Thediathesis–stress model, also known as thevulnerability–stress model, is apsychological theory that attempts to explain a disorder, or its trajectory, as the result of an interaction between apredispositional vulnerability, the diathesis, and stress caused by life experiences. The term diathesis derives from theGreek term (διάθεσις) for a predisposition or sensibility. A diathesis can take the form of genetic, psychological, biological, or situational factors.[1] A large range of differences exists among individuals' vulnerabilities to the development of a disorder.[1][2]
The diathesis, or predisposition, interacts with the individual's subsequentstress response. Stress is a life event or series of events that disrupt a person's psychological equilibrium and may catalyze the development of a disorder.[3] Thus the diathesis-stress model serves to explore how biological or genetic traits (diatheses) interact with environmental influences (stressors) to produce disorders such as depression, anxiety, or schizophrenia.[4] The diathesis-stress model asserts that if the combination of the predisposition and the stress exceeds a threshold, the person will develop adisorder.[5]The use of the termdiathesis in medicine and in the specialty of psychiatry dates back to the 1800s. However, the diathesis-stress model was not introduced and used to describe the development ofpsychopathology until it was applied to explainingschizophrenia in the 1960s byPaul Meehl.[6]
The diathesis-stress model is used in many fields ofpsychology, specifically for studying the development of psychopathology.[7] It is useful for the purposes of understanding the interplay ofnature and nurture in the susceptibility topsychological disorders throughout the lifespan.[7] Diathesis-stress models can also assist in determining who will develop a disorder and who will not.[8] For example, in the context ofdepression, the diathesis-stress model can help explain why Person A may become depressed while Person B does not, even when exposed to the same stressors.[7] More recently, the diathesis-stress model has been used to explain why some individuals are more at risk for developing a disorder than others.[9] For example, children who have a family history of depression are generally more vulnerable to developing a depressive disorder themselves. A child who has a family history of depression and who has been exposed to a particular stressor, such asexclusion or rejection by their peers, would be more likely to develop depression than a child with a family history of depression that has an otherwise positive social network of peers.[9] The diathesis-stress model has also served as useful in explaining other poor (but non-clinical) developmental outcomes.
Protective factors, such as positive social networks or high self-esteem, can counteract the effects of stressors and prevent or curb the effects of the disorder.[10] Many psychological disorders have a window of vulnerability, during which time an individual is more likely to develop a disorder than others.[11] Diathesis–stress models are often conceptualized as multi-causal developmental models, which propose that multiple risk factors over the course of development interact with stressors and protective factors contributing to normal development or psychopathology.[12] Thedifferential susceptibility hypothesis is a recent theory that has stemmed from the diathesis–stress model.[13]
The term diathesis is synonymous withvulnerability, and variants such as "vulnerability-stress" are common within psychology.[7] Avulnerability makes it more or less likely that an individual will succumb to the development ofpsychopathology if certain stress is encountered.[1] Diatheses are considered inherent within the individual and are typically conceptualized as being stable, but not unchangeable, over the lifespan.[3][2] They are also often considered latent (i.e., dormant) because they are harder to recognize unless provoked by stressors.[1]
Diatheses are understood to includegenetic,biological,physiological,cognitive, andpersonality-related factors.[7] Some examples of diatheses include genetic factors, such as abnormalities in some genes or variations in multiple genes that interact to increase vulnerability. Other diatheses include early life experiences such as the loss of a parent[8] or high neuroticism.[14] Diatheses can also be conceptualized as situational factors, such as lowsocioeconomic status or having a parent with depression.
Stress can be conceptualized as a life event that disrupts the equilibrium of a person's life.[3][15] For instance, a person may be vulnerable to becoming depressed but will not develop depression unless he or she is exposed to a specific stress, which may trigger a depressive disorder.[16] Stressors can take the form of a discrete event, such as thedivorce of parents or adeath in the family, or can be more chronic factors such as having along-term illness or ongoing marital problems.[8] Stresses can also be related to more daily hassles, such as school assignment deadlines. This also parallels the popular (and engineering) usage of stress, but note that some literature defines stress as theresponse to stressors, especially where usage in biology influences neuroscience.
It has been long recognized that psychological stress plays a significant role in understanding how psychopathology develops in individuals.[17] However, psychologists have also identified that not all individuals who are stressed, or go through stressful life events, develop a psychological disorder. To understand this, theorists and researchers explored other factors that affected the development of a disorder[17] and proposed that some individuals under stress develop a disorder and others do not. As such, some individuals are more vulnerable than others to developing a disorder once the stress has been introduced.[1] This led to the formulation of the diathesis-stress model.
Stress is known to be amast cell activator.[18] Mast cells are long-lived tissue-resident cells with an important role in many inflammatory settings, including host defense against parasitic infection and in allergic reactions.[19]
There is evidence that "children exposed to prenatal stress may experience resilience driven by epigenome-wide interactions".[20] Early life stress interactions with the epigenome show potential mechanisms driving vulnerability towards psychiatric illness.[21] Ancestral stress alters lifetime mental health trajectories via epigenetic regulation.[22]
Carriers ofcongenital adrenal hyperplasia have a predisposition to stress[23] due to the unique nature of this gene.[24] True rates of prevalence are not known, but common genetic variants of the human Steroid 21-Hydroxylase Gene (CYP21A2) are related to differences in circulating hormone levels in the population.[25]
Psychological distress significantly impacts the quality of life of affected individuals. It is a known feature of generalizedjoint hypermobility (gJHM), as well as of its most common syndromic presentation, namelyEhlers–Danlos syndrome, hypermobility type (also known asjoint hypermobility syndrome, JHS/EDS-HT). Interestingly, in addition to the confirmation of a tight link between anxiety and gJHM, preliminary connections with depression,attention deficit hyperactivity disorder (ADHD),autism spectrum disorders, andobsessive–compulsive personality disorder (OCPD) were also found.[26]
Sensory processing sensitivity (SPS) is apersonality trait involving "an increased sensitivity of thecentral nervous system and a deepercognitive processing of physical, social and emotional stimuli".[27] The trait is characterized by "a tendency to 'pause to check' in novel situations, greater sensitivity to subtle stimuli, and the engagement of deeper cognitive processing strategies for employing coping actions, all of which are driven by heightened emotional reactivity, both positive and negative".[28] SPS captures sensitivity to the environment in a heritable, evolutionary-conserved trait associated with increased information processing in the brain, moderating sensitivity to environments in a for-better-and-for-worse fashion. Interaction with negative experiences increases the risk forpsychopathology, whereas interaction with positive experiences (including interventions) increases positive outcomes.[29]
Protective factors, while not an inherent component of the diathesis–stress model, are of importance when considering the interaction of diatheses and stress. Protective factors can mitigate or provide a buffer against the effects of major stressors by providing an individual with developmentally adaptive outlets to deal with stress.[10] Examples of protective factors include a positive parent-childattachment relationship, a supportive peer network, and individual social and emotional competence.[10]
Many models ofpsychopathology generally suggest that all people have some level of vulnerability towards certain mental disorders but posit a large range of individual differences in the point at which a person will develop a certain disorder.[1] For example, an individual with personality traits that tend to promote relationships, such asextroversion andagreeableness, may engender strong social support, which may later serve as a protective factor when experiencing stressors or losses that may delay or prevent the development of depression. Conversely, an individual who finds it difficult to develop and maintain supportive relationships may be more vulnerable to developing depression following a job loss because they do not have protective social support. An individual's threshold is determined by the interaction of diatheses and stress.[3]
Windows of vulnerability for developing specific psychopathologies are believed to exist at different points of the lifespan. Moreover, different diatheses and stressors are implicated in different disorders. For example, breakups and other severe or traumatic life stressors are implicated in the development of depression. Stressful events can also trigger the manic phase ofbipolar disorder, and stressful events can then prevent recovery and trigger relapse. Having a genetic disposition for becoming addicted and later engaging inbinge drinking in college are implicated in the development ofalcoholism. A family history ofschizophrenia combined with the stressor of being raised in a dysfunctional family raises the risk of developing schizophrenia.[11]
Diathesis-stress models are often conceptualized as multi-causal developmental models, which propose that multiplerisk factors over the course of development interact with stressors and protective factors contributing to normal development or psychopathology.[12] For example, a child with a family history of depression likely has a genetic vulnerability to depressive disorder. This child has also been exposed to environmental factors associated with parental depression that increase their vulnerability to developing depression as well. Protective factors, such as a strong peer network, involvement in extracurricular activities, and a positive relationship with the non-depressed parent, interact with the child's vulnerabilities in determining the progression to psychopathology versus normative development.[30]
Some theories have branched from the diathesis-stress model, such as thedifferential susceptibility hypothesis, which extends the model to include a vulnerability to positive environments as well as negative environments or stress.[13] A person could have a biological vulnerability that, when combined with a stressor, could lead to psychopathology (diathesis–stress model); but that same person with a biological vulnerability, if exposed to a particularly positive environment, could have better outcomes than a person without the vulnerability.[13]
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