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”?
Yes, I do believe a similar phenomenon exists in humans and this truly reveals the interaction and nature and nurture. I also think that there are many critical developmental periods where parent-child interaction can influence epigenetic mechanisms. For example, kangaroo care or skin-to-skin contact in the first few days of life as well as breastfeeding are both parent-child interactions in early life that have been shown to improve health outcomes. Additionally, parental interaction and warmth during childhood has also been associated with health outcomes, with poor health in adults who received very little loving interaction from their parents during childhood. The proposed mechanism for this long-term effect is physiologic differences in response to stress, similar to that proposed in the Weaver article (Carroll et al. PNAS 2013).
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.
I think that the mechanisms proposed by Weaver and Gruenewald both occur and that they are not mutually exclusive. Gruenewald and colleagues show that lifetime exposure to socioeconomic disadvantage is associated with increased markers of physiologic stress in adulthood. This hypothesis makes sense, but it is also possible that positive behavioral interactions (like parental warmth and affection) may reduce the biologic impact of such socio-economic stressors.
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?
Gene-environment interactions clearly occur and the effect of this interaction on health and disparity have been hypothesized and studied for some time. I do think the interplay of the two greatly contribute to health disparity. Evaluating how this relationship affects disparity along different dimensions of disparity is an interesting thought. As I was reading the H&B article, I started to think of different low SES communities and how their known health risks and outcomes are different even when all are exposed to low SES and to racial/ethnic disparities. Take for example, new immigrants to the US versus tight-knit religious based communities (eg Ashkanazi Jewish or Amish) versus Africans in small communities in rural Africa. All could be said to be “low SES” risk, all have racial/ethnic differences and yet their overall and long-term health risks are all very different. Understanding how the GxE interaction differs from one group (however you define it) to the next could be informative in how we may address/improve the quality of life for another group. Easier said than done of course…