OBJECTIVE: In a randomized controlled trial, we assessed the effect of daily moderate alcohol intake on glycemic control in the fasting and postprandial states in patients with type 2 diabetes who previously had abstained from alcohol.
RESEARCH DESIGN AND METHODS: We randomly assigned 109 patients (41-74 years old) with established type 2 diabetes who abstained from alcohol to receive 150 ml wine (13 g alcohol) or nonalcoholic diet beer (control) each day during a 3-month multicenter trial. The beverages were consumed during dinner. Diet and alcohol consumption were monitored.
RESULTS: During the intervention, 17% of participants (12% from the alcohol group) dropped out, leaving 91 who completed the trial. Within the alcohol group, fasting plasma glucose (FPG) decreased from 139.6 +/- 41 to 118.0 +/- 32.5 mg/dl after 3 months compared with 136.7 +/- 15.4 to 138.6 +/- 27.8 mg/dl in the control subjects (P(v) = 0.015). However, alcohol consumption had no effect on 2-h postprandial glucose levels (difference of 18.5 mg/dl in the control group vs. 17.7 mg/dl in the alcohol group, P(v) = 0.97). Patients in the alcohol group with higher baseline A1C levels had greater reductions in FPG (age-adjusted correlation -0.57, P(v) < 0.001). No significant changes were observed in the levels of bilirubin, alkaline phosphatase, alanine aminotransferase, or aspartate aminotransferase, and no notable adverse effects were reported. Participants in the alcohol group reported an improvement in the ability to fall asleep (P(v) < 0.001).
CONCLUSIONS: Among patients with type 2 diabetes who had previously abstained from alcohol, initiation of moderate daily alcohol consumption reduced FPG but not postprandial glucose. Patients with higher A1C may benefit more from the favorable glycemic effect of alcohol. Further intervention studies are needed to confirm the long-term effect of moderate alcohol intake.
Objective: The objective of this study was to investigate the association of four-year changes in alcohol consumption with subsequent risk of type 2 diabetes.
Research Design and Methods: We prospectively examined 38,031 men from the Health Professionals Follow-up Study free of diagnosed diabetes or cancer in 1990. Alcohol consumption was reported on food frequency questionnaires and updated every four years.
Results: A total of 1905 cases of type 2 diabetes occurred during 428,497 person-years of follow-up. A 7.5 g/day ( approximately half a glass) increase in alcohol consumption over four years was associated with lower diabetes risk among initial nondrinkers (multivariable hazard ratio [HR] 0.78; 95% confidence interval [CI] 0.60-1.00) and drinkers initially consuming /=15 g/day (HR 0.99; 95% CI 0.95-1.02; P(interaction) < 0.01). A similar pattern was observed for levels of total adiponectin and hemoglobin A(1c), with a better metabolic profile among abstainers and light drinkers who modestly increased their alcohol intake, compared with men who either drank less or among men who were already moderate drinkers and increased their intake. Likewise, compared to stable light drinkers (0-4.9 g/day), light drinkers who increased their intake to moderate levels (5.0-29.9 g/day) had a significantly lower risk of type 2 diabetes (HR 0.75; 95% CI 0.62-0.90).
Conclusions: Increases in alcohol consumption over time were associated with lower risk of type 2 diabetes among initially rare and light drinkers. This lower risk was evident within a four-year period following increased alcohol intake.
OBJECTIVE: Moderate alcohol consumption is associated with reduced incidence of type 2 diabetes and cardiovascular mortality and increases adiponectin concentrations, but effects might differ according to sex and beverage consumed.
RESEARCH DESIGN AND METHODS: A total of 72 healthy individuals (22-56 years) were enrolled in this randomized controlled crossover trial. After washout, two interventions for 3 weeks followed: ethanol (concentration 12.5%), beer (5.6%), or red wine (12.5%) equivalent to 30 g ethanol/day for men and 20 g/day for women or the same de-alcoholized beverages or water. Adiponectin was measured by sandwich enzyme-linked immunosorbent assay.
RESULTS: Among women, adiponectin significantly increased after consuming red wine (29.8%, P < 0.05) and increased among men after ethanol solution (17.4%, P < 0.05) and consuming beer (16.1%, P < 0.05). De-alcoholized beverages had no substantial effect on adiponectin concentrations.
CONCLUSIONS: Moderate amounts of ethanol-containing beverages increased adiponectin concentrations, but sex-specific effects might depend on type of beverage consumed.
OBJECTIVE: The purpose of this study was to investigate whether adiponectin concentrations and biomarkers of inflammation, endothelial dysfunction, and insulin resistance mediate the association between alcohol consumption and diabetes.
RESEARCH DESIGN AND METHODS: In a nested case-control study of 705 women with incident diabetes and 787 matched control subjects, we examined the adjusted relationship between baseline alcohol consumption and risk of diabetes before and after adjustment for markers of inflammation/endothelial dysfunction (C-reactive protein, vascular cell adhesion molecule-1, intercellular adhesion molecule-1, E-selectin, tumor necrosis factor-alpha receptor 2, and interleukin-6), fasting insulin, and adiponectin concentrations.
RESULTS: Alcohol consumption was associated with a decreased risk of diabetes (odds ratio per 12.5 g/day increment in alcohol use 0.58; 95% CI 0.49-0.69; P < 0.001). Adjustment for BMI attenuated the association by 25%. None of the markers of inflammation or fasting insulin appeared to account for >2% of the observed relationship. Without adjustment for BMI, these biomarkers individually explained slightly more of the association, but <10% in all cases. Adiponectin accounted for 25% in a fully adjusted model and for 29% without adjustment for BMI.
CONCLUSIONS: In this population of women, alcohol consumption was inversely associated with risk of type 2 diabetes. Adiponectin appeared to be a mediator of this association, but circulating biomarkers of inflammation, endothelial dysfunction, and fasting insulin did not explain this association. These results suggest that further research is needed into the potentially mediating roles of other biomarkers affected by alcohol consumption.