Alcohol consumption as a cause of cancer

Connor, Jennie

doi:10.1111/add.13477

Cited by 170 publications

(120 citation statements)

References 35 publications

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“…8,48 Recent findings do not support an overall protective effect from alcohol consumption. 18,50-52 Flawed study designs have been implicated in earlier findings of "protective effects" 53-58 -however, a great deal of controversy on this topic remains. 51,55,[59][60][61][62] A large proportion of participants in this study reported light-moderate drinking (0.1 to 29.9 g of ethanol/day or < 1 to 2 drinks/day), and may be unaware of the potential harm associated with even small Continued on the following page but regular amounts of alcohol.…”

Section: Discussionmentioning

confidence: 99%

“…14,17 However, recent evidence has challenged these findings and suggest that there is no safe limit of consumption, especially for cancer. [18][19][20][21] Despite the controversy, identifying a safe threshold based on sound methodology which accounts for beverage type, the frequency and volume of consumption and patterns of use for alcohol remains an important research question. 21 Recent reviews on the topic suggest that even light-to-moderate alcohol use may not be protective for chronic disease.…”

Section: Introductionmentioning

confidence: 99%

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Alcohol consumption and low-risk drinking guidelines among adults: a cross-sectional analysis from Alberta’s Tomorrow Project

Brenner

Haig

Poirier

et al. 2017

Health Promot Chronic Dis Prev Can

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Introduction Moderate to heavy alcohol consumption is a risk factor for all-cause mortality and cancer incidence. Although cross-sectional data are available through national surveys, data on alcohol consumption in Alberta from a large prospective cohort were not previously available. The goal of these analyses was to characterize the levels of alcohol consumption among adults from the Alberta’s Tomorrow Project in the context of cancer prevention guidelines. Furthermore, we conducted analyses to examine the relationships between alcohol consumption and other high-risk or risk-related behaviours. Methods Between 2001 and 2009, 31 072 men and women aged 35 to 69 years were enrolled into Alberta’s Tomorrow Project, a large provincial cohort study. Data concerning alcohol consumption in the past 12 months were obtained from 26 842 participants who completed self-administered health and lifestyle questionnaires. We conducted cross-sectional analyses on daily alcohol consumption and cancer prevention guidelines for alcohol use in relation to sociodemographic factors. We also examined the combined prevalence of alcohol consumption and tobacco use, obesity and comorbidities. Results Approximately 14% of men and 12% of women reported alcohol consumption exceeding recommendations for cancer prevention. Higher alcohol consumption was reported in younger age groups, urban dwellers, those with higher incomes and those who consumed more red meat. Moreover, volume of daily alcohol consumption was positively associated with current tobacco use in both men and women. Overall, men were more likely to fall in the moderate and high-risk behavioural profiles and show higher daily alcohol consumption patterns compared to women. Conclusion Despite public health messages concerning the adverse impact of alcohol consumption, a sizeable proportion of Alberta’s Tomorrow Project participants consumed alcohol in excess of cancer prevention recommendations. Continued strategies to promote low-risk drinking among those who choose to drink could impact future chronic disease risk in this population.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Alcohol consumption and low-risk drinking guidelines among adults: a cross-sectional analysis from Alberta’s Tomorrow Project

Brenner

Haig

Poirier

et al. 2017

Health Promot Chronic Dis Prev Can

View full text Add to dashboard Cite

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“…Epidemiological evidence strongly suggests that moderate to heavy alcohol consumption increases the risk of cancer of the oral cavity, pharynx, larynx, esophagus, liver, colon, rectum and female breast [1][2][3]. Recent estimates indicate that the relative risk for heavy drinkers compared with nondrinkers and occasional drinkers is 5.13 for oral and pharyngeal cancer, 4.95 for esophageal 2 cancer, 2.65 for laryngeal cancer, 2.07 for liver cancer, 1.44 for colorectal cancer and 1.61 for breast cancer [3].…”

Section: Introductionmentioning

confidence: 99%

“…It has been estimated that 5.8% of cancer deaths world-wide are attributable to alcohol use [5]. However, the biological mechanism by which alcohol causes cancer is unclear [1,2,6,7]; this is often raised as an objection to accept the strong epidemiological link between alcohol consumption and cancer [2].…”

Section: Introductionmentioning

confidence: 99%

A local mechanism by which alcohol consumption causes cancer

López‐Lázaro

2016

Oral Oncology

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Epidemiological data indicate that 5.8% of cancer deaths world-wide are attributable to alcohol consumption. The risk of cancer is higher in tissues in closest contact on ingestion of alcohol, such as the oral cavity, pharynx and esophagus. The risk of these cancers is increased even in people who have only one alcoholic drink per day. However, since ethanol is not mutagenic and the carcinogenic metabolite of ethanol (acetaldehyde) is mostly produced in the liver, it is not clear why alcohol use preferentially exerts a local carcinogenic effect. It is well known that ethanol causes cell death at the concentrations present in alcoholic beverages; however, this effect has been overlooked probably because dead cells cannot give rise to cancer. Here I discuss that the cytotoxic effect of ethanol on the cells lining the oral cavity, pharynx and esophagus activates the division of the stem cells located in deeper layers of the mucosa to replace the dead cells. Every time stem cells divide, they become exposed to unavoidable errors associated with cell division (e.g., mutations arising during DNA replication and chromosomal alterations occurring during mitosis) and also become highly vulnerable to the genotoxic activity of endogenous and exogenous DNA-damaging agents (e.g., reactive oxygen species, acetaldehyde and tobacco carcinogens). Alcohol consumption probably increases the risk of developing cancer of the oral cavity, pharynx and esophagus by promoting the accumulation of cell divisions in the stem cells that maintain these tissues in homeostasis. Because the cytotoxic activity of ethanol is concentration-dependent, the risk of these cancers will not only increase with increasing amounts of ethanol, but also with increasing concentrations; an ounce of whisky is probably more carcinogenic when taken undiluted than when taken mixed with non-alcoholic beverages. The local cytotoxic effect of ethanol can also explain the known synergistic effect of alcohol and tobacco use on the risk of these cancers. Understanding the mechanisms of carcinogenicity of alcohol is important to reinforce the epidemiological evidence and to raise public awareness of the strong link between alcohol consumption and cancer.

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“…Connor makes a cogent argument for 'having it both ways' [1]. We agree that it is entirely plausible that alcohol causes cancer but does not afford drinkers a cardiovascular benefit.…”

mentioning

confidence: 94%