Vitamin B3

Clinical Studies
References

Vitamin B3, also known a nicotinic acid, is a water-soluble vitamin that plays essential roles in energy metabolism in the living cell, DNA repair and many other essential functions.  Nicotinic acid is a vasodilator, helping to increase blood flow to extremeties and is therefore included in our formula specifically to help improve sexual function and performance.

As well as sexual and reproductive function and impotence, vitamin B3 can also be helpful for the following:  high cholesterol/cholesterol imbalance, osteoarthritis, rheumatoid arthritis, alcoholism, cancer, schiophrnia, senility and circulatory disorders.

 


Published Clinical Studiesclin
Vitamin B3

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]

back

 

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]

back

 

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]

back to top


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.