Showing posts with label Lovaas. Show all posts
Showing posts with label Lovaas. Show all posts

Tuesday 15 December 2020

Fine tuning Social Behavior in Autism with an existing pediatric drug, Desmopressin?


There are two closely related hormones, vasopressin and oxytocin, that have been extensively researched in autism. 

With oxytocin you can modify social-bonding behavior. You can increase oxytocin in the brain either via a nasal spray containing oxytocin, or you can add a specific bacterium to your gut that triggers a signal to the brain to produce more of its own oxytocin.  The latter is my preferred method, because you can produce a mild long-lasting effect throughout the day.

Oxytocin has a very short life and it does not cross the blood brain barrier.

There is even a new study in the works that will compare these two methods of treating autism.


Probiotics and oxytocin nasal spray as neuro-social-behavioral interventions for patients with autism spectrum disorders: a pilot randomized controlled trial protocol

Autism spectrum disorder (ASD) is a complex neurodevelopmental disorder characterized by impairments in social interaction and communication. Oxytocin (OXT), as a neuropeptide, plays a role in emotional and social behaviors. Lactobacillus reuteri (L. reuteri) supplementation led to an OXT-dependent behavioral improvement in ASD mouse models. Despite some promising results from animal studies, little is known about the efficacy of supplementation with L. reuteri, alone or with exogenous OXT therapy, on social-behavioral functions in ASD patients. This paper presents a protocol for a pilot randomized controlled trial to evaluate the feasibility of conducting a full trial comparing oral supplementation of L. reuteri probiotics and intranasal OXT spray to placebo on the effect of social and behavioral functions in ASD patients. The study will also capture preliminary estimates of the efficacy of the proposed interventions in ASD patients.


This pilot trial is a two-staged, randomized, double-blind, placebo-controlled, parallel-group study. Throughout the study (0–24 weeks), 60 patients with ASD will be randomly assigned to receive either oral L. reuteri probiotics or placebo. In the second study stage (13–24 weeks), all participants will receive intranasal OXT spray. As primary outcomes, serum OXT levels will be assayed and social behaviors will be assessed via the Autism Behavior Checklist and the Social Responsiveness Scale which are validated questionnaires, an objective emotional facial matching test, and a new video-based eye-tracking test. Secondary outcomes include the GI-severity-index and Bristol Stool Chart to assess GI function and gut microbiome/short-chain fatty acids. All the outcomes will be assessed at baseline and weeks 12 and 24.


This pilot study will provide important information on the feasibility of recruitment, blinding and concealment, treatment administration, tolerability and adherence, specimen collection, outcome assessment, potential adverse effects, and the preliminary efficacy on both primary and secondary outcomes. If successful, this pilot study will inform a larger randomized controlled trial fully powered to examine the efficacies of oral L. reuteri probiotics and/or intranasal OXT spray on social-behavioral improvement in ASD patients. 

My conclusion was to add two drops of L.Reuteri DSM 17938 (Biogaia Protectis) into the liquid part of my son's Polypill therapy. That way there are no extra pills to swallow and in theory the bottle should last 50 days, so I am not forever looking to buy more.  If you want a bigger effect, just add more drops.  The producer suggests a daily dose of 5 drops for babies, to promote GI health - the original intended purpose.

When it comes to Vasopressin it looks like you cannot avoid a nasal inhaler, unless you want to try transcutaneous electrical acupoint stimulation (TEAS).  There is a debate as to whether Vasopressin and its analogs (man-made modified versions) can cross the blood brain barrier and to what extent. 

There are 4 previous posts that looked at Vasopressin. 

The Vasopressin showing good results in the trials at Stanford is the injectable pharmaceutical version of the hormone made into a nasal spray.  This kind of spray could be made easily at a compounding pharmacy.

It turns out that a synthetic analog of vasopressin, called desmopressin, has been widely used for over 40 years to treat nocturnal enuresis (night-time bed-wetting) among other more serious conditions.


Desmopressin in Autism 

Nocturnal enuresis is common in individuals with but to our knowledge, there are no reports that desmopressin enhances social functioning in ASD (or in any other clinical population). This may be because desmopressin is typically administered at bedtime (so prosocial effects would be less evident) and orally (oral desmopressin does not cross the blood-brain barrier). The most likely explanation, however, is that desmopressin acts selectively on AVPR2, rather than on AVPR1A”



A randomized placebo-controlled pilot trial shows that intranasal vasopressin improves social deficits in children with autism


Desmopressin N=1 example 

I was recently contacted by the father of a young boy with autism who has been prescribed Desmopressin nasal spray by his neurologist.

The father noted major positive behavioral changes from the first dose.

This is of course great news.

Desmopressin is a widely available drug, seen as safe, and that is why it is prescribed to children.

In the US the nasal spray version is no longer widely used for children and they use the oral version.

In some countries it is used for people with MS (Multiple Sclerosis) with nocturnal enuresis.


Desmopressin Shortage

Before readers get too excited, Ferring Pharmaceuticals, the big producer of Desmopressin nasal sprays did voluntarily withdraw its brands (Minirin, DDAVP Nasal Spray, Desmopressin Acetate Nasal Spray) from the market in August 2020 due to a quality problem.


There is now a shortage and so what was an easy to obtain drug, may be more difficult to get.  There is a Pfizer version called Presinex.  

From the above paper on vasopressin for autism:-

Vasopressin benefits 

“In conclusion, the present pilot study determined that 4-week intranasal AVP treatment compared to placebo enhanced social communication abilities, diminished anxiety symptoms, and reduced repetitive behaviors in children with ASD. On nearly all behavioral measures, participants with the highest pre-treatment blood AVP concentrations benefitted the most from AVP treatment, suggesting that pre-treatment blood AVP concentrations may be useful for setting dosing guidelines for this medication. Last, intranasal AVP treatment was well tolerated with minimal side effects in this pediatric study population. These preliminary findings suggest that intranasal AVP treatment has potential to enhance social abilities in an ASD patient population characterized by currently intractable social impairments” 

Transcutaneous electrical acupoint stimulation (TEAS) to raise vasopressin 

“there is evidence that nonpharmacological interventions may facilitate endogenous AVP release, for example, electroacupuncture stimulation increases brain AVP concentrations in rats. Transcutaneous electrical acupoint stimulation (TEAS) therapy improves social functioning and anxiety symptoms in children with ASD, particularly in those with the largest post-treatment increase in blood AVP concentrations. The authors of this prior report theorized that increased AVP signaling may be the mechanism by which the prosocial and anxiolytic benefits of TEAS treatment were achieved” 


Vasopressin with Bumetanide  - take great care

A while back, one reader did ask me about taking intranasal Vasopressin with Bumetanide.  His doctor in California thought this might not be wise since the two drugs have opposing effects.

·        Bumetanide (a diuretic) makes you pee more.

·        Vasopressin (the anti-diuretic hormone) makes you pee less.

The real problem is the risk of low sodium, hyponatremia.  This is always a risk with vasopressin and the risk might well increase if you took Bumetanide.  The risk is going to be dose dependent.

If you take Vasopressin and then drink large amounts of water this will disturb the volume of fluids in your body and in particular it will lower the level of sodium.  This may lead to seizures and ultimately worse.

Bumetanide does disturb the level of electrolytes, but nearly all the change usually occurs in Potassium, this is why you need to add back potassium via diet and add a supplement.  Sodium is not normally a problem, but always check all electrolytes when taking a blood draw.

If someone adds vasopressin to their existing bumetanide therapy, the doctor should definitely monitor the level of sodium.

In most people’s diet, sodium is one thing you are likely to have too much of and it is very easy to add a bit more sodium if the blood test suggests it is necessary.  In extreme cases of low sodium you need to use a special re-hydration drink, or an intravenous saline solution.  Monty has a relative who keeps going to hospital for the latter.

The diuretic action of Bumetanide is a side effect of the "autism effect" and so if you can reduce the diuresis of bumetanide that would be good thing.  Researchers are trying to find a better-bumetanide and their goal is to have no diuresis.

If combining vasopressin with Bumetanide is accompanied by both reduced diuresis and a matching reduction in fluid intake, this might actually work well.  Clearly, extra care needs to be taken and what might be perfectly safe in one person may not be safe in another person.



I do have to give a big thank-you to our reader who shared his experience with Desmopressin and to the neurologist for suggesting it.

Desmopressin looks like one of those autism therapies that needs only a very short trial to determine whether it is beneficial.  This is a big advantage.

You would hope the Stanford vasopressin researchers make a short trial of Desmopressin, just to compare the effect.  They probably will not.

All you have to decide is whether it is going to be the left nostril, or the right nostril.  With intranasal insulin there was a problem with irritation inside the nose, so alternating left and right sides might be best.  You hold your breath and then squirt the spray; the objective is not to breath the spray into your lungs.  An easy mistake to make.

Note that I am referring to the 10 mcg/0.1mL Desmopressin nasal spray.  The one used to treat kids that wet their bed at night.

There is also a much more potent 1.5 mg/mL version, called Stimate in the US.  This is used to treat von Willebrand’s Disease (Type I) and hemophilia/haemophilia.  You do not want that version.  This version is 15 times more potent than the anti bed-wetting variant. 

I have been suggesting to Aspies living in the US that they give Vasopressin a trial to counter the social deficits that some find troubling.  I think they are able to obtain this via a compounding pharmacy, with a helpful doctor’s prescription.

I think outside the US your doctor will think you are mad if you ask for a specially compounded vasopressin nasal spray, or indeed a compounded  oxytocin spray.

For people unable to get the intranasal vasopressin prescribed/compounded, Desmopressin is on option to discuss with your doctor. Maybe time to develop a bed wetting problem?

The Aspies in the Netherlands have the legal option of a tiny non-hallucinogenic dose of Psilocybin once a month, which seems an effective way to target Serotonin 5-HT2A receptor-mediated pathways and so improve social behavior. What caught my attention was that the effect of this tiny dose lasts a month and it can also be used to treat severe, otherwise untreatable, cluster headaches.

Psilocybin is the fancy name for magic mushrooms.

Psilocybin is also legal in Brazil and not surprisingly in Jamaica.  It looks like the US is moving in the same direction - medicinal magic mushrooms!

FDA grants Breakthrough Therapy Designation to Usona Institute's psilocybin program for major depressive disorder

The “medical” dose of Psilocybin is a tiny fraction of the “recreational” dose and is only taken when the effect of previous dose fades to zero.  It is not a crazy idea at all, just not currently a legal therapy in most countries.  More than half a century ago Lovaas was researching something very similar at UCLA, but using LSD.

All told, there are several potential ways to fine-tune social behavior in autism. Sulforaphane is yet another option.


Monday 3 August 2020

Why is the evidence for Early Intensive Behavioral Intervention for Autism so weak?

One to one autism therapy is pricey – is it worth it?

Only a handful of countries widely apply behavioral interventions to treat toddlers diagnosed with autism.  Behavioral interventions include Applied Behavioral Analysis (ABA), Verbal Behavior (VB), Pivotal Response Treatment (PRT) and the Denver model.

Even after several decades, the published evidence that these interventions actually work is quite weak.  This explains why most countries do not readily provide public funds for ABA.

In the US, efforts are being made to diagnose autism at younger and younger ages, because the child can then benefit from these “proven” interventions, that other countries do not believe work.  Who is right?  

You can read Manuel Casanova’s perspective at the end of this post.  He is not such a fan of expensive US developed therapies and concludes:-
"spending time with your children and group socialization, in my experience, have provided the most favorable outcomes"

Does ABA work?  If so, why can’t you prove it?

From my personal experience, behavioral intervention was very beneficial as a teaching method, but it does not make autism go away.

In today’s study the aim was to determine if behavioral intervention is cost effective.  The conclusion based on all the studies considered is that there is no conclusive evidence that behavioral intervention is cost effective.  So logically the countries that do not widely fund it, like the UK, can be reassured that they are on the “right side” of the argument.

My view is that is that autism is so heterogeneous you can prove almost nothing, with any degree of certainly.  It is always going to be a case of ifs, buts and maybes.  This also very much applies to clinical trials of drugs to treat autism.

Why did ABA ever catch on in the first place?  People want hope and the more expensive something is, the more people want it.  Forty hours a week of ABA is very expensive and nice to have, if someone else is paying.  

We saw in an earlier post that Lovaas (the founding father of ABA) later admitted to selectively retiring non-responders from his clinical trials, to improve the apparent success of his methods.  This pretty much means you have to ignore all his data and his papers should be retracted. 

Many parents want curative treatments for autism.

Lovaas claimed that ABA is curative and that the treated kids end up like typical kids.  Sadly, this is an exaggeration.

Is two years of ABA cost effective for severe autism?  I guess it depends whose money is paying for it.  Is two years of ABA going to be life changing for a person with severe autism?  Unfortunately, even after 20 years of ABA, that person will likely still have severe autism, if you have not treated their underlying biological problems.

Some parents rave about ABA and make comments like “after two years of ABA my son now makes eye contact”.  Great, but would you pay $120,000 of your own money for that?  I think not.  Should your local government regard that as money well spent?  I think they should be more demanding; the results of just $1,000 spent on the right personalized medicine will be much more impressive.

Today most people currently being diagnosed with autism have mild cases.  If they can talk and do not have intellectual disability (ID) / mental retardation (MR), they will likely see little benefit from 40 hours a week of discrete trial training.  It would be a huge waste of money and probably just annoy the child.  

Many children with mild autism need a different kind of therapy, they need to learn social and emotional skills they may not naturally possess - how to make friends, how to avoid making enemies and so how not to get bullied at school.  This will only be effective started very young, before being a victim becomes a badge of honour.

Autism is a lifelong condition that affects how people understand the world and interact with others. Early intensive applied behaviour analysis-based interventions are an approach designed to help young (preschool) autistic children. This approach is often delivered on a one-to-one basis, for 20–50 hours per week, over a period of several years.
This project obtained and analysed the original data from studies of early intensive applied behaviour analysis-based interventions, to determine whether or not these interventions are beneficial. It also investigated whether or not the interventions represent good value for money.
The results suggest that early intensive applied behaviour analysis-based interventions may improve children’s intelligence, communication, social and life skills more than standard approaches. However, some results could be inaccurate or incorrect, and there was no evidence about other important outcomes, such as the severity of autism and where children went to school. Most studies lasted for around 2 years, which means that it is not known if early intensive applied behaviour analysis-based interventions have meaningful long-term benefits.
It was not possible to fully assess whether or not these interventions provided value for money, as the benefits of early intensive applied behaviour analysis-based interventions were unclear, although the available evidence suggested that they did not. Early intensive applied behaviour analysis-based interventions may, however, provide value for money if their effects were to last into adulthood, or if receiving early intensive applied behaviour analysis had a large impact on the type of school children attended.
Future studies of early interventions may be helpful, but should consider looking at which components of early applied behaviour analysis-based interventions are the most important, rather than at whether or not they work better than other interventions. Future studies should also follow best current research practice and evaluate outcomes that matter to autistic people and their families. 

Economic evaluation

Using National Institute for Health and Care Excellence decision rules to benchmark the results of the cost-effectiveness analysis and adopting a £30,000 (USD 40,000) per quality-adjusted life-year threshold, these results indicate that early intensive applied behaviour analysis-based interventions would need to generate either further benefits or cost savings to be considered cost-effective.

Implications for service provision

Although individual participant data meta-analyses have shown small to moderate improvements in child cognitive ability and adaptive behaviour for early intensive applied behaviour analysis-based interventions relative to treatment as usual or eclectic approaches, all of the identified studies were at risk of bias, limiting the strength of conclusions that can be drawn from these results. Furthermore, results from individual studies varied considerably, with some showing no relative benefit of early intensive applied behaviour analysis-based interventions. 


For cases of severe autism, if you can afford intensive (and expensive) 1:1 intervention of any credible kind (Floortime, ABA, Denver etc - whatever works best in your case) it makes sense to use it.  It should improve skill acquisition and will make the parents feel better.

None of these interventions are curative, the child will still have autism.  When you no longer pay for the 1:1 intervention, the effects most definitely will start to fade away.  Don’t mortgage your house to pay for ABA.

Nothing stops you making your own 1:1 intervention program using family, friends and volunteers.  This does not cost much and is sustainable over many years; it is likely to be much for effective that 2 years of "professional" therapy.

I do find it odd that in the US there is free early intervention for toddlers and then provision just stops, as if it suddenly is no longer needed.

If you use ABA to teach a child to tie shoe laces, he/she will retain the skill as long as you keep buying shoes with laces.  If you do not practice/apply the skill for 6 months, do not be surprised if it has to be re-taught.

Our final ABA consultant was very experienced, she worked for 10+ years in the US before moving home to Athens, Greece.  She told me that in her experience all children with autism benefit from ABA, but the level of progress they make varies widely.  If a child does not respond to ABA, it very likely is not being done correctly.  ABA should be seen as fun, not like a punishment. If your child hates ABA sessions, they have no chance of working.

I come back to my earlier recommended strategy. Find your most effective novel medical treatment, which will inevitably be a polytherapy and combine this with a method of learning that works best for your particular child.

Then just keep going and let time do its work.

In countries like the UK, with free health and education provision, the government does not generally pay for early intervention because their medical advisors do believe it to be cost effective, which really means they think it does not work and so do not want to pay for it.  The cynic might just say they do not want to fund it. 

The idea was supposed to be that by investing upfront in ABA during the early years, you save money later on, by having a more functional child and then adult who requires less expensive provision.  Unfortunately, there is absolutely no proof this is true.  

If you go from early intervention, to an ABA special school and then ABA college, things clearly did not work out.

In the US early intervention is assumed to be very effective and the current idea is that doctors should hurry to diagnose autism before 24 months so as to get into the intervention program as soon as possible.  Where is the evidence to support the US view?  Are US outcomes any better?

We saw in recent research from UC Davis that looked at outcomes over time in autism that the best outcomes are not associated with any particular therapy.  The best outcomes happen because of the biological characteristics of that child, rather than any amount of behavioral intervention.

I expected the UC Davis study to show a relative benefit for those who received ABA therapy, but it did not.  We do have to take note.  I am actually pro-ABA and have spent a vast amount of money on this kind of therapy and 1:1 instruction.   

Ignoring treating the biological dysfunctions in autism while spending hundreds of thousands of dollars on 1:1 therapy and special education does not make a lot of sense.

Here is a relevant excerpt from a recent post by the neurologist, autism researcher and autism Grandfather, Manuel Casanova, from his Cortical Chauvinism blog: -

Despite marked differences in geography, non-Westernized countries see autism as a social responsibility rather than a medical condition.  These countries offer a collectivist perspective that downplays individuality and prioritizes maintaining relationships within a given group of people.  In this regard, I have often marveled as to how vastly different countries, like Colombia and the more desolate regions of Eastern Russia (Siberia), share similar perspectives regarding autism. Indeed, due to a lack of resources, interventions in these countries are usually parent-mediated and heavily influenced by cultural norms.  Lack of personnel trained in behavioral analysis has been supplanted by art and music instruction.  Classes are provided in group settings where outperforming other members is not seen as conductive to the overall benefit of the group. Members are encouraged to adopt the norms of the group while teachers emphasize cooperation and nurturing. Students arrive early to school to participate in team building exercises.

I have often marveled at the achievements of troupes of autistic children performing autochthonous musicals and their accompanying choreography.  Adopting the norms of the group have served them far better than any Westernized behavioral intervention.  Participants in these groups seem genuinely happy; in part, given the sense of achievement at contributing to a piece of artistic expression.  In addition, the structured activities in such groups offer norms that minimize uncertainty.  Participants feel a sense of security in a group that fast becomes their extended family.

Autism is a medical condition but, without a cause that we can target, treatment options have remained symptomatic.  This is one of the reasons for looking at other countries and learning what has worked for them.  Indeed,  I believe that we can gain from adopting the cultural perspective of other countries to benefit our own children. Whether it is an improvisation on an autism chair, electroacupuncture, or using a zen bowl, spending time with your children and group socialization, in my experience, have provided the most favorable outcomes.

Manuel is one of a very small group of thoughtful researcher-clinicians, who have been working in the field of autism for decades, like Dr Kelley from Johns Hopkins and that psychologist Dr Siegel who wrote the Politics of Autism and revealed how Lovaas really did his "research". 

Manuel's researcher son-in-law is interested in precision medicine and drug re-purposing, I guess driven by his own young son's rare genetic "autism", NGLY1 deficiency. This very severe condition leads to the body not being able to breakdown and remove damaged and misfolded proteins.  You would think that reducing Endoplasmic Reticulum (ER) stress, that produces misfolded proteins, might be useful. This was covered here, along with a long list of possible therapeutics:-

Some readers are following the details of the Covid-19 situation.

The Indian Experiment rather than the Swedish Experiment

A recent study suggests that more than half of the 6 million slum dwellers in Mumbai have had Covid-19; another 6 million do not live in slums. Government research showed that in the capital Delhi 23% have Covid-19 antibodies.

Mumbai slums have an extremely high population density, extreme poverty and so not much social distancing. So they show what Covid-19 does with no serious intervention, better than Sweden does.  Mumbai has reported 6,200 deaths in total.

You can extrapolate from the data (57% of slum dwellers and 16% of non slum dwellers with Covid antibodies) for the total 12 million population of Mumbai.  4.4 million had the virus and 0.14% died.  In the worst case scenario, when everyone finally gets infected in the next few years, there would be another 7.4 million with the virus and another 10,800 deaths.  The death/mortality rate for the city would be 0.14%.  (In reality it will probably be less than 0.14%, because some people will not get the virus)

The 0.14% Covid-19 mortality rate compares to the 2.5% mortality rate of the 1918/9 global flu pandemic; worse still that flu pandemic affected fit young people the most, making the demographic impact huge. 

The crude death rate from all causes in the US is around 0.8% each year (just 0.7% in India).  That puts the 0.14% from Covid-19 into some perspective. If Americans are as healthy as Indians and India did not under-report the number of Covid deaths in Mumbai (both are big ifs), you could apply the 0.14% mortality from Covid-19  to 330 million Americans and get 460,000 people. I think the realistic number would be higher, given deaths to date in the US.  

I think the world has been very lucky to have been affected by a pandemic that has such a low mortality rate.  It could easily have been 20 times worse, perhaps next time?  In the Middle Ages, the Black Death killed hundreds of millions of people - a truly apocalyptic pandemic.

There is no certainty that a vaccine is going solve the Covid-19 problem, indeed the UK government is buying 12 different vaccines, in the hope that one is effective.  Vaccines are often least effective in older people, who are main risk group for Covid-19.

If no vaccine turns out to be 90% effective, the Mumbai slum dwellers and the Swedes will have been the smart ones.

Controlled Infection vs Vaccination

If I was a dentist I would be seriously worried about Covid-19. I would favor a small infection today, caught from my party-going offspring, rather than in two year's time catch it while peering into a stranger's mouth during an hour long procedure, and get a huge initial exposure, leading to a more severe infection.  The fact that Mumbai policemen, London bus drivers and of course doctors and nurses without good PPE have had so many fatalities does suggest the amount of virus you are initially exposed to is a critical factor to the outcome.  This would be logical anyway.

I am really glad at least my older son and myself have had Covid-19.  If I was a dentist, I would be hugely relieved. A few months ago we assumed Covid-19 was both highly infectious and often deadly, now we know the reality.  If you are youngish, slim and healthy the risk is very low.  Many in rich societies are old, overweight and in poor health.

I did take my younger son Monty, aged 17 with autism, for a visit to the dentist two months ago and I really felt sorry for her.  She was wearing a mask, but that is no guarantee of her safety.  


Thursday 4 April 2019

A 15 year Longitudinal Study of French Autism and a look at Early Diagnoses of US Autism that Resolved

Today’s post is all about what to expect in the future; it covers a detailed look at 2 different studies that I think are best considered in a single post.

Forewarned is forearmed.

How high to set the bar?

In a recent post I highlighted the need for long term (longitudinal) studies showing what happened to people diagnosed with autism back in the 1990s in California and New York, when an autism diagnosis was much more meaningful and yet early intervention was already available. We could then see what the outcome was 20 years after diagnosis and this might help parents decide their own autism strategies for today.

I was encouraged to subsequently come across today’s study from France that traces the progress made over 15 years by a group diagnosed with autism.  I also include my take on a popular recent study that showed what “Optimal Outcome” looks like in American autism, but that looks just over a 4 year period.

Don’t raise your hopes.

All this leads to the practical question of how far to raise the bar? What should parents expect at diagnosis? What should clinicians be telling parents? and what kind of value is being delivered by hundreds of millions of dollars spent on early intervention and special schooling by each of many municipal authorities all over world. Is their spending delivering its potential return? Today's post suggests not.

Today we come across 2 autism rating scales. The Childhood Autism Rating Scale (CARS) is my long-time favourite; in this scale above 30 means autistic and if you get above 36.5 it is severe autism. If you come at 29 you have some features of autism but not enough to be diagnosed with even mild autism.

The Vineland Scale is a very scientific way to measure adaptive behaviour (life skills). These are really the most important skills you need to live semi-independently and have some kind of job.

The Vineland results really reflect what you are taught at school/home, rather than how “autistic” you are.  Vineland is not a measurement of IQ. You can be a functional adult who is still well and truly autistic and have had a CARS score of above 30 from diagnosis at 3 years old all the way to 18 years old.

If you are a genuine Aspie reading this, I very much doubt your CARS score was above 30 when you left high school. This is why Asperger’s has to be considered as a separate category.

The French Study

The way autism was treated in the 1990s and early 2000s in big cities in California was very different to how it was, and is, treated in France. In France hospitals and psychotherapy played a major role, whereas in the US it was and remains all about ABA early intervention.

The outcomes in France for the top 20% are not stellar, but they are actually quite OK, they end up at 20 years old with the adaptive life skills of a 13 year old. The results for the remaining 80% in the lower group show adaptive behaviour / living skills of a 2-3 years old at the age of 20.  The percentage with severe ID/MR (IQ less than 70) increased from 49% to 78.2% at the age of 20.  In effect virtually the entire lower group, that makes up 80% of the study participants, leave school with mental retardation / intellectual disability.  That is a lot.  I did highlight in earlier posts that people with severe autism usually see their IQ fall as they get older, because IQ tests gets harder as you get older and people with severe autism acquire skills more slowly than their typical peers, so they inevitably fall further behind.  

The good news was that 5.4% of the cohort lost their autism diagnosis by age 20 and all without any ABA. Time and time again we see that some people age out of their autism.

Not surprisingly, the higher your IQ and verbal skills at diagnosis the better your outcome will be.  The most dramatic progress occurs before the age of 8.  This we already knew and it is attributed to the brain being more plastic in early childhood, allowing a greater degree of self-repair.

The average CARS total score of the entire group was 35.7 on diagnosis. On CARS autism scale 30 is the threshold for an autism diagnosis. Mild to moderate autism is 30 to 36.5.

You cannot make the case that this group performed poorly because they were all profoundly autistic, some were, but that was balanced by some with mild autism. As a group they were likely more severe than a group diagnosed with autism aged 3 in California in 2019.

By diagnosing at 2 years old and sometimes even younger, there will be a sub-group included whose very plastic brains were on track to self-repair, so that they would never have been diagnosed with autism in most countries, which wait till 3, 4 or even 5 years old to make a diagnosis.

Another key point here is that very likely a large proportion of 2019 autism diagnoses in the United States would correspond to a CARS score less than 30, but nobody bothered to measure it. As Dr Siegel suggests, their parents are now incentivized to want a diagnosis.  It is like a quirky badge of honour, with benefits.

There is limited data on long-term outcome of ASD with co-occurring intellectual disabilities (ID) and challenging behaviours in France. The EpiTED period cohort is a 15 years longitudinal study of the developmental trajectories of 281 children initially recruited at mean age of 5 years. Two contrasted developmental trajectories were identified. Low cognitive level, absence of language, and higher ASD scores at baseline were predictive of low growth at follow-up. As adults the participants were predisposed to persistent co-occurring challenging behaviours as well as underlying ID impacting their ability to function independently. The results underscore the need for development of services and supports for adults with ASD in France who may also have already lacked access to adequate interventions and support services.

The inclusion criteria in the EpiTED cohort were: (a) index child age below 7 years; (b) parental informed consent; (c) diagnosis of childhood autism, atypical autism, or Asperger Syndrome according to ICD-10 criteria (atypical autism corresponded to at least two domains of impairment according to ICD-10 criteria) (World Health Organization 1993) (autism will be subsequently referred to as ASD unless specifically signifying subtype). All diagnoses were validated by two independent, experienced child and adolescent psychiatrists among the research staff (including AB), on the basis of medical records, as well as videotaped observations during enrolment. Subjects for whom a consensual diagnosis could not be obtained or those for whom the date of appearance of ICD-10 autism symptoms emerged after 3 years were not enrolled. Between 1997 and 1999, among 362 eligible children, 281 with ASD (77%) aged between 3 and 7  years fulfilled the research inclusion criteria (T1); 62 children were excluded as they did not meet research inclusion criteria; 19 children (families) had moved away prior to enrolment and were also excluded.
The index children were followed prospectively over 15 years with four assessment points: ages 5 (T1), 8 (T2), 15 (T3), and 20 (T4) years (see flow chart, Fig. 1). At T2, from 2000 to 2002, 219 of children were reassessed; at T3, from 2007 to 2009, 152 adolescents were reassessed; and at T4, from 2012 to 2015, 106 young adult subjects were reassessed.

The primary outcome measures of the study were the standard scores in the three domains of the vineland adaptive behavior scale (VAB-S) (Sparrow et al. 1984). This scale is widely used to assess adaptive skills in different areas (daily living, communication, socialization and motor skills) in individuals from birth to adulthood including those affected by intellectual disabilities or ASD. VABS scores recorded at each of the follow-up times were used to identify developmental trajectories in communication, socialization, and daily living skills

ASD symptom severity was assessed using the total score of the childhood autism rating scale (CARS) (Eric Schopler et al. 2002), with scoring based on a 20 min and standardized video clip of the child interacting with an adult.

The diagnosis of ASD was stable (see Table 3): 94 (88.7%) subjects received a diagnosis of childhood autism and 12 subjects a diagnosis of atypical autism at T1; at 15 years follow up (T4), 82.6% of the cohort remained above the ADOS ASD threshold; 5.4% of the cohort lowered their ADOS scores under the ASD threshold; 12% of the cohort became “atypical autism”. Whereas the ASD diagnosis was remarkably stable between T1 and T2 follow up stages, most diagnostic changes occurred between T2 and T3. The ratio of participants without ID ranged between 7.5 and 22.5 according to measurement steps. Among the subjects with childhood autism, 59.6% were non-verbal at T1, with 39% remaining non-verbal at T4. With respect to comorbid ID, most changes occurred between 4 and 8 years of age. The proportion of children with either word/sentence language at T4 was 61%. The ratio of combined moderate and severe ID (IQ 20–25 to 50–55) measured by “best estimate” assessment of intellectual functioning was stable across time (around 80%), but the ratio of moderate ID (IQ 35–55 to 50–55) decreased from 27 to 5%, while that of severe ID (20–25 to 35–40) increased from 49 to 78.2% between T1 and T4.

Vineland Scale

Here below is an example tracking the adaptive development of a child with a disability.

If the child progressed 100% as a typical child in all three domains (communication, daily living skills and socialization) he/she would follow the sold black line at 45 degrees. If the child falls below expected level, then the line will track below the straight line at 45 degrees.

In the French data, the top 20% group reached the level of about 150 months of age by 20 years old. The Low growth group, which comprised almost 80% of the sample, reached the functional age of 24 months by the age of 20.

Fig. 2 Trajectories of adaptive level through adulthood among 94 participants of the EpiTED Cohort diagnosed as children. The figure shows the mean adaptive scores (CI 95%) over time for participants assigned to the two trajectory groups: _______Low growth group; ……………… lower CI 95%; - - - - - - - - upper CI 95%

The EpiTED is a unique prospective cohort of children with well-characterized ASD referred to five Departments in France. At the time of the cohort’s inception, the participating centers were the only public sites diagnosing and treating preschool children with ASD in the country. Although the cohort exhibited considerable rate of co-occurring ID, it must be noted that 20 years ago early diagnosis of high functioning children with ASD and interventions for them were not the norm in France. Therefore, children with ASD with more severe co-occurring levels of ID, communication, and adaptive impairments, so identified, were more likely to be referred to the study collaborating sites.
 Among the 106 study participants at the four collection time points, diagnostic stability was dominant, but not constant, and associated with a general improvement of ASD characteristics. However, the emerging trend in intellectual abilities, as measured by the best estimate procedure, was more unstable, with an increase of severe ID from 49 to 78.2%. This could result either from an actual decline of intellectual abilities, potentially and consequentially due to minimal exposure to educational interventions and learning opportunities (many children with ASD were historically excluded from mainstream education lacking access to support services), or alternatively as a result of lower performance scores on identical measures with advancing age, or both. While an improvement in adaptive skills measured by the VABS was the rule for the entire group, two contrasted developmental trajectories in adaptive functioning were identified. The majority of participants (around 80%) followed a low-growth developmental trajectory, with the remainder following a high-growth trajectory. Again, for majority of participants, a lower cognitive level, absence of functional speech, and increased CARS scores at T1 predicted a low-growth trajectory in communication, socialization, and daily living skills. Other studies have reported a similar relationship with IQ, non-verbal mental age, ASD severity and speech (Bal et al. 2015; Smith et al. 2012; Szatmari et al. 2015). Nonetheless, in the absence of studies on long-term effect of intervention, one cannot decide if this poor outcome is intrinsic to a fraction of the ASD population, or an effect of absence of interventions or limited exposure to learning opportunities. As regards co-occurring challenging behaviors, our results suggest that behavioral problems in children with ASD persist in early adulthood and are related to core symptom severity, levels of cognitive and language impairments, as well as medical comorbidities. The results also affirm that ASD symptom severity among adult subjects was a significant predictor of co-occurrence of challenging behaviors (Baghdadli et al. 2003, 2008). Another significant predictor was the presence of GI disorders. This is consistent with reports of a high correlation between the presence of pain and the frequency and severity of stereotypies (Courtemanche et al. 2016), as well as challenging behaviors in general (Chaidez et al. 2014). Nonetheless, these combined variables only explained at most 30% of the developmental variance observed in the study sample. Invariably, this means that other factors, not identified here, might explain the presence of challenging behaviors in adults with ASD. Additional research is needed to examine other influences, with particular relevance for the services and interventions in the community provided. It is of interest that for children with ASD, the main risk factors for self-injurious behaviour (SIB) were ASD symptom severity and cognitive level (Baghdadli et al. 2003, 2008). In the present study, the symptom severity remained a significant risk factor, but language skills instead of cognitive level predicted the presence of SIB. One possible explanation for this might be that SIB at adulthood may reflect a relationship with communicative deficits. This finding emphasizes the crucial role of communicative abilities and the need for targeted behavioural interventions for children with ASD aiming at developing better communication in order to prevent as well as manage subsequent challenging behaviours. The impact of having a child with ASD on parental QoL was strong with several implications not only on daily life but also on parental emotional well-being, lasting through adolescence through young adulthood. The results did not affirm that raising a child with ASD often leads to the breaking up of the parental relationship, as has been commonly believed. Overall, parental QoL at early adulthood appears to be mainly predicted by the presence of co-occurring challenging behaviours, whereas at adolescence parental QoL was also predicted by the children’s adaptive level, namely in communication and daily living skills. Again, the impact of co-occurrence of challenging behaviours on family life argues for the importance of implementing specific interventions targeting them at a younger age. In a functional behavioural assessment perspective (O’neill and Jones 1997), challenging behaviours are described as a way to obtain reinforcement or escape a negative experience, which is most of the time related to poor communication. From our perspective, the best way to prevent subsequent development of adverse behaviours is to propose specific treatment aiming at the development of communicative abilities in the very early years. It is also crucial to provide parental training and disability support guidance as parental involvement and knowledge is key predictive factor of parental satisfaction and performance (Renty and Roeyers 2006). We can hypothesize that the participants of the EpiTED cohort had limited access to this type of interventions, as the educational approaches have considerably changed since the children were included in this follow-up study 20 years ago (Happé and Charlton 2012). Finally, the EpiTED as a “period” cohort reflects the ASD diagnostic practices in France in the mid-1990s and in the ensuing two decades. High-functioning verbal individuals were frequently not given ASD diagnoses, due to the dominant use of alternative diagnoses in the French classification of mental health disorders (Classification Française des Troubles Mentaux de l’Enfant et de l’Adolescent, CFTMEA), particularly for verbal subjects, and the dominant influence of psychoanalysis. An important limitation of the EpiTED cohort therefore is that the prevalence of co-occurring challenging behaviours, ID, as well as associate medical comorbidity, including epilepsy cannot be representative of a contemporary profile of children with ASD that will be currently recruited from child and adolescent psychiatry services and ASD evaluation clinics in public centers. Nonetheless, the EpiTED cohort provides a distinctive portrait of French children with official diagnosis of ASD enrolled in public centers and how they fared over a 20-years follow-up as they became young adults. While there was improvement in their adaptive skills, the substantial social and communication difficulties among the children in the cohort tended to persist in adulthood reflecting the salient effects of non-specific, delayed or Journal of Autism and Developmental Disorders 1 3 absent interventions. As adults the subjects in the EpiTED cohort were noted to be predisposed to persistent challenging behaviours impacting their ability to be independent and have acceptable QoL. As the Government of France is increasingly recognizing the widespread shortcomings in services and supports for children with ASD and their families, the current EpiTED analyses underscore the need for service provision for adults with ASD as an urgent policy priority. This is a unique and relevant finding not only for researchers and clinicians but for policy makers in planning for the next National Autism Plan.

Conclusion on the French Study

This is French data that I think can be best considered as tracking outcome from DSM3-like autism. So it is Strictly Defined Autism (SDA), not the much broader 2019 type of American autism.

Based on my earlier review of the epidemiology of autism I found it roughly splits into 0.3% of all kids have Strictly Defined Autism (SDA), 0.3% have true Asperger’s (genuine little professors) and 0.4% have something in between. That takes us to 1% prevalence. In my opinion today’s figures of even greater than 2% prevalence include many people will very mild symptoms of ASD, so a likely CARS score of 25 to 29.  Beyond 1% is likely over-diagnosis, diagnosing for dollars, self-diagnosis, educational autism (school diagnosed), private psychologist diagnosis or whatever you choose to call it.

The Big Question

Would a 15 year longitudinal study in California (the home of ABA) look any better? In the next study at age 7 even the optimal outcome group did not look in any way “recovered”.  Perhaps by 20 years old things would look much better.

I would love to know and I keep an open mind.

Is French Autism therapy so much worse than in most developed countries? Different, yes; but is the result at age 20 any better in Germany, Italy, the United Kingdom or the United States?  How about some facts?

Now to the study on Optimal Outcome in US Autism

The sad news is that the US study only looks at outcomes of those with early diagnosis up to the age of about 7. The French study looked at all the way up to 20 years old.

Given those limitations of the US study, it does at least show us what the star performers look like at age 7. These are the ones that technically lost their autism diagnosis, but as you will read are still far from typical kids at the age of 7.

The study concerns the outcome for children diagnosed with DSMIV autism when then were 2.6 years old and then entered an early intervention program. Four years later about 9% no longer met the criteria for an autism diagnosis.

This loss of diagnosis is what we now seem to call “optimal outcome”. Today we get to see what optimal outcome means for those 9%, which accounts for the 38 children in the study.  So did 9% essentially “recover”?  Not really.

In research papers I usually skip to the data and what I saw was that of the 38 kids with “optimal outcome” only 10 were in mainstream school, without needing an assistant; that is what I would see as “recovery”. Those 10 kids are about 2% of all the 569 kids with an initial autism diagnosis.

Only 1% were free of any psychiatric diagnosis (ADHD, anxiety, OCD, MR/ID etc).  So, even optimal outcome does not look such a great place to be.

I wonder how many will be in mainstream school, without an assistant, when they are 16?  I think it will be more than 2%, I certainly hope so. I was expecting at least 10% would be mainstreamed without an assistant before they turned 7 years old.

Inner city New York is doing well diagnosing children so young and putting them into their early intervention program, but their results four years later look nothing like Lovaas suggested.

I am really surprised that more people did not lose their diagnosis. This sample is from New York where you might expect autism to be over-diagnosed and to have the best early intervention offerings.

Recall in the old post on autism with tics (Tourette’s type autism) that 6% of kids lost their diagnosis without any intervention.

If at 2 years old CARS is above 30 you have autism, if at 6 years old it has fallen below 30, you have lost your diagnosis and achieved “optimal outcome”.

A chart review was performed of 38 children diagnosed with autism spectrum disorder (ASD) by 3 years of age at an inner-city developmental program who subsequently experienced resolution of ASD symptomatology and no longer met diagnostic criteria for ASD at follow-up an average of 4 years later. 

Demographic, developmental/cognitive data, Childhood Autism Rating Scale, and Autism Diagnostic Observation Schedule data as available were reviewed from the initial diagnostic evaluation and at the time of follow-up. Services received by the children between the time of diagnosis and follow-up, educational setting at the time of follow-up, and emotional/behavioral and learning diagnoses made by the multidisciplinary team at follow-up were reviewed. The findings indicate that residual emotional/behavioral and learning problems were present at follow-up in the vast majority of children in this group and that the majority continued to require educational support.

Although autism spectrum disorder (ASD) has generally been considered a lifelong condition, it has been acknowledged for more than 40 years that some individuals with an early diagnosis of ASD do not meet criteria for the diagnosis at a later age. Lovaas used the term recovery to characterize the outcome of this group of children who received intensive behavioral intervention and later could be educationally mainstreamed and had average Intelligence Quotient (IQ). The term optimal outcome was coined by Fein to characterize a group of 34 individuals with early ASD whose later social functioning could not be distinguished from typical controls and who appeared to be cured of ASD. Follow-up studies have spoken of varying degrees of learning or emotional vulnerability that continue in the “positive outcome” populations, including attention problems and language problems. More recently, a long-term follow-up study of 198 children diagnosed with ASD at ages 2 to 4.5 years found that 17 children no longer met the criteria for ASD at the 2-year follow-up. Later, when the children were about 10 years of age, parents were interviewed by phone regarding the children’s school age needs. Based on parent report, all 17 children continued to have some type of ongoing developmental and/or neuropsychiatric challenge.

The goals of the current study were to further characterize the residual learning, cognitive, and emotional/behavioral diagnoses as well as the range of educational supports required at school age in a group of children with a history of an early diagnosis of ASD that resolved.

Demographics The 38 subjects of this study represented 7% of the 569 children receiving an early diagnosis at the center in a 10-year period. (In order to provide a real denominator for calculating the percentage of children no longer meeting criteria for ASD at follow-up, we need to know the number of children of the 569 who actually came for follow-up. Unfortunately, a change in our program’s clinical affiliation since the original cohort was studied with resultant changes in the charting system does not allow us to establish the exact number of the 569 children who came for follow-up. Our best estimate of the follow-up rate is on the basis of a prior study involving a subset of 108 children from this group of 569 who were diagnosed by 24 months. The follow-up rate for that group was 71%. Utilizing the 71% follow-up rate, the 38 children no longer meeting criteria for ASD would represent 9.4% of the sample.) The mean age of the sample was 2.6 + 0.9 years of age at initial diagnosis and 6.4 + 2.8 years at follow-up. The sample was 80% male with a diverse demographic representative of the community served: 36% self-identifying as Caucasian, 44% Hispanic, and 10% African American. Forty-six percent of the sample had Medicaid, and 42% were bilingual (Spanish and English). Eighty percent of the children received Early Intervention services (most commonly weekly special instruction for 1 hour per week and twice-weekly speech and occupational therapies) and 39% had received Applied Behavioral Analysis.

The above chart shows that the CARS evaluation of autism severity fell below the cut-off point of 30 and generally there was an increase in IQ of about 10.  So the kids became less autistic and a bit smarter. Severe autism starts at a CARS score of 36.5, you can see that these kids were only mild to moderate autistic at the time of their initial diagnosis.

One child went from CARS of 38 to CARS of 27. His parents should be very happy. He went from very serious autism to trivial autism.

Follow-up Evaluation Results

At follow-up, it was the clinical impression of the multidisciplinary team using DSM IV that none of the participants continued to meet criteria for an ASD diagnosis. Mean Childhood Autism Rating Scale score at follow-up for the group was 25+ 4, with 30 being the cutoff for ASD (Table 1). On the Autism Diagnostic Observation Schedule (available in 23 of the 38), all available scores were in the non-autistic range. However, other diagnoses were present (Table 2). Only 8% (n ¼ 3) of the children warranted no diagnosis other than having had a history ofASD. Sixty-eightpercent (n¼26) had language/ learning disabilities, 49% (n ¼ 19) of the children were diagnosed with externalizing behavior problems (attention-deficit hyperactivity disorder [ADHD], oppositional defiant disorder, disruptive behavior disorder), 24% (n¼9) were diagnosed with internalizing problems (mood disorder, anxiety disorder, obsessive compulsive disorder [OCD], selective mutism), and 5% (n ¼2) were given a significant mental health diagnosis (psychotic disorder not otherwise specified). Sixty percent (n ¼ 23) of the children received 2 diagnoses, with the most common combination being language/learning disability and ADHD. Follow-up cognitive testing, available in 33 of the 38 participants (Table 1), revealed that none of the children functioned in the range of intellectual disability, including those who previously tested as delayed on the Bayley. The average Full Scale IQ of the sample at follow-up was 93+14; 6% (n ¼ 2) scored in the borderline category; 27% (n ¼ 9) in the low average range; and 67% (n ¼ 22) in the average range (Table 1). The mean Verbal IQ of the sample at follow-up was 92+14 and mean Nonverbal IQ was 95+12 (Figure 1).

Follow-Up Educational/Academic Setting
Information regarding academic setting at follow-up was available for 34 of the 38 children: 26% of the children (n ¼ 10) were in a mainstream class, 13% (n¼5) were in a mainstream class with assistant teacher support, 29% (n ¼ 11) were in an integrated co-teaching (ICT) or collaborative team teaching (CTT) class/or received resource room, and 21% (n ¼ 8) were in a self-contained classroom (Table 2).


A given for this study is that there is a subset of children with an early ASD diagnosis who show a categorical improvement in their original social communicative impairment, such that they no longer manifest a social communicative impairment impacting on their functioning at some later point. Such a phenomenon has been repeatedly documented for a small group of children with ASD. Less clear has been whether children with this history continue to experience residual learning and emotional/behavioral problems. The findings of this small sample suggest that at least in the early elementary years, such residual problems are very common for this group. In this sample, although the loss of the ASD diagnosis was associated with gains in cognition, the vast majority of these children who experienced resolution of ASD continued to manifest symptoms of other emotional/behavioral and/or learning diagnoses (92%) and continued to require educational supports (74%).

Though it has been reported in multiple studies that a small subset of children with early ASD improve in terms of their social functioning and no longer warrant a diagnosis of autism,11 this persistent finding continues to beg severalquestions: Was autism overcalled in these children to begin with? Are some children better able to respond to intervention? Does the specific intervention the child receives contribute to outcome? All are possible. Based on our experience, our sense is that the symptoms evolve—in some children in response to intervention, in others due to their individual developmental trajectories. And who is most likely to evolve in this positive direction? Those with the mildest symptoms to begin with. This study as well as previous studies all support that it is the children with milder autistic symptoms who are most likely to follow this pattern of resolution of autistic symptoms. The milder forms of autism likely serve as a holding area. There, children await the emergence of the signs and symptoms of a more specific developmental or emotional-behavioral condition—whether that is language/learning disability or emotional-behavioral disorders that require more language, cognition, and increased behavioral expectations in order to be specifically identified and diagnosed. A 2-year-old simply does not have sufficient language or cognition to manifest the signs of schizophrenia, or to give voice to anxiety

Conclusions on the US and French Studies

I think that clinicians and therapists can too easily take cover behind the accepted mantra that each case of autism is unique, to justify why little Charlie did not make the hoped for miraculous “recovery” or achieve what Lovaas claimed as the outcome for 50% of such kids.  

In the wider world there is a concept of benchmarking performance, so you can see how your product or service compares.

Whoever is paying all these hundreds of millions of dollars in early intervention should demand proof of their effect. I myself do not see any proof.  The results overall look pretty terrible. Time to start treating severe autism medically?

By studying the trajectories of just a thousand kids from diagnosis to adulthood, you could reliably say what is typical and what you might expect in the upper and lower quartiles. Then you could look at the effect of different types of therapy and schooling. Nobody has done this, clearly too much bother and it would take many years.

My conclusion is that the bar has been set very low, too low. To be a star performer you do not have to be as dramatically improved as you might think.

I would love to know what percentage of these 569 kids from New York will go on to get a driver’s license.

Apparently, in the US we can expect about a third of those with an autism diagnosis, but no learning disability, to go on to pass their driving test.  I fail to see how you can safely drive a car in a busy city if you could not attend mainstream school without an assistant.

People diagnosed with autism at 3 years old versus 11, 21 or even 51 years of age have a completely different scale of disorder. I do not believe many of those diagnosed in later years would have ever had a CARS score of more than 30. 

I think if CARS needs to be 30 or greater to warrant an autism diagnosis, people with a lower score should not be given an autism diagnosis. I think this would immediately reduce the incidence of autism in the US by half, back down to the 1 in 100.

Why are not all children given a CARS assessment as part of their diagnosis? An ancestor of mine created a scale (the Baron score) used today to assess the severity of ulcerative colitis when carrying out an endoscopy. If a gastroenterologist can be bothered to give your ulcers a score, why cannot the developmental pediatrician or child psychiatrist?

Perhaps we should add a new label for CARS between 25 and 29; perhaps a “teeny tiny bit autistic”. Yes, you too can be on the spectrum, but don’t confuse your case with that of people with CARS above 36.