(Nicotinic acid, B3)
GENERAL:
Vitamin B3 (Niacin) is necessary for proper circulation, healthy skin, and is important for the proper functioning of the nervous system. It is involved in the normal formation of stomach fluids and secretion of bile, along with the synthesis of the sex hormones.
It may help lower triglycerides, cholesterol and is considered helpful for schizophrenia and other mental illnesses. Note: A "flush" may occur after intaking niacin. It is usually harmless, diminishes after 30 minutes or so, and can be reduced by taking niacin with a meal and an extra glass of water. A no-flush variety of niacin (inositol hexaniacinate) does not cause flushing, but is more expensive. Niacinamide (a synthetic form of niacin) also does not cause flushing, however there is some disagreement as to whether niacinamide would yield all the benefits of niacin.
Niacin is a water-soluble nutrient that participates in over 50 metabolic functions in the body important in the release of energy from carbohydrates?
Deficiency Symptoms: Headaches, insomnia, loss of appetite, low blood sugar, dizziness, halitosis, diarrhea, depression, canker sores, fatigue, and dementia. Pellagra is the most well-known deficiency disease.
Absorption Enhancers: B-Complex, vitamin B1, vitamin B2, vitamin C, phosphorus.
Absorption Antagonists: Alcohol, coffee, caffeine, excess sugar/carbohydrate intake, antibiotics, sulfa drugs.
Best Food Sources: Whole grains; organ meats, especially liver; fish; nuts; eggs; green vegetables such as broccoli; carrots; brewer’s yeast; legumes.
Hypoglycemic
Both nicotinic acid (NA) and the adenosine receptor agonist phenylisopropyladenosine (PIA) are potent antilipolytic agents. We have evaluated the ability of these compounds to lower plasma glucose concentration in 450-g male diabetic rats. Diabetes was induced by intravenous streptozotocin, and the rats were studied 7-10 days later. Mean (+/- SE) fasting glucose decreased 4 h after subcutaneous injections of PIA at 0 and 2 h. A similar change in plasma glucose level was also seen in rats injected with NA. The decrease in the concentration of plasma glucose in both instances was preceded by marked sustained reductions in plasma free fatty acid (FFA) concentrations; FFA decreased in PIA-injected rats and in response to NA. With injection of normal saline, neither plasma glucose nor FFA concentrations decreased in diabetic rats. There was no change in the plasma insulin concentration of rats that had hypoglycemic responses to PIA or NA. In vitro glucose uptake was determined in isolated adipocytes, and both PIA and NA were shown to increase basal and maximal insulin-stimulated glucose uptake. The stimulating effect of the two compounds was similar, and the magnitude of the effect was comparable in adipocytes from either normal or diabetic rats. As a result, neither NA nor PIA could restore the defects in glucose transport to normal in adipocytes from diabetic rats. Insulin-stimulated glucose uptake was assessed in vivo by determining the steady-state glucose response of diabetic rats to a continuous infusion of insulin and glucose and was found to be significantly enhanced in response to NA compared with NaCl.(ABSTRACT TRUNCATED AT 250 WORDS)
PMID: 2962514
Glucocorticoids, oral contraceptives and nicotinic acid are associated with glucose intolerance, and the main cause of the glucose intolerance induced by these drugs is insulin resistance
PMID: 10707579
In this study the effect of two drugs [etomoxir and nicotinic acid (NA)] on plasma glucose, free-fatty acid (FFA), and triglyceride (TG) concentrations was determined in rats with streptozocin (STZ)-induced diabetes. The two compounds modify FFA metabolism by different mechanisms, etomoxir (ethyl-2-[6-(4-cholorophenoxyl)-hexyl]oxirane-2-carboxylate) by inhibiting hepatic fatty acid oxidation, and NA by inhibiting lipolysis in adipose tissue.
The acute administration of either etomoxir or NA lowered plasma glucose concentrations in diabetic rats by approximately 150 mg/dl (P less than .001) in 4 h.
Because plasma insulin concentrations did not change in response to either drug, whether administered singly or in combination, these metabolic effects do not result from a change in insulin secretion. These results suggest that modulation of FFA metabolism at the level of the adipocyte or the liver can have dramatic effects on carbohydrate and lipid metabolism.
PMID: 3275556
BACKGROUND: High doses of niacin have been shown to impair glucose control in patients with non--insulin-dependent diabetes mellitus (NIDDM). We undertook a study to determine if low-dose niacin has a similar effect.
CONCLUSION: Low-dose [500 mg three times daily for 2 months ] niacin increases fasting blood sugar in patients with stable NIDDM. [non--insulin-dependent diabetes mellitus] (they call that low dose?!?)
PMID: 11862304
NA significantly reduced the glucose infusion rate required to maintain euglycaemia in all subjects (placebo vs NA; 31.5+/-4.2 vs. 26.2+/-4.6 micromol/kg/min, P = 0.002) associated with a decrease in non-oxidative glucose disposal.
PMID: 10980588
ingestion of niacin-bound chromium and natural antioxidants such as grape seed proanthocyanidin extract has been demonstrated to improve insulin sensitivity and/or ameliorate free radical formation and reduce the signs/symptoms of chronic age-related disorders including syndrome X.
PMID: 12074977
Nicotinamide is being used in trials to prevent or delay the development of clinical IDDM. A related compound, niacin, has been shown to cause insulin resistance in normal subjects, resulting in increased insulin secretion. This study was designed to answer the question: Does the short-term administration of nicotinamide cause insulin resistance in subjects who have a high risk of developing IDDM? Eight islet cell antibody-positive (ICA+) relatives of IDDM patients were given nicotinamide at a dose of 2 g/day for 2 weeks. Measurements of first-phase insulin release, insulin sensitivity, glucose effectiveness, and the constant for glucose disappearance (Kg) were measured at baseline, at the end of 2 weeks of therapy, and after subjects had been off therapy for at least 2 weeks. Nicotinamide administration caused a 23.6% decrease in insulin sensitivity (P = 0.02). This decrease was associated with a fall in Kg despite increased insulin secretion.
PMID: 8866571
To determine whether downregulation of Gi proteins is associated with insulin resistance, we incubated isolated adipocytes with N6-(2-phenylisopropyl)adenosine (PIA; an A1-adenosine receptor agonist; 300 nM), prostaglandin E1 (PGE1; 3 microM), or nicotinic acid (1 mM) for 4 days in primary culture. The cells were washed, and the rate of glucose transport (2-deoxy-[3H]glucose uptake) was measured after incubation with various concentrations of insulin for 45 min. Both PIA and PGE1 (which downregulate Gi) decreased the maximal responsiveness of the cells to insulin by approximately 30% and caused a rightward shift in the dose-response curve. By contrast, nicotinic acid (which does not downregulate Gi) did not alter the insulin sensitivity of the cells. Prolonged treatment of adipocytes with either PIA or PGE1 (but not nicotinic acid) rendered the cells completely resistant to the antilipolytic effect of insulin. The ability of insulin to stimulate autophosphorylation of the beta-subunit of the insulin receptor was decreased by approximately 30% in PIA-treated cells, and the dose-response curve was shifted to the right. Similarly, the ability of the receptor to phosphorylate poly(Glu4-Tyr1) was decreased by approximately 35%. This decrease in tyrosine kinase activity of the receptor may account for the decrease in insulin sensitivity of glucose transport but cannot account for the complete loss of antilipolysis. The findings suggest both a direct and indirect involvement of Gi proteins in insulin action.
PMID: 9277377
NA-induced insulin resistance in this study is (a) less than previously reported; (
not associated with changes in insulin secretory responsiveness, but is © influenced by an individually variable NA effect on fasting NEFA levels.PMID: 8903118
Hyperinsulinemia, in association with NA infusion (NA study) brings about a significantly greater stimulation of total glucose disposal in both pregnant (approximately 30%) and nonpregnant (approximately 35%) rabbits compared with the control study. A more pronounced inhibition of hepatic glucose production occurred in NA study in pregnant rabbits (approximately 30 vs. approximately 10%) but it did not reach a statistical significance, whereas there was a total inhibition in nonpregnant rabbits.
PMID: 8476036
The literature seams a bit confused, some sources claim and increase in insulin levels while other claim no change. While it acts to both lower glycerides and glucose levels, it appears to in most cases to induct insulin resistance [although I didn’t really see a good explanation as to why… perhaps this could be counteracted] and as one study mentioned it decreases lipolysiswhich of course would be bad.
It is said that increases in fat intake lead to an increase in insulin concentrations…. Perhaps lowering glycerides effects this equation in some manner?
The “niacin-bound chromium and natural antioxidants such as grape seed proanthocyanidin extract” sounds interesting and should be looked into further although I do not know what compounds specifically they are referring to.
Leptin stimulant
The effect of 3 days of intensive treatment with acipimox, an antilipolytic nicotinic acid derivative, on plasma leptin levels was studied in eight patients with Type 2 diabetes mellitus in a double-blind, placebo-controlled, cross-over study. Acipimox reduced plasma free fatty acids (FFA) markedly and lowered plasma triglycerides, glucose and insulin. Plasma leptin levels were elevated in all eight patients during 3 days of acipimox treatment (mean increase+/-s.e.: 2.38+/-0.57ng/ml, P<0.005) and the 24h mean effect of acipimox on leptin levels increased during the experimental period (P<0.03). The effect on plasma insulin and glucose resembled a mirror image of the effect on plasma leptin during 3 days of treatment. The suggestion that leptin mediates insulin resistance and may be involved in the development of the diabetic syndrome cannot be supported by the present results. It has been reported that FFA stimulates leptin secretion. Surprisingly, despite a markedly reduced FFA level, leptin concentration increased in the present study. We suggest that a primary acipimox effect is to increase leptin secretion, and that this prevails over the reduced FFA stimulus.
PMID: 11022182
Significantly, antilipolytic agents other than insulin (adenosine, nicotinic acid, acipimox, and orthovanadate) did not mimic the acute stimulatory effects of insulin on leptin secretion under these conditions. We conclude that norepinephrine specifically inhibits insulin-stimulated leptin secretion not only via the low-affinity beta3-adrenoceptors but also via the high-affinity beta1/beta2-adrenoceptors. Moreover, it is suggested that 1) activation of phosphodiesterase III by insulin represents an important metabolic step in stimulation of leptin secretion, and 2) lipolytic hormones competitively counterregulate the stimulatory effects of insulin by activating the adenylate cyclase system.
PMID: 12055093
This was about all there was on leptin, once I know what the niacin-bond chromium compound is I will look to see if it has any effect on leptin like the analogue does.
Growth Hormone stimulant
Recent studies in adult volunteers have demonstrated that the free fatty acid reduction induced by acipimox, a nicotinic acid analog, stimulated GH secretion per se and enhanced in an additive manner the GH secretion elicited by such different stimuli as pyridostigmine, GHRH and GHRP-6.
These results indicate that: 1) following the administration of a single oral dose of acipimox, significant GH secretion was elicited in healthy short prepubertal children; 2) the combined administration of acipimox plus L-Dopa did not, however, enhance the GH secretion of this group of children; 3) acipimox was well tolerated with minimal side effects
PMID: 11085190
It has previously been shown that nicotinic acid (NA)-induced depression of free fatty acids (FFA) stimulates the secretion of GH and glucagon. To evaluate this hormonal response further, we studied the influence of different doses of glucose administered by continuous iv infusion on the GH and glucagon increase during NA-induced FFA depression. In ten male non-obese volunteers, FFA depression by the infusion of NA (2.3 g over a period of 210 min) resulted in a late rise (from 150 min on) of GH (From 1.1 to 25.9 ng/ml) and an early increase (from 30 min on) of glucagon (from 71.7 to 138.2 pg/ml). When glucose was infused (approximately 60, 120 and 180 g, respectively, over a period of 270 min) during NA-induced FFA depression, the GH rise was reduced and delayed in relation to the amount of glucose infused, but could not be completely abolished (maximal GH concentration during the three NA-plus-glucose infusions: 16.5, 8.0 and 6.1 ng/ml, respectively). The glucagon rise was entirely reversed by the high glucose dose. Insulin did not rise during NA infusion alone. Its secretion in response to glucose infusion was not significantly influenced by FFA depression. Thus, during NA-induced FFA depression the secretion of two lipolytic hormones--GH and glucagon--is stimulated while the secretion of the lipogenetic hormone insulin remains low. Glucose has an inhibitory effect on the GH and glucagon response which, however, is different for each of the hormones.
PMID: 838844
Perhaps increased Glucagon is the cause of the insulin sensitivity?
Two chemically unrelated inhibitors of lipolysis were used in order to differentiate between the effect of FFA depression and a possible FFA-unrelated drug effect, respectively, on the plasma concentrations of GH, cortisol, and glucagon. Saline infusion served as a control experiment. In eight healthy male volunteers, a similar FFA depression by either iv infusion of nicotinic acid (3-pyridine-carboxylic acid, NA) or oral intake of an adenosine derivative, N(6)-allyl-N(6)-cyclohexyl-adenosine (AD-D), was followed by a significant GH increase (to 22.1 +/- 6.2 and 9.6 +/- 2.9 ng/ml at 240 and 270 min, respectively). Due to the large scatter of the GH concentrations during NA infusion, these responses were not significantly different. No GH increase occurred when the FFA depression was prevented by addition of a lipid infusion. In contrast, plasma cortisol and glucagon both increased significantly (by 107.4 micrograms/liter at 270 min and by 48.4 pg/ml at 60 min, respectively) during NA- but not during AD-D-induced FFA depression. Addition of the lipid infusion abolished the cortisol increase during NA infusion but had no influence on basal cortisol concentrations during AD-D intake. It lowered glucagon to values slightly below basal concentrations when added to the NA infusion and more markedly during AD-D administration. The results provide evidence that 1) depression of plasma FFA per se stimulates the secretion of GH, and 2) the increase of cortisol and glucagon during NA infusion is probably unrelated to the FFA depression. Hence, the stimulatory effect of FFA lack on glucagon secretion needs to be reconsidered.
PMID: 6345570
The influence of ketone body infusion on the serum GH and glucagon response to FFA depression and insulin hypoglycemia was investigated in 10 healthy men. Intravenous infusion of nicotinic acid induced suppression of both FFA and ketone bodies. This was accompanied by a delayed GH increase to 21.1 +/- 6.9 ng/ml (at 300 min). During an additional beta-hydroxybutyrate (OHB) infusion, FFA remained depressed, but ketone bodies were elevated, and the GH response was abolished (maximum 5.6 +/- 1.6 ng/ml). During infusion of OHB alone, FFA were suppressed. GH increased significantly, although less markedly than during suppression of both FFA and ketone bodies (to 9.3 +/- 3.1 ng/ml at 270 min). No GH rise occurred when both FFA and ketone bodies were kept elevated by the addition of a lipid infusion. The GH rise in response to insulin hypoglycemia was not changed by an OHB infusion (43.2 +/- 4.6 vs. 48.0 +/- 7.3 ng/ml). However, OHB increased the net GH output by significantly delaying the return to basal concentrations in the presence of a reduced FFA rebound. An effect of OHB infusion on the plasma glucagon concentration during all experiments was small, and its physiological significance is doubtful. These results confirm that FFA depression induces delayed GH secretion. They suggest that this is not wholly dependent on concomitant depression of ketone bodies. On the other hand, when ketone bodies are elevated, the GH response to FFA depression is diminished or absent. The net GH response to changes in lipid substrates probably depends on the concentration of both FFA and ketone bodies.
PMID: 6348066
The purpose of this study was to assess how selected physiological and performance responses are affected when the normal increase in plasma free fatty acid concentration during exercise is blunted by ingesting nicotinic acid. On four occasions, 10 subjects cycled at 68 +/- 1% VO2peak for 120 min followed by a timed 3.5-mile performance task. Every 15 min during exercise, subjects ingested 3.5 ml.kg LBM-1 of one of four beverages: 1) water placebo (WP), 2) WP + 280 mg nicotinic acid.l-1 (WP + NA), 3) 6% carbohydrate-electrolyte beverage (CE), and 4) CE + NA. Ingestion of nicotinic acid (WP + NA and CE + NA) blunted the rise in FFA associated with WP and CE; in fact, NA ingestion effectively prevented FFA from rising above rest values. The low FFA levels with NA feeding were associated with a 3- to 6-fold increase in concentrations of human growth hormone throughout exercise. The mean performance time for CE (10.7 min) was significantly less than for WP (12.2 min) and WP + NA (12.8 min), but did not differ from CE + NA (11.4 min). The results indicate that blunting the normal rise in FFA alters the hormonal response to exercise and reduces the capacity to perform high-intensity exercise.
PMID: 7564973
Glucagon
Total glucose uptake during exercise was greater (P <.05) in NA (1,876 +/- 161 micromol.kg(-1)) than in CON (1,525 +/- 107 micromol.kg(-1)). Total fat oxidation was reduced (P <.05) by approximately 32% during exercise in NA. Total carbohydrate oxidized was approximately 42% greater (P <.05) in NA (412 +/- 40 mmol) than CON (290 +/- 37 mmol), of which, approximately 16% (20 +/- 10 mmol) could be attributed to glucose. Plasma insulin and glucagon were similar between trials. Catecholamines were higher (P <.05) during exercise in NA. In summary, during prolonged moderate exercise in untrained women, reduced FFA availability results in a compensatory increase in carbohydrate oxidation, which appears to be due predominantly to an increase in glycogen utilization, although there was a small, but significant, increase in whole body glucose uptake.
PMID: 11288047
In order to assess the ability of nicotinic acid to decrease plasma glucose concentration, normal individuals were given continuous four hour infusions of either nicotinic acid (NA), somatostatin (SRIF), NA + SRIF, or 0.9% NaCl (Saline). Plasma non-esterified fatty acid (NEFA) concentration decreased to about one-fourth of the basal value in response to either NA or NA + SRIF, associated with statistically significant decreases in plasma glucose concentration. The ability of NA and NA + SRIF to decrease plasma glucose concentration was seen despite the fact that plasma insulin concentrations also fell significantly during both infusions. Although plasma glucose concentration fell significantly in response to both NA and NA + SRIF, the effect of NA + SRIF was approximately twice as great as that seen with NA alone. The augmented hypoglycaemic effect of NA + SRIF as compared to NA alone was associated with a concomitant fall in plasma glucagon concentration. In contrast, plasma glucose concentration did not change following Saline, and was actually higher than baseline after the infusion of SRIF alone. These results provide evidence that NA can lower plasma glucose concentration in normal volunteers, and suggests that this is mediated by the NA-associated decrease in plasma NEFA concentration.
PMID: 1358776
Lowering of the plasma FFA level in intact fasted rats by infusion of nicotinic acid (NA) caused essentially complete ablation of insulin secretion (IS) in response to a subsequent intravenous bolus of arginine, leucine, or glibenclamide (as previously found using glucose as the beta-cell stimulus). However, in all cases, IS became supranormal when a high FFA level was maintained by co-infusion of lard oil plus heparin. Each of these secretagogues elicited little, if any, IS from the isolated, perfused "fasted" pancreas when tested simply on the background of 3 mM glucose, but all became extremely potent when 0.5 mM palmitate was also included in the medium. Similarly, IS from the perfused pancreas, in response to depolarizing concentrations of KCl, was markedly potentiated by palmitate. As was the case with intravenous glucose administration, fed animals produced an equally robust insulin response to glibenclamide regardless of whether their low basal FFA concentration was further reduced by NA. In the fasted state, arginine-induced glucagon secretion appeared to be independent of the prevailing FFA concentration. The findings establish that the essential role of circulating FFA for glucose-stimulated IS after food deprivation also applies in the case of nonglucose secretagogues. In addition, they imply that (i) a fatty acid-derived lipid moiety, which plays a pivotal role in IS, is lost from the pancreatic beta-cell during fasting; (ii) in the fasted state, the elevated level of plasma FFA compensates for this deficit; and (iii) the lipid factor acts at a late step in the insulin secretory pathway that is common to the action of a wide variety of secretagogues.
PMID: 9616208
NA has no direct effect on GNG. [gluconeogenesis]
This was the limited info I could find on NA acting directly with glucagons, as you can see it does not seam to stimulate it indirectly so that would rule out glucagons as being the cause if insulin resistance. While theory is knocked down another question has become apparent.
The NA clears the blood of fatty acids and then suppresses their use for energy, this led to a decrease in exercise performance in women but what about their metabolism? Is it being slowed down or is the glycolysis substituting completely for the lost energy? My understanding is that glucose provides fast energy then fat which is why you slow down after you have been working for a while, so I would assume then that the glucose getting used here is not getting used fast enough to compensate for the lack in lipolysis .
I also do not understand the method by which NA inhibits lipolysis , is it from the adipose tissue receiving and in flux of FA or by some other means?
It appears that insulin is can counteract the anitlipolytic action of NA although to what extent I can’t say and I am not sure if this is directly or indirectly through the stimulate of GH which would then promote fat burning, but this hints that if we can find a way around the other negative (NA causing insulin resistance) then using this with and insulin spiking meal could be still have potential.
To go off subject for a moment, they mention arginine releasing glucagons as mentioned here as well
Arg exerts its vascular actions also through NO-independent effects, including membrane depolarization, syntheses of creatine, proline and polyamines, secretion of insulin, growth hormone, glucagon and prolactin, plasmin generation and fibrinogenolysis, superoxide scavenging and inhibition of leukocyte adhesion to nonendothelial matrix.
PMID: 11053497
Now if arginine stimulates both insulin and glucagons I wonder which one wins out? Perhaps they effect of it alone gives no net increase in either making its use as an insulin potentiator rather useless.
PMID: 9927497
Vasodilator
The next property of NA we will look at is the vasodialation or flush it causes. Pharocopia has this information.
Niacin: A flush occurs due to histamine release from mast cells, 20 minutes after ingestion lasting up to 1 to 1 and ˝ hours. This usually lessens after 3 days and may disappear at higher doses. Decrease by taking niacin with meals, raising dosage slowly, or taking 300mg aspirin 15 - 30 minutes before ingestion of niacin. Can raise uric acid levels by competing with uric acid for renal excretion. Gouty symptoms or uric acid stone formation is rare though. Can see deterioration in oral glucose tolerance. Hepatic toxicity is rare but may occur with doses over 3 gm/day. Can see with sustained-release niacin, which can also cause bleeding with a prolonged thrombin time and lactic acidosis with nausea and vomiting. Other side effects reported with niacin include pruritus, hyperpigmentation, rash, acanthosis nigricans, nausea, diarrhea, aggravation of peptic ulcers, hypotension and atrial fibrillation.
Cardiostimulation produced by noradrenaline, glucagon, or tachycardia on the isolated perfused rat heart produced a metabolic coronary dilatation that was potentiated by nicotinic acid or its amide [NIC; 0.05-1.0 mM] without affecting the cardiostimulation. Reactive hyperaemia to brief coronary occlusion was unaffected by NIC, thus confirming that its vasodilator mechanism is of a different nature than that leading to metabolic coronary dilatation. It is suggested that NIC may be of significance as an adjuvant in the treatment of certain types of coronary insufficiencies.
PMID: 6232626
From personal experience I can tell you that a strong histamine flush (from 1gram) causes extreme redness to the entire body, you feel pressure in your face from it, and when you rub against anything it prickles. At only 250 I have had the flush occur at virtually the same magnitude. I personally do not find it all that uncomfortable as long as I don’t move around a lot, It gives you a warm but not hot feeling that can be actually quiet pleassent.
Now for those of you who follow my posts you have probably seen me mention my theory before but I will restate it here.
Wearing socks to stimulate vassodialtion in the extremities helps one fall asleep
A cold room helps one to fall asleep
Anithistamines specifically H1 antagonists causes drowsiness
H1 stimulation (I may have my receptors confused here) causes vassodialation of the extremities
Niacin causes vassodialation
Sleep depravation is related to niacin deficiency (PMID: 2062264, PMID: 1809857)
Melatonin peaks at the same time in which body temperature is at its lowest.
Do I have to draw you a picture?
Unfortunately I can find little research to directly support that there is indeed a direct connection between melatonin and histamine.
Liver toxicity
The final consideration on NA is liver toxicity
Marked lowering of plasma total and low-density lipoprotein cholesterol levels that occur during treatment of dyslipidemia with pharmacologic doses of nicotinic acid result from hepatotoxicity. Therefore, a marked reduction in low-density lipoprotein may suggest generalized liver toxicity and drug treatment should be discontinued.
PMID: 9527102
We report a case of severe liver injury occurring on two occasions in a patient ingesting large doses of nicotinic acid. The liver architecture was markedly distorted, with both massive and submassive lobular collapse and marked cholestasis. Complete resolution of biochemical and histologic abnormalities occurred after withdrawal of these drugs.
PMID: 6823602
A 46-year-old man began taking nicotinic acid, 3 g daily, for hypercholesterolemia. A month later, he developed clinical and biochemical evidence of modest hepatocellular injury, and therapy was stopped. It was restarted 6 weeks later, and 10 weeks after that, the patient presented with fulminant hepatic failure, which resolved rapidly after cessation of nicotinic acid therapy. We suggest that nicotinic acid was the cause of his liver disease, that this case is of particular note because of the rather short period of therapy before the onset of liver injury and the severity of the hepatic failure, and that the probable increased use of nicotinic acid for serum cholesterol control makes it especially important for physicians and their patients to be alert to the signs of hepatotoxicity.
PMID: 3680913
Nicotinic acid has a proven efficacy in the treatment of hypercholesterolemia. Therapeutic use of this water-soluble B vitamin has resulted in a survival benefit among patients enrolled in the Coronary Drug Project. Conversely, nicotinic acid has been associated with a high side-effect profile when used at therapeutic doses. Nevertheless, there are no previously reported cases of hematemesis temporally associated with nicotinic acid use. The authors report the case of a previously healthy 20-year-old man who developed hematemesis and hepatitis 1 week after self-initiating the daily consumption of 6 g of nicotinic acid. Supportive therapy and discontinuing nicotinic acid resulted in rapid clinical improvement in this patient. The clinical circumstances suggest a possible causal relationship between nicotinic acid consumption and his presenting problems. The use of large doses of nicotinic acid may be rapidly complicated by hematemesis and hepatitis.
PMID: 2801756
I do not know minimum dose at which live function becomes impaired, nor do I know the lowest effective dose for causing glucose uptake or GH secretion although the study witth the women would have had them taking around 2.5 grams. The RDA for B3 is 15mg, the minimum dose at which flush can occur is 50mg. Most Niacin supplements I have seen are 250mg pills. I would assume that the effects are dose dependant and that one could therefore utilize NA at a dose lower then what would cause liver problems and still get some of the benefits.
For anyone who whishes to try the flush, I would assume that repeated flushing could deplete histamine stores in the mast cells faster then they could be replenished, I do not know the consequences of this but taking l-histadine would likely help to maintain histamine levels.
