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  • July 4, 2015
  • 05:19 AM

A viral 'cause' of obesity?

by Paul Whiteley in Questioning Answers

I must thank Leah Hardy (@LeahFHardy) for bringing to my attention the paper by Qinglong Shang and colleagues [1] (open-access available here) reporting that: "Ad36 [Human adenovirus 36] infection is associated with an increased risk of obesity development."Based on a meta-analysis of the available research literature examining whether Ad-36 - "a nonenveloped icosahedral virus comprised of double-stranded DNA and is one of 56 serotypes in 7 subgroups of human adenoviruses" - might be linked to obesity, researchers concluded that the weight of evidence from 11 studies did favour "an association between Ad36 infection and a significantly increased risk of obesity development, especially in children." Such findings can be added to other meta-analyses [2] that have also previously suggested that there may be more to see in this 'infectobesity' area [3].I have to say that I was quite unaware of the links being made between Ad-36 and obesity prior to reading the Shang paper. I've previously tackled the idea that the obesity might have some important microbiological links (see here) before on this blog but never considered the possibility of a viral infection as showing involvement until now. Obviously one has to be a little guarded against making any sweeping statements that for example, Ad-36 is the primary cause of all obesity, because in all likelihood the issue is likely to be rather more complex than that. Appreciating that the old 'energy in, energy out' hypothesis is itself likely to be an over-simplification of why we are faced with growing rates of overweight and obesity, I'm sure that Ad-36 probably fits into a rather large jigsaw puzzle - somewhere. The requirement for a greater understanding of the hows and whys of any viral - obesity link is also strong alongside the idea that even if proved, any viral link should not absolve responsibility for eating and exercising right as part of maintaining a healthy weight.Research such as that from Berger and colleagues [4] suggesting that "Ad36(+) may be associated with biomarkers implicated in inflammation but not with greater levels of fat mass" offers some cautionary data on why there may be quite a bit more research needed looking at Ad-36 and obesity. If one considers that inflammation seems to be part and parcel of obesity, the whole thing starts to get quite a bit more complicated.Still, if science does start to get closer to the idea that Ad-36 (or other agents) might indeed heightened the risk of obesity and perhaps even suggest 'transferability' from person-to-person, this may open up new ways of tackling this issue [5] even with the prospect of immunising against infection-induced weight gain [6].Music: Babies by Pulp.----------[1] Shang Q. et al. Serological data analyses show that adenovirus 36 infection is associated with obesity: a meta-analysis involving 5739 subjects. Obesity (Silver Spring). 2014 Mar;22(3):895-900.[2] Yamada T. et al. Association of Adenovirus 36 Infection with Obesity and Metabolic Markers in Humans: A Meta-Analysis of Observational Studies. PLoS One. 2012; 7(7): e42031.[3] Valiquette L. et al. A microbiological explanation for the obesity pandemic? Can J Infect Dis Med Microbiol. 2014 Nov-Dec;25(6):294-5.[4] Berger PK. et al. Association of adenovirus 36 infection with adiposity and inflammatory-related markers in children. J Clin Endocrinol Metab. 2014 Sep;99(9):3240-6.[5] Esposito S. et al. Adenovirus 36 infection and obesity. J Clin Virol. 2012 Oct;55(2):95-100.[6] Na HN. & Nam JH. Proof-of-concept for a virus-induced obesity vaccine; vaccination against the obesity agent adenovirus 36. Int J Obes (Lond). 2014 Nov;38(11):1470-4.----------Shang Q, Wang H, Song Y, Wei L, Lavebratt C, Zhang F, & Gu H (2014). Serological data analyses show that adenovirus 36 infection is associated with obesity: a meta-analysis involving 5739 subjects. Obesity (Silver Spring, Md.), 22 (3), 895-900 PMID: 23804409... Read more »

  • July 3, 2015
  • 04:37 PM

REM sleep critical for young brain development; medication interferes

by Dr. Jekyll in Lunatic Laboratories

Rapid eye movement or REM sleep actively converts waking experiences into lasting memories and abilities in young brains reports a new study. The finding broadens the understanding of children’s sleep needs and calls into question the increasing use of REM-disrupting medications such as stimulants and antidepressants.

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Michelle C. Dumoulin Bridi, Sara J. Aton, Julie Seibt, Leslie Renouard, Tammi Coleman1, & Marcos G. Frank. (2015) Rapid eye movement sleep promotes cortical plasticity in the developing brain. Science Advances. info:/10.1126/sciadv.1500105

  • July 3, 2015
  • 11:47 AM

Smile at a party and people are more likely to remember seeing your face there

by BPS Research Digest in BPS Research Digest

When you smile at a party, your facial expression is emotionally consistent with the happy context and as a consequence other guests will in future be more likely to remember that they've seen your face before, and where you were when they saw you. That's according to a team of Italian researchers led by Stefania Righi who have explored how memory for a face is affected by the emotion shown on that face and the congruence between that emotional expression and its surrounding context.The researchers first presented 30 participants (11 men) with 64 unfamiliar face and scene pairings. The faces were either smiling or fearful and they were either presented alongside an image of a happy scene (e.g. a party) or a fear-inducing scene (e.g. a car crash). The participants' task at this stage was simply to indicate whether each face-scene pairing was emotionally congruent or not.Next came the memory test. Different faces (some previously seen, some new) were flashed up on-screen against a black background and the participants had to say whether they'd seen the face before or if it was entirely new. After each face, three scenes appeared of the same genre (e.g. three party scenes), and the participants had to say which specific scene the face had previously appeared alongside.Previously seen happy faces were better remembered than fearful faces, but only when they appeared alongside a happy scene. Memory for fearful faces, by contrast, was unaffected by the congruence of the accompanying scene. Why should smiling faces at a party or other happy context be better remembered than a fearful face? The researchers think the combination of a smiling face and happy scene has a broadening effect on observers' attention, enhancing their memories for the face. From a methodological point of view, it's shame the study didn't also feature neutral faces: without these, we can't be certain whether smiling faces in a happy context were enhancing memory or if fearful faces in that context were harming memory, or a bit of both.Figure 3 from Righi et al, 2015.The researchers also propose that smiling faces have a "unitising effect" whereby the face and its context are bound together in memory. This idea also appeared to be supported by the results: participants were better at remembering the accompanying scenes (happy and fearful) for smiling faces than fearful faces.Put these two key results together and it means that we're particularly likely to remember a smiling face we saw at a party, and the specific context we saw it in. Righi and her colleagues said it made sense for memory to work this way. "A smiling person communicates a social bond and the ability to remember, not only the face identity, but also the context of the first encounter with that 'potential friend', could reflect an adaptive behaviour in view of future social relations." The new results also complement past research on memory for face-name pairings: presented with a name, participants were better at remembering when it was earlier paired with a happy face than a neutral one._________________________________ Righi, S., Gronchi, G., Marzi, T., Rebai, M., & Viggiano, M. (2015). You are that smiling guy I met at the party! Socially positive signals foster memory for identities and contexts Acta Psychologica, 159, 1-7 DOI: 10.1016/j.actpsy.2015.05.001 Post written by Christian Jarrett (@psych_writer) for the BPS Research Digest.

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  • July 3, 2015
  • 09:55 AM

Evidence for "Unconscious Learning" Questioned

by Neuroskeptic in Neuroskeptic_Discover

Can we learn without being aware of what we're learning? Many psychologists say that 'unconscious', or implicit, learning exists.

But in a new paper, London-based psychologists Vadillo, Konstantinidis, and Shanks call the evidence for this into question.

Vadillo et al. focus on one particular example of implicit learning, the contextual cueing paradigm. This involves a series of stimulus patterns, each consisting of a number of "L" shapes and one "T" shape in various orientations. For ... Read more »

  • July 3, 2015
  • 06:02 AM

5 Tips For Better Sleep

by Elisabeth Buhl Thubron in United Academics

Adding some ‘worry time’ to your day could work better than pills.... Read more »

  • July 3, 2015
  • 04:56 AM

Vitamin D metabolic gene variants and risk for autism

by Paul Whiteley in Questioning Answers

I was really rather happy to see the "preliminary evidence" reported by Rebecca Schmidt and colleagues [1] when it came to examining whether selected vitamin D metabolic gene variants might show linkage to autism spectrum disorder (ASD) based on data derived from the CHARGE initiative.For quite a while now I've discussed the various peer-reviewed science on the topic of vitamin D deficiency / insufficiency with autism in mind on this blog (see here and see here for example). Specifically, how a diagnosis of ASD seems to offer little protection against issues with vitamin D appearing and what that could mean for important issues such as bone health (see here) for example.A key component that seemed to be missing from the growing volume of research looking at vitamin D and autism was some discussion about whether the genetics of vitamin production and usage might offer some further clues to how vitamin D might more directly be 'linked' to [some] autism. Schmidt et al have started to put some flesh on to the scientific bones in this area following their previous research discussions on vits and SNPs with autism in mind (see here) .So: "Maternal, paternal, and child DNA samples for 384 (81%) families of children with ASD and 234 (83%) families of TD [typically developing] children were genotyped for: TaqI, BsmI, FokI, and Cdx2 in the vitamin D receptor (VDR) gene, and CYP27B1 rs4646536, GC rs4588, and CYP2R1 rs10741657." In effect, researchers looked for potential genetic 'issues' with the vitamin D receptor (VDR) gene that have previously been linked to various health issues. They found some potentially interesting information including: "Paternal VDR TaqI homozygous variant genotype was significantly associated with ASD in case-control analysis." Homozygous by the way, refers to the concept of zygosity and the fact we have pairs of chromosomes. Further: "A significant association between decreased ASD risk and child CYP2R1 AA-genotype was found in hybrid log-linear analysis."This is early days research insofar as the genetics of vitamin D and autism only being mentioned once before in the research literature as per the report from Yan and colleagues [2]. I'm excited at the Schmidt data but am not going to go all out on this very preliminary inspection of vitamin D receptor gene functioning without further large-scale replication and validation studies being carried out including discussions on things like cognitive ability in light of other recent data [3]. Whilst we are however, on the topic of vitamin D and its potential extra-skeletal activities, I'm minded to also bring in the paper by Kaneko and colleagues [4] and their results implying that "vitamin D affects brain serotonin concentrations" with mention of autism among other labels. Reporting on a particularly interesting enzyme - tryptophan hydroxylase (TPH)2 - which has an important role in serotonin metabolism (see here) I'll be watching closely on how vitamin D research with autism in mind also develops in this area.And then there are the Raftery results [5] to bring to your attention putting further scientific flesh on to the bones about the possibility of a relationship between vitamin D levels and intestinal permeability (see here). Given what has been mentioned about 'leaky gut' and autism in the peer-reviewed literature so far (see here) one might also add this to further investigations in this area...Music: I am the Monarch of the Sea.----------[1] Schmidt RJ. et al. Selected vitamin D metabolic gene variants and risk for autism spectrum disorder in the CHARGE Study. Early Hum Dev. 2015 Jun 11;91(8):483-489.[2] Yan J. et al. Vitamin D receptor variants in 192 patients with schizophrenia and other psychiatric diseases. Neurosci Lett. 2005 May 20-27;380(1-2):37-41.[3] Jorde R. et al. Vitamin D and cognitive function: The Tromsø Study. J Neurol Sci. 2015 Jun 7. pii: S0022-510X(15)00350-0.[4] Kaneko I. et al. 1,25-Dihydroxyvitamin D regulates expression of the tryptophan hydroxylase 2 and leptin genes: implication for behavioral influences of vitamin D. FASEB J. 2015 Jun 12. pii: fj.14-269811.[5] Raftery T. et al. Effects of vitamin D supplementation on intestinal permeability, cathelicidin and disease markers in Crohn's disease: Results from a randomised double-blind placebo-controlled study. United European Gastroenterol J. 2015 Jun;3(3):294-302.----------Schmidt RJ, Hansen RL, Hartiala J, Allayee H, Sconberg JL, Schmidt LC, Volk HE, & Tassone F (2015). Selected vitamin D metabolic gene variants and risk for autism spectrum disorder in the CHARGE Study. Early human development, 91 (8), 483-489 PMID: 26073892... Read more »

Schmidt RJ, Hansen RL, Hartiala J, Allayee H, Sconberg JL, Schmidt LC, Volk HE, & Tassone F. (2015) Selected vitamin D metabolic gene variants and risk for autism spectrum disorder in the CHARGE Study. Early human development, 91(8), 483-489. PMID: 26073892  

  • July 2, 2015
  • 08:00 AM

Want Better Group Performance? Try a Standing Meeting

by Jeremiah Stanghini in Jeremiah Stanghini

In keeping with the theme of “standing” being better for us from earlier this week, I thought I’d tackle another journal article discussing the merits of standing. This time, the research included participants well-beyond the 2nd and 3rd grade, but still used students … Continue reading →... Read more »

  • July 2, 2015
  • 05:36 AM

How social anxiety manifests on Facebook

by BPS Research Digest in BPS Research Digest

For many shy people, online social networking sites have an obvious appeal – a way to socialise without the unpredictable immediacy of a face-to-face encounter. However, a new study finds that people who are socially anxious betray their awkwardness on Facebook, much as they do in the offline world. The researchers Aaron Weidman and Cheri Levinson said their findings could hint at ways for socially anxious people to conceal their nervousness and attract more online friends.Seventy-seven students (average age 19; 77 per cent of them female) completed a measure of social anxiety. High scores were given to those who agreed with statements like "I have difficulty talking with other people" and "I am tense mixing in a group". Before the students left the psych lab, the researchers took screen grabs of their Facebook pages.Several aspects of the students' Facebook pages correlated with their social anxiety scores. Unsurprisingly perhaps, those with fewer Facebook friends had higher social anxiety scores, so too did those who showed their relationship status as "single" (versus married or status not shown) and those whose page did not show a status update or quote (a sign of self-disclosure). These markers largely reflect offline signs of social anxiety – it's well established for example that people who are socially anxious share less information and tell fewer stories in conversation.So, socially anxious people betray signs of their personalities on their Facebook pages, but would a stranger looking at their page pick up on these cues? Next, the researchers showed the students' Facebook pages to six other students and asked them to rate the social anxiety of the owners of the pages (if the observing students recognised any of the people in the Facebook pages, they didn't rate those pages).There was a modest correlation between the observers' ratings of the Facebook owners' social anxiety and the owners' actual (self-reported) social anxiety scores. The observers picked up on some cues correctly, including lack of Facebook friends. But other cues they misread. Observers tended to rate Facebook pages with fewer photos and fewer people in the profile photo as more socially anxious, even though neither of these factors actually correlated with the owners' social anxiety scores. Observers also failed to pick up on the significance of a lack of self-disclosure or the owners' relationship status. Unfortunately, some of the tell-tale signs of social anxiety can lead shy people to appear awkward and to make a negative impression on people they meet – the very outcome that they fear. These new results suggest the same problem may apply on Facebook, but they also point at a way to help by addressing the signs that strangers will read as evidence of social awkwardness.The researchers said people high in social anxiety "may benefit from interventions aimed at forcing them to befriend more individuals on Facebook, post more photos of themselves, and to choose a profile picture that depicts them in the presence of others, all of which might cause observers to view [them] more positively as potential friends."_________________________________ Weidman, A., & Levinson, C. (2015). I’m still socially anxious online: Offline relationship impairment characterizing social anxiety manifests and is accurately perceived in online social networking profiles Computers in Human Behavior, 49, 12-19 DOI: 10.1016/j.chb.2014.12.045 --further reading--The Psychology of Facebook, DigestedPost written by Christian Jarrett (@psych_writer) for the BPS Research Digest.

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  • July 2, 2015
  • 02:34 AM

Acute bipolar depression and immune alterations

by Paul Whiteley in Questioning Answers

"Individuals with acute bipolar depression show immune alterations. Some of the alterations are similar to those found in acute mania."That was the bottom line reported by Faith Dickerson and colleagues [1] following their analysis of blood samples provided by "82 individuals with acute bipolar depression, 147 with acute mania, and 280 controls." Looking for the presence of various antibodies to "human herpesviruses, gliadin, Toxoplasma gondii, and endogenous retroviruses as well as for C-reactive protein (CRP) and pentraxin-3" in said samples, researchers reported a few potentially important findings.So: "The levels of CRP and IgG antibodies to an endogenous retrovirus, Mason-Pfizer monkey virus (MPMV), were significantly elevated in the bipolar depressed group." Further: "Levels of pentraxin-3 were reduced in both psychiatric groups." Researchers also reported that for 32 individuals who were hospitalised (and I assume treated) for bipolar depression, they "showed a significant decrease in the levels of MPMV antibodies, but not a change in the other markers."Looking through the list of antigens included for analysis, without looking at the authorship list, I could have told you that the authors Faith Dickerson and/or Robert Yolken were involved in this study based on what has been discussed before on this blog (see here and see here for example). The work coming out of Johns Hopkins has been particularly interesting with their focus on "the role of infectious and inflammatory processes in complex psychiatric disease such as schizophrenia, bipolar disorder, and autism." Their most recent work on pentraxin-3 looks very interesting indeed (see here) and complements their most recent results.The finding of elevations in the levels of CRP in the "bipolar depressed group" fits in well with the idea of inflammation being somehow involved in psychiatry (see here) and seemingly crossing diagnostic labels (see here). One might reasonable ask whether the research voices are indeed getting stronger for the potential usefulness of 'treating inflammation' when it comes to something like depression (see here) bearing in mind no clinical or medical advice is given or intended.Finally, is that "endogenous retrovirus" finding reported by Dickerson et al. Regular readers of this blog might already know that I'm an avid [amateur] follower of the idea that all those fossil viruses that lurk in our genomes might be some much more than just junk DNA. With schizophrenia in mind (see here), with attention-deficit hyperactivity disorder (ADHD) in mind (see here), with autism in mind (see here), even with chronic fatigue syndrome / myalgic encephalomyelitis (CFS/ME) in mind (see here), I've covered the topic a few times on this blog. Although never coming across MPMV before, this is not the first time that antibodies to non-human primate viruses have been talked about with psychiatric / behavioural conditions in mind [2]. Indeed a previous paper from Dickerson and colleagues [3] even went as far as suggesting that as part of suite of inflammatory markers, the presence and elevation of MPMV antibodies is likely derived "from the activation of homologous endogenous retroviruses and to be a reflection of immune activation." Similar sentiments seem to carry over to the most recent results too.Music: Doves - There Goes The Fear.----------[1] Dickerson F. et al. Immune alterations in acute bipolar depression. Acta Psychiatr Scand. 2015 Jun 9.[2] Lillehoj EP. et al. Serum antibodies reactive with non-human primate retroviruses identified in acute onset schizophrenia. J Neurovirol. 2000 Dec;6(6):492-7.[3] Dickerson F. et al. A combined marker of inflammation in individuals with mania. PLoS One. 2013 Sep 3;8(9):e73520.----------Dickerson F, Katsafanas E, Schweinfurth LA, Savage CL, Stallings C, Origoni A, Khushalani S, Lillehoj E, & Yolken R (2015). Immune alterations in acute bipolar depression. Acta psychiatrica Scandinavica PMID: 26061032... Read more »

Dickerson F, Katsafanas E, Schweinfurth LA, Savage CL, Stallings C, Origoni A, Khushalani S, Lillehoj E, & Yolken R. (2015) Immune alterations in acute bipolar depression. Acta psychiatrica Scandinavica. PMID: 26061032  

  • July 1, 2015
  • 02:19 PM

New epigenetic mechanism revealed in brain cells

by Dr. Jekyll in Lunatic Laboratories

For decades, researchers in the genetics field have theorized that the protein spools around which DNA is wound, histones, remain constant in the brain, never changing after development in the womb. Now, researchers from the Icahn School of Medicine at Mount Sinai have discovered that histones are steadily replaced in brain cells throughout life – a process which helps to switch genes on and off.... Read more »

Maze, I., Wenderski, W., Noh, K., Bagot, R., Tzavaras, N., Purushothaman, I., Elsässer, S., Guo, Y., Ionete, C., Hurd, Y.... (2015) Critical Role of Histone Turnover in Neuronal Transcription and Plasticity. Neuron, 87(1), 77-94. DOI: 10.1016/j.neuron.2015.06.014  

  • July 1, 2015
  • 06:24 AM

Offspring autism risk and advancing parental age (differences)

by Paul Whiteley in Questioning Answers

Parental age at offspring conception/birth in relation to offspring autism risk has been a recurrent theme in autism research circles for quite a few years now. I've covered it more than once on this blog (see here for example) and the various suggestions that advancing parental age in particular, might elevate the risk of offspring autism.Set in this context, the paper by Sven Sandin and colleagues [1] (open-access) (a name not unfamiliar to this blog) adds to the research evidence based on their analysis of some 5.7 million children born between 1985 - 2004 resident in one of five countries (Denmark, Israel, Norway, Sweden and Western Australia). Including data on some 30,000 children diagnosed with an autism spectrum disorder (ASD): "Parental ages, sex and birth year were obtained from birth or civil registers."After quite a bit of statistical modelling and controlling for various potentially confounding variables, several findings were reported pertinent to the authors' data being "the strongest evidence to date supporting the hypothesis that advanced parental ages at the time of birth are independently associated with risk for ASD in the offspring." Outside of "no support for any modification by the sex of the child" researchers also noted a "combined parental age effect" whereby there "was a joint effect of maternal and paternal age with increasing risk of ASD for couples with increasing differences in parental ages."A few of the finer details of this study have been covered elsewhere (see here). I'll draw your attention to one or two statistics unearthed during the study:"relative to fathers aged 20–29 years, fathers 50 years or older had a statistically significantly increased risk for offspring with ASD (RR=1.66 95% CI:1.49–1.85)","Relative to mothers aged 20–29 years, mothers younger than 20 years had a statistically significantly increased risk for offspring with ASD (RR=1.18 95% CI:1.08–1.29)" and the "lowest risk corresponded to couples that generated the majority of births, specifically, 29–39-year-old fathers and 25–35-year-old mothers." Those estimates of relative risk (RR) statistics translate into an estimated 66% increased risk for offspring autism if a dad was over 50 years old compared with a dad in their 20s, an 18% increased risk for offspring autism for teen mums compared to 20-something mums and the lowest statistical risk of offspring autism being reported when dads conceive in their 30s coupled with a mid-20 to mid-30 year old mum. The authors also note that "Similar patterns of association, but with slightly higher RRs for the highest parental ages, were evident for AD [autistic disorder]" so completing the message about older parental ages at conception and differing parental ages being relevant across the autism spectrum.Accepting that this was a huge study in terms of participant numbers and spanning different geographical locations, the authors rightly offer a few words of caution about their methods and data. So: "we lack information about potentially confounding variables such as SES [socio-economic status] and parental psychiatric history" is something to keep in mind [2]. Further: "We cannot rule out the possibility that other factors associated with parental age (for example, length of marriage or partnership, obstetric complications, gestational age and birth weight) have an important role in explaining our results" and "We did not have individual level information on co-morbid ID [intellectual disability] in ASD cases." I'd also suggest that given the growing emphasis on autism or ASD not existing in some sort of diagnostic vacuum (see here) one might reasonably ask whether other comorbidity outside of ID might also play a role in risk estimates.As to the possible mechanism(s) of effect, well, the authors go through the usual older parents - older sperm and eggs mantra although perhaps bypassing an emerging area outside of just de novo mutations based on the role of epigenetic mechanisms (see here). They do suggest that the 'difference in parental age' factor might suggest "that the increase in risk is not attributable to advancing parental age per se, and that the risk increase cannot be explained solely by an accumulation of point mutations or other genomic alterations in the parents" but say little more on the basis of their collected data.I might be wrong but I also didn't seem too much in the way of discussion of how parental nutrition might impact on offspring autism risk as per the proposed factor from other work by authors on the Sandin paper in relation to the inter-pregnancy interval (IPI) and autism risk (see here and see here). Although the idea that parental age might affect autism offspring risk, I'd be minded to suggest that this is only the first stage in a journey towards elucidating the particular mechanisms of any effect.Music: The Pixies - Gigantic.----------[1] Sandin S. et al. Autism risk associated with parental age and with increasing difference in age between the parents. Mol Psychiatry. 2015 Jun 9.[2] Lehti V. et al. Maternal socio-economic status based on occupation and autism spectrum disorders: A national case-control study. Nord J Psychiatry. 2015 Mar 3:1-8.----------Sandin S, Schendel D, Magnusson P, Hultman C, Surén P, Susser E, Grønborg T, Gissler M, Gunnes N, Gross R, Henning M, Bresnahan M, Sourander A, Hornig M, Carter K, Francis R, Parner E, Leonard H, Rosanoff M, Stoltenberg C, & Reichenberg A (2015). Autism risk associated with parental age and with increasing difference in age between the parents. Molecular psychiatry PMID: 26055426... Read more »

Sandin S, Schendel D, Magnusson P, Hultman C, Surén P, Susser E, Grønborg T, Gissler M, Gunnes N, Gross R.... (2015) Autism risk associated with parental age and with increasing difference in age between the parents. Molecular psychiatry. PMID: 26055426  

  • July 1, 2015
  • 04:45 AM

What kind of a person volunteers for a free brain scan?

by BPS Research Digest in BPS Research Digest

When psychologists scan the brains of a group of people, they usually do so in the hope that the findings will generalise more widely. For example, if they find that there are correlations between localised brain shrinkage and mental performance in a group of healthy older participants, they will usually infer that such correlations apply in healthy older people more generally. But there's an important problem with this logic (one that applies to other fields of psychology): what if the people who volunteer for brain scans are systematically different from those who don't?To explore this issue, Mary Ganguli and her colleagues turned to 1,982 older participants (aged 65+) who were participating in a large, long-running study into ageing. This study excluded participants who were severely mentally impaired or in long-term care.Helpfully, the researchers already had a good deal of data from all the participants, including their demographics, health and mental skills. Next they asked the participants if they'd be interested in taking part in a free brain scan study at their local hospital in return for a cash incentive.Nearly half the sample (46.2 per cent) stated flat out that they would not be interested. The others gave answers ranging from definitely to maybe. Those who expressed an interest in volunteering for a brain scan differed from those who were definitely not keen in many ways: the willing were more likely to be younger, male, better educated, married, employed, free from depressive symptoms, mentally fitter, subjectively healthier, on fewer meds and living unsupervised. There were no differences between the groups in terms of subjective memory concerns or ethnicity.Next, the researchers conducted an actual brain scan on 48 of those participants who'd expressed an earlier interest. This revealed the expected correlations between grey matter volume in specific brain areas and cognitive performance.Now the researchers made some adjustments so that the results from each brain scan participant were weighted according to how similar they were to the averaged group of 1,982 participants involved in the larger ageing study. This was a proof of principle, to see if it's possible to correct for the bias introduced by relying on volunteers rather than truly random samples. The adjustment certainly made a difference to the findings – now grey matter volume in fewer regions showed correlations with cognitive test scores, which the researchers attributed to a reduction in bias.This isn't the most exciting brain scan study you'll read about this year, and the specific findings might only apply to older adults, but it addresses an important issue in neuroimaging and contributes to the gradual refining of psychological methods, helping our science become more reliable by avoiding biased results._________________________________ Ganguli, M., Lee, C., Hughes, T., Snitz, B., Jakubcak, J., Duara, R., & Chang, C. (2015). Who wants a free brain scan? Assessing and correcting for recruitment biases in a population-based sMRI pilot study Brain Imaging and Behavior, 9 (2), 204-212 DOI: 10.1007/s11682-014-9297-9 --further reading--Just how representative are the people who volunteer for psychology experiments?Beware the "super well" - why the controls in psychology research are often too healthyHow burnt-out students could be skewing psychology researchPost written by Christian Jarrett (@psych_writer) for the BPS Research Digest.

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  • July 1, 2015
  • 01:43 AM

Technologies and Generations

by Aurametrix team in Health Technologies

Children no longer obey their parents; every man wants to write a book and the end of the world is evidently approaching. So said a clay tablet inscribed almost 5 thousand years ago. But the world still stands, although we do go through golden and dark ages and societies rise and fall. Technology's golden age is now. or so we hope. How are current generations influenced by it and how will they shape the future world? Even as they age, Baby Boomers embrace emerging technologies such as smartphones and social networking. They will be the driving and demanding force behind innovation in healthcare. In the past, they drove economy by spending and borrowing, boosting housing and stock prices, increasing demand for products and services. Then the bubble burst. America's neglected middle child, Generation X is now the quiet driving force behind enterprise, media and information consumption. Xers endured lots of destruction, but were able to adapt and sparked a renaissance of entrepreneurship. They bring to the table a significant amount of buying power, but are less eager to spend money. Nielsen poll suggests they prefer a good deal over a social statement with their purchase.Millennial Generation, alternatively dubbed the Net Generation, Generation Y (or Why?), Echo-boomers, Nexters, and Digital Natives is now the largest generation in U.S history. Fueled by immigration, they outgrew the outsized Baby Boomer population and continue to grow.  Raised on a steady diet of video games, in a world where almost everything can be done with an app, fanned by economic slowdown, they are choosing to live differently and embrace the sharing economy. Since the second world war, purchases of new cars and suburban houses have propelled economic recoveries. Millennials may have lost interest in both, spending on smartphones instead. "The cheapest generation" burdened by student loans is renting instead of buying. They are demanding better integration of technology into public services, prefer healthy, natural, socially and environmentally conscious products.Perhaps auto brands and home builders just need to leverage mobile and environmental sustainability to attract this generation? Manufacturers do think so trying to turn cars into "giant docking stations with wheels". Tesla is one example of a brand adapting to millennials - and it's the top automotive stock among this generation. What about smart residences? Companies are betting on the Internet of Things - embedding objects we interact with in daily lives with electronics, software, sensors and connectivity. One-in-four Millennials (23%) already installed at least one of these products in their homes, compared to 12% of the total population. But building a true "smart home" - like the one owned by the Jetson's  -  integrating and managing multiple devices, and dealing with their eminent malfunctions needs a a lot of patience. Perhaps companies like IOTAS - creating smart homes for today's renters  - have taken the right first step? In the coming years, current generations will serve as a testbed for emerging technology concepts. Millennials will continue to drive the growth in the Internet of Things, connected cars and wearables markets. Generation Z will inherit technology rigorously honed through human testing. What will be their signature product and signature means of communication? We'll know soon enough.No doubt, we live in interesting timesJoin our conference "The Rise of the Millenials – Emerging Disruptive Trends". It will take place on September 19th 2015, at the Intel Auditorium in Santa Clara. REFERENCESPutre L (2013). The march of the Millenials. Your hospital staff in 2025: the same, only different. Hospitals & health networks / AHA, 87 (9) PMID: 24260968The “Not so Young” Millennial Consumer“Americans and their gadgets” (2010) ... Read more »

Costanza, D., Badger, J., Fraser, R., Severt, J., & Gade, P. (2012) Generational Differences in Work-Related Attitudes: A Meta-analysis. Journal of Business and Psychology, 27(4), 375-394. DOI: 10.1007/s10869-012-9259-4  

Becton, J., Walker, H., & Jones-Farmer, A. (2014) Generational differences in workplace behavior. Journal of Applied Social Psychology, 44(3), 175-189. DOI: 10.1111/jasp.12208  

  • July 1, 2015
  • 12:05 AM

The Power of the Mind May not be as Well Utilized as it could be

by Kyle Harris in Sports Medicine Research (SMR): In the Lab & In the Field

Of 1283 survey respondents, only 27% of athletes reported using mental skills such as goal setting, positive self-talk, imagery, and relaxation. Of the 249 respondents who used mental skills 72% reported they felt it helped expedite their recovery process.... Read more »

Arvinen-Barrow M, Clement D, Hamson-Utley JJ, Zakrajsek RA, Lee SM, Kamphoff C, Lintunen T, Hemmings B, & Martin SB. (2015) Athletes' use of mental skills during sport injury rehabilitation. Journal of Sport Rehabilitation, 24(2), 189-97. PMID: 25996227  

  • June 30, 2015
  • 02:56 PM

Women’s faces get redder at ovulation, but human eyes can’t pick up on it

by Dr. Jekyll in Lunatic Laboratories

Previous studies have shown that men find female faces more attractive when the women are ovulating, but the visual clues that allow this are unclear. Now, new research investigating whether it might be to do with subtle changes in skin colour has shown that women’s faces do increase in redness during ovulation, but the levels of change are just under the detectable range of the human eye.... Read more »

Hannah Rowland, & Robert Burriss. (2015) Women’s faces get redder at ovulation, but human eyes can’t pick up on it. PLOS ONE. info:/

  • June 30, 2015
  • 10:43 AM

What the textbooks don't tell you about psychology's most famous case study

by BPS Research Digest in BPS Research Digest

Image: Photograph by Jack Wilgus ofa daguerreotype of Phineas Gagein the collection of Jack and Beverly Wilgus.It's a remarkable, mythical tale with lashings of gore – no wonder it's a favourite of psychology students the world over. I'm talking about Phineas Gage, the nineteenth century railway worker who somehow survived the passing of a three-foot long tamping iron through the front of his brain and out the top of his head. What happened to him next?If you turn to many of the leading introductory psychology textbooks (American ones, at least), you'll find the wrong answer, or a misleading account. Richard Griggs, Emeritus Professor of Psychology at the University of Florida, has just analysed the content of 23 contemporary textbooks (either released or updated within the last couple of years), and he finds most of them contain distortions, omissions and inaccuracies.It needn't be so. Thanks to painstaking historical analysis of primary sources (by Malcolm Macmillan and Matthew Lena) – much of it published between 2000 and 2010 – and the discovery during the same time period of new photographic evidence of post-accident Gage (see image, right), it is now believed that Gage made a remarkable recovery from his terrible injuries. He ultimately emigrated to Chile where he worked as a horse-coach driver, controlling six horses at once and dealing politely with non-English speaking passengers. The latest simulations of his injury help explain his rehabilitation – it's thought the iron rod passed through his left frontal lobe only, leaving his right lobe fully intact.Image: From Van Horn et al 2012Yet, the textbooks mostly tell a different story. Of the 21 that cover Gage, only 4 mention the years he worked in Chile. Only three detail his mental recovery. Fourteen of the books tell you about the first research that attempted to identify the extent of his brain injuries, but just four of the books give you the results from the most technically advanced effort, published in 2004, that first suggested his brain damage was limited to the left frontal lobe (watch video). Only 9 of the books feature either of the two photos to have emerged of Gage in recent times.So the textbooks mostly won't tell you about Gage's rehabilitation, or provide you with the latest evidence on his injuries. Instead, you might hear how hear never worked again and became a vagrant, or that he became a circus freak for the rest of his life, showing off the holes in his head. "The most egregious error," says Griggs, "seems to be that Gage survived for 20 years with the tamping iron embedded in his head!".Does any of this matter? Griggs argues strongly that it does. There are over one and half million students enrolled in introductory psychology courses in the US alone, and most of them are introduced to the subject via textbooks. We know from past work that psychology textbook coverage of other key cases and studies is also often distorted and inaccurate. Now we learn that psychology's most famous case study is also misrepresented, potentially giving a misleading, overly simplistic impression about the effects of Gage's brain damage. "It is important to the psychological teaching community to identify inaccuracies in our textbooks so that they can be corrected, and we as textbook authors and teachers do not continue to 'give away' false information about our discipline," Griggs concludes._________________________________ Griggs, R. (2015). Coverage of the Phineas Gage Story in Introductory Psychology Textbooks: Was Gage No Longer Gage? Teaching of Psychology, 42 (3), 195-202 DOI: 10.1177/0098628315587614 --further reading--Phineas Gage - Unravelling the MythCoverage of Phineas Gage in "Great Myths of the Brain"Foundations of Sand - the lure of academic myths and their place in classic psychology.Post wr... Read more »

  • June 30, 2015
  • 05:06 AM

Low glycemic index diet reduces symptoms of mouse autism

by Paul Whiteley in Questioning Answers

A quote to begin: "Overall, the manuscript supports the idea that ASD [autism spectrum disorder] results from gene–environment interactions and that in the presence of a genetic predisposition to ASD, diet can make a large difference in the expression of the condition."The manuscript in question was by Antonio Currais and colleagues [1] reporting some rather interesting results based on the 'dangermouse' that is the BTBR mouse model of autism. Researchers from the Salk Institute for Biological Studies showed that "the dietary glycemic index has a significant impact on the ASD phenotype." The dietary glycemic index (GI) by the way, is concerned with how particular foods / foodgroups affect blood glucose levels and the crux of the research was to see what happened to pregnant mice when fed either a high GI or low GI diet in terms of offspring outcomes. Offspring also followed the same diet diet post weaning.To quote from the paper and some associated media: "The two groups of animals consumed the same number of calories and were identical in weight. But mice that ate a high-glycemic index diet showed all of the expected behavioral symptoms of autism. Their social interactions were impaired, they repeated actions that served no apparent purpose, and they groomed extensively."Various other differences were present across the different dieting mice as per the findings that: "diet modulates plasma metabolites, neuroinflammation and brain markers of neurogenesis in a manner that is highly reflective of ASD in humans." This included the finding that "the brains of the high-glycemic index diet mice appeared to have greater numbers of activated microglia, the resident immune cells of the brain" and various inflammation-related genes being more readily expressed in comparison to the low-glycemic index diet mice. Microglia and autism remains a complex topic (see here) but with the advent of recent research findings [2] complete with headlines such as ''Missing link' between brain and immune system discovered' I dare say that we'll be hearing more about this is times to come.The compound doublecortin also receives a mention in the Currais results as per the suggestion that those mice living on the high-glycemic diet had less of the stuff and the significance of this finding given the link between doublecortin and neurogenesis for example [3]. Bearing in mind the BTBR mouse model of autism might already be more prone to reductions in the levels of doublecortin [4] it might be useful to see how this finding pans out when applied to real people in the real world."The new study found that the diet might directly influence the ecosystem of bacteria in the gut." It perhaps goes without saying that any sort of dietary change is likely to affect the composition of those trillions of wee beasties that call our gastrointestinal (GI) tract home. This also applies to mice and probably every other type of animal. "'We were really surprised when we found molecules in the blood that others had reported could only be generated by gut bacteria,' Maher says. 'There were big differences in some of these compounds between the two diets.'" Metabolites of gut bacteria found in general circulation... does this imply intestinal permeability (leaky gut) might be part and parcel of any effect? If so, would that perhaps also tie into the findings reported by Elaine Hsaio and colleagues a while back on leaky mice guts, gut bacteria and autism? Add in also the idea that high glycemic index foods tend to include things like wheat and various other grains and we start to get something looking rather familiar to autism research that may well show some relationship [5]."The group plans to analyze the gut bacteria, and its potential link with features of autism, more directly. They also hope to better understand the role of inflammation in the ability to generate new neurons." I'm very much looking forward to seeing these results, bearing in mind that mice are mice not people [6] and autism (or rather the autisms) is/are [a] very complicated condition(s).Music: The Jesus And Mary Chain - Just Like Honey.----------[1] Currais A. et al. Dietary glycemic index modulates the behavioral and biochemical abnormalities associated with autism spectrum disorder. Molecular Psychiatry. 2015. June 9.[2] Louveau A. et al. Structural and functional features of central nervous system lymphatic vessels. Nature. 2015 Jun 1.[3] Couillard-Despres S. et al. Doublecortin expression levels in adult brain reflect neurogenesis. Eur J Neurosci. 2005 Jan;21(1):1-14.[4] Stephenson DT. et al. Histopathologic characterization of the BTBR mouse model of autistic-like behavior reveals selective changes in neurodevelopmental proteins and adult hippocampal neurogenesis. Mol Autism. 2011 May 16;2(1):7.[5] Lammers KM. et al. Gliadin induces an increase in intestinal permeability and zonulin release by binding to the chemokine receptor CXCR3. Gastroenterology. 2008 Jul;135(1):194-204.e3.[6] Wong AH. & Josselyn SA. Caution When Diagnosing Your Mouse with Schizophrenia: The Use and Misuse of Model Animals for Understanding Psychiatric Disorders. Biol Psychiatry. 2015 May 6. pii: S0006-3223(15)00361-3.----------Currais A, Farrokhi C, Dargusch R, Goujon-Svrzic M, & Maher P (2015). Dietary glycemic index modulates the behavioral and biochemical abnormalities associated with autism spectrum disorder. Molecular psychiatry PMID: 26055422... Read more »

  • June 29, 2015
  • 01:51 PM

The fear you experience playing video games is real, and you enjoy it

by Dr. Jekyll in Lunatic Laboratories

With the advent of video games, a frequently asked question has been whether we get as engrossed in them emotionally as we do when we see a scary movie. The answer is yes and many game players enjoy the fear caused by the zombies, disfigured humans and darkness they often encounter, the researchers found.... Read more »

  • June 29, 2015
  • 04:57 AM

Fermented foods and social anxiety?

by Paul Whiteley in Questioning Answers

Stumbling across a headline that reads: 'Study Finds Decreased Social Anxiety Among Young Adults Who Eat Fermented Foods' was bound to pique my blogging interest. When I eventually tracked down the source paper behind the headline I became more and more intrigued as today I bring to your attention the study findings reported by Matthew Hilimire and colleagues [1].Implementing "a cross-sectional approach to determine whether consumption of fermented foods likely to contain probiotics interacts with neuroticism to predict social anxiety symptoms" researchers asked over 700 students - psychology students - to self-report on "fermented food consumption, neuroticism, and social anxiety." Fermented foods by the way, cover a range of foods "that contain probiotics" including yogurt and sauerkraut (a particular favourite of mine). Researchers also enquired about various other variables such as fruit and vegetable intake and the amount of exercise taken over the past 30 days.Bearing in mind that this was a study based on self-report and that psychology students might not be entirely representative of the population in general, the results of an "interaction model, controlling for demographics, general consumption of healthful foods, and exercise frequency" did seem to suggest that there may be more to see when it comes fermented food consumption and social anxiety: "Fermented foods should be further investigated as an intervention for social anxiety."I'm not falling hook, line and sinker for these results - correlation is not the same as causation - despite my continuing interest in the science of psychobacteriomics (my word creation) and the idea that those trillions of wee beasties that inhabit our deepest, darkest [gut] recesses might be doing so much more than just helping to digest food and making the odd nutrient or two. I do however think that we need to dedicate quite a few more resources to the idea that psychology and behaviour might not be solely rooted in the grey-pink matter floating in our skull [2] as recent news articles seem to imply.Finally, and without wishing to make too many sweeping generalisations from the Hilimire results, I did think about whether such findings may be particularly 'useful' for certain groups of people where social anxiety might be over-represented. Autism is an obvious label given the suggestion that at least a quarter of those on the autism spectrum might also fulfil the diagnostic criteria for social anxiety disorder (see here). That such anxiety might also have knock-on effects to the presentation of more core autism symptoms (see here) is also noteworthy bearing in mind that a diet rich in fermented foods might not be for everyone and that social anxiety with or without autism is bound to be a very complicated process.We await further research in this area.Music: The Flaming Lips - Do You Realize??----------[1] Hilimire MR. et al. Fermented foods, neuroticism, and social anxiety: An interaction model. Psychiatry Res. 2015; 228: 203-208.[2] Dinan TG. et al. Collective unconscious: how gut microbes shape human behavior. J Psychiatr Res. 2015 Apr;63:1-9.----------Hilimire MR, DeVylder JE, & Forestell CA (2015). Fermented foods, neuroticism, and social anxiety: An interaction model. Psychiatry research, 228 (2), 203-8 PMID: 25998000... Read more »

Hilimire MR, DeVylder JE, & Forestell CA. (2015) Fermented foods, neuroticism, and social anxiety: An interaction model. Psychiatry research, 228(2), 203-8. PMID: 25998000  

  • June 29, 2015
  • 04:35 AM

We're more likely to cheat when we think it's our last chance to do so

by BPS Research Digest in BPS Research Digest

Imagine spending your school half-term week with a forgetful relative who always leaves money scattered around the house. Would you pinch any? If so, when, and why? A new paper suggests that we are most likely to “cheat at the end”, and uses a neat method to find out why.A number of theories predict we are likelier to cheat later than earlier. Perhaps we award ourselves moral credits for being good earlier, and later spend them like Catholic indulgences for guilt-free sin. Or maybe the struggle with temptation wears down our self-control, or we become desensitised to the thought of cheating. The job of psychological science is to distinguish between explanations, and Daniel Effron’s team developed a method that argues against these, in favour of an alternative that’s based on “anticipatory regret” or the fear of missing out.Participants sat alone in a room and tossed a coin 13 times, supposedly as part of an experiment on psychokinesis (the ability to control objects with the mind). Before each toss, participants predicted whether the coin would land heads or tails and then they recorded the outcome themselves using a computer. They were told each “correct” toss would earn them 10 cents. Crucially, the experimenters made it clear that they were depending on the participants to honestly report their successes. So, cheating was both possible and profitable.The researchers looked for signs of cheating, not in any one individual, but by examining average performance across all 847 participants. For any given toss, when the group’s average success rate exceeded the 50/50 success rate you’d expect based on chance, this was taken as a sign that cheating was at play.Effron’s team were particularly interested in the success rate on the seventh coin toss. They’d told some participants they would have 13 tosses in total: their seventh toss had a similar success rate to the previous six, at around chance. This suggests that the first six tosses hadn’t eroded willpower, or built up moral credits ready to be cashed in. By contrast, the researchers had told other participants they would only have seven tosses of the coin. What was striking was that these participants appeared to cheat more on the seventh toss, collectively achieving significantly more successes than would be expected based on chance. This result suggests it wasn’t the build-up of prior events that mattered, but the fact that this seemed to be the final opportunity… and if they didn’t act now, they never could.Indeed, when these cheating participants were informed there would in fact be more tosses to follow, their honesty suddenly popped back up on toss eight and onwards. This suggests their willpower hadn’t been used up, nor were they desensitised to cheating. The researchers also conducted a meta-analysis taking in data from this experiment, a further replication, and other work, with the overall results suggesting that we are three times more likely to cheat at what we believe to be the final opportunity than at any other time.This may remind some of you of research using the “Prisoner’s Dilemma” economic game, which shows that “defection” or mistreatment of others rises towards the end of a period of interaction. But as Efron’s team notes, that pattern is due to the to-and-fro of the game: if I swindle you at the start of our interaction, I can expect the same from you every time. Here, there was no ongoing interaction and so no reason why cheating on trial one or seven should have any different consequences. So this "cheating at the end" effect isn’t about how others treat you, but how you expect to feel about yourself.The authors conclude that knowing when cheating is likely to occur – on the last day of a period where a work supervisor is absent, for instance – could be useful in organising the timing and targeting of anti-cheating strategies, such as reminding people of moral standards just before a “peak time” period._________________________________ Effron, D., Bryan, C., & Murnighan, J. (2015). Cheating at the End to Avoid Regret. Journal of Personality and Social Psychology DOI: 10.1037/pspa0000026 Post written by Alex Fradera (@alexfradera) for the BPS Research Digest.

... Read more »

Effron, D., Bryan, C., & Murnighan, J. (2015) Cheating at the End to Avoid Regret. Journal of Personality and Social Psychology. DOI: 10.1037/pspa0000026  

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