Beyond Diathesis Stress: Differential Susceptibility to Environmental Influences

Institute for the Study of Children, Families and Social Issues, Birkbeck University of London, 7 Bedford Square, London WC1B 3RA, United Kingdom.
Psychological Bulletin (Impact Factor: 14.76). 11/2009; 135(6):885-908. DOI: 10.1037/a0017376
Source: PubMed


Evolutionary-biological reasoning suggests that individuals should be differentially susceptible to environmental influences, with some people being not just more vulnerable than others to the negative effects of adversity, as the prevailing diathesis-stress view of psychopathology (and of many environmental influences) maintains, but also disproportionately susceptible to the beneficial effects of supportive and enriching experiences (or just the absence of adversity). Evidence consistent with the proposition that individuals differ in plasticity is reviewed. The authors document multiple instances in which (a) phenotypic temperamental characteristics, (b) endophenotypic attributes, and (c) specific genes function less like "vulnerability factors" and more like "plasticity factors," thereby rendering some individuals more malleable or susceptible than others to both negative and positive environmental influences. Discussion focuses upon limits of the evidence, statistical criteria for distinguishing differential susceptibility from diathesis stress, potential mechanisms of influence, and unknowns in the differential-susceptibility equation.

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    • "The intervention's protective findings suggests that participation in efficacious intervention programs may have the potential to intervene on stress processes at a biological level and promotes the role of intervention programs among youth living in high conflict or stressful environments . While prevention programs may benefit all youth to a degree, there is a growing appreciation and literature on individual differences in sensitivity to one's environment , both positive and negative (Belsky and Pluess 2009). These differences may be partly explained by genetic predispositions. "
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    ABSTRACT: Parent–child relationships with high conflict and low warmth and support are associated with later adverse behavioral and physiological child outcomes. These outcomes include shorter telomere lengths, the repetitive sequences at the ends of chromosomes that have been utilized as a biomarker for chronic stress. Our research group furthered this by exploring telomere length outcomes following a family-based prevention program and identified reduced telomere shortening 5 years post intervention among those originally exposed to nonsupportive parenting and randomized to the intervention condition. However, not all individuals respond equally, and a growing literature suggests genetic sensitivity to one's environment, with variations in the oxytocin receptor gene (OXTR) potentially influencing this sensitivity. We utilized data from African American youths (mean age 17) randomized to intervention (n = 100) or control condition (n = 91) with baseline assessments of genetic status and nonsupportive parenting, and 5-year follow-up assessments of telomere length. We found a significant three-way interaction between nonsupportive parenting, intervention condition, and OXTR rs53576 genotype. OXTR GG individuals, who are suggested to be more sensitive to their social environment, exhibited significantly more variability, evidencing the shortest telomeres when exposed to nonsupportive parenting and randomized to the control condition, and similar telomere lengths to non at-risk groups when randomized to the intervention. In contrast, those with the A allele showed no statistical difference in telomere lengths across parental and intervention conditions. Subsequent analyses suggest that these findings may be mediated through chronic anger, whereby GG individuals exposed to nonsupportive parenting and randomized to the control condition had a greater increase in chronic anger by study follow-up, compared to those in the intervention, and this change associated with greater telomere shortening. These findings highlight the importance of individual differences and potential role of genetic status in moderating the relationship between environmental contexts and biological outcomes.
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    • "However, an accumulation of evidence later indicated that vulnerable individuals identified in diathesis–stress models might instead be viewed as sensitive, developmentally plastic, and malleable vis-à-vis environmental influences, regardless of their valence. This alternate perspective led to the biological sensitivity to context model (Boyce and Ellis, 2005) and the differentialsusceptibility hypothesis (Belsky and Pluess, 2009), both of which share features with the concept of sensory processing sensitivity (Aron and Aron, 1997) from the personality literature. These independently developed but complementary and influential models have been joined under the umbrella term neurobiological susceptibility (Ellis et al., 2011; see also Moore and Depue, in press, Pluess (in press), and Stamps (2015) for highly relevant reviews of this general concept). "
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    ABSTRACT: Adolescence has been characterized as a period of heightened sensitivity to social contexts. However, adolescents vary in how their social contexts affect them. According to neurobiological susceptibility models, endogenous, biological factors confer some individuals, relative to others, with greater susceptibility to environmental influences, whereby more susceptible individuals fare the best or worst of all individuals, depending on the environment they encounter (e.g., high vs. low parental warmth). Until recently, research guided by these theoretical frameworks has not incorporated direct measures of brain structure or function to index this sensitivity. Drawing on prevailing models of adolescent neurodevelopment and a growing number of neuroimaging studies on the interrelations among social contexts, the brain, and developmental outcomes, we review research that supports the idea of adolescent neurobiological susceptibility to social context for understanding why and how adolescents differ in development and well-being. We propose that adolescent development is shaped in part by brain-based individual differences in sensitivity to social contexts–be they positive or negative–such as those created through relationships with parents/caregivers and peers. As such, we recommend that future research measure brain function and structure to operationalize susceptibility factors that moderate the influence of social contexts on developmental outcomes.
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    • "According to Belsky's differential susceptibility hypothesis (Belsky, 1997, 2005), infants with negative or difficult temperaments have a heightened susceptibility to caregiving quality (Belsky et al., 1998). Temperament is a phenotypic marker of underlying genetic characteristics that often follows a differential susceptibility pattern in the empirical literature (Belsky & Pluess, 2009). Children with a ''difficult'' temperament (i.e., high negative affectivity) are at an increased risk for subsequent social–emotional maladjustment when they experience a poor-quality caregiving environment (i.e., low-quality childcare or parenting; see Belsky & Pluess, 2009) – but, in contexts of high-quality caregiving, are better adjusted than even those children low in negative affectivity (Boyce & Ellis, 2005). "
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    ABSTRACT: The paper reports on a study which tested whether infants high in negative affectivity are differentially susceptible to observed coparenting behavior in relation to their subsequent social–emotional development. Data came from a longitudinal study of 182 US dual-earner, primiparous couples and their infant children. At nine-months postpartum, child negative affectivity was reported by mothers and fathers and supportive and undermining coparenting behavior were assessed from mother-father-infant observations. At 27-months mothers reported on toddlers’ externalizing behavior and dysregulation using a clinical assessment tool designed to identify competencies and areas of concern in toddlers’ social–emotional development. Hierarchical regression analyses revealed partial support for the differential susceptibility hypothesis. Specifically, infants high in negative affectivity had lower levels of dysregulation when embedded in a more supportive coparenting context, and higher levels of dysregulation when embedded in a less supportive coparenting context. In contrast, supportive coparenting behavior was not relevant for the dysregulation of infants initially low in negative affectivity.
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