Health Disparities Forum

OnonoMaricianah_Assignment: #2 

Questions Related to Week 3 Readings:

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 believe this mechanism is relevant in humans and that an example of that critical period is early teenagehood.  One of the objectives of my dissertation work will look at parenting stress and intra-household functioning and how this affects adolescent psychosocial well-being and sexual risk taking. Studies have shown that HIV-affected adolescents defined as adolescents with at least one or both parents infected with HIV have poor psychosocial functioning and are much more likely to get HIV when compared to similar households in which parents don't have HIV. The burden and stress of the disease make most caregivers unable to provide the necessary “licking and grooming” at this crucial age resulting in adverse sexual reproductive health outcomes including HIV infection.

In this field that I am greatly interested in because traditionally parenting was communal but with urbanization – those structures have been eroded. There is some evidence that suggests that maternal behaviors that can influence adolescent health and risky health behaviors include1) type of discipline (consistent versus inconsistent), 2) level of maternal involvement, 3) level of maternal monitoring, 4) type of communication and 5) parenting style. In this case, the maternal licking and grooming levels can be paralleled to the different parenting styles namely demandingness (control) and responsiveness (acceptance). In a study looking at the relationships between maternal parenting style and adolescent sexual behavior in a sample of 253 British adolescent-mother dyads*, maternal parenting style was found to be directly associated with the delay of the first sexual experience for the adolescent between the ages of 15-16 years of age. For the older adolescent, this was not true. These findings suggest that parental styles have a greater influence on the adolescent's sexual attitude and behavior in the early teen years verses the later years and that parental influences decrease for the older adolescent.

Reference:

*Taris TW, Semin GnR. How mothers' parenting styles affect their children's sexual efficacy and experience. J Gen Psychol. 1998; 159(1): 68-81

2.  Provide a brief proposal for a study that would allow you to assess whether epigenetic modifications in humans in response to maternal behavior influence subsequent health of the human (feel free to choose any health or behavioral outcome you think you can do this with, e.g., dementia or depression or smoking). Bonus if you can explain how you would approach this if we assume that the relevant epigenetic changes are tissue specific and occur in the brain. 

Borrowing from my dissertation proposal: one of my aims is to assess the impact of an income generating agricultural intervention on parenting stress and psychosocial functioning among caregivers. Within each household in which there is an adolescent, I will measure maternal 1) stress, 2) support, 3) involvement, 4) communication and 5) limit setting using the parenting stress index and the parent-child relationship inventory. I hypothesize that the income generating agricultural intervention will result in less maternal parenting stress and better psychosocial functioning and less sexual risk-taking among adolescents. In this case- I am looking at maternal parenting stress/dysfunction as the key pathway by which this intervention will operate.

My primary outcomes: incidence of HSV-2 (primary outcome for males) and unintended pregnancy (co-primary outcome for females), less HIV transmission risk behaviors (unprotected sex, multiple sexual partnerships, transactional sex and early sexual debut), and higher utilization of HIV testing, HIV prevention, and reproductive health services.

Methods:

Enroll mother-adolescent dyads. I plan to enroll adolescents aged 13-21 years and their mothers. I will stratify them by gender and by age group 13-15 16-18 and then 19-21.  This stratification will allow me to see the differential effects of this “maternal stress reliever” and be able to know at which age to start intervening.

Measurement: I will combine both

1. Biomarkers of stress e.g. HPA axis activity, immune activation. Here I can measure a) plasma/salivary cortisol, blood/salivary inflammatory cytokine levels such as cytokine IL-6, ACTH, heart rate variability, adrenaline and noradrenaline levels.  Heart rate variability provides a window into the balance between the sympathetic and parasympathetic and can now be easily done using relatively small ECG epochs.
2. Psychological effects and assess both cognitive performance and subjective effects.
3. Use standardized and validated tools to measure at baseline 1) stress, 2) support, 3) involvement, 4) communication and 5) limit setting, for example, using the parenting stress index and the parent-child relationship inventory

I would do this at baseline before randomization into intervention and control and then repeat quarterly over a period of 24 months plus endline.

1. Gruenewald, in contrast to Weaver, emphasizes 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 Weaver findings.  The Weaver findings talk about definitive and stable bio-structural changes that occur secondary to maternal behavior such as the methylation and alteration of sequences. It is clear that the early environment regulates the activity of the specific genes in the brain, which in turn influences hormonal and behavioral responses to stress which then influence vulnerability/resilience to disease. The Gruenewald findings extend this work to show that these genotypic changes in the brain due to maternal or environmental issues such as social, economic status/position are not static but dynamic and cumulative throughout the course of one’s life but when they do, they start off with the base those Weaver findings. It’s almost like the gardener's story. The early life determines which kind of soil you grow. Subsequent exposures only build on it, sometimes even changing the soil and reversing.

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?

I am not sure I understood the question, but I think that GxE interactions can contribute to major disparities along racial/ethnic, socioeconomic, or geographic dimensions.

In my opinion, the relationship between gene and environment is syndemic. Syndemicity implies a synergistic effect of problems that are not only linked but are also mutually enhancing. The influence of genes depends on the interplay between contextual and generic factors. Interplay refers to how contextual and genetic factors combine over time to change the likelihood of specific behaviors. Behavior in most part reflects the cumulative history of a person’s social experiences as they combine with his or her genetic makeup. To put it into context using an example adults of higher SES (regardless of race) are more likely to have grown up in childhood homes with better nutrition, fewer health risk behaviors, safer neighborhoods and more economic resources. Now because poverty and social inequality in America are racialised, we find that African Americans in the US are typically more likely to have fewer economic resources, live in unsafe education, and be engaged in risky behavior. In the superficial form, GxE overemphasizes the role of genetics while its really a socio-political issue. The manifestation of poor health and poor health outcomes in African Americans in America is more a direct consequence of the racialization of impoverishment and social inequality from a historical standpoint MORE THAN it is a genetic issue. In other words, blacks are more likely to be hypertensive not because of their genetic makeup but because of the societal issues.   

The disparities as regards possession, access to and ability to accumulate wealth is not a racial issue but because certain races are more likely to be affected than others  - it looks like it's a race issue. Unfortunately, I don't see how GxE  definitions/ interactions can help to disambiguate this