AOR GABA is a neurotransmitter that inhibits the activity of excitatory neuronal impulses to prevent the overstimulation of the brain. GABA has been referred to as the brain's natural calming agent, inducing relaxation and reducing anxiety.
| EN
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Product Code
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Size
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Weight Per Capsule
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Vegetarian
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| 144963
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AOR01400
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60 Vegi-Caps
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600 mg
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100% Vegetarian
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| Supplement Facts
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| Serving Size: 1 Capsule
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Amount Per Serving
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| Gamma Amino Butyric Acid
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600mg
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| Non-medicinal ingredients: Capsule; hypromellose, water.
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AOR guarantees that
no ingredients not listed on the label have been added to AOR GABA.
AOR GABA contains no wheat, gluten, corn, nuts, dairy, soy, eggs, fish, shellfish
or any animal byproducts.
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 of AOR GABA
Pharmaceutical synthesis
Cautions:
None Known
Pregnancy/Nursing:
Do not use AOR GABA if pregnant or nursing
GABA, or Gamma-aminobutyric Acid, is a non-essential amino acid
that is generally classified as a neurotransmitter. GABA is not found in
significant amounts in food. Its status as an amino acid stems from the
fact that it is a by-product of the decarboxylation of glutamic acid by
vitamin B6. GABA's neurotransmitter status has been sub-categorized to
define it as an inhibitory neurotransmitter.
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.
Role of Gamma-aminobutyric Acid in Anxiety.
Psychopathology. 1984;17(Suppl1):15-24.
Enna SJ.
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.