Heavy Alcohol Use Causes Long-Term Brain Damage

/in /by

The physiological mechanisms thought to underlie this ethanol potentiation were reviewed by Morikawa and Mornsett (2010) and include reductions of a barium-sensitive potassium and M-type currents. Ethanol facilitates action potential firing of midbrain dopamine neurons (Figure 2A) difference between aa and na and increases extracellular dopamine levels in the VTA (Deehan et al., 2016) (Figure 2C). Clearly, the SK channel has important roles in neuroadaptations that alter ethanol-related behaviors.

How much is too much for alcohol to start affecting the brain? From the earliest traces of brewing, which happened about 10,000 years ago, to former trade negotiations and family celebrations – the use of alcohol intertwined with people’s everyday life. But researchers have a lot to say about how alcohol affects the brain in the long run. People with severe addictions or a long history of alcohol misuse may suffer serious withdrawal symptoms when quitting.

How Alcohol Affects the Brain and Behavior

For the first time researchers demonstrate in an animal how heavy alcohol use leads to long-term behavioral issues by damaging brain circuits critical for decision-making. Alcohol can impair your ability to think, damage your brain cells, and increase your risk of long-term conditions such as memory loss and addiction. If you feel you’re at risk of suicide due to heavy drinking, consult a mental health professional. Studies indicate a link between chronic alcohol consumption and long-term neurological complications. Heavy alcohol consumption can also potentially contribute to cognitive impairment, memory deficits, and mood disorders.

Fetal alcohol syndrome

Studies have shown that the heavy, prolonged consumption of alcohol can trigger mental health issues, including anxiety and depression, and can lead to alcohol use disorder. There is no lack of literature exposing the long-term effects of alcohol on the brain. The amount of alcohol someone drinks, how often they drink, at what age they started drinking, family history, gender, genetics and health status are some of the most common triggers. With time, increasing the BAC levels might be enough to create long-term effects on the brain. And when someone drinks, the alcohol reaches crucial areas of the brain — cerebral cortex, frontal lobe, hippocampus, hypothalamus, cerebellum — which impairs a person’s balance, judgment, speech and memory, and forces the brain to work harder. The effects of alcohol on the brain vary depending on the dose and on individual factors, such as overall health.

Cognitive and Behavioral Disorders

The brain mediates our motivation to repeat behaviors that lead to pleasurable, rewarding states or reduce uncomfortable, distressing physical or emotional states. Save my name, email, and website in this browser for the next time I comment. Understanding the molecular mechanisms and network-level changes provides opportunities for targeted interventions and the development of novel pharmacological treatments. Alcohol’s influence on brain chemistry is multifaceted, involving interactions with multiple neurotransmitter systems, modulation of neural pathways, and induction of neuroplastic changes. Neuroplasticity refers to the brain’s ability to reorganize itself by forming new neural connections throughout life. While not a perfect analogue to specific ligands, alcohol can interact with the ligand-binding sites of various neurotransmitter receptors, modulating their activity.

Low levels of alcohol consumption have historically been viewed as harmless or even beneficial due to its potentially favorable effects on cardiovascular health , as described in more detail elsewhere in this special issue. These come in many different forms such as the consequences of damage during intoxication, e.g., from falls and fights, damage from withdrawal, damage from the toxicity of alcohol and its metabolites and altered brain structure and function with implications for behavioral processes such as craving and addiction. Alcohol dependence, also known as alcoholism, is characterized by a craving for alcohol, possible physical dependence on alcohol, an inability to control one’s drinking on any given occasion, and an increasing tolerance to alcohol’s effects (American Psychiatric Association APA 1994). Such confluence of information can provide evidence linking structural damage, functional alterations, and the specific behavioral and neuropsychological effects of alcoholism.

Depression, a group of conditions that lower a person’s mood, affects about 80 percent of alcoholics at some point. It also affects your body’s hormonal systems and can cause or exacerbate mental health problems. Symptoms of Korsakoff syndrome are typically more severe than those of alcoholic dementia.

Alcohol use can damage the hippocampus, the part of your brain responsible for memory and learning. Research indicates that heavy alcohol use can also increase the risk of suicide. Any amount of alcohol can diminish your judgment and functioning, and even low or moderate alcohol use can have harmful effects on different organs. Oftentimes, we aren’t thinking about how much or how often we consume alcohol or its effects on the body. Although rates of drinking and binge drinking have been going down over recent decades, national surveys show that among youth and young adults, one in five report drinking alcohol in the past 30 days, and one in 10 report binge drinking.

Whether you’re a casual drinker, someone struggling with addiction, or a concerned friend or family member, knowledge is power. It’s also worth noting that alcohol addiction often doesn’t occur in isolation. One area of particular interest is the potential for brain plasticity to aid in recovery. For those already struggling with alcohol-related issues, it’s crucial to recognize that help is available. Strategies for improving decision-making and impulse control often involve mindfulness techniques and cognitive training exercises.

For example, in rats exposed to alcohol for up to 5 days, there was an increase in histone 3 lysine 9 acetylation in the pronociceptin promoter in the brain amygdala complex. This may cause CNS depression leading to acute tolerance to these withdrawal effects. One of the proposed mechanisms for alcohol’s neurotoxicity is the production of nitric oxide (NO), yet other studies have found alcohol-induced NO production to lead to apoptosis (see Neuroinflammation section). An MRI brain scan found that levels of N-acetylaspartate (NAA), a metabolite biomarker for neural integrity, was lower in binge drinkers. This integration between the two cerebral hemispheres and cognitive function is affected.

The more we know about how alcohol affects the adolescent brain, the more we can inform the conversations about alcohol that we have with teens. The good news is that the special ability of the brain to change with experience during adolescence seems to also lend itself to recovery from some alcohol-induced changes.2 The more alcohol a person consumes, the more significant the memory impairment.4 If a person drinks enough, particularly if they do so quickly, alcohol can produce a blackout. Research suggests that the patterns in adolescent brain development may increase the likelihood of adolescents engaging in unsafe behaviors such as alcohol use.1 For example, the systems of the brain that respond to rewards and stressors are very active in adolescence. These learning experiences, complemented by the adolescent brain’s your ultimate biofeedback therapy toolkit increased ability to readily change in response to experiences (also known as brain plasticity), are key to developing the skills and knowledge to become independent.

However, though MRI research will be important in advancing our understanding of the impact of alcohol on the brain we cannot infer harm solely from alterations to brain structure. Quantitative analyses of brain macrostructure in FASD have repeatedly found lower grey and white matter volume along with increased thickness and density of cortical grey matter . Early case studies highlighted striking morphological anomalies, most notably thinning of the corpus callosum and enlargement of ventricles, but subsequent radiological investigations have highlighted there is considerable variability in the impact of FASD on brain development . 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. These effects are found in prefrontal, cingulate, and temporal regions as well as the corpus callosum and may reflect an acceleration of typical age-related developmental processes similar to what we have described in adults with alcohol dependence.

While much of the past focus has been on ethanol effects on molecules and synapses, there has been increasing realization that these targets must be considered in the context of micro- and larger circuits. Further study is required to understand the effect of ethanol on midbrain dopamine neurons, especially in light of recent findings on the anatomical and biochemical diversity of dopamine neurons (Lammel et al., 2008; Poulin et al., 2014). Thus, plasticity deficits in the NAc and hippocampus may contribute to behavioral adaptations to chronic ethanol (Coune et al., 2017). These changes could explain the effect of chronic ethanol exposure on striatal LTP, as paired activation of the mPFC and BLA inputs induces robust LTP of the corticostriatal input to the DMS (Ma et al., 2017). With novel optogenetic and transgenic tools, scientists can now study pathway-specific ethanol effects.

Neuroimaging studies have also dramatically advanced our understanding of the brain’s response to alcohol and the neurochemical basis of alcohol dependence. At the behavioral level, alcohol intoxication has been shown to increase risky behaviors such as risky driving, criminal behavior, and sexual promiscuity , whilst trait impulsivity has often been found to be increased in alcohol dependent individuals . 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 . For example, naltrexone, a µ-opioid receptor antagonist, can attenuate the increased BOLD response to alcohol-related cues in the putamen and reduce risk of relapse .

Impulsive Behavior

  • From the earliest traces of brewing, which happened about 10,000 years ago, to former trade negotiations and family celebrations – the use of alcohol intertwined with people’s everyday life.
  • Approximately one third of all babies born to alcoholic mothers will develop Fetal Alcohol Syndrome or Effects (FAS or FAE), causing central nervous system (CNS) dysfunctions including Attention Deficit Disorder (ADD) and impaired IQ.
  • This rapidly evolving field is providing information that will be valuable in addressing the large public health problem created by this small drug.
  • Mice lacking the GlyR alpha 2 subunit show reduced ethanol intake, but GlyR alpha 3 knockout mice show increased intake (Mayfield et al., 2016).
  • It should be noted that the impact of alcohol on the cerebellar structure has been relatively understudied and most MRI research has focused on cortical and subcortical structures.
  • These findings reinforce the idea that signaling through AC and PKA is involved in ethanol’s actions and are in accord with findings from invertebrate models (Moore et al., 1998).

Longitudinal MRI studies further showed that changes to volume follow a non-linear pattern with greater increases occurring in the early stages of abstinence 22,23,24. It should be noted that the impact of alcohol on the cerebellar structure has been relatively understudied and most MRI research has focused on cortical and subcortical structures. The emergence of magnetic resonance imaging (MRI) brought vast improvements to image resolution and allowed for differentiation of brain tissue. The link between alcohol use and cerebral atrophy goes back decades, with early findings coming from post-mortem investigations and subsequent in vivo examinations of gross morphology using computerized tomography (CT) 8,9,10. In order to improve treatment outcomes, a detailed understanding of the neurobiological mechanisms responsible for vulnerability, relapse and successful recovery and the identification of novel biomarkers to develop more efficacious therapeutic targets are warranted.

Additionally, while alcohol might provide temporary euphoria, drinking regularly may worsen depression and anxiety. The problem is that once your brain realizes it likes the effects of alcohol, it wants more to keep the good feeling going. Many people use a nightcap as a way to help them drift off to bed after a busy or stressful day, but drinking is likely to have a negative effect on your Prevent Drug Misuse sleep. If you’ve become alcohol-dependent, your brain can’t function normally without some amount of alcohol in your system.

This article discusses everything you need to know about the short-term effects of alcohol. As a central nervous system depressant, alcohol slows the body’s systems and leads to noticeable changes in cognitive and physical functions. Through a complex process of cell membrane ion pumps and neurotransmitter stimulation, the multi-faceted effects of alcohol and alcohol withdrawal are becoming better understood. Mice that have been exposed to chronically elevated levels of alcohol reveal increased numbers of NMDA receptors and NMDA related seizure activity. In vitro studies have demonstrated an increase in the binding sites for MK801 (dizocilpine) in neurons chronically exposed to alcohol.

  • The physiological consequences of these effects of ethanol are not fully clear, but roles in the effects of drugs on synaptic transmission are emerging, as discussed later in this review.
  • Another mechanism by which thiamine deficiency leads to cytotoxicity is by affecting carbohydrate metabolism leading to the reduction of the enzyme α-Ketoglutarate Dehydrogenase, leading to mitochondrial damage, which in turn induces necrosis .
  • Future research should help to clarify the importance of many neurochemical effects of alcohol consumption.
  • In a society where alcohol is a highly popular substance, if you don’t drink, you probably know someone who does.
  • “We now have a new model for the unfortunate cognitive changes that humans with alcohol use disorder show,” said author Patricia Janak, a Johns Hopkins University neuroscientist who studies the biology of addiction.

Following chronic ethanol exposure, LTD is altered such that D1-negative MSNs show LTD while D1-positive MSNs lose LTD, and sometimes show LTP (Jeanes et al., 2014; Renteria et al., 2017) (Figure 3O). Acute and chronic ethanol-induced changes in plasticity have also been extensively studied in the NAc, a region implicated in the rewarding effects of ethanol (reviewed in Renteria et al., 2016), and will only be briefly summarized here. It will be interesting to determine how these plasticity changes contribute to ethanol-induced cognitive impairment. Although studies have investigated the acute effects of ethanol on PFC NMDARs (Weitlauf and Woodward, 2008), few have investigated the effect on synaptic plasticity in this area. Indeed, high-dose ethanol treatment can transiently abolish NMDA-dependent LTD in hippocampal neurons and elicit cognitive deficits in rats (Silvestre de Ferron et al., 2015). Ethanol alters learning and memory (Oslin and Cary, 2003; White, 2003), and this may involve effects on synaptic plasticity, including long-term depression (LTD) and long-term potentiation (LTP) (reviewed in Zorumski et al., 2014).

The exact mechanism by which various concentrations of ethanol either activates or inhibits TLR4/IL-1RI signaling is not currently known, though it may involve alterations in lipid raft clustering or cell adhesion complexes and actin cytoskeleton organization. Ethanol can trigger the activation of astroglial cells which can produce a proinflammatory response in the brain. Additionally, abnormal brain metabolism, a loss of white brain matter in the frontal lobe, and higher parietal gray matter NAA levels were found. This dysfunction causes an increase in the neurotransmitter GABA in cerebellar Purkinje cells, granule cells, and interneurons leading to a disruption in normal cell signaling.