Niacin cholesterol reduction

The immediate-release formulation of phytosterols is made by Endurance Products Company, based outside of Portland, Oregon. Its Web site is www.endur.com. This is the same company that makes the best formulation of my favorite method of cholesterol control, niacin. Place orders outside the United States at www. endur.com click on Customer Service page. International Orders. Take two 450 mg tablets at the start of two major meals daily to block the absorption of cholesterol in the foods you eat, inhibit the recycling of bile made of cholesterol, and achieve a cholesterol reduction in your bloodstream of up to 10 percent. 

In a study of patients with hyperlipidaemia, niacin was shown to reduce triglyceride and VLDL significantly, while also being shown to decrease the transport rate (synthesis) of VLDL-TG (Ganji et al. 2003). It also increased hepatic excretion of biliary cholesterol, which may in part explain the reason why cholesterol is lost from the body (Grundy et al. 1981), which may be due to increased reverse cholesterol transport (RTC). Also, as cholesterol reduction is the result of niacin s effect on LDL, reduction of LDL from VLDL will play an active role in niacin-mediated plasma cholesterol reduction (Grundy et al. 1981). 

The first hypotheses for cholesterol reduction with niacin pointed toward a steep niacin-induced decrease in non-esterified fatty acid (NEFA) mobilization from adipose tissue via inhibition of lipolysis (reviewed by Carlson 2005). Hormone sensitive lipase mediates lipolysis in response to increased cyclic adenosine monophosphate in adipocytes. A G-protein-coupled cell surface receptor (GPR) inhibiting adenylyl cyclase was proposed, and in 2003, three independent groups identified the human niacin receptors as the low-affinity... 

Combination drug therapy is an effective means to achieve greater reductions in LDL cholesterol (statin + ezetimibe or bile acid resin, bile acid resin + ezetimibe, or three-drug combinations) as well as raising HDL cholesterol and lowering serum triglycerides (statin + niacin or fibrate). 

Niacin (vitamin B3) has broad applications in the treatment of lipid disorders when used at higher doses than those used as a nutritional supplement. Niacin inhibits fatty acid release from adipose tissue and inhibits fatty acid and triglyceride production in liver cells. This results in an increased intracellular degradation of apolipoprotein B, and in turn, a reduction in the number of VLDL particles secreted (Fig. 9-4). The lower VLDL levels and the lower triglyceride content in these particles leads to an overall reduction in LDL cholesterol as well as a decrease in the number of small, dense LDL particles. Niacin also reduces the uptake of HDL-apolipoprotein A1 particles and increases uptake of cholesterol esters by the liver, thus improving the efficiency of reverse cholesterol transport between HDL particles and vascular tissue (Fig. 9-4). Niacin is indicated for patients with elevated triglycerides, low HDL cholesterol, and elevated LDL cholesterol.3... 

Some patients, in particular those with genetic forms of hypercholesterolemia (Table 9-2), will require three or more drugs to manage their disorder. Regimens using a statin, resin, and niacin were found to reduce LDL cholesterol up to 75%.42 These early studies were conducted with lovastatin, so larger reductions would be expected with the more potent statins available today. 

In general, a statin plus a BAR or niacin plus a BAR provide the greatest reduction in total and LDL cholesterol. 

Niacin deficiency is known to produce pellagra, which presents dermatological, gastrointestinal, and neurological symptoms (19,93,96). Niacin has also been implicated in several nonvitamin functions, which are still under investigation. These include the reduction of serum cholesterol levels, vasodilation, and modulation of the effects of cancer and diabetes (93,96-99). 

Prior to 1987, the lipid-lowering armamentarium was limited essentially to dietary changes (reductions in saturated fats and cholesterol), the bile acid sequestrants (cholestyramine and colestipol), nicotinic acid (niacin), the fibrates, and probucol. Unfortunately, all of these treatments have limited efficacy or tolerability or both. Substantial reductions in LDL cholesterol (up to 47%) accompanied by increases in HDL cholesterol of up to 32% could be achieved by the combination of a lipid-lowering diet, a bile acid sequestrant, and the subsequent addition of nicotinic acid (Illingworth et al., 1981). However, this therapy is not easy to administer or tolerate and was therefore often unsuc-... 

It is well established that HMG-CoA reductase inhibitors and bile acid sequestrants can be used together safely, with a greater reduction in LDL cholesterol than is obtainable when either drug is used alone. Unfortunately, bile acid sequestrants are often poorly tolerated, which limits the usefulness of this combination. Relatively low doses of niacin, when used in combination with statins, produce a very attractive effect on the lipoprotein profile (Gardner et al., 1996 Stein et al., 1996) the ability of niacin to substantially increase HDL cholesterol is additive, with the profound reduction in LDL cholesterol produced by the statin, and there is also a moderate reduction in triglycerides. However,... 

Low HDL cholesterol is a strong independent risk predictor of CHD. ATP III redefined low HDL cholesterol as <40 mg/dL but specified no goal for HDL cholesterol raising. In low HDL, the primary target remains LDL, but treatment emphasis shifts to weight reduction, increased physical activity, smoking cessation, and to fibrates and niacin if drug therapy is required. 

The manufacturer does not recommend use of the fixed combination as initial therapy of primary hypercholesterolemia or mixed dyslipidemia. It is specifically Indicated in patients receiving lovastatin alone plus diet who require an additional reduction in triglyceride levels or increase in HDL cholesterol levels it is also Indicated In those treated with niacin alone who require additional decreases in LDL cholesterol. 

In a long-term follow-up of the Coronary Drug Project, Canner et al. (54) found in 8,341 men with established CHD that treatment with niacin resulted in an 11% relative risk reduction for mortality compared with placebo. Interestingly, despite beneficial effects on HDL cholesterol levels, treatment with estrogen was halted early in this trial for an increase in adverse effects and outcomes (55). 

Combination therapy with niacin and a statin has also been shown to produce clinical and angiographic benefits. Brown et al. (56) evaluated the effects of simvastatin in combination with niacin on patients with documented coronary disease in the HATS trial and demonstrated a significant reduction in nonfatal MI or death from cardiovascular causes compared to placebo, albeit with a relatively small number of patients. In the treatment arm, HDL cholesterol increased by 26% over the three years of treatment and was also associated with a slight regression (0.4%) in coronary mean percent stenosis in the proximal arteries by invasive arteriography the placebo arm experienced a 3.9% increase in stenoses. 

Neomycin is indicated for the suppression of intestinal bacteria of the bowel as a preoperative prophylaxis for elective colorectal surgery. The treatment begins 3 days prior to surgery with liquid diets with minimum residue, oral capsule of bisacodyl, magnesium sulfate, enema, and repeated oral administration of neomycin and erythromycin (1 gram of each). Neomycin has been used as an adjunctive therapy in hepatic coma by reduction in the ammonia-forming bacteria in the intestinal tract. The subsequent reduction in blood ammonia has resulted in neurologic improvement. Neomycin combined with niacin reduces the cholesterol level. 

A. Mectianism and Effects Niacin (but not nicotinamide) directly reduces the secretion of VLDL fixjm the liver (Figure 35-2) and inhibits hepatic synthesis of apolipoproteins or cholesterol. Consequently, LDL formation is reduced and there is a decrease in LDL cholesterol (Table 35-3). Increased clearance of VLDL by lipoprotein lipase in the periphery has also been demonstrated and probably accounts for the reduction in serum triglyceride concentrations. In addition, the levels of HDL may increase. Finally, niacin decreases circulating fibrinogen and increases tissue plasminogen activator. 

Bile acid sequestrants are indicated for the treatment of hypercholesterolemia in patients who do not adequately respond to dietary modifications. They may be used either alone or in combination with HMGRIs or niacin. These combinations often can achieve a 50% reduction in plasma LDL levels. Cholestyramine, but neither colestipol nor colesevelam, also is approved for the relief of pruritus associated with partial biliary obstruction. Bile acid sequestrants should not be used to treat hypertriglyceridemias or mixed hyperlipoproteinemias in which hypertriglyceridemia is the primary concern. These compounds also are contraindicated in patients with cholelithiasis or complete biliary obstruction because of the impaired secretion of bile acids caused by these conditions. Finally, cholestyramine and colestipol are contraindicated in patients with primary biliary cirrhosis, because this can further raise serum cholesterol (7,15,21). 

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