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”?
There is an interesting theory that is under investigation here at UCSF regarding the apparent increased risk of diabetes / metabolic syndrome among filipinos who emigrated to the US, compared to both native filipinos as well as filipino americans that were born and raised in the states. Certainly, there are multiple cultural / societal effects at play, but one theory is based on the idea that there are “imprinting” metabolic events in utero that impacts the child’s future metabolism and risk of developing diabetes. If a mother in the Philippines was subject to less fatty foods, and then the offspring were exposed to higher caloric nutrition during lifetime, obesity and diabetes would more likely occur.
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 Gruenewald’s findings are consistent to the Weaver findings. To use my example, there are many significant SES impacts (access to healthy food options, physical activity levels, and stress) that most certainly increase the risk of developing diabetes. However, as far-fetched as the above theory is, I do think there is “weight” behind the fact that some folks are just pre-disposed to obesity and weight gain then others. I do believe that some people can eat whatever they want and not gain a pound, while others cannot. The idea that there is a critical window early in development that impacts this later-in-life tendency to pick up weight is compelling to me.
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?
I think my example can be an illustration of this gene-by-environment concept. If a filipino mother comes from a low SES in the Philippines, and has poor nutrition during pregnancy, the child may be at increased risk of packing on the pounds when (s)he lives in a nutrient dense environment like the US. This concept is so critical to the idea that SES disparities can have biological plausibility in impacing lifelong (and intergenerational) pathways.