Protecting your genetic “Hard Drive”

February 7th, 2010

“If your genome was like a computer hard drive…”

DNA code is a sequence of chemicals that encode all the data you need to build and operate a human and it is written with only 4 DNA digits. It is a digital code but it is not binary like computers, but quaternary with 4 distinct items. The encoding information in an ordered sequence of 4 different symbols called “bases”, typically denoted A, C, G, and T.

* A: adenosine
* C: cytosine
* G: guanine
* T: thymine

These 4 substances are the fundamental “bits” of information in the genetic code, and are called “base pairs” because there are actually 2 substances per “bit.”

The entirety of human DNA code, called the “human genome”, runs about 3 billion bases in total. Every human being has 2 copies of this code, one copy from each parent, so a human’s cell DNA contains a total of around 6 billion bases. In computer terms, this is around 6 Gigabytes of symbols per cell that need to be copied and distributed to each daughter cell in a process of cell division or “mitosis”

mitosis_500

Luckily, both computer drives and DNA copying have very efficient error detection and correction mechanisms. The most important error corrector for biological data is the p53 enzyme, which will be featured in the future post, “All along the watchtower”

But unlike computers, there is a single critical step in every cell division in which 23 double pairs of chromosomes are simultaneously pulled apart to impart 23 single pairs for each of the two new cells.  This occurs in the miraculous kinetechore:

Kinetochore_428w

Think of this as a huge Virginia Reel of chromosomes but with pairs of siamese twins instead of men and women.  That way, it doesn’t matter which chromosome goes to which daughter cell. This dance party happens 50 billion times a day in your body.

Unfortunately, DNA sequences, like Scarlet and Rhett, can be attracted to complimentary DNA strands even if they are not supposed to be paired with them. If they don’t follow the music or “dance with the ones that brung ‘em” you can get an improper number if chromosomes or new and abnormal fused chromosomes.

But even without taking into consideration the crash-prone event of the kinetochore “mosh pit ,” consider that there are 50 billion cell divisions x 6 billion base pairs copied per cell division every day. This means there are 300 quintillion chances for errors every day. That’s 300,000,000,000,000,000,000 chances to make a mistake every day.  Wow.

That makes me feel lucky to have woken up this morning.

You should feel even more fortunate because for the first time in history, you can protect your genetic code, like I have, by lengthening the telomeres with TA-65.  Visit RechargeBiomedical.com and schedule a consultation soon. Don’t wait for your genetic hard drive to crash. Be proactive.

Good health to all,

Dr. Ed Park

(adapted  from “Introduction to Genes and DNA”)

P.S.:  Please check your inbox each Sunday for a new post. Here are some of the upcoming posts:

  • “Telomerase is like an old-school Dymo labeler”
  • “If you are what you eat, where are all the smart zombies?”
  • “Taking antioxidants is worse than useless”
  • “Vitamins that can kill you- ADEK that’s stacked”
  • “Premature aging syndromes – what’s the common denominator?”
  • “9,500 year old trees”
  • “G.U.T check.: A Grand Unified Theory of Aging”
  • “AIDS is AGING and vice versa”
  • “Family history, cancer risk, and other flat-earth theories”
  • “Fourth and longer – lengthen your chromosomes to make it to overtime”
  • “The Age of Aquarius and the End of Time – Hippies and Mayans and why we’ve got to get ourselves back to the garden
  • “Cancer Stem Cells- a new paradigm”
  • “You are already a cancer survivor, many times over!”
  • “Telomerase activation and Cancer (these amps go to eleven…)”
  • “The Philadelphia Experiment – what REALLY causes cancer”
  • “p53 – All along the watchtower”
  • “Roseanne Rosannadanna and the truth about life insurance”

Exercise is associated with longer telomeres

February 1st, 2010

Everyone knows exercise keeps you younger.
Telomere shortening causes aging.

Now even the “Grey Lady” is interested in dying her metaphorical hair!

http://well.blogs.nytimes.com/2010/01/27/phys-ed-how-exercising-keeps-your-cells-young/?emc=eta1

Unfortunately, this isn’t exactly “breaking news.”  But at least the NYT blog is ahead of 99% of medical doctors, who don’t even know what the heck 2009’s Nobel Prize in Medicine was for.  Can you imagine 99% of Economists or Physicists not having any clue about what their Nobel Prize was for?

I even heard a line about telomere shortening and stress in a Kate Winslet Romantic comedy, “The Holiday.”  (A great movie, BTW)

Here is a quick smattering of the many articles linking exercise and telomere shortening:

1. Skeletal muscle telomere length in healthy, experienced, endurance runners.
Rae DE, Vignaud A, Butler-Browne GS, Thornell LE, Sinclair-Smith C, Derman EW, Lambert MI, Collins M.
Eur J Appl Physiol. 2010 Jan 26. [Epub ahead of print]PMID: 20101406 [PubMed - as supplied by publisher]Related articles

2. Leukocyte telomere length is preserved with aging in endurance exercise-trained adults and related to maximal aerobic capacity.Larocca TJ, Seals DR, Pierce GL.
Mech Ageing Dev. 2010 Jan 11. [Epub ahead of print]PMID: 20064545 [PubMed - as supplied by publisher]Related articles

3. Coupling Aging Immunity with a Sedentary Lifestyle: Has the Damage Already Been Done? – A Mini-Review.
Simpson RJ, Guy K.
Gerontology. 2009 Dec 19. [Epub ahead of print]PMID: 20029165 [PubMed - as supplied by publisher]Related articles

4. The biology of satellite cells and telomeres in human skeletal muscle: effects of aging and physical activity.

Kadi F, Ponsot E.
Scand J Med Sci Sports. 2009 Sep 17. [Epub ahead of print]PMID: 19765243 [PubMed - as supplied by publisher]Related articles

5. The association between leukocyte telomere length and cigarette smoking, dietary and physical variables, and risk of prostate cancer.
Mirabello L, Huang WY, Wong JY, Chatterjee N, Reding D, Crawford ED, De Vivo I, Hayes RB, Savage SA.
Aging Cell. 2009 Aug;8(4):405-13. Epub 2009 Jun 1.PMID: 19493248 [PubMed -


6. Relationship between physical activity level, telomere length, and telomerase activity.
Ludlow AT, Zimmerman JB, Witkowski S, Hearn JW, Hatfield BD, Roth SM.
Med Sci Sports Exerc. 2008 Oct;40(10):1764-71.PMID: 18799986 [PubMed - indexed for MEDLINE]Related articlesFree article

7. Inreased telomerase activity and comprehensive lifestyle changes: a pilot study.
Ornish D, Lin J, Daubenmier J, Weidner G, Epel E, Kemp C, Magbanua MJ, Marlin R, Yglecias L, Carroll PR, Blackburn EH.
Lancet Oncol. 2008 Nov;9(11):1048-57. Epub 2008 Sep 15. Erratum in: Lancet Oncol. 2008 Dec;9(12):1124. PMID: 18799354 [PubMed - indexed for MEDLINE]Related articles

8. Effects of physical exercise on myocardial telomere-regulating proteins, survival pathways, and apoptosis.
Werner C, Hanhoun M, Widmann T, Kazakov A, Semenov A, Pöss J, Bauersachs J, Thum T, Pfreundschuh M, Müller P, Haendeler J, Böhm M, Laufs U.
J Am Coll Cardiol. 2008 Aug 5;52(6):470-82.PMID: 18672169 [PubMed - indexed for MEDLINE]Related articles

9. Increased abdominal obesity, adverse psychosocial factors and shorter telomere length in subjects reporting early ageing; the MONICA Northern Sweden Study.
Nordfjäll K, Eliasson M, Stegmayr B, Lundin S, Roos G, Nilsson PM.
Scand J Public Health. 2008 Sep;36(7):744-52. Epub 2008 Jul 22.PMID: 18647789 [PubMed - indexed for MEDLINE]Related articles

Telomere shortening causes aging

January 31st, 2010

Telomere shortening causes aging!

I can make this statement but how do you objectively establish causation versus association?  In epidemiology, we use the NINE BRADFORD-HILL criteria, which represent common sense rules of logic.   The more of the criteria you have, the more likely something is actually CAUSING something else and not just associated.

  1. STRENGTH
  2. CONSISTENCY
  3. SPECIFICITY
  4. TEMPORALITY
  5. GRADIENT
  6. PLAUSABILITY
  7. COHERENCE
  8. EXPERIMENTAL EVIDENCE
  9. ANALOGY

Anyone can come up with a theory.  Here are some popular ones: the sun travels around the earth, gods roll dice to decide our destinies, evil spirits can cause madness.

By using the Nine Bradford-Hill criteria, we can assess causation for just about anything. Let’s say I have a theory that “having four wheels on a vehicle causes lethal motor vehicle accidents.” After all, almost all of the lethal MVA’s are associated with four-wheel vehicles. Intuition tells us this is association and not causation but let’s go through the process to show you how the criteria work:

STRENGTH –  good.  Most accidents involve cars with four wheels.
CONSISTENCY – again good, given most MVA’s involve passenger cars
SPECIFICITY    - poor.  Motorcycles and 18-wheelers are more lethal than four wheel accidents.
TEMPORALITY: fair. You usually need four-wheels to get into an MVA
GRADIENT: poor in either direction.  Fewer wheels (Motorcycles) and more wheels (trucks) are more lethal.
PLAUSABILITY: poor. Why would four wheels do this?
COHERENCE: poor. Why would four wheels do this?
EXPERIMENTAL EVIDENCE: poor.  NTSB tests have not been done comparing four wheels with two wheels because the outcome is obvious. Just ask any ER physician.
ANALOGY: poor.  Who is more nimble, you or your dog or cat? Four legs, like four wheels is a good foundation.

What about the theory that telomere shortening causing aging?

STRENGTH – excellent. The older you are, the shorter your telomeres. The fastest shortening comes with premature aging syndromes (Progerias)

CONSISTENCY – excellent. All humans age and all humans show telomere shortening as they age.

SPECIFICITY – excellent. Shortening telomeres is a hallmark of all the Progerias

TEMPORALITY- good.  Shortening telomeres occurs before aging appears

GRADIENT – excellent.  The older you get, the shorter they get

PLAUSABILITY – excellent.  Loss of protection of the ends of chromosomes allows for DNA rearrangement

COHERENCE – excellent. Loss of protection of the ends of chromosomes allows for DNA rearrangement and subsequent disease

EXPERIMENTAL EVIDENCE – Nature has done these experiments in the form of the Progerias which involve DNA repair deficiencies. See: http://en.wikipedia.org/wiki/Dyskeratosis_congenita

ANALOGY: excellent.  Telomeres protect the tips like aglets on shoelaces.  Another analogy is that aging chromosomes are like candles burning on both ends.

And what about the theory that Resveratrol is good for your health?
Surprisingly, it only fulfills one of the criteria, weakly:

A few experiments have shown that Resveratrol extends the life of fruit flies, nematode worms, and short-lived fish, possibly because of its toxicity. There has been A LOT of good scientific study of Resveratrol in humans it but all show negative results.  Resveratrol is simply a “cure in search of a disease.” Yet Americans spend millions taking it because people like red wine and because we trust Oprah and Dr. Oz.

So if telomere shortening causes aging in humans, what can we do to slow it?  The good news is that your body has always done it by activating telomerase in its stem cells.  In fact, all plants and animals above bacteria require telomerase to protect their chromosomes.  The better news is that we now have a safe nutraceutical called TA-65 that safely enhances your own natural telomerase anti-aging mechanism.

To learn more about the role of shortening telomeres in aging read about our Dr. Park’s  theory of aging:
http://www.rechargebiomedical.com/aging.html

Also, if my New Year’s resolution holds firm, please expect a new blog posting from me every Sunday afternoon.

Upcoming topics include (in no particular order and with working titles):

  • “Telomerase is like an old-school Dymo labeler”
  • “If you are what you eat, where are all the smart zombies?”
  • “Taking antioxidants is worse than useless”
  • “Vitamins that can kill you- ADEK that’s stacked”
  • “Premature aging syndromes – what’s the common denominator?”
  • “9,500 year old trees”
  • “G.U.T check.: A Grand Unified Theory of Aging”
  • “If your genome was like a computer hard drive…”
  • “AIDS is AGING and vice versa”
  • “Family history, cancer risk, and other flat-earth theories”
  • “Fourth and longer – lengthen your chromosomes to make it to overtime”
  • “The Age of Aquarius and the End of Time – Hippies and Mayans and why we’ve got to get ourselves back to the garden
  • “Cancer Stem Cells- a new paradigm”
  • “You are already a cancer survivor, many times over!”
  • “Telomerase activation and Cancer (these amps go to eleven…)”
  • “The Philadelphia Experiment – what REALLY causes cancer”
  • “p53 – All along the watchtower”
  • “Roseanne Rosannadanna and the truth about life insurance”

“Nobel, Schnobel, where did the Dow close?”

December 8th, 2009

Congratulations to the winners of the 2009 Nobel prizes:

  • Economics: Elinor Ostrom (governance of the commons) &   Oliver Williamson (corporate governance)
  • Peace:          Barack Obama (for international diplomacy)
  • Literature:    Herta Muller (Poetry of the dispossessed)
  • Chemistry:   Ramakrishnan, Steitz, Yonath (Ribosomes)
  • Physics:       Charles Kao (Fiberoptic communication) &  Willard Boyle and George Smith (the CCD imaging sensor)
  • Medicine:    Greider, Blackburn, Szostak (the discovery of telomerase)

I find it notable that from the six categories,  an average person with a college degree would have some idea of what the first five prizes were awarded for.

But the prize in Medicine was for the discovery of something unknown to 99% of its own expert practitioners.

Why? Is telomerase biology an obscure backwater of the field?  Hardly. A simple PubMed literature search brings up 16,385 citations for “telomere or telomerase”

A search of telomere + (other search words) yields these results:

  • +Arthritis:                             56
  • +Atherosclerosis:                  90
  • +Neurological Disease:        644
  • +Aging:                            1,375
  • +Cancer:                          3,590

Someday, clinical physicians may have heard of a telomere, even though most all diseases they treat may be causally related to failures of protecting the tips of chromosomes.

With every day that passes, you will get older, but your doctor won’t get any wiser to telomere biology.  Even a Nobel Prize in their chosen profession isn’t enough for 99% of them to “Wikipedia it”  or take their eyes off of Health Care Reform or CNBC.

So maybe it’s time you did your own due diligence about what causes illness and aging?  It is a lot simpler than exercise, diet, and anti-oxidants.  It’s all about the telomeres.

To take the first step towards a longer and healthier life, go to www.rechargebiomedical.com/aging.html

Postscipt: Before you dismiss this newsletter, consider that telomerase is THE essential enzyme that protects the tips of DNA in all plants and animals.  That’s EVERY SINGLE CHROMOSOME in every single plant and animal!  That seems like a pretty significant discovery well worthy of a Nobel Prize.  After all,  Seven Billion other people were in the running for the Nobel Peace Prize just by virtue of not being George Bush ;-)

Telomeres are longer in healthier, older people

November 20th, 2009
Hello subscribers, I’m passing along this press release from TA Sciences. It is more evidence that telomeres are a critical factor in staying young and healthy.

This study shows that people “who have lived to a very old age have inherited mutant genes that make their telomerase-making system extra active.” For those of us who have not inherited such genes, TA-65 is the only known product that can activate telomerase.

“Longevity Tied to Genes That Preserve Tips of Chromosomes
November 11, 2009; Bronx, NY ­ A team led by researchers at Albert Einstein College of Medicine of Yeshiva University has found a clear link between living to 100 and inheriting a hyperactive version of an enzyme that rebuilds telomeres -­ the tip ends of chromosomes. The findings appear in the latest issue of the Proceedings of the National Academy of Sciences. Yousin Suh, Ph.D.

Telomeres play crucial roles in aging, cancer and other biological processes. Their importance was recognized last month, when three scientists were awarded the 2009 Nobel Prize in Physiology and Medicine for determining the structure of telomeres and discovering how they protect chromosomes from degrading.

Telomeres are relatively short sections of specialized DNA that sit at the ends of all chromosomes. One of the Nobel Prize winners, Elizabeth Blackburn, Ph.D., of the University of California at San Francisco, has compared telomeres to the plastic tips at the ends of shoelaces that prevent the laces from unraveling. Each time a cell divides, its telomeres erode slightly and become progressively shorter with each cell division. Eventually, telomeres become so short that their host cells stop dividing and lapse into a condition called cell senescence. As a result, vital tissues and important organs begin to fail and the classical signs of aging ensue.

In investigating the role of telomeres in aging, the Einstein researchers studied Ashkenazi Jews because they are a homogeneous population that was already well studied genetically. Three groups were enrolled:  86 very old ­ but generally healthy people (average age 97); 175 of their offspring; and 93 controls (offspring of parents who had lived a normal lifespan). Gil Atzmon, Ph.D. “Telomeres are one piece of the puzzle that accounts for why some people can live so long,” says Gil Atzmon, Ph.D., Assistant Professor of Medicine and of Genetics at Einstein, Genetic Core Leader for The LonGevity Project at Einstein’s Institute for Aging Research, and a lead author of the paper. “Our research was meant to answer two questions: Do people who live long lives tend to have long telomeres? And if so, could variations in their genes that code for telomerase account for their long telomeres?”
The answer to both questions was “yes.”

“As we suspected, humans of exceptional longevity are better able to maintain the length of their telomeres,” said Yousin Suh, Ph.D., associate professor of medicine and of genetics at Einstein and senior author of the paper. “And we found that they owe their longevity, at least in part, to advantageous variants of genes involved in telomere maintenance.”
More specifically, the researchers found that participants who have lived to a very old age have inherited mutant genes that make their telomerase-making system extra active and able to maintain telomere length more effectively. For the most part, these people were spared age-related diseases such as cardiovascular disease and diabetes, which cause most deaths among elderly people.

“Telomeres are one piece of the puzzle that accounts for why some people can live so long.” Gil Atzmon,  Ph.D.

“Our findings suggest that telomere length and variants of telomerase genes combine to help people live very long lives, perhaps by protecting them from the diseases of old age,” says Dr. Suh. “We’re now trying to understand the mechanism by which these genetic variants of telomerase maintain telomere length in centenarians. Ultimately, it may be possible to develop drugs that mimic the telomerase that our centenarians have been blessed with.”

The study, “Genetic Variation in Human Telomerase is Associated with Telomere Length in Ashkenazi Centenarians,” appears in the November 9th on-line issue of the Proceedings of the National Academy of Sciences. In addition to Drs. Atzmon and Suh, the study’s other Einstein researchers were co-lead author Miook Cho, M.S., Temuri Budagov, M.S., Micol Katz, M.D., Xiaoman Yang, M.D., Glenn Siegel, M.D., Aviv Bergman, Ph.D., Derek M. Huffman, Ph.D., Clyde B. Schechter, M.D., and Nir Barzilai, M.D.

Maximum Lifespan- The Graphic Novel

November 3rd, 2009

After over three years, we’re proud to announce that the E-Book publication of Maximum Lifespan is ready for download!

Ken Garrett, a dying scientist, lures his estranged son home by revealing that his mother was never really dead, but in hiding. Dr. Garrett will gamble with his children, his own body, and the future of the human race to achieve immortality.

An original, full-color, 185 page graphic novel in the style of Philip K. Dick (Blade Runner, Total Recall) or Alejandro Amenábar (Vanilla Sky, The Sea Inside, Agora)

Please see our Graphic Novel trailer and download the first 53 pages, which is yours to read and share widely with friends.

Maximum Lifespan

Maximum Lifespan

Hard data that TA-65 works!

September 23rd, 2009

Although I’ve been taking TA-65 for two years, this pdf ( 6mos_telomeres ) that is attached shows the 6 month results from my first three Patton Protocol clients. Everyone feels great and the gains are nothing short of a home run.

If you can, please join us for tomorrow’s TA-65 webinar at 4pm PST (7pm EST):

“FROM TA Sciences- For IMMEDIATE RELEASE:

We’ll have Bill Andrews, PhD, co-discoverer of the hTERT telomerase gene, delivering a powerful presentation on Telomere Biology as it applies to your patients through the use of TA-65. We’ll also have an important discussion about “Resveratrol versus TA-65.”

There will also be docs on board for this webinar who are taking TA-65 themselves as well as using it in their practice. There will be ample opportunity for Q&A.

Plan to listen and/or participate in the webinar Thursday the 24th, from 7-9 PM (4PM PST)  by going to http://tasciences.com/live”

Thursday, Sept. 24, 4:00pm (Pacific) or 7PM (Eastern Standard): Telomere Talk

September 16th, 2009

FROM TA Sciences- For IMMEDIATE RELEASE:

“Telomere Biology is rapidly advancing our ability to live longer and better. The discovery of TA-65, a safe-for-human- consumption Telomerase Activator has opened a new door– a new paradigm.

Best selling anti-aging author Michael Fossel, M.D. Ph.D. has likened the discovery of the first Telomerase Activator to the day humans learned how to grow crops for food! But so many doctors and health care professionals know little or nothing about telomeres and Telomerase Activators, even in the face of a hugely important article recently published in the August 17th edition of Scientific American.

Scientific American spotlighted our company, T.A. Sciences and our product, TA-65, asking: “Could the secrets to anti-aging be at the tips of our chromosomes?”

We’ll have Bill Andrews, PhD, co-discoverer of the hTERT telomerase gene, delivering a powerful presentation on Telomere Biology as it applies to your patients through the use of TA-65. We’ll also have an important discussion about “Resveratrol versus TA-65.”

There will also be docs on board for this webinar who are taking TA-65 themselves as well as using it in their practice. There will be ample opportunity for Q&A.

Please RSVP to : marissa@tasciences.com or call 212 588 8805 for further information.

Plan to listen and/or participate in the webinar Thursday the 24th, from 7-9 PM (4PM PST)  by going to http://tasciences.com/live

TA-65 in Scientific American

August 29th, 2009
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.

Why hair turns gray

August 8th, 2009

(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.