Biological explanations and treatments

Biological Explanation: Genetic Factors

One possible explanation of schizophrenia may be heredity i.e. genetics. Schizophrenia tends to run in families, but only among individuals who are genetically related rather than related by marriage. The risk of developing the disorder among individuals who have family members with schizophrenia is higher than it is for those who do not. No one gene is thought to be responsible for this disorder – it’s more likely that different combinations of genes make individuals more vulnerable to schizophrenia. Having these genes does not necessarily mean an individual will develop schizophrenia.

Family Studies

Family studies have established that schizophrenia is more common among biological relatives of a person with schizophrenia, and that the closer the degree of genetic relatedness, the greater the risk.

Gottesman and Shield’s (1991)

Children with two schizophrenic parents had a concordance rate of 40%, children with one schizophrenic parent a rate of 12% and siblings (where a brother or sister had schizophrenia) a concordance rate of 9%.

Twin Studies

If monozygotic (MZ – genetically identical) twins are more concordant than dizygotic (DZ – who share only (on average) 50% of their genes), then this suggests that the greater similarity is due to genetic factors.

Hilker et al. (2017) — Danish Twin Study of Schizophrenia

This study used data from the Danish Twin Register which included over 30,000 twin pairs. They also combined this data with psychiatric records from the Danish Psychiatric Central Register (to collect information about schizophrenia diagnoses).

Hilker found a concordance rate of approximately 33% for schizophrenia in monozygotic (MZ) twins, compared to around 7% for dizygotic (DZ) twins.

However, using these twin data, Hilker et al. estimated the heritability of schizophrenia to be approximately 79%. This does not mean that 79% of people with schizophrenia inherited it. Instead, it means: Approximately 79% of the variation in schizophrenia risk within the population can be attributed to genetic differences between individuals.

Adoption Studies

Because of the difficulties of disentangling genetic and environmental influences for individuals who share genes and environment, studies of genetically related individuals who have been reared apart are used.

Tienari et al. (2000)

found that 6.7% of adoptees with biological mothers diagnosed with schizophrenia later developed the disorder, compared to 2% of controls. This supports a genetic contribution to schizophrenia; however, the researchers emphasised that environmental factors also play an important role, suggesting an interaction between genetic vulnerability and upbringing.

Polygenic

Meaning schizophrenia is influenced by many genes, each contributing a small amount to the overall risk of developing the disorder.

Polygenic:

“Like adding drops of dye to water  — one drop does nothing, but many change the colour.”

Genetic vulnerability:

Genes load the gun, environment pulls the trigger.”

Evaluation of genetic explanation: Strengths:

• Supporting research: There is overwhelming evidence to suggest that genetic factors make some people much more vulnerable to developing the disorder than others (see all research above).

• Applications/Determinism: Understanding genetic vulnerabilities enable researchers to make predictions of mental illness. This deterministic view can help to direct early interventions, support, or treatment. You can use evidence from treatments that are stated at the bottom of this page.

Weaknesses:

• Alternative explanation – Nature/Nurture: There are a number of factors in the environment associated with risk of the disorder (which could account for concordance rates of less than 100%) and other research on expressed emotion (seen later) has shown that the negative emotional climate in some families may lead to stress beyond an individual’s coping mechanisms, thus triggering a schizophrenic episode.

• Issues with supporting research: Cause and effect may be difficult to establish with twin, family and adoption studies due to a lack of control, it is difficult to suggest that genetics is the only cause of schizophrenia. Use the Gottesman research for this point. 

Biochemical explanation: The Dopamine Hypothesis

Hyperdopaminergia = Excessive levels of dopamine activity

Hyperdopaminergia refers to excessive dopamine activity, particularly in the mesolimbic pathway. This is associated with positive symptoms of schizophrenia such as auditory hallucinations.

The main roles of the mesolimbic pathway:

Reward processing & Assigning importance to stimuli. In simple terms: it helps you decide what matters and what is relevant in your environment.

There is too much dopamine activity in this pathway and this is thought to lead to faulty processing where everything feels important or meaningful. This can link to auditory hallucinations as internal thoughts are mistakenly tagged as important external stimuli. Therefore, the brain interprets them as real voices!

Delusions can also be linked, as individuals misinterpret insignificant events as highly meaningful. For example, a person with schizophrenia, could see someone talking on the phone, and think that they are plotting against them.

Hypodopaminergia = Low levels of dopamine

The prefrontal cortex is located at the front of the frontal lobe and is responsible for planning complex cognitive behaviour, decision making, and regulating goal-directed actions. In schizophrenia, reduced dopamine activity (hypodopaminergia) in this region is associated with negative symptoms. For example, low dopamine levels may lead to avolition, as individuals find it difficult to initiate and sustain goal-directed behaviour.

Biostructure Explanation: Neural Correlates 

Neural correlates are patterns of activity in the brain that occur with a schizophrenic experience. As they occur simultaneously, this could lead us to believe that the patterns observed are implicated in causing schizophrenia.

Neural correlates are patterns of brain activity that are associated with specific experiences of schizophrenia. Although these patterns occur alongside symptoms, they represent correlations rather than direct causes.

superior temporal gyrus and anterior cingulate cortex:

The superior temporal gyrus contains the auditory cortex and is involved in processing sounds, while the anterior cingulate cortex (ACC) is associated with higher-level cognitive functions such as emotion regulation, decision-making, and impulse control.

Allen et al. (2007)

used fMRI scans to compare brain activity in patients experiencing auditory hallucinations with controls. They found reduced activation in areas such as the superior temporal gyrus and ACC, with lower activity being negatively correlated with increased severity of hallucinations.

ventral striatum:

Additionally, the ventral striatum, which is involved in reward anticipation, has been linked to negative symptoms. Research has found a negative correlation between activity in the ventral striatum and avolition, such that lower activity is associated with more severe avolition.

However, as these findings are correlational, they cannot establish causation.

Evaluation of dopamine explanation

• Supporting research: Allen et al (2007) scanned patients with auditory hallucinations, compared to a control. A negative correlation was found – lower neural activation levels were found in superior temporal gyrus and anterior cingulate gyrus and were correlated with an increase in positive symptoms such as auditory hallucinations. 

• Useful Applications – Much of the evidence supporting the dopamine hypothesis comes from the success of drug treatments that attempt to change levels of dopamine activity in the brain. The basic mechanism of anti-psychotic drugs is to reduce the effects of dopamine and so reduce the symptoms of schizophrenia. Therefore, this explanation is useful in helping to develop treatments for schizophrenia. You can use evidence from the treatments section below. 

• Reductionist – a simplistic explanation that is easy to explain to patients. Schizophrenia is a complex disorder with multiple neurotransmitter systems implicated. The dopamine hypothesis might oversimplify the intricate neural mechanisms involved in the disorder. 

• Inconsistencies in Dopamine Levels: Not all studies consistently find elevated dopamine levels in individuals with schizophrenia. This inconsistency raises questions about the reliability of dopamine dysregulation as the sole explanation. For example in the Allen study, not all participants will fit the correlation.

• Deterministic – helps patients to realise that it is not their fault that they have this illness. Neurotransmitters are not something an individual can control, so it provides a sense of relief to the individual. 

Biological Treatments for Schizophrenia

Anti-psychotics

Anti-psychotics help the person with the disorder function as well as possible in their life, while at the same time increasing their feelings of subjective well-being. Anti-psychotics are usually recommended as the initial treatment for the symptoms of schizophrenia, after which clinicians will tend to use a combination of medication and psychological therapies. All anti-psychotics work by reducing dopaminergic transmission, i.e. reducing the action of dopamine in areas of the brain associated with schizophrenic symptoms.

• Typical antipsychotics (such as chlorpromazine) are used primarily to combat the positive symptoms such as hallucinations and thought disturbances, but doesn’t tend to work very well with negative symptoms.

• Atypical antipsychotics (such as clozapine) also combat these positive symptoms but they are also claimed to have some beneficial effects on negative symptoms as well.

Typical Anti-psychotics

Chlorpromazine pronounced as (klor pro ma zeen) is a typical antipsychotic drug used to treat schizophrenia. It works by blocking D2 dopamine receptors on the postsynaptic neuron, reducing the transmission of dopamine in the brain. This decreases dopamine activity, which is important as schizophrenia is associated with hyperdopaminergia.

As a result, chlorpromazine is effective in reducing positive symptoms such as hallucinations and delusions. It also has a sedative effect, which can help calm patients.

However, typical antipsychotics are associated with a high frequency of side effects, such as extrapyramidal symptoms (e.g. involuntary movements). This led to the development of atypical antipsychotics, which aim to reduce these side effects.

Typical Anti-psychotic side effects

Common side effects:

• dizziness

• drowsiness

• anxiety

• sleep problems (insomnia)

• breast swelling or discharge

• changes in menstrual periods

• weight gain

• swelling in hands or feet

• blurred vision

• constipation

• impotence or trouble having an orgasm

Serious long-term side effects

Extrapyramidal side effects (EPS) are movement disorders caused by the blockade of dopamine in the nigrostriatal pathway. This pathway is involved in motor control, so reducing dopamine activity can disrupt normal movement.

Symptoms of EPS include tremors, muscle stiffness, restlessness, and involuntary movements. Some of these effects, particularly the involuntary movements may be irreversible.

In rare cases, antipsychotic drugs can cause Neuroleptic Malignant Syndrome (NMS), a serious condition characterised by muscle rigidity, high fever, and reduced consciousness, which can be life-threatening if untreated.

Due to the severity of side effects, newer atypical antipsychotics were developed. Some, such as clozapine, require regular blood monitoring due to the risk of serious side effects such as agranulocytosis.

Atypical anti-psychotics

Clozapine is an atypical antipsychotic that works by blocking dopamine receptors and serotonin receptors. By reducing dopamine activity in subcortical areas, it helps to reduce positive symptoms such as hallucinations and delusions.

By blocking serotonin receptors, particularly 5-HT2A receptors, clozapine may help modulate dopamine activity in certain brain regions, including the prefrontal cortex. Increased dopamine transmission in the prefrontal cortex is thought to contribute to improvements in negative symptoms, such as avolition, reduced emotional expression, and social withdrawal.

Atypical Common side effects:

• blurred vision

• confusion

• dizziness

• irregular heart beat

• fever

• sleepiness or unusual drowsiness

• sweating

• trembling or shaking of the hands or feet

Rare side effects:

• convulsions

• problems in urination

• hyperventilation

• loss of interest, pleasure or appetite

• muscle spasm or jerking of the arms or legs

• sudden loss of consciousness

• decreased sexual ability

Evaluation: Strengths:

• You only need to chose one of these studies to learn as research to support. Research to support – Thornley et al. (2003) reviewed studies on the drug treatments of schizophrenics by comparing groups who were taking Chlorpromazine to groups who were taking a placebo drug. Chlorpromazine was associated with better overall functioning, reduced symptom severity and fewer relapses in comparison to the placebo. Leucht et al (2012) carried out a meta-analysis of 65 studies published between 1959 and 2011, and involving nearly 6000 patients. All patients had been stabilised on either typical or atypical anti-psychotics. Some of these patients were taken off their medication and given a placebo instead. The remaining patients remained on there regular anti-psychotic. Within 12 months, 64% of those patients who had been given the placebo had relapsed compared to 27% of those who stayed on the anti-psychotic drug.

• Research to support effectiveness –Melter (2012) concluded that Clozapine is more effective than typical antipsychotics and is effective in 30-50% of treatment-resistant cases where typical antipsychotics have failed.

• Usefulness –  Crossley et al (2010) carried out a meta-analysis for 15 studies to examine the efficacy and side effects of atypical drugs vs typical drugs in the early phase treatment of schizophrenia. Patients on atypical anti-psychotics gained more weight than those on typicals, whereas those on typicals experienced more extrapyramidal side effects. This could highlight the usefulness in terms of which drugs are more ethical. The usefulness of drug treatments should consider side effects, as if one form of drug has an increased risk in creating more problems in the individual than what they started with, this drug can be classed as more effective as a treatment.

Weaknesses:

• Usefulness: Research suggests that more than half of the patients taking typical anti-psychotics experience Parkison’s or extrapyramidal problems. These side effects can be so distressing for the patient that other drugs have to be given to control them, or the patient may stop taking their anti-psychotic medication.
  

  Alternative explanation: Drug treatments are shown to be less beneficial when taken as a sole treatment. Tarrier et al. (2000) focused on people with schizophrenia receiving 20 sessions of CBT in 10 weeks. Those who participated in CBT and drugs had a better reduction in symptoms compared to those who were just taking drugs.

• Lack of Freewill – Ross and Read (2004) argue that when people are prescribed anti-psychotic medication, it reinforces the view that there is ‘something wrong with them.’ This prevents the individual from thinking about possible stressors (such as life history or current circumstances) that might be possible for their condition. In turn this reduces their motivation to look for possible solutions that might alleviate these stressors and reduce their suffering. By taking a drug it takes away their freewill, this may make them feel out of control or that the treatment is being done to them. This could encourage a vicious cycle where individuals stop and start medication again and again.