It began with a conversation.
Two decades ago, Dr. Sarah Crawford met a young woman whose mind worked in both mysterious and fascinating ways. The encounter sparked a question that would shape years of research. Now, the Southern Connecticut State University biology professor is challenging conventional thinking about autism’s origins — proposing a new model that focuses not on one cause, but many.
“Many have used vaccines as a starting point for the causes of autism. My model looks at quantitative exposure—multiple factors contributing to the development of the disorder with an additive effect,” Crawford said.
In other words, there is no one cause of autism.
“That’s my model,” she said.
Crawford’s research notes that vaccines, under certain circumstances, may contribute to autism—but only as part of a much broader picture. An individual’s genetic background, she notes, may include inherited differences that increase susceptibility to the disorder.
“It’s the seed in the soil. Autism originates from a genetic background that is still not well understood,” she said.
Autism spectrum disorder is a developmental condition with symptoms typically emerging within the first three years of life. The term “spectrum” reflects the broad range of experiences—every individual with autism has a unique combination of strengths, symptoms, and challenges.
While autism was first studied in the 1940s, it wasn’t formally defined as a distinct diagnosis until the 1980s. Today, the Centers for Disease Control and Prevention estimate that autism affects one in 54 children in the United States. Despite decades of research, the disorder remains both widely misunderstood and unresolved.
Crawford hopes to change that.
Her research focuses on epidemiological studies that explore common factors among individuals with autism—documenting maternal health during pregnancy, early infant life, and key developmental milestones that might influence brain development. From there, researchers assess whether any identified links are modifiable.
Given the heightened interest in vaccines during the COVID-19 pandemic, Crawford emphasizes that her model is about the cumulative effect of multiple influences. She likens it to an “avalanche effect” that can push a vulnerable system to the edge.
This means recognizing that vaccines have a protective effect—stimulating the immune system. If the system is highly dysfunctional, a vaccine could play a role. Still, vaccines have no primary role in the development of autism.
Instead, her model examines how a range of factors—some still unidentified—might affect the developing brain. “Vaccines are just one of many environmental exposures, like a child catching the flu or a mother having gestational diabetes,” she said.
Crawford emphasizes the importance of studying the combination of a dysregulated immune system and the events that disrupt it.
“The idea is to identify individuals who may be at risk—either prenatally or in early life—and determine if interventions like diet or environmental changes could help. We don’t know; we haven’t done the studies yet.”
Crawford’s model breaks the research into three categories: maternal, fetal, and neonatal. Among the factors her research examines are inflammatory differences such as immune system disorders, or infections during pregnancy. In the newborn category, the research considers whether young infants under the age of two have been hospitalized with severe infections. Research has shown a higher rate of autism among children who experience early respiratory infections, she said.
Crawford’s research is shifting into its next phase, studying early brain development from the earliest stage of embryogenesis to the development of the brain. Joining her this fall is junior biology major Connor Poudrie, who is focusing on genetics. Diagnosed with autism at the age of five, Poudrie brings both personal insight and academic passion to the project.
“I was lucky to be diagnosed early,” he said. “I had trouble with speech and social cues. As I grew older, I started to get better with that but was interested in what was the cause of it. It’s a complex order; it’s different for everyone.”
He recalled recognizing his own differences in elementary school.
“I’d do multiplication problems differently than everyone else. I noticed over time, I think differently than most people. I had to learn to figure myself out,” he said.
When Poudrie approached Crawford about advising his thesis on autism, the timing was perfect.
“I told him, ‘You’ve come to the right place. We’re just developing this brain model now,’” she said.
The model incorporates diverse environmental factors that can occur early in life. The research will use Drosophila—a genetics research tool—to study how the brain develops in response to microbial agents that may trigger immune responses at different stages.
“We try to define autism by behavior. If we can show that combined effects affect early events during the brain’s formation, then we have a more potent argument for identifying risk and protecting vulnerable populations, especially infants and pregnant women,” Crawford said.
Future phases of the study may examine specific environmental exposures, including vaccines, but always as part of a broader landscape of risk.
“Maybe we’re going to change behavioral patterns in ways that are protective for a short period of time, whether in pregnancy or newborn year of life—that encourages normal brain maturation and development and have an influence in bringing down these incredibly high incidents of the disorder,” she said.
