As the number of children diagnosed with autism continues to rise at alarming rates, researchers have been working hard to figure out what environmental and/or genetic factors might be contributing to the disorder.
Now, based on the findings of a new study, researchers from the University of Central Florida (UCF) may be a step closer to establishing a link between processed food and specific changes in the fetal brain tied to behaviors in autism.
Their findings, published in the journal Scientific Reports, show that when fetal-derived neural stem cells are exposed to high levels of Propionic Acid (PPA), an additive commonly found in processed foods, it decreases neuron development.
PPA is often used in the commercial food industry to increase the shelf life of packaged foods and to inhibit mold in processed cheese and bread. The acid also occurs naturally in the gut, and when a mother’s microbiome changes during pregnancy, it can cause an increase in the acid.
However, the researchers say that eating packaged foods containing the acid can further increase PPA in the woman’s gut, which then crosses to the fetus.
Researcher Dr. Saleh Naser, who specializes in gastroenterology research at the College of Medicine’s Burnett School of Biomedical Sciences, began the study after reports showed that children with autism often suffer from gastric issues such as irritable bowel syndrome.
He wondered about a possible link between the gut and the brain and began examining how the microbiome, or gut bacteria, differed between people with autism and those who do not have the condition.
“Studies have shown a higher level of PPA in stool samples from children with autism and the gut microbiome in autistic children is different,” Naser said. “I wanted to know what the underlying cause was.”
In the lab, the scientists discovered that exposing neural stem cells to excessive PPA damages brain cells in several ways: First, the acid disrupts the natural balance between brain cells by reducing the number of neurons and over-producing glial cells. And although glial cells help develop and protect neuron function, too many glia cells disturb connectivity between neurons. They also cause inflammation, which has been noted in the brains of autistic children.
In addition, excessive amounts of the acid shorten and damage pathways that neurons use to communicate with the rest of the body. This combination of reduced neurons and damaged pathways hinder the brain’s ability to communicate, resulting in behaviors that are often found in children with autism, including repetitive behavior, mobility issues and inability to interact with others.
Previous research has found links between autism and environmental and genetic factors, but this study is the first to discover the molecular link between elevated levels of PPA, proliferation of glial cells, disturbed neural circuitry and autism.
More research needs to be conducted before drawing clinical conclusions. Next, the team will attempt to validate its findings in mice models by seeing if a high PPA maternal diet causes autism in mice genetically predisposed to the condition. There is no cure for autism, which affects about 1 in 59 children, but the scientists hope their findings will advance studies for ways to prevent the disorder.
Naser conducted the 18-month study with Dr. Latifa Abdelli and UCF undergraduate research assistant Aseela Samsam. The research was self-funded by UCF.
“This research is only the first step towards better understanding of autism spectrum disorder,” the UCF scientists concluded. “But we have confidence we are on the right track to finally uncovering autism etiology.”
Source: University of Central Florida