Taking issue with language that only loosely links alcohol consumption to increased cancer incidence, an article in the July 2016 issue of Addiction suggests that 5.8 percent of all cancer deaths worldwide are caused by alcohol-attributable cancers of the oropharynx, larynx, esophagus, liver, colon, rectum, and female breast. Jennie Connor, “Alcohol consumption as a cause of cancer,” Addiction, July 2016. After reviewing “meta- analyses identified from the Medline database and the archives of the International Agency for Research on Cancer,” a researcher with the University of Otago’s Department of Preventive and Social Medicine reports a “dose–response relationship” between alcohol consumption and cancer, “without evidence of threshold of effect” and regardless of beverage type.
“Expressions such as ‘alcohol-related cancer’, ‘alcohol-attributable cancer’ and the effect of alcohol on ‘the risk of cancer’ incorporate an implicit causal association, but are easily interpreted as something less than cancer being caused by drinking,” opines the study author, who cites the example of a U.S. scientist purportedly employed by “an alcohol industry body” to dispute the effect of moderate alcohol consumption on cancer risk. “In this context, some confusion and skepticism about whether alcohol causes cancer may seem understandable, but in some cases doubt is also being generated by dissemination of misinformation, which undermines research findings and contradicts evidence-based public health messages.”
In addition, the article calls into question research that describes the protective effect of alcohol on cardiovascular disease (CVD). Connor notes the limitations of such studies, including the use of self-reported consumption measures; lack of consumption pattern measurements; the inclusion of former or occasional consumers of alcohol in an abstainer reference group; and residual confounding factors that vary by cancer types. As the article explains, “While residual confounding of the alcohol and cancer associations may reduce or increase the magnitude of the harmful effect, residual confounding of the CVD association is plausibly responsible for the whole of the observed protective effect, and particularly in combination with the bias caused by misclassification of former drinkers as abstainers.”
“The highest risks are associated with the heaviest drinking, but a considerable burden is experienced by drinkers with low to moderate consumption, due to the distribution of drinking in the population,” concludes Connor. “Thus, population-wide reduction in alcohol consumption will have an important effect on the incidence of these conditions, while targeting the heaviest drinkers alone has limited potential.”