Vitamins

Niacin (Vitamin B3)

By All The Nutrients Editorial Team Published: 7 min read

Niacin (vitamin B3) is a water-soluble B-vitamin that functions as the precursor to two essential coenzymes — NAD (nicotinamide adenine dinucleotide) and NADP (nicotinamide adenine dinucleotide phosphate) — found in every living cell. These coenzymes participate in over 400 enzyme reactions, making niacin central to energy metabolism, DNA repair, and cell signalling. Niacin can be synthesised in the body from the amino acid tryptophan (approximately 60 mg tryptophan yields 1 mg niacin equivalent), but dietary intake remains essential for adequate NAD levels. The richest dietary sources are poultry, fish, peanuts, mushrooms, and fortified grains.

Daily Value

16.0 mg

FDA 2020

Upper Limit

35.0 mg

per day

Top Source

Yeast extract spread

128 mg

What Does Niacin (Vitamin B3) Do?

  • Energy metabolism: NAD and NADP are the central electron carriers in cellular respiration. In glycolysis, the TCA cycle, and fatty acid β-oxidation, NAD⁺ accepts electrons (becoming NADH) from fuel oxidation; NADH then donates those electrons to the mitochondrial electron transport chain to generate ATP. Without NAD, no fuel — carbohydrate, fat, or protein — can be efficiently converted to usable energy.
  • DNA repair and genomic stability: PARP-1 (poly-ADP ribose polymerase), which detects and repairs single-strand DNA breaks, consumes enormous quantities of NAD⁺ during DNA repair. Severe niacin deficiency depletes NAD below the threshold for PARP activity, impairing DNA repair and genomic stability. This is thought to underlie the skin and mucosal lesions of pellagra (the deficiency disease), where rapidly dividing tissues are most vulnerable.
  • NAD⁺ as a longevity-related signalling molecule: NAD⁺ is the substrate for sirtuins (SIRT1–7) — a family of deacylases linked to metabolic regulation, stress resistance, mitochondrial biogenesis, and ageing. NAD⁺ levels decline with age, and this decline has been causally linked to hallmarks of ageing in animal models. Precursor supplementation (NMN, NR) is an active research area in longevity science, though human clinical translation is still early.
  • Lipid metabolism at pharmacological doses: At doses 50–100× the RDA (1,000–3,000 mg/day of nicotinic acid), niacin is a potent pharmacological agent — the most effective currently available drug for raising HDL cholesterol (by 15–35%), lowering triglycerides (by 20–50%), and shifting LDL from small, dense (atherogenic) to large, buoyant particles. This pharmacological effect is distinct from nutritional niacin function and requires medical supervision due to side effects (flushing, hepatotoxicity).
Horizontal bar chart of niacin per 100g: beef liver 14.9mg, peanuts dry roasted 12.1mg, chicken breast cooked 13.7mg, tuna cooked 13.3mg, turkey roasted 11mg, salmon cooked 10.6mg, portobello mushrooms 3.9mg. FDA DV reference line at 16mg.
Poultry, fish, and peanuts are the everyday niacin champions — a single chicken breast covers the full daily value.
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Signs of Niacin (Vitamin B3) Deficiency

Pellagra is the classic niacin deficiency disease, historically associated with populations subsisting on maize (corn) as a staple without lime treatment (nixtamalisation) or supplementary tryptophan sources. The "4 Ds" define pellagra:

  • Dermatitis — symmetrical, sun-exposed skin lesions that begin as erythema (redness) resembling sunburn, progress to hyperpigmentation, thickening, and eventually cracking ("crazy pavement" skin); the Casal's necklace (necklace-like skin lesion around the neck) is pathognomonic
  • Diarrhoea — inflammation of the gastrointestinal mucosa causing nausea, vomiting, and watery or bloody diarrhoea; intestinal villi atrophy in severe cases
  • Dementia / neuropsychiatric symptoms — anxiety, depression, disorientation, memory loss, and in severe cases, psychosis and hallucinations; reflect NAD depletion in the central nervous system
  • Death — untreated pellagra has a high mortality rate; the fourth D of classical teaching
  • Glossitis and angular stomatitis — inflammation of the tongue (beefy red, painful) and cracks at the mouth corners; seen in less severe B3 deficiency and often co-occurs with B2 and B6 deficiency
  • Pellagra-like syndrome from drug interactions — isoniazid (TB medication), 5-fluorouracil, and hartnup disorder (tryptophan absorption defect) can cause pellagra-like presentations by blocking tryptophan → niacin conversion despite adequate dietary intake

Upper Limit: The Tolerable Upper Intake Level (UL) for niacin is 35 mg/day for adults from supplements or fortified foods. The UL applies only to supplemental nicotinic acid or nicotinamide — not to naturally occurring niacin in whole foods. Above the UL: nicotinic acid causes prostaglandin-mediated flushing (uncomfortable but not harmful). At pharmacological doses (≥1,000 mg/day): sustained-release nicotinic acid has been associated with severe hepatotoxicity requiring liver transplant in rare cases. Regular monitoring of liver enzymes is required for anyone using niacin therapeutically.

Consider supplementing

B-Complex supplement

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How to Get the Most from Niacin (Vitamin B3)

Niacin from most food sources is well absorbed (nearly complete), but bioavailability varies between food matrices:

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Alkaline cooking (nixtamalisation) unlocks niacin in corn

Niacin in untreated maize is almost entirely bound to niacytin — a niacin-polysaccharide complex that is unabsorbable. Traditional lime-water soaking (nixtamalisation) of corn for tortillas, tamales, and hominy breaks these bonds, releasing free niacin and increasing bioavailability by 6–10 fold. This is why pellagra historically affected populations eating non-nixtamalised corn but not Mesoamerican populations with centuries of nixtamalisation practice.

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Tryptophan-rich protein contributes niacin equivalents

About 60 mg dietary tryptophan is converted to 1 mg niacin (1 niacin equivalent, NE). This conversion depends on riboflavin, B6, and iron as cofactors. Foods rich in tryptophan — turkey, chicken, milk, eggs, cheese — therefore contribute to niacin status even when not high in preformed niacin. When calculating intake, tryptophan contribution should be included in total niacin equivalents.

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Nicotinic acid supplement form causes flushing — take with food

The immediate-release nicotinic acid form of niacin (but not nicotinamide / niacinamide, or the timed-release forms) causes prostaglandin-mediated skin flushing — a harmless but uncomfortable vasodilation of skin capillaries — within 15–30 minutes of ingestion. Taking nicotinic acid supplements with food and starting with low doses (100 mg) greatly reduces flushing. Aspirin (325 mg) taken 30 minutes before also blunts flushing by blocking prostaglandin synthesis. Flush-free niacin (inositol hexanicotinate) does not cause flushing but also lacks the lipid-modifying effects of true nicotinic acid.

Common Niacin (Vitamin B3) Questions

How much niacin do I need per day?

The FDA Daily Value for niacin is 16 mg NE (niacin equivalents) per day. The National Academies RDA is 16 mg NE/day for adult men and 14 mg NE/day for adult women. During pregnancy: 18 mg NE/day; breastfeeding: 17 mg NE/day. The Tolerable Upper Intake Level (UL) is 35 mg/day for adults from niacin supplements or fortified foods (not from naturally occurring niacin in whole foods, which is not associated with adverse effects). The UL is based on the flushing threshold. Pharmacological doses (1,000–3,000 mg/day of nicotinic acid) for lipid management far exceed this UL and require medical supervision.

What foods are highest in niacin?

Per 100 g: beef liver (14.9 mg), chicken breast cooked (13.7 mg), tuna cooked (13.3 mg), turkey roasted (11.0 mg), salmon cooked (10.6 mg), peanuts dry roasted (12.1 mg), portobello mushrooms (3.9 mg), fortified breakfast cereals (up to 20 mg per serving). Many grains in the US and Canada are enriched with niacin — enriched white bread provides about 3 mg per slice, contributing substantially to average intakes. A diet including poultry, fish, peanuts, or fortified grains daily reliably meets the RDA.

Does niacin lower cholesterol?

At pharmacological doses (nicotinic acid 1,500–3,000 mg/day), niacin is a potent lipid modifier: it raises HDL by 15–35%, lowers triglycerides by 20–50%, and shifts LDL particles toward the less atherogenic large-buoyant type. Historically used as a first-line lipid therapy, it fell out of favour after the AIM-HIGH trial (2011) found that adding high-dose niacin to statin therapy did not reduce cardiovascular events despite improving the lipid panel. The HPS2-THRIVE trial (2014) confirmed no cardiovascular benefit when added to statins. Current role: primarily in patients who cannot tolerate statins or require additional triglyceride or HDL management. Niacin at dietary or supplement-RDA doses has no clinically meaningful effect on lipids.

What is pellagra?

Pellagra is the clinical syndrome of severe niacin deficiency, characterised by the "4 Ds": Dermatitis (sun-exposed skin lesions with hyperpigmentation and thickening), Diarrhoea, Dementia (neuropsychiatric symptoms), and Death if untreated. Historically, pellagra was epidemic in the US South (1906–1940) and in parts of Europe wherever populations depended on non-nixtamalised corn as a dietary staple. The disease was eradicated in developed countries by mandatory grain fortification with niacin (begun in the US in 1938–1941) and dietary diversification. Today, pellagra still occurs in parts of sub-Saharan Africa, among people with alcoholism, in malabsorption disorders, and in patients taking isoniazid or other niacin-antagonist drugs.

What is the difference between niacin and niacinamide?

Both are forms of vitamin B3 that the body converts to NAD and NADP and both prevent and treat pellagra at nutritional doses. The key difference lies in the side effects and pharmacological applications. Nicotinic acid (niacin) causes the prostaglandin-mediated skin flush and has potent lipid-modifying effects at doses above 1 g/day. Nicotinamide (niacinamide) does not cause flushing and lacks lipid-modifying effects but has other clinical uses: topical niacinamide is used in dermatology for acne, rosacea, and hyperpigmentation; oral niacinamide at 500 mg twice daily has shown modest benefit in reducing non-melanoma skin cancer recurrence in an Australian RCT. Neither form can substitute for the other in pharmacological (lipid-lowering) applications.