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  • April 29, 2017
  • 05:18 AM

When grandmothers smoked during pregnancy...

by Paul Whiteley in Questioning Answers

Please, do not smoke during pregnancyALSPAC - the Avon Longitudinal Study of Parents and Children - continues to give in research terms as today I want to mention the findings reported by Jean Golding and colleagues [1] (open-access) observing "an association between maternal grandmother smoking in pregnancy and grand daughters having adverse scores in Social Communication and Repetitive Behaviour measures that are independently predictive of diagnosed autism."The study results have garnered quite a bit of media interest (see here for example) with calls for quite a bit more research to be carried out on this important topic. I might also give a hat-tip to Jill Escher and the Escher Fund for Autism who were instrumental in this study. Indeed, her analysis of the Golding results (see here) will no doubt trump my contribution.The Golding paper is open-access but a few details are worth mentioning:As I noted, ALSPAC provided the source data for the study (as it has on quite a few autism research occasions). This time around researchers looked at autistic traits among some of their 14,000 strong cohort comprising "a social communication score, a speech coherence score, a sociability temperament scale, and a repetitive behaviour score." Mothers and fathers of children involved in ALSPAC also provided information about pregnancy including answering questions on whether mothers themselves were/had smoked during pregnancy and also whether their mother (the child's grandmothers on both sides) smoked during pregnancy.The data obtained from the autistic traits measures (delivered at various times of the child's development) and the smoking histories were analysed. Data on some 170 participating children actually diagnosed with an autism spectrum disorder (ASD) were also thrown into the statistical mix.Results: "We found that two of the four autistic traits in the grandchild (F2) were increased in prevalence if the maternal grandmother (F0) smoked in pregnancy especially if the mother herself (F1) did not herself smoke." Researchers also noted a particular association between grandmother pregnancy smoking and grand-daughters over grandsons, and several potentially important confounding variables were also taken into account. They also concluded that "diagnosed autism was also associated with the maternal grandmother smoking in pregnancy" but express some caution in light of the smaller numbers included in this part of the analysis."These results are intriguing" say the authors. Indeed they are. Accepting the reliance on parental report, acceptance of the myriad of other factors that might affect any relationship and the fact that "sets of trait questions were not designed as measures of autistic traits but rather to identify the child’s performance in regard to a large number of attributes at different ages" as a consequence of researchers not originally expecting the prevalence of autism to be anything like it is today(!), further research is indicated. I say this in the context that research looking at any link between maternal pregnancy smoking and offspring autism risk has not consistently found any correlation (see here).Then to the question of mechanism of effect. Well, researchers talk about "two plausible candidate mechanisms" to account for results. First is "transmission of damage to mitochondrial DNA (mtDNA)" where mitochondria DNA is subject to 'mutation' as a result of exposure to tobacco smoke. The researchers noted that: "Mitochondrial transmission across the generations is exclusively via the mother, so is compatible with our observed associations between maternal prenatal tobacco exposure and adverse scores on Social Communication and Repetitive Behaviour measures in her granddaughters." The second possible mechanism is that of "epigenetic inheritance from one generation to the next." This builds upon something of a continuing debate where structural DNA issues (i.e. mutations) are put to one side in favour of chemical alterations to genes (e.g. the addition of methyl groups) affecting gene expression. It's a topic that has been talked about quite a bit on this blog with reference to autism (see here for example) but still needs a lot more science done on it specifically on transgenerational epigenetic inheritance. Smoking is known to have effects on DNA methylation (see here) but the suggestion is that these or other epigenetic effects could continue down into future generations.The potential effects of tobacco smoking during pregnancy in relation to second (or even third generation) autism or autistic traits risk requires quite a bit more study. Importantly, if such results are confirmed in future investigations, it opens up a whole myriad of possibilities in terms of how other previous generational exposures outside of just tobacco smoking during pregnancy might have affected future generations. This research area could get very, very complicated indeed.----------[1] Golding J. et al. Grand-maternal smoking in pregnancy and grandchild's autistic traits and diagnosed autism. Sci Rep. 2017 Apr 27;7:46179.----------Golding J, Ellis G, Gregory S, Birmingham K, Iles-Caven Y, Rai D, & Pembrey M (2017). Grand-maternal smoking in pregnancy and grandchild's autistic traits and diagnosed autism. Scientific reports, 7 PMID: 28448061... Read more »

Golding J, Ellis G, Gregory S, Birmingham K, Iles-Caven Y, Rai D, & Pembrey M. (2017) Grand-maternal smoking in pregnancy and grandchild's autistic traits and diagnosed autism. Scientific reports, 46179. PMID: 28448061  

  • April 28, 2017
  • 07:00 AM

Friday Fellow: Hooker’s Lips

by Piter Boll in Earthling Nature

by Piter Kehoma Boll We are always fascinated by plants that have some peculiar shape that resemble something else. And certainly one of them is the species I’m introducing today, Psychotria elata, also known as hooker’s lips or hot lips. Found … Continue reading →... Read more »

  • April 28, 2017
  • 03:04 AM

Autism, pregnancy maternal immune activation and vitamin D?

by Paul Whiteley in Questioning Answers

Today's post is a bit of a mash-up, drawing on two articles quite recently published in the peer-reviewed science domain.The first is by Stephanie Vuillermot and colleagues [1] (open-access) suggesting that "early dietary supplementation with vitamin D may open new avenues for a successful attenuation or even prevention of neurodevelopmental disorders following maternal inflammation during pregnancy." These findings have also received some media attention (see here for example) and continues a research theme focused on vitamin D (the sunshine vitamin/hormone) and [some] autism (see here for example).The second paper is by Michael Lombardo and colleagues [2] (open-access) and also covers the topic of maternal immune activation (MIA) and its potential effects on offspring outcomes, concluding that: "MIA may confer increased risk for ASD [autism spectrum disorder] by dysregulating key aspects of fetal brain gene expression that are highly relevant to pathophysiology affecting ASD."What are the connections between these papers? Well, obviously both deal with the concept of maternal immune activation (MIA) where infection, or possibly/rather 'inflammatory' responses to infection, during critical periods of pregnancy seem to be able to affect offspring developmental and other outcomes. This bearing in mind that pregnancy represents a time of 'reprogrammed immune function' such that the maternal immune system does not mount a response to the genetically dissimilar organism growing inside the body. Both papers model MIA in rodents (mice and rats respectively) given the ethics of undertaking such experimental studies in humans. Both studies concluded that (a) there is evidence that MIA is a real phenomenon and (b) bearing in mind rodents are not necessarily the same as humans (see here) (a shocker I know), MIA seems to invoke specific biochemical changes pertinent to the expression of genes *linked* to autism that are also potentially amenable to intervention.The Vuillermot findings in particular, offer some rather intriguing prospects for further study as a function of their conclusion that: "maternal VitD co-administration blocked the emergence of the ASD-relevant deficits in social interaction, stereotyped behavior, and emotional learning and memory." I appreciate that 'blocking the emergence' of autistic behaviours is not something that everyone is going to unanimously welcome (the implication being that every single autistic trait is somehow something to be eradicated). The idea however that aspects of even something like certain stereotyped behaviours under certain conditions and with certain intensity might 'set someone up' for the presentation of truly disabling conditions such as anxiety [3] (see here too) offers a degree of support for the idea of intervention targeting such behaviours in particular circumstances.But there is a potential research spanner in the works when it comes the idea that vitamin D might 'offset' some of the changes associated with exposure to MIA. The authors note: "VitD does not alter maternal or fetal inflammatory cytokine production." This statement was made on the basis that "prenatal administration of vitamin D had no effect on pro-inflammatory cytokine levels in dams or in fetal brains." Cytokines are those chemical messengers of the immune system. How then, you might ask? Well, back to the Lombardo paper and the possibility that vitamin D is not necessarily an 'anti-inflammatory' of choice under such circumstances but might - MIGHT - act on some of the mechanisms related to those genes expressed under MIA conditions. It's pretty well-known for example, that vitamin D does influence gene expression (see here for example) as our knowledge of the biological duties of the sunshine vitamin/hormone expand (see here). It is logical to assume that the next research step would be to see whether vitamin D administration *might* at certain times and under certain circumstances, affect the expression of those genes 'highly relevant to pathophysiology affecting ASD' under MIA conditions. This, in the context that maternal vitamin D levels during pregnancy again *might* have an important impact on the presentation of offspring autistic traits (see here).And since we're on the topic of vitamin D and autism (yet again), how about reading a new hypothesis paper on some potentially important connections [4]?----------[1] Vuillermot S. et al. Vitamin D treatment during pregnancy prevents autism-related phenotypes in a mouse model of maternal immune activation. Molecular Autism. 2017; 8: 9.[2] 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. Mar 21.[3] 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.[4] Gillberg C. et al. The role of cholesterol metabolism and various steroid abnormalities in autism spectrum disorders: A hypothesis paper. Autism Res. 2017. April 12.----------Vuillermot, S., Luan, W., Meyer, U., & Eyles, D. (2017). Vitamin D treatment during pregnancy prevents autism-related phenotypes in a mouse model of maternal immune activation Molecular Autism, 8 (1) DOI: 10.1186/s13229-017-0125-0Lombardo, M., Moon, H., Su, J., Palmer, T., Courchesne, E., & Pramparo, T. (2017). Maternal immune activation dysregulation of the fetal brain tran... Read more »

  • April 27, 2017
  • 08:49 AM

Code Orange for the Bengal Tiger!

by Jente Ottenburghs in Evolutionary Stories

Genetic study highlights challenging conservation of the Bengal Tiger in India.... Read more »

  • April 27, 2017
  • 02:57 AM

Is screen time a risk factor for ADHD?

by Paul Whiteley in Questioning Answers

The findings reported by Vivien Suchert and colleagues [1] observing that "screen time, but not other non-screen-based sedentary activities should be considered as being a risk factor for ADHD [attention-deficit hyperactivity disorder]" taps into long-running debates on whether our societal obsession with watching, clicking and swiping might not be 'a totally positive thing' when it comes to psychological development, health and wellbeing.Yes, I know this is a complicated area full of big personalities, sweeping generalisations, half-truths and soundbites (see here for example). But I talk about peer-reviewed science on this blog, and am dealing with presented evidence specifically looking at the issue of screen time and ADHD on this particular occasion.So, taking a not insignificant sample number of over 900 young adults aged 13-17 years old, researchers assessed various parameters in relation to "screen-based and non-screen-based sedentary behavior and ADHD symptoms." When I say 'assessed', immediately one potentially big issue stands out when it comes to measures of sedentary behaviour used in the study and the inclusion of the questionnaire method over and above the use of more objective measures such as physical activity monitors (see here). No mind, researchers analysed the collected data and determined a few key observations not least that: "Screen time was related to the total ADHD score (p < 0.001) as well as to the subscales inattention (p ≤ 0.016) and hyperactivity/impulsivity (p ≤ 0.008)." Further: "Sedentary time without screens was virtually not associated with ADHD."OK, to reiterate sweeping generalisations are not required on the basis of these results alone. There are a myriad of other methodological issues outside of just objective measures of sedentary behaviour that could skew the Suchert results and these should be taken into consideration. But set in the context that this is not the first time that screen use has been *corrrelated* with something like ADHD or ADHD-type behaviours [2] (or indeed the second time [3]) I'm minded to suggest that quite a more investigation is indicated. Of course, there are other factors to include in the research mix. The findings reported by Tong and colleagues [4] are potentially pertinent: "children with ADHD symptoms were likely to spend more time using a computer during school days; they were also more likely to eat while using a computer." This implies that ADHD or ADHD-type behaviours might predispose to increased screen time rather than the other way around. The relationship is likely to be complex.In terms of the potential 'hows and whys' of any connection between screen time and ADHD-type behaviours, well, there are already some clues. I'd perhaps suggest that the effects of screen time on sleep could be a good place to start given other peer-reviewed research clues [5]. The relationship between sleep and ADHD is a complicated one, but it is known that sleep interventions can [modestly] affect the presentation of some ADHD behaviours (see here). There are no doubt other research avenues worth looking into also.Should anyone act on the Suchert findings as they stand? Well, I don't do medical or clinical advice on this blog but I'm minded to suggest that some sensible advice provided by others might come into play: "No screens in the child’s bedroom. Pay attention to the content of the games, especially to violence. Set limits on screen time, and look for other ways to manage family interactions." With my 'what if' research hat on, I am also wondering whether the rise and rise of screens and screen time in the context of autism might also need some particular research examination, in light of the idea that autism and ADHD is not an unfamiliar diagnostic combination (see here)...To close, although perhaps most famous as a 'rat tickler', the passing away of Jaak Panksepp a few days back deserves mention given his notable ideas about autism and the influence they had and continue to have...----------[1] Suchert V. et al. Relationship between attention-deficit/hyperactivity disorder and sedentary behavior in adolescence: a cross-sectional study. Atten Defic Hyperact Disord. 2017 Apr 4.[2] Chan PA. & Rabinowitz T. A cross-sectional analysis of video games and attention deficit hyperactivity disorder symptoms in adolescents. Ann Gen Psychiatry. 2006 Oct 24;5:16.[3] Montagni I. et al. Association of screen time with self-perceived attention problems and hyperactivity levels in French students: a cross-sectional study. BMJ Open. 2016 Feb 26;6(2):e009089.[4] Tong L. et al. Attention-Deficit/Hyperactivity Disorder and Lifestyle-Related Behaviors in Children. PLoS One. 2016 Sep 22;11(9):e0163434.[5] Engelhardt CR. et al. Media use and sleep among boys with autism spectrum disorder, ADHD, or typical development. Pediatrics. 2013 Dec;132(6):1081-9.----------Suchert V, Pedersen A, Hanewinkel R, & Isensee B (2017). Relationship between attention-deficit/hyperactivity disorder and sedentary behavior in adolescence: a cross-sectional study. Attention deficit and hyperactivity disorders PMID: 28378132... Read more »

  • April 26, 2017
  • 03:02 AM

Hornig, Lipkin and chronic fatigue syndrome again

by Paul Whiteley in Questioning Answers

Drs Mady Hornig and Ian Lipkin once again provide some fodder for this blog, continuing one of their important research themes on how chronic fatigue syndrome (CFS) (sometimes also referred to as myalgic encephalomyelitis, ME) might show some important immune-related issues [1].This research tag-team and the teams of dedicated scientists who surround them are making some real progress with regards to the idea that ME/CFS is a physical condition (not psychosomatic and not 'biopsychosocial') with some readily identifiable biological features potentially accompanying cases. Of course we're not there just yet when it comes to a biological test for ME/CFS but science has at least started down that particular research path...With accompanying media attention in tow (see here), the focus of the most recent results were on how disease sub-types might be important to CFS and specifically, how: "Immune signatures in the central nervous system of ME/CFS patients with atypical features may be distinct from those with more typical clinical presentations."Authors described how cerebrospinal fluid (CSF) samples from "32 ME/CFS cases with classical features and presentations and 27 ME/CFS cases with atypical features or clinical presentations" were included for analysis. On what basis was 'typical' and 'atypical' described? Well: "The ‘classical’ (C-ME/CFS) group had acute onset of disease marked by a prodrome consistent with infection; ‘atypical’ (A-ME/CFS) ME/CFS patients met full diagnostic criteria for ME/CFS at onset of their illness, but had a less standard onset of ME/CFS and/or developed other disorders after illness onset of ME/CFS." Interestingly one person included in the A-ME/CFS group was described as having Gulf-War Illness (another important condition talked about on this blog).The results: various cytokines (chemical messengers of the immune system) were assayed for and with some nifty statistical 'corrections' authors reported some potentially important differences between the groups. So: "We found discrete differences in immune signatures of the CNS in ME/CFS subjects with atypical presentations that included sparse inter-cytokine networks and lower levels of two inflammatory mediators, the Th17 cytokine, IL17A, and the IFNγ- and TLR4-induced chemokine, CXCL9." All-in-all results suggested a "less robust CNS immune activation in A-ME/CFS."Much more research is required in this area for sure. But these results are interesting and pertinent to the idea that within the heterogeneity (where have a I heard that before?) of CFS/ME, there may be quite a few phenotypes and subgroups that might be readily separable with a little biological research effort. Does this therefore mean when we talk about the pluralisation of lots of labels (the autisms, the schizophrenias, the depressions, etc), we might also one day called it 'the chronic fatigue syndromes'? Well, I've kinda speculated about this before in the peer-reviewed domain...----------[1] Hornig M. et al. Immune network analysis of cerebrospinal fluid in myalgic encephalomyelitis/chronic fatigue syndrome with atypical and classical presentations. Transl Psychiatry. 2017 Apr 4;7(4):e1080.----------Hornig M, Gottschalk CG, Eddy ML, Che X, Ukaigwe JE, Peterson DL, & Lipkin WI (2017). Immune network analysis of cerebrospinal fluid in myalgic encephalomyelitis/chronic fatigue syndrome with atypical and classical presentations. Translational psychiatry, 7 (4) PMID: 28375204... Read more »

  • April 25, 2017
  • 01:46 PM

Editors of Brazilian journals – a hard life that is getting harder! [Originally published as the editorial in Anais da Academia Brasileira de Ciências vol. 89 no. 1]

by SciELO in SciELO in Perspective

The financing of journals of Brazil can be improved by extending the validity period of research grants, in order to allow publishers a better plan for articles publication. An editorial written by Alexander Kellner in the first issue of 2017 of Anais da Academia Brasileira de Ciências examines the challenge faced by editors of journals of Brazil and highlights their hard work in attracting relevant manuscripts, seeking to achieve ever greater levels of excellence and internationalization. … Read More →... Read more »

CORDEIRO, Y., & SCHUCK, P. (2015) Hot Topics in Biomedical Sciences. Anais da Academia Brasileira de Ciências, 87(2), 1271-1272. DOI: 10.1590/0001-376520158722  

Vasconcelos, S., Sorenson, M., Watanabe, E., Foguel, D., & Palácios, M. (2015) Brazilian Science and Research Integrity: Where are We? What Next?. Anais da Academia Brasileira de Ciências, 87(2), 1259-1269. DOI: 10.1590/0001-3765201520150165  

  • April 25, 2017
  • 07:02 AM

The Brightness Temperature of the Quiet Solar Chromosphere at 2.6 mm by Kazumasa Iwai et al

by CESRA in Solar Radio Science

The brightness temperature of the Sun constitutes a basic property of the solar atmosphere. The main emission mechanism of the Sun at millimeter and submillimeter wavelengths is thermal free–free emission from the chromosphere, which is an atmospheric layer with a temperature ranging between 6000 to 20,000 K. The opacity of thermal free–free emission depends on the temperature and density in the emission region. In addition, the Rayleigh– Jeans law is applicable [...]... Read more »

Iwai, K., Shimojo, M., Asayama, S., Minamidani, T., White, S., Bastian, T., & Saito, M. (2017) The Brightness Temperature of the Quiet Solar Chromosphere at 2.6 mm. Solar Physics, 292(1). DOI: 10.1007/s11207-016-1044-5  

  • April 25, 2017
  • 03:15 AM

Who'd have thunk it: physical activity inversely associated with BMI and body fat percentage

by Paul Whiteley in Questioning Answers

"In this sample of middle-aged adults, drawn from the general population, physical activity was inversely associated with BMI [body mass index] and body fat percentage. For people with the same BMI, those who were more active had a lower body fat percentage."Those were the conclusions made by Kathryn Bradbury and colleagues [1] (open-access) drawing on data derived from "cross-sectional analysis of participants recruited into UK Biobank in 2006–2010." Said results continue a research theme where physical activity figures in the aforementioned dataset.So: "119 230 men and 140 578 women aged 40–69 years, with complete physical activity information, and without a self-reported long-term illness, disability or infirmity" were included for study - not an under-powered study by any means. Height and weight of participants were measured by trained staff "using standardised techniques." Physical activity estimates were gathered via self-report; specifically the use of 'touchscreens' as information gatherers regarding "walking, moderate physical activity and vigorous physical activity" and how often in a typical week participants "did each of the activities for 10 min or more" then onward for how many minutes during a day. Such data was number-crunched to provide something called "excess metabolic equivalent (MET)-hours/week of physical activity during work and leisure time." The authors also report on some efforts to off-set the potential unreliability of self-reported physical activity and several other variables (whether occupation involved primarily sitting or standing, tobacco smoking status, alcohol consumption, etc) were also thrown into the statistical mixer.Results: well, who'd have thunk it? Those reporting higher levels of physical activity (via questionnaire responses) tended to have a lower BMI and a lower body fat percentage. They were also likely to eat more fruit and vegetables that those with low levels of physical activity. Diet, occupation type and education level did not however seem to affect the primary findings.Accepting again that self-reported physical activity is not a great substitute for more objective measures and that BMI, whilst a good rough-and-ready indication of weight status, tends not to differentiate between fat and muscle, these are important results. They imply that far from not being able to outrun a bad diet (see here) physical activity still has an important place in maintaining a sensible weight and thus reducing the risk of a myriad of adverse health outcomes. Added to other findings indicating that we all really need to move quite a bit more (see here), the message seems to be that the human body was made for moving so move it. And the latest figures on obesity and physical activity highlight the challenges being faced in this area.And so to close,  a song to help with that 'move it' sentiment...----------[1] Bradbury KE. et al. Association between physical activity and body fat percentage, with adjustment for BMI: a large cross-sectional analysis of UK Biobank. BMJ Open 2017; 7: e011843.----------Bradbury, K., Guo, W., Cairns, B., Armstrong, M., & Key, T. (2017). Association between physical activity and body fat percentage, with adjustment for BMI: a large cross-sectional analysis of UK Biobank BMJ Open, 7 (3) DOI: 10.1136/bmjopen-2016-011843... Read more »

  • April 25, 2017
  • 02:16 AM

Will technology make language rights obsolete?

by Dave Sayers in Language on the Move

Something has been nagging at me recently. I read a lot of tech news, and it seems automated translation is...... Read more »

  • April 24, 2017
  • 04:22 AM

Promising mouse model for Ngly1 deficiency

by adam phillips in It Ain't Magic

A recent study of Ngly1 deficient mice used a secondary knockout to create double knockouts with symptoms similar to human NGLY1 deficiency.... Read more »

  • April 24, 2017
  • 03:05 AM

Sensory issues in adult ADHD controlling for autistic symptoms...

by Paul Whiteley in Questioning Answers

I was intrigued to read the paper by Bijlenga and colleagues [1] reporting on "the prevalence of sensory hyper- and hyposensitivity among adults with ADHD [attention-deficit hyperactivity disorder], controlling for autistic symptoms."The authors concluded that among their cohort of over 100 adults diagnosed with ADHD, both sensory hyper- and hyposensitivity symptoms as described by response to the Adolescent/Adult Sensory Profile-NL (AASP-NL), were over-represented compared with population norm data. Interestingly, authors also took a snapshot of 'autistic symptoms' based on responses to the Autism-spectrum Quotient (AQ) and reported that: "Adults with ADHD had more autistic symptoms" but: "Sensory hypo- and hypersensitivity were both related to an increased ADHD score, even showing a dose-response relationship, but not to any autistic symptom or comorbid disorder."My intrigue stems from a few implications of such findings, with the requirement for much more study. First is the quite important overlap between autism and ADHD (see here) confirmed symptom-wise in the Bijlenga paper. Second is the idea that, within this cohort at least, adults with ADHD may variably present with sensory issues. Third, assuming that the AQ 'does what it says on the tin' with regards to screening for autistic symptoms (see here), the lack of a notable connection between autistic symptoms and sensory sensitivities in the context of adult ADHD might have some important implications related to my first point when autism and ADHD appear simultaneously. Indeed it poses the question: are sensory issues, now noted in specific relation to autism via at least one diagnostic schedule (see here) actually 'a core part of all autism' or perhaps a feature of something else for some?Reiterating that more research is required (not least more formal screening for autism over and above the use of AQ or related screening schedules) that last point/question might actually make more sense than many people might first realise. If, for example, we take the view that autism rarely exists in some sort of diagnostic vacuum (see here and see here) and that science and clinical practice really needs to be more proactive when it comes to an autism diagnosis being a starting point not the finishing line (see here), it's not beyond the realms of possibility that sensory issues for some might have been spuriously linked to autism when in fact other comorbid labels/symptoms better account for their presentation. This not only has implications for screening/diagnosis but also management of said sensory symptoms, as per other reports talking about the use of stimulant medication indicated for ADHD 'affecting' aspects of odour sensitivities for example [2]. By saying that I'm not making any sweeping judgements about pharmacotherapy for ADHD treating sensory issues present alongside autism, merely that new avenues might open up.A final quick glance at some of the other peer-reviewed literature on the topic of sensory issues and ADHD reveals that there is some history in this area [3]. Said sensory issues have also been *linked* to some of the other behavioural facets noted in cases of ADHD [4]. Perhaps, in light of such data, it is time for ADHD - whether in symptoms or in label - to be taken into account when sensory issues are discussed in the context of autism in the science literature and in clinical practice?----------[1] Bijlenga D. et al. Atypical sensory profiles as core features of adult ADHD, irrespective of autistic symptoms. Eur Psychiatry. 2017 Feb 21;43:51-57.[2] Romanos M. et al. Improved odor sensitivity in attention-deficit/hyperactivity disorder. Biol Psychiatry. 2008 Dec 1;64(11):938-40.[3] Clince M. et al. Comparing and Exploring the Sensory Processing Patterns of Higher Education Students With Attention Deficit Hyperactivity Disorder and Autism Spectrum Disorder. Am J Occup Ther. 2016 Mar-Apr;70(2):7002250010p1-9.[4] Shimizu VT. et al. Sensory processing abilities of children with ADHD. Braz J Phys Ther. 2014 Jul-Aug;18(4):343-52.----------Bijlenga D, Tjon-Ka-Jie JY, Schuijers F, & Kooij JJ (2017). Atypical sensory profiles as core features of adult ADHD, irrespective of autistic symptoms. European psychiatry : the journal of the Association of European Psychiatrists, 43, 51-57 PMID: 28371743... Read more »

Bijlenga D, Tjon-Ka-Jie JY, Schuijers F, & Kooij JJ. (2017) Atypical sensory profiles as core features of adult ADHD, irrespective of autistic symptoms. European psychiatry : the journal of the Association of European Psychiatrists, 51-57. PMID: 28371743  

  • April 22, 2017
  • 11:30 PM

Intrinsic Motivation Is Caused by Achievement

by Joshua Fisher in Text Savvy

Education interventions (specifically those dealing with mathematics education) designed to increase achievement may be better uses of time than those designed to increase intrinsic motivation.... Read more »

  • April 22, 2017
  • 06:14 AM

Autistic adults as critical autism experts (with research caveats)

by Paul Whiteley in Questioning Answers

"Findings suggest that autistic adults should be considered autism experts and involved as partners in autism research."That was the conclusion reached in the paper by Kristen Gillespie-Lynch and colleagues [1] (open-access) reporting on the results of an online survey assessing "autism knowledge and stigma among 636 adults with varied relationships to autism, including autistic people and nuclear family members." Among the various groups of people who contributed to the survey, several viewpoints emerged. The message primarily however was that: "autistic people are autism experts through their lived experiences." I don't think many people would quibble with such findings.A few other details emerged from the Gillespie-Lynch study that merit discussion. Many participants showed a "reduced tendency to view autism through a deficit-defined medical model compared with non-autistic people." This is perhaps not an unexpected finding given the history of applying the medical model to autism and the rise and rise of the neurodiversity movement that "challenges the medical model" in particular respect over the question of deficit vs. difference and implications thereof. Although the medical model provides the means to identify and diagnose autism or autism spectrum disorder (ASD) (on the basis of deficits), it's not unexpected that for some, once those tasks have been completed, the 'treatment' side of the model is not necessarily a top priority; or at least not as important as addressing the various inequalities that seem to stem from a diagnosis. That being said, I do agree with the authors sentiments that: "the neurodiversity movement and the medical model overlap in recognizing that supports are needed to ameliorate challenges associated with autism." Those challenges are variable and person-dependent but include the effects of both core and peripheral signs and symptoms and the various over-represented comorbidities that seem to follow a diagnosis of autism (see here). I would, at this point, also caution on using the words 'biopsychosocial model' in the context of autism as the authors have included in their discussions, given what it has meant for other labels (see here) and the potential 'psychologising' of some important medical symptoms.I added the words 'with research caveats' to the title of this post to ensure that such a positive message about autism and the autism spectrum is not just given a 'free pass' when it comes to scrutiny of the scientific method, the way the study was carried out and the applicability of the results to the entire autism spectrum. This was an online survey not a face-to-face piece of research (other related research has similarly used such a method and on more than one occasion) and the authors acknowledge that they: "did not verify diagnosis of participants who self-identified as autistic" for example. Given what we are beginning to see when it comes to some of the 'self-screening' instruments out there regarding possible autism or not (see here), I'm always a little cautious that self-diagnosis / self-identification does not necessarily mean [eventual] clinician-diagnosed autism and how important this is when it comes to correctly ascertaining the wants and wishes of those diagnosed as being on the spectrum.On the point about the representativeness of this research, the authors also note: "Findings may not generalize to autistic participants who lack the verbal and computer skills needed to complete the survey." Yet another example it seems of this important issue.I have to say that I'm also a little disheartened that yet again an important group that was once very firmly on the autism spectrum aren't really given the credit they deserve according to the Gillespie-Lynch findings: "Autistic participants were more likely to recognize that most children cannot outgrow autism." The 'optimal outcome' children and adults it seems, still represent one of the most maligned groups associated with the autism spectrum (assuming that optimal outcome occurring in up to 9% of the autism population is not an insignificant figure). This despite the fact that even the diagnostic stability of the most 'high-functioning' cases of autism can wobble it seems (see here) even into adulthood. One of the premier experts on autism also seems to agree according to some recent media (see here). I often wonder if the seeming lack of acceptance of this group/feature might have something to do with the 'identity' side of autism and the idea that within the vast heterogeneity of autism (or the plural autisms if you prefer) the use of 'them and us descriptions' like 'neurotypical' are perhaps not as binary or long-lasting as many would believe or want to believe?Within the context of [approximate] phrases such as 'if you've met one person with autism, you've met one autistic person' there is caution in over-generalising these latest results but they are nonetheless important. I think it would be rather fitting to end with a few choice phrases from the Gillespe-Lynch paper: "As many of our survey respondents indicated, each person, regardless of whether or not they are autistic, is unique" and: "Some autistic people seek out factual knowledge about autism while others believe that they can only be experts in their own particular form of autism." Either way, the insights provided by people on the autism spectrum (all parts of the autism spectrum and indeed, across the age ranges) should be valued, and where possible, incorporated into research and practice.And one voice from the autism spectrum carries some rather sensible messages...----------[1] Gillespie-Lynch K. et al. Whose Expertise Is It? Evidence for Autistic Adults as Critical Autism Experts. Front. Psychol. 2017. March 28.----------Gillespie-Lynch, K., Kapp, S., Brooks, P., Pickens, J., & Schwartzman, B. (2017). Whose Expertise Is It? Evidence for Autistic Adults as Critical Autism Experts Frontiers in Psychology, 8 DOI: 10.3389/fpsyg.2017.00438... Read more »

Gillespie-Lynch, K., Kapp, S., Brooks, P., Pickens, J., & Schwartzman, B. (2017) Whose Expertise Is It? Evidence for Autistic Adults as Critical Autism Experts. Frontiers in Psychology. DOI: 10.3389/fpsyg.2017.00438  

  • April 21, 2017
  • 07:00 AM

Friday Fellow: Crystalline crestfoot

by Piter Boll in Earthling Nature

by Piter Kehoma Boll Even in the smallest pools or ponds of freshwater lost in a field, the diversity of lifeforms is amazing. Sadly, these environments are one of the most damaged of all ecosystems on earth and we probably … Continue reading →... Read more »

  • April 21, 2017
  • 06:26 AM

History of neuroscience: John Hughlings Jackson

by neurosci in Neuroscientifically Challenged

In 1860, when John Hughlings Jackson was just beginning his career as a physician, neurology did not yet exist as a medical specialty. In fact, at that time there had been little attention paid to developing a standard approach to treating patients with neurological disease. Such an approach was one of Jackson's greatest contributions to neuroscience. He advocated for examining each patient individually in an attempt to identify the biological underpinnings of neurological disorders. This examination, Jackson asserted, should be guided by the tenets of localization of function, which had been popularized by Franz Joseph Gall in the decades before Jackson was born. Concordant with these tenets, Jackson believed that neurological dysfunction could be traced back to dysfunction in specific foci of the nervous system, and the ability to identify the part of the nervous system that was affected to produce a disease was critical for making an accurate diagnosis.Jackson's perspective on understanding neurological diseases is exemplified by his efforts to elucidate the neurobiological origins of epilepsy---the work he is probably best known for. Jackson's observations on epilepsy date back to the very beginning of his medical career. At that time, the most popular explanation for epileptic seizures was that they were associated with abnormal function in a region of the brain known as the corpus striatum, a term that refers to a composite structure consisting of the striatum and the globus pallidus. The corpus striatum was known to be involved with motor functions, which caused it to be implicated in epileptic seizures as well.Jackson, however, began to suspect that the cerebral cortex participated in creating the convulsions that epileptics suffered from during seizures. To support this hypothesis, he cited cases where patients experienced convulsions that primarily struck one side of the body. Very often, Jackson argued, these patients upon autopsy would display damage to the cerebral hemisphere on the opposite side of the body that was affected by seizures.
Watch this 2-Minute Neuroscience video to learn more about epilepsy.Jackson approached the idea that there were certain areas of the cortex devoted to movement with hesitancy for multiple reasons. First, at the time the prevailing view was still that the cortex was unexcitable, and thus would be unlikely to be affected by what Jackson considered to be a disease of increased excitability. Additionally, it was still common in Jackson's time to consider the cortex to be homogenous. Although the concept of localization of function was challenging this idea, many still held the belief that all gray matter in the cortex was equivalent and there were no areas of functional specialization. According to this view, the entire mass of the cortex had to act together to produce some sort of response. Jackson's idea that seizures could be linked to increased excitability in one half of the cortex did not conform to this perspective.In addition to his observations about the link between hemispheric damage and seizures on the other side of the body, Jackson also noted a unique feature of some of the seizures he observed. He pointed out that in certain patients convulsions started in one specific area of the body and then proceeded to travel outward from that area in a predictable fashion. For example, convulsions might begin in the hand and then move up the arm to the face, and then down the same leg on the same side of the body. Or they might start in the foot and travel up the leg, then down the arm and into the hand on the same side of the body.This process, later called the Jacksonian march, would help Jackson to formulate some of his most important ideas about the brain. He hypothesized that there were areas of the cortex that were devoted to controlling the movement of different parts of the body. When excitation spreads throughout the cortex, Jackson posited, it stimulates these different areas one by one, creating the Jacksonian march of convulsions through the patient's body. Furthermore, Jackson suggested that the parts of the body that were capable of the most diverse movements (e.g. hand, face, foot) likely had the most space in the cortex devoted to them.With his observations on epilepsy Jackson was essentially predicting the existence of the motor cortex as well as anticipating the functional arrangement of the gray matter that the motor cortex is made up of. His hypothesis that there was a distinct region of the cerebral cortex devoted to motor function was confirmed in 1870 when Gustav Fritsch and Eduard Hitzig provided experimental evidence of a motor cortex in dogs. The arrangement Jackson envisioned, where one part of the cortex is devoted to one part of the body, we now call somatotopic arrangement. It has been verified by a series of experiments, capped by Wilder Penfield's electrical stimulation studies of the 1930s. It is now common neuroscience knowledge that there are regions of the motor cortex that seem to be devoted specifically to movement of the hands, other regions devoted to the movement of the face, and so on. As Jackson predicted, areas of the body that are involved in more diverse movements generally have more cortical area devoted to them.Jackson's clinical observations of epilepsy and his hypotheses about the motor regions in the cortex accurately predicted what would soon be discovered through experimentation, and acted as a guide for researchers like Fritsch and Hitzig. Thus, Jackson's work contributed significantly to a better understanding of the organization of the cortex, a region that we now consider to be functionally diverse and intricately arranged---a far cry from the idea of cortical homogeneity common in Jackson's time. Additionally, Jackson's development of a more formalized methodology of observation in neurology has caused him to be considered one of the founding fathers of the field.Jackson's contributions to neuroscience, however, were much more extensive than there is room to cover here. He wrote copiously on diverse topics ranging from the evolution of the nervous system to aphasia. At a time when our understanding of the brain was still so lacking in comparison to today, Jackson had a brilliant mind that seemed capable of comprehending brain function in a way that has rarely been replicated in the history of neuroscience.Finger, S. Origins of Neuroscience. New York, NY: Oxford University Press; 1994.York GK, Steinberg DA. An Introduction to the Life and Work of John Hughlings Jackson: Introduction. Med Hist Suppl. 2007; (26): 3–34.... Read more »

York GK, Steinberg DA. (2007) An Introduction to the Life and Work of John Hughlings Jackson. Med Hist Suppl., 3-34. info:/

  • April 21, 2017
  • 04:32 AM

Parental exposures and risk of offspring autism: some curious details

by Paul Whiteley in Questioning Answers

"Overall, our results were consistent with no positive association between parental asthmagen exposure and ASD [autism spectrum disorder] in the children."So said the findings reported by Alison Singer and colleagues [1] (open-access) continuing a research theme from this group [2] looking at whether "parental workplace exposures to risk factors for asthma (“asthmagens”)" might have relevance to offspring risk for autism.Based on data derived from some of those oh-so-important Scandinavian research registries (this one based in Denmark), researchers initially looked at some 12,000 cases (where autism was mentioned in medical records) compared with over 48,000 controls (not autism) to ascertain whether parental work exposures might play some role in autism risk. This numbers were eventually boiled down somewhat.Despite the opening line to the post, there were some curious details to emerge from the collected analyses. So: "We observed an inverse association between any maternal occupational asthmagen exposure and ASD in the children." Researchers reported that maternal occupational exposure actually seemed to be protective against the development of offspring autism according to their findings. They note that this finding was "largely explained by latex exposures" on the basis of linking occupational codes "to an asthma-specific job exposure matrix (JEM)." In other words, they didn't specifically look at latex exposure in every single case but rather relied on the probability that a particular occupation would entail this or other exposure.A few other curious details also emerged: "Some paternal occupational asthmagen categories were positively associated with ASD, including bioaerosols..., pharmaceutical drugs (manufacturing or extensive handling)..., and metals." The authors tend to talk down these findings as per the suggestion that: "Some of these associations could be chance findings resulting from multiple comparisons or could reflect bias, such as unmeasured confounding" but I would perhaps be a little more cautious about rejecting them outright. Indeed the authors note on one point in relation to maternal exposures: "While adjustment for unmeasured confounding could bring the association to the null, the confounding would need to be implausibly strong to mask a positive association."I've covered the topic of parental (occupational) exposures and offspring autism risk before on this blog (see here) alongside associated research (see here). The current take-away message from quite a bit of this research is that there may be target classes of compounds to 'look out for' when it comes to offspring autism risk, but as of yet there is no smoking gun. One also needs to read such research in the context of the myriad of 'associations' that have been made with offspring autism risk down the years (see here for example) and how genes and environment might mix in relation to the plural autisms. Cumulative effects are more likely over single factors.Insofar as the current Singer results, I do feel that the authors might have been a little premature in making the sweeping claims that they have on the basis of their findings: "this large population-based case-control study does not suggest a positive measurable association between parental occupational asthmagen exposure and ASD." I say this in the context that 'asthmagen' exposure could be incurred via several routes (see here). I don't doubt that the correlations/findings reported by Singer could be 'due to chance', but until such claims can be independently verified in direct study (see here for one idea) and perhaps tested in animal models for example, they should really just report what they found without fear, favour or complication...----------[1] Singer AB. et al. Parental exposures to occupational asthmagens and risk of autism spectrum disorder in a Danish population-based case-control study. Environmental Health. 2017 16: 31.[2] Singer AB. et al. Maternal Exposure to Occupational Asthmagens During Pregnancy and Autism Spectrum Disorder in the Study to Explore Early Development. J Autism Dev Disord. 2016 Nov;46(11):3458-3468.----------Singer, A., Burstyn, I., Thygesen, M., Mortensen, P., Fallin, M., & Schendel, D. (2017). Parental exposures to occupational asthmagens and risk of autism spectrum disorder in a Danish population-based case-control study Environmental Health, 16 (1) DOI: 10.1186/s12940-017-0230-8... Read more »

  • April 20, 2017
  • 05:19 AM

DHM attenuates obesity-induced slow-twitch-fiber decrease via FLCN/FNIP1/AMPK pathway

by Joana Guedes in BHD Research Blog

Obesity is often associated with decreases in the proportion of skeletal muscle slow-twitch fibers and insulin sensitivity. Slow-twitch fibers are rich in mitochondria and utilize fatty acid oxidative phosphorylation for energy production. In their new study, Zhou et al. (2017) explore the role of the FLCN/FNIP1/AMPK signalling pathway in obesity-induced reductions in slow-twitch fibers and insulin sensitivity in skeletal muscle using high-fat-diet-induced (HFD) obese mice, ob/ob mutant mice, and palmitate-treated C2C12 myotubes. The authors also assess the effects of dihydromyricetin (DHM) on the obesity-induced decrease in slow-twitch fibers, and the molecular mechanisms responsible for this effect.... Read more »

  • April 20, 2017
  • 04:37 AM

"a gradual decline in recorded diagnoses of CFS/ME since 2001"?

by Paul Whiteley in Questioning Answers

The quote forming the title of today's post comes from the paper by Simon Collin and colleagues [1] (open-access available here) who, based on analysis of the UK "Clinical Practice Research Datalink (CPRD), formerly known as the General Practice Research Database (GPRD)" set out to look at the "Incidence of CFS/ME [chronic fatigue syndrome/ myalgic encephalomyelitis], FM [fibromyalgia], post-viral fatigue syndrome (PVFS), and asthenia/debility." I say incidence but that last sentence should really read as  'recorded incidence'.Searching the research database between January 2001 and December 2013, researchers looked at the [recorded] incidence (that's incidence not prevalence) of the various fatigue-related conditions/labels recorded by participating GP (general practice) surgeries.Recorded diagnoses of CFS/ME showed a soft but noticeable decline over the period of study: "Annual incidence of CFS/ME decreased from 17.5 [per 100,000 people] in 2001 to 12.6 in 2013." A similar decline was also noted in respect of PVFS and asthenia/debility. When however it came to FM, there was an overall increase in cases between 2001 and 2013 (albeit characterised by peaks and troughs in recorded diagnoses across specific years).Some other important data were also reported on. So: "All diagnoses showed strong evidence of variation by age and sex" and estimated socio-economic status (SES). Further: "Incidence rates of CFS/ME were 2.4-fold higher among women... with peak incidence in the 40–49 years age group." Women were also more likely to be over-represented in relation to a diagnosis of FM too.This is potentially important data. It suggests that at least among participating GP practices in the CPRD, recorded diagnoses of CFS/ME seem to be going down. The caveats however mentioned by the researchers do need to be highlighted, not least that they "examined recorded data rather than actual incidence, i.e. we are describing incidence rates of GPs’ recording of diagnostic codes" and "diagnoses were not independently validated." In other words, this is data based on "GPs enter[ing] medical diagnoses and symptoms as Read codes." I might also add in another quote from the authors too: "In 2005, 48% of GPs in one English region did not feel confident about making a diagnosis of CFS/ME, and 28% did not recognise CFS/ME as a legitimate illness." A bit of an issue by all accounts if one would like to get accurate data on incidence or prevalence.I also have a to raise a point in relation to this latest data and how it compares with other data produced by the same research group (see here). Keeping in mind that incidence is not the same as prevalence, I bring back to your attention the findings reported by Collin and colleagues [2] on another occasion suggesting that nearly 2% of 16-year olds in the ALSPAC cohort were affected by CFS. More work needs to be done when it comes to official monitoring of the numbers of cases of CFS/ME (and FM) outside of just reliance on GP practice recordings in order to get a true picture of numbers of cases. Of course, there is another possible explanation for the fall in recorded diagnoses: GPs are increasingly understanding that some of the symptoms included under the banner of CFS/ME overlap with various other conditions/labels too...----------[1] Collin SM. et al. Trends in the incidence of chronic fatigue syndrome and fibromyalgia in the UK, 2001-2013: a Clinical Practice Research Datalink study. J R Soc Med. 2017 Jan 1:141076817702530.[2] Collin SM. et al. Chronic Fatigue Syndrome at Age 16 Years. Pediatrics. 2016 Feb;137(2):e20153434.----------Collin SM, Bakken IJ, Nazareth I, Crawley E, & White PD (2017). Trends in the incidence of chronic fatigue syndrome and fibromyalgia in the UK, 2001-2013: a Clinical Practice Research Datalink study. Journal of the Royal Society of Medicine PMID: 28358988... Read more »

  • April 19, 2017
  • 04:31 AM

Allergy and ADHD meta-analysed and guess what...

by Paul Whiteley in Questioning Answers

"Reports of frequent manifestation of allergic diseases in children with attention deficit hyperactivity disorder (ADHD) have been the subject of mounting clinical interest."OK, go on."The objective of this study was to compile and assess available studies on the association between ADHD and allergic diseases in children."And your findings... "children with ADHD are more likely to have asthma, allergic rhinitis, atopic dermatitis, and allergic conjunctivitis than their counterparts. Interventions including strategies for managing allergies in children with ADHD would be beneficial."So said the systematic review and meta-analysis published by Celine Miyazaki and colleagues [1] (open-access) who provide quite a good 'where we're at' update when it comes to a potentially important intersection between a developmental condition (ADHD) and a series of somatic, immune-based conditions (allergy).Regular readers of this blog might already know that I have a blogging interest in all-things immune system and behaviour (see here for example). Indeed, acknowledging that the immune system may be doing so much more than protecting us from the multitude of viral, bacterial and other insults we face each day is gaining some real [peer-reviewed] scientific momentum.Boiling down the peer-reviewed literature to five studies meeting the meta-analysis criteria laid out by authors, cumulatively including some 60,000 research participants (including data derived from that wonderful Taiwanese research registry that I keep going on about), researchers set to work on the examining the various findings. Nearly 8,000 of the 61,811 children included for study were diagnosed with ADHD and various allergic diseases were 'examined' in the context of the ADHD label or without the label. The results were as mentioned in the first paragraph.When it came to looking at which specific allergic disease diagnoses were most strongly linked to ADHD a familiar theme emerged: "children with ADHD have an 80% increased odds of asthma compared with children without ADHD." I'm beginning to lose track of the number of times I've covered this association down the blogging years (see here and see here and see here). Indeed, these results add to other reviews on this topic [2] previously covered on this blog (see here).The nature of the association? Well, more studies are still required. The authors talk about some work looking at possible overlapping genetic issues with autoimmunity in mind, and that is probably going to be quite important. More than that however is the idea that other less-genetic factors might also play a role. Y'know how social factors such as poverty might figure (see here) for example. I'm also minded to bring in the possibility of an 'association' between food allergy and behavioural symptoms (see here) in light of other work. Such a connection might also implicate all-manner of other bodily systems including the [hyped-up] field of microbiomics for example. Suffice to say that connections are likely to be complex and potentially numerous.The other implication from the Miyazaki results is another thing I've been going on about for some years on this blog: preferential screening. Y'know, when a diagnosis of asthma for example, is received, how about screening for ADHD and related developmental issues? Or, the other way around, screen for allergic diseases when a diagnosis of ADHD is received? And then there's the intervention angle, and some potentially useful data from both other developmental/behavioural diagnoses and allergy symptoms (see here) and some rather more direct evidence (see here)?To close, my brood have just discovered Little Britain and the laughter has gone on and on and on...----------[1] Miyazaki C. et al. Allergic diseases in children with attention deficit hyperactivity disorder: a systematic review and meta-analysis. BMC Psychiatry. 2017; 17: 120.[2] Schans JV. et al. Association of atopic diseases and attention-deficit/hyperactivity disorder: A systematic review and meta-analyses. Neurosci Biobehav Rev. 2017 Mar;74(Pt A):139-148.----------Miyazaki, C., Koyama, M., Ota, E., Swa, T., Mlunde, L., Amiya, R., Tachibana, Y., Yamamoto-Hanada, K., & Mori, R. (2017). Allergic diseases in children with attention deficit hyperactivity disorder: a systematic review and meta-analysis BMC Psychiatry, 17 (1) DOI: 10.1186/s12888-017-1281-7... Read more »

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