What are your thoughts on Blastocystis carriage and age? Please comment!... Read more »
Forsell J, Granlund M, Samuelsson L, Koskiniemi S, Edebro H, & Evengård B. (2016) High occurrence of Blastocystis sp. subtypes 1-3 and Giardia intestinalis assemblage B among patients in Zanzibar, Tanzania. Parasites , 9(1), 370. PMID: 27356981
Poulsen CS, Efunshile AM, Nelson JA, & Stensvold CR. (2016) Epidemiological Aspects of Blastocystis Colonization in Children in Ilero, Nigeria. The American journal of tropical medicine and hygiene, 95(1), 175-9. PMID: 27139454
A new mechanism that affects how our immune cells perform - and hence their ability to prevent disease - has been discovered by an international team of researchers. To date, researchers have identified hundreds of genetic variants that increase or decrease the risk of developing diseases from cancer and diabetes to tuberculosis and mental health disorders.
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M Zaeem Cader, Katharina Boroviak, Qifeng Zhang, Ghazaleh Assadi, Sarah L Kempster, Gavin W Sewell, Svetlana Saveljeva, Jonathan W Ashcroft, Simon Clare, Subhankar Mukhopadhyay, Karen P Brown, Markus Tschurtschenthaler, Tim Raine, Brendan Doe, Edwin R Chilvers, Jules L Griffin, Nicole C Kaneider, R Andres Floto, Mauro D'Amato, Allan Bradley, Michael J O Wakelam.... (2016) C13orf31 (FAMIN) is a central regulator of immunometabolic function. Nature Immunology. info:/10.1038/ni.3532
'Physical activity boosts kids' brain power and academic prowess' went the press release accompanying the consensus statement published by Jens Bangsbo and colleagues  (open-access).The consensus statement brought together researchers from around the world "and from a variety of academic disciplines" to emphasise how undertaking all-manner of different kinds of exercise "are still a good investment in academic achievement" when it comes to children aged between 6-18 years of age.The statement is open-access but a few choice passages are particularly worthy of highlighting including the idea that there are various positive physical effects from exercise (as if you needed telling): "Frequent moderate-intensity and, to a lesser extent, low-intensity exercise improves cardiometabolic fitness in children and youth." I might at this point also refer you to the findings by Ekelund and colleagues  that made some headlines recently suggesting that about 65-70 minutes of "moderate intensity physical activity" a day might be something to aim for across different age groups. Yes, move more.Perhaps just as important are the various associations being made between exercise and other important areas of health and well-being including that: "Physical activity before, during and after school promotes scholastic performance in children and youth" and: "Mastery of fundamental movement skills is beneficial to cognition and scholastic performance in children and youth." Being careful not to fall into the trap that is 'those who exercise are more 'smarter' than those who don't' the idea that mastering movement skills might be another positive from exercise is an important point to make. As I've said before on this blog (see here) one particular pastime ticks a lot of boxes in terms of exercise and a particular focus on fine and gross motor skills: the martial arts. Added to the fact that some important life skills can be gained from disciplines such as karate (e.g. self-confidence) and I'd be the first to advocate more children and young adults getting involved in such activities. Indeed, this is something else covered in the Bangsbo article: "Physical activity-based positive youth development programmes that have an intentional curriculum and deliberate training are effective at promoting life skills (eg, interpersonal, self-regulation skills) and core values (eg, respect and social responsibility) in children and youth."Finally, I leave you with another important point raised in the consensus statement: "Social inclusion can be promoted by providing equal access to opportunities within physical activity and sports settings regardless of children and young people's social, cultural, physical and demographic characteristics." Wearing my autism research hat, I might agree with the tenets of this point (see here) applied to the autism spectrum and how participation in sports and exercise can be a really important part of social inclusion strategies.Now, added to exercise potentially improving academic outcomes, how about some outdoor learning too and importantly, making sure that children and young people get enough [quality] sleep?---------- Bangsbo J. et al. The Copenhagen Consensus Conference 2016: children, youth, and physical activity in schools and during leisure time. Br J Sports Med. 2016 Jun 27. pii: bjsports-2016-096325. Ekelund U. et al. Does physical activity attenuate, or even eliminate, the detrimental association of sitting time with mortality? A harmonised meta-analysis of data from more than 1 million men and women. Lancet. 2016. July 27.----------Bangsbo J, Krustrup P, Duda J, Hillman C, Andersen LB, Weiss M, Williams CA, Lintunen T, Green K, Hansen PR, Naylor PJ, Ericsson I, Nielsen G, Froberg K, Bugge A, Lundbye-Jensen J, Schipperijn J, Dagkas S, Agergaard S, von Seelen J, Østergaard C, Skovgaard T, Busch H, & Elbe AM (2016). The Copenhagen Consensus Conference 2016: children, youth, and physical activity in schools and during leisure time. British journal of sports medicine PMID: 27354718... Read more »
Bangsbo J, Krustrup P, Duda J, Hillman C, Andersen LB, Weiss M, Williams CA, Lintunen T, Green K, Hansen PR.... (2016) The Copenhagen Consensus Conference 2016: children, youth, and physical activity in schools and during leisure time. British journal of sports medicine. PMID: 27354718
One of the main mysteries confounding development of an HIV vaccine is why some people infected with the virus make the desired antibodies after several years, but a vaccine can't seem to induce the same response.
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M. Anthony Moody1,2,3,*,†, Isabela Pedroza-Pacheco4,†, Nathan A. Vandergrift1,5, Cecilia Chui4, Krissey E. Lloyd1, Robert Parks1, Kelly A. Soderberg1, Ane T. Ogbe4, Myron S. Cohen6, Hua-Xin Liao1,5, Feng Gao1,5, Andrew J. McMichael, David C. Montefiori, Laurent Verkoczy, Garnett Kelsoe, Jinghe Huang, Patrick R. Shea, Mark Connors, Persephone Borrow, & Barton F. Haynes. (2016) Immune perturbations in HIV-1–infected individuals who make broadly neutralizing antibodies. Science Immunology . info:/10.1126/sciimmunol.aag0851
A diet high in saturated fat can make your brain struggle to control what you eat. If people are looking to lose weight, stay clear of saturated fat. Consuming these types of fatty food affects a part of the brain called the hypothalamus, which helps regulate hunger.
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Viggiano, E., Mollica, M., Lionetti, L., Cavaliere, G., Trinchese, G., De Filippo, C., Chieffi, S., Gaita, M., Barletta, A., De Luca, B.... (2016) Effects of an High-Fat Diet Enriched in Lard or in Fish Oil on the Hypothalamic Amp-Activated Protein Kinase and Inflammatory Mediators. Frontiers in Cellular Neuroscience. DOI: 10.3389/fncel.2016.00150
I was really, really pleased to read the paper by Melanie Uhde and colleagues  (open-access) I don't mind telling you. Covering a topic close to my blogging and research heart - sensitivity to wheat or gluten but not coeliac disease - the authors provide some much needed scientific clarification when it comes to how gluten or wheat might impact on some of those "who reported symptoms in response to wheat intake and in whom coeliac disease and wheat allergy were ruled out." Some media interest in the paper can also be seen here.With an authorship list including some of the great and good on this issue (see here for example) researchers included 80 participants presenting with non-coeliac wheat sensitivity (NCWS) according to "criteria recently proposed by an expert group" . These NCWS participants reported "experiencing intestinal and/or extraintestinal symptoms after ingestion of gluten-containing foods, including wheat, rye or barley. The reported symptoms in all subjects improved or disappeared when those foods were withdrawn for a period of 6 months, and recurred when they were re-introduced for a period of up to 1 month." All 80 provided serum samples for analysis that were compared with similar samples from 40 participants with "biopsy-proven active coeliac disease" and 40 samples from asymptomatic controls on a non-restrictive diet.The sort of information sought from those serum samples included quite a bit. Not only were "established markers" of coeliac disease (CD) assayed for - including IgA antibody to TG2 - but various immunological markers towards gluten were also included for study. Based also on the idea that "intestinal cell damage and systemic immune response to microbial components" might be an important feature of NCWS, researchers also markers associated with "compromised intestinal epithelial barrier integrity."Results: well, as per the media interest in this paper: "The findings suggest that these individuals [with NCWS] have a weakened intestinal barrier, which leads to a body-wide inflammatory immune response."A few further details are worthwhile discussing. First, the genetics of coeliac disease (those DQ2 and/or DQ8 heterodimers) were present in about a quarter of those with NCWS "a rate not substantially different than in the general population." Second, most of those with NCWS did not show the characteristic mucosal signs of CD as per the Marsh gradings (0 or 1) throughout the cohort. This was in direct contrast to the CD participants who all "expressed HLA DQ2 and/or DQ8 and presented with Marsh 3 grade intestinal histological findings." The conclusion: CD and NCWS participants are not one and the same (just in case you needed telling).Next: "Serum levels of both LBP [lipopolysaccharide (LPS)-binding protein (LBP)] and sCD14 were significantly elevated in individuals with NCWS in comparison with patients with coeliac disease and healthy individuals." This implies that there is 'systemic immune activation' on-going in those participants with NCWS not seen to the same extent in the other groups. These findings were also complemented by results indicative of that compromised intestinal epithelial barrier integrity previously discussed. The final picture emerging being one where NCWS participants seem to be in a state of 'immune activation' "linked to increased translocation of microbial and dietary components from the gut into circulation, in part due to intestinal cell damage and weakening of the intestinal barrier." I might add that some smaller scale analysis of serum samples from those NCWS participants "both before and after 6 months of a self-monitored diet free of wheat, rye and barley" suggested "a significant decline in the markers of immune activation and gut epithelial cell damage, in conjunction with the improvement of symptoms."And rest.For those as interested in this area of research as I am, I'm sure that you can understand my happiness in seeing the Uhde results and what it might mean for many, many people who've been perhaps been 'fobbed off' down the years with regards to their gluten ills. I can't help but see a possible connection between these findings and others reported with autism in mind for example (see here and see here). The added suggestion that 'intestinal cell damage' might be a feature of NCWS also possibly ties in with all that talk about 'leaky gut' and some autism (see here) but I don't doubt it may go well beyond just [some] autism . Not looking so tree-hugging now eh?Of course there is more to do in this area: "Further research is needed to investigate the mechanism responsible for the intestinal damage and breach of the epithelial barrier, assess the potential use of the identified immune markers for the diagnosis of affected individuals and/or monitoring the response to specific treatment strategies, and examine potential therapies to counter epithelial cell damage and systemic immune activation in affected individuals." I might also add in a role for those trillions of wee beasties that call our gut home (the gut microbiota) as potentially also being a target for further scientific research too (see here for example).I await further studies...---------- Uhde M. et al. Intestinal cell damage and systemic immune activation in individuals reporting sensitivity to wheat in the absence of coeliac disease. Gut. 2016. July 25. Catassi C. et al. Diagnosis of Non-Celiac Gluten Sensitivity (NCGS): The Salerno Experts’ Criteria. Nutrients. 2015;7(6):4966-4977. Whiteley P. Nutritional management of (some) autism: a case for gluten- and casein-free diets? Proc Nutr Soc. 2015 Aug;74(3):202-7.----------Uhde, M., Ajamian, M., Caio, G., De Giorgio, R., Indart, A., Green, P., Verna, E., Volta, U., & Alaedini, A. (2016). Intestinal cell damage and systemic immune activation in individuals reporting sensitivity to wheat in the absence of coeliac disease Gut DOI: 10.1136/gutjnl-2016-311964... Read more »
Uhde, M., Ajamian, M., Caio, G., De Giorgio, R., Indart, A., Green, P., Verna, E., Volta, U., & Alaedini, A. (2016) Intestinal cell damage and systemic immune activation in individuals reporting sensitivity to wheat in the absence of coeliac disease. Gut. DOI: 10.1136/gutjnl-2016-311964
A new study, which followed 180 preterm infants from birth to age seven, found that babies who were fed more breast milk within the first 28 days of life had had larger volumes of certain regions of the brain at term equivalent and had better IQs, academic achievement, working memory, and motor function.
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Mandy B. Belfort, MD, Peter J. Anderson, PhD, Victoria A. Nowak, MBBS, Katherine J. Lee, PhD, Charlotte Molesworth, Deanne K. Thompson, PhD, Lex W. Doyle, MD, & Terrie E. Inder, MBChB, MD. (2016) Breast Milk Feeding, Brain Development, and Neurocognitive Outcomes: A 7-Year Longitudinal Study in Infants Born at Less Than 30 Weeks' Gestation. The Journal of Pediatrics. DOI: http://dx.org/10.1016/j.jpeds.2016.06.045
In a Brain Post from 2012 I reviewed a study of fatigue in elite athletic performance. This study supported a key role in the brain insula in regulating the perception of exercise-induced fatigue. You can access this post by clicking HERE.An update on this topic was recently published in PloS One by a research team in Australia.This study compared performance on a cognitive task after extreme 20 minute cycling time trial. Professional cyclists were compared to recreational cyclists on the Stroop test that requires inhibitory control.The results of the study were that elite cyclists performed significantly better on the Stroop test (more correct responses) following exercise than non-elite cyclists. This is indicative of a greater resistance effects of fatigue on brain performance.The authors note in the discussion section:"These finding suggest that successful endurance performance may require superior inhibitory control and resistance to mental fatigue."This resistance to mental fatigue at high levels of exercise may be a key component in successful performance at the elite level.Inhibitory control has been shown to have a significant genetic association and to be stable over time. It is possible that training interacts with genetic factors to produce brain fatigue resistance in the elite cyclist population.Readers with more interest in this topic can access the free full-text research manuscript by clicking on the PMID link in the citation below.Follow the author on Twitter HERE.Photo of non-elite cyclist participating in triathlon is from the author's files. Martin K, Staiano W, Menaspà P, Hennessey T, Marcora S, Keegan R, Thompson KG, Martin D, Halson S, & Rattray B (2016). Superior Inhibitory Control and Resistance to Mental Fatigue in Professional Road Cyclists. PloS one, 11 (7) PMID: 27441380... Read more »
Martin K, Staiano W, Menaspà P, Hennessey T, Marcora S, Keegan R, Thompson KG, Martin D, Halson S, & Rattray B. (2016) Superior Inhibitory Control and Resistance to Mental Fatigue in Professional Road Cyclists. PloS one, 11(7). PMID: 27441380
Science headlines eh? Who would trust them and their sometimes inflated press releases?I start today with a science headline taken from the BBC website reading: "Pregnancy multivitamins 'are a waste of money'" based on the findings of a review article  published in the journal Drug and Therapeutics Bulletin.In it we are told that complex multi-vitamin and mineral supplements are 'unlikely to be needed and are an unnecessary expense' during the nine months that made us. Further that certain vitamins are not indicated for supplementation during pregnancy including that contributory to excess vitamin A. All pregnant women have to do, we are told is "to have a healthy, varied diet including fresh fruit and vegetables" and avoid the old phrase 'eating for two'. What could be simpler?The irony behind such findings and those BBC and other media headlines is that although one needs to be careful about one's vitamin and mineral intake (treat them as what they are, medicines) there is a long tradition of vitamin supplementation being indicated when it comes to that special time called pregnancy. Indeed, and I quote from the BBC article: "pregnant women should make sure they take folic acid and vitamin D, as well as eating a well-balanced diet, as per NHS guidelines, they add."So let me get this straight: don't take a multi-vitamin supplement but makes sure that you take a (multi) supplement containing folic acid and vitamin D? You can perhaps see how confusing such headlines are and how grandiose ideas that every woman pre-conceptual and during pregnancy is feasting down on 5-a-day (or even 8-a-day if you actually believe it will make you happier!) are not necessarily based in reality. We would all love to think that important health messages about maternal fruit and vegetable consumption during pregnancy for example, are being heard loud and clear but the reality is that they aren't for everyone. The reality is that people are using vitamin and mineral supplements to supplement their dietary needs for whatever reasons and headlines further confusing the population about such supplementation being a 'waste of money' is only likely to put more people off using them without perhaps giving greater thought about the ways and means to help people alter their diet accordingly. The net result: more pregnant women potentially becoming deficient in certain core nutrients during pregnancy and more potential effects/risks for her and her offspring.I do have a bee in my bonnet about this issue because time after time the research evidence points to how important pregnancy nutrition is for a variety of maternal and offspring outcomes . Outside of folic acid and vitamin D, various other nutrients are also pretty important during pregnancy (i.e. iodine - 'good for baby, good for the economy') and the unfortunate reality is that most people can't or don't get enough of them from their diet alone. The late David Barker was a pioneer in the area of foetal programming including that related to pregnancy nutrition; one can only wonder what he would make of the suggestion that universally, supplementary multivitamin use during pregnancy is a 'waste of money'?And finally, you want more people to eat fruit and vegetables? Don't focus too much on just price and positioning at the supermarket, focus on home economics (or just cookery!) classes at school  for starters and make fruit and vegetables interesting...---------- Vitamin supplementation in pregnancy. Drug & Therapeutics Bulletin. 2016. July 11. Harding JE. The nutritional basis of the fetal origins of adult disease. Int J Epidemiol. 2001 Feb;30(1):15-23. McMorrow L. et al. Perceived barriers towards healthy eating and their association with fruit and vegetable consumption. J Public Health (Oxf). 2016 May 24.----------Drug and Therapeutics Bulletin (2016). Vitamin supplementation in pregnancy Drug and Therapeutics Bulletin DOI: 10.1136/dtb.2016.7.0414... Read more »
Medication roulette, if you have ever had to deal with depression or other types of mental illness you know what I'm talking about. You take a pill that could help or could cause all sorts of horrid side effects. You cross your fingers as you take that first pill and in the 4-6 weeks it takes to start working you cross your fingers, hope, wish and probably even dread the outcome. But why does it take so long for antidepressants to start working in the first place and what could be done to change that?
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Erb, S., Schappi, J., & Rasenick, M. (2016) Antidepressants Accumulate in Lipid Rafts Independent of Monoamine Transporters to Modulate Redistribution of the G protein, Gα . Journal of Biological Chemistry. DOI: 10.1074/jbc.M116.727263
Deep space missions could increase the chances of cardiovascular diseases, thereby increasing the chances of deaths in astronauts.
NASA’s Apollo program sent 9 manned missions and 24 astronauts above the low Earth orbit (LEO) during decades of 1960s and 1970s. Those missions also included Apollo 11, which was used to take Neil Armstrong and Buzz Aldrin to the moon. However, it appears that such beyond Earth missions have their own problems.
A 1969 crew portrait of Apollo astronauts Neil Armstrong, left, Michael Collins, centre, and Buzz Aldrin. (Photograph: AP-Nasa)
A 1969 crew portrait of Apollo astronauts Neil Armstrong, left, Michael Collins, centre, and Buzz Aldrin. (Photograph: AP-Nasa)
In a study, researchers worked on the fate of Apollo astronauts and found that the chances of death from cardiovascular diseases is 4-5 times more than that found for astronauts of the same time, who only went in low Earth orbits, or never went to any orbital mission. Researchers found that the Earth’s magnetic field is protective to human body and moving beyond that protective field could result in long-lasting damage to the cardiovascular system, and deep space radiation is one of the most important reasons in that damage. Various radiations and radiation sources are present in the space such as galactic cosmic rays, radiation in the Van Allen belts, and solar particle events. Protons are among the most abundant type of radiation in space. All these start affecting the body, especially cardiovascular system of astronauts.
Although the sample size of the study is small, the results show that about 45% of the Apollo astronauts died from cardiovascular problems as compared to only 11% of low Earth orbit astronauts and 9% of non-flight astronauts. Researchers found that the rate of death from cardiovascular diseases can be compared to that of the general population, but it could be due to very fit and healthy body of astronauts and the presence of diseased conditions in general public.
Heart related system (Source: FDA)
Heart related system (Source: FDA)
“In summary, results from the present study reveal that Apollo lunar astronauts have a significantly higher mortality rate due to CVD (cardiovascular disease) than either the cohort of astronauts who never flew an orbital space mission or astronauts who never flew beyond LEO (low Earth orbit),” Researchers noted in the study.
This is the first study to look at the long-term health consequences of people moving out into deep space. It has important implications for future space missions as many space agencies with NASA are planning to move to the moon and beyond the moon to the Mars by the decade 2030.
Space missions (Image source: NASA)
Space missions (Image source: NASA)
Delp, M., Charvat, J., Limoli, C., Globus, R., & Ghosh, P. (2016). Apollo Lunar Astronauts Show Higher Cardiovascular Disease Mortality: Possible Deep Space Radiation Effects on the Vascular Endothelium Scientific Reports, 6 DOI: 10.1038/srep29901... Read more »
Delp, M., Charvat, J., Limoli, C., Globus, R., & Ghosh, P. (2016) Apollo Lunar Astronauts Show Higher Cardiovascular Disease Mortality: Possible Deep Space Radiation Effects on the Vascular Endothelium. Scientific Reports, 29901. DOI: 10.1038/srep29901
The paper by Traolach Brugha and colleagues  makes for some blogging fodder today and the suggestion that: "The combined prevalence of autism in adults of all ages in England was 11/1000."Just before going through the Brugha paper it is perhaps appropriate to put it into some context based on other work from this group previously covered on this blog (see here) and the findings again by Brugha and colleagues  (a further report on their findings that time around can be seen here).On that last occasion published in 2011, the estimated prevalence of adult autism in the UK - living in the community - was reported on, arriving at a figure of 9.8/1000. That finding was based on data from the 2007 Adult Psychiatric Morbidity Survey (APMS) and whilst important, was not without it's methodological weaknesses including the fact that: "Sampling excluded institutional residents and adults with intellectual disability severe enough to prevent them from participating in the assessment." I'll come back to the 'weakness' issues shortly also with one of the screening instruments in mind...Anyhow, the Adult Psychiatric Morbidity Survey (2007) once again formed the basis for the recent paper by Brugha added to "a population case-register survey of 290 adults with intellectual disability". Those additional 290 adults have already been discussed in another publication from this group (see here) and were collectively termed the IDCR cohort (Intellectual Disability Case Register study). I have to admit that at first I thought it was the 2014 reincarnation of the APMS that formed the bulk of the data for this latest paper - data from the publication of which is due out soon - but this was not the case as we are told that: "The sample from the first general population study was extended with the inclusion of representative samples of adults with intellectual disability omitted from the earlier survey" i.e. those additional 290 adults included as part of the IDCR study. The value added bit to the latest Brugha paper was the inclusion of adults both living in both private households or in communal care both "sampled from learning disability case registers."The 2-stage screening affair held with the 2007 APMS cohort where the the Autism-Spectrum Quotient (AQ) - the AQ20 - was the starting point, followed by the ADOS (Autism Diagnostic Observation Schedule) (module 4) as and when required. ADOS module 1 was actually the preferred assessment scheme for those IDCR study participants (module 1 "is designed for individuals who do not consistently use phrase speech") and the AQ initial screen did not seem to figure.The results: well, I've already indicated that the estimated prevalence was around 1.1% of the adult population, up from the previous 0.9% estimate. This was based on "14 men and 4 women with autism in the APMS subsample, and 49 men and 40 women with autism in the IDCR subsample." It should be noted that of the original 290 participants interviewed from the IDCR cohort, only 276 were eventually assessed for autism as a consequence of some presenting with quite profound difficulties not conducive to a "confident assessment".The authors report that estimated autism prevalence was higher in those with moderate to profound learning (intellectual) disability and that there was a 'gradient' of autism prevalence by learning disability status. A quote by the authors relays this finding perfectly: "almost two in five adults with moderate to profound intellectual disability had autism." Indeed, the link between autism and learning disability is something that has also been discussed in recent posts (see here) on this blog. Authors also observed that: "Male gender was a strong predictor of autism only in those with no or mild intellectual disability" so highlighting how the gender ratio for autism in those with moderate or profound intellectual disability was nowhere near the traditional 4:1 ratio commonly touted.Although important data filling a very important gap in terms of the estimated adult prevalence of autism here in Blighty, I would like to return to the potential 'weakness' aspect of the last and latest Brugha papers. For those who follow this blog you'll probably know that I have a few issues with one of the primary screening instruments put forward with 'autistic traits' in mind: the Autism Spectrum Quotient (AQ). It's nothing personal when it comes to my growing unease with the instrument but in these days of the 'are you autistic?' pop psychology survey (see here) I'm not convinced that (a) it is all that reliable as an accurate screening measure  for autism and (b) that it is specifically 'tuned into autism' at the expense of other possible diagnoses (see here). The fact that the AQ20 was the first stage screener for those potentially requiring subsequent ADOS-ing at least in the APMS 2007 cohort does bring into question exactly how accurate the Brugha findings are in terms of the final estimated prevalence of adult autism among those where learning disability does not feature. Indeed, even the authors in a further relevant publication have even questioned their 2-stage methodology used : "The AQ-20 was only a weak predictor of ADOS-4 cases." Hmm.To reiterate, I don't want to come down to hard on the Brugha findings because they are some of the best data we currently have when it comes to estimates of numbers of cases of adult autism in the UK. The fact that the data - systematically collected on this and the previous testing occasion - seemed to be pointing towards a significant role for learning disability when it comes to autism alongside an increase in cases when this factor is taken into consideration also plays into all those debates about whether autism is truly on the rise (see here) and what further planning and resources are going to be needed in future years. It is however only with time and continued monitoring that we will see what trends become apparent with regards to autism prevalence in adults here in the UK and what more we will see when APMS 2014 finally begins to report...To close, having watched the fantastic film Ant-Man with my brood recently, we're never going to look at Thomas the Tank Engine in quite the same light...---------- Brugha TS. et al. Epidemiology of autism in adults across age groups and ability levels. Br J Psychiatry. 2016 Jul 7. Brugha TS. et al. Epidemiology of autism spectrum disorders in adults in the community in England. Arch Gen Psychiatry. 2011 May;68(5):459-65. Ashwood KL. et al. Predicting the diagnosis of autism in adults using the Autism-Spectrum Quotient (AQ) questionnaire. Psychol Med. 2016 Jun 29:1-10. Brugha TS. et al. Validating two survey methods for ... Read more »
Brugha TS, Spiers N, Bankart J, Cooper SA, McManus S, Scott FJ, Smith J, & Tyrer F. (2016) Epidemiology of autism in adults across age groups and ability levels. The British journal of psychiatry : the journal of mental science. PMID: 27388569
A team of Toronto scientists has found similarities in brain impairments in children with autism spectrum disorder (ASD), attention deficit hyperactivity disorder (ADHD) and obsessive compulsive disorder (OCD). The study involved brain imaging of white matter in 200 children with autism, ADHD, OCD or no diagnosis.
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Ameis, S., Lerch, J., Taylor, M., Lee, W., Viviano, J., Pipitone, J., Nazeri, A., Croarkin, P., Voineskos, A., Lai, M.... (2016) A Diffusion Tensor Imaging Study in Children With ADHD, Autism Spectrum Disorder, OCD, and Matched Controls: Distinct and Non-Distinct White Matter Disruption and Dimensional Brain-Behavior Relationships. American Journal of Psychiatry. DOI: 10.1176/appi.ajp.2016.15111435
"The meta-analysis provided evidence for higher blood glutamate levels in ASD [autism spectrum disorder]."That was the research bottom-line reported by Zhen Zheng and colleagues  (open-access available here) who surveyed the current peer-reviewed science literature in this area and found something to see based on: "Twelve studies involving 880 participants and 446 incident cases."Drawing on the idea that glutamate is a rather important amino acid that plays a role in various biological processes including that related to the manufacture of GABA (see here), Zheng et al observed higher circulating blood levels of the stuff; a sort-of proxy for what might also be going on with regards to brain levels of glutamate. That "excess glutamate has been shown to be a potent neurotoxin that leads to neuronal cell death and plays a role in the pathophysiology of some neuropsychiatric disorders" is an important point to make as to the potential implications from the Zheng meta-analysis.Zheng et al do mention how important glutamate is for the purposes of GABA production and in particular, how issues with glutamate decarboxylase (GAD) - a key enzyme that converts glutamate into GABA - described in some cases of autism  might account for the elevated levels of glutamate yet the generally lower levels of GABA seen in autism (see here). I'd be inclined to agree that this is perhaps one of the more important implications for glutamate in autism; particularly when added to the whole 'glutamate linked to epilepsy' bit knowing how close a relationship autism and epilepsy seem to share (see here).Where next with this research area I hear you ask? Well, I'd like to know a little more not just about glutamate but also another linked amino acid called glutamine. It has already been talked about in the autism research literature a while back (see here) but a lot more follow-up work is required on these two important compounds and what their differing ratio might mean. I'd also like to see more work done on the idea that "the mood stabilizer valproic acid, which exerts neuroprotective effects against glutamate-induced excitotoxicity, is effective in ASD [autism spectrum disorder] with seizures." Yes, I know that valproic acid a.k.a valproate is a bit of a double-edged sword when it comes to autism and other offspring developmental issues under certain circumstances (see here) but much like another research story in autism (see here) timing of exposure seems to be a key issue and one wonders whether other unrelated compounds might also exert a similar neuroprotective effect.As to the idea that "blood glutamate levels may serve as a potential biomarker in the diagnosis of ASD" made by Zheng and colleagues, we'll wait and see...---------- Zheng Z. et al. Blood Glutamate Levels in Autism Spectrum Disorder: A Systematic Review and Meta-Analysis. PLoS One. 2016 Jul 8;11(7):e0158688. Yip J. et al. Decreased GAD65 mRNA levels in select subpopulations of neurons in the cerebellar dentate nuclei in autism: an in situ hybridization study. Autism Res. 2009 Feb;2(1):50-9.----------Zheng Z, Zhu T, Qu Y, & Mu D (2016). Blood Glutamate Levels in Autism Spectrum Disorder: A Systematic Review and Meta-Analysis. PloS one, 11 (7) PMID: 27390857... Read more »
Zheng Z, Zhu T, Qu Y, & Mu D. (2016) Blood Glutamate Levels in Autism Spectrum Disorder: A Systematic Review and Meta-Analysis. PloS one, 11(7). PMID: 27390857
Everyone does it ...no, not poop, but fart. Passing gas, fuming, crop dusting, cracking a rat -- no matter what you call it -- everyone fart, but why? Researchers have published an article devoted to the review of gaseous neurotransmitters of microbial origin and their role in the human body.
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Oleskin, A., & Shenderov, B. (2016) Neuromodulatory effects and targets of the SCFAs and gasotransmitters produced by the human symbiotic microbiota. Microbial Ecology in Health . DOI: 10.3402/mehd.v27.30971
I going to assume that readers have some background knowledge about probiotics, gut bacteria, bacterial dysbiosis and coeliac disease before reading this post. I'd love to be able to give detailed descriptions of each here but fear that this would turn a short post into a much longer one...So... in a previous post titled: 'Probiotics degrading gluten peptides?' I covered the potentially important suggestion that certain types of bacteria might have the ability to breakdown (degrade) immunogenic gluten peptides. This may be particularly relevant to conditions like coeliac disease where specific peptides derived from gluten are involved in a cascade of biological processes that can and do affect a sizeable proportion of the population.In this part 2 post I'm turning my attention to the findings reported by Alberto Caminero and colleagues  who observed that: "Small intestinal bacteria exhibit distinct gluten metabolic patterns in vivo, increasing or reducing gluten peptide immunogenicity." Further that: "This microbe-gluten-host interaction may modulate autoimmune risk in genetically susceptible persons and may underlie the reported association of dysbiosis and CeD [coeliac disease]."How did they arrive at such conclusions? Well, it all started with some bacterial seeding, where "bacteria isolated from the small intestine of CeD patients or healthy controls" was implanted into a germ-free mouse/mice. Said mice were given gluten (gluten gavage) and various measures of gliadin content and the extent of breakdown of gluten proteins were measured. The specific peptides "produced by bacteria used in mouse colonization" were subjected to analysis via one of the gold-standards of analytical chemistry: LC-MS/MS. Said peptides were then evaluated for their immunogenic potential "using peripheral blood mononuclear cells from celiac patients after receiving a 3-day gluten challenge."Results: well I've already mentioned that different types of intestinal bacteria seemed to have different patterns of gluten protein degradation. This is rather important because not 10-15 years ago most people in the know would have suggested that gluten protein degradation is solely under the control of the body's biological systems designed for this purpose. Now it appears, there may be bacterial helping hands also at work. So: "Lactobacillus spp. from the duodenum of non-CeD controls degraded gluten peptides produced by human and Psa [Pseudomonas aeruginosa] proteases, reducing their immunogenicity." But for every 'good guy' there must be a 'bad guy' and in this case Psa assumes that role: "Psa-modified gluten peptides activated gluten-specific T-cells from CeD patients."One still has to be a little cautious about this and other related work as things stand but such results are promising. Not only because more and more the gut microbiome is being implicated in conditions like coeliac disease (see here for example) but also because there may be something that can be done about it  and science has the technology to identify other potential gluten-digesting bacteria  too. Indeed, alongside a suite of other potential intervention options (see here for example) the management of conditions like coeliac disease by avoidance of dietary gluten may eventually not be the only option. Whether this may also extend to the slightly more grey areas of gluten sensitivity (see here) remains to be seen as does the idea that certain bacteria might also 'work' on accompanying issues such as those linked to gut barrier integrity ...---------- Caminero A. et al. Duodenal bacteria from patients with celiac disease and healthy subjects distinctly affect gluten breakdown and immunogenicity. Gastroenterology. 2016 Jun 30. pii: S0016-5085(16)34713-8. Duar RM. et al. Identification and characterization of intestinal lactobacilli strains capable of degrading immunotoxic peptides present in gluten. J Appl Microbiol. 2015 Feb;118(2):515-27. Berger M. et al. Rapid isolation of gluten-digesting bacteria from human stool and saliva by using gliadin-containing plates. Exp Biol Med (Maywood). 2015 Jul;240(7):917-24. Orlando A. et al. Lactobacillus GG restoration of the gliadin induced epithelial barrier disruption: the role of cellular polyamines. BMC Microbiol. 2014 Jan 31;14:19.----------Caminero, A., Galipeau, H., McCarville, J., Johnston, C., Bernier, S., Russell, A., Jury, J., Herran, A., Casqueiro, J., Tye-Din, J., Surette, M., Magarvey, N., Schuppan, D., & Verdu, E. (2016). Duodenal bacteria from patients with celiac disease and healthy subjects distinctly affect gluten breakdown and immunogenicity Gastroenterology DOI: 10.1053/j.gastro.2016.06.041... Read more »
Caminero, A., Galipeau, H., McCarville, J., Johnston, C., Bernier, S., Russell, A., Jury, J., Herran, A., Casqueiro, J., Tye-Din, J.... (2016) Duodenal bacteria from patients with celiac disease and healthy subjects distinctly affect gluten breakdown and immunogenicity. Gastroenterology. DOI: 10.1053/j.gastro.2016.06.041
The fountain of youth may reside in an embryonic stem cell gene named Nanog. In a series of experiments, the gene kicked into action dormant cellular processes that are key to preventing weak bones, clogged arteries and other telltale signs of growing old. The findings also show promise in counteracting premature aging disorders such as Hutchinson-Gilford progeria syndrome.
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Mistriotis, P., Bajpai, V., Wang, X., Rong, N., Shahini, A., Asmani, M., Liang, M., Wang, J., Lei, P., Liu, S.... (2016) NANOG Reverses the Myogenic Differentiation Potential of Senescent Stem Cells by Restoring ACTIN Filamentous Organization and SRF-Dependent Gene Expression. STEM CELLS. DOI: 10.1002/stem.2452
I very carefully approach the findings reported by Jennifer Fairthorne and colleagues  today detailing "the occurrence of hospital admissions and treatment/services for cancer in mothers of children with ASD [autism spectrum disorder] with or without ID [intellectual disability] compared with other mothers." Appreciating that families touched by autism probably have enough on their plate without additional talk about the 'big C', I do however think that this kind of research is important if not only as part of the process of 'caring for the carers'.Based on the analysis of various "Western Australian administrative health databases" (something gaining research ascendancy), researchers sought to estimate the odds, sorry hazard ratios, of hospitalisation and/or use of services in relation to cancer when it came to mums of children with autism (with and without learning disability) "compared with other mothers." They concluded that there may be something more to see when it comes to elevated use of cancer services among mothers of children with autism. Mothers of children with autism but not with accompanying learning disability in particular seemed to be a group in need of quite a bit more scientific investigation.Minus any sweeping generalisations nor scaremongering, this is important work. I've kinda touched upon the idea that risk of cancer might be something to look at in first degree relatives of those with autism (see here) before. As per reports such as the one by Erin Ingudomnukul and colleagues  the risk is not wildly increased similar to the risk of cancer among people with autism themselves (see here), but certainly enough to start asking more research questions about possible mechanisms and the potential applicability of preferential screening services. Indeed, on the topic of possible mechanisms it might be useful to note the growing interest in the idea that autism genes are not necessarily just genes for autism (see here) and that just outside of structural genetics, there is another branch of science ripe for further dual inquiry ...---------- Fairthorne JC. et al. Mothers of Children with Autism have Different Rates of Cancer According to the Presence of Intellectual Disability in Their Child. Journal of Autism and Developmental Disorders. 2016. July 6. Ingudomnukul E. et al. Elevated rates of testosterone-related disorders in women with autism spectrum conditions. Horm Behav. 2007 May;51(5):597-604. Latham KE. et al. The epigenetic lorax: gene-environment interactions in human health. Epigenomics. 2012 Aug;4(4):383-402.----------Fairthorne, J., de Klerk, N., Leonard, H., & Whitehouse, A. (2016). Mothers of Children with Autism have Different Rates of Cancer According to the Presence of Intellectual Disability in Their Child Journal of Autism and Developmental Disorders DOI: 10.1007/s10803-016-2847-9... Read more »
Fairthorne, J., de Klerk, N., Leonard, H., & Whitehouse, A. (2016) Mothers of Children with Autism have Different Rates of Cancer According to the Presence of Intellectual Disability in Their Child. Journal of Autism and Developmental Disorders. DOI: 10.1007/s10803-016-2847-9
Capitalizing on experimental genetic techniques, researchers have demonstrated that temporarily turning off an area of the brain changes patterns of activity across much of the remaining brain. The research suggests that alterations in the functional connectivity of the brain in humans may be used to determine the sites of pathology in complex disorders such as schizophrenia and autism.
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Grayson, D., Bliss-Moreau, E., Machado, C., Bennett, J., Shen, K., Grant, K., Fair, D., & Amaral, D. (2016) The Rhesus Monkey Connectome Predicts Disrupted Functional Networks Resulting from Pharmacogenetic Inactivation of the Amygdala. Neuron, 91(2), 453-466. DOI: 10.1016/j.neuron.2016.06.005
The brain's reward centers in severely obese women continue to respond to food cues even after they've eaten and are no longer hungry, in contrast to their lean counterparts. The study compared attitudes and the brain activity of 15 severely obese women (those with a body mass index greater than 35) and 15 lean women (those with a BMI under 25).
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Puzziferri, N., Zigman, J., Thomas, B., Mihalakos, P., Gallagher, R., Lutter, M., Carmody, T., Lu, H., & Tamminga, C. (2016) Brain imaging demonstrates a reduced neural impact of eating in obesity. Obesity, 24(4), 829-836. DOI: 10.1002/oby.21424
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