: Type 1 diabetes is a condition that can lead to serious long-term complications and can have significant psychological and quality of life implications. Its incidence is increasing in all parts of the world, but the reasons for this are incompletely understood. Genetic factors alone cannot explain such a rapid increase in incidence; therefore, environmental factors must be implicated. : Lifestyle factors have been classically associated with type 2 diabetes. However, there are data implicating obesity and insulin resistance to type 1 diabetes as well (accelerator hypothesis). Cholesterol has also been shown to be correlated with the incidence of type 1 diabetes; this may be mediated by immunomodulatory effects of cholesterol. There is considerable interest in early life factors, including maternal diet, mode of delivery, infant feeding, childhood diet, microbial exposure (hygiene hypothesis), and use of anti-microbials in early childhood. : Distance from the sea has recently been shown to be negatively correlated with the incidence of type 1 diabetes. This may contribute to the increasing incidence of type 1 diabetes since people are increasingly living closer to the sea. Postulated mediating mechanisms include hours of sunshine (and possibly vitamin D levels), mean temperature, dietary habits, and pollution. Ozone, polychlorinated biphenyls, phthalates, trichloroethylene, dioxin, heavy metals, bisphenol, nitrates/nitrites, and mercury are amongst the chemicals which may increase the risk of type 1 diabetes. : Another area of research concerns the role of the skin and gut microbiome. The microbiome is affected by many of the factors mentioned above, including the mode of delivery, infant feeding, exposure to microbes, antibiotic use, and dietary habits. Research on the reasons why the incidence of type 1 diabetes is increasing not only sheds light on its pathogenesis but also offers insights into ways we can prevent type 1 diabetes.

Diabetes mellitus is a major risk factor for cardiovascular disease and mortality. Diabetic patients have a two- to fourfold increased risk of developing cardiovascular disease. There is convincing evidence that tight glycemic control aimed at lowering HbA(1c) reduces cardiovascular risk. However, even well-controlled diabetic patients remain at increased risk. The reason is that, although antihyperglycemic agents have been available for many years, we have been unable to mimic physiological insulin secretion. Type 2 diabetic patients typically lose the first phase of insulin secretion very early in the course of their disease, resulting in increased postprandial glucose excursions (PPGEs). This has, until recently, been largely neglected. This review will discuss the physiological control of postprandial glucose, as well as the causes of increased PPGEs and of other features of postprandial dysregulation seen in subjects with abnormal glucose tolerance. It will also discuss the effects of increased PPGE on the endothelium and review the epidemiological data linking postprandial hyperglycemia to cardiovascular disease. Finally, the effectiveness of a number of therapeutic options in lowering postprandial glucose and their effect on the endothelium and outcome will be reviewed. However, the possible role of PPG in cancer risk and in cognitive function is beyond the scope of this review and will not be discussed.

OBJECTIVE—To investigate whether the DD genotype is a predictor of mortality and of the decline in renal function in patients with type 2 diabetes and established nephropathy. RESEARCH DESIGN AND METHODS—A total of 56 such patients of Maltese Caucasian descent were recruited, and their ACE genotype was determined. Serum creatinine was estimated approximately every 4 months. The glomerular filtration rate (GFR) was calculated according to the Cockroft-Gault formula, and rate of change was determined by regression analysis. RESULTS—The rate of change in calculated GFR was −7.76 ml · min^–1 · year^–1 in those with the DD genotype (n = 31) and −1.17 ml · min^–1 · h^–1 in those with the ID or II genotype (n = 25) (P < 0.01). The 3-year mortality was 45.2% in the DD group compared with 20.0% in the ID/II group (P < 0.05). CONCLUSIONS—The DD genotype of the ACE gene polymorphism is associated with a more rapid decline in renal function and higher mortality in type 2 diabetic patients with established nephropathy.