Abstract Alcohol drinking patterns encompass various dimensions of consumption. However, most studies have focused narrowly on the quantity of alcohol consumed. This study aimed to identify alcohol-drinking patterns in middle-aged population using alcohol-related variables and to examine their relationship with coronary heart disease (CHD), stroke, and all-cause-mortality risk. The present population-based study included adults from the Danish Health Examination Survey (DANHES) cohort who were ≥40 years old and free of CHD and stroke at baseline (n = 46 141). Latent Class Analysis (LCA) was used to identify distinct subpopulations based on six alcohol-related variables (amount, frequency, binge episodes, type, within meals, at home and alone). Cox proportional hazard models were used to estimate hazard ratios (95% confidence interval) between drinking patterns and CHD, stroke, and all-cause mortality during a median follow-up of 11.8 years. Four classes of drinking patterns were identified in both sexes (labeled as “low drinkers,” “low-to-moderate drinkers,” “moderate-regular drinkers,” and “frequent-heavy drinkers”). The more frequent drinking pattern was a median of 3 (2–5) drinks per week. Frequent heavy drinking was associated with a higher risk of stroke. Individuals in the low-to-moderate male drinking class and the moderate-regular female drinking class not under heart medication had a lower risk of all-cause mortality than low-level drinkers. Four distinct drinking patterns were identified. Among individuals 40 years and older, frequent-heavy drinking was associated with a higher risk of stroke, while low-to-moderate regular drinking might be associated with a lower all-cause mortality risk compared to low drinkers.
Marta Trius-Soler, M. Guasch-Ferré, Cristina Valle-Hita et al.· European Journal of Public H...· 0 citations
BACKGROUND AND AIMS
All apolipoprotein B-containing lipoproteins are established causal factors for coronary artery disease (CAD). This study aimed to identify robust proteomic signatures of low-density lipoprotein (LDL), triglyceride-rich lipoproteins (TRL), and lipoprotein(a) [Lp(a)] and to evaluate whether these signatures illuminate biological processes underlying differences in per-particle atherogenicity.
METHODS
Plasma proteins associated with LDL, TRL, and Lp(a) concentrations were identified using multivariable-adjusted regression across 2918 proteins in a primary prevention cohort based on UK Biobank (n=35,269), and findings were corroborated using one-sample Mendelian randomization. Proteins consistently identified by both approaches were summarized into lipoprotein-specific multi-protein scores and associated with incident CAD (n=1599 events) using Cox regression. High-dimensional mediation analysis quantified the proportion of lipoprotein-associated CAD risk explained by proteomic alterations. Findings were replicated in the Multi-Ethnic Study of Atherosclerosis (n=5915).
RESULTS
Requiring concordance between observational and Mendelian randomization analyses (both Bonferroni-adjusted P<0.05), 30 proteins were identified as associated with LDL, 471 with TRL, and 53 with Lp(a). The TRL and Lp(a) signatures were distinct from the LDL signature yet overlapped substantially with each other (36 shared proteins), with common enrichment in inflammatory pathways. After adjustment for potential confounders and measured lipoprotein concentrations, the multi-protein scores for TRL (hazard ratio per 1-SD [HRSD], 1.16; 95% confidence interval [95%CI]: 1.08-1.24) and Lp(a) (HRSD, 1.09; 95%CI: 1.03-1.15), but not LDL (HRSD, 0.95; 95%CI: 0.89-1.02), were associated with incident CAD. Mediation analysis was consistent with immune activation and vascular remodeling markers mediating TRL-associated CAD risk (proportion mediated, 62%) and, in part, Lp(a)-associated risk (14%).
CONCLUSIONS
Beyond arterial lipid deposition, TRL and Lp(a) converge on inflammatory and vascular remodeling pathways that, under the assumptions of observational mediation analysis, may explain their excess per-particle atherogenicity compared with LDL.
J. Morze, E. Björnson, Michael Y. Mi et al.· European Heart Journal· 0 citations
We use cookies to run the site and, with your consent, for analytics and to show ads.
See our Cookie Policy.
