Effects of moderate alcohol consumption on subclinical femoral atherosclerosis in smokers and non-smokers.

Abstract

We read with great interest the published article ‘Association between alcohol consumption and subclinical femoral atherosclerosis in smoking and non-smoking men: the AWHS study’, by Moreno-Franco et al. [1]. We wish to share our views on the published article. The authors investigated the potential influence of alcohol intake on subclinical atherosclerosis in femoral arteries among 2099 healthy middle-aged male workers of the Opel Spain automobile assembly factory recruited between 2009 and 2014. The workers were categorized as ever smokers and never smokers. The ever smokers consisted of current smokers (reported to have smoked in the past 1 year) and former smokers (reported to have smoked at least 50 cigarettes in their life-time, but none for the past 1 year). Past studies have reported several positive changes upon quitting smoking, including an improvement in endothelium-dependent vasodilation within 2–12 weeks following quitting smoking [2]. The excess risks of myocardial infraction are reduced to half after a year from abstinence [3]. The risk of stroke is reduced to that of non-smokers after 5–15 years of smoking cessation [4]. Hence, we urge future studies to classify the subjects who are still smoking separately from those who have quit smoking (at least a year from the date of recruitment). In the present study, the authors reported moderate alcohol consumption (2–30 g/day) reducing the prevalence of subclinical atherosclerosis in the femoral arteries of ever smokers. However, the prevalence of femoral plaques was still greater than never smokers with similar alcohol intake. Hence, the authors speculated that moderate drinking might benefit heavy smokers. Several studies have reported benefits of low or moderate alcohol intake [5, 6], whereas some have disagreed [7, 8]; therefore, the notion is somewhat inconsistently reported to date, due to various reasons. There is a wealth of information associating genetic variance in enzymes that metabolize alcohol, such as alcohol dehydrogenase [9, 10], aldehyde dehydrogenase [11, 12] and cytochrome P450 [13] with atherosclerosis. Hence, regardless of the amount of alcohol consumed, different individuals may respond differently to alcohol intake, which should be taken into account when studying the effects of alcohol intake on physiological events. In the current investigation, Moreno and colleagues [1] also reported no benefits of moderate alcohol consumption in the never smoker group, which adds more credence to the existing belief [7, 8, 14] that the ‘protective effects’ of moderate alcohol consumption on overall cardiovascular profile are more limited than once thought. In line with these findings, the limitations, which we have listed in this letter, should also be carefully considered for a more robust approach in future studies.