Suggested Use
Take one to two capsules daily without food, or as directed by a qualified health practitioner. Do not use if pregnant or nursing.

Main Applications
• Anxiety
• Insomnia
• Mood Disorders
• Epilepsy

Source
Pharmaceutical synthesis

Cautions:
None Known

Pregnancy/Nursing:
Do not use if pregnant or nursing

*These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease.

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.

The development of anxioselective agents has made it possible to examine the biochemical basis of anxiety. Electrophysiological analysis revealed that benzodiazepines selectively enhance gamma-aminobutyric acid (GABA) neurotransmission. Subsequent work demonstrated the presence of a specific population of benzodiazepine binding sites on neuronal membranes. These sites appear to be linked to certain GABA receptors such that occupation of the benzodiazepine component reveals a group of GABA recognition sites that may be more sensitive to the neurotransmitter. These data, coupled with the findings that barbiturates may act, at least in part, by interacting with the GABA receptor-coupled chloride channel, suggest that pharmacological manipulations of the GABA system can alleviate the symptoms of anxiety. The anxioselectivity of the benzodiazepines may be related to the fact that they activate only a certain population of GABA receptors, whereas barbiturates can potentiate the majority of these sites. These discoveries point to the possibility that alterations in the GABA system may partially explain the neurochemical basis of anxiety.

Subtype-specific alterations of gamma-aminobutyric acid and glutamate in patients with major depression.
Arch Gen Psychiatry. Jul2004;61(7):705-13.
Sanacora G, Gueorguieva R, Epperson CN, Wu YT, Appel M, Rothman DL, Krystal JH, Mason GF.

BACKGROUND: Measurement of cortical gamma-aminobutyric acid (GABA) and glutamate concentrations is possible using proton magnetic resonance spectroscopy. An initial report, using this technique, suggested that occipital cortex GABA concentrations are reduced in patients with major depressive disorder (MDD) relative to healthy comparison subjects. OBJECTIVES: To replicate the GABA findings in a larger sample of MDD patients, to examine the clinical correlates of the GABA reductions in these subjects, and to examine other critical metabolite levels. DESIGN: Study for association. SETTING: Academic clinical research program. PARTICIPANTS: The GABA measurements were made on 38 healthy control subjects and 33 depressed subjects. INTERVENTIONS: Occipital cortex metabolite levels were measured using proton magnetic resonance spectroscopy. MAIN OUTCOME MEASURES: The levels of occipital cortex GABA, glutamate, N-acetylaspartate, aspartate, creatine, and choline-containing compounds, along with several measures of tissue composition, were compared between the 2 groups. RESULTS: Depressed subjects had significantly lower occipital cortex GABA concentrations compared with healthy controls (P =.01). In addition, mean glutamate levels were significantly increased in depressed subjects compared with healthy controls (P<.001). Significant reductions in the percentage of solid tissue (P =.009) and the percentage of white matter (P =.04) in the voxel were also observed. An examination of a combined database including subjects from the original study suggests that GABA and glutamate concentrations differ among MDD subtypes. CONCLUSIONS: The study replicates the findings of decreased GABA concentrations in the occipital cortex of subjects with MDD. It also demonstrates that there is a change in the ratio of excitatory-inhibitory neurotransmitter levels in the cortex of depressed subjects that may be related to altered brain function. Last, the combined data set suggests that magnetic resonance spectroscopy GABA measures may serve as a biological marker for a subtype of MDD.

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.
Cavagnini F, Invitti C, Pinto M, Maraschini C, Di Landro A, Dubini A, Marelli A

A single oral dose of 5 g gamma aminobutyric acid (GABA) was given to 19 subjects and serial venous blood samples were obtained before and 3 h after drug administration. A placebo was administered to 18 sbjects who served as controls. GABA caused a significant elevation of plasma growth hormone levels (P less than 0.001), but did not consistently alter plasma prolactin concentration since only 5 out of 15 subjects showed an increase of the hormone. Eight additional subjects were submitted to an insulin tolerance test before and after per os administration of 18 g GABA daily for 4 days. Protracted GABA treatment significantly blunted the response of growth hormone and enhanced that of prolactin to insulin hypoglycaemia (P less than 0.01). These results indicate that pharmacological doses of GABA affect growth hormone and prolactin secretion in man. The precise nature of GABA's effects as well as its mechanism of action remains to be clarified.

GABA(A) Receptors in the Lateral Hypothalamus as mediators of satiety and body weight regulation
Brain Res. 2009 Jan 20. [Epub ahead of print]
Turenius CI, Htut MM, Prodon DA, Ebersole PL, Ngo PT, Lara RN, Wilczynski JL, Stanley BG.

In the lateral hypothalamus (LH), the inhibitory amino acid neurotransmitter, GABA, has had a long-standing presumptive role as an inhibitor of food intake. However, minimal investigation has been focused on GABA, especially as compared to the attention received by many peptide transmitters. To begin to address this deficiency in the understanding of the role of GABA in the LH and feeding, we report that antagonism of GABA(A) receptors in the rat LH elicits feeding, consistent with previous findings, and provide evidence for the behavioral selectivity of this effect. We extend previous findings that activation of LH GABA(A) receptors suppresses feeding, in particular by showing that nighttime and deprivation-induced eating are dramatically suppressed. Finally, we show that chronic activation, but not blockade, of the LH GABA(A) receptors leads to a reduction in 24h food intake with concomitant body weight loss. These data collectively suggest that activation of GABA(A) receptors plays a fundamental role in controlling food intake and body weight, a role that has previously been somewhat underestimated.