Rechârge Biomedical Clinic

On March 30th, some Über-geeks fired up their Large Hadron Collider in Switzerland in an effort to move one huge step closer to Einstein’s elusive lifelong dream of a G.U.T. or Grand Unified Theory.  That ‘theory of everything’ is a somewhat verifiable way to explain how the particles of the Standard Model of particle physics fit with our understanding of Electromagnetism, Strong and Weak nuclear forces, and Gravity.

I know what you’re thinking:

“Zzzzzzzz…BOh–ring”

But WAKE UP! To paraphrase the Baby-Boomers’-Bard, “The future now, will later be past.”

The story of how firing up the big blaster didn’t end the universe was eclipsed in the headlines because 1) it didn’t affect the survivors of Oceanic 815 and 2) it’s not as riveting as Kate Gosselin’s fate on Dancing with the Stars. I get that. But explaining the whole universe is pretty good for a species of “Monkey-boy” hominids that have only been in existence for a mere 200k of the universe’s 13.7 billion years, or 0.000014 of its creator’s existence. This would be probably as likely one of your dust mites writing your entire life story into a Tony-award winning musical during a commercial break of Dancing with the Stars.

So if these acne-stricken, Toblerone-scarfing smarties find their Higgs Boson particle (or Dan Brown’s ‘God Particle’ from Angels and Demons) they’ll be closer to unifying their models and better still, their mom’s get to tell their ‘Frenemies’ how their kid turned out to be smarter than Einstein.

I know what you’re thinking:

“Where the $*@! is he going with this?”

In 1986, Sean Connery played a 14th century theologian/gumshoe named William of Ockham in a pretty cool whodunit movie called The Name of the Rose.

He (Sir William of Ockham, not the greatest James Bond of all time) is best known for his principle of “Ockham’s Razor,”  which has been a close companion of scientists and detectives from Carolus Linnaeus to Lieutenant Columbo:

pluralitas non est ponenda sine necessitate

“plurality should not be posited without necessity”

In other words, don’t evoke a whole bunch of reasons when only one will do just fine.

So that’s really the point of this posting.   To explain aging, theorists often focus on the results of human aging, not its root cause, which is likely to be telomere erosion.

Since telomere erosion allows the ends of all DNA to be exposed and injured, it is sufficient to explain and encompass all the other theories such as:

• Error Accumulation
• Somatic mutation
• Accumulative-Waste
• Free Radical theory
• Mitohormesis
…etc.

To paraphrase another pretty cool movie “One theory to rule them all, one theory to bind them…”

It seems logical that if every living creature with non-circular DNA uses telomerase to protect their DNA libraries, despite having evolved a variety of different repeating sequences, then the evolutionary conservation of telomerase must be a necessary condition for the survival of any species that carries the entire library in every cell nucleus.

Since the “Grand Inquisitors” these days are physicists and not sadistic zealots, anyone can come up with a theory. Even I did. If you want to check out my theory of aging, go to: http://www.rechargebiomedical.com/aging.html

And if you want to do something logical and positive towards living healthier and longer, you should do what hundreds of MD’s, PhD’s, and CEO’s have already done: take TA-65 to activate your telomerase and repair your critically short telomeres. You have our MONEY-BACK GUARANTEE!

Bacteria are simple and all their functions are limited to that one tiny cell. In contrast, Eukaryotes (those with nuclei) are complex and each cell has many specialized organelles that perform different functions compartmentalized by membranes.

Bacteria have a circular DNA that is small and easy to copy. Each bacterium is like a simple robot with a shopping list of things it can do. The robots can overrun but they can’t organize themselves into organs, let alone larger creatures.

In contrast, eukaryotic cells, which make up ALL plants and animals, have hugely convoluted, linear DNA, comprising many chromosomes protected by a nuclear membrane. Unlike a robot with the list, they are like a person bearing the complete library (thousands of genes for proteins and RNA) that the entire society (the organism) requires to function. Although that particular cell may only actively need a fraction of the genes, they carry the entire library.

As you know, Darwin’s evolutionary theory emphasized competitive reproductive advantage created by mutations in the creation of species. Ironically, the biggest evolutionary inflections involved two cooperative milestones known as “Symbiogenesis” (the creation of new life from combination of species and the fictional name of the biotech giant in my new graphic novel, Maximum Lifespan.)

Some scientists believe that Eukaryotes were created when DNA viruses with membranes were incorporated into primitive bacteria, forming the first nucleated cells.

Next, those primitive single cell eukaryotes, the Protozoa, incorporated bacteria into their cytoplasm to produce energy, such as mitochondria for animals, and chloroplasts for plants.

But there are three problems with carrying huge DNA libraries:

1. inefficiency
2. errors: 50 billion cell divisions daily, each requiring 6 billion base pairs to be copied, yielding 300 quintillion chances for transcription errors
3. non-circular DNA shortens each time it divides leading to REPLICATIVE SENESCENCE.

Click here to read Carolyn Abraham’s article and wonderful video explaining this process:
http://www.theglobeandmail.com/life/article965900.ece

So really, we exist only because long ago, little bacteria, the mitochondria, were given a nice place to live inside our cells. In exchange for that cozy hideaway, those bacteria generate our fuel. But like “Manuchrian Candidates,” they can also morph into assassins at the end of life, as we’ll describe in a future blog posting.

To learn how TA-65 is reversing chromosome deterioration for hundreds of pioneers and making us younger, go to http://www.rechargebiomedical.com/

The two oldest trees known were Bristlecone Pine trees in Nevada (Prometheus-5000 years old) and Prometheus in California (4800 years old)

a Bristlecone pine

Like all living things more evolved that bacteria, trees need to lengthen their telomeres with telomerase otherwise they’ll die from critically shortened chromosome tips, the telomeres. The difference between us and trees is that their telomeres are seven base pairs repeating (TTTAGGG) rather than the six that we use (TTAGGG.)

Bacteria all have circular DNA, which can be easily reproduced without shortening. In contrast, each cell from a EUKARYOTE (yeast, plants, and animals) houses the entire vast library of thousands of genes in its nucleus. The variable expression of those genes determines the form and function cells in their organs.

Evidence shows that trees with more telomerase activity live longer. With high telomerase activation, 2000- to 5000-year lifespans are possible. With moderate activity comes medium lifespans (400- to 500 years) and with little activation, the pine trees are short-lived (100- to 200-years.) †

You are fortunate to live in a time after the discovery of TA-65, a nutraceutical substance that can activate telomerase and thereby delay aging. Start your Patton Protocol now and you can experience rejuvenation so that someday, you can be “as old as the trees.”

† Flanary and Kletetschka published these results in Rejuvenation Research (2006 Spring; 9(1): 61-63

To learn more, go to:
Rechargebiomedical.com

“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”



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:



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”

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”

(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.

A recent study suggests that critically-short telomeres may allow harmful changes. This study is like a ‘smoking gun’ in the understanding of cancer. Compared with similar but unaffected people, women who had developed breast cancer showed more worn-out telomeres. Since telomeres protect the tips of chromosomes, longer is better.

We’ve known for a long time that when the end of Chromosome 9 gets too short and crosses over to the end of Chromosome 22, you get a Philadelphia Chromosome and a kind of leukemia. When the telomeres shorten, this sort of crossing over is more likely to occur.

All it takes is one single end of one single chromosome in one single stem cell to produce a lethal process known as cancer.

Let’s keep those telomeres long with TA-65!

——————————————————————————————————-

“Chromosome 9 Arm-Specific Telomere Length and Breast Cancer Risk
Yun-Ling Zheng, Christopher A. Loffredo, Peter G. Shields and Sahar Selim

Cancer Genetics and Epidemiology Program, Lombardi Comprehensive Cancer Center, Georgetown University, Washington DC

Correspondence author: Yun-Ling Zheng, Cancer Genetics and Epidemiology Program, Lombardi Comprehensive Cancer Center, Georgetown University, 3800 Reservoir Road, NW, Box 571465, Washington, DC20057. Phone: (202) 687-6654; Fax: (202) 784-3034; E-mail: yz37@georgetown.edu

BACKGROUND: Telomere dysfunction is involved in the development of breast cancer and very short telomeres are frequent genetic alterations in breast tumors. However, the influence of telomere lengths of specific chromosomal arms on the breast cancer risk is unknown. METHODS: We conducted a case-control study of breast cancer to examine the associations of the telomere length on chromosome 9 short arms (9p) and long arms (9q) with risk of breast cancer. Chromosome 9 arm specific telomere lengths were measured by quantitative fluorescent in situ hybridization (FISH) using cultured blood lymphocytes. RESULTS: Telomere length on chromosome 9p was significantly shorter in breast cancer patients than in control subjects (P < 0.001). Using the 50th percentile value in controls as a cut point, women who have short 9p telomeres had an increased risk of breast cancer (adjusted odds ratio [OR] = 2.6; 95% confidence interval [CI], 1.5 – 4.3). When the 9p telomere length was divided into quartiles, a significant inverse dose-response relationship between 9p telomere length and breast cancer risk was observed (Ptrend < 0.001), with a quartile ORs of 3.0 (95% CI, 1.2-7.5), 3.9 (95% CI, 1.6-9.5), and 6.6 (95% CI, 2.8-15.9) for third, second and first quartile respectively when compared with women in the forth quartile. CONCLUSIONS: Short telomere length on chromosome 9p is strongly associated with the risk of breast cancer. If confirmed by future studies, chromosome 9p telomere length has the potential to be incorporated into the current prediction models to significantly enhance breast cancer risk prediction.”

In the 1930′s, twenty years before Watson and Crick described the DNA’s double helix, Herman Muller was irradiating fruit flies at Woods Hole to produce mutants with deletions and inversions involving the ends of chromosomes. High energy rays produce DNA breaks, which is why UV exposure gives us skin cancer.

Of note, he never found mutants with deletions or inversions
involving the natural ends of the chromosomes and concluded that:

‘‘. . . the terminal gene must have a special function, that of sealing the end of the chromosome, so to speak, and that for some reason a chromosome cannot persist indefinitely without having its ends thus sealed.’’

Muller coined the term telomere for this terminal gene from the Greek, meaning simply ‘‘end part,’’ but the fact that this region of the chromosome deserved a specific name was a recognition that something unusual was going on there.”

(The above was excerpted from: The Plant Cell, Vol. 16, 794–803, April 2004,)

Muller used experiment and observation to correctly deduce the function of telomeres long before we even knew the structure of DNA.

All too often, truth often has to wait for consensus and dogma to catch up. In the case of telomerase activation science, let’s hope it doesn’t take the seventy years that it took for Herman Muller to be vindicated by Maria Blasco’s work.

Can you really afford NOT to take TA-65?

Great health to all,
Dr. Park

P.S. To see experimental proof of telomerase’s role in preventing chromosomal damage, go to http://www.rechargebiomedical.com/stemcells.html