Questions Related to Week 5 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”?
Example: Reading to children. The affect of reading to your child on a regular basis in the first 2 years of life have been shown to make a difference their verbal IQ later on. Reading to your child later in life likely does not have the same effect.
Example: Stunting. Poor macro and micro nutrition under the age of 2 has been associated with decreased height potential or stunting later in life. Even after normalization of nutrient intake at ages >2 years we see children never gain their height potential.
Example: Visual defect: Infants who have a visual defect such as strabismus, that is not corrected early on with glasses never are able to develop that part of the visual cortex despite correction with glasses later in life.
Example: RSV exposure in early childhood. There is increasing evidence that early RSV infections predispose children to more severe asthma later in life. Whereas adults who get RSV do not suddenly develop asthma, or a worsening of their asthma.
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 that Gruenwald’s findings are somewhat unrelated to the Weaver findings. Weaver’s findings do not exclude the possibility that cumulative effects of low SES, and stress might increase allostatic load. Instead, Weaver discusses the effect of specific stressors at specific times on specific outcomes. I suspect that both Gruenwald and Weaver would agree that their two mechanisms of injury likely have two different biologic pathways.
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 think that GxE interactions play a large role in major disparities along racial/ethnic, socioeconomic and geographic dimensions. This postulate brings together a lot of what we have been discussing in class. That social disparities have a strong effect on health through multiple mechanisms they find their way under the skins surface and result in poorer outcomes when faced with similar splay of genetic predispositions. Modern medicine has welcomed in various modifiers of genetic predisposition to explain phenotypic presentation. Why not consider environment as one of these modifiers. I agree with previous students who hope that environment does not provoke too many heritable genetic changes for an environment-by-genes (ExG) interaction as this would make alleviating /reversing the effects of social disparities so much more difficult.