1. Yes, the mechanism is clearly relevant to humans. The primary human analog to maternal licking and grooming is child-caregiver attachment security, which has been persuasively demonstrated as a salient predictor of later childhood and adult emotional and interpersonal function and parenting style. One difference between humans and rats, however, is the capacity of humans to recover from the adverse effects of insecure early attachment through therapeutic processes (measured, for example, by the Adult Atttachment Interview), leading most child developmental researchers to conceive of key junctures in early life as "sensitive" rather than "critical" periods, in light of the former’s scope for plastic reorganization.
2. “Dyadic infant-caregiver meditation training modifies epigenetic transmission of insecure attachment-based emotional dysregulation: A longitudinal neurogenomic investigation of trauma-exposed low-income families.” The objective of the study is to determine whether a mindfulness-based dyadic parenting intervention in which parents and young children in a high trauma-exposed community and in which dyads engage in conjoint yogic and other age-appropriate contemplative practices reduces emotional dysregulation in early adolescence. A neurogenomic approach involving bioinformatics, genomics and neuroimaging will be used to investigate the role of epigenetic processes in the developmental maturation of key substrates of emotional self-regulation functions in the frontal executive and limbic systems.
3. In conceptual terms Gruenewald’s findings are consistent and complementary to Weaver’s. Adversity-related alterations in stress physiology are certainly conceivable as the outcome both of deficits in critical periods and cumulative load over time: that is, these ideas are not mutually exclusive. However, I’m not familiar with the extent to which the empirical literature in human development necessarily supports this conceptual possibility.
4. Racial and socio-economic health disparities reflect gene-environment interactions because environmental stressors such as oppression, food insecurity, and environmental toxins etc. disproportionately affect historically marginalized communities. Genetic risk factors for negative health outcomes are more likely to result in actual negative outcomes when they interact with environments that amplify their risk-promoting impacts through psychosocial mediation of epigenetic gene transcription processes.