In an attempt to judge the effects of alcohol on the risk of coronary heart disease (CHD), the authors have carried out analyses using a sample of subjects from the National Epidemiologic Survey on Alcohol and Related Conditions III (NESARC-III). They based their exposure to current alcohol use on a single assessment at baseline of self-reported consumption during the past year, when the subjects were an average of 38.9 years of age. In addition they asked subjects if they had consumed larger amounts of alcohol when they were younger.
Their assessment of CHD was based on answers to questions at baseline as to having been told by a doctor that they had chest pain or CHD, apparently within the same 12-month period when they were asked about current alcohol consumption. Nothing in the paper indicates that the authors had data on the subsequent development of CHD during a follow-up period. When relating reported alcohol intake to CHD, they excluded 1,671 who reported “previous CHD,” although for this relatively young group it is questionable how many actually had CHD, as no data on validation of the diagnosis was done. For unclear reasons, for their comparison group they excluded any subjects with conditions that “may increase the risk of CHD (e.g., pneumonia, influenza, tuberculosis, liver disease, neurologic conditions, osteoporosis, arthritis, STD) and can be viewed as comorbid conditions related to alcohol consumption.”
Given that the exposure (alcohol) and outcome (CHD) were apparently from the same time period, there is reason to worry about reverse causation (i.e., subjects may have developed CHD and changed, either decreased or increased, their alcohol consumption during the same period).. As for using the self-reported amount of alcohol consumed at some time in the past as the exposure, there is a large chance of serious misclassification of exposure due to recall bias and bias according to current alcohol intake (as subjects currently reporting greater amounts of alcohol were more likely to report even higher intake in the past).
With only a single assessment of current alcohol intake, an inadequate assessment of long-term alcohol intake, a lack of data during a follow-up period for the main outcome, CHD, and no validation of the outcome, Forum members considered that this was an unusual cohort to use when attempting to judge the relation of changes in alcohol consumption to the development of CHD. The necessary elements for a useful analysis were not available to these investigators using this population sample. In any case, results from many well-done long-term cohort studies with repeated assessments of alcohol and validated CHD outcomes during follow up have already provided key data on this topic: they almost uniformly demonstrate that light-to-moderate drinkers who do not binge drink have significantly lower risk of developing CHD. The present analysis does not provide data that would question such findings.
Reference: Fan AZ, Ruan WJ, Chou SP. Re-examining the relationship between alcohol consumption and coronary heart disease with a new lens. Pre-publication. Preventive Medicine 2019;118:336=343.