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  • July 31, 2014
  • 08:10 AM
  • 7 views

Tough Talking Apes

by Mark E. Lasbury in The 'Scope

The new Planet of the Apes movie has talking apes! In the old Charleton Heston versions, the apes had thousands of years to evolve speech capabilities, but Dawn of the Planet of the Apes takes place only 10 years after their escape from the lab. Anatomical differences between human and ape hyoid position, rib musculature and tongue show us why speech is not possible for Cesar and his friends. In addition, new research points out the importance of the foxp2 protein for speech and auditory function. ... Read more »

  • July 31, 2014
  • 05:31 AM
  • 14 views

The voices heard by people with schizophrenia are friendlier in India and Africa, than in the US

by Christian Jarrett in BPS Research Digest

When a patient with schizophrenia hears voices in their head, is the experience shaped by the culture they live in? Tanya Luhrmann and her colleagues investigated by interviewing twenty people diagnosed with schizophrenia living in San Mateo, California; twenty in Accra, Ghana; and twenty others in Chennai India. There were similarities across cultures, including descriptions of good and bad voices, but also striking differences.In San Mateo the interviewees talked about their condition as a brain disease, they used psychiatric diagnostic terms to describe themselves, and their experiences were almost overwhelmingly negative. Fourteen described hearing voices that told them to hurt others or themselves. Eight people didn't know the identity of their voices and few described having a personal relationship with their voices.By contrast, in Chennai, the interviewees frequently spoke of their relationships with their voices - that is, they heard the voices of relatives or friends, giving them advice or scolding them. These patients rarely used diagnostic terms, and rarely talked of voices instructing them to commit violence. Instead, distress, when it occurred, usually arose from their voices talking about sex. Nine interviewees described voices that were significantly good - in terms of being playful or entertaining.In Accra, yet another picture emerged. Most of the interviewees here mentioned hearing God. This isn't simply a case of this sample being more religious - the interview groups in all three locations were predominantly religious. Half the interviewees in Accra reported that their voice hearing was mostly or entirely positive. Others frequently emphasised the positive. Use of diagnostic labels was rare, as were incitements to violence by voices.Luhrmann and her team said their most striking finding was that the experiences of voice hearing in the two non-Western samples were less harsh and more "relational" - that is, patients perceived their voices as other people, who could not be controlled. The researchers believe this difference is likely due to Western cultures emphasising independence and individuality - in which case heard voices are experienced as a violation - whereas African and Asian cultures emphasise how each person's mind is interwoven with others. "We believe that these social expectations about minds and persons may shape the voice-hearing experience of those with serious psychotic disorder," the researchers said.These results need to be replicated with larger samples matched more precisely for illness severity, and with more tightly controlled measures (the current study was deliberately qualitative and exploratory). If replicated, the findings would imply the experience of hearing voices in schizophrenia is to some extent malleable, which could have exciting therapeutic implications. Indeed, it's notable that the outcomes for patients with schizophrenia outside the West, especially in India, are known to be more positive - perhaps because of the way patients relate to their voices. "The harsh violent voices so common in the West may not be an inevitable feature of schizophrenia," the researchers said._________________________________Luhrmann, T., Padmavati, R., Tharoor, H., & Osei, A. (2014). Differences in voice-hearing experiences of people with psychosis in the USA, India and Ghana: interview-based study The British Journal of Psychiatry DOI: 10.1192/bjp.bp.113.139048 --further reading--What's it like to hear voices that aren't there?The same voices, heard differently?Psychosis isn't always pathologicalPost written by Christian Jarrett (@psych_writer) for the BPS Research Digest.

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  • July 31, 2014
  • 04:18 AM
  • 10 views

Dipeptidyl peptidase (DPP) IV and autism: supporting opioid-excess?

by Paul Whiteley in Questioning Answers

Serum levels of dipeptidyl peptidase (DPP) IV were found to be lower in children with autism compared to asymptomatic controls according to the study by Shahid Bashira & Laila AL-Ayadhi [1]. Based on analysis by ELISA, researchers concluded that "alterations in the plasma level of DPP IV play a role in the pathophysiology of autism".A sailor went to sea, sea, sea... @ Wikipedia Anyone who has followed the autism research scene for any length of time might have already heard about DPP-IV and autism. The paper by Hunter and colleagues [2] (open-access here) and subsequent response [3] highlights some of the discussions in this area relating to the use of the opioid-excess hypothesis [4] as a means to potentially explain some autism. The idea stemming from some earlier work (see here) being that a defect in the functioning of DPP-IV with regards to its ability to degrade proline-rich proteins such as gliadin (gluten) might account for the build-up of gluten derived opioid peptides suggested as part of the opioid-excess theory. Earlier accounts of issues with DPP-IV in relation to the classic gluten-related autoimmune condition coeliac disease (see here for an overview) kinda set the tone [5] for some analysis with autism in mind. Indeed, at least one trial of enzyme-based therapy has also talked about the potential involvement of DPP-IV in some cases of autism [6].The Bashira paper did not specifically set out to look at the relationship between DPP-IV and dietary elements potentially linked to autism. Instead their focus seemed to be on the involvement of this peptidase in brain physiology and "its possible link to neuroinflammation in autism". DPP-IV has, for example, been discussed with cerebral ischemia in mind as per the results from Röhnert and colleagues [7] although I hasten to add that I am not equating autism and brain ischemia.I personally feel that quite a bit more research effort is needed in the area of DPP-IV. Lower plasma levels of DPP-IV have been noted in cases of other conditions such as depression [8]. The recent results from Simone Peters and colleagues [9] which talked about "Short-term exposure to gluten specifically induced current feelings of depression" in their cohort (see this post) could fit well with the reduction in gluten peptide degrading abilities potentially present as a consequence of something like lower DPP-IV levels. Indeed, one might also speculate that the suggestion of non-coeliac gluten sensitivity (NCGS) may actually reflect involvement of opioid peptides on the basis of such a correlation...I'm also taken back to some work by Vojdani and colleagues [10] which talked about anti-CD26 autoantibodies being present in a "significant percentage of children with autism". CD26, a surface glycoprotein used synonymously with DPP-IV, was suggested to show involvement as a function of "dietary peptides, bacterial toxins and xenobiotics bind[ing] to lymphocyte receptors and/or tissue enzymes, resulting in autoimmune reaction in children with autism". Their follow-up study [11] further added to the literature in this area and how "Dysfunctional membrane peptidases and autoantibody production may result in neuroimmune dysregulation and autoimmunity" in relation to autism. Autoimmunity and autism y'say?As per the cycles of scientific research, where research areas fall in and out of favour, it does appear that there is a resurgence of interest in elements of the opioid-excess theory with a specific focus on the role of food-derived peptides in relation to at least some autism. The Roy review looking at naltrexone for autism (see here) is one element given the opioid antagonistic effects of this pharmaceutic. The Sokolov paper (with its flaws) looking at beta-casomorphin - the opioid peptide derived from the casein protein - in relation to autism is another. The Trivedi paper (see here) on exogenous opioid peptides and DNA methylation levels adds to the research bundle. Dare I even mention the camel milk and autism connection also being made in the research literature too as a function of different milks and different protein/peptide configurations?Music to close. Epic by Faith No More.----------[1] Bashir S. & AL-Ayadhi L. Alterations in plasma dipeptidyl peptidase IV in autism: A pilot study. Neurology, Psychiatry and Brain Research. 2014; 20: 41-44.[2] Hunter LC. et al. Opioid peptides and dipeptidyl peptidase in autism. Dev Med Child Neurol. 2003 Feb;45(2):121-8.[3] Shattock P. et al. Opioid peptides and dipeptidyl peptidase in autism. Dev Med Child Neurol. 2004 May;46(5):357.[4] Shattock P. & Whiteley P. Biochemical aspects in autism spectrum disorders: updating the opioid-excess theory and presenting new opportunities for biomedical intervention. Expert Opin Ther Targets. 2002 Apr;6(2):175-83.[5] Smith MW. & Phillips AD. Abnormal expression of dipeptidylpeptidase IV activity in enterocyte brush-border membranes of children suffering from coeliac disease. Exp Physiol. 1990 Jul;75(4):613-6.[6] Brudnak MA. et al. Enzyme-based therapy for autism spectrum disorders -- is it worth another look? Med Hypotheses. 2002 May;58(5):422-8.[7] Röhnert P. et al. Dipeptidyl peptidase IV, aminopeptidase N and DPIV/APN-like proteases in cerebral ischemia. J Neuroinflammation. 2012 Feb 28;9:44.[8] Maes M. et al. Alterations in plasma dipeptidyl peptidase IV enzyme activity in depression and schizophrenia: effects of antidepressants and antipsychotic drugs. Acta Psychiatr Scand. 1996 Jan;93(1):1-8.[9] Peters SL. et al. Randomised clinical trial: gluten may cause depression in subjects with non-coeliac gluten sensitivity - an exploratory clinical study. Aliment Pharmacol Ther. 2014 May;39(10):1104-12.[10] Vojdani A. et al. Infections, toxic chemicals and dietary peptides binding to lymphocyte receptors and tissue enzymes are major instigators of autoimmunity in autism. Int J Immunopathol Pharmacol. 2003 Sep-Dec;16(3):189-99.[11] Vojdani A. et al. Heat shock protein and gliadin peptide promote development of peptidase antibodies in children with autism and patients with aut... Read more »

  • July 30, 2014
  • 01:31 PM
  • 31 views

Suicide, it might be in the blood

by Gabriel in Lunatic Laboratories

I tried to kill myself, more than once in fact. It was a troubling time for me and as a former active duty Marine that might not be too surprising […]... Read more »

  • July 30, 2014
  • 09:19 AM
  • 27 views

Higher Implicit Self-Esteem Linked to Positive Evaluation of Spouses

by amikulak in Daily Observations

It’s often said that we can’t love others unless we love ourselves.  According to a new study, this may be true, but perhaps in a different way than we expect: […]... Read more »

  • July 30, 2014
  • 08:30 AM
  • 21 views

The Attentive Look of a Dog in Training

by CAPB in Companion Animal Psychology Blog

Researchers investigate the body language of a dog that is performing well in training.Photo: Markus Balint / ShutterstockA new study puts dogs through the first stage of a basic training task and analyzes eye contact and posture in the most successful dogs. The research by Masashi Hasegawa et al (Azabu University School of Veterinary Medicine) is motivated by a desire to improve people’s training abilities by helping them recognize the posture associated with successful learning. One of the neat things about this paper is that the study was done with completely untrained dogs. For obvious reasons, many canine science studies use well-behaved pet dogs of the kind that is calm when taken to a strange location like a university laboratory. While these studies are valuable, not all dogs are well-socialized and it’s important that research considers all kinds of dogs. What better dog for a study of dogs-in-training than one that is totally untrained?!The dogs live at a place called the World Ranch in Osaka, Japan. 46 dogs took part, aged 1 to 6.5 (average 3 years), and a wide mix of breeds. Training was carried out by someone previously unknown to the dogs, in sessions of 5 minutes each that took place in the dogs’ exercise yard. The handler used food to lure the dog into a sit position. He only did this when he had the dog’s attention, but he did it as many times as he could in the 5 minute session. After this, there was a 3 minute rest, followed by a test in which the hand signal was performed on its own (without food) 20 times. Every time the dog sat on request, whether in the training session or the test, it was given a piece of food.Each dog had three sessions like this a day, for three days, to make a total of nine sessions. The sessions were videoed so that the dogs’ body language could be analyzed.The results showed a positive correlation between the number of trials in the training session and the number of correct responses in the tests. In other words, practice makes perfect: the more practice a dog had, the better it performed on the test. In addition, the age of the dog was not linked to the number of correct responses; dogs could learn at any age.The dogs were divided into two groups for further analysis: those that had performed especially well on the tests, and the rest. This meant the body language of dogs that are successfully learning could be compared to those that are performing less well.The high-achieving dogs had their eyes wide open, their mouths closed, their ears forward, and their tails were high but not wagging. Surprisingly, the researchers consider this in terms of dominance, the open eyes being seen as dominant but the other aspects of the posture not. It does not make sense to consider the relationship between dog and trainer as one of dominance; the dog is trying to understand how to earn the treat, and if it hasn’t figured it out yet then it shows a need for the trainer to make it clear.The most interesting finding is that the wide eyes occurred mostly when the dog looked up at the handler’s face, showing that gaze from the dog to the handler is important in training. This is in line with Braem and Mills (2010), who also found a positive association between dogs looking at the handler and their performance in learning. Deldalle and Gaunet (2014) found that dogs trained using positive reinforcement gaze more at their owners during the sit command and when walking on leash than dogs trained using negative reinforcement, demonstrating a better relationship between dog and owner in the R+ group.  This study only looked at the stage of using a lure. Dogs did not progress beyond this, even though they responded to the lure many times. One Papillion had 194 trials! (That must have been a happy dog). Even starting with a completely untrained dog, it is possible to teach ‘sit’ quickly. It would be nice to see the research repeated using an incremental training plan that progresses via hand signal to a verbal command. It's also possible body language will change in response to continued training, and future research could follow dogs as they learn a set of commands. In fact the initial lure, although exactly where you would start, is too difficult for some dogs. When this is the case, it would be more appropriate just to expect their head to follow the lure, without going into a full sit at the beginning.  We should be able to say that any dog training book will explain how to teach your dog the basics, but sadly this is not the case. Some books still recommend the use of unnecessary aversive techniques; if a book suggests hitting your dog, jerking the leash, or doing a so-called ‘alpha’ roll, discard it and choose another book instead! For an excellent example of how to fade the food lure when teaching sit, see this post on fading food lures and adding a verbal cueby Lori Nanan at Your Pit Bull and You. If you’re a keen trainer and want to get into the techie details, you’ll like Train Your Dog Like a Pro by Jean Donaldson. What’s your favourite dog training book and why?ReferenceBraem, M., & Mills, D. (2010). Factors affecting response of dogs to obedience instruction: A field and experimental study Applied Animal Behaviour Science, 125 (1-2), 47-55 DOI: 10.1016/j.applanim.2010.03.004Deldalle, S., & Gaunet, F. (2014). Effects of 2 training methods on stress-related behaviors of the dog (Canis familiaris) and on the dog–owner relationship Journal of Veterinary Behavior: Clinical Applications and Resear... 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  • July 30, 2014
  • 07:02 AM
  • 1 view

We agree and thus, I am certain we shall prevail

by Doug Keene in The Jury Room

The American Bar Association is seeking nominations until August 8, 2014 to help it decide on the Top 100 law blogs (“Blawgs”). We have been in the ABA Top 100 for the past 4 years and would like to make it 5! If you like this blog, please nominate us (it’s fast and free) here. THANKS! […]

Related posts:
“Reactions vary along traditional partisan lines”
I want to be special: The desires of the conservative and the liberal
Politics and prejudice? Nope. It’s about ideology!


... Read more »

  • July 30, 2014
  • 05:35 AM
  • 48 views

When the cuddle hormone turns nasty - oxytocin linked with violent intentions

by Christian Jarrett in BPS Research Digest

For many years, the hormone oxytocin was caricatured as the source of all human goodness - trust, altruism, love, and morality. Among the findings that contributed to this picture were the discovery that sniffing oxytocin increases people's trust and generosity in financial games; that it aids face recognition; and that its release is associated with maternal bonding; and with orgasm.However, the picture has grown a lot more complicated of late, with findings showing that oxytocin has a "dark side" - for example, boosting envy and shadenfreude. Now a team of researchers led by Nathan DeWall has further sullied the reputation of this once idolised molecule. They've demonstrated that for certain people in particular circumstances, exposure to oxytocin might actually lead to increased violence.The researchers split 93 undergraduates (47 men) into two groups - one group sniffed oxytocin, the other group sniffed a salt water solution. The students didn't know whether they'd received the oxytocin or the placebo, and the researchers were also blinded to who'd received what. Next the students completed two tasks designed to make them stressed, including giving a public presentation to an unfriendly audience. Finally, they answered two questions about their tendency to be physically aggressive, and further questions about how likely it was that they'd engage in violence towards a current or former romantic partner based on how they currently felt.Here's the main finding - oxytocin boosted the self-confessed likelihood of being violent towards a partner, specifically in those students who admitted that they have a proclivity for physical aggression. DeWall's team think this fits with an emerging, more nuanced understanding of oxytocin's effects. It remains true that the hormone plays an important role in maintaining human relationships, but this isn't always an innocent function. Previous research shows oxytocin can increase intolerance and aggression towards outsiders. Now we learn that for people who typically resort to aggression to keep hold of their romantic partners, stress plus increased oxytocin nudges them towards violence."Our findings add to the understanding of the 'prickly side of oxytocin'," said DeWall and his team. "Far from being a panacea for all social ills, oxytocin may have a much more diversified effect, as in the current case."_________________________________  DeWall, C., Gillath, O., Pressman, S., Black, L., Bartz, J., Moskovitz, J., & Stetler, D. (2014). When the Love Hormone Leads to Violence: Oxytocin Increases Intimate Partner Violence Inclinations Among High Trait Aggressive People Social Psychological and Personality Science, 5 (6), 691-697 DOI: 10.1177/1948550613516876 --further reading--A social 'Viagra' for shy people?Why do some men insult their partners?Post written by Christian Jarrett (@psych_writer) for the BPS Research Digest.

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  • July 30, 2014
  • 04:52 AM
  • 27 views

Immunological effects from risperidone treatment in autism

by Paul Whiteley in Questioning Answers

The findings from Jai Eun Choi and colleagues [1] suggesting that use of the antipsychotic risperidone may impact on levels of certain cytokines - messenger cells of the immune system - in some cases of autism spectrum disorder (ASD) grabbed my attention recently. I've always been pretty interested in the complexity of the immune system when it comes to something like autism (see here) as well as the various examples of how many of the medications used to 'manage' aspects of autism appear to have quite a few more biological effects over and above those listed on the patient information leaflet. Think melatonin for example, and what a molecular handyperson this pharmaceutic has turned out to be (see here).Could it be magic... @ Wikipedia The Choi paper worked on the assumption that use of risperidone and other antipsychotics have previously been shown to correlate with changes to serum levels of certain cytokines as per examples of work in the area of schizophrenia [2] and here [3]. Some of this research even hinted that part of the reason why antipsychotics might 'work' in some cases of schizophrenia was to do with their potential effect on "the inflammatory-like situation" present [4]. Certainly it's been noted before on this blog how inflammation may very well play some role when it comes to psychiatry (see here) particularly in light of some of the research on the various inflammatory markers (see here) accepting the chicken-and-egg question of what comes first: inflammation or symptoms?Anyhow, based on a small-ish sample (n=45), Choi et al looked at plasma levels of "27 different cytokines" both before risperidone treatment was introduced and after 8 weeks on the drug. Interestingly the words 'responders' and 'nonresponders' were included in the analyses undertaken to look for any changes/trends following antipsychotic use (something which I think more studies should head towards). As it happens, "2 of the 27 plasma cytokines showed statistically significant decreases in median levels" - eotaxin and monocyte chemoattractant protein-1 (MCP-1). Further, when those responders and non-responders were separated out "the median values of interleukin (IL)-5 were significantly higher (p=0.005) in the overall responder group than in nonresponders".Obviously one has to be a little bit guarded about the conclusions reached from this fairly small and fairly short study. Whilst risperidone does have a place in the medicines cabinet for some people with autism (see here), paediatric use (as was the case in the Choi study) is not without risks as per a recent entry on the SFARI website (see here). The guidance from NICE here in the UK (well, England at least) also mentioned how cautious physicians must be when using antipsychotics "for behaviour that challenges" with autism in mind.I was quite interested in the Choi findings particularly that of the elevations in IL-5 in the responder group. I'm no expert on IL-5 but some light reading around the topic (see here) seems to imply that elevations of this cytokine are probably not going to be a great thing from the point of view of their involvement in the activation of eosinophils [5]. I've talked before on this blog about some of the work looking at eosinophils and autism (see here) and some potentially interesting correlations with other research (see here). I'd perhaps like to see more about this correlation in future studies particularly building on other findings in relation to IL-5 and autism [6] (open-access here) including as part of being a risk factor for offspring autism [7] (open-access here).Insofar as the eotaxin and MCP-1 findings, well, again there is probably a lot more work to do on these compounds as a function of their mention in other autism research [8] (open-access here). The paper by Paul Ashwood [9] (who incidentally was an author on the Choi paper) looking at Fragile X syndrome (FXS) with and without autism also caught my eye: "significant differences were observed between the FXS group with autism and the FXS without autism for IL-6, eotaxin, MCP-1" as another avenue for further study.So then... somewhere the drinks are free (or should that be all-inclusive).----------[1] Choi JE. et al. Change in Plasma Cytokine Levels During Risperidone Treatment in Children with Autism. J Child Adolesc Psychopharmacol. 2014 May 14.[2] Zhang XY. et al. Changes in serum interleukin-2, -6, and -8 levels before and during treatment with risperidone and haloperidol: relationship to outcome in schizophrenia. J Clin Psychiatry. 2004 Jul;65(7):940-7.[3] Kim DJ. et al. Effect of risperidone on serum cytokines. Int J Neurosci. 2001;111(1-2):11-9.[4] Cazzullo CL. et al. Cytokine profiles in schizophrenic patients treated with risperidone: a 3-month follow-up study. Prog Neuropsychopharmacol Biol Psychiatry. 2002 Jan;26(1):33-9.[5] Takatsu K. & Nakajima H. IL-5 and eosinophilia. Curr Opin Immunol. 2008 Jun;20(3):288-94.[6] Suzuki K. et al. Plasma cytokine profiles in subjects with high-functioning autism spectrum disorders. PLoS One. 2011;6(5):e20470.[7] Goines PE. et al. Increased midgestational IFN-γ, IL-4 and IL-5 in women bearing a child with autism: A case-control study. Mol Autism. 2011 Aug 2;2:13.[8] Ashwood P. et al. Associations of impaired behaviors with elevated plasma chemokines in autism spectrum disorders. J Neuroimmunol. 2011 Mar;232(1-2):196-9.[... Read more »

Choi JE, Widjaja F, Careaga M, Bent S, Ashwood P, & Hendren RL. (2014) Change in Plasma Cytokine Levels During Risperidone Treatment in Children with Autism. Journal of child and adolescent psychopharmacology. PMID: 24828014  

  • July 29, 2014
  • 01:15 PM
  • 47 views

Can’t Handle the Stress? Blame your Brain

by Gabriel in Lunatic Laboratories

Do you rise to the occasion, or do you fold under the pressure? No matter which side of the fence you’re, you can thank [or blame] your brain. Some people […]... Read more »

  • July 29, 2014
  • 12:32 PM
  • 39 views

Are silly superstitions useful because they are silly?

by neuroecology in Neuroecology

(Attention warning: massive speculation ahead.) Auguries often seem made up, useless. Is that why they are useful? Dove figured that the birds must be serving as some kind of ecological indicator. Perhaps they gravitated toward good soil, or smaller trees, or some other useful characteristic of a swidden site. After all, the Kantu’ had been […]... Read more »

  • July 29, 2014
  • 07:35 AM
  • 38 views

Is Twitter Ruining Our Proper English?

by Katja Keuchenius in United Academics

“Hey al im on my way 2wrk but i totes 4got 2bring ur ipod sori il hav 2 bring it nxt tym ur workin. Hav a nice day xo”
Gives you the cramps? Maybe you should read this article.... Read more »

  • July 29, 2014
  • 07:30 AM
  • 36 views

Is homosexuality "natural"?

by Bill Sullivan in The 'Scope

In the beginning, there was no sex. That’s because in the beginning, there was no Barry White. A playful look at examples of homosexuality in nature.... Read more »

Van Houdenhove E, Gijs L, T'sjoen G, & Enzlin P. (2014) Asexuality: A Multidimensional Approach. Journal of sex research, 1-10. PMID: 24750031  

  • July 29, 2014
  • 05:30 AM
  • 13 views

Remembering together - How long-term couples develop interconnected memory systems

by Christian Jarrett in BPS Research Digest

Although it might seem a good idea to work with other people to remember important information, the evidence suggests that this typically isn't so. Individual recall is most efficient whereas social remembering comes with drawbacks, tripping up our flow and inhibiting memories. But this evidence mostly comes from asking people to collaborate with a stranger. What happens when you know each other really, really well?Celia Harris and colleagues at Macquarie University recently reviewed their previously published and new research on social remembering by long-term intimate couples. Their data showed that on standard tasks, such as reproducing words from studied lists, couples working together often did as well as when they worked alone. This lack of a penalty from social remembering is itself notable, but it's just a gateway into more intriguing findings.During another study, the researchers noticed that although couples did more poorly at listing their shared holidays when recalling together, these social sessions were filled with anecdotes and tangents that weren't generated in the solo sessions. This inspired them to depart from testing memory for lists of words and events, and to explore the amount of rich, in-depth information remembered by couples about experienced events. They found these social exchanges led to clear collaborative memory benefits, which could take three forms:“New information” such as finally snatching an elusive name of a musical thanks to a chain of prompts between the two parties.Richer, more vivid descriptions of events including sensory information.Information from one partner painting things in a new light for the other.Differences between the couples were crucial. Those who structured their approach together and were more prepared to riff off the other's contributions did better than those who were more passive or critical. Richer events were also better remembered by partners who rated their intimacy as higher.The authors note that older adults tend to experience the greatest memory difficulties with first-hand autobiographical information, rather than abstracted facts. This is exactly where the couples gained the biggest benefit from remembering together, as evidenced by performance on the in-depth event recall task and the spontaneously emerging anecdotes. It's possible that as we grow older, we offset the unreliability of our own episodic systems by drawing on the memorial support offered by a trusted partner. This might explain why when one member of an older couple experiences a drop in cognitive function, the other soon follows. Our memory systems are more of a shared resource than we realise._________________________________ Harris, C., Barnier, A., Sutton, J., & Keil, P. (2014). Couples as socially distributed cognitive systems: Remembering in everyday social and material contexts Memory Studies, 7 (3), 285-297 DOI: 10.1177/1750698014530619 Post written by Alex Fradera (@alexfradera) for the BPS Research Digest.

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  • July 29, 2014
  • 04:04 AM
  • 39 views

Ketogenic diet and the valproate mouse model of autism

by Paul Whiteley in Questioning Answers

A brief entry today and yet another blog post that starts with a quote (sorry)... "The offspring exposed to VPA [valproic acid] prenatally demonstrated a significant decrease in the number of play initiations/attacks and this was reversed with the KD [ketogenic diet]".Gloucester Old Spot @ Wikipedia That finding reported in the paper by Ahn and colleagues [1] continues my interest in all-things related to prenatal VPA exposure and the reported effects on some offspring (see here). The added bonus of including some discussion about how the use of a ketogenic diet might reverse some of the effects of VPA exposure (in rats at least) is also worthwhile mentioning.A couple of pointers perhaps...Rats, Sprague-Dawley mother rats, were given VPA or saline (as a control) during pregnancy and their pups (VPA-exposed vs. controls) were subjected to measures looking at "juvenile play behavior" and eventually "mitochondrial bioenergetic analysis" as a function of the use of a ketogenic or standard diet.Results: "Prenatal VPA exposure also disrupted the pattern of play responses". Not a great surprise there given everything else that has been linked to VPA exposure in-utero. But.. use of the ketogenic diet "was able to modify complex social behaviors and mitochondrial respiration". As noted previously, the reduction in play initiations made by the VPA exposed mice was to some degree rescued following use of the ketogenic diet.Yes, I know that this was a study of rats, and whilst useful, rats are rats not humans. But I am nevertheless intrigued by the suggestion that something like a ketogenic diet - more typically indicated for some types of treatment resistant epilepsy - might to some degree, affect the behaviour and physiology of animals exposed to a traditional anticonvulsant like valproate during the nine months that made them. Does anyone else find that a little ironic? Also throw in mention of the words 'autism spectrum disorder' alongside that animal VPA exposure model alongside the ketogenic diet (see here) and I'm sure there's some more research to be done in this area.Mode of action? I dunno. I will draw your attention to some interesting work on carnitine homoeostasis as a function of valproate administration [2] which might be relevant. Carnitine plays a role in mitochondrial function [3] and there is some suggestion that a ketogenic diet might help maintain carnitine levels in the presence of VPA [4]. Whether this applies to brain structures or neurochemistry potentially already affected by prenatal exposure to VPA is a question not yet asked or answered. Bearing in mind the gastrointestinal (GI) effects also noted in VPA exposure models (see here) I might also be inclined to 'look to the bowels' in terms of any potential effects from the ketogenic diet in that organ too.Music to close and I was taken aback by the performance from Pumeza at the opening to the 2014 Commonwealth Games and her version of Freedom Come All Ye...----------[1] Ahn Y. et al. The Ketogenic Diet Modifies Social and Metabolic Alterations Identified in the Prenatal Valproic Acid Model of Autism Spectrum Disorder. Dev Neurosci. 2014 Jul 8.[2] Morand R. et al. Effect of short- and long-term treatment with valproate on carnitine homeostasis in humans. Ther Drug Monit. 2012 Aug;34(4):406-14.[3] Zammit VA. et al. Carnitine, mitochondrial function and therapy. Adv Drug Deliv Rev. 2009 Nov 30;61(14):1353-62.[4] Coppola G. et al. Plasma free carnitine in epilepsy children, adolescents and young adults treated with old and new antiepileptic drugs with or without ketogenic diet. Brain Dev. 2006 Jul;28(6):358-65.----------Ahn Y, Narous M, Tobias R, Rho JM, & Mychasiuk R (2014). The Ketogenic Diet Modifies Social and Metabolic Alterations Identified in the Prenatal Valproic Acid Model of Autism Spectrum Disorder. Developmental neuroscience PMID: 25011527... Read more »

  • July 28, 2014
  • 07:55 PM
  • 49 views

Attention Deficit Hyperactivity Disorder & Eating Disorders: Is There a Link?

by Tetyana in Science of Eating Disorders


Attention deficit hyperactivity disorder (ADHD), characterized by inattention, hyperactivity, and impulsivity, is a common childhood disorder. ADHD can often persist into adolescence and adulthood. The prevalence of ADHD is thought to be between 6-7% among children and adolescents and ~5% among adults (Willcutt, 2012).
Increasingly, evidence from multiple studies has pointed to comorbidity between ADHD and eating disorders (EDs). For example, one study found that young females with ADHD were 5.6 times more likely to develop clinical (i.e., diagnosable according to DSM-5) or subthreshold (i.e., sub-clinical) bulimia nervosa (BN) (Biederman et al., 2007). Another study found that found that 21% of female inpatients at an ED unit had six or more ADHD symptoms (Yates et al., 2009).
However, most previous studies are limited by the fact that they assessed comorbidity between ADHD and EDs among patients. This limits our ability to generalize these findings to community samples, where many may experience symptoms of the disorders at subthreshold levels. Moreover, most studies focused on bingeing/purging behaviours and did not investigate differences between ADHD subtypes.
In the current study, Jennifer Bleck …

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  • July 28, 2014
  • 09:05 AM
  • 72 views

The mistakes that lead therapists to infer psychotherapy was effective, when it wasn't

by Christian Jarrett in BPS Research Digest

How well can psychotherapists and their clients judge from personal experience whether therapy has been effective? Not well at all, according to a paper by Scott Lilienfeld and his colleagues. The fear is that this can lead to the continued practice of ineffective, or even harmful, treatments.The authors point out that, like the rest of us, clinicians are subject to four main biases that skew their ability to infer the effectiveness of their psychotherapeutic treatments. This includes the mistaken belief that we see the world precisely as it is (naive realism), and our tendency to pursue evidence that backs our initial beliefs (the confirmation bias). The other two are illusory control and illusory correlations - thinking we have more control over events than we do, and assuming the factors we're focused on are causally responsible for observed changes.These features of human thought lead to several specific mistakes that psychotherapists and others commit when they make claims about the effectiveness of psychological therapies. Lilienfeld's team call these mistakes "causes of spurious therapeutic effectiveness" or CSTEs for short. The authors have created a taxonomy of 26 CSTEs arranged into three categories.The first category includes 15 mistakes that lead to the perception that a client has improved, when in fact he or she has not. These include palliative benefits (when the client feels better about their symptoms without actually showing any tangible improvement); confusing insight with improvement (when the client better understands their problems, but does not actually show recovery); and the therapist's office error (confusing a client's presentation in-session with their behaviour in everyday life).The second category consists of errors that lead therapists and their clients to infer that symptom improvements were due to the therapy, and not some other factor, such as natural recovery that would have occurred anyway. Among these eight mistakes are a failure to recognise that many disorders are cyclical (periods of recovery interspersed with phases of more intense symptoms); ignoring the influence of events occurring outside of therapy, such as an improved relationship or job situation; and the influence of maturation (disorders seen in children and teens can fade as they develop).The third and final category of errors are those that lead to the assumption that improvements are causes by unique features of a therapy, rather than factors that are common to all therapies. Examples here include not recognising placebo effects (improvements stemming from expectations) and novelty effects (improvements due to initial enthusiasm).To counter the many CSTEs, Lilienfeld's group argue we need to deploy research methods including using well-validated outcome measures, taking pre-treatment measures, blinding observers to treatment condition, conducting repeated measurements (thus reducing the biasing impact of irregular everyday life events), and using control groups that are subjected to therapeutic effects common to all therapies, but not those unique to the treatment approach under scrutiny. "CSTEs underscore the pressing need to inculcate humility in clinicians, researchers, and students," conclude Lilienfeld and his colleagues. "We are all prone to neglecting CSTEs, not because of a lack of intelligence but because of inherent limitations in human information processing. As a consequence, all mental health professionals and consumers should be sceptical of confident proclamations of treatment breakthroughs in the absence of rigorous outcome data."_________________________________ Lilienfeld, S., Ritschel, L., Lynn, S., Cautin, R., & Latzman, R. (2014). Why Ineffective Psychotherapies Appear to Work: A Taxonomy of Causes of Spurious Therapeutic Effectiveness Perspectives on Psychological Science, 9 (4), 355-387 DOI: 10.1177/1745691614535216 --further reading--When therapy causes harmPost written by Christian Jarrett (@psych_writer) for the BPS Research Digest.

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  • July 28, 2014
  • 04:24 AM
  • 80 views

Prenatal and neonatal blood mercury levels and autism

by Paul Whiteley in Questioning Answers

Acknowledging that some topics have the ability to furrow brows when it comes to autism research, mercury and autism is becoming something of a frequent talking point on this blog as a function of a whole slew of articles appearing in the peer-reviewed domain. If I were to [very tentatively] summarise the collected literature so far, it would be to say something like:Mosaic of mercury @ Wikipedia (i) there is quite a bit more research to be done on some sources of mercury being 'linked' to cases of autism i.e. air pollution, fish consumption (see here),and(ii) the body burden of mercury for some on the autism spectrum is elevated (see here) compared to other groups and potentially linked to "a decreased ability to excrete mercury due to a combination of lowered reduced glutathione, emergence of oxidative stress, and excessive use of oral antibiotics" according to the review by Francesca Gorini and colleagues [1] (open-access).I know some people may not like hearing that summary but that's my interpretation of the various reviews and meta-analyses conducted so far. I should add that I'm not though passing any specific comment on whether mercury 'causes' autism bearing in mind what we know about the developmental consequences of exposure.The paper by Vincent Yau and colleagues [2] looking at maternal serum and infant newborn bloodspot levels of mercury adds to that literature with their conclusion: "levels of total mercury in serum collected from mothers during mid-pregnancy and from newborn bloodspots were not significantly associated with risk of ASD [autism spectrum disorder]". I believe we had seen this data presented before at the 2011 IMFAR conference too (see here).A few details first:Based on data obtained from the EMA (Early Markers of Autism) study, a cohort "identified from the California Department of Developmental Services (DDS)" records, mid-pregnancy maternal serum samples and the wonderful resource that is the neonatal bloodspots related to some 84 children diagnosed with an ASD were analysed for total mercury content (inorganic and organic mercury). Blinded results were compared with 159 population controls (asymptomatic) and 49 children diagnosed with a learning (intellectual) disability or developmental delay.ICP mass spectrometry was the name of the analytical game, which as I've talked about before, is one of the methods of choice when it comes to the analysis of the metallome. Archived blood spot samples were subject to laser ablation as a function of their mounting. Results: "Maternal serum and infant blood mercury levels were significantly correlated among all study groups". In other words, maternal mercury burden seemed to be associated with neonatal offspring burden (albeit with a correlation coefficient ~0.4 which is OK but not exactly great).Further: "Results for mercury levels in newborn blood samples were similar" across the groups. Ergo, at birth, levels of total mercury from neonatal bloodspots "were not significantly associated with risk of ASD". That's not to say that there weren't some differences in average levels of blood mercury levels across the groups, just that such differences were not deemed to elevate the risk of ASD overall.Like quite a lot of the science in this area, there are several ways you could interpret these results. You could, for example say that the maternal burden of mercury during pregnancy was not associated with offspring risk of autism. You could also say that 'at or shortly after birth' (remember those words), blood mercury levels do not seem to correlate with the risk of autism. Therefore mercury is not a factor in relation to autism as per other results in this area [3]. You could say those things, as you might for several other variables supposedly related to autism... vitamin D for example? (see here and then see here).But you might also consider the bank of research which has reported elevated levels of mercury in various biofluids and tissues particularly focused on slightly older infants and children with autism as illustrative of something potentially important: increasing exposure to mercury with age. Take for example the paper by Majewska and colleagues [4] and their findings reporting: "Autistic children significantly differed from healthy peers in the concentrations of mercury in hair: younger autistics had lower levels, while older - higher levels than their respective controls". The results from Hertz-Picciotto and colleagues [4] (open-access here) also implied that behaviour might play a role in blood mercury levels: "Interestingly, although few children had Hg amalgams, those who did and who also either chewed gum or had bruxism appeared to have experienced sufficient release of inorganic Hg to be measurable in blood". I say this noting that not every child with autism has mercury amalgams, as neither do they all partake in teeth grinding.The Yau results make an important contribution to the issue of mercury and autism in terms of maternal contribution and mercury load at birth. As part of some further investigations, and bearing in mind that participants in the EMA initiative might also be involved in other State initiatives (beincharge!), I would like to see further follow-up of participants and if and how their mercury load might have changed as they matured. Analysis of other parameters mentioned in that Gorini review paper - such as glutathione measures for example - might also offer some important accompanying data on whether excretion factors are part of the issue here and what might be done to help relieve any excess burden of the troublesome heavy metal that is mercury. Oh, and given that genetic factors might also play some role in mercury accumulation as per the findings by Llop and colleagues [5] (open-access), there may also be more research to do here too...----------[1] Gorini F. et al. The Role of Heavy Metal Pollution in Neurobehavioral Disorders: a Focus on Autism. Review Journal of Autism... Read more »

Yau VM, Green PG, Alaimo CP, Yoshida CK, Lutsky M, Windham GC, Delorenze G, Kharrazi M, Grether JK, & Croen LA. (2014) Prenatal and neonatal peripheral blood mercury levels and autism spectrum disorders. Environmental research, 294-303. PMID: 24981828  

  • July 26, 2014
  • 05:59 AM
  • 115 views

Temperatures make our global warming opinions change like the weather

by Andy Extance in Simple Climate

Our experience of current warmth can override our scientific knowledge in driving beliefs about climate change, which is part of the reason we struggle to take the resulting risks seriously, underlines Columbia University’s Elke Weber. ... Read more »

  • July 25, 2014
  • 12:00 PM
  • 139 views

The Friday Five 07/25/14

by Bill Sullivan in The 'Scope

Five of the coolest news stories from the past week... Read more »

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