1. 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? Please consider this both in general and in respect to your particular area of interest.
It is important to first note that the argument presented by Hertzmann and Boyce concerns only a subset of interactions that contribute to major health disparities. They acknowledge that there are a wealth of factors, including but not limited to structural inequalities, involved in creating and maintaining such health disparities. However their focus is on the phenomenon of biological embedding, and more often than not, on biological embedding during critical periods of development. Can early childhood experiences affect long-term health outcomes independently of structural inequalities, and if so how? Experiments with rodents have provided huge insight into potential mechanisms, including but not limited to epigenetics, methylation and regulation of the HPA axis. It is widely recognized that there exists a specific window in childhood during which children are particularly susceptible to environmental and social influences. Some even describe this neuroplasticity as being “like a sponge”. This is seen through language acquisition and through adverse childhood experiences (ACE) that affect individual health outcomes for years to decades after the fact. Thus there must be a way that this neuroplasticity is modulated by environmental influences during this critical period. These GxE interactions then shape an individual’s responses (for example regulation of their HPA axis) to environmental influences such as structural inequalities, not only creating a vicious cycle but also becoming rooted in and accentuating the pathways that lead to the major disparities we observe all around us.
The phenomenon of biological embedding can potentially play a role in the association between atopic dermatitis and depression in children. Interestingly, children of higher SES are more likely affected by atopic dermatitis (AD), and dysregulation of the HPA axis has been linked to the development of AD and depression. This does raise questions about the pervasive nature of biological embedding and the potential for early targeting of risk factors that could affect long term health outcomes.
2. Discuss implications of epigenetic mechanisms of disease for intergenerational effects on health disparities, as well as for interventions designed to address health disparities.
The Barcelona De Mendoza article about epigenetic changes and perceived racial discrimination raises several interesting points. The first is that epigenetic mechanisms of disease, for example methylation of CpG sites, may be associated with the accumulation of discriminatory experiences rather than the type of discriminatory experiences, echoing the concept of social causation and cumulative influences discussed by Hertzmann and Boyce. The second is that this mechanism provides insight into how certain health disparities are passed down from generation to generation. Epigenetic changes, although modulable, are transmitted to offspring. The offspring of those having suffered from structural, racial/ethnic, socioeconomic, and/or geographic inequalities are thus at a disadvantage right out of the womb. This in turn exacerbates their own responses to the inequalities they will face in life, which will lead to epigenetic changes, and perpetuate the cycle of health disparities. However having elucidated these epigenetic mechanisms also allows for ways to target these ‘biological disparities’ and potentially reverse what would have been a lifetime of socially partitioned health outcomes.
3. Discuss how the findings in the Robinette paper relate to socioecological model we are using in this course – e.g. briefly describe how the different levels displayed in this model are related to each other in this paper.
The Robinette paper explains that neighborhood SES affects allostatic load through multiple pathways that can directly translate to the RWJ Foundation framework. Lower income neighborhoods (= “living and working conditions in homes and communities”) are linked to various health behaviors including diet, physical activity, and smoking (= “behaviors”), which in turn affect allostatic load and thus health outcomes. The paper also sought to further analyze the subtleties of the apparent association between lower income neighborhoods and allostatic load, more specifically by a pathway mediated by perceived stress and anxiety. This would correspond to another category, at the same level of the “behaviors” category in the RWJ framework, which could be defined as “affective” (or we could also reasonably envision this “affective” category as a subset of the “behaviors” category). Thus the findings of this study demonstrate a major pathway in the socioecological model and shed light on potential parallel pathways that may also play a significant role.