Explanations for schizophrenia (Schizophrenia Model Answers) (Paper 3 Model Answers)

Describe and evaluate biological explanations of schizophrenia ( 16 marks) 

The biological explanation of schizophrenia encompasses components such as candidate genes and the dopamine hypothesis. Dopamine, an important neurotransmitter, functions differently in the brains of individuals with schizophrenia. Schizophrenics exhibit abnormally high numbers of D2 receptors in their neurons, resulting in increased dopamine binding and neuronal firing. These disturbances in dopamine functioning can impact attention, perception, and thoughts, potentially leading to disordered thinking. Hyperdopaminergia, characterized by high levels or activity of dopamine in the subcortex, may manifest as symptoms like speech poverty or auditory hallucinations. On the other hand, hypodopaminergia in the prefrontal cortex, responsible for thinking and decision making, has been associated with the negative symptoms of schizophrenia, such as avolition.

Genetic factors also play a role in the development of schizophrenia, as evidenced by Gottesman's investigation, which revealed genetic similarities among family members associated with the likelihood of developing the disorder. For instance, first-degree relatives like identical twins, who share 100% of the same genes, have a 48% chance of developing schizophrenia, while second-degree relatives like grandchildren, who share 25% of genes, have a 5% chance. These findings suggest the presence of candidate genes that increase the risk of inheritance, and the closer the degree of genetic relatedness, the higher the likelihood of developing schizophrenia. Studies by Tienari et al and Ripke et al further support the genetic vulnerability to schizophrenia, providing substantial evidence for the influence of genetic factors.

However, one evaluation of the biological explanation of schizophrenia is that it is overly reductionist. The explanation simplifies the complex processes of schizophrenia, focusing mainly on neural correlations and overlooking potential environmental factors. This limited perspective fails to consider the broader context in which schizophrenia emerges. Another issue with the dopamine hypothesis is its reliance on correlational evidence, preventing causal inferences. The question of whether excess dopamine causes schizophrenia or schizophrenia leads to an excess of dopamine remains unanswered, indicating an incomplete explanation. Moreover, factors such as drug abuse can impact dopamine levels, adding further complexity to the relationship between dopamine and schizophrenia.

Additionally, there is mixed support for the dopamine hypothesis. While drugs like amphetamines and antipsychotics provide some evidence, they can induce schizophrenic symptoms. For example, L-Dopa, used to treat Parkinson's disease caused by dopamine deficiency, can trigger schizophrenic symptoms in individuals without a history of schizophrenia. This indicates that dopamine alone cannot offer a comprehensive explanation, as other factors, including candidate genes coding for the production of other neurotransmitters like glutamate, are involved.

Overall, the biological explanation of schizophrenia provides valuable insights into the role of genetic and neurotransmitter factors, particularly dopamine. However, it is important to recognize the limitations of this explanation, including its reductionist nature, the reliance on correlational evidence, and the existence of other contributing factors beyond dopamine. A more comprehensive understanding of schizophrenia necessitates considering the interplay between biological, environmental, and psychological factors.

 

Describe the interactionist approach to both explain schizophrenia and as a treatment for schizophrenia (16)

Model Answer

The interactionist approach offers an explanation of schizophrenia as a combination of genetic vulnerability and a triggering stressor, known as the diathesis-stress model. The original diathesis model, proposed by Meehl, attributed schizophrenia solely to a biological cause, specifically the presence of a "schizogene." According to this model, individuals who were not genetically vulnerable would not develop schizophrenia, regardless of the amount of stress they experienced.

However, a limitation of the original model is its oversimplified nature. It is now understood that multiple genes contribute to an increased vulnerability to schizophrenia. There is no single gene that serves as the sole cause of the illness, as recognized in the modern understanding of the diathesis-stress model. This limitation highlights the weakness of the original model and the strength of the updated approach.

In the contemporary understanding of vulnerability (diathesis), it is acknowledged that there is no specific "schizogene" as initially proposed by Meehl. Instead, there are numerous genes that can increase the risk of developing schizophrenia. Research by Ripke et al. identified 108 variations in genetic coding associated with the condition. Additionally, vulnerability may also stem from childhood trauma, such as sexual abuse. The modern understanding also considers the role of the hypothalamic-pituitary-adrenal system, which, when overactive, may increase the likelihood of stress-related factors in developing schizophrenia.

Moreover, the current understanding of stress emphasizes its interaction with genetic vulnerability, as it can act as a trigger for schizophrenia. Houston et al. found that cannabis use, for instance, functions as a stressor and significantly increases the likelihood of developing schizophrenia, as it interferes with the dopamine system.

Turkington et al. suggest that a combination of treatments, including medications and cognitive-behavioral therapy (CBT), should be employed for more effective results. However, the successful implementation of this approach relies on adopting an interactionist perspective. While the USA primarily relies on drug treatments alone, the UK combines drugs with CBT.

One strength of the interactionist approach is its effectiveness as a treatment. Tarrier et al. conducted a study where patients were randomly assigned to different groups receiving medications, therapies, or a control group with medication only. The results showed that patients in the combined treatment group exhibited lower symptoms compared to those in the control group. This finding demonstrates the practical advantage of applying an interactionist approach that combines multiple treatments for improved outcomes.

Another strength of the interactionist approach is its consideration of vulnerability. For example, Tienari et al.'s research on Finnish adoptees revealed that genetic vulnerability from biological parents, combined with stressors from adoptive families, could trigger schizophrenia. This finding supports the interactionist approach by highlighting that the presence of both stress and genetic vulnerability increases the likelihood of developing schizophrenia.

However, a weakness of the interactionist approach is the lack of understanding regarding the mechanisms through which the diathesis-stress model operates. For instance, the specific process by which schizophrenia manifests and how vulnerability and stress "interact" to produce symptoms remains unknown. This limitation reduces the explanatory validity of the interactionist approach, as it provides limited information about the causal mechanisms of schizophrenia in relation to genetic vulnerability and stress.

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