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”?
The authors show that the maternal behavior alters the HPA responses in rats and such response has been documented in other mammals. However, to my reading, these effects have not been reported in other primates. That said, it is not unreasonable to extrapolate that parental behavior can influence a child response to stress. Children with a better SES during the first few years of life have fewer behavioral problems. Behaviors most analogous to “maternal licking and grooming” in humans may include contact time (i.e holding and carrying, touching and interacting).
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.
The findings in this paper by Gruenewald et.al. are not inconsistent or unrelated to those of Weaver et. al. Gruenewald et.al. uses a comprehensive measure which they called allostatic load consisting of SNS, PNS, HPA, cardiovascular, glucose metabolism, lipid, and inflammation risk indices. They include HPA and some of the other measures likely are modulated by epigenetic mechanisms. So the two papers measure similar outcomes. In Weaver et. al. measure the exposure at one time-point – care at an early age of childhood, whereas Gruenewald et.al. measure the exposure as a cumulative variable.
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 authors argue that the interaction of genes and environment contribute to health disparaties and have supported their arguments with example – child development and how it effects health, differences between Swedish and Lithuanian men in terms of heart disease, effect of life experiences on four major biological systems (HPA, ANS, memory/attention, social affiliation).
Genetic differences among race/ethnicity are well known. We also know that health issues are modified by the environment. For example, Japanese-Americans have a lower rate of gastric cancers than those living in Japan. This not only demonstrate interaction of environment with race/ethnicity, but also with geographical differences. Another study Hamdi et.al. 2015 looked at the interaction of alcohol use among twins in relation to SES/environment. The study found that in low-SES environment, the alcohol use varies considerably and this is largely explained by genetic factors. Ref: Hamdi NR, Krueger RF, et.al. Socioeconomic status moderated Genetic and Environmental Effects on the Amount of Alcohol Use. Alcohol Clinic Exp Res, 39(4):603-610, 2015.