Niacin (Nicotinic Acid)


Article Author:
Soraya Djadjo


Article Editor:
Tushar Bajaj


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Mayank Singhal


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James Hughes
Beata Beatty
Nazia Sadiq
Hajira Basit
Phillip Hynes
Tehmina Warsi


Updated:
5/15/2019 9:35:54 PM

Indications

Niacin (a combination of nicotinic acid and nicotinamide), a B vitamin (vitamin B3), is a pharmacotherapeutic agent that has been used since 1955, making it the oldest, pleiotropic hypolipidemic agent.[1] The vitamin plays a role in both neuroprotection and neuronal death, giving it utmost importance in the proper functioning of the central nervous system (CNS), neuronal development, and function.[2]

Niacin has seen extensive use, alone or in combination, with statin medications (hydroxymethyl glutaryl coenzyme A reductase inhibitors) in the reducing of total cholesterol, triglycerides, low-density lipoprotein (LDL) cholesterol, very low-density lipoprotein (VLDL), and lipoprotein levels.  Moreover, niacin is the most potent agent used to increase plasma high-density lipoprotein (HDL) cholesterol.[3][1][4] In patients with diabetes mellitus or mixed dyslipidemia, niacin has demonstrated in clinical trials that it can counterbalance cardiovascular risk in this patient population, hence decreasing cardiovascular morbidity and mortality, especially when used in combination with statin drugs.[1][4]

Niacin being such a pleiotropic agent still possesses properties that are yet to be fully uncovered.  Some other studied uses of niacin other than the ones stated above are[5][6][7][8][9][10][11][12][13][14][15]:

  • Decreases  the incidence of cardiovascular events, premature aging, age-associated neurological disorders such as:
    • Alzheimer disease
    • Huntington's disease
    • Amyotrophic lateral sclerosis
    • Muscular atrophy
    • Parkinson disease
    • Squamous cell carcinoma
  • It also has therapeutic use in the treatment of diabetic encephalopathy, schizophrenia, malignant glioma, neurodegenerative diseases, hyperphosphatemia in chronic kidney disease and arthritis[14]
  • Circadian rhythm and metabolism regulation through sirtuins
  • Intracellular calcium regulation

Mechanism of Action

Niacin, after undergoing biochemical reactions in the mitochondria with nicotinamide, and tryptophan forms nicotinamide adenine dinucleotide (NAD) and NAD phosphate (NADP). NAD and NADP are the active forms of niacin which when reduced to NAD(H) and NADP(H) respectively, participates in catabolic redox reactions, and are cofactors in anabolic redox reactions.

Although niacin has been in use for many years, its useful pleiotropic effects make it a challenge to grasp its mechanism of action fully. However, a targeted mechanism of action based on certain effects niacin has in the human body are:

  1. Lipid metabolism: Lipid-lowering ability of niacin is very diverse and still under investigation. One proposed mechanism is the action of niacin’s antilipolytic effect, thought to be mediated via nicotinic acid receptors. An alternate mechanism recently uncovered is the ability of niacin to speed up the intracellular degradation of Apolipoprotein B (ApoB) containing lipoproteins, such as VLDL and LDL by inhibiting triglyceride synthesis. Also, niacin inhibits diacylglycerol acyltransferase 2 (DGAT2), thereby decreasing hepatic triglyceride synthesis. A suggested mechanism for the increase of HDL-cholesterol levels is the fact that niacin decreases the degradation of ApoA-I-containing lipoproteins, increases peroxisome proliferator-activated receptor γ (PPARγ) expression and enhances PPARγ transcriptional activity in macrophages.[16] Levels of free fatty acids are lowered via niacin’s downregulating action of cyclic adenosine monophosphate. By doing so, it decreases the most important intracellular mediator of pro-lipolytic stimuli.[17]
  2. Increased fasting glycemia: This is thought to be through roles of niacin-responsive G protein-coupled receptor (GPR109a) and plasma free fatty acids (FFAs). Though details of the mechanism are yet to be fully uncovered, research has observed a direct relationship has between insulin resistance in muscles and high FFA (in the form of lipid overload) concentrations in non-adipose tissues.  Also, intestinal cells in vivo are showed to increase their local glucose uptake when GPR109a gets stimulated by niacin, an effect which is thought to contribute to loss of glycemic control.[18]
  3. Aging-related process and pathologies: Though still yet to be fully uncovered, the mechanism of action through current research is thought to be the inverse relation between Nicotinamide adenine dinucleotide (NAD) concentrations and dietary niacin intake.  Researchers have demonstrated that reduced intracellular NAD concentrations lead to loss of a cell's power to undergo division and growth leading to cell aging and death.[6] NAD-dependent enzymes such as sirtuin proteins and poly(ADP-ribose) polymerase (PARP) not only provide continuous protection of the genome but are also necessary for the repair of damaged DNA. Cancer incidence and reactive oxygen species increase were observed with decreased PARP. Also, lifespan-extending effects of caloric restriction which are mediated by sirtuins, have been associated with premature aging and disorders like Huntington and other age-associated neurological disorders, in cells with defective sirtuins.[6][18]
  4. Malignant glioma:  Niacin is thought to inhibit glioma cell invasion both in vivo and in vitro.  Epithelial-mesenchymal transition (EMT) is involved in the process of cell migration, adhesion, and polarity; it also has involvement in the downregulation of E-cadherin, an epithelial marker and upregulation of Snail1, a mesenchymal marker, both processes which are important to the normal developmental of mesoderm and neural crest migration. Tumor cells are found to have EMT-like processes, which not only gives them the ability to recur but to cause immunosuppression and cell invasion. The degradation of Snail1, an EMT-promoting transcription factor that leads to invasion of U251 glioblastoma multiforme cells was found to be facilitated in cells with niacin treatment, thus leading to a decrease in tumor invasion.[12][13]

Administration

Niacin is available in two chemical forms. As nicotinic acid only, used for hyperlipoproteinemia or peripheral vascular disease. Another form is both nicotinic acid and nicotinamide (niacinamide), used for nutritional supplementation or pellagra. Oral extended-release tablets come in  250mg, 500mg, 750mg, 1000mg, 3000mg. Dosing of 1 to 3 grams/day was found to reduce serum LDL cholesterol and increase serum HDL cholesterol.[18][19]

A formulation of modified release niacin and with crystalline immediate-release niacin was found to offer similar results.[5]

 Immediate release tablets come dosages ranging from 50mg to 500mg. Initial dosing should be as low as possible to decrease adverse effect reactions and slowly titrated preferably no more than 500 mg over 4 weeks to patient’s response and tolerance.

Reverses in insulin resistance induced by lipid overload and rapid reduction of plasma FFA were observed with acute administration of niacin.[18]

At the time of niacin administration, alcohol should be avoided as it may increase the risk of pruritus and flushing. Niacin therapy is not recommended in patients who are chronic alcohol abusers due to increased risk of hepatotoxicity.

Recommended dosage:

Pellagra:

Oral dosage (nicotinic acid or nicotinamide/niacinamide)

Adults

Up to 500 mg/day orally, depending on the severity of niacin deficiency.

Intravenous or Intramuscular dosage

50 to 100 mg intramuscular 5 times daily, or 25 to 100 mg given by slow intravenous infusion twice daily, depending on the severity of niacin deficiency. Maximum: 500 mg/daily.

Children

Dosing is up to 300 mg/day given by slow intravenous infusion, depending on the severity of niacin deficiency.

Hypercholesterolemia, mixed dyslipidemia or hypertriglyceridemia, type IV or V:

Dosing is 1500 to 3000 mg/day orally, divided either as two or three times daily.

Starting dose: 250 mg orally at bedtime, with a gradual increase of 250 mg/day every 4 to 7 days up to 2000 mg/day.

After 2 months, the dosage may be increased to 250 to 500 mg/day every 2 to 4weeks, with a maximum of 6000 mg/day. 

Of note: 325 mg aspirin 30 minutes before a dose may reduce flushing;

Medication should be given without food.

Niacin is FDA Pregnancy Category C. When used at high doses to treat conditions such as dyslipidemia, niacin may cause harm to an unborn fetus.

Niacin has no black box warning.

Adverse Effects

Adverse effects of pharmacological doses of nicotinic acid are continuously under research in clinical research trials.

Some common reactions are:

Flushing: Niacin often causes generalized pruritus, and a burning sensation is usually limited to the face and chest and lasts 20 to 30 minutes.  This side effect, however, is one that decreases not only in frequency but severity with time.[5] Pretreatment of 30 minutes with aspirin (up to 325mg) can be used to counter this side effect. Laropiprant, a potent, selective antagonist of prostaglandin D2( PGD2)-receptor subtype-1 not only helps reduce this side effect of niacin but allows for optimal pharmacological dosing if needed.[20]

One reaction to consider is niacin’s effects, (whether used alone or in combination with statin medications) on glycemic control, in patients with dyslipidemia, regardless of their diabetes mellitus status who are undergoing niacin therapy.

In non-diabetic patients with dyslipidemia, on average, 5 years of niacin therapy, whether used alone or in laropiprant combination therapy, was associated with a 34% increased risk of developing diabetes.[21] 

Also, niacin has been shown to increase fasting glycemic levels in patients with diabetes. Avoiding niacin therapy has been recommended in patients with metabolic syndrome or diabetes.[18][4]

Other side effects include hyperuricemia, gastrointestinal disorders, rash, increase in homocysteine levels, hypotension, dyspepsia, elevations in AST and ALT, nausea, vomiting, and paresthesias.[4][1]

Some serious adverse reaction:

Peptic ulcer disease, arrhythmias, anaphylaxis, hepatotoxicity, hepatic necrosis, fulminant, macular edema.[1]

Contraindications

Contraindications to niacin include the following conditions:

  • Patients with active peptic ulcer disease
  • Patients who have active liver disease or present with unexplained and persistent elevations in hepatic transaminases
  • Patients with hypersensitivity to niacin or any component of this medication
  • Patients with arterial bleeding

Monitoring

Laboratory monitoring is recommended in patients on niacin therapy due to its diverse side effects.

In pre-diabetes or diabetic patients, frequent monitoring of blood glucose is necessary as niacin can increase fasting blood glucose.

In patients on diabetic medications, such as acarbose, albiglutide, alogliptin, glipizide, or insulin should also have blood glucose monitors as niacin has an antagonistic effect on blood glucose.

Niacin can cause an increase in uric acid, thus exerting an antagonist on medications for gout, such as pegloticase and allopurinol.

Niacin exerts an additive reaction with blood pressure medications (amlodipine clozapine, bisoprolol, diltiazem) opioids (morphine, oxycodone, tramadol, methadone) antipsychotics (quetiapine, risperidone) phosphodiesterase type 5 inhibitor (tadalafil) thus leading to hypotension. Frequent blood pressure check is recommended. Also, niacin, in combination with some beta blockers may decrease its antihyperlipidemic efficacy.

Niacin can increase the risk of bleeding by exerting an additive effect. Niacin has been shown to not only cause a reduction in platelet counts (mean of -11% with 2000 mg) but to increase prothrombin time (mean of approximately +4%); leading to bleeding, especially when combined with anticoagulants such as apixaban, caplacizumab, or warfarin. Thus, a blood coagulation panel should be a routine test.

Niacin also exerts an additive effect when combined with ceritinib, diazoxide leading to hyperglycemia.

Phosphorus levels also require monitoring in patients at risk for hypophosphatemia as niacin can cause a decrease in phosphorus levels (mean of -13% with 2000 mg).

Harm may result in a nursing baby as niacin can pass into breast milk; therefore it should be avoided.

Toxicity

In pharmacological doses (example 1000 to 3000 mg/day), flushing reaction associated with its crystalline nicotinic acid component (not nicotinamide) is the most common and studied the toxicity of niacin, which is both person-to-person and dose-dependent.

Other symptoms of toxicity may include dizziness, upset stomach, redness, itching, nausea, and vomiting.

Enhancing Healthcare Team Outcomes

Niacin is a pharmacotherapeutic pleiotropic agent with properties still yet to be fully understood. It is encouraged that individuals in the healthcare field (pharmacist, nurse practitioner, primary care provider) stay updated on niacin's properties and side effects uncovered by ongoing research. Niacin can cause flushing, a significant adverse effect that significantly affects its compliance in patients. Knowing how to titrate, from a minimal dose, will not only help minimize such adverse effects but will surely benefit patient health outcomes. Close monitoring and periodic blood work on initiating or increasing the dosage of niacin should be obtained as it is known to increase the risk of bleeding, hypotension, hyperuricemia, and cause alterations in glycemic control. Its adverse effect on glycemic control in patients with dyslipidemia both with or without diabetes is one of its most concerning effects as it may cause diabetes in predisposed patients or make the management of diabetes a challenge. 


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Niacin (Nicotinic Acid) - Questions

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A 45-year-old man comes to the clinic for a routine health exam. He has no medical problems, He smokes two packs of cigarettes daily but does not drink alcohol. He has a family history of hypertension and diabetes. His blood pressure is 129/55 mmHg and body mass index is 31 kg/m2. Laboratory results are: total cholesterol 254 mg/dl, triglycerides 150 mg/dl, high-density lipoprotein 37 mg/dl and low-density lipoprotein 180 mg/dl. Which vitamin depresses the synthesis of fatty acids?



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Which amino acid is the precursor of niacin synthesis?



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A 68-year-old white man with a history of hyperlipidemia, myocardial infarction, hypertension presents to the clinic for a wellness exam. The patient states that he is currently on atorvastatin, aspirin 81mg, labetalol, hydrochlorothiazide and another medication which he cannot recall the name but states that the doctor who prescribed it said it would help with his hyperlipidemia. The patient states that one of his medications makes his skin turns red is itchy and sometimes burns. Upon physical exam, blood pressure 145/67 mmHg, body mass index 33 kg/m2, total cholesterol 231 mg/dl, triglycerides 152 mg/dl, high-density lipoprotein 19 mg/dl, and low-density lipoprotein 180 mg/dl. What is the most effective medication to increase the HDL level?



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A 40-year-old man is found to have severe hypertriglyceridemia on routine evaluation. He has no present complaints. He has a history of hypertension and asymptomatic gall stones. Medication is hydrochlorothiazide and vitamin D. His mother had a non-fatal myocardial infarction at age 57. The patient neither smokes nor drink alcohol. His blood pressure is 130/75 mm Hg and his pulse is 82/min. He has been prescribed niacin for his hypertriglyceridemia. The patient returns to the clinic 2 weeks later complaining of intensive flushing and pruritis. What is the most likely cause of the complaint?



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A 67-year-old man with a history of dyslipidemia and myocardial infarction five years ago presents to the clinic for a wellness checkup. His current fasting lipid profile is high-density lipoprotein 21 mg/dl total cholesterol 267 mg/dl triglycerides 195mg/dl and low-density lipoprotein 211 mg/dl . The patient is currently on simvastatin and aspirin 81 mg. The patient is also encouraged to exercise. The patient states that he did some research and found that an over the counter vitamin helps to increase high-density lipoprotein and he started the regimen two months ago. Which is an FDA approved use for the regimen he started two months ago?



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A 47-year-old man with a history of dyslipidemia decides to, along with lifestyle modification, take a supplement, which he read on the internet, helps with lowering fats, and, increasing the levels of high-density lipoproteins. He has not visited a physician in 20 years because he does not trust doctors. He goes to a health food store and buys and over the counter supplement, and decides to take twice as much as the label recommends. What side effect is very likely to manifest with his approach?



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A 50-year-old Caucasian woman with a history of hyperlipidemia presents to the clinic for a wellness exam. The patient states she was diagnosed with hyperlipidemia about a year ago and started on atorvastatin which the patient stated she is tolerating well. The patient is also taking labetalol. A couple of months ago patient states a new medication was added. The patient states that since she started the new medication, her skin turns red, is itchy and sometimes burns. Upon physical exam, blood pressure 189/67mmHg, body mass index 37kg/m2, total cholesterol 241mg/dl, triglycerides 158mg/dl, high-density lipoprotein 22mg/dl and low-density lipoprotein 180mg/dl. What is the best next step at this time?



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A 45-year–old man with a history of hyperlipidemia and hypertension presents to the clinic for a wellness exam. He was diagnosed with hyperlipidemia 6 months ago and was started on a medication which he does not recall. Today the patient is wondering if he can be prescribed a different medicine as he stopped taking his previous medication months ago due to muscle cramping. Upon physical exam, blood pressure 139/77mmHg, body mass index 31kg/m2, total cholesterol 254mg/dl, triglycerides 150mg/dl, high-density lipoprotein 23mg/dl and low-density lipoprotein 155mg/dl. What is the best treatment at this time?



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A 25-year-old man with no significant past medical history presents to the clinic for a wellness checkup. During his last visit, the patient was diagnosed with hyperlipidemia, and his lipid profile at the time was high-density lipoprotein 22 mg/dl, total cholesterol 260mg/dl, triglycerides 190mg/dl, and low-density lipoprotein 210mg/dl. The patient was started on simvastatin and encouraged to exercise. He states that after some online research he found that an over the counter vitamin helps increase high-density lipoprotein which he started 2 months ago. Which describes the mechanism of action on this supplement?



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Niacin (Nicotinic Acid) - References

References

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Fricker RA,Green EL,Jenkins SI,Griffin SM, The Influence of Nicotinamide on Health and Disease in the Central Nervous System. International journal of tryptophan research : IJTR. 2018;     [PubMed]
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Florentin M,Liberopoulos EN,Kei A,Mikhailidis DP,Elisaf MS, Pleiotropic effects of nicotinic acid: beyond high density lipoprotein cholesterol elevation. Current vascular pharmacology. 2011 Jul 1;     [PubMed]
Wierzbicki AS, Niacin: the only vitamin that reduces cardiovascular events. International journal of clinical practice. 2011 Apr;     [PubMed]
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Motawi TK,Darwish HA,Hamed MA,El-Rigal NS,Naser AFA, A Therapeutic Insight of Niacin and Coenzyme Q10 Against Diabetic Encephalopathy in Rats. Molecular neurobiology. 2017 Apr;     [PubMed]
Xu XJ,Jiang GS, Niacin-respondent subset of schizophrenia – a therapeutic review. European review for medical and pharmacological sciences. 2015;     [PubMed]
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Li J,Qu J,Shi Y,Perfetto M,Ping Z,Christian L,Niu H,Mei S,Zhang Q,Yang X,Wei S, Nicotinic acid inhibits glioma invasion by facilitating Snail1 degradation. Scientific reports. 2017 Mar 3;     [PubMed]
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HOFFER A, Treatment of arthritis by nicotinic acid and nicotinamide. Canadian Medical Association journal. 1959 Aug 15;     [PubMed]
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Meyer-Ficca M,Kirkland JB, Niacin. Advances in nutrition (Bethesda, Md.). 2016 May;     [PubMed]
Farnier M,Chen E,Johnson-Levonas AO,McCrary Sisk C,Mitchel YB, Effects of extended-release niacin/laropiprant, simvastatin, and the combination on correlations between apolipoprotein B, LDL cholesterol, and non-HDL cholesterol in patients with dyslipidemia. Vascular health and risk management. 2014;     [PubMed]
Parhofer KG, Review of extended-release niacin/laropiprant fixed combination in the treatment of mixed dyslipidemia and primary hypercholesterolemia. Vascular health and risk management. 2009;     [PubMed]
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