Introduction to schizophrenia

Schizophrenia is a serious mental disorder characterised by disturbances in thought, perception, emotion, and behaviour. Symptoms are often divided into positive symptoms (additions to normal experience, such as hallucinations and delusions) and negative symptoms (losses from normal experience, such as reduced emotional expression and social withdrawal). Understanding its causes involves exploring both biological and psychological factors.

Biological explanations of schizophrenia

Biological explanations suggest that schizophrenia arises from physical factors within the body, such as genetics or brain chemistry. These views emphasise innate predispositions rather than purely environmental influences. As a result, they point towards treatments like medication that target these biological mechanisms.

Genetic explanation

Genes are units of DNA that carry instructions for traits and can be passed from parents to offspring. The genetic explanation proposes that schizophrenia can be inherited, meaning certain individuals have a higher risk due to their family background.

Key evidence comes from studies comparing family members:

• Family studies - These show that relatives of people with schizophrenia have a higher risk of developing the disorder, suggesting a hereditary component.
• Twin studies - Monozygotic (MZ) twins share 100% of their genes, while dizygotic (DZ) twins share about 50%. A higher concordance rate (the likelihood both twins have the disorder) in MZ twins supports a genetic basis.
  • For example, research by Gottesman and Shields (1966) found a concordance rate of 42 per cent for MZ twins and 9 per cent for DZ twins.

More recent research uses genome-wide association studies (GWAS), which scan entire genomes to identify variations linked to disorders.

GWAS findings:

• GWAS have identified certain alleles (different forms of a gene) that are more common in people with schizophrenia, such as those related to dopamine and GABA.
• Gene deletions, like in the COMT gene, can increase risk by disrupting normal brain function.

This genetic predisposition does not mean schizophrenia is inevitable; it interacts with other factors.

Biochemical explanation: the dopamine hypothesis

Neurotransmitters are chemical messengers that transmit signals between neurons in the brain. The dopamine hypothesis focuses on imbalances in dopamine, proposing that abnormal levels contribute to schizophrenia symptoms.

Originally, researchers thought excess dopamine caused the disorder. However, this idea evolved because treatments like dopamine antagonists were found not to reduce negative symptoms and did not work for some people.

An updated version from the 1990s suggests:

• Low dopamine in the mesocortical pathway causes negative and cognitive symptoms.
• Excess dopamine in the mesolimbic pathway may result from upregulation.

This hypothesis explains why symptoms vary and highlights the brain's complex chemistry.

Psychological explanation of schizophrenia

While biological explanations focus on the body, psychological ones emphasise cognitive processes – how people think, perceive, and interpret information. The cognitive explanation views schizophrenia as resulting from faulty information processing in the brain, leading to misinterpretations of reality.

This occurs because individuals with schizophrenia may struggle with monitoring their own thoughts or understanding others.

Key cognitive problems and related symptoms

• Self-monitoring error - Individuals mistakenly attribute their own internal thoughts (sub-vocal speech) to external sources, perceiving them as voices from outside, leading to auditory hallucinations.
• Difficulties with mentalising - There is trouble inferring others' intentions or mental states (theory of mind deficits), so neutral actions seem threatening, causing distress and isolation, leading to paranoia and social withdrawal.
• Counter-evidence bias - Beliefs form without enough evidence, and they persist despite contradictory information, as the person fails to revise their thinking, leading to delusions.

These cognitive glitches disrupt normal mental functioning, leading to the distorted experiences characteristic of schizophrenia.

Evaluation of explanations for schizophrenia

Evaluation of the biological explanation

• Supporting evidence from animal studies - Rats given amphetamines (which boost dopamine) display behaviours similar to schizophrenia, such as unusual movements and withdrawal, suggesting dopamine's role.
• Contradictory evidence - Apomorphine, a drug that activates dopamine receptors, does not worsen symptoms in people with schizophrenia or induce them in healthy individuals, challenging the dopamine hypothesis.

Evaluation of the cognitive explanation

• Supporting evidence - People with schizophrenia are less accurate at recognising recordings of their own voices compared to healthy controls, aligning with self-monitoring errors.
• Causality issues - It is unclear if cognitive problems cause schizophrenia or result from it, as brain changes from the disorder might impair thinking (a validity concern).

Overall, no single explanation fully accounts for schizophrenia, suggesting a combined approach is needed.

Issues and debates in explanations of schizophrenia

Explanations of schizophrenia raise broader questions in psychology about what causes mental disorders. These debates compare individual traits with environmental influences and consider how nature and nurture interact.

Individual and situational explanations

Individual explanations focus on personal factors, like genetic makeup, that make someone prone to schizophrenia.

Situational explanations highlight external influences, such as stress from life events, drug use, or cultural factors (e.g., higher rates in some immigrant groups due to discrimination).

In reality, schizophrenia often stems from a mix: individual genetics combined with situational triggers like poverty or trauma.

Nature versus nurture

Nature refers to biological inheritance, while nurture involves environmental experiences.

Support for nature:

• Twin studies, like Gottesman and Shields (1966), show higher concordance in MZ twins, pointing to genetic factors.
• However, even MZ twins do not have 100% concordance, and shared environments may confound results (shared environment fallacy).

Support for nurture:

• The cognitive explanation does not explain why some people have faulty thinking, such as through biochemical differences (nature) or modelling family members (nurture).

Schizophrenia likely involves both, through epigenetics – where environmental factors influence whether genes are expressed (turned on) or silenced.

The diathesis-stress model

This model integrates nature and nurture, proposing that some people have a genetic diathesis (vulnerability) to schizophrenia, but symptoms only emerge under stress (nurture factors).

For example, a person with certain gene variations might develop the disorder after experiencing traumatic events, discrimination, or poverty. This explains why not everyone with genetic risks gets schizophrenia, emphasising the role of life circumstances in triggering it.

Understanding these interactions supports holistic treatments, combining medication with therapy to address both biological and environmental aspects.