Nurishing Beginnings: The Role of Prenatal Nutrition in Offsetting Stress-Related Developmental Risks

Maternal prenatal stress and nutrition influence fetal growth and long-term child outcomes. Maternal perceived stress and undernutrition frequently co-occur and affect overlapping biological stress pathways related to oxidative stress, Still, little is known about the interactive effects of maternal prenatal stress and nutrition on fetal and long-term child outcomes and neurological development. The proposed R00 research will leverage data from the “Enhancing Nutrition and Antenatal Infection Treatment for Maternal and Child Health” (ENAT) trial to examine interactive effects of maternal prenatal stress and nutrition intervention on long-term child outcomes. The ENAT study randomized n=2390 pregnant women to receive an “enhanced nutrition” package or “standard care” and collected data on maternal prenatal stress (Cohen’s Perceived Stress Scale) throughout the pre- and postnatal period. Using data from ENAT, we will determine independent and interactive effects of maternal prenatal perceived stress and nutrition intervention on children’s cognitive and neural developmental at 24 months of age. Child outcomes will include stress-sensitive outcomes previously shown to be sensitive to early life adversity, including attention, memory, and language. We will also use electroencephalography (EEG) to examine neural oscillation across different frequency bands as an index of neural maturation. To study underlying biological pathways, we will use maternal and infant blood samples examine whether maternal and newborn telomere lengths may serve as biomarkers of in-utero programming of birth and child outcomes in relation to maternal prenatal perceived stress and nutrition. We hypothesize that higher levels of maternal prenatal stress will be associated with poorer cognitive and neural oscillatory child outcomes. Telomeres are non-coding tandem repeats at the end of the chromosomes that maintain genome and cell integrity. Telomeres erode over time and stress and poor nutrition can lead to accelerated erosion and cellular aging. Children with low birthweight have been found to have shorter telomeres. We therefore hypothesize that effects of prenatal stress on birth and child outcomes will be mediated by maternal and newborn telomere length, but that such associations will be attenuated in offspring of women who received nutrition intervention This R00 will enable me to lead an innovative research program in child neurodevelopment and establish me as a leader and innovative scholar utilizing advanced methods to uncover mechanistic processes that shape childhood development in domestic and global settings. The proposed research aligns with NICHD’s goal to set a foundation for healthy pregnancies and lifelong living. We will generate epidemiologic and biologic evidence linking maternal prenatal nutrition and stress with newborn and childhood outcomes that are sensitive to prenatal stress and form long-term outcomes related to school achievement and mental health. We will use this knowledge to guide public health decisions regarding pre- and postnatal intervention both domestically and globally, and to develop future intervention to support optimal child development and health. Project Number: 4R00HD110651-03 | Fiscal Year: 2026 | NIH Institute/Center: Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD) | Principal Investigator: Sarah Jensen | Institution: WOMEN AND INFANTS HOSPITAL-RHODE ISLAND, PROVIDENCE, RI | Award Amount: $248,999 | Activity Code: R00 | Study Section: NSS View on NIH RePORTER: https://reporter.nih.gov/project-details/11490335