Treating Adults with Autism?

 

Almost the entire focus of treating autism is targeted at young children; only rarely do you hear about clinical trials involving adults, yet we are often reminded that autism is a lifelong condition.

For those of you that read the proposed guidelines to drug companies developing autism therapies, this issue raised its head again.  Will therapies effective in children be effective in adults (and vice versa)?

There are many issues here.  On the one hand there is great caution about giving drugs to very young children, but there is the realization that many therapies may only be effective if given at an extremely young age.

I only started treating the biological dysfunctions in Monty, now aged 12, when he was 9 years old.  By good fortune the first therapy (bumetanide) I tried was highly effective, otherwise this blog would not exist.

Had that Bumetanide clinical trial been published 5 years earlier, would I have given my then 4 year old son that same drug?  Probably not.

With what I now know, I would be happy to give Bumetanide as soon after birth that autism was even suspected.  (To the trained eye, this is but a few months old)

The effect of no treatment

For three years I have been developing a personalized autism treatment, Monty’s Polypill, and I think it works well, but a few weeks ago we decided to see what happens with no treatment at all.

This did provide some useful insights into treating young adults, as opposed to young children.

The first thing is that all the new skills that have been acquired, at close to neurotypical speed, in the last three years, did not just fade away. 

The old obvious repetitive behaviors/stimming/stereotypy did not return, but more subtle new ones did.  (no NAC)

He could still play his piano nicely with his teacher, but his interest in playing out of lessons faded away as did his skill level out of lessons.

He showed an occasional aversion to doing anything new, for example when his assistant came in the afternoon, I told him to go outside and meet her.  He could happily open the front door (his normal routine) but was not able to walk though it and meet her by the gate.  (no statin)

When I offered to go with him, he had a brief tantrum. 

He started asking permission to do things he knew how to do, which some people saw as a positive.  When lying in bed at 9pm he called out “Mum can I read a book”, rather than just picking one from the shelf by his bed and when at a small birthday party he had to bend down to light the candles, he turned round and said “can I squat?”  Most people thought that was good use of vocabulary, I was thinking “just do it”.  (statin effect)

I received comments like “how patient he is”, or at school  words like “peace” and “peaceful”.  I was thinking how passive he was. (no bumetanide/low dose clonazepam)

While there was no glaring loss of cognitive function and spelling tests and maths test at school were not showing any deficit, I noticed a loss of ability to develop new skills. 

We use an excellent online program called Math Whizz and one thing we were learning was to how to use the calendar.

Typical questions would be:-

“What date is the second Friday in May?”

“What date if the first Monday in December?”

“What day (of the week) is the last day in June?”

You first have to click on “May” to get the calendar to turn to the correct month and then you can figure out the answer.

To my surprise, while still on the Polypill, Monty was getting pretty good at this exercise, on his first attempt.

However, a few days later, when we tried with no Polypill, he was struggling and as the days passed he got worse and worse.  (chloride levels gradually rising?)

There was even a return of the sensory overload that causes many problems for some people with autism and also Asperger’s.  Even the sound of a crow became disturbing.  Both Acetazolamide and Bumetanide are used to treat Hypokalemic Periodic Paralysis, which is a more severe form of Hypokalemic Sensory Overload and at least some types of Autistic Sensory Overload are a subset of this.

After two weeks of Bumetanide and Potassium the sound over-sensitivity has gone again.  It did not go away immediately.

Pleiotropic effect of Verapamil

While I initially identified the calcium channel blocker, Verapamil, as an effective inhibitor of aggression and SIB triggered by allergy/mast cell degranulation, I was once asked if I thought Verapamil might have pleiotropic effects in Monty.  Having stopped using Verapamil and then restarted it, all outside of the problematic allergy season, I have all the proof I need in my n=1 case.  Life is better with a little Verapamil; his calcium channel dysfunction goes beyond those in mast cells.

Verapamil was the last element of the Polypill that I re-started; I was rather hoping it would show no effect outside the allergy season.  Only after adding it back did things really return to what has become our "normal".

There is after all a vast amount of evidence linking calcium ion channel dysfunction and autism.

My Verdict

I think many people would be very happy to have a passive child, who can sit for two hours in restaurant.

Most people do not notice the fading of good behavior, because their overriding concern is the lack of any “bad” behavior.  So a bad behavior is followed by a “is this better?”, rather than a “Wow, do you know Monty did today …”.

I prefer a child who can learn, even if that means he may get fed up from time to time, and show it.

I was pleased to come home earlier this week and find Monty sitting alone playing his piano beautifully (no prompting, no reinforcement needed), with his music book laid out in front of him, playing one melody, turning the page and playing the next one, while his big brother had gone upstairs to play his computer games, because little brother does not need him. 

  

Intervention in Adults

Other than halting self injurious behavior (SIB), I am far from convinced that most people would even notice the difference if you took an adult with classic autism and started to treat him.

At that age, passive and patient is what most caregivers want.

So I see little prospect that “corrective biological therapy” will ever be initiated in many adults with more serious autism;  they will continue to be “tranquilized”.

Many adults with Asperger’s and high IQ do their own research and self-treat; some even read this blog. For them, even a small biological "improvement" can have a welcome effect on well-being. Good for them.

Intervention in Young Children

The best way forward is to intervene immediately after diagnosis.  In the US/Canada that might be two years old, but more like four years old in Europe.

If I was a Roche or Novartis, this would be my target:- non-verbal, non toilet-trained toddlers who make no eye contact, possibly cry a lot and tend to be kept at home.

Buy Arbaclofen for Autism? Perhaps try Pantogam Aktiv?

             

An Enantiomer is like a mirror image,

so there are two versions of the “same” molecule one called R- and one called  S-

Some people are still looking to obtain Arbaclofen to treat autism and Fragile-X, they regularly stumble upon this blog.

A couple of years ago there was a lot of interest in Arbaclofen (R-baclofen), a GABA_B drug, which is, in effect, a special version of a cheap existing drug called Baclofen.  Baclofen is generally used to treat spasticity, but also alcoholism and even hiccups.

As we saw in earlier posts, the drug Baclofen is a mixture of R-Baclofen and S-Baclofen. The research showed that their action is different and that S-Baclofen reduced the effect of R-baclofen.  So in some modes of action, pure R-Baclofen would have much greater effect than the regular Baclofen mixture.

If you use the "index by subject" on this blog, which is a tab at the top, you can find the posts that relate to Arbaclofen.

Arbaclofen

1.   4G and Autism - Glutamine, Glutamate, GABA & GAD

2.   Autism Clinical Trials, Arbaclofen (STX209), Curemark CM-AT and the Clever Chiropractor

3.   Human Growth Factors, Autism and the Centenarian Nobel Laureate

Arbaclofen Research in Autism/Fragile X

This very expensive episode was triggered by one child with autism being prescribed regular Baclofen, for an unrelated issue.  That child’s autism had dramatically improved, this then led to the interest of Seaside Therapeutics, who already had another prospective autism drug.

After tens of millions of dollars spent, everything stopped a couple of years ago.  The developer, Seaside Therapeutics, appears to have been shut down, although in its clinical trial a substantial minority found the drug was effective.  The way the trial had been structured, the drug did not achieve is “primary endpoint” and so Roche, the potential follow-on investor, deemed the trial a failure.

This led to many unhappy parents seeking alternative sources of R-Baclofen, which they believed had been effective.

Baclofen for Asperger’s?

At least one regular reader of this blog finds that Baclofen is very helpful for himself.

Yesterday before completing this post I had some exchanges with a UK pediatrician (spelled paediatrician in the UK) who is prescribing Baclofen to eight children with Asperger’s to treat anxiety. The results are very positive.  I do wonder is this a 100% response rate,  or are the eight a subset of all the children that have tried the drug?

One of our Australian readers of this blog is very interested in minimizing anxiety in his child with high functioning autism.  He did forward me some research, a while back,  that links GABA_B to Somatostatin, also called Growth Hormone Inhibiting Hormone (GHIH) .  The research from Carnegie Mellon shows that GHIH changes the way the brain functions. 

This does get very complicated the more you dig and, until today, I did not start to write up my findings.  This is just some initial thoughts/links for scientists.

Intermediary Neuron Acts as Synaptic Cloaking Device, Says Carnegie Mellon Study

“Furthermore, by silencing certain parts of the neuronal network, the activity of the somatostatin neurons also can change the way the brain functions, heightening some perceptual pathways and silencing others.” 

Neocortical Somatostatin Neurons Reversibly Silence Excitatory Transmission via GABAb Receptors

“If the levels of human growth hormone in circulation in the brain and the blood get too high, then special cells called somatostatin neurons detect this. These neurons then trigger the creation of more GHIH in the brain. This then in turn slows down the secretion of human growth hormone.”

Autism-linked gene guides growth of subtype of neurons

 “Mature interneurons from this brain region mainly express either parvalbumin or somatostatin, which serve as markers of these subtypes. Parvalbumin neurons tend to fire quickly in response to signals, whereas the somatostatin ones respond more slowly.

In control mice, the ratio of these two subtypes is about 50:50. By contrast, the mutant mice show a dramatic decrease in the number of interneurons expressing somatostatin. This results in an excess of abnormally large cells expressing parvalbumin.

Despite an overall loss of interneurons, the mice have more inhibitory signals than controls do, skewing the signaling balance to excitation.” 

We do know that the various growth factors in people with autism can be disturbed, but in different types of autism that disturbance varies, just to complicate things.

Various therapies based on this are under development (one uses IGF-1 and NNZ-256 is another).  We also know that many people with classic autism have accelerated growth (both body and head) in the first two years.  We also know that brain growth is also accelerated.

We know from the genetic research that many of the anomalies relate to GABA.

We know that targeting the GABA_A receptor can be hugely beneficial in classic autism (bumetanide and micro-dose clonazepam).  We can also fine tune the structure of the GABA_A receptor and potentiate it using allosteric modulators (like Pregnenolone or progesterone).  This also gets very complicated.

Baclofen for Classic Autism?

Baclofen is a spasticity drug:

Spasticity (from Greek spasmos-, meaning "drawing, pulling") is a feature of altered skeletal muscle performance with a combination of paralysis, increased tendon reflex activity and hypertonia. It is also colloquially referred to as an unusual "tightness", stiffness, or "pull" of muscles.

People with (classic) autism as opposed to Asperger’s can have all sorts of fine and gross motor issues, particularly as young children.

They can “toe walk”, walk with their feet pointing in different directions, they can have “claw hand”.  They can struggle to control a pencil and even when they learn, their handwriting can be very sloppy.

Are these spasticity issues?  I think they probably are.

When people’s autism flares up, an early sign is worsening handwriting.

When my son’s Polypill begins to wear off in spring/summer at school at around 11 am, the claw hand returns.

I did indeed try Baclofen about a year ago.  There is an effect - no claw hand.

The problem with Baclofen is tolerance, the more you use it the higher the effective dose becomes, just like benzodiazepines.

So I noted that there was an effect, but chose to move on.

Meanwhile over in Russia

For many years in Russia they have had their own GABA_B drug, similar to Baclofen, it is called Pantogam.  Pantogam has been used for years as a therapy for neurological conditions including autism.

Just as Baclofen is “racemic mixture” of left-baclofen and right-baclofen, so is Pantogam.  There is S-Pantogam and R-Pantogam.

Enantiomers

There is nothing strange about these left and right versions of a drug

Here is from Wikipedia:-

Enantiomers of each other often show different chemical reactions with other substances that are also enantiomers. Since many molecules in the bodies of living beings are enantiomers themselves, there is sometimes a marked difference in the effects of two enantiomers on living beings. In drugs, for example, often only one of a drug's enantiomers is responsible for the desired physiologic effects, while the other enantiomer is less active, inactive, or sometimes even responsible for adverse effects.

Owing to this discovery, drugs composed of only one enantiomer ("enantiopure") can be developed to enhance the pharmacological efficacy and sometimes do away with some side effects. An example of this kind of drug is eszopiclone (Lunesta), which is enantiopure and therefore is given in doses that are exactly 1/2 of the older, racemic mixture called zopiclone. In the case of eszopiclone, the S enantiomer is responsible for all the desired effects, though the other enantiomer seems to be inactive; while an individual must take 2 mg of zopiclone to get the same therapeutic benefit as they would receive from 1 mg of eszopiclone, that appears to be the only difference between the two drugs.

Another good example is a common antihistamine:-

Levocetirizine (Xyzal) and cetirizine (Zyrtec)

Cetirizine, an effective H1-receptor antagonist, is a racemate mixture of two enantiomers: levocetirizine (R enantiomer) and dextrocetirizine (S enantiomer).  Chemically, levocetirizine is the active enantiomer of cetirizine. It is the L-enantiomer of the cetirizine racemate.

Cetirizine is sold as Zyrtec and Levocetirizine is sold as Xyzal.

If you prefer Claritin:

Claritin is loratadine.  The active half of this mixture is desloratadine.

So they have separated this out and produced a single-enantiomer drug made exclusively of desloratadine.  You can buy this as Clarinex/Aerius, depending on where you live.

In many cases the single-enantiomer drug works no better, it just costs more and may allow for a patent to be extended, which may mean billions of extra dollars.

Single-enantiomer drugs: elegant science, disappointing effects.

Abstract

Most new drugs are marketed as single enantiomers but many older agents are still available in racemic form. As these drugs reach the end of their patent life manufacturers become interested in marketing single enantiomer equivalents. This is called 'chiral switching' and it has been claimed that it will bring clinical benefits in terms of improved efficacy, more predictable pharmacokinetics or reduced toxicity. We reviewed the clinical evidence and prices for three recently marketed single enantiomer versions of widely used racemic drugs: escitalopram, esomeprazole and levosalbutamol. Claims of increased efficacy were based on comparisons of non-equivalent doses and any advantages seemed small and clinically unimportant. Prices of esomeprazole and levosalbutamol were higher than their racemic alternatives and we predict that these prices will remain high despite the market presence of generic versions of the racemates. Patent protection and a perception of superiority based on promotion rather than evidence will maintain price premiums for single enantiomer drugs that are not justified on the basis of clinical performance

Back to Russia

In Russia they have now marketed the single enantiomer drug of Pantogam, which is called Pantogam Aktiv.

Does Pantogam Aktiv work “better” than Pantogam, or does it just cost more?

Is Pantogam Aktiv equivalent to R-baclofen (arbaclofen)?

How would those eight kids with Asperger's in the UK fare on Pantogam Aktiv, as opposed to Baclofen?  Is tolerance an issue with Pantogam Aktiv? 

“Failed” Arbaclofen Trial

Rather than spend tens of millions of dollars on Arbaclofen, why did not someone just think of first trying Pantogam and Pantogam Aktiv on that very first child who responded to Baclofen?

When they closed the trial (and the company) why did they not suggest to those unhappy parents to try Pantogam and Pantogam Aktiv?

Pantogam Research

Most research is in Russian, but there is some in English.  Interestingly this drug affects both GABA_A and GABA_B.

While its main effect is on GABA_B. like Baclofen, it also has the effect of modulating the GABA_A response.  This effect means that when combined with benzodiazepines, where normally people build up a tolerance, and so the dose needs to be increased, no tolerance develops.  We saw this very effect on GABA_A with tiny doses of other drugs in earlier posts.

Attention Deficit Hyperactivity Disorder: Selection ofthe Optimum Duration of Medical Treatment

 A total of 32 children aged 6–12 years with attention deficit hyperactivity disorder (ADHD) were monitored during prolonged (6–8 months) treatment with Pantogam (homopantothenic acid) at daily doses of 500–1000 mg. Treatment results were assessed using the DSM-IV core ADHD symptom scales and the WFIRS-P (parental) scale every two months. Decreases in core symptoms on the DSM-IV core ADHD symptom scale were seen at two months of treatment. Significant changes on the WFIRS-P scale took longer: improvements in self-concept, socialization, and social activity were seen at four months and in behavior and schoolwork, basic life skills, along with decreases in risk-associated behavior, at six months. Thus, in contrast to regression of core ADHD symptoms, overcoming impairments in social-psychological adaptation required longer treatment periods.

Pantogam in daily psychiatric practice

Role of Combat Stress in the Formation of Chronic Pain Syndrome in Combatants and Its Treatment with Pantogam Active

Conclusion

Arbaclofen (R-Baclofen) failed its clinical trial, so it is no wonder drug for Fragile X and classic autism, but is was effective in a minority of people. 

It is possible that it would have been much more effective on people at the other end of the spectrum, those with Asperger’s – like the reader of this blog and the UK pediatrician using cheap Baclofen.

The people behind the Arbaclofen trial were super-brainy types from MIT, dig a bit deeper and I recall family links to Fragile-X.  So objectivity went out of the window, along with all those millions of dollars.

I do not suppose Pantogam and Pantogam Aktiv are autism wonder drugs, but they must help in some cases, otherwise the Russians would not be prescribing them. 

For those who found Arbaclofen really did help, why not try Pantogam and Pantogam Aktiv?  Just use Google:- “Buy Pantogam” in place of “Buy Arbaclofen”.

You would have thought someone smart at the US NIMH would have thought of this.  There are some very clever Russians and they do have autism over there too.

Traumatic Brain Injury and Autism, linked again, but not in a good way

It came as no surprise to me that many people involved in high profile mass shootings suffer from mild autism (Asperger’s).  What did surprise me was that so many people with TBI (Traumatic Brain Injury) also commit such crimes.  Indeed in a recent study (see later) of 239 killers, 28% appear to have autism and 21% suffered from TBI.

Indeed the name used by the Austrian, Hans Asperger, in 1943 for his newly identified condition was “Autistic Psychopathy”, it was only many decades later when his work was discovered for the English-speaking world by Lorna Wing in 1981, that the condition became known as Asperger’s.  Wing did not like the term “Autistic Psychopathy” that Asperger had chosen, because she thought it would apply sociopathic (violent) behaviour to the lay public.

Wing recently passed away and the New York Times wrote a nice article about her.

Dr. Lorna Wing, Who Broadened Views of Autism, Dies at 85

Her paper, that first established Asperger’s syndrome, is here:-

Asperger’s syndrome a clinical account

Since this paper was published only in 1981, it is hardly surprising that so few older adults have been diagnosed with Asperger’s.  Indeed it was a full ten years later, in 1991, that an authoritative English translation of Asperger's work was made by Uta Frith; before that Asperger’s Syndrome (AS) remained virtually unknown.

As we have noted before, Psychiatrists and Psychologists like to take their time; no Space Race or Manhattan Project in their little world.  Still, half a century is pretty slow.

People suggesting an autism “epidemic” might take note that only 25 years ago, absolutely nobody bothered to diagnose mild cases of autism, they did not even have a word for it.  Those of you still wondering why your doctor still knows so little about autism, might also take note.

Now I understand why there were no Aspies in my school, when I was a child.  They had not been invented.  I had assumed that Asperger’s syndrome was of the same era as the man himself, but Hans Asperger died in 1980.

I had no idea it took Psychiatrists, Psychologists, and yes, Doctors, half a century to absorb, accept, and begin to act on a new idea;  all because Asperger spoke/wrote in that “extremely rare” German language.  Incidentally, 50 million Americans claim German ancestry, not to mention that the British royal family is actually German; the House of Windsor is really the House of Saxe-Coburg-Gotha, before some image building took place in 1917 during WW1.

So don’t raise your expectations of these people too high, for the next half century.  Hopefully they have figured out Google Translate.

Here is the Pediatrician, Professor Hans Asperger at work in Austria; nice drawing on the black board:-

  

Die„Autistischen Psychopathen“ im Kindesalter (1943)

Autistic Psychopathy in Childhood  1943 (translated from Germanin 1991)

Asperger and his Syndrome, by Uta Frith

  

Asperger’s (Autistic  Psychopathy) and  TBI among Mass Murderers

In the recent study of 239 mass murderers almost 50% had either ASD or head injury /TBI, the other half suffered from “psychological stresses”.

Neuro-developmental and psychosocial risk factors in serial killers and mass murderers

At least the author has clearly read about Hans Asperger, he suggests a new diagnosis, Criminal Autistic Psychopathy, as a subcategory of Asperger's syndrome.

I will not dwell on the murder angle, other than to say that perhaps if people with Asperger’s were actively included at school, they would ultimately lead happier and more successful lives.  The percentage that currently go on to have very violent thoughts, might not then do so, and the tiny percentage of those might not act on those very thoughts.

I should point out that I do not find it odd at all that the boy with Asperger’s in my elder son’s class keeps telling him “I will kill you and your parents”, to which Ted, now 14,  says “but I won’t let you” and the response is “but I will wait until you are not there”.  I am not seriously worried that he will do this, but if I was his parent, I would be very concerned that he says/thinks such things.

Fortunately there are no serial killers with Classic Autism, so no need to lock up Ted’s brother.

ASD, TBI & PTSD

We have come across TBI several times in this blog, and I note that many people coming to this blog are TBI sufferers.

Both ASD and TBI are associated various degrees of mood disorder.  These feelings are driven by neurological changes that are usually ignored, or treated rather crudely with drugs that rarely seem to work entirely as intended. 

I think the world of autism could learn much from the mood disorders that follow TBI.

Epilepsy occurs very frequently in both ASD and TBI.

The third condition that we might usefully consider is Post Traumatic Stress Disorder (PTSD).  This condition is also associated with severely affected mood.  Army veterans returning from recent conflicts can be greatly affected by PTSD.  We came across the military type of PTSD in the post about the hormone TRH.  One of the many roles of TRH in the body seems to be linked to mood, and very specifically suicide.  The US military is funding development of a TRH nasal spray to reduce the incidence of suicide.  They cannot give antidepressants, like Prozac, because a well-known side effect is suicidal thought.  TRH is included in my autism PolyPill.

People with Asperger’s do have an elevated risk of suicide, another reason to sniff some TRH, perhaps?

The Link between ASD, TBI and PTSD

The above conditions are very different, but they share some similar symptoms relating to mood disorders.  By understanding the neurological underpinnings of the mood disorder in one condition, we might well learn something useful for the others.

The research into TBI seems to focus on better surviving the first few hours.  We saw in earlier posts that by giving intravenously either statins, or the female hormone progesterone, in the Emergency Room, there was a marked increase in survivability.  Progesterone and statins are both highly neuroprotective.

When Michael Schumacher had his TBI in a recent skiing accident, I was saying to myself “give him progesterone”, I very much doubt the French neurologists did.  They probably do not read American/English research.

In the case of autism, very recent research has shown an excess of male hormones in the amniotic fluid of mothers who give birth to a baby that will later be diagnosed with autism.  We also have seen how some people with mild autism treat themselves with progesterone to feel better.

Many years ago pregnant women were often prescribed progesterone and/or estrogen, now it seems to be limited to some women undergoing infertility treatment.  Perhaps giving progesterone might reduce the incidence of autism?

Statins are a known treatment for cytokine storms and are included in my autism PolyPill.

Once back home, people recovering from TBI and PTSD do seem to face similar treatment to adults with autism; they get ignored.

Due to all the recent conflicts in Iraq and Afghanistan, we do hear quite frequently about the consequences of untreated PTSD.  There are also very many cases of TBI, resulting from motor vehicle accidents (cars, bikes, quad bikes etc), sports accidents (skiing) and shootings (particularly in the US).  It seems that in many cases there can outwardly be a physical recovery, but personality has altered.  As we have seen in this blog, all the various hormones and neurotransmitters are interrelated and so any neurological damage will have multiple knock-on effects.  This will consequently transform, for better or worse, someone’s personality.  I used to know a person once, who was about to marry for the third time.  The second wife had been hit by a bus while crossing the street, and I remember how odd it sounded what he said next, “when she got better, she was a different person and I had to divorce her”.  The change in personality makes perfect sense, we are all the result of the particular homeostasis our brains settled at.  So some people are gregarious, others are loners, and a very small number become psychopaths.

If we more fully understood how the brain works, most types of mood disorder would likely be treatable.  Since people with TBI and mild autism are now easily identifiable, there is yet another reason to accelerate this research.  A frequent justification for the low expenditure on autism research is that “you don’t die from autism”.  Well, the above research shows that plenty of people do die from autism, just not the ones you expected.

Just to give the full picture, sadly people with severer types of autism have substantially elevated risk of mortality in their early years, due to seizures, drowning and other accidents.  There is research showing this, but it also shows up any time you see cause of death on the samples from brain tissue banks, used in autism studies.  This is why it is very important to teach people with severer autism to be confident swimmers, however hard it might seem.

Mastocytosis Mistaken for Aspergers

One of the features I have in this blog is that I get to see what search terms people use to find this site.  Sometimes these search terms tell you some very interesting things.

Here is one such interesting search, somebody used today:-

    mastocytosis mistaken for aspergers

Even though I expect 90+% visitors to this blog are interested in more severe types of ASD than Asperger's, much here is likely to be applicable to some people with Asperger's.

There are several posts in this blog about the role of mast cells and how allergies cause them to degranulate.  In some people mast cell degranulation actually leads to pain.  Some people have an over-expression of mast cells, this is called Mastocytosis.

I made by own theory about seasonal autism flare-ups and mast cells, which I called Seasonal Autistic Mastocytosis.

Now we know that at least one person thinks their mastocytosis was mistaken for Asperger's. 




 

Bumetanide Dosage & Effectiveness in Autism & Asperger's

The clinical trial of Bumetanide in autism, published in 2012, was what triggered my interest in using drugs to treat autism.

A randomised controlled trial of bumetanide in the treatment of autism in children

In that trial on children aged 3-11 years, the dosage used was 1mg a day, split in two doses.

In my trial, I found 1mg in the morning effective, while splitting the dose rendered it ineffective. 

I was surprised to hear that the French researchers find the treatment effective in 90% of cases of autism, including Asperger’s.  The reason is that while Monty, now aged 10 with ASD, is a responder, it seems that most people I know who have tried it have not responded.  Only one did respond, and that was when the father upped the dosage.

Now I hear that Lemmonier’s standard dosage has doubled to 2mg a day, with 1mg in the morning and 1mg at 5pm.  He tries for three months, before assuming the drug to be ineffective.

So to anyone who tried Bumetanide without success, maybe it is time to try again at the revised dosage and see if you are in the 90%.

The researchers are also suggesting Bumetanide is given from a very early age, as soon as autism is suspected.