Key result
Higher alcohol intake was significantly associated with an increased risk of carotid plaque (OR 1.42; 95% CI 1.14-1.76 per 280 g/week) and higher plaque burden, but not with cIMT.
Why the study?
The causal relevance of alcohol intake to measures of carotid artery thickness and atherosclerosis in Chinese adults required investigation.
Does higher alcohol intake increase the risk of subclinical carotid atherosclerosis in Chinese adults?
Observational (n=22,384)
Does higher alcohol intake increase the risk of subclinical carotid atherosclerosis in Chinese adults?
Odds Ratio: 1.42 (95% CI 1.14–1.76)
Higher alcohol intake is causally associated with increased carotid plaque burden, supporting the atherogenic effect of alcohol and challenging notions of cardiovascular benefit from drinking.
Higher alcohol intake may promote subclinical carotid atherosclerosis; supports atherogenic effects but leaves causal and practice implications open.
BACKGROUND AND AIMS: We investigated the causal relevance of alcohol intake with measures of carotid artery thickness and atherosclerosis in Chinese adults. METHODS: The study included 22,384 adults from the China Kadoorie Biobank, with self-reported alcohol use at baseline and resurvey, carotid artery ultrasound measurements, and genotyping data for ALDH2-rs671 and ADH1B-rs1229984. Associations of carotid intima media thickness (cIMT), any carotid plaque, and total plaque burden (derived from plaque number and size) with self-reported (conventional analyses) and genotype-predicted mean alcohol intake (Mendelian randomization) were assessed using linear and logistic regression models. RESULTS: Overall 34.2% men and 2.1% women drank alcohol regularly at baseline. Mean cIMT was 0.70 mm in men and 0.64 mm in women, with 39.1% and 26.5% having carotid plaque, respectively. Among men, cIMT was not associated with self-reported or genotype-predicted mean alcohol intake. The risk of plaque increased significantly with self-reported intake among current drinkers (odds ratio 1.42 [95% CI 1.14-1.76] per 280 g/week), with directionally consistent findings with genotype-predicted mean intake (1.21 [0.99-1.49]). Higher alcohol intake was significantly associated with higher carotid plaque burden in both conventional (0.19 [0.10-0.28] mm higher per 280 g/week) and genetic analyses (0.09 [0.02-0.17]). Genetic findings in women suggested the association of genotype-predicted alcohol with carotid plaque burden in men was likely to due to alcohol itself, rather than pleiotropic genotypic effects. CONCLUSIONS: Higher alcohol intake was associated with a higher carotid plaque burden, but not with cIMT, providing support for a potential causal association of alcohol intake with carotid atherosclerosis.
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Zhou et al. (2023) conducted an observational in subclinical carotid atherosclerosis (n=22,384). Alcohol intake vs. Lower or no alcohol intake was evaluated on Any carotid plaque (OR 1.42, 95% CI 1.14-1.76). Higher alcohol intake was significantly associated with an increased risk of carotid plaque (OR 1.42; 95% CI 1.14-1.76 per 280 g/week) and higher plaque burden, but not with cIMT.
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