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  • 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
  • 09:52 AM

Stop Worrying, Good-Looking Dudes: Your Sperm Is Fine

by Elizabeth Preston in Inkfish

You may have seen headlines over the past week proclaiming that handsome men have lower-quality sperm. If this made you panic because you happen to be a great-looking guy, you can stop. (If you’re an un-handsome man who’s been gloating—sorry.) This scientific study did say a few interesting things about Spaniards, Colombians, and cheekbones. But […]The post Stop Worrying, Good-Looking Dudes: Your Sperm Is Fine appeared first on Inkfish.... Read more »

Soler C, Kekäläinen J, Núñez M, Sancho M, Alvarez JG, Núñez J, Yaber I, & Gutiérrez R. (2014) Male facial attractiveness and masculinity may provide sex- and culture-independent cues to semen quality. Journal of evolutionary biology, 27(9), 1930-8. PMID: 25056484  

  • 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
  • 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
  • 11:36 AM

Altruism and AlAnon: in helping we are helped

by DJMac in Recovery Review

“Giving implies to make the other person a giver also.” So said Eric Fromm whose quote starts this research paper which travels to the heart of mutual aid. The clear message? In helping other, we help ourselves. The recovery saying “We only keep what we have by giving it away” hits the mark in this respect. What [...]
The post Altruism and AlAnon: in helping we are helped appeared first on Recovery Review.
... Read more »

  • September 10, 2014
  • 09:40 AM

Midi-chlorians gave Jedi knights their power. Is there something like this on Earth?

by Bill Sullivan in The 'Scope

A strange and provocative paper by Alexander Panchin and colleagues proposes an unorthodox new idea called the “biomeme hypothesis”, which posits that the impulse behind some religious rituals could be driven by mind-altering parasites.... 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
  • 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
  • 09:37 AM

Elderly Seabirds Dive Just as Well as Young Ones

by Elizabeth Preston in Inkfish

If your grandma got up from the sofa, did a couple toe-touches, and then ran a mile at her college track pace, she might be approaching the athletic skill of a thick-billed murre. These seabirds make incredibly deep, long dives to catch prey. As they age, their bodies slow and change like ours. But the […]The post Elderly Seabirds Dive Just as Well as Young Ones appeared first on Inkfish.... Read more »

  • 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
  • 09:05 PM

The atmosphere and what we eat: significant increases in greenhouse gas emissions predicted for high-calorie diets recommended by USDA

by Jonathan Trinastic in Goodnight Earth

New research shows that shifting to recommended, high-calorie USDA diets could increase GHG emissions due to the dairy required to make up for reduced meat/poultry calories. What we eat impacts our long-term environment!... Read more »

  • 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
  • 04:40 PM

“If I do that, I’ll be in more pain and won’t sleep and …” Tampa Scale of Kinesiophobia reformulated

by Bronwyn Thompson in Healthskills: Skills for Healthy Living

The TSK has been used for many years now as a good measure of kinesiophobia. Usually scores of above 45 (from a possible 68) suggest that the person has beliefs that their pain represents ongoing damage (Somatic focus) and that they should avoid doing anything that provokes pain (Activity avoidance). High scores have been associated with a wide range of negative outcomes including pain intensity, disability, distress – and in a wide range of individuals including people with chronic low back pain, acute low back pain, osteoarthritic knees and hips, shoulder pain and so on. Originally the measure was believed to tap into the idea that pain represents damage or harm, and also to measure the belief that activities should be avoided.

In people who have been well ‘educated’ in pain neurophysiology, intellectually they know that their pain isn’t about what goes on in the tissues, so they may score fairly low on the Somatic scale of the TSK. Yet they avoid – and when asked about this, they say things like “I know if I do things it’s going to increase my pain and I’ll have a really bad night’s sleep” or “I’ll have a rotten day” or “I’ll be grumpy with my kids”. It’s not the potential damage that’s the problem – instead the problem is really about the way they see that pain will get in the way of what they want to do.... Read more »

  • 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 […]
The post Coping with Stress – Some Essential Constructs appeared first on The UberBrain.
... Read more »

  • September 8, 2014
  • 04:22 AM

Homocysteine, MTHFR and schizophrenia studied AND meta-analysed

by Paul Whiteley in Questioning Answers

"Our study suggests that increased plasma total homocysteine levels may be associated with an increased risk of schizophrenia". Further: "The meta-analysis of the Japanese genetic association studies demonstrated a significant association between the MTHFR C677T polymorphism and schizophrenia".MTHFR (again!) @ Paul WhiteleySo said the results of the study and meta-analysis carried out by Akira Nishi and colleagues [1] (open-access) looking at the 'big H' alongside everyone's genetic Scrabble favourite MTHFR (methylenetetrahydrofolate reductase (NAD(P)H)).The Nishi paper represents pretty good scientific value for money given that authors not only looked at plasma levels of total homocysteine in nearly 400 participants diagnosed with schizophrenia compared with nearly 1000 controls, they also genotyped for the MTHFR C677T polymorphism [2] (describing an amino acid substitution which reduces the activity of the enzyme methylenetetrahydrofolate reductase and results in elevated homocysteine levels) in a further 1700 participants with schizophrenia compared against over 3000 asymptomatic controls. For good measure, the authors then carried out a meta-analysis of the scientific literature looking at homocysteine and schizophrenia as a function of gender. Phew.As per the opening paragraph, authors reported "significantly elevated plasma total homocysteine levels in patients with schizophrenia compared with controls, in both male and female subjects". The results of their meta-analysis confirmed such elevations in homocysteine "although antipsychotic medication might influence this outcome". Combined with the association made between a diagnosis of schizophrenia and the MTHFR SNP studied, all adds up to "disrupted 1-carbon metabolism [having] an important role in the pathophysiology of schizophrenia".I don't mind saying that the Nishi results are really rather interesting to me. The links between schizophrenia and homocysteine have been talked about previously on this blog (see here) including the potential usefulness of folic acid and vitamin B12 for some cases of schizophrenia (see here). Nishi et al also talk about another potentially important part of their results with some mention of DNA methylation, something which also crosses over into other areas of research interest too (see here).And so the evidence continues to stack up for the big H and MTHFR in some cases of schizophrenia...Music then. The Pixies and Debaser.----------[1] Nishi A. et al. Meta-analyses of Blood Homocysteine Levels for Gender and Genetic AssociationStudies of the MTHFR C677T Polymorphism in Schizophrenia. Schizophrenia Bulletin. 2014; 40: 1154-1163.[2] Gilbody S. et al. Methylenetetrahydrofolate reductase (MTHFR) genetic polymorphisms and psychiatric disorders: a HuGE review. Am J Epidemiol. 2007 Jan 1;165(1):1-13.----------Nishi A, Numata S, Tajima A, Kinoshita M, Kikuchi K, Shimodera S, Tomotake M, Ohi K, Hashimoto R, Imoto I, Takeda M, & Ohmori T (2014). Meta-analyses of Blood Homocysteine Levels for Gender and Genetic Association Studies of the MTHFR C677T Polymorphism in Schizophrenia. Schizophrenia bulletin PMID: 24535549... Read more »

  • September 7, 2014
  • 01:46 PM

A new Hope for Muscle Wasting Diseases

by Gabriel in Lunatic Laboratories

Muscle wasting diseases can be difficult to watch. They are typically slow and have a very painful progression, some to the point of not even being able to breath on ones own. But new research might change all that. Scientists have developed a novel technique to promote tissue repair in damaged muscles. The technique also creates a sustainable pool of muscle stem cells needed to support multiple rounds of muscle repair.... Read more »

Vittorio Sartorelli, & Alessandra Sacco. (2014) STAT3 signaling controls satellite cell expansion and skeletal muscle repair. Nature Medicine. info:/10.1038/nm.3656

  • September 7, 2014
  • 10:03 AM

Fist Bump, Don't Handshake

by Viputheshwar Sitaraman in Draw Science

Fist bumps minimize contact time and surface area, diminishing germ transfer in terms of greetings--especially compared to handshakes.... Read more »

  • September 6, 2014
  • 06:22 PM

Is the Internet of Things the Real Thing?

by Aurametrix team in Health Technologies

The Internet of Things: an exciting new world with a digital nervous system or a nightmare where objects take decisions while we are unconscious?15 years ago, when the term was first coined, it was about assigning everything around us a unique identity with RFID tags, to enable all material things to talk to each other and save us time for gathering and using information. As RFID tags dropped below 1 cent cost, and sensors, modems and devices are getting smaller, smarter and cheaper, this vision is moving closer to reality.The latest Gartner's Hype Cycle (August 2014) places the Internet of Things at the peak of Inflated Expectations, while Big Data evolving in tandem with IoT has already started to fall into the through of disillusionment, getting ready to join mobile health and cloud computing right there on the bottom of the through. Consumers are not ready to embrace the flood of smart wearables and appliances - as they don't really know what to do with them, don't perceive their value and are concerned about privacy and prices.Clay Christensen's theory of "disruptive technology" emphasizes that technologies tend to get better at a faster rate than users' needs increase. Next Big Thing often starts as an expensive "toy". When the telephone was first introduced it could only be afforded by the rich and it could only carry a signal over a short distance. If Watson really had said in 1943 that "there is a world market for maybe five computers", as Gordon Bell pointed out much later, it would have held true for some ten years.The first generation of IoT devices fell short of user needs and was rather primitive. Over a third of people who bought a smart wearable abandoned it a few months later. Yet, the "new" has never been hotter. It seems a new wearable is launching every week and we are constantly waiting for something newer and better, hoping it will finally answer the question "what can we do now that we could not do before?"However, the current generation of "smart things" is focused mostly on better designed hardware and higher-end consumers. Fashionable elegant-looking devices are supposed to make wearables more appealing and "design thinking" is one of today's hottest buzzwords. Withings Activité, Fitbit pendants from Tory Burch,  Yves Béhar's designed Vessyl, Diane Von Furstenberg's Google glass, Rebecca Minkoff's tech-enabled jewelry, and the new bracelet from Intel - MICA  - highlighted by pearls and other precious stones - are getting ready to conquer attention of consumers and developers. Especially developers - as the size of the market will depend on the number of developer-entrepreneurs creating value in it.The app economy taught hardware manufacturers that when people experiment they find ways to create value, often in unexpected ways.  But it also taught developers that they need to invest considerable time to build a marketable app and the chances of that app to make money are about 1 in 25,000. As the average age of developers keeps decreasing getting into the middle and high school years, the main benefit of app development becomes education and learning by itself. But will this be sufficient for the Internet of Things or will inter-networked things remain a toy for the wealthy? ReferencesAshton K. (2009). That 'Internet of Things' Thing, in the real world things matter more than ideas RFID Journal (June 22)Gartner's "Hype Cycle for Emerging Technologies, 2014" at's Clayton Christensen on the economics of 'disruption' ( G (2014). The internet of things for personalized health. Studies in health technology and informatics, 200, 22-31 PMID: 24851958Perera, C., Zaslavsky, A., Christen, P., & Georgakopoulos, D. (2014). Sensing as a service model for smart cities supported by Internet of Things Transactions on Emerging Telecommunications Technologies, 25 (1), 81-93 DOI: 10.1002/ett.2704Anderson J. amd Rainie L. (2014) The Internet of Things Will Thrive by 2025. Pew researchMackinlay M. (2013). Phases of Accuracy Diagnosis: (In)visibility of System Intersect, Vol 6, No 2... Read more »

Ashton K. (2009) That 'Internet of Things' Thing, in the real world things matter more than ideas. RFID Journal. info:/

Schreier G. (2014) The internet of things for personalized health. Studies in health technology and informatics, 22-31. PMID: 24851958  

Perera, C., Zaslavsky, A., Christen, P., & Georgakopoulos, D. (2014) Sensing as a service model for smart cities supported by Internet of Things. Transactions on Emerging Telecommunications Technologies, 25(1), 81-93. DOI: 10.1002/ett.2704  

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