze a slipway for the DUKWs, speeding up the crossing, and 129th Brigade got about a battalion and a half across in total, setting up a perimeter along the escarpment above the bridging site.The Wessex field companies now began work under fire on a Class 9 (9 tonne maximum load) Folding Boat Equipment (FBE) bridge while the infantry fought to expand the bridgehead and clear Vernonnet. The Worcesters got over the broken bridge, and light rafts began to get 6-pounder anti-tank guns and armoured cars of the recce regiment across, but work on the bridge was halted by heavy fire until 5th DCLI and 7th Somerset LI from newly-arrived 214th Brigade struggled across the broken road bridge into Vernonnet. By nightfall the bridgehead was reasonably secure, the FBE bridge named 'David' was complete and 15th (Kent) GHQTRE's rafting troops were arriving to get a tank ferry into operation before morning. 7th Army Troops Royal Engineers had also arrived to begin a Class 40 Bailey Bridge.Next morning (27 August) a squadron each of 15th/19th Hussars' Cromwells and 4th/7th DGs' Shermans were rafted across and held off an armoured counter-attack, the infantry and 43rd Recce cleared the banks and pushed through the forest until they were firmly established on the heights. By 28 August, 7th ATRE working under shellfire had built their Class 40 bridge, codenamed 'Goliath', and 11th Armoured was beginning to pour across to spearhead XXX Corps' advance. A second Class 40 named 'Saul' was built by 15th (Kent) GHQRE. After the Seine crossing, 43rd (Wessex) Division was 'grounded' while the rest of XXX Corps raced across northern France and Belgium. The division rested and received reinforcements (many of them experienced men drafted from the disbanded 59th (Staffordshire) Division).
Market Garden
When 43rd (Wessex) Division next moved, the war was now 250 miles (400 km) away. The first elements moved up to Brussels to protect headquarters and carry out engineering works, then the division concentrated at Diest to take part in Operation Market Garden, beginning on 17 September. In 'Garden', the ground part of the operation, XXX Corps was to link river crossings up to the Nederrijn at Arnhem via a 'carpet' of airborne troops. 43rd (Wessex) Division accompanied by 8th Armoured Bde was to follow Guards Armoured Division, carrying out assault crossings if any of the bridges were found to be destroyed, and guarding the 'corridor' to Arnhem. The advance up the only road ('Club Route') was slow but on 21 September 43rd (Wessex) Division caught up with the Guards at Nijmegen. Further progress was blocked by strong German forces, and 1st Airborne Division holding out at Arnhem was in a desperate plight. 43rd (Wessex) Division was ordered to pass through the Guards the following morning and make an all-out effort to reach the Nederrijn by a side road. The Germans were found to be dug in at Oosterhout and the countryside was so boggy that it was impossible to move vehicles off the road, making outflanking moves too slow. Despite the shortage of artillery ammunition coming up the precarious line of communication, the whole of the divisional artillery and heavy mortars were used, but it was evening before the division got through. 5th DCLI, supported by a squadron of 4th/7th DG, was ordered to make a dash over the last 10 miles (16 km) to get in touch with the Polish Parachute Brigade at Driel on the south bank of the Nederrijn. The journey took only 30 minutes, but the road behind the column was cut by German tanks that had to be hunted down and destroyed before support could be brought up. Attempts to launch DUKWs with supplies for 1st Airborne were unsuccessful.The whole of 23 September was taken up with getting support through to 5th DCLI and the Poles and in clearing the main road, though 43rd Recce Rgt was able to exploit westwards. During the night 5th Dorsets and the divisional engineers ferried a few hundred Poles across the Nederrijn in assault boats to reinforce 1st Airborne Division's shrinking perimeter. 4th Dorsets and the engineers made another assault crossing on the night of 24/25 September, suffering heavy casualties and getting few supplies across. By now 1st Airborne had been effectively destroyed, and the only course now was to evacuate the survivors. Their radios had been inoperable, and the only communication link had been through 64th (London) Medium Regiment, RA, attached to 43rd (Wessex) Division. Through this link the code word for the evacuation was passed, and during the night of 25/26 September a feint attack was made by 5th Wiltshires while around 2300 survivors of 1st Airborne and the Poles were ferried back to the south bank; few of 4th Dorsets made it back.The division was blamed by many airborne soldiers for its dilatory advance to the river, though the Corps commander, Lt-Gen Horrocks, defended the division, pointing out that it could not deploy any armoured vehicles (either 8th Armoured Bde or 43rd Recce Rgt's armoured cars and half-tracks) off the single road, nicknamed 'Hell's Highway', which was cut behind them on several occasions, and praising the division's hard fighting. Nevertheless, Maj-Gen Thomas replaced the commanding officer of 43rd Recce immediately after the battle.In the aftermath of Market Garden, 43rd (Wessex) Division was stationed on 'the Island' (between the Rivers Waal and Nederrijn). 43rd Recce Rgt, with 12th Battalion King's Royal Rifle Corps from 8th Armoured Bde under command, protected the division's open western flank. The concealed squadrons sent back reports, but were forbidden to engage the enemy in order to hide the extent of the position. However, on the night of 26/27 September a furious firefight broke out when the Germans crossed the river in strength and attempted to emplace anti-tank guns in 43rd Recce's hidden positions.The Germans launched a serious counter-attack from the east on 1 October, attacking 129th Bde strung out guarding the road from Nijmegen to the Nederrijn. 4th Somerset LI and 5th Wiltshires fought them off at Elst for 48 hours, the divisional artillery breaking up some of the attacks, and RAF medium bombers following up. Further north, 5th Dorsets beat off 116th Panzer Division and 7th Hampshires had to dislodge enemy troops who fortified themselves in some brick kilns, with the help of RAF Typhoons. On 5 October 43rd (Wessex) handed most of its positions over to the US 101st Airborne Division, leaving the anti-tank and mortar platoons and 5th DCLI, the divisional reserve, to help out. The attacks ended after one last attempt on 6 October. 43rd Wessex continued to hold the western part of the Island. The divisional historian records that "While the Division faced the monotony inseparable from static defence, the Reconnaissance Regiment fought a different type of war". This involved guarding the western end of the Island, cooperating with the Dutch Resistance and facilitating the escape across the river of British paratroops who had evaded capture.
Operation Clipper
43rd (Wessex) Division was then shifted east with XXX Corps to cooperate with the US Ninth Army by capturing the Geilenkirchen salient (Operation Clipper). XXX Corps had 43rd Wessex and 84th US Divisions under command for this attack, which entailed breaching the Siegfried Line defences and capturing a string of fortified villages. 84th US Division attacked on the morning of 18 November, supported by British specialist armour, and was through the line of pillboxes by midday. 214th Brigade then attacked on its left in the afternoon, led by 7th Somerset LI and tanks of 4th/7th DG, and took its first objective, the village of Neiderheide. But many of the tanks and most of the supply vehicles got bogged down while 1st Worcesters were threading their way through Gilrath to form up for the second phase towards Tripsrath. Without tanks, and the artillery having shifted to another target, 1st Worcesters struggled forward under shellfire and forced their way into the village at nightfall. The traffic jam of bogged vehicles disrupted the attacks by 5th Dorsets and 5th DCLI, but they got into Bauchem and Hocheide respectively, and patrols reached Geilenkirchen itself, which was surrounded. After driving off some counter-attacks by 15th Panzer Grenadier Division during the night, Geilenkirchen was captured after a stiff fight next day. But thereafter heavy rain turned the whole battlefield into mud while the infantry struggled to consolidate their positions under heavy shellfire from the Siegfried Line guns. One wood captured and grimly held first by 4th Dorsets and then 5th Dorsets for seven days became known as 'Dorset Wood'. On 22 November 5th DCLI suffered heavy casualties trying to take the high ground near Hoven to deny the enemy observation over the two Allied divisions. Overnight both sides shared the village of Hoven, before counter-attacks came in at dawn from 10th SS Panzer Division and 21st Panzer Division. Horrocks himself authorised the withdrawal of the DCLI before they were overwhelmed. Any further attempt to take Hoven was impossible due to the waterlogged state of the country, which then had to be defended in conditions resembling the worst of the Western Front in the First World War. Horrocks organised an ad hoc battalion from XXX Corps' service units to relieve Wessex infantry for rest. Planning was under way to renew the offensive when the Germans attacked in the Ardennes (the Battle of the Bulge) on 16 December.
Operation Blackcock
The division then later played a comparatively small part in the mainly American Battle of the Bulge, where it was placed on the River Meuse as a reserve. Once the German Ardennes Offensive had been halted, 43rd (Wessex) Division returned to the offensive in early 1945 in Operation Blackcock to reduce the Roer Triangle, though exploitation was prevented by bad weather.
Operation Veritable
The 43rd later played a large part in Operation Veritable attached to First Canadian Army, through the month-long fighting in the Reichswald to capture Kleve, roll up the Siegfried Line defences, cross the Goch escarpment and seize Xanten on the Rhine.
Across the Rhine
43rd (Wessex) Division was given a follow-up task in the assault crossing of the Rhine (Operation Plunder). Its leading brigade crossed the river on 25 March behind 51st (Highland) Division, which had carried the assault on the night of 23/24 March. It found itself in immediate combat, but had broken through by 29 March. During the subsequent pursuit, 43rd (Wessex) Division was given the task of opening 'Club Route' for XXX Corps. The division was divided into five battle groups for the first 25 miles (40 km) drive, incorporating units of 8th Armoured Brigade. The advance began on 30 March: German rearguards were either overcome or bypassed, and the Twente Canal was crossed, with troops of 129th Infantry Bde and 8th Armoured Bde liberating Lochem on 1–2 April. The pursuit continued through April and ended with the capture of Bremen and XXX Corps' drive into the Cuxhaven peninsula. Hostilities ended on 5 May after the German surrender at Lüneburg Heath.After a period as occupation forces in XXX Corps' district, 43rd (Wessex) Division's HQ and TA units were demobilised at the war's end. Throughout the North West Europe Campaign the 43rd (Wessex) Division, like so many other Allied divisions that fought from Normandy to Germany, had suffered very heavy casualties with the majority of them, 80% in some units, being suffered by the average Tommy in the infantry battalions. From June 1944 to May 1945 the 43rd (Wessex) Division, or the Yellow Devils or British SS Division as known by the Germans, had suffered well over 12,500 casualties, with almost 3,000 killed in action.
43rd (Wessex) Infantry Division Order of Battle 1939–1945128th Infantry Brigade (left 6 June 1942)
1/4th Battalion, Hampshire Regiment
2/4th Battalion, Hampshire Regiment
5th Battalion, Hampshire Regiment
128th Infantry Brigade Anti-Tank Company (formed 19 June 1940, disbanded 20 December 1941)129th Infantry Brigade
4th Battalion, Somerset Light Infantry
4th Battalion, Wiltshire Regiment
5th Battalion, Wiltshire Regiment
129th Infantry Brigade Anti-Tank Company (formed 14 May 1940, disbanded 20 December 1941)130th Infantry Brigade
7th Battalion, Hampshire Regiment
4th Battalion, Dorsetshire Regiment
5th Battalion, Dorsetshire Regiment
130th Infantry Brigade Anti-Tank Company (formed 17 May 1940, disbanded 20 December 1941)25th Tank Brigade (from 1 June 1942, left 2 September 1942)
51st (Leeds Rifles) Royal Tank Regiment
11th Royal Tank Regiment
142nd Regiment Royal Armoured Corps34th Tank Brigade (from 3 September 1942, left 10 September 1943)
North Irish Horse (left 3 September 1942)
147th Regiment Royal Armoured Corps
153rd Regiment Royal Armoured Corps
151st Regiment Royal Armoured Corps (from 3 September 1942)214th Infantry Brigade (from 5 September 1943)
7th Battalion, Somerset Light Infantry
5th Battalion, Duke of Cornwall's Light Infantry
9th Battalion, Somerset Light Infantry (left 30 September 1943)
1st Battalion, Worcestershire Regiment (from 30 September 1943)Divisional Troops
1/8th Battalion, Middlesex Regiment (joined as Machine Gun Battalion from 18 November 1941, redesignated 8th Battalion May 1942, left 1 October 1942, rejoined as Support Battalion 1 October 1943, again as MG Battalion 28 February 1944)
48th Battalion, Reconnaissance Corps (converted from 5th Battalion, Gloucestershire Regiment 20 November 1941, redesignated 43rd Battalion 1 January 1942, later 43rd Regiment 6 June 1942, finally 43rd (Wessex) Reconnaissance Regiment (The Gloucestershire Regiment), Royal Armoured Corps 1 January 1944)
94th (Queen's Own Dorset Yeomanry) Field Regiment, Royal Artillery
112th (Wessex) Field Regiment, Royal Artillery
141st (Queen's Own Dorset Yeomanry) Field Regiment, Royal Artillery (left 8 June 1942)
179th Field Regiment, Royal Artillery (from 9 June 1942)
59th (Duke of Connaught's Own) Anti-Tank Regiment, Royal Artillery
110th Light Anti-Aircraft Regiment, Royal Artillery (converted from 7th Battalion, Dorsetshire Regiment, joined 23 March 1941)
43rd (Wessex) Divisional Engineers204th (Wessex) Field Company, Royal Engineers
260th Field Company, Royal Engineers
553rd Field Company, Royal Engineers (from 13 January 1940)
207th (Wessex) Field Park Company, Royal Engineers
13th Bridging Platoon, Royal Engineers (from 1 October 1943)
43rd (Wessex) Divisional Signals, Royal Corps of Signals
Royal Army Service Corps
54, 504, 505, 506 Companies
Royal Army Medical Corps
129, 130, 213 Field Ambulances
14, 15, 38 Field Dressing Stations
38 Field Hygiene Section
Royal Army Ordnance Corps
43 Ordnance Field Park
306 Mobile Laundry and Bath Unit
Royal Electrical and Mechanical Engineers
129, 130, 214 Infantry Brigade Workshops
43 Wessex Division Provost Company, Royal Military Police
57 Field Security Section
Postal Unit
Postwar
The TA was reconstituted from 1 January 1947 and its units and formations including 43rd (Wessex) Infantry Division were reformed. However, the TA saw large numbers of amalgamations from 1950 onwards. In 1961 the division became a district headquarters as 43rd (Wessex) Division/District, and it was disbanded on the reduction of the TA into the Territorial and Army Volunteer Reserve on 1 April 1967, when many individual TA units lost their identities. The district headquarters itself formed the core of the structure for the creation of South West District under HQ UK Land Forces in 1972.
43rd (Wessex) Infantry Division Order of Battle 1947128 Infantry Brigade
4th Battalion, Royal Hampshire Regiment at Winchester
4th Battalion, Oxfordshire and Buckinghamshire Light Infantry at Oxford
4th/6th Battalion, Royal Berkshire Regiment at Reading129 Infantry Brigade
4th Battalion, Somerset Light Infantry at Bath
5th Battalion, Gloucestershire Regiment at Gloucester
4th Battalion, Wiltshire Regiment at Trowbridge130 (West Country) Infantry Brigade
4th Battalion, Devonshire Regiment at Exeter
5th (Prince of Wales's) Battalion, Devonshire Regiment at Plymouth
4th/5th Battalion, Duke of Cornwall's Light Infantry at Truro
4th Battalion, Dorsetshire Regiment at DorchesterRoyal Armoured Corps
Royal Wiltshire Yeomanry at SwindonRoyal Artillery
294 (Queen's Own Dorset Yeomanry) Field Regiment at Sherborne
296 (Royal Devon Yeomanry) Field Regiment at Exeter
387 (Queen's Own Oxfordshire Hussars) Field Regiment at Oxford
383 (Duke of Connaught's Royal Hampshire) Anti-Tank Regiment at Portsmouth
396 (Devon) Light Anti-Aircraft Regiment at Devonport
883 Locating Battery at BristolRoyal Engineers
110 Field Engineer Regiment204 Field Squadron
226 Field Squadron
260 Field Squadron
207 Field Park SquadronRoyal Corps of Signals
43rd (Wessex) Infantry Division Signal Regiment at Taunton 1 Squadron at Exeter
2 Squadron at Taunton
3 Squadron at Torquay, later BristolRoyal Army Service Corps
43 (Wessex) Infantry Divisional Column at Bristol504 Company at Swindon
505 Company at Didcot
506 Company at Plymouth
1567 Company at Plymouth
43 Ordnance Field Park, Royal Army Ordnance Corps
43 Divisional Royal Electrical and Mechanical Engineers
43 Divisional Royal Army Medical Corps
Commanders
The following officers commanded the division at various times:
Insignia
The banner of the kings of Wessex bore a golden Wyvern, a dragon with two eagle-like legs and the barbed tail of a snake. The 43rd (Wessex) Division adopted the golden wyvern on a blue square as its formation sign in 1935.
Memorials
The Hill 112 memorial was erected by the divisional engineers and later taken over by the Commonwealth War Graves Commission with an endowment from the Memorial Fund. The first memorial in England was at Castle Hill, Mere, in Wiltshire, acquired on a 199-year lease from the Duchy of Cornwall and entrusted to the Parish Council of Mere. Next the fund acquired Wynyard's Gap near Crewkerne, Somerset. Finally, Sir Richard Onslow (formerly of the Duke of Cornwall's Light Infantry) presented Rough Tor on Bodmin Moor to the National Trust as a memorial. The Roll of Honour is in the War Memorial Chapel in Salisbury Cathedral.A memorial stone stands at the end of a lane named 'Somerset' in Lochem, Netherlands, showing the Wessex Wyvern and listing 4th Bn Somerset Light Infantry, 4th Bn Wiltshire Regiment and units of 8th Armoured Bde who liberated Lochem on 1–2 April 1945. The horizontal inscription reads 'All the way from Normandy'.
See also
List of British divisions in World War I
List of British divisions in World War II
British Army Order of Battle (September 1939)
Notes
References
Bibliography
External links
Mark Conrad, The British Army, 1914 (archive site)
British Army units from 1945 on
Divisional insignia
The Long, Long Trail
Orders of Battle at Patriot Files
Graham Watson, The Territorial Army 1947
World War II Armed Forces
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The 43rd (Wessex) Infantry Division was an infantry division of Britain's Territorial Army (TA). The division was first formed in 1908, as the Wessex Division. During the First World War, it was broken-up and never served as a complete formation. It was reformed in the TA in 1920, and then served in the campaign in North West Europe from June 1944 until May 1945, during the Second World War. The division suffered heavy casualties and gained an excellent reputation. After the Second World War, the division formed part of the postwar TA, and became the 43rd (Wessex) Division/District in 1961. It was finally disbanded in 1967.
Formation
The Territorial Force (TF) was formed on 1 April 1908 following the enactment of the Territorial and Reserve Forces Act 1907 (7 Edw.7, c.9) which combined and re-organised the old Volunteer Force, the Honourable Artillery Company and the Yeomanry. On formation, the TF contained 14 infantry divisions and 14 mounted yeomanry brigades. One of the divisions was the Wessex Division.The Wessex Division was formed in Southern Command from TF units in the south-western counties of Cornwall, Devon, Dorset, Hampshire, Somerset and Wiltshire. In peacetime, the divisional headquarters was at 19 Cathedral Close in Exeter.
Wessex Division Order of Battle 1908–1914Divisional HQ at Exeter
Hampshire Brigade at Southampton
4th Battalion, Hampshire Regiment at Winchester (joined 12th Indian Division and served in Mesopotamia)
5th Battalion, Hampshire Regiment at Southampton (served in Third Afghan War)
6th (Duke of Connaught's Own) Battalion, Hampshire Regiment at Portsmouth (joined 15th Indian Division and served in Mesopotamia)
7th Battalion, Hampshire Regiment at Bournemouth (served in Aden)South-Western Brigade at Taunton
4th Battalion, Somerset Light Infantry at Bath (joined 37th Indian Brigade and served in Mesopotamia)
5th Battalion, Somerset Light Infantry at Taunton (joined 75th Division and served in Palestine)
4th Battalion, Dorsetshire Regiment at Dorchester (joined 42nd Indian Brigade and served in Mesopotamia)
4th Battalion, Wiltshire Regiment at Trowbridge (joined 75th Division and served in Palestine)Devon & Cornwall Brigade at Exeter
4th Battalion, Devonshire Regiment at Exeter (joined 41st Indian Brigade and served in Mesopotamia)
5th (Prince of Wales's) Battalion, Devonshire Regiment at Plymouth (joined 75th Division and served in Palestine)
6th Battalion, Devonshire Regiment at Barnstaple (joined 36th Indian Brigade and served in Mesopotamia)
4th Battalion, Duke of Cornwall's Light Infantry at Truro (served in Aden, later with 75th Division in Palestine)Divisional Royal Artillery
I Wessex Brigade, Royal Field Artillery at Portsmouth (joined 3rd (Lahore) Division and served in Mesopotamia)
1st Hampshire Battery
2nd Hampshire Battery
3rd Hampshire Battery
1st Wessex Ammunition Column
II Wessex (Howitzer) Brigade, Royal Field Artillery at Ryde, Isle of Wight
4th Hampshire (Howitzer) Battery (served in Aden)
5th Hampshire (Howitzer) Battery (joined 6th (Poona) Division and served in Mesopotamia; captured at Kut)]
2nd Wessex Ammunition Column
III Wessex Brigade, Royal Field Artillery at Swindon (served in Third Afghan War)
6th Hampshire Battery
Dorsetshire Battery
Wiltshire Battery
3rd Wessex Ammunition Column
IV Wessex Brigade, Royal Field Artillery at Exeter
1st Devonshire Battery
2nd Devonshire Battery
3rd Devonshire Battery (served in Third Afghan War)
4th Wessex Ammunition Column
Wessex (Hampshire) Heavy Battery, Royal Garrison Artillery and Ammunition Column at Cosham (served on the Western Front)Wessex Divisional Engineers (joined 27th Division and served at Salonika)
1st Wessex Field Company at Bath (became 500th Field Company)
2nd Wessex Field Company at Weston-super-Mare (became 501st Field Company)
Wessex Divisional Telegraph Company ('Signal Company' from 1910) at ExeterDivisional Royal Army Medical Corps (joined 8th Division and served on the Western Front)
1st Wessex Field Ambulance at Exeter (became 24th Field Ambulance)
2nd Wessex Field Ambulance at Plymouth (became 25th Field Ambulance)
3rd Wessex Field Ambulance at Portsmouth (became 26th Field Ambulance)
Wessex Clearing Hospital at ExeterWessex Divisional Transport & Supply Column, Army Service Corps, at Exeter (joined 29th Division and served at Gallipoli)
Divisional Company at Andover (became 246 Company)
Devonshire and Cornwall Company at Plymouth (became 247 Company)
South Western Brigade Company at Bridgwater (became 248 Company)
Hampshire Brigade Company at Aldershot (became 249 Company)
First World War
On 29 July 1914, the Wessex Division was on Salisbury Plain carrying out its annual training camp when 'precautionary orders' were received, and next day the division took up emergency war stations in Somerset, Devon and Cornwall. The order to mobilise arrived on the evening of 4 August. Between 10 and 13 August the division concentrated on Salisbury Plain and began war training.On 24 September, at the special request of the Secretary of State for War, Earl Kitchener of Khartoum the Wessex Division accepted liability for service in British India to relieve the Regular Army units there for service on the Western Front. The division's infantry battalions (without their brigade headquarters) and artillery brigades embarked at Southampton on 8 October and were convoyed to Bombay, disembarking on 9 November. The engineers, medical units, transport, heavy battery and brigade ammunition columns also remained in the UK and joined formations composed of Regular units brought back from India and other imperial garrisons. Meanwhile, the battalions and batteries were immediately distributed to garrisons across India, reverting to peacetime service conditions, and the Wessex Division never saw service as a whole, though it was formally numbered the 43rd (1st Wessex) Division in 1915 and the brigades were designated 128th (Hampshire) Brigade, 129th (South Western) Brigade and 130th (Devon and Cornwall) Brigade.As soon as the Wessex Division had left for India, the home depots began raising 2nd Line units, distinguished from the 1st Line by a '2/' prefix. Recruitment and training of the 2nd Wessex Division proceeded so well that it was also sent to India in December 1914, and later received the notional title of 45th (2nd Wessex) Division.By early 1915 the need was growing for troops to be sent to various theatres of war, and the first drafts and formed units from the 1st Wessex Division began to go on active service, particularly to the Mesopotamian Front. By the end of the war only one battalion and five batteries remained in India, and most of these then participated in the Third Anglo-Afghan War.
Second World War
Mobilisation and training
43rd (Wessex) Division was reformed in 1920 and became part of the Territorial Army, which replaced the TF. In the period of international tension preceding the outbreak of the Second World War, the existing territorial divisions (known as the first-line) helped form new formations, known as the second-line. This process was known as duplicating. The division's duplicate was the 45th Infantry Division.
The TA was mobilised on the outbreak of war in September 1939 and the division began training in its home area. In May 1940 it was preparing to go overseas to join the British Expeditionary Force (BEF) in France, but the German invasion of the Low Countries on 10 May ended the 'Phoney War' before the division was ready. When the Battle of France was lost and the BEF was being evacuated from Dunkirk, 43rd (W) Division was one of the few reasonably well-equipped formations left in Home Forces to counter a German invasion of the United Kingdom. It formed part of the mobile GHQ Reserve disposed on the line from Northampton through North London to Aldershot, from which brigade groups could be despatched to any threatened area. During the period when invasion was most threatened, the division was stationed just north of London.By the end of 1940 the division was stationed under XII Corps in East Kent, where it remained for the next four years, first in defensive mode, later training intensively. It was later noted that its habitual training area round Stone Street, outside Folkestone, bore a marked resemblance to the Bocage countryside in Normandy where it would later fight.
In 1942, however, after the German invasion of the Soviet Union and the entrance of the United States into the war, the situation changed and the 43rd Division started training for offensive operations to return to mainland Europe. Throughout most of 1942, the division was part of XII Corps, serving alongside the 46th Infantry Division and 53rd (Welsh) Infantry Division. XII Corps was, at the time, commanded by Lieutenant-General Bernard Montgomery.In March 1942, the division also gained a new General Officer Commanding (GOC) in the form of Major-General Ivor Thomas. Thomas was a decorated officer who had served as a young battery commander in the Royal Artillery on the Western Front during the First World War where he was twice wounded and awarded the Military Cross and the Distinguished Service Order. He would command the 43rd Division until September 1945. Thomas was an effective but hard-driving commander, humourless and not universally liked, sometimes known as 'Butcher', or more jocularly by Lt-Gen Brian Horrocks and others as 'Von Thoma', after the German Lt-Gen Wilhelm Ritter von Thoma captured after the Battle of Alamein. (Horrocks also jokingly referred to Thomas's command as the 'Wicked Wyvern'). Critics of his training methods regarded 43rd (Wessex) Division as 'the most over-exercised in the Army'.
In June 1942, the 128th Infantry Brigade (consisting of three battalions of the Hampshire Regiment) was transferred to 46th Infantry Division. It was replaced first by 25th and later 34th Army Tank Brigade as part of an experiment with 'Mixed Divisions'. However the experiment was abandoned (deemed unsuitable for the type of terrain in North-western Europe) in late 1943 and the 34th Tank Brigade was replaced, in October 1943, by the 214th Independent Infantry Brigade, a Home Defence formation raised during the war that had been serving in Hampshire and Dorset District. After service in the Isle of Wight, 214th Brigade had received specialised training in combined operations under the Royal Marines at Inverary, and retained an individuality within the division. 214th Brigade would remain with the 43rd Division for the rest of the war.
Operation Overlord
XII Corps and 43rd (Wessex) Division were assigned to 21st Army Group for the Allied invasion of Normandy (Operation Overlord). They were follow-up formations, with 43rd (Wessex) Division scheduled to complete its landings 14 days after D Day (D +14, 20 June). However, shipping delays and a storm between 19 and 22 June delayed its arrival; the division finally concentrated round Bayeux on 24 June.HQ, A and C Squadrons of 43rd (Wessex) Reconnaissance Regiment were aboard the troopship Derrycunihy, which arrived off Sword Beach on the evening of 20 June. High seas and enemy shelling prevented unloading for three days and it was decided to move to Juno Beach for disembarkation. As the ship started engines it detonated an acoustic mine, splitting the ship in two, and the after part, packed with sleeping men of 43rd Recce Regiment, sank rapidly. Worse still, an ammunition lorry caught fire, and oil floating on the water was set alight. Landing craft and gunboats came alongside and picked up survivors, but the regiment lost 183 men, with another 120 evacuated wounded. Most of 43rd Recce Rgts's vehicles were landed from the beached fore part of the "Derrycunihy", and reinforcements were sent from England, but the regiment was not fully up to strength until the end of July 1944.
Operation Epsom
The division's first action, Operation Epsom starting on 26 June, involved following 15th (Scottish) Division's advance and then securing the captured objectives. However, this entailed some heavy fighting by 5th Battalion Duke of Cornwall's Light Infantry (DCLI) against a Panzer counter-attack at Cheux on 27 June. The supporting 17-pounder anti-tank guns were knocked out and the infantry had to stalk Panther tanks with their lighter 6-pounder anti-tank guns and hand-held PIATs. Other battalions mopped up the important objective of Manvieux. On 28 June 1st Battalion Worcestershire Regiment made an attack from Cheux against Mouen: they had to cross open cornfields, but had support from the whole divisional artillery and heavy mortars plus two medium artillery regiments. The infantry followed the Creeping barrage of smoke and High explosive shells and forced their way into the houses and gardens, using PIATs against those German tanks that had survived the barrage. On 29 June 129 Brigade advanced under fire to ford the River Odon and dug in, a German counter-attack against them in the evening being destroyed by the divisional artillery.
Hill 112
The division's first major offensive action of its own was Operation Jupiter, to take Hill 112, which had been briefly captured by British armour during 'Epsom' but had to be abandoned. The attack on 10 July was supported by all the divisional artillery and mortars, plus the artillery of 15th (Scottish) Division and 11th Armoured Division and 3rd and 8th Army Groups Royal Artillery (AGRAs). In the first phase 129th Brigade on the right, with all three battalions in line, and 130th Brigade on the left with one battalion, were to capture the hill and the road from it to Château de Fontaine. They were supported by Churchill tanks from 31st Tank Brigade. Then, while 129th Brigade formed a secure south-west flank, 130th Brigade and Churchill Crocodile flamethrowing tanks from 79th Armoured Division were to advance from Château de Fontaine to capture Eterville and Maltot and the high ground to the south-east. Finally, 214th Brigade in Kangaroo armoured personnel carriers accompanied by 4th Armoured Brigade was supposed to break through to the River Orne and seize bridgeheads.The massive barrage stunned but failed to suppress the defenders from 10th SS Panzer Division. When the Wessex infantry went forward they came under heavy fire and had to clear defenders from the dugouts and defensive positions of their outpost line on the forward slopes. 5th Battalion Dorsets and 9th Royal Tank Regiment, leading 130th Brigade against the farms on the lower ground, made quick progress, 7th Somerset Light Infantry passing through with the Churchills and Crocodiles to deal with Chateau de Fontaine. But 129th Brigade was slowed in its advance on Hill 112 itself, suffering heavy casualties on the open slopes, and then running into the recently-arrived Tiger I tanks of 102nd SS Heavy Panzer Battalion, which the Churchills and corps anti-tank guns of 86th (Devon) Anti-Tank Regiment, Royal Artillery, struggled to deal with. By mid-morning 129th Brigade only had a slender toehold on the edge of the plateau. Attempting to continue 130th Brigade's advance on Maltot, 7th Hampshires and 9th RTR came under crossfire from Hill 112, while some of the Tigers reached the village first. The leading Hampshire penetrated the village, leaving strongpoints to be mopped up later by the following Dorsets, but they were driven out by counter-attacks. 4th Dorsets, making a second attack, suffered heavy casualties. Two battalions of 214th Brigade had already been drawn into the fighting around Chateau de Fontaine, leaving 5th DCLI as the last uncommitted battalion. It attacked up the slopes of Hill 112, described as 'one of the most tragic acts of self-sacrifice in the entire North West European Campaign'. Launched at 20.30 towards 'The Orchard' on the crest of the hill, and supported by a squadron of 7th Royal Tank Regiment and all available guns, including the divisional light anti-aircraft guns, the attack reached the orchard, but could get no further. The infantry and anti-tank guns held off counter-attacks through the night from the newly-arrived 9th SS Panzer Division, and were reinforced in the morning by a company of 1st Worcesters and briefly by a squadron of Sherman tanks from the Royal Scots Greys. By mid-afternoon all the anti-tank guns on the hill had been knocked out, the tanks had to retire to the reverse slope, and the defence was almost over. The order was given to withdraw and 60 survivors of 5th DCLI were brought down. Both sides remained dug in on the slopes, with the hilltop left in No man's land. The division had to hold its positions under mortar fire for another 14 days, described by the commander of 214th Brigade as comparable only 'to the bombardment at Passchendaele'. This defence was followed by a final set-piece attack, Operation Express, in which 4th and 5th Wiltshires and 7th RTR succeeded in capturing Maltot on 22 July.
Overall, 43rd (Wessex) Division performed well in Normandy and was considered by many senior British officers to be one of the best divisions of the British Army during the war. For the rest of the war Bernard Montgomery, commanding all British and Canadian troops in the campaign, preferred to use formations such as 43rd (Wessex) and 15th (Scottish) to spearhead his assaults. This was mainly due to issues of morale because veteran formations such as the 7th Armoured and 51st (Highland), both of which had seen extensive service in North Africa and Italy (and fought poorly in Normandy, according to senior officers), were judged as tired and war-weary with morale being almost dangerously fragile. With formations that had spent years in the United Kingdom training such as the 43rd (Wessex), 15th (Scottish), 11th Armoured and 59th (Staffordshire) Divisions the problem of morale was less of an issue.
Mont Pinçon
After a short rest 43rd (Wessex) Division moved to XXX Corps to launch an attack towards the dominating height of Mont Pinçon as part of Operation Bluecoat. 8th Armoured Brigade was assigned to support the infantry. Starting at 08.00 on 30 July, the division was to force its way through enemy positions at Briquessard and advance through Cahagnes towards Ondefontaine. 130th Brigade led, reinforced by 4th Somerset Light Infantry and Sherman tanks of the Sherwood Rangers Yeomanry, followed by 214th Brigade and then 129th Brigade. Initial casualties were heavy, particularly from mines, and the advance achieved only 1,000 yards (910 m) on the first day. It took until the following morning to clear the mines and restart the advance with 214th Brigade and the tanks of 4th/7th Dragoon Guards. At 17.30 the brigade broke through, and 1st Worcesters riding on the tanks got beyond Cahagnes by nightfall. 7th Somerset Light Infantry cleared the village in the dark and, with the aid of the divisional artillery, fought off a counter-attack accompanied by heavy armour (probably Jagdpanthers) that had to be stalked with PIATs.The division fought its way forward during 1 August, then at 02.00 on 2 August 129th Brigade began its advance on Ondefontaine. It was a day of slow but steady progress against rifle and machine gun fire from commanding positions on the ridge in front, followed by another pre-dawn attack towards Ondefontaine, while 214th Brigade began working its way towards Mont Pinçon. 5th DCLI and B Squadron 4th/7th DG, supported by the divisional artillery and mortars, reached the top of the ridge and engaged enemy infantry and armour, while 1st Worcesters worked round the flank and took the crest. 43rd Recce Regiment (reformed after the Derrycunihy disaster) then went through to unhinge the Ondefontaine defences. The division was now facing east, with Mont Pinçon only 4 miles (6.4 km) away.
At 08.00 on 5 August, 4th Wiltshires moved out with B Squadron 13th/18th Royal Hussars, picking their way through the narrow lanes, while A Sqn took a parallel route carrying 5th Wiltshires. 4th Wiltshires found a bridge blown and went ahead without their tanks towards the strongly-held village of St Jean-le-Blanc, breaking up a counter-attack by calling down artillery fire. About 16.00 the battalion pioneers managed to bridge the stream and a Troop of B Sqn crossed, but withdrew to 'harbour' at dusk. Meanwhile, 5th Wiltshires got to the bridge over the Druance at the foot of Mont Pinçon but failed to capture it by the end of the day. Generals Ivor Thomas and Brian Horrocks (who had just taken command of XXX Corps) were anxious to push on, and had already cancelled Operation Blackwater, designed to reach the River Noireau, because it was too risky with Mont Pinçon still in enemy hands.A new attack was planned for 6 August, with 130th Brigade making a feint to the north, while 129th Brigade continued from the west. In the end, the dominating position fell to a surprise attack. 4th Somerset Light Infantry and the reduced 5th Wiltshires fought their way forward through sweltering weather all day. 5th Wiltshires secured the crossroads at La Variniere and 4th Wiltshires was due to pass through them, when at about 18.00 A Sqn 13th/18th Hussars managed to get two Troops up a steep track to the top of the hill. By 18.30, seven Shermans were on the summit, attempting to mount an all-round defence and calling for infantry support. A staff officer ran up to Lt-Gen Horrocks at XXX Corps HQ, shouting 'We've got it, sir!' As fog descended on the hill, the 4th Wiltshires and the rest of A and B Sqns of the Hussars picked their way up the almost undefended track, followed by 4th Somerset LI. By daybreak the summit was firmly held, despite heavy German bombardment, and 5th Wiltshires and C Sqn still held the crossroads below. 214th Brigade relieved the exhausted troops that morning.Having taken and then defended Mont Pinçon, 43rd (Wessex) Division participated in XXX Corps' advance. It crossed the Noireau on 15 August by a broken railway bridge and by wading, whereupon 204 Field Company RE set to work with a waterproofed bulldozer to build a tank ford and a trestle bridge named 'Genesis'. 553 Field Company and 207 Field Park Company then built the division's first Bailey bridge across the site of the railway bridge. The main opposition came from mortars and booby-trapped mines. Next morning 43rd Recce and the Sherwood Foresters were ready to continue the pursuit of the broken enemy, who were soon caught in the Falaise pocket.
Vernon Bridge
The breakout achieved, XXX Corps drove flat out for the River Seine (Operation Loopy), with 43rd (W) Division sent ahead to make an assault crossing at Vernon. For this operation it was assisted by the bridging specialists of 15th (Kent) GHQ Troops Royal Engineers, a medium artillery regiment and the Cromwell tanks of 15th/19th The King's Royal Hussars, the armoured reconnaissance regiment of 11th Armoured Division. US troops had already reached the west bank of the Seine, so the convoys of assault troops and bridging material moving eastwards had to be carefully coordinated to cross with US convoys repositioning to the south. The first convoy, Group One, consisted of nearly 1500 vehicles of 129th Brigade with its usual proportion of divisional artillery, engineers and support services, reinforced by 1st Worcesters. Some of the assault infantry rode in the DUKW amphibious trucks that were to carry them over the river. The group arrived at Vernon on the afternoon of 25 August, ready to begin the assault that evening against the defenders from 49th German Infantry Division.15th (Kent) GHQTRE was tasked with manning the DUKWs during the initial assault and then operating rafts until the first bridge could be laid. They also had storm boats in reserve but these had to be used in the first wave because launching points for DUKWs were hard to find. A 15-minute bombardment by the guns of 94th (Dorset Yeomanry) Field Regiment, 121st (West Riding) Medium Regiment (further back in Group Two) and C Sqn, 15th/19th Hussars, together with the heavy mortars of 8th Middlesex, was followed by a smoke barrage to cover the crossing at 19.00. On the right, 5th Wiltshires began crossing in eight storm boats manned by 15th (Kent) GHQTRE, but they grounded before reaching the far side, and were raked by machine gun fire. By the end of an hour only one boat remained. Only about a company had got across, and they were overrun during the night. Three of the four available DUKWs also grounded, the survivor ferrying across the rest of 5th Wiltshires in the dark. On the left, 4th Somerset LI got across in the storm boats relatively easily, but found that their bridgehead was on an island, and they were still cut off from the east bank, apart from a few men who scrambled over the wreckage of the railway bridge. 1st Worcesters failed to get over the broken road bridge into the village of Vernonnet, which was strongly held. In the dark 260th Field Company managed to bulldoze a slipway for the DUKWs, speeding up the crossing, and 129th Brigade got about a battalion and a half across in total, setting up a perimeter along the escarpment above the bridging site.The Wessex field companies now began work under fire on a Class 9 (9 tonne maximum load) Folding Boat Equipment (FBE) bridge while the infantry fought to expand the bridgehead and clear Vernonnet. The Worcesters got over the broken bridge, and light rafts began to get 6-pounder anti-tank guns and armoured cars of the recce regiment across, but work on the bridge was halted by heavy fire until 5th DCLI and 7th Somerset LI from newly-arrived 214th Brigade struggled across the broken road bridge into Vernonnet. By nightfall the bridgehead was reasonably secure, the FBE bridge named 'David' was complete and 15th (Kent) GHQTRE's rafting troops were arriving to get a tank ferry into operation before morning. 7th Army Troops Royal Engineers had also arrived to begin a Class 40 Bailey Bridge.Next morning (27 August) a squadron each of 15th/19th Hussars' Cromwells and 4th/7th DGs' Shermans were rafted across and held off an armoured counter-attack, the infantry and 43rd Recce cleared the banks and pushed through the forest until they were firmly established on the heights. By 28 August, 7th ATRE working under shellfire had built their Class 40 bridge, codenamed 'Goliath', and 11th Armoured was beginning to pour across to spearhead XXX Corps' advance. A second Class 40 named 'Saul' was built by 15th (Kent) GHQRE. After the Seine crossing, 43rd (Wessex) Division was 'grounded' while the rest of XXX Corps raced across northern France and Belgium. The division rested and received reinforcements (many of them experienced men drafted from the disbanded 59th (Staffordshire) Division).
Market Garden
When 43rd (Wessex) Division next moved, the war was now 250 miles (400 km) away. The first elements moved up to Brussels to protect headquarters and carry out engineering works, then the division concentrated at Diest to take part in Operation Market Garden, beginning on 17 September. In 'Garden', the ground part of the operation, XXX Corps was to link river crossings up to the Nederrijn at Arnhem via a 'carpet' of airborne troops. 43rd (Wessex) Division accompanied by 8th Armoured Bde was to follow Guards Armoured Division, carrying out assault crossings if any of the bridges were found to be destroyed, and guarding the 'corridor' to Arnhem. The advance up the only road ('Club Route') was slow but on 21 September 43rd (Wessex) Division caught up with the Guards at Nijmegen. Further progress was blocked by strong German forces, and 1st Airborne Division holding out at Arnhem was in a desperate plight. 43rd (Wessex) Division was ordered to pass through the Guards the following morning and make an all-out effort to reach the Nederrijn by a side road. The Germans were found to be dug in at Oosterhout and the countryside was so boggy that it was impossible to move vehicles off the road, making outflanking moves too slow. Despite the shortage of artillery ammunition coming up the precarious line of communication, the whole of the divisional artillery and heavy mortars were used, but it was evening before the division got through. 5th DCLI, supported by a squadron of 4th/7th DG, was ordered to make a dash over the last 10 miles (16 km) to get in touch with the Polish Parachute Brigade at Driel on the south bank of the Nederrijn. The journey took only 30 minutes, but the road behind the column was cut by German tanks that had to be hunted down and destroyed before support could be brought up. Attempts to launch DUKWs with supplies for 1st Airborne were unsuccessful.The whole of 23 September was taken up with getting support through to 5th DCLI and the Poles and in clearing the main road, though 43rd Recce Rgt was able to exploit westwards. During the night 5th Dorsets and the divisional engineers ferried a few hundred Poles across the Nederrijn in assault boats to reinforce 1st Airborne Division's shrinking perimeter. 4th Dorsets and the engineers made another assault crossing on the night of 24/25 September, suffering heavy casualties and getting few supplies across. By now 1st Airborne had been effectively destroyed, and the only course now was to evacuate the survivors. Their radios had been inoperable, and the only communication link had been through 64th (London) Medium Regiment, RA, attached to 43rd (Wessex) Division. Through this link the code word for the evacuation was passed, and during the night of 25/26 September a feint attack was made by 5th Wiltshires while around 2300 survivors of 1st Airborne and the Poles were ferried back to the south bank; few of 4th Dorsets made it back.The division was blamed by many airborne soldiers for its dilatory advance to the river, though the Corps commander, Lt-Gen Horrocks, defended the division, pointing out that it could not deploy any armoured vehicles (either 8th Armoured Bde or 43rd Recce Rgt's armoured cars and half-tracks) off the single road, nicknamed 'Hell's Highway', which was cut behind them on several occasions, and praising the division's hard fighting. Nevertheless, Maj-Gen Thomas replaced the commanding officer of 43rd Recce immediately after the battle.In the aftermath of Market Garden, 43rd (Wessex) Division was stationed on 'the Island' (between the Rivers Waal and Nederrijn). 43rd Recce Rgt, with 12th Battalion King's Royal Rifle Corps from 8th Armoured Bde under command, protected the division's open western flank. The concealed squadrons sent back reports, but were forbidden to engage the enemy in order to hide the extent of the position. However, on the night of 26/27 September a furious firefight broke out when the Germans crossed the river in strength and attempted to emplace anti-tank guns in 43rd Recce's hidden positions.The Germans launched a serious counter-attack from the east on 1 October, attacking 129th Bde strung out guarding the road from Nijmegen to the Nederrijn. 4th Somerset LI and 5th Wiltshires fought them off at Elst for 48 hours, the divisional artillery breaking up some of the attacks, and RAF medium bombers following up. Further north, 5th Dorsets beat off 116th Panzer Division and 7th Hampshires had to dislodge enemy troops who fortified themselves in some brick kilns, with the help of RAF Typhoons. On 5 October 43rd (Wessex) handed most of its positions over to the US 101st Airborne Division, leaving the anti-tank and mortar platoons and 5th DCLI, the divisional reserve, to help out. The attacks ended after one last attempt on 6 October. 43rd Wessex continued to hold the western part of the Island. The divisional historian records that "While the Division faced the monotony inseparable from static defence, the Reconnaissance Regiment fought a different type of war". This involved guarding the western end of the Island, cooperating with the Dutch Resistance and facilitating the escape across the river of British paratroops who had evaded capture.
Operation Clipper
43rd (Wessex) Division was then shifted east with XXX Corps to cooperate with the US Ninth Army by capturing the Geilenkirchen salient (Operation Clipper). XXX Corps had 43rd Wessex and 84th US Divisions under command for this attack, which entailed breaching the Siegfried Line defences and capturing a string of fortified villages. 84th US Division attacked on the morning of 18 November, supported by British specialist armour, and was through the line of pillboxes by midday. 214th Brigade then attacked on its left in the afternoon, led by 7th Somerset LI and tanks of 4th/7th DG, and took its first objective, the village of Neiderheide. But many of the tanks and most of the supply vehicles got bogged down while 1st Worcesters were threading their way through Gilrath to form up for the second phase towards Tripsrath. Without tanks, and the artillery having shifted to another target, 1st Worcesters struggled forward under shellfire and forced their way into the village at nightfall. The traffic jam of bogged vehicles disrupted the attacks by 5th Dorsets and 5th DCLI, but they got into Bauchem and Hocheide respectively, and patrols reached Geilenkirchen itself, which was surrounded. After driving off some counter-attacks by 15th Panzer Grenadier Division during the night, Geilenkirchen was captured after a stiff fight next day. But thereafter heavy rain turned the whole battlefield into mud while the infantry struggled to consolidate their positions under heavy shellfire from the Siegfried Line guns. One wood captured and grimly held first by 4th Dorsets and then 5th Dorsets for seven days became known as 'Dorset Wood'. On 22 November 5th DCLI suffered heavy casualties trying to take the high ground near Hoven to deny the enemy observation over the two Allied divisions. Overnight both sides shared the village of Hoven, before counter-attacks came in at dawn from 10th SS Panzer Division and 21st Panzer Division. Horrocks himself authorised the withdrawal of the DCLI before they were overwhelmed. Any further attempt to take Hoven was impossible due to the waterlogged state of the country, which then had to be defended in conditions resembling the worst of the Western Front in the First World War. Horrocks organised an ad hoc battalion from XXX Corps' service units to relieve Wessex infantry for rest. Planning was under way to renew the offensive when the Germans attacked in the Ardennes (the Battle of the Bulge) on 16 December.
Operation Blackcock
The division then later played a comparatively small part in the mainly American Battle of the Bulge, where it was placed on the River Meuse as a reserve. Once the German Ardennes Offensive had been halted, 43rd (Wessex) Division returned to the offensive in early 1945 in Operation Blackcock to reduce the Roer Triangle, though exploitation was prevented by bad weather.
Operation Veritable
The 43rd later played a large part in Operation Veritable attached to First Canadian Army, through the month-long fighting in the Reichswald to capture Kleve, roll up the Siegfried Line defences, cross the Goch escarpment and seize Xanten on the Rhine.
Across the Rhine
43rd (Wessex) Division was given a follow-up task in the assault crossing of the Rhine (Operation Plunder). Its leading brigade crossed the river on 25 March behind 51st (Highland) Division, which had carried the assault on the night of 23/24 March. It found itself in immediate combat, but had broken through by 29 March. During the subsequent pursuit, 43rd (Wessex) Division was given the task of opening 'Club Route' for XXX Corps. The division was divided into five battle groups for the first 25 miles (40 km) drive, incorporating units of 8th Armoured Brigade. The advance began on 30 March: German rearguards were either overcome or bypassed, and the Twente Canal was crossed, with troops of 129th Infantry Bde and 8th Armoured Bde liberating Lochem on 1–2 April. The pursuit continued through April and ended with the capture of Bremen and XXX Corps' drive into the Cuxhaven peninsula. Hostilities ended on 5 May after the German surrender at Lüneburg Heath.After a period as occupation forces in XXX Corps' district, 43rd (Wessex) Division's HQ and TA units were demobilised at the war's end. Throughout the North West Europe Campaign the 43rd (Wessex) Division, like so many other Allied divisions that fought from Normandy to Germany, had suffered very heavy casualties with the majority of them, 80% in some units, being suffered by the average Tommy in the infantry battalions. From June 1944 to May 1945 the 43rd (Wessex) Division, or the Yellow Devils or British SS Division as known by the Germans, had suffered well over 12,500 casualties, with almost 3,000 killed in action.
43rd (Wessex) Infantry Division Order of Battle 1939–1945128th Infantry Brigade (left 6 June 1942)
1/4th Battalion, Hampshire Regiment
2/4th Battalion, Hampshire Regiment
5th Battalion, Hampshire Regiment
128th Infantry Brigade Anti-Tank Company (formed 19 June 1940, disbanded 20 December 1941)129th Infantry Brigade
4th Battalion, Somerset Light Infantry
4th Battalion, Wiltshire Regiment
5th Battalion, Wiltshire Regiment
129th Infantry Brigade Anti-Tank Company (formed 14 May 1940, disbanded 20 December 1941)130th Infantry Brigade
7th Battalion, Hampshire Regiment
4th Battalion, Dorsetshire Regiment
5th Battalion, Dorsetshire Regiment
130th Infantry Brigade Anti-Tank Company (formed 17 May 1940, disbanded 20 December 1941)25th Tank Brigade (from 1 June 1942, left 2 September 1942)
51st (Leeds Rifles) Royal Tank Regiment
11th Royal Tank Regiment
142nd Regiment Royal Armoured Corps34th Tank Brigade (from 3 September 1942, left 10 September 1943)
North Irish Horse (left 3 September 1942)
147th Regiment Royal Armoured Corps
153rd Regiment Royal Armoured Corps
151st Regiment Royal Armoured Corps (from 3 September 1942)214th Infantry Brigade (from 5 September 1943)
7th Battalion, Somerset Light Infantry
5th Battalion, Duke of Cornwall's Light Infantry
9th Battalion, Somerset Light Infantry (left 30 September 1943)
1st Battalion, Worcestershire Regiment (from 30 September 1943)Divisional Troops
1/8th Battalion, Middlesex Regiment (joined as Machine Gun Battalion from 18 November 1941, redesignated 8th Battalion May 1942, left 1 October 1942, rejoined as Support Battalion 1 October 1943, again as MG Battalion 28 February 1944)
48th Battalion, Reconnaissance Corps (converted from 5th Battalion, Gloucestershire Regiment 20 November 1941, redesignated 43rd Battalion 1 January 1942, later 43rd Regiment 6 June 1942, finally 43rd (Wessex) Reconnaissance Regiment (The Gloucestershire Regiment), Royal Armoured Corps 1 January 1944)
94th (Queen's Own Dorset Yeomanry) Field Regiment, Royal Artillery
112th (Wessex) Field Regiment, Royal Artillery
141st (Queen's Own Dorset Yeomanry) Field Regiment, Royal Artillery (left 8 June 1942)
179th Field Regiment, Royal Artillery (from 9 June 1942)
59th (Duke of Connaught's Own) Anti-Tank Regiment, Royal Artillery
110th Light Anti-Aircraft Regiment, Royal Artillery (converted from 7th Battalion, Dorsetshire Regiment, joined 23 March 1941)
43rd (Wessex) Divisional Engineers204th (Wessex) Field Company, Royal Engineers
260th Field Company, Royal Engineers
553rd Field Company, Royal Engineers (from 13 January 1940)
207th (Wessex) Field Park Company, Royal Engineers
13th Bridging Platoon, Royal Engineers (from 1 October 1943)
43rd (Wessex) Divisional Signals, Royal Corps of Signals
Royal Army Service Corps
54, 504, 505, 506 Companies
Royal Army Medical Corps
129, 130, 213 Field Ambulances
14, 15, 38 Field Dressing Stations
38 Field Hygiene Section
Royal Army Ordnance Corps
43 Ordnance Field Park
306 Mobile Laundry and Bath Unit
Royal Electrical and Mechanical Engineers
129, 130, 214 Infantry Brigade Workshops
43 Wessex Division Provost Company, Royal Military Police
57 Field Security Section
Postal Unit
Postwar
The TA was reconstituted from 1 January 1947 and its units and formations including 43rd (Wessex) Infantry Division were reformed. However, the TA saw large numbers of amalgamations from 1950 onwards. In 1961 the division became a district headquarters as 43rd (Wessex) Division/District, and it was disbanded on the reduction of the TA into the Territorial and Army Volunteer Reserve on 1 April 1967, when many individual TA units lost their identities. The district headquarters itself formed the core of the structure for the creation of South West District under HQ UK Land Forces in 1972.
43rd (Wessex) Infantry Division Order of Battle 1947128 Infantry Brigade
4th Battalion, Royal Hampshire Regiment at Winchester
4th Battalion, Oxfordshire and Buckinghamshire Light Infantry at Oxford
4th/6th Battalion, Royal Berkshire Regiment at Reading129 Infantry Brigade
4th Battalion, Somerset Light Infantry at Bath
5th Battalion, Gloucestershire Regiment at Gloucester
4th Battalion, Wiltshire Regiment at Trowbridge130 (West Country) Infantry Brigade
4th Battalion, Devonshire Regiment at Exeter
5th (Prince of Wales's) Battalion, Devonshire Regiment at Plymouth
4th/5th Battalion, Duke of Cornwall's Light Infantry at Truro
4th Battalion, Dorsetshire Regiment at DorchesterRoyal Armoured Corps
Royal Wiltshire Yeomanry at SwindonRoyal Artillery
294 (Queen's Own Dorset Yeomanry) Field Regiment at Sherborne
296 (Royal Devon Yeomanry) Field Regiment at Exeter
387 (Queen's Own Oxfordshire Hussars) Field Regiment at Oxford
383 (Duke of Connaught's Royal Hampshire) Anti-Tank Regiment at Portsmouth
396 (Devon) Light Anti-Aircraft Regiment at Devonport
883 Locating Battery at BristolRoyal Engineers
110 Field Engineer Regiment204 Field Squadron
226 Field Squadron
260 Field Squadron
207 Field Park SquadronRoyal Corps of Signals
43rd (Wessex) Infantry Division Signal Regiment at Taunton 1 Squadron at Exeter
2 Squadron at Taunton
3 Squadron at Torquay, later BristolRoyal Army Service Corps
43 (Wessex) Infantry Divisional Column at Bristol504 Company at Swindon
505 Company at Didcot
506 Company at Plymouth
1567 Company at Plymouth
43 Ordnance Field Park, Royal Army Ordnance Corps
43 Divisional Royal Electrical and Mechanical Engineers
43 Divisional Royal Army Medical Corps
Commanders
The following officers commanded the division at various times:
Insignia
The banner of the kings of Wessex bore a golden Wyvern, a dragon with two eagle-like legs and the barbed tail of a snake. The 43rd (Wessex) Division adopted the golden wyvern on a blue square as its formation sign in 1935.
Memorials
The Hill 112 memorial was erected by the divisional engineers and later taken over by the Commonwealth War Graves Commission with an endowment from the Memorial Fund. The first memorial in England was at Castle Hill, Mere, in Wiltshire, acquired on a 199-year lease from the Duchy of Cornwall and entrusted to the Parish Council of Mere. Next the fund acquired Wynyard's Gap near Crewkerne, Somerset. Finally, Sir Richard Onslow (formerly of the Duke of Cornwall's Light Infantry) presented Rough Tor on Bodmin Moor to the National Trust as a memorial. The Roll of Honour is in the War Memorial Chapel in Salisbury Cathedral.A memorial stone stands at the end of a lane named 'Somerset' in Lochem, Netherlands, showing the Wessex Wyvern and listing 4th Bn Somerset Light Infantry, 4th Bn Wiltshire Regiment and units of 8th Armoured Bde who liberated Lochem on 1–2 April 1945. The horizontal inscription reads 'All the way from Normandy'.
See also
List of British divisions in World War I
List of British divisions in World War II
British Army Order of Battle (September 1939)
Notes
References
Bibliography
External links
Mark Conrad, The British Army, 1914 (archive site)
British Army units from 1945 on
Divisional insignia
The Long, Long Trail
Orders of Battle at Patriot Files
Graham Watson, The Territorial Army 1947
World War II Armed Forces
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Commons category
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The 43rd (Wessex) Infantry Division was an infantry division of Britain's Territorial Army (TA). The division was first formed in 1908, as the Wessex Division. During the First World War, it was broken-up and never served as a complete formation. It was reformed in the TA in 1920, and then served in the campaign in North West Europe from June 1944 until May 1945, during the Second World War. The division suffered heavy casualties and gained an excellent reputation. After the Second World War, the division formed part of the postwar TA, and became the 43rd (Wessex) Division/District in 1961. It was finally disbanded in 1967.
Formation
The Territorial Force (TF) was formed on 1 April 1908 following the enactment of the Territorial and Reserve Forces Act 1907 (7 Edw.7, c.9) which combined and re-organised the old Volunteer Force, the Honourable Artillery Company and the Yeomanry. On formation, the TF contained 14 infantry divisions and 14 mounted yeomanry brigades. One of the divisions was the Wessex Division.The Wessex Division was formed in Southern Command from TF units in the south-western counties of Cornwall, Devon, Dorset, Hampshire, Somerset and Wiltshire. In peacetime, the divisional headquarters was at 19 Cathedral Close in Exeter.
Wessex Division Order of Battle 1908–1914Divisional HQ at Exeter
Hampshire Brigade at Southampton
4th Battalion, Hampshire Regiment at Winchester (joined 12th Indian Division and served in Mesopotamia)
5th Battalion, Hampshire Regiment at Southampton (served in Third Afghan War)
6th (Duke of Connaught's Own) Battalion, Hampshire Regiment at Portsmouth (joined 15th Indian Division and served in Mesopotamia)
7th Battalion, Hampshire Regiment at Bournemouth (served in Aden)South-Western Brigade at Taunton
4th Battalion, Somerset Light Infantry at Bath (joined 37th Indian Brigade and served in Mesopotamia)
5th Battalion, Somerset Light Infantry at Taunton (joined 75th Division and served in Palestine)
4th Battalion, Dorsetshire Regiment at Dorchester (joined 42nd Indian Brigade and served in Mesopotamia)
4th Battalion, Wiltshire Regiment at Trowbridge (joined 75th Division and served in Palestine)Devon & Cornwall Brigade at Exeter
4th Battalion, Devonshire Regiment at Exeter (joined 41st Indian Brigade and served in Mesopotamia)
5th (Prince of Wales's) Battalion, Devonshire Regiment at Plymouth (joined 75th Division and served in Palestine)
6th Battalion, Devonshire Regiment at Barnstaple (joined 36th Indian Brigade and served in Mesopotamia)
4th Battalion, Duke of Cornwall's Light Infantry at Truro (served in Aden, later with 75th Division in Palestine)Divisional Royal Artillery
I Wessex Brigade, Royal Field Artillery at Portsmouth (joined 3rd (Lahore) Division and served in Mesopotamia)
1st Hampshire Battery
2nd Hampshire Battery
3rd Hampshire Battery
1st Wessex Ammunition Column
II Wessex (Howitzer) Brigade, Royal Field Artillery at Ryde, Isle of Wight
4th Hampshire (Howitzer) Battery (served in Aden)
5th Hampshire (Howitzer) Battery (joined 6th (Poona) Division and served in Mesopotamia; captured at Kut)]
2nd Wessex Ammunition Column
III Wessex Brigade, Royal Field Artillery at Swindon (served in Third Afghan War)
6th Hampshire Battery
Dorsetshire Battery
Wiltshire Battery
3rd Wessex Ammunition Column
IV Wessex Brigade, Royal Field Artillery at Exeter
1st Devonshire Battery
2nd Devonshire Battery
3rd Devonshire Battery (served in Third Afghan War)
4th Wessex Ammunition Column
Wessex (Hampshire) Heavy Battery, Royal Garrison Artillery and Ammunition Column at Cosham (served on the Western Front)Wessex Divisional Engineers (joined 27th Division and served at Salonika)
1st Wessex Field Company at Bath (became 500th Field Company)
2nd Wessex Field Company at Weston-super-Mare (became 501st Field Company)
Wessex Divisional Telegraph Company ('Signal Company' from 1910) at ExeterDivisional Royal Army Medical Corps (joined 8th Division and served on the Western Front)
1st Wessex Field Ambulance at Exeter (became 24th Field Ambulance)
2nd Wessex Field Ambulance at Plymouth (became 25th Field Ambulance)
3rd Wessex Field Ambulance at Portsmouth (became 26th Field Ambulance)
Wessex Clearing Hospital at ExeterWessex Divisional Transport & Supply Column, Army Service Corps, at Exeter (joined 29th Division and served at Gallipoli)
Divisional Company at Andover (became 246 Company)
Devonshire and Cornwall Company at Plymouth (became 247 Company)
South Western Brigade Company at Bridgwater (became 248 Company)
Hampshire Brigade Company at Aldershot (became 249 Company)
First World War
On 29 July 1914, the Wessex Division was on Salisbury Plain carrying out its annual training camp when 'precautionary orders' were received, and next day the division took up emergency war stations in Somerset, Devon and Cornwall. The order to mobilise arrived on the evening of 4 August. Between 10 and 13 August the division concentrated on Salisbury Plain and began war training.On 24 September, at the special request of the Secretary of State for War, Earl Kitchener of Khartoum the Wessex Division accepted liability for service in British India to relieve the Regular Army units there for service on the Western Front. The division's infantry battalions (without their brigade headquarters) and artillery brigades embarked at Southampton on 8 October and were convoyed to Bombay, disembarking on 9 November. The engineers, medical units, transport, heavy battery and brigade ammunition columns also remained in the UK and joined formations composed of Regular units brought back from India and other imperial garrisons. Meanwhile, the battalions and batteries were immediately distributed to garrisons across India, reverting to peacetime service conditions, and the Wessex Division never saw service as a whole, though it was formally numbered the 43rd (1st Wessex) Division in 1915 and the brigades were designated 128th (Hampshire) Brigade, 129th (South Western) Brigade and 130th (Devon and Cornwall) Brigade.As soon as the Wessex Division had left for India, the home depots began raising 2nd Line units, distinguished from the 1st Line by a '2/' prefix. Recruitment and training of the 2nd Wessex Division proceeded so well that it was also sent to India in December 1914, and later received the notional title of 45th (2nd Wessex) Division.By early 1915 the need was growing for troops to be sent to various theatres of war, and the first drafts and formed units from the 1st Wessex Division began to go on active service, particularly to the Mesopotamian Front. By the end of the war only one battalion and five batteries remained in India, and most of these then participated in the Third Anglo-Afghan War.
Second World War
Mobilisation and training
43rd (Wessex) Division was reformed in 1920 and became part of the Territorial Army, which replaced the TF. In the period of international tension preceding the outbreak of the Second World War, the existing territorial divisions (known as the first-line) helped form new formations, known as the second-line. This process was known as duplicating. The division's duplicate was the 45th Infantry Division.
The TA was mobilised on the outbreak of war in September 1939 and the division began training in its home area. In May 1940 it was preparing to go overseas to join the British Expeditionary Force (BEF) in France, but the German invasion of the Low Countries on 10 May ended the 'Phoney War' before the division was ready. When the Battle of France was lost and the BEF was being evacuated from Dunkirk, 43rd (W) Division was one of the few reasonably well-equipped formations left in Home Forces to counter a German invasion of the United Kingdom. It formed part of the mobile GHQ Reserve disposed on the line from Northampton through North London to Aldershot, from which brigade groups could be despatched to any threatened area. During the period when invasion was most threatened, the division was stationed just north of London.By the end of 1940 the division was stationed under XII Corps in East Kent, where it remained for the next four years, first in defensive mode, later training intensively. It was later noted that its habitual training area round Stone Street, outside Folkestone, bore a marked resemblance to the Bocage countryside in Normandy where it would later fight.
In 1942, however, after the German invasion of the Soviet Union and the entrance of the United States into the war, the situation changed and the 43rd Division started training for offensive operations to return to mainland Europe. Throughout most of 1942, the division was part of XII Corps, serving alongside the 46th Infantry Division and 53rd (Welsh) Infantry Division. XII Corps was, at the time, commanded by Lieutenant-General Bernard Montgomery.In March 1942, the division also gained a new General Officer Commanding (GOC) in the form of Major-General Ivor Thomas. Thomas was a decorated officer who had served as a young battery commander in the Royal Artillery on the Western Front during the First World War where he was twice wounded and awarded the Military Cross and the Distinguished Service Order. He would command the 43rd Division until September 1945. Thomas was an effective but hard-driving commander, humourless and not universally liked, sometimes known as 'Butcher', or more jocularly by Lt-Gen Brian Horrocks and others as 'Von Thoma', after the German Lt-Gen Wilhelm Ritter von Thoma captured after the Battle of Alamein. (Horrocks also jokingly referred to Thomas's command as the 'Wicked Wyvern'). Critics of his training methods regarded 43rd (Wessex) Division as 'the most over-exercised in the Army'.
In June 1942, the 128th Infantry Brigade (consisting of three battalions of the Hampshire Regiment) was transferred to 46th Infantry Division. It was replaced first by 25th and later 34th Army Tank Brigade as part of an experiment with 'Mixed Divisions'. However the experiment was abandoned (deemed unsuitable for the type of terrain in North-western Europe) in late 1943 and the 34th Tank Brigade was replaced, in October 1943, by the 214th Independent Infantry Brigade, a Home Defence formation raised during the war that had been serving in Hampshire and Dorset District. After service in the Isle of Wight, 214th Brigade had received specialised training in combined operations under the Royal Marines at Inverary, and retained an individuality within the division. 214th Brigade would remain with the 43rd Division for the rest of the war.
Operation Overlord
XII Corps and 43rd (Wessex) Division were assigned to 21st Army Group for the Allied invasion of Normandy (Operation Overlord). They were follow-up formations, with 43rd (Wessex) Division scheduled to complete its landings 14 days after D Day (D +14, 20 June). However, shipping delays and a storm between 19 and 22 June delayed its arrival; the division finally concentrated round Bayeux on 24 June.HQ, A and C Squadrons of 43rd (Wessex) Reconnaissance Regiment were aboard the troopship Derrycunihy, which arrived off Sword Beach on the evening of 20 June. High seas and enemy shelling prevented unloading for three days and it was decided to move to Juno Beach for disembarkation. As the ship started engines it detonated an acoustic mine, splitting the ship in two, and the after part, packed with sleeping men of 43rd Recce Regiment, sank rapidly. Worse still, an ammunition lorry caught fire, and oil floating on the water was set alight. Landing craft and gunboats came alongside and picked up survivors, but the regiment lost 183 men, with another 120 evacuated wounded. Most of 43rd Recce Rgts's vehicles were landed from the beached fore part of the "Derrycunihy", and reinforcements were sent from England, but the regiment was not fully up to strength until the end of July 1944.
Operation Epsom
The division's first action, Operation Epsom starting on 26 June, involved following 15th (Scottish) Division's advance and then securing the captured objectives. However, this entailed some heavy fighting by 5th Battalion Duke of Cornwall's Light Infantry (DCLI) against a Panzer counter-attack at Cheux on 27 June. The supporting 17-pounder anti-tank guns were knocked out and the infantry had to stalk Panther tanks with their lighter 6-pounder anti-tank guns and hand-held PIATs. Other battalions mopped up the important objective of Manvieux. On 28 June 1st Battalion Worcestershire Regiment made an attack from Cheux against Mouen: they had to cross open cornfields, but had support from the whole divisional artillery and heavy mortars plus two medium artillery regiments. The infantry followed the Creeping barrage of smoke and High explosive shells and forced their way into the houses and gardens, using PIATs against those German tanks that had survived the barrage. On 29 June 129 Brigade advanced under fire to ford the River Odon and dug in, a German counter-attack against them in the evening being destroyed by the divisional artillery.
Hill 112
The division's first major offensive action of its own was Operation Jupiter, to take Hill 112, which had been briefly captured by British armour during 'Epsom' but had to be abandoned. The attack on 10 July was supported by all the divisional artillery and mortars, plus the artillery of 15th (Scottish) Division and 11th Armoured Division and 3rd and 8th Army Groups Royal Artillery (AGRAs). In the first phase 129th Brigade on the right, with all three battalions in line, and 130th Brigade on the left with one battalion, were to capture the hill and the road from it to Château de Fontaine. They were supported by Churchill tanks from 31st Tank Brigade. Then, while 129th Brigade formed a secure south-west flank, 130th Brigade and Churchill Crocodile flamethrowing tanks from 79th Armoured Division were to advance from Château de Fontaine to capture Eterville and Maltot and the high ground to the south-east. Finally, 214th Brigade in Kangaroo armoured personnel carriers accompanied by 4th Armoured Brigade was supposed to break through to the River Orne and seize bridgeheads.The massive barrage stunned but failed to suppress the defenders from 10th SS Panzer Division. When the Wessex infantry went forward they came under heavy fire and had to clear defenders from the dugouts and defensive positions of their outpost line on the forward slopes. 5th Battalion Dorsets and 9th Royal Tank Regiment, leading 130th Brigade against the farms on the lower ground, made quick progress, 7th Somerset Light Infantry passing through with the Churchills and Crocodiles to deal with Chateau de Fontaine. But 129th Brigade was slowed in its advance on Hill 112 itself, suffering heavy casualties on the open slopes, and then running into the recently-arrived Tiger I tanks of 102nd SS Heavy Panzer Battalion, which the Churchills and corps anti-tank guns of 86th (Devon) Anti-Tank Regiment, Royal Artillery, struggled to deal with. By mid-morning 129th Brigade only had a slender toehold on the edge of the plateau. Attempting to continue 130th Brigade's advance on Maltot, 7th Hampshires and 9th RTR came under crossfire from Hill 112, while some of the Tigers reached the village first. The leading Hampshire penetrated the village, leaving strongpoints to be mopped up later by the following Dorsets, but they were driven out by counter-attacks. 4th Dorsets, making a second attack, suffered heavy casualties. Two battalions of 214th Brigade had already been drawn into the fighting around Chateau de Fontaine, leaving 5th DCLI as the last uncommitted battalion. It attacked up the slopes of Hill 112, described as 'one of the most tragic acts of self-sacrifice in the entire North West European Campaign'. Launched at 20.30 towards 'The Orchard' on the crest of the hill, and supported by a squadron of 7th Royal Tank Regiment and all available guns, including the divisional light anti-aircraft guns, the attack reached the orchard, but could get no further. The infantry and anti-tank guns held off counter-attacks through the night from the newly-arrived 9th SS Panzer Division, and were reinforced in the morning by a company of 1st Worcesters and briefly by a squadron of Sherman tanks from the Royal Scots Greys. By mid-afternoon all the anti-tank guns on the hill had been knocked out, the tanks had to retire to the reverse slope, and the defence was almost over. The order was given to withdraw and 60 survivors of 5th DCLI were brought down. Both sides remained dug in on the slopes, with the hilltop left in No man's land. The division had to hold its positions under mortar fire for another 14 days, described by the commander of 214th Brigade as comparable only 'to the bombardment at Passchendaele'. This defence was followed by a final set-piece attack, Operation Express, in which 4th and 5th Wiltshires and 7th RTR succeeded in capturing Maltot on 22 July.
Overall, 43rd (Wessex) Division performed well in Normandy and was considered by many senior British officers to be one of the best divisions of the British Army during the war. For the rest of the war Bernard Montgomery, commanding all British and Canadian troops in the campaign, preferred to use formations such as 43rd (Wessex) and 15th (Scottish) to spearhead his assaults. This was mainly due to issues of morale because veteran formations such as the 7th Armoured and 51st (Highland), both of which had seen extensive service in North Africa and Italy (and fought poorly in Normandy, according to senior officers), were judged as tired and war-weary with morale being almost dangerously fragile. With formations that had spent years in the United Kingdom training such as the 43rd (Wessex), 15th (Scottish), 11th Armoured and 59th (Staffordshire) Divisions the problem of morale was less of an issue.
Mont Pinçon
After a short rest 43rd (Wessex) Division moved to XXX Corps to launch an attack towards the dominating height of Mont Pinçon as part of Operation Bluecoat. 8th Armoured Brigade was assigned to support the infantry. Starting at 08.00 on 30 July, the division was to force its way through enemy positions at Briquessard and advance through Cahagnes towards Ondefontaine. 130th Brigade led, reinforced by 4th Somerset Light Infantry and Sherman tanks of the Sherwood Rangers Yeomanry, followed by 214th Brigade and then 129th Brigade. Initial casualties were heavy, particularly from mines, and the advance achieved only 1,000 yards (910 m) on the first day. It took until the following morning to clear the mines and restart the advance with 214th Brigade and the tanks of 4th/7th Dragoon Guards. At 17.30 the brigade broke through, and 1st Worcesters riding on the tanks got beyond Cahagnes by nightfall. 7th Somerset Light Infantry cleared the village in the dark and, with the aid of the divisional artillery, fought off a counter-attack accompanied by heavy armour (probably Jagdpanthers) that had to be stalked with PIATs.The division fought its way forward during 1 August, then at 02.00 on 2 August 129th Brigade began its advance on Ondefontaine. It was a day of slow but steady progress against rifle and machine gun fire from commanding positions on the ridge in front, followed by another pre-dawn attack towards Ondefontaine, while 214th Brigade began working its way towards Mont Pinçon. 5th DCLI and B Squadron 4th/7th DG, supported by the divisional artillery and mortars, reached the top of the ridge and engaged enemy infantry and armour, while 1st Worcesters worked round the flank and took the crest. 43rd Recce Regiment (reformed after the Derrycunihy disaster) then went through to unhinge the Ondefontaine defences. The division was now facing east, with Mont Pinçon only 4 miles (6.4 km) away.
At 08.00 on 5 August, 4th Wiltshires moved out with B Squadron 13th/18th Royal Hussars, picking their way through the narrow lanes, while A Sqn took a parallel route carrying 5th Wiltshires. 4th Wiltshires found a bridge blown and went ahead without their tanks towards the strongly-held village of St Jean-le-Blanc, breaking up a counter-attack by calling down artillery fire. About 16.00 the battalion pioneers managed to bridge the stream and a Troop of B Sqn crossed, but withdrew to 'harbour' at dusk. Meanwhile, 5th Wiltshires got to the bridge over the Druance at the foot of Mont Pinçon but failed to capture it by the end of the day. Generals Ivor Thomas and Brian Horrocks (who had just taken command of XXX Corps) were anxious to push on, and had already cancelled Operation Blackwater, designed to reach the River Noireau, because it was too risky with Mont Pinçon still in enemy hands.A new attack was planned for 6 August, with 130th Brigade making a feint to the north, while 129th Brigade continued from the west. In the end, the dominating position fell to a surprise attack. 4th Somerset Light Infantry and the reduced 5th Wiltshires fought their way forward through sweltering weather all day. 5th Wiltshires secured the crossroads at La Variniere and 4th Wiltshires was due to pass through them, when at about 18.00 A Sqn 13th/18th Hussars managed to get two Troops up a steep track to the top of the hill. By 18.30, seven Shermans were on the summit, attempting to mount an all-round defence and calling for infantry support. A staff officer ran up to Lt-Gen Horrocks at XXX Corps HQ, shouting 'We've got it, sir!' As fog descended on the hill, the 4th Wiltshires and the rest of A and B Sqns of the Hussars picked their way up the almost undefended track, followed by 4th Somerset LI. By daybreak the summit was firmly held, despite heavy German bombardment, and 5th Wiltshires and C Sqn still held the crossroads below. 214th Brigade relieved the exhausted troops that morning.Having taken and then defended Mont Pinçon, 43rd (Wessex) Division participated in XXX Corps' advance. It crossed the Noireau on 15 August by a broken railway bridge and by wading, whereupon 204 Field Company RE set to work with a waterproofed bulldozer to build a tank ford and a trestle bridge named 'Genesis'. 553 Field Company and 207 Field Park Company then built the division's first Bailey bridge across the site of the railway bridge. The main opposition came from mortars and booby-trapped mines. Next morning 43rd Recce and the Sherwood Foresters were ready to continue the pursuit of the broken enemy, who were soon caught in the Falaise pocket.
Vernon Bridge
The breakout achieved, XXX Corps drove flat out for the River Seine (Operation Loopy), with 43rd (W) Division sent ahead to make an assault crossing at Vernon. For this operation it was assisted by the bridging specialists of 15th (Kent) GHQ Troops Royal Engineers, a medium artillery regiment and the Cromwell tanks of 15th/19th The King's Royal Hussars, the armoured reconnaissance regiment of 11th Armoured Division. US troops had already reached the west bank of the Seine, so the convoys of assault troops and bridging material moving eastwards had to be carefully coordinated to cross with US convoys repositioning to the south. The first convoy, Group One, consisted of nearly 1500 vehicles of 129th Brigade with its usual proportion of divisional artillery, engineers and support services, reinforced by 1st Worcesters. Some of the assault infantry rode in the DUKW amphibious trucks that were to carry them over the river. The group arrived at Vernon on the afternoon of 25 August, ready to begin the assault that evening against the defenders from 49th German Infantry Division.15th (Kent) GHQTRE was tasked with manning the DUKWs during the initial assault and then operating rafts until the first bridge could be laid. They also had storm boats in reserve but these had to be used in the first wave because launching points for DUKWs were hard to find. A 15-minute bombardment by the guns of 94th (Dorset Yeomanry) Field Regiment, 121st (West Riding) Medium Regiment (further back in Group Two) and C Sqn, 15th/19th Hussars, together with the heavy mortars of 8th Middlesex, was followed by a smoke barrage to cover the crossing at 19.00. On the right, 5th Wiltshires began crossing in eight storm boats manned by 15th (Kent) GHQTRE, but they grounded before reaching the far side, and were raked by machine gun fire. By the end of an hour only one boat remained. Only about a company had got across, and they were overrun during the night. Three of the four available DUKWs also grounded, the survivor ferrying across the rest of 5th Wiltshires in the dark. On the left, 4th Somerset LI got across in the storm boats relatively easily, but found that their bridgehead was on an island, and they were still cut off from the east bank, apart from a few men who scrambled over the wreckage of the railway bridge. 1st Worcesters failed to get over the broken road bridge into the village of Vernonnet, which was strongly held. In the dark 260th Field Company managed to bulldoze a slipway for the DUKWs, speeding up the crossing, and 129th Brigade got about a battalion and a half across in total, setting up a perimeter along the escarpment above the bridging site.The Wessex field companies now began work under fire on a Class 9 (9 tonne maximum load) Folding Boat Equipment (FBE) bridge while the infantry fought to expand the bridgehead and clear Vernonnet. The Worcesters got over the broken bridge, and light rafts began to get 6-pounder anti-tank guns and armoured cars of the recce regiment across, but work on the bridge was halted by heavy fire until 5th DCLI and 7th Somerset LI from newly-arrived 214th Brigade struggled across the broken road bridge into Vernonnet. By nightfall the bridgehead was reasonably secure, the FBE bridge named 'David' was complete and 15th (Kent) GHQTRE's rafting troops were arriving to get a tank ferry into operation before morning. 7th Army Troops Royal Engineers had also arrived to begin a Class 40 Bailey Bridge.Next morning (27 August) a squadron each of 15th/19th Hussars' Cromwells and 4th/7th DGs' Shermans were rafted across and held off an armoured counter-attack, the infantry and 43rd Recce cleared the banks and pushed through the forest until they were firmly established on the heights. By 28 August, 7th ATRE working under shellfire had built their Class 40 bridge, codenamed 'Goliath', and 11th Armoured was beginning to pour across to spearhead XXX Corps' advance. A second Class 40 named 'Saul' was built by 15th (Kent) GHQRE. After the Seine crossing, 43rd (Wessex) Division was 'grounded' while the rest of XXX Corps raced across northern France and Belgium. The division rested and received reinforcements (many of them experienced men drafted from the disbanded 59th (Staffordshire) Division).
Market Garden
When 43rd (Wessex) Division next moved, the war was now 250 miles (400 km) away. The first elements moved up to Brussels to protect headquarters and carry out engineering works, then the division concentrated at Diest to take part in Operation Market Garden, beginning on 17 September. In 'Garden', the ground part of the operation, XXX Corps was to link river crossings up to the Nederrijn at Arnhem via a 'carpet' of airborne troops. 43rd (Wessex) Division accompanied by 8th Armoured Bde was to follow Guards Armoured Division, carrying out assault crossings if any of the bridges were found to be destroyed, and guarding the 'corridor' to Arnhem. The advance up the only road ('Club Route') was slow but on 21 September 43rd (Wessex) Division caught up with the Guards at Nijmegen. Further progress was blocked by strong German forces, and 1st Airborne Division holding out at Arnhem was in a desperate plight. 43rd (Wessex) Division was ordered to pass through the Guards the following morning and make an all-out effort to reach the Nederrijn by a side road. The Germans were found to be dug in at Oosterhout and the countryside was so boggy that it was impossible to move vehicles off the road, making outflanking moves too slow. Despite the shortage of artillery ammunition coming up the precarious line of communication, the whole of the divisional artillery and heavy mortars were used, but it was evening before the division got through. 5th DCLI, supported by a squadron of 4th/7th DG, was ordered to make a dash over the last 10 miles (16 km) to get in touch with the Polish Parachute Brigade at Driel on the south bank of the Nederrijn. The journey took only 30 minutes, but the road behind the column was cut by German tanks that had to be hunted down and destroyed before support could be brought up. Attempts to launch DUKWs with supplies for 1st Airborne were unsuccessful.The whole of 23 September was taken up with getting support through to 5th DCLI and the Poles and in clearing the main road, though 43rd Recce Rgt was able to exploit westwards. During the night 5th Dorsets and the divisional engineers ferried a few hundred Poles across the Nederrijn in assault boats to reinforce 1st Airborne Division's shrinking perimeter. 4th Dorsets and the engineers made another assault crossing on the night of 24/25 September, suffering heavy casualties and getting few supplies across. By now 1st Airborne had been effectively destroyed, and the only course now was to evacuate the survivors. Their radios had been inoperable, and the only communication link had been through 64th (London) Medium Regiment, RA, attached to 43rd (Wessex) Division. Through this link the code word for the evacuation was passed, and during the night of 25/26 September a feint attack was made by 5th Wiltshires while around 2300 survivors of 1st Airborne and the Poles were ferried back to the south bank; few of 4th Dorsets made it back.The division was blamed by many airborne soldiers for its dilatory advance to the river, though the Corps commander, Lt-Gen Horrocks, defended the division, pointing out that it could not deploy any armoured vehicles (either 8th Armoured Bde or 43rd Recce Rgt's armoured cars and half-tracks) off the single road, nicknamed 'Hell's Highway', which was cut behind them on several occasions, and praising the division's hard fighting. Nevertheless, Maj-Gen Thomas replaced the commanding officer of 43rd Recce immediately after the battle.In the aftermath of Market Garden, 43rd (Wessex) Division was stationed on 'the Island' (between the Rivers Waal and Nederrijn). 43rd Recce Rgt, with 12th Battalion King's Royal Rifle Corps from 8th Armoured Bde under command, protected the division's open western flank. The concealed squadrons sent back reports, but were forbidden to engage the enemy in order to hide the extent of the position. However, on the night of 26/27 September a furious firefight broke out when the Germans crossed the river in strength and attempted to emplace anti-tank guns in 43rd Recce's hidden positions.The Germans launched a serious counter-attack from the east on 1 October, attacking 129th Bde strung out guarding the road from Nijmegen to the Nederrijn. 4th Somerset LI and 5th Wiltshires fought them off at Elst for 48 hours, the divisional artillery breaking up some of the attacks, and RAF medium bombers following up. Further north, 5th Dorsets beat off 116th Panzer Division and 7th Hampshires had to dislodge enemy troops who fortified themselves in some brick kilns, with the help of RAF Typhoons. On 5 October 43rd (Wessex) handed most of its positions over to the US 101st Airborne Division, leaving the anti-tank and mortar platoons and 5th DCLI, the divisional reserve, to help out. The attacks ended after one last attempt on 6 October. 43rd Wessex continued to hold the western part of the Island. The divisional historian records that "While the Division faced the monotony inseparable from static defence, the Reconnaissance Regiment fought a different type of war". This involved guarding the western end of the Island, cooperating with the Dutch Resistance and facilitating the escape across the river of British paratroops who had evaded capture.
Operation Clipper
43rd (Wessex) Division was then shifted east with XXX Corps to cooperate with the US Ninth Army by capturing the Geilenkirchen salient (Operation Clipper). XXX Corps had 43rd Wessex and 84th US Divisions under command for this attack, which entailed breaching the Siegfried Line defences and capturing a string of fortified villages. 84th US Division attacked on the morning of 18 November, supported by British specialist armour, and was through the line of pillboxes by midday. 214th Brigade then attacked on its left in the afternoon, led by 7th Somerset LI and tanks of 4th/7th DG, and took its first objective, the village of Neiderheide. But many of the tanks and most of the supply vehicles got bogged down while 1st Worcesters were threading their way through Gilrath to form up for the second phase towards Tripsrath. Without tanks, and the artillery having shifted to another target, 1st Worcesters struggled forward under shellfire and forced their way into the village at nightfall. The traffic jam of bogged vehicles disrupted the attacks by 5th Dorsets and 5th DCLI, but they got into Bauchem and Hocheide respectively, and patrols reached Geilenkirchen itself, which was surrounded. After driving off some counter-attacks by 15th Panzer Grenadier Division during the night, Geilenkirchen was captured after a stiff fight next day. But thereafter heavy rain turned the whole battlefield into mud while the infantry struggled to consolidate their positions under heavy shellfire from the Siegfried Line guns. One wood captured and grimly held first by 4th Dorsets and then 5th Dorsets for seven days became known as 'Dorset Wood'. On 22 November 5th DCLI suffered heavy casualties trying to take the high ground near Hoven to deny the enemy observation over the two Allied divisions. Overnight both sides shared the village of Hoven, before counter-attacks came in at dawn from 10th SS Panzer Division and 21st Panzer Division. Horrocks himself authorised the withdrawal of the DCLI before they were overwhelmed. Any further attempt to take Hoven was impossible due to the waterlogged state of the country, which then had to be defended in conditions resembling the worst of the Western Front in the First World War. Horrocks organised an ad hoc battalion from XXX Corps' service units to relieve Wessex infantry for rest. Planning was under way to renew the offensive when the Germans attacked in the Ardennes (the Battle of the Bulge) on 16 December.
Operation Blackcock
The division then later played a comparatively small part in the mainly American Battle of the Bulge, where it was placed on the River Meuse as a reserve. Once the German Ardennes Offensive had been halted, 43rd (Wessex) Division returned to the offensive in early 1945 in Operation Blackcock to reduce the Roer Triangle, though exploitation was prevented by bad weather.
Operation Veritable
The 43rd later played a large part in Operation Veritable attached to First Canadian Army, through the month-long fighting in the Reichswald to capture Kleve, roll up the Siegfried Line defences, cross the Goch escarpment and seize Xanten on the Rhine.
Across the Rhine
43rd (Wessex) Division was given a follow-up task in the assault crossing of the Rhine (Operation Plunder). Its leading brigade crossed the river on 25 March behind 51st (Highland) Division, which had carried the assault on the night of 23/24 March. It found itself in immediate combat, but had broken through by 29 March. During the subsequent pursuit, 43rd (Wessex) Division was given the task of opening 'Club Route' for XXX Corps. The division was divided into five battle groups for the first 25 miles (40 km) drive, incorporating units of 8th Armoured Brigade. The advance began on 30 March: German rearguards were either overcome or bypassed, and the Twente Canal was crossed, with troops of 129th Infantry Bde and 8th Armoured Bde liberating Lochem on 1–2 April. The pursuit continued through April and ended with the capture of Bremen and XXX Corps' drive into the Cuxhaven peninsula. Hostilities ended on 5 May after the German surrender at Lüneburg Heath.After a period as occupation forces in XXX Corps' district, 43rd (Wessex) Division's HQ and TA units were demobilised at the war's end. Throughout the North West Europe Campaign the 43rd (Wessex) Division, like so many other Allied divisions that fought from Normandy to Germany, had suffered very heavy casualties with the majority of them, 80% in some units, being suffered by the average Tommy in the infantry battalions. From June 1944 to May 1945 the 43rd (Wessex) Division, or the Yellow Devils or British SS Division as known by the Germans, had suffered well over 12,500 casualties, with almost 3,000 killed in action.
43rd (Wessex) Infantry Division Order of Battle 1939–1945128th Infantry Brigade (left 6 June 1942)
1/4th Battalion, Hampshire Regiment
2/4th Battalion, Hampshire Regiment
5th Battalion, Hampshire Regiment
128th Infantry Brigade Anti-Tank Company (formed 19 June 1940, disbanded 20 December 1941)129th Infantry Brigade
4th Battalion, Somerset Light Infantry
4th Battalion, Wiltshire Regiment
5th Battalion, Wiltshire Regiment
129th Infantry Brigade Anti-Tank Company (formed 14 May 1940, disbanded 20 December 1941)130th Infantry Brigade
7th Battalion, Hampshire Regiment
4th Battalion, Dorsetshire Regiment
5th Battalion, Dorsetshire Regiment
130th Infantry Brigade Anti-Tank Company (formed 17 May 1940, disbanded 20 December 1941)25th Tank Brigade (from 1 June 1942, left 2 September 1942)
51st (Leeds Rifles) Royal Tank Regiment
11th Royal Tank Regiment
142nd Regiment Royal Armoured Corps34th Tank Brigade (from 3 September 1942, left 10 September 1943)
North Irish Horse (left 3 September 1942)
147th Regiment Royal Armoured Corps
153rd Regiment Royal Armoured Corps
151st Regiment Royal Armoured Corps (from 3 September 1942)214th Infantry Brigade (from 5 September 1943)
7th Battalion, Somerset Light Infantry
5th Battalion, Duke of Cornwall's Light Infantry
9th Battalion, Somerset Light Infantry (left 30 September 1943)
1st Battalion, Worcestershire Regiment (from 30 September 1943)Divisional Troops
1/8th Battalion, Middlesex Regiment (joined as Machine Gun Battalion from 18 November 1941, redesignated 8th Battalion May 1942, left 1 October 1942, rejoined as Support Battalion 1 October 1943, again as MG Battalion 28 February 1944)
48th Battalion, Reconnaissance Corps (converted from 5th Battalion, Gloucestershire Regiment 20 November 1941, redesignated 43rd Battalion 1 January 1942, later 43rd Regiment 6 June 1942, finally 43rd (Wessex) Reconnaissance Regiment (The Gloucestershire Regiment), Royal Armoured Corps 1 January 1944)
94th (Queen's Own Dorset Yeomanry) Field Regiment, Royal Artillery
112th (Wessex) Field Regiment, Royal Artillery
141st (Queen's Own Dorset Yeomanry) Field Regiment, Royal Artillery (left 8 June 1942)
179th Field Regiment, Royal Artillery (from 9 June 1942)
59th (Duke of Connaught's Own) Anti-Tank Regiment, Royal Artillery
110th Light Anti-Aircraft Regiment, Royal Artillery (converted from 7th Battalion, Dorsetshire Regiment, joined 23 March 1941)
43rd (Wessex) Divisional Engineers204th (Wessex) Field Company, Royal Engineers
260th Field Company, Royal Engineers
553rd Field Company, Royal Engineers (from 13 January 1940)
207th (Wessex) Field Park Company, Royal Engineers
13th Bridging Platoon, Royal Engineers (from 1 October 1943)
43rd (Wessex) Divisional Signals, Royal Corps of Signals
Royal Army Service Corps
54, 504, 505, 506 Companies
Royal Army Medical Corps
129, 130, 213 Field Ambulances
14, 15, 38 Field Dressing Stations
38 Field Hygiene Section
Royal Army Ordnance Corps
43 Ordnance Field Park
306 Mobile Laundry and Bath Unit
Royal Electrical and Mechanical Engineers
129, 130, 214 Infantry Brigade Workshops
43 Wessex Division Provost Company, Royal Military Police
57 Field Security Section
Postal Unit
Postwar
The TA was reconstituted from 1 January 1947 and its units and formations including 43rd (Wessex) Infantry Division were reformed. However, the TA saw large numbers of amalgamations from 1950 onwards. In 1961 the division became a district headquarters as 43rd (Wessex) Division/District, and it was disbanded on the reduction of the TA into the Territorial and Army Volunteer Reserve on 1 April 1967, when many individual TA units lost their identities. The district headquarters itself formed the core of the structure for the creation of South West District under HQ UK Land Forces in 1972.
43rd (Wessex) Infantry Division Order of Battle 1947128 Infantry Brigade
4th Battalion, Royal Hampshire Regiment at Winchester
4th Battalion, Oxfordshire and Buckinghamshire Light Infantry at Oxford
4th/6th Battalion, Royal Berkshire Regiment at Reading129 Infantry Brigade
4th Battalion, Somerset Light Infantry at Bath
5th Battalion, Gloucestershire Regiment at Gloucester
4th Battalion, Wiltshire Regiment at Trowbridge130 (West Country) Infantry Brigade
4th Battalion, Devonshire Regiment at Exeter
5th (Prince of Wales's) Battalion, Devonshire Regiment at Plymouth
4th/5th Battalion, Duke of Cornwall's Light Infantry at Truro
4th Battalion, Dorsetshire Regiment at DorchesterRoyal Armoured Corps
Royal Wiltshire Yeomanry at SwindonRoyal Artillery
294 (Queen's Own Dorset Yeomanry) Field Regiment at Sherborne
296 (Royal Devon Yeomanry) Field Regiment at Exeter
387 (Queen's Own Oxfordshire Hussars) Field Regiment at Oxford
383 (Duke of Connaught's Royal Hampshire) Anti-Tank Regiment at Portsmouth
396 (Devon) Light Anti-Aircraft Regiment at Devonport
883 Locating Battery at BristolRoyal Engineers
110 Field Engineer Regiment204 Field Squadron
226 Field Squadron
260 Field Squadron
207 Field Park SquadronRoyal Corps of Signals
43rd (Wessex) Infantry Division Signal Regiment at Taunton 1 Squadron at Exeter
2 Squadron at Taunton
3 Squadron at Torquay, later BristolRoyal Army Service Corps
43 (Wessex) Infantry Divisional Column at Bristol504 Company at Swindon
505 Company at Didcot
506 Company at Plymouth
1567 Company at Plymouth
43 Ordnance Field Park, Royal Army Ordnance Corps
43 Divisional Royal Electrical and Mechanical Engineers
43 Divisional Royal Army Medical Corps
Commanders
The following officers commanded the division at various times:
Insignia
The banner of the kings of Wessex bore a golden Wyvern, a dragon with two eagle-like legs and the barbed tail of a snake. The 43rd (Wessex) Division adopted the golden wyvern on a blue square as its formation sign in 1935.
Memorials
The Hill 112 memorial was erected by the divisional engineers and later taken over by the Commonwealth War Graves Commission with an endowment from the Memorial Fund. The first memorial in England was at Castle Hill, Mere, in Wiltshire, acquired on a 199-year lease from the Duchy of Cornwall and entrusted to the Parish Council of Mere. Next the fund acquired Wynyard's Gap near Crewkerne, Somerset. Finally, Sir Richard Onslow (formerly of the Duke of Cornwall's Light Infantry) presented Rough Tor on Bodmin Moor to the National Trust as a memorial. The Roll of Honour is in the War Memorial Chapel in Salisbury Cathedral.A memorial stone stands at the end of a lane named 'Somerset' in Lochem, Netherlands, showing the Wessex Wyvern and listing 4th Bn Somerset Light Infantry, 4th Bn Wiltshire Regiment and units of 8th Armoured Bde who liberated Lochem on 1–2 April 1945. The horizontal inscription reads 'All the way from Normandy'.
See also
List of British divisions in World War I
List of British divisions in World War II
British Army Order of Battle (September 1939)
Notes
References
Bibliography
External links
Mark Conrad, The British Army, 1914 (archive site)
British Army units from 1945 on
Divisional insignia
The Long, Long Trail
Orders of Battle at Patriot Files
Graham Watson, The Territorial Army 1947
World War II Armed Forces
|
conflict
|
{
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43510
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"text": [
"World War II"
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|
Al Barsha (Arabic: البرشاء) is a collection of sub-communities in Dubai, United Arab Emirates (UAE). Al Barsha is one of the newer residential developments, and is located in west Dubai, south of Al Sufouh. Al Barsha is bounded by E 11 (Sheikh Zayed Road) and E 311 (Sheikh Mohammad Bin Zayed Road).
Schools
Dubai American Academy
American School of Dubai
Dubai International Academy
Global Indian International School
Nord Anglia International School Dubai
Al Mawakeb School - Al Barsha
Dwight School Dubai
Attractions
Dubai Miracle Garden
Mall of the Emirates
Ski Dubai
Dubai Butterfly Garden
Al Jaber Gallery
Al Barsha Pond Park
Al Barsha Mall
Dreamscape
History of Cinema Museum
Dubai Community Theater and Arts Centre
== References ==
|
country
|
{
"answer_start": [
73
],
"text": [
"United Arab Emirates"
]
}
|
Al Barsha (Arabic: البرشاء) is a collection of sub-communities in Dubai, United Arab Emirates (UAE). Al Barsha is one of the newer residential developments, and is located in west Dubai, south of Al Sufouh. Al Barsha is bounded by E 11 (Sheikh Zayed Road) and E 311 (Sheikh Mohammad Bin Zayed Road).
Schools
Dubai American Academy
American School of Dubai
Dubai International Academy
Global Indian International School
Nord Anglia International School Dubai
Al Mawakeb School - Al Barsha
Dwight School Dubai
Attractions
Dubai Miracle Garden
Mall of the Emirates
Ski Dubai
Dubai Butterfly Garden
Al Jaber Gallery
Al Barsha Pond Park
Al Barsha Mall
Dreamscape
History of Cinema Museum
Dubai Community Theater and Arts Centre
== References ==
|
Commons category
|
{
"answer_start": [
0
],
"text": [
"Al Barsha"
]
}
|
Al Barsha (Arabic: البرشاء) is a collection of sub-communities in Dubai, United Arab Emirates (UAE). Al Barsha is one of the newer residential developments, and is located in west Dubai, south of Al Sufouh. Al Barsha is bounded by E 11 (Sheikh Zayed Road) and E 311 (Sheikh Mohammad Bin Zayed Road).
Schools
Dubai American Academy
American School of Dubai
Dubai International Academy
Global Indian International School
Nord Anglia International School Dubai
Al Mawakeb School - Al Barsha
Dwight School Dubai
Attractions
Dubai Miracle Garden
Mall of the Emirates
Ski Dubai
Dubai Butterfly Garden
Al Jaber Gallery
Al Barsha Pond Park
Al Barsha Mall
Dreamscape
History of Cinema Museum
Dubai Community Theater and Arts Centre
== References ==
|
width
|
{
"answer_start": [
233
],
"text": [
"11"
]
}
|
Clement Lowell Harriss (1912–2009) was an American economist, a past president of the National Tax Association and a former executive director of the Academy of Political Science. He was one of the United States' leading tax experts and the author of highly regarded economics textbooks and other books on economic subjects. He was professor emeritus of economics at Columbia University and taught there for 43 years. He was the professor for whom the C. Lowell Harriss Professorship of Economics and International Affairs at the School of International and Public Affairs at Columbia was named.
Early life
Harriss was born in Fairbury, Nebraska. He was the son of Riley Clement Harriss and Alice Mary Hunt. He was a summa cum laude graduate of Harvard. Upon graduating from Harvard, he was awarded a Sheldon Fellowship which funded his travel for 13 months throughout Europe, Turkey, the Balkans, and Northern Africa. He arrived in Berlin the day Hitler began his presidency. He also undertook graduate study at the University of Chicago and earned a Ph.D. from Columbia University.
Teaching career
In addition to his long affiliation with Columbia University, Harriss taught at Stanford University, the University of California at Berkeley, Princeton University, and Yale. He also held posts at the Wharton School, the New School for Social Research and Pace University. He accepted the posthumous 1996 Nobel Prize in Economics for his colleague at Columbia, William Vickrey, because the announcement of the prize occurred just three days before Vickrey died. Vickrey had been awarded the prize along with James Mirrlees for research on the economic theory of incentives.
Books
Gift Taxation in the U.S. (1940)
History and Policies of the Home Owners Loan Corporation (1951)
The American Economy: Principles, Practices, Policies (1953)
The Good Earth of America (1974)
Money and Banking (1961)
Economics (1966)
Constitutional Restrictions on Property Taxing and Borrowing Powers In New York (1967)
Innovations in Tax Policy and Other Essays (1972)
Inflation: Long-Term Problems (1973)
Government Spending and Land Values (1973)
The Property Tax and Local Finance (1983)The Control of Federal Spending (1985)
Professional associations
He was a member of the American Economic Association, the Mont Pelerin Society and the Royal Economic Society. In 1979 he served on the board of directors of the Institute for Research on the Economics of Taxation. He was a past president of the National Tax Association. He was Executive Director (1981–87) of the Academy of Political Science. He worked as a consultant to both the U.S. Treasury and the Agency for International Development.
Personal
On June 1, 1936 he married Agnes Bennett Murphy, and they had two daughters and two sons. He served in the U.S. Air Corps (1943-1946). His party affiliation was Republican. He was a member of the University Club of New York and Philadelphia Society. Agnes Harriss predeceased her husband in 1992.
Death and legacy
Harriss died of natural causes on December 14, 2009 at his home in Bronxville, New York, at the age of 97. He was one of the few remaining economists to have experienced the American Great Depression. Writing for Fortune shortly after Harriss's death, Ben Stein recalled that Harriss had been one of his most influential professors at Columbia. Stein wrote that "a huge amount of what is my stock in trade as an economist and writer about economics came from that man."The American Institute for Economic Research established a memorial scholarship program in his honor to be "given to enrolled students who have demonstrated innovative and creative accomplishments in businesses they are operating while attending college." The Lincoln Institute of Land Policy, where Harriss had served on the board of directors, established a dissertation fellowship program in his name.
== References ==
|
place of birth
|
{
"answer_start": [
628
],
"text": [
"Fairbury"
]
}
|
Clement Lowell Harriss (1912–2009) was an American economist, a past president of the National Tax Association and a former executive director of the Academy of Political Science. He was one of the United States' leading tax experts and the author of highly regarded economics textbooks and other books on economic subjects. He was professor emeritus of economics at Columbia University and taught there for 43 years. He was the professor for whom the C. Lowell Harriss Professorship of Economics and International Affairs at the School of International and Public Affairs at Columbia was named.
Early life
Harriss was born in Fairbury, Nebraska. He was the son of Riley Clement Harriss and Alice Mary Hunt. He was a summa cum laude graduate of Harvard. Upon graduating from Harvard, he was awarded a Sheldon Fellowship which funded his travel for 13 months throughout Europe, Turkey, the Balkans, and Northern Africa. He arrived in Berlin the day Hitler began his presidency. He also undertook graduate study at the University of Chicago and earned a Ph.D. from Columbia University.
Teaching career
In addition to his long affiliation with Columbia University, Harriss taught at Stanford University, the University of California at Berkeley, Princeton University, and Yale. He also held posts at the Wharton School, the New School for Social Research and Pace University. He accepted the posthumous 1996 Nobel Prize in Economics for his colleague at Columbia, William Vickrey, because the announcement of the prize occurred just three days before Vickrey died. Vickrey had been awarded the prize along with James Mirrlees for research on the economic theory of incentives.
Books
Gift Taxation in the U.S. (1940)
History and Policies of the Home Owners Loan Corporation (1951)
The American Economy: Principles, Practices, Policies (1953)
The Good Earth of America (1974)
Money and Banking (1961)
Economics (1966)
Constitutional Restrictions on Property Taxing and Borrowing Powers In New York (1967)
Innovations in Tax Policy and Other Essays (1972)
Inflation: Long-Term Problems (1973)
Government Spending and Land Values (1973)
The Property Tax and Local Finance (1983)The Control of Federal Spending (1985)
Professional associations
He was a member of the American Economic Association, the Mont Pelerin Society and the Royal Economic Society. In 1979 he served on the board of directors of the Institute for Research on the Economics of Taxation. He was a past president of the National Tax Association. He was Executive Director (1981–87) of the Academy of Political Science. He worked as a consultant to both the U.S. Treasury and the Agency for International Development.
Personal
On June 1, 1936 he married Agnes Bennett Murphy, and they had two daughters and two sons. He served in the U.S. Air Corps (1943-1946). His party affiliation was Republican. He was a member of the University Club of New York and Philadelphia Society. Agnes Harriss predeceased her husband in 1992.
Death and legacy
Harriss died of natural causes on December 14, 2009 at his home in Bronxville, New York, at the age of 97. He was one of the few remaining economists to have experienced the American Great Depression. Writing for Fortune shortly after Harriss's death, Ben Stein recalled that Harriss had been one of his most influential professors at Columbia. Stein wrote that "a huge amount of what is my stock in trade as an economist and writer about economics came from that man."The American Institute for Economic Research established a memorial scholarship program in his honor to be "given to enrolled students who have demonstrated innovative and creative accomplishments in businesses they are operating while attending college." The Lincoln Institute of Land Policy, where Harriss had served on the board of directors, established a dissertation fellowship program in his name.
== References ==
|
place of death
|
{
"answer_start": [
3076
],
"text": [
"Bronxville"
]
}
|
Clement Lowell Harriss (1912–2009) was an American economist, a past president of the National Tax Association and a former executive director of the Academy of Political Science. He was one of the United States' leading tax experts and the author of highly regarded economics textbooks and other books on economic subjects. He was professor emeritus of economics at Columbia University and taught there for 43 years. He was the professor for whom the C. Lowell Harriss Professorship of Economics and International Affairs at the School of International and Public Affairs at Columbia was named.
Early life
Harriss was born in Fairbury, Nebraska. He was the son of Riley Clement Harriss and Alice Mary Hunt. He was a summa cum laude graduate of Harvard. Upon graduating from Harvard, he was awarded a Sheldon Fellowship which funded his travel for 13 months throughout Europe, Turkey, the Balkans, and Northern Africa. He arrived in Berlin the day Hitler began his presidency. He also undertook graduate study at the University of Chicago and earned a Ph.D. from Columbia University.
Teaching career
In addition to his long affiliation with Columbia University, Harriss taught at Stanford University, the University of California at Berkeley, Princeton University, and Yale. He also held posts at the Wharton School, the New School for Social Research and Pace University. He accepted the posthumous 1996 Nobel Prize in Economics for his colleague at Columbia, William Vickrey, because the announcement of the prize occurred just three days before Vickrey died. Vickrey had been awarded the prize along with James Mirrlees for research on the economic theory of incentives.
Books
Gift Taxation in the U.S. (1940)
History and Policies of the Home Owners Loan Corporation (1951)
The American Economy: Principles, Practices, Policies (1953)
The Good Earth of America (1974)
Money and Banking (1961)
Economics (1966)
Constitutional Restrictions on Property Taxing and Borrowing Powers In New York (1967)
Innovations in Tax Policy and Other Essays (1972)
Inflation: Long-Term Problems (1973)
Government Spending and Land Values (1973)
The Property Tax and Local Finance (1983)The Control of Federal Spending (1985)
Professional associations
He was a member of the American Economic Association, the Mont Pelerin Society and the Royal Economic Society. In 1979 he served on the board of directors of the Institute for Research on the Economics of Taxation. He was a past president of the National Tax Association. He was Executive Director (1981–87) of the Academy of Political Science. He worked as a consultant to both the U.S. Treasury and the Agency for International Development.
Personal
On June 1, 1936 he married Agnes Bennett Murphy, and they had two daughters and two sons. He served in the U.S. Air Corps (1943-1946). His party affiliation was Republican. He was a member of the University Club of New York and Philadelphia Society. Agnes Harriss predeceased her husband in 1992.
Death and legacy
Harriss died of natural causes on December 14, 2009 at his home in Bronxville, New York, at the age of 97. He was one of the few remaining economists to have experienced the American Great Depression. Writing for Fortune shortly after Harriss's death, Ben Stein recalled that Harriss had been one of his most influential professors at Columbia. Stein wrote that "a huge amount of what is my stock in trade as an economist and writer about economics came from that man."The American Institute for Economic Research established a memorial scholarship program in his honor to be "given to enrolled students who have demonstrated innovative and creative accomplishments in businesses they are operating while attending college." The Lincoln Institute of Land Policy, where Harriss had served on the board of directors, established a dissertation fellowship program in his name.
== References ==
|
educated at
|
{
"answer_start": [
367
],
"text": [
"Columbia University"
]
}
|
Clement Lowell Harriss (1912–2009) was an American economist, a past president of the National Tax Association and a former executive director of the Academy of Political Science. He was one of the United States' leading tax experts and the author of highly regarded economics textbooks and other books on economic subjects. He was professor emeritus of economics at Columbia University and taught there for 43 years. He was the professor for whom the C. Lowell Harriss Professorship of Economics and International Affairs at the School of International and Public Affairs at Columbia was named.
Early life
Harriss was born in Fairbury, Nebraska. He was the son of Riley Clement Harriss and Alice Mary Hunt. He was a summa cum laude graduate of Harvard. Upon graduating from Harvard, he was awarded a Sheldon Fellowship which funded his travel for 13 months throughout Europe, Turkey, the Balkans, and Northern Africa. He arrived in Berlin the day Hitler began his presidency. He also undertook graduate study at the University of Chicago and earned a Ph.D. from Columbia University.
Teaching career
In addition to his long affiliation with Columbia University, Harriss taught at Stanford University, the University of California at Berkeley, Princeton University, and Yale. He also held posts at the Wharton School, the New School for Social Research and Pace University. He accepted the posthumous 1996 Nobel Prize in Economics for his colleague at Columbia, William Vickrey, because the announcement of the prize occurred just three days before Vickrey died. Vickrey had been awarded the prize along with James Mirrlees for research on the economic theory of incentives.
Books
Gift Taxation in the U.S. (1940)
History and Policies of the Home Owners Loan Corporation (1951)
The American Economy: Principles, Practices, Policies (1953)
The Good Earth of America (1974)
Money and Banking (1961)
Economics (1966)
Constitutional Restrictions on Property Taxing and Borrowing Powers In New York (1967)
Innovations in Tax Policy and Other Essays (1972)
Inflation: Long-Term Problems (1973)
Government Spending and Land Values (1973)
The Property Tax and Local Finance (1983)The Control of Federal Spending (1985)
Professional associations
He was a member of the American Economic Association, the Mont Pelerin Society and the Royal Economic Society. In 1979 he served on the board of directors of the Institute for Research on the Economics of Taxation. He was a past president of the National Tax Association. He was Executive Director (1981–87) of the Academy of Political Science. He worked as a consultant to both the U.S. Treasury and the Agency for International Development.
Personal
On June 1, 1936 he married Agnes Bennett Murphy, and they had two daughters and two sons. He served in the U.S. Air Corps (1943-1946). His party affiliation was Republican. He was a member of the University Club of New York and Philadelphia Society. Agnes Harriss predeceased her husband in 1992.
Death and legacy
Harriss died of natural causes on December 14, 2009 at his home in Bronxville, New York, at the age of 97. He was one of the few remaining economists to have experienced the American Great Depression. Writing for Fortune shortly after Harriss's death, Ben Stein recalled that Harriss had been one of his most influential professors at Columbia. Stein wrote that "a huge amount of what is my stock in trade as an economist and writer about economics came from that man."The American Institute for Economic Research established a memorial scholarship program in his honor to be "given to enrolled students who have demonstrated innovative and creative accomplishments in businesses they are operating while attending college." The Lincoln Institute of Land Policy, where Harriss had served on the board of directors, established a dissertation fellowship program in his name.
== References ==
|
field of work
|
{
"answer_start": [
267
],
"text": [
"economics"
]
}
|
Clement Lowell Harriss (1912–2009) was an American economist, a past president of the National Tax Association and a former executive director of the Academy of Political Science. He was one of the United States' leading tax experts and the author of highly regarded economics textbooks and other books on economic subjects. He was professor emeritus of economics at Columbia University and taught there for 43 years. He was the professor for whom the C. Lowell Harriss Professorship of Economics and International Affairs at the School of International and Public Affairs at Columbia was named.
Early life
Harriss was born in Fairbury, Nebraska. He was the son of Riley Clement Harriss and Alice Mary Hunt. He was a summa cum laude graduate of Harvard. Upon graduating from Harvard, he was awarded a Sheldon Fellowship which funded his travel for 13 months throughout Europe, Turkey, the Balkans, and Northern Africa. He arrived in Berlin the day Hitler began his presidency. He also undertook graduate study at the University of Chicago and earned a Ph.D. from Columbia University.
Teaching career
In addition to his long affiliation with Columbia University, Harriss taught at Stanford University, the University of California at Berkeley, Princeton University, and Yale. He also held posts at the Wharton School, the New School for Social Research and Pace University. He accepted the posthumous 1996 Nobel Prize in Economics for his colleague at Columbia, William Vickrey, because the announcement of the prize occurred just three days before Vickrey died. Vickrey had been awarded the prize along with James Mirrlees for research on the economic theory of incentives.
Books
Gift Taxation in the U.S. (1940)
History and Policies of the Home Owners Loan Corporation (1951)
The American Economy: Principles, Practices, Policies (1953)
The Good Earth of America (1974)
Money and Banking (1961)
Economics (1966)
Constitutional Restrictions on Property Taxing and Borrowing Powers In New York (1967)
Innovations in Tax Policy and Other Essays (1972)
Inflation: Long-Term Problems (1973)
Government Spending and Land Values (1973)
The Property Tax and Local Finance (1983)The Control of Federal Spending (1985)
Professional associations
He was a member of the American Economic Association, the Mont Pelerin Society and the Royal Economic Society. In 1979 he served on the board of directors of the Institute for Research on the Economics of Taxation. He was a past president of the National Tax Association. He was Executive Director (1981–87) of the Academy of Political Science. He worked as a consultant to both the U.S. Treasury and the Agency for International Development.
Personal
On June 1, 1936 he married Agnes Bennett Murphy, and they had two daughters and two sons. He served in the U.S. Air Corps (1943-1946). His party affiliation was Republican. He was a member of the University Club of New York and Philadelphia Society. Agnes Harriss predeceased her husband in 1992.
Death and legacy
Harriss died of natural causes on December 14, 2009 at his home in Bronxville, New York, at the age of 97. He was one of the few remaining economists to have experienced the American Great Depression. Writing for Fortune shortly after Harriss's death, Ben Stein recalled that Harriss had been one of his most influential professors at Columbia. Stein wrote that "a huge amount of what is my stock in trade as an economist and writer about economics came from that man."The American Institute for Economic Research established a memorial scholarship program in his honor to be "given to enrolled students who have demonstrated innovative and creative accomplishments in businesses they are operating while attending college." The Lincoln Institute of Land Policy, where Harriss had served on the board of directors, established a dissertation fellowship program in his name.
== References ==
|
occupation
|
{
"answer_start": [
51
],
"text": [
"economist"
]
}
|
Clement Lowell Harriss (1912–2009) was an American economist, a past president of the National Tax Association and a former executive director of the Academy of Political Science. He was one of the United States' leading tax experts and the author of highly regarded economics textbooks and other books on economic subjects. He was professor emeritus of economics at Columbia University and taught there for 43 years. He was the professor for whom the C. Lowell Harriss Professorship of Economics and International Affairs at the School of International and Public Affairs at Columbia was named.
Early life
Harriss was born in Fairbury, Nebraska. He was the son of Riley Clement Harriss and Alice Mary Hunt. He was a summa cum laude graduate of Harvard. Upon graduating from Harvard, he was awarded a Sheldon Fellowship which funded his travel for 13 months throughout Europe, Turkey, the Balkans, and Northern Africa. He arrived in Berlin the day Hitler began his presidency. He also undertook graduate study at the University of Chicago and earned a Ph.D. from Columbia University.
Teaching career
In addition to his long affiliation with Columbia University, Harriss taught at Stanford University, the University of California at Berkeley, Princeton University, and Yale. He also held posts at the Wharton School, the New School for Social Research and Pace University. He accepted the posthumous 1996 Nobel Prize in Economics for his colleague at Columbia, William Vickrey, because the announcement of the prize occurred just three days before Vickrey died. Vickrey had been awarded the prize along with James Mirrlees for research on the economic theory of incentives.
Books
Gift Taxation in the U.S. (1940)
History and Policies of the Home Owners Loan Corporation (1951)
The American Economy: Principles, Practices, Policies (1953)
The Good Earth of America (1974)
Money and Banking (1961)
Economics (1966)
Constitutional Restrictions on Property Taxing and Borrowing Powers In New York (1967)
Innovations in Tax Policy and Other Essays (1972)
Inflation: Long-Term Problems (1973)
Government Spending and Land Values (1973)
The Property Tax and Local Finance (1983)The Control of Federal Spending (1985)
Professional associations
He was a member of the American Economic Association, the Mont Pelerin Society and the Royal Economic Society. In 1979 he served on the board of directors of the Institute for Research on the Economics of Taxation. He was a past president of the National Tax Association. He was Executive Director (1981–87) of the Academy of Political Science. He worked as a consultant to both the U.S. Treasury and the Agency for International Development.
Personal
On June 1, 1936 he married Agnes Bennett Murphy, and they had two daughters and two sons. He served in the U.S. Air Corps (1943-1946). His party affiliation was Republican. He was a member of the University Club of New York and Philadelphia Society. Agnes Harriss predeceased her husband in 1992.
Death and legacy
Harriss died of natural causes on December 14, 2009 at his home in Bronxville, New York, at the age of 97. He was one of the few remaining economists to have experienced the American Great Depression. Writing for Fortune shortly after Harriss's death, Ben Stein recalled that Harriss had been one of his most influential professors at Columbia. Stein wrote that "a huge amount of what is my stock in trade as an economist and writer about economics came from that man."The American Institute for Economic Research established a memorial scholarship program in his honor to be "given to enrolled students who have demonstrated innovative and creative accomplishments in businesses they are operating while attending college." The Lincoln Institute of Land Policy, where Harriss had served on the board of directors, established a dissertation fellowship program in his name.
== References ==
|
employer
|
{
"answer_start": [
367
],
"text": [
"Columbia University"
]
}
|
Clement Lowell Harriss (1912–2009) was an American economist, a past president of the National Tax Association and a former executive director of the Academy of Political Science. He was one of the United States' leading tax experts and the author of highly regarded economics textbooks and other books on economic subjects. He was professor emeritus of economics at Columbia University and taught there for 43 years. He was the professor for whom the C. Lowell Harriss Professorship of Economics and International Affairs at the School of International and Public Affairs at Columbia was named.
Early life
Harriss was born in Fairbury, Nebraska. He was the son of Riley Clement Harriss and Alice Mary Hunt. He was a summa cum laude graduate of Harvard. Upon graduating from Harvard, he was awarded a Sheldon Fellowship which funded his travel for 13 months throughout Europe, Turkey, the Balkans, and Northern Africa. He arrived in Berlin the day Hitler began his presidency. He also undertook graduate study at the University of Chicago and earned a Ph.D. from Columbia University.
Teaching career
In addition to his long affiliation with Columbia University, Harriss taught at Stanford University, the University of California at Berkeley, Princeton University, and Yale. He also held posts at the Wharton School, the New School for Social Research and Pace University. He accepted the posthumous 1996 Nobel Prize in Economics for his colleague at Columbia, William Vickrey, because the announcement of the prize occurred just three days before Vickrey died. Vickrey had been awarded the prize along with James Mirrlees for research on the economic theory of incentives.
Books
Gift Taxation in the U.S. (1940)
History and Policies of the Home Owners Loan Corporation (1951)
The American Economy: Principles, Practices, Policies (1953)
The Good Earth of America (1974)
Money and Banking (1961)
Economics (1966)
Constitutional Restrictions on Property Taxing and Borrowing Powers In New York (1967)
Innovations in Tax Policy and Other Essays (1972)
Inflation: Long-Term Problems (1973)
Government Spending and Land Values (1973)
The Property Tax and Local Finance (1983)The Control of Federal Spending (1985)
Professional associations
He was a member of the American Economic Association, the Mont Pelerin Society and the Royal Economic Society. In 1979 he served on the board of directors of the Institute for Research on the Economics of Taxation. He was a past president of the National Tax Association. He was Executive Director (1981–87) of the Academy of Political Science. He worked as a consultant to both the U.S. Treasury and the Agency for International Development.
Personal
On June 1, 1936 he married Agnes Bennett Murphy, and they had two daughters and two sons. He served in the U.S. Air Corps (1943-1946). His party affiliation was Republican. He was a member of the University Club of New York and Philadelphia Society. Agnes Harriss predeceased her husband in 1992.
Death and legacy
Harriss died of natural causes on December 14, 2009 at his home in Bronxville, New York, at the age of 97. He was one of the few remaining economists to have experienced the American Great Depression. Writing for Fortune shortly after Harriss's death, Ben Stein recalled that Harriss had been one of his most influential professors at Columbia. Stein wrote that "a huge amount of what is my stock in trade as an economist and writer about economics came from that man."The American Institute for Economic Research established a memorial scholarship program in his honor to be "given to enrolled students who have demonstrated innovative and creative accomplishments in businesses they are operating while attending college." The Lincoln Institute of Land Policy, where Harriss had served on the board of directors, established a dissertation fellowship program in his name.
== References ==
|
given name
|
{
"answer_start": [
452
],
"text": [
"C."
]
}
|
Alan Ernest Owen FRSE FRSC FIP (7 October 1928 – 28 January 1999) was an English physicist specialising in glass technology.
Life
He was born on 7 October 1928 in Hastings on the Sussex coast. He studied science at the Brighton College of Technology 1949 to 1953. His initial role was as a research chemist for the English China Clay Research Laboratories at St Austell in Cornwall. He then moved to the University of Sheffield, researching the electronic qualities of glass, and gained a doctorate there (DSc). In 1959 he went to Westinghouse Electronic Systems in Baltimore in the United States, where he stayed until 1962. He then worked at CNRS in Toulouse and at the Center for Solid State Electronics Research at Arizona State University.In 1967 he settled in Edinburgh as a senior lecturer at the University of Edinburgh He was promoted to Reader in 1969 and Professor of physical electronics in 1981.In 1981 he was elected a Fellow of the Royal Society of Edinburgh. His proposers were William Cochran, William Farvis, Robert Allan Smith, Gordon Craig, Nicholas Kemmer and Richard Sillitto.He retired in 1985 and died of a heart attack on 28 January 1999.
Publications
Electric Conduction and Dielectric Relaxation in Glass (1963)He was editor of Physics and Chemistry of Glasses, published by the Society of Glass Technology.
== References ==
|
occupation
|
{
"answer_start": [
81
],
"text": [
"physicist"
]
}
|
Alan Ernest Owen FRSE FRSC FIP (7 October 1928 – 28 January 1999) was an English physicist specialising in glass technology.
Life
He was born on 7 October 1928 in Hastings on the Sussex coast. He studied science at the Brighton College of Technology 1949 to 1953. His initial role was as a research chemist for the English China Clay Research Laboratories at St Austell in Cornwall. He then moved to the University of Sheffield, researching the electronic qualities of glass, and gained a doctorate there (DSc). In 1959 he went to Westinghouse Electronic Systems in Baltimore in the United States, where he stayed until 1962. He then worked at CNRS in Toulouse and at the Center for Solid State Electronics Research at Arizona State University.In 1967 he settled in Edinburgh as a senior lecturer at the University of Edinburgh He was promoted to Reader in 1969 and Professor of physical electronics in 1981.In 1981 he was elected a Fellow of the Royal Society of Edinburgh. His proposers were William Cochran, William Farvis, Robert Allan Smith, Gordon Craig, Nicholas Kemmer and Richard Sillitto.He retired in 1985 and died of a heart attack on 28 January 1999.
Publications
Electric Conduction and Dielectric Relaxation in Glass (1963)He was editor of Physics and Chemistry of Glasses, published by the Society of Glass Technology.
== References ==
|
employer
|
{
"answer_start": [
805
],
"text": [
"University of Edinburgh"
]
}
|
Alan Ernest Owen FRSE FRSC FIP (7 October 1928 – 28 January 1999) was an English physicist specialising in glass technology.
Life
He was born on 7 October 1928 in Hastings on the Sussex coast. He studied science at the Brighton College of Technology 1949 to 1953. His initial role was as a research chemist for the English China Clay Research Laboratories at St Austell in Cornwall. He then moved to the University of Sheffield, researching the electronic qualities of glass, and gained a doctorate there (DSc). In 1959 he went to Westinghouse Electronic Systems in Baltimore in the United States, where he stayed until 1962. He then worked at CNRS in Toulouse and at the Center for Solid State Electronics Research at Arizona State University.In 1967 he settled in Edinburgh as a senior lecturer at the University of Edinburgh He was promoted to Reader in 1969 and Professor of physical electronics in 1981.In 1981 he was elected a Fellow of the Royal Society of Edinburgh. His proposers were William Cochran, William Farvis, Robert Allan Smith, Gordon Craig, Nicholas Kemmer and Richard Sillitto.He retired in 1985 and died of a heart attack on 28 January 1999.
Publications
Electric Conduction and Dielectric Relaxation in Glass (1963)He was editor of Physics and Chemistry of Glasses, published by the Society of Glass Technology.
== References ==
|
award received
|
{
"answer_start": [
934
],
"text": [
"Fellow of the Royal Society of Edinburgh"
]
}
|
Alan Ernest Owen FRSE FRSC FIP (7 October 1928 – 28 January 1999) was an English physicist specialising in glass technology.
Life
He was born on 7 October 1928 in Hastings on the Sussex coast. He studied science at the Brighton College of Technology 1949 to 1953. His initial role was as a research chemist for the English China Clay Research Laboratories at St Austell in Cornwall. He then moved to the University of Sheffield, researching the electronic qualities of glass, and gained a doctorate there (DSc). In 1959 he went to Westinghouse Electronic Systems in Baltimore in the United States, where he stayed until 1962. He then worked at CNRS in Toulouse and at the Center for Solid State Electronics Research at Arizona State University.In 1967 he settled in Edinburgh as a senior lecturer at the University of Edinburgh He was promoted to Reader in 1969 and Professor of physical electronics in 1981.In 1981 he was elected a Fellow of the Royal Society of Edinburgh. His proposers were William Cochran, William Farvis, Robert Allan Smith, Gordon Craig, Nicholas Kemmer and Richard Sillitto.He retired in 1985 and died of a heart attack on 28 January 1999.
Publications
Electric Conduction and Dielectric Relaxation in Glass (1963)He was editor of Physics and Chemistry of Glasses, published by the Society of Glass Technology.
== References ==
|
given name
|
{
"answer_start": [
0
],
"text": [
"Alan"
]
}
|
Ebrahim Moosa is the Mirza Family Professor of Islamic Thought & Muslim Societies at the University of Notre Dame with appointments in the Department of History and in the Kroc Institute for International Studies in the Keough School of Global Affairs. He is co-director of the Contending Modernities program at Notre Dame. He was previously Professor of Religion and Islamic Studies at Duke University. He is considered a leading scholar of contemporary Muslim thought. Moosa has been named as one of the top 500 Influential Muslims in the World.
Life and career
Moosa completed his theological training in the early 1980s in India, graduating with specialization in the traditional Islamic sciences from Darul Ulum Nadwatul Ulama in Lucknow, India. His Ph.D. is from the University of Cape Town, where he taught until the late 1990s. He was visiting professor of Islamic studies at Stanford University from 1998 to 2001. From 2001 to 2014, he taught in the Religion department at Duke University. In the Fall of 2014 he moved to Notre Dame.According to the contemporary scholar Adis Duderija, Moosa is "one of the most prominent intellectual theoreticians behind progressive Muslim thought." According to UCLA Professor Khaled Abou El Fadl, Moosa is "a formidable Muslim intellectual and scholar."Moosa served as a professor of Religion and Islamic Studies at the Duke University. In 2007, he was invited to deliver his lecture, "Ethical Challenges in Contemporary Islamic Thought," in Morocco, which was attended by King Muhammad VI.Moosa specializes in classical and medieval Muslim thought, Islamic ethics/law, and religion and modernity.
Publications
Moosa has contributed articles to Middle East Law and Governance, Journal of the American Academy of Religion, Journal for Islamic and Near Eastern Law, The Journal of Law and Religion, Islamic Studies, History of Religions, Islamic Law and Society, and Der Islam, among others. He authored Ghazali and the Poetics of Imagination (UNC Press, 2005), which won the American Academy of Religion's Best First Book in the History of Religions Award in 2006. He authored What Is a Madrasa?, an introduction to madrasas in India and Pakistan, which according to Maryam Kashani, "contributes a South Asian perspective to the rich scholarship on Islamic education."He edited and wrote the introduction to Fazlur Rahman's Revival and Reform in Islam: A Study of Islamic Fundamentalism (Oneworld, 1999), Islam in the Modern World (with Jeffrey Kenney; Routledge, 2013), and Muslim Family Law in Sub-Saharan Africa: Colonial Legacies and Post-colonial Challenges (with Shamil Jeppie and Richard Roberts; Amsterdam University Press, 2010).
References
Citations
General bibliography
Carl W. Ernst and Richard Martin (eds.) Rethinking Islamic Studies: From Orientalism to Cosmopolitanism (University of South Carolina Press, 2010).
Adis Duderija. Constructing a Religiously Ideal "Believer" and "Woman" in Islam: Neo-traditional Salafi and Progressive Muslims' Methods of Interpretation (New York: Palgrave Macmillan, 2011)
Omid Safi (ed.) Progressive Muslims: On Justice, Gender, and Pluralism (Oxford: Oneworld, 2003)
Deborah Caldwell, "Hajj in a Time of War: An Interview with Ebrahim Moosa" in Michael Wolfe, Taking Back Islam: American Muslims Reclaim Their Faith (Rodale, 2004)
James Boyd White (ed.) How Should We Talk about Religion?: Perspectives, Contexts, Particularities (Notre Dame: University of Notre Dame Press, 2006)
External links
Official website
Duke University Department of Religious Studies Website
Duke Theologian on Scholarship, Advocacy, and Activism
Deleuzian Musings on Ghazali and the Poetics of Imagination
Ebrahim Moosa's page at The Immanent Frame Archived 2014-11-26 at the Wayback Machine
Ebrahim Moosa on the Challenges Facing Islam
|
educated at
|
{
"answer_start": [
775
],
"text": [
"University of Cape Town"
]
}
|
Ebrahim Moosa is the Mirza Family Professor of Islamic Thought & Muslim Societies at the University of Notre Dame with appointments in the Department of History and in the Kroc Institute for International Studies in the Keough School of Global Affairs. He is co-director of the Contending Modernities program at Notre Dame. He was previously Professor of Religion and Islamic Studies at Duke University. He is considered a leading scholar of contemporary Muslim thought. Moosa has been named as one of the top 500 Influential Muslims in the World.
Life and career
Moosa completed his theological training in the early 1980s in India, graduating with specialization in the traditional Islamic sciences from Darul Ulum Nadwatul Ulama in Lucknow, India. His Ph.D. is from the University of Cape Town, where he taught until the late 1990s. He was visiting professor of Islamic studies at Stanford University from 1998 to 2001. From 2001 to 2014, he taught in the Religion department at Duke University. In the Fall of 2014 he moved to Notre Dame.According to the contemporary scholar Adis Duderija, Moosa is "one of the most prominent intellectual theoreticians behind progressive Muslim thought." According to UCLA Professor Khaled Abou El Fadl, Moosa is "a formidable Muslim intellectual and scholar."Moosa served as a professor of Religion and Islamic Studies at the Duke University. In 2007, he was invited to deliver his lecture, "Ethical Challenges in Contemporary Islamic Thought," in Morocco, which was attended by King Muhammad VI.Moosa specializes in classical and medieval Muslim thought, Islamic ethics/law, and religion and modernity.
Publications
Moosa has contributed articles to Middle East Law and Governance, Journal of the American Academy of Religion, Journal for Islamic and Near Eastern Law, The Journal of Law and Religion, Islamic Studies, History of Religions, Islamic Law and Society, and Der Islam, among others. He authored Ghazali and the Poetics of Imagination (UNC Press, 2005), which won the American Academy of Religion's Best First Book in the History of Religions Award in 2006. He authored What Is a Madrasa?, an introduction to madrasas in India and Pakistan, which according to Maryam Kashani, "contributes a South Asian perspective to the rich scholarship on Islamic education."He edited and wrote the introduction to Fazlur Rahman's Revival and Reform in Islam: A Study of Islamic Fundamentalism (Oneworld, 1999), Islam in the Modern World (with Jeffrey Kenney; Routledge, 2013), and Muslim Family Law in Sub-Saharan Africa: Colonial Legacies and Post-colonial Challenges (with Shamil Jeppie and Richard Roberts; Amsterdam University Press, 2010).
References
Citations
General bibliography
Carl W. Ernst and Richard Martin (eds.) Rethinking Islamic Studies: From Orientalism to Cosmopolitanism (University of South Carolina Press, 2010).
Adis Duderija. Constructing a Religiously Ideal "Believer" and "Woman" in Islam: Neo-traditional Salafi and Progressive Muslims' Methods of Interpretation (New York: Palgrave Macmillan, 2011)
Omid Safi (ed.) Progressive Muslims: On Justice, Gender, and Pluralism (Oxford: Oneworld, 2003)
Deborah Caldwell, "Hajj in a Time of War: An Interview with Ebrahim Moosa" in Michael Wolfe, Taking Back Islam: American Muslims Reclaim Their Faith (Rodale, 2004)
James Boyd White (ed.) How Should We Talk about Religion?: Perspectives, Contexts, Particularities (Notre Dame: University of Notre Dame Press, 2006)
External links
Official website
Duke University Department of Religious Studies Website
Duke Theologian on Scholarship, Advocacy, and Activism
Deleuzian Musings on Ghazali and the Poetics of Imagination
Ebrahim Moosa's page at The Immanent Frame Archived 2014-11-26 at the Wayback Machine
Ebrahim Moosa on the Challenges Facing Islam
|
employer
|
{
"answer_start": [
388
],
"text": [
"Duke University"
]
}
|
Ebrahim Moosa is the Mirza Family Professor of Islamic Thought & Muslim Societies at the University of Notre Dame with appointments in the Department of History and in the Kroc Institute for International Studies in the Keough School of Global Affairs. He is co-director of the Contending Modernities program at Notre Dame. He was previously Professor of Religion and Islamic Studies at Duke University. He is considered a leading scholar of contemporary Muslim thought. Moosa has been named as one of the top 500 Influential Muslims in the World.
Life and career
Moosa completed his theological training in the early 1980s in India, graduating with specialization in the traditional Islamic sciences from Darul Ulum Nadwatul Ulama in Lucknow, India. His Ph.D. is from the University of Cape Town, where he taught until the late 1990s. He was visiting professor of Islamic studies at Stanford University from 1998 to 2001. From 2001 to 2014, he taught in the Religion department at Duke University. In the Fall of 2014 he moved to Notre Dame.According to the contemporary scholar Adis Duderija, Moosa is "one of the most prominent intellectual theoreticians behind progressive Muslim thought." According to UCLA Professor Khaled Abou El Fadl, Moosa is "a formidable Muslim intellectual and scholar."Moosa served as a professor of Religion and Islamic Studies at the Duke University. In 2007, he was invited to deliver his lecture, "Ethical Challenges in Contemporary Islamic Thought," in Morocco, which was attended by King Muhammad VI.Moosa specializes in classical and medieval Muslim thought, Islamic ethics/law, and religion and modernity.
Publications
Moosa has contributed articles to Middle East Law and Governance, Journal of the American Academy of Religion, Journal for Islamic and Near Eastern Law, The Journal of Law and Religion, Islamic Studies, History of Religions, Islamic Law and Society, and Der Islam, among others. He authored Ghazali and the Poetics of Imagination (UNC Press, 2005), which won the American Academy of Religion's Best First Book in the History of Religions Award in 2006. He authored What Is a Madrasa?, an introduction to madrasas in India and Pakistan, which according to Maryam Kashani, "contributes a South Asian perspective to the rich scholarship on Islamic education."He edited and wrote the introduction to Fazlur Rahman's Revival and Reform in Islam: A Study of Islamic Fundamentalism (Oneworld, 1999), Islam in the Modern World (with Jeffrey Kenney; Routledge, 2013), and Muslim Family Law in Sub-Saharan Africa: Colonial Legacies and Post-colonial Challenges (with Shamil Jeppie and Richard Roberts; Amsterdam University Press, 2010).
References
Citations
General bibliography
Carl W. Ernst and Richard Martin (eds.) Rethinking Islamic Studies: From Orientalism to Cosmopolitanism (University of South Carolina Press, 2010).
Adis Duderija. Constructing a Religiously Ideal "Believer" and "Woman" in Islam: Neo-traditional Salafi and Progressive Muslims' Methods of Interpretation (New York: Palgrave Macmillan, 2011)
Omid Safi (ed.) Progressive Muslims: On Justice, Gender, and Pluralism (Oxford: Oneworld, 2003)
Deborah Caldwell, "Hajj in a Time of War: An Interview with Ebrahim Moosa" in Michael Wolfe, Taking Back Islam: American Muslims Reclaim Their Faith (Rodale, 2004)
James Boyd White (ed.) How Should We Talk about Religion?: Perspectives, Contexts, Particularities (Notre Dame: University of Notre Dame Press, 2006)
External links
Official website
Duke University Department of Religious Studies Website
Duke Theologian on Scholarship, Advocacy, and Activism
Deleuzian Musings on Ghazali and the Poetics of Imagination
Ebrahim Moosa's page at The Immanent Frame Archived 2014-11-26 at the Wayback Machine
Ebrahim Moosa on the Challenges Facing Islam
|
religion or worldview
|
{
"answer_start": [
47
],
"text": [
"Islam"
]
}
|
Ebrahim Moosa is the Mirza Family Professor of Islamic Thought & Muslim Societies at the University of Notre Dame with appointments in the Department of History and in the Kroc Institute for International Studies in the Keough School of Global Affairs. He is co-director of the Contending Modernities program at Notre Dame. He was previously Professor of Religion and Islamic Studies at Duke University. He is considered a leading scholar of contemporary Muslim thought. Moosa has been named as one of the top 500 Influential Muslims in the World.
Life and career
Moosa completed his theological training in the early 1980s in India, graduating with specialization in the traditional Islamic sciences from Darul Ulum Nadwatul Ulama in Lucknow, India. His Ph.D. is from the University of Cape Town, where he taught until the late 1990s. He was visiting professor of Islamic studies at Stanford University from 1998 to 2001. From 2001 to 2014, he taught in the Religion department at Duke University. In the Fall of 2014 he moved to Notre Dame.According to the contemporary scholar Adis Duderija, Moosa is "one of the most prominent intellectual theoreticians behind progressive Muslim thought." According to UCLA Professor Khaled Abou El Fadl, Moosa is "a formidable Muslim intellectual and scholar."Moosa served as a professor of Religion and Islamic Studies at the Duke University. In 2007, he was invited to deliver his lecture, "Ethical Challenges in Contemporary Islamic Thought," in Morocco, which was attended by King Muhammad VI.Moosa specializes in classical and medieval Muslim thought, Islamic ethics/law, and religion and modernity.
Publications
Moosa has contributed articles to Middle East Law and Governance, Journal of the American Academy of Religion, Journal for Islamic and Near Eastern Law, The Journal of Law and Religion, Islamic Studies, History of Religions, Islamic Law and Society, and Der Islam, among others. He authored Ghazali and the Poetics of Imagination (UNC Press, 2005), which won the American Academy of Religion's Best First Book in the History of Religions Award in 2006. He authored What Is a Madrasa?, an introduction to madrasas in India and Pakistan, which according to Maryam Kashani, "contributes a South Asian perspective to the rich scholarship on Islamic education."He edited and wrote the introduction to Fazlur Rahman's Revival and Reform in Islam: A Study of Islamic Fundamentalism (Oneworld, 1999), Islam in the Modern World (with Jeffrey Kenney; Routledge, 2013), and Muslim Family Law in Sub-Saharan Africa: Colonial Legacies and Post-colonial Challenges (with Shamil Jeppie and Richard Roberts; Amsterdam University Press, 2010).
References
Citations
General bibliography
Carl W. Ernst and Richard Martin (eds.) Rethinking Islamic Studies: From Orientalism to Cosmopolitanism (University of South Carolina Press, 2010).
Adis Duderija. Constructing a Religiously Ideal "Believer" and "Woman" in Islam: Neo-traditional Salafi and Progressive Muslims' Methods of Interpretation (New York: Palgrave Macmillan, 2011)
Omid Safi (ed.) Progressive Muslims: On Justice, Gender, and Pluralism (Oxford: Oneworld, 2003)
Deborah Caldwell, "Hajj in a Time of War: An Interview with Ebrahim Moosa" in Michael Wolfe, Taking Back Islam: American Muslims Reclaim Their Faith (Rodale, 2004)
James Boyd White (ed.) How Should We Talk about Religion?: Perspectives, Contexts, Particularities (Notre Dame: University of Notre Dame Press, 2006)
External links
Official website
Duke University Department of Religious Studies Website
Duke Theologian on Scholarship, Advocacy, and Activism
Deleuzian Musings on Ghazali and the Poetics of Imagination
Ebrahim Moosa's page at The Immanent Frame Archived 2014-11-26 at the Wayback Machine
Ebrahim Moosa on the Challenges Facing Islam
|
family name
|
{
"answer_start": [
8
],
"text": [
"Moosa"
]
}
|
Ebrahim Moosa is the Mirza Family Professor of Islamic Thought & Muslim Societies at the University of Notre Dame with appointments in the Department of History and in the Kroc Institute for International Studies in the Keough School of Global Affairs. He is co-director of the Contending Modernities program at Notre Dame. He was previously Professor of Religion and Islamic Studies at Duke University. He is considered a leading scholar of contemporary Muslim thought. Moosa has been named as one of the top 500 Influential Muslims in the World.
Life and career
Moosa completed his theological training in the early 1980s in India, graduating with specialization in the traditional Islamic sciences from Darul Ulum Nadwatul Ulama in Lucknow, India. His Ph.D. is from the University of Cape Town, where he taught until the late 1990s. He was visiting professor of Islamic studies at Stanford University from 1998 to 2001. From 2001 to 2014, he taught in the Religion department at Duke University. In the Fall of 2014 he moved to Notre Dame.According to the contemporary scholar Adis Duderija, Moosa is "one of the most prominent intellectual theoreticians behind progressive Muslim thought." According to UCLA Professor Khaled Abou El Fadl, Moosa is "a formidable Muslim intellectual and scholar."Moosa served as a professor of Religion and Islamic Studies at the Duke University. In 2007, he was invited to deliver his lecture, "Ethical Challenges in Contemporary Islamic Thought," in Morocco, which was attended by King Muhammad VI.Moosa specializes in classical and medieval Muslim thought, Islamic ethics/law, and religion and modernity.
Publications
Moosa has contributed articles to Middle East Law and Governance, Journal of the American Academy of Religion, Journal for Islamic and Near Eastern Law, The Journal of Law and Religion, Islamic Studies, History of Religions, Islamic Law and Society, and Der Islam, among others. He authored Ghazali and the Poetics of Imagination (UNC Press, 2005), which won the American Academy of Religion's Best First Book in the History of Religions Award in 2006. He authored What Is a Madrasa?, an introduction to madrasas in India and Pakistan, which according to Maryam Kashani, "contributes a South Asian perspective to the rich scholarship on Islamic education."He edited and wrote the introduction to Fazlur Rahman's Revival and Reform in Islam: A Study of Islamic Fundamentalism (Oneworld, 1999), Islam in the Modern World (with Jeffrey Kenney; Routledge, 2013), and Muslim Family Law in Sub-Saharan Africa: Colonial Legacies and Post-colonial Challenges (with Shamil Jeppie and Richard Roberts; Amsterdam University Press, 2010).
References
Citations
General bibliography
Carl W. Ernst and Richard Martin (eds.) Rethinking Islamic Studies: From Orientalism to Cosmopolitanism (University of South Carolina Press, 2010).
Adis Duderija. Constructing a Religiously Ideal "Believer" and "Woman" in Islam: Neo-traditional Salafi and Progressive Muslims' Methods of Interpretation (New York: Palgrave Macmillan, 2011)
Omid Safi (ed.) Progressive Muslims: On Justice, Gender, and Pluralism (Oxford: Oneworld, 2003)
Deborah Caldwell, "Hajj in a Time of War: An Interview with Ebrahim Moosa" in Michael Wolfe, Taking Back Islam: American Muslims Reclaim Their Faith (Rodale, 2004)
James Boyd White (ed.) How Should We Talk about Religion?: Perspectives, Contexts, Particularities (Notre Dame: University of Notre Dame Press, 2006)
External links
Official website
Duke University Department of Religious Studies Website
Duke Theologian on Scholarship, Advocacy, and Activism
Deleuzian Musings on Ghazali and the Poetics of Imagination
Ebrahim Moosa's page at The Immanent Frame Archived 2014-11-26 at the Wayback Machine
Ebrahim Moosa on the Challenges Facing Islam
|
given name
|
{
"answer_start": [
0
],
"text": [
"Ebrahim"
]
}
|
Ebrahim Moosa is the Mirza Family Professor of Islamic Thought & Muslim Societies at the University of Notre Dame with appointments in the Department of History and in the Kroc Institute for International Studies in the Keough School of Global Affairs. He is co-director of the Contending Modernities program at Notre Dame. He was previously Professor of Religion and Islamic Studies at Duke University. He is considered a leading scholar of contemporary Muslim thought. Moosa has been named as one of the top 500 Influential Muslims in the World.
Life and career
Moosa completed his theological training in the early 1980s in India, graduating with specialization in the traditional Islamic sciences from Darul Ulum Nadwatul Ulama in Lucknow, India. His Ph.D. is from the University of Cape Town, where he taught until the late 1990s. He was visiting professor of Islamic studies at Stanford University from 1998 to 2001. From 2001 to 2014, he taught in the Religion department at Duke University. In the Fall of 2014 he moved to Notre Dame.According to the contemporary scholar Adis Duderija, Moosa is "one of the most prominent intellectual theoreticians behind progressive Muslim thought." According to UCLA Professor Khaled Abou El Fadl, Moosa is "a formidable Muslim intellectual and scholar."Moosa served as a professor of Religion and Islamic Studies at the Duke University. In 2007, he was invited to deliver his lecture, "Ethical Challenges in Contemporary Islamic Thought," in Morocco, which was attended by King Muhammad VI.Moosa specializes in classical and medieval Muslim thought, Islamic ethics/law, and religion and modernity.
Publications
Moosa has contributed articles to Middle East Law and Governance, Journal of the American Academy of Religion, Journal for Islamic and Near Eastern Law, The Journal of Law and Religion, Islamic Studies, History of Religions, Islamic Law and Society, and Der Islam, among others. He authored Ghazali and the Poetics of Imagination (UNC Press, 2005), which won the American Academy of Religion's Best First Book in the History of Religions Award in 2006. He authored What Is a Madrasa?, an introduction to madrasas in India and Pakistan, which according to Maryam Kashani, "contributes a South Asian perspective to the rich scholarship on Islamic education."He edited and wrote the introduction to Fazlur Rahman's Revival and Reform in Islam: A Study of Islamic Fundamentalism (Oneworld, 1999), Islam in the Modern World (with Jeffrey Kenney; Routledge, 2013), and Muslim Family Law in Sub-Saharan Africa: Colonial Legacies and Post-colonial Challenges (with Shamil Jeppie and Richard Roberts; Amsterdam University Press, 2010).
References
Citations
General bibliography
Carl W. Ernst and Richard Martin (eds.) Rethinking Islamic Studies: From Orientalism to Cosmopolitanism (University of South Carolina Press, 2010).
Adis Duderija. Constructing a Religiously Ideal "Believer" and "Woman" in Islam: Neo-traditional Salafi and Progressive Muslims' Methods of Interpretation (New York: Palgrave Macmillan, 2011)
Omid Safi (ed.) Progressive Muslims: On Justice, Gender, and Pluralism (Oxford: Oneworld, 2003)
Deborah Caldwell, "Hajj in a Time of War: An Interview with Ebrahim Moosa" in Michael Wolfe, Taking Back Islam: American Muslims Reclaim Their Faith (Rodale, 2004)
James Boyd White (ed.) How Should We Talk about Religion?: Perspectives, Contexts, Particularities (Notre Dame: University of Notre Dame Press, 2006)
External links
Official website
Duke University Department of Religious Studies Website
Duke Theologian on Scholarship, Advocacy, and Activism
Deleuzian Musings on Ghazali and the Poetics of Imagination
Ebrahim Moosa's page at The Immanent Frame Archived 2014-11-26 at the Wayback Machine
Ebrahim Moosa on the Challenges Facing Islam
|
notable work
|
{
"answer_start": [
2125
],
"text": [
"What Is a Madrasa?"
]
}
|
Padre nuestro (Spanish for "Our Father") can refer to:
Padre nuestro (2007 film), a 2007 American–Argentine film
Padre nuestro (1925 film), a 1925 Argentine film
Our Father (1953 film), a 1953 Mexican film
Padre nuestro (1985 film), a 1985 Spanish film
Padre nuestro (2005 film), a 2005 Chilean film
"Padre Nuestro," a song by E Nomine
|
instance of
|
{
"answer_start": [
76
],
"text": [
"film"
]
}
|
Padre nuestro (Spanish for "Our Father") can refer to:
Padre nuestro (2007 film), a 2007 American–Argentine film
Padre nuestro (1925 film), a 1925 Argentine film
Our Father (1953 film), a 1953 Mexican film
Padre nuestro (1985 film), a 1985 Spanish film
Padre nuestro (2005 film), a 2005 Chilean film
"Padre Nuestro," a song by E Nomine
|
original language of film or TV show
|
{
"answer_start": [
15
],
"text": [
"Spanish"
]
}
|
Padre nuestro (Spanish for "Our Father") can refer to:
Padre nuestro (2007 film), a 2007 American–Argentine film
Padre nuestro (1925 film), a 1925 Argentine film
Our Father (1953 film), a 1953 Mexican film
Padre nuestro (1985 film), a 1985 Spanish film
Padre nuestro (2005 film), a 2005 Chilean film
"Padre Nuestro," a song by E Nomine
|
title
|
{
"answer_start": [
0
],
"text": [
"Padre nuestro"
]
}
|
Padre nuestro (Spanish for "Our Father") can refer to:
Padre nuestro (2007 film), a 2007 American–Argentine film
Padre nuestro (1925 film), a 1925 Argentine film
Our Father (1953 film), a 1953 Mexican film
Padre nuestro (1985 film), a 1985 Spanish film
Padre nuestro (2005 film), a 2005 Chilean film
"Padre Nuestro," a song by E Nomine
|
country of origin
|
{
"answer_start": [
288
],
"text": [
"Chile"
]
}
|
John Bird Burnham (1869-1939) was a conservationist and entrepreneur who founded the Crater Club off of Whallons Bay on Lake Champlain in 1899.Born in Newcastle, Delaware, he worked in New York City as editor of Forest and Stream from 1881 to 1887, where he wrote many articles advocating for game protection. In 1898 he bought a home in Willsboro, New York, and turned it into the Highlands Game Preserve. Despite lacking training as an architect or as a builder, he nevertheless designed and built some seventy cabins and cottages, along with club buildings. By 1905, he also established a maple sugar and maple candy business, the Adirondack Mountain Creams factory Essex, New York.He led a campaign for passage of a federal migratory bird law, the Weeks-McLean Law (passed in 1913) as well as a migratory bird treaty with Canada.
Burnham was also a noted adventurer, having traveled the Yukon as a young man, and in his fifties he led an expedition to Siberia to collect specimens of the Marco Polo sheep in 1921.
== References ==
|
given name
|
{
"answer_start": [
0
],
"text": [
"John"
]
}
|
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