| Dietary sources | |
| GABA is an inhibitory neurotransmitter that can be formed from glutamic acid. Many protein foods contain glutamic acid, but GABA is only present in traces in the diet. | |
| Physiological effects | |
| Nervous system |
|
| Pancreas |
|
| GABA metabolism |
| Gamma-aminobutyric acid (GABA) is the most important central inhibitory neurotransmitter in the brain. It is synthesized endogenously from the amino acid glutamic acid and from ammonia with the help of the vitamin B6-dependent enzyme glutamate decarboxylase (1). GABA is partly transported into neighboring glial cells. There it is converted to glutamine by GABA transaminase, which can returned to the presynaptic cell if required and converted to glutamate (glutamine cycle). |
| The function of GABA in nerve tissue |
| GABA binds to different specific receptors on the membranes of nerve cells. The GABAA receptor is ionotropic. When GABA opens the chloride ion channel in the cell membrane, which leads to an increased influx of chloride ions into the cell. The increase of the intracellular chloride concentration triggers and inhibitory signal which leads to a reduced excitability of the cell through hyperpolarization. The GABAB receptor has a metabotropic effect. GABA docking increase opening of the potassium channels and reduces the opening of the calcium channels. This also leads to hyperpolarization of the cell membrane, which inhibits the presynaptic release of the transmitter. |
| Calculating effect of GABA |
| GABA has a calming and smoothing effect on the nerves. Other calming pharmacologically active substances such as Valium and other benzodiazepine-containing drugs have an effect by stimulating the formation of GABA in the brain. GABA also seems to play an important role in the development of the nervous system in the growing organism. For example, an additional supply of GABA in young rats can increase the concentration of growth hormone in the plasma and thus intensify protein synthesis in the brain (2). In addition, the GABAB receptor can also have a stimulating effect in the young organism, which is important for the development of neurons (3). Various clinical patterns are associated with a malfunction of GABA metabolism. Insufficient GABA homeostasis, especially during neuron formation, can lead to anxiety and anxiety disorders (4). GABAA-receptor dysfunction is discussed as a possible cause of epilepsy (5). |
| GABA and diabetic neuropathies |
| The possible applications of GABA in diabetes mellitus concern two independent body systems in which the GABA mechanism of action shows different results. On the one hand the peripheral nervous system and associated diabetic neuropathies, on the other hand the pancreas and associated production of insulin. The GABA analogues pregabalin or gabapentin have long been successfully used for the treatment of pain and diabetic neuropathies (6). GABA appears to be able to influence pain in neuropathies by modulating the nerve stimuli in the region of the spinal ganglia (7). Therefore, GABA substitution is a serious therapeutic alternative in the treatment of neuropathies and in pain therapy. |
| Possible pancreatic secretion by GABA |
| GABA is found in all tissues of endocrine organs and plays a role in the pathophysiology of hormone-related diseases (8). Recent studies have shown that GABA can also stimulate DNA synthesis in the endocrine tissue of the pancreas, thereby stimulating the activity, new formation and growth of insulin-producing islet cells (9). The increase in GABA concentration in the hypothalamus, observed in animal experiments, suggests that pancreatic regeneration processes may be related to higher-level regulatory mechanisms (10). GABA receptors are also involved in glucose homeostasis. A reduced number of receptors leads to a negative influence on glucose status (11). Presumably, the release of insulin is intensified by the Ca2+ ion currents in the insulin-producing cells (12). However, earlier studies have found conflicting results (13). |
| Parameter | Substrate | Reference value | Description |
| GABA | Urine | 1.0 - 9.7 nmol/g creatinine | 2.morning urine, acidified |
| Impact on | Symptoms |
| General well-being | Accelerated pulse, night sweating, impatience, craving for carbohydrates |
| Nervous system | Anxiety disorders Sleep disorders |
| Hormone system | Premenstrual Syndrome (PMS) |
| Effect | Indication | Dosage |
| Physiological effects at a low intake |
States of agitation, irritability, anxiety | 500 mg/d |
| Complementary treatment of neurological and neuropsychiatric diseases | 500 mg/d | |
| Complementary therapy for treatment of diabetic neuropathies | 500 mg/d | |
| Complemetary therapy for diabetes mellitus to improve insulin secretion | 500 mg/d | |
| General mode of administration | |
| When |
GABA should be taken outside of meal times. Notes:
|
| Side effects | |
| In rare cases, very high doses can lead to a harmless and temporary increase in heart rate, shortness of breath, tingling skin sensations or paradoxical effects (increase in anxiety). | |
| Contraindications | |
| Severe liver damage | |
| Drug or nutrient interactions | |
| None | No relevant interactions are known to date. |
| Description |
| Endogenous substances (gamma amino acid) |
| Related substances |
| Gamma-aminobutyric acid |
| References |
|
1) Gröber U: Orthomolekulare Medizin. 2002. |
