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  • November 11, 2014
  • 11:54 AM
  • 106 views

Recovering from an Eating Disorder in a Society that Loves Fat Shaming (and Dieting)

by Tetyana in Science of Eating Disorders

Is ED recovery easier when your body is “normative or stereotypically desirable”? The anon asking the question implied that recovery could be more difficult because “an obese person … will never stop hearing hearing extremely triggering stuff about their body type.” Anon asked, “Have there been any studies on this?” Andrea tackled this question in her last post (it might be helpful to read it first if you haven’t yet); in this post, I will expand on my original answer.

Assuming anon meant, “Have there been anything studies assessing whether recovery is harder for individuals who do not fit the normative body type (because of fat phobia/fat shaming/diet culture)?” Then, my answer is: Not really, or at least I couldn’t find anything evaluating this question directly.... Read more »

Bulik, C.M., Marcus, M.D., Zerwas, S., Levine, M.D., & La Via, M. (2012) The changing "weightscape" of bulimia nervosa. The American Journal of Psychiatry, 169(10), 1031-6. PMID: 23032383  

McKisack, C., & Waller, G. (1997) Factors influencing the of group psychotherapy for bulimia nervosa. The International Journal of Eating Disorders, 22(1), 1-13. PMID: 9140730  

  • November 11, 2014
  • 11:13 AM
  • 123 views

Anorexia Nervosa: Brain Connectivity Abnormalities

by William Yates, M.D. in Brain Posts

Functional magnetic resonance imaging is providing a new tool for understanding brain circuitry in normal brain development and in brain disorders. Anorexia nervosa is an restrictive calorie eating disorder often resistant to treatment.No effective drug treatment for anorexia nervosa currently exists and psychotherapy is often only partially effective. A better understanding of the brain pathophysiology in anorexia nervosa is needed to aid in treatment development.Stephanie Kullman along with colleagues at the University of Tubingen recently published a study of brain connectivity in twelve women with anorexia nervosa.This study used a resting state functional connectivity approach with magnetic resonance imaging. In functional connectivity studies, the brain is studied during rest and levels of coherent activity between brain regions measured. The authors of this study noted anorexia nervosa commonly includes motor hyperactivity and so they used both a non-athlete and athlete female control group for comparision.The primary findings from this study included the following:The brain inferior frontal gyrus (IFG) in both the left and right sides demonstrated reduced effective connectivity Decreased effective connectivity was noted between the right IFG and the cingulateIncreased effective connectivity was noted between the right IFG and the bilateral orbitofrontal gyrus regionIncreased effective connectivity was noted between the left IFG and the bilateral insular cortexThe authors note the inferior frontal cortex is a key region for executive functions, or control of complex cognitive functions. Disturbance of executive function in anorexia nervosa may contribute to food consumption and activity decision making.The authors note their study found a link between level of physical hyperactivity in individual patients with anorexia nervosa and reduced IFG connectivity. Women with the highest level of physical activity had the lowest levels of IFG connectivity.The areas of increased connectivity in this sample of patients with anorexia contribute to processing of the salience of stimuli. The authors note the insular cortex is a "multisensory neural node" involved in integration of "perception, emotion, interoceptive awareness, cognition and gustation". Disturbance of connectivity balance between the IFG and insular cortex may contribute to anxiety and fear related to somatic sensations.The findings in this imaging study occurred in the context of active illness in anorexia nervosa. It would be interesting to follow these findings with recovery and weight restoration.Additionally, modification of functional connectivity disturbances in anorexia may hold promise for new drug development and more effective psychological interventions.Readers with more interest in this study can access the free full-text manuscript by clicking on the citation link below.Image of brain with highlighted inferior frontal gyrus is from a screen shot from the Brain Tutor app for the iPad from the author's files.Follow the author on Twitter @WRY999Kullmann S, Giel KE, Teufel M, Thiel A, Zipfel S, & Preissl H (2014). Aberrant network integrity of the inferior frontal cortex in women with anorexia nervosa. NeuroImage. Clinical, 4, 615-22 PMID: 24936412... Read more »

  • November 11, 2014
  • 04:50 AM
  • 357 views

Psychiatric comorbidity in post H1N1 vaccination narcolespy?

by Paul Whiteley in Questioning Answers

I can imagine that the paper by Atilla Szakács and colleagues [1] is likely to draw some rather differing opinions about potential importance based on their subject matter and methods/participant numbers looking at the frequency of psychiatric comorbidity among those with narcolepsy including narcolepsy post H1N1 vaccination. The fact that autism - "pervasive developmental disorder not otherwise specified (i.e., atypical autism)" - is mentioned as one of the comorbidity in the post-vaccination narcolepsy group, albeit only present in some 3% of the 31 participants (one person by my reckoning), potentially moves us into some contentious territory.I can't go back to yesterday because I was a different person then.That being said, the finding that nearly half of the post-vaccination narcolepsy cases presented with some kind of psychiatric comorbidity and the lion's share of that comorbidity was represented by a diagnosis of attention-deficit hyperactivity disorder (ADHD) (~30%) is perhaps the bigger headline from this study. Or is it?OK, it might be worthwhile taking this one step at a time. The report by the European Centre for Disease Prevention and Control (ECDC) [2] provides a good overview on the correlation between the use of the Pandemrix influenza vaccine and risk of narcolepsy in children and adolescents based on European data. The paper by Miller and colleagues [3] put a UK perspective on this, concluding that: "The increased risk of narcolepsy after vaccination with ASO3 adjuvanted pandemic A/H1N1 2009 vaccine indicates a causal association, consistent with findings from Finland". These findings and others suggested that there may be quite a bit more to see when it came to any relationship and, as a result, the door was opened to possible compensation as a vaccine-damage case (see the BBC report on this here). But, and it is an important point, other studies in other parts of the world have not reported a similar connection [4] and indeed, whether influenza infection (including 2009 H1N1 infection) itself could have been a risk factor for narcolepsy [5] has been discussed in the peer-reviewed literature.The hows and whys of any relationship between the H1N1 influenza vaccine and [some] narcolepsy are still under discussion. The hypocretins have been the source of quite a bit of speculation [6] although the research road linking processes related to these compounds and the possible effects of vaccination has not run so smoothly (see here). Autoimmunity, or rather some of the genetics of autoimmunity, has also been highlighted as being a potentially revealing mechanism of involvement [7] perhaps shadowing some recent work in an unrelated area (see here). Indeed, another publication from Szakács and colleagues [8] hinted as much: "All patients in the postvaccination group were positive for human leukocyte antigen (HLA)-DQB1*0602".Insofar as narcolepsy not related to vaccine administration, there is already a body of work to suggest quite a few comorbidities might already be elevated in risk following a diagnosis. The paper by Ohayon [9] detailed various somatic and psychiatric/behavioural issues to be over-represented alongside a diagnosis of narcolepsy. Of particular note to the psychiatric side of things were reports that: "major depressive disorder (MDD)... and social anxiety disorder" affected around 20% of people with the diagnosis. Both these conditions were noted in the Szakács study. Modestino & Winchester [10], based on the use of "a retrospective self-report questionnaire indicating the presence of childhood ADHD symptomatology in adults" suggested that "childhood ADHD symptomatology history among adult narcoleptics is common". Ideas about mis-diagnosis of ADHD covering for a condition like narcolepsy have also been suggested elsewhere (see here).I will reiterate that the Szakács study only looked at 38 children and adolescents, and 31 of those participants fitted that post-vaccination narcolepsy criteria. This is a very small study where even the authors highlight that this means little can be conclusively taken from their findings. Insofar as that autism - atypical autism - finding, it is not beyond the realms of statistical possibility that such detection of a single case is entirely a fluke finding or indeed, something that might be expected given the increasing prevalence rate/estimates (see here). Indeed, I'll draw your attention to an earlier report on this matter [11].The ADHD findings ("29% had attention deficit hyperactivity disorder (ADHD) inattentive type") are a little more difficult to explain away taking account of my previous chatter on the sample size of the Szakács paper. I've talked before on this blog about the paediatric ADHD prevalence figures/estimates (see here) and their hovering between 5-8% in the general population based on the collected work so far published in this area. Diagnoses like autism do seem to carry a greater risk of ADHD (see here) but given that only one case of autism was detected in the Szakács sample, I don't think we can say that this factor accounts for the results reported.I draw back from suggesting that ADHD (in any or all its forms) is definitely related to narcolepsy post 2009 H1N1 vaccination or indeed natural infection on the strength of the current data and small (unevenly distributed) participant groups. What however the Szakács findings do perhaps impress, is the need for greater scrutiny of this possible variable; if anything else, to potentially highlight any possible mechanisms of response and possibly offer some further insights into the underlying genetics and biochemistry of [at least some] ADHD.I close with the official (UK) advice on flu vaccination (see here).Music: Wild Honey by Hugh Laurie (House).----------[1] Szakács A. et al. Psychiatric Comorbidity and Cognitive Profile in Children With Narcolepsy With or Without Association to the H1N1 Influenza Vaccination. Sleep. 2014 Oct 17. pii: sp-00241-14.[2] European Centre for Disease Prevention and Control. Narcolepsy in association with pandemicinfluenza vaccination (a multi-country European epidemiological investigation) Stockholm: ECDC; September 2012.[3] Miller E. et a... Read more »

  • November 10, 2014
  • 04:51 PM
  • 132 views

Intestinal Parasites: Friends, Foes and Shades of Gray

by Aurametrix team in Irritable Bowel Blog

Parasite is a bad word with negative connotations. Yet, "bad things" can be good for you - and every situation is different. About one third of people in the world carry at least one parasite in their gastrointestinal tract, and the relationship between health and intestinal parasites is not as straightforward as one might think.... Read more »

  • November 10, 2014
  • 03:57 PM
  • 122 views

A new way to look at Global Warming

by Gabriel in Lunatic Laboratories

Global warming, nothing new with that and it’s here to stay for now. But while computer models churn out bleak forecasts for the planet’s future, we also have a more conceptual understanding of what is happening as humans pump carbon dioxide into the air. Unfortunately the traditional conceptual understanding of carbon dioxide wrapping the planet in a sort of blanket that traps more heat is not quite right.... Read more »

  • November 10, 2014
  • 10:05 AM
  • 117 views

Eating Disorders Linked to Higher Autoimmune Disease Rates

by William Yates, M.D. in Brain Posts

There is increasing evidence for inflammation contributing to risk for a variety of psychiatric disorders.I previously summarized research supporting use of anti-inflammatory drugs in the treatment of depression.A recent study from Finland supports an inflammation link to the eating disorder categories.The key elements of the design of this study included:Subjects: 2342 subjects admitted for treatment in the Eating Disorders Unit at the central hospital in Finland. Four controls were identified for each case matched by age, gender and place of residenceIdentification of presence for autoimmune diseases: Cases and controls were examined for the presence of one of 30 autoimmune diagnoses in their Hospital Discharge RegisterStatistical analysis: Period and lifetime rates for autoimmune disorders were compared between eating disorder cases and control using logistic regression modeling with calculation of odds ratios and 95% confidence intervals. Here are the important findings from the study:Eating disorders subjects had a 5.6% rate for presence of any autoimmune disease compared to only 2.8% of controls (Odds ratio 2.13, 95% confidence interval 1.71-2.65)Rates for autoimmune disorders were increased across all eating disorder diagnostic categories including anorexia nervosa, bulimia nervosa and binge eating disorderWithin autoimmune disease subtypes, endocrinological and gastroenterological diseases were statistically increased in eating disordersType I diabetes and Crohn's disease were individual autoimmune disorders found at higher rates in eating disorders The authors note there are several methods that could explain the association between autoimmunity and eating disorder risk. Higher rates of autoantibodies against peptides that control appetite and stress response could contribute to eating disorder risk.Additionally, the authors note disturbed eating may contribute to disturbance of the microbiome of the gut. Gut microbiome is a known regulator of autoimmunity and a contributor to allergies and type I diabetes risk.The authors noted additional specific autoimmune disorders may be increased in eating disorders but due to small sample size their study may have not found a statistical association.Systemic lupus erythematosis rates were increased in the eating disorder group but this was one of the individual disorders that failed to reach statistical significance.The take home message for clinicians treating eating disorder patients is to be vigilant for the presence of autoimmune medical disorders in this population. Accurate and early detection of autoimmune disorders in those with eating disorders may contribute to improved medical outcomes.Readers with more interest can access the free full text manuscript by clicking on the PMID link below.Photo of street scene in Dingle, Ireland is from the author's files.Follow the author on Twitter @WRY999Raevuori A, Haukka J, Vaarala O, Suvisaari JM, Gissler M, Grainger M, Linna MS, & Suokas JT (2014). The increased risk for autoimmune diseases in patients with eating disorders. PloS one, 9 (8) PMID: 25147950... Read more »

Raevuori A, Haukka J, Vaarala O, Suvisaari JM, Gissler M, Grainger M, Linna MS, & Suokas JT. (2014) The increased risk for autoimmune diseases in patients with eating disorders. PloS one, 9(8). PMID: 25147950  

  • November 10, 2014
  • 03:01 AM
  • 112 views

Metabolomics and autism: the continuing search for biomarkers

by Paul Whiteley in Questioning Answers

I'm always a happy bunny when some of my own research findings receive something like independent replication. So it was when I read the monster paper from Paul West and colleagues [1] (open-access) reporting results based on not one, not two, not three, not even four, but five mass spectrometric methods looking for potential biomarkers for autism. Metabolomics in action (see here for an introduction to this topic).Rosina @ Wikipedia The particular reason for my excitement was the quote: "Creatinine was decreased in children with ASD [autism spectrum disorder] and is consistent with the findings of Whitely et al, who observed similar changes in urinary creatinine in children diagnosed with PDD [pervasive developmental disorder]" based on the results of our paper a few years back [2] (see here for further details of how I spend my spare time talking about urine). The caveat being that we (the Royal We) looked in urine and West et al looked at blood (plasma). I can also forgive the authors for spelling my name wrong too... WHITELEY.The West paper is open-access but I'm gonna give you a few pointers nonetheless. Stick with me on this one because although quite a long post, this is important work...So: "The aim of the study was to perform a broad evaluation of small molecules in blood plasma to discover metabolites that may lead to biomarkers associated with ASD." The value-added bit was that this was study from the MIND Institute which meant that participant groups were very well-defined in terms of diagnosis and presenting symptoms. Indeed, as per other studies of biomarkers (see here), the talk was all about study groups (ASD vs. asymptomatic controls denoted as 'typically developing' TD) and also the use of training and test sets, where: " 82 patient samples (52 ASD and 30 TD samples) were split into two sets, (1) a training set of 61 samples (39 ASD and 22 TD) for identification of statistically significant features and classification modeling and (2) a 21-sample independent validation set (13 ASD and 8 TD) used to evaluate performance of the classification models."So, then to the interesting bit... the mass spec methods used and data handling. A combination of liquid chromatography-high resolution mass spectrometry (LC-HRMS) and gas chromatography-mass spectrometry (GC-MS) were used. Actually the LC-HRMS was based on separation using C8 and HILIC column chromatography (the LC part) on both occasions coupled to "electrospray ionization" (the MS part) in positive and negative ion mode so giving "4 separate data acquisitions per sample." That and the GC-MS data makes 5 methods. Various methods/software were used to identify potential metabolites of interest including a couple of programs we use in our lab such as "Agilent Technologies MassHunter Qualitative Analysis software" and the METLIN database.Results: as one might imagine, quite a few compounds/metabolites/signals were picked up across the 5 methods used. Table 2 of the paper gives you some idea of the sorts of numbers talked about. That being said, assigning a molecular formula to all those metabolites is rather another matter as per the authors note: "... 179 features comprised 3% of the LC-HRMS and 8% of the GC-MS preprocessed set of features". 'Features' by the way referred to "a moiety detected by the mass spectrometer that is defined by 2 properties 1) the detected mass-to-charge ratio (m/z) and 2) the chromatographic retention time".Those 179 'features' formed the basis of the statistical analyses used to try and differentiate autism from control samples. These were subsequently whittled down to: "an 80 feature set [that] exhibited the best combined classification performance metrics... with an average accuracy of 90%, an average sensitivity of 92%, an average specificity of 87%, and an average AUC [area under the curve] of 0.95."When moving from training to validation sets, the previous 80 feature model did not work as well. Indeed, some further statistical modelling was used and: "The results suggest that at least 40 features are needed to reach an accuracy of 70% and that a range of 80 to 160 features had the best performance with this independent validation sample set as well as the training set of samples."To get to the juicy details of which compounds might be the ones to watch with autism biomarkers in mind, well: "a variety of molecular classes including amino acids, organic acids, sterols, and fatty acids" came up. I've already mentioned creatinine but other prominent mentions were given to "aspartate, glutamate, DHEAS, citric acid, succinic acid, methylhexa-, tetra- and hepta-decanoic acids, isoleucine, glutaric acid, 3-aminoisobutyric acid" and homocitrulline. The authors provide a handy overview of where their results might fit with other autism research areas (e.g. mitochondrial dysfunction, the gut microbiome) which I would encourage interested readers to further peruse. I'm gonna highlight isoleucine as one example where a form of autism has already been talked about with the words 'branched chain amino acids' in mind (see here).The authors conclude with a need for quite a bit more study in this area: "This initial study provides proof of concept to further pursue development of metabolic biomarkers of ASD." Personally, I'd like to think that proof-of-concept is perhaps too preliminary a way of introducing metabolomics to autism research given previous research forays (see here and see here and see here) and their potentially important findings. Certainly, things need to be scaled up in terms of participant ... Read more »

  • November 9, 2014
  • 09:02 PM
  • 119 views

Using Specific Bacteria to Treat Antibiotic-Induced Diarrheal Disease (C. difficile)

by Geoffrey Hannigan in Prophage

There has been a lot of talk about the microbiome and Clostridium difficile infections. This is because patient antibiotic or chemotherapeutic exposure (both of which can destroy your commensal bacterial communities) increases the risk of C. difficile infection. This observation suggests a role for commensal bacteria in mediating infection resistance. The exact commensal bacteria that mediate protection against C. difficile infection are not known, but luckily for us, scientists are working on it. A paper, recently published in Nature, describes a study that sheds light on what bacteria might be offering protection against C. difficile infection.... Read more »

  • November 9, 2014
  • 12:48 PM
  • 140 views

If being sad is “bad”, then why is there sad music?

by Gabriel in Lunatic Laboratories

We tell children not to look so sad. We tell adults to wipe that sad look off their face and smile. We even worry that if you are sad too long, you might need medical attention. Yet, for most of us, when life gets you down, you put on some sad music. So if sadness is such a negative, why do we spend our money and time wallowing in these sad tunes?... Read more »

  • November 8, 2014
  • 12:55 PM
  • 138 views

When it comes to sleep recommendations, what about the children?

by Gabriel in Lunatic Laboratories

Sleep is a hot topic lately, are we getting too much, too little, how much is enough? However, most of these questions are for adults, so what about children? Well as it turns out a new study used activity monitors to track how sleep habits changed in younger and older teens as they grew during a two-year period. Key findings from this study has also lent t0 new support to recent recommendations by the American Academy of Pediatrics that middle and high schools avoid starting earlier than 8:30 a.m.... Read more »

  • November 8, 2014
  • 04:51 AM
  • 111 views

UK Millennium Cohort Study: School and the disabled child

by Paul Whiteley in Questioning Answers

Quite recently the BBC News online ran with the headline: "Disabled children's behaviour 'deteriorates at school'". The story revolved around the findings reported by Rebecca Fauth and colleagues [1] (open-access) looking at "the extent to which the associations between disability and behaviour are linked to children’s developmental stage and thus may be ‘grown out of’ as children enter school and move out of the early years". I should add that, at the time of writing, the Fauth paper is described as a 'working paper' and further "Citation of such a paper should account for its provisional character". So noted.But why Earth, Jor-El? They're primitives...With apologies for all the quotations included in this entry, participants for this trial were drawn from the UK Millennium Cohort Study (MCS) [2] which has previously reported on the topic of autism [3] - "Pre-diagnostic data showed early health problems differentiated children later diagnosed with autism from non-diagnosed peers" - Mmm.In the Fauth paper it included over 6000 UK children covering various ages at different times over the course of the study (referred to as 'sweeps'). Children without reported disability were compared against 3 primary groups defined as 'disabled':Children with developmental delay (DD) at 9 months of age. This was assessed via "a set of 8 questions... that were taken from the Denver Developmental Screening Test" and "five items from an UK adaptation of the MacArthur Communicative Development Inventories (CDI) were used to identify early communicative gestures".Children with a "Long-standing limiting illness [LSLI] at 3, 5 or 7 years". LSLI was defined "if they had an LSLI at one or more of the occasions it was asked between age 3 and age 7" and included various conditions covering 'mental health' and physical health (asthma, type 1 diabetes and vision impairment).Children with Special Educational Needs (SEN) at age 7. Those familiar with the UK system will probably already know about SEN, but for those that don't, it covers "those children who need additional support with their learning" (see here). Further: "SEN may relate to learning difficulties or impairments such as hearing loss, ADHD or dyslexia".Researchers tracked participants looking at various measures covering areas of "children's emotional, relationship and behavioural issues at the ages of three, five and seven" according to the BBC report. Fauth and colleagues list the dependent variables as being derived from "the four ‘problem’ subsets of the parent-reported Strengths and Difficulties Questionnaire (SDQ)". They also took into account various other factors based on family background and constitution, the parent-child relationship (including discipline practices) and child characteristics.Based on some nifty statistical modelling, the authors reported on a few key points:So: "in their early preschool years disabled children do suffer from more challenging expressions of behaviour". With some caveats: "disabled children exhibit a divergent trajectory from the ‘average’ child, showing increases over time in peer problems, hyperactivity and emotional problems, but not for conduct problems".Also: "family and individual characteristics that are associated with both disability and behaviour (such as poverty, family structure, cognitive ability and home environment) mediate the effects of disability in these instances".The authors talk about sex differences in their results: "overall girls face lower levels of peer, conduct and hyperactivity behavioural problems across the early years than boys". This is perhaps not an unexpected result as any parent with both boys and girls will perhaps tell you. But: "disabled boys consistently demonstrated more hyperactive problems than non disabled boys, and that these differences grew over time for boys with LSLI and SEN". Additionally: "The differences between disabled and non-disabled children is much greater for boys than for girls, and this divergence between disabled and non-disabled boys grows more over time than it does for girls".Parenting styles also get a mention in the results: "harsh discipline being consistently associated with higher levels of problem behaviours, and parent-child closeness being linked to lower rates of problem behaviours". With disability in mind however, the authors saw: "very little evidence of parenting moderating the relationship between disability and problem behaviours, either at age 3 or over time".I should also add that when it came to looking at developmental delay (DD) the authors noted: "the developmental trajectories of children identified as DD did not diverge from those without DD" although measurement of peer and hyperactivity issues for example, did still not 'close the gap' compared with non-DD participants.The authors conclude: "Child behavioural difficulties can have far reaching consequences and hence, without appropriate support or intervention, young disabled children may face an accumulation of adverse consequences that serve to compromise their well-being in adolescence and adulthood".I'm sure you can appreciate how important this work is in terms of both how disability impacts on childhood and what strategies might be put in place to reduce some of the more adverse effects of such issues and lessen any inequality as a result. I note for example, that the BBC write-up of this research has given quite a lot of weight with regards to bullying and the notion that schools should adopt "more stringent anti-bullying strategies for those identified as different" as a result of the findings. I would very much agree with this position; with the caveat of ensuring that children with disability are not further plunged into the 'victim' label as a result of any strategies. This can sometimes itself have consequences for things like future independence and self-esteem; thus helping individuals to help themselves - instilling confidence and resilience and building up feelings of self-worth - is another strand to any discussions (and I have a few ideas on that without making any sweeping generalisations). I'm also wondering whether the debate on home-schooling might also come into play here too?I'd finally also like to pass some comment about the issue of parenting styles discussed in the findings. Although no large effect appeared to be observed from parenting style and problem behaviours in those with disability, the more general association between harsh parenting style and hyperactive behaviours for example, offers a fascinating opportunity and potentially offers some, more general lessons on child development and rearing. I might add that the parenting style - disability non-event - "does not have much role in modifying the specific trajectories of problem behaviours associated with disability" - might also carrying some lessons for particular conditions like autism for example too (see here).Now, how about looking at other potential mediators of behaviour such as adequate sleep [4], ... Read more »

Connelly R, & Platt L. (2014) Cohort Profile: UK Millennium Cohort Study (MCS). International journal of epidemiology. PMID: 24550246  

  • November 7, 2014
  • 07:39 PM
  • 152 views

Friends with Benefits

by Abena Edugyan in Your Active Edge

Two studies that look at motivation and physical activity. ... Read more »

Janssen, I., Dugan, S., Karavolos, K., Lynch, E., & Powell, L. (2013) Correlates of 15-Year Maintenance of Physical Activity in Middle-Aged Women. International Journal of Behavioral Medicine., 21(3), 511-518. DOI: 10.1007/s12529-013-9324-z  

  • November 7, 2014
  • 10:05 AM
  • 131 views

The Friday Five for 11/7/14

by Bill Sullivan in The 'Scope

A fun way to learn the latest cool science news! Crazy science stunts, the chemistry of fire breathing, bugs in the brain.... Read more »

Yolken, R., Jones-Brando, L., Dunigan, D., Kannan, G., Dickerson, F., Severance, E., Sabunciyan, S., Talbot, C., Prandovszky, E., Gurnon, J.... (2014) Chlorovirus ATCV-1 is part of the human oropharyngeal virome and is associated with changes in cognitive functions in humans and mice. Proceedings of the National Academy of Sciences. DOI: 10.1073/pnas.1418895111  

  • November 7, 2014
  • 04:11 AM
  • 150 views

Treating depression: exercise or anti-inflammatory meds?

by Paul Whiteley in Questioning Answers

Reiterating my primary caveat on this blog about not giving anything that looks, sounds or smells like medical and/or clinical advice, I'm bringing three papers to the research blogging table today, all published in the JAMA journal family and all talking about depression / depressive symptoms.See my hat... @ Wikipedia First up is the paper by Ole Köhler and colleagues [1] reviewing "the antidepressant and possible adverse effects of anti-inflammatory interventions". Some media interest in this study can be found here. For those who might not know, there is a growing 'feeling' that the various links being made between inflammation or inflammatory mechanisms and psychiatry (see here) may well also extend into the area of depression or depressive symptoms. Far be it from me to say that inflammation and depression is a 'done deal' in scientific terms, but when reading research papers with titles like: 'So depression is an inflammatory disease, but where does the inflammation come from?' by Michael Berk and colleagues [2] (open-access) one kinda gets the impression that quite a lot of opinion has already come down on the side of a probable link.The Köhler paper looked at the combined peer-reviewed literature on the use of various anti-inflammatory medication strategies previously trialled "in adults with depressive symptoms, including those who fulfilled the criteria for depression" including the use of "nonsteroidal anti-inflammatory drugs (NSAIDs)" and "cytokine inhibitors". Cytokines, inflammation and psychology is a topic which has graced this blog on previous occasions (see here). The authors concluded that whilst there is quite a bit more to do in this area: "This study supports a proof-of-concept concerning the use of anti-inflammatory treatment in depression. Identification of subgroups that could benefit from such treatment might be warranted". Touché.Next up are the papers by Snehal M. Pinto Pereira and colleagues [3] and Umar Toseeb and colleagues [4] both talking about a possible role for physical activity and exercise when it comes to the presentation of depression. The results were a little mixed; Pinto Pereira et al concluding that during adult life "activity may alleviate depressive symptoms in the general population" as a function of "a trend of fewer depressive symptoms with more frequent activity". By contrast, Toseeb et al looking at physical activity (PA) "and depressive symptoms during 3 years of adolescence" noted no "longitudinal association between objectively measured PA and the development of depressive symptoms". Indeed they quite prominently recorded a lack of support for PA being protective against developing depressive-type symptoms in their teenage group.There are some differences in the way that the Pinto Pereira and Toseeb research groups went about looking at their respective cohorts and the differences in age between their participants is certainly worth noting. Just correlating two variables is also likely to omit other significant factors (such as inflammation!) which might also show some involvement in the onset or continuation of depression/depressive symptoms. That being said I hark back to other reviews on this topic such as the meta-analysis by Mammen & Faulkner [5] as detailing the bigger picture, denoting some "promising evidence that any level of PA, including low levels (e.g., walking <150 minutes/weeks), can prevent future depression".If we are to assume that anti-inflammatory medication and physical activity (at least for some) can impact on depression or depressive symptoms, the next question really needs to be: what could unite these two findings if anything? Yes, anti-inflammatory meds impact on inflammatory processes, but does this mean that exercise could be doing the same? I found quite a bit of peer-reviewed literature in this area talking about acute and chronic exercise and its short- and long-term effects on inflammation and inflammatory markers (see here for a summary). The long-and-short of it is that nobody really knows at present and, once again, there is quite a lot of merit for the N=1 in this area of study.I might however also advance a couple of other ideas potentially worth looking into. First is the impact that inflammation / anti-inflammatory techniques and exercise have on an important region: the gut microbiota. Those trillions of wee beasties which reside in our deepest, darkest recesses doing so much more than just helping us digest our food are seemingly cropping up everywhere these days (see here for example). The idea that certain elements of our bacterial passengers might also show involvement with something like depression in a sort of gut-brain axis manner is by no means a new concept as per previous discussions on this blog (see here). Research hinting that exercise may also impact on the gut microbiota [6] particularly when it comes to the diversity of bacteria to be present, offers something a glimpse into how exercise may provide effects. Gut bacteria diversity and depression is however still wanting in research terms...Second up, and potentially related to the gut microbiota [7] is the introduction of some epigenetic effect from both anti-inflammatory strategies and exercise when it comes to depression. The science of epigenetics has again been something of a talking point on this blog (see here and see here) from quite a few behavioural perspectives down the years. The idea being that above and beyond your structural genome, there is an added layer of chemical complexity pertinent to the switching on or off of genes which might influence risk for all manner of things. Hype aside, there is growing evidence looking at epigenetic mechanisms being potentially pertinent to depression [8] (open-access) although the precise hows and whys remain somewhat elusive. At the same time, the epigenetics of exercise is also an up-coming area [9] albeit with further investigation needed. Marrying the two concepts together - the epigenetics of exercise and depression - might be a good research idea because at present, there is something of a void in this area. That being said, the epigenetics of immune functions is an area of some note (see here).I really hope that I've not gone beyond my blogging remit with this post in emphasising the potential links between depression, inflammation and physical activity. By no means did I intend to boil something like... Read more »

Ole Köhler, Michael E. Benros, Merete Nordentoft, Michael E. Farkouh, Rupa L. Iyengar, Ole Mors, & Jesper Krogh. (2014) Effect of Anti-inflammatory Treatment on Depression, Depressive Symptoms, and Adverse Effects. JAMA Psychiatry. info:/doi:10.1001/jamapsychiatry.2014.1611

Snehal M. Pinto Pereira, Marie-Claude Geoffroy, & Christine Power. (2014) Depressive Symptoms and Physical Activity During 3 Decades in Adult Life. JAMA Psychiatry. info:/doi:10.1001/jamapsychiatry.2014.1240

Toseeb, U., Brage, S., Corder, K., Dunn, V., Jones, P., Owens, M., St Clair, M., van Sluijs, E., & Goodyer, I. (2014) Exercise and Depressive Symptoms in Adolescents. JAMA Pediatrics. DOI: 10.1001/jamapediatrics.2014.1794  

  • November 6, 2014
  • 09:42 PM
  • 130 views

Diving into Energy Drinks

by Wiley Asia Blog in Wiley Asia Blog - Life Sciences

How much do you know about energy drinks? We always consume energy drinks to boost our mood in general and to enhance our physical endurance. Being consumed since 1960s in Europe and Asia, we are uncertain about the side effects that energy drinks could produce.

While energy drinks are consumed by general consumers, teenagers and young adults are targeted group of consumers. The researchers analysed various ingredients that usually contain in energy drinks as well as the market size and safety.... Read more »

  • November 6, 2014
  • 05:53 PM
  • 203 views

A Possible Genetic “Cure” for HIV… Maybe

by Gabriel in Lunatic Laboratories

Let’s face it, a cure for HIV probably won’t be coming around for awhile. That slippery little virus manages to avoid everything we throw at it. Well researchers at Massachusetts General (MGH) and Boston Children’s hospitals (BCH) tried to take another crack at the problem. For the first time they have used a relatively new gene-editing technique to create what could prove to be an effective technique for blocking HIV from invading and destroying patients’ immune systems.... Read more »

Mandal, P., Ferreira, L., Collins, R., Meissner, T., Boutwell, C., Friesen, M., Vrbanac, V., Garrison, B., Stortchevoi, A., Bryder, D.... (2014) Efficient Ablation of Genes in Human Hematopoietic Stem and Effector Cells using CRISPR/Cas9. Cell Stem Cell, 15(5), 643-652. DOI: 10.1016/j.stem.2014.10.004  

  • November 6, 2014
  • 04:30 AM
  • 103 views

Neurotensin, autism and tail-chasing Bull Terrriers?

by Paul Whiteley in Questioning Answers

I'm not kidding.The paper by Tsilioni and colleagues [1] (open-access) did indeed look at serum levels of neurotensin and corticotropin-releasing hormone (CRH) in a cohort of children diagnosed with an autism spectrum disorder (ASD) alongside levels in tail-chasing Bull Terrier dogs as compared to unaffected [non tail-chasing] Bull Terriers (BTs) and Labrador Retriever dogs. You may well smirk or even laugh at such research but, as per the recent [preliminary] broccoli chemical - autism study (see here), unusual research may yet offer some interesting insights into some of the biology of at least some of the autism spectrum.Meg's gravy is famous.Mention of neurotensin and autism really can only mean the involvement of one researcher: Prof. Theoharis Theoharides and his continuing interest in this area [2]. Indeed, the only thing seemingly missing from the Tsilioni paper is some analysis of another of Prof. Theoharides' interests: mast cells and autism (see here); although I do note that the authors mention how: "NT [neurotensin] is a vasoactive peptide isolated from the brain and is implicated in immunity. It is increased in the skin following acute stress, triggers skin mast cells (MCs) and increases skin vascular permeability in rodents through MC activation".The Tsilioni paper is open-access but a few pointers might be in order:Greek children diagnosed with an ASD (N=40) fulfilling quite a few inclusion criteria provided a fasting blood sample. Similar samples were also provided by "normotypic" controls (I assume this means asymptomatic for ASD)."Serum from unaffected (n=18) and affected BTs (n=14) and unaffected Labrador retriever dogs (n=6) was collected at various facilities accessible to the owners and was sent to the senior Author’s laboratory on dry ice". Apparently a behavioural survey was used to classify Bull Terriers into affected and unaffected groups.Analysis for NT and CRH levels was completed on samples based on ELISA preceded by some clean-up steps. Results were presented to also include: "whether there is any relationship between the number of ASD children with GI [gastrointestinal] symptoms and high serum NT levels and whether it is more than expected by chance".So: group serum NT levels were significantly elevated in the cohort of children with ASD compared to controls (see here). As per the scatterplot shown in that last link however, this elevation was not noted for every child with autism; by my count about 11 children in the ASD group showed results above the upper 95% confidence interval (CI) for that particular group. The presence of GI symptoms also seemed to moderate this relationship: "There is a strong correlation between the number of ASD children with GI symptoms and high serum NT levels".Group serum CRH levels were also elevated for the ASD group compared to controls (see here) (12 of which seemed to show a similar pattern to that previously described).Bull Terriers affected by that tail-chasing behaviour - "reminiscent of stereotypic spinning exhibited by autistic children" - also showed group elevations in the levels of serum NT and CRH when compared to control dogs. The authors suggest that this: "supports the premise that these dogs could represent at least an autism endophenotype" from an animal model point of view (see this table for further information).Outside of trying to model autism or more precisely behaviours associated with autism in another animal model other than rodents (see here) or monkeys (see here), the authors provide other clues for their report of a [potential] canine model: "This dog breed may be useful in the investigation of the diagnosis, pathogenesis and treatment of ASD. NTR and/or CRHR-1 antagonists, as well as MC blockers, could provide possible therapeutic approaches for stress-induced ASD. For instance, the natural flavonoid luteolin is known to inhibit mast cell-mediated allergic inflammation, and a dietary supplement containing luteolin was recently reported to significantly benefit children with ASD". That last sentence on luteolin as a potential intervention option for autism comes from other work published by the authors [3] in need of further, controlled study.The evidence is starting to stack up suggesting that there may be more to see when it comes to NT and CRH levels in relation to at least some cases of autism (the autisms?). That GI symptoms (which are becoming much more readily accepted as being elevated in frequency when it comes to autism) might be a moderating variable of the presence of those peptide hormones is another potentially important feature in terms of how such pathology seems to interplay with behavioural symptoms (see here). I would like to see a little more focus on how other behavioural signs and symptoms (autism+) might also be affecting NT and/or CRH levels when it comes to cases of autism, and indeed, how this work overlaps with other reports of NT for example, in other conditions [4] potentially acting as "an endogenous antipsychotic drug" and more [5]Music then. The Sound of Silence by S & G.----------[1] Tsilioni I. et al. Elevated serum neurotensin and CRH levels in children with autistic spectrum disorders and tail-chasing Bull Terriers with a phenotype similar to autism. Transl Psychiatry. 2014 Oct 14;4:e466.[2] Angelidou A. et al. Neurotensin is increased in serum of young children with autistic disorder. J Neuroinflammation. 2010 Aug 23;7:48.[3] Theoharides TC. et al. A case series of a luteolin formulation (NeuroProtek®) in children with autism spectrum disorders. Int J Immunopathol Pharmacol. 2012 Apr-Jun;25(2):317-23.[4] Boules M. et al. Diverse roles of neurotensin agonists in the central nervous system. Front Endocrinol (Lausanne). 2013 Mar 22;4:36.[5] Boules MM. et al. Elucidating the Role of Neurotensin in the Pathophysiology and Management of Major Mental Disorders. Behav. Sci. 2014; 4: 125-153.----------... Read more »

  • November 5, 2014
  • 04:08 PM
  • 113 views

A Big Break for Bio-Gasoline

by Gabriel in Lunatic Laboratories

While the world waits for a better battery (and a energy grid system that doesn't require constant power making), scientists are hard at work trying to teach old fuels a new trick. Thankfully an international team of bioengineers has boosted the ability of bacteria to produce isopentenol, a compound with desirable gasoline properties. The finding, if it is not obvious, is a significant step toward developing a bacterial strain that can yield industrial quantities of renewable bio-gasoline.... Read more »

  • November 5, 2014
  • 12:19 PM
  • 122 views

Anorexia Nervosa as a Disorder of Perception

by William Yates, M.D. in Brain Posts

A key feature in anorexia nervosa is the disturbance in perception of the body.This perceptual disturbance is encapsulated in criteria 3 from DSM-5: "Disturbance in the way in which one's body weight or shape is experienced, undue influence of body weight or shape evaluation, or denial of the seriousness of the current low weight" Santino Guadio from Italy and colleagues recently published a nice summary of the support for body image disturbance in anorexia nervosa. This study focused on research in the neuropsychology of anorexia nervosa.This review is informative in outlining the components involved in sensory perception.Here are the key findings from their review following their perception components outline.Tactile perceptionWhat it is: identifying touch stimuli and discriminating differences in stimuliHow it is tested: finger identification test, tactile estimation task (estimating distance between two tactile stimuli in different body sitesFindings in anorexia nervosa: Patients with anorexia nervosa perform poorly on identifying finger perception when blindfolded and two fingers are stimulated. Anorexia nervosa is also associated with overestimation of distance between stimulation sites over multiple body partsHaptic perceptionWhat it is: ability to identify shapes by touch when no visual input is availableHow it is tested: Identifying figures and shapes with eyes closed using hands for sensory inputFindings in anorexia nervosa: Patients with anorexia nervosa perform more poorly than controls on correctly identify shape and form when unable to see an object. This deficit appears to be present during both active illness with weight loss and persists following weight restoration.PropioceptionWhat it is: identification of body and limb position in spaceHow it is tested: identification of right-left orientation, ability to place a rod in a vertical postion as body position is modified and no visual sensation is providedFindings in anorexia nervosa: Patients with anorexia nervosa show impaired spatial orientation perception as well as deficits in correctly identifying right-left orientation.Haptic-visual-proprioception integration:What it is: Ability to estimate correct physical properties using both haptic and visual stimuliHow it is tested: Two objects of identical weight but difference size are presented for touch and sight input. Subjects estimate weight of two objects relative to each otherFindings in anorexia nervosa: Subjects with anorexia nervosa show reduction in size-weight performance and reduction integration of visual and haptic information.Visual-tactile-proprioception integration:What it is: use and integration of three sensory modalities, sight, touch and body positionHow it is tested: rubber hand test where subjects estimate position of left index finger before and after visuotactile stimulations.Findings in anorexia nervosa: Patients with anorexia nervosa show impairment in two components of visuo-tactile-propioception integrationInteroceptive perception:What it is: ability to identify and process internal bodily sensations such as heartbeart, intestinal activity, hunger, painHow it is tested: participants are asked to count their own heartbeats and this count is compared to actual heart rate. Findings in anorexia nervosa: Patients with anorexia nervosa show impaired perception of heartbeat compared to controlsThe authors note they found a relatively few well-designed studies of perception in anorexia nervosa. Although the number of studies is small, this review supports a multi-modal impairment in perception in patients with anorexia nervosa compared to controls.The authors note perception is known to be processed through the brain parietal lobe. They propose that parietal lobe dysfunction may impair perception in anorexia nervosa. This perceptual impairment may contribute to the body image disturbance found in the illness.Look for an expansion of studies of perception in anorexia nervosa. Pairing neuropsychological perception studies with advanced brain imaging research techniques may be powerful strategy.Readers with more interest in this topic can access the free full-text manuscript by clicking on the citation link below.Figure of parietal lobe is from an iPad screenshot from the app Brain Tutor.Follow the author on Twitter WRY999.Gaudio S, Brooks SJ, & Riva G (2014). Nonvisual multisensory impairment of body perception in anorexia nervosa: a systematic review of neuropsychological studies. ... Read more »

  • November 5, 2014
  • 10:30 AM
  • 103 views

Neury Thursday: Sleep and the Blood Brain Barrier, with some hesitation

by Allison in Dormivigilia

Researchers found that the permeability of the blood brain barrier is compromised with chronic sleep deprivation. However, the methods section brings these findings into question. Scientists, do your job and make those methods detailed. ... Read more »

He, J., Hsuchou, H., He, Y., Kastin, A., Wang, Y., & Pan, W. (2014) Sleep Restriction Impairs Blood-Brain Barrier Function. Journal of Neuroscience, 34(44), 14697-14706. DOI: 10.1523/JNEUROSCI.2111-14.2014  

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