Statin Use Correlates With Higher Telomerase Activity

There has been interest in extending increasing telomerase expression as a means to slow aging for some years. The available tools other than gene therapy are sparse on the ground, however. Telomerase extends telomere length, the caps of repeating DNA sequences at the ends of chromosomes that shorten with each cell division. Telomerase may have other roles that more directly impact aging, however, such as an influence on mitochondrial function.

Shorter telomeres in at least some tissues correlate with stress and ill health and aging, but this is a very dynamic system - average telomere length can change in either direction on a short time scale. It is far from clear that progressively shorter telomere length is a cause of aging rather than just a reflection of other changes and damage, and the same goes for natural variations in levels of telomerase in the body. While increasing expression of telomerase is shown to extend life in mice, that may or may not have anything to do with telomere length, and mouse telomerase biology is quite different from that of humans.

So all this said, it was only a matter of time before researchers evaluated all the existing approved drugs for treatment of age-related conditions to see if any of them altered telomerase activity. There are regulatory incentives to beware of here, however, in that it is much cheaper for research institutions to try to find marginal new uses of already approved drugs than to work on new and radically better medical technologies that would then have to go through the exceedingly and unnecessarily expensive approval process. So don't expect anything of great practical use to result from this:

Not only do statins extend lives by lowering cholesterol levels and reducing the risks of cardiovascular disease, but new research [suggests] that they may extend lifespans as well. Specifically, statins may reduce the rate at which telomeres shorten, a key factor in the natural aging process. This opens the door for using statins, or derivatives of statins, as an anti-aging therapy. "By telomerase activation, statins may represent a new molecular switch able to slow down senescent cells in our tissues and be able to lead healthy lifespan extension."

To make this discovery, Paolisso and colleagues worked with two groups of subjects. The first group was under chronic statin therapy, and the second group (control), did not use statins. When researchers measured telomerase activity in both groups, those undergoing statin treatment had higher telomerase activity in their white blood cells, which was associated with lower telomeres shortening along with aging as compared to the control group. This strongly highlights the role of telomerase activation in preventing the excessive accumulation of short telomeres.

"The great thing about statins is that they reduce risks for cardiovascular disease significantly and are generally safe for most people. The bad thing is that statins do have side effects, like muscle injury. But if it is confirmed that statins might actually slow aging itself - and not just the symptoms of aging - then statins are much more powerful drugs than we ever thought."

Link: http://www.eurekalert.org/pub_releases/2013-08/foas-sms082913.php

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