Niacin deficiency – Niacin is a component of two important glycolytic enzymes — Nicotinaminde adenine dinucleotide (NAD) and NAD phosphate, as well as a regulator of DNA synthesis and repair. Nutritionally, it is available as —

a) Preformed niacin or nicotinic acid, mainly in non- vegetarian foods e.g. meat and fish; or

b) Synthesized from its precursor – Tryptophan, which is mainly present in milk and eggs (60 mg trytophan yields —1 mg of niacin).

Cereals and vegetarian diet are poor sources of free niacin as well as tryptophan.


Niacin deficiency is prevalent in maize-eating populations, due to its high leucine content that interferes with endogenous conversion of typtophan into niacin (amino acid imbalance). However in India, it is mainly seen in jowar-eating population of Telangana district in Andhra Pradesh, due to same reason.

Niacin deficiency

Clinically, prototype manifestation of niacin deficiency – Pellagra, presents with a triad of 3 D’s, as follows —

a) Dermatitis i.e. photosensitive rashes on exposed parts of body, often described as pellagrous glove (hands), boot (legs), necklace (neck) etc. Chronic cases may develop vesicobullous, weeping, desquamating or hyperpigmented lesions.

b) Chronic Diarrhea with/without vomiting.

c) Dementia with depression, dizziness, disorientation, delirium & burning sensation/numbness (parasthesia).


It rests on typical clinical triad, dietary history and response to niacin therapy. Reduced urinary excretion of N-methyl nicotinamide (a metabolite) has been used as an indicator of subclinical Niacin deficiency.


The treatment of Niacin deficiency includes oral niacin supplementation (50-300 mglday). TV niacin (TOO mg) may be given in severe cases, though it lead to an unpleasant sensation of local heat & flushing and rarely, the cholestatic jaundice. Avoidance of sun exposure, soothing topical agents over skin lesions and treatment of co-existing vitamin deficiencies is also necessary.