03 June 2019 In Cancer

Alcohol consumption has been established to be a major factor in the development and progress of cancer. Genetic polymorphisms of alcohol-metabolism genes result in differences between individuals in exposure to acetaldehyde, leading to possible carcinogenic effects. Arg47His (rs1229984 G > A) in ADH1B have been frequently studied for its potential effect on carcinogenesis. However, the findings are as yet inconclusive. To gain a more precise estimate of this potential association, we conducted a meta-analysis including 66 studies from 64 articles with 31999 cases and 50964 controls. The pooled results indicated that ADH1B Arg47His polymorphism is significantly associated with the decreased risk of overall cancer (homozygous model, odds ratio (OR) = 0.62, 95% confidence interval (CI) = 0.49-0.77; heterozygous model, OR = 0.71, 95% CI = 0.60-0.84; recessive model, OR = 0.83, 95% CI = 0.76-0.91; dominant model, OR = 0.62, 95% CI = 0.53-0.72; and allele comparison, OR = 0.82, 95% CI = 0.75-0.89). Stratified analysis by cancer type and ethnicity showed that a decreased risk was associated with esophageal cancer and head and neck cancer amongst Asians. In conclusion, our meta-analysis suggested that ADH1B Arg47His polymorphism was significantly associated with decreased overall cancer risk. These findings need further validation in large multicenter investigations.

03 June 2019 In Cancer

PURPOSE: It is unknown whether alcohol intake is associated with the risk of lethal (metastatic or fatal) prostate cancer. We examine (1) whether alcohol intake among men at risk of prostate cancer is associated with diagnosis of lethal prostate cancer and (2) whether intake among men with nonmetastatic prostate cancer is associated with metastasis or death.

METHODS: This prospective cohort study uses the Health Professionals Follow-Up Study (1986 to 2012). Our analysis of alcohol intake among men at risk of prostate cancer included 47,568 cancer-free men. Our analysis of alcohol intake among men with prostate cancer was restricted to 5,182 men diagnosed with nonmetastatic prostate cancer during follow-up. We examine the association of total alcohol, red and white wine, beer, and liquor with lethal prostate cancer and death. Multivariate Cox proportional hazards regression estimated hazard ratios (HRs) and 95% CIs.

RESULTS: Alcohol drinkers had a lower risk of lethal prostate cancer (any v none: HR, 0.84 [95% CI, 0.71 to 0.99]) without a dose-response relationship. Total alcohol intake among patients with prostate cancer was not associated with progression to lethal prostate cancer (any v none: HR, 0.99 [95% CI, 0.57 to 1.72]), whereas moderate red wine intake was associated with a lower risk (any v none: HR, 0.50 [95% CI, 0.29 to 0.86]; P trend = .05). Compared with none, 15 to 30 g/d of total alcohol after prostate cancer diagnosis was associated with a lower risk of death (HR, 0.71 [95% CI, 0.50 to 1.00]), as was red wine (any v none: HR, 0.74 [95% CI, 0.57 to 0.97]; P trend = .007).

CONCLUSION: Cancer-free men who consumed alcohol had a slightly lower risk of lethal prostate cancer compared with abstainers. Among men with prostate cancer, red wine was associated with a lower risk of progression to lethal disease. These observed associations merit additional study but provide assurance that moderate alcohol consumption is safe for patients with prostate cancer.

03 June 2019 In Cardiovascular System

BACKGROUND AND AIMS: The interrelationship between alcohol consumption and depression is complex, and the direction of the association is unclear. We investigated whether alcohol consumption influences the risk of depression while accounting for this potential bidirectionality.

METHODS: A total of 10 441 individuals participated in the PART study in 1998-2000, 8622 in 2001-2003, and 5228 in 2010. Participants answered questions on their alcohol consumption, symptoms of depression, childhood adversity, and sociodemographic, socioeconomic, psychosocial, and lifestyle factors. A total of 5087 participants provided repeated information on alcohol consumption. We used marginal structural models to analyze the association between alcohol consumption and depression while controlling for previous alcohol consumption and depressive symptoms and other time-varying confounders.

RESULTS: Non-drinkers had a higher depression risk than light drinkers (</=7 drinks/week) (risk ratio: 1.7; 95% confidence interval 1.3-2.1). Consumers of seven-fourteen drinks/week had a depression risk similar to that of light drinkers. Hazardous drinking was associated with a higher risk of depression than non-hazardous alcohol consumption (risk ratio: 1.8, 95% confidence interval: 1.4-2.4).

CONCLUSION: Light and moderate alcohol consumption and non-hazardous drinking were associated with the lowest risk of subsequent depression after accounting for potential bidirectional effects. Hazardous drinking increased the risk of depression.

03 June 2019 In Cardiovascular System

BACKGROUNDS: Views on the relationship between alcohol consumption and stroke risk remain controversial. Moreover, data on cumulative alcohol intake are limited. We examined the potential impact of cumulative alcohol consumption on the risk of total stroke and its subtypes in men.

METHODS: This prospective study included 23,433 men from the Kailuan Study. Cumulative alcohol consumption was taken as the primary exposure by calculating self-reported alcohol consumption from three consecutive examinations (in 2006, 2008, and 2010). The first occurrence of stroke was confirmed by reviewing medical records from 2010 to 2016. We used Cox proportional hazards regression to analyze the data.

RESULTS: During the 5.9 +/- 0.8 years of follow-up, 678 total strokes were identified, including 595 ischemic stroke (IS), 90 intracerebral hemorrhage and 19 subarachnoid hemorrhage cases. The adjusted hazard ratios (95% confidence intervals) of total stroke for light, moderate and heavy cumulative alcohol consumption were 1.23 (1.01-1.51), 1.49 (1.13-1.97), and 1.50 (1.21-1.86), respectively, compared with those of nondrinkers. The results were similar for IS. Cumulative alcohol consumption was not associated with intracerebral hemorrhage risk (hazard ratio 1.46; 95% confidence interval, 0.74-2.08).

CONCLUSIONS: Cumulative alcohol consumption is an independent risk factor of total stroke and IS in men in a community-based cohort. Even light alcohol intake increases the risk of total stroke and IS.

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