Questions Related to Week 4 Readings:
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.
Hertzmann and Boyce present some evidence on gene x environment interactions. Certainly, a genetic predisposition can be mitigated or activated by certain environmental factors, including the role of methylation. In the most obvious way, racism is a context that is most harmful to the individuals whom are most discriminated against early on, as these groups may be given fewer social/educational benefits and others’ expectations of them directly influences their behavior. However, given that genetic variation is not less within v. between racial/ethnic groups, it’s not clear to me how a genes x environment interaction would contribute to racial/ethnic disparities. I can see clearly from the research that certain environmental factors will be particularly damaging for those who are more biologically sensitive to context, and that there will be group differences by race/ethnicity in context, but that simply points to environmental factors, which are associated with race/ethnicity. It feels the same to think about that with respect to socioeconomic context. That being said, perhaps with socioeconomic level, this connection is more easily made because there are both genetic and environmental factors that influence intelligence, which may impact academic achievement, but SES will impact the extent to which environmental influences mediate the relation between intelligence and education, which will likely impact SES. For my area of interest (eating disorders), the link between genes and environment feels easier to understand. Although everyone in Western culture is exposed to dieting culture through others’ behavior and media, as well as a preference towards the “thin ideal” body type (to different extents based on exposure to these factors and protective factors in cultural views on ideal body type that can differ by race/ethnicity), and most people have been on a diet, only a few people develop an eating disorder. Extremely few people (less than 1%) develop anorexia nervosa, despite widespread prevalence of dieting, desire to lose weight, and idealization of a thin (women) or muscular/toned (men) body. This points to the heavy role of genetics (about 70%) in eating disorder development, while environment potentially just provides the spark. Given differences in the ideal body type between racial/ethnic groups, there is the possibility that some body cultures may serve as protective factors against the development of an eating disorder. There is a role for genetics in obesity and how overweight can be a risk factor for certain eating disorders, but given the lack of evidence for differences in eating disorder prevalence across SES or racial/ethnic groups, it’s also hard for me to apply this concept to the development of an eating disorder.
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 experience of discrimination as one example of an environmental influence that may modify gene expression suggests that risk for epigenetic changes continues to increase across the lifespan as increasing instances of discrimination are encountered, which may increase risk for children born under increased risk factors (e.g., maternal physical and mental health). However, I am not entirely clear how strong the science is around how gene expression in a parent impacts genes in an offspring, and I’ve seen some research that non-genetic inheritance is likely rare. It would be helpful to understand this better.
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.
Braveman et al’s model demonstrates how genetic or biological factors interact with the environment (built environment—living and working conditions, and social environment—social opportunities and resources, economic opportunities and resources), one’s own health behaviors, and medical care. Robinette et al. found that neighborhood income (over and above individual income, demographics, health behaviors) was associated with greater allostatic load. The relation was relatively small in relation to the other associations in the model (e.g., exercise) but nevertheless demonstrated a link between neighborhood income and allostatic load. However, it’s hard to separate neighborhood income from additional factors related to the built environment (access to parks, convenience stores/fast food v. fresh fruits/vegetables) and social environment (local social cohesion/social support), which was discussed to some extent in the article. Should the lack of opportunity be less than in other neighborhoods, one would imagine that this would impact change in individual SES given the impact of stress on mental/physical health and how this may impact job performance and continued earning potential.