Supplementation with omega 3 from fish oil could slow biological aging
Omega-3 fatty acid supplements: an aid against aging
A surprising finding shows that reducing the ratio of omega-6 to omega-3 in the body through supplementation with high-dose fish oil could slow cellular aging and by 15 percent slow oxidative stress in healthy adults. Highlighting this new effect of omega-3 fatty acids found in fish oil is research published by Janice Kiecolt-Glaser and colleagues at Ohio State University (Columbus, USA) in the journal Brain, Behavioue, and Immunity.
Telomeres, an indicator of biological aging
U.S. researchers looked at the length of telomeres, which is the end of the chromosomes that contain the cells' Dna, as an indicator of aging.
Several researches have shown that in diseases associated with aging, these structures are shorter than normal. Not only that, shorter telomeres are associated with unhealthy lifestyles and earlier mortality. This study focused on their length in the white blood cells of individuals who took either 2.5 grams or 1.25 grams of the Omega-3 EPA (eicosapentaenoic acid) and DHA (docosahexaenoic acid) daily for 4 months in a ratio of 7:1. This parameter was compared with telomere length in people who, instead, consumed a mixture representative of the average fat consumption in the typical American diet. Simply considering the amount of Omega-3 intake, the researchers found no significant difference in telomere length in the different individuals who participated in the study.
However, focusing on the ratio of Omega-6 to Omega-3 showed that lower values (associated, therefore, with higher amounts of Omega-3) were associated with longer telomeres. Similar results were also obtained by analyzing the activity of telomerase, the enzyme on which telomere length depends. Taken together, these data indicate that the lower the Omega-6/Omega-3 ratio, the less cells age.
Omega-3 and Omega-6: two opposing effects The results obtained reiterate how important it is to ensure a diet such that Omega-6 and Omega-3 levels are maintained in an optimal balance. In fact, although both are essential fatty acids for the body, their action is mostly opposite, and while in most cases Omega-6 promotes inflammatory phenomena, Omega-3 has a marked anti-inflammatory effect. Unfortunately, modern Western diets are particularly high in Omega-6. Many experts believe that the increased consumption of these fatty acids at the expense of the healthier Omega-3s is at least partly responsible for the increase in certain diseases such as, for example, cardiovascular disease. The results of this new study reaffirmed how a targeted approach to reducing the ratio of Omega-6 to Omega-3 based on increasing the consumption of the latter may be effective in improving health status. Not only that, Kiecolt-Glaser commented on the finding of the influence of Omega-3 on telomere length by pointing out that it supports the hypothesis that dietary supplement intake can indeed influence aging processes.
Anti-aging and anti-inflammatory In addition to the protective effect against telomere shortening, the researchers found that both doses of Omega-3 tested reduced oxidative stress, a factor associated with several disorders, including cardiovascular and neurodegenerative disorders, by about 15 percent. These results join those obtained earlier by the same researchers, who have shown that Omega-3 intake is effective in reducing levels of inflammation, another important factor in determining health status. Based on all this evidence, the authors concluded that Omega-3 supplements could represent a rare case in which a single nutritional intervention can help reduce the risk of several diseases associated with aging: from coronary heart disease to diabetes and Alzheimer's.
Source:
Kiecolt-Glaser JK, Epel ES, Belury MA, Andridge R, Lin J, Glaser R, Malarkey WB, Hwang BS, Blackburn E, "Omega-3 fatty acids, oxidative stress, and leukocyte telomere length: A randomized controlled trial," Brain Behav Immun. 2012 Sep 23. pii: S0889-1591(12)00431-X. doi: 10.1016/j.bbi.2012.09.004. [Epub ahead of print].
