Treatment of Schizophrenia

Hoffer, A.

doi:10.1016/b978-0-08-021533-4.50023-2

Cited by 6 publications

(6 citation statements)

References 9 publications

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“…For correcting dyslipidemia and order to obtain the known and established proper clinical therapeutic benefit for the NAD precursor, niacin, it has been repeatedly determined that it is necessary to have high doses of 1-3g/day. In trials involving over 1,000 patients with regimens of at least 1.5g/day for at least 3 months with no appreciable side effects [115]. After analysis, it was clear that the risk to benefit for nicotinamide therapy is highly favorable should the drug prove to be efficacious in preventing diabetes.…”

Section: Nicotinamide (Nam)mentioning

confidence: 96%

“…Unfortunately, pharmacological approaches for diabetes trials have not always followed the necessary high levels of NAD precursors for therapeutic benefit. It is critical to maintain high levels of NAD to achieve efficacy [115,116]. The NAD precursors are all water soluble and typically cleared in several hours.…”

Section: Autoimmune Disease Ido and Nad Precursor Based Therapeuticsmentioning

confidence: 99%

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Pharmacological Targeting of IDO-Mediated Tolerance for Treating Autoimmune Disease

Penberthy

2007

CDM

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Cells at the maternal-fetal interface express indoleamine 2,3 dioxygenase (IDO) to consume all local tryptophan for the express purpose of starving adjacent maternal T cells of this most limiting and essential amino acid. This stops local T cell proliferation to ultimately result in the most dramatic example of immune tolerance, acceptance of the fetus. By contrast, inhibition of IDO using 1-methyl-tryptophan causes a sudden catastrophic rejection of the mammalian fetus. Immunomodulatory factors including IFNgamma, TNFalpha, IL-1, and LPS use IDO induction in responsive antigen presenting cells (APCs) also to transmit tolerogenic signals to T cells. Thus it makes sense to consider IDO induction towards tolerance for autoimmune diseases in general. Approaches to cell specific therapeutic IDO induction with NAD precursor supplementation to prevent the collateral non-T cell pathogenesis due to chronic TNFalpha-IDO activated tryptophan depletion in autoimmune diseases are reviewed. Tryptophan is an essential amino acid most immediately because it is the only precursor for the endogenous biosynthesis of nicotinamide adenine dinucleotide (NAD). Both autoimmune disease and the NAD deficiency disease pellagra occur in women at greater than twice the frequency of occurrence in men. The importance of IDO dysregulation manifest as autoimmune pellagric dementia is genetically illustrated for Nasu-Hakola Disease (or PLOSL), which is caused by a mutation in the IDO antagonizing genes TYROBP/DAP12 or TREM2. Loss of function leads to psychotic symptoms rapidly progressing to presenile dementia likely due to unchecked increases in microglial IDO expression, which depletes neurons of tryptophan causing neurodegeneration. Administration of NAD precursors rescued entire mental hospitals of dementia patients literally overnight in the 1930's and NAD precursors should help Nasu-Hakola patients as well. NAD depletion mediated by peroxynitrate PARP1 activation is one of the few established mechanisms of necrosis. Chronic elevation of TNFalpha leading to necrotic events by NAD depletion in autoimmune disease likely occurs via combination of persistent IDO activation and iNOS-peroxynitrate activation of PARP1 both of which deplete NAD. Pharmacological doses of NAD precursors repeatedly provide dramatic therapeutic benefit for rheumatoid arthritis, type 1 diabetes, multiple sclerosis, colitis, other autoimmune diseases, and schizophrenia in either the clinic or animal models. Collectively these observations support the idea that autoimmune disease may in part be considered as localized pellagra manifesting symptoms particular to the inflamed target tissues. Thus pharmacological doses of NAD precursors (nicotinic acid/niacin, nicotinamide/niacinamide, or nicotinamide riboside) should be considered as potentially essential to the therapeutic success of any IDO-inducing regimen for treating autoimmune diseases. Distinct among the NAD precursors, nicotinic acid specifically activates the g-protein coupled receptor (GPCR) GPR109a to produce the...

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Section: Nicotinamide (Nam)mentioning

confidence: 96%

Section: Autoimmune Disease Ido and Nad Precursor Based Therapeuticsmentioning

confidence: 99%

Pharmacological Targeting of IDO-Mediated Tolerance for Treating Autoimmune Disease

Penberthy

2007

CDM

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“…A number of healthcare providers have suggested niacin as a therapy for schizophrenia, citing a reduction in the conversion of norepinephrine to epinephrine and other mechanisms as beneficial for this psychiatric disorder (16)(17)(18)20,22,29). A probe of the World Wide Web with the search engine Google produced over 12,000 hits on the search for sites having both "niacin" and "schizophrenia."…”

Section: Discussionmentioning

confidence: 98%

“…Data have demonstrated a high prevalence of the use of over the counter vitamin products for healthcare and disease management, often without the advice or awareness of the user's allopathic or traditional healthcare providers (12)(13)(14)(15). Some healthcare providers have advocated high-dose niacin as a treatment for schizophrenia, although controlled outcome trial data are limited (16)(17)(18)(19)(20)(21)(22)(23)(24). In this case, our patient followed advice available on the World Wide Web that advocated the use of high doses of niacin for treatment of schizophrenia.…”

Section: Introductionmentioning

confidence: 97%

Treatment Advice on the Internet Leads to a Life-Threatening Adverse Reaction: Hypotension Associated with Niacin Overdose

Mularski¹,

Grazer

Santoni

et al. 2006

Clinical Toxicology

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We describe a case of massive oral niacin overdose that resulted in severe persistent hypotension without the manifestation of cutaneous flushing. This case is the highest overdose of niacin reported in the literature to date and the first time severe persistent hypotension has been attributed to niacin. A 56-year-old male with a history of schizophrenia presented to the emergency department after orally ingesting 11,000 mg of niacin. The patient cited an Internet resource that recommended high-dose niacin for therapy of schizophrenia as the reason for his ingestion. He stopped his psychiatric medications several weeks prior to his niacin overdose. At presentation, the patient was alert and normothermic. His pulse was 68 beats per minute and his blood pressure was initially 92/41 mmHg. Hypotension with a blood pressure of 58/40 developed over the next few hours and persisted despite intravenous infusion of over 4 liters of normal saline. The physical exam was otherwise unremarkable, specifically without signs of an allergic reaction or cutaneous flushing. He required intravenous dopamine infusion for 12 hours to support a mean arterial blood pressure greater than 60 mmHg. Evaluation for other etiologies of hypotension was unrevealing. Serum niacin levels were 8.2 ug/ mL and 5.6 ug/mL at 48 and 96 hours post ingestion, respectively, giving an apparent T1/2 of 87 hours. Massive overdose of niacin appears to be capable of causing severe, persistent hypotension in the absence of cutaneous flushing. In this case, the ingestion of a dietary supplement based on Internet advice led to a severe adverse reaction.

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“…Abram Hoffer has found that he could cure schizophrenia (as he claimed) with high doses of Niacin (vitamin B3), Omega 3 and Vitamin C [33][34][35]. I have followed this approach for about 10 years and found it very beneficial.…”

mentioning

confidence: 99%

Suggestions for Treatment of Schizophrenia

Beyer¹

2019

Biomedical Journals

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Treatment of Schizophrenia

Cited by 6 publications

References 9 publications

Pharmacological Targeting of IDO-Mediated Tolerance for Treating Autoimmune Disease

Pharmacological Targeting of IDO-Mediated Tolerance for Treating Autoimmune Disease

Treatment Advice on the Internet Leads to a Life-Threatening Adverse Reaction: Hypotension Associated with Niacin Overdose

Suggestions for Treatment of Schizophrenia

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