Beyond Profound Autism - Towards More Useful Ways to Classify Autism

 

A new paper continues to refine the concept of Profound Autism to define how should we describe autistic people who require lifelong, round-the-clock care. 

Developing a consensus research definition for profound autism using a modified Delphi method

 

Using a modified Delphi process involving researchers, clinicians, caregivers and autistic individuals, the authors developed a consensus research definition of profound autism. Their goal is admirable. By encouraging researchers to use a common definition, studies become easier to compare and the subgroup with the greatest support needs is less likely to be overlooked.

I welcome that goal, but …

 

Research definition or clinical reality?

The authors are careful to emphasise that "profound autism" is intended as a research definition rather than a new clinical diagnosis.

That distinction is important.

Researchers need consistent definitions so that studies include comparable participants. A research definition helps ensure that one study of "profound autism" is investigating a similar population to another.

Parents, however, have often been asking for something completely different.

Many families caring for autistic people who require lifelong support argue that the autism spectrum has become so broad that it no longer communicates the reality of their child's disability. They are looking for terminology that helps explain prognosis, support needs and, in some countries, eligibility for services.

A research-only definition does not solve those problems.

Indeed, by combining autism severity, intellectual disability and adaptive functioning into a single category, it may create new sources of confusion outside the research setting.

 

This is in marked contrast to Asperger's syndrome. In 1994, Asperger's syndrome was introduced into the DSM-IV as a recognised clinical diagnosis, not merely as a research category. It was used by clinicians, educators and families to describe a distinctive presentation of autism. When it was removed in 2013 and absorbed into the broader diagnosis of Autism Spectrum Disorder, the spectrum expanded to encompass individuals ranging from those living entirely independently to those requiring lifelong, round-the-clock care.

It is therefore unsurprising that researchers are once again looking for ways to subdivide this very broad spectrum.

However, unlike Asperger's syndrome, profound autism is not intended to become a clinical diagnosis. It is a tool for research, not for clinical practice.

Perhaps what is really needed are two complementary frameworks:

·        A research framework that allows scientists to compare studies using consistent and well-defined populations.

·        A clinical framework that describes an individual's autism severity, intellectual ability, adaptive functioning, language, medical complications and support needs separately.

The second approach may be far more useful for families because it paints a richer and more accurate picture of the individual than any single label ever could.

The authors deserve credit for recognising that the current autism spectrum has become too broad for many research questions and their perseverance. Whether "profound autism" is the best way to address that problem remains open to debate, but they have undoubtedly started an important conversation.

How Has the Diagnosis Changed?

It is easy to forget how much the diagnosis of autism has changed over the past quarter of a century.

In 2000, clinicians were still using the DSM-IV classification, which recognised several distinct pervasive developmental disorders: Autistic Disorder, Asperger's syndrome and PDD-NOS (Pervasive Developmental Disorder – Not Otherwise Specified).

To receive a diagnosis of Autistic Disorder, a child had to meet at least six diagnostic criteria spanning social interaction, communication and restricted or repetitive behaviours, with symptoms present before three years of age. Most children diagnosed with Autistic Disorder had significant language delay, many had intellectual disability, and a large proportion required substantial lifelong support.

By contrast, individuals with average or above-average intelligence and no clinically significant language delay were generally diagnosed with Asperger's syndrome, while those who showed autistic features but did not fully satisfy the criteria for either diagnosis often received a diagnosis of PDD-NOS.

This changed dramatically in 2013 when DSM-5 replaced these separate diagnoses with a single diagnosis of Autism Spectrum Disorder (ASD). The intention was to improve diagnostic consistency, recognising that there were no clear biological boundaries separating the previous categories. However, the consequence was the creation of an exceptionally broad diagnostic spectrum.

Today, the same diagnosis encompasses people living entirely independently—including university professors, engineers, scientists and other professionals—as well as individuals who cannot communicate verbally, require assistance with every aspect of daily living and need lifelong, round-the-clock care.

This historical perspective helps explain why researchers are once again attempting to identify meaningful subgroups within autism. In many respects, the proposal for profound autism represents an effort to recover some of the distinctions that were lost when Asperger's syndrome and PDD-NOS were merged into a single spectrum. 

Why do we need a better classification of autism?

Autism has become an extraordinarily broad diagnosis.

At one end of the spectrum are university professors, software engineers, airline pilots and people who require little or no formal support.

At the other end are individuals who cannot communicate verbally, cannot dress or feed themselves, may have epilepsy, severe gastrointestinal disease, self-injurious behaviour and require lifelong supervision.

Although these individuals all satisfy the behavioural criteria for autism spectrum disorder, they clearly do not represent the same clinical condition.

When research studies combine such diverse populations under one diagnostic label, interpreting the results becomes increasingly difficult. A treatment that benefits one subgroup may have no effect—or even be harmful—in another.

Recognising this enormous heterogeneity is one of the greatest strengths of the new paper.

 

The proposed definition of profound autism

After two rounds of expert consultation, the Delphi panel proposed that profound autism should be defined by several key characteristics.

The individual should:

• meet the diagnostic criteria for autism spectrum disorder
• be at least eight years old
• require continuous adult supervision to ensure health, safety and wellbeing
• demonstrate adaptive functioning well below age expectations

and also have either:

• severe intellectual impairment (typically reflected by an IQ below 50), or
• minimal verbal communication, consisting mainly of single words or fixed phrases used to communicate basic needs.

Importantly, this is intended as a research definition, not a new clinical diagnosis.

The intention is not to create another subtype of autism but to ensure that studies investigating those with the highest support needs are describing comparable populations.

That is an entirely reasonable objective.

 

What the Paper Gets Right

Several aspects of the paper deserve praise.

First, it openly acknowledges that autism is not one disorder.

The current autism spectrum encompasses people with enormously different abilities, medical problems, educational outcomes and support requirements.

Recognising that these individuals should not always be analysed together is long overdue.

Secondly, the authors move away from relying solely on IQ.

Instead, they give much greater emphasis to adaptive functioning—the practical skills needed for everyday life.

Being able to dress, wash, communicate needs, recognise danger, prepare food or manage daily routines often determines independence far more than an IQ score.

In many ways, adaptive functioning is a better measure of the help a person actually requires.

Finally, the authors recognise that research involving those with the greatest support needs has declined over recent decades.

That imbalance deserves to be corrected.

 

Where I think the definition falls short

Although I agree with the motivation behind the paper, I am less convinced by the solution.

My concern is that the proposed definition combines three different concepts into a single label:

• autism severity
• intellectual disability
• adaptive functioning

These are related, but they are not identical.

A person may have extremely severe autistic symptoms while having an IQ of 120.

Another may have equally severe autistic symptoms together with profound intellectual disability.

A third may have only moderate autistic features but such poor adaptive functioning that lifelong supervision is still required.

These individuals have very different developmental trajectories, medical needs and treatment priorities.

Grouping them together under one behavioural label risks obscuring those important differences.

 

James Coplan's alternative framework

More than twenty years ago, pediatric neurologist James Coplan proposed a remarkably elegant way of thinking about autism prognosis. I wrote about it in my book on page 90.

Instead of asking a single question—

"How severe is the autism?"

—he separated prognosis into independent dimensions.

His framework considered:

• severity of autistic features
• intellectual ability
• age

 

 

 

 

 

His diagrams illustrate two children who initially appear equally autistic.

Child A has profound intellectual disability.

Child B has normal intelligence.

Both improve with age and both still have autism. But child B’s intelligence allows him to break up the troubling aspects of autism into smaller more manageable pieces. Child A never manages to overcome these barriers and remains disabled.

Their long-term outcomes become completely different.

The difference is not autism alone.

It is autism combined with intellectual disability.

I have always thought this framework was one of the clearest ways of explaining why prognosis varies so enormously across the autism spectrum.

If I were updating Coplan's model today, I would start with a fourth independent dimension, adaptive functioning. Later we can add some additional dimensions to narrow down sub-groups of autism.

 

 

 

 

Autism severity is not the same as IQ

One recurring source of confusion is the assumption that severe autism automatically means low intelligence. It does not.

Many autistic people experience severe sensory difficulties, severe social disability and marked repetitive behaviours while having average, or even exceptionally high, IQ.

Conversely, many autistic people also have severe intellectual disability.

These are different dimensions.

This distinction matters because one reason the term "profound autism" has generated debate is that many autistic people with severe autistic symptoms but normal intelligence feel it reinforces the misconception that intellectual disability is simply part of autism, rather than a common but separate co-occurring condition.

The authors of the Delphi paper were clearly aware of this problem.

Interestingly, the expert panel could not reach consensus on the most appropriate IQ threshold.

An IQ below 50 received the greatest support but still failed to reach the predefined level required for formal consensus.

That illustrates just how difficult it is to reduce a complex clinical picture to a single number.

 

The taboo of low IQ

One recurring issue when discussing autism today is the reluctance to talk openly about impaired cognitive function, or low IQ.

This is not an entirely new phenomenon. In 1973 the IQ threshold traditionally associated with what was then called mental retardation (now intellectual disability) became more stringent. Whereas an IQ below about 80 had been used previously, the emphasis shifted to an IQ below 70, approximately two standard deviations below the population mean. Although this appears to be a relatively small numerical change, it reduced the proportion of the population meeting the criterion from roughly 16% to about 2.3% today.

Today we seem to be moving in opposite directions. The diagnostic boundaries for autism and ADHD have broadened considerably, while the definition of intellectual disability become narrower.

Unfortunately, IQ has become an uncomfortable subject. Rather than asking why some children have impaired cognitive development—and whether it might be prevented or treated—we often focus on finding more acceptable terminology, such as intellectual disability or learning difficulty. Changing the name may reduce stigma, but it does not change the underlying biology.

IQ is not determined by genetics alone. It is influenced by prenatal health, nutrition, education, environmental factors and many medical conditions. The remarkable increase in average IQ observed in countries such as South Korea over the past several decades demonstrates that cognitive performance can improve substantially across a population as living conditions, health and education improve.

South Korea provides one of the world's clearest examples of how environmental factors can influence measured cognitive ability. During the country's rapid economic development, researchers documented exceptionally large gains in IQ test performance—around 7–8 points per decade for cohorts born between 1970 and 1990. These gains are far too rapid to be explained by genetics and instead reflect the powerful effects of improved nutrition, healthcare, education and childhood development.

Average IQ in sub-Saharan Africa is reported to be around 80, but it is not a politically correct subject to discuss.

Perhaps the most encouraging development is the growing recognition that some forms of intellectual disability are treatable. This indeed ended up being one of the goals of my son’s autism therapy.

I was surprised to later discover the excellent Treatable-ID.org project, which catalogues hundreds of inherited metabolic and genetic disorders in which early diagnosis and targeted treatment can prevent or reduce intellectual disability. The database is not yet complete, but it highlights how understanding the biology of cognitive impairment can lead to meaningful interventions.

Parents often face a difficult dilemma. When applying for educational or social support, they may need to provide evidence that their child has intellectual disability. Yet, understandably, they also want to emphasise their child's strengths and abilities. That tension can make honest discussions about cognitive ability surprisingly difficult.

Ultimately, our goal should not simply be to find kinder terminology. It should be to understand why intellectual disability develops and, wherever possible, to prevent or treat it.

 

CARS, IQ and Adaptive Functioning Measure Different Things

One lesson from this discussion is that we should stop expecting a single measurement to describe everything.

Autism researchers already have well-established tools for measuring different aspects of an individual's condition.

The Childhood Autism Rating Scale (CARS) is widely used in clinical trials to quantify the severity of autistic symptoms. It allows researchers to determine whether a treatment has reduced the core behavioural features of autism.

IQ tests measure cognitive ability.

Adaptive behaviour scales, such as the Vineland Adaptive Behavior Scales, measure how well a person functions in everyday life.

Language assessments measure communication.

These are not competing measurements.

They answer different questions.

 

Question	Measurement Tool	What It Isolates
How severe are the autistic features?	CARS (Childhood Autism Rating Scale)	Core behavioral features & symptom severity
How well does the brain solve problems?	IQ Tests	Cognitive and intellectual ability
How independently can the person function?	Vineland (Adaptive Behavior Scales)	Practical, real-world everyday life skills
How well can they communicate?	Language Assessment	Structural and functional communication levels

 

No single score can replace the others.

For example, two children may both have a CARS score of 46, indicating similarly severe autistic symptoms.

One may have an IQ of 110.

The other an IQ of 35.

Their autism severity is similar.

Their prognosis is not.

Likewise, two people with identical IQs may have very different adaptive functioning. One may travel independently and prepare meals, while another may require constant supervision because of poor judgement or inability to communicate in dangerous situations.

Each measurement adds a different piece of the puzzle.

Although adaptive functioning may ultimately predict support needs better than IQ, IQ remains a concept that most people readily understand. Saying that someone has an IQ below 50 immediately conveys severe cognitive impairment. Saying that adaptive functioning is "three standard deviations below the mean" is scientifically precise but far less intuitive.

For parents, describing an eight-year-old as having adaptive skills comparable with those of an eighteen-month-old child may actually communicate the situation more clearly, even though psychologists generally avoid age-equivalent scores because of their statistical limitations.

Rather than trying to compress all of these dimensions into a single label, we should recognise that each contributes valuable information.

 

What About Self-Injury and Aggression?

One of the most surprising findings from the Delphi process is not what was included—but what was deliberately excluded.

The expert panel decided that self-injurious behaviour (SIB), aggression and other severe challenging behaviours should not form part of the definition of profound autism.

Their reasoning is understandable.

Although these behaviours are common among autistic people requiring lifelong care, they are not universal. Some profoundly disabled autistic people never become aggressive or self-injurious, while others with less severe intellectual impairment do.

From the perspective of defining a research population, that makes sense.

However, from the perspective of improving lives, I think something important risks being overlooked.

Self-injury and severe aggression are among the greatest causes of:

• family stress
• school exclusion
• psychiatric admission
• physical injury
• use of restrictive practices
• reduced quality of life

These behaviours are not simply unfortunate complications.

They are major clinical problems in their own right.

They also almost certainly represent important biological processes that deserve investigation.

Whether driven by pain, epilepsy, anxiety, executive dysfunction, sensory overload, catatonia, immune activation or other mechanisms, severe behavioural dysregulation should not disappear from autism research simply because it does not define a diagnostic subgroup.

Instead, it should become a major research priority.

 

Towards a Multidimensional Framework

Rather than inventing another umbrella label, I believe autism research would benefit from routinely describing individuals across several independent dimensions.

For example:

Dimension	Example measure
Autism severity	CARS-2
Intellectual ability	IQ
Adaptive functioning	Vineland
Language	Single words, phrases, fluent speech
Behaviour	Self-injury, aggression, catatonia
Medical complexity	Epilepsy, gastrointestinal disease, sleep disorder
Development	Age and developmental trajectory

 

This immediately creates a far richer description than any single label.

Instead of saying:

"This study included children with profound autism."

Researchers could report:

• Mean CARS score
• Mean IQ
• Mean adaptive functioning
• Language level
• Prevalence of epilepsy
• Frequency of self-injury
• Frequency of aggression
• Presence of regression
• Known genetic diagnoses

Readers would immediately understand precisely which population had been studied.

 

 

 

Then, for example, we have some Aspies with IBD (irritable bowel disease). The IBD does share a biological basis with their autism. Treat the IBD and watch their autism symptoms mellow.

The future lies in studying better subgroups

Perhaps the greatest opportunity is not to invent another autism label, but to identify clinically and biologically meaningful subgroups.

Many of these already exist.

Examples include:

• Autism with profound intellectual disability
• Autism with average or high intelligence
• Autism with severe self-injury
• Autism with severe aggression
• Autism with epilepsy
• Autism with catatonia
• Autism with developmental regression
• Autism associated with mitochondrial dysfunction
• Autism with severe gastrointestinal disease
• Autism with chronic sleep disorders
• Autism associated with immune dysregulation
• Autism following hypoxic brain injury
• Autism following congenital infection
• Autism associated with connective tissue disorders
• Autism associated with specific genetic syndromes such as SCN2A, SHANK3, CACNA1C, SCN8A, SYNGAP1, Phelan-McDermid syndrome, Rett syndrome, Fragile X syndrome, Tuberous Sclerosis Complex and many others.

 

Even these subgroups are not mutually exclusive.

A child may belong to several simultaneously.

That is perfectly acceptable.

The purpose is not to create dozens of new diagnoses.

The purpose is to identify people who are likely to share similar biology—and therefore similar treatment opportunities.

Interestingly, autism research is already moving in this direction.

Clinical trials increasingly recruit specific subgroups rather than "all autism."

Examples include:

• minimally verbal autism
• autism with epilepsy
• Fragile X syndrome
• Rett syndrome
• tuberous sclerosis
• Phelan-McDermid syndrome
• SCN2A-related autism

The field has already recognised that autism is biologically heterogeneous.

Perhaps our classification systems should catch up.

 

Precision medicine needs better descriptions

The real promise of precision medicine is not simply to identify ever smaller genetic subgroups.

It is to understand why individuals who satisfy the same behavioural diagnosis often have completely different biology.

One child may have mitochondrial dysfunction.

Another an ion channel disorder.

Another chronic neuroinflammation.

Another an underlying metabolic disease.

Another significant prenatal hypoxic brain injury.

Behaviour alone cannot distinguish these individuals.

Yet these biological differences may determine prognosis far more accurately than behavioural scores.

They may also determine which treatments are most likely to work.

The future of autism research therefore lies not in inventing broader behavioural labels but in combining behavioural assessment with genetics, neurobiology, metabolism, electrophysiology and careful clinical phenotyping.

That is the essence of precision medicine.

 

Conclusion

The new consensus definition of profound autism represents an important step forward.

It recognises that autism encompasses individuals with enormously different abilities and support needs, and that research should no longer treat them as one homogeneous population.

I fully support that objective.

However, I am not convinced that another behavioural label is the final answer.

Autism severity, intellectual ability, adaptive functioning, language, challenging behaviour and medical complexity are all independent dimensions.

They should be measured independently.

James Coplan recognised this more than twenty years ago when he separated autism severity from intellectual ability and developmental trajectory.

Today I would simply extend that framework by adding adaptive functioning, language, behaviour and medical complexity.

Most importantly, I believe the future lies beyond behavioural classification altogether.

The greatest advances in autism research are increasingly coming from the identification of biologically meaningful subgroups—whether defined by genetics, epilepsy, mitochondrial dysfunction, immune abnormalities, catatonia, regression or other underlying mechanisms.

These subgroups are far more likely to reveal targeted treatments than any single behavioural label.

The future of autism research is therefore unlikely to be shaped by a new definition such as profound autism.

It will be shaped by understanding why two people with the same autism diagnosis can have completely different biology, completely different outcomes and, ultimately, completely different treatments.

Labels describe people. Biology explains them.

 

The average IQ of South Koreans has risen dramatically over the past half century, largely through improvements in nutrition, healthcare and education. Whether the same can be said for autism researchers is perhaps more debatable. In our enthusiasm to develop new classifications, we should not overlook the valuable work carried out decades ago. James Coplan's multidimensional framework remains remarkably relevant today and arguably aligns more closely with the goals of precision medicine than many more recent attempts to subdivide the autism spectrum. Hans Asperger was 50 years ahead of his time.

 

 

Note on Hans Asperger

A 2023 investigation concluded that there was no evidence Hans Asperger knew that Am Spiegelgrund was operating a child euthanasia programme when he referred patients there in 1941. Around 800 children were ultimately killed at the institution during the Nazi period, including two of Asperger's former patients.

https://pubmed.ncbi.nlm.nih.gov/36239413/

Following the end of the Second World War, Ernst Illing, the director of Am Spiegelgrund, was arrested and tried by an Austrian court in 1946. He was convicted of murders committed at the institution, sentenced to death, and executed by hanging on 30 November 1946.

The historical record surrounding Hans Asperger continues to be debated. New evidence should always be considered carefully, but historical interpretations should be revised only when supported by robust evidence. Replacing one oversimplified narrative with another risks introducing new biases rather than improving our understanding of the past.

It is striking that some people are deeply concerned about the former diagnosis of Asperger syndrome because of ongoing historical debates about Hans Asperger and yet many give little thought to buying products from companies with well-documented links to the Nazi regime, such as Hugo Boss, whose founder was a Nazi Party member and whose company manufactured uniforms for Nazi organisations while using forced labour during the Second World War.  

In 1938, the Nazi government even awarded Henry Ford the Grand Cross of the German Eagle, the highest honour it could bestow on a foreign civilian.

Henry Ford was a pioneering industrialist, but he also promoted antisemitic views through his newspaper, the Dearborn Independent. These articles were later collected into the four-volume series The International Jew in the early 1920s. It was translated into at least 12 languages. The writings spread antisemitic conspiracy theories about Jewish people and influenced extremist movements internationally, including Nazi Germany. Adolf Hitler openly admired Ford and mentioned him favourably in Mein Kampf. Ford was the only American mentioned positively by Hitler in Mein Kampf, and Hitler later stated that he regarded Ford as an inspiration.

It does illustrate that society often applies historical scrutiny inconsistently.

I hope Simon Baron-Cohen never bought a Ford!

Is it relevant today? Not to most people.

Ordinary Gifted or Gifted with Asperger’s Syndrome? And Treatment options for Aspies

Asperger with his Little Professors

This blog is focused more on severe autism, but today it is turn for the Aspies.  The post does rather ramble, because I included some old unused material on micro-dose LSD that may be Aspie-relevant.

Most people diagnosed with autism these days do not have severe autism and so their ideal medical therapy may be very different to the Polypill, I developed for my son.

For a young Aspie he might just need a single intervention like Sertraline (Zoloft) and nothing else, or perhaps Amantadine.

There is more than twenty years of experience medically treating people with Asperger’s, but it very much remains a case of trial and error to find what works.

It does look like most translational research in autism is now focused on those without problems with speech or cognition. That is good news for people with Asperger’s, not so good for the other end of the spectrum.

The paper below is 20 years old, but the medical treatment has not become out of date.

Gifted children with Asperger's Syndrome

Behavior Problems. Children with AS usually have some behavior problems. They may be compulsive or hyperactive. They may be prone to tantrums or aggressive outbursts. They may routinely hit other children without provocation or touch people in inappropriate ways. Some AS children suffer from anxiety attacks or specific phobias. They may be sensitive to teasing, but consistently demonstrate provocative behaviors that invite teasing. Some AS children will engage adults in endless arguments if given the opportunity. Parents especially may find themselves trapped in repeated discussions about the same events or disagreements. Adults should not attempt to reason for more than a minute with such children (Barron & Barron, 1992; Dewey, 1991; Klin & Volkmar, 1995). Brief, concrete directives are most effective. Visual supports like pictograms can be posted on a child's notebook, desk, or on the wall to visually cue the child regarding expected behaviors. The addition of visual supports can be remarkably effective in helping AS students organize their behavior. Teachers and parents should consult with an augmentative communication specialist to learn more about visual supports.

In addition to behavioral and educational approaches, medications may be helpful in treating specific problematic behaviors. Medications can significantly improve the quality of life of AS children when they exhibit compulsive or aggressive behaviors that interfere with school adjustment or family life. Medication may also be needed to alleviate symptoms of depression, thought disorder, or anxiety attacks. Tofranil and Prozac have been recommended (Grandin, 1992). Beta blockers have been helpful for some aggressive AS children, and Anafranil, Luvox, or one of the SSRIs (e.g., Zoloft) can be useful in reducing obsessive-compulsive tendencies (Gragg & Francis, 1997; Rapoport, 1989).

If you now look at what is recommend today, two decades later it is pretty much the same.

From the Kennedy Krieger Institute:

What Anxiety Treatments Work for People with Autism?

  

For core anxiety symptoms, her group listed four possible SSRI antidepressants, sertraline (Zoloft), Prozac, Celexa, or escitalopram (Lexapro). That listing was based upon data on children and teenagers who do not have a developmental disorder. The researchers noted that youth with autism often report one particular side effect with SSRI drugs: "behavioral activation," which may appear as hyperactivity, impulsiveness, or trouble sleeping.¹⁴ Other possible side effects, which are not unique to autism, are suicidal thoughts in adolescents, or worsening of mood problems in people with bipolar disorder. So these drugs "should be prescribed cautiously in youth with ASD, with close monitoring," the researchers advised. Their article, in the journal Pediatrics, includes starting and maximum doses for doctors to consider. (See Additional Resources below for a link to the article, to share with your health care provider.)

Over at the MIND Institute at UC Davis:-

Specifying and Treating Anxiety in Autism Research (STAAR) Study

At least 50 percent of children with autism spectrum disorder (ASD) exhibit clinically significant anxiety symptoms. These are associated with increased social deficits, depression, irritability, and stereotyped and self-injurious behaviors. While it is clear that anxiety represents a substantial problem for those with ASD, there are important issues that need to be clarified before effective treatment becomes widespread. This project of the ACE will explore better ways to detect anxiety in children with ASD and determine whether cognitive behavioral therapy or medication can better alleviate their symptoms

  

Studies often appear to show no benefit, but it depends what you choose to measure (the primary outcome) and how large the sample is.

Prozac proves no better than a placebo in treating kids with autism

At first, the fluoxetine group appeared to show a slight but significant easing of obsessive-compulsive symptoms after four months compared with the placebo. But after the researchers controlled for factors including age, sex and the severity of symptoms at the start of the trial, the difference vanished. Fluoxetine did no better than the placebo.

The relatively small sample size could have limited the researchers’ ability to detect a benefit from the drug, Neumeyer says. “It’s possible that, with higher numbers, they would’ve found subgroups who benefit from SSRIs,” she says. “That’s the painful part of this [kind of] research though; you’re left wondering.”

Interesting to see low dose Prozac (fluoxetine) used successfully in severe French autism:-

Low-Dose Fluoxetine in Four Children with Autistic Spectrum Disorder Improves Self-Injurious Behavior, ADHD-Like Symptoms, and Irritability

In this article, the authors present four clinical cases of ASD-diagnosed children with ADHD-like symptoms and/or SIB and/or other heteroaggressive behaviors and/or irritability and impulsivity. Each was treated with low doses of fluoxetine, specified as follows: 2.5 mg/d (liquid formulation) in the morning for the first week, followed by a flexible titration schedule based on weight and tolerability. The Hollander et al. protocol [3] is reproduced here, in which children with ASD were given low doses of fluoxetine. Patients were assessed using the Clinical Global Impression Scales (CGI) [12] during the time of fluoxetine introduction and observation. None had tried an SSRI treatment before the reported trial.

In conclusion, in these case reports, we found that the prescription of fluoxetine, in addition to valproate and cyamemazine (Case 1) or to risperidone (Cases 2, 3 and 4), could be effective on severe behavioral symptoms associated with ASD in children. It is important to inform child psychiatrists about this therapeutic possibility even if it would be difficult to predict the rate of responders on the basis of this cases and the literature. The role of comedication remains unanswered as none of our cases was on fluoxetine monotherapy.

  

Recall this old post:- 

When is an SSRI not an SSRI? Low dose SSRIs as Selective Brain Steroidogenic Stimulants (SBSSs) via Allopregnanolone modifying GABAa receptors and neonatal KCC2 expression

Micro-dosing LSD for Aspies?

Since we are on the subject of Aspies, I will insert a post that I never finished.  It is very much for the genuine Aspie, the one with a high IQ, the type working over at Google HQ. Usually male, does not strictly need any medical treatment, but may seek some out nonetheless.

Even though LSD was used at high doses in people with severe autism in the 1960s at UCLA, current interest involves micro-doses taken by people without any severe disability. 

A trial is about to start at Imperial College in London that may particularly interest Californian and Dutch Aspies.

First ever trials on the effects of microdosing LSD set to begin

Silicon Valley geeks say it sharpens their thinking and enhances creativity. Other people say it lifts the fog of depression. A novel experiment launching 3 September 2018 will investigate whether microdosing with LSD really does have benefits – or whether it’s all in the mind.

Microdosing using psychedelic drugs – either LSD or magic mushrooms – is said to have become very popular, especially with people working in the Californian digital tech world, some of whom are said to take a tiny amount one or more days a week as part of their routine before heading to work. It’s not for a psychedelic high, though – it’s to make them more focused.

Microdosers tend to use either tiny amounts of LSD – as little as one-fifteenth of a tab – or of psilocybin, the active ingredient in magic mushrooms. The study is recruiting just those who use LSD, because of the difficulty in disguising even ground-up mushrooms in a capsule.

But it’s illegal. So how many people are microdosing is unknown and there is only anecdotal evidence of the effects and any downsides. In a bid to learn more, the Beckley Foundation, which was set up to pioneer research into mind-altering substances, and the unit it funds at Imperial College London, will launch the first ever placebo-controlled trial of microdosing on Monday, 3 September 2018.

It will be unique, says Balázs Szigeti, the study leader. The cost and the illegality of LSD would make a conventional study prohibitively expensive. So he has hit on a way of running it by inviting those who already microdose to join a “self-blinded” study. They will take either what they usually use in a capsule or an identical dummy capsule instead, without knowing which is which. They will complete questionnaires and tests and play cognitive games online, and only at the end will they learn whether they were happy and focused because of LSD or because they thought they were using LSD.

The trial itself:-

https://selfblinding-microdose.org/

Conclusion

The big difference between treating mild autism (Asperger’s) and severe autism is whether cognitive function is a target.  For severe autism raising cognitive function is the most important target, because it has the potential to improve all other behavioral issues. 

Aspies have been self-treating for decades and in some countries have a helpful psychiatrist happy to prescribe off-label (SSRIs, bet-blockers etc).  They often seem to like 5HT2A agonists.

The effective drugs for mild autism (Asperger’s) may have only limited value to those with severe autism.  Unless you resolve cognitive impairment, you will not transform the developmental trajectory.

It would be helpful if during the initial observational autism diagnosis, the doctor made clear to parents, what kind of autism the child has.   This often is not the case.

It is clear that most people diagnosing autism in very young children do not attempt to measure IQ, or even use an autism ratings scale, like CARS.  There are understandable reasons for this, but it still looks lazy to me.  Nowadays people struggle less hearing the word “autism”, but nobody wants to hear about MR/ID in their 3 year old.  So better to keep silent and avoid parents bursting into tears.

You really do need to be told where you are on the scale from Aspie to the other extreme of Autistic disorder/ Kanner’s/Classic/SDA.  You might think this would be obvious, but it is not.  If you have a 4 year old Aspie, start with Aspie therapies, not therapies for severe autism.

We saw in Catherine Lord’s study that all of those in her 20 year longitudinal study of children with an autism diagnosis, also had an IQ , when measured, indicating MR/ID.  Her study group was a random selection of those diagnosed with autism where she worked.  Back then autism meant autism.  Her “top performing” 40% have normal IQ as adults, but even in that group their measured IQ at age 3 or 4 was less than 70.  This group are not Aspies, they would have had normal/high IQ when tested at the age of 3 or 4.

The meaning of the diagnosis has changed so much in 20 years that the research now talks of autism with a developmental disorder and autism without a developmental disorder.

Actually, “autism” is supposed to be a developmental disorder; that was the whole point. But never mind.

Aspies have had a wide range of treatment options for more than 20 years and they also stand to benefit for the new generation of “autism” drugs, which are actually mainly for mild autism.

As with severe autism, treating an Aspie will also require personalized medicine, or just call it trial and error.  Prozac might be hopeless, but Zoloft work wonders.  ADHD meds might help, or just make things worse.  Oxytocin might improve empathy, or do absolutely nothing.  Perhaps the study at Imperial will show micro-dose LSD does have a benefit.  Since you are fully verbal and have a high IQ it is not hard to establish whether there is a benefit or not, move on and perfect your personal therapy.

It is the other end of the spectrum, where there is a big problem.  You may need to look at the new drugs being developed for Down Syndrome, Fragile-X and the numerous rare single gene autisms. Those drugs will not be cheap.