Development and Psychopathology

Biological sensitivity to context: II. Empirical explorations of an evolutionary–developmental theory

a1 University of Arizona
a2 University of Wisconsin
a3 University of California, Berkeley

Article author query
ellis bj   [PubMed][Google Scholar] 
essex mj   [PubMed][Google Scholar] 
boyce wt   [PubMed][Google Scholar] 


In two studies comprising 249 children and their families, the authors utilized secondary, exploratory data analyses to examine Boyce and Ellis' (this issue) evolutionary–developmental theory of biological sensitivity to context. The theory proposes that individual differences in stress reactivity constitute variation in susceptibility to environmental influence, both positive and negative, and that early childhood exposures to either highly protective or acutely stressful environments result in heightened reactivity. In Study 1, 127 3- to 5-year old children were concurrently assessed on levels of support/adversity in home and preschool environments and on cardiovascular reactivity to laboratory challenges. In Study 2, 122 children were prospectively assessed on familial stress in both infancy and preschool and on autonomic and adrenocortical reactivity to laboratory challenges at age 7. In both studies, a disproportionate number of children in supportive, low stress environments displayed high autonomic reactivity. Conversely, in Study 2, a relatively high proportion of children in very stressful environments showed evidence of heightened sympathetic and adrenocortical reactivity. Consistent with the evolutionary–developmental theory, the exploratory analyses also generated the testable hypothesis that relations between levels of childhood support/adversity and the magnitude of stress reactivity are curvilinear, with children from moderately stressful environments displaying the lowest reactivity levels in both studies. a

c1 Address correspondence and reprint requests to: Bruce J. Ellis, Division of Family Studies and Human Development, University of Arizona, PO Box 210033, Tucson, AZ 85721-033; E-mail:


a The research on which this paper was based was supported by grants from the John D. and Catherine T. MacArthur Foundation's Research Network on Psychopathology and Development, the National Institute of Child Health and Human Development (1RO1 HD 24718), and the National Institute of Mental Health (R01-MH44340 and P50-MH53524). We thank Jay Belsky and David Bjorklund for comments on an earlier draft of this paper.