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Book Title:



The Telomerase Revolution


Michael Fossel
Ben Bella Books

Why do we age? — There have been many theories of aging. The followings are a short list of the feasible causes: free radicals, mutations, waste-product accumulation, cross-linkage, errors of repair, wear and tear, aging by design for evolution, etc.

Cells were once considered to be immortal since Alexis Carrel grew cells from a chicken heart and found no signs of cell aging. Carrel's theory stood undisputed for decades. — But it was wrong; new cells were inadvertently introduced in his experiment. In the early of 1960s, Leonard Hayflick showed that cells divide a finite number of times and reach a scenesent state in which they will no longer divide and become quiescent or die. Because of this finite times of cell division, human lifespan has been limited to about 120 years so far. As we age, we humans encounter a plethora of age-related diseases: Alzheimer's disease, atherosclerosis, osteoporosis, osteoarthritis, skin aging, immune aging, heart attacks, strokes, and cancers. We have been struggling to cope with those age-related diseases without much success.

By the turn of the 21st century, knowledge of a telomere and telomerase had been accumulated. Telomeres consist of a repeated sequence of nucleotides TTAGGG, in mammals, at the both ends of DNAs. Since a sequence TTAGGG does not correspond to any protein or enzyme, it was once considered to be a junk DNA. But since DNA polymerases cannot replicate all the nucleotides to the end of telomeres that they can't hold, telomere shortening occurs every time cells divide and duplicate DNAs — losing a portion of telomeres, thereby protecting DNAs. That is a role of telomeres. About 15000 telomeres at birth become shorter and shorter after each division, and cells finally become scenesent when telomeres become about five to six thousand bases. Thus, Hayflick limit is represented by nothing but a ticking biological clock of telomere shortening, for which we could do nothing. On the other, it was known that telomeres are reset in stem cells and germ cells through activated telomerase gene. Telomerase was shown to exist by Elizabeth Blackburn and Carol Greider, who were awarded the Nobel Prize in medicine and physiology for their work on telomerase in 2009. (Incidentally, Shinya Yamanaka was awarded the Nobel Prize for iPS cells in 2012. iPS cells will be used to develope tissues and organs for replacement.)

Shown in the publication disclosed in 1999 by a biotechnology company Geron, when telomerase was used to reset telomere length in an old cell to a length typical in a young cell, the old cell became indistinguishable from a young one. In short, changes in telomere length did not simply correlate with cell aging, but they were responsible for cell aging, and they could be reset by activating telomerase gene. Telomerase genes are turned on in stem cells and germ cells, but turned off in our somatic cells. In the few years immediately following the turn of the century, several experiments showed that researchers could reverse aging both in cells and in the tissues made from those cells. Similar results occur with human vascular and bone cells, using old cells to grow young vascular tissue and using old human bone cells to grow young bone tissue. In all cases, when we restore telomere lengths to the lengths seen in young cells, we can grow young cells from old cells; tissue that looks and functions like young tissue.

From these evidences, Michael Fossel proposed the telomere theory of aging in the cells as the fundamental cause of all age-related diseases, and currently searches for the effective intervention by the telomerase therapy. He states as follows:
We now have the knowledge and the ability to intervene in aging and its diseases. Strangely, few people are aware of the changes that have already been underway for the past two decades. Over the next decade, we began the first trials of oral agents that promised to at least partially reset the aging process at the clinical level in human beings. Reversing aging has been accomplished by re-lengthening the telomeres, thereby resetting the pattern of gene expression, resulting in healthier and younger function not only in tissues, but for the entire organism.

By actually reversing aging, we extend lifespan and we will drastically cut the costs of medical care, erasing the need for nursing homes, preventing age-related diseases, and leaving people healthy, whole, and fully capable of living their lives completely. We have done almost everything we can to increase lifespan for the aging; the only way to further increase human lifespan is not to prolong disabilities, but to improve health.

If we reverse aging, and if we can prevent age-related diseases, then how long will we actually live? That is difficult to predict. We won't really know until long after we begin to prevent aging — until people have lived as long as they will, whatever that might be. Given what we do know of human biology and clinical medicine, and from the little information we have from animal models and tissue experiments, we can make a guess. Within the next decade or two, the projected mean human lifespan may very well move into the range of several centuries of active, healthy life, with far better control of diseases such as cancer, Alzheimer's, and atherosclerosis. We are about to change human medicine — as well as our lives and our society — forever.

We don't know what happens to the medical segment related to telomeres and telomerase activation in the next decades, but if 100% activation of telomerase gene or telomerase is achieved through whatever safe means — a drug: 'elixir of life', viral vectors, telomerase protein, mRNA, or gene editings, a new human history may well begin with healthy and long human lifespan. A wonderful thing is that this is neither a science fiction nor a mantra, but a telomere science based on concrete evidences. The implications are truly profound as connoted in the title.

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Although telomerase activation in human tissues and small animals had been observed, there had been no human trials until Sept. 2015, when Liz Parrish dared to inject hTERT into her body by use of viral vector. It was reported as follows:
In September 2015, telomere data taken from Parrish's white blood cells (leukocytes) at SpectraCell's testing laboratory in Houston, Texas, immediately before therapies were administered, revealed that Parrish's telomeres were unusually short for her age: 6.71kb. When the same test was taken again in March 2016, telomere length was found to be 7.33kb, which implied that telomeres of Parrish's white blood cells have become longer, meaning biologically younger about 20 years in only 6 months. When she had her telomere length examined again in 2018, it was found that her telomeres further increased from 7.33kb in 2016 to 8.12kb in 2018 --- without any additional treatment. She said that the outcome exceeded her expectations, with no adverse effect, such as cancer --- the alleged danger with activating the telomerase enzyme since cancer cells have hyper-activated telomerase genes for their own survival. But, because stem and germ cells have activated telomerase genes, Michael Fossel insists that there be no danger (--- otherwise, babies are born with cancers) and stabilized cells' functions rather prevent cancers.
Liz Parrish also stated that although the exciting telomere length improvement was shown in her white blood cells, she doesn't yet know if it is happening in all cells inside her body. The precisely tuned dose might be or must be determined through a series of examinations.