Alcohol and GABA Receptors: Interactions, Effects & Withdrawal

The relationship between GABA and alcohol is intricate.

GABA (gamma amino-butyric acid) is an amino acid. Unlike most other aminos though, it is not used primarily for protein synthesis.

Instead, it serves largely as a neurotransmitter in the brain and central nervous system (CNS). More specifically, GABA is the primary inhibitory neurotransmitter in the body.

It is responsible for regulating sedative and calming effects and balancing the effects of various excitatory neurotransmitters, like Glutamate and Adrenaline.

GABA and alcohol have some similar effects on the brain, with alcohol serving as an indirect agonist of GABA receptors. Alcohol binds to a subset of GABA receptor sites in the brain and mimics the effects of this neurotransmitter.

This results in the characteristic inhibitory effects of GABA and suppresses the effects of glutamate, the brain’s most important excitatory neurotransmitter.

By agonizing GABA receptors and inhibiting glutamate, alcohol induces multiple depressive effects on the brain and CNS. However, because of this it is important not to combine GABA and alcohol due to the risk of interactions.

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GABA and Alcohol

Besides suppressing Glutamate and activating the sub-type of GABA-B receptors, alcohol also causes increased amounts of Serotonin and Dopamine to be released in the brain.

Even small amounts of alcohol will increase Serotonin and Dopamine concentrations within the brain’s nucleus accumbens (one of the brain’s reward centers).

The result of these effects on the nucleus accumbens and in the amygdala create feelings of pleasure when small amounts of alcohol are consumed.

Both depressive and excitatory components of the reward system are activated by alcohol.

In the short term, the neurochemical effects of Glutamate, GABA, and alcohol combine to cause various states of euphoria – from getting a weak buzz, to laughing, to being boisterous, to the loosening of inhibitions, to having slower reaction times.

While low levels of alcohol consumption may not be problematic, drinking too much can cause excess sedation of the Central Nervous System by over-stimulating GABA pathways.

Past a certain point, which is dependent on each individual, this can develop into a state of alcohol toxicity leading to adverse physical and mental states. This will be especially exacerbated if taking alcohol in conjunction with GABA supplements or drugs that work on GABAergic pathways in the brain.

For example, anti-anxiety drugs like benzodiazepines or the herbal supplement Lemon Balm are also known to stimulate GABA receptors in the brain and are contraindicated with alcohol use.

GABA’s Role in Alcohol Addiction

Over time, with continued drinking, tolerance to alcohol’s effects may develop. GABA receptors can become desensitized to the effects of alcohol and other GABA agonists. This can result in increased stress levels, which may lead to a desire to drink larger and larger quantities of alcohol.

Increases in tolerance to alcohol lead to overdrinking. Habitual overdrinking may lead to the drinker’s inability to control his need for alcohol; possible leading to alcohol dependence.

Essentially, the body becomes used to increased states of GABA stimulation and when the agonist (alcohol) is not present, the body feels a higher levels of stress and excitatory stimulation from the effects of Glutamate. Dependence causes the individual to drink more regularly, in greater quantities, to achieve the same results.

If alcohol is again removed from the system, the result is serious withdrawal symptoms. In very serious cases, withdrawal from alcohol can cause death due to over-stimulation and the inability of GABA to regulate neurotransmission in the brain.

In addition to this, chronic overdrinking can lead to the onset of numerous adverse health conditions and diseases.

GABA and Stress in the Brain

Interactions between glutamate, GABA and alcohol can activate the brain’s stress defence systems.

When the amygdala and other related areas of the brain detect alcohol toxicity, they initiate synthesis and secretion of CRF (corticotropin-releasing factor).

CRF subsequently stimulates certain behavioral and sympathetic responses to the stress. The normal, logical response of CRF to such stress would be to call on the brain to adapt to the stress.

However, alcohol acutely reduces CRF. Over time, the CRF system and the brain’s stress management mechanisms become more tolerant of alcohol.

As CRF persists at unnecessarily high levels over time, neurotransmission effectiveness in the brain’s reward centers diminishes. In alcoholics, these effects become even more pronounced and may result in downregulation of neurotransmitter sensitivity.

Put differently, chronic overconsumption of alcohol causes the brain to reset its recognition levels of reward; meaning an alcoholic will have to drink more and more to achieve the same desired reward effects.

Then, when an alcoholic cannot or does not drink enough to stimulate the reward centers, he or she may feel ill. The brain and body may become unable to easily reverse the artificially elevated CRF levels.

In many cases, this imbalance between Glutamate, GABA, and alcohol causes the alcoholic to consume in excess levels.

Overdrinking chronically depletes GABA functioning within the brain, and may also cause hyperexcitation of the glutamate system. As long as an alcoholic in such a state continues to drink he may feel normal, though other health problems can begin to occur.

However, when drinking ceases, the body needs to rapidly readjust. This also places significant burdens on the liver, kidneys, and other filtration systems; possibly causing the onset of diseases like liver scarring (cirrhosis), kidney disease, and more.

GABA for Treatment for Alcoholism

Gamma amino-butyric acid is a neuroamine substance that acts to regulate body rhythms including heartbeat, breathing, sleeping, and more.

It has been theorized that taking exogenous GABA supplements may increase endogenous levels in the brain and reverse the GABA depletion that can occur from alcohol withdrawal. This may help to counteract the resulting hyperactivation of the glutamatergic system when an alcoholic stops drinking.

How this process works exactly is still unknown, as current scientific knowledge has shown that GABA cannot cross over the blood-brain barrier and cause an effect there. There are theories that some people may have a more permeable blood-brain barrier, or that the supplemental GABA interacts with receptors in the rest of the body (possibly the enteric nervous system in the gastrointestinal tract) and causes signals to be sent to the brain.

GABA supplements are believed to help ameliorate many of the symptoms of alcohol withdrawal. However, alcohol withdrawal should only be conducted under the supervision of a qualified healthcare provider as there may be serious complications, including death.

Certain side effects and interactions are also possible. Speak with a doctor about better understanding the intricate relationship between GABA and alcohol or to learn about safely withdrawal from regular alcohol use.

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