Aims/hypothesis Type 2 diabetes is associated with reduced antioxidant defence. Only a few human studies have investigated the role of antioxidants in the pathogenesis of diabetes. This study aimed to examine whether α-tocopherol or β-carotene affected the occurrence of type 2 diabetes. Methods In the Alpha-Tocopherol, Beta-Carotene Cancer Prevention (ATBC) Study, a double-blind, controlled trial, 29,133 male smokers aged 50-69 years were randomised to receive either α-tocopherol (50 mg/day) or β-carotene (20 mg/day) or both agents or placebo daily for 5-8 years (median 6.1 years). Baseline serum samples were analysed for α-tocopherol and β-carotene using HPLC. Cases of diabetes were identified from a nationwide Finnish registry of patients receiving drug reimbursement for diabetes. Of 27,379 men without diabetes at baseline, 705 men were diagnosed with diabetes during the follow-up of up to 12.5 years. Results Baseline serum levels of α-tocopherol and β-carotene were not associated with the risk of diabetes in the placebo group: the relative risk (RR) between the highest and lowest quintiles of α-tocopherol was 1.59 (95% CI 0.89-2.84) and that for β-carotene was 0.66 (95% CI 0.40-1.10). Neither supplementation significantly affected the incidence of diabetes: the RR was 0.92 (95% CI 0.79-1.07) for participants receiving α-tocopherol compared with nonrecipients and 0.99 (95% CI 0.85-1.15) for participants receiving β-carotene compared with non-recipients. Conclusions/interpretation Neither α-tocopherol nor β-carotene supplementation prevented type 2 diabetes in male smokers. Serum levels of α-tocopherol and β-carotene were not associated with the risk of type 2 diabetes.ClinicalTrials.gov ID no. NCT00342992
Background/Objectives: Oxidative stress may induce insulin resistance in peripheral tissues and impair insulin secretion from pancreatic b-cells. Antioxidants are suggested to decrease the risk of diabetes through reduction of oxidative stress. However, only a few studies exist on dietary antioxidants and the risk of type 2 diabetes. We investigated the association of dietary antioxidants with incident type 2 diabetes in the a-Tocopherol, b-Carotene Cancer Prevention Study cohort. Subject/Methods: The study cohort included 29 133 male smokers aged 50-69 years. During a median follow-up of 10.2 years 660 incident cases of diabetes were observed among the 25 505 men with a completed baseline food frequency questionnaire. Results: Dietary a-tocopherol, b-tocopherol and b-tocotrienol were positively associated with the risk of diabetes when adjusted for age and supplementation (relative risk (RR) 1.17 (95% confidence interval (CI) 0.91-1.51) P for trend 0.02; RR 1.31 (95% CI 1.02-1.68) P for trend 0.01; RR 1.28 (95% CI 1.00-1.63) P for trend 0.01, respectively), but the association disappeared after multivariate adjustment (RR 0.92 (95% CI 0.71-1.19) P for trend 0.97; RR 1.06 (95% CI 0.82-1.36) P for trend 0.48; RR 1.04 (95% CI 0.80-1.35) P for trend 0.46, respectively). Other tocopherols and tocotrienols as well as vitamin C, carotenoids, flavonols and flavones had no association with risk of diabetes. Conclusions: Dietary antioxidants were not associated with a decreased risk of incident diabetes in middle-aged male smokers.
Relatively small lifestyle modifications related to weight reduction, physical activity and diet has been shown to decrease the risk of type 2 diabetes. Connected with diet, low consumption of meat has been suggested as a protective factor of diabetes. The aim was to examine the association between the consumption of total meat or the specific types of meat and risk of type 2 diabetes. The ATBC cohort included middle aged male smokers. During up to 12 years of follow-up, 1098 incident cases of diabetes were diagnosed from 24,845 participants through the nationwide register. Food consumption was assessed by a validated food frequency questionnaire. In the age and intervention group adjusted model, high total meat consumption was a risk factor of type 2 diabetes (relative risk (RR) 1.50, 95% confidence interval (CI): 1.23, 1.82, highest vs. lowest quintile). The result was similar after adjustment for environmental factors and foods related to diabetes and meat consumption. The RR of type 2 diabetes was 1.37 for processed meat (95% CI: 1.11, 1.71) in the multivariate model. The results were explained more by intakes of sodium than intakes of saturated fatty acids, protein, cholesterol, heme iron, magnesium and nitrate, and were not modified by obesity. No association was found between red meat, poultry and the risk of type 2 diabetes. In conclusion, it may help to prevent the global epidemic of type 2 diabetes by reducing the consumption of processed meat. It seems that sodium of processed meat may explain the association.
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