By Cassandra Forsythe-Pribanic, PhD, RD
It starts sometime after you hit 30: you get out of bed one morning and your back feels like a stiff branch and your knees are more creaky than they’ve ever been. For at least a few seconds, you take slow steps, one by one, until your body loosens up and feels no pain, like it normally felt when you were a younger person.
That morning, when you got out of bed, you realized that the hill you’ve been climbing is starting to get a bit rockier. All those past years of jumping off rooftops, or lifting extremely heavy weights, is starting to feel it’s damaging effects. Today you realize it: you’re getting old.
The realization of stiffness, and perhaps even the start of arthritis or joint degeneration, is even worse than finding your first grey hair – at least with the hair you can cover it up. But, this stiffness in your back and achiness in your knees is a bit harder to hide; and you know it’s going to get worse.
Age-spots, wrinkles, thinning skin, aching joints; these are all signs of the proverbial time bomb that is our lifespan. We all want to go out with a bang, but how fast we go and how good we feel during this process all depends on how we treat our bodies from day one. Everything from nutrition, to our choice of exercise, to our choice of “recreational activities”, has an influence on our bodies’ aging lifeline.
How old are you, really?
Recently, scientists have discovered a truly unique way to measure how old your body really is. In 2009, the Nobel Prize in medicine was awarded to molecular scientists for uncovering unique proteins in our bodies, called Telomeres, and their enzymes, telomerases, that play an important role in the aging process.
Telomeres are snippets of DNA at the end of our chromosomes that function like little end-caps, providing stability and protection to our genetic material. The enzyme telomerase is responsible for rebuilding and maintaining telomere structure and is found within our cells. Most normal human adult cells, however, do not have enough active telomerase to maintain telomere length indefinitely, and therefore undergo telomere attrition with age.
Our telomeres shorten as a normal process of cellular division (which occurs all the time within our bodies). Each time a cell divides, the telomere is decreased in length until a critical length is reached, signaling cell death. This process of telomere shortening represents a ‘molecular clock’ that underlies aging. Usually telomerase enzymes rebuild your telomeres, but as we noted above, they have their own life span too.
Measuring age with telomeres
Telomere length is currently the best measure of your actual biological age compared to chronological age. It is also an important barometer of your overall health. Obesity is closely associated with chronic diseases, several cancers and premature death. Obese adults are found to have shorter telomeres than their normal weight counterparts. These findings support the notion that excess body fat may accelerate aging. Exercise, on the other hand, is found to up-regulate telomerase activity, which may provide the underlying molecular mechanism for the anti-aging effects of regular physical exercise.
Many human diseases of different origins that are associated with aging, as well as late stages of cancer are characterized by the presence of short telomeres. It then stands to reason that therapies directed at preserving telomere length may slow aging and retard the onset of age-related diseases.
Preserving telomeres with omega-3s
When people think of omega-3 fats from seafood, they often think heart health and fat loss. However, they can now associate a new benefit to omega-3s: Longevity.
New research suggests that these special essential fatty acids may actually preserve telomerase activity, and in turn, prevent shortening of telomeres themselves.
Cardiologists from the University of California, San Francisco, and other hospitals measured telomere length over five years in 608 patients who had coronary-artery blockage and previous heart attacks. Researchers found that people with high levels of omega-3 fatty acids in their white blood cells experienced significantly less shortening of telomeres over five years, as compared with patients with lower omega-3 levels.
This study focused on levels of omega-3s from marine sources, not from vegetable sources like flaxseed or walnuts. Omega-3 from plants don’t have the same effect on telomere length as seafood omega-3s, but still have other benefits, like improving the blood cholesterol profile.
Although all these patients had experienced some cardiac event, those with longer telomeres have less cellular aging and are most likely to live the longest with the most vitality.
The researchers in this study hypothesized that omega-3s work via two mechanisms to protect telomeres and preserve cellular health. First, omega-3s protect your cells against oxidative stress, a process that occurs in every one’s body and accelerates the aging process (free radicals and oxidative stress are one of the causes of age spots, wrinkles, joint pain and disease through cell damage). Second, omega-3s increase the activity of telomerase enzymes so that telomeres are always being rebuilt and preserved.
Marine Omega-3s for Healthy Longevity
Omega-3s from marine sources may be one way to preserve your youthfulness and protect against the damaging effects of aging. Think of omega-3 fatty acids (EPA and DHA) like little super heroes of the fat world: in one punch they knock down free radical enemies while helping telomerases keep your telomeres healthy and long.
References:
Blackburn, E. H. Switching and signaling at the telomere. Cell 106, 661–673 (2001).
Shay, J. W. & Wright, W. E. Telomerase: a target for cancer therapeutics. Cancer Cell 2, 257–265 (2002).
Kim S, Parks CG, et al. Obesity and weight gain in adulthood and telomere length. Cancer Epidemiol Biomarkers Prev. 2009 Mar; 18(3):816-20
Wermer C, Furster T, et al. Physical Exercise Prevents Cellular Senescence in Circulating Leukocytes and in the Vessel Wall. Circulation. 2009 Nov 30.
Jeanclos E, Krolweski A, et al. Shortened telomere length in white blood cells of patients with IDDM. Diabetes 1998;47:482-6.
Gardner JP, Li S, Srinivasin SR, et al. Rise in insulin resistance is associated with escalated telomere attrition. Circulation 2005;111:2171-7.
Samani NJ, Boutby, R, et al. Telomere shortening in atherosclerosis. Lancet 2001;358:472-3.
Morla M, Busquet X, et al. Telomere shortening in smokers with and without COPD. Eur Respir J 2006; 27:525-528.
Farzeneh-Far R, Lin J, Epel E, et al. Association of Marine Omega-3 Fatty Acids with Telomeric aging in patients with Coronary Heart Disease. JAMA. 2010; 303(3):250-257
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