What Is It?
And Where Does It Come From?
Phenibut (beta-phenyl-gamma-aminobutyric acid) 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.
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What Does It Do?
And What Scientific Studies Give Evidence To Support This?
Phenibut has a long history of clinical use in Russia. It has been used to help reduce stress, relieve tension, prevent anxiety, improve sleep, as well as potentate pre and post-operative medications.2 Psychiatrists frequently use phenibut in the treatment of psychiatric and psychological disorders such as depression, PTSD (post-traumatic stress disorder) and stuttering.3
Phenibut is effective as a psychiatric treatment method because it helps to elevate mood, relieve anxiety4,5,6 enhance thinking abilities, protect the brain from stress7 and induce sleep and relaxation. In fact, phenibut has proven so effective at treating psychiatric and psychological disorders that its effectiveness has been compared to diazepam.
Phenibut has apparent anti-addictive properties as well. Clinical research has demonstrated that smokers going through withdrawal find it easier to cope when supplementing with phenibut.8 Smokers report that the relaxation they experience as a result of taking phenibut helps them to avoid the anxiety that can come from an urge to relapse.
Because phenibut can induce mild relaxation (as a derivative of GABA) it has found wide use amongst the athletic community. Phenibut acts on some (but not all) GABA receptors, and this mild agonist effect is responsible for the relaxation that it can induce.
Who Needs It?
And What Are Some Symptoms Of Deficiency?
All persons can benefit from phenibut supplementation due to its ability to induce relaxation and improve mental function. Phenibut supplementation may be especially efficacious for athletes and people living hectic, stress filled lifestyles.
No symptoms of deficiency exist.
How Much Should Be Taken?
And Are There Any Side Effects?
Strictly adhere to label recommendations.
Tolerance is a side effect of chronic administration. Tolerance is a phenomenon whereby the body either:
- Down regulates the endogenous production of a substance in response to elevated levels arising from exogenous introductions.Or
- Reduces the affinity of its receptor sites to a ligand of exogenous origin
With respect to the chronic administration of phenibut, the body down regulates the affinity of its receptors to phenibut. This will result in a decrease of phenibuts efficiency over time. This will require increasingly larger doses to be administered to maintain the original effects seen with the first dosage.
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.
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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.