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”?
Perhaps the effects of maternal influences on HPA development and behavioral responses to stress discovered in rats translate to humans through maternal behaviors of skin-to-skin or kangaroo care postpartum. Research has established that skin-to-skin contact particularly in the first week postpartum enhances brain development and calms newborns. What is interesting is the positive effects of skin-to-skin aren’t only reaped by the newborn but studies showed fewer symptoms of depression and lower levels of salivary cortisol vs mothers who did not have skin-to-skin contact with their babies.
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.
Considering Link & Phelan (1996) propose SES as a fundamental cause of health outcomes, I do not think the Gruenewald paper contradicts the findings of Weaver. Behaviors such as maternal behaviors during infancy, could act as a potential mediator of health outcomes related to SES. For example, a postpartum woman currently experiences a low SES context may not have maternity leave from work in order to fully engages in skin-to-skin care. Individual behavior factors or choices of parenting can be directly influenced by the larger SES adversity context.
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 described the phenomenon of genes by environment well in their paper. The authors conclude that biologically sensitive people are distributed across social classes but the environment of low SES context with the probability of higher adversity contexts aggravates risk of the expression of these genes resulting in poor health outcomes. Whereas biologically sensitive individuals growing up in privileged environments will experience more protective effects on these genes resulting in better health outcomes. The interplay is dependent on context and therefore create disparities between SES groups from childhood.