The World Health Organization recognizes schizophrenia as a widespread disorder affecting numerous people world wide. The International Classification of Diseases and Health Related Problems is a publication of the World Health Organization in which recognized psychological disorders are listed and briefly described. The description provided for schizophrenia states that, affected persons suffer from a distortion in thinking and perception. Common symptoms include hallucinations, usually auditory in nature, and delusions, commonly manifested in the patient believing there is a plot against them. According to the Diagnostic and Statistical Manual (DSM) disorganized behavior and speech that exist for a prolonged period of time are also common symptoms. The DSM identifies the usual age of onset around adolescence to early adulthood and a stressful event or events are viewed as the preliminary cause of a schizophrenic episode. The etiology of schizophrenia has been explained using the diathesis-stress modelfor over 30 years (Walker & Diforio, 1997).
Numerous theories have been developed in an attempt to explain the etiology of schizophrenia. The diathesis-stress model stands out from other theories because of its integration of both the nature and nurture viewpoints. The nature aspect of the model says that there is a genetic deficit in persons with schizophrenia that leads to a vulnerability or oversensitivity to stress. The nurture aspect has to do with the amount of stress that the vulnerable person is exposed to (Rosenthal, 1970). Past research generally separates stress into two categories, prenatal stress and postnatal stress (Read, Perry, Moskowitz & Connolly, 2001). Prenatal stress generally refers to the biological or nature related aspects of the model, while, postnatal stress refers to the environmental or nurture aspects. The following review of research will make clear how nature and nurture related stressors result in the behavioral manifestation of schizophrenia in persons who are biologically at risk for developing the disorder; or in other words the effectiveness of the diathesis-stress model in explaining the etiology of schizophrenia.
The Biological Threat of Developing Schizophrenia Explained by Prenatal Stress
Schizophrenia is a biologically based mental disorder (Chua & Murray, 1996). When a person is exposed to stressors their neuroendocrine and autonomic nervous systems are activated. In schizophrenia these systems are overactive leading to an imbalance. The hypothalamic-pituitary-adrenal-axis (HPA) is affected by this imbalance resulting in the release of excessive amounts of glucocorticoid. The glucocorticoid reacts with the hippocampus which is in charge of adjusting the activation of the HPA (Jones & Fernyhough, 2007). Hippocampal damage is common in schizophrenia and is due to the neurotoxic effect of excessive glutamate which results from the high glucocoricoid levels (Walker & Diforio, 1997). Persistent heightened levels of glucocorticoid can cause a decrease in the activity of the negative feedback system. In other words, the HPA always receives signals to activate but never receives a signal to stop when the stressor is gone (Sapolsky, 1992). Because the HPA is overactive in persons with schizophrenia they become overly sensitive to stressors, that is, their bodies react easily to stress. Normal adults who experience stressors over a prolonged period of time habituate to that stressor. However, research has shown that prenatal and early childhood stressors often lead to sensitization rather then habituation.
Excessive glucocorticoid exposure while in the womb has been show to cause hippocampus damage and hinder its proper development (Walker et. al, 1997). An expecting mother does not herself have to be a schizophrenic; she just has to be presented with a series of stressful events that lead to increased dopamine activity. Research in this area has focused primarily on animal subjects due to ethical constraints. Walker and Diforio (1997) reported that in a study accomplished by using newborn infants there were significantly higher cortisol levels and lower hippocampal activity in some infants as compared to others. A damaged hippocampus or one with less than average volume is commonly found in schizophrenic patients (Bogerts, Meerz, & Schonfeldt-Bausch, 1985). It follows that prenatal stressors leading to irregular hippocampal development result in children with a biological predisposition to develop schizophrenia. Excessive glucocorticoid is just one example of a prenatal stressor. Others such as viral infection, nutritional deficiency, RH factor incompatibility and hypoxia are thought be influential as well, further research is still needed to be certain.
Postnatal Stressors the Environmental Vulnerability to Schizophrenia
There are certain experiences in early childhood that have been linked to a higher prevalence of schizophrenia later in life. This is because the brain, along with the rest of the nervous system, is still developing in early childhood. People diagnosed with schizophrenia often report being abused as children. Recent studies have found that the abnormal neurobiological structure found in schizophrenia can be explained by the effects of traumatic events on a child’s neurodevelopment (Read, et al., 2001). In fact, traumatic events such as child abuse produce the same type of biological effects that pre natal stressors produce. Psychotic experiences are more common in people who have experienced trauma or abuse in their life (Kinderman et. al. 2000). Persons who have suffered from child sexual or physical abuse are significantly more likely to experience hearing voices, visual hallucinations, thoughts of reading others minds, and paranoid delusions (Ross, Anderson, & Clark, 1994). Neurodevelopment continues throughout childhood and stressors in childhood affect the HPA axis in the same way that they affect an unborn fetus. The HPA axis is supposed to be self-regulatory, that is, it is supposed to return to its baseline level when a stressor is no longer present. Repeated stressors or a single severe stressor can change the HPA axis baseline so that it will have a higher level of response in the future (Read, et. al, 2001). Heim et al. (2000) found that “hypothalamic-pituitary-adrenal axis and autonomic nervous system hyperreactivity, presumably due to cortical releasing factor hypersecretion, is a persistent consequence of childhood abuse that may contribute to the diathesis for adulthood psychopathological conditions” (Pg. 593). As mentioned before this increased activity of the HPA axis leads to hippocampus damage and may explain the schizophrenic episodes experienced by victims of child abuse.
Understanding How Prenatal and Postnatal Stressors Interact
Comparing the effects of prenatal and postnatal stressors will aid with a complete understanding of the diathesis-stress-model. The model can be broken down into three parts, external factors, neural mechanisms and behavioral outcome. External factors would be prenatal stressors or insults, and psychosocial stress, also known as a postnatal stressor. If the external factor was a prenatal stressor the hippocampal structure and or function are damaged. If the external factor was a psychosocial stressor the HPA axis activation level will be altered and cortisol release will increase. In the prenatal stressor condition the hippocampal abnormality causes the HPA axis to change reactivity and increases cortisol levels. In the postnatal condition since the HPA axis and cortisol levels are already affected they will result in the damage of the hippocampus. Both external factors lead to disturbances in the neural mechanisms the main difference is the order in which they are affected. Once the mechanisms previously mentioned have been altered the subcortical dopamine system is activated. It is the excessive activation of the dopamine system that leads to the behavioral outcome of schizophrenic behaviors episodes (Walker, et. al, 1997).
Conclusion
The diathesis-model provides some hope for the future prevention of schizophrenia. Hope lies in the fact that psychosocial stressors experienced by children can be, if not prevented, at least lessened. During such a crucial time of neurodevelopment children need a nurturing environment free of traumatic stressors such as abuse and neglect. If a child has been subjected to trauma cognitive or behavioral therapy to help the child respond in an emotionally and biologically appropriate way may lessen the likelihood they will become a victim of adult onset schizophrenia. This of course is an idea that will require further research. The prenatal stressor or nature aspect of the diathesis-stress-model provides less hope due to the fact that biologically the person is considered at risk from birth. Walker et al (1997) reported that the longer Schizophrenia was left untreated the less effective medicine was at helping the symptoms. In other words, the high activity level of the dopaminergic system in the brain when left for a prolonged period of time does more permanent damage. In this respect knowing the symptoms associated with prenatal stressors would allow for doctors to test infants and either start treatment early or at least monitor the child closely. The diathesis-stress-model does not take into account the effects that illegal drugs have on the brain and it focuses very little on the effect that personality differences can have in the way different persons handles stress. In general it is a good starting point in understanding the etiology from the nature and nurture viewpoints. It has been supported by countless research studies and I would encourage researchers to now expand on the basic ideas of the model including aspects of social psychology and personality psychology.
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