Diathesis-Stress Model Research Paper

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The premise underlying the “diathesis-stress” model is that a person is more likely to suffer an illness if he or she has a particular diathesis (i.e., vulnerability or susceptibility) and is under a high level of stress. Diathesis factors that have been studied include family history of substance abuse or mental illness; individual psychological characteristics such as hostility or impulsivity; biological characteristics (e.g., cardiovascular reactivity, hypothalamic-pituitary-adrenal responsivity); and environmental characteristics such as childhood maltreatment or low socioeconomic status. Diathesis factors are generally assumed to be relatively stable but not necessarily permanent.

The term stress refers to events and experiences that may cause psychological distress. Stress can influence mechanisms that help to maintain the stability of an individual’s cognition, physiology, and emotion. Although the notion that stress can influence the development of illness has been held since the mid-nineteenth century, it was not until theories of schizophrenia proposed during the 1960s that the concepts of stress and diathesis were combined. In studies of depression that found empirical support for the model, stress has most commonly been operationalized as having experienced major negative events within the past year.

An implication of the diathesis-stress model is that the greater the vulnerability an individual has, the less stress is required for that individual to become ill. It is necessary to consider both the presence of a diathesis and a person’s level of stress in order to determine the degree of risk for the onset or reoccurrence of an illness. For example, a study of depression showed that among subjects with a diathesis in the form of genetic risk, 10 percent developed depression at low stress levels but 33 percent developed depression at high levels. For those without the diathesis, the figures were 10 percent and 17 percent, respectively.

Other health problems to which the diathesis-stress model has been widely applied include substance use, schizophrenia, and heart disease. Studies have investigated a broad range of both environmental and psychological vulnerabilities, as well as biological vulnerabilities, some of which involve genetic expression. Interest in the role of genetics in disease onset has also led to studies on geneenvironment interaction, which suggest that elevation of disease risk by an environmental factor occurs primarily for individuals with a susceptible genotype.

Empirical support for the applicability of the diathesis-stress model is robust and has warranted preventive interventions targeting those at highest risk of developing negative health outcomes. For example, psychological interventions address the way a person with high vulnerability appraises and responds to stressful life events. Researchers seek to refine measures of vulnerability, provide suggestions for preventive strategies, and gather empirical evidence for the effectiveness of preventive interventions. Overall, the diathesis-stress model has provided researchers and clinicians with a framework in which knowledge about biological, environmental, and psychological processes can be used to decrease the likelihood that an illness will develop or reoccur.


  1. Caspi, Avshalom, Karen Sugden, Terrie E. Moffitt, Alan Taylor, et al. 2003. Influence of Life Stress on Depression: Moderation by a Polymorphism in the 5-HTT Gene. Science 301 (5631): 386–389.
  2. Hankin, Benjamin L., and John R. Z. Abela, eds. 2005. Development of Psychopathology: A Vulnerability-Stress Perspective. Thousand Oaks, CA: Sage.
  3. Monroe, Scott M., and Anne D. Simons. 1991. Diathesis-Stress Theories in the Context of Life Stress Research: Implications for the Depressive Disorders. Psychological Bulletin 110 (3): 406–425.
  4. Scher, Christine D., Rick E. Ingram, and Zindel V. Segal. 2005. Cognitive Reactivity and Vulnerability: Empirical Evaluation of Construct Activation and Cognitive Diathesis in Unipolar Depression. Clinical Psychology Review 25: 487–510.

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