The Effects Of Alcohol On Neurotransmission (And What To Do About It)
We've all probably had some sort of relationship with alcohol. Early in the relationship, it may be all about fun: partying, being crazy, relieving social anxiety, etc. But as we get older, alcohol can play a much more insidious role. Want to have a few beers or glasses of wine once in a while? I'm not going to stop you, but I am going to educate you, specifically in what is happening in you brain when you drink.
It has been said that if alcohol had been introduced in modern times, it would have been classified a poison. That being said, it's probably here to stay, so now we have to do the clean-up work of ingesting poison. There are the well-known effects of drinking: addiction, slurred speech, decreased reaction time, loss of motor function, loss of inhibitions, vomiting, etc., but let's look at the lesser talked about neurological effects.
It has been said that if alcohol had been introduced in modern times, it would have been classified a poison. That being said, it's probably here to stay, so now we have to do the clean-up work of ingesting poison. There are the well-known effects of drinking: addiction, slurred speech, decreased reaction time, loss of motor function, loss of inhibitions, vomiting, etc., but let's look at the lesser talked about neurological effects.
Effect |
Result |
Decreased transmission in Acetylcholine systems: |
literally slowing down/ shrinking of the brain |
Increased turnover of Norepinephrine and Dopamine: |
sapping energy and false-triggering our reward system |
Increased transmission in GABA systems: |
a short-term relief from anxiety followed by anxiety from GABA depletion, which leads to more drinking |
Extended toxic effects on Serotonin transmitters: |
eventually requiring alcohol to feel happy |
Increased production of Beta-Endorphin in the hypothalamus: |
possibly contributing to adrenal fatigue |
Excerpt from "The Science of Alcohol Addiction" on the Harvard Science Review:
"Why is the ethanol molecule so addictive? Ethanol (C2H5OH) first binds to a GABA-a receptor responsible for creating gamma-aminobutyric acid (GABA). GABA inhibits neuron activity by an increase of chlorine ion release into neurons. (2,3). This dramatic increase in negative charge causes the membrane potential of the neurons to be very negative, thus making it difficult for neurons to cross the threshold membrane potential required for activation. To a similar effect, alcohol inhibits glutamate, the counterpart molecule to GABA used to excite neuron activity. The combined consequences of GABA stimulation and glutamate inhibition cause the calming effects of alcohol that is typically associated with an “optimal buzz.” However, Professor Gutlerner cites that prolonged alcohol use makes the GABA-a receptor less sensitive to activation, which is partially responsible for many of the effects during alcohol withdrawal such as anxiety disorders, panic attacks- the combined result of a hyper-activated central nervous system. As a result, many addicts find themselves drinking to simply feel “normal.”
Reward Pathway
Although the damage to the GABA pathway is important, a significant consequence of alcohol is its interference with the reward pathway. The reward pathway is essentially nature’s way of reinforcing good behaviors and eliminating bad behaviors by generating the neurotransmitter dopamine in the ventral tegmental area (VTA), a group of neurons located in the midbrain. Alcohol’s major interaction with the reward pathway comes through its stimulation of beta-endorphins, which activates opioid peptides, a chain of amino acids that modify the activity of nearby neurons (4). These peptides control feelings of euphoria. Alcohol also increases the concentration of neurotransmitter dopamine, which stimulates desire in the body’s reward center, the nucleus accumbens, an area not too far away from the VTA. Simultaneously, alcohol binds to acetylcholine and serotonin (responsible for inhibition) receptors and alters their respective pathways. After prolonged use, more and more alcohol is needed to achieve the same level of euphoria as before. The changed neurochemistry of the addict’s brain can be seen following figure, showing the increase of positive reinforcement in the nucleus accumbens in non-dependents and the increase of negative reinforcement in the amygdala independents."
"Why is the ethanol molecule so addictive? Ethanol (C2H5OH) first binds to a GABA-a receptor responsible for creating gamma-aminobutyric acid (GABA). GABA inhibits neuron activity by an increase of chlorine ion release into neurons. (2,3). This dramatic increase in negative charge causes the membrane potential of the neurons to be very negative, thus making it difficult for neurons to cross the threshold membrane potential required for activation. To a similar effect, alcohol inhibits glutamate, the counterpart molecule to GABA used to excite neuron activity. The combined consequences of GABA stimulation and glutamate inhibition cause the calming effects of alcohol that is typically associated with an “optimal buzz.” However, Professor Gutlerner cites that prolonged alcohol use makes the GABA-a receptor less sensitive to activation, which is partially responsible for many of the effects during alcohol withdrawal such as anxiety disorders, panic attacks- the combined result of a hyper-activated central nervous system. As a result, many addicts find themselves drinking to simply feel “normal.”
Reward Pathway
Although the damage to the GABA pathway is important, a significant consequence of alcohol is its interference with the reward pathway. The reward pathway is essentially nature’s way of reinforcing good behaviors and eliminating bad behaviors by generating the neurotransmitter dopamine in the ventral tegmental area (VTA), a group of neurons located in the midbrain. Alcohol’s major interaction with the reward pathway comes through its stimulation of beta-endorphins, which activates opioid peptides, a chain of amino acids that modify the activity of nearby neurons (4). These peptides control feelings of euphoria. Alcohol also increases the concentration of neurotransmitter dopamine, which stimulates desire in the body’s reward center, the nucleus accumbens, an area not too far away from the VTA. Simultaneously, alcohol binds to acetylcholine and serotonin (responsible for inhibition) receptors and alters their respective pathways. After prolonged use, more and more alcohol is needed to achieve the same level of euphoria as before. The changed neurochemistry of the addict’s brain can be seen following figure, showing the increase of positive reinforcement in the nucleus accumbens in non-dependents and the increase of negative reinforcement in the amygdala independents."
Differences By Gender
In a study that links depression and alcohol problems showed evidence suggesting that in men alcohol use precedes the depression, whereas in women, the depression precedes the alcohol use.
"But I Don't Get Drunk"
It doesn't matter. Alcohol crosses the blood-brain barrier even when consumed in relatively small amounts (or in large amounts consumed slowly over longer periods of time). Whether it takes you two hours or all day to finish off that 12-pack, you still consumed 144 oz.
In a study that links depression and alcohol problems showed evidence suggesting that in men alcohol use precedes the depression, whereas in women, the depression precedes the alcohol use.
"But I Don't Get Drunk"
It doesn't matter. Alcohol crosses the blood-brain barrier even when consumed in relatively small amounts (or in large amounts consumed slowly over longer periods of time). Whether it takes you two hours or all day to finish off that 12-pack, you still consumed 144 oz.
What To Do About It
The simple answer is to stop drinking or severely reduce the amount and frequency of drinking. (If you are capable of doing so without withdrawal, congratulations.) Let's look at some strategies to mitigate the withdrawal symptoms:
The simple answer is to stop drinking or severely reduce the amount and frequency of drinking. (If you are capable of doing so without withdrawal, congratulations.) Let's look at some strategies to mitigate the withdrawal symptoms:
Anti-Alcohol Support Supplements are products designed to replenish and detoxify. |
Supplement for the mental/ emotional symptoms at the time when you would otherwise be drinking. Replace the nightly glass of scotch with l-tryptophan and lemon balm. Take l-phenylalanine or a caffeine + l-theanine supplement before going out with friends. If your brain is happy and satisfied, it won't care if it came from a glass bottle or a plastic supplement bottle. |
If you are a beer drinker, switch to non-alcoholic beer. Studies have shown that the first sip of beer produces a release of Dopamine even before the alcohol reaches the brain. Trick your brain into thinking you're drinking. |
Get outside for low-impact exercise like walking in nature. Teach your body to produce GABA instead of needing alcohol to fake its effects. |
The cure for addiction is connection. Reach out to friends, family, spouses, AA... anyone whom you can healthfully spend time with who will support you in this major life change. |
More:
"Neurohacking": An Overview
Self Assessment
Braverman Assessment
Supplements & Adaptogens
Effects of Alcohol on Neurotransmission
Dig Deeper
"Neurohacking": An Overview
Self Assessment
Braverman Assessment
Supplements & Adaptogens
Effects of Alcohol on Neurotransmission
Dig Deeper
Disclaimer: This document is for informational purposes only and is not intended to interfere with or supersede the guidance of medical or psychiatric professionals. You are responsible for your own body, including how you treat it and what you choose to put in it.