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”?
This study was very thorough and I was impressed that they were able to show reversibility of the epigenetic changes by central infusion of a histone deacetylase inhibitor. While these particular behaviors is not directly applicable to humans, there is a possibility that a “sensitive period” exists for humans where social behaviors are key for epigenetic modification of the newborn’s genome. It is already established that behaviors around key developmental periods in childhood will affect outcomes such as attachment behaviors as the child grows. Some behaviors that may be analogous to licking/grooming and arched back nursing may be skin-to-skin contact, smiling, talking/singing/reading to the child, and positive affirmations. The challenge is to identify the key behaviors, genes, and time period in the context of human development.
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.
The Gruenewald study indicates that SES adversity accumulated over the course of a lifetime correlates with greater allostatic load. This differs from the key “sensitive period” indicated in the Weaver study. As the two studies are investigating very different research contexts (mouse epigenetic changes vs. surveying a large human cohort) I do not think that they refer to the same populations. However both could be true: there could be key sensitive periods in human development as well as a cumulative load of SES adversity.
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?
Hertzmann and Boyce cite numerous examples of instances where gene’s affect on developmental outcomes is only present under certain environmental conditions. For example, the low monoamine oxidase A (MOA) activity polymorphism was associated with antisocial outcomes in males only in the context of severe childhood maltreatment. I think that GxE interactions may contribute to a small amount of the disparities we observe along social gradients, but the majority is probably largely determined by social factors.