The effect of moderate alcohol intake on serum apolipoprotein A-I-containing lipoproteins and lipoprotein (a)☆
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Cited by (78)
Alcohol drinking patterns and biomarkers of coronary risk in the Spanish population
2014, Nutrition, Metabolism and Cardiovascular DiseasesCitation Excerpt :As regards irregular heavy drinking, it has been associated with a 45% increase in CHD risk after adjustment for the volume of alcohol consumed; thus, it seems that any cardioprotective effect of moderate alcohol consumption may be negated by irregular heavy drinking occasions [4]. The mechanisms of the cardiovascular effect of heavy drinking are poorly understood; while a few clinical trials suggest that heavy drinking increases HDL-cholesterol [5–7], it may also exert a detrimental effect on thrombosis, blood pressure and atrial fibrillation [8,9]. Short-term trials may not be appropriate to characterize the effect of long-term drinking patterns.
Beyond HDL-cholesterol increase: Phospholipid enrichment and shift from HDL<inf>3</inf> to HDL<inf>2</inf> in alcohol consumers
2007, Journal of Lipid ResearchCitation Excerpt :However, comparison between the groups and multivariate analysis showed no influence of alcohol consumption on the ratio of apoA-I to apoA-II (Tables 4, 6), which allows the conclusion that LpA1 and LpA1/A2 are increased in a similar manner. This conclusion is in accordance with two studies directly showing an alcohol-related increase of both lipoprotein species (24, 45). Yet, other data suggest that alcohol consumption mainly increases LpA1/A2 (18, 46).
Alcohol and Stroke
2005, Comprehensive Handbook of Alcohol Related PathologyLifestyle determinants of high-density lipoprotein cholesterol: The National Heart, Lung, and Blood Institute Family Heart Study
2004, American Heart JournalCitation Excerpt :Many investigators have studied the mechanisms by which alcohol increases HDL-C. Okamoto et al23 showed that high serum levels of HDL-C in habitual alcohol drinkers are mainly dependent on an increase of apolipoprotein A-1 (Apo A-1) synthesis in the liver. With the administration of 60 g per day of ethanol to healthy volunteers for 3 weeks, Valimaki et al24 found that Apo A-1, HDL-C2, and HDL-C3 each increased by 17% and fell to near baseline levels after 3 weeks of abstinence. Nishiwaki et al25 attribute the increase in HDL-C following alcohol consumption primarily to an increase in lipoprotein lipase (LPL), while Goldberg et al26 report no increase in LPL but a marked decrease in hepatic lipase and possible acute inhibition of the catabolism of HDL-C following alcohol administration.