I thought these articles were really interesting. I am familiar with the content, but hadn't read the studies.
The mechanism described in Weaver et al is relevant in humans – one way we typically identify it as the bond between mothers and their children which can be a result of the care taking behavior by mothers. This can include physical touch meant to sooth or show affection as well as responding to the needs of a child such as hunger or discomfort. The idea that because stress has biological and/or hormonal effects, soothing or affection which impacts stress can go on to effect these biological or hormonal effects makes sense. And it is logical that this can have significant impacts on the growing brain of a child. To test this idea, a cohort study comparing two groups of children – those raised in eastern European orphanages, a resource limited setting, with those raised at home as the first born child. These groups could be followed up and monitored for cases of coronary artery disease related to the HPA axis as referenced in Hertzmann and Boyce.
According to Gruenewald, there are physiological differences, later in life, between groups with differing levels of SES adversity. I think this is in accordance with Weaver et al and the differences in comparison can be attributed to measurement. Lab science, at the moment, allows for discrete biological findings while human subjects research relies on examination of a range of markers, the specificity of which in relation to SES has not yet been demonstrated.
Hertzmann and Boyce report that about 15% of children are more highly biologically reactive to their environment. This leads me to conclude that the relevance of the gene times environment interactions occurs over a range. There is not a dose-response relationship between levels of SES adversity and health, but it is a significant contributor to disparities between communities when examined across racial, SES, and geographical contexts.