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”?
The assumption that early changes to DNA methylation and other epigenetic processes could have similar mechanisms in humans as the rat models described in the Weaver paper. One example of similar maternal infant bonding could be during initial skin to skin contact with a newborn especially in preterm infants. Early breastfeeding may also be a similar behavior that could impact the infant’s genetic material. However, I doubt that there is only one critical window for genetic change through the lifespan of a human being.
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 major difference appears that Weaver et al focused on specific individual maternal behaviors at a specific, early timepoint in child/pup development, while Gruenewald describes a cumulative impact of multiple stressors or time. An individual’s response to these stressors may be impacted by early epigenetic changes (ie viia the HPA pathway, cortisol response), so the two topics do appear loosely related. The major inconsistency appears to be that Gruenewald suggests an individual’s response to stress changes over time as these adverse events accumulate which does appear to be different than Weaver’s ascertain that early maternal behaviors are the primary driver of how an individual’s regulation of their stress response is formed.
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?
This appears to be the “middle of the road” seeking to combine a strictly biological and strictly behavioral explanation for individual variation in stress response. For individuals we a genetic predisposition to a specific disorder lower SES and the accompanying discrimination and chronic stress that can be associated, may lead an individual to be more likely to have the illness or have a more severe phenotype. However, this model fails to include the structural, societal impact on individuals including historical oppression, racism, and discrimination.