November 8, 2016
06:41 AM
19 views

The Brain Basis of Hating Cheese?

by Neuroskeptic in Neuroskeptic_Discover

Do you find gruyère gross? Are you repelled by roquefort?

Neuroscientists are now investigating why this might be. A new paper claims to reveal The Neural Bases of Disgust for Cheese.

French (heh) researchers Jean-Pierre Royet and colleagues used fMRI to scan 15 people who liked cheese and 15 who "hated" it. During the scan, the participants were shown images of cheese and were exposed to cheese odors.

The six neuro-cheeses were blue cheese, cheddar, goat cheese, gruyère, parmesan, ... Read more »

Royet JP, Meunier D, Torquet N, Mouly AM, & Jiang T. (2016) The Neural Bases of Disgust for Cheese: An fMRI Study. Frontiers in human neuroscience, 511. PMID: 27799903

November 8, 2016
02:57 AM
23 views

"A Putative Blood-Based Biomarker for Autism Spectrum Disorder-Associated Ileocolitis"

by Paul Whiteley in Questioning Answers

Contrary to Murphy's Law - 'never repeat a successful experiment' - replication or reproducibility is a cornerstone of good science. Today, I'm blogging about a piece of research that aimed to do just that as per the findings reported by Stephen Walker and colleagues [1] (open-access).The title of this post has been borrowed from the title of the Walker paper to illustrate how moving on from the quite widely known 'fact' that functional gastrointestinal (GI) symptoms are over-represented when it comes to the label of autism (see here for example) so further research focus is required on more pathological bowel conditions potentially linked to autism too (see here). Yes, I know this potentially takes us into some uncomfortable territory but for those with autism suffering with various bowel issues (and I do mean suffering) this marks some important science for them and their families onward to the resolution of any further health inequalities.The latest Walker paper follows on from their original findings [2] which have been previously covered on this blog (see here) observing that: "ASDGI children have a gastrointestinal mucosal molecular profile that overlaps significantly with known inflammatory bowel disease (IBD), yet has distinctive features that further supports the presence of an ASD-associated IBD variant, or, alternatively, a prodromal phase of typical inflammatory bowel disease." ASDGI by the way, referred to their small grouping of "twenty five consecutive ASDGI cases (6 autism; 19 autism spectrum disorder) with histopathologic findings of ileitis, colitis, or both."This latest time around authors report on the extending of their 'initial findings' in "an additional case/control cohort." Further they "report a gene expression profile in peripheral blood that may reflect the presence of ASD-associated ileocolitis and provide a putative surrogate biomarker that, upon validation, would be of significant clinical relevance." Potentially, big words.The paper is open-access but here are a few choice details:Biopsy samples - "a specimen from each of seven anatomic locations (from the terminal ileum to rectum)" - and blood samples were provided by 21 participants (patients) diagnosed with an autism spectrum disorder (ASD). All presented with gastrointestinal (GI) symptoms and all had "a history of normal development for at least 12 months followed by developmental regression and onset of gastrointestinal symptoms." All also had "histologically-confirmed ileitis, colitis, or both in at least one of seven collected and archived colonic biopsies." A control group of 21 'typically-developing' children "without ASD who had gastrointestinal symptoms... but no identifiable histologic inflammation on any biopsies in either the ileum or colon" were also included for analysis.Part 1 of the study "compared whole genome gene expression profiles of inflamed ASD GI mucosal tissue (ASDIC+) to non-inflamed TD mucosal tissue (TDIC−) in biopsies from both the terminal ileum and colon." This is pretty much what was done by the authors during their first research voyage in this area. Part 2 was more novel insofar as blood gene expression profiles were compared between the groups. It's also important to note that: "blood was obtained from the same patients, and at the same time, as their respective mucosal tissue samples."Results: applying a statistical technique called Principal Component Analysis (PCA) looking at gene expression in those mucosal (bowel) samples, authors were again able to say that there were differences between inflamed and non-inflamed samples/groups. They also observed some potentially important differences in those blood samples too: "Nine of these DETs [gene transcripts that are differentially-expressed] were also differentially expressed in blood in our most recent cohort." You might ask what does this actually tell us about the autism+GI group? Well, nothing and something, insofar as it is not really being ethical to start taking bowel biopsies from children with autism without any indication to do so, which means that comparisons between non-GI and GI+ children with autism were not possible. The data do however suggest that a "putative peripheral marker could provide a proxy for gastrointestinal inflammation and also provide functional insights."Insofar as the details of what genes were being differentially expressed in ASDIC+ vs. TDIC- samples and how these overlapped with the previous study from the authors, there were some interesting candidates including "a key mitochondrial folate pathway gene, MTHFD2 (methylenetetrahydrofolate dehydrogenase (NADP + dependent) 2, methenyltetrahydrofolate cyclohydrolase)" hinting at an effect beyond just immune function and inflammation/inflammatory signalling. Authors modelled various combinations of these genes expressed (or not) to try and come up with some preliminary Receiver Operating Characteristic (ROC) curve analysis. Regular readers of this blog will probably have heard me talk about ROC analyses before (see here for example) with regards to the search for potential classifiers or biomarker profiles associated with autism. Bearing in mind the small participant numbers included in this study and the final figures arrived at, I'd suggest that quite a bit more work is required before anyone takes the reported findings as gospel just yet. But they are interesting...So, there you have it. This is important work for two reasons: (i) more pathological bowel states can and do present alongside autism [3] (the diagnosis of autism is seemingly protective of very little as science is learning) and (ii) with the strong requirement for further investigations in this area, science is seemingly starting on a path to potentially identifying blood-based 'biomarkers' possibly useful in identifying those who might benefit from further screening for such bowel issues.Given the history and debate in the area of bowel disease accompanying some autism, I'm not expecting giant fanfares to greet these results nor any big rush to try and prove/disprove these latest findings. That is an unfortunate truth and in the end, it is the children/adults with autism and significant GI issues who lose out as a consequence. The fact that this and the previous work by the authors is peer-reviewed science and not just speculation however will I think eventually be important, as talk about medical comorbidity accompanying autism continues at a pace [4] (see here too) and further moves towards 'what can we do about such issues?' eventually start to come to the forefront.And just before I go, there may also be other research uses for biopsies as and when they have to be taken from children/adults under clinical investigation [5]...To close, I note there is an election across the Pond. With all the nastiness that has followed the campaign, surely there's an easier way to pick the Leader of the Free World...----------[1] Walker SJ. et al. A Putative Blood-Based Biomarker for Autism Spectrum Disorder-Associated Ileocolitis. Sc... Read more »

Walker SJ, Beavers DP, Fortunato J, & Krigsman A. (2016) A Putative Blood-Based Biomarker for Autism Spectrum Disorder-Associated Ileocolitis. Scientific reports, 35820. PMID: 27767057

November 7, 2016
01:57 PM
33 views

Neuroteratogenic Viruses: ZIKV, the placenta and IUGR

by thelonevirologist in Virology Tidbits

In humans, the most common infectious neuroteratogenic agents are summarised by the mnemonic “TORCH(S)” (Toxoplasmosis, Others, Rubella, (Human) Cytomegalovirus, Herpes Simplex, Syphilis) with ZIKV either classified as “Others” or by expanding the mnemonic to TORCHSZ and indeed health authorities in affected countries regularly test cases of microcephaly suspected to be associated with neurological infections not only for ZIKV but also for the presence of TORCH(S). Microcephaly however is only one outcome of CNS defects that are associated with the infection of foetal neural cells with infectious agents, as illustrated by the wide range of symptoms of neonate that include hydrocephalus, cerebellar dysplasia, hypomyelinogenesis or microphthalmia.
Common to all pathogens is, that they infect the foetus in utero rather than intra partum or vertical by breastfeeding, suggesting that the infection of neural precursor or mature neurons during the development of the foetal brain causes abnormal foetal brain development. Therefore, it is crucial to examine both the ability of neuroteratogenic viruses to infect and replicate in vaginal tissue as well to examine the mechanism of transplacental transmission and thus infection of embryonic and/or foetal cells. Here the mechanism of foetal ZIKV infection via the maternal placenta is discussed. ... Read more »

Yockey LJ, Varela L, Rakib T, Khoury-Hanold W, Fink SL, Stutz B, Szigeti-Buck K, Van den Pol A, Lindenbach BD, Horvath TL.... (2016) Vaginal Exposure to Zika Virus during Pregnancy Leads to Fetal Brain Infection. Cell, 166(5), 1247-12560000. PMID: 27565347

Bayless NL, Greenberg RS, Swigut T, Wysocka J, & Blish CA. (2016) Zika Virus Infection Induces Cranial Neural Crest Cells to Produce Cytokines at Levels Detrimental for Neurogenesis. Cell host , 20(4), 423-428. PMID: 27693308

El Costa H, Gouilly J, Mansuy JM, Chen Q, Levy C, Cartron G, Veas F, Al-Daccak R, Izopet J, & Jabrane-Ferrat N. (2016) ZIKA virus reveals broad tissue and cell tropism during the first trimester of pregnancy. Scientific reports, 35296. PMID: 27759009

Tabata T, Petitt M, Puerta-Guardo H, Michlmayr D, Wang C, Fang-Hoover J, Harris E, & Pereira L. (2016) Zika Virus Targets Different Primary Human Placental Cells, Suggesting Two Routes for Vertical Transmission. Cell host , 20(2), 155-66. PMID: 27443522

Quicke KM, Bowen JR, Johnson EL, McDonald CE, Ma H, O'Neal JT, Rajakumar A, Wrammert J, Rimawi BH, Pulendran B.... (2016) Zika Virus Infects Human Placental Macrophages. Cell host , 20(1), 83-90. PMID: 27247001

Bayer A, Lennemann NJ, Ouyang Y, Bramley JC, Morosky S, Marques ET Jr, Cherry S, Sadovsky Y, & Coyne CB. (2016) Type III Interferons Produced by Human Placental Trophoblasts Confer Protection against Zika Virus Infection. Cell host , 19(5), 705-12. PMID: 27066743

Ning F, Liu H, & Lash GE. (2016) The Role of Decidual Macrophages During Normal and Pathological Pregnancy. American journal of reproductive immunology (New York, N.Y. : 1989), 75(3), 298-309. PMID: 26750089

Lash GE, Pitman H, Morgan HL, Innes BA, Agwu CN, & Bulmer JN. (2016) Decidual macrophages: key regulators of vascular remodeling in human pregnancy. Journal of leukocyte biology, 100(2), 315-25. PMID: 26819320

Salamonsen LA, Hannan NJ, & Dimitriadis E. (2007) Cytokines and chemokines during human embryo implantation: roles in implantation and early placentation. Seminars in reproductive medicine, 25(6), 437-44. PMID: 17960528

Olagnier D, Amatore D, Castiello L, Ferrari M, Palermo E, Diamond MS, Palamara AT, & Hiscott J. (2016) Dengue Virus Immunopathogenesis: Lessons Applicable to the Emergence of Zika Virus. Journal of molecular biology, 428(17), 3429-48. PMID: 27130436

November 7, 2016
03:13 AM
25 views

8.6% of children with autism have epilepsy?

by Paul Whiteley in Questioning Answers

"Epilepsy was reported to co-occur in 8.6 % of ASD [autism spectrum disorder] cases."That was the headline conclusion reported by Shiny Thomas and colleagues [1] as they drew on data from "the most recent U.S. National Survey of Children's Health, 2011-2012" to add to the extensive literature looking at how common epilepsy is when it comes to autism.Including some 1600 children/young adults diagnosed with autism - equivalent to a prevalence of 1.8% of the entire 85,000-strong cohort - researchers "examined parent-reported prevalence of co-occurring epilepsy" and eventually came up with that 8-9% figure. Further, they also observed that: "the co-occurrence of epilepsy was associated with increasing child age, female gender, intellectual disability, speech problems and lower socioeconomic status."This is important work. Epilepsy or seizure disorder is not something to be taken lightly under any circumstances; more so when applied to autism and the 'burden' of medical comorbidity that seems to be over-represented following a diagnosis (see here). The use of the U.S. National Survey of Children's Health (NSCH), 2011-2012 also has some significant strengths in terms of numbers of participants and has previously informed quite a few areas of autism research (see here for example).There is another important detail attached to the Thomas paper that is also worthy of comment in relation to how their prevalence figure compares with other independent studies in terms of epilepsy appearing comorbid to autism (readers should click on the 'Supplementary material' attachment shown here). Bearing in mind their data was derived from children "ages 2-17" and includes the term 'parent-reported' (as opposed to medical records reported) the 8.6% figure seems to be quite a conservative one. I say this on the basis that previous data from NSCH has observed slightly higher rates of epilepsy (see here) and other data sources have even talked about 1 in 5 children on the autism spectrum manifesting with a seizure or seizure disorder (see here). I of course realise that the word 'epilepsy' covers quite a bit of diagnostic ground and seizures/seizure disorder can present for a variety of reasons, but nonetheless I stand by the 8.6% comorbidity figure as perhaps being one of the lower values published in the peer-review domain.The additional observations that 'increasing age' and presence of intellectual (learning) disability might influence the presence of epilepsy in relation to autism are interesting but by no means novel findings. They do however offer something of a roadmap to monitoring those on the autism spectrum who may be at some enhanced risk of developing epilepsy and indeed, implementing the relevant strategies in a timely fashion to ensure that epilepsy is managed safely.Many questions still remain concerning the hows and whys of epilepsy intersecting with autism (and indeed, autism intersecting with epilepsy) including those related to more 'non-traditional' aspects (see here for example). What however is abundantly clear from the peer-reviewed and other literature in this area is that epilepsy is an important part of life for quite a few people on the autism spectrum and as many resources as possible should be pumped into looking at the relationship and offsetting / averting the potentially life-changing consequences that epilepsy can have on a person and their loved ones (see here).To close, when one mentions 'God Save the Queen' one should really specify which version one requires?----------[1] Thomas S. et al. Brief Report: Prevalence of Co-occurring Epilepsy and Autism Spectrum Disorder: The U.S. National Survey of Children's Health 2011-2012. J Autism Dev Disord. 2016 Oct 17.----------Thomas S, Hovinga ME, Rai D, & Lee BK (2016). Brief Report: Prevalence of Co-occurring Epilepsy and Autism Spectrum Disorder: The U.S. National Survey of Children's Health 2011-2012. Journal of autism and developmental disorders PMID: 27752862... Read more »

Thomas S, Hovinga ME, Rai D, & Lee BK. (2016) Brief Report: Prevalence of Co-occurring Epilepsy and Autism Spectrum Disorder: The U.S. National Survey of Children's Health 2011-2012. Journal of autism and developmental disorders. PMID: 27752862

November 7, 2016
12:30 AM
38 views

What The Future Will Hold

by Aurametrix team in Aurametrix Blog

Elections are bad for your health. More than half of Americans, independently of their party preference, are stressed about upcoming elections, especially the oldest and the youngest voters. Social media is one of the major factors making this stress even worse. ... Read more »

Stanton SJ, Beehner JC, Saini EK, Kuhn CM, & Labar KS. (2009) Dominance, politics, and physiology: voters' testosterone changes on the night of the 2008 United States presidential election. PloS one, 4(10). PMID: 19844583

Markey, P., & Markey, C. (2011) Pornography-seeking behaviors following midterm political elections in the United States: A replication of the challenge hypothesis. Computers in Human Behavior, 27(3), 1262-1264. DOI: 10.1016/j.chb.2011.01.007

Waismel-Manor I, Ifergane G, & Cohen H. (2011) When endocrinology and democracy collide: emotions, cortisol and voting at national elections. European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology, 21(11), 789-95. PMID: 21482457

Blanton, H., Strauts, E., & Perez, M. (2012) Partisan Identification as a Predictor of Cortisol Response to Election News. Political Communication, 29(4), 447-460. DOI: 10.1080/10584609.2012.736239

Neiman J, Giuseffi K, Smith K, French J, Waismel-Manor I, & Hibbing J. (2015) Voting at Home Is Associated with Lower Cortisol than Voting at the Polls. PloS one, 10(9). PMID: 26335591

November 6, 2016
09:05 PM
40 views

Obama invades Europe: “Yes, we can!”

by Piter Boll in Earthling Nature

by Piter Kehoma Boll This information was known by me and some other people for quite a while, but only recently has caught attention of the general public. Obama is the newest threat in Europe. No, I’m not talking about the … Continue reading →... Read more »

Álvarez-Presas, M., Mateos, E., Tudó, À., Jones, H., & Riutort, M. (2014) Diversity of introduced terrestrial flatworms in the Iberian Peninsula: a cautionary tale. PeerJ. DOI: 10.7717/peerj.430

Boll, P., & Leal-Zanchet, A. (2016) Preference for different prey allows the coexistence of several land planarians in areas of the Atlantic Forest. Zoology, 119(3), 162-168. DOI: 10.1016/j.zool.2016.04.002

Carbayo, F., Álvarez-Presas, M., Jones, H., & Riutort, M. (2016) The true identity of Obama (Platyhelminthes: Geoplanidae) flatworm spreading across Europe. Zoological Journal of the Linnean Society, 177(1), 5-28. DOI: 10.1111/zoj.12358

November 5, 2016
04:20 AM
63 views

Sensory subtypes and anxiety and autism

by Paul Whiteley in Questioning Answers

"This is the first study to identify the existence of sensory subtypes among older children and adolescents with ASD [autism spectrum disorder] and explore their association with anxiety levels."Far be it from me to question the above quote provided in the paper by Mirko Uljarević and colleagues [1] but I'm inclined to suggest that there has already been some research published on the link between sensory issues and anxiety in the context of the autism spectrum before (see here and see here). Indeed, I do wonder whether the assertions put forward by Mazurek and colleagues [2] on how gastrointestinal (GI) issues (yes, they are over-represented) might be an important part of any sensory/anxiety mix in autism could be something that is further looked at by Uljarević in their cohort?Anyhow, the Uljarević paper is an interesting one given the idea that within the vast heterogeneity that is autism (or even the autisms) sensory issues as measured by "the short sensory profile" are notuniform in their presentation (a shocker, I know). The finding that anxiety scores, as measured by the Spence anxiety scales, were potentially a little different according to sensory subtype (sensory adaptive, sensory moderate, sensory severe) particularly when it came to the sensory adaptive grouping - "Children and adolescents from the adaptive subtype had significantly lower anxiety scores when compared with other two subtypes" - is important. The implication being that with various other variables not differing (chronological age, expressive language, or severity of autism diagnostic features) sensory issues might be one important driver of the presentation of anxiety when it comes to autism.As I've mentioned quite a few times on this blog, the topic of anxiety and autism is an important one (see here for example). There are a few different 'types' of anxiety (or anxiety diagnoses) that might be more applicable to autism alongside some discussion about how to measure anxiety when it comes to autism (see here). But the primary messages are: (i) anxiety is pretty rife in terms of accompanying a diagnosis of autism and (ii) the effects of anxiety can be absolutely, utterly disabling. Set in this light, if there are things that can be done to overcome anxiety over and above what might be traditionally offered (see here) by for example, 'affecting' those sensory issues, many people potentially stand to benefit.Next question: how does one go about 'intervening' when sensory issues are present alongside autism? Well, the science is still a little sparse here outside of the odd case report on something like bumetanide showing a potential effect [3] for example. I might draw your attention to some preliminary work on how visual sensory issues might be a target for other interventions (see here) but there is still some way to go in that area too and one needs to be mindful of how ophthalmologic disorder(s) may also contribute (see here). Going back to the Mazurek paper and the 'triad' of sensory issues, anxiety and bowel problems hinted at with at least some autism in mind, one could speculate that treating said bowel issues *might* have further positive effects on sensory and anxiety issues too. Indeed, in the more general context of how anxiety and another important label - depression - may well have a functional bowel issue link (see here), there is plenty of research fodder to draw on hinting at a 'gut-brain' link in some cases. No doubt there are other ways and means to tackle sensory issues as and when they impact on quality of life and by the sounds of other research [4] sensory issues in autism as described by the DSM-5 are going to be pretty widespread.To close, it's 'Remember, remember the 5th of November, gunpowder, treason and plot..' day here in the UK today. So here's V and his revolutionary chatter again and please, be careful this Bonfire night.----------[1] Uljarević M. et al. Sensory subtypes and anxiety in older children and adolescents with autism spectrum disorder. Autism Res. 2016 Oct;9(10):1073-1078.[2] Mazurek MO. et al. Anxiety, sensory over-responsivity, and gastrointestinal problems in children with autism spectrum disorders. J Abnorm Child Psychol. 2013 Jan;41(1):165-76.[3] Grandgeorge M. et al. The effect of bumetanide treatment on the sensory behaviours of a young girl with Asperger syndrome. BMJ Case Rep. 2014 Jan 31;2014. pii: bcr2013202092[4] Green D. et al. Brief Report: DSM-5 Sensory Behaviours in Children With and Without an Autism Spectrum Disorder. J Autism Dev Disord. 2016 Nov;46(11):3597-3606.----------Uljarević M, Lane A, Kelly A, & Leekam S (2016). Sensory subtypes and anxiety in older children and adolescents with autism spectrum disorder. Autism research : official journal of the International Society for Autism Research, 9 (10), 1073-1078 PMID: 26765165... Read more »

Uljarević M, Lane A, Kelly A, & Leekam S. (2016) Sensory subtypes and anxiety in older children and adolescents with autism spectrum disorder. Autism research : official journal of the International Society for Autism Research, 9(10), 1073-1078. PMID: 26765165

November 4, 2016
09:13 AM
79 views

Study shows that articles published in English attract more citations

by SciELO in SciELO in Perspective

Among the many factors that influence citation practice in scholarly communication, the language of publication plays a key role. A study by Argentine researchers showed that English articles receive more citations than those published in other languages. Despite being perceived by many as of lower quality and relevance, articles in Spanish from two Latin American journals were blind evaluated and were not, in fact, underqualified. … Read More →... Read more »

Di Bitetti, M., & Ferreras, J. (2016) Publish (in English) or perish: The effect on citation rate of using languages other than English in scientific publications. Ambio. DOI: 10.1007/s13280-016-0820-7

Meneghini, R., Packer, A., & Nassi-Calò, L. (2008) Articles by Latin American Authors in Prestigious Journals Have Fewer Citations. PLoS ONE, 3(11). DOI: 10.1371/journal.pone.0003804

Letchford, A., Moat, H., & Preis, T. (2015) The advantage of short paper titles. Royal Society Open Science, 2(8), 150266. DOI: 10.1098/rsos.150266

Meneghini, R., & Packer, A. (2007) Is there science beyond English? Initiatives to increase the quality and visibility of non-English publications might help to break down language barriers in scientific communication. EMBO reports, 8(2), 112-116. DOI: 10.1038/sj.embor.7400906

November 4, 2016
06:12 AM
62 views

Two recent case reports on BHD – Epidemiologic study of patients in Asia and new FLCN mutation

by Joana Guedes in BHD Research Blog

Furuya et al. (2016) present a new study describing genetic, epidemiologic and clinicopathologic features of 312 Asian individuals with BHD manifestations based on data from 120 probands from different families (119 Japanese and 1 Taiwanese), 36 siblingss with genetic testing and 156 siblings without genetic testing.... Read more »

Furuya M, Yao M, Tanaka R, Nagashima Y, Kuroda N, Hasumi H, Baba M, Matsushima J, Nomura F, & Nakatani Y. (2016) Genetic, epidemiologic and clinicopathologic studies of Japanese Asian patients with Birt-Hogg-Dubé syndrome. Clinical genetics, 90(5), 403-412. PMID: 27220747

November 4, 2016
05:00 AM
30 views

Friday Fellow: Silvergreen Moss

by Piter Boll in Earthling Nature

by Piter Kehoma Boll Found throughout most of the world, you probably have encountered this fellow many times in your life, but did not pay any attention. After all, it is just a moss! Scientifically known as Bryum argenteum and popularly … Continue reading →... Read more »

Sabovljevic, A., Sokovic, M., Sabovljevic, M., & Grubisic, D. (2006) Antimicrobial activity of Bryum argenteum. Fitoterapia, 77(2), 144-145. DOI: 10.1016/j.fitote.2005.11.002

Shaw, A., & Albright, D. (1990) Potential for the Evolution of Heavy Metal Tolerance in Bryum argenteum, a Moss. II. Generalized Tolerances among Diverse Populations. The Bryologist, 93(2), 187. DOI: 10.2307/3243622

November 4, 2016
04:03 AM
69 views

Hyperhomocysteinemia as a significant risk factor for autism?

by Paul Whiteley in Questioning Answers

The findings reported by Naushad Shaik Mohammad and colleagues [1] provide some blogging fodder today and the suggestion of a link between some of the genetics of the folate pathway and the finding of elevated levels of homocysteine with [some] autism in mind.OK, from the start, the genetics of folate metabolism mentioned in the context of autism typically means reference to the quite well replicated finding of issues with the gene methylenetetrahydrofolate reductase (MTHFR) (see here for some background). This gene (product) serves an important purpose in relation to the conversion of 5,10-methylenetetrahydrofolate to 5-methyltetrahydrofolate; the latter helping to convert the amino acid homocysteine to methionine. Outside of the importance of methionine to the process of DNA methylation (yep, some of that epigenetics stuff that you keep hearing about), there is quite a body of literature emerging to suggest that elevated levels of homocysteine might also have some important health effects.For quite a few years now, a specific genetic issue with MTHFR - MTHFR C677T - has been reported in quite a few people on the autism spectrum (see here). This allied to other independent research suggesting that the downstream effects of issues with MTHFR linked to elevations in levels of homocysteine may not also be an uncommon finding (see here). Shaik Mohammad et al therefore set about looking at the relationship between genetic issues with MTHFR and hyperhomocysteinemia in the context of autism.They did this by use of an "artificial neural network (ANN) model" where data initially from "138 autistic and 138 nonautistic children" on various genetic issues linked to folate metabolism (including MTHFR) were used as potential "predictors of autism risk." We are also told that: "Meta-analyses were carried out on 1361 ASD children and 6591 nonautistic children to explore the association of MTHFR C677T and homocysteine with the risk for ASD [autism spectrum disorder]."Results: well, the model wasn't exactly brilliant at predicting the risk of autism (63.8% accuracy). The authors call this a 'moderate' finding but I'd probably suggest that their results are yet another very good example of how heterogeneous the autism spectrum actually is. The idea of not using the term 'autism' as a research starting point in this context (see here) also receives support. Perhaps of greater importance were their findings linked to homocysteine and autism and how: "Hyperhomocysteinemia was observed in autistic children" to a greater extent that controls. They did also confirm that the MTHFR C677T genetic polymorphism was linked to 'inflating homocysteine levels' alongside another genetic issue called MTRR A66G (methionine synthase reductase). This is not an unusual finding in the context of what is already known about MTRR and homocysteine. The MTRR bit potentially linked to autism is however, something that this research group have previously suggested to 'reduce the risk' of autism [2].In terms of what these results mean in the context of autism, there are a few possibilities. First, screening. Knowing what we now seem to know about MTHFR and homocysteine in relation to quite a lot of people with autism, I would have thought it would be good practice to screen genetics/biochemistry. Minus any scaremongering or sweeping generalisations, the observation that hyperhomocysteinemia 'may' have links to cardiovascular disease and other adverse states for example, also perhaps implies screening save any further charges of health inequality when it comes to the label of autism. Next management. Far from being a 'nothing can be done about it' state, there is some good evidence that small adjustments to nutrition can potentially have positive effects on some of these parameters. With no medical or clinical advice given or intended, high levels of homocysteine seem in some cases, to be reactive to certain vitamin supplementation. The focus on vitamin B12 could also be set in the context of other recent studies of this vitamin (and its vitamers) with autism in mind (see here) (but I am careful not to link the two parameters just yet). And just recently there is news that there is a new way of assaying for vitamin B12 on the horizon which could also be useful. Finally, more research is indicated. As per my discussions not so long ago about another potentially important link to folate metabolism and autism (see here), there does appear to be quite a bit more to see when it comes to the folate cycle intersecting with homocysteine metabolism (and it's downstream effects). Yes, we can talk about whether folate is 'protective' or not when it comes to 'risk' of autism (see here and see here) but what this latest work suggests is that this area is complicated and potentially includes many genetic/epigenetic/biochemical variables that need to be taken into account.----------[1] Shaik Mohammad N. et al. Clinical utility of folate pathway genetic polymorphisms in the diagnosis of autism spectrum disorders. Psychiatr Genet. 2016 Oct 17.[2] Mohammad NS. et al. Aberrations in folate metabolic pathway and altered susceptibility to autism. Psychiatr Genet. 2009 Aug;19(4):171-6.----------Shaik Mohammad N, Sai Shruti P, Bharathi V, Krishna Prasad C, Hussain T, Alrokayan SA, Naik U, & Radha Rama Devi A (2016). Clinical utility of folate pathway genetic polymorphisms in the diagnosis of autism spectrum disorders. Psychiatric ge... Read more »

Shaik Mohammad N, Sai Shruti P, Bharathi V, Krishna Prasad C, Hussain T, Alrokayan SA, Naik U, & Radha Rama Devi A. (2016) Clinical utility of folate pathway genetic polymorphisms in the diagnosis of autism spectrum disorders. Psychiatric genetics. PMID: 27755291

November 3, 2016
11:10 PM
86 views

Stereotyped ethnic names as a barrier to workplace entry

by Ingrid Piller in Language on the Move

Who of the three women in this image do you think German employers are most likely to consider as a...... Read more »

Arai, M., Bursell, M., & Nekby, L. (2016) The Reverse Gender Gap in Ethnic Discrimination: Employer Stereotypes of Men and Women with Arabic Names. International Migration Review, 50(2), 385-412. DOI: 10.1111/imre.12170

Piller, I. (2016) Language at work. Linguistic Diversity and Social Justice. DOI: 10.1093/acprof:oso/9780199937240.003.0004

November 3, 2016
01:49 PM
76 views

Does The Motor Cortex Inhibit Movement?

by Neuroskeptic in Neuroskeptic_Discover

A new paper could prompt a rethink of a basic tenet of neuroscience. It is widely believed that the motor cortex, a region of the cerebral cortex, is responsible for producing movements, by sending instructions to other brain regions and ultimately to the spinal cord. But according to neuroscientists Christian Laut Ebbesen and colleagues, the truth may be the opposite: the motor cortex may equally well suppress movements.

Ebbesen et al. studied the vibrissa motor cortex (VMC) of the rat, ... Read more »

Ebbesen CL, Doron G, Lenschow C, & Brecht M. (2016) Vibrissa motor cortex activity suppresses contralateral whisking behavior. Nature Neuroscience. PMID: 27798633

November 3, 2016
04:10 AM
91 views

Antibiotic brain part 3

by Paul Whiteley in Questioning Answers

"This study demonstrates an association between antibiotic use in the first year of life and subsequent neurocognitive outcomes in childhood."So said the findings reported by Slykerman and colleagues [1] who relied on data from the Auckland Birthweight Collaborative Study (an initiative set up to determine whether "internationally recognized risk factors for small-for-gestational-age (SGA) term babies were applicable in New Zealand") to examine the suggestion that early life antibiotic use might be associated with a "detrimental effect on later neurocognitive outcomes."Relying on maternal report of antibiotic use among offspring "between 12 months and 3.5 years of age" researchers compared data with that derived from "Intelligence test scores and measures of behavioural difficulties" when children were 3.5, 7 and 11 years of age. They found that antibiotic use during the first 12 months of life was high in their cohort (70%) and that: "Those who had received antibiotics had more behavioural difficulties and more symptoms of depression at follow up." I've highlighted the 'relying on maternal report' bit because although parents are typically the experts on their own children (yes, they are), the reliance on parental report is not the same as reliance on objective medical or prescribing records for antibiotic use and important information on antibiotic type, dose and reason for such use that they typically contain. Indeed, I might also stress that correlating antibiotic use and developmental outcome whilst interesting should also be mindful of the myriad of other variables that might play a role, including the idea that 'behavioural difficulties' often don't present until later infancy for whatever reason. Be careful with single associations.But... I've labelled this post 'Antibiotic brain part 3' because I feel that the Slykerman findings are another important piece of evidence potentially pertinent to the idea that antibiotics may be pretty good at tackling bacterial infection but that also that they may have some quite potent effects on behaviour and development as well as physiology (see here for antibiotic brain part 1 and antibiotic brain part 2).What's the possible mode of action linking [early] antibiotic use and behaviour and development? Well, far be it from me to speculate too much but I'm minded to bring in the idea that those trillions of wee beasties that inhabit our deepest, darkest recesses (the gut microbiome) might play some role in any process. Minus hype [2] we're for example, already finding out how gut bacteria 'might' show some important behavioural connections (see here for example) and specifically how certain strains of bacteria might link to important states such as depression (see here and see here). It's not outside the realms of possibility that 'swallowing a grenade' (although not literally) designed to kill bacteria rather willy-nilly, might influencing either bacterial diversity in the gut or impact on specific strains that could be consider more rather than less beneficial.One more idea for science to perhaps consider relates to why antibiotics were given in the first place. If for example we assume that ear infection might be a common reason, could it not be that the actual symptoms over and above the [antibiotic] treatment might be the more important variable in relation to 'behavioural difficulties'? [3]There is much more to do in this area, but alongside the dangers of antibiotic resistance perhaps science might also be more open to the idea that antibiotics might do so much more than just impact on physiology?To close, for those in Blighty who might remember Hastings, 1066 and a certain Tapestry, things were a whole lot more complicated/gory that you might have expected...----------[1] Slykerman RF. et al. Antibiotics in the first year of life and subsequent neurocognitive outcomes. Acta Paediatr. 2016 Oct 4.[2] Bik EM. The Hoops, Hopes, and Hypes of Human Microbiome Research. Yale J Biol Med. 2016 Sep 30;89(3):363-373.[3] Niclasen J. et al. Associations between otitis media and child behavioural and learning difficulties: Results from a Danish cohort. Int J Pediatr Otorhinolaryngol. 2016 May;84:12-20.----------Slykerman RF, Thompson J, Waldie KE, Murphy R, Wall C, & Mitchell EA (2016). Antibiotics in the first year of life and subsequent neurocognitive outcomes. Acta paediatrica (Oslo, Norway : 1992) PMID: 27701771... Read more »

Slykerman RF, Thompson J, Waldie KE, Murphy R, Wall C, & Mitchell EA. (2016) Antibiotics in the first year of life and subsequent neurocognitive outcomes. Acta paediatrica (Oslo, Norway : 1992). PMID: 27701771

November 2, 2016
04:56 PM
84 views

When I read things like this...

by Craig Payne in Running Research Junkie

When I read things like this...... Read more »

Hollander K, Heidt C, van der Zwaard B, Braumann KM, & Zech A. (2016) Long-Term Effects of Habitual Barefoot Running and Walking: A Systematic Review. Medicine and science in sports and exercise. PMID: 27801744

Medicine

November 2, 2016
11:09 AM
81 views

Weight Training Boosts Brain Size and Performance

by William Yates, M.D. in Brain Posts

Aerobic exercise increases brain blood flow and has demonstrated beneficial effects on cognition.The effects of weight training exercise on the brain is less frequently studied. Hence, we know little about the effect and mechanism of weight training on brain function and performance.A recent study provides some needed insight on this topic.A study by C Suo and colleagues from Australia examined the effects of resistance training and cognitive skills training on brain structure and function.The key elements of design in their study included the following features:Subjects: 100 elderly subjects of average age 70 years with mild cognitive impairmentIntervention: 6 months of progressive resistance training (PRT), computerized cognitive training (CCT), both interventions or neither intervention (sham control group)Cognitive assessments: MMSE, Clinical Dementia Rating Scale and a battery of neuropsychological testsImaging: Pre- and post- 3T MRI voxel-based quantitative assessments of brain regions and resting state fMRIStatistical Analysis: SPSS linear mixed model studying three main effects, time, PRT and CCT The findings in this study were quite remarkable:PRT: Increased performance on global cognitionPRT: Increased brain gray matter volume in the posterior cingulate cortex (see image)PRT: Increase in cigulate gray matter volume correlated with improvement in global cognitionPRT: Reversed progression of brain white matter intensities, a biomarker of cerebrovasular diseaseCCT: Slowed progression of decline in overall memory performanceCCT: Enhanced connectivity between brain hippocampus and superior frontal cortex This is one of the first studies finding a significant improvement in cognitive function in elderly subjects after progressive resistance training.Additionally, the study supports PRT's potential benefit in reversing brain white matter intensities (WMI). I have previously written a blog post on the association of WMI with increased rates of dementia and premature death. You can find that post HERE.The take home message here is that both PRT and CCT appear to have beneficial effects on slowing the effects of aging on the brain. They each appear to have unique mechanisms and brain targets. A smart preventative program for brain health in the elderly would combine the two interventions.Readers with more interest in this study can access the free full-text manuscript by clicking on the link in the citation below.Image showing cingulate cortex is an iPad screen shot from the app 3D BrainFollow me on Twitter by clicking WRY999Suo C, Singh MF, Gates N, Wen W, Sachdev P, Brodaty H, Saigal N, Wilson GC, Meiklejohn J, Singh N, Baune BT, Baker M, Foroughi N, Wang Y, Mavros Y, Lampit A, Leung I, & Valenzuela MJ (2016). Therapeutically relevant structural and functional mechanisms triggered by physical and cognitive exercise. Molecular psychiatry, 21 (11) PMID: 27090304... Read more »

Suo C, Singh MF, Gates N, Wen W, Sachdev P, Brodaty H, Saigal N, Wilson GC, Meiklejohn J, Singh N.... (2016) Therapeutically relevant structural and functional mechanisms triggered by physical and cognitive exercise. Molecular psychiatry, 21(11), 1645. PMID: 27090304

November 2, 2016
10:30 AM
80 views

Testing an Automated and Humane Way to Resolve Barking

by CAPB in Companion Animal Psychology Blog

Teaching a quiet behaviour using an automatic feeder is a promising solution to barking problems.Some dogs bark when their owner is out and they are left home alone. A recent study by Alexandra Protopopova (Texas Tech University) et al investigates the effectiveness of a humane, automated approach to solving barking problems.The research was conducted because some owners use citronella or shock collars to try and prevent their dogs from barking. While the devices may sometimes work, there are concerns they may also have adverse effects.For example, if a dog barks when they see people going by the window and then receives a burst of citronella or an electric shock, they may associate the unpleasant experience with people and become fearful and/or aggressive. Because of these welfare concerns, some organizations recommend against their use (see the AVSAB position statement on the use of punishment).This study used a humane approach that rewarded dogs with food (via a PetSafe remote-activated feeder) for periods of quiet. It was not a fully-automated system as the researcher logged barks and activated a remote control, but it shows the possibility of an automated system in future.Eight dogs were initially recruited to take part in the study, but three were almost immediately excluded when they failed to bark during the first two sessions. The remaining five dogs ranged in age from 8 months to 6 years.Rewarding the dog for being quiet is what is known as a DRO – differential reinforcement of other behaviour, i.e. other to barking.The period of time dogs were expected to be quiet for was different for each dog, based on observations of the frequency of barking. For two of the dogs, it was as little as 5 seconds, and for another it was 7 seconds. For these three dogs, each session was only 10 minutes long so that they did not eat too much; the other two dogs had 20 minute sessions.The design of the study involved a baseline period in which the dog is left alone and barking is monitored but nothing happens, followed by a test period in which the feeding system was used to reward periods of quiet, and then a repeat of both sessions.The owner left the dog, either shutting the dog in a room or crate as they usually did when leaving home. The researcher was in another room where they could hear barking and activate the remote control when the software told them it was time to give a treat.During the test sessions, the interval for which each dog was required to be quiet before getting a treat remained the same for the entire time.For example, a dog called Nina barked every 4.4 seconds on average during the two baseline periods. During the test sessions, every time she went 5 seconds without barking, she was given a treat. During these 10 minute sessions, she barked on average every 26.6 seconds – but in fact she did not bark at all during the second test session.The protocol worked for three of the five dogs. It did not work for one dog, and for the other dog it was not easy to tell.In a second experiment with just the three dogs for whom it worked, the length of time they had to be quiet before earning a treat was increased by doubling the time from one session to the next. Two of the dogs were quiet for the longest period tested (600 seconds and 1,200 seconds). The third dog (Nina) showed big improvements in the early stages but then began to sometimes bark again; this may or may not have been related to a mistake that increased the duration more rapidly than planned.One thing to note is that the dogs could have been barking for any reason to be accepted into the study. In fact the paper says four of the dogs (all except for Nina) potentially showed signs of separation anxiety.The time intervals were chosen based on what it seemed a dog would be able to easily achieve, based on their barking record, but the smallest time interval used was 5 seconds. Maybe a shorter interval would have been better for some dogs. Also, it would be more efficient to have a protocol for adjusting the time intervals throughout, but that was not part of this study.The scientists conclude “This study provides evidence of the efficacy of an alternative (DRO) to the devices that deliver aversive stimulation to decrease home alone excessive barking for at least some dogs.”Think about it: just two 10- or 20 minute sessions were enough to teach three of the dogs to be quiet for a certain length of time. Further research can investigate the best training protocol to use, and the most efficient way to increase the duration of the quiet behaviour.This study has a very small sample size, but the results are promising. Perhaps in the future there will be a range of automated reward-based anti-barking devices on the market.People who buy citronella or electronic anti-bark collars might be just as willing to buy an automated anti-bark feeder and use it to provide their dog’s meals, giving them an easy solution without welfare concerns. It is already possible to buy such a device (although not the version used in the study which was designed by the researchers).A good reward-based dog trainer will devise a training plan that takes into account the reason why the dog is barking (e.g. excitement, fear, separation anxiety). If you think your dog has separation anxiety, you will find useful information via the website of Malena DeMartini.Does your dog bark a lot?ReferenceProtopopova, A., Kisten, D., & Wynne, C. (2016). Evaluating a humane alternative to the bark collar: Automated differential reinforcement of not barking in a home-alone setting Journal of Applied Behavior Analysis DOI: 10.1002/jaba.334Photos: Susan Schmitz (top) and Jennay Hitesman (Shutterstock.com)... Read more »

Protopopova, A., Kisten, D., & Wynne, C. (2016) Evaluating a humane alternative to the bark collar: Automated differential reinforcement of not barking in a home-alone setting. Journal of Applied Behavior Analysis. DOI: 10.1002/jaba.334

November 2, 2016
04:30 AM
90 views

What Came First the Concussion Or the Lower Extremity Musculoskeletal Injury?

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

Athletes who reported sustaining a concussion were 1.6 to 2.9 times more likely to have also sustained a lower extremity musculoskeletal injury at the end of their intercollegiate athletic careers.... Read more »

Gilbert, F., Burdette, G., Joyner, A., Llewellyn, T., & Buckley, T. (2016) Association Between Concussion and Lower Extremity Injuries in Collegiate Athletes. Sports Health: A Multidisciplinary Approach, 8(6), 561-567. DOI: 10.1177/1941738116666509

November 2, 2016
03:55 AM
110 views

ADHD (symptoms) and pain

by Paul Whiteley in Questioning Answers

If a primary goal of medicine is to relieve pain and suffering then the paper by Andrew Stickley and colleagues [1] might provide an important insight into how medicine might be missing some important groups when it comes to the experience of pain "assessed by the degree to which it interfered with work activity in the previous month."Drawing on data from the English 2007 Adult Psychiatric Morbidity Survey (APMS) (a resource that has cropped up on this blog before), authors set about examining "the association between ADHD [attention-deficit hyperactivity disorder] symptoms and pain in the general adult population" to ascertain any connection or not. Bearing in mind a 'screener' was employed when it came to ADHD symptoms (and the problems that other screeners have had when it comes to APMS (see here)) authors concluded that even after adjustment for "comorbid common mental disorders" those adults presenting with self-reported ADHD symptoms had "higher odds for experiencing pain."This is of course not the first time that pain has been suggested to be more frequent where ADHD symptoms or even ADHD is concerned. Fuller-Thomson and colleagues [2] reported that women diagnosed with ADHD were quite a bit more likely to report 'chronic pain' than not-ADHD controls alongside a spectrum of other adversities and issues. Even children / young adults with 'attention problems' have been reported to show a higher frequency of "chronic multisite pain" [3] thus potentially extending the relationship further through the age-groups.So what could be the reason(s) behind such an association? Well, outside of the large body of peer-reviewed evidence suggesting that the risk of injury is enhanced in relation to ADHD (see here) and what influence this might have, other work is potentially revealing. So, traumatic dental injuries and ADHD [4], the persistence of headaches and ADHD [5], the list goes on with regards to potential factors that could influence the presentation of pain. I might also draw your attention to the idea that the perception of pain may be 'altered' [6] when it comes to ADHD or the presentation of ADHD symptoms as demonstrated under experimental conditions. Indeed, this side of things might have some rather important implications for autism too (see here) given the 'over-representation' of ADHD in autism (see here). The idea also that use of something like methylphenidate, traditionally indicated for ADHD, might affect pain responses in ADHD is also worthy of greater research consideration [7].Finally, I'm also minded to suggest that rather than 'blaming it all on ADHD' pain accompanying ADHD or ADHD symptoms could also be due to other coexisting conditions. It's not for example, completely unknown for ADHD to coexist alongside conditions such as fibromyalgia for example [8] bearing in mind that fibromyalgia has a very definite connection to pain. I'm also wondering whether the quite strong link between ADHD and something like asthma (see here), might also be an additional source of pain either directly or indirectly too?The bottom line: yet another case of screening for / asking about other things when a psychiatric / behavioural diagnosis is given and treating / managing accordingly. Screen don't assume.----------[1] Stickley A. et al. ADHD symptoms and pain among adults in England. Psychiatry Res. 2016 Oct 3;246:326-331.[2] Fuller-Thomson E. et al. Attention-deficit/hyperactivity disorder casts a long shadow: findings from a population-based study of adult women with self-reported ADHD. Child Care Health Dev. 2016 Jul 20.[3] Skrove M. et al. Chronic multisite pain in adolescent girls and boys with emotional and behavioral problems: the Young-HUNT study. Eur Child Adolesc Psychiatry. 2015 May;24(5):503-15.[4] Sabuncuoglu O. & Irmak MY. The ADHD modeL for traumatic dental injuries: A critical review and update of the last 10 years. Dent Traumatol. 2016 Oct 17.[5] Parisi P. et al. Headache and attention deficit and hyperactivity disorder in children: common condition with complex relation and disabling consequences. Epilepsy Behav. 2014 Mar;32:72-5.[6] Treister R. et al. Alterations in pain response are partially reversed by methylphenidate (Ritalin) in adults with attention deficit hyperactivity disorder (ADHD). Pain Pract. 2015 Jan;15(1):4-11.[7] Wolff N. et al. Reduced pain perception in children and adolescents with ADHD is normalized by methylphenidate. Child Adolesc Psychiatry Ment Health. 2016 Jul 22;10:24.[8] Derksen MT. et al. High frequency of adult attention deficit hyperactivity disorder among fibromyalgia patients in the Netherlands: should a systematic collaboration between rheumatologists and psychiatrists be sought? Clin Exp Rheumatol. 2015 Jan-Feb;33(1 Suppl 88):S141.----------Stickley A, Koyanagi A, Takahashi H, & Kamio Y (2016). ADHD symptoms and pain among adults in England. Psychiatry research, 246, 326-331 PMID: 27750114... Read more »

Stickley A, Koyanagi A, Takahashi H, & Kamio Y. (2016) ADHD symptoms and pain among adults in England. Psychiatry research, 326-331. PMID: 27750114

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