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”?
The mechanism does appear relevant to humans, given the research demonstrating linkages between adverse childhood events/experiences and chronic HPA dysregulation/elevated cortisol levels (supposing the opposite, supportive/nurturing environments help regulate HPA/promote resiliency). Maternal licking/grooming in rats could be equated to human bonding/nurture, such as skin-to-skin, breastfeeding, in addition to general care/bathing/singing/soothing of newborns. “Baby friendly” hospitals, promote skin-to-skin and early breastfeeding interventions in an effort to promote mother-newborn bonding and breastfeeding. I am not aware of studies that have shown that such measures also increase resiliency/protect against future stress responses, but it seems to be an area of interest/current research; nor am I aware of there being a well-defined critical time period, such as the Weaver article reports for rats.
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.
Gruenewald’s findings relate and are consistent w/Weaver’s findings. The two articles take 2 different approaches (and subjects), but both appear aimed at looking at factors contributing to future stress/HPA dysregulation. Where Weaver focuses on factors that may be protective against future HPA dysregulation, Gruenewald focuses on the impact of repeat SES stressors with HPA dysregulation. As noted above, both are important for furthering our understanding of how to protect against and intervene early to improve patients’ stress responses and resiliency. Neither article is disproving or arguing against the other, but they are two approaches to a common goal.
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?
The gene-by-environment interactions (GxE) can have huge impact on disparities, given the disparities starting early in life that can impact future development. The authors list multiple examples, and it is easy to see how adverse life experiences starting in the womb would impact development of infants through adulthood. Given continued institutional racism, segregation and growing disparities in SES (and often along geographic lines), it is easy to imagine that the widening of disparities can have a snowballing effect, as communities are in a cycle of stress and poverty. Ideally, we would have the social policies and resources to combat racism, improve patients’ SES, and reduce the stress and toxin exposures that can start in the prenatal period and impact a person’s development.