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 is an interesting study and theory, and it’s certainly conceivable that epigenetic changes during infancy affect humans as well as rats. However, studies also suggest that epigenetic changes continue over a lifetime as a result of environmental and social factors. The relative importance of epigenetic changes in infancy compared to those occurring throughout a lifetime would be more impactful, as this comparison would help us understand the “clinical significance” of each type of epigenetic change on an individual’s life experiences. Analogous behaviors in infancy could include breastfeeding, cuddling, and soothing behaviors (cooing, rocking).
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 findings are consistent with Weaver’s findings; the scope of these two studies is just quite different. Gruenewald creates a broad framework of socioeconomic measures that impact the allostatic load developing over an individual’s lifetime. In contrast, Weaver focuses on two very specific behavioral activities that occur during a specific time period. Weaver’s findings could fit within the broader framework of Gruenwald’s study as one critical point in development that contributes to the multi-system allostatic load measures.
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 theory takes into account that genetic phenotypes predispose individuals to illness, but the life stressors associated with lower SES may increase the likelihood of developing the disease or result in a more severe presentation. It’s difficult to ascribe the “extent” of the impact of GxE interactions, but I believe that an individual’s developmental trajectory is impacted by these interactions. For example, depression and schizophrenia have genetic predispositions, but life stressors can trigger development of the disease. Higher SES may be protective against these stressors and prevent individuals with more socioeconomical support from developing the disease. Genetically predisposed individuals from lower SES environments are thus at a double disadvantage, first from developing the disease and second from having fewer support structures to help manage it.