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.
PURPOSE: To examine the acute and chronic effects of alcohol on blood pressure (BP) and the incidence of hypertension. We discuss the most current understanding of the mechanisms underlining these effects and their associations with the putative cardioprotective effects of consumption of low-to-moderate amounts of alcoholic beverages.
RECENT FINDINGS: A recent meta-analysis confirmed findings of experimental studies, demonstrating an acute biphasic effect of ethanol on BP, decreasing up to 12 h of ingestion and increasing after that. This effect is mediated by vagal inhibition and sympathetic activation. A meta-analysis found that chronic consumption of alcoholic beverages was associated with a high incidence of hypertension in men and women; it also found that, in women, the risk begins at moderate alcohol consumption. The risks of alcohol consumption are higher in Blacks than in Asians or Caucasians. The mechanism underlying the chronic effects of alcohol on BP, and particularly the differential effect on Blacks, is still unknown. Short-term trials showed that alcohol withdrawal promotes BP reduction; however, the long-term effectiveness of interventions that aim to lower BP through the restriction of alcohol consumption has not been demonstrated.
The harmful effects of alcohol on BP do not support the putative cardioprotective effect of low-to-moderate consumption of alcoholic beverages. The absence of a tangible mechanism of protection, and the possibility that this beneficial effect is biased by socioeconomic and other characteristics of drinkers and abstainers, calls into question the hypothesis that consuming low amounts of alcoholic beverages improves cardiovascular health. The evidence from investigations with various designs converge regarding the acute biphasic effect of ethanol on BP and the risk of chronic consumption on the incidence of hypertension, particularly for Blacks. These effects do not support the putative cardioprotective effect of consumption of low-to-moderate amounts of alcoholic beverages. Mechanisms of chronic BP increase and the demonstration of long-term benefits of reducing alcohol intake as a means to treat hypertension remain open questions.
BACKGROUND: The association between Parkinson's disease (PD) risk and alcohol intake is a controversial topic.
OBJECTIVES: To systematically assess the association between PD risk and alcohol intake.
METHODS: PubMed and Embase databases were searched for eligible studies with prospective design on PD risk and alcohol intake. A meta-analysis with a random-effects model and dose-response analysis was performed. Relative risk ratios (RRs) with 95% CIs were calculated.
RESULTS: Eleven prospective studies were included. Overall, a higher intake of alcohol was inversely associated with PD risk (RR: 0.81, 95% CI: 0.70-0.95, I (2) = 73.7%). Significant differences existed between the specific types of alcoholic beverages and geographic area. Specifically, a significant association existed for beer (RR: 0.78, 95% CI: 0.65-0.94, I (2) = 0.0%) and studies conducted in Asia (RR: 0.66, 95% CI: 0.55-0.80, I (2) = 37.3%). Dose-response analysis indicated a nonlinear relationship between PD risk and alcohol exposure. No evidence for publication bias was detected.
CONCLUSIONS: In summary, our meta-analysis suggests that alcohol consumption was associated with a decreased risk of PD, with a nearly U-shaped association. Future studies are warranted to clarify the question of a specific type of alcoholic beverage-dependent association, geographic area effect, and possible threshold effects regarding both the adverse and beneficial effects of alcohol.