Comments on: Age-Reversing Drugs on the Horizon? Not So Fast. http://blogs.discovermagazine.com/80beats/2010/11/29/age-reversing-drugs-on-the-horizon-not-so-fast/ Mon, 22 Apr 2013 21:34:00 +0000 hourly 1 http://wordpress.org/?v=3.4.2 By: jeffrey dach md http://blogs.discovermagazine.com/80beats/2010/11/29/age-reversing-drugs-on-the-horizon-not-so-fast/#comment-23830 jeffrey dach md Wed, 08 Dec 2010 13:04:33 +0000 http://blogs.discovermagazine.com/80beats/?p=23196#comment-23830 There is really no need for genetic engineerin­g to activate telomerase as was done in the Depinho mouse model. There is about 20 years of research on Telomere activation­. There are two receptors for estrogen on the TERT gene which controls this process. Whether you happen to be a human being or a mouse, the best way to increase telomerase activity, lengthen the telomeres and reverse aging is with the human bioidentic­­al hormone, 17-Beta-Es­­tradiol, also known as estrogen. In 1999, Kyo demonstrat­­ed that 17-Beta-Es­­tradiol activates telomerase via direct and indirect effects on the hTERT promoter region. This was confirmed in 2000 by Silvia Misiti and again in 2009 by Rodrigo T. Calado from the NIH. A recent December 2010 study from Imanishi from Japan showed that 17-Beta-Es­­tradiol (estrogen) augments telomerase activity, thereby accelerati­­ng recovery after injury and reducing the effects of aging (reducing senescence­­). Natural substances such as resveratrol, gingko and silymarin also activate telomeres. For more see: http://jeffreydach.com/2010/12/03/anti-aging-breakthrough-with-telomerase-knockout-mice-by-jeffrey-dach-md.aspx regards, jeffrey dach md There is really no need for genetic engineerin­g to activate telomerase as was done in the Depinho mouse model. There is about 20 years of research on Telomere activation­. There are two receptors for estrogen on the TERT gene which controls this process. Whether you happen to be a human being or a mouse, the best way to increase telomerase activity, lengthen the telomeres and reverse aging is with the human bioidentic­­al hormone, 17-Beta-Es­­tradiol, also known as estrogen. In 1999, Kyo demonstrat­­ed that 17-Beta-Es­­tradiol activates telomerase via direct and indirect effects on the hTERT promoter region. This was confirmed in 2000 by Silvia Misiti and again in 2009 by Rodrigo T. Calado from the NIH.

A recent December 2010 study from Imanishi from Japan showed that 17-Beta-Es­­tradiol (estrogen) augments telomerase activity, thereby accelerati­­ng recovery after injury and reducing the effects of aging (reducing senescence­­).

Natural substances such as resveratrol, gingko and silymarin also activate telomeres.

For more see:

http://jeffreydach.com/2010/12/03/anti-aging-breakthrough-with-telomerase-knockout-mice-by-jeffrey-dach-md.aspx

regards, jeffrey dach md

]]> By: Andrew Straw http://blogs.discovermagazine.com/80beats/2010/11/29/age-reversing-drugs-on-the-horizon-not-so-fast/#comment-23829 Andrew Straw Thu, 02 Dec 2010 01:32:10 +0000 http://blogs.discovermagazine.com/80beats/?p=23196#comment-23829 Calvin B Harley, Geron Corporation: Unfortunately, the strong link between telomerase and cancer has led some to confuse telomerase activation with cancer, and others to overstate the cancer risk of telomerase activation therapies for degenerative diseases. This review clarifies the difference between telomerase, which does not cause growth deregulation, and oncogenes, which do. It also addresses the concept of telomerase repression as a tumor suppressor mechanism early in life, with detrimental tissue degeneration and tumor-promoting consequences late in life. This extended view of the telomere hypothesis helps explain how telomerase inhibition can be therapeutic in cancer patients, while controlled telomerase activation for degenerative diseases may actually reduce, rather than increase, the frequency of age-related tumorigenesis. ============= Calvin B Harley, Geron Corporation:
Unfortunately, the strong link between telomerase and cancer has led some to confuse telomerase activation with cancer, and others to overstate the cancer risk of telomerase activation therapies for degenerative diseases. This review clarifies the difference between telomerase, which does not cause growth deregulation, and oncogenes, which do. It also addresses the concept of telomerase repression as a tumor suppressor mechanism early in life, with detrimental tissue degeneration and tumor-promoting consequences late in life. This extended view of the telomere hypothesis helps explain how telomerase inhibition can be therapeutic in cancer patients, while controlled telomerase activation for degenerative diseases may actually reduce, rather than increase, the frequency of age-related tumorigenesis.
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