Autism detectable in brain long before symptoms appear
I quit a high flying job to research ASD when my son was diagnosed years ago and have read every single paper and website I could find.<p>My broad conclusion from this is that ASD is a condition caused by lots of different factors with common symptoms.<p>This makes treatments tough as ASD caused by oxidative stress would respond badly to treatments that work great on ASD caused by reductive stress for example (eg ASD symptoms that seem to get &#x27;better&#x27; when taking paracetamol vs ASD made worse by it).<p>Thus when treatments are tried across the population you get odd results if you&#x27;re not sub-dividing the groups into likely etiology, I&#x27;ve tried to look for statistically significant sets taking this into account.<p>The key dysfunctional system in most ASD seems to be the balance between the excitatory and inhibitory neurotransmitters GABA and Glutamate.<p>The two broad groups for this appear to reflect &#x27;classical&#x27; autism, ie same from birth vs &#x27;regressive&#x27; ASD, for example secondary to mitochondrial dysfunction where there is a sudden loss of ability.<p>For the former, a common cause appears to be GABA dysfunction, which the blog epiphanyasd.blogspot.com does a great job pulling together the research on.<p>In this case GABA doesn&#x27;t flip to inhibitory from excitatory at birth and this could show up in brain scans for this subset of children with ASD..<p>The treatment options are interesting in this regard, but the &#x27;safest&#x27; trial to check this dysfunction I&#x27;ve found is micro-dosage clonazepam (40mcg), which is already prescribed to children with anxiety (at 500-1000mcg doses). At this subclinical dosage, it should have no impact unless there is a dysfunction, but if it does (which it has in several families I know), then the research into other drugs that could treat this dysfunction becomes far more interesting (eg current trials in France by Ben Ari and Lemmonier on bumetanide).