Vitamin B3 (Niacinamide)

Clinical Studies
References


A vitamin important in carbohydrate metabolism, the formation of testosterone and other hormones, the formation of red blood cells and maintaining the integrity of all cells. Niacinamide helps your body to utilize protein, fats and carbohydrates. It is necessary for a healthy nervous system and digestive system. Niacinamide is a peripheral vascular dilator, which may be helpful in hypertension. Deficiency may cause listlessness, headache, weight loss, loss of appetite, rough cracked skin and ulceration.

Niacinamide may be helpful in poor appetite, ulcerative colitis, chronic diarrhea, disorders of the digestive system, as an insect repellent, in diabetic neuropathy, AIDS, maintaining a positive mental attitude, enhancing learning abilities, heart disease, alcoholism, stress, improving athletic performance and aging. It may also be used for canker sores (syphilis), immuno-depression, memory loss including Alzheimer's disease, vision problems such as cataracts and glaucoma, motion sickness and increasing energy.

Published Clinical Studiesclin
Vitamin B3 (Niacinamide)

Advances in the understanding and management of dyslipidemia: using niacin-based therapies.1

Ito MK.

 

University of the Pacific, Thomas J. Long School of Pharmacy and Health Sciences, 3350 La Jolla Village Drive, San Diego, CA 92161-0002, USA. uopito@aol.com

The use of niacin, alone and in combination, for the treatment of dyslipidemia in patients with or at risk for coronary heart disease (CHD), is discussed. Cardiovascular risk is independently predicted not only by high levels of low-density lipoprotein cholesterol (LDL-C), but also low levels of high-density lipoprotein cholesterol (HDL-C) and elevated triglycerides. Moreover, we now understand that LDL particle size and number are associated with differing levels of atherogenicity. Metabolic syndrome, increasingly being recognized as a marker for elevated cardiovascular risk, is associated with atherogenic dyslipidemia characterized by low HDL-C, high triglycerides, and small, dense LDL particles. Controlled clinical studies have shown that niacin therapy effectively increases HDL-C and lowers triglyceride and LDL-C levels while causing a shift toward larger, less atherogenic LDL particles. Niacin, alone or in combination, prevents progression and promotes regression of coronary atherogenic lesions and significantly reduces CHD-related morbidity and mortality. Statin monotherapy causes modest increases in HDL-C and decreases triglycerides, while more potently reducing LDL-C. Combinations of lipid-modifying agents may better address the full spectrum of lipoprotein abnormalities in some patients. Investigations have shown that combining statin therapy with niacin results in additive improvement in the major lipids and lipoproteins and improves clinical outcome. With recently broadened treatment recommendations, it seems likely that combination therapy will be increasingly deemed the appropriate choice for addressing a range of lipid abnormalities.

Publication Types:

  • Congresses

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Sustained-release niacin for prevention of migraine headache.2

Velling DA, Dodick DW, Muir JJ.

 

Division of Pain Management Mayo Clinic, Scottsdale, Ariz 85259, USA.

Considerable advances in the diagnosis and treatment of migraine headache have occurred during the past decade, but treatment options for acute migraine attacks have expanded at a faster rate than those for prophylaxis. We describe a patient whose migraine headaches responded dramatically to sustained-release niacin as preventive treatment. Niacin is not generally considered to be effective for migraine prevention. However, low plasma levels of serotonin have been implicated in migraine pathogenesis, and niacin may act as a negative feedback regulator on the kynurenine pathway to shunt tryptophan into the serotonin pathway, thus increasing plasma serotonin levels. Sustained-release niacin merits further study as a potentially useful preventive therapy for migraine headache.

Publication Types:

  • Case Reports

PMID: 12934790 [PubMed - indexed for MEDLINE]

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Antiatherothrombotic effects of nicotinic acid.3

Rosenson RS.

 

Preventive Cardiology Center, Northwestern University, The Feinberg School of Medicine, 201 East Huron Street, Galter Pavilion 11-120, Chicago, IL 60612, USA. r-rosenson@northwestern.edu

Cardiovascular event reduction in hypercholesterolemic subjects appropriately emphasizes the prominent role of statin therapy; however, niacin (nicotinic acid) is also an effective lipid-altering agent that prevents atherosclerosis and reduces cardiovascular events. Niacin has multifarious lipoprotein and anti-atherothrombosis effects that improve endothelial function, reduce inflammation, increase plaque stability, and diminish thrombosis. Niacin reduces the atherogenicity of low-density lipoprotein (LDL) by changing the distribution of small LDL to large LDL subclass, and the susceptibility of LDL to oxidative modification. It is the most effective agent for increasing high-density lipoprotein cholesterol. Moreover, it favorably alters high-density lipoprotein composition, increasing apolipoprotein AI relative to apolipoprotein AII. Niacin reduces blood viscosity through a variety of mechanisms, thus improving blood flow and perfusion through stenotic segments of the vasculature. Finally, niacin has cardioprotective effects that may limit ischemia-reperfusion injury. By preserving glycolysis during periods of ischemia and improving subendocardial blood flow during reperfusion, niacin can improve the functional recovery of the myocardium.

PMID: 14642410 [PubMed - in process]

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Pharmacotherapy for dyslipidaemia--current therapies and future agents.4

Bays H, Stein EA.

 

L-MARC Research Center, 3288 Illinois Avenue, Louisville, KY 40213, USA. HBaysMD@aol.com

Current lipid-altering agents that lower low density lipoprotein cholesterol (LDL-C) primarily through increased hepatic LDL receptor activity include statins, bile acid sequestrants/resins and cholesterol absorption inhibitors such as ezetimibe, plant stanols/sterols, polyphenols, as well as nutraceuticals such as oat bran, psyllium and soy proteins; those currently in development include newer statins, phytostanol analogues, squalene synthase inhibitors, bile acid transport inhibitors and SREBP cleavage-activating protein (SCAP) activating ligands. Other current agents that affect lipid metabolism include nicotinic acid (niacin), acipimox, high-dose fish oils, antioxidants and policosanol, whilst those in development include microsomal triglyceride transfer protein (MTP) inhibitors, acylcoenzyme A: cholesterol acyltransferase (ACAT) inhibitors, gemcabene, lifibrol, pantothenic acid analogues, nicotinic acid-receptor agonists, anti-inflammatory agents (such as Lp-PLA(2) antagonists and AGI1067) and functional oils. Current agents that affect nuclear receptors include PPAR-alpha and -gamma agonists, while in development are newer PPAR-alpha, -gamma and -delta agonists, as well as dual PPAR-alpha/gamma and 'pan' PPAR-alpha/gamma/delta agonists. Liver X receptor (LXR), farnesoid X receptor (FXR) and sterol-regulatory element binding protein (SREBP) are also nuclear receptor targets of investigational agents. Agents in development also may affect high density lipoprotein cholesterol (HDL-C) blood levels or flux and include cholesteryl ester transfer protein (CETP) inhibitors (such as torcetrapib), CETP vaccines, various HDL 'therapies' and upregulators of ATP-binding cassette transporter (ABC) A1, lecithin cholesterol acyltransferase (LCAT) and scavenger receptor class B Type 1 (SRB1), as well as synthetic apolipoprotein (Apo)E-related peptides. Fixed-dose combination lipid-altering drugs are currently available such as extended-release niacin/lovastatin, whilst atorvastatin/amlodipine, ezetimibe/simvastatin, atorvastatin/CETP inhibitor, statin/PPAR agonist, extended-release niacin/simvastatin and pravastatin/aspirin are under development. Finally, current and future lipid-altering drugs may include anti-obesity agents which could favourably affect lipid levels.

Publication Types:

  • Review
  • Review, Academic

PMID: 14596646 [PubMed - indexed for MEDLINE]

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Niacin, lipids, and heart disease.5

Malik S, Kashyap ML.

 

Atherosclerosis Research Center, Department of Veterans Affairs Healthcare System, Division of Cardiology, University of California at Irvine, 5901 East Seventh Street (11-111-I), Long Beach, CA 90822, USA.

Niacin is the most effective medication in current clinical use for increasing high-density lipoprotein (HDL) cholesterol. It has the broadest effect on the lipid profile, reducing all atherogenic apolipoprotein (apo) B and increasing all antiatherogenic apo AI-containing lipoproteins, resulting in significant reduction in atherosclerotic complications and total mortality in trials. Recent research indicates novel major target sites of action in the liver to 1) directly inhibit diacylglycerol acyltransferase 2 (DGAT2), explaining its effect on triglycerides and apo B lipoproteins, and 2) inhibit the HDL apo AI catabolism pathway, resulting in higher HDL levels. Such information may lead to new drug discovery and supply the rationale for combination with other lipid regulators that are known to have different mechanisms of action. Trial evidence shows that niacin is not only safe to use in persons with diabetes, but that its combination with 3-hydroxy-3-methyl-glutaryl coenzyme A (HMG CoA) reductase inhibitors (statins) is also safe and effective. Recently, a new formulation of niacin has made it easier to tolerate and administer. Clinical trials are needed to determine whether niacin in combination with other lipid-modulating agents decreases the risk of cardiovascular events beyond the approximately 30% that has been noted with monotherapy.

PMID: 14558989 [PubMed - in process]

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Niacin as a component of combination therapy for dyslipidemia.6

Miller M.

 

Center for Preventive Cardiology, University of Maryland Medical Center, Baltimore 21201, USA. mmiller@heart.umaryland.edu

Dyslipidemia is one of the most important modifiable risk factors for coronary disease. Despite the availability of highly effective lipid-modifying agents, many patients still do not reach lipid targets established by national guidelines. Niacin has been known to be an effective treatment of dyslipidemia for almost half a century. Niacin substantially increases high-density lipoprotein cholesterol (HDL-C) levels while lowering levels of low-density lipoprotein cholesterol (LDL-C), triglycerides, and lipoprotein(a). In addition, niacin converts small LDL particles into more buoyant, less atherogenic LDL particles. Combined with other agents, niacin offers an important treatment option for patients with dyslipidemia. In particular, niacin complements LDL-C-lowering drugs; it is the most effective agent available for increasing HDL-C levels while lowering levels of LDL-C and triglycerides and improving other lipid risk factors such as lipoprotein(a). Combining niacin with statins or bile acid sequestrant therapy is safe and effective for improving lipid levels and decreasing coronary risk. Differences in niacin formulations dictate tolerability profiles and should be considered when selecting niacin as part of lipid therapy. Furthermore, adverse effects on glucose and insulin sensitivity should be considered when selecting candidates for niacin therapy. Adding niacin to lipid-lowering regimens is a valuable option for physicians treating patients with dyslipidemia and should be considered in appropriate patients.

Publication Types:

  • Review
  • Review, Tutorial

PMID: 12934785 [PubMed - indexed for MEDLINE]

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 7
Effects of an oral mixture containing glycine, glutamine and niacin on memory, GH and IGF-I secretion in middle-aged and elderly subjects.

Arwert LI, Deijen JB, Drent ML.

 

Department of Endocrinology, VU University Medical Center, de Boelelaan 1117, 1081 HVAmsterdam, The Netherlands.

Aging is associated with declining activity of the growth hormone-insulin-like growth factor-I (GH-IGF-I) axis and with a decrease in cognitive function. The stimulatory effect of an orally administered nutritional supplement, mainly containing glycine, glutamine and niacin on the GH-IGF-I axis and on mood and cognition was investigated. Forty-two healthy subjects (14 men and 28 women, aged 40-76 years) were enrolled in a randomised, double blind, placebo-controlled trial. They received 5 g of a nutritional supplement or placebo, twice daily orally for a period of 3 weeks. At baseline and after 3 weeks, blood was collected for measurement of serum GH and IGF-I levels and mood and cognitive function were tested. The nutritional supplement ingestion for 3 weeks was found to increase serum GH levels with 70% relatively to placebo, whereas circulating IGF-I levels did not change. Mean GH (+/- SD) increased in this group from 3.23 (+/- 4.78) to 4.67 mU/l (+/- 5.27) (p = 0.03). GH increase was not associated with improvement in mood or memory. Correlation analyses, however, revealed that individual increases in IGF-I, but not GH, were associated with improved memory and vigour. It is concluded that an oral mixture of glycine, glutamine and niacin can enhance GH secretion in healthy middle-aged and elderly subjects.

Publication Types:

  • Clinical Trial
  • Randomized Controlled Trial

PMID: 14609312 [PubMed - indexed for MEDLINE]

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Nutritional cofactor treatment in mitochondrial disorders.8

Marriage B, Clandinin MT, Glerum DM.

 

Department of Medical Genetics, University of Alberta, Edmonton, Alberta, Canada. Barbara.Marriage@abbott.com

Mitochondrial disorders are degenerative diseases characterized by a decrease in the ability of mitochondria to supply cellular energy requirements. Substantial progress has been made in defining the specific biochemical defects and underlying molecular mechanisms, but limited information is available about the development and evaluation of effective treatment approaches. The goal of nutritional cofactor therapy is to increase mitochondrial adenosine 5'-triphosphate production and slow or arrest the progression of clinical symptoms. Accumulation of toxic metabolites and reduction of electron transfer activity have prompted the use of antioxidants, electron transfer mediators (which bypass the defective site), and enzyme cofactors. Metabolic therapies that have been reported to produce a positive effect include Coenzyme Q(10) (ubiquinone); other antioxidants such as ascorbic acid, vitamin E, and lipoic acid; riboflavin; thiamin; niacin; vitamin K (phylloquinone and menadione); creatine; and carnitine. A literature review of the use of these supplements in mitochondrial disorders is presented.

Publication Types:

  • Review
  • Review, Tutorial

PMID: 12891154 [PubMed - indexed for MEDLINE]

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Referencesref

  1. Zema MJ. Gemfibrozil, nicotinic acid and combination therapy in patients with isolated hypoalphalipoproteinemia: a randomized, open-label, crossover study. J Am Coll Cardiol 2000;35:640-6.
  2. Conly JM, Stein K, Worobetz L, Rutledge-Harding S. The contribution of vitamin K2 (menaquinones) produced by the intestinal microflora to human nutritional requirements for vitamin K. Am J Gastroenterol 1994;89(6):915-23.
  3. McKevoy GK, ed. AHFS Drug Information. Bethesda, MD: American Society of Health-System Pharmacists, 1998.
  4. Cordes I, Buchmann S, Scheffner D. Vitamin K deficiency with erythromycin. Observation of a boy treated with valproate. Monatsschr Kinderhdilkd 1990;138(2):85-7.
  5. Lipsky JJ. Antibiotic-associated hypoprothrombinemia. J Antimicrob Chemother 1988;21(3):281-300.
  6. Alitalo R, Ruutu M, Valtonen V, et al. Hypoprothrombinemia and bleeding during administration of cefamandole and cefoperazone. Report of three cases. Ann Clin Res 1985;17(3):116-9.
  7. Shimada K, Matsuda T, Inamatsu T, et al. Bleeding secondary to vitamin K deficiency in patients receiving parenteral cephem antibiotics. J Antimicrob Chemother 1984;14(Suppl B):325-30.
  8. Blumenthal M, Goldberg A, Brinckmann J (eds). Herbal Medicine Expanded Commission E Monographs. Newton, MA: Integrative Medicine Communications, 2000.
  9. Conly J, Stein K. Reduction of vitamin K2 concentrations in human liver associated with the use of broad spectrum antimicrobials. Clin Invest Med 1994;17(6):531-9.
  10. Brenner A. The effects of megadoses of selected B complex vitamins on children with hyperkinesis: controlled studies with long-term follow-up. J Learn Disabil 1982;15:258-64.
  11. Kastrup EK. Drug Facts and Comparisons. 1998 ed. St. Louis, MO: Facts and Comparisons, 1998.
  12. Garg R, Malinow M, Pettinger M. Niacin treatment increases plasma homocyst(e)ine levels. Am Heart J 1999;138:1082-7.
  13. Reimund E. Sleep deprivation-induced dermatitis: further support of nicotinic acid depletion in sleep deprivation. Med Hypotheses 1991;36(4):371-3.
  14. DiPiro JT, Talbert RL, Yee GC, et al, Eds. Pharmacotherapy: A pathophysiologic approach. 4th ed. Stamford, CT: Appleton & Lange, 1999.
  15. Garg R, Malinow MR, Pettinger M, et al. Niacin treatment increases plasma homocysteine levels. Am Heart J 1999;138:1082-7.
  16. Honma N. The effect of lactic acid bacteria, Part 1: biological significance. New Medicines and Clinics 1986;35(12):1-3.
  17. Gorbach SL. Bengt E. Gustafsson memorial lecture. Function of the normal human microflora. Scand J Infect Dis Suppl 1986;49:17-30.
  18. Hill MJ. Intestinal flora and endogenous vitamin synthesis. Eur J Cancer Prev 1997;6:S43-5.
  19. Cummings JH, Macfarlane G. Role of intestinal bacteria in nutrient metabolism. J Parenter Enteral Nutr 1997;21(6):357-65.
  20. Micromedex Healthcare Series. Englewood, CO: MICROMEDEX Inc.