What is GABA
Dr. Bieger Report: Gamma Amino-Butyric Acid (GABA): Neurotransmitter with an anxiety-relieving effect
Gamma-aminobutyric acid (GABA) is the main inhibitory neurotransmitter of the central nervous system. After glutamate, the most important excitatory neurotransmitter, the GABA concentration in the CNS is highest. Paradoxically, both GABA and glutamate are made from the same amino acid precursor. Glutamine is oxidized to glutamate by glutamate synthase, which is converted to GABA in GABA-ergic neurons by GAD (glutamate decarboxylase; GAD: cofactor vitamin B6). GABA cannot be synthesized directly from glutamine.
The outstanding importance of GABA as an inhibitory neurotransmitter was recognized as early as 1960. It has a modulating effect on numerous neuronal processes in the CNS, mostly directly antagonistic to the excitatory glutamate. 40% of all neuronal synapses are GABAerg. The majority of these GABA neurons are so-called "interneurons" that control the activity of other neurons. In addition, however, there are also effectoric GABAergic neurons projecting into the periphery. Primarily peripheral GABA neurons are also known today, especially in the enteral nervous system.
GABA acts via interneuronal synapses primarily by inhibiting the presynaptic release of excitatory neurotransmitters. Benzodiazepines and barbiturates have an accessory effect via the so-called GABA-A receptor and strengthen the GABA effect. Important GABA enhancers are the pregnane steroids, synthesized intracerebrally or imported through the blood-brain barrier. The sleep-promoting and sedating effect of oral progesterone is largely based on its GABA-A receptor affinity. When administered orally, it is even more effective in the liver or in the CNS itself, the main metabolite allo-pregnanolone.
The neurotransmitter serotonin, which stimulates the GABA synthesis and increases the GABA receptor affinity, is of particular importance for the effectiveness of GABA. If there is a serotonin deficiency, the effectiveness of GABA is also limited. Other GABA mimetics are theanine, taurine and rhodiola, which also attack the GABA receptor and increase the GABA effect. In addition, some, such as taurine, have a glutamate-antagonistic effect.
GABA has an anxiolytic, analgesic, relaxing, anticonvulsant and blood pressure stabilizing effect. In addition, GABA has a level that goes beyond serotonin and melatonin sleep-promoting effect. Very low GABA concentrations are found in severe disorders of the neurotransmitter network, high pressure, chronic pain, irritable colon, premenstrual syndrome, depression, epilepsy or schizophrenia.
Complications of the GABA deficiency are cravings for sugar / sweets, paresthesia, muscle tension, ringing in the ears (tinnitus), changed olfactory sensations, night sweats, hyperventilation, tachycardia, memory loss, impulsiveness, impatience, fears. Above all, the anti-anxiety effect of GABA is used clinically. However, since GABA itself cannot cross the blood-brain barrier, lipophilic GABA derivatives such as gabapentin, pregabalin, etc. are used and are considered first-line medication for generalized anxiety syndrome.
In addition to its neural effects, GABA has a variety of paracrine and endocrine functions. It acts centrally on the hypothalamic secretion of releasing factors, GABA-ergic neurons innervate the pituitary gland and GABA has a paracrine effect via the portal vein system on the pituitary production of prolactin, ACTH, TSH and LH. Above all, it stimulates growth hormone secretion via activation of the hypothalamic HGH-releasing hormone and immediately after synthesis in the pituitary gland. GABA is also produced locally in the pancreatic islet cells and modulates insulin secretion.
Finally, GABA has immunomodulatory effects. Via GABA receptors on T cells, GABA blocks the secretion of proinflammatory cytokines and inhibits T cell activation and proliferation.
There are several options for treating GABA deficits:
1. Treatment with the glutamate / GABA precursor glutamine, which is also extremely important for detoxifying the CNS. We use Glutamine in combination with the GABA modulators taurine and theanine and the GABA inducer 5HTP / serotonin in the preparation GABAmax, which is also responsible for neurotransmitter synthesis contains important enzyme cofactors from the B vitamin group, vitamin C and tocopherols, which have a glutamate-neutralizing effect. In addition, GABAmax contains a small amount of tyrosine as a catecholamine precursor, which better balances the inhibitory valences.
2. Treatment with Glutamine in combination with glycine, the smallest amino acid that also functions as a neurotransmitter in some brain regions and has a predominantly GABA-like effect. Glutamine / GABA and glycine work synergistically to promote sleep, relax and pave the way for the nocturnal regeneration of the endocrine system. In the preparation GABAnight are glutamine and glycine combined with 5HTP / serotonin, the modulators taurine, choline and passion flower as well as the enzyme cofactors from the B vitamin series.
3. GABA itself When administered orally, it is due to a blockage by the blood-brain barrier only marginal central effectsHowever, its peripheral effects on endocrine organs and the immune system are not impaired - provided they are caused by paracrine GABA. In these cases, if the GABA effect on the adrenal gland, pituitary gland, islet organ and the metabolism is to be used, GABA itself is used in doses of 500 - 2000 mg daily used.
4. Limited central effects from GABA even with a modified, sublingual preparation GABAcalm can be achieved, which can reach the brain via the oral mucosa "on secondary routes". Due to its quick effect, which starts within minutes, it is suitable for the immediate treatment of anxiety states and has proven itself many times. In addition, the effectiveness of GABAtropen preparations can be tested in advance with GABAcalm.
5. Eventually exist lipophilic GABA derivatives such as the preparation Kavinace, which contains GABA coupled to niacin, as a highly effective GABA variant. However, due to the strong induction of degradation enzymes, its duration of action is limited to 10-14 days. However, after a break in treatment of a few days, it is fully effective again.
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