Biological Explanations of Schizophrenia

There are alleles from multiple genes that increase the risk of developing schizophrenia. 

These alleles are heritable, meaning that people are more likely to develop schizophrenia if their family members also have schizophrenia. 

The more genetic risk alleles a person has, the more likely they are to develop schizophrenia. 

One strength of the genetic explanation of schizophrenia is that it is supported by twin studies. 

Gottesman and Shields conducted a twin study looking at the concordance rate for schizophrenia in MZ and DZ twins. 

The concordance rate for MZ twins was 74% and the concordance rate for DZ twins was 24%.

This large difference in concordance rate betwen MZ and DZ twins, indicates a genetic contribution to developing schizophrenia. 

Therefore, this research strongly supports the genetic vulnerability to schizophrenia explanation. 

However, environmental influences must also be present in schizophrenia development as the concordance rate for MZ twins is not 100%. 

One weakness of Gottesman and Shields' study is that, like other twin studies, it assumes that MZ twins and DZ twins have a similar amount of shared environment. 

However, this may not be true, as identical twins are often treated as the same person more often than DZ twins.

Therefore, it would be wrong to assume that individuals in a DZ twin pair have an equal amount of shared environment compared to MZ twins.

It is likely that MZ twins are treated more similarly to each other than DZ twins. 

This means that the high concordance rates for schizophrenia observed in MZ twins in this study are most likely caused by genetic as well as environmental factors. 

Therefore, Gottesman and Shield's study over-exaggerates the role of genetics in schizophrenia development, and so, weakens the genetic explanation of schizophrenia. 

One strength of the genetic explanation for schizophrenia is that it is supported by adoption studies. 

Tiernari et al compared adopted children whose biological mothers had schizophrenia to a control group of adopted children whose biological mothers did not have schizophrenia. 

Tiernari found that adopted children of biological mothers with schizophrenia were more likely to develop schizophrenia themselves. 

Since these children were adopted at birth, any similarity between the adopted child and its biological mother must be due to genetics and not the environment. 

This study shows that genetics has more influence on schizophrenia development than the environment, supporting the genetic explanation.

One limitation of Tiernari's study, like many adoption studies, is that they assume that similarities between biological parents and adopted child is due to genetics only. 

However, children are often matched with adoptive parents that are similar to their biological parents (e.g. similar area, similar social background) and so, these adopted children experience the same environmental factors as they would have with their biological parents. 

This means that similarities between a child and their biological parents may be due to shared environmental factors as well as genetics. 

Therefore, Tiernari's study over-exaggerates the role of genetics in schizophrenia development, and weakens the genetic explanation of schizophrenia. 

Genes influence our behaviour by controlling brain processes, so they may cause abnormalities in the brain that cause schizophrenia. 

There are two main explanations for this suggestion: 

• Neural Correlates Hypothesis

• Dopamine Hypothesis

The neural correlates explanation of schizophrenia states that schizophrenia is caused by abnormal brain structures. 

For instance, some research has shown that schizophrenics have larger ventricles in the brain and a smaller frontal cortex than normal. 

Therefore, these observed brain abnormalities that are correlated with schizophrenia, may be the cause of schizophrenia. 

Torrey conducted MRI scans to look at the brains of schizophrenia patients compared to those of a healthy control group. 

It was found that, on average, the ventricles of schizophrenia patients were 15% larger than the control group's. 

Therefore, this study supports the idea that abnormal brain structures correlated with schizophrenia, may be causing schizophrenia, proposed by the neural correlates explanation. 

One limitation of the neural correlates explanation is that the correlation between schizophrenia and abnormal brain structures , such as enlarged ventricles, does not necessarily mean that brain abnormalities cause schizophrenia. 

For instance, it is possible that abnormal brain structures often observed in schizophrenia patients are caused by taking medication that alters brain structure in treating schizophrenia.

And so, the medication may actually be causing the abnormal brain structures, rather than schizophrenia. 

This means that, we do not have sufficient evidence to conclude a cause-effect relationship between abnormal brain structures and schizophrenia because supporting evidence obtained from MRI studies is only correlational. and because the drugs that patients take to treat schizophrenia may act as a confounding variable in studies of neural correlates. 

Therefore, these two facts, weaken support for the neural correlates explanation of schizophrenia. 

A second limitation of the neural correlates hypothesis is that there are individual differences in the abnormal brain structures displayed across patients with schizophrenia. 

For instance, some research has found no significant difference in the size of ventricles of schizophrenia patients and control groups. Other research has reported different brain abnormalities are more significant, such as brain shape, rather than size of ventricles. 

This indicates that results have not always replicated to support the neural correlates explanation, casting doubt on its reliability as a possible explanation for schizophrenia. 

The dopamine hypothesis states that abnormal brain function causes schizophrenia. 

The dopamine hypothesis states that

• abnormally high levels of dopamine

• in the mesolimbic system

• leads to neural overactivity in this region

• which causes the positive symptoms of schizophrenia, such as hallucinations and delusions. 

Side note: the mesolimbic system is made up of the basal ganglia and surrounding brain regions 

The revised dopamine hypothesis states that abnormal brain function causes schizophrenia. 

 The dopamine hypothesis states that

• abnormally high levels of dopamine
• in the mesolimbic system
• leads to neural overactivity in this region
• which causes the positive symptoms of schizophrenia, such as hallucinations and delusions. 

Also, the

• abnormally low levels of dopamine
• in the frontal cortex
• leads to neural underactivity in this region
• which causes the negative symptoms of schizophrenia such as avolition and speech therapy. 

One strength of the dopamine hypothesis is that it is supported by drug studies. 

Several drug studies have demonstrated that drugs that increase dopamine (e.g. amphetamines) can cause hallucinations and delusions in healthy people, which are the positive symptoms of schizophrenia. 

And also have shown that, drugs that decrease dopamine, decrease the likelihood of experiencing hallucinations and delusions in schizophrenia patients (i.e. a reduction in positive symptoms) 

In these studies, altering dopamine levels has a clear effect on the experience of positive symptoms of schizophrenia, suggesting a cause-effect relationship. 

Therefore, these studies support the dopamine hypothesis. 

One limitation of the dopamine hypothesis is that it cannot explain positve symptoms in all schizophrenics.

Noll reviewed 15 drug studies in which patients that had schizophrenia were given drugs that reduced dopamine levels. 

It was found that for 1/3 of patients, the drugs that decreased dopamine, did not prevent positive symptoms, like hallucinations and delusions. 

This shows that though the majority of schizophrenics had their positive symptoms reduced by taking dopamine-reducing drugs, some schizophrenics positive symptoms are still are unaffected by altering dopamine levels. 

Therefore, this shows that abnormal dopamine levels may not be the only cause of schizophrenia, and exposes the limits of the dopamine hypothesis. 

One weakness of the dopamine hypothesis is that the evidence supporting it is not always conclusive. 

Montcrieff conducted a review of the evidence supporting the dopamine hypothesis and claims that the evidence is inconclusive

Found that drugs, like amphetamines, that cause positive symptoms of schizophrenia, also affect other neurotransmitters as well as dopamine such as noradrenaline and serotonin.

This means that we cannot be conclude that it is the increased dopamine that is causing these positive symptoms of schizophrenia, and not another neurotransmitter. 

Therefore, this limits the support provided from drug studies and so, weakens the dopamine hypothesis.