EGO

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.

Inattentional Blindness is the failure to notice an unexpected object in a visual display.

Cognitive Psychology is an approach to understanding human cognition by observing behaviour of people performing cognitive tasks. It is concerned with the internal processes involved in making sense of our environment, and deciding what behaviour to be appropriate. These processes include attention, perception, learning, memory, language, problem-solving, reasoning, and thinking.

The most famous experiment that shows evidence for inattentional blindness is the Simons and Chabris (1999) experiment where an audience or viewer watches a group of people pass a ball to one another wearing either black or white, and a woman dressed as a gorilla enters the frame for 9 seconds, then walks off. Results reported that 50% of the observers did not notice the gorilla enter the frame. In all honesty, when I saw the video for the first time at university, I did not see the gorilla enter the frame either.

In reality, we are often aware of changes in our visual environment because we detect motion cues accompanying the change. This information suggests that our ability to detect visual changes is not only due to the detection of movement. An obvious explanation of the gorilla experiment findings is that the visual representations we form in our mind are sparse and incomplete because they depend on our limited attentional focus. Simons and Rensick (2005) point out that there are other explanations, such as: detailed and complete representations may exist initially but may either decay rapidly or be overwritten by a subsequent stimulus. It needs to be said that in the gorilla experiment, the observers are instructed to count how many times the ball passes, so really, our attention is deliberately compromised. The real-life implications of inattentional blindness reveals the role of selective attention in human perception. Inattentional blindness represents a consequence of this critical process that allows us to remain focused on important aspects of our world without distraction from seemingly irrelevant objects and events.

Being present, in the moment (mindfulness) can help aid our attention. Distractions such as using our mobile phones, advertising material, other people, “multi-tasking” and internal emotional states all contribute to our lack of focus and attention. Think of a magician’s ability to manipulate their audiences attention in order to prevent them from seeing how a trick is performed. There are also safety implications, as you would know … if you’ve been paying attention, haha.

Just food for thought, my readers, and friends 🙂

Social psychological models of behaviour attempt to explain why individuals act the way they do in various social contexts. These models integrate individual, interpersonal, and societal factors to provide insights into behaviour. Here’s an overview of some key models:

1. Theory of Planned Behaviour (TPB) proposes that behaviour is influenced by:

– Attitudes toward the behaviour

– Subjective norms (perceptions of others’ approval)

– Perceived behavioural control (i.e., confidence in one’s ability to perform the behaviour [self-efficacy])

2. Social Cognitive Theory (SCT) suggests that behaviour is the result of:

– Reciprocal interaction between personal factors (beliefs, attitudes), environmental factors (social norms), and behaviour itself

– Concepts like self-efficacy (belief in one’s ability) play a major role.

3. Health Belief Model (HBM), designed to predict health-related behaviours. Behaviour is driven by factors such as perceived:

– Susceptibility (risk of harm)

– Severity (consequences of harm)

– Benefits (advantages of action)

– Barriers (obstacles to action)

4. Cognitive Dissonance Theory explains how people strive for consistency between their beliefs, attitudes, and behaviours. When inconsistency arises, they feel dissonance (mental discomfort) and are motivated to reduce it by changing their attitudes or actions.

5. Social Identity Theory examines how individuals define themselves within social groups. Behaviour is influenced by group membership, including in-group favouritism and out-group bias.

6. Attribution Theory focuses on how people explain their own and others’ behaviours. Explains behaviour as being attributed either to internal (dispositional) or external (situational) factors. For example, it is common for people to attribute negative outcomes in their life to external factors rather than internal factors.

7. Elaboration Likelihood Model (ELM) explains how people process persuasive messages and what determines whether those messages will change attitudes or behaviour. It’s often applied in areas like marketing, communication, and public health campaigns. The ELM identifies two primary routes through which persuasion can occur:

– Central Route; this route involves deep, thoughtful consideration of the content and logic of a message. People are more likely to take the central route when they are motivated to process the message (e.g., the topic is personally relevant or important to them) and they can understand and evaluate the arguments (e.g., they aren’t distracted, and they have enough knowledge about the subject). Persuasion through the central route tends to result in long-lasting attitude change that is resistant to counterarguments. Example: A person researching the pros and cons of electric cars before deciding to buy one.

– Peripheral Route, which relies on superficial cues or heuristics (mental shortcuts) rather than the message’s content. People are more likely to take the peripheral route when they are not highly motivated or lack the ability to process the message deeply, and when they focus on external factors like the attractiveness or credibility of the speaker, emotional appeals, or catchy slogans. Persuasion through this route tends to result in temporary attitude change that is less resistant to counterarguments. Example: A person choosing a product because their favourite celebrity endorsed it.

8. Self-Determination Theory (SDT) emphasizes intrinsic and extrinsic motivation. It emphasizes the role of intrinsic motivation—doing something for its inherent satisfaction—over extrinsic motivation, which is driven by external rewards or pressures. It suggests that behaviour is influenced by the need for:

– Autonomy (control over one’s actions); When people perceive they have a choice and are acting in alignment with their values, their motivation and satisfaction increase.

– Competence; Refers to the need to feel effective, capable, and successful in achieving desired outcomes. People are motivated when tasks challenge them at an appropriate level and provide opportunities for growth and mastery. Example: A gamer progressing through increasingly difficult levels, gaining skills and confidence along the way.

– Relatedness; Refers to the need to feel connected to others and experience a sense of belonging. Supportive relationships and positive social interactions enhance motivation and well-being. Example: Employees feeling a bond with their colleagues in a collaborative work environment.

9. Social Learning Theory proposes that behaviour is learned through observation and imitation. Role models and reinforcement play a key role in shaping actions.

10. Transtheoretical Model (Stages of Change) explains behaviour change as a process occurring in stages: precontemplation, contemplation (ambivalence), preparation, action, and maintenance

These models provide frameworks to understand behaviours in contexts like health, decision-making, group dynamics, and social influence.