NO EXCESS 12-YEAR MORTALITY IN MEN WITH IMPAIRED GLUCOSE-TOLERANCE WHO PARTICIPATED IN THE MALMO PREVENTIVE TRIAL WITH DIET AND EXERCISE

Impaired glucose tolerance (IGT) is associated with increased mortalit y due to ischaemic heart disease (IHD), but as it is not known whether this excess mortality can be reduced by preventing or delaying the de velopment of non-insulin-dependent diabetes mellitus (NIDDM), a long-t erm NIDDM prevention trial of dietary counselling and physical exercis e was launched at Malmo, Sweden, the 12-year follow-up of which is rep orted here. At 12-year follow-up of 6956 men who underwent health scre ening at 48 years of age, an IGT intervention group (n = 288) who part icipated in a long-term NIDDM prevention programme were compared with an IGT non-randomised routine treatment group (n = 135), a diabetic gr oup (n = 144), and the remainder, the normal glucose tolerance (NGT) g roup (n = 6389). The variables studied included the levels of blood gl ucose, plasma insulin, blood pressure, blood lipids, lung function and maximum oxygen uptake. Subjects with IGT were characterised by overwe ight, poor vital capacity, hypertension, hypertriglyceridaemia and hyp erinsulinaemia. The mortality rate in the IGT intervention group was s imilar to that in the NGT group (6.5 vs 6.2 per 1000 person years at r isk) and lower than that in the IGT routine treatment group (6.5 vs 14 .0, p = 0.009). In the two IGT groups taken together, intervention but not body mass index, systolic blood pressure, smoking, cholesterol or the 2-h glucose level predicted mortality. Systolic blood pressure wa s a predictor of IHD mortality among IGT subjects; and in the cohort a s a whole, body mass index, systolic blood pressure, hypercholesterola emica, diabetes and smoking were predictors of IHD mortality. The find ings suggest that a long-term intervention programme, with an emphasis on lifestyle changes, including dietary counselling and physical exer cise, will reduce mortality in subjects with IGT who are at an increas ed risk of both developing NIDDM and of premature death due to II-ID a nd other causes.