Accounting for Fetal Death: Vital Statistics and the Medicalization of Pregnancy in the United States

Recent reports by the Centers for Disease Control and Prevention have decried the high rate of fetal mortality in the contemporary United States. Much of the data about fetal and infant deaths, as well as other poor pregnancy outcomes, are tabulated and tracked through vital statistics. In this article, I demonstrate how notions of fetal death became increasingly tied to the surveillance of maternal bodies through the tabulating and tracking of vital statistics in the middle part of the twentieth century. Using a historical analysis of the revisions to the United States Standard Certificate of Live Birth, and the United States Standard Report of Fetal Death, I examine how the categories of analysis utilized in these documents becomes integrally linked to contemporary ideas about fetal and perinatal death, gestational age, and prematurity. While it is evident that there are relationships between maternal behavior and birth outcomes, in this article I interrogate the ways in which the surveillance of maternal bodies through vital statistics has naturalized these relationships. Copyright 2013 Elsevier Ltd. All rights reserved.

Embryonic exposure to corticosterone modifies the juvenile stress response, oxidative stress, and telomere length.

Early embryonic exposure to maternal glucocorticoids can broadly impact physiology and behaviour across phylogenetically diverse taxa. The transfer of maternal glucocorticoids to offspring may be an inevitable cost associated with poor environmental conditions, or serve as a maternal effect that alters offspring phenotype in preparation for a stressful environment. Regardless, maternal glucocorticoids are likely to have both costs and benefits that are paid and collected over different developmental time periods. We manipulated yolk corticosterone (cort) in domestic chickens (Gallus domesticus) to examine the potential impacts of embryonic exposure to maternal stress on the juvenile stress response and cellular ageing. Here, we report that juveniles exposed to experimentally increased cort in ovo had a protracted decline in cort during the recovery phase of the stress response. All birds, regardless of treatment group, shifted to oxidative stress during an acute stress response. In addition, embryonic exposure to cort resulted in higher levels of reactive oxygen metabolites and an over-representation of short telomeres compared with the control birds. In many species, individuals with higher levels of oxidative stress and shorter telomeres have the poorest survival prospects. Given this, long-term costs of glucocorticoid-induced phenotypes may include accelerated ageing and increased mortality.