Understanding Schizophrenia Based on the Biopsychosocial Model

In this article, schizophrenia and its onset are discussed on the basis of the biopsychosocial model. Schizophrenia is a serious mental illness “that causes people to lose contact with reality” (Comer, 2010, p. 25). People with schizophrenia often illustrate bizarre behavior accompanied with distorted mind, disorganized perceptions, or withdrawn emotions. Their neurocognitive deficits aggravate over time (Seidman et al., 2012). Common symptoms of schizophrenia, either positive or negative, as listed by Comer (2010) include “hallucinations, delusions, disorganization, abnormal movements, restricted emotional expression, avolition, impaired cognition, depression, and mania” (p. 445).

In tradition, the biomedical model is commonly used by scientists to study diseases and disorders with emphasis on individuals’ biological factors including the genetic materials and physiological function and structure. Today many researchers have come to recognize that aspects of individuals such as their histories, social relationships, lifestyles, personalities, mental processes, and biological processes should be considered in a full conceptualization of risk factors for mental disorders. As a result, the biopsychosocial model has emerged as an alternative to the biomedical approach to address holistic aspects of biological, psychological, and social systems each interrelated with and producing changes in the others (Sarafino & Smith, 2011).

The Biopsychosocial Model

The core concept of biopsychosocial model is that abnormal behavior and mental disorder can be understood and treated more completely if considerations are given to the biological, psychological, and sociocultural aspects of a person’s problem rather than only one of them. Based on this model, the biopsychosocial theories have been developed to study mental disorder including schizophrenia. Many studies confirmed that “abnormality results from the interaction of genetic, biological, developmental, emotional, behavioral, cognitive, social, cultural, and societal influences” (Comer, 2010, p. 79).

According to biopsychosocial model, health and illness influence and result from the interplay of biological, psychological, and social aspects of people’s lives. Biopsychosocial model may be thought as an extension of the biomedical model because by adding a person’s background to the biomedical perspective, a different and broader picture of the person’s health and illness can be perceived with connections of biological factors to psychological and social factors (Sarafino & Smith, 2011). The biopsychosocial model weighs all three factors to assess how they affect and interact with people’s health.

Brains of People with Schizophrenia

Two hundred years ago phrenologists raised concerns of localization of functions in the brain. Scientists in the past have identified localization of function on the cortex (Hergenhahn, 2009). Research showed that schizophrenia and other mental disorders may be related to dysfunctions or abnormal structures of localized units of the brain. Based on studies of abnormal brains during last ten years, scientists connected schizophrenia, especially cases dominated by negative symptoms, to structural abnormalities of the brain. From brain images, researchers identified that schizophrenic patients usually have enlarged ventricles, the brain cavities that contain cerebrospinal fluid (Comer, 2010).

Recent studies also linked schizophrenia to abnormalities of the hippocampus, amygdala, and thalamus, among other brain structures. In a study on cortical thickness, gray matter volume, and white matter diffusivity and anisotropy in schizophrenia, Murakami et al. (2011) concluded that schizophrenic patients had significantly decreased hippocampal volume compared with healthy controls and “that progressive hippocampal volume loss occurs in the early course of illness in schizophrenic patients but not in the more chronic stages” (p. 859). Another research by Pinkham (2012) showed that schizophrenia is associated with aberrant brain responses in the neural network involved in cognition-emotion interaction. These findings point to neurophysiological alterations in brain networks associated with cognitive control over emotion processing, which may underlie impairments in many aspects of goal-directed behavior in people with schizophrenia.

Even though psychologists today can associate schizophrenia with disturbances in identifiable brain regions and the chemicals located there, the research of schizophrenia should not be restricted simply to these regions and chemicals (Toates, 2011). As Toates (2011) suggested, further studies should address “the psychological phenomena of schizophrenia, such as apathy and hallucinations, emerge from a whole brain that contains such local disturbances” (p. 12).

The Genetic Factors

In genetic research, scientists found that a biological predisposition to schizophrenia could be inherited by some people who might develop this disorder later when they experience extreme stress, usually during late adolescence or early adulthood. Genetic Factors are often viewed on the basis of principles of the diathesis stress perspective. As Comer (2010) stated, the influence of genetic factors had been confirmed by “studies of (1) relatives of people with schizophrenia, (2) twins with this disorder, (3) people with schizophrenia who are adopted, and (4) genetic linkage and molecular biology” (p. 433).

According to Joober, Boksa, Benkelfat, and Rouleau (2002), researchers have found neither major genes that cause schizophrenia nor a gross neuropathological signature of schizophrenia. However, recent findings in genetic epidemiological research demonstrated additive and interactive genes could only place small effects from each but coherently manifest the genetic vulnerability for schizophrenia. To fully understand the genetics of schizophrenia, Joober et al. (2002) suggested further studies on the complex classic factors in relation to the inheritance of schizophrenia in non-mendelian mode and construction of “a phenotypic definition based on objective, reliable and reproducible measurements” (p. 343).

Taking advantage of salient progress in neuroscience in recent years, scientists have used neuroimaging to study the neurobiological processes that convey the mental disorder risk from the genes to the complex phenotypes. These studies resulted that “schizophrenia is highly heritable with a pattern consistent with both common and rare allelic variants and gene x environment interaction” (Hirvonen & Hietala, 2011, p. 89). In a study of schizophrenic genetics related to neurotransmitters, Hirvonen and Hietala (2011) revealed that people with a risk of schizophrenia share neurotransmitter abnormalities with changes in the dopamine system. Molecular imaging studies have shown that potential intermediate phenotypes that carry the risk for schizophrenia include increased striatal presynaptic synthesis, increased striatal D2 receptors, and increased cortical D1 receptors.

The Environmental Factors

As explained by Solli and Barbosa Da Silva (2012), environmental factors include “life events, interactions in social environments, abuse, neglect, trauma, etc.” (p. 287). Although genetic factors mainly impose an individual’s risk of schizophrenia, the actual onset of schizophrenia may be triggered by multiple environmental factors. Solli and Barbosa Da Silva (2012) further explained that environmental exposures may influence the expression of genes by affecting a number of neurotransmitter systems. Environmental factors can also trigger schizophrenic behavior by disturbing brain functions of hypothalamic-pituitary-adrenal axis, the autonomic nervous system, and the immune system.

When a person’s immune system is impaired by environmental conditions, the immune system dysfunction may play a role in the etiology of schizophrenia and cause an incidence of schizophrenia. According to Richard and Brahm (2012), clinical studies on schizophrenic patients showed that genetic, environmental, and neurobiological factors are related to immunologic influences on schizophrenia. Therefore, the onset of schizophrenia may be prevented or controlled by manipulation of environmental factors to protect and enhance the immune system for individuals with high risk of this disease.

Among environmental factors, unhealthy communication patterns within family have been thought to contribute to psychological problems and mental disorders. Past researches attempted to make connections between particular communication patterns and pathological outcomes in the case of schizophrenia; however these factors had been over-emphasized. For example, early studies introduced theories that schizophrenic symptoms with a child were caused by a family environment where a cold, authoritarian mother dominated an ineffectual father. It was suggested that schizophrenia could eventually occur when a child’s brain functions were disturbed by inescapable mixed-message commands consistently given by parents in this type of environment. Today, these theories are “neither widely held nor empirically supported, especially as findings regarding the biological factors underlying schizophrenia have been strongly established” ((Pomerantz, 2011, p. 351).

Discussion

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.

References

Comer, R. J. (2010). Abnormal psychology (8th ed.). New York, NY: Worth Publishers.

Hergenhahn, B. R. (2009). An introduction to the history of psychology (6th ed.). Mason, OH: Cengage Learning.

Hirvonen, J., & Hietala, J. (2011). Dysfunctional brain networks and genetic risk for schizophrenia: specific neurotransmitter systems. CNS Neuroscience & Therapeutics, 17(2), 89-96. doi:10.1111/j.1755-5949.2010.00223.x

Joober, R., Boksa, P., Benkelfat, C., & Rouleau, G. (2002). Genetics of schizophrenia: from animal models to clinical studies. Journal Of Psychiatry & Neuroscience, 27(5), 336-347.

Murakami, M., Takao, H., Abe, O., Yamasue, H., Sasaki, H., Gonoi, W., & ... Ohtomo, K. (2011). Cortical thickness, gray matter volume, and white matter anisotropy and diffusivity in schizophrenia. Neuroradiology, 53(11), 859-866. doi:10.1007/s00234-010-0830-2

Pinkham, A. E., Sasson, N. J., Beaton, D., Abdi, H., Kohler, C. G., & Penn, D. L. (2012). Qualitatively distinct factors contribute to elevated rates of paranoia in autism and schizophrenia. Journal Of Abnormal Psychology, 121(3), 767-777. doi:10.1037/a0028510

Pomerantz, A. M. (2011). Clinical psychology: Science, practice, and culture (2nd ed.). Thousand Oaks, CA: Sage.

Richard, M. D., & Brahm, N. C. (2012). Schizophrenia and the immune system: Pathophysiology, prevention, and treatment. American Journal Of Health-System Pharmacy, 69(9), 757-766. doi:10.2146/ajhp110271

Sarafino, E. P. & Smith, T. W. (2011). Health psychology: Biopsychosocial interactions (7th ed.). Hoboken, NJ: John Wiley & Sons.

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

Solli, H. M. & Barbosa Da Silva, A.(2012). The Holistic Claims of the Biopsychosocial Conception of WHO’s International Classification of Functioning, Disability, and Health (ICF): A Conceptual Analysis on the Basis of a Pluralistic–Holistic Ontology and Multidimensional View of.. Journal Of Medicine & Philosophy, 37(3), 277-294.

Toates, F. (2011). Biological psychology (3rd ed.). Saddle River, NJ: Pearson Education.

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

Literature Abstract

Introduction

The study by Murakami et al. (2011) was to determine differences in cortical thickness, gray matter volume, and white matter integrity between normal subjects and schizophrenic patients. Gray and white matters were evaluated simultaneously for hypothesized disruption of neural circuits in schizophrenic mechanism with both gray and white matter involved.

Methodology

The research sample includes 21 schizophrenic patients (15 males and 6 females, mean age 32.65) and 21 healthy comparisons with matched ages and genders. Psychiatric symptoms were evaluated using the Positive and Negative Syndrome Scale within 3 days prior to MR scanning. A MRI brain scanner (Signa HDx) was used to acquire T1-weighted images. Cortical thickness and gray matter volume were estimated using FreeSurfer software. White matter was calculated using TBSS software. General linear models were used for analyzing cortical thickness at each vertex. Statistical analyses include ANCOVA for gray matter volume and two t tests for white matter volume.

Results

Research found no significant differences in cortical thickness evaluated for both hemispheres using general linear models at each vertex between schizophrenia and healthy controls. Gray matter volume measurements of hippocampus, amygdala, caudate, pallidum, putamen, and thalamus proper showed that hippocampal volume was significantly smaller in the schizophrenia group (9.75±0.94 mL) than in the healthy control group (10.32±0.77 mL). Voxel-wise analysis for white matter revealed no significant differences in FA, AD, or RD regions between schizophrenia and healthy controls. Stepwise multivariate analysis (independent variables: sex, age, duration; dependent variable: hippocampal volume) revealed positive relationship between hippocampal volume and duration of illness.

Conclusion

Scientists at University of Tokyo assessed gray and white matter changes in schizophrenia patients using combined analyses of cortical thickness, gray matter volume, and white matter diffusivity and anisotropy. They concluded that hippocampal volume decreases in schizophrenic patients and the loss of white matter occurs in early course of schizophrenia.