primaFORCE Phenibut can help support relaxation, restful sleep and feelings of well being

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Phenibut can help support relaxation, restful sleep patterns and feelings of well being PHENIBUT

Can help support relaxation, restful sleep and feelings of well being.

Support Relaxation
Support Restful Sleep
Support Feelings of Well Being

Phenibut Capsules
Tested for Potency & Purity
90 Capsules

RRP £25.99
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BUY TWO FOR £24.99

LAB TESTED FOR POTENCY AND PURITY

SUPPORT RELAXATION
SUPPORT RESTFUL SLEEP
SUPPORT FEELINGS OF WELL BEING

Primaforce Phenibut, lab tested for potency and purity, can help support relaxation, restful sleep and feelings of well being.

Supplement Facts
Serving Size: 1 Vegetarian Capsule
Servings Per Container: 90

Amount Per Serving
Phenibut (B-phenyl-y-Aminobutyric acid) 250 MG†

† Daily Value Not Established.

Suggested Use
As a dietary supplement, take 1-2 vegetarian capsules 2-4 times per day. For use as a sleep aid, consume 2-6 vegetarian capsules before bed. Start at the lower dose to assess tolerance. Do not take for more than 3 days in a row with out 2-3 day wash out.

Phenibut (beta-phenyl- gamma-aminobutyric acid, also spelled fenibut, originally known as phenigamma) is a derivative of the neurotransmitter GABA that crosses the blood-brain barrier [1]. It was developed in Russia, and there it has been used clinically since the 1960's for a range of purposes. Phenibut has both nootropic and anxiolytic (anxiety-reducing) properties, and it is commonly compared to diazepam (Valium), baclofen, and piracetam, and it has similarities to and differences from all of these substances.

Structurally, phenibut is similar to GABA, baclofen (p-Cl-phenibut), and beta-phenylethylamine (PEA). GABA is the primary inhibitory neurotransmitter in the brain. The addition of the phenyl ring to GABA allows the compound to more easily cross the blood-brain barrier, but also changes its activity profile [1-2]. Baclofen is a drug commonly used in studies on GABA(B) receptors, and also clinically used to treat severe spasticity of cerebral origin [3]. PEA is a naturally occuring biogenic amine which is similar in structure to amphetamine, and like amphetamine, it is a stimulant that causes the release of dopamine, and also promotes anxiety in high enough amounts.

Phenibut is a GABA receptor agonist and also causes the release of GABA. Similar to baclofen, phenibut is an agonist at GABA(B) receptors, although it does have some effect on GABA(A) receptors as well [2]. It is possible that phenibut has a higher activity at central GABA(B) receptors than peripheral ones [4]. The role of the GABA(B) receptor is not well-established, although research in the last seven years has significantly increased our understanding of this receptor. The most well-established role of GABA(B) receptors is inhibition of the release of some neurotransmitters, and it may also serve as a negative feedback mechanism for GABA release [5-6].

Because of the structural similarity to PEA, phenibut may share some similarities and differences with it. When phenibut is administered along with PEA, it antagonizes many of its effects, such as promotion of anxiety, promotion of seizures, and hyperthermia. This has lead some to postulate that antagonism of PEA, rather than the GABA-mimetic activity, may be the important mechanism of action for tha anxiolytic effect of phenibut [2, 7]. Phenibut also increases dopamine levels, and it has been postulated that the structural similarity to PEA may play a role in this effect [2].

There is one report in the literature of serotonergic effects of phenibut [8], but it does not look as though this has been followed up on.

Effects of phenibut

Anxiety reduction. Phenibut is effective in many animal models of anxiety phenibut has a mechanism of action similar to that of many drugs which are known to reduce anxiety in humans. Animal studies have compared the profile of phenibut to diazepam (Valium), which has pronounced anxiolytic properties, and piracetam, which has weak anxiolytic properties. One study found phenibut had a tranquilizing effect similar to, but weaker than diazepam. It also caused sedation and muscle relaxation (whereas piracetam did not), but again these effects were weaker than those caused by diazepam [2].

In Russia, phenibut is commonly used to treat many neuroses, including post-traumic stress disorder, stuttering, and insomnia. In double blind placebo-controlled studies, phenibut has reportedly been found to improve intellectual function, improve physical strength, and reduce fatigue in neurotic and psychotic patients [2].

Nootropic effects. Although phenibut does not meet all the requirements of a nootropic, it does have many similarities to piracetam. In mice, phenibut causes significant improvement on the passive avoidance test [2]. In this test of memory, animals are put in an undesirable area (such as a lighting situation or height from the floor that that species dislikes), and then given a negative stimulus (such as a shock) when they exit that area. Their ability to stay in the original area reflects how well they remember that if they exit it, they will receive the undesirable stimulus. Phenibut also improves performance on the swimming and rotarod tests and antagonizes the amnestic effect of chloramphenicol [2]. It also has an antihypoxic effect, a trait commonly seen among nootropics [17]. However, in one study, phenibut was ineffective in the water maze and shuttle box tests, while piracetam was [18]. Other research supports the idea that phenibut has nootropic activity similar to that of piracetam, but not as strong [19]. Nootropic activity has also been reported in humans [2], but it was not specified whether these were healthy adult humans, and they were probably elderly or psychiatric patients.

Another trait phenibut shares with nootropics is neuroprotection. Multiple animal studies have indicated that phenibut administration increases resistance to the detrimental effects of edema on mitochondria and energy production in the brain [20-22]. Phenibut also normalizes brain energy metabolism changes caused by chronic stress [23]. It was found to prevent changes in plasma electrolytes caused by cerebral injury [24]. Phenibut also protects dopaminergic neurons, and improved the condition of patients being treated with antiparkinsonic drugs [25].

Other effects. Phenibut has anticonvulsant activity against some drugs or conditions, but not others. It also potentiates the action of some other anticonvulsant drugs, and has been used to treat patients with epilepsy [2]. Phenibut has been reported to reduce motion sickness, and used in the treatment of alcohol and morphine withdrawal [2, 26]. One study indicated that phenibut increased resistance to heat stress and improved working capacity in humans [27].

Some studies indicate that phenibut has anti-arrhythmic properties in humans [28-29]. It also has other cardioprotective properties [30-31]. Finally, phenibut showed promise in experimental models of gastric lesions [32-33].

Tolerance develops to many of the effects of phenibut, although it is reported that it does not develop to the nootropic effect. The first signs of tolerance may be seen within as little as five days. For this reason, it is commonly used for one to two week periods, or dosage is increased by 25-30% after two weeks [2]. This makes phenibut ideal for short periods of stress or anxiety, but not ideal for chronic use. It is possible that taking only one dose daily may partially reduce the development of tolerance.

Phenibut ~ 90 Capsules

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1. CNS Drug Rev. 2001 Winter;7(4):471-81. Phenibut (beta-phenyl-GABA): a tranquilizer and nootropic drug. Lapin I.
2. Pavlov J Biol Sci. 1986 Oct-Dec;21(4):129-40. On neurotransmitter mechanisms of reinforcement and internal inhibition. Shulgina GI.
3. Curr Drug Target CNS Neurol Disord. 2003 Aug;2(4):248-59. GABA(B) receptors as potential therapeutic targets. Vacher CM, Bettler B.
4. Eur J Pharmacol. 1993 Mar 16;233(1):169-72. R-(-)-beta-phenyl-GABA is a full agonist at GABAB receptors in brain slices but a partial agonist in the ileum. Ong J, Kerr DI, Doolette DJ, Duke RK, Mewett KN, Allen RD, Johnston GA.
5. Am J Physiol Gastrointest Liver Physiol. 2001 Aug;281(2):G311-5. Receptors and transmission in the brain-gut axis: potential for novel therapies. IV. GABA(B) receptors in the brain-gastroesophageal axis. Blackshaw LA.
6. Prog Neurobiol. 1995 Jul;46(4):423-62. A physiological role for GABAB receptors and the effects of baclofen in the mammalian central nervous system. Misgeld U, Bijak M, Jarolimek W.
7. Farmakol Toksikol. 1985 Jul-Aug;48(4):50-4. [Differences and similarity in the interaction of fenibut, baclofen and diazepam with phenylethylamine] [Article in Russian]. Lapin IP.
8. Farmakol Toksikol. 1980 May-Jun;43(3):288-91. [Effect of structural analogs of gamma-aminobutyric acid on serotonin- and dopaminergic mechanisms] [Article in Russian]. Nurmand LB, Otter MIa, Vasar EE.
9. Pharmacol Biochem Behav. 1981;14 Suppl 1:53-9. Pharmaco-ethological analysis of social behaviour of isolated mice. Poshivalov VP.
10. Biull Eksp Biol Med. 1987 Nov;104(11):588-90. [Role of the GABAergic system in the mechanism of the stress-regulating action of phenibut] [Article in Russian]. Kovalev GV, Spasov AA, Bogachev NA, Petrianik VD, Ostrovskii OV.
11. Pharmacol Toxicol. 1990 Jan;66(1):41-4. Stress-protection action of beta-phenyl(GABA): involvement of central and peripheral type benzodiazepine binding sites. Rago L, Kiivet RA, Adojaan A, Harro J, Allikmets L.
12. 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.
13. 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.
14. 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.
15. Eksp Klin Farmakol. 2000 Jan-Feb;63(1):14-8. [The neurochemical profile of the caudate nucleus in the anxiolytic action of benzodiazepine and nonbenzodiazepine tranquilizers on different models of anxiety] [Article in Russian]. Talalaenko AN, Gordienko DV, Markova OP.
16. Ross Fiziol Zh Im I M Sechenova. 1997 Mar;83(3):88-94. [Neurochemical analysis of the amygdala basolateral nucleus of rats during anxiety tests] [Article in Russian] Talalaenko AN, Babii IuV, Perch NN, Vozdvigin SA, Panfilov VIu.
17. Biull Eksp Biol Med. 1984 Feb;97(2):170-2. [Nootropic properties of gamma-aminobutyric acid derivatives] [Article in Russian]. Ostrovskaia RU, Trofimov SS.
18. Farmakol Toksikol. 1984 Jan-Feb;47(1):20-3. [Comparative characteristics of the nootropic action of fenibut and fepiron] [Article in Russian]. Kovaleva EL.
19. Farmakol Toksikol. 1987 Jul-Aug;50(4):18-22. [Normalizing effect of GABA derivatives on late behavioral disorders occurring in rats with early postnatal suppression of protein synthesis] [Article in Russian]. Burov IuV, Ostrovskaia RU, Smol'nikova NM, Trofimov SS, Savchenko NM.
20. Eksp Klin Farmakol. 1994 Mar-Apr;57(2):13-6. [The effect of fenibut on the ultrastructure of the brain mitochondria in traumatic edema and swelling] [Article in Russian]. Novikov VE, Naperstnikov VV.
21. Farmakol Toksikol. 1991 Nov-Dec;54(6):44-6. [The effect of GABA-ergic agents on oxidative phosphorylation in the brain mitochondria in traumatic edema] [Article in Russian]. Novikov VE, Sharov A.
22. Farmakol Toksikol. 1984 May-Jun;47(3):35-8. [Effect of benzodiazepine and GABA derivatives on the energy metabolism indices in brain edema] [Article in Russian]. Novikov VE, Kozlov SN, Iasnetsov VS.
23. 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.
24. Eksp Klin Farmakol. 1992 May-Jun;55(3):70-2. [The effect of GABA-ergic agents on the blood electrolyte balance in acute craniocerebral trauma] [Article in Russian]. Novikov VE, Chemodurova LN.
25. Zh Nevropatol Psikhiatr Im S S Korsakova. 1986;86(8):1146-8. [Phenibut potentiation of the therapeutic action of antiparkinson agents] [Article in Russian]. Gol'dblat IuV, Lapin IP.
26. 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.
27. Eksp Klin Farmakol. 1997 Jan-Feb;60(1):68-71. [The enhancement of human thermal resistance by the single use of bemitil and fenibut] [Article in Russian]. Makarov VI, Tiurenkov IN, Klauchek SV, Nalivaiko IIu, Antipova AIu.
28. Kardiologiia. 1987 May;27(5):48-52. [Differential psychopharmacotherapy of heart rhythm disorders] [Article in Russian]. Skibitskii VV.
29. Ter Arkh. 1986;58(11):97-101. [Clinico-hemodynamic effects of psychotropic preparations and psychosomatic correlations in cardiac rhythm disorders] [Article in Russian]. Petrova TR, Skibitskii VV.
30. Farmakol Toksikol. 1983 May-Jun;46(3):41-4. [Effect of tranquilizers on myocardial function in stress injury] [Article in Russian]. Kovalev GV, Gurbanov KG, Tiurenkov IN.
31. Farmakol Toksikol. 1983 Jan-Feb;46(1):38-41. [Effect of tranquilizers on the course of myocardial ischemia and on myocardial resistance to hypoxia in coronary artery occlusion] [Article in Russian]. Kovalev GV, Gurbanov KG, Tiurenkov IN, Naidenov SI.
32. Patol Fiziol Eksp Ter. 1995 Jan-Mar;(1):21-3. [Central mechanisms of neurogenic gastric lesion and its pharmacologic correction] [Article in Russian]. Bul'on VV.
33. Biull Eksp Biol Med. 1990 Nov;110(11):504-6. [The effect of GABA-ergic agents on the development of a neurogenic stomach lesion in rats] [Article in Russian]. Bul'on VV, Zavodskaia IS, Khnychenko LK.
34. Farmakol Toksikol. 1989 Jul-Aug;52(4):37-9. [Effect of fenibut and seduxen on fetal development in the second half of pregnancy] [Article in Russian]. Filimonov VG, Sheveleva GA, Strel'chenko NV, Sizov PI, Iasnetsov VS.
35. Biull Eksp Biol Med. 1985 Jun;99(6):698-700. [Effect of fenibut on the GABA B receptors of the spinal motor neurons] [Article in Russian]. Abramets II, Komissarov IV.
36. 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.
37. Med Tr Prom Ekol. 1997;(5):35-8. [Experimental bases of the use of pharmacologic agents aimed at higher heat resistance of humans as means of individual protection] [Article in Russian]. Makarov VI, Tiurenkov IN, Klauchek SV, Nalivaiko IO, Antipova AIu.

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