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  • February 23, 2017
  • 02:59 AM
  • 32 views

"Autoimmune epilepsy is an underrecognized condition..."

by Paul Whiteley in Questioning Answers

"Among adult patients with epilepsy of unknown etiology, a significant minority had detectable serum Abs [autoantibodies] suggesting an autoimmune etiology."So said the findings reported by Divyanshu Dubey and colleagues [1] continuing a research theme previously discussed on this blog (see here) on how epilepsy / seizure-type disorder(s) for some might have more to do with immune function than many people might think.OK, a brief bit of background: epilepsy is a blanket term covering a wide variety of different presentations that affect the brain and specifically, 'the electrics' of the brain. Seizures are the most common symptom. Treatment typically comes in the form of anti-epileptic medicines (although other options are being considered for some). It's been known for a while that outside of the 'brain' focus of epilepsy, other biological systems might also play a role in the development/maintenance of the condition(s); specifically the immune system and quite often in cases where traditional anti-epileptic medicines don't seem to be able to control seizures effectively. The details are still a little sketchy but studies like the one from Dubey et al are trying to put some scientific flesh on to the bones of what facets of the immune system are potentially involved, specifically under 'autoimmune' conditions where the body fails to recognise 'self' as self and mounts an immune response against the body's own tissue(s).Dubey and colleagues looked at a group of participants "presenting to neurology services with new-onset epilepsy or established epilepsy of unknown etiology" and tested donated serum samples "for Abs reported to be associated with autoimmune epilepsy (NMDAR-Ab, VGKCc-Ab, leucine-rich glioma-inactivated protein 1 [LGI1] Ab, GAD65-Ab, γ-aminobutyric acid type B receptor [GABAB] Ab, α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic receptor [AMPAR] Ab, antineuronal nuclear antibody type 1 [ANNA-1 or anti-Hu] Ab, Purkinje cell cytoplasmic antibody type 2 [PCA-2] Ab, amphiphysin Ab, collapsin-response mediator protein 5 [CRMP-5] Ab, and thyroperoxidase [TPO] Ab)." Quite a lot of those autoantibodies probably sound like gibberish to the lay reader but some of them have been discussed in other contexts on this blog (see here and see here for examples).Results: some (15) of the 127 participants initially enrolled in the study were "subsequently excluded after identification of an alternative diagnosis." This in itself is interesting, as diagnoses such as "hypoxic or anoxic injury following cardiac arrest" and "ischemic stroke" are mentioned, illustrating how several different roads can lead to epilepsy and/or the presentation of seizures.Then: "Serum Abs suggesting a potential autoimmune etiology were detected in 39 (34.8%) cases." Over a third of the cohort showed serological evidence of autoantibodies and some presented with more than one type of autoantibody as being present. Breaking down those serologically positive participants, we are told that: "19 patients (48.7%) had new-onset epilepsy and 20 patients (51.3%) had established epilepsy." The authors did also subsequently limit their findings to those cases excluding TPO-Ab and low-titer GAD65-Ab (autoantibodies where a specific role to epilepsy is unclear or not specific) but even then reported that: "23 patients (20.5%) with unexplained epilepsy had positive serologic findings strongly suggestive of an autoimmune cause of epilepsy." There is also a final part to the Dubey paper which also merits mention: "Among the 23 patients who were seropositive, 15 (65.2%) received some sort of immunotherapy. Better seizure outcome was associated with use of immunomodulatory therapy... especially with use of intravenous methylprednisolone... or plasmapheresis."Alongside other (independent) studies in this area, the peer-reviewed evidence does seem to growing to suggest that within the wide (and heterogeneous) 'spectrum' that is epilepsy, at least some of that epilepsy might have an important immune component to it. To quote again from Dubey: "The data presented here suggest that autoimmune encephalitis may explain at least 20% of adult-onset epilepsies of unknown etiology." Aside from the importance of screening for said autoantibodies when certain cases of epilepsy appear at clinic, there are a few other potentially important points that could be raised about such data. Autism is area that I would be interested to see some further investigations carried out on with the Dubey findings in mind. Epilepsy is an important comorbidity 'over-represented' when it comes to autism (see here) and given the suggestions down the years that immune function (specifically autoimmunity) might be a facet of 'some' autism (see here for example) it's not beyond the realms of possibility that comorbid epilepsy might be a further facet of any autoimmune processes. Birds of an autoimmune feather tend to stick together and all that (see here). Add in the findings specifically talking about 'anti-NMDA-receptor encephalitis "mimicking an autistic regression"' (see here) and how methlyprednisolone might not be an uncommon medicine for some types of (autoimmune-related autistic presentation) and the hypotheses to be tested are laid out in front of you. By saying that, I don't want to take anything away from the more typical forms of epilepsy that can present (either alone or alongside autism) but rather point to the expanding knowledge base suggesting that immune functions may extend much further than just protecting the host from infection et al...To close, slightly related to some of the content included in this post, the trailer for the film Brain on Fire (from the book of the same name) is out and looking like required viewing.----------[1] Dubey D. et al. Neurological Autoantibody Prevalence in Epilepsy of Unknown Etiology. JAMA Neurol. 2017 Feb 6.----------Dubey D, Alqallaf A, Hays R, Freeman M, Chen K, Ding K, Agostini M, & Vernino S (2017). Neurological Autoantibody Prevalence in Epilepsy of Unknown Etiology. JAMA neurology PMID: 28166327... Read more »

Dubey D, Alqallaf A, Hays R, Freeman M, Chen K, Ding K, Agostini M, & Vernino S. (2017) Neurological Autoantibody Prevalence in Epilepsy of Unknown Etiology. JAMA neurology. PMID: 28166327  

  • February 22, 2017
  • 04:20 AM
  • 54 views

History of bipolar disorder = elevated risk of dementia: is vitamin D important?

by Paul Whiteley in Questioning Answers

"History of BD [bipolar disorder] is associated with significantly higher risk of dementia in older adults."So said the systematic review and meta-analysis published by Breno Diniz and colleagues [1] taking in the accumulated peer-reviewed literature on this topic. Including data for some 3000 individuals diagnosed with bipolar disorder and nearly 200,000 controls (without bipolar disorder), authors calculated something of a significantly higher risk of dementia in those with a documented history of bipolar disorder. They note that there is more research to do in this area, specifically on mechanisms and "to evaluate interventions that may reduce the risk of dementia in this population."Outside of the literature included in the Diniz study, similar findings have been reported in the science literature. The paper by Almeida and colleagues [2] noted that: "Bipolar disorder in later life is associated with increased risk of dementia" based on their analysis of ~38,000 older men (65-85 years old) and their "13-year risk of dementia." Perhaps more worryingly were their findings that: "Bipolar disorder was also associated with increased mortality" in relation to "death by suicide, accidents, pneumonia or influenza, and diseases of the liver and digestive system." Other data looking more generally at clinical depression paints a similar picture [3] suggesting something of a connection between various types of depression and risk of various types of dementia: "depressive symptomatology is associated with pathological mechanisms associated with neurodegeneration."I've tackled the topic of dementia a couple of times on this blog; most recently in relation to how incidental vitamin D deficiency *could be* something important when it comes to at least some cases of dementia (see here). Minus any sweeping generalisations and accepting that there may be many different roads leading to dementia and/or bipolar disorder, I am intrigued at the possibility that the sunshine vitamin might be something to consider as a 'connector' between elements of the depression and dementia spectrums as per other findings (see here for example). At the very least, it invites lots more targeted investigation, including whether vitamin D might indeed be a nootropic of choice for some (see here)...----------[1] Diniz BS. et al. History of Bipolar Disorder and the Risk of Dementia: A Systematic Review and Meta-Analysis. The American Journal of Geriatric Psychiatry. 2017. Jan 4.[2] Almeida OP. et al. Risk of dementia and death in community-dwelling older men with bipolar disorder. Br J Psychiatry. 2016 Aug;209(2):121-6.[3] Cherbuin N. et al. Dementia risk estimates associated with measures of depression: a systematic review and meta-analysis. BMJ Open. 2015 Dec 21;5(12):e008853.----------Diniz BS, Teixeira AL, Cao F, Gildengers A, Soares JC, Butters MA, & Reynolds CF 3rd (2017). History of Bipolar Disorder and the Risk of Dementia: A Systematic Review and Meta-Analysis. The American journal of geriatric psychiatry : official journal of the American Association for Geriatric Psychiatry PMID: 28161155... Read more »

Diniz BS, Teixeira AL, Cao F, Gildengers A, Soares JC, Butters MA, & Reynolds CF 3rd. (2017) History of Bipolar Disorder and the Risk of Dementia: A Systematic Review and Meta-Analysis. The American journal of geriatric psychiatry : official journal of the American Association for Geriatric Psychiatry. PMID: 28161155  

  • February 22, 2017
  • 04:01 AM
  • 49 views

Do twitter or facebook activity influence scientific impact?

by Richard Kunert in Brain's Idea

Are scientists smart when they promote their work on social media? Isn’t this a waste of time, time which could better be spent in the lab running experiments? No. An analysis of all available articles published by PLoS journals suggests otherwise. My own twitter activity might best be thought of as learning about science (in […]... Read more »

Peoples BK, Midway SR, Sackett D, Lynch A, & Cooney PB. (2016) Twitter Predicts Citation Rates of Ecological Research. PloS one, 11(11). PMID: 27835703  

  • February 21, 2017
  • 03:39 AM
  • 66 views

Neuropsychiatric disorder onset "temporally related to prior vaccinations"?

by Paul Whiteley in Questioning Answers

"Given the modest magnitude of these findings in contrast to the clear public health benefits of the timely administration of vaccines in preventing mortality and morbidity in childhood infectious diseases, we encourage families to maintain vaccination schedules according to CDC guidelines."The quote opening this post comes from the paper published by Douglas Leslie and colleagues [1] (open-access) and offers not a conclusion from their study looking at the possibility that "the onset of some neuropsychiatric disorders may be temporally related to prior vaccinations in a subset of individuals" but a caution that cause-and-effect were not 'proven' in their study. Anyone with any knowledge about previous occasions where administration of vaccines have been correlated with specific psychiatric or behavioural outcomes (see here and see here for examples) will recognise how important such a caution is, bearing in mind that vaccines are medicines (albeit preventative) and are subject to similar monitoring for safety and the small possibility of adverse effects as other medicines.Based on the examination of "the MarketScan® Commercial Claims and Encounters database", a US drug and medical insurance claims database, researchers looked at various diagnoses of interest including OCD (obsessive compulsive disorder), AN (anorexia nervosa), anxiety disorder, tic disorder, major depression, bipolar disorder and ADHD (attention-deficit hyperactivity disorder) in children/young adults aged 6-15 years old. This alongside several other classes of diagnosis including broken bones and 'open wounds'. Participants were matched one-to-one with controls without said neuropsychiatric diagnoses and exposure(s) to various vaccinations - "influenza, tetanus and diphtheria (TD), hepatitis A, hepatitis B, meningitis, and varicella" - were 'tracked'. Interestingly, this is not the lead authors' first foray into using the MarketScan database [2], where autism was the previous topic of analysis (specifically healthcare service use and costs).Results: bearing in mind that samples sizes varied according to those diagnoses under investigation, the authors report: "Receipt of any vaccine in the previous 6 months was highest for children with AN (21.4%), followed by OCD (15.9%) and tic disorder (15.8%), and was lowest for children with open wounds (10.3%)." This information needs to be treated carefully because - again - it tells us nothing about any cause-and-effect relationship, just correlation and trend; trends that could be there for all-manner of different reasons outside of the variables looked at. Further: "HRs [hazard ratio] associated with receipt of any vaccine were highest for children with AN... followed by OCD."The authors also looked at specific vaccinations in relation to those neuropsychiatric disorders included in their study. They report: "Influenza vaccinations during the prior 3, 6, and 12 months were... associated with incident diagnoses of AN, OCD, and an anxiety disorder." Conversely: "children with major depression were less likely to have received the influenza vaccine in the previous 3 months" and "children with bipolar disorder were also less likely to have received the influenza vaccine in the previous 3 or 6 months."OK, it is worth reiterating - yet again - that this was a study looking at possible associations and not necessarily cause-and-effect. Indeed, judging by that last paragraph and the table of HRs produced by the authors (see here) one might easily claim that flu vaccination might potentially shield someone from developing major depression as much as 'cause' AN, OCD and/or anxiety disorder. Such is the nature of such studies and the findings being reported. And indeed someone has actually looked at depressive symptoms (symptoms that is, not depression as a clinical diagnosis) before and after an influenza vaccination and found very little...I note that with specific regard to the influenza vaccine and the findings that "children with AN, OCD, or a tic disorder were more likely to have received the influenza vaccine in the preceding periods" the authors head into the research talking about narcolepsy and the "AS03-adjuvanted H1N1 vaccine" as a possible template for their findings. This despite not covering the diagnosis of narcolepsy in their study (they could have). I've touched upon this area of research before on this blog (see here) (something that continues to appear in media discussions) and whilst not disputing the findings, do for example, wonder why in the work of Szakács and colleagues [3] ADHD was picked up as a comorbidity present in their "post-H1N1 vaccination (PHV) narcolepsy group" but in the Leslie data the HRs showed little evidence of any relationship. Yes, H1N1 vaccination is not necessarily the same as influenza vaccination reported in the Leslie data (we don't actually know what specific influenza vaccines were administered), but surely if discussions turn to an 'autoimmune' element as a possible mechanistic feature potentially linking vaccination and [some] neuropsychiatric disorder(s), one would expect to see the same/similar pattern of conditions being represented and reported? For balance, I should also point out that other independent study has talked about eating disorders potentially having "immune-mediated mechanisms" connected, particularly those associated with autoimmunity [4] although I don't doubt such a connection is likely complicated and probably not universally applicable.It's not difficult to find issues with the Leslie paper and no doubt these will be emphasised in any further discussions about the data reported even when the authors stress throughout that "findings do not demonstrate a causal role of vaccination in the pathoetiology of any of these conditions." The strengths of the data - e.g. the use of that administrative database for confirming diagnoses and vaccine exposure - are worth mentioning again in light of other debates on data sources from other 'disappearing' manuscripts in this area. I might also add that by focusing in on various diagnoses but not autism (which again, they could have done) and not a certain vaccine, the authors seem well aware of the history in this area - "the association of the measles, mumps, and rubella vaccine with autism spectrum disorder has been convincingly disproven" - and probably either thought nothing more of it or chose to steer well clear of it (or perhaps a combination of both).Is there a 'where next' when it comes to the Leslie data? To quote again from the paper: "findings require replication in a larger population-based sample, possibly including assessments of various potentially important host factors, e.g., the individual’s ... Read more »

  • February 20, 2017
  • 10:56 AM
  • 62 views

The Science of the Rorschach Blots

by Neuroskeptic in Neuroskeptic_Discover

When the psychiatrist Hermann Rorschach blotted ink onto paper to produce a series of abstract patterns, could he have known that nearly 100 years later, the Rorschach test would be a household name?



Although the use of the Rorschach to diagnose mental illness is mostly a thing of the past, research on the test continues. Last week, two new papers were published on the Rorschach blots, including a fractal analysis of the images themselves and a brain scanning study using fMRI.



The ... Read more »

Taylor RP, Martin TP, Montgomery RD, Smith JH, Micolich AP, Boydston C, Scannell BC, Fairbanks MS, & Spehar B. (2017) Seeing shapes in seemingly random spatial patterns: Fractal analysis of Rorschach inkblots. PloS one, 12(2). PMID: 28196082  

  • February 20, 2017
  • 04:33 AM
  • 79 views

Catatonic symptoms and autism

by Paul Whiteley in Questioning Answers

"Catatonic symptoms are more prevalent in young people with autism than previously thought" said the article recently published by Breen and Hare [1]. Continuing a research theme of at least one of the authors [2], the idea that catatonic symptoms - primarily manifesting as stupor, unresponsiveness to light, noise or touch, mutism, etc - might be over-represented when it comes to autism is not a new one by any means.Breen & Hare set about looking for "the presence and nature of such attenuated behaviours in children and adolescents with autism" based on something called the Attenuated Behaviour Questionnaire. This was delivered to parents/caregivers online alongside looking at information from other measures based on the presence of repetitive behaviour and depression."Attenuated behaviour indicative of catatonia was relatively common in young people with autism with up to 20.2% having an existing diagnosis of catatonia and evidence of a relationship between attenuated behaviours and measures of depression and repetitive and restricted behaviours." Such findings as I said, are by no means novel but once again highlight how a diagnosis of autism or autism spectrum disorder (ASD) is seemingly protective of nothing when it comes to comorbidity. To quote another author on this topic: "an unabashed drumroll for increased recognition and treatment of catatonia in autism spectrum disorders (ASD)" [3] is needed.Catatonia appearing alongside [some] autism leads into a number of areas in relation to the 'closeness' of any relationship (some people have talked about 'autistic catatonia') and the management strategies that may be subsequently indicated. On the issue of management, guidance is available [4] albeit including a strategy - electroconvulsive therapy (ECT) - that is probably not going to win any awards in terms of popularity given its historical basis. Accepting that still today ECT as an 'intervention' option when it comes to autism still courts heated discussion (see here), there is the requirement for much greater study of catatonic symptoms in relation to autism and whether there may be several presentations ripe for more novel intervention [5] (in light of a growing area of research interest). Said intervention might also take into account the plurality of autism too (see here)...To close, yet another song for my brood and a very proud father who saw some real talent in the karate competition yesterday (those first place trophies are proof that team kata and team kumite are definitely the way forward)...----------[1] Breen J. & Hare DJ. The nature and prevalence of catatonic symptoms in young people with autism. J Intellect Disabil Res. 2017 Feb 1.[2] Hare DJ. & Malone C. Catatonia and Autistic Spectrum Disorders. Autism. 2004; 8: 183-195.[3] Dhossche DM. Decalogue of Catatonia in Autism Spectrum Disorders. Frontiers in Psychiatry. 2014;5:157.[4] Mazzone L. et al. Catatonia in patients with autism: prevalence and management. CNS Drugs. 2014 Mar;28(3):205-15.[5] Kiani R. et al. Anti-NMDA-receptor encephalitis presenting with catatonia and neuroleptic malignant syndrome in patients with intellectual disability and autism. BJPsych Bull. 2015 Feb;39(1):32-5.----------Breen J, & Hare DJ (2017). The nature and prevalence of catatonic symptoms in young people with autism. Journal of intellectual disability research : JIDR PMID: 28150394... Read more »

  • February 19, 2017
  • 01:01 PM
  • 84 views

Using Discourse Analysis to Assess Cognitive Decline

by The Neurocritic in The Neurocritic

Figure from Gauthier et al. (2005).

Alzheimer's Disease (AD) and other dementias are progressive neurodegenerative conditions that unfold over time. Subtle symptoms such as forgetfulness and word finding problems may progress to mild cognitive impairment (MCI), and then escalate to full-blown dementia. Recent efforts to classify prodromal states have included automated analysis of spontaneous... Read more »

Fraser, K., Meltzer, J., & Rudzicz, F. (2015) Linguistic Features Identify Alzheimer’s Disease in Narrative Speech. Journal of Alzheimer's Disease, 49(2), 407-422. DOI: 10.3233/JAD-150520  

Thomas, C., Keselj, V., Cercone, N., Rockwood, K., . (2005) Automatic detection and rating of dementia of Alzheimer type through lexical analysis of spontaneous speech. IEEE International Conference, 1569-1574. info:/10.1109/ICMA.2005.1626789

  • February 18, 2017
  • 04:30 AM
  • 135 views

Social interaction and autism: it takes two to tango

by Paul Whiteley in Questioning Answers

Psychology experiments are not generally fodder for this blog when it comes to autism. The main reason being that quite a few appearing in the peer-reviewed literature tend to look at quite abstract features perhaps somewhat removed from the daily lives of autistic people and their significant others. A few also seem to struggle with the idea that grand over-arching psychological theories (that seem to inevitably follow psychological findings in particular) are not required when it comes to autism in these days of heterogeneity and plurality.I am making an exception today however with the paper by Noah Sasson and colleagues [1] (open-access) and their findings suggesting advocating "for a broader perspective of social difficulties in ASD [autism spectrum disorder] that considers both the individual’s impairments and the biases of potential social partners." In other words, it takes two to [socially, interactively] tango. I might add that a doctoral thesis by one of the co-authors on the Sasson paper (Daniel Faso) is also available for further inspection too (see here).Based on the idea that issues with social interaction "quantity and quality" might not be something exclusively under the control of those diagnosed with autism, Sasson et al devised a series of experiments to test their hypothesis: "three studies conceived and conducted independently by three research groups assessing observers’ first impressions of—and intentions to socially engage with— children and adults with ASD based upon “thin slices” of their real-world social behavior." I'm not going to go into too much detail about the experiments because the paper is open-access and you can read about them for yourselves. 'Thin slices' in the context of the experiments carried out referred to media that were rated pertinent to "observers’ first impressions of individuals with ASD engaging in real-world social behavior."The results make for some important reading as across the different experiments undertaken the key messages were that: "first impressions of individuals with ASD are significantly less favorable than those of matched TD [typically developing] controls, and are associated with greater reluctance on the part of observers to pursue social engagement." Further: "social interaction difficulties in ASD are not solely an individual impairment but also a relational one, and consideration of both of these factors is necessary for a full understanding of social impairment in ASD." I relay all of that bearing in mind that these were experiments carried out under controlled conditions (I don't know about you, but I don't generally rate people at first contact using a "0-3" Likert scale or a "non-graduated slider" on 'how approachable' they were or the likelihood of a friendship developing).Although important, I don't think anyone should be too surprised by the results reported in the context of how first impressions count and how people are generally quick to judge from "personality and character traits" whether social engagement with a person or group of people is going to be a short or longer-term thing. I say this also bearing in mind that minus any psychobabble, people generally take into account things like context, familiarity and similarity when it comes to their social interaction decisions too [if for example, you happen to be a fan of Star Wars or a Shotokan karateka, I might be more inclined to chat with you than say if you talked about the goings-on on various reality TV shows]. Indeed, the authors note: "these studies present only group-wise comparisons and do not address individual differences among those with ASD, nor whether individual characteristics of the raters (e.g., gender, personality, etc.) affect the results reported here." I'd also forward the idea that they might also include important concepts such as self-monitoring for example when it comes to future studies in this area. Similarly, it would also be handy to see if 'comorbidity counts' when it comes to further investigations on this topic in light of expanding links between different labels and traits (see here).The question of what to do about the Sasson findings similarly provide some food for thought. The authors suggest that: "intervention and education approaches that target both those with ASD as well as their TD [typically developing] peers may offer a more comprehensive approach for improving social and functional outcomes in autism." In the context of other studies looking at social interaction and autism particularly in the school setting (see here) I can see how this might work in terms of raising awareness of how people are not always the same when it comes to the presentation of their social persona. Intervening with a wider group (i.e. peers) and taking the onus off 'just the person with autism' is a win-win situation and will no doubt have other positive knock-on effects in terms of self-esteem and helping to remove barriers around the 'disability' framing of autism. I might add that in these days of the potential virality of personality traits, it makes sense to include everyone.In a wider context - outside of school - and in the big, wide [adult] world however, I'm slightly less sure of how such intervention is going to be achieved. Yes, we would all love people to be more understanding and less 'judgemental' in their first (and subsequent) impressions, but when it comes to influencing aspects such as views on "awkwardness, attractiveness, [and] likability" I'm not so sure that this can be universally achieved. Indeed, facets such as attractiveness and likability are probably going to be influenced by lots of variables outside of those just linked to an autism diagnosis and its presentation (frank or not). By saying all that, I'm not suggesting that we shouldn't try to educate and perhaps even move people away from the whole 'first impressions last' [2] thing, but rather am looking at the realistic prospect of achieving such a societal goal, mindful that it takes two to tango...And on the topic of first impressions, at least get the handshake right (i.e. let go)...----------[1] Sasson NJ. et al. Neurotypical Peers are Less Willing to Interact with Those with Autism based on Thin Slice Judgments. Sci Rep. 2017 Feb 1;7:40700.[2] Gunaydin G. et al. Impressions Based on a Portrait Predict, 1-Month Later, Impressions Following a Live Interaction. Social Psychological and Personality Science. 2017. 8: 36-44.----------Sasson NJ, Faso DJ, Nugent J, Lovell S, Kennedy DP, & Grossman RB (2017). Neurotypical Peers are Less Willing to Interact with Those with Autism based on Thin Slice Judgments. Scientific reports, 7 PMID: 28145411... Read more »

  • February 17, 2017
  • 07:02 AM
  • 141 views

Changing your name after marrying, bias at home and  work, and smart-phone blindness

by Rita Handrich in The Jury Room

It’s time again for another combination post featuring fascinating tidbits you may have missed were it not for our eagle eyes and constant efforts to keep you informed. And yes, we’ll start at the end since we know you are wondering if smart-phone blindness is really a thing. Would we steer you wrong? Smart-phone blindness […]... Read more »

Share, EF. (2017) Hillary Rodham versus Hillary Clinton: Consequences of surname choice in marriage. Gender Issues. info:/

  • February 17, 2017
  • 07:01 AM
  • 130 views

Why does music training increase intelligence?

by Richard Kunert in Brain's Idea

We know that music training causes intelligence to increase, but why? In this post I 1) propose a new theory, and 2) falsify it immediately. Given that this particular combination of activities is unpublishable in any academic journal, I invite you to read the whole story here (in under 500 words). 1) Proposing the ISAML Incredible but […]... Read more »

Jones, M., & Boltz, M. (1989) Dynamic attending and responses to time. Psychological Review, 96(3), 459-491. DOI: 10.1037//0033-295X.96.3.459  

Kunert R, & Jongman SR. (2017) Entrainment to an auditory signal: Is attention involved?. Journal of experimental psychology. General, 146(1), 77-88. PMID: 28054814  

Glenn Schellenberg, E. (2004) Music Lessons Enhance IQ. Psychological Science, 15(8), 511-514. DOI: 10.1111/j.0956-7976.2004.00711.x  

  • February 16, 2017
  • 03:14 AM
  • 157 views

"early medical events are associated with clinical ASD phenotypes"

by Paul Whiteley in Questioning Answers

The paper by Charlotte Willfors and colleagues [1] (open-access) provides some food for thought today and the observation that various individual and cumulative medical events - "early medical events likely to be caused by environmental factors" - may be important to at least some autism.Researchers "scrutinized the early medical histories of a rare and informative sample of 13 MZ [monozygotic] twin pairs discordant for clinical ASD [autism spectrum disorder]" also including "13 MZ typically developing (TD) control pairs (n=52) matched for sex" as an 'exploratory step. Discordant for autism means that one twin had autism and the other did not.This research first step looked at medical events (likely to be caused by environmental factors!) included things like delivery and neonatal variables (e.g. foetal distress, hypoxia), minor and frequent infections (e.g. ear infections), allergy and epilepsy to name a few. Data was acquired from a few sources including medical records and medical history "assessed from a parent reported questionnaire." They examined exposure to the medical events "in relation to either quantitative or qualitative discordance for ASD." Qualitative discordance referred to when "only one twin within a pair meeting the diagnostic criteria of ASD." A 'confirmatory' study was also carried out whereby a larger, independent cohort of 100 twin pairs "quantitatively discordant for autistic traits" were also quizzed and findings cross-validated.Results: a few non-shared environmental (NSE) events seemed to be important based on their analysis. So: "Single early medical factors, likely to be caused by NSE, that discriminated between twins in qualitative ASD discordant pairs were dysregulation during the first year of life (comprising feeding and sleeping problems, excessive crying and worrying) and birth weight." Authors also reported that cumulatively, the appearance of early medical events were significantly different in MZ twins with autism compared with their non-ASD co-twin. It's worth mentioning that some of those 'dysregulation' events have been talked about in the earliest descriptions of autism (see here). Birth weight too has something of a long-standing connection to [some] autism (see here). When it came to analysis based on autistic traits (the confirmatory study) it seemed that "early dysregulation and the cumulative load of a variety of early adverse medical events" continued to be important variables (although birth weight linked to ASD traits lost its significance).These are important findings. The focus on MZ twins (who share a common structural genetic blueprint) means that the genetics side of things is to a large extent 'controlled for' and the results are more likely to reflect some environmental or, more accurately, non-genetic influence. There is a caveat to this though, as per the authors recognition: "with the exception of putative post-twinning de novo mutations." I might also add that MZ twins are also not necessarily epigenetically the same too so gene expression can (and does) differ. What causes these epigenetic differences is still the source of some debate but I might chime in with one idea (see here) out of many possibilities."Our data indicate that taking into account the cumulative load of early medical factors might strengthen or discourage a suspicion of ASD, at least in a minority of cases." This is an interesting thought provided by the authors based on their findings. It ties in well with the idea that although behavioural presentation is core to autism presentation and diagnosis, behaviour might not be the only important feature present in relation to autism. I do have to express a degree of caution however with such an approach based on the idea that various types of regression have been noted in the peer-reviewed literature to accompany some autism (see here) and with it, the concept of 'acquired autism' should really be properly recognised (see here for example) in these days of the plural 'autisms'. Indeed, there's a research study idea for anyone out there: looking at MZ twins discordant for autism with onset of said autism tied into a regression of skills?Scientific replication is the name of the [future] game in this area of study, drawing on larger cohorts and perhaps based in other geographical areas outside of Sweden. We also need to find out what mechanisms might be potentially associating something like 'early dysregulation' with the onset of autism, taking into account how factors such as early feeding practices/issues for example, might provide at least one avenue for future study (see here).To close, in light of some recent media headlines about the 'myth' that autism rates are on the up (and quite significantly so over past two decades), I offer some past posts suggesting that the word 'myth' should be reserved for other [non-peer-reviewed] matters (see here and see here and see here) and not this particular branch of epidemiological science. As to what may be 'causing' the upswing in numbers of diagnosed cases, well, it's likely to be very, very, very complicated (and without any need for sweeping generalisations please)...----------[1] Willfors C. et al. Medical history of discordant twins and environmental etiologies of autism. Transl Psychiatry. 2017 Jan 31;7(1):e1014.----------Willfors C, Carlsson T, Anderlid BM, Nordgren A, Kostrzewa E, Berggren S, Ronald A, Kuja-Halkola R, Tammimies K, & Bölte S (2017). Medical history of discordant twins and environmental etiologies of autism. Translational psychiatry, 7 (1) PMID: 28140403... Read more »

Willfors C, Carlsson T, Anderlid BM, Nordgren A, Kostrzewa E, Berggren S, Ronald A, Kuja-Halkola R, Tammimies K, & Bölte S. (2017) Medical history of discordant twins and environmental etiologies of autism. Translational psychiatry, 7(1). PMID: 28140403  

  • February 15, 2017
  • 12:00 PM
  • 144 views

"Dominance" Training Deprives Dogs of Positive Experiences

by CAPB in Companion Animal Psychology Blog

Dominance is an outdated approach to dog training – and it also means dogs miss out on fun.Approaches to dog training based on dominance rely on the idea that you have to be the ‘alpha’ or pack leader. Unfortunately, this type of dog training is not just out-of-date and potentially risky, but modern approaches to dog training are also a lot more fun – for you and the dog.What is dominance in dog training?We sometimes hear the phrase ‘my dog is being dominant.’ ‘Your dog is being dominant’ can even be an insult because it implies you are not confident enough.What people mean by ‘dominant’ can be anything from your dog walking through a door in front of you, to jumping on you, or relaxing on the sofa, growling at you or winning a game of tug. For that reason alone, it’s not a very helpful description.Let’s unpack these examples for a moment, because using a framework of dominance is taking away the person’s choice about things. It’s perfectly fine for your dog to walk in front of you, and it’s up to you if they jump on you to greet you or are allowed on the sofa (some people like it, some people don’t – of course strangers probably don’t like to be jumped on).If your dog growls at you, it’s important not to punish them because this is their way of telling you they are uncomfortable; instead you should stop what you are doing and reconsider how you can fix it so you and your dog are both happy. A dominance-based approach would potentially put you in danger of getting bitten.As for tug… dogs who win at tug are more involved in the game (suggesting they enjoy it more) and show more playful attention-seeking afterwards, such as nuzzling and pawing at their owner (Rooney & Bradshaw 2002). Games of tug can be fun for you and the dog, and are a useful way to entertain your dog at times when walks are limited. Arbitrarily saying people should not play tug or should not let the dog win is doing a disservice to both dogs and people.Problems with dominance in dog trainingWhen people apply dominance to dog training, it usually results in them using aversive methods, such as alpha rolls, because they think they have to make their dog submit. This can cause a range of issues.Here are just a few examples:There is a risk of an aggressive response with the use of confrontational methods (Herron, Shofer & Reisner, 2009). 31% of people who did an alpha roll, 39% who forced the dog to let go of something from their mouth, and 43% of people who hit or kicked the dog reported an aggressive response. If people use aversive training techniques, their dogs are 2.9 times more likely to be aggressive to a family member and 2.2 times more likely to be aggressive to a stranger outside the home than if the dog had been trained using reward-based methods (Casey et al 2014). Greater frequency of punishment is associated with an increased prevalence of aggression and excitability (Arhant et al 2010) Dogs trained to sit and walk on leash using leash jerks or tugs and pushing the dog into a sit position showed more signs of stress (mouth-licking, yawning, and lowered body posture) than those taught with reward-based techniques. They also gazed less at their owner, suggesting the human-canine relationship is not as good (Deldalle and Gaunet, 2014). Photo: Grigorita Ko; top, alexei_tm; below, oneinchpunch (all Shutterstock.com)What do scientists think about dominance and dogs?“Dominance” as applied by so many people in dog training is not the same as “dominance” when used by scientists, which is a much more nuanced term. Even so, it does not adequately describe the relationship between dogs and people.Writing in his Psychology Today blog, John Bradshaw, author of Dog Sense, explains that for dogs to think about dominance would actually require some important cognitive abilities – knowing that other creatures can think about us – which we have no evidence that dogs have.He says,“It is more parsimonious to interpret dogs’ behaviour as if they were simply trying to maintain access to essential resources, perhaps the most important being, uniquely for this species, access to one or more human attachment figures.”So how does this relate to dog training? In the same post, Bradshaw says,“Both for their own safety and to be acceptable to society, companion dogs need to be kept under control, but that can be achieved by reward-based training, without reference to their position in some illusory “hierarchy”.”Now, you can find some scientists who think dogs have dominance hierarchies between themselves, and Marc Bekoff summarizes some of them in his blog. But he also says,“I don't think that dogs need to be forced into submission to train or to teach them how to live harmoniously with other dogs, with other animals, or with humans. I favor positive training/teaching methods and they have been shown to be highly effective in achieving these goals.”Let’s be clear about this: these two scientists have very different views about dominance and dogs, but they both say it’s not the way to train a dog.It’s unfortunate that some people mistakenly believe the dominance or pack leader approach to dog training is based in science, especially since it has negative consequences.Alexandra Horowitz, author of Inside of a Dog and Being a Dog, explains the problems with the alpha dog myth in this recent video for Business Insider. var playerParam = {'pcode':'BhdmY6l9g002rBhQ6aEBZiheacDu','playerBrandingId':'6e12e8b3387a44daacfb73afba25a76e','skin': {'config': '//player.ooyala.com/static/v4/stable/latest/skin-plugin/skin.json'} };OO.ready(function() {window.pp = OO.Player.create('container', 'FhcGNpOTE6WIqG3Z_mtM86QulBlrVMaQ', playerParam); }); Luckily, there is an excellent alternative to the dominance approach: reward-based dog training.   Reward-Based Dog Training: Many Things to LikeLet’s look at reward-based training from the dog’s perspective. First of all, it teaches the dog what to do, instead of just what not to do. With reward-based training yo... Read more »

  • February 15, 2017
  • 07:02 AM
  • 134 views

Tell it to the judge 

by Doug Keene in The Jury Room

Anyone who has been in court more than a few times, has likely heard a judge “rehabilitate” a potential juror who has expressed bias by asking the juror if they will, in judging “this case”, be “fair, impartial and unbiased”. Why yes, your Honor (say almost all of them). Mykol Hamilton and Kate Zephyrhawke, researchers, […]... Read more »

Charles G. Lord, Lee Ross, & Mark R. Lepper. (1979) Biased Assimilation and Attitude Polarization: The Effects of Prior Theories on Subsequently Considered Evidence. Journal  of Personality and Social Psychology, 37(11), 2098-2109. info:/

Lord CG, Lepper MR, & Preston E. (1984) Considering the opposite: a corrective strategy for social judgment. Journal of Personality and Social Psychology, 47(6), 1231-43. PMID: 6527215  

  • February 15, 2017
  • 04:30 AM
  • 141 views

"Androgens were not associated with autistic traits at 12 months of age"

by Paul Whiteley in Questioning Answers

EARLI - the Early Autism Risk Longitudinal Investigation study - has been mentioned on this blog before (see here) with the aim of the initiative to "examine possible environmental risk factors for autism and study whether there is any interplay between environmental factors and genetic susceptibility."In this post I'm bringing the paper by Bo Park and colleagues [1] (open-access) to your attention and the observation(s) that umbilical cord blood levels of testosterone and other related androgens were seemingly not associated with autistic traits at 12 and 36 months of age in their cohort. Such findings represent yet another biological research blow (see here) to facets of the Extreme Male Brain (EMB) theory of autism and the suggestion that "ASD [autism spectrum disorder] is an extreme presentation of a typical male cognitive profile where the drive to “systemize” is stronger than the drive to empathize."So, looking at cord blood samples from 137 children recruited on to EARLI - "a high autism-risk cohort following pregnant mothers with an older child diagnosed with an ASD (autistic disorder, Asperger syndrome, or pervasive developmental disorder not otherwise specified)" - researchers looked at whether measures of various androgens might correlate with scores on the Autism Observation Scales for Infants (AOSI) and Social Responsiveness Scale (SRS). Said schedules were administered at 12 months and 36 months respectively and various potentially confounding variables were taken into account when it came to looking at any associations. It's also worth pointing out that the technology of choice when it came to those measures of cord blood levels of androgens was an old favourite of this blog: liquid chromatography-tandem mass spectrometry (LC-MS/MS).Results: well as per the title of this post, and after adjustment for potentially confounding variables - "maternal age, gestational age, and cesarean delivery" - there wasn't a great deal to see in terms of levels of androgens and the presence of autistic traits. Indeed, the title of this post only tells half the story as testosterone was also found not to be associated with the SRS scores at 36 months too. The authors do note that: "Male infants (n=75) showed significantly higher umbilical cord testosterone levels and greater social deficits at 36 months of age" than females, but after adjustment for confounders this observation was left wanting. They also talk about some interesting observations about when a child had an older female sibling diagnosed with autism - "androgen levels and autistic traits may depend on sex of the older affected sibling" - but I'm not so sure about the strength of such findings and whether other mechanisms might also be at work. I might reiterate that autistic traits were the name of the research game in this study not a diagnosis of autism.As mentioned, the Park findings represent another setback for the generalisability of the role of androgens (prenatal and beyond) in relation to autism and/or autistic traits. I guess that in these days of the plural 'autisms' (see here) it's perhaps not entirely unexpected that grand theories of autism seem doomed to fail when put up to scientific scrutiny. Indeed someone recently has talked about this [2]. I still however remain interested in the discussions around the EMB theory of autism, and although this and other research has not been entirely kind to the hypothesis, it is still perhaps deserving of further study in order to see who it may be most relevant to in these days of plural autisms and subgroupings...To close, isn't this why Twitter was invented?----------[1] Park BY. et al. Umbilical cord blood androgen levels and ASD-related phenotypes at 12 and 36 months in an enriched risk cohort study. Molecular Autism. 2017; 8: 3.[2] Müller R-A. & Amaral DG. Editorial: Time to give up on Autism Spectrum Disorder? Autism Res. 2017. Jan 27.----------Park, B., Lee, B., Burstyn, I., Tabb, L., Keelan, J., Whitehouse, A., Croen, L., Fallin, M., Hertz-Picciotto, I., Montgomery, O., & Newschaffer, C. (2017). Umbilical cord blood androgen levels and ASD-related phenotypes at 12 and 36 months in an enriched risk cohort study Molecular Autism, 8 (1) DOI: 10.1186/s13229-017-0118-z... Read more »

Park, B., Lee, B., Burstyn, I., Tabb, L., Keelan, J., Whitehouse, A., Croen, L., Fallin, M., Hertz-Picciotto, I., Montgomery, O.... (2017) Umbilical cord blood androgen levels and ASD-related phenotypes at 12 and 36 months in an enriched risk cohort study. Molecular Autism, 8(1). DOI: 10.1186/s13229-017-0118-z  

  • February 14, 2017
  • 12:13 PM
  • 168 views

The Complexities of “The Love Hormone”

by Miss Behavior in The Scorpion and the Frog

New York street art. Photo inWikimedia Commons posted by Pedroalmovar.Oxytocin, commonly known as “the love hormone”, is a small chemical that is produced in the brain of mammals, but can both act as a neurotransmitter and enter the blood stream and act as a hormone. It has long been heralded for its role in both maternal and romantic love, but more recent research is showing us just how complicated the physiology of love can be.Oxytocin is released in mammalian mothers after birth. It promotes nursing and bonding between a mother and her young. As children grow, oxytocin is involved in how both mothers and fathers “baby-talk” and mirror their children. It is involved in pro-social behaviors in both young and adults: trust, generosity, cooperation, hugging, and empathy. And of course, oxytocin promotes positive communication and pair bonding in romantic couples. Countless studies have found these relationships between affiliation and oxytocin in many mammalian species, giving oxytocin its commonly used nickname “the love hormone”.But more recent studies show that it’s not so simple.In a number of recent studies, people have been given oxytocin nasal sprays and tested for various behavioral effects in different contexts… and the context really seems to matter. Oxytocin increases trust, generosity, cooperation, and empathy towards people we already know and like. But it decreases trust, generosity, cooperation, and empathy towards strangers. When we play games with strangers, oxytocin makes us more jealous when we lose and it makes us gloat more when we win. It also seems to enhance many attributes relating to ethnocentrism: It increases our ability to read facially-expressed emotions in people of our own race while making it harder to read facial expressions of people of a different race. When forced to choose between being nice to a stranger of our own race versus a stranger of another race, oxytocin makes us more likely to choose the person of our own race. In studies of both people and rodents, oxytocin decreases aggression towards our families and friends, but increases aggression towards strangers.Oxytocin is not the universal love hormone we once understood it to be. It helps us direct our positive support towards our “in-groups” (our family and friends) and defend them from our “out-groups” (individuals we don’t know). It is a delicate balance: Too little of it can cause social impairment and make it difficult to connect with loved-ones; Too much of it can increase our anxiety towards strangers and racist tendencies. And to make things more complicated, each of us has a slightly different oxytocin system: sex, gender, social history, history of childhood trauma or neglect, psychiatric illnesses and genetic variations all have profound effects on the oxytocin system.There is much we don’t know about the role of oxytocin and love. But they are a good fit, because both, it seems, are complicated.Want to know more? Check these out:Shamay-Tsoory SG, & Abu-Akel A (2016). The Social Salience Hypothesis of Oxytocin. Biological psychiatry, 79 (3), 194-202 PMID: 26321019 Zik JB, & Roberts DL (2015). The many faces of oxytocin: implications for psychiatry. Psychiatry research, 226 (1), 31-7 PMID: 25619431 ... Read more »

Shamay-Tsoory SG, & Abu-Akel A. (2016) The Social Salience Hypothesis of Oxytocin. Biological psychiatry, 79(3), 194-202. PMID: 26321019  

  • February 14, 2017
  • 03:27 AM
  • 141 views

Relative age and ADHD medication

by Paul Whiteley in Questioning Answers

"Youngest children in class 'more likely to be given ADHD drugs'" went the NHS Choices headline that led me to the short report produced by Martin Whitely and colleagues [1] (open-access).ADHD - attention-deficit hyperactivity disorder - is something of interest to this blog; not least the idea that relative age (age relative to peers in the same school year group) might be an important variable when it comes to at least some diagnoses of the condition (see here).The Whitely paper draws on data from a research favourite place - Western Australia (WA) - and focused on "the proportions of WA children born in the early and late months of a recommended school-year intake who received at least one Pharmaceutical Benefits Scheme [PBS] prescription for an ADHD medication in 2013."The results: from a starting population of some 300,000 children, about 6,000 of them (~2%) were in receipt of a state-recognised prescription of an ADHD medication. The article does not actually mention which ADHD medication was given but methylphenidate (a.k.a Ritalin) is listed in the PBS directory and is the typically indicated medication used for ADHD (see here). Boys, we are told, were more likely to be prescribed ADHD medication than girls (2.9% vs. 0.8% respectively).Then to the headline: when splitting the children into two age groups - 6-10 year olds and 11-15 year olds - researchers noted that those born in June (the last birth month influencing year of school intake) were more likely to be prescribed ADHD medication than those born in July. This trend was noted in both age groups. The conclusion being that the youngest children in a year group at school were more likely to be in receipt of prescribed medication for ADHD compared to older children in the year group.Alongside the caveats linked to the Whitely report made by NHS Choices, there is a need for further investigation in this area and in particular, whether the results generalise to places outside of just WA. I've already linked to my previous discussion about relative age and ADHD diagnosis/medication (see here again) and from comparisons with the Taiwanese data [2] on this topic, including the fact that Taiwan have a different cut-off month for school entry (August 31). On that basis, yes the trend appears to generalise across geographies...----------[1] Whitely M. et al. Influence of birth month on the probability of Western Australian children being treated for ADHD. MJA. 2017; 206: Feb 6.[2] Chen MH. et al. Influence of Relative Age on Diagnosis and Treatment of Attention-Deficit Hyperactivity Disorder in Taiwanese Children. J Pediatr. 2016 May;172:162-167.e1.----------Martin Whitely, Leanne Lester, John Phillimore, & Suzanne Robinson (2017). Influence of birth month on the probability of Western Australian children being treated for ADHD The Medical Journal of Australia... Read more »

Martin Whitely, Leanne Lester, John Phillimore, & Suzanne Robinson. (2017) Influence of birth month on the probability of Western Australian children being treated for ADHD. The Medical Journal of Australia. info:/

  • February 13, 2017
  • 07:02 AM
  • 129 views

Simple Jury Persuasion: The “bad is black” effect 

by Rita Handrich in The Jury Room

It is hard to believe that more than two decades have passed since the controversial Time magazine cover featuring OJ Simpson with his skin intentionally darkened was distributed. It was published in 1994 and people were so upset that the magazine’s managing editor issued a public apology for publishing the cover photo. Today, we are […]... Read more »

Alter, A., Stern, C., Granot, Y., & Balcetis, E. (2016) The “Bad Is Black” Effect. Personality and Social Psychology Bulletin, 42(12), 1653-1665. DOI: 10.1177/0146167216669123  

  • February 13, 2017
  • 04:28 AM
  • 153 views

Depression, SMILES and Modified Mediterranean diet (advice)

by Paul Whiteley in Questioning Answers

SMILES in the title of this post refers to the SMILES trial - Supporting the Modification of lifestyle In Lowered Emotional States - and results recently published by Felice Jacka and colleagues [1] (open-access) pertinent to the idea that "dietary improvement" might be something to consider when a diagnosis of major depressive episode (MDE) is received.Having previously published their study protocol [2], researchers set about looking at whether under "single blind, randomised controlled" conditions, the application of advice pertinent to a diet - the 'ModiMedDiet' - focused on increasing diet quality along Mediterranean diet lines, might be useful for those diagnosed with MDE. The results (which had already been revealed before peer-reviewed publication) said 'yes', such an intervention might be something to consider based on scoring of the Montgomery–Åsberg Depression Rating Scale (MADRS) after 3 months of "individual nutritional consulting sessions delivered by a clinical dietician."Looking at two groups, those randomly allocated to dietary advice/intervention (n=31 completing) and those allocated to a control condition (social support) (n=25 completing), researchers noted improvements in the MADRS scores more frequently in the diet intervention group. To quote: "At 12 weeks, 32.3% (n = 10) of the dietary support group and 8.0% (n = 2) of the social support control group achieved remission criteria of a score less than 10 on the MADRS." Similar differences were also noted on other study schedules: the Hospital Anxiety and Depression Scale (HADS)-depression subscale.Caveats? Well as a seasoned veteran of research looking at how dietary intervention for labels generally thought to be outside of the somatic domain can go, I can testify to the limitations attached to this kind of work associated with a lack of double-blindedness and issues associated with dietary compliance. This was also a study providing dietary support and so was not necessarily making study controlled meals for each participant over the course of the study (lessons from other recent research show that advice and prompts can only go so far in dietary studies). The authors also note that they "recruited participants on the basis of existing ‘poor’ quality diet" and how "this may limit the generalisability of our findings to the wider population of individuals with depression." An important point indeed.But this study represents important work and provides yet more evidence that 'nutritional medicine' should perhaps be part of mainstream psychiatry (see here). You can um-and-ah about whether 'food is medicine' and all that jazz (have you never heard of pharmacognosy?) but I'm firmly with the idea that what we eat might, on occasion and for some people, have some pretty profound implications for things other than our physical health and that includes depression (included in several forms)...To close, a note to any would-be ageing karateka, middle-aged hips tend to take a little more time to get used to perfecting yoko geri kekomi (pass the ibuprofen please). But practice does (eventually) make perfect...----------[1] Jacka F. et al. A randomised controlled trial of dietary improvement for adults with major depression (the ‘SMILES’ trial). BMC Medicine. 2017; 15: 23.[2] O'Neil A. et al. A randomised, controlled trial of a dietary intervention for adults with major depression (the “SMILES” trial): study protocol. BMC Psychiatry. 2013; 13: 114.----------Jacka, F., O’Neil, A., Opie, R., Itsiopoulos, C., Cotton, S., Mohebbi, M., Castle, D., Dash, S., Mihalopoulos, C., Chatterton, M., Brazionis, L., Dean, O., Hodge, A., & Berk, M. (2017). A randomised controlled trial of dietary improvement for adults with major depression (the ‘SMILES’ trial) BMC Medicine, 15 (1) DOI: 10.1186/s12916-017-0791-y... Read more »

Jacka, F., O’Neil, A., Opie, R., Itsiopoulos, C., Cotton, S., Mohebbi, M., Castle, D., Dash, S., Mihalopoulos, C., Chatterton, M.... (2017) A randomised controlled trial of dietary improvement for adults with major depression (the ‘SMILES’ trial). BMC Medicine, 15(1). DOI: 10.1186/s12916-017-0791-y  

  • February 11, 2017
  • 04:43 AM
  • 138 views

Pregnancy exposure to SSRIs and offspring autism risk: debate continues

by Paul Whiteley in Questioning Answers

"It remains unclear whether the association between first trimester SSRI [selective serotonin reuptake inhibitor] exposure and child autism that was present in the case-control studies even after adjustment for MMI [maternal mental illness] is a true association or a product of residual confounding."So said the results of the systematic review and meta-analysis undertaken by Hilary Brown and colleagues [1] looking at a potentially important association between pregnancy use of a class of medicines typically used as antidepressants (albeit with some caveats [2]) and risk of offspring autism. This topic has previously received some airtime on this blog (see here and see here) and specifically, how maternal mental health - as per the question 'why were mothers taking SSRIs during pregancy?' - might be a rather large confounding variable affecting any possible correlation.Unfortunately even with the Brown paper, the debates will continue as to whether the SSRI-offspring autism correlation is a 'true' correlation or not. Based on the results of 6 studies - "4 case-control studies and 2 cohort studies" - where MMI was adjusted for/restricted to, authors reported some interesting trends. So in their meta-analysis of the data where results from case-control studies were adjusted for a potential impact from MMI, researchers observed that "first trimester exposure remained statistically significant." In "MMI-restricted analyses" covering the same study type, the collected studies did not show any connection between pregnancy SSRI use and offspring autism during either the first trimester or 'any time during pregnancy'. Similar results were found in the cohort studies included in the Brown paper (although both first trimester and 'any point during pregnancy' SSRI use both showed significant correlations to offspring autism in adjusted studies). I might also add that the Brown meta-analysis on this topic is not the only recent addition to the peer-reviewed literature [3]; indeed, there are several [4] others."Future studies require robust measurement of MMI prior to and during pregnancy" said Brown et al. I would agree with this sentiment added to the caveat that we may never truly know whether there is a definitive connection between pregnancy SSRI use and offspring autism risk on the basis of observational studies alone. Yes, I know it is unethical to withhold treatment such as SSRIs when clinically indicated even during pregnancy and so investigations utilising this kind of 'interventionist' study design are not likely to be undertaken anytime soon. But it does strike me that we could do quite a bit more modelling any potential effects (or not) in animal studies for example, as per some investigations with fish a while back (see here) as a start.And finally, although it is not my place to give clinical or medical advice on this blog, I should point out that much like investigations on another medicine prescribed during pregnancy potentially linked to offspring outcomes (see here), SSRIs are not generally given willy-nilly to pregnant women; there are very valid reasons for managing mum's psychiatric health particularly during pregnancy. If anyone is in doubt, please consult your doctor (and not just Dr Google).To close, before 'fake news' there was The Day Today (and they did it oh so well)...----------[1] Brown HK. et al. The Association Between Antenatal Exposure to Selective Serotonin Reuptake Inhibitors and Autism: A Systematic Review and Meta-Analysis. J Clin Psychiatry. 2017 Jan;78(1):e48-e58.[2] Jakobsen JC. et al. Selective serotonin reuptake inhibitors versus placebo in patients with major depressive disorder. A systematic review with meta-analysis and Trial Sequential Analysis. BMC Psychiatry. 2017; 17: 58.[3] Kaplan YC. et al. Prenatal selective serotonin reuptake inhibitor use and the risk of autism spectrum disorder in children: A systematic review and meta-analysis. Reprod Toxicol. 2016 Dec;66:31-43.[4] Kobayashi T. et al. Autism spectrum disorder and prenatal exposure to selective serotonin reuptake inhibitors: A systematic review and meta-analysis. Reprod Toxicol. 2016 Oct;65:170-178.----------Brown HK, Hussain-Shamsy N, Lunsky Y, Dennis CE, & Vigod SN (2017). The Association Between Antenatal Exposure to Selective Serotonin Reuptake Inhibitors and Autism: A Systematic Review and Meta-Analysis. The Journal of clinical psychiatry, 78 (1) PMID: 28129495... Read more »

  • February 10, 2017
  • 07:02 AM
  • 118 views

Teaching AI to be prejudiced, the “bamboo ceiling”,  overcoming unconscious bias, snap judgments and racial fears

by Doug Keene in The Jury Room

Time for another one of those combination posts on things much too good to overlook. This time we are almost all about various sorts of bias to keep you up to speed on the different ways we make (and teach) biased judgments. Bias is taught—even to artificial intelligence We hear a lot about how parents […]... Read more »

Azevedo, R., Garfinkel, S., Critchley, H., & Tsakiris, M. (2017) Cardiac afferent activity modulates the expression of racial stereotypes. Nature Communications, 13854. DOI: 10.1038/ncomms13854  

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