Alcohol and Steatotic Liver Disease Exhibit Divergent Associations with High Plasma Small Dense LDL-C Concentration.

Authors

Yasuhiro Matsubayashi, Kiminori Kato, Mao Watanabe, Yasuki Ito, Noriyuki Satoh, Takaaki Sato, Masaru Kitazawa, Takaho Yamada, Hirohito Sone

Published in

The Journal of clinical endocrinology and metabolism. Jun 19, 2026. Epub Jun 19, 2026.

Abstract

Within the metabolic dysfunction-associated steatotic liver disease (MASLD)/MASLD with increased alcohol intake (MetALD)/alcohol-associated liver disease (ALD) framework, cardiovascular risk varies by alcohol exposure. As small dense low-density lipoprotein cholesterol (sdLDL-C) is highly atherogenic, this study assessed the relative effects of steatotic liver disease (SLD) and alcohol consumption on sdLDL-C elevation and the effects of conventional fasting lipids [low-density lipoprotein cholesterol (LDL-C)/high-density lipoprotein cholesterol (HDL-C)/triglycerides (TGs)] on these associations.
This cross-sectional study enrolled 55,745 participants who underwent health screenings in Niigata, Japan between April 2024 and March 2025. Alcohol consumption was self-reported as low, moderate, or excessive. Participants were grouped by SLD status and alcohol consumption. sdLDL-C was directly measured, with high sdLDL-C defined as ≥35 mg/dL. Multivariable linear regression (sdLDL-C) and logistic regression (high sdLDL-C) analyses used two models: model 1 was adjusted for age, sex, body mass index, smoking, lipid-lowering medication, antihypertensive medication, and diabetes, and model 2 was further adjusted for LDL-C, HDL-C, and TGs. Marginal standardized prevalence and standardized prevalence differences (PDs) were estimated using g-computation with 2000 bootstrap iterations.
The crude prevalence of high sdLDL-C was influenced by SLD and alcohol consumption, being highest in the SLD(+)/excessive alcohol consumption group (76.4%). In model 2, SLD-related associations were attenuated, whereas alcohol-related associations remained robust, as the PD was lower for SLD(+) than for SLD(-) within each alcohol category.
Alcohol exposure contributes to an atherogenic sdLDL-C phenotype beyond conventional fasting lipids within contemporary SLD categories, indicating potential relevance for risk profiling in MetALD/ALD.

PMID:
42319754
Bibliographic data and abstract were imported from PubMed on 19 Jun 2026.

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