Sources and Physiologic Functions Sources: Niacin is located in unrefined and enriched grain and cereal, milk, and hard working liver, especially liver.Yeast, poultry, salt water fish, nuts, legumes, coffee, tea, dairy foods, and potatoes are fantastic reasons for Niacin.
Populations vulnerable: In alcoholics, deficiency may be caused by decreased intake, reduced absorption, or impaired capability to utilize the absorbed vitamin. Chronic diarrhea, cirrhosis with the liver, diabetes mellitus, and malignant disease may result in niacin deficiency. Niacin deficiencies are rare in western world, because body can make niacin in the aminiacid tryptophan. However, the antituberculosis drug isoniazid impairs the conversion of tryptophan to niacin and could produce the signs of niacin deficiency. Patients with Tuberculosis receiving INH therapy ought to be supplemented with niacin.
Signs and Symptoms of Deficiency: Severe niacin deficiency may lead to an ailment called Pellagra. This disease is seen as severe dermatitis and fissured scabs, diarrhea, and mental depression. The disease is assigned to "the four Ds": dermatitis, diarrhea, dementia, and ultimately, death. Another manifestation of Pellagra is Casal's collar, which is a rough red dermatitis. Achlorhydria, retarded growth and pigmentation in the tongue, is also another symptoms.
Safety: Many clinicians have extensive experience with using niacin for your management of hyperlipidemias. The adverse events associated with niacin may be split into along side it effects: flushing, diarrhea, indigestion, nausea, and vomiting. The more severe adverse events are hepatotoxicity, exacerbation of gout, and possible worsening of glucose intolerance. There are three available forms of niacin: the short acting or crystalline, the intermediate acting, and also the long acting forms. In general, the flushing and gastrointestinal unwanted effects tend to occur using the short or intermediate acting forms at doses as low as 50 to 100mgs, and usually resolve with continued use from the drugs. The more severe toxicity is usually seen with all the longer acting forms in doses of 2-6 gm/day. From the clinical study data it would appear that an intake of under 500mg is associated with no identifiable risk.
Toxicity is normally noticed in patients helped by high doses for hypercholesterolemia. Hypotension and dermatitis include the most frequent symptoms. Other symptoms of toxicity include increased pulse and respiratory rate, increased cerebral the flow of blood, and nerves inside the body stimulation. Peripheral vasodilation, fatty liver, and decreased serum cholesterol, can also be seen.
Biochemistry: The term niacin identifies both nicotinic acid and niacinamide. The biologically active coenzyme forms are niacinamide adenine dinucleotide (NAD+) as well as phosphorylated derivative, niacinamide adenine dinucleotide phosphate (NADP+). NAD and NADP are utilized in the catalysis of oxidation and reduction reactions. The coenzyme functions to just accept and donate electrons. NAD is used in energy-producing reactions concerning the degradation of carbohydrates, essential fatty acids, ketone bodies, amino acids, and alcohol. NADP is usually associated with biosynthetic reactions much like the pentose phosphate pathway, fatty acid biosynthesis, cholesterol synthesis, and by ribonucleotide reductase. Niacin is also important for growth, conversion of vitamin A to retinal, and prevention of Pellagra. Nicotinic acid can often be used as being a vasodilator.
Recommendations: Recommendations: RDA in mg




* Infants birth to six mos - 5 mg

* Infants 6 mos to at least one yr - 9 mg

* Children 1 yr to 3 yr - 9 mg

* Children 4 yr to 6 yr - 12 mg

* Children 7 yr to 10 yr - 13 mg

* Adolescent males 11yr to 14 yr - 17 mg

* Adolescent females 11 yr to 14 yr - 15 mg

* Adolescent males 15 yr to 18 yr - 20 mg

* Adolescent females 15 yr to 18 yr - 15 mg

* Adult males 19 yr to 50 yr - 19 mg

* Adult females 19 yr to 50 yr - 15 mg

* Adult males 51 yr plus - 15 mg

* Adult females 51 yr plus - 13 mg

* Pregnant Women - 17 mg

* Lactating Mothers (1st a few months) - 20 mg

* Lactating Mothers (2nd 6 months) - 20 mg

Niacin B3

Food Source Serving Size/Amount # of mg/serving

Wheat Flour (whole wheat) 1 cup 7.6 mg

Wheat Flour (white enriched) 1 cup 7.4 mg

Milk 2% fat 8 fl. oz 0.2 mg

Liver (beef braised) 3.5 oz 10.7 mg

Yeast (brewer's) 1.0 oz 10.7 mg

Turkey (dark meat) 3.5 oz 3.6 mg

Chicken (dark meat) 3.5 oz 1.26 mg

Chicken (light meat) 3.5 oz 1.03 mg

Atlantic cod (raw) 3 oz 1.8 mg

Atlantic salmon (raw) 3 oz 6.7 mg

Almonds (lightly roasted) 1 oz 1.0 mg
Literature: Cholesterol:
Niacin is employed in the treatment of hypercholesterolemia. The efficacy and safety of lovastatin and niacin were compared in the controlled, randomized, open-label study of the 26 week duration in 136 patients with primary hypercholesterolemia. Lovastatin and niacin both exerted favorable dose-dependent changes around the concentrations of plasma lipids and lipoproteins. Lovastatin was more effective in cutting LDL cholesterol concentrations, whereas niacin was more efficient in increasing high-density lipoprotein cholesterol concentrations and decreasing the Lp(a) lipoprotein level. Lovastatin was better tolerated than niacin, in large part because from the common cutaneous unwanted effects of niacin. The dosages used were lovastatin 20mg/d and niacin 1.5 g/d for 10 weeks. Similar outcome was noticed in another study where the two drugs reduced low-density lipoprotein-high-density lipoprotein ratios with a similar level, although these effects were obtained in another way. In this study 27 beyond 37 patients finished the trial having a dose of four years old.5 g/d of nicotinic acid. In another study in renal transplant patients, nicotinic acid significantly reduced the entire cholesterol and also the low-density lipoprotein cholesterol and significantly increased the high-density lipoprotein cholesterol. The triglyceride level was reduced by about 100 but was not significant (P = 0.09). There were no significant changes in the triglyceride and high-density lipoprotein blood choleseterol levels in the lovastatin treated group. Flushing created in 67%, but there are no dropouts because of unwanted side effects.
The long-term safety and efficacy of the new extended-release once-a-night niacin preparation, Niaspan, inside the treatments for hypercholesterolemia was determined. Niaspan produced favorable changes in LDL and HDL cholesterol, triglycerides, and lipoprotein(a). Adverse hepatic effects were minor and occurred at rates just like those reported for statin therapy. Intolerance to flushing, ultimately causing discontinuation of Niaspan, happened in 4.8% of patients.
In one study conducted in 110 patients observed in a personal medical clinic throughout a 5-year period, 43% of men and women given regular nicotinic acid and 42% of the given sustained-release nicotinic acid were expected to discontinue the medication due to side effects. However, some unwanted side effects necessitating discontinuing nicotinic acid would not occur until the patient ended up utilizing the drug for a couple of years.
In the Coronary Drug Project, Niacin treatment showed modest benefit in decreasing definite nonfatal recurrent myocardial infarction but failed to decrease total mortality. With a mean follow-up of many years, nearly 10 years after termination with the trial, mortality all causes within the niacin group was 11% under within the placebo group (52.0 versus 58.2%; p = 0.0004). This late benefit of niacin, occurring after discontinuation with the drug, could be a result of an translation in a mortality benefit over subsequent years from the early favorable effect of niacin in decreasing nonfatal reinfarction or perhaps a result of the cholesterol-lowering effect of niacin, or both.
Lipoprotein(a)
Seman et. al. discussed the importance of treatments for elevated degrees of Lipoprotein (a) levels. Recent data have supported Lp(a) just as one independent risk factor for coronary heart disease (CHD). In vitro studies declare that Lp(a) leads to atherogenesis directly by cholesterol uptake and indirectly with the inhibition of fibrinolysis. A study with the Mayo Clinic demonstrated the association between electrophoretic detection of Lp(a) from fresh plasma and CHD in both men and women, causing relative risks for people of a single.9 and 1.6, respectively. This is further sustained by Framingham Heart Study. In some studies, Lp(a) is proven to be a risk facor for CHD in men and not ladies. In both studies, below half as much new cases of CHD happened women as in men, which may have affected these results. The Scandinavian Simvastatin Survival Study indicated that Lp(a) predicted major coronary events and death in secondary prevention in simvastatin and in controls. This somewhat contrasts with studies that declare that Lp(a) attributes risk only if the LDL cholesterol is high. Angiographic studies also suggest that Lp(a) can predict lumen diameter, but only inside setting of either high LDL cholesterol or low HDL cholesterol. Cross-sectional data on Lp(a) and CHD have provided some comprehension of the connection between high Lp(a) levels and vascular disease in blacks versus whites, with a positive correlation between Lp(a) and CHD in some black population.
Lp(a) levels, however would not are most often beneficial in predicting post-procedure outcomes. Lp(a) failed to predict occlusion over half a year in ruthless cardio-arterial stenting or percutaneous transluminal coronary angioplasty, or older 5 years following coronary artery bypass grafting. Furthermore, a role for accelerating atherogenesis in patients with diabetes hasn't been successfully associated with Lp(a).
Mechanisms which can be viewed as involved with Lp(a) and CHD range from the uptake of Lp(a) by foam cells, selective trapping of Lp(a) by artery wall proteoglycans, and aggregation of LDL with Lp(a). Accelerated atherogenesis necessitates the inhibition of plasmin formation around the endothelial surface: hence, lowering the activation of transforming growth factor bmay cause migration and proliferation of smooth muscle cells in the vascular intima. Plasmin suppression may be caused in part with the transcription damaging plasminogen activator inhibitor-1 with the uptake of Lp(a) and extremely bad (VLDL) in the endothelial cells. In addition, Lp(a) induced endothelial dysfunction may promote vascular occlusion.
In patients with CHD or possibly a significant risk for CHD, you should consider measuring Lp(a) and treating with either niacin or estrogen when the patient has Lp(a) levels of cholesterol of more than 10 mg/dL or even an Lp(a) mass in excess of 30 mg/dL.
Diabetes:
Treatment with nicotinamide may prevent or delay the start insulin dependent diabetes mellitus. In a population based diabetes prevention trial, 20,195 young children were screened for islet cell antibodies. Risk might be determined by measuring the number of antibodies to islet cells (ICA antibody test). Of these, 185 had islet cell antibodies and met the factors for treatment with nicotinamide. 173 received botox cosmetic injections. The study population has an average follow-up period of 7.1 years. The incidence of diabetes in children who tested positive for ICA antibodies, and who were given niacinamide, was reduced by about 60%. Nicotinamide features a protective effect up against the development of insulin dependent diabetes in this setting, though the size in the effect features a wide confidence interval. In recent onset type 1 diabetes, niacinamide may prolong the "honeymoon period". Another study demonstrated that nicotinamide improves insulin secretion and metabolic control in lean type 2 diabetic patients with secondary failure to sulphonylureas. bandar qq improves C-peptide release in type 2 diabetic patients with secondary failure of sulphonylureas, leading to some metabolic control just like patients given insulin.
Peripheral vascular disease:
Several double-blind studies demonstrated that inositol hexaniacinate can improve walking distance in patients with intermittent claudication. In one with the studies, 120 patients received either placebo or 2 g of inositol hexaniacinate daily. Over a period of three months, the inositol hexaniacinate treated group showed a significant improvement in walking distance.
Raynaud's disease:
The effects of 4 g/day of Hexopal (Hexanicotinate inositol) or placebo was examined in 23 patients with primary Raynaud's disease during winter. The Hexopal group felt subjectively better and had demonstratively shorter and fewer attacks of vasospasm through the trial period. Serum biochemistry and rheology had not been significantly different between the two groups. Although the mechanism of action remains unclear, Hexopal is safe and it is effective in lessening the vasospasm of primary Raynaud's disease throughout the winter months.
Osteoarthritis:
In a double-blind placebo controlled study, 72 patients with osteoarthritis were randomized for treatment with niacinamide or perhaps an identical placebo for 12 weeks. Niacinamide improved the world impact of osteoarthritis, improved joint flexibility, reduced inflammation, and allowed for decline in standard anti-inflammatory medications when compared with placebo. This study shows that niacinamide may have a job inside treatments for osteoarthritis.
Summary: Vitamin B3 (Niacin) is found in unrefined and enriched grain and cereal, milk, and liver organ, especially liver.Yeast, poultry, salt water fish, nuts, legumes, coffee, tea, milk products, and potatoes are fantastic causes of Niacin. Chronic diarrhea, alcoholism, cirrhosis of the liver, diabetes mellitus, and malignant disease can result in niacin deficiency. Niacin deficiencies are rare in developed countries, since the body may make niacin. Significant studies have shown that Niacin can increase HDL levels reducing LP(a) which improves one's cardiac risk profile. Research shows the benefit of Niacin supplementation carries a protective effect against the growth and development of insulin dependent diabetes (Type I) as well as in Type II diabetics improves C-peptide release in patients with secondary failure of sulphonylureas, leading to some metabolic control comparable to patients treated with insulin. Additional research indicates potential benefit inside treatments for Raynaud's disease, peripheral vascular disease and osteoarthritis.
Hypotension and dermatitis will be the most typical symptoms of hypervitaminosis. Other the signs of toxicity include increased pulse and respiratory rate, increased cerebral the circulation of blood, and nerves inside the body stimulation. Peripheral vasodilation, fatty liver, and decreased serum cholesterol, can be seen.