Week 2 Discussion On Use Of Niacin
Week 2 Discussion On Use Of Niacin
Discussion post on the use of herbal/supplement Niacin
Niacin
Key Concepts Learned:
Evidence for effectiveness:
How can I Incorporate Natural Standard/Medicine in my Practice:
APA format, use the format above, in text citation, provided document with information on Niacin, no plagiarism,
Citation for attached document:
Natural Medicines. (2016). Niacin. Retrieved from https://naturalstandardce.therapeuticresearch.com/monographs/html/niacin.html#effectivenessBriefBackground (Links to an external site.)
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· Combination product examples: ADVICOR® (niacin extended-release/lovastatin tablets), CordaptiveTM (niacin/laropiprant).
Clinical Bottom Line/Effectiveness
Brief Background
· Vitamin B3 is composed of niacin (nicotinic acid) and its amide, niacinamide, and may be found in many foods, including yeast, meat, fish, milk, eggs, green vegetables, and cereal grains. Dietary tryptophan, found in protein-containing foods such as red meat, poultry, eggs, and dairy products, is also converted to niacin after ingestion. Vitamin B3 is frequently found in combination with other B vitamins, including thiamine, riboflavin, pantothenic acid, pyridoxine, cyanocobalamin, and folic acid.
· According to numerous clinical trials, niacin (not niacinamide) appears to be a relatively safe, inexpensive, and effective treatment for hyperlipidemia. Niacin supplementation is a lipid-modifying therapy that specifically addresses the triglyceride/high-density lipoprotein cholesterol axis (1). Niacin is also a widely used lipid-regulating agent in dyslipidemic patients (2;3;4;5). Niacin elicits significant increases in HDL, up to 20-30% at doses of 1-2g daily, with greater effects than other drugs (including 3-hydroxy 3-methylglutarylCoA; HMG-CoA reductase inhibitors/statins) (6;7;8;9). Niacin also causes mild reductions (~5-20%) in low-density lipoproteins (LDL), with stronger effects occurring at higher doses (3-4.5g daily) (10;11;12;13;14). Additional decreases in LDL levels may be achieved by combining niacin with an HMG-CoA reductase inhibitor or bile acid sequestrant (9). Preliminary evidence suggests that niacin therapy may reduce the incidence of atherosclerosis and secondary cardiovascular events (15). Niacin decreases lipoprotein (a) and fibrinogen levels; both have been associated with a decreased risk of coronary artery disease (16;17;18;4). Niacin may also decrease the carotid intima-media thickness (4;9). However, niacin therapy has also been found to increase plasma homocysteine levels by up to 55% (19;20), possibly negating any positive effects on serum lipids and increasing the risk of adverse cardiac events. Due to the adverse effects associated with niacin use, it is not often used in the treatment of pediatric dyslipidemia (21).
· Niacin therapy has a high incidence of initial minor adverse events, including cutaneous flushing, pruritus, and gastrointestinal upset (22;23;24;25;26;27;28;29;30;31;32;33;34;35;36). Concomitant NSAIDs or aspirin are often recommended during the first 1-2 weeks to reduce flushing (likely prostaglandin mediated); aspirin (325mg), ibuprofen (200mg), naproxen, indomethacin, and laropiprant have been shown to significantly reduce the incidence of flushing experienced after niacin administration (37;38;39;40;41;42;43;44;45;46;47;48;49;50;51;52;3;53). Use of an antihistamine 15 minutes prior to a niacin dose may also suppress cutaneous flushing (54;55). The flushing response often spontaneously diminishes after 1-2 weeks of therapy. Numerous case reports have been published concerning the development of hepatotoxicity following niacin therapy, ranging from elevated aminotransferase levels to jaundice, ascites, and hepatitis (56;57;58;39;59;60;61;62;63;64;65;66;67;68;69;70;71;72;31;73;74;75;76;77;78;79;80;81). Concomitant use of niacin or niacinamide and other agents that elevate transaminases or elicit hepatotoxicity may have additive hepatotoxic effects. Both niacin and HMG-CoA reductase inhibitors may elevate liver function tests or result in hepatotoxicity, and transaminase levels should be monitored. Immediate-release nicotinic acid may pose less risk of hepatotoxicity than extended-release formulations. Niacin, particularly in large doses, may cause insulin resistance, hyperglycemia, and hyperinsulinemia (82;56;58;24;25;83;60;84;85;28;86;29;87;88;89;90;12;91;32;92;93;94;95;96;97;98;99).
· Niacinamide (not niacin) has been investigated for the prevention and delay of type 1 diabetes mellitus, possibly mediated through the protection and preservation of pancreatic beta-islet cell function. Initial human research has been equivocal. Preliminary evidence suggests potential for niacinamide as a treatment for osteoarthritis.
· In preliminary studies, inositol hexanicotinate, an ester of niacin and inositol, has also been shown to share some beneficial effects with niacin without causing the adverse effects associated with niacin administration (100;101).
· Nicotinic analog hypolipidemic medications, such as 5-methylpyrazine carboxylic acid 4-oxide (Acipimox®), have been developed for lipid modification in individuals with hyperlipoproteinemia and cardiovascular disease (102;103;104;105;106). Acipimox® is not available in the United States. Skin rash, headache, transient low blood pressure, altered thyroid hormone levels, and elevated blood levels of uric acid have also been noted with nicotinic acid therapy.
· Niacin consumption for treatment of a condition should be monitored by a healthcare professional (107). Week 2 Discussion On Use Of Niacin
