02 August 2016 In Cancer

BACKGROUND AND AIMS: There is increasing research evidence about the causal role of alcohol in cancer, accompanied by unclear and conflicting messages in the media. This paper aimed to clarify the strength of the evidence for alcohol as a cause of cancer, and the meaning of cause in this context.

METHODS: Recent epidemiological and biological research on alcohol and cancer was reviewed and summarized, drawing upon published meta-analyses identified from the Medline database and the archives of the International Agency for Research on Cancer. More recent epidemiological studies not included in these publications were also reviewed. A brief description of the nature of causal inference in epidemiology was used to frame discussion of the strength of the evidence that alcohol causes cancer, and contrast this with the case for a protective association of alcohol with cardiovascular disease.

RESULTS: The usual epidemiological understanding of a cause is a factor that increases the incidence of a condition in the population. In the context of a body of epidemiological evidence of an association of alcohol consumption with a disease, the inference that it is a causal association requires alternative explanations of the observed finding to be judged unlikely. Even without complete knowledge of biological mechanisms, the epidemiological evidence can support the judgement that alcohol causes cancer of the oropharynx, larynx, oesophagus, liver, colon, rectum and breast. The measured associations exhibit gradients of effect that are biologically plausible, and there is some evidence of reversibility of risk in laryngeal, pharyngeal and liver cancers when consumption ceases. The limitations of cohort studies mean that the true effects may be somewhat weaker or stronger than estimated currently, but are unlikely to be qualitatively different. The same, or similar, epidemiological studies also commonly report protection from cardiovascular disease associated with drinking but a high level of scepticism regarding these findings is now warranted.

CONCLUSIONS: There is strong evidence that alcohol causes cancer at seven sites in the body and probably others. Current estimates suggest that alcohol-attributable cancers at these sites make up 5.8% of all cancer deaths world-wide. Confirmation of specific biological mechanisms by which alcohol increases the incidence of each type of cancer is not required to infer that alcohol is a cause.

17 May 2016 In Cancer

BACKGROUND: We investigated four factors, height, weight gain since age 20, physical activity, and alcohol drinking, for associations with risk of breast cancer (BC) according to menopausal status, using the latest data of the Japan Collaborative Cohort Study (JACC Study).

MATERIALS AND METHODS: We confined the analysis to 24 areas available of cancer incidence information, excluding women with a previous diagnosis of BC. Baseline data were collected from 38,610 (9,367 premenopausal, and 29,243 postmenopausal) women during 1988 and 1990. The study subjects were followed-up at the end of 2009, and 273 (84 premenopausal, and 189 postmenopausal) cases of BC were newly diagnosed in 501,907 person-years. The Cox model was used to estimate a hazards ratio (HR) and its 95% confidence interval (CI) of BC risk.

RESULTS: As a result of the multivariate analysis adjusting for age at baseline survey, age at menarche, number of live births, and, age at first delivery, weight gain since age 20 of 6.7 kg-9.9 kg, and >/=10.0 kg were significantly associated with increased risk for postmenopausal BC (HR=2.48, 95% CI 1.40-4.41, and, HR=2.94, 95% CI 1.84-4.70, respectively). Significantly increased trend of BC risk was also observed in weight gain since age 20 (p for trend, p<0.001). Amount of ethanol intake per day>/=15.0 g was significantly associated with increased risk for postmenopausal BC in the multivariable-adjusted analysis (HR=2.74, 95% CI 1.32-5.70).

CONCLUSIONS: Higher weight gain in adulthood and larger amounts of ethanol intake were significantly associated with increased risk of BC in Japanese postmenopausal women. None of the investigated factors were significantly associated with BC risk in Japanese premenopausal women.

17 May 2016 In Cancer

The objective of this study was to outline the biological pathways of alcohol-attributable breast cancer, the epidemiological risk relationship between alcohol consumption and breast cancer, and the global burden of breast cancer incidence and mortality attributable to alcohol consumption, with a focus on light drinking. First, the literature regarding the biological mechanisms of how alcohol affects the risk of breast cancer was reviewed and summarized. Second, a search of meta-analyses that evaluated the risk relationship between alcohol consumption and breast cancer was conducted. Last, the burden of alcohol-attributable breast cancer incidence and mortality was estimated by means of a Population-Attributable Fraction methodology. Data on alcohol consumption were obtained from the Global Information System on Alcohol and Health, and data on cancer incidence and mortality were obtained from the GLOBOCAN database. Alcohol consumption affects breast cancer risk through the alteration in hormone levels and the associated biological pathways, the metabolism of ethanol resulting in carcinogens, and the inhibition of the one carbon metabolism pathway. The systematic review found 15 meta-analyses on the risk relationship between alcohol consumption (also light consumption) and the risk of breast cancer. All but 2 of these analyses showed a dose-response relationship between alcohol consumption and the risk of breast cancer. An estimated 144,000 (95% confidence interval [CI]: 88,000 to 200,000) breast cancer cases and 38,000 (95% CI: 2,400 to 53,000) breast cancer deaths globally in 2012 were attributable to alcohol, with 18.8% of these cases and 17.5% of these deaths affecting women who were light alcohol consumers. All levels of evidence showed a risk relationship between alcohol consumption and the risk of breast cancer, even at low levels of consumption. Due to this strong relationship, and to the amount of alcohol consumed globally, the incidence of and mortality from alcohol-attributable breast cancer is large.

17 May 2016 In Cancer

OBJECTIVE: To test the hypothesis that postmenopausal women who increase their alcohol intake over a five year period have a higher risk of breast cancer and a lower risk of coronary heart disease compared with stable alcohol intake.

DESIGN: Prospective cohort study.

SETTING: Denmark, 1993-2012.

PARTICIPANTS: 21?523 postmenopausal women who participated in the Diet, Cancer, and Health Study in two consecutive examinations in 1993-98 and 1999-2003. Information on alcohol intake was obtained from questionnaires completed by participants.

MAIN OUTCOME MEASURES: Incidence of breast cancer, coronary heart disease, and all cause mortality during 11 years of follow-up. Information was obtained from the Danish Cancer Register, Danish Hospital Discharge Register, Danish Register of Causes of Death, and National Central Person Register. We estimated hazard ratios according to five year change in alcohol intake using Cox proportional hazards models.

RESULTS: During the study, 1054, 1750, and 2080 cases of breast cancer, coronary heart disease, and mortality occurred, respectively. Analyses modelling five year change in alcohol intake with cubic splines showed that women who increased their alcohol intake over the five year period had a higher risk of breast cancer and a lower risk of coronary heart disease than women with a stable alcohol intake. For instance, women who increased their alcohol intake by seven or 14 drinks per week (corresponding to one or two drinks more per day) had hazard ratios of breast cancer of 1.13 (95% confidence interval 1.03 to 1.23) and 1.29 (1.07 to 1.55), respectively, compared to women with stable intake, and adjusted for age, education, body mass index, smoking, Mediterranean diet score, parity, number of births, and hormone replacement therapy. For coronary heart disease, corresponding hazard ratios were 0.89 (0.81 to 0.97) and 0.78 (0.64 to 0.95), respectively, adjusted for age, education, body mass index, Mediterranean diet score, smoking, physical activity, hypertension, elevated cholesterol, and diabetes. Results among women who reduced their alcohol intake over the five year period were not significantly associated with risk of breast cancer or coronary heart disease. Analyses of all cause mortality showed that women who increased their alcohol intake from a high intake (=14 drinks per week) to an even higher intake had a higher mortality risk that women with a stable high intake.

CONCLUSION: In this study of postmenopausal women over a five year period, results support the hypotheses that alcohol intake is associated with increased risk of breast cancer and decreased risk of coronary heart disease.

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