An Editorial on Telomeres and Longevity
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Telomeres are the ends of the chromosome, caps of repeating DNA sequences that shorten with each cell division and lengthen according to the activity of the enzyme telomerase - this is a very dynamic process, responding differently to circumstances in different cells and tissue types. Telomere length somewhat acts as a countdown clock, moving a cell towards shutdown after a certain number of divisions rather than permitting continued replication, but as for all matters biological the telomere-telomerase-chromosome system considered as a whole is exceedingly complex. It influences and is influenced by many other important cellular systems and feedback loops: mitochondrial damage, for example, appears tied to telomere length and telomerase activity. Thus even as data rolls in ever faster in this age of biotechnology, the telomere story has stubbornly remained that telomeres generally become shorter on average with age or ill health or stress, and that this shortening might be a contribution to aging or it might only be a marker for other cellular changes and damage that occurs with aging.

This is an important distinction to draw: we should find ways to fix and reverse the changes that are fundamental, that are causes of aging. But we don't have to fix and reverse the markers and secondary changes. If we repair the root causes, the many other line items should take care of themselves. But biology is complicated - obtaining the answers for processes that are right down there in the depths of the cellular machinery, central to everything and touching on everything, takes time.

Here's a good editorial from Impact Aging, very readable for the layperson:

Not surprisingly, given that species differ in many other relevant aspects of their biology, including the pattern of activity of the telomere-restoring enzyme telomerase simple comparisons of average telomere length across species do not map directly onto interspecific variation in maximum lifespan. In relatively long-lived species, telomerase is downregulated in most somatic cells, thought to have evolved as a mechanism to counteract an increased risk of tumour formation, particularly in endotherms. One potential cost of this is that tissue renewal capacity is limited, resulting in somatic deterioration with age.

However, within a given long-lived species, there is good reason to predict that variation in average telomere length in somatic cells will be related to potential lifespan. Examining this link is fraught with difficulties, not least of which is that studies covering the entire lifespan of a cohort of long lived animals take a very long time. Circumventing this by looking at telomere length and subsequent survival in individuals that are already old omits all the individuals who died early in life (and who may have had the shortest telomeres). The alternative approach of comparing average telomere length in a cross sectional sample of individuals of different ages suffers from a related bias; mean telomere length could actually appear to increase with age if individuals with short telomeres die and so drop out of the sample. Furthermore, since telomere length is a dynamic character, if it is predictive of lifespan, we also need to know at what life history stage the relationship is strongest. Longitudinal studies are therefore essential.

Time is the most precious thing for us, and it is unfortunate that finding the necessary information that would allow the research community to be more effective in addressing the causes of aging - by eliminating potential mechanisms from the "must fix" list - might at this point take up more time than it would save.

Comments

The author is wrestling with symptoms vs causes in relation to telomere length and aging across species. His zebra finches were useful due to their relatively short lifespan. His results were consistent with other telomere length/aging condition studies. He concludes that variances in telomere length can be detected very early at 25 days which points to another precondition other than the Hayflick limit as the cause of shortened telomeres.

Let's return to the Human cohort. The disease Progeria is known to have rapid aging effects with extremely short telomeres. Studies of Ashkenazi Centenarians showed a healthy telomere length. Elizabeth Blackburn showed that individuals under chronic stress had shortened telomeres. Dogs and horses have similar telomeres to humans and would be a better indicator. Man's best friend could shorten the timeline required for longitudinal study.

Assuming that all of this study confirms or denies the causes of telomere shortening then what are we to do about it? There seems to be a benefit to strenuous exercise, meditation, calorie restriction and nutrients. My own experience with TA-65 showed definite improvements in health and mood. Atheletes are taking TA-65 and reporting improved performance and quicker recovery time. They stress there bodies and telomeres much more and at an earlier age. I am convinced that aging is actually a replication problem.

Stem cells have ability to repair our bodies provided that their telomeres are healthy. This adds leverage to any improvement to their telomere length. Taking your own stem cells and culturing them and reintroducing them is becoming a popular offshore therapy. The FDA does not allow this and other promising techniques to be practiced in the US. Where is the outrage? I will have to meditate on that.

Posted by: Bernie Kitts at February 27, 2012 4:47 AM
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