Nutritional and Dietary Supplementation during Pregnancy
“Bert” Bertis Britt Little in 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).
Nutrition and Nutritional Supplements in the Management of Dyslipidemia and Dyslipidemia-Induced Cardiovascular Disease
Stephen T. Sinatra, Mark C. Houston in Nutritional and Integrative Strategies in Cardiovascular Medicine, 2022
The effective dosing range of niacin is from 500 to 4,000 mg/day. The niacin dose should be gradually increased, starting at 100 mg/day and administered at meal time. Niacin-induced flushing can be reduced by giving a daily dose of 81 mg aspirin and taken with a quercetin supplement at 500–1,000 mg/day. Niacin should not be taken within 6 hours of alcohol [5]. Only vitamin B3 niacin is effective for dyslipidemia. The no-flush (inositol hexanicotinate (IHN)) does not improve lipid profiles and is not recommended [5]. The potential side effects of niacin include hyperglycemia, hyperuricemia, gout, hepatitis, flushing, rash, pruritus, hyperpigmentation, hyper-homocysteinemia, gastritis, ulcers, bruising, tachycardia, and palpitations [5,121,122]. At lower doses of niacin, these side effects are not common.
Micronutrients
Chuong Pham-Huy, Bruno Pham Huy in Food and Lifestyle in Health and Disease, 2022
Niacin (nicotinic acid), but not niacinamide, has been used for decades as a lipid-lowering drug. Niacin is considered a valuable therapeutic agent to boost levels of high-density lipoprotein cholesterol (HDL-C) or good cholesterol. It also lowers levels of low-density lipoprotein cholesterol (LDL-C) or bad cholesterol, as well as decreases hypertriglyceridemia and high lipoprotein A (33, 39, 42). These effects are only observed in high amounts of niacin (two to three g/day). However, the clinical use of niacin to treat hyperlipidemic diseases is limited by its side effects, such as flushing of the skin, liver damage, itching, burning sensation, stomach upset, headache, dizziness, blurred vision, glucose intolerance, paresthesia (tingling), rashes, nausea, mouth pain, and runny nose (33, 39, 42). Moreover, it remains unclear whether niacin, either in the setting of well-controlled LDL-Cholesterol or in combination with other lipid-lowering agents, confers any therapeutic benefit, and if so, by which mechanism (42). The results of recent trials reject the hypothesis that simply raising HDL-Cholesterol is cardioprotective (42). It is of note that nicotinamide does not have the pharmacologic action of the nicotinic acid that is used at high doses to lower blood lipids (3). Therefore, the use of niacin at high doses for the treatment of hypercholesterolemia and hyperlipidemia must be supervised by a cardiologist to calculate the benefits and risks of the treatment.
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.
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