Archive for February, 2010

28 FebRoseanne Rosannadanna and the truth about life insurance

As a physician, I’ve noticed that people explain health and disease in three main ways:

Heredity: “My mother’s brother had that.”
Luck: “These things come in threes”
Cosmic retribution for something we did or didn’t do: “I ate a lot of junk food as a teenager and that’s why I got colon cancer.”

But if you think about your body like a car, you wouldn’t bring a car with 300,000 miles to the mechanic and insist:

“I knew the engine block was going to blow because Toyota Corollas in my family have done that in the past.” (Heredity)

“My transmission broke because nothing good ever happens to me since I bet against my own Red Sox to win the World Series.” (Luck)

“My transmission is shot because I have a lead foot.” (Karma)

If we extend the car analogy, then here are some failures in our bodies and our cars:

Heart attack———→ Engine trouble
Osteoporosis——-→ chassis deterioration
Hip and Knee replacement ——-→ struts and shocks
Wrinkles and skin cancer ——→ Dings and paint damage
Alzheimers——–→ Electrical failure
Colon Cancer—–→ Muffler ;-)

Now I’m not trying to say that heredity and abuse/maintenance aren’t huge factors in causing disease. They are. But when a car has 300,000 miles, are any of those explanations even called for?

With cars, the problem is the wear and tear that comes with mileage. With people, the problem is replicative senescence that comes with aging. But for both, Roseanne Rosannadanna’s old saying applies:
roseanne_rosanna_dana
“If it’s not one thing, it’s another.”

It’s true. Did you you realize that in retrospect, 3 out of 4 people who develop a cancer have NO FAMILY HISTORY for that cancer!

Ironically, Gilda Radner may be the exception that proves the rule when it comes to family history and cancer: she was a carrier for BRCA1 mutation and therefore had an 85% lifetime chance of breast cancer and a 45% chance of ovarian cancer.

WHY, you ask? Well, BRCA1 codes for an enzyme that repairs our DNA. Mutations in that crucial nanomachine make it hard to fix the inevitable errors that occur with copying stem cell DNA millions of times over.

But even without that genetic time bomb, Gilda, like all of us, had a theoretical 100% chance of developing every cancer if she had only lived to hundreds of years old. In keeping with the metaphor, a car driven forever will eventually develop a problem in every system.

Luckily, your body is far superior to any mere machine. It is endowed with the ability to self-renew and self-repair using its own immortalized stem cells.

So don’t focus on which organ is going to “go rogue.” Focus on keeping those organs well maintained by protecting nuclear DNA before the damage can occur. With TA-65 and telomerase activation, you are living in the first generation of humans who can roll back their odometers and maximize their healthy lifespans.

Start today by going to : http://www.rechargebiomedical.com/index.html

20 FebAIDS is Aging, and vice versa

We know that Immune health deteriorates as you age. But did you know that the aging of your immune system may be an important CAUSE of aging in general?

The thymus is a small but essential organ overlying your breastplate where fresh immune cells from the bone marrow, aka the “T Cells” (for thymus), become mature. It is like a “West Point” for T-cells which will be selected for their ability to learn the host’s unique password, the MHC-1 (or Major Histocompatibility Complex 1), that almost every cell in your body possesses. In the diagram below, this “positive selection” takes place in the outer cortex. MHC-1 critical for fighting cancer and viruses-infected cells.

The thymus is the heart of the adaptive immune system

The thymus is the heart of the adaptive immune system



Before they graduate, the majority of T-cells are killed off by apoptosis (programmed cell death) because they react too strongly to the MHC 1 and might escape to wreak havoc on host cells by creating autoimmune diseases. This “negative selection” takes place in the central medulla of the thymus.

Until the 1960′s, scientists considered the thymus to be a useless organ, a graveyard for immune cells. This was probably because the organ was withered by the time their older patients went to autopsy.

On the other hand, the ancient Greek physician, Galen (AD 129-200) considered the thymus the “seat of the soul” and “that mystical organ.” We now realize that the thymus is literally and figuratively the center of the adaptive immune system. Galen noted that the relative size was greatest as an infant and that after puberty, the organ shrinks. But the “thymic West Point” probably withers because of lack of enrollment from eligible young T-cells, not from self-destruction.

Advanced HIV infection, aka AIDS, results in a premature burning-out of the host’s immune system. That is why HIV patients keep track of their “T-cell count” as a gauge of how much immune function remains. CD28 (+) cells are “naive T-cells” and are thus able to adapt to new immune threats. With AIDS, the immune system loses its capacity to respond to new threats as the proportion of CD 28(-) (pronounced ‘cee-dee-negative’) T-cells increases. CD28 (-) T-cells, stretching the military metaphor, are 4F, or not suitable for military service.
immune deficiency allows cancer to develop and thrive

immune deficiency allows cancer to develop and thrive

Previously an extremely rare cancer occurring in elderly Mediterranean men, Kaposi’s sarcoma (shown above) was one of the first phenomena of AIDS before scientists had identified HIV in the early 1980′s. So what is the relationship between cancer, viruses and immune deficiency?

You body is constantly fighting new cancers and latent viruses like an army waging war on many fronts. When all the T cells (West Point officers) and the Natural Killers (enlisted men) are used up, the war is lost.

To understand why AIDS is a form of Aging and vice versa, go to:
http://www.rechargebiomedical.com/immunehealth.html

14 FebCancer “stem cells”: a new paradigm.

Is there really such a thing as a Cancer Stem Cell (CSC) ?

The traditional view of carcinogenesis was that any run-of-the-mill cell could become cancerous by accomplishing three things:

  1. The deactivation of a tumor suppressor gene,
  2. A proto-oncogene becoming an oncogene,
  3. Reversion to a more primitive, stem-like state allowing them to activate telomerase, the enzyme that allows the ends of chromosomes (telomeres) to lengthen and make the cell immortal.

This theory is analogous to a long-time worker bee transforming itself into a Queen Bee without all the special diet and preparation that is normally required.

Burning the candle at both ends

Once upon a time, scientists thought that all cells in a dish could grow forever, like cancers. But experiments showed that differentiated (aka non-stem) cells only divide about 50 times before the colony dies out. The destiny of these differentiated cells is a product of two fundamental rules: non-stem cells don’t activate telomerase and the replication of non-circular DNA always results in some shortening of DNA at the telomeres. This aging your chromosomes is like burning a candle at both ends and is known as REPLICATIVE SENESCENCE.

When the telomeres inevitably become critically short on any of the 92 chromosomal tips in every cell, the informational DNA is exposed and will be damaged. Telomerase is your stem cells’ way of manufacturing new telomere DNA to keep your chromosomes capped and protected.


The Cancer Stem Cell model


The new paradigm is that cancers, like the cells in your healthy organs, are maintained by very rare Cancer Stem Cells (CSC’s). Using the beehive metaphor, if you get the carcinogenic mutations in the Queen Bee (stem cell), the resulting new CSC is already an immortalized, telomerase-active cell. That may help explain why highly toxic radiation and chemotherapy sometimes kills off the “worker bees,” but since the robust Queen survives, she can recreate a whole new colony

Whether none, some, or all of clinical malignancies have CSC’s is a matter of ongoing investigation and controversy. What seems clear is that by telomerase activation, TA-65 safely adds more “wick” to the candles that are your telomeres. By delaying the damage to our cellular DNA, we delay the ravages of time. At the cellular level, we call those ravages REPLICATIVE SENESCENCE. At the human level, we call it getting old.

For more information about CSC’s go to: http://rechargebiomedical.com/cancer.html

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
  • “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”

07 FebProtecting your genetic “Hard Drive”

“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”

01 FebExercise is associated with longer telomeres

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

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