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 that epigenetic mechanisms have a relevant effect on human health. A clear example was the winter of Dutch famine in the Second World War. It was an intervention (dramatic for war) in a specific period of time that modified pregnant women being exceptionally vulnerable, and the children they gave birth were influenced by epigenetic changes resulting from hunger throughout their lives. When they became adults, they ended up weighing a few kilos more than the average. In middle age, they had higher levels of triglycerides and LDL cholesterol. They also experienced higher rates of diseases such as obesity, diabetes and schizophrenia.[1] So if the dietary factors can contribute to the epigenetic alterations and, in some cases, they could potentially reverse the abnormal epigenetic states. This may provide a reason to consume products that show the ability to stimulate beneficial epigenetic modifications, including increased consumption of fruits, vegetables.
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 the findings in Gruenewald's study may be complementary to Weaver's findings. Gruenwald's study shows an effect of increased SES adversity on the average multi-system allostatic load in a "period of life" and in all "periods of life", a greater adversity of SES was associated with a higher multi-system allostatic load average among the study participants. Weaver's findings, on the other hand, could be extrapolated to the fact that experiencing adversity (from SES for example) in key periods of time during a person's life can prepare him / her to develop physical / psychological risk, as opposed to experiencing the same adversity by SES in other periods of time less critical of its development.
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 interaction is an important mechanism in health along with other mechanisms. The process of controlling gene expression is complex and the research that examines epigenetic processes provides a specific place, time, conditions where the intersection of genes/gene expression and the environment occurs.I think that adversity or enrichment in early life has far-reaching effects throughout life. The interactions between the gene and the environment between the specific genetic variants and the early social environments that generate risk may be related to the differences in the epigenetic processes, which explains the variation between individuals in the expression of related genes, for example, with neurodevelopment disorders. On the other hand, knowing that these mechanisms are reversible we could generate interventions that could be accompanied by analysis and changes of epigenetic markers.
[1] Ekamper et al., “Independent and Additive Association of Prenatal Famine Exposure and Intermediary Life Conditions with Adult Mortality between Age 18–63 Years.”