While the detrimental effects of binge drinking are well recognized, low-to-moderate alcohol consumption may be beneficial to health, although the underlying mechanism(s) remains elusive. In this opinion article, we will examine the effects of low dose alcohol consumption from the perspective of epigenetic modulation. Biochemically, alcohol is metabolized into acetate and subsequently to acetyl-coA, which can modulate histone acetylation levels. While elevated levels of acetyl-CoA are detrimental for longevity, we argue that diminished acetyl-CoA also negatively affects fatty acid biosynthesis and histone acetylation, which play a critical role in gene expression and, ultimately, health span. Since mitochondrial function and glucose metabolism, which provide the main source of nucleocytoplasmic acetyl-CoA, are compromised with age, alcohol-derived acetate could be an alternative source of acetyl-CoA to compensate. Hence, the health benefits of low ethanol consumption may be more pronounced after midlife, since mitochondrial function and/or glucose metabolism are diminished in this phase of the life course.
Indeed, various clinical alcohol consumption studies concur with this notion, and have shown that a low dose of regular alcohol intake after midlife brings about various health and survival benefits. The requirement for regular alcohol intake may also reflect the transient nature of ethanol-induced histone acetylation. Conversely, ethanol may also stimulate carcinogenesis by inhibiting DNA methylation, as it was shown to reduce various pathways leading to DNA and histone methylation. However, unlike acetylation, where ethanol directly increases the substrate for acetylation, this effect was only observed in the high alcohol exposure cohort. While alcohol-derived acetate may be beneficial for health after midlife, various detrimental effects of alcohol consumption remain, and hence, we do not advocate excessive drinking to increase acetate. This opinion article establishes a possible role of ethanol-derived acetate in achieving homeostasis and sustaining an organism's health span.
BACKGROUND: Favorable association between modest alcohol consumption and cardiovascular disease had been reported in general population, however, whether observed benefit extend to men with established fatty liver disease remains unknown.
METHODS: Cross-sectional study of 10,581 consecutive male participants aged 30 years or older undergoing abdominal ultrasonography and carotid artery ultrasonography were screened. Non-alcoholic fatty liver disease (NAFLD) was diagnosed with ultrasonography and exclusion of secondary causes for fat accumulation or other causes of chronic liver disease. Modest alcohol use was defined as consumption of less than 20 g of alcohol per day.
RESULTS: There were total 2280 men diagnosed with fatty liver, and the mean age was 51.8 years old. Among them, 1797 were modest alcohol drinkers. The prevalence of carotid plaques (55.3% vs. 43.4%, p < 0.001) and carotid artery stenosis (11.0% vs. 5.5%, p < 0.001) was higher in non-drinkers than modest drinkers. Modest alcohol consumption had the independent inverse association with carotid plaques [odd ratio (OR): 0.74, 95% confidence interval (CI): 0.60-0.92] and carotid artery stenosis (OR: 0.62, 95% CI: 0.43-0.90), adjusted for age, smoking and metabolic syndrome.
CONCLUSIONS: Modest alcohol consumption had a favorable association with carotid plaque or CAS in men with NAFLD
BACKGROUND: In January 2016, the UK announced and began implementing revised guidelines for low-risk drinking of 14 units (112 g) per week for men and women. This was a reduction from the previous guidelines for men of 3-4 units (24-32 g) per day. There was no large-scale promotion of the revised guidelines beyond the initial media announcement. This paper evaluates the effect of announcing the revised guidelines on alcohol consumption among adults in England.
METHODS: Data come from a monthly repeat cross-sectional survey of approximately 1700 adults living in private households in England collected between March 2014 and October 2017. The primary outcomes are change in level and time trend of participants' Alcohol Use Disorders Identification Test-Consumption (AUDIT-C) scores.
RESULTS: In December 2015, the modelled average AUDIT-C score was 2.719 out of 12 and was decreasing by 0.003 each month. After January 2016, AUDIT-C scores increased immediately but non-significantly to 2.720 (beta=0.001, CI -0.079 to 0.099) and the trend changed significantly such that scores subsequently increased by 0.005 each month (beta=0.008, CI 0.001 to 0.015), equivalent to 0.5% of the population increasing their AUDIT-C score by 1 point each month. Secondary analyses indicated the change in trend began 7 months before the guideline announcement and that AUDIT-C scores reduced significantly but temporarily for 4 months after the announcement (beta=-0.087, CI -0.167 to 0.007).
CONCLUSIONS: Announcing new UK drinking guidelines did not lead to a substantial or sustained reduction in drinking or a downturn in the long-term trend in alcohol consumption, but there was evidence of a temporary reduction in consumption.