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How the world got lost on
the road to an anti-aging pill
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August 30, 2011: by Bill Sardi
They die, one every minute.
A sudden blockage of blood circulation in one or more coronary arteries results in damage to heart muscle that many cannot survive.
They represent as many as 1 in every 6 deaths in the U.S.
They are American adults whose lives should have been saved but weren’t.
There are 16 million of them at high risk who have been diagnosed with coronary artery disease.
The baby aspirin tablets, the statin cholesterol-lowering drugs, the streptokinase clot busters and inserted catheter balloons that break up clots in coronary arteries aren’t saving as many lives as advertised. Baby aspirin doesn’t sufficiently inhibit clots in heart arteries and a standard aspirin tablet induces bleeding gastric ulcers that can be mortal in themselves.
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August 23, 2011: by ResveratrolNews
So why is resveratrol averting mortal heart attacks in the animal lab, in preliminary studies restoring vision to humans who are battling an otherwise hopeless eye disease, and is considered to be the most promising anti-cancer molecule on the planet — and therefore addresses the three most feared health problems of humanity — yet relatively few Americans have adopted res-pills into their daily health regimens?
These questions and more are answered by Bill Sardi in his most recent e-book THE CASE FOR RESVERATROL: Why Aren’t More Americans Taking Resveratrol Pills?
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August 19, 2011: by Bill Sardi
Sirtris’ re-emergence with its Sirtuin1-gene activating SRT1720 drug gains the attention of the pharma world and health seekers. Most striking was that high-fat-fed mice did not gain weight, something that was only demonstrated in rodents with a supra-high dose of resveratrol (21,000 mg human equivalent dose). However, to produce this effect and overcome fatty liver SRT1720 had to be given in a 100 mg/kilogram dose, equivalent in human terms to 7000 mg for a 160-lb human. I’m not sure healthy humans are going to want to take seven 1000 mg pills a day, and at what cost? Lower dose (2100 mg human equivalent dose) SRT1720 produced a much more tempered effect and a modest improvement in life span. So maybe humans who are killing themselves by eating high-fat diets would benefit from this drug, but maybe not healthy people. Recognize the lab mice in this experiment were fed a 60% fat-calorie diet whereas humans generally consume 20-25% fat calorie diets. As a scientific achievement, SRT1720 is notable, but it doesn’t yet translate into a practical or affordable medicine for humans. The claim was these so-called new chemical entities under development by Sirtris were 1000-fold more powerful than resveratrol, but the dose required to produce a 44% increase in life span (about what a limited calorie diet achieves) is still quite high. And while there were no signficant side effects, this was true for mega-dose resveratrol in animal models of treatment for multiple myeloma (bone marrow cancer), but when 5000 mg of resveratrol was given to humans with this type of cancer it rapidly induced kidney failure. Bottom line, SRT1720 is a scientific achievement that is a long way from becoming an anti-aging drug. – Bill Sardi, ResveratrolNews.com
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August 18, 2011: by Bill Sardi
The announcement today, published in The New York Times, that a synthetic drug, SRT1720, produced by Sirtris Pharmaceuticals, mimics resveratrol and overcomes fatty liver which results in a 44% increase in the life span of laboratory animals, is the re-emergence of this company’s visibility since its failed (but half-hearted) venture to market a resveratrol pill. GlaxoSmithKline, the parent to Sirtris, abandoned further research and development for its SRT501 resveratrol (rez-vair-ah-trol) drug when mega-doses induced kidney failure in a human trial among bone marrow cancer patients.
The quest to develop these small-molecule drugs began in 2003 when Harvard researchers linked a resveratrol, a red wine molecule, with a key gene — Sirtuin1 – thought to be activated in calorie restricted animals that results in prolongation of life span.
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July 4, 2011: by Bill Sardi
A scientific review reveals resveratrol (rez-vair-aw-troll), known as a red wine molecule, simultaneously removes fatty plaques from arteries and the brain via its ability to control copper.
In 2009 researchers demonstrated resveratrol’s ability to inhibit cholesterol plaque accumulation (atherosclerosis) in arteries by its ability to promote efflux (exit) of cholesterol from the liver rather than interfere with cholesterol production in the liver as statin drugs do. Via its ability to bind with copper, resveratrol negates unbound copper’s susceptibility to harden cholesterol and form arterial plaque.
In a lab dish, resveratrol’s ability to reduce oxidation (hardening) of cholesterol (LDL- low-density lipoproteins) “was found to be mainly due to its capacity to chelate copper.”
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June 30, 2011: by Bill Sardi
* SOD = superoxide dismutase
Genes they be — a Sirtuin family of seven “silent information regulators” that are guardians of the cell. Sirtuins have been linked with prolonged lifespan in various life forms, starting with yeast cells, fruit flies and roundworms.1
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June 2, 2011: by Bill Sardi
Researchers at the Ottawa Research Institute report that resveratrol still exerts anti-cancer action, sometimes in profound ways, but that the Sirtuin1 gene is not always required to produce such an effect. Mice bred without a functioning Sirtuin1 gene did not develop fewer intestinal polyps (see graphic below).
The assumption is that Sirtuin1 is a survival gene that is switch on in calorie restricted animals who have double the lifespan of animal fed a normal diet. Resveratrol is a molecule that is purported to activate the Sirtuin1 gene. But subsequent studies don’t always validate the idea that the Sirtuin1 gene is a strong anti-cancer gene. In fact, Sirtuin1 gene proteins are produced at a high level in lymph gland tumors (B-cell lymphomas) and are accompanied by a poor prognosis in B-cell lymphomaand breast cancer.
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May 31, 2011: by Bill Sardi
Resveratrol continues to edge closer to becoming the safest and most effective alternative to estrogen replacement during menopause.
The idea behind using resveratrol or any phyto (plant) estrogen is for this molecule’s ability to seat itself on estrogen cell receptors (doorways of entry into cells), thus blunting the effect of natural estrogen.
A recent animal study conducted at Michigan State University revealed that slow-release/low-dose estrogen given to laboratory rats generated the superoxide radical, a form of oxygen free radical that can harm tissues and produce mutations in DNA. Estrogen supplementation also produced unfavorable changes such as elevated blood pressure and faster heart rate. The phytoestrogen resveratrol completely reversed all of these adverse effects. Science Daily published a report about resveratrol’s counteraction against estrogen, found here.
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: by Bill Sardi
Researchers report that resveratrol (rez/vair-ah-trol), known as a red wine molecule, helps to reverse what are called somatic cells (cells that have already been converted into muscle, heart, brain, etc. cells) back into being stem cells better than five other molecules tested for such capability. These converted stem cells can then be harvested for insertion into living tissues to replace damaged or aged cells. This discovery is published in an early online edition of the journal Aging Cell.
Such a maneuver, to reverse already developed cells, had already been demonstrated by researchers in Japan about five years ago. But this approach is fraught with drawbacks, namely that viruses used to insert reprogramming factors into cells can induce gene mutations and activate genes that promote cancer. So-called reverse induced pluripotent stem cells have remained a research tool rather than a therapeutic technology. Researchers have been searching for the next big milestone in making stem cells without viruses, which set the stage for resveratrol.
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May 13, 2011: by Bill Sardi
Gone are the jaw-dropping days when a Harvard scientist captivated audiences on CBS’s 60-Minutes program and on the front pages of The New York Times and The Wall Street Journal, talking about the promise of a bona fide anti-aging pill and how his laboratory had found the holy grail of aging, a survival gene known as Sirtuin1, and its molecular activator, resveratrol.
Initial testing showed mega-dose resveratrol prolonged the life of rodents fed a fat-laden diet, but failed to do so for animals on a standard-fat calorie diet. More disconcerting was the widely acclaimed discovery that resveratrol activated the Sirtuin1 survival gene when in fact it was a fluorescent compound used in this assay that was the actual agent that stimulated Sirtuin1, not resveratrol. This only meant that the gene target was off base, not that resveratrol is less promising. But the science was correctly called into question.
Subsequent studies provide mixed results for resveratrol as an activator of the Sirtuin1 gene. [Free Radical Medicine & Biology, The controversial links among calorie restriction, SIRT1, and resveratrol, in press 2011] In mammals neither the over-expression of Sirtuin1 protein nor administration of Sirtuin1 activators could extend the lifespan of mice on a standard-calorie diet.
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