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9990 · 1.1.2

Explanations of schizophrenia — practice questions

Practice and worked examples for 9990 Explanations of schizophrenia. Short previews only — attempt the full question in MarkScheme against the official scheme.

Worked example 1

The lifetime risk of schizophrenia in the general population is approximately 1%. Gottesman's (1991) research found a concordance rate of 48% for monozygotic (MZ) twins. Calculate how many times more likely an individual is to develop schizophrenia if their identical twin has the disorder, compared to someone in the general population. Show your working and explain the implication.

Show solution outline

Step 1: Identify the relevant probabilities.

  • Risk for an individual with an affected MZ twin (P_MZ) = 48% or 0.48
  • Risk for the general population (P_GenPop) = 1% or 0.01

Step 2: Formulate the calculation for relative risk.

  • Relative Risk = Probability in exposed group / Probability in unexposed group
  • Relative Risk = P_MZ / P_GenPop

Step 3: Perform the calculation.

  • Relative Risk = 0.48 / 0.01
  • Relative Risk = 48

Step 4: State the answer and implication.

  • Answer: An individual is 48 times more likely to develop schizophrenia if their identical twin has the disorder compared to the general population.
  • Implication: This large increase in relative risk provides strong quantitative evidence for a significant genetic component in the aetiology of schizophrenia, as MZ twins share 100% of their genes.

Worked example 2

Explain how genetic and environmental factors may interact in schizophrenia. Refer to Gottesman (1991) and Tienari et al. (2004). Evaluate the dopamine hypothesis. [10 marks]

Show solution outline

AO1 — Genetic vulnerability (Gottesman, 1991):

  • Meta-analysis of twin studies: MZ concordance ~48%, DZ ~17%.
  • Shows substantial heritability — schizophrenia runs in families.
  • Concordance below 100% implies environmental contribution.

AO1 — Gene–environment interaction (Tienari et al., 2004):

  • Finnish adoption study: children with genetic risk (biological mother had schizophrenia) raised in high-EE or dysfunctional adoptive families showed highest rates of schizophrenia-spectrum disorders.
  • Low-risk adoptees in same environments less affected — supports diathesis-stress.

AO1 — Dopamine hypothesis:

  • Mesolimbic hyperdopaminergia → positive symptoms (hallucinations, delusions).
  • Supported by effectiveness of D2-blocking antipsychotics.

AO3 — Evaluation of dopamine hypothesis:

  • Strength: Drug evidence and post-mortem studies offer biological plausibility.
  • Limitation: Not all patients respond to antipsychotics; negative symptoms poorly explained — reductionist if used alone.
  • Alternative: Glutamate/NMDA dysfunction (phencyclidine model) suggests dopamine is partial account.

Judgement: Best explanation is interactionist — Gottesman shows genetic diathesis; Tienari shows environment modulates expression; dopamine explains mechanism but not full aetiology.

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