Rechârge Biomedical Clinic

Q: Does aging prevent cancer?
A: No, yes, no, no, and huh?

I’ve tossed together a quick posting about the question “Does Aging prevent cancer?”

We’ll take this question on Five levels:

1) The Molecular Level – No!
Replicative senescence causes telomeric DNA to shorten each cell division.
Unprotected telomeres allow for DNA damage which is the sina qua non of cancer.
So at the level of the DNA, it’s quite the opposite: aging of the DNA causes cancer.

2) Nuclear Level -Yes
Yes.  A wonderful experiment created a custom p53 enzyme (the policeman of the genome) that could no longer kill (apoptosis) but COULD shut down (senescence) critically damaged telomeres.  They proved that in real-life mice, p53 prevention of skin cancer required the forced-aging of old dysfunctional cells possessed of critically-short telomeres.  Surprisingly, the p53 prevention of skin cancer in these mice was not mediated by killing those cells.

3) Organism level – No
Obviously, older people get more cancer, premature aging syndrome kids (progerics) get more cancer, and aging immune systems (i.e. AIDS) area associated with more cancer.

4) Evolution of the Species level – No.
From aging conferences and reading editorials, I’ve heard some intelligent scientists suggest that aging is Nature’s way of preventing cancer. Dubious at best.

Hominid evolution never included aging because the fossil record doesn’t even show any of our ancestors made it much past 30.  Since cancer never occurred (because aging was uncommon,) it couldn’t have be a factor in natural selection.  Those scientists need to brush up on their Darwin and Dawkins, and put down the Genesis and Grimm brothers.

5) Cosmic – huh?

Isn't it Ironic?

Grimm Brothers are a good model for much of what passes for theories on Aging.  Deeply ingrained in our core values is the ironic comeuppance, which serves as a karmic gyroscope in what is essentially a magical and personal view of living.  “Be careful what you wish for” they say, the Monkey’s Paw, Vampirism, the Twilight Zone episode where Burgess Meredith has all the time in the world to read books but breaks his glasses.

But let’s face it, in the real world, the bad guys often come out on top and usually, Grace gives us more than we truly deserve.

In my opinion, the universe doesn’t concern itself with ‘aging’ or ‘cancer’.  These terms are abstractions that emerge from human biology and consciousness. Scientists who suggest that aging prevents cancer should concern themselves more with the mechanics of the watch, than whether the watchmaker was blind, deaf, or in a foul mood when he wove the tapestry of our lives.

As Alexander Pope pointed out: “The proper study of mankind is Man” and the experts there are the storytellers, musicians, and artists.

The experts on God and the Metaphysical “meaning of it all” are clergy and philosophers.

In my opinion, scientists should stick to science and avoid hand-waving and trying to interpret the cosmic ‘meaning of it all’

The news yesterday was of a new class of drug to fight melanoma using a new mechanism: it boosts your immune system instead of destroying it.

I created this diagram to illustrate the treatment of cancer as of 2010:

But as with many things, best treatment for cancer is prevention. If you protect the tips of the chromosomes (the TELOMERES), you don’t get the recombination and breaks that cause cancer.

The second best the p53 enzyme, the “watchman of the genome”, which repairs DNA, causes damaged cells to stop dividing, or destroys them outright.

The third line is the adaptive immune system of the T Cells, especially the Natural Killer cells. Check out this link to see how your body has possibly cured you of cancer millions of times already.

Once cancer becomes clinically-evident (like the weeds above ground in this diagram,) treatment becomes increasingly destructive from precision surgery, to local radiation, to systemic chemotherapy.

The efficacy of radiation and chemotherapy comes from targeting rapidly-producing cells.  Unfortunately, your own body’s stem cells are also rapidly-producing. So the cure is often worse than the disease and at the very least, it makes it harder to fight the disease

Would you put down a student protest....

.... by dropping napalm on campus?

Returning to our pyramid diagram, an ounce of prevention is better than a pound of weed-killer, or scorched earth.

Telomerase activation occurs with rest, exercise, good diet, and taking TA-65.

To learn more about the link between cancer and telomeres check out this link.

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!

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“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.”