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  • May 24, 2017
  • 04:33 AM
  • 9 views

Irritable bowel syndrome (IBS) as a risk factor for bipolar disorder

by Paul Whiteley in Questioning Answers

"Only irritable bowel syndrome (IBS) emerged as a risk factor for BD [bipolar disorder] supported by convincing evidence."So said the results of the umbrella review of systematic reviews and meta-analyses by Beatrice Bortolato and colleagues [1] looking at the various environmental risk factors potentially linked to the diagnosis of bipolar disorder. I might add that this is a topic that has been discussed before on this blog (see here and see here for examples).If the systematic review / meta-analysis represents the top of the research methodology hierarchy, a review including a number of systematic reviews and meta-analyses represents the cherry on top. Indeed, there is a growing trend of this kind of research (see here).The authorship names included on the Bortolato paper are not unfamiliar to this type of study methodology (see here) and specifically, the focus on psychiatric and somatic variables often being intertwined. This time around attentions turned to bipolar disorder, previously called manic depression, and a survey of 16 research publications identified listing over 50 "unique environmental risk factors for BD." The report of a possible link (with 'convincing evidence') between IBS and BD consolidates the idea of a gut-brain axis. Authors also detailed a few other factors as showing weaker but not necessarily less important connections to BD including childhood adversity, obesity and asthma. Focusing in on asthma in particular - a condition again previously talked about in the context of BD - I am wondering whether there are quite a few more generalisations connected to this diagnosis within the context of psychiatric labels (see here and see here)?Of course, more science is indicated on the hows-and-whys of connections such as the one between IBS and BD and the tantalising prospect of new intervention avenues if such a relationship is further confirmed. Minus any medical or clinical advice, I'm specifically thinking about how alterations to the gut microbiome accompanying cases of IBS might mean that talk of things like probiotics affecting the symptoms of IBS (see here) could be applicable to the presentation of [some] BD too. That and the idea that certain dietary elements might also be important to cases (see here and see here)...To close, I know that the past few days have not exactly been ones for smiling, but if some smiles and laughter are what you need, then the animal kingdom can provide them...----------[1] Bortolato B. et al. Systematic assessment of environmental risk factors for bipolar disorder: an umbrella review of systematic reviews and meta-analyses. Bipolar Disord. 2017; 00: 1–13.----------Bortolato, B., Köhler, C., Evangelou, E., León-Caballero, J., Solmi, M., Stubbs, B., Belbasis, L., Pacchiarotti, I., Kessing, L., Berk, M., Vieta, E., & Carvalho, A. (2017). Systematic assessment of environmental risk factors for bipolar disorder: an umbrella review of systematic reviews and meta-analyses Bipolar Disorders DOI: 10.1111/bdi.12490... Read more »

  • May 23, 2017
  • 12:38 PM
  • 24 views

Dismantle the Poverty Trap by Nurturing Community Trust

by Jalees Rehman in The Next Regeneration

Understanding the precise reasons for why people living in poverty often make decisions that seem short-sighted, such as foregoing more education or taking on high-interest short-term loans, is the first step to help them escape poverty. The obvious common-sense fix is to ensure that the basic needs of all citizens – food, shelter, clothing, health and personal safety – are met, so that they no longer have to use all new funds for survival. This is obviously easier in the developed world, but it is not a trivial matter considering that the USA – supposedly the richest country in the world – has an alarmingly high poverty rate. It is estimated that more than 40 million people in the US live in poverty, fearing hunger and eviction from their homes. But just taking care of these basic needs may not be enough to help citizens escape poverty. A recent research study by Jon Jachimowicz at Columbia University and his colleagues investigated “myopic” (short-sighted) decision-making of people with lower income and identified an important new factor: community trust.... Read more »

Jachimowicz, J., Chafik, S., Munrat, S., Prabhu, J., & Weber, E. (2017) Community trust reduces myopic decisions of low-income individuals. Proceedings of the National Academy of Sciences, 201617395. DOI: 10.1073/pnas.1617395114  

  • May 23, 2017
  • 07:06 AM
  • 27 views

Multi-Loop Structure of Nonthermal Microwave Sources in a Major Long-Duration Flare by V. Grechnev et al.*

by CESRA in Solar Radio Science

Hard X-ray (HXR) and microwave observations of flares show only a few nonthermal sources. They are simple and compact, especially in impulsive flares, suggesting involvement of one to two loops. Hanaoka (1996) and Nishio et al. (1997) interpreted these observations in terms of double-loop flares. This view was later extended up to long-duration flares (Tzatzakis, Nindos, and Alissandrakis, 2008). A concept of a simple flare loop became dominant. However, observations [...]... Read more »

  • May 23, 2017
  • 02:54 AM
  • 42 views

"there is no single way for a brain to be normal" (or how 'neurotypical' is a nonsense)

by Paul Whiteley in Questioning Answers

I'm not usually so forthright with my posts on this blog, but today I'm being a little more bullish as I talk about an editorial from Simon Baron-Cohen [1] titled: "Neurodiversity – a revolutionary concept for autism and psychiatry."The crux of the SBC paper is the suggestion that use of the term 'disorder' specifically with autism in mind might have certain connotations - "Disorder should be used when there is nothing positive about the condition" - and until the "biomedical mechanistic cause of a disorder becomes known" some thought should go into the way autism for example, is described.The author seems to come down on something between 'difference' and 'disability' as being valid replacements, bearing in mind the wide - very wide - heterogeneity that is the autism spectrum and the fact that 'disorder' is still very prominent in the formal clinical descriptions of autism and related diagnoses (see here). Indeed on the topic of 'biomedical mechanistic causes' and [some] autism, well, there is already some evidence for this (see here)...Personally, I don't want to get involved in such disorder/difference debates. I say this on the basis that (a) people have their own ideas, descriptions and motivations for talking about what autism is and isn't to them (and who I am to question them and their views) and (b) from a research and clinical point of view, such linguistic differences make little difference when it comes to whether someone does or does not reach critical cut-off points for being on the autism spectrum and the subsequent help and support required. These are cultural issues not fundamental research or clinical ones (although I daresay some people would argue against that last point).What I do however want to mention about the Baron-Cohen article is that specific sentence described in the title of this post - "there is no single way for a brain to be normal" - in relation to neurodiversity [2] and how said phrase helps dismantle a problematic term present in various autism circles: neurotypical (NT).I see the word neurotypical (NT) banded about a lot these days including in the peer-reviewed domain. I assume from the name that the term describes 'others' who within the vast spectrum of diversity - neuro and otherwise - are, in relation to autism, not positioned on the autism spectrum. It's basically an 'us-and-them' term, which means not-autism (or other condition where similarly applied).The problem I have with this term relates to the questions: what exactly is neurotypical? and who actually falls under such a description?OK, we have the first bit - neuro - which is also used/misused a lot these days (together with some scepticism) I assume referring to the brain. Autism is often described in terms of the brain (structure, connectivity, 'wiring') as mentioned in the Baron-Cohen text, with some groups even talking about the possibility of an 'autistic brain' (see here). More precisely 'neuro' probably better describes the nervous system so one might instead look to the term 'autistic nervous system' as being more accurate (bearing in mind the brain is but one thinking organ in the body!). The second part - 'typical' - on it's own means just that: classic, quintessential, representative. Put them both together and the suggestion is that there is an 'average, representative brain / nervous system' in the population that is distinct from the 'autistic brain / nervous system'.Why is this problematic? Well, this is where the concept of 'identity' has I think perhaps overstretched itself.The 'autistic brain'? Bullshit (pardon my language). As I've said before on this blog, there is nothing in the peer-reviewed science literature to yet say that the brains / nervous system of everyone diagnosed as being on the autism spectrum are in any way universally different from those not reaching thresholds for the autism spectrum (see here). Nothing. Not one article. Indeed, with the greater recognition that autism is probably a plural condition covered by a singular label (see here), the likelihood that something / anything will universally define the 'autistic brain' is becoming even more distant. Y'know, much like the fading concept of an autistic gene that's taken so long to consign to the research dustbin/trashcan. I say all this even before we start to add-in the idea that autism rarely exists in some sort of diagnostic vacuum (see here) in these days of ESSENCE (see here).OK, you might say that 'typical' could be stretched to include a wider spectrum of brains / functioning / thinking rather than just one singular thing? Well, that's true but here's another issue: at what point does 'typical' then turn into 'atypical'? The inference is that alongside the neurotypical there is something akin to the neuroatypical. Where are these boundaries of neurotypical and neuroatypical? Do the boundaries shudder to an abrupt halt the moment cut-off points for a diagnosis of autism are reached or surpassed? Does this also mean that other labels such as attention-deficit hyperactivity disorder (ADHD) are also outside of the term neurotypical? Really? On what evidence?Then also there are the various observations that the presentation(s) of autism - the symptoms / characteristics / label - might actually be quite fluid across different people according to variables such as age or environment and how that further complicates the neurotypical concept. I've talked for example, before about how something like diagnostic stability is perhaps not as stable as many people might think when it comes to some autism (see here) and indeed, in relation to other over-represented comorbidity too (see here). Does this mean that those for example, currently not fulfilling the diagnostic criteria for autism but having previously done so at some previous point have somehow 'transitioned' from autism to neurotypical? Again, really? On what evidence?I could go on (and on) about the other problems with the concept of neurotypical (e.g. the problem of objectively measuring thinking styles, etc) but I won't. All I'll say is that in the age of 'show me the evidence' please do show me the evidence - any evidence - that neurotypical is anything other than an alternative phrase to 'not-autism' or at least not meeting the current cut-off thresholds for a diagnosis of autism or related label.And, on the basis of the points I've raised in today's post, how then can science continue to justify it's use when the description of neurotypical is, by all accounts, a nonsense?----------[1] Baron-Cohen S. Editorial Perspective: Neurodiversity - a revolutionary concept for autism and psychiatry. J Child Psychol Psychiatry. 2017 Jun;58(6):744-747.[2] Armstrong T. The myth of the normal brain: embracing neurodiversity. AMA J Ethics. 2015 Apr 1;17(4):348-52.----------... Read more »

  • May 22, 2017
  • 03:00 PM
  • 71 views

Unraveling the Mysteries of Mischievous Microbiome

by Aurametrix team in Aurametrix Blog

Science explains why some people smell worse than others despite keeping themselves squeaky clean. The body is crawling with bacteria increasing the risk for diseases for which we have unreserved levels of sympathy. It can also lead to ​unlikable conditions such as unpredictable and embarrassing outbursts of body odor - so bad it ruins social lives and careers.  But there is no cure for metabolic body odor ... Read more »

  • May 22, 2017
  • 05:13 AM
  • 45 views

"a gluten-related subgroup of schizophrenia"?

by Paul Whiteley in Questioning Answers

A quote to begin this post: "this preliminary study demonstrates that altered AGDA [antibodies against gliadin-derived antigen] levels in the circulation are associated with schizophrenia and could serve as biomarkers for the identification of a schizophrenia subgroup that may need an alternative therapy or precision treatment."So said the findings reported by McLean and colleagues [1] (open-access) looking at an area of some interest to this blog (see here) on how dietary gluten might show something of an important relationship to at least some cases of schizophrenia. Just in case you weren't aware, there is quite a history when it comes to gluten and schizophrenia (see here) as per the very forward-thinking of people such as Curt Dohan and Karl Reichelt.Researchers on this latest occasion set about looking in a little more detail at the suggestion that circulating anti-gliadin antibodies (AGAs) reflective of an immune response to a component of dietary gluten might show some connection to schizophrenia. Indeed they note that "all the tests for circulating AGAs in schizophrenia have been developed with mixtures of full-length native gliadins consisting of ~300 amino acid residues" suggesting that such a scatter gun approach may have included epitopes "that are unlikely to survive digestion in the gut." So, they instead "measured plasma levels of IgG and IgA against indigestible peptide fragments derived from γ- and α-gliadins" in archived plasma samples from "169 patients with schizophrenia and 236 control subjects."The results - based on the use of an "In-house ELISA for antibodies against gliadin-derived antigens" - were rather intriguing. So: "There was no significant difference in the levels of plasma antibodies against native gliadins between the patient group and the control group." If I'm reading this right, this finding is in contrast to other independent research occasions [2]. Indeed, when it came to looking at both IgA and IgG plasma anti-gliadin antibodies, there was no significant difference between the schizophrenia and non-schizophrenia participants as groups.But... when it came to a specific gliadin (γ-Gliadin) derived fragment  - AAQ6C - with the amino acid sequence HPKCSIMRAPFASIVAGIGGQYRD - researchers reported on something potentially important to see: "patients with schizophrenia had significantly higher levels of plasma anti-AAQ6C IgG than control subjects." Importantly too, authors also noted that anti-psychotic medication did not appear to influence their antibody results. This was important given that seemingly all of the participants diagnosed with schizophrenia were taking one or more of this class of medicine. In line with the opening quote to this post, the authors make a preliminary foray into the possible 'biomarker' usefulness of the various anti-gluten antibodies for schizophrenia. I have to say on this point however, that the data is not that impressive as things currently stand.There is more to do when it comes to the possible effects of dietary elements containing gluten (and casein) in relation to cases of schizophrenia. This work adds something to the idea that diet can affect psychiatry/behaviour/development but what is perhaps missing is the recognition that schizophrenia is probably a heterogeneous and plural condition (see here and see here for examples) and as such, not every case is going to be gluten and/or casein-related. I do agree with the authors that more research is needed in this area alongside the idea that intervention via either dietary changes [3] and/or other options might also be on the research agenda...----------[1] McLean RT. et al. Differential antibody responses to gliadin-derived indigestible peptides in patients with schizophrenia. Translational Psychiatr. 2017. May 9.[2] Dickerson F. et al. Markers of gluten sensitivity and celiac disease in recent-onset psychosis and multi-episode schizophrenia. Biol Psychiatry. 2010 Jul 1;68(1):100-4.[3] Jackson J. et al. A gluten-free diet in people with schizophrenia and anti-tissue transglutaminase or anti-gliadin antibodies. Schizophrenia Res. 2012;140(0):262-263.----------McLean RT, Wilson P, St Clair D, Mustard CJ, & Wei J (2017). Differential antibody responses to gliadin-derived indigestible peptides in patients with schizophrenia. Translational psychiatry, 7 (5) PMID: 28485731... Read more »

  • May 22, 2017
  • 04:30 AM
  • 38 views

Should Athletic Trainers Add Anxiety Surveys to Preseason Baseline Testing?

by Jane McDevitt in Sports Medicine Research (SMR): In the Lab & In the Field

An athlete with anxiety symptoms during preseason was more likely to get injured during a season than an athlete without symptoms.... Read more »

  • May 21, 2017
  • 10:50 AM
  • 50 views

Predictive Processing: the role of confidence and precision

by Sergio Graziosi in Writing my own user manual - Sergio Graziosi's Blog

This is the second post in a series inspired by Andy Clark’s book “Surfing Uncertainty“. In the previous post I’ve mentioned that an important concept in the Predictive Processing (PP) framework is the role of confidence. Confidence (in a prediction)…Read more ›... Read more »

Kanai R, Komura Y, Shipp S, & Friston K. (2015) Cerebral hierarchies: predictive processing, precision and the pulvinar. Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 370(1668). PMID: 25823866  

  • May 21, 2017
  • 07:55 AM
  • 77 views

A Survey of Our Secret Lives

by Neuroskeptic in Neuroskeptic_Discover

What kinds of secrets does the average person keep? In a new paper, Columbia University researchers Michael L. Slepian and colleagues carried out a survey of secrets.



Slepian et al. developed a 'Common Secrets Questionnaire' (CSQ) and gave it to 600 participants recruited anonymously online. Participants were asked whether they'd ever had various secrets, at any point in their lives. The results are a monument to all our sins:

It turns out that extra-relational thoughts - meaning "thou... Read more »

Slepian, M., Chun, J., & Mason, M. (2017) The Experience of Secrecy. Journal of Personality and Social Psychology. DOI: 10.1037/pspa0000085  

  • May 20, 2017
  • 06:12 AM
  • 72 views

Gastrin-releasing peptide and autism continued

by Paul Whiteley in Questioning Answers

Yet another 'continued' or 'part 2' short post for you today, building on some previous - very preliminary research - talking about the use of gastrin-releasing peptide (GRP) and autism (see here).The authors included on the paper by Josemar Marchezan and colleagues [1] are familiar ones to this part of the autism research landscape as per the other occasions that members of this group have looked at / talked about GRP and autism in the peer-reviewed domain.GRP is all about a compound that 'does what it says on the tin' insofar as stimulating the release of gastrin from specialist cells in the stomach. This in turn leads to the secretion of gastric acid among other things and onward aids the digestion of food.This time around Marchezan et al describe the results of a controlled trial on the use of GRP (vs. placebo) in a small group of boys (N=10) diagnosed with autism. This is a step-up from their previous research efforts in this area talking about a case series report and an open (non-blinded, non-placeboed?) study. Participants were given the same amount of GRP (160 pmol/kg) over the same number of days (4 consecutive days) as that detailed in their previous studies. This time around, the Aberrant Behavior Checklist (ABC) scale was the outcome measure of choice.Results: well, let's put it one way, they weren't exactly astounding in terms of any positive effects from the use of GRP over such a short space of time. This was exemplified by the authors use of "no statistical difference" when it came to looking at quite a lot of the data obtained during the investigation comparing GRP to placebo. On the plus side there were "no adverse effects, changes in vital signs, or laboratory abnormalities associated with the use of GRP" so the whole 'first do no harm' bit seems to be intact, at least in the short-term.Whilst it would be easy to sweep such results under the 'did not work' carpet, I am however minded to go with the authors' suggestion that "further research with other designs and a larger sample size to evaluate the efficacy and safety of GRP in children with autism" would be a step forward. I say this on the basis that hypochlorhydria - low levels of gastric acid - is not something completely unknown to parts of the autism spectrum (see here) and does suggest some *possible* involvement for something like GRP in specific cases of autism.----------[1] Marchezan J. et al. A Placebo-Controlled Crossover Trial of Gastrin-Releasing Peptide in Childhood Autism. Clin Neuropharmacol. 2017 Apr 27.----------Marchezan, J., Becker, M., Schwartsmann, G., Ohlweiler, L., Roesler, R., Renck, L., Gonçalves, M., Ranzan, J., & Riesgo, R. (2017). A Placebo-Controlled Crossover Trial of Gastrin-Releasing Peptide in Childhood Autism Clinical Neuropharmacology DOI: 10.1097/WNF.0000000000000213... Read more »

Marchezan, J., Becker, M., Schwartsmann, G., Ohlweiler, L., Roesler, R., Renck, L., Gonçalves, M., Ranzan, J., & Riesgo, R. (2017) A Placebo-Controlled Crossover Trial of Gastrin-Releasing Peptide in Childhood Autism. Clinical Neuropharmacology, 1. DOI: 10.1097/WNF.0000000000000213  

  • May 19, 2017
  • 10:21 PM
  • 58 views

The warmer the dangerouser, at least if you are a caterpillar

by Piter Boll in Earthling Nature

by Piter Kehoma Boll Scientist all over the world agree that species diversity is higher at the tropics than at polar regions, i.e., the closer you get to the equator, more species you will find. But apart from making food … Continue reading →... Read more »

Roslin, T., Hardwick, B., Novotny, V., Petry, W., Andrew, N., Asmus, A., Barrio, I., Basset, Y., Boesing, A., Bonebrake, T.... (2017) Higher predation risk for insect prey at low latitudes and elevations. Science, 356(6339), 742-744. DOI: 10.1126/science.aaj1631  

  • May 19, 2017
  • 07:00 AM
  • 62 views

Friday Fellow: Common Stinkhorn

by Piter Boll in Earthling Nature

by Piter Kehoma Boll Today things are getting sort of pornographic again. Some time ago I introduced a plant whose flowers resemble a woman’s vulva, the asian pigeonwing, and now is time to look at something of the other sex. … Continue reading →... Read more »

  • May 19, 2017
  • 05:13 AM
  • 73 views

Characterization of a FLCN mutation associated with RCC

by Joana Guedes in BHD Research Blog

Mutations in the FLCN gene are the cause of Birt-Hogg-Dubé (BHD) syndrome, a rare disease characterized by renal cell carcinoma (RCC), pneumothorax and fibrofolliculomas. In their new study, Bartram et al. (2017) identify a heterozygous mutation in the FLCN gene in a patient with RCC. DNA from tumour and a metastasis was analysed and the authors demonstrated skipping of exon 11 as the consequence of this mutation leading to a shift in the reading frame and the insertion of a premature stop codon. The FLCN protein was still expressed but it was strongly destabilized and had a different subcellular localization. Both altered protein stability and subcellular localization could be partly reversed by blocking proteasomal and lysosomal degradation.... Read more »

Bartram MP, Mishra T, Reintjes N, Fabretti F, Gharbi H, Adam AC, Göbel H, Franke M, Schermer B, Haneder S.... (2017) Characterization of a splice-site mutation in the tumor suppressor gene FLCN associated with renal cancer. BMC medical genetics, 18(1), 53. PMID: 28499369  

  • May 19, 2017
  • 04:26 AM
  • 66 views

Injury risk and ADHD: part 2

by Paul Whiteley in Questioning Answers

Consider this short post a sort of follow-on to a previous entry on this blog concerning the elevated risk of injury following a diagnosis of attention-deficit hyperactivity disorder (ADHD). The paper in question today is that by Wu-Chien Chien and colleagues [1] who yet again [2], brought the quite significant scientific weight of the "National Health Insurance Research Database in Taiwan" to bear on this topic.In this latest paper, Chien et al relied on data from a 'subset' of the main insurance research database and found some not unexpected things: "The patients with ADHD had a 143% increased risk of overall injuries than the controls after considering all the confounding factors" and "the use of methylphenidate was associated with a 22.6% decrease in the risk of injuries in the patients with ADHD."What's more to say? Well, yet again risk of adverse issues *correlating* with a diagnosis of ADHD comes to the forefront (see here for another example). Yet again the idea that 'tackling' ADHD is a worthy goal (for many reasons) if not only to mitigate such elevated risks being presented, bearing in mind that medication "approved solely for ADHD treatment" is not some sort of magic bullet [3]. There are also other potentially important intervention options to look at (see here for example). I'm minded at this point to also bring in the recent findings reported by Borschuk and colleagues [4] talking about how comorbid asthma accompanying ADHD (yes, there is a surprisingly strong relationship between the two diagnoses) might play a role in the expression of ADHD and onwards provide some 'interesting' directions when it comes to tackling ADHD and it's elevated risk for various adverse outcomes...To close, appreciating a talent...----------[1] Chien WC. et al. The risk of injury in adults with attention-deficit hyperactivity disorder: A nationwide, matched-cohort, population-based study in Taiwan. Res Dev Disabil. 2017 Apr 27;65:57-73.[2] Kang JH. et al. Attention-deficit/hyperactivity disorder increased the risk of injury: a population-based follow-up study. Acta Paediatr. 2013 Jun;102(6):640-3.[3] Fleming M. et al. Educational and Health Outcomes of Children Treated for Attention-Deficit/Hyperactivity Disorder. JAMA Pediatr. 2017. May 1.[4] Borschuk AP. et al. The influence of comorbid asthma on the severity of symptoms in children with attention-deficit hyperactivity disorder. J Asthma. 2017 May 1:1-7.----------Chien WC, Chung CH, Lin FH, Yeh CB, Huang SY, Lu RB, Chang HA, Kao YC, Chiang WS, Chou YC, Tsao CH, Wu YF, & Tzeng NS (2017). The risk of injury in adults with attention-deficit hyperactivity disorder: A nationwide, matched-cohort, population-based study in Taiwan. Research in developmental disabilities, 65, 57-73 PMID: 28458048... Read more »

  • May 18, 2017
  • 04:40 AM
  • 80 views

On vaccinated and un-vaccinated homeschooled children: the disappearing-reappearing-disappearing-reappearing studies

by Paul Whiteley in Questioning Answers

I originally began writing this post in the last week of November 2016 following first sight of the study abstract by Anthony Mawson and colleagues [1] and their journey into a topic that has had its fair share of discussion/argument* (*delete as appropriate) with autism in mind down the years: are vaccines or immunisation patterns potentially linked to [some] autism?As it happened, this post was shelved for some time because (a) only an abstract appeared despite a publication date accompanying the initial open-access submission in a Frontiers journal and (b) the subsequent sudden disappearance of the abstract from the publishers website following some discussions on social media about the paper and the review process (see here and see here for more information).The study then appeared in a different journal (April 2017) before once again disappearing.Now it's back - for now - in the same journal, so once again it's fodder for this blog...As I always do when it comes to any chatter specifically on this topic, I should reiterate a few things: (a) the prime directive of this blog - no clinical or medical advice is given or intended - and (b) that vaccines save lives. I know some people attribute other factors to that 'life-saving' angle when it comes to vaccines over the longer term (better health, better environment, etc), but one really only needs to look at the protective effect of the various meningitis vaccines for example, to see their results in something like real-time. I repeat again: vaccines save lives.What however does seem to be missing from at least some of the general discussion about vaccines as a whole and their very positive health effects is the fact that they are medicines. As such they are not somehow impervious to potentially producing side-effects for some people, albeit a small proportion of people who use them. The problem at the moment is, that we don't really know everything there is to know about which people might be at greater risk of side-effects than others (although some clues are emerging) and importantly, how all those side-effects may manifest. Science - metabolomic science - is however starting to tackle some aspects of these issues [2] minus too much hype at the present time.As per the title of this post, Mawson et al set about examining whether there were differences between those children who were vaccinated and those un-vaccinated across "a broad range of health outcomes." In line with the previous history hypothesising about autism and specific vaccination, the authors focused on any 'association' between vaccination status and neurodevelopmental disorders (NDD) taking into account other potentially confounding variables.The source data for those vaccinated / un-vaccinated children participants (N=666) was an anonymous online questionnaire completed by mothers of children who were members of various homeschooling organisations in four regions of the United States. Homeschooling refers to a situation where a child is educated at home outside of the mainstream education system choices. Homeschoolers were selected for study because, according to the authors, a "higher proportion are unvaccinated compared to public school children."Results: around 40% of the participants were indeed described as un-vaccinated in the Mawson cohort. This is quite a bit higher than other estimates [3] specifically looking at homeschooled children. Then to some of the details: "Vaccinated children were significantly less likely than the unvaccinated to have been diagnosed with chickenpox and pertussis." If you needed more evidence that vaccines work, that last sentence kinda provides you with it, particularly in light of what diseases like pertussis can potentially do to the most vulnerable.And then some potential controversies: vaccinated children were significantly more likely to have been diagnosed with pneumonia, otitis media, allergies and NDDs (defined as autism spectrum disorder, attention deficit hyperactivity disorder, and/or a learning disability). After some statistical adjustment for potentially confounding variables, authors reported that "vaccination, nonwhite race, and male gender were significantly associated with NDD after controlling for other factors." I might also draw your attention to the reported finding that: "preterm birth and vaccination combined was strongly associated with NDD in the final adjusted model with interaction, more than doubling the odds of NDD compared to vaccination alone." This might suggest that there are synergistic variables at work influencing any identified risk continuing a research theme [4]. Indeed, the same authors have devoted a whole other article to this finding [5] (this paper also went through the same disappearing-reappearing act too).Wearing the objective blinkers of science, this is by no means perfect research. Not only are there potential issues related to the use of an on-line questionnaire (and anonymous at that), the focus on subjective reports over inspection of more objective medical records (even though parents were asked to obtain and use their child's vaccination record(s) when completing the questionnaire), and problems associated with recall (including possible telescoping effects), there are a whole host of other issues that one could cite in relation to such research and potential biases that could/might have influenced the results (including factors such as this one). I might also add that the Mawson study did not appear to 'name names' when it came to which individual vaccines may or may not have been involved in their findings despite asking questions about if and when specific immunisations were administered to participants. Indeed authors noted: "We did not set out to test a specific hypothesis about the association between vaccination and health." Then there is also the 'reaction' angle to papers such as this one to mention; bearing in mind that science these days does not exist in some sort of social/cultural vacuum as per other very recent and very relevant examples. Cumulatively, you can see that there ... Read more »

Anthony R Mawson, Brian D Ray, Azad R Bhuiyan, & Binu Jacob. (2017) Pilot comparative study on the health of vaccinated and unvaccinated 6- to 12-year-old U.S. children. Journal of Translational Science. info:/10.15761/JTS.1000186

  • May 17, 2017
  • 03:08 PM
  • 106 views

Paper About Plagiarism Contains Plagiarism

by Neuroskeptic in Neuroskeptic_Discover

Regular readers will know that I have an interest in plagiarism. Today I discovered an amusing case of plagiarism in a paper about plagiarism.

The paper is called The confounding factors leading to plagiarism in academic writing and some suggested remedies. It recently appeared in the Journal of the Pakistan Medical Association (JPMA) and it's written by two Saudi Arabia-based authors, Salman Yousuf Guraya and Shaista Salman Guraya.



Here's an example of the plagiarism: a 2015 paper by ... Read more »

  • May 17, 2017
  • 12:00 PM
  • 89 views

Epigenetic Marks Associated to Severe Obesity

by Delphine Fradin in EpiBeat

There is growing evidence that DNA methylation might contribute to obesity. Candidate gene methylation studies in animal models and humans have demonstrated methylation changes in promoters of various genes that are implicated in obesity, appetite control and/or metabolism, insulin signaling, immunity, growth and circadian clock regulation.

Severe obesity in children is defined as greater than or equal to 99th percentile of body mass index (BMI) for age and gender or a BMI z-score ≥3.5. Population surveys demonstrate a significant increase in obesity prevalence among children, where severe obesity is the most rapidly growing paediatric obesity subgroup. Compared to youth with BMI in the obese range, those with severe obesity have higher rates of immediate and long-term diseases. It stands to reason that youth with obesity and severe obesity may also differ in aetiological factors and consequences, including epigenetic.... Read more »

Fradin, D., Boëlle, P., Belot, M., Lachaux, F., Tost, J., Besse, C., Deleuze, J., De Filippo, G., & Bougnères, P. (2017) Genome-Wide Methylation Analysis Identifies Specific Epigenetic Marks In Severely Obese Children. Scientific Reports, 46311. DOI: 10.1038/srep46311  

  • May 17, 2017
  • 11:24 AM
  • 90 views

Dad's Impact in Infant Development

by William Yates, M.D. in Brain Posts

Mother's interaction with their infants play a key role in infant development.The independent role of fathers in infant development is less well known and studied.A recent study from the United Kingdom supports a important role for father-child interactions in infant development.Here are the main elements of the design of this study:Subjects: Families of infants with typical deliveries were recruited from maternity wards in two hospitals in the United Kingdom.Design: Home assessments were completed at 3 months and 24 months following birth making this a longitudinal study design. Assesment at 3 months included observation of father-child interaction.Key outcome measures: 24 month score on the Mental Development Index (MDI) of the Bayley Scales of Infant DevelopmentStatistical analysis: Correlational analysis of paternal interaction measures at 3 and 24 months was completed. Additionally, independent simple linear analyses and PROCESS macro tool modeling were done to examine effects of covariates.The important finding from the study was that paternal-infant interaction at 3 months of age predicted important dimensions of infant mental development.Fathers who demonstrated more engagement, sensitivity and less control at 3 months had infants with greater scores on the Mental Development Index at 24 months.That authors note in the discussion section "The results of this study indicate that specific dimensions of father-child interactions at both time points are associated with MDI scores even when adjusting for paternal depression, age and education, and maternal sensitivity and infant age."The take home message in this study is that Dad's make a difference in infant development. As the authors note, supporting paternal interaction may be a key prevention measure in infant development.Readers with more interest in this study can access the free full-text manuscript by clicking on the PMID link in the citation below.Follow me on Twitter @WRY999Photo of paternal spider monkey and infant is from my photography files. Follow me on Instagram at WRY999You can find all my Brain Post blog posts and highlight Twitter posts on my Facebook Page Neuroscience Medicine.Sethna V, Perry E, Domoney J, Iles J, Psychogiou L, Rowbotham NEL, Stein A, Murray L, & Ramchandani PG (2017). FATHER-CHILD INTERACTIONS AT 3 MONTHS AND 24 MONTHS: CONTRIBUTIONS TO CHILDREN'S COGNITIVE DEVELOPMENT AT 24 MONTHS. Infant mental health journal PMID: 28449355... Read more »

  • May 17, 2017
  • 07:02 AM
  • 80 views

Those who only kill children are neuro-psychologically different from other murderers

by Doug Keene in The Jury Room

Of course it isn’t a surprise that they are gravely disturbed, but who knew it was neuropsychological?  This is an article from researchers at Northwestern University and looks very specifically at similarities and differences in the neuropsychological test scores of those who killed only children and those who killed some adults as well as children. […]... Read more »

Azores-Gococo, N., Brook, M., Teralandur, S., & Hanlon, R. (2017) Killing A Child. Criminal Justice and Behavior., 2147483647. DOI: 10.1177/0093854817699437  

  • May 17, 2017
  • 04:30 AM
  • 85 views

Another Feather in the Cap of the FIFA 11 Injury Prevention Program

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

Implementing the FIFA 11 injury prevention program decreases the risk of injury among collegiate male soccer players.... Read more »

Silvers-Granelli HJ, Bizzini M, Arundale A, Mandelbaum BR, & Snyder-Mackler L. (2017) Does the FIFA 11  Injury Prevention Program Reduce the Incidence of ACL Injury in Male Soccer Players?. Clinical orthopaedics and related research. PMID: 28389864  

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