One species-general life history (LH) principle posits that challenging childhood environments are coupled with a fast or faster LH strategy and associated behaviors, while secure and stable childhood environments foster behaviors conducive to a slow or slower LH strategy. This coupling between environments and LH strategies is based on the assumption that individuals’ internal traits and states are independent of their external surroundings. In reality, individuals respond to external environmental conditions in alignment with their intrinsic vitality, encompassing both physical and mental states. The present study investigated attachment as an internal mental state, examining its role in mediating and moderating the association between external environmental adversity and fast LH strategies. A sample of 1169 adolescents (51% girls) from 9 countries was tracked over 10 years, starting from age 8. The results confirm both mediation and moderation and, for moderation, secure attachment nullified and insecure attachment maintained the environment-LH coupling. These findings suggest that attachment could act as an internal regulator, disrupting the contingent coupling between environmental adversity and a faster pace of life, consequently decelerating human LH.

Extrinsic mortality risks calibrating fast life history (LH) represent a species-general principle that applies to almost all animals including humans. However, empirical research also finds exceptions to the LH principle. The present study proposes a maternal socialization hypothesis, whereby we argue that the more human-relevant attachment system adds to the LH principle by up- and down-regulating environmental harshness and unpredictability and their calibration of LH strategies. Based on a longitudinal sample of 259 rural Chinese adolescents and their primary caregivers, the results support the statistical moderating effect of caregiver–child attachment on the relation between childhood environmental adversities (harshness and unpredictability) and LH strategies. Our theorizing and findings point to an additional mechanism likely involved in the organization and possibly the slowdown of human LH.