It’s been an unanswered question for years – Is autism an autoimmune disorder? Recent science suggests that it may very well be.
Immune dysregulation and autism is the topic of an interesting opinion article published in the New York Times this week.
A 20 year study from Denmark indicates that if the mother experiences a bacterial or viral infection during pregnancy, the risk for autism may double or triple.
However, it’s not the bug, it’s the maternal immune response to the invader and the ensuing inflammation that is the culprit.
If the mother has some dysregulation of her immune system, whether it be from viruses during pregnancy or from her own immune balance problems, this can affect the developing child’s brain.
It appears that it is the mother’s response to a trigger is what is important.
Research by Paul Patterson, an expert in neuroimmunity at Caltech, shows that causing inflammation in pregnant mice results in behavioral problems in the offspring.
Paul Patterson has a blog and a book that may be of interest.
Another large study from Denmark has shown associations between autoimmune diseases in the parents (especially the mother) and the elevated risk of autism in the child.
Another Danish study, which included nearly 700,000 births over a decade, found that if a mother had rheumatoid arthritis, this elevated a child’s risk of autism by 80 percent.
They found that if the mother had celiac disease, (an inflammatory disease triggered by proteins in wheat and other grains), the risk for autism increased 350 percent.
That is a huge risk, especially in view of the fact that many people with celiac disease go undiagnosed for years. I wonder if gluten intolerance carries a similar risk and/or if a grain-free diet in the mother alleviates some of the risk…
Genetics also has something to do with autism.
However, it is the gene variants that are associated with autoimmune disease that appear to increase the risk of autism, especially if it comes from the mother’s side.
The common denominator here is the problem of inflammation.
This begs the million dollar question of why we are experiencing so many inflammatory conditions.
Modern cultures who still live close to the earth – actually have little if any autoimmune diseases and they have no autism.
The hygiene hypothesis is becoming more and more accepted and medicine is embracing the inherent therapeutic possibilities of using bacateria, viruses and even helminths (worms) as a therapeutic modality.
Inflammation in autistic children was first identified by Dr. Andrew Wakefield.
He observed that autistic children had inflammation in their bowels.
He did endoscopy exams on all the autistic children he saw in his gastroenterology practice and he noticed that they all had a new kind of inflammatory bowel disease that he called autistic enterocolitis.
He has been persecuted for this work, but it appears that others have found similar problems in the guts of autistic children.
Here again, inflammation is at work.
There is current research that suggests that inflammation in the amniotic fluid may influence the development of the child’s brain.
Brain cells called astroglia and microglia — get enlarged from chronic immune activation.
Pro-inflammatory chemicals and cytokines are present. Genes involved in inflammation are switched on. Amniotic fluid collected from Danish newborns who later developed autism looked mildly inflamed according to a study presented this year.
All the associations and relationships of autism with various other diseases and conditions as noted above, revolve around inflammation.
Inflammation is the basis for many disease conditions.
Civilization has created a clean and sterile world for us, but we have lost our old friends (parasites, worms and other microbes that should be part of our microbiome) and we need them back.
Amazingly, scientists at Montefiore Medical Center and the Albert Einstein College of Medicine are investigating the use of pig whipworm (Trichuris suis) in autistic adults.
T suis has been used successfully to treat inflammatory bowel disease and is currently being studied in other universities (NYU is one) for that condition.
We know that our uncivilized ancestors coexisted with parasites, worms and other microbes that helped regulate the two arms of the immune system – Th1 and TH2.
When the immune system becomes damaged, one of the two arms (TH1 and TH2) becomes dominant.
This causes the development of chronic allergies, autoimmune diseases and recurrent infections. The more unbalanced the relationship between Th1 and Th2, the more damage to the healthy tissue occurs and the more advanced the autoimmune disease may become.
In healthy individuals, TH1 and TH2 responses are balanced and able to switch back and forth according to the body’s requirements. These responses will activate when appropriate to eradicate a threat and then it will calm down appropriately until the next time an invader appears.
What does all this have to do with inflammation?
Every time an immune response is activated, chemicals called cytokines are released.
These cytokines are purveyors of inflammation. Therefore, each time an immune response is initiated, inflammation occurs under the radar. If the person’s immune response is unbalanced in the two arms (Th1 and TH2) the response may be inappropriate and will create inflammation.
Inflammation is destructive and chronic inflammation is the basis of all kinds of degenerative diseases.
I have already talked about the effects of gluten on susceptible individuals. But there are many other triggers because we are all individuals biochemically.
The author of this very interesting opinion article is Moises Velasquez-Manoff. He is the author of “An Epidemic of Absence: A New Way of Understanding Allergies and Autoimmune Diseases.”
That is a book I will be reading.
My only complaint is that he did not give references for the research he quoted and that is why I do not have those references here. I guess an opinion piece does not require that type of documentation but I kind of wish he did include that information.
Are you as interested in this topic of research as I am? Leave a comment and let me know!