Diabetes mellitus is a disease of antiquity (see Chapter 1). A treatment was described in the Ebers papyrus and as long ago as 600 BC two main types were distinguished. Perhaps the most famous description was by Arateus the Cappadocian who talked of the melting down of flesh into urine and of the end being speedy. Over the ensuing centuries sporadic descriptions were noted, with Maimonides in Egypt pointing out its relative rarity. It was attributed to a salt-losing state although the sweetness of the urine had long been known. Undoubtedly, virtually all of these accounts referred to type 1 (T1DM) or late type 2 diabetes (T2DM).

Diabetes was better recognized in the 17th and 18th centuries, with the association with obesity noted in some cases. The obvious breakthrough came in the 17th century with the demonstration of excess glucose in the urine and later also in blood.

The presence of excess ketones was shown in the 19th century. A clear description of the two main types of diabetes appeared at the end of the 19th century, with the distinction being made between that occurring in young people with a short time course before ketoacidosis supervened, and that found in older people who were obese. Over the next decades these became known as juvenile-onset diabetes and maturity-onset diabetes, although it was generally stated that the latter was just a milder form of the disease. Diagnosis now depended on glucose measurement with some using glucose tolerance tests. There were no standard criteria for these initially, although glucose levels were clearly above normal. Diagnosis usually occurred after clinical development of the disease with the combination of symptoms with raised glucose in the blood or glycosuria being diagnostic, together with ketonuria in the juvenile-onset form.

A further breakthrough occurred with the work of Himsworth in 1936. Himsworth’s work showed that people with diabetes could be divided into insulin-resistant and insulin-sensitive types, with the former much more common in those with the maturity-onset variety [1]. The next milestone was the development of the radioimmunoassay for insulin which allowed the unequivocal demonstration of insulin deficiency, or indeed absence, in those with juvenile-onset diabetes while levels were apparently normal or raised in those with maturity-onset diabetes.

At that time, diabetes was still considered to be a relatively uncommon disorder occurring predominantly in Europids. The World Health Organization (WHO) began to take note and held its first Expert Committee meeting in 1964 [2]. The real breakthrough, however, in terms of diagnosis and classification came in 1980 with the publication of the second Expert Committee report [3] shortly after the report from the National Diabetes Data Group (NDDG) in the USA in 1979 [4]. These events form the starting point for the diagnostic criteria and classification used today.

Diabetes mellitus is a metabolic disorder of multiple etiologies. It is characterized by chronic hyperglycemia together with disturbances of carbohydrate, fat and protein metabolism resulting from defects of insulin secretion, insulin action or both [6]. The relative contribution of these varies between different types of diabetes. These are associated with the development of the specific microvascular complications of retinopathy, which can lead to blindness, nephropathy with potential renal failure, and neuropathy. The latter carries the risk of foot ulcers and amputation and also autonomic nerve dysfunction. Diabetes is also associated with an increased risk of macrovascular disease.

The characteristic clinical presentation is with thirst, polyuria, blurring of vision and weight loss. This can lead to ketoacidosis or hyperosmolar non-ketotic coma (see Chapter 19). Often, symptoms are mild or absent and mild hyperglycemia can persist for years with tissue damage developing, although the person may be totally asymptomatic.

There was awareness of different grades of severity of diabetes for many centuries; however, the possibility that there were two distinct types only emerged at the beginning of the 20th century. Even then there was no real clue to distinct etiologies. In the 1930s, Himsworth suggested that there were two phenotypes. The first real attempt to classify diabetes came with the first WHO Expert Committee on Diabetes Mellitus which felt that the only reliable classification was by age of onset and divided diabetes into juvenile-onset and maturity-onset disease [2]. There were many other phenotypes in vogue at that time including brittle, gestational, pancreatic, endocrine, insulin-resistant and iatrogenic diabetes, but for most cases there was no clear indication of etiology. Clarity began to emerge in the 1970s with the discovery of the human leukocyte antigen (HLA) genotypes common in juvenile-onset diabetes and the discovery of islet call antibodies. This gave a clear indication that younger patients with diabetes, all of whom required insulin therapy, had an autoimmune disorder.

The beginning of the modern era came with the second WHO Expert Committee [3] which reviewed and modified the revised classification published by the National Diabetes Data Group [4]. This proposed two main classes of diabetes: insulin-dependent diabetes mellitus (IDDM; type 1) and non-insulin-dependent diabetes (NIDDM; type 2) together with “other types” and gestational diabetes. There were also two risk classes: previous abnormality of glucose intolerance (PrevAGT) and potential abnormality of glucose tolerance (PotAGT) which replaced previous types known as pre-diabetes or potential diabetes.

The 1980 classification was revised further in 1985 [5] and reverted to clinical descriptions with retention of IDDM and NIDDM but omission of type 1 and type 2. Malnutrition-related diabetes mellitus was also introduced in recognition of a different phenotype found particularly in Asia and sub-Saharan Africa. Impaired glucose tolerance (IGT) was also introduced as a high risk class.