The Roles of Telomeres and Telomerase in Attaining the Full Life Span of 120
By Edmund Chein
Palm Springs, California
April 8, 2014 6:22am CST
Telomere length is one of the best indicators of aging. This is true of any organism at any age, including humans, and it is the reason why telomere length is such an effective way to estimate the biological age. To take this a step further, we need to understand that all humans do not have telomeres of ideal length—if we did, we would all live to 120 . . . or longer. Telomeres shorten (erode progressively, to use more scientific terminology) as a result of cumulative cycles of cell regeneration over the course of an organism’s lifetime. That is, telomeres become shorter as we age. Therefore, lengthening our telomeres is the most effective way to live longer and in better health. The best way to lengthen telomeres is to activate telomerase, the enzyme that maintains and repairs them. However, in addition to enabling longevity, telomeres and telomerase play a significant role in cancer biology. More than 95 percent of all types of malignant tumors activate telomerase during their formation; as a result, telomerase is considered necessary to sustain cancer growth. Scientists have begun clinical trials and tests exploring ways to inhibit telomerase activity, and breakthroughs are likely to be forthcoming. This is important information to know, but even more important is our understanding that the therapeutic modality and medical method recommended in this book are not known to increase cancer risk. Medical studies continue to show that short telomeres are responsible for causing aging, as well as age-related disease and debilitation. Without telomerase repair, critically short telomeres can—and will—severely harm the cell, often causing permanent damage. Because every cell has telomeres capping the ends of the chromosomes in its nucleus, it’s essential to determine telomere length. A majority of short telomeres in an individual will result in premature aging, disease (particularly a greater risk of developing problems with the cardiovascular and central nervous systems), and failure to attain the full life span. Of course, lifestyle and genetics are also key factors that contribute to aging and disease. And, not surprisingly, obesity, smoking, psychological and emotional stress, and other unhealthy states of being and habitual behaviors all contribute to telomere shortening. These behaviors and states increase physical stress, harm the immune system, and create inflammations—factors all known to contribute to decreased well-being and shorter life spans. Conversely, diet (nutrition and supplementation), exercise, and sleep all can decrease the effects of stress, strengthen the immune system, reduce the amount of inflammations in the body, and inhibit telomere shortening. A majority of short telomeres in an individual will result in premature aging, disease, and failure to attain the full life span. To underscore its importance, let’s reemphasize that healthy diet (with appropriate supplementation); regular exercise (appropriate for existing health conditions); sufficient sleep (seven to nine hours a night); and positive supporting habits (meditation, yoga, breathing exercises, journaling [see part 2]) all will encourage better health—to a great extent by limiting telomere shortening. Thus, by promoting telomere lengthening through telomerase activation, we can further improve these results. (Again, we will explore the method in greater detail in chapter 5). As the foregoing clearly shows, telomeres are the key to longevity—to attaining the full life span of 120. It’s as simple as that. Medical Studies That Support the Benefits of Telomerase Activation As stated above, there had been some speculation within the medical/scientific community that lengthening telomeres in normal human cells could potentially increase the risk of cancer. However, studies over the last ten years have consistently refuted these doubts. Several publications by Jerry Shay and Wooding Wright at the University of Texas Southwest Medical Center, as well as Calvin Harley, who reviewed 86 publications on the relationship between telomerase and cancer, concluded that (1) telomerase was not a cancer-causing oncogene, and (2) telomerase did not cause cells to lose growth control and become cancerous.10 In 2001, Drs. Keith Williams and Kimberly Boggess at the University of North Carolina demonstrated that progesterone (not progestin or medroxy-progesterone) inhibits endometrial telomerase.11 (The findings and conclusions of Drs. Williams and Boggess validated my own long-standing position that progesterone prevents breast, uterine, and prostate cancers.) In 2005, Dr. Gomez Sanchez and his group at La Paz University in Spain showed that the growth hormone directly activates telomerase.12 Also in 2005, Dr. Michael Sheppard affirmed, “Growth hormone therapy does not induce cancer.”13 Again in 2005, the California—based biotech company Geron discovered and patented TA-65, a telomerase activator. (The New York-based supplement company T.A. Sciences manufactures TA-65, which is made from the Chinese herb Astragalus membranaceus.*) In 2007, Dr. Scott Brouillette and his group in Scotland demonstrated that telomere length is a predictor of the onset of coronary disease.14 In 2008, Dr. L. Kaszubowska at the University of Gdnask in Poland showed that centenarians have long telomeres in their lymphocytes (cells of the lymphatic system, most notably white blood cells).15 (Dr. Kaszubowska’s findings and conclusions proved my own long-held position that lengthening telomeres does not cause cancer.) In 2009, a joint study by Georgetown University and the National Cancer Institute concluded that short telomeres lead to chromosome instabilities, which in turn lead to cancer.16 Also in 2009, Dr. H. Xu and his group at the National Human Genome Research Institute (part of the National Institutes of Health [NIH]) demonstrated that the use of multivitamins is associated with longer telomere length among women.17 Needless to say, the most significant achievement of 2009 was the already mentioned awarding of the Nobel Prize in Medicine to Drs. Blackburn, Greider, and Szostak for their telomere and telomerase research.18 In July 2010, an international team of scientists compared telomere length with incidences of cancer in 787 patients, finding that those patients who had short telomeres had three times the incidence of cancer as patients with long telomeres. These researchers suggested that keeping telomeres at their optimal length through telomerase activation could likely prevent cancer.19 During this time frame, Dr. Maria Blasco continued her studies on mice. A prolific scientist who heads the Telomeres and Telomerase Group at the Spanish National Cancer Research Centre, Dr. Blasco concluded that in the group of genetically engineered mice studied, TA-65 rescued cells in jeopardy and improved health without increasing cancer incidence (a risk when cells can divide for longer periods of time). In her study, a group of middle-aged and old mice ate food enhanced with TA-65, while the control group ate plain food. After three months, Blasco’s team took blood samples from both groups in order to measure telomere length. Sure enough, the mice that ingested the TA-65 had a lower percentage of “very short telomeres.” However, the changes did not last, overall longevity did not change, and average telomere length of the treated mice did not change.