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Autistic Adults & Autoimmunity: A Research Perspective on an Emerging Connection

Every so often, a topic pulls me deep into a research rabbit hole—especially when it intersects with lived experience. Recently, that topic was the relationship between autism and autoimmune conditions. And while the science is still evolving, what I found suggests this connection deserves far more scientific attention than it currently receives.


The central question that kept resurfacing was this:


Is there a causal relationship between autism and autoimmune conditions, or are we observing a complex correlation shaped by multiple biological and environmental factors?


As it turns out, the answer isn’t simple—and that’s precisely why it’s worth exploring.


What Early Research Revealed: Immune Irregularities and Autoimmunity


One of the earlier pieces of research pointing toward this connection comes from Enstrom, Van de Water & Ashwood (2009). Their work examined immune profiles in autistic individuals and found patterns of:


  • Altered cytokine levels,

  • immune activation, and

  • the presence of autoantibodies.


These findings didn’t claim causation, but they opened the door to a critical hypothesis: the immune system may play a role—direct or indirect—in the biological landscape of autism.


At the time, this idea was controversial. Today, it’s part of a growing body of inquiry.


Where the Research Stands Now: Neuroinflammation and Innate Immune Function


Fast-forward to more recent work, and the conversation becomes even more interesting. In Hughes, Moreno & Ashwood (2024), the investigators highlight:


  • Innate immune dysfunction,

  • increased inflammatory signaling, and

  • evidence of chronic neuroinflammation in some autistic individuals.


This work doesn’t imply that autism is an autoimmune disorder. Instead, it suggests that some autistic people may have immune phenotypes that make them more susceptible to inflammatory or autoimmune conditions.


This aligns with clinical observations of higher rates of:


  • Hashimoto’s and other thyroid disorders

  • gastrointestinal inflammation

  • co-occurring autoimmune diagnoses


But again: association ≠ causation. What this means is that immune activity appears to be part of the broader biological picture for at least a subset of autistic individuals.


A Neuroimmune Perspective: Why the Connection Makes Biological Sense


The nervous system and immune system continuously communicate—a bidirectional process often referred to as the neuroimmune axis. Disruptions in one can influence the other.


Some factors that may interact within autistic physiology include:


  • chronic sympathetic activation (fight-or-flight patterns),

  • long-term stress from sensory overload or masking,

  • gut dysbiosis affecting immune signaling,

  • genetic predispositions toward immune reactivity.


None of these are unique to autism, but the combination may lead to a distinct risk profile.


This theory aligns with what many autistic adults report anecdotally: symptoms dismissed as “stress” or “behavioral,” but which may have genuine physiological roots.


Nutrition as a Modifiable Variable (Not a Cure, Not a Replacement for Care)


In research terms, nutrition is considered a modifiable factor that can influence immune function and inflammation. For example:


  • Specific dietary patterns can support or hinder gut barrier function.

  • Micronutrient status affects immune resilience and oxidative stress.

  • Dietary inflammation can exacerbate immune dysregulation.


Nutrition does not cure autism or autoimmune conditions—nor does the research suggest it should be viewed that way.


But from a systems biology perspective, nutrition is one of several accessible levers that may influence neuroimmune health, quality of life, and symptom burden.

This is an area in need of more targeted research, especially in autistic populations.


Where the Evidence Leaves Us


Right now, the autism–autoimmunity link fits into a category researchers call “emerging but not yet conclusive.”


Here’s what the current literature supports:


  • ✔ Immune irregularities appear in a subset of autistic individuals.

  • ✔ Autoimmune conditions occur at higher-than-average rates in autistic adults.

  • ✔ Neuroinflammation is being increasingly documented in autism research.

  • ✔ The neuroimmune axis provides a plausible biological pathway.

  • ✔ More research is urgently needed to understand mechanisms and variability.


Here’s what the evidence does not currently support:


  • ✘ Autism is caused by autoimmunity.

  • ✘ Autoimmunity is caused by autism.

  • ✘ Nutrition alone can “treat” these conditions.


The real picture is likely multidimensional—genetics, environment, immune function, neurological patterns, and lived stress interacting over time.


Why This Matters for Future Research and Care


If autistic individuals are indeed more vulnerable to specific immune or inflammatory processes, this should influence:


  • diagnostic frameworks,

  • screening practices,

  • integrative treatment models,

  • and long-term health guidance.


It could also reduce the decades-long cycle of dismissal many autistic adults experience when reporting chronic health symptoms.

In other words:


Understanding the neuroimmune landscape in autism isn’t just a research pursuit—it’s a path toward better care, better validation, and better outcomes.


References


  1. Enstrom AM, Van de Water JA, Ashwood P. Autoimmunity in autism. Curr Opin Investig Drugs. 2009;10(5):463–473.

  2. Hughes HK, Moreno RJ, Ashwood P. Innate Immune Dysfunction and Neuroinflammation in Autism Spectrum Disorder (ASD). Focus (Am Psychiatr Publ). 2024;22(2):229–241. doi:10.1176/appi.focus.24022004

 
 
 

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