Successful treatment of schizophrenia requires optimal daily doses of vitamin [B.sub.3]

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Authors: Abram Hoffer and Jonathan Prousky
Date: Dec. 2008
From: Alternative Medicine Review(Vol. 13, Issue 4)
Publisher: Thorne Research Inc.
Document Type: Article
Length: 2,440 words

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For over 50 years Dr. Abram Hoffer has been educating clinicians about the need to correctly (optimally) dose schizophrenics with vitamin [B.sub.3] (niacin; niacinamide). For the past 10 years I have, likewise, educated numerous naturopathic and medical doctors about the very same thing. For some reason, both types of clinicians routinely treat schizophrenic patients with plenty of vitamins, minerals, and other natural health products, but they never provide enough vitamin [B.sub.3]. In these authors opinions, schizophrenic patients cannot get well if not provided with optimal doses of vitamin [B.sub.3]. This prevents the real acceptance of nutritional treatment since clinicians will not observe favorable results when inadequate treatment is provided; their schizophrenic patients will continue to suffer needlessly.

To understand the importance of vitamin [B.sub.3] treatment, some background information is needed. Schizophrenia is characterized by a combination of perceptual changes (e.g., hallucinations) and thought disorders (e.g., delusions). (1) These aberrant mental states, which can lead to psychotic behavior, cause a tremendous amount of emotional and psychological suffering. The cause of schizophrenia, the subject of much debate, is considered a biochemical imbalance, although certain genetic factors most certainly play a role.

The majority of scientists and psychiatrists subscribe to the dopamine excess theory of schizophrenia; i.e., that too much dopamine is largely responsible for the symptoms of psychosis. However, since 1952, Hoffer, the founding father of orthomolecular medicine, has researched, published, and expanded on the adrenochrome theory of schizophrenia. (1,2) He and his colleagues, Drs. Osmond and Smythies, arrived at this theory by studying and researching the effects of substances such as mescaline, lysergic acid diethylamide (LSD), and amphetamines--all of which can cause a clinical syndrome in normal individuals that would be clinically indistinguishable from schizophrenia.

Osmond and Smythies noted that mescaline had a similar chemical structure to that of adrenaline. Hoffer, Osmond, and Smythies concluded that since both can be converted to indoles in the body, the potential schizophrenic toxin might be an indole derivative of adrenaline with similar neurochemical properties to that of mescaline or LSD. They eventually deduced that the schizophrenic toxin was an oxidized derivative of adrenaline known as adrenochrome. Since the early 1950s, the adrenochrome theory has been validated by the following findings:

1. Adrenochrome and its close relatives--dopaminochrome (from dopamine) and noradrenochrome (from noradrenaline)--are present in the human brain. (3-5)

2. These compounds probably induce a combination of neurotoxic and mind-mood-altering effects. (3-5)

3. Reducing adrenochrome, dopaminochrome, and noradrenochrome is therapeutic for the treatment of schizophrenia. (6)

To reduce the production of adrenochrome, Hoffer and his team decided on the methyl acceptor vitamin [B.sub.3]. This vitamin, previously used to treat pellagra (a disease clinically indistinguishable from schizophrenia) had relevant biochemical properties. (1,2) Hoffer and his team researched the metabolism of adrenaline. They knew that the reaction involving noradrenaline to adrenaline required the addition of one methyl group. Because vitamin [B.sub.3] was known to function as a methyl acceptor, Hoffer's team theorized that an optimum dose of niacin might decrease the amount of noradrenaline that would be converted to adrenaline....

Source Citation

Source Citation
Hoffer, Abram, and Jonathan Prousky. "Successful treatment of schizophrenia requires optimal daily doses of vitamin [B.sub.3]." Alternative Medicine Review, vol. 13, no. 4, Dec. 2008, pp. 287+. Accessed 30 Nov. 2021.

Gale Document Number: GALE|A192485096