May 16, 2006
Telomeres Wear Down Quicker In Men Than Women
Men live fewer years on average than women do. Telomeres - cap structures on the ends of chromosomes - shorten with age and their shortening may be one cause of aging. A new study finds that telomeres wear down in the cells of aging men more rapidly than in the cells of aging women.
This new study published in the journal “Cytogenetic and Genome Research” shows significantly shorter telomeres and higher erosion rates in men than in women, which likely causes a shorter life expectancy of male cells and tissues.
Human telomeres form the terminal structures of human chromosomes and play a pivotal role in the maintenance of genomic integrity and function. During aging, telomeres gradually shorten, eventually leading to cellular senescence. Therefore, in humans, short telomeres are considered to be a sign of advanced age.
In this study, the authors investigated human telomere length differences on single chromosome arms of 205 individuals in different age groups and sexes by T/C-FISH (telomere/centromere-fluorescence in situ hybridization), which allows precise measurement of individual telomeres.
In all chromosome arms there was a linear correlation between telomere length and donor age. Generally, the men had shorter telomeres and higher attrition rates than the women.
Even if we could lengthen our telomeres doing that might not increase life expectancy. Why? Wearing down of telomeres protects against cancer by reducing the number of times that cells can divided. Lift that limit and our risk of cancer would probably rise.
The development of effective and easy treatments to cure cancer would make telomere lengthening a much more attractive goal.
Actually, the restoring telomere length vs cancer risk should be viewed with extreme skeptical mindset.
Stem cells clearly exceed the Hayflick limit by about 1-3 orders of magnitude. This suggests that the safety edge on divisions is out past the 1000 division mark. Cancer, at the cell level, is a DNA failure. But cancer, as disease, is a failure of systemic immunosurveillance. Improve/restore immunosurveillance and off you go. I spent 3 years showing this can be achieved simply by removal of soluble receptors, TGF-beta overshoot and most recently, the identification of IL-23 as the cancer-defensive cytokine that stops immunosurveillance.
I believe you could safely double up and get an extra 50 divisions out of the bulk of cells without increase in the cancer risk.
Wish I had the dollars to go prove it.
In the meantime, increasing SOD, high dose reservatrol, is the most one can do. Hopefully, more SENS to follow!
I've recently read estimates that 30% to 40% of cancers might come from stem cells.
At the same time, stem cells wearing out are a major cause of aging. Lots of stuff stops working when stem cells can no longer come in and supply repair cells.
Would lengthening telomeres in stem cells make them more youthful? Do old stem cells fail to lengthen their telomeres?
Immunosurveillance: very interesting and good for you! I've read a couple of recent reports about methods to get immune systems to recognize cancer cells as enemies. One boosts the efficacy of anti-cancer vaccines. I should have done a post on it. Maybe I can still find the reports.
Thanks. We'll see if the damnable therapy makes it to market! The stuff routinely crushes solid tumors but translation to human study has been tripped up mostly at the business level, not the clinical level.
What truly sucks, if the reports are to be believed, a lot of stem cells croak without ever seeing the light of day. E.g. The resevoirs, mostly in the bone marrow, just do the apoptotic dance over time.
I am almost convinced that we should put everyone thru plasmapheretic bone marrow extraction at 22, make 4 aliquotes of the stuff, toss it in liquid nitrogen, and every 20 years you go and reinfuse the stem cells.
And yes, and 30-40% is the conservative, reasonable scientist level. But I have the sinking sensation that a stem cell lands in an inflamed area, gets caught in a chronic inflammatory cycle, maybe it does that nuclear fusion/gene swapping thing, and bam! cancer. This may suck, but certainly on the solid tumor side, I would not be shocked if 10 years from now we up that number to 95%