Re: [GRG] are short telomeres a cause or a result of aging?

Dear GRG,

Further to the conversation about short Telomeres, Josh Mittledorf has published an excellent article on his blog that details a new human hTERT and Myostatin therapy from Bioviva! This is very big news indeed.

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From: Dr. Harold Katcher To: Gerontology Research Group ; Sent: Tuesday, 17 March 2015, 19:02Subject: Re: [GRG] are short telomeres a cause or a result of aging?

Wow C David!
That’s an awful lot of good data you provide us. Of course that’s your field of expertise – but it definitely rules out telomere length as a function of cell divisions alone. Endurance training (reminds me to go the the gym today) up-regulated telomerase  and endurance-trained older adults have longer telomeres on the leukocyte chromosomes. So endurance training seems to me more likely to cause the production of new blood cells from hematopoietic progenitor cells (a few thousand in people) – and that should accelerate telomere attrition?  And yet telomeres are longer.  That endurance-trained older adults have longer telomeres  could be explained by say the elimination of short-telomere-ed cells through rough usage. But the induction of telomerase in the heart with endurance training explains that it is the addition onto extant telomeres that is the cause – probably. So where in the heart was telomerase expressed (and how did they know)? In the cardiac stem cells self-renewing? (That would be nice.) The fact that leukocyte telomere length is preserved in endurance trained adults is both encouraging and discouraging ; encouraging, because we, with our own efforts, can affect our lifespan length, and discouraging because endurance-trained adults do not live appreciably (in terms of multiples of the normal lifespan (as in C. elegans – where we can produce a ten-times normal lifespan by mutations to nutrient receptors and sensors)), longer.  I think the telomere length is more important in keeping certain populations of cycling cells at certain levels – tissue homeostasis, but it clearly is responsible for some diseases of aging as numbers of cells reach replicative senescence send signals throughout the body and convert to senescent cells and increase the body’s inflammation. Or they die (apoptose – is that a verb?) and so lead to cytopenia. So I don’t think telomere attrition is the cause of aging – again there exists a remedy for it (telomerase) and the fact that it’s not used can have two explanations: 1) that it cannot be used, because say a mutation has eliminated the telomerase TERT gene, or 2) that it is simply not called upon after what would normally be self-renewal to keep the telomeres long. The likelihood that the TERT genes are randomly knocked out by mutations (while most other genes are not) – or made inaccessible by epigenetic mutations – again while other genes are not- in all stem cell populations at particular adult lifestages – is about as likely as tossing a quarter and having land on its edge. So explanation 2) is the correct one – the cell has functional telomerase but doesn’t use it. Why not  – did it ever – in young bodies, when stem cells self-renew, do they use telomerase to maintain their telomere lengths? I believe they do, but eventually do not in aging. If that is the case why do they stop? My own thinking leads me to the conclusion that they are either ordered not to, or lose their orders to do so. In either case I think their environments determine this. I believe this is non-cell autonomous. 




About Johnny Adams

My full-time commitment is to slow and ultimately reverse age related functional decline to increase healthy years of life. I’ve been active in this area since the 1970s, steadily building skills and accomplishments. I have a good basic understanding of the science of aging, and have many skills that complement those of scientists so they can focus on science to advance our shared mission. Broad experience Top skills: administration, management, information technology (data and programming), communications, writing, marketing, market research and analysis, public speaking, forging ethical win-win outcomes among stakeholders (i.e. high level "selling"). Knowledge in grant writing, fundraising, finance. Like most skilled professionals, I’m best described as a guy who defines an end point, then figures out how to get there. I enjoy the conception, design, execution and successful completion of a grand plan. Executive Director Gerontology Research Group (GRG). Manages Email discussion forum, web site, meetings and oversees supercentenarian (oldest humans, 110+ years) research. CEO / Executive Director Carl I. Bourhenne Medical Research Foundation (Aging Intervention Foundation), an IRS approved 501(c)(3) nonprofit. Early contributor to Supercentenarian Research Foundation. Co-Founder Geroscience Healthspan Forum. Active contributor to numerous initiatives to increase healthy years of life. Co-authored book on conventional, practical methods available today to slow the processes of aging – nutrition, exercise, behavior modification and motivation, stress reduction, proper supplementation, damage caused by improper programs, risk reduction and others. Fundamental understanding of, and experience in the genomics of longevity (internship analyzing and curating longevity gene papers). Biological and technical includes information technology, software development and computer programming, bioinformatics and protein informatics, online education, training programs, regulatory, clinical trials software, medical devices (CAT scanners and related), hospital electrical equipment testing program. Interpersonal skills – good communication, honest, well liked, works well in teams or alone. Real world experience collaborating in interdisciplinary teams in fast paced organizations. Uses technology to advance our shared mission. Education: MBA 1985 University of Southern California -- Deans List, Albert Quon Community Service Award (for volunteering with the American Longevity Association and helping an elderly lady every other week), George S. May Scholarship, CA State Fellowship. BA psychology, psychobiology emphasis 1983 California State University Fullerton Physiological courses as well as core courses (developmental, abnormal etc). UCLA Psychobiology 1978, one brief but fast moving and fulfilling quarter. Main interest was the electrochemical basis of consciousness. Also seminars at the NeuroPsychiatric Institute. Other: Ongoing conferences, meetings and continuing education. Aging, computer software and information technology. Some molecular biology, biotech, bio and protein informatics, computer aided drug design, clinical medical devices, electronics, HIPAA, fundraising through the Assoc. of Fundraising Professionals. Previous careers include: Marketing Increasing skill set and successes in virtually all phases, with valuable experience in locating people and companies with the greatest need and interest in a product or service, and sitting across the table with decision makers and working out agreements favorable to all. Information Technology: Management, data analysis and programming in commercial and clinical trials systems, and bioinformatics and protein informatics. As IT Director at Newport Beach, CA based technology organization Success Family of Continuing Education Companies, provided online software solutions for insurance and financial professionals in small to Fortune 500 size companies. We were successful with lean team organization (the slower moving competition was unable to create similar software systems). Medical devices: At Omnimedical in Paramount CA developed and managed quality assurance dept. and training depts. for engineers, physicians and technicians. Designed hospital equipment testing program for hospital services division. In my early 20’s I was a musician, and studied psychology and music. Interned with the intention of becoming a music therapist. These experiences helped develop valuable skills used today to advance our shared mission of creating aging solutions.
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