Comprehensive Library Of Resveratrol News

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  • Resveratrol News Roundup, September 2014

    September 2, 2014: by Bill Sardi

    Arsenic and Resveratrol

    Arsenic is ubiquitous in groundwater supplies throughout the U.S.  The Environmental Protection Agency permits 10 micrograms of arsenic per liter of drinking water.  [US Geological Survey] The health risks posed by small amounts of arsenic have been described.  [] ancer from pooling of arsenic in the bladder has been reported.  [Journal Epidemiology Community Health 2006]  The Environmental Protection Agency habitually over-warns about even the lowest exposure to potentially toxic molecules like arsenic.  Arsenic exposure needs to be reviewed in light of experimental evidence showing low-dose arsenic may activate internal antioxidant defenses in the human body (what is called hormesis).  [Human Experimental Toxicology Nov 2007]  However, health risks associated with accumulated lifetime exposure are unknown.  In regard to arsenic antidotes, resveratrol has recently undergone testing in an animal model of arsenic poisoning and was found to reverse liver damage and elevate antioxidant defenses such as glutathione.  [Biomedical Research International July 2, 2014]

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  • Resveratrol Inhibits Sight-Threatening New Blood Vessels At the Back Of The Eyes While Simultaneously Promoting New Blood Vessels That Repair The Heart After A Heart Attack

    August 29, 2014: by Bill Sardi

    There is a clear dichotomy in the treatment of patients who battle the loss of their vision due to wet (neovascular) macular degeneration while simultaneously attempting to mend scarred muscle tissue after a heart attack.

    This may be a greater problem than realized as ophthalmologists who commonly instill anti-growth factor drugs (anti vascular endothelial growth factor or anti-VEGF drugs) directly into the eye to induce abnormal blood vessels to recede may be completely unaware how many of their retinal degeneration patients have had a heart attack that requires the formation of new blood vessels to heal scarred muscle tissue.

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  • Clears Up Confusion Instigated By ConsumerLab About Whether Orally Consumed Resveratrol Activates The Sirtuin1 Survival Gene

    August 28, 2014: by Bill Sardi


    Does resveratrol really activate SIRT1 – the “longevity” gene? Answer:

    Resveratrol has been shown to activate the SIRT1 gene in the laboratory. However, it is not yet clear if oral supplementation with resveratrol has the same effect. [ posted August 27, 2014]

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  • Update: How To Put Your Anti-Aging Pill To The Test

    August 26, 2014: by Bill Sardi

    Despite the fact a Harvard researcher has recently been quoted to say the secret to halting the aging process is much closer than we think and that “there is no limit on the human lifespan,” [Yahoo News Aug 19, 2014], it is difficult if not impossible to conclusively prove so-called anti-aging pills will produce superlongevity because a 100-year study would be required.

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  • Longevity Seekers: Is This Your Future? Lessons From The World’s Oldest Man

    August 21, 2014: by Bill Sardi

    Sakari Momoi, age 111, is being honored by the Guinness Book of World Records as the oldest man on earth. [The Japan News Aug 21, 2014] His recent photographs don’t serve as motivation for younger adults to surpass his age. The primary reason: he looks old, very old. What youth-seekers really want, to their very last day, is thick hair, smooth skin and “Viagra baby.” They don’t want to look as parched as Sakari Momoi.

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  • Why Your Great, Great Grandchildren May Live Longer By Taking A Longevity Pill Like Longevinex®

    August 3, 2014: by Bill Sardi

    People who have long-lived parents and grandparents often believe they will live exceptionally long too due to inherited longevity.  And now there is evidence for that, but not from the classic inheritability we were likely taught in college biology class.

    This report deals with two biological terms: genotypes and phenotypes.  The genotype is the genetic makeup of an individual and is usually used to explain a particular trait.  When that particular trait is expressed or materializes, then that is known as the phenotype.

    What we inherit are two sets of genetic information.  The first are the better-known inherited traits that emanate from sequences of what are called nucleotides (adenine, guanine, cytosine, thymine amino acids) on the DNA ladder.  An example of a phenotype is hair color or blood type.

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  • Let’s Let Charles Darwin Sort-Out A Modern Debate In Biology

    July 28, 2014: by Bill Sardi

    An immense federal project that involved 440 scientists from 32 laboratories from around the world, a project known as ENCODE, concluded that 80% of the library of human genes (known as the human genome) is biologically functional.  The results of ENCODE were reported in September of 2012 and strong criticism of its “extremely loose definition of ‘biologically functional’ soon followed.”  [Proceedings National Academy Sciences April 2, 2013; Time Magazine Sept 6, 2012]

    ENCODE stunned the world of human genetics at that time as it was believed that only a small fraction (~3%) of genes actually produce proteins.

    Yet in another a scientific reversal, just 22-months later scientists at Oxford University report only 8.2% of our DNA is biologically active.  Oxford researchers say the rest of the genome is leftover evolutionary material that has undergone mutational losses or gains in the DNA code.  [Science Daily July 24, 2014; PLoS Genetics July 24, 2014]

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  • Cancer Investigators Search For Mitochondrial Antioxidants Nature Already Provides

    July 19, 2014: by Bill Sardi

    Researchers at Cold Spring Harbor Laboratory, writing in a recent edition of The New England Journal of Medicine, claim a reason why supplemental antioxidants have failed to consistently reduce the risk for cancer is that they don’t target the precise location where 90% of oxidation takes place – in cellular power plants called mitochondria. [New England Journal Medicine July 10, 2014; Medscape July 11, 2014]

    These researchers are calling for the development of “synthetic” strategies to target the mitochondria and negate the protective effect dietary antioxidants provide cancer cells, ignoring the fact there are many natural antioxidant molecules that already target mitochondria and promote cancer cell death.

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  • The Next Big Thing For Humanity: The First Anti-Aging Drug. But Wait A Minute. Last Year It Was A Nutraceutical.

    July 14, 2014: by Bill Sardi

    The prospect of the world’s first FDA-approved anti-aging drug is now being discussed (again).  Researchers, writing in the journal AGING CELL point to a survival gene, Sirtuin1 (sir-two-in), as the molecular target to achieve extended healthspan and lifespan and a synthetic drug, SRT2014 (Sirtris Pharmaceuticals) that docks-up to that gene to produce health benefits similar to those achieved with restricted calorie diets.

    The first report of aged lab animals maintaining bone (averting osteoporosis) and muscle mass (averting sarcopenia) throughout their lifetime by taking an oral Sirtuin1 activating pill are now reported with the prospect of doing the same in humans. Researchers claim animal experiments demonstrate “that it is possible to design a small molecule that can slow aging and delay multiple age-related diseases in mammals.”  [Aging Cell June 16, 2014]

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  • Researchers Confirm Overmineralization Theory Of Aging With Discovery Sirtuin-3 Gene Controls Iron

    July 7, 2014: by Bill Sardi

    In confirmation of the overmineralization theory of aging Harvard Medical School Researchers report that the Sirtuin-3 survival gene, which has been positively linked with longevity in humans, controls iron metabolism in living cells. [Oncogene June 9, 2014]

    The Sirtuin-3 gene is known as a mitochondrial gene.  There are a few hundred mitochondria in living cells.  They produce cellular energy in the form of adenotriphosphate (ATP).

    By virtue of its ability to control iron the Sirtuin-3 gene reduces oxidation, suppresses tumor growth and helps to renew old mitochondria in a process called mitogenesis.

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