Biological reactivity to psychological stressors comprises a complex,
integrated, and highly conserved repertoire of central neural and
peripheral neuroendocrine responses designed to prepare the organism for
challenge or threat. Developmental experience plays a role, along with
heritable, polygenic variation, in calibrating the response dynamics of
these systems, with early adversity biasing their combined effects toward
a profile of heightened or prolonged reactivity. Conventional views of
such high reactivity suggest that it is an atavistic and pathogenic legacy
of an evolutionary past in which threats to survival were more prevalent
and severe. Recent evidence, however, indicates that (a) stress reactivity
is not a unitary process, but rather incorporates counterregulatory
circuits serving to modify or temper physiological arousal, and (b) the
effects of high reactivity phenotypes on psychiatric and biomedical
outcomes are bivalent, rather than univalent, in character, exerting both
risk-augmenting and risk-protective effects in a context-dependent manner.
These observations suggest that heightened stress reactivity may reflect,
not simply exaggerated arousal under challenge, but rather an increased
biological sensitivity to context, with potential for negative
health effects under conditions of adversity and positive effects under
conditions of support and protection. From an evolutionary perspective,
the developmental plasticity of the stress response systems, along with
their structured, context-dependent effects, suggests that these systems
may constitute conditional adaptations: evolved psychobiological
mechanisms that monitor specific features of childhood environments as a
basis for calibrating the development of stress response systems to
adaptively match those environments. Taken together, these theoretical
perspectives generate a novel hypothesis: that there is a curvilinear,
U-shaped relation between early exposures to adversity and the development
of stress-reactive profiles, with high reactivity phenotypes
disproportionately emerging within both highly stressful and
highly protected early social environments.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 by
the Division of Intramural Research of NICHD. The first author is
particularly indebted to Dr. Steve Suomi and Dr. Jan Genevro for a series
of conversations that directly influenced the ideas upon which this paper
is based. We also thank Dr. Jay Belsky and Dr. David Bjorklund for their
helpful comments on an earlier draft of this paper.