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Written by
Sabrina Freudenmann
In 2009 the Nobel Prize in Physiology or Medicine was awarded jointly to Elizabeth H. Blackburn, Carol W. Greider and Jack W. Szostak “for the discovery of how chromosomes are protected by telomeres and the enzyme telomerase.”
Inside the nucleus of a cell, our genes are arranged along twisted, double-stranded molecules of DNA called chromosomes. At the ends of the chromosomes there are cap like structures of DNA called telomeres. These telomeres protect our genetic data and make it possible for our cells to divide.
Telomeres have been compared with the plastics tips on shoelaces, because they keep chromosome ends from fraying and sticking to each other, which would destroy or scramble an organism’s genetic information. Not exactly something we want! Overtime, due to ongoing cell division telomeres actually shorten in length. Telomere length appears to be an indication of age and the general health status of an individual.
The enzyme called telomerase is counteracting this process by delaying or even reversing the cellular aging process. Telomerase can lengthen the telomeres by adding back lost DNA. Unfortunately, the enzyme is insufficient to completely restore the lost DNA of the telomeres and therefore cannot fully stop cellular aging. The enzymes task is to slow down cellular death/aging but doesn’t have the capacity to immortalise cells. It has been observed that accelerated telomeres shortening is associated with premature aging with increased organ deterioration and a shortened patient lifespan.
Humans with shorter than average telomere length are at an increased risk of heart disease, stroke or infection. Individuals with chronic stress or infections have accelerated telomere shortening compared to age-matched counterparts.
Why is our telomere length such a good predictor of longevity when too much telomerase can be bad?
While increased telomerase activity could bring youth to aging cells too much of it can be damaging for an individual. Just as youthful stem cells use telomerase to offset telomere length loss, cancer cells employ telomerase to maintain their aberrant and destructive growth. Augmenting and regulating telomerase function will have to be performed with precision, walking a narrow line between cell rejuvenation and a heightened risk for cancer development.
Therefore, drug development to increase indiscriminately telomerase activity isn’t desired at all.
Telomere lengths measured can reflect our genetic makeup but also the history of a cell. Our environment also plays a major role in regulating telomeres. If our cells are exposed to a lot of stress and injury – even at a young age – then they are forced to divide more often and shorten their telomeres.
Oxidative stress, stress hormones and inflammatory stress are all factors which will cause strain on a molecular level, subsequently damaging proteins and other essential components of a cell.
Prolonged inflammation, for example, can cause cells to activate a cell-death program. Recent studies in mice have shown that activation of inflammation pathways in the brain can suppress cognitive function, muscle strength and overall longevity. All of these stressors are often interconnected and therefore causing premature aging of cells.
How do these stressors lead to premature aging? The shortening of telomeres could be a major factor in aging. However, the molecular understanding of cellular aging is ultimately more complex and many pathways are responsible for aging and disease. So whatever we do to minimise stressors will stimulate telomerase activity or at least hinder premature aging.
Here are some factors that research has discovered to be linked to telomere length and telomerase activity:
A diet which contains fresh vegetables and fruits (high antioxidants), low sugar and unprocessed meats is associated with longer telomeres.
Several different extracts from the Astralagus membranaceus root have been documented to activate telomerase activity in human T cells.
Resveratrol has been shown to activate telomerase in epithelial an endothelial progenitor cells.
Researchers from the University of California studied more than 600 patients and found that the higher the blood levels of fish-derived omega 3 acids in patients with coronary heart disease, the longer the telomeres.
Furthermore, higher vitamin D concentrations, which are easily modifiable through nutritional supplementation were found to have longer telomere length.
A 2008 study published in the Archives of Internal Medicine of more than 2400 twins compared the telomere length in those that exercised versus the sedentary ones. After one year, they found – based on telomere length – that those who exercised were biologically younger than those who didn’t. The telomeres of the most active subjects were 200 nucleotides longer than those of the least active subjects.
“The good news is you don’t have to go to the gym three hours a day or run a marathon a week. People who do moderate aerobic exercise – about three times a week for 45 minutes – have telomeres pretty much as long as marathon runners. Mixing things up seems to be good too. One study showed the more different kinds of exercise people did, the longer their telomeres. Many studies looking at people under severe chronic stress find their telomere shortness relates to how severely that stress is experienced. But that relationship seems particularly strong in sedentary people. Even 10-15 minutes of light exercise daily appeared, in one study, to buffer the effect.”
The Telomere Effect: A Revolutionary Approach to Living Younger, Healthier, Longerby Dr. Elizabeth Blackburn and Elissa Epel
Some forms of meditation, which reduce stress and increase positive mindsets and well-being are able to lengthen telomeres.
Telomeres length is associated with chronic inflammation so anything that lowers inflammation will indirectly influence telomere length and reduces aging.
A healthy diet, frequent exercise and a low everyday stress profile has been associated with a healthier inflammatory status as many studies have shown. As stated above, the same lifestyle factors are also connected with longer telomeres and/or higher telomerase activity while psychiatric disorders, obesity, etc. are associated with deregulated telomere/telomerase physiology.
A German study in 2002 showed that higher levels of extracellular superoxide dismutase (a crucial antioxidant) slowed telomere shortening thus mellowing the aging process. Ozone stimulates superoxide dismutase production, protects and promotes greater telomerase activity. But that’s not all, ozone increases nitric oxide – a powerful vasodilator in our endothelial cells.
These are the cells that line our arteries. And higher nitic oxide levels increase telomerase activity.
Repetitive ozone treatments have been shown to act as a potent anti-oxidant to boost telomerase activity, protect the mitochondria from damage of free radicals and therefore prevent DNA deterioration.
As Dr. Rowen said in a recent interview: “The best anti-aging medicine is a healthy diet, proper detoxification, reduced stress levels and Ozone therapy.”
References:
Effros, R. B., & Valenzuela, H. F. (2013). Functional Assessment of Pharmacological Telomerase Activators in Human T Cells, 57–66. https://doi.org/10.3390/cells2010057
Shin, D., Shin, J., & Lee, K. W. (2019). Effects of Inflammation and Depression on Telomere Length in Young Adults in the United States.
Passos, F., Oakley, F., Correia-melo, C., Greaves, L., Jurk, D., Wilson, C., … Zglinicki, T. Von. (2014). Chronic inflammation induces telomere dysfunction and accelerates ageing in mice, (May). https://doi.org/10.1038/ncomms5172
Ayse Gul Mutlu. (n.d.). Telomerase Inhibitors and Activators: Pharmaceutical Importance. https://doi.org/http://dx.doi.org/10.5772/65933
Investigation, O. (2015). The Association Between Physical Activity in Leisure Time and Leukocyte Telomere Length, 168(2), 154–158.
Richards, J. B., Valdes, A. M., Gardner, J. P., Paximadas, D., Kimura, M., Nessa, A., … Aviv, A. (2007). Higher serum vitamin D concentrations are associated with longer leukocyte telomere length in women 1 – 3, 1420–1425.
Blackburn, E. (2011). NIH Public Access, (415), 34–53. https://doi.org/10.1111/j.1749-6632.2009.04414.x.Can
Diseases, I., Kordinas, V., Ioannidis, A., & Chatzipanagiotou, S. (n.d.). The Telomere / Telomerase System in Chronic. https://doi.org/10.3390/genes7090060
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