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Thermal Physiology and Thermoregulation
Published in James Stewart Campbell, M. Nathaniel Mead, Human Medical Thermography, 2023
James Stewart Campbell, M. Nathaniel Mead
Niacin is a B-vitamin that can be obtained from dietary sources. Dietary niacin supplying 50 to 100 mg per day does not appear to have significant thermographic effects. At pharmacologic doses of 1000 to 3000 mg, however, niacin has definite effects on skin blood flow (Figure 5.16). Flushing of the face is one of the most common side-effects associated with ingestion of niacin as well as nitrate medicines (nitroglycerine, isosorbide dinitrate, etc.) and PDE5 inhibitor drugs (sildenafil, etc.). Pharmacologic heat dissipation may be triggered by these vasodilating drugs. All forms of niacin should be avoided for about 8–12 hours before a thermographic exam.
Triglycerides/Hypertriglyceridemia
Published in Charles Theisler, Adjuvant Medical Care, 2023
Nicotinic Acid (Vitamin B3): Niacin is a first-line pharmacologic agent for treating hypertriglyceridemia.1 Niacin blocks the release of free fatty acid from adipose tissue and reduces the rate of secretion of very-low-density lipoprotein particles.4 Clinically, niacin reduces triglycerides by 30%–50%, raises HDL cholesterol by 20%–30%, and lowers LDL cholesterol levels by 5%–25%.1 Niacin is not as potent as fibrates for lowering triglyceride levels but is more effective at raising HDL cholesterol levels.1 Patients on nicotinic acid are usually started on low daily doses and gradually increased to an average daily dose of 1.5–3 gm/day to avoid hepatotoxicity.2 Flushing from nicotinic acid can be decreased by taking the extended-release form and by taking niacin during or after meals, or by the use of an aspirin 30 minutes before niacin ingestion.5 Patients should be made aware that niacin can interact with other medications and cause side effects. Low-dose niacin combined with a statin has been associated with a significant decrease in cardiovascular events.6
Nutritional and Dietary Supplementation during Pregnancy
Published in “Bert” Bertis Britt Little, Drugs and Pregnancy, 2022
Niacin is a B complex vitamin that is metabolized to niacinamide, the active form of B3, in humans. Niacin is naturally present in a wide variety of foods. Treatment for hyperlipidemia with niacin usually is for doses 200–400 times the RDA. In a unique study of niacin deficiency, it was eloquently shown that niacin deficiency is associated with birth defects in humans and mice (Shi et al., 2017). No increased frequency of congenital anomalies was found in rats and rabbits born to mothers given large doses of niacin during organogenesis (Takaori et al., 1973). The frequency of orofacial clefts was not increased in infants whose mothers took niacin during the first trimester in a large case-control study of 98,787 births (Yoshida et al., 2020).
Safety and efficacy of therapies for chylomicronemia
Published in Expert Review of Clinical Pharmacology, 2022
Isabel Shamsudeen, Robert A. Hegele
Niacin has been used clinically since the 1970s as a lipid lowering therapy and has multiple effects on the lipid profile. Although its mechanism of action is still uncertain, niacin is known to increase the expression of adipose tissue lipase, which improves tissue TG uptake and inhibits intracellular diacylglycerol O-acyltransferase 2, which in turn, decreases hepatic VLDL synthesis [43]. Niacin can lower TG levels by 5–35% [44]. Clinical experience indicates that in MCS patients who have HTG due to high levels of chylomicrons and VLDL, niacin lowers total TG primarily by lowering VLDL [1]. Experience also indicates that effects in FCS patients are minimal. Niacin has several side effects, including insulin resistance, flushing, pruritis, and light-headedness [44]. Furthermore, niacin failed to reduce ASCVD in clinical trials, leading to its withdrawal from many markets [45].
Lipoprotein(a) in atherosclerosis: from pathophysiology to clinical relevance and treatment options
Published in Annals of Medicine, 2020
Andreja Rehberger Likozar, Mark Zavrtanik, Miran Šebeštjen
Niacin (i.e. vitamin B3) was for a long time the only approved lipid-lowering drug that showed potent reductions in Lp(a) levels [10]. Niacin lowers Lp(a) by silencing apo(a) gene expression in hepatocytes, which encodes glycoprotein apo(a), a crucial element in the Lp(a) structure [91]. The effects of niacin were dose-dependent and led to 25 and 38% decreases in Lp(a) levels with 2 and 4 g niacin daily, respectively [92]. A similar efficacy of niacin was seen in a meta-analysis of extended-release niacin preparations [93]. However, despite large reductions in Lp(a) levels, the treatment effects of niacin have not been mirrored in any overall reduction of CV events [70, 72]. Indeed, a randomized double-blind trail of niacin in patients with low HDL cholesterol levels who were receiving intensive statin therapies (i.e. AIM-HIGH) found no differences in a comparison of simvastatin with placebo or with extended-release niacin in patients with established CVD, in terms of the endpoint of CV events [73]. Also, addition of laropiprant to extended-release niacin did not improve the outcomes in the ‘Effects of extended-release niacin with laropiprant in high-risk patients’ (HPS2-THRIVE) study [71]. Another limitation of the wider prescription of niacin is the high prevalence of side-effects. In particular, at the higher doses that are effective in reducing Lp(a) levels, niacin is poorly tolerated, and is often discontinued by patients.
Preparation of stabilized submicron fenofibrate crystals on niacin as a hydrophilic hydrotropic carrier
Published in Pharmaceutical Development and Technology, 2020
Rasha A. Alshaikh, Ebtessam A. Essa, Gamal M. El Maghraby
Niacin is being employed as an atheroprotective agent. This use was based on the ability of niacin to reduce the fatty acid influx to the liver. This subsequently reduces secretion of very low density lipoproteins which are the precursors of anxious lipids that lead to atherogenesis. In addition, niacin can increase the level of HDL cholesterol (Bruckert et al. 2010; Ito 2015; Catapano et al. 2016). This was clinically reflected as enhanced lipid profile with a reduction in the cardiovascular events. Indeed, current recommendations for minimizing the risk of hypertriglyceridemia induced acute pancreatitis are to use fibrates or niacin in addition to dietary control (Chapman et al. 2011; Ito 2015; Catapano et al. 2016). Additionally, combination of dietary modification, fenofibrate, and niacin provided maximal benefit in improving the lipid profile of HIV-patients (Balasubramanyam et al. 2011). Taking this into consideration, combination of fenofibrate with niacin can be beneficial therapeutic scheme. The benefit will become even greater if the two drugs were developed as a fixed dose combination.