Role of Perinatal Biological Factors in Delayed Lactogenesis II Among Women With Pre-pregnancy Overweight and Obesity.

Abstract

Pre-pregnancy overweight and obesity are negatively associated with delayed onset of lactogenesis II (OL), but the mechanisms by which these conditions affect OL are still unclear. To identify biological factors related to pre-pregnancy overweight/obesity and determine whether these biological factors were associated with delayed OL in this population. In this prospective observational study, we assigned 72 primipara to a pre-pregnancy overweight/obese group (n = 36) and a normal-weight group (n = 36). Blood samples were collected at 37 w of gestation and 48 h postpartum and assayed for levels of the following hormones: leptin, insulin, estradiol, prolactin (PRL), progesterone, and oxytocin. The primary outcome was timing of OL, estimated by maternal perception of breast fullness. We used linear-regression analysis to determine associations between hormones and delayed OL. Sixty-three participants (87.5%) had complete data. OL occurred later in overweight/obese than in normal-weight women (p < .001). Compared with the normal-weight group, the overweight/obese group showed higher leptin levels at both times of observation and exhibited a slower drop in estrogen concentrations from 37 w of gestation to 48h postpartum (all p < .05). After adjusting for confounding factors, leptin concentrations in late pregnancy and the magnitudes of decline in estrogen concentrations at 48h postpartum were correlated with OL. Women who were overweight/obese before pregnancy had elevated leptin levels in late pregnancy and a delayed decline in estrogen concentrations at 48h postpartum. Both of these phenomena were related to delayed OL in this population.