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    Fetal programming and adult obesity


    Mary Jane is a 28-year-old G2P1 whom you are seeing for prenatal care at 8 weeks' gestation. She is 5 ft 6 in tall and weighs 105 lb. She works in a highly visible technology position and strongly desires to maintain her body image during pregnancy. In her first pregnancy, she gained only 10 lb and delivered a healthy infant at 39 weeks weighing 4.85 lb. How should you counsel the patient regarding nutrition and weight gain in this pregnancy?

    Prenatal care

    Formalized prenatal care in the United States originated in the early 1900s with a program of just 3 pregnancy visits. Maternal mortality rates at the beginning of the 20th century approached 1% of pregnancies, with the principle etiologies being that of preeclampsia, infection, and hemorrhage. Accordingly, prenatal care focused on 3 complications: Patients’ blood pressure and urine protein were measured at each visit for the diagnosis of preeclampsia, urinalysis was performed for urinary tract infection, and hematocrit was determined to prevent anemia and consequences of hemorrhage. These interventions as well as other healthcare improvements (blood banking, attention to asepsis, antibiotics) resulted in a dramatic reduction in maternal mortality, to rates now approaching 1 per 10,000 pregnancies in the United States. With this dramatic reduction in maternal mortality, the goals of prenatal care shifted to the reduction of fetal and neonatal morbidity and mortality, prematurity,1 and more recently to the diagnosis (diagnostic ultrasound, biomarkers, amniocentesis), prevention (folate supplementation), and treatment (in utero and neonatal surgery) of congenital anomalies.

    Developmental programming     

     Prenatal care is just now beginning to focus on the longer-term consequences of optimizing fetal health so as to prevent childhood and adult disease. Developmental programming may be defined as the permanent alteration in tissue structure or function as a result of the in utero environment. The concept of fetal programming has gained increased credence supported by strong findings from human epidemiologic studies and animal models.2,3 Specifically, in utero exposures to altered maternal nutrition (excess and deficient), stress (eg, glucocorticoids), or environmental toxins, among others, may alter organ structure or function. As approximately 50% of all cell divisions for growth occur from conception to birth, it is not surprising that environmental stresses may impact cell number. Although the genotype of programmed offspring does not change, modified gene expression may be a consequence of exposure-mediated epigenetic changes, thus altering the expression of regulatory peptides and organ function (Figure 1). In fact, 2 common historical obstetrical “teratogens” act via epigenetic programming. Thalidomide, which was prescribed in the 1950s as a sedative and morning sickness prescription, and included in more than 50 over-the-counter products, acts to truncate limb development by an epigenetic process that inhibits angiogenesis.4 Of equal concern, diethylstilbestrol (DES) was used off label in women with a history of miscarriage prior to US Food and Drug Administration (FDA) approval in 1947. Only in 1971 did the FDA respond to evidence that DES-programmed female offspring have an increased risk of vaginal clear cell carcinoma, a response that occurs via an epigenetic process of gene hypermethylation in utero.5


    Michael G. Ross, MD, MPH
    Dr. Ross is a professor in the Department of Obstetrics and Gynecology, Geffen School of Medicine, University of California, Los Angeles ...
    Mina Desai, MSc, PhD
    Dr. Desai is an associate professor in the Department of Obstetrics and Gynecology, Geffen School of Medicine, University of California, ...


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