Function

Mnemonic

Active forms of Niacin are NAD+ and NADP+.

Cofactor for redox reactions (e.g., alcohol dehydrogenase, isocitrate dehydrogenase, G6PD)
Required for the metabolism of fats, carbohydrates, and proteins.
Synthesized endogenously from the amino acid tryptophan. Requires vitamins B2 (riboflavin) and B6 (pyridoxine) as cofactors.

Therapeutic use

Dyslipidemia: Niacin lowers VLDL and increases HDL serum levels (See Lipid-lowering agents)

Malnutrition: Most common cause worldwide (e.g., alcohol use disorder, diets heavy in corn).
Hartnup disease: Autosomal recessive disorder causing defective intestinal and renal absorption of neutral amino acids, including tryptophan. t
Malignant carcinoid syndrome: Increased metabolism of tryptophan to serotonin leads to less tryptophan available for niacin synthesis.
Isoniazid (INH) therapy: INH depletes vitamin B6 (pyridoxine), a required cofactor for niacin synthesis.
Prolonged diarrhea: Malabsorption.

Dermatitis:
- Photosensitive hyperpigmented rash on sun-exposed areas. t
- Casal necklace: Broad collar-like rash on the neck (C3/C4 dermatome).
- Thick, scaly skin on hands/feet (“glove and stocking”).
Diarrhea: Atrophy of columnar epithelium of GI tract.
Dementia: Neuronal degeneration (hallucinations, insomnia, anxiety, memory loss).
Glossitis: Swollen, beefy-red tongue.

Mnemonic

The 3 D’s of B₃.: Dermatitis, Diarrhea, and Dementia.

3 for tree: dermatitis, dementia

Facial flushing: due to prostaglandin release and NOT due to histamine (typically seen when niacin therapy is started, can be avoided by coadministration of aspirin)
Hyperuricemia, podagra
- Niacin decreases renal uric acid excretion.
Hyperglycemia