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”?
I believe this mechanism has some relevance to humans, although I think it is unlikely that there is one critical time period but rather several periods throughout development that influence the stress response. Probably the most analogous phenomenon is related to diet and obesity prior to puberty having a lasting impact on risk of diabetes and the metabolic syndrome. This is likely a combination of both learned behaviors but may also reflect physiologic “imprinting”. Similarly, part of the motivation of skin-to-skin contact and 24 hour rooming-in post-partum are reduction in stress hormones. It is possible that levels of stress hormones in this early period could influence future response to stress via an epigenetic mechanism.
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.
Gruenewald provides a broader framework to understand the cumulative impact of negative factors on health. Weaver’s findings are not incompatible but rather focus on specific developmental or vulnerable periods in which specific psychosocial exposures may have a larger impact. This theory that there are important developmental periods in which exposures/responses to stress may be more influential is also reflected in Gruenewald’s findings in which SES adversity in childhood appears to account for much of the cumulative SES adversity score.
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?
The gene-by-environment interaction approach recognizes that there are genetic differences that may predispose individuals to specific phenotypes (for example increased risk of diabetes as mentioned in the first example, or in my field of research there are a set of genetic mutations that seem to predispose individuals to developing progressive fibrotic lung disease later in life). However the environment can substantially modify the phenotype by genetic-environment interactions. In the fibrotic lung disease example, some individuals are born with certain mutations that predispose them to fibrotic lung disease. However subsequent exposures in their environment (early exposure to secondhand smoke, mold/mildewed living environments, etc) influence the trajectory. The gene-environment interaction approach is similar to many “two hit” disease models in which you are thought to be born with a genetic predisposition to a specific outcome, but a second factor determined by your environment influences whether the outcome/disease state occurs. As race, SES and geographic differences all strongly impact environment it is not hard to see how the GxE interaction can lead to disparities along these lines. However I do think we should be careful that we do not consider genes and environment equally. In fibrotic lung diseases, genetic differences account for <5% of variation suggesting that environment plays a much larger role in determining the disease state.