Alcohol is calorie dense, but unlike food products, alcoholic drinks tend to be exempt from nutritional labelling laws that require energy content information to be displayed on packaging or at point of purchase. This review provides a perspective on the likely efficacy of alcoholic drink energy labelling as a public health policy to reduce obesity and discusses key questions to be addressed by future research.
First, the contribution that alcohol makes to population level daily energy intake and obesity is outlined. Next, consumer need for alcohol energy labelling and the potential impacts on both consumer and industry behavior are discussed. Pathways and mechanisms by which energy labelling of alcoholic drinks could reduce obesity are considered, as well as possible unintended consequences of alcoholic drink energy labelling. Would widespread energy labelling of alcoholic drinks reduce obesity? The unclear effect that alcohol has on population level obesity, the modest contribution calories from alcohol make to daily energy intake and limited impact nutritional labelling policies tend to have on behavior, suggest alcohol energy labelling may have limited impact on population obesity prevalence as a standalone policy. However, there are a number of questions that will need to be answered by future research to make definitive conclusions on the potential for alcohol energy labelling policies to reduce obesity.
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: It has already been established that the consumption of alcoholic beverages increases high-density lipoprotein cholesterol (HDL-C) levels in dose-response.
METHODS AND RESULTS: A cross-sectional analysis was carried out with 6132 participants of both sexes aged between 35 and 74 years, who were active and retired workers from six Brazilian states. Heavy drinkers were categorized by sex: men > 210 g/week and women > 140 g/week; moderate drinkers: men /=83 mg/dL).
We used binary logistic regression to assess associations between baseline alcohol intake and HDL-C, which were adjusted for sex, age, income, physical activity, kilocalories and body mass index (BMI), and we found an positive association between extremely high HDL-C and the excessive consumption of alcoholic beverages. These participants were mostly women with a high income, lower waist circumference, kilocalorie consumption and also a higher consumption in all categories of alcoholic beverages. CONCLUSION: Excessive alcohol consumption was associated with a higher probability of extremely high HDL-C.
PURPOSE: Previous observational studies have shown that alcohol and coffee were associated with colorectal cancer (CRC) risk, but the causal relationships have not been adequately explored. This study aimed to assess the potential causal associations of alcohol and coffee with CRC risk using Mendelian randomization (MR) analyses in an East Asian population.
METHODS: Publicly available summary-level genome-wide association studies data on ever/never alcohol drinker (n = 165,084), alcohol consumption (n = 58,610), coffee consumption (n = 152,634), and CRC (7062 cases and 195,745 controls) were obtained from the BioBank Japan (BBJ). Single-nucleotide polymorphisms (SNPs) that were significantly related to the exposures were identified as instrumental variables.
Five, two, and six SNPs were used for ever/never alcohol drinkers, alcohol consumption, and coffee consumption, respectively. The inverse variance weighted method was used as the main MR method to calculate the odds ratios (ORs) and 95% confidence intervals (95% CIs) of CRC risk per one-unit change in exposures.
RESULTS: Genetically predicted ever/never alcohol drinkers (OR: 1.08; 95% CI 1.06, 1.11; P < 0.001) and alcohol consumption (OR: 1.39; 95% CI 1.21, 1.60; P < 0.001) were positively associated with CRC risk. Conversely, genetically predicted coffee consumption was inversely related to CRC risk, with an OR (95% CI) of 0.80 (0.64, 0.99) (P = 0.037). CONCLUSION: Genetically predicted alcohol use and consumption were risk factors for CRC while genetically predicted coffee consumption was a protective factor.
Our findings highlight the effectiveness of keeping healthy dietary habits to prevent CRC. Further studies with more valid SNPs and CRC cases are needed. Validation of our findings is also recommended.