PLT Test Blog

  Regular readers of this blog will see that there is an underlying logic behind recent posts.   We know levels of the cytokine IL-6 are raised in autism and we know that high levels of IL-6 in mice produces a baby with autism and we know this can be reversed by giving IL-6 antibodies to the mother, prior to birth. We also know from numerous previous posts that growth hormone (GH) and the growth factor IGF-1 are implicated in autism.   Both GH and IGF-1 are used in clinical trials for autism. Today’s post draws all this together.   It turns out that IL-6 disrupts the GH-IGF-1 axis.   The hormone GH is supposed to control the release of IGF-1; so a little more GH should produce a little more IGF-1.   The problem is that the cytokine IL-6 disrupts this relationship.   In the presence of elevated amounts of IL-6, which is characteristic of autism, and regressive autism in particular, GH does not produce the expected increase in IGF-1; IGF-1 levels are act...

  We have noted in earlier posts that autism is a dynamic encephalopathy and this may help explain why a therapy that works in a child aged 10, may be of little help to another child aged 3.   Not only are there many sub-types of autism, but each sub-type is evolving, as the child matures. None of the autism drug therapies I have implemented have permanent disease changing effects, they all seem to work, but the effect is lost once you stop taking them.   Today’s post is about drugs that you take just once.   For a parent trying to find a drug that works in the sub-type affecting their child, this has a big advantage.   No need to keep trying for months to see if the drug has any effect. Perhaps the most important time to intervene with drug therapy is as soon as possible after the diagnosis; but with what? In an earlier post on trying to get a non-verbal child to talk, I suggested the use of corticosteroids to arrest on-going neuroinflammation.   Drugs li...