No abstract

Introduction: Maternal underweight and obesity are prevalent conditions, associated with chronic, low-grade inflammation, poor fetal development, and long-term adverse outcomes for the child. The placenta senses and adapts to the pregnancy environment in an effort to support optimal fetal development. However, the mechanisms driving these adaptations, and the resulting placental phenotypes, are poorly understood. We hypothesised that maternal underweight and obesity would be associated with increased prevalence of placental pathologies in term and preterm pregnancies. Methods: Data from 12,154 pregnancies were obtained from the Collaborative Perinatal Project, a prospective cohort study conducted from 1959 to 1974. Macro and microscopic placental pathologies were analysed across maternal prepregnancy body mass index (BMI) to assess differences in the presence of pathologies among underweight, overweight, and obese BMI groups compared to normal weight reference BMI at term and preterm. Placental pathologies were also assessed across fetal sex. Results: Pregnancies complicated by obesity had placentae with increased fetal inflammation at preterm and increased maternal inflammation at term. In term pregnancies, increasing maternal BMI associated with increased maternal vascular malperfusion (MVM), odds of an appropriate mature placenta for gestational age, and placental weight, and decreased placental efficiency. Male placentae, independent of maternal BMI, had increased inflammation, MVM, and placental efficiency than female placentae, particularly at term. Discussion: Maternal underweight and obesity are not inert conditions for the placenta, and the histomorphological changes driven by suboptimal maternal BMI may serve as indicators of adversities experienced in utero and potential predictors of future health trajectories.

Malnutrition and infectious disease often coexist in socially inequitable contexts. Malnutrition in the perinatal period adversely affects offspring development and lifelong non-communicable disease risk. Less is known about the effects of infectious disease exposure during critical windows of development and health, and links between in utero HIV-exposure in the absence of neonatal infection, perinatal nutritional environments, and infant development are poorly defined. In a pilot feasibility study at Kalafong Hospital, Pretoria, South Africa, we aimed to better understand relationships between maternal HIV infection and the early nutritional environment of in utero HIV exposed uninfected (HEU) infants. We also undertook exploratory analyses to investigate relationships between food insecurity and infant development. Mother-infant dyads were recruited after delivery and followed until 12 weeks postpartum. Household food insecurity, nutrient intakes and dietary diversity scores did not differ between mothers living with or without HIV. Maternal reports of food insecurity were associated with lower maternal nutrient intakes 12 weeks postpartum, and in infants, higher brain-to-body weight ratio at birth and 12 weeks of age, and attainment of fewer large movement and play activities milestones at 12 weeks of age, irrespective of maternal HIV status. Reports of worry about food runout were associated with increased risk of stunting for HEU, but not unexposed, uninfected infants. Our findings suggest that food insecurity, in a vulnerable population, adversely affects maternal nutritional status and infant development. In utero exposure to HIV may further perpetuate these effects, which has implications for early child development and lifelong human capital.