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 mechanism seems to also be relevant in humans. One analogy would be research that has demonstrated that mothers of newborns with immediate skin-to skin contact release higher levels of oxytocin than mothers without immediate skin-to-skin contact with their newborns. Higher levels of oxytocin have been associated with promoting maternal/fetal bonding, reducing newborn stress, promoting newborn breast feeding and duration of breast feeding.
2. Provide a brief proposal for a study that would allow you to assess whether epigenetic modifications in humans in response to maternal behavior influence subsequent health of the human (feel free to choose any health or behavioral outcome you think you can do this with, e.g., dementia or depression or smoking). Bonus if you can explain how you would approach this if we assume that the relevant epigenetic changes are tissue specific and occur in the brain.
One way to test this hypothesis would be to measure levels of oxytocin in mothers with immediate skin to skin and then in mothers without immediate contact with their newborns. In adulthood, maternal levels of oxytocin could be used to determine the presence or absence of anxiety in adulthood. The null hypothesis would be that adults whose mothers had low levels of maternal oxytocin are more likely to have anxiety in adulthood. While you could potentially then assess for this connection between the predictor and outcome, it is difficult to control for many external factors that could also lead to anxiety in adulthood.
3. Gruenewald, in contrast to Weaver, emphasizes 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.
Despite use of different measures (biological markers vs. cumulative effects of SES), the Gruenwald findings seem to be consistent with the Weaver findings/ One exception being that in the Weaver article, the authors suggested that maternally mediated epigenetic markings may not be reversible in adulthood, whereas the Gruenwald article proposes many pathways through which social status is linked to health and as such, intervening on any step could potentially lead to improved health
4. 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?
Genetics, early environments and experiences are all important in building the foundation for how individuals respond to future environmental exposures (cumulative SES, stress, diet, etc.). In twin studies (ex. Sickle cell disease), even with similar genetics, when exposed to different environments, twins have different phenotypic expressions of the same disease which is why I believe that the interaction of genetics and environment contributes to health disparities. As a researcher with an interest in this area, this intersection provides many opportunities for interventions over a person’s lifetime to affect health outcomes.