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  • January 15, 2015
  • 05:10 AM

Maternal thyroid autoantibody and offspring autism risk

by Paul Whiteley in Questioning Answers

I have, on this blog, previously mentioned the paper by Alan Brown and colleagues [1] suggesting that: "The prevalence of maternal TPO-Ab+ [thyroid peroxidase antibody] was significantly increased in pregnancies giving rise to autism cases (6.15%) compared to controls (3.54%)." It was during some discussion on the suggested diagnosis of Down syndrome disintegrative disorder (see here) and the idea that some signs and symptoms of regressive autism (?) might overlap with TPO antibodies in some cases of Down syndrome.You've got a playdate with destiny!I've had a few weeks to further reflect on the Brown paper and decided that their suggestion of: "the first biomarker-based evidence that a class of known maternal autoimmune disorders is related to autism in offspring" is worthy of a post all of its own.A quick recap first: thyroid peroxidase antibodies translates as the body mounting an immune response against thyroid peroxidase, an important enzyme in the production of the thyroid hormones. As per another mention of TPO based on research suggestive of a tentative link between anti-TPO antibodies and [some] depressive disorder (see here), the more usual clinical occasion regarding detection of such antibodies is in relation to something like Hashimoto's thyroiditis, an autoimmune condition.Brown and colleagues drew upon collected data from the Finnish Prenatal Study of Autism (FiPS-A) [2], an initiative which had at its disposal "archived maternal serum specimens from virtually the entire pregnant population of Finland beginning in 1983". Alongside quite a bit of other registry based information on things like an ICD-10 diagnosis of autism in offspring, Brown et al set to work analysing those archived serum specimens for some "967 matched case-control pairs" (autism cases matched 1:1 with sex and date of birth linked asymptomatic controls) for the presence of thyroid peroxidase antibody (TPO-Ab).As per the previous sentence, serum samples from mums who went on to have a child with autism were significantly more likely to present with TPO-Ab; indeed: "The odds of autism were increased by nearly 80% among offspring of mothers who were TPO-Ab+ during pregnancy" compared with those antibody negative. Perhaps just as important, authors also reported that: "Measures of maternal thyroid hormones did not differ between groups" suggesting that the actual antibodies might be the more important factor over and above a thyroid hormone link (see here for discussion on other work in this area).For those who follow this blog, the idea that [some] autism and [some] autoimmunity / autoimmune conditions might show [some] linkage is not a new one. If one delves deeper into the peer-reviewed research arena one finds other hints that other maternal antibodies might also show a connection to offspring autism risk as per the idea of MAR autism (see here), that is, maternal autoantibody-related autism. Granted, the research road has not run entirely smoothly when it comes to any possible connection (see here) and there are still questions to be answered, not least when it comes to the effects of comorbidity common to autism and how they may likewise have an autoimmune connection too (see here for example). The Brown results however cannot be readily brushed under the scientific carpet given their origin and pretty powerful participant numbers used in the current study alongside some prior research 'form in the inflammatory area (see here). I for one, am keenly awaiting further investigations perhaps including a study or two on offspring autism risk among mothers with autoimmune thyroiditis [3]...?To close: California Über Alles. Let moshing commence...----------[1] Brown AS. et al. Maternal thyroid autoantibody and elevated risk of autism in a national birth cohort. Prog Neuropsychopharmacol Biol Psychiatry. 2015 Mar 3;57:86-92.[2] Lampi KM. et al. Finnish Prenatal Study of Autism and Autism Spectrum Disorders (FIPS-A): overview and design. J Autism Dev Disord. 2011 Aug;41(8):1090-6.[3] Molloy CA. et al. Familial autoimmune thyroid disease as a risk factor for regression in children with Autism Spectrum Disorder: a CPEA Study. J Autism Dev Disord. 2006 Apr;36(3):317-24.----------Brown, A., Surcel, H., Hinkka-Yli-Salomäki, S., Cheslack-Postava, K., Bao, Y., & Sourander, A. (2015). Maternal thyroid autoantibody and elevated risk of autism in a national birth cohort Progress in Neuro-Psychopharmacology and Biological Psychiatry, 57, 86-92 DOI: 10.1016/j.pnpbp.2014.10.010... Read more »

Brown, A., Surcel, H., Hinkka-Yli-Salomäki, S., Cheslack-Postava, K., Bao, Y., & Sourander, A. (2015) Maternal thyroid autoantibody and elevated risk of autism in a national birth cohort. Progress in Neuro-Psychopharmacology and Biological Psychiatry, 86-92. DOI: 10.1016/j.pnpbp.2014.10.010  

  • January 14, 2015
  • 03:54 PM

The hidden neurological impact of explosions on military members

by Dr. Jekyll in Lunatic Laboratories

More bad news for war Veterans, the brains of some Iraq and Afghanistan combat veterans who survived blasts from improvised explosive devices (IEDs) and died later of other causes show a distinctive honeycomb pattern of broken and swollen nerve fibers throughout critical brain regions, including those that control executive function. The pattern is different from brain damage caused by car crashes, drug overdoses or collision sports, and may be the never-before-reported signature of blast injuries suffered by soldiers as far back as World War I.... Read more »

Ryu J, Horkayne-Szakaly I, Xu L, Pletnikova O, Leri F, Eberhart C, Troncoso JC, & Koliatsos VE. (2014) The problem of axonal injury in the brains of veterans with histories of blast exposure. Acta neuropathologica communications, 2(1), 153. PMID: 25422066  

  • January 14, 2015
  • 05:11 AM

Autism research in Jamaica

by Paul Whiteley in Questioning Answers

For the past couple of years I've been tracking some rather interesting publications coming out of data from Jamaica on the topic of autism / autism spectrum disorder (ASD) specifically looking at the possible overlap between genes and various environmental factors. I thought now would be a good time to bring this collection of papers to the blogging table and summarise their findings based on the analysis of data collected from The Jamaican Autism study. The fact that their latest research foray mentions some of the genetics of glutathione [2] with autism in mind is very interesting in light of some other findings in this area (see here). There's more on this shortly.You're not Absolem. I'm Absolem. Stupid girl.So:Study 1: Maternal and paternal age are jointly associated with childhood autism in Jamaica [2].Higher parental age - both mother and father age - seemed to be associated with a diagnosis of autism/ASD in offspring. Higher maternal age in particular, survived further statistical analysis as being a potentially important factor. This is a topic which has cropped up in autism research circles before (see here).Study 2: Seafood consumption and blood mercury concentrations in Jamaican children with and without autism spectrum disorders [3]."Our findings do not support an association between blood mercury concentrations measured in Jamaican children 2–8 years of age and ASD case status." Such a conclusion was based on the analysis of blood mercury concentrations between ASD cases and a control group, and took into account important factors such as seafood consumption bearing in mind what is known about such a foodstuff and environmental exposures (see here).Study 3: The role of drinking water sources, consumption of vegetables and seafood in relation to blood arsenic concentrations of Jamaican children with and without Autism Spectrum Disorders [4].Blood arsenic levels were the focal point of this study, and a familiar conclusion to the previous study: "Our results do not support an association between postnatal total blood arsenic measured in Jamaican children 2-8 years of age and ASD case status." Again the consumption of certain foodstuffs seemed to be important correlates related to any elevated levels of arsenic detected.Study 4: Role of fruits, grains, and seafood consumption in blood cadmium concentrations of Jamaican children with and without Autism Spectrum Disorder [5].Cadmium levels this time around, and again: "we did not find any significant differences between ASD cases and typically developing (TD) controls with respect to the 75th percentile of blood cadmium concentrations." Food (yes again) seemed to be a good correlate linked to differences in blood cadmium levels.Study 5: Blood manganese concentrations in Jamaican children with and without autism spectrum disorders [6].Manganese, and wait for it... "Our results do not indicate a relationship between postnatal BMC [blood manganese concentrations] and ASD case status of Jamaican children ages 2–8 years."Study 6: Blood Lead Concentrations in Jamaican Children with and without Autism Spectrum Disorder [7].Lead (Pb), a favourite topic of this blog, was the metal of choice when it came to analysis to see if there was any connection between the stuff and autism. Er,... "Our results do not support an association between postnatal blood lead concentration measured in Jamaican children 2–8 years of age and ASD case status."I think you can see the trend coming out of this data examining samples of children living in Jamaica with and without autism. Perhaps just as important are the various discussions about the ways and means that participants might have been exposed to these various metals and how one needs to be aware of how food in particular, could be a significant source of exposure. This perhaps puts a new slant on previous studies which have suggested an increased body burden of certain metals to be associated with autism (see here) and the question of whether dietary sources of such metals have adequately been taken into account. Don't get me wrong, I'm still very keen to see more 'metallomics' applied to autism research (see here), perhaps just controlling for a few more potentially important confounders.The Jamaican Autism study also provides quite a nice template for setting up further geographically distinct initiatives to compare and contrast with/against. I note for example that the recent study from Hodgson and colleagues [8] looking at autism in Oman (itself the topic of quite a few peer-reviewed publications) suggested some rather different results for their cohort: "Mercury levels were markedly elevated in the hair of autistic subjects vs. control subjects" albeit based on hair analysis not blood. With the previous caveat about confounders in operation, one wonders whether there may be more to see across different countries particular when bringing into play the potential importance of that glutathione connection which has also previously received some mention in the Jamaican autism studies [9].And then some music. Jamaica and music, mmm... One Love.----------[1] Rahbar MH. et al. nteraction between GSTT1 and GSTP1 allele variants as a risk modulating-factor for autism spectrum disorders. Research in Autism Spectrum Disorders. 2015; 12: 1-9.[2] Rahbar MH. et al. Maternal and paternal age are jointly associated with childhood autism in Jamaica. J Autism Dev Disord. 2012 Sep;42(9):1928-38.[3] Rahbar MH. et al. Seafood consumption and blood mercury concentrations in Jamaican children with and without autism spectrum disorders. Neurotox Res. 2013 Jan;23(1):22-38.[4] Rahbar MH. et al. The role of drinking water sources, consumption of vegetables and seafood in relation to blood arsenic concentrations of Jamaican children with and without Autism Spectrum Disorders. Sci Total Environ. 2012 Sep 1;433:362-70.[5] Rahbar MH. et al. Role of fruits, grains, and seafood consumption in blood cadmium concentrations of Jamaican children with and without Autism Spectrum Disorder. Res Autism Spectr Disord. 2014 Sep 1;8(9):1134-1145.[6] Rahbar MH. et al. Blood manganese concentrations in Jamaican children with and without autism spectrum disorders. Environ Health. 2014 Aug 23;13:69.[7] Rahbar MH. et al. Blood Lead Concentrations in Jamaican Children with and without Autism Spectrum Disorder. Int J Environ Res Public Health. 2014 Dec 23;12(1):83-105.[8] Hodgson NW. et al. Decreased glutathione and elevated hair mercury levels are asso... Read more »

Rahbar MH, Samms-Vaughan M, Loveland KA, Pearson DA, Bressler J, Chen Z, Ardjomand-Hessabi M, Shakespeare-Pellington S, Grove ML, Beecher C.... (2012) Maternal and paternal age are jointly associated with childhood autism in Jamaica. Journal of autism and developmental disorders, 42(9), 1928-38. PMID: 22230961  

  • January 13, 2015
  • 02:07 PM

Genetic brain disorders start at the synapse

by Dr. Jekyll in Lunatic Laboratories

As we’ve seen from research featured here at the lab, there are many genetic disorders that cause intellectual disability and autism. Historically, these were viewed as untreatable. However, in recent years we have shown via animal models that it is possible to reverse the effects of these gene mutations. But the question remained whether different gene mutations disrupt common physiological processes. If this were the case, a treatment developed for one genetic cause of autism and intellectual disability might be useful for many others.... Read more »

  • January 13, 2015
  • 04:58 AM

Autism diagnosis as a predictor of slow colonic transit

by Paul Whiteley in Questioning Answers

Slow colonic transit is all about issues with the speed of gastrointestinal (GI) motility and how as well as deriving nourishment from our food/drink, the other important task which our gut undertakes is the removal of waste, which it generally does pretty well. The paper by Zainab Ridha and colleagues [1] suggested that a diagnosis of autism might be over-represented when it came to their review of children referred for "nuclear transit studies", that is measuring bowel transit by means of using a radiotracer. Indeed the authors note: "Neuropsychiatric disorders, in particular autism, are useful predictors of STC [slow transit constipation] and FFR [functional fecal retention] in children". I think we might have previously seen snippets of these results in another publication too [2].You might feel a sharp scratch...It's not new news that functional bowel disorders such as constipation and diarrhoea tend to be quite frequent issues accompanying quite a few cases of autism. I've covered some of the research on this topic before on this blog (see here). I might in particular, draw your attention to the meta-analysis by Barbara McElhanon and colleagues [3] (open-access) that concluded: "Children with ASD [autism spectrum disorder] experience significantly more general GI symptoms than comparison groups".Although there is now pretty widespread acceptance that bowel issues can and often do accompany autism, there is still a degree of reticence to talk about what might be causing such issues and what *might* be done about them [4], specifically when approached in the context of more serious underlying bowel disorders potentially being linked to said functional bowel issues (see here). I hark back to one of my first ramblings on this topic which was titled: 'Should I mention gastrointestinal symptoms in autism?' as an example of how delicate an area of investigation this was/is.I'd like to think that the paper from Ridha et al might however continue to open this research area up and highlight how the so-called gut-brain axis is growing in both acceptance and understanding. The additionally interesting data from the authors suggesting that: "15.8 % of patients with constipation were obese, compared to 6.4 % in the general Australian paediatric population" whilst not necessarily autism-exclusive might also stimulate further interest in light of the analysis of weight and activity with autism in mind too (see here). Oh, and that nutritional deficiency and a higher body mass index (BMI) might also be another curious combination for some on the autism spectrum [5].I'm going to chance my [speculating] luck and say that among the many factors potentially involved in these combined factors, a role for those trillions of wee beasties that call us home (the gut microbiome) might also show some involvement...Music: Joe Cocker - With A Little Help From My Friends (RIP).----------[1] Ridha Z. et al. Predictors of slow colonic transit in children. Pediatr Surg Int. 2014 Dec 31.[2] Croaker D. et al. PO-0110 Predictors Of Slow Colonic Transit In Children. Arch Dis Child 2014; 99: A285.[3] McElhanon BO. et al. Gastrointestinal symptoms in autism spectrum disorder: a meta-analysis. Pediatrics. 2014 May;133(5):872-83.[4] Coccolrullo P. et al. Lactobacillus reuteri (DSM 17938) in Infants with Functional Chronic Constipation: A Double-Blind, Randomized, Placebo-Controlled Study. J Peds. 2010; 157: 598-602.[5] Shmaya Y. et al. Nutritional deficiencies and overweight prevalence among children with autism spectrum disorder. Res Dev Disabil. 2014 Dec 19;38C:1-6.----------Ridha Z, Quinn R, & Croaker GD (2014). Predictors of slow colonic transit in children. Pediatric surgery international PMID: 25549892... Read more »

Ridha Z, Quinn R, & Croaker GD. (2014) Predictors of slow colonic transit in children. Pediatric surgery international. PMID: 25549892  

  • January 12, 2015
  • 08:26 PM

Volcanic eruptions partially explain global warming hiatus

by Jonathan Trinastic in Goodnight Earth

The well-known global warming hiatus since 2000 has been partially explained by recent data from satellite measurements showing that sulfate emissions from volcanic eruptions is reflecting incoming sunlight.... Read more »

Santer, B., Solomon, S., Bonfils, C., Zelinka, M., Painter, J., Beltran, F., Fyfe, J., Johannesson, G., Mears, C., Ridley, D.... (2014) Observed multi-variable signals of late 20th and early 21st century volcanic activity. Geophysical Research Letters. DOI: 10.1002/2014GL062366  

  • January 12, 2015
  • 05:08 PM

Study shows rise in mass die-offs

by Dr. Jekyll in Lunatic Laboratories

You really don’t hear much about mass die-offs from mainstream news outlets; this might make you think they don’t happen that often. However, an analysis of 727 mass die-offs of nearly 2,500 animal species from the past 70 years has found that such events are increasing among birds, fish, and marine invertebrates. At the same time, the number of individuals killed appears to be decreasing for reptiles and amphibians, and is unchanged for mammals.... Read more »

Samuel B. Fey, Adam M. Siepielski, Sébastien Nusslé, Kristina Cervantes-Yoshida, Jason L. Hwan, Eric R. Huber, Maxfield J. Fey, Alessandro Catenazzi, & Stephanie M. Carlson. (2015) Recent shifts in the occurrence, cause, and magnitude of animal mass mortality events. Proceedings of the National Academy of Sciences of the United States of America. info:/10.1073/pnas.1414894112

  • January 12, 2015
  • 10:24 AM

Collective Personality and Our Environment

by Miss Behavior in The Scorpion and the Frog

We are all familiar with the concept of the personality of an individual. We are less familiar with group- or collective personalities (although most teachers can tell you at length about the personalities of each of their classes). The concept is the same: whereas an individual personality relates to an individual’s consistent behaviors across time and contexts, a collective personality relates to a group’s consistent behaviors across time and contexts. Collective personalities can be strongly influenced by the composition and size of the animal group, but also by the environment. A social spider web by Harvey Barrison at Wikimedia Commons. This week at Accumulating Glitches I talk about how the environment influences group personalities in social spiders. Check it out here. And to learn more, check this out: Modlmeier, A., Forrester, N., & Pruitt, J. (2014). Habitat structure helps guide the emergence of colony-level personality in social spiders Behavioral Ecology and Sociobiology, 68 (12), 1965-1972 DOI: 10.1007/s00265-014-1802-z ... Read more »

  • January 11, 2015
  • 08:02 PM

Police Brutality And The Efficacy Of Body-Worn Cameras

by Alexis Delanoir in How to Paint Your Panda

In a study entitled "The Effect of Police Body-Worn Cameras on Use of Force and Citizen's Complaints Against the Police: A Randomized Controlled Trial," published in the Journal of Quantitative Criminology, Ariel et al. review what is the first scientific report on the topic of whether or not police body-worn cameras work in terms of decreasing the rate of excessive force by police. As the title suggests, it also reviewed the effects of body-worn cameras on the rate of complaints raised by citizens against the police for excessive use of force.... Read more »

  • January 11, 2015
  • 03:10 PM

Being angry might be good for your health

by Dr. Jekyll in Lunatic Laboratories

In the US and many Western countries, people are urged to manage feelings of anger or suffer its ill effects. We are raised to, for a large part, stifle our emotions and to “not be so angry.” However, new research with participants from the US and Japan suggests that anger may actually be linked with better, not worse, health at least in certain cultures.... Read more »

Kitayama S., J. M. Boylan, Y. Miyamoto, C. S. Levine, H. R. Markus, M. Karasawa, C. L. Coe, N. Kawakami, G. D. Love, & C. D. Ryff. (2015) Expression of Anger and Ill Health in Two Cultures: An Examination of Inflammation and Cardiovascular Risk. Psychological Science. DOI:  

  • January 10, 2015
  • 03:54 PM

Experiment showcasing humanity’s ‘dark side’ may offer a way to control it

by Dr. Jekyll in Lunatic Laboratories

It was an infamous experiment, one on obedience and reprehensible behavior done in 1961. With memories of Holocaust atrocities and the prosecution of Nazi officials at Nuremberg still fresh, psychologist Stanley Milgram made history. You may not remember the name per say, but chances are you know his work.... Read more »

  • January 10, 2015
  • 10:31 AM

Neuromyths and the disconnect between science and the public

by neurosci in Neuroscientifically Challenged

When the movie Lucy was released in the summer of 2014, it was quickly followed by a flurry of attention surrounding the idea that we only use 10% of our brains. According to this perspective, around 90% of our neurons lie dormant, all the while teasing us by reminding us that we have only achieved a small fraction of our human potential. In the movie, Scarlet Johansson plays a woman who takes an experimental new drug that makes her capable of using upwards of 90% of her brain. Due to this sudden enhancement in brain utilization, she develops unprecedented cognitive abilities, as well as some extrasensory capabilities like telepathy and telekinesis. Thus, the plot of the movie actually hinges on the accuracy of the 10% of the brain idea. Unfortunately, it is an idea that has at this point been thoroughly debunked. In truth, it appears that all of our brain is active fairly constantly. Although some areas may be more active at times than others, there are no areas that ever go completely dark.Despite this understanding of full-brain utilization being widely endorsed throughout the scientific community, the 10% of the brain myth is still accepted as true by a significant proportion of the public (which might explain why Lucy was able to rake in close to $460 million worldwide). In fact, a recent survey of educators in five different countries--the United Kingdom, The Netherlands, Turkey, Greece, and China--found that the percentage of teachers who believe in the 10% of the brain myth ranges from a low of 43% in Greece to a high of 59% in China.The same survey identified a number of other inaccurate beliefs about the brain held by educators--beliefs that have come to be categorized as neuromyths. For example, 44-62% of teachers believed that consuming sugary drinks and snacks would be likely to affect the attention level of their students. The idea that sugar intake can decrease children's attention and increase their hyperactivity has been around since the 1970s. The first formal study to identify a relationship between sugar and hyperactivity was published in 1980, but it was an observational study without the ability to make any determination of a causal relationship. Since then more than a dozen placebo-controlled studies have been conducted, but a relationship between sugar and hyperactivity has not been supported. In fact, some studies found sugar to be associated with decreased activity. Yet, if you spend an afternoon at a toddler's birthday party, your chances of overhearing a parent attributing erratic toddler behavior to cake are around 93% (okay, that's a made-up statistic but the chances are high).According to the survey, a large percentage (ranging from 71% in China to 91% in the U.K.) of teachers in the countries mentioned above also believe that hemispheric dominance is an important factor in determining individual differences in learning styles. In other words, they believe that some people think more with their "left brain" and others more with their "right brain," and that this lateralization of brain function is reflected in personalities and learning styles. The concept of hemispheric dominance has been an oft-discussed one in neuroscience since the 1860s when Paul Pierre Broca identified a dominant role for the left hemisphere (in most individuals) in language. Since the middle of the twentieth century, however, the concept of hemispheric dominance has been extrapolated to a number of functions other than language. Many now associate the right side of the brain with creativity and intuitive thinking, while the left side of the brain is linked to analytical and logical thought. By extension, people who are creative are sometimes said to be more "right-brained," while those who are more analytical are said to be "left-brained."These broad characterizations of individuals using one side of their brain more than the other, however, are not supported by research. Although there are certain behaviors that seem to rely more on one hemisphere than the other--language and the left hemisphere being the best example--overall the brain functions as a whole and in general an individual doesn't preferentially use one hemisphere more based on his personality. Still, this myth has become so pervasive that a recommendation that children be identified as right-brained or left-brained and teaching approaches be modified accordingly has even made its way into educational texts.Where do neuromyths come from?Neuromyths are not generally created nor spread with malicious intent. Although there may be instances where inaccurate neuroscience information is used by entrepreneurs hoping to convince the public of the viability of a dubious product, usually neuromyths arise out of some genuine scientific confusion. For example, the misconception that sugar causes hyperactivity in children was bolstered by a study that did detect such an effect. The scientific status of the hypothesis, however, was forced to remain in limbo for a decade until more studies could be conducted. Those subsequent, better-designed studies failed to find a relationship, but by that time the myth had taken on a life of its own. The fact that it was so easy for parents to mistakenly attribute poor behavior to a previous sugary treat helped to sustain and propagate the inaccuracy.So, some neuromyths are born from a published scientific finding that identifies a potential relationship and grow simply because it then takes time--during which faulty information can spread--to verify such a finding. Many myths also arise, however, from inherent biases--both personal and cultural--or the misinterpretation of data. At times, the sheer complexity of the field of neuroscience may be a contributing factor, as it may cause people to seek out overly simplistic explanations of how the brain works. These oversimplifications can be alluring because they are easy to understand, even if at times they are not fully accurate. For example, the explanation of depression--a disorder with a complex, and still not understood etiology--as being attributable to an imbalance of one neurotransmitter (i.e. serotonin) was popular in scientific and public discourse for decades before being recognized as too simplistic. After the scientific community has untangled any confusion that may have led to the creation of a neuromyth, it still takes quite a long time for the myth to die out. In part, this is because there is a disconnect between the information that is readily available to the public and that which is accessible to the scientific community. Most of the general public do not read academic journals. So, if several studies that serve to debunk a neuromyth are published over the course of a few years, the public may be unaware of these recent developments until the findings are communicated to them in some other form (e.g. a website or magazine that has articles on popular science topics).Eventually this knowledge does find its way into the public discourse, though, it's just a question of when. The 10% of the brain myth, for example, has probably lasted for at least a century. But by 2014 enough of the non-scientific community was aware of the inaccuracies in the plot of Lucy to raise something of an uproar about them. There are other neuromyths, however, that have more recently become part of public knowledge, and thus we are likely to see them come up again and again over the next several years before widespread appreciation of their erroneousness emerges.The myth of three, a current neuromythOne example of a (relatively) recently espoused neuromyth is sometimes referred to as the "myth of three." The underlying idea of the myth of three is that there is a critical period between birth and three years of age, during which most of the major events of early brain development occur. This is a time when there is extensive synaptogenesis--a term for the formation of new connections between neurons--occurring. According to the myth of three, if the external environment during this time isn't conducive to learning or healthy brain development, the effects can range from a missed--and potentially lost--opportunity for cognitive growth to irreversible damage. Conversely, by enriching a child's environment during these first three years, you can increase the chances he will grow up to be the next Doogie Howser, MD. In other words, ages 0 to 3 represent the most important years of a child's learning life and essentially determine the course for his or her future cognitive maturation. Hillary Clinton summarized the myth of three appropri... Read more »

Howard-Jones, P. (2014) Neuroscience and education: myths and messages. Nature Reviews Neuroscience, 15(12), 817-824. DOI: 10.1038/nrn3817  

  • January 9, 2015
  • 04:36 PM

Humans keep the memories accurate by forgetting

by Dr. Jekyll in Lunatic Laboratories

Your brain is a memory powerhouse, constantly recording experiences in long-term memory. Those memories help you find your way through the world: Who works the counter each morning at your favorite coffee shop? How do you turn on the headlights of your car? What color is your best friend’s house? But then your barista leaves for law school, you finally buy a new car and your buddy spends the summer with a paint brush in hand. Suddenly, your memories are out of date. So what do you do, forget about it.... Read more »

Kim G, Lewis-Peacock JA, Norman KA, & Turk-Browne NB. (2014) Pruning of memories by context-based prediction error. Proceedings of the National Academy of Sciences of the United States of America, 111(24), 8997-9002. PMID: 24889631  

  • January 8, 2015
  • 05:33 PM

Music takes the pain away post surgery

by Dr. Jekyll in Lunatic Laboratories

In today’s society, when it is so easy to over medicate children and adults alike it is nice to finally read something that looks for an alternative option. This particular case deals with pain management in children post surgery and the study shows that pediatric patients who listened to 30 minutes of songs by Rihanna, Taylor Swift and other singers of their choosing — or audio books — had a significant reduction in pain after major surgery.... Read more »

  • January 8, 2015
  • 04:49 AM

Abdominal discomfort syndrome in a subset of ME/CFS

by Paul Whiteley in Questioning Answers

"The findings show that ADS [abdominal discomfort syndrome] is a characteristic of a subset of patients with ME/CFS [Myalgic Encephalomyelitis / Chronic Fatigue Syndrome] and that increased bacterial translocation (leaky gut) is associated with ADS symptoms."Right there. God does not build in straight lines.So said the study by Michael Maes and colleagues [1] looking at both gastrointestinal (GI) symptom presentation in diagnosed cases of ME/CFS and "the IgA and IgM responses directed against commensal bacteria" - rough translation: an immune system response against some of those microscopic beasties that call us home (residing in our deepest, darkest recesses). Leaky gut by the way, is something that I'm particularly interested in on this blog for quite a few different reasons (see here) and refers to potential issues with the barrier separating the contents of our GI tract from the wider body and the ever-vigilant immune system. Dysfunction of said barrier might mean that an immune response against bacteria are more likely as per a certain Sutterella finding in autism research a few years back. And before you ask, yes, leaky gut is a real concept despite some who would say otherwise...The term 'abdominal discomfort syndrome' akin, I think, to something around irritable bowel syndrome based on the results of the cluster analysis "performed on gastro-intestinal symptoms" by Maes et al, is an interesting finding. It is not necessarily new news that there may be sub-groups of people described under the label of ME/CFS, one of which might be a 'gut related subgroup' (see here). Indeed, gut inflammation has been mentioned on more than one occasion [2] with something of a connection to the presentation of more functional bowel issues.What is perhaps novel about the Maes findings is the authors' assertion that their study results point to: "a pathway phenotype, i.e bacterial translocation, that is related to ME/CFS and ADS/IBS and that may drive systemic inflammatory processes." This comes on the back of other evidence suggesting that issues with gut permeability associated with the process of bacterial translocation may be present in cases of ME/CFS and potentially amenable to intervention [3] (although I hasten to add that further research is required on this topic).Michael Maes is quite a prolific peer-reviewed author when it comes to ME/CFS tapping into some really, really interesting areas of research such as mitochondrial dysfunction [4], oxidative stress [5] and autoimmunity [6]. This latest research venture adds further to the notion that genetics and biology are the drivers of quite a large proportion of cases covered under the umbrella term 'overlapping fatigue syndromes' [7].And then some music. How about Yellow from Coldplay?----------[1] Maes M. et al. Evidence for the existence of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) with and without abdominal discomfort (irritable bowel) syndrome. Neuro Endocrinol Lett. 2014 Nov 2;35(6):445-453.[2] Lakhan SE. & Kirchgessner A. Gut inflammation in chronic fatigue syndrome. Nutr Metab (Lond). 2010 Oct 12;7:79.[3] Maes M. et al. Normalization of the increased translocation of endotoxin from gram negative enterobacteria (leaky gut) is accompanied by a remission of chronic fatigue syndrome. Neuro Endocrinol Lett. 2007 Dec;28(6):739-44.[4] Morris G. & Maes M. Mitochondrial dysfunctions in myalgic encephalomyelitis/chronic fatigue syndrome explained by activated immuno-inflammatory, oxidative and nitrosative stress pathways. Metab Brain Dis. 2014 Mar;29(1):19-36.[5] Morris G. & Maes M. Oxidative and Nitrosative Stress and Immune-Inflammatory Pathways in Patients with Myalgic Encephalomyelitis (ME)/Chronic Fatigue Syndrome (CFS). Curr Neuropharmacol. 2014 Mar;12(2):168-85.[6] Morris G. et al. The emerging role of autoimmunity in myalgic encephalomyelitis/chronic fatigue syndrome (ME/cfs). Mol Neurobiol. 2014 Apr;49(2):741-56.[7] Whiteley P. et al. Correlates of Overlapping Fatigue Syndromes. Journal of Nutritional and Environmental Medicine. 2014; 14: 247-259.----------Maes M, Leunis JC, Geffard M, & Berk M (2014). Evidence for the existence of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) with and without abdominal discomfort (irritable bowel) syndrome. Neuro endocrinology letters, 35 (6), 445-453 PMID: 25433843... Read more »

  • January 7, 2015
  • 09:06 PM

New antibiotic may help slow drug resistance

by Dr. Jekyll in Lunatic Laboratories

Antibiotic resistance, a hot topic lately here at the labs, as evidence by this recent post. So it is fortuitous that I stumbled upon this little bit of research that suggests scientists (using a “revolutionary” approach) have devised an antibiotic that may offset the mounting problem of drug resistance for decades… hopefully.... Read more »

Ling LL, Schneider T, Peoples AJ, Spoering AL, Engels I, Conlon BP, Mueller A, Schäberle TF, Hughes DE, Epstein S.... (2015) A new antibiotic kills pathogens without detectable resistance. Nature. PMID: 25561178  

  • January 7, 2015
  • 04:55 AM

Inflaming inflammation and autism: linking microglial activation and neuronal activity

by Paul Whiteley in Questioning Answers

It has been quite a few weeks since the publication of the paper by Simone Gupta and colleagues [1] (open-access) talking about "observations [that] provide pathways and candidate genes that highlight the interplay between innate immunity and neuronal activity in the aetiology of autism."I'm a wrecker. I wreck things, professionally. I mean.At the time of publication in early December (2014), there was quite a bit of media interest in the findings as per reports such as this one and this one. The watch-words were 'inflammation', 'brain' and 'immune response' as per the discovery that microglia - the constant gardeners - might play quite an important role in the process of inflammation or at least "implicating dysregulated microglial responses in concert with altered neuronal activity-dependent genes in autism brains."The Gupta paper is open-access so no need for the long explanation from me. Still a few points are worth mentioning bearing in mind my novice status in this area:The name of the game was transcriptomics, yet another -omic to add to your growing -omic dictionary, this time looking at "the complete set of RNA transcripts that are produced by the genome, under specific circumstances or in a specific cell."Said method was applied to RNA sequencing in "autism brains" or at least specific parts of the brain donated by families of 32 deceased people with autism and 40 asymptomatic controls. If you are really interested, cortical samples were analysed looking at some regions already discussed in the autism research literature (see here). I apologise for the cold, scientific discussions by the way given first and foremost those brain samples were very precious offerings.Differences in genetic expression were found between the groups which were further examined via gene ontology (GO!) and something called "weighted gene correlation network analysis" which as the name suggests looks at correlating genes which are co-expressed "to identify discrete gene modules based on co-expression between genes." One of the best hits the authors got was in relation to "enrichment for M2-microglial cell states... and the GO term ‘Type I Interferon pathway’". The type I Interferon pathway includes the name 'interferon' which implicates immune function (see here).Ergo, "evidence for type I interferon and M2-activation state abnormalities in autism that may lead to a variety of pathologic and phenotypic consequences." The authors speculate that "M2-activation state microglia genes" are potentially 'driven' by the interferon response which brings us back to those headlines about brain inflammation being 'common' in autism. The idea that neuronal activity-dependent genes might also be 'affected' by this state unites immune function and brain development with at least the cohort of cases of autism in mind. I might also add that whilst interest focused on the microglia - interferon connection, the GO category enrichment data also picked up a few other potentially interesting connections including "defense response to virus" and "response to virus". Indeed, the authors summarised by suggesting: "These data provide support for a mechanistic connection for viral-infection hypotheses... for autism with neural over-growth hypotheses... through the novel identification of exaggerated M2 activation states in autism brain tissue." Parts of Johns Hopkins, where quite a few of the authors are based, have some speciality in this area as per other research teams (see here) so are perhaps ideally placed to follow this work up as and when required.Accepting that studying brains from the deceased is still an area fraught with some methodological issues not least because the diagnosis of autism very rarely exists in clinical isolation some comorbidity of which can impact on the reasons for early mortality, inflammation and autism already has quite a bit of research history when it comes to the peer-reviewed arena. The genetics of the immune system being implicated in autism is also not new news as per other entries on this blog (see here) and my already linking to some discussions about the Nardone paper [2] last year (2014) also implicating epigenetic processes too. Microglia and autism? Well again, been there and seen that similarly applies (see here).Interestingly, in some of the accompanying press attached to the Gupta study is the suggestion that future work might look to "find out whether treating the inflammation could ameliorate symptoms of autism." Approaching such a sentiment with some degree of caution, I'd be minded to suggest that such ideas seem to follow a pattern in psychiatry these days (see here) further to the idea that the chemistry of inflammation seems to be connected to at least some autism [3] (see here and see here too). Peter over at the Epiphany blog has, as well as covering the Gupta study, talked about quite a few ways and means that one might go about 'treating' such inflammation. What I would perhaps add - alongside my caveat about this blog not giving medical or clinical advice - is that rather than just focusing on the agents potentially 'causing' inflammation, one might also look at the counter-balance systems also present, as per my discussions on some fairly recent work from Harumi Jyonouchi and colleagues [4] and the so-called anti-inflammatory cytokines such as IL-10 (see here). Just a thought...The Blue Danube to close... (music starts at 1min 40secs)----------[1] ... Read more »

  • January 6, 2015
  • 06:11 PM

Tropical forests absorbing more carbon dioxide than previously thought

by Jonathan Trinastic in Goodnight Earth

New analyses of theoretical models backed by experimental measurements indicate that tropical forests are absorbing much more CO2 than previously known!... Read more »

Schimel D, Stephens BB, & Fisher JB. (2014) Effect of increasing CO2 on the terrestrial carbon cycle. Proceedings of the National Academy of Sciences of the United States of America. PMID: 25548156  

  • January 6, 2015
  • 01:16 PM

Lots of selfies may suggest you’re a narcissist

by Dr. Jekyll in Lunatic Laboratories

Well I’ve got some bad news to all you selfie fanatics out there, a new study showed that men who posted more online photos of themselves than others scored higher on measures of narcissism and psychopathy. The study looked exclusively at men, however the men out there should have no fear, there is a follow up study being done with women as well.... Read more »

  • January 6, 2015
  • 04:40 AM

Olanzapine, gut bacteria and weight gain in mice

by Paul Whiteley in Questioning Answers

"These results collectively provide strong evidence for a mechanism underlying olanzapine-induced weight gain in mouse and a hypothesis for clinical translation in human patients."That was the summary statement derived from data published by Andrew Morgan and colleagues [1] (open-access) looking at how some of those trillions of wee beasties which colonise humans and animals (the microbiome) may very well influence response to medicines... at least in mice. The authors' specific focus on one of the important side-effects of taking neuroleptics (antipsychotics) - weight gain - also potentially invites some new research directions when it comes to curbing such an important issue.I had so many evil plans in the works - the illiteracy beam, typhoon cheese, robo-sheep...I want to get one thing straight before I go further into the Morgan results: this is not a post designed to 'bash' pharmaceutics such as antipsychotics. Not many people would really want to spend [part of] their lives taking antipsychotics if they could really help it, but this class of medicines, with all their faults, quite a few by all accounts [2], do provide something of a service in terms of their impact on symptom presentation in certain states/diagnoses and perhaps most importantly, a "decreased mortality" compared with no treatment [3]. That all being said, I'm very much in favour of research getting to the core reasons why a condition like schizophrenia (one of the conditions managed by antipsychotic use) may present in the first place over and above just managing symptoms by pharmacotherapy and/or other means as and when they occur. I think most people would agree with that sentiment. That and ensuring that antipsychotics are not over-used [4].Back to the Morgan paper which is open-access but for which I'd like to summarise a few salient points before passing further comment:This was a mouse study. I'll repeat that: this was a mouse study. Researchers started from the idea that "the commensal microbiome of the mammalian gut in health and disease has become a topic of intense study". I can't disagree with that given my previous ramblings on this topic over the years (see here). The idea that said gut microbiota may play a role in for example, how we metabolise certain foods and medicines, is also gaining popularity as per the notion of pharmacometabonomics [5] coined in part, by a few authors who's work has been previously talked about on this blog (see here).So: "After establishing that C57BL/6J mice gain considerable weight while consuming olanzapine" (i.e. a good mouse model) researchers set about searching for evidence that gut bacteria are "necessary and sufficient for olanzapine-induced weight gain". They did find it by the way, based on the weight differences noted in mice raised on a high-fat diet + olanzapine compared with animals raised on a high-fat diet without medication.They also looked at "the effects of olanzapine on the gut microbiome" based on the examination of faecal pellets (nice!) and "high-throughput sequencing of the bacterial 16S ribosomal RNA gene". The results again based on the diet + medication compared to just diet suggested that the medication-treated mice presented with a gut bacteria pattern that "has previously been associated with obesity in mouse and human". That and some interesting findings suggesting that: "Gut microbiota composition is correlated with weight gain" bearing in mind that correlation is not the same as causation.Finally, another important suggestion from Morgan et al: "olanzapine has direct antibacterial activity in vitro against two bacterial isolates (E. coli NC101 and E. faecalis OGIRF) derived from the mammalian gut." As per other related findings, don't just assume that medicines just have 'one mode of action' as per that listed on the package insert. Indeed other antipsychotics seem to have for example, anti-parasitic activity [6] which may be relevant to another research area of interest (see here).The authors conclude that: "In light of evidence that olanzapine has intrinsic antimicrobial activity, we propose that its actions in the gut may be analogous to the chronic low-dose antibiotic regimens used to promote weight gain in livestock." The idea also being that targeting gut bacteria during something like olanzapine therapy might have the potential to 'off-set' side-effects like weight gain as and when it occurs.Although this is very early-days research focused on mice not people, I am really quite interested in the Morgan results and where they may eventually lead. Weight gain following antipsychotic use is an important side-effect which, according to other research literature [7], can have sometimes profound effects on things like "long-term cardiac safety". Indeed, when one considers that heart health is for example, a sorely under-appreciated area when it comes to something like schizophrenia (see here), one senses that a degree of urgency is perhaps required to replicate the Morgan findings and see whether they translate into human beings also.Then comes the speculation: is there any way to mitigate the gut bacteria effects that something like olanzapine might have? I note the Morgan study relied on olanzapine being "compounded into high fat (45 kcal%) food" to simulate the oral route of administration. I do wonder whether the same effects would be observed if other administration routes were trialled, say by injection or via transdermal application [8]? Second question: do the results imply that formulating a probiotic or a pill with the bacterial species seemingly affected by olanzapine may be useful in reducing weight gain? I can't readily answer that last question but certainly there are quite a few studies out there looking at gut bacteria and issues like obesity as per my previous chatter on Akkermansia muciniphila (see here) as one example. Finally, and again with mucho mucho emphasis on my blogging caveat about not giving medical or clinical advice, is there any role to play for the not-so-nice-to-think-about intervention that is the poo transplant? I know, I know... it sounds like the stuff of nightmares but more and more, science is coming around to the idea that particularly when your life is on the line as per Clostridium difficile infection, the faecal microbiota transplantation might offer some real hope. And C. diff infection seems to be on... Read more »

Morgan AP, Crowley JJ, Nonneman RJ, Quackenbush CR, Miller CN, Ryan AK, Bogue MA, Paredes SH, Yourstone S, Carroll IM.... (2014) The Antipsychotic Olanzapine Interacts with the Gut Microbiome to Cause Weight Gain in Mouse. PloS one, 9(12). PMID: 25506936  

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