I think the wrong people are in charge of autism research; forensic scientists or even air-crash investigators might do much better.
We have seen
in this blog that many drugs have a positive effect in specific types of
autism. In many, but not all cases, the mechanism of that drug and its effect
on the pathology of autism is understood.
If you have
followed an ABA programme, you will know that an experienced autism therapist
would very easily be able to give a long list of behavioral issues that occur
in varying combinations among her clients.
From reading
the research, it is clear that the people who understand the biology, often do
not understand the psychology and the behavioral issues they are trying to
treat - but perhaps they should. Only
then can you target treatments for specific problems. There can be no single drug for autism, but
there can be a drug for obsessive behaviours, and another for self-injury. You cannot say a low dose of X helps with
social cognition, but for aggression you need a high dose of X. To me at least, this is complete nonsense and
shows a complete failure to understand the underlying psychology.
Just as most
people struggle with all the jargon of biochemistry, I suppose the medical
researchers fail to grasp the nuances of the psychologists’ jargon. We need to match both sides, because we need
science to solve a complex problem that presents itself in hard to describe, odd
behaviours and not as nice neat equation to solve.
It is difficult
to accurately describe and quantify the behavioral issues of a child with
ASD. It is very hard for a parent, but
it is definitely possible for a psychologist using tools like ABBLS and others. Then you can move towards seeing precisely
what behavioral effects a drug has and stop expecting improvements in areas
that are completely unrelated.
Having
produced the list of deficit areas you can then try and understand the
underlying pathology as to why a drug is effective.
I make no
claims to have great expertise in this area, but it looks like nobody else does
either.
Here are
some examples:
Obsessions
Obsessive
compulsive behaviours are well known to affect some people with autism. This is a type of behaviour that most people
would understand and would notice if they saw it, although they might find it
hard to quantify.
Oxidative
stress is a measurable pathological condition that is present in some people
with autism. Oxidative stress exists in
other medical conditions and has a known therapy, an antioxidant like NAC.
By chance, it
was found that treating someone with obsessive compulsive behaviours with NAC,
greatly reduced those behaviours.
In the case
of people with autism and obsessive compulsive behaviours, it would be good to
know if other deficit areas were also impacted.
Clearly, taking away the obsessive compulsive behaviours, you would
expect to see a general improvement, since the person is now much calmer and
better able to function and so many behaviours should improve to a certain
extent. But does NAC reduce head banging
and other SIB? I think not.
So we can
then conclude that oxidative stress triggers obsessive compulsive behaviours
and NAC should be prescribed. Oxidative
stress may exist to a lesser degree in subjects that do not (yet) display
obsessive behaviours.
Anxiety
I have not
tried to treat anxiety in autism, but many people have. Anxiety lies on the axis running from happy
to depressed. By raising the level of serotonin
in the brain you move from depressed towards happy. The antidepressant Prozac is given to many
children with ASD to reduce anxiety. Prozac is a selective
serotonin reuptake inhibitor (SSRI).
The problem with
such drugs is their side effects and use can result in dependency. If that was not the case, the advice would be
simple.
I think a
better and safer way exists to raise brain serotonin levels in autism.
Seizures and SIB
Not all
people with SIB (Self-injurious Behavior) have seizures, but I expect many
people with seizures have SIB. Both
conditions appear to be channelopathies (ion channel/transporter dysfunctions);
but there is more to it than that, what triggers the channelopathy? It would seem that in both cases the message
comes via inflammatory signalling from the vagus nerve. So to treat these conditions you can block
the inflammatory signalling (vagus nerve stimulation), or you can treat the resulting
ion channel/transporter dysfunction in the brain; doing both may be quite
unnecessary.
If you have
neither seizures nor SIB, then using any of the above therapies would be of
little effect.
Many open questions remain
All is not
clear; for example, where does hyperactivity fit in? Where does anger fit in? Is anger just a mild version of SIB? It is extreme anxiety? Is it something entirely different?
An
interesting finding of mine was that showing affection appears to be
pathologically related to self-confidence and lack of inhibition. The pathology linking them appears to be
neuroinflammation, or rather the control of it.