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  • October 21, 2016
  • 04:37 AM

One more time: asthma and autism

by Paul Whiteley in Questioning Answers

I'm actually getting a little bored of talking about the various peer-reviewed research looking at a possible connection between asthma and autism on this blog. It's not that it isn't an interesting topic but rather that the data is coming in thick and fast suggesting that behaviour and physiology are not completely separate anymore.I did however want to direct you to the paper by Alessandro Tonacci and colleagues [1] who, following a systematic review "according to the PRISMA guidelines" suggested that "Autism Spectrum Disorder and asthma could be associated conditions, as evidenced by the higher prevalence of asthma in autistic children with respect to typically developed controls." I might add that this is not the first time that this authorship group have examined the coincidence of allergic disease with autism (see here).The idea that asthma and autism might be connected is an important finding because not so long ago I talked about another paper [2] - a meta-analysis - that came up with a slightly different conclusion to that listed by Tonacci (see here). OK, a systematic review and a meta-analysis whilst related are not necessarily one and the same and so one has to be a little careful. That being said, I did raise a few 'issues' with that previous meta-analysis by Zheng and colleagues [2] around what they did and did not seemingly include in their paper. A meta-analysis or systematic review is only as good as the number and quality of the studies it includes.The strength of the Tonacci review is that it followed those PRISMA guidance - the Preferred Reporting Items for Systematic reviews and Meta-Analyses - and also that "Methods for study selection and inclusion criteria were specified in advance and documented in PROSPERO protocol #CRD42014012851." In other words, much like when study protocols for clinical trials are pre-registered to avoid any 'massaging' of results or changing/switching outcomes, so their aims and objectives were on record for all to see.Where next for the suggestion of a possible link between asthma and autism? Well, how about taking into account a role for comorbidity as per the increasingly strong evidence coming out about how asthma and attention-deficit hyperactivity disorder (ADHD) may be linked (see here) and what that means for the over-representation of ADHD in autism or vice-versa (see here). I might once again suggest that immune function (i.e. inflammation or inflammatory processes) could be a common variable requiring further study too (see here for example). Such research may wish to take into account overlapping genetics/epigenetics as being important as well as the more functional biochemistry of immune system processes.Given also the specific focus on "allergic asthma" by Tonacci et al I'm also wondering whether the various research on allergy symptoms affecting autism presentation might be important for some (see here). Indeed, with no medical advice given or intended, the idea of treating allergic disease in cases of ADHD for example (see here) is perhaps an area ripe for further investigation when it comes to autistic presentation too...To close: Guardians of the Galaxy is back (and the soundtrack will be as cool as ever I guess).----------[1] Tonacci A. et al. A systematic review of the association between allergic asthma and autism. Minerva Pediatr. 2016 Oct 5.[2] Zheng Z. et al. Association between Asthma and Autism Spectrum Disorder: A Meta-Analysis. PLoS One. 2016 Jun 3;11(6):e0156662.----------Tonacci A, Billeci L, Ruta L, Tartarisco G, Pioggia G, & Gangemi S (2016). A systematic review of the association between allergic asthma and autism. Minerva pediatrica PMID: 27706122... Read more »

Tonacci A, Billeci L, Ruta L, Tartarisco G, Pioggia G, & Gangemi S. (2016) A systematic review of the association between allergic asthma and autism. Minerva pediatrica. PMID: 27706122  

  • October 20, 2016
  • 04:32 AM

"Folinic acid improves communication in childhood autism"

by Paul Whiteley in Questioning Answers

A quote to begin: "... in this small trial of children with non-syndromic ASD [autism spectrum disorder] and language impairment, treatment with high-dose folinic acid for 12 weeks resulted in improvement in verbal communication as compared with placebo, particularly in those participants who were positive for FRAAs [folate receptor-α autoantibody]."Those were the findings reported by Richard Frye and colleagues [1] (open-access) continuing a research theme from this group looking at how folinic acid - a reduced form or vitamer of folate - may "markedly" improve symptoms in some children diagnosed with ASD (see here). Some media reporting about these latest results are available (see here for example) but if you're sticking with my interpretation there are a few important points to note.So:This was a gold-standard "double-blind, randomized placebo-controlled" study meaning that as well as pitting folinic acid against a placebo, both researchers and participants were blind to 'who got what' during the 12 weeks of study. The aim was to compare a "target dose" of folinic acid "(2 mg kg−1 per day)" with said placebo formulation. It also appears that the authors went to some lengths to ensure that folinic acid and placebo capsules were "indistinguishable by sight and feel" as well as odour and taste.Participants (~7 years old) (N=48) were allocated to the folinic acid (n=23) or placebo group (n=25). All had a diagnosis of ASD and importantly, "Reconfirmation of the diagnosis using the lifetime version of the Autism Diagnostic Interview-Revised by an independent research reliable rater was requested from all participants." Participants were also required to have "documentation of language impairment" accompanying their autism as well as being free from current antipsychotic medication use alongside various other inclusion/exclusion criteria."Verbal communication was the primary outcome" we are told, offering a rather refreshing prospect insofar as the focus being on symptoms rather than syndromes. That's not to say that various behavioural schemes pertinent to the presentation of autism and other general 'adaptive behaviours' weren't also included, but this was a study looking specifically at what happened to verbal communication.Results: well, first and foremost folinic acid seemed to be pretty safe and well tolerated as we are told that "no serious adverse effects" were recorded for the folinic acid group when blinding was broken. First, do no harm and all that. As per the opening sentence of this post, there were some significant group improvements noted for the group taking folinic acid in relation to verbal communication ("an important core ASD symptom") compared with the placebo group.Going back to the whole 'positive for FRAAs' there were also some results to be seen. "This study suggests that FRAAs predict response to high-dose folinic acid treatment. This is consistent with the notion that children with ASD and FRAAs may represent a distinct subgroup." Without turning this post into some grand explanation of what FRAAs are (bearing in mind I'm barely getting my head around this myself), this ties into other findings (see here) and how these autoantibodies work to impair folate transport and 'block' or 'bind' to the folate receptor. One explanation is that folinic acid is able to 'bypass the FRα [folate receptor-α] when it is blocked and/or dysfunctional' particularly at higher doses. The use of the term "distinct subgroup" when it comes to autism is music to many ears in these days of the more plural 'autisms' and recognition that certain inborn errors of metabolism seem to be associated with 'some types' of autism [2] (more on this paper to come soon).Of course there is more to do in this area as the authors themselves identify the small participant numbers as one limitation and the future requirement to "determine the optimal folinic acid dose". Although no adverse effects were reported during the 12-week period, I'd also suggest that longer-term follow-up is needed to make sure that this effect extends a little longer too. Given the folate connection evident in this line of research, I'd for example, also be interested to see a little more work done on whether everyone's favourite scrabble gene - methylenetetrahydrofolate reductase (MTHFR) - potentially linked to some autism (see here) might also be an important player with regards to folinic acid use and response. Finally, minus any sweeping generalisations, the idea that FRAAs might also extend across labels to schizophrenia (see here) for example, is also potentially worthy of further investigation insofar as the 'links' that still remain when it comes to the autism and schizophrenia spectrums (see here) (remembering too the important work of Mildred Creak).Having said all that, these are important results as they stand. Not least because under rigorous methodological conditions, folinic acid has seemingly passed yet another scientific hurdle with regards to its potential relevance to at least some autism. We will no doubt see more on this topic in the peer-reviewed literature in times to come...----------[1] Frye RE. et al. Folinic acid improves verbal communication in children with autism and language impairment: a randomized double-blind placebo-controlled trial. Molecular Psychiatry. 2016. Oct 18.[2] Simons A. et al. Can psychiatric childhood disorders be due to inborn errors of metabolism? European Child & Adolescent Psychiatry. 2016. Sept 30.----------Frye, R., Slattery, J., Delhey, L., Furgerson, B., Strickland, T., Tippett, M., Sailey, A., Wynne, R., Rose, S., Melnyk, S., Jill James, S., Sequeira, J., & Quadros, E. (2016). Folinic acid improves verbal communication in children with autism and language impairment: a randomized double-blind placebo-controlled trial Molecular Psychiatry DOI: 10.1038/mp.... Read more »

  • October 19, 2016
  • 11:30 AM

A Windstorm is a Reminder of Disaster Preparation for Pets

by CAPB in Companion Animal Psychology Blog

The best time to start disaster preparation for your pet is now.Recently, like many people in this part of the world, we heard there was a big storm on the way. The third of three windstorms was said to be the most powerful. Since we live in an area with many beautiful trees and the power lines are above ground, it does not take much to knock out the power.In the end, we were lucky. The storm was not as strong as predicted, and it changed track and went further north. But it’s a reminder that we all need to be prepared for emergencies. And pets are an important part of our emergency preparedness.Planning starts with thinking about the kinds of emergencies you might face. Maybe you live in an area that is prone to floods or forest fires, or has the potential for big earthquakes. It’s helpful to think about smaller events too, that might impact you without affecting others: house fires, job losses, illnesses. These could all have an impact on your ability to care for your pet.You could come to arrangements with friends and family about how you will care for each other’s pets if something happens. It helps to talk about these things in advance.For me, with an incoming storm I wanted to be sure I had enough pet food and cat litter, and to charge up my cellphone. A bad storm last year knocked the power out for more than a day, and I can tell you that by day 2 the novelty was really wearing off. It was long enough that once the power came back, local stores had to stay closed to throw out ruined food. Also some roads were blocked with fallen trees, making travel more difficult for a short while. In this part of the world, the big risk we are meant to be prepared for is an earthquake. The official advice is to have enough supplies that you can manage on your own for at least 72 hours, preferably longer.That means food and water supplies for your pets as well as yourself, flashlights and spare batteries, and a radio so that you know what’s happening in the world. (A wind-up and/or solar-powered one that you can use to charge a cellphone seems like a good idea).Don’t forget to include some of your dog or cat’s favourite treats.A harness and leash would be handy so you don't run out of the house without them. A towel or blanket could be useful as a temporary bed for your dog or cat. Bowls for food and water, washing up liquid and some garbage bags would all be useful too.Having some cash in small notes is sensible in case of power being out at ATMs. This is a habit you can get into, or you can keep a small amount at home.What about copies of important documents, not just your own but also your pets’ vaccination records? Keep them in a plastic wallet or container that will keep them dry, and add them to your ‘grab bag’ that you will grab and take with you in an emergency.Identification for your pet is sometimes overlooked (tattoo, microchip, collar tag). As well as making sure your pet has id, ensure the people who keep the microchip/tattoo records have an up-to-date address and phone number for you.Helping your pet to be well-socialized and to be calm and well-behaved in ordinary life pays off in an emergency too. After the M9 earthquake in Fukushima, those who had trained and socialized their pets were more likely to be able to take them with them when they evacuated (Yamazaki 2015).Training your cat or dog to go in a carrier is useful in ordinary life, since it means you can take them to the vet. In an emergency, it’s easy to see that it might make the difference to being able to take them with you.Heath and Linnabary (2015) also say that having a good starting point for animals is part of emergency planning. While they are thinking about the broader societal level, we can apply this to our individual situations too. If your dog or cat is fearful or has other struggles in ordinary life, finding ways to solve those issues is worthwhile (if you need help from a certified trainer or behaviourist, this could be the moment to make that call).This post is not a guide to how to prepare for emergencies; rather it’s intended to encourage you to think about the kinds of events you might have to prepare for, and get started. It’s not a solo activity; discuss it with your family and friends. And you might be kind enough to also consider neighbours who are seniors or who might need a little help for other reasons.You can also put a regular date in your diary to review your plans and update your supplies (even bottled water has a sell-by date). Pick a date that you will remember, either because it’s meaningful to you or because it’s the date your city carries out earthquake drills (thus you will be reminded by the media). For me, that's tomorrow: ShakeOut BC is on 20th October.You can find more information about emergency planning for pets in this ASPCA guide.ReferencesHeath SE, & Linnabary RD (2015). Challenges of Managing Animals in Disasters in the U.S. Animals : an open access journal from MDPI, 5 (2), 173-92 PMID: 26479228Yamazaki, S. (2015). A Survey of Companion-Animal Owners Affected by the East Japan Great Earthquake in Iwate and Fukushima Prefectures, Japan Anthrozoös, 28 (2), 291-304 DOI: 10.1080/08927936.2015.11435403Photo: Josh Powell ( Read more »

  • October 19, 2016
  • 02:51 AM

Paracetamol for fever 'associated' with autism?

by Paul Whiteley in Questioning Answers

"In this study, we again show that acetaminophen use is associated with ASD [autism spectrum disorder]."That was one of the results reported by Stephen Schultz & Georgianna Gould [1] (open-access available here) as part of their survey of the US "National Database for Autism Research (NDAR) of the National Institute of Mental Health (NIMH)" looking at "whether ASD is associated with acetaminophen use." Acetaminophen by the way, is another name for paracetamol, the over-the-counter pain relief medication that is going through some turbulent times at the moment (see here for example).Shultz & Gould - one of whom has some research form in this area [2] - eventually relied on information for 118 children diagnosed with an ASD and 79 'non-ASD' children with an average age of about 11 years old. The sorts of data they looked at surrounded the parental choice of medication to treat fevers (I think) including whether paracetamol, ibuprofen or aspirin were used. I have to say that the authors could have made the methodology behind their analysis a little bit clearer in terms of how the questions were posed and to whom rather than just referring to another study with regards to participant selection for example. I had to go fishing for various details which is guaranteed to furrow my brow...Results: well, I'm slightly puzzled it has to be said. When it came to questions about paracetamol use (I use the term paracetamol 'cos that's what us Limeys are used to) between the ASD and non-ASD groups I didn't see too much difference overall. Take for example the questions about 'only using paracetamol' for fever or 'first choice' use for fever. The percentage figures for the ASD and non-ASD group were 15% and 12% respectively for 'only use this' and 35% and 46% respectively for 'first choice'. Given the participant numbers, I'm not sure that these stats are so wildly different. Yes, I appreciate that when it came to the question about 'rarely or never using' paracetamol to treat fever, 17% of those with ASD reported positive to this question compared with only 3% of controls, but does this really tell us much about very different patterns of paracetamol use?Further, the authors report results based on "age-adjusted models for levels of fever medication use". They observe that using "acetaminophen as a first choice was 83% less likely in children with ASD... while use of acetaminophen if other medication doesn’t bring down fever was 82% less likely in children with ASD." They interpret this to mean that compared with their previous results [2] findings were reversed in that "older children with ASD compared to control children were significantly less likely to use acetaminophen for fever; whereas, in our 2008 study, younger children with ASD compared to control children were significantly more likely to use acetaminophen at 12-18 months of age and after the MMR vaccination." The mention of immunisation in that last sentence was based on their 2008 paper suggesting that "acetaminophen use after measles-mumps-rubella vaccination was associated with autistic disorder" but I have to say that I'm left a little wanting in terms of these recent findings by Shultz & Gould.I do think there is a 'where next?' discussion to be had when it comes to the idea that paracetamol use might be linked to 'some' autism. Given the growing research interest in paracetamol use and a 'hyperactive phenotype' of autism (see here), this stalwart of pain relief is deserving of much further inspection in relation to autism. Shultz & Gould do offer one possible research direction based on some speculation about the how the endocannabinoid system might fit into this (something mentioned by other authors too). I am interested in the hypothetical situation they conclude their paper with implicating the endocannabinoid system and how paracetamol might affect 'endocannabinoid tone' but to what extent is perhaps another question.Just before I finish on this topic I'm minded to bring to your attention another detail from the Shultz / Gould paper with regards to the sentence: "children with ASD vs. non-ASD children are significantly more likely to show an increase in sociability when they have a fever." I've always thought the observations on behaviour and fever when it comes to [some] autism to be quite important (see here). Speculation that "this increase [in sociability] is due to anandamide activation of the endocannabinoid system in ASD children" is also ripe for further scientific investigation...It's been a while but here is some music to close: Mrs Robinson.----------[1] Schultz ST. & Gould GG. Acetaminophen Use for Fever in Children Associated with Autism Spectrum Disorder. Autism Open Access. 2016 Apr;6(2). pii: 170.[2] Schultz ST. et al. Acetaminophen (paracetamol) use, measles-mumps-rubella vaccination, and autistic disorder: the results of a parent survey. Autism. 2008 May;12(3):293-307.----------Schultz ST, & Gould GG (2016). Acetaminophen Use for Fever in Children Associated with Autism Spectrum Disorder. Autism-open access, 6 (2) PMID: 27695658... Read more »

  • October 18, 2016
  • 04:32 AM

Chronic fatigue syndrome and the detrimental application of the 'biopsychosocial model'

by Paul Whiteley in Questioning Answers

'The times they are a changin'' said a Nobel prize winner and that's also a sentiment that seems true when it comes to chronic fatigue syndrome / myalgic encephalomyeltis (CFS/ME) too (see here for example).Anyone who has followed the tos-and-fros of the PACE trial - the one that suggested that CBT (cognitive behavioural therapy) and GET (graded exercise therapy) might provide some significant relief of symptoms associated with CFS/ME - will probably have heard the quite open claims being made that "the study was bad science." Scientific dirty laundry continues to be aired in public as a result of the focus on the wrongs and rights of PACE and with it, precious money that might well have been used for CFS/ME science has instead seemingly been used in legal disputes.Outside of the methodological points potentially associated with the PACE trial/results, at the heart of the issue on whether CBT for example, might influence the progression of CFS/ME is the continued idea in some quarters that ME/CFS is part of a spectrum of conditions primarily centred in the domain of the biopsychosocial (BPS) model. Here, the suggestion is that a biological agent or agents act to trigger the condition but thereafter psychological and sociological factors play a major part in 'maintaining' the condition. For many people who suffer (yes, suffer) with ME/CFS the application of the BPS model to their symptoms has been likened to charges of malingering and subsequently many patients feel let down by medicine and indeed, that their symptoms have been trivialised.The paper by Keith Geraghty & Aneez Esmail [1] puts some scientific flesh on to the idea that continued use of the BPS model applied to CFS/ME might be detrimental to many patients and particularly their interactions with healthcare providers. Including reference to the quite extensive literature suggesting that all-manner of biological factors may be at work on the various experiences of CFS/ME (see here for example), the authors question "whether or not the BPS model generates ‘harms’ for CFS patients." The conclusion: yes, applying the logic of the BPS model during healthcare consultation is probably not doing much for quite a few patients with ME/CFS who are often in real distress and don't really want to be told it's 'all psychological' and treated as such.This is an important piece of work. Irrespective of your personal viewpoint of what ME/CFS is (and isn't) it tells us that healthcare interactions are important to people diagnosed with the condition and that "an over-emphasis on the 'psycho' (and only then with regard to alleged causation, rather than impact), at the expense of 'bio' and 'social' aspects of their impairments" has done little to either treat or manage or improve symptoms or quality of life for many people. It also tells us to respect the concept that CFS/ME is a heterogeneous condition and perhaps offer some viable alternatives to the BPS model. Not least is the idea that screening for conditions known to influence fatigue (see here) might be a good starting point and then taking things from there.I do however think it is important that we don't minimise the psychological effects that ME/CFS can have on a person. Sometimes being bed-bound with only limited contact with the 'outside world' trapped in a spiral of fatigue and rest, fatigue and rest is unlikely to do anyone any good. Indeed, when researchers talk about depression and other psychiatric features being potentially over-represented in cases of CFS/ME, I'm not surprised given how severe fatigue and other symptoms can sometimes be. A good physician should be screening for such accompanying issues and offering the appropriate treatment for them, mindful that these are not necessarily a core part of CFS/ME [2].I get the impression that the BPS model (in its current form [3]) is coming to the end of its reign when applied to a label like CFS/ME on the basis of more research resources being pumped into looking at the biology/biological course of the condition and less emphasis on the psychological 'treatment' of the condition (see here). This perhaps follows a more general trend where psychogenic explanations for physical illness are starting to receive some critical commentary [4] including critically looking at the idea that "psychogenic illnesses are believed to be more responsive to psychological interventions than comparable "organic" illnesses". This is of course, little consolation for those patients with ME/CFS who've had to face the BPS model even in light of contrary indication [5] and perhaps not had the best experience of it. Indeed, I wonder if there will come a point where a formal apology will be issued about the way science and medicine has treated many people with ME/CFS and the sometimes needless suffering that the BPS model in particular, has had on many aspects including the doctor-patient relationship.----------[1] Geraghty KJ. & Esmail A. Chronic fatigue syndrome: is the biopsychosocial model responsible for patient dissatisfaction and harm? Br J Gen Pract. 2016 Aug;66(649):437-8.[2] Taylor AK. et al. 'It's personal to me': A qualitative study of depression in young people with CFS/ME. Clin Child Psychol Psychiatry. 2016 Oct 14. pii: 1359104516672507.[3] Maes M. & Twisk FN. Chronic fatigue syndrome: Harvey and Wessely's (bio)psychosocial model versus a bio(psychosocial) model based on inflammatory and oxidative and nitrosative stress pathways. BMC Med. 2010 Jun 15;8:35.[4] Wilshire CE. & Ward T. Psychogenic Explanations of Physical Illness: Time to Examine the Evidence. Perspect Psychol Sci. 2016 Sep;11(5):606-631.[5] Twisk FN. & Maes M. A review on cognitive behavorial therapy (CBT) and graded exercise therapy (GET) in myalgic encephalomyelitis (ME) / chronic fatigue syndrome (CFS): CBT/GET is not only ineffective and not evidence-based, but also potentially harmful for many patients with ME/CFS. Neuro Endocrinol Lett. 2009;30(3):284-99.----------... Read more »

Geraghty KJ, & Esmail A. (2016) Chronic fatigue syndrome: is the biopsychosocial model responsible for patient dissatisfaction and harm?. The British journal of general practice : the journal of the Royal College of General Practitioners, 66(649), 437-8. PMID: 27481982  

  • October 17, 2016
  • 03:00 AM

Maternal obesity and offspring autism meta-analysed (again)

by Paul Whiteley in Questioning Answers

Meta-analyses eh? You spend ages waiting for one and two come along in quick succession. Well today I'm posting about yet another meta-analysis of the peer-reviewed scientific literature suggesting that "excessive maternal BMI [body mass index] is associated with an increased ASD [autism spectrum disorder] risk in offspring." [1]The review by Ying Wang et al follows hot on the heels of the meta-analysis by Li and colleagues [2] (see here for my take) but further looked at "the potential association of different category of BMI including overweight and underweight with ASD risk" among other things. BMI by the way, is a rough and ready way to quantify how much of a person there is according to height and weight. Whilst a useful statistic, it is not without its issues.After taking into account data from "6 cohort studies and 1 case-control study involving 8,403 cases and 509,167 participants" the authors unsurprisingly came to the same conclusion as Li and colleagues that a higher BMI seems to confer more [relative] risk for offspring autism as an outcome. Authors even included a nice graphic (see here) suggesting something of a dose-response relationship between the two variables (based on data from four of the studies included in their meta-analysis).What's more to say? Well, 'The maternal body as environment in autism science' returns into the frame and questions about possible mechanisms need to be asked/answered. No, such findings don't mean (a) every mum with a child with autism was overweight or obese before or during pregnancy or (b) every overweight or obese mum will have a child with autism: "Compared with children whose mothers were at normal weight, children born to overweight and obese mothers have a 28% and 36% higher risk of developing ASD, respectively." Such data does however open the door to the idea of foetal programming when it comes to potential offspring outcomes and how elevated BMI as possibly linking to facets of metabolic syndrome for example, might have some role to play for some (see here).More investigations are indicated.----------[1] Wang Y. et al. Maternal Body Mass Index and Risk of Autism Spectrum Disorders in Offspring: A Meta-analysis. Scientific Reports. 2016; 6: 34248.[2] Li YM. et al. Association Between Maternal Obesity and Autism Spectrum Disorder in Offspring: A Meta-analysis. J Autism Dev Disord. 2016 Jan;46(1):95-102.----------Wang, Y., Tang, S., Xu, S., Weng, S., & Liu, Z. (2016). Maternal Body Mass Index and Risk of Autism Spectrum Disorders in Offspring: A Meta-analysis Scientific Reports, 6 DOI: 10.1038/srep34248... Read more »

  • October 16, 2016
  • 08:58 PM

Call me: female zebra finches prefer their mate’s call

by Emily Makowski in Sextraordinary!

Social interactions are highly sought-after and rewarding in many animals... Even when social interactions involve only one of our senses, they are still rewarding. For example, we like looking at photos of our friends on Facebook, or hearing the voice of a faraway relative via telephone. It’s the same with other animals; not only is socialization rewarding and can be used as an incentive for learning, but just the sights, sounds, and even smells of others are also rewarding. Hernandez et al. explored this concept with female zebra finches, who were shown to prefer the calls of their mate.... Read more »

  • October 16, 2016
  • 02:18 PM

Female brains change in sync with hormones

by Dr. Jekyll in Lunatic Laboratories

Although it has already been known for some time that the brain does not remain rigid in its structure even in adulthood, scientists have recently made a surprising discovery. The brain is not only able to adapt to changing conditions in long-term processes, but it can do this every month.

... Read more »

Barth, C., Steele, C., Mueller, K., Rekkas, V., Arélin, K., Pampel, A., Burmann, I., Kratzsch, J., Villringer, A., & Sacher, J. (2016) In-vivo Dynamics of the Human Hippocampus across the Menstrual Cycle. Scientific Reports, 32833. DOI: 10.1038/srep32833  

  • October 16, 2016
  • 09:14 AM

Web of lies and the public

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

In the previous two posts I’ve gone through the depressing exercise of exploring the misconstrued world-view that led the UK to leave the EU. The picture that emerges is not limited to the UK, but is a paradigm example of…Read more ›... Read more »

  • October 15, 2016
  • 05:47 AM

Know your brain: Suprachiasmatic nucleus

by neurosci in Neuroscientifically Challenged

Where is the suprachiasmatic nucleus?

the suprachiasmatic nucleus is represented by a small green area within the hypothalamus (indicated by red arrow).

The suprachiasmatic nuclei are two small, paired nuclei that are found in the hypothalamus. Each suprachiasmatic nucleus only contains approximately 10,000 neurons. The nuclei rest on each side of the third ventricle, just above the optic chiasm. The location provides the rationale for the naming of the structure, as supra means above and chiasmatic refers to its proximity to the optic chiasm. What is the suprachiasmatic nucleus and what does it do?Circadian rhythms are biological patterns that closely follow a 24-hour cycle. The term circadian comes from the Latin for around (circa) and day (diem), and circadian rhythms govern a large number of biological processes including sleeping, eating, drinking, and hormone release. In the 1960s, researchers noticed that damage to the anterior hypothalamus of the rat caused a disruption in the animal's circadian rhythms. Several years later, the specific nucleus in the hypothalamus whose integrity was necessary for maintaining circadian rhythms was identified as the suprachiasmatic nucleus.We now know that the suprachiasmatic nucleus houses a type of biological clock that is able to keep our circadian rhythms on close to a 24-hour cycle, even without the help of external cues like daylight. Thus, if you were to lock someone in a room with no external light and no other way of telling the time, her body would still maintain a circadian rhythm of around 24 hours. The mechanism that regulates this biological clock was first elucidated in Drosophila, more commonly known as the fruit fly.In Drosophila, the timekeeping of the circadian clock appears to be controlled by a cycle of gene expression that has an ingenious negative feedback mechanism built into it. Cells in the suprachiasmatic nuclei of Drosophila produce two proteins called Clock and Cycle. Clock and Cycle bind together and act to promote the expression of two genes called period (per) and cryptochrome (cry). The protein products of these two genes, Per and Cry, then bind together and proceed to inhibit the actions of Clock and Cycle, an action which in turn suppresses the production of Per and Cry. Gradually, however, the Per and Cry proteins begin to break down. When Per and Cry degrade fully, Clock and Cycle are free to act again; they go back to promoting the expression of per and cry, starting the cycle anew. The process consistently takes around 24 hours to complete before it repeats. Thus, it is thought that this cycle of gene expression is what acts as the molecular clock in Drosophila suprachiasmatic nucleus cells.This understanding of the timekeeping mechanism in Drosophila laid the foundation for elucidating the process in mammals, where it is thought to be similar but more complex. The mammalian version of Cycle is called BMAL1 (which stands for brain and muscle ARNT-like 1). When CLOCK and BMAL1 bind together, they enhance the transcription of a family of genes that includes multiple period (Per1, Per2, and Per3) and cryptochrome (Cry1 and Cry2) genes. The resultant PER and CRY proteins form complexes along with other proteins to inhibit the activity of CLOCK and BMAL1 until the PER and CRY proteins degrade (as above). We know that this process of gene expression and inhibition acts to keep a 24-hour clock within the neurons of the suprachiasmatic nucleus, but less is known about how the timekeeping within these neurons leads to the regulation of rhythmic activity throughout the body. It is believed, however, that the molecular clocks found within the neurons of the suprachiasmatic nuclei regulate neural activity within the nuclei, which in turn coordinates the activity of multiple signaling pathways as well the stimulation of projections to neuroendocrine neurons in the hypothalamus involved with hormone release.Additionally, the suprachiasmatic nucleus helps to maintain circadian rhythms by coordinating the timing of billions of other circadian clocks found in cells throughout the rest of the brain and body. Not long after the discovery of the suprachiasmatic nucleus, it was also learned that similar types of molecular clocks exist in most other peripheral tissues and in many areas of the brain. These clocks, sometimes called slave oscillators (while the suprachiasmatic nucleus is considered the master oscillator) appear to depend on signals generated by the suprachiasmatic nucleus to synchronize their time-keeping with that of the suprachiasmatic nucleus. These signals can be associated with rhythms that the suprachiasmatic nucleus helps to establish, like feeding patterns, rest and activity behaviors, etc., or by direct neuronal or hormonal output from the suprachiasmatic nucleus.Although the suprachiasmatic nucleus is capable of maintaining circadian rhythms independently of any environmental signals (e.g. daylight), it does rely on cues from the environment to make adjustments to the circadian clock. For example, when you fly across multiple time zones, your body's circadian clock becomes significantly out of sync with the timing of the day (e.g. your body might be preparing for sleep when it is still light out). To make adjustments to the circadian clock in such instances, the suprachiasmatic nucleus relies on information it receives from the retina about light in the environment. Such information travels from the retina to the suprachiasmatic nucleus along a path called the retinohypothalamic tract. Additional inputs to the suprachiasmatic nucleus provide more information about light in the environment and other non-photic information about time of day to help to adjust the circadian clock.Due to the importance of our circadian rhythms to normal functioning, the integrity of the suprachiasmatic nucleus is essential to health. Disrupted function of the suprachiasmatic nucleus is being explored as a potential influence in a variety of psychiatric disorders as well as a factor in age-related decline in healthy sleep. Thus, although we have much more to learn about the suprachiasmatic nucleus, it is clear that it plays a very critical role in healthy brain and bodily function.Colwell, C. (2011). Linking neural activity and molecular oscillations in the SCN Nature Reviews Neuroscience, 12 (10), 553-569 DOI: 10.1038/nrn3086Dibner, C., Schibler, U., Albrecht, U. (2010). The mammalian circadian timing system: organization and coordination of central and peripheral clocks Annual review of physiology, 72 (1), 517-549.... Read more »

  • October 15, 2016
  • 04:50 AM

Atopic dermatitis and the "increased risk of developing ADHD and ASD later in life"

by Paul Whiteley in Questioning Answers

I'm not gonna dwell too much on the findings reported by Lee and colleagues [1] talking about how "toddlers who suffer from AD [atopic dermatitis] at the age younger than 3 years are at a higher risk of developing ADHD [attention-deficit hyperactivity disorder] and ASD [autism spectrum disorder] during later childhood" because science already seems to understand that there may be an important connection between early allergic disease and later offspring behavioural/developmental outcomes (see here for example).That the Lee data is derived once again from the 'big data' powerhouse that is Taiwan - specifically the National Health Insurance Research Database (NHIRD) - makes the findings that little bit more 'believable' given the numbers and processes involved in collecting said information."Children from the AD group with 3 comorbidities together, namely, allergic rhinitis, allergic conjunctivitis, and asthma, had the greatest risk of developing ADHD and ASD." Within statements like that it is getting progressively more difficult to downplay the impact that immune function (or immune response?) might have to quite a few people diagnosed as on the autism spectrum or with ADHD (or both). Further, that for some the 'treatment' of certain allergic symptoms might also impact on behaviour/development (see here and see here for examples) provides an important roadmap for further investigations in this area and the identification of who might be 'best responders' for such intervention (with no medical advice given or intended)."Pediatricians taking care of toddlers with AD should have knowledge of this increased risk of developing ADHD and ASD later in life, especially when children have certain comorbidities such as allergic rhinitis, allergic conjunctivitis, and asthma." Who would disagree, bearing in mind that the spectrum of potential correlates linked to early life allergy may be pretty wide?To close, some words of wisdom: "there is no good reason for self-conscious farters to avoid fibre."----------[1] Lee CY. et al. Longitudinal association between early atopic dermatitis and subsequent attention-deficit or autistic disorder: A population-based case-control study. Medicine (Baltimore). 2016 Sep;95(39):e5005.----------Lee CY, Chen MH, Jeng MJ, Hsu JW, Tsai SJ, Bai YM, Hung GY, Yen HJ, Chen TJ, & Su TP (2016). Longitudinal association between early atopic dermatitis and subsequent attention-deficit or autistic disorder: A population-based case-control study. Medicine, 95 (39) PMID: 27684861... Read more »

  • October 14, 2016
  • 02:58 AM

Yet more on potential biomarkers and chronic fatigue syndrome

by Paul Whiteley in Questioning Answers

'Thick and fast' is probably the best way that I can describe the flurry of peer-reviewed scientific papers recently appearing (see here and see here for examples) talking about how chronic fatigue syndrome (CFS) (also linked to the diagnosis of myalgic encephalomyelitis, ME) might have some important biological processes attached to it.Now we can add the findings reported by Federica Ciregia and colleagues [1] (open-access) to the list and their observations that "the identification of biomarkers present in particular subgroups of CFS patients may help in shedding light upon the complex entity of CFS."The Ciregia paper is open-access but well-worth a few inches of discussion on this blog. Not least because (a) the word 'mitochondria' is part and parcel of the their findings in line with other research in this area, (b) one of the gold standards of analytical chemistry - liquid chromatography mass spectrometry -  was used, and (c) some of the findings are based on a study of twins: "a patient suffering from CFS in comparison with his healthy monozygotic twin." This mirrors other similar published work from this authorship group [2].So, using a discovery/training and validation approach similar to other biomarker studies in other areas, researchers initially set out to "study the mitochondria extracted from platelets of the twins" using "nano-liquid chromatography electrospray ionization mass spectrometry (nano-LC-MS)." They were looking for evidence of different compounds being presented/expressed in those twins diagnosed with CFS compared with their non-affected twin and eventually came up with 41 proteins - "34 were upregulated in CFS and 7 were downregulated" (see here for the list of compounds).Using a process called Ingenuity Pathway Analysis (IPA) "to retrieve the known functions of each protein" authors were able to visualise where each compound 'fitted' in terms of specific biological functions. The top three included: "metabolism of isocitric acid..., metabolism of NADH... and metabolism of nucleic-acid component or derivative." Certainly NADH has some 'history' when it comes to CFS/ME (see here).Then came the validation side of the study where "the most promising biomarkers were validated by western blot [WB] analysis in a big cohort of patients, using whole saliva (WS)." Here some 45 patients diagnosed with CFS ("based on the classification criteria of Fukuda et al") were recruited alongside 45 not-CFS controls and spit samples from all were analysed for "aconitate hydratase (ACON), ATP synthase subunit beta (ATPB) and malate dehydrogenase (MDHM)." Two proteins, ACON and ATPB. were replicated or at least "consistent with the results from nano-LC-MS."Finally, researchers looked at whether presented clinical features as described in various questionnaires delivered to participants might play a role in the presentation of their biological results. They did see something (see here) - "For each marker, the values were actually higher in the group of patients who had clinical features similar to the ill twin" - but I would be minded to suggest that quite a bit more work is needed before anyone reads too much into this as the results stand.So, there you have it. A little bit more evidence to suggest that science is edging a little closer to potentially identifying some of the biology behind (or least associated with) at least some CFS (and ME). A little bit more peer-reviewed evidence moving the discussions away from 'psychosomatic' [3] to something a little more testable/analysable with CFS/ME in mind (I'll be coming to the paper by Geraghty & Esmail soon enough on this blog by the way). Independent replication is the next step, onwards to potentially "developing tailored treatments." That bearing in mind, we already have some emerging data in this area too (see here) (with no medical advice given or intended).And just in case you want yet more potential biomarker research for CFS, here's another paper that has just been published [4]. Thick and fast people, thick and fast.So, there is a new trailer for Rogue One (A Star Wars story)...----------[1] Ciregia F. et al. Bottom-up proteomics suggests an association between differential expression of mitochondrial proteins and chronic fatigue syndrome. Transl Psychiatry. 2016 Sep 27;6(9):e904.[2] Ciregia F. et al. A multidisciplinary approach to study a couple of monozygotic twins discordant for the chronic fatigue syndrome: a focus on potential salivary biomarkers. J Transl Med. 2013 Oct 2;11:243.[3] Geraghty KJ. & Esmail A. Chronic fatigue syndrome: is the biopsychosocial model responsible for patient dissatisfaction and harm? Br J General Practitioners. 2016. Aug 1.[4] Yamano E. et al. Index markers of chronic fatigue syndrome with dysfunction of TCA and urea cycles. Scientific Reports. 2016; 6: 34990.----------Ciregia F, Kollipara L, Giusti L, Zahedi RP, Giacomelli C, Mazzoni MR, Giannaccini G, Scarpellini P, Urbani A, Sickmann A, Lucacchini A, & Bazzichi L (2016). Bottom-up proteomics suggests an association between differential expression of mitochondrial proteins and chronic fatigue syndrome. Translational psychiatry, 6 (9) PMID: 27676445... Read more »

  • October 13, 2016
  • 11:37 AM

Social Priming - Does It Work After All?

by Neuroskeptic in Neuroskeptic_Discover

"Social priming" has been the punching-bag of psychology for the past few years.

The term "social priming" refers to the idea that subtle cues can exert large, unconscious influences on human behaviour. The classic example of a social priming effect was the "professor priming" study in which volunteers who completed a task in which they had to describe a typical professor, subsequently performed better on a general knowledge task. In other words, as the authors put it, "priming a stereotype o... Read more »

Payne BK, Brown-Iannuzzi JL, & Loersch C. (2016) Replicable effects of primes on human behavior. Journal of experimental psychology. General, 145(10), 1269-1279. PMID: 27690509  

  • October 13, 2016
  • 02:56 AM

ADHD and conduct disorder long-term

by Paul Whiteley in Questioning Answers

Today I'm once again blogging about peer-reviewed research suggesting that when it comes to the long-term effects of attention-deficit/hyperactivity disorder (ADHD) on a person, there is some pretty solid evidence that addressing symptoms early could "potentially avert a wide range of future adverse outcomes."The paper making such a conclusion is the one from Holly Erskine and colleagues [1] who conducted a systematic review and meta-analysis pertinent to this topic; also taking into account the potential effects of a diagnosis of conduct disorder (CD) in the long-term. Including nearly 100 studies "linking ADHD and CD with a range of health and psychosocial outcomes" authors were able to say with some degree of confidence that issues with academic achievement, risk of comorbid "mental and substance use disorders", employment prospect likelihood and risk of criminality (i.e. being arrested) were all seemingly linked to a diagnosis of ADHD. Similar findings were also reported for CD. I know this is kind of research is not exactly great PR for ADHD (or CD) but it is nonetheless important.Accepting that (i) sweeping generalisations about ADHD/CD do no-one any good and (ii) there may be multiple variables attached to the 'adverse' outcomes detailed outside of just diagnosis, there are some important points to be acted upon following the Erskine review. I might for example, advocate the position that academic achievement is a particularly important area when it comes to the symptoms of ADHD (see here) and moves to address the impact of ADHD on education should perhaps be a priority.Minus any medical and/or clinical advice being dished out on this blog (I don't do that), there are several intervention options that have been discussed in the collected science literature to think about. Medication is one possibility as per what is known about the effectiveness of something like methylphenidate on ADHD signs and symptoms (see here). Sleep training is something else that appears to be quite useful when it comes to [some] ADHD (see here) too and could probably tie into research looking at physical activity levels and ADHD (see here). And then we have the collected literature pointing to dietary elements as possibly showing some connection to some facets of ADHD as per the whole fatty acid story (see here) and even something potentially linked to milk allergy for at least some (see here). This nutrition research building on the almost forgotten studies on a few foods diet and ADHD (see here) for example, which seems to have ground to a shuddering halt in research strategy terms. The list is long and getting longer (immune system, nutritional supplements, etc) of where to look when it comes to potentially important intervention routes for something like ADHD. Discussions with physicians need to be had and further investment in research is needed.And perhaps one might also be inclined to take more note of the research suggesting that various 'somatic disease' might also be more likely when a diagnosis of ADHD is received [2] and how, for a start, preferential screening might be undertaken?----------[1] Erskine HE. et al. Long-Term Outcomes of Attention-Deficit/Hyperactivity Disorder and Conduct Disorder: A Systematic Review and Meta-Analysis. J Am Acad Child Adolesc Psychiatry. 2016 Oct;55(10):841-50.[2] Instanes JT. et al. Adult ADHD and Comorbid Somatic Disease: A Systematic Literature Review. J Atten Disord. 2016 Sep 22. pii: 1087054716669589.----------Erskine HE, Norman RE, Ferrari AJ, Chan GC, Copeland WE, Whiteford HA, & Scott JG (2016). Long-Term Outcomes of Attention-Deficit/Hyperactivity Disorder and Conduct Disorder: A Systematic Review and Meta-Analysis. Journal of the American Academy of Child and Adolescent Psychiatry, 55 (10), 841-50 PMID: 27663939... Read more »

Erskine HE, Norman RE, Ferrari AJ, Chan GC, Copeland WE, Whiteford HA, & Scott JG. (2016) Long-Term Outcomes of Attention-Deficit/Hyperactivity Disorder and Conduct Disorder: A Systematic Review and Meta-Analysis. Journal of the American Academy of Child and Adolescent Psychiatry, 55(10), 841-50. PMID: 27663939  

  • October 12, 2016
  • 08:30 AM

Training is Purrfect Enrichment for Frustrated Shelter Cats

by CAPB in Companion Animal Psychology Blog

A new study finds that training shelter cats leads to more contentment and better health.The study, by Nadine Gourkow and Clive Phillips (University of Queensland), tested the effects of training sessions on cats that were frustrated when they arrived at an animal shelter. The cats in the training group became more content and were healthier compared to the cats who just experienced normal shelter conditions.Prof. Clive Phillips says,“Confining a cat into a small cage after it has been roaming free, in someone’s home or as a stray, is a huge challenge for any cat. A significant proportion of them develop serious behaviour problems and one of these is extreme frustration, manifested by trying to escape or turning their cage contents upside down. “We can help these cats adapt by training them to do a task, taking time with them and encouraging them to have trust in human contact. Then they will be happier, healthier and more likely to get adopted.”The study took place at the Vancouver branch of the BCSPCA. Cats were assessed within an hour of arriving at the shelter. Out of 250 cats that were assessed, 15 were deemed frustrated and were eligible to take part in this study.Signs that the cats were frustrated include pacing, meowing, tipping out the contents of food bowls and litter trays, and trying to escape the cage by biting the bars or putting their paw through. Cats were defined as frustrated if these signs were apparent more than 10% of the time.8 cats were assigned to the control condition and experienced normal shelter life for the next ten days. 7 cats were put in the training condition. Four times a day, they had an individual 10-minute reward-based training session with the experimenter.The training took place in a room next door to the room with the cat cages. Initially the cats were carried there, but most soon learned to walk to the room with the experimenter once she let them out of their cage.The cats were given two minutes to explore the room, then the clicker training session started. The aim of the training plan was to teach them to do a hi-five.The cats were first conditioned to the clicker and then shaped to do a hi-five. Once they had learned the behaviour they were taught to do it on cue (“Give me five”).  Whiskas Temptations cat treats in tuna flavour were used as the reward.Throughout the study, stool samples were collected from cats in both the training and control groups. Video cameras were also mounted in the cat cages so that behaviour could be monitored, and evaluations were made for 10 minutes every hour. The researcher also noted whether the experimental cats were friendly or not at the end of each training session.The behavioural results showed that cats in the training group were more likely to be content than those in the control group, who remained frustrated for longer. Signs of contentment included normal grooming, lying on their side in a relaxed posture, rubbing the head or body on things in the cage, and sitting calmly at the front of the cage.Over time, the control group of cats became apathetic, typically after 6 days of trying to escape. They did not eat as much or groom themselves properly, and spent a lot of time sleeping.The stool samples showed that cats in the training group had higher levels of Immunoglobulin A, which can protect against upper respiratory infections. In line with this, the control group was significantly more like to get an upper respiratory infection during the time of the study.The training activity involved several aspects that may have been beneficial to the cat – time out from the cage and time spent with a human as well as the training itself. It could be any of these, or the combination, that caused these results.The sample is small, but it represents all of the frustrated cats that were available at the shelter at that time. Further research with a larger sample is needed. The authors point out that cats may also become frustrated after being at a shelter for a while, so potentially many more cats could benefit.These results are promising and suggest that training is good for frustrated cats. Shelters could incorporate this kind of enrichment into their regular practice. Cat training might be an attractive program for volunteers.Would you like to try training a cat?ReferenceGourkow, N., & Phillips, C. (2016). Effect of cognitive enrichment on behavior, mucosal immunity and upper respiratory disease of shelter cats rated as frustrated on arrival Preventive Veterinary Medicine, 131, 103-110 DOI: 10.1016/j.prevetmed.2016.07.012Photo: Esin Deniz ( cat stories:Interview with Dr. Sarah Ellis on The Trainable CatYour cat would like food puzzle toysEnrichment tips for cats (that many people miss)... Read more »

  • October 12, 2016
  • 03:02 AM

Obesity in adolescent chronic fatigue syndrome (CFS)

by Paul Whiteley in Questioning Answers

"At 13 years, adolescents who had received a diagnosis of chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) who were attending specialist CFS/ME services were more than two times more likely to be obese than adolescents in the general population."At first reading, I wasn't particularly surprised by the findings reported by Norris and colleagues [1] (open-access) drawing on data partly derived from everyone's favourite UK longitudinal birth cohort: ALSPAC (Avon Longitudinal Study of Parents and Children). If one assumes that those suffering (yes, people do suffer from CFS/ME) might not be engaging in an optimal exercise regime nor eating the best of diets one can perhaps see how the condition might be a susceptibility factor for issues with weight. That being said, and after some further thought, the Norris findings might not be something entirely representative of the effects of CFS/ME either given documented cases of malnutrition and sadly, death (see here). Sweeping generalisations are, yet again, not required.So, the Norris group findings... well, some of the authors are not completely unknown to the idea that eating habits might be perturbed in cases of CFS/ME as per other entries on this blog (see here). This time around ALSPAC data was joined by "data collected from all National Health Service (NHS) paediatric specialist services that participated in the CFS/ME National Outcomes Database (NOD) between August 2004 and October 2014." The aim was to "obtain prevalence estimates for obesity at two time points during adolescence (ages 13 years and 16 years), in three groups of adolescents representing a continuum of CFS/ME severity (healthy population, CFS/ME based on responses to questionnaires and clinically diagnosed CFS/ME)." In case your a little confused, the CFS/ME by questionnaire response group were derived from ALSPAC. The categorisation of obesity or not was made by clinical height and weight measurements from the ALSPAC data but was a little less 'formalised' for the more detailed diagnosis CFS/ME group (in clinic) including measurement "in the clinic or GP surgery or obtained from parental report." Body mass index (BMI) was calculated from said measurements.Results: well, aside from that opening sentence on 13 year olds, the authors also reported that for those with CFS/ME: "At 16 years, they were more than 4 times more likely to be obese compared to those in the general population." The authors noted that the association between CFS/ME and obesity was 'driven' in the most part by "those attending the specialist services, thus representing those with CFS/ME severe enough to be referred for specialist treatment.""Health professionals should be aware of this association to encourage appropriate screening for obesity and its possible complications when assessing patients with CFS/ME." I agree with the authors conclusions stemming from their findings but I think a word of caution also needs to be applied too.For those who've followed the CFS/ME research scene for the past few years, you'll probably already have heard about the PACE trial and the 'suggestion' among other things that graded exercise therapy (GET) might be something to consider "to gradually increase how long you can carry out a physical activity." PACE has stumbled in recent times following a long and drawn out (and expensive) 'battle' to access the data behind the headlines; having already seen a 'downgrading' of effect from some agencies. Now, think to yourself what would be a health professional's response to being presented by a patient who is obese? Change your diet? Maybe do a little more exercise? Hmm...I'm not saying that young people with CFS/ME who present with weight issues shouldn't be provided with the same appropriate medical advice and care as everyone else with such issues. I'm not saying that every health professional would be prescribing pounding the treadmill or anything related given the quite unique issues associated with CFS/ME. I do however think that set within the research history created partly as a result of initiatives such as the PACE trial, there are sensitivities that need to be observed before sweeping healthcare advice is provided en-masse. That also 'not out-running' a bad diet is gaining some traction is an important point to make as other areas of research could yet be explored bearing in mind how exercise might impact on the gut microbiome of some CFS/ME (see here) for example. That might also includes the gut virome [2] too...----------[1] Norris T. et al. Obesity in adolescents with chronic fatigue syndrome: an observational study. Arch Dis Child. 2016 Sep 21. pii: archdischild-2016-311293.[2] Giloteaux L. et al. A Pair of Identical Twins Discordant for Myalgic Encephalomyelitis/Chronic Fatigue Syndrome Differ in Physiological Parameters and Gut Microbiome Composition. Am J Case Rep. 2016 Oct 10;17:720-729.----------Norris T, Hawton K, Hamilton-Shield J, & Crawley E (2016). Obesity in adolescents with chronic fatigue syndrome: an observational study. Archives of disease in childhood PMID: 27655658... Read more »

Norris T, Hawton K, Hamilton-Shield J, & Crawley E. (2016) Obesity in adolescents with chronic fatigue syndrome: an observational study. Archives of disease in childhood. PMID: 27655658  

  • October 11, 2016
  • 03:01 AM

Taekwondo training and balance in autism

by Paul Whiteley in Questioning Answers

"TKD [Taekwondo] training can help children with ASD [autism spectrum disorder] improve their balance."Go on."Our findings suggest that TKD can be a fun, feasible, and effective therapeutic option for balance improvement of children with ASD."So said the results of the study by Yumi Kim [1] (open-access) looking at whether the Korean martial art might be able to help with aspects of some of the very important movement issues that can be associated with a diagnosis of autism.Based on quite a small participant group (N=14) where 8 children diagnosed with an ASD "completed the TKD intervention twice per week for eight weeks (50 min per session)" and 6 served as a 'no intervention' control group, researchers looked at various measures of balance using the "NeuroCom Balance Master."Again keeping in mind the small participant groups, there did appear to be some short-term benefit on aspects of balance following the use of TKD training. Specifically: "Following the TKD intervention, children with ASD showed balance improvement during right single leg stance under eyes closed condition compared to those who did not participate in the intervention." Also: "Children with ASD in the TKD group also improved their balance during left single leg stance under eyes open condition compared to their baseline performance" bearing in mind that there were some changes to balance variables for the control group too (albeit not significant). Insofar as what happened to autistic traits/symptoms as a consequence of the intervention (or not), well the words "we did not have any clinical measures of symptom severity of ASD" tell you all you need to know.Regular readers to this blog might have already know that I am a bit of a fan of how participation in the martial arts might be something suited to at least some people on the autism spectrum (see here for example). Several components of the martial arts might be useful outside of just 'knowing how to handle yourself' including: (a) the focus on repetition and routine (certainly in karate there is a lot of this with respect to kata and kumite) all bound to 'specific rules', (b) the combination of aerobic and anaerobic exercise being pretty good for keeping physically and mentally active (important for some autism or at least some comorbidities) and (c) the 'motor' advantages of the martial arts; something that is being talked about a lot more these days with autism in mind. As a sport or pastime, the martial arts have some significant draws for many groups of people.There is more research to do in this area not least to work on improving the research methodologies of studies on the use of martial arts when it comes to autism. So say for example, rather than just having a 'treatment as usual' arm, how about pitting some of the martial arts against each other (for science of course) or even comparing them with some of the 'softer edges' of the arts (see here) to provide some more detailed information. As per some of the various studies looking at karate training and autism, I'd also be minded to say that monitoring the presentation of autism (or comorbidities) over the course of training might be a good thing too as is some further inspection on whether particular movement diagnoses potentially accompanying autism might also be important [2]. There is lots more to see and do in this area.To close, some karate kata set to music and a question: how many kata can you name? I'll start you off.. Enpi.----------[1] Kim Y. et al. Effects of Taekwondo intervention on balance in children with autism spectrum disorder. J Exerc Rehabil. 2016 Aug 31;12(4):314-9.[2] McAuliffe D. et al. Dyspraxia in ASD: Impaired coordination of movement elements. Autism Res. 2016 Sep 21.----------Kim Y, Todd T, Fujii T, Lim JC, Vrongistinos K, & Jung T (2016). Effects of Taekwondo intervention on balance in children with autism spectrum disorder. Journal of exercise rehabilitation, 12 (4), 314-9 PMID: 27656628... Read more »

Kim Y, Todd T, Fujii T, Lim JC, Vrongistinos K, & Jung T. (2016) Effects of Taekwondo intervention on balance in children with autism spectrum disorder. Journal of exercise rehabilitation, 12(4), 314-9. PMID: 27656628  

  • October 10, 2016
  • 04:39 AM

"Learning difficulties linked with winter conception"

by Paul Whiteley in Questioning Answers

Having recently mentioned the BBC headline that makes up the title of this entry in a related post (see here) I'm pleased to be finally able to bring the paper by Daniel Mackay and colleagues [1] (open-access) to your attention.Observing that in Scotland at least, "that season of conception is strikingly associated with the subsequent risk of special educational needs in the offspring" there are various potential implications to come from such data covering both learning (intellectual) disability and also the autism spectrum.So, take over 800,000 school children who attended a school in Scotland between 2006 and 2011 and whose data could be linked to maternity records (again, held in Scotland). Examine date of conception as per the formula "date of delivery minus gestational age at delivery plus 2 weeks" and plot "monthly incidence rates of children with special educational needs... by month of conception." Include "special educational needs attributed to intellectual disabilities, dyslexia, other specific learning difficulties, visual impairment, hearing impairment, deafness and blindness individually combined, physical or motor impairments, language or speech disorder, ASD [autism spectrum disorder], and social, emotional, and behavioral difficulties" for a more detailed breakdown of how month of conception might be linked to said labels.Results: well, I've already mentioned about the 'striking association' that was made between season of conception for starters. The trends across various labels covered under special educational needs (SEN) were remarkably consistent where conception in quarter 1 (January–March) seemed to show a peak in terms of incidence compared with those conceived in quarter 3 (July–September). Even when researchers re-ran the data taking into account only children who were born at 40 weeks gestation (n=246,594), they got pretty much the same results coming back; "suggestive of an environmental exposure that occurs at a critical developmental stage before labor and delivery rather than secondary to seasonal variation in the gestational age at delivery."So what might account for the possible link between winter conception and the presence of various labels headed under SEN? Well, it's not beyond the realms of possibility that winter, the season of coughs, colds and sneezes might imply some infective agent as potentially exerting an effect. There is a pretty sizeable volume of peer-reviewed literature suggesting that something like maternal influenza might influence offspring behaviour and development [2]. This line of research is all the more convincing given the continued drive to look at the [reprogrammed] maternal immune system during pregnancy and what effects infection might have on it. The maternal pregnancy body as 'environment' eh?The authors also discuss another potentially equally important factor as also being something to look at: vitamin D. So: "In our study, the incidence of special educational needs peaked among children conceived in February whose mothers would have experienced low levels of ultraviolet B radiation and therefore produced low levels of vitamin D in early pregnancy and experienced higher levels in late pregnancy." Regular readers are probably pretty sick and tired of me going on (and on) about how vitamin D is potentially linked to so much more that just bone health. I was really happy to see that UK Government policy is starting to change when it comes to the 'sunshine' vitamin/hormone (see here) as it's importance is at last being recognised. Bearing in mind that because of their location, the people of Scotland are not exactly blessed with loads of solar radiation conducive to the synthesis of lots of year-round vitamin D, one can see how this stuff might be an important feature of the relationship observed by Mackay et al. But, as per recent headlines, one needs to be a little cautious when it comes to ideas about supplementation...More research is however implied given that there could be other important factors potentially also at work, although I'd be minded to suggest we already have two important variables with infection and vitamin D.To close, the UK Office of National Statistics (ONS) has some interesting data on how popular your birthday might be. Mine is rather less popular...----------[1] Mackay DF. et al. Month of Conception and Learning Disabilities: A Record-Linkage Study of 801,592 Children. Am J Epidemiol. 2016 Sep 20.[2] Cai L. et al. Gestational Influenza Increases the Risk of Psychosis in Adults. Med Chem. 2015;11(7):676-82.----------Mackay DF, Smith GC, Cooper SA, Wood R, King A, Clark DN, & Pell JP (2016). Month of Conception and Learning Disabilities: A Record-Linkage Study of 801,592 Children. American journal of epidemiology PMID: 27651381... Read more »

  • October 10, 2016
  • 04:30 AM

Therapist-Directed Cognitive Rehabilitation Improved Functional Cognitive Outcomes

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

Four treatment strategies for chronic symptoms after a mild traumatic brain injury (mTBI) improved symptoms; however, those with therapist-directed cognitive rehabilitation demonstrated superior improvements in functional cognitive scores compared with standard of care and computer-based rehabilitation.... Read more »

  • October 8, 2016
  • 02:31 PM

Concentrating on the social billions

by Dr. Jekyll in Lunatic Laboratories

Using online social media does not lead to long-term problems with our ability to concentrate, according to new research. We are social animals, so it is really no surprise that billions of us now use online tools to communicate, educate and inform each other. The advent of social media and social networking has nevertheless been phenomenally rapid.

... Read more »

Doss, S., Carstens, D., & Kies, S. (2016) Episodic social media impact on users. International Journal of Social Media and Interactive Learning Environments, 4(3), 273. DOI: 10.1504/IJSMILE.2016.079505  

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