EGO

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

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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

Albert Ellis, in his Rational Emotive Behaviour Therapy (REBT), identified a number of dysfunctional beliefs that people often hold. Ellis intentionally adopts extreme views to emphasize how people often exaggerate their perspectives irrationally. He referred to this tendency as “awfulizing,” where we negatively overgeneralise situations. This behaviour can stem from a strong desire for certainty, causing us to perceive things in extreme terms rather than viewing them as part of a nuanced spectrum. Consequently, this leads to the formation of self-stereotypes.

A self-stereotype refers to the process of applying generalised beliefs or stereotypes about a group to oneself, especially when one identifies as part of that group. For instance, if someone belongs to a specific cultural or social group (gay men) and internalises the commonly held stereotypes about that group (partying and casual sex), they may unconsciously start viewing and behaving in ways that align with those generalisations.

1. Alcohol (ethanol) enters the body through the oral cavity (i.e., the mouth). The inner surface of the oral cavity is mucosal tissue to keep the cavity lubricated and it is capable of absorbing alcohol into the bloodstream. This absorption is considered “insignificant”.

2. Alcohol flows down the oesophagus to the stomach where 10-20% of ethanol will be absorbed into the bloodstream. Alcohol enters the bloodstream via the mucosal tissue of the stomach wall, and travels straight to the liver. Alcohol can take 5-10 minutes to reach the brain because of the ethanol absorbed via the stomach. If you drink alcohol on an empty stomach, the pyloric sphincter [gateway between the stomach and the small intestine] is going to be more open, and the alcohol is going to immediately enter the small intestine after reaching the stomach. If food is also present in the stomach, the sphincter will open and close at a rate that allows food to enter the small intestine gradually, therefore if alcohol is also in the stomach, it will gradually enter the small intestine.

3. Alcohol flows through the pyloric sphincter into the small intestines where most alcohol absorption occurs. Human intestines are attached the to the posterior abdominal wall by a fold of membrane called the mesentery. Alcohol is absorbed into the mesentery via veins and then travels to the liver.

4. One function of the liver is that it detoxifies toxic elements into non-toxic elements before passing it to the heart and then the rest of the body. The liver sustains considerable “abuse” from a variety of toxic elements and chemicals, and therefore it needs to be capable of full regeneration. NOTE: Many diseases and exposures can harm it beyond the point of repair. These include cancer, hepatitis, certain medication overdoses, and fatty liver disease.

In the liver, ethanol is met with an enzyme called alcohol dehydrogenase and converts ethanol into acetaldehyde [ass-eh-tal-de-hide]. This chemical is more toxic than ethanol, so the liver uses another enzyme to convert acetaldehyde into acetate, which is non-toxic to the human body. NOTE: the amount of alcohol consumed + the timeframe it is consumed [and a variety of other factors] will influence the ability of the liver to effectively convert acetaldehyde all the way into acetate. The liver can’t handle the entire workload effectively therefore ethanol (before being metabolised) will go straight from the liver to the bloodstream and make its way directly to the heart.

NOTE: Genetics will play a role! Certain people do not produce the liver enzymes in enough quantity to properly breakdown ethanol.

5. Blood leaves the liver through the hepatic veins. The hepatic veins carry blood to the inferior vena cava—the largest vein in the body—to the right side of the heart. The heart will beat and send the incoming blood to the lungs to oxygenate and expel carbon dioxide as we breath out. This is how ethanol can be on your breath. Inside the lungs, at the very end of the bronchioles, are hollow air sacs called alveoli where there is a gas exchange. Ethanol evaporates through capillaries into the air sacs and exhaled out of the body. Breathalysers can detect the quantity of ethanol in a person’s system based on the quantity of ethanol in our breath.

6. Not all the ethanol will expel from the body via the breath. The rest will flow back to the heart, with newly oxygenated blood, and then get pumped all the way up to the brain and around the body. NOTE: Ethanol is water soluble. It will be distributed to every cell in the body except bone and fatty tissue [some will enter fat cells but not easily]. Ethanol will interact with every other cell i.e., every organ, gland, nerve, muscle etc.

7. Ethanol will affect and compromise protein synthesis inside muscle tissue. Therefore, if you have been training at the gym, running, swimming etc., your muscles will not effectively be able to repair.

8. Once ethanol has reached the brain, it will cross the blood-brain barrier and begin to affect chemical messengers [neurotransmitters] in the grey matter of the brain. It affects serotonin, dopamine, gamma-amino-butyric-acid (aka GABA), glutamate, endorphins etc. The person will experience pleasure, euphoria, lowered inhibitions [related to dopamine], lowered cognitive ability (e.g., decision making/problem solving, emotion regulation) and lowered coordination and reflexes.

The more ethanol ingested, the more dopamine is secreted and communicated between neurons (i.e., nerve cells). One of dopamine’s functions is to make you feel pleasure or ‘rewarded’ for doing things that are good for humans, hence, from an evolutionary perspective, we are likely to do them again to help us thrive in our environment and social world. Dopamine is secreted when we:

• eat healthy foods (but also recently developed processed foods that are high in sugar and salt)
• exercise
• achieve goals
• be productive (e.g., finish a task like cleaning, cooking, work-related tasks)
• master new skills (e.g., learning an instrument or a new talent), and
• have positive and stimulating social interactions

Ethanol influences so much dopamine secretion and communication that the brain becomes unable to make responsible decisions cognitively. The simultaneous experience of euphoria and lowered cognitive ability means we are more likely to be “happy” about making irresponsible decisions.

Increased dopamine is how drinking alcohol “blocks” unpleasant emotions like fear, stress, anxiety, and insecurity. When we don’t feel these unpleasant, yet necessary, emotions we will behave in ways that are dangerous, abnormal, potentially embarrassing, and generally problematic.

Another significant brain region affected by ethanol is the hypothalamus and the pituitary glad [together known as the hypothalamic-pituitary axis]. These structures control the entire hormonal system. The hypothalamus monitors the body, and it will send instructions to the pituitary gland based on information it receives from the hypothalamus. The hypothalamus is aware that ethanol is flooding the brain and it starts adjusting the secretion of hormones via the pituitary gland.

One of the instructions it gives the pituitary gland is to start modulating the adrenal glands to secrete cortisol (i.e., stress hormone) and epinephrine and norepinephrine (i.e., adrenaline).

Now, our cognitive capacity is diminished, inhibitions are lowered, and we will experience a rush of stress hormones and adrenaline coursing through the body. Cortisol and adrenaline will provide a boost of energy. It will increase the heart rate, blood pressure, body sweat, sugar levels in the bloodstream, and enhances the brain’s ability to use glucose. Glucose is a “fuel” source for brain functioning, including the generation of neurotransmitters. Behaviourally, we can see this in children when we say they are “hyperactive” because they’ve ingested too much sugar.

The pituitary gland will also slow the secretion of anti-diuretic hormone (aka. vasopressin). A diuretic is something that makes us urinate. If the anti-diuretic hormone (also called vasopressin) slows down, then we won’t be “holding on” to water as effectively, hence we begin to urinate more. People call this “breaking the seal”.

9. South of the body, blood is pumped into the kidneys via the renal artery which spreads through the renal cortex. The blood is then filtered into urine and expelled from the body. The lowered anti-diuretic hormone will dilate (become wider/bigger or more open) blood vessels in the kidneys which means more blood gets passed through and filtered, but it also means we lose a lot more body water which leads to dehydration. Vasopressin is essential in the control of osmotic balance, blood pressure regulations, and kidney function, therefore, when vasopressin is lowered, we are losing essential water and minerals/electrolytes. Electrolytes are involved in urination because the kidneys need them to make the process of filtering blood more efficient.

The loss of water and electrolytes will contribute to a hangover. Electrolytes play a role in cellular water absorption so if we are losing more water than we are bringing in, and we are losing the electrolytes that support the absorption of water, we become dehydrated very quickly.

10. The Hangover

Symptoms: nausea, fatigue, diarrhoea, vomiting, paranoia, anxiety, anorexia (i.e., loss of appetite), increased thirst, muscle weakness, irritability, sweating, increased blood pressure, and headache.

The exact cause of a “hangover” is not yet known however variables affecting the hangover are:

• individual differences such as sex, size, body fat, genetics etc
• lack of sleep
• general health
• drinking behaviour e.g., frequency, duration, quantity
• food intake before and during
• water intake before and after
• your body’s ability to metabolise alcohol i.e., excessive amounts of acetaldehyde due to fewer enzymes to metabolise alcohol in the liver before entering the bloodstream
• general behaviour while drinking e.g., poly-substance use, dancing, sexual activity, risk-taking behaviours etc.

Strategies for Controlled Drinking

• Setting personal drinking limits and sticking to it
• Alternating alcoholic drinks with soft drinks i.e., one alcoholic drink then a water, soft drink, or juice
• Have a meal before drinking
• Switching to low alcohol drinks
• Having regular alcohol-free days/weeks/months
• Identifying high risk situations for heavy drinking and creating a management plan

Engaging in alternative activities to drinking