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BACKGROUND: Breast cancer aetiology may differ by estrogen receptor (ER) status. Associations of alcohol and folate intakes with risk of breast cancer defined by ER status were examined in pooled analyses of the primary data from 20 cohorts.

METHODS: During a maximum of 6-18 years of follow-up of 1 089 273 women, 21 624 ER+ and 5113 ER- breast cancers were identified. Study-specific multivariable relative risks (RRs) were calculated using Cox proportional hazards regression models and then combined using a random-effects model.

RESULTS: Alcohol consumption was positively associated with risk of ER+ and ER- breast cancer. The pooled multivariable RRs (95% confidence intervals) comparing >/= 30 g/d with 0 g/day of alcohol consumption were 1.35 (1.23-1.48) for ER+ and 1.28 (1.10-1.49) for ER- breast cancer (Ptrend /= 0.26). Dietary (from foods only) and total folate intakes were not associated with risk of overall, ER+ and ER- breast cancer; pooled multivariable RRs ranged from 0.98 to 1.02 comparing extreme quintiles. Following-up US studies through only the period before mandatory folic acid fortification did not change the results. The alcohol and folate associations did not vary by tumour subtypes defined by progesterone receptor status.

CONCLUSIONS: Alcohol consumption was positively associated with risk of both ER+ and ER- breast cancer, even among women with high folate intake. Folate intake was not associated with breast cancer risk.

This is the first study specifically estimating the proportion of new cancer cases that could be attributable to alcohol consumption in the year 2012 in Brazil. The proportion of exposed cases and the association between alcohol and lip and oral cavity, nasopharynx, other pharynx, larynx, esophagus, colorectum, female breast, liver, and intrahepatic bile ducts cancers was based on data made available by the Integrator System of Hospital Cancer Registries. The cancer incidence was obtained from the estimates produced by GLOBOCAN. In 2012 there were 437,592 new cancer cases in Brazil, excluding non-melanoma skin cancers. Of these, alcohol consumption was responsible for 4.8% of all new cases. The alcohol-attributable fraction was higher for men (7.0%) than for women (2.6%). A total of 21,000 new cancer cases, 15,554 in men and 5,646 in women, could be attributable to alcohol consumption. In Brazil, a significant fraction of cancer cases can be attributed to alcohol consumption, and public health measures to prevent heavy alcohol use should be implemented.

Alcohol consumption is often a comorbid condition in other chronic liver diseases. It has been shown to act in synergy to increase liver injury in viral hepatitis, hereditary hemochromatosis, and nonalcoholic fatty liver disease (NAFLD), leading to an increased risk of cirrhosis, hepatocellular carcinoma, and liver-related mortality. Data suggest that modest alcohol consumption may be inversely related to the risk of developing NAFLD and lower rates of progression of NAFLD to nonalcoholic steatohepatitis (NASH). This article reviews data on the relationship between alcohol consumption and other chronic liver diseases.

BACKGROUND: Fatty liver (hepatic steatosis) is one of the most common diseases globally, with increasing prevalence. The role of alcohol consumption in the development of hepatic steatosis has not been systematically examined. METHODS: We searched Medline, Embase, and ProQuest Dissertations & Theses Global for original data on the relationship between alcohol consumption and hepatic steatosis measured by non-invasive imagery, excluding studies conducted in participants <18years, or subgroups related to viral and drug-induced liver disease. We identified 18 articles reporting adjusted data (Japan=11, other high-income countries=7). Random-effect categorical meta-analyses (<20g/day pure alcohol consumption vs non-drinkers) and dose-response meta-analyses for the whole range of alcohol consumption were conducted. RESULTS: In total, 99,370 participants and 25,662 cases of hepatic steatosis were included. In Japan, low alcohol consumption was consistently associated with substantially reduced incidence and prevalence of hepatic steatosis compared to non-drinkers (RR for <20g pure alcohol/day=0.75, 95% CI: 0.71-0.79, I(2)=0%). No overall association was found in other countries (RR=1.05, 95% CI: 0.86-1.30, I(2)=84%). Dose-response analyses in Japan (up to 80g/day) showed an inverse relationship in men and a J-shape in women. CONCLUSIONS: Alcohol consumption showed a complex association with hepatic steatosis with substantial differences by ethnicity and sex. Low alcohol consumption was beneficial in Japan with good epidemiological evidence, whereas there was no association in other countries. However, heterogeneity was large in countries other than Japan. More and higher quality research in diverse ethnic populations is needed to further clarify this relationship