Fish oil lengthens telemeres

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Telomere length could explain effects of fish oil in CHD

JANUARY 19, 2010 | Nainggolan

San Francisco, CA - 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).

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. "