Archive for August, 2009

29 AugTA-65 in Scientific American

Telomerase Activation Sciences, Inc.
Dear T.A. Sciences Friend,

As a member of our mailing list you have received updates over the past two years about the world of telomerase activation.  We wanted to be sure that you saw this current article below from Scientific American.  It is further validation of the work we do and the exciting promise of telomerase activation.  Feel free to email or call us anytime with your questions about TA-65.

Thanks for your interest in lengthening our Healthspans.
The T.A. Sciences Team!

SCIENTIFIC AMERICAN

News -  August 17, 2009
Anti-Aging Pill Targets Telomeres at the Ends of Chromosomes
Could the secrets to anti-aging be at the tips of our chromosomes?
By Mandy Kendrick

Peter Pan stayed forever young in Neverland. In real life, some scientists are looking at telomeres, or regions of repetitive DNA at the ends of our chromosomes, to try to arrive at something like a real version of this story.

Telomeres consist of up to 3,300 repeats of the DNA sequence TTAGGG. They protect chromosome ends from being mistaken for broken pieces of DNA that would otherwise be fixed by cellular repair machinery. But every time our cells divide, the telomeres shrink. When they get short enough, our cells no longer divide and our body stops making those cells. Over time, this leads to aging and death.

New York-based T.A. Sciences claims to be the only company in the world manufacturing a supplement in a pill form that has been lab tested and shown to stop telomeres from shortening, in hopes of halting the aging process. The product, TA-65, comes from extracts of the Chinese herb astragalus, which has been used for medicinal purposes for more than 1,000 years, says Noel Patton,chief executive officer of the company.

TA-65 is produced at very low levels in the astragalus plant, but the company purifies and concentrates the substance, which is thought to “turn on” the enzyme telomerase (hTERT) that acts to maintain or lengthen telomeres. hTERT is usually “off” in adult cells, except in immune, egg and sperm cells, and in malignant cancer-forming cells.

The TA-65 pill requires no approval from the U.S. Food and Drug Administration because it is marketed as a supplement and not a drug. Therefore, T.A. Sciences cannot make claims about the drug’s efficacy at curing disease. But Patton and Calvin Harley, the chief scientific officer at Geron-the company that discovered TA-65-go on to note that researchers have found a correlation between telomere length and susceptibility to certain aging-related diseases.

T.A. Sciences did five years of testing on TA-65, beginning in 2002.  Results from an anti-aging trial can be found at the company’s Web site. Patton says he has been taking the supplement for two years and that everyone at T.A. Sciences over the age of 40 takes the product.

William Andrews has worked on telomere biology for the past 15 years.  He is the chief executive officer of Sierra Sciences, LLC, a rival company that is screening for chemicals to activate telomerase, but also a T.A. Sciences client for the past two-and-a-half years. He thinks that “taking a telomerase inducer is safer than driving my car to work” but acknowledges that there are some unknown risks with taking the product.
For example, telomerase is the same enzyme that allows cancer cells to stop aging or to become immortal, so there is a chance that TA-65 could keep alive cancer cells that would otherwise die, notes Andrews.

However, telomerase activation should keep all telomeres longer in the first place, and that actually reduces the chances of cells becoming cancerous, Andrews notes. He also says that the enzyme should keep immune cells, which can fight off most cancerous cells, alive longer.

Another problem facing telomere science is that no suitable model organism is available for testing. Animals do not age through telomere shortening in the same way that humans do, Harley notes, adding that “not even mice or monkeys have the same telomere aging system. The best system to ultimately test is going to be the human.”

The potential benefits of the supplement seem to outweigh the risk for patients like Andrews. “People such as myself who elect to take TA-65 and look forward to taking even stronger telomerase inducers in the future must act totally on gut feelings,” Andrews notes.

For those who are less adventurous, other researchers have identified lifestyle changes that can help optimize telomerase activity, without the $14,000-per-year price tag of the TA-65 treatment.

08 AugWhy hair turns gray

(Adapted from a posting by Edyta Zielinska on GernTalk, dated 11th June 2009:)

“Researchers have identified the mechanism for why hair goes gray with age and stress in the June 12, 2009 issue of Cell.

It’s generally thought that accumulated DNA damage is a likely culprit in aging phenotypes such as graying hair, but researchers have been unable to show a direct link, said David Fisher chairman of the department of dermatology at the Massachusetts General Hospital, who was not involved in the study. “Hair follicles are very deep,” said Fisher, so it’s unlikely that DNA damage would be caused by UV radiation from sunlight, for example.”


In order to understand the process involved in graying hair, scientists used radiation and other chemical inducers of DNA damage on pigment stem cells called melanocyte stem cells in mice. DNA damage resulted in premature graying in mice.

Dr. Park’s comment: As in every organ, the  main reason for DNA damage is telomere shortening, allowing the genetic code to be corrupted when the chromosomal ends are unprotected.

DNA damage normally causes two outcomes — cell death or shut down.  Scientist showed that induced DNA damage can also elicit a third pathway – forcing stem cells into terminal differentiation. As a result, stem cells lost their ability to replenish pigmented cells.

Dr. Park again: The source article goes on to evoke a teleological hand-waving that is sadly typical in science. They suggest that the “third pathway” of differentiation represents the body’s effort to “protect” itself from cancer.  In my opinion, evolution would never have allowed people to take advantage of such an “intelligent design” because humans never evolved in conditions where they could even survive long enough to exhibit cancer.

Loss of differentiation is, ex post facto, a good thing but is merely the unintended result of knocking out the established programming that was allowing appropriate, “asymmetric division,” or the production of a perfect master copy and a more differentiated cell.  That asymmetric division, along with immortalization, are the two hallmarks of  “stemness.”

The bottom line: cellualar dysfunction is caused by genetic aging caused by insufficient telomerase activation and its saltatory protection of your genetic code.
What is frightening is that even one end, of one chromosome, in one immortal stem cell, can spell disaster because of the unlimited reproduction of that defective stem cell’s faults.

To learn more about stem cells and their role in aging, visit our website at RechargeBiomedical.com.