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  • March 28, 2017
  • 04:34 AM
  • 35 views

Presenting with the symptoms of autism and then diagnosed with phenylketonuria (PKU)

by Paul Whiteley in Questioning Answers

The case report from Betül Mazlum and colleagues [1] (open-access available here) illustrates once again that (a) the plural 'autisms' exist (see here) and (b) screening for inborn errors of metabolism (IEM) should be an important part of any autism assessment (see here). Indeed, screening for IEM should really be part of assessments for many different labels...Detailing a case report wherein a 3-year old child came to clinical attention for "speech delay and social problems", the authors describe how following a diagnosis of "autism according to DSM-IV criteria" further investigations were undertaken. Said investigations included analysis of blood and urine amino acid levels and, voilà, high levels of phenylalanine were detected and a diagnosis of phenylketonuria (PKU) made. Initiation of a low phenylalanine diet (the treatment of choice for PKU) followed and was accompanied by some important [positive] changes to behaviour and cognition. Of particular note to the presentation of autism we are told that: "At 4 months follow-up improvement was noticed in his eye contact, joined attention and speech."The authors further note: "This case was not at particular risk for PKU at first thought, being born to non-consanguineous parents and during a period when newborn screening with Guthrie test was widely applied in Turkey. Although the child had a heel prick in the hospital where he was delivered, the results are unavailable and therefore whether his sample was analyzed is questionable."OK, this was a case report and whilst an important 'N=1' is not necessarily generalisable to all autism (or rather all autisms). Insofar as the methods talked about for establishing raised phenylalanine - "Blood and urine amino acid chromatography" - I would have liked to have seen a little more detail in relation to the specific 'chromatography' methods used and any results related to another aromatic amino acid (tyrosine). We don't also have any data on follow-up either (repeat biological testing)...PKU is an important but quite rare IEM. This is not however the first time that PKU has been linked to autism or the presentation of autistic traits (see here) particularly in cases of 'untreated' PKU. Aside from PKU providing quite a good template for how diet - certain aspects of diet - can affect behaviour and mental state for some (see here) there are other potential implications and 'correlations' on the back of this work. Not least is the intersection between another intervention measure potentially indicated for PKU - tetrahydrobiopterin (sapropterin or BH4) - and research suggesting that the 'mopping up phenylalanine' properties of this compound might be potentially effective for some cases and facets of autism too (see here) based on double-blind, placebo-controlled trial results [2]."The possibility of a metabolic disorder including PKU should be considered in any child presenting with symptoms of autism, learning or speech problems and PKU should be tested unless the newborn screening results are available." I wouldn't argue with those sentiments [3], allowing for the fact that other correlates should also be considered (see here for example) particularly it seems, when autism appears alongside something like intellectual (learning) disability. The question of whether the quite restrictive low phenylalanine diet typically indicated for PKU might also impact autistic signs and symptoms is something that science still perhaps needs to look into...Music to close, and how about something lively from The King?----------[1] Mazlum B. et al. A late-diagnosed phenylketonuria case presenting with autism spectrum disorder in early childhood. Turk J Pediatr. 2016;58(3):318-322.[2] Klaiman C. et al. Tetrahydrobiopterin as a treatment for autism spectrum disorders: a double-blind, placebo-controlled trial. J Child Adolesc Psychopharmacol. 2013 Jun;23(5):320-8.[3] Bilder DA. et al. Neuropsychiatric comorbidities in adults with phenylketonuria: A retrospective cohort study. Mol Genet Metab. 2017 Mar 6. pii: S1096-7192(17)30052-5.----------Mazlum B, Anlar B, Kalkanoğlu-Sivri HS, Karlı-Oğuz K, Özusta Ş, & Ünal F (2016). A late-diagnosed phenylketonuria case presenting with autism spectrum disorder in early childhood. The Turkish journal of pediatrics, 58 (3), 318-322 PMID: 28266201... Read more »

Mazlum B, Anlar B, Kalkanoğlu-Sivri HS, Karlı-Oğuz K, Özusta Ş, & Ünal F. (2016) A late-diagnosed phenylketonuria case presenting with autism spectrum disorder in early childhood. The Turkish journal of pediatrics, 58(3), 318-322. PMID: 28266201  

  • March 27, 2017
  • 04:38 AM
  • 55 views

Detecting stereotypic behaviours through technology

by Paul Whiteley in Questioning Answers

"We have designed an Internet-of-Things (IoT) framework named WearSense that leverages the sensing capabilities of modern smartwatches to detect stereotypic behaviors in children with autism."So said the paper by Amir Mohammad Amiri and colleagues [1] (open-access available here) and, I have to say, something that really piqued my [research] attention. Describing how authors managed to design and construct a smartwatch with the ability to "detect three behaviors, including hand flapping, painting, and sibbing [hitting themselves on the top of their head] that are commonly observed in children with autism" they report some preliminary findings.When I say these are preliminary findings, I do indeed mean preliminary, as a two-phase preliminary trial included data from "12 healthy subjects aged between 23–33" and "two subjects (ages 15 and 16) diagnosed with autism." Aside from the implication that young adults with autism are somehow 'not healthy' (I think the correct terminology should be 'not diagnosed with autism/autism spectrum disorder'), you can perhaps see that much of the data for this study came from artificial, induced behaviours not necessarily produced by those on the spectrum - "The tasks that the subjects were invited to do included three different types for 20 s." I do have some other quibbles about the write-up of this study as per very generalised sentences like: "These stereotypic behaviors happen when a child is trying to regulate the sensory input from their surrounding environment."But I don't want to take anything away from the potential of this kind of research and where, with a bit more study and refinement, it could take many areas of autism research and practice. Accepting the argument that stereotypic behaviours that can accompany autism are not always something that needs to be tinkered with, I can perhaps see a use for this technology when it comes to screening and assessment. If for example, this kind of technology could be applied to something like an ADOS assessment, you could perhaps see how there may be additional information to be garnered (and indeed, built up coincidental to the 'objectivity' linked to such an exam). Coupled with other technology in relation to things like gaze monitoring for example, the potential gets even more exciting. And then also are the potentials of this kind of tracking software in relation to monitoring physical activity and autism (see here for example) or even in the context of epilepsy occurring alongside autism (see here for another WearSense use). There may be lots more to see when it comes to such technology and autism...----------[1] Amiri AM. et al. WearSense: Detecting Autism Stereotypic Behaviors through Smartwatches. Healthcare (Basel). 2017 Feb 28;5(1).----------Amiri AM, Peltier N, Goldberg C, Sun Y, Nathan A, Hiremath SV, & Mankodiya K (2017). WearSense: Detecting Autism Stereotypic Behaviors through Smartwatches. Healthcare (Basel, Switzerland), 5 (1) PMID: 28264474... Read more »

Amiri AM, Peltier N, Goldberg C, Sun Y, Nathan A, Hiremath SV, & Mankodiya K. (2017) WearSense: Detecting Autism Stereotypic Behaviors through Smartwatches. Healthcare (Basel, Switzerland), 5(1). PMID: 28264474  

  • March 25, 2017
  • 01:06 PM
  • 49 views

Native multilinguals

by Madalena Cruz-Ferreira in Being Multilingual

P { margin-bottom: 0.08in; } Some of my language teaching students sometimes express out loud their heartfelt desire to become native speakers. I was quite baffled the first time I heard this: we’re all native speakers, surely, and we can’t become natives, if we take the word “native” to mean what I supposed it is meant to mean, ‘from birth’. But does it? It turned out that my students’ previous teacher training had included the mantra that “native” means ‘flawless’ in this collocation, and flawless, whatever we take this word to mean, is certainly something that all of us can at least aspire to become. This latter meaning of the word “native” has in fact been made quite explicit in the literature about “second” (or “foreign”) languages – with my profuse apologies for the scare quotes that will crop up all over this post: I’ve no idea what the scared words might mean, in this literature. This meaning explains, for example, why some of us think it a worthwhile endeavour to compare school language learners to “native speakers”, for purposes of language quality assessment. But there is a snag: if learning languages from birth entails flawless use of those languages, how come multilinguals across the board, including simultaneous multilinguals who learn more than one language from Day One, go on being compared to “native speakers”? The thing is that “native speaker” has yet a third meaning, ‘monolingual’, this time a covert one, which nevertheless heeds the overt, systematic practice of comparing any multilinguals to monolinguals. This meaning explains, for example, the virtual absence of acknowledgement that multilinguals can be “native” users of their languages. If we accept that multilingual proficiency should be assessed through comparison with “native” proficiency, then we’re saying that multilinguals and natives are two distinct kinds of language users, since we can’t compare a thing to itself.But there is another snag. If multilinguals aren’t native users of their languages, then they must be “non-native”, by the logic of the assumedly useful labels which populate research on language uses. However, they aren’t, because multilinguals get compared to non-natives, too. In addition, simultaneous multilinguals can’t be “non-native”, if their languages are there for them from Day One, which is one of the meanings of “native”. Multilinguals, in sum, appear to inhabit a Linguistic No Man’s Land.“Day One”, unfortunately, may not be what clinches the issue either. If the language(s) in which we’re brought up from birth happen to be imported languages, then those languages aren’t “ours”. And if we learn a new language in early childhood, though not exactly from Day One, how many days should we count to count as a native user of it? Can I, for example, claim French as native language, having lived with it from just before age 3? Or was I then already way past my native learning prime, as I must have been when I learned my other languages several years later? If you’re interested in the mysteries of “critical periods” which snipe at “native” language learning abilities, Carmen Muñoz and David Singleton’s state of the art discussion, A critical review of age-related research on L2 ultimate attainment, is a must-read. Scare-quoted terminological acrobatics about multilingualism would be hilarious, of course, if it didn’t appear in “serious” research, thereby proving that we’ve no idea what we’re talking about. Have a look in my article First language acquisition and teaching, to see what I mean. The muddle got compounded when researchers developed a preference for labelling the languages of a multilingual by means of numbers, possibly on the belief that identifying things by numbers makes them look scientifically unquestionable. There’s always some “L1” lurking in there somewhere, which means that there must be rankings of L2, ... Ln, where the numbers apparently serve the purpose of showing that languages either politely follow one another or should do so. But what do these numbers mean when, say, simultaneous multilinguals learn one or more new languages in school? Not much, it seems, because we prefer to stick to labels rather than acknowledge their undefinable uselessness. Since “L1” represents an inherently singular concept (in more than one sense of “singular”), the logic of cardinal and ordinal numbering requires that L1 = “first language”, whereby everyone must have a single “first” language, endowed with rights of primogeniture associated with other firstborns. If there’s no single chronological first language, no problem: we just assign one to children, for reasons of administrative expediency, and call it their “mother tongue”. Finally, by the logic that first = “best”, we end up talking about “dominant” and “balanced” languages, and about all the other hopeless labels which do no more than betray our hopeless beliefs that multilinguals are, in fact, funny monolinguals. This state of affairs may well explain why multilingualism goes on being blamed for anything that deviates from monolingualism, to which I’ll return some other day. Meanwhile, the next post, a guest post, goes back to where this post started, to report vivid encounters with “nativeness” from a language teacher who’s also had plenty of reasons to wonder about the meaning of this word.... Read more »

  • March 25, 2017
  • 12:40 PM
  • 51 views

Sign-speech multilinguals

by Madalena Cruz-Ferreira in Being Multilingual

P { margin-bottom: 0.08in; } Opinions and decisions about multilingualism involving sign languages suffer from the same resilient fantasies which have plagued multilingualism in general over the past 100 years or so. With sign languages, however, there’s the aggravating factor that fantasies about them join the chorus. Only the other week, for example, I had a couple of (speech-speech) multilingual friends wonder why all the fuss about sign languages among linguists like me, since these languages are but a set of universal gestural primitives, like rubbing your tummy to indicate you’re hungry, as they put it. Aren’t they?, they nevertheless asked at the end of their reasoning. No, I replied. This would be roughly equivalent to saying that spoken languages are but a set of universal groany primitives to indicate your mood, as I put it. I took this chance to dispel their other illusion, that sign languages are straightforward fingerspelling systems, which draws on the interesting assumption that all signers must be literate. Many sign languages do include fingerspelling components, but the fact that, say, BSL (British Sign Language) and ASL (American Sign Language) use two-handed and one-handed spelling, respectively, for the same printed language, should help reassess the presumed straightforwardness of fingerspelling. In addition, BSL and ASL are as mutually unintelligible as other sign languages around the world. My friends are well educated, cosmopolitan professionals. Their take reflects the overarching myth that sign languages really aren’t languages at all, which goes on shaping policies devised by other professionals, those who have been empowered to deal with language education and who therefore aren’t in the habit of asking questions at the end of their reasonings. In a book chapter discussing The British Sign Language community up to the early 1990s, Paddy Ladd gives a distressing review of the ignorance and associated prejudice which, among other rulings, sanctioned physical violence to ‘cure’ deaf children of their signing ‘compulsion’. Just like, as I reported elsewhere, multilingualism came to be beaten out of hearing schoolchildren, the hands of deaf schoolchildren were tied behind their backs in order to force them to use spoken language. Just like, as I also reported elsewhere, multilingualism came to be medicalised, the language of deaf people was “pathologised” (Ladd’s word). Small wonder, then, that sign-speech multilinguals came to be viewed as doubly ‘handicapped’. When sign languages finally became legitimised, as it were, as objects of linguistic enquiry, sign multilingualism turned out, unsurprisingly, to match speech multilingualism. It comes complete with mixes, as David Quinto-Pozos reports for LSM (Lengua de Señas Mexicana) and ASL in Sign language contact and interference, for example, and with a lingua franca, International Sign, which Anja Hiddinga and Onno Crasborn discuss in Signed languages and globalization. But sign multilingualism remained the business of signers, so hearing communities needn’t bother with the eccentricities of deaf communities. Dealing with sign-speech multilingualism, however, appears to invite regression to hand-tied Fantasy Land: sign languages may be languages after all, but they are less so than spoken ones and should therefore not take priority in (so-called) multilingual education. It may help to understand that we’re talking about difference here, not winner-takes-it-all competition of gradable merits. It is as useful to compare the contexts of use of distinct linguistic modes as it’s useful to compare multilinguals and monolinguals. Insisting on doing so fails to recognise one of the many paradoxes reflecting our perennial difficulty in defining what languages are: do we want to say that speech beats sign, hands down, because we’re persuaded that auditory resources rank higher than visual ones in linguistic sophistication? Or should we rank those resources the other way around, because we believe that spoken languages are subsidiary to spelt ones? Language is as independent of the modes we’ve found to represent it – whether natural, sense-bound ones like sight, hearing, touch, or artificial ones like print – as music is independent of the instruments (our voice included) through which we produce it. What’s more, our senses seldom serve us to the exclusion of other senses. Manual gestures, for example, are intrinsic to spoken interaction, where attention to both visual and sound clues necessarily assists (de)coding. There’s even evidence that adequate gesturing enhances learning, as Martha W. Alibali and colleagues showed for a speech-based maths class in Students learn more when their teacher has learned to gesture effectively. In this sense, speakers and signers alike are multimodal users of language, and so are all of us, speakers or signers, who are literate. There may be some overlap between gestural uses in spoken and signed interaction, as Trevor Johnston argued for pointing gestures in Towards a comparative semiotics of pointing actions in signed and spoken languages, but the fundamental issue is that signs and speech belong to two different linguistic modes, each with their rules, standards and practices. Precisely for this reason, sign-speech multilinguals can avail themselves of means of linguistic expression which monomodal interaction lacks, in that “distinct modalities allow for simultaneous production of two languages”, as Karen Emmorey and colleagues discuss in Bimodal bilingualism. This means that sign-speech multilinguals, like any language users, must draw on the whole of their linguistic resources in order to be able to develop as human beings. The Position Statement on Early Cognitive and Language Development and Education of Deaf and Hard of Hearing Children, adopted by the NAD (National Association of the Deaf, USA) in June this year, makes for as engrossing reading as Paddy Ladd’s chapter – with many thanks to Beppie van den Bogaerde, who brought this publication to my attention on Twitter, @HU_DeafStudies. The document examines the relationship between sign, speech and print modes, debunking the usual myths about minority languages causing delayed development of mainstream languages (why never the other way around, one wonders?), about the primacy of spoken languages over signed ones, about reading abilities presupposing “... Read more »

Alibali, M., Young, A., Crooks, N., Yeo, A., Wolfgram, M., Ledesma, I., Nathan, M., Breckinridge Church, R., & Knuth, E. (2013) Students learn more when their teacher has learned to gesture effectively. Gesture, 13(2), 210-233. DOI: 10.1075/gest.13.2.05ali  

  • March 25, 2017
  • 05:37 AM
  • 80 views

Including the "full intellectual range" in autism vision research

by Paul Whiteley in Questioning Answers

The paper by Alyse Brown and colleagues [1] (open-access available here) is probably not going to gain any significant media headlines (unlike other recent studies - see here and see here) but does cover a rather important question regarding the autism research landscape: how representative is autism research?Specifically looking at the collected research on visual processing (distinct from physical issues with the eyes that still require greater awareness) with autism in mind, the authors surveyed the research literature to determine "what extent the ASD with-ID [intellectual disability] population has been excluded from visual research." Intellectual or learning disability is one of the more frequently over-represented comorbidities that can accompany a diagnosis of autism or autism spectrum disorder (ASD). Their answer: "our searches indicate that 80% of the vision research associated with ASD is representative of less than 60% of the appropriate population, i.e., those with ASD without ID while the ASD with ID group who we argue currently represent 42% of the ASD population, have not been adequately considered."You may well quibble with the "recalculation of ASD prevalence figures, using the criteria of DSM-5" as a means of calculating that '~40% of those with autism have ID too' figure. For me however, the message is quite stark: autism research - specifically related to visual processing issues - is not yet representative of  'all autism'."Reluctance to test individuals who are below 80 in IQ is presumably a practical stance as the data collected from these individuals are often hard to obtain, and often close to floor level performance." The authors note however that the presence of ID alongside autism in the area of visual processing is not something that cannot be 'overcome' by researchers with some creative thinking and a few modification(s) to their experimental designs. Indeed, visual processing research lends itself well to quite a few alterations to methods [2]...How applicable might these results be to other areas of autism research? Well, we just don't know. I daresay that quite a lot of the 'psychology' based autism research in particular might show a bias towards autism without intellectual disability for just those reasons listed above. The problem then of grand, over-arching generalisations to 'all autism' on the basis of results from the more 'cognitively-able' becomes apparent. Of course, in these days of the plural 'autisms' (see here) and the realisation that 'heterogeneity means heterogeneity' when it comes to autism (see here) one could argue that even characterisations based on the presence of ID or not when it comes to autism are equally 'simplistic' and equally 'useless'. How many autisms might well have an ID element to them? Is ID a comorbidity or something rather more central to some of the autisms? These questions and related others are ones that autism research as a whole will eventually have to start looking at and taking into account.And going back to the issue of eye disorders being potentially over-represented and under-diagnosed in relation to autism, the paper by Mouridsen and colleagues [3] reiterates that intellectual ability when accompanying autism needs more health equality: "The rate of eye disorder was particularly high (24.5%) in those with a co-occurring profound or severe learning disability (IQ < 50)."----------[1] Brown AC. et al. Vision Research Literature May Not Represent the Full Intellectual Range of Autism Spectrum Disorder. Front Hum Neurosci. 2017 Feb 14;11:57.[2] Boot FH. et al. Delayed visual orienting responses in children with developmental and/or intellectual disabilities. J Intellect Disabil Res. 2013 Dec;57(12):1093-103.[3] Mouridsen SE. et al. Eye Disorders among Adult People Diagnosed with Infantile Autism in Childhood: A Longitudinal Case Control Study. Ophthalmic Epidemiol. 2017 Mar 15:1-4.----------Brown AC, Chouinard PA, & Crewther SG (2017). Vision Research Literature May Not Represent the Full Intellectual Range of Autism Spectrum Disorder. Frontiers in human neuroscience, 11 PMID: 28261072... Read more »

  • March 24, 2017
  • 01:00 PM
  • 37 views

Lines that do not meet? Different perspectives of psychology upon organizations and work

by SciELO in SciELO in Perspective | Press Releases

Is it possible to attach a single label to the different approaches and professional practices of Psychology regarding work? Are there irreconcilable differences between psychology approaches, for example, an approach with a concentrated focus on management and another focused on the health of workers? … Read More →... Read more »

  • March 24, 2017
  • 03:46 AM
  • 101 views

Autism and anxiety disorder: zooming in on the details

by Paul Whiteley in Questioning Answers

Although it is not necessarily new news that (a) autism rarely exists in some sort of diagnostic vacuum, and (b) that some of the comorbidity 'over-represented' when it comes to autism can actually be more disabling than autism itself, there are still more investigations to be done.The paper by Vicki Bitsika & Christopher Sharpley [1] represents an example of how autism science is starting to go past the whole 'is there a connection between...' bit when it comes to autism and various comorbidity, specifically focused on the issue of anxiety. Looking at parental responses on "the Social Responsiveness Scale (SRS) and the GAD subscale of the Child and Adolescent Symptom Inventory (CASI-4 GAD) about their sons" researchers reported some rather interesting trends when it came to the two based on a cohort of young males diagnosed with autism. The authors used the term 'high-functioning' to describe the particular 'type' of autism being looked at in their study but I'm rather less sure this is an appropriate description ('high- and low-functioning' tend to be very generalised terms).I should back-track slightly and point out that the reasoning behind this research was to "assist in treatment or avoidance of GAD [generalised anxiety disorder] by identifying ASD [autism spectrum disorder]-related behaviours as 'targets' for intervention with anxious children as well as for preventative treatments that could be implemented into daily routines before children become anxious." Of all the debates past and present in relation to autism, specifically on the topic of 'treatment' (or even 'cure'), I don't think anyone would be opposed to the idea that anxiety (whether symptoms or disorder) should be treated and potentially 'cured' in this context. Anxiety can be absolutely disabling including when tied into autism.Results: bearing in mind their focus on only two parameters (SRS scores and GAD scores) in this study, there are some interesting trends in need of further investigation. So: "For pre-adolescents, high levels of tension in social situations were associated with 3.5-times greater likelihood of having GAD; for adolescents, experiencing difficulty in changes in routine was associated with a 10-fold increase in risk of GAD." The pre-adolescents and adolescents bit in that sentence was due to the division of their cohort on the basis of age. The results suggest therefore that anxiety (or at least GAD) might express itself for various different reasons potentially linked to the age/maturity of the person.I know some people might be shrugging their shoulders at such a finding and saying 'we already knew that'. Well, I'm not one of them. Take for example the 'change in routines' as being a possible factor in the expression of GAD in adolescents. The recent work by Joyce and colleagues [2] looking at another important term relevant to this issue - intolerance of uncertainty - adds an additional layer to the Bitsika/Sharpley findings as per their conclusion that: "replicated previous findings based on parent report showing a significant positive relationship between RRB [restricted and repetitive behaviours] and anxiety." RRBs can, amongst other things, include responses to routine (and changes to said routines).As to the question of what such findings might mean in the context of intervention, the authors talk about how intervening in the symptoms of GAD (a kind of reactionary approach) might also benefit from also trying to focus intervention on certain autistic symptoms too. Outside of the [careful] use of some of the talking/behavioural therapies and perhaps the whiff of some effect from certain pharmacological interventions when it comes to RRBs and autism, there isn't a great deal on offer at the moment in autism science and practice in this area. Indeed, if the relationship between RRBs and anxiety is further confirmed (and I mean confirmed [3]), I'd perhaps suggest that moves to target RRBs in the context of autism could/should be a research priority if only to potentially reduce the effects of anxiety.And the inquiry continues [4]...----------[1] Bitsika V. & Sharpley CF. The association between parents' ratings of ASD symptoms and anxiety in a sample of high-functioning boys and adolescents with Autism Spectrum Disorder. Res Dev Disabil. 2017 Mar 1;63:38-45.[2] Joyce C. et al. Anxiety, Intolerance of Uncertainty and Restricted and Repetitive Behaviour: Insights Directly from Young People with ASD. J Autism Dev Disord. 2017 Feb 25.[3] Wang S. et al. Sex Differences in Diagnosis and Clinical Phenotypes of Chinese Children with Autism Spectrum Disorder. Neurosci Bull. 2017 Feb 25.[4] South M. et al. Symptom overlap on the srs-2 adult self-report between adults with asd and adults with high anxiety. Autism Res. 2017. March 7.----------Bitsika, V., & Sharpley, C. (2017). The association between parents’ ratings of ASD symptoms and anxiety in a sample of high-functioning boys and adolescents with Autism Spectrum Disorder Research in Developmental Disabilities, 63, 38-45 DOI: 10.1016/j.ridd.2017.02.010... Read more »

  • March 23, 2017
  • 04:02 AM
  • 114 views

Congenital cytomegalovirus (CMV) infection and autism continued

by Paul Whiteley in Questioning Answers

I wanted to briefly talk about the paper by Francesca Garofoli and colleagues [1] on congenital cytomegalovirus (CMV) infection and autism not because it contains any novel data (see here), but because it reminds us that the potential 'pathways' to a diagnosis of autism are multiple and not necessarily 'pre-programmed' as per the 'it's all genetic' arguments that frequently figure in various domains.Congenital CMV infection refers to the transmission of CMV - "a common virus that belongs to the herpes family of viruses" - from mother to foetus during pregnancy. The details are still under investigation as to how and why CMV affects a foetus (bearing in mind this is quite a common virus) but autism as a consequence of [some] congenital CMV infection has growing evidence-based support [2].Garofoli et al included 70 'proven' cases of CMV "congenitally-infected infants" in their study; specifically looking "to correlate congenital cytomegalovirus (CMV) infection with autism spectrum disorder (ASD) and to define its prevalence." They determined that 2 of their 70 strong cohort met criteria for an ASD at the age of 3 years. Two of 70 translated as 2.8% of their cohort and contrasts with [estimated] autism prevalence "in general Italian population (0.66-1.36%)." The figure of 2.8% is also not a million miles away from other estimates of autism suggested via congenital CMV infection [3].Although 2.8% of the cohort (2/70) might not sound like a lot I'm inclined to suggest that it does prompt quite a lot more additional investigation. Not least is the question: 'why was autism/ASD not diagnosed in the other 68 children?' and onward whether other factors (genetics(!), biology, infection timing, immunologic response, etc) might come into play [4] in relation to the congenital CMV infection - autism association? Taking also into account the estimated prevalence of ASD in Italy, these figures (estimates) do seem to be a little lower than that described in other geographical locations (see here and see here for examples). Indeed, bearing in mind the research evidence already looking at estimated ASD prevalence in Italy [5] it's not unfair to say that 'under-estimation' might be a familiar theme...----------[1] Garofoli F. et al. An Italian Prospective Experience on the Association Between Congenital Cytomegalovirus Infection and Autistic Spectrum Disorder. J Autism Dev Disord. 2017 Mar 3.[2] Ornoy A. et al. Prenatal factors associated with autism spectrum disorder (ASD). Reprod Toxicol. 2015 Aug 15;56:155-69.[3] Engman ML. et al. Prenatal acquired cytomegalovirus infection should be considered in children with autism. Acta Paediatr. 2015 Aug;104(8):792-5.[4] Lombardo MV. et al. Maternal immune activation dysregulation of the fetal brain transcriptome and relevance to the pathophysiology of autism spectrum disorder. Mol. Psychiatr. 2017. March 21.[5] Ferrante M. et al. Prevalence and age at diagnosis of Autism Spectrum Disorder in south Italy, 2004–2014. Eur J Public Health. 2015; 25 (suppl_3).----------Garofoli F, Lombardi G, Orcesi S, Pisoni C, Mazzucchelli I, Angelini M, Balottin U, & Stronati M (2017). An Italian Prospective Experience on the Association Between Congenital Cytomegalovirus Infection and Autistic Spectrum Disorder. Journal of autism and developmental disorders PMID: 28258350... Read more »

  • March 22, 2017
  • 04:08 AM
  • 118 views

On genotype and environmental exposure patterns

by Paul Whiteley in Questioning Answers

I was rather interested to read the paper by Michela Traglia and colleagues [1] (open-access available here) concluding that: "maternal and fetal genetic make-up are important determinants of mid-gestational maternal circulating levels of some environmental organohalogens." Interested because, in these days of gene-environment interactions being applied to just about everything, the detail that is missing - which genes might potentially be linked to which environmental factors - has not yet been suitably addressed in the peer-reviewed science literature.So, based on data - "serum levels of a set of 21 organohalogens in a subset of 790 genotyped women and 764 children" - derived from participants included in the Early Markers for Autism (EMA) Project, researchers set about assessing how genetics might impact on environmental pollutant exposure profiles. Maternal blood samples were collected at around 15-20 weeks pregnancy. Children provided blood samples via the fabulous resource that is the newborn screening program, where: "Newborn blood spots were collected on filter paper 1-2 days after birth." Maternal samples were analysed for various environmental pollutants and both sets of samples were analysed for the genetic material they contained pertinent to whether "circulating mid-gestational levels of organohalogens would be driven by common maternal genetic determinants, and that these results could shed light on the observed associations between the organohalogens and ASD [autism spectrum disorder]."Results: yes, the authors "found evidence that a large proportion of maternal circulating levels of BB-153, BDE-47, -100, -153 [polybrominated congeners] and their sum was significantly controlled by common genetic factors." Those 'common genetic factors' typically referred to the presence of point mutations (SNPs) that litter everyone's genome and on occasion, can affect the function/production of specific biological processes. So: "Genome-wide association analyses identified significant maternal loci for p,p'-DDE... in the CYP2B6 gene and for BDE-28... near the SH3GL2 gene, both involved in xenobiotic and lipid metabolism." In other words, although the environmental pollutants measured are not great products in the first place (in terms of safety), a person's genetic make-up can influence how such products are eventually dealt with by the body and potentially onwards, what subsequent effects they might have.Additionally: "results suggest that the maternal circulating levels of some compounds were more highly influenced by fetal genetic factors than maternal genetics." This leads into another aspect of the current study whereby foetal genetic factors might also play a part in "controlling the toxicant disposition between mother and fetus." Specifically, authors noted that aspects of the individual genetics of a foetus (distinct from its mother) "contributed to the levels of BDE-100... and PCB187... near the potential metabolic genes LOXHD1 and PTPRD, previously implicated in neurodevelopment."And finally: "We confirmed that the serum levels of BDE-100, -153 and the total sum of PBDEs were significantly lower in mothers of ASD-affected children compared to mothers of control children." This is interesting in light of other discussions about PBDEs and autism in particular (see here). The authors do discuss various scenarios to account for their results not least that "transplacental transfer of organohalogens during pregnancy may be driven by the fetal genome expressed in placenta." Further analyses of the 'placentome' might therefore be indicated.To reiterate, this is interesting research. It tells us that many [adverse] environmental exposures, whilst typically to be avoided, don't act on the body in a uniform way as a function of differing genomes and differences in the ways that the body 'handles' such exposures. With autism in mind, this is not necessarily new news (remember paraoxonase gene variants and organophosphate metabolism [2] and air pollution and offspring autism?) but is a useful reminder. Such work also provides a template for looking at the myriad of other environmental factors put forward to influence autism risk and whether individual product safety is necessarily the only or most important factor when it comes to assessing relative risk profiles.I might finally also draw your attention to a recent interesting meta-analysis of the various environmental risk factors potentially linked to autism [3] (open-access) and another article talking about similar things [4] (open-access) (thanks Annabelle). Genes and environment, genes and environment...Music: Petula Clark sings the Beatles? Personally, I think it's better than the original...----------[1] Traglia M. et al. Independent Maternal and Fetal Genetic Effects on Mid-gestational Circulating Levels of Environmental Pollutants. G3 (Bethesda). 2017 Feb 24. pii: g3.117.039784.[2] D'Amelio M. et al. Paraoxonase gene variants are associated with autism in North America, but not in Italy: possible regional specificity in gene-environment interactions. Mol Psychiatry. 2005 Nov;10(11):1006-16.[3] Modabbernia A. et al. Environmental risk factors for autism: an evidence-based review of systematic reviews and meta-analyses. Molecular Autism. 2017; 8: 13.[4] Parker W. et al. The role of oxidative stress, inflammation and acetaminophen exposure from birth to early childhood in the induction of autism. Journal of International Medical Research. 2017. Jan 20.----------Traglia M, Croen LA, Lyall K, Windham GC, Kharrazi M, DeLorenze GN, Torres AR, & Weiss LA (2017). Independent Maternal and Fetal Genetic Effects on Mid-gestational Circulating Levels of Environmental Pollutants. G3 (Bethesda, Md.) PMID: 28235828... Read more »

  • March 21, 2017
  • 01:00 PM
  • 112 views

Study proposes fruition as a new attribute of information representation for works of contemporary art

by SciELO in SciELO in Perspective | Press Releases

It discusses information and art starting from the books of artists, from the collection of the Núcleo de Arte Contemporânea da Paraíba (NAC/UFPB), analyzing the performance of CI through the representation of information, in a collaborative working relationship between professionals. The representation of information could help in the treatment and organization of information, softening the complexity of these objects in the face of their possibilities of abstraction and fruition. … Read More →... Read more »

  • March 21, 2017
  • 10:04 AM
  • 165 views

The Weirdest Animals on Earth: 12 Amazing Facts About Platypuses

by Miss Behavior in The Scorpion and the Frog

What IS that? A photo by Stefan Kraft at Wikimedia Commons.1. Platypuses are so strange, that when British scientists first encountered one, they thought it was a joke: A Governor of New South Wales, Australia, sent a platypus pelt and sketch to British scientists in 1798. Even in their first published scientific description of the species, biologists thought that this duck-beaked, beaver-bodied, web-footed specimen may be some Frankenstein-like creation stitched together as a hoax. But this is only the beginning of their oddities…2. Platypuses are egg-laying mammals. Mammals are animals that have a backbone, are warm-blooded, and females produce milk for their young. Most females that nurse their young also carry their developing babies in their bodies and give birth to live young… But platypuses don’t play by those rules. Platypuses are monotremes, egg-laying mammals that include the platypus and four species of echidna. Most female mammals have two functional ovaries, but female platypuses, like most female birds, only have a functional left ovary. Once a year, a female platypus may produce a clutch of two or three small, leathery eggs (similar to reptile eggs), that develop in her uterus for 28 days. Because female platypuses don’t even have a vagina, when the eggs are ready, she lays them through her cloaca, an opening that serves for reproduction, peeing and pooping. (In fact, monotreme comes from the Greek for “one hole”). She then curls around them and incubates them for another 10 days until they hatch. 3. Platypuses sweat milk! Not only do female platypuses not have vaginas, they don’t have nipples either! Instead, lactating mothers ooze milk from pores in their skin, which pools in grooves on their bellies so the babies can lap it up. …And they’re not even embarrassed about it! 4. Adult platypuses are toothless. Baby platypuses (that is the actual technical term for them, by the way… not “puggles”, which would be way more fun) are born with teeth but they lose them around the time that they leave the breeding burrow. In their place are rigid-edged keratinized pads that they use as grinding plates. When they catch their prey (worms, bugs, shrimp, and even crayfish), they store it in their cheek pouches and carry it to the surface, where they use gravel to crush it in their toothless maw.5. The platypus “duck bill” is a sensory organ used to detect electric fields. Muscles and neurons use electrical impulses to function, and these impulses can be detected by electroreceptors. Although common in shark and ray species, electroreception is rare in mammals, only having been discovered in monotremes and the Guiana dolphin. Platypuses have rows of around 40,000 electroreceptors on their highly sensitive bill, which they wave back and forth in the water, much like a hammerhead shark, to determine the location of their prey. It’s a good thing this sense is so sensitive, since they close their eyes, nose and ears every time they dive. 6. Platypuses don’t use their tails like beavers do. Whereas beavers use their large, flat, leathery tails for swimming and slapping the water to send signals, platypuses don’t use their tails for any of that. Platypuses have large, flat tails for storing fat in case of a food shortage. Unlike beaver tails, platypus tails are covered in fur, which the mothers use to snuggle with their incubating eggs.A platypus ankle spur. Photo by E.Lonnon at Wikimedia Commons.7. Male platypuses have venomous ankle spurs. Their venom is strong enough to kill small animals and to create excruciating pain in humans. Since only males have it and they produce more venom during the breeding season, we think its main function may be to compete for mates and breeding territories.8. Platypuses are knuckle-walkers with a reptilian gait. Although they are well-built for swimming with their webbed feet and legs on the sides of their bodies, these traits make it quite awkward to get around on dry land. To walk, they pull in their webbing and walk on their knuckles, exposing their claws. Like reptiles and salamanders, platypuses flex their spines from side-to-side, supported by their sprawling legs. 9. Platypuses have unusually low body temperatures. As unusual as they are, platypuses are still mammals, which are defined, in part, by their ability to generate most of their own body heat with their metabolism. Platypuses do this as well, but whereas most mammals maintain body temperatures between 37-40 degrees C (99-104 degrees F), platypuses are happy with a body temperature of 32 degrees C (90 degrees F). This lower metabolism reduces the amount of calories they need to eat.10. They have no stomach. Stomachs are specialized protein-digesting chambers of digestive tracts that contain protein-digesting enzymes and acids to activate them. Not all animals have them, but most carnivores do. The most common exceptions to this rule are fish… and platypuses. Why? We don’t know for sure, but many of these animals consume diets high in calcium carbonate, which is a natural antacid. If their own diet would constantly neutralize their stomach acid, then the stomach really isn’t going to do them any good anyway.11. They have 10 sex chromosomes! Most mammals have two sex chromosomes, one from each parent. An individual that has two X chromosomes is usually female and an individual that has one X and one Y chromosome is usually male. Thus, female mammals pass along an X chromosome to each offspring and males can pass along an X or a Y. But platypuses are not content to be normal in any way…They have 10 sex chromosomes: 5 from mom and 5 from dad. All 5 chromosomes from mom are Xs, whereas a male sperm either contains 5 Xs or 5 Ys. Birds also have two sex chromosomes, but in birds, individuals with two of the same type are usually male and individuals with different chromosomes are usually female. Their system is called ZW, where the mammalian system is XY. The platypus X chromosome is more similar than the X chromosome of other mammals to the bird Z chromosome.12. The platypus genome is as much of a hodgepodge as its body. Only 80% of the platypus’ genes are like other mammals. Some of their genes have only previously been found in birds, reptiles, fish, or amphibians.To learn about more weird animals, go here.References: ... Read more »

Scheich, H., Langner, G., Tidemann, C., Coles, R., & Guppy, A. (1986) Electroreception and electrolocation in platypus. Nature, 319(6052), 401-402. DOI: 10.1038/319401a0  

Warren, W., Hillier, L., Marshall Graves, J., Birney, E., Ponting, C., Grützner, F., Belov, K., Miller, W., Clarke, L., Chinwalla, A.... (2008) Genome analysis of the platypus reveals unique signatures of evolution. Nature, 453(7192), 175-183. DOI: 10.1038/nature06936  

  • March 21, 2017
  • 03:57 AM
  • 140 views

PACE trial recovery data and chronic fatigue syndrome - a reply

by Paul Whiteley in Questioning Answers

I'd encourage readers interested in the background to the response paper by Michael Sharpe and colleagues [1] to have a look at a previous blogging occasion when the topic of the PACE trial, chronic fatigue syndrome (CFS) and 'recovery' were discussed (see here).Suffice to say that this latest paper is a reply to one published by Carolyn Wilshire and colleagues [2] who concluded that: "The claim that patients [with CFS] can recover as a result of CBT [cognitive behaviour therapy] and GET [graded exercise therapy] is not justified by the data, and is highly misleading to clinicians and patients considering these treatments." Said discussions linking back to some quite extensive debates on how one should (and shouldn't) treat/manage conditions like CFS (see here).I wanted to highlight the latest Sharpe paper because (a) I anticipated a reply from these authors following the Wilshire paper criticism of their recovery paper [3], and (b) although the debates in this area have been quite extensive already, the use of the scientific peer-reviewed medium to discuss and even argue is an important avenue. The authors have a right to scientific reply.So how did Sharpe et al respond? Well the words 'recovery', 'threshold' and ''no generally agreed measure of recovery" when it comes to CFS form the crux of the response to the Wilshire paper. They address the issue of recovery thresholds that have been a real source of discussion in relation to the PACE trial secondary analysis concluding that: "No participant met our full criteria for recovery at baseline." They point out that whilst "13% of participants met the recovery criterion of being within the normal range... for physical functioning when entering the trial" physical functioning was but one measure they used to determine recovery.They also approach the topic of 'changing thresholds' when it came to the definition of recovery in the PACE trial. To quote: "We changed these thresholds for our detailed analysis plan because after careful consideration and consultation, we concluded that they were simply too stringent to capture clinically meaningful recovery." They also report that elements of their assessment - the PACE walking test - are "not comparable with data collected in other studies" as a function of their reliance on personal motivation/ability over and above the use of encouragement as in other studies.Finally, authors also talk about 'what other studies have found regarding recovery' when it comes to CFS. They note that their findings in relation to the use of standard medical care (SMC) for CFS in the PACE trial were similar to other reports [4]. They also point to research suggesting that the use of CBT in independent study for CFS show similar rates of recovery [5] to theirs originally reported. In other words, they make a case for their findings fitting in with some of the other literature on this topic.A quick trawl of PubMed with the terms 'chronic fatigue syndrome' and 'recovery' reveals that there is indeed quite a bit more to do in this area of science. To quote from one paper (a critical review) [4]: "Estimates of recovery ranged from 0 to 66 % in intervention studies and 2.6 to 62 % in naturalistic studies." What this tells us is that (a) how recovery is reported in relation to CFS is still in need of some clarification [6] and perhaps more importantly, agreed uniformity is still required in its assessment; (b) some of the measures used to form judgements of recovery when it comes to CFS are not necessarily fit for purpose [7] (bearing in mind not everyone agrees with this); and (c) further efforts need to go into looking at many more aspects of CFS recovery outside of just a reliance on the fatigue parameter (see here and see here for examples). In short, science does not really know what recovery looks like in relation to CFS [8] despite it seemingly happening for all manner of reasons...Where do we go from here? This is a difficult question to answer. It is doubtful that the response from Sharpe and colleagues is going to change too many opinions about PACE given the strength of feeling on the topic and the various goings-on that have occurred around debate in this area (see here). Still today, other comments on the PACE trial continue to emerge in the peer-reviewed domain [9] from notable CFS researchers and there are even calls to retract the original recovery paper (see here). Yes, there are lessons to be learned from the PACE trial (e.g. stick to your "original protocol thresholds", make your data 'open-access' and think about how to do this in the planning/recruitment stages of your trial, be mindful that short-term gains don't necessarily translate into long-term ones, work with the ME/CFS community (rather than labelling elements of them 'vexatious' or worse when they ask questions or request data) but I can't see how these factors will immediately and positively affect the lives of people living with CFS/ME here and now. That recommendations on the use of CBT for CFS have already altered in some parts of the world (see here) - "The strength of evidence on global improvement is downgraded from moderate to low when considering CBT separately from other counseling and behavioral interventions" - and are potentially likely to change here in Blighty perhaps signifies that science and medicine is moving on when it comes to this topic. Science should be doubling its efforts to expand its research boundaries when it comes to managing CFS outside of just a reliance on the [outdated?] psychosomatic model and indeed, it is...And on the topic of other CFS research avenues, I've already talked about a few interesting avenues on this blog (see here and see here and see here) mindful that when we talk about CFS/ME, we're probably not talking about just one entity (see here). Also alongside, that there seems to be an awful lot of 'over-represented' comorbidity accompanying quite a lot of CFS/ME (see here for example) to also contend with...Music: Lush Life (even if you don't know the song title, you might rec... Read more »

M Sharpe, T Chalder, AL Johnson, KA Goldsmith, & PD White. (2017) Do more people recover from chronic fatigue syndrome with cognitive behaviour therapy or graded exercise therapy than with other treatments?. Fatigue: Biomedicine, Health , 1-5. info:/10.1080/21641846.2017.1288629

  • March 20, 2017
  • 04:31 PM
  • 146 views

Why ear plugs are great for clubbing and concerts

by Richard Kunert in Brain's Idea

I enjoy clubbing and pop/rock concerts exclusively with my ear plugs in. Does that mean I miss out? No, I enjoy the music exactly as it is meant to be. Picture by Melianis at fi.wikipedia (CC BY 2.5) Since 2004 the urban dictionary includes the term ‘deaf rave’ to describe a ‘rave, or party, organised […]... Read more »

Huang J, Gamble D, Sarnlertsophon K, Wang X, & Hsiao S. (2013) Integration of auditory and tactile inputs in musical meter perception. Advances in experimental medicine and biology, 453-61. PMID: 23716252  

Russo FA, Ammirante P, & Fels DI. (2012) Vibrotactile discrimination of musical timbre. Journal of experimental psychology. Human perception and performance, 38(4), 822-6. PMID: 22708743  

Zhao F, Manchaiah VK, French D, & Price SM. (2010) Music exposure and hearing disorders: an overview. International journal of audiology, 49(1), 54-64. PMID: 20001447  

  • March 20, 2017
  • 01:00 PM
  • 95 views

Research analyzes use of TRS in organizational studies

by SciELO in SciELO in Perspective | Press Releases

Bibliometric research analyzes the use of Social Representation Theory (SRT) in Organizational Studies (OS). We investigated 90 papers published in journals and scientific events from 2001 to 2014. The results indicate that the use of SRT in OS is incipient, superficial and presents theoretical and methodological inconsistencies. … Read More →... Read more »

  • March 20, 2017
  • 07:02 AM
  • 135 views

Simple Jury Persuasion: The SPOT (Spontaneous Preference  for Own Theories) effect 

by Doug Keene in The Jury Room

It’s been a while since we’ve had a new cognitive bias to share with you. Previously we’ve blogged on many different biases and here are a handful of those posts. Today’s research paper combines three biases—two of which we’ve blogged about before: the better-than-average effect, confirmation bias and also, the endowment effect. The endowment effect […]... Read more »

Gregg AP, Mahadevan N, & Sedikides C. (2017) The SPOT effect: People spontaneously prefer their own theories. Quarterly Journal of Experimental Psychology, 70(6), 996-1010. PMID: 26836058  

  • March 20, 2017
  • 04:13 AM
  • 141 views

ALSPAC says no to cat ownership - psychosis risk hypothesis but...

by Paul Whiteley in Questioning Answers

"While pregnant women should continue to avoid handling soiled cat litter, given possible T. gondii exposure, our study strongly indicates that cat ownership in pregnancy or early childhood does not confer an increased risk of later adolescent PEs [psychotic experiences]."So said the findings reported by Francesca Solmi and colleagues [1] (open-access) who brought a smile to any reader of the title of their paper: "Curiosity killed the cat: no evidence of an association between cat ownership and psychotic symptoms at ages 13 and 18 years in a UK general population cohort." For those who might not be aware of the hypothesis, cat ownership has been previously linked to 'adverse' psychological outcomes (see here) tied into some peer-reviewed evidence on one possible environmental factor linked to psychosis and conditions manifesting psychosis: Toxoplasma gondii.ALSPAC - Avon Longitudinal Study of Parents and Children - brought it's quite significant scientific prowess to bear on the question of whether "cat ownership in pregnancy and childhood (ages 4 and 10 years) was associated with psychotic experiences (PEs) in early (age 13, N = 6705) and late (age 18, N = 4676) adolescence, rated from semi-structured interviews." Having a cat in the house was not the only question asked by Solmi et al as the presence of other pets were also investigated: "dogs, rabbits, rodents, birds (all waves), and tortoises and fish (from 21 months)." PEs were assessed at approximate ages of 13 and 18 years old via responses to the "psychotic-like symptoms interview (PLIKSi), a semi-structured interviewer-rated screening assessment for PEs." Various other variables were also factored into the examination of any effect or not.Results: well, as per the opening sentence to this post, cat ownership did not seem to be related to later PEs. The potential caveat being that in some of their analyses there did seem to be a possible association - "Owning a cat at age 4 years was associated with higher odds of having PEs at age 13 years in univariable models" - but the significance of this association disappeared when adjustments for other potentially confounding variables were made. Obviously this kind of study can't control for every single potentially confounding variable but they did at least try.Why the disparity between these results and the previous ones suggestive of a possible connection between childhood cat ownership and later adverse psychological health? Well, an important point is made by Solmi and colleagues: "Our study was based on PEs in early and late adolescence, unlike other studies which were based on a clinical diagnosis of schizophrenia." In other words. psychotic experiences might be part and parcel of schizophrenia but not necessarily all that schizophrenia encompasses and not necessarily just enough to merit a diagnosis of schizophrenia. They do also go on to highlight how the previous report on the association may also not have included the range of potentially confounding variables that were included and controlled for in the current study as another possibility for the differences reported. Having said that [2]...Does the T. gondii - schizophrenia hypothesis fall as a result of the Solmi results? Probably not. Solmi et al hint that even though cat ownership probably isn't related to PEs, they do not totally debunk the idea that there may be a connection. They did not for example, look for the presence of contact with T. gondii in this particular study (others have) as per serological examination of participants. I say this bearing in mind that not every moggy is necessarily infected with T. gondii or anything else. Sweeping generalisations on all cats are not required.Music to close, and containing the lyric 'Caringosity killed the Kerouac cat', a chirpy little number from a band with quite a contentious name...----------[1] Solmi F. et al. Curiosity killed the cat: no evidence of an association between cat ownership and psychotic symptoms at ages 13 and 18 years in a UK general population cohort. Psychol Med. 2017 Feb 22:1-9.[2] Fuller Torrey E. et al. The antecedents of psychoses: a case-control study of selected risk factors. Schizophr Res. 2000 Nov 30;46(1):17-23.----------Solmi F, Hayes JF, Lewis G, & Kirkbride JB (2017). Curiosity killed the cat: no evidence of an association between cat ownership and psychotic symptoms at ages 13 and 18 years in a UK general population cohort. Psychological medicine, 1-9 PMID: 28222824... Read more »

  • March 19, 2017
  • 11:14 PM
  • 142 views

3 Study Habits of Successful Students in College

by Winston Sieck in Thinker Academy

Can’t wait to break out of high school and dash off to college? College is a lot of fun. Late nights, parties, sporting events with thousands of people, on-campus concerts and thousands of potential new friends combine to make college some of the best years of a person’s life. Yet, in the midst of all […]
Check out 3 Study Habits of Successful Students in College, an original post on Thinker Academy.
... Read more »

  • March 18, 2017
  • 04:58 AM
  • 148 views

HSV-2 gestational infection and offspring autism risk

by Paul Whiteley in Questioning Answers

"In our cohort, high levels of antibodies to herpes simplex virus 2 at midpregnancy were associated with an elevated risk of autism spectrum disorder in male offspring. These findings provide support for the hypothesis that gestational infection may contribute to the pathogenesis of autism spectrum disorder and have the potential to drive new efforts to monitor women more closely for cryptic gestational infection and to implement suppressive therapy during pregnancy."That was the conclusion reached in the paper published by Milada Mahic and colleagues [1] including the research tag-team that is Mady Hornig and Ian 'virus hunter' Lipkin in the list of contributing authors. Having already received some media attention (see here), it doesn't need much more from me but I do want to include a few details and relevant points in this blog entry.So, the Autism Birth Cohort was the starting point, and "442 mothers of children with ASD... and 464 frequency-matched controls" who all provided plasma samples "(903 samples acquired at midpregnancy and 878 acquired after delivery)." Said samples were analysed for IgG antibodies to ToRCH agents: "Toxoplasma gondii, rubella virus, cytomegalovirus (CMV), and herpes simplex viruses 1 (HSV-1) and 2 (HSV-2)." Some of those viruses and parasites have previously been mentioned with [some] autism in mind (see here and see here and see here).Results: well, an important detail first: "Because rubella vaccination is part of the routine child vaccination schedule in Norway, almost all individuals had IgG antibodies to rubella virus." Indeed, other authors have speculated that rubella vaccination has actually "prevented substantial numbers" of autism as a knock-on effect of reducing the numbers of cases of congenital rubella syndrome [2]. Vaccination doing more than just saving lives eh?Next: "Our data suggest that the presence of high levels of anti-HSV-2 antibodies at midpregnancy increases the risk of ASD [autism spectrum disorder] in boys." The authors complemented this finding by some rather neat statistical wizardry whereby odds ratios were calculated based on "four different anti-HSV-2 reference levels (60, 120, 180, and 240 arbitrary units [AU]/ml)." Having said that: "High levels of antibodies, which are typically indicative of recent infection, were found in only a small number of subjects." They also reported "no statistically significant association with risk was found with high levels of HSV-2 antibodies at delivery" and saw nothing significant when it came to the other infections examined. These important points have been picked up in the NHS Choices entry on this study (see here).These are interesting findings and, as far as I can see, represent something quite novel to the quite vast autism research landscape (assuming you count maternal HSV-2 levels and not antibody levels in actual people diagnosed with autism). The reliance on data from an initiative like the Autism Birth Cohort ensured some rigour in terms of the diagnosis of autism [3] and with the reputations following Drs Hornig and Lipkin, one would have to be pretty brave to question their virus-hunting credentials also with autism in mind [4].Then to the million-dollar question: how might elevated HSV-2 antibodies during pregnancy affect offspring risk of autism? There is a familiar theme offered by the authors to this question as per statements like: "ASD risk associated with high levels of antibodies to HSV-2 is not specific to HSV-2 but instead reflects the impact of immune activation and inflammation on a vulnerable developing nervous system." I know some people still have a bit of a problem with the idea that something like maternal immune activation (MIA) might up the risk for various offspring outcomes [hint: if an article contains the word 'truth' in the title, step away] but please, stop with the 'it can never happen' generalisations and instead look to the existing peer-reviewed evidence on the topic [5]. Yes, science needs to do more on the topic of MIA and autism but clues are emerging all the time...Oh, and I'll be coming to research talking about another member of the herpesviruses in relation to autism quite soon on this blog.To close, operation hardtack and other videos (best viewed in full-screen mode).----------[1] Mahic M. et al. Maternal Immunoreactivity to Herpes Simplex Virus 2 and Risk of Autism Spectrum Disorder in Male Offspring. mSphere. 2017. Feb 22.[2] Berger BE. et al. Congenital rubella syndrome and autism spectrum disorder prevented by rubella vaccination - United States, 2001-2010. BMC Public Health. 2011; 11: 340.[3] Stoltenberg C. et al. The Autism Birth Cohort (ABC): A Paradigm For Gene-Environment-Timing Research. Molecular Psychiatry. 2010;15(7):676-680.[4] Hornig M. et al. Lack of association between measles virus vaccine and autism with enteropathy: a case-control study. PLoS One. 2008 Sep 4;3(9):e3140.[5] Careaga M. et al.  Maternal Immune Activation and Autism Spectrum Disorder: From Rodents to Nonhuman and Human Primates. Biol Psychiatry. 2017 Mar 1;81(5):391-401.----------Milada Mahic, Siri Mjaaland, Hege Marie Bøvelstad, Nina Gunnes, Ezra Susser, Michaeline Bresnahan, Anne-Siri Øyen, Bruce Levin, Xiaoyu Che, Deborah Hirtz, Ted Reichborn-Kjennerud, Synnve Schjølberg, Christine Roth, Per Magnus, Camilla Stoltenberg, Pål Surén, Mady Hornig, & W. Ian Lipkin (2017). Maternal Immunoreactivity to Herpes Simplex Virus 2 and Risk of Autism Spectrum Disorder in Male Offspring. mSphere : ... Read more »

Milada Mahic, Siri Mjaaland, Hege Marie Bøvelstad, Nina Gunnes, Ezra Susser, Michaeline Bresnahan, Anne-Siri Øyen, Bruce Levin, Xiaoyu Che, Deborah Hirtz.... (2017) Maternal Immunoreactivity to Herpes Simplex Virus 2 and Risk of Autism Spectrum Disorder in Male Offspring. mSphere. info:/10.1128/mSphere.00016-17

  • March 17, 2017
  • 07:02 AM
  • 147 views

Don’t do this at work, beards, ear worms, narcissists, &  discarding advances in knowledge

by Rita Handrich in The Jury Room

Here’s another this-and-that post documenting things you need to know but that we don’t want to do a whole post about–so you get a plethora of factoids that will entertain your family and entrance your co-workers. Or at least be sort of fun to read and (probably) as awe-inspiring as the stack of vegetables and […]... Read more »

Beaman, CP, Powell, K, & Rapley, E. (2015) Want to block eagworms from conscious awareness? Buy gum! . The Quarterly Journal of Experimental Psychology,, 68(6), 1049-1057. info:/

Hepper EG, Hart CM, & Sedikides C. (2014) Moving Narcissus: Can Narcissists Be Empathic?. Personality , 40(9), 1079-1091. PMID: 24878930  

  • March 17, 2017
  • 03:39 AM
  • 137 views

Fatty acids and autism meta-analysed yet again (with a different result?)

by Paul Whiteley in Questioning Answers

OK I'm a little confused right now.Not so long ago I talked about the paper from Horvath and colleagues [1] (see here) concluding that "the limited data currently available suggest that ω-3 FA [omega-3 fatty acid] supplementation does not enhance the performance of children with ASD [autism spectrum disorder]." Such a conclusion was based on the application of a systematic review and meta-analysis of the available peer-reviewed literature up to August 2016.Now however, another systematic review and meta-analysis on the topic has emerged from Mazahery and colleagues [2] and reported something a little bit different: "Populations with ASD have lower n-3 LCPUFA status and n-3 LCPUFA supplementation can potentially improve some ASD symptoms." Don't you just love science!OK, so what could be the reason(s) for the differing conclusions reached by the reviews on this topic? Well, Mazahery and colleagues (the most recent review) actually conducted two meta-analyses: "meta-analysis 1 compared blood levels of LCPUFA and their ratios arachidonic acid (ARA) to docosahexaenoic acid (DHA), ARA to eicosapentaenoic acid (EPA), or total n-6 to total n-3 LCPUFA in ASD to those of typically developing individuals (with no neurodevelopmental disorders), and meta-analysis 2 compared the effects of n-3 LCPUFA supplementation to placebo on symptoms of ASD." Horvath et al only conducted one meta-analysis in their study roughly equivalent to meta-analysis 2 presented by Mazahery looking at the effects of fatty acid supplementation on the presentation of autism. Mazahery and colleagues also surveyed the literature up to May 2016 and found four randomised-controlled trials (RCTs) (N=107) whereas Horvath et al (who published earlier!) surveyed the literature up to August 2016 and found five RCTs (N=183). Indeed, it appears that based on that last 'difference' one might see how the grand 'top of the scientific hierarchy' meta-analysis is yet again, only as good as the data it contains. And a certain celebrity in science circles seems to agree...Where next I hear you ask? Well, I'd be tempted to follow the recommendations of Mazahery and colleagues when they suggest that: "Further research with large sample size and adequate study duration is warranted to confirm the efficacy of n-3 LCPUFA." Indeed, there are already studies to watch in this area. That and recognising that within the vast plurality that is the autisms it is not totally outside the realms of possibility that specific parts of the autism spectrum might be more vulnerable to fatty acid issues than others. Oh, and don't forget that outside of impacting autistic 'performance' (or not), fatty acid supplementation does seem to have other health-related properties too...----------[1] Horvath A. et al. ω-3 Fatty Acid Supplementation Does Not Affect Autism Spectrum Disorder in Children: A Systematic Review and Meta-Analysis. J Nutr. 2017 Jan 11. pii: jn242354.[2] Mazahery H. et al. Relationship between Long Chain n-3 Polyunsaturated Fatty Acids and Autism Spectrum Disorder: Systematic Review and Meta-Analysis of Case-Control and Randomised Controlled Trials. Nutrients. 2017 Feb 19;9(2). pii: E155.----------Mazahery H, Stonehouse W, Delshad M, Kruger MC, Conlon CA, Beck KL, & von Hurst PR (2017). Relationship between Long Chain n-3 Polyunsaturated Fatty Acids and Autism Spectrum Disorder: Systematic Review and Meta-Analysis of Case-Control and Randomised Controlled Trials. Nutrients, 9 (2) PMID: 28218722... Read more »

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