Depression niacin

Niacin Nicotinic acid, nicotinamide Coenzyme in oxidation and reduction reactions, functional part of NAD and NADP Pellagra—photosensitive dermatitis, depressive psychosis... 

Nicotinate and nicotinamide, together referred to as niacin, are required for biosynthesis of the coenzymes nicotinamide adenine dinucleotide (NAD"") and nicotinamide adenine dinucleotide phosphate (NADP" ). These both serve in energy and nutrient metabolism as carriers of hydride ions (see pp. 32, 104). The animal organism is able to convert tryptophan into nicotinate, but only with a poor yield. Vitamin deficiency therefore only occurs when nicotinate, nicotinamide, and tryptophan are all simultaneously are lacking in the diet. It manifests in the form of skin damage (pellagra), digestive disturbances, and depression. 

Pellagra is often characterized by mental abnormalities such as anxiety, irritability, and depression. The classic symptoms of pellagra are known as the 4 Ds -dementia, diarrhea, dermatitis, and death. Inflammation of mucosal surfaces, weakness, anorexia, and other gastrointestinal disturbances are also seen. Niacin (300 to 500 mg per day) is the definitive therapy. 

Gram doses of nicotinamide have been used in so-called orthomolecular psychiatry as a treatment for schizophrenia, originally because of the similarities between schizophrema and the depressive psychosis of pellagra. The underlying rationale for this use is that such high doses of niacin may deplete methyl donors, and at least one of the theories of the biochemical basis of schizophrenia was that the condition is caused by inappropriate methylation of neurotransmitter metabolites to yield psychotogenic compounds (Hoffer et al., 1957). There is no independent confirmation of the efficacy of nicotinamide in the treatment of schizophrenia. 

Nicotinic acid (niacin) Nicotinamide adenine dinucleotide (NAD+) Oxidation-reduction Pellagra (dermatitis, depression, diarrhea)... 

A diet deficient in niacin (as well as byptophan) leads to glossitis of the tongue, dermatitis, weight loss, diarrhea, depression and dementia. 

A precursor to the neurotransmitter serotonin, which promotes relaxation and sleep, tryptophan reduces anxiety and helps some forms of depression. It converts to niacin, lowers cholesterol, helps migraine headaches, and stimulates growth hormone. 

Niacin Deficiency. Niacin deficiency, manifested as pellagra, is characterized by the four Ds dermatitis, diarrhea, depression, and death. The dermatitis is characterized by a pigmented rash developing on skin exposed to... 

Hudson CJ, Lin A, Cogan S, Cashman F, Warsh JJ. The niacin challenge test Chnical manifestation of altered transmembrane signal transduction in schizophrenia Biol Psychiatry 1997 41 507-513. Ikonomov OC, Manji HK. Molecular mechanisms underlying mood stabilization in manic-depressive ill-... 

The earliest neurologic symptoms of pellagra are reminiscent of neurasthenia, with insomnia, fatigue, nervousness, irritability, and depression with memory loss (Victor et al, 1971). A progressive dementia can develop, but this seems unlikely to be caused solely by the absence of niacin. An acute confusional syndrome also occurs in human pellagra, and this is reversible with niacin therapy. A central neuritis is prominent in the large motor cortex cells (the Betz cells). This is not a demyelinating process like Bj2 deficiency but a primary involvement of the whole neuron. 

ADP-ribosylation reactions such as DNA repair, calcium mobilization and deacetylation (Kirkland 2009). In addition, at pharmacological concentrations, niacin is an effective agent for the treatment of dislipidemias and atherosclerosis (Prousky et al. 2011). Furthermore, evidence exists that niacin ameliorates acute migraine, chronic tension-type headaches, depression and schizophrenia (Prousky et al. 2011). This chapter focuses on chemical and biochemical aspects of the vitamin. 

Niacin deficiency leads to unwanted multisystemic problems that are often associated with dermatological changes. Pellagra is a condition in which niacin deficiency causes a symmetrical pigmented rash, thickened skin and superficial scaling which are found in sun-exposed body areas. The classic triad of niacin deficiency are the three D s—dermatitis, diarrhoea and dementia (Hegyi et al. 2004). Some of the effects on the central nervous system include depression, anxiety, restlessness and poor concentration. In addition, alcoholic individuals with poor nutrition can develop pellagroid encephalopathy (Cook et al. 1998). The role of niadn deficiency in cardiovascular disease and lipid metabolism remains to be fully explored. 

Earlier scientific Kterature reveals that niacin deficiency has been associated with three main types of psychiatric manifestations, which are (a) schizophreniform, (b) manic depressive types and (c) anxiety and depressive disorders (Rudin 1981). Schizophreniform manifestations include auditory hallucinations and persecutory delusions. 

The depressive psychosis is superficially similar to schizophrenia and the organic psychoses, but clinically distinguishable by the sudden lucid phases that alternate with the most florid psychiatric signs. It is probable that these mental symptoms can be explained by a relative deficit of the essential amino acid tryptophan, and hence reduced synthesis of the neurotransmitter serotonin, and not to a deficiency of niacin per se. 

Other claims for megadoses of nicotinic acid or nicotinamide, such as the claim that abnormalities associated with schizophrenia, Down s syndrome, hyperactivity in children, etc. can be reduced, have so far failed to win general acceptance. Clearly niacin deficiency or dependency can exacerbate some types of mental illness such as depression or dementia. There have been a number of attempts to treat depression with tryptophan or niacin, or both, on the basis that the correction of depressed brain levels of serotonin would be advantageous. However, these have met with only limited success. Schizophrenics have been treated with nicotinic acid on the basis that their synthesis of NAD is impaired in some parts of the brain, and that the formation of hallucinogenic substances such as methylated indoles may be controlled. 

Many tissues are affected by riboflavin deficiency (aribofla-vinosis). Riboflavin deficiency requires 3-4 months of deprivation to manifest and symptoms include lesions on the lips, inflammation of the tongue, lowered levels of white and red blood cells, excessive sensitivity to pain and vascu-larisation of the cornea. Deficiency also results in decreased conversion of tryptophan into niacin. A test for deficiency is to measure glutathione reductase levels, which are depressed when riboflavin levels are low as are xanthine oxidase levels. There is a link between riboflavin deficiency in pregnancy and the development of pre-eclampsia. However, supplementation with riboflavin in a trial indicated that there was no effect on the prevention of pre-eclampsia. Alcoholics are at increased risk of riboflavin deficiency as... 

There is some evidence that niacin can reduce the incidence of cancers of the mouth and throat. Niacin has been used to protect (3-cells in the pancreas in insulin-dependent diabetics and has been reported to increase insulin sensitivity. The effects of niacin in lowering cholesterol and low density lipoprotein have been studied extensively. High doses up to 1 g per day are required but the evidence for effectiveness is not wholly conclusive. There is some evidence that high doses of niacin improve survival rates in HIV infection. In conjunction with tryptophan, niacin has been used to treat depression. 

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