Questions Related to Week 5 Readings:
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”?
In infants, there is thought to be a “golden hour” where just after the baby is born, skin-to-skin contact between the infant and the mother is important to both the mother and the infant. For infants, this includes both physiologic benefits and benefits having to do with breast-feeding. Studies have shown that this skin-to-skin contact improves the likelihood of successful breast feeding at their first feed, these infants have higher glucose levels and more stability of the cardio-respiratory system. (Moore et al. “Early skin-to-skin contact for mothers and their healthy newborn infants” in Cochrane Database Syst Rev 2016) One study even showed that this golden hour improved the stabilization of multiple parameters of very low birth weight pre-term infants. (Castrodale & Rinehart “The golden hour: improving the stabilization of the very low birth-weight infant” in Adv Neonatal Care 2014) Mothers who had this skin-to-skin contact were more likely to exclusively breast-feed and continue breastfeeding longer Moore et al. “Early skin-to-skin contact for mothers and their healthy newborn infants” in Cochrane Database Syst Rev 2016).
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.
You could examine whether babies who were breastfed during the first year of life were more or less likely to develop depression later in life. You could design this as a cohort study of adults – one group who had been exclusively breastfed, and one group who had been formula-fed. Then evaluate how many in each group developed depression by a pre-defined time-point. You could sample their brain tissue via biopsy or after death, in order to examine for the epigenetic changes.
3. 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.
I think that the Grunewald findings are consistent with the Weaver findings. Importantly, the Gruenwald study uses different metrics so the outcomes are not directly comparable. Gruenwald evaluates association between lifetime stressors and biological markers, as compared with evaluation of actual epigenetic modifications by Weaver. Ultimately, however, they are both evaluating the impact that the exposure to stressors has on future health, with differences in where they are measuring this impact in the downstream pathway.
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?
I think that GxE interactions have a huge potential to impact disparities among all of these dimensions. Take geographic, where living in a certain geographic area will give individuals different exposures. We know of instances where these exposures can lead to genetic diseases in those individuals’ offspring, for example. In other words, just by living in a certain geographic region could result in exposures that result in genetic modifications that cause differences in downstream health. Ultimately, it seems that the way these GxE interactions could be linked to major disparities is really through disparities in exposure… certain races, SES classes, or geographically-located groups being in contact with different exposures than other groups. These environmental exposures then have the ability to interact with genes to impact those individuals’ trajectories and, in our interest, health outcomes.