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  • Humans Would Live 600 Years If Aging Process Could Be Halted

    June 30, 2017: by Bill Sardi

    A debate broke out recently between biologists who study human aging.  One side of the argument claims the number of people reaching a theoretical maximum lifespan (~115 years) has not increased.  On the other side of the argument biologists argue there is no scientific support for the claim the maximum lifespan is fixed ~115 years.  [Nature June 29, 2017]

    Between 1969 and 1995 there was an uninterrupted increase in maximum reported age at death.  But that advance in longevity appears to have reached a plateau.

    Limitless lifespan

    But in recent times biologists have begun to recognize a limitless or indefinitely long human lifespan is biologically achievable, though they have stopped short of predicting biological immortality.

    Yet Johnny Andersen, an anti-aging investigator, says extreme life extension is probably only 15-25 years away. [Quora.com Feb 17, 2017]  He notes that 80-year olds now have a 95% chance of blowing out the candles on their 81st birthday cake.

    Andersen says immortality is impossible because of accidental death.  “But cure aging and the average lifespan would be ~600 years,” he writes.  Life insurance actuaries agree with Andersen, saying the removal of aging as a cause of death would produce indefinitely long survival.

    Andersen says while anti-aging medicine is moving tremendously fast, longevity seekers would likely need to travel overseas to avail themselves of any such breakthroughs as the US Food & Drug Administration and the Medicines & Healthcare Products Regulatory Agency in the UK move at a snail’s pace and demand endless trials before they place their imprimatur on any anti-aging pill.

    But precisely what new synthetic molecules is pharmacology going to cook up that can exert a stronger anti-aging effect than natural molecules that already exist?  Humanity may not have to wait at all.

    New pathway: “road to immortality”

    A new biological pathway in the arms race to produce superlongevity has now been identified and one recent landmark report is saying it is a “road to immortality.”

    Longevity hounds have certainly become familiar with the Sirtuin1 survival gene incomparably activated by the red wine molecule resveratrol, mTOR inhibitors like the anti-autoimmune drug Sirolimus (rapamycin), or the Klotho gene activated by vitamin D.  But a new “road to immortality” has been discovered, transposon inhibitors.

    Transposons or “jumping genes” were first identified in the 1940s by Barbara McClintock.  They were once classified as junk DNA.

    Transposons (a sequence of DNA) can transpose themselves and change their position within the library of ~25,000 human genes (genome) and therefore alter a cell’s genetic identity and genome size.  Transposons can create or reverse genetic mutations.

    Since transposons induce gene mutations usually by inserting themselves in the wrong position on the DNA ladder, they lead to cell death that biologists surmise is a protection against cancer.

    The human genome must be protected from transposons or gene mutations will run wild.

    Transposons are controlled by microRNA.  [International Journal Molecular Science July 31, 2013]  MicroRNA are small strings of nucleotides (steps on the DNA ladder). (See diagram below)

    More specifically it is short interacting microRNA (PIWI microRNA) that control transposons. [Advances Experimental Medicine Biology 2016]

    Geneticists explain that the age-related disintegration of the human genome (library of genes) that results from “jumping genes” (transposons) is “silenced” (i.e. blocked) by PIWI MicroRNA.  [Cellular & Molecular Life Science May 2015; Molecular Reproduction & Development Aug 2013]  The PIWI MicroRNA pathway appears to play a critical role in cellular immortality.  [Aging Cell June 27, 2017]

    Inactivation of the process of that produces gene mutations via MicroRNA slows the rate of aging.  A key feature of aging is instability of the genome (unrepaired mutations).  Mutations can emanate from nucleotides being inserted in the wrong order or being absent entirely.  These are mutations of insertion or deletion.  Genomic instability increases with advancing age in the adult year.

    Transposons (“jumping genes”) can result in the disintegration of DNA and can overwhelm the DNA repair system.

    Biologists don’t often use the word “immortality.”  Here it is used accurately.  This mechanism is a big deal in the pursuit of longevity.  If cells mutate, grow old and die off, premature aging results.

    While biological aging may not be completely halted, apparently humans are living far short of their plausible lifespan (70-90 years vs. ~600 years) solely due to the aging process.  A major biological process has been uncovered (transposons) that destabilize DNA.  Block that process and biologists theorize cellular immortality.

    Nature’s pharmacy: small molecules control transposons

    Small molecules (polyphenols) found in apple peel (phloretin), pomegranate, grape skins (resveratrol), onions (quercetin), and spices (curcumin) are small molecules that can activate microRNA.  [Molecules Sept 21, 2016; Current Pharmaceutical Biotechnology 2014]

    Longevinex® is the only branded resveratrol-based nutraceutical that has been tested for microRNA activation.

    Longevinex® exhibits a unique influence over microRNA in a demonstrable manner over plain resveratrol.   Longevinex® was tested after an experimentally induced heart attack in laboratory animals.  Here is the comparison between resveratrol and Longevinex® on a microRNA basis.

    ACTIVATION OF MicroRNA BY RESVERATROL & LONGEVINEX®

    Fold change of selected microRNA

    Heart attack

    No treatment

    Heart attack +
    Resveratrol

    Heart attack + Longevinex®

    microRNA 539

    + 214.3

    +172.4

    +314.6

    microRNA 20b

    – 112.9

    – 189.0

    – 1366.0

    microRNA 21

    – 4.0

    +61.5

    + 59.3

    Source: PLoS One 2010

    Over 90% of the influence of Longevinex® over microRNA was exerted on a single microRNA 20b which inhibits the hypoxia inducing factor (HIF-1) gene, a gene that induces cells to cease using oxygen for energy and inhibits vascular endothelial growth factor (VEGF) that limits the formation of new abnormal blood vessels (angiogenesis or neovascularization) that facilitate solid tumor growth and destruction of the visual center the back of the eyes (macula).  [PLoS One Oct 29, 2009] Longevinex® may be the most powerful anti-angiogenesis agent ever tested.  ©2017 Bill Sardi, ResveratrolNews.com

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