The Cost of Approving an Old Generic Drug as a New Autism Drug

Some readers of this blog are commenting how hard it is to obtain prescription only drugs for “off-label” use in autism.

None of the drugs mentioned in this blog are actually approved for use in autism.  There is some science showing that they might be effective, but there is no mention of autism on the “label” approved by the regulator.

This means that your doctor will not know how to prescribe it and your insurer will not want to pay for it.

So how do I access these drugs?

This is a frequent question.  In theory you do not need to wait for the drug to be approved, you can apply to the national drug agency in your home country for permission to use a drug based on the experimental use that showed it might be effective.

Better still, in many countries like the USA, doctors are not banned from prescribing “off-label” drugs.  If the doctor follows the new research, he is permitted to apply it on his own patients.  If he does it recklessly, he might eventually lose his license.

In cancer therapy, many drugs are used off-label.

Why not just approve a new use for an old drug?

This would seem an obvious question and this is what is being done with bumetanide, one of drugs described in this blog.

The problem is the cost and the time taken: EUR 4 million  (USD 5 million) and four years.

As you can see below, in the case of Bumetanide, the French Government will contribute EUR 1 million and it appears the Simons Foundation another EUR 1.5 million.

RECHERCHES PARTENARIALES ET INNOVATION BIOMEDICALE (RPIB) 2012 : projet CURE AUTISM

Curing autism with the diuretic bumetanide 

Since Bumetanide is available today as a cheap generic drug, they cannot really ever get their money back.  Only if they modified the molecule slightly, patented it, and got that new drug approved could they recoup their USD 5 million, which would then be even more, since they would have even higher costs.

The last I heard, Bumetanide will only be approved for autism in Europe, not the USA, due to cost issues.

So with this kind of financial logic, you can see why off-label uses of old generic drugs are likely to stay off-label.  

Best find yourself an off-label doctor.

NAC for Long Term Use in Autism

One of the post popular subjects on this blog is the use of NAC (N-acetyl cysteine) for autism. There are numerous earlier posts explaining how and why it works.

Just look up NAC in the index by subject; there are 19 posts, for those with plenty of time. (the labels function just gives the recent posts)

NAC was shown in a clinical trial at Stanford to be an effective treatment for autism.  You might have expected that this would be quickly followed by further research, but since NAC is widely available as a cheap supplement, there is not much financial incentive for further research.  Without that research, mainstream doctors will never prescribe it.

Beginner's guide to NAC 

Highly respected researchers have shown that in many types of autism, oxidative stress is present and considered that NAC might be an effective therapy.

In the past, some DAN-type doctors have used NAC, but the Stanford trial was the first mainstream trial for autism.

For oxidative stress in asthma and in particularly severe types, like COPD, NAC has long been used.  Oxidative stress stops asthma drugs from working, which is why NAC is used.

In autism, as in asthma, it appears that oxidative stress is a long term condition.  NAC controls oxidative stress, but it does not cure it.

Just as asthma research has shown that smoking triggers irreversible oxidative stress, the same appears to be true for autism.  NAC will rebuild the level of body’s own antioxidant, GSH, but as soon as you stop taking the NAC, oxidative stress reappears.  Many years after people quit smoking, the asthma research showed that oxidative stress remains, and so the asthma drugs do not work.

Will NAC be effective?

In cases of classic autism, NAC has been effective for almost everyone who has given me feedback.

The effect is usually noticed as being a reduction/elimination of stereotypy/stimming and obsessive compulsive behavior.  Other people have seen a reduction in aggression and even in sleeping problems.  The reduction in stereotypy makes way for good behaviours, like increased speech and better mood.

Some types of autism are not associated with oxidative stress; anecdotally, it seems to be some regressive types of autism.

When effective, NAC should change behaviour within a couple of days.  Equally, when you stop taking it, the same behaviours should return with a day or two.  This is a good way to check that you are not just imagining the effect.

NAC has “stopped working”

After a period of months you may find, as I did, that NAC has “stopped working”.  If this happens, most likely it is not that NAC has stopped working, but rather that something else has started working and is making the autism worse.  You need to identify what has happened, treat it, and then NAC will appear to start working again.

Possible reasons for NAC appearing to stop working include:-

·        Effect of an allergy (pollen or food)
·        Flare-up in an existing auto-immune disease
·        New auto-immune condition

For example, if the person has a history of GI problems and these get worse just as NAC “stops working”, you would know what to do.

NAC dosage

From what people tell me, in a three year old children 600mg once per day is effective.

In older children higher doses, going up to 2,400 mg or 3,000 mg are being used. 

There will come a point where increasing NAC will have no further behavioural effect and then there will be more likelihood of side effects.

You can experiment to find the lowest effective dose.  It is logical to split larger doses over the day, to maximize effectiveness and minimize any side effects.

In my son (33kg/73 lbs) I give 1,200mg at breakfast, 600mg at lunch and 600mg in the evening.  I started about 20 months ago.

Quality of NAC

There is both cheap NAC in gelatin capsules and foil-packed NAC.  Over time NAC will react with the air and lose its potency; as this happens a smell of rotten eggs is produced.  The foil-packed NAC is called Fluimucil in Europe and PharmaNAC in the US.

Side effects

Almost everything has side effects of some kind, but in the doses used for autism, NAC does not seem to cause anything troubling to occur.  

NAC will also reduce homocysteine, which is linked to various heart problems in adults.  As an antioxidant, NAC will also help remove any metals that should not be present. NAC has also been shown to improve outcomes in some types of cancer.

Double-tap Autism – perhaps an important variant

In spite of the recent drive to improve autism awareness, mainly in North America, very much more could be done to understand the condition itself.  

Rather than just giving it different names (now ASC rather than ASD, for example) and broadening the “catchment area” of the autism diagnosis, would it not be wise to better study the “disease” itself?

In most countries, people with autism are not treated by any doctor, so a huge pool of possible information is lost forever.  We just have anecdotal evidence, and much of that can be emotionally distorted by care givers.

Whether I want to or not, I just can’t keep noticing things in the media that make me take note.  I do get lots of people writing to me, sending me links to articles and I do admit to looking at some other people’s blogs.

The clever researchers studying autism, and the handful of clinicians writing about it, do not seem to notice the same things as me.  So I will go a little further and define a new type of autism that I would have thought must have been noticed many times before.

Double-tap Autism

I am here referring to the more severe types of autism, not high functioning autism (HFA) and definitely not Asperger’s.  Double-tap autism is a variant of what I call “disabling autism”.

The younger generation of gamers, will all know where I got the name from.  So in my case, Ted, aged 14 and very neurotypical, is the inspiration.

There does seem to be a substantial group of children who are diagnosed with autism (very) early, i.e. younger than 36 months and sometimes younger than 24 months.  They then start their intensive ABA program, since they are either North American, affluent, or both.  All goes well and little Charlie, or Billy, is responding well to his therapy and the parents are even beginning to think that autism is not as bad as they had feared.  Then along comes a viral, perhaps flu-like, infection and all of a sudden things go into reverse and Charlie is no longer the little ABA star he once was and he regresses further. Progress thereafter remains painfully slow.

I do keep noticing very similar descriptions in blogs and newspaper reports.  I just read another example in the UK’s Daily Telegraph, with a father describing his son’s double-tap and descent thereafter. Hence this post.

Rapha boss Simon Mottram: my life with autism

Understanding the Underlying Science

While your family doctor likely knows absolutely nothing about autism, there is actually a great deal of scientific knowledge out there in the literature.

By observing clinical changes in the progression of a disease, you really should be able to learn something about it.  But if nobody is making observations, little progress can be made.

Monty, aged 11 with autism, has only ever seen a doctor, with some knowledge of autism, once in his life; indeed his regular paediatrician believes that a child has the “right not to speak” until he is five years old.  For Europe, once in a lifetime would be average and for much of the world, that would be one more than normal.  In parts of North America the situation is very much better, with EEGs, neurologists, genetic testing, diagnosis before 24 months and even free early intensive behavioural intervention on request.

I am certainly not the most qualified to hypothesize as to what is going on in double-tap autism; my son has “single-tap” autism, after all.  Nonetheless I think it would very interesting to understand the mechanism behind the second tap, and then to reverse it.  I do not believe you can necessarily reverse damage caused years ago in utero, but the effects of a viral infection aged 3-4 should be treatable, if you know what to treat.

The term “regressive autism” means very different things to different people, just as the term “autism” has now been devalued by the ever widening of its definition by, not so clever, psychiatrists in the US.   

             

Regressive autism is something different to double-tap autism.  Double-tap autism is like a further regression, after classic autism has already been noticed, diagnosed and become stable.

It is possible that in some cases nobody noticed the first tap and then you would confuse severe regressive autism with double-tap autism.  I think that regressive autism, where initial development was genuinely “normal”, is a different phenomenon to early-onset classic autism. 

I do not believe the brain abnormalities found in post mortem autism studies are necessarily present in regressive autism.  In fact I believe that science has got a distorted view from the post mortem studies, since they are by definition hugely skewed towards severe classic autism, with seizures and indeed MR.  Think where they get the samples from.  

All this does matter; the current scientific belief, based on post-mortem brain samples, is that the autistic brain is damaged prior to birth.  As a result any kind of therapy is based on optimizing the function of a fundamentally damaged brain and hoping to take advantage of the plasticity of the young brain.

If the brain has developed normally to the age of 3 years old, it has already substantially completed its development.  If thereafter things go wrong, it cannot be because of the kind of malformations found in the post-mortem samples.  So there is a much higher chance of being able to reverse those changes.  Just as in PANDAS and PANS, a perfectly developed brain can, in certain circumstances, produce odd autistic-like behaviours.  PANDAS and PANS are treatable and autistic-like behaviours can be reversed.

So serious thought should be given to treating people with double-tap autism.  It should be treatable and it should be possible to revert to the state the child was in, prior to the second tap.

Possible Treatment

I would think that the immunomodulatory therapy that I have been talking about in recent posts would be a good place to start.  Somebody like Dr Swedo, the PANDAS lady, would be needed to do some experiments.  Therapies for PANDAS already include:-

·        Steroids

·        IVIG

·       Plasmapheresis

and, if all that is claimed about it was really true:-

·        Gc-MAF (Gc protein-derived macrophage activating factor)

Another possibility is that the virus is just a trigger for a genetic or epigenetic process.  If it is an inherited genetic anomaly, it was always present, like the gene that often leads to breast cancer, it is like a ticking time bomb; it may or may not explode in your lifetime.  If it is epigenetic then the process is like a bookmark, rather than a genetic defect, that turns on something that should be off, or vice versa.  Regardless of genetic or epigenetic, once you know what gene is affected, you may be able to figure out a way to counter it.  Just like in my PolyPill research, I read that it was already known in autism there may be a defect in the CACNA1C gene. The CACNA1C gene produces the calcium channel Cav1.2.  So I just needed to look at this Cav1.2 channel and figure out how to modify its behavior, just in case it was linked to my son’s particular type of autism.  This only took a few hours to figure out; it took longer to test it and even longer to write about it.

It is quite likely that many of the people with double-tap autism have the same underlying dysfunctions, and so what helps one could help many.  This was also the case with PANDAS/PANS.

I hope somebody, vaguely scientific, eventually does try and help people with this kind of autism.  It should be less difficult than classic autism, which turns out to be treatable after all.  But don’t hold your breath and, as I tell my older son, if a job is worth doing, best do it yourself.  That is unless you have Dr Swedo on your case.

Immunomodulatory Therapy in Autism - Potassium Channel Kv1.3, Parasitic Worms, and their ShK–related peptides

Regular readers of this post will know that I believe that Immunomodulatory therapy has great promise for treating various subtypes of autism.  In effect, I want to bring the over-activated immune system back under control.  Two methods that appeal are:-

·        The steroid, Prednisone, because it is cheap and though it has side effects, they are very well understood. It also has been shown to be effective in autism and related conditions like PANDAS and Landau-Kleffner syndrome (LKS)

·        Parasitic worms appeal because they are known to have beneficial effect in many auto-immune conditions ranging from arthritis to autism, but nobody really understood why.  Until now.

This post is about the worms and recent research which has established that it is likely that they work by blocking the potassium channel Kv1.3.

You will have noted that this blog keeps going on about ion channel dysfunctions and autism.  We already know that Cl^-, Ca²⁺ , K⁺ and Na²⁺ are all implicated.

When researching calcium channel blockers for autism, one reason I picked Verapamil was that it is also a potassium channel blocker.  My earlier experiments have shown that hypokalemic sensory overload exists in autism, I showed that oral potassium could treat sensory overload.

Hypokalemic Autistic Sensory Overload

 

This blog is (slowly) working its way through the ion channel dysfunctions known to exist in autism.

Well, it appears that Verapamil also blocks Kv1.3.

Block of the lymphocyte K+ channel mKv1.3 by the phenylalkylamine verapamil

Research Down Under

Researchers in Australia have identified the chemicals released by parasitic worms that have the effect of subduing the immune system.  They identified a large family of Stichodactyla helianthus toxin (ShK)–related peptides in parasitic worms, they showed that these peptides acted to inhibit Kv1.3 channels in human T cells.

Kv1.3 channel-blocking immunomodulatory peptides from parasitic worms: implications for autoimmune diseases

Abstract

The voltage-gated potassium (Kv) 1.3 channel is widely regarded as a therapeutic target for immunomodulation in autoimmune diseases. ShK-186, a selective inhibitor of Kv1.3 channels, ameliorates autoimmune diseases in rodent models, and human phase 1 trials of this agent in healthy volunteers have been completed. In this study, we identified and characterized a large family of Stichodactyla helianthus toxin (ShK)–related peptides in parasitic worms. Based on phylogenetic analysis, 2 worm peptides were selected for study: AcK1, a 51-residue peptide expressed in the anterior secretory glands of the dog-infecting hookworm Ancylostoma caninum and the human-infecting hookworm Ancylostoma ceylanicum, and BmK1, the C-terminal domain of a metalloprotease from the filarial worm Brugia malayi. These peptides in solution adopt helical structures closely resembling that of ShK. At doses in the nanomolar–micromolar range, they block native Kv1.3 in human T cells and cloned Kv1.3 stably expressed in L929 mouse fibroblasts. They preferentially suppress the proliferation of rat CCR7⁻ effector memory T cells without affecting naive and central memory subsets and inhibit the delayed-type hypersensitivity (DTH) response caused by skin-homing effector memory T cells in rats. Further, they suppress IFNγ production by human T lymphocytes. ShK-related peptides in parasitic worms may contribute to the potential beneficial effects of probiotic parasitic worm therapy in human autoimmune diseases

A less heavy summary is here:-

'Wormpill' could ease autoimmune disease symptoms

  

The researchers noted that Kv1.3 is widely regarded as a therapeutic target for immunomodulation in autoimmune diseases.

So it seems that they have identified the mechanism of action of the worms.

Earlier posts have mentioned intentionally swallowing TSO parasites (Helminthic therapy) for autism and the trials now ongoing by Coronado Biosciences.   Here is part of one post:-

I think that TSO is very interesting.  It is now being developed by Coronado Biosciences as a therapy for several inflammatory conditions including:-

·        Crohn’s disease

·        Ulcerative Colitis

·        Autism

Here is a link to all the clinical trials they are running.

The idea behind TSO is that the parasites have evolved a method of ensuring their survival in their host, by subduing the immune system, so that they are not killed/ejected.  By down-regulating the immune system, they become a therapy for diseases featuring an over active immune system.

This all started a few years ago when one autism Dad figured all this out and tried it on his own son.  Then began the long process of clinical trials, which then ended up with Coronado Biosciences.  The Dad’s website is here.

The Australians have the idea of making their (ShK)–related peptides into a drug therapy.  So no need to swallow those worms after all.

Verapamil or Stichodactyla helianthus toxin (ShK)–related Peptides

Just as the Australians may have trumped Coronado Bioscience with their better-than-a-worm peptide pill, has Verapamil the ability to trump the Ozzies?

We know that Verapamil is neutralizing many allergic reactions affecting autism all over the body.  This appears to be a combination of mast cell stabilization and a possible effect on pancreatic function that reduces GI problems.  But is Verapamil’s inhibitory effect on Kv1.3 also providing a broader immunomodulatory effect as well?  It does indeed look possible.

We would need somebody using TSO worms for autism, to see if Verapamil was effective for them too.  Any volunteers?

Unlike the TSO worms and the ShK peptides, Verapamil is cheap and sitting on the shelf in your local pharmacy.

Cognitive Function Restored, with Bumetanide

Regular readers will know that every summer Monty, aged 11 with ASD, has a “flare-up” in his autism.  Behaviour gets very much worse and now we notice that also cognitive function is impaired.

In my last post I repeated how the aggression and SIB (self-injurious behaviour) was very effectively suppressed by Verapamil and I was pondering how to solve the, now visible, cognitive decline.

I suppose some readers may be thinking all this sounds fanciful.  Once a child with autism is verbal and has got as far as basic maths, it is very easy to measure cognitive function.  For years I have asked Monty what he had for lunch at school that day, to check how “switched-on” he was.  Now, I just need to ask him something like “what is five times five”.

Ted, Monty’s older brother, has also noticed these changes and has recently delighted in showing how his brother does not know six times six, or even twelve plus five.  He would ask him questions when we are all in the car, and then I would have to start making excuses for his brother.  Well with Verapamil, at least Ted is not going to get punched by Monty, as they sit in the back of the car.

We know that for most of the year Monty knows the right answer to all these questions, but from July to early October he may get them wrong, or does not answer.  This was all traced back to the effect of a mild pollen allergy.

Rather than look for something new, I decided that as a first step I would just increase the dose of one of his existing Polypill ingredients and “hey presto” the problem was solved.  A nice surprise, indeed.

I increased the Bumetanide dose from 1mg once a day, to 1mg twice a day.

Every time since that I ask Monty five times five, or six times four he gets the right answer, even if he is in the middle of doing something else, like jumping into the swimming pool.  That is proof enough for me.  Even Ted has noticed.

In previous posts I did complain about the effectiveness of autism rating scales and suggested that measuring academic performance (in older kids) might be more reliable.   In the case of Bumetanide this really is the case.

As to the relationship between bumetanide and allergy, there are various possibilities.  I did yesterday highlight this impact to the French researchers currently working to get Bumetanide approved officially as drug for autism, since it could be useful for them to know.

Conclusion

So, the current summertime allergy solution is:-

Aggression and SIB – Verapamil three times a day

Cognitive impairment – Bumetanide one extra daily dose of 1mg

All that is left of the “autism flare-up” is a very occasional rapid mood swing from happy to sad.

Compared to last summer, the difference is profound and now the difference between behaviour in summer and winter is very small.

  

Allergies, Autism and Cognitive Impairment

Previous posts showed how pollen allergies can lead to summertime flare-ups in autism; most noticeable are violent/aggressive behaviours, but there is actually much more going on.

I established that Verapamil, the calcium channel blocker, and surprisingly also a mast cell stabilizer, can very effectively extinguish the aggression, but without really solving the usual allergy symptoms like itchy eyes.  As a result, you need to use a convention anti-allergy treatment as well.

Asthma/Pollen Hot Spots

Any asthma suffer will be able to tell you about the places that make them feel worse and the places that places that reduce their symptoms.  It seems that pine forests high in the mountains and on certain coastlines are best.

Forested areas around cities are not good for asthma, Berlin being an example. So you can easily check if you live in an asthma hot spot, or in a better place.

Cognitive Impairment

We just spent two weeks under the olive trees beside the sea in Greece, which I would classify as a low pollen location.  Having returned home to a big city and a house directly opposite a forest, we could see the effect of an asthma/pollen hot spot.

Monty, aged 11 with ASD, mild pollen allergy and mild asthma, did change his behaviour almost immediately.

The Verapamil does continue to block aggressive behaviour, but what changed was an immediate return of mild atopic dermatitis (red patches behind knees) and what Monty’s brother Ted, aged 14, described as Monty became “more stupid”.  It is not a nice way to describe it, but when you look closely, it is there.  The allergy has effectively lowered his cognitive function.  It is very easy to check, just ask some simple maths questions or memory questions (what did you have for breakfast?).  It is as if he is very mildly intoxicated (drunk), he is not staggering around, but he is not as sharp as he was in Greece, or at home in the spring.

Faced with an aggressive child, the last thing you would bother about is how good he is at mental maths, and so you would probably never notice it.  But having solved the aggression we are left with the observation that the allergy causes some temporary cognitive impairment.  I say temporary, because if you take away the allergens, everything improves and returns to where it was.

What is going on?

We know that allergens cause mast cell degranulation, which releases histamine, IL-6, and other pro-inflammatory substances in a chain reaction.  We know that these cross the BBB (blood brain barrier) where there are several types of histamine receptor.  The body has at least 4 types: - H1, H2, H3 and H4, and maybe more not yet identified.

Typical anti-histamines only block H1, and the newer ones are specifically designed not to cross the BBB, so as not to make you drowsy.  We later discovered that most H1 anti-histamines have moderate mast cell stabilizing properties, meaning they do reduce the release of histamine itself.

Calcium channel signaling is known to be disturbed in autism and there is excess physical calcium found in the autistic brain.  This did suggest that modifying calcium channel behaviour might be of benefit.  A known genetic variation in autism does affect the L-type calcium channels.  This suggested that blocking the L-channels might be helpful.  This was shown to be true in Timothy syndrome and I showed it to be true in Monty.

Other research has shown that Verapamil is an effective mast cell stabilizer, which did come as a surprise.

Now we come back to the effect of the allergy.  If untreated, it will “dumb down” the child and also lead to extreme behaviours like aggression, but also even odd physical tics, like moving the head forwards and backwards like a pigeon.

Perhaps there is a two stage process going on, which ultimately leads to the aberrant signaling of the L-type calcium channels and aggression.  Or is it just a progression from mild to severe?

Is it a coincidence that a calcium channel blocker can stabilize mast cells?  I think it unlikely.

Autism as an Allergy of the Brain

The idea put forward by Professor Theoharides, that autism is, at least in part, an allergy of the brain, looks more and more valid.  It was the subject of an earlier post.

Is a Subtype of Autism an Allergy of the Brain?

I do wonder how much mental retardation (MR) / cognitive impairment is also caused by the same mechanism.  Depending on how you define “autism” and whose figures you use, between 20% and 50% of people with autism have MR.  MR is defined as an IQ of 70 or less.

·        Mild retardation: Mild retardation: IQ level 50-55 to approximately 70 (85% of people with mental retardation are in this category)
·        Moderate retardation: IQ level 35-40 to 50-55 (10% of people with mental retardation)
·        Severe retardation: IQ level 20-25 to 35-40 (3 - 4% of people with mental retardation)
·        Profound retardation: IQ level below 20 or 25 (1 - 2% of people with mental retardation)

I would suggest that many people with autism might be “cognitively impaired” by allergies, be they caused by pollen, cats, dust, food, detergents, pollution or anything else.  Maybe they just dropped from a potential IQ of 120 to 110, or maybe they dropped from 80 to 35 and are now known as severely retarded.

Verapamil treats more than aggression and SIB

Based on my sample of one, it would be conceivable that Verapamil merely treats aggression and self-injurious behaviour (SIB), and that allergies are a side issue.  But thanks to the feedback on this blog, it is clear that Verapamil is treating the allergy.  One reader gave very extensive feedback showing how Verapamil greatly reduced her child’s GI problems (caused by food intolerance/allergies) and improved behaviour.  So based on a sample of two, Verapamil’s effect does seem to be related to mast cell degranulation and allergies.

Conclusion

I am very happy to have discovered the benefits of Verapamil, but I will continue to look into how further to reduce the “brain allergy effect”.  Perhaps the allergy is somehow affecting the excitatory/inhibitory balance of the Neurotransmitter GABA, I say this because Monty’s behaviour somehow resembles life without Bumetanide.  

Bumetanide’s role in autism is to lower brain Cl^- concentration and to switch GABA to be inhibitory.  A recent comment on one of my Bumetanide posts was from somebody highlighting a paper that questioned whether enough Bumetanide crosses into the brain to switch GABA to be inhibitory.  

Note that a recently published comprehensive review on the use of bumetanide in the treatment of neonatal seizures indicates that theres is no evidence to support the use of this drug in the treatment of central nervous system disorders via the NKCC1-dependent mechanism described above, as at the very low doses that are given to infants and children bumetanide does not reach sufficient levels in the brain.

direct link to the original review:
http://onlinelibrary.wiley.com/doi/10.1111/epi.12620/pdf

It is conceivable that allergies affect the blood brain barrier (BBB), although you might expect allergies to weaken the BBB, rather than strengthen it; but the body does plenty of strange things.  So a second daily dose of Bumetanide just might help.  In France, the autism researchers working with Bumetanide do give it twice a day.

The simplest method to reduce the “brain allergy effect” would be to just avoid the allergen(s).  In the case of Monty, this would be to go and live in a low pollen environment, and perhaps even avoid cats.

Since 30+% of people with autism apparently suffer from asthma, then 30% of people with autism might also find behavioral relief by avoiding pollen.  Those suffering from aggression and SIB would very likely benefit dramatically from Verapamil.

This might also suggest that residential facilities for people with severe autism should be in low pollen areas.

Incidentally, our local special needs school used to be surrounded by a rampant overgrowth of ragweed/ambrosia.  This is one of the most notorious plants for causing allergies in humans.  The current number 1 in the ATP world tennis rankings then gave them some money to tidy up the grounds.  Coincidentally, like many of the “inmates”, he also favors a gluten free diet.