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Abstract

Addiction is a complex, multifaceted phenomenon that has been described variously as a disease, disorder, syndrome, obsessive-compulsive behaviour, learned behaviour, or spiritual malady. Modern scientific understanding emphasises addiction as a chronic brain disorder shaped by neurobiological changes, learning, and social context. This article examines each conceptualisation and presents an integrated definition that aligns with current neuroscience, psychological, and public health evidence.

Conceptualising Addiction: Labels and Their Accuracy

No single label fully captures addiction’s complexity; each highlights certain truths while overlooking others.

Disease

From a medical perspective, disease is the closest match. Addiction involves persistent neurobiological changes in reward, stress, and self-control circuits, increases relapse risk over years, and shows substantial genetic vulnerability (~50–60%) (NIDA, 2018; Heilig et al., 2021). Treatments improve outcomes but rarely “cure” the condition. This framing is used by the American Society of Addiction Medicine (ASAM), NIDA, WHO ICD-11, and DSM-5-TR (as “Substance Use Disorder”) (NIDA, 2018).

Disorder

Disorder is also scientifically accurate and slightly less medicalised. DSM-5’s “Substance Use Disorder” captures behavioural, psychological, and biological criteria and recognises functioning and harm rather than framing addiction strictly as a lifelong disease (Heather, n.d.; Heilig et al., 2021).

Syndrome

Addiction may be described as a syndrome because it is a cluster of symptoms with behavioural and physiological manifestations, without a single causative factor. However, the term is too generic for practical use outside clinical texts (Blithikioti et al., 2025).

Obsessive and Compulsive Learned Behaviour

Addiction involves learning, habit formation, and compulsion through reinforcement of rewarding behaviours (Hyman, 2005; Hausotter, 2013). Yet describing it solely as learned behaviour ignores genetic predisposition, neuroadaptation, withdrawal, and social factors.

Spiritual Malady

Some mutual-aid traditions characterise addiction as a spiritual malady. While this may be meaningful for individuals, it is not scientifically explanatory: addiction can be adequately explained via biological, psychological, and social mechanisms (Lewis, 2017).

Modern Integrative Definition

The most accurate contemporary description of addiction is:
“A chronic, relapsing disorder of brain circuits involved in reward, stress, and self-control, shaped by learning, environment, and social context”.

This definition encompasses:

• Disease/disorder: medical accuracy
• Learned behaviour and compulsion: neuroscience and behavioural accuracy
• Social determinants: public health relevance
• Flexibility for personal or spiritual interpretations

In short, addiction is best understood as a bio-psycho-social condition that is treatable and sometimes reversible, rather than a deterministic, lifelong curse.

Neurobiology: Why Addiction Is Considered a Brain Disorder

Repeated substance use alters structural and functional brain circuits involved in reward, stress, motivation, memory, and self-control (Nwonu et al., 2022; NIDA, 2018). These changes can persist long after use stops, explaining why addiction is more than a matter of “bad habits” or weak will (NIDA, 2025).

Chronicity and Relapse

Addiction is often chronic and relapsing. Even after long periods of abstinence, cues and stressors can trigger relapse (Meurk et al., 2014; SAMHSA, 2023). Key regions implicated include the basal ganglia (habit formation), extended amygdala (stress), and prefrontal cortex (decision-making) (Kirby et al., 2024). Nevertheless, many individuals achieve stable remission, highlighting heterogeneity in clinical outcomes (Heilig et al., 2021).

Learning, Memory, and Habit Formation

Addiction exploits neural mechanisms of learning and memory: rewarding behaviours are repeated and consolidated into habits, with cues triggering compulsive responses even when the substance’s reward diminishes (Hausotter, 2013; Lewis, 2017). This intertwines biological disorder and learned behaviour.

Critiques and Limitations

Some scientists caution that framing addiction strictly as a brain disease is simplistic:

• Brain changes may resemble those from other motivated behaviours (Lewis, 2017).
• Many recover without formal treatment (Heilig et al., 2021).
• Social, environmental, and psychological factors are crucial to understanding addiction (Blithikioti et al., 2025).

Thus, while the disease model is powerful, it does not fully represent addiction’s heterogeneity or socio-psychological dimensions.

Implications for Treatment

Addiction is treatable, not simply curable. Interventions combining pharmacological and behavioural approaches, alongside social support, can foster long-term recovery (Liu & Li, 2018; Heilig et al., 2021). Like other chronic conditions, management — rather than elimination — is often the realistic goal (NIDA, 2018). Neural circuits can gradually readjust, particularly when environmental and personal factors support recovery.

Conclusion

Addiction is a learned, compulsive brain disorder with chronic potential, shaped by neurobiological, psychological, social, and environmental factors. Recognising addiction as both a disorder and a behavioural learning condition avoids extremes: it is neither an unchangeable fate nor merely a moral failing. This integrated perspective supports nuanced understanding, compassionate care, and effective treatment strategies.

References

Blithikioti, C., Fried, E. I., Albanese, E., Field, M., & Cristea, I. A. (2025). Reevaluating the brain disease model of addiction. The Lancet Psychiatry, 12(6), 469–474. https://doi.org/10.1016/S2215-0366(25)00060-4

Hausotter, W. (2013). Neuroscience and understanding addiction. Addiction Technology Transfer Center (ATTC) Network. https://attcnetwork.org/neuroscience-and-understanding-addiction

Heather, N. (n.d.). What’s wrong with the brain disease model of addiction (BDMA)? Addiction Theory Network. https://addictiontheorynetwork.org/brain-disease-model-of-addiction

Heilig, M., MacKillop, J., Martinez, D., Rehm, J., Leggio, L., & Vanderschuren, L. J. M. J. (2021). Addiction as a brain disease revised: Why it still matters, and the need for consilience. Neuropsychopharmacology, 46(10), 1715–1723. https://doi.org/10.1038/s41386-020-00950-y

Hyman, S. E. (2005). Addiction: A disease of learning and memory. The American Journal of Psychiatry, 162(8), 1414–1422. https://doi.org/10.1176/appi.ajp.162.8.1414

Kirby, E. D., Glenn, M. J., Sandstrom, N. J., & Williams, C. L. (2024). Neurobiology of addiction (Section 14.5). In Introduction to Behavioral Neuroscience. OpenStax. https://socialsci.libretexts.org/…/14.05:_Neurobiology_of_Addiction

Leshner, A. I. (1997). Addiction is a brain disease, and it matters. Science, 278(5335), 45–47. https://doi.org/10.1126/science.278.5335.45

Lewis, M. (2017). Addiction and the brain: Development, not disease. Neuroethics, 10(1), 7–18. https://doi.org/10.1007/s12152-016-9293-4

Liu, J. F., & Li, J. X. (2018). Drug addiction: A curable mental disorder? Acta Pharmacologica Sinica, 39(12), 1823–1829. https://doi.org/10.1038/s41401-018-0180-x

Meurk, C., Carter, A., Partridge, B., Lucke, J., & Hall, W. (2014). How is acceptance of the brain disease model of addiction related to Australians’ attitudes towards addicted individuals and treatments for addiction? BMC Psychiatry, 14, 373. https://doi.org/10.1186/s12888-014-0373-x

National Institute on Drug Abuse. (2018). Drugs, brains, and behavior: The science of addiction (Rev. ed.). https://irp.nida.nih.gov/…/NIDA_DrugsBrainsAddiction

Nwonu, C. N. S., Nwonu, P. C., & Ude, R. A. (2022). Neurobiological underpinnings in drug addiction. West African Journal of Medicine, 39(6), 874–884. https://pubmed.ncbi.nlm.nih.gov/36063103

Substance Abuse and Mental Health Services Administration. (2023). What is substance use disorder? U.S. Department of Health and Human Services. https://www.samhsa.gov/substance-use/what-is-sud

To answer that question, I’ll need to explain a part of the brain called the Limbic System.

Within the brain there is a set of structures called the limbic system. There are several important structures within the limbic system: the amygdala, hippocampus, thalamus, hypothalamus, basal ganglia, and cingulate gyrus. The limbic system is among the oldest parts of the brain in evolutionary terms. It’s not just found in humans and other mammals, but also fish, amphibians, and reptiles.

The limbic system is the part of the brain involved in our behavioural and emotional responses, especially when it comes to behaviours we need for survival: feeding, reproduction and caring for our young, and fight or flight responses (https://qbi.uq.edu.au/brain/brain-anatomy/limbic-system).

The limbic system contains the brain’s reward circuit or pathway. The reward circuit links together several brain structures that control and regulate our ability to feel pleasure (or “reward”). The sensation of pleasure or reward motivates us to repeat behaviours. When the reward circuit is activated, each individual neuron (nerve cell) in the circuit relays electrical and chemical signals.

In a healthy world without addictive manufactured drugs, humans survive and thrive when they are rewarded for certain behaviours (cleaning, hard work, sex, eating, achieving goals etc), hence evolution has provided us with this feel-good chemical so that we will repeat pleasurable behaviours.

There is a gap between neurons called the synapse. Neurons communicate with each other by sending an electro-chemical signal from one neuron (pre-synaptic neuron) to the next (post-synaptic neuron). In the reward circuit, neurons release several neurotransmitters (chemical messengers). One of these is called dopamine. Released dopamine molecules travel across the synapse and link up with proteins called dopamine receptors on the surface of the post-synaptic neuron (the receiving nerve cell). When the dopamine binds to the dopamine receptor, it causes proteins attached to the interior part of the post-synaptic neuron to carry the signal onward within the cell. Some dopamine will re-enter the pre-synaptic nerve cell via dopamine transporters, and it can be re-released.

When a reward is encountered, the pre-synaptic nerve cell (neuron) releases a large amount of dopamine in a rapid burst. Dopamine transporters will remove “excessive” amounts of dopamine naturally within the limbic system. Dopamine surges like this help the brain to learn and adapt to a complex social and physical world.

Drugs like methamphetamine (a stimulant drug) are able to “hijack” this process contributing to behaviours which can be considered unnatural or potentially dysfunctional. A range of consequences can follow.

When someone uses methamphetamine, the drug quickly enters the brain, depending on how the drug is administered. Nevertheless, meth or ice is quick acting. Meth blocks the re-entry of dopamine back into the pre-synaptic neuron – which is not what happens naturally. This is also what cocaine does to the brain. However, unlike cocaine, higher doses of meth increase the release of dopamine from the presynaptic neuron leading to a significantly greater amount of dopamine within the synapse. Higher doses of cocaine will not release “more dopamine” from the pre-synaptic neuron like meth does. This is why after about 30 minutes or so, people who use cocaine will need more to maintain the high.

Dopamine gets trapped in the synapse (space between nerve cells) because the meth (like cocaine) prevents “transporters” from removing it back into the cell it came from. The postsynaptic cell is activated to dangerously high levels as it absorbs so much dopamine over a long period of time. The person using meth experiences powerful feelings of euphoria, increased energy, wakefulness, physical activity, and a decreased appetite.

When an unnatural amount of dopamine floods the limbic system like this over a long period of time, without reabsorption, then our brain is not replenished with dopamine, hence people who use meth often (even on a single occasion) may feel unmotivated, depressed, joyless, and/or pointlessness when they stop using. Figuratively speaking, the brain is “empty” or low on dopamine fuel, and it will take time to for dopamine to return to baseline levels and replenish itself. This may motivate the user to seek more methamphetamine to return to “normal”.

Methamphetamine can also cause a variety of cardiovascular problems, including rapid heart rate, irregular heartbeat, and increased blood pressure. Hyperthermia (elevated body temperature) and convulsions may occur with methamphetamine overdose, and if not treated immediately, can result in death (What are the immediate (short-term) effects of methamphetamine misuse? | National Institute on Drug Abuse (NIDA) (nih.gov))

SIGNS OF SUBSTANCE MISUSE OR ADDICTION

• Finding it difficult to meet responsibilities.
• Withdrawing from activities or not enjoying activities that used to provide satisfaction e.g. work, family, hobbies, sports, socialising.
• Taking part in more dangerous or risky behaviours e.g., drink driving, unprotected sex, using dirty needles, criminal behaviour.
• Behaviour changes e.g., stealing, exhibiting violence behaviour toward others.
• Conflict with partner/family/friends, losing friends.
• Experiencing signs of depression, anxiety, paranoia, or psychosis.
• Needing more substance to experience the same effects
• Cravings and urges to use the substance and symptoms of withdrawal when not using the substance.
• Having difficulty reducing or stopping substance use.
• Regretting behaviours while under the influence and continuing to use again.

(Substance abuse, misuse and addiction | Lifeline Australia | 13 11 14)