We examined whether the often-reported protective association of alcohol with cardiovascular disease (CVD) risk could arise from confounding. Our sample comprised 908 men (56-67 years), free of prevalent CVD. Participants were categorized into 6 groups: never drinkers, former drinkers, and very light (1-4 drinks in past 14 days), light (5-14 drinks), moderate (15-28 drinks), and at-risk (>28 drinks) drinkers. Generalized linear mixed effect models examined the associations of alcohol use with three established CVD risk scores: The Framingham Risk Score (FRS); the atherosclerotic CVD (ASCVD) risk score; and the Metabolic Syndrome (MetS) Severity score, adjusting for group differences in demographics, body size, and health-related behaviors. In separate models we additionally adjusted for several groups of potentially explanatory factors including socioeconomic status, social support, physical and mental health status, childhood factors, and prior history of alcohol misuse. Results showed lower CVD risk among light and moderate alcohol drinkers, relative to very light drinkers, for all CVD risk scores, independent of demographics, body size, and health-related behaviors. Alcohol-CVD risk associations were robust to further adjustment for several groups of potential explanatory factors. Study limitations include the all-male sample with limited racial and ethnic diversity, and the inability to adjust for sugar consumption and for patterns of alcohol consumption. Although this observational study does not address causation, results show that middle-aged men who consume alcohol in moderation have lower CVD risk and better cardiometabolic health than men who consume little or no alcohol, independent of a variety of health, behavioral, psychosocial, and earlier life factors.
OBJECTIVE: To assess the prevalence of metabolic syndrome (MetS) in Chinese adults living in Ningbo and to examine the association between alcohol consumption and MetS and its medical components.
DESIGN: A representative survey in Ningbo was conducted in 2015 covering socio-demography. A FFQ together with additional questionnaires was used to collect information on alcohol consumption, diet, demography, lifestyle and medical information. Multivariable logistic regression and generalised linear models were used to examine the association between alcohol consumption and both MetS and its medical components, respectively.
SETTING: Ningbo, China.
PARTICIPANTS: A total of 2853 adults >/= 20 years (44 % men) in this final analysis.
RESULTS: The prevalence of frequent alcohol drinkers and MetS was 29.9 % and 28.0 %, respectively. Significantly higher prevalence of MetS and mean values of medical components were found in the group of frequent alcohol drinkers with an exception for HDL-cholesterol, compared with less or non-alcohol drinkers. Frequent alcohol consumption was associated with higher odds of developing MetS and positively associated with medical components excepting waist circumference.
CONCLUSIONS: Frequent alcohol consumption contributed to a higher prevalence of MetS and unfavourable influence on MetS and its medical components among Chinese adults. A public health intervention on alcohol restriction is necessary for the prevention and control of the ongoing epidemic MetS.
The causal effects of alcohol-in-moderation on cardiometabolic health are continuously debated. Mendelian randomization (MR) is an established method to address causal questions in observational studies. We performed a systematic review of the current evidence from MR studies on the association between alcohol consumption and cardiometabolic diseases, all-cause mortality and cardiovascular risk factors. We performed a systematic search of the literature, including search terms on type of design and exposure. We assessed methodological quality based on key elements of the MR design: use of a full instrumental variable analysis and validation of the three key MR assumptions. We additionally looked at exploration of non-linearity. We reported the direction of the studied associations. Our search yielded 24 studies that were eligible for inclusion. A full instrumental variable analysis was performed in 17 studies (71%) and 13 out of 24 studies (54%) validated all three key assumptions. Five studies (21%) assessed potential non-linearity. In general, null associations were reported for genetically predicted alcohol consumption with the primary outcomes cardiovascular disease (67%) and diabetes (75%), while the only study on all-cause mortality reported a detrimental association. Considering the heterogeneity in methodological quality of the included MR studies, it is not yet possible to draw conclusions on the causal role of moderate alcohol consumption on cardiometabolic health. As MR is a rapidly evolving field, we expect that future MR studies, especially with recent developments regarding instrument selection and non-linearity methodology, will further substantiate this discussion.
BACKGROUND: Alcohol consumption and cardiovascular disease (CVD) have a complex relation.
OBJECTIVES: We examined the associations between alcohol consumption, fasting plasma proteins, and CVD risk.
METHODS: We performed cross-sectional association analyses of alcohol consumption with 71 CVD-related plasma proteins, and also performed prospective association analyses of alcohol consumption and protein concentrations with 3 CVD risk factors (obesity, hypertension, and diabetes) in 6745 Framingham Heart Study (FHS) participants (mean age 49 y; 53% women).
RESULTS: A unit increase in log10 transformed alcohol consumption (g/d) was associated with an increased risk of hypertension (HR = 1.14; 95% CI: 1.04, 1.26; P = 0.007), and decreased risks of obesity (HR = 0.80; 95% CI: 0.71, 0.91; P = 4.6 x 10-4) and diabetes (HR: 0.68; 95% CI: 0.58, 0.80; P = 5.1 x 10-6) in a median of 13-y (interquartile = 7, 14) of follow-up. We identified 43 alcohol-associated proteins in a discovery sample (n = 4348, false discovery rate <0.05) and 20 of them were significant (P <0.05/43) in an independent validation sample (n = 2397). Eighteen of the 20 proteins were inversely associated with alcohol consumption. Four of the 20 proteins demonstrated 3-way associations, as expected, with alcohol consumption and CVD risk factors. For example, a greater concentration of APOA1 was associated with higher alcohol consumption (P = 1.2 x 10-65), and it was also associated with a lower risk of diabetes (P = 8.5 x 10-6). However, several others showed unexpected 3-way associations.
CONCLUSIONS: We identified 20 alcohol-associated proteins in 6745 FHS samples. These alcohol-associated proteins demonstrated complex relations with the 3 CVD risk factors. Future studies with integration of more proteomic markers and larger sample size are warranted to unravel the complex relation between alcohol consumption and CVD risk.