OBJECTIVE:To assess the association between allostatic load, as an estimate of chronic stress, and adverse pregnancy outcomes. METHODS:This was a secondary analysis of nuMoM2b (Nulliparous Pregnancy Outcomes Study: Monitoring Mothers-to-Be), a prospective observational cohort study. Our primary exposure was dichotomous high allostatic load in the first trimester, defined as 4 or more of 12 biomarkers in the "worst" quartile. The primary outcome was a composite adverse pregnancy outcome: hypertensive disorders of pregnancy (HDP), preterm birth, small for gestational age (SGA), and stillbirth. Secondary outcomes included components of the composite. Multivariable logistic regression was used to test the association between high allostatic load and adverse pregnancy outcomes, adjusted for potential confounders. Mediation and moderation analyses were conducted to assess the role of allostatic load along the causal pathway between racial disparities and adverse pregnancy outcomes.RESULTS: Among 4,266 individuals, 34.7% had a high allostatic load. Composite adverse pregnancy outcome occurred in 1,171 (27.5%): 14.0% HDP, 8.6% preterm birth (48.0% spontaneous and 52.2% indicated), 11.0% SGA, and 0.3% stillbirth. After adjustment for maternal age, gravidity, smoking, bleeding in the first trimester, and health insurance, high allostatic load was significantly associated with a composite adverse pregnancy outcome (adjusted odds ratio [aOR] 1.5, 95% CI 1.3, 1.7) and HDP (aOR 2.5, 95% CI 2.0-2.9), but not preterm birth or SGA. High allostatic load partially mediated the association between self-reported race and adverse pregnancy outcomes. The association between allostatic load and HDP differed by self-reported race, but not for a composite adverse pregnancy outcome, preterm birth, or SGA.CONCLUSION: High allostatic load in the first trimester is associated with adverse pregnancy outcomes, particularly HDP. Allostatic load was a partial mediator between race and adverse pregnancy outcomes. The association between allostatic load and HDP differed by self-reported race.

Objective: To assess the relationship between allostatic load, a measure of cumulative chronic stress in early pregnancy and cardiovascular disease risk, 2-7 years postpartum, and pathways contributing to racial disparities in cardiovascular disease risk. Design: Secondary analysis of a prospective cohort study. Setting Multicenter Population: Pregnant women. Methods: Our primary exposure was high allostatic load in the first trimester, defined as at least 4 of 12 biomarkers (systolic blood pressure, diastolic blood pressure, body mass index, cholesterol, low-density lipoprotein, high-density lipoprotein, high-sensitivity C-reactive protein, triglycerides, insulin, glucose, creatinine and albumin) in the unfavourable quartile. Logistic regression was used to test the association between high allostatic load and main outcome adjusted for confounders: time from index pregnancy and follow up, age, education, smoking, gravidity, bleeding in the first trimester, index adverse pregnancy outcomes, and health insurance. Each main outcome component and allostatic load were analysed secondarily. Mediation and moderation analyses assessed the role of high allostatic load in racial disparities of cardiovascular disease risk. Main outcome measure: Incident cardiovascular disease risk: hypertension, or metabolic disorders. Results: Cardiovascular disease risk was identified in 1462/4022 individuals (hypertension: 36.6%, metabolic disorder: 15.4%). After adjustment, allostatic load was associated with cardiovascular disease risk (adjusted odds ratio [aOR] 2.0, 95% CI 1.8-2.3), hypertension (aOR 2.1, 95% CI 1.8-2.4) and metabolic disorder (aOR 1.7, 95% CI 1.5-2.1). Allostatic load was a partial mediator between race and cardiovascular disease risk. Race did not significantly moderate this relationship. Conclusions: High allostatic load during pregnancy is associated with cardiovascular disease risk. The relationships between stress, subsequent cardiovascular risk and race warrant further study.

shed some light regarding the best LMWH protocol for pregnant people with a history of VTE. The study did not stratify regarding those with inherited thrombophilias, but was well-powered to identify a clinically significant difference of recurrent VTEs. Although there was not a statistically significant difference seen, there was a higher rate of postpartum VTEs in the 2 groups. Unfortunately, the data do not provide the answer for what is the best approach. Based on these data, I think it would be reasonable to use low-dose LMWH, given that there were no statistical differences, and the lowest dose to achieve an outcome can be prudent. However, one might also choose to use intermediate dosing given that there was a 1% risk of VTE postpartum in that group compared with 2% in the low-dose group, and there were no differences in bleeding complications. However, a third approach, which was not studied, might be to use low-dose LMWH during pregnancy and increase to intermediate postpartum. That way, one would minimize the bleeding risks during the antepartum and intrapartum periods, but gain a bit more thromboprophylaxis during the time that seems highest risk. Such an approach was not studied, but one can see the logic behind it. Thus, we continue with less evidence-based guidance than we truly need, but for now know that any of these approaches are likely effective and perhaps can be adjusted based on individual risk.-ABC)