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Yes, alcohol releases dopamine in the nucleus accumbens, the brain area that assigns value to rewards, as PET imaging studies in humans show. It does so indirectly and alongside other chemical messengers, and with chronic drinking that system responds less and less to other rewards.
That double face explains why the first drink feels pleasant and why some people find it harder and harder to stop.
Does alcohol produce dopamine?
Alcohol does not make dopamine, because that neurotransmitter is synthesized by the neurons themselves. What it does is increase its release in the nucleus accumbens, a region of the ventral striatum linked to motivation and pleasure.
One of the classic pieces of evidence came from experiments with rats. In 1988, Di Chiara and Imperato used microdialysis to show that ethanol, like opiates, nicotine, amphetamine, and cocaine, raised extracellular dopamine above all in the accumbens (Di Chiara and Imperato, 1988).
In humans, confirmation came with PET scanning and the tracer [11C]raclopride, which competes with dopamine for D2 and D3 receptors. Boileau and colleagues gave alcohol with orange juice to six healthy volunteers and measured more dopamine in the ventral striatum than when they drank juice alone (Boileau et al., 2003).
In that study, the size of the change correlated with each participant’s impulsivity and with the rise in heart rate, considered a marker of alcohol’s stimulant effects. The finding adds to other work on the brain region that is activated by beer.
The table summarizes the human brain imaging studies cited in this article.
| Study | Participants | What they measured | Result |
|---|---|---|---|
| Boileau et al., 2003 | 6 healthy adults | Dopamine after drinking alcohol | Increase in the ventral striatum and nucleus accumbens |
| Urban et al., 2010 | 21 young social drinkers | Dopamine after drinking alcohol | Release throughout the striatum, greater in the ventral striatum, with differences between men and women |
| Mitchell et al., 2012 | Heavy drinkers and controls | Endogenous opioids after drinking | Release in the nucleus accumbens and orbitofrontal cortex |
| Volkow et al., 1996 | 10 people with alcoholism and 17 controls | Dopamine D2 receptors | Fewer available receptors in the alcoholism group |
| Volkow et al., 2007 | 20 detoxified people with alcoholism and 20 controls | Dopamine released by methylphenidate | 70% smaller increase in the ventral striatum |
How does alcohol reach the reward system?
Ethanol is a small molecule that easily crosses the blood-brain barrier, the filter that separates the blood from brain tissue. That is why it acts on the brain shortly after reaching the bloodstream.
Unlike cocaine, which blocks one specific target, the dopamine transporter, alcohol has no single target. It acts on several systems at once, including GABA (gamma-aminobutyric acid), glutamate, endogenous opioids, and serotonin, and dopamine is only one piece of that circuit (Gilpin and Koob, 2008).
One of the proposed pathways runs through GABA, the brain’s main chemical brake. By strengthening GABA signaling onto the interneurons that normally restrain dopamine neurons, alcohol could silence them and leave the dopamine neurons freer to fire (Gilpin and Koob, 2008).
Another pathway involves endogenous opioids, such as endorphins. In 2012, a PET study showed that drinking alcohol releases these molecules in the nucleus accumbens and in the orbitofrontal cortex (Mitchell et al., 2012).
Among the heavy drinkers in that study, release in the orbitofrontal cortex correlated with feelings of euphoria and with problem drinking.
Is alcohol a stimulant or a depressant?
It is both, depending on the moment. While blood alcohol concentration is rising, euphoria and disinhibition dominate, and as it falls, sedation and tiredness set in, which is known as the biphasic response.
King and colleagues gave 34 young people a drink containing 0.4 or 0.8 g of ethanol per kilogram of body weight, or a placebo. Heavy drinkers felt the stimulant effects more strongly, especially while blood alcohol concentration was rising, and felt less sedation than light drinkers (King et al., 2002).
To get a sense of the high dose, just calculate it for a 70 kg person and compare it with a 355 ml can of 5% beer. Ethanol has a density of 0.789 g/ml.
[math]70 \times 0.8 = 56 \ \text{g of ethanol}[/math]
[math]355 \times 0.05 \times 0.789 \approx 14.0 \ \text{g per can}[/math]
[math]\dfrac{56}{14.0} \approx 4 \ \text{cans}[/math]
The low dose in the trial is equivalent to about two cans for that same person. The sedative phase is the one many people mistake for good rest, something that alcohol actually worsens during the night.
What changes in the brain with chronic drinking?
With repeated drinking, the reward system adapts. People with alcoholism have fewer dopamine D2 receptors available in the striatum, and in Volkow’s 1996 study that reduction was not related to the number of days since the last drink (Volkow et al., 1996).
The amount of dopamine released also decreases. In 2007, the same group gave methylphenidate, a stimulant, to 20 people with alcoholism who had already been detoxified and to 20 controls, and the increase in dopamine in the ventral striatum was 70% smaller in the first group (Volkow et al., 2007).
Volkow, Wise, and Baler group the roles of dopamine in reinforcement, motivation, and self-control under the name dopamine motive system. With repeated exposure, cues associated with drinking gain strength while the response to other rewards and the capacity for self-control weaken (Volkow et al., 2017).
Koob and Le Moal describe addiction as a cycle in which the reward system works worse and worse while stress systems that counteract it become activated (Koob and Le Moal, 2008). In that state, drinking increasingly serves to stop feeling bad.
The same authors note that genetic and developmental factors influence who is more vulnerable to that cycle.
That reward deficit is part of the withdrawal state that appears after stopping drinking, along with anxiety and irritability (Gilpin and Koob, 2008). The same review describes persistent neuronal deficits with chronic drinking, some of which can recover completely after long periods of abstinence.
Does dopamine explain everything?
No, and its role should not be overstated. Nutt and his colleagues reviewed 40 years of research and concluded that there is strong evidence that stimulants raise dopamine in the human striatum, and only some evidence that alcohol does too (Nutt et al., 2015).
The same authors note that receptor availability and dopamine release are reduced in alcohol dependence. They also point out that viewing addiction as a dopamine disorder has not led to new treatments.
The medications with the strongest support act on other systems. A review of 122 clinical trials found that acamprosate and oral naltrexone, which blocks opioid receptors, reduce the return to drinking, with 12 and 20 patients treated for each relapse prevented (Jonas et al., 2014).
The fact that naltrexone works fits with the role of endogenous opioids described earlier. There are also more recent lines of research, such as psychedelics to treat alcoholism, which are still being studied.
Frequently Asked Questions (FAQ)
1. How long does it take the brain to recover its dopamine after quitting alcohol?
There is no established figure. The reduction in D2 receptors in people with alcoholism was not related to the number of days since the last drink (Volkow et al., 1996), and people who had already been detoxified showed, compared with controls, a 70% smaller increase in dopamine in the ventral striatum after receiving methylphenidate (Volkow et al., 2007). Some of those deficits can recover completely after long periods of abstinence (Gilpin and Koob, 2008).
2. Is alcohol a stimulant or a depressant?
It has a biphasic effect. While blood alcohol concentration is rising, euphoria and disinhibition dominate, and as it falls, sedation and tiredness set in. Heavy drinkers feel the stimulant part more and the sedative part less than light drinkers (King et al., 2002).
3. Why doesn’t coffee sober you up?
Caffeine blocks the adenosine receptors that mediate part of the drowsiness and motor clumsiness caused by alcohol, so the person feels more alert without their blood alcohol concentration going down. A 2011 review also proposes that caffeine may enhance the effect of the dopamine released by alcohol and encourage people to drink more (Ferré and O’Brien, 2011).
4. Are people with ADHD at higher risk of alcoholism?
Yes, according to a meta-analysis of studies that followed children with and without ADHD into adolescence or adulthood. Children with ADHD were not more likely to have tried alcohol, but they were more likely to develop abuse or dependence (Lee et al., 2011). The idea that they drink to make up for a dopamine deficit is a hypothesis that those studies do not test.
5. Does alcohol release the same dopamine in men and women?
Not exactly. A PET study of 21 young social drinkers found significant sex differences in dopamine release after drinking, and only in men was that release related to the feeling of activation (Urban et al., 2010). The authors frame this as a possible clue to the differences in vulnerability to alcoholism between men and women.
References
1. Boileau, I., Assaad, J. M., Pihl, R. O., Benkelfat, C., Leyton, M., Diksic, M., Tremblay, R. E., & Dagher, A. (2003). Alcohol promotes dopamine release in the human nucleus accumbens. Synapse, 49, 226-231. https://doi.org/10.1002/syn.10226
2. Di Chiara, G., & Imperato, A. (1988). Drugs abused by humans preferentially increase synaptic dopamine concentrations in the mesolimbic system of freely moving rats. Proceedings of the National Academy of Sciences, 85, 5274-5278. https://doi.org/10.1073/pnas.85.14.5274
3. Ferré, S., & O’Brien, M. C. (2011). Alcohol and caffeine. The perfect storm. Journal of Caffeine Research, 1, 153-162. https://doi.org/10.1089/jcr.2011.0017
4. Gilpin, N. W., & Koob, G. F. (2008). Neurobiology of alcohol dependence. Focus on motivational mechanisms. Alcohol Research & Health, 31, 185-195.
5. Jonas, D. E., Amick, H. R., Feltner, C., Bobashev, G., Thomas, K., Wines, R., et al. (2014). Pharmacotherapy for adults with alcohol use disorders in outpatient settings. A systematic review and meta-analysis. JAMA, 311, 1889-1900. https://doi.org/10.1001/jama.2014.3628
6. King, A. C., Houle, T., de Wit, H., Holdstock, L., & Schuster, A. (2002). Biphasic alcohol response differs in heavy versus light drinkers. Alcoholism, Clinical and Experimental Research, 26, 827-835. https://doi.org/10.1111/j.1530-0277.2002.tb02611.x
7. Koob, G. F., & Le Moal, M. (2008). Addiction and the brain antireward system. Annual Review of Psychology, 59, 29-53. https://doi.org/10.1146/annurev.psych.59.103006.093548
8. Lee, S. S., Humphreys, K. L., Flory, K., Liu, R., & Glass, K. (2011). Prospective association of childhood attention deficit/hyperactivity disorder (ADHD) and substance use and abuse/dependence. A meta-analytic review. Clinical Psychology Review, 31, 328-341. https://doi.org/10.1016/j.cpr.2011.01.006
9. Mitchell, J. M., O’Neil, J. P., Janabi, M., Marks, S. M., Jagust, W. J., & Fields, H. L. (2012). Alcohol consumption induces endogenous opioid release in the human orbitofrontal cortex and nucleus accumbens. Science Translational Medicine, 4, 116ra6. https://doi.org/10.1126/scitranslmed.3002902
10. Nutt, D. J., Lingford-Hughes, A., Erritzoe, D., & Stokes, P. R. (2015). The dopamine theory of addiction. 40 years of highs and lows. Nature Reviews Neuroscience, 16, 305-312. https://doi.org/10.1038/nrn3939
11. Urban, N. B., Kegeles, L. S., Slifstein, M., Xu, X., Martinez, D., Sakr, E., et al. (2010). Sex differences in striatal dopamine release in young adults after oral alcohol challenge. A positron emission tomography imaging study with [11C]raclopride. Biological Psychiatry, 68, 689-696. https://doi.org/10.1016/j.biopsych.2010.06.005
12. Volkow, N. D., Wang, G. J., Fowler, J. S., Logan, J., Hitzemann, R., Ding, Y. S., et al. (1996). Decreases in dopamine receptors but not in dopamine transporters in alcoholics. Alcoholism, Clinical and Experimental Research, 20, 1594-1598. https://doi.org/10.1111/j.1530-0277.1996.tb05936.x
13. Volkow, N. D., Wang, G. J., Telang, F., Fowler, J. S., Logan, J., Jayne, M., et al. (2007). Profound decreases in dopamine release in striatum in detoxified alcoholics. Possible orbitofrontal involvement. Journal of Neuroscience, 27, 12700-12706. https://doi.org/10.1523/JNEUROSCI.3371-07.2007
14. Volkow, N. D., Wise, R. A., & Baler, R. (2017). The dopamine motive system. Implications for drug and food addiction. Nature Reviews Neuroscience, 18, 741-752. https://doi.org/10.1038/nrn.2017.130
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