Health Disparities Forum

1.  Yes. Research from both developmental psychology and neuroscience suggests that the early years of a child’s development are critical in establishing the functional neural networks involved in emotion and attention regulation. Thus, early adverse experiences such as abuse, neglect, isolation, or lack of meaningful social bonds with both caregivers and peers have significant impact on outcomes later in life. Separation from parental figures during acute stress during early development can lead to hyperactive HPA responses that if not addressed through some form of clinical intervention can be maintained and be seen to continually manifest decades later. In humans, there is significant researching suggesting that like licking in mice, behaviors such as breast feeding and continuous chest/body contact with the mother during the first months are key factors that facilitates bonding and a sense of security during infant development. Furthermore, reading and language development in children has demonstrated life-long benefits pertaining to communication facilitation that act as buffers during stressful social and environmental events. 

2. While the interaction of genes and environment is relatively established in modern scientific literature, Gruenewald argues for the cumulative effects of SES adversity on this multi-system allostatic load, implying higher levels of allostatic load in middle and later adulthood for the individuals who have experienced a greater level of SES adversity across their entire life course. Gruenewald’s arguments are relevant in that they pertain to the ‘broader picture’ and emphasize the fact that consecutive adverse experiences that occurs both within and outside the critical windows of development may render an individual more vulnerable to adverse outcomes. I suppose what this argument speaks to is more the degree to with which an individual can change, and whether, as Weaver argues, epigenetic patterns are established during this time and therefore later experiences have less gain. While not necessarily in contradiction, research has shown that individuals who engage in certain self-regulatory practices like meditation which involves practicing techniques that alter the cognitive and emotional responses to thoughts and experiences, have been shown to shorten telomere length, increase structural grey matter, increase white matter and alter functional connectivity in the associated networks, respectively, along with considerable reports of behavioral change (improvement). In that context, I do not disagree with either Weaver or Gruenewald’s findings, however I think the both lack the incorporation of more recent findings in epigenetic research suggesting that significant changes to both the brain and behavior can persist throughout adulthood. 

 3. Hertzmann and Boyce argue the gene by environment interaction, and that the psychiatric and biomedical outcomes of being a highly reactive individual are bivalent in that they are sometimes protective, and in others, risk-augmenting. In this sense, their argument from my perspective, is the most nuanced in that they address the fact that individuals may be biologically sensitive across social partitions, however those coming from a more adverse/at risk environment are will be in a higher risk-augmenting context. However, what they fail to discuss is the additive factor of the influence of available resources such as mental/health care and the institutional roles that are at work in buffering against these GxE interactions. The lack of available and accessible preventative health/medical interventions are a major dimension of (in my opinion) what facilitate these disparities along racial/ethnic, socioeconomic, and geographic dimensions. The institutionalized stratifiers (i.e., lack of universal healthcare, institutionalized racism) can thus be highlighted and considered the significant contributors that they are to these disparities, exactly because of these GxE interactions.