The latest critique from The ISFAR casts its eye over research from Finland

The latest critique from The ISFAR casts its eye over research from Finland

Observational epidemiologic studies relating alcohol consumption to health and disease have been remarkably consistent over many decades: light to moderate alcohol intake is related to improved cardiovascular health and less diabetes, while heavy intake and binge drinking relate primarily to adverse cardiovascular and other disease outcomes.

A multitude of animal experiments have identified many mechanisms by which moderate drinking affects cardiovascular disease, including beneficial effects on lipids, coagulation factors, fibrinolysis, glucose metabolism, inflammation, and endothelial function. The mechanisms for a direct effect of heavy drinking on upper airway cancers and liver disease have also been delineated, and suggested mechanisms given for the slight increase in breast cancer risk from even moderate drinking seen in most epidemiologic studies.

The specific metabolic effects of alcohol, however, have been little studied.

The investigators in a recent study collected a large amount of metabolic data from population-based cohorts of relatively young and healthy men and women in Finland. Their analysis provides a wealth of information by relating such data to the reported alcohol intake of subjects.

In the analysis - among almost 10,000 young adults from three population-based cohorts in Finland - associations of alcohol intake with 86 metabolic measures were assessed. Circulating lipids, fatty acids and metabolites were quantified by high-throughput nuclear magnetic resonance metabolomics and biochemical assays. The investigators found that alcohol consumption was associated with a complex metabolic signature, including aberrations in multiple biomarkers for reduced as well as elevated cardiometabolic risk; many factors showed different associations according to the estimated amount of alcohol consumed.

Among key associations found for greater alcohol intake were increases in HDL-cholesterol and its subclasses, decreases in LDL size, an increase in monounsaturated fatty acids and a decrease in omega-6 fatty acids, as well as lower concentrations of glutamine and citrate. For reasons that were not explained, the changes in fatty acids from alcohol in this study were similar to those occurring following the administration of canola oil in other research.

Some ISFAR reviewers pointed out that the analyses were not theory-driven, and should only be used to generate hypotheses that would need to be tested in future experiments. As stated by one reviewer, one result of this paper could be that it ignites the interest for experimental studies and provides new variables to be evaluated in prospective studies. In any case, the findings of this study provide valuable clues to the biological effects on health, both favourable and adverse, related to alcohol consumption.

While not discussed by the authors, ISFAR members considered that the results of this paper might also be useful in providing a new approach for judging the level of alcohol intake of individuals in epidemiologic studies. At present, alcohol intake is judged almost exclusively from self-reports by subjects. Previous attempts designed to identify subjects more likely to be under-reporting their intake have shown that they may sharpen relations between estimated intake and health outcomes.

ISFAR members believe that approaches that identify sources of bias for self-reported data, whether based on genetic, behavioural, physiological, or other information (preferably on all), might allow epidemiologists to have more precise and accurate information on alcohol intake when relating such to disease outcomes. A new approach for providing more accurate and unbiased estimates of alcohol intake is suggested by this excellent analysis.

To read the full critique, click here.

These critiques are published with the permission of The ISFAR.