Chill with GABA

GABA (gamma-aminobutyric acid) is an amino acid that is the primary inhibitory neurotransmitter in the brain. Think of it as the “brakes” that keep the brain from getting overactive. For optimal functioning, the brain must balance the excitatory and inhibitory influences: excessive excitation can lead to seizures, insomnia, anxiety, and many other clinical conditions; excessive inhibition of neurons can result in lack of coordination, sedation, and anesthesia. Under normal conditions, GABA is released when the brain’s activity level needs to be calmed down and is reabsorbed when an optimal activity level is reinstated.

How does GABA work in the brain?
Image credit goes to Dr. Carlo Carandang, https://www.youtube.com/watch?v=M_QQD9NdJcU

GABA cell receptors are located on the cell surfaces of almost every region of the brain and especially on the hypothalamus, the pituitary gland, and the amygdala. They are like satellite dishes that allow only certain molecules to attach to them. Several types of molecules are allowed to attach to them, including: actual GABA neurotransmitters (molecules that travel from one nerve cell/neuron to another and are released by the body); and other molecules (benzodiazepines, barbiturates, alcohol, GABA supplements, and others) that have been externally introduced.

GABA nerve cells (neurons) connect with nerve cells on an organ across a synapse. In the image here, a GABA neuron is connected to a nerve call on the surface of the amygdala (the fear center of the brain). A synapse is the space between nerve cells where neurotransmitters mediate the transmission of nerve impulses that either facilitate or inhibit electrical impulses in the target cell. The purpose of a release of GABA neurotransmitter molecules in the brain is for those molecules to attach to GABA receptors and inhibit (stop, calm down) electrical impulses in the target cells. In this case, for example, calming electrical impulses to nerve cells on the amygdala quiets anxiety.

Under normal circumstances, GABA neurotransmitters are released and act through the cell receptors to quiet the brain activity to an optimal level. This occurs because the binding of the GABA neurotransmitter to the GABA receptor causes a channel to open up to the nucleus/inside of the cell. Chloride ions from the fluid around the cell flow into the channel and inhibit electrical activity inside the cell. When the cell activity is sufficiently calmed, the GABA molecules are then reabsorbed back into the GABA nerve cell by a reuptake pump mechanism so that they can be recycled.

GABA’s high concentration in the hypothalamus suggests it also plays a significant role in hypothalamic-pituitary function. The hypothalamus is a region of the posterior section of the brain that is the regulating center for visceral (instinctive) functions such as sleep cycles, body temperature, and the activity of the pituitary gland. The pituitary gland is the master endocrine gland affecting all hormone functions of the body.

The keys to an optimal level of brain activity, therefore, are (1) sufficient GABA released into the synapse, (2) GABA cell receptors that are in good working order and channels that open up to let the chloride ions in, and (3) a properly working reuptake pump system to receive the GABA neurotransmitters when GABA’s work is done.

What happens when non-GABA molecules attach to GABA receptors?

GABAA receptors allow other molecules to bind to them besides naturally generated GABA neurotransmitters.

  • Benzodiazapines – cannot work without the presence of at least some natural GABA; work to stimulate the activity of GABA (examples of benzodiazapines are Xanax, Valium, Klonapin, Neurontin); not advised for long-term continued use because of potential for addiction/dependency, especially in the elderly. Their sites are on the outside of the receptor facing the synapse.
  • Barbiturates – drugs that act as central nervous system depressants and cause prolonged opening of the chloride ion channel to the nucleus of the cell without the presence of GABA; heightened risk of addiction and no known antidote, but necessary for certain surgeries and to control seizures. Their sites are on the inside of the ion channel close to the top of the channel.
  • Neuroactive Steroids – Endogenous (made by the body) steroid actions on GABAA receptors may underlie important effects on mood and behavior. Exogenous (made outside the body) neuroactive steroids have potential as anesthetics, anticonvulsants, and neuroprotectants. (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2047817/). Their sites are on the inside of the ion channel below those for the barbiturates.
  • Picrotoxins – Toxic plant substance, used mostly in research. Their sites are inside the ion channel toward the cell nucleus.
  • Alcohol – alcohol mimics the effect of GABA, so the effect when they are both present is much stronger than when either is present by itself; excessive alcohol consumption can lead to desensitization of GABA receptors and the person’s need to drink more and more for the same effect; this also explains why withdrawal from alcohol can sometime leads to significant symptoms (https://www.therecoveryvillage.com/alcohol-abuse/faq/alcohol-and-gaba/). Their sites are inside the ion channel.
  • GABA supplements – mimic the activity of a benzodiazepine on a GABA receptor; they are the ONLY outside substances that can actually add GABA to the body.

What happens when GABA isn’t reabsorbed after its natural calming activity has been completed?

The natural cycle is the GABA neurotransmitters are reabsorbed when their work is complete. If they are not, the concentration of GABA in the synapse increases, leading to more GABA receptors with open chloride ion channels and an even greater decrease in electrical activity in the brain. This can be done artificially by the introduction of certain drugs and oral supplements (GABA Reuptake Inhibitors, GRIs). GRIs may be used in the clinical treatment of seizures, convulsions, or epilepsy as anticonvulsants/antiepileptics, anxiety disorders such as generalized anxiety disorder (GAD), social phobia (SP) also known as social anxiety disorder (SAD), and panic disorder (PD) as anxiolytics, insomnia as hypnotics, muscle tremors or spasms as muscle relaxants, and chronic pain as analgesics. They may also potentially be used as anesthetics in surgery. For a list of common GRIs, go to:
https://mentalhealthdaily.com/2014/12/02/gaba-reuptake-inhibitors-list/

What happens when natural GABA is not present in sufficient quantities or is not present at all?

Low GABA levels have been found in cases of panic, anxiety, depression, alcoholism, and bipolar disorders and in the brains of patients with multiple sclerosis, action tremors, tardive dyskinesia, & other disorders of movement. Causes may include: inadequate diet, prolonged stress, and genetics.

Even if GABA levels are sufficient, GABA receptor function may be reduced because of a genetic polymorphism in the GABA receptor that reduces the efficiency of GABA neurotransmission, the presence of GABA receptor inhibitors, or low serotonin levels. Serotonin is a positive regulator of GABA-GABA receptor interaction.
https://www.integrativepsychiatry.net/natural_gaba.html

As mentioned earlier, insufficient GABA leads to hyperactivity in the brain. Benzodiazapines cannot work if there is no GABA present.

What are good foods to eat to increase natural GABA availability in the brain?

Foods with the highest GABA content, according to a May 2018 review published in Nutrients, include:

  • Cruciferous vegetables (broccoli, cabbage, cauliflower, Brussels sprouts)
  • Soy beans
  • Adzuki beans
  • Mushrooms
  • Spinach
  • Tomatoes
  • Buckwheat
  • Peas
  • Chestnuts
  • Sweet potatoes
  • Sprouted grains
  • Rice (specifically brown rice)
  • White tea

Note: Not all of these foods are recommended for all blood types. Wellness Made Simple can help you to determine which are best for your personal diet.

Certain bacterial strains found in your gut, Lactobacillus and Bifidobacterium, produce GABA and may increase the neurotransmitter in your enteric nervous system, which may increase concentration of the neurotransmitter in the cerebrospinal fluid, report the authors of this review in Frontiers in Psychology: https://www.frontiersin.org/articles/10.3389/fpsyg.2015.01520/full

How much GABA is safe to take as a supplement?

According to https://www.livestrong.com/article/548115-the-maximum-dosage-of-gaba/, there is no safe dosage amount established for GABA in the treatment of anxiety, but doctors generally recommend 500 to 750 mg per day, starting as low as 100-200 mg and working up as needed. An excessive level of GABA in the bloodstream can cause the exact symptoms you are trying to quell. This is one of the most common side effects. Called a “paradoxical reaction” by doctors, too much of the amino acid can lead to patients feeling edgy, anxious, and it may even lead to insomnia. Most experts advise taking a small dose of GABA at first, to see how your body chemistry reacts to it, before moving up to a clinical dosage.
https://www.livestrong.com/article/63549-side-effects-much-gaba/

Is there a safe, effective supplement that includes GABA?

While there are many GABA supplements on the market, Wellness Made Simple can suggest doTERRA’s Adaptiv Calming Blend© capsules for home use. Each capsule is one serving and contains 100 mg of GABA plus an essential oil blend of Lavender flower/leaf/stem oil, Coriander seed oil, Wild Orange peel oil, and Fennel seed oil, Ahiflower seed oil, and Sceletium aerial parts extract, all known for their calming properties. For more information for yourself and your healthcare provider on this cutting edge supplement, go to:
https://media.doterra.com/us/en/pips/doterra-adaptiv-essential-oil-blend-capsules.pdf

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