Niacin (patient information)

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Niacin, also known as nicotinic acid or vitamin B3, is a water-soluble vitamin whose derivatives such as NADH, NAD, NAD+, and NADP play essential roles in energy metabolism in the living cell and DNA repair.[1] The designation vitamin B3 also includes the corresponding amide nicotinamide (or "niacinamide"), whose chemical formula is C6H6NO2.

Other functions of niacin include removing toxic chemicals from the body,[2] and assisting in the production of steroid hormones made by the adrenal gland, such as sex hormones and stress-related hormones.


Niacin was first discovered from the oxidation of nicotine to form nicotinic acid. When the properties of nicotinic acid were discovered, it was thought prudent to choose a name to dissociate it from nicotine, in order to avoid the perception that vitamins or niacin-rich food contain nicotine. The resulting name 'niacin' was derived from nicotinic acid + vitamin.

Niacin is also referred to as Vitamin B3 because it was the third of the B vitamins to be discovered. It has historically been referred to as "vitamin PP", a name derived from the term "pellagra-preventing factor", because the disease pellagra is due to a deficiency of niacin in the diet.

Dietary needs

The recommended daily allowance of niacin is 2-12 mg a day for children, 14 mg a day for women, 16 mg a day for men, and 18 mg a day for pregnant or breast-feeding women.[3]

Severe deficiency of niacin in the diet causes the disease pellagra, whereas mild deficiency slows down the metabolism, causing decreased tolerance to cold.

Dietary niacin deficiency tends to occur only in areas where people eat corn (maize), the only grain low in niacin, as a staple food, and that don't use lime during meal/flour production. Alkali lime releases the tryptophan from the corn in a process called nixtamalization so that it can be absorbed in the intestine, and converted to niacin.[2]

Pharmacological uses

Niacin, when taken in large doses, blocks the breakdown of fats in adipose tissue, thus altering blood lipid levels. Niacin is used in the treatment of hyperlipidemia because it reduces very low density lipoprotein (VLDL), a precursor of low density lipoprotein (LDL) or "bad" cholesterol. Because niacin blocks breakdown of fats, it causes a decrease in free fatty acids in the blood and consequently, decreased secretion of VLDL and cholesterol by the liver.[4]

By lowering VLDL levels, niacin also increases the level of high density lipoprotein (HDL) or "good" cholesterol in blood, and therefore it is sometimes prescribed for patients with low HDL, who are also at high risk of a heart attack.[5] An extended release formulation of niacin for this indication is marketed by Abbott Laboratories under the trade name Niaspan.

Niacin is sometimes consumed in large quantities by people who wish to fool drug screening tests, particularly for lipid soluble drugs such as marijuana.[6] It is believed to "promote metabolism" of the drug and cause it to be "flushed out". However, scientific studies have shown it does not affect drug screenings and can pose a risk of overdose, causing arrhythmias, metabolic acidosis, hyperglycemia, and other serious problems (see below).


People taking pharmacological doses of niacin (1.5 - 6 g per day) often experience a syndrome of side-effects that can include one or more of the following:[7]

Facial flushing is the most commonly reported side effect.[8] It lasts for about 15-30 minutes, and is sometimes accompanied by a prickly or itching sensation. This effect is mediated by prostaglandins and can be blocked by taking 300 mg of aspirin half an hour before taking niacin, or by taking one tablet of ibuprofen per day. Taking the niacin with meals also helps reduce this side effect. After 1 to 2 weeks of a stable dose, most patients no longer flush. Slow or "sustained" release forms of niacin have therefore been developed to lessen these side effects.[9][10] [11] One study showed the incidence of flushing was 4.5x lower (1.9 vs. 8.6 episodes in the first month) with a sustained-release formulation.[12]

Doses above 2 g per day have been associated with liver damage, particularly with slow-release formulations. [13]

High-dose niacin may also elevate blood sugar, thereby worsening diabetes mellitus.[14] Hyperuricemia is another side effect of taking high-dose niacin; thus niacin may worsen gout[citation needed].

Niacin at doses used in lowering cholesterol has been associated with birth defects in laboratory animals and should not be taken by pregnant women.[15]

Niacin at extremely high doses can have life-threatening acute toxic reactions. One patient suffered vomiting after taking eleven 500-milligram niacin tablets over 36 hours, and another was unresponsive for several minutes after taking five 500-milligram tablets over two days.[16][17] Extremely high doses of niacin can also cause niacin maculopathy, a thickening of the macula and retina which leads to blurred vision and blindness.[18]

Inositol hexanicotinate

One popular form of dietary supplement is inositol hexanicotinate, usually sold as "flush-free" or "no-flush" niacin (although those terms are also used for regular sustained-release.) While this form of niacin does not cause the flushing associated with the nicotinic acid form, it is not clear whether it is pharmacologically equivalent in its positive effect [19].


The liver can synthesize niacin from the essential amino acid tryptophan (see below), but the synthesis is extremely inefficient; 60 mg of tryptophan are required to make one milligram of niacin.[20]

The 5-membered aromatic heterocycle of the essential amino acid, tryptophan, is cleaved and rearranged with the alpha amino group of tryptophan into the 6-membered aromatic heterocycle of niacin by the following reaction:

Food sources

Animal products: Fruits and vegetables: Seeds: Fungi:


  1. Northwestern University Nutrition
  2. 2.0 2.1 Vitamin B3 University of Maryland Medical Center.
  3. Template:Pauling
  4. T. Katzung, Basic and Clinical Pharmacology, 9th ed. p. 570.
  5. Postgraduate Medicine
  6. Niacin abuse in the attempt to alter urine drug tests. Pharmacist's Letter/Prescriber's Letter 2007;23(6):230606.
  7. J.G. Hardman et al., eds., Goodman and Gilman's Pharmacological Basis of Therapeutics, 10th ed., p.991.
  8. NIH Medline Plus: Niacin.
  9. J.G. Hardman et al., eds., Goodman and Gilman's Pharmacological Basis of Therapeutics, 10th ed., p.991.
  10. T. Katzung, Basic and Clinical Pharmacology, 9th ed. p. 570.
  11. Options for therapeutic intervention: how effective are the different agents? European Heart Journal Supplements Vol 8 Suppl F Pp. F47-F53 [1]
  12. Chapman M, Assmann G, Fruchart J, Sheperd J, Sirtori C. Raising high-density lipoprotein cholesterol with reduction of cardiovascular risk: the role of nicotinic acid - a position paper developed by the European Consensus Panel on HDL-C. Cur Med Res Opin. 2004 Aug;20(8):1253-68. PMID 15324528
  13. J.G. Hardman et al., eds., Goodman and Gilman's Pharmacological Basis of Therapeutics, 10th ed., p.992.
  14. J.G. Hardman et al., eds., Goodman and Gilman's Pharmacological Basis of Therapeutics, 10th ed., p.991.
  15. J.G. Hardman et al., eds., Goodman and Gilman's Pharmacological Basis of Therapeutics, 10th ed., p.992.
  16. Hazards: Niacin to Pass a Drug Test Can Have Dangerous Results, By ERIC NAGOURNEY, New York Times, April 17, 2007[2]
  17. Mittal MK, Florin T, Perrone J, Delgado JH, Osterhoudt KC. Toxicity From the Use of Niacin to Beat Urine Drug Screening. Ann Emerg Med. 2007 Apr 4. PMID 17418450[3]
  18. JD Gass, Nictonic Acid Maculopathy, Am. J. Opthamology, 1973;76:500-10
  19. No-Flush Niacin for the Treatment of Hyperlipidemia
  20. Oxidization Reactions of Niacin from the Linus Pauling Institute at Oregon State University Linus Pauling Institute.

External links

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