PLT Test Blog

Some readers of this blog have developed quite advanced personalized medication for their child with autism.  As you might expect, given the wide variety of autism sub-types, the medical therapies found to be effective vary widely.  It is interesting that many people see fluctuations in cognitive function and some develop strategies to counter them. I came across another form of variable cognitive dysfunction, “Chemo-brain”, that occurs in people after cancer treatment.  Chemo brain can also be called chemo fog, chemotherapy-related cognitive impairment or just cognitive dysfunction. It is interesting for readers of this blog because chemo brain is thought to be caused by changes in inflammatory cytokine expression within the brain, over a few years the symptoms usually fade away.  Some people’s autism just fades away, although tell-tale signs usually remain. Cytokine expression appears to be both a cause of autism and a consequence of it.  One clever researcher...

I think most lay people would be surprised to know that literally tens of thousands of scientific papers have been published on autism and yet not a single drug has been approved to treat core autism. Surely there must be some value in all this research, that can be extracted today? A reader recently sent me a link to an excellent lecture about propionic acid in autism.  The first part of the lecture was much more general and concisely summarizes what we know about autism.  We know a vast amount; it just has not been translated (applied).  Click below for the video. Source:- American College of Nutrition Translation Alli from Switzerland, a medical reader of this blog did raise this issue a while back.  Why has the vast knowledge about autism not been translated across into medical therapies? Her conclusion was the same as mine; don’t wait, do the translation yourself.  This is of course easier said than done, because there are wide variations in what causes aut...

In this composite image, a human nerve cell derived from a patient with Rett syndrome shows significantly decreased levels of KCC2 compared to a control cell.  This will be equally true of about 50% people with classic autism, people with Down syndrome, many with TBI and many with epilepsy In a recent post I highlighted an idea from the epilepsy research to treat a common phenomenon also found in much classic autism.  Neurons are in an immature state with too much intracellular chloride, the transporter that brings it in, called NKCC1, is over-expressed and the one that takes it out, KCC2, is under-expressed.  The net result is high levels of intracellular chloride and this leaves the brain in an over-excited state (GABA working in reverse) reducing cognitive function and with a reduced threshold to seizures. The epilepsy research noted that increased BDNF is one factor that down regulates KCC2, which would have taken chloride out of the cells.  So it was suggested ...

It is not always easy to decide which subjects to study, never mind if you have autism. For Monty, aged 12 with autism, it has been me choosing what he studies.  At the beginning it was rather overwhelming for his 1:1 assistant, because there was so much to learn and never enough time.  It takes years to learn very simple things that typical kids just pick up naturally. One big change after three and half years of Polypill use, is that Monty follows the standard academic curriculum, albeit for kids two years his junior. An excellent but not very user friendly curriculum/skill list is in a book called ABLLS ( assessment of basic language and learning skills).  It is both a curriculum and an assessment tool.  It covers all the very basic skills that kids need as a foundation for future learning. We were working from this list of simple skills for four years, until the age of eight.  These are skills most kids effortlessly pick up in the first three or four years...

Caution:- Ponstan (Mefenamic Acid) contains a warning:- Caution should be exercised when treating patients suffering from epilepsy. At lower doses Ponstan is antiepileptic, but at high doses it can have the opposite effect.  This effect depends on the biological origin of the seizures. In an earlier post I wrote about a paper by Knut Wittkowski who applied statistics to interpret the existing genetic data on autism.   “Autism treatments proposed by clinical studies and human genetics are complementary” & the NSAID Ponstan as a Novel AutismTherapy His analysis suggested the early use of Fenamate drugs could potentially reduce the neurological anomalies that develop in autism as the brain develops.  The natural question arose in the comments was to whether it is too late to use Fenamates in later life. Knut was particularly looking at a handful of commonly affected genes ( ANO 2/4/7 & KCNMA1) where defects should partially be remedied by use of fenamates. I rec...