January 15, 2014

The Effects of Fish Oil on Aging

Commentary considers the possible link between longer lifespan and omega-3-fatty acids


Farzaneh-Far R, Lin J, Epel ES, Harris WS, Blackburn EH, Whooley MA. Association of marine omega-3 fatty acid levels with telomeric aging in patients with coronary heart disease. JAMA. 2010;303(3):250-257.


This was a prospective cohort study of 608 ambulatory outpatients with stable coronary artery disease recruited from the Heart and Soul Study between September 2000 and December 2002 and followed up to January 2009 (median: 6.0 years; range: 5.0–8.1 years). Leukocyte telomere length was measured at baseline and again after 5 years of follow-up. Multivariable linear and logistic regression models were used to investigate the association of baseline levels of omega-3 fatty acids (docosahexaenoic acid [DHA] and eicosapentaenoic acid [EPA]) with subsequent change in telomere length.

Key Findings

Individuals 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 5 years; 95% confidence interval [CI], 0.09–0.17), whereas those in the highest quartile experienced the slowest rate of telomere shortening (0.05 T/S units over 5 years; 95% CI, 0.02–0.08; p < 0.001 for linear trend across quartiles). Levels of DHA+EPA were associated with less telomere shortening before (unadjusted β coefficient x 10−3 = 0.06; 95% CI, 0.02–0.10) and after (adjusted β coefficient x 10−3 = 0.05; 95% CI, 0.01–0.08) sequential adjustment for established risk factors and potential confounders. Each 1-standard deviation increase in DHA+EPA levels was associated with a 32% reduction in the odds of telomere shortening (adjusted odds ratio, 0.68; 95% CI, 0.47–0.98). Among a cohort of patients with coronary artery disease, there was an inverse relationship between baseline blood levels of marine omega-3 fatty acids and the rate of telomere shortening over 5 years.


What is the possible link between longer lifespan and omega-3-fatty acids? Is reduced telomere shortening the key? During cell division there is a progressive loss of tandem repeat DNA sequences (telomeres), which form the protective caps at the end of chromosomes, eventually leading to cell death. Since short telomeres are associated with cardiovascular disease and death, can it be assumed that this mechanism is the reason omega-3 fatty acids have shown a prolonged lifespan in this segment of the population?
A critic might state that there is not enough information to draw this conclusion; however I would state that there may never be enough information to draw that conclusion, as the body and disease simply exist on too many levels.
 A critic might state that there is not enough information to draw this conclusion; however I would state that there may never be enough information to draw that conclusion, as the body and disease simply exist on too many levels. Omega-3 fatty acids promote antiplatelet aggregation, a beneficial effect in preventing cardiovascular events.1 Omega-3 fatty acids have an anti-inflammatory effect on the body and have been reported to reduce C-reactive protein, which may be the leading marker in the prediction of vascular (cardiovascular) event and disease.2 Decreased tissue levels of minerals and antioxidants have been associated with cardiovascular risk.3,4 So which effect is it? In the end it may be shown that the collective effect of omega-3 supplementation and dietary intake may be the key to the telomere effect, not a single attributable physiologic effect. This would coincide in theory to the broad range of medical conditions that are positively affected by the intake of omega 3s. One note: Omega-3 fatty acids vary greatly in quality; some oils may be rancid, or they may be contaminated either by pollution or the manufacturing process. As a clinician, a simple telomere or CRP benefit would not be enough to recommend supplementation without an intimate knowledge of the origin and manufacturing quality of the source of omega-3. As oxidation is an intimate part of cardiovascular disease, the rancidity and potential toxicity of the product must come into question.5

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1. Phang M, Garg ML, Sinclair AJ. Inhibition of platelet aggregation by omega-3 polyunsaturated fatty acids is gender specific-redefining platelet response to fish oils. Prostaglandins Leukot Essent Fatty Acids. 2009;81(1):35-40.
2. Micallef MA, Munro IA, Garg ML. An inverse relationship between plasma n-3 fatty acids and C-reactive protein in healthy individuals. Eur J Clin Nutr. 2009;63(9):1154-1156.
3. Johnson CJ, Peterson DR, Smith EK. Myocardial tissue concentrations of magnesium and potassium in men dying suddenly from ischemic heart disease. Am J Clin Nutr. 1979;32(5):967-970.
4. Stephens NG, Parsons A, Schofield PM, Kelly F, Cheeseman K, Mitchinson MJ. Randomised controlled trial of vitamin E in patients with coronary disease: Cambridge Heart Antioxidant Study (CHAOS). Lancet. 1996;347(9004):781-786.
5.Navab M, Hama SY, Reddy ST, et al. Oxidized lipids as mediators of coronary heart disease. Curr Opin Lipidol. 2002;13(4):363-372.