Vitamin B3 (niacin)

Vitamin B3 is not one compound but a family. Niacin (nicotinic acid) and nicotinamide (also called niacinamide) are the two dietary forms, and both are converted in the body to NAD: a coenzyme so central to metabolism that essentially every cell depends on it for turning food into usable energy, and for a set of repair and signalling enzymes that consume NAD as a substrate. The two forms share that destination and behave very differently on the way there, which is the single most useful thing to understand about B3 and the reason advice about it so often contradicts itself.

As a nutrient the story is short. Requirements are modest, B3 is present in meat, fish, wholegrains, legumes and fortified foods, and the body can also make a little from the amino acid tryptophan. Frank deficiency, pellagra, the classic triad of dermatitis, diarrhoea and dementia, is essentially absent in developed countries outside of alcohol dependence, severe malabsorption and a few rare metabolic conditions. For almost everyone eating a mixed diet, dietary needs are already covered and a supplement adds nothing.

The interest therefore comes from pharmacological doses, which are one to two orders of magnitude above nutritional intake, and at that level niacin stops being a vitamin and starts being a drug. It shifts blood lipids convincingly, raising HDL substantially, lowering triglycerides and lowering LDL, and on that basis it was prescribed for decades. Then the outcome trials arrived. AIM-HIGH randomised 3,414 patients on statins to extended-release niacin or placebo; the lipids moved as expected and cardiovascular events did not fall. HPS2-THRIVE followed with 25,673 patients and found the same absence of benefit, alongside significant excess harm: more new-onset diabetes and worse control in existing diabetes, plus gastrointestinal, musculoskeletal and skin adverse events. Niacin for lipid-lowering has since largely disappeared from guidelines.

That sequence is a useful lesson in its own right: it is one of the clearest demonstrations that improving a blood marker is not the same as improving health, and it is part of why HDL is now widely read as a marker of good metabolic health rather than a target to raise. More recently, work published in Nature Medicine identified 4PY, a terminal breakdown product of excess niacin, as associated with higher cardiovascular event rates, with laboratory evidence that it directly promotes vascular inflammation. That finding is early and concerns excess rather than dietary intake, but it points in the same direction as the trials rather than against them.

Nicotinamide is the non-flushing form and has a different profile again. It does not meaningfully shift lipids, and its best evidence is dermatological: topical niacinamide has clinical-trial support for pigmentation, blotchiness and barrier function, and oral nicotinamide has been trialled for skin-cancer chemoprevention in people at high risk under medical supervision; a finding that does not transfer to the general population. It is also the form used in the NAD-boosting supplements sold for longevity, usually as nicotinamide riboside or nicotinamide mononucleotide. Those reliably raise blood NAD levels; whether raising NAD produces any clinical benefit in healthy humans remains unsettled, and a raised biomarker is precisely what the niacin story cautions against reading as a result.

The practical position is straightforward. If you eat a mixed diet you do not need supplemental B3. If you are considering the doses used for lipids, that is a medical decision with poor outcome evidence and real harms behind it. And the flush, the intense, uncomfortable reddening and prickling that niacin causes at higher doses, is a genuine physiological effect, not an impurity or a sign the product is working.

Sources

• PubMed: niacin nicotinamide vitamin B3 supplementation lipids NAD (research overview)
• HPS2-THRIVE Collaborative Group. Effects of extended-release niacin with laropiprant in high-risk patients. N Engl J Med 2014;371:203–212
• AIM-HIGH Investigators. Niacin in patients with low HDL cholesterol levels receiving intensive statin therapy. N Engl J Med 2011;365:2255–2267
• Ferrell M, et al. A terminal metabolite of niacin promotes vascular inflammation and contributes to cardiovascular disease risk. Nat Med 2024;30:424–434; PMID 38374343