Omega-3 supplements linked to younger biological age in older people


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Omega-3 supplements linked to younger biological age in older people
Supplements of omega-3s may slow cellular ageing in older people with mild cognitive impairment, according to results of a pilot randomized clinical trial

DHA (docosahexaenoic acid) was associated with reduced shortening of telomeres, DNA sequences at the end of chromosomes that shorten as cells replicate and age,  report researchers from Australia in Nutrition​.

The aging and lifespan of normal, healthy cells are linked to the so-called telomerase shortening mechanism, which limits cells to a fixed number of divisions. During cell replication, the telomeres function by ensuring the cell's chromosomes do not fuse with each other or rearrange, which can lead to cancer. Elizabeth Blackburn, a telomere pioneer at the University of California San Francisco, likened telomeres to the ends of shoelaces, without which the lace would unravel.

With each replication the telomeres shorten, and when the telomeres are totally consumed, the cells are destroyed (apoptosis). Previous studies have also reported that telomeres are highly susceptible to oxidative stress.

“It is becoming increasingly evident that damage specific to the telomeric ends of chromosomes is one of the most critical events that initiate genome instability leading to accelerated ageing, cognitive decline and neurodegenerative disease,” ​explained the authors of the new paper.

Observational vs intervention studies

This is not the first time that omega-3s have been linked to reduced telomere shortening, with findings from a study by researchers from the University of California, San Francisco indicating that high blood levels of omega-3 fatty acids may slow cellular ageing in people with coronary heart disease (JAMA​, Vol. 303, pp. 250-257).

The UCSF study was epidemiological, however, while the new study, performed by scientists from the Commonwealth Scientific and Industrial Research Organisation (CSIRO), the University of South Australia, and the University of Newcastle is an intervention study, albeit on a pilot scale.

Led by Nathan O’Callaghan, the researchers recruited 33 people over the age of 65 with mild cognitive impairment, and randomly assigned them to one of three groups: The first group received EPA (eicosapentaenoic acid) omega-3 supplements (1.67g EPA+0.16g DHA/day); the second group received DHA omega-3 supplements (1.55g DHA+0.40g EPA/day), or omega-6 linoleic acid (LA, 2.2g/day) for six months.

Results of the study showed that the omega-6 group exhibited the greatest shortening of telomere length, compared to the DHA and EPA groups. Increased levels of DHA in red blood cells was significantly associated with reduced telomere shortening in the DHA group, said O’Callaghan and his co-workers.

“Although underpowered to detect significant differences between treatment groups, this study provides interesting pilot data that indicates telomere shortening may be modified by nutritional means over a six month period,” ​they wrote.

“Specifically, increasing n-3 PUFA intake via supplementation may attenuate telomere shortening that occurs with age. These data build on current epidemiological evidence and recent reports linking increased marine n-3 PUFA with decreased telomere attrition.

“Further investigation is needed to understand the effects observed here, particularly deciphering whether telomere length is modified through an increase in n-3 PUFA or (and/or) a decrease in n-6 PUFA.”


Commenting on the results, Harry Rice, PhD, VP of regulatory & scientific affairs for the Global Organization for EPA and DHA Omega-3s (GOED), was not impressed with the study. "If not for the 2010 JAMA publication reporting an inverse relationship between baseline blood levels of marine omega-3 fatty acids and the rate of telomere shortening over 5 years, in addition to the 2012 publication reporting that average telomere length increases with omega-3 supplementation, I might be quick to dismiss the present results,"​ he told us.

"Given that Apolipoprotein-ε4 (APOE-ε4) is a major genetic risk factor for cognitive decline and Alzheimer's Disease and recent research demonstrated that APOE-ε4 carriers demonstrated marked telomere attrition over two years, future subject recruitment for research investigating the effect(s) of Omega-3s on telomere length in cognitively impaired individuals should focus on APOE-ε4 carriers."

Source: Nutrition
Published online ahead of print, doi: 10.1016/j.nut.2013.09.013
“Telomere shortening in elderly people with mild cognitive impairment may be attenuated with omega-3 fatty acid supplementation: A randomised controlled pilot study”
Authors: N. O’Callaghan, N. Parletta, Catherine M. Milte, Bianca Benassi-Evans, Michael Fenech, Peter RC. Howe

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