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Having described what schizophrenia is, clinical psychology asks what causes it. Biological explanations locate the origins of the disorder in physiological processes: the neurotransmitter dopamine, genetic inheritance, and structural and functional differences in the brain (neural correlates and neuroanatomy). These explanations rest on a substantial and methodologically diverse body of evidence, and they underpin the drug treatments studied later in the topic. They have also attracted sustained criticism for being reductionist and deterministic, and for the difficulty of establishing cause rather than mere correlation. This lesson examines the dopamine hypothesis in both its original (hyperdopaminergia) and revised (hyper- and hypodopaminergia) forms, the genetic evidence from family, twin and adoption studies, and the principal neural correlates, all discussed in the measured, evidence-based register appropriate to clinical psychology.
Key Definition: Biological explanations propose that schizophrenia arises primarily from physiological factors — dysregulation of neurotransmitters (especially dopamine), inherited genes, and differences in brain structure and function — rather than from psychological or social factors alone.
This lesson addresses the Edexcel 9PS0 — Paper 2, Topic 5: Clinical Psychology content on the biological explanations of schizophrenia: the dopamine hypothesis (the original hyperdopaminergia account and the revised account distinguishing subcortical hyperdopaminergia from prefrontal hypodopaminergia), genetic explanations (evidence from family, twin and adoption studies), and neural correlates and neuroanatomy (structural and functional brain differences associated with the disorder). It builds on the symptoms-and-features lesson — the positive/negative distinction maps directly onto the revised dopamine hypothesis — and it provides the rationale for the drug treatments (antipsychotics) covered later in the topic. In assessment-objective terms, you should be able to describe the dopamine hypothesis, the genetic evidence and the neural correlates (AO1), apply this to scenarios such as interpreting a family-risk figure or a described drug effect (AO2), and evaluate the biological explanations — their evidential strength, the correlation-versus-causation problem, reductionism and determinism, and their integration with psychological factors (AO3).
Connects to…
The dopamine hypothesis is the most influential neurochemical explanation of schizophrenia. Dopamine is a neurotransmitter — a chemical messenger that crosses the synapse to influence the next neuron — and the hypothesis proposes that abnormal dopaminergic transmission underlies the disorder's symptoms. It exists in an original and a revised form.
The original dopamine hypothesis proposed that schizophrenia results from excessive dopamine activity (hyperdopaminergia), particularly at D2 receptors in subcortical regions such as the mesolimbic pathway. Three independent lines of evidence supported it:
The original account was later refined into a more sophisticated, two-part version distinguishing where in the brain the abnormality lies. On this revised view, schizophrenia involves:
This revision matters because it explains an otherwise puzzling clinical fact: standard (typical) antipsychotics, which reduce dopamine, relieve positive symptoms but do little for — and may even worsen — negative symptoms. If positive and negative symptoms reflect opposite dopamine abnormalities in different brain regions, a drug that uniformly lowers dopamine cannot fix both. The revised hypothesis thus links directly to the positive/negative distinction described in the previous lesson.
graph LR
A["Dopamine pathways<br/>in schizophrenia"] --> B["Subcortex / mesolimbic<br/>HYPERdopaminergia<br/>(excess at D2)"]
A --> C["Prefrontal cortex<br/>HYPOdopaminergia<br/>(too little dopamine)"]
B --> D["POSITIVE symptoms<br/>hallucinations, delusions"]
C --> E["NEGATIVE symptoms<br/>avolition, cognitive deficits"]
style B fill:#2563eb,color:#fff
style C fill:#7c3aed,color:#fff
The early support for the hypothesis was indirect — it relied on the effects of drugs rather than on direct measurement of dopamine in patients. More recently, PET (positron emission tomography) imaging has allowed dopamine activity to be estimated in living people, and this work broadly reports elevated dopamine synthesis capacity in the striatum of patients, particularly those experiencing acute positive symptoms, with some evidence that the elevation can be detected even in individuals at high clinical risk before a full disorder develops. This strengthens the hypothesis in two ways: it moves the evidence from inference-from-drug-action towards direct biological measurement, and finding the abnormality in the pre-onset (prodromal) phase makes it less likely that the dopamine change is merely a consequence of having the illness or of taking medication. The dopamine account also connects to the genetic evidence, since some of the genes implicated in schizophrenia are part of the dopamine system (notably the gene coding for the D2 receptor) — a convergence that makes the whole biological picture more coherent.
Exam Tip: State the revised hypothesis precisely: different dopamine abnormalities (excess subcortically, deficiency in the prefrontal cortex) for different symptom types. Writing simply that "schizophrenia is caused by too much dopamine" gives only the original version and misses the mark that distinguishes a developed answer. Note too that the drug evidence shows dopamine is involved, not that it is the whole cause.
Schizophrenia tends to run in families, which prompted researchers to investigate its genetic component using family, twin and adoption studies. Each design is intended to separate the contribution of shared genes from that of shared environment.
Family studies compare the rate of schizophrenia among the biological relatives of a diagnosed individual (the proband). The general finding, from the widely cited pooled family-study data (Gottesman, 1991), is that risk rises with genetic closeness:
| Relationship | Shared genes (approx.) | Approximate lifetime risk |
|---|---|---|
| General population | — | ~1% |
| Sibling of a person with schizophrenia | 50% | ~9% |
| Child of one affected parent | 50% | ~13% |
| Dizygotic (DZ) twin | 50% | ~17% |
| Monozygotic (MZ) twin | 100% | ~48% |
The pattern is clear: the more genes an individual shares with an affected relative, the higher their risk. The crucial limitation is equally clear: relatives who share genes also typically share environments, so family studies on their own cannot disentangle nature from nurture.
Twin studies exploit the fact that monozygotic (MZ, identical) twins share essentially 100% of their DNA, whereas dizygotic (DZ, non-identical) twins share on average about 50% — the same as ordinary siblings. If genes matter, MZ concordance should exceed DZ concordance. A classic review by Gottesman and Shields (1966) examined twin pairs in which at least one twin had a diagnosis of schizophrenia and found concordance of roughly 42% for MZ twins and 9% for DZ twins. The substantially higher MZ figure strongly implies a genetic contribution.
Two features of these data deserve emphasis. First, the gap between MZ and DZ concordance is the evidence for genetic influence. Second, the fact that MZ concordance is far below 100% is decisive evidence that genes are not the whole story: if schizophrenia were wholly genetic, MZ twins (who are genetically identical) would always be concordant. They are not — so environmental factors must also contribute, which is exactly the logic behind the diathesis-stress model studied later.
Adoption studies separate genes from environment by studying children raised apart from their biological parents. The best-known is Tienari et al. (2004), who followed adopted-away offspring of Finnish mothers diagnosed with schizophrenia and compared them with adopted-away offspring of mothers without the diagnosis. The high-genetic-risk adoptees developed schizophrenia at a higher rate (around 6.7%) than the low-risk controls (around 2%) — evidence for a genetic contribution, since the elevated risk travelled with the high-risk children even though they were raised in unrelated families. Critically, the elevated risk was concentrated in those raised in dysfunctional adoptive family environments, while low-risk adoptees in such families were largely unaffected. Tienari's study is therefore cited as evidence both for genetic vulnerability and for the diathesis-stress model: genes raised susceptibility, but a stressful family environment was needed to express it.
Key Definition: Concordance is the probability that, if one twin has a condition, the other twin also has it. Higher concordance in MZ than in DZ twins indicates a genetic contribution; concordance below 100% in MZ twins indicates that genes are not sufficient on their own.
The genetic studies are often summarised in a single figure — the heritability of schizophrenia is frequently estimated at around 80% — and this figure is widely misunderstood. Heritability is a population statistic: it describes the proportion of the variation in a trait, within a particular population, that can be statistically attributed to genetic variation. It does not mean that any individual's schizophrenia is "80% caused by genes", nor that 80% of people with the relevant genes will develop the disorder. A high heritability estimate is entirely compatible with the environment playing a decisive role, because heritability says nothing about the causes of the disorder in a single person — only about the sources of differences across a group. This distinction is examinable and is a reliable way to demonstrate sophisticated understanding: it lets you accept the strong genetic evidence while still insisting, correctly, that environment matters.
Modern molecular genetics has searched directly for the genes involved, using genome-wide association studies (GWAS) that compare the genomes of very large numbers of patients and controls. This work has identified many genetic loci associated with schizophrenia — including genes involved in dopamine signalling (notably the gene coding for the D2 receptor), as well as genes involved in glutamate signalling and immune function. The key finding is that no single gene "causes" schizophrenia; the disorder is highly polygenic, arising from the combined small effects of very many genetic variants, which is one reason there is no usable single-gene test. The involvement of dopamine-system genes is a striking convergence, because it links the genetic evidence directly to the dopamine hypothesis: two independent lines of evidence — pharmacological and genetic — both implicate dopamine, which is more persuasive than either alone. At the same time, the polygenic, small-effect picture reinforces the point that genetic risk is a matter of vulnerability rather than destiny, and helps explain why the same diagnosis may rest on genetically different foundations in different people — a further echo of the heterogeneity and validity concerns raised in the symptoms lesson.
Neuroimaging (MRI, fMRI and PET) has identified structural and functional brain features that are statistically associated with schizophrenia. These are termed neural correlates — patterns that co-occur with the disorder, which is not the same as having caused it.
The ventricles are fluid-filled cavities in the brain; in many people with schizophrenia they are enlarged relative to controls. Enlarged ventricles imply a loss of surrounding brain tissue (reduced grey matter), and the finding has been replicated widely, being associated especially with negative symptoms. However, two qualifications limit its value: enlarged ventricles are not specific to schizophrenia (they appear in other conditions, including some dementias), and not every patient shows them. Enlarged ventricles are therefore associated with the disorder but are neither necessary nor sufficient for it.
The prefrontal cortex supports executive functions such as planning, working memory and the regulation of behaviour. Many patients show reduced blood flow and metabolic activity here — termed hypofrontality. Hypofrontality fits the revised dopamine hypothesis well, since reduced prefrontal dopamine (hypodopaminergia) would be expected to impair prefrontal function and produce negative and cognitive symptoms — an example of two biological strands (neurochemistry and neuroanatomy) converging.
Further reported differences include reduced grey matter in several regions, and altered activity in temporal-lobe areas involved in language (linked to auditory hallucinations, consistent with the idea that hallucinations may involve self-generated inner speech misattributed to an external source). Collectively these findings suggest schizophrenia is associated with widespread, if subtle, differences in brain structure and function rather than a single focal lesion.
It is worth being clear about how neural correlates relate to the dopamine and genetic strands, because a strong answer integrates them rather than listing them separately. Hypofrontality is not an isolated finding: it is precisely what the revised dopamine hypothesis predicts, since reduced prefrontal dopamine (hypodopaminergia) should impair the executive functions the prefrontal cortex supports, producing negative and cognitive symptoms. Enlarged ventricles, by contrast, index a loss of tissue whose cause is unknown — it may reflect the neurodevelopmental disruption discussed in "Going Further", the illness process itself, or the effects of long-term treatment. So the neural evidence is best read as converging with the neurochemical account in some respects (hypofrontality) while raising fresh causal questions in others (ventricular enlargement). This is a more sophisticated use of the neuroanatomical evidence than treating each finding as a free-standing "brain difference".
Key Definition: Neural correlates are measurable patterns of brain structure or activity associated with a mental state or disorder. Because they are correlational, they cannot by themselves establish that the brain feature caused the disorder.
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