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Niacin stimulates Growth Hormone

While extolling the benefits of niacin, one frequently overlooked “side effect” is that niacin is a powerful and inexpensive releaser of growth hormone. (Quabbe, et al, 1983) (Fig. 3).

Quabbe and colleagues administered 500 mg niacin intravenously to humans, and noted a dramatic rise in growth hormone. In a second phase of their study, they simultaneously administered an infusion of fatty acids. Note that the fat completely blunted any rise in growth hormone. The practical take-home lesson of this study is that anyone using niacin as a growth hormone stimulant should take it on an empty stomach (glucose and insulin also inhibit growth hormone, as well as fatty acids).

Niacin favorably altered several cardiovascular risk factors as well. Apolipoprotein (a) levels were significantly (20%) reduced by niacin, but were not altered by gemfibrozil. Both substances reduced serum apolipoprotein (b) levels by the same amount. Fibrinogen, a third risk factor, was reduced by niacin, but increased 6-9% by gemfibrozil. The authors concluded, “Niaspan, 2,000 mg, had a significantly better effect on fibrinogen levels than gemfibrozil.”

These results support many previous studies on the use of niacin as a lipid-lowering nutrient

Side Effects and Contraindications to High-Dose Niacin

High dose niacin is very safe. Its most frequent “adverse effect” is a harmless flushing of the skin, accompanied by itching. This effect usually resolves over a few days or weeks of use. Taking an aspirin 30 minutes or so before the niacin also helps to reduce this effect. Another way to minimize the flushing is to start with low doses (50-100 mg) and gradually increase the dose as tolerated. Finally, inositol hexanicotinate (IHN)—another non-flushing form of niacin—can also be used. IHN, while a bit more costly than niacin, is effective in somewhat lower doses, thereby remaining cost effective. Another side effect is the potential for elevation of liver enzymes or liver toxicity. Liver toxicity is rare, and occurs most frequently with timed release preparations.

Anyone contemplating high dose niacin therapy probably should have their liver enzymes checked within several months of achieving therapeutic levels (1,500-3,000 mg). The only absolute contraindication to niacin therapy is insulin-dependent diabetes. Niacin aggravates blood sugar problems in insulin dependent diabetics, further worsening their lipid problems, usually causing their triglycerides to skyrocket. Alternatively, I recommend niacinamide (also contained in Optimum D) in doses up to three grams daily for insulin dependent diabetics. Although niacinamide does not normally effect lipid levels in non-diabetics, because of its glucose-stabilizing affect in diabetics, it tends to normalize their blood lipids—especially, the triglycerides.


Niacin once again emerges as a low-cost, highly effective agent to reduce cholesterol, raise HDL, and lower LDL and triglycerides. In addition, it has the added benefits of lowering apolipoproteins a and b, and fibrinogen, and raising growth hormone. Muntoni (1974) stated that “lipostatic” substances are the agents of choice to retard aging, and niacin may very well be the best substance in this class (Dilman and Dean, 1992).


Canner, P.L., Berge, K.G., Wenger, N.K., et al. Fifteen year mortality in Coronary Drug Project patients: long-term benefit with niacin. J Am Coll Cardiol, 1986, 8: 1245-1255.

Dilman, V., and Dean, W. The Neuroendocrine Theory of Aging and Degenerative Disease, 1992, The Center for Bio-Gerontology, Pensacola.

Guyton, John R., Blazing, Michael A., Hagar, James, et al. Extended-release niacin vs Gemfibrozil for the treatment of low levels of high density lipoprotein cholesterol. Arch Intern Med, 2000, 160: 1177-1184.

Horowitz, N. Link niacin to longevity after an MI. Medical Tribune, 1985, 26: 12, pp. 1, 17.

Muntoni, S. Inhibition of fatty acid oxidation by biguanides: implication for metabolic physiopathology. Adv Lipid Res, 1974, 12: 311-377.

Quabbe, H.J., Ramek, W., and Luyckx, A.S. Growth hormone, cortisol and glucagon concentration during plasma free fatty acid depression. Different effects of nicotinic acid and an adenosine derivative. J Clin Endocr Metab, 1983, 57: 410-414.






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