Inositol Nicotinate (Inositol Hexanicotinate): A Comprehensive Reference
1. Identity, Chemistry, and Nomenclature
Inositol nicotinate, also known as inositol hexanicotinate or inositol hexaniacinate, is a compound of niacin (vitamin B3) and inositol. More precisely, it is the hexanicotinic acid ester of meso-inositol. The compound consists of six molecules of nicotinic acid (niacin) linked to a central inositol molecule. Its molecular formula is C₄₂H₃₀N₆O₁₂ (PubChem CID 3720).
In chemical nomenclature it is sometimes designated myo-inositol hexanicotinate, reflecting the specific stereoisomeric form of inositol involved — the myo-form, which is the predominant biologically active stereoisomer of inositol and the structural basis for a number of secondary messengers.
The terms "no-flush niacin" and "flush-free niacin" are conventionally used for inositol hexanicotinate; in this compound, six molecules of nicotinic acid (niacin) are covalently attached to inositol by ester bonds.
The compound's CAS registry number is 6556-11-2. Its systematic IUPAC name for the mononicotinate metabolic intermediate is (1R,2S,3R,4R,5S,6S)-2,3,4,5,6-pentahydroxycyclohexyl pyridine-3-carboxylate, reflecting the pyridine ring of nicotinic acid esterified at a hydroxyl position of inositol.
Niacin is available as a dietary supplement in the forms of nicotinic acid, nicotinamide, and inositol hexaniacinate. In the dietary supplement market, inositol nicotinate is most commonly sold as oral tablets or capsules. In the European Union and United Kingdom, inositol hexanicotinate (also known as inositol hexaniacinate) is authorized by the European Food Safety Authority (EFSA) as a source of niacin (vitamin B3) for addition to food supplements, following a 2009 scientific opinion confirming its safety and bioavailability under specified conditions. In Europe, it is also prescribed under the trade name Hexopal for peripheral vascular conditions, where it helps alleviate symptoms such as pain and cold sensitivity in the extremities.
2. Natural Sources and Occurrence
Inositol nicotinate is a compound made of niacin (vitamin B3) and inositol; inositol occurs naturally in the body and can also be made in the laboratory. Niacin itself is endogenously produced in the body from the amino acid tryptophan and obtained from the diet from such foods as meats, grains, milk, and eggs. Inositol, in its myo-form, is widely distributed in plant-based foods — particularly in fruits, beans, grains, and nuts, primarily as phytic acid (inositol hexaphosphate) and as free inositol.
Inositol hexanicotinate itself, however, is not a naturally occurring food compound. It consists of niacin esterified with inositol, allowing for a slow release of niacin in the body. While traditional niacin is found naturally in foods like meat, fish, and grains, IHN is a manufactured compound. It was developed synthetically as a pharmaceutical and dietary supplement form of niacin with the intent of achieving gradual release and reduced adverse effects.
3. Traditional and Historical Use
Unlike many botanical dietary supplements with centuries of documented ethnobotanical use, inositol nicotinate has no ancient or traditional medicinal history. Its use is exclusively a product of twentieth-century pharmaceutical development. Early synthesis focused on linking six molecules of nicotinic acid to one inositol molecule, aiming for sustained release and reduced acute adverse effects. Key clinical investigations began in the late 1950s and 1960s, primarily targeting peripheral artery disease and related circulatory impairments.
A 1963 Italian study evaluated inositol hexanicotinate in patients with peripheral arteriopathies, reporting improvements in symptoms such as claudication through enhanced vasodilation and lipid modulation without significant side effects. Subsequent trials in the 1960s, including those by Welsh and Ede (1961), demonstrated its use in Raynaud's disease and hyperlipidemia, with doses up to 1,800 mg daily promoting peripheral circulation and reducing cholesterol levels in over 150 patients, outperforming niacin in tolerability. These early efforts established inositol nicotinate as a viable option for vascular conditions, though studies were often small-scale and observational.
From the 1960s through the 1980s, inositol nicotinate was employed clinically in parts of Europe — notably the United Kingdom, Germany, and Scandinavia — primarily for peripheral vascular disease, intermittent claudication, and Raynaud's phenomenon. It was marketed under various trade names including Hexopal, Hexanicit, and Linodil. Lipid-lowering applications were investigated in European clinical settings from the early 1960s onward, with early published data in German-language pharmacological journals (Dorner and Fischer, 1961; Wilke and Frahm, 1976). In the United States, inositol hexanicotinate rose in popularity as a dietary supplement during the 1990s and 2000s, primarily marketed as "no-flush niacin" for cardiovascular support.
4. Key Constituents, Active Compounds, and Mechanisms of Action
4.1 Component Compounds
Inositol nicotinate is itself the active compound of interest, but its pharmacological actions are understood primarily through the activity of its hydrolytic products. Inositol nicotinate undergoes hydrolysis by plasma esterases, releasing free nicotinic acid and inositol in a sustained manner. This process takes more than 48 hours; the bloodstream enzymatic hydrolysis of inositol hexanicotinate was found to be slower in the first ester linkage than in subsequent linkages. Sequential hydrolytic steps form one nicotinic acid molecule in each step, producing eventually six molecules of nicotinic acid and one inositol moiety.
4.2 Mechanisms of Action
When ingested, inositol nicotinate breaks down into inositol and niacin; the niacin component helps widen blood vessels (vasodilation), lowers blood lipid levels (including cholesterol), and inhibits a protein involved in blood clotting.
The primary mechanism of action for niacin involves inhibiting hepatic diacylglycerol acyltransferase-2, which reduces triglyceride synthesis and decreases the secretion of very-low-density lipoprotein (VLDL) from the liver. This process ultimately leads to a reduction in LDL cholesterol and an increase in HDL cholesterol. Niacin also interacts with the GPR109A receptor, which mediates both its lipid-modifying effects and the prostaglandin-mediated vasodilation responsible for flushing.
Inositol nicotinate mediates a vasodilatory, lipid-lowering, and fibrinolytic effect on the cardiovascular system. Like other niacins, inositol nicotinate is a lipid-regulating agent that reduces plasma triglycerides, atherogenic apolipoprotein B (apoB)-containing lipoproteins (VLDL, LDL, and lipoprotein(a)), while increasing antiatherogenic apoA-I-containing HDL levels.
Research has suggested that the therapeutic effect of inositol nicotinate is not merely due to vasodilation, but that other mechanisms such as enhanced fibrinolysis and lowering of serum lipids may play a significant part in its overall effect.
Mechanistically, any clinical effects from IHN stem from nicotinic acid ultimately binding to niacin receptors on adipocytes, immune cells, and vascular tissue, as well as downstream changes in lipid metabolism and vasodilation mediated by prostaglandins. Because IHN releases nicotinic acid slowly, vasodilation is milder and less likely to trigger intense flushing. The inositol portion serves chiefly as the carrier; at typical IHN doses, inositol's independent effects are minimal compared with dedicated myo-inositol supplements.
4.3 The Bioavailability Controversy
A pivotal and contested question in the scientific literature concerns whether IHN actually releases enough free niacin in the bloodstream to produce pharmacological effects. The evidence on this point is conflicting and directly shapes the interpretation of all IHN efficacy data.
In 2009, the European Food Safety Authority (EFSA) Scientific Panel on Food Additives and Nutrient Sources Added to Food concluded that nicotinate from IHN is a bioavailable source of niacin. The EFSA panel confirmed that inositol hexanicotinate is absorbed intact and hydrolysed in the body, releasing free nicotinic acid and inositol. Gastrointestinal absorption of inositol hexanicotinate varies widely, with an average of 70 per cent of an orally ingested dose absorbed into the bloodstream. It is metabolized slowly, with nicotinic acid levels reaching a peak approximately 6–10 hours after intake, compared to intake of free nicotinic acid where plasma levels peak after 0.5–1 hour.
However, the EFSA opinion's conclusion of bioavailability has not translated into demonstrated clinical efficacy. The available data suggest that intestinal absorption of IHN varies widely, with an average of 70 percent of the administered dose being absorbed into the bloodstream, but the majority of IHN that is absorbed appears to remain intact after absorption. No published study has demonstrated that inositol hexanicotinate releases free niacin, demonstrably increases circulating niacin, or alters plasma lipid levels. Thus, there is no evidence that niacin in this formulation is bioavailable (Meyers et al., 2006). IHN is absorbed and metabolized more slowly than nicotinic acid, leading to lower peak plasma levels of free niacin and a significant reduction in flushing.
Enzymatic hydrolysis in the bloodstream was demonstrated by Harthon and Brattsand (1979). The results indicated that the plasma hydrolysis of the first ester linkage in inositol hexanicotinate proceeded more slowly than the hydrolysis of the subsequent linkages. This kinetic limitation may explain why circulating levels of free niacin sufficient for pharmacological action may not be reliably achieved.
5. Scientific Evidence by Area of Use
5.1 Raynaud's Phenomenon
Raynaud's phenomenon — a vasospastic disorder characterized by episodic digital ischemia in response to cold or stress — represents the area of use for IHN with the most consistent body of clinical evidence, though the studies are predominantly small and dated.
Inositol nicotinate is used to treat blood circulation problems and some research shows it can improve symptoms of Raynaud's phenomenon over several weeks.
A notable controlled investigation was that of Holti (1979), published in the Journal of International Medical Research. The vaso-active effects of inositol nicotinate (Hexopal®) were investigated in thirty patients with primary and secondary Raynaud's phenomenon using several non-invasive experimental techniques under controlled conditions. The earlier formed impression that this drug requires a prolonged "build-up" period was confirmed. Recording the time required to induce Raynaud's phenomenon, as well as assessments of total and nutrient digital blood flow, showed significant beneficial therapeutic effects upon the skin's microcirculation. Smokers responded slower than non-smokers, but even elderly patients with longstanding vasospastic disease showed measurably improved digital circulation.
Ring and Bacon (1977) published a quantitative thermographic assessment in Journal of International Medical Research (volume 5, pp. 217–22) reporting improvements in digital blood flow with IHN therapy.
A randomized, double-blind, placebo-controlled trial by Sunderland et al. (1988) — Sunderland GT, Belch JJ, Sturrock RD, et al., "A double-blind, randomized, placebo-controlled trial of hexopal in primary Raynaud's disease," published in Clin Rheumatol 1988;7:46–9 — evaluated the compound in primary Raynaud's disease. This trial is widely cited in systematic reviews of Raynaud's treatments.
A systematic review published in PubMed (Raynaud's phenomenon [primary], 2009) identified inositol nicotinate among the interventions reviewed for primary Raynaud's phenomenon. The review found 15 systematic reviews, RCTs, or observational studies that met its inclusion criteria, and performed a GRADE evaluation of the quality of evidence for interventions.
Evidence assessment: The evidence for IHN in Raynaud's phenomenon is preliminary and limited. Positive studies exist (Holti 1979, Ring & Bacon 1977, Sunderland et al. 1988) and point toward potential benefit in symptom reduction and improved digital circulation. However, the studies are small, predominantly from the 1970s–1980s, and use heterogeneous outcome measures. No large, well-powered, modern RCT exists. Historically, IHN has been tried for peripheral circulation complaints including Raynaud's phenomenon. Much of the clinical literature is decades old, with modest sample sizes and mixed results. Contemporary vascular care emphasizes supervised exercise therapy, smoking cessation, and agents with stronger evidence for symptom relief.
5.2 Intermittent Claudication (Peripheral Arterial Disease)
Intermittent claudication — exercise-induced leg pain due to peripheral arterial disease — was the other primary indication for Hexopal in European clinical practice.
Multiple small controlled trials from the 1980s examined IHN in this setting. O'Hara et al. (1988) published "The therapeutic efficacy of inositol nicotinate (Hexopal) in intermittent claudication: a controlled trial" in Br J Clin Pract 42(9):377–383. An earlier double-blind, placebo-controlled study by O'Hara (1985) in J Int Med Res 13(6):322–7 also examined Hexopal for intermittent claudication. Kiff and Quick (1988) published "Does inositol nicotinate (Hexopal) influence intermittent claudication? A controlled trial" in Br J Clin Pract 42(4):141–145. Head (1986) published "Treatment of intermittent claudication with inositol nicotinate" in Practitioner 230(1411):49–54.
Evidence assessment: The clinical trials in intermittent claudication are small, conducted predominantly in the 1980s, and have not been followed up with modern, large-scale RCTs. The results were mixed across trials. In some places inositol hexanicotinate is prescribed for the symptomatic relief of Raynaud's phenomenon and severe intermittent claudication. However, the overall evidence base for intermittent claudication is considered insufficient to recommend IHN in contemporary vascular disease guidelines, which emphasize supervised exercise rehabilitation and pharmacological agents with robust RCT data.
5.3 Dyslipidemia (Cholesterol and Triglyceride Effects)
The use of IHN as a lipid-lowering agent — particularly as an alternative to niacin for patients who cannot tolerate flushing — has been a persistent area of investigation and commercial promotion, though the evidence is deeply mixed and the question of adequate bioavailability is central.
Early German-language studies from the 1960s and 1970s reported positive lipid effects. Dorner and Fischer (1961) in Arzneim-Forsch published one of the first observations of IHN's influence on serum lipids and lipoproteins. Wilke and Frahm (1976) in Dtsch Med Wochenschr 101:401–5 studied IHN in combination with clofibrate for hyperlipoproteinemia types IIa, IIb, IV, and V.
A pivotal and methodologically strong study by Keenan (2013), published in the Journal of Clinical Lipidology (PMID 23351578), was a 6-week, blinded, placebo-controlled trial. The study compared 1,500 mg/day of wax-matrix extended-release niacin (WMER) with 1,500 mg/day of IHN. Subjects with mild-to-moderate dyslipidemia (LDL = 130–190 mg/dL) were randomized, after a 4-week diet lead-in period, to three parallel study arms (40 subjects per arm). Results: WMER demonstrated significant improvements in total cholesterol (−11%), LDL (−18%), HDL (+12%), and non-HDL (−15%) (P < .001), whereas IHN and placebo showed no significant improvement in lipids. Pharmacokinetics demonstrated an intermediate release and absorption rate for WMER over 6 hours, and IHN showed no evidence of bioavailability. IHN was well tolerated but was no better than placebo in lipid improvement and showed no evidence of bioavailability.
By contrast, a more recent uncontrolled prospective study presented at an American Heart Association meeting (Circulation, 2019 abstract) examined 43 patients with dyslipidemia. Forty-three patients with age ≥30 years with dyslipidemia comprising females with HDL-C <50 mg/dL and males with HDL-C <40 mg/dL were included in the study. Treatment with IHN resulted in a significant reduction in triglycerides (146.10±88.34 to 119.08±64.27) mg/dL, p<0.001; VLDL (29.18±17.70 to 25.76±17.26) mg/dL, p=0.002; total cholesterol (126.69±40.84 to 116.60±33.97) mg/dL, p=0.03; and LDL cholesterol (70.84±35.62 to 62.00±26.90) mg/dL, p=0.01. A highly significant increase (p<0.001) was found in HDL cholesterol levels (34.02±6.05 to 37.37±6.12) mg/dL after 12 weeks of therapy. However, this was a conference abstract without a placebo control, limiting its interpretive value.
The Meyers et al. (2003) study in Annals of Internal Medicine 139:996–1002, which examined free nicotinic acid content in over-the-counter niacin preparations, found that IHN products contained negligible levels of free nicotinic acid and provided no evidence of functional niacin bioavailability at doses used in supplements. Nicotinic acid has long been used for the treatment of dyslipidemia; wax-matrix extended-release niacin and IHN have both been formulated to increase patient tolerability. Several trials of WMER demonstrated good efficacy in improving dyslipidemia; however, there are few scientific data on the use of IHN.
Evidence assessment: The evidence for IHN as a lipid-lowering agent is weak and contradictory. The most rigorously designed placebo-controlled RCT (Keenan 2013) found IHN no better than placebo for lipid outcomes and showed no pharmacokinetic evidence of niacin bioavailability. Earlier European studies reporting benefits were generally uncontrolled or used IHN in combination with other agents, making attribution difficult. There are few scientific data on the use of IHN, and there is no good scientific evidence to support its use for high cholesterol.
5.4 Inositol Component and Metabolic Effects
A broader body of RCT evidence exists for myo-inositol as a standalone supplement — particularly in the contexts of polycystic ovary syndrome (PCOS), insulin resistance, gestational diabetes, and metabolic syndrome. However, this evidence pertains to free myo-inositol supplementation, not to inositol hexanicotinate.
Inositol supplementation's findings hold particular clinical significance for conditions marked by cardiometabolic dysfunction, including obesity, metabolic syndrome, type 2 diabetes, and PCOS. These conditions share common pathological features such as hyperglycemia, insulin resistance, dyslipidemia, hypertension, and central obesity — all of which showed improvement with inositol supplementation to some extent in meta-analytic analysis. Future research should involve large-scale, rigorous trials with standardized protocols, longer follow-up, and diverse populations.
As noted above, the inositol portion of IHN serves chiefly as the carrier; at typical IHN doses, inositol's independent effects are minimal compared with dedicated myo-inositol supplements. Therefore, the metabolic inositol evidence base cannot be directly extrapolated to inositol hexanicotinate at supplement doses.
5.5 "No-Flush" Claim
IHN is marketed as "no-flush" niacin, but research suggests that the lack of flushing may be due to its limited conversion to active niacin. Nicotinamide and inositol hexanicotinate do not appear to be associated with flushing. Some inositol nicotinate products are promoted as "no-flush" niacin because some people think they don't cause as much flushing as regular niacin, but this possible benefit has not been proven in research studies. The absence of flushing may therefore reflect reduced pharmacological activity rather than a superior delivery mechanism.
6. Body Systems and Health Areas Associated with Inositol Nicotinate
- Cardiovascular/Peripheral Vascular System: The niacin component helps widen blood vessels (vasodilation), lowers blood lipid levels (including cholesterol), and inhibits a protein involved in blood clotting. IHN has been studied for Raynaud's phenomenon, intermittent claudication, and general peripheral vascular disease.
- Lipid Metabolism: Like other niacins, inositol nicotinate is classified as a lipid-regulating agent that reduces the levels of plasma triglycerides, atherogenic apolipoprotein B-containing lipoproteins (VLDL, LDL, and lipoprotein(a)), while increasing antiatherogenic apoA-I-containing HDL levels. However, this classification is based on the theoretical mechanism of its niacin component; clinical evidence for actual lipid modification at supplement doses is lacking (see Section 5.3).
- Hemostatic/Fibrinolytic System: Inositol nicotinate has fibrinolytic effects, which may increase the risk of bleeding when used concomitantly with anticoagulant/antiplatelet drugs.
- Niacin (Vitamin B3) Nutritional Status: It is used as a dietary supplement acting as a source of niacin (vitamin B3), one of the essential human nutrients. Although the inositol hexanicotinate complex does not represent an essential nutrient itself, niacin is pivotal to cellular metabolism, playing the important role in coenzyme function and oxidation-reduction reactions.
- Glucose Metabolism: Via the released niacin component, IHN is associated with potential effects on blood sugar levels (see Safety, Section 8).
7. Dosage Forms and Dosages Reported in Studies
Inositol nicotinate is available in the form of oral tablets and capsules.
The following dosages have been specifically reported in cited studies and regulatory documents:
- 1,500 mg/day — used in the Keenan (2013) placebo-controlled RCT comparing IHN to wax-matrix extended-release niacin for dyslipidemia (6-week trial). This was a 6-week blinded, placebo-controlled trial comparing 1,500 mg/day of WMER with 1,500 mg/day IHN.
- Up to 4,000 mg/day for 3 months — the dose range used in clinical trials cited by the Council for Responsible Nutrition (CRN). IHN does not cause a flushing reaction. Clinical trials using IHN of up to 4,000 mg daily for 3 months do not demonstrate adverse effects (Sunderland et al. 1988). No meaningful adverse effects have been noted in several well-designed clinical trials using IHN in amounts that range from 600 to 4,000 mg.
- 900 mg/day — used in combination with 1.5 g clofibrate in a 19-patient study of hypercholesterolemia over 24 weeks (Hutt trial). This sequential control design study examined the effectiveness of a combination of 900 mg of inositol nicotinate and 1.5 g of clofibrate daily in 19 patients with hypercholesterolemia during a period of 24 weeks.
- Up to 1,800 mg/day — reported in early 1960s trials (Welsh and Ede, 1961) for peripheral circulation and cholesterol reduction. Doses up to 1,800 mg daily were used in those trials promoting peripheral circulation and reducing cholesterol levels in over 150 patients.
- Regulatory nutritional dose context: Nicotinic acid given as inositol hexanicotinate in a dose of 10 mg per day would amount to a daily dose of 11 mg inositol hexanicotinate. EFSA concluded that inositol hexanicotinate is a safe source of niacin in supplements "provided that use levels are in compliance with the defined upper safe use level for nicotinic acid (10 mg/day)." However, the panel noted that use levels proposed by petitioners were 40 and 495 mg/day, which would provide levels of nicotinic acid 4 to 45 times higher than the tolerable upper intake level.
Gastrointestinal absorption of inositol hexanicotinate varies widely, with an average of 70% of an orally ingested dose absorbed from the stomach and upper small intestines into the bloodstream as the intact form. The maximum serum levels of nicotinic acid are reached approximately 6–10 hours after oral ingestion.
8. Safety Considerations and Drug Interactions
8.1 General Tolerability
Inositol nicotinate is possibly safe for most people when taken by mouth. It can cause some side effects such as stomach upset, headache, nausea, burping, and hiccups. It might also cause liver damage like other niacin products in some people.
8.2 Hepatotoxicity
High doses of inositol nicotinate, particularly over extended periods, may lead to liver toxicity. Symptoms of liver issues include jaundice (yellowing of the skin and eyes), dark urine, fatigue, and abdominal pain. In numerous case reports, patients given 3,000–9,000 mg/day niacin for months to years to treat hyperlipidemia developed liver toxicity. While these reports relate primarily to pharmaceutical-dose nicotinic acid, the risk is relevant to IHN given that niacin is its hydrolytic product. Medical supervision should be provided for patients using more than 1,000 mg/day nicotinic acid. Inositol nicotinate is contraindicated in patients with active liver disease or unexplained elevated liver enzymes.
8.3 Blood Glucose Elevation
Long-term use of inositol nicotinate might increase blood sugar. Diabetes medications are used to lower blood sugar. By increasing blood sugar, inositol nicotinate might decrease the effectiveness of diabetes medications. Monitoring of blood sugar is closely recommended.
8.4 Flushing and Skin Reactions
Flushing is a common side effect in people treated with 30 mg/day or more nicotinic acid by mouth and is characterized by a burning, tingling, and itching sensation primarily on the face, arms, and chest, that can be accompanied by pruritus, headaches, and increased intracranial blood flow. Nicotinamide and inositol hexanicotinate do not appear to be associated with flushing. However, research suggests that the lack of flushing may be due to its limited conversion to active niacin rather than an intrinsically superior pharmacological profile.
8.5 Bleeding Risk
Inositol nicotinate might slow blood clotting. In theory, inositol nicotinate might increase the risk of bleeding and make bleeding disorders worse. Bleeding disorders: Inositol nicotinate may slow blood clotting, increasing the risk of bleeding for individuals with clotting disorders or those undergoing surgery.
8.6 Interactions with Anticoagulants and Antiplatelet Drugs
Concomitant use of inositol nicotinate with anticoagulant or antiplatelet drugs might theoretically increase the risk of bleeding. Inositol nicotinate has fibrinolytic effects, which may increase the risk of bleeding when used concomitantly with anticoagulant/antiplatelet drugs. Inositol nicotinate may increase the risk of bleeding when taken with drugs that increase the risk of bleeding. Some examples include aspirin, anticoagulants such as warfarin (Coumadin®) or heparin, antiplatelet drugs such as clopidogrel (Plavix®), and nonsteroidal anti-inflammatory drugs such as ibuprofen.
8.7 Interactions with Antihypertensive Drugs
Antihypertensive medications can also interact with inositol nicotinate. Since niacin has vasodilatory effects, it can potentiate the blood pressure-lowering effects of these drugs, leading to hypotension.
8.8 Interactions with Statins
Inositol nicotinate may interact with statins including simvastatin and atorvastatin. This interaction is relevant because combination niacin–statin therapy has been associated with a risk of myopathy in case reports involving high-dose nicotinic acid.
8.9 Interactions with Bile Acid Sequestrants
Inositol nicotinate may affect the absorption and efficacy of certain medications, such as bile acid sequestrants (used to lower cholesterol).
8.10 Interactions with Antidiabetes Drugs
Inositol nicotinate may interact with diabetes medicines such as metformin and glibenclamide. The mechanism is niacin-mediated impairment of insulin secretion and glucose tolerance, which may reduce the effectiveness of blood-glucose-lowering medications.
8.11 Allergies and Niacin Sensitivity
Niacin, a chemical that is released when inositol nicotinate breaks down in the body, might make allergies worse by releasing histamine. If a person is sensitive to niacin, they should not use inositol nicotinate.
8.12 Uric Acid
Inositol nicotinate may cause a high uric acid level in the blood (hyperuricemia), among other potential adverse effects. This is consistent with the known effect of high-dose nicotinic acid on uric acid metabolism and is a relevant consideration for patients with gout or a predisposition to it.
8.13 Pregnancy and Lactation
There is not enough reliable information about the safety of taking inositol nicotinate if a person is pregnant or breast-feeding; caution is advised.
8.14 EFSA Upper Intake Level
EFSA concluded that nicotinate from inositol hexanicotinate is bioavailable and a source of niacin, and that inositol hexanicotinate is a safe source of niacin in supplements provided that use levels are in compliance with the defined upper safe use level for nicotinic acid (10 mg/day). The EFSA Panel determined that nicotinate from inositol hexanicotinate is bioavailable and a source of niacin; the Panel used the already established nicotinic acid UL of 10 mg per day from the EC SCF (2002) evaluation to derive the UL for IHN. This stands in stark contrast to the gram-level doses used in most efficacy trials, indicating that the doses employed in clinical studies substantially exceed European regulatory safe use levels when IHN is used as a food supplement.
References
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