Based on a prospective cohort study of adults from southwest China with heterogeneity in their demographical characteristics and lifestyles, we aimed to explore the association between drinking patterns and incident hypertension under the interaction of these confounding factors. The Cox proportional hazard model was used to estimate the hazard ratios (HR) and 95% confidence intervals (95% CI).
Subgroup analysis was performed according to sex, ethnicity, area, occupation, smoking, and exercise to compare the differences in the association between drinking patterns and the incidence of hypertension. Blood pressure was higher in participants with a high drinking frequency than those with a low drinking frequency (p < 0.001). We found that total drinking frequency, liquor drinking frequency, rice wine drinking frequency, and alcohol consumption were significantly associated with an increased risk of hypertension.
Compared with the non-drinking group, a heavy drinking pattern was positively correlated with hypertension. Drinking can increase the risk of hypertension, especially heavy drinking patterns, with a high frequency of alcohol intake and high alcohol consumption. From the analysis results of the longitudinal data, drinking alcohol is still an important risk factor for hypertension among Chinese subjects, especially for men, the rural population, the employed, the Han nationality, smokers, and certain exercise populations.
IMPORTANCE: Observational studies have consistently proposed cardiovascular benefits associated with light alcohol consumption, while recent genetic analyses (ie, mendelian randomization studies) have suggested a possible causal link between alcohol intake and increased risk of cardiovascular disease. However, traditional approaches to genetic epidemiology assume a linear association and thus have not fully evaluated dose-response estimates of risk across different levels of alcohol intake.
OBJECTIVES: To assess the association of habitual alcohol intake with cardiovascular disease risk and to evaluate the direction and relative magnitude of cardiovascular risk associated with different amounts of alcohol consumption.
DESIGN, SETTING, and PARTICIPANTS: This cohort study used the UK Biobank (2006-2010, follow-up until 2016) to examine confounding in epidemiologic associations between alcohol intake and cardiovascular diseases. Using both traditional (ie, linear) and nonlinear mendelian randomization, potential associations between alcohol consumption and cardiovascular diseases (eg, hypertension and coronary artery disease) as well as corresponding association shapes were assessed. Data analysis was conducted from July 2019 to January 2022.
EXPOSURES: Genetic predisposition to alcohol intake.
MAIN OUTCOMES AND MEASURES: The association between alcohol consumption and cardiovascular diseases, including hypertension, coronary artery disease, myocardial infarction, stroke, heart failure, and atrial fibrillation.
RESULTS: This study included 371463 participants (mean [SD] age, 57.0 [7.9] years; 172400 [46%] men), who consumed a mean (SD) 9.2 (10.6) standard drinks per week. Overall, 121708 participants (33%) had hypertension. Light to moderate alcohol consumption was associated with healthier lifestyle factors, adjustment for which attenuated the cardioprotective epidemiologic associations with modest intake. In linear mendelian randomization analyses, a 1-SD increase in genetically predicted alcohol consumption was associated with 1.3-fold (95% CI, 1.2-1.4) higher risk of hypertension (P < .001) and 1.4-fold (95% CI, 1.1-1.8) higher risk of coronary artery disease (P = .006). Nonlinear mendelian randomization analyses suggested nonlinear associations between alcohol consumption and both hypertension and coronary artery disease: light alcohol intake was associated with minimal increases in cardiovascular risk, whereas heavier consumption was associated with exponential increases in risk of both clinical and subclinical cardiovascular disease.
CONCLUSIONS and RELEVANCE: In this cohort study, coincident, favorable lifestyle factors attenuated the observational benefits of modest alcohol intake. Genetic epidemiology suggested that alcohol consumption of all amounts was associated with increased cardiovascular risk, but marked risk differences exist across levels of intake, including those accepted by current national guidelines.
This Data in Brief article contains further sensitivity analysis data related to the article "Alcohol consumption and mortality: the Ludwigshafen Risk and Cardiovascular Health (LURIC) study" [1]. Alcohol consumption data of participants in LURIC was collected using a questionnaire. This data was used to calculate the amount of alcohol consumption in g ethanol per day by using standard volumes and standard vol-% in different beverages in Germany.
The data shown here provide results from the LURIC study stratified by gender. Furthermore, the LURIC study results were reproduced using other classifications, which were stratified in different literature data. In addition, our analysis provides data of alcohol consumption for smokers and non-smokers in the LURIC study cohort separately.
The relationship between alcohol consumption and cardiovascular disease risk is complex. Low-to-moderate daily alcohol consumption (1-2 drinks/day) is associated with reduced risk, whereas greater amounts of alcohol consumption and a "binge" pattern of drinking are associated with increased cardiovascular risk and mortality. Arterial stiffness may help explain the complex relationship.
This integrated review summarizes data from studies examining the associations between alcohol consumption and pulse wave velocity, a gold standard measure of arterial stiffness. We also briefly review the concept and methodology of pulse wave velocity measurement as well as the mechanisms of alcohol-induced arterial stiffening.
Findings among the different studies reviewed were inconsistent with methodological challenges related to alcohol use assessment. While making specific conclusions regarding this relationship is tenuous; the data suggest that excessive alcohol consumption or a binge drinking pattern is associated with increased arterial stiffness.