- Questions Related to Week 3 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”?
I believe this mechanism is relevant to human development. A similar example would be the acquisition of spoken language. Similar to the example from Weaver et al, when looking at the acquisition of spoken language of in congenitally deaf children we see that obvious deficits in early vocalization. The same was previously reported in an extreme and horrible case of a child being isolated in near complete language deprivation until the age of 13 and was subsequently noted to have significant deficits in communication. The precise pathway involved in not completely known but I can imagine there may be similar processes at work.
reference: https://www.ncbi.nlm.nih.gov/books/NBK11007/
2. Provide a brief proposal for a study that would allow you to assess whether epigenetic modifications in humans in response to maternal behavior influence subsequent health of the human (feel free to choose any health or behavioral outcome you think you can do this with, e.g., dementia or depression or smoking). Bonus if you can explain how you would approach this if we assume that the relevant epigenetic changes are tissue specific and occur in the brain.
For this I will have limited knowledge in the brain (very far from the GU system) and for this example will put the obvious ethics issues aside:
You could examine the relationship between control of maternal diabetes and congenital hearing loss. You could compare mothers without diabetes, those with well controlled diabetes and those with uncontrolled diabetes and compare rates of congenital hearing loss.
In order to approach the testing of brain tissue you could sample tissue from the auditory centers in the brain of babies from each category, measuring the degree of signaling and identify changes in methylation and histone acetylation in each.
3. Gruenewald, in contrast to Weaver, emphasizes 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 from both articles are related although the outcomes measured are not directly comparable. The Weaver paper shows there are epigentic modifications due to stressors, while the Gruenewald paper demonstrates an association between reported lifetime stressors and biomarker levels. The outcome measures of the Gruenewald paper are far downstream from the genome level of effect described in the Weaver paper. They both support an overall message that stressors have effects on multiple systems although they are not consistent in showing clear genomic level modifications in both instances.
4. 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 racial/ethnic, socioeconomic or geographic dimensions are the situations and environments in which the GxE interactions are generated. Based upon the varied conditions of the dimensions, the effects of the GxE interactions are reduced or magnified and thereby dictating the degree of the observed disparity.