Key Points Question What are the prenatal risk factors and perinatal and postnatal outcomes associated with maternal opioid use during pregnancy? Findings In this cohort study based on data from 8509 mother-child pairs in the Boston Birth Cohort, in utero opioid exposure was significantly associated with higher risks of fetal growth restriction, preterm birth, lack of expected physiological development, childhood conduct disorder or emotional disturbance in preschool-aged children, and attention-deficit/hyperactivity disorder in school-aged children. Meaning Prenatal opioid exposure was associated with higher risks of adverse perinatal and postnatal physical health and neurodevelopmental outcomes, suggesting that efforts to mitigate the health consequences of the opioid epidemic require more intergenerational research.
This study aimed to identify actual and perceived barriers to postpartum care among a probability sample of women who gave birth in Los Angeles County, California in 2007. Survey data from the 2007 Los Angeles Mommy and Baby (LAMB) study (N = 4,075) were used to identify predictors and barriers to postpartum care use. The LAMB study was a cross-sectional, population-based study that examined maternal and child health outcomes during the preconception, prenatal, and postpartum periods. Multivariable analyses identified low income, being separated/divorced and never married, trying hard to get pregnant or trying to prevent pregnancy, Medi-Cal insurance holders, and lack of prenatal care to be risk factors of postpartum care nonuse, while Hispanic ethnicity was protective. The most commonly reported barriers to postpartum care use were feeling fine, being too busy with the baby, having other things going on, and a lack of need. Findings from this study can inform the development of interventions targeting subgroups at risk for not obtaining postpartum care. Community education and improved access to care can further increase the acceptability of postpartum visits and contribute to improvements in women's health. Postpartum care can serve as a gateway to engage underserved populations in the continuum of women's health care.
This study examines racial/ethnic, nativity, and sociodemographic disparities in the prevalence of pre-pregnancy obesity and overweight in the United States. Logistic regression was fitted to the 2012–2014 national birth cohort data to derive unadjusted and adjusted differentials in pre-pregnancy obesity (BMI ≥30), severe obesity (BMI ≥40), and overweight/obesity (BMI ≥25) prevalence among 10.4 million US women of childbearing age. Substantial racial/ethnic differences existed, with pre-pregnancy obesity rates ranging from 2.6% for Chinese and 3.3% for Vietnamese women to 34.9% for American Indians/Alaska Natives (AIANs) and 60.2% for Samoans. Pre-pregnancy overweight/obese prevalence ranged from 13.6% for Chinese women to 61.7% for AIANs and 86.3% for Samoans. Compared to non-Hispanic whites, women in all Asian subgroups had markedly lower risks of pre-pregnancy obesity, severe obesity, and overweight/obesity, whereas Samoans, Hawaiians, AIANs, blacks, Mexicans, Puerto Ricans, and Central/South Americans had significantly higher risks. Immigrant women in each racial/ethnic group had lower rates of pre-pregnancy obesity than the US-born. Sociodemographic risk factors accounted for 33–47% of racial/ethnic disparities and 12–16% of ethnic-immigrant disparities in pre-pregnancy obesity and overweight/obesity. Further research is needed to assess the effects of diet, physical inactivity, and social environments in explaining the reported ethnic and nativity differences in pre-pregnancy obesity.
Leptin is a pro-inflammatory cytokine that plays an important role in energy homeostasis. Emerging evidence suggests that leptin levels are altered in children with autism spectrum disorder (ASD); however this has not been studied prospectively. Rapid growth during infancy and early childhood has been implicated in ASD, but the evidence is inconsistent. Since leptin is involved in growth and is a potential risk factor for ASD, we explored the associations between 1) cord, early childhood leptin and ASD; and 2) birth weight for gestational age, early childhood weight gain and ASD. We also assessed the mediating role of leptin in the relationship between weight gain during infancy and ASD. This study was conducted in a sample of 822 subjects from the Boston Birth Cohort. ASD was defined from diagnostic codes in electronic medical records. Extremely rapid weight gain during infancy was associated with a greater ASD risk and this persisted after adjusting for potential confounders (aOR: 3.11; 95% CI: 1.37, 7.07). Similarly, children that had higher plasma leptin levels, prior to ASD diagnosis, had an increased ASD risk in both unadjusted and adjusted models (aOR: 7.87; 95% CI: 2.06, 30.04). Further, early childhood leptin indirectly mediated the relationship between rapid weight gain and ASD. No associations were found between birth weight for gestational age, cord leptin and risk of ASD. Our findings provide a basis to further explore whether the combination of early life growth pattern and a biomarker such as leptin can predict ASD earlier.
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