PLT Test Blog

Regular readers of this and similar blogs will have noticed that the human body functions in quite irrational ways.  We know why this is; we are the product of a very slow evolutionary process, rather than being a clean-sheet design like your smart phone or iPad. As a result, nothing is ever quite as simple as it seems and at times the cleverer you are, the less likely you are to find a medical therapy effective in humans. Such is the case with autism, inflammation and microglia. It might seem that you can track back inflammation in autism to its “root cause”, which could appear to be those immune cells in the brain, called microglia.  We know they are “activated” in autism and we know that autism is typified by an “over-activated” immune response. Working with the assumption that autism is a brain dysfunction, you would assume that the effective therapy should be inside the so-called blood brain barrier (BBB). You would then just look for a potent drug that could “stabilize” ...

Today’s post answers a question left un-answered in earlier posts about the best way to treat the imbalance (excitatory vs inhibitory or just E/I) that exists in the function of the key neurotransmitter GABA in many types of autism. I first started this blog after the pleasant shock of seeing the positive behavioral and cognitive effect caused by Bumetanide. This was just copying a recent French clinical trial on humans. Later on in this blog we came across Professor Catterall who made two experiments in mice to show that the same E/I imbalance could be treated using tiny doses of a drug called Clonazepam.  At doses a hundred time higher, Clonazepam is used to treat seizures and anxiety, but at those doses it dose have side effects. The mechanism is different to Bumetanide, by the effect was claimed to be the same. Since Bumetanide has actually been shown effective in a human trial, most readers of this blog have this as their first choice. I commented that in Monty, aged 11 with A...

Apple users may have to click here Instead of giving you my rather heavy post about epigenetics and autism, today’s post is much more down to earth. Medical opinion in North America has long been very much in favour of ABA (Applied Behavioural Analysis) as the only “scientifically proven” therapy for the core symptoms of autism. This evidence is actually quite flaky, so much so that in the very "evidence driven" United Kingdom, their highly regarded National Institute for Health and Care Excellence (NICE) does not even mention ABA, let alone endorse it, in their guidance note in how to manage autism. The management and support of children and young people on the autism spectrum ABA is a potent tool to manage autism and provides a flexible framework to teach people who do not respond to traditional teaching methods.  However, it is no cure for autism and the old studies suggesting that almost 50% of kids going to an intensive ABA program will lose their autism diagnosis after ...

Today’s post was driven by another attempt not to take a statin. Statins are among the world’s most prescribed, and yet most maligned, drugs.  Hundreds of millions of people take a statin drug every day to lower their cholesterol, but a small, vocal minority complain about muscle pains, memory loss and even type 2 diabetes. Since my Polypill is evidently a therapy, and not a cure, for autism, the odds are that it will be needed life-long.  Regardless of the apparent lack of side-effects, nobody should be taking drugs/supplements that are not really needed.  Atorvastatin (Lipitor/Sortis) is part of my Polypill for the type of autism affecting Monty, aged 11, with ASD. Every time I stop the statin part of my Polypill therapy, I end up starting it again after only a one day break.  I notice all sorts of little behavioral changes that I really do not want to see.    These changes involve loss of initiative, flexibility and motivation.  I really do not see...

CAPE ( caffeic acid phenethyl ester ) is a substance known to be an inhibitor of PAK1.   PAK1 has been shown at MIT to be implicated in various disorders including Fragile X and schizophrenia.   PAK1 inhibitors are also effective in research models of various cancers, including leukemia. There are currently no approved PAK1 inhibitor drugs, although several are in development. PAK1 is also implicated in Neurofibromatosis, and clinicians have researched various alternative PAK1 inhibiting substances.  The two most interesting ones that I have already written posts about are:- ·         Ivermectin , an old anti-parasite drug (also shown effective in  leukemia) ·         BIO 30 propolis, rich in CAPE Ivermectin is already used as an autism treatment by “alternative” doctors who think autism is caused by parasites.   We saw in a recent post that a study looking for parasites in people with autis...