Telomeres, Exercise, Lifestyle and their Relationship to Longevity
Recent research over the last few decades has paid increasing attention to aging at the molecular level. In particular, a genetic component called telomeres, has garnered much attention over the last few decades. Chromosomes are long strands of deoxyribonucleic acid or DNA. DNA is our molecular blueprint of who we are, being the genetic blueprint for forming our genome. Telomeres are found at the end of the chromosome, looking like a cap that helps prevent other chromosomes from fusing together. In essence, a telomere is a part of the DNA found in the nucleus of the cell, made up of six repeating nucleotide bases-- thymine (T), adenine (A), and cytosine (C), or a TTAGGG sequence. Under normal conditions, when cells divide, telomeres and their repeating nucleotide sequence shorten with each cell division. Therefore, similar to determining a tree's age by cutting the tree and examining the number of rings that exist, examining telomere length on the molecular level can provide an indication of the age of the person.
As cells continue to shorten, the cell and ultimately the human being age, a process referred to as senescence. If the telomere shortens too much, the DNA can be damaged. Furthermore, as the telomere shortens to very short lengths, cell division ultimately stops. Certain cells need to naturally die off for proper health. However as individuals age, all of their body cells' genetic material are ultimately undergoing a telomeric reduction. Conversely, with cancer, the reverse is often witnessed. Certain cells in the body do not die off naturally and continue an unending life cycle due to enzymatic telomerase production and a tumor-type agglutination of unhealthy cells.
Given the information that has been presented so far, it appears that aging is an inevitable feature that is determined by the molecular structure of our genetic blueprint. Furthermore, although truth for this proposition appears to be found in what has come to be referred to as the Hayflict Phenomenon, which is the programmed capacity for cells to divide, even under optimal conditions, no more than approximately 50 to 60 times, setting a genetic upper limit to our lifespan, this does not mean human beings have no control in how long they can live. In fact, recent information has provided important knowledge on how we may ultimately slow aging down through the perseveration of telomere integrity.
A recent study that was led by Dean Ornish, Professor of Medicine as the University of California, San Franciso followed 35 men over five years. All 35 men had been diagnosed with low-risk prostate cancer. Of the 35 men, 10 of the men in the study were assigned to engage in a healthy lifestyle that was composed of a vegetarian diet, regular exercise and regular sessions of stress reduction through use of meditation and yoga. This served as the experimental group. The other individuals who did not experience lifestyle changes served as controls.
The study demonstrated some interesting results. Until recently most have assumed that the telomeric shortening was ultimately inevitable with aging, give or take some level of individual variation in the speed or progression of the shortening of the telomere, leading to individual differences in how fast one ages. However, in the Ornish study, at the end of five years, the researchers found that those that adopted the healthier lifestyle habits mentioned above demonstrated a younger looking DNA in terms of the degree of its shortening (Raffensperger, 2013). Not only was telomere shortening slowed, but it was actually reversed. In the 10 men who made lifestyle changes, telomere length grew by an average of 10 percent over the five year study period. Moreover, the quantitatively greater number of healthier lifestyle changes made was associated with more telomere growth. Conversely, the control group experienced a three percent reduction, or shortening in telomere length over the five year length of the study. The study results do have to be interpreted cautiously since the study was far from representative, quite small, with a fairly loose level of control. Yet, they do present some very interesting results that need further investigation, results that are quite inspiring and salubrious to say the least.
Telomere shortening is also related with many diseases. However, whether the diseases are caused by the shortening of the telomere or the telomere shortening causes the disease needs to be further studied. Furthermore, centenarians were found to have longer telomeres than those who were 85 years of age. Here again the question is whether the longer telomere led to centenarians reaching their status or was it due to their health being better, leading to greater telomere length, and subsequently greater age (Knox, 2013). Nevertheless, there does appear to be a connection between telomere length, disease and aging.
Overall however, there is increasing evidence that exercise, better nutrition, and subsequently enhanced health leads to a reduction in the rate of telomere degradation. Both younger and other marathon runners and track athletes demonstrated upregulation of telomere-stabilizing proteins. They also demonstrated decreased expression of apoptosis regulators. Both of these features were not found in more sedentary controls.
Both younger track-and-field athletes and the older runners had up-regulation of telomere-stabilizing proteins and decreased expression of vascular apoptosis regulators in circulating leukocytes compared with individuals who did not exercise frequently. Furthermore, other research has found that subjects who spent more than three hours each week in vigorous physical activity had longer telomere length as compared to subjects who were 10 years younger than them and who exercised less than 16 minutes each week (Giuliano, 2010). Even with mice that were subjected to increased exercise levels in the laboratory as compared to those that were sedentary controls, telomere length was enhanced among the more active mice (WebMD).
Genetics may also be susceptible to the anti-aging effects of exercise. One would anticipate that identical twins, given that they share the same genetic information, would be an ideal group to see if exercise has a telomeric-enhancing effect that could trump genetic blueprint they are born with and is part of their DNA. What in fact was found is that when one twin was active and one was sedentary and telomere lengths were compared, the identical twin with the greater activity had longer telomeres. This is quite compelling since identical twins share exactly the same genetic material.
Given what has been reviewed in this article, it appears that we are not just prisoners of our biology. It has been known for some time that exercise, healthy diets and healthy lifestyles can enhance our health and possibly even our longevity. However, now we are seeing increasing evidence for the health-enhancing effects of exercise and nutrition on the molecular level. It appears that exercise, a healthy diet, and a healthy overall lifestyle may have an epigenetic effect on our telomeres that exogenously can have a very beneficial impact on our immanent genetic profile, and potentially on our health and longevity.
Giuliano, V. (2010/Jan). Exercise, telomerase and telomeres. http://www.anti-agingfirewalls.com/2010/01/14/exercise-telomerase-and-telomeres/
Knox, R. (2013/Sept). Healthful Living May Lengthen Telomeres And Lifespans. http://www.npr.org/blogs/health/2013/09/17/223386084/healthful-living-may-lengthen-telomeres-and-lifespans
Neale, T. (2009/Nov). Exercise May Slow Telomere Shortening, Aging. http://www.medpagetoday.com/PrimaryCare/ExerciseFitness/17221
Raffensperger, L. (2013/Sept). Healthy Diet and Exercise Can Reverse Aging in Our Cells. http://blogs.discovermagazine.com/d-brief/2013/09/17/healthy-diet-and-exercise-can-reverse-aging-in-our-cells/
WebMD. Molecular Proof: Exercise Keeps You Young
Intense Activity Keeps Telomeres Long. http://www.webmd.com/fitness-exercise/news/20091201/molecular-proof-exercise-keeps-you-young