Cause of Classic Autism

Peter Hypothesis Regarding the Cause of Autism,

 The Predisposition of some Children towards it and Implications for Treatment

Autism is a spectrum of behaviours and disorders that result from damage and subsequent malformation of the developing cerebellum.  The damage in classic autism occurs in utero, whereas in the case of regressive autism, there is a second oxidative shock that occurs around a key point in brain development, triggering the onset of autism.  The cause of the cerebral damage is an oxidative shock from one or more of a variety of possibilities, not limited to, maternal stress and infection during pregnancy and toxins such as mercury crossing the blood brain barrier (BBB).  Individuals with autism, and many of their close relatives, have a predisposition to the condition, due to an inherited over-reactive immune system.

The immune system may have become over-reactive to infection partly due to a lack of the on-going attacks, for which it has evolved.  This may be another case for the well documented “Hygiene Hypothesis”, in which a little bit of dirt, rather than an apple a day, keeps the doctor away.

The result is that while in modern society the likelihood of an oxidative shock has increased, the immune system has become so relaxed, due to a sterile environment, that it becomes over-activated when confronted by a severe oxidative shock.  A cytokine storm then rages and the resulting severe neuroinflammation and oxidative damage causes permanent brain damage.  The brain tries to repair itself, but as it continues to grow, it deforms.  A milder neuroinflammation typically continues throughout life and this aggravates the observed autistic behaviours.

In very rare individuals with mild autism, a “recovery” can be observed.  This is most likely the result of successful behavioural therapy of some kind and the on-going neuroinflammation subsiding, for reasons unknown.    In cases where brain damage is substantial, as is generally reported to be the case in classic autism, “recovery” is somewhat fanciful; optimal outcome is the realistic goal of therapy.

A secondary inherited/genetic factor may eventually be proved to be the permeability of the BBB (blood brain barrier).  This would play a role in both the initial oxidative shock reaching the cerebellum and in the following cytokine storm.  Cytokine molecules are particularly large and those released from outside the brain should struggle to enter it.

Vaccination damage is just one of many possible causes of oxidative shock that could trigger regressive autism; it cannot be the cause of classic early onset autism.  Milder cases of autism, and indeed ADHD, are caused by milder cerebral damage and milder on-going neuroinflammation.

Implications of the Hypothesis

1.       At risk mothers should avoid possible oxidative attack

The overactive immune system is measurable (the simplest and cheapest test is the C-reactive protein test; but cytokine testing would be conclusive) and this knowledge could be used to reduce further cases of autism, by identifying at risk mothers.  The threat of oxidative damage could be reduced by de-sensitizing the immune system during pregnancy (risky, but possible), or perhaps better, by meticulously avoiding oxidative damage during pregnancy, in those in the high risk group.  Most likely, the lack of a “successful” oxidative attack during pregnancy would reduce the likelihood of a secondary shock later on that could tip the balance towards regressive autism.

Oxidative damage can be caused by a wide range of environmental factors including, pollution, living too close to high voltage electricity cables or powerful radio/TV transmitters or even mobile phone transmitters.  Maternal stress and even extreme weather events have been shown to do oxidative damage.  There is a great deal of research on this subject, but it is poorly reported; just search on Google Scholar. 

2.       Reset the immune system

Increased exposure to pets, mild intestinal parasites and dirt in general, would reverse the modern trend towards an unprepared and then over-reactive immune system.

This would have the secondary benefit of reducing the prevalence of a wide range of 21st century conditions including asthma, food allergies, eczema and even gastrointestinal sensitivity and arthritis.  These are all linked to neuroinflammation and/or an overactive immune system.

3.       Therapy & Treatment

Once the brain damage has occurred we are left with the challenge of how best to manage it and achieve “optimal outcome”.  Now that we have a plausible hypothesis, this will greatly help us (me) finding effective therapies, some of which will be novel.

Therapy needs to take advantage of neuroplasticity, particularly in the very early years, to maximize the potential of the damaged brain.  Intensive early behavioural intervention has been proved to be effective and neurological explanation is that the brain’s own plasticity is being exploited to develop new pathways within it.  In other words, start an ABA programme.

Targets for pharmacological intervention:- 
  •     Reduce the on-going neuroinflammation / oxidative stress   

  •    Treat secondary issues arising from the malformation of the brain

            ·         Ion channel and neurotransmitter (GABA, glutamate etc.)  malfunction

            ·         Hippocampus malfunction, leading to a cascade of hormone errors (CRH, 
                      TRH, AVP, Oxytocin, Cortisol etc.)


  1. Hi,
    This is Seth Bittker again. Your hypotheses sound reasonable. I alos agree oxidative stress plays a signficant role. I think the underlying cause is too much oral supplementation of vitamin D given to the young. There are good reasons for this if you look at syndromes that are comorbid with autism they feature over-active calcium channels (i.e. too much calcium).
    Vitamin D promotes calcium absorption. Also Th2 immune skew in autism is characteristic of excessive consumption of vitmain D. Oxidative stress can be the result of too much vitamin D. Also the functional deficiency of potassium in autism points to too much vitamin D. Most importantly whenever we adjusted the amount of vitmain D upward that babies get in our society, autism rates go up. Since Cuba does not fortify or supplement with vitamin D and neither do the Amish, we would expect them to have low rates, and they do. There is more. I have a book about this on amazon and would gladly discuss further.

    1. How to find what is the problem with our kid and if we know the problem means then only we can give supplements right..... - downregulation of TH1 through upregulation of IL-10 and downregulation of IL-17
      This prevents autoimmune phenomena and cytokine flares which affect cognition in certain subtypes of to find it?

    2. Hi Seth, I am eager to read your paper and i have purchased it, interestingly vitamin d is also a treatment for autoimmune disease. I give my kids both calcium and vitamin d - due to dairy free diet mostly and also because of the research between vitamin d/autoimmunity/anti-cancer. How much is too much vitamin d in blood marker in your opinion. We try to keep it around 100-135.

    3. Seth, I have read your book. Some parents say Vitamin D supplement helps their children. So like many other supplements it works for some?What about children with VDR Taq and VDR Foq (+/+). My 30 months old grandson has this. His 25 OH Vit D level is 27 ng/ml. I understand he needs vitamin D supplement. Am I wrong? Do we need to test for 1, 25 OH vit D also? We give 2000iu daily dose for the past 2 weeks. He has no adverse reaction. Do we need to add K2 also? I would like to know more about the relationship between polymorphism in vit D receptor gene and D supplement. Also the relationship between Cholesterol, Vitamin D and ferritin. All the three are low in my grandson. Thank you.

  2. Excellent! Our philosophy is that every person or family dealing with Autism Spectrum Disorders is entitled to the best support from their community. By providing a portal of information, ratings and reviews and making it accessible between families, caregivers, professionals, businesses and service providers, we will support all persons living with an Autism Spectrum Disorder and ensure they are cared for by their community at large. Thank you for this great article!

  3. I also had an epiphany about 4 years ago. I began to research everything we knew about autism rates. If I am right it explains many things starting with why it was first detected in the early 1940's and took an upturn in the 1990's. Other things that it explains is why, more males than females, higher rates west of the Cascade Mountains, lack of autism among the Amish, the seasonal rate variation in Alaska, Japan and the UK have the highest rates. I may be totally wrong but it's interesting how many things make sense if I am right. With all the bad press on this environmental condition I'm amazed that no one else has made the connection.

  4. Peter, one very important topic that I hope you cover in your book or in this blog, is a suggested "order of interventions".
    To me, it is obvious that one need to recognize/address allergy, mast cell problems, epilepsy and GI problems before you move further to treatments for cognition and core autism. One reason is of course that there might be less autism to treat after that. But the most important reason is that all these comorbidities might induce adverse effects on some core treatments. We have seen the wrong brand of bumetanide giving allergy problems and NSAIDs making GI problems worse, adding histamines or even enhance risk of seizures. "Severe autism" is probably often autism + comorbidity, and for those affected also alternative (that is, GI friendly, histamine-less etc) substances/treatments need to be mentioned.


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