Summary of GABA
Primary Information, Benefits, Effects, and Important Facts
GABA is the most potent depressive neuroamine in human brains. It regulates many of the depressive and sedative actions in brain tissue and is critical for relaxation.
GABA is a highly regulated compound in vivo (in living), and is able to balance itself out in body tissues due to a myriad of factors.
Due to these regulation factors, GABA as a supplement does not exert many depressive effects on its own. The human body is too adept at regulation, and orally ingested GABA cannot alter human physiology to much of a degree.
GABA, however, is a target for many other compounds that can act vicariously (in a multitude of ways) to increase GABA levels, which ultimately causes depressive effects.
Things To Know & Note
GABA is a depressive neurotransmitter, but supplementation with GABA does not seem to exert depressive effects unless overdosed to an inadvisable level.
How to Take GABA
Recommended dosage, active amounts, other details
Supplemental GABA has been used in humans (for the purpose of enhancing growth hormone metabolism) in the dosage range of 3,000-5,000mg GABA. It is unsure if this is the optimal dosage.
Scientific Research on GABA
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GABA (Gamma-Aminobutyric Acid) is one of the more potent depressive neuroactive peptides in human brain tissue. It is involved in a wide range of suppressive and depressive activities intimate with the parasympathetic nervous system (PNS). It is synthesized directly from the excitatory neurotransmitter glutamate via the enzyme glutamate decarboxylase and can be reverse transformed to glutamate via the tricarboxylic acid cycle.
It appears that changes in brain GABA concentrations and systemic GABA concentrations can be reflective of each other, and that changes in one of these markers induces changes in the other.
Its uptake into the brain is high at nonphysiologically low levels and has low uptake rates at higher nonphysiological concentrations. This phenomenon is caused by GABA being a self-inhibitor of its transport into the brain, able to block its own transport in doses above what is normal. By this mechanism, neurological GABA levels stay constant.
Self-inhibition of GABA cannot stop all transport into the brain, and the highest recorded value of inhibition has been 80%. Therefore superloading GABA might be able to overcome self-inhibition by passive diffusion.
In cases of supraphysiological GABA levels in the brain, the brain is able to eject excess GABA. The blood brain barrier's efflux rate for GABA is approximately 16 times as potent as the uptake rate, and is activated during periods of excessive GABA concentrations in neurological tissue as to prevent excessive depressive effects.
In adults, GABA in systemic circulation seems to have very minimal uptake rates into brain tissue. Youth seem to have greater blood brain barrier (BBB) permeability. It appears to suppress its own entry across the blood brain barrier when in systemic excess, and shares this ability with beta-alanine, although GABA was more potent in this regard.
Nitric oxide (NO) seems to be able to increase blood brain barrier permeability to GABA significantly.
It was initially thought that GABA ingestion increases Growth Hormone secretion, although this is true to a degree earlier studies have clarified 'Growth Hormone' into a more specific subset of analogues. Immunoreactive Growth hormone (irGH) and Immunofunctional Growth Hormone (ifGH) are two analogues which appear to be elevated in vivo after oral administration of GABA.
Despite GABAs inefficacy in passing the BBB, it appears to induce these changes via neurological means, more specifically a reaction which is mediated via dopamine release at a suprapituitary level.
GABAs influence on GH secretion seems to be changed with resistance exercise. A greater overall area-under-curve and higher peak values are noted with the pairing. Interestingly, the peak value with exercise occurs 30 minutes after ingestion yet 75 minutes during rest. These augmenting effects may be due to exercise-induced NO potentiating GABA entry into the brain, as alluded to in the previous section.
Although it was not concluded in the previous study that the effects of GABA on growth hormone were direct (as hepatic biotransformation of GABA to other amines is a possibility), the researchers suspect it may be so.
It should be noted that Growth Hormone exists in over 100 different isoforms, and that irGH and ifGH may not exert the same benefits typically associated with the most common (22kDa) isoform of Growth Hormone.
- Petroff OA. GABA and glutamate in the human brain. Neuroscientist. (2002)
- GABA in plasma and cerebrospinal fluid of different species. Effects of γ-acetylenic GABA, γ-vinyl GABA and sodium valproate.
- Transport of GABA at the Blood-CSF Interface.
- Al-Sarraf H. Transport of 14C-gamma-aminobutyric acid into brain, cerebrospinal fluid and choroid plexus in neonatal and adult rats. Brain Res Dev Brain Res. (2002)
- Efflux of a suppressive neurotransmitter, GABA, across the blood–brain barrier.
- Blood-brain barrier to H3-γ-aminobutyric acid in normal and amino oxyacetic acid-treated animals.
- Shyamaladevi N, et al. Evidence that nitric oxide production increases gamma-amino butyric acid permeability of blood-brain barrier. Brain Res Bull. (2002)
- Cavagnini F, et al. Effect of acute and repeated administration of gamma aminobutyric acid (GABA) on growth hormone and prolactin secretion in man. Acta Endocrinol (Copenh). (1980)
- Cavagnini F, et al. Effect of gamma-aminobutyric acid on growth hormone and prolactin secretion in man: influence of pimozide and domperidone. J Clin Endocrinol Metab. (1980)
- Powers ME, et al. Growth hormone isoform responses to GABA ingestion at rest and after exercise. Med Sci Sports Exerc. (2008)
- Nindl BC, et al. Growth hormone molecular heterogeneity and exercise. Exerc Sport Sci Rev. (2003)
- De Palo EF, et al. Growth hormone isoforms, segments/fragments: does a link exist with multifunctionality. Clin Chim Acta. (2006)