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”?
This mechanism may be relevant in humans. Epigenetics refers to the chemical modifications that lead to changes in gene expression without any alteration in the DNA structure itself. In humans, it has been shown that early postnatal life is a sensitive phase that is important for future infant neuroplasticity. During the early postnatal period, the infant brain is vulnerable to the quality of experiences, and as such, it has been suggested that early stress can have a profound effect on the immature brain as it is organizing itself (Montiross and Provenzi, JOGNN, 2015). For example, Smith et al. (Annals Neurology, 2011) showed that early chronic exposure to painful stimulation is associated with altered neuroendocrine response and long-lasting brain alterations. Smith also showed that the number of skin-breaking and invasive procedures during a NICU stay is associated with thicker cortical volume in 7 year old preterm-born children. I believe that the behaviors most analogous to “maternal licking and grooming” in rats are “skin-to-skin contact” and swaddling in human infants.
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 believe that the conclusions that Gruenewald draws are somewhat consistent to those that Weaver draws in that both authors seem to suggest the importance of stressful events that occur in childhood. According to Weaver, stress experienced during “critical” or “sensitive” periods of life early on contribute to permanent epigenetic changes later in life. According to Gruenewald, it is more the “accumulation” of life stressors (allostatic load) that is important to the development of changes later on, as opposed to stressful events at critical time periods. While Gruenewald discusses the accumulation of stressors over the life, concluding that there is a higher level of allostatic load in middle and later adulthood in individuals who have experienced greater level of SES adversity across the life course from childhood to adulthood, she seems to emphasize the importance of childhood experiences, which is similar to Weaver. One important difference is that, while Weaver suggests that “critical periods” during childhood are more important, Gruenewald suggests that an accumulation of stressful life events is more important.
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 believe that genes, environment, and experiences all likely combine to contribute to major disparities along racial/ethnic, SES, and geographical dimensions. An example of this can be seen in twin studies in childhood obesity. In a systematic review performed by Silventoinen et al. (Int J Obes, 2010), the authors conclude that adoption studies support the role of family environment in childhood obesity, as correlations were found between adoptees and adoptive parents; however, correlations were substantially stronger between parents and biological offspring, further supporting the importance of genetic factors. It is possible that stressors associated with poverty during childhood could be associated with environmental factors that then alter genes contributing to worsening obesity later in life.