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.”


Issue 612

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