Scientists May Have Actually Found One Of The Causes Of Autism
The importance of our gut microbiota to our health has become increasingly clear in recent years as more and more studies have been released.
Everything from how we react to fear and negative stimuli to our weight and mental health to our susceptibility to autoimmune disorders like type 1 diabetes and lupus can be impacted.
A groundbreaking study recently published in The Journal of Immunology has uncovered a fascinating link between the gut microbiota and autism, a neurodevelopmental disorder. The research, conducted on animals, reveals that the microbiota of our mothers may play an even more significant role in influencing our risk of developing autism than our own gut microbiota.
John Lukens, PhD candidate at the University of Virginia School of Medicine and lead researcher, explained, “The microbiome can shape the developing brain in multiple ways.” He further emphasized that the microbiome is crucial in determining how an offspring’s immune system responds to infection, injury, or stress.
In terms of autism, the study suggests that this relationship might be driven by a specific immune molecule, interleukin-17a (IL-17a), which could have a pivotal role in the disorder’s development.
The molecule interleukin-17a (IL-17a), already known to be associated with diseases like psoriasis, multiple sclerosis, and rheumatoid arthritis, has now been linked to the development of autism. This molecule plays a crucial role in defending against infections, particularly fungal infections, but it also influences brain development during fetal growth.
To test their hypothesis, the research team suppressed IL-17a in lab mice to explore its potential connection to autism. They selected female mice from two different labs: one group had gut microbiota that predisposed them to an inflammatory response triggered by IL-17a, while the second group (the control) did not. When IL-17a was artificially suppressed in both sets of mice, the offspring from both groups displayed neuro-typical behaviors at birth, suggesting that preventing IL-17a-induced inflammation may protect against autism-related behaviors.
Despite the initial success in suppressing IL-17a, the pups born to the mothers in the first group eventually developed a neurological disorder that mirrored autism, affecting their social and repetitive behaviors, once they were allowed to grow without further human interference.
To investigate the cause, the researchers performed a fecal transplant using the stool from the first group and transferred it to the mice in the second group. The goal was to see if altering the second group’s microbiota to resemble that of the first group would trigger similar outcomes. As expected, the offspring from the second group developed a neurological disorder resembling autism.
While these are early studies and may not directly apply to human pregnancies, they provide an intriguing direction for autism research. They offer compelling evidence that a mother’s gut health may play a significant role in the development of neurodevelopmental disorders.
The next step, according to Lukens, is to determine what aspect of the mother’s microbiome is linked to the development of autism and see whether they can find such correlations in people.
There are a number of more molecules to look at. IL-17a might be a single component in a much bigger picture, Lukens suggested.
