Excessive consumption of alcohol has been commonly linked to a higher risk of several disorders including hypertension, depression, and even cancer. Drinking alcohol can also affect neurological function resulting in reduced memory, poor judgement, impulsivity, impaired motor coordination, respiratory depression, and even coma.
However, does alcohol really kill brain cells?
Let’s find out what happens to the brain when you drink alcohol and whether it actually kills brain cells.
Alcohol is a psychoactive substance that impacts many neurotransmitter systems in the brain including those systems that employ the neurotransmitters gamma-aminobutyric acid (GABA), serotonin, glycine, glutamate, and acetylcholine. The by-products of alcohol metabolism, including acetaldehyde, can also have neurological effects and produce many of the symptoms of alcoholic hangovers. However, the primary intoxicating effects are due to alcohol’s effect on the GABA, opioid, and dopamine systems. GABA is the predominant inhibitory neurotransmitter in the nervous system. Alcohol enhances and magnifies the effects of GABA causing sedation and slowing of many neurological functions such as reflexes, motor coordination, and cortical higher-order thinking. In large enough quantities, alcohol can lead to suppression of the respiratory drive center of the brain causing a decline of the respiratory rate and unconsciousness. The euphoric effects of alcohol are due to increases in endogenous opioids and dopamine in the “pleasure center” of the brain called the nucleus accumbens.
Consuming occasional, sub-intoxicating amounts of alcohol is unlikely to cause neuronal harm or death. However, frequent binge drinking and chronic intoxication for extended periods of time are completely different scenarios with diffferent outcomes. The totality of the evidence strongly suggests that high dose, high frequency use of alcohol causes significant disruption of normal brain functions, alterations of brain structures, and neuronal cell death. (Oscar-Berman, 2003) However, not all exposures are the same. The degree of brain damage is also dependent on mutliple other variables besides dose, frequency, and duration; including age of exposure, genetics, associated diseases, vitamin and nutirional deficiencies, and even the number of untreated alcohol withdrawal episodes.
Let us find out more about how alcohol affects brain health.
Exposure to excessive amounts of alcohol is more detrimental to younger users. Basically, the younger the brain, the greater the vulnerability. This increased vulnerability is due to the dynamic changes in function and morphology (structure) of the brain during periods of rapid growth. During development, neurogenesis (growth of new brain cells), myelination of neurons, and synaptogenesis (creation of new connections between neurons), and synaptic pruning (elimination of un-needed connections), are all progressing synergistically in a very rapid fashion. Like a multi-piece orchestra playing a symphony, the timing and coordination of these developmental events are critical to the outcome of a mature, properly functioning nervous system. If one, or a few, of these processes are disrupted, inhibited, or impinged by a substance at toxic levels, the necessary developmental events cannot occur at the proper time within the proper sequence. As described by Stiles and Jernigan, “Rather, brain development is aptly characterized as a complex series of dynamic and adaptive processes that operate throughout the course of development to promote the emergence and differentiation of new neural structures and functions. These processes operate within highly constrained and genetically organized, but constantly changing contexts that, over time, support the emergence of the complex and dynamic structure of the human brain.” 
The relative greater harm delivered by insults to the developing nervous system are not only seen in alcohol exposure,  but also in other types of exposure including marijuana use. Adolescent exposure to alcohol has shown degeneration in brain structures such as the frontal lobe and hippocampi leading to difficulties with memory formation, executive functions, judgement, and impulsivity. Fetal alcohol syndrome is another example of the greater harm to normal development from alcohol exposure. The fetal cells from which brain cells are derived degenerate upon exposure to alcohol and those that do survive cannot migrate to the proper location to create normal brain structures.  Whether alcohol use predisposes people to Alzheimer’s Disease and other types of dementia is under investigation.  Two types of global cognitive impairment due to alcohol have been described, one due to the direct neurotoxic effects of alcohol named Alcohol-Related Dementia, and the other being related to thiamine deficiency due to alcoholism called Wernicke-Korsakoff syndrome (WKS).
Nutritional deficiencies in the context of chronic alcoholism is common and well described. When alcohol use becomes consistent, every day throughout the day, loss of appetite and a reliance on alcohol as an energy source can lead to a decline in alternative sources of calories, even to the point where alcohol constitutes the vast majority of daily caloric intake. Vitamin deficiencies can result due to both a lack of intake and alcohol’s ability to alter the function of those vitamins that remain. The most commonly seen vitamin deficiencies in alcoholism include vitamin B12 (cobalamin) vitamin B1 (Thiamine) and vitamin B9 (folate).
Thiamine deficiency in the context of alcoholism can produce a neurological syndrome called Wernicke’s Encephalopathy (W.E.). The syndrome consists of the acute onset of confusion, decreased attention, disorientation, ocular abnormalities, and unsteady gait (ataxia). Another syndrome, called Korsakoff’s Psychosis, commonly occurs with W.E. in 80% of cases and is characterized by chronic symptoms of psychosis, retrograde and anterograde amnesia, confabulation, and personality changes. Alcohol causes both an absolute and relative thiamine deficiency in alcoholism. Absolute thiamine deficiency results from both lower dietary intake and poor absorption from the gastrointestinal tract. However, alcohol also inhibits the normal functioning of this vitamin rendering the thiamine that is still present in the body useless. Since thiamine is critical to the energy production processes of cells, those cells with high metabolic needs, such as those found in the brain, are more susceptible to cellular disruption and apoptosis (cellular death). Brain lesions are often found in the thalamus, mammillary bodies, brain stem, and frontal lobes. These lesions are found to be due to neuronal degeneration, edema (swelling), and hemorrhage of capillaries.
Genetic predisposition for alcoholism is well characterized. Evidence also exists to suggest that the impulsivity commonly linked to alcoholism has a possible genetic component, as well as the susceptibility to neurological consequences of alcohol exposure. For example, a certain type of alcohol-related neurodegeneration called proinflammatory cytokine mediated (alcohol-related) brain damage, is thought to have a genetic susceptibility from the same genes that predispose someone to alcohol use disorder and impulsivity.
Neurological systems become extremely hyperactive during untreated alcohol withdrawal. This excitatory state is a physiologic rebound that occurs after the depressant effects of the alcohol are removed. Alcohol causes a suppression of excitatory neurotransmitters, such as glutamate, and enhances the activity of inhibitory neurotransmitters such as GABA. Overtime, a new homeostatic state is achieved as a new paradigm of molecular and cellular activity is locked in place by the chronic exposure and activity of the alcohol. The brain and the body make the necessary cellular and molecular “adjustments” to adapt and tolerate the presence of an abnormally high blood alcohol concentration. The diverse effects that alcohol has on the brain and body causes changes in levels of receptors, enzymes, neurotransmitters, and various other proteins that leads to changes in synaptic (electrical) activity. Many of these changes are an effort to “counter” the sedating and depressant effects of the alcohol. Thus, in order for the individual to remain functional in the face of a high blood alcohol content, molecular and cellular systems that promote alertness, reflexes, heart rate, blood pressure, attention, respiratory rate, and others, must be increased in equal measure. Like a seesaw trying to maintain balance, if alcohol adds weight to one side, additional force must be applied to the opposite side. However, if and when the blood alcohol drops, it’s suppressive effects are withdrawn, leaving the overly enhanced excitatory systems to unleash a flood of excitatory neurotransmitters and cause the typical symptoms of alcohol withdrawal (elevated blood pressure, increased heart rate, agitation, hyper-alertness, sweats, tremors, anxiety, and in some cases, seizures and delirium.
Experiencing untreated alcohol withdrawal symptoms is not only distressing and life-threatening, but evidence suggests that the extreme physiological reactions are potentially damaging to the nervous system. One theory posits that high glutamate and N-Methyl-D-Aspartate receptor (NMDA) activity causes cellular injury by increasing intra-cellular calcium levels and creating reactive oxygen species.  Vulnerable areas include the cerebral cortex, hippocampus, and cerebellum.
Electromagnetic (EEG, MEG, MRI, fMRI) and hemo-dynamic (PET, SPECT) scans are the most common ways that anatomical, functional, and biochemical changes due to alcohol abuse are measured. Electromagnetic imaging allows for “real-time” measurements of brain function including changes to a “stimulus” or intervention while the subject is being scanned. These scans are especially helpful in identifying changes in brain function over time. Hemo-dynamic scans are most helpful in measuring chemical activity (oxygen consumption) or blood flow changes in various brain structures. Positron emission tomography (PET) and single photon emission computed tomography (SPECT) often use a radioactively labelled molecule such as glucose to track the changes in cellular activity. Various PET and SPECT scan studies have confirmed prior studies that have found a decrease in metabolism in the area of the brain that helps control impulses called the prefrontal cortex in alcoholics. MRI and fMRI can also be used to measure functional changes in specific brain regions. An MRI study examining the effects of binge drinking found that, after three years of binging, MRI scans could detect loss of frontal lobe white matter and lower neural integrity. One technique called diffusion tensor imaging (DTI) can actually measure the orientation and integrity of specific neuronal pathways to detect damage. One study demonstrated disruption of the microstructure of nerve fibers after heavy alcohol use.
Alcohol is a neurotoxin that can, in high doses and frequency, cause brain damage. Various studies have demonstrated that alcohol impacts neurological function, structure, and biochemistry.