The brain transfers signals by way of neurons sending impulses to one another through a network of junctions or gaps between nerve cells called synapses. GABA acts as an inhibitor of such impulses within the synapses of the human brain and spinal cord, effectively creating a ‘calming effect' by preventing the overstimulation of the brain. The mechanism of action by which this is achieved depends on the binding of GABA to specific trans-membrane receptors within the plasma membrane of the neurons themselves, inhibiting both their pre- and post-synaptic impact.

Research with GABA supplementation has focused on addressing conditions of anxiety, growth hormone deficiency, depression, epilepsy, and various other disorders of the central nervous system. In the early 1980's, researchers believed that manipulating GABA receptors could alleviate the symptoms of anxiety, and supplementation with GABA itself was one such form of manipulation. This conclusion has since been strengthened by numerous studies confirming a direct correlation between major depressive disorder (MDD) and significantly decreased GABA concentrations in the occipital cortex of MDD subjects. This well-established correlation has led to the use of supplemental GABA as a means of addressing not only the symptoms of anxiety, but also of depression, premenstrual dysphoric disorder and manic-depressive (bipolar affective) disorder. The strategy is relatively straightforward; GABA inhibits the production of excitatory impulses from reaching the brain, including those that enhance panic, alarm, and/or fear. Anti-anxiety drugs such as benzodiazepine that are normally prescribed for such conditions can become addictive, a risk that is non-existent with GABA supplementation. Indeed, some research even supports using GABA to facilitate withdrawal from benzodiazepine medications.

In addition to mood disorders, GABA research has also been applied to the study of epilepsy, particularly in regard to how GABA supplementation can reduce the frequency and intensity of seizures. GABA is the major inhibitory neurotransmitter in the brain, and anticonvulsant drugs for the treatment of epileptic seizures are designed to enhance endogenous GABA levels (i.e. Vigabatrin) or mimic its effects (i.e. Gabapentin). This emphasis on maintaining high levels of GABA has once again led to the formularized justification of GABA supplementation, this time to offset epileptic seizures.

Finally, researchers have long believed that GABA can alleviate the symptoms of insomnia due to its ability to generate calm (via its inhibition of excitatory neural impulses) and thus induce sleep. The increase of plasma growth hormone (which also rises naturally during sleep) is yet another capability that has been attributed to exogenous GABA supplementation. This capability has made GABA a relative staple of the life-extensionist movement, which is always concerned with halting and/or reversing the inverse relationship between age and growth hormone levels. Research to support this exists in both human and animal studies, with one trial showing that a single 5-gram oral dose can raise growth hormone levels by as much as 550% within 90 minutes of ingestion. Elevated growth hormone levels play an important role in the prevention of a multitude of age-related conditions, including sarcopenia, metabolic syndrome, osteoporosis, and an overall impaired quality of life.

References:

Enna SJ, et al. Role of Gamma-aminobutyric Acid in Anxiety. Psychopathology. 1984;17(Suppl1):15-24.

Sanacora G, Gueorguieva R, Epperson CN, et al. Subtype-specific alterations of gamma-aminobutyric acid and glutamate in patients with major depression. Arch Gen Psychiatry. Jul2004;61(7):705-13.

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). Feb1980;93(2):149-54.

Treiman DM. Gabaergic mechanisms in epilepsy. Epilepsia. 2001;42(Suppl3):8-12.

Braverman ER, et al. The Healing Nutrients Within. New Canaan,CT: Keats Publishing, Inc; 1997:257-58.

Gamma-aminobutyric acid, Monograph. Altern Med Rev. 2007 Sep;12(3):274-9.