
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.
Our responses to fear and negative stimuli, our weight and mental health, and even our vulnerability to autoimmune disorders such as type 1 diabetes and lupus—all of these can be influenced.

A recent study published in The Journal of Immunology has uncovered a potential link between the gut microbiota and autism, based on research conducted on animals. Principal researcher and PhD candidate John Lukens from the University of Virginia School of Medicine explained, “The microbiome can shape the developing brain in multiple ways.”
Lukens also emphasized that the microbiome plays a vital role in how an offspring’s immune system responds to infection, injury, or stress. In the case of autism, this connection may be tied to a specific molecule known as interleukin-17a (IL-17a), a key player in the immune system’s response.

The molecule IL-17a has already been implicated in diseases such as psoriasis, multiple sclerosis, and rheumatoid arthritis. It is also crucial in defending against infections, particularly fungal ones, and has been shown to influence brain development while still in the womb.
To explore its potential role in autism, the research team suppressed IL-17a in lab mice. They selected female mice from two different labs: the first lab had mice with gut microbiota that made them more prone to an inflammatory response triggered by IL-17a, while the second lab provided control mice without this predisposition. The offspring from both groups of mice displayed neuro-typical behaviors at birth when IL-17a was suppressed, effectively preventing the inflammatory response associated with the molecule and its potential link to autism.

However, as the pups born to the mothers in the first group matured, they developed neurological behaviors resembling autism, particularly in social interactions and repetitive actions, once they were allowed to grow without further human intervention.
To confirm that this was linked to the distinct microbiota of the first group, the researchers performed a fecal transplant using the feces from these mice and transferred it to the mice in the second group. The aim was to alter the microbiota of the second group to more closely resemble that of the first group. As expected, the pups from the second group later developed neurological issues that mirrored autism.
While these studies are still in their early stages and may not directly apply to human pregnancies, they open an intriguing avenue for autism research. They offer compelling evidence that a mother’s gut health could play a role in the development of neurodevelopmental disorders.

The next step, according to Lukens, is to identify which specific aspect of the mother’s microbiome is linked to autism development and to explore whether similar correlations can be found in humans.
Lukens also pointed out that IL-17a might only be one part of a much larger picture, suggesting that there are many more molecules to examine in this complex relationship.