Effects of ethanol intake on lipoproteins and atherosclerosis.
Abstract
PURPOSE OF REVIEW: This article reviews published studies regarding effects of ethanol intake on lipoprotein levels and function as they relate to atherosclerosis, with special emphasis on recent publications in the past 2 years. RECENT FINDINGS: Some recent studies have explored novel mechanisms of ethanol on atherogenesis via effects on HDL composition and function. Other studies have focused on changes in levels of LDL cholesterol (LDL-C), triglyceride, and other factors such as inflammatory markers C-reactive protein (CRP) and lipoprotein-associated phospholipase A2 (LpPLA2). Other areas of emphasis have been the effects within specific populations and between genders, as well as contributions of genetic polymorphisms in prediction of response to ethanol. Surprisingly, results of recent studies are often at odds with prior, seemingly well established findings. SUMMARY: The association between moderate ethanol consumption and favorable changes in lipoproteins and lipoprotein-related factors in atherosclerosis continues to become better established with the publication of new studies in this field. Continued progress is being achieved in understanding the well established link between moderate intake and reduced risk of cardiovascular disease (CVD). Nevertheless, it remains difficult to implement these findings in clinical practice due to the ongoing lack of randomized, blinded clinical trial data, and the well known hazards of excess ethanol consumption.
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Alcohol intake increases hepatic fatty acid synthesis and decreases fatty acid oxidation, with a net effect to stimulate hepatic VLDL triglyceride secretion.
“Alcohol intake increases hepatic fatty acid synthesis and decreases fatty acid oxidation, with a net effect to stimulate hepatic VLDL triglyceride secretion.”
From Evaluation and Treatment of Hypertriglyceridemia: An Endocrine Society Clinical Practice Guideline (2012) · cites this paper as [106]
The effects of alcohol on triglycerides are dose-dependent.
“The effects of alcohol vary interindividually, tend to be amplified in subjects with underlying lipid disorders, are dose-dependent (106), and may be related to the mode of intake (107).”
From Evaluation and Treatment of Hypertriglyceridemia: An Endocrine Society Clinical Practice Guideline (2012) · cites this paper as [106]
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References 46 · Cited by 95
- Authors
- Brinton, E. A.
- Affiliations
- University of Utah (US)
- Corresponding author
- Brinton, Eliot A
- ORCID
- Brinton, Eliot A
- Venue
- Current Opinion in Lipidology
- Published
- 2010-08
- Volume
- 21
- Issue
- 4
- Pages
- 346-351
- ISSN
- 0957-9672 (ISSN-L)
- OpenAlex
- W1987232383
- Cited by
- 95
- References
- 46
- Citations by year
- 2025: 5 · 2024: 8 · 2023: 4 · 2022: 3 · 2021: 3 · 2020: 2 · 2019: 4 · 2018: 8 · 2017: 1 · 2016: 9 · 2015: 7 · 2014: 3 · 2013: 8 · 2012: 19
- FWCI
- 1.50
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Current Opinion in Lipidology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- National Institute on Aging (R01AG18734, R01AG018734)
- Topics
- Health Sciences › Medicine › Pathology and Forensic Medicine › Alcohol Consumption and Health Effects
- Health Sciences › Medicine › Surgery › Lipoproteins and Cardiovascular Health
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipid metabolism and disorders
- Keywords
- ethanol consumption, moderate drinking, lipoproteins, atherosclerosis, HDL cholesterol, LDL cholesterol, triglycerides, C-reactive protein, lipoprotein-associated phospholipase A2, inflammation, sex differences, genetic polymorphism, cardiovascular risk
- MeSH terms
- Alcohol Drinking, Ethanol, Animals, Humans, Inflammation, Lipoproteins, Triglycerides, Atherosclerosis
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