Questions Related to Week 5 Readings:
- 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 same or a similar mechanism likely operates in how humans develop traits like trust and confidence from their interactions with individuals and the broader environment at critical stages in life (e.g. sense of security from parent during infancy or with sense intimacy/affection with social network in young adulthood). The article made me think of Erikson’s stages of psychosocial development and how Weaver et al. provide a potential explanation for how environmental interactions elicit genetic changes that manifest as personality traits. Erikson’s theory proposes that we develop virtues like hope, will, purpose, and love based on the successful completion of developmental challenges at each stage of life. He argued that failing to master a developmental task may lead to psychosocial problems in the future. An example that’s analogous to the Weaver et al. experiments is how Erikson proposed that if primary caregivers are unable to provide for an infant’s basic needs, the child may grow to become distrustful of others and have a warier view of their world.
- 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 Greenwald’s work on allostatic load is consistent and complementary to the concepts proposed by Weaver et al. Whereas Greenwald provides insight on how experiences of SES adversity accumulate across the life course to impact physiological functioning, Weaver attempts to understand how social interactions that are partly (or mostly) shaped by SES adversity (e.g. provision of food or amount of time that a parent spends with her child) elicit changes at the genetic level. An extension to allostatic load is the concept of resilience, which refers to the mechanism that protects individuals against risks associated with high allostatic load. Weaver’s work on how maternal behavior produces changes to gene expression might provide insight on how positive social interactions at critical life stages can have a protective effect against future life adversities.
- 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?
Although gene-by-environment interactions remain controversial and some have voiced skepticism about the methodologies of these studies, I think it’s a positive progression in our attempt to understand how the broader social context can elicit biological changes that can predispose vulnerable subgroups to poorer health outcomes. In an article examining the last decade of GxE research, Duncan and Keller noted that genotypes do not exist in a vacuum and that their expression must depend, to some extent, on the environment. I do think that GxE interaction is a contributor to health disparities; but to what extent, I’m not sure. It would be disheartening if indeed all or most of it can be attributed to GxE interactions that provoke heritable genetic changes – that would just make work eliminating disparities so much harder!