Niacin Benefits and Side
Effects
What are the benefits of niacin as a medical therapy? How does it work?

Drs Kamanna VS, and Kashyap ML. have a detailed description about the benefits and its
adverse side effects in their review article. Nicotinic acid (niacin) has long been used for the
treatment of lipid disorders and cardiovascular disease. Niacin favorably affects
apolipoprotein (apo) B-containing lipoproteins (eg, very-low-density lipoprotein [VLDL], low-
density lipoprotein [LDL], lipoprotein[a]) and increases apo A-I-containing lipoproteins (high-
density lipoprotein [HDL]).

They summarize the recent findings: Niacin directly and noncompetitively inhibits hepatocyte
diacylglycerol acyltransferase-2, a key enzyme for triglyceride synthesis. The inhibition of
triglyceride synthesis by niacin results in accelerated intracellular hepatic apo B degradation
and the decreased secretion of VLDL and LDL particles. Previous human and test-tube
studies findings indicate that niacin retards mainly the hepatic catabolism of apo A-I (vs apo A-
II) but not scavenger receptor BI-mediated cholesterol esters. Decreased HDL-apo A-I
catabolism by niacin explains the increases in HDL half-life and concentrations of lipoprotein
A-I HDL subfractions, which augment reverse cholesterol transport. Initial data suggest that
niacin, by inhibiting the hepatocyte surface expression of beta-chain adenosine triphosphate
synthase (a HDL-apo A-I holoparticle receptor), inhibits the removal of HDL-apo A-I. Niacin
increases vascular endothelial cell redox state, resulting in the inhibition of oxidative stress
and vascular inflammatory genes, key cytokines involved in atherosclerosis.

The niacin flush (its major side effect) results from the stimulation of prostaglandins D(2) and E
(2) by subcutaneous Langerhans cells via the G protein-coupled receptor 109A niacin
receptor. Although decreased free fatty acid mobilization from adipose tissue via the G
protein-coupled receptor 109A niacin receptor has been a widely suggested mechanism of
niacin to decrease triglycerides, physiologically and clinically, this pathway may be only a
minor factor in explaining the lipid effects of niacin. [Am J Cardiol. 2008 Apr 17;101(8A):20B-
26B]


Niacin's Potential Benefits on Cardiovascular Diseases
Dr. Lardizabal and Deedwania, UCSF, explains in their article, "Cardiovascular disease still
ranks as the top cause of mortality worldwide. Lipid-modifying therapy has revolutionized the
treatment of the disease and is partly responsible for the recent decline in deaths due to
cardiovascular disease. Treatment strategies have evolved since the introduction of the
earlier lipid-lowering agents (fibrates, niacin, bile acid resins) to the advent of statins, which
have become the standard drugs in cholesterol therapy." [Cardio Clin. 2011 Feb, 29(1):87-
103.]

In a rat study, the rats (group II) were fed with a lipogenic diet consisting of 2% cholesterol,
0.5% cholic acid and 20% sunflower oil added to the pellet chow, and given 3% alcoholic
water for 60 days. Two other groups fed with the same lipogenic diet and treated with
chromium and niacin. Researchers found heart LPO, serum GGT activity and serum PCC
were increased; serum PON activity and heart GSH levels were decreased in hyperlipidemic
rats. Treatment with combined niacin and chromium reversed these effects. [Hum Exp Toxicol.
2010 Dec 22. ] Similarly, in a clinical study, Insull W Jr. from Baylor College, Texas, found
combination of niacin extended-release and simvastatin results in a less atherogenic lipid
profile than atorvastatin monotherapy in a study of patients with dyslipidemia. [Vasc Health
Risk Manag. 2010 Nov 24;6:1065-75.]

Niacin's Potential Benefits on Metabolic Syndrome
Patients with metabolic syndrome are at increased risk for cardiovascular disease. Niacin
improves lipid abnormalities associated with metabolic syndrome, but is underused, mainly
because of flushing (its side effect). Laropiprant reduces niacin-induced flushing and, in
combination with extended-release niacin, improves lipid levels.

Niacin's Potential Benefits on Diabates - Reduced Risk in Cardiovascular Events
Patients with type 2 diabetes have increased expression of cell adhesion molecules (CAMs).
CAMs and monocyte adhesion mediate essential processes in atherogenesis. Dr Tavintharan
S. and co-workers from Khoo Teck Puat Hospital found niacin 1500mg daily raised HDL-
cholesterol from 0.8mmol/l (95% CI: 0.7-0.9) to 0.9mmol/l (95% CI: 0.8-1.1) and monocytes
isolated from patients on niacin had reduced adhesion to endothelial cells. [Atherosclerosis.
2010 Dec 25.]

The Relationship of Niacin and Fat Cells
Niacin is converted to NAD and NADP in tissues, whose products are involved in a number of
cellular processes; and it is associated with the regulation of adipogenesis. Dr. Fujimori K
from Osaka University, Japan, found niacin promoted adipogenesis by suppressing the
production of the anti-adipogenic PGF(2α) through down-regulation of C/EBPβ-activated
cyclooxygenase-2 expression in adipocytes. [Prostaglandins Other Lipid Mediat. 2011 Jan 12]

What is adipogenesis? Adipogenesis is the process of cell differentiation by which
preadipocytes become adipocytes. Adipocytes, also known as lipocytes and fat cells, are the
cells that primarily compose adipose tissue, specialized in storing energy as fat.

Niacin may cause side effects:
Its side effects may include: itching, stinging, tingling, or burning of the skin, headache, blurred
vision, nausea, vomiting, diarrhea, heartburn and bloating.
Discuss with your doctor before taking any alternative medicine. This article is for
reference only, it is not a medical advice. All rights reserved. Do not copy this article to
other website or blog.