A model of psychopathology in which the emergence of psychological disorders results from an interaction between an individual’s inherent vulnerability for developing the disorder and the individual’s experience of stressful events.
The diathesis-stress model of psychopathology is a framework for understanding the development of psychological disorders. According to the general model, each individual possesses some degree of inherent vulnerability (i.e., diathesis) for developing a given disorder. Onset of a disorder can then be triggered by environmental stress; however, the amount or intensity of stress required to trigger a disorder depends on the extent to which the individual is inherently vulnerable. For example, the greater an individual’s vulnerability to a disorder, the smaller the amount of stress needed to trigger the development of the disorder. This interaction between diathesis and stress can help to explain why some individuals develop a disorder while others do not.
Although both stress and vulnerability factors have long been associated with the development of psychopathology, the two components were not integrated within a unified model of psychopathology until theories of schizophrenia were proposed in the 1960s (e.g., Meehl 1962). According to Meehl’s model of schizophrenia, an inherited genetic vulnerability (which he termed schizotaxia) predisposes individuals to develop a schizotypic personality which has the potential of decompensating into clinical schizophrenia. Meehl believed that schizophrenia would only manifest in a small subset of these individuals. Specifically, he proposed that decompensation is more likely to occur in the presence of additional inherited risk factors (e.g., anxiety-proneness) and an unfavorable social environment. As such, Meehl’s model suggests that schizophrenia results from an interaction between individuals’ inherited characteristics and their environmental experiences.
Within the context of schizophrenia, the conceptualization of a diathesis-stress interaction was further developed by Bleuler (1963) and Rosenthal (1963). Contrary to the earlier belief that there was a single cause of the disorder, Bleuler (1963) proposed that the development of schizophrenia is caused by the interaction between various dispositional factors and environmental stressors. According to this conceptualization, while all individuals possess some degree of inherent vulnerability, development of schizophrenia will occur only if environmental factors cause sufficient stress to trigger the onset of the disorder. Furthermore, Bleuler (1963) stated that the onset of schizophrenia may be triggered by “a disharmonic personality which creates disharmonic and dissociated human relations” (p. 950). In other words, dispositional factors can influence the individual’s environment in such a way that contributes to the development of the disorder.
Since its original conceptualization, the diathesis-stress stress model has since been adapted to theories of other types of psychopathology, such as depression (Monroe and Simons 1991) and post-traumatic stress disorder (McKeever and Huff 2003). Furthermore, while the diathesis component originally referred to a biologically based vulnerability, the definition has been broadened in more recent models to include various psychological and social factors (Monroe and Simons 1991).
Sullivan et al. (2003) conducted a meta-analysis to examine the impact of genetic and environmental factors on liability to schizophrenia. Based on published results from twelve twin studies of schizophrenia, Sullivan et al. (2003) found a heritability estimate of 81%, indicating a strong genetic component associated with the disorder. In addition, they found a small but significant effect of shared environmental factors, thus supporting the view that the development of schizophrenia is influenced by both genetic and environmental factors.
Diathesis-stress interactions have also been demonstrated in relation to other types of psychopathology. For example, Kendler et al. (1995) found that genetic risk and stressful life interacted to predict the onset of major depressive episodes in a study of female-female twin pairs. Specifically, in comparison to individuals with low genetic risk, individuals with high genetic risk were significantly more likely to develop depression after experiencing a stressful life event. In addition to a significant interaction, their results also indicated that genetic risk predicted depression onset even in the absence of stressful life events, and that stressful life events predicted depression onset across all levels of genetic risk. The authors concluded that individuals at higher genetic risk are more vulnerable to the depressive effects of stressful life events.
Although the diathesis-stress model provides a valuable conceptual framework for developing theories of psychopathology, the general model alone may represent an overly simplistic view of how psychological disorders develop. Monroe and Simons (1991) outlined several notable limitations of the original model. For instance, early diathesis-stress models assumed that a disorder manifests when stress activates a diathesis. Such models did not adequately consider how the diathesis might influence stress, or how the diathesis and stress might interact over time. Furthermore, the general model does not specify the types of diatheses and stressors that are most relevant for the prediction of a given disorder. Due to the loosely defined terminology, Monroe and Simons recommended that researchers develop empirically based hypotheses regarding the specific nature of diathesis-stress interactions for a given disorder. In regards to defining stress, Monroe and Simons emphasized the importance of differentiating between different types of life stress and determining which types are most likely to trigger the onset of a given disorder.
The diathesis-stress model posits that psychological disorders result from an interaction between inherent vulnerability and environmental stressors. Such interactions between dispositional and environmental factors have been demonstrated in psychopathology research. Despite limitations of the general model, the diathesis-stress framework continues to be a valuable heuristic that can be used to further develop etiological theories of psychopathology.
- Kendler, K. S., Kessler, R. C., Walters, E. E., MacLean, C., Neale, M. C., Heath, A. C., & Eaves, L. J. (1995). Stressful life events, genetic liability, and onset of an episode of major depression in women. The American Journal of Psychiatry, 152(6), 833–842. https://doi.org/10.1176/ajp.152.6.833.CrossRefPubMedGoogle Scholar
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