As a vitamin, requirements are low. High doses for lipids are a medical matter.
Niacin lowers apolipoprotein B (≈ −24 mg/dL) and raises apoA1 (≈ +8 mg/dL) in randomized trials; the effect is greater with doses >1,500 mg/day and with extended-release niacin. It improves lipid markers, although its real cardiovascular clinical benefit remains debated.
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Niacin, or vitamin B3, is a water-soluble B vitamin with a peculiar pharmacological profile and historically important clinical applications; it exists in two main chemical forms with clinically distinct properties: nicotinic acid (niacin proper) and nicotinamide or niacinamide (the form used for dermatological indications and to avoid the characteristic vasodilating effect of nicotinic acid); both forms are converted into the enzymatic cofactor NAD/NADP, central to hundreds of reactions in energy metabolism and DNA repair.
Historically, severe niacin deficiency causes pellagra, a disease with classic manifestations in the "three Ds" (diarrhea, dermatitis, dementia) that was endemic in populations consuming diets based on non-nixtamalized corn (where niacin is present but not bioavailable) in the southern United States in the early 20th century and in other regions; traditional nixtamalization of Mesoamerican corn and modern fortification of cereals have practically eliminated pellagra as a public health problem.
The most studied pharmacological indication of nicotinic acid is the treatment of dyslipidemia: at high doses (1,000-2,000 mg/day), nicotinic acid significantly reduces LDL cholesterol (15-25 percent), triglycerides (20-50 percent), and lipoprotein(a) (a specific cardiovascular risk factor), and raises HDL cholesterol (15-35 percent), a remarkably broad lipid-modulating profile that for decades positioned niacin as the second drug of choice for lowering lipids after statins.
However, the large modern clinical trials (AIM-HIGH, HPS2-THRIVE) have shown disappointing results: although lipid numbers improve as expected, they do not translate into significant reductions in hard cardiovascular events (heart attack, stroke, cardiovascular mortality) when niacin is added to optimal statin treatment; these data, together with the profile of significant side effects (especially flushing), have led to a major reduction in the clinical use of pharmacological niacin in dyslipidemia, although it retains a place in people with complex dyslipidemia or statin intolerance in specific circumstances.
Topical nicotinamide (not oral nicotinic acid) has documented efficacy in inflammatory acne, especially in 4-5 percent formulations; several trials have shown efficacy comparable to topical 1 percent clindamycin without the bacterial resistance problems associated with topical antibiotics, a dermatological indication with interesting clinical support.
An Australian randomized trial published in NEJM in 2015 showed that oral nicotinamide supplementation at 500 mg twice a day for 12 months significantly reduced the incidence of non-melanoma skin cancer (basal cell and squamous cell carcinoma) in people with a prior history of these cancers, a specific indication with solid clinical support and growing use in preventive dermatology in people with high cumulative sun exposure.
Oral nicotinic acid at therapeutic doses produces a characteristic cutaneous vasodilating effect called flushing: intense redness, a sensation of heat, itching, and sometimes palpitations that appear 15-30 minutes after the dose and last 30-60 minutes; although benign, this effect is very bothersome and significantly limits clinical adherence; nicotinamide does not cause flushing but also lacks the lipid-lowering effects; "no-flush" formulations such as inositol hexanicotinate partially retain the pharmacological activity with less flushing but also with less clear clinical efficacy.
Nutritional doses are 14-16 mg/day in adults; therapeutic doses for dyslipidemia are 1,000-3,000 mg/day of nicotinic acid (with gradual escalation to improve tolerance of flushing), ideally in sustained-release formulations with medical monitoring; for topical acne, 4-5 percent formulations applied according to the product's directions; for prevention of non-melanoma skin cancer, 500 mg of nicotinamide twice a day as in the reference trial's regimen.
Precautions are important with therapeutic doses of nicotinic acid: the flushing discussed above; hepatotoxicity with sustained-release formulations at high doses (immediate-release formulations have a better liver profile but worse flushing); increased blood glucose and insulin resistance with prolonged use at high doses; increased uric acid with possible precipitation of gout; gastrointestinal discomfort; people with active liver disease, active peptic ulcer, severe gout, or poorly controlled diabetes should avoid high doses; in pregnancy and breastfeeding, nutritional doses are safe but high therapeutic doses are not recommended; nicotinamide has a significantly more favorable safety profile than nicotinic acid and is preferable for indications where the lipid-lowering effect is not required (acne, skin cancer prevention); commercial products labeled "flush-free niacin" may vary in actual clinical efficacy, and it is advisable to read the specific composition.
Information, not medical advice. Scientific evidence reflects the quality of the studies.