Telomere Length Could Explain Effects of Fish Oil in CHD

January 20, 2010

January 19, 2010 (San Francisco, California) — A new study in patients with coronary artery disease (CAD) has uncovered an inverse association between baseline blood levels of fish oil and the rate of telomere shortening over five years, suggesting a possible explanation for the protective effects of omega-3 fatty acids [1].

Telomeres are the extreme ends of chromosomal DNA that shorten with age. Telomere shortening is seen as an indicator of biological aging, and telomere length has been shown to independently predict morbidity and mortality in patients with cardiovascular diseases, Dr Ramin Farzaneh-Far (San Francisco General Hospital, CA) and colleagues explain in their paper published in the January 20, 2010 issue of the Journal of the American Medical Association.

This is yet another reason for cardiologists to try to convince their patients to take either a fish-oil supplement or eat regular fatty-fish meals.

"This suggests the existence of a novel mechanism for why omega-3 fatty acids are effective in this patient population--an area that has not been well worked out previously; it suggests they could be acting through telomeres," Farzaneh-Far told heartwire . "It's also the first study that shows that a dietary factor may be able to slow down telomere shortening," he observes.

However he stresses that this was, "at its heart, an observational study" and that a randomized trial will be needed to prove causality. But in the meantime, the results "underscore and reinforce the American Heart Association guidelines that patients with CAD should be taking 1 g a day of omega-3 fatty acids for secondary prevention," he says. "This is yet another reason for cardiologists to try to convince their patients to take either a fish-oil supplement or eat regular fatty-fish meals."

Those With Lowest Levels of Fatty Acids Had Fastest Rate of Telomere Shortening

The researchers recruited 608 outpatients with stable CAD taking part in the Heart and Soul Study between 2000 and 2002 and measured telomere length at baseline in the blood and again after five years of follow-up, using a standard telomere-length assay. They also assessed baseline blood levels of the marine omega-3 fatty acids docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), expressed as a percentage of total fatty-acid methyl esters, "a relatively new blood test," Farzaneh-Far explains.

Patients were divided into quartiles on the basis of their marine omega-3 fatty-acid levels, with means of 2.3%, 3.3%, 4.3%, and 7.3% in the four groups, respectively. Farzaneh-Far says an important point to note is that omega-3 fatty acids "can be obtained only from the diet; there is no endogenous production." The optimal level of omega-3 fatty acids is not firmly established but is thought to be around 7% to 8%, "with most people on Western diets likely having levels way below what is optimal," he says.

Those in the lowest quartile of DHA+EPA experienced the fastest rate of telomere shortening, 0.13 telomere-to-single-copy-gene ratio [T/S] units over five years, whereas those in the highest quartile experienced the slowest rate, 0.05 T/S units over five years (p<0.001 for linear trend across the quartiles).

Novel Study, With Two Measures of Telomere Length

Farzaneh-Far says the research is "one of the few . . . that has two measurements of telomere length, so we were able to measure the actual rate of change, which gives us a sense of the rate at which biological aging is taking place. From a scientific point of view, that is one of the novel elements of this study."

Also, "from the telomere point of view, this is the first study to show an effect of a dietary factor, that this may be able to slow down telomere shortening," he notes.

Even after extensive statistical adjustments for confounding factors, "we found a dose-dependent decrease in the rate of telomere shortening according to the level of baseline omega-3 fatty acids," he reiterates, "suggesting that the association is causal."

However, he acknowledges, "To prove this, you would need a randomized trial. This would entail taking patients and measuring their telomere length at baseline, then randomizing half to omega-3 fatty acids and half to placebo and measuring the telomere length again to see whether the treatment group had less shortening of their telomeres: that would be the gold-standard way to prove causality."

Could Omega-3 Fatty Acids Be a Risk Factor for CHD?

Farzaneh-Far says the research also highlights a possible new concept: that omega-3 fatty acids could be used as a marker for coronary artery disease, in much the same way as cholesterol, for example.

"The idea is that the omega-3 index, the percentage of fatty acids in the blood, could be measured and that low levels would predict worse outcomes. So the omega-3 index might be useful for risk stratification in the future."

Coauthor Dr William S Harris (University of South Dakota, Sioux Falls) is an advisor and speaker for and has received research grants from companies with interests in omega-3 fatty acids, including GlaxoSmithKline and Monsanto. In addition, he has recently founded a company, OmegaQuant Analytics, to offer blood omega-3 fatty-acid testing. Farzaneh-Far and the other authors report no disclosures.

Comments

3090D553-9492-4563-8681-AD288FA52ACE
Comments on Medscape are moderated and should be professional in tone and on topic. You must declare any conflicts of interest related to your comments and responses. Please see our Commenting Guide for further information. We reserve the right to remove posts at our sole discretion.
Post as:

processing....