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 do think this mechanism is relevant in humans. When I read the article, the first mechanism or theory that I could think of was John Bowlby’s attachment theory. While it may not be the best example, I think the resemblance is quite intriguing. Bowlby’s work suggests that children’s attachment styles are influenced by their mother’s presence—both physical and emotional presence—at critical stages of a newborn’s child (~birth day to 6-8 months). The four attachment styles that were described by Bowlbly are secure, anxious-avoidant, ambivalent, and disoriented. Secure attachment refers to children who have developed a safe, secure attachment with their primary caregiver—they are happy and eager to explore their surroundings. While distressed when the mother is gone, they are assured she will return; this attachment is influenced by the mother’s consistent emotional and physical presence. Anxious-avoidant attachment refers to children who do not fully trust their mothers to provide them with their needs—they are quite insecure and anxious due to the mother being emotionally distant. Ambivalent attachment styles refer to children that developed insecurity and helplessness around their mother’s due to the mother’s inconsistent and sometimes neglectful behavior. Lastly disorganized/disoriented attachment style refers to children who do not fit in any of the aforementioned attachment styles and are often angry, passive, and apathetic due to the mother’s extreme behavior that varies between passivity and aggression. Thus, maternal emotional presence (i.e., behaviors including physical connection, physical presence, attending to child’s needs, etc.) is most analogous to maternal licking and grooming.
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.
It almost seems like Gruenewald findings are inconsistent with the Weaver findings. Gruenewald, as mentioned, emphasizes the cumulative effects of issues in SES on a multi-system allostatic load measure, but no emphasis on an early sensitive period that highly influences future outcomes. The latter explanation is consistent with Weaver findings. Essentially the two arguments are related—both looking at the influence of genetic and social factors contributing to future health outcomes. Both seem plausible and can be applied to different research questions.
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?
This is a really interesting question, and I liked the way Hertzmann and Boyce developed and conveyed their argument. While I cannot come up with a generalized answer, I do actually think GxE interactions can potentially contribute to major disparities along racial/ethnic, socioeconomic, or geographic dimensions. I think the best way to explain that is via an example. The way I think of the interactions between genes and the environment is by linking it to the diathesis-stress model, which is a psychological theory that attempts to explain the occurrence of a disorder/illness as a result of an interaction between a predispositional vulnerability (analogous to genetics) and a stress caused by experiences in life (i.e., the environment). This theory asserts that human beings have a certain disease-occurrence threshold that once exceeded the disorder would be developed. The predisposed vulnerability kind of dictates the strength of the environmental stimulus/stressor that is needed for a disorder to occur. For example, lets say there is a predetermined genetic factor associated with anxiety (e.g., serotonin-related). If a particular racial group has that genetic factor, then members of that group would not need that strong of an environmental stressor (e.g., economical issues, social issues, etc.) to develop anxiety because the genetic factor already influenced that disease-occurrence threshold. In contrast, a racial group without that genetic factor has more leeway and can tolerate stronger stimuli or environmental stressors before expressing a particular disorder because that disease-occurrence threshold is unaffected by the genetic factor. I find this theory is quite intriguing, and I think the best way to fully understand it is by conducting more research. Otherwise, it would be difficult to come up with solid conclusions.