View source for Philosophy:Diathesis–stress model

{{Short description|Psychological theory}}
[[File:Diathesisstressdualriskmodel.JPG|upright=1.35|thumb|Schematic of diathesis–stress model]] The '''diathesis-stress model''', also known as the '''vulnerability–stress model''', is a psychological theory that attempts to explain a disorder, or its trajectory, as the result of an interaction between a predispositional vulnerability, the diathesis, and stress caused by life experiences. The term diathesis derives from the [[Social:Ancient Greek|Greek]] term (διάθεσις) for a predisposition or sensibility. A diathesis can take the form of genetic, psychological, biological, or situational factors.<ref name="Ingram">Ingram, R. E. & Luxton, D. D. (2005). "Vulnerability-Stress Models." In B.L. Hankin & J. R. Z. Abela (Eds.), ''[https://books.google.com/books?id=1Fd0LneB724C&q=Development+of+Psychopathology%3A+A+vulnerability+stress+perspective&pg=PR7 Development of Psychopathology: A vulnerability stress perspective]'' (pp. 32-46). Thousand Oaks, CA: Sage Publications Inc.</ref> A large range of differences exists among individuals' vulnerabilities to the development of a disorder.<ref name="Ingram" /><ref name="Ormel2013">{{cite journal |author1=Ormel J.|author2=Jeronimus, B.F.|author3=Kotov, M.|author4=Riese, H.|author5=Bos, E.H.|author6=Hankin, B. | year = 2013 | title = Neuroticism and common mental disorders: Meaning and utility of a complex relationship | journal = Clinical Psychology Review | volume = 33 | issue = 5 | pages = 686–697 | doi=10.1016/j.cpr.2013.04.003 | pmid=23702592 | pmc=4382368}}</ref>
The diathesis, or predisposition, interacts with the individual's subsequent stress 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.<ref name="Oatleyb" /> 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.<ref name="PreventionAction">{{Cite web|url=http://www.preventionaction.org/reference/diathesis-stress-models|archiveurl=https://web.archive.org/web/20120603201839/http://www.preventionaction.org/reference/diathesis-stress-models|url-status=dead|title= Resources and Information|archivedate=June 3, 2012|website=www.preventionaction.org}}</ref> The diathesis-stress model asserts that if the combination of the predisposition and the stress exceeds a threshold, the person will develop a disorder.<ref name="Lazarus">{{cite journal |last1=Lazarus |first1=R. S. |title=From Psychological Stress to the Emotions: A History of Changing Outlooks |journal=Annual Review of Psychology |date=January 1993 |volume=44 |issue=1 |pages=1–22 |doi=10.1146/annurev.ps.44.020193.000245 |pmid=8434890 |doi-access=free }}</ref>
The use of the term ''diathesis'' 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 of [[Philosophy:Psychopathology|psychopathology]] until it was applied to explaining [[Medicine:Schizophrenia|schizophrenia]] in the 1960s by Paul Meehl.<ref>{{cite journal |last1=Meehl |first1=P. E. |title=Schizotaxia, schizotypy, schizophrenia |journal=American Psychologist |year=1962 |volume=17 |issue=12 |pages=827–838 |doi=10.1037/h0041029}}</ref>

The diathesis-stress model is used in many fields of [[Social:Psychology|psychology]], specifically for studying the development of psychopathology.<ref name="Sigelman">Sigelman, C. K. & Rider, E. A. (2009). [https://books.google.com/books?id=8smBuRecmDsC&pg=PT656 Developmental psychopathology.] ''Life-span human development'' (6th ed.) (pp. 468-495). Belmont, CA: Wadsworth Cengage Learning.</ref> It is useful for the purposes of understanding the interplay of nature and nurture in the susceptibility to psychological disorders throughout the lifespan.<ref name="Sigelman"/> Diathesis-stress models can also assist in determining who will develop a disorder and who will not.<ref name="Oatleya">Oatley, K., Keltner, D., & Jenkins, J. M. (2006a). "Emotions and mental health in adulthood." ''[https://books.google.com/books?id=RGHghPqIO_8C Understanding Emotions]'' (2nd ed.) (pp. 353-383). Oxford, UK: Blackwell Publishing.</ref> For example, in the context of [[Medicine:Depression (mood)|depression]], 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.<ref name="Sigelman"/> More recently, the diathesis-stress model has been used to explain why some individuals are more at risk for developing a disorder than others.<ref name="Gazelle">{{cite journal |last1=Gazelle |first1=Heidi |last2=Ladd |first2=Gary W. |title=Anxious Solitude and Peer Exclusion: A Diathesis-Stress Model of Internalizing Trajectories in Childhood |journal=Child Development |date=February 2003 |volume=74 |issue=1 |pages=257–278 |doi=10.1111/1467-8624.00534 |pmid=12625449 }}</ref> 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 as exclusion 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.<ref name="Gazelle"/> 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.<ref name="ACF"/> Many psychological disorders have a window of vulnerability, during which time an individual is more likely to develop a disorder than others.<ref name="Barlow"/> 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.<ref name="Masten"/> The [[Philosophy:Differential susceptibility hypothesis|differential susceptibility hypothesis]] is a recent theory that has stemmed from the diathesis–stress model.<ref name="Belsky"/>

==Diathesis==
[[File:Diathesis_stress_model_cup_analogy.svg|upright=1.35|thumb|A cup analogy demonstrating under the same amount of stressors, person 2 is more vulnerable than person 1, because of their predisposition]]
The term diathesis is synonymous with vulnerability, and variants such as "vulnerability-stress" are common within psychology.<ref name="Sigelman"/> A vulnerability makes it more or less likely that an individual will succumb to the development of [[Philosophy:Psychopathology|psychopathology]] if certain stress is encountered.<ref name="Ingram"/> Diatheses are considered inherent within the individual and are typically conceptualized as being stable, but not unchangeable, over the lifespan.<ref name="Oatleyb">Oatley, K., Keltner, D. & Jenkins, J. M. (2006b). "Emotions and mental health in childhood."''[https://books.google.com/books?id=RGHghPqIO_8C Understanding emotions]'' (2nd ed.) (pp. 321-351). Oxford, UK: Blackwell Publishing.</ref><ref name="Ormel2013"/> They are also often considered latent (i.e., dormant) because they are harder to recognize unless provoked by stressors.<ref name="Ingram"/>

Diatheses are understood to include [[Biology:Heredity|genetic]], biological, physiological, cognitive, and [[Philosophy:Personality|personality]]-related factors.<ref name="Sigelman"/> 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<ref name="Oatleya"/> or high neuroticism.<ref name="NeuroticismMA">{{cite journal |last1=Jeronimus |first1=B. F. |last2=Kotov |first2=R. |last3=Riese |first3=H. |last4=Ormel |first4=J. |title=Neuroticism's prospective association with mental disorders halves after adjustment for baseline symptoms and psychiatric history, but the adjusted association hardly decays with time: a meta-analysis on 59 longitudinal/prospective studies with 443 313 participants |journal=Psychological Medicine |date=15 August 2016 |volume=46 |issue=14 |pages=2883–2906 |doi=10.1017/S0033291716001653 |pmid=27523506 |s2cid=23548727 |url=https://zenodo.org/record/895885 }}</ref> Diatheses can also be conceptualized as situational factors, such as low socioeconomic status or having a parent with depression.

==Stress==
Stress can be conceptualized as a life event that disrupts the equilibrium of a person's life.<ref name="Oatleyb"/><ref name="Jeronimus2013">{{cite journal |last1=Jeronimus |first1=B. F. |last2=Ormel |first2=J. |last3=Aleman |first3=A. |last4=Penninx |first4=B. W. J. H. |last5=Riese |first5=H. |title=Negative and positive life events are associated with small but lasting change in neuroticism |journal=Psychological Medicine |date=15 February 2013 |volume=43 |issue=11 |pages=2403–2415 |doi=10.1017/S0033291713000159 |pmid=23410535 |s2cid=43717734 }}</ref> 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.<ref name="Nolen">Nolen-Hoeksema, S. (2008). "Suicide". ''[https://books.google.com/books?id=wYIsQAAACAAJ Abnormal Psychology]'' (4th ed.) (pp. 350-373). New York, NY: McGraw-Hill.</ref> Stressors can take the form of a discrete event, such as the [[Social:Divorce|divorce]] of parents or a [[Biology:Death|death]] in the family, or can be more chronic factors such as having a long-term illness or ongoing marital problems.<ref name="Oatleya"/> 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 the [[Medicine:Stress|response]] 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.<ref name="Monroe">{{cite journal |last1=Monroe |first1=Scott M. |last2=Simons |first2=Anne D. |title=Diathesis-stress theories in the context of life stress research: Implications for the depressive disorders. |journal=Psychological Bulletin |date=1991 |volume=110 |issue=3 |pages=406–425 |doi=10.1037/0033-2909.110.3.406 |pmid=1758917 }}</ref> 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<ref name="Monroe"/> 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.<ref name="Ingram"/> This led to the formulation of the diathesis-stress model.

==Genetics==
Stress is known to be a [[Biology:Mast cell|mast cell]] activator.<ref>{{cite book |last1=Baldwin |first1=AL |title=Mast Cells |chapter=Mast cell activation by stress |series=Methods in Molecular Biology |date=2006 |volume=315 |pages=349–60 |doi=10.1385/1-59259-967-2:349 |pmid=16110169 |isbn=1-59259-967-2 }}</ref> 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.<ref>{{Cite web | url=https://www.immunology.org/public-information/bitesized-immunology/cells/mast-cells |title = Mast Cells &#124; British Society for Immunology}}</ref>

There is evidence that "children exposed to prenatal stress may experience resilience driven by epigenome-wide interactions".<ref>{{cite journal |last1=Serpeloni |first1=Fernanda |last2=Radtke |first2=Karl M. |last3=Hecker |first3=Tobias |last4=Sill |first4=Johanna |last5=Vukojevic |first5=Vanja |last6=Assis |first6=Simone G. de |last7=Schauer |first7=Maggie |last8=Elbert |first8=Thomas |last9=Nätt |first9=Daniel |title=Does Prenatal Stress Shape Postnatal Resilience? – An Epigenome-Wide Study on Violence and Mental Health in Humans |journal=Frontiers in Genetics |date=16 April 2019 |volume=10 |pages=269 |doi=10.3389/fgene.2019.00269 |pmid=31040859 |pmc=6477038 |doi-access=free }}</ref> Early life stress interactions with the epigenome show potential mechanisms driving vulnerability towards psychiatric illness.<ref>{{cite journal |last1=Lewis |first1=Candace Renee |last2=Olive |first2=Michael Foster |title=Early life stress interactions with the epigenome: potential mechanisms driving vulnerability towards psychiatric illness |journal=Behavioural Pharmacology |date=2014 |volume=25 |issue=5 0 6 |pages=341–351 |doi=10.1097/FBP.0000000000000057 |pmid=25003947 |pmc=4119485 }}</ref> Ancestral stress alters lifetime mental health trajectories via epigenetic regulation.<ref>{{cite journal |last1=Ambeskovic |first1=Mirela |last2=Babenko |first2=Olena |last3=Ilnytskyy |first3=Yaroslav |last4=Kovalchuk |first4=Igor |last5=Kolb |first5=Bryan |last6=Metz |first6=Gerlinde A. S. |title=Ancestral Stress Alters Lifetime Mental Health Trajectories and Cortical Neuromorphology via Epigenetic Regulation |journal=Scientific Reports |date=23 April 2019 |volume=9 |issue=1 |pages=6389 |doi=10.1038/s41598-019-42691-z |pmid=31011159 |pmc=6476877 |bibcode=2019NatSR...9.6389A }}</ref>

Carriers of [[Medicine:Congenital adrenal hyperplasia|congenital adrenal hyperplasia]] have a predisposition to stress<ref>{{cite journal |title=Psychological vulnerability to stress in carriers of congenital adrenal hyperplasia due to 21-hydroxylase deficiency |journal=Hormones |date=12 May 2017 |volume=16 |issue=1 |pages=42–53 |doi=10.14310/horm.2002.1718 |pmid=28500827 |last1=Kyritsi |first1=E. M. |last2=Koltsida |first2=G. |last3=Farakla |first3=I. |last4=Papanikolaou |first4=A. |last5=Critselis |first5=E. |last6=Mantzou |first6=E. |last7=Zoumakis |first7=E. |last8=Kolaitis |first8=G. |last9=Chrousos |first9=G. P. |last10=Charmandari |first10=E. |doi-access=free }}</ref> due to the unique nature of this gene.<ref>{{cite journal |last1=Concolino |first1=Paola |title=Issues with the Detection of Large Genomic Rearrangements in Molecular Diagnosis of 21-Hydroxylase Deficiency |journal=Molecular Diagnosis & Therapy |date=17 July 2019 |volume=23 |issue=5 |pages=563–567 |doi=10.1007/s40291-019-00415-z |pmid=31317337 |s2cid=197543506 }}</ref> 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.<ref>{{cite journal |last1=Doleschall |first1=Márton |last2=Szabó |first2=Julianna Anna |last3=Pázmándi |first3=Júlia |last4=Szilágyi |first4=Ágnes |last5=Koncz |first5=Klára |last6=Farkas |first6=Henriette |last7=Tóth |first7=Miklós |last8=Igaz |first8=Péter |last9=Gláz |first9=Edit |last10=Prohászka |first10=Zoltán |last11=Korbonits |first11=Márta |last12=Rácz |first12=Károly |last13=Füst |first13=George |last14=Patócs |first14=Attila |title=Common Genetic Variants of the Human Steroid 21-Hydroxylase Gene (CYP21A2) Are Related to Differences in Circulating Hormone Levels |journal=PLOS ONE |date=11 September 2014 |volume=9 |issue=9 |pages=e107244 |doi=10.1371/journal.pone.0107244 |pmid=25210767 |pmc=4161435 |bibcode=2014PLoSO...9j7244D |doi-access=free }}</ref>

Psychological distress significantly impacts the quality of life of affected individuals. It is a known feature of generalized joint hypermobility (gJHM), as well as of its most common syndromic presentation, namely [[Medicine:Ehlers–Danlos syndromes|Ehlers–Danlos syndrome]], hypermobility type (also known as ''joint hypermobility syndrome'', JHS/EDS-HT). Interestingly, in addition to the confirmation of a tight link between anxiety and gJHM, preliminary connections with depression, [[Medicine:Attention deficit hyperactivity disorder|attention deficit hyperactivity disorder]] (ADHD), [[Medicine:Autism spectrum|autism spectrum]] disorders, and [[Medicine:Obsessive–compulsive personality disorder|obsessive–compulsive personality disorder]] (OCPD) were also found.<ref>{{cite journal |last1=Sinibaldi |first1=Lorenzo |last2=Ursini |first2=Gianluca |last3=Castori |first3=Marco |date=March 2015 |title=Psychopathological manifestations of joint hypermobility and joint hypermobility syndrome/ Ehlers-Danlos syndrome, hypermobility type: The link between connective tissue and psychological distress revised |journal=American Journal of Medical Genetics Part C: Seminars in Medical Genetics |volume=169 |issue=1 |pages=97–106 |doi=10.1002/ajmg.c.31430 |pmid=25821094 |s2cid=8543532}}</ref>

[[Philosophy:Sensory processing sensitivity|Sensory processing sensitivity]] (SPS) is a [[Social:Trait theory|personality trait]] involving "an increased sensitivity of the [[Biology:Central nervous system|central nervous system]] and a deeper [[Cognition|cognitive]] processing of physical, social and emotional stimuli".<ref name="Boterberg2016">{{cite journal |last1=Boterberg |first1=Sofie |last2=Warreyn |first2=Petra |title=Making sense of it all: The impact of sensory processing sensitivity on daily functioning of children |journal=Personality and Individual Differences |date=April 2016 |volume=92 |pages=80–86 |doi=10.1016/j.paid.2015.12.022 |hdl=1854/LU-7172755 |url=https://biblio.ugent.be/publication/7172755 |hdl-access=free }}</ref> 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".<ref name="Booth2015">{{citation |title=Sensory-processing sensitivity moderates the association between childhood experiences and adult life satisfaction |first1=Charlotte |last1=Booth |first2=Helen |last2=Standage |first3=Elaine |last3=Fox |date=1 Dec 2015 |journal=Personality and Individual Differences |volume=87 |pages=24–29 |doi=10.1016/j.paid.2015.07.020 |pmid=26688599 |pmc=4681093 }}</ref> 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 for [[Philosophy:Psychopathology|psychopathology]], whereas interaction with positive experiences (including interventions) increases positive outcomes.<ref>{{cite journal |last1=Greven |first1=Corina U. |last2=Lionetti |first2=Francesca |last3=Booth |first3=Charlotte |last4=Aron |first4=Elaine N. |last5=Fox |first5=Elaine |last6=Schendan |first6=Haline E. |last7=Pluess |first7=Michael |last8=Bruining |first8=Hilgo |last9=Acevedo |first9=Bianca |last10=Bijttebier |first10=Patricia |last11=Homberg |first11=Judith |title=Sensory Processing Sensitivity in the context of Environmental Sensitivity: A critical review and development of research agenda |journal=Neuroscience & Biobehavioral Reviews |date=1 March 2019 |volume=98 |pages=287–305 |doi=10.1016/j.neubiorev.2019.01.009 |pmid=30639671 |doi-access=free |hdl=2066/202697 |hdl-access=free }}</ref>

==Protective factors==
{{Annotated image|caption=Equipped with more resource, the effect from different life stressors is buffered|image=Diathesis stress model graph.svg|width=512|height=300|image-width=512|image-left=0|image-top=0|annotations={{Annotation|480|290|Time|font-weight=bold|font-size=12}}
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{{Annotation|340|220|Predisposition|font-weight=bold|font-size=25|color=green}}}}{{See also|Coping (psychology)}}
[[Medicine:Protective factor|Protective factor]]s, 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.<ref name="ACF">{{Cite web |url=http://www.childwelfare.gov/pubs/guide2012/guide.pdf#page=9 |title=Administration for Children and Families (2012). ''Preventing child maltreatment and promoting well-being: A network for action''. Department of Health and Human Services. Retrieved from www.childwelfare.gov |access-date=2012-10-31 |archive-date=2020-06-19 |archive-url=https://web.archive.org/web/20200619192646/http://www.childwelfare.gov/pubs/guide2012/guide.pdf#page=9 |url-status=dead }}</ref> Examples of protective factors include a positive parent-child [[Philosophy:Attachment theory|attachment relationship]], a supportive peer network, and individual social and emotional competence.<ref name="ACF" />

==Throughout the lifespan==
Many models of [[Philosophy:Psychopathology|psychopathology]] 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.<ref name="Ingram"/> For example, an individual with personality traits that tend to promote relationships, such as extroversion and [[Philosophy:Agreeableness|agreeableness]], 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.<ref name="Oatleyb"/>

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 of [[Medicine:Bipolar disorder|bipolar disorder]], and stressful events can then prevent recovery and trigger relapse. Having a genetic disposition for becoming addicted and later engaging in binge drinking in college are implicated in the development of [[Medicine:Alcoholism|alcoholism]]. A family history of [[Medicine:Schizophrenia|schizophrenia]] combined with the stressor of being raised in a dysfunctional family raises the risk of developing schizophrenia.<ref name="Barlow">Barlow, D. H. & Durand, V. M. (2009). ''[https://books.google.com/books?hl=en&lr=&id=yITxaqlS_yMC&oi=fnd&pg=PT6 Abnormal psychology: An integrative approach.]'' Belmont, CA: Wadsworth Publishing Company.{{page needed|date=May 2020}}</ref>

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.<ref name="Masten">{{cite journal |last1=Masten |first1=Ann S. |title=Ordinary magic: Resilience processes in development. |journal=American Psychologist |date=2001 |volume=56 |issue=3 |pages=227–238 |doi=10.1037/0003-066x.56.3.227 |pmid=11315249 }}</ref> 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.<ref name="Cummings">Cummings, M. E., Davies, P. T., & Campbell, S. B. (2000). ''[https://books.google.com/books?id=5SyyeX-yVbAC&pg=PA1 Developmental psychopathology and family process: Theory, research, and clinical implications.]'' New York, NY: The Guilford Press.{{page needed|date=May 2020}}</ref>

Some theories have branched from the diathesis-stress model, such as the [[Philosophy:Differential susceptibility hypothesis|differential susceptibility hypothesis]], which extends the model to include a vulnerability to positive environments as well as negative environments or stress.<ref name="Belsky">{{cite journal |last1=Belsky |first1=Jay |last2=Pluess |first2=Michael |title=Beyond diathesis stress: Differential susceptibility to environmental influences. |journal=Psychological Bulletin |date=2009 |volume=135 |issue=6 |pages=885–908 |doi=10.1037/a0017376 |pmid=19883141 }}</ref> 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.<ref name="Belsky"/>

==See also==
* [[Unsolved:Biopsychosocial model|Biopsychosocial model]]
* [[Philosophy:Environmental sensitivity|Environmental sensitivity]]
* [[Philosophy:Gene–environment interaction|Gene–environment interaction]]
* [[Philosophy:Heritability|Heritability]]
* Human behavior genetics

==References==
{{reflist|2}}

==External links==

{{DEFAULTSORT:Diathesis-stress model}}
[[Category:Psychological theories]]

{{Sourceattribution|Diathesis–stress model}}