Summary: New research from Oregon Health & Science University indicates that when mothers consume a high‑fat diet during pregnancy, their offspring may face a higher risk of anxiety and depressive symptoms later in life. In a controlled nonhuman primate model, researchers linked maternal high‑fat diet exposure to disrupted development of the central serotonin system. Notably, switching offspring to a healthier diet early in life did not fully reverse these effects.
Source: Oregon Health and Science University
OHSU researchers are the first to demonstrate a causal relationship using a nonhuman primate model.
A high‑fat diet during pregnancy can do more than affect maternal weight and metabolic health. New controlled research in nonhuman primates shows it can alter brain and endocrine development in offspring and produce persistent behavioral changes associated with anxiety and depression. These findings point to diet as a significant environmental factor shaping long‑term mental health across generations.
The study, published in the journal Frontiers in Endocrinology, was led by Elinor L. Sullivan, Ph.D., assistant professor in the Division of Neuroscience at the Oregon National Primate Research Center at OHSU. Researchers were able to tightly control maternal diets—an experimental advantage not possible in human populations—and then follow neurobehavioral and physiological outcomes in the juvenile offspring.
Researchers assigned 65 female Japanese macaques to either a high‑fat diet or a control diet during pregnancy and early development. They monitored 135 juvenile offspring for anxiety‑like behavior and other neurodevelopmental measures. Both male and female offspring exposed to a maternal high‑fat diet displayed higher levels of anxiety‑related behavior compared with control animals. In addition to behavioral differences, the team documented impairments in the development of serotonin‑producing neurons—cells that synthesize the neurotransmitter serotonin, which plays a key role in mood regulation and brain development.
“Given the high level of dietary fat consumption and maternal obesity in developed nations, these findings have important implications for the mental health of future generations,” the authors write. The study’s controlled design demonstrates a causal link between maternal high‑fat diet exposure and lasting changes to offspring behavior and brain chemistry.
Joel Nigg, Ph.D., professor of psychiatry, pediatrics, and behavioral neuroscience in the OHSU School of Medicine, described the results as striking. He noted that while obesity’s links to cardiovascular and metabolic disease are well known, this study provides a clear demonstration that maternal diet can produce substantial effects on offspring brain development and behavior.
Key findings include:
- Persistent increases in anxiety‑like behaviors among juveniles exposed to maternal high‑fat diet.
- Postweaning consumption of a high‑fat diet also increased anxiety and contributed independently to repetitive, stereotypic behaviors in juveniles.
- Altered stress hormone (cortisol) responses tied to maternal and early postnatal diet exposure.
- Impaired development of the central serotonergic system, including changes to tryptophan hydroxylase‑2 mRNA expression in brainstem raphe nuclei and reduced serotonergic markers in prefrontal cortex regions.
- Early nutritional intervention at weaning—switching offspring to a control diet—was not sufficient to fully reverse many anxiety‑related behavioral changes induced by maternal high‑fat diet.
Sullivan and first author Jacqueline R. Thompson emphasize that the goal is not to blame mothers, but to inform public health efforts and support families. They recommend promoting access to healthy food, prenatal care, and policies that encourage healthier lifestyles for people of reproductive age. Thompson noted that increased public awareness of early life contributors to neuropsychiatric disorders could improve identification, prevention, and management at both individual and community levels.
Funding: This work was supported by the National Institute of Mental Health grant R01MH107508, the Murdock Charitable Trust and Murdock College Research Program for Life Science (grant 2011273:HVP), and the Oregon Clinical and Translational Research Institute (UL1TR000128) from the National Center for Advancing Translational Sciences at the NIH. Operation of the Oregon National Primate Research Center (ONPRC) and core facilities were supported by P51 OD011092.
Source and authorship: Press materials from Oregon Health and Science University. Original research titled “Exposure to a High‑Fat Diet during Early Development Programs Behavior and Impairs the Central Serotonergic System in Juvenile Non‑Human Primates” was authored by Jacqueline R. Thompson, Jeanette C. Valleau, Ashley N. Barling, Juliana G. Franco, Madison DeCapo, Jennifer L. Bagley, and Elinor L. Sullivan, and published in Frontiers in Endocrinology (published online July 21, 2017; doi:10.3389/fendo.2017.00164).
Perinatal exposure to maternal obesity and a high‑fat diet increases not only metabolic risk but also impacts brain development and behavior. In a nonhuman primate model, maternal high‑fat diet produced a lasting increase in juvenile anxiety, altered cortisol stress responses, and impaired development of central serotonin synthesis—changes observed in both brainstem and prefrontal regions. Postweaning consumption of a high‑fat diet further contributed to anxiety and repetitive behaviors, but switching to a control diet at weaning did not fully reverse the effects induced by maternal diet. These findings indicate that perinatal high‑fat diet exposure programs the developing brain and endocrine system in ways that raise the risk of mental health and neurodevelopmental disorders in offspring.
These conclusions derive from a rigorously controlled animal study. While findings highlight important biological mechanisms and public health implications, translation to humans requires continued research that accounts for complex genetic, environmental, and social factors affecting maternal and child health.