What are the risk factors for the development of DM

Type 1 DM is due, in the majority of cases, to an autoimmune destruction of the insulin producing b-cells of the pancreatic islets (Type 1A DM) in contrast to the extremely infrequent non-autoimmune type (Type 1B DM). The process of autoimmune destruction presents in genetically predisposed individuals, is probably triggered by (presently unknown) environmental factors (viruses? antigens of diet?) and proceeds over a period of months to years. The genetic indices are present from birth and the immunologic ones (pancreatic auto-antibodies) present after the beginning of the autoimmune process. The metabolic indices can be detected with sensitive tests when enough destruction of the b-cell has occurred, but before the appearance of symptomatic hyperglycaemia (reduction of the first phase of insulin secretion during the intravenous glucose tolerance test). Thus, high-risk groups for the development of Type 1 DM are individuals with a certain genetic predisposition (certain combinations of genes of the Human Leukocytes Antigens [HLAs: DR3 and DR4]) and with existence of antibodies against certain pancreatic proteins (see also Chapter 2). The risk is increased in individuals with first degree relatives suffering from Type 1 DM, and is bigger when the sick relative is the father (diabetes risk 6 percent) or a sibling (risk 5 percent), rather than the mother (risk 2 percent), for unknown reasons (it is worth noting that the risk of Type 1 DM in the general population, when there are no first degree relatives who are Type 1 diabetics, is roughly 0.4 percent). The combination of family history of Type 1 DM with the presence of aggravating genes of the HLA system increases the risk much more (up to 25-50 percent).

For Type 2 DM, epidemiologic studies as well as data from its pathophysiology and natural history, have shown various factors that are related to an increased frequency of its appearance. These factors are age > 45 years, obesity (BMI > 25 kg/m2), family history of DM, a sedentary life-style, certain racial groups and nationalities (African Americans or Hispanics, Native Americans, Pacific Islanders, etc.), history of gestational DM or birth of a child > 4 kg (8.8 lb), history of hypertension or dyslipidaemia and the polycystic ovary syndrome. Also, a low birth weight and cigarette smoking have been associated epidemiologically with the risk of developing DM. However, the most powerful association has been found with the presence of Impaired Fasting Glucose (IFG) and/ or Impaired Glucose Tolerance (IGT). IFG is defined as the presence of fasting plasma glucose levels between 110-125 mg/dl [6.1-6.9 mmol/L] for Europe 100-125 mg/dl [5.6-6.9 mmol/L] for America), and IGT is the presence of plasma glucose levels between 140-200 mg/dl (7.811.1 mmol/L) two hours after the intake of 75 g glucose by mouth during an oral glucose tolerance test. The individuals with IFG or IGT (conditions that only overlap in 20-25 percent of cases) have a probability of around 30 percent of developing clinically evident DM in the next five years. The presence of both of these conditions raises the risk to around 50 percent. Thus, these two conditions are rightly considered as a pre-clinical stage of DM and are called 'pre-diabetes'. The presence of IGT is usually also associated with other components of the metabolic syndrome (hypertension, dyslipidaemia, obesity) and with increased cardiovascular risk.

The studies of DM prevention have consequently been mainly focused on these high-risk groups.

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