Fish Oil Fails To Prevent Heart Disease

For as long as I have been involved in cardiovascular research, the story of how the n–3 fatty acids found in fish oil can potentially help improve cardiovascular risk factors – by positively influencing everything from arrhythmias, elevated triglyceride levels, atherosclerotic plaque, impaired endothelial function, platelet aggregation, to inflammation.

Benefits of consuming fish oil was also suggested by epidemiologic studies that showed a reduced risk of cardiovascular events among persons who consume fish regularly or who take supplements containing n–3 fatty acids.

But now, according to the results of the ORIGIN trial, presented yesterday at the 72nd American Diabetes Association Scientific Conference, the daily ingestion of 1 g of n–3 fatty acids has zero impact on preventing heart disease.

Thus, in this study published by the ORIGIN investigators in the New England Journal of Medicine, 12,536 individuals who were at high risk for cardiovascular events and had impaired fasting glucose, impaired glucose tolerance, or diabetes were randomly assigned to 1-g capsule containing at least 900 mg (90% or more) of ethyl esters of n–3 fatty acids or placebo daily and followed for 6.2 years.

Virtually exactly the same number of participants in the n–3 fatty acids and placebo groups experienced cardiovascular complications or death. Nor was there any difference between the groups in deaths from any cause.

So much for fish-oil supplements – readers may recall, that a similar randomised controlled study (incidentally, by the same investigators), also failed to demonstrate any benefits (and possible harm) from taking vitamin e capsules.

As to the lack of efficacy of n-3 fatty acids in this study, the author offer the following possible explanations:

“First, two of the largest trials recruited patients who had had a myocardial infarction within the past 3 months or who had heart failure. Such participants might have been more likely to benefit from any possible antiarrhythmic effect of n–3 fatty acids than were participants in our study.

Second, participants in our trial were taking more concomitant cardioprotective therapies than were those in many previously published trials. These therapies may have reduced the incidence of death from cardiovascular causes, thereby reducing the statistical power to detect any effect of n–3 fatty acids.

Third, participants in some of the other trials may have had a daily dietary intake of n–3 fatty acids that differed from the intake in our study population (median, 210 mg per day) and thus might have derived greater benefit from supplementation.

Fourth, our study was restricted to patients with impaired fasting glucose, impaired glucose tolerance, or diabetes, and n–3 fatty acids may not be effective in such patients.”

While these may all well be reasons, I am more willing to consider the most plausible explanation – n-3 fatty acid supplements just don’t have all that dramatic effect as the supplement makers will have you believe.

For me, a key learning is once again, that epidemiological studies that suggest that people eat more of one thing than another live longer, is hypothesis generating at best. So far, most of such associations have failed to stand up to rigorous double-blind randomised controlled trials.

Not that this is likely to matter much to those who sell these supplements (a $13 billion annual market according to a recent report) or perhaps to the many who take them religiously.

Even I have a supply of fish oil capsules at home, which I guess I can now throw out.

Toronto, Ontario