Doctor In Italy Quells Parkinson’s With Overlooked Vitamin Cure

Doctor In Italy Quells Parkinson’s With Overlooked Vitamin Cure

By Bill Sardi

January 12, 2017

In recent weeks the world has learned the news media creates fake news and/or completely shuns significant news stories to match its own politically correct agendas. So an unequivocal cure for a major brain disease goes unreported. Shame on CNN, CBS, ABC, NBC, the BBC, Reuters, Associated Press and the New York Times.

For a disease considered incurable, a physician in Italy has begun to provide a common B vitamin to successfully treat a debilitating motor-nerve disease commonly known as Parkinson’s disease. The importance of this startling discovery has escaped major news outlets. It should be heralded on television and in newspapers worldwide. But it has only been reported by an obscure European news source. [Ultima Edizione.eu] (Be sure to click the before-and-after video tabs.)

History of vitamin B1 and Parkinson’s

Physician James Parkinson first described a “shaking palsy” in 1817. [Cold Spring Harbor Perspectives in Medicine 2011] Today, 200 years later Parkinson’s disease is still considered an incurable disease.

Parkinson’s disease emanates from the loss of dopamine-producing cells in the brain. Approximately 60-80% of dopamine-producing cells are damaged before symptoms arise. Dopamine is a nerve-transmitting chemical in the brain.

It has taken two centuries for a vitamin-phobic medical profession to hesitantly begin to treat Parkinson’s disease with vitamin B1 (thiamin).

Historically the link between Parkinson’s disease and thiamin deficiency has been agonizingly slow.

Thiamin, vitamin B1, was the first vitamin to be discovered. Vitamin B1 was first synthesized in 1936. [Annals New York Academy Sciences April 1962] So dietary supplementation was possible from that point forward.

It took till 1967 for the first published report that a decline in brain dopamine levels of pigeons was due to experimentally induced thiamin deficiency. [International Journal Neuropharmacology July 1967]

A link between thiamin deficiency and low dopamine levels was discussed in 1987 in an experiment that attempted to determine why rats tend to eat mice (muricide). Low dopamine levels induced by a shortage of thiamin in the diet were linked to this abnormal animal behavior. [Pharmacology Biochemistry Behavior 1987]

In 1988 researchers noted a thiamin-deficient diet decreased dopamine concentration and synthesis in the brain (striatum). The provision of alcohol to lab animals also decreased dopamine levels. The brain region most susceptible to damage (the hypothalamus) in thiamin deficient animals is the very same region of the brain that produces dopamine. [Drug Alcohol Dependency 1988]

In 1999 it was observed that low levels of thiamin in the cerebrospinal fluid were related to Parkinson’s disease. [Neuroscience Letters 1999]

In 2013 researchers reviewed all prior published scientific reports and concluded that thiamin plays a role in Parkinson’s disease. [CNS Neuroscience Therapy2013]

First therapeutic trials report

In 2013 the first reports were published the use of high-dose thiamin among Parkinson’s disease sufferers resulted in considerable improvement in measured motor function (31.3% to 77.3%). Injection of high-dose thiamin was effective in reversing symptoms. [BMJ Case Reports 2013]

Then another study published in 2015 confirmed that injectable thiamin treatment (100 mg twice a week) improves motor nerve function among Parkinson’s patients. [Journal Alternative Complementary Medicine 2015]

In 2016 researchers in Italy reported on the successful use of high-dose thiamin among Parkinson’s patients. Notably, all of the patients had normal blood levels of thiamin yet thiamin therapy led to significant improvement in Parkinson’s symptoms. There were no adverse events. [Neural Regeneration Research2016]

Loss of sense of smell is earliest sign

Finally, in January of 2017 researchers noted that the sense of smell declines years prior to the onset of Parkinson’s disease. Scented strips were used to test scent among individuals with Parkinson’s disease. Almost half of the individuals tested (47%) scored low on this test and dietary thiamin was also low in these subjects.

The main finding of the study was an association between low thiamin in the diet reported 2-8 years prior to the onset of symptoms and diagnosis. Impairment of olfaction (sense of smell) is a characteristic and early feature of Parkinson’s disease these researchers wrote. Involvement of many B- family vitamins appears to be involved in the decline of smell. Therefore, a decline in the sense of smell may serve as an early screening tool for Parkinson’s disease. [European Journal Clinical Nutrition Jan 2017]

Because of a change in western diets, Dr. Derrick Lonsdale, the reigning clinical authority on vitamin B1, says the high sugar/carbohydrate diet of today results in a return of the scourge of beri beri. The problem is, modern medicine observes symptoms of this nutrient deficiency disease and treats those instead of its cause.

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Western populations are paying a high price for poor absorption or depletion of thiamin due to consumption of alcohol, drugs like diuretics (water pills), refined sugar, carbohydrates, even coffee and tea. [Evidence Based Complementary Alternative Medicine 2006]

The ordeal of undetected thiamin deficiency is only exacerbated by the modern paradigm of treating symptoms of disease as if they emanate from the drug deficiency, not a nutrient deficiency.

So we now have 60,000 Americans diagnosed with Parkinson’s disease annually and 10 million worldwide living with the disease. More than 23,000 die of Parkinson’s disease annually in the U.S. [Parkinsons Disease Foundation]

Levodopa, the main drug prescribed for Parkinson’s disease, costs ~$2500/year. [Parkinson’s Disease Foundation]

As of 2014 there were 23 medicines under development for Parkinson’s disease. Drugs only serve as a distraction for a disease that may emanate from a vitamin deficiency.

Thiamin deficiency is associated with other age-related brain diseases such as Alzheimer’s and Huntington’s disease. [The Scientist Oct 2013]

Alzheimer’s too

This author penned an earlier report linking Alzheimer’s disease to thiamin deficiency. [Knowledge of Health]

The earliest sign of Alzheimer’s disease is also a decline in the sense of smell. [Neuropsychiatric Disease Treatment 2016] That was first reported in 1974. [Acta Psychiatric Scandinavia 1974]

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The startling problem with Alzheimer’s disease is that there is no proven cure for this brain disease either and only 1 in 244 drugs undergoing trials for this brain disease have achieved FDA approval.

Accumulation of beta amyloid plaque in the brain begins up to 20 years before symptoms occur. With so many Americans now living into their eighth, ninth and tenth decade of life and 44% of age 75-84 adults affected, it is too late to conduct a long-term controlled study to head off this anticipated Alzheimer’s plague. We are going to have close to half of the senior adult population living with Alzheimer’s memory loss and the other half of that population taking care of them!

Rx: B vitamins

The provision of the entire family of supplemental B vitamins, in particular thiamin (B1), pyridoxine (B6), folic acid (B9), and cobalamin (B12) appears to be important in the theoretical model of these diseases. Disturbed sense of smell has been reversed with vitamin B12 supplementation. [International Forum Allergy Rhinology 2016; Psychosomatics 2014]

The best way to achieve this proposed prophylaxis is either a B-vitamin complex or a multivitamin. In most instances the provision of B vitamins in these formulas is marginal, often not exceeding the outdated Daily Value or the Recommended Daily Allowance.

A progressive fall off in the absorption of these B vitamins due to a decline in secretion of stomach acid with advancing age, or in the case of thiamin the blockage of absorption by drugs, antacids, alcohol, sugar and carbohydrates and even presumably healthy beverages like tea and coffee, serve as sufficient evidence doses of B vitamins need to be updated in most multivitamins if a universal attempt is to be made to head off Parkinson’s and Alzheimer’s disease epidemic.

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Because of poor absorption of water-soluble forms of B1, vitamin B1 in fat-soluble form (Benfotiamine) is the preferred form in dietary supplements but is generally not provided in B-complex or multivitamins. [Clinical Therapeutics Oct 2016; International Journal Clinical Pharmacology Therapeutics 1998] Fat- soluble benfotiamine is about almost 6 times more biologically available than water-soluble thiamin hydrochloride, the common form used in dietary supplements. [Journal Clinical Pharmacology 2014]

Furthermore, gut bacteria has now been shown to regulate movement disorders like Parkinson’s disease in laboratory mice and represents a risk factor. [Cell2016; World Journal Gastroenterology 2015] Ditto for Alzheimer’s disease. [Science China/Life Science 2016] Multivitamins need to incorporate ingredients that promote healthy gut bacteria.

As for the doctor in Italy who has reported on the successful use of thiamin/vitamin B1 for Parkinson’s disease symptoms we can only say bravo and wonder when the Nobel Prize committee will take notice.

A newly available multivitamin that incorporates amply dosed B-vitamins in forms that maximize absorption and other ingredients that beneficially modify gut bacteria has been formulated by this author. [MolecularMulti]