In this abnormal psychology episode of The Psychology World Podcast, we’re going to be looking at What Causes Schizophrenia? This is a great clinical psychology topic you’ll love.
This episode has been sponsored by Abnormal Psychology: The Causes and Treatments for Depression, Anxiety and More Third Edition. Available on all major eBook retailers and you get order the paperback, large print and hardback copies from Amazon, your local bookstore or your local library.
Clinical Psychology: What Causes Schizophrenia?
There are a lot of different causes of Schizophrenia and there is no one cause so everything below; for lack of a better term; interacts together to cause the condition.
The Dopamine Hypothesis:
This hypothesis was proposed by Meltzer & Stahl (1976) and they thought schizophrenia was caused by excess activity of dopamine synapses in certain areas of the brain.
This I think is interesting since we tend to associate dopamine with positive behaviours so the thought that dopamine can do us harm is weird at first. Yet in Biological Psychology I discuss how much damage various neurotransmitters can do to us.
So, this hypothesis is interesting, to say the least.
Furthermore, this hypothesis is supported by several key pieces of evidence. For example, drugs that provoke a similar state to schizophrenia (like amphetamines) increase stimulation of dopamine synapses. (Martinez et al, 2007) Meaning there’s a link between stimulation of the synapses and schizophrenia.
Additionally, drugs that alleviate schizophrenia block postsynaptic dopamine receptors. (Dimitilis & Shanker, 2016) and drugs that are the most effective at blocking dopamine receptors also are the most effective against schizophrenia.
Overall, this evidence provides good evidence for this theory and I quite like the hypothesis since it’s logical and it makes sense.
However, there is evidence against this hypothesis. Such as: drugs that block postsynaptic dopamine receptors don’t always alleviate schizophrenia for all patients, and there are inconsistent results about the measurements of dopamine or its metabolites.
On the whole, I want to add that this hypothesis is quite good but it’s similar to the serotonin hypothesis in depression. Because it’s just a biological factor and it doesn’t take the cognitive or social factors into account.
The Glutamate hypothesis:
Another biological hypothesis for the cause of schizophrenia is the Glutamate hypothesis proposed by Moghaddam & Javitt (2012). This propose schizophrenia is partially caused by a lack of Glutamate activity.
This is a problem because Glutamate inhibits dopamine release so this hypothesis builds upon the dopamine hypothesis and explains why the excess dopamine levels occur.
Saying that the lack of Glutamate activity occurs because Phencyclidine blocks the glutamate synapses. Preventing it from being released into the synaptic gap. (Murray, 2002) as well as Schizophrenia is associated with lower than normal release of glutamate and fewer receptors in the prefrontal cortex and hippocampus (Harrison et al., 2003)
Leading to this interaction of both positive and negative symptoms of schizophrenia.
Especially, in people already predisposed to the condition.
Overall, I believe these two hypotheses largely build upon one another and these are good explanations for the biological explanation of schizophrenia.
Genetic and Prenatal Factors:
For a long time, schizophrenia has been known to run in families. As supported by Andreasen and Black (1996) as it found that a sibling of a person with schizophrenia is four times more likely to develop schizophrenia than the general population.
Nevertheless, there are always problems with the research.
However, whilst the evidence above could be perceived to be down to environmental factors.
The results from twin studies show that the likelihood of identical twins developing schizophrenia if the other twin has it is between 41%- 65% and 6%-28% for non-identical twins. (Cardno and Gottesman, 2000)
In addition, genetics aren’t the only possible cause of schizophrenia as prenatal influences; influences during pregnancy; can cause schizophrenia as well.
Such as prenatal influences include a diminished supply of oxygen to the brain as well as a number of prenatal infections can contribute to schizophrenia.
Furthermore, the evidence suggests that schizophrenia is a neurodevelopmental disorder. Meaning that from a young age the brain doesn’t develop as it’s meant to; also this means that schizophrenia could be detected in early adulthood.
Finally, stress is another contributing factor to the development of schizophrenia as explained in the introduction. Stress can trigger a genetic disposition to cause a condition.
This explains the higher prevalence of schizophrenia in people with a lower socioeconomic status.
Other biological causes of schizophrenia include:
· Poor nutrition for mother
· Extreme maternal stress during pregnancy
· Season of birth effect
· Viral infections and influenzas.
· Premature birth, low birth weight and complications in delivery.
In addition, to the biological causes of this condition, a new line of thinking is starting to develop to consider there might be a neurodevelopmental cause of schizophrenia. Yet it isn’t firmly established currently.
For instance, some psychologists believe damage to an infant’s dorsolateral prefrontal cortex could be a factor. Since at one year old there is little effect of the brain lesion, as well as infants perform as well as undamaged monkeys when performing tasks.
However, at 2 years old, the effects of the lesion are clear and the 2-year-old infant performs a lot worse than undamaged monkeys.
I really hoped you enjoyed this clinical psychology episode. If you want to support the podcast, please check out the following links:
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Abnormal Psychology Reference:
Whiteley, C (2021) Abnormal Psychology: The Causes and Treatments of Depression, Anxiety and More Third Edition, CGD Publishing
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