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PURPOSE: To compare acute effects of moist snuff with or without nicotine and red wine with or without alcohol on prandial hormones and metabolism.

BASIC PROCEDURES AND METHODS: Two deciliters of wine, with or without alcohol, were taken together with a standardized supervised meal in 14 healthy women and men. All participants also combined the meal with usage of with moist snuff, with or without nicotine. The snuff was replaced hourly at each of the four settings, i.e. snuff with or without nicotine combined with red wine with or without alcohol, that started at 0800 o'clock and were finished at noon.

MAIN FINDINGS: We found ghrelin levels to be more efficiently suppressed when drinking red wine with alcohol compared to non-alcoholic wine by analyzing area under the curve (AUC). AUC for regular wine was 370 +/- 98 pg/ml x hours and 559 +/- 154 pg/ml x hours for de-alcoholized red wine, p < 0.0001 by general linear model. The postprandial metabolic rate was further elevated following alcohol containing red wine compared with non-alcoholic red wine (p = 0.022). Although glucose levels were not uniformly lower after alcoholic red wine, we found lowered glucose levels 3 h after the meal (mean glucose wine: 4.38 +/- 0.96 mmol/l, non-alcoholic wine: 4.81 +/- 0.77 mmol/l, p = 0.005). Nicotine-containing moist snuff (AUC: 1406 +/- 149 nmol/ml x hours) elevated the levels of serum cortisol compared with nicotine-free snuff (AUC: 1268 +/- 119 nmol/ml x hours, p = 0.005). We found no effects of nicotine or alcohol on feelings of satiety.

CONCLUSIONS: Alcohol in red wine augmented the postprandial suppression of ghrelin and it also lowered postprandial glucose 3 h post-meal. These effects are in line with observational trials linking regular intake of moderate amounts of red wine with lower risk for diabetes.

BACKGROUND AND AIMS: Alcohol consumption has complex effects on myocardial infarction (MI) and ischemic stroke. We investigated the difference in associations according to drinking patterns (drinking frequency vs. amount per occasion) and sex.

METHODS: This population-based retrospective study included 11,595,191 subjects participating in national health examinations between 2009 and 2010. Using Cox regression analyses, we calculated MI and ischemic stroke risk according to weekly alcohol consumption, drinking frequency, and amount per occasion.

RESULTS: For MI, all weekly alcohol consumption amounts showed lower risk compared to non-drinkers: mild (adjusted hazard ratio [aHR], 0.78; 95% confidence intervals [CI], 0.77-0.79), moderate (aHR, 0.71; 95% CI, 0.70-0.73), and heavy (aHR, 0.74; 95% CI, 0.72-0.76). Drinking frequency and amount per occasion did not differ in MI risk. However, women showed increased risk with heavy drinking and >/=8 drinks per occasion. For ischemic stroke, a J-shaped association was observed for weekly alcohol consumption: mild (aHR, 0.91; 95% CI, 0.90-0.92), moderate (aHR, 0.94; 95% CI, 0.93-0.96), and heavy (aHR, 1.04; 95% CI, 1.02-1.06). Among women, ischemic stroke risk began to increase with moderate drinking. Given similar weekly alcohol consumption levels, ischemic stroke risk increased with higher frequency of drinking, not with amount per occasion.

CONCLUSIONS: Drinking frequency may be a more important risk factor for ischemic stroke than amount per occasion. Among women, the protective effect of alcohol against MI was not evident in heavy amounts, and the risk of ischemic stroke began to increase at lower levels compared to men.

We examined associations between sex-specific alcohol intake trajectories and alcohol-related cancer risk using data from 22 756 women and 15 701 men aged 40 to 69 years at baseline in the Melbourne Collaborative Cohort Study. Alcohol intake for 10-year periods from age 20 until the decade encompassing recruitment, calculated using recalled beverage-specific frequency and quantity, was used to estimate group-based sex-specific intake trajectories. Hazard ratios (HR) and 95% confidence intervals (CI) were estimated for primary invasive alcohol-related cancer (upper aerodigestive tract, breast, liver and colorectum). Three distinct alcohol intake trajectories for women (lifetime abstention, stable light, increasing moderate) and six for men (lifetime abstention, stable light, stable moderate, increasing heavy, early decreasing heavy, late decreasing heavy) were identified. 2303 incident alcohol-related cancers were diagnosed during 485 525 person-years in women and 789 during 303 218 person-years in men. For men, compared with lifetime abstention, heavy intake (mean >/= 60 g/day) at age 20 to 39 followed by either an early (from age 40 to 49) (early decreasing heavy; HR = 1.75, 95% CI: 1.25-2.44) or late decrease (from age 60 to 69) (late decreasing heavy; HR = 1.94, 95% CI: 1.28-2.93), and moderate intake (mean <60 g/day) at age 20 to 39 increasing to heavy intake in middle-age (increasing heavy; HR = 1.45, 95% CI: 1.06-1.97) were associated with increased risk of alcohol-related cancer. For women, compared with lifetime abstention, increasing intake from age 20 (increasing moderate) was associated with increased alcohol-related cancer risk (HR = 1.25, 95% CI: 1.06-1.48). Similar associations were observed for colorectal (men) and breast cancer. Heavy drinking during early adulthood might increase cancer risk later in life.

Fetal alcohol exposure can lead to a range of developmental disorders, including impaired fetal growth and development of multiple organ systems. These disorders are grouped under the term fetal alcohol spectrum disorders (FASDs). Adequate nutrition and a conducive intrauterine environment are essential for healthy fetal development. Nutrient deficiencies resulting from inadequate maternal nutrient ingestion may be compounded by alcohol-induced altered nutrient metabolism, placental clearance, and malabsorption. Alcohol-induced alteration of the intrauterine environment is the main source of developmental deficits and nutritional insufficiencies can worsen the effects on fetal development. In this review, we discuss studies examining the collective and interactive effects of nutrition (specifically iron, selenium, vitamin A, thiamine, zinc, folate, vitamin B12, choline, and amino acids) relative to gestational alcohol consumption and its effects on fetal growth and development. We also summarize scientific reports that tested potential benefits of micronutrient supplementation in animal models of fetal alcohol spectrum disorders and in humans. In summary, the deleterious effects of alcohol exposure in relation to nutrient homeostasis further validate that avoidance of alcohol consumption during pregnancy is the most effective way to mitigate the teratogenic effects of alcohol.