Neurology Center

According to a major new report from Australia, social and family factors associated with autism are associated with a lower risk of intellectual disability - and vice versa. But why?


The paper is from Leonard et al and it's published in PLoS ONE, so it's open access if you want to take a peek. The authors used a database system in the state of Western Australia which allowed them to find out what happened to all of the babies born between 1984 and 1999 who were still alive as of 2005. There were 400,000 of them.

The records included information on children diagnosed with either an autism spectrum disorder (ASD), intellectual disability aka mental retardation (ID), or both. They decided to only look at singleton births i.e. not twins or triplets.

In total, 1,179 of the kids had a diagnosis of ASD. That's 0.3% or about 1 in 350, much lower than more recent estimates, but these more recent studies used very different methods. Just over 60% of these also had ID, which corresponds well to previous estimates.

There were about 4,500 cases of ID without ASD in the sample, a rate of just over 1%; the great majority of these (90%) had mild-to-moderate ID. They excluded an additional 800 kids with ID associated with a "known biomedical condition" like Down's Syndrome.

So what did they find? Well, a whole bunch, and it's all interesting. Bullet point time.

• Between 1984 to 1999, rates of ID without ASD fell and rates of ASD rose, although there was a curious sudden fall in the rates of ASD without ID just before the end of the study. In 1984, "mild-moderate ID" without autism was by far the most common diagnosis, with 10 times the rate of anything else. By 1999, it was exactly level with ASD+ID, and ASD without ID was close behind. Here's the graph; note the logarithmic scale:
  

• Boys had a much higher rate of autism than girls, especially when it came to autism without ID. This has been known for a long time.
  
• Second- and third- born children had a higher rate of ID, and a lower rate of ASD, compared to firstborns.
  
• Older mothers had children with more autism - both autism with and without ID, but the trend was bigger for autism with ID. But they had less ID. For fathers, the trend was the same and the effect was even bigger. Older parents are more likely to have autistic children but less likely to have kids with ID.
  

• Richer parents had a strongly reduced liklihood of ID. Rates of ASD with ID were completely flat, but rates of ASD without ID were raised in the richer groups, though it was not linear (the middle groups were highest. - and effect was small.)
  

Neurology and psychiatry are related fields - if for no other reason, because neurological disorders can often manifest as, and get misdiagnosed as, psychiatric ones.

But what's the borderline between neurology and psychiatry? What makes one disease "neurological" and another "mental"? Are some psychiatric disorders more "neurological" than others?

It's a rather philosophical question and you could discuss it for as long as you wanted. Rather than doing that I thought I'd have a look to see which disorders are, at the moment, considered to fall into each category.

To do this I did a quick search the archives of two journals, Neurology which the world's leading journal of... well, guess, and the American Journal of Psychiatry. I looked to see how many papers from the past 20 years had either a Title or an Abstract which referred to various different diseases. You can see the results above. Note that the total number of papers varied, obviously, and I've only plotted the proportion.

Some interesting results. Schizophrenia, which is probably considered "the most neurological" psychiatric disorder, is in fact the least talked about in Neurology. Depression is top amongst the "core" psychiatric ones.

Autism occupies a middle ground, discussed by psychiatrists at 70% and neurologists at 30%. That didn't surprise me, but what did was that ADHD is almost as neurological as autism. Mental retardation is also intermediate, though it's 30:70 in favour of neurology. Whether autism is really less neurological than mental retardation, is a good question.

Then out of the disorders with a known neuropathology, Alzheimer's disease, Huntington's disease and "dementia" (which overlaps with Alzheimer's) are a bit psychiatric while stuff like headache and epilepsy is almost 100% neurological. Why this is, is not entirely clear, since both dementia and epilepsy are caused by neurological damage, and they can both cause "psychiatric" symptoms.

I suspect the difference is that it's just much harder to treat Alzheimer's, Huntington's and dementia. With epilepsy or meningitis, neurologists have a very good chance of controlling the symptoms and few patients will be left with ongoing psychiatric problems. But with the neurodegenerative disorders, neurologists can't really do much, leaving a large pool of people for psychiatrists to study.

Someone once said that neurologists take all of the curable diseases and leave psychiatrists with the ones they can't help. These figures suggest that there may be some truth in this.

Note: This book quotes me approvingly, so this is not quite a disinterested review.

Cordelia Fine's Delusions of Gender is an engaging, entertaining and powerfully argued reply to the many authors - who range from the scientifically respectable to the less so - who've recently claimed to have shown biological sex differences in brain, mind and behaviour.

Fine makes a strong case that the sex differences we see, in everything from behaviour to school achievements in mathematics, could be caused by the society in which we live, rather than by biology. Modern culture, she says, while obviously less sexist than in the past, still contains deeply entrenched assumptions about how boys and girls ought to behave, what they ought to do and what they're good at, and these - consciously or unconsciously - shape the way we are.

Some of the Fine's targets are obviously bonkers, like Vicky Tuck, but for me, the most interesting chapters were those dealing in detail with experiments which have been held up as the strongest examples of sex differences, such as the Cambridge study claiming that newborn boys and girls differ in how much they prefer looking at faces as opposed to mechanical mobiles.

But Delusions is not, in Steven Pinker's phrase, saying we ought to return to "Blank Slatism", and it doesn't try to convince you that every single sex difference definately is purely cultural. It's more modest, and hence, much more believable: simply a reminder that the debate is still an open one.

Fine makes a convincing case (well, it convinced me) that the various scientific findings, mostly from the past 10 years, that seem to prove biological differences, are not, on the whole, very strong, and that even if we do accept their validity, they don't rule out a role for culture as well.

This latter point is, I think, especially important. Take, for example, the fact that in every country on record, men roughly between the ages of 16-30 are responsible for the vast majority of violent crimes. This surely reflects biology somehow; whether it's the fact that young men are physically the strongest people, or whether it's more psychological, is by the by.

But this doesn't mean that young men are always violent. In some countries, like Japan, violent crime is extremely rare; in other countries, it's tens of times more common; and during wars or other periods of disorder, it becomes the norm. Young men are always, relatively speaking, the most violent but the absolute rate of violence varies hugely, and that has nothing to do with gender. It's not that violent places have more men than peaceful ones.

Gender, in other words, doesn't explain violence in any useful way - even though there surely are gender differences. The same goes for everything else: men and women may well have, for biological reasons, certain tendencies or advantages, but that doesn't automatically explain (and it doesn't justify) all of the sex differences we see today; it's only ever a partial explanation, with culture being the other part.

A new study has provided the strongest evidence yet that the rate of autism in children rises with the father's age: Advancing paternal age and risk of autism. But questions remain.

The association between old fathers and autism has been known for many years, and the most popular explanation has been genetic: sperm from older men are more likely to have accumulated DNA damage, which might lead to autism.

As I've said before, this might explain some other puzzling things such as the fact that autism is more common in the wealthy; it might even explain any recent increases in the prevalence of autism, if people nowadays are waiting longer to have kids.

But there are other possibilities. It might be that the fathers of autistic people tend to have mild autistic symptoms themselves (which they do), and this makes them likely to delay having children, because they're socially anxious and so take longer to get married, or whatever. It's not implausible.

The new study aimed to control for this, by looking at parents who had two or more children, at least one of them with autism, and at least one without it. Even within such families, the autistic children tended to have older fathers when they were born - that is to say, they were born later. See the graphs below for details. This seems to rule out explanations based on the characteristics of the parents.

However, there's another objection, the "experienced parent" theory. Maybe if parents have already had one neurotypical child, they're better at spotting the symptoms of autism in subsequent children, by comparison with the first one.

The authors tried to account for this as well, by controlling for the birth-order ("parity") of the kids. They also controlled for the mother's age amongst several other factors such as year of birth and history of mental illness in the parents. The results were still highly significant: older fathers meant a higher risk of autism. As if that wasn't enough, they also did a meta-analysis of all the previous studies and confirmed the same thing.

So overall, this is a very strong study, but there's a catch. The study population included over a million children (1,075,588) born in Sweden between 1983 and 1992. Of these, there was a total of 883 diagnosed cases of autism. That's a rate of 0.08%. In other words, although older fathers raised the risk of autism by quite a lot relatively speaking, the absolute rate was still tiny.

The most recent estimates of autism prevalence in Britain have put the figure at somewhere in the region of between 1% and 2% e.g. Baird et al (2006) and Baron-Cohen et al (2009) with American studies, using slightly different methods, generally coming in just below 1%. So the Swedish figure is more than 10 times lower than modern estimates. Whether this reflects different criteria for diagnosis, national differences, or increased prevalence over time, is debatable but it does raise the question of whether these findings still apply today.

The only way to know for sure would be to do a randomized controlled trial - get half your volunteer men to wait 10 years before having children - but I don't think that's going to happen any time soon...

Hultman CM, Sandin S, Levine SZ, Lichtenstein P, & Reichenberg A (2010). Advancing paternal age and risk of autism: new evidence from a population-based study and a meta-analysis of epidemiological studies. Molecular psychiatry PMID: 21116277

How do you know whether a scientific idea is a good one or not?


The only sure way is to study it in detail and know all the technical ins and outs. But good ideas and bad ideas behave differently over time, and this can provide clues as to which ones are solid; useful if you're a non-expert trying to evaluate a field, or a junior researcher looking for a career.

Today's ideas are the basis for tomorrow's experiments. A good idea will lead to experiments which provide interesting results, generating new ideas, which will lead to more experiments, and so on.

Before long, it will be taken as granted that it's true, because so many successful studies assumed it was. The mark of a really good idea is not that it's always being tested and found to be true; it's that it's an unstated assumption of studies which could only work if it were true. Good ideas grow onwards and upwards, in an expanding tree, with each exciting new discovery becoming the boring background of the next generation.

Astronomers don't go around testing whether light travels at a finite speed as opposed to an infinite one; rather, if it were infinite, their whole set-up would fail.

Bad ideas generate experiments too, but they don't work out. The assumptions are wrong. You try to explain why something happens, and you find that it doesn't happen at all. Or you come up with an "explanation", but next time, someone comes along and finds evidence suggesting the "true" explanation is the exact opposite.

Unfortunately, some bad ideas stick around, for political or historical reasons or just because people are lazy. What tends to happen is that these ideas are, ironically, more "productive" than good ideas: they are always giving rise to new hypotheses. It's just that these lines of research peter out eventually, meaning that new ones have to take their place.

As an example of a bad idea, take the theory that "vaccines cause autism". This hypothesis is, in itself, impossible to test: it's too vague. Which vaccines? How do they cause autism? What kind of autism? In which people? How often?

The basic idea that some vaccines, somewhere, somehow, cause some autism, has been very productive. It's given rise to a great many, testable, ideas. But every one which has been tested has proven false.

First there was the idea that the MMR vaccine causes autism, linked to a "leaky gut" or "autistic enterocolitis". It doesn't, and it's not linked to that. Then along came the idea that actually it's mercury preservatives in vaccines that cause autism. It doesn't. No problem - maybe it's aluminium? Or maybe it's just the Hep B vaccine? And so on.

At every turn, it's back to square one after a few years, and a new idea is proposed. "We know this is true; now we just need to work out why and how...". Except that turns out to be tricky. Hmm. Maybe, if you keep ending up back at square one, you ought to find a new square to start from.

An unusually gripping genetics paper from Biological Psychiatry: Pagnamenta et al.

The authors discuss a family where two out of the three children were diagnosed with autism. In 2009, they detected a previously unknown copy number variant mutation in the two affected brothers: a 594 kb deletion knocking out two genes, called DOCK4 and IMMP2L.

Yet this mutation was also carried by their non-autistic mother and sister, suggesting that it wasn't responsible for the autism. The mother's side of the family, however, have a history of dyslexia or undiagnosed "reading difficulties"; all of the 8 relatives with the mutation "performed poorly on reading assessment".

Further investigation revealed that the affected boys also carried a second, entirely separate, novel deletion, affecting the gene CNTNAP5. Their mother and sister did not. This mutation came from their father, who was not diagnosed with autism but apparently had "various autistic traits".

Perhaps it was the combination of the two mutations that caused autism in the two affected boys. The mother's family had a mutation that caused dyslexia; the father's side had one that caused some symptoms of autism but was not, by itself, enough to cause the disorder per se.

However, things aren't so clear. There were cases of diagnosed autism spectrum disorders in the father's family, although few details are given and DNA was only available from one of the father's relatives. So it may have been that the autism was all about the CNTNAP5, and this mutation just has a variable penetrance, causing "full-blown" autism in some people and merely traits in others (like the father).

In order to try to confirm whether these two mutations do indeed cause dyslexia and autism, they searched for them in several hundred unrelated autism and dyslexia patients as well as healthy controls. They detected the a DOCK4 deletion in 1 out of 600 dyslexics (and in his dyslexic father, but not his unaffected sister), but not in 2000 controls. 3 different CNTNAP5 mutations were found in the affected kids from 3 out of 143 autism families, although one of them was also found in over 1000 controls.

This is how psychiatric genetics is shaping up: someone finds a rare mutation in one family, they follow it up, and it's only carried by one out of several hundred other cases. So there are almost certainly hundreds of genes "for" disorders like autism, and it only takes a mutation in one (or two) to cause autism.

Here's another recent example: they found PTCHD1 variants in a full 1% of autism cases. It seems to me that autism, for example, is one of the things that happens when something goes wrong during brain development. Hundreds of genes act in synchrony to build a brain; it only takes one playing out of tune to mess things up, and autism is one common result.

Mental retardation and epilepsy are the other main ones, and we know that there are dozens or hundreds of different forms of these conditions each caused by a different gene or genes. The million dollar question is what it is that makes the autistic brain autistic, as opposed to, say, epileptic.

The "rare variants" model has some interesting implications. The father in the Pagnamenta et al. study had never been diagnosed with anything. He had what the authors call "autistic traits", but presumably he and everyone just thought of those as part of who he was - and they could have been anything from shyness, to preferring routine over novelty, to being good at crosswords.

Had he not carried the CNTNAP5 mutation, he'd have been a completely different person. He might well have been drawn to a very different career, he'd probably never have married the woman he did, etc.

Of course, that doesn't mean that it's "the gene for being him"; all of his other 23,000 genes, and his environment, came together to make him who he was. But the point is that these differences don't just pile up on top of each other; they interact. One little change can change everything.

Link: BishopBlog on why behavioural genetics is more complicated than some people want you to think.

Pagnamenta, A., Bacchelli, E., de Jonge, M., Mirza, G., Scerri, T., Minopoli, F., Chiocchetti, A., Ludwig, K., Hoffmann, P., & Paracchini, S. (2010). Characterization of a Family with Rare Deletions in CNTNAP5 and DOCK4 Suggests Novel Risk Loci for Autism and Dyslexia Biological Psychiatry, 68 (4), 320-328 DOI: 10.1016/j.biopsych.2010.02.002

Young children with autism prefer looking at geometric patterns over looking at other people. At least, some of them do. That's according to a new study - Preference for Geometric Patterns Early in Life As a Risk Factor for Autism.

Pierce et al took 110 toddlers (age 14 to 42 months). Some of them had autism, some had "developmental delay" but not autism, and some were normally developing.

The kids were shown a one-minute video clip. One half of the screen showed some kids doing yoga, while the other was a set of ever-changing complex patterns. A bit like a screensaver or a kaleidoscope. Eye-tracking apparatus was used to determine which side of the screen each child was looking at.

What happened? Both the healthy control children, and the developmentally delayed children, showed a strong preference for the "social" stimuli - the yoga kids. However, the toddlers with an autism spectrum disorder showed a much wider range of preferences. 40% of them preferred the geometric patterns. Age wasn't a factor.

This makes intuitive sense because one of the classic features of autism is a fascination with moving shapes such as wheels, fans, and so on. The authors conclude that

A preference for geometric patterns early in life may be a novel and easily detectable early signature of infants and toddlers at risk for autism.

We live in societies where some people are richer than others - though the extent of wealth inequality varies greatly around the world.

In general, it's sad but true that poor people suffer more diseases. Within a given country almost all physical and mental illnesses are more common amongst the poor, although this isn't always true between countries.

So if a certain disease is more common in rich people within a country, that's big news because it suggests that something unusual is going on. Autism spectrum disorders (ASDs) have long been known to show this pattern, at least in some countries, but this has often been thought to be a product of diagnostic ascertainment bias. Maybe richer and better-educated parents are more likely to have access to services that can diagnose autism. This is a serious issue because autism often goes undiagnosed and diagnosis is rarely clear-cut.

An important new PLoS paper from Wisconsin's Durkin et al suggests that, while ascertainment bias does happen, it doesn't explain the whole effect in the USA: richer American families really do have more autism than poorer ones. The authors made use of the ADDM Network which covers about 550,000 8 year old children from several sites across the USA. (This paper also blogged about here at C6-H12-O6 blog.)

ADDM attempts to count the number of children with autism based on

So the draft of DSM-V is out.

If, as everyone says, the Diagnostic and Statistical Manual is the Bible of Psychiatry, I'm not sure why it gets heavily edited once every ten years or so. Perhaps the previous versions are a kind of Old Testament, and only the current one represents the New Revelation from the gods of the mind?

Mind Hacks has an excellent summary of the proposed changes. Bear in mind that the book won't be released until 2013. Some of the headlines:

• Asperger's Syndrome is out - everyone's going to have an "autistic spectrum disorder" now.
  
• Personality Disorders are out - kind of. In their place, there's 5 Personality Disorder Types, each of which you can have to varying degrees, and also 6 Personality Traits, each of which you can have to varying degrees.
• Hypoactive Sexual Desire Disorder - the disease which failed-antidepressant-turned-aphrodisiac flibanserin is supposed to treat - is out, to be replaced by Sexual Interest and Arousal Disorder.
• Binge Eating Disorder, Hypersexuality Disorder, and Gambling Addiction are in. Having Fun is not a disorder yet, but that's on the agenda for DSM-VI.

A. A behavioral or psychological syndrome or pattern that occurs in an individual

B. The consequences of which are clinically significant distress (e.g., a painful symptom) or disability (i.e., impairment in one or more important areas of functioning)

C. Must not be merely an expectable response to common stressors and losses...

D. That reflects an underlying psychobiological dysfunction

E. That is not primarily a result of social deviance or conflicts with society

J. When considering whether to add a mental/psychiatric condition to the nomenclature, or delete a mental/psychiatric condition from the nomenclature, potential benefits (for example, provide better patient care, stimulate new research) should outweigh potential harms (for example, hurt particular individuals, be subject to misuse)

The diagnosis of bipolar [in children] "is being given, we believe, too frequently," said Dr. David Shaffer, a member of the work group on disorders in childhood and adolescence. In reality, when such children are tracked into adulthood, very few of them turn out to be bipolar, he said.

It was about this time two years ago that my faith in the British media died. It had never been in the best of health, but up until then I believed that the (non-tabloid) newspapers were written by professionals trying to find out and communicate the truth as best they could.

Journalists might be wrong, I thought, but they did their best to ensure that they weren't. And they might have a bad habit of focussing on sensational stories that "sold papers", but such stories would at least be accurate. A career in journalism was something that strongly appealed to me.

What happened on July 8th 2007 was that The Observer printed a front-page article so demented that I’ve never been able to take that newspaper at face value since. And if you can't trust The Observer, which sat on my family's breakfast table every Sunday since before I can remember, you can't trust any of them (at least, I can’t.)

The article was about autism, and it claimed to be a report on a new research study carried out at Cambridge by the famous Professor Simon-Baron-Cohen. The upshot was that Baron-Cohen’s team had found the rate of autism to be 1 in 58 children, much higher than the previous study from a few years earlier, which found a rate of about 1 in 86. Furthermore, The Observer said, two of the team, “world experts” in autism, thought that this “dramatic rise” (i.e. a rise of 50% in a few years!) might be something to do with the much-maligned MMR vaccine.

The original article no longer exists on the Observer’s website, but the WayBack Machine has it.

It was pulled after Ben Goldacre, amongst many others (including Baron-Cohen and even the Government), criticized the piece vociferously and it was, eventually, replaced by an unsatisfactory “clarification”. Goldacre’s take on things was chronicled in a astonishing series of articles (1, 2, 3, 4, et al.) which revealed some horrific journalism, including, amongst much else, attributing opinions to people who didn’t hold them and failing to reveal conflicts of interest. If for some reason you’re not already a Goldacre fan, read those posts, and you’ll see what all of the fuss is about. But you need to know one other thing – he is literally the only journalist in the country who does what he does.

The most damning criticism at the time, however, was that the research in question could not possibly have found an increase in autism rates, let alone a “big surge”, a “dramatic rise”, or an “upward trend”. The new research, quite deliberately, used more extensive assessment criteria than previous studies. It was specifically designed to find the highest possible estimate. So only a fool would try to compare it to other sets of data and see this as evidence of rising rates. Also, even if there had been a real increase, it couldn’t have been because of MMR, because the kids in both studies will have had the MMR vaccine. The oldest kids in the Baird et al study of 9-10 year olds were born in 1991, a few years after MMR was introduced, while the youngest in the Baron-Cohen study were born in 2000, when MMR uptake was, if anything, lower, thanks to the MMR-autism scare.

Now, two years after The Observer’s “scoop”, the research is finally out in the British Journal of Psychiatry: Prevalence of autism-spectrum conditions: UK school-based population study. I’ll be examining this paper in detail in the next post, but here’s what you need to know if you remember the story from 2007:

The paper doesn’t mention the Observer affair but it’s obvious that the authors had the article in mind while they were writing up their results. They repeatedly emphasise that their prevalence estimate cannot be compared to previous ones. They make it very clear (to the point of seeming a bit stilted) that they believe that the apparent rise in prevalence of autism over time is due to better detection and diagnosis, rather than a real “epidemic”. And they do not mention MMR – not that they had any reason to, of course. The highest estimate they arrive at, which they say is probably somewhat too high but close enough, is 1 in 64 children. 1 in 58 doesn’t appear in the paper.

What’s most interesting about the paper is who wrote it. The author list includes Simon Baron-Cohen (obviously) and Fiona Scott. The Observer named Scott as an MMR-autism theorist, something she strongly denied, in 2007. However, fascinatingly, Carol Stott is not an author, although she receives a massive acknowledgement at the end of the paper – “Carol Stott was a member of the research team throughout the main phase of the study and contributed to the coordination and running of the study, data management and data collection. She also made valued contributions to team discussions.” On the basis of this, she clearly had a right to be listed as an author – but wasn’t. We can only assume that she chose not to be, because if the other authors had left her off the list without her permission they would have been guilty of a serious breach of trust.

Carol Stott, you’ll remember, played a role in the Observer autism story. Unlike Fiona Scott, she does (or at least did in 2007) believe that MMR is linked to autism, and she had very close links with Andrew Wakefield as well as displaying a, er, penchant for the scatological in some bizarre emails to journalist Brian Deer. (Goldacre does say he “genuinely warmed to her, and she regrets that many people have fallen into entrenched positions on MMR on both sides” though, so she’s not all bad!)

So, questions remain. How did the preliminary research get leaked in 2007? What happened to make 1 in 58 become 1 in 64? What’s the deal with Stott? We don’t know. But we do know a bit more about autism thanks to this paper, and in the next post I’ll be discussing that.

[BPSDB]

Children with autism often shown repetitive behaviours, ranging from repeated movements to compulsively collecting or arranging objects and desiring that daily routines are always done in the exact same way. Repetitive behaviour is often considered one of the three core features of autistic disorders (alongside difficulties in social interaction, and difficulties in communication).

SSRI antidepressants are often used to try to treat repetitive behaviours. Unfortunately, they don't work, at least according to a new study - Lack of Efficacy of Citalopram in Children With Autism Spectrum Disorders and High Levels of Repetitive Behavior.

The trial included 149 American children with autism aged from 5 to 17 years old, all of whom had moderate or severe repetitive behaviours. They were randomly assigned to get either citalopram, an SSRI, or placebo, and were followed up for 12 weeks to see if it had any effect on their repetitive behaviours. The dose of citalopram started at 2.5 mg and gradually increased to, in most cases, 20 mg, which is the dose that an adult person with depression would most commonly take - for a kid, this is a high dose.

The results were unequivocal - citalopram had absolutely no benefit over placebo. Zilch. On the other hand, it did cause side effects in some children - gastrointenstinal problems like diarrehea, skin rashes, and, most worryingly, hyperactivity - "increased energy levels", insomnia, "Attention and concentration decreased", and so forth. (Two children in the citalopram group also experienced seizures, but it's not clear that this was related to the drug, as citalopram is not known for causing seizures in adults.)

So, citalopram was not just useless, but actually harmful, in these children. This is the largest trial of an SSRI for repetitive behaviours in autism so far; there have been a few others, including one double-blind study of Prozac finding some benefit, but this is by far the most compelling.

But there's a big question here - why would anyone think that citalopram would work? Citalopram was designed to treat adults with... depression. Hence why it's called an antidepressant. Depression in adults is no more like compulsive behaviour in autistic children than is having a broken leg or heart disease. They're completely different conditions.

The main reason why SSRIs are used to try to treat repetitive behaviour is that they also work quite well against obsessive-compulsive disorder (OCD). People with OCD have repetitive behaviours, "compulsions". They might wash their hands ten times after going to the toilet. Or check that the fridge door is closed and the oven is switched off every time they leave the kitchen. Or count up to one hundred in their head whenever they see the number 13. And so forth.

SSRIs do work against OCD. Does this mean that they ought to also work against the repetitive behaviors in autism? Only if you think all repetitive behaviours are the same, with the same causes.

People with OCD feel compelled to perform their ritualistic behaviours as a way of coping with their "obsessions" - intrusive, unpleasant thoughts that they can't otherwise get out of their heads. Someone might be obsessed with the thought of germs and disease whenever they go to the toilet, and the only way to feel clean is to wash their hands 10 times. They might be obsessed with the idea that their family will die whenever they see the unlucky number 13, unless they "cancel it out" by counting to 100. The repetitive behaviours, in other words, are a consequence of the obsessions, which are unwanted, anxiety-provoking thoughts. SSRIs probably work by making the obsessions seem less troubling, so there is less need for the compulsions.

People with autism are often described as having "obsessions" too, but in the sense of "Things they are very interested in", not "Thoughts they cannot get rid of". Likewise, autistics may show "compulsive behaviours", but not as a way of dealing with obsessions. The words are the same, but the reality is different.

Maybe autistic people just like sameness and routine. That's part of who they are, and it's not something that can be treated with drugs. People with OCD hate having it - they don't like their obsessions or compulsions, they feel stuck with them. The compulsions are a coping mechanism. But in autism, at least most of the time, that's not how it works. An autistic child "compulsively" playing with the same toy over and over, or reading yet another book about their "obsession", dinosaurs, may be perfectly happy. In which case, why give them happy pills? And this is what the authors of the paper eventually suggest -

It may be that the repetitive behavior in children with ASDs is fundamentally different from what is observed among children with obsessive-compulsive disorder in its behavioral picture and in its biologic underpinnings.

The media's all too often shabby treatment of neuroscience and psychology research doesn't just propagate bad science - it means that the really interesting and important bits go unreported. This is what's just happened with the controversy surrounding a paper from the Autism Research Center (ARC) at Cambridge University - Bonnie Aeyeung et. al.'s Fetal Testosterone and Autistic Traits. For research published in a journal with an impact factor of 1.538 (i.e. not good), it's certainly attracted plenty of attention - but for all the wrong reasons.


The Autism Research Center is headed by the dashing Simon Baron-Cohen, also one of the authors on the paper. He's probably the world's best-known autism researcher, and the author of some excellent books on the subject including the classic Mindblindness and The Essential Difference. Mindblindness, in particular, probably deserves a lot of the credit for interesting a generation of psychologists in autism. A big cheese, in other words. Surely his greatest achievement, however, is being Borat's cousin.

Baron-Cohen is famous for his theory that the characteristic features of autism are exaggerated versions of the allegedly characteristic features of male, as opposed to female, cognition. Namely, autistic people have difficulties understanding the emotions and behaviour of other people ("empathizing"), but may show excellent rote memory and understanding of abstract, mathematical or mechanical systems ("systematizing"). He and his colleagues have also hypothesised that an excess of the well-known masculinizing hormone testosterone, could be responsible for the hyper-male brains of autistics, just as testosterone is responsible for the development of masculine traits in boys. Amongst other things this would explain why rates of diagnosed autistic spectrum disorders are several times higher in boys than in girls.

Now, this is one of those wide-ranging theories which serves to drive research, rather than strictly following from the evidence. It's a bold idea, but there is, at the moment, not enough data to confirm or reject this idea. The simple view that testosterone = maleness = autism is almost certainly wrong, but it's a neat theory, there's clearly something to it, and, as one of the commentators on the paper puts it

The new research was not about autism screening; the new research has not discovered that a high level of testosterone in prenatal tests is an indicator of autism; autism spectrum disorder has not been linked to high levels of testosterone in the womb; and tests (of autism) in the womb do not allow termination of pregnancies.