Schizophrenia is a destructive mental illness with no answer to what causes it. In the nineteenth century Wilhelm Wundt postulated that the breakdown of apperception ability could result in schizophrenia (Hergenhanhan, 2009). Today scientists intend to explain mental disorders by considering more than one kind of cause at a time. Using the biopsychosocial model, researchers study biological, psychological, and social factors and their interactions that affect schizophrenic pathology and onset.
Brain research showed that people with schizophrenia suffer abnormalities in certain regions of the brain. For example, the hippocampal volume was found significantly decreased for schizophrenic patients. Such abnormalities may be caused by genetic factors. Although epidemiological studies indicate that schizophrenia is highly heritable, schizophrenia is “neither a purely genetic disorder, nor caused by a single gene” (Hirvonen & Hietala, 2011, p. 89). Instead, both rare and common genetic variants combined with environmental risk factors and their interactions together could probably cause schizophrenia.
Because Schizophrenia is regarded as neurodevelopmental disorder, neurocognitive dysfunction becomes a core component of Schizophrenia (Seidman et al., 2012). From the neuroscience approach, molecular imaging studies provided solid evidences of links between dopaminergic abnormalities and schizophrenia. These studies suggest that dopaminergic mechanisms may function as intermediate phenotypes because similar alterations have been identified in both schizophrenia patients and people at genetic risk but with no expression of the illness.
Genetic scientists found that people could inherit a biological predisposition to schizophrenia but the development of the disorder might be influenced by social and environment factors which impose extreme stress and social conflict during late adolescence or early adulthood. Environment factors may trigger onset schizophrenia in many ways. For instance, an environment condition may weaken a person’s immune system and apply immunologic influences on schizophrenia.
By implementing social and environmental factors, scientists and mental health service providers are able to find new approaches for managing and remedying schizophrenia. For example, therapeutic yoga classes were found to be effective by providing a calm environment, friendly social atmosphere, and regulated routine for schizophrenic inpatients to reduce stress and modulate autonomic nervous system (Visceglia & Lewis, 2011). As concluded by Visceglia and Lewis (2011), yoga therapy resulted in significant outcomes such as reduced psychopathology and improved aspects of quality of life.
In summary, schizophrenia is a complicated mental disease characterized by a diverse set of symptoms and affected by a multifactorial etiology including both environmental and genetic influences. Recent researches indicate that schizophrenia is linked to brain abnormalities, neuropsychological deficit, genetic conditions, and social environment. However, no definite cause has been found to this disorder. Because the onset of schizophrenia may be triggered by interactions of biological, psychological, and social factors together, the biopsychosocial approach is a proper model for understanding and studying schizophrenia. This model may help scientists and care givers better understand, predict, prevent, control, and possibly cure schizophrenia.
Hirvonen, J., & Hietala, J. (2011). Dysfunctional brain networks and genetic risk for schizophrenia: specific neurotransmitter systems. CNS Neuroscience &
Seidman, L. J., Meyer, E. C., Giuliano, A. J., Breiter, H. C., Goldstein, J. M., Kremen, W. S., & ... Faraone, S. V. (2012). Auditory working memory impairments in individuals at familial high risk for schizophrenia. Neuropsychology, 26(3), 288-303. doi:10.1037/a0027970
Visceglia, E., & Lewis, S. (2011). Yoga Therapy as an Adjunctive Treatment for Schizophrenia: A Randomized, Controlled Pilot Study. Journal Of Alternative & Complementary Medicine, 17(7), 601-607. doi:10.1089/acm.2010.0075