Interactionist explanations and treatments | AQA A-Level Psychology Revision

Revision Notes
Aug 6
34 min read

Updated: Aug 14

For 7182 specification, first teach in September 2025

AQA A-Level Psychology | Free Revision Notes

Estimated study time: 60 minutes

Interactionist explanations argue that schizophrenia cannot be understood through biology or experience alone. These Interactionist explanations and treatments A-Level Psychology revision notes examine the diathesis-stress model, in which an underlying vulnerability combines with environmental stress to increase the likelihood of symptoms.

The same interactionist logic can guide treatment. Antipsychotic medication may address biological processes, while CBT or family therapy addresses psychological and environmental factors. AQA explicitly requires the importance of an interactionist approach in both explaining and treating schizophrenia, together with the diathesis-stress model.

Learning Objectives 🎯

By the end of this revision page, you should be able to:

Explain the diathesis-stress model of schizophrenia.
Distinguish a diathesis from an environmental stressor.
Explain the original and modern versions of the model.
Apply the model to unfamiliar scenarios.
Explain why an interactionist explanation is important.
Explain how biological and psychological treatments may be combined.
Evaluate interactionist explanations and combined treatments.

Revision Notes 📚

Interactionist explanations and treatments overview

An interactionist approach proposes that schizophrenia develops through the interaction of several influences.

These may include:

Genetic vulnerability.
Neural or neurochemical functioning.
Early developmental experiences.
Psychological trauma.
Dysfunctional cognitive processing.
Family stress.
Major life events.
Workplace stress.
Cannabis use.

The key principle is:

No single influence necessarily produces schizophrenia by itself.

Instead:

underlying vulnerability + sufficient environmental stress → increased probability of schizophrenia

The approach therefore combines:

nature, such as inherited genetic risk
nurture, such as stressful life experiences

It also connects different levels of explanation:

Biological.
Cognitive.
Psychological.
Social.
Environmental.

What does interactionist mean?

Interactionist means that the effect of one factor depends partly on another factor.

This is different from simply listing several possible causes.

Additive account

An additive account might say:

Genes increase risk, and stress separately increases risk.

Interactionist account

An interactionist account says:

The effect of stress depends partly on the person’s vulnerability, and the effect of vulnerability depends partly on the stress experienced.

For example:

A major life event may not lead to schizophrenia in a person with little underlying vulnerability.
A person with substantial vulnerability may never develop schizophrenia if sufficient stress is not experienced.
The same stressful event may have different effects on different people.
The same vulnerability may produce different outcomes in different environments.

The relationship between the factors is therefore central.

The diathesis-stress model

What is a diathesis?

A diathesis is an underlying vulnerability or predisposition.

It makes a person more susceptible to developing schizophrenia.

A diathesis does not mean:

The person currently has schizophrenia.
Symptoms are inevitable.
One gene directly causes hallucinations.
The person will become unwell at a particular age.

It means that the person may be more vulnerable than someone without the same predisposition.

What is stress?

A stressor is an environmental experience or demand that places psychological or biological pressure on the person.

Possible stressors accepted within AQA’s 2025 mark scheme include:

A major life event.
Family stress.
Workplace stress.
Cannabis use.

Other stressful experiences may contribute where they are relevant to the person and model.

The interaction

The model proposes:

A diathesis creates vulnerability, while stress contributes to triggering the development or return of symptoms.

AQA assessed the basic relationship directly in 2022. The correct statement was that stressful conditions trigger schizophrenia in people with an underlying predisposition.

A simple pathway

vulnerability exists → stress is experienced → coping systems are overwhelmed → symptoms emerge

This sequence is simplified.

The exact pathway may involve interactions among:

Genes.
Dopamine.
Brain development.
Cognition.
Stress responses.
Social relationships.

Predisposition is not inevitability

The model is probabilistic.

It predicts increased probability rather than certainty.

Consider two people with a family history of schizophrenia.

One experiences major and continuing stress.
One experiences a relatively stable environment.

The model predicts that the first person may be more likely to develop symptoms.

It does not predict with certainty that:

The first person will develop schizophrenia.
The second person will remain symptom-free.

Other vulnerabilities and experiences may also matter.

The threshold idea

The model is often understood through the idea of a threshold.

A person may accumulate vulnerability and stress.

Symptoms are more likely when the combined influence reaches a sufficient level.

A simplified pattern is:

Underlying vulnerability	Environmental stress	Predicted risk
Low	Low	Relatively low
High	Low	Increased vulnerability, but symptoms may not develop
Low	High	Stress is present, but vulnerability may be insufficient
High	High	Greatest likelihood of symptoms

This table illustrates probability rather than an exact mathematical rule.

Different routes to the threshold

Person A may have:

High genetic vulnerability.
Moderate environmental stress.

Person B may have:

Lower genetic vulnerability.
Severe and prolonged environmental stress.

Both may reach a level at which symptoms become more likely.

The model can therefore explain why people with different histories may receive the same diagnosis.

The original diathesis-stress model

Meehl’s early account

The early version of the model is associated with Meehl.

It treated the diathesis primarily as a genetic vulnerability and proposed that one gene could create predisposition.

Environmental stress was then required for schizophrenia to develop.

The basic early model was:

single genetic vulnerability + environmental stress → schizophrenia

AQA’s 2025 mark scheme contrasts Meehl’s single-gene account with the later polygenic model.

Strength of the original account

The original account improved on a purely genetic explanation.

It recognised that:

Inherited risk is not sufficient by itself.
Environmental experience affects whether vulnerability is expressed.
People with similar biological vulnerability can have different outcomes.

Limitation of the original account

Schizophrenia is not now understood as resulting from one simple gene.

The original version was too narrow because:

Genetic vulnerability is polygenic.
Different people may inherit different combinations of risk variants.
Non-genetic experiences can also create lasting vulnerability.
Stress is more complex than one single event.

The modern diathesis-stress model

The modern model broadens both parts.

Modern diathesis

A diathesis may involve:

Polygenic vulnerability.
Prenatal experience.
Early psychological trauma.
Dysfunctional cognitive processing.
Other lasting developmental vulnerabilities.

Modern stress

Stress may involve:

Major life events.
Family conflict.
High expressed emotion.
Workplace stress.
Cannabis use.
Continuing environmental pressure.

The current account is therefore better represented as:

one or more vulnerabilities + one or more stressors → increased probability of schizophrenia

Polygenic vulnerability

What does polygenic mean?

Polygenic means that many genes contribute to vulnerability.

A person may inherit:

Several risk alleles.
A particular combination of variants.
Greater or lower genetic loading.

Different combinations may affect:

Brain development.
Dopamine functioning.
Sensitivity to stress.
Cognitive processing.

The details of inherited vulnerability are covered in polygenic risk and family evidence [Genetic explanations].

Ripke and polygenic risk

AQA’s 2025 mark scheme identifies Ripke’s work as an example supporting the modern polygenic understanding of diathesis.

The central exam point is:

Modern genetic vulnerability involves many genes rather than one schizophrenia gene.

Neural vulnerability

Genetic differences may contribute to altered neural development or neurotransmitter functioning.

Possible biological vulnerabilities may involve:

Dopamine activity.
Brain structure.
Neural communication.
Sensitivity of stress-related biological systems.

A person may therefore possess a neural vulnerability before symptoms become severe.

This links the interactionist model with neural correlates and the dopamine hypothesis [Neural correlates and the dopamine hypothesis].

Possible pathway

polygenic vulnerability → altered neural functioning → increased sensitivity to environmental stress → symptoms

This does not mean that every neural correlate is necessarily present before schizophrenia develops.

The direction of causality remains difficult to establish.

Early experiences as a diathesis

A major development in the modern model is that a diathesis does not have to be purely genetic.

AQA’s 2025 mark scheme recognises:

Prenatal experiences, such as maternal exposure to influenza during pregnancy.
Postnatal experiences, such as psychological trauma or childhood abuse.

as possible sources of lasting vulnerability.

Prenatal vulnerability

A prenatal event may affect:

Brain development.
Neural organisation.
Later biological sensitivity.

The event occurs before birth but may create a vulnerability that remains throughout development.

Postnatal trauma

Severe early trauma may produce lasting changes in:

Stress sensitivity.
Trust.
Emotional regulation.
Cognitive processing.
Interpretation of threat.

The trauma may therefore function as a diathesis because it creates enduring vulnerability rather than operating only as a short-term trigger.

Trauma as diathesis or stress

The classification depends on the proposed role.

Trauma as a diathesis

An early traumatic experience produces long-term vulnerability.

early abuse → lasting psychological vulnerability → later stress triggers symptoms

Trauma as a stressor

A traumatic event occurs later and triggers symptoms in someone already vulnerable.

genetic vulnerability → traumatic life event → symptoms emerge

The same broad type of experience can therefore play different roles according to:

Timing.
Duration.
Psychological effect.
Position in the causal pathway.

Cognitive processing as a diathesis or trigger

AQA’s 2025 mark scheme identifies an important discussion question:

Are dysfunctional thought processes best regarded as a diathesis or as a trigger?

Cognitive processing as a diathesis

A person may have a relatively enduring difficulty involving:

Source monitoring.
Metacognition.
Executive functioning.
Interpreting ambiguous information.

This creates vulnerability before severe symptoms develop.

Cognitive processing as a trigger or maintaining factor

Alternatively:

Stress produces an unusual experience.
The person interprets it as threatening.
The interpretation increases fear.
The belief becomes stronger.
Symptoms are maintained.

The cognitive process may therefore help convert stress into a particular symptom rather than being the original vulnerability.

The relevant processing difficulties are explored in dysfunctional thought processing [Cognitive explanations].

Environmental stressors

Major life events

Major changes may place substantial pressure on the person.

Examples include:

Bereavement.
Moving home.
Beginning university.
Relationship breakdown.
Unemployment.
Serious illness within the family.

A major event is not automatically harmful.

Its effect depends on:

The person’s vulnerability.
The meaning of the event.
Other stressors.
Available support.
Coping resources.

Family stress

Family stress may include:

Persistent criticism.
Hostility.
Emotional over-involvement.
Repeated conflict.
Contradictory communication.

These factors may:

Trigger the emergence of symptoms.
Worsen existing symptoms.
Increase the likelihood of relapse.

The psychological mechanisms are examined in family communication and expressed emotion [Family dysfunction].

Workplace stress

Pressure at work may involve:

High demands.
Conflict.
Low control.
Insecurity.
Long working hours.
Fear of losing employment.

The model does not claim that workplace stress alone normally causes schizophrenia.

It may trigger symptoms where sufficient underlying vulnerability exists.

Cannabis use

AQA identifies cannabis use as one possible environmental stressor within the modern model.

Within the diathesis-stress approach:

Cannabis does not affect every user in the same way.
Its effect may depend on underlying vulnerability.
It may interact with other stressors.
It should be understood as one possible trigger rather than a universal cause.

Family history and stressful events

The specimen assessment provides a clear application.

Louise has:

A grandfather and aunt diagnosed with schizophrenia.
Recently lost her father.
Moved away to begin university.
Begun experiencing hallucinations and delusions.

The mark scheme identifies:

Her family history as evidence of genetic vulnerability.
Bereavement and moving to university as stressful life events.
The interaction as the explanation for the emergence of symptoms.

Complete application

Louise may have inherited a genetic predisposition because schizophrenia occurs among her biological relatives. Losing her father and moving away to begin university are major stressful events. According to the diathesis-stress model, these environmental pressures may have triggered her underlying vulnerability, resulting in hallucinations and delusions.

Weak application

Louise became schizophrenic because she was stressed.

This is incomplete because it ignores:

The diathesis.
The interaction.
The evidence from the family history.

Worked scenario: high vulnerability and moderate stress

Lucas has several biological relatives with schizophrenia. His symptoms begin after continuing conflict at home.

The model would suggest:

Family history indicates possible genetic loading.
This creates an underlying diathesis.
Continuing family conflict acts as environmental stress.
The interaction raises the likelihood that symptoms will emerge.

Do not state that either factor proves causation.

Worked scenario: severe stress without known family history

Meera has no known family history of schizophrenia but experienced severe childhood trauma and later develops symptoms after losing her job.

A modern interactionist explanation could suggest:

Childhood trauma created a lasting psychological vulnerability.
Job loss acted as a later environmental stressor.
The interaction contributed to symptom development.
The absence of known family history does not rule out genetic vulnerability, but genetic risk does not need to be the only possible diathesis.

Worked scenario: vulnerability without symptoms

Aaron’s identical twin has schizophrenia, but Aaron has never experienced hallucinations or delusions.

The model would suggest:

Aaron may possess substantial genetic vulnerability.
Vulnerability is not sufficient by itself.
He may not have experienced the required combination of stressors.
Other developmental differences may also have affected the outcome.

This supports a probabilistic rather than deterministic interpretation.

Worked scenario: relapse

After successful treatment, Imani returns to a highly critical household and her symptoms begin to worsen.

The model can be applied to relapse:

Biological vulnerability remains.
Treatment previously reduced symptom severity.
High expressed emotion increases environmental stress.
Stress interacts with continuing vulnerability.
Symptoms return or worsen.

The diathesis-stress model is therefore relevant to both:

Initial development.
Later relapse.

Why an interactionist approach is important

It avoids single-cause explanations

A purely genetic explanation cannot fully explain why:

Identical twins can have different outcomes.
Some people with family histories never develop symptoms.
Symptoms sometimes follow major stressful events.

A purely environmental explanation cannot fully explain why:

People react differently to similar stress.
Schizophrenia clusters within some biological families.
Neural and genetic evidence exists.

The interactionist approach recognises both patterns.

It integrates nature and nurture

The model does not treat nature and nurture as competing explanations.

Instead:

inherited characteristics affect responses to environments, while environments affect whether vulnerability is expressed

This connects directly with the relative roles of heredity and experience [The nature-nurture debate].

It works across levels of explanation

The approach may combine:

Genes.
Neurotransmitters.
Cognition.
Family relationships.
Social stress.

This is more complete than reducing schizophrenia to one receptor or one family interaction.

It connects with levels of explanation and the value of holism [Holism and reductionism].

It explains individual differences

People differ in:

Genetic loading.
Neural functioning.
Early experiences.
Cognitive processing.
Stress exposure.
Symptom profile.

The model can explain why:

Similar stress produces different outcomes.
Similar vulnerability produces different outcomes.
The amount of stress needed to trigger symptoms may vary.
Treatments work differently for different patients.

It produces cautious predictions

The model does not state:

“This person will develop schizophrenia.”

It states:

“This combination of vulnerability and stress may increase the probability.”

This is scientifically and ethically more appropriate than treating family history as destiny.

Explaining different symptom patterns

Interactionism may help explain why people experience different combinations of symptoms.

For example:

Genetic and dopamine vulnerability may increase the likelihood of unusual perceptual experiences.
Source-monitoring difficulties may affect whether inner speech becomes a hallucination.
Family hostility may increase the threat attached to experiences.
Repeated stress may worsen avolition or cognitive disorganisation.

The exact symptom may depend on the combination of:

Biological vulnerability.
Cognitive interpretation.
Environmental context.

Biological vulnerability and psychological meaning

Consider a person who experiences internally generated speech as unusually vivid.

A biological explanation might propose:

altered neural or dopamine functioning increases the intensity of the experience

A cognitive explanation might propose:

the person fails to recognise it as self-generated

An environmental explanation might propose:

continuing stress increases the frequency or threat of the experience

Together:

neural vulnerability + source-monitoring difficulty + stress → distressing auditory hallucination

The accounts describe different parts of the same pathway.

Evaluating the diathesis-stress model

Strength: genetic evidence supports vulnerability

Family, twin and adoption research indicates that schizophrenia risk is related to biological family history.

Higher concordance among more genetically similar relatives supports the existence of an inherited diathesis.

This evidence is consistent with the interactionist model because:

Genes increase vulnerability.
Concordance is not perfect.
Environmental factors are therefore also required.

AQA identifies family, twin and adoption evidence as relevant evaluation of the diathesis component.

Why incomplete concordance supports interactionism

Identical twins share nearly all their genetic material.

If genes alone caused schizophrenia, identical twin concordance should be complete.

It is not.

Discordance suggests that:

Stress exposure differs.
Prenatal environments can differ.
Early experiences differ.
Cognitive and social factors matter.

The finding therefore challenges a purely genetic account while supporting biological vulnerability within an interactionist model.

Strength: evidence supports the role of life events

AQA identifies Hultman’s research concerning episodes precipitated by life events as evidence relevant to stress.

This supports the model because symptom onset or recurrence appears connected with environmental pressure.

However, a life event occurring before an episode does not prove that it caused the episode.

The person might also have experienced:

Early signs before the recorded event.
Changes in behaviour that created the stressful event.
Other unmeasured stressors.

Strength: physiological evidence of stress

AQA also identifies Walker’s finding of high levels of cortisol among people with schizophrenia.

Cortisol is associated with the body’s stress response.

High levels are consistent with the claim that stress is involved.

Limitation of cortisol evidence

The direction is uncertain.

Possible explanations include:

Stress contributes to schizophrenia symptoms.
Experiencing severe symptoms raises cortisol.
Hospitalisation or medication affects cortisol.
Another factor affects both cortisol and symptoms.

The evidence demonstrates association rather than simple causation.

Limitation: causality cannot be demonstrated experimentally

Researchers cannot ethically assign people to:

Childhood abuse.
Severe bereavement.
Family hostility.
Cannabis use.
Deliberately intense workplace stress.

They also cannot manipulate:

Genetic inheritance.
Prenatal exposure.
Family history.

Evidence therefore usually comes from:

Natural experiments.
Quasi-experiments.
Correlational studies.
Longitudinal studies.
Retrospective reports.

AQA’s 2025 mark scheme identifies the difficulty of demonstrating cause and effect as a central criticism.

Limitation: reverse causality

The model often assumes:

stress → symptoms

The reverse may also occur:

early symptoms → stressful events

For example:

Suspiciousness may damage relationships.
Avolition may lead to job loss.
Confused behaviour may increase family conflict.
Social withdrawal may reduce support.

The stressful experience may partly result from the developing condition.

The relationship may be bidirectional:

stress worsens symptoms → symptoms create more stress → further symptoms emerge

Strength: the modern model is more flexible

The modern account is stronger than the original because it recognises that:

Vulnerability can be polygenic.
Different people have different genetic pathways.
Early experiences can create lasting diathesis.
Stress can take several forms.
Cognitive processing can influence symptom development.
Biological and psychological factors can interact.

This broader model reflects the complexity of schizophrenia more effectively.

Limitation: flexibility can reduce precision

A model becomes difficult to test if almost any factor can be labelled:

A diathesis.
A stressor.
A trigger.
A maintaining factor.

For example, trauma might be classified as:

An early vulnerability.
A later stressor.
Both.

This flexibility helps the model accommodate different cases, but it can make predictions less precise.

A good scientific explanation should clarify:

Which factor plays which role.
When the factor occurs.
How it affects the person.
What outcome is predicted.

Limitation: the threshold is difficult to measure

The model often refers to stress exceeding a threshold.

In practice, psychologists cannot easily calculate:

A person’s exact genetic vulnerability.
The precise amount of stress experienced.
The point at which symptoms will develop.

Different stressors also cannot be compared through one simple unit.

For example:

Bereavement.
Workplace pressure.
Family hostility.
Cannabis use.

may affect people in different ways.

The threshold is therefore a useful concept rather than a directly observable boundary.

Strength: it explains why neither component is sufficient

The model accounts for two important findings:

Many people exposed to severe stress do not develop schizophrenia.
Many people with biological relatives affected by schizophrenia do not develop the condition.

A single-factor theory struggles with one or both findings.

Interactionism explains them by proposing that risk emerges from the combination.

Limitation: diagnosis may weaken evidence

Research into vulnerability and stress depends on accurately identifying schizophrenia.

However, diagnosis may be affected by:

Co-morbidity.
Symptom overlap.
Culture bias.
Gender bias.

These issues are examined in co-morbidity, overlap and diagnostic bias [Issues in diagnosis].

If samples contain people with different conditions or symptom patterns:

Genetic findings may be inconsistent.
Stress relationships may vary.
Treatment effects may appear weaker.
The model may be difficult to evaluate.

Nature-nurture evaluation

The model is an interactionist resolution of the nature-nurture debate.

Strength

It avoids the false choice between:

Biological inheritance.
Environmental experience.

Both influence the outcome.

Limitation

Simply stating that “both matter” is not enough.

A useful explanation must identify:

The specific biological vulnerability.
The relevant stressor.
The mechanism through which they interact.
The predicted symptom or outcome.

Otherwise, interactionism can become a vague compromise rather than a precise theory.

Determinism

Biological determinism

A purely genetic account may imply that inherited biology determines schizophrenia.

Environmental determinism

A purely family or trauma account may imply that experiences determine schizophrenia.

Soft determinism

The diathesis-stress model is closer to soft determinism.

It proposes that:

Biology and experience strongly influence outcomes.
Neither necessarily guarantees the condition.
Different combinations produce different probabilities.
Treatment and environmental change may alter the course.

This avoids the fatalism associated with a hard deterministic explanation.

Reductionism and holism

Reductionist explanations

A biological account may reduce schizophrenia to:

Genes.
Dopamine.
Brain regions.

A psychological account may reduce it to:

Cognitive failures.
Family communication.

Interactionist explanation

The diathesis-stress model is more holistic because it combines several levels.

It considers the person within:

A biological system.
A cognitive system.
A family.
A wider environment.

Remaining limitation

Even an interactionist model may omit:

The person’s subjective experience.
Cultural meaning.
Wider social inequality.
Individual protective factors.
Differences in treatment access.

It is broader, but not necessarily complete.

Social sensitivity

The model can reduce blame because it avoids claiming that:

The person chose their symptoms.
The family alone caused schizophrenia.
Genes make the condition inevitable.

However, careless use may still create stigma.

For example:

Relatives may be viewed as genetically defective.
People with childhood trauma may be treated as permanently vulnerable.
People using cannabis may be blamed entirely for becoming unwell.
Families may still be held responsible for stress.

Responsible conclusions use probabilistic language and recognise several interacting influences.

Interactionist treatment

The interactionist approach also has implications for treatment.

The central principle is:

If schizophrenia involves biological and psychological or environmental factors, treatment may need to address more than one level.

A combined treatment programme might involve:

Antipsychotic medication.
Cognitive behaviour therapy.
Family therapy.
Appropriate social support.

Biological treatment

Antipsychotic medication

Typical and atypical antipsychotics affect neurotransmitter activity.

They may:

Reduce hallucinations.
Reduce delusions.
Lower severe psychotic agitation.
Reduce relapse risk while treatment continues.
Make psychological engagement easier.

Relevant lessons include:

dopamine receptor blockade [Typical antipsychotics]
dopamine and serotonin receptor action [Atypical antipsychotics]

Biological target

Medication mainly targets:

Neurotransmitter activity.
The biological expression of vulnerability.
Severe positive symptoms.

It does not directly teach the person how to:

Question a persecutory belief.
Manage a voice.
Improve family communication.
Respond to stress.

Psychological treatment

Cognitive behaviour therapy

CBT may help the person:

Identify beliefs.
Examine evidence.
Develop alternative interpretations.
Reduce fear associated with voices.
Develop coping strategies.
Reduce avoidance.

This is examined in challenging beliefs and interpretations [Cognitive behaviour therapy].

Family therapy

Family therapy may:

Reduce criticism.
Reduce hostility.
Reduce emotional over-involvement.
Improve communication.
Develop realistic expectations.
Reduce relapse-related stress.

This is examined in reducing expressed emotion and improving communication [Family therapy].

Combining medication and CBT

A combined programme may operate as follows:

Antipsychotic medication reduces severe positive symptoms.
The person becomes better able to concentrate and communicate.
CBT examines beliefs that remain.
The person develops alternative interpretations and coping strategies.
Reduced distress improves functioning.

Example

Omar hears a threatening voice and believes it must always be obeyed.

Medication may:

Reduce the intensity or frequency of the voice.

CBT may:

Examine whether the voice is all-powerful.
Review occasions when it was wrong.
Develop positive self-talk.
Reduce obedience and avoidance.

The treatments address different aspects of the same problem.

Combining medication and family therapy

A combined programme may operate as follows:

Medication reduces current symptoms.
The person returns to the family home.
Psychoeducation helps relatives understand symptoms and side effects.
Communication training reduces criticism and hostility.
Reduced expressed emotion lowers environmental stress.
Relapse becomes less likely.

Example

Carla’s delusions improve with medication, but arguments and constant monitoring begin after she returns home.

Medication may continue to reduce dopamine-related symptoms.

Family therapy may:

Reduce emotional over-involvement.
Develop agreed boundaries.
Improve communication.
Create a relapse-prevention plan.

Combining medication, CBT and family therapy

A more comprehensive programme could involve:

Treatment	Main target
Antipsychotic medication	Neurotransmitter activity and severe symptoms
CBT	Beliefs, interpretations, coping and avoidance
Family therapy	Expressed emotion, communication and environmental stress

The treatment plan may therefore address:

Diathesis-related biological processes.
The cognitive meaning of symptoms.
Environmental stress and relapse.

Combined treatment is not identical for every patient

An interactionist approach does not mean that every person automatically receives every treatment.

Treatment should consider:

Dominant symptoms.
Severity.
Previous response.
Side effects.
Family circumstances.
Ability to engage in CBT.
Personal preference.
Co-morbid conditions.
Current relapse risk.

For example:

A person with severe hallucinations may initially need medication.
A person distressed by persistent beliefs may benefit from CBT.
A person returning to a high-EE home may benefit from family therapy.
A person without safe family contact may not be suited to family therapy.

Evidence for combined treatment

AQA’s 2025 mark scheme identifies Tarrier’s research as relevant evidence concerning the effectiveness of combined treatments.

The exam-relevant implication is:

Outcomes may improve when psychological therapy is added to biological treatment rather than relying on medication alone.

This supports interactionist treatment because:

Biological processes are addressed.
Cognitive or environmental processes are addressed.
Different maintaining factors can be treated simultaneously.

Caution

Evidence that a combined treatment is effective does not prove that the diathesis-stress explanation is correct.

A combined treatment may help because:

Each treatment independently reduces different symptoms.
Extra professional contact improves adherence.
Participants have higher expectations.
One component is responsible for most improvement.

Treatment evidence supports practical usefulness more directly than it proves causal theory.

AQA’s combined-therapy research scenario

The June 2022 paper compared:

Drug therapy alone.
Drug therapy combined with cognitive therapy.

The combined-treatment group had a higher mean mood score after therapy, although AQA’s question correctly highlighted that post-treatment means alone did not allow proper conclusions without baseline results or measures of dispersion.

Research-methods lesson

When comparing combined treatment with medication alone, researchers need:

Pre-treatment measures.
Post-treatment measures.
Measures of dispersion.
Appropriate statistical testing.
Information about dropout.
Equivalent groups.

A higher post-treatment mean does not prove greater improvement if the groups differed before therapy began.

Evaluating combined treatments

Strength: several mechanisms are addressed

Schizophrenia involves different types of difficulty.

Medication may target:

Dopamine activity.
Severe positive symptoms.

CBT may target:

Delusional interpretation.
Voice-related distress.
Coping.

Family therapy may target:

Criticism.
Hostility.
Relapse-related stress.

A combination may therefore provide greater explanatory and therapeutic coverage.

Strength: medication may enable psychological therapy

A person experiencing severe psychosis may struggle to:

Concentrate.
Trust a therapist.
Discuss beliefs.
Complete homework.
Participate in family sessions.

Medication may reduce symptom intensity sufficiently for psychological work to begin.

This creates a practical sequence:

biological stabilisation → psychological engagement → longer-term coping and relapse prevention

Strength: psychological therapy may address medication limitations

Medication may reduce hallucinations while leaving:

Fear of the voice.
Established delusional interpretations.
Social avoidance.
Family conflict.

CBT and family therapy can address these remaining difficulties.

Combined treatment may therefore improve:

Quality of life.
Social functioning.
Coping.
Treatment adherence.

rather than merely reducing a symptom score.

Limitation: treatment burden

A combined programme can be demanding.

The person may need to:

Take medication regularly.
Attend CBT.
Complete between-session activities.
Attend family sessions.
Attend medical monitoring.

This may be difficult where the person experiences:

Avolition.
Cognitive disorganisation.
Sedation.
Financial or travel difficulties.
Distrust of services.

Adding treatment is not automatically better if the programme becomes impossible to follow.

Limitation: side effects remain

Adding psychological therapy does not remove medication side effects.

The person may still experience:

Tremors.
Muscle stiffness.
Sedation.
Weight gain.
Other drug-specific risks.

These may reduce:

Quality of life.
Engagement.
Adherence.
Long-term effectiveness.

An interactionist treatment plan must still include a cost-benefit judgement.

Limitation: access and cost

Combined treatment requires:

Prescribing and monitoring.
Trained CBT practitioners.
Trained family therapists.
Suitable facilities.
Repeated sessions.
Coordination between services.

This can create:

Long waiting lists.
Higher initial costs.
Unequal access.
Difficulty maintaining continuity.

Counterargument

Higher initial costs may be justified if treatment leads to:

Fewer relapses.
Fewer hospital admissions.
Better community functioning.
Reduced crisis-service use.

Cost-effectiveness must be assessed over an appropriate period.

Limitation: identifying the active component

Suppose a person receives medication and CBT and improves.

Researchers may not know whether improvement resulted from:

Medication.
CBT.
The interaction.
Extra clinical attention.
Greater treatment adherence.
Natural recovery.

A well-designed trial requires comparison groups such as:

Medication alone.
Psychological therapy plus medication.
Another active psychological condition.
Usual care.

Limitation: not every combination is appropriate

Family therapy may be unsuitable where:

Family contact is limited.
Relationships are unsafe.
The person does not consent.

CBT may be difficult where:

Cognitive disorganisation is severe.
Insight is limited.
Avolition prevents engagement.

Medication may be unsuitable where:

Side effects outweigh benefits.
Physical-health risks are substantial.
The person refuses treatment.

Interactionist treatment means selecting an appropriate combination, not imposing every available intervention.

Ethical issues in combined treatment

Consent

The person should understand:

The purpose of each treatment.
Possible benefits.
Possible side effects.
Alternatives.
Who will be involved.
What information will be shared.

Privacy

Combining individual and family treatment may create uncertainty about:

What the CBT therapist shares.
What relatives are told.
What remains confidential.
How risk information is managed.

Control

A large treatment team may make the person feel that:

Decisions are being made for them.
Refusal is not respected.
Every aspect of life is monitored.

An interactionist approach should increase personalisation rather than becoming a more extensive system of control.

Interactionist treatment and relapse

The diathesis may remain after symptoms improve.

For example:

Genetic vulnerability is not removed.
Stress sensitivity may continue.
Cognitive-processing difficulties may persist.

Treatment therefore often includes relapse prevention.

Biological relapse prevention

Medication may continue to reduce neurotransmitter-related symptom processes.

Cognitive relapse prevention

CBT may help the person:

Identify unusual thoughts.
Recognise triggers.
Use coping strategies.
Seek help early.

Family relapse prevention

Family therapy may help relatives:

Recognise early warning signs.
Respond calmly.
Reduce criticism.
Contact professionals appropriately.

The combined plan addresses several possible routes to relapse.

Interactionist case formulation

Consider the following scenario:

Zara has a strong biological family history of schizophrenia. She experiences increasing workplace pressure and conflict at home. She begins hearing voices and develops the belief that colleagues are monitoring her. Medication reduces the voices, but she remains frightened and her family continually criticises her absence from work.

Diathesis

Zara’s family history suggests possible genetic vulnerability.

Stressors

Workplace pressure.
Family conflict.

Symptoms

Auditory hallucinations.
Persecutory delusion.

Biological treatment

An antipsychotic may reduce dopamine-related positive symptoms.

CBT

CBT may:

Examine the belief that colleagues are monitoring her.
Reduce the power attached to the voices.
Develop coping strategies.

Family therapy

Family therapy may:

Explain the effect of symptoms on work.
Reduce critical comments.
Improve communication.
Lower relapse-related stress.

This is a complete interactionist formulation because the explanation and treatment both involve interacting levels.

Evaluating interactionism as an approach

More comprehensive than one-factor theories

Interactionism incorporates evidence that:

Schizophrenia has biological associations.
Stress can precipitate episodes.
Cognition affects symptom interpretation.
Family climate affects relapse.

Its breadth is a major strength.

Risk of becoming descriptive rather than explanatory

A model that states:

“Many things interact.”

may describe complexity without explaining the mechanism.

A strong interactionist explanation must still specify:

Which vulnerability.
Which stressor.
How they interact.
Which outcome is predicted.

Practical value

The approach leads to combined treatment.

This is useful because it encourages clinicians to assess:

Symptoms.
Medication response.
Beliefs.
Stress.
Family interaction.
Personal circumstances.

The patient is not reduced to dopamine levels or one dysfunctional thought.

Scientific difficulty

Interactions are harder to investigate than simple relationships.

Researchers may need to measure:

Genetic risk.
Childhood experience.
Current stress.
Cognitive processing.
Symptoms.
Treatment history.

Large samples and complex analyses may be required.

More realistic explanations are often harder to test cleanly.

Early and modern models compared

Early model	Modern model
Diathesis mainly genetic	Diathesis may be genetic, developmental or psychological
One gene associated with Meehl	Polygenic vulnerability associated with modern research
Stress treated relatively broadly	Several types of environmental stress considered
Simpler and easier to describe	More complex and more representative
More biologically focused	Integrates biological and psychological vulnerability
Limited account of individual pathways	Allows several routes to schizophrenia

AQA’s 2025 examiner report noted that stronger answers explained both the original model and the development of modern understandings of diathesis and stress.

How to apply the model in an exam

Step 1: identify the diathesis

Look for:

Biological relatives with schizophrenia.
Genetic vulnerability.
Prenatal risk.
Early trauma.
Lasting cognitive vulnerability.

Step 2: identify the stressor

Look for:

Bereavement.
Moving.
University.
Workplace pressure.
Family conflict.
Cannabis use.
Another major stressful experience.

Step 3: state the interaction

Use:

“The stressor may have triggered the underlying vulnerability.”

Step 4: link to the symptom

Identify:

Hallucination.
Delusion.
Speech difficulty.
Avolition.
Relapse.

Complete application sentence

“Amir’s biological mother has schizophrenia, suggesting inherited genetic vulnerability. The recent loss of his job and continuing family conflict provide environmental stress. According to the diathesis-stress model, these pressures may have triggered the vulnerability, contributing to the onset of his delusions.”

How to explain combined treatment

Use the following structure:

biological process → biological treatment → psychological or environmental process → psychological treatment → combined benefit

Example:

“The antipsychotic reduces dopamine activity and may lessen hallucinations. CBT then helps the person examine the threatening meaning attached to the voices and develop coping strategies. The treatments therefore address different parts of the condition.”

Structuring a 16-mark diathesis-stress essay

The June 2025 question allocated:

AO1: 6 marks
AO3: 10 marks

Evaluation therefore carries more weight than description.

Paragraph 1: interactionist overview

Define interactionism.
Define diathesis and stress.
Explain that the combination produces risk.

Paragraph 2: original model

Meehl.
Single genetic vulnerability.
Environmental stress required.

Paragraph 3: modern diathesis

Polygenic vulnerability.
Ripke.
Prenatal or early-trauma vulnerability.

Paragraph 4: modern stress

Life events.
Family or workplace stress.
Cannabis use.
Explain interaction rather than listing.

Paragraph 5: evidence for vulnerability

Family, twin or adoption findings.
Explain incomplete concordance.

Paragraph 6: evidence for stress

Hultman and life events.
Walker and cortisol.
Consider causality.

Paragraph 7: conceptual evaluation

Nature-nurture interaction.
Reductionism and holism.
Determinism.
Difficulty measuring threshold.

Paragraph 8: implications

Combined treatment.
Tarrier as supporting evidence.
Explain that treatment evidence does not prove the model.

What not to do in a 16-mark answer

The 2025 examiner report identified three major problems.

Problem 1: answers were too brief

Many students had insufficient descriptive and evaluative material.

Problem 2: excessive focus on treatment

Treatment is relevant evaluation, but an essay about the model must remain focused on explaining schizophrenia.

Problem 3: treating diathesis and stress as separate essays

Students sometimes described vulnerability and stress independently without explaining their interaction.

The examiner report emphasised that this missed the central point of an interactionist approach.

A stronger paragraph pattern

Use:

Point: Genetic evidence supports the diathesis component.Evidence: Risk generally rises with biological relatedness, but identical-twin concordance is below complete agreement.Explanation: This supports inherited vulnerability while showing that genes alone are insufficient.Interaction: Environmental stress is needed to explain why genetically similar people can have different outcomes.Conclusion: The evidence is more consistent with interactionism than with hard genetic determinism.

The interaction sentence is what prevents the paragraph becoming a mini genetic essay.

Overall conclusion

The diathesis-stress model proposes that schizophrenia develops when an underlying vulnerability interacts with environmental stress.

The early model emphasised:

A single genetic vulnerability.
An external trigger.

The modern model recognises:

Polygenic risk.
Prenatal and postnatal vulnerability.
Cognitive vulnerability.
Several forms of environmental stress.

The approach is important because it:

Integrates nature and nurture.
Explains individual differences.
Avoids simple genetic or environmental determinism.
Connects biological, cognitive and social levels.
Supports combined treatment.

Biological and psychological treatments may be combined so that:

Medication addresses neural and neurotransmitter processes.
CBT addresses beliefs, interpretations and coping.
Family therapy addresses communication and environmental stress.

The most defensible conclusion is:

Schizophrenia is best understood and treated through interacting biological, psychological and environmental influences rather than through one universal cause or one universal treatment.

Key Words 🔑

Key word	Student-friendly definition	How it may be used in an exam
Interactionist approach	Explanation combining influences whose effects depend on one another	Introduce the overall account
Diathesis-stress model	Model proposing that vulnerability interacts with environmental stress	State the central theory
Diathesis	Underlying vulnerability or predisposition	Identify genetic or psychological risk
Stress	Environmental pressure that may trigger vulnerability	Identify life events or family stress
Stressor	A particular event or experience producing stress	Apply a scenario
Predisposition	Increased susceptibility rather than certainty	Avoid deterministic claims
Vulnerability	Characteristic making a person more likely to develop a condition	Explain the diathesis
Trigger	Factor contributing to the emergence or return of symptoms	Explain environmental stress
Threshold	Point at which combined vulnerability and stress become sufficient for symptoms	Explain individual differences
Probabilistic	Changing the likelihood of an outcome rather than guaranteeing it	Evaluate determinism
Genetic loading	Degree of inherited vulnerability	Apply family history
Polygenic	Influenced by many genes	Explain the modern model
Meehl	Psychologist associated with the early single-gene version	Describe the original model
Ripke	Researcher associated with evidence for polygenic vulnerability	Explain the modern account
Prenatal vulnerability	Risk created by an experience before birth	Explain an expanded diathesis
Psychological trauma	Severe distressing experience that may create lasting vulnerability or act as stress	Explain modern diathesis
Life event	Major change that may produce stress	Apply bereavement or moving
Family stress	Pressure arising from criticism, hostility or conflict	Link with family dysfunction
Workplace stress	Pressure associated with demands or conflict at work	Give a stressor example
Cannabis use	Possible environmental trigger identified in interactionist accounts	Explain one modern stressor
Cognitive vulnerability	Lasting dysfunctional processing increasing susceptibility	Link with cognitive explanations
Cortisol	Hormone associated with the stress response	Explain Walker’s evidence
Relapse	Return or worsening of symptoms after improvement	Apply interactionism to treatment
Nature-nurture interaction	Heredity and environment affecting each other’s influence	Evaluate the model
Soft determinism	Position recognising causal influence without inevitability	Evaluate the model
Biological reductionism	Explaining schizophrenia through genes or neural processes alone	Contrast with interactionism
Environmental reductionism	Explaining schizophrenia through environmental experience alone	Contrast with interactionism
Holism	Considering several interacting aspects of a person	Evaluate the model’s breadth
Combined treatment	Use of biological and psychological interventions together	Explain interactionist treatment
Antipsychotic medication	Biological treatment affecting neurotransmitter activity	Target biological processes
Cognitive behaviour therapy	Treatment examining beliefs, interpretations and coping	Target cognitive processes
Family therapy	Treatment improving understanding and family interaction	Target environmental stress
Adjunctive treatment	Treatment added to another intervention	Explain psychological therapy alongside medication
Tarrier	Researcher cited by AQA in relation to combined treatments	Support practical implications
Cause and effect	Whether one factor directly produces another	Evaluate stress research
Reverse causality	Possibility that symptoms produce stress	Evaluate the model
Longitudinal study	Research following participants over time	Explain investigation of onset
Quasi-experiment	Comparison using naturally occurring differences	Describe vulnerability research
Treatment burden	Combined practical demands of several interventions	Evaluate combined therapy
Active treatment component	Part of a combined intervention responsible for improvement	Evaluate treatment studies

Hints from the Examiner Reports 💡

Examiner hint: Always explain the interaction.

The model is not:

one paragraph on genes + one paragraph on stress

It is:

vulnerability affects response to stress, and stress affects whether vulnerability is expressed

The 2025 examiner report specifically warned that separating the two components missed the central point.

Examiner hint: Learn both versions of the model.

Stronger 2025 answers discussed:

Meehl’s original single-gene version.
Modern polygenic vulnerability.
Early experiences as possible diatheses.
Broader understandings of stress.

Examiner hint: Do not describe only genetic vulnerability.

AQA’s 2022 multiple-choice assessment required both:

An underlying predisposition.
Stressful conditions that trigger development.

Examiner hint: Use cautious causal language.

Write:

“May trigger.”
“Increases vulnerability.”
“Is consistent with.”
“Raises the likelihood.”

Avoid:

“Definitely causes.”
“Everyone with the gene develops schizophrenia.”
“Stress alone creates schizophrenia.”

Examiner hint: Apply every scenario clue.

In the specimen Louise question:

Family history was the diathesis.
Bereavement and moving to university were the stressors.
Hallucinations and delusions were the resulting symptoms.

Examiner hint: Use evidence for both parts.

Possible evidence includes:

Twin, adoption and family research for vulnerability.
Hultman for life events.
Walker for cortisol and stress.
Tarrier for implications involving combined treatment.

Examiner hint: Do not overfocus on treatment in an essay asking about the explanation.

Treatment is a useful evaluation point, but the 2025 report noted that some students appeared to answer a different question because combined treatment dominated their response.

Examiner hint: Evaluate evidence rather than naming it.

Weak:

“Walker supports the model.”

Stronger:

“Higher cortisol among people with schizophrenia is consistent with stress involvement, but symptoms or hospitalisation could themselves increase cortisol, so direction of causality remains uncertain.”

Examiner hint: Use the original-modern comparison as evaluation.

The modern account is more comprehensive, but its greater flexibility can make diathesis and stress harder to define and test precisely.

Examiner hint: For treatment questions, state what each treatment targets.

Medication → neurotransmitter activity.
CBT → beliefs and coping.
Family therapy → communication and environmental stress.

Compare changes from pre-treatment baselines and include measures of dispersion.

Exam-Style Questions ✍️

Questions

1. What is meant by a diathesis?[2 marks]

2. What is meant by a stressor in the diathesis-stress model?[2 marks]

3. Explain the diathesis-stress model of schizophrenia.[4 marks]

4. Explain one difference between the original and modern versions of the diathesis-stress model.[4 marks]

5. Rosa has a biological parent and sibling who have experienced schizophrenia. After a close friend dies and Rosa begins a demanding new job, she starts hearing voices.

Explain Rosa’s experience using the diathesis-stress model.[4 marks]

6. Amir experienced severe childhood trauma. Many years later, continuing family conflict occurs shortly before he develops persecutory delusions.

Explain how the modern diathesis-stress model could account for Amir’s symptoms.[4 marks]

7. Explain why identical-twin concordance below 100% supports an interactionist explanation of schizophrenia.[4 marks]

8. Explain one strength and one limitation of the diathesis-stress model.[6 marks]

9. Explain how antipsychotic medication and CBT may be combined in an interactionist treatment programme.[6 marks]

10. Explain how antipsychotic medication and family therapy may be combined.[6 marks]

11. Researchers compare medication alone with medication plus CBT. They record the following results:

Treatment	Participants showing substantial improvement	Number beginning treatment
Medication alone	28	50
Medication plus CBT	38	50

a) Calculate the percentage showing substantial improvement with medication alone.[2 marks]

b) Calculate the percentage showing substantial improvement with combined treatment.[2 marks]

c) Explain one conclusion and one limitation of the findings.[4 marks]

12. Louise has a family history of schizophrenia. Her father has recently died, and she has moved away from home to start university. She has now begun experiencing hallucinations and delusions.

Using your knowledge of schizophrenia, explain why Louise is now showing symptoms.[4 marks]

13. Evaluate the use of combined biological and psychological treatments for schizophrenia.[8 marks]

14. Discuss the diathesis-stress model as a way of explaining schizophrenia.[16 marks]

15. Discuss interactionist explanations and treatments of schizophrenia. Refer to the following scenario in your answer.

Ethan has several biological relatives who have experienced schizophrenia. Following the loss of his job and months of conflict at home, he develops hallucinations and persecutory delusions. An atypical antipsychotic makes the voices quieter, but Ethan still believes that they control him. His relatives frequently criticise him and closely monitor everything he does.

[16 marks]

Answers and Mark Scheme

Question 1

Award up to two marks:

A diathesis is an underlying vulnerability or predisposition.
It increases the likelihood of developing schizophrenia but does not guarantee it.

Question 2

Award up to two marks:

A stressor is an environmental event or pressure.
It may trigger or worsen schizophrenia where an underlying vulnerability is present.

Question 3

Award up to four marks:

The model is interactionist.
A person possesses an underlying diathesis or vulnerability.
The vulnerability may be biological, genetic, psychological or developmental.
Environmental stress interacts with the vulnerability.
Schizophrenia becomes more likely when the combined influence is sufficient.
Neither diathesis nor stress is necessarily enough by itself.

Question 4

Award up to four marks:

The original model treated the diathesis primarily as a single genetic vulnerability.
Meehl is associated with this early account.
The modern model regards schizophrenia as polygenic.
It also allows prenatal or postnatal experiences, such as trauma, to create lasting vulnerability.
The modern model therefore uses a broader understanding of diathesis and stress.

Question 5

Award up to four marks:

Schizophrenia among Rosa’s parent and sibling suggests inherited genetic vulnerability.
The death of her friend is a major stressful life event.
Beginning a demanding job provides further stress.
These stressors may have triggered the underlying diathesis.
The voices are auditory hallucinations resulting from the interaction.

Question 6

Award up to four marks:

Severe childhood trauma may have created a lasting psychological diathesis.
The continuing family conflict acts as a later environmental stressor.
The stress interacts with the existing vulnerability.
This increases the likelihood of schizophrenia symptoms.
Amir’s unsupported belief that others intend harm is a persecutory delusion.

Question 7

Award up to four marks:

Identical twins share nearly all their genetic material.
One twin may have schizophrenia while the other does not.
Genes therefore create vulnerability but are not sufficient.
Different environmental or developmental experiences must influence whether symptoms develop.
This supports an interaction between inherited risk and stress.

Question 8

Award up to three marks for a developed strength and three for a developed limitation.

Possible strength:

The model explains why genetic evidence supports vulnerability but identical-twin concordance is below 100%. Inherited risk contributes to schizophrenia, while environmental differences account for discordant outcomes.

Possible limitation:

Cause and effect is difficult to establish because researchers cannot manipulate severe stress or genetic vulnerability ethically. Life events may trigger symptoms, but early symptoms could also create job loss, relationship conflict or other recorded stressors.

Alternative creditworthy points include:

Evidence concerning life events.
Cortisol evidence.
Modern flexibility.
Lack of precise measurement.
Nature-nurture integration.
Holism.
Combined-treatment implications.

Question 9

Award up to six marks:

Antipsychotic medication affects neurotransmitter activity.
It may reduce positive symptoms such as hallucinations and delusions.
Symptom reduction may allow the person to concentrate and participate more effectively.
CBT examines beliefs and interpretations that remain.
It may challenge the power attributed to voices and develop coping strategies.
The combination addresses biological symptom processes and psychological responses.
It may improve both symptom management and everyday functioning.

Question 10

Award up to six marks:

Antipsychotic medication may reduce severe psychotic symptoms.
Family therapy works with the person and relatives.
Psychoeducation can improve understanding of symptoms and treatment.
Communication training can reduce criticism and hostility.
Boundaries may reduce emotional over-involvement.
Reduced expressed emotion lowers environmental stress.
The combination therefore addresses biological processes and relapse-related family stress.

Question 11a

5028×100=56%

Award:

One mark for appropriate working.
One mark for 56%.

Question 11b

5038×100=76%

Award:

One mark for appropriate working.
One mark for 76%.

Question 11c

Award up to four marks.

Possible conclusion:

A greater percentage improved with medication plus CBT.
The difference was 20 percentage points.
This is consistent with combined treatment providing an additional benefit.

Possible limitation:

No inferential-test result is provided, so statistical significance cannot be claimed.
The figures do not show pre-treatment severity.
Dropout or adherence information is absent.
Improvement may have been defined subjectively.
The results do not establish which treatment component produced the effect.

Question 12

Award up to four marks:

Louise’s family history indicates possible inherited genetic vulnerability.
Her grandfather and aunt provide evidence of biological family risk.
The death of her father is a major stressful life event.
Moving away to start university provides additional stress.
These stressors may have triggered the underlying diathesis.
The resulting hallucinations and delusions are consistent with schizophrenia.

This reflects the application specified in the AQA sample mark scheme.

Question 13

A strong answer should include:

Combined treatments address several levels of schizophrenia.
Medication may reduce severe positive symptoms.
CBT may address beliefs, interpretations and coping.
Family therapy may reduce expressed emotion and relapse-related stress.
Medication may enable psychological engagement.
Psychological therapy may address difficulties left by medication.
AQA identifies Tarrier as evidence relevant to combined-treatment effectiveness.
Combined treatment does not prove the diathesis-stress explanation.
Programmes may be costly and time-consuming.
Treatment burden may increase dropout or non-adherence.
Medication side effects remain.
Not every therapy is suitable for every person.
Family therapy requires safe and willing family participation.
CBT requires sufficient motivation and concentration.
Researchers may struggle to identify the active treatment component.
Individualised treatment is more appropriate than automatically providing every intervention.
Long-term quality of life should be considered alongside symptom reduction.

Question 14

A strong response should include:

Knowledge and understanding

Interactionist explanation.
Diathesis as vulnerability.
Stress as environmental trigger.
Interaction rather than separate effects.
Predisposition does not guarantee symptoms.
Threshold or differing levels of vulnerability.
Meehl’s original single-gene account.
Environmental stress in the original model.
Modern polygenic vulnerability.
Ripke.
Prenatal experience as possible diathesis.
Postnatal trauma as possible diathesis.
Life events.
Family stress.
Workplace stress.
Cannabis use.
Possible role of cognitive processing.

Discussion

Family, twin and adoption evidence for vulnerability.
Incomplete identical-twin concordance.
Hultman and life events.
Walker and cortisol.
Correlation does not establish causation.
Symptoms may create stressful events.
Ethical barriers to experimental research.
Original model compared with modern understanding.
Modern model is more comprehensive.
Flexibility may reduce precision.
Diathesis and stress are difficult to measure.
Nature-nurture interaction.
Soft determinism.
Greater holism than single-factor explanations.
Possible remaining omissions.
Diagnostic validity problems.
Practical implication of combined treatment.
Tarrier and combined treatments.
Treatment effectiveness does not prove explanation.

AQA’s June 2025 question allocated six AO1 marks and ten AO3 marks, so discussion should be detailed and sustained.

Question 15

A strong response should include:

Knowledge and understanding

Interactionist explanation.
Genetic or biological diathesis.
Environmental stress.
Threshold and probabilistic risk.
Modern polygenic vulnerability.
Life events and family stress.
Antipsychotic medication.
CBT.
Family therapy.
Combined biological and psychological treatment.

Application

Ethan’s affected biological relatives suggest genetic vulnerability.
Job loss is a major life stressor.
Months of conflict provide continuing family stress.
These pressures may trigger the diathesis.
Hearing voices is an auditory hallucination.
Believing the voices control him may involve a delusion of control.
The atypical drug reduces the voices, showing some biological treatment benefit.
The belief about their power remains, so CBT may examine this interpretation.
CBT could review occasions when the voices were wrong or ignored.
Family criticism demonstrates high expressed emotion.
Close monitoring suggests emotional over-involvement.
Family therapy may reduce criticism and agree boundaries.
The combined plan addresses biological, cognitive and environmental factors.

Evaluation

Genetic evidence supports biological vulnerability.
Incomplete concordance shows that genes are insufficient.
Stress evidence supports environmental triggering.
Cause and effect remains uncertain.
Job loss may be a consequence of emerging symptoms.
The modern model is more comprehensive than a single-gene account.
Its flexibility makes precise testing difficult.
The model integrates nature and nurture.
It is less reductionist than one-level explanations.
Medication may enable Ethan to engage with CBT.
CBT addresses beliefs that medication has not removed.
Family therapy may lower relapse-related stress.
Medication side effects and adherence must be considered.
Combined treatment is demanding and costly.
Treatment success does not prove the model.
Personalised combined treatment is preferable to one universal programme.

Higher-level responses will keep the interaction central throughout, rather than presenting genetic, environmental and treatment material as three unrelated mini-essays.