Wednesday, November 9, 2022 from 1 - 2 PM

Chair: Elinor L. Sullivan, Associate Professor in Psychiatry, Oregon Health & Science University, Portland, USA

Co-Chair & Discussant: Elizabeth K. Wood, Ph.D., Post-doctoral Trainee, Psychiatry Department, Oregon Health & Science University, Portland, OR:

Symposium Abstract: 

The influence of prenatal nutrition on offspring neurobehavioral development is an emerging and exciting area of research. This symposium highlights recent preclinical and clinical work examining the impact of prenatal dietary intake on offspring neurobehavioral outcomes from early infancy to adolescence, using state-of-the-art measures of nutrition, offspring neurobehavior, and their potential mechanistic pathways. First, Dr. Elizabeth Wood will present data on the independent effects of the prenatal dietary glycemic index of pregnant persons on temperament outcomes in six-month-old human infants, proposing a unique and modifiable target for intervention. Second, Jose Murgueitio will present neuroimaging data showing that the prenatal obesogenic nutrition of pregnant persons leads to altered brain volumes in their two-week-old human infants, pointing to possible neural mechanisms of prenatal dietary effects on risk for offspring psychopathology. Third, Dr. Elinor Sullivan will describe the influence of maternal prenatal Western-style diet, inflammation, and metabolic profile on juvenile nonhuman primate offspring behavioral outcomes, suggesting that inflammation may be a common pathway for multiple prenatal programming effects. Finally, Dr. Kellie Tamashiro will describe the influence of maternal prenatal high-fat/high-sugar diet on the gut-microbiome and cognitive development in rodent offspring. She will also highlight the utility of a prenatal exercise intervention for ameliorating prenatal dietary effects. Bridging preclinical and clinical efforts, this symposium will summarize and examine recent work investigating how prenatal nutrition shapes offspring development and the mechanistic pathways underlying these relationships, including altered neurodevelopment, peripheral inflammation, changes in metabolic hormones, and the gut-microbiome.

List of abstracts and presenters


Elizabeth K. Wood, Ph.D., Post-doctoral Trainee, Psychiatry Department, Oregon Health & Science University, Portland, OR

The dietary glycemic index (GI) is a measure of the rate of plasma glucose generation from food consumption, with higher GI foods leading to rapid increases in blood sugar. While prenatal consumption of high-GI foods has been linked to offspring risk for obesity and metabolic disorders, the impact of prenatal GI on infant neurodevelopment is unclear. The independent effects of prenatal dietary GI, fasting plasma glucose and adiposity during pregnancy, and pre-gravid body mass index (BMI) on infant negative affect in 308 mother-infant dyads were examined. During the 2nd trimester, participants completed 24-hour dietary recalls conducted by trained nutritionists and adiposity was assessed via air displacement plethysmography. Pre-gravid BMI and fasting plasma glucose values were extracted from medical records. Infant temperament was evaluated at six months using the Infant Behavior Questionnaire-Revised. Results from structural equation models accounting for the interdependence of dietary GI, pre-gravid BMI, and maternal adiposity and metabolic measures showed that higher 2nd trimester dietary GI predicted higher infant negative affect at 6 months (β=.13, p=.05), including higher distress to limitations (β=.14, p=.04), sadness (β=.16, p=.02), and lower falling reactivity (β=-.13, p=.052). Fasting plasma glucose also predicted infant sadness at 6 months (β=.24, p=.001). Interestingly, there were no other significant relationships between maternal pre-gravid BMI, adiposity, and metabolic measures and infant negative affect or its subscales. These results suggest that prenatal dietary GI is a critical intervention target for improving infant neurodevelopmental outcomes and are an important step toward elucidating the relationship between prenatal nutrition and infant neurodevelopment.


Jose N. Murgueitio, Graduate Student, University of North Carolina at Chapel Hill, Chapel Hill, NC

Prenatal obesogenic nutrition (PON) has been linked to offspring outcomes, suggesting that high-fat prenatal diet is related to increased mice anxiety and depressive-like behavior, and high sugar consumption prenatally has been linked to human brain tissue organization in offspring. While there seems to be a relation between PON and offspring outcomes, no study has examined the relation between PON and human brain subcortical volumes. The present study follows a longitudinal cohort of mother-child dyads (n=103) from pregnancy. Mothers completed 24-hour diet recall prenatally using the Nutrition Data System for Research software, and at 2 weeks, neonates were scanned using 3T MRI during natural sleep. We tested whether fat, saturated fatty-acids (SFAs), sugar, and added sugar were associated with subcortical brain volumes, controlling for relevant covariates. Our results show that higher total fat intake was associated with decreased right [β= -0.75(0.32), p=0.023] and left amygdala [β= –0.73(0.35), p=0.038], and intracranial volumes [β= -862.03(423.88), p=0.045]. Higher SFAs were associated with increased right [β =1.23(0.46), p=0.008] and left amygdala [β=1.46(0.49), p=0.004] volumes. Total sugar was associated with decreased right caudate nucleus volume [β= -2.69(0.97), p=0.007]. Total added sugar was associated with increased right caudate nucleus volume [β= 2.19, (0.85), p=0.01]. These results support evidence suggesting that PON impacts offspring development. Additionally, volumetric differences of the structures associated with PON in this study, have been associated with several aberrant behaviors later in development in other studies. Future research should explore longitudinal associations as well as the mechanisms linking PON to neonatal brain volumes.


Elinor L. Sullivan, Associate Professor in Psychiatry, Oregon Health & Science University, Portland, OR

The prevalence of pediatric neurodevelopmental disorders has risen dramatically in recent decades. To varying degrees, maternal diet, metabolic state, and inflammation have each been shown to influence offspring neurodevelopment in humans and animal models. However, the complex interaction between nutrition and metabolic and inflammatory systems makes it difficult to identify targets for intervention. Using a longitudinal non-human primate model of chronic Western-style diet (WSD) exposure, we have previously shown that maternal physiological factors, including third trimester inflammation, uniquely alter offspring negative affect. This study investigates the influence of maternal WSD, inflammatory and metabolic profile on offspring behavior. Dams were fed either a WSD or control diet for a year prior to gestation and throughout lactation. Metabolic state and inflammation were measured during the third trimester. Social behavior was measured in offspring at 6.5 months of age (n=39) using the Novel Peer Introduction task. WSD increased IL-12 (p=.004) and decreased in MDC (p=.014) in the third trimester in adult females. WSD offspring displayed decreased social engagement as indicated by decreased initiation of proximity (p=.023) and affiliative contact (p=.048) by WSD offspring. Maternal IL-12 mediated the association between WSD and reduced social behavior. WSD increased IL-12 (β= 0.36) which was negatively associated with initiation of proximity (β= -0.35) and affiliative contact (β= -0.65; ps<0.05). Additionally, WSD increased repetitive behavior (β=0.63, p=.03), which was unrelated to any inflammation markers. Given the increasing global prevalence of a WSD and neurodevelopmental disorders, these findings can help direct future investigations to alleviate this public health risk.


Kellie Tamashiro, Ph.D., Associate Professor of Psychiatry & Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, MD

The intrauterine and early postnatal environments are sensitive periods during development and insults during this time can have profound adverse effects on offspring health. Rodent models have demonstrated that maternal consumption of a diet high in fat or sugar affects maternal metabolic state and negatively impacts offspring brain development. In addition to increased susceptibility to metabolic disease, rat offspring have delayed achievement of some developmental milestones and lasting deficits in cognitive function and reward responses. Progress has been made in elucidation of the underlying cellular and molecular mechanisms that may be responsible for altered brain development and negative behavioral outcomes, including gut dysbiosis and increased inflammation prior to weaning. The gut-brain axis has a well-known role in the controls of feeding and regulation of body weight. There is now greater appreciation for its additional roles in mood, cognitive function, and reward processes. Maternal high-fat diet during the perinatal period may have a critical role in establishment of offspring microbiota and development of the gut-brain axis, to have direct and indirect impacts on brain and behavior. Finally, identification of potential interventions to mitigate or prevent adverse consequences is critical for improving offspring health. Our data in rats suggest that maternal exercise during the gestation period is sufficient to have beneficial long-term effects on offspring brain development and behavior.

Symposium Discussant

Elizabeth K. Wood, Ph.D., Post-doctoral Trainee, Psychiatry Department, Oregon Health & Science University