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 dysfunction or failure exists in that structure, what effects will that have on our brains? Biological explanations for schizophrenia explore the various aspects of schizophrenia from a biological perspective, including investigating a genetic basis, the dopamine hypothesis, and neural correlates.
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Jetzt kostenlos anmeldenHow 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 dysfunction or failure exists in that structure, what effects will that have on our brains? Biological explanations for schizophrenia explore the various aspects of schizophrenia from a biological perspective, including investigating a genetic basis, the dopamine hypothesis, and neural correlates.
Fig. 1 - Schizophrenia has biological explanations, Joshua Fuller
Research suggests that schizophrenia may have a biological cause. Biological causes and explanations for schizophrenia, therefore, focus on our biology, including our genes, the dopamine hypothesis, and neural correlates. Biological explanations assume that our thoughts and behaviours are due to certain aspects of our biology.
One explanation for schizophrenia is that it may have a genetic basis. Schizophrenia tends to run in families. A genetic argument 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.
Gottesman (1991) supports the genetic predisposition argument. Gottesman (1991) 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%.
The result 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%.
Fig. 2 - Schizophrenia is a polygenic disorder.
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, specialised receptors receive them, and each neurotransmitter has different types. 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.
Hallucinations can be vivid and manifest in an auditory or visual way. To patients, these hallucinations are as real as anything those who don't have schizophrenia see in the world.
Researchers argue that the dopamine hypothesis is often associated with the positive symptoms of schizophrenia, including hallucinations. Too much dopamine in the limbic system increases the activation of dopamine 2 receptors (D2), and too little dopamine in different areas of the brain can result in negative symptoms. Dopamine imbalances may manifest as visual or auditory hallucinations for patients, depending on the area of the brain it affects.
Neural correlates describe 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. Torrey (2002) found that the ventricles of schizophrenia patients are, on average, 15% larger than those 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, Gottesman (1991) demonstrated that genetics must have some influence.
According to Tienari et al. (2004), adopted children with schizophrenic biological mothers were likelier to develop schizophrenia than control participants. A genetic (i.e., biological) component to schizophrenia is thus also suggested. They suggested children raised in an adverse environment with these biological links were more likely to develop schizophrenia than adopted children with no biological links.
Seeman and Kapur (2000) found that people with schizophrenia had more dopamine receptors in their brains on post-mortem examination than control participants, supporting the dopamine hypothesis. Seeman and Kapur (2000) support 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. Suddath et al. (1990) support the biological approach, as it clearly shows how a biological factor (eg, brain structure) presents differently in people with and without mental disorders.
Fig. 3 - There is a genetic component to schizophrenia.
The biological and psychological explanations for schizophrenia share and disagree on various aspects of the arguments for what causes schizophrenia.
While the biological explanation tends to focus on the genetic basis of schizophrenia, the dopamine hypothesis, and neural correlates, the psychological explanation for schizophrenia focuses more on family dysfunctions and cognitive explanations.
Interestingly, although the psychological explanation for schizophrenia explores how family environments and relationships can facilitate the development of schizophrenia in individuals, the theories acknowledge a genetic or biological vulnerability needs to exist more often than not in these individuals for schizophrenia to occur. The explanations highlight the biological and psychological similarities in the explanation for schizophrenia.
In evaluating biological explanations for schizophrenia, we ought to consider their main limitations. Let us have a look.
Biological explanations can be deterministic.
Deterministic research and theories are characterised 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 colour of our eyes or skin colour. Biological deterministic explanations are 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 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 their upbringing (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, supported by twin and adoption studies. Schizophrenia is a polygenic disorder.
The dopamine hypothesis states that schizophrenia results from an imbalance of the neurotransmitter dopamine in the brain.
Neural correlates suggest 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, and psychological explanations for schizophrenia highlight how the environment can impact the development of schizophrenia.
We can narrow down the biological causes of schizophrenia to three potential explanations:
Schizophrenia has both biological and psychological explanations. 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 and dysfunctional thought processing issues (e.g., faulty attention systems) 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.
What is dopamine?
A neurotransmitter associated with the rewards system of our brains.
What is a synapse?
A small gap between neurons across which messages are fired through neurotransmitters.
Issues with dopamine production in the ________ nigra contributes to symptoms of schizophrenia.
substantia.
What did Farde et al. (1990) find in their study into the dopamine hypothesis?
No difference in dopamine (D2) receptor levels between schizophrenic and non-schizophrenic participants.
The dopamine hypothesis is a deterministic theory. Why is this a limitation?
Deterministic theories have their limitations, as they are not compatible with societal notions of responsibility and self-control, on which many of our legal and moral norms are based.
How does Parkinson's treatment, L-Dopa, support the dopamine hypothesis?
Some patients are given levodopa (L-Dopa) when treating Parkinson’s disease, a drug that increases dopamine levels in the brain. These patients are reported to experience psychotic side effects similar to schizophrenia symptoms. This supports the role that dopamine plays in the development of schizophrenic symptoms.
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