AQA A-level Psychology (7182): Paper 3 – Addiction — Study Guide

This guide follows the AQA AS and A-level Psychology (7181, 7182) specification, Version 1.4 (1 September 2025), for teaching from September 2025. It covers section 4.3.10 Addiction, one of the three topics in Option 3 (Aggression, Forensic Psychology, Addiction). The specification places Addiction in Paper 3: Issues and Options in Psychology, where it is assessed in Section D.

Use it with the 7182 subject hub, the 7182 topic checklist, the Addiction revision notes and the Addiction practice questions.

How Paper 3 is set up

The specification prints Paper 3 as follows. What’s assessed: compulsory content 8 (Issues and debates in Psychology) and optional content, “one from option 1, 9–11, one from option 2, 12–14, one from option 3, 15–17”. It is a written exam of 2 hours, 96 marks in total, 33.3% of A-level. Section A has multiple choice, short answer and extended writing questions worth 24 marks and is not tied to an option. Sections B, C and D each cover one topic from options 1, 2 and 3 respectively, with multiple choice, short answer and extended writing, 24 marks each. So if you study Addiction, it is your Section D topic, and you cannot also answer Aggression or Forensic Psychology for that section.

The specification also says that research methods, practical research skills and mathematical skills are assessed in Paper 3, and that you should be able to “evaluate therapies and treatments including in terms of their appropriateness and effectiveness”. So be ready for data, research design and therapy evaluation questions on Addiction, not only essays.

Coverage table

Syllabus reference	What you must know or be able to do (from the specification)	Where assessed
4.3.10 Describing addiction	Physical and psychological dependence, tolerance and withdrawal syndrome	Paper 3, Section D
4.3.10 Risk factors	Genetic vulnerability, personality and social influences	Paper 3, Section D
4.3.10 Nicotine addiction	Brain neurochemistry, including the role of dopamine; learning theory, including cue reactivity	Paper 3, Section D
4.3.10 Gambling addiction	Learning theory, including partial and variable reinforcement; cognitive theory, including cognitive bias	Paper 3, Section D
4.3.10 Reducing addiction	Drug therapy; behavioural interventions, including aversion therapy and covert sensitisation; cognitive behaviour therapy	Paper 3, Section D
4.3.10 Behaviour change	The application of Prochaska’s six-stage model of behaviour change	Paper 3, Section D

Describing addiction

Key terms

• Physical dependence: the body has adapted to the substance, so stopping produces physical withdrawal symptoms.
• Psychological dependence: a compulsion to use the substance or behaviour because it brings pleasure or relief. Cravings are the classic sign. Gambling shows psychological dependence without a drug.
• Tolerance: over time the person needs more of the substance (or a bigger bet) to get the same effect, because the body or brain responds less to the same amount.
• Withdrawal syndrome: the set of unpleasant symptoms when use stops or is cut down. For nicotine these include irritability, poor concentration, restlessness and cravings.

Evaluation. The distinction is useful but blurred. Withdrawal is physical, yet the craving that comes with it is psychological. Behavioural addictions such as gambling show tolerance (larger stakes) and withdrawal-like irritability with no drug at all, which suggests the brain’s reward system, not the substance itself, is the common factor.

Worked example (AO2). Scenario: Ola now vapes twice as often as a year ago to feel calm, and feels shaky and snappy on long flights. “Ola shows tolerance [knowledge], because she needs twice the amount for the same calming effect [application]. The shakiness and irritability on flights are withdrawal syndrome, which points to physical dependence [analysis]. However, her need to vape ‘to feel calm’ also suggests psychological dependence, so the two are hard to separate in a real person [evaluation].”

Risk factors in the development of addiction

Genetic vulnerability. Some people inherit a greater risk, probably through many genes that affect reward and drug metabolism. Vink, Willemsen and Boomsma (2005) studied 1,572 Dutch twin pairs. They estimated that smoking initiation was explained by genes (44%), shared environment (51%) and unique environment (5%). Nicotine dependence was explained by genes (75%) and unique environment (25%).

Personality. Eysenck linked addiction to high neuroticism and psychoticism, and Zuckerman’s sensation-seeking trait (a drive for new and intense experience) is often linked to drug use and gambling. A difficulty is direction: drug use may also change personality.

Social influences. Family and peers model use, supply the substance and set norms (beliefs about what is normal). Christakis and Fowler (2008) analysed 12,067 people in the Framingham Heart Study network from 1971 to 2003. When a spouse quit smoking, a person’s chances of smoking fell by 67%; for a friend the figure was 36% and for a sibling 25%. Smokers clustered together and quit together.

Evaluation.

• Twin data support genes, but even 75% heritability is a population figure. It does not tell you how much of one person’s addiction is genetic.
• Risk factors interact. The diathesis-stress idea fits: genetic vulnerability may only lead to addiction if social pressure or stress triggers it.
• Christakis and Fowler’s data are correlational. People choose friends like themselves, so clustering may reflect selection as well as influence.
• Practical value: knowing risk factors helps target prevention, for example at young people with smoking peers.

Worked example (AO3). “Twin research supports genetic vulnerability: Vink et al. found that genes explained 75% of the variation in nicotine dependence among Dutch twins. However, genes explained only 44% of starting to smoke, with shared environment explaining 51%. This suggests social influences decide whether someone starts, and genes then shape whether use becomes dependence, an interactionist account.”

Explanations for nicotine addiction

Brain neurochemistry and dopamine

Nicotine binds to nicotinic acetylcholine receptors on dopamine neurons in the ventral tegmental area. This triggers dopamine release in the nucleus accumbens, part of the mesolimbic reward pathway, producing pleasure. Nicotine has a short half-life in the blood (about two hours), so its effects wear off within hours of the last cigarette. With repeated use, receptors become desensitised (tolerance) and the brain adjusts, so without nicotine the person feels low and irritable (withdrawal). Smoking again relieves this.

Evaluation.

• Support from treatment: drugs that act on the same receptors, such as varenicline (a partial agonist), help people quit, which fits the dopamine explanation.
• It explains the speed of addiction to smoking, because inhaled nicotine reaches the brain fast.
• It is reductionist. It cannot explain why many people relapse long after withdrawal has ended, which needs learning and cue reactivity.

Learning theory and cue reactivity

Initiation can be explained by social learning (modelling and vicarious reinforcement). Maintenance uses operant conditioning: the dopamine rush is positive reinforcement, and relief from withdrawal is negative reinforcement. Relapse uses classical conditioning. Places, people, smells and the lighter become secondary reinforcers through repeated pairing with nicotine. Cue reactivity is the craving and physiological arousal these cues produce on their own.

Evaluation.

• Carter and Tiffany (1999) meta-analysed 41 cue-reactivity studies. Drug cues produced strong increases in self-reported craving (effect sizes of about 1.2 to 1.3 for smokers, cocaine and heroin users) and smaller physiological changes such as heart rate. This supports the conditioning account.
• It explains relapse years after quitting, which neurochemistry alone does not.
• Cue exposure therapy, based on extinguishing these associations, has had mixed results, so conditioning may not be the whole story.

Worked example (AO2). “For Dev, the walk from the station to his office was paired with a cigarette every morning for years. The walk became a conditioned stimulus, so it now produces craving on its own. This cue reactivity explains why Dev relapses on workdays but not on holiday, which a purely dopamine-based account cannot explain.”

Explanations for gambling addiction

Learning theory: partial and variable reinforcement

Wins act as positive reinforcement, but they are unpredictable. Under partial reinforcement only some bets are rewarded. Under a variable ratio schedule the number of bets between wins changes. This schedule produces fast, steady responding that is very resistant to extinction, because the next bet could always be the winner. Near misses and the lights and sounds of machines act as secondary reinforcers.

Evaluation. Clark et al. (2009) used a simplified slot-machine task. Near misses felt less pleasant than full misses but increased players’ desire to keep gambling, though only when players had personal control over arranging the gamble. Near misses also activated brain areas (striatum and insula) that respond to monetary wins. This supports learning theory. A limitation is that most people who gamble on these schedules do not become addicted, so individual differences such as cognition must matter too.

Cognitive theory: cognitive bias

Gamblers hold distorted beliefs that keep them betting. Examples are the illusion of control (believing skill or rituals influence chance), the gambler’s fallacy (believing a win is “due” after losses) and reading near misses as signs of improvement.

Griffiths (1994) compared 30 regular and 30 non-regular fruit-machine gamblers in an arcade, using a “thinking aloud” method. Regular gamblers made more irrational verbalisations (about 14% of their verbalisations, compared with 2.5% for non-regular gamblers) and were more skill-oriented on self-report measures. On objective measures they were not significantly more skilful.

Evaluation. Griffiths’ field setting gives ecological validity, but coding verbalisations is subjective. Cognitive theory explains why gamblers continue despite losses. It does not explain why only some people develop the biases, and it struggles to say whether biases cause gambling or develop from it.

Worked example (AO3). “Cognitive theory is supported by Griffiths, whose regular gamblers made more irrational statements than non-regular gamblers despite showing no greater skill. This suggests distorted thinking, not real skill, keeps them playing. But the study shows a difference, not a cause; heavy play may create the biases. A combined account, in which variable reinforcement builds the habit and biases justify it, is more complete.”

Reducing addiction

Drug therapy

• Nicotine replacement therapy (patches, gum) supplies nicotine without smoke, reducing withdrawal so the person can tackle the habit.
• Varenicline is a partial agonist at nicotinic receptors. It gives a smaller dopamine effect and blocks the full reward of smoking.
• Naltrexone is an opioid antagonist that may reduce the reward of gambling. Kim et al. (2001) ran an 11-week double-blind trial with people diagnosed with pathological gambling: at the end, 75% of those taking naltrexone were rated much or very much improved, compared with 24% on placebo. Nausea was common in the first week.

Evaluation. Easy to use and supported by controlled trials. But it treats symptoms, not the learned or cognitive causes, and side effects lead some people to drop out.

Behavioural interventions

• Aversion therapy pairs the addictive behaviour with an unpleasant stimulus (for example a nausea-inducing drug or “rapid smoking”) so the behaviour becomes linked with discomfort.
• Covert sensitisation does the same in imagination. The person pictures the behaviour followed by a vivid unpleasant consequence.

Evaluation. A Cochrane review by Hajek and Stead (2004) concluded that the evidence was insufficient to judge whether rapid smoking works, because most trials had serious methodological problems, and that milder aversive methods seemed to lack specific effect. Aversion therapy also raises ethical issues because it causes deliberate discomfort. Covert sensitisation avoids physical harm, but it depends on the person’s ability to imagine vividly.

Cognitive behaviour therapy

CBT starts with a functional analysis (when and why the behaviour happens). The therapist then challenges distorted beliefs, such as “I’m due a win”, and teaches skills such as coping with cues and refusing offers. Petry et al. (2006) randomly allocated 231 gamblers to Gamblers Anonymous referral alone, referral plus a CBT workbook, or referral plus eight sessions of individual CBT. CBT reduced gambling more than GA referral alone during treatment, with some effects maintained at follow-up, and individual CBT improved some outcomes compared with the workbook.

Evaluation. CBT targets causes and teaches lasting skills. It needs motivation, time and a trained therapist, and some people find it hard to talk through cognitive distortions.

Worked example (AO3, appropriateness). “For a heavy smoker, NRT is appropriate first because it reduces withdrawal quickly. However, NRT leaves conditioned cues untouched, so combining it with CBT to manage cue reactivity is more appropriate for long-term change.”

Prochaska’s six-stage model of behaviour change

The six stages are precontemplation (no intention to change), contemplation (thinking about it, aware of pros and cons), preparation (planning soon), action (has changed within the last six months), maintenance (change sustained for more than six months, guarding against relapse) and termination (no temptation, certain they will not relapse). People can move back as well as forward, so relapse is part of the cycle. The model’s application is to match the intervention to the stage: for example, raising awareness in precontemplation and teaching coping skills in action.

Evaluation. The model treats relapse as normal and encourages services to support people who are not yet ready. However, a Cochrane review by Cahill, Lancaster and Green (2010) found that stage-based self-help and counselling interventions for smoking were neither more nor less effective than non-stage-based equivalents. Critics also argue that the stage boundaries are arbitrary and that people can move from no intention to quitting very quickly.

Common errors

• Defining tolerance as “getting used to it” without saying that more is needed for the same effect.
• Treating withdrawal as proof of psychological dependence. Withdrawal syndrome is the sign of physical dependence.
• Writing “variable reinforcement” without saying what varies (the number of bets between wins).
• Explaining cue reactivity with operant conditioning. Cue reactivity is classical conditioning.
• Describing aversion therapy and covert sensitisation as the same thing. Covert sensitisation happens in imagination.
• Listing five of Prochaska’s stages and forgetting termination, or forgetting to apply the model to an intervention.
• Evaluating therapies only on effectiveness. The specification also asks for appropriateness.

Links onward

Revise the learning theory you need from the approaches revision notes and the Approaches in Psychology guide. Use the Issues and debates study guide to sharpen evaluation points such as reductionism and nature-nurture. Then turn to the Addiction revision notes and test yourself with the Addiction practice questions.

Official syllabus

AQA AS and A-level Psychology (7181, 7182) specification, Version 1.4 (1 September 2025), for teaching from September 2025, section 4.3.10 Addiction and the Paper 3 scheme of assessment. Check aqa.org.uk/7182 for the current version.