What is the Differential Susceptibility Hypothesis?


The differential susceptibility hypothesis proposed by Jay Belsky is another interpretation of psychological findings that are usually discussed according to the diathesis-stress model.

Both models suggest that people’s development and emotional affect are differentially susceptible to experiences or qualities of the environment. Where the Diathesis-stress model suggests a distinct and mostly negativity-sensitive group, Belsky describes a group that is sensitive to negative experiences but also to positive experiences. These models may be complementary, if some individuals are dually or uniquely positivity-sensitive, while other people are uniquely negativity-sensitive.

Differential Susceptibility versus Diathesis-Stress

The idea that individuals vary in their responsivity to negative qualities of the environment is generally framed in diathesis-stress or dual-risk terms. That is, some individuals, due to their biological, temperamental and/or behavioural characteristics (i.e. “diathesis” or “risk 1”), are more vulnerable to the adverse effects of negative experiences (i.e., “stress” or “risk 2”), whereas others are relatively resilient with respect to them (see Figure 1, an adaptation of Bakermans-Kranenburg and van IJzendoorn’s (2007) Figure 1). A fundamentally different, even if not competing view, of the very same phenomenon is central to Belsky’s differential susceptibility hypothesis and Boyce and Ellis’ (2005) related notion of biological sensitivity to context: Individuals do not simply vary in the degree to which they are vulnerable to the negative effects of adverse experience but, more generally, in their developmental plasticity.

On this hypothesis, more “plastic” or malleable individuals are more susceptible than others to environmental influences in a for-better-and-for-worse manner. That is, susceptible to both the adverse developmental sequelae associated with negative environments and the positive developmental consequences of supportive ones. Less susceptible individuals, in contrast, are less affected by rearing conditions, be they presumptively supportive or undermining of well being (see Figure 2, an adaptation of Bakermans-Kranenburg and Van IJzendoorn’s (2007) Figure 1).

Figure 1. The diathesis-stress/dual-risk model. Developmental outcome as it relates to environmental quality. A “vulnerable” group experiences negative outcome when exposed to a negative environment, although this group is identical to the other, “resilient” group in a positive environment.
Figure 2. The differential susceptibility model. The lines depict two categorical groups that differ in their responsiveness to the environment: the “plastic” group is disproportionately more affected by both negative and positive environments compared to the “fixed” group.

Theoretical Background

Belsky suggests that evolution might select for some children who are more plastic, and others who are more fixed in the face of, for example, parenting styles.

Belsky offers that ancestral parents, just like parents today, could not have known (consciously or unconsciously) which childrearing practices would prove most successful in promoting the reproductive fitness of offspring – and thus their own inclusive fitness. As a result, and as a fitness optimising strategy involving bet hedging, natural selection might have shaped parents to bear children varying in plasticity. This way, if an effect of parenting had proven counterproductive in fitness terms, those children not affected by parenting would not have incurred the cost of developing in ways that ultimately proved “misguided”.

Importantly, natural selection might favour genetic lines with both plastic and fixed developmental and affective patterns. In other words, there is value to having both kinds at once. In light of inclusive-fitness considerations, children who were less malleable (and more fixed) would have “resistance” to parental influence. This could be adaptable some times, and maladaptive other times. Their fixedness would not only have benefited themselves directly, but even their more malleable siblings indirectly. This is because siblings, like parents and children, have 50% of their genes in common. By the same token, had parenting influenced children in ways that enhanced fitness, then not only would more plastic offspring have benefited directly by following parental leads, but so, too, would their parents and even their less malleable siblings who did not benefit from the parenting they received, again for inclusive-fitness reasons. The overall effect may be to temper some of the variability in parenting. That is, to make more conservative bets.

This line of evolutionary argument leads to the prediction that children should vary in their susceptibility to parental rearing and perhaps to environmental influences more generally. As it turns out, a long line of developmental inquiry, informed by a “transactional” perspective, has more or less been based on this unstated assumption.

Criteria for the Testing of Differential Susceptibility

Belsky, Bakermans-Kranenburg, & Van IJzendoorn, (2007) delineated a series of empirical requirements – or steps – for evidencing the differential susceptibility hypothesis. Particularly they identify tests that distinguish differential susceptibility from other interaction effects including diathesis-stress/dual-risk.

While diathesis-stress/dual-risk arises when the most vulnerable are disproportionately affected in an adverse manner by a negative environment but do not also benefit disproportionately from positive environmental conditions, differential susceptibility is characterised by a cross-over interaction: the susceptible individuals are disproportionately affected by both negative and positive experiences. A further criterion that needs to be fulfilled to distinguish differential susceptibility from diathesis-stress/dual-risk is the independence of the outcome measure from the susceptibility factor: if the susceptibility factor and the outcome are related, diathesis-stress/dual-risk is suggested rather than differential susceptibility. Further, environment and susceptibility factor must also be unrelated to exclude the alternative explanation that susceptibility merely represents a function of the environment. The specificity of the differential-susceptibility effect is demonstrated if the model is not replicated when other susceptibility factors (i.e. moderators) and outcomes are used. Finally, the slope for the susceptible subgroup should be significantly different from zero and at the same time significantly steeper than the slope for the non- (or less-) susceptible subgroup.

Susceptibility Markers and Empirical Evidence

Characteristics of individuals that have been shown to moderate environmental effects in a manner consistent with the differential susceptibility hypothesis can be subdivided into three categories:

  • Genetic factors;
  • Endophenotypic factors; and
  • Phenotypic factors.

Bakermans-Kranenburg and Van IJzendoorn (2006) were the first to test the differential susceptibility hypothesis as a function of Genetic Factors regarding the moderating effect of the dopamine receptor D4 7-repeat polymorphism (DRD4-7R) on the association between maternal sensitivity and externalising behaviour problems in 47 families. Children with the DRD4-7R allele and insensitive mothers displayed significantly more externalising behaviours than children with the same allele but with sensitive mothers. Children with the DRD4-7R allele and sensitive mothers had the least externalising behaviours of all whereas maternal sensitivity had no effect on children without the DRD4-7R allele.

Endophenotypic Factors have been examined by Obradovic, Bush, Stamperdahl, Adler and Boyce’s (2010). They investigated associations between childhood adversity and child adjustment in 338 5-year-olds. Children with high cortisol reactivity were rated by teachers as least prosocial when living under adverse conditions, but most prosocial when living under more benign conditions (and in comparison to children scoring low on cortisol reactivity).

Regarding characteristics of the category of Phenotypic Factors, Pluess and Belsky (2009) reported that the effect of child care quality on teacher-rated socioemotional adjustment varied as a function of infant temperament in the case of 761 4.5-year-olds participating in the NICHD Study of Early Child Care and Youth Development (NICHD Early Child Care Research Network, 2005). Children with difficult temperaments as infants manifest the most and least behaviour problems depending on whether they experienced, respectively, poor or good quality care (and in comparison to children with easier temperaments).

Table 1: List of Proposed Susceptibility Factors that emerge across studies, according to Belsky and colleagues.

What is the 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 a stress caused by life experiences. The term diathesis derives from the Greek term (διάθεσις) for a predisposition, or sensibility. A diathesis can take the form of genetic, psychological, biological, or situational factors. A large range of differences exists among individuals’ vulnerabilities to the development of a disorder.

The diathesis, or predisposition, interacts with the individual’s subsequent stress response. Stress is a life event or series of events that disrupts a person’s psychological equilibrium and may catalyse the development of a disorder. 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. The diathesis-stress model asserts that if the combination of the predisposition and the stress exceeds a threshold, the person will develop a disorder. 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 psychopathology until it was applied to explaining schizophrenia in the 1960s by Paul Meehl.

The diathesis-stress model is used in many fields of psychology, specifically for studying the development of psychopathology. It is useful for the purposes of understanding the interplay of nature and nurture in the susceptibility to psychological disorders throughout the lifespan. Diathesis-stress models can also assist in determining who will develop a disorder and who will not. For example, in the context of 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. More recently, the diathesis-stress model has been used to explain why some individuals are more at risk for developing a disorder than others. 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 his or her 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. 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 disorder. Many psychological disorders have a window of vulnerability, during which time an individual is more likely to develop disorder than others. Diathesis-stress models are often conceptualised 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. The differential susceptibility hypothesis is a recent theory that has stemmed from the diathesis-stress model.

Refer to Differential Susceptibility Hypothesis.


The term diathesis is synonymous with vulnerability, and variants such as “vulnerability-stress” are common within psychology. A vulnerability makes it more or less likely that an individual will succumb to the development of psychopathology if a certain stress is encountered. Diatheses are considered inherent within the individual and are typically conceptualised as being stable, but not unchangeable, over the lifespan. They are also often considered latent (i.e. dormant), because they are harder to recognise unless provoked by stressors.

Diatheses are understood to include genetic, biological, physiological, cognitive, and personality-related factors. 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, or high neuroticism. Diatheses can also be conceptualised as situational factors, such as low socio-economic status or having a parent with depression.


Stress can be conceptualised as a life event that disrupts the equilibrium of a person’s life. For instance, a person may be vulnerable to become depressed, but will not develop depression unless they are exposed to a specific stress, which may trigger a depressive disorder. Stressors can take the form of a discrete event, such the divorce of parents or a death in the family, or can be more chronic factors such as having a long-term illness, or ongoing marital problems. 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 response to stressors, especially where usage in biology influences neuroscience.

It has been long recognised that psychological stress plays a significant role in understanding how psychopathology develops in individuals. 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 affect the development of a disorder and proposed that some individuals under stress develop a disorder and others do not. As such, some individuals are more vulnerable than others to develop a disorder once stress has been introduced. This led to the formulation of the diathesis-stress model.


Sensory processing sensitivity (SPS) is a temperamental or personality trait involving “an increased sensitivity of the central nervous system and a deeper cognitive processing of physical, social and emotional stimuli”. The trait is characterised 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 is driven by heightened emotional reactivity, both positive and negative”.

Sensory processing sensitivity captures sensitivity to 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 risk for psychopathology. Whereas interaction with positive experiences (including interventions), increases positive outcomes. Mast cells are long-lived tissue-resident cells with an important role in many inflammatory settings including host defence to parasitic infection and in allergic reactions. Stress is known to be a mast cell activator.

There is evidence that children exposed to prenatal stress may experience resilience driven by epigenome-wide interactions.” Early life stress interactions with the epigenome show potential mechanisms driving vulnerability towards psychiatric illness. ancestral stress alters lifetime mental health trajectories via epigenetic regulation.

Carriers of congenital adrenal hyperplasia have a predeposition to stress, due to the unique nature of this gene. 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.

Psychological distress is a known feature of generalised joint hypermobility (gJHM), as well as of its most common syndromic presentation, namely Ehlers-Danlos syndrome, hypermobility type (a.k.a. joint hypermobility syndrome – JHS/EDS-HT), and significantly contributes to the quality of life of affected individuals. Interestingly, in addition to the confirmation of a tight link between anxiety and gJHM, preliminary connections with depression, attention deficit (and hyperactivity) disorder, autism spectrum disorders, and obsessive-compulsive personality disorder were also found.

Protective Factors

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. Examples of protective factors include a positive parent-child attachment relationship, a supportive peer network, and individual social and emotional competence.

Throughout the Lifespan

Many models of 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. For example, an individual with personality traits that tend to promote relationships such as extroversion and 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.

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 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 alcoholism. A family history of schizophrenia combined with the stressor of being raised in a dysfunctional family raises the risk of developing schizophrenia.

Diathesis-stress models are often conceptualised 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. 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 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.

Some theories have branched from the diathesis-stress model, such as the differential susceptibility hypothesis, which extends the model to include a vulnerability to positive environments as well as negative environments or stress. 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.