Wine Information Council

Alcohol consumption remains prevalent among pregnant and nursing mothers despite the well-documented adverse effects this may have on the offspring. Moderate-to-high levels of alcohol consumption in pregnancy result in fetal alcohol syndrome (FAS) disorders, with brain defects being chief among the abnormalities. Recent findings indicate that while light-to-moderate levels may not cause FAS, it may contribute to epigenetic changes that make the offspring prone to adverse health outcomes including metabolic disorders and an increased propensity in the adolescent-onset of drinking alcohol. On the one hand, prenatal alcohol exposure (PAE) causes epigenetic changes that affect lipid and glucose transcript regulating genes resulting in metabolic abnormalities. On the other hand, it can program offspring for increased alcohol intake, enhance its palatability, and increase acceptance of alcohol's flavor through associative learning, making alcohol a plausible second hit for the development of alcohol-induced liver disease. Adolescent drinking results in alcohol dependence and abuse in adulthood. Adolescent drinking results in alcohol dependence and abuse in adulthood. Alterations on the opioid system, particularly, the mu-opioid system, has been implicated in the mechanism that induces increased alcohol consumption and acceptance. This review proposes a mechanism that links PAE to the development of alcoholism and eventually to alcoholic liver disease (ALD), which results from prolonged alcohol consumption. While PAE may not lead to ALD development in childhood, there are chances that it may lead to ALD in adulthood.

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

Low-risk thresholds for alcohol use differ across various national guidelines. To assess the novel WHO risk drinking levels in light of alcohol-sensitive common laboratory tests, we analysed biomarkers of liver status, inflammation and lipid profiles from a population-based survey of individuals classified to abstainers and different WHO risk drinking levels defined in terms of mean alcohol consumption per day. The study included 22,327 participants aged 25-74 years from the National FINRISK Study. Data on alcohol use, health status, diet, body weight and lifestyle (smoking, coffee consumption and physical activity) were recorded from structured interviews. Alcohol data from self-reports covering the past 12 months were used to categorize the participants into subgroups of abstainers and WHO risk drinking categories representing low, moderate, high and very high risk drinkers. Serum liver enzymes (GGT, ALT), C-reactive protein (CRP) and lipid profiles were measured using standard laboratory techniques. Alcohol risk category was roughly linearly related with the occurrence of elevated values for GGT, ALT and CRP. Alcohol drinking also significantly influenced the incidence of abnormalities in serum lipids. Significantly higher odds for abnormal GGT, ALT and altered lipid profiles remained in alcohol drinkers even after adjustment for age, waist circumference, physical inactivity, smoking and coffee consumption. A more systematic use of laboratory tests during treatment of individuals classified to WHO risk drinking categories may improve the assessment of alcohol-related health risks. Follow-ups of biomarker responses may also prove to be useful in health interventions aimed at reducing alcohol consumption.

There is no available abstract for this article.