Social Determinants of Health and Health Disparities
Reading Reflection for Biological Mechanisms Lecture
Due: 2/2/16
Questions Related to Week 5 Readings:
- 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”?
There is some evidence that maternal behaviors in humans may epigenetically influence infant and toddler outcomes. Breastfeeding, which allows for bonding also provides antibodies important for immune regulation. There is growing interest in the possible epigenetic influence of breast milk via immunomodulation. Verduci et al point to Neonatal Necrotizing Enterocolitis (NEC), an intestinal inflammatory disorder found in neonates as an example of epigenetic modification of breast milk. NEC is common in formula feed infants and breastfeeding has been association with a 77% reduction in risk for NEC. One explanation for this difference is that breast milk may be enhancing the production of secretory IgA, an Immunoglobin that is associated with bacterial rearrangement in the intestine, in addition to inhibiting the activation of B-cell signaling pathways associated with the regulation of proinflammatory cytokine genes (Verduci, 2014). Studies on premature infants have shown a benefit of skin-to-skin contact in reducing infant cortisol stress response (Mörelius, 2005). In addition, skin-to-skin contact has been shown to reverse the effects of high maternal cortisol levels in utero (Feldman, 2010). Although there is some evidence that skin-to-skin contact is influencing cortisol levels via epigenetic modification in animal models, it is yet to be shown in humans.
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 contradictory to Weavers. Gurenewald found that there is a cumulative effect of low SES influences has consistent, inconsistent, or unrelated to the Weaver findings? Explain.
Gruenewald’s findings are inconsistent with Weaver’s findings. Weaver argues that early childhood exposures within a critical window of susceptibility may be having epigenetic influence that impact long-term outcomes. The critical window in this case appears to be within one week post-natal (Meaney, 1996), and exposures before or after this critical window will not have an effect. Gruenewald on the other hand argues that social, environmental, and behavioral factors, driven by SES, have a cumulative effect on long-term outcomes. These influences may be exerted through a variety of mechanisms (i.e. stress pathways, metabolic pathway, and maybe even epigenetically). There is no critical window of exposure but rather an additive effect of SES; the greater the number and/or magnitude of these exposures the worse the outcomes. These findings have different implications for intervention. Based on Weaver’s findings the intervention may be at the point of delivery. Programs that encourage postnatal behaviors, specifically within this critical window, may be more effective. Whereas based on Gruenewald’s findings interventions that influence SES (e.g. educational interventions, which also influence the other indicators of SES) may be more effective. These educational interventions may need to be initiated early and may need to be sustained through college or greater.
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 environmental exposures (e.g. toxins, food, violence, etc.) are racial/ethnically, socioeconomically, and geographically patterned. For example, individuals who are African American or Hispanic/Latino tend to be concentrated in deprived neighborhoods therefore they may be more likely to be exposed to the exposures mentioned above. There is some evidence that environmental factors exert biological influence that result in higher rates of chronic illnesses such as heart disease, obesity, and cancer. Although I don’t believe that there are underlying genetic differences between racial/ethnic groups, I do believe that there is some environmental modification of gene expression that is driving some of the disparities that we see. How much of the disparities can be accounted for through epigenetic modification may depend on the environmental factor and the disease outcome (I’m pretty sure this hasn’t been quantified and don’t really know if it can be). I also think that disparities are largely driven by a combination of epigenetic mediated biological processes, non-epigenetic biological processes, and behaviors that are driven by larger social determinants.
Feldman, R., Singer, M., & Zagoory, O. (2010). Touch attenuates infants’ physiological reactivity to stress. Developmental science, 13(2), 271-278.
Meaney, M.J. et al. Early environmental regulation of forebrain glucocorticoid recep- tor gene expression: implications for adrenocortical responses to stress. Dev. Neurosci. 18, 49–72 (1996).
Mörelius, E., Theodorsson, E., & Nelson, N. (2005). Salivary cortisol and mood and pain profiles during skin-to-skin care for an unselected group of mothers and infants in neonatal intensive care. Pediatrics, 116(5), 1105-1113.
Verduci, E., Banderali, G., Barberi, S., Radaelli, G., Lops, A., Betti, F., ... & Giovannini, M. (2014). Epigenetic effects of human breast milk. Nutrients, 6(4), 1711-1724.