Alcohol and Dopamine: How Does Alcohol Affect Dopamine Levels

This complex interaction is part of what makes alcohol’s effects on the brain so intricate and potentially problematic. Dopamine, often referred to as the “feel-good” neurotransmitter, plays a vital role in our brain’s functioning. When we engage in activities that our brain perceives as rewarding, such as eating delicious food, having sex, or experiencing the initial effects of alcohol, dopamine is released, creating feelings of pleasure and reinforcing the behavior. Understanding the basics of the dopamine system provides a foundation for exploring how alcohol interacts with this crucial neurotransmitter. By grasping the intricate mechanisms involved in dopamine transmission and regulation, we can better comprehend how alcohol affects the delicate balance of dopamine in the brain.

• Partial dopamine D2 agonists, therefore, offer the opportunity to treat the dysregulated dopamine activity during acute alcohol consumption as well as alcohol dependence.
• Thus, MOR antagonist medication may be more effective in reducing cravings and delaying the onset of drinking in women than in men.
• Furthermore, understanding how individuals react differently to glutamate depending on age, sex, and duration of cannabis use, among other factors, may enable clinicians to customize treatments according to each patient’s needs.
• Literature search, data extraction, and assessment of risk of bias were performed by Nathalie Barrios, Will Riordan, and Yasmin Zakiniaeiz.
• One abstract (Colizzi et al. 2019) was combined with its full article (Colizzi et al. 2020), resulting in a total of 9 randomized studies.

Preclinical as well as clinical studies have shown that substances indirectly targeting the mesolimbic dopamine system may be potential targets for attenuation of alcohol reward. Several studies have demonstrated a dose-response relationship between alcohol intake and dopamine release in the nucleus accumbens, indicating that a higher dose of alcohol leads to greater dopamine release 7. This discrepancy may be due to methodological differences in the studies, such as varying alcohol concentrations of 10% 40 compared to 20% 44 of alcohol w/v per delivery, and the binge drinking design in one study 44. These findings also suggest that at high enough doses, dopamine responses may be low, indicating that alcohol can be aversive and presumably less reinforcing. This is consistent with reports of lowered or ‘blunted’ dopamine responses in people with chronic alcohol use relative to non-drinking counterparts 13, 32, 66.

What treatments target dopamine receptors to help with alcohol addiction?

These observations indicate that alcohol stimulates the activity of endogenous opioid peptides, leading indirectly to the activation of dopaminergic neurons. Opioid peptide antagonists would interfere with this process, thereby reducing dopamine release. Moreover, individual differences in personality traits, stress levels, and environmental factors can all influence how alcohol affects dopamine function.

Imaging protocol used in each study

Additionally, genetic variations in nAChR subunit genes, such as CHRNA5, have been linked to differences in alcohol sensitivity and risk for alcohol use disorder. While alcohol can initially produce feelings of pleasure and relaxation due to increased dopamine release, chronic alcohol use can lead to dopamine dysregulation, potentially contributing to or exacerbating mental health issues such as depression and anxiety. The cycle of increased drinking to combat negative emotions, followed by worsening mood due to dopamine depletion, can be particularly challenging for individuals with co-occurring mental health and alcohol use disorders. Some individuals may have genetic variations that affect their dopamine receptors or the enzymes involved in dopamine metabolism. For example, certain alcohol gene mutations can influence dopamine function and potentially alter an individual’s susceptibility to alcohol addiction. These genetic differences can affect how a person responds to alcohol, including the intensity of the dopamine response and the likelihood of developing alcohol use disorders.

Two more studies examined the prefrontal cortex under conditions of stress 42 and prenatal alcohol exposure 45 and thus cannot be directly compared to the first study. More studies are needed to examine the impact of sex on the relationship between alcohol use and dopamine, as well as to investigate the involvement of other brain regions in the dopaminergic pathways. Indeed, our analysis of dopamine transient dynamics revealed faster dopamine uptake in caudate and putamen of alcohol-consuming female, but not male, macaques. Thus, any apparent dopamine uptake differences in the male macaque groups presented here are a function of faster clearance times due to decreased dopamine release and not faster dopamine clearance rates per se. Interestingly, across multiple studies, chronic alcohol use resulted in enhanced dopamine uptake rates, though this effect has been found to vary between species and striatal subregions (for review, see 10).

The Link Between Dopamine Deficiency and Depression in Alcohol Dependence

Two studies assessed relationships between dopamine and alcohol-related behavior 40, 44 or cognitive functioning 44. Another study, conducted in alcohol withdrawal conditions did not observe any relationships between ex vivo FSCV dopamine concentration in the nucleus accumbens and alcohol intake, active lever presses, or decision-making outcome measures in male and female rats that completed a gambling task 44. The dopamine deficiency hypothesis is supported by a study showing decreased dopamine receptor gene expression after several months of voluntary alcohol drinking 103. In addition, microdialysis studies in freely moving outbred rats show a decreased dopamine output in the NAc, compared to age‐matched alcohol‐naïve controls, following 7 weeks 104 and 10 months 29 of voluntary alcohol consumption. Furthermore, after 10 months of drinking, a blunted dopamine response following a systemic alcohol challenge has been found in long‐term drinking, compared to alcohol‐naïve rats 29. These results indicate that long‐term drinking attenuates the responsiveness of the system to external dopamine stimulation, in addition to decreasing baseline levels of dopamine.

The dopamine system and alcohol dependence

Given dopamine’s pivotal role in the development and maintenance of alcohol dependence, medications targeting dopamine does constitute an important area of research. Although promising preclinical results, the majority of results from the clinical studies with dopamine‐acting medications have thus far been discouraging. The side effects profile of many of the evaluated compounds, including typical antipsychotic drugs, render them clinically unfavourable. On the other hand, newer dopamine agents, without complete antagonism or agonism, especially the dopamine stabilizers show promise and deserve further investigation in alcohol‐dependent patients. The hypothesis that atypical antipsychotics may does alcohol release dopamine decrease alcohol intake are supported by two separate studies with risperidone and olanzapine in high‐alcohol‐preferring rats 154, 155.

Increased Urination & Dehydration

Before we dive into alcohol’s impact, it’s important to remember that the amount you drink completely changes its overall effect on your brain health. But, there is some evidence showing that light and moderate drinking may have its upsides too. The chemicals in alcohol actually reduce the production of GABA in the brain and throughout the body. When people do not have enough GABA to regulate their emotions, they often experience more mental health issues such as stress, depression, and paranoia.

Avoiding alcohol during a dopamine reset helps us reap the full benefits of the practice. Skipping the drink not only prevents disruption of dopamine levels, but it also supports other neurotransmitters such as serotonin, which is responsible for feelings of happiness. However, in our world today, there are so many things that can give us an artificial dopamine boost and oversaturate our brain that we continue to chase these highs. Data reports show that the average time people spend on social media per day skyrocketed from 90 minutes in 2013 to 143 minutes in 2024. The National Center for Drug Abuse Statistics reports that 13.5% of Americans 12 and over used drugs in the last month, which is a 3.8% increase year-over-year.

• A study has also investigated the effect of dopamine D2 receptor agonist administration into VTA on alcohol intake.
• For example, alcohol modulates the serotonin levels in the synapses and modifies the activities of specific serotonin receptor proteins.
• Dopamine uptake was also enhanced in females, but not males (regardless of abstinence state).
• Based on the hypothesis that OSU6162 can counteract both hyper‐ and hypo‐dopaminergic states, the compound has recently been evaluated in both animal models modulating alcohol‐mediated behaviours as well as in a placebo‐controlled human laboratory study in alcohol‐dependent patients.

Here, we aim to review the animal and human data describing the role of dopamine and the mesolimbic dopamine system during acute and chronic alcohol exposure. Finally, preclinical and clinical studies evaluating the potential of available dopaminergic agents as well as indirect dopamine modulators as novel medications for alcohol dependence are discussed. Alcohol dependence is a chronic relapsing psychiatric disorder significantly contributing to the global burden of disease 1 and affects about four percent of the world’s population over the age of 15 (WHO). In the fifth edition of the diagnostic and statistical manual of mental disorders (DSM), the term alcohol use disorder was introduced and grossly defined as problem drinking that has become severe. The characteristics of this disorder include loss of control over alcohol intake, impaired cognitive functioning, negative social consequences, physical tolerance, withdrawal and craving for alcohol. To date, there are three medications approved by both the European Medicines Agency (EMA) and the Food and Drug Administration (FDA) for the treatment of alcohol dependence; disulfiram, naltrexone and acamprosate.

In the next section, we will explore strategies and approaches for treating alcohol addiction by modulating dopamine and the reward system. It’s important to note that the effects of alcohol on dopamine can vary among individuals. Genetic factors, previous alcohol exposure, and other individual characteristics can influence how an individual’s brain responds to alcohol.

4, the final quinpirole treatment time points (i.e., after 30 min in quinpirole) were analyzed with a two-factor ANOVA (treatment group and region). The atypical antipsychotic tiapride has been found to be efficacious in reducing alcohol drinking two placebo‐controlled clinical trials 158, 159. A small study in twenty alcohol‐dependent individuals, with significant levels of anxiety or depression, showed that tiapride treatment causes a reduced alcohol intake as well as prolonged periods of abstinence 158. In the largest of the studies 159, 100 recently abstinent alcohol‐dependent patients were randomized to 300 mg of tiapride or placebo for a 3‐month treatment period.

Furthermore, studies with intra‐VTA alcohol infusions highlight that different subregions within the heterogeneous VTA might have different ability to modulate the alcohol‐induced dopamine response. Specifically, rats voluntarily self‐administer alcohol, as well as acetaldehyde (an alcohol metabolite) into the posterior, but not anterior, part of the VTA 80–85, indicating that alcohol is reinforcing only within the posterior VTA. In corroboration are the findings that the sensitivity of the posterior VTA to the reinforcing effects of alcohol is enhanced in alcohol‐preferring rats 88.

How does alcohol affect the brain and neurotransmitters?

The mesocortical system also originates primarily in the A10 cell group and affects various regions of the cerebral cortex. Chronic alcohol consumption induces compensatory upregulation of NMDA receptors, heightening excitatory signaling and contributing to tolerance. Upon cessation, this heightened glutamatergic activity leads to withdrawal symptoms such as agitation, anxiety, and, in severe cases, seizures and delirium tremens. This hyperexcitable state underscores NMDA receptor dysregulation’s role in alcohol dependence and withdrawal syndromes.

Criteria being met indicate a low risk of bias, while criteria not being met indicate a high risk of bias. An unclear response indicates insufficient details have been reported to properly assess the risk of bias. Studies were assessed by the first and second authors independently, with inconsistencies being resolved by the senior author. A dopamine detox is a temporary solution that uses abstinence to reduce the risk of alcohol dependence.