Obesity rates in women of childbearing age is now at 29%, according to recent CDC reports. It is known that obesity is associated with oxidative stress and inflammation, including disruptions in cellular function and cytokine levels. In pregnant women who are obese, associated placental dysfunction can lead to small for gestational age (SGA) infants. More frequently, however, maternal obesity is associated with large for gestational age (LGA) newborns, who also have higher incidence of metabolic disease and asthma due to elevated levels of inflammation. In addition, anthropogenic environmental exposures to “endocrine disrupting” and “forever” chemicals affect obesity, as well as maternal physiology, the placenta, and fetal development. Placental function is intimately associated with the control of inflammation during pregnancy. There is a large amount of literature examining the relationship of placental immunology, both cellular and humoral, with pregnancy and neonatal outcomes. Cells such as placental macrophages and NK cells have been implicated in spontaneous miscarriage, preeclampsia, preterm birth, perinatal neuroinflammation, and other post-natal conditions. Differing levels of placental cytokines and molecular inflammatory mediators also have known associations with preeclampsia and developmental outcomes. In this review, we will specifically examine the literature regarding maternal, placental, and fetal immunology and how it is altered by maternal obesity and environmental chemicals. We will additionally describe the relationship between placental immune function and clinical outcomes, including neonatal conditions, autoimmune disease, allergies, immunodeficiency, metabolic and endocrine conditions, neurodevelopment, and psychiatric disorders.

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ObjectiveMore women are obese at their first prenatal visit and then subsequently gain further weight throughout pregnancy than ever before. The impact on the infant’s development of neonatal hypoxic ischemic encephalopathy (HIE) has not been well studied. Using defined physiologic and neurologic criteria, our primary aim was to determine if maternal obesity conferred an additional risk of HIE.Study DesignData from the New York State Perinatal Data System of all singleton, term births in the Northeastern New York region were reviewed using the NIH obesity definition (Body Mass Index (BMI) ≥ 30 kg/m2). Neurologic and physiologic parameters were used to make the diagnosis of HIE. Physiologic criteria included the presence of an acute perinatal event, 10-min Apgar score ≤ 5, and metabolic acidosis. Neurologic factors included hypotonia, abnormal reflexes, absent or weak suck, hyperalert, or irritable state or evidence of clinical seizures. Therapeutic hypothermia was initiated if the infant met HIE criteria when assessed by the medical team. Logistic regression analysis was used to assess the effect of maternal body mass index on the diagnosis of HIE.ResultsIn this large retrospective cohort study we evaluated outcomes of 97,488 pregnancies. Infants born to obese mothers were more likely to require ventilatory assistance and have a lower 5-min Apgar score. After adjusting for type of delivery and maternal risk factors, infants of obese mothers were diagnosed with HIE more frequently than infants of non-obese mothers, OR 1.96 (1.33–2.89) (p = 0.001).ConclusionInfants of obese mothers were significantly more likely to have the diagnosis of HIE.

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