Post List

Psychology posts

(Modify Search »)

  • April 17, 2014
  • 09:14 AM

What Do You Want to Hear First: Good News or Bad News?

by Jeremiah Stanghini in Jeremiah Stanghini

As it turns out, our answer to this question is different depending on whether we’re the one delivering the news or we’re the one receiving the news. If we’re delivering the news, we’re more likely to want to lead with … Continue reading →... Read more »

  • April 17, 2014
  • 09:00 AM

A poor excuse for removing a peer-reviewed publication

by Katharine Blackwell in Contemplating Cognition

I became disenchanted with the idea of e-books when Amazon reached into scores of Kindles and removed copies of (of all possible books) 1984 and Animal Farm. The notion that a major company had the power to deny access to any content they deemed problematic simply presented too many visions of reactive, totalitarian control.

I never considered that those very concerns might apply to the publishers of scientific research, who – in this age of online-only publications – have the power to remove properly vetted research articles at their whim. Now, it is not a nightmare vision but a grim reality.... Read more »

  • April 17, 2014
  • 07:49 AM

Cannabis use and structural changes in the brain

by Robb Hollis in Antisense Science

“One or two spliffs a week could mess up your brain” – Metro, 16 April 2014

Spark your interest? This headline caught the eyes of the Antisense team, so we chased down the original article in the Journal of Neuroscience and took a closer look!

Cannabis is the most commonly used illegal drug in the US, and the ‘casual use’ culture surrounding marijuana is a subject of great debate and controversy, with arguments for drug legalisation making their way into our headlines more and more often. But what are the effects of this kind of casual infrequent drug abuse?... Read more »

  • April 17, 2014
  • 04:31 AM

Mitochondrial dysfunction as a neurobiological subtype of autism

by Paul Whiteley in Questioning Answers

The paper by Suzanne Goh and colleagues [1] reporting on "a possible neurobiological subtype of mitochondrial dysfunction in ASD [autism spectrum disorder]" is a worthy addition to the research roll call which has graced this blog down the years. Based on the analysis of brain lactate levels - a potential marker of mitochondrial dysfunction - via the analysis of lactate doublets on brain magnetic resonance spectroscopic imaging (MRSI), authors picked up a significantly higher rate of lactate in cases of autism spectrum disorder (ASD) when compared to age and sex-matched asymptomatic controls. I've talked lactate and autism before on this blog (see here) so very much welcomed this research looking specifically at brain levels of this stuff.I'm writing this post having already scheduled a blog entry on the recent paper by Rose and colleagues [2] (open-access here) on the increasing complexity of mitochondrial dysfunction being seemingly present in some cases of autism. Given the findings from Goh et al I've decided to publish this entry first (just to confuse everyone even further) as yet again, my confusion on the topic of all-things mitochondrial has an opportunity to shine through.So then, a few details from the Goh paper:Based on imaging and other data derived from 75 participants diagnosed with an ASD (aged 5-60 years) contrasted with 96 typically-developing controls, the authors set about "assessing in-vivo evidence of mitochondrial dysfunction directly in the brains of a large sample of children and adults with ASD".Whilst not an imaging man, I can tell you that they used proton multiplanar spectroscopic imaging (MPSI) to quantify endogenous brain chemistry and "regional cellular metabolism and function" specifically towards the detection of lactate. Actually, the talk of [lactate] doublets is not a million miles away from the results one gets as a consequence of a related chemical analytical technique, NMR, which brings back memories of some work from days gone by.After laying down quite a few ground rules for what was and wasn't a readable result, the authors concluded that: "Lactate doublets were present at a significantly higher rate in participants with ASD (13%) than in typically developing controls (1%) (P = .001), providing in vivo evidence for the presence of mitochondrial dysfunction in the brains of individuals with ASD". In-vivo by the way, means in the living and contrasts with science done in a test-tube (in-vitro).Age was a factor when it came to lactate levels, with elevations reported more often in adults than in children. This phenomenon has been talked about before in the research literature [3].The authors go on to discuss the implications of their results. Bearing in mind the various situations where elevated brain lactate levels have been noted outside of just ageing, including as a result of issues like anxiety or panic disorder [4], they reiterate how their "strict exclusion critera and careful scanning procedures made such explanations less likely". Further they highlight how: "individuals with ASD should undergo evaluation for mitochondrial dysfunction, as novel and promising treatments are under development for mitochondrial disorders".As per my link above, this is not the first time that lactate has appeared in the autism research literature. I'll for example, draw your attention to the paper by Al-Mosalem and colleagues [4] and their reporting that: "Lactate as an important energy metabolite for the brain was significantly higher in autistic patients compared to control showing about 40% increase". Bear in mind however that this and other results [5] have tended to look in plasma rather than directly what's going on in the brain as Goh et al did.There's little more for me to say on this area of research aside from the need for further replicative investigations and perhaps a little more inquiry into the subgroup of people with autism who fall into this mitochondrial dysfunction category bearing in mind the continued focus on the plurality of autism (the autisms). That there may be interventions available for mitochondrial disorder when present [6] is another important point. As per related research in other conditions with a potential mitochondrial aspect to them (see here), at least one of the interventions - Coenzyme Q10 (ubiquinol) - is being looked at with some autism in mind [7] (open-access here) bearing in mind no medical or clinical advice is given or intended.Music then to close. I'm thinkin' of something with a candy orientation given the time of year, so again, ladies and gentlemen, Mr Sammy Davis Jnr and The Candy Man.. (he can you know).-----------[1] Goh S. et al. Mitochondrial Dysfunction as a Neurobiological Subtype of Autism Spectrum Disorder. Evidence From Brain Imaging. JAMA Psychiatry. 2014. April 9.[2] Rose S. et al. Oxidative stress induces mitochondrial dysfunction in a subset of autistic lymphoblastoid cell lines. Transl Psychiatry. 2014 Apr 1;4:e377.[3] Ross JM. et al. High brain lactate is a hallmark of aging and caused by a shift in the lactate dehydrogenase A/B ratio. PNAS. 2010; 10.1073/pnas.1008189107[4] Al-Mosalem OA. et al. Metabolic biomarkers related to energy metabolism in Saudi autistic children. Clin Biochem. 2009 Jul;42(10-11):949-57.[5] Oliveira G. et al. Mitochondrial dysfunction in autism spectrum disorders: a population-based study. Dev Med Child Neurol. 2005 Mar;47(3):185-9.[6] Parikh S. et al. A Modern Approach to the Treatment of Mitochondrial Disease. Curr Treat Options Neurol. Nov 2009; 11(6): 414–430.[7] Gvozdjáková A. et al. Ubiquinol improves symptoms in children with autism. Oxid Med Cell Longev. 2014;2014:798957.----------Goh, S., Dong, Z., Zhang, Y., DiMauro, S., & Peterson, B. (2014). Mitochondrial Dysfunction as a Neurobiological Subtype of Autism Spectrum Disorder JAMA Psychiatry DOI: 10.1001/jamapsychiatry.2014.179... Read more »

  • April 16, 2014
  • 08:29 PM

What makes music groovy?

by Henkjan Honing in Music Matters

Today PLOS ONE publishes a study that uses an often criticized research method: questionnaire and web-based research (cf. Honing & Ladinig, 2008). This study, however, is a good example of how an unspectacular method (i.e. compared to, e.g., controlled experiments, brain imaging techniques or computational modelling) can still be quite informative.... Read more »

Witek, M., Clarke, E., Wallentin, M., Kringelbach, M., & Vuust, P. (2014) Syncopation, Body-Movement and Pleasure in Groove Music. PLoS ONE, 9(4). DOI: 10.1371/journal.pone.0094446  

Honing, H., & Reips, U.-D. (2008) Web-based versus lab-based studies: a response to Kendall (2008). Empirical Musicology Review, 3(2), 73-77. info:/

  • April 16, 2014
  • 05:04 PM

What Do Preschoolers Learn from Fantastical Picture Books?

by Rebecca Schwarzlose in Garden of the Mind

One of the new picture books making the bedtime rounds at our house is How Do Dinosaurs Say Goodnight?, which describes and depicts dinosaurs doing such un-dinosaurly things as tucking themselves into bed or kissing their human mothers good night. The book is whimsical, gorgeously illustrated, and includes a scientific angle, as the genus names of the dinosaurs are included in the pictures. I’m always careful to read these genus names aloud as we look at each picture. But is this book actually teaching my daughter anything about dinosaurs? And does the misinformation get in the way of her learning these facts? A new study suggests that it might.... Read more »

  • April 16, 2014
  • 08:30 AM

Does Animal-Assisted Therapy Help At-Risk Boys?

by CAPB in Companion Animal Psychology Blog

If existing behavioural programs aren’t working, can therapeutic sessions with a dog help boys who have problems at school?Photo: criben / ShutterstockA new paper by Abbey Schneider et al (2014) investigates the success of a program designed to help boys who are considered ‘at-risk’ – by matching them up with a specially trained dog and handler.In Colorado, a group of elementary schools take part in a program called the Human Animal Bond in Colorado (HABIC). It is designed to help girls and boys who have problems such as hyperactivity, aggression, anxiety, or depression. These children are usually given an Individualized Education Plan to help them in school, and several behavioural support systems are also available. When these supports are not enough, children can be referred to HABIC.The Animal Assisted Therapy program matches each child to a specific dog and handler, with whom they spend 10-12 sessions. The first is a meet-and-greet, and in this and subsequent sessions the child helps the handler teach new commands to the dog, learns how to give the dog commands it already knows, and also has unstructured time in which they can play with or cuddle the dog. The dog and handler are specially trained to work in the program, and the sessions are designed for each child with specific behavioural and emotional aims.Dogs are great for a program like this because they are not judgmental, they are available to be petted and cuddled, the child can try out different pro-social behaviours with the dog, and the relationship does not rely on verbal skills. Within the framework of attachment theory, the child can develop a secure attachment with the dog (and the dog’s handler) that will enable them to feel safe and to develop emotionally and behaviourally.Nine boys took part in this study. The researchers conducted a set of assessments before, during and after the animal-assisted therapy sessions. This included observations of the child and dog interacting that were designed to assess the emotional bond between them, the child’s self-reports about the relationship with the dog, teacher and parent assessments of the child’s behaviour, and data about the child’s absences from school and referrals to the principal for bad behaviour.The researchers say the “results suggest that children are able to create more emotionally positive relationships with both animals and adults over the course of the intervention.”  In addition, although there was no change in being absent from school, there was a significant reduction in the number of times the boys were referred to the principal’s office for problem behaviour.Interestingly, teachers did not rate the boys’ behaviour as better in the classroom. The researchers think it is possible their ratings were clouded by previous experiences with the boys. Independent classroom observations could be a useful addition to future evaluations.A nice thing about this study is that in evaluating emotional attachment between the child and dog, observations were also made of the dog, such as the time spent in close proximity to the boy, and whether the dog’s mouth was open in a happy expression or closed, suggesting tension.The researchers say one advantage of the scheme is that, while social skills can be taught, the desire to connect emotionally with others is harder to inspire. The dog provides encouragement to the child to connect with another being. It also seems that unstructured time is important for the development of the bond between them, and this is something that warrants future research.This study is an important formal evaluation of an existing scheme. Without research like this, we would not know if such schemes work or how they could be improved. It is small-scale, and a larger evaluation that included girls as well as boys would be helpful. The results are very encouraging, and suggest that animal-assisted therapy can be beneficial for children with a range of behavioural problems.The HABIC program is just one way in which animals can potentially help children. For example, work by Maggie O’Haire suggests that a classroom program with guinea pigs can help children with autism as well as their normal peers. This is a fascinating topic and we look forward to future work by these and other researchers in the field.If you would like to know more about the study, the full paper is open-access (registration required).Is there an animal-assisted therapy program in your community?ReferenceSchneider, A.A.,, Rosenberg, J., Baker, M., Melia, N., Granger, B., & Biringen, Z. (2014). Becoming relationally effective: High-risk boys in animal-assisted therapy Human-Animal Interaction Bulletin, 2 (1), 1-18... Read more »

Schneider, A.A.,, Rosenberg, J., Baker, M., Melia, N., Granger, B., & Biringen, Z. (2014) Becoming relationally effective: High-risk boys in animal-assisted therapy. Human-Animal Interaction Bulletin, 2(1), 1-18. info:/

  • April 16, 2014
  • 01:54 AM

Joined by HDAC (inhibitors)

by Paul Whiteley in Questioning Answers

I'm treading quite carefully with this post which came about following my [non-expert] reading of the paper abstract from Anand Venkatraman and colleagues [1] on a potential downside to the use of HDAC (histone deacetylase) inhibitors for treating spinocerebellar ataxia type 1 (SCA1), a progressive disease affecting movement and other knock-on functions. This follows other work suggesting that certain HDAC inhibitors might offer some important new lines of investigation when it comes to at least some of the various types of spinocerebellar ataxia (SCA). For those who thought this was a blog about autism research, bear with me on this one...HDACs represent a group of enzymes which go to work removing acetyl groups on histone tails which, as the paper by Patrick Grant [2] (open-access) very nicely illustrates, has the potential to do some rather important things to processes like gene expression (condensing chromatin and repressing transcription). I have kinda touched upon histones and the so-called histone code in a previous introductory post on the rise and rise of epigenetics (see here) with autism in mind.The Venkatraman results focused on a mouse model, and how depletion/loss of a particular type of HDAC - HDAC3 - was in some cases: "highly deleterious both behaviorally, with mice showing early onset ataxia, and pathologically, with progressive histologic evidence of degeneration". They talk about "cautionary evidence that this approach could produce untoward effects" when it comes to the employment of "pharmacologic inhibition of HDAC3" via HDAC inhibitors in SCA.Not to make too many sweeping generalisations or form associations which might not be there, but two things from the Venkatraman paper got my old(ish) grey matter fired up: (i) mention of HDAC inhibitors and the emerging story when it comes to prenatal exposure to valproate with a HDAC slant, and (ii) the focus on Purkinje cell function; as their paper title states: "The histone deacetylase HDAC3 is essential for Purkinje cell function". Both these points bring me back to some potentially important issues which might apply to at least some autism and related neurodevelopmental outcomes.It is still very much an emerging picture but pregnancy use of valproate and 'adverse' offspring events/development is turning into something of a quite important association in recent times. So much so that the US FDA and UK MHRA have issued some guidance on this matter. Valproate has some history as a potential teratogen [3] bearing in mind my offering no medical or clinical advice on this matter aside from saying 'don't mess with epilepsy'. That valproate is also an HDAC inhibitor [4] (open-access) is another mechanism through which the drug might (a) find some new markets for conditions other than epilepsy, but also (b) impact on development and functions. Readers are invited to have a look through the paper by Katie Lloyd [5] (open-access) for a well-rounded overview of potential effects.Then to the Purkinje cell story. I'm sure most people with an interest in autism will have heard about the cerebellum in relation to the condition at some point. Indeed, the paper by Fatemi and colleagues [6] (open-access) kinda sums up where we're at when it comes to the 'little brain' bearing in mind the need for further investigation and the greater focus on the plural 'autisms'. To talk about the cerebellum and autism also brings into the play those Purkinje cells which have also featured on several occasions on the autism research menu [7] and quite recently, with an epigenetic slant to the research (see here). Indeed, the paper by Jill James and colleagues [8] (open-access) on epigenetics and EN-2 is something I'd very much like to see more work on.Again, not to make mountains out of molehills, but I did wonder whether there may be some science to do covering these potentially overlapping areas. I'm not necessarily saying that valproate = HDAC inhibition = impact on Purkinje cell numbers/maturation/functions = autism because I very much doubt it's going to be that simple or generalised despite some emerging [rodent] data [9]. With the increasing interest in all-things epigenetic however, also crossing over to autism research [10] (open-access), one might consider more inquiry into the HDACs, their inhibitors and effectors (and exposure timing) to be a potentially important part of that particular autism research tide? Whether even important ecosystems e.g. "the [gut] microbiota itself may be viewed as an epigenetic entity" [11] may also tie into some of the work in this area too?----------[1] Venkatraman A. et al. The histone deacetylase HDAC3 is essential for Purkinje cell function, potentially complicating the use of HDAC inhibitors in SCA1. Hum Mol Genet. 2014 Mar 4.[2] Grant PA. A tale of histone modifications. Genome Biology 2001, 2:reviews0003-reviews0003.6[3] Alsdorf R. & Wyszynski DF. Teratogenicity of sodium valproate. Expert Opin Drug Saf. 2005 Mar;4(2):345-53.[4] Göttlicher M. et al. Valproic acid defines a novel class of HDAC inhibitors inducing differentiation of transformed cells. EMBO J. 2001; 20(24): 6969–6978.[5] Lloyd KA. A scientific review: mechanisms of valproate-mediated teratogenesis. Bioscience Horizons 2013; 6 : hzt003[6] Fatemi SH. et al. Consensus paper: pathological role of the cerebellum in autism. Cerebellum. 2012 Sep;11(3):777-807.[7] Skefos J. et al. Regional alterations in purkinje cell density in patients with autism. PLoS One. 2014 Feb 24;9(2):e81255.[8] James SJ. et al. Complex epigenetic regulation of engrailed-2 (EN-2) homeobox gene in the autism cerebellum. Transl Psychiatry. 2013 Feb 19;3:e232.[9] Moldrich RX. et al. Inhibition of histone deacetylase in utero causes sociability deficits in postnatal mice. Behav Brain Res. 2013 Nov 15;257:253-64.[10] Lasalle JM. Autism genes keep turning up chromatin. OA Autism. 2013 Jun 19;1(2):14.[11] Stilling RM. et al. Microbial genes, brain & behaviour - epigenetic regulation of the gut-brain axis. Genes Brain Behav. 2014 Jan;13(1):69-86.----------... Read more »

  • April 14, 2014
  • 10:51 PM

Disordered Eating and Athletic Performance: Where’s the Line?

by Emma in Science of Eating Disorders

If a person severely restricts his diet and exercises for hours each day, he has an eating disorder. If another does exactly the same but it is because she wants to make the lightweight rowing team (which has an upper weight limit), she’s a committed athlete. When the two overlap, and an athlete presents with eating disorder symptoms, how do we distinguish between the demands of the sport and the illness?
I’ve been interested in the distinctions we make between disordered and non-disordered eating and exercise behaviours for a while now. Recently, when I was browsing through articles, I came across a literature review by Werner et al. (2013) (open access) of studies examining weight-control and disordered eating behaviours in young athletes.
The authors start by noting the sheer lack of research that has actually been done in this area. This is worrying: typical onset of eating disorders is during adolescence, and research indicates that athletes are more likely to develop these disorders, leaving young athletes in what appears to be a high-risk position.
Werner et al. searched for …

You May Also Like:
Demystifying the Genetic and Environmental Influences on Disordered Eating
Diabulimia: Disordered Eating in Type 1 Diabetic Patients
Shared Genetics Between Disordered Eating and Periods (Menses)

... Read more »

  • April 14, 2014
  • 10:24 AM

Some exploratory evidence that wait-list conditions may act as a nocebo in psychotherapy trials

by Kristoffer Magnusson in R Psychologist

The hypothesis that wait-lists could be nocebo conditions was investigated by Furukawa et al (2014). The authors performed a network meta-analysis of 49 RCT that involved cognitive-behaviour therapy for depression. ... Read more »

Furukawa TA, Noma H, Caldwell DM, Honyashiki M, Shinohara K, Imai H, Chen P, Hunot V, & Churchill R. (2014) Waiting list may be a nocebo condition in psychotherapy trials: a contribution from network meta-analysis. Acta psychiatrica Scandinavica. PMID: 24697518  

  • April 14, 2014
  • 09:12 AM

Why Humanistic Psychology is Still Relevant

by Jeremiah Stanghini in Jeremiah Stanghini

The development of humanistic psychology began in the late 1950s and was ‘born‘ in the early 1960s. Given the time that humanistic psychology grew, there’s no doubt that it informed the civil rights movement. However, some say that humanistic psychology peaked in the 1970s. An … Continue reading →... Read more »

DeRobertis, E. M. (2013) Humanistic Psychology: Alive in the 21st Century?. Journal of Humanistic Psychology, 53(4), 419-437. DOI: 10.1177/0022167812473369  

  • April 14, 2014
  • 09:00 AM

How practicing compassion alters the brain

by Katharine Blackwell in Contemplating Cognition

As tempting as it is to hope that one meditation practice could be a panacea within the mind – meditate, and become more mindful! improve your attention! cure your depression! notice when those around you need help! – I have to admit that I know the brain doesn’t work this way. The skills you practice are the skills you strengthen, and compassion in particular is a skill that requires more than just a general awareness of your environment.... Read more »

Weng HY, Fox AS, Shackman AJ, Stodola DE, Caldwell JZ, Olson MC, Rogers GM, & Davidson RJ. (2013) Compassion training alters altruism and neural responses to suffering. Psychological science, 24(7), 1171-1180. PMID: 23696200  

  • April 14, 2014
  • 07:02 AM

A new neurolaw caveat to minimize punishment

by Doug Keene in The Jury Room

Just say his brain made him do it! That is the conclusion of new research on the relationship between gruesomeness of the crime and the harshness of the sentence. In case you can’t intuit this one, the more gruesome (and disturbing) the crime, the harsher the sentence tends to be. But if the assault was […]

Related posts:
Neurolaw Update: Who’s in charge here—me or my brain?
When identifying punishment—will jurors focus on intent or outcome?
Simple Jury Persuasion: Anger + Disgust = Moral Outrage

... Read more »

  • April 14, 2014
  • 03:58 AM

Neurology of inflammatory bowel diseases

by Paul Whiteley in Questioning Answers

The paper by Ben-Or and colleagues [1] talking about a neurologic profile present in a small participant cohort of children and adolescents diagnosed with an inflammatory bowel disease (IBD) caught my eye recently. Their findings reporting that over two-thirds of their paediatric participant group diagnosed with IBD also "exhibited neurologic manifestations" provides some compelling preliminary evidence for further investigation in this area.Outside of reports of headache and dizziness, the presentation of attention-deficit hyperactivity disorder (ADHD), hypotonia and "sensory complaints" comorbid to IBD shines a spotlight on the so-called 'gut-brain axis'. That being said the fact that "seizures and neuropsychiatric disorders were less characteristic" between IBD cases and asymptomatic controls may also have some important implications for various conditions including the primary topic of this blog, the autism spectrum conditions.I'm not on this occasion going to dissect the Ben-Or findings too much aside from pointing you in the direction of some other research which may very well tie into their findings. I've talked before about research on other bowel-related conditions suggestive of potentially important neurological and behavioural links. Think coeliac disease and the the ataxia story as one example mentioned in a previous post (see here). I'd also draw your attention to some work in the autism research domain talking about a possible link between functional bowel habit issues and the presentation of anxiety and sensory symptoms (see here). Granted, it is a leap from a diagnosis of IBD to the presentation of constipation or diarrhoea not necessarily due to an IBD (or at least that's what was thought) but one might imagine that further investigation would be indicated in light of the Ben-Or data.Reiterating the gut-brain link which seems to be appearing with ever-greater frequency these days, I'm minded to suggest that further research be directed to looking at the possible mechanisms to account for any relationship. The usual triad of issues: intestinal (gut) permeability, the gut microbiota and the gut mucosal immune system spring to mind as potential players in any relationship, but that's all I'll say on the matter for now.----------[1] Ben-Or O. et al. The Neurologic Profile of Children and Adolescents With Inflammatory Bowel Disease. J Child Neurol. 2014 Apr 2.----------Ben-Or O, Zelnik N, Shaoul R, Pacht A, & Lerner A (2014). The Neurologic Profile of Children and Adolescents With Inflammatory Bowel Disease. Journal of child neurology PMID: 24700662... Read more »

  • April 12, 2014
  • 11:54 PM

Early brain development and heat shock proteins

by in Neuroscientifically Challenged

The brain development of a fetus is really an amazing thing. The first sign of an incipient nervous system emerges during the third week of development; it is simply a thickened layer of tissue called the neural plate. After about 5 more days, the neural plate has formed an indentation called the neural groove, and the sides of the neural groove have curled up and begun to fuse together (see pic to the right). This will form the neural tube, which will eventually become the brain and spinal cord. By around 10 weeks, all of the major structures of the brain are discernible, even if they are not yet fully mature. So, in a matter of two months, the framework for the human brain is built from scratch. If that doesn't put you in awe of nature, nothing will.Although the process of neural development is amazing, it is also very sensitive. There are indications that a number of environmental exposures during prenatal development may increase the risk of disorders like autism, schizophrenia, and epilepsy. Some of these dangerous environmental exposures are well known (e.g. alcohol consumption during pregnancy increasing the risk of developing fetal alcohol syndrome). However, there are a number of other factors whose detrimental effects on fetal neural development are still debated or have not yet been fully elucidated. For example, the effects on a fetus of substances like phthalates (plasticizers that are likely found in a number of products throughout your home), bisphenol A (another substance used in the production of plastics - found frequently in food and drink containers), and even tobacco smoke, are still being investigated. But a pregnancy free from exposure to any potentially harmful substances doesn't guarantee normal neural development. Even factors that are natural and more difficult to control, like maternal infection during pregnancy, are suspected of being detrimental in some cases.To complicate the issue even further, it is difficult to predict who will be affected by these environmental insults and who will not. It seems that there may be a genetic susceptibility to neurodevelopmental damage that causes a particular exposure to be detrimental to one fetus, while it may not have a major impact on another with a different genetic makeup. This complication, however, also provides an opportunity to learn more about the etiology of neurodevelopmental disorders. For, if we can learn what mechanism is failing in the fetus who is affected, but functioning in the fetus who is not, then our understanding of the origin of these disorders will be drastically improved.In a paper published last week in Neuron, Hashimoto-Torii et al. approached the problem from this angle and examined the role of heat shock proteins in neurodevelopmental problems. Heat shock proteins are peptides whose expression is increased during times of stress. They earned their name when it was discovered in the early 1960s that high levels of heat increased their expression in Drosophila (fruit flies). Since, it has been learned that heat shock protein expression is increased during all sorts of stress, including infection, starvation, hypoxia (lack of oxygen), and exposure to toxins like alcohol. Thus, some also refer to heat shock proteins as stress proteins.To investigate the role of heat shock proteins in neurodevelopmental disorders, Hashimoto-Torii et al. exposed mouse embryos to three different types of environmental insults. They injected pregnant mice with either alcohol, methylmercury, or a seizure-inducing drug. Then, they looked to see how the brains of the embryos reacted. As they hypothesized, they saw a significant increase in the expression of a transcription factor (heat shock factor 1 or HSF1) that promotes the production of heat shock proteins.When the researchers investigated the effects of prenatal exposure to the insults listed above in mice who lacked an HSF1 gene (HSF1 knockout mice), they saw that the exposed moms had smaller litters than control mice. The mice that were born, however, also displayed malformations consistent with neurodevelopmental damage, greater susceptibility to seizures after birth, and reduced brain size. The reduction in brain volume seemed to be due to decreased neurogenesis after the insult.To make a clearer connection between heat shock protein activation and human disease, the researchers exposed stem cells derived from schizophrenic patients to methylmercury and alcohol, and compared the response of the "schizophrenic cells" to the response of cells from non-schizophrenic (control) patients. They didn't see an overall difference in heat shock protein expression between the two types of cells, but they did see significant variability in expression among the schizophrenic cells. In other words, both schizophrenic and control cells increased expression of heat shock protein after an insult, but some of the schizophrenic cells appeared to increase expression more or less than others. The control cells all displayed a relatively similar increase in expression. This suggests that there may be an abnormal response involving heat shock proteins in individuals with a certain genetic predisposition; perhaps this abnormal response makes the individual more susceptible to disrupted neurodevelopment.Thus, the study by Hashimoto-Torii et al. points to heat shock proteins as a potential culprit behind what goes wrong in early brain development to lead to psychiatric disorders like schizophrenia and autism. More research will need to be done, however, to verify this role for heat shock proteins. And, even if future research supports this finding, it is likely that heat shock proteins are still only part of the puzzle. But the puzzle is complex, and so we will need to add many of these little pieces before we can begin to comprehend the whole picture.Hashimoto-Torii, K., Torii, M., Fujimoto, M., Nakai, A., El Fatimy, R., Mezger, V., Ju, M., Ishii, S., Chao, S., Brennand, K., Gage, F., & Rakic, P. (2014). Roles of Heat Shock Factor 1 in Neuronal Response to Fetal Environmental Risks and Its Relevance to Brain Disorders Neuron DOI: 10.1016/j.neuron.2014.03.002
... Read more »

  • April 11, 2014
  • 06:25 PM

Dad's obesity and risk of offspring autism

by Paul Whiteley in Questioning Answers

In this post I'm talking about the paper by Pål Surén and colleagues [1] and their suggestion that "paternal obesity is an independent risk factor for ASDs [autism spectrum disorders] in children". I do so not with the intent of stigmatising parents and specifically parents with weight issues, which tend to be present for many more reasons than just food and exercise (see here), but merely to highlight how parental physical health may show some relationship to offspring cognitive and developmental progress. Indeed, the findings from Surén et al are to viewed in the context of some other related research in this area (see here).By the water @ Renoir @ Wikipedia Quite a nice summary of the Surén work can be found here and here. The basics are: MoBa (see here), questioning parents particularly fathers about their physical health while their partner was pregnant, following up offspring and their subsequent development - specifically whether they had received a diagnosis of "autistic disorder", Asperger syndrome or pervasive developmental disorder not otherwise specified (PDD-NOS).The results: well, the rate of autism reported (0.45%) was interesting. Certainly compared to other prevalence estimates we've been hearing about recently, quite a different figure was noted altogether (see here) allowing for age differences in case ascertainment. Then to the primary findings: "The risk of autistic disorder was 0.27% (25 of 9267) in children of obese fathers and 0.14% (59 of 41 603) in children of fathers with normal weight (BMI <25), generating an adjusted OR of 1.73 (95% CI: 1.07–2.82)". And with regards to Asperger syndrome: "The risk was 0.38% (18 of 4761) in children of obese fathers and 0.18% (42 of 22 736) in children of normal-weight fathers, and the adjusted OR was 2.01 (95% CI: 1.13–3.57)". Ergo, potentially double the risk of offspring autism when fathers were categorised as overweight or obese based on body mass index (BMI).It goes without saying that the suggestion of a link between paternal weight and offspring risk of autism is by no means proved by this latest research. Think correlation not being the same as causation as one reason why we should not just accept the results of this work at face value irrespective of how enthusiastic researchers might be about their data and what they were able to control for as potential interfering variables. That also BMI has it's 'issues' when it comes to defining healthy weight is another reason for caution where muscle mass for example, is not accounted for in such a simplistic formula.But all that doesn't mean the results are not interesting...In recent times I've noticed quite a bit more research looking at the potential role of father's health and wellbeing on offspring development treading in the footsteps of how ageing might play a role. Take for example the recent opinion piece in Nature titled 'Sins of the father' which introduces another side to the Surén results: the science of epigenetics. The paper by Lambrot and colleagues [2] is as good an example as any on how a father's nutritional status with folate in mind, might impact on offspring health. I'm not asking you to take this as fact; merely that the focus on maternal nutrition and offspring outcome might not be the only important variable in any relationship.Harking back to another paper by the Surén research group (including Drs Hornig and Lipkin) [3] reveals nutrition to be something that the authors had probably thought about with the current results in mind. On that occasion, the focus was on the elevated risk of autism in cases of a short inter-pregnancy interval (see here) and mention of a "depletion of micronutrients" as a possible factor. Shadows indeed of the work of the late David Barker and his foetal programming hypothesis.I do believe there are more investigation to be done building on the Surén results. I've already made mention of folate in the father-offspring relationship given the link between the folate cycle and the availability of methyl groups for the process of DNA methylation, an important epigenetic process. One might also wonder about the body of work looking at more traditional genetic issues in the genes involved in that cycle such as everyone's favourite Scrabble gene and enzyme:  Methylenetetrahydrofolate reductase (MTHFR) and its growing links with some autism (see here). Could issues with MTHFR present in fathers confer susceptibility to offspring autism, or weight issues pertinent to an elevated risk via epigenetic mechanisms? That being said, I'm sure that any relationship is going to be complicated and not necessarily relevant to every child diagnosed with an autism spectrum condition.Music to close. In memory of author Sue Townsend and her Adrian Mole series of books... Profoundly in Love with Pandora.----------[1] Surén P. et al. Parental Obesity and Risk of Autism Spectrum Disorder. Pediatrics. 2014. April 7.[2] Lambrot R. et al. Low paternal dietary folate alters the mouse sperm epigenome and is associated with negative pregnancy outcomes. Nature Comms. 2013; 4: 2889.[3] Gunnes N. et al. Interpregnancy interval and risk of autistic disorder. Epidemiology. 2013 Nov;24(6):906-12.----------... Read more »

Suren, P., Gunnes, N., Roth, C., Bresnahan, M., Hornig, M., Hirtz, D., Lie, K., Lipkin, W., Magnus, P., Reichborn-Kjennerud, T.... (2014) Parental Obesity and Risk of Autism Spectrum Disorder. PEDIATRICS. DOI: 10.1542/peds.2013-3664  

  • April 11, 2014
  • 07:02 AM

Smiling and credibility: Is it different for male and female witnesses at trial?

by Rita Handrich in The Jury Room

Women smile more than men. Men are typically seen as more credible than women. So these researchers decided to see if there was a relationship between smiling and assessments of credibility on actual witnesses in the courtroom.  The researchers used the Witness Credibility Scale to assess actual witnesses overall credibility. They thought that if smiling […]

Related posts:
Women as Expert Witnesses: The good, the sad, and the ugly
Which is the more moral negotiator? The male or the female?
Stereotypes happen all the time if you are neither pale nor male

... Read more »

  • April 11, 2014
  • 03:48 AM

Brain Scans: Don’t Throw Out The Baby With The Dead Salmon

by Neuroskeptic in Neuroskeptic_Discover

Is neuro-skepticism in danger of going too far? Is it time to take a critical look at critiques of neuroscience? Martha Farah of the University of Pennsylvania says yes, in a Hastings Center Report just published: Brain Images, Babies, and Bathwater: Critiquing Critiques of Functional Neuroimaging Farah covers a broad spectrum of criticisms, ranging from […]The post Brain Scans: Don’t Throw Out The Baby With The Dead Salmon appeared first on Neuroskeptic.... Read more »

  • April 10, 2014
  • 03:56 AM

Gluten exposure and "feelings of depression"?

by Paul Whiteley in Questioning Answers

Could exposure to dietary gluten affect a person's moods or emotional state?Well, if the paper by Simone Peters and colleagues [1] (open-access here) is to be believed the answer may very well be yes, at least in some cases, as they report a link between gluten consumption and feelings of depression under [short-term] experimental conditions. If replicated, such a finding may have profound consequences for how we view our relationship between food and mental health and wellbeing.Bread Ma'am? @ Wikipedia I was initially drawn to the Peters paper as a function not only of the subject matter but also the authorship team. Mention of Jessica Biesiekierski in amongst the list of contributors immediately brought back memories of another ground-breaking paper of hers [2] reporting that "Non-celiac gluten intolerance may exist" (see here).For those who might not know about non-coeliac gluten sensitivity (NCGS), this is a suggestion that outside of the classical connection between gluten and the autoimmune condition coeliac (celiac) disease, there exists something of a spectrum of gluten-related health issues. Some of these issues might have far-reaching implications for an array of conditions including that of autism... at least some autism (see here).The Peters paper is open-access but a few details might be worthwhile mentioning:This was a gold-standard trial in terms of being randomised, double-blind, placebo-controlled and including a cross-over component. What this means is that participants with irritable bowel syndrome (IBS) who were negative for coeliac disease (CD) (though not necessarily tested for the serology of CD) were "asked that they continue on a GFD [gluten-free diet] low in FODMAPS [Fermentable, Oligo-, Di-, Mono-saccharides And Polyols]" for the study duration. Participants were then divided up into groups to receive one of three dietary challenges to their gluten-free diet: gluten supplement (16g/day), whey supplement (16g/day) or placebo for 3 days followed by a wash-out period and then onto the next dietary supplement regime. Neither participants nor researchers knew who got what challenge when.As well as adherence to the gluten-free diet and gastrointestinal (GI) symptoms being assessed, salivary cortisol secretions were measured alongside mental state as per the use of the State Trait Personality Inventory (STPI), a self-report measure.Results: bearing in mind the relatively small participant group examined (n=22) and the various complications one might expect from undertaking a dietary trial, there was an "increase in [the] STPI state depression score following gluten ingestion compared to placebo". The depression scores were also higher when comparing gluten and whey supplements but did not reach statistical significance. No differences were found with regards to cortisol concentrations across the groups and time-frames nor for GI symptoms.The authors conclude that: "Short-term exposure to gluten specifically induced current feelings of depression with no effect on other indices or on emotional disposition". They added: "Such findings might explain why patients with non-coeliac gluten sensitivity feel better on a gluten-free diet despite the continuation of gastrointestinal symptoms".I have to say that as preliminary as these results might be, I'm quite excited at the implications from them. Yes, I have some professional interest in the relationship between gluten and our mental health / psychology and the so-called gut-brain axis (see here) so am perhaps biased, but to see some research utilising the gold-standard of evidence-based medicine coming up with the findings that they did is something rather grand. As per my opening sentences, replication, replication, replication is the next stop and then we can get really excited.I note the authors do speculate on why they got the results they did. Cortisol is kinda ruled out as a cause as a function of their findings of no significant change. I might however draw your attention to other findings in this area which should be kept in mind. Serotonin (5-HT) also gets a mention as a potential explanatory reason, which is also interesting bearing in mind the mood connection with this neurotransmitter with appropriate caveats.Then to some other interesting avenues for further study such as those trillions of beasties which call us and our gut home: the gut microbiota and their potential connection to our mood and psychology (see here). And how about a possible role for gluten exorphins and further the suggestion that opiate antagonists such as naltrexone might be a useful thing to look at? I'd perhaps also be minded to suggest that another possibility not discussed by the authors might be that of intestinal hyperpermeability (leaky gut) also playing a potential role given what we know about gut permeability and gluten [3]. More investigations like this please.----------[1] Peters SL. et al. Randomised clinical trial: gluten may cause depression in subjects with non-coeliac gluten sensitivity – an exploratory randomised clinical study. Alimentary Pharmacology & Therapeutics. 2014. doi: 10.1111/apt.12730[2] Biesiekierski JR. et al. Gluten causes gastrointestinal symptoms in subjects without celiac disease: a double-blind randomized placebo-controlled trial. Am J Gastroenterol. 2011 Mar;106(3):508-14.[3] Vazquez-Roque MI. et al. A controlled trial of gluten-free diet in patients with irritable bowel syndrome-diarrhea: effects on bowel frequency and intestinal function. Gastroenterology. 2013 May;144(5):903-911.e3.----------... Read more »

  • April 10, 2014
  • 12:29 AM

Atheists and Their Capacity for Awe at Life

by Scott McGreal in Eye on Psych

Many people think of awe as a particularly religious emotion and therefore seem to assume that people with no religious beliefs at all, e.g. atheists are closed to the experience of awe. This assumption is quite false and reflects a wider prejudice against atheists. Research has shown that people who reject supernatural beliefs actually are capable of experiencing a sense of awe. In fact, the experience of awe may be particularly beneficial for those who do not believe in an afterlife.... Read more »

join us!

Do you write about peer-reviewed research in your blog? Use to make it easy for your readers — and others from around the world — to find your serious posts about academic research.

If you don't have a blog, you can still use our site to learn about fascinating developments in cutting-edge research from around the world.

Register Now

Research Blogging is powered by SMG Technology.

To learn more, visit