THE INTERACTIONIST APPROACH TO SCHIZOPHRENIA
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THE IMPORTANCE OF AN INTERACTIONIST APPROACH IN EXPLAINING AND TREATING SCHIZOPHRENIA; THE DIATHESIS-STRESS MODEL
Schizophrenia is often explained using the diathesis-stress model (DSM), which posits that the disorder results from a combination of biological vulnerabilities and environmental stressors. This model views schizophrenia as resulting from damage or dysfunction in specific brain areas involved in language, thought, and cognitive functions. For example, dopamine D2 receptors are implicated in both hyperactivity and hypoactivity in different brain regions, particularly in areas like Broca’s area (associated with language production). These imbalances may contribute to the differences seen in positive symptoms (e.g., hallucinations, delusions) and negative symptoms (e.g., language difficulties, flat affect) in schizophrenia.
The DSM suggests that the causes of this brain dysfunction include a complex interaction of genetic factors, prenatal factors (e.g., infections, malnutrition), birth complications (e.g., hypoxia), and other biological risks. These vulnerabilities interact with environmental stressors such as abuse, bullying, family conflict, or other life stressors, which can trigger or exacerbate the onset of schizophrenia
THE ORIGINAL DIATHESIS-STRESS MODEL
The original diathesis-stress model posits that schizophrenia arises from the interaction between an underlying genetic vulnerability (diathesis) and environmental stressors. Genetic predispositions alone are insufficient to cause schizophrenia; rather, they require environmental triggers to activate them. Twin studies by Gottesman and Shields (1972) demonstrated higher concordance rates for schizophrenia in monozygotic (MZ) twins compared to dizygotic (DZ) twins, reinforcing the genetic component. However, since MZ twins only show a 48% concordance rate, environmental factors must play a crucial role in determining whether the disorder develops.
RISK FACTORS: ORIGINAL MODEL (BIOLOGICAL AND ENVIRONMENTAL)
Biological factors:
Genetic predisposition: Family history of schizophrenia
Perinatal complications: Difficult birth, hypoxia
Prenatal exposure to pathogens: Maternal infections during pregnancy
Abnormal brain structures: Enlarged ventricles, reduced grey matter
Neurochemical imbalances: Dopamine dysregulation
Environmental stressors:
Early childhood trauma: Abuse, neglect
Family dysfunction: Marital schism, high expressed emotion
Substance abuse: Cannabis use, alcohol
Socioeconomic stressors: Poverty, unstable living conditions
Urban living environments: Higher incidence in urban areas
CRITIQUE OF THE ORIGINAL MODEL
The original model simplifies genetic vulnerability, treating it as fixed. It does not account for the complex interplay of epigenetic factors—where genes can be turned on or off by environmental influences—or neuroplasticity, which involves changes in brain structure and function over time. Additionally, the term "stress" is too broad and vague, failing to account for specific types of environmental factors that can activate genetic vulnerabilities.
THE UPDATED DIATHESIS-STRESS MODEL
The updated model recognises that genetic vulnerability is dynamic and subject to change based on environmental influences. This model incorporates research on epigenetics—the process by which environmental factors can switch genes on or off—affecting how they are expressed. Rather than a simple vulnerability-stressor relationship, the updated model considers factors such as negative neuroplasticity, where harmful experiences (like trauma or substance abuse) lead to detrimental changes in the brain's structure and function.
HOW ENVIRONMENTAL RISK FACTORS TURN GENES ON
The key idea in the updated model is that environmental factors do more than simply trigger the onset of schizophrenia—they can actively modify gene expression. This occurs through epigenetic changes, which can be influenced by factors such as abuse, cannabis use, and other stressors. These epigenetic changes alter the way certain genes function, potentially increasing the risk of schizophrenia.
RISK FACTORS: BIOLOGICAL AND PSYCHOLOGICAL
Biological risk factors include those that can affect gene expression during critical periods of brain development, such as:
Cannabis use: Cannabis use in adolescence can increase schizophrenia risk by affecting dopamine signalling through epigenetic changes (Di Forti et al., 2019).
Prenatal infections: Maternal infections, such as influenza during the third trimester, can disrupt foetal brain development, as Brown & Patterson (2011) highlight. These infections can induce epigenetic changes that affect cortical development.
Low vitamin D levels during pregnancy may also impact foetal brain development, increasing schizophrenia risk.
Psychological risk factors focus on trauma and stress:
Trauma and abuse: Chronic childhood trauma, such as abuse, can lead to lasting epigenetic changes in genes associated with the stress response and brain development (Read et al., 2005).
Chronic stress: Prolonged stress alters cortisol regulation and can dysregulate brain regions like the hippocampus, leading to negative plasticity and increased vulnerability to schizophrenia.
CANNABIS USE
Cannabis, particularly in adolescence, has been strongly linked to the development of schizophrenia in individuals with a genetic predisposition. Research suggests that cannabis use can cause epigenetic changes that affect dopamine signalling, a key neurotransmitter involved in schizophrenia. Studies like those by Di Forti et al. (2019) have shown that regular use of high-potency cannabis is associated with a higher risk of developing psychosis.
Cannabis use may also induce negative neuroplasticity, wherein it disrupts normal brain development during adolescence, a critical period for brain maturation. This plasticity, once negatively altered, may lead to lasting changes in dopamine receptor functioning, exacerbating genetic vulnerabilities. In this way, cannabis use can "turn on" or amplify the expression of schizophrenia-related genes by interfering with neurotransmitter systems and brain development.
CHILDHOOD TRAUMA AND ABUSE
Experiencing trauma or abuse during childhood can also influence gene expression through epigenetic mechanisms. Research by Read et al. (2005) found a strong correlation between early life trauma and the later development of psychosis, including schizophrenia. The chronic stress from such experiences can lead to changes in the hypothalamic-pituitary-adrenal (HPA) axis, which regulates the body's response to stress.
Chronic stress and trauma are thought to activate genes linked to schizophrenia by altering the brain’s stress response systems. Prolonged stress may result in dysregulation of cortisol, which affects brain areas like the hippocampus and prefrontal cortex. This interaction between stress and gene expression can lead to negative plasticity, where structural and functional changes in the brain make it more vulnerable to schizophrenia.
EPIGENETICS AND STRESS
Epigenetics explains how genes related to schizophrenia can be switched on by environmental factors like stress. For instance, Tost and Meyer-Lindenberg (2012) found that early life stress alters the epigenetic regulation of genes related to the HPA axis, which controls stress responses. These epigenetic changes may increase an individual’s sensitivity to future stress, making them more likely to develop schizophrenia when exposed to significant stressors later in life.
Maternal stress during pregnancy is also a significant risk factor. Studies have shown that high levels of maternal stress can lead to epigenetic changes in the developing foetus, affecting genes involved in brain development and stress regulation. This prenatal exposure to stress can increase the risk of schizophrenia by predisposing the child to abnormal neurodevelopment.
RETROVIRUSES
Recent research has suggested that retroviruses, which are remnants of ancient viruses embedded in our genome, may be activated by environmental stressors. Keller et al. (2014) proposed that these retroviruses, when activated by stress or infection, may contribute to schizophrenia by affecting neural development or immune responses. These viruses remain dormant in the genome but can be "turned on" under certain conditions, such as stress, leading to brain damage or altered brain function, potentially triggering psychosis.
THE IMPORTANCE OF AN INTERACTIONIST APPROACH IN EXPLAINING AND TREATING SCHIZOPHRENIA
The interactionist approach highlights the dynamic interplay between genetic predispositions and environmental influences in explaining schizophrenia. This approach emphasises the importance of addressing both biological and environmental factors in treatment. For example, treatments should include antipsychotic medications targeting biological dysfunctions (e.g., dopamine imbalances), alongside psychosocial interventions like cognitive-behavioural therapy (CBT) to manage stress and trauma.
REFERENCES
Original Diathesis-Stress Model:
Gottesman, I. I., & Shields, J. (1972). Schizophrenia and Genetics: A Twin Study Vantage Point. Academic Press.
Updated Diathesis-Stress Model:
Brown, A. S., & Patterson, P. H. (2011). The role of maternal infection in schizophrenia risk. Schizophrenia Bulletin, 37(2), 284–290.
Di Forti, M., Quattrone, D., Freeman, T. P., Tripoli, G., Gayer-Anderson, C., & Quigley, H. (2019). The contribution of cannabis use to variation in the incidence of psychotic disorder across Europe. The Lancet Psychiatry, 6(5), 427-436.
Keller, J., Fusar-Poli, P., & Ffytche, D. H. (2014). Epigenetic mechanisms in schizophrenia. Progress in Neuro-Psychopharmacology & Biological Psychiatry, 54, 88-102.
Read, J., van Os, J., Morrison, A. P., & Ross, C. A. (2005). Childhood trauma, psychosis and schizophrenia: A literature review with theoretical and clinical implications. Acta Psychiatrica Scandinavica, 112(5), 330-350.
Tost, H., & Meyer-Lindenberg, A. (2012). Environmental influences in schizophrenia: The role of epigenetics. Schizophrenia Bulletin, 38(3), 432–437.
FURTHER READING
Howes, O. D., & Kapur, S. (2009). The dopamine hypothesis of schizophrenia: Version III—The final common pathway. Schizophrenia Bulletin, 35(3), 549–562.
van Os, J., Kenis, G., & Rutten, B. P. (2010). The environment and schizophrenia. Nature, 468(7321), 203–212.
McGrath, J. J., & Mortensen, P. B. (2020). The interplay between genetics and environmental exposures in schizophrenia. Annual Review of Public Health, 41, 81-101.
