The prevalence of autism spectrum disorder (ASD) is on the rise.
According to the Centers for Disease Control and Prevention (CDC), in 2000, 1 in 150 children had ASD, but by 2012, that number had risen to 1 in 68.
As of 2018, 1 in 59 children have ASD.
Although researchers do not yet know exactly what causes ASD, they think that a combination of genes, environmental influences, and issues with the maternal immune system in the early stages of pregnancy may contribute to its development.
Recently, some studies have pointed to the gut microbiome as a potential key player in the development of ASD.
For instance, some researchers found that the microbiota of autistic children lacked the beneficial strains of bacteria Bifidobacteria and Prevotella, while other studies found “a significant increase in the Firmicutes/Bacteroidetes ratio” and higher levels of the bacterial taxa Escherichia/Shigella and Clostridium cluster XVIII.
Studying a common food preservative
So, researchers Prof. Saleh Naser and Latifa Abdelli — together with undergraduate research assistant Aseela Samsam, from the University of Central Florida (UCF) in Orlando — set out to further examine the link between gut bacteria and ASD.
Specifically, the team focused on the link between propionic acid (PPA) and autism.
“Studies have shown a higher level of PPA in stool samples from [autistic children] and the gut microbiome in autistic children is different,” explains Prof. Naser, also of the Burnett School of Biomedical Sciences at UCF. “I wanted to know what the underlying cause was,” he adds.
PPA is a naturally occurring short-chain saturated fatty acid with antifungal properties. Also, many manufacturers use it as a food preservative and flavoring agent for packaged and processed products.
What is the link between PPA and autism?
Experiments with cultured neural stem cells have revealed that very high PPA levels reduce the number of cells that go on to differentiate into neurons and increase the number of cells that go on to become glial cells.
In the new study, too much PPA also damaged the molecular pathways that normally enable neurons to send information to the rest of the body.
The researchers suggest that such disruption in the brain’s ability to communicate may explain ASD-related characteristics such as repetitive behavior and difficulties with social interaction.
They also suggest that eating processed foods likely to have high levels of PPA during pregnancy may increase PPA levels in the maternal gut, which could then transfer to the fetus.
“In the current study,” write the authors, “we are linking maternal PPA exposure to disturbed neural patterning during early stages of embryonic neural development leading to overproliferation of glial cells, abnormal neural architecture, and increased inflammatory profile; possible precursors for autism.”
However, PPA is naturally present in the gut, and the pregnancy changes that occur in the maternal microbiome can naturally cause PPA to increase. Prof. Nasar and team acknowledge the fact that more research is necessary before they can reach any clinical conclusions.
“This is an intriguing finding and a first in the field,” write the researchers. Their next steps include replicating the findings in mice and determining whether a high-PPA maternal diet leads to offspring with ASD-like behavior. Prof. Naser and colleagues conclude:
“This research is only the first step toward [a] better understanding of [ASD]. But we have confidence we are on the right track to finally uncovering autism etiology.”