Table of Contents > Interactions & Depletions > Niacin (vitamin B3, nicotinic acid), Niacinamide Print

Niacin (vitamin B3, nicotinic acid), Niacinamide



Interactions

Niacin and Niacinamide/Drug Interactions:
  • AlcoholAlcohol: According to numerous clinical trials, niacin treatment frequently produces cutaneous flushing (391; 292; 56; 333; 284; 326; 22; 23; 24; 26; 27; 250; 293; 294; 392; 319; 28; 86; 29; 393; 88; 12; 30; 394; 312; 31; 32; 395; 33; 34; 35; 384; 96; 36; 98; 396; 397; 287; 386; 322; 309; 323; 320; 62; 306; 398; 399; 400); theoretically, niacin-induced flushing may be magnified by concomitant ingestion of alcohol (424). According to a case report, coadministration of alcohol and niacin may increase the risk of hepatotoxicity (375)
  • AndrogensAndrogens: Niacinamide has been shown to increase the solubility of testosterone in vitro (423), which may affect the toxicity or efficacy of testosterone administration in vivo (423).
  • AntibioticsAntibiotics: According to secondary sources, antibiotics may lead to decreased production of B vitamins through the destruction of normal gastrointestinal flora.
  • Anticoagulants and antiplateletsAnticoagulants and antiplatelets: According to case reports, niacin therapy may increase the risk of bleeding (263). In addition, thrombocytopenia has been observed in clinical trials of niacin therapy (264; 27; 88).
  • Anticonvulsant agentsAnticonvulsant agents: According to animal and human evidence, niacinamide may increase plasma levels of anticonvulsants, including carbamazepine, diazepam, and sodium valproate (425). In patients with epilepsy, nicotinamide increased the half-life of carbamazepine (426).
  • Antidiabetic agentsAntidiabetic agents: In numerous human studies, niacin increased blood glucose levels (82; 56; 58; 24; 25; 83; 60; 84; 85; 28; 86; 29; 87; 88; 89; 90; 12; 32; 92; 93; 94; 95; 96; 97; 98). On the contrary, the concomitant administration of niacinamide and insulin has been shown to lead to a reduction in insulin requirements in children newly diagnosed with type 1 diabetes mellitus (152; 352; 351). Some studies have found no difference (427; 352; 350). Dosing adjustments of antidiabetic agents may be needed.
  • Antigout agentsAntigout agents: In clinical research, niacin therapy has been shown to increase serum uric acid levels (54; 58; 24; 25; 26; 266; 250; 60; 254; 255; 84; 85; 28; 86; 29; 88; 12; 258; 259; 260; 261; 257; 98; 262).
  • AntihistaminesAntihistamines: In human research, use of an antihistamine 15 minutes prior to a niacin dose suppressed cutaneous flushing (54; 55). The flushing response often spontaneously diminishes after 1-2 weeks of therapy.
  • AntihypertensivesAntihypertensives: In human evidence, nicotinic acid lowered blood pressure values in patients with hypertension (181). Nicotinic acid may act similarly to calcium channel blockers, according to principal component analysis and factor analysis of molecular properties (428).
  • Antilipemic agents, bile acid sequestrantsAntilipemic agents, bile acid sequestrants: In human research, concomitant administration of niacin and bile acid sequestrants (cholestyramine, colestipol) enhanced lipid-lowering effects, reduced niacin absorption, and increased the risk of adverse effects, such as myopathy (412; 135; 335; 277; 278; 19; 26; 429; 430; 431; 280; 395; 432; 433; 434).
  • Antilipemic agents, fibratesAntilipemic agents, fibrates: In humans, taking niacin and fibrates, such as gemfibrozil, clofibrate, or fenofibrate, increased the risk of adverse effects (412), altered the pharmacokinetics of either agent (435), or enhanced the cholesterol-lowering effects of the antilipemic (171; 172; 286; 335; 436; 304; 437).
  • Antilipemic agents, HMG-CoA reductase inhibitorsAntilipemic agents, HMG-CoA reductase inhibitors: In humans, taking niacin and HMG-CoA reductase inhibitors, such as pravastatin, lovastatin, and atorvastatin, increased the risk of adverse effects, namely myopathy and rhabdomyolysis (413; 319; 414; 415; 416). This combination may also elevate liver function tests, result in hepatotoxicity, enhance the reduction of serum cholesterol levels (276; 438; 319; 439; 440; 393; 441; 442; 30; 325; 395; 299; 324; 35; 15; 443; 444; 445; 446), or increase plasma HDL levels (440; 393; 35; 444; 446).
  • Antithyroid agentsAntithyroid agents: Decreases in total serum thyroxine and free thyroxine levels and increases in triiodothyronine uptake ratios have been reported in humans after niacin therapy (22; 25; 406; 407; 264; 408).
  • AspirinAspirin: Concurrent use of aspirin has been shown to reduce the tingling, itching, flushing, and warmth associated with oral niacin administration in humans (37; 38; 39; 40; 41; 42; 43; 44; 45; 46; 47; 48; 49; 50; 51; 52).
  • BenzodiazepinesBenzodiazepines: Niacinamide has been shown to increase the solubility of diazepam in vitro, which may or may not affect the toxicity or efficacy of diazepam and possibly other benzodiazepines (423).
  • Calcium-channel blockersCalcium-channel blockers: Nicotinic acid is similar to medications in the class of drugs known as dihydropyridine calcium channel blockers, according to principal component analysis and factor analysis of molecular properties (428).
  • Cardiovascular agentsCardiovascular agents: In humans, niacin therapy increased plasma homocysteine levels by up to 55% from baseline, possibly increasing the risk of adverse cardiac events (19; 20). Circulatory collapse following intravenous administration of nicotinic acid has been reported in one patient who was suspected of being chronically ill and poorly nourished (381). Abnormal heart rhythms and heart palpitations have occurred in niacin studies, according to unconfirmed reports.
  • Contraceptives (oral)Contraceptives (oral): Niacinamide has been shown to increase the solubility of 17-beta-estradiol in vitro, which may affect the toxicity or efficacy of 17-beta-estradiol and possibly other estrogens (423). Oral contraceptives may stimulate tryptophan oxygenase and increase the amount of tryptophan that is converted into niacin, thus lowering the doses of niacin that may be necessary to attain a specific clinical effect (447; 432).
  • Cytochrome P450 metabolized agentsCytochrome P450 metabolized agents: Nicotinamide decreased the conversion of primidone to phenobarbital in both animals and epileptic patients, likely due to the inhibition of cytochrome P450 (426).
  • EpinephrineEpinephrine: Anaphylactic shock necessitating the administration of epinephrine has been described in two women and one man after receiving intravenous niacin (380; 381). The subcutaneous administration of a single 250mg/kg dose of niacin in rats inhibited normal fasting epinephrine, norepinephrine, and theophylline-induced free fatty acid release (448).
  • EstrogensEstrogens: Niacinamide has been shown to increase the solubility of 17-beta-estradiol in vitro (423), which may affect the toxicity or efficacy of 17-beta-estradiol and possibly other estrogens. Oral contraceptives may stimulate tryptophan oxygenase and increase the amount of tryptophan that is converted into niacin (447; 432), thus theoretically lowering the doses of niacin that may be necessary to attain a specific clinical effect.
  • Ganglionic blocking drugsGanglionic blocking drugs: In human research, nicotinic acid had ganglionic-like effects (449), and theoretically it may potentiate the effects of ganglionic blocking agents, thereby resulting in postural hypotension.
  • GriseofulvinGriseofulvin: Niacinamide has been shown to increase the solubility of griseofulvin in vitro (423), which may theoretically affect the toxicity or efficacy of griseofulvin administration in vivo.
  • HepatotoxinsHepatotoxins: Niacin administration has been reported to cause significant but reversible elevation of serum transaminase concentrations in clinical trials (56; 326; 24; 25; 26; 250; 60; 392; 62; 319; 65; 254; 28; 86; 29; 251; 393; 90; 71; 312; 394; 258; 75; 260; 261; 257; 79; 96; 98; 81; 322; 398; 332). Numerous case reports detail the development of hepatotoxicity, including jaundice, hepatitis, ascites, fulminant hepatic failure, and liver structural changes after niacin administration (58; 24; 250; 61; 63; 64; 66; 67; 68; 251; 87; 70; 90; 71; 46; 74; 76; 77; 78; 79; 96; 80; 81; 409; 60; 62; 69). Theoretically, concomitant use of niacin with other hepatotoxic agents may increase the risk of liver damage.
  • NeomycinNeomycin: Concomitant use of neomycin and niacin may result in additive effects on the lowering of lipoprotein (a), low-density lipoprotein, and total cholesterol levels (450; 295).
  • NicotineNicotine: Worsening of flushing and dizziness has been reported in humans with the use of transdermal nicotine and niacin (451).
  • Nonsteroidal anti-inflammatory agents (NSAIDs)Nonsteroidal anti-inflammatory agents (NSAIDs): In humans, use of aspirin or other NSAIDs reduced the tingling, itching, flushing, and warmth associated with oral niacin administration (37; 38; 39; 40; 41; 43; 44; 46; 47; 50; 51; 52; 42; 45; 48; 49; 3).
  • PrimidonePrimidone: In animals, nicotinamide increased the half-life of primidone by 47.6%, and the conversion to phenobarbital and phenylethylmalonamide was decreased by 32.4% and 14.5%, respectively (426). Nicotinamide also decreased the conversion of primidone to phenobarbital in patients with epilepsy.
  • ProbucolProbucol: Concomitant administration of niacin and probucol in patients resulted in enhanced cholesterol-lowering effects and may allow lower doses of each medication to be used (452).
  • ProcetofeneProcetofene: In humans, a combination of procetofene and niacin normalized triglyceride levels (453).
  • ProgestinsProgestins: Niacinamide has been shown to increase the solubility of progesterone in vitro (423), which may affect the toxicity or efficacy of progesterone administration in vivo.
  • PyrazinamidePyrazinamide: In humans, pellagra occurred with use of pyrazinamide and niacin due to structural similarities between pyrazinamide and nicotinamide (454). The administration of a diet rich in pyrazinamide has been shown to significantly increase the metabolism of tryptophan to niacin in rats (455), which may have implications for the concurrent use of niacin and pyrazinamide in humans.
  • TheophyllineTheophylline: The subcutaneous administration of a single 250mg/kg dose of niacin in rats inhibited normal fasting epinephrine, norepinephrine, and theophylline-induced free fatty acid release (448).
  • Thyroid hormonesThyroid hormones: Decreases in total serum thyroxine and free thyroxine levels and increases in triiodothyronine uptake ratios have been reported in humans after niacin therapy (22; 25; 406; 407; 264; 408).
  • VasodilatorsVasodilators: Niacin induces a vasodilatory response in humans (391; 292; 56; 333; 284; 326; 22; 23; 24; 26; 27; 250; 293; 294; 392; 319; 28; 86; 29; 393; 88; 12; 30; 394; 312; 31; 32; 395; 33; 34; 35; 384; 96; 36; 98; 396; 397; 287; 386; 322; 309; 323; 320; 62; 306; 398; 399).

Niacin and Niacinamide/Herb/Supplement Interactions:
  • Amino acidsAmino acids: Basic scientific research has revealed that interactions among certain amino acids, such as lysine and tryptophan, may play a role in niacin synthesis (456)
  • AndrogensAndrogens: Niacinamide increases the solubility of testosterone in vitro (423), which may affect the toxicity or efficacy of testosterone administration in vivo.
  • AntibacterialsAntibacterials: According to secondary sources, antibacterial herbs or supplements may lead to a decreased production of B vitamins through the destruction of normal gastrointestinal flora.
  • Anticoagulants and antiplateletsAnticoagulants and antiplatelets: In theory, niacin therapy may increase the risk of bleeding (263). In addition, thrombocytopenia has been observed in clinical trials of niacin therapy (264; 27; 88).
  • AnticonvulsantsAnticonvulsants: According to animal and human research, niacinamide may alter plasma levels of anticonvulsants (425).
  • Antigout herbs and supplementsAntigout herbs and supplements: In clinical research, niacin therapy has been shown to increase serum uric acid levels (54; 58; 24; 25; 26; 266; 250; 60; 254; 255; 84; 85; 28; 86; 29; 88; 12; 258; 259; 260; 261; 257; 98; 262).
  • AntihistaminesAntihistamines: In human research, 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.
  • AntilipemicsAntilipemics: In humans, niacin increased the risk of side effects (413; 319; 414; 412; 415; 416) and increase lipid-lowering effects (457; 438; 413; 319; 440; 414; 393; 441; 442; 30; 325; 395; 324; 299; 35; 415; 15; 443; 444; 445; 446; 416; 458) when used with antilipemic agents.
  • AntioxidantsAntioxidants: In human research, there is conflicting evidence as to whether antioxidants decrease niacin's beneficial effects on cholesterol levels and heart disease (459; 276; 458; 460; 461; 462; 463).
  • Cardiovascular herbs and supplementsCardiovascular herbs and supplements: Niacin therapy has been shown to increase plasma homocysteine levels by up to 55% from baseline in humans, possibly increasing the risk of adverse cardiac events (19; 20). Circulatory collapse following intravenous administration of nicotinic acid has been reported in one patient who was suspected of being chronically ill and poorly nourished (381). Abnormal heart rhythms and heart palpitations have occurred in niacin studies, according to unconfirmed reports.
  • ChromiumChromium: In humans, chromium and nicotinic acid had synergistic effects on blood glucose control in the elderly (464; 465).
  • Cytochrome P450 metabolized herbs and supplementsCytochrome P450 metabolized herbs and supplements: Nicotinamide decreases the conversion of primidone to phenobarbital in both animals and epileptic patients, likely due to inhibition of cytochrome P450 (426).
  • ContraceptivesContraceptives: Niacinamide has been shown to increase the solubility of 17-beta-estradiol in vitro (423), which may affect the toxicity or efficacy of 17-beta-estradiol and possibly other estrogens. Oral contraceptives may stimulate tryptophan oxygenase and increase the amount of tryptophan that is converted into niacin, thus lowering the doses of niacin that may be necessary to attain a specific clinical effect (447; 432).
  • Grape seedGrape seed: Concomitant administration of chromium polynicotinate (niacin-bound chromium) and grape seed proanthocyanidin has been shown to result in greater improvements in the lipid profile of hypercholesterolemic subjects than either agent alone (466), suggesting an additive effect.
  • Hepatotoxic herbs and supplementsHepatotoxic herbs and supplements: Niacin administration has been reported to cause significant but reversible elevation of serum transaminase concentrations in clinical trials (56; 326; 24; 25; 26; 250; 60; 392; 62; 319; 65; 254; 28; 86; 29; 251; 393; 90; 71; 312; 394; 258; 75; 260; 261; 257; 79; 96; 98; 81; 322; 398; 332). Numerous case reports detail the development of hepatotoxicity, including jaundice, hepatitis, ascites, fulminant hepatic failure, and liver structural changes after niacin administration (58; 24; 250; 61; 63; 64; 66; 67; 68; 251; 87; 70; 90; 71; 46; 74; 76; 77; 78; 79; 96; 80; 81; 409; 60; 62; 69). Theoretically, concomitant use of niacin with other hepatotoxic agents may increase the risk of liver damage.
  • HypoglycemicsHypoglycemics: In human research, niacin has been shown to increase blood glucose levels and may require dosing adjustments of hypoglycemic agents (82; 56; 58; 24; 25; 83; 60; 84; 85; 28; 86; 29; 87; 88; 89; 90; 12; 32; 92; 93; 94; 95; 96; 97; 98). On the contrary, the concomitant administration of niacinamide and insulin has been shown to lead to a reduction in insulin requirements in children newly diagnosed with type 1 diabetes mellitus (152; 352; 351). Some studies have found no difference (427; 82; 56; 58; 24; 25; 83; 60; 84; 85; 28; 86; 29; 87; 88; 89; 90; 12; 32; 92; 93; 94; 95; 96; 97; 98).
  • HypotensivesHypotensives: In patients with hypertension, nicotinic acid lowers blood pressure values (181). Thus, additive effects with hypotensive agents are possible. Nicotinic acid may act similarly to calcium channel blockers, according to principal component analysis and factor analysis of molecular properties (428).
  • Inositol hexanicotinateInositol hexanicotinate: Inositol hexanicotinate may be a source of nicotinic acid therapy (101).
  • KavaKava: It has been suggested that kava-induced dermopathy is due to niacin deficiency in humans (467).
  • Minerals (zinc sulfate)Minerals (zinc sulfate): Oral administration of zinc sulfate to alcoholics with pellagra has been shown to increase the urinary excretion of niacin metabolites, suggesting its ability to affect the metabolism of tryptophan to niacin; this has possible implications for the concurrent administration of zinc and niacin (468).
  • Pantothenic acidPantothenic acid: The results of one crossover study in adolescents found that supplementation with pantothenic acid increased urinary secretion of niacin and may have implications for the concomitant use of the two B-complex vitamins (469).
  • PhytoestrogensPhytoestrogens: Interactions may theoretically occur between estrogens and niacin or niacinamide, but it is not clear if these interactions apply to herbs or supplements with phytoestrogenic constituents (chemical components that possess estrogen receptor agonist or antagonist properties, or exert estrogen-like effects clinically but may not be structurally similar to estrogens). Niacinamide has been shown to increase the solubility of 17-beta-estradiol in vitro (423), which may affect the toxicity or efficacy of 17-beta-estradiol and possibly other estrogens. Oral contraceptive drugs may stimulate tryptophan oxygenase and increase the amount of tryptophan that is converted into niacin, thus lowering the doses of niacin that may be necessary to attain a specific clinical effect (447; 432).
  • PhytoprogestinsPhytoprogestins: Niacinamide has been shown to increase the solubility of progesterone in vitro (423), which may affect the toxicity or efficacy of progesterone administration in vivo.
  • Salicylate-containing herbsSalicylate-containing herbs: Concurrent use of aspirin has been shown to reduce the tingling, itching, flushing, and warmth associated with oral niacin administration in humans (37; 38; 39; 40; 41; 42; 43; 44; 45; 46; 47; 48; 49; 50; 51; 52), an effect that may also result from use of salicylate-containing herbs. Aspirin significantly reduced the intensity and duration of niacin-induced flushing, using a specially formulated low-flushing niacin. However, levels of salicylates in herbs may vary or be too low to attain desired clinical effects.
  • SitosterolsSitosterols: In humans, concomitant administration of niacin and a 20% suspension of beta-sitosterol and dihydro-beta-sitosterol resulted in an additive decrease in plasma cholesterol compared to each agent alone (22).
  • Thyroid agentsThyroid agents: Decreases in total serum thyroxine and free thyroxine levels and increases in triiodothyronine uptake ratios have been reported in humans after niacin therapy (22; 25; 406; 407; 264; 408).
  • Tryptophan: Tryptophan: As a precursor to niacin, supplementation with tryptophan may theoretically increase niacin levels. During pregnancy, the catabolism of tryptophan is accelerated, and niacin supplementation may not be needed (348).
  • Vasodilator herbs and supplementsVasodilator herbs and supplements: Niacin induces a vasodilatory response in humans (391; 292; 56; 333; 284; 326; 22; 23; 24; 26; 27; 250; 293; 294; 392; 319; 28; 86; 29; 393; 88; 12; 30; 394; 312; 31; 32; 395; 33; 34; 35; 384; 96; 36; 98; 396; 397; 287; 386; 322; 309; 323; 320; 62; 306; 398; 399). Theoretically, the vasodilatory effects of niacin by other vasodilatory agents.
  • Vitamins (vitamin E, vitamin Avitamin B5/pantothenic acidvitamin B6)Vitamins (vitamin E, vitamin A, vitamin B5/pantothenic acid, vitamin B6): In clinical research, concomitant administration of vitamin E and niacin may have additive effects on the lowering of serum cholesterol levels (470). The addition of vitamin A to this combination may also contribute (463). However, a number of studies have demonstrated no benefits of antioxidants (vitamin E) on cardiovascular outcomes (471; 472; 473; 474). In addition, it has been suggested that antioxidants may blunt niacin's beneficial effects on cholesterol levels and heart disease, possibly by interfering with niacin's effects on proteins involved with the formation of high-density lipoproteins (HDL) (458; 460; 461; 463; 470). Niacin in combination with vitamin A has been suggested as a possible therapy to ameliorate dysgeusia (loss of taste or a metallic taste) (236). The results of one crossover study in adolescents found that supplementation with pantothenic acid increased urinary secretion of niacin and may have implications for the concomitant use of the two B-complex vitamins (469). Supplementary vitamin B6 may interfere with niacin metabolism.

Niacin and Niacinamide/Food Interactions:
  • GeneralGeneral: Taking niacin with food may decrease stomach upset and the risk of peptic ulcer in humans (39).
  • CoffeeCoffee: Coffee is a source of niacin (475). Concomitant use may increase levels of niacin.
  • Hot beveragesHot beverages: Niacin has been shown to induce flushing (424); theoretically, hot beverages ingested concomitantly may magnify niacin-induced flushing (424).
  • Oat branOat bran: One trial involving combination treatment found no added effect with the use of oat bran and niacin therapy (394).
  • SorghumSorghum: Human niacin status may be affected by eating sorghum (Sorghum gramineae) grain in ready-to-eat breakfast cereals (476).
  • Tryptophan-containing foodsTryptophan-containing foods: As the precursor to niacin, supplementation with tryptophan may increase niacin levels. During pregnancy, the catabolism of tryptophan is accelerated, and niacin supplementation may not be needed (348).

Niacin and Niacinamide/Lab Interactions:
  • ApolipoproteinsApolipoproteins: In clinical trials, niacin was shown to reduce apolipoprotein C-I, C-II, C-III, and E levels (315; 316).
  • Blood pressureBlood pressure: In hypertensive individuals, nicotinic acid lowered blood pressure values (181).
  • Coagulation panelCoagulation panel: There are three published case reports of patients who developed a reversible coagulopathy while taking sustained-release niacin (263). O'Brien et al. reported on the development of leukopenia in two patients taking niacin for the treatment of hypercholesterolemia (264). Mild eosinophilia was observed in six of seven subjects given sustained-release niacin (1g three times daily) for a period of two weeks (410). Thrombocytopenia has been observed in clinical trials of niacin therapy (264; 27; 88). Treatment with niacin has been shown to cause a significant decrease in plasma fibrinogen levels in humans (16; 17). Niacin therapy may also lead to clotting factor synthesis deficiency and coagulopathy, which may result in prolonged prothrombin times (263). In clinical trials, treatment with niacin has been shown to cause a significant decrease in plasma prothrombin levels (285).
  • CortisolCortisol: Intravenous niacin administration caused a significant increase in plasma cortisol in healthy male volunteers (477).
  • Creatine kinaseCreatine kinase: In humans, niacin therapy has been associated with increases in creatine kinase levels (319; 88; 395; 98; 322).
  • Fibrinogen levelsFibrinogen levels: Treatment with niacin has been shown to cause a significant decrease in plasma fibrinogen levels in humans (16; 17; 285).
  • GlucagonGlucagon: Intravenous niacin administration caused a significant increase in plasma glucagon in healthy male volunteers (477).
  • Glucose levelsGlucose levels: Niacin may cause significant increases in blood glucose concentrations, glucose intolerance, and insulin resistance, necessitating monitoring of niacin therapy, especially in diabetic patients, as insulin or hypoglycemic medications may require dosing alterations (56; 58; 24; 25; 83; 60; 84; 85; 28; 86; 29; 87; 88; 89; 90; 12; 91; 32; 92; 93; 94; 95; 96; 98). Niacinamide was shown to cause a significant 23.6% increase in insulin resistance in a group of eight subjects at high risk of developing diabetes mellitus (type 1) (390). Seven of 11 subjects were glucose-intolerant after extended-release (ER) niacin therapy; for three of these subjects, this was a new finding (99). In a clinical trial, nicotinic acid increased plasma glucose levels in both those with or without a family history of type 2 diabetes (478).
  • Homocysteine levelsHomocysteine levels: Concomitant administration of colestipol and niacin therapy as part of the Cholesterol Lowering Atherosclerosis Study (CLAS) resulted in increased homocysteine levels in humans, which may also be attributable to niacin therapy alone (19). An analysis of 52 participants in the Arterial Disease Multiple Intervention Trial (ADMIT) also showed niacin therapy to cause a 55% increase in plasma homocysteine levels from baseline (p=0.001) (20). Periodic monitoring of homocysteine levels may be warranted (20).
  • Human growth hormoneHuman growth hormone: Nicotinic acid has been shown to increase human growth hormone levels (479).
  • Lactic acid testLactic acid test: Two case reports have been published detailing the development of lactic acidosis after ingestion of sustained-release niacin, one involving concurrent ethanol ingestion (376; 375).
  • Lipid profileLipid profile: At a dose of 2g daily, Niaspan® was shown to cause a significant decrease in serum lipoprotein (a) and triglyceride concentrations in humans (327; 328; 18). Niacin induced a small but significant increment in hepatic secretion of biliary cholesterol (11). Significant increases in high-density lipoproteins (HDL) have been shown in clinical trials using niacin (306; 307; 298; 308; 10; 262; 11; 12; 309; 310; 311). In clinical trials, niacin reduced low-density lipoprotein (LDL) levels (313; 306; 10; 11; 12; 311; 310). In clinical trials, niacin administration caused significant decreases in serum cholesterol (333; 334; 335; 24; 250; 336; 337; 92; 338; 339; 257; 340; 341; 10). In clinical trials, niacin reduced very-low-density lipoprotein (VLDL) and small LDL (314; 311; 313) and increased HDL (311).
  • Liver function testsLiver function tests: Niacin and niacinamide administration may increase human serum bilirubin, alanine aminotransferase, aspartate aminotransferase, and lactate dehydrogenase concentrations (56; 326; 24; 25; 26; 250; 60; 392; 62; 319; 65; 254; 28; 86; 29; 251; 393; 90; 71; 312; 394; 258; 75; 260; 261; 257; 79; 96; 98; 81; 322). One patient receiving 2,000mg of niacin plus 40mg of lovastatin experienced reversible elevations in liver transaminases (320). Periodic monitoring of liver function tests, especially transaminase values, is recommended (every three months initially) (58; 24; 250; 61; 63; 64; 66; 67; 68; 251; 87; 70; 90; 71; 46; 74; 76; 77; 78; 79; 96; 80; 81; 480).
  • Plasma uric acidPlasma uric acid: Elevated serum uric acid levels have been observed with niacin therapy in humans (54; 58; 24; 25; 26; 266; 250; 60; 254; 255; 84; 85; 28; 86; 29; 88; 12; 258; 259; 260; 261; 257; 98; 262; 481). The development of gout has reportedly occurred in some patients due to hyperuricemia following high doses of niacin (54; 284; 266; 250; 259; 395).
  • Thyroid function testsThyroid function tests: Decreases in total serum thyroxine and free thyroxine levels and increases in triiodothyronine uptake ratios have been reported after niacin therapy in humans (22; 25; 406; 407; 264; 408).

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The information in this monograph is intended for informational purposes only, and is meant to help users better understand health concerns. Information is based on review of scientific research data, historical practice patterns, and clinical experience. This information should not be interpreted as specific medical advice. Users should consult with a qualified healthcare provider for specific questions regarding therapies, diagnosis and/or health conditions, prior to making therapeutic decisions.

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