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...Do you think this mechanism is relevant in humans? If so, what behaviors are most analogous to “maternal licking and grooming”?
Yes, I believe that particular maternal behaviors during the peripartum/early infancy have an effect on infant development. As the article notes: “...maternal effects on the expression of defensive responses, such as increased HPA activity, are a common theme in biology.” It would stand to reason that humans would be no exception to such a common theme. I think we see this acknowledged to some degree in the encouragement of new parents to participate in skin-to-skin contact and other bonding/soothing behaviors for the benefit of the infant such as reading or singing. It seems possible that the infant would be able to pick up on if its needs are being met, and the responsiveness or timeliness of the parent to those needs, and that may have an effect on how the infant will handle distressing periods later.
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.
These findings are consistent with the Weaver article. Both articles highlight the possibility of a biological consequence to social interaction/stressors. Gruenewald’s main finding was that higher levels of allostatic load in middle/late adulthood correlated with those who experienced higher SES adversity across the life course. I think this is consistent with the Weaver article, in particular to Weaver’s comment on the reversal of the epigenetic markings with cross-fostering. I think that plays well into Grunewald’s discussion on allostatic load and the buildup of the SES adversity. However, they were not looking at exactly the same measurements and, therefore, it is only the idea of this as a larger concept that rings true for these two studies.
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 research up to this point in investigating the “whether and how” has reached the point that we can at say “whether” they interact is clear, but “how” they interact is up for interpretation. My concern is if the "how" even matters at all. It is clear that these mechanisms are complex and are not perfectly studied. The “gene by environment” idea plays by Weaver’s findings of the epigenetic markers being reversible, as well as Gruenewald’s allostatic load theory. The example in this H&B article of how environmental factors like “urban vs rural can interact with serotonin receptor gene expression” is an example of how GxE interactions can contribute to disparities related to geographic dimensions.
In short, I think the article is convincing, however, (and maybe I’m just feeling cynical at the moment) I question the utility of spending so much energy looking into the "how" and these micro-changes in genes, when the full reality of the consequences of people’s environment/SDH is right in front of us and waiting for change. Do we need more studies on rat licking to add to the evidence, or do we need more studies on intervention and implementation?