As we age, we tend to notice a loss of muscle mass, strength, bone mass, and energy potential. Meanwhile, body fat increases, skin wrinkles, mood changes occur, and immunity declines. New scientific research is shedding light on why we age and how we may be able to slow the process.

There are numerous theories explaining the aging process; however, most of these theories eventually come to the same conclusion: Aging is a process of accumulated damage to our genetic blueprint, our DNA. If the DNA in one of your cells was to unwind completely, it would stretch over one metre in length. However, it is tightly fitted into compact units–DNA packages–called chromosomes.

Over the last few years, longevity researchers have focused their attention on the caps at the ends of these chromosomes, called telomeres. Every time our cells divide, the telomere gets a little shorter until cellular division comes to a halt. Once a cell has run its full potential of cellular divisions, it is referred to as a senescent (old) cell.

In the aging process, the body becomes increasingly unable to repair accumulated cell damage. Cellular senescence may be one of the key causes of aging, with telomere damage leading the way. Research presented in the Journal of the American Geriatric Society (August 2001) indicated that telomere shortening is directly associated with accumulated DNA damage and cellular aging.

According to Dr. Judith Campisi, a pioneer in the field of cell aging, senescent cells don’t die once they stop dividing, but instead continue to emit harmful proteins to neighbouring cells, eventually leading to their malfunction. Research presented in the Journal of Experimental Gerontology (November 2001) showed that cells with dysfunctional telomeres could contribute to cancer and aging, as telomeres are essential for maintaining the integrity and stability of our genes.

It is widely known that as we age, we often become more insulin resistant. This condition and accumulated body fat can also predispose people to cardiovascular disease and a shorter lifespan. The mechanisms behind this have not been well understood–perhaps until now. Research published in the journal Circulation (May 2005), showed that increased insulin resistance along with a higher body fat content results in greater telomere shortening over time. This study is the first to show tangible evidence that insulin resistance and excess body fat lead to premature aging.

A Little Help Along the Way

Aside from the usual healthy weight-loss advice–follow a sensible low-glycemic diet, exercise, get plenty of sleep–supplementing with a natural compound called carnosine (beta-alanylhistamine) has shown promise when it comes to the health of your telomeres. Research in 2004 from the Chinese Academy of Sciences showed that when carnosine was added to a human cell culture, the cells showed much slower telomere shortening and a greatly extended lifespan. Daily suggested dosages for carnosine are 50 to 250 mg/day.

About the Author

Brad J. King, MS, MFS, is a nutritional researcher and author of five books, including the international best-seller Fat Wars (Wiley, 2004). Subscribe to his free monthly newsletter at fatwars.com.