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”?
I think that this mechanism could be relevant in humans to some extent, although it is hard for me to believe that there is only one critical time period which what happens after and what happens before does not matter. Rather I think that there may be several time periods where there is a change in stress response. I don’t believe that the mechanism happens at the epigenetic level, but I could be wrong. But certainly experiences throughout one’s childhood including interactions with parent after birth, during infancy, being read to, language tone that is used with kids all impact how stress is internalized or responded to later in life. However there are also structural factors outside of direct parental relationships that oppress individuals and likely impact the way they respond to stress later in life.
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 think that there are pieces of the Weaver findings that could be relevant here, however overall I think of them as being more unrelated. Weavers findings might fit into the psychosocial exposures/processes domain of Gruenwald’s theoretical framework. Gruenwald has a broader framework to understand these processes, and does not try to isolate one piece of adversity to understand the effect on health.
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 don’t think that gene by environment interactions contribute to major disparities along racial/ethnic, socioecononomic, or geographic dimensions. I think I find this model problematic because it places fault on individuals (at the genetic level) instead of on structures of oppression. While this model may be plausible and account for some disparities I think major structural factors of oppression and inequality are more likely to play a major role in health disparities.