AQA A-Level Psychology: Schizophrenia, Aggression, Forensic Psychology and Addiction

AQA A-Level Psychology Paper 3 (7182/3) is where you sit the option topics, and four of the most popular choices are Schizophrenia, Aggression, Forensic Psychology, and Addiction. Each appears as one section of Paper 3 worth 24 marks, alongside the compulsory Issues and Debates section and two other options. To perform well you need precise knowledge of explanations, therapies, and studies -- but you also need to evaluate critically, because the 16-mark essay in each section demands well-supported analysis, not just description.

For broader guidance on exam structure and question types across all three papers, see the AQA A-Level Psychology Exam Guide.

Paper 3 at a Glance

Paper 3: Issues and Options in Psychology is a 2-hour exam worth 96 marks (33.3% of the A-Level):

Section A: Issues and Debates in Psychology -- 24 marks, compulsory.
Sections B, C, and D -- each worth 24 marks. You answer one option topic per section, choosing from: Relationships, Gender, Cognition and Development, Schizophrenia, Eating Behaviour, Stress, Aggression, Forensic Psychology, and Addiction.

Each option section typically includes short-answer questions and one 16-mark essay.

Schizophrenia

Schizophrenia is one of the most content-rich option topics on the specification. You need to understand classification, biological and psychological explanations, therapies, and the interactionist approach.

Classification and Diagnosis

Schizophrenia is characterised by a disruption of cognition and emotion, affecting language, thought, perception, and sense of self. Symptoms are divided into two categories:

Positive symptoms -- experiences added to normal functioning, including hallucinations (most commonly auditory, such as hearing voices) and delusions (irrational beliefs that are often paranoid or grandiose in nature).
Negative symptoms -- a reduction of normal functioning, including avolition (a severe loss of motivation to carry out everyday tasks), speech poverty (a reduction in the amount and quality of speech), and affective flattening (reduced range and intensity of emotional expression).

Diagnosis raises significant issues of reliability and validity. Symptom overlap with conditions like bipolar disorder makes differential diagnosis difficult. Cultural differences mean that what counts as delusional varies across societies, raising questions about cultural bias in diagnostic criteria. High co-morbidity with depression and substance abuse further complicates the picture and suggests schizophrenia may not be a single, clearly defined disorder.

Biological Explanations

Genetics: Family studies show risk increases with genetic closeness. Gottesman found ~48% concordance in MZ twins versus ~17% in DZ twins. Adoption studies (e.g., Tienari et al.) confirm elevated risk in adopted children of affected biological parents. Candidate gene research points to dopamine-related genes, though schizophrenia is polygenic.

The dopamine hypothesis: The original version proposed excessive dopamine activity causes schizophrenia, supported by the effectiveness of dopamine-blocking drugs and the psychotic effects of amphetamines. The updated version is more nuanced: hyperdopaminergia in subcortical areas drives positive symptoms, while hypodopaminergia in prefrontal areas contributes to negative symptoms and cognitive deficits.

Neural correlates: Brain imaging reveals enlarged ventricles, reduced grey matter, and lower prefrontal cortex activity during cognitive tasks -- though whether these are causes or consequences remains unclear.

Psychological Explanations

Family dysfunction: Bateson's double bind theory proposes that contradictory parental messages produce disordered thinking. Expressed emotion -- hostility, criticism, and emotional over-involvement from family members -- is strongly linked to relapse rates rather than initial onset.

Cognitive explanations: Dysfunctional thought processing, particularly impaired metarepresentation (the ability to reflect on one's own thoughts), may explain hallucinations and delusions. Frith's model proposes that patients cannot distinguish inner speech from external voices.

Biological Therapies

Typical antipsychotics: Chlorpromazine was the first widely used antipsychotic. It works as a dopamine antagonist, binding to dopamine D2 receptors and blocking their action. This is effective at reducing positive symptoms such as hallucinations and delusions. However, typical antipsychotics are associated with significant side effects including drowsiness, weight gain, and -- with long-term use -- tardive dyskinesia (involuntary facial movements).

Atypical antipsychotics: Clozapine was developed as an improvement over typical antipsychotics. It also acts on dopamine receptors but additionally affects serotonin activity, which may account for its effectiveness in treating negative symptoms as well as positive ones. Clozapine is particularly important for treatment-resistant schizophrenia, but carries a risk of agranulocytosis (a dangerous drop in white blood cell count), requiring regular blood monitoring.

Psychological Therapies

CBT for psychosis (CBTp) helps patients identify and challenge distorted beliefs. For example, a patient experiencing paranoid delusions may be guided to test the evidence for and against their belief. CBTp does not aim to eliminate symptoms entirely but to reduce distress and improve functioning. Family therapy aims to reduce expressed emotion through psychoeducation, communication training, and problem-solving skills. Studies show that family therapy significantly reduces relapse rates. Token economies use operant conditioning in institutional settings, where patients earn tokens for desirable behaviours and exchange them for rewards. While effective for managing behaviour, token economies address symptoms rather than causes and raise ethical concerns about conditioning vulnerable individuals.

The Interactionist Approach

The diathesis-stress model proposes that schizophrenia results from biological vulnerability interacting with environmental stressors. Modern versions recognise that diathesis can include early trauma and that stress can be biological (e.g., cannabis use). This supports combining medication with psychological therapies.

Aggression

Neural and Hormonal Mechanisms

Serotonin normally inhibits aggression via the prefrontal cortex; low levels are linked to impulsive aggression, supported by studies using serotonin-depleting drugs. Testosterone correlates with dominance and aggression -- Dabbs et al. found higher testosterone in violent prisoners -- though the relationship may be bidirectional.

Genetic Factors

Twin studies show higher concordance for aggression in MZ than DZ twins. The MAOA gene ("warrior gene") is a key focus: Brunner et al. linked a MAOA mutation to aggression in a Dutch family, while Caspi et al. demonstrated a gene-environment interaction where the low-activity MAOA variant predicted antisocial behaviour only when combined with childhood maltreatment.

The Ethological Explanation

Lorenz proposed aggression is innate and adaptive. Innate releasing mechanisms trigger aggression via fixed neural pathways. Fixed action patterns are stereotyped aggressive sequences (demonstrated in stickleback fish). Ritualised aggression limits harm within species, but Lorenz argued human weapons have outpaced our evolved inhibitory mechanisms.

Evolutionary Explanations

Jealousy and infidelity: Sexual jealousy is an evolved response -- Buss found men are more distressed by sexual infidelity, women by emotional infidelity. Male-male aggression reflects reproductive competition, explaining why young males show the highest rates of physical aggression.

Social Psychological Explanations

Frustration-aggression hypothesis (Dollard): Frustration always produces aggression; Berkowitz later revised this, arguing frustration is one of many aversive stimuli creating readiness for aggression. Social learning theory (Bandura): The Bobo doll studies showed children imitate observed aggression, especially when the model is rewarded (vicarious reinforcement). Deindividuation (Zimbardo): Loss of personal identity in crowds reduces social constraints, increasing aggression.

Institutional Aggression

The importation model (Irwin and Cressey) explains prison aggression through characteristics inmates bring with them. The deprivation model (Sykes) attributes it to frustrations of prison life -- loss of liberty, autonomy, and security. The Lucifer effect (Zimbardo) argues situational factors, deindividuation, and dehumanisation can make ordinary people aggressive, as demonstrated in the Stanford Prison Experiment.

Media Influences on Aggression

Desensitisation reduces emotional responses to real violence through repeated media exposure. Disinhibition weakens social norms when violence is shown without consequences. Cognitive priming activates aggressive thoughts and behavioural scripts, making aggressive responses more accessible.

Forensic Psychology

Offender Profiling

Top-down approach (FBI typology): Developed from interviews with convicted serial offenders in the United States. The profiler begins with a pre-existing classification and applies it to the crime scene. The key distinction is between organised offenders (planned crimes, high intelligence, socially competent, controlled crime scene) and disorganised offenders (impulsive, lower intelligence, socially inadequate, chaotic crime scene). The approach has been criticised for being based on a small, unrepresentative sample and for assuming offenders fit neatly into one category.

Bottom-up approaches: These are data-driven and use statistical analysis. Investigative psychology (Canter) applies psychological theory to analyse crime patterns, including interpersonal coherence -- the idea that offenders behave consistently across different situations. Geographical profiling (Rossmo) analyses the spatial pattern of linked crimes to identify the likely area where the offender lives, based on the principle that most offenders commit crimes close to their base.

Biological Explanations of Offending

Lombroso's atavistic form proposed criminals are evolutionary "throwbacks" identifiable by physical features -- now discredited but historically significant. Genetic explanations are supported by twin and adoption studies (e.g., Mednick et al.); the XYY karyotype was initially linked to aggression but later research found XYY men are not more violent. Neural explanations focus on prefrontal cortex dysfunction -- Raine et al. found reduced glucose metabolism in the prefrontal cortex of murderers using PET scans.

Psychological Explanations of Offending

Eysenck's criminal personality theory links offending to high extraversion, neuroticism, and psychoticism, arguing these traits make individuals harder to condition into prosocial behaviour. Cognitive distortions include hostile attribution bias (interpreting ambiguous actions as hostile) and minimalisation (downplaying offence severity). Differential association theory (Sutherland) proposes criminal behaviour is learned when exposure to pro-criminal definitions outweighs pro-social ones. Psychodynamic explanations link offending to an inadequate or over-harsh superego and disrupted early attachment (Bowlby's maternal deprivation hypothesis).

Dealing with Offending

Custodial sentencing aims to deter, incapacitate, punish, and rehabilitate -- but recidivism rates are high and imprisonment may worsen offending through criminal exposure and institutionalisation. Behaviour modification (token economies) rewards desirable behaviour with tokens but shows limited transfer outside institutions. Anger management teaches cognitive preparation, skill acquisition, and application practice -- moderately effective when offenders are motivated. Restorative justice brings offenders and victims together to build empathy and accountability, with meta-analyses supporting its effectiveness for reducing reoffending.

Addiction

Describing Addiction

Physical dependence: The body adapts to the presence of a substance, and cessation produces physical withdrawal symptoms such as tremors, nausea, and sweating.
Psychological dependence: A perceived need for the substance or behaviour to function normally or cope with stress, even in the absence of physical symptoms.
Tolerance: Over time, increasing amounts of the substance are needed to achieve the same effect as the body adapts to its presence.
Withdrawal: The unpleasant physical and psychological symptoms that occur when the addictive substance or behaviour is stopped.

Risk Factors

Genetic vulnerability: Family and twin studies indicate a heritable component to addiction. Research on alcoholism, for example, has identified genes involved in dopamine receptor sensitivity.
Stress: Chronic stress is associated with increased vulnerability, partly through its effects on cortisol and dopamine systems.
Personality: Traits such as high sensation-seeking, impulsivity, and neuroticism are associated with greater addiction risk.
Family influences: Parental modelling of substance use, poor attachment, and family conflict all increase risk.
Peers: Peer influence is one of the strongest predictors of substance use initiation in adolescence, operating through social norms and direct pressure.

Explanations of Nicotine Addiction

Brain neurochemistry: Nicotine binds to nicotinic acetylcholine receptors, stimulating dopamine release in the mesolimbic reward pathway. Tolerance develops as dopamine receptors downregulate. Learning theory: Smoking is maintained through positive reinforcement (dopamine) and negative reinforcement (relieving withdrawal). Cue reactivity -- conditioned responses to smoking-related stimuli -- triggers cravings via classical conditioning.

Explanations of Gambling Addiction

Learning theory: Variable reinforcement schedules produce highly resistant behaviour patterns. Environmental cues become conditioned stimuli triggering the urge to gamble. Cognitive bias: The gambler's fallacy (believing past losses make wins more likely) and illusion of control (believing skill can influence random outcomes) maintain gambling by distorting perceived odds.

Reducing Addiction

Drug therapy: Nicotine replacement therapy (NRT) eases withdrawal by providing nicotine without smoking. Opioid antagonists such as naloxone and naltrexone may reduce gambling's rewarding effects. Behavioural interventions: Aversion therapy pairs the addictive behaviour with an unpleasant stimulus; covert sensitisation uses imagined negative consequences. Both show short-term effects but high relapse rates. CBT challenges distorted thoughts maintaining addiction and teaches relapse prevention skills.

The Theory of Planned Behaviour (Ajzen)

This model proposes that the immediate determinant of behaviour is the individual's intention, which is shaped by three factors:

Attitudes: The individual's overall evaluation of the behaviour (e.g., "Smoking is harmful and I want to stop").
Subjective norms: The individual's perception of social pressure regarding the behaviour (e.g., "My friends and family want me to quit").
Perceived behavioural control: The individual's belief in their ability to perform the behaviour, similar to self-efficacy (e.g., "I believe I can quit if I use NRT").

The model recognises the role of cognition and social factors in addiction. A key limitation is the intention-behaviour gap -- intentions do not always translate into action.

Prochaska's Six-Stage Model of Behaviour Change

This model describes addiction recovery as a process involving six stages:

Pre-contemplation: The individual is not considering change and may not recognise they have a problem.
Contemplation: The individual is aware of the problem and is considering change but has not committed to action.
Preparation: The individual makes plans and may take small steps such as setting a quit date.
Action: The individual actively modifies their behaviour.
Maintenance: The individual works to sustain the change and prevent relapse.
Termination: The addictive behaviour is no longer a temptation.

The model usefully recognises that relapse is a normal part of the process rather than a failure, and that individuals may cycle through the stages multiple times. It has been criticised for assuming behaviour change is always a conscious, rational process and for lacking clear criteria for distinguishing between stages.

Prepare with LearningBro

These four option topics demand both breadth and depth -- you need to know the key theories, studies, and evaluations, and write structured essays under timed conditions. The best preparation is active retrieval practice rather than passive re-reading.

LearningBro offers structured courses with exam-style questions to help you revise effectively:

Use these resources alongside your own revision to build the knowledge and exam technique you need for Paper 3.