Xanthinol Nicotinate is a form of Niacin that passes easily through cell membranes; Xanthinol Nicotinate is the most potent form of Niacin available.
Xanthinol Nicotinate has been shown to increase brain glucose metabolism, improve brain ATP levels and improve brain blood flow (it acts as a vasodilator). As such, Xanthinol Nicotinate has been used to treat short-term memory disorders, mental flagging (i.e. lack of brain energy that compromises vigilance, concentration and attention) and insufficient blood flow to the arteries and the extremities. Furthermore Xanthinol Nicotinate has been clinically shown to improve the reaction speed of the elderly.
The activity of nicotinic acid at the cell membrane has shown to improve neurological transmission inside the cell and aslo enhances cell metabolism and oxygen supply in the brain.
Why is this so important to athletes?
Increased blood flow to these areas of the brain may help to increase performance during exercise that require specific tasks and boost mental alertness. Cereral vasodialation will also increase glucose delivery to the brain that leads to less Central Nervous System fatigue during short and long term activity.
When it enters the cell the rate of metabolism of glucose speeds up and ATP prodcution is increased. This directly affects brain energy and this means better neurological transmission between the barin and msucles.
Xanthinol Nicotinate is mostly used in Brain functionin formulas; however is being studied as part of our CNS Technology research.
Refferences:
Cervantes-Laurean D, McElvaney NG, Moss J. Niacin. In: Shils M, Olson JA, Shike M, Ross AC, eds. Modern Nutrition in Health and Disease. 9th ed. Baltimore: Williams & Wilkins; 1999:401-411.
Jacob R, Swenseid M. Niacin. In: Ziegler EE, Filer LJ, eds. Present Knowledge in Nutrition. 7th ed. Washington D.C: ILSI Press; 1996:185-190.
Jacobson MK, Jacobson EL. Discovering new ADP-ribose polymer cycles: protecting the genome and more. Trends Biochem Sci. 1999;24(11):415-417.
Park YK, Sempos CT, Barton CN, Vanderveen JE, Yetley EA. Effectiveness of food fortification in the United States: the case of pellagra. Am J Public Health. 2000;90(5):727-738. (PubMed)
Gregory JF, 3rd. Nutritional Properties and significance of vitamin glycosides. Annu Rev Nutr. 1998;18:277-296. (PubMed)
Fu CS, Swendseid ME, Jacob RA, McKee RW. Biochemical markers for assessment of niacin status in young men: levels of erythrocyte niacin coenzymes and plasma tryptophan. J Nutr. 1989;119(12):1949-1955. (PubMed)
Food and Nutrition Board, Institute of Medicine. Niacin. Dietary Reference Intakes: Thiamin, Riboflavin, Niacin, Vitamin B6, Vitamin B12, Pantothenic Acid, Biotin, and Choline. Washington, D.C.: National Academy Press; 1998:123-149. (National Academy Press)
Jacobson EL, Jacobson MK. Tissue NAD as a biochemical measure of niacin status in humans. Methods Enzymol. 1997;280:221-230.
Jacobson EL, Shieh WM, Huang AC. Mapping the role of NAD metabolism in prevention and treatment of carcinogenesis. Mol Cell Biochem. 1999;193(1-2):69-74. (PubMed)
Hageman GJ, Stierum RH. Niacin, poly(ADP-ribose) polymerase-1 and genomic stability. Mutat Res. 2001;475(1-2):45-56. (PubMed)
Boyonoski AC, Spronck JC, Gallacher LM, et al. Niacin deficiency decreases bone marrow poly(ADP-ribose) and the latency of ethylnitrosourea-induced carcinogenesis in rats. J Nutr. 2002;132(1):108-114. (PubMed)
Gensler HL, Williams T, Huang AC, Jacobson EL. Oral niacin prevents photocarcinogenesis and photoimmunosuppression in mice. Nutr Cancer. 1999;34(1):36-41. (PubMed)
Weitberg AB. Effect of nicotinic acid supplementation in vivo on oxygen radical-induced genetic damage in human lymphocytes. Mutat Res. 1989;216(4):197-201. (PubMed)
Brody T. Nutritional Biochemistry. 2nd ed. San Diego: Academic Press; 1999.