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
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.