I’ve been reading the new book by Michael Fossel, The Telomerase Revolution: The Enzyme That Holds the Key to Human Aging and Will Soon Lead to Longer, Healthier Lives. I think anyone who finds the material on this site to be of interest will find the book an enlightening, enjoyable read.
Fossel’s thesis in the book is that telomeres are the ultimate cause of aging. Telomeres are caps on the ends of chromosomes, and with each cell replication, the caps become shorter. Once the telomeres become short enough, all kinds of cellular malfunction occurs, and ultimately the cell becomes senescent. Since all aging and the diseases associated with it are ultimately caused at the cellular level, shortening of telomeres provides a mechanism for the phenomenon of aging.
Aging is associated with the accumulation of cellular damage. When we’re young, the constituents of our cells turn over at a high rate; essentially, the constituents — proteins, lipids, organelles – are broken down and replaced often. As we age, this process slows, allowing for the accumulation of damaged cell parts, and they don’t function as well. Fossel ascribes this to shortened telomeres leading to changes in gene expression, in turn leading to lower turnover of cell constituents.
Several companies are at work researching how to lengthen telomeres. One product (that I’m aware of) has been developed: TA-65, an expensive supplement that activates telomerase, the telomere-lengthening enzyme. (For what it’s worth, many of the Amazon reviewers say it works well. I’m tempted to try it.)
Meanwhile, what can you do to keep telomeres from shortening at a faster rate than normal?
For starters — and maybe the most important thing — keep iron levels low.
While users of multivitamin supplements had about a 5% longer telomere length than non-users, those who took iron supplements had 9% shorter telomeres.(3)
People with iron overload also have shorter telomeres.(4)
Excess iron, and in fact, probably any level of iron, also causes DNA damage. Since telomeres are made of the same bases as DNA, damage to DNA not can cause cancer or other diseases of aging, but directly promote aging itself.
It’s been shown that body iron stores are highly correlated to the amount of DNA damage.(5) See the chart below, taken from the paper that found this result. Urinary 8-OHdG is a measure of DNA damage.
Of more than passing interest in this paper, the subjects were divided into tertiles (thirds) of ferritin levels. Among fertile women, the lowest tertile was a ferritin of <17, the highest >36; among men, the lowest tertile repesented those with a ferritin of <98, the highest >180. This shows the much greater levels of iron that men normally have, and is connected to their higher rates of disease and earlier death than women.
So, for now, it looks like the best thing to keep telomeres longer is to keep iron low. We already know that iron is a strong driver of aging, and shortening of telomeres could be the proximate cause.
Of interest, if the way that telomere shortening causes aging is through decreased turnover of cellular constituents, speeding up the turnover to more youthful levels may counteract this effect. The best way to do that is through intermittent fasting, which promotes autophagy, the cellular self-cleansing process, and speeds turnover of damaged cellular constituents.