26 June 2020 In Cancer

Introduction: Alcohol is a carcinogen for human cancer. This contribution summarizes the relationships between alcohol use and gastrointestinal cancers, and implications for prevention.

Methods: Comparative risk assessment and narrative literature review.

Results: The following gastrointestinal cancer sites were found to be causally impacted by alcohol use: lip and oral cavity, pharynx other than nasopharynx, esophagus, colon and rectum, and liver. Globally, 368,000 deaths (304,000 men and 64,000 women) and more than 10 million disability-adjusted life years (DALYs) lost (10.1 million; 8.4 million men and 1.6 million women) in 2016 were attributable to alcohol use, making up about 10% of all deaths and DALYs lost due to these cancers, respectively.

There are effective and cost-effective alcohol control policies available to reduce this burden, namely the best buys of increasing taxation, reducing availability, and banning advertisement. In addition, public knowledge about the alcohol-cancer link should be increased. Discussion: There are a number of assumptions underlying these estimates, but overall all of them seem to be conservative.

26 June 2020 In Cancer
There is no available abstract for this article. You can read the erratum here .
05 June 2020 In Liver Disease

BACKGROUND & AIMS: Moderate alcohol intake is associated with reduced prevalence or incidence of fatty liver. However, whether or not the association is independent of dietary patterns remains unclear. We aimed to evaluate the cross-sectional association of alcohol intake with fatty liver after accounting for dietary patterns and obesity.

METHODS: We assessed 4579 adults aged 30-79 years who participated in routine clinical examinations in St. Luke's International Hospital, Japan (January to March, 2015). We assessed their habitual diet using diet-history questionnaire, estimated alcohol intake, and derived dietary pattern variables using factor analysis. Fatty liver was ascertained using ultrasonography. Linear and U-shaped associations of alcohol intake with fatty liver were evaluated using Poisson regression, and a post hoc analysis was conducted after detecting potential outliers for alcohol intake and excluding them using sex-specific statistics (median plus 2 x interquartile range).

RESULTS: Fatty liver was ascertained in 1120 participants (24.5%). Whereas no significant association of alcohol intake with fatty liver was observed when potential outliers of alcohol intake were included (p = 0.25), a significant U-shaped association was observed after excluding the outliers with and without adjustment for dietary patterns (p = 0.003 and 0.02, respectively). The lowest prevalence was estimated when alcohol consumption was approximately 7% of energy, with a prevalence ratio of 0.72 (95% confidence interval = 0.59-0.86) compared to non-drinkers. The association became imprecise and attenuated toward the null after further adjustment for body mass index (p = 0.06).

CONCLUSIONS: Alcohol intake showed a U-shaped association with fatty liver prevalence. This association was independent of underlying dietary patterns, while it was sensitive to excessive alcohol intake and obesity status, providing clinical implications for the prevention of fatty liver.

05 June 2020 In Liver Disease

Alcohol and obesity are the main risk factors for alcoholic liver disease and nonalcoholic fatty liver disease (NAFLD), respectively, and they frequently coexist. There are considerable synergistic interaction effects between hazardous alcohol use and obesity-associated metabolic abnormalities in the development and progression of fatty liver disease.

Intermittent binge-drinking has been shown to promote steatohepatitis from obesity-related steatosis, and binge-drinking is associated with progression to cirrhosis even when average alcohol intake is within the currently used criteria for a NAFLD diagnosis.

Recent longitudinal studies in NAFLD have shown that light-to-moderate alcohol use is associated with fibrosis progression and incident clinical liver disease, suggesting that there is no liver-safe limit of alcohol intake in the presence of NAFLD; a J: -shaped association between alcohol and all-cause mortality remains controversial.

The interaction effects between alcohol and obesity make the present strict dichotomization of liver disease into alcoholic and NAFLD inappropriate, and require attention in future research, public health policy, individual counseling, and risk stratification.

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