W. Thomas Boyce

TL;DR: A scientific consensus is emerging that the origins of adult disease are often found among developmental and biological disruptions occurring during the early years of life as mentioned in this paper, and that these early experiences can affect adult health in 2 ways: cumulative damage over time or by the biological embedding of adversities during sensitive developmental periods.

TL;DR: 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.

TL;DR: The differential susceptibility paradigm has far-reaching implications for understanding whether and how much child and adult development responds, for better and for worse, to the gamut of species-typical environmental conditions.

TL;DR: This paper found that the effects of high reactivity on behavior and health are bivalent rather than univalent in character, exerting both risk-augmenting and risk-protective effects depending on the context.

TL;DR: It was found that a model's capacity to explain SES-health relationships varied across health outcomes, and the authors proposed a developmental approach to exploring mechanisms that link SES and child health.