HW Week 4

HW Week 4

by Andrew -
Number of replies: 1

Questions Related to Week 4 Readings:

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 think the mechanism of epigenetic changes during critical period of infancy are important, however, I would not say they are not as important outside of the sensitive period. Rather, it may be equally as important. Studies have shown epigenetic changes (e.g. acetylation and methylation) continue throughout an individuals life time due to environmental interactions, social interactions and own personal emotions. These epigenetic changes can not only change the way we presently behave, but also effect our next generation (i.e. epigenetic changes in germ cells). 

Human behaviors that may be analogous to a murine models maternal licking and grooming pups could be kissing the infant, stroking the child, and breast feeding. Other closely related behaviors could be diet and language. Studies have shown these aforementioned factors not only may play a role in a child’s psychosocial development but also in their epigenetic markers/embryological development.

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 Grunewald’s finding are generally consistent with Weaver’s finding. The ideas are similar, they differ at the level of change In the literature, Weaver’s epigenetic changes may effect down stream gene expression of offspring, while Grunewald’ discusses what are the [present] resulting physiological changes due to the changes in gene expression. In addition, they also slightly differ on the epigenetic outcomes, Weaver focuses on postive attributes [licking/grooming], whereas Grunewald focus on negative attributes [SES adversity]. 

For example, an individual who grows up in SES adversity may be living in a low income neighborhood where they have to watch their surrounding, and have access to poor public education and food resources. Hence, they are constantly in a state of stress, where chronic stress causes increased levels of cortisol, which is a steroid hormone that may enter the nucleus of cells freely and cause epigenetic modifications (Weaver). Genetic changes then causes differential gene expression of vital protein association to cellular/homeostatic regulations leading to small and gradual cell/tissue/organ stress and eventual accumulated damages associated to cardiovascular diseases, hence, poorer health outcomes (Gruenewald). Although these “associations” are merely speculative, and the aforementioned example is not implying correlation with causation, one could see how these two papers could be related on a biological level with a focus on different outcomes (postive vs negative) that merits further investigation. 

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?

As alluded to my previous response, I believe gene by environment may play a small-medium role in contributing to major disparities along racial/ethnic, socioeconomic and geographic dimensions. I think another way of thinking GxE on major disparities is observing the intergenerational epigenetic effects. Studies have shown epigenetic changes in an individual’s life such as through extreme environmental stress are potentially “heritable” through methylation and acetylation of the individual’s germ cells. During the formation of the zygote, these epigenetic changes may persist, with further accumulate with the other epigenetic changes from the partnered germ cell, and lead to a small but potentially significant changes in neuroanatomy growth, and hence, the offspring's mental development. Although the exact mechanism is unclear and to what exact degree does epigenetic changes contribute to embryological development, it would not be too far off to think that starting off in life already at a physiological disadvantage may hinder future biological and psychosocial growth. This may lead to less opportunities for intragenerational mobility which may further reinforce or widen the gap of major disparities that the offspring parents has already experienced in their life time. 

In reply to Andrew

Re: HW Week 4

by Maria Glymour -

Thanks Andrew. "Epigenetics" should really be filed under the concepts of environment, rather than genetic per se.  So, the debate about the role of GxE is more about how the health effects coding variants depend on environmental context (and epigenetic modifications may be one mechanism of this).