The basis of addiction is training the brain’s reward system to release dopamine (a feel-good neurotransmitter) based on a repeated stimulus. That could be an exogenous (outside the body) chemical such as alcohol or THC or cocaine or it could be a repeated behavior that results in the release of dopamine such as gambling or sex or social media scrolling on a smart phone. The takeaway here is that all roads lead to dopamine.
The problem with repeated use of substances or engagement in behaviors in pursuit of dopamine is that, over time, the same amount of the substance or behavior results in the need for more dopamine, which requires either more frequent use/activity, greater potency, or both. This applies to both substances and behaviors. Not only do we have to “up the ante” to achieve a similar level of dopamine—this is called tolerance—the receptors in neurons that are activated by dopamine become less sensitive as well, so the “feeling” is less intense. When we experience big, frequent releases of dopamine, our brain actually tries to force our reward system back into balance by releasing other neurotransmitters such as dynorphin and GABA, among others, that counteract dopamine, sending the pleasure system into a dopamine deficit.[1] At this point, we often use a substance or engage in a behavior just to feel “normal,” or less bad, rather than to feel good. Although most people are able to fully recover dopamine (D2) receptor sensitivity with extended abstinence, in some cases, over time, the brain’s effort to maintain homeostasis may result in a long-term dulling of the perception of pleasure (anhedonia) regardless of the substance or behavior, and, in rare cases, it appears this can be permanent.
Additional factors that may contribute to or mitigate against addiction include genetic propensity, environment, chronic stress, and age of initial use.
From a mental health perspective, when we choose to use a substance or engage in a behavior that causes significant problems in our lives—work, financial, relationships, etc.—and we keep using/doing it, along with a few other things like increasing tolerance and withdrawal symptoms[2] in the absence of the stimulus, that is referred to as “disordered” use, which is a diagnosis called “substance use disorder.”
Another important point related to addiction, and particularly withdrawal, is that substances that create psychoactive releases of dopamine also usually affect other neurotransmitters in the brain as well. For example, alcohol is a central nervous system depressant and a disinhibitory (we say and do things when inebriated that we wouldn’t when sober). Cocaine is a stimulant and an analgesic. Opioids are central nervous system depressants and powerful analgesics for which we have specific synaptic receptors that when activated, dramatically decrease the transmission of pain signals. Ironically, we have endogenous chemicals in the brain called endorphins that fit into the same receptors and also dull the perception of pain. Endorphins play a role, for example, in a runner’s “high” and often result in feeling diminished pain when an injury is first incurred.
A really important point about addiction is that when substance use and behaviors are used as coping mechanisms (self-medicating) for psychological distress or mental health symptoms, the user tends to experience more than just chemical addiction. There are frequently also psychological implications related to the addictive use and behaviors whether the individual knows they are self-medicating or not. For example, drinking heavily or gambling or playing video games for hours on end may be a means of avoiding the pain of previous trauma or shame or depression or a way of dulling social anxiety. The problem, of course, is that even when substances or behavior temporarily provide relief, the underlying cause of the symptoms we are medicating for often worsen and even the symptoms themselves may become more intense when we enter a dopamine deficit. In some cases we also get a “rebound” effect related to other neurotransmitters in which the symptom or feeling we are trying to avoid returns more intensely when the substance we are medicating with begins to wear off. This is true for both “recreational” and prescription drugs. This dynamic has significant implications for cessation of and recovery from substance use and behavioral addictions because it is very hard to stop self-medicating without a “backfill” for the substance or behavior we are using to “treat” the symptom(s).
The Good News about Dopamine (and other neurotransmitters)
Many activities and substances can generate modest releases of dopamine (and other feel-good neurotransmitters such as oxytocin, endorphins, norepinephrine, adrenalin, serotonin, etc.) that, due to lower amounts of dopamine and less frequent releases, provide pleasure without addiction or counter measures in pursuit of homeostasis in the reward centers of the brain. A beautiful sunset, a hike, intense exercise, lovemaking, a great song, or even a really good meal, all tend to produce feel good moments without risk of addiction. In some cases, one might experience low level “dependence,” which simply means that in the absence of the substance or activity (sugar, caffeine, sex, skiing) one is conscious of not having the positive feeling, and may even long for it, but that is different than addiction, which also includes increasing tolerance, neurobiological withdrawal, and the choice to continue using a substance or engage in a behavior despite it causing clinically significant negative outcomes in one’s life. Repeated hikes in the woods are not likely to lead to significant, negative outcomes and maladaptive behavior!
Figure 1. Neurochemical Responses to Dopamine Spikes (created by ChatGPT)
Summary
Addiction develops when repeated substance use or behaviors train the brain to release dopamine. Over time, tolerance builds—requiring more of the substance/behavior to achieve the same effect—while dopamine receptors become less sensitive. The brain counteracts excessive dopamine with opposing neurotransmitters, creating a deficit where people use just to feel normal rather than good. While most recover with abstinence, some experience long-term or permanent anhedonia.
Risk factors include genetics, environment, stress, and age of first use. Continued substance use or engagement in destructive behaviors despite significant negative outcomes, combined with increased tolerance and withdrawal symptoms, suggest a substance use or behavioral disorder.
Many substances affect multiple neurotransmitter systems beyond dopamine (alcohol depresses the CNS, opioids activate pain-relief receptors, cocaine stimulates). When substances are used to self-medicate psychological distress, addiction becomes more complex—underlying issues often worsen, symptoms intensify during dopamine deficits, and rebound effects occur. Recovery requires addressing both the addiction and the underlying issues being medicated.
The good news: Natural pleasures (exercise, nature, relationships, music) release modest amounts of dopamine without triggering addiction’s tolerance-withdrawal-compulsion cycle. Low-level dependence (missing your morning coffee) differs fundamentally from addiction, which involves escalating use despite serious negative consequences.
[1] It’s not possible in this article to go into detail about all of the ways the brain attempts to counteract dopamine, but the process includes releasing other hormones, “down regulating” dopamine (D2) receptors, and activating the HPA Axis (fight or flight system) to increase the presence of stress hormones among other actions. An infographic of this process is provided in this article.
[2] Withdrawal, sometimes called “detox,” refers to potentially intense negative, physical and psychological symptoms that are basically a response to a neurochemical imbalance that occurs when a substance the brain has become accustomed to is no longer present in the brain. Withdrawal symptoms are different depending on the drug, but in most cases, the brains plasticity will eventually achieve recalibration. Some substances present such intense withdrawal symptoms that they may need to be medically managed depending on the intensity of the chemical dependence.