The Biological Residue of Childhood Poverty

Abstract

Children raised in poverty are prone to physical health problems late in life. To understand these findings and address the scientific challenge they represent, we must formulate integrative conceptual frameworks at the crossroads of behavioral and biomedical science, with a strong developmental emphasis. In this article, we outline such a framework and discuss research bearing on its validity. We address how childhood poverty gets under the skin, at the level of tissues and organs, in a manner that affects later disease risks. We also tackle questions about resilience; Even with lengthy exposure to childhood poverty, why do only a subset of people acquire diseases? Why are some individuals protected while others remain vulnerable? Maternal nurturance might be a source of resilience, buffering children from the long-term health consequences of poverty. We conclude with research priorities.

Figure 1

Model depicting how early disadvantage brings about pro-inflammatory phenotype and subsequent vulnerability to health problems.

Figure 2

The peripheral blood mononuclear cells of adults reared in low-SES families have more pronounced IL-6 responses to poly I:C (a viral analogue, upper left) and flagellin (a bacterial product, upper right), compared with adults from high-SES families. Those raised in low-SES families also display upregulation of genes with response elements for NF-κB, the molecular lynchpin of inflammation, and downregulation of genes with response elements for the anti-inflammatory glucocrticoid receptor (bottom panel).

Figure 3

Maternal nurturance buffers against higher counts of MetS components in those from low-SES backgrounds. The top panel displays counts of MetS components as a function of childhood SES and maternal nurturance, which is depicted at lower (−1 SD), typical (sample mean), and higher (+1 SD) levels of the sample distribution. The bottom panel displays counts of MetS components by childhood SES. For illustration, the sample has been stratified into tertiles on maternal nurturance.

Figure 4

Early-life family climate and inflammatory trajectory in adolescence. To the extent that they were raised in a harsh family climate,, participants had increasing stimulated IL-6 production over the followup (upper panel), and became less sensitive (more resistant) to cortisol’s anti-inflammatory properties (lower panel). Family harshness depicted at lower (−1 SD), typical (sample mean), and higher (+1 SD) levels of the sample distribution. IL-6 was measured in whole blood cultures incubated with the bacterial product lipopolysaccharide for 6 hours.