Chemistry and Forms

Niacin and niacinamide are the two principal forms of the water-soluble B-complex vitamin, B3. Nicotinic acid and nicotinamide are alternate names for niacin and niacinamide, respectively. Niacin was initially isolated from rice bran in 1911. Later, in 1934, Warburg and Christian isolated niacinamide, the amide of niacin, when coenzyme II (NADP) was extracted from equine erythrocytes. The structure of niacinamide consists of a pyridine ring with an amide group in position three. Inositol hexaniacinate is the hexanicotinic acid ester of meso-inositol; it also called inositol hexanicotinate or inositol nicotinate.

Niacin is extremely stable to heat, light, acid, alkali, and oxidation.

Physiology and Function

Although niacin and niacinamide have divergent pharmacological activities, they share the fundamental function that identifies them as B3, the vitamin activity that prevents pellagra. However, niacin does not meet the criteria for being defined as a vitamin in the strictest sense because it can be derived from tryptophan. However, at a 60:1 ratio for biosynthesis, this process is highly inefficient and depends on vitamins B1, B2, and B6as essential cofactors.

Niacin, as either nicotinamide or nicotinic acid, is rapidly absorbed in the proximal small intestine by facilitated diffusion (at low concentrations) and by passive diffusion (at high concentrations). A small proportion of niacinamide is metabolized to niacin, primarily through the activity of enteric flora. The pharmacokinetics of niacinamide vary significantly depending on dose, species, gender, and route of administration. In humans, peak serum concentrations of niacinamide are attained within 1 hour of oral ingestion because it is rapidly cleared from circulation and distributed. Niacin is primarily eliminated via the urine, but also appears in breast milk.

Nicotinamide adenine dinucleotide (NAD+, coenzyme I) and nicotinamide adenine dinucleotide phosphate (NADP+, coenzyme II) are the active forms of nicotinamide. The nicotinamide component of NAD and NADP plays a key role in hydrogen transfer reactions by acting as a hydride ion acceptor or donor in numerous intracellular oxidation-reduction (redox) reactions. Thus, they are required for the activity of more than 200 enzymes participating in a broad range of metabolic processes, including glycolysis, tissue respiration, and lipid, amino acid, and purine metabolism. Notably, NAD is required for the redox reactions in glycolysis and in Krebs cycle during oxidative phosphorylation, through which biological systems derive most of their energy from carbohydrates. NADPH is also involved in fatty acid and steroid synthesis as well as the pentose phosphate shunt pathway, one pathway by which ribose is synthesized. Consequently, niacin is essential to biosynthesis of hormones such as estrogen, progesterone, testosterone, and insulin, along with stress-related hormones in the adrenals. Niacinamide is known to stimulate gamma-aminobutyric acid (GABA) receptors, without binding to the receptor sites, an effect likened to that of benzodiazepines. Both NAD+ and NADP+ function as cofactors for numerous dehydrogenase enzymes (e.g., lactate and malate dehydrogenases) responsible for innumerable biochemical reactions in the body, including detoxifying alcohol and utilizing carbohydrates, fats, and proteins. Niacin is a precursor of glucose tolerance factor, and niacinamide facilitates beta-cell regeneration in vivo and in vitro.

Nicotinamide adenine dinucleotide is the substrate for mono–adenosine diphosphate (ADP)–ribosyltransferases and poly-ADP-ribose polymerase (PARPs), two classes of enzymes that separate the niacin moiety from NAD and transfer ADP-ribose units from NAD to acceptor proteins. Although their functions are not yet well understood, PARPs also appear to play an important role in DNA replication and repair, as well as cell differentiation. Niacinamide inhibits free-radical formation and acts as an antioxidant, at least in part by preventing NAD depletion during DNA repair by inhibiting PARP. In particular, niacinamide protects pancreatic islet cell lysis (e.g., after exposure to oxygen free radicals and nitric oxide) and suppresses cytokine-mediated induction of nitric oxide synthase. Through its inhibition of PARP, niacinamide also modulates major histocompatibility complex (MHC) class II expression and exerts an anti-inflammatory action affecting neutrophil chemotaxis.

Known or Potential Therapeutic Uses

Within conventional medical practice, vitamin B3usage, typically as niacinamide, is primarily framed in terms of prophylaxis and treatment of frank vitamin B3deficiency states, particularly pellagra. However, the most common clinical application of niacin is treatment of primary hyperlipidemia, specifically type IIa/IIb, III, IV, or V hyperlipoproteinemia, where it is a first-line therapy, often in combination with an HMG-CoA reductase inhibitor, for reducing low-density lipoprotein cholesterol (LDL-C) concentrations and triglycerides and increasing high-density lipoprotein cholesterol (HDL-C) concentrations.

Supplementation with vitamin B3can play an essential role in treatment of individuals with malabsorption syndromes associated with pancreatic insufficiency and diseases of the small intestine, such as celiac and tropical sprue. Diabetes mellitus, hyperthyroidism, malignant carcinoid syndrome, and other pathophysiological states can increase metabolic requirements for B3and carry a significant risk for B3deficiency. Hartnup's disease is a rare autosomal recessive tryptophan metabolism disorder wherein inborn errors of metabolism cause tryptophan absorption and transport to be impaired and tryptophan to be diverted to form 5-hydroxytryptamine, thereby impairing conversion of tryptophan to niacin and increasing risk of niacin deficiency and the need for niacin (and tryptophan) intake.

Historical/Ethnomedicine Precedent

The use of lime or other alkalinating agents in the diets and cooking practices of many traditional cultures represents an institutionalized application of the empirical observation that bound niacin in many food sources, especially maize, needs to be liberated to supply adequate dietary intake of niacin.

Possible Uses

General

Burns, human immunodeficiency virus (HIV) support, postpartum support, pregnancy, schizophrenia, skin cancer.

Niacin

Anxiety, atherosclerosis, Bell's palsy, diabetes mellitus, dysmenorrhea, Hartnup's disease, high hypercholesterolemia, hyperlipidemia, hyperlipoproteinemia (type IIa/IIb, III, IV, V), hypertriglyceridemia, hypothyroidism, intermittent claudication, hypothyroidism, migraines, multiple sclerosis, myocardial infarction (recurrence), photosensitivity, Raynaud's disease, smoking cessation, tardive dyskinesia.

Niacinamide

Acne (topical), alcohol withdrawal support, anxiety, bursitis, cataracts, dermatitis herpetiformis (with tetracycline), diabetes mellitus (type 1; prevention), Hartnup's disease, hypoglycemia, osteoarthritis, pellagra, photosensitivity, Raynaud's disease, tardive dyskinesia.

Inositol Hexaniacinate

Hypercholesterolemia, intermittent claudication, peripheral vascular disease, Raynaud's disease.

Deficiency Symptoms

Niacin deficiency manifests pervasively, affecting every cell in the body. Symptoms of mild niacin deficiency include indigestion, fatigue, canker sores, vomiting, and depression. In its classic presentation as pellagra, severe niacin deficiency is characterized by cutaneous, mucous membrane, central nervous system (CNS), and gastrointestinal (GI) symptoms, alone or in combination; a pattern commonly described as the “four Ds”: dermatitis, diarrhea, dementia, and death. Nutritionally based pellagra usually involves a simultaneous tryptophan deficiency. The dermatitis caused by a niacin deficiency is characterized by cracked, thick, scaly skin forming a symmetrical, darkly pigmented rash and exacerbated by sun exposure, a phenomenon known as “mal del sol.” This condition is often complicated by other B-vitamin deficiencies. Scarlet glossitis and stomatitis are characteristic of acute deficiency. The tongue and mouth become inflamed, painful with a burning sensation, and take on a bright, beefy red appearance. Diarrhea results from decreased hydrochloric acid secretion accompanied by inflammation of the GI tract. Dementia caused by a lack of niacin begins with irritability, headaches, and insomnia, followed by mental confusion, amnesia, hallucinations, and severe depression. If untreated, pellagra is ultimately fatal.

The most common causes of niacin deficiency are alcoholism and inadequate intake of niacin (and tryptophan) with sufficient bioavailability; genetic, pathophysiological, and iatrogenic factors also constitute significant risks. High dietary intake of cereals (e.g., sorghum, corn) not processed with lime, to increase tryptophan bioavailability, is a common cause of niacin deficiency in settings of poverty and poor diet. However, a broad nutritional deficit is usually required, especially involving protein, tryptophan and/or thiamine, riboflavin, and pyridoxine. Excessive leucine intake (e.g, with high millet intake, as common in India) can lead to a niacin deficiency even with normal intake because leucine blocks NAD synthesis. Diarrhea, cirrhosis, and inadequate or imbalanced nutrient infusions during postoperative recovery are common causes of secondary niacin deficiency.

Dietary Sources

Liver, poultry, meat, fish, eggs, peanuts, brewer's yeast, torula yeast, rice bran, rice polishings, and wheat bran are rich dietary sources of vitamin B3. Legumes, mushrooms, nuts, sunflower seeds, and wheat germ can also serve as significant nutrient sources. In general, however, although whole grains and cereal products may contain some vitamin B3, fortification of white flour is the primary means of ensuring that commonly consumed grain products provide adequate niacin nutriture. Niacin tends to be bound to glycosides in mature cereal grains, such as corn and wheat, which significantly decreases its bioavailability. Alkali treatment of grains, such as with alkaline-cooking process using lime, may result in release of the bound niacin and increase its bioavailability; however, this has been disputed. Dietary tryptophan can be converted to niacin and can enhance available supplies, but evidence indicates that the 60:1 conversion ratio may be overly optimistic. ¹

Food sources of B3often also contain thiamine, riboflavin, pantothenic acid, pyridoxine, cyanocobalamin, and folic acid. B-complex vitamins (especially B1, B2, and B6), vitamin C, magnesium, zinc, protein, and essential fatty acids enhance absorption of vitamin B3, whereas alcohol, coffee, excess sugar, antibiotics, and steroids reduce niacin absorption.

Nutrient Preparations Available

Vitamin B3as a nutritional supplement is primarily available as niacinamide (nicotinamide) or niacin (nicotinic acid). Multivitamin formulations typically contain some form of B3. Nicotinamide is the form of niacin most often used in nutritional supplements and in food fortification. Nicotinate and inositol hexaniacinate (the hexanicotinic acid ester of meso-inositol) are also available as nonprescription forms. Timed-release supplemental niacin (OTC) can produce fewer superficial adverse effects (e.g., flushing) but can also be more hepatotoxic. Nicotinic acid in a shorter-acting, timed-release preparation, sometimes referred to as “intermediate release” or “extended release,” is available by prescription. Limited but relatively consistent evidence indicates that inositol hexaniacinate may be the best-tolerated form of niacin, with minimal incidence of skin flushing, nausea, vomiting, agitation, and hepatotoxicity. ^2-4

Within conventional medical practice the crystalline, immediate-release form (usually taken two to four times daily) and the extended-release form (once daily) are the two prescription formulations of niacin approved for treatment of dyslipidemia. The American Heart Association advises against using OTC supplemental niacin. ⁵

Note: Niacin dosage values for requirements and foods are described in niacin equivalents (NE), which are calculated by combining nicotinic acid and niacinamide intake and adding an estimate for tryptophan conversion. Niacin (mg equivalents)=Nicotinic acid (mg) + Nicotinamide (mg) + Tryptophan (mg)/60

Dosage Forms Available

Capsule, liquid, powder, tablet, effervescent tablet. Injectable forms are sometimes administered by health care professionals.

Source Materials for Nutrient Preparations

All B vitamins are predominantly synthesized, except for the “food form,” in which synthesized B vitamins are added to nutrient broth for yeast, which (supposedly) incorporates higher amounts of them into the cells, which are then dried and tableted.

Dosage Range

Adult

• Dietary:   The U.S. dietary reference intake (DRI) for niacin is 16 mg niacin equivalents per day for men and 14 mg equivalents daily for women. ⁶ Pregnant or lactating women: 18 mg daily.

• Supplemental/Maintenance:   100 mg daily, combined forms.

• Pharmacological/Therapeutic:   500 mg three times daily.

• Toxic:   U.S. tolerable upper limit (UL) established for nicotinic acid in adults is 35 mg per day; this level was selected to avoid the adverse effect of flushing in the general population, even though flushing and other adverse effects from nicotinamide are significantly less common. No separate tolerable UL has been established for nicotinamide. Reports of nicotinamide overdosage are not present in the literature.

• Nicotinic acid/niacin:   Transient acute flushing symptoms can occur at 100 to 200 mg niacin. Elevated liver enzymes, jaundice, and other signs of hepatotoxicity have been observed at nicotinic acid intakes as low as 750 mg/day for less than 3 months. Timed-release nicotinic acid has been associated with chemical hepatitis at levels as low as 500 mg/day for 2 months, although most cases have involved significantly higher doses and longer periods of intake,

• Nicotinamide/niacinamide:   Low toxicity generally characterizes the safety profile of nicotinamide. Intake of 3 g/day of nicotinamide for longer than 3 months has been associated with adverse effects such as nausea, vomiting, elevated liver enzymes, and jaundice. However, rare occurrences of liver toxicity have been reported at doses in excess of 1000 mg/day.

Pediatric (<18 Years)

Dietary:

• Infants, birth to 6 months: 2 mg/day (AI, adequate intake)
• Infants, 7 to 12 months: 4 mg/day (AI)
• Children, 1 to 3 years: 6 mg/day (RDA)
• Children, 4 to 8 years: 8 mg/day (RDA)
• Children, 9 to 13 years: 12 mg/day (RDA)
• Adolescents, 14 to 18 years: 14 mg (females) or 16 mg (males) daily (RDA)

• Supplemental/Maintenance:   Usually not recommended for children under 12 years of age. Avoid extended-release forms.

• Pharmacological/Therapeutic:   Usually not recommended for children under 12 years of age. Niacinamide has been administered in research and clinical settings involving prevention of type 1 diabetes mellitus in “high-risk” individuals at daily doses of 150 to 300 mg per year of the child's age, or 25 mg per kilogram body weight daily. Avoid extended-release forms.

• Toxic:   No tolerable UL for niacin in infants has been proposed. The U.S. tolerable UL established for niacin in children age 1 to 8 years is 10 to 15 mg daily and 20 mg daily for children 9 to 13 years; for adolescents (14-18 years) it is 30 mg daily. These levels were selected to avoid the adverse effect of flushing in the general population; flushing from nicotinamide is unreported and not considered an associated effect.

Laboratory Values

Cellular NAD and NADP content: Some clinicians and researchers suggest this test may provide the most clinically relevant indicators of niacin nutritional status. ⁷

• Erythrocyte nicotinamide adenine nucleotide (NAD):   This test can provide a sensitive indicator of niacin status.

• Red blood cell (RBC) NAD/NADP ratio:   A ratio of RBC NAD to RBC nicotinamide nucleotide phosphate (NADP) less than 1.0 may indicate deficiency.

• Urinary 1- N-methyl-nicotinamide (NMN) and 2- N-pyridone (2-N-P):   Excretion of less than 0.8 mg NMN per day and/or less than 1.0 mg 2-N-P per day indicates niacin deficiency. Although this measurement of excretion levels of major niacin metabolites can provide relatively accurate indices of niacin status, the results are often not conclusive.

• Whole-blood niacin:   Reference range 1.2 to 2.9 µg/mL.

• Abnormal liver function studies:   All individuals taking pharmacological doses of niacin should be monitored for liver function and enzyme levels; elevations in AST (SGOT) and ALT (SGPT) are common.

• Lymphocytic growth response.

Niacin or nicotinic acid administration can alter findings from several laboratory tests.

Urinary catecholamine concentration measurements by fluorimetric methods may be falsely elevated by niacin.

• Urine glucose determination using Benedict's reagent (cupric sulfate) may produce false-positive reactions. However, nicotinic acid may elevate blood glucose levels.
• Nicotinic acid may falsely elevate blood growth hormone levels.
• High-dose nicotinic acid may elevate blood uric acid levels.
• Niacin may falsely elevate homocysteine (Hcy) levels (by interference with the assay). It can also truly elevate Hcy levels by consuming methyl donor nutrients in its metabolism.

Niacin may decrease high-sensitivity C-reactive protein (hsCRP).

Overview

The safety profile for pharmacological preparations of vitamin B3varies significantly for different forms of the nutrient and exhibits a major differentiation between short-term, nonthreatening but uncomfortable adverse effects and longer-term toxicity. Evaluation of vitamin B3toxicity is further complicated by over 50 years of research findings and clinical observations that use varied preparations and poor methodology or that are inadequately powered, rendering contradictory and inconsistent conclusions, and that are often simply obsolete or clinically irrelevant.

Generally, adverse effects (predominantly flushing and itching) are significantly more likely with nicotinic acid than with nicotinamide, and, conversely, nicotinamide is better tolerated than nicotinic acid. Moreover, adverse reactions to niacinamide, at doses less than 1000 mg/day, are rare (and possibly linked to impure materials), and as such the nutrient is generally considered safe in most situations. ^8-11However, the possibility exists that adverse effects of niacinamide have not been adequately documented because significantly fewer clinical trials have involved niacinamide and the lack of data simply reflects a study bias. No adverse effects are associated with intake of niacin from food sources in typically consumed forms. ⁶ Adverse effects ranging from minor discomfort to severe toxicity are possible with nicotinic acid. Close supervision and regular monitoring are warranted when administering doses of niacin greater than 1000 mg/day.

Nutrient Adverse Effects

General Adverse Effects

Niacin often causes skin flushing with burning and tingling sensations, especially in the face, at levels more than 100 mg, although some sensitive individuals can experience flushing with as low a dose as 10 to 20 mg. These symptoms are of rapid onset and limited duration and may be accompanied by stomach distress, itching, and headache. The vasodilatory response involved constitutes a significant mechanism of action in the therapeutic action of niacin and is considered beneficial by many who self-administer niacin. However, many patients who discontinue or refuse niacin do so to avoid this unpleasant effect. These niacin-induced adverse effects typically resolve with discontinuation. Tachyphalaxis also develops with continued daily use, although tolerance may disappear with breaks of just a few days, but is usually quickly reestablished shortly after daily intake is resumed.

Nausea and GI upset are usually the first signs of toxicity with both niacin and niacinamide. Niacin is excreted as methylated pyridones, the formation of which uses S-adenosylmethionine (SAMe), the primary physiological methyl donor. The resulting niacin-induced interference with methionine metabolism and depletion of SAMe impairs detoxification processes and contributes to many of niacin's adverse effects, including decreased levels of vitamin B6and increased plasma homocysteine concentrations. Changes in hepatic transaminase enzyme levels, indicating liver inflammation, are often the second detectable sign of niacin toxicity. Prudence warrants that aspartate transaminase (AST, SGOT) and alanine transaminase (ALT, SGPT) be monitored regularly during therapy with any form of niacin. Elevated liver enzymes, jaundice, and other signs of hepatotoxicity have been observed at nicotinic acid intakes as low as 500 mg/day for less than 3 months, although doses of 1500 to 3000 mg/day are more typically associated with clinically significant adverse effects. A significant body of evidence indicates that slow-release or extended-release forms of niacin are more likely to cause adverse effects and hepatic toxicity reactions. Niacin administration needs to be discontinued or the dose significantly reduced at first indication of adverse effects on liver function. When initiating pharmacological doses of time-release niacin, beginning with 500 mg and increasing by 500 mg each month up to the target dose (usually 1.5-3.0 g) improves tolerance to the therapy.

Other symptoms rarely or infrequently associated with niacin intake include headache, dizziness, anxiety, panic attacks, hypothyroidism, abnormal cardiac rhythms, heart palpitations, difficult breathing, lactic acidosis, myopathy, elevated creatine kinase levels, tooth or gum pain, macular swelling, blurred vision, and toxic amblyopia.

In a multicenter randomized, placebo-controlled trial, Garg et al. ¹² found that niacin therapy, at 1000 mg or more per day, can substantially increase plasma homocysteine levels.

Niacinamide, at high dosage levels, has been associated with nausea, heartburn, vomiting, flatulence, and diarrhea. Parenteral administration of niacinamide has been reported to cause mild headaches and dizziness.

Rare occurrences of anaphylactic shock have been reported following intravenous or oral niacin therapy.

Adverse Effects Among Specific Populations

Individual characteristics that increase susceptibility to adverse effects from excess nicotinic acid intake include abnormal liver function or a history of liver disease, active peptic ulcer disease, alcohol abuse, diabetes, hypoglycemia, gout, cardiac arrhythmias, severe hypotension, inflammatory bowel disease, and migraine headaches.

Pregnancy and Nursing

Use of niacin supplementation during pregnancy or breastfeeding is not recommended because research on safety and effectiveness is insufficient. No problems have been reported.

Children

Use of niacin supplementation in children is not recommended because of insufficient research on safety and effectiveness and diminished hepatic detoxification capacity. No problems have been reported.

Contraindications

Vitamin B3is contraindicated in persons with hypersensitivity or allergy to niacin or niacin-containing substances and in children under 12 years of age, especially time-release forms.

Precautions and Warnings

Niacin should be avoided, or used only under close supervision and with appropriate monitoring, in patients with liver disease or compromised hepatic function, especially time-release forms.

Concomitant use of niacin and HMG-CoA reductase inhibitors (statins) significantly increases the risk of adverse effects, ranging from mild and reversible to severe and potentially fatal, especially in patients with compromised renal or hepatic function (see later discussion).

For decades, warnings have been voiced regarding potential risks for individuals with diabetes or hypoglycemia. Nicotinic acid can induce elevation in blood glucose and depletion of glycogen stores. Recent clinical trials found that niacin does not appear to raise blood glucose levels in patients with type 2 diabetes. ^13,14Thus, although niacin may cause significant alterations in blood sugar levels and insulin, such effects warrant clinical management rather than avoidance. (See Nutrient-Drug Interactions.)

Niacin can increase uric acid production and elevate blood uric acid concentrations. Individuals with gout, or predisposition to gout, should be administered niacin only under close supervision, preferably within the context of a comprehensive approach to dietary change and risk reduction. This adverse effect is primarily theoretical and evidence preliminary or inconsistent.

Niacin may elevate plasma homocysteine levels and should only be used under close supervision and with appropriate monitoring by patients with hyperhomocysteinemia or elevated risk of stroke or heart disease.

High-dose niacin intake can aggravate peptic ulcer and should be avoided in these patients except under close supervision and with appropriate monitoring.

Rare occurrences of leukopenia and slightly increased blood eosinophils have been reported in individuals taking niacin. Caution is advised in patients with bleeding disorders or undergoing anticoagulant therapy.

Strategic Considerations

With its long-standing role within standard practice of cardiovascular care, niacin is a nutrient that belies the labels of “alternative” and “conventional” and demonstrates the importance of an integrative approach to risk reduction and therapeutic intervention based on scientific evidence and clinical outcomes. The use of niacin with statins, resins, and fibrates is well established in conventional medicine. As such, niacin confirms the need for a multidisciplinary and collaborative model in both the benefits it conveys and the risks it amplifies when coadministered with various drug regimens and in the ways in which a strategic approach employing multiple nutrients can reduce adverse effects, optimize efficacy, and expand benefits.

Vitamin B3is among the most frequently researched nutrients in conventional medicine. However, a review of the available evidence illustrates that the combination of widespread usage and scientific research of limited character and narrow focus has resulted in an incomplete and unevenly distributed set of data characterized by many more speculative, ill-founded, or inadequately investigated “interactions” than thoroughly researched and well-documented ones.

Niacin can play an important role in a comprehensive strategy for reducing dyslipidemia and the risk of coronary disease, but low doses may be safer and just as effective as high doses. Also, there is an even greater need to coadminister vitamins B6and B12and folate, as well as methyl donor support through nutrients such as SAMe and betaine, to counter the tendencies to hepatoxicity and hyperhomocysteinemia, especially if statins are also employed. The issue of how antioxidants, singly or as networks, may interact with niacin to impair some of its therapeutic activity deserves focused research.

Two primary issues consistently arise regarding clinical application of niacin: toxicity and glucose control. The issue of toxicity is inherent to the nature of niacin and manifests primarily in adverse effects on the liver and interference with B6-tryptophan-methionine metabolism, leading to elevation of homocysteine (Hcy). The use of low-dose niacin or the alternative administration of nontoxic inositol hexaniacinate may adequately address the former. Coadministration of B2, B6, B12, folic acid, SAMe, and possibly betaine may diffuse the adverse effect on methyl donor supply and Hcy regulation.

The issue of interference with glucose control, particularly the often-asserted possibility of interference with oral hypoglycemic medications, may have been resolved with recent evidence indicating a lack of clinically significant interaction; nevertheless, continued research into potential benefits, drawbacks, and clinical implementation of coadministration is needed. Regular monitoring of liver enzyme levels, specifically AST and ALT, as well as plasma Hcy, is critical whenever administering niacin, especially in conjunction with statins.

The multiple concerns with niacin-induced toxicity highlight the need for further research into the efficacy of inositol hexaniacinate, or low-dose niacin, for treatment of dyslipidemias.

Likewise, the role of niacinamide in relation to insulin sensitivity, glucose tolerance, and dysglycemia suggests the need for integrative strategies that can both prevent the progression of dysfunction to disease and evolve within a multidisciplinary treatment strategy that responds flexibly to improvement or decline in the patient's condition.

In almost all its uses, vitamin B3exemplifies several fundamental principles operative in the clinical practice of integrative medicine. Less may do more, or enough, for any given agent. Static monotherapy using any agent is often less effective than flexible, personalized, and synergistic polypharmacy/polynutrient strategies crafted to the individual patient and evolving with their changing condition. Moreover, the spectrum of clinical applications for niacin and niacinamide and these agents’ interactions with various drugs emphasize the importance of the guiding principles in the management of most clinically significant interactions: the centrality of physician-patient trust and dialogue, the importance of collaboration among health care professionals bringing together various perspectives and expertises, the continuum of dosage from nutrient support to pharmacological intervention, the opportunities to emphasize therapeutic actions or mitigate adverse effects through combinations and dosage manipulation, and the essential need for ongoing supervision, monitoring, and titration.

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