Peter Hypothesis Regarding the Cause of 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.

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 21^st 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.)