Game Changer or Fine Tuning? It depends on severity of Autism

 

There are so many possible autism interventions discussed in this blog, it clearly is not always easy to know their relative merit.

There are so many people now diagnosed with autism it is no longer such a meaningful term.  The most extreme autism I think I will have to start calling really severe autism.  A scale of 1 to 100 would be much more helpful than the current levels 1, 2 or 3. I suppose Elon Musk and Greta are level 1.

One reader did recent describe the effects of bumetanide in his child as being game changing.  I think it is an excellent description to use.  For our reader Roger, Leucovorin was a game changer.

Another reader wrote to me to give an update about his three year old

“After 3 months of bumetanide treatment I've seen improvement on his cognition, like, he is now able to finish an apple and take the end to the trash by himself or enter in his room, turn the lights on, take some toy, turn lights off and close the door or eat his lunch by himself. He is smarter now.”

This reader is well on his way to finding the additional elements for his son’s personalized polytherapy and the way he is going about it is likely to yield optimal results. Most of what you need is tucked away in this blog somewhere.  It is a case of who dares wins.

Using my scale of 1 to 100, with Elon and Greta in low single digits and many people referred to at the blog of the US National Council of Severe Autism mainly at 80-100, we can put interventions into a bit more perspective.

It is still far from perfect because most people with really severe autism reach a plateau in development at a very young age.  This matters because as a three year old they do not look/behave so differently to a typical child, but by the time they reach 18 years old, the difference is gigantic.

If you could delay the onset of this developmental plateau for a decade the result would be transformative.  Based on the longitudinal studies to adulthood, it looks like about 80% of severe autism reaches a plateau at the level of a 2-3 year old.  The other 20% continue to learn, but at a slower rate than typical children. 

In the case of the autism which is <10, like Greta and Elon, very small issues can still become very troubling.  There was inevitably bullying at school from mild to severe, there likely was (and still is) anxiety, perhaps an eating disorder, perhaps some self harming or even suicidal thoughts.

If you fine tune the brain a little to reduce anxiety and improve social/emotional responsiveness, you can trim someone’s score from a 15 to a 9 and make them feel much better.  Job done.

For someone with an IQ of 50 (i.e. severe intellectual disability), non-verbal, non-literate, who is sometimes aggressive and exhibits autistic behaviors, you are going to need much more than fine tuning, you need a game changer.  Then you can go on and fine tune things to give further incremental improvement.

One doctor reader did suggest to me that, in effect, five moderately effective interventions might equal one game changer.

In the case of autism that I deal with, the most important step was raising cognitive function, not treating what people consider to be autism.  I think that this applies to almost all people with a score 50 to 100.  Even if it was never actually diagnosed, the barrier to progress is low cognitive function and a severely reduced ability to learn and acquire new skills.  This has to be fixed and for many people the tools already exist.

 

Improving cognitive function

Game Changer

·      Bumetanide  (also Azosemide, KBr and, possibly, Betaine with the same effect of lowering chloride inside neurons)

Fine tuning

·      Atorvastatin, reducing cognitive inhibition

·      Micro-dose Clonazepam, shift E/I imbalance

·      Low-dose Roflumilast, raising IQ

 

Reducing autistic behaviors

Fine tuning

·      NAC

·      Sulforaphane

·      Verapamil

·      Oxytocin

·      BHB

·      Pentoxifylline

·      Agmatine

·      Clemastine

·      DMF

·      Leucovorin (Calcium Folinate)

 

Interventions with a slow course of action

Some interventions, for example pro-myelinating therapies (like clemastine and Tyler’s N-acetylglucosamine), or pro-autophagy therapies, may take a long time to show effect. I think you may need to first see very tangible results from other therapies, which are much easier to assess.

As Roger will want to point out, in the case of Cerebral Folate Deficiency Leucovorin was the game changer.

In the case of other metabolic autisms, a single therapy may also be the game changer, like the Greek boy for whom high dose biotin resolved his previously severe autism.

In the case of Fragile-X, there seem to be potential game changers galore.  The latest is plugging the leaky membrane in mitochondria that is allowing ATP to leak out, using a research drug dexpramipexole, or potentially the related and already approved variant Mirapex ER (pramipexole).  Mirapex is used to treat the symptoms of Parkinson Disease and Restless Legs Syndrome. 

If our occasional reader and bio-statistician Knut Wittkowski is correct, Mefenamic Acid (the NSAID Ponstan) could be a real game changer, if taken around 2-3 years of age.  He suggests this will block the progression to severe non-verbal autism. Knut has been upsetting YouTube with some of his interviews about Covid-19 and his deal with Q-Biomed to develop Mefenamic Acid fell through. You can buy Ponstan very cheaply, outside of the US, even as a pediatric syrup.

Hopefully, Dr Naviaux's Suramin will be a game changer for some.  More of that in the coming post on leaky ATP.

Conclusion

I am told where we live that Monty’s autism is “fixed”, or by one autism Grandad we know, “he’s 80% fixed”.

If you started life with (really) severe autism, even 80% fixed means you are still pretty autistic, much more so than Elon and Greta, but far less so than the now adult “children” over at the National Council for Severe Autism, who have really severe autism and often had a very early plateau in development.

Monty has finished his year-end exams.  Overall, the grades of his NT classmates are pretty terrible, maybe due to Covid disruptions.  I told Monty’s assistant that if he can come somewhere in the middle, without her doing the tests for him or having extra time, that is a great result, regardless of the grade itself.  In all his subjects he comes in the middle. In the English educational system, Monty is now a C student, maybe even with the odd B or D; so not something to boast about.  What really is amazing  is this person could not figure out  9 – 2 = 7,  at the age of 9 years old, prior to starting bumetanide and his Polypill therapy.  Now he is nearly 18 years old.

If you find that your young child is a genuine bumetanide responder, but later struggle to source it, take a close look at what untreated severe autism looks like by adulthood.  Then you may choose to redouble your efforts to get hold of your game changer. Some readers are getting it from Egypt, Pakistan, Nigeria, China, Austria and many from Mexico and Spain.  In Brazil you can buy it only in a compounding pharmacy. The lucky ones get it at their local pharmacy, which is what should be possible for everyone and one day that might even happen.

There are countless fine-tuning therapies that may be potentially effective in a particular person.  They are certainly worth having; you just have to look at what is available and cost effective.

There will soon be a post about leaky ATP in Fragile X and autism.

Two readers have highlighted the research suggesting that Betaine might have a similar effect to Bumetanide.  It does not block the NKCC1 transporter, but it may reduce the mRNA that produces them, so the net effect may potentially be similar.  At much lower doses, Betaine is a common autism supplement.  This will be covered in the next post.

 

Update on Roflumilast/Daxas as a PDE4 inhibitor for Autism

 

There is already quite a lot in this blog about using a PDE (Phosphodiesterase) inhibitor to potentially treat autism.

Readers might have seen the recent article below, in which a PDE-4D inhibitor raised cognition in adults with Fragile-X.

Drug boosts cognition in men with fragile X syndrome 

The study drug, BPN14770, is developed by Tetra Therapeutics, a clinical-stage biotechnology company in Grand Rapids, Michigan. It blocks the activity of phosphodiesterase-4D, an enzyme in the brain that degrades cyclic AMP. In a mouse model of fragile X, BPN14770 increased cyclic AMP and eased several fragile-X-related traits.

 

For the new work, 30 men with fragile X participated in a 24-week double-blind crossover study of the drug. The researchers randomly assigned each man to one of two treatment sequences: 12 weeks on the drug followed by 12 weeks on a placebo, or 12 weeks of placebo crossing over to 12 weeks on the drug. Researchers assessed all of the participants at the start of the study and during week 6 and week 12 of each trial sequence. They also asked parents and caregivers to rate changes in the men’s language, daily function and anxiety.

The treatment produced “significant improvement in the language and daily function measures that the families were rating, in conjunction with improvement on this objective test [NIH Toolbox] that’s very hard to have a placebo effect on,” says Elizabeth Berry-Kravis, professor of child neurology at Rush University Medical Center in Chicago, Illinois, who led the study.

 

Later on in the post is the science, which it does help to read. if you want apply it.

The research drug BPN14770 used in the Fragile-X trial is not something you can buy at the pharmacy, but there are PDE inhibitors available today.

I have written a post recently about the use of Pentoxifylline, which is a very cheap drug that is not selective, if affects many types of PDE not just PDE-4D. 

Pentoxifylline – Clearly an Effective add-on Autism Therapy for some

 

Today I am looking at Roflumilast/Daxas which mainly affects PDE-4.  There are 4 sub-types (isoforms) A, B, C and D.  Drugs that affect all these sub-types are called PDE4 pan inhibitors and they usually cannot be used in humans. due to severe nausea.

Roflumilast/Daxas is used to treat COPD/severe asthma at a dose just on the limit, where it begins to be effective and inhibit PDE in the lungs but before the nausea makes it unusable. There is research to make an inhaled version, which would make a lot of sense.

We are interested in PDE4 in the brain, not the lungs.  The effect of Roflumilast on PDE4 is unusual in that it is very dose dependent; too little and there is no effect, too much and there is no effect.  So, the amount of Roflumilast and its metabolites in your blood stream need to be within a tight range.

The median plasma half lives of Roflumilast and its N-oxide metabolite are approximately 17 and 30 hours, respectively.

This means if you give the same dose every day, the level of the metabolites will reach a steady state only after about 5 days.

As mentioned in an early post, roflumilast is not soluble in water, but it is in alcohol.  This means you can make a tincture, just like they do with bee propolis.  In fact, I am using an old propolis bottle, the type with a screw-on pipette.

We know from the research that in healthy adults a dose of 100mcg may be cognitive enhancing.

My target dose was 80mcg, but I wanted to be able to easily vary it.

Take an old propolis bottle and clean it with alcohol/ethanol/vodka.

In a small glass, dissolve 5 tablets (5 x 500mcg Daxas) in 15ml of vodka.  The tablets slowly dissolve; mix well and then use the pipette to transfer the fluid to the bottle and also figure out where on the pipette equates to 0.5ml. When I recently did this it took me 31 squirts, so by eye I was giving on average 83 mcg.

When I first started there was one day of dramatically increased speech, which I could not reproduce.  The first day of Pentoxifylline also had this effect. Pentoxifylline has a very short half-life.

Since at school Monty is having his year-end exams, I decided to focus on cognition.  I think my original dose was too high, more like 100 mcg.  Giving a little extra is something you have to resist.

Being a bit stingy (ungenerous) with the pipette, is what you have to be.

At close to 80 mcg a day, I am getting feedback from school that cognition is great.

Exams started and Monty is doing really well.  They are 90-minute exams and the fact that he is even there is amazing to me; that is down to 8 years of Bumetanide.

It looks like 80 mcg of Roflumilast does give an extra boost to cognition in a 60 kg boy.

Is it worth it?

One pack of 30 x 500mcg Roflumilast/Daxas tablets costs about EUR 40 (about 50 USD) in Europe, but at the 80 mcg daily dose it will last 6 months.

Monty has had been no side effects (nausea, GI etc), but this is very specific to the person. I myself did get GI side effects from 100 mcg.

   

Science that supports the use of a PDE4 inhibitor

There are many different types of PDE (Phosphodiesterase) and there has been a lot of research looking at their relevance to a wide range of neurological conditions.

The table below gives a useful summary, by disorder.

 

Neurodevelopmental disorders are highlighted in red. AD Alzheimer disease; ASD autism spectrum disorder; BP bipolar disorder; DS down syndrome; HD Huntington disease; ID intellectual disability; FXS fragile X syndrome; MDD major depression disorder, RTT Rett syndrome, SCZ schizophrenia.

 

This table is from an excellent paper published earlier this year.

 

Role of phosphodiesterases in the pathophysiology of neurodevelopmental disorders

Phosphodiesterases (PDEs) are enzymes involved in the homeostasis of both cAMP and cGMP. They are members of a family of proteins that includes 11 subfamilies with different substrate specificities. Their main function is to catalyze the hydrolysis of cAMP, cGMP, or both. cAMP and cGMP are two key second messengers that modulate a wide array of intracellular processes and neurobehavioral functions, including memory and cognition. Even if these enzymes are present in all tissues, we focused on those PDEs that are expressed in the brain. We took into consideration genetic variants in patients affected by neurodevelopmental disorders, phenotypes of animal models, and pharmacological effects of PDE inhibitors, a class of drugs in rapid evolution and increasing application to brain disorders. Collectively, these data indicate the potential of PDE modulators to treat neurodevelopmental diseases characterized by learning and memory impairment, alteration of behaviors associated with depression, and deficits in social interaction. Indeed, clinical trials are in progress to treat patients with Alzheimer’s disease, schizophrenia, depression, and autism spectrum disorders. Among the most recent results, the application of some PDE inhibitors (PDE2A, PDE3, PDE4/4D, and PDE10A) to treat neurodevelopmental diseases, including autism spectrum disorders and intellectual disability, is a significant advance, since no specific therapies are available for these disorders that have a large prevalence. In addition, to highlight the role of several PDEs in normal and pathological neurodevelopment, we focused here on the deregulation of cAMP and/or cGMP in Down Syndrome, Fragile X Syndrome, Rett Syndrome, and intellectual disability associated with the CC2D1A gene.

  

It looks like idiopathic autism has the least research, but there is an interesting old paper.

  

Expression of Phosphodiesterase 4 is altered in brain of subjects with autism

 

The cyclic adenosine monophosphate-specific phosphodiesterase-4 (PDE4) gene family is the target of several potential therapeutic inhibitors and the PDE4B gene has been associated with schizophrenia and depression. Little, however, is known of any connection between this gene family and autism, with limited effective treatment being available for autism. We measured the expression of PDE4A and PDE4B by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and Western blotting in Brodmann's area 40 (BA40, parietal cortex), BA9 (superior frontal cortex), and cerebellum from subjects with autism and matched controls. We observed a lower expression of PDE4A5, PDE4B1, PDE4B3, PDE4B4, and PDE4B2 in the cerebella of subjects with autism when compared with matched controls. In BA9, we observed the opposite: a higher expression of PDE4AX, PDE4A1, and PDE4B2 in subjects with autism. No changes were observed in BA40. Our results demonstrate altered expressions of the PDE4A and PDE4B proteins in the brains of subjects with autism and might provide new therapeutic avenues for the treatment of this debilitating disorder.

  

Conclusion

It looks like Roflumilast/Daxas should join Pentoxifylline on the to-trial list for people with autism.

In my opinion the actions of Pentoxifylline and Roflumilast/Daxas are sufficiently different that conceivably some people might benefit from taking both.

I cannot see why someone with Fragile X should wait another decade for BPN14770 to maybe get commercialized.

There are PDE4 inhibitors in the pipeline for Alzheimer’s.  In my opinion the focus should be more on prevention.  By the time people get diagnosed with Alzheimer’s, it is too late to reverse it.

 

 

 

Autism Videos - Personalized Medicine to treat Autism using off-label Generic Drugs

 

Today’s post contains three autism videos.  I was asked to give a presentation about treating autism with off-label drugs.  This turned out to be quite easy to write, but it kept getting longer and longer.  I think most people would need to watch it in two sittings and you do need to have a deep interest in the subject.  I could have gone on for hours longer, there is much more to tell.  

Click on the settings to watch in HD, then you can read the slides clearly.  In the lower right corner of YouTube, click on the white cog shape, select quality and then HD.

 

I also include two very good videos by Tony Attwood, which are much lighter going, but really explain why Asperger’s and Autism are better understood when considered separately, albeit that they really are part of the same spectrum.  They should be required viewing by anyone new to the subject of autism, parents in particular.

  

 

Personalized Medicine to treat Autism using off-label generic drugs

https://youtu.be/jlv6nxrSWiQ

 

This video was presented at the conference: -

 

Autism - Challenges and Solutions 

Moscow 18 May 2021

 

by Peter Lloyd-Thomas

EpiphanyASD

 

 

Here are the excellent videos from Tony Attwood:-

 

 

Could It Be Asperger’s?

https://www.youtube.com/watch?v=LuZFThlOiJI

 

 Could It Be Autism?

https://www.youtube.com/watch?v=HIrxgD3oqYc&t=1228s

 

 

 

Self-Injurious Behavior (SIB) in Autism– if all else fails, why not ECT?

 

I did mention Electroconvulsive Therapy (ECT) in a recent post as a therapy for Self-Injurious Behavior (SIB) in autism and since there has been a review paper published very recently, it is the topic of today’s post.

There was a previous post on this subject:-

Electro Convulsive Therapy (ECT) and Cannabidiol (CBD) in Autism

By coincidence, Mr Electric, Elon Musk, has just revealed that he has Asperger's Syndrome. I don't think he will be fitting ECT to his Tesla vehicles anytime soon.  ECT is likely only going to be used by those at the other extreme end of the autism spectrum, the ones who do not know was money is, let alone cryptocurrencies.

There are many possible ways to treat someone who self-injures or indeed is aggressive towards others. From a psychiatric unit you might get various psychiatric drugs (antipsychotics etc), protective and restraining devices and in some cases Electroconvulsive Therapy (ECT).

Some literature on ECT suggests that it is effective in almost all cases of SIB.

This blog is mainly about novel personalized medicine and in the case of SIB there are multiple choices, which may, or may not be effective in any one case. In my son’s case the SIB was driven by an ion channel dysfunction which is fully treatable with a cheap little yellow pill, Verapamil.

  

Electroconvulsive Therapy (ECT)

ECT is a psychiatric treatment where seizures in the brain are electrically induced in patients to provide relief from mental disorders.  There are no muscular convulsions.  ECT involves multiple administrations, typically given two or three times per week until the patient is no longer suffering symptoms. ECT is administered under anesthesia with a muscle relaxant.

ECT is often used with informed consent as an intervention for major depressive disorder, mania, and catatonia.

Unfortunately, in autism, maintenance ECT therapy is required.  It is a treatment, not a cure.

The study below refers to catatonia, which you may not be familiar with.

Catatonia is a group of symptoms that usually involve a lack of movement and communication, and also can include agitation, confusion, and restlessness. Until recently, it was thought of as a type of schizophrenia.

Source: https://www.verywellmind.com/what-is-catatonic-schizophrenia-2794979

 

  

Electroconvulsive Therapy (ECT) for Autism Spectrum Disorder Associated with Catatonia and Self-Injury: A Clinical Review 

 

Objectives

We reviewed published clinical reports that evaluated treatment effects of electroconvulsive therapy (ECT) with children, adolescents, and adults who had autism spectrum disorder (ASD), catatonia, and self-injury.

Methods

Published reports were identified from an internet search and summarized according to seven review criteria: (a) participant description, (b) clinical presentation, (c) previous treatments, (d) course of ECT, (e) treatment outcome, (f) side effects, and (g) evaluation methodology.

Results

ECT was associated with clinical improvement in all participants. Most notable benefits included decreased self-injury, acquisition or recovery of functional life skills, elimination of catatonic symptoms, and return to baseline functioning. Maintenance ECT was typically required to sustain improved clinical status in the months and years following acute ECT.

Conclusions

There appears to be sufficient evidence that supports therapeutic benefits from ECT in persons with ASD, catatonia, and self-injury. However, measurement methods and evaluation design vary greatly among reports, there may be a publication bias towards cases with positive findings, and more rigorous clinical research is necessary particularly concerning optimization of maintenance ECT to maximize benefit and monitor for any adverse response.

 

The reports and summarized results are presented in Table 1. Among the participants (N=14), 28.5% were female and 71.4% were male ranging in age from 8 to 33 years old. From this sample, 35.7% were children, 28.5% were adolescents, and 35.7% were adults. Beyond the primary diagnoses of ASD and catatonia, the participants had comorbid conditions of intellectual disability, attention-deficit hyperactivity disorder, bipolar disorder, major depressive disorder, Tourette’s disorder, Addison’s disease, and neuroleptic malignant syndrome. The clinical presentation of participants at the time of referral for ECT was uniformly debilitating. Many participants refused to feed themselves, were significantly underweight and malnourished, and required nasogastric or gastrostomy tube feeling. Their general level of adaptive functioning was typically compromised, described as “needing assistance with feeding, getting dressed, brushing his teeth, and combing his hair”, displaying “significant mood instability characterized by irritability, tantrumming, alternating laughing and crying episodes as well as intermittent insomnia and anorexia”, and exhibiting “spontaneous episodes of punching, kicking, and biting, often requiring her to be restrained by several adults”. Self-injury was severe and long-standing, for example, a child, adolescent, and adult who had a “five year history of self-injury” that “included slapping and punching his head as well as banging his head or his knees and shoulders”, performed “hand-to-head, knee-to-head, and hand-to-body self-injury”, and “struck knees against his head, hit his head against a fixed surface or object, punched his face and head with hands, pressed fingers against his eyes, and bit any part of his body”. The seriousness of cases was reflected in participants who required inpatient hospitalization and were no longer able to attend school, live at home, or participate in the community. Use of protective equipment such as hard and soft helmets, padded gloves, arm and body guards, and rigid arm restraints restricting flexion at the elbow was uniform across reports.

Access to ECT in the USA varies greatly among states based on the presence or absence of procedural restrictions, practice regulations, administrative requirements, and stipulations regarding consent. This variability from state-to-state impacts patient care and evaluation of effectiveness of ECT when procedures and protocols are not uniform and administered consistently.

Maintenance ECT in which the number of treatment sessions was gradually decreased during the hospital stay preceding and then following discharge was indicated in nearly all clinical reports. Haq and Ghaziuddin  wrote that “withdrawal of maintenance-ECT in patients with autism and catatonia often precipitates relapse of symptoms, perhaps more rapidly and predictably than in the treatment of mood disorders”. They advised that m-ECT be continued as long as clear evidence shows it benefits the patient. Similarly, Wachtel, Hermida, and Dhossche proposed that ECT should be considered a “treatment rather than a cure” and that patient relapse remains a concern even with m-ECT in place. Indeed, many of the reports we reviewed found that participants relapsed quickly when ECT was discontinued or treatment frequency reduced, requiring a readjusted m-ECT schedule and/or concomitant pharmacotherapy to confer therapeutic benefit, While our review demonstrates that there are presently no precise parameters and guidelines for administering m-ECT to persons with ASD, the demonstration that ECT regimens must be tailored to unique patient circumstances is in line with m-ECT paradigms among neurotypical individuals.

 

 

Conclusion

Self-injury and aggression in autism can become overwhelming and, one way or another, have to be treated.  Electroconvulsive Therapy (ECT) clearly is one option that may be available, depending on where you live.

If you stop the maintenance therapy, the behaviors will return.  Ideally you live near the hospital. 

In terms of what it is actually doing, I think we can compare it to an old computer whose screen keeps freezing, you just restart it and hope for the best.  Then you know it is time to look around for a new computer, before you lose whatever is on the hard drive.  ECT is like a system reset, without knowing what the underlying problem is. 

In the absence of an effective alternative, why not ECT?

Is there a pharmacological "reset button" for at least some aspects of some autism? A short course of steroids does something along these lines; you can even have a single dose, as in therapy for an asthma attack/exacerbation.  Suramin is not really a monthly "reset", because the drug has a very long half-life and so it is there all month long, just at a slowly reducing level.  

Holiday Injection … Done! Getting “Pfizered” for Greece

 

Some parts of the world are trying to get back to some sort of Covid normal, while others are in crisis.  Where we live 40% have been vaccinated and likely 50% have already had the virus.

Monty, aged 17 with ASD, is a big fan of swimming in the sea and where we live that means crossing borders.  Crossing borders is much easier if you have had a Covid-19 vaccine and it looks like for children the best option is the one from Pfizer-BioNTech.  BioNTech is the clever company set up by a Turkish husband and wife team in Germany. They licensed their vaccine to Pfizer for distribution outside of China, in China they have a deal with Fosun Pharma.

Last week Monty had the opportunity, at very short notice, to go and get the Pfizer inoculation. I collected him from school and took him to a clinic in the city centre, that he has never been to and which undoubtedly would have a long line of people queuing outside it.

Monty knows all about injections and syringes, courtesy of his dental marathon a couple of years ago. He even knows about antibodies from Biology classes. The most rational explanation I came up with while driving, for why he was going to see the “doctor” was that it was for his “holiday injection”.  Monty’s school assistant had some more scientific explanations, but the problem is then you are left wondering why you still need to wear a mask at school, after you have been “Pfizered”.

“Do you like swimming in the sea, on holiday?” …   “Yes” was reply.

“This year, because of Covid, you need to get a holiday injection in your arm.  It doesn’t hurt and we’ve all had ours.”

“After 2 holiday injections, you’re ready for summer holidays.”

Bad news became good news.  Holidays … nice!

 

Children traveling without a covid Vaccine

In many cases children can travel without a covid vaccine, but you may need a PCR test before the trip out and the trip back.  You might well develop covid whilst you are abroad and then you are stuck.

A classmate of Monty was traveling with his vaccinated parents and the border policeman was not sure whether to let him through, since he had no PCR test, or vaccine certificate.

The Pfizer vaccine does look the best choice for a healthy 17-year-old.  For them, safety is more important than efficacy, because they are at almost zero risk from the current variants of the virus.  This may very well change in the coming years.

  

Covid risk for those with autism

Whether you are at elevated risk from Covid depends on what kind of autism you have.  I think my son is at even lower risk than his peers; he very rarely gets sick and another reason is his steroid inhaler for asthma; this actually reduces the chance of mild covid becoming severe covid.  Steroids are now widely used in hospital treatment, but really should be started before you even think about going to hospital.

People with MS (multiple sclerosis) taking disease modifying therapy may be another group who are protected from severe Covid.  These therapies block the cytokine storm that takes you from mild covid to severe covid.  The studies are somewhat contradictory, so you can believe whichever you want.   

The expensive drug Remdesivir, was approved as a therapy even though it has no effect on mortality, which makes you seriously wonder about its benefit.  Not surprisingly, the cheap oral steroid drug, Dexamethasone, substantially reduces mortality.

What happened to hydroxychloroquine (HCQ) and Didier Raoult, the French Professor who promoted it?  He still thinks he is right, even though great efforts were made to prove him wrong, including using data later shown to have been faked.

A recently published study looking at 28,759 adults with mild COVID 19 in Iran actually supports Raoult:

https://www.sciencedirect.com/science/article/pii/S1567576921002721

Early administration of HCQ reduced the odds of hospitalization by 38%.

Early administration of HCQ reduced the odds of death by 73%.

Serious HCQ adverse drug reactions were not reported in any of the age groups with or without comorbidities.

 

Does hydroxychloroquine have an anti-viral benefit in Covid-19?  Only you can decide.  The scare stories about dangerous side effects were evidently grossly overstated, which makes you wonder what else was made up by the naysayers.

I think this shows that you can find data to support whichever side you favour.  This seems to happen quite often, when a medical issue becomes politicized.

My own Covid therapy was hydroxychloroquine as the antiviral, to which I would have added prednisone if necessary.  As a local doctor told me, you do not want to go to hospital with Covid.

Back to autism.

Some types of autism are associated with comorbidities elsewhere in your body.  These can include problems with your lungs, as in the case of Down syndrome. If you have Prader Willi syndrome, you will present with autism and obesity.  The obesity is the covid risk.

Intellectual disability is put forward as a Covid risk, which makes sense.  People with ID/MR are likely to live in group homes or institutions, where they may be exposed to the virus and they may not follow all the protective measures.  People taking psychiatric drugs are likely to be overweight, which is a bigger risk factor than age.  People with ID/MR are likely to get worse healthcare than typical people, even when there is no health crisis.  The study below seems very credible'. 

After old age, intellectual disability is greatest risk factor for death from COVID-19, study finds

The results showed that those with intellectual disabilities were 2.5 times more likely to contract COVID-19, were about 2.7 times more likely to be admitted to the hospital and 5.9 times more likely to die from the infection than the general population.

Nowadays most people diagnosed with autism do not have any intellectual disability, so it makes sense that in some countries they have made people with intellectual disability, rather than just autism, as a priority group for vaccination.  

On a practical level, an overstretched hospital is not going to be a good place for an adult with intellectual disability, with or without autism.  They should indeed be prioritized for vaccination

When it comes to autism parents there seem to be three groups: -

1.     Desperate to get the vaccine

2.     Desperate to avoid the vaccine

3.     Desperate to go on holiday

 

 

 

 

Autism – Awareness and Acceptance

 

There is a lot of talk this month about autism awareness and acceptance.  Some people get very excited about this and some people get quite upset about it; it seems to depend on how old the person with autism is and how severely impaired, if at all, they are. 

For much of the confusion we have to thank the psychiatrists who keep broadening the definition of autism and their lack of using one of the standard ratings scales to tell people just how autistic they actually are (like on a scale of 1 to 100, not 1 to 3).  The result is a widespread misunderstanding of what the word autism means.  Nowadays it means very little.

I think that bubbles better represent autism than pieces of a puzzle.

People with any difference, from mild to severe, tend to live in their own little bubble; but bubbles do have a nasty habit of bursting and then a different reality may present itself. Also, if you live in a bubble you generally only hear people with similar opinions to your own – the social media echo chamber effect.

Monty, aged nearly 18, continues to live happily in his enchanted bubble. School is online currently, but hopefully back to normal again next week. Online school is pretty good because his assistant comes to our house.  Easter was celebrated and a couple of girls from his class came to hunt for chocolate eggs with him in our garden.

We visited some of Monty’s distant relatives who are usually looking after their grandson with severe non-verbal autism.  The boy has been out of school for a year, because his special school closed due to Covid.  He lives in a very different kind of bubble. Grandad was wondering where the boy will be in 10 years’ time, presuming it likely to be in an institution, a very different kind of bubble and not an attractive one.

On Sunday we were invited by friends for lunch beside the river. Their adult children do not come, likewise our adult son, they all have better things to do.  Monty was invited and we are beyond the stage where you would leave him at home, out of sight, with a babysitter. Our friends are aware that Monty has autism and they “accept it”, or else they would not invite him.

It is easy to accept a young man who sits nicely for two hours, eats his soup and then devours his fish, carefully avoiding the bones and a little later, asks what is for dessert.  He makes his own way to the restroom, we are not worried he will go the women’s rather than the men’s by mistake, or that he will run out of the building, or jump into the river. So, what is there not to accept?

Can you bring a non-verbal 11-year-old boy, with severe untreated autism and a very limited diet, to a two hour lunch in a busy restaurant, surrounded by people he does not know?  I don’t think so, it would not be accepted.

Even when Monty had quite challenging behaviors, when much younger, he did get taken everywhere.  Fortunately, small children can get away with a lot - we are programmed to be sympathetic and make allowances for them.  When children become more adult-like, we expect different behavior.  If your development plateaus at the level of a 2-year-old, strangers are going to want to keep their distance when you get bigger.

Rather than blame the strangers for their lack of tolerance, why not do more to ensure development does not stall at such an early age?  How about some awareness of that?

I keep asking why special schools where we live do not teach any alternative method of communication to non-verbal autistic children.  Schools for the deaf do teach sign language, but with a diagnosis of autism you are left with nothing.  No use is made of augmentative communication devices.  No use is made of the Picture Exchange Communication System (PECS).

Clearly awareness can be a first step towards acceptance, but there are limits to what people can accept.

My elder son told me about a boy in his circle who is very obviously gay and yet his father remains unaware, even his wife has not broken the news to him.  The news would not be well accepted, so it is just hidden away.

Now that most autism diagnosed is very mild, it is beginning to get drawn into the trending gender dysphoria topic.  Being autistic is being equated to being gay and just another difference to celebrate with rainbow colours.  It is put forward as something you can choose to mask, with your built-in cloaking device, if you want, but then you risk damaging your “mental health”.

Not surprisingly some parents of children with severe autism want a new descriptive word for their child’s condition. Autism has lost any clear meaning.  I guess they would love to buy one of those cloaking devices to mask their child’s autism, then they too could go for lunch at a fancy restaurant.

Among the least accepting adults I have met were parents at a musical performance put on by children with autism.  The parents made no allowances for interruptions made by younger siblings in the audience, it was a case of “remove your screaming child!”.  I assumed they would be more sympathetic than regular parents, but not at all.

The next question is whether acceptance is enough. At a recent parent teacher meeting at Monty's school, one new teacher was telling me how he identified with our situation, because his young niece has autism and some physical disability. He thought acceptance was the key issue at school and told me how well Monty is accepted by his class.  I did not disagree, but in my mind I was thinking "well actually, how about some learning?".  One advantage that Monty has developed since taking his PolyPill therapy, is that he has learnt many new skills that help to make him accepted.  He skis well, swims well, plays the piano well and is better at mathematics than many of his peers, so they know he is more than just a token autistic.  I think he earned some respect.  On the inclusion - delusion scale regarding mainstream schooling he is doing well.

 

What to do?

In some people’s bubbles, they are already doing a lot to improve their situation. These are the bubbles to be made aware of.

People tend to want to peer inside other people’s bubbles but then step back.  The author of a book on ECT (electro-convulsive therapy) to successfully treat her son’s severe self-injurious behavior (SIB), is bemused as to why other parents do not follow her example.  I told her that for most people ECT would be a step too far.

You would think there should be a basic standard of care available to all.  If the parents do not have a grip on the situation, at least the school should and ideally so should the pediatrician.  This probably does exist somewhere, perhaps in Scandinavia.

Acceptance has different aspects, of course it is good that people can accept others with differences and include them.  If parents just accept that their child is severely disabled by autism and then assume that nothing can be done, that would be really bad. Who ever did well by giving up?

As usual a lot of harm can be done with the best of intentions.  At both ends of the spectrum there are very one-sided views.  From the very severe end come the “horror stories” of their daily life and the conviction that there is an explosion in the incidence of their very severe autism.  At the ever-booming, slightly affected end of the spectrum is a small vocal group who are anti anything that can treat autism, whether it is behavioral therapy or pharmaceuticals. 

You might wonder what happens to all those neurodivergent people with Schizophrenia or Bipolar – don’t they get celebrated?  I do not see anyone lobbying for awareness and acceptance of them.  Why is that?  Too scary perhaps.

In many parts of the world the child with untreated severe autism is going to end up living in the same place as the adult diagnosed with Schizophrenia. Autism comes home to its big brothers Schizophrenia and indeed Bipolar, with all their overlapping miss-expressed genes.

Choose your bubble wisely.

 

What should be done?

The psychiatrists paid to write the diagnostic manuals (DSM5) need to step into the 21^st century and start doing the job properly.

An observation of autistic behaviors in a patient needs to be evaluated and graded, for example with the Childhood Autism Rating Scale (CARS).  If the child is below the threshold of 30, they should not be diagnosed with autism.  Yes, that means that the school does not get extra payments and indeed neither do the parents – this often is the desire behind a diagnosis.

The people who actually have an autism score above the threshold should be the focus of the autism budget.  The bigger their challenges, the more support they should get.

One in five school children have special education needs of one sort or another and these clearly should be addressed, but not by misdiagnosing some of them with autism.

People who have a genuine autism diagnosis, should then start a process of determining what are its biological foundations and what can be done to reduce the damaging consequences that led to seeking a medical diagnosis in the first place.

If there are no damaging consequences, how can this be a case worthy of a medical diagnosis?  It isn’t autism, perhaps it is sub-clinical autism.  It is likely quirky, nerdy, introvert, anxious or even gay (ouch!) etc - all perfectly normal traits.

 

What will be done?

Nothing.

Choose your bubble on that basis and make it as enchanted as you can.