By Michaela Carrick
Telomeres and Aging – the Connection

Inside the cell, at the end of each chromosome is a section called a telomere. Young cells have longer telomeres than older cells because everwy time a cell divides, the telomere becomes shorter. Shorter telomeres have been associated with age-related diseases and early mortality1. Once a telomere becomes too short, the cell dies through a process called apoptosis. This means, by slowing down the shortening of telomeres, we may be able to slow down the aging process2.

In addition to telomere shortening, DNA suffers increased damage as we age and the cell’s energy supply becomes less efficient. Inflammation plays a vital role in the process of aging. Inflammation is a normal response of the immune system to the invasion of bacteria and viruses. Life expectancy has increased greatly and this means our immune system must remain active for much longer than it was designed to.

This has led to chronic inflammation, a major risk factor for age-related diseases such as Alzheimer’s, diabetes and atherosclerosis3. Research also suggests that molecules called reactive oxygen species damage the mitochondria of cells and telomeres of mitochondrial DNA, causing a decline in their function and leading to age-related diseases4. Managing inflammation is critical to cellular health.

Omega-3s and Inflammation

Omega-3s and omega-6 work together to balance inflammation in the body. Omega-3 is anti-inflammatory whereas omega-6 is inflammatory. These two molecules are constantly competing in the human body for the same enzymatic pathways. As anti-inflammatory molecules, omega-3s reduce inflammation and oxidative stress and by doing so omega-3s protect telomeres9.

Higher omega-3 levels have also been linked to lower all-cause mortality10,11,12. Omega-3’s anti-inflammatory and antioxidant properties may explain why individuals with higher blood omega-3 levels have a reduced mortality risk. Previous papers have reported omega-3 supplementation significantly reduced inflammation, an underlying mechanism of many chronic diseases. For example, the ATTICA Study, a health and nutrition survey of healthy Greek adults reported higher omega-6:omega-3 ratios were associated with higher TNF-α and IL-6, markers of inflammation13.

The Ohio State Study

A study conducted at The Ohio State University investigated if omega-3 supplementation could affect inflammation, telomere length and oxidative stress9. Researchers also assessed if the ratio of omega-6 to omega-3 fatty acids explained the differences between individuals in response to omega-3 supplementation. OmegaBrite donated both placebo and control material for this study.

106 sedentary and overweight adults aged 40-85 were split into three groups for 4 months. Group one took 2.5g of omega-3 daily; group two took 1.25g of omega-3 daily; and group three took a placebo supplement daily that represented the fatty acids in the average American’s diet.

In this study, F2-isoprostanes were used to measure levels of oxidative stress. The results were F2-isoprostanes were 15% lower in individuals who took an omega-3 supplement daily compared to the placebo group9. The study concluded that omega-3s can impact cell aging in addition to inflammation and oxidative stress9.

Lower omega-6:omega-3 ratios were associated with longer telomeres at the end of the study and telomere length increased with decreasing omega-6:omega-3 ratio9. There was no significant effect of omega-3 directly related to telomere length or telomerase but this study gave scientists a deeper understanding of the importance of an omega-6 to omega-3 balance9. These results agree with findings from other studies that have reported a link between omega-3 and omega-6 ratios and telomere length14,15,16.

Short telomeres can be predictive of early disease17, thus by altering the omega-3 and omega-6 ratio, immune cell aging and the onset of age-related diseases could be slowed down.

The findings of this study suggest that levels of omega-6 and the omega-3 should be considered when designing nutritional intervention9. It was also reported that individuals with higher omega-6:omega-3 ratios benefit most from supplementation, meaning the supplementation of poorer diets may have a greater positive effect9. By increasing our intake of omega-3s, we can lower oxidative stress, inflammation and telomere length.


  1. Jaskelioff M, Muller FL, Paik JH, et al. Telomerase reactivation reverses tissue degeneration in aged telomerase-deficient mice. Nature. 2011;469(7328):102-106.
  2. Cawthon RM, Smith KR, O’Brien E, Sivatchenko A, Kerber RA. Association between telomere length in blood and mortality in people aged 60 years or older. Lancet. 2003;361(9355):393-395.
  3. Bruunsgaard H, Pedersen M, Pedersen BK. Aging and proinflammatory cytokines. Curr Opin Hematol. 2001;8(3):131-136.
  4. Payne BA, Chinnery PF. Mitochondrial dysfunction in aging: Much progress but many unresolved questions. Biochim Biophys Acta. 2015;1847(11):1347-1353.
  5. Balk EM, Lichtenstein AH, Chung M, Kupelnick B, Chew P, Lau J. Effects of omega-3 fatty acids on serum markers of cardiovascular disease risk: a systematic review. Atherosclerosis. 2006;189(1):19-3.
  6. Parker G, Gibson NA, Brotchie H, Heruc G, Rees AM, Hadzi-Pavlovic D. Omega-3 fatty acids and mood disorders. Am J Psychiatry. 2006;163(6):969-978.
  7. Mohebi-Nejad A, Bikdeli B. Omega-3 supplements and cardiovascular diseases. Tanaffos. 2014;13(1):6-14.
  8. Zivkovic AM, Telis N, German JB, Hammock BD. Dietary omega-3 fatty acids aid in the modulation of inflammation and metabolic health. Calif Agric (Berkeley). 2011;65(3):106-111.
  9. Kiecolt-Glaser JK, Epel ES, Belury MA, et al. Omega-3 fatty acids, oxidative stress, and leukocyte telomere length: A randomized controlled trial. Brain Behav Immun. 2013;28:16-24.
  10. Lee JH, O’Keefe JH, Lavie CJ, Harris WS. Omega-3 fatty acids: cardiovascular benefits, sources and sustainability. Nat Rev Cardiol. 2009;6(12):753-758.
  11. Pottala JV, Garg S, Cohen BE, Whooley MA, Harris WS. Blood eicosapentaenoic and docosahexaenoic acids predict all-cause mortality in patients with stable coronary heart disease: the Heart and Soul study. Circ Cardiovasc Qual Outcomes. 2010;3(4):406-412.
  12. Marchioli R, Barzi F, Bomba E, et al. Early protection against sudden death by n-3 polyunsaturated fatty acids after myocardial infarction: time-course analysis of the results of the Gruppo Italiano per lo Studio della Sopravvivenza nell’Infarto Miocardico (GISSI)-Prevenzione. Circulation. 2002;105(16):1897-1903.
  13. Kalogeropoulos N, Panagiotakos DB, Pitsavos C, et al. Unsaturated fatty acids are inversely associated and n-6/n-3 ratios are positively related to inflammation and coagulation markers in plasma of apparently healthy adults. Clin Chim Acta. 2010;411(7-8):584-591.
  14. Farzaneh-Far R, Lin J, Epel E, Lapham K, Blackburn E, Whooley MA. Telomere length trajectory and its determinants in persons with coronary artery disease: longitudinal findings from the heart and soul study. PLoS One. 2010;5(1):e8612.
  15. Cassidy A, De Vivo I, Liu Y, et al. Associations between diet, lifestyle factors, and telomere length in women. Am J Clin Nutr. 2010;91(5):1273-1280.
  16. Kang JX. Differential effects of omega-6 and omega-3 fatty acids on telomere length. Am J Clin Nutr. 2010;92(5):1276-1277; author reply 1277.
  17. Calado R, Young N. Telomeres in disease. F1000 Med Rep. 2012;4:8.