1. Weaver et al propose that among rats, maternal behavior towards newborn pups influences their cortisol response to stress via epigenetic mechanisms that change the expression of glucocorticoid receptor gene for the rest of the pup’s life. They argue that because epigenetic patterns are established at specific developmental periods, there is extreme time sensitivity to when the pup is exposed to particular maternal behaviors (licking and grooming, in this case), and maternal behavior before or after that sensitive period window is not as important. Do you think this mechanism is relevant in humans? If so, what behaviors are most analogous to “maternal licking and grooming”?
Weaver proposes that behavioral programming during early critical period altered GR gene promoter and were reversible through cross-fostering, thus a mechanism for life-long offspring effects by maternal behavior through gene expression. I would think LG and ABN would be analogous to early mother behavior and child interaction, such as early skin-to-skin contact, innate emotions (smiling, laughing, singing) and feeding/latching. Roth et al 2013 (PMC4080409) reports relevant epigenetic examples among humans with varying early critical period experiences, such as epigenetic regulation linked to childhood experiences (sexual abuse, institutional care and maternal stress level).
2. Gruenewald, in contrast, emphasize the cumulative effects of SES adversity on a multi-system allostatic load measure. Do you think that the Gruenewald findings are consistent, inconsistent, or unrelated to the Weaver findings? Explain.
I believe Gruenewald and Weaver’s models are overlapping, but vary is scope and modifiability. Both involve exposure factors affect on biological regulatory systems. Weaver proposes that the external impact to epigenetics occurs during a defined ‘critical period’ early in life, and although there is degree of reversibility, the impact mostly occurs during these early years. Alternatively, Gruenwald suggests a cumulative effect of environment throughout a life course, including adulthood (measured by AL). They do note that childhood health was not measured, and that perhaps negative interaction during ‘critical period’ could have led to worse childhood health, worse life course SES and outcomes. Within the cumulative model, environmental factors (SES) may impact epigenetics and gene expression; Weaver would seem to suggest this occurs mostly during critical period while Gruenewald would suggest this is a life long process.
3. Hertzmann and Boyce argue that “it is not genes or environment, nor is it genes and environment, but rather it is gene-by-environment interactions that influence developmental trajectories.” To what extent do you think that GxE interactions can contribute to major disparities along racial/ethnic, socioeconomic, or geographic dimensions?
I believe they could likely play a significant role – varying exposure experiences by race/ethnicity, SES, neighborhood, etc can impact epigenetics (as outlined above), impact biological regulatory systems (HPA axis) and lead to varying health outcomes. Through the cumulative model, this could occur through a life course and lead to increasingly widened disparities with continued exposure. The article uses example of increased cortisol exposure by early stressor (ie time in Romanian orphanage) with future developmental outcomes. They raise an interesting paradox where those from lower SES, who may be more ‘biological sensitive through early adversity, will find themselves in risk-augmented settings through life that will drive a deeper disparity. This model offers a potential causal framework to potentially intervene upon (early interventions).