A prospective study of drinking patterns in relation to risk of type 2 diabetes among men.
ABSTRACT Using data from a 12-year prospective study, we determined the importance of the pattern of alcohol consumption as a risk factor for type 2 diabetes in a cohort of 46,892 U.S. male health professionals who completed biennial postal questionnaires. Overall, 1,571 new cases of type 2 diabetes were documented. Compared with zero alcohol consumption, consumption of 15-29 g/day of alcohol was associated with a 36% lower risk of diabetes (RR = 0.64; 95% CI 0.53-0.77). This inverse association between moderate consumption and diabetes remained if light drinkers rather than abstainers were used as the reference group (RR = 0.60, CI 0.50-0.73). There were few heavy drinkers, but the inverse association persisted to those drinking >/=50 g/day of alcohol (RR = 0.60, CI 0.43-0.84). Frequency of consumption was inversely associated with diabetes. Consumption of alcohol on at least 5 days/week provided the greatest protection, even when less than one drink per drinking day was consumed (RR = 0.48, CI 0.27-0.86). Compared with infrequent drinkers, for each additional day per week that alcohol was consumed, risk was reduced by 7% (95% CI 3-10%) after controlling for average daily consumption. There were similar and independent inverse associations for beer, liquor, and white wine. Our findings suggested that frequent alcohol consumption conveys the greatest protection against type 2 diabetes, even if the level of consumption per drinking day is low. Beverage choice did not alter risk.
American Journal of Epidemiology 05/2004; 159(10):935-944. DOI:10.1093/aje/kwh134 · 4.98 Impact Factor
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ABSTRACT: The association between alcohol and blood glucose levels, and whether it is modified by other variables, was examined in a cross-sectional survey of 5518 staff aged 40–65 years at worksites in Auckland and Tokoroa, New Zealand. Diabetes was determined by oral glucose-tolerance tests using 1999 WHO criteria. Usual alcohol intake in the previous 3 months, measured by food frequency questionnaire, was related positively with fasting triglycerides and high-density-lipoprotein (HDL)-cholesterol, and unrelated with fasting glucose, but had an approximate U-shaped relationship with 2-h glucose, which varied from an adjusted mean (S.E.) of 5.62 (0.08) mmol/l in non-drinkers, down to 5.34 (0.08) mmol/l in light alcohol drinkers (alcohol <5 g per day), and back up to 5.52 (0.09) mmol/l in heavy drinkers (≥20 g per day). Adjusting further for triglycerides increased the mean difference in 2-h glucose for all drinking categories compared with non-drinkers, particularly for heavy drinkers (≥20 g per day), from −0.22 (S.E.=0.10) to −0.37 (0.10) mmol/l. The confounding effect of triglycerides suggests alcohol may affect the diabetes risk by a mechanism related to the triglyceride metabolism, which in heavy drinkers may counteract the protective effect of improved insulin sensitivity, resulting in the U-shaped relationship between alcohol and diabetes described in previous studies.Diabetes Research and Clinical Practice 05/2004; DOI:10.1016/S0168-8227(04)00068-3 · 2.54 Impact Factor
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ABSTRACT: Chronic ethanol consumption is well established as a major risk factor for type-2 diabetes (T2D), which is evidenced by impaired glucose metabolism and insulin resistance. However, the relationships between alcohol consumption and the development of T2D remain controversial. In particular, the direct effects of ethanol consumption on proliferation of pancreatic β-cell and the exact mechanisms associated with ethanol-mediated β-cell dysfunction and apoptosis remain elusive. Although alcoholism and alcohol consumption are prevalent and represent crucial public health problems worldwide, many people believe that low-to-moderate ethanol consumption may protect against T2D and cardiovascular diseases. However, the J- or U-shaped curves obtained from cross-sectional and large prospective studies have not fully explained the relationship between alcohol consumption and T2D. This review provides evidence for the harmful effects of chronic ethanol consumption on the progressive development of T2D, particularly with respect to pancreatic β-cell mass and function in association with insulin synthesis and secretion. This review also discusses a conceptual framework for how ethanol-produced peroxynitrite contributes to pancreatic β-cell dysfunction and metabolic syndrome.