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”?
Yes, I do believe that this epigenetic mechanism of programming by maternal behavior (in a critical time period) is relevant in humans as well. There has been evidence showing that the epigenome is susceptible to changes in nutrients and diets that the infant is exposed to in the prenatal and early postnatal period1. A more recent translational study that was inspired by Weaver et al. tried to replicate their work in humans, using breast feeding as the maternal behavior in question2. They found that similar to the results in the animal study, breast feeding in 5-month-old infants decreased DNA methylation of the glucocorticoid receptor promoter (i.e. it changed the epigenetic pattern through behavioral programming) and decreased HPA stress reactivity2. The authors proposed that these results could explain some of the positive effects of breastfeeding on infant development. In the above two examples, human behaviors of diet and breastfeeding were analogous to “maternal licking and grooming” in rats.
1. Remely, M., Stefanska, B., Lovrecic, L., Magnet, U., & Haslberger, A. G. (2015). Nutriepigenomics: The role of nutrition in epigenetic control of human diseases. Current Opinion in Clinical Nutrition and Metabolic Care, 18(4), 328-333.
2. Lester, B. M., Conradt, E., LaGasse, L. L., Tronick, E. Z., Padbury, J. F., & Marsit, C. J. (2018). Epigenetic Programming by Maternal Behavior in the Human Infant. Pediatrics, 142(4), e20171890.
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 the Gruenewald findings are consistent with the Weaver findings to a moderate extent. While Weaver focused on the positive determinants of health (i.e. maternal grooming in influencing stress in offspring), Gruenewald looked at models of negative determinants of health (i.e. the effect of SES adversity on allostatic load). Both studies found that these determinants that occur early on in an individual’s life have an effect on their health in adulthood. Weaver focused on the epigenetic mechanism by which this may occur, where there is a critical period during which these maternal behaviors influence the epigenetic pattern in the offspring (very early on after birth), after which this persists into adulthood and affects the stress response of the individual. Similarly, the accumulation of risk model that Gruenewald investigated has a lifecourse approach, whereby those with greater SES adversity across the life course (childhood and adulthood) have greater negative effect on the biological functioning in later adulthood. As such, the critical period in the Weaver findings is analogous to the childhood and early adulthood period in the Gruenewald findings, although they are not exactly the same.
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?
Gene-by-environment interaction is the idea that (instead of genetic only or environmental effects only) certain genotypes may result in systematically different phenotypes, as a result of the individual’s environment. Since an individual’s racial background, socioeconomic status and geographic location all play important roles in shaping that person’s social environment, I think that gene-by-environment interactions can contribute to major disparities to a large extent along these lines. An example of this is can be seen in schizophrenia, which is known to have a strong hereditary component (with multiple genes of small effect sizes contributing to the disease) but also is heavily influenced by environmental effects (such as social stress and drug abuse). Indeed, twin studies have shown a concordance rate of 50%3, which further demonstrates that even if an individual has a genetic predisposition for schizophrenia, the expression of the disorder is dependent on the environment which they are living in. For someone who is already genetically predisposed to the disorder, lower SES, discrimination due to racial/ethnic background and living in a poorer neighbourhood/country may increase the risk for encountering its environmental triggers throughout the life course (eg. maternal stress and malnutrition, poor parenting, drug abuse and lack of social support). As such, schizophrenia is an appropriate example of showing how gene-by-environment can contribute to major disparities.
3. Karl, T., & Arnold, J. C. (2014). Schizophrenia: a consequence of gene-environment interactions?. Frontiers in behavioral neuroscience, 8, 435. doi:10.3389/fnbeh.2014.00435