Telomerase activation is presently thought to improve the genetic stability of human cells against cancer.
The danger of cancer goes up in humans after cells become senescent, especially in epithelial tissue and
in lymphocytes. After the cell has become cancerous, then telomerase inhibition becomes attractive as therapy,
because cancer cells often activate telomerase as part of their growth strategy. This sometimes fails, however,
because cancer cells may use the ALT mechanism instead of activating hTERT to produce telomerase.
I note that germ cells such as sperm and egg have high continuous levels of telomerase,
and show no cancer problems. Similarly, stem cells intermittantly activate telomerase so that they
can have many more cellular divisions than the normal somatic 50 cellular divisions from the embyonic.
stage of human development, up to 1000 cell divisions. Furthermore, cultured human cells
in vitro typically
become immortal without cancerous effect when exogenous telomerase is applied to the culture.
The good news is that hTERT is not thought to be an oncogene causing cancer. In my opinion, telomerase
activation as anti aging strategy is only worrisome when no guard band is included
to catch cancer cells activated by carcinogens in cases in which the cancer uses hTERT activation.
That is, it seems safe enough to use cyclic telomerase activation such as suggested by Noel Patton
at
TA Sciences in connection with therapy using TA-65, a telomerase activator based on astragalus
extract and present as a minor component (cycloastragenol?), or chemically obtained from astragalus extracts
or constituents such as astragaloside iv, as described in Geron patent literature.
See
http://greenwood.s5....gevity.html#(7) to study other small molecule telomerase activators and also see Michael Fossel's MD-PhD book
Cells, Aging, and Human Disease.
I think cyclic telomerase activation will make our genes more stable against cancer, and that our
strategy in life extension should include cyclic telomerase activation as a matter of course, so that we do not
suffer much from the presence of senescent cells in our bodies. This also requires limiting cellular wastes
such as lipofuscin, and avoiding other mechanisms that can trigger senescence, such as high levels of
oxidative radicals that damage telomeric DNA in the absence of transcription, which tends to repair
transcribed DNA. It may also be required, as shown by Zs-Nagy, to keep the cell membrane permeability to
potassium in nerve cells within acceptable range by the use of DMAE, Centrophenoxine, or other drugs, if
we mean to obtain extremely long life spans approaching physical immortality with rejuvenation included. Similar
considerations may apply to chlorine in muscle cells. Improving DNA shielding with antioxidants and
antiglycating drugs such as carnosine should help ward off senescence effects due to telomeric DNA damage, and
DNA repair may be accelerated by other mechanisms such as application of Cat's Claw Extract or Pero's AC-11.
Incidentally, I still think extra vitamin C should be useful to 2500 mg/day. The aging of mitochondrial DNA
is better protected against when telomeres are long, as then the cell automatically generates higher
levels of endogenous antioxidants. I note that alpha lipoic acid plus acetyl L-carnitine has been effective
in mitochondrial recovery, and that treatment with NO using arginine supplements and endogenous nitric oxide synthetase
effectively promotes mitochondrial genesis. Otherwise, observe that membrane-damaging peroxynitrites generated by NO
are effectively countered with the gamma tocopherol form of vitamin E.
Edited by jamesagreen, 10 January 2008 - 10:36 PM.
