Vitamin B3 (Niacin)

What is niacin and what does it do in the body?

Niacin is the general name for nicotinic acid (pyridine-3-carboxylic acid), nicotinamide, and related derivatives such as nicotinamide riboside. Tissues convert absorbed niacin into NAD (nicotinamide adenine dinucleotide), the main active form; NAD is then also converted into NADP (in all tissues except skeletal muscle). According to NIH, more than 400 enzymes require NAD, a number not seen for any other vitamin-derived coenzyme. ^[1]

NAD takes part mainly in breakdown reactions that transfer the potential energy in carbohydrates, fats, and proteins to ATP, the cell’s energy unit; the enzymes needed for maintaining genome integrity, controlling gene expression, and cell signaling also use NAD. NADP supports building reactions such as cholesterol and fatty acid synthesis and the cell’s antioxidant function. ^[1] NAD and NADP taken in with food are converted to nicotinamide in the intestine and absorbed. ^[1]

Tryptophan is also a source of niacin: by the most commonly used estimate, 60 mg of tryptophan is converted into 1 mg of niacin (niacin equivalent, NE). The efficiency of the conversion varies widely between people. If riboflavin (B2), pyridoxine (B6), or iron is insufficient, the conversion decreases. ^[1]

How much niacin is needed per day?

The US Food and Nutrition Board, on which NIH relies, gives the RDA for adults over 19 years as 16 mg NE for men and 14 mg NE for women; it is 18 mg NE in pregnancy and 17 mg NE in breastfeeding. The values are based on urinary excretion of niacin metabolites in adults. ^[1] EFSA (in the summary report published in 2017) ties niacin requirement to energy requirement: the average requirement (AR) is 1.3 mg NE/MJ and the population reference intake (PRI) is 1.6 mg NE/MJ (about 6.6 mg NE/1,000 kcal); these values apply to adult groups, including pregnancy and breastfeeding, and hold if other nutrients (iron, riboflavin, B6, protein) are adequate. ^[2] In Türkiye, a 2008 book published on the HSGM (Ministry of Health, General Directorate of Health Promotion) website also gives the daily niacin requirement as 6.6 mg per 1,000 calories. ^[10]

NIH reports that, according to NHANES 2015–2016, mean niacin intake from food and beverages in the US was 31.4 mg in men and 21.3 mg in women, and that in 2009–2012 data only 1% of adults had an intake below the EAR; in the US many breads and cereals are fortified with niacin, and these products should not be assumed to have the same content in Türkiye. ^[1]

Which foods contain niacin?

Animal foods (poultry, beef, fish) provide about 5–10 mg of niacin per serving; nuts, legumes, and grains provide 2–5 mg. In some grains, natural niacin is bound to polysaccharides and glycopeptides, so its bioavailability is about 30%; free niacin added for fortification is well absorbed. ^[1]

The table shows NIH’s US servings; the values do not include what is formed from tryptophan, and the US daily value (DV) is 16 mg for adults. 20% and above counts as a “high source.” ^[1] In Türkiye, the book on the Ministry of Health’s HSGM website lists meat, fish, poultry, liver, yeast, grains, dried legumes, and green leafy vegetables as niacin sources. ^[10]

What are pellagra and niacin deficiency?

According to NIH, severe niacin deficiency causes pellagra: a pigmented, scaly rash on sun-exposed skin, a bright red tongue, vomiting, constipation or diarrhea, and neurological symptoms such as depression, apathy, headache, fatigue, memory loss, and hallucinations. Pellagra is rare in industrialized societies; it is mostly seen in refugees and displaced people who eat a very limited diet poor in niacin and protein. In the early 20th century it was common in the southern US and parts of Europe among people whose diet was based mainly on corn. ^[1] In Türkiye, the book on the HSGM website also states that pellagra is seen mostly in societies with a one-sided diet, especially those consuming only corn. ^[10]

NIH reports that the World Health Organization addresses pellagra with medical treatment using nicotinamide and B complex or yeast products over weeks; this guide gives no regimen. The risk of niacin insufficiency increases in the following situations: ^[1]

• Inadequate nutrition: Poverty, anorexia, alcohol use disorder, AIDS, inflammatory bowel disease, or liver cirrhosis. ^[1]
• Riboflavin, B6, or iron insufficiency: The conversion of tryptophan to niacin decreases. ^[1]
• Hartnup disease: A rare genetic disease that impairs tryptophan absorption and increases its loss in urine. ^[1]
• Carcinoid syndrome: Tryptophan is diverted to serotonin instead of niacin. ^[1]
• Isoniazid and pyrazinamide: According to NIH, these tuberculosis drugs block niacin production from tryptophan; pellagra can develop and can be prevented by increasing niacin intake. ^[1]

Blood niacin level is not a reliable indicator of status. The most sensitive and reliable measure is urinary excretion of the two methylated metabolites (N1-methylnicotinamide and N1-methyl-2-pyridone-5-carboxamide): in adults, more than 17.5 µmol per day reflects adequate status, 5.8–17.5 µmol low status, and less than 5.8 µmol deficient status. ^[1]

Does niacin lower cholesterol or protect the heart?

The right distinction has two layers: lipid values and clinical outcomes. According to NIH, nicotinic acid doses more than 100 times the RDA are effective in treating dyslipidemia over months to years; nicotinamide does not show this effect because it does not bind to the receptors that mediate the lipid effect. In studies since the late 1950s, these doses have raised HDL by 10–30% and lowered LDL by 10–25%, triglycerides by 20–50%, and lipoprotein(a) by 10–30%. ^[1]

Cardiovascular events are a separate question. In HPS2-THRIVE, 25,673 adults with vascular disease (all on statin-based LDL-lowering therapy) received 2 g/day of extended-release niacin with the flushing-preventing laropiprant, or placebo; over a median 3.9 years of follow-up, LDL was on average 10 mg/dL lower and HDL 6 mg/dL higher, but there was no significant effect on major vascular events (13.2% and 13.7%; rate ratio 0.96; 95% CI 0.90–1.03). In the niacin group, the absolute excess was 3.7 points for serious diabetes control disorders, 1.3 points for new diabetes diagnosis, 1.0 for serious gastrointestinal events, 0.7 for musculoskeletal events, 0.3 for skin events, 1.4 for infection, and 0.7 for bleeding. The study was funded by sources including the manufacturer; the formulation tested is a combination of niacin and laropiprant. ^[5]

NIH also reports that a study of 3,414 patients (1,500–2,000 mg/day extended-release niacin added to a statin) was stopped after 3 years because of no additional benefit and an increase in the risk of ischemic stroke. ^[1] In a large study in the 1970s (8,341 people who had previously had a myocardial infarction, 3,000 mg/day of nicotinic acid, mean 6.2 years), nonfatal infarctions decreased but arrhythmia increased; total and cause-specific mortality did not fall over the years, while a 11% reduction in all-cause mortality was reported 9 years after the study ended. ^[1]

The Cochrane review (Schandelmaier et al., 2017; 23 RCTs published between 1968 and 2015, 39,195 participants; median dose 2 g/day, median duration 11.5 months) reported that niacin did not reduce all-cause mortality (RR 1.05; 95% CI 0.97–1.12), cardiovascular mortality (RR 1.02; 0.93–1.12), fatal or nonfatal infarction (RR 0.93; 0.87–1.00), or stroke (RR 0.95; 0.74–1.22). Discontinuation because of side effects was more frequent with niacin (RR 2.17; 1.70–2.77). The authors concluded that niacin is unlikely to be beneficial for preventing cardiovascular events. ^[4]

NIH reports that the 2018 ACC/AHA guideline states that niacin may be useful in some cases of severe hypertriglyceridemia but lowers LDL only mildly, and that it does not recommend it as an add-on to a statin. ^[1] For this reason, this guide assigns grade B to niacin for lipid values and grade E to its reducing cardiovascular events when added on top of a statin.

Does nicotinamide prevent skin cancer?

This question is separate from niacin’s lipid effect and belongs to the nicotinamide form. In ONTRAC (phase 3, double-blind), 386 people who had had at least two nonmelanoma skin cancers in the previous 5 years received 500 mg of nicotinamide twice daily or placebo for 12 months. The rate of new nonmelanoma skin cancers was 23% lower in the nicotinamide group (95% CI 4–38; p=0.02); there was a 20% reduction (−6 to 39) in basal cell carcinoma and a 30% reduction (0 to 51) in squamous cell carcinoma, and the number of actinic keratoses decreased. No benefit was seen after the drug was stopped. ^[6] In immunosuppressed organ transplant recipients, ONTRANS (158 people, stopped early) showed no difference in the number of new keratinocyte cancers at 12 months (RR 1.0; 95% CI 0.8–1.3). ^[7] A 2023 meta-analysis pooling four studies, combining immunocompetent and immunosuppressed patients, found RR 0.82 (0.61–1.12) for nonmelanoma skin cancer and judged the evidence that oral nicotinamide significantly reduces the number of keratinocyte cancers to be insufficient. ^[8]

The 1,000 mg/day in ONTRAC is above the SCF’s adult nicotinamide upper limit of about 900 mg/day; NIH states that upper limits do not apply to niacin given under medical supervision. ^{[3] [1]} For this reason, the result cannot be carried over to a supplement taken on its own.

On the question of preventing type 1 diabetes, in ENDIT (Europe, Canada, US; 552 first-degree relatives of people with type 1 diabetes who were islet cell antibody positive, 5 years, modified-release nicotinamide or placebo), there was no difference in the development of diabetes (unadjusted HR 1.07; 95% CI 0.78–1.45). ^[9]

Niacin supplements and high-dose risks

No adverse effects have been reported from natural niacin intake through food. As a supplement or drug, nicotinic acid at 30–50 mg and above usually causes flushing: redness, burning, tingling, and itching of the face, arms, and chest; these symptoms are considered uncomfortable rather than toxic, but headache, rash, dizziness, and a drop in blood pressure may accompany them. Nicotinamide does not cause flushing. Inositol hexanicotinate is labeled “flush-free”; NIH notes that its mean absorption is about 30% lower than that of nicotinic acid and nicotinamide and that it is highly variable. ^[1]

1,000–3,000 mg/day of nicotinic acid causes more serious effects: hypotension that raises the risk of falls, fatigue, impaired glucose tolerance and insulin resistance, nausea, heartburn and abdominal pain, blurred vision, and macular edema. High doses over months to years can raise liver enzymes and lead to hepatitis and acute liver failure; hepatotoxicity is more likely with extended-release forms. With nicotinamide, nausea, vomiting, and liver toxicity have been reported at 3,000 mg/day; in dialysis patients, diarrhea and thrombocytopenia were most common at 500–1,500 mg/day. ^[1]

NIH reports that ACC/AHA recommends measuring liver transaminases, fasting blood sugar or HbA1c, and uric acid at baseline, while the dose is being raised, and every 6 months afterward in people using nicotinic acid supplements. It is recommended that it not be used when transaminases exceed 2–3 times the upper limit of normal, or when there is persistent hyperglycemia, acute gout, unexplained abdominal pain, new atrial fibrillation, weight loss, or persistent severe skin reactions. ^[1] In people using antidiabetic drugs, monitoring is needed because high-dose nicotinic acid raises blood sugar; this effect is most likely at doses of 1.5 g/day and above. ^[1]

The upper limits are framed differently by the two institutions and should not be confused. The UL of the Food and Nutrition Board, on which NIH relies, applies only to supplemental niacin and is 35 mg/day in adults (30 mg for ages 14–18; excluding use under medical supervision); it is based on flushing and applies to both forms. ^[1] The SCF (2002), in contrast, assessed the two forms separately: 10 mg/day for free nicotinic acid (applying an uncertainty factor of 3 to 30 mg, at which flushing is seen) and about 900 mg/day for nicotinamide (12.5 mg/kg/day; NOAEL 25 mg/kg/day and a factor of 2); these values do not apply in pregnancy and breastfeeding because of insufficient data. ^[3] According to NIH, in NHANES 2003–2006, total niacin intake reached or exceeded the UL in 10% of supplement users aged 2 years and older. ^[1]

NMN and nicotinamide riboside (NR) are not labeled as niacin sources; NIH writes that FDA decided in November 2022 that NMN cannot be lawfully marketed as a dietary supplement in the US because it had been authorized for investigation as a new drug. ^[1] In its letter dated December 2, 2025, FDA, in turn, stated that it changed its interpretation on this issue on September 29, 2025 and determined that NMN is not excluded from the supplement definition, thereby superseding the November 2022 letter; this is a regulatory classification, not a safety or efficacy assessment. ^[12]

What is niacin’s status in Türkiye?

As a supplement, niacin falls under the Ministry of Agriculture and Forestry’s Turkish Food Codex Communiqué on Food Supplements (2013/49). According to the current text with amendments incorporated, the Communiqué requires that, of the vitamins and minerals, only those listed in Annex-1 be used in the forms specified in Annex-2, and that daily maximum limits comply with Annex-3; it does not permit statements in labeling, presentation, and advertising claiming to prevent, treat, or cure disease, and it prohibits the production and placing on the market of food supplements for infants and young children under 2 years of age (before the amendment of November 21, 2015, this limit was 4 years); the Ministry evaluates products aimed at the 2–4 age group separately. ^[11]

Evidence table: claim, population, and limits

This guide does not set personal doses; the use of high-dose nicotinic acid or nicotinamide, in the presence of statins, antidiabetic and tuberculosis drugs, liver disease, or gout, depends on the decision of the treating physician.