ABOVE: Dopamine is often presented as the happiness chemical, but scientists have proven that the truth is much more complicated. ©istock, pepifoto
In the late 2010s, dopamine detoxing or fasting emerged as the latest scientific-sounding wellness trend. The exact definition of a dopamine detox has always been somewhat fluid. Some practitioners recommend abstaining from eating, talking, using the internet, watching TV, playing video games, and consuming alcohol, nicotine, or other drugs and claim that a detox will reset dopamine levels. Others, like psychologist Cameron Sepah, the author of “The Definitive Guide to Dopamine Fasting 2.0,” maintain that the practice is not actually about reducing dopamine, but instead is a catchy name for a cognitive behavioral therapy-based technique to help people reduce compulsive behaviors.
Despite Sepah’s assertions, the popularization of the term has nonetheless spawned various podcasts, books, and supplements to help people “optimize dopamine,” to the exasperation of many scientists who have spent their entire careers studying this multifaceted molecule. It’s not that researchers are necessarily opposed to any of the suggested behaviors: taking a break from activities like scrolling through social media, drinking alcohol, or binge-watching reality TV could even be helpful for many people. However, they argue that it’s incorrect to present dopamine as the underlying agent of the potential benefits for well-being.
“Maybe if you break your routine, you might notice certain things as more novel, and maybe then enjoy them more,” said Talia Lerner, a neuroscientist at Northwestern University. “[One of] the reasons it’s appealing to people is because it builds on experiences in the world that are familiar to us, and that have been recognized truly for millennia.” As Lerner pointed out, periods of fasting or abstaining from certain behaviors are common in religious traditions around the world, including Judaism, Hinduism, Christianity, Islam, and Buddhism.1
“This is something that has existed, and that people have recognized value in, for a long time,” said Lerner. “But the question of what neural circuits might make some of those practices valuable is not well defined. It’s probably not all dopamine, and it’s certainly not as simple as just ‘lowering your dopamine.’ So, the name is a weird, catchy thing that I think rubs scientists the wrong way, because it's not particularly precise. And it's kind of confusing public perception of what this molecule does.”
Indeed, the dopaminergic system, with its many circuits, receptor subtypes, and modulators, is so complex and varied as to render phrases like “lowering dopamine” essentially meaningless. And although dopamine is arguably one of the most extensively studied neurotransmitters, scientists still have several questions about how it functions and what role it plays in behavior.
Humble beginnings
Dopamine hasn’t always been such a media darling; scientists once thought it was simply an intermediate molecule, formed as the brain converted the amino acid tyrosine into adrenaline and noradrenaline.2 Pioneering work in the 1950s identified dopamine as a neurotransmitter in its own right and demonstrated its crucial role in movement.2 Soon afterwards, post-mortem studies of human brains revealed that dopamine was depleted in specific regions in patients with Parkinson’s disease and by 1961, trials of L-DOPA, a dopamine precursor, were underway in patients.2
It was only later that dopamine came to be known as the canonical reward molecule. Experiments in the 1970s and early 1980s showed that low-level electrical stimulation of certain brain regions was a reinforcing stimulus for rats.3 When the implanted electrode was near dopaminergic cell bodies in the midbrain, the rats pushed the lever to deliver the stimulation with great enthusiasm—clocking in at up to 110 pushes per minute.
In agreement with these findings, Wolfram Schultz, now a neurophysiologist at the University of Cambridge, demonstrated in the 1980s that presenting monkeys with a tasty treat—or a cue that they had learned to associate with a treat—increased the firing rate of dopaminergic neurons in the midbrain.4
Almost immediately, however, it was clear that dopamine and its associated signaling pathways were far from straightforward. Once animals learned that a certain cue predicted a certain reward, these midbrain dopaminergic neurons only increased their firing rate in response to the cue—when the animals actually received the reward, these neurons ignored it completely, maintaining their usual baseline levels of chatter.5 If the animals were given a cue that predicted a reward, but then did not receive the promised reward, the neurons briefly went completely silent. This led scientists to hypothesize that the purpose of these dopaminergic signals was not necessarily to encode reward, but to encode reward prediction error—the difference between expected reward and actual reward.
Although perhaps not strongly emphasized at the time, these early experiments also revealed substantial heterogeneity even within a single population of dopaminergic neurons. For example, a 1992 study by Schultz and colleagues reported that the majority of the recorded neurons fired more in response to a reward-predicting cue, but this “majority” was only 58 percent, suggesting that perhaps the reward prediction error hypothesis did not fully explain the function of these neurons.6
Down the Rabbit Hole: Adventures in Dopamine-land
As technology improved by leaps and bounds, researchers were able to investigate dopaminergic systems in greater depth, mapping synaptic connections and assessing patterns of transcription in individual cells. The deeper they dug, the more complexity they found.
While there are relatively few dopamine-producing neurons in the human brain—only about 400,000-600,000 out of more than 80 billion neurons—they send projections widely throughout the brain.7 “Dopamine obviously has different functions depending on what brain region it is released in,” said Stephanie Borgland, who studies the neurobiology of addiction and obesity at the University of Calgary.
Moreover, said Borgland, over the past fifteen years, researchers have come to appreciate differences between the dopamine neurons themselves. “Dopamine neurons come in all shapes and sizes; some dopamine neurons [also] release other neurotransmitters. Some populations behave really differently: classically, dopamine incentivizes and makes animals work harder for reward… but other people have shown that some dopamine neurons that project to a different part of the nucleus accumbens are actually involved in aversive responses.”
Further muddying the waters, according to Lerner, is evidence that dopamine may be involved not just in reward error predictions, but in predictions in general.8 “Maybe it helps you learn that cue A predicts cue B, even if either of those cues have explicit value,” she said.
Scientists are making progress in teasing apart the different elements of the dopaminergic system that might help account for these seemingly disparate effects. Collectively, dopamine researchers around the world have identified five different dopamine receptor subtypes and are studying their different dynamics.9 They have begun to classify dopaminergic neurons based on gene expression and are exploring differences in function and vulnerability to disease in some of these genetically-defined subpopulations.10–12
However, the full picture of dopamine physiology and function is far from complete. And while dopamine is certainly an important molecule, it’s essentially never acting in isolation. The activity of other neuronal populations mediates the activity of dopaminergic neurons, and other neurotransmitters, including endogenous opioids, orexin, and serotonin, are also implicated in many of the behaviors popularly attributed to dopamine. “The more we know, the more we come up with other questions to ask,” said Lerner.
DIY Dopamine?
Even though there’s still more work to be done, Borgland and Lerner said that the idea of a dopamine fast or detox doesn’t really line up with the current scientific understanding of this molecule.
While taking a short break from a daily treat or pleasant activity might make those things more enjoyable later, this likely isn’t due to a “resetting” of the dopamine system and, said Borgland, it’s probably not going to be sufficient to unlearn certain behaviors or prevent cravings.
“The challenge with dopamine fasting is that they're making the assumption that you're going to rewire your brain over this period of time in the absence of dopamine,” she said. “When, in fact, you're just not being reinforced for that period of time. But you still have all the habits and things like that present.” She also referenced research showing that after rats were repeatedly exposed to drugs of abuse, like cocaine, various parts of their brains’ dopaminergic systems remained altered for a month or more of abstinence—a long time for an animal with a two to three year lifespan.13
“Dopamine is complicated and nuanced,” said Borgland. “And dopamine fasting is probably not going to really do anything for you. To change a habit, you need to have new learning, which takes time.”
Some researchers are concerned that dopamine fasting is not only a dubiously effective practice and an incorrect invocation of an important neurotransmitter, but that it also has the potential to be harmful.
“Where I worry is if people start [trying to] to deplete their dopamine in [non-behavioral] ways,” said Nandakumar Narayanan, a neurologist at the University of Iowa. As a physician scientist who treats patients with Parkinson’s disease and other neurological disorders, he is acutely aware of the risks of pharmacologically elevating or depleting dopamine. “There are dangers in messing with this system,” he said.
“I think there's a role for scientific communication to inspire and to cultivate curiosity. Those are important things that we do as publicly-funded scientists,” he said. “But where I have a problem is where that revelry turns to recommendations.” This is especially true when the recommendations involve supplements or other products that are not evidence-based.
“I live in the world of randomized, double blind, placebo-controlled, high quality medical evidence,” he said. “We spend, as a society, lots of money—and I [as a researcher] spend most of my time—trying to figure out what evidence is real, and then we publish it so that people can read it… So that’s where we should look.”
- Trabelsi K, et al. Religious fasting and its impacts on individual, public, and planetary health: Fasting as a “religious health asset” for a healthier, more equitable, and sustainable society. Front Nutr. 2022;9:1036496.
- Björklund A, Dunnett SB. Fifty years of dopamine research.Trends Neurosci. 2007;30(5):185-187.
- Corbett D, Wise RA. Intracranial self-stimulation in relation to the ascending dopaminergic systems of the midbrain: A moveable electrode mapping study. Brain Res. 1980;185(1):1-15.
- Schultz W. Responses of midbrain dopamine neurons to behavioral trigger stimuli in the monkey. J Neurophysiol. 1986;56(5):1439-1461.
- Schultz W. Dopamine reward prediction error coding. Dialogues Clin Neurosci. 2016;18(1):23-32.
- Ljungberg T, et al. Responses of monkey dopamine neurons during learning of behavioral reactions. J Neurophysiol. 1992;67(1):145-163.
- Volpicelli F, et al. Molecular regulation in dopaminergic neuron development. Cues to unveil molecular pathogenesis and pharmacological targets of neurodegeneration. Int J Mol Sci. 2020;21(11):3995.
- Sharpe MJ, et al. Dopamine transients do not act as model-free prediction errors during associative learning. Nat Commun. 2020;11(1):106.
- Bhatia A, et al. Biochemistry, Dopamine Receptors. In: StatPearls. StatPearls Publishing; 2024.
- Poulin JF, et al. Classification of midbrain dopamine neurons using single-cell gene expression profiling approaches. Trends Neurosci. 2020;43(3):155-169.
- Azcorra M, et al. Unique functional responses differentially map onto genetic subtypes of dopamine neurons. Nat Neurosci. 2023;26(10):1762-1774.
- Kamath T, et al. Single-cell genomic profiling of human dopamine neurons identifies a population that selectively degenerates in Parkinson’s disease. Nat Neurosci. 2022;25(5):588-595.
- Saddoris MP, et al. Cocaine self-administration experience induces pathological phasic accumbens dopamine signals and abnormal incentive behaviors in drug-abstinent rats. J Neurosci. 2016;36(1):235-250.