Does Drinking Alcohol Kill Brain Cells?

This damage is often irreversible, emphasizing the long-term consequences of alcohol abuse on physical functioning. Underage drinking increases the risk of anxiety, depression, and low self-esteem, which can affect the brain long term. Heavy drinking may weaken parts of the brain that are responsible for cognitive function and emotion regulation. Research shows that heavy drinking can speed up memory loss and cognitive decline compared with those who did not drink, had quit drinking, or were light-to-moderate drinkers.

• A diet rich in antioxidants, omega-3 fatty acids, and vitamins, particularly B vitamins, can aid in reducing inflammation and supporting neuronal health.
• This damage is often irreversible, emphasizing the long-term consequences of alcohol abuse on physical functioning.
• Alcohol is the most commonly used recreational beverage and drug of abuse among the adult population, alcohol-related death is the third leading preventable cause of death in the United States which accounts for more than 3.3 million global deaths annually 1,2.
• Transmission electron microscopy (TEM) analysis revealed significant alterations in mitochondrial morphology in alcohol-exposed cells.
• For instance, chronic heavy drinkers may experience a loss of up to 10% of their brain’s white matter, which is essential for communication between brain regions.
• In alcohol-related brain damage, ethanol and its metabolites have the potential to disrupt glial physiology and neurobiology in gray and white matter.

How Does Alcohol Affect Brain Development?

Further studies are required to elucidate receptor changes in response to alcohol consumption and dependence across all known neurotransmitter systems. While alcohol does not permanently kill brain cells, chronic abuse can cause lasting damage to the brain’s structure and function, including memory loss, reduced cognitive abilities, and increased risk of neurological disorders. However, chronic heavy drinking can lead to brain atrophy, reduced brain volume, and impaired cognitive function due to damage to neural pathways and supporting structures. Importantly, while short-term alcohol use does not typically destroy brain cells, it can cause temporary shrinkage or atrophy due to dehydration and altered brain chemistry. However, repeated episodes of short-term damage can cumulatively increase the risk of long-term harm, including potential cell loss. Thus, while brain cells are not immediately destroyed by a single instance of drinking, the acute effects of alcohol on neural function are profound and serve as a precursor to more severe consequences with prolonged use.

How Does Alcohol Affect Your Brain?

These free radicals, in turn, activate Rho kinase(ROCK/JNK) signaling to induce the release of vascular endothelial growth factor (VEGF) and inflammatory cytokines in brain endothelial cells (e.g. upregulation of ICAM-1and E-selectin, the release of IL-6) 36,37. In addition to thiamine-deficiency and acetaldehyde related toxicity, alcohol can also cause damage via peripheral and neuro-inflammatory mechanisms. Studies in rodents have demonstrated that alcohol stimulates intestinal inflammation by irritating the stomach and gut, causing the release of the nuclear protein high-mobility group box 1 (HMGB1), which subsequently activate Toll-like receptor 4 (TLR4) and makes the gut “leaky” 80.

Roles

• To this end, neuroblastoma cells were exposed to millimolar (mM) ethanol for up to 24 hours.
• Increased MOR binding could be due to higher receptor levels or reduced release of endogenous endorphins.
• Animal experimental studies demonstrate the presence of cytochrome p4502E1 in the smooth endoplasmic reticulum of brain cells that are capable of Ethanol metabolism in brain by catalyzing the H2O2 with catalase enzyme 34.
• Teenagers are likely to engage in high-risk behaviors, such as driving under the influence and using other substances.

MRS studies of the human brain have revealed a reduced level of NAA in several brain regions of patients with AUD which indicates neuronal injury. Similarly, studies in AUD patients have shown an elevated level of choline-containing compounds that usually provide evidence of demyelination but it is not consistent with alcohol withdrawal syndrome 71,11. According to Alcohol and Brain Cells earlier studies, alcohol withdrawal seizures commonly occur due to an imbalance between glutamatergic and GABAergic neurotransmission which can be detected by MRS of the human brain 107. Multimodal imaging may be useful in predicting the cognitive outcomes and therapeutic success of substance use induced neurological disorder.

While less studied in the context of cognitive impairment, the brainstem’s exposure to alcohol can disrupt its regulatory functions, contributing to respiratory depression and other life-threatening conditions, particularly during severe intoxication or withdrawal. Teenagers are likely to engage in high-risk behaviors, such as driving under the influence and using other substances. Damaged regions of the brain can start to “light up” on brain scans after you cut back on drinking, but there are limits.

Regions of the brain most affected by alcohol

Several controversial studies implicated that NMDA receptors are strongly involved with excitotoxicity which contributes to cell death and hamper the longevity of the cells 42,58. Recent evidence supports the hypothesis that excitotoxic events of NMDA receptors play a role in the formation of neurodegenerative diseases like Alzheimer’s and Huntington’s disease and affect normal brain function 11. In contrast, prior studies had shown that ethanol-induced blockage of the NMDA receptor could increase neurotoxicity by decreasing the expression of brain-derived neurotrophic factor (BDNF) during chronic alcohol administration 62. Therefore, more studies are needed to establish the role of the NMDA receptor in the mechanism of neurodegeneration or neuro-regeneration in patients with AUD. Alcohol-related functional differences in the brain are not exclusively observed in dependent individuals.

Alcohol and Memory Loss

Alcohol consumption, particularly in excessive amounts, has been shown to have detrimental effects on the brain, including the destruction of brain cells, or neurons. While the exact number of brain cells destroyed by alcohol varies depending on factors such as the amount and frequency of consumption, as well as individual differences in tolerance and metabolism, research suggests that chronic heavy drinking can lead to significant neuronal damage. Studies have found that long-term alcohol abuse can result in the loss of up to 10% of the brain’s total neurons, particularly in regions such as the cerebellum, hippocampus, and prefrontal cortex, which are responsible for motor coordination, memory, and decision-making, respectively. This neuronal damage can contribute to a range of cognitive and behavioral impairments, including memory loss, learning difficulties, and impaired executive function, highlighting the importance of understanding the potential consequences of excessive alcohol consumption on brain health. The µ-opioid receptor (MOR) binds β-endorphins and enkephalins which, in turn, increase dopamine release in the NAc 140. 11CCarfentanil is a PET tracer that can be used to define MOR receptor availability and is also sensitive to endogenous endorphin release.

Despite these detrimental effects, the brain retains some capacity for recovery if alcohol consumption is ceased. Abstinence from alcohol has been shown to partially restore neurogenesis and improve cognitive function over time. However, the extent of recovery depends on the duration and severity of alcohol use, as well as individual factors such as age and overall health.

Acetaldehyde is known to be toxic active metabolite, it is implicated in; the induction of alcoholic cardiomyopathy 75, the development of cancers 76 and to have some neurobehavioral effects 77. During intoxication the production of acetaldehyde can cause flushing, increased heart rate, dry mouth, nausea and headache 78. Notably, Acetaldehyde contributes to toxic effects of chronic alcohol on the brain leading to neuronal degeneration 79. Acetaldehyde induces cell damage and cytotoxicity by inducing DNA malfunction and protein adducts 78. Additionally, this protein adduct formation can also induce an immune response which can further damage tissues. As previously mentioned, thiamine is an essential cofactor required for the synthesis and function of several essential enzymes.

Alcohol’s Impact: How Many Brain Cells Does It Destroy?

Thiamine requires phosphorylation by thiamine pyrophosphokinase to be converted to its active co-enzyme form. Thiamine pyrophosphokinase is inhibited by alcohol, which also increases the rate of thiamine metabolism 63. This phosphorylation step requires magnesium as a cofactor, which is also depleted in alcoholism 70. Cumulatively, alcoholism leads to thiamine deficiency via the reduction of intake, uptake, and utilization.

After the first-pass metabolism, alcohol metabolites are distributed throughout the body, it goes to the brain through the blood vessels then it enters into the endothelial cells from the blood and alters the expression of signaling molecules which adhere to the BMVEC 33. The metabolism of EtOH in the brain is controversial than the metabolism of acetaldehyde due to undetectable evidence of homogenous ADH activity in the whole brain. Animal experimental studies demonstrate the presence of cytochrome p4502E1 in the smooth endoplasmic reticulum of brain cells that are capable of Ethanol metabolism in brain by catalyzing the H2O2 with catalase enzyme 34. However, the oxidation of acetaldehyde in brain cell is established because of ALDH (aldehyde dehydrogenase) have been well known to be found in mitochondria of brain cells 35.

Alcohol use can also cause thiamine deficiency by disrupting absorption in the gastrointestinal tract. Studies in both humans and rodents have demonstrated that thiamine is transported via an active sodium independent transporter and therefore requires both energy and a normal pH level 66,67,68, both of which are reduced in alcoholism. Additionally, thiamine absorption can further be depleted by diarrhoea or vomiting which are common occurrences in alcoholism. It is also important to note that thiamine absorption in the gut can be altered by several genetic variants that affect thiamine transport and metabolism 69. The cerebellum, located at the base of the brain, is also highly susceptible to alcohol’s effects. Prolonged alcohol use can cause degeneration of cerebellar neurons, leading to symptoms such as unsteady gait, tremors, and impaired fine motor skills.

Astrocytes maintain the BBB integrity by forming paracrine interactions to coordinates the CNS blood flow and neural function between pericytes and CNS vasculature 45. Alcohol-induced tight junction disassembly is usually mediated via activation of expression protein kinase C (PKC) which subsequently allows toxic substances to enter the brain which in turn affects CNS homeostasis. Loss of astrocytes function to maintain the neurovascular coupling is not recovered by the proliferation of adjacent astrocytes resulting in long-term effect in neurovascular damage. In summary, MRI studies have offered invaluable insight into the effects of alcohol and have typically found a loss of volume and reduced myelination throughout the brain. The findings described here fit the notion that alcohol affects healthy brain aging and this effect becomes more pronounced with higher levels of consumption. It also suggests that there may be a greater vulnerability to the effects of alcohol on brain health with old age.

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