Because of a lapse in government funding, the information on this website may not be up to date, transactions submitted via the website may not be processed, and the agency may not be able to respond to inquiries until appropriations are enacted. There’s also more of an effect on your brain and its development if you’re younger — one that can have a lasting impact. But as you drink more — and you don’t need to drink that much more — eventually, the enzymes that break down the alcohol get saturated.
Binge drinking
This inflammatory response can temporarily impair brain cell function and contribute to symptoms like headaches, fatigue, and cognitive fog. However, in the short term, this inflammation is generally reversible and does not lead to significant cell death. Magnetic resonance spectroscopy (MRS) provides additional information about the molecular concentration and ethanol metabolites in the brain 104. Proton-MRS can explore region-specific neurobiological status in combination with genetic mediated neurocognitive decline which has potential efficacy for future clinical management of AUD 105. The largest MRS signals arise from N-acetyl aspartate (NAA), glutamate, glutamine, and choline-containing compounds (Cho) which are considered to measure neuronal integrity and normal brain function 106,70.
Health Conditions
Despite the negative consequence of drinking alcohol, there is still hope for the recovery of alcohol-induced neurodegeneration. Neuro-regeneration (neuronal stem cell proliferation and formation of new neurons) generally depends on alcohol dosage, drinking duration, nutritional deficiency, stage of neuronal damage, and cellular components that correspond with cognitive functioning impairment. In AUD, alcohol alters the physiological status of the nervous system, may cause interruption of neuroprotective functions, and interfere with the absorption of certain nutrients which are necessary to maintain CNS homeostasis and brain cell development 111. These factors may then result in loss of structure and function of multiple brain regions which induce alcoholic neurodegeneration 6. Surprisingly alcohol abstinence could help individuals recover from the pathological state as well as improve cognitive function with sustained abstinence 67.
- The National Institute on Alcohol Abuse and Alcoholism notes that a number of factors influence how alcohol affects the brain, including how much and how often a person drinks, how long the individual has been drinking, prenatal exposure to alcohol, and the overall state of a person’s health.
- In conclusion, while alcohol does not directly destroy brain cells, its impact on neurogenesis is severe and multifaceted.
- Additionally, alcohol triggers the release of pro-inflammatory cytokines, creating a hostile environment for neural stem cells.
- Multimodal imaging may be useful in predicting the cognitive outcomes and therapeutic success of substance use induced neurological disorder.
- “Generally, over time, there have been new studies that show that chronic alcohol use — at very heavy use — can lead to brain damage, both gray and white matter.
2. Neurotoxicity of Acetaldehyde
Additionally, alcohol triggers the release of pro-inflammatory cytokines, creating a hostile environment for neural stem cells. This inflammatory response further suppresses the brain’s regenerative capacity, exacerbating the loss of cognitive function observed in heavy drinkers. Alcohol’s impact on brain cell regeneration is a critical area of study, as chronic alcohol consumption can significantly impair the brain’s ability to repair and regenerate neurons.
Blackouts are gaps in a person’s memory of events that occurred while they were intoxicated. These gaps happen when a person drinks enough alcohol that it temporarily blocks the transfer of memories from short-term to long-term storage—known as memory consolidation—in a brain area called the hippocampus. So, if you drink before the age of 14, there’s about a 50% chance you’re going to develop an alcohol use disorder in your adulthood,” explains Dr. Anand. For starters, too much alcohol can interfere with neurogenesis, which is your body’s ability to make new brain cells.
Effects on brain development can be long-lasting
Initial transcriptome studies indicated that alcohol increased levels of TSPO (18 kDa translocator protein, that is upregulated in activated microglia). However, when TSPO binding was analyzed using PET in alcohol dependent individuals and individuals undergoing detoxification these findings were not replicated 96,97. Cumulatively, this evidence suggests that alcohol is clearly an activator of microglia, and as previously described upregulation of microglial activation can result in neurotoxicity. However, the extent of alcohol induced microglial activation may well be dependent on the extent and pattern of alcohol exposure. Besides, immune therapy, N terminus-based antibodies immunization has a significant role in clearing the misfolded protein (Aβ and tau protein) but it is only effective at the earliest stage of disease 77.
- Alcohol enhances GABA’s effects, leading to slowed neural activity, which manifests as reduced inhibitions, impaired coordination, and slurred speech.
- 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.
- Studies on the rodent and human brain delineated that excessive ethanol intake induces neuronal injury during various developmental stages including neurodegeneration and this type of ethanol-induced neurodegeneration seems to be connected with glial activation and neuroinflammation 23,63,64.
- Strength of evidence to show direction of effects on receptor radioligand binding in human PET imaging studies in alcohol dependence.
Neuroimaging studies have also dramatically advanced our understanding of the brain’s response to alcohol and the neurochemical basis of alcohol dependence. Positron emission tomography (PET) and single photon emission computed tomography (SPECT) use radiotracers that bind specifically to key receptors of interest, to quantify receptor location and availability. Neurotransmitter release can also be indirectly quantified using PET, through measurement of the amount of tracer that is ‘displaced’ from the receptor when endogenous neurotransmitter is released in response to a pharmacological (or other) challenge. Such techniques have been instrumental in the investigation of key neurotransmitter systems and identification of molecular dysfunction in the human brain. The use of PET to study the effects of chronic alcohol consumption has advanced our understanding of reward mechanisms, neuroadaptations resulting from chronic use that led to tolerance and withdrawal and has identified key regions and circuits implicated in loss Alcohol and Brain Cells of control and motivation to drink. This section summarizes PET studies that investigate the key neurotransmitter systems and review the evidence in case-control studies (summarized in Table 1).
On top of that are peripheral factors that compound brain damage such as poor diet, vitamin deficiencies leading to Wernicke-Korsakoff syndrome. Prenatal alcohol exposure can also have a profound impact on brain development and lead to irremediable changes of fetal alcohol syndrome. This chapter briefly reviews aspects of these with a particular focus on recent brain imaging results. Cardiovascular effects of alcohol that lead to brain pathology are not covered as they are dealt with elsewhere in the volume.
Lifestyle modification is also one of the most promising initiatives to reduce alcohol or age-related neurodegeneration as well as possible intervention strategies to control chronic disease or prevent the onset of dementia. Several lifestyle factors like aerobic and anaerobic exercise, an antioxidant-rich diet, limited alcohol consumption, neuropsychological therapy, and cognitive training have been demonstrated to improve cognitive function or postpone disease progression in AUD 141,142. The association between lifestyle modification and neurodegeneration in AUD is outlined in Table 2.
Choice impulsivity, the tendency to make choices that lead to suboptimal, immediate or risky outcomes is often measured using a delay discounting task to assess an individual’s preference for a smaller, immediate reward compared with a larger, delayed reward 112. Individuals who scored higher in trait impulsivity measures exhibited greater choice impulsivity than their lower trait impulsive counterparts 115. In summary, alcohol can contribute to neurotoxicity via thiamine deficiency, metabolite toxicity and neuroinflammation. Alcohol reduces the uptake and metabolism of thiamine, the essential co-factor without which glucose breakdown and the production of essential molecules cannot occur. The metabolism of alcohol itself can also lead directly to neurotoxicity as the metabolite acetaldehyde is toxic and can lead to neurodegeneration.
A single night of heavy drinking is unlikely to kill brain cells, but it can cause temporary cognitive impairment and damage to brain function. The reversibility of alcohol-induced brain cell destruction is not absolute and depends on several factors, including the duration and severity of alcohol use, the individual’s overall health, and their genetic predisposition. Chronic, heavy drinkers may face more challenges in recovery compared to those who have engaged in moderate drinking. Additionally, the age at which alcohol consumption began plays a crucial role, as the developing brains of adolescents are more susceptible to damage and may have a reduced capacity for recovery. Early intervention and cessation of alcohol use are therefore critical in maximizing the potential for brain repair. In summary, while alcohol does not directly “kill” brain cells in large numbers, it causes widespread damage to critical regions of the brain, including the cerebral cortex, hippocampus, cerebellum, brainstem, and prefrontal cortex.
ALDH converts acetaldehyde to acetate, acetate has further effects on brain including increase lipid peroxidation and free radicals production. EtOH exposure induces the catalytic expression of oxidative metabolizing enzymes which is parallel to enhancing the production of ROS (Figure 1). Alcohol works on the brain to produce its desired effects, e.g., sociability and intoxication, and hence the brain is an important organ for exploring subsequent harms.
Conversely, microglial activation and neurodegeneration were clearly shown in rats exposed to intermittent alcohol treatment 91. Indeed two-photon microscopy has been used to demonstrate the rapid response of microglia to even single acute alcohol exposure 92. Microglial activation has also been investigated in response to heavy session intermittent drinking in rodents 93. It has been suggested that peripheral inflammation could be caused by stimulation of systemic monocytes and macrophages or by causing gastrointestinal mucosal injury 93. This innate response was linked to the perpetuation of the immune cascade via microglial activation which produces neuroinflammation 94 this, in turn has been shown to affect cognitive function 93.