This article is more than 5 years old. Information may no longer be current.
Omega-3 fatty acids may protect against cellular aging in patients with CHD
Click Here to Manage Email Alerts
Researchers have identified an inverse relationship between baseline marine omega-3 fatty acid blood levels and the rate of leukocyte telomere shortening, an emerging marker of biological age, giving researchers some of the first clues into the mechanisms underlying the protective effects of increased oily fish intake for patients with CHD.
“Marine omega-3 fatty acid supplementation has been associated with improved survival after MI in observational studies and randomized clinical trials,” the researchers wrote. “Although the mechanisms involved remain incompletely understood, there is increasing evidence that omega-3 fatty acids exert direct effects on aging and age-related diseases.”
Between September 2000 and December 2002, researchers recruited 608 patients with stable CAD from the Heart and Soul Study. They measured leukocyte telomere length and omega-3 fatty acid levels (docosahexaenoic acid and eicosapentaenoic acid) at baseline and again at five-year follow-up, and used multivariable linear and logistic regression models to investigate the relationship between the two over time.
Data indicated that after five years those in the lowest quartile of omega-3 fatty acid levels had the fastest rate of telomere shortening (0.13 telomere-to-single-copy gene ratio [T/S] units; 95% CI, 0.09-0.17), whereas those in the highest quartile experienced the slowest rates of shortening (0.05 T/S units; 95% CI, 0.02-0.08).
When the researchers sequentially adjusted for established risk factors and potential confounders, including demographics, comorbidities, BP, serum lipids, inflammatory biomarkers, medications and baseline telomere length, higher baseline omega-3 fatty acid levels were associated with an increase in absolute telomere length over time (adjusted B coefficient=0.05; 95% CI, 0.01-0.08).
The researchers observed a 32% reduction in the odds of telomere shortening with each 1-SD increase in omega-3 fatty acid levels (adjusted OR=0.68; 95% CI, 0.47-0.98).
Despite these findings, no significant associations existed between baseline levels of the two. The researchers hypothesized that factors such as systemic inflammation, obesity, oxidative stress and lack of physical activity may play a cumulative role in determining telomere length throughout life.
“The present findings identify deceleration of telomere attrition as a potentially novel pathway for the anti-aging effects of marine omega-3 fatty acids,” they wrote.
The researchers emphasized that the observational nature of the study precludes any definite conclusions regarding causality and that other unmeasured confounding covariates cannot be excluded. Results may not be generalizable to a wide patient population, as the majority of study participants were outpatient men with CAD. “To definitely address the question of whether omega-3 fatty acids inhibit cellular aging, a double-blind, randomized, placebo-controlled trial would be necessary,” they wrote.
Farzaneh-Far R. JAMA. 2010;303:250-257.