Eating Disorders DSM-5

Addiction is a chronic, relapsing disorder involving changes in brain reward, motivation, learning, stress and executive control systems. While different substances (and behaviours) act through distinct primary mechanisms, they converge on common neurobiological pathways — particularly the mesocorticolimbic dopamine system.

Below is an overview in Australian English of the core mechanisms and then substance-specific and behavioural addiction processes.

Core Neurobiological Pathways in Addiction

1. The Mesocorticolimbic Dopamine System

The central pathway implicated in addiction is the mesocorticolimbic circuit, involving:

• Ventral tegmental area (VTA)
• Nucleus accumbens (NAc)
• Prefrontal cortex (PFC)
• Amygdala
• Hippocampus

All addictive drugs increase dopamine transmission in the nucleus accumbens, either directly or indirectly. Dopamine does not simply produce pleasure — it encodes reward prediction, salience and learning. With repeated exposure:

• Drug-related cues gain exaggerated salience
• Natural rewards become less reinforcing
• Behaviour becomes increasingly habitual and compulsive

2. Neuroadaptation and Allostasis

Repeated substance exposure produces:

Tolerance — Reduced response due to receptor downregulation or neurotransmitter depletion.

Dependence — Neuroadaptations that produce withdrawal when the substance is removed.

Allostatic shift — The brain’s reward set point shifts downward, mediated by stress systems (e.g. corticotropin-releasing factor), resulting in dysphoria during abstinence.

3. Habit Formation and Loss of Control

With repeated use:

• Control shifts from ventral striatum (goal-directed) to dorsal striatum (habit-based)
• Prefrontal cortex regulation weakens
• Impulsivity and compulsivity increase

Substance-Specific Mechanisms

Alcohol

Alcohol acts on multiple neurotransmitter systems:

• Enhances GABA-A receptor function (inhibitory)
• Inhibits NMDA glutamate receptors (excitatory)
• Increases dopamine release in nucleus accumbens
• Affects endogenous opioid systems

Chronic exposure leads to:

• GABA downregulation
• NMDA upregulation
• Hyperexcitable state during withdrawal (risk of seizures, delirium tremens)

Alcohol dependence also involves stress system activation and impaired frontal cortical control.

Methamphetamine

Methamphetamine is a potent psychostimulant that:

• Enters presynaptic terminals
• Reverses the dopamine transporter (DAT), causing carrier-mediated dopamine efflux
• Inhibits vesicular monoamine transporter 2 (VMAT2), releasing dopamine from synaptic vesicles into the cytoplasm
• Causes massive dopamine release into the synapse

It also increases noradrenaline and serotonin.

Chronic use causes:

• Dopamine neurotoxicity (particularly to dopaminergic terminals)
• Reduced dopamine transporter availability
• Structural changes in striatum and PFC
• Persistent cognitive deficits

Methamphetamine produces particularly strong sensitisation of cue-driven craving.

Cocaine

Cocaine:

• Blocks the dopamine transporter (DAT), preventing reuptake
• Increases synaptic dopamine concentration

Unlike methamphetamine, cocaine acts by blocking DAT rather than reversing it, and does not cause large presynaptic vesicular release — the elevation in synaptic dopamine arises from impaired clearance.

Repeated use leads to:

• Dopamine receptor downregulation
• Enhanced cue reactivity
• Rapid cycling between intoxication and crash
• Strong psychological dependence

Opioids (e.g. heroin, morphine, oxycodone)

Opioids act primarily at mu-opioid receptors (MORs), which are expressed throughout the brain, including in the VTA. Their dopaminergic effects arise through multiple mechanisms:

• MORs on GABAergic interneurons in the VTA suppress inhibitory tone, thereby disinhibiting dopamine neurons (the classical disinhibition mechanism)
• MORs are also expressed on VTA dopamine neurons and projection targets directly, contributing additional excitatory drive beyond the disinhibition pathway

They also act in brainstem respiratory centres, which underlies the risk of respiratory depression in overdose.

Chronic use produces:

• Receptor desensitisation and internalisation
• Reduced endogenous opioid production
• Severe physical withdrawal mediated by noradrenergic rebound in the locus coeruleus
• Strong negative reinforcement (use to avoid withdrawal)

Cannabis

Δ9-tetrahydrocannabinol (THC):

• Activates CB1 receptors (the primary psychoactive cannabinoid receptor)
• Modulates GABA and glutamate release at presynaptic terminals
• Indirectly increases dopamine in NAc via disinhibitory mechanisms

Cannabis produces:

• Altered endocannabinoid system function
• CB1 receptor downregulation with chronic use
• A mild to moderate withdrawal syndrome (irritability, sleep disturbance, appetite changes)
• Effects on hippocampal memory circuits

While addiction risk is generally considered lower than for opioids or stimulants, it remains clinically significant and may be underestimated, particularly given the widespread availability of high-potency THC products (e.g. concentrates and high-THC flower), which are associated with greater dependence risk and more severe withdrawal.

MDMA (Ecstasy)

MDMA:

• Reverses the serotonin transporter (SERT), causing massive serotonin efflux — this is its primary mechanism
• Also increases dopamine and noradrenaline

Neurobiological consequences include:

• Acute empathogenic and entactogenic effects driven by serotonin release
• Post-use serotonin depletion, which may contribute to dysphoria in the days following use
• Potential serotonergic neurotoxicity, though this evidence comes largely from high-dose or repeated animal studies; the clinical significance in typical human recreational use remains under debate and is not definitively established
• Moderate addictive potential relative to psychostimulants, partly because dopaminergic effects are less prominent than with cocaine or methamphetamine

Prescription Psychoactive Medications

Certain prescribed medications also have addictive potential:

Benzodiazepines — Enhance GABA-A receptor activity. Cause tolerance via receptor downregulation. Dependence is primarily a GABAergic adaptation. Withdrawal can be protracted and, in cases of high-dose or long-term use, may produce seizures.

Prescription stimulants — Act via similar mechanisms to amphetamine, increasing dopamine and noradrenaline. Risk of misuse exists in susceptible individuals, though therapeutic doses in appropriately diagnosed patients are associated with substantially lower addiction risk than recreational use.

Behavioural (Process) Addictions

Gambling Disorder

Gambling disorder is recognised in DSM-5-TR as a non-substance-related addictive disorder. Although no substance is ingested, similar neurobiological mechanisms are involved.

Dopamine and reward prediction error — Near misses activate the nucleus accumbens similarly to wins. Variable ratio reinforcement schedules (as in poker machines) generate strong, unpredictable dopamine prediction error signalling that powerfully drives continued behaviour.

Cue reactivity — Gambling-related cues activate the same mesocorticolimbic circuitry as drug cues, with increased striatal activation and reduced prefrontal inhibitory control.

Habit circuitry — A shift from ventral to dorsal striatal control contributes to compulsive betting despite continued losses.

Other Emerging Behavioural Addictions

Conditions such as internet gaming disorder, compulsive sexual behaviour disorder, and problematic social media use share overlapping neurobiological features including:

• Dopamine dysregulation and sensitisation to cue salience
• Reduced executive control
• Stress system activation

However, the evidence base for most of these conditions is still developing, and their classification as formal addictive disorders remains an area of active research and debate. Internet gaming disorder is currently listed in DSM-5-TR as a condition for further study.

Shared Neurobiological Themes Across Addictions

Across substances and behaviours, addiction involves:

• Dopamine sensitisation to cues
• Reduced sensitivity to natural rewards
• Impaired prefrontal inhibitory control
• Stress system overactivation (particularly corticotropin-releasing factor)
• Habit circuitry dominance (dorsal striatum)
• Neuroplastic changes in glutamatergic signalling

Why Some Substances Are More Addictive

Addictive potential is influenced by multiple interacting factors. The speed of dopamine rise is one of the most studied — faster onset of dopamine elevation (e.g. via smoking or intravenous administration) is associated with stronger reinforcement. This framework, developed largely through the work of Volkow and colleagues, has strong empirical support, though it represents a mechanistic model rather than an established universal law. Other important factors include:

• Intensity of dopamine release
• Pharmacokinetics (e.g. route of administration)
• Withdrawal severity (which drives negative reinforcement)
• Social and environmental context
• Genetic vulnerability (heritability of addiction is estimated at 40–60% across substances)

Conclusion

Addiction is not simply about pleasure seeking. It reflects maladaptive neuroplasticity in reward, stress, learning and executive control circuits. While alcohol, methamphetamine, cannabis, opioids, cocaine and MDMA each act through different primary molecular mechanisms, they converge on common neural pathways that drive craving, tolerance, withdrawal and compulsive use. Behavioural addictions such as gambling engage these same circuits despite the absence of an ingested substance.

The neurobiological understanding of addiction continues to evolve, and where evidence is still emerging — particularly regarding emerging behavioural addictions and the long-term neurotoxic effects of substances like MDMA — clinical interpretation should be appropriately cautious.

There have been various theories and models proposed over time to help us understand why individuals use alcohol and other drugs, and why some people become dependent or ‘addicted’ but not others. The following are several models or theories of addiction. They reflect the political, medical, spiritual, and social forces of those times in history.

The Moral Model

Alcohol and tobacco was introduced in the Western countries during the 1500’s. The widespread use and misuse of chemical substances resulted in a range of social problems and it was thought by some that substance use was “problematic” and “morally wrong” (Lassiter & Spivey, 2018). The moral model viewed AOD dependency as a moral and personal weakness that involved a lack of self-control, and was often viewed as a potential danger to society (Stevens & Smith, 2014).

The moral model considered addiction a “sin” and a result of free, yet irresponsible, choice. Therefore, many politically conservative groups, religious groups, and legal systems tended to punish the individual who uses AOD. The moral model or attitude towards addiction can still be seen today in certain cultures. Those who still believe addiction is morally “wrong” tend to perceive the most appropriate way to treat the individuals who use AOD are through legal sanctions, such as imprisonment and fines. For example, in many countries, drivers who are caught under the influence of alcohol or other drugs are not considered for treatment programs but instead receive court sentences as punishments (Fisher & Harrison, 2017).

This model has been rejected by alcohol and other drugs professionals as unscientific and contributes to the stigma surrounding addiction and substance use (White, 1991, cited in Fisher & Harrison, 2017).

The Disease Model

This model takes up the medical viewpoint and proposes addiction as a disease or illness that an individual has. It proposed that addiction is a disease that is progressive and chronic whereby the individual holds no control as long as the substance use continues. In other words, their addiction will continue to deteriorate with the continuous AOD (Thombs & Osborn, 2019). It also proposes that individuals who uses AOD can never be cured from addiction, though it can be readily treated through sustained abstinence such as self-help fellowships and treatment community. 

In the 1940s, Jellinek proposed a disease model in relation to alcoholism, arguing that it is a disease caused by a physiological deficit in an individual, making the person permanently unable to tolerate the effects of alcohol (Stevens & Smith, 2014). Jellinek identified signs and symptoms and clustered them into stages of alcoholism, as well as progression of the disease, which form the basis of 12-step or Anon-type programs (e.g., Alcoholics Anonymous and Narcotics Anonymous; Stevens & Smith, 2014). 

Under the disease model, treatment requires complete abstinence. Once an individual has accepted the reality of their addiction and ceased substance use, they are labelled as being in recovery, but are never ‘cured’ (e.g., “Once an alcoholic, always an alcoholic”; Thombs & Osborn, 2019). Whilst originally applied to alcohol dependency, it has now been generalised to other substances and many traditional substance use treatment models are based on this model (Capuzzi & Stauffer, 2020; Stevens & Smith, 2014).

The disease model offered an alternative to the moral theory, helping to remove the moral stigma attached to addiction and replacing it with an emphasis on treatment of an illness (Capuzzi & Stauffer, 2020). Disease theory helped to explain how some people experience the physiological effects of addiction such as dependence, tolerance, and withdrawal more than others, and how these mechanisms are caused by a biochemical abnormality in an individual which increases their likelihood of developing a dependency (DiClemente, 2018). 

While the disease model was well received by a range of professionals, many criticised it because research did not find that the progressive, irreversible progression of addiction through stages always occurs as predicted (Capuzzi & Stauffer, 2020). Additionally, many in the AOD field argued that the model did not address the complex interrelated factors that accompany dependency (Stevens & Smith, 2014). Finally, some professionals argued that the concept of addiction being a disease may also convey the impression to some individuals that they are powerless over their dependency and/or not responsible for the consequences of destructive addictive behaviours, which can be counteractive to treatment (Capuzzi & Stauffer, 2020).

Genetic and Neurobiological Theories

These theories suggest that some people may be genetically predisposed to develop drug dependency. For example, individuals usually begin substance use on an experimental basis. They then continue using because there is some reinforcement for doing so (e.g., a reduction of pain, experience of euphoria, social recognition, and/or acceptance, etc.). Some people may continue to use substances in a controlled or recreational manner with limited consequences while others progress to non-medical use and eventually develop a dependency. Why? Genetic and neurobiological theories propose that this is the result of a genetic predisposition to drug dependency (Fisher & Harrison, 2017). 

Factors being considered by researchers in the genetic transmission of dependency on alcohol include neurobiological features such as an imbalance in the brain’s production of ‘feel good’ neurotransmitters or in the metabolism of ethanol, which is the key component of alcohol (Stevens & Smith, 2014). Other researchers explored genetic differences in temperament and personality traits which they argued may lead to certain individuals becoming more vulnerable in the face of challenging environmental circumstances, leading to AOD use (Stevens & Smith, 2014). Genetic predispositions such as these may explain why some individuals develop dependency on AOD while others in similar situations do not.

The Psycho-dynamic Model

This model proposes that substance use may be due to an unintentional response to some difficulties that an individual experienced in their childhood. This explanation is based on the theory that was put forward by Sigmund Freud, whereby the problems of whether we are able to cope with difficulties as adults are linked to our childhood experience. Many counselling approaches today are based on this theory which aim to seek understanding of people’s unconscious motivations and to enhance how they view themselves (Capuzzi & Stauffer, 2020).

The Psycho-dynamtic model also believes that AOD use is often secondary to a primary psychological issue. In other words, alcohol and other drugs is a symptom rather than a disorder, and AOD use is a means to temporarily relieve or numb emotional pain. For example, an individual suffering from depression might self-medicate with stimulants to relieve the enervating effects of depression or manage their anxiety by using benzodiazepines (Fisher & Harrison, 2017). 

There is evidence to support this model, whereby childhood traumatic events are associated with mental health problems and substance use disorders. Wu et al. (2010) conducted a study among 402 adults who were receiving substance use disorder treatments. They revealed that almost all (95%) of the participants experienced one or more childhood traumatic events, and 65.9% of them experienced emotional abuse and neglect from their childhood. The authors also reported that the higher the number of childhood traumatic events experienced, the higher the risk of substance use disorders and mental health problems such as post-traumatic stress disorder. 

Personality Traits

Some theorists suggest that certain individuals have certain personality traits that are linked to AOD dependency. For example, dependency on alcohol has been associated with traits such as developmental immaturity, impulsivity, high reactivity and emotionality, impatience, intolerance, and inability to express emotions (Capuzzi & Stauffer, 2020).

Social Learning Model

This model suggests that social learning processes such as observing other peoples behaviours (i.e., modelling) and cultural norms are important in the process of learning behaviours. Albert Bandura proposed Social Learning Theory which would argue that substance use is initiated by environmental stressors or modelling people around you with “perceived status”. For example, a child observes their parents use alcohol in social situations and the child is therefore more likely to perceive that AOD use for social situations is appropriate (Harrison & Fisher, 2017); the association between socialisation and alcohol has been established.

The social learning model also recognises the influence of cognitive processes such as coping, self-efficacy, and outcome expectancies. Some researchers are currently focusing on how an individuals expectation of the effects of drugs influence the pattern of AOD use and resulting dependency. Russell (1976, cited in Wise & Koob, 2013) suggested that dependency on substance is not only chemical (biological) but also behavioural and social in nature. 

It has also been suggested that substance use occurs when an individual thinks substance use is a coping mechanism. This can be learned from television and film, social medial, peer influence, or messages from caregivers during childhood. The individual hopes the AOD use will relieve from them from stress (Stevens & Smith, 2014). 

Socio-cultural Model

Different from the previous models, the socio-cultural model perceives substance use as an issue of society as a whole instead of focusing only on the individual. People tend to overestimate the influence of internal and psychological factors while underestimating the external and environmental factors, even among some alcohol and other drugs workers (Gladwell, 2000, cited in Lewis, Dana, & Blevins, 2015). Thus, this model highlights the importance of how society shapes substance use behaviours, such as cultural attitudes, peer pressures, family structures, economic factors, and more (Bobo & Husten, 2000). For example, Coffelt et al. (2006) found that parents’ alcohol use are associated with their children’s drinking behaviour, whereby when the adult’s alcohol problems increased, the likelihood of their adolescent child’s alcohol use increased. 

The Biopsychosocial Model

Substance use behaviour cannot be explained or understood scientifically or spiritually based on a single variable, antecedent, or “cause”. Biological, psychological, learning, social and cultural context all contributes to explaining why addiction develops and maintains. The interactions between these factors are presented in The Biopsychosocial Model – arguably the most commonly used model to explain addiction today. The model suggests that substance use and the progression of substance dependency can be explained by recognising that the body and mind are connected within a social and cultural context (Skewes & Gonzalez, 2013).

The model allows any combination of biological, psychological, social and cultural factors to contribute to AOD misuse and dependency, rather than a single dominating factor. This is much more holistic and integrative when attempting to understand the determinant of addiction (Stevens & Smith, 2014).

References:

1. Bobo, J. K., & Husten, C. (2000). Sociocultural influences on smoking and drinking. Alcohol Research and Health, 24(4), 225-232. 
2. Capuzzi, D., & Stauffer, M. D., Sharpe, C. W. (2020). History and etiological models of addiction. In D. Capuzzi, & M. D. Stauffer (Eds.), Foundations of addictions counseling (pp. 1-22). Pearson Education.
3. Coffelt, N. L., Forehand, R., Olson, A. L., Jones, D. J., Gaffney, C. A., Zens, M. S. (2006). A longitudinal examination of the link between parent alcohol problems and youth drinking: The moderating roles of parent and child gender. Addictive Behaviours, 31, 4, 593-605. https://doi.org/10.1016/j.addbeh.2005.05.034 
4. DiClemente, C. C. (2018). Addiction and change: How addictions develop and addicted people recover. The Guilford Press.
5. Fisher, G. L., & Harrison, T. C. (2017). Substance abuse: Information for school counsellors, social workers, therapists, and counsellors. Pearson Education. 
6. Lassiter, P. S., & Spivey, M. S. (2018). Historical perspectives and the moral model. In P. S. Lassiter, & J. R. Culbreth (Eds.), Theory and practice of addiction counselling. (pp. 27-46). Sage Publications. 
7. Lewis, J. A., Dana, R. Q., & Blevins, G. A. (2015). Substance abuse counselling. Cengage Learning.
8. Skewes, M. C., & Gonzalez, V. M. (2013). The biopsychosocial model of addiction. In P. M. Miller, A. W. Blume, D. J. Kavanagh, K. M. Kampman, M. E. Bates, M. E. Larimer, N. M. Petry, P. D. Witte, S. A. Ball (Eds.), Principles of addiction: Comprehensive addictive behaviours and disorders (pp. 61-70). Academic Press.
9. Stevens, P., & Smith, R. L. (2014). Substance abuse counselling: Theory and practice. Pearson Education. 
10. Teesson, M., Hall, W., Proudfoot, & Degenhardt, L. (2012). Addictions. Taylor & Francis Group.
11. Thombs, D. L., & Osborn, C. J. (2019). Introduction to addictive behaviours. The Guilford Press. 
12. Wise, R. A., & Koob, G. F. (2013). The development and maintainance of drug addiction. Neuropsychopharmacology, 39, 254-262.
13. Wu, N. S., Schairer. L. C., Dellor, E., & Grella, C. (2010). Childhood trauma and health outcomes in adults with comorbid substance abuse and mental health disorders. Addictive Behaviors, 35(1). 68-71. https://doi.org/10.1016/j.addbeh.2009.09.003