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Posted July 8, 2013: by Bill Sardi
This investigator’s report about a vitamin remedy to quell the ongoing epidemic of Alzheimer’s memory loss suggests Big Pharma must have known all along that a vitamin B1 (thiamin) deficiency is associated with or is a cause of abnormalities (brain plaque) observed in both laboratory animals and humans.
A shortage of thiamin had been linked to Down’s Syndrome as far back as 1976. Down’s syndrome subjects develop an early form of Alzheimer’s disease.
That pharmaceutical companies must have known all this but failed to report it is consistent with their narrow profit-making mission to produce synthetic molecules and gain their approval as drugs.
Lamenting over the fact pharmaceutical companies have not been able to come up with a pill to prevent or treat Alzheimer’s disease, an online investment website asks “Can’t anyone tackle Alzheimer’s?” Not if you are trying to develop synthetic patentable drugs to conquer what is a vitamin deficiency disease!
The news media creates great drama and often misdirected anticipation for every Alzheimer’s drug trial, only aiding and abetting the misdirection by Big Pharma. In the quest to produce multi-billion dollar blockbuster drugs, which agency in the medical community speaks for simpler, less costly and problematic cures like vitamins? Not the National Institutes of Health (NIH), not the FDA.
Big Pharma gets away with this as it faces no real competition because vitamins, minerals, amino acids and herbal remedies are not on the same footing.
What is needed is an anti-trust action against the pharmaceutical companies to allow a free market to exist where natural remedies can compete with synthetic drugs.
Private enterprise has a mandate to produce the most profitable cures, but public health authorities need to serve in the public’s interest, to promote and develop the most economical remedies. Safe, inexpensive and effective is not the objective of Big Pharma nor public health agencies today.
Just how did public health authorities at the National Institutes of Health (NIH) not know about the B-vitamin linkage to Alzheimer’s disease?
A recently published report says “there is debate about the relative contributions of the direct toxic effect of alcohol, and the impact of thiamine deficiency, to lasting brain damage.” How long will the debate continue before a human clinical trial is launched?
Over a decade ago the prestigious Cochrane Center that judges whether there is sufficient scientific data to substantiate various treatments for diseases, concluded in that there was insufficient evidence (only 50 reported cases where thiamin levels were obtained) to determine whether a shortage of thiamin results in Alzheimer’s disease. This is just another evidence that the National Institutes of Health has drug its feet over the link between thiamin deficiency and Alzheimer’s.
NIH should have been launched human trials involving thiamin’s role in Alzheimer’s disease years ago. Of the 40 NIH-funded clinical trials presently listed, none involve vitamins. Thiamin has not been a priority at the NIH’s National Institute on Mental Health. Its researchers are all trying to cash in just like Big Pharma. The revolving door between Big Pharma and public agencies is well known.
Vitamins are not profitable enough to fund a human clinical study. Vitamin makers certainly can’t fund a study. Only the National Institutes of Health has sufficient funds to take thiamin through trials to prove it would serve as a remedy for this horrific brain disease.
The fact that a recent animal study and a human case report now unequivocally demonstrate that brain aging is accelerated by a simple vitamin deficiency suggests at least a segment of the research community is ready to break ranks given there are currently no useful drugs to treat or prevent Alzheimer’s disease.
And there is another big hidden sin. Big Pharma knows that many of its drugs actually hasten Alzheimer’s disease. For example, drugs that deplete thiamin such as diuretics and digoxin may increase the long-term risk for memory loss of the Alzheimer’s type. This places Big Pharma in the role of creating a drug-induced disease and then cooking up a remedy to solve a problem of their own doing.
The Alzheimer’s Association projects Alzheimer’s disease will affect 13.8 million by 2050 (5 million currently diagnosed) unless new ways to stop the disease are discovered and brought to market. Current medications do not treat Alzheimer’s or stop it from progressing; they only attempt lessen symptoms, such as memory loss and confusion.
Then there are practicing physicians. All doctors need do now is prescribe benfotiamine (no Rx needed however), the fat-soluble form of thiamin. But will they? Big Pharma exerts subtle pressure on doctors not to recommend vitamin therapy.
It is said that most cases of thiamin-deficiency induced memory loss “are missed by clinicians.” It has only recently been said that “physicians should have a high index of suspicion” for alcohol/thiamin-deficiency induced brain disease and “dose thiamin accordingly.” This problem may be a result of doctors addressing most modern maladies as drug deficiencies, not nutrient deficiencies.
Doctors consider anything short of an FDA-approved drug to be unproven. Another example is a dietary supplement demonstrated to rescue otherwise hopeless patients with a sight-robbing eye disease called wet-macular degeneration who have failed injectable drug therapy. Eye doctors have simply elected to ignore this development and permit an estimated 30,000 people to enter the ranks of the legally blind rather than prescribe a dietary supplement on a compassionate care basis.
So, will the Down’s syndrome kids continue on without doctor-guided vitamin therapy? Will there be no impetus behind an effort to supplement the diet of pregnant women to reduce the risk of giving birth to Down’s syndrome babies? Will at-risk seniors continue to receive millions of dollars of ineffective drugs for memory loss rather than benfotiamine?
For the self-guided public, plain water-soluble vitamin B1 (thiamin hydrochloride) may not be effective. The fat-soluble vitamin B1 (benfotiamine) is what is needed. In laboratory animals, thiamin-treated animals experienced a 4-fold increase in red blood cell thiamin levels whereas benfotiamine-treated animals experienced a 25-fold increase in thiamin.
Alzheimer’s patients and their families should not be reticent to start their own trial use of benfotiamine. A year-long trial is suggested. Mega-dose thiamin pills (80-300 mg) are widely sold as benfotiamine, a fat-soluble version of thiamin. The risk for side effects with mega-dose thiamin is nil.
The FDA permits hundreds of millions of dollars of ineffective and problematic anti-Alzheimer’s drugs to be sold today. One anti-Alzheimer’s drug (Aricept) racks up $800 million annual sales. Yet it works no better than an inactive placebo pill. The British Medical Journal reviewed 22 published studies and concluded the three top selling drugs for Alzheimer’s disease were simply ineffective.
Families of Alzheimer’s patients may clamor for doctors to “do something” for their loved ones who are losing their minds. But this is no excuse to deceive patients and families and plunder insurance funds.
The horror show continues. The public remains clueless. My report linking Alzheimer’s disease and Down’s syndrome to a B vitamin deficiency will likely remain in obscurity, even in the era where online communication permits global distribution of information.
The role of alcohol in Alzheimer’s disease is well known but inexplicably separated from non-alcohol-induced memory loss. Yet thiamin deficiency is highly prevalent among alcohol abstainers.
The idea that alcohol-induced brain disease (known as Wernicke’s, encephalopathy) which is unarguably induced by thiamin deficiency, is a distinct disease entity apart from Alzheimer’s disease has prevailed. But a recent review of 53 published reports found 43 of these 53 reports were non-alcohol related. Some of these cases exhibited normal brain scans (magnetic resonance imaging or MRI) and a small percentage even had normal blood thiamin levels, which suggests the normal range for this vitamin needs to be re-evaluated.
For whatever reasons modern medicine has categorized alcohol induced amnesia as a separate disorder apart from Alzheimer’s disease. Yet in 1985 researchers said there are “some similarities in the memory disorders of alcoholic Korsakoff and Alzheimer patients.”
A report published in the Journal of the American Medical Association says “alcoholic dementia” and early Alzheimer’s dementia are “not mutually exclusive.” The report concluded that the role of alcohol “can be difficult to determine” because population studies suggest moderate alcohol consumption reduces the risk for Alzheimer’s disease.
The lack of a straightforward relationship between Alzheimer’s disease and alcohol consumption may be explained a recent study. Not only are red wine molecules protective for the brain, it has been demonstrated in laboratory animals that plain alcohol, but not modest red wine intake, inhibits absorption of thiamin.
A report published in 1993 stated that alcoholism is “a common disease in older patients, affecting 10% of those living at home and as many as 40% of those in nursing homes.” Common observed symptoms included “diarrhea and dementia,” two of the three hallmark symptoms of thiamin deficiency. The report went on to say that “alcohol-induced brain injury can resemble Alzheimer’s disease.”
The diagnosis of Alzheimer’s disease is tenuous because there is no blood test or other marker that conclusively confirms this disease. Usually diagnosis is made solely based upon symptoms.
Yet over a dozen years ago it was noted the protrusions from the underside of the human brain known as mammillary bodies, shrink in size as a result of vitamin B1 deficiency. One study showed the mean volume of the mamillary bodies is reduced by 60% in cases with chronic thiamin deficiency induced by alcohol. Progressive shrinkage of mammillary bodies on the underside of the brain can be visualized by magnetic resonance imaging (MRI).
It has long been known that mammillary bodies are among the first brain regions implicated in amnesia.
Wikipedia says damage to mammillary bodies due to thiamine deficiency produce symptoms of memory loss consistent with Alzheimer’s disease.
The association between diabetes and Alzheimer’s is strong. One explanation for that is in diabetes the kidneys excrete more vitamin B1 (thiamin) due to decreased production of molecules that recycle thiamin once it reaches the kidneys.
A survey of subjects on a gluten-free diet reveals they frequently exhibit vitamin deficiencies, with thiamin deficiency actually being more common after a gluten-free diet is implemented.
Let us not forget that it was Russian physician S.S. Korsakoff who over 100 years ago initially described a syndrome named after him associated with amnesia associated with thiamin deficiency. Everyone else is late to the party. ©2013 Bill Sardi, Knowledge of Health, Inc.
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