Alcohol Drinking, Apolipoprotein Polymorphisms and the Risk of Cardiovascular Diseases

Abstract

Lipoprotein disorders are a major risk factor for atherosclerotic neuro-cardiovascular disease (ACVD) and are heavily influenced by lifestyle, including alcohol drinking. Moderate drinkers have a lower ACVD risk than abstainers due to their higher levels of high-density lipoprotein (HDL) cholesterol, an important protective factor against ACVD. On the contrary, heavy drinking increases ACVD risk. According to an extensive literature body, ethanol intoxication modifies lipid serum profile and induces endothelial dysfunction. Single nucleotide polymorphisms may influence the relationship between alcohol drinking, HDL cholesterol level, and atherosclerotic risk. The risk of ACVD in heavy drinkers seems enhanced in patients with apolipoprotein E4 allele, interleukin- 6-174 polymorphism, and cholesteryl ester transfer protein TaqIB polymorphism. Apolipoprotein E4 is a known risk factor for ACVD, while apolipoprotein E2 has mixed effects. Therefore, even if a "protective role" may be attributed to moderate drinking, this effect cannot be extended to everyone.

Keywords: Alcoholism; adiponectin.; apolipoprotein E; atherosclerotic cardiovascular disease; genetic polymorphism.

Fig. (1)

Scheme of one molecule LDL, a particle with a diameter of 22 nm surrounded by a single lipid layer composed of around 800 phospholipids and 500 unesterified cholesterol molecules accompanied by one apolipoprotein B100 (ApoB-100) molecule and by minor apolipoproteins like apolipoprotein E (ApoE). In the core of the LDL particle are stored 1500 molecules of esterified cholesterol and about 170 triglycerides. LDL particles are a high-risk factor for developing cardiovascular disease. Modified from ref. [3].

Fig. (2)

Effects of alcohol abuse on atherosclerotic plaque formation. Excessive alcohol consumption is a risk factor for atherosclerotic disease. In particular, exposure of the endothelium to ethanol (EtOH) increases the production of reactive oxygen species that oxidize low-density lipoproteins (LDL) to oxidized LDL. The subsequent phagocytosis of ox-LDL by macrophages in the intima leads to the accumulation of foam cells, chronic inflammation of the intima, and the formation of atherosclerotic plaque. Over time, this hemodynamic alteration results in coronary artery disease, stroke, peripheral artery disease, kidney problems, heart attack, and aneurysm.