Will Coffee Crack your Chromosomes?

Bloggers were amused by the Daily Mail's latest crap science article - a scary cancer story about research that hadn't even been done yet. The article is about a study to be conducted by some University of Leicester scientists, which will investigate whether coffee intake by pregnant women is correlated with DNA changes in babies, similar to those seen in leukemia. In other words: coffee-drinking might be associated with some molecular changes which might point to a risk of leukemia. We should ban the stuff, clearly.

What did scare me though was this line:

Previous research has shown that caffeine damages DNA, cutting cells’ ability to fight off cancer triggers such as radiation.

Hold on, caffeine is genotoxic? That would be pretty worrying. It wouldn't mean that coffee causes cancer, but it would make it highly plausible. But does caffeine in fact damage DNA? That might sound like a simple question to answer. Sadly not. It turns out that caffeine is one of the most researched chemicals in all of genotoxicology, and after over 1000 studies there's no consensus on what, if anything, it does to DNA. The story is remarkably complex and has all the good elements of a scientific intrigue. This review by Steven D'Ambrosio , for example, convincingly argues that:

A number of [genotoxic] effects have been observed [in the lab]. However, they usually appear after very high doses (> 1 mM) of caffeine in combination with genotoxins, and are usually specific to certain cell types and/or cellular parameters. Humans, on the other hand, consume much less caffeine in the diet...thus, it is difficult to implicate caffeine, even at the highest levels of dietary consumption, as a genotoxin to humans.

That's a relief. But right at the end we find that "This work was supported by the National Coffee Association"! If the author was in the pocket of Big Java, how can we trust him? Was he being bribed, perhaps with sacks of top-grade Columbian beans...? There's good evidence that high concentrations of caffeine can enhance the DNA damage produced by genotoxic agents such as radiation. But most of these experiments used caffeine concentrations hundreds of times higher than most coffee-drinkers are likely to experience. And contrary to the Mail's claim, this doesn't mean that coffee damages DNA - it probably works by deregulating the cell replication cycle to prevent DNA repair, which means that in theory, caffeine could even make cancer cells more vulnerable to chemotherapy (but again, only at extreme doses.) There's little epidemiological evidence of any association between coffee drinking and cancer; what evidence there is seems to suggest that coffee might even protect against some cancers...

Still, one comforting lesson from all this is that it's not just neuroscience in which seemingly simple questions (like is there are an area of the brain for recognizing faces?) can turn out to be much more complicated than one might hope...

S Dambrosio (1994). Evaluation of the Genotoxicity Data on Caffeine Regulatory Toxicology and Pharmacology, 19 (3), 243-281 DOI: 10.1006/rtph.1994.1023

I'm So Depressed

We use the word depression to refer to a wide range of states of mind, from severe "clinical depression" to just feeling a bit miserable. A "depressing movie" is not one which is going to make you clinically depressed if you watch it.

But the words "mania" and "psychosis" are not like this. People don't often talk about being manic when they're happy - I've heard people describe themselves as "a bit manic", but the bit makes all of the difference. People do use these words wrongly, e.g. some people seem to use "psychotic" when they mean "psychopathic". But even so, these words are always associated with abnormality and pathology. Depression is talked about as "normal" in a way in which mania and psychosis aren't.

This is misleading. True, depression can be hard to distinguish from sadness, stress, ennui, angst and other emotions. But it is a mistake to think that clinical depression is nothing more than a kind of inappropriate or excessive sadness. Being manic is not just being very happy, even if feeling very happy is one of the aspects of mania in some people (but not in all). Depression is not just feeling very sad. In fact, depression can be much more like mania and psychosis than most people tend to think.

In my experience of depression, it's little like sadness. Most people that I've spoken to who have suffered from depression agree; the distinctive thing about depression in most cases seems to be a feeling of lack, or a lack of feeling, in which things lose their value and worth. Textbooks call this anhedonia, a lack of pleasure, which is as good a description as any. Whereas, if you're sad about something, at least you value it.

It's interesting to imagine what things would be like if depression were today a word like mania, as it was 50 years ago.

The British are Incredibly Sad

Or so says Oliver James(*) on this BBC radio show in which he also says things like "I absolutely embraces the credit crunch with both arms".

Oliver James is a British psychologist best known for his theory of "Affluenza". This is his term for unhappiness and mental illness caused, he thinks, by an obsession with money, status and possessions. Affluenza, James thinks, is especially prevanlent in English-speaking countries, because we're more into free-market capitalism than the people of mainland Europe. In fact, he regularly makes the claim that we in Britain, the U.S., Australia etc. are today twice as likely to be mentally ill as "the Europeans". This is because rates of mental illness supposedly surged in the English-speaking world due to 1980s Reagan/Thatcher free market policies. Hence why he welcomes the current economic unpleasantness.

Were all of this true, it would be incredibly important. Certainly important enough to justify writing three books about it and seemingly endless articles for the Guardian. But is it true? Well, this is Neuroskeptic, so you can probably guess. Also, bear in mind that James is someone who is on record as thinking that

[The Tears for Fears song] Mad World. With the chilling line "The dreams in which I'm dying are the best I've ever had", in some respects it is up there with TS Eliot's Prufrock as a poetic account of bourgeois despair.

Obviously poetic taste is entirely subjective etc., but honestly.

Anyway, where did James get the twice-as-bad-as-Europe (or, in some articles, three times as bad) idea from? He says the World Health Organization. Presumably he is referring to one of the World Health Organization's World Mental Health Surveys, such as the analysus presented in this JAMA paper.

At first glance, you can see what he means. This paper reports that the % of people reporting suffering from at least one mental illness over the last year was far higher in the US (26.4%) than in say Italy (8.2%), or Nigeria (4.7%). But on closer inspection, even this data includes some incongruous numbers. Why is Beijing (9.1%) twice as bad as Shanghai (4.3%)? Worse, why does France have a rate of 18.4% while across the border in Germany it's just 9.1%? Are the French twice as materialistic as the Germans? The answer, of course, is that these numbers are more complicated than they appear. In fact, if you believe those figures at face value, you are...well, you're probably Oliver James.

These numbers come from structured interviews, conducted by trained lay researchers, of a random sample of the population. In other words, some guy asked some random people a series of fairly personal questions, reading them off a list, and if they said "Yes" to questions like "Have you ever in your life had a period lasting several days or longer when most of the day you felt sad, empty or depressed?" they might get a tick for "depression". We know this because the interviews used the WHO-CIDI screening questionaire, the first part of which is here.

As part of my own research, I have been that guy asking the questions (in a slightly different context). At some point I'll write about this in more detail, but suffice to say that it's hard to trying to retrospectively diagnose mental illness in someone you've never met before. The potential for denial, mis-remembering, malingering, forgetting or just plain failure to understand the questions is enormous, although it doesn't come across in the final data, which looks lovely and neat.

The authors of the JAMA paper are well aware of this which is why they're skeptical of the apparantly large cross-national differences. In fact, most of their comment section consists of caveats to that effect. Just a few (edited, emphasis mine - see the full paper for more, it's free):

An important limitation of the WMH surveys is their wide variation in response rate. In addition, some of the surveys had response rates below normally accepted standards [i.e. many people refused to participate]... performance of the WMH-CIDI could be worse in other parts of the world either because the concepts and phrases used to describe mental syndromes are less consonant with cultural concepts than in developed Western countries [almost certainly they are] or because absence of a tradition of free speech and anonymous public opinion surveying causes greater reluctance to admit emotional or substance-abuse problems than in developed Western countries. [again, almost certainly, and Europeans are generally more reserved than Americans in this regard.] ... some patterns in the data (e.g. the much lower estimated rate of alcoholism in Ukraine than expected from administrative data documenting an important role of alcoholism in mortality in that country) raise concerns about differential validity.

There's another, more fundamental problem with this data. On any meaningful criterion of "mental illness", a society in which 25% people were mentally ill in any given year would probably collapse. The WHO survey, however, is based on the DSM-IV criteria of mental illness. These are are increasingly regarded as very broad; for example, DSM-IV does not distinguish between feeling miserable & down for two weeks because your boyfriend leaves you, and spending a month in bed hardly eating for no apparant reason. Both are classed as "depression", and hence a "mental illness", although 50 years ago, only the second would have been considered a disease. For someone who styles himself a rebel in the mould of R. D. Laing, it's baffling that James accepts the American Psychiatric Association's dubious criteria.

What other data could we look at? Ideally, we want a measure of mental illness which is meaningful, objective and unambigious. Well, there aren't any, but suicide rates might be the next best thing - they're nice hard numbers which are difficult to fudge (although in cultures in which suicide is strongly taboo, suicides may be reported as deaths from other causes.) Although not everyone who commits suicide is mentally ill, it is fair to say that if Britain really were twice as unhappy as the rest of Europe, we would have a relatively high suicide rate.

What's the data? Well, according to Chishti et. al. (2003) Suicide Mortality in the European Union, we don't.
In fact suicide rates in the UK are boringly middle of the road. They're higher than in places like Greece and Spain, but well below rates in France, Sweden and Germany. Suicide rates are not a direct measure of rates of mental illness, because not everyone who commits suicide is mentally ill, and the rate of succesful suicide depends upon access to lethal means. But does this data look compatible with James's claim that rates of "mental illness" are twice as high in Britain as on "the Continent"? - or indeed with James's implicit assumption that "the Continent" is monolithic?

What's odd is that James clearly knows a bit about suicide, or at least he does now, because just today he wrote a remarkably sensible article about suicide statistics for the Guardian. So he really ought to know better.

Drug sales are another nice, hard number. Of course, medication rates do not equal illness rates - in any field of medicine, but especially psychiatry. Doctors in some countries may be more willing to use drugs, or patients may be more willing to take them. With that in mind, the fact that population-adjusted (source, also here) British sales of antidepressants drugs are twice those of Ireland and Italy, equal to those of Spain, and half those of France, Norway and Sweden does not necessarily mean very much. But it hardly supports James's theory either.

Interestingly, although James holds up Denmark as an example of the kind of happy, "unselfish capitalism" that we should aspire to, the Danes take 50% more antidepressants than we do! (They also have a much higher suicide rate.) True, sales of anxiety drugs and sleeping pills are relatively high in the UK, but still less than Denmark's. Most interestingly, sales of antipsychotics are very low in the UK - roughly the same as in Germany and Italy but less than a quarter of the sales in Ireland and Finland!

So cheer up, Anglos. We're not twice as sad as the French. More likely, we are just more open about talking our problems in the interests of scientific research. However, the French, to their credit, didn't give the world Oliver James.

[BPSDB]

(*) This is Oliver James, psychologist. Not to be confused with: Oliver James, heartthrob actor; Oliver James, Fleet Foxes song, and Oliver James, Ltd.

The WHO World Mental Health Survey Consortium (2004). Prevalence, Severity, and Unmet Need for Treatment of Mental Disorders in the World Health Organization World Mental Health Surveys JAMA: The Journal of the American Medical Association, 291 (21), 2581-2590 DOI: 10.1001/jama.291.21.2581

Autism, Testosterone and Eugenics

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

To date, no theory of autism has provided such a connecting thread linking etiology, neuropsychology and neural bases of autism.

Anyway, the paper reports on an association between testosterone levels in the womb and later "autistic traits" in childhood. 235 healthy children were studied; for all of these kids, the levels of testosterone in the womb during pregnancy were known, because their mothers had had amniocentesis, collecting a sample of fluid from the womb. Amniocentesis is not risk-free and it can't be done for research purposes, but the mothers here got amniocentesis for medical reasons and then agreed to take part in research as well. Testosterone levels in the amniotic fluid were measured; notably, this probably represents testosterone produced by the fetus itself, rather than the mother.

The headline finding was that fetal testosterone (fT) levels were correlated with later "autistic traits", as judged by the mothers, who filled out questionaires about their kid's behaviour at the age of about 8. Here's a nice plot showing the correlation. The vertical axis, "AQ-child total", is the parent's total reported score on the "Autism Quotient" questionaire. Higher scores are meant to indicate autism-like traits (although see below). You'll also notice that fT levels are much higher in the boy fetuses than in the girl fetuses - not surprisingly. That's it - a statistically significant association, but there is still a lot of scatter on the plot. The correlation was still significant if the very high-scoring children were ignored. A similar pattern emerged using a different autism rating scale, but was less significant - probably because many scores were very low.
So, this was a perfectly decent study with an interesting result, but it's only a correlation, and not an especially strong one. How did this get written up? New research brings autism screening closer to reality puffed the Guardian's front page! They suggested that measuring fetal testosterone levels might be a way of testing for autism pre-natally, thus sparking off an entirely formulaic debate about the ethics of selective abortion, the usual denunciations of "eugenics", etc. Long story short - Catholics are against it, the National Autistic Society say it's a dilemma, while a family doctor on Comment is Free is unsure about the "test" because she can't read the article: she doesn't have access to the journal.

Lest it be said that the ethical debate is important in itself, even if the details of the testosterone-based screening test might be inaccurate, bear in mind that "testing for autism" is likely to raise unique issues. Are we talking about a test which could distinguish "low-functioning autism" - which can leave children unable to lead anything like a normal life - from "high-functioning autism", sometimes associated with incredible intellectual achievement? Would the test distinguish classical high-functioning autism from Asperger's? When and if a test is developed, these will be crucial questions. You cannot simply speculate about "a test for autism" in the abstract.

Anyway, after a few days of this nonsense Baron-Cohen rightly protested that the paper had nothing to do with prenatal testing, and that such testing isn't on the horizon yet.

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.

Most importantly, there were no autistic kids in the study - all of the children were "normal", although some were rated highly on the autism measures. Moreover, as the plot above shows, any testosterone-based screening test would be very inaccurate. Which is why no experts proposed one.

Just like last time. Back in 2007 the Observer (the Sunday version of the Guardian) ran a front-page article about Simon Baron-Cohen's work on the epidemiology of autism. They said that he'd found that autism rates in Britain were "surging"; they probably aren't, and Baron-Cohen's data didn't show that they were, but despite this the Observer took weeks to clarify the issue (for details of the saga, see Bad Science.) In both cases, some important research about autism from Cambridge ended up on the front page of the newspaper, but the debate which followed completely missed the real point. It would have been better for all concerned if the research had never caught the attention of journalists at all.

The actual study in this case is very interesting, as are the three academic commentaries and a response from the authors published alongside it. I can't cover all of the nuances of the debate, but some of the points of interest include: the question of whether the Autism Quotient (AQ) questionaire actually measures autistic behaviours, or just male behaviours; the point that it may be testosterone present in baby boys shortly after birth, not in the womb, which is most important; and the interesting case of children suffering from Congenital Adrenal Hyperplasia, a genetic disorder leading to excessive testosterone levels; Baron-Cohen et. al. suggest that girls with this disorder show some autism-like traits, but this is controversial. Clearly, this is a crucial point.

Overall, while it's too soon to pass judgement on the extreme male brain theory or the testosterone hypothesis, both must be taken seriously. As for autism prenatal testing, I suspect that this will only come when more of the genetic causes of autism are identified. There is no single "gene for autism"; currently a couple of genes responsible for a small % of autism cases are known: CNTNAP2, for example.

Once we have a good understanding of the many genes which can lead to the many different forms of autistic-spectrum disorders, genetic testing for autism will be possible; I doubt that testosterone levels or anything else will serve as a non-genetic marker, because autism almost certainly has many different causes, and many different associated biochemical abnormalities. Maybe I'm wrong, but even so, if you're worried about hypothetical people aborting hypothetical autistic fetuses, you don't have to worry quite yet. Actual children are dying in Zimbabwe - worry about them.

[BPSDB]

Bonnie Auyeung, Simon Baron-Cohen, Emma Ashwin, Rebecca Knickmeyer, Kevin Taylor, Gerald Hackett (2009). Fetal testosterone and autistic traits British Journal of Psychology, 100 (1), 1-22 DOI: 10.1348/000712608X311731

Prozac and Old Mice

A while back, I wrote about an important paper which cast doubt on the "neurogenesis hypothesis" of antidepressant drug action, which I summarized as

...the proposal that antidepressants work by promoting the survival and proliferation of new neurones in certain areas of the brain - the "neurogenesis hypothesis". Neurogenesis, the birth of new cells from stem cells, occurs in a couple of very specific regions of the adult brain, including the elaborately named subgranular zone (SGZ) of the dentate gyrus (DG) of the hippocampus. Many experiments on animals have shown that chronic stress, and injections of the "stress hormone" corticosterone, can suppress neurogenesis, while a wide range of antidepressants block this effect of stress and promote neurogenesis. (Other evidence shows that antidepressants probably do this by inducing the expression of neurotrophic signalling proteins, like BDNF.)

It's a popular theory at the moment, not least because it's the only real alternative to the older, much-maligned and certainly incomplete monoamine hypothesis of antidepressants. But the neurogenesis hypothesis has problems of its own. A new paper claims to add to what seems like a growing list of counter-examples: Ageing abolishes the effects of fluoxetine on neurogenesis.

The researchers, Couillard-Despres et. al. from the University of Regensburg in Germany, found that fluoxetine (Prozac) enhances hippocampal neurogenesis in mice - as expected - but found in addition that this only holds true in young mice. In middle-aged and older mice, there was no such effect. That's a new finding, and a very important one.

More specifically, the (male) mice were given injections of Prozac for two weeks each. Compared to mice given placebo injections, the mice on Prozac showed

increased survival and the frequency of neuronal marker expression in newly generated cells of the hippocampus in the young adult group (that is 100 days of age) only. No significant effects on neurogenesis could be detected in fluoxetine-treated adult and elderly mice (200 and over 400 days of age).

For mice, 100 days old corresponds to a human age of about 20 years; 200 days is 35 and 400 days is 65 years. The graph here shows the number of BrdU-labelled cells in the dentate gyrus, a measure of neural progenitor cell survival. As you can see, although Prozac robustly increased BrdU+ cell counts in the 100 day old mice, this effect was much less prominent (although perhaps still present a bit?) in the older mice.

It's already well known that hippocampal neurogenesis is age dependent. Young animals (and people) have lots of new neurones being generated, but the rate progressively and inevitably declines with age. This has always been a problem for the simple hypothesis that reduced neurogenesis causes depression, because if that were the case, we'd all be paralyzed by despair by the age of 50. Despite this, it remained plausible that antidepressants worked by increasing neurogenesis, but this new evidence suggests otherwise.

Or does it? What if it turns out that fluoxetine has no antidepressant-like effects in old rodents? In that case, the neurogenesis hypothesis would be supported, not weakened, by this evidence. The author's of the paper don't even consider this possibility, which is a little odd. They do note that antidepressants are effective in older people with depression, but given that this is a paper about mice that's not the same thing. Someone needs to find out whether Prozac has anti-depressant-like effects in the same kind of old mice as those used in this study. If so, the neurogenesis hypothesis will be looking pretty fragile.

This should also serve as a reminder that lab mice are animals, not research robots. They get old, like the rest of us, and research done only on young mice, or male mice, or a certain breed of mice, may not be applicable to others. I have two cats: if you stroke the grey one on the belly, she'll purr contentedly. But if you foolishly assume that the tabby one is the same, you'll get bitten pretty quickly...

S Couillard-Despres, C Wuertinger, M Kandasamy, M Caioni, K Stadler, R Aigner, U Bogdahn, L Aigner (2009). Ageing abolishes the effects of fluoxetine on neurogenesis Molecular Psychiatry DOI: 10.1038/mp.2008.147

Biases, Fallacies and other Distractions

One of the pitfalls of debate is the temptation to indulge in tearing down an opponent's arguments. It's fun, if you're stuck behind a keyboard but still feeling the primal urge to bash something's head in with a rock. Yet if you're interested in the truth about something, the only thing that should concern you is the facts, not the arguments that happen to be made about them.

Plenty has been written about arguments and how they can be bad: sins against good sense are called "fallacies" and there are many lists of them. Some of the more popular fallacies have become household names - ad hominem attacks, the appeal to authority, and everyone's favorite the straw man argument.

Likewise, cognitive psychologists have done much to name and catalogue the various ways in which our minds can decieve us. Under the blanket name of "biases" many of these are well known - there's confirmation bias, cognitive dissonance, rationalization, and so on.

There's a reason why so much has been said about fallacies and biases. They're out there, and they're a problem. When you set your mind to it, you can find them almost anywhere - no matter who you are. This, for example, is written by someone who believes that HIV does not cause AIDS. By most standards, this makes him a kook. And he probably is a kook, about AIDS, but he’s not stupid. He makes some perfectly sensible points about cognitive dissonance and the psychology of science. And here, he offers further words of wisdom:

I have no satisfactory answer to offer, unfortunately, for how AIDStruthers could be brought to useful mutual discussion.
...
Here’s a criterion for whether a discussion is genuinely substantive or not, directed at clarification and increased understanding: no personal comments adorn the to-and-fro. If B appears not to understand what A is saying, then A looks for other ways of presenting the case, A doesn’t simply keep repeating the same assertions spiced with “Why can’t you…?”, and the like. [Added 28 December: Another hallmark of the non-substantive comments is that the commentator not only keeps harping on the same thing but does so by return e-mail, leaving no time to consider what s/he is replying to; see Burun's admission of suffering from that failing.]
...
One lesson from experience is that the aim of Rethinkers cannot be to convince the AIDStruthers. It soon becomes a sheer waste of time to attempt to argue substance with them; a waste of time because you can’t learn anything from them, and they are incapable of learning anything from you. Rethinkers and Skeptics should address the bystanders, onlookers, the unengaged “silent majority”. There seem always to be with us some people who cheerfully continue to believe that the Earth is only about 6,000-10,000 years old, and many other things that most of us judge to be utterly disproved by factual evidence.

That could have come straight from the pen of such pillars of scientific respectability as Carl Sagan or Orac - until you remember that by "Rethinkers" and "Skeptics" he means people who don't believe that HIV causes AIDS, while "AIDStruthers" is his term for those who do, that is, almost every medical and scientific professional.

The lesson here is that you don't have to be right in order to notice that people who disagree with you are irrational, or that much of the opposition to your belief is dogmatic. The sad fact is that stubborness and a tendency to dogmatism are a part of human nature and it's very hard to escape from them; likewise, it's very hard to make a complex argument without saying something at least technically fallacious (that witty aside? Ad hominem attack!)

The point is that none of this matters. If something is true, then it's true even if everyone who believes it is a dogmatic maniac. So it's certainly true even if the only people you know who believe it are idiots. What's the chance that you've argued with the smartest Christian ever, or the best informed opponent of homeopathy? In which case - the fallacies and biases of the people you have argued with certainly don't matter. In an argument, the only thing of importance is what the facts are, and the way to find out is to look at the evidence.

If you're taking the time to name and shame the fallacies in someone's reasoning or to diagnose their biases, then you're not talking about the evidence - you're talking about your opponent(s). Why are you so fascinated by him...? To spend time lamenting the irrationality of your opponents is unhealthy. The only people who have a reason to care about other people’s fallacies and biases are psychologists. Daniel Kahneman got half a Nobel Prize for his work on cognitive biases - it's his thing. But if your thing is HIV/AIDS, or evolution, or vaccines and autism, or whatever, then it's far from clear that you have any legitimate interest in your opponent's flaws. In all likelihood, they are no more flawed than anyone else - or even if they are, their real problem is not that they're making ad hominem attacks (or whatever), but that they're wrong.

So when barely-coherent columnist Peter Hitchens writes in the Daily Mail about wind farms

If visitors from another galaxy really are going round destroying wind turbines, then it is the proof we have been waiting for that aliens are more intelligent than we are.

The swivel-eyed, intolerant cult, which endlessly shrieks – without proof – that global warming is man-made, has produced many sad effects.

The point is not that people who believe that global warming is man made are not a cult. They're not, but even if they were, it wouldn't matter. The swiveliness of their eyes or the pitch of their voice is not obviously relevant either.

Of course, if you're out to have fun bashing heads, or writing columns for the Daily Mail, then go ahead. Learn the names of as many fallacies and biases as you can (including the Latin names if possible - that's always extra impressive) and go nuts. But if you're serious about establishing or discussing the truth about something, then there is only one set of biases and fallacies you ought to care about – your own.

[BPSDB]

NOS1 - An Impulsivity Gene?

Neuroskeptic has warned before of the pitfalls of candidate gene association studies. With small sample sizes and multiple comparisons, false positive results are all too common, especially in behavioural genetics. Yet it's not all bad. The renowned Klaus-Peter Lesch and colleagues have just produced a paper which is a cut above the rest. They report on an association between a promoter region polymorphism in the gene NOS1 and "impulsive" traits.

NOS1 codes for the enzyme nitric oxide synthase 1, which is expressed in neurones and makes nitric oxide (Nitrogen monoxide, NO). NO is a small molecule with various roles in animals, most famously the ability to induce erections - Viagra works by enhancing this effect. NO is also known to act as a neurotransmitter, with widespread but poorly understood functions in the brain. It's therefore plausible that altered nitric oxide synthase function could affect behaviour, and several animal studies suggest that indeed it does.

The new paper, published in the Archives of General Psychiatry, reports on the characterization of a functional variant in the human NOS1 gene, and its association with behaviour in several large human samples. The polymorphism, which Lesch et. al. previously discovered and called NOS1 Ex1f VNTR, is a Variable Number Tandem Repeat in a promoter region of DNA. It can be either "short" (S) or "long" (L) (although note that these are arbitrary categories, since the length of the region varies along a range.)

The authors first established that Ex1f is a functional (biologically meaningful) variant, by showing that shorter forms of the Ex1f promoter are less active than the longer forms in vitro (see graphs). They then examined human brain tissue from post-mortem samples and found that the short/long polymorphism was associated with significant differences in the expression of a large number of proteins. Although most of the proteins in question were nothing to do with NO, this shows that the polymorphism does something, which is a start (many don't).

They then report on the association between the short form of the gene and what they call "impulsivity". Here's the exciting bit:

In two separate control samples of normal German adults (most of whom) were screened to exclude psychiatric disorders (n=640 and 1314), 21 and 20% carried two copies of the short allele (SS). I've helpfully highlighted that in green above. Then, in samples of German people who displayed various forms of impulsive behaviour, the SS genotype was more common: in 383 adults with ADHD (28% SS), 189 adults who had attempted suicide (25% SS), and adults with "Cluster B" personality disorders 26% SS, but not those with "Cluster C" disorders representing anxious traits. Also, in a sample of 182 criminals referred to a forensic psychiatry unit, those who had been assessed as "violent" were more likely to carry the SS genotype than those not (p=0.04). In a nutshell, SS is bad. There was a negative result in a family-wise association study in childhood ADHD, however.

As if that weren't enough data, in 1099 healthy volunteers, those carrying the S allele scored lower on the "Conscientiousness" factor of the NEO personality questionnaire than LL people, although the difference was only significant in women. Low conscientiousness could be seen as impulsiveness - although note that there are 5 personality factors on the NEO and the authors presumably checked for a genetic effect on all 5, so that's at least 5 comparisons.

Finally, they managed to work a bit of neuroimaging into the paper in the form of an EEG study in which SS subjects showed a greater posteriorization of the "no-go" centroid during a continuous performance task. The no-go centroid is an electrical signal which occurs in the brain during inhibition of an action; the authors claim that the fact that this signal occurred further back in the brain in SS subjects points "toward impaired function of the medial prefrontal cortex in these subjects, which probably underlies an improper cognitive control of initiated responses resulting in impulsive behaviors", but to be honest, that's very optimistic. What, if anything, this finding means is unclear.

Still, despite a couple of dodgy bits, the paper as a whole offers pretty good evidence that the NOS1 Ex1f variant is functional and influences personality. This is the first report linking NOS1 to behaviour in humans, although since the paper includes data from a number of different samples, it's more than just preliminary evidence. On the other hand, nothing in this field should be considered a fact until the exact effect in question has been replicated by independent researchers - at least, that's my rule of thumb.

The nature of the effect (the associated phenotype) is also unclear. The authors interpret it as increased "impulsivity", but that's a vague concept. Impulsivity in all situations? Only in social situations? Only when stressed? We don't know. Also, the authors seem to have only looked for associations with impulsive conditions. Were someone to look for an association with, say, depression, or schizophrenia, they might well find one, in which case this might be best seen as a resilience gene rather than an impulsivity one. No doubt someone will be doing such a study as we speak, so hopefully, we'll know soon.

History note: Klaus-Peter Lesch first attained fame as the lead author on the first paper associating the 5HTTLPR variant with personality. In the 12 years since this polymorphism has attracted more attention than any other in the field of behavioural genetics with several hundred papers at last count. So if that's anything to go by, we'll be hearing a lot more about NOS1. Stay tuned.

Andreas Reif, MD; Christian P. Jacob, MD; Dan Rujescu, MD; Sabine Herterich, PhD; Sebastian Lang, MD;, Lise Gutknecht, PhD; Christina G. Baehne, Dipl-Psych; Alexander Strobel, PhD; Christine M. Freitag, MD;, Ina Giegling, MD; Marcel Romanos, MD; Annette Hartmann, MD; Michael Rösler, MD; Tobias J. Renner, MD;, Andreas J. Fallgatter, MD; Wolfgang Retz, MD; Ann-Christine Ehlis, PhD; Klaus-Peter Lesch, MD (2009). Influence of Functional Variant of Neuronal Nitric Oxide Synthase on Impulsive Behaviors in Humans Archives of General Psychiatry, 66 (1), 41-50

Special issue on the Neuropsychology of Faces

Just a tip-off: if you liked my discussion of the brain and faces, you'll love the latest issue of the Journal of Neuropsychology.

Dorothy Rowe Wronged, also Wrong

(Via Bad Science) Here's the curious story of what happened when clinical psychologist Dorothy Rowe was interviewed for a BBC radio show about religion. She gave a 50 minute interview in which she said that religion was bad. The BBC, in their wisdom, edited this down to 2 minutes of audio which made her sound as if she was saying religion was good. She was annoyed, and complained. The BBC admitted that they'd misrepresented her and apologized. Naughty.

But that's not the point of this post. Because the BBC not only offered Rowe an apology, they also agreed to let her write about what she really believes and put it up on bbc.co.uk. Here is the result. Oh dear. It's, well, it's confused.

"Neuroscience proves the existence of free will" would be an extraordinary media headline, and, perhaps even more extraordinary, it would be true.

No it wouldn't Rowe - it wouldn't even mean anything. It gets worse from there on in. Read it if you can, but it's pretty bad. Not Bono-bad, but bad, especially in the way that she inserts references to the brain and to neuroscience seemingly at random which add literally nothing to her argument. Her argument being that we interpret reality, rather than directly percieving it. Which is true enough, but that idea's been around since the time of ancient Greece, where the cutting edge of neuroscience was the theory that the brain was made of semen. It's philosophy, not neuroscience.

This kind of neuro-fetishism happens a lot nowadays, but what's really weird is that Rowe is one of those psychologists who is convinced that depression (and indeed all mental illness) is not a "brain problem". Even one such as she clearly isn't immune to the lure of neuroscience explanations.

[BPSDB]

Mice, Math and Drugs: On Science without Understanding

The latest issue of Neuropsychopharmacology is chock full of goodies - not only one of the first ever controlled trials of medical marijuana, but also a surprise gem from an American-Israeli collaboration, called A Data Mining Approach to In Vivo Classification of Psychopharmacological Drugs. Yet despite being an excellent paper, it raises some worrying questions about what is and isn't science.

In a nutshell, the authors sought to discover a way of efficiently determining what a drug does. There are several broad classes of psychoactive drugs, such as stimulants, e.g. cocaine, and opioids, e.g. morphine. If you want to find out whether an unknown drug has opioid-like painkilling effects, for example, you have to test for them specifically - e.g. by measuring how the drug alters a mouse's pain threshold in a test called the Hot Plate test (guess what that involves.) If you want to test whether the same compound has antidepressant effects, you would have to do a different test entirely, like the Porsolt test. And so on.

The authors tried - and claim to have succeeded - to find a way of detecting the effects of drugs in a single, simple test. The test involved putting a mouse onto an empty circular platform (an "open field") and just allowing it to run around for an hour. A camera records the movements of the mouse, and a computer analyzes the video to give the mouse's position every 1/30th of a second. The result is a series of numbers showing the path which the mouse took around the area.

The clever bit follows: from this path data, one can derive various other numbers - for example, the mouse's velocity, acceleration, and direction of movement relative to the wall of the platform, at any given point in time. An hour of a mouse's life can be broken down into a veritable mountain of data (especially since there are 30 x 60 seconds x 60 minutes = 108,000 time points.)

The authors then used a technique called data mining to discover patterns in this data which could be useful in discovering drugs. Data mining is nothing complicated - it essentially means taking a lot of data and searching it all for anything interesting. In this case, they injected mice with various doses of various different drugs from three different classes - stimulants, opioids, and "psychotomimetics" such as phencyclidine (angel dust) and ketamine. They recorded their movement over the course of an hour and analyzed it to get 10 numbers ("attributes") at each of the 108,000 time points. They then considered the combination of up to 4 different attributes simultaneously in a procedure they call (and have no doubt patented as) "Pattern Array Analysis".

The single-attribute pattern coded P{*,*,3,*,*,*,*,*,*,*} is defined only by the third bin (40-60 cm/s) of the third attribute (speed), ie the animal is moving moderately fast... as more attributes are added to the definition of a pattern it becomes more and more specific, eg the four-attribute pattern P{*,*,1,2,*,1,5,*,*,*} means moving very slowly while slightly decelerating in the direction of the arena wall but turning sharply away from it.

They then took every one of this huge number of possible "behaviour patterns" (there were 73,042), measured how many times each mouse did each one over the course of the hour, and worked out which patterns became more or less common after giving each of the different drugs. They ended up with this:
This is a plot with 73,042 dots on it. Each dot represents a pattern of mouse movement behaviour. Dots further to the right represent behaviours which are more common, while dots higher up represent behaviours the frequency of which is most significantly different between mice given opioids and mice given other drugs (or no drugs). Most of the dots are low down the plot, showing that the opioids had little effect on them. But the dot with an arrow pointing at it represents a behaviour which is both common, and much, much less common in mice injected with opioids; in fact the significance p value of the difference is below 0.00000000000001 (that's 15 zeroes).

What is this behaviour? It's P{*,*,*,*,4,*,*,*,*,*} (‘moderately positive jerk’), meaning that the mouse's acceleration was increasing at a certain point in time (for those who know calculus: the second derivative of speed was positive & quite high). So, give a mouse morphine, and you can be pretty sure that its acceleration won't be increasing very often. Hmm. A similar procedure was performed for the other two classes of drugs.

Now, what on earth does that mean? Why do opioids suppress the ‘moderately positive jerk’? No-one knows - and the odd thing is that we don't need to know. Once we've identified the pattern of behaviour to look for, we could use it to determine whether drugs have opioid-like activity, even if you haven't got any idea why it works. And it does work - the authors report that by looking for the right behaviours, they could successfully classify a range of other drugs, including a couple of mystery drugs for which the person running the experiment didn't know what they were. This plot shows the success rate; the three classes of drugs are in different colours, and they clearly occupy three distinct regions of the "space", the two dimensions of which are frequency of two different patterns of behaviour. Overall, this is a very impressive paper, and the practical implications are potentially very great - soon, it might be possible to tell what effects a newly designed drug has, all in a single mouse test. This could greatly speed up, and reduce the cost, of drug discovery. For drug companies, it could be very useful indeed.

But is it "science"? This paper doesn't really add to our understanding of the world - all it does is tell us that a seriously obscure aspect of mouse movement, 'moderately positive jerk’, is altered by opioids. This is a potentially useful fact, especially if you're a drug company, but it's a completely uninterpretable one - it doesn't help us to explain, or understand, anything about mice, or opioids, or anything. It's not a theory or a hypothesis, and it will probably never give rise to one. It's just an isolated, brute fact. This is the kind of "science" that the most hard-core logical positivist would be happy with.

And this kind of thing is becoming popular in neuroscience. Essentially similar techniques are becoming widely used in fMRI data analysis. Here's a diagram from another paper from 2007 reporting on a method of using genetic algorithms to data-mine MEG data (a way of recording changes in the magnetic field surrounding the brain) to discover patterns which could be used to diagnose various neurological and psychiatric illnesses. It works:
It's an elegant technique and it's a nice result. But again, no-one has any idea what this diagram really "means" and almost certainly no-one never will. The fact that the schizophrenia patients and the Alzheimer's disease patients occupy different areas of this imaginary 2D "space" defined by two complex variables somehow derived from a huge mountain of numbers is potentially useful, if you want to diagnose a disease, but it tells you absolutely nothing about that disease. It's like going to a witch-doctor and asking if someone is ill; she's always right, but if you ask her how she knows, she just says "By magic".

Data mining's cool, but when it's done like this, it's not science...

Neri Kafkafi, Daniel Yekutieli, Greg I Elmer (2008). A Data Mining Approach to In Vivo Classification of Psychopharmacological Drugs Neuropsychopharmacology, 34 (3), 607-623 DOI: 10.1038/npp.2008.103


Apostolos P Georgopoulos, Elissaios Karageorgiou, Arthur C Leuthold, Scott M Lewis, Joshua K Lynch, Aurelio A Alonso, Zaheer Aslam, Adam F Carpenter, Angeliki Georgopoulos, Laura S Hemmy, Ioannis G Koutlas, Frederick J P Langheim, J Riley McCarten, Susan E McPherson, José V Pardo, Patricia J Pardo, Gareth J Parry, Susan J Rottunda, Barbara M Segal, Scott R Sponheim, John J Stanwyck, Massoud Stephane, Joseph J Westermeyer (2007). Synchronous neural interactions assessed by magnetoencephalography: a functional biomarker for brain disorders Journal of Neural Engineering, 4 (4), 349-355 DOI: 10.1088/1741-2560/4/4/001

Medical Marijuana Helps HIV Pain

There have long been anecdotal reports that marijuana can have pain-killing (analgesic) effects in types of chronic pain which are otherwise difficult to treat. This has led to great enthusiasm about the prospect of "medical marijuana" - but, attractive as that might sound, there has always been a lack of hard evidence showing that marijuana in fact works. Being highly illegal in the U.S.A (more illegal than cocaine in fact), it's hard to study.

A paper out today in Neuropsychopharmacology aimed to test the analgesic power of smoked marijuana vs. placebo and found that it was moderately effective. The work was done at the University of California (where else?) San Diego, and the subjects were all men with HIV. Like many such patients, they all suffered from chronic pain due to nerve cell damage, caused by either the virus itself or certain anti-HIV drugs. The patients in this study had all been diagnosed with "distal sensory predominant polyneuropathy" (DSPN), and were already taking standard painkillers such as aspirin and/or opiates such as morphine. This was pain that wouldn't go away.

30 volunteers were randomly assigned to smoke four times per day for 5 days; they smoked either marijuana cigarettes or placebo cigarettes which were similar in appearance but which lacked the active chemicals of marijana. After a two week break the subjects got the other kind for cigarette for five days (a cross-over design). Most, but not all, of the patients had some experience with (illegal) cannabis previously.

The results - After smoking marijuana, the patients rated their pain as being significantly less than when they were on placebo. The difference was significant although not enormous at first glance - a median difference in pain reduction of 3.3 "DDS points" (starting score median was 11.1) which translated into a standardized effect size of 0.60 ("medium" to "large"). So marijuana didn't completely kill the pain, but it was a decent help, and the effect was comparable to that seen with other drugs used in neuropathic pain such as anti-convulsants.

There was one snag, however. Although the side effects of the cannabis were generally minor, one of the patients, who had never tried cannabis before, developed "cannabis-related psychosis" on the first day they smoked the real cannabis.

One cannabis-naive subject had an acute, cannabis-induced psychosis at the start of the second smoking week; unblinding revealed that he had received placebo during the first week and active cannabis during the second.

Marijuana use has been correlated with an increased risk of psychosis. Whether the link is a causal one is hotly debated, but it's plausible that it could be, so it's something to bear in mind. The problem is that, frustratingly, the authors don't tell us anything about what "an acute, cannabis-induced psychosis" actually means. Is this just their melodramatic way of describing the unpleasant but fairly harmless experience of "pulling a whitey"? How long did it last? Did the patient require psychiatric treatment? Full-blown psychosis from the first dose of cannabis sounds rather implausible. Also, a number of drugs currently on the market can cause psychosis in rare cases, such as L-dopa - it shouldn't be seen as the end of the world for a drug, especially if it's one which fills an important niche.

So, this is evidence that marijuana can be helpful in one form of chronic neuropathic pain. Although it was a small, short study in a fairly narrowly defined group of patients, this is a believable result, given the anecdotal evidence and given the fact that mountains of animal studies show that marijuana-like drugs (CB1 receptor agonists) are analgesic in animals. It's a cliché that medical research papers always end with a call for further study on the question at hand, but in this case, I think that really is warranted. If marijuana can help treat intractable chronic pain, we need to know about it, and that means we need more randomized controlled trials.

Ronald J Ellis, Will Toperoff, Florin Vaida, Geoffrey van den Brande, James Gonzales, Ben Gouaux, Heather Bentley, J Hampton Atkinson (2008). Smoked Medicinal Cannabis for Neuropathic Pain in HIV: A Randomized, Crossover Clinical Trial Neuropsychopharmacology, 34 (3), 672-680 DOI: 10.1038/npp.2008.120

The British Media's Favorite Diagnoses

I was bored again last night, so time for some more graphs.
This shows the total number of LexisNexis UK News Search hits in the "UK Broadsheets" category from 1st January of each year to 1st January of the next year, for four terms. A hit represents a broadsheet newspaper article containing the specified string(s). (This article might not be "about" that condition e.g., a report about a crime committed by someone with schizophrenia which be a hit for "schizophrenia".)This is the same data for schizophrenia, bipolar/manic depression and autism/Asperger's, but shown as the ratio of hits compared to the number of hits for "Epilepsy" in the same year. I did this because hits for all conditions increase over time, which probably represents the fact that newspapers are getting longer & maybe that they're getting more interested in health (speculation.) Assuming that coverage of epilepsy is relatively immune to "fashion", which seems plausible, this allows trends in the "popularity" of the other three conditions to be seen more clearly.

What's the story? Firstly, the popularity of schizophrenia has remained fairly stable relative to epilepsy since 1985; this is what you'd expect, since rates of schizophrenia haven't changed much over that time. I was a little surprised that the recent cannabis-causes-schizophrenia theme, which some British papers have been pushing quite hard, hasn't had much effect. Hmm.

Bipolar disorder has become much more popular since about 2000; it's now close to being as popular as schizophrenia. Given that the true rates of these two disorders have probably not changed for 30 years, this points to some kind of cultural, as opposed to medical, trend; bipolar is almost certainly more diagnosed and less stigmatized today than in the past - indeed in some circles it's more trendy than just plain depression. (Note that "bipolar" will also give hits for articles using it in the political sense ("bipolar world"), but this is pretty uncommon.)

As for autism, coverage spiked in 2001-2002, the height of the British MMR-causes-autism scare. So no surprise there, but what did surprise me is that the popularity of autism has continued to increase since, with no sign of having peaked yet. Despite the fact that even the most stubborn armchair developmental neurologists have now largely stopped using the British newspapers to argue that vaccines cause autism, autism still gets more mentions than ever before.

So British newspaper readers can expect to hear plenty more about autism in 2009. Just remember that if you want in-depth discussions of this topic you might be better off reading LeftbrainRightbrain. That the newspapers are devoting increasing space to serious illnesses such as autism and bipolar disorder is in many ways a good thing, but quantity isn't quality, as MMR and the media's deeply uncritical coverage of the Kirsch et. al. (2008) antidepressant meta-analysis showed (more on that soon...)

Feel free to draw more conclusions from these coloured lines, as the mood takes you.

P.S I would have liked to do "depression", but that word has many meanings, e.g. in economics. "Clinical depression", on the other hand, seems to me increasingly old-fashioned; people just call it depression. Any ideas as to the best thing to search for?

[BPSDB]

Links You Might Like #2, and a note on Powerwatch

The Chronicle of Higher Education has a must-read piece about the integration of sociology and behavioral genetics. In it we learn that the American Journal of Sociology has just run a special issue devoted to that theme - wow. Looks fascinating (I haven't read it yet). As John Hawks notes, however, the traditional feuding between biological and social theorists of behaviour doesn't seem to be over yet...

There was an interesting discussion of the psychology of philosophy over at The Garden of Forking Paths.

Finally, Powerwatch UK have, very decently, included a link to my December 21st criticisms of a paper about leukemia and power lines, in their coverage of that study.

Critiquing a Classic: "The Seductive Allure of Neuroscience Explanations"

One of the most blogged-about psychology papers of 2008 was Weisberg et. al.'s The Seductive Allure of Neuroscience Explanations.

As most of you probably already know, Weisberg et. al. set out to test whether adding an impressive-sounding, but completely irrelevant, sentence about neuroscience to explanations for common aspects of human behaviour made people more likely to accept those explanations as good ones. As they noted in their Introduction:

Although it is hardly mysterious that members of the public should find psychological research fascinating, this fascination seems particularly acute for findings that were obtained using a neuropsychological measure. Indeed, one can hardly open a newspaper’s science section without seeing a report on a neuroscience discovery or on a new application of neuroscience findings to economics, politics, or law. Research on nonneural cognitive psychology does not seem to pique the public’s interest in the same way, even though the two fields are concerned with similar questions.

They found that the pointless neuroscience made people rate bad psychological "explanations" as being better. The bad psychological explanations were simply descriptions of the phenomena in need of explanation (something like "People like dogs because they have a preference for domestic canines"). Without the neuroscience, people could tell that the bad explanations were bad, compared to other, good explanations. The neuroscience blinded them to this. This confusion was equally present in "normal" volunteers and in cognitive neuroscience students, although cognitive neuroscience experts (PhDs and professors) seemed to be immune.

But is this really true?

This kind of research - which claims to provide hard, scientific evidence for the existence of a commonly believed in psychological phenomenon, usually some annoyingly irrational human quirk - is dangerous; it should always be read with extra care. The danger is that the results can seem so obviously true ("Well of course!") and so important ("How many times have I complained about this?") that the methodological strengths and weaknesses of the study go unnoticed. People see a peer-reviewed paper which seemingly confirms the existence of one of their pet peeves, and they believe it - becoming even more peeved in the process.(*)

In this case, the peeve is obvious: the popular media certainly seem to inordinately keen on neuroimaging studies, and often seem to throw in pictures of brain scans and references to brain regions just to make their story seem more exciting. The number of people who confuse neural localization with explanation is depressing. Those not involved in cognitive neuroscience must find this rather frustrating. Even neuroimagers roll their eyes at it (although some may be secretly glad of it!)

So Weisberg et al. struck a chord with most readers, including most of the potentially skeptical ones - which is exactly why it needs to be read very carefully critiqued. Personally, having done so, I think that it's an excellent paper, but the data presented only allow fairly modest conclusions to be drawn, so far. The authors have not shown that neuroscience, specifically, is seductive or alluring.

Most fundamentally, the explanations including the dodgy neuroscience differed from the non-neurosciencey explanations in more than just neuroscience. Most obviously, they were longer, which may have made them seem "better" to the untrained, or bored, eye; indeed the authors themselves cite a paper, Kikas (2003), in which the length of explanations altered how people perceived them. Secondly, the explanations with added neuroscience were more "complex" - they included two separate "explanations", a psychological one and a neuroscience one. This complexity, rather than the presence of neuroscience per se, might have contributed to their impressiveness.

Perhaps the authors should have used three conditions - psychology, "double psychology" (with additional psychological explanations or technical terminology), and neuroscience (with additional neuroscience). As it stands, the authors have strictly shown is that longer, more jargon-filled explanations are rated as better - which is an interesting finding, but is not necessarily specific to neuroscience.

In their discussion (and to their credit) the authors fully acknowledge these points (emphasis mine)

Other kinds of information besides neuroscience could have similar effects. We focused the current experiments on neuroscience because it provides a particularly fertile testing ground, due to its current stature both in psychological research and in the popular press. However, we believe that our results are not necessarily limited to neuroscience or even to psychology. Rather, people may be responding to some more general property of the neuroscience information that encouraged them to find the explanations in the With Neuroscience condition more satisfying.

But this is rather a large caveat. If all the authors have shown is that people can be "Blinded with Science" (yes...like the song) in a non-specific manner, that has little to do with neuroscience. The authors go on to discuss various interesting, and plausible, theories about what might make seemingly "scientific" explanations seductive, and why neuroscience might be especially prone to this - but they are, as they acknowledge, just speculations. At this stage, we don't know, and we don't know how important this effect is in the real world, when people are reading newspapers and looking at pictures of brain scans.

Secondly, the group differences - between the "normal people", the neuroscience students, and the neuroscience experts - are hard to interpret. There were 81 normal people, mean age 20, but we don't know who they were or how they were recruited - were they students, internet users, the authors' friends? (10 of them didn't give their age and for 2 gender was "unreported" -?) We don't know whether their level of education, their interests, or values were different from the cognitive neuroscience students in the second group (mean age 20), who may likewise have been different in terms of education, intelligence and beliefs from the expert neuroscientists in the third group (mean age 27). Maybe such personal factors, rather than neuroscience knowledge, explained the group similarities and differences?

Finally, the effects seen in this paper were, on the face of it, small - people rated the explanations on a 7 point scale from -3 (bad) to +3 (excellent), but the mean scores were all between -1 and +1. The dodgy neuroscience added about 1 point on a 7 point scale of satisfactoriness. Is that "a lot" or "a little"? It's impossible to say.

All of that said - this is still a great paper, and the point of this post is not to criticize or "debunk" Weisberg et. al.'s excellent work. If you haven't read their paper, you should read it, in full, right now, and I'm looking forward to further stuff from the same group. What I'm trying to do is to warn against another kind of seductive allure, probably the oldest and most dangerous of all - the allure of that which confirms what we already thought we knew.

(*)Or do they? Or is this just one of my pet peeves? Maybe I need to do an experiment about the allure of psychology papers confirming the allure of psychologist's pet peeves...

Deena Skolnick Weisberg, Frank C. Keil, Joshua Goodstein, Elizabeth Rawson, Jeremy R. Gray (2008). The Seductive Allure of Neuroscience Explanations Journal of Cognitive Neuroscience, 20 (3), 470-477 DOI: 10.1162/jocn.2008.20040