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How the world got lost on
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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.”
Earlier studies, conducted in the late 1990s, show that trans resveratrol, but to a much lesser extent cis resveratrol (its less active molecular cousin that has been altered due to exposure to UV light), works to prevent oxidation of lipoproteins (protein-bound cholesterol) at very low concentration. It was found that low-dose trans resveratrol is “by far the most potent chelators of copper and does not chelate iron.” It “may contribute to the protective effects of wine by removal of copper from LDL particles and arterial tissue.”
Resveratrol appears to reduce fatty deposits in arteries at relative low dose – about the amount provided in 3 glasses of dark red wine (180-300 mg). Quercetin works even better in this regard and is a good companion to resveratrol.
This may help explain why resveratrol was found to reduce arterial plaque formation in arteries without lowering circulating cholesterol numbers in animals. In fact, with more cholesterol exiting the body, it may even raise circulating levels of cholesterol.
In 2007 researchers also showed that HDL cholesterol complexes with beta amyloid plaque to remove it from the brain and final disposal through its exit from the liver. Resveratrol has been shown to raise HDL cholesterol and reduce beta amyloid in animal brains.
A major misdirection by modern medicine may be in the design of drugs that inhibit production of fatty plaques in the liver and brain.
It has been difficult to scientifically justify the use statin drugs among healthy adults who have elevated circulating cholesterol levels and no other risk factors for arterial disease (smoking, high blood pressure, angina chest pain, elevated blood sugar, family history of heart disease).
A review of the ten largest studies of cholesterol-lowering statin drugs did not reveal a significant reduction in mortality. Statin drugs DO reduce mortality among high-risk individuals, but again, 80 healthy people (Jupiter study) or 95 healthy people (ALLHAT-LLT study) have to take a statin drug over a 5-year period for one person to avoid a heart attack (see chart below). That is less than 2% effectiveness! Only when the 10-year risk for heart attack is greater than 20% are statin drugs useful for “primary prevention.” But primary prevention candidates are generally health and do not have these risk factors. individuals.
Beta amyloid plaque buildup in the brain is suspected of contributing to Alzheimer’s disease, which is technically defined as early loss of memory (50s and 60s) rather than true senile dementia (70s and 80s).
Because cholesterol in the diet promotes production of beta amyloid plaque (Alzheimer’s plaque) in the brain, a cholesterol-lowering drug was tested as a preventive measure against Alzheimer’s memory loss. But the drug failed miserably. In fact, in a definitive study only 1046 of 1684 patients could even continue taking an experimental drug due to the side effects (which went unreported because the patients stopped taking the pills). The study, published in the Journal of the American Medical Association in 2009 concluded that a drug designed to reduce beta amyloid plaque in the brain “did not slow cognitive decline or the loss of activities of daily living in patients with mild Alzheimer’s disease.”
The authoritative Cochrane review board concluded, that while statins drugs do, in fact, reduce circulating cholesterol levels, they do not improve memory or thinking among above that provided by an inactive placebo pill.
A consensus statement issued from the the British Association for Psychopharmacology says: “To date, results of pivotal studies have been equivocal and no disease-modifying agents are either licensed or can be currently recommended for clinical use.” This includes all of the cholinesterase inhibitors (Tacrin, Aricept) that are uselessly prescribed for Alzheimer’s disease. The reason why this is mentioned here is that disproven drugs for Alzheimer’s disease are broadly prescribed. Yet if a physician receives an inquiry from a patient concerning resveratrol pills for this disease, he will dismiss the idea because it is “unproven.”
Researchers now believe an age-related decline in brain metabolic activity and inflammation occurring at the synapse (the gap between brain cells where brain chemicals [aka: neurotransmitters] must jump from one brain cell to another for proper thinking and memory to occur), are primary in Alzheimer’s disease and that the deposition of beta amyloid is secondary to that. Beta amyloid exacerbates Alzheimer’s disease but is not the primary cause.
Along this line of thinking, resveratrol has been shown to improve brain metabolism in the mitochondria of brain cells. Resveratrol has been shown to reduce all three major markers of inflammation (tumor necrosis factor-TNF, C-reactive protein-CRP, and cyclooxygenase2 (COX2). Resveratrol inhibits TNF, the major marker of brain inflammation. Injection of TNF-inhibiting drugs rapidly resolves Alzheimer’s symptoms for a short time. So the concept of employing TNF-inhibiting agents has already been proven in humans. Just human trials with resveratrol are lacking.
An added advantage of resveratrol over any other man-made cholesterol drugs is that it has broad biological action and also beneficially inhibits blood clotting and inflammation and dilates (widens) blood vessels that normally narrow with advancing age. Resveratrol even regenerates vitamin E.
Furthermore, resveratrol works like a statin drug. In fact, it inhibits the same cholesterol-producing enzyme that statin drugs do, only without liver toxicity.
One report written a decade ago made the biological connection between circulating oxidized arterial lipoproteins (cholesterol) in arteries and beta amyloid plaque in the brain and proposed that “neuronal cell death due to oxidized brain lipids (fats) could be ameliorated by resveratrol, a polyphenolic compound known for its antioxidant properties.”
Ten years later not one human trial of resveratrol for Alzheimer’s disease has taken place. In fact, this author is personally aware of one drug company blocking such a study that was sponsored by the National Institutes of Health. You can see below that two studies involving resveratrol and Alzheimer’s disease have been agonizingly delayed for over 4 years. The public is going to have to proceed ahead with self-care regimens if they are to obtain the health benefits proposed by resveratrol.
National Institutes of Health: Ongoing Clinical Trials/ Resveratrol
|1||Active, not recruiting||Randomized Trial of a Nutritional Supplement in Alzheimer’s Disease
|2||Unknown †||Pilot Study of the Effects of Resveratrol Supplement in Mild-to-Moderate Alzheimer’s Disease
|3||Recruiting||Effects of Dietary Interventions on the Brain in Mild Cognitive Impairment (MCI)
Resveratrol is the double-duty natural medicine that quells cholesterol plaque in arteries and brain. Take advantage of it by supplementing daily with this miracle molecule.
© 2011 Bill Sardi ResveratrolNews.com Not for posting on other websites