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  • August 29, 2014
  • 03:52 AM

Oxytocin and autism: the hype?

by Paul Whiteley in Questioning Answers

Consider some excerpts from two recent papers looking at oxytocin (OXT) - the "love hormone"(!) - and the autism spectrum disorders (ASDs)...“It’s not the years, honey. It’s the mileage”"These findings indicate that dysregulated OXT biology is not uniquely associated with ASD social phenotypes as widely theorized, but instead variation in OXT biology contributes to important individual differences in human social functioning, including the severe social impairments which characterize ASD" according to Karen Parker and colleagues [1]. Some media accompanying this paper can be found here.and"Participants who received oxytocin showed no benefit following treatment on primary or secondary outcomes" according to the findings reported by Adam Guastella and colleagues [2].For those who have followed the autism research scene over the years, you'll know that discussions about some connection between the neuropeptide oxytocin and autism have figured quite prominently. Indeed, I've covered OXT and autism before on this blog (see here). Media headlines like the one from the BBC suggesting that the "Love hormone 'helps autistic brain'" have been quite a regular feature, building up OXT to almost Saintly proportions. Unfortunately, as has often been the case with autism (sorry, the autisms) the science has not exactly followed the hype. Take for example the paper by Dadds and colleagues [3] who, prior to Guastella et al, reported that: "Compared to placebo, intranasal oxytocin did not significantly improve emotion recognition, social interaction skills, or general behavioral adjustment in male youths with autism spectrum disorders".I'm not saying that all the research on OXT and autism is bunk because that's obviously not true [4]. As per the meta-analysis by Preti and colleagues [5] there may, for example, be some merit in continuing looking at where and when OXT use might be indicated including that related to important comorbidity [6]. The route of administration - intranasal (via the nose) - is for me, also a really interesting drug delivery method which may be applicable to many, many different medicines indicated for autism or peripheral symptoms/conditions.But what the Parker and Guastella studies do tell us, is that once again, grand over-arching theories of autism seemingly serve no-one well. The study by Bedford and colleagues [7] perhaps said it best with their data arguing: "against cognitive theories of ASD which propose that a single underlying factor has cascading effects across early development leading to an ASD outcome". Replace cognitive theories with biological ones and science seems to be getting a little closer to what looks like the real nature of the autisms, heterogeneity, comorbidity and all... Oh, and then there is some interesting data on how oxytocin might be affecting the "second brain" (gastrointestinal function) as well as the grey-pinkish matter [8]. Move over melatonin (see here)?Music to close and I'm happy to be stuck with you... (stick with the video, the music does eventually kick in).----------[1] Parker KJ. et al. Plasma oxytocin concentrations and OXTR polymorphisms predict social impairments in children with and without autism spectrum disorder. PNAS. 2014. August 4.[2] Guastella AJ. et al. The effects of a course of intranasal oxytocin on social behaviors in youth diagnosed with autism spectrum disorders: a randomized controlled trial. J Child Psychol Psychiatry. 2014 August 2.[3] Dadds MR. et al. Nasal oxytocin for social deficits in childhood autism: a randomized controlled trial. J Autism Dev Disord. 2014 Mar;44(3):521-31.[4] LoParo D. & Waldman ID. The oxytocin receptor gene (OXTR) is associated with autism spectrum disorder: a meta-analysis. Mol Psychiatry. 2014 August 5.[5] Preti A. et al. Oxytocin and autism: a systematic review of randomized controlled trials. J Child Adolesc Psychopharmacol. 2014 Mar;24(2):54-68.[6] Hall SS. et al. Effects of intranasal oxytocin on social anxiety in males with fragile X syndrome. Psychoneuroendocrinology. 2012 Apr;37(4):509-18.[7] Bedford R. et al. Additive effects of social and non-social attention during infancy relate to later autism spectrum disorder. Dev Sci. 2014 Jul;17(4):612-20.[8] Welch MG. et al. Oxytocin regulates gastrointestinal motility, inflammation, macromolecular permeability, and mucosal maintenance in mice. Am J Physiol Gastrointest Liver Physiol. 2014 Aug 21. pii: ajpgi.00176.2014.----------Parker, K., Garner, J., Libove, R., Hyde, S., Hornbeak, K., Carson, D., Liao, C., Phillips, J., Hallmayer, J., & Hardan, A. (2014). Plasma oxytocin concentrations and OXTR polymorphisms predict social impairments in children with and without autism spectrum disorder Proceedings of the National Academy of Sciences DOI: 10.1073/pnas.1402236111... Read more »

Parker, K., Garner, J., Libove, R., Hyde, S., Hornbeak, K., Carson, D., Liao, C., Phillips, J., Hallmayer, J., & Hardan, A. (2014) Plasma oxytocin concentrations and OXTR polymorphisms predict social impairments in children with and without autism spectrum disorder. Proceedings of the National Academy of Sciences. DOI: 10.1073/pnas.1402236111  

Guastella AJ, Gray KM, Rinehart NJ, Alvares GA, Tonge BJ, Hickie IB, Keating CM, Cacciotti-Saija C, & Einfeld SL. (2014) The effects of a course of intranasal oxytocin on social behaviors in youth diagnosed with autism spectrum disorders: a randomized controlled trial. Journal of child psychology and psychiatry, and allied disciplines. PMID: 25087908  

  • August 28, 2014
  • 07:56 AM

Feminism Not Funny? Women In American Sitcoms

by Nura Rutten in United Academics

Compared to the beginning of the sitcom-area, in the 1950′s/1960′s, the roles of women and men sometimes seem to be reversed. However, in every sitcom, the woman who wants to be funny has only two options.... Read more »

  • August 28, 2014
  • 04:29 AM

Minocycline for schizophrenia?

by Paul Whiteley in Questioning Answers

"Minocycline may improve the psychopathology of schizophrenia, especially the negative symptoms, and seems to be well tolerated".A Bachelors Drawer (apparently) @ Wikipedia That was the finding from the systematic review and meta-analysis undertaken by Oya and colleagues [1] looking at the collected literature on the use of "minocycline augmentation therapy in patients with schizophrenia receiving antipsychotic agents". Augmentation therapy by the way, refers to the addition of minocycline to existing pharmacotherapy for schizophrenia.I wasn't all that surprised to read the Oya paper given that for some time now, there have been scientific rumblings about how antibiotics might do quite a bit more than just 'killing bacteria' [2]. "Scientists shocked" was how one media report has previously talked about this area of research; which conjures up all-manner of visions of stunned science-types walking around with lab coats on and mouths and eyes wide open in amazement.The reports that minocycline might act on the negative symptoms of schizophrenia (see here) is also quite an important detail, because these are often the symptoms which affect daily living skills, potentially manifesting as "losing interest and motivation in life and activities, including relationships and sex... [and a] lack of concentration, not wanting to leave the house and changes in sleeping patterns". These are also the symptoms which tend to respond less well to traditional management strategies like medication.The final question(s) are how and why does minocycline affect cases of schizophrenia? The paper from Zhang and Zhao [3] (open-access) provides quite a good overview of the various hypotheses put forward. Unsurprisingly, some effect on inflammation figures quite strongly in the suggestions put forward. I could go on and on and on about the various research in this area (see here for example) but won't on this occasion. Instead, I'll direct you to a previous post I wrote on minocycline and Fragile X syndrome (see here) which mentions some effect from minocycline on matrix metalloproteinase-9 (MMP-9). I'd like to think that this is a potentially important point because of the tie-in with something like homocysteine (see here), the big H, which has also been mentioned with schizophrenia in mind (see here). Just speculatin' of course.Music to close. Frank Sinatra and something about a lot of coffee in Brazil?----------[1] Oya K. et al. Efficacy and tolerability of minocycline augmentation therapy in schizophrenia: a systematic review and meta-analysis of randomized controlled trials. Hum Psychopharmacol. 2014 Aug 4.[2] Levkovitz Y. et al. A double-blind, randomized study of minocycline for the treatment of negative and cognitive symptoms in early-phase schizophrenia. J Clin Psychiatry. 2010 Feb;71(2):138-49.[3] Zhang L. & Zhao J. Profile of minocycline and its potential in the treatment of schizophrenia. Neuropsychiatr Dis Treat. 2014 Jun 17;10:1103-11.----------Oya K, Kishi T, & Iwata N (2014). Efficacy and tolerability of minocycline augmentation therapy in schizophrenia: a systematic review and meta-analysis of randomized controlled trials. Human psychopharmacology PMID: 25087702... Read more »

  • August 27, 2014
  • 07:35 PM

(False?) Positive Psychology Meets Genomics

by Neuroskeptic in Neuroskeptic_Discover

Academic bunfight ahoy! A new paper from Nick Brown – famed debunker of the “Positivity Ratio” – and his colleagues, takes aim at another piece of research on feel-good emotions. The target is a 2013 paper published in PNAS from positive psychology leader Barbara Fredrickson and colleagues: A functional genomic perspective on human well-being. The […]The post (False?) Positive Psychology Meets Genomics appeared first on Neuroskeptic.... Read more »

Brown, N., MacDonald, D., Samanta, M., Friedman, H., & Coyne, J. (2014) A critical reanalysis of the relationship between genomics and well-being. Proceedings of the National Academy of Sciences. DOI: 10.1073/pnas.1407057111  

  • August 27, 2014
  • 09:45 AM

Is it really possible for someone to turn into THE HULK? Don’t make me angry.

by Bill Sullivan in The 'Scope

Could epigenetics provide a bit of a biological explanation behind THE HULK?... Read more »

  • August 27, 2014
  • 07:02 AM

Just how diverse is this group, really?

by Doug Keene in The Jury Room

We often make assumptions when discussing diversity that we all perceive a group’s diversity in the same way. Today’s research shows that simply isn’t so. That is, you and I (depending on our racial in-group) can look at the same group and you might say it is diverse while I say it is not. What […]

Related posts:
Improving working relationships in your ethnically diverse jury
Religion, ethnicity and Asian-American’s voting patterns
Proof we don’t hire the most qualified candidate!

... Read more »

  • August 27, 2014
  • 05:33 AM

Gaming Against Depression: It Can Really Help

by Katja Keuchenius in United Academics

A meta-analysis of 19 different studies of game-based interventions shows encouraging results. And besides the big amount of games for youngsters, the researchers specifically point out much can be done with with therapeutic gaming for older adults.... Read more »

  • August 27, 2014
  • 03:56 AM

Prenatal SSRI exposure and autistic traits

by Paul Whiteley in Questioning Answers

A quote to start today's post: "Our results suggest an association between prenatal SSRI exposure and autistic traits in children". That was a primary finding reported by Hanan El Marroun and colleagues [1] who looked at whether maternal depressive symptoms or a class of quite commonly used pharmaceutics - the selective serotonin reuptake inhibitors (SSRIs) - used to manage depressive symptoms, during pregnancy might impact on offspring development."Everything the light touches is our kingdom" Before progressing through some of the details around this area, I'm going to also direct your attention to a couple of important accompanying commentaries on the Marroun findings from Jones & McDonald [2] and Petersen and colleagues [3] (open-access). Both caution about reading too much too soon into the reported association between SSRIs and offspring outcomes, and the very real outcomes that can come about if psychiatric issues such as depression are not properly managed. Something I think most people might have heard about recently.A few details about the Marroun paper might be useful:Following some previous discussions correlating maternal SSRI use during pregnancy and offspring outcome with autism in mind (see here) including the quite recent papers by Harrington and colleagues [4] and Rai and colleagues [5], the authors looked to "prospectively determine whether intra-uterine SSRI exposure is associated with childhood autistic symptoms in a population-based study". "A total of 376 children prenatally exposed to maternal depressive symptoms (no SSRI exposure), 69 children prenatally exposed to SSRIs and 5531 unexposed children were included" for study. The commentary from Petersen et al notes how small a group were actually exposed to SSRIs and how "these numbers rapidly dwindled when it came to the measurement of the outcome".The Child Behavior Checklist and Social Responsiveness Scale (SRS) were used to assess "pervasive developmental and affective problems" and "autistic traits" respectively. Results: aside from an association between prenatal selective serotonin reuptake inhibitor (SSRI) exposure and autistic traits in children, researchers also reported that: "Prenatal exposure to maternal depressive symptoms without SSRIs was related to both pervasive developmental (odds ratio (OR) = 1.44, 95% CI 1.07-1.93) and affective problems (OR = 1.44, 95% CI 1.15-1.81)". The suggested link between maternal depressive symptoms and autistic traits was to some degree weaker than the SSRI exposure correlation.The authors conclude that: "Long-term drug safety trials are needed before evidence-based recommendations are possible" as once again I'll direct you to the Jones and Petersen commentaries.In the same way that the emerging data on prenatal valproate exposure *might* link into offspring outcome including the presence of autism (see here), so the Marroun paper potentially adds another medicine to the list. I would perhaps temper that last sentence by adding that the valproate story is perhaps a little further along in terms of rodent models of prenatal valproate exposure mimicking some features of autism (see here) and the data providing something like mechanisms to be looked at with further investigations in mind [6]. Still, the CDC Treating for Two initiative might be once again relevant.The added complication with the SSRI-autism correlation is the discussion about maternal depressive symptoms also potentially mediating any link with offspring autism or autistic traits. The paper by Sørensen and colleagues [7] (open-access here) kinda hinted that this and other important confounding factors might impact on any studies of association, including details like: "paternal antidepressant use during the time of pregnancy was not associated with an increased risk of autism spectrum disorders, except for a 30% increase when the fathers took SSRI". Even more recently Clements and colleagues [8] talked about how maternal "major depression" confounded any medication relationship with offspring presentation. They also talked about a link with ADHD which brings me back to yesterday's post on comorbidity (see here)...One would do well not to discount such confounding factors at this stage. Indeed, if one assumes that depression might have a physiological link to something like inflammation for example [9] we then start to arrive at the increasingly important research looking at maternal inflammation as being a risk factor for offspring autism (see here). And before you ask, yes, C-reactive protein (CRP) has been linked to depressive symptoms as per the meta-analysis by Valkanova and colleagues [10].The Marroun results are interesting and add something to an increasing bank of peer-reviewed literature [11] suggestive of a possible link between SSRI use during pregnancy and offspring outcomes. On the basis of the current existing literature and with my blogging caveat of no medical advice given or intended, I would be minded to conclude that there is quite a bit more experimental investigation to be done on this category of medicines. But I don't yet think there is enough clear evidence to conclusively put an elevated risk of offspring autism on the list of potential side-effects of these medicines.Music then. Scissor Sisters and Laura.----------[1] Marroun HE. et al. Prenatal exposure to selective serotonin reuptake inhibitors and social responsiveness symptoms of autism: population-based study of young children. The British Journal of Psychiatry. 2014; 205: 95-102.[2] Jones I. & McDonald L. Living with uncertainty: antidepressants and pregnancy. The British Journal of Psychiatry. 2014; 205: 103-104.[3] Petersen I. et al. Prenatal exposure to selective serotonin reuptake inhibitors and autistic symptoms in young children: another red herring? The British Journal of Psychiatry. 2014; 205: 105-106.[4] Harrington RA. et al. Prenatal SSRI Use and Offspring With Autism Spectrum Disorder or Developmental Delay. Pediatrics. 2014 Apr 14.[5] Rai D. et al. Parental depression, maternal antidepressant use during pregnancy, and risk of autism spectrum disorders: population base... Read more »

  • August 26, 2014
  • 05:17 AM

Drinking small amounts of alcohol boosts people's sense of smell

by BPS Research Digest in BPS Research Digest

As our modern world relies overwhelmingly on sight and sound to transmit information, it might not strike you quite how acute our sense of smell is. In fact we humans can outperform the most sensitive measuring instruments in detecting certain odours, and distinguish smells from strangers from those of our blood relations. Now new research suggests our natural olfactory talents may be even greater when we use modest amounts of alcohol to reduce our inhibitions.A team led by Yaara Endevelt-Shapira tested participants on two days: on one, tests took place before and after drinking a cup of grape juice, and on the other day, before and after a drink containing a dose of alcohol (vodka). Even though the alcohol dose was based on a single measure (35ml) adjusted for the participants’ weight, differences in how people’s bodies process alcohol meant that breathalyser measures of Blood Alcohol Content (BAC) varied from as low as 0.01 to as high as 0.1 across participants.A smell-detection experiment involved participants indicating which of three jars of oil contained a highly diluted scent. Higher BAC did not influence performance, but when a dose of alcohol produced a low BAC (below .06), participants were able to identify more highly diluted scents than they could on their no-booze day.In a second experiment, participants sniffed three scents and tried to tell which one differed from the other (identical) two. High BAC made this discrimination task harder, but again, low BAC had a facilitative effect, making it easier to determine the odd smell out. This task was also replicated in a field experiment, pulling people aside at a bar to test their discrimination for trios of scratch-and-sniff stickers: those punters who had already had a drink (all had a low BAC) performed significantly better than those who had not.Taken together the findings suggest that low alcohol doses improve smelling ability, but why does it have this effect? We can’t yet be certain, however the study offers some clues that it has to do with removing people’s inhibition.First, smell detection was worse for candidates who scored highly on an aspect of motivation called “baseline inhibitory state”, which refers to a person’s tendency to avoid or prevent negative outcomes (it was measured with items such as "I worry about making mistakes"). Participants who were inclined to hold back in this way were poorer at detecting smells.Second, alcohol-fuelled improvement in smell discrimination correlated with how much participants’ performance dropped on the Stroop task when under the influence. This classic task involves inhibiting the meaning of a colour word in order to complete the challenge of naming the ink colour that the word is printed in. Smell discrimination improved more for participants who displayed weaker inhibitory powers on the Stroop.The authors explained that the prefrontal cortex has inhibitory connections to the olfactory cortex, our smell centre. And cases exist where frontal brain injury has led to near-immediate improvements in olfactory ability. This evidence signature presents a reasonable case that we are constantly suppressing a superior sense of smell, but that this inhibition can be reduced by various means…including a drop of the hard stuff._________________________________ Endevelt-Shapira, Y., Shushan, S., Roth, Y., & Sobel, N. (2014). Disinhibition of olfaction: Human olfactory performance improves following low levels of alcohol Behavioural Brain Research, 272, 66-74 DOI: 10.1016/j.bbr.2014.06.024 Post written by Alex Fradera (@alexfradera) for the BPS Research Digest.

... Read more »

  • August 26, 2014
  • 04:39 AM

Brian Hooker's Hooked Hoax: Measles-Mumps-Rubella (MMR) Vaccination and Autism Spectrum Disorder

by Alexis Delanoir in How to Paint Your Panda

10 years after the initial study by DeStefano et al. (2004) was conducted, famous anti-vaccine alarmist Brian Hooker, along with Andrew Wakefield, are talking about a "whistleblower" in the CDC claiming that the original data was fraudulent, and was masking a 336% increased risk in ASD in African American boys receiving the MMR vaccine "on time." Did Hooker prove anything in his new study, however? Only that he doesn't understand epidemiology or statistics.... Read more »

  • August 26, 2014
  • 03:55 AM

76% of youths with autism meet ADHD diagnostic criteria?

by Paul Whiteley in Questioning Answers

Autism is not normally a stand-alone diagnosis. I've mentioned that point a few times on this blog, stressing how a clinical diagnosis of autism appears to increase the risk of various other behavioural, psychiatric and somatic diagnoses also [variably] being present over a lifetime. Part of that comorbidity has been talked about in discussions about ESSENCE (see here) and the excellent document produced by Treating Autism on medical comorbidities occurring alongside autism (see here) for example. Prof. Gillberg's recent scientific publication called 'Autism Plus Versus Autism Pure' [1] kinda adds to this notion and his very strongly worded sentiments: "It is high time that the comorbidities, sometimes even more important than the autism, came back on the diagnostic agenda".Cheeky... @ Wikipedia Outside of the more traditional comorbidities mentioned in the same breath as some autism, such as learning disability (intellectual disability) and epilepsy or seizure-type disorders, quite a lot of attention is being focused on the overlap between autism and attention-deficit hyperactivity disorder (ADHD). Indeed, the paper by Gagan Joshi and colleagues [2] very much thrusts ADHD into the autism diagnostic arena with their assertion of: "A high rate of comorbidity with ADHD was observed in psychiatrically referred youth with ASD [autism spectrum disorder], with a clinical presentation typical of the disorder".The Joshi paper sought to "compare the clinical presentation of ADHD between youth with autism spectrum disorder (ASD) and ADHD and a sample of youth with ADHD only". What they found is something remarkably similar to the typical presentation of ADHD (without autism) insofar as age of onset and "distribution of diagnostic subtypes, the qualitative and quantitative symptom profile, and symptom severity". I might add that their participant group was classified as "High-Functioning" (their words not mine) so one needs to be mindful that only one part of the autism spectrum was surveyed.What is perhaps slightly worrying from the Joshi results was the finding that: "a significant majority of ASD youth with ADHD failed to receive appropriate ADHD treatment". ADHD treatment, as I've mentioned in previous posts, normally implies pharmacotherapy but can also include other intervention options as per discussions on things like dietary changes potentially being useful for some (see here). Indeed, I've talked about the some of the results from things like the use of a gluten- and casein-free (GFCF) diet when applied to autism and how ADHD-type symptoms might be the more important targets for intervention (see here). The idea also that outside of just affecting ADHD symptom profiles, intervention might also have knock-on effects for other areas as per the review by Daley and colleagues [3] is similarly important.I don't want to linger further on this issue aside from reiterating that the presentation of autism is, more often than not, part of a complex tapestry of presentation which can cover various other diagnostic categories. ADHD or sub-threshold ADHD-type symptoms are being realised as fairly frequent companions to a diagnosis of autism. The changes to the diagnostic criteria for ADHD (see here) will no doubt further expand the link between autism and ADHD, placing yet more emphasis on how autism is not normally a stand-alone diagnosis.Music to close. Ray Charles and You Don't Know Me.----------[1] Gillberg C. & Fernell E. Autism Plus Versus Autism Pure. J Autism Dev Disord. 2014 Jun 24.[2] Joshi G. et al. Symptom Profile of ADHD in Youth With High-Functioning Autism Spectrum Disorder: A Comparative Study in Psychiatrically Referred Populations. J Atten Disord. 2014 Aug 1. pii: 1087054714543368.[3] Daley D. et al. Behavioral Interventions in Attention-Deficit/Hyperactivity Disorder: A Meta-Analysis of Randomized Controlled Trials Across Multiple Outcome Domains. J Am Acad Child Adolesc Psychiatry. 2014 Aug;53(8):835-847.e5.----------Joshi G, Faraone SV, Wozniak J, Tarko L, Fried R, Galdo M, Furtak SL, & Biederman J (2014). Symptom Profile of ADHD in Youth With High-Functioning Autism Spectrum Disorder: A Comparative Study in Psychiatrically Referred Populations. Journal of attention disorders PMID: 25085653... Read more »

  • August 25, 2014
  • 12:02 PM

Spoiler Alert!: Are You Wasting Your Time Avoiding Spoilers?

by Melissa Chernick in Science Storiented

Lately I have been cranking though a lot of media – TV, movies, books, podcasts, etc. To the point that I start to wonder how I have time for actual life. During this mass consumption of media, I've been thinking about, and discussing with friends, the topic of spoilers. Bring up this topic with just about anyone and you’ll find that it’s actually a pretty controversial one. As for me, I fall in the no spoilers category. Spoil one of my beloved TV shows and you will go from friend to “friend” just that fast. But I know that there are those out there that don’t mind being spoiled or actually prefer it. That got me to thinking back to a study from few years ago about this topic. The study got quite a bit of attention from the media, specifically applying the findings to film and TV. After doing some searches on Web of Science for similar studies, I can see why. There just aren’t any – to the point that even this older study has only been cited 3 times, and not by other media related studies. So, well, what the heck?In 2011, a short little study published in Psychological Science by Leavitt and Christenfeld asked if spoiling a story decreased peoples’ pleasure in it. The universal element of all types of media is story. When you talk about spoilers you are inherently talking about changing someone’s enjoyment of the story. The study asked 176 males and 643 females (just a little sex biased and not broken down by any other demographics) to take part in three experiments in which they read three different sorts of short stories selected from anthologies: (1) Ironic-twist stories, (2) Mysteries, and (3) Evocative literary stories. For each of the stories, some of the participants’ stories included a spoiler paragraph that summarized the story and gave the outcome. Afterwards, the participants were asked to rate the story for enjoyment on a 10 point scale – a “hedonic rating.” They found that the participants significantly preferred spoiled over unspoiled stories in all categories and reported that the spoiler paragraph was not out of place or jarring.Figure 1 from the study. These are hedonic ratings of the individual spoiled and unspoiled stories.Considering all of the attention this study got when it was published and the applications made to a variety of media, I’m going to throw in a little more personal critique than I do normally. Start out by asking: Are their data wrong? Well, no. But there are some methodologies and assumptions that I questions. First is that they assume that I have the same experience each time I read a story. The authors do focus on that first reading but also state that “people’s ability to reread stories with undiminished pleasure, and to read stories in which the genre strongly implies the ending, suggests that suspense regarding the outcome may not be critical to enjoyment and may even impair pleasure by distracting attention from a story’s relevant details and aesthetic qualities.” As someone who rereads her favorite books over and over again, I say “not so!” Their statement suggests that I did not enjoy the shock of a scene the first time around when in fact I did. You know what I mean: that “holy-crap-did-that-just-happen?!!!” moment. Am I saying that twist is all there is? Of course not, but one of the memorable parts of the first reading - the surprise - would not have been the same without it. Upon rereads, my undiminished pleasure comes from the writing and spending more time in a world with characters that I love (or love to hate).The study’s authors conclude that “people are wasting their time avoiding spoilers,” but go on to say that that their data “do not suggest that authors err by keeping things hidden.” They point out that readers who read stories that open with the outcomes still anticipate additional revelations at the end. To me, this statement suggests that readers still expect twists in the story even though they've just read all of them, that they are waiting for the shock, the twist. A good example might be someone who is seeing a film adaptation of a book they've read; they are looking for the differences in the movie. Considering this, I think would have liked more detail in the methods about how their spoilers were presented. I wonder if a big “Spoiler Alert” warning on that summary paragraph would have made a difference – one that labeled and explained it as something that spoiled everything. Perhaps this would remove this erroneous anticipation? Or what about a before questionnaire that scored anticipation levels? Personally, I am way more upset if someone spoils something I've been looking forward to compared to something I could care less about. What about gauging viewpoints on spoilers by asking a simple question like: Do you read the last chapter of a book first to see what happens?Did I come into this paper with some preconceived notions? Sure, but I seem to have more problems with this study than most. Upon reflection, I think that stems from problems I have with the study's methodology added to the attention it has gotten (it hasn't escaped me that I’m giving it even more with this post). It has been used to justify spoiling a story – a behavior that I typically find to be one of smug superiority. I think it is important to keep in mind that this is a single small study, and one that had I been a reviewer for would have gotten hacked to pieces. I''m a fan of a nice, simple study but I'm not a fan of lack-of-detail, particularly in the methods.But I'm not a psychologist, what do I know? What do you think? Do you love or hate spoilers? How would you have done a study on this topic?Leavitt, J., & Christenfeld, N. (2011). Story Spoilers Don't Spoil Stories Psychological Science, 22 (9), 1152-1154 DOI: 10.1177/0956797611417007Here's some of the media attention this study received and a couple other articles on the topic. Spoiler Alert - some of these contain spoilers.Film School Rejects: "How Bad Do Spoilers Spoil?: A Super Scientific StudySmithsonian: "Are Spoilers Misnamed?"UC San Diego News Release: "Spoiler Alert: Stores Are Not Spoiled by 'Spoilers'"/Film: "Spoilers Are Good For You, Says Study"The Atlantic: "Here's the Twist: Good Films Are Good Even If They've Been 'Spoiled'"io9: "The Cultural Curse of Knowledge and Movie Spoilers"io9: "Why I refuse to watch movies without spoilers"Vulture: "Spoilers: In Defense of the American Watercooler"Vulture: "Spoilers: The Official Vulture Statutes of Limitations" (I like this proposes a stature of limitations on spoilers based on the media type) "Spoiler Alert: A Survival Guide to All Things" (also the source of the image)... Read more »

Leavitt, J., & Christenfeld, N. (2011) Story Spoilers Don't Spoil Stories. Psychological Science, 22(9), 1152-1154. DOI: 10.1177/0956797611417007  

  • August 25, 2014
  • 09:00 AM

Awe and the supernatural

by Katharine Blackwell in Contemplating Cognition

Majestic mountains, vibrant vistas, stunning scenery – and, perhaps, the transformation of a blob of molten glass into a rearing horse – these are sights that can truly be awe-inspiring, generating those feelings of reverence and wonder. They make time seem to slow down. But do they also make it seem more likely that there must be some creator or supernatural being behind it all?... Read more »

Valdesolo P, & Graham J. (2014) Awe, uncertainty, and agency detection. Psychological Science, 25(1), 170-178. PMID: 24247728  

  • August 25, 2014
  • 07:02 AM

Women are easily misled so why not lie to them in negotiations?

by Rita Handrich in The Jury Room

Back in 2012, we wrote about which gender was the more moral in negotiations. (Spoiler alert: it was women.) Now we have a new article on why women get lied to in negotiations. Not when or if–but why. Basically, people believe women are more easily misled than men and people believe women to be less […]

Related posts:
Which is the more moral negotiator? The male or the female?
Negotiating Salary 101 for Women Only
Negotiations: Starting high and ending with nothing

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Kray, LJ, Kennedy, JA, & Van Zant, AB. (2014) Not competent enough to know the difference? Gender stereotypes about women’s ease of being misled predict negotiator deception. . Organizational Behavior and Human Decision Processes. info:/

  • August 25, 2014
  • 04:41 AM

Your angry face makes you look stronger

by BPS Research Digest in BPS Research Digest

No matter where you travel on earth, you'll likely have no problem recognising when someone is angry with you. From the plains of Russia to the beaches of Brazil, anger shows itself in a tell-tale facial display involving lowered brow, snarled nose, raised chin and thinned lips.A popular view has it that, besides reliably conveying anger, this particular constellation of facial movements is arbitrary and serves no other function. A team of evolutionary psychologists led by Aaron Sell disagrees. They think the anger face also makes the angry person look stronger. This fits their "recalibration theory of anger" that sees the emotion as an aggressive threat. An angry animal or person is communicating the costs that they will inflict on others if they do not get what they want. By making an angry person look stronger, so the theory goes, the facial expression gives weight to the threat of aggression, likely influencing the target's judgment about the seriousness of the threat.To test this, Sell and his colleagues created pairs of faces using a computer programme. They began with a 20-year-old male face, morphed from averages of many faces, and then calibrated it so that for each of the seven distinguishing features of anger (lowered brow, raised lips, raised mouth, widened nose, enlarged chin, lips thinned, lips pushed forward), they created a pair of contrasting faces. One face in each pair displayed one angry feature, the other face showed the opposite feature. For example, one face showed lowered brows, the other face in the pair showed raised brows. In this way, the seven distinguishing features of anger were isolated.Thirty-five student participants then looked at the facial pairs and indicated in each case which face they thought looked stronger. The key finding? Each anger-related facial feature when displayed on its own attracted higher ratings of perceived strength. This implies each element of the anger expression contributes to making a person appear stronger.Further experiments ruled out an alternative explanation - perhaps angry faces actually serve to make a person look older, and this leads to ratings of greater strength because observers assume a slightly older man is stronger than a 20-year-old. One way the researchers tested this was to show participants pairs of morphed faces of a 60-year-old man, in which case looking older presumably wouldn't be associated with greater strength. Three of the angry facial features actually led him to being rated as younger, with only two prompting ratings of being older. Moreover, participants rated the man as stronger when he displayed six of the seven angry facial features."The current study is the first systematic test of the individual components of the anger expression," the researchers said. "And in so doing it confirms that these features are improbably well-designed to solve the adaptive problem of bargaining with threats of force." The results are also consistent with a range of other research, including the finding that several features of an angry expression tend to be more prominent in men than women (this fits with the idea that aggression is a more important bargaining tool for men); that stronger and bigger men get angry more easily; and that men's fighting ability can be discerned from the shape of their face. Looking at the study's limitations, it's a shame the researchers didn't investigate women's expressions of anger, and that they relied on student participants._________________________________ Sell, A., Cosmides, L., & Tooby, J. (2014). The human anger face evolved to enhance cues of strength Evolution and Human Behavior, 35 (5), 425-429 DOI: 10.1016/j.evolhumbehav.2014.05.008 Post written by Christian Jarrett (@psych_writer) for the BPS Research Digest.

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Sell, A., Cosmides, L., & Tooby, J. (2014) The human anger face evolved to enhance cues of strength. Evolution and Human Behavior, 35(5), 425-429. DOI: 10.1016/j.evolhumbehav.2014.05.008  

  • August 25, 2014
  • 04:40 AM

mTOR-regulated autophagy and autism mouse models

by Paul Whiteley in Questioning Answers

I was intrigued to read the paper by Guomei Tang and colleagues [1] (open-access) and their assertion that: "mTOR [mammalian target of rapamycin]-regulated autophagy is required for developmental spine pruning, and activation of neuronal autophagy corrects synaptic pathology and social behavior deficits in ASD [autism spectrum disorder] models with hyperactivated mTOR"."Re-verify our range to target... one ping only".If that opening paragraph sounds like scientific gibberish, I'll refer you to one of the many media write-ups of the study (see here) describing how, among other things, researchers looked at brain tissue from the deceased with autism compared with those asymptomatic for autism and counted 'spines' (dendritic spines) - protrusions from a neuron. They reported "increased dendritic spine density with reduced developmental spine pruning in layer V pyramidal neurons in postmortem ASD temporal lobe". This is interpreted as "an oversupply of synapses" in certain parts of the brain and lead to headlines such as: "Scientists discover people with autism have too many brain 'connections'". All of this ties into the debates about brain connectivity in autism [2].The next part of the Tang findings revolve around one of the possible 'whys' for their surplus of synapses findings talking about possible issues with the process of autophagy [3] - a sort of cellular housekeeping. The idea being that there are processes at work which clear out cells which we don't need or that are damaged including synaptic pruning. Here, the authors focused on something called mTOR (which has been previously discussed on this blog) specifically with it's link to autophagy [4]. Based on a mouse model of tuberous sclerosis (see here), a condition associated with autistic-like behaviour [5], researchers reported issues with mTOR activity which seemed to overlap with the findings of synaptic oversupply noted in brain samples from those with autism. Further "the medication rapamycin both restores normal synaptic pruning and reduces autism-like behaviors in a mouse model of autism" according to another commentary on the Tang study.The NHS Choices website has already given the Tang study the once-over (see here) and noted: "this research is in its very early stages. It mainly helps our understanding of the brain changes that may be involved in this condition. It is too soon to say whether it could lead to any treatment for autism spectrum disorders, and even if it does it is likely to be a long way off". I'd echo those sentiments as well as adding a few of my own.First, although no expert on the analysis of neural tissue, I note some more knowledgeable commentators have talked about how careful one has to be when drawing too many conclusions based on postmortem studies (see here). This also means taking into account the effect of any comorbidity that appeared alongside the diagnosis of autism and what role that might play in any results obtained. Second, is the reliance on a mouse model of autism (emphasis on 'mouse model') which, although overlapping with some autistic behaviours and with possibly related findings [6], is not necessarily representative of quite a lot of autism. Tuberous sclerosis for example, does seem to show some kind of relationship with autism [7] but as with other proposed less idiopathic types of autism (see here) one has to be a little bit careful in over-extrapolating any connection. Same goes for when one talks about increased spine density being found in all autism [8]. Finally, rapamycin is not exactly what one might call a desirable medication as a consequence of it's primary use and possible side-effects. I'm not saying that it doesn't have it's uses, just that when applied to real people with autism (not mouse models), the peer-reviewed literature is currently very, very sparse when it comes to efficacy and importantly safety. That being said, there may be other ways to inhibit mTOR [9] bearing in mind my caveat about not giving medical or clinical advice on this blog...Music then. Rather Be...----------[1] Tang G. et al. Loss of mTOR-Dependent Macroautophagy Causes Autistic-like Synaptic Pruning Deficits. Neuron. 2014. August 21.[2] Uddin LQ. et al. Reconceptualizing functional brain connectivity in autism from a developmental perspective. Front Hum Neurosci. 2013 Aug 7;7:458.[3] Glick D. et al. Autophagy: cellular and molecular mechanisms. J Pathol. 2010 May;221(1):3-12.[4] Jung CH. et al. mTOR regulation of autophagy. FEBS Lett. 2010 Apr 2;584(7):1287-95.[5] Reith RM. et al. Loss of Tsc2 in Purkinje cells is associated with autistic-like behavior in a mouse model of tuberous sclerosis complex. Neurobiol Dis. 2013 Mar;51:93-103.[6] Isshiki M. et al. Enhanced synapse remodelling as a common phenotype in mouse models of autism. Nat Commun. 2014 Aug 21;5:4742.[7] Smalley SL. Autism and tuberous sclerosis. J Autism Dev Disord. 1998 Oct;28(5):407-14.[8] Wei H. et al. The therapeutic effect of memantine through the stimulation of synapse formation and dendritic spine maturation in autism and fragile X syndrome. PLoS One. 2012;7(5):e36981.[9] Theoharides TC. et al. Focal brain inflammation and autism. J Neuroinflammation. 2013 Apr 9;10:46.----------... Read more »

Tang, G., Gudsnuk, K., Kuo, S., Cotrina, M., Rosoklija, G., Sosunov, A., Sonders, M., Kanter, E., Castagna, C., Yamamoto, A.... (2014) Loss of mTOR-Dependent Macroautophagy Causes Autistic-like Synaptic Pruning Deficits. Neuron. DOI: 10.1016/j.neuron.2014.07.040  

  • August 25, 2014
  • 02:39 AM

Autobiographical Memory for a Life-Threatening Airline Disaster

by The Neurocritic in The Neurocritic

“My attention shifts to the fact that the comforting engine hum is eerily gone. Where has the comforting hum of the engines gone. Something has gone very, very wrong, the plane continued to shake.” -Daniel Goncalves, recalling the terror of Air Transat Flight 236I'm sitting here in an airport, reading a harrowing first person account of Air Transat Flight 236, which fell out of the sky when it lost all power on Aug. 24, 2001.The plane was bound from Toronto, Ontario to Lisbon, Portugal when a fuel leak in the right engine began 3 hrs and 46 min after takeoff (at 04:38 UTC). The leak went undetected by the flight crew for over an hour, when it finally became apparent that the remaining fuel was insufficient to reach their destination in Lisbon. At 05:45 UTC, the pilot diverted the flight to Lajes Field on Terceira Island in the Azores, a cluster of islands about 850 miles west of Portugal.Image: Humberta Augusto/AP – via The Globe and MailAir Transat Flight 236 with its emergency slides deployed, sitting on the tarmac of Lajes Field in the Azores island of Terceira, after an emergency landing on Friday, Aug, 24, 2001.Here, Mr. Goncalves' gripping narrative should speak for itself.“All lights turn off, TV's off, P.A. system off, emergency lights light up the floors marking the emergency exit door. What the hell is going on? Is this a joke? Another clearly tense voice takes over and tried to address the 300+ passengers without the aid of a P.A. system. "Everyone put on their life vest and prepare for emergency ditching at sea." Huh? What the hell does that mean? Are you kidding me? Disbelief. "The captain has informed us that we are two hours away from Lisbon and we will not make it. We are preparing for an emergency ditch at sea. When you hear BRACE, BRACE, BRACE, lean against the seat in front of you, fold your arms and brace yourself." WHAT WHAT WHAT WHAT????? Oh my God, what is happening. We're going into the cold and black Atlantic? Now? Why? Is this a Joke? Are we part of that Just for Laughs show? Stop playing, come on. No joke. I was in denial. This fully loaded Airbus A330 was going into the ocean and all I knew was that my poor family were there with me. It hit me. This wasn't going to go away. This was it. This really was it. The end. Unimaginable death by catastrophe.”-Daniel Goncalves, My Air Transat flight 236 storyI'm reading this story because of a very unique paper published recently in Clinical Psychological Science (McKinnon et al. 2014), a study of  post-traumatic stress disorder (PTSD) and memory in survivors of the near-fatal Air Transat flight. Fifteen of the individuals WHO WERE ACTUALLY ON THAT FLIGHT participated in an experiment of autobiographical memory for the event, a shared horror of impending death. The comparison events were the terrorist attacks of September 11, 2001 (9/11) and a neutral event from around the same time.1 Seven of the survivors had been diagnosed with PTSD, six did not have PTSD, and the status of the remaining two was unknown. This immediately raises the caveat of very small comparison groups, further complicated by the fact that some of the assessment instruments were missing from various participants (e.g., the NEO-Five Factor Inventory of personality was missing from four).The study was conducted in the lab of Dr. Brian Levine, a well-known memory researcher at the Rotman Research Institute in Toronto. Adding another unexpected twist, the first author of the paper, Dr. Margaret C. McKinnon, was a passenger on Flight AT236!Now I'm flying in an Airbus 319, returning home. The setting sun to my right is blinding across the aisle.Here is the series of events on AT236 as recounted by Goncalves:Timeline: 4:38am-fuel started leaking5:45am- diverted to Lages Air Base in Azores5:48am- emergency declared6:13am- engine no 2 flamed out 217 km from Lages Air Base, full thrust to engine #1 on left wing and plane descended 6,000 feet (this was scary and when when the passengers first found out something was very wrong).6:23am- Mayday declared6:26am- engine no 1 flamed out 120 km from Lages Air Base6:45am- plane touched down hard on runway 33Then a flight attendant came over the PA system on my flight: “Ladies and gentlemen, we are experiencing a little turbulence, please return to your seats and fasten your seat belts.”OK, there's the turbulence, good thing I took an anti-emetic...But the bumpiness was quite short-lived, so back to our main story.Image via ... Read more »

  • August 25, 2014
  • 01:00 AM

Does Nature Influence How We Think?

by Rodney Steadman in Gravity's Pull

Connectedness with nature may influence cognitive styles.... Read more »

Rodney Steadman. (2014) Does Nature Influence How We Think?. Gravity's Pull. info:/

  • August 24, 2014
  • 04:51 PM

How does chronic pain management work? A hypothesis to ponder

by Bronwyn Thompson in Healthskills: Skills for Healthy Living

What DOES change in chronic pain management is people's self efficacy or belief that they CAN do what's important in their lives - by hook or by crook. And even more importantly, they have something to DO that's important to them. Maybe something that hasn't been studied in sufficient detail is what a person wants to be able to do, what's their motivation, what are their valued occupations? That's a hypothesis about therapeutic change I think we need to ponder.... Read more »

  • August 24, 2014
  • 03:06 PM

Correcting the Critics of Nicholas Wade & MAOA

by nooffensebut in The Unsilenced Science

Geneticists are not the leading experts on behavioral genetics, and they and other critics have made numerous errors and misjudgments about Nicholas Wade’s book A Troublesome Inheritance, as well as MAOA or warrior gene research.... Read more »

Bevilacqua L, Doly S, Kaprio J, Yuan Q, Tikkanen R, Paunio T, Zhou Z, Wedenoja J, Maroteaux L, Diaz S.... (2010) A population-specific HTR2B stop codon predisposes to severe impulsivity. Nature, 468(7327), 1061-6. PMID: 21179162  

Cases O, Seif I, Grimsby J, Gaspar P, Chen K, Pournin S, Müller U, Aguet M, Babinet C, & Shih JC. (1995) Aggressive behavior and altered amounts of brain serotonin and norepinephrine in mice lacking MAOA. Science (New York, N.Y.), 268(5218), 1763-6. PMID: 7792602  

Tuinier S, Verhoeven WMA, Scherders MJWT, Fekkes D, & Pepplinkhuizen L. (1995) Neuropsychiatric and biological characteristics of X-linked MAO-A deficiency syndrome. A single case intervention study. New Trends in Experimental and Clinical Psychiatry, 99-107. info:/

Zhu B, Chen C, Moyzis R, Dong Q, Chen C, He Q, Li J, Lei X, & Lin C. (2012) Association between the HTR2B gene and the personality trait of fun seeking. Personality and Individual Differences, 53(8), 1029-1033. DOI: 10.1016/j.paid.2012.07.026  

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