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  • September 12, 2014
  • 09:52 PM

The Re-emergence of the Minimal Running Shoe

by Craig Payne in Running Research Junkie

The Re-emergence of the Minimal Running Shoe ... Read more »

Davis IS. (2014) The Re-emergence of the Minimal Running Shoe. The Journal of orthopaedic and sports physical therapy, 1-19. PMID: 25211531  

  • September 12, 2014
  • 03:44 PM

Inflammation of the Brain and Memory Problems

by Gabriel in Lunatic Laboratories

Neurological disorders typically involve memory issues. Most of the problems are attributed to plaques that build up in the brain (which are typically prions), yet some causes are unknown. New research however sheds some light on at least one cause of memory problems. As it turns out brain inflammation can rapidly disrupt our ability to retrieve complex memories of similar but distinct experiences.... Read more »

  • September 12, 2014
  • 11:47 AM

Insulin, growth hormone and risk of schizophrenia?

by Paul Whiteley in Questioning Answers

"Overall, the present findings suggest that metabolic and hormonal disturbances such as effects on insulin and growth hormone may represent a vulnerability factor to develop mental disorders". That was the conclusion reported by van Beveren and colleagues [1] (open-access) looking at "disruption of insulin and growth factor signaling pathways as an increased risk factor for schizophrenia"."Years ago you served my father in the Clone Wars"Drawing on data derived from participants taking part in the Genetic Risk and Outcome of Psychoses (GROUP) study [2] researchers looked at blood serum samples "to measure the levels of 184 molecules in serum from 112 schizophrenia patients, 133 siblings and 87 unrelated controls". Multiplex immunoassay was the analytical weapon of choice.The results indicated that "10 proteins were present at significantly different levels between schizophrenia patients and controls" which can be seen here. The insulin synthesis pathway showed more than a passing connection to group differences as per the appearance of insulin and precursor molecules such as proinsulin and C-peptide (connecting peptide). Some of these pathway molecules were also reported to be altered in the sibling group(s) too. Growth hormone also featured as a potentially distinguishing marker, as did adiponectin among others.The authors conclude (again) their findings for "the presence of a molecular endophenotype involving disruption of insulin and growth factor signaling pathways as an increased risk factor for schizophrenia". Perhaps even more interesting is their view of the body of work [3] suggesting that "antipsychotic drugs are known to increase peripheral glucose levels" and how, in light of their findings, "these effects may be intrinsically related to the therapeutic mechanism of action by increasing the peripheral blood glucose levels and thereby increasing glucose availability in the brain".As the authors point out, there is still quite a bit more to do in this area including examining larger samples sizes and importantly, looking at blood glucose levels as a measure of insulin resistance to further complement their findings. I note however that issues with insulin function being potentially related to mood and other psychiatric conditions are nothing new as per the various literature in this area. Anderson and colleagues [4] for example, talked about a diagnosis of diabetes doubling the odds of comorbid depression. Bearing in mind, the possible interfering effect of medication, Verma and colleagues [5] found that in drug-naive (unmedicated) patients with first-episode psychosis there was a significantly increased likelihood of diabetes to be present compared with age and sex-matched asymptomatic control participants. I don't doubt however, that any relationship is going to be complicated.Finally, and bearing in mind the prime directive of this blog (no medical or clinical advice given or intended), there is the question of how this research might translate into therapeutic intervention. A final quote from the authors on this and the possibility of: "novel disease prevention approaches, which could involve nutrition modification, stress reduction and pharmaco-therapeutic interventions, including the application of well-tolerated drugs that combat insulin resistance". Alongside the dietary aspect (which is something very favourable to this blog for lots of reasons), I am wondering whether we could also learn something from times gone by [6]? Perhaps even the appliance of prophylactic psychiatry [7]?Music to close and Andrea Bocelli sings Funiculì, Funiculà...----------[1] van Beveren NJM. et al. Evidence for disturbed insulin and growth hormone signaling as potential risk factors in the development of schizophrenia. Translational Psychiatry. 2014; 4: e430.[2] Korver N. et al. Genetic Risk and Outcome of Psychosis (GROUP), a multi-site longitudinal cohort study focused on gene-environment interaction: objectives, sample characteristics, recruitment and assessment methods. Int J Methods Psychiatr Res. 2012 Sep;21(3):205-21.[3] Wirshing DA. et al. The effects of novel antipsychotics on glucose and lipid levels. J Clin Psychiatry. 2002 Oct;63(10):856-65.[4] Anderson RJ. et al. The prevalence of comorbid depression in adults with diabetes: a meta-analysis. Diabetes Care. 2001 Jun;24(6):1069-78.[5] Verma SK. et al. Metabolic risk factors in drug-naive patients with first-episode psychosis. J Clin Psychiatry. 2009 Jul;70(7):997-1000.[6] Anderson K. et al. Salsalate, an old, inexpensive drug with potential new indications: a review of the evidence from 3 recent studies. Am Health Drug Benefits. 2014 Jun;7(4):231-5.[7] Sawa A. & Seidman LJ. Is Prophylactic Psychiatry around the Corner? Combating Adolescent Oxidative Stress for Adult Psychosis and Schizophrenia. Neuron. 2014; 83: 991-993.----------van Beveren NJ, Schwarz E, Noll R, Guest PC, Meijer C, de Haan L, & Bahn S (2014). Evidence for disturbed insulin and growth hormone signaling as potential risk factors in the development of schizophrenia. Translational psychiatry, 4 PMID: 25158005... Read more »

  • September 12, 2014
  • 09:15 AM

The Friday Five for 09/12/2014

by Bill Sullivan in The 'Scope

Get caught up quick on the hottest science news from this week!... Read more »

Denoeud, F., Carretero-Paulet, L., Dereeper, A., Droc, G., Guyot, R., Pietrella, M., Zheng, C., Alberti, A., Anthony, F., Aprea, G.... (2014) The coffee genome provides insight into the convergent evolution of caffeine biosynthesis. Science, 345(6201), 1181-1184. DOI: 10.1126/science.1255274  

  • September 11, 2014
  • 08:21 PM

"Barefoot Running and Hip Kinematics: Good News for the Knee?"; what about "Bad News for the Ankle"?

by Craig Payne in Running Research Junkie

"Barefoot Running and Hip Kinematics: Good News for the Knee?"; what about "Bad News for the Ankle"?... Read more »

McCarthy C, Fleming N, Donne B, & Blanksby B. (2014) Barefoot Running and Hip Kinematics: Good News for the Knee?. Medicine and science in sports and exercise. PMID: 25207927  

  • September 11, 2014
  • 12:45 PM

The Origami Brain and a new marker for Schizophrenia

by Gabriel in Lunatic Laboratories

Anyone who has seen pictures or models of the human brain (like the one above) is aware that the outside layer, or cortex, of the brain is folded in an intricate pattern of “hills”, called gyri, and “valleys”, called sulci which give the brain it’s distinctive look. It turns out that the patterns of cortical folding are largely consistent across healthy humans, broadly speaking. However, disturbances in cortical folding patterns suggest deeper disturbances in brain structure and function.... Read more »

Nanda P, Tandon N, Mathew IT, Giakoumatos CI, Abhishekh HA, Clementz BA, Pearlson GD, Sweeney J, Tamminga CA, & Keshavan MS. (2014) Local gyrification index in probands with psychotic disorders and their first-degree relatives. Biological psychiatry, 76(6), 447-55. PMID: 24369266  

  • September 11, 2014
  • 09:55 AM

Treating autism in the first year of life

by Paul Whiteley in Questioning Answers

I had been waiting y'know. Waiting a while for the paper by Sally Rogers and colleagues [1] to finally appear quite a few days after the media headlines about 'reducing', 'reversing' and even 'eliminating' the signs and symptoms of autism in early infancy had appeared. Personally, I prefer the New Scientist headline: 'Early autism intervention speeds infant development' given the text of the paper. I should perhaps also add the words 'for some' to that sentence as you will hopefully see...I'm sure most people have already read about the study ins and outs: take an intervention called 'Infant Start' (IS), a relation of the Early Start Denver Model (ESDM), and apply it with a small (very small) group of "symptomatic" young infants (n=7, aged between 6-15 months old) showing signs and symptoms of autism. Plot baseline measures and progress of those children under IS using various psychometric tools including something like the Autism Observation Scale for Infants (AOSI) and old reliable: the ADOS (the Autism Diagnostic Observation Schedule) compared against four comparison groups. One of those control groups included those with similar early autism symptoms as judged by "elevated AOSI scores and clinician concerns" but who did not receive IS; a so-called "declined referral (DR) group" (n=4). Record results and report outcome based on said 12-week program and added extra sessions a few months down the line.The headline conclusion: "At 36 months, the treated group had much lower rates of both ASD [autism spectrum disorder] and DQs [developmental quotients] under 70 than a similarly symptomatic group who did not enroll in the treatment study". Further: "the pilot study outcomes are promising". I should add that when it came to the "final visit" and "based on standardized assessments and clinical judgement" 2 of the 7 children in the IS group did eventually receive a diagnosis of ASD/PDD-NOS (pervasive developmental disorder not otherwise specified). This compared with 3 of the 4 children in the DR group who met criteria for ASD/PDD-NOS (the other child "presented with intellectual disability"). Insofar as DQ - specifically "overall DQ at or below 70 at 36 months" - well, one child in the IS group fell into this category compared with 3 children in the DR group (note to authors, you've called this the 'DE' group... sorry to be pedantic). You can um-and-ah about the links between ASD and PDD-NOS for example, but suffice to say that any effect from IS was not universal across all participants included in the trial. If you'd like a few more details about the trial and results, I'll refer you to the press release from UC Davis (see here).Of course this is not the first time that this type of very early intervention has been discussed in the peer-reviewed domain. Take for example another paper by Rogers and colleagues [2] (open-access) talking about the use of ESDM with a cohort of 14-24 month old toddlers "at risk for autism spectrum disorders". The results on that occasions were slightly less dramatic than the more recent ones with the caveat that "both younger child age at the start of intervention and a greater number of intervention hours were positively related to the degree of improvement in children's behavior for most variables". I talked about this in a previous post (see here). Indeed it appears that age at start of intervention might be an important variable after all.So, where next with this research? Well, aside from some discussions reiterating how useful it would be to have something to aid early diagnosis (see here) bearing in mind that it has not been conclusively proven that all autism is present from birth (see here), discussions have turned to why such early intervention might have had the effect that it had. Brain plasticity has been mentioned, and how critical periods in early development might be particularly amenable to such intensive intervention. Of course, without the all-important "testing the treatment’s efficacy" under more controlled conditions and with larger groups, one cannot discount some role for chance in the recent findings. Not buying that as an answer? How about differing developmental trajectories then?----------[1] Rogers SJ. et al. Autism Treatment in the First Year of Life: A Pilot Study of Infant Start, a Parent-Implemented Intervention for Symptomatic Infants. Journal of Autism and Developmental Disorders. 2014. 12 September.[2] Rogers SJ. et al. Effects of a brief Early Start Denver model (ESDM)-based parent intervention on toddlers at risk for autism spectrum disorders: a randomized controlled trial. J Am Acad Child Adolesc Psychiatry. 2012 Oct;51(10):1052-65.----------S. J. Rogers, L. Vismara, A. L. Wagner, C. McCormick, G. Young, & S. Ozonoff (2014). Autism Treatment in the First Year of Life: A Pilot Study of Infant Start, a Parent-Implemented Intervention for Symptomatic Infants Journal of Autism and Developmental Disorders : 10.1007/s10803-014-2202-y... Read more »

S. J. Rogers, L. Vismara, A. L. Wagner, C. McCormick, G. Young, & S. Ozonoff. (2014) Autism Treatment in the First Year of Life: A Pilot Study of Infant Start, a Parent-Implemented Intervention for Symptomatic Infants. Journal of Autism and Developmental Disorders. info:/10.1007/s10803-014-2202-y

  • September 11, 2014
  • 04:42 AM

Omega-3 fatty acids rescues Fragile X phenotypes in Fmr1-Ko mice

by Paul Whiteley in Questioning Answers

"These results demonstrate that n-3 PUFAs dietary supplementation, although not a panacea, has a considerable therapeutic value for FXS [Fragile X syndrome] and potentially for ASD [autism spectrum disorder], suggesting a major mediating role of neuroinflammatory mechanisms".A view @ Wikipedia That was the conclusion reached by Susanna Pietropaolo and colleagues [1] who "evaluated the impact of n-3 PUFA dietary supplementation in a mouse model of fragile X syndrome (FXS), i.e., a major developmental disease and the most frequent monogenic cause of ASD". Looking at the Fmr1-KO mouse model of FXS, a mouse specifically bred to mimic the silencing of the FMR1 gene noted in FXS (see here) with onwards adverse effects for the production of FMRP, researchers looked at what happened when diets were "enriched or not with n-3 PUFAs from weaning until adulthood when they were tested for multiple FXS-like behaviors". The results seemed to indicate that "n-3 PUFA supplementation rescued most of the behavioral abnormalities displayed by Fmr1-KO mice, including alterations in emotionality, social interaction and non-spatial memory, although not their deficits in social recognition and spatial memory". Neuroinflammatory imbalances noted in the knock-out mice were also positively affected by omega-3 supplementation.I don't need to remind you that the Pietropaolo study was a study of mice and one needs to be quite careful about extrapolating animal results when it comes to humans. That being said, given the quite extensive work that has been done on FXS and the detailing of it's molecular background, one might assume that the current results are treated with a little less scepticism than in relation to other more idiopathic 'types' of autism. Still, proper trials with people are indicated as per other research.Omega-3 fatty acids have been discussed before on this blog with autism in mind (see here). The collected literature on their usefulness as supplements for autism is rather mixed at present [2] despite some emerging evidence on their involvement in various biological processes in cases of autism (see here). That being said, I'm not getting too down on omega-3 fatty acids in light of some associations being made with specific skills over and above any condition-specific relationship and some new light being shed on their use in other conditions [3]. I'm yet to find anything like an experimental trial of fatty acids in real people with FXS but did chance(!) upon the study by Lachance and colleagues [4] (open-access) talking about the use of fenretinide (N-(4-hydroxyphenyl) retinamide (4HPR)) in the test-tube and effects "associated with the normalization of arachidonic acid/docosahexaenoic acid ratio in macrophages". The effect talked about translates as a down-regulation in the "production of arachidonic acid (AA), a pro-inflammatory omega-6 polyunsaturated fatty acid, and to increase levels of omega-3 polyunsaturated docosahexaenoic acid (DHA), which has an anti-inflammatory effect". Mmm... possibly some new targets to replace quite a few disappointments when it comes to FXS therapeutics (see here).Music to close. Fontella Bass and Rescue Me.----------[1] Pietropaolo S. et al. Dietary supplementation of omega-3 fatty acids rescues fragile X phenotypes in Fmr1-Ko mice. Psychoneuroendocrinology. 2014 Jul 9;49C:119-129.[2] James S. et al. Omega-3 fatty acids supplementation for autism spectrum disorders (ASD). Cochrane Database Syst Rev. 2011 Nov 9;(11):CD007992.[3] Hawkey E. & Nigg JT. Omega-3 fatty acid and ADHD: Blood level analysis and meta-analytic extension of supplementation trials. Clin Psychol Rev. 2014 Jun 2;34(6):496-505.[4] Lachance C. et al. Fenretinide corrects the imbalance between omega-6 to omega-3 polyunsaturated fatty acids and inhibits macrophage inflammatory mediators via the ERK pathway. PLoS One. 2013 Sep 12;8(9):e74875.----------Pietropaolo S, Goubran MG, Joffre C, Aubert A, Lemaire-Mayo V, Crusio WE, & Layé S (2014). Dietary supplementation of omega-3 fatty acids rescues fragile X phenotypes in Fmr1-Ko mice. Psychoneuroendocrinology, 49C, 119-129 PMID: 25080404... Read more »

Pietropaolo S, Goubran MG, Joffre C, Aubert A, Lemaire-Mayo V, Crusio WE, & Layé S. (2014) Dietary supplementation of omega-3 fatty acids rescues fragile X phenotypes in Fmr1-Ko mice. Psychoneuroendocrinology, 119-129. PMID: 25080404  

  • September 10, 2014
  • 08:26 PM

Patellofemoral Joint Stress during Running with Alterations in Foot Strike Pattern

by Craig Payne in Running Research Junkie

Patellofemoral Joint Stress during Running with Alterations in Foot Strike Pattern... Read more »

  • September 10, 2014
  • 06:00 PM

Anecdotes and the Appearance of Improvement

by Rogue Medic in Rogue Medic

We like to give treatments that produce results that we can see and logically attribute to the treatments we gave.

We like to give IV (IntaVenous) furosemide (Lasix – frusemide in Commonwealth countries) for CHF (Congestive Heart Failure).

1. The patient had CHF.
2. I gave IV furosemide.
3. The patient produced urine.... Read more »

  • September 10, 2014
  • 02:26 PM

Multiple Sclerosis and Myelin loss

by Gabriel in Lunatic Laboratories

Multiple sclerosis (MS) is an unpredictable, often disabling disease of the central nervous system that disrupts the flow of information within the brain, and between the brain and body. The exact cause is unknown, however people with multiple sclerosis lose myelin in the gray matter of their brains and the loss is closely correlated with the severity of the disease, according to a new magnetic resonance imaging (MRI) study.... Read more »

Vasily L. Yarnykh, James D. Bowen, Alexey Samsonov, Pavle Repovic, Angeli Mayadev, Peiqing Qian, Beena Gangadharan, Bart P. Keogh, Kenneth R. Maravilla, & Lily K. Jung Henson. (2014) Fast Whole-Brain Three-dimensional Macromolecular Proton Fraction Mapping in Multiple Sclerosis. Radiological Society of North America . info:/10.1148/radiol.14140528

  • September 10, 2014
  • 09:36 AM

Video Tip of the Week: #Docker, shipping containers for software and data

by Mary in OpenHelix

Breaking into the zeitgeist recently, Docker popped into my sphere from several disparate sources. Seems to me that this is a potential problem-solver for some of the reproducibility and sharing dramas that we have been wrestling with in genomics. Sharing of data sets and versions of analysis software is being tackled in a number of […]... Read more »

  • September 10, 2014
  • 08:00 AM

Return of Results from Next-gen Sequencing

by Daniel Koboldt in Massgenomics

The rapid adoption of next-gen exome and genome sequencing for clinical use (i.e. with patient DNA) raises some difficult questions about the return of results to patients and their families. In contrast to traditional genetic testing, which usually checks for variants in specific genes, high-throughput sequencing has the potential to reveal a number of secondary […]... Read more »

  • September 10, 2014
  • 05:01 AM

Donepezil and D-cycloserine rescue behaviours in VPA exposed animals

by Paul Whiteley in Questioning Answers

In a post not-so-long-ago I talked about an interesting piece of research by Ahn and colleagues [1] suggesting that a ketogenic diet might yet hold some promise to "modify complex social behaviors and mitochondrial respiration" affected in the "prenatal valproic acid (VPA) rodent model of ASD [autism spectrum disorder]". The idea being that exposure to valproic acid (valproate) during the nine months that made us might carry some heightened risk for adverse effects on offspring development (see here) and a dietary change might rescue some functions."Daisy, Daisy, give me your answer do"Well, the floodgates have well and truly opened when it comes to looking at various pharmacological agents that 'might' also rescue abilities thought to be affected by prenatal valproate exposure as today I discuss two papers.First up is the paper by Wellmann and colleagues [2] which reported that: "D-cycloserine normalized the VPA-induced increase in play fighting in males and also increased social motivation in females". Second is the paper by Kim and colleagues [3] (open-access here) who observed: "Subchronic treatment of donepezil improved sociability and prevented repetitive behavior and hyperactivity of VPA-treated mice offspring".Aside from reiterating that these were studies of rodents and not humans, I was slightly taken aback by the reported findings. Cycloserine is normally packaged as an antibiotic but, as with many medicines these days, the pharmacological effects of the compound seem to extend far beyond the intended (antimicrobial) action [4]. I've talked about D-cycloserine before on this blog (see here) and some rather interesting research linking administration to several conditions. With autism in mind, I'll bring to your attention the paper by Urbano and colleagues [5] as one example of how far and wide this pharmaceutic is venturing. As to mode of action, well, I'd be clutching at straws if I was to hazard any guess. I might suggest that something around glutamate metabolism might be something to look at [6] which coincides with one of the proposed actions of D-cycloserine [7].Donepezil (Aricept®) falls under the category of acting as a reversible acetylcholinesterase inhibitor (AChEI). More usually indicated for dementia and particularly Alzheimer's disease [8] Kim et al describe how "prenatal exposure of valproic acid (VPA) induced dysregulation of cholinergic neuronal development, most notably the up-regulation of acetylcholinesterase (AChE) in the prefrontal cortex of affected rat and mouse offspring". You can, therefore, perhaps see the logic in using donepezil as an AChEI particularly when one takes into account how other AChE inhibitors have been studied with autistic behaviours in mind [9]. Indeed, this is not the first time that donepezil has specifically been talked about in relation to autism, mouse models of autism, as per the findings from Karvat & Kimchi [10] and their discussions based on the BTBR 'dangermouse' where: "i.p. [intraperitoneal] injection of AChEI to BTBR mice significantly relieved autism-relevant phenotypes, including decreasing cognitive rigidity, improving social preference, and enhancing social interaction, in a dose-dependent manner". And there is the promise of more to come with this medicine.Reiterating that the Wellmann and Kim results (and the Ahn results) are based on studies of rodents not people, these are an interesting datasets crying out for further replication and study. Scientific glimmers are appearing which provide further data on what biological functions might be affected by prenatal valproate exposure and importantly, what might be done to [safely] rescue certain functions. But we're not there yet... and I haven't even mentioned epigenetics [11] ...An unusual song from Ween to close... Push th' Little Daisies. Having said that, Ween are/were an unusual band...----------[1] Ahn Y. et al. The Ketogenic Diet Modifies Social and Metabolic Alterations Identified in the Prenatal Valproic Acid Model of Autism Spectrum Disorder. Dev Neurosci. 2014 Jul 8.[2] Wellmann KA. et al. D-Cycloserine Ameliorates Social Alterations That Result From Prenatal Exposure To Valproic Acid. Brain Res Bull. 2014 Aug 14. pii: S0361-9230(14)00120-8.[3] Kim JW. et al. Subchronic Treatment of Donepezil Rescues Impaired Social, Hyperactive, and Stereotypic Behavior in Valproic Acid-Induced Animal Model of Autism. PLoS One. 2014 Aug 18;9(8):e104927.[4] Rodrigues H. et al. Does D-cycloserine enhance exposure therapy for anxiety disorders in humans? A meta-analysis. PLoS One. 2014 Jul 3;9(7):e93519.[5] Urbano M. et al. A trial of D-cycloserine to treat stereotypies in older adolescents and young adults with autism spectrum disorder. Clin Neuropharmacol. 2014 May-Jun;37(3):69-72.[6] Bristot Silvestrin R. et al. Animal model of autism induced by prenatal exposure to valproate: altered glutamate metabolism in the hippocampus. Brain Res. 2013 Feb 7;1495:52-60.[7] Hashimoto K. Targeting of NMDA receptors in new treatments for schizophrenia. Expert Opin Ther Targets. 2014 Sep;18(9):1049-63.[8] McGleenon BM. et al. Acetylcholinesterase inhibitors in Alzheimer’s disease. British Journal of Clinical Pharmacology. 1999; 48: 471-480.[9] Ghaleiha A. et al. Galantamine efficacy and tolerability as an augmentative therapy in autistic children: A randomized, double-blind, placebo-controlled trial. J Psychopharmacol. 2013 Oct 15;28(7):677-685.[10] Karvat G & Kimchi T. Acetylcholine elevation relieves cognitive rigidity and social deficiency in a mouse model of autism. Neuropsychopharmacology. 2014 Mar;39(4):831-40.[11] Tordjman S. et al. Gene × Environment interactions in autism spectrum disorders: role of epigenetic mechanisms. Front Psychiatry. 2014 Aug 4;5:53.----------... Read more »

  • September 9, 2014
  • 05:10 PM

Genetics and Running Economy

by Craig Payne in Running Research Junkie

Genetics and Running Economy... Read more »

Bertuzzi R, Pasqua LA, Bueno S, Lima-Silva AE, Matsuda M, Marquezini M, & Saldiva PH. (2014) Is the COL5A1 rs12722 Gene Polymorphism Associated with Running Economy?. PloS one, 9(9). PMID: 25188268  

  • September 9, 2014
  • 02:35 PM

Autism and Testosterone

by Gabriel in Lunatic Laboratories

As a male we are at higher risk for heart disease, we are also at higher risk for stroke. It’s that pesky testosterone, sure it has its benefits, don’t get me wrong I think testosterone over all is great. Estrogen has it’s own downsides too, things like certain cancers for example. Well estrogen has some other benefits and as it turns out, the same sex hormone that helps protect females from stroke may also reduce their risk of autism.... Read more »

Amanda Crider,, Roshni Thakkar,, Anthony O Ahmed, & Anilkumar Pillai. (2014) Dysregulation of estrogen receptor beta (ERβ), aromatase (CYP19A1), and ER co-activators in the middle frontal gyrus of autism spectrum disorder subjects. Molecular Autism . info:/10.1186/2040-2392-5-46

  • September 9, 2014
  • 04:35 AM

The gondii and generalised anxiety disorder

by Paul Whiteley in Questioning Answers

Toxoplasma gondii (T. gondii) has been absent from discussions on this blog for a while now. I'm going to remedy that today with this post talking about the paper from Markovitz and colleagues [1] who concluded: "T. gondii infection may play a role in the development of GAD [generalized anxiety disorder]"."You have saved our lives. We are eternally grateful"Based on participants taking part in the Detroit Neighborhood Health Study exposure to T. gondii "defined by seropositivity and IgG antibody levels" was measured in approaching 500 people. Psychiatric diagnoses including depression, PTSD (posttraumatic stress disorder) and GAD were ascertained and data analysed to see if there was anything correlation-wise between T. gondii exposure and the various conditions.The results suggested that T. gondii exposure was "associated with a 2 times greater odds of GAD" when taking into account various potential confounding variables. Those with some of the highest antibody levels to T. gondii were over three times at greater risk of GAD, potentially suggesting a dose-response relationship. Ergo, "T. gondii infection is strongly and significantly associated with GAD" but with more research to do.Although no expert on GAD, I was a little puzzled by the Markovitz results. My previous musings on T. gondii and how it manages to alter rodent behaviour would seem to imply that this protozoan has an opposite effect on animal anxiety (i.e. reducing or modifying anxiety and predation-related fear [2]). Of course mice/rats are mice/rats and not humans but one might have expected something of an opposite effect [3].That being said, this is not the first time that anxiety (human anxiety) has been mentioned alongside T. gondii as per the paper by Groër and colleagues [4] (open-access). In that case authors concluded that: "Higher T gondii immunoglobulin G titers in infected women were related to anxiety and depression during pregnancy". Some clarification is perhaps needed in this area...To close, music I've probably linked to before but it's so good I'm gonna do it again: REM and It's the End of the World...----------[1] Markovitz A. et al. Toxoplasma gondii and anxiety disorders in a community-based sample. Brain Behav Immun. 2014 Aug 11. pii: S0889-1591(14)00418-8.[2] Kaushik M. et al. The role of parasites and pathogens in influencing generalised anxiety and predation-related fear in the mammalian central nervous system. Horm Behav. 2012 Aug;62(3):191-201.[3] Gonzalez LE. et al. Toxoplasma gondii infection lower anxiety as measured in the plus-maze and social interaction tests in rats A behavioral analysis. Behav Brain Res. 2007 Feb 12;177(1):70-9.[4] Groër MW. et al. Prenatal depression and anxiety in Toxoplasma gondii-positive women. Am J Obstet Gynecol. 2011 May;204(5):433.e1-7.----------Markovitz A, Simanek AM, Yolken R, Galea S, Koenen KC, Chen S, & Aiello AE (2014). Toxoplasma gondii and anxiety disorders in a community-based sample. Brain, behavior, and immunity PMID: 25124709... Read more »

Markovitz A, Simanek AM, Yolken R, Galea S, Koenen KC, Chen S, & Aiello AE. (2014) Toxoplasma gondii and anxiety disorders in a community-based sample. Brain, behavior, and immunity. PMID: 25124709  

  • September 8, 2014
  • 06:07 PM

Genes Smash! An Oxytricha trifallax story

by Gabriel in Lunatic Laboratories

In DNA mutation is often a bad thing. It’s sort of like building a car, there are far more wrong ways to one together than there are right ways. Still, mutation happens often which brings with it good (and more often bad) things. Usually mutation is spontaneous, it has no real rhyme or reason (in a broad sense) and while it brings things like cancers, it also can bring amazingly beneficial traits too.... Read more »

Chen X, Bracht JR, Goldman AD, Dolzhenko E, Clay DM, Swart EC, Perlman DH, Doak TG, Stuart A, Amemiya CT.... (2014) The Architecture of a Scrambled Genome Reveals Massive Levels of Genomic Rearrangement during Development. Cell, 158(5), 1187-98. PMID: 25171416  

  • September 8, 2014
  • 10:41 AM

Coping with Stress – Some Essential Constructs

by Vivek Misra in The UberBrain

Anxiety, insomnia, muscle tension, fatigue, high blood pressure, and anger are just some of the symptoms of stress. Stress not only affects our body, but also our behavior that can lead to social withdrawal. This presentation will explore the nature of our mind and the various factors in our lives that cause us stress. We will learn simple meditation techniques that can nourish the mind which will lead to increased focus, greater productivity, and improved relationships. ~ Pandi Gadadhara Pandi, an author, meditation teacher, inspirational speaker, and lecturer at Columbia University gave a talk organized by Google . Pandi talks about stress management for work-life balance – something we could probably all stand to be a little better at. Pandit uses his life experience and decades of in-depth studies to aid people in overcoming the various stress factors in their own lives. The medical field now knows that stress leads to anxiety, insomnia, muscle tension, high blood pressure, and anger. Pandit’s unique approach applies Eastern wisdom and meditation techniques to help the audience gain deeper insight into their mind and understand the reasons we becomes stressed, anxious, and angry. An Integrative Approach  for Preventing and Managing Stress: A number of strategies can help in stress management. Some of these techniques are validated at Neurokrish 1. Develop Social Support Systems: Support from friends and family provides emotional sustenance, tangible resources, aid and information Membership of club or societies: hobby or interest group, illness support groups, religious groups, sports and recreational clubs Owning a pet can be […]
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  • September 8, 2014
  • 08:00 AM

I’ll Wager That You Bet On Football, Or Maybe Football

by Mark E. Lasbury in The 'Scope

Betting on American football and football proper is a trillion dollar a year industry. Why do only 4% of gamblers become addicted. Some of it is actually due to the games themselves. New research is showing that a belief in your knowledge of the game and the “near miss” wherein you almost win your bet, are strong factors in dopamine signaling in the reward centers of the brain.... Read more »

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Khazaal Y, Chatton A, Billieux J, Bizzini L, Monney G, Fresard E, Thorens G, Bondolfi G, El-Guebaly N, Zullino D.... (2012) Effects of expertise on football betting. Substance abuse treatment, prevention, and policy, 18. PMID: 22578101  

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