Obesity Before Pregnancy Linked to Autism-Like Behavior in Kids

Obese pregnant woman feeling cheerful

A mother’s weight before pregnancy could be linked to autism-like behaviors in her children.

This is the conclusion of a study by researchers at the University of Hawaiʻi at Mānoa, who found that obesity can trigger metabolic shifts that cause lasting epigenetic changes in a mother’s eggs.

These changes are passed on to the developing embryo and affect genes involved in brain development, including “Homer1,” a protein important for regulating synaptic signaling, learning, memory and response to neural activity.

Obesity and autism spectrum disorder (ASD) rates are increasing worldwide (though for autism this could be because of increased awareness).

More than 2 in 5 adults (42.4 percent) are diagnosed as obese in the U.S., while 1 in 31 children and 1 in 45 adults are living with ASD across the country.

While ASD is not an illness—and just means people’s brains work differently from others’—the researchers said their findings mark a “significant advancement” in understanding how early life factors can shape long-term brain development.

Excited young woman covering her mouth and screaming while looking at a positive pregnancy test in the bedroom.

Antonio_Diaz/Getty Images

Conducting experiments in mice models, the team detected increased levels of a specific Homer1 gene isoform that is known to interfere with neural connections—and is associated with behaviors linked to ASD—in male offspring of obese female mice.

“This work highlights how a mother’s health prior to pregnancy, not just during gestation, can shape her child’s brain development in profound ways,” said paper author and epigeneticist professor Alika K. Maunakea in a statement.

“We were surprised to find that even without direct maternal contact after conception, these epigenetic imprints from the egg carried enough weight to alter behavior.”

To isolate the effects of pre-pregnancy obesity away from those during gestation, the time between conception and birth, the researchers used an in vitro fertilization (IVF) and embryo transfer model. This approach allowed them to study early epigenetic programming more precisely.

Behavioral assessments of adolescent male mice revealed impaired social interactions and repetitive behaviors. These traits, which mirror characteristics of ASD, were linked to altered gene regulation in the brain, the researchers explained.

“By leveraging our institute’s expertise in developmental biology, reproductive science and epigenetics we are beginning to understand how early-life programming can ripple through generations,” said paper author and reproductive biologist professor Monika Ward in a statement.

The researchers say the findings may lead to early interventions, potentially even before conception. However, they hope future studies will explore nutritional or pharmacological therapeutic strategies that may reverse or mitigate these effects.

There is no single known ’cause’ for autism, but research suggests it could develop from a combination of genetic and environmental factors.

“Brain scans show differences in the shape and structure of the brain in people with autism compared to in neurotypical development. Researchers do not know the exact cause of autism but are investigating a number of theories, including the links among heredity, genetics, and medical problems,” the Autism Society website outlines.

“There has been misinformation about the cause of autism. It is not caused by vaccines or due to parenting style or nutrition.”

Newsweek has reached out to the researchers for additional comment.

Do you have a tip on a health story that Newsweek should be covering? Do you have a question about autism? Let us know via health@newsweek.com.

Reference

Allan, N. P., Torres, A., Corley, M. J., Yamamoto, B. Y., Balaan, C., Yamauchi, Y., Peres, R., Qin, Y., Khadka, V. S., Deng, Y., Ward, M. A., & Maunakea, A. K. (2025). Pre-Conception Maternal Obesity Confers Autism Spectrum Disorder-like Behaviors in Mice Offspring Through Neuroepigenetic Dysregulation. Cells, 14(15), 1201. https://doi.org/10.3390/cells14151201

Leave a Reply

Your email address will not be published. Required fields are marked *