Cognitive Impairment in Schizophrenia, Bipolar & Autism

Neurological/neuropsychiatric disorders are often poorly described and poorly treated, but adult-onset conditions have historically been taken much more seriously and so the research is more advanced .  I find myself quite often looking at research on schizophrenia and bipolar; many of the same genes and metabolic dysfunctions common in autism show up in those conditions.

Many people really dislike the term Mental Retardation (MR), which is actually a very accurate descriptive term, meaning that someone is cognitively behind their peers.  Most lay people have no idea what Intellectual Disability (ID) means.

It is interesting that about 90% of people with schizophrenia and 50% of people with bipolar are cognitively behind their peers.  I suspect the figure for autism would also be about 90%, if someone measured it.  Most people with Asperger’s are not top of the class.

Only in extreme cases of being cognitively behind their peers, when their IQ is less than 70, does a person get diagnosed with MR/ID.

So the clinical diagnosis of MR/ID is just an arbitrary cut-off point.  The idea that if IQ is greater than 70 there is no cognitive deficit is entirely flawed.

It seems than in autism, as in schizophrenia and bipolar we should assume that cognitive dysfunction is present; the only question is how much and what to do about it.

Having treated the cognitive dysfunction(s), the person is then in a better place to compensate for the other dysfunctions they might have.

Even though the psychiatrists and psychologists will tell you that autism is all about the triad of impairments, I think they are missing the most important element, which is cognitive dysfunction.

As people with autism age, many find their symptoms associated with the above “triad of impairments” mellow.  The substantial minority who experience untreated flare-ups driven by inflammation caused by things like allergy, GI problems and even juvenile arthritis may not be so lucky.

I imagine that cognitive function in adulthood remains at the level it reached as a teenager.

Cognitive Function as the Therapeutic Target

Since many children with autism do eventually overcome many of their challenges in childhood, perhaps cognitive function really should be given a higher priority in treatment and research.

Many caregivers and educators are mainly focused on minimizing bad/disruptive behaviors (and bruises) rather than the emergence of good behaviors and learning.  This is sad but true.

As the child matures, in many cases these bad/disruptive behaviors may fade without any clever interventions.

So an intervention that stops stereotypy in a toddler, which was blocking learning, may have very much less impact in an adolescent.  Or at least the impact may be much less obvious.

I remember reading about a parent with two children with Fragile-X who was very upset when the Arbaclofen trials were halted, since her kids had responded well.  But two years later in another article it was clear that things were going fine without Arbaclofen.  The son whose violence towards his mother had been controlled by Arbaclofen, was no longer aggressive.  He continued to suffer cognitively, being a male with Fragile-X, the sister was much less affected  (females with fragile X syndrome have two X chromosomes and only one of the chromosomes usually have an abnormal gene, so usually females are less affected).   

The advantage of using cognitive function as a target is that it is much easier to measure than subjective behavioral deficits.  For the majority of people it is likely to be the most important factor in their future success and well-being.

In the substantial minority of cases where there are seizures and/or factors causing autism flare-ups, the behavioral deficits may remain undiminished into adulthood.  These people would also benefit from maximized cognitive function.

Cognitive Deficit in Schizophrenia & Bipolar (BPD)

To most lay people schizophrenia is characterized by abnormal social behavior and failure to recognize what is real. Common symptoms include false beliefs, unclear or confused thinking, hearing voices, reduced social engagement and emotional expression, and a lack of motivation. People often have additional mental health problems such as major depression, anxiety disorders, or substance use disorder. Symptoms typically come on gradually, begin in early adulthood, and last a long time.

Cognitive impairments and psychopathological parameters in patients of the schizophrenic spectrum.

  

Abstract

Cognitive impairment is a core feature of schizophrenia and it is considered by many researchers as one of the dimensional components of the disorder. Cognitive dysfunction occurs in 85% of schizophrenic patients and it is negatively associated with the outcome of the disorder, the psychosocial functioning of the patients, and non-compliance with treatment. Many different cognitive domains are impaired in schizophrenia, such as attention, memory, executive functions and speech. Nowadays, it is argued that apart from clinical heterogeneity of schizophrenia, there is probable heterogeneity in the accompanying neurocognitive dysfunction. Recent studies for cognitive dysfunction in schizophrenia employ computerized assessment batteries of cognitive tests, designed to assess specific cognitive impairments. Computerized cognitive testing permits for more detailed data collection (e.g. precise timing scores of responses), eliminates researcher's measurement errors and bias, assists the manipulation of data collected, and improves reliability of measurements through standardized data collection methods. The aims of the present study are: the comparison of cognitive performance of our sample of patients and that of healthy controls, on different specific cognitive tests, and the testing for possible association between patients' psychopathological symptoms and specific cognitive impairments, using the Cogtest computerized cognitive assessment battery. 71 male inpatients diagnosed with schizophrenia or other psychotic spectrum disorders (mean = 30.23 ± 7.71 years of age), admitted in a psychiatric unit of the First Department of Psychiatry, Athens University Medical School, Eginition Hospital (continuous admissions) were studied. Patients were excluded from the study if they suffered from severe neurological conditions, severe visual or hearing impairment, mental retardation, or if they abused alcohol or drugs.

Bipolar disorder, also known as bipolar affective disorder or manic depression, is a mental disorder characterized by periods of depression and periods of elevated mood. The elevated mood is significant and is known as mania or hypomania depending on the severity or whether symptoms of psychosis are present. During mania an individual feels or acts abnormally happy, energetic, or irritable. They often make poorly thought out decisions with little regard to the consequences. The need for sleep is usually reduced. During periods of depression there may be crying, poor eye contact with others, and a negative outlook on life

It also turns out that cognitive deficit is generally present in bipolar disorder (BPD).

Understanding Cognitive Impairments in Bipolar Disorder and Psychosis

  

“One area that Dr. Burdick is exploring is the frequency of neurocognitive impairment in BPD. Research shows that approximately 90 percent of schizophrenic patients suffer from cognitive deficits compared to only 40 to 60 percent of BPD patients. Understanding why certain patients develop significant cognitive difficulties while others do not is critical in optimizing patients’ quality of life, she says.”

Bipolar is probably not something you would connect with autism.  Being an observational diagnosis you would not tend to look at the biological underpinnings. The biological basis of both bipolar and schizophrenia are far better studied than autism and do significantly overlap with it.

In a recent post I looked at epigenetics and autism, when it comes to schizophrenia and bipolar the role of epigenetics is far more in the mainstream.

There is an approved epigenetic therapy (the HDAC inhibitor Valproate) for Bipolar mania and there is a clinical trial to improve cognitive function in schizophrenia using ather epigenetic therapy (the HDAC inhibitor Sodium Butyrate.)

Butyrate is also showed promise in a mouse model (D-AMPH) of Bipolar.

Sodium Butyrate For Improving Cognitive Function In Schizophrenia

Epigenetic mechanisms in schizophrenia

Effects of sodium butyrate on oxidative stress and behavioral changes induced by administration of D-AMPH

Conclusion

I think people should be more open to discuss cognitive deficits and not hide behind politically correct terminology.

It seems that in both bipolar and schizophrenia cognitive deficits are recognized to be at the core of the disorder, even though 99% will not have an IQ<70 and so not be labelled with MR/ID.

Autism therapies which clearly improve cognitive function, like Bumetanide and low-dose Clonazepam, should be promoted as such.  Clinical trials should measure the cognitive improvement separately from autism measures.  As the person ages I think the benefit will often be more noticeable/measurable cognitively than behaviorally.

Treatable ID and Some Autism

Vancouver is one of the most attractive cities I have visited.  It is home to BC Children’s Hospital and Dr Sylvia Stöckler-Ipsiroglu and Dr Clara van Karnebeek. Together they have produced a remarkably thorough website called Treatable-ID, which sets out information on 82 treatable forms of Intellectual Disability (ID), formerly known as Mental Retardation (MR).

  

This excellent resource was recently brought to my attention by a reader of this blog from Down Under, another place well worth visiting.  Thanks, Alexandria.

ID/MR and Autism

ID/MR is defined as having an IQ less than 70; this means the cognitively weakest 2.2% of the population.

Classic Autism, Autistic Disorder or what we might now also call Strict Definition Autism affects about 0.3% of the population.  It is likely that about half of this group would score <70 in an IQ test.  I do not suggest they take one.

It is clear that an overlap might exist between the causes of MR/ID and the cause of some Strict Definition Autism.

In earlier posts I have referred to improving cognitive function in autism using Bumetanide.  We even saw that it should also improve cognitive function in Down Syndrome.

I suggested that Diamox/ Acetazolamide, another diuretic, could also have a similar effect (via the AE3 cotransporter).  One reader of this blog, Agnieszka, has been sharing her use of Acetazolamide, in the comments on the previous post.

People with RASopathies often have autism and MR/ID.  There are potential RAS therapies, one of which is a cheap statin drug.

We saw how dendritic spine morphology could be modulated and how that could affect cognitive function.  PAK inhibitors can, in theory, achieve this.

So I am already sold on the idea of some cognitive dysfunction being treatable, but I thought I was in a minority of a few dozen. Apparently not.

A friend recently highlighted my suggested autism therapies to a leading Spanish Neurologist, who clearly thinks I am just dreaming.  What would he make of Sylvia and Clara, the BC Duo?  Too much medicinal marijuana, perhaps? 

Science is all about remaining open-minded.  This should also be true for Medicine, but very often it is not. Combine this with the reality that kids with ID/MR/autism are bottom of the list of most people's priorities and you will see why things do not change, unless YOU make the changes, for your n=1 at home. 

81 inborn errors of metabolism related to Intellectual Disability and amenable to therapy

The BC Duo have collated the data on 81 treatable forms of ID/MR.

Not surprisingly some of these 81 also lead to “autism”, so they must also be treatable.  Roger, one this blog’s followers, has at least one of these 81.

So I suggest that anyone interested in a type of autism with some degree of cognitive impairment takes a good look at their site.

Treatable-ID.org

These are the 81 inborn errors:-

- A -
Aceruloplasminemia
(X-Linked) Adrenoleukodystrophy
AGAT Deficiency
α-Mannosidosis
l.o. Argininemia
l.o. Argininosuccinic Aciduria
Aspartylglucosaminuria

- B -
β-Ketothiolase Deficiency
Biotin Responsive Basal Ganglia Disease
Biotinidase Deficiency

- C -
Cerebral Folate Receptor-α Deficiency
Cerebrotendinous Xanthomatosis
l.o. Citrullinemia
Citrullinemia Type II
Co Enzyme Q10 Deficiency
Cobalamin A Deficiency
Cobalamin B Deficiency
Cobalamin C Deficiency
Cobalamin D Deficiency
Cobalamin E Deficiency
Cobalamin F Deficiency
Cobalamin G Deficiency
Congenital Intrinsic Factor Deficiency
l.o. CPS Deficiency
Creatine Transporter Defect

- D -
DHPR Deficiency (Biopterin Deficiency)

- E -
Ethylmalonic Encephalopathy

- G -
GAMT Deficiency
Gaucher Disease Type III
GLUT1 Deficiency Syndrome
l.o. Glutaric Acidemia I
Glutaric Acidemia II
GTPCH1 Deficiency (Biopterin Deficiency)

- H -
HHH Syndrome:
(Hyperornithinemia, Hyperammonemia, Homocitrullinuria)
HMG-CoA Lyase Deficiency
Holocarboxylase Synthetase Deficiency
Homocystinuria
Hunter Syndrome (MPS II)
Hurler Syndrome (MPS I)
Hyperinsulinism Hyperammonemia Syndrome

- I -
Imerslund Gräsbeck Syndrome
l.o. Isovaleric Acidemia

- M -
Maple Syrup Urine Disease (Variant)
MELAS
Menkes Disease Occipital Horn Syndrome
l.o. Metachromatic Leukodystrophy
3-Methylcrotonylglycinuria
3-Methylglutaconic Aciduria Type I
l.o. Methylmalonic Acidemia
MHBD Deficiency
mHMG-CoA Synthase Deficiency
Molybdenum Cofactor Deficiency Type A
l.o. MTHFR Deficiency

- N - l.o. NAGS Deficiency Niemann Pick Disease Type C l.o. Non-Ketotic Hyperglycinemia - O - l.o. OTC Deficiency - P - PCBD Deficiency (Biopterin Deficiency) PDH Complex Deficiency Phenylketonuria PHGDH Deficiency (Serine deficiency) PSAT Deficiency (Serine deficiency) l.o. Propionic Acidemia PSPH Deficiency (Serine deficiency) PTS Deficiency (Biopterin Deficiency) Pyridoxine Dependent Epilepsy Pyrimidine 5-Nucleotidase Superactivity - S - Sanfilippo Syndrome A (MPS IIIa) Sanfilippo Syndrome B (MPS IIIb) Sanfilippo Syndrome C (MPS IIIc) Sanfilippo Syndrome D (MPS IIId) SCOT Deficiency Sjögren Larsson Syndrome Sly Syndrome (MPS VII) Smith Lemli Opitz Syndrome SPR deficiency (Biopterin deficiency) SSADH Deficiency - T - Thiamine Responsive Encephalopathy Tyrosine Hydroxylase Deficiency Tyrosinemia Type II - W - Wilson Disease

Not to confuse Sylvia and Clara with the other dynamic duo, your kids may know, from DC, rather than BC.

With so many treatable forms of MR/ID/Autism out there, is it not a little strange that thorough metabolic testing and Whole Exome Sequencing (WES) are not standard procedures after diagnosis?

By the way, WES is only as good as its interpretation.  Even world leading centres can be very weak in this respect. Insist on receiving the extended report and check all the possibly dysfunctional genes yourself.  It is not so hard.

Bumetanide “reverses” MR/ID in Down Syndrome

You probably know what Down Syndrome looks like, but you probably never expected the above life expectancy data.  It used to be the case that kids with this disorder were institutionalized after birth.

Source:  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4445685/figure/F2/

In an earlier post I suggested that some types of Mental Retardation (MR)/Intellectual Disability (ID) should be treatable.  I was thinking about RASopathies, dendritic spine morphology and the GABA E/I (Excitatory/Inhibitory) imbalance found in autism.  I even suggested to the autism researchers working on the bumetanide approval process that the simplest measure of effectiveness would be to measure IQ before and after treatment.

Recent research has shown that in Down Syndrome GABA is also excitatory.  GABA should be inhibitory, otherwise the brain cannot function properly and there will be a large risk of seizures.  In many people with autism GABA is excitatory; this reduces their cognitive function and leads to almost 80% having unusual epileptiform activity (like “pre-epilepsy”) and about 35% going on to developing seizures.

In the Down Syndrome mouse model the researchers found that Bumetanide improved cognitive function, via the shifting of GABA from excitatory to inhibitory.

Our findings demonstrate that GABA is excitatory in adult DS mice and identify a new therapeutic approach for the potential rescue of cognitive disabilities in individuals with DS.

I thought that was great news.  Perhaps other types of MR/ID are also the result of GABA E/I imbalance, they too would be treatable with Bumetanide.

The question remains, does anyone care enough to bother about these people?  Take a look at the life expectancy chart at the top of this post.  Things have got much better, but there is a long way to go.

Down Syndrome

Most people have heard about Down Syndrome (DS) and I certainly knew more about what DS looked like than what autism looked like.

People with DS look different, are short, and 99% have some degree of MR/ID.  About 10% also have autism and half will develop epilepsy.

Down syndrome is caused by having three copies of the genes on chromosome 21, rather than the usual two.  The extra genetic material present in DS results in overexpression of a portion of the 310 genes located on chromosome 21. This overexpression has been estimated at around 50%.

Some adults with DS lose the ability to use speech when they are about 30 years old.

Until 1970 children with DS used to live for just 10 years, whereas today most survive into their 50s.

About 92% of pregnancies in Europe with a diagnosis of Down Syndrome are terminated. In the United States, termination rates are around 67%.  When non-pregnant people are asked if they would have a termination if their fetus tested positive only 23–33% said yes.

Reversing excitatory GABA_AR signaling restores synaptic plasticity and memory in a mouse model of Down syndrome

Down syndrome (DS) is the most frequent genetic cause of intellectual disability, and altered GABAergic transmission through Cl⁻-permeable GABA_A receptors (GABA_ARs) contributes considerably to learning and memory deficits in DS mouse models. However, the efficacy of GABAergic transmission has never been directly assessed in DS. Here GABA_AR signaling was found to be excitatory rather than inhibitory, and the reversal potential for GABA_AR-driven Cl⁻ currents (E_Cl) was shifted toward more positive potentials in the hippocampi of adult DS mice. Accordingly, hippocampal expression of the cation Cl⁻ cotransporter NKCC1 was increased in both trisomic mice and individuals with DS. Notably, NKCC1 inhibition by the FDA-approved drug bumetanide restored E_Cl, synaptic plasticity and hippocampus-dependent memory in adult DS mice. Our findings demonstrate that GABA is excitatory in adult DS mice and identify a new therapeutic approach for the potential rescue of cognitive disabilities in individuals with DS.

Conclusion

It would appear that excitatory GABA may be more common than anyone thought.  I wonder how many other people with MR/ID might be affected and be potential beneficiaries of this very inexpensive therapy.

I did ask one of my doctor relatives if she has any patients with DS; I said that there may be a treatment for their MR/ID.  She is not going to prescribe her patients anything off-label, so unless Ben-Ari decides he wants to help people with DS, as well as ASD, people will DS will remain untreated.  I will ask him.

Also, given the large amount of money going into the genetics of autism, perhaps it would be worth looking at those 310 genes located on chromosome 21 to see if the overexpression of one may trigger speech loss in people with regressive autism and/or might be present from birth in people with classic autism.  One of them must trigger the speech loss in that sub-group of adults with DS.

Reassessing Cognitive Impairment in Autism – Improving the Prognosis

When Monty, now aged 11 with ASD, was diagnosed aged three and a half we were told that he had autism and “this may be indicative of the presence of an associated learning disability, but it is impossible at this stage to give a prognosis as to his future difficulties” and also “he is not yet able to take part in formal assessments of his cognitive ability. When his skills and ability to share interests with adults and to follow direction/instruction develop, it will be possible to formally assess his cognitive skills using standard measures.”

Off the record, we were also told that he might develop epilepsy.

We never measured his IQ and he has never had a seizure.

With hindsight, it is interesting what they said about it being pointless to try and measure his IQ.  Apparently it is not uncommon to do just that.

Improving Cognitive Function

This post is about cognitive improvement, so do not be put off by the introduction to MR/ID.  Several regular readers who are using some of the suggested drugs discussed in this blog are now also commenting on the resulting cognitive improvement, so it really is not just a case of N=1.

Nobody here is measuring the change in their child’s IQ, so these remain anecdotes.

To start on a happy note

Monty, aged 11 and diagnosed with classic autism, has been learning the piano for three years.  At the start he was not very cooperative with his teacher and after a few months the lessons stopped.  

27 months ago he started on bumetanide, the first part of his autism Polypill.  After years of ABA, slow but solid development appeared to have reached a plateau; but then he began to accelerate.  We restarted piano lessons again, with a new teacher.  Having added Atorvastatin, from the very next day he began to practice daily, playing without his teacher.  He has had two 40 minutes lessons most weeks since.  Two years later this is the result:-

 Click the image to play, turn up the volume (video may not work on Apples)

  

  

So there is no doubt that Monty got smarter.  When I heard him playing this piece, I thought it was the piano teacher, but she was recording Monty on her phone.

Big brother also did not believe little brother was playing this, until he saw the full video (with moving fingers).

Reading, writing, and numeracy have all improved and are now at a similar level to those of many of his NT classmates (who are 2 to 3 years younger than him).  Rather unexpectedly, he was recently the only one in class who understood how to multiply fractions; this was never taught at home.   

Prior to starting the Polypill drugs, I had spent three years, on and off, trying to teach Monty prepositions, without much progress.  This is almost always a difficult area for those with classic autism.  In the end he figured it all out by himself, with a little help from Bumetanide.

Recently yet another cognitive step forward seems to have have occurred, which appears to be the result of PAK 1 inhibiting propolis and/or the tangeretin flavonoid.  Monty's assistant in school was today proudly showing me his latest school test result, "73% and it was all his own work".  She thinks it is the tangeretin.

In earlier years school was for “socialization”, not learning.  This is fine as long as the learning takes place at home, otherwise inclusion means no education.

Cognitive Function, IQ, MR/ID

I prefer to talk about cognitive function, and its improvement or enhancement.  Drugs that achieve this are usually called Nootropic.

I think that many people remain skeptical about Nootropics.

Psychiatrists, Pediatricians and Psychologists prefer to think about IQ, MR/ID.

People affected do not like the old term of Mental Retardation (MR) and so quite recently, in English speaking countries, it was replaced by the term Intellectual Disability (ID).  The World Health Organization still use the old term, as does almost everybody else.

Somebody is diagnosed with MR or ID if their IQ is below 70.  In a typical group of 100 people, two people (2.2%) would be expected to fall into that category.  The average IQ (mean, median and mode) is 100.

In theory as you progress through childhood and into adulthood your IQ is expected to stay the same.  So the tests used adjust for your age.  There are special non-verbal tests.

If you acquire new skills at a lower rate than typical, your IQ would appear to fall over time.  This does not mean that you have lost skills just that you are acquiring new skills at a slower rate than your peers.  This explains why parents of kids with ASD, who do have their IQ tested, often find their score goes down as they get older.

Measuring IQ in Autism

I think it is generally a bad idea to measure IQ in people with autism.

There is anecdotal evidence to show that the results are often not valid, because the test is based on the assumption of compliance and that the child is actually doing his/her best.  Not surprisingly, the experts have found that children undergoing an ABA program improve their measured IQ by 10s.  After a few months of ABA the previously unfocused child has been trained to sit down, sit still, pay attention and work.  Of course they then get a higher score, but are they now more intelligent?

One reason put forward for not measuring IQ, is that while people will go a long way to help a child with autism to learn, once you add a diagnosis of MR/ID, some people will try much less hard.

Nonetheless people do measure IQ in autism and it is worth a quick look at what is known.

Some people are saying that 50% of people with autism have MR/ID.  I always found that odd, and what exactly do they mean by autism?

Using the previous US DSM definitions, Asperger’s was a part of the autistic spectrum but had the precondition that there was no MR/ID and no language delay.  Then you had the middle group with the odd name of PDD-NOS    (Pervasive Developmental Disorder Not Otherwise Specified).  This groups the people with more issues than Asperger’s, but without many of the problems experienced by those diagnosed with Autism.

So in the old US system there were 3 main categories, plus 2 minor ones:-

1.     Asperger’s

2.     PDD-NOS

3.     Autism

4.     Retts Syndrome

5.     Childhood Disintegrative Disorder (CDD)

Very few people have Retts or CDD.

The Autistic Spectrum was, in effect, also called PDD (Pervasive Developmental Disorder) just to confuse people a little more.  PDD = ASD = the above five conditions.

The latest version DSM5 went several steps backwards.  Everybody affected in the US is now just ASD, all five categories were merged.  

Hopefully nobody else in the world will pay any attention.

Unfortunately being Psychiatrists, they again have to muddy the water and all the future data/statistics.  A portion of people formerly diagnosed with PDD-NOS, will now get diagnosed with SCD (Social Communication Disorder) which is set outside the new definition of ASD.

“Congratulations you are off the Spectrum” 

I really do wonder about the IQ of these Psychiatrists.

Reliable Data on ASD

I do like to have some reliable data.  The quality of data in the field of autism is usually very poor and incompatible (i.e. rubbish).  Most data, like that from the CDC in the US, is unreliable.  It seems that richer “Ethnic European” parents push to get an autism diagnosis much harder than poorer “Hispanic” and “African American” parents.  Perhaps hard to believe as an outsider, but in the US poverty equals low diagnosis of autism and wealth equals high diagnosis.  Incidence does not equal diagnosis.  CDC data is just who got diagnosed; in the US many poorer people do not get diagnosed.  If you live in a country with free socialized healthcare, as in Europe, this will look strange.

I have chosen a highly regarded, and very highly cited, Canadian source for my data.

Éric Fombonne  is a French psychiatrist and epidemiologist based at McGill University in Montreal.  He co-authored a pair of studies in 2001 and 2005 with Suniti Chakrabarti, that examined the entire preschool and early school population of one large area of the United Kingdom (falling under the South Staffordshire Health Authority).

There is a stable population of indigenous British people with a small (1.4%), mostly Asian, immigrant population. The total population living in the area was 320 000 people.

The studies are:-

Pervasive Developmental Disorders in Preschool Children, 2001

Pervasive Developmental Disorders in Preschool Children: Confirmation of High Prevalence, 2005

All children from 2.5 to 6.5 years old were screened, a total of 15,500 children in total 97 children (79.4% male)  were found to have a PDD (i.e. be somewhere on the autistic spectrum)

Of the 97 children, 29 (29.9%) had no functional use of language defined as the daily spontaneous use of 3-word phrases. The proportion of children without functional language was however strongly associated with diagnostic subtype (AD, 69.2%; Asperger syndrome, 0%; PDD-NOS, 16.1%).

Of the 97 children, 37 children underwent Merrill-Palmer testing and 56, Wechsler Preschool and Primary Scale of Intelligence testing. Four children could not be tested for practical reasons. Overall, 24 (25.8%) of 93 children had some degree of mental retardation. The 2 children with childhood disintegrative disorder and Retts syndrome scored in the moderate range of mental retardation.

Side-note about shoddy research

To show those of you still unconvinced that published, and moderately highly cited, autism research can be rubbish, the authoritative sounding paper written by a Professor of Psychology below also reviewed the above research data.

Are the Majority of Children With Autism Mentally Retarded? A Systematic Evaluation of the Data

The author commented:-

“Recent epidemiological surveys have shown that the prevalence rates of MR in children with autism is between 40% and 55% (e.g., Chakrabarti & Fombonne, 2001), much lower than the typical rates cited in the literature.”

The Chakrabarti & Fombonne 2001 paper clearly shows 69% of people with the narrow diagnosis of “autism” had MR whereas 25.8% of those with the broader diagnosis of ASD/PDD.

More than 100 other papers now cite the author’s incorrect readings of the original research.

I do not know what IQ you need to have to be a Professor of Psychology, but it clearly needs to be increased.

Back to the Fombonne studies

Four years later they repeated the same study on the next cohort of English school children:-

The rate of mental retardation in the autistic disorder group was 66.7%, compared to 12.0% in the group with pervasive developmental disorder not otherwise specified and 0.0% in the Asperger's disorder group

So I will take the average of the two studies

            Autism                       68% with MR/ID

            PD-NOS                     10% with MR/ID

            Asperger’s                    0% with MR/ID

What surprised me was the breakdown of the children by PDD.  Most kids (>50%) were PD-NOS, I did not expect that.

  Autism                        31%

            PD-NOS                     52%

            Asperger’s                  16%

            CDD/Retts                    1%

So the percentage all PDD (i.e. all ASD) with MR was 27%

Combining this as a graphic:-  

  

So now when people tell me that 50% of kids with autism have MR/ID, at least I know the likely reality.  It is either more, or less, depending on what you mean by “autism”; but is not 50%.

Conclusion

Most people think you cannot change your IQ.

The reality is that testing a young child with severer ASD is highly likely to underestimate their IQ, since the test assumes that the child will comply with the tester.  Most young children with autism do not comply with their parents, let alone an IQ tester.

ABA will improve compliance and hence improve an IQ test result.

Long term ABA use will, in many cases, gradually improve the child’s ability to learn and hence boost cognitive function and by implication an IQ test result.  You will find references to people saying ABA raised their kids IQ score by one or two dozen.

Correcting the biological dysfunctions underlying autism undermines the whole shaky DSM system.

PDD-NOS is, in effect, milder classic autism without the stereotypy .

Take some N-acetyl cysteine pills, you lower oxidative stress and you can stop the stereotypy.  So then your “expert” diagnosis would change from classic autism to PDD-NOS?

Take a few more pills and instead being in the 68%, with an IQ of less than 70, you can move up to 85 and, who knows, maybe much higher.

But it has to be said that the concept of IQ is something many people think they understand.

If one day, I were to make a clinical trial of my autism Polypill, I would definitely include a before and after measurement of IQ, alongside all the usual behavioral measures that most people would not understand.

And then …

“Wonder drug rescues people with autism from mental retardation”

In the meantime, we can continue correcting the remaining biological dysfunctions underlying autism and thus improving cognitive function.

Note the rocket, for those with classic autism doing just this and changing their prognosis.