Effects of Alcohol on HDL and Cardiovascular Risk

Multiple studies have established a known J-shaped relationship between alcohol intake and cardiovascular risk including coronary heart disease and ischaemic stroke (Krenz and Korthuis 2012). The term 'drink' is imprecise; however, the amount of alcohol in one drink is similar for wine, spirits or beer. Thus, a 100 ml glass of table wine at 13 % alcohol, 35 ml of distilled spirits at 40 % alcohol and 300 ml of beer at 5 % alcohol all contain around 10–12 g of pure ethyl alcohol. The general consensus is that men consuming two standard alcoholic drinks per day and women consuming half that intake appear to have a lower cardiovascular event rate than persons abstaining from alcohol (Krenz and Korthuis 2012). Estimates of the risk reduction associated with moderate alcohol intake drinkers compared with those abstaining from alcohol range from 25 to 30 % (Krenz and Korthuis 2012).

Alcohol Intake and HDL-C

Several plausible mechanisms have been proposed to explain the positive moderate alcohol intake-mediated effects on CVDs: reduced thrombogenic and coagulation factors (platelet aggregation and fibrinogen levels), low plasma concentrations of inflammation markers (C-reactive protein, interleukin-6 and adiponectin), lowered blood pressure, increased insulin sensitivity and lipoprotein profile via a lowering of LDL-C and increase in HDL-C (Klatsky 2010). However, this alcohol–CVD relationship is nonlinear, and excessive alcohol consumption has adverse effects on hypertension and other pro-inflammatory factors, despite increasing HDL-C (Foerster et al. 2009).

Some reports have suggested that wine carries a lower risk of mortality than beer or spirits and that this may be related to the ability of nonalcoholic phenolic compounds to inhibit LDL oxidation and its pro-inflammatory effects (Frankel et al. 1993; Gronbaek et al. 2000; Klatsky et al. 2003). However, other studies have failed to identify an additional advantage associated with red wine (Di Castelnuovo et al. 2002; Mukamal et al. 2003), thereby suggesting that ethyl alcohol is the main factor for the cardioprotective effect.

A recent meta-analysis demonstrated that alcohol exerts favourable effects on several cardiovascular biomarkers (higher HDL-C, apoA-I and adiponectin levels and lower fibrinogen levels) which seems to be independent of the alcoholic beverage type (Brien et al. 2011). This systematic review found that 1–2 drinks per day increased HDL-C by 0.10 mmol/L (Brien et al. 2011). However, the contribution of alcohol-induced HDL-C-raising effects to cardiovascular risk remains largely unknown. Early studies indicated that the atheroprotective effects were mediated, largely, by the increase in HDL-C, since the addition of HDL-C to the multivariate model attenuated the inverse association between alcohol intake and myocardial infarction (Gaziano et al. 1993). Nevertheless, one recent report describing a large Norwegian cohort with extensive control for confounding factors showed that HDL-C levels were not on the causal pathway connecting alcohol to the lower risk of death from coronary heart disease (Magnus et al. 2011). These findings raise the question of which specific HDL subpopulation particles are affected by alcohol intake and their significance for coronary heart disease protection.

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