Addicted to Addiction
When does a harmful behaviour become a disorder?
Posted July 10, 2025 | Reviewed by Margaret Foley
Addiction can be a loaded term. The word originated in the 16th century to denote an abnormal attachment , typically to alcohol , and was derived from the Latin term for legally binding someone into a debt (Rosenthal & Faris, 2019).
Its use as a medical diagnosis has long been contentious. The more circumscribed “substance use disorder” was preferred by the American Psychiatric Association to classify dependence on drugs of abuse up until the fifth edition of the Diagnostic and Statistical Manual (DSM-5), which introduced the section “Substance-Related and Addictive Disorders.”
In everyday use, addiction has the broader meaning of an irresistible urge or compulsion that overwhelms self-control and degrades quality of life. Within that definition, addiction has been applied to a great many things: sugar, fasting, gaming, shopping, extreme sports, exercise, love, sex , and pornography , to name a few. The idea of being “addicted to dopamine ” has even been proposed as a catch-all term for the addictive nature of modern life (online life in particular). Given that disruption of dopamine transmission is the biological basis of addictive behaviour, this essentially means being addicted to addiction.
Symptoms vs. mechanisms
Part of the reason why the use of addiction as a medical term is contested is that it is often defined by symptoms, rather than biological mechanisms. Addiction involves insatiable desire, compulsions, obsessive thoughts, impulsiveness, and withdrawal pain when trying to break the habit. Addicts also display characteristic behaviours: neglect of responsibilities, secrecy, lying to protect supply, and prioritising the addiction over all other concerns.
From a psychiatric perspective, it is difficult to disentangle these symptoms of addiction from other conditions in a definitive way. Lots of disorders involve obsessive thoughts, compulsive behaviours, and difficulties with impulse control, and you can’t realistically diagnose a medical condition from so abstracted a behaviour as “being secretive.”
In contrast, addictive substances like cocaine, heroin, and alcohol have detectable effects on brain physiology. They disrupt the operation of the reward system in the brain, resulting in persistent functional changes: increased dopamine and opiate signalling in response to addiction-related cues, reduced response to other rewards, and weakened feedback regulation from the “executive” prefrontal cortex (Robinson & Berridge, 2003). Changes can even be detected at the molecular level as long-lasting alterations in gene transcription and epigenetic regulation (Robison & Nestler, 2011)
Those mechanistic changes in neurobiology define addiction as a distinct phenomenon rooted in neurological dysregulation, not just a matter of symptoms. How, then, does this relate to the many behaviours and habits that have become popularly described as addictions?
Behavioural addictions
The concept underlying behavioural, or process, addictions is that some natural rewards can drive the reward system into the same dysregulated state as addictive substances.
There is one behaviour for which direct evidence for this effect has been found: compulsive gambling. The same upregulation of reward transmission for gambling rewards, coupled with diminished responsiveness to alternative rewards, and associated genetic changes, have been identified. As a consequence, gambling is listed in the DSM-5 as an addictive disorder.
For other behaviours, the evidence base is thinner—although food, sex, and exercise addiction have increasing research to support them (Olsen, 2011).
Where does that leave all the other harmful behaviours that might fall into the category?
An obvious limitation for defining behavioural addictions is that it is very hard to measure those characteristic mechanistic changes in living people. For gambling, food, sex, and exercise, there are at least animal models that can be used to directly test for neuroplasticity and gene expression, and so it’s feasible to gather data.
This isn’t always possible.
For example, I’m fascinated by the phenomenon of limerence— obsessive, romantic infatuation with another person. The symptoms of limerence map closely to the euphoric highs, insatiable desires, intrusive thoughts, and involuntary cravings of addiction, but it’s challenging to see how an animal model of “addiction to another person” could be developed.
More broadly, limerence illustrates a difficult grey area in therapeutic practice: behaviours that are clearly harmful to the individual, cause psychological distress, and need support, but don’t fit into a designated psychiatric category. Therapists have to find a way to proceed.
Is limerence an attachment disorder, an impulse control disorder , a mood disorder , or a behavioural addiction? Should they dismiss the concept outright because it’s not listed in the DSM? It’s Carl Sagan’s famous dictum: Absence of evidence is not evidence of absence.
This uncertainty is partly why we have the parallel everyday use of addiction to mean “a behaviour that has symptoms similar to substance misuse disorders.”
Many of the proposed new addictions seem to fit the pattern; how many will turn out to have the same grounding in neurobiology remains to be seen.
Rosenthal, RJ & Faris, SB. (2019). The etymology and early history of ‘addiction.’ Addiction Research & Theory , 27(5): 437–449.
Robinson, TE & Berridge, KC. (2003). Addiction. Annual Review of Psychology , 54: 25-53.
Robison AJ & Nestler EJ. (2011) Transcriptional and epigenetic mechanisms of addiction. N ature Reviews Neuroscience , 12(11): 623-37.
Olsen CM. (2011). Natural rewards, neuroplasticity, and non-drug addictions. Neuropharmacology, 61(7): 1109-22.
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Tom Bellamy, Ph.D., is a neuroscientist and honorary Associate Professor at the University of Nottingham, UK.
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