Alcohol and the Brain: An Overview National Institute on Alcohol Abuse and Alcoholism NIAAA

As ions move through the receptor channels, an electrical current is spread over the cell membrane. Globally an estimated 237 million men and 46 million women have alcohol use disorders, according to WHO’s 2018 Global status report on alcohol and health. Excessive drinking also inhibits the pituitary secretion of anti-diuretic hormone (ADH), which acts on the kidney to reabsorb water. When ADH levels drop, the kidneys do not reabsorb as much water; consequently, the kidneys produce more urine. Alcohol depresses the nerve centers in the hypothalamus that control sexual arousal and performance.

1. Surprisingly however, Gsk3β in the NAc is inhibited by alcohol in rats [40], emphasizing the region-specificity of alcohol’s action.
2. Accordingly, it was natural to assume that ethanol would act on GABAA receptors in a manner similar to other sedative drugs.
3. Alcohol’s actions on inhibitory neurotransmission in this lower area of the central nervous system may cause some of alcohol’s behavioral effects.
4. The study had a large population sample (36,678 healthy adults ages 40-60) adjusted for age, sex, height, socioeconomic status, and country of residence, etc.
5. Another area requiring further research relates to individual differences in resilience and susceptibility to AUD.

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. Recent advances in neurotechnologies have opened new avenues of investigation into how alcohol-induced alterations in neural circuit activity influence ongoing behaviors and decision-making (Figure 2) [4,68].

Furthermore, GIRK channels (Herman et al., 2015) and the hyperpolarization-activated and cyclic nucleotide-gated (HCN) channel current (Ih) (Appel et al., 2003; McDaid et al., 2008; Nimitvilai et al., 2016b) may also be involved in ethanol stimulation of dopamine neuron firing. It is now clear that dopamine neurons are heterogeneous, and recent reports have identified a subset of VTA dopamine neurons with greater sensitivity to ethanol’s effects (Avegno et al., 2016; Mrejeru et al., 2015; Tateno and Robinson, 2011) (Figures 2A and ​and2D).2D). The chronic and withdrawal effects of ethanol on dopamine neuron firing are mixed, with decreases observed in anesthetized rats (Diana et al., 1996) but no change (Okamoto et al., 2006; Perra et al., 2011) or increases (Didone et al., 2016) detected in slices. Repeated in vivo ethanol downregulates Ih density in dopamine neurons (Okamoto et al., 2006) and induces adaptations in the dopamine D2 receptor and GIRK channels (Perra et al., 2011) (Figure 3C). Thus, while changes in dopamine neuron firing are among the most consistent effects of ethanol, more work is needed to pin down the mechanisms underlying this effect. Ethanol distribution in the body and brain is similar to water, with equilibration throughout organs and cells within a few minutes of drinking.

Having multiple tools to minimize stress and anxiety is necessary for good mental health. Still, you should not rely on alcohol as a primary source of nutrients as it won’t provide enough of each nutrient to meet your needs. Whole foods ultimately are better sources of nutrients without the added risks of alcohol. For instance, drinking excess alcohol can impair nutrient absorption and metabolism of vitamins. Drinking too much alcohol, or more than recommended limits per week, can cause health problems over time.

Core Resource on Alcohol

Some of the neurological pathways known to be affected by alcohol consumption include the dopaminergic, serotoninergic, γ-amino butyric acid (GABA) and glutamate pathways. The particular symptom of intoxication will depend on where in the brain the suppression of neuron activity is there a difference between a sober house and a halfway house occurs. As the blood alcohol concentration increases, new symptoms of intoxication emerge (Figure 2.1). The medulla, or brain stem, controls or influences all of the bodily functions that are involuntary, like breathing, heart rate, temperature and consciousness.

3. Alcohol and Neuroinflammation

For instance, the protein tyrosine kinase (PTK) Fyn, through the phosphorylation of GluN2B in the dorsomedial striatum (DMS) of rodents, contributes to molecular and cellular neuroadaptations that drive goal-directed alcohol consumption [51,52]. Interestingly, Fyn also plays a role in heroin use [53], suggesting a more generalized role of the kinase in addiction. Furthermore, GsDREADD-dependent activation of the serine/threonine kinase protein kinase A (Pka) in the DMS of mice activates Fyn specifically in D1R MSNs to enhance alcohol consumption, suggesting that Pka is upstream of Fyn [54]. Indeed, a large body of evidence supports the role of Pka signaling in the actions of alcohol [3]. Interestingly, phosphodiesterase 4 and 10a (Pde4 and Pde10a), enzymes required for the termination of Pka activity [55], have also been implicated in AUD [56]. Furthermore, a genome-wide association study identified PDE4B as a risk factor in elevated alcohol consumption [6,7].

These dual, powerful reinforcing effects help explain why some people drink and why some people use alcohol to excess. With repeated heavy drinking, however, tolerance develops and the ability of alcohol to produce pleasure and relieve discomfort decreases. Long-term, heavy drinking causes alterations in the neurons, such as reductions in their size. Alcohol is the first thing people go for when they are at a social gathering and are looking to have a pleasant time. It is the first choice in the long list of things which can make a person feel intoxicated and give that feeling of high.

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Voltage-sensitive calcium channels are pores in the cell membrane that admit calcium into the neuron in response to changes in electrical currents generated in the neuron.2 Short-term alcohol consumption inhibits calcium flow through these channels. Long-term alcohol exposure results, however, in a compensatory increase in calcium flow, which becomes excessive when alcohol consumption ceases. Evidence suggests that medications that inhibit calcium channel function (i.e., calcium channel blockers such as nimodipine) can relieve the seizures accompanying alcohol withdrawal (Valenzuela and Harris 1997). Alcohol might also increase inhibitory neurotransmission by increasing the activity of inhibitory neuromodulators, such as adenosine. Activation of the adenosine system causes sedation, whereas inhibition of this system causes stimulation.

Alcohol Consumption and Changes in the Brain

This property contributed to the idea that many of ethanol’s effects involve its occupation of water-filled cavities in proteins and subsequent alteration of function. Considering the ubiquity of distribution and low drug potency, ethanol acts on numerous molecular targets in neurons and synapses throughout the brain. This lack of specificity can be daunting to those who study potent and specific drugs, including drugs of abuse with circumscribed primary molecular targets (e.g., opiates). However, even these target-specific drugs produce complex secondary neuroadaptations that contribute to drug use disorders.

However, there has been debate about the mechanisms involved in this tonic current effect. In the cerebellum, there is evidence that ethanol’s enhancement of interneuron firing is a key factor underlying increased tonic current (Valenzuela and Jotty, 2015), but this may not be the case in other brain regions. Although ethanol potentiates the firing of dopamine neurons, it inhibits the firing of midbrain GABAergic neurons (Adermark stages of alcoholism et al., 2014; Burkhardt and Adermark, 2014; Stobbs et al., 2004) (Figure 2G). Interneurons of the striatum are also differentially affected by acute ethanol (Blomeley et al., 2011; Clarke and Adermark, 2015). Ethanol decreases the tonic firing frequency of cholinergic interneurons in the striatum, which then affects the activity of medium spiny neurons (MSNs) (Adermark et al., 2011b; Blomeley et al., 2011) (Figure 2H).

However, neuroimaging studies on the effects of alcohol use and dependence have either excluded women or shown low female enrolment [154]. Consideration of gender- and sex-related effects has also been limited, in part due to a lack of power [154]. Rates of alcohol dependence have increased drastically in women and many of the harmful health effects are more severe and occur more rapidly in women [155]. This underscores the need to examine sex- and gender-related alterations on brain function and structure in alcohol use; improving our understanding of these effects may enable tailoring of pharmacotherapeutic treatments to improve outcomes. Impulsivity, a term used to describe a lack of inhibitory control characterized by reckless behavior in the absence of premeditation, has multiple domains including choice, trait, and response inhibition [106].

It is important to keep in mind, however, that frontal brain systems are connected to other regions of the brain, and frontal abnormalities may therefore reflect pathology elsewhere (Moselhy et al. 2001). Brain cells (i.e., neurons) communicate using specific chemicals called neurotransmitters. Specialized synaptic receptors on the surface of neurons are sensitive to specific neurotransmitters.

On the other hand, top-down approaches begin with ethanol-related physiological or behavioral changes leading to the study of specific molecular mechanisms and brain circuits contributing to these effects. Dopaminergic function following chronic alcohol consumption has been extensively investigated with several targets for potential therapeutics being discovered. 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].

Functional MRI brain scans were used to assess brain changes in the participants and the control group. The researchers found negative associations between alcohol intake and brain macrostructure and microstructure, global brain volume, regional gray matter volume, and white matter microstructure. About 90% of gray matter (which serves to process information in the brain) showed a negative association with alcohol intake. The most affected brain regions were the frontal lobe (responsible for our executive functions), parietal lobe (involved in sensory perception and integration), and insular part of the brain (involved in processing positive and negative emotions). However, changes were also seen in the brain stem (regulates automatic body functions essential for life), putamen (involved in learning and motor control), and amygdala (regulates emotions such as fear and aggression).

Alcohol doesn’t kill brain cells, but it does have both short- and long-term effects on your brain, even in moderate amounts. But if you find yourself drinking heavily or binge drinking often, consider reaching out for help. Alcohol can have additional effects on developing brains, which are more vulnerable to the effects of alcohol. While the long-term effects of alcohol on the brain can be quite serious, most of them of the damage is reversible is you stop drinking.

FASDs interfere with the brain’s growth and development, leading to lifelong physical, mental, and behavioral problems. FASDs are an umbrella term for different conditions caused by exposure to alcohol in utero. Schematic representation of alcohol’s effects on the balance of inhibitory signs of a functioning alcoholic and excitatory neurotransmission in the brain. Schematic drawing of the human brain, showing regions vulnerable to alcoholism-related abnormalities. According to this hypothesis, alcoholism accelerates natural chronological aging, beginning with the onset of problem drinking.