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.
I do agree with this concept, that it's not nature or nurture that influences who we are and our health outcomes, but rather the interplay between nature and nurture (or genes and environment) throughout our lives and especially during the first few decades of life that manifest in our behaviors and how people live their lives in this complicated world. I first came across these ideas reading Robert Sapolsky's book Monkeyluv, a collection of essays putting into context the science of behavioral and genetic developmental biology that were written in a more pop science, lay audience format. The Body Keeps the Score by van der Kolk also discusses how the effects of trauma in one's lifetime can have significant biological effects on our neuroanatomy, how the brain perceives threats, and how this trauma is then also passed along to later generations. It makes sense then that stresses and traumas experienced as a result of racism, SES disparities, and other SDOH inequities would have physiological and biologic repercussions that then lead to poorer outcomes that exacerbate stress and trauma, perpetuating this cycle. Reading the article by Hertzmann and Boyce put these ideas in more academic and nuance terms which was helpful. In my particular area of interest in addiction medicine, this idea helps also support trauma-informed care, where providers should understand that prior trauma and stresses of a patient's circumstances may affect a person's physiologic and sociologic behaviors long after these stresses have occurred, and remains a helpful way to provide empathic and patient centered care for patients with substance use disorders.
2.
Discuss implications of epigenetic mechanisms of disease for
intergenerational effects on health disparities, as well as for
interventions designed to address health disparities.
While there is evidence that epigenetic mechanisms of disease can be passed down to later generations, I'm also encouraged by the evidence that when mammals are taken out of their maladaptive environments, some of the damage can be reversed (e.g., the rats from low-licking geneologies developed high-licking behaviors as mothers when raised by high-licking mothers themselves) and therefore may provide an opportunity to counterbalance epigenetic damage over time. This represents an opportunity where if we improve people's environments and reduce their health disparities, while not all of the damage done can be erased for them, some of the damage can be reversed such that the allostatic load is gradually reduced with each sequential generation.
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.
Based on the Braveman et al model, genetic or other biological factors are interacting with all of the other factors, including health, behaviors, medical care, living and working conditions in homes/committees, and economic and social opportunities/resources. The findings in the Robinette paper support this in that it looked at allostatic load, a biological variable capturing the physiologic damage and risk for worse health outcomes at later stages of life, and how allostatic load is related to SES including income, neighborhood-associated factors, perceived anxiety/stress around SES, and behaviors like smoking, exercise, and fast food consumption. It reinforced the idea that factors related to poor SES are linked to allostatic load possibly in a bidirectional way, lending support to the GxE interactions concept.