Historical aspects of type 1 diabetes

The first recognisable reports of type 1 diabetes – a condition presenting in children or young adults and terminating in fatal ketoacidosis – appeared towards the end of the 19th century. Clinicians were soon able to distinguish this aggressive form of diabetes from the more indolent late-onset type, but the link between insulin sensitivity, susceptibility to diabetic ketoacidosis and body-build was not made until the mid-20th century. Final acceptance that there were two main forms of diabetes was delayed until the 1970s, by which time juvenile diabetes was seen to have the characteristic hallmarks of an autoimmune disease.

Diabetes presenting in children or young adults and terminating in fatal ketoacidosis first appeared in the medical literature in the 19th century, but this was a very rare clinical condition. Physicians were already aware that there were different types of diabetes. Harley commented in 1866 that 'there are at least two distinct forms of the disease requiring diametrically opposing forms of treatment', and Etienne Lancereaux made the distinction between fat (diabete gras) and thin (diabete maigre) diabetes.

At that time, overweight adults could manage reasonably well with diet restriction, but there was no effective treatment for children. The starvation regimen introduced by Frank Allen in 1911 could prolong a miserable life, but the children typically died of ketoacidosis, tuberculosis or starvation within months of diagnosis.

The discovery of insulin in 1921–2 was one of the closest approaches to a secular miracle in the history of medicine.[1] Survival was closely related to age at diagnosis (see Figure).

Dublin JI, 1951: Life expectancy by age of diagnosis
Dublin JI, 1951: Life expectancy by age of diagnosis

Clinicians struggled to understand the difference between young thin patients who required insulin for life, and the older fatter individuals who could manage without it. The discovery by Houssay[2] that diabetes improved in animals following removal of the pituitary (hypophysectomy) suggested to many that the adult form of diabetes, in which the pancreas often appeared normal at autopsy, was due to overproduction of growth hormone, and some made the distinction between 'pancreatic' and 'pituitary' diabetes; there were even efforts to treat the latter by irradiation of the pituitary gland.

Others considered a genetic explanation, whereby homozygous individuals with two copies of a hypothetical 'diabetes gene' developed juvenile onset diabetes, whereas those who were heterozygous (i.e. with a single copy) developed late onset disease.

The Viennese physician Falta made the first attempts to link the clinical features of diabetes with responsiveness to insulin in the 1930s,[3] but it was Harold Himsworth who demonstrated the point by an elegant experiment in which he tested the effect of insulin injection in patients who swallowed a simultaneous dose of glucose (see Figure). Younger patients and non-diabetic individuals suppressed the rise in plasma glucose, but overweight adults showed a rise in glucose. From this he correctly inferred that there are two main forms of the disease: an insulin-deficient form in lean young people and an insulin-resistant form in overweight adults.[4]

Bioassay of the insulin content of post mortem human pancreas in the 1950s added support to this concept, since the amount of insulin was reduced to below 10% of normal in early-onset patients, but remained at about 50% in late-onset diabetes.[5].

Coincidentally, there was a vogue for a technique called somatotyping that reached its peak in the 1930s and 1940s. William Sheldon, for example, photographed nude subjects and made a set of nine standard measurements against a grid. Based on this technique, he classified people as ectomorphs, mesomorphs or endomorphs according to the supposed preponderance of the three germ layers.

Others sought to use this technique to establish a link between physique and susceptibility to disease – so-called constitutional medicine. Draper, a New York physician, recruited an anthropologist called Dupurtuis to somatotype his diabetic patients, and was somewhat perplexed when Dupurtuis returned to say that there was not one somatotype of diabetes, but two. These they referred to as Group 1 and Group 2.[6]

John Lister, a young doctor in London, combined the Himsworth test with somatotyping, and identified a characteristic body build that was associated with insulin insensitivity. He concluded in 1951 that there were 'two broad groups of diabetics – the young, thin, non-arteriosclerotic group with normal blood pressure and usually an acute onset to the disease, and the older, obese, arteriosclerotic group with hypertension and usually an insidious onset. ... These types we have provisionally designated type I and type II, respectively.'[7]

The somatotype of type 2 diabetes
The somatotype of type 2 diabetes

The terminology did not catch on, however, and the terms juvenile- and maturity-onset diabetes were widely used for decades until the term type 1 diabetes was re-introduced by Andrew Cudworth (who learned of it from John Lister) in 1976.[8] By this time the concept of autoimmune disease had become well established, and it had become clear that juvenile diabetes qualified for inclusion in this category. From this point onwards the view that diabetes was a single spectrum of disease rapidly lost favour, and the two major forms became enshrined in the literature. Initially, most clinicians preferred to subdivide these according to the perceived need for insulin into insulin-dependent and non-insulin dependent diabetes mellitus (IDDM and NIDDM). By 1996, however, the World Health Organization (WHO) opted for a classification based upon aetiology rather than therapy, and type 1 and type 2 diabetes became the accepted terms.

The history of the discovery of type 1 diabetes and of the recognition of type 1 diabetes as an immune-mediated disorder is related in more detail in the two daughter pages that follow this.

See also: Discovery of type 1 diabetes


  1. ^ Bliss M. The Discovery of Insulin. Paul Harris, Edinburgh, 1983

  2. ^ Houssay BA, Biasotti A. The hypophysis, carbohydrate metabolism and diabetes. Endocrinology 1931;15:511–23

  3. ^ Falta W, Boller R. Insularer und insulinresistenter diabetes. Klin Wochenschr 1931;10:438–43

  4. ^ Himsworth HP Diabetes its differentiation into insulin-sensitive and insulin-insensitive types. Lancet 1936;1:127–30

  5. ^ Wrenshall GA, Bogoch A, Ritchie R. Extractable insulin of pancreas. Diabetes 1952;1:87–107

  6. ^ Draper G, Dupurtuis CW, Caughey JL. Human Constitution in Clinical Medicine. New York, Harper, 1944

  7. ^ Lister J, Nash J, Ledingham U. Constitution and insulin sensitivity in diabetes mellitus. Br Med J 1951;1(4703):376–9

  8. ^ Cudworth AG: The aetiology of diabetes mellitus. Br J Hosp Med 1976;16:207–16


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    Russel Kirkby added a compliment on 7 September 2016 at 11:51AM
    Thanks for a wonderful insight. All your hard work much appreciated and valuable
  2. no profile image
    Russel Kirkby added a compliment on 7 September 2016 at 11:50AM
    Thanks for a wonderful insight. All your hard work much appreciated and valuable
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