Differential Susceptibility


Theoretical background of the differential susceptibility hypothesis

Because the future is and always has been inherently uncertain, ancestral parents, just like parents today, could not have known (consciously or unconsciously) what 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 optimizing strategy involving bet hedging[6]natural selection would 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, in light of inclusive-fitness considerations, these less malleable children’s “resistance” to parental influence would not only have benefited themselves directly, but even their more malleable sibs-indirectly, given that sibs, like parents and children, have 50% of their genes in common. By the same token, had parenting influenced children in ways that enhancedfitness, 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 sibs who did not benefit from the parenting they received, again for inclusive-fitness reasons.
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. Criteria for the testing of differential susceptibility
Belsky, Bakermans-Kranenburg, & van IJzendoorn, (2007) delineated a series of empirical requirements-or steps-for convincingly establishing evidence of differential susceptibility to environmental influences and distinguishing 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 characterized by a cross-over interaction: the susceptible inpiduals 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 inpiduals that have been shown to moderate environmental effects in a manner consistent with the differential susceptibility hypothesis can be subpided into three categories[9]:

  1. Genetic Factors
    E.g., Bakermans-Kranenburg and van IJzendoorn (2006) were the first to test the differential susceptibility hypothesis as a function of genes regarding the moderating effect of thedopamine receptor D4 7-repeat polymorphism (DRD4-7R) on the association between maternal sensitivity and externalizing behavior problems in 47 families. Children with the DRD4-7R allele and insensitive mothers displayed significantly more externalizing behaviors than children with the same allele but with sensitive mothers. Children with the DRD4-7R allele and sensitive mothers had the least externalizing behaviors of all whereas maternal sensitivity had no effect on children without the DRD4-7R allele.
  2. Endophenotypic Factors
    E.g., Obradovic, Bush, Stamperdahl, Adler and Boyce’s (2010) investigated associations between childhood adversity and child adjustment in 338 5-year olds. Children with highcortisol 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).
  3. Phenotypic Factors
    E.g., 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 behavior problems depending on whether they experienced, respectively, poor or good quality care (and in comparison to children with easier temperaments).


Ellis et al. 2011 Differential susceptibility to the environment: An evolutionary–neurodevelopmental theory, pdf file
Bakermans-Kranenburg, VanIJzendoorn 2007 Genetic vulnerability or differential susceptibility in child development: the case of attachment, pdf file
Bakermans-Kranenburg, VanIJzendoorn 2006 Gene-Environment Interaction of the Dopamine D4 Receptor (DRD4), pdf file
Bakermans-Kranenburg, VanIJzendoorn 2011 Differential susceptibility: New evidence and meta-analysis, pdf file
Belsky et al. 2007 Differential Susceptibility to Environmental Influences, pdf file