According to the 2018-National Survey on Drug Use and Health (NSDUH), 14.4 million people suffered from alcohol use disorder (AUD) in the US, and over 100,000 deaths were attributable to alcohol 3. The World Health Organization reported that more than 200 health conditions including cancer, liver cirrhosis, and neurocognitive impairment were also attributed to alcohol consumption 2. These chronic health conditions are progressive, cause a heavy economic burden to society, and decrease the quality of life for both patients and caregivers 4. To this end, alcohol exposure significantly increased the accumulation of oxidatively damaged proteins in both differentiated and undifferentiated cells after 12 or 24 hours of exposure.
- (VTA), dopaminergic projections extend through the striatum and prefrontal regions of the brain.
- 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.
- FASDs interfere with the brain’s growth and development, leading to lifelong physical, mental, and behavioral problems.
- In AUD, brain immune defense cells, microglia, are activate and express many proinflammatory genes including tumor necrotic factor α (TNF α), cyclo-oxygenase, NADPH enzymes which change the brain immune system and nerve cell functions 67,68.
- Lower BDNF levels impair the brain’s ability to recover from injury and adapt to new information, contributing to long-term cognitive impairments.
Long-Term Effects of Heavy Drinking
Emerging therapies, including pharmacological interventions and lifestyle changes, aim to enhance brain cell regeneration in recovering alcoholics, offering hope for mitigating long-term damage. Short-term alcohol exposure can also cause inflammation in the brain, though this is more pronounced with chronic use. Acute inflammation occurs as the brain responds to alcohol as a toxin, triggering the release of pro-inflammatory cytokines.
Neuroimaging evidence of alcohol-induced neuroinflammation and neurodegeneration
Before you reach for your next drink, Dr. Anand explains how alcohol can affect your brain — not only in the short term, but also in the long run. Consuming alcohol while pregnant can cause permanent damage to the developing brain and other organs of the fetus. Before getting into the effects of alcohol on the brain, it’s important to understand how experts talk about alcohol use. The toll that frequent alcohol use can have on your body can be severe but in some cases, the damage can be reversible.
It may take several months of complete abstinence from alcohol to give your brain time to heal. People who drink regularly may notice that alcohol does not have the same effect on them as it used to. You build up a tolerance over time and do not feel as good as you once did with the same amount of alcohol. Serious complications include irreversible brain damage, psychiatric disorders (e.g., depression, anxiety), and increased risk of other neurodegenerative conditions, such as Alzheimer’s disease.
Empirical studies further show that ethanol-induced brain damage is mainly related to oxidative stress response from proinflammatory cytokines activated during alcohol intoxication. Proinflammatory cytokines NF-kB (transcription factor) mediate oxidative stress plays a role in the induction of anti-inflammatory and immune response signals, which appear to underlie neuronal degeneration and tissue atrophy 46,47. Cytokines are large families of secreted proteins that are transported from blood serum to neuronal tissue in response to oxidative stress-related alcohol neuroinflammation 47.
Structural and Volumetric Changes
- The reward system is responsible for goal-directed behavior by means of reinforcement and responds to conventional rewards such as food and money, as well as all known drugs of abuse.
- Astrocytes and oligodendrocytes play a crucial role in the molecular mechanism of signal conduction and neurotransmission in both gray and white matter.
- Chronic, heavy drinkers may face more challenges in recovery compared to those who have engaged in moderate drinking.
- Analysis of post-mortem brains of patients with Alcohol Use Disorder showed in increase in microglial markers (Iba1 and GluT5) compared with controls 82.
To better characterize brain function and behavior following exposure to alcohol both acute and chronic, as well as improve treatment outcome and reduce risk of relapse, it is imperative that large-scale studies with longitudinal designs are conducted. The dopamine, GABA and opioid systems are by far the most researched using PET and SPECT imaging techniques to measure neurochemical dysfunction in alcohol dependence, due to the availability of selective radiolabeled tracers for the targets of DRD2/3, GABA-A and MOR receptors, respectively. Well validated tracers for other targets such as those in the serotonergic system do exist, but their use in alcohol dependent individuals is not well characterized. Studies using novel radioligands to assess other receptor targets and neurochemical systems including the endocannabinoid and glutamatergic systems is less advanced, but a few selective tracers do exist. It must be acknowledged that PET/SPECT is somewhat limited as a technique because of its radioactivity meaning that young people and repeat scanning cannot be carried out. Nevertheless, PET/SPECT imaging is still the only way to directly image neurotransmitter receptors and neurotransmitter release (when sensitive tracers are available) in the living human brain.
We and our partners process data to provide:
The researchers noted that people with alcohol use disorder (AUD) had less brain matter than others. The affected brain regions controlled skills like attention, language, memory, and reasoning. Intermittent ethanol treatment causes a decrease in expression of the dopamine receptor type 2 (D2R) and a decrease in phosphorylation of 2B subunit of the NMDA receptor (NMDAR2B) in the prefrontal cortex, hippocampus, nucleus accumbens, and for only D2R the striatum.
Brain Shrinkage
Alcohol consumption, especially in excess, has a profound impact on the brain, affecting various regions and their functions. While the notion that alcohol kills brain cells is somewhat simplistic—as it primarily damages the connections between neurons (synapses) rather than the cells themselves—it is clear that certain areas of the brain are more vulnerable to its effects. One of the most affected regions is the cerebral cortex, responsible for higher-order cognitive functions such as decision-making, problem-solving, and memory. Chronic alcohol use impairs the cerebral cortex’s ability to process information efficiently, leading to difficulties in learning, attention, and impulse control. This region’s reduced functionality is a key factor in the cognitive deficits observed in long-term drinkers.
Prenatal Alcohol Exposure
Endorphin release in the NAc and OFC was measured in light versus heavy drinkers through displacement of 11CCarfentanil following acute alcohol consumption of an alcoholic drink. Changes in OFC binding correlated significantly with problematic drinking and subjective high in heavy drinkers but not in controls 141. In abstinent alcohol dependent individuals a greater MOR availability in the ventral striatum, as measured by 11CCarfentanil, compared with healthy controls was correlated with a greater craving for alcohol 142. Increased MOR binding could be due to higher receptor levels or reduced release of endogenous endorphins. It was later postulated that greater 11CCarfentanil binding could be related to reduced β-endorphins in alcoholism.
Less is Alcohol and Brain Cells known about the dose-response mechanism, though it has been suggested moderate drinking lies somewhere intermediate 52,53. This would again imply that the impact of alcohol consumption on brain structure is not limited to heavy alcohol consumption. However, it has been noted there are differences in brain structure that predate alcohol initiation and may predispose individuals to heavy alcohol use. Structural precursors have mostly been found in the prefrontal cortex and fronto-limbic white matter and show considerable overlap with structural differences found in individuals with a family history of alcohol dependence 54. Nevertheless, there are studies that have suggested differences are not solely attributable to familial risk 55,56, and more research is needed to better understand these risk factors.
When comparing the neural response of light (consuming ~0.4 drinks per day) and heavy (consuming ~5 drinks per day) drinkers to alcohol cues, light drinkers have been found to have a higher BOLD signal in VS, while heavy drinkers show an increased BOLD signal in DS 102. The DS response in the heavy drinkers suggests the initiation of a shift from experimental to compulsive alcohol use during which a shift in neural processing is thought to occur from VS to DS control 103. However, such cross-sectional studies are unable to establish whether such differences are prodromal or consequential of alcohol exposure. A recent longitudinal study in adolescents showed that blunted BOLD response to non-drug reward was predictive of subsequent problematic alcohol use 104. These results suggests that certain functional differences in reward processing may predate problematic alcohol consumption.
Regular physical exercise is another powerful tool, as it promotes neurogenesis and enhances cognitive function. Cognitive-behavioral therapies and mindfulness practices can further support recovery by improving mental health and reducing the risk of relapse. These holistic approaches, combined with medical supervision and support, can significantly enhance the brain’s ability to heal. Furthermore, alcohol disrupts the blood-brain barrier (BBB), which normally protects the brain from harmful substances.
