On the Erosion of Telomeres

Going forward, NIH funded medical research is open access, the full papers being freely available at PubMed Central. This is one modest part of a very necessary evolution in the way in which information is handled and organized in the broader scientific community. Dropping the cost of access to scientific data to near zero is a requirement to evolve the next generation of correlators, synthesists, research automation and toolsets. The level of complexity in the life sciences is so great, and growing so rapidly, that effective progress in the years ahead depends upon the development of a powerful organizational layer above the raw mass of scientific data.

But back to PubMed Central. You should take a drive around the site, see what's out there. A paper on telomere erosion caught my eye while I was doing just that, an illustration that we there is a way to go yet to fully understand how telomere shortening relates to longevity, health and life circumstances:

Telomeres - the terminal caps of chromosomes - become shorter as individuals age, and there is much interest in determining what causes telomere attrition since this process may play a role in biological aging. The leading hypothesis is that telomere attrition is due to inflammation, exposure to infectious agents, and other types of oxidative stress, which damage telomeres and impair their repair mechanisms. Several lines of evidence support this hypothesis, including observational findings that people exposed to infectious diseases have shorter telomeres.

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Our results show that repeated Salmonella infections cause telomere attrition in [white blood cells (WBCs)], and particularly for males, which appeared less disease resistant than females. Interestingly, we also found that individuals having long WBC telomeres at early age were relatively disease resistant during later life. Finally, we found evidence that more rapid telomere attrition increases mortality risk, although this trend was not significant.

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Our results indicate that infectious diseases can cause telomere attrition, and support the idea that telomere length could provide a molecular biomarker for assessing exposure and ability to cope with infectious diseases.

Funnily enough, it's a PLoS One paper - open access twice over. Now, one might cast telomere erosion in white blood cells, a component of the immune system, as one of the more direct biological forms of wear and tear through repeated usage. More infections, more work for the immune system, more immune cell division, and so forth. This is probably quite separate from other mechanisms relating to telomere length in other tissues in the body - for example the link between oxidative stress due to mitochondrial free radicals and telomere shortening.

I'd be willing to wager that changes in telomere length will turn out to be a very complex topic across the body as a whole, with many different dominant mechanisms, circumstances and degree and type of effect on health. The one thing we can point to is a consensus that accelerated shortening of telomeres is not a good thing for the normal operation of your body.

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