Questions Related to Week 4 Readings:
- 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”?
Analogous human behaviors could include breastfeeding, holding, cuddling, and talking/singing to infants. The stress mechanism in the rats is similar to the stress response process in humans via the hypothalamic-pituitary-adrenal axis. It makes sense to me that we would especially sensitive to stressors during certain developmental periods that could lead to long-term, learned physiologic and emotional response patterns.
- 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 don’t think Gruenewald is inconsistent with Weaver. In fact, Gruenewald found that greater SES adversity at each time period was a significant predictor of higher allostatic load. In other words, our current health is determined in part by stressors both during childhood and cumulative over time. The good news is the adverse effect of childhood stress can, at least in theory, be attenuated by lower SES adversity during adulthood.
- 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?
It seems to me that GxE interactions can contribute to a vicious cycle that worsens disparities over time. Low SES in children adversely affects the HPA axis (e.g. dysregulation) leading to social-emotional, cognitive, and developmental disturbances that directly affect health and also contribute to continued or worsening low SES that in turn lead to even poorer health. The modification in gene expression that occurs in this process can be passed on to offspring producing an intergenerational pattern of growing health disparities.