Effects of Alcohol on the Cardiovascular System in Women

Abstract

Alcohol use has complex effects on cardiovascular (CV) health. The associations between drinking and CV diseases such as hypertension, coronary heart disease, stroke, peripheral arterial disease, and cardiomyopathy have been studied extensively and are outlined in this review. Although many behavioral, genetic, and biologic variants influence the interconnection between alcohol use and CV disease, dose and pattern of alcohol consumption seem to modulate this most. Low-to-moderate alcohol use may mitigate certain mechanisms such as risk and hemostatic factors affecting atherosclerosis and inflammation, pathophysiologic processes integral to most CV disease. But any positive aspects of drinking must be weighed against serious physiological effects, including mitochondrial dysfunction and changes in circulation, inflammatory response, oxidative stress, and programmed cell death, as well as anatomical damage to the CV system, especially the heart itself. Both the negative and positive effects of alcohol use on particular CV conditions are presented here. The review concludes by suggesting several promising avenues for future research related to alcohol use and CV disease. These include using direct biomarkers of alcohol to confirm self-report of alcohol consumption levels; studying potential mediation of various genetic, socioeconomic, and racial and ethnic factors that may affect alcohol use and CV disease; reviewing alcohol–medication interactions in cardiac patients; and examining CV effects of alcohol use in young adults and in older adults.

Evaluating the effects of alcohol and tobacco use on cardiovascular disease using multivariable Mendelian randomization

“…Importantly, in our main analysis we failed to find a cardioprotective effect of alcohol use on CVD outcomes, suggesting that previously reported reductions in CVD risk due to other lifestyle differences that are associated with more light-to-moderate drinking patterns, such as healthier lifestyles 37 , are contributing to these effects. Our total weekly consumption instrument may have failed to differentiate between light-to-moderate drinking and heavier consumption, which are reported to have inverse associations with CVD disease risk in observational literature 14 . More likely, however, previous research may not have accounted for smoking, which we found to be significantly associated with increased CVD risk.…”

“…Expanding upon their single stroke variable, which may mask differential associations between alcohol and stroke subtypes 11 further strengthens our conclusions. Failing to replicate the instrumental variable estimates Millwood et al 2019 found among participants in the China Kadoorie Biobank sample supports the hypothesized differential effect of alcohol consumption on CVD risk across ethnic backgrounds 14,39 . East Asia has the highest prevalence of stroke worldwide 40 , and generally lower alcohol consumption behaviors than European countrie.…”

“…In general, our findings support previous observational research showing a relationship between alcohol, smoking, and CVDs 5,13 , and the consistent estimates across complementary MR methods and after controlling alcohol consumption for smoking (and smoking for alcohol consumption) strengthen causal inference. Finding robust increases in HDL-C with no corresponding reduction in CVD risk calls into question the mechanism through which observational literature attributed any cardioprotective effect of light-to-moderate alcohol consumption 14 . Similarly, our results, when combined with traditional RCTs and MR studies that failed to find CVD risk reduction of increased HDL-C [34][35][36] suggests that there is no cardioprotective effect of alcohol consumption.…”

“…Meta-analyses and short-term trials suggest alcohol consumption is associated with CVD risk factors including increased high-density lipoprotein-cholesterol (HDL-C) 13 ; however, the association with low-density lipoprotein cholesterol (LDL-C) and triglycerides (TRG) are less clear 14 . Variation in size, density, concentrations and composition of circulating lipids, which traditional measures are unable to distinguish, are thought to have contrasting effects to CVD risk 15 .…”

“…Despite its public health importance 13 , nearly all human data evaluating the alcohol-CVD relationship is from conventional epidemiological studies 14 , and thus, the causal effect of alcohol consumption patterns on CVD risk factors and outcomes has not been fully elucidated. Triangulating evidence from different study designs is needed to improve our understanding of the alcohol-CVD relationship 16 .…”