The biological approach to schizophrenia

The biological approach in psychology explains mental disorders like schizophrenia by focusing on physical factors within the body. This approach assumes that these symptoms arise from issues at the biological level, such as problems with brain chemicals, genes, or brain structure.

Categories of biological explanations

• Biochemical factors - Involving the function of neurotransmitters (chemical messengers that transmit signals between neurons in the brain).
• Genetic factors - Related to inherited traits that increase vulnerability.
• Brain structure factors - Concerning physical differences in the brain's anatomy.

Biochemical factors in schizophrenia

Biochemical explanations suggest that schizophrenia results from imbalances in brain chemicals, particularly neurotransmitters. If schizophrenia has a genetic basis, these chemical differences should be detectable in affected individuals. Research points to overactivity in certain neurotransmitter systems as a key cause, leading to disrupted brain signalling that produces schizophrenic symptoms.

The dopamine hypothesis

Dopamine is a neurotransmitter that enables neurons (nervous cells) to communicate by causing them to fire. The dopamine hypothesis proposes that schizophrenia is linked to excessive dopamine activity in the brain. This overactivity causes neurons using dopamine to fire too frequently, overwhelming the system with messages. As a result, this "message overload" can trigger symptoms like hallucinations or paranoia.

Two main versions of this hypothesis:

• Excessive dopamine production - Some individuals produce too much dopamine, leading to heightened neural activity.
• Increased dopamine receptors - Others may have a normal amount of dopamine but more receptors (specialised sites on neurons that receive dopamine signals), causing more frequent firing and overproduction of messages.

Genetic factors in schizophrenia

Genetic explanations view schizophrenia as partly inherited, meaning certain genes increase a person's vulnerability to developing the disorder. This vulnerability can be passed down through families. Evidence from family and twin studies shows that the closer the genetic relationship, the higher the risk, indicating a hereditary component.

Evidence from family and twin studies

Schizophrenia tends to run in families, with the risk increasing based on genetic similarity.

Examples of genetic risk patterns:

• If one identical twin has schizophrenia, the other has a higher chance of developing it compared to fraternal twins.
• The severity of a parent's disorder influences the child's likelihood; more severe cases in parents correlate with higher risk in offspring.
• Within the same family, individuals may inherit a general vulnerability but develop different forms of schizophrenia, such as paranoid or catatonic.

Twin and family studies provide reliable evidence that the degree of risk of developing schizophrenia increases with the degree of genetic relatedness.

Structural brain abnormalities in schizophrenia

Structural explanations focus on physical differences in the brains of people with schizophrenia compared to those without the disorder. Brain imaging techniques, such as MRI, have revealed consistent differences, including reduced brain weight and issues in specific regions.

Negative symptoms are often linked to these structural changes, which is why they may not respond to dopamine-based medications. In contrast, positive symptoms are more associated with biochemical factors like dopamine imbalances.

Enlarged brain ventricles

Ventricles are fluid-filled cavities in the brain that contain cerebrospinal fluid. One of the most common findings in schizophrenia is enlarged ventricles, which may indicate loss of brain tissue or incomplete development of certain areas. This enlargement is not universal – it is more prevalent in men and those with long-term schizophrenia.

Abnormalities in the frontal lobes

Research shows abnormalities in the frontal lobes of people with schizophrenia. The frontal lobes also contain major dopamine pathways, linking structural issues to the dopamine hypothesis.

Research study: Weinberger et al. (1972):

• Method - Compared MZ twins where one had schizophrenia and the other did not, using tasks that activate the frontal lobes, combined with MRI scans.
• Results - Schizophrenic twins showed enlarged ventricles and lower activity in frontal lobe areas compared to their non-schizophrenic twins.
• Conclusions - These structural differences suggest frontal lobe abnormalities contribute to schizophrenia, potentially explaining cognitive symptoms.
• Evaluation - The use of MZ twins controls for genetics, strengthening the evidence for structural causes, but the study is limited to a small sample and does not prove causation.

Abnormalities in brain asymmetry

In healthy individuals, structures like the amygdala are typically smaller on the left than the right. However, in schizophrenia, this asymmetry may be absent or reversed.

Research study: Young et al. (1991):

• Method - Used brain scans to compare structural asymmetry in schizophrenic patients and a control group (people without schizophrenia).
• Results - Controls showed expected asymmetry (e.g., smaller left amygdala), but schizophrenic patients lacked this asymmetry, with more uniform sizes across brain sides.
• Conclusions - Loss of normal asymmetry indicates structural abnormalities that may underlie schizophrenic symptoms, particularly those affecting emotion.
• Evaluation - Provides objective evidence through scans, but does not explain why asymmetry is lost; individual differences limit generalisability.