Natural Sources of Vitamin B-3 Niacin
Vitamin-B3-Niacin Rich Foods
Vitamin-B3-Niacin Rich Foods

What is Niacin

Niacin is a water-soluble vitamin that occurs in many animal and plant tissues. Niacin belongs to the vitamin B family also known as vitamin B3 or nicotinamide, a type of B vitamin and niacin deficiency causes pellagra. It is water-soluble, which means it is not stored in the body. Water-soluble vitamins dissolve in water. Leftover amounts of the vitamin leave the body through the urine. That means you need a regular supply of such vitamins in your diet. Niacin helps the digestive system, skin, and nerves to function. It is also important for converting food to energy.

Niacin can cause mild-to-moderate serum aminotransferase elevations and high doses and certain formulations of niacin have been linked to clinically apparent, acute liver injury which can be severe as well as fatal.

Niacin is converted to its active form niacinamide, which is a component of two coenzymes, nicotinamide adenine dinucleotide (NAD) and its phosphate form, nicotinamide adenine dinucleotide phosphate (NADP). These coenzymes play an important role in tissue respiration and in glycogen, lipid, amino acid, protein, and purine metabolism 2)), 3). Nicotinamide does not appear to exert antilipemic effects; the activity of other metabolites on lipoprotein fractions currently are unknown 4).

The principal antilipemic effect of niacin appears to result mainly from decreased production of very low density lipoprotein cholesterol (VLDL-cholesterol) 5). Decreased production of VLDL-cholesterol by niacin may be related to the partial inhibition of free fatty acid release from adipose tissue, a decreased delivery of free fatty acids to the liver, and a decrease in triglyceride synthesis and VLDL-triglyceride transport. Enhanced clearance of VLDL-cholesterol and chylomicron triglycerides also may occur, possibly as a result of enhanced activity of lipoprotein lipase. Reductions in LDL-cholesterol concentrations may be related to decreased production and enhanced hepatic clearance of LDL-cholesterol precursors (i.e., VLDL-cholesterol). The mechanism by which niacin increases HDL-cholesterol concentrations has not been fully elucidated but may be related to a decreased hepatic clearance of apo A-I-containing particles and decreased synthesis of apo A-II. Niacin has no effect on cholesterol synthesis or fecal excretion of fats, sterols, or bile acids.

Humans are able to synthesize nicotinic acid from tryptophan – the liver can synthesize niacin from the essential amino acid tryptophan, but the synthesis is extremely slow and requires vitamin B6; 60 mg of tryptophan are required to make one milligram of niacin 6). Bacteria in the gut may also perform the conversion but are inefficient.Another source for nicotinic acid is the gut flora. In humans there is no deamidation of nicotinamide to nicotinic acid in the gut. Nicotinamide is rapidly absorbed in stomach and small intestine. In plasma both the acid and the amide form are found. Erythrocytes take up the acid by a sodium dependent saturable transport system. Both the acid and the amide are able to pass the blood-brain barrier, however separate systems for uptake have been identified. Brain cells have a high affinity for nicotinamide, but not for nicotinic acid. Nicotinamide is the main substance that is transported between the different tissues as a precursor of NAD synthesis. The liver, kidneys, brain and erythrocytes prefer nicotinic acid as a precursor for NAD synthesis, but testes and ovaries prefer nicotinamide. NAD nucleosidase cleaves NAD with nicotinamide as one of the products. This can be deamidated to form nicotinic acid (and re-converted to NAD) or methylated and released via urine. Excretion of the amide (and its metabolites) tends to be more extensive compared to the acid 7).

A deficiency of this vitamin causes pellagra, a disease characterized by dermatitis, diarrhea, and dementia that is endemic today in parts of India and China, and may result in death in severe cases 8)). Other symptoms include irritability, loss of appetite, weakness, and dizziness. Niacin deficiency is rare in the United States but may still be seen in alcoholics, dietary cultists, and patients with malabsorption syndrome 9). Some clinicians prefer niacinamide for the treatment of pellagra because it lacks vasodilating effects 10). As a precursor of pyridine nucleotides (nicotinamide adenine dinucleotide (NAD) and nicotinamide adenine dinucleotide phosphate (NADP), niacin participates in the function of numerous enzymatic pathways, which are critical for normal cell metabolism, involving, for example redox reactions and those that consume NAD.

NAD (or Nicotinamide adenine dinucleotide) is used extensively in glycolysis and the citric acid cycle of cellular respiration. The reducing potential stored in NADH can be converted to ATP through the electron transport chain or used for anabolic metabolism. ATP “energy” is necessary for an organism to live. Green plants obtain ATP through photosynthesis, while other organisms obtain it by cellular respiration. (wikipedia). Nicotinamide adenine dinucleotide is a A coenzyme composed of ribosylnicotinamide 5′-diphosphate coupled to adenosine 5′-phosphate by pyrophosphate linkage. It is found widely in nature and is involved in numerous enzymatic reactions in which it serves as an electron carrier by being alternately oxidized (NAD+) and reduced (NADH) 11).

Niacin and its metabolites are rapidly excreted in urine. Following oral administration of single and multiple doses of an immediate-release (Niacor) or extended-release (Niaspan) niacin preparation, approximately 88 or 60-76% of the dose, respectively, was excreted in urine as unchanged drug and inactive metabolites 12).

Niacin Antihyperlipidemic Activity

Although the exact mechanism of action by which niacin lowers cholesterol is not fully understood, it may act by inhibiting the synthesis of very low density lipoprotein (VLDL), inhibiting the release of free fatty acids from adipose tissue, increasing lipoprotein lipase activity, and reducing the hepatic synthesis of very low density lipoprotein cholesterol (VLDL-C) and low density lipoprotein cholesterol (LDL-C) 13).

When Niacin is given in high doses alone or in combination with other medicines, it’s effective in lowering low density lipoprotein (LDL) cholesterol and triglyceride and raising high density lipoprotein (HDL) cholesterol, which makes this agent of unique value in the therapy of dyslipidemia. This may help prevent the development of pancreatitis (inflammation of the pancreas) and other problems caused by high levels of cholesterol and triglycerides in the blood. Niacin is also used to help lower risk of heart attack in patients with a history of heart attack and hyperlipidemia 14), 15).

Uses of Niacin

  • Niacin and niacinamide are indicated for prevention and treatment of vitamin B3 deficiency states.
  • Vitamin B3 (Niacin) when given in high doses, is effective in lowering low density lipoprotein (LDL) cholesterol, triglycerides, and raising high density lipoprotein (HDL) cholesterol, which makes this agent of unique value in the therapy of dyslipidemia. The magnitude of individual lipid and lipoprotein responses may be influenced by the severity and type of underlying lipid abnormality. The increase in total high density lipoprotein (HDL) “good” cholesterol is associated with a shift in the distribution of HDL subfractions with an increase in the HDL2:HDL3 ratio and an increase in apolipoprotein A-I content. Vitamin B3 (Niacin) treatment also decreases the serum levels of apolipoprotein B-100 (apo B), the major protein component of the VLDL (very low-density lipoprotein) and LDL fractions, and of lipoprotein-a, a variant form of low density lipoproteins cholesterol (LDL) independently associated with coronary risk 16), 17).
  • When given at these doses (1000 mg – 6000 mg daily), niacin has been shown to increase HDL and lower LDL cholesterol levels and to decrease rates of cardiovascular events in high risk individuals 18). The mechanism of action of niacin in hyperlipidemia is not well understood, but is believed to be related to inhibition of cAMP signaling pathways in adipocytes, which results in decreased release of lipids from fat cells. Niacin was officially approved for use in the United States in 1957 and is still widely used, although its role in management of hyperlipidemia in patients taking statins and other cholesterol lowering agents remains uncertain and controversial 19), 20).
  • Niacin comes as a tablet and an extended-release (long-acting) tablet to take by mouth. The regular tablet usually is taken two to three times a day with meals, and the extended-release tablet is taken once a day, at bedtime, after a low-fat snack. Follow the directions on your prescription label or package label carefully, and ask your doctor or pharmacist to explain any part you do not understand. Swallow the extended-release tablets whole; do not split, chew, or crush them. Take niacin exactly as directed. Do not take more or less of it or take it more often than prescribed by your doctor. For many years, doses of 1 to 3 grams of nicotinic acid per day has been a treatment option for low HDL cholesterol and high LDL cholesterol and triglyceride levels.
  • Regular niacin is available in multiple generic forms, under several brand names (including Niacor), in many concentrations as either tablets or capsules from 50 to 1,000 mg each. When used to treat hyperlipidemia, regular niacin is generally referred to as intermediate release [IR] niacin. IR-niacin must be taken several times daily and is associated with a high rate of cutaneous flushing. The recommended dosage for hyperlipidemia is 1 to 6 grams daily, starting at low doses (100 mg three times daily) and increasing at weekly intervals based upon tolerance and effect.
  • Sustained release [SR] formulations of niacins have been developed which are available over-the-counter. SR niacin can be taken once daily and is less likely to cause flushing, but is not approved for use in hyperlipidemia and has been associated with a high rates of hepatotoxicity in some studies.
  • Extended release (ER) capsules and tablets of niacin are available in concentrations ranging from 125 to 1,000 mg, which are approved for use in hyperlipidemia and have not been associated with a higher rate of hepatotoxicity compared to regular niacin. Niacin ER is available by prescription and over-the-counter in generic forms and under several brand names such as Niaspan and Niobid. The recommended daily dosage of niacin ER ranges from 500 to 2,000 mg generally given once daily at bedtime. Niacin is also available in combination with other lipid lowering drugs such as lovastatin (Advicor). Common side effects of niacin include nausea, fatigue, pruritus and flushing; flushing being a major dose-limiting side effect.
  • Niacin and niacinamide are also used to prevent niacin deficiency and to treat pellagra. Some clinicians prefer niacinamide for the treatment of pellagra because it lacks vasodilating effects. Pellagra may result from dietary deficiency, isoniazid therapy, or from decreased conversion of tryptophan to niacin in Hartnup disease or carcinoid tumors.

Although niacin and niacinamide have not been shown by well-controlled trials to have therapeutic value, the drugs have been used for the management of schizophrenic disorder, drug-induced hallucinations, chronic brain syndrome, hyperkinesis, unipolar depression, motion sickness, alcohol dependence, livedoid vasculitis, acne, and leprosy 21).

Niacin Food Sources

Niacin  is found in:

  • Milk
  • Eggs
  • Enriched breads and cereals
  • Rice
  • Fish
  • Lean meats
  • Legumes
  • Peanuts
  • Poultry

Dietary Reference Intakes for Niacin:

The best way to get the daily requirement of essential vitamins is to eat a balanced diet that contains a variety of foods.


  • 0 to 6 months: 2* milligrams per day (mg/day)
  • 7 to 12 months: 4* mg/day*Adequate Intake (AI)

Children (RDA)

  • 1 to 3 years: 6 mg/day
  • 4 to 8 years: 8 mg/day
  • 9 to 13 years: 12 mg/day

Adolescents and Adults (RDA)

  • Males age 14 and older: 16 mg/day
  • Females age 14 and older: 14 mg/day, 18 mg/day during pregnancy, 17 mg/day during lactation

Specific recommendations depend on age, gender, and other factors (such as pregnancy). Women who are pregnant or breast-feeding need higher amounts. Ask your health care provider which amount is best for you.

Niacin Supplement

Niacin is a component of most multivitamin and vitamin B preparations in concentrations close to the minimum daily requirement, which are not effective in lowering lipid levels. Niacin is also found in many herbal mixtures and energy drinks, but generally in low or modest doses.

The recommended dietary allowance (RDA) of this vitamin is 14 to 16 mg daily in adults, and slightly more for pregnant women (18 mg) and less for children (2 to 12 mg). Niacin given at or around these doses is not associated with significant side effects or liver injury 22).

Niacin is also used to prevent and treat pellagra (niacin deficiency), a disease caused by inadequate diet and other medical problems.

Side Effects of Niacin As Prescription Drug To Treat Dyslipidemia

Dyslipidemia, defined as elevated total or low-density lipoprotein (LDL) cholesterol levels, or low levels of high-density lipoprotein (HDL) cholesterol, is an important risk factor for coronary heart disease (CHD) and stroke.

Niacin as a prescription medicine can be used in a number of situations including the following:

  • Alone or in combination with other medications, such as HMG-CoA inhibitors (statins) or bile acid-binding resins;
  • to decrease the risk of another heart attack in patients with high cholesterol who have had a heart attack;
  • to prevent worsening of atherosclerosis (buildup of cholesterol and fats along the walls of the blood vessels) in patients with high cholesterol and coronary artery disease;
  • to reduce the amount of triglycerides (other fatty substances) in the blood in patients with very high triglycerides who are at risk of pancreatic disease (conditions affecting the pancreas, a gland that produces fluid to break down food and hormones to control blood sugar).

Results of a clinical study in people with heart disease and well-controlled cholesterol levels that compared people who took niacin and simvastatin with people who took simvastatin alone and found similar results for the two groups in the rate of heart attacks or strokes. Taking niacin along with simvastatin or lovastatin also has not been shown to reduce the risk of heart disease or death compared with the use of niacin, simvastatin, or lovastatin alone 23). Talk to your doctor if you have questions about the risks and benefits of treating increased amounts of cholesterol in your blood with niacin and other medications.

Side effects only occur for prescription medication to treat hyperlipidemia are far higher than the recommended dietary allowance (RDA) and are generally in the range of 1 to 6 grams  (1000 mg – 6000 mg daily) daily.

Depending on the strength of the medicine and also the number of doses you take each day, the time allowed between doses, common side effects are:

Although not all of these side effects may occur, if they do occur they may need medical attention.

Check with your doctor immediately if any of the following side effects occur:

  • Darkening of urine
  • light gray-colored stools
  • loss of appetite
  • severe abdominal or stomach pain
  • yellow eyes or skin
  • cough
  • diarrhea
  • feeling of warmth
  • flushing or redness of the skin, especially on the face and neck
  • headache
  • nausea or vomiting
  • rash or itching
  • runny nose
  • sneezing
  • stuffy nose

Other side effects not listed may also occur in some patients. If you notice any other effects, check with your healthcare professional.

Large doses of niacin can cause:

For high cholesterol and triglycerides:

  • For oral dosage forms (extended-release capsules, oral solution, or regular tablets):
    Adults—500 to 2000 milligrams (mg) one to three times a day.
  • For oral dosage form (extended-release tablets):
    Adults and children older than 16 years of age—At first, 500 milligrams (mg) per day, taken at bedtime. After 4 weeks, your doctor will increase your dose to 1000 mg per day, taken at bedtime. However, the dose is usually not more than 2000 mg per day.


  • Increased blood sugar (glucose) level
  • Liver damage
  • Peptic ulcers
  • Skin rashes
  • Rhabdomyolysis (serious muscle problem when used with statin medicine)

This medicine may make you dizzy. Do not drive or do anything else that could be dangerous until you know how this medicine affects you. Stand or sit up slowly.

If you need to stop taking extended-release niacin, even for a short time, talk to your doctor before you start taking it again. You may need to start back on a lower dose.

Tell any doctor or dentist who treats you that you are using this medicine. This medicine may affect certain medical test results.

Your doctor will do lab tests at regular visits to check on the effects of this medicine.

Niacin and Hepatotoxicity (Liver Injury & Toxicity) 24)

Niacin in doses above 500 mg daily causes transient, asymptomatic elevations in serum aminotransferase levels in up to 20% of people. The elevations are rarely greater than 3 times the upper limit of the normal range and usually resolve spontaneously even with continuation of the drug. The effect is partially dose related and is more common with doses above 3 g/day. In some patients, there is an overall decrease in serum proteins synthesized by the liver and, in some instances, coagulopathy with an increase in prothrombin time and decline in serum albumin, coagulation factors and apolipoproteins. These changes resolve rapidly upon stopping therapy and may not recur with lower doses.

Niacin can also cause serious hepatotoxicity, but this is uncommon. Significant hepatotoxicity is particularly common with high doses of sustained release niacin. In many cases, the injury becomes apparent after a dose increase or after switching from the regular crystalline to a sustained release form. The pattern is primarily hepatocellular, although cases with a cholestatic pattern have been described. The patients present with jaundice, itching, nausea, vomiting and fatigue. When the injury is the result of switching from the crystalline to the sustained release form, the injury may present acutely within days or a few weeks with a prodromal period of nausea, vomiting and abdominal pain, that is followed by jaundice and pruritus. Early during the injury serum aminotransferase levels are very high and then usually fall rapidly with discontinuation or dose lowering. The clinical phenotype resembles acute hepatic necrosis, suggesting a direct toxic effect. Imaging studies of the liver may reveal areas of hypodensity (“starry sky liver”) interpreted as focal fatty infiltration that resolves after stopping the drug. Liver biopsy typically shows varying degrees of centrolobular necrosis with only mild inflammation.

Mechanism of Injury

The mechanism of hepatotoxicity is assumed to be an intrinsic toxic reaction related to high serum levels of niacin that overwhelm the high affinity, low concentration nicotinic acid receptors (that are responsible for the flushing response). The finding that niacin can be restarted at lower doses after an episode of clinically apparent injury indicates that the hepatic damage is unlikely to be idiosyncratic or due to hypersensitivity.

Outcome and Management

Niacin hepatotoxicity appears to be dose dependent and more common with the sustained release form of the drug. Hepatotoxicity is less common with regular, crystalline niacin or extended release niacin. Most cases are mild and resolve rapidly upon stopping the medication, although in some instances, the injury is acute and severe and progresses to liver failure that is fatal or requires emergency liver transplantation. Complete resolution of the clinical symptoms is expected within days of stopping niacin, whereas serum enzyme elevations may require several weeks or months to resolve. Rechallenge with the same form leads to rapid recurrence and should be avoided. If the injury occurred after switching to a SR formulation, the crystalline form of niacin may be restarted at a lower dose and with caution.

A Niacin Deficiency causes Pellagra. The symptoms include:

  • Digestive problems
  • Inflamed skin
  • Mental impairment

Even normal doses can be associated with feeling warmth, redness, itching or tingling of the face, neck, arms or upper chest. This is called “flushing”. In most cases, this problem will get better after taking niacin on a regular basis for a while. To prevent flushing, do not drink hot beverages or alcohol at the same time you take niacin. New forms of nicotinic acid reduce this side effect. Nicotinamide does not cause these side effects. Some clinicians prefer niacinamide for the treatment of pellagra because it lacks vasodilating effects 25).

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