There are some things that science can tell me that I’m not sure I want to know. For example, I’m not sure I want to know the sequence of my own genome and my projected risk of developing any particular, currently incurable diseases. There are some things it is better not to know, particularly if there is nothing you can do about it anyway. Until recently I would have put telomere length into this category as well. Short telomeres are an indicator of biological age and are associated with increased susceptibility to diseases of aging. And stress, such as could be caused by worrying about how short your telomeres are, is known to make them even shorter. So why find out? It turns out that there are some things under our control that can positively affect telomere length.
Telomeres are nucleoprotein structures at the end of chromosomes that protect them from damage and ensure that genetic information is not lost during cell division. DNA polymerases cannot replicate DNA at the ends of chromosomes effectively, and without the protective effects of telomeres a small amount of chromosomal DNA would be lost with each cycle of cell division. The stretches of repetitive telomere DNA prevent progressive shortening of the chromosome, but are themselves shortened with each cell division. Telomere shortening limits the number of times that a cell can divide. Somatic cells are capable of a finite number of divisions, a number known as the Hayflick limit. Once cells reach that limit, they die. This limit is associated with telomere length. Once telomeres reach a critical length, cellular senescence is triggered, and a cell stops dividing and dies. Because of this, telomere length can act as a gauge of cellular or “biological” age.
I recently watched the episode “Decoding Immortality” on the Smithsonian Channel, which gave a fascinating account of the work of Elizabeth Blackburn, Carol Greider, and Jack Szostak, who were awarded the 2009 Nobel Prize in Physiology or Medicine for their discovery of (and ongoing work on) the enzyme telomerase. Telomerase counteracts telomere shortening by restoring length. The program covered a lot of material in 45 minutes: the discovery of telomerase; the relationship with the Hayflick limit; the tragic consequences of inherited telomerase mutations; and the delicate balance between finding the optimal telomerase dose (healthy aging) and getting too much (cancer).
One fact that I learned from the Smithsonian program was that lobsters are not susceptible to diseases of aging—apparently old lobsters are as sprightly and agile as young ones. It turns out that the key to this good fortune is an unusually high level of telomerase maintained throughout their long lifespan. Could telomerase be the key to the fountain of youth? Maybe—at the very least it seems like it could hold some of the secrets of healthy aging.
Research into the relationship between telomere length, telomerase activity, oxidative stress and other age-related effects has revealed fascinating insights into the biology of cellular aging. For example, a 2004 study showed that telomere shortening is associated with a high-stress lifestyle. Women with high levels of perceived stress had telomeres that were on average 10 years “older” than those of controls, suggesting a biological reason why stressful lives may promote earlier onset of age-related diseases. A 2012 study, published in Molecular Pain also identified a connection between the stress caused by chronic pain and shortened telomere length, and a 2011 study published in Nature identified a connection between telomere dysfunction and metabolic and mitochondrial damage associated with cell death.
But it’s not all bad news. A 2010 PloS One paper found that exercise can protect cells from the deleterious effects of chronic stress. In that study, participants who exercised vigorously for as little as 40 minutes over a 3-day period were protected from the telomere-shortening effects of stress. And in the Smithsonian episode, studies were highlighted showing that meditation, regular exercise and a low-fat diet all counteracted the telomere-shortening effects of stress.
So eat right, engage in consistent exercise, and avoid stress. Darn it!! Those are things that I know I should be doing anyway, but have trouble fitting in to my hectic lifestyle. I was hoping for a pill or something I could add to my diet (but not the green tea again please). Instead I will have to to carry on making time for exercise, continue to cram a few extra vegetables into my diet, and lay off the donuts. While it may be providing a familiar recipe for healthy aging, telomerase research is helping us understand the story of how these lifestyle choices affect us at the cellular level. Perhaps the day will come when we can also pop an optimal dose of telomerase to give us an additional boost and make us feel as good as an old lobster.
- Decoding Immortality: Smithsonian Channel
Esper, E.S., et al. (2004) Accelerated telomere shortening in response to life stress. Proc. Natl. Acad. Sci. USA, 101, 17312-17315.
- Sahin, E., et al. (2011) Telomere dysfunction induces metabolic and mitochondrial compromise. Nature 470, 359-365
- Sibille, K. et al. (2012) Chronic pain, perceived stress and cellular aging: an exploratory study. Molecular Pain. 8, 12-17.
- Puterman, E., et al. (2010) The Power of exercise: Buffering the effect of chronic stress on telomere length. Plos ONE, 5, e10837.
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