Taking the MBTI with HFA

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Back in the early 2000s I was working in America for Cable & Wireless. One of my colleagues was Craig, a Duke University professor of psychiatry; his wife, Dee Ann, was also trained in psychotherapy. I remember talking to her at one of our works dinners about the Myers-Briggs classification scheme and when it didn't work. She replied that it tended to give erratic results with people who exhibited abnormal mental conditions, such as schizophrenia and Asperger's syndrome.

And I left it there.

Today I'm wondering what happens if a person with High-Functioning Autism (formerly Asperger's syndrome) takes the Myers-Briggs Inventory. How does their MBTI come out?

ChatGPT tells me...

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How HFA People Score on the Myers–Briggs Type Indicator

The Myers–Briggs Type Indicator rests on population averages of neurotypical psychology. It was never built to describe autistic cognition. When people with high-functioning autism (HFA) take the MBTI, the results often wobble or misclassify. The same is true of the Five Factor Model, though in a different way.

Take the S/N dimension. Some autistic people live in concrete domains: bus timetables, mechanical systems, the fine grain of sensory detail. They look like S. Others immerse themselves in mathematics, philosophy, speculative worlds. They look like N. Both are common.

The test assumes the two poles are exclusive; autism ignores that rule. A developer who can design high-performance real-time transaction systems may come out as a classic N for abstract thinking. Yet ask him about politics or engage in small talk and he seems incurious, even obtuse - answers that tilt back toward S.

Extraversion is another fault line. HFA people can be talkative, sometimes performatively gregarious, yet maintain no close friends. The MBTI interprets their verbal energy as E, while their lived experience is solitary. A literal answer to “Do you enjoy going to parties?” might be “Yes, I like the food and the noise,” even if the same person leaves early, interacts with no one, and has no social bonds. The test confuses stimulus-seeking with sociability.

On the T/F scale, many answer as T. They rely on explicit reasoning, exploiting rules and consistency. That does not mean they lack affect, only that their affect is not measured in the MBTI’s idiom. Similarly, the J/P axis is confounded: autism’s need for sameness, its preference for routine, shows up as J. But this is neurology, not “personality preference”.

If you shift to the Big Five, the pattern persists. “Openness” can score high if interests are abstract, or low if they are repetitive and concrete. “Conscientiousness” may appear strong on orderliness but weak on adaptive planning. “Agreeableness” is pulled down by low empathy-related items, though fairness and honesty are often high. “Neuroticism” is inflated by anxiety, a frequent comorbidity. Instability is the rule.

The real problem is structural. These instruments assume traits cluster as they do in the neurotypical bell curve. Autism reshuffles the deck. Literal answering, context-bound interpretations, and construct mismatch ensure that the outputs are noisy. What looks like inconsistency is the wrong measurement framework.

Better alternatives exist. The Empathising–Systemising Quotient, the RAADS-R, and sensory processing profiles capture dimensions orthogonal to MBTI and FFM. They measure the axes on which autistic cognition varies.

So when an HFA person emerges from the MBTI as ENTJ one month and ISFP the next, it is not a crisis of self-knowledge. It is the instrument failing to fit the mind it tries to describe.

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Chris Packham: coming out as an Aspie

Chris Packham

The BBC recently showed Chris Packham's hour-long documentary where he discusses his Asperger's syndrome (iPlayer till 27th October).

Strictly speaking you don't have Asperger's, you are Asperger's. This makes treatment problematic - are you signing up to erase, or profoundly modify, your personality?

Packham wasn't a fan, particularly as this seemed to be the dominant objective of the American 'therapies' he was taken to see.

His partner, Charlotte, who was on camera seemed to be a Myers-Briggs NT, maybe INTJ. She came across as cool, composed and eminently cerebral: a meeting of minds.

There's another kind of partner an 'Asperger's sufferer' can have: here's Paul Dirac's wife:

"Given his lack of interest in his fellow humans, most colleagues assumed Dirac was shut off sexually, or perhaps gay and repressed. So they got a bit of a shock when, in 1934, he met a chatty Hungarian divorcee called Manci Balazs and three years later married her.

Manci was his opposite: where Dirac hardly spoke, she never stopped; he found empathy difficult, she had friends coming out of her ears; he was very literal-minded, she was subjective and passionate.

Needless to say, it was she who was forced to woo him, but somehow it worked. As a friend once put it: 'He gave her status and she gave him a life.' They were married for 50 years and had two children.

A year after their marriage, he wrote Manci a lovely letter saying: 'You have made me human. I shall be able to live happily with you even if I have no more success in my work.'

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I was surprised to hear Packham pronounce his condition 'Asperjers'; surely he, more than anyone, would know that Hans Asperger was Austrian, and as a consequence the 'g' is hard.

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Asperger's (and Autism in general) is highly heritable, although Packham's documentary - more impressionistic and personal - made no mention of it. This means that most population variation along the autism spectrum, from normal (non-autistic) to extreme, is a consequence of individual genomic variation, rather than differential input from the environment.

So although your parents made you autistic, it was through their genes, not their parenting.

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Autism and IQ

From Time:

"When Asperger’s was first described in 1944 by Austrian pediatrician Hans Asperger, he referred to children with the syndrome as “little professors” because of their prodigious vocabularies and precocious expertise, and because they tended to lecture others endlessly without being aware of their own tediousness. Poor social skills and obsessive interests characterize the condition.

Yet, despite the obvious similarities, very little research has been done on the connection between autism and extreme talent. One previous study, published in 2007, did find that close relatives of prodigies — like close relatives of people with autism — tended to score higher on autistic traits, particularly in problems with social skills, difficulty switching attention and intense attention to detail. Other than that, however, the issue hasn’t been studied systematically, beyond the observation that autism is often seen in savants, or people with exceptional abilities who have other simultaneous impairments. ..."

"... the intense world theory of autism, which posits how the disorder may arise. The theory holds that certain patterns of brain circuitry cause autistic symptoms, including excessive connectivity in local brain regions, which can heighten attention and perception, and diminished wiring between distant regions, which can lead to a sort of system overload. In both animal and human studies, this type of brain wiring has been associated with enhanced memory and also with amplified fear and sensory overstimulation. The former is usually a good thing; the latter may cause disability.

The intense world theory propounds that all autism carries the potential for exceptional talent and social deficits. The social problems, the theory suggests, may ensue from the autistic person’s dysfunctional attempts — social withdrawal and repetitive behaviors, for instance — to deal with his heightened senses and memory.

It’s possible, then, that the wiring in prodigies’ brains resembles that of an autistic person’s, with tight local connections, except without the reduction in long-distance links. Or, their brains may function just like those with autism, but their high intelligence allows them to develop socially acceptable ways of coping with the sensory overload."

I was struck by a TV programme some years ago about the Maths Olympiad. This is usually won by East Asians; Ashkenazim are also well-represented in winning teams. The British team was composed of pleasant, well-adjusted and extremely smart Ashkenazim .. and Anglo-Saxons who all seemed to be Aspies.

In the Gregory Cochran, Jason Hardy, and Henry Harpending paper it was suggested that the Ashkenazim had undergone extreme selection for high IQ over the last millennium due to the social niche of finance into which they were forced for so many centuries by the Christian proscription of usury. This, they argued, had also increased the frequency of specific mutations which increased brain efficiency at the cost of new debilitating genetic diseases (in the homozygous cases).

I suspect Asperger's may be somewhat similar, although with a more diffuse and sprawling etiology. As the causation is polygenic (+ CNV?) we are still some way from a definitive account.

A polygenic risk for autism spectrum disorders

The full title of the paper in the news today is "Genetic risk for autism spectrum disorders and neuropsychiatric variation in the general population" authored by a cast of thousands. It's published in Nature Genetics - here's the abstract.

"Almost all genetic risk factors for autism spectrum disorders (ASDs) can be found in the general population, but the effects of this risk are unclear in people not ascertained for neuropsychiatric symptoms. Using several large ASD consortium and population-based resources (total n > 38,000), we find genome-wide genetic links between ASDs and typical variation in social behavior and adaptive functioning.

"This finding is evidenced through both LD score correlation and de novo variant analysis, indicating that multiple types of genetic risk for ASDs influence a continuum of behavioral and developmental traits, the severe tail of which can result in diagnosis with an ASD or other neuropsychiatric disorder. A continuum model should inform the design and interpretation of studies of neuropsychiatric disease biology."

At some level this is not too surprising, there's not a 'gene for autism or Asperger Syndrome' any more than there's a gene for height or intelligence. Instead a number of alleles of small effect push the genome towards or away from autism spectrum traits, with de novo negative mutations adding a sprinkling of gratuitous damage.

There is a dataset of families where one family member has an ASD (autism spectrum disorder) while the the rest are not so classified. This is the Simons Simplex Collection (SSC):

"The Simons Simplex Collection (SSC) is a core project and resource of the Simons Foundation Autism Research Initiative (SFARI). The SSC achieved its primary goal to establish a permanent repository of genetic samples from 2,600 simplex families, each of which has one child affected with an autism spectrum disorder, and unaffected parents and siblings."

There is a test, similar to an IQ test, which measures the level of difficulty experienced by people with an ASD. It's called the Vineland Adaptive Behavior Rating Scale (VABS):

"Raw scores are converted to IQ-type standard scores (mean: 100 sd: 15) for each domain and for the composite adaptive behavior score. Score ranges are as follows:

• 70-80 borderline adaptive functioning; 
• 51-55 -70: mildly deficient adaptive functioning ; 
• 35-50: moderately deficient adaptive behavior; 
• 20-35: severely deficient adaptive behavior; 
• less than 20: markedly or profoundly deficient adaptive behavior. 

Scores above 80 are classified in approximately the same ranges (low average, average, above average, superior) as IQ scores."

When you test the SSC non-ASD people (controls) vs. SSC people with ASD (cases) using the VABS, this is what you see:

Figure 2 from the Nature Genetics paper 

You plainly observe the overlap between non-ASD and ASD people on a scale designed to measure degrees of autistic behaviour.

While this histogram does not directly exhibit the underlying genetic analysis, it's exactly what you expect to see from a polygenic syndrome.