title: Antidepressants may lead to a decrease in niacin and NAD in patients with poor dietary intake.
abstract: The term niacin is the generic name for the two compounds nicotinic acid and nicotinamide, the major dietary precursors for two important coenzymes, nicotinamide adenine dinucleotide (NAD) and its phosphorylated form, NADP. Niacin is important for the maintenance of cellular integrity and energy production and is involved in more than 500 intracellular reactions. Deficiencies of niacin may contribute to neuropsychiatric and neurodegenerative disorders. Patients who develop nutritional deficiencies as a result of poor dietary intake, especially inadequate intake of proteins and vitamins, could potentially suffer from niacin deficiency and NAD depletion. However, de novo synthesis of niacin and NAD in the kynurenine pathway of tryptophan metabolism may compensate for impaired dietary intake. The rate of synthesis of NAD and niacin from tryptophan oxidation depends on the induction of the enzyme indoleamine 2,3-dioxygenase (IDO) by pro-inflammatory cytokines such as interferon-gamma. Niacin synthesis is not limited by a decrease in tryptophan and excessive IDO activity may therefore lead to a decline in tryptophan levels. Antidepressants have an anti-inflammatory effect, including reduction of interferon-gamma and therefore inhibition of IDO, the rate-limiting enzyme of the kynurenine pathway. In theory, this could account for increased serotonin as more tryptophan becomes available for serotonin synthesis. However, the downside may be that less NAD and niacin are synthesised downstream, which could exacerbate common psychiatric problems. It is our hypothesis that patients with poor dietary intake, who are treated with antidepressants, are at risk of developing niacin/NAD deficiency with possible development of associated neuropsychiatric symptoms. We therefore propose that niacin supplementation be considered in patients with inadequate diets who are treated with antidepressants. We believe that if this does not happen, a subclinical niacin deficiency may result, which would be difficult to detect as it would cause the same symptoms of the original illness (e.g. depression). Niacin deficiency should be considered and ruled out in all patients with treatment-resistant depression, who have a poor response to antidepressants. This is potentially a cost-effective and easy intervention, which could be examined in a randomized controlled trial.
authors.affiliation: Department of Psychiatry, School of Medicine, Faculty of Health Sciences, University of Pretoria, South Africa. Electronic address: mviljoen@webafrica.org.za.
authors.forename: Margaretha
authors.initials: M
authors.lastname: Viljoen
authors.affiliation: East Herts Child and Adolescent Mental Health Service (CAMHS), Hertfordshire Partnership University NHS Foundation Trust, United Kingdom.
authors.forename: Annie
authors.initials: A
authors.lastname: Swanepoel
authors.affiliation: Department of Physiology, School of Medicine, Faculty of Health Sciences, University of Pretoria, South Africa.
authors.forename: Priyesh
authors.initials: P
authors.lastname: Bipath
mesh_terms: D000928:Antidepressive Agents / Q000009:adverse effects*; D019587:Dietary Supplements; D006801:Humans; D044342:Malnutrition / Q000378:metabolism* / Q000473:pathology; D008954:Models, Biological; D009243:NAD / Q000172:deficiency / Q000378:metabolism*; D009422:Nervous System Diseases / Q000517:prevention & control*; D009525:Niacin / Q000172:deficiency / Q000378:metabolism*
chemical_list: D000928:Antidepressive Agents; D009243:NAD; D009525:Niacin