How Alcohol Compounds Its Damage to the Brain

a clean brain vs a brain with drugs and alcohol

Even when people are subjected to the same environmental conditions, their responses to a given dose of alcohol vary significantly on metabolic, physiological, subjective, cognitive, motor, and other measures (Reed 1985). The pharmacokinetics (time course of absorption, distribution, metabolism, and excretion of ethanol) varies significantly when alcohol is administered orally, but much less so when alcohol is given intravenously (Grant et al. 2000). Alcoholism has devastating consequences, but not all alcoholics are equally at risk for brain changes and neurobehavioral deficits.

What do healthcare professionals who work with adolescents need to know about alcohol?

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]. Work in animal models has also shown that exercise changes gene expression by altering both histones and the molecular tags directly attached to DNA. This increases the activity of genes important to the activity and plasticity of neurons, supporting the idea that exercise improves learning and memory and can decrease the risk of dementia.

Learn More About the Adolescent Brain and Substance Use

In the CeA, for example, CRF levels and GABA transmission are increased and remain so during acute withdrawal. Interestingly, acute ethanol exposure following chronic ethanol treatment has the same effect as acute ethanol in naive animals, suggesting that acute ethanol-induced facilitation of GABA transmission does not undergo tolerance (Roberto et al., 2004a) (Figure 3G). While the most immediate effects of alcohol usually subside within a week, some symptoms like sleep disturbances and mood changes can persist. Dr. Mathis explains, “This happens because the brain downregulates the neurotransmitters and their receptors.” Essentially, during heavy drinking episodes, the brain is overwhelmed with high levels of dopamine and serotonin. Once alcohol consumption ceases, this change results in a deficiency of neurotransmitters and takes a toll on your mental health.

Level 3: Alcohol’s effects on transcriptional activity

a clean brain vs a brain with drugs and alcohol

Just as drugs produce intense euphoria, they also produce much larger surges of dopamine, powerfully reinforcing the connection between consumption of the drug, the resulting pleasure, and all the external cues linked to the experience. Large surges of dopamine “teach” the brain to seek drugs at the expense of other, healthier goals and activities. Some drugs like opioids also disrupt other parts of the brain, such as the brain stem, alcoohol is better than drugs which controls basic functions critical to life, including heart rate, breathing, and sleeping. Here, we outline a framework for understanding alcohol-induced changes in the brain, which can help you appreciate the challenges faced by many patients with AUD when they try to cut back or quit drinking. We then describe evidence-based treatments you can recommend to patients to help the brain, and the patient as a whole, to recover.

a clean brain vs a brain with drugs and alcohol

  • 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).
  • “Additional behaviors such as drinking on an empty stomach or polysubstance use also interfere with how the body processes alcohol [and] further increase risk for alcohol-related blackouts.”
  • Accordingly, it was natural to assume that ethanol would act on GABAA receptors in a manner similar to other sedative drugs.

These ideas first were developed in a series of articles from the laboratory of Virginia Davis, including articles published in Science and Nature (Davis and Walsh 1970; Yamanaka et al. 1970). The idea that alcohol is only a “pro-drug” and that acetaldehyde is the effective agent has a boomerang quality because it is discarded every few years, only to return later. In fact, evidence continues to accumulate that alcohol consumption can result in brain acetaldehyde levels that may be pharmacologically important (Deng and Deitrich 2008). However, the role of acetaldehyde as a precursor of alkaloid condensation products is less compelling. In addition to structural alterations, evidence suggests that chronic exposure to alcohol can lead to functional dysregulation of key brain systems that control behaviour such as reward processing, impulse control and emotional regulation.

Understanding convergence and divergence between mechanisms in males and females will continue to be critical moving forward [111,112]. The kinase mTOR in complex 1 (mTORC1) plays a crucial role in synaptic plasticity, learning and memory by orchestrating the translation of several dendritic proteins [39]. MTORC1 is activated by alcohol in discrete brain regions resulting in the translation of synaptic proteins such as Collapsin response-mediated protein 2 (CRMP2) [40] and ProSap-interacting protein 1 (Prosapip1) [41], as well as Homer1 and PSD-95, GluA2 and Arc [40,42,43]. Through the translation of these transcripts and others, mTORC1 contributes to mechanisms underlying alcohol seeking and drinking as well as reconsolidation of alcohol reward memories and habit [44–46]. Further, protein translation plays a role in additional alcohol-dependent phenotypes (Figure 1). For example, the activity of mRNA binding protein fragile-X mental retardation protein (Fmrp), which plays an important role in translation [47], is enhanced by alcohol in the hippocampus of mice resulting in alteration in the expression of synaptic proteins [48].

Furthermore, the CeA and BNST regions are anatomically connected, and inhibition of CRF neurons projecting from the CeA to the BNST decreases escalation of alcohol intake and somatic withdrawal symptoms in rats [87]. The frontal lobes are connected with the other lobes of the brain, and through multiple interconnections, they receive and send fibers to numerous subcortical structures as well (Fuster 1997, 2006). The anterior region of the frontal lobes (prefrontal cortex) plays a kind of executive regulatory role within the brain (Goldberg 2001; Lichter and Cummings 2001). Executive functions (which depend upon many of our cognitive abilities, such as attention, perception, memory, and language) are defined differently by different theorists and researchers.

  • Cumulatively, alcoholism leads to thiamine deficiency via the reduction of intake, uptake, and utilization.
  • While these approaches are just beginning to be applied within the field, there are some intriguing findings.
  • Furthermore, the size of the corpus callosum is notably reduced with age in alcoholic men (Pfefferbaum et al. 1996).
  • Thus, excessive alcohol use impairs the executive and motivational functions that determine self-regulation and goal-directed behavior and can, in turn, result in a further increase in alcohol intake, tolerance, and dependence.
  • In summary, alcohol can contribute to neurotoxicity via thiamine deficiency, metabolite toxicity and neuroinflammation.

It also fits the description of people with lesions of the frontal lobes, who are characterized as “impulsive, inconsiderate, uninhibited, inflexible, or ill-mannered….” (Brewer 1974, p. 41). As a group, alcoholics share this constellation of behaviors characteristic of frontal lobe dysfunction, which also can include impaired judgment, blunted affect, poor insight, distractibility, cognitive rigidity, and reduced motivation. To probe impulsiveness through fMRI, response inhibition tasks are commonly used, such as the Go/no-go (GNG) task and Stop Signal Task (SST). Such studies have found that adolescents who later transitioned into heavy drinking had lower BOLD activation at baseline and increased activation in frontal regions when subsequently drinking heavily compared with continuous non-drinkers [110,111].

How health care leaders can prioritize health equity for the LGBTQIA2+ community

  • No significant relationships were found between cortical thickness changes and current substance abuse (including drugs other than alcohol), or psychiatric disorders, or past cigarette smoking.
  • “Drinks with higher alcohol content will cause a stronger and faster response than drinks with low alcohol content,” notes Samuel Mathis, MD, a board-certified family medicine doctor and assistant professor of family medicine at the University of Texas Medical Branch.
  • These ideas first were developed in a series of articles from the laboratory of Virginia Davis, including articles published in Science and Nature (Davis and Walsh 1970; Yamanaka et al. 1970).
  • Another example is the transcriptional regulator, LIM Domain Only 4 (Lmo4), which was shown to drive vast changes in gene expression in the basolateral amygdala (BLA) of mice in response to repeated exposure to alcohol and to the regulation of alcohol intake [30].
  • Advances in neuroscience continue to shed light onto regulatory mechanisms relevant for alcohol use.

Ethanol’s actions on these channels were not defined until the mid 1990s (e.g., Dopico et al. 1996). In flies, a high sugar diet can reprogram the ability to taste sweetness by tapping into a gene expression network involved in development. High amounts of alcohol use are causal risk factors in the development of disease in the heart, liver, pancreas, and brain (including the brains of children in utero). When it comes to adults, excessive alcohol use can cause multiple well-defined brain issues ranging from short-term confusion to dementia. In an acute sense, consumption of alcohol can lead to uninhibited behavior, sedation, lapses in judgment, and impairments in motor function.

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