Mediating Effects of High-density Lipoprotein for Alcohol Consumption and Myocardial Infarction: The Multi-Ethnic Study of Atherosclerosis (OR19-07-19). (13th June 2019)

• Record Type: Journal Article
• Authors: Huang, Shue; Gao, Xiang; Li, Shanshan; Shearer, Gregory
• Is Part Of: Current developments in nutrition. Volume 3(2019)Supplement 1
• Publication Date: 2019-06-13
• Subjects: Nutrition -- Periodicals; Nutritional Physiological Phenomena; Nutrition; Periodicals; Periodicals; Fulltext; Internet Resources; Periodicals; 612.3
• DOI: 10.1093/cdn/nzz046.OR19-07-19
• Languages: English
• ISSNs: 2475-2991

Abstract

Abstract: Objectives: The aim of this study was to investigate whether and to what extent the association between alcohol intake and incident myocardial infarction (MI) is mediated through high density lipoprotein cholesterol (HDL-C), and HDL particles (HDL-P). Methods: A total of 6, 704 participants from the Multi-Ethnic Study of Atherosclerosis were included in the analysis. Alcohol consumption information was assessed via a questionnaire at baseline (exam 1). HDL-C concentrations and HDL-P were both measured at exam 1. Cox regression was used to model the association of habitual alcohol intake and risk for MI before and after adjusting HDL-C and HDL-P, in addition to adjustment of all potential covariates. Mediated effects through HDL-C, and HDL-P were estimated using the causal mediation analysis. Results: After a median of 8 years follow-up, 171 incident MI cases were documented. Alcohol intake was associated with a lower risk for incident MI (adjusted Hazard Ratio (HR) = 0.69, 95% Confidence Interval (CI): 0.50-0.95), relative to non-drinkers. The relation between alcohol intake and MI became nonsignificant after further adjusting HDL-P. The HRs of the indirect effect of alcohol through HDL-C and HDL-P were 0.97 (95% CI: 0.93, 1.01) (P = 0.16) and 0.94 (95% CI: 0.90, 0.99) (P = 0.02), indicating that on average, alcohol intake reduced the risk of MI by 6% through its effect on HDL-P and not through HDL-C. The proportion of the effect of alcohol on MI mediated by HDL-P was 14.6%. Conclusions: This study indicates that the lower risk of MI related to alcohol intake appears to partially work through increasing HDL-P, however, the mechanism for much of alcohol's effect to reduce MI risk remains unexplained. This suggests that HDL-P can be a target for MI prevention, however the mediating effect of HDL-P is very moderate. Funding Sources: N/A.