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![]() Phenibut Info And Products Improves Relaxation And Mental Function ![]()
Phenibut is derived from the neurotransmitter GABA.1 GABA is a neurotransmitter responsible for nerve signal transmission efficiency, and elevated GABA levels are necessary for sound sleep. What does it do and what scientific studies give evidence to support this? Phenibut (beta-phenyl-gamma-aminobutyric acid) has a long history of clinical use in Russia. Learn more about the benefits of Phenibut on Clayton South's Health Facts.
No symptoms of deficiency exist.
Strictly adhere to label recommendations. Tolerance is a side effect of chronic administration. Tolerance is a phenomenon whereby the body either:
For this reason phenibut is typically cycled. Meaning: users of this supplement use phenibut for a period of one to two weeks and then cease administration for an equal amount of time. This allows for maximum benefit and minimal down regulation. The toxicity of phenibut is very low. No reports of overdose have been reported when used in moderation, and no reports of dependency have emerged in scientific literature. Persons on MAOI inhibitors or epilepsy medications like tegretol or trileptal should consult with their psychiatrist / physician prior to supplementation with phenibut. Clinical research has demonstrated that phenibut can potentate or inhibit the function of some epilepsy medications. REFERENCES
1. Pavlov J Biol Sci. 1986 Oct-Dec;21(4):129-40. On neurotransmitter mechanisms of reinforcement and internal inhibition. Shulgina GI.
2. Arch Immunol Ther Exp (Warsz). 1975;23(6):733-46. Pharmacological properties of gamma-animobutyric acid and it derivatives. IV. Aryl gaba derivatives and their respective lactams. Chojnacka-Wojcik E, Hano J, Sieroslawska J, Sypniewska M.
3. Lapin I. Phenibut (beta-phenyl-GABA): a tranquilizer and nootropic drug. CNS Drug Rev. 2001 Winter;7(4):471-81.
4. Neurosci Behav Physiol. 2003 Mar;33(3):255-61. Neurochemical characteristics of the ventromedial hypothalamus in mediating the antiaversive effects of anxiolytics in different models of anxiety. Talalaenko AN, Pankrat'ev DV, Goncharenko NV.
5. Eksp Klin Farmakol. 2002 Sep-Oct;65(5):22-6. [Monoaminergic and aminoacidergic mechanisms of the posterior hypothalamus in realization of the antiaversive effects of anxiosedative and anxioselective agents in various anxiety models] [Article in Russian]. Talalaenko AN, Pankrat'ev DV, Goncharenko NV.
6. Ross Fiziol Zh Im I M Sechenova. 2001 Sep;87(9):1217-26. [Neurochemical characteristics of the ventromedial hypothalamus and anti-aversive effects of anxiolytic agents in various anxiety models] [Article in Russian]. Talalaenko AN, Pankrat'ev DV, Goncharenko NV.
7. Ukr Biokhim Zh. 1984 Nov-Dec;56(6):637-41. [Mg2+-ATPase activity of brain mitochondria fractions in chronic stress and its correction by psychotropic agents] [Article in Russian]. Kresiun VI.
8. Farmakol Toksikol. 1991 Sep-Oct;54(5):14-6. [The adequacy of a new method for assessing the vestibular protective effect of biologically active substances] [Article in Russian]. Karkishchenko NN, Dimitriadi NA.
Republished from Clayton South's Health Facts.
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