Finally, Hard Evidence Against The "Autism Epidemic"?

The idea of an 'autism epidemic' has a lot of people very worried.

No-one disputes that diagnosed rates of autism have increased enormously over the past 15 years or so, around the world. However, other people write it off as essentially a cultural phenomenon: we're getting better at detecting the disorder and more willing to label kids as having it.

I subscribe to the latter view, but there's very little hard evidence for it. To prove that diagnostic changes have occurred, rather than a true increase in autism, you'd have to know what would have happened to today's kids, say, 20 years ago. Would they have been diagnosed? We have no way of knowing. At least not until someone invents a time machine.

However, a new study just out offers a valuable new perspective on the debate: Spatial clusters of autism births and diagnoses point to contextual drivers of increased prevalence.

According to authors Soumya Mazumdar and colleagues, there's a zone of high autism prevalence in California, areas where kids aged 0-4 years old are more likely to be diagnosed with the condition. The epicentre is L.A.; there's actually three overlapping hotspots centred on Santa Monica, Alhambra and North Hollywood.

In these clusters, autism rates are between 2 and 6 times higher than the rest of the state.

Now an interesting thing about these areas was that they're rich in paediatricians, autism advocacy organizations, and money. In other words, there's better access to health services and probably more awareness of autism. This is suggestive evidence that the reason lots of kids get diagnosed here is about diagnosis, not autism per se.

But the blockbuster result is that children born outside the cluster, who later moved home into one, had a higher chance of getting a diagnosis than those who stayed out. The effect was smaller than for kids born inside the hot zone, but it was significant.

That's also consistent with the idea that the clusters are clusters of diagnosis, not autism.

It's not proof. You could argue that there's some toxic chemical, say, present in the rich parts of L.A. that causes autism, even if you move into the toxic area only at age 3 or 4, and that's been getting worse recently, leading to rising rates.

But it seems a stretch. What's the chemical? And why hypothesize one, when the diagnostic services hypothesis nicely accounts for these findings? As the authors say:

The findings reported in this article do not fully reject the possibility that environmental toxicants drive some of the risk of autism ... since there are a plethora of possible toxicants, it is impossible to falsify all hypotheses that researchers have started to explore.

 Mazumdar S, Winter A, Liu KY, and Bearman P (2012). Spatial clusters of autism births and diagnoses point to contextual drivers of increased prevalence. Social Science And Medicine PMID: 23267775

Mental Illness and Crime, Yet Again

As if on cue, a major study about the relationship (if any) between mental disorder and crime has appeared just when everyone's talking about that.

Although having said that, people seem to be interested in that issue most of the time nowadays, in the UK at any rate, with schizophrenia topping the list of supposedly scary syndromes.

So - should we be worried?

The new research, from Australian team Morgan et al, surveyed everyone born in the state of Western Australia between 1955 and 1969. About 1.6 million people lived there over the course of the study so this was a big project.

By linking local records of arrests over the period 1985 to 1996 to the database of psychiatric diagnosis, the researchers were able to examine disorder-crime correlations in the entire population - meaning that there was no possibility of bias.

So what happened? Here's some highlights:

• 32% of psychiatric patients had been arrested at least once. Unfortunately, it's not clear what the rate was in the general population, but that falls into the range of overall arrest rates in most countries.
• 11% of those arrested had a psychiatric diagnosis. This rose to 20% of arrests for violent offences.
• 0.8% of suspects had schizophrenia, rising to 1.7% for violent offences.
• The number of arrests in people without a disorder fell over the period 1985-1996, reflecting the well-known fact that people commit fewer crimes as they get older. However, in psychiatric patients, there was no change over time.
• For murder, 30% of suspects had a psychiatric history while 3% had a diagnosis of schizophrenia.
• Both substance abuse and personality disorders were associated with higher arrest rates than schizophrenia, but schizophrenia in turn was higher than depression, anxiety, and other miscellaneous disorders.
• Although only 1.7% of violent offenders had schizophrenia, those with the disorder were somewhat more likely to involve strangers, and to take place in public places, and less likely to target family and partners.

Overall this confirms that the great majority of crimes, including violent ones, are not committed by people with mental illness, and that your chance of getting 'murdered by a lunatic' is incredibly low. This strikes me as the only statistic that matters to most people.

There's a long-standing debate over whether people with various disorders are more likely to commit crimes than they would be if they didn't have one, the relative risk. While interesting, this is a purely academic question. What the rest of us need to know is the absolute risk, and this is low.

Morgan VA, Morgan F, Valuri G, Ferrante A, Castle D, and Jablensky A (2012). A whole-of-population study of the prevalence and patterns of criminal offending in people with schizophrenia and other mental illness. Psychological medicine, 1-12 PMID: 23234722

Religion Rises After Disaster Strikes

People turn to religion after natural disasters - but it doesn't actually provide much solace.

So say researchers Sibley and Bulbulia, who examined the population of Christchurch, New Zealand, before and after the 2011 earthquake. 185 died and many city landmarks were damaged in the disaster.

The paper, Faith after an Earthquake, opens with a Biblical quote.

Sibley and Bulbulia took advantage of the fact that a longitudinal study of the 'health and values' of the New Zealanders was already underway when the quake struck, and the survey included questionnaires about religious beliefs.

They found that, compared to before the event, residents of the affected Canterbury region were more likely to report becoming religious (8.6%) than of losing their faith (5.3%); in the rest of the country religion declined from 2009 to 2011, so the earthquake-hit area was exceptional.

The authors say:

Philosophers have plausibly argued that natural disasters such as the Christchurch earthquake are rationally incompatible with the existence of an all-powerful, all-loving God, because natural disasters cause pointless suffering to innocents... though faith eroded elsewhere in New Zealand, there was a significant upturn in religious faith among those who experienced the misery of New Zealand's most lethal natural disaster in eighty years.

But did faith help people cope with the disaster?

No - believers reported no better subjective well-being compared to the non-religious, either before or after the earthquake, although those who both lost their faith (apostates) during the period and were personally affected suffered a decline.

What's rather odd about this, however, is that other results showed that apart from the apostates, well-being wasn't affected by the earthquake at all. So it's no surprise that the religious coped no better: the irreligious already coped very well, so there was no room for improvement.

Sibley, C., and Bulbulia, J. (2012).Faith after an Earthquake: A Longitudinal Study of Religion and Perceived Health before and after the 2011 Christchurch New Zealand Earthquake PLoS ONE, 7 (12) DOI: 10.1371/journal.pone.0049648

How Intelligent is IQ?

"If your IQ is somewhere around 60 then you are probably a carrot'', according to a British spokesman for high-IQ club Mensa.

IQ's in the news at the moment thanks to a paper called Fractionating Human Intelligence from Canadian psychologists Adam Hampshire and colleagues. Some say it 'debunks the IQ myth' - but does it?

The study started out with a huge online IQ test...

Behavioral data were collected via the Internet between September and December 2010. The experiment URL was originally advertised in a New Scientist feature, on the Discovery Channel web site, in the Daily Telegraph, and on social networking web sites including Facebook and Twitter.

The test involved 12 different cognitive tasks, based on the usual IQ test kind of things, and they got a huge 45,000 usable responses.

However, the main part of the study used functional MRI (fMRI) to measure brain activity caused by each of the 12 tasks. There were only 16 volunteers in the brain scan study, which is pretty small.

The key finding was that although each of the 12 tasks made a different pattern of brain regions light up, there were two main components of this: one lit up mostly in response to tasks requiring short-term memory, and the other was associated with reasoning and logic: (EDIT: Picture corrected, oops.)

They did various other analyses that confirmed this, and they also found evidence for a third network responsible for language (verbal) skill.

Finally, the killer conclusion was that there was no reason to introduce the imfamous  'g factor' - a number representing general intelligence affecting performance on all tasks. Although there was a 'g factor' statistically, it was explained by the fact that tasks required both the memory and the logic networks (although to different degrees).

g is the most controversial aspect of IQ testing, because if it exists, that means that some people are just smarter than others across the board - not just better at a particular kind of thing. So has this study killed g?

Well, not by itself. There's a huge literature on IQ and g, going back almost 100 years. This stuff is not based on brain imaging, but just on IQ test scores, and it's a complex topic. I don't think one brain study with 16 people can really overturn that, although it does lend weight to the anti-g camp who have been arguing against g for decades.

There's a sense, though, in which it doesn't matter. If all tasks require both memory and reasoning (and all did in this study), then the sum of someone's memory and reasoning ability is in effect a g score, because it will affect performance in all tasks.

If so, it's academic whether this g score is 'really' monolithic or not. Imagine that in order to be good at basketball, you need to be both tall, and agile. In that case you could measure someone's basketball aptitude, even though it's not really one single 'thing'...

Hampshire, A., Highfield, R., Parkin, B., and Owen, A. (2012). Fractionating Human Intelligence Neuron, 76 (6), 1225-1237 DOI: 10.1016/j.neuron.2012.06.022

Why (And How) To Write Less

I said a couple of times during my recent trip to UPenn that "Most writing is too long". People seemed to nod appreciatively at this, so here's some more on that topic...

Most writing is too long and the most common reason is that it's not written for the reader's benefit. Readers want the important stuff, as clearly as possible, in the shortest possible space. If you remember that and let it guide your writing, you won't go far wrong. The reader's favourite bits are the ones you don't write.

The problem is that it's tempting to write for your own benefit, not the reader's, and this almost always ends up making things too long. This can take many forms:

Some write to help themselves understand the material, such that the end product is a record of their learning process. Others will insert details that the reader doesn't need, because it's a topic the writer's fond of. Other fear making tough decisions about what to include, so they say everything and hope some of it's good: "Write it all and let God sort them out."

This is common because formal education teaches you to write poorly. Specifically, it encourages people to overwrite. Teachers and professors give assignments and they set a minimum word count. This sends the message that where writing's concerned, more is better.

Teachers have their reasons. They want a brain-dump to show that the student's done the homework, pretty much the opposite of good writing. That's fair enough for school, but if you internalize that philosophy, you will end up writing to show off rather than for the reader's benefit.

Once you put the reader's interests first, you'll naturally start to find your own ways to achieve that. Everyone's style is different, but here's a few I've learned:

• If it starts "On that note...", "Also...", or "Furthermore...", you should probably cut it.
• Join Twitter - writing to a 140 character limit is a great form of discipline. Then imagine that every paragraph you write must become a tweet. You may find you can compress that paragraph into one sentence.
• Just as Twitter is good, other artificial constraints are good. Set yourself a word limit; if you're blogging, make it 500 words.
• Unless the article's about you, sentences that include the word "I" or "we" can usually be cut.
• Think of your piece as a nuclear missile: it has a payload, the message you want the reader to grasp, and a rocket motor, the introduction and other stuff you need to ensure it reaches the reader. Every missile needs a motor, but designers try to make the payload as big as possible, given the size of the motor. Identify what your payload is, and what your motor is. Then think, is my motor too big? (It probably is.) In this paragraph the missile analogy is the motor.
• As a rule of thumb, by writing it better, you can cut it down by half.

When "Mental" Illness Isn't

 

There's a theory that 'psychiatric diseases' like depression and schizophrenia aren't diseases because they're not diagnosed on the basis of any kind of biological abnormality, but purely on symptoms - unlike 'real' diseases like cancer and AIDS.

Now, in my view there's quite a bit of truth in that - but there's also a serious flaw in the argument. Sometimes, disorders diagnosed on the basis of psychiatric symptoms do turn out to have had a clear biological cause. So the original diagnosis of a psychiatric disease was correct: there was indeed a disease.

This is happening more and more often now because of biomedical advances.

A group of German neurologists and psychiatrists recently wrote about a case of a man diagnosed with bipolar disorder:

In February 2009, a 28-year-old presented to our clinic with a first episode of depression. He reported depressed mood, anhedonia, decreased drive, reduced alertness and concentration. The symptoms responded well to quetiapine 100 mg.

Fourteen months later, a first manic episode with logorrhea [excessive speech], aggressive and disinhibited behavior occurred... it completely remitted after treatment with quetiapine 1000mg. A diagnosis of bipolar I disorder was made.

Two months later, the patient presented with another depressive episode... Despite treatment with quetiapine, aripiprazole, lithium, valproate and escitalopram, the patient did not improve...

So far, seems like a fairly typical case of bipolar. However, it turned out that...

Neurological examination was remarkable for extrapyramidal symptoms with left-sided rigor and bradykinesia [slowed movements]. On initial and concurrent magnetic resonance imaging (MRI), numerous subcortical lesions in the frontal lobes were detected... Screening for autoimmune antibodies detected NMDAR antibodies.

It turned out the guy had autoimmune encephalitis: his body was generating antibodies that blocked the brain's key NMDA receptors; the drug ketamine does that too. Treatment with immunosuppressant drugs was started and he recovered fairly quickly. For a first-hand account of the disease, in which it was also diagnosed as a psychiatric disorder initially, see the recent book Brain On Fire.

Now, let's imagine that this had happened in 1960. What would the guy's story have been then?

He'd have been seen by a psychiatrist and diagnosed with bipolar, just as he was today. Depending on how severe the depression was, and whether or not he had any more episodes, he might well have ended up in a psychiatric hospital.

But he probably wouldn't have been diagnosed with a neurological disorder. He'd have tested negative for all the neurological diseases known at the time. No-one tested for NMDA antibodies back then, because NMDA receptors weren't even discovered until 1981.

It's true that his neurological exam showed a movement disorder (left-sided rigor and bradykinesia)  but this might well have been written off as a side effect of the high dose antipsychotics he was taking, which cause similar movement disorders.

50 years ago this guy, and many others like him, could well have ended up committed to an asylum. 100 years ago, I think it would have been almost certain he'd have been deemed 'insane' and locked up at some point.

If so, some of the people in psychiatric hospitals 50 or 100 years ago will have had this disease - or others. And if we didn't know about anti-NMDA encephalitis until recently, who's to say what we'll discover next?

Choe CU, Karamatskos E, Schattling B, Leypoldt F, Liuzzi G, Gerloff C, Friese MA, and Mulert C (2012). A clinical and neurobiological case of IgM NMDA receptor antibody associated encephalitis mimicking bipolar disorder. Psychiatry research PMID: 23246244

Ketamine: Magic Antidepressant Or Illusion? Revisited

There's a lot of interest in the idea that ketamine provides unparalleled rapid, powerful antidepressant effects, even in people who haven't responded to conventional antidepressants.

Earlier this year, I asked:

Ketamine - Magic Antidepressant, or Expensive Illusion?
There have now been several studies finding dramatic antidepressant effects of ketamine, the "club drug" aka "horse-tranquilizer". Great news? If you believe it. But hold your, er, horses... there's a problem.

My concern was that although depressed patients certainly do report feeling better after an injection of ketamine, compared to people given placebo, that doesn't prove that the drug is actually an antidepressant.

Rather, patients might be experiencing an enhanced, 'active' placebo effect, because ketamine causes subjectively powerful hallucinogenic experiences. So the placebo-controlled trials weren't really blinded.

To settle the question, I suggested a three-way trial comparing it both to an inert placebo, and to some other hallucinogen; if ketamine has a specific antidepressant effect, it should produce more improvement than the comparison drug.

This has never been done.

Given this background, a new trial from NIMH's Ketamine King, Carlos Zarate, makes interesting reading: A Randomized Trial of a Low-Trapping Nonselective N-Methyl-D-Aspartate Channel Blocker in Major Depression.

Zarate et al tried a novel drug, AZD6765 in depressed people. AZD6765 works much like ketamine in that it blocks brain NMDA receptors. But it is a less powerful trapping blocker than ketamine, meaning that AZD6765 causes less dramatic effects on the target receptors, in some respects.

In practice, this makes AZD6765, much less hallucinogenic than ketamine.

So it's interesting that, compared to placebo, the new drug only produced small benefits. On the MADRS depression symptom scale, patients felt a little better on AZD6765, but the boost only lasted a few hours.

The effect was far smaller than in an earlier ketamine trial as my crudely-mashed-up graph shows (although note that the patient populations were somewhat different, one bipolar and one unipolar depression, although their baseline severity was the same.)

While on ketamine people experienced significant subjective effects, with AZD6765 they didn't, and couldn't tell whether they got drug or placebo. Is that why they got a smaller benefit?

This is what we'd see if NMDA blockers do have a modest antidepressant effect but the dramatic improvements seen on ketamine are largely active placebo phenomena. Then again, it's also consistent with ketamine being a powerful antidepressant and AZD6765 just being less effective because it's a milder blocker of NMDA - effectively, a low dose of ketamine.

To tell the difference, we need... an active placebo controlled trial, like I've been banging on about for ages. But I wasn't the first one to suggest it - that was none other than Carlos Zarate et al in 2006.


Zarate CA Jr, Mathews D, Ibrahim L, Chaves JF, Marquardt C, Ukoh I, Jolkovsky L, Brutsche NE, Smith MA, and Luckenbaugh DA (2012). A Randomized Trial of a Low-Trapping Nonselective N-Methyl-D-Aspartate Channel Blocker in Major Depression. Biological psychiatry PMID: 23206319

My Breakfast With "Scientism"

One morning, I awoke convinced that science was the only source of knowledge. I had developed a case of spontaneous scientism.

The first challenge I faced was deciding what to eat for breakfast. Muesli, or cornflakes? Which would be the more scientific choice? I decided to go on the internet to look up the nutritional value of the different cereals, to see which one would be healthiest.

My computer was off. So first I'd need to turn it on - but how? From past experience, I suspected that pressing the big green power button on the front would do it - but then I remembered, that's merely anecdotal evidence. I needed scientific proof.

So I made a mental note to run a double-blind, randomized controlled trial of "turning my computer on" tomorrow.

Lacking nutritional data, I decided to pick a cereal by taste. I like muesli more than cornflakes. At last, a choice! Muesli it is, I thought - until I realized that I didn't actually know which one I preferred more. I had a gut feeling I liked muesli, but that's not science. What if, in fact, I hated muesli? Science couldn't tell me, at least not yet.

Another mental note: conduct cereal taste preference study, day after tomorrow. No breakfast for me, today.

By now, I was hungry, confused and annoyed. "This is getting ridiculous!", I tried to exclaim to no-one in particular - but then I realized - I could not even speak because I knew next to nothing scientific about the English language.

Sure, I had vague intuitions about how to put words together to express meaning, but that's just unscientific hearsay that I'd picked up as a child (no better than a religion, really!) In order to communicate, I'd need to study some proper science about semantics and grammar... but, oh no, how could I even read that literature?

Faced with the impossibility of doing anything whatsoever purely guided by science, I decided to go back to bed... yet with no scientific basis for controlling my own muscles, I collapsed where I stood, bashing my head on the breakfast table as I fell. 

Luckily, the bump on the noggin cured me of my strange obsession, and I lived to tell the tale.

---

Many people will tell you that "scientism", the belief that science is the only way to know anything, is a serious problem, a misunderstanding that threatens all kinds of nasty consequences.

It's not, because it doesn't exist - no-one believes that. If they did, they would end up like the unfortunate narrator in my story.

Everyday, we make use of many sources of information, from personal experience and learning to simply looking at things, whether they be right in front of your eyes or on TV. This is knowledge, and no-one thinks that we ought to replace it with "science", if that were even possible.

"Scientism" is a fundamentally unhelpful concept. Scientists are often wrong, and sometimes they're wrong about things that other non-scientists are right about. But each such case is different and must be judged on its own merits.

Neither Drugs Nor Therapy Prevent Psychosis

Neither medication nor psychotherapy is effective in improving the prognosis for youngsters considered to be at high risk of developing psychosis, according to a major study just published.

The idea of identifying and treating young people at risk of becoming psychotic - because of a family history of schizophrenia, or because they're showing some mild symptoms - has become very fashionable lately. But can we really do anything to pre-empt the disorder?

In this trial, 115 "ultra-high risk" Australian subjects were randomized to three different treatment conditions, or if they didn't agree to treatment, they were just followed up to see what happened.

The treatments didn't work. Here's the smoking gun, showing the proportion who didn't go psychotic over time:

This shows all four of the subject groups did pretty much the same in terms of their likelihood of becoming psychotic. Neither cognitive therapy, nor the antipsychotic drug risperidone (at a low dose) had any effect: those given 'supportive therapy' (basically: sympathetic chats) and a placebo pill did just as well.

There probably wasn't even a placebo effect: none of the three treatment groups did better than people who got no treatment at all (monitoring group), although people weren't randomly assigned to that group, so that's a little less clear.

Is this a surprise? Yes, if you believed the early studies to examine this question which claimed great things for drugs and therapy. But the current findings are no shock if you've been following the (much larger) recent trials - for example the British one from earlier in the year, which found zero benefit of cognitive therapy.

Early small trials have a nasty habit of not working out in the long run.

The other lesson here is that even "ultra-high risk" folks usually don't get psychotic: only about 10-20% of them, in fact, became ill in the first two years of this study; the British results I mentioned are very similar.

So is this really "ultra high"? Relatively, yes it is; even a 10% risk is far higher than the chance that a random person on the street would have. But in absolute terms, perhaps not.

A concern here is that rounding these folks up, labelling and 'treating' them might make their lives worse, or even increase the risk of psychosis. That's not just my opinion: that's what the very cognitive therapists who eagerly run these trials believe (or ought to, if they're being consistent with their own theories).

One of the key ideas in cognitive accounts of psychosis is that the belief and fear that one is 'going crazy', or that you're otherwise abnormal, is itself a major source of stress that actually leads to worsening of symptoms.

What could be scarier than being told you're at "ultra high risk"?

Preventing psychosis is a great idea in theory. But most bad ideas are.

McGorry, P., Nelson, B., Phillips, L., Yuen, H., Francey, S., Thampi, A., Berger, G., Amminger, G., Simmons, M., Kelly, D., Thompson, A., and Yung, A. (2012). Randomized Controlled Trial of Interventions for Young People at Ultra-High Risk of Psychosis The Journal of Clinical Psychiatry DOI: 10.4088/JCP.12m07785

Search Trends Reveal The Most Suicidal States

US states with more Google searches for suicide-related things actually have a higher suicide rate, according to a study just out.

Researchers Gunn and Lester write that, across the 50 US states,

The association between suicide rates and the search volume for ‘‘commit suicide’’ was significant and positive[r=0.31, p=0.01]... ‘‘how to suicide’’ was marginally significant and positive [r=0.21, p=0.07]... Finally, ‘‘suicide prevention’’ was significant and positive [r=0.61, p=0.001].

This seems pretty convincing although it's hard to know whether this represents suicidal people making the searches, as opposed to people searching in response to local suicides that already happened.

The fact that "suicide prevention" was the closest correlated with suicides while "how to suicide" was weakest makes the latter seem more plausible to me.

Previous suicide-search research has given mixed findings:

Sueki (2011) looked at variations in the volume of Google searches about suicide and depression in Japan by month from 2004–2012 and found that the monthly search volume for‘‘suicide’’and‘‘suicide method’’was not significantly correlated with the monthly suicide rate. However, searches for‘‘depression’’ were positively associated with the monthly suicide rate especially with a time lag of 1–3 months.

Over the past couple of years there's been a flurry of studies based on analyzing Google and Twitter trends. What's interesting to me is that we're really in the early days of this, when you think about likely future technologies. What will happen when everyone's wearing a computer 24/7 that records their every word and move, and even what they see?

Eventually, psychology and sociology might evolve (or degenerate) into no more than the analysis of such data...

Gunn III, J., & Lester, D. (2012). Using google searches on the internet to monitor suicidal behavior Journal of Affective Disorders DOI: 10.1016/j.jad.2012.11.004

The Case Of The Missing Parasites

Collembola or "Springtails" are a common group of bugs - they're technically not insects although much like them - found all over the world.

There's no evidence that these critters are parasites for humans - except for one strange scientific report claiming to have found Collembola body parts in skin scrapings from people diagnosed with delusional parasitosis - a psychiatric disorder characterised by the belief that one is infested with parasites.

According to said 2004 paper by Altschuler et al, these patients are not delusional after all. This paper has been popular in the delusional parasitosis community.

However, insect expert Matan Shelomi says that Altschuler et al's best photo of the so-called Springtails was probably Photoshopped. He explains that in the only pic to clearly show anything resembling a 'bug' (there were many others, but none look convincing), the raw microscope image shows nothing but a blurry blob.

Altschuler et al claimed to have enhanced the contrast, but when Matan did that, there was still no visible critter. However, in the published image, a rather sinister bug is clearly seen. How did it get there?

Either the image contrast was somehow selectively enhanced just for the 'bug' part - which, of course, presumes that the bug was there, and is quite invalid - or more likely,

The level of detail present in Altschuler et al.’s enhanced image, particularly in the areas of the legs and a very odd pair of stripes along the abdomen, does not appear when contrast is applied equally. Such detail, however, can easily be created using functions such as Burn, Dodge, and Colorize on Photoshop®,when applied to select portions of the image manually as if via paintbrush.

However, Shelomi says, even if such fraud is proven, there may be nothing anyone can do: the journal the original paper was published in has since folded, so it would be impossible to retract it, and the author runs an independent non-profit and is hence not subject to scientific misconduct regulations.

Thanks very much to @benmeg for sending me a copy of this paper.

Shelomi M (2012). Evidence of Photo Manipulation in a Delusional Parasitosis Paper. The Journal of parasitology PMID: 23198757

The Onion Makes Mental Illness Ridiculous

Despite being entirely fictional, The Onion offer some of the most perceptive political analysis anywhere.

Less well known, but likewise brilliant, is its coverage of mental health. The Onion's approach is to satirize the beliefs and perceptions that characterize psychiatric illness. The result is hilarious, but also insightful and, in a weird way, empathetic:

Local Anorexic Still Way Too Fat

Despite years of intense dieting and vigorous exercise, local anorexic Lisa Kimmel is still way too fat, it was reported Monday... Though Kimmel could stand to lose a few pounds in nearly every area of her body, worst of all are her arms. "I've got this totally disgusting flab on the back of my arms that swings back and forth when I move," said Kimmel, wearing an oversized Champion sweatshirt to conceal her obesity. "My arms totally look like my grandmother's."

Making matters worse is the fact that Kimmel's mother wants her to be overweight, constantly trying to get her to eat fatty foods like ravioli, mashed potatoes and broiled chicken with the skin still on. Other family members, as well as Kimmel's friends and doctors, also entreat her to eat because they want her to be fat, repulsive and unliked.

Pharmaceutical Company Says Its New Anti-Depressant Is 'Worthless And Dumb'

At a press conference Monday, Peter Cafazzo, CEO of Brunley-Hunt Pharmaceuticals (BHP), introduced his company's latest anti-depressant, Cyntrex, a product he described as "a totally stupid waste of time that probably nobody will ever want ever." ...

According to reports, top BHP researchers began having doubts about the drug during the early development stages, when they realized they couldn't do anything right ever ever ever, and that none of the pharmaceutical-industry leaders cared whether they lived or died. But work on the project continued, despite BHP's growing conviction that Cyntrex would be the worst product in pharmaceutical history.

Is The Government Spying On Paranoid Schizophrenics Enough?

Panelists discuss ways to care for the nation's paranoid schizophrenics, such as hiding cameras in their homes or audio transmitters in their ears. e.g. "We need to hide cameras everywhere they go, in the street, in their homes, in the eyes of people at the stores where they shop."

Some people might see this as making fun of the mentally ill, but I don't: it's making fun of the illness.

Suffering from a psychiatric disorder is a tragedy, but the disorder itself, and the distorted cognitions associated with it are, well, ridiculous. It's ridiculous to see yourself as fat when you're dangerously underweight. It's laughable to think you're worthless when you're successful and respected.

Coming to realize the absurdity of such beliefs is an important part of recovery, and an explicit goal of cognitive behavioural therapy although therapists don't tend to emphasize the funny side, it is certainly there.