The association of diabetes mellitus and mental illness, in particular, schizophrenia, has been remarked upon for over a century. Recentepidemiological studies have shown the age- and sex-matched prevalence of diabetes in patients with schizophrenia to be 1.5–2 times those in the general population. This difference is particularly noticeable in younger patients. The explanation for this finding probably resides in both environmental and biological factors. Patients with schizophrenia tend to be sedentary and have a poor diet, which are both known risk factors for diabetes. However, familial studies have indicated a heritable component to the risk of diabetes in patients with schizophrenia. A number of biological mechanisms have been proposed to explain this, including neuroendocrine changes and neurodevelopmental anomalies, but none are entirely satisfactory. In addition, it has been suggested that treatment with antipsychotic medication may potentially increase the risk of diabetes and account for some of the increased prevalence seen in patients with schizophrenia. It has been suggested that different antipsychotic drugs may differ in their ability to facilitate the emergence of poor glycaemic control in patients with schizophrenia. However, the situation is far from clear and more work is required to accurately assess the potential risk associated with different antipsychotic drugs.

Raised blood pressure (BP) is a major cause of CHD and the leading cause of stroke. Although BP rises with age in most populations, there are remote populations around the world where BP does not rise with age and where the high prevalence of high BP and frank hypertension seen in the UK and other Western countries in the older age-groups is not found. However, when such populations migrate to urban settings, their BPs rise, indicating that the population-wide BP problem is largely environmental in origin. Thus, a substantial body of evidence has accumulated on the importance of dietary factors in BP (Na and alcohol intakes (direct relationship) and K intake (inverse relationship)) as well as body weight (direct relationship). More recently, attention has shifted to other dietary factors that might affect BP. Data from studies of vegetarians (who tend to have lower BP than meat-eating populations) as well as clinical data on the adverse effects of protein intake in patients with renal insufficiency led to the view in Western countries that dietary (animal or total) protein had an adverse effect on BP. By contrast, studies in Japan and China suggested that dietary protein might be protective of high BP and stroke. Recent epidemiological studies have found inverse associations between dietary protein intake and BP, consistent with this view, and supported by some evidence from animal studies. Recent controlled clinical trials of soyabean supplementation have also suggested a BP-lowering effect of protein intake. Results of further large-scale epidemiological studies of protein and BP are awaited.