Addiction — AQA A-Level Psychology
Test yourself on Addiction with AQA A-Level practice questions.
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Addiction explained
Addiction is a disorder in which someone keeps using a substance, or repeating a behaviour, despite knowing what it costs them.
Read the full explanation
Physical dependence is a bodily adaptation: the nervous system has recalibrated around the drug, so stopping it throws the body out of balance and produces withdrawal, a cluster of symptoms usually opposite in direction to the drug’s own effects. Stopping nicotine brings irritability, anxiety and craving that peak at 24 to 72 hours. Psychological dependence is the compulsion side, the craving and the sense of not coping without it. Tolerance is why the dose climbs: repeated use downregulates receptors, so the same amount does less than it used to. Evaluate the split, because it leaks. Gambling involves no ingested chemical yet produces craving and withdrawal-like symptoms, which is why DSM-5 (2013) moved gambling disorder in with the substance disorders.
Risk factors in the development of addiction, including genetic vulnerability, personality and social influences.
The development of addiction is rarely caused by a single trigger; rather, it emerges from interacting risk factors. Genetic vulnerability suggests individuals inherit a predisposition, such as possessing the A1 variant of the DRD2 gene, which reduces dopamine receptor density and drives compensatory substance use. Personality traits also elevate risk; for instance, high levels of neuroticism or impulsivity can lead individuals to self-medicate or engage in risky behaviours. Furthermore, social influences play a critical role through mechanisms like social learning. If an adolescent observes peers or family members receiving social rewards for smoking, they may imitate this behaviour, increasing their likelihood of developing an addiction.
Explanations for nicotine addiction: brain neurochemistry, including the role of dopamine, and learning theory as applied to nicotine addiction, including reference to cue reactivity.
Nicotine addiction can be explained through both biological and behavioural mechanisms. Brain neurochemistry focuses on how nicotine binds to nicotinic acetylcholine receptors in the ventral tegmental area. This stimulates the release of dopamine in the nucleus accumbens, activating the brain's reward pathway and producing intense pleasure. Conversely, learning theory applies operant conditioning, where nicotine use is positively reinforced by these rewarding sensations and negatively reinforced by the avoidance of withdrawal symptoms. Classical conditioning further explains relapse through cue reactivity; neutral environmental stimuli, such as a lighter or a specific social setting, become associated with nicotine's effects, triggering intense cravings.
Explanations for gambling addiction: learning theory as applied to gambling, including reference to partial and variable reinforcement; cognitive theory as applied to gambling, including reference to cognitive bias.
Gambling is the awkward case for learning theory: gamblers lose far more often than they win, yet the behaviour is unusually hard to extinguish. The answer is the reinforcement schedule. Wins arrive on a variable ratio schedule, unpredictably after a varying number of bets, and Skinner showed that this schedule produces high, steady responding and the greatest resistance to extinction of all, because no run of losses tells the gambler the reward has stopped coming. Near misses reinforce too, being processed almost like wins. Cognitive theory explains the beliefs that keep the schedule working: the gambler’s fallacy that a loss makes a win due, an illusion of control from choosing numbers, and a recall bias that remembers wins vividly and losses barely. Griffiths (1994) had 60 fruit-machine players think aloud; regular gamblers produced far more irrational verbalisations.
Reducing addiction: drug therapy; behavioural interventions, including aversion therapy and covert sensitisation; cognitive behaviour therapy.
Three routes, each attacking a different part of the problem. Drugs work on the chemistry: agonists such as methadone occupy the same receptors as heroin more slowly and safely, antagonists such as naltrexone block the receptors so a relapse produces no high, and aversives such as disulfiram stop alcohol being fully broken down, so drinking brings nausea and vomiting. Aversion therapy is classical conditioning, pairing the substance with a genuinely unpleasant experience until it provokes disgust on its own. Covert sensitisation does the same in imagination, the client rehearsing a vivid scene of vomiting over themselves, which avoids the ethical objections to an emetic or a shock. Cognitive behaviour therapy targets the beliefs, challenging the gambler’s biases and rehearsing relapse prevention: Petry et al. (2006) found eight CBT sessions beat Gamblers Anonymous referral alone.
The application of Prochaska’s six-stage model of behaviour change.
Prochaska’s six-stage model explains how individuals overcome addiction through a cyclical process. The stages are pre-contemplation (no intention to change), contemplation (aware of the problem but uncommitted), preparation (intending to act soon), action (modifying behaviour), maintenance (preventing relapse), and termination (zero temptation). Application involves tailoring interventions to the client's current stage. For example, a smoker in pre-contemplation benefits from education about health risks, whereas someone in the action stage requires behavioural strategies like avoiding triggers. This stage-matched approach increases the effectiveness of addiction treatments by providing targeted, timely support.
Your focus
- Describe withdrawal syndrome as symptoms opposite in direction to the drug's own effects, using nicotine at 24 to 72 hours.
- Distinguish physical from psychological dependence in a given case by whether stopping brings bodily symptoms or craving alone.
- Apply tolerance to a climbing dose, explaining receptor downregulation as why the original amount now does less.
Show all 22 objectives
- Explain why gambling makes the physical and psychological split hard to sustain, given DSM-5 reclassified it in 2013.
- Describe how genetic vulnerability contributes to the development of addiction.
- Explain the relationship between specific personality traits and addiction risk.
- Evaluate the role of social influences, including peers and family, in addictive behaviours.
- Outline the role of dopamine and the reward pathway in nicotine addiction.
- Apply principles of operant and classical conditioning to explain smoking behaviour.
- Describe the phenomenon of cue reactivity and its role in triggering nicotine cravings.
- Explain how variable ratio reinforcement and near misses together make gambling unusually resistant to extinction.
- Describe Griffiths' think-aloud comparison of 30 regular and 30 non-regular fruit machine players and what he found.
- Identify which cognitive bias a gambler's statement shows, choosing between gambler's fallacy, illusion of control and recall bias.
- Evaluate learning theory against cognitive theory on the first bet and on why most regular gamblers never become disordered.
- Describe how agonists, antagonists and aversives each work, naming methadone, naltrexone and disulfiram.
- Explain aversion therapy as classical conditioning and distinguish it from covert sensitisation by where the pairing happens.
- Outline what a CBT programme for addiction covers, from functional analysis of triggers to relapse prevention planning.
- Apply Petry's trial of 231 gamblers as evidence that eight CBT sessions beat Gamblers Anonymous referral alone.
- Evaluate drug therapy and aversion therapy on relapse, side effects and the ethical objection each raises.
- Outline the six stages of Prochaska's model of behaviour change.
- Apply the model to select appropriate interventions for individuals at different stages of addiction recovery.
- Evaluate the strengths and limitations of the six-stage model in the context of addiction treatment.
Addiction exam tips
Marking Points
- Physical dependence: the body has adapted to the substance, so its absence produces a physiological withdrawal state and use continues partly to avoid that state.
- Psychological dependence: a compulsion to experience the effect again, shown in craving, preoccupation and the belief that one cannot function without it.
- Tolerance: a reduced response to the same dose after repeated use, explained by receptor downregulation, so the user escalates the amount to get the original effect.
- Withdrawal syndrome: symptoms appearing on cessation or reduction, typically the opposite of the drug’s acute effects (a stimulant leaves fatigue and low mood).
- Named illustration: nicotine withdrawal produces irritability, anxiety, poor concentration and craving, peaking within roughly 24 to 72 hours of the last cigarette.
- Evaluation: the physical/psychological distinction is hard to sustain, since gambling has no ingested substance yet shows tolerance, craving and withdrawal-like distress, and DSM-5 (2013) reclassified gambling disorder with the substance use disorders.
- Explain genetic vulnerability using specific mechanisms, such as inherited variations in dopamine receptor genes (e.g., DRD2).
- Describe how personality traits, particularly impulsivity and neuroticism, correlate with higher rates of substance misuse.
- Outline social influences, distinguishing between peer pressure (normative social influence) and family influences (observational learning).
- Evaluate the interaction of these risk factors using the diathesis-stress model, noting that genetics alone do not guarantee addiction.
- Detail the neurochemical process: nicotine binds to nAChRs, leading to dopamine release in the mesolimbic pathway.
- Explain positive and negative reinforcement in the maintenance of nicotine addiction.
- Define cue reactivity as a classical conditioning process where environmental cues trigger physiological cravings.
- Evaluate the neurochemical explanation by discussing the success of treatments like nicotine replacement therapy, which targets nicotinic acetylcholine receptors to manage withdrawal.
- Contrast the biological and learning approaches, noting how learning theory better explains relapse after physical withdrawal has ceased.
- Operant conditioning: a win delivers money and excitement immediately after the bet, positively reinforcing gambling; for some, gambling also removes boredom or low mood, negatively reinforcing it.
- Partial reinforcement: only some responses are rewarded, and partially reinforced behaviour is far more resistant to extinction than continuously reinforced behaviour.
- Variable reinforcement specifically: wins come after an unpredictable number of bets (variable ratio), which produces a high, steady rate of responding and the strongest resistance to extinction, so losing runs do not signal that reward has ceased.
- Near misses: two jackpot symbols and a third just off the payline are processed as near-wins and reinforce continued play despite being losses.
- Cognitive bias, gambler’s fallacy: believing independent events are linked, so a run of losses means a win is "due".
- Cognitive bias, illusion of control: believing skill, ritual or choosing one’s own numbers influences a chance outcome.
- Cognitive bias, recall and attributional bias: wins are remembered and attributed to skill, losses are minimised, forgotten or blamed on bad luck, so experience never corrects the belief.
- Evidence: Griffiths (1994) compared 30 regular and 30 non-regular fruit-machine gamblers using a think-aloud method and found regular gamblers made significantly more irrational verbalisations, such as treating the machine as having moods.
- Evaluation: learning theory struggles to explain the very first bet and why most regular gamblers never become disordered, whereas cognitive theory explains persistence but rests on self-report; its strength is practical, since challenging these beliefs is what cognitive behaviour therapy does.
- Drug therapy, agonists: methadone substitutes for heroin at the same receptor sites, satisfying the craving with a controlled dose that allows stabilisation and gradual reduction.
- Drug therapy, antagonists: naltrexone blocks opioid receptors so the drug produces no reward, breaking the reinforcement link.
- Drug therapy, aversives: disulfiram prevents the full breakdown of alcohol, so drinking causes an immediate build-up of acetaldehyde and severe nausea, flushing and vomiting.
- Nicotine replacement therapy delivers nicotine without the tar and the smoking ritual, reducing withdrawal while the behavioural habit is tackled separately.
- Aversion therapy: classical conditioning in which the addictive stimulus is repeatedly paired with an aversive unconditioned stimulus (an emetic, or shock in gambling studies) so it becomes a conditioned stimulus for disgust.
- Covert sensitisation: the same pairing carried out in imagination, the therapist guiding a vivid aversive scene, so no drug or shock is administered and dropout and ethical objections are reduced.
- Cognitive behaviour therapy: functional analysis of triggers, challenging cognitive biases such as the illusion of control, plus skills training and relapse prevention planning.
- Evidence: Petry et al. (2006) randomised 231 pathological gamblers and found those given eight sessions of CBT alongside Gamblers Anonymous referral showed significantly better outcomes than referral alone.
- Evaluation: drug therapy treats the symptom rather than the cause, carries side effects and depends on compliance, so relapse is common once it stops; aversion therapy shows poor long-term effects and raises ethical objections; CBT demands motivation and effort, which is why dropout rates are high.
- Identify and define the six stages: pre-contemplation, contemplation, preparation, action, maintenance, and termination.
- Explain that the model is dynamic and cyclical, acknowledging that individuals may move back and forth between stages due to relapse.
- Apply the model to a novel scenario by matching specific therapeutic interventions to the individual's current stage of change.
- Evaluate the model's usefulness, such as its practical application in creating stage-matched interventions that improve treatment outcomes.
- Discuss limitations, such as the arbitrary division between stages or the difficulty in accurately assessing which stage a client is currently in.
Examiner Tips
- 💡In a "distinguish between" question, define both terms and then supply one contrasting example each. The mark is for the contrast, so an answer defining only the first term caps itself.
- 💡Given a scenario, quote the stem back: if the person "needs three cans to feel what one used to do" that is tolerance, and if they are "shaky and irritable by lunchtime" that is withdrawal. Labelling the evidence is where the AO2 marks sit.
- 💡Do not spend an evaluation paragraph listing symptoms. AO3 here is the argument that the physical/psychological boundary is blurred, with gambling as the worked case.
- 💡Use the diathesis-stress model as a synoptic evaluation point to explain how genetic vulnerability interacts with social influences.
- 💡When discussing personality, explicitly name traits like impulsivity or antisocial personality disorder rather than just saying 'a bad personality'.
- 💡Support your explanation of social influences with psychological concepts like vicarious reinforcement or normative social influence.
- 💡Use specific brain anatomy, such as the ventral tegmental area (VTA) and nucleus accumbens, to elevate your neurochemical explanation.
- 💡When evaluating learning theory, use cue reactivity to explain why smokers often relapse in familiar environments like pubs.
- 💡Combine both explanations for a strong conclusion, suggesting that neurochemistry initiates the addiction while learning theory maintains it.
- 💡Use the word "unpredictable" explicitly when explaining variable reinforcement; examiners look for it as the feature that resists extinction.
- 💡A scenario naming someone who "feels a win is due" or "picks their own numbers" is handing you the gambler’s fallacy and the illusion of control. Name the bias, then apply it to that person’s detail.
- 💡If asked to compare the two explanations, make the point that they operate at different levels, the schedule maintaining the behaviour and the biases maintaining the belief, rather than declaring one simply better.
- 💡If the question asks about one named therapy, resist writing about the other two; only the named one earns AO1, and the rest is wasted time.
- 💡In an applied question, prescribe for the person in the stem. A gambler with strong cognitive distortions points to CBT; someone in acute opioid withdrawal points to methadone, and saying why that fits is the AO2.
- 💡Ethics is a genuine AO3 line for aversion therapy, but make it specific: informed consent and protection from harm when an emetic or shock is used, and note that covert sensitisation was designed to answer exactly that.
- 💡When given a stem, look for temporal clues (such as 'planning to quit next week' or 'has been clean for two months') to accurately identify the person's current stage.
- 💡Use the concept of 'stage-matched interventions' to explain why a specific treatment might fail if applied at the wrong time.
- 💡Remember to evaluate the model's cultural validity, noting that its focus on individual decision-making may not apply as effectively in collectivist cultures.
Common Mistakes
- Treating tolerance and dependence as the same thing. Tolerance is a shrinking response to a given dose; dependence is needing the substance to feel or function normally, and an examiner wants them separated.
- Describing withdrawal as simply "feeling ill" or "wanting it badly". Credit comes from naming symptoms and noting they typically oppose the drug’s own effects, not from vague discomfort.
- Equating addiction with heavy use. Someone can drink a great deal without tolerance, withdrawal or loss of control, and the term describes the pattern of dependence rather than the quantity.
- Claiming behavioural addictions such as gambling are "only psychological" and therefore not real addiction, which ignores the DSM-5 reclassification and the physiological craving evidence.
- Error: Claiming there is a single 'addiction gene'. Correction: Explain that genetic vulnerability involves multiple genes (polygenic) interacting with environmental triggers.
- Error: Confusing peer pressure with family influences. Correction: Clearly separate peer conformity from parental modelling and perceived parental approval.
- Error: Assuming personality traits cause addiction directly. Correction: State that personality traits are correlational risk factors, not deterministic causes.
- Error: Stating that dopamine directly causes addiction. Correction: Explain that dopamine creates a reward signal that reinforces the behaviour, rather than acting as a direct cause.
- Error: Confusing positive and negative reinforcement in smoking. Correction: Specify that positive reinforcement is the euphoric feeling, while negative reinforcement is the removal of withdrawal symptoms like irritability.
- Error: Describing cue reactivity without linking it to classical conditioning. Correction: Explicitly identify the environmental cue as a conditioned stimulus that produces a conditioned response (craving).
- Describing partial reinforcement as "sometimes being rewarded" without saying why that matters. The creditworthy point is resistance to extinction, so a losing streak does not stop the behaviour.
- Confusing variable ratio with variable interval. Gambling pays after an unpredictable number of bets, not after an unpredictable amount of time.
- Explaining the gambler’s fallacy backwards, saying a winner expects to keep winning. The fallacy is that past losses make a future win more likely when the events are independent.
- Presenting Griffiths (1994) as showing regular gamblers are more skilful. Objectively the two groups performed similarly; the difference was in how they talked about the machine.
- Treating think-aloud verbalisations as proven beliefs, when they may be commentary produced for the researcher rather than the thinking that drives play.
- Confusing agonists with antagonists. An agonist activates the receptor as a substitute (methadone); an antagonist blocks it so use brings no reward (naltrexone).
- Describing covert sensitisation as a mild form of aversion therapy. The difference is that the aversive experience is imagined rather than actually experienced, which is the whole point of it.
- Calling disulfiram a punishment. It works as classical conditioning, pairing alcohol with an unconditioned nausea response, and the term matters when the question asks for the mechanism.
- Evaluating all three therapies with one generic line about side effects. Each has its own weakness: relapse after withdrawal of the drug, poor durability for aversion, and dropout for CBT.
- Confusing the contemplation and preparation stages. Correction: Ensure contemplation is described as thinking about change without commitment, while preparation involves actively planning to take action within the next month.
- Treating the model as a strictly linear process. Correction: Describe the model as cyclical, explicitly stating that individuals often relapse and return to earlier stages before achieving termination.
- Omitting the termination stage because it is rarely achieved. Correction: Always include termination as the final stage of the six-stage model, even if noting that many people remain in maintenance permanently.