(and Other Diseases)
Linking Telomeres and Disease
Patients with shorter leukocyte telomeres had a 3-fold higher mortality rate from heart disease and a 8.5-fold higher mortality rate from infectious diseases. (Cawthorne, Lancet, 2003).
Another study showed that younger individuals with shorter telomeres had a 2.8-3.2 fold higher risk of premature myocardial infarction (heart attack). (Brouilette, 2003).
Other studies showed the same cardiovascular risk effect in older individuals. (Starr, 2007).
Finally, a study showed that peripheral blood leukocyte telomere length was shown to have predictive value as a test for advanced cardiovascular disease. (Willeit, 2010).
More recently, telomere length was shown to be an independent risk factor for cancer. (Willeit, 2010).
In a 10-year Italian study, those with the longest telomeres had the lowest risk of cancer (5.1 cases per 1,000 person-years).
those with the shortest telomeres had the highest risk of cancer (22.5 cases pre 1,000 person-years).
In summary, there is a clear link between short telomeres and disease risk.
Telomere biology: Cancer firewall or aging clock?
(Josh Mitteldorf, Sept 2013
It has been a decade since the first surprising discovery that longer telomeres in humans are statistically associated with longer life expectancies. Since then, it has been firmly established that telomere shortening imposes an individual fitness cost in a number of mammalian species, including humans. But telomere shortening is easily avoided by application of telomerase, an enzyme which is coded into nearly every eukaryotic genome, but whose expression is suppressed most of the time. This raises the question how the sequestration of telomerase might have evolved. The predominant assumption is that in higher organisms, shortening telomeres provide a firewall against tumor growth.
A more straightforward interpretation is that telomere attrition provides an aging clock, reliably programming lifespans. The latter hypothesis is routinely rejected by most biologists because the benefit of programmed lifespan applies only to the community, and in fact the individual pays a substantial fitness cost. There is a long-standing skepticism that the concept of fitness can be applied on a communal level, and of group selection in general.
But the cancer hypothesis is problematic as well. Animal studies indicate that there is a net fitness cost in sequestration of telomerase, even when cancer risk is lowered…
…If telomeres are an aging clock, then telomerase makes an attractive target for medical technologies that seek to expand the human life- and health-spans.
“Telomeres do not cause cancer.
Telomerase, the enzyme that lengthens them does not cause cancer.
The over expression of telomerase in many but not all human cancers is merely another step in the cancer process.
Turning on telomerase to lengthen telomeres may actually prevent cancer in the long run because it’s the short telomeres that allow the DNA in your chromosomes to fragment.
This makes them more likely to cause the dangerous mutations we equate to cancer. This is one of the hopes for TA-65.” (Dr. Dave)
Cancer can use a different mechanism we’re still studying today called ALT – Alternative Lengthening of Telomeres.
About 10-15% of cancers appear to deploy ALT to survive.
Withholding Telomerase appears to have no effect on these ALT Cancers.
Cancer and Telomeres- Studies
“The telomerase activator TA-65 elongates short telomeres and increases health span of adult old mice without increasing cancer incidence“
“A Natural Product Telomerase Activator As Part of a Health Maintenance Program“
“Telomerase at the intersection of cancer and aging“
Personal Telomeromics: “Can You Turn Back the Clock” Series Links