Objective: To derive and test the implications of a sex-specific fetal growth standard. Design: Secondary analysis of a prospective observational cohort. Setting: Eight U.S. centers. Population or Sample: Nulliparas followed longitudinally through pregnancy. A lower-risk subgroup (exclusions: chronic hypertension, pre-gestational diabetes, suspected aneuploidy, preterm delivery) was selected for fetal growth equation derivation. Methods: Fetal weights at 14-20 weeks, 22-29 weeks, and birth were used to derive a sex-specific fetal growth equation. We compared rates of SGA and LGA by sex using the sex-specific and sex-neutral (Hadlock) standards. Using the full unselected cohort, we assessed outcomes and clinical management according to SGA and LGA status. Main outcome measures: Proportion considered SGA and LGA; obstetric interventions relevant to SGA and LGA. Results: We derived a sex-specific equation using 7,280 infants. The sex-neutral standard diagnosed SGA more often in female and LGA more often in male newborns. The sex-specific standard resolved these disparities. Using the full unselected cohort (N=8,339), newborns reclassified from SGA to AGA by the sex-specific standard were more likely to be delivered for growth restriction with comparable risk of morbidity compared to newborns considered AGA by both methods. Newborns reclassified from AGA to LGA by the sex-specific standard had higher rates of cesarean for arrest of descent, cesarean for arrest of dilation, and shoulder dystocia than newborns considered AGA by both methods. Conclusions: The sex-neutral standard generates sex disparities in SGA and LGA at birth. A sex-specific standard resolves these disparities and may improve growth pathology risk stratification.

OBJECTIVE To assess the relationship between allostatic load in early pregnancy and CVD, 2 to 7 years postpartum, and potential pathways contributing to racial disparities in CVDs. DESIGN Secondary analysis of an observational cohort study. SETTING nuMom2b Heart Health Study. POPULATION Pregnant individuals. METHODS Our primary exposure was dichotomous high allostatic load in the first trimester, defined as four or more out of 12 biomarkers in the “worst” quartile. The primary outcome was new diagnosis of composite CVD, consisting of HTN and or MD (fasting glucose greater than 100 mg/dL or medication for diabetes). Each outcome and allostatic load component was analyzed secondarily. Multivariable logistic regression was used to test the association between high allostatic load and CVD adjusted for potential confounders. Mediation and moderation analyses assessed the role of high allostatic load in racial disparities of CVD. MAIN OUTCOME MEASURE Composite CVD. RESULTS Among 4,022 individuals, CVD was identified in 1,462 (36.4%); 26.6% had HTN, and had 15.4% MD. High allostatic load was present in 33.0%. After adjustment for covariates, high allostatic load was associated with CVD (aOR 2.0, 1.8-2.3), HTN (2.1, 1.8-2.4), and MD (1.7, 1.5-2.1). There was a reduction in the magnitude of the relationship between race and CVD with the addition of allostatic load. Self-reported race did not significantly moderate the relationship between allostatic load and CVD. CONCLUSION High allostatic load is associated with CVD. Allostatic load was a partial mediator between race and CVD. Race did not moderate the relationship between allostatic load and CVD.