Statins may slow human aging by protecting against telomere shortening: A feature of senescent cells

Posted By News On August 29, 2013 - 3:30pm

Bethesda, MD—Not only do statins extend lives by lowering cholesterol levels and reducing the risks of cardiovascular disease, but new research in the September 2013 issue of The FASEB Journal 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," said Giuseppe Paolisso, M.D., Ph.D., a researcher involved in the work from the Department of Internal Medicine, Surgical, Neurological Metabolic Disease and Geriatric Medicine at Second University of Naples in Naples, Italy.

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," said Gerald Weissmann, M.D., Editor-in-Chief of The FASEB Journal. "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."

This is fascinating research. However, statins are not slowing telomere shortening as a result of telomerase activation. They are doing so via some as-of-yet unknown mechanism. This is because it has already been shown that telomerase activation by itself can lengthen critically short telomeres but does nothing to slow down the long-term shortening of average telomeres (see http://www.terraternal.com/Products/ProductDetails/cx/TA-65/645/182.aspx and http://www.terraternal.com/Products/ProductDetails/cx/Telomere-Guard/616/155.aspx). This is primarily related to the dynamics of telomerase access as mediated by the 'shelterin' complex. Statins appear to have made a critical breakthrough in this area and sound very promising.

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