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by Neuroskeptic in Neuroskeptic
There was quite the stir a few weeks back about a psychology paper claiming that rich people aren't very nice: Higher social class predicts increased unethical behavior. The article, in PNAS, reported that upper class individuals were more likely to lie, cheat, and break traffic laws.However, these results have been branded "unbelievable" in a Letter to PNAS just published. Psychologist Gregory Francis notes that the paper contains the results of 7 seperate experiments, and they all found statistically significiant socioeconomic effects on unethical behaviour.Those 7 replications of the effect "might appear to provide strong evidence for the claim" - one study good, 7 studies better, right? - but Francis says that actually, it's too good to be believed.Each of the studies was fairly small, and the effects they found were modest, and only just significant. So the observed power of the studies - the probability that a study of that size would detect the effect that they did, in fact, find - was only about 50-88% in each case.Think of it this way: if you took a pack of cards and discarded half of the black ones, then shuffled the remainder, a random card from the deck would most likely be red. But even so, it would still be very unlikely that you'd pick 10 reds in a row.The chances of all 7 studies finding a positive result - even assuming that the effect claimed in the paper was real - is just 2%, by Francis's calculations.Ow.He concludes "The low probability of the experimental findings suggests that the data are contaminated with publication bias. Piff et al. may have (perhaps unwittingly) run, but not reported, additional experiments that failed to reject the null hypothesis (the file drawer problem), or they may have run the experiments in a way that improperly increased the rejection rate of the null hypothesis (4)".What might have happened? Maybe there were more than 7 studies and... maybe they peeked at the data before deciding on the same size, took other outcome measures unreported. See also the 9 Circles of Scientific Hell.Piff et al respond, firmly denying that they ran any other unpublished experiments, and saying that they "scrutinized our data collection procedures, coding protocols, experimental methods, and debriefing responses. In no case have we found anything untoward." They go on to criticize the method Francis used to get his magic 2% figure, which they point out relies on some debatable assumptions.Even if you buy the 2% figure, it doesn't mean that the true effect is zero; it might be real, but exaggerated. Ultimately it all becomes rather murky and subjective, which is why I think we need preregistration of research, which would prevent any possibility of such data fiddling, and also remove the possibility of false accusations of it... but that's another story.Francis, G. (2012). Evidence that publication bias contaminated studies relating social class and unethical behavior Proceedings of the National Academy of Sciences DOI: 10.1073/pnas.1203591109... Read more »
Francis, G. (2012) Evidence that publication bias contaminated studies relating social class and unethical behavior. Proceedings of the National Academy of Sciences. DOI: 10.1073/pnas.1203591109
by Neuroskeptic in Neuroskeptic
The media are gleefully reporting a recent paper showing that "gaydar is real" - we can tell who's gay just by looking: The Roles of Featural and Configural Face Processing in Snap Judgments of Sexual OrientationWhile it's a fine paper, I'm afraid that the results really aren't that exciting.American undergraduate students were able to classify people as gay or straight with better than chance accuracy, based purely on photos of their face. For male photos, the hit rate was 0.57; for women it was better with an accuracy of 0.65.However, that's on a scale where you get 0.50 by flipping a coin. So saying that gaydar is '65% accurate', as almost everyone has, is misleading. Still, the numbers seem solid. The sample sizes were large and the effect was replicated very convincingly in two experiments.However... this tells us very little about real world "gaydar", and it wasn't intended to. There are reasons to think it could underestimate the accuracy:Most importantly - people only saw the pictures for 50 milliseconds each. 1/20th of a second. Followed by a backward mask. That's right on the threshold of conscious perception, almost 'subliminal' but not quite. With longer viewing times, they might have done better.All the faces were black and white photos with the hair and ears cropped out (see above - and I think those two photos from the paper are the authors, although I may be wrong!). Anyone with facial hair, glasses, or any other 'accessories' wasn't used. In the real world, we have that extra information.In real life, we get clues from facial expressions, body language, voice, clothes. You could argue that these are being used (consciously or not) specifically as signals of sexuality, so they don't count as 'gaydar' - but more on that later. But it could also overestimate gaydar's powers:These were photos that people chose for their Facebook profiles. We all know how much effort some people put into that choice. We also know that different photos of the same person can often seem like two different people. Your Facebook pic is probably the most "selected" photo of you in existence. It would be better - but also much harder - to use passport photos.All of the gays in the study were out of the closet: they broadcast their sexuality on Facebook. But lots of gay people don't do that. Now those cases are probably where 'gaydar' is most likely to be of interest to most people, I think; those people might be harder to spot.As far as I can tell, this study wasn't intended to "prove that gaydar works". It was meant to examine how it works, by seeing whether it works very quickly (yes - in 50 ms in some cases). The authors also tested how accuracy was changed by flipping the photos upside down; this reduced accuracy but it was still well above chance. Ultimately, we need to ask what "gaydar" means and why we find it so interesting.On a superficial level, it just means being able to sense, from someone's appearance, if they're gay. That certainly does 'work' - if you see a guy coming out of a gay club in a tight pink Boy George t-shirt then yeah, he's probably gay. But he's (effectively) told you so, by being in that club and wearing those clothes, so that's not very interesting. That's an extreme case, but clearly people advertise their sexuality (and much else of course) all the time. Gaydar, in a weak sense, is just perception.I think what makes "gaydar" intriguing is the stronger idea that it can go beneath such adverts. That we can see who's really gay, whether or not they admit it, even to themselves. If that were possible, then it would seem to mean that homosexuality is part of the essence of some people - in other words, that it's a biological trait.So gaydar in a strong sense is risque. It calls to mind un-PC ideas such as physiognomy and would seem to validate various stereotypes which are the stuff of dirty jokes more than polite discussion.Does gaydar in this strong, exciting sense exist? That's another question. This study doesn't tell us.Tabak, J., and Zayas, V. (2012). The Roles of Featural and Configural Face Processing in Snap Judgments of Sexual Orientation PLoS ONE, 7 (5) DOI: 10.1371/journal.pone.0036671... Read more »
Tabak, J., & Zayas, V. (2012) The Roles of Featural and Configural Face Processing in Snap Judgments of Sexual Orientation. PLoS ONE, 7(5). DOI: 10.1371/journal.pone.0036671
by Neuroskeptic in Neuroskeptic
Yet another "promising" novel antidepressant has failed to actually treat depression.That's not an uncommon occurrence these days, but this time, the paper reporting the findings is almost as rubbish as the drug: Translational evaluation of JNJ-18038683, a 5-HT7 receptor antagonist, on REM sleep and in major depressive disorderSo, Pharma giant Janssen invented JNJ-18038683. It's a selective antagonist at serotonin 5HT-7 receptors, making it pharmacologically rather unusual. They hoped it would work as an antidepressant. It didn't - in a multicentre randomized controlled trial of 230 depressed people, it had absolutely no benefits over placebo. A popular existing drug, citalopram, failed as well:About the only thing JNJ-18038683 did do in humans was to reduce the amount of dreaming REM sleep per night. This REM suppressing effect is also seen with other antidepressants and this is evidence that the drug does do something - just not what it's meant to. Being charitable you could call this a failed trial.Ouch! But it gets better. Unhappy that JNJ-18038683 bombed, Janssen reached for their copy of the Cherrypicker's Manifesto. This is a new statistical method, proposed by fellow Pharma company GSK in a 2010 paper, which consists of excluding data from study centres with a very high (or very low) placebo response rate.Anyway, after applying this "filter" JNJ-18038683 seemed to do a bit better than placebo, but the benefit over placebo still wasn't statistically significant - with a p value of 0.057, the wrong side of the sacred p=0.05 line (on page 33).Yet Page 33's "trend towards statistical significance" magically becomes "significant" - in the Abstract:[with] a post hoc analyses (sic) using an enrichment window strategy... there was a clinically meaningful and statistically significant difference between JNJ-18038683 and placebo.Well, no, there wasn't actually. It was only a trend. Look it up.That aside, the problem with the whole filter idea is that it could end up biasing your analysis in favour of the drug, leading to misleading results. The original authors warned that "data enrichment is often perceived as a way of improperly introducing a source of bias... In conventional RCTs, to overcome the bias risk, the enrichment strategy should be accounted for and pre-planned in the study protocol." They should know, as they invented it, but Janssen rather oddly say the exact opposite: "This methodology cannot be included in a protocol prospectively as it will introduce operational bias in that scheme."Hmm.Anyway, even after the filter technique, citalopram didn't work either... bad news for citalopram, except, was it citalopram at all? This is really unbelievable: Janssen don't seem clear on whether they compared their drug to citalopram, or to escitalopram - a quite different drug.They say "citalopram" in most cases, but they have "escitalopram" instead, in three places, including, mysteriously, in a "hidden" text box in that graph I showed earlier:I'm not making this up: I stumbled upon a text box which is invisible, but if you select it with the cursor, you find it contains "escitalopram"! I have no idea what the story behind that is, but at best it is seriously sloppy.Come on Janssen. Raise your game. In the glory days of dodgy antidepressant research, your rivals were (allegedly) concealing data on suicides and brushing whole studies under the carpet, to make their drugs look better. Despicable, but at least it had a certain grandeur to it.Bonaventure, P., Dugovic, C., Kramer, M., De Boer, P., Singh, J., Wilson, S., Bertelsen, K., Di, J., Shelton, J., Aluisio, L., Dvorak, L., Fraser, I., Lord, B., Nepomuceno, D., Ahnaou, A., Drinkenburg, W., Chai, W., Dvorak, C., Carruthers, N., Sands, S., and Lovenberg, T. (2012). Translational evaluation of JNJ-18038683, a 5-HT7 receptor antagonist, on REM sleep and in major depressive disorder Journal of Pharmacology and Experimental Therapeutics DOI: 10.1124/jpet.112.193995... Read more »
Bonaventure, P., Dugovic, C., Kramer, M., De Boer, P., Singh, J., Wilson, S., Bertelsen, K., Di, J., Shelton, J., Aluisio, L.... (2012) Translational evaluation of JNJ-18038683, a 5-HT7 receptor antagonist, on REM sleep and in major depressive disorder. Journal of Pharmacology and Experimental Therapeutics. DOI: 10.1124/jpet.112.193995
by Neuroskeptic in Neuroskeptic
I've got another guest post over at Discover magazine: Is the Purpose of Sleep to Let Our Brains “Defragment,” Like a Hard Drive?It's an expanded version of two Neuroskeptic posts(1,2) about the theory that the job of slow-wave sleep is to prune connections in the brain, connections which tend to become stronger while we're awake and might become too strong without periodic resetting.One of the commenters on the Discover post pointed out that this idea a bit like a much older idea about sleep, from Francis Crick (of discovering-the-structure-of-DNA fame). Back in 1983, Crick and Graeme Mitchison proposed that dreaming sleep serves to help us "unlearn": The Function of Dream SleepTheir idea was a bit different, but it was really very elegant. During dreaming, they noted, the brain is cut off from real sensory input, and is subject only to essentially random activity variations. However, sometimes these meaningless inputs may be 'interpreted' as having meaning, activating representations (concepts, thoughts, memories) that we've learned to recognize when awake.These "patterns" that the brain wrongly "sees" in noise are what we experience as dreams.Crick and Mitchison's point is that, ideally, a pattern recognition system (like the brain) shouldn't be picking up patterns from random noise because that would be a sign that it was biased in favor of those patterns - "obsessed" with them, as it were, and liable to see them everywhere. So it would be good if there were some way of identifying the brain's biases and (partially) unlearning them.That's what dreams do, somehow, according to Crick. It's like if dreams are a self-administered Rorschach test that the brain uses to work out what's "weighing on its mind"! Incidentally, this is an idea I once suggested (much less clearly) myself.It's a beautiful and ingenious theory, although as the authors admitted, it would be very hard to test and it leaves wide open the question of how dreams could cause memories to be "unlearned" or indeed whether unlearning is even possible in the brain. It's also not very similar to the modern "defrag" theory, because Crick was talking about the dreaming rapid eye movement stage of sleep, not slow-wave sleep.Francis Crick and Graeme Mitchison (1983). The Function of Dream Sleep Nature, 304, 111-114... Read more »
Francis Crick and Graeme Mitchison. (1983) The Function of Dream Sleep. Nature, 111-114. info:/
by Neuroskeptic in Neuroskeptic
People think of "social anxiety disorder" as more serious than "social phobia" - even when they refer to exactly the same thing.Laura C . Bruce et al did a telephone survey of 806 residents of New York State. They gave people a brief description of someone who's uncomfortable in social situations and often avoids them. The question was: should they seek mental health treatment for this problem?When the symptoms were labelled as "social anxiety disorder", 83% of people recommended treatment. But when the same description was deemed "social phobia", it dropped to 75%, a statistically significant difference.OK, that's only an 8% gap. It's a small effect, but then the terminological difference was a small one. "Anxiety disorder" vs "Phobia" is about a subtle a distinction as I can think of actually. Imagine if one of the options had been a label that didn't imply anything pathological - "social anxiety" or "shyness". That would probably have had a much bigger impact.This matters, especially in regards to current debates over the upcoming DSM-5 psychiatric diagnostic manual. Lots of terminological changes are planned. This study is a reminder that even small changes in wording can have an impact on how people think about mental illness. Last week I covered another recent piece of research showing that beliefs about other people's emotions affect how people rate their own mental health.My point is: DSM-5 will not merely change how professionals talk about the mind. It will change how everyone thinks and behaves.Bruce, L. (2012). Social Phobia and Social Anxiety Disorder: Effect of Disorder Name on Recommendation for Treatment American Journal of Psychiatry, 169 (5) DOI: 10.1176/appi.ajp.2012.11121808... Read more »
Bruce, L. (2012) Social Phobia and Social Anxiety Disorder: Effect of Disorder Name on Recommendation for Treatment. American Journal of Psychiatry, 169(5), 538. DOI: 10.1176/appi.ajp.2012.11121808
by Neuroskeptic in Neuroskeptic
According to University of Iowa researchers Vincent A. Magnotta and colleagues, any neuroscientist with an MRI scanner could soon be able to measure the acidity (pH) of the human brain in great detail: Detecting activity-evoked pH changes in human brain. If it works out, it would open up a whole new dimension of neuroimaging - and might be able to answer some of the biggest questions in the field.The method relies on measuring T1 relaxation in the rotating frame (T1ρ). Essentially, it's about the rate at which protons are swapped between water molecules and proteins. That rate is known to depend on pH.Anyway. It certainly looks impressive. Using a standard 3 Tesla MRI scanner, they were able to image the whole brain once every 6.6 seconds - only slightly slower than conventional fMRI measurements of brain activity, where 2 or 3 seconds is more usual. The spatial resolution was comparable to fMRI.Here's how it did on some bottles of jelly -Then they moved onto mouse brains (the differences are smaller here)...And finally they scanned some people. They were able to detect the (very small) pH changes caused by hyperventilation, which raises pH, and breathing air enriched in carbon dioxide, which lowers it.Lovely pictures I'm sure you agree, and it's a very clever methodology from a technical point of view. But what will it mean for neuroscience?Well, for one thing, it might be able to help resolve some of the debates over what conventional fMRI is actually measuring. For example, some neuroscientists believe that many (seemingly) interesting fMRI results may actually be (at least partially) reflections of subtle changes in breathing rate. Measuring acidity, an indirect proxy for breathing, could start to answer such questions.The main question though is, what are we going to call the new method? "T1ρ MRI"... not a terribly catchy name.Maybe MRalkalI?Magnotta, V., Heo, H., Dlouhy, B., Dahdaleh, N., Follmer, R., Thedens, D., Welsh, M., and Wemmie, J. (2012). Detecting activity-evoked pH changes in human brain Proceedings of the National Academy of Sciences DOI: 10.1073/pnas.1205902109... Read more »
Magnotta, V., Heo, H., Dlouhy, B., Dahdaleh, N., Follmer, R., Thedens, D., Welsh, M., & Wemmie, J. (2012) Detecting activity-evoked pH changes in human brain. Proceedings of the National Academy of Sciences. DOI: 10.1073/pnas.1205902109
by Neuroskeptic in Neuroskeptic
Bipolar disorder usually strikes between the ages of 15 and 25, and is extremely rare in preteens, according to a major study: Age at onset versus family history and clinical outcomes in 1,665 international bipolar-I disorder patientsThe findings are old hat. It's long been known that manic-depression most often begins around the age of 20, give or take a few years. Onset in later life is less common while earlier onset is very unusual.The main graph could have been lifted from any psychiatry textbooks of the last century:The red bars are the data. Ignore the black line, that just shows an imaginary 'even' distribution over the lifespan.Why am I blogging about these remarkably unremarkable results? Because they undermines the theory, popular in certain quarters but highly controversial, that 'child bipolar' or 'pediatric bipolar' is a major health problem.The study confirmed that early-onset bipolar I does exist, but just 5% of the bipolar I patients had an onset before the age of 15. Assuming a lifetime prevalence of 1% for bipolar I disorder, which is about right, that makes about 0.05%, 1 in 2000 kids, about the same prevalence as Down's Syndrome. Even that's an overestimate, though, because this sample was enriched for early-onset cases: some of the participating clinics were child and adolescent only.There's a few caveats. This was a retrospective study, that took adults diagnosed bipolar, and asked when their symptoms first appeared. It's possible that early onset cases were under-sampled, if they were less likely to survive to adulthood, or get treated. The generally milder bipolar II might also be different from the bipolar I studied here. But in general, these numbers support the traditional view that childhood bipolar is just not very prevalent.Baldessarini, R., Tondo, L., Vázquez, G., Undurraga, J., Bolzani, L., Yildiz, A., Khalsa, H., Lai, M., Lepri, B., Lolich, M., Maffei, P., Salvatore, P., Faedda, G., Vieta, E., and; Tohen, M. (2012). Age at onset versus family history and clinical outcomes in 1,665 international bipolar-I disorder patients World Psychiatry, 11 (1), 40-46 DOI: 10.1016/j.wpsyc.2012.01.006... Read more »
Baldessarini, R., Tondo, L., Vázquez, G., Undurraga, J., Bolzani, L., Yildiz, A., Khalsa, H., Lai, M., Lepri, B., Lolich, M.... (2012) Age at onset versus family history and clinical outcomes in 1,665 international bipolar-I disorder patients. World Psychiatry, 11(1), 40-46. DOI: 10.1016/j.wpsyc.2012.01.006
by Neuroskeptic in Neuroskeptic
Whether we think of ourselves as "depressed" or "anxious" depends on what we think about other people's emotional lives, rather than our own, according to an important paper just published: Am I Abnormal? Relative Rank and Social Norm Effects in Judgments of Anxiety and Depression Symptom SeverityThe work appears in the obscure Journal of Behavioural Decision Making, which is downright criminal. It deserves to be in the British Journal of Psychiatry ... and it's not often I think that about a paper.In the first experiment, the authors quizzed people how many days per month they felt “depressed, sad, blue, tearful” or had “excessive anxiety about a number of events or activities.” They then asked them a series of questions designed to work out how they thought other people would answer than question. So they could work out where each individual thought they ranked within the general population, in terms of depression or anxiety symptoms.Take a look. The top panel shows someone who felt depressed on 5 days a month, but believed this put him in the most depressed 70% of people. The second person felt depressed twice as often, but she thought she was below average. They found that perceived rank was strongly correlated with whether people thought they "had depression" or "had anxiety" - much more strongly than actual frequency of symptoms. "Having depression" meant "being more depressed than other people".That's just a correlation and doesn't prove causation, but in the second experiment, they randomly assigned people to get different versions of a survey which manipulated perceived rank, and they confirmed that rank was indeed associated with how "disabling" they felt a given level of symptoms would be.Now, this is just common sense, in a way. Of course whether you think of yourself as abnormal will depend on what you think of as normal - that's what "abnormal" means. We understand ourselves in the context of other people.But this common sense is maybe not so common nowadays; you can read a hundred papers about the chemistry, genetics or causes of "depression" without a consideration of what "depression" (i.e. "abnormal" as opposed to "normal" mood) is.The implications are big. Here's my main concern. Right now a lot of people think that promoting the idea that mental illness is very common is a good idea. Their stated goal is that by 'normalizing' mental illness, we'll destigmatize it. This will both help the mentally ill to cope, and encourage people to talk about their own mental health and get help.All very nice. I've accused such campaigns of being based on dodgy stats, but this paper suggests that such campaigns could end up having exactly the opposite effect from that intended - they could lead to under-diagnosis, and increased stigma.Suppose being depressed or anxious becomes seen as more 'normal'. According to these data, this will make people who are depressed or anxious less likely to seek help, for any given level of symptoms. Change people's perceptions of other people, and you'll change how they see themselves.Worse, normalizing distress could - paradoxically - make those who do seek help seem more abnormal. Think about it: if depression and anxiety are normal, surely only an abnormal person would need special help to deal with them. It's a small step from this to the idea that mental illness is mere personal weakness, laziness, attention-seeking, or scrounging. 'What's your problem? Everyone feels down or worried sometimes... most of us just deal with it.' If everyone is mentally ill, then no-one is really mentally ill... so the "mentally ill" must have something else wrong with them. Not very nice.I'm not sure if this has happened, or will ever happen, but it's something to think about.Melrose, K., Brown, G., and Wood, A. (2012). Am I Abnormal? Relative Rank and Social Norm Effects in Judgments of Anxiety and Depression Symptom Severity Journal of Behavioral Decision Making DOI: 10.1002/bdm.1754... Read more »
Melrose, K., Brown, G., & Wood, A. (2012) Am I Abnormal? Relative Rank and Social Norm Effects in Judgments of Anxiety and Depression Symptom Severity. Journal of Behavioral Decision Making. DOI: 10.1002/bdm.1754
by Neuroskeptic in Neuroskeptic
Many fMRI studies could be giving false-positive results according to an important new paper from Anders Eklund and colleagues: Does parametric fMRI analysis with SPM yield valid results?—An empirical study of 1484 rest datasets.The authors examined the SPM8 software package, probably the most popular tool for analyzing neuroimaging data.Their approach was beautifully simple. They wanted to check how often conventional analysis of fMRI would "find" a signal when there wasn't really anything happening. So they took data from nearly 1,500 people who were scanned when they were just resting, and saw what would happen if you looked for "task related" activations in those scans, even though there was in fact no task. It's a very clever use of the resting state data.Eklund et al ran the analysis many thousands of times, under various different conditions. This is the key finding:This shows the proportion of analyses which produced significant "activations" associated with various different "tasks". In theory, the false positive rate should be way down at the bottom at 5% in each case. That's the error rate they told SPM8 to provide. As you can see, it was often much higher. Oh dear.The error rate depended on two main things. Most important was the task design. Block designs were much worse than event-related designs (see the labels at the bottom: B1,2,3,4 are block, E1,2,3,4 are event.) The longer the blocks, the more errors. B4, the most error-ridden design of all, corresponds to 30 second blocks.That's bad news because that's a very common design.Secondly, the repeat time (TR) mattered, especially for block designs. The TR is how long it takes to scan the whole brain once. The longer the TR, the better, the data showed: 1 second TRs are really dodgy. Luckily, they are rarely used. 2 seconds is OK for most event-related designs, but block designs really suffer. 3 seconds is even better.Because most fMRI studies today use 2-3 second TRs, this is somewhat reassuring, but for block design B4 the error rate was still up to 30% even with TR=3. Oh dear, oh dear.So what went wrong? It's complicated, and you should read the paper, but in a nutshell the problem is that fMRI data analysis assumes that there are only two sources of data: the real brain activation signal, and white noise. The key assumption is that it's white noise, which essentially means that it is random at any moment in time: knowing about what the noise did in the past tells you nothing about what it will do in the future. "Random" noise that's actually correlated with itself over time is not white noise.Now noise in the brain is certainly not white, for various reasons, including the effects of breathing and heart rate (which of course are cyclical, not random.) All fMRI analysis packages try to correct for this - but Eklund et al have shown that SPM8's approach doesn't manage to do that, at least for many designs.What about rival fMRI software like FSL or BrainVoyager? We don't know. They use different approaches to noise modelling, which might mean they do better, but maybe not.And the really big question: does this mean we can't trust published SPM8 results? Does SPM stand for Spurious Positive Mapping? Well, that's also not clear. All of Eklund et al's analyses were based on single subject data. But most fMRI studies pool the results from more like 20 or 30 subjects. Averaging over many subjects might make the false positives cancel out, but we don't yet know if that would solve the problem or only lessen it.Eklund, A., Andersson, M., Josephson, C., Johannesson, M., and Knutsson, H. (2012). Does parametric fMRI analysis with SPM yield valid results?—An empirical study of 1484 rest datasets NeuroImage DOI: 10.1016/j.neuroimage.2012.03.093... Read more »
Eklund, A., Andersson, M., Josephson, C., Johannesson, M., & Knutsson, H. (2012) Does parametric fMRI analysis with SPM yield valid results?—An empirical study of 1484 rest datasets. NeuroImage. DOI: 10.1016/j.neuroimage.2012.03.093
by Neuroskeptic in Neuroskeptic
The concept of "autism" is widely believed to have been first proposed by Leo Kanner in his 1943 article, Autistic Disturbances Of Affective Contact.But did Kanner steal the idea? That's the question raised in a provocative paper by Nick Chown: ‘History and First Descriptions’ of Autism: A response to Michael Fitzgerald. The piece stems from a debate between Chown and Irish autism expert Michael Fitzgerald, who first made the accusation in a book chapter.On the evidence presented, I don't think there's good reason to believe that Kanner did "steal" autism, and Chown doesn't seem convinced either. But there's an interesting story here anyway.Fitzgerald says that in 1938, Hans Asperger - of Asperger's Syndrome fame - gave a series of lectures in Vienna. These were published in a Vienna journal called Wiener Klinischen Wochenzeitschrift as an article called "Das psychisch abnorme kind" ("The mentally abnormal child").In this article, Asperger put forward the concept of autism. The term was coined by Eugen Bleuler in 1911 in reference to symptoms seen in 'schizophrenia' (he came up with that word too), but that was nothing to do with children.In 1943, Kanner published his landmark paper, in which he did not mention Asperger. Asperger published his first major description of 'autistic psychopathy' in 1944. The big question, then, is - had Kanner read or heard of Asperger's ideas before 1943?Asperger was working in Austria while Kanner, although Austrian-born, was in the USA. WW2 would have made it impossible for them to have communicated directly - however, word of Asperger's ideas could have reached Kanner via one of the many European doctors who fled to America, over that period.There is however no direct evidence that this happened. Fitzgerald makes much of the fact that Kanner opened his 1943 paper by saying "Since 1938, there have come to our attention a number of children..." This could be a reference to Asperger's 1938 work - but Kanner said it referred to his first "diagnosis" of autism, Donald T.This leaves us with a fluke: two Austrian-born psychiatrists independently discovered the syndrome we now call childhood autism, decided to borrow Bleuler's term "autism" for it, made their first observations in 1938 and first published properly in 1943-1944.Personally, I think that while that is a remarkable coincidence, such things are not uncommon in science. I see no reason to think that Kanner plagiarized Asperger, although it remains possible. If someone were to discover a copy of Asperger's 1938 article tucked away in one of Kanner's old notebooks, then I'd change my mind, but not before...Chown, N. (2012). ‘History and First Descriptions’ of Autism: A response to Michael Fitzgerald Journal of Autism and Developmental Disorders DOI: 10.1007/s10803-012-1529-5... Read more »
Chown, N. (2012) ‘History and First Descriptions’ of Autism: A response to Michael Fitzgerald. Journal of Autism and Developmental Disorders. DOI: 10.1007/s10803-012-1529-5
by Neuroskeptic in Neuroskeptic
There's little evidence that antidepressants are useful in reducing repetitive behaviors in autism - but there is evidence of bias in the published literature. That's according to Carrasco, Volkmar and Bloch in an important report just out in Pediatrics: Pharmacologic Treatment of Repetitive Behaviors in Autism Spectrum Disorders: Evidence of Publication BiasThey looked at all of the published trials examining whether antidepressant drugs (mostly SSRIs, like Prozac) were better than placebo in reducing repetetive behaviours in children or adults with an autism spectrum disorder (ASD).A meta-analysis showed that there was a statistically significant benefit of the drugs overall, but it was marginal, with a small effect size d=0.22, and it was driven mainly by two old, very small studies that found big benefits. One of them only had 12 subjects. By far the largest study, King et al (2009) with 149 people, showed zero effect.This plot shows all of the studies, with the red line being no benefit of drug vs placebo. The further to the right of the line, the bigger the benefit, but the grey horizontal lines show the uncertainty. As you can see, two small, messy studies found big effects, the others didn't.Worse yet, although there were 5 published studies, the authors also found that there had been 5 studies that had been completed, but never published. Carrasco, Volkmar and Bloch wrote to the people in charge of those studies and asked for data; only one out of 5 replied. The data showed no benefit.We don't know what the other 4 unpublished studies found, but the way science works means they probably came out negative. If we assume that they did, then even the small benefit seen in the published studies disappears.This paper, incidentally, is great example of why trial registration is a great thing. Without mandatory pre-registration on clinicaltrials.gov, no-one would know about the 6 unpublished trials at all. It would have been even better if the researchers had been forced to make public the results, as well as the existence, of the unpublished trials; but it's a lot better than nothing.Finally, the authors of this paper stress that this doesn't mean antidepressants don't help at all in autism - just that they probably don't help with repetitive behaviors.Carrasco, M., Volkmar, F., and Bloch, M. (2012). Pharmacologic Treatment of Repetitive Behaviors in Autism Spectrum Disorders: Evidence of Publication Bias Pediatrics, 129 (5) DOI: 10.1542/peds.2011-3285... Read more »
Carrasco, M., Volkmar, F., & Bloch, M. (2012) Pharmacologic Treatment of Repetitive Behaviors in Autism Spectrum Disorders: Evidence of Publication Bias. Pediatrics, 129(5). DOI: 10.1542/peds.2011-3285
by Neuroskeptic in Neuroskeptic
A fun little study from 2008 looked at rates of self-reported mental illness in mental health professionals: Psychologists' And Social Workers' Self-Descriptions Using DSM-IV PsychopathologyThe authors did an anonymous survey of clinical psychologists and social workers in Israel. They found thatThe sample of 128 professionals included 63 psychologists and 65 social workers. The presence of Axis I traits (i.e. mental illness) was reported by 81.2%, the three most frequent traits being mood, obsessive-compulsive disorder, and eating disorder. Axis II traits (personality disorders) were reported by 73.4% of subjects, the three most frequent conditions being narcissistic, avoidant, and obsessive-compulsive personality traits.Take a look:There were few differences between the two professions although for what it's worth, social workers were more likely to report psychosis and substance abuse problems, while clinical psychologists were more narcisstic, with a full 40% of them admitting to having narcisstic traits. On that note the authors (perhaps unwisely) comment:While speculative, it may be suggested that narcissistic traits include some important factors in motivating individuals to choose to enter the mental health care profession. In a psychotherapeutic relationship, the ability to influence and understand another person's psyche may include features of "narcissistic gratification".Ouch!The problem with all this, though, is that it's not clear what reporting "DSM-IV psychopathology" means; people rated their symptoms on a 5 point scale where 1 = "no evidence of the disorder" and 5 is "greatest severity". Most of the reported symptoms were low in severity, but we don't know what "low" is relative to.If you said that your narcissism was rated "2" out of 5, you might just mean that you have some narcissistic traits sometimes. That's how I'd interpret the question, anyway.But in that case, what exactly are you saying? Not much. You're not saying you're very narcissistic. You're not saying you're more narcissistic than average: you might well think that most other people would also score a "2", or even higher. You're not actually saying "I am narcissistic" at all, just admitting that you're not wholly un-narcissistic... and who of us can really say that?The same goes for all the questions. I think this study would have been much more interesting if they'd just asked people whether, in their clinical judgement, they meet criteria for the disorder. Or whether, if they had to assess a patient who was just like them, what would they diagnose them with? Because criteria are what professionals use on their patients, not 5 point scales.Nachshoni, T., Abramovitch, Y., Lerner, V., Assael-Amir, M., Kotler, M., and Strous, R. (2008). Psychologists' And Social Workers' Self-Descriptions Using DSM-IV Psychopathology Psychological Reports, 103 (1), 173-188 DOI: 10.2466/pr0.103.1.173-188... Read more »
Nachshoni, T., Abramovitch, Y., Lerner, V., Assael-Amir, M., Kotler, M., & Strous, R. (2008) Psychologists' And Social Workers' Self-Descriptions Using Dsm-Iv Psychopathology . Psychological Reports, 103(1), 173-188. DOI: 10.2466/pr0.103.1.173-188
by Neuroskeptic in Neuroskeptic
Do people from different cultures express emotions differently?A new paper says yes: Facial expressions of emotion are not culturally universal. But as far as I can see the data show that at least some of them very much are universal.First some background. The authors, Rachael Jack and colleagues of Glasgow, have published before on this theme. Back in 2009 I blogged about one of their previous papers, which showed that East Asians were less accurate than Westerners at categorizing certain emotions.But although there were cultural differences in ability to classify some emotions, East Asians still did much better than just guessing. To me, this said that there are fundamental universal emotional expressions, albeit culture can subtly modify them.That's my verdict on this study as well.The authors adopted a new (and very clever) method this time. Rather than just showing people photos of actors posing expressions, and asking subjects to label them with an emotion, they generated virtual faces using a 3D modelling software, and made the faces display "expressions", with their 41 virtual facial muscle groups.Subjects (either white Westerners, or recent East Asian immigrants) saw 4,800 random assortments and had to label each one; the authors could therefore work back to calculate their "mental model" of that emotion based on the set of facial movements that best fit, individually (it reminds me of this method).What happened? The Westerners mental models clustered into the classic 6 "basic emotions" of happy, sad, disgust, fear, anger, and surprise. The Asians however didn't; although they were pretty much the same on happy and sad, they were less clear about the other 4.But how much less? Take a look:Cluster analysis and dissimilarity matrices of the Caucasian and Asian models of facial expressions. In each panel, vertical color coded bars show the k means (k = 6) cluster membership of each model. Each 41-dimensional model (n = 180 per culture) corresponds to the emotion category labelled above (30 models per emotion). The underlying grayscale dissimilarity matrices represent the Euclidean distances between each pair of models, used as inputs to k-means clustering. Note that, in the Caucasian group, the lighter squares along the diagonal indicate higher model similarity within each of the six emotion categories compared with the East Asian models. Correspondingly, k-means cluster analysis shows that the Western Caucasian models form six emotionally homogenous clusters... In contrast, the Asian models show considerable model dissimilarity within each emotion category and overlap between categories.This shows that yes, Asians "confused" some emotions more than Westerners but the basic emotional distinctions seemed to be intact, with Happy and Sad especially solid.And look at these examples of the "mental model" for one subject of each group: yes they're different, but not very.These are fine results, and I think there are real questions over whether the Ekman 6 emotions model really captures the essence of human emotions (especially negative ones.)But, especially in the context of previous work from the same authors, I don't think these data really justify the paper's title ("Facial expressions of emotion are not culturally universal"), or the statement thatOur data directly show that across cultures, emotions are expressed using culture-specific facial signals. Although some basic facial expressions such as fear and disgust originally served as an adaptive function... facial expression signals have since evolved and diversified to serve the primary role of emotion communication during social interaction. As a result, these once biologically hardwired and universal signals have been molded by the diverse social ideologies and practices of the cultural groups who use them for social communication.Overall, (ahem) I'm happy to admit that these data show some surprising cultural differences, but I'm afraid that the authors' overblown rhetoric makes me disgusted, sad and angry.Jack, R., Garrod, O., Yu, H., Caldara, R., & Schyns, P. (2012). Facial expressions of emotion are not culturally universal Proceedings of the National Academy of Sciences DOI: 10.1073/pnas.1200155109... Read more »
Jack, R., Garrod, O., Yu, H., Caldara, R., & Schyns, P. (2012) Facial expressions of emotion are not culturally universal. Proceedings of the National Academy of Sciences. DOI: 10.1073/pnas.1200155109
by Neuroskeptic in Neuroskeptic
Can we prevent psychosis? In a major study just published, Early detection and intervention evaluation for people at risk of psychosis, 288 young British adults who were deemed to be 'at risk of psychosis' were randomized to get cognitive therapy (CT) or a control condition. The hope was that it could prevent transition to serious psychotic illness.The primary outcome measure was how many of them later went on to get diagnosed with full-blown psychosis. 2 years later, 7% of the CT group and 9% of the controls had, so that's no significant benefit of treatment. CT slightly reduced the level of mild psychotic-like symptoms, but not how much distress they caused.So, in other words, no we can't prevent psychosis, not with CT alone at any rate. But there's lots more interesting stuff here... Now a transition rate of some 8% over 2 years is lower than in previous studies and might suggest that the concept of the 'psychosis risk syndrome' or 'at-risk mental state' (under consideration for inclusion in DSM-5) is a bit dodgy. The venerable Prof. Allen Frances thinks so. But he misses the fact that the rate was 18% when you also count the people who went psychotic during the baseline assessments (to be fair to Frances, the authors buried that bombshell quite deep in the Discussion).Still, that's still 82% false positives. Is that too high?We can't tell, from a study like this. As in any disease screening program, we need to know the relative costs and benefits of true and false 'hits', as well as the percentages of them.Here's some food for thought on that note. One of the key tenets of the CT model of psychosis is that 'psychotic' symptoms are a more or less normal response to stress, and that psychosis is maintained by a cycle of thoughts and feelings in which these experiences are themselves a source of concern, because they're felt to be abnormal, pathological, or otherwise threatening, thus leading to more stress, and more symptoms, and hence more concern... and so on. CT aims to break that cycle.Check it out (image from here, coauthored by Graham Dunn, senior author of the present work.)If you accept that, then it seems that literally the worst possible thing you could say to someone in the 'at risk mental state' is "Watch out! You're at risk of going psychotic!" According to CT, exactly that line of thinking is the root of the whole problem.The authors of this paper indeed write that "Key ingredients of the approach [include] a focus on normalising psychotic-like experience". But who deemed them abnormal in the first place? The patient, all by themselves... or some well-meaning professional? It's not clear.We are told that the patients were "seeking help for symptoms", but why? Of their own accord, or after someone else raised concerns? 45 people were referred to the study but excluded because they said that they didn't want help. So there was at least some degree of professional 'railroading', driven by the idea that people with such symptoms ought to seek help If you accept the CT account of psychosis, then I'd say you ought to think very seriously about whether this whole thing isn't equivalent to giving everyone an X-ray to detect cancers. The X-rays might end up causing more tumours than they find.I wonder if the authors of this study considered this.Anyway. Keith Laws of LawsNeuroBlog has a good post about the study and the rather overexcited way it's been received in the press (even, er, the BMJ...)Despite the authors not being able to make any claims about CT positively affecting transition rates... and the lack of any medication analysis (in fact all patients were unmedicated as an entry requirement) they conclude: "On the basis of low transition rates, high responsiveness to simple interventions such as monitoring, a specific effect of cognitive therapy on the severity of psychotic symptoms, and the toxicity associated with antipsychotic drugs, we would suggest that antipsychotics are not delivered as a first line treatment to people meeting the criteria for being in an at risk mental state" So the article in the UK Guardian entitled Drugs not best option for people at risk of psychosis, study warns is not simply misunderstanding by a journalist, but what looks like author spinning.... The BMJ press release itself is headlined Cognitive therapy helps reduce severity of distress among psychotic patients - even though the paper (and the press release itself!) clearly states: "Cognitive therapy did not significantly affect distress related to these psychotic experiences...nor levels of depression, social anxiety, or satisfaction with life..."Morrison, A., French, P., Stewart, S., Birchwood, M., Fowler, D., Gumley, A., Jones, P., Bentall, R., Lewis, S., Murray, G., Patterson, P., Brunet, K., Conroy, J., Parker, S., Reilly, T., Byrne, R., Davies, L., and Dunn, G. (2012). Early detection and inte... Read more »
Morrison, A., French, P., Stewart, S., Birchwood, M., Fowler, D., Gumley, A., Jones, P., Bentall, R., Lewis, S., Murray, G.... (2012) Early detection and intervention evaluation for people at risk of psychosis: multisite randomised controlled trial. BMJ, 344(apr05 1). DOI: 10.1136/bmj.e2233
by Neuroskeptic in Neuroskeptic
In 1997, American artist Katherine Sherwood was 44 when she suffered a major stroke. She writes about her experience and how it changed her work in a fascinating article just out, How a Cerebral Hemorrhage Altered My ArtAll of the images below are examples of her work, taken from the paper.Sherwood writes that she had long been interested in the brain. She incorporated neuroscience themes into her work even before the stroke. Here's a 1990 piece: Then, out of the blue, her life was changed:The next May I experienced a cerebral hemorrhage affecting the parietal lobe of the dominant hemisphere [i.e. the left side of the brain, which controls the right side of the body]. I lost my ability to walk, talk, read, and think as my right side became paralyzed within the course of 2 min. It happened during a graduate student’s critique... I do not recall saying this but one of my colleagues reported that the last thing I said was “Oh no, not again.” I was referring to the death of my father at age 33 from an aneurysm. This was when my life caught up to my art...Six months later after my brain had absorbed my spilled blood I had a cerebral angiogram. Relieved that it was over and the possible second stroke had not occurred, I sat up on the gurney and looked at the computer screen in the corner of the room. The images of the arterial system of my brain both stunned and reminded me of the Southern Song Dynasty Chinese landscape paintings that I had deeply admired. I immediately said without thinking, “I need those images.” The room broke out in laughter which I still do not understand. I repeated, “No, I am an artist and I really need those images.”Sherwood never regained the use of her right hand. She had previously relied on her right hand to pain with, and she was forced to learn to use her left, and this led to changes in her style.To compensate for the loss of fine dexterity from using her off hand, she started to paint on larger canvasses, using different materials and a "freer" approach.As a neuroscientist, the main question at the back of my mind reading this was, did damage to her left parietal lobe have a "direct" effect on her mind and personality which altered her artistic process, beyond making her use her left hand etc? Sherwood writes that she's just not sure: [some writers] proposed that my new success came from changes in my brain, particularly in the disruption of “the interpreter.” My artist friends vehemently disagreed with this assessment, preferring to believe it had something to do with the 20-years of painting I had done before my cerebral hemorrhage and my ample time to paint while I was recovering. I leave it up to mystery, a category that drives my doctors crazy. Link: On a slightly different note see the Neurocritic's Suffering For Art Is Still Suffering Sherwood, K. (2012). How a Cerebral Hemorrhage Altered My Art Frontiers in Human Neuroscience, 6 DOI: 10.3389/fnhum.2012.00055... Read more »
Sherwood, K. (2012) How a Cerebral Hemorrhage Altered My Art. Frontiers in Human Neuroscience. DOI: 10.3389/fnhum.2012.00055
by Neuroskeptic in Neuroskeptic
Are personality tests any more accurate than astrology?A lovely study I just came across examined this question: Science Versus the Stars. The researchers took 52 college students and got them to complete a standard NEO personality questionnaire. They also had to state the date, time and place of their birth.Three weeks later, the participants were then given two personality summaries - one based on the personality tests, and one on their astrological chart generated with a computer program.The trick was that everyone also got a pair of bogus summaries, one of each kind. These were simply someone else's results, picked at random from the other 51 volunteers. They weren't told which were the fakes and which were real - they had to work it out, based on which one matched them best.The results showed that the subjects were no better than guessing when trying to tell which of the two astrology charts was theirs. They were able to pick their own personality scores better than chance, although only 80% of them got it right, and guesswork gets you to 50% - so this is not all that impressive. Psychology beat astrology, but hardly by a landslide.This study is a modern update of Shawn Carlson's classic 1985 Nature paper, A double-blind test of astrology. In Carlson's experiment, though, people weren't even able to accurately pick out their own personality scores.When asked to say which of the four reports was the best match overall match to their personality, 55% of the participants picked their own real personality one - but no fewer than 35% preferred one of the astrology charts, and 10% went for someone else's personality scores. Hmm.The authors say the present results represent less of an endorsement of psychological measures than a further indictment of astrology. but I think it's interesting that even under very favorable conditions (only one fake personality test), people were well short of perfect accuracy at spotting their own psychological scores - which they had themselves produced by filling out a questionnaire, just weeks before. Whether that tells us more about the NEO test, the participants' memory, or the fact that all the students at Conneticut College are pretty much the same, I'll leave it for you to judge...Wyman, A., and Vyse, S. (2008). Science Versus the Stars: A Double-Blind Test of the Validity of the NEO Five-Factor Inventory and Computer-Generated Astrological Natal Charts The Journal of General Psychology, 135 (3), 287-300 DOI: 10.3200/GENP.135.3.287-300... Read more »
Wyman, A., & Vyse, S. (2008) Science Versus the Stars: A Double-Blind Test of the Validity of the NEO Five-Factor Inventory and Computer-Generated Astrological Natal Charts. The Journal of General Psychology, 135(3), 287-300. DOI: 10.3200/GENP.135.3.287-300
by Neuroskeptic in Neuroskeptic
Evolutionary psychologist Satoshi Kanazawa has never been far from controversy. When he's not having his blog cancelled for saying black women are unattractive, he's arguing that some nations just aren't smart enough to be monogamous.Given which, his latest work, saying that gay people are smarter on average, is probably his most politically correct paper in years, strange as that may sound.In three large population surveys (USA's AddHealth and GSS, UK's NCDS), Kanazawa found a small positive correlation between estimated IQ and self-reported homosexual behaviour or identity. Now I'm not sure what to make of this. He controlled for confounds such as race, religion and political orientation (and those correlations are interesting in themselves), but you can never measure and correct for everything in a study like this.Kanazawa interprets all this in terms of the Savanna hypothesis, essentially the idea that intelligence allows us to transcend our evolutionary programming (according to which we ought to all be straight, amongst many other things) -The Savanna-IQ Interaction Hypothesis (Kanazawa, 2010a), implies that the human brain’s difficulty with evolutionarily novel stimuli may interact with general intelligence, such that more intelligent individuals have less difficulty with [evolutionarily novel] stimuli than less intelligent individuals...Evolutionarily novel entities that more intelligent individuals are better able to comprehend and deal with may include ideas and lifestyles that form the basis of their preferences and values; it would be difficult for individuals to prefer or value something that they cannot truly comprehend...However, it could be that in America and the UK today, smarter people tend to end up in the kind of social circles where being gay is (for whatever reason) more acceptable.The main problem with this is that the effects are very small. For example, in the AddHealth study, IQ in childhood was correlated with later adult sexual identity with a coefficent of 0.013... but the association of homosexuality with political attitude (liberalism) of 0.613, 60 times as high.The Savanna hypothesis is all very well, but does it predict such small effects? Isn't there a point where very weak evidence in favor of a theory actually becomes evidence against it...? Kanazawa, S. (2012). Intelligence and Homosexuality Journal of Biosocial Science, 1-29 DOI: 10.1017/S0021932011000769... Read more »
KANAZAWA, S. (2012) INTELLIGENCE AND HOMOSEXUALITY. Journal of Biosocial Science, 1-29. DOI: 10.1017/S0021932011000769
by Neuroskeptic in Neuroskeptic
An interesting report in (believe it or not) Medical Hypotheses - Alternating gender incongruity: A new neuropsychiatric syndrome providing insight into the dynamic plasticity of brain-sex. Bigender individuals report alternating between male, female, and (sometimes) mixed gender states. Case and Ramachandran - that's V.S. Ramachandran of phantom limb fame - write:Under the transgender umbrella, a distinct subset of "Bigender" individuals report blending or alternating gender states. It came to our attention that many (perhaps most) bigender individuals experience involuntary alternation between male and female states, or between male, female, and additional androgynous or othergendered identities ("Multigender")...But almost no-one's studied the bigender phenomenon - A survey of the transgender community by the San FranciscoDepartment of Public Health found that about 3% of genetic malesand 8% of genetically female transgendered individuals identifiedas bigender. To our knowledge, however, no scientific literature has attempted to explain or even describe bigenderism; a search ofPsychInfo and PubMed databases returned zero results... the study of this condition could proveilluminating to scientific understanding of gender, body representation,and the nature of self.No scholarly paper would be complete without some elaborate new jargon, of course -For the purposes of our research we are calling this condition "alternating gender incongruity" (AGI). We seek to establish AGI as a nosological entity based in an understanding of dynamic brain representations of gender and sex.So they designed a survey (details in the paper) and sent it to members of a bigender internet forum. The forum had 600 members, although many were lurkers; they got a total of 39 replies. So it's a highly self-selected sample, then, but that's inevitable I think. Here's what they had to say -Of the 32 alternating bigender respondents included [some were excluded for diagnoses of DID etc], 11 were anatomically female (identified as female at birth)... One respondent identified as intersex, but only for reasons of androgynous facial appearance...10/32 respondents agreed that their gender switches were "predictable." The period of gender switches was highly variable, ranging from multiple times per day to several times per year. A majority (23/32) of respondents, however, reported that their gender switched at least weekly [with 14 saying it switched at least once per day]. What are the switches like? Some respondents are quoted -"I still have the same values and beliefs, but a change in gender is really a change in the filter through which I interact with the world and through which it interacts with me.""My voice usually ends up being higher than other times, I’ll be more emotional, my views on things like politics tend not to change, but how I react to certain things does. Like if I’m in male mode and I see someone crying I’ll think more along the lines of, 'Man up...' while if I’m in girl mode I’ll think more along the lines of ‘Oh sweety!’"This being Ramachandran, the paper also touches on left handedness, brain hemispheres, phantom genitals and more, but it's fair to say that all this is pretty speculative -In myth, art, and tradition throughout the world the left side of the body (and hand) – and therefore the right hemisphere – is regarded as more "feminine" – intuitive and artistic. One wonders therefore whether gender alternation may reflect alternation of control of the two hemispheres. Such alternation is seen to a limited extent even in normal individuals but may be exaggerated (and more directly involve the gender aspect) in AGI...Personally, what I find most interesting about this is the question of what would have happened to 'bigender' people before the term 'bigender' came along; it seems to be newer, and certainly less widely used, than 'transgender'/'transsexual'.Would they have been identified as transgender? Maybe... but maybe not. Would they have had any label at all?Case, L., and Ramachandran, V. (2012). Alternating gender incongruity: A new neuropsychiatric syndrome providing insight into the dynamic plasticity of brain-sex Medical Hypotheses, 78 (5), 626-631 DOI: 10.1016/j.mehy.2012.01.041... Read more »
Case, L., & Ramachandran, V. (2012) Alternating gender incongruity: A new neuropsychiatric syndrome providing insight into the dynamic plasticity of brain-sex. Medical Hypotheses, 78(5), 626-631. DOI: 10.1016/j.mehy.2012.01.041
by Neuroskeptic in Neuroskeptic
Do you wish you were smarter? Are you often baffled by puzzles?According to Australian neuroscientists Chi and Snyder, all you need is a bit of electric assistance: Brain stimulation enables the solution of an inherently difficult problem.In their study, 22 volunteers were faced with the 9 dots problem, a notoriously difficult puzzle. The goal here is to draw exactly four straight lines connecting all nine of these dots, without retracing any line, or lifting your pen from the page.Can you do it? If not, don't worry; not many people can. None of Chi and Snyder's 22 subjects did it in the 3 minutes before the stimulation was turned on.But 5 of the 11 volunteers later managed to do it, after 5 minutes of transcranial direct current stimulation (tDCS), a simple form of neurostimulation in which a weak electric current is passed through the head via electrodes attached to either side. The "L− R+" current was designed to boost the right temporal lobe while inhibiting the left, on the hypothesis that the right side of the brain helps us "think outside the box" (literally.)None of the 11 volunteers in the placebo control group succeeded. They were given tDCS but after 30 seconds, it was gradually turned off; this is intended to produce the same tingling sensations as real tDCS, but without affecting the brain. That's statistically significant (p=0.018, one tail fisher’s exact test), although the numbers are small.The authors also refer to other unpublished data:We would like to emphasize the robustness of our finding. The finding that tDCS enabled more than 40% of participants to solve the ‘unsolvable’ nine-dot problem is consistent with our pilot study (see Section 2), which shows that whereas no one solved the nine-dot problem in the sham stimulation condition, 3 out of 7 participants in the L−R+ stimulation condition did so after stimulation. It is also strongly supported by subsequent studies where we, for curiosity, included the nine-dot problem at the end of an unrelated experiment. In fact, of all the data we have ever collected by 2 different experimenters over eight months, we found that 0 out of 29 participants in the sham stimulation condition solved the nine-dots problem, whereas 14 out of 33 participants (naïve to the problem) in the L−R+ stimulation condition did so. The probability that by chance 14 out of 33 participants solved the problem is less than 1 in a billion, according to analysis using binominal distribution (assuming that the expected solution rate without stimulation is 5%).Hmm. When these guys published similar tDCS results with a different puzzle last year, not everyone was convinced. Critics said that 'Thinking caps' are pseudoscience masquerading as neuroscience:Chi and Snyder's participants solved maths puzzles that the researchers claim required "insight", yet crucially the subjects did not perform any other tasks to show that only puzzles requiring "insight" were influenced by the brain stimulation... Rather than encouraging novel thinking, maybe brain stimulation made participants less cautious in reaching a decision, or maybe it helped them recall a similar problem seen a few minutes earlier, or maybe it made them temporarily less distractable (or even dulled their hearing), or maybe it boosted general alertness.The point is that without appropriate experimental controls, the results are virtually meaningless...Personally I don't think this is all that concerning because the 9 dots problem is really hard and I find it implausible that general alertness would help much; in this study, Chi and Snyder did give people a mental arithmetic task as well to try to control for such non-specific effects. Everyone did it three times - before,... Read more »
Chi, R., & Snyder, A. (2012) Brain stimulation enables the solution of an inherently difficult problem. Neuroscience Letters. DOI: 10.1016/j.neulet.2012.03.012
by Neuroskeptic in Neuroskeptic
I've just come across a striking example of why correcting for confounding variables in statistics might not sound exciting, but can be a matter of life and death.Imagine you're a doctor or researcher working with HIV/AIDS. You're taking a sample of blood from a HIV+ patient when you slip and, to your horror, jab yourself with a bloodied needle.What do you do?In a 1997 study, researchers Cardo et al studied hundreds of cases of this kind of accidental HIV exposure ("needlestick injuries") in medical and scientific workers. They wanted to find differences between the people who contracted the virus, and the ones who didn't.One factor they considered was post-exposure prophylaxis - taking HIV drugs as soon as possible after a suspected exposure. Now these drugs were still pretty new in 1997, and it wasn't clear how well they prevented infection, as opposed to just delaying symptoms. Many people with needlestick injuries were offered a course of drugs - but did they work?Cardo et al's raw data found no significant benefitBy univariate analysis, there was no significant difference between case patients and controls in the use of zidovudine [AZT, the first HIV drug] after exposure.But it turned out that this was due to confounding variables. When they corrected for other factors...Infected case patients were significantly less likely to have taken zidovudine than uninfected controls (odds ratio 0.19, P=0.003). This is a classic example of confounding, since the adjusted odds ratio differed from the crude odds ratio (0.7) because zidovudine use was more likely among both case patients and controls after exposure characterized by one or more of the four risk factors in the model.So while people who took zidovudine were just as likely to catch HIV than ones who didn't, they were also more severely exposed to the virus i.e. by being exposed to a greater quantity of blood, or a deeper wound. People were more likely to decide to take it after severe exposures. Zidovudine actually dramatically reduced the risk.Post-exposure prophylaxis has since become standard procedure and it has undoubtedly saved many lives since. Without statistical correction, it might have taken longer for people to see the benefits.In summary, I guess what I'm saying is, remember to correct for confounds - or die.Cardo DM, Culver DH, Ciesielski CA, Srivastava PU, Marcus R, Abiteboul D, Heptonstall J, Ippolito G, Lot F, McKibben PS, and Bell DM (1997). A case-control study of HIV seroconversion in health care workers after percutaneous exposure. Centers for Disease Control and Prevention Needlestick Surveillance Group. The New England journal of medicine, 337 (21), 1485-90 PMID: 9366579... Read more »
Cardo DM, Culver DH, Ciesielski CA, Srivastava PU, Marcus R, Abiteboul D, Heptonstall J, Ippolito G, Lot F, McKibben PS.... (1997) A case-control study of HIV seroconversion in health care workers after percutaneous exposure. Centers for Disease Control and Prevention Needlestick Surveillance Group. The New England journal of medicine, 337(21), 1485-90. PMID: 9366579
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