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  • Inhibit One Gene Among 25,000 And Add 12 Years To Your Lifespan & Healthspan

    January 28, 2015: by Bill Sardi

    Researchers have added 15% to the lifespan of laboratory mice by deleting the second copy of a tumor-promoting gene known as MYC.  In human equivalent terms if that could be done in humans it would add about 12 more healthy years to the lifespan of Homo sapiens.

    The problem is we can’t remove a copy of the MYC gene from every cell in the human body.  But we can inhibit the activation (gene protein-making) of the MYC gene and possibly achieve the 12 extra years of life like the lab mice did.

    Such a powerful effect from just one gene is a headline news story today.  Inhibition of MYC increased male lifespan by 10% and female lifespan by 20% (15% average).

    As background information, the size of the human and mouse genome (library of genes) is about the same – 25,000.  The mouse and human genomes are homologous, that is, presented in a similar order.  Networks of genes are switched on or off (expressed or silenced) as aging progresses.  So the biological impact of deletion of a second copy of just one gene is quite remarkable.

    Even more extraordinary is these MYC-inhibited mice were far healthier.  The bones were not withering with advancing years.  Striking graphic images of this effect are reproduced (above) in this report.

    All of the organs and tissues in these mice aged slower.  These MYC-inhibited mice were smaller but otherwise suffered no other untoward consequences, exhibiting strong mating activity in old age!  (Here, here!)  This is in contrast to calorie-restricted diets whose anti-aging effects are offset by reduced ability to reproduce.

    As they aged these mice did not develop bone loss (osteoporosis), their immune system remained responsive and they had less scarring (fibrosis) in heart muscle tissue.  They were more active and maintained their balance on a rotating rod longer compared to mice whose redundant MYC gene was not deleted. [Science Daily Jan 26, 2015]

    However, the crossover of common genes activated by the anti-diabetic drug metformin, and the red wine molecule resveratrol and a calorie-restricted diet, all known as anti-aging strategies, was not remarkably similar to that of the mice with the deleted MYC gene.

    Genes Crossover

    Cross-over of genes activated or inhibited by various anti-aging agents (metformin anti-diabetic drug, a calorie-restricted diet or the red wine molecule resveratrol) compared with laboratory mice with a deleted MYC gene.

    Despite that finding, resveratrol has been widely reported to inhibit the MYC gene. [Toxicological Applied Pharmacology March 1, 2012]

    MYC is known to be abnormally active in cancer.  [Oncogene Feb 20, 2014] In fact, MYC is considered one of the most potent activators of cancer. [Cell Cycle Dec 15, 2010]

    Researchers have reported the demonstrable manner in which resveratrol controls Myc in a report entitled: “C-Myc down-regulation: a critical molecular event in resveratrol-induced cell cycle arrest and apoptosis of human medulloblastoma cells.”  This report suggests inhibition of the Myc gene by a widely available natural molecule (resveratrol) demonstrably halts the growth of brain tumors (medulloblastoma).  [Journal Neurooncology Nov 2006]

    It is interesting to learn what overactivates this gene – metallic minerals such as iron and copper that tend to accumulate in living tissues with advancing age.

    Here is just some of the evidence that metals over-activate the MYC gene:

    • MYC activation induces loss of control iron, a major growth factor for tumor cells. [Science Jan 29, 1999]
    • Increased Myc activity would lead to increased intracellular concentrations of iron essential for tumor cell growth. [Oncogene May 13, 1999]

    It is not like scientists don’t know how to de-activate or suppress the MYC gene.  Mineral controlling molecules called chelators (key-lay-tors) switch off the MYC gene.  Here is some of the evidence:

    • A copper chelating, iron controlling metal chelator can decrease the growth of cancer by inhibition of MYC. [Cancer Research Feb 1, 2001]
    • In a form of cancer called neuroblastoma the cancer promoter gene MYC is inhibited by iron and copper chelators. [com]
    • An iron chelator is documented to inhibit the spread (metastasis) of liver cancer via the MYC gene. [Oncotarget Sept 2014]
    • In one study just 50% reduction of MYC gene expression resulted in a greater than 10-fold reduction in susceptibility to tumor-promoting (RAS) proteins. [Cancer Research Feb 1, 2001]

    So it is not completely unexpected that the deletion or inhibition of this gene would be reported to increase the lifespan and healthspan of laboratory mice.  [Cell Jan 26, 2015]  Nor is it surprising to find resveratrol as a copper chelator inhibits the MYC gene. [Biochemical Pharmacology May 9, 1997]

    Twelve more healthy years is not the superlongevity (120 healthy years) promised by molecularly mimicking a calorie restricted diet, but I don’t think there is human living into old age who wouldn’t want to remain healthy and independent AND continue to actively mate with the opposite sex.  This recently published report serves to provide further evidence for the overmineralization theory of aging. [] © 2015 Bill Sardi,

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