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How we think and behave may be due to either psychological or physiological factors. Is it the structure of our brains that dictates how we think? Or is there something else governing our thoughts? And if there is a dysfunction or failure in that structure, what effects will that have on our brains?
Biological explanations for schizophrenia (and disorders, in general) assume that our thoughts and behaviours are due to certain aspects of our biology. There are three major biological causes of schizophrenia that we will discuss in this article: genetics, the dopamine hypothesis, and neural correlates.
One explanation for schizophrenia is that it may have a genetic basis. Schizophrenia tends to run in families. This means that the closer the relationship to a person with schizophrenia, the more likely they are to have it. However, schizophrenia is a polygenic disorder not caused by a single ‘schizophrenia gene’.
Polygenic means that many genes contribute to the development of schizophrenia, but each gene increases a person’s risk of developing schizophrenia by only a tiny amount.
This genetic predisposition is supported by a 1991 study by Gottesman, which found that in identical twins (monozygotic, MZ) who share 100% of their DNA, the concordance rate (the rate that one twin will develop schizophrenia if the other twin also has the disorder) is 48%. This is significantly higher than non-identical twins (dizygotic, DZ), who share only 50% of their DNA. The concordance rate for DZ twins was 17%.
This study suggests that there must be a genetic component in the development of schizophrenia. However, it is unlikely that schizophrenia is entirely genetic, as the concordance rate for MZ twins was not 100%.
Another biological explanation for schizophrenia is the dopamine hypothesis. The dopamine hypothesis states that schizophrenia results from an imbalance of the neurotransmitter dopamine in the brain.
Neurotransmitters are chemicals that allow the brain to transmit messages between neurons.
Small, specialized receptors receive them, and there are different types for each neurotransmitter. Dopamine is a neurotransmitter associated with the reward system in our brain and some areas of the brain that are important for speech and movement. The dopamine hypothesis states that too much or too little dopamine or dopamine receptors in the brain develop schizophrenia.
Too much dopamine is associated with positive symptoms such as hallucinations and delusions. Too little dopamine is related to negative symptoms such as poor speech.
Neural correlates is a term used when a particular structural difference in the brain is associated with a psychological disorder. Concerning schizophrenia, the main neural correlate we focus on is the difference in ventricle size between schizophrenic and control participants.
Ventricles are small hollow vessels in the brain that transport cerebrospinal fluid to, from, and around the brain.
The cerebrospinal fluid helps supply the brain with vital nutrients and also helps remove toxins and waste products from the brain. A 2002 study by Torrey found that the ventricles of schizophrenia patients are on average 15% larger than those of people without schizophrenia.
The dopamine hypothesis and its evidence support the biological approach to schizophrenia because it shows that biological factors such as brain structure can influence the onset of schizophrenia.
Here are some critical studies that support the idea that biological factors have at least some influence on the development of schizophrenia. Many of these studies are discussed in more detail in our articles on individual biological explanations of schizophrenia.
Gottesman (1991) determined using the twin study mentioned earlier, that there must be a genetic component to schizophrenia. Since MZ twins had higher concordance rates than DZ twins and other family members, it was demonstrated that genetics must have some influence.
According to Tienari et al. (2004), adopted children with schizophrenic biological mothers were more likely to develop schizophrenia than control participants. A genetic (i.e., biological) component to schizophrenia is thus also suggested.
This study found that people with schizophrenia had more dopamine receptors in their brains on post-mortem examination than control participants, supporting the dopamine hypothesis. This supports the biological approach as the dopamine hypothesis provides a biological explanation for schizophrenia.
Suddath et al. (1990) found differences in ventricle size in 12 out of 15 pairs of twins, one of which had schizophrenia, and the other did not. This supports the biological approach, as it clearly shows how a biological factor (eg, brain structure) presents differently in people with and without mental disorders.
In evaluating biological explanations for schizophrenia, we ought to consider their main limitations. Let us have a look.
Biological explanations such as those in this article are usually deterministic.
Deterministic research and theories are characterized by the idea that factors we cannot choose control our thoughts and behaviour.
Biological determinism states that we cannot choose our neurobiology and how it shapes our thoughts and behaviour, just as we cannot choose the color of our eyes or skin colour. This is a limited view because it contradicts our typical societal belief that we have free will and can control our actions. Without this belief, our justice systems and other ways in which our society functions would not work.
Biological explanations of schizophrenia are evidence of biological determinism. They assume that biological factors (e.g., our genes or brain structure) determine schizophrenia, which does not consider free will.
Biological approaches often favour the side of ‘nature’ in the ‘nature vs nurture’ debate. The ‘nature’ side of this debate holds that people’s behaviour is due to their nature (biological factors, evolutionary factors, etc.) rather than how they were raised (education, external factors, life experience).
Twin studies of schizophrenia show that we cannot rely entirely on nature’s explanation. The concordance rate in identical twins (sharing 100% of DNA) was not 100% (Gottesman 1991), suggesting that there must be some influence from external factors.
A significant application of these biological explanations is antipsychotic drugs. These drugs are widely used to help schizophrenic patients manage their symptoms through typical and atypical antipsychotic drugs. Antipsychotics can help patients regain control of their daily lives, improve their quality of life, and in some cases, support non-biological treatment plans. However, they do not ‘cure’ schizophrenia.
There are three primary biological explanations for schizophrenia: genetics, neural correlates, and the dopamine hypothesis.
The genetic explanation states that schizophrenia tends to run in families.
The dopamine hypothesis states that schizophrenia results from an imbalance of the neurotransmitter dopamine in the brain.
Neural correlates is the idea that specific structural differences in the brain are associated with schizophrenia.
There is much research on biological approaches, but they do not fully explain how and why schizophrenia develops.
We can narrow down the biological causes of schizophrenia to three potential explanations:
Schizophrenia has both biological and psychological causes. People can be genetically predisposed to developing schizophrenia and have structural and chemical differences in their brains. However, they can also be more susceptible to developing schizophrenia due to psychological reasons. For instance, hostile family environments, dysfunctional thought processing issues (e.g., faulty attention systems) and issues with central control and meta-representation are also associated with developing and maintaining schizophrenia.
It is somewhat reductionist since it dismantles the complex disorder and states that simple components such as genetics cause schizophrenia. Reductionism often offers physiological explanations without considering all the variables that have been proven to influence disorders such as schizophrenia.
The three biological risk factors for schizophrenia are genetic predispositions, such as schizophrenia running in the family, neural correlates (differences in brain structure), and dopamine imbalances.
Dopamine is both an excitatory and inhibitory neurotransmitter. When too much dopamine exists in the limbic regions of the brain, it increases the activation of dopamine two receptors (D2), and positive symptoms such as hallucinations begin to develop. Similarly, negative symptoms develop when the function of dopamine receptors is reduced in the prefrontal cortex.
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