BACKGROUND AND OBJECTIVE: Changes in lipoproteins and hemostasis only incompletely explain the reduced cardiovascular mortality associated with light to moderate alcohol consumption. Since increasing evidence suggests that atherosclerosis can be considered to be a chronic inflammatory process, we sought to assess the association between daily alcohol consumption and levels of sensitive markers of inflammation. STUDY PARTICIPANTS AND METHODS: 478 voluntary blood donors (358 men, 120 women) aged 40 to 68 years were categorized into four groups according to their self-reported amount of daily alcohol consumption: 0 g/day, >0 - 20 g/day, >20 - 40 g/day, and > 40 g/day. Means of various sensitive markers of inflammation (C-reactive protein (CRP), serum amyloid A (SAA), interleukin-6 (IL-6), intercellular adhesion molecule-1, plasma viscosity und albumin) were calculated and compared by bivariate and multivariate analyses. RESULTS: More than 80 % of the study participants reported to consume alcohol, mainly beer. We found statistically significantly decreased levels of SAA, CRP, and plasma viscosity in subjects with light-to-moderate alcohol intake (>0 - 20 g/day and > 20 - 40 g/day, respectively), and a trend for increased levels of albumin in these subjects compared to non-drinkers. After multivariable adjustment for potential confounders (age, gender, body mass index, cigarette smoking, years of school education, and physical activity) a significant U-shaped association (p = 0.02) between levels of SAA and the amount of daily alcohol intake remained: there were 0.75 mg/l and 0.70 mg/l lower mean levels, respectively, of SAA in subjects with light-to-moderate alcohol intake compared to those of non-drinkers. Subjects with an alcohol intake of > 40 grams per day showed a statistically significant increase in levels of interleukin-6 (0.50 pg/ml) compared to non-drinkers. CONCLUSION: Potential anti-inflammatory properties of moderate alcohol consumption might represent an additional mechanism to explain its atheroprotective effect.
BACKGROUND AND OBJECTIVE: Changes in lipoproteins and hemostasis only incompletely explain the reduced cardiovascular mortality associated with light to moderate alcohol consumption. Since increasing evidence suggests that atherosclerosis can be considered to be a chronic inflammatory process, we sought to assess the association between daily alcohol consumption and levels of sensitive markers of inflammation. STUDY PARTICIPANTS AND METHODS: 478 voluntary blood donors (358 men, 120 women) aged 40 to 68 years were categorized into four groups according to their self-reported amount of daily alcohol consumption: 0 g/day, >0 - 20 g/day, >20 - 40 g/day, and > 40 g/day. Means of various sensitive markers of inflammation (C-reactive protein (CRP), serum amyloid A (SAA), interleukin-6 (IL-6), intercellular adhesion molecule-1, plasma viscosity und albumin) were calculated and compared by bivariate and multivariate analyses. RESULTS: More than 80 % of the study participants reported to consume alcohol, mainly beer. We found statistically significantly decreased levels of SAA, CRP, and plasma viscosity in subjects with light-to-moderate alcohol intake (>0 - 20 g/day and > 20 - 40 g/day, respectively), and a trend for increased levels of albumin in these subjects compared to non-drinkers. After multivariable adjustment for potential confounders (age, gender, body mass index, cigarette smoking, years of school education, and physical activity) a significant U-shaped association (p = 0.02) between levels of SAA and the amount of daily alcohol intake remained: there were 0.75 mg/l and 0.70 mg/l lower mean levels, respectively, of SAA in subjects with light-to-moderate alcohol intake compared to those of non-drinkers. Subjects with an alcohol intake of > 40 grams per day showed a statistically significant increase in levels of interleukin-6 (0.50 pg/ml) compared to non-drinkers. CONCLUSION: Potential anti-inflammatory properties of moderate alcohol consumption might represent an additional mechanism to explain its atheroprotective effect.