Further thoughts on spiteful mutants

I’ve had two requests recently, one for opinions about the spiteful mutant hypothesis, the other about Kaczynski’s work. These are related concepts, of course, in that they both deal with the structure of society.

It took me a little while to realize that the “spiteful mutant” hypothesis has to do with bioleninism, not just studies about mice (clearly I haven’t been reading the right things). Bioleninism is the idea that elites may prefer to hire/promote unqualified people because these people will then be more loyal to the regime because they know they couldn’t get as good a job elsewhere.

The problem with this theory is that the “unqualified” people being hired by the elites are not grateful or loyal at all. If anything, they are resentful, malicious, petty, and greedy, ready to tear down everyone who “gave them a chance,” especially if they think they can promote themselves at the same time.

The difficulty with the mouse models is that they deal with autistic-model mice and their effects on the social structure of a normal mouse colony, but in real life, the people throwing wrenches into society are not autistic–if anything, they are hyper-social. (Or as Ted would say, they are oversocialized.)

Humans, obviously, are not mice. Humans build things. (Mice build things, too, but much less than humans.) We build lots of things, especially those of us in the modern, industrialized world.

I’m sure I’ve harped this over and over, but I still find the modern, industrial world amazing (and slightly disconcerting). I am amazed that our homeless are fat, that ordinary people have toilets, that infant mortality is below 1%. On the scale of human history, we as a species have changed almost everything about our lives in the blink of an eye, and we have yet to see how all of this works out for us. Certainly we are not adapted to it, but that doesn’t necessarily make it bad.

Building our modern world has required the development of new mental skills that our ancestors didn’t possess, like reading, writing, and arithmetic. 10,000 years ago, before the invention of the alphabet, these skills didn’t exist; today almost everyone has mastered them.

Language, both oral and written, requires the ability to generalize. Take something as simple as the letter “A”. It comes in three standard forms, A, a, and the little a used in handwriting. It also comes in many different fonts, in sloppy and neat handwriting, in cursive and smudged ink. You can read the letter “a” even when part of the letter is missing.

Even worse than the variability in the mere shape of the letter, “A” does not consistently refer to a particular sound. It sounds like it is supposed to in “apple,” but sounds like a U in “was.”

Now multiply by the whole alphabet and all of the different voices and accents, noisy rooms and distorted audio, and it’s a wonder that we can understand each other at all, much less read sentences like, “Rpie rsapebrreis are delciiuous in the smmuertmie,” and “Gosts luv cookies b_t candy iz b_ttr.”

Our understanding of language relies on a lot of processing to fill in the gaps between what we hear/see and what was meant. A similar effect is at play with optical illusions.

Both of these faces, for example, are red. Your brain takes the raw data from your eyes, does some processing and color-correction to account for the other colors in the image, and ends up concluding that one screamer is actually orange.

Our brains do this because real life has shifting patterns of color and shade, and our brains are trying to figure out the “real” color if you remove those effects.

One of the interesting things about autistic people is that they are less likely to “see” optical illusions. This might turn out to be one of those amusing psychological findings that doesn’t replicate, but assuming it’s sound, it seems to be because their brains do less processing of the raw data the receive. This means they see the world more as it actually is and less as they think it should be.

The advantage to seeing the world as it actually is and not as you want it to be obviously lies in professions that autists or semi-aspie people excel in, like math and engineering. Unlike reading, you can’t just go filling in missing data in mathematical equations. Lewis Carol could write poems by stringing together things that sound like words, but you can’t build a circuit by wiring together a bunch of capacitors into something that looks generally like the idea of a circuit. An equation that is missing a digit isn’t solvable, a measurement with a misplaced decimal is useless (and potentially deadly), and a misplaced image tag in a post’s code once completely messed up my blog’s layout.

If reading and talking require being good at adding information until you get the general gist of what is meant, math and engineering require carefully not adding information. Humans aren’t very good at this, because it’s a very new skill.

Modern industrial civilization is only possible because of precision engineering. You cannot fit a billion transistors on a microchip without precision. You cannot send communication and navigation satellites into space without building complicated rockets that have to not explode on the launchpad (a surprisingly difficult task) and then precisely calculating their trajectories (otherwise they will veer off disastrously. These computations are complex enough that they tax the limits of human abilities–as Drozdov et al wrote in Fundamentals of Computer Technology in 1964:

Assume that we are to determine the trajectory of a guided space rocket. For this purpose we must calculate the points of the trajectory lying far ahead in the direction of motion of the rocket; only in that case can we estimate the deviation of the rocket from the prescribed direction and apply the necessary midcourse corrections. Such a calculation can be made only by an electronic computer, since workers would require tens of days or several months to calculate a single trajectory, while a rocket takes only three days to reach the moon. The computer will calculate the trajectory in minutes or tens of minutes.

Computers allow us to be more precise, much faster.)

Back in the 1700s, sailors faced a daunting problem: they had no reliable way to measure longitude while at sea. In 1707, inability to determine their position led to four British warships crashing and sinking, causing the deaths of over a thousand sailors. The British Parliament subsequently offered a reward of 20,000 pounds (that would be about 3 million pounds today,) to anyone who could solve the problem.

Early attempts focused on old fashioned methods of finding one’s way and telling time: the heavens. The board awarded 3,000 pounds, for example, to the widow of Tobias Mayer for his lunar tables. Just as the shadows cast by the sun or the height of the north star could be used to determine one’s latitude, so, they hoped, could the moon assist with longitude. Unfortuantely, this method is clunky, difficult, and relies too much on being able to see the moon.

The clockwork in Harrison’s H4 watch

John Harrison came up with a radically new solution: a watch. So long as your watch shows Greenwich time, you can compare it to the local time (observable via the sun or stars,) and the difference shows your longitude. Unfortunately, clocks that kept time precisely enough to accurately determine one’s latitude far from land didn’t exist in Harrison’s day: he had to build them himself. The resulting clocks are masterpieces, incredibly accurate for their day:

Harrison began working on his second ‘sea watch’ (H5) while testing was conducted on the first, which Harrison felt was being held hostage by the Board. After three years he had had enough; Harrison felt “extremely ill used by the gentlemen who I might have expected better treatment from” and decided to enlist the aid of King George III. He obtained an audience with the King, who was extremely annoyed with the Board. King George tested the watch No.2 (H5) himself at the palace and after ten weeks of daily observations between May and July in 1772, found it to be accurate to within one third of one second per day. King George then advised Harrison to petition Parliament for the full prize after threatening to appear in person to dress them down. Finally in 1773, when he was 80 years old, Harrison received a monetary award in the amount of £8,750 from Parliament for his achievements, but he never received the official award (which was never awarded to anyone). He was to survive for just three more years. …

Captain James Cook used K1, a copy of H4, on his second and third voyages, having used the lunar distance method on his first voyage.^[22] K1 was made by Larcum Kendall, who had been apprenticed to John Jefferys. Cook’s log is full of praise for the watch and the charts of the southern Pacific Ocean he made with its use were remarkably accurate.

Okay, so that was a bit of an aside, but it’s a great story.

Societies with primitive technology have much less need for precision. It is difficult to imagine what a John Harrison would have dedicated his life to in a tribe of nomadic goat herders: they would have no need for second-level time-keeping precision. Primitive people didn’t even need fancy numbers like “12;” our lovely base-10 number system is a recent invention. Primitive people generally got by with tally marks; many had number systems that essentially stopped at 3: 1, 2, 3, lots.

We discussed this back in my review of Numbers and the Making of Us; the author spent much of his childhood among the Piraha of the Amazon, who have almost no words for numbers and no sense of number bigger than three (the first three are instinctual; many animals can count to three).

The author’s parents (missionaries) have actually tried to teach the Piraha to count, but after many years of training they still struggled to grasp concepts like “7” and 1-to-1 correspondence (that is, if I set up a line of 7 cans, can you set up a matching line that also contains 7 cans?)

In short, the advance of technology over the past 200 years has required the development of much higher levels of mental precision than our ancestors used.

Most people, of course, want to be precise sometimes and generalize at other times, and our brains naturally switch between the two modes depending on what we’re doing, but there is obviously a trade-off between being exceptionally good at either variety. (Smart people may have enough brains to do both well, but the rest of us have to pick one side or the other.)

In the “spiteful mutants” experiment, mouse society is inherently social, and the mutants who disrupt it are “autistic” (or what passes for autism in mice). In real life, much of our modern world was built by thing-obsessed people like John Harrison or Bill Gates. Our society isn’t “autistic” by any means, but there is a place for them that wouldn’t exist in other societies. By contrast, the “spiteful mutants” in our society are oversocialized folks like this guy:

@wesyang is the only non-black author on my list. The truth is that the subject of race in 21st-century America is far from simply black and white. We need to think hard about the complicated and liminal space in which Asian American identity is made and contested.

— Thomas Chatterton Williams 🌍 🎧 (@thomaschattwill) June 27, 2020

No one who was busy trying to get the tolerances on their widget-producing machines down to less than a tenth of a millimetre ever had time to worry about the “liminal space” in which anyone’s identity is made.

In short, these people are trying to make us more social, more hierarchical, more like the original mouse community with all of the mice focused on reading social cues from each other and less like the “mutant” community with its focus on social cues and things.

As for where Ted fits into all of this, well, I suppose blowing people up is pretty spiteful, but he might not have in the first place if people had just left his woods alone.

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The Autism Matrix

Just a thought this morning, but I think the “autism spectrum” would be better characterized as a “matrix” with intelligence running along one axis and impairment on the other.

We can divide this into four useful quadrants, representing high IQ & high impairment, high IQ & low impairment, low IQ & high impairment, and low IQ and low impairment.

Of course these are not entirely unrelated measures–the impairment that causes autism can also cause low IQ, but it makes a functional distinction because different quadrants suffer different challenges and limitations.

The traditional distinction was between “autism” and “asperger’s,” with asperger’s generally reserved for the smarter, higher functioning kids. Asperger’s has been dropped as a diagnosis due to this distinction being not the most useful–there are high-functioning dumb kids with autism and low-functioning smart kids. (And adults.)

Just a little thought.

Can Autism be Cured via a Gluten Free Diet?

I’d like to share a story from a friend and her son–let’s call them Heidi and Sven.

Sven was always a sickly child, delicate and underweight. (Heidi did not seem neglectful.) Once Sven started school, Heidi started receiving concerned notes from his teachers. He wasn’t paying attention in class. He wasn’t doing his work. They reported repetitious behavior like walking slowly around the room and tapping all of the books. Conversation didn’t quite work with Sven. He was friendly, but rarely responded when spoken to and often completely ignored people. He moved slowly.

Sven’s teachers suggested autism. Several doctors later, he’d been diagnosed.

Heidi began researching everything she could about autism. Thankfully she didn’t fall down any of the weirder rabbit holes, but when Sven’s started complaining that his stomach hurt, she decided to try a gluten-free diet.

And it worked. Not only did Sven’s stomach stop hurting, but his school performance improved. He stopped laying his head down on his desk every afternoon. He started doing his work and responding to classmates.

Had a gluten free diet cured his autism?

Wait.

A gluten free diet cured his celiac disease (aka coeliac disease). Sven’s troublesome behavior was most likely caused by anemia, caused by long-term inflammation, caused by gluten intolerance.

When we are sick, our bodies sequester iron to prevent whatever pathogen is infecting us from using it. This is a sensible response to short-term pathogens that we can easily defeat, but in long-term sicknesses, leads to anemia. Since Sven was sick with undiagnosed celiac disease for years, his intestines were inflamed for years–and his body responded by sequestering iron for years, leaving him continually tired, spacey, and unable to concentrate in school.

The removal of gluten from his diet allowed his intestines to heal and his body to finally start releasing iron.

Whether or not Sven had (or has) autism is a matter of debate. What is autism? It’s generally defined by a list of symptoms/behaviors, not a list of causes. So very different causes could nonetheless trigger similar symptoms in different people.

Saying that Sven’s autism was “cured” by this diet is somewhat misleading, since gluten-free diets clearly won’t work for the majority of people with autism–those folks don’t have celiac disease. But by the same token, Sven was diagnosed with autism and his diet certainly did work for him, just as it might for other people with similar symptoms. We just don’t have the ability right now to easily distinguish between the many potential causes for the symptoms lumped together under “autism,” so parents are left trying to figure out what might work for their kid.

Interestingly, the overlap between “autism” and feeding problems /gastrointestinal disorders is huge. Now, when I say things like this, I often notice that people are confused about the scale of problems. Nearly every parent swears, at some point, that their child is terribly picky. This is normal pickiness that goes away with time and isn’t a real problem. The problems autistic children face are not normal.

Parent of normal child: “My kid is so picky! She won’t eat peas!”

Parent of autistic child: “My kid only eats peas.”

See the difference?

Let’s cut to Wikipedia, which has a nice summary:

Gastrointestinal problems are one of the most commonly associated medical disorders in people with autism.^[80] These are linked to greater social impairment, irritability, behavior and sleep problems, language impairments and mood changes, so the theory that they are an overlap syndrome has been postulated.^[80][81] Studies indicate that gastrointestinalinflammation, immunoglobulin E-mediated or cell-mediated food allergies, gluten-related disorders (celiac disease, wheat allergy, non-celiac gluten sensitivity), visceral hypersensitivity, dysautonomia and gastroesophageal reflux are the mechanisms that possibly link both.^[81]

A 2016 review concludes that enteric nervous system abnormalities might play a role in several neurological disorders, including autism. Neural connections and the immune system are a pathway that may allow diseases originated in the intestine to spread to the brain.^[82] A 2018 review suggests that the frequent association of gastrointestinal disorders and autism is due to abnormalities of the gut–brain axis.^[80]

The “leaky gut” hypothesis is popular among parents of children with autism. It is based on the idea that defects in the intestinal barrier produce an excessive increase of the intestinal permeability, allowing substances present in the intestine, including bacteria, environmental toxins and food antigens, to pass into the blood. The data supporting this theory are limited and contradictory, since both increased intestinal permeability and normal permeability have been documented in people with autism. Studies with mice provide some support to this theory and suggest the importance of intestinal flora, demonstrating that the normalization of the intestinal barrier was associated with an improvement in some of the ASD-like behaviours.^[82] Studies on subgroups of people with ASD showed the presence of high plasma levels of zonulin, a protein that regulates permeability opening the “pores” of the intestinal wall, as well as intestinal dysbiosis (reduced levels of Bifidobacteria and increased abundance of Akkermansia muciniphila, Escherichia coli, Clostridia and Candida fungi) that promotes the production of proinflammatory cytokines, all of which produces excessive intestinal permeability.^[83] This allows passage of bacterial endotoxins from the gut into the bloodstream, stimulating liver cells to secrete tumor necrosis factor alpha (TNFα), which modulates blood–brain barrier permeability. Studies on ASD people showed that TNFα cascades produce proinflammatory cytokines, leading to peripheral inflammation and activation of microglia in the brain, which indicates neuroinflammation.^[83] In addition, neuroactive opioid peptides from digested foods have been shown to leak into the bloodstream and permeate the blood–brain barrier, influencing neural cells and causing autistic symptoms.^[83] (See Endogenous opiate precursor theory)

Here is an interesting case report of psychosis caused by gluten sensitivity:

 In May 2012, after a febrile episode, she became increasingly irritable and reported daily headache and concentration difficulties. One month after, her symptoms worsened presenting with severe headache, sleep problems, and behavior alterations, with several unmotivated crying spells and apathy. Her school performance deteriorated… The patient was referred to a local neuropsychiatric outpatient clinic, where a conversion somatic disorder was diagnosed and a benzodiazepine treatment (i.e., bromazepam) was started. In June 2012, during the final school examinations, psychiatric symptoms, occurring sporadically in the previous two months, worsened. Indeed, she began to have complex hallucinations. The types of these hallucinations varied and were reported as indistinguishable from reality. The hallucinations involved vivid scenes either with family members (she heard her sister and her boyfriend having bad discussions) or without (she saw people coming off the television to follow and scare her)… She also presented weight loss (about 5% of her weight) and gastrointestinal symptoms such as abdominal distension and severe constipation.

So she’s hospitalized and they do a bunch of tests. Eventually she’s put on steroids, which helps a little.

Her mother recalled that she did not return a “normal girl”. In September 2012, shortly after eating pasta, she presented crying spells, relevant confusion, ataxia, severe anxiety and paranoid delirium. Then she was again referred to the psychiatric unit. A relapse of autoimmune encephalitis was suspected and treatment with endovenous steroid and immunoglobulins was started. During the following months, several hospitalizations were done, for recurrence of psychotic symptoms.

Again, more testing.

In September 2013, she presented with severe abdominal pain, associated with asthenia, slowed speech, depression, distorted and paranoid thinking and suicidal ideation up to a state of pre-coma. The clinical suspicion was moving towards a fluctuating psychotic disorder. Treatment with a second-generation anti-psychotic (i.e., olanzapine) was started, but psychotic symptoms persisted. In November 2013, due to gastro-intestinal symptoms and further weight loss (about 15% of her weight in the last year), a nutritionist was consulted, and a gluten-free diet (GFD) was recommended for symptomatic treatment of the intestinal complaints; unexpectedly, within a week of gluten-free diet, the symptoms (both gastro-intestinal and psychiatric) dramatically improved … Despite her efforts, she occasionally experienced inadvertent gluten exposures, which triggered the recurrence of her psychotic symptoms within about four hours. Symptoms took two to three days to subside again.

Note: she has non-celiac gluten sensitivity.

One month after [beginning the gluten free diet] AGA IgG and calprotectin resulted negative, as well as the EEG, and ferritin levels improved.

Note: those are tests of inflammation and anemia–that means she no longer has inflammation and her iron levels are returning to normal.

She returned to the same neuro-psychiatric specialists that now reported a “normal behavior” and progressively stopped the olanzapine therapy without any problem. Her mother finally recalled that she was returned a “normal girl”. Nine months after definitely starting the GFD, she is still symptoms-free.

This case is absolutely crazy. That poor girl. Here she was in constant pain, had constant constipation, was losing weight (at an age when children should be growing,) and the idiot adults thought she had a psychiatric problem.

This is not the only case of gastro-intestinal disorder I have heard of that presented as psychosis.

Speaking of stomach pain, did you know Curt Cobain suffered frequent stomach pain that was so severe it made him vomit and want to commit suicide, and he started self-medicating with heroin just to stop the pain? And then he died.

Back to autism and gastrointestinal issues other than gluten, here is a fascinating new study on fecal transplants (h/t WrathofGnon):

Many studies have reported abnormal gut microbiota in individuals with Autism Spectrum Disorders (ASD), suggesting a link between gut microbiome and autism-like behaviors. Modifying the gut microbiome is a potential route to improve gastrointestinal (GI) and behavioral symptoms in children with ASD, and fecal microbiota transplant could transform the dysbiotic gut microbiome toward a healthy one by delivering a large number of commensal microbes from a healthy donor. We previously performed an open-label trial of Microbiota Transfer Therapy (MTT) that combined antibiotics, a bowel cleanse, a stomach-acid suppressant, and fecal microbiota transplant, and observed significant improvements in GI symptoms, autism-related symptoms, and gut microbiota. Here, we report on a follow-up with the same 18 participants two years after treatment was completed. Notably, most improvements in GI symptoms were maintained, and autism-related symptoms improved even more after the end of treatment.

Fecal transplant is exactly what it sounds like. The doctors clear out a person’s intestines as best they can, then put in new feces, from a donor, via a tube (up the butt or through the stomach; either direction works.)

Unfortunately, it wasn’t a double-blind study, but the authors are hopeful that they can get funding for a double-blind placebo controlled study soon.

I’d like to quote a little more from this study:

Two years after the MTT was completed, we invited the 18 original subjects in our treatment group to participate in a follow-up study … Two years after treatment, most participants reported GI symptoms remaining improved compared to baseline … The improvement was on average 58% reduction in Gastrointestinal Symptom Rating Scale (GSRS) and 26% reduction in % days of abnormal stools… The improvement in GI symptoms was observed for all sub-categories of GSRS (abdominal pain, indigestion, diarrhea, and constipation, Supplementary Fig. S2a) as well as for all sub-categories of DSR (no stool, hard stool, and soft/liquid stool, Supplementary Fig. S2b), although the degree of improvement on indigestion symptom (a sub-category of GSRS) was reduced after 2 years compared with weeks 10 and 18. This achievement is notable, because all 18 participants reported that they had had chronic GI problems (chronic constipation and/or diarrhea) since infancy, without any period of normal GI health.

Note that these children were chosen because they had both autism and lifelong gastrointestinal problems. This treatment may do nothing at all for people who don’t have gastrointestinal problems.

The families generally reported that ASD-related symptoms had slowly, steadily improved since week 18 of the Phase 1 trial… Based on the Childhood Autism Rating Scale (CARS) rated by a professional evaluator, the severity of ASD at the two-year follow-up was 47% lower than baseline (Fig. 1b), compared to 23% lower at the end of week 10. At the beginning of the open-label trial, 83% of participants rated in the severe ASD diagnosis per the CARS (Fig. 2a). At the two-year follow-up, only 17% were rated as severe, 39% were in the mild to moderate range, and 44% of participants were below the ASD diagnostic cut-off scores (Fig. 2a). … The Vineland Adaptive Behavior Scale (VABS) equivalent age continued to improve (Fig. 1f), although not as quickly as during the treatment, resulting in an increase of 2.5 years over 2 years, which is much faster than typical for the ASD population, whose developmental age was only 49% of their physical age at the start of this study.

Important point: their behavior matured faster than it normally does in autistic children.

This is a really interesting study, and I hope the authors can follow it up with a solid double-blind.

Of course, not all autists suffer from gastrointestinal complaints. Many eat and digest without difficulty. But the connection between physical complaints and mental disruption across a variety of conditions is fascinating. How many conditions that we currently believe are psychological might actually be caused a by an untreated biological illness?

Does the DSM need to be re-written?

I recently came across an interesting paper that looked at the likelihood that a person, once diagnosed with one mental disorder, would be diagnosed with another. (Exploring Comorbidity Within Mental Disorders Among a Danish National Population, by Oleguer Plana-Ripoll.)

This was a remarkable study in two ways. First, it had a sample size of 5,940,778, followed up for 83.9 million person-years–basically, the entire population of Denmark over 15 years. (Big Data indeed.)

Second, it found that for virtually every disorder, one diagnoses increased your chances of being diagnosed with a second disorder. (“Comorbid” is a fancy word for “two diseases or conditions occurring together,” not “dying at the same time.”) Some diseases were particularly likely to co-occur–in particular, people diagnosed with “mood disorders” had a 30% chance of also being diagnosed with “neurotic disorders” during the 15 years covered by the study.

Mood disorders includes bipolar, depression, and SAD;

Neurotic disorders include anxieties, phobias, and OCD.

Those chances were considerably higher for people diagnosed at younger ages, and decreased significantly for the elderly–those diagnosed with mood disorders before the age of 20 had a +40% chance of also being diagnosed with a neurotic disorder, while those diagnosed after 80 had only a 5% chance.

I don’t find this terribly surprising, since I know someone with at least five different psychological diagnoses, (nor is it surprising that many people with “intellectual disabilities” also have “developmental disorders”) but it’s interesting just how pervasive comorbidity is across conditions that are ostensibly separate diseases.

This suggests to me that either many people are being mis-diagnosed (perhaps diagnosis itself is very difficult,) or what look like separate disorders are often actually one, single disorder. While it is certainly possible, of course, for someone to have both a phobia of snakes and seasonal affective disorder, the person I know with five diagnoses most likely has only one “true” disorder that has just been diagnosed and treated differently by different clinicians. It seems likely that some people’s depression also manifests itself as deep-rooted anxiety or phobias, for example.

While this is a bit of a blow for many psychiatric diagnoses, (and I am quite certain that many diagnostic categories will need a fair amount of revision before all is said and done,) autism recently got a validity boost–How brain scans can diagnose Autism with 97% accuracy.

The title is overselling it, but it’s interesting anyway:

Lead study author Marcel Just, PhD, professor of psychology and director of the Center for Cognitive Brain Imaging at Carnegie Mellon University, and his team performed fMRI scans on 17 young adults with high-functioning autism and 17 people without autism while they thought about a range of different social interactions, like “hug,” “humiliate,” “kick” and “adore.” The researchers used machine-learning techniques to measure the activation in 135 tiny pieces of the brain, each the size of a peppercorn, and analyzed how the activation levels formed a pattern. …

So great was the difference between the two groups that the researchers could identify whether a brain was autistic or neurotypical in 33 out of 34 of the participants—that’s 97% accuracy—just by looking at a certain fMRI activation pattern. “There was an area associated with the representation of self that did not activate in people with autism,” Just says. “When they thought about hugging or adoring or persuading or hating, they thought about it like somebody watching a play or reading a dictionary definition. They didn’t think of it as it applied to them.” This suggests that in autism, the representation of the self is altered, which researchers have known for many years, Just says.

N=34 is not quite as impressive as N=Denmark, but it’s a good start.

Learning in Numbers

There is strength in numbers, but is there wisdom?

I’ve heard from multiple sources the claim that parenting, paradoxically, gets easier after the fourth child. There are several simple explanations for this phenomenon: people get more skilled at parenting after lots of practice; the older kids start helping out with the younger ones, etc.

But what if the phenomenon rests on something much more basic about human psychology–our desire to imitate others?

(Perhaps you don’t, dear reader. There are always exceptions.)

As Aristotle put it, man is a political animal–by which he meant that we are inherently social and prone to building communities (polities) together, not that we are inherently prone to arguing about who should govern North Carolina, though that may be political, too. In Aristotle’s words, a man who lives entirely alone is either a beast (living like an animal) or a god (able to fulfill all of his own needs without recourse to other humans.) Normal humans depend in many ways on other humans.

Compared to our pathetic ability to learn math (just look at most people’s SAT-math scores) and inability to read without direct instruction, humans learn socially-imparted skills like the ability to speak multiple languages, play games, assert dominance over each other, which clothes are fashionable, and how to crack a socially-appropriate joke with ease.

Social learning comes so naturally to people that we only notice it in cases of extreme deficit–like autism–or when parents protest that their children are becoming horribly corrupted by their peers.

So perhaps households with more than 4 children have hit a threshold beyond which social learning takes over and the younger children simply seem to “absorb” knowledge from their older siblings instead of having to be explicitly taught.

Consider learning to eat, a hopefully simple task. We are born with instincts to nurse, put random things in our mouths, and swallow. Preventing babies from eating random non-food objects is a bit of a problem for new parents. But learning things like “how to get this squishy food into your mouth with a spoon without also getting it everywhere else in the room” is much more complicated–and humans take food rituals to much more complicated heights than strained peas and carrots.

Parents of new children put a great deal of effort into teaching them to eat (something that ought to be an instinct.) Those with means puree fresh veggies, chop bits of meat, show a sudden interest in organics, and sit down to spoon every single last bit into their infants’ mouths. It is as if they are convinced that kids cannot learn to eat without at least as much instruction as a student learning to wield a welding torch. (And based on my own experience, they’re probably right.)

By contrast, parents of multiple children have–by necessity–relaxed. As a popular comic once depicted (though I can’t find it now,) feeding at this point becomes throwing Cheerios at the highchair as you run by.

Yet I’ve never seen any evidence that the younger children in large families are likely to be malnourished–they seem to catch the Cheerios on the fly and do just fine.

What if imitation is a strong factor in larger families, allowing infants and young children to learn skills like “how to eat” without needing direct parental instruction just by watching their older siblings? You might object that even infants in single parent households could learn to eat by imitating their parents (and they probably do,) but having more people around probably enforces the behavior more strongly, and having younger children around gives an example that is much more similar to the infant. We adults are massive compared to children, after all.

If basic learning of life skills proceeds more easily in an environment with more peers,(for infants or adults,) then what effects should we expect from our current trend toward extreme atomization?

I recently came across an essay about life in a trailer park vs sturdier housing:

To me, growing up in that trailer park meant playing until dark with neighborhood kids, building tree houses and snow forts. Listening out my bedroom window for the sound of my dad’s pickup truck leaving for work in the early morning. Riding my bike down the big hill at the top of the lot, avoiding potholes and feeling safe because there wasn’t much traffic and if I fell and skinned my knee, someone would come out on their front porch and ask if I was okay.

Some of the only happy memories I have of my childhood were from that time in my life, before my parents were thrust into insurmountable debt, before my mother was hospitalized, before I had to go live with my grandmother. Nana had a real house. She didn’t live in a trailer. But when she would scream at me or try to attack me as I squeezed by her and fled upstairs, I wished I had neighbors close by to hear her — to believe me, and to perhaps even help.

The most dysfunctional and unstable years of my life were spent in a real house, with four walls and a slanted roof — where fences went up between the houses so that no one ever had to feel responsible for what went on behind their neighbor’s front door.

This is more about atomization than learning, but still interesting. Is it good for humans to be so far apart? To live far from relatives, in houses with thick walls, as single children or single adults, working and commuting every day among strangers?

Certainly the downsides of being among relatives are well-documented. Many tribal societies have downright cruel customs directed at relatives, like sati or adult circumcision. But that doesn’t mean that the extreme opposite–total atomization–is perfect. Atomization carries other risks. Among them, staying indoors and not socializing with our neighbors may cause us to lose some of our social knowledge, our ability to learn how to exist together.

We might expect that physical atomization due to technological change (sturdier houses, more entertaining TV, comfier climate control systems,) could cause symptoms in people similar to those caused by medical deficits in social learning, like autism. A recent study on the subject found an interesting variation between the brains of normies and autists:

So great was the difference between the two groups that the researchers could identify whether a brain was autistic or neurotypical in 33 out of 34 of the participants—that’s 97% accuracy—just by looking at a certain fMRI activation pattern. “There was an area associated with the representation of self that did not activate in people with autism,” Just says. “When they thought about hugging or adoring or persuading or hating, they thought about it like somebody watching a play or reading a dictionary definition. They didn’t think of it as it applied to them.” This suggests that in autism, the representation of the self is altered, which researchers have known for many years, Just says.

This might explain the high rates of body dysmorphias in autism. It might also explain the high rates in society.

I remember another study which I read ages ago which found that people basically thought about “God” in the same parts of their brain where they thought about themselves. This explains why God tends to have the same morals as His believers. If autists have trouble imagining themselves, then they may also have trouble imagining God–and this might explain rising atheism rates.

Even our rising autism rates, though probably driven primarily by shifts in diagnostic fads, might be influenced by shrinking families and greater atomization, as kids with borderline conditions might show more severe symptoms if they are also more isolated.

On the other hand, social media is allowing people to come together and behave socially in new and ever larger groups.

For all their weaknesses, autists are probably better at normies at certain kinds of tasks, like abstract reasoning where you don’t want to think too much about yourself. I have long suspected that normies balk at philosophical dilemmas such as the trolley problem because they over-empathize with the subjects. Imagining themselves as one of the victims of the runaway trolley causes them distress, and distress causes them to attack the person causing them distress–the philosopher.

And so the citizens of Athens condemned Socrates to death.

But just as people can overcome their natural and very sensible fear of heights in order to work on skyscrapers, perhaps they can train themselves not to empathize with the subjects of trolley problems. Spending time on problems with no human subjects (such as mathematics or engineering) may also help people practice ways of approaching problems that don’t immediately resort to imagining themselves as the subject. On the converse, perhaps a bit of atomization (as seen historically in countries like Britain and France, and recently AFAIK in Japan,) helps equip people to think about difficult, non-human related mathematical or engineering problems.

Thoughts?

A theory of male and female Sociopathy, pt 2

Note: this is just a theory, developed in reaction to recent conversations. 

As we were discussing Friday, one form of female sociopathy (at least relevant to this conversation) likely involves manipulating or coercing others into providing resources for her children.

There are a couple of obvious tropes:

1. The evil stepmother, who shunts resources away from a man’s first child, toward his later children. 
2. The cuckoldress, who tricks or convinces a man to care for another man’s children (this is not always seen as evil, since the male drive to provide for children is triggered at least partly by their proximity, since men cannot give birth, and thus men feel genuine affection for children who happen to be around them,)
3. The crazy ex, who sues a man for all he is worth, doing her best to prevent him from being able to provide for any future children. 

How crazy are women? 

22%–slightly more than 1 in 5–women have been diagnosed with a mental illness, at least according to all of the data I’ve seen. Since mental illness peaks during the childbearing ages and falls off quickly after menopause, we can also assume that this rate is closer to 1 in 4 during these years. 

(The dramatic problems our Native American communities are facing is a separate matter, deserving of its own post.)

The odd thing about this data is that mental illness rates are higher for women than men, despite the fact that mental retardation and mental disability rates are higher for men than women. Men are more likely than women to have serious conditions like non-verbal autism and schizophrenia, more likely to be homeless or commit suicide. When things go terribly wrong, the sufferers are disproportionately male (an unfortunate side effect of the Y chromosome causing greater male variability than female variability on a variety of traits.) 

So why on earth do more women than men suffer from mental illness? 

Perhaps some forms of mental illness confer some unexpected benefits on women. 

Many (perhaps most) “mental illnesses” correlate with a single personality trait–neuroticism: 

“Previously we thought that mental illnesses such as depression, schizophrenia, bipolar disorder, and substance abuse, were completely separate diseases,” Ystrøm says.

But research has now shown that these illnesses are often linked. If you suffer from one mental illness, you are more likely to develop another. And if someone in your immediate family has a psychiatric illness, your risk increases not only for this disorder, but for all other disorders.

These findings have led researchers to suspect that there could be a common underlying factor that increases an idividual’s risk of mental illness, overall. … 

Ystrøm and colleagues have used new statistical methods to look for patterns in personality, mental disorders, genes, and environmental factors, among the twins in the Twin Register. 

And the answer to the question the researchers asked is: yes, neuroticism seems to be the personality trait that best describes the risk of all mental disorders. …

“This one trait doesn’t explain everything. Anyone can develop a mental illness…”

And in women, neuroticism correlates with… more surviving offspring (in at least one study): 

Taking an evolutionary approach, we use data from a contemporary polygynous high-fertility human population living in rural Senegal to investigate whether personality dimensions are associated with key life-history traits in humans, i.e., quantity and quality of offspring. We show that personality dimensions predict reproductive success differently in men and women in such societies and, in women, are associated with a trade-off between offspring quantity and quality. In women, neuroticism positively predicts the number of children, both between and within polygynous families. Furthermore, within the low social class, offspring quality (i.e., child nutritional status) decreases with a woman’s neuroticism, indicating a reproductive trade-off between offspring quantity and quality. 

What is neuroticism, in the Big 5 Personality Traits* sense? 

*Note: I am not endorsing or denying all five traits one way or another.

It’s worrying. Mothers who worry more about their offspring have more offspring–though it’s quite easy to imagine that the causality points in the opposite direction as the study’s authors conclude–poor women with lots of skinny babies have more reason to worry about their children than women with a few fat babies. 

When are women most likely to experience mental illness?

Immediately after the birth of a child. It’s called post-partum depression, and it can be very bad–one woman in my moms’ group ended up in the mental hospital after developing post-partum psychosis. Andrea Yates famously drowned her five children during a bout of post-partum depression/psychosis.

Why on earth would women develop a debilitating mental illness at the most vulnerable time in their offspring’s life? Wouldn’t natural selection select rather quickly against anything that makes women worse at taking care of their offspring? 

Let’s turn to everyone’s favorite genetic disease, sickle cell anemia. SCA is famous for being a relatively simple genetic mutation of the sort where if you have one copy of the sickle cell gene, you are less likely to get malaria, and if you have two copies, you tend to die. In areas where malaria is common, the cost of having a quarter of your children die from SCA is lower than the cost of loosing them to malaria. 

Personality traits, including neuroticism, generally exist on a continuum. People may become more neurotic when life warrants it, and less neurotic when they don’t need to worry. A mother with a new baby is in a very vulnerable state–she has just lost a good deal of blood, may not be able to walk, and has an infant to care for every other hour, day and night. It is not a normal state by any measure. It is a time when being extra attentive and extra aware of threats and predators is in a woman’s interest.

It is also a time when women are most in need of help from their mates, relatives, or other friends. Increased neuroticism may also prompt others to attend more closely to the new mother, helping her out. . Increased neuroticism may be so helpful during this time period that a few women getting way too much neuroticism and becoming extremely depressed or even killing their children is a cost outweighed by the increased survival of babies whose mothers had moderate levels of neuroticism. 

Let us note that nature doesn’t care about your feelings. Male praying mantises who allow themselves be eaten by their mates have more offspring than the ones who don’t, but that doesn’t mean male praying mantises enjoy getting eaten. Children who die of sickle

cell anemia don’t much appreciate that their siblings were protected from malaria, either.

An increase in neuroticism immediately after the birth of a baby may prompt a mother to take better care of it, but that doesn’t mean she enjoys the neuroticism. Neither does it mean that post-partum depression is healthy, any more than sickle cell anemia is healthy just because it’s a side effect of a trait that helps people avoid malaria. 

But wait, I have more studies!

Reproductive Fitness and Genetic Risk of Psychiatric Disorders in the General Population: 

The persistence of common, heritable psychiatric disorders that reduce reproductive fitness is an evolutionary paradox. Here, we investigate the selection pressures on sequence variants that predispose to schizophrenia, autism, bipolar disorder, major depression and attention deficit hyperactivity disorder (ADHD) using genomic data from 150,656 Icelanders, excluding those diagnosed with these psychiatric diseases. … Higher polygenic risk of autism is associated with fewer children and older age at first child whereas higher polygenic risk of ADHD is associated with having more children. We find no evidence for a selective advantage of a high polygenic risk of schizophrenia or bipolar disorder. Rare copy-number variants conferring moderate to high risk of psychiatric illness are associated with having fewer children and are under stronger negative selection pressure than common sequence variants. …

In summary, our results show that common sequence variants conferring risk of autism and ADHD are currently under weak selection in the general population of Iceland. However, rare CNVs that also impact cognition are under stronger selection pressure, consistent with mutation-selection balance. The hypothesis that a selective advantage accounts for the prevalence of sequence variants conferring risk of schizophrenia and bipolar disorder is unproven, but rather this empirical evidence suggests that common sequence variants largely escape selection as their individual effect sizes are weak.

Unfortunately, this study mostly looks at the data in aggregate, instead of breaking it down by males and females. (And I don’t know why they would bother excluding people who actually have the conditions they are trying to study, but perhaps it doesn’t make much difference.) 

Thankfully, they did break down the data by male/female in the tables–Table 1 and Table 2. These tables are confusing, but the takeaway is that mental illness has a bigger effect on male fertility than female fertility. 

Also: Fecundity of Patients with Schizophrenia, Autism, Bipolar Disorder, Depression, Anorexia Nervosa, or Substance Abuse vs. their Unffected Siblings: 

Results Except for women with depression, affected patients had significantly fewer children (FR range for those with psychiatric disorder, 0.23-0.93; P < 10⁻¹⁰). This reduction was consistently greater among men than women, suggesting that male fitness was particularly sensitive. Although sisters of patients with schizophrenia and bipolar disorder had increased fecundity (FR range, 1.02-1.03; P < .01), this was too small on its own to counterbalance the reduced fitness of affected patients. Brothers of patients with schizophrenia and autism showed reduced fecundity (FR range, 0.94-0.97; P < .001). Siblings of patients with depression and substance abuse had significantly increased fecundity (FR range, 1.01-1.05; P < 10⁻¹⁰). In the case of depression, this more than compensated for the lower fecundity of affected individuals.

Conclusions Our results suggest that strong selection exists against schizophrenia, autism, and anorexia nervosa and that these variants may be maintained by new mutations or an as-yet unknown mechanism. Bipolar disorder did not seem to be under strong negative selection. Vulnerability to depression, and perhaps substance abuse, may be preserved by balancing selection, suggesting the involvement of common genetic variants in ways that depend on other genes and on environment.

Now, this study gets interesting in its graphs: 

From Fecundity of Patients with Schizophrenia, Autism, Bipolar Disorder, Depression, Anorexia Nervosa, or Substance Abuse vs their Unaffected Siblings

In every case, mental illness has a bigger effect on male fertility than female–and in the case of depression, it has no effect on female fertility. 

But wait: 

Same source.

This graph is confusingly labeled, but it is breaking down the correlation on the brothers and sisters of people with mental disorders. So the first dot represents the brothers of people with schizophrenia; the second dot represents the sisters of people with schizophrenia. 

None of these effects are huge, and some of them changed when “comorbidities were included in the analysis,” though it’s not clear exactly what that means–the word comorbidity in this context refers to people with more than one diagnosis. 

For the objectives of this study, we first analyzed each disorder separately without accounting for comorbidities. A secondary analysis was then performed that corrected for comorbidities by analyzing all disorders simultaneously.

So when you analyze all of the disorders together, sisters of schizophrenics had no increased fertility, and neither did the siblings of people with bipolar. Depressed men had average fertility, while depressed women actually had slightly above average fertility. The results for anorexia, substance abuse, and autism didn’t change. 

And from Spain: Seven Dimensions of Personality Pathology are Under Sexual Selection in Modern Spain: 

Personality variation is increasingly thought to have an adaptive function. This is less clear for personality disorders (PDs)—extreme variants of personality that cause harm in most aspects of life. However, the possibility that PDs may be maintained in the population because of their advantages for fitness has been not convincingly tested. In a sample of 959 outpatients, we examined whether, and how, sexual selection acts on the seven main dimensions of personality pathology, taking into account mating success, reproductive success, and the mediating role of status. We find that, to varying extents, all personality dimensions are under sexual selection. Far from being predominantly purifying, selective forces push traits in diverging, often pathological, directions. These pressures differ moderately between the sexes. Sexual selection largely acts in males through the acquisition of wealth, and through the duration (rather than the number) of mates. This gives a reproductive advantage to males high in persistence–compulsivity. Conversely, because of the decoupling between the number of mates and offspring, the promiscuous strategy of psychopaths is not so successful. Negative emotionality, the most clinically detrimental trait, is slightly deleterious in males but is positively selected in females, which can help to preserve variation. 

It’s interesting that the invention of birth control may have inadvertently selected against promiscuous psychopaths–rather similar to the theory that abortion is responsible for the decrease in crime since the early 90s. 

“Negative emotionality” is likely equivalent to “neuroticism.”

There are two obvious reasons why mental illness might have more of an effect on males than females–one is that mental illness might simply be mores severe for males than females, on average. The second is that mental illness interferes more with holding down a job than with being a housewife, so women with mental illnesses have more options than men. 

Less obvious, though, is that some of these traits might actually be beneficial–in small quantities–for women.

That’s enough for now; let’s continue this discussion on Friday. (Wednesday is book club.) 

Testosterone metabolization, autism, male brain, and female identity

I began this post intending to write about testosterone metabolization in autism and possible connections with transgender identity, but realized halfway through that I didn’t actually know whether the autist-trans connection was primarily male-to-female or female-to-male. I had assumed that the relevant population is primarily MtF because both autists and trans people are primarily male, but both groups do have female populations that are large enough to contribute significantly. Here’s a sample of the data I’ve found so far:

A study conducted by a team of British scientists in 2012 found that of a pool of individuals not diagnosed on the autism spectrum, female-to-male (FTM) transgender people have higher rates of autistic features than do male-to-female (MTF) transgender people or cisgender males and females. Another study, which looked at children and adolescents admitted to a gender identity clinic in the Netherlands, found that almost 8 percent of subjects were also diagnosed with ASD.

Note that both of these studies are looking at trans people and assessing whether or not they have autism symptoms, not looking at autists and asking if they have trans symptoms. Given the characterization of autism as “extreme male brain” and that autism is diagnosed in males at about 4x the rate of females, the fact that there is some overlap between “women who think they think like men” and “traits associated with male thought patterns” is not surprising.

If the reported connection between autism and trans identity is just “autistic women feel like men,” that’s pretty non-mysterious and I just wasted an afternoon.

Though the data I have found so far still does not look directly at autists and ask how many of them have trans symptoms, the wikipedia page devoted to transgender and transsexual computer programmers lists only MtFs and no FtMs. Whether this is a pattern throughout the wider autism community, it definitely seems to be a thing among programmers. (Relevant discussion.)

So, returning to the original post:

Autism contains an amusing contradiction: on the one hand, autism is sometimes characterized as “extreme male brain,” and on the other hand, (some) autists (may be) more likely than neurotypicals to self-identify as transwomen–that is, biological men who see themselves as women. This seems contradictory: if autists are more masculine, mentally, than the average male, why don’t they identify as football players, army rangers, or something else equally masculine? For that matter, why isn’t a group with “extreme male brains” regarded as more, well, masculine?

(And if autists have extreme male brains, does that mean football players don’t? Do football players have more feminine brains than autists? Do colorless green ideas sleep furiously? DO WORDS MEAN?)

*Ahem*

In favor of the “extreme male brain” hypothesis, we have evidence that testosterone is important for certain brain functions, like spacial recognition, we have articles like this one: Testosterone and the brain:

Gender differences in spatial recognition, and age-related declines in cognition and mood, point towards testosterone as an important modulator of cerebral functions. Testosterone appears to activate a distributed cortical network, the ventral processing stream, during spatial cognition tasks, and addition of testosterone improves spatial cognition in younger and older hypogonadal men. In addition, reduced testosterone is associated with depressive disorders.

(Note that women also suffer depression at higher rates than men.)

So people with more testosterone are better at spacial cognition and other tasks that “autistic” brains typically excel at, and brains with less testosterone tend to be moody and depressed.

But hormones are tricky things. Where do they come from? Where do they go? How do we use them?

According to Wikipedia:

During the second trimester [of pregnancy], androgen level is associated with gender formation.^[13] This period affects the femininization or masculinization of the fetus and can be a better predictor of feminine or masculine behaviours such as sex typed behaviour than an adult’s own levels. A mother’s testosterone level during pregnancy is correlated with her daughter’s sex-typical behavior as an adult, and the correlation is even stronger than with the daughter’s own adult testosterone level.^[14]

… Early infancy androgen effects are the least understood. In the first weeks of life for male infants, testosterone levels rise. The levels remain in a pubertal range for a few months, but usually reach the barely detectable levels of childhood by 4–6 months of age.^[15][16] The function of this rise in humans is unknown. It has been theorized that brain masculinization is occurring since no significant changes have been identified in other parts of the body.^[17] The male brain is masculinized by the aromatization of testosterone into estrogen, which crosses the blood–brain barrier and enters the male brain, whereas female fetuses have α-fetoprotein, which binds the estrogen so that female brains are not affected.^[18]

(Bold mine.)

Let’s re-read that: the male brain is masculinized by the aromatization of testosterone into estrogen.

If that’s not a weird sentence, I don’t know what is.

Let’s hop over to the scientific literature, eg, Estrogen Actions in the Brain and the Basis for Differential Action in Men and Women: A Case for Sex-Specific Medicines:

Burgeoning evidence now documents profound effects of estrogens on learning, memory, and mood as well as neurodevelopmental and neurodegenerative processes. Most data derive from studies in females, but there is mounting recognition that estrogens play important roles in the male brain, where they can be generated from circulating testosterone by local aromatase enzymes or synthesized de novo by neurons and glia. Estrogen-based therapy therefore holds considerable promise for brain disorders that affect both men and women. However, as investigations are beginning to consider the role of estrogens in the male brain more carefully, it emerges that they have different, even opposite, effects as well as similar effects in male and female brains. This review focuses on these differences, including sex dimorphisms in the ability of estradiol to influence synaptic plasticity, neurotransmission, neurodegeneration, and cognition, which, we argue, are due in a large part to sex differences in the organization of the underlying circuitry.

Hypothesis: the way testosterone works in the brain (where we both do math and “feel” male or female) and the way it works in the muscles might be very different.

Do autists actually differ from other people in testosterone (or other hormone) levels?

In Elevated rates of testosterone-related disorders in women with autism spectrum conditions, researchers surveyed autistic women and mothers of autistic children about various testosterone-related medical conditions:

Compared to controls, significantly more women with ASC [Autism Spectrum Conditions] reported (a) hirsutism, (b) bisexuality or asexuality, (c) irregular menstrual cycle, (d) dysmenorrhea, (e) polycystic ovary syndrome, (f) severe acne, (g) epilepsy, (h) tomboyism, and (i) family history of ovarian, uterine, and prostate cancers, tumors, or growths. Compared to controls, significantly more mothers of ASC children reported (a) severe acne, (b) breast and uterine cancers, tumors, or growths, and (c) family history of ovarian and uterine cancers, tumors, or growths.

Androgenic Activity in Autism has an unfortunately low number of subjects (N=9) but their results are nonetheless intriguing:

Three of the children had exhibited explosive aggression against others (anger, broken objects, violence toward others). Three engaged in self-mutilations, and three demonstrated no aggression and were in a severe state of autistic withdrawal. The appearance of aggression against others was associated with having fewer of the main symptoms of autism (autistic withdrawal, stereotypies, language dysfunctions).

Three of their subjects (they don’t say which, but presumably from the first group,) had abnormally high testosterone levels (including one of the girls in the study.) The other six subjects had normal androgen levels.

This is the first report of an association between abnormally high androgenic activity and aggression in subjects with autism. Although a previously reported study did not find group mean elevations in plasma testosterone in prepubertal autistic subjects (4), it appears here that in certain autistic individuals, especially those in puberty, hyperandrogeny may play a role in aggressive behaviors. Also, there appear to be distinct clinical forms of autism that are based on aggressive behaviors and are not classified in DSM-IV. Our preliminary findings suggest that abnormally high plasma testosterone concentration is associated with aggression against others and having fewer of the main autistic symptoms.

So, some autists have do have abnormally high testosterone levels, but those same autists are less autistic, overall, than other autists. More autistic behavior, aggression aside, is associated with normal hormone levels. Probably.

But of course that’s not fetal or early infancy testosterone levels. Unfortunately, it’s rather difficult to study fetal testosterone levels in autists, as few autists were diagnosed as fetuses. However, Foetal testosterone and autistic traits in 18 to 24-month-old children comes close:

Levels of FT [Fetal Testosterone] were analysed in amniotic fluid and compared with autistic traits, measured using the Quantitative Checklist for Autism in Toddlers (Q-CHAT) in 129 typically developing toddlers aged between 18 and 24 months (mean ± SD 19.25 ± 1.52 months). …

Sex differences were observed in Q-CHAT scores, with boys scoring significantly higher (indicating more autistic traits) than girls. In addition, we confirmed a significant positive relationship between FT levels and autistic traits.

I feel like this is veering into “we found that boys score higher on a test of male traits than girls did” territory, though.

In Polymorphisms in Genes Involved in Testosterone Metabolism in Slovak Autistic Boys, researchers found:

The present study evaluates androgen and estrogen levels in saliva as well as polymorphisms in genes for androgen receptor (AR), 5-alpha reductase (SRD5A2), and estrogen receptor alpha (ESR1) in the Slovak population of prepubertal (under 10 years) and pubertal (over 10 years) children with autism spectrum disorders. The examined prepubertal patients with autism, pubertal patients with autism, and prepubertal patients with Asperger syndrome had significantly increased levels of salivary testosterone (P < 0.05, P < 0.01, and P < 0.05, respectively) in comparison with control subjects. We found a lower number of (CAG)_n repeats in the AR gene in boys with Asperger syndrome (P < 0.001). Autistic boys had an increased frequency of the T allele in the SRD5A2 gene in comparison with the control group. The frequencies of T and C alleles in ESR1 gene were comparable in all assessed groups.

What’s the significance of CAG repeats in the AR gene? Apparently they vary inversely with sensitivity to androgens:

Individuals with a lower number of CAG repeats exhibit higher AR gene expression levels and generate more functional AR receptors increasing their sensitivity to testosterone…

Fewer repeats, more sensitivity to androgens. The SRD5A2 gene is also involved in testosterone metabolization, though I’m not sure exactly what the T allele does relative to the other variants.

But just because there’s a lot of something in the blood (or saliva) doesn’t mean the body is using it. Diabetics can have high blood sugar because their bodies lack the necessary insulin to move the sugar from the blood, into their cells. Fewer androgen receptors could mean the body is metabolizing testosterone less effectively, which in turn leaves more of it floating in the blood… Biology is complicated.

What about estrogen and the autistic brain? That gets really complicated. According to Sex Hormones in Autism: Androgens and Estrogens Differentially and Reciprocally Regulate RORA, a Novel Candidate Gene for Autism:

Here, we show that male and female hormones differentially regulate the expression of a novel autism candidate gene, retinoic acid-related orphan receptor-alpha (RORA) in a neuronal cell line, SH-SY5Y. In addition, we demonstrate that RORA transcriptionally regulates aromatase, an enzyme that converts testosterone to estrogen. We further show that aromatase protein is significantly reduced in the frontal cortex of autistic subjects relative to sex- and age-matched controls, and is strongly correlated with RORA protein levels in the brain.

If autists are bad at converting testosterone to estrogen, this could leave extra testosterone floating around in their blood… but doens’t explain their supposed “extreme male brain.” Here’s another study on the same subject, since it’s confusing:

Comparing the brains of 13 children with and 13 children without autism spectrum disorder, the researchers found a 35 percent decrease in estrogen receptor beta expression as well as a 38 percent reduction in the amount of aromatase, the enzyme that converts testosterone to estrogen.

Levels of estrogen receptor beta proteins, the active molecules that result from gene expression and enable functions like brain protection, were similarly low. There was no discernable change in expression levels of estrogen receptor alpha, which mediates sexual behavior.

I don’t know if anyone has tried injecting RORA-deficient mice with estrogen, but here is a study about the effects of injecting reelin-deficient mice with estrogen:

The animals in the new studies, called ‘reeler’ mice, have one defective copy of the reelin gene and make about half the amount of reelin compared with controls. …

Reeler mice with one faulty copy serve as a model of one of the most well-established neuro-anatomical abnormalities in autism. Since the mid-1980s, scientists have known that people with autism have fewer Purkinje cells in the cerebellum than normal. These cells integrate information from throughout the cerebellum and relay it to other parts of the brain, particularly the cerebral cortex.

But there’s a twist: both male and female reeler mice have less reelin than control mice, but only the males lose Purkinje cells. …

In one of the studies, the researchers found that five days after birth, reeler mice have higher levels of testosterone in the cerebellum compared with genetically normal males³.

Keller’s team then injected estradiol — a form of the female sex hormone estrogen — into the brains of 5-day-old mice. In the male reeler mice, this treatment increases reelin levels in the cerebellum and partially blocks Purkinje cell loss. Giving more estrogen to female reeler mice has no effect — but females injected with tamoxifen, an estrogen blocker, lose Purkinje cells. …

In another study, the researchers investigated the effects of reelin deficiency and estrogen treatment on cognitive flexibility — the ability to switch strategies to solve a problem⁴. …

“And we saw indeed that the reeler mice are slower to switch. They tend to persevere in the old strategy,” Keller says. However, male reeler mice treated with estrogen at 5 days old show improved cognitive flexibility as adults, suggesting that the estrogen has a long-term effect.

This still doesn’t explain why autists would self-identify as transgender women (mtf) at higher rates than average, but it does suggest that any who do start hormone therapy might receive benefits completely independent of gender identity.

Let’s stop and step back a moment.

Autism is, unfortunately, badly defined. As the saying goes, if you’ve met one autist, you’ve met one autist. There are probably a variety of different, complicated things going on in the brains of different autists simply because a variety of different, complicated conditions are all being lumped together under a single label. Any mental disability that can include both non-verbal people who can barely dress and feed themselves and require lifetime care and billionaires like Bill Gates is a very badly defined condition.

(Unfortunately, people diagnose autism with questionnaires that include questions like “Is the child pedantic?” which could be equally true of both an autistic child and a child who is merely very smart and has learned more about a particular subject than their peers and so is responding in more detail than the adult is used to.)

The average autistic person is not a programmer. Autism is a disability, and the average diagnosed autist is pretty darn disabled. Among the people who have jobs and friends but nonetheless share some symptoms with formally diagnosed autists, though, programmer and the like appear to be pretty popular professions.

Back in my day, we just called these folks nerds.

Here’s a theory from a completely different direction: People feel the differences between themselves and a group they are supposed to fit into and associate with a lot more strongly than the differences between themselves and a distant group. Growing up, you probably got into more conflicts with your siblings and parents than with random strangers, even though–or perhaps because–your family is nearly identical to you genetically, culturally, and environmentally. “I am nothing like my brother!” a man declares, while simultaneously affirming that there is a great deal in common between himself and members of a race and culture from the other side of the planet. Your  coworker, someone specifically selected for the fact that they have similar mental and technical aptitudes and training as yourself, has a distinct list of traits that drive you nuts, from the way he staples papers to the way he pronounces his Ts, while the women of an obscure Afghan tribe of goat herders simply don’t enter your consciousness.

Nerds, somewhat by definition, don’t fit in. You don’t worry much about fitting into a group you’re not part of in the fist place–you probably don’t worry much about whether or not you fit in with Melanesian fishermen–but most people work hard at fitting in with their own group.

So if you’re male, but you don’t fit in with other males (say, because you’re a nerd,) and you’re down at the bottom of the highschool totem pole and feel like all of the women you’d like to date are judging you negatively next to the football players, then you might feel, rather strongly, the differences between you and other males. Other males are aggressive, they call you a faggot, they push you out of their spaces and threaten you with violence, and there’s very little you can do to respond besides retreat into your “nerd games.”

By contrast, women are polite to you, not aggressive, and don’t aggressively push you out of their spaces. Your differences with them are much less problematic, so you feel like you “fit in” with them.

(There is probably a similar dynamic at play with American men who are obsessed with anime. It’s not so much that they are truly into Japanese culture–which is mostly about quietly working hard–as they don’t fit in very well with their own culture.) (Note: not intended as a knock on anime, which certainly has some good works.)

And here’s another theory: autists have some interesting difficulties with constructing categories and making inferences from data. They also have trouble going along with the crowd, and may have fewer “mirror neurons” than normal people. So maybe autists just process the categories of “male” and “female” a little differently than everyone else, and in a small subset of autists, this results in trans identity.*

And another: maybe there are certain intersex disorders which result in differences in brain wiring/organization. (Yes, there are real interesx disorders, like Klinefelter’s, in which people have XXY chromosomes instead of XX or XY.) In a small set of cases, these unusually wired brains may be extremely good at doing certain tasks (like programming) resulting people who are both “autism spectrum” and “trans”. This is actually the theory I’ve been running with for years, though it is not incompatible with the hormonal theories discussed above.

But we are talking small: trans people of any sort are extremely rare, probably on the order of <1/1000. Even if autists were trans at 8 times the rates of non-autists, that’s still only 8/1000 or 1/125. Autists themselves are pretty rare (estimates vary, but the vast majority of people are not autistic at all,) so we are talking about a very small subset of a very small population in the first place. We only notice these correlations at all because the total population has gotten so huge.

Sometimes, extremely rare things are random chance.

Species of Exit: Israel

Israel is–as far as I can tell–one of the sanest, least self-destructive states in the entire West. (Note: this is not to say that I love everything about Israel; this is actually a pretty low bar, given what’s happening everywhere else.) Their people are literate and healthy, they have a per capita GDP of 36.5k, (33rd in the world,) and they’re 18th globally on the Human Development Index. They don’t throw people off of buildings or have public floggings, and despite the fact that they have birth control and the state actually pays for abortions, the Jewish population still has a positive fertility rate:

The fertility rates of Jewish and Arab women were identical for the first time in Israeli history in 2015, according to figures released by the Israel Central Bureau of Statistics on Tuesday….Jewish and Arab women had given birth to an average of 3.13 children as of last year.

According to Newsweek:

This high fertility rate is not simply an artifact of Israel’s growing ultra-Orthodox or Haredi population; the non-Haredi fertility rate is 2.6. (This is, by the way, a far higher fertility rate than that of American Jews, which is 1.9; the replacement rate is 2.3.)

And they’ve managed to resist getting conquered by their aggressive and numerically superior neighbors several times in the past century.

Not bad for a country that didn’t exist 100 years ago, had to be built from the sand up, and is filled with people whom conventional wisdom holds ought to have been rendered completely useless by multi-generational epigenetic trauma.

Now, yes, Israel does get a lot of support from the US, and who knows what it would look like (or if it would exist at all,) in an alternative timeline where the US ignores it. Israel probably isn’t perfect, just interesting.

Harking back to my Measures of Meaning post, I propose that Israel has 4 things going for it:

Ethiopian Jewish member of the IDF

1. Israelis have meaningful work. Their work has been, literally, to build and secure their nation. Israelis have had to build almost the entire infrastructure of their country over the past hundred years, from irrigation systems to roads to cities. Today, Tel Aviv is a city with a population of 430,000 people. In 1900, Tel Aviv didn’t exist.

Unlike the US, Israel has a draft: every Israeli citizen, male and female, has to serve in the Israeli army. (Obviously exceptions exist.) This is not seen as state-run slavery but part of making sure the entire society continues to exist, because Israel faces some pretty real threats to its borders.

The IDF even has a special division for autists:

Many autistic soldiers who would otherwise be exempt from military service have found a place in Unit 9900, a selective intelligence squad where their heightened perceptual skills are an asset. …

The relationship is a mutually beneficial one. For these young people, the unit is an opportunity to participate in a part of Israeli life that might otherwise be closed to them. And for the military, it’s an opportunity to harness the unique skill sets that often come with autism: extraordinary capacities for visual thinking and attention to detail, both of which lend themselves well to the highly specialized task of aerial analysis.

I suspect–based on personal conversations–that there is something similar in the US military, but have no proof.

My anthropological work suggests that one of the reasons people enter the military is to find meaning in their lives, (though this doesn’t work nearly as well when your country does things like invade completely irrelevant countries you don’t actually care about like Vietnam.)

2. Like I said, Israelis have above-replacement total fertility–meaning that many Israelis hail from large families, with lots of children, siblings, and cousins. Israelis appear to have managed to achieve this in part by subsidizing births (which probably will have some long-term negative effects for them,*) and in part by explicitly advocating high birth rates in order to prevent themselves from being out-bred by the Palestinians and to show that Hitler what for.

*ETA: See the comments for a discussion of dysgenic fertility on Israel.

3. Religion is so obviously a unifying force in Israeli life that I don’t think I need to detail it.

What about that fourth thing? Oh yes: Many of the Jews who don’t like the idea of “nations” and “ethno states” and “religion” probably moved to the US instead of Israel. The US got the SJW Jews and Israel got the nationalist Jews.

4. A sense of themselves as a distinct nation. As I’ve discussed before, this is not exactly genetic, due to different Jewish groups having absorbed about 50% of their DNA from the folks around them during the diaspora years, and of course a big part of the country is Arab/Palestinians, but there is still much genetically in common.

There is probably a lot I’m missing.

Of course there are religious Jews in the US (and their numbers are growing relative to the secular Jewish population.) While Jews as a whole voted 70% for Hillary, only 56% of the Orthodox supported her. (I’ve seen different numbers elsewhere, but these are the ones I’ve been able to find a source for.)

(I suspect that America’s high-IQ secular Jews suffer from being in America instead of Israel. They don’t have religion to guide them, children to focus them, nor (in many cases) meaningful work. Without something positive to work towards, they turn to politics/ideology to provide meaning in their lives, while simultaneously suffering the psychological stress of knowing that the Holocaust was directed at people like them.)

But that’s irrelevant to Israeli Jews.

Long-term, I’m not bullish on Israel, given its precarious location, surrounded by nations that aren’t very fond of it–and I am not offering any opinions about the Israeli/Palestinian situation–but as first world nations go, it at least desires to keep existing.

Autism

Isaac Newton

The autist’s greatest strength–and weakness–is his deficiency in the neural mechanisms of mimicry. Without the necessary feedback loops, he fails to subconsciously adopt of his peers’ words, actions, and beliefs, leaving him is free to develop his own–caring little about how strange they seem to everyone else.

At his most unfortunate, the infant autist lacks even the instincts necessary to imitate the mouth-shapes and mouth-sounds of his parents, leaving him unable to develop speech. Some of these autists understand speech perfectly well, but simply cannot produce it.

At his most fortunate, the autist, immune to other people’s preconceived notions, revolutionizes some field of science or math–or both:

Here is buried Isaac Newton, Knight, who by a strength of mind almost divine, and mathematical principles peculiarly his own, explored the course and figures of the planets, the paths of comets, the tides of the sea, the dissimilarities in rays of light, and, what no other scholar has previously imagined, the properties of the colours thus produced. Diligent, sagacious and faithful, in his expositions of nature, antiquity and the holy Scriptures, he vindicated by his philosophy the majesty of God mighty and good, and expressed the simplicity of the Gospel in his manners. Mortals rejoice that there has existed such and so great an ornament of the human race! He was born on 25 December 1642, and died on 20 March 1726/7.—Translation from G.L. Smyth, The Monuments and Genii of St. Paul’s Cathedral, and of Westminster Abbey (1826), ii, 703–4.^[115]

What Mental Traits does the Arctic Select for?

Apropos Friday’s conversation about the transition from hunting to pastoralism and the different strategies hunters employ in different environments, I got to thinking about how these different food-production systems could influence the development of different “intelligences,” or at least mental processes that underlie intelligence.

Ingold explains that in warm climes, hunter-gatherers have many food resources they can exploit, and if one resource starts running low, they can fairly easily switch to another. If there aren’t enough yams around, you can eat melons; if not enough melons, squirrels; if no squirrels, eggs. I recall a study of Australian Aborigines who agreed to go back to hunter-gatherering for a while after living in town for several decades. Among other things (like increased health,) scientists noted that the Aborigines increased the number of different kinds of foods they consumed from, IIRC, about 40 per week to 100.

By contrast, hunters in the arctic are highly dependent on exploiting only a few resources–fish, seals, reindeer, and perhaps a few polar bears and foxes. Ingold claims that there are (were) tribes that depended largely on only a few major hunts of migrating animals (netting hundreds of kills) to supply themselves for the whole year.

If those migrating change their course by even a few miles, it’s easy to see how the hunters could miss the herds entirely and, with no other major species around to exploit, starve over the winter.

Let’s consider temperate agriculture as well: the agriculturalist can store food better than the arctic hunter (seal meat does not do good things in the summer,) but lacks the tropical hunter-gatherer’s flexibility; he must stick to his fields and keep working, day in and day out, for a good nine months in a row. Agricultural work is more flexible than assembly line work, where your every minute is dictated by the needs of the factory, but a farmer can’t just wander away from his crops to go hunt for a months just because he feels like it, nor can he hope to make up for a bad wheat harvest by wandering into his neighbor’s fields and picking their potatoes.

Which got me thinking: clearly different people are going to do better at different systems.

But first, what is intelligence? Obviously we could define it in a variety of ways, but let’s stick to reasonable definitions, eg, the ability to use your brain to achieve success, or the ability to get good grades on your report card.

A variety of mental traits contribute to “intelligence,” such as:

1. The ability to learn lots of information. Information is really useful, both in life and on tests, and smarter brains tend to be better at storing lots and lots of data.
2. Flexible thinking. This is the ability to draw connections between different things you’ve learned, to be creative, to think up new ideas, etc.
3. Some form of Drive, Self Will, or long-term planning–that is, the ability to plan for your future and then push yourself to accomplish your goals. (These might more properly be two different traits, but we’ll keep them together for now.)

Your stereotypical autistic, capable of memorizing large quantities of data but not doing much with them, has trait #1 but not 2 or 3.

Artists and musicians tend to have a lot of trait #2, but not necessarily 1 or 3 (though successful artists obviously have a ton of #3)

And an average kid who’s not that bright but works really hard, puts in extra hours of effort on their homework, does extra credit assignments, etc., has a surfeit of #3 but not much 2 or 1.

Anyway, it seems to me like the tropical hunting/gathering environment, with many different species to exploit, would select for flexible thinking–if one food isn’t working out, look for a different one. This may also apply to people from tropical farming/horticulturalist societies.

By contrast, temperate farming seems more likely to select for planning–you can’t just wander off or try to grow something new in time for winter if your first crop doesn’t work out.

Many people have noted that America’s traditionally tropical population (African Americans) seems to be particularly good at flexible thinking, leading to much innovation in arts and music. They are not as talented, though, at Drive, leading to particularly high highschool dropout rates.

America’s traditionally rice-farming population (Asians,) by contrast, has been noted for over a century for its particularly high drive and ability to plan for the future, but not so much for contributions to the arts. East Asian people are noted for their particularly high IQ/SAT/PISA scores, despite the fact that China lags behind the West in GDP and quality of life terms. (Japan, of course, is a fully developed country.) One potential explanation for this is that the Chinese, while very good at working extremely hard, aren’t as good at flexible thinking that would help spur innovation. (I note that the Japanese seem to do just fine at flexible thinking, but you know, the Japanese aren’t Chinese and Japan isn’t China.)

(I know I’m not really stating anything novel.) But the real question is:

What kind of mental traits might pastoralism, arctic pastoralism, or arctic hunting select for?