Association of Habitual Alcohol Intake With Risk of Cardiovascular Disease.
Association of Habitual Alcohol Intake With Risk of Cardiovascular Disease.
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DOI:
10.1001/jamanetworkopen.2022.3849
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发表时间:
2022-03-01
影响因子:
13.8
通讯作者:
Aragam KG
中科院分区:
文献类型:
--
作者:
Biddinger KJ;Emdin CA;Haas ME;Wang M;Hindy G;Ellinor PT;Kathiresan S;Khera AV;Aragam KG
What is the risk of cardiovascular disease associated with different amounts of habitual alcohol consumption? In this cohort study of 371 463 individuals, genetic evidence supported a nonlinear, consistently risk-increasing association between all amounts of alcohol consumption and both hypertension and coronary artery disease, with modest increases in risk with light alcohol intake and exponentially greater risk increases at higher levels of consumption. In this study, alcohol consumption at all levels was associated with increased risk of cardiovascular disease, but clinical and public health guidance around habitual alcohol use should account for the considerable differences in cardiovascular risk across different levels of alcohol consumption, even those within current guideline-recommended limits. This cohort study assesses the association between habitual alcohol intake and cardiovascular disease risk and evaluates the direction and relative magnitude of cardiovascular risk associated with different amounts of alcohol consumption. 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. 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. 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. Genetic predisposition to alcohol intake. The association between alcohol consumption and cardiovascular diseases, including hypertension, coronary artery disease, myocardial infarction, stroke, heart failure, and atrial fibrillation. This study included 371 463 participants (mean [SD] age, 57.0 [7.9] years; 172 400 [46%] men), who consumed a mean (SD) 9.2 (10.6) standard drinks per week. Overall, 121 708 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. 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.
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DOI:
10.1016/s0140-6736(18)32203-7
发表时间:
2018-11-10
期刊:
Lancet (London, England)
影响因子:
--
作者:
GBD 2017 Causes of Death Collaborators
通讯作者:
GBD 2017 Causes of Death Collaborators
影响因子:
2.1
作者:
Staley JR;Burgess S
通讯作者:
Burgess S
影响因子:
2.9
作者:
Visontay R;Sunderland M;Slade T;Wilson J;Mewton L
通讯作者:
Mewton L
DOI:
10.1016/s0140-6736(18)32225-6
发表时间:
2018-11-10
期刊:
Lancet (London, England)
影响因子:
--
作者:
GBD 2017 Risk Factor Collaborators
通讯作者:
GBD 2017 Risk Factor Collaborators
影响因子:
37.8
作者:
Arvanitis M;Qi G;Bhatt DL;Post WS;Chatterjee N;Battle A;McEvoy JW
通讯作者:
McEvoy JW