AGING RESEARCH – ARUN’S VIEW 1

Self link
These are notes to self, made available in hope they will attract tough comments, reveal my directions and their reason; are not intended to hurt any views – I am a stoic, perhaps buddhist, consider all not so to be noxious vermin, but see no reason to propagate my views. Some people who can discern scholastic approach to questions (hard stoic but not skeptic) requiring a rational conclusion for all questions rangfing over UNinteresting to besides the point to sophistry if unrational, Rational stoic (not a persistent skeptic!) to distance from pure scientist.

the fellows referenced have a common theme

approach is scientific path to amortality

consider empirical studies on humans to be gold standard

are in possesion of data on models

have narratives on why applicable to humans

experiment on self first

have reasons to believbe they are honest

are not commercially driven (OK after studies only)

hence can be emulated pre-proof

FORGET THE BLOOD OF TEENS. THIS PILL PROMISES TO EXTEND LIFE FOR A NICKEL POP.

 

Nir Barzilai,

Dr. Nir Barzilai is the director of the Institute for Aging Research at the Albert Einstein College of Medicine and the Director of the Paul F. Glenn Center for the Biology of Human Aging Research and of the National Institutes of Health’s (NIH) Nathan Shock Centers of Excellence in the Basic Biology of Aging. He is the Ingeborg and Ira Leon Rennert Chair of Aging Research, professor in the Departments of Medicine and Genetics, and member of the Diabetes Research Center and of the Divisions of Endocrinology & Diabetes and Geriatrics.

Dr. Barzilai’s research interests are in the biology and genetics of aging. One focuses on the genetic of exceptional longevity, where we hypothesize and demonstrated that centenarians have protective genes, which allows the delay of aging or for the protection against age-related diseases. In a Program he is leading we take full advantage of phenotypes, DNA, and cells from the Ashkenazi Jewish families with exceptional longevity and the appropriate controls and his group have established at Einstein (over 2600 samples of which ~670 are centenarians) and discovered underling genomic differences associated with longevity. Longevity Genes Project (LGP) is a cross-sectional, on-going collection of blood and phenotype from families with centenarian proband. LonGenity is a longitudinal study of 1400 subjects, half offspring of parents with exceptional longevity, validating and following their aging in relationship to their genome. The second direction, for which Dr. Barzilai is holding an NIH Merit award that focuses on the metabolic decline of aging, and his team hypothesize that the brain leads this decline. His lab has identified several central pathways that specifically alter body fat distribution and insulin action and secretion by intraventricular or hypothalamic administration of several peptides that are modulated by aging including: Leptin, IGF-1, IGFBP3 and resveratrol.

He has received numerous grants, among them ones from the National Institute on Aging (NIA), American Federation for Aging Research, the Ellison Medical Foundation and The Glenn Medical foundation. He has published over 230 peer-reviewed papers, reviews, and textbook chapters. He is an advisor to the NIH on several projects and serves on several editorial boards and is a reviewer for numerous other journals. Dr. Barzilai is in the board of the American Federation for Aging Research, is its co-scientific director, and has served on several NIA study section. He is also a founder of CohBar Inc., a biotech that develops mitochondrial derived peptides as therapy for aging and its diseases. He is co-PI on the R24 Geroscience (Apollo) grant that is an effort to move the field of aging to translation. Dr. Barzilai has been the recipient of numerous prestigious awards, including the Beeson Fellow for Aging Research, the Ellison Medical Foundation Senior Scholar in Aging Award, the Paul F. Glenn Foundation Award, the NIA Nathan Shock Award, and the 2010 Irving S. Wright Award of Distinction in Aging Research.

He is currently leading an international effort to approve drugs that can target aging. Targeting Aging with METformin (TAME) is a specific study designed to prove the concept that multi-morbidities of aging can be delayed by metformin, working with the FDA to approve this approach which will serve as a template for future efforts to delay aging and its diseases in humans.

Born in Israel, Dr. Barzilai served as chief medic and physician in the Israel Defense Forces. He graduated from The Ruth and Bruce Rappaport Faculty of Medicine at the Technion-Israel Institute of Technology in Haifa and completed his residency in internal medicine at Hadassah Medical Center in Jerusalem. He served in a refugee camp during the war in Cambodia (1979-1980) and built a nutritional village in the homeland of the Zulu (1983 – Kwazulu). He has completed 2 fellowships at Yale (metabolism) and Corenell (Endocrinoology and molecular Medicine). He was an invited speaker to the 4th Israeli President Conference (2012) and a Vatican conference on efforts to enhance cures (2013, 2016). He has also taken part in Global initiatives and spoke at The Milken Global Institute, Asian Megatrends and is an advisor for the Prime Minister of Singapore on Aging. Dr. Barzilai has been on the ‘Forward 50, top 50 influence Jews in the US (2011). His work has been profiled by major outlets, including the New York Times, the BBC and PBS' NOVA science now, TEDx talk Science and is the leading feature on the Ron Howard/Jonathan Silberberg/National Geographic film about the Age of Aging.

 Matt Kaeberlein,

Matt Kaeberlein (born 1971^[1]) is an American biologist and biogerontologist best known for his research on evolutionarily conserved mechanisms of aging. He is currently a Professor of Pathology at the University of Washington in Seattle.

 James Kirkland, and

The major research focus of James L. Kirkland, M.D., Ph.D., is the impact of cellular aging (senescence) on age-related dysfunction and chronic diseases, especially developing methods for removing these cells and alleviating their effects. Senescent cells accumulate with aging and in such diseases as dementias, atherosclerosis, cancers, diabetes and arthritis.

The goal of Dr. Kirkland's current work is to develop methods to remove these cells to delay, prevent, alleviate or partially reverse age-related chronic diseases as a group and extend health span, the period of life free of disability, pain, dependence and chronic disease.

Focus areas

·         Cellular senescence. Dr. Kirkland's team developed the idea that removing senescent cells may enhance health span, partly based on the observation that mice with mutations that increase life span have lower senescent cell burden than normal mice, and that short-lived mice have more of these cells. To test this idea, Dr. Kirkland and his team, in collaboration with others at Mayo Clinic, eliminated senescent cells from genetically modified mice, in which a drug-activated "suicide" gene was expressed only in senescent cells. They found that this process enhanced health span, at least in the context of an accelerated aging-like disease. This gave proof of principle for the notion that clearing senescent cells with a drug in non-genetically-modified individuals might be beneficial. They continue to work on developing interventions that selectively target senescent cells.

·         Diabetes, other chronic diseases and cellular senescence. Diabetes and obesity are associated with accumulation of senescent cells in fat and other tissues. Dr. Kirkland's group is working on ways to reduce severity and alleviate the complications of diabetes by clearing senescent cells or blocking them from producing factors that cause or exacerbate dysfunction. Effects of eliminating senescent cells or the factors they release are being investigated on frailty and a range of other chronic disorders in Dr. Kirkland's laboratory and with collaborators at Mayo and other institutions.

Significance to patient care

Dr. Kirkland's work is important in developing methods to enhance health span and delay onset of the chronic age-related diseases as a group, rather than one at a time. These conditions, including diabetes, dementias, atherosclerosis, cancers and arthritis, among others, account for the bulk of morbidity, mortality and health costs in most of the world.

 David Sinclair 

he Sinclair Lab studies the processes that drive aging and age-related diseases, and works toward discovering methods for slowing down or reversing these processes. Work ranges from dissecting novel pathways and identifying target genes, to assessing small molecules that may slow the pace of aging and increase healthspan. The overarching goal is to establish new biological approaches that can be translated into radically different medicines to promote longer, more productive lives. A focus is on how genetic and epigenetic changes drive aging, common diseases and disorders such as cancer, heart disease, inflammation, neurodegeneration, infertility and diabetes. To advance our studies we use a wide range of genetic, genomic and proteomic tools. In addition we employ several unique mouse models to assess the role of these factors and how well genetic and pharmacological agents may impact them. We are a team with a broad range of skill sets, who work together and complement each other to solve key scientific questions about mammalian biology and human health. Skills in the lab range from enzymology and biochemistry, to genetics, genomics, proteomics and systems biology.

Their recommendations compress to two – metformin and NMN. I add a third - MITOQ. Here is my reasoning – pointless to debate but med MD-PhD. ALL life is cellular, all animals age. So aging is cellular – mitochondria based. MITOQ feeds COQ10 to Mitochondria bypassing all, to be greatly bio-available. No wittig-like Carrier for NMN or metformin. Metformin good for actual diabetic and aging pseudo-diabetics. Insulin promotes aging as do high sugars! Sublingual administration of 500 mg of NMN per day is twice the dose taken by Sinclair! Metformin is dirt cheap. MITOQ is $1 per day, so is NMN. That plus NMN and exercise is to be given up, if no benefits in 3 month. The drugs should enable you to do exercise! If you attribute your health to exercise, don’t forget what enabled you!