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The Diathesis-Stress Model suggests that psychological disorders arise from the interaction of an underlying vulnerability (diathesis) and external stressors. An individual may have a predisposition to a disorder, but it’s the combination of this vulnerability and adverse life events that triggers its manifestation.
What is Diathesis?
The term “diathesis” comes from the Greek word for disposition (“diathesis”). In the context of the diathesis-stress model, this disposition is a factor that makes it more likely that an individual will develop a disorder following a stressful life event.
A diathesis can be a biological factor, like abnormal variations in one or more genes. But other sorts of factors, even if not genetically hard-wired, can also be considered diatheses so long as they form early on and are stable across a person’s life.
For example, traumatic early life experiences, such as the loss of a parent, can act as longstanding predispositions to a psychological disorder. In addition, personality traits like high neuroticism are sometimes also referred to as diatheses.
Finally, diatheses can be situational factors — like living in a low-income household or having a parent with mental illness (Theodore, 2020).
Some of these factors might matter more for some psychological disorders compared to others (for example, a particular genetic variation might increase one’s risk of developing depression but not schizophrenia).
It’s important to note that not all diatheses are created equal. For example, some genetic variations only slightly increase an individual’s risk of a mental disorder, while others increase one’s risk substantially.
As a result, in the diathesis-stress model, different diatheses give rise to different responses to stress.
To conceptualize this, consider the “cup analogy.” Imagine several cups filled with different amounts of marbles; when water is poured into those cups, the cups with more marbles will overflow more easily.
Diatheses are like marbles, and stress is like water: the greater the diathesis, the less stress is needed to cause “overflow” (i.e., give rise to mental illness) (Theodore, 2020).
Diathesis-Stress Model
The diathesis-stress model is a concept in psychiatry and psychopathology that offers a theory of how psychological disorders emerge.
It intervenes in the debate about “nature vs. nurture” in psychopathology — whether disorders are predominantly caused by innate biological factors (“nature”) or by social and situational factors (“nurture”) — by providing an account of how both might coincide in giving rise to a disorder.
According to the diathesis-stress model, the emergence of a psychological disorder requires first the existence of a diathesis, or an innate predisposition to that disorder in an individual, and second, stress, or a set of challenging life circumstances that trigger the disorder’s development.
Furthermore, individuals with greater innate predispositions to a disorder may require less stress to trigger that disorder, and vice versa.
In this way, the diathesis-stress model explains how psychological disorders might be related to both nature and nurture and how those two components might interact with one another (Broerman, 2017).
The diathesis-stress model is a modern development of a longstanding debate about the causes of mental illness. This debate began as early as ancient Greece and Rome when theories included imbalances in bodily fluids and interactions with the devil.
Later, this evolved into the “nature vs. nurture” debate. By the late 20th century, it became clear that nature interacted with nurture to produce disorder, and the diathesis-stress model came to the forefront (Theodore, 2020).
The model has been useful in explaining why some individuals with biological dispositions to mental illness do not develop a disorder and why some individuals living through stressful life circumstances nonetheless remain psychologically healthy.
It has also opened the door to research into protective factors: positive elements that counteract the effects of diathesis and stress to prevent the onset of a disorder.
Finally, it has proven particularly useful in the context of specific disorders, such as schizophrenia and depression.
Diathesis and Stress Interactions
According to the diathesis-stress model, diatheses interact with stress to bring about mental illness. In this context, “stress” is an umbrella term encompassing any life event that disrupts an individual’s psychological equilibrium — their normal, healthy regulation of thoughts and emotions.
In the diathesis-stress model, these challenging life events are thought to interact with individuals’ innate dispositions to bring psychological disorders to the surface.
Stress comes in many different forms. It may be a single traumatic event, like the death of a close relative or friend. But stress can also be an ongoing, sustained challenge in one’s life, like a chronic illness or an abusive relationship.
It can even be more mundane, the sorts of things we usually mean when we talk about “stress” — like anxiety from work or school (Theodore, 2020).
These events or situations can profoundly impact individual psychology and interact with diatheses to foment mental illness.
The role of stress in the diathesis-stress model is nuanced. For one, some life circumstances may constitute both a diathesis and stress. For instance, a child with a parent who suffers from mental illness may both be genetically predisposed to that illness and may also undergo stress as a result of her parent’s condition (Theodore, 2020).
Second, the timing of stress within an individual’s lifespan may be important; certain disorders are thought to have “windows of vulnerability” during which they are more likely to be brought about by stressful life events (Lokuge, 2011)
Moreover, positive life circumstances, called protective factors, may counteract stress, which decrease the likelihood that a disorder will emerge in response to stress.
Finally, different stresses are thought to play different roles across mental disorders — in other words, a particular form of stressful life event may play an especially pronounced role in depression, or schizophrenia, etc. These last two points will be explored in the sections below.
Protective Factors
Just as negative elements in one’s life make the onset of a psychological disorder more likely, there can also be positive elements that make the onset of a disorder less likely. These positive elements are called protective factors.
Protective factors help explain why some people who have both significant diatheses and stresses nonetheless remain psychologically healthy — in these cases, protective factors prevent a disorder from coming to the surface (Theodore, 2020).
Protective factors can be conditions, meaning beneficial life circumstances that protect against mental illness. They can also be attributes: traits or behaviors of an individual that make them more resilient against psychological disorders (“Protective Factors”).
Conditions that act as protective factors include strong parental and social support and assistance from psychotherapists or counselors. Attributes that act as protective factors include social and emotional competence and the use of healthy coping strategies and stress management techniques (Theodore, 2020).
By itself, the diathesis-stress model does not necessarily include protective factors in its assessment of the causes of psychological disorders.
As a result, the model has been updated in recent years to accommodate protective factors. This updated model is sometimes called the stress-vulnerability-protective factors model (Theodore, 2020).
Examples
The diathesis-stress model has proven useful in illuminating the causes of specific psychological disorders. One area where the model has had considerable success is schizophrenia, a disease with both genetic and environmental causes.
Schizophrenia
While schizophrenia has a strong genetic component, some individuals with genetic susceptibilities to the disorder nonetheless remain healthy.
As a result, the view currently held by many psychiatrists is that schizophrenia requires a genetic predisposition in combination with stress later on in life, which then triggers the emergence of the disorder.
Some researchers have also put forth a neural diathesis-stress model of schizophrenia, in which they attempt to explain how brain changes resulting from diatheses and stresses give rise to the disorder (Jones and Fernyhough, 2007).
Thus, the diathesis-stress model does well to explain the origins of schizophrenia and has even been supported by evidence from neuroscience.
Depression
The diathesis-stress model has also been used to explain the origins of depression. Similarly to schizophrenia, genetic risk factors for depression have been identified, but not all people with those risk factors go on to develop the disorder.
According to the diathesis-stress model of depression, stressful life events interact with genetic predispositions to bring about depressive symptoms.
This model of depression has been validated by research — a study found there to be an interaction effect between genetic risk factors for depression and scores on an inventory of stressful life events in predicting depressive symptoms (Colodro-Conde et al., 2018).
The model has also proven useful in explaining suicidal behavior. Early models of suicidal behavior tended to focus exclusively on stress, which failed to account for why some individuals exposed to extreme stress nonetheless refrain from engaging in suicidal behavior.
Since suicidal behavior likely also relies on an interaction between genetic and early childhood dispositions with stress later in life, researchers have suggested that efforts to treat and prevent suicidal behavior should utilize a diathesis-stress model (van Heeringen, 2012).
Different psychological disorders have different causes. Some may rely more strongly on hard-wired predispositions, while others may respond more to stressful events later in life.
Nevertheless, the diathesis-stress model has been shown to have wide applicability across many areas of psychiatry.
It offers a powerful explanation of how nature and nurture might come together to give rise to mental illness, a much-needed advancement over earlier theories that took one or the other to be completely determinative.
References
Broerman, R. (2017). Diathesis-Stress Model. In V. Zeigler-Hill & T. K. Shackelford (Eds.), Encyclopedia of Personality and Individual Differences (pp. 1–3). Springer International Publishing. https://doi.org/10.1007/978-3-319-28099-8_891-1
Colodro-Conde, L., Couvy-Duchesne, B., Zhu, G., Coventry, W. L., Byrne, E. M., Gordon, S., Wright, M. J., Montgomery, G. W., Madden, P. a. F., Major Depressive Disorder Working Group of the Psychiatric Genomics Consortium, Ripke, S., Eaves, L. J., Heath, A. C., Wray, N. R., Medland, S. E., & Martin, N. G. (2018). A direct test of the diathesis-stress model for depression. Molecular Psychiatry, 23(7), 1590–1596. https://doi.org/10.1038/mp.2017.130
DIATHESIS | Meaning & Definition for UK English | Lexico.com. (n.d.). Lexico Dictionaries | English. Retrieved February 23, 2022, from https://www.lexico.com/definition/diathesis
Jones, S. R., & Fernyhough, C. (2007). A new look at the neural diathesis–stress model of schizophrenia: The primacy of social-evaluative and uncontrollable situations. Schizophrenia Bulletin, 33(5), 1171–1177. https://doi.org/10.1093/schbul/sbl058
Lokuge, S., Frey, B. N., Foster, J. A., Soares, C. N., & Steiner, M. (2011). Depression in women: Windows of vulnerability and new insights into the link between estrogen and serotonin. The Journal of Clinical Psychiatry, 72(11), e1563-1569. https://doi.org/10.4088/JCP.11com07089
Protective Factors to Promote Well-Being and Prevent Child Abuse & Neglect—Child Welfare Information Gateway. (n.d.). Retrieved February 23, 2022, from https://www.childwelfare.gov/topics/preventing/promoting/protectfactors/
Theodore. (2020, April). Diathesis-Stress Model (Definition + Examples). Retrieved from https://practicalpie.com/diathesis-stress-model/.
van Heeringen, K. (2012). Stress–Diathesis Model of Suicidal Behavior. In Y. Dwivedi (Ed.), The Neurobiological Basis of Suicide. CRC Press/Taylor & Francis. http://www.ncbi.nlm.nih.gov/books/NBK107203/
Walker, E. F., & Diforio, D. (1997). Schizophrenia: a neural diathesis-stress model. Psychological review, 104(4), 667.