Addiction — AQA A-Level Psychology
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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, stress, personality, family influences and peers.
A risk factor raises the probability that someone becomes addicted; it does not make it inevitable, and that distinction earns marks on its own. Genetics come first: twin and adoption work puts the heritability of alcohol dependence near 50%, and Blum et al. (1990) found the A1 variant of the DRD2 gene in 69% of severe alcoholics against about 20% of controls, a variant linked to fewer type-2 dopamine receptors and so to a blunted reward system. Stress works through self-medication, using the substance to damp down anxiety or the after-effects of childhood trauma. Personality contributes through impulsivity, neuroticism and sensation-seeking rather than one "addictive personality". Family and peers supply social learning: children copy parental models, and adolescents systematically overestimate how much their friends use, then drink or smoke up to that imagined norm.
Explanations for nicotine addiction: brain neurochemistry, including the role of dopamine, and learning theory as applied to smoking behaviour, including reference to cue reactivity.
Neurochemically, nicotine reaches the brain in ten seconds, binding nicotinic acetylcholine receptors on neurons in the ventral tegmental area. These fire and flood the nucleus accumbens with dopamine along the mesolimbic reward pathway. Repeated flooding desensitises receptors and the brain upregulates their number. Without nicotine, dopamine falls below normal; the smoker feels irritable. Learning theory adds conditioning: the dopamine surge positively reinforces smoking, relief of withdrawal negatively reinforces it, and neutral things paired with smoking become conditioned stimuli. This is cue reactivity. Carter and Tiffany’s (1999) meta-analysis found dependent smokers show measurable craving and arousal to smoking cues alone.
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 the following theories of behaviour change to addictive behaviour; the theory of planned behaviour and Prochaska’s six-stage model of behaviour change.
Both models answer the same question: what actually turns wanting to stop into stopping? Ajzen says intention is the immediate cause of behaviour, and intention is built from three things. Personal attitude, whether the person judges quitting worthwhile; subjective norms, what they believe important others think and do; and perceived behavioural control, how easy they believe it would be, which also predicts behaviour directly because confidence sustains effort. Prochaska treats change as a sequence instead, moving through precontemplation, contemplation, preparation, action, maintenance and termination, with relapse expected rather than treated as failure, so treatment is matched to the stage actually reached. Evaluate with the intention-behaviour gap: Webb and Sheeran (2006) found a medium-to-large shift in intention produced only a small-to-medium shift in behaviour.
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 27 objectives
- Explain why gambling makes the physical and psychological split hard to sustain, given DSM-5 reclassified it in 2013.
- Explain what a risk factor is, stating that it shifts probability and is neither necessary nor sufficient for addiction.
- Describe genetic vulnerability using the 50 per cent heritability estimate and Blum's DRD2 A1 finding of 69 against 20 per cent.
- Apply stress, personality or peer risk to a given case, naming self-medication or overestimated peer use as the route.
- Evaluate the risk factor evidence as correlational and explain why diathesis-stress handles the interaction better.
- Describe nicotine's route from inhalation to nicotinic receptors in the ventral tegmental area and dopamine in the nucleus accumbens.
- Explain why a smoker feels flat without a cigarette, using desensitisation and upregulation dropping dopamine below baseline.
- Apply positive and negative reinforcement to distinguish an early cigarette from one smoked only to end withdrawal.
- Explain why a lighter or a coffee triggers craving, using cue reactivity and Carter and Tiffany's meta-analysis of 41 studies.
- Evaluate the neurochemical account using relapse after nicotine replacement therapy and the many who try cigarettes without dependence.
- 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.
- Describe the three components of the theory of planned behaviour and state which one also predicts behaviour directly.
- Apply Prochaska's six stages to a given smoker and say which intervention matches the stage they have actually reached.
- Explain why relapse in the six-stage model returns a person to an earlier stage rather than counting as failure.
- Evaluate the theory of planned behaviour using Webb and Sheeran's intention-behaviour gap across 47 experimental tests.
- Discuss West's objection that the stage boundaries cut arbitrarily across a continuum and that many people quit unplanned.
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.
- A risk factor increases vulnerability and shifts probability; it is neither necessary nor sufficient, so an explanation must be stated in those terms rather than as a cause.
- Genetic vulnerability: heritability of alcohol dependence estimated around 50% from twin and adoption studies; Blum et al. (1990) reported the DRD2 A1 allele in 69% of severe alcoholics compared with roughly 20% of non-alcoholic controls.
- Mechanism for the genetic finding: fewer type-2 dopamine receptors means a weaker response to ordinary reward, so the person seeks a stronger source of dopamine (reward deficiency).
- Stress: both acute stress and childhood trauma raise risk, explained by self-medication, where the substance is used to relieve anxiety and its relief negatively reinforces further use.
- Personality: impulsivity, high neuroticism and sensation-seeking predict onset, and antisocial personality disorder is over-represented among dependent users.
- Family influences and peers: social learning through parental modelling and perceived approval, plus adolescent overestimation of peer use, which normalises heavier consumption.
- Evaluation: the evidence is overwhelmingly correlational, so direction of causation is uncertain (stress may follow addiction as easily as precede it), and a diathesis-stress framing handles the interaction better than any single factor.
- Nicotine reaches the brain within roughly ten seconds of inhalation and binds nicotinic acetylcholine receptors on dopaminergic neurons in the ventral tegmental area.
- Those neurons project to the nucleus accumbens (the mesolimbic reward pathway), where the resulting dopamine release produces the pleasurable, rewarding effect.
- Desensitisation/upregulation: chronic nicotine desensitises receptors and their number upregulates, so in the drug’s absence dopamine function dips below baseline, producing withdrawal and craving.
- Learning theory, positive reinforcement: the dopamine reward follows the behaviour immediately, which is precisely the schedule operant conditioning strengthens.
- Learning theory, negative reinforcement: later cigarettes are smoked mainly to remove the aversive withdrawal state, which maintains the habit after the initial pleasure has faded.
- Cue reactivity via classical conditioning: stimuli repeatedly paired with smoking (a lighter, coffee, the pub, a break at work) become conditioned stimuli that trigger craving and physiological arousal on their own.
- Evidence: Carter and Tiffany (1999) meta-analysed 41 cue reactivity studies and found dependent smokers reported significantly higher craving and showed greater physiological arousal to smoking-related cues than to neutral ones.
- Evaluation: neurochemistry alone cannot explain why most people who try cigarettes never become dependent, and nicotine replacement therapy leaves most smokers relapsing, which implies the conditioned cues matter as much as the drug.
- 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.
- Theory of planned behaviour: behaviour follows from intention, and intention is determined by three components, so an intervention must shift the components rather than lecture about the behaviour.
- Personal attitude: the individual’s own weighing of the costs and benefits of the addictive behaviour and of giving it up.
- Subjective norms: the person’s belief about what significant others approve of and how much they themselves do it, which is why correcting overestimated peer use changes behaviour.
- Perceived behavioural control: how much control the person believes they have, which feeds intention and also predicts behaviour directly, since belief in success sustains the attempt.
- Prochaska’s six stages in order: precontemplation (no intention, may deny a problem), contemplation (weighing change), preparation (intends to act soon), action (actively changing), maintenance (sustaining change), termination (no temptation remains).
- The model is dynamic and cyclical, not a one-way staircase; relapse returns the person to an earlier stage and is treated as a normal part of change rather than as failure.
- Practical strength: matching the intervention to the stage, so someone in precontemplation gets awareness-raising rather than a quit plan they are not ready for.
- Evaluation of the theory of planned behaviour: Webb and Sheeran (2006) meta-analysed 47 experimental tests and found a medium-to-large change in intention produced only a small-to-medium change in behaviour, the intention-behaviour gap, so intention is a weaker cause than the model implies.
- Evaluation of the six-stage model: West (2005) argued the stage boundaries are arbitrary cuts across a continuum, and many people quit suddenly with no planning stage at all, which the model cannot accommodate.
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.
- 💡Scenario questions almost always plant two or three risk factors in the stem. Find them, name each one with AQA’s own term, then explain how that factor operates for that person.
- 💡Use "vulnerability" and "increases the likelihood" rather than "makes them an addict"; the careful wording is itself creditworthy in evaluation.
- 💡Keep one correlational criticism ready to deploy against whichever factor the question names, since it applies to nearly all of the research base here.
- 💡If the question asks for explanations in the plural, cover both neurochemistry and learning theory and show how each explains the same addictive behaviour.
- 💡For a scenario about someone who relapses on returning to an old pub or a work break, name the cue as a conditioned stimulus and the craving as a conditioned response rather than just calling it a trigger.
- 💡In an extended response, evaluate both explanations using evidence about nicotine replacement, individual differences in dependence and the practical value of cue-exposure work.
- 💡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.
- 💡Name all three components of the theory of planned behaviour every time, even in a short answer; questions are routinely written so each component carries a mark.
- 💡In an applied question, locate the person in the stem at a specific stage and justify it from their words. Someone insisting they could stop any time is in precontemplation, and saying so is the AO2.
- 💡In an extended response, describe both models accurately, then evaluate the intention-behaviour gap, the boundaries between stages and the practical value of stage-matched treatment.
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.
- Writing that a gene "causes" addiction. No single gene does; the finding is an association with a variant that alters dopamine receptor density, and overclaiming here loses the evaluation mark.
- Listing all five risk factors in one line each and stopping. A question worth more than four marks wants the mechanism for each factor named, not a shopping list.
- Confusing family influences with genetics when the parent is the source of both. Say which route is being claimed, inherited vulnerability or modelling and exposure.
- Asserting an "addictive personality" as an established trait. The evidence supports specific traits such as impulsivity and sensation-seeking, not a unified personality type.
- Saying nicotine "releases dopamine" and stopping there. The marks are in the pathway: receptors in the ventral tegmental area, projection to the nucleus accumbens, then desensitisation/upregulation explaining withdrawal.
- Mixing up the two conditioning processes. Cue reactivity is classical conditioning of a stimulus to a craving response; reinforcement is operant, about consequences that strengthen the behaviour.
- Treating positive and negative reinforcement as reward and punishment. Negative reinforcement removes an unpleasant state (withdrawal) and therefore increases smoking; punishment would decrease it.
- Ignoring cue reactivity entirely, even though AQA names it in the specification, which forfeits marks that are effectively guaranteed.
- 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.
- Listing the six stages out of order or omitting maintenance and termination. The sequence itself is the AO1 here, so an incomplete list is directly penalised.
- Confusing subjective norms with the person’s own attitude. Subjective norms are beliefs about what other people think and do, not what the individual personally believes about the behaviour.
- Treating perceived behavioural control as actual control. It is the person’s perception, and in the model that perception does the work whether or not it is accurate.
- Describing relapse as the model breaking down, when the cyclical structure builds relapse in as expected and is one of its acknowledged strengths.
- Writing an evaluation that only praises the models as "useful" without the intention-behaviour gap or the arbitrariness of the stages, which leaves the AO3 marks unclaimed.