Our Neurotoxin of Choice: Alcohol and the Gradual Descent of the Brain (by Danielle Steinbach)
Sep 17, 2025Heavy metals like mercury and arsenic.
Perchloroethylene.
Trichloroethylene.
Toluene.
These chemicals are all neurotoxins that have been confirmed to accelerate cognitive decline upon inhalation. Among the symptoms that arise from repeated exposure to these substances are cerebellar dysfunction and associated coordination troubles, white matter decline, memory loss, and dopaminergic signaling degeneration. These are chemicals I would recommend limiting exposure to as much as possible.
Well, those chemicals and alcohol.
Alcohol, a substance that can induce every one of the above listed symptoms, has been widely normalized as a treat to ingest at the end of the day to reduce stress. Well, of course we perceive alcohol to limit stress – it damages the parts of your brain that allow you to remember and respond to stressful events.
However, just as I would advise against consuming paint riddled with perchloroethylene or having a glass of toluene before you sleep, I would also advise against intaking alcohol into your body. Unfortunately, alcohol has proven to be a curious and powerful substance that we can’t seem to phase out even with all the accumulating evidence of its short-term and long-term destructiveness.
Over the course of history, humans have unwittingly ingested toxic compounds believing them to have neutral or even beneficial effects. In the medieval days of Europe, salves containing deadly tropane alkaloids in the belladonna plant were applied to women’s skin in order to reduce birthing pains, cast enchantments, and improve their desirability. However, as we discovered its neurodegenerative, hallucinogenic, and acetylcholine-inhibiting effects, we turned against the use of raw belladonna in humans. In ancient Asia and Africa, the unwitting ingestion of tetrodotoxin in improperly prepared, raw pufferfish resulted in numerous accidental deaths. Then, we learned about the neurotoxic side effects of tetrodotoxin, and only chefs qualified to remove the dangerous substance are permitted to serve pufferfish for human consumption.
Now, after decades of research, we can claim with certainty the neurotoxic effects of alcohol. And yet, alcohol breaks the pattern - we haven’t phased it out. Although significant strides have been made in reducing alcohol consumption worldwide, about 10% of Americans report struggling with disordered, excessive alcohol consumption. The unique difficulties we have encountered with reducing alcohol consumption despite its known neurotoxicity speak to the chilling efficacy of alcohol as an addictive substance, both in its capacity as a stimulant and a depressant.
Given how quickly alcohol circulates to the brain, the presence of alcohol will activate enzymes such as Cytochrome P450 2E1, which will oxidize alcohol and transfer the removed electrons to freely circulating oxygen, creating reactive oxygen species (ROS). The accumulation of ROS in the brain can then induce macromolecule damage, with DNA and protein damage being the most notable consequences. Therein lies the neurochemistry behind neurodegeneration with long-term excessive alcohol consumption.
At the level of neurotransmission, alcohol also inhibits glutamate, a neurotransmitter known for promoting memory consolidation through binding to a special class of receptors called NMDA receptors. Regular consumption of alcohol thus directly prevents processes significant in learning at the neurochemical level. On the flip side to alcohol’s effects on excitatory neurotransmitters, inhibitory GABA (gamma-amino-butyric acid) actually spikes in the presence of alcohol, leading to hesitant movement and poor coordination. A critical rule of the brain – and the body in general – is that if our environment shifts such that we cannot naturally maintain homeostasis and specific ranges of chemicals, our bodies tend to respond by manufacturing ways to force our bodies back into equilibrium. In this case, jolts of GABA beyond typical ranges will induce a decline in GABA receptors to maintain a specific frequency of GABAergic neuronal signal reception. However, the long-term result of this decline in GABA receptors is that, even when someone is not actively drinking alcohol, they still exhibit a lack of inhibition. This disinhibition can lead to consequences such as behavioral issues and seizures.
On a larger structural scale, alcohol consumption proves particularly detrimental to the frontal lobe, and fMRI studies suggest that alcohol selectively inhibits blood oxygenation in the prefrontal cortex. In so doing, alcohol consumption detracts from our judgement, planning, and decision-making skills, and its effects are particularly pronounced when introduced to the still developing neuronal circuitry of adolescents.
MRI and CT imaging have also confirmed the link between excessive alcohol consumption and volume decline through gray matter reduction in the cerebellum and limbic system. Eventually, damage to the cerebellum can cause irreversible motor coordination and balance problems. Meanwhile, damage to the limbic system incurs consequences in emotional regulation and memory. Eventually, damage to the limbic system will cause temporary mood swings to transition to long-term behavioral dysregulation.
In severe cases, alcohol can even induce Wernicke-Korsakoff syndrome, a condition characterized primarily by insufficient stores of thiamine (vitamin B1) due to alcohol consumption. As alcohol makes its way into the gut, its metabolic byproducts can damage the cells of the gastrointestinal tract, reducing nutrient absorption. Furthermore, oxidized byproducts of alcohol destroy thiamine as it passes to the liver. Thiamine serves a critical role in a myriad of fundamental cognitive functions and molecular neuronal functions. One of these critical roles of vitamin B1 is supporting the jumping (or saltatory propagation) of action potentials along the axon. Additionally, thiamine serves to drive the production of ATP (‘energy’ molecules) from carbohydrates to power basic neuronal functioning. Thus, as thiamine is depleted, as is the case in Wernicke-Korsakoff syndrome, afflicted patients often exhibit ataxia, which can be described as an inability to control the precision of one’s movements. Furthermore, this condition is characterized by premature impairments in learning and recall skills.
However, even in less extreme cases of alcohol consumption, given the way that metabolites produced from alcohol bear the potential to break down proteins in the brain and create aggregate protein bundles, alcohol consumption increases one’s risk for neurodegenerative diseases such as Alzheimer’s and Parkinson’s. The accumulation of DNA damage from ROS byproducts of alcohol can also induce neuronal cell death, contributing to neurodegeneration and overall gray matter decline in the brain.
Alcohol places an extraordinary array of burdens on the brain, from vitamin depletion, to protein accumulation, to DNA damage, to neurotransmitter imbalances, and many other side effects. Yet, we normalize alcohol consumption so easily, and it remains our neurotoxin of choice when we go out for dinner or attend a party or come home from a long day at work.
Well, my view is that our brains are precious enough, too precious to poison on purpose. I think that a sober clarity of thought serves as a better long-term protector against anxiety and depression than a neurotoxin that limits your ability to confront your fears and troubles in life. And, as the number of young people who regularly drink alcohol dwindles, I have more and more hope that maybe we are moving away from this toxin and looking towards facing life in its purest form, with all our cognitive faculties about us.
-- Danielle Steinbach
Sources:
https://www.sciencedirect.com/science/article/pii/S0378427410015808
https://www.frontiersin.org/journals/cellular-neuroscience/articles/10.3389/fncel.2020.00282/full
https://www.sciencedirect.com/science/article/pii/S0278691518302242
https://americanaddictioncenters.org/rehab-guide/addiction-statistics-demographics
https://pmc.ncbi.nlm.nih.gov/articles/PMC6668884/
https://www.frontiersin.org/journals/cellular-neuroscience/articles/10.3389/fncel.2020.00282/full
Stay connected with news and updates!
Join our mailing list to receive the latest news and updates from our team.
Don't worry, your information will not be shared.
We hate SPAM. We will never sell your information, for any reason.