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  • March 22, 2017
  • 04:08 AM
  • 30 views

On genotype and environmental exposure patterns

by Paul Whiteley in Questioning Answers

I was rather interested to read the paper by Michela Traglia and colleagues [1] (open-access available here) concluding that: "maternal and fetal genetic make-up are important determinants of mid-gestational maternal circulating levels of some environmental organohalogens." Interested because, in these days of gene-environment interactions being applied to just about everything, the detail that is missing - which genes might potentially be linked to which environmental factors - has not yet been suitably addressed in the peer-reviewed science literature.So, based on data - "serum levels of a set of 21 organohalogens in a subset of 790 genotyped women and 764 children" - derived from participants included in the Early Markers for Autism (EMA) Project, researchers set about assessing how genetics might impact on environmental pollutant exposure profiles. Maternal blood samples were collected at around 15-20 weeks pregnancy. Children provided blood samples via the fabulous resource that is the newborn screening program, where: "Newborn blood spots were collected on filter paper 1-2 days after birth." Maternal samples were analysed for various environmental pollutants and both sets of samples were analysed for the genetic material they contained pertinent to whether "circulating mid-gestational levels of organohalogens would be driven by common maternal genetic determinants, and that these results could shed light on the observed associations between the organohalogens and ASD [autism spectrum disorder]."Results: yes, the authors "found evidence that a large proportion of maternal circulating levels of BB-153, BDE-47, -100, -153 [polybrominated congeners] and their sum was significantly controlled by common genetic factors." Those 'common genetic factors' typically referred to the presence of point mutations (SNPs) that litter everyone's genome and on occasion, can affect the function/production of specific biological processes. So: "Genome-wide association analyses identified significant maternal loci for p,p'-DDE... in the CYP2B6 gene and for BDE-28... near the SH3GL2 gene, both involved in xenobiotic and lipid metabolism." In other words, although the environmental pollutants measured are not great products in the first place (in terms of safety), a person's genetic make-up can influence how such products are eventually dealt with by the body and potentially onwards, what subsequent effects they might have.Additionally: "results suggest that the maternal circulating levels of some compounds were more highly influenced by fetal genetic factors than maternal genetics." This leads into another aspect of the current study whereby foetal genetic factors might also play a part in "controlling the toxicant disposition between mother and fetus." Specifically, authors noted that aspects of the individual genetics of a foetus (distinct from its mother) "contributed to the levels of BDE-100... and PCB187... near the potential metabolic genes LOXHD1 and PTPRD, previously implicated in neurodevelopment."And finally: "We confirmed that the serum levels of BDE-100, -153 and the total sum of PBDEs were significantly lower in mothers of ASD-affected children compared to mothers of control children." This is interesting in light of other discussions about PBDEs and autism in particular (see here). The authors do discuss various scenarios to account for their results not least that "transplacental transfer of organohalogens during pregnancy may be driven by the fetal genome expressed in placenta." Further analyses of the 'placentome' might therefore be indicated.To reiterate, this is interesting research. It tells us that many [adverse] environmental exposures, whilst typically to be avoided, don't act on the body in a uniform way as a function of differing genomes and differences in the ways that the body 'handles' such exposures. With autism in mind, this is not necessarily new news (remember paraoxonase gene variants and organophosphate metabolism [2] and air pollution and offspring autism?) but is a useful reminder. Such work also provides a template for looking at the myriad of other environmental factors put forward to influence autism risk and whether individual product safety is necessarily the only or most important factor when it comes to assessing relative risk profiles.I might finally also draw your attention to a recent interesting meta-analysis of the various environmental risk factors potentially linked to autism [3] (open-access) and another article talking about similar things [4] (open-access) (thanks Annabelle). Genes and environment, genes and environment...Music: Petula Clark sings the Beatles? Personally, I think it's better than the original...----------[1] Traglia M. et al. Independent Maternal and Fetal Genetic Effects on Mid-gestational Circulating Levels of Environmental Pollutants. G3 (Bethesda). 2017 Feb 24. pii: g3.117.039784.[2] D'Amelio M. et al. Paraoxonase gene variants are associated with autism in North America, but not in Italy: possible regional specificity in gene-environment interactions. Mol Psychiatry. 2005 Nov;10(11):1006-16.[3] Modabbernia A. et al. Environmental risk factors for autism: an evidence-based review of systematic reviews and meta-analyses. Molecular Autism. 2017; 8: 13.[4] Parker W. et al. The role of oxidative stress, inflammation and acetaminophen exposure from birth to early childhood in the induction of autism. Journal of International Medical Research. 2017. Jan 20.----------Traglia M, Croen LA, Lyall K, Windham GC, Kharrazi M, DeLorenze GN, Torres AR, & Weiss LA (2017). Independent Maternal and Fetal Genetic Effects on Mid-gestational Circulating Levels of Environmental Pollutants. G3 (Bethesda, Md.) PMID: 28235828... Read more »

  • March 21, 2017
  • 10:04 AM
  • 56 views

The Weirdest Animals on Earth: 12 Amazing Facts About Platypuses

by Miss Behavior in The Scorpion and the Frog

What IS that? A photo by Stefan Kraft at Wikimedia Commons.1. Platypuses are so strange, that when British scientists first encountered one, they thought it was a joke: A Governor of New South Wales, Australia, sent a platypus pelt and sketch to British scientists in 1798. Even in their first published scientific description of the species, biologists thought that this duck-beaked, beaver-bodied, web-footed specimen may be some Frankenstein-like creation stitched together as a hoax. But this is only the beginning of their oddities…2. Platypuses are egg-laying mammals. Mammals are animals that have a backbone, are warm-blooded, and females produce milk for their young. Most females that nurse their young also carry their developing babies in their bodies and give birth to live young… But platypuses don’t play by those rules. Platypuses are monotremes, egg-laying mammals that include the platypus and four species of echidna. Most female mammals have two functional ovaries, but female platypuses, like most female birds, only have a functional left ovary. Once a year, a female platypus may produce a clutch of two or three small, leathery eggs (similar to reptile eggs), that develop in her uterus for 28 days. Because female platypuses don’t even have a vagina, when the eggs are ready, she lays them through her cloaca, an opening that serves for reproduction, peeing and pooping. (In fact, monotreme comes from the Greek for “one hole”). She then curls around them and incubates them for another 10 days until they hatch. 3. Platypuses sweat milk! Not only do female platypuses not have vaginas, they don’t have nipples either! Instead, lactating mothers ooze milk from pores in their skin, which pools in grooves on their bellies so the babies can lap it up. …And they’re not even embarrassed about it! 4. Adult platypuses are toothless. Baby platypuses (that is the actual technical term for them, by the way… not “puggles”, which would be way more fun) are born with teeth but they lose them around the time that they leave the breeding burrow. In their place are rigid-edged keratinized pads that they use as grinding plates. When they catch their prey (worms, bugs, shrimp, and even crayfish), they store it in their cheek pouches and carry it to the surface, where they use gravel to crush it in their toothless maw.5. The platypus “duck bill” is a sensory organ used to detect electric fields. Muscles and neurons use electrical impulses to function, and these impulses can be detected by electroreceptors. Although common in shark and ray species, electroreception is rare in mammals, only having been discovered in monotremes and the Guiana dolphin. Platypuses have rows of around 40,000 electroreceptors on their highly sensitive bill, which they wave back and forth in the water, much like a hammerhead shark, to determine the location of their prey. It’s a good thing this sense is so sensitive, since they close their eyes, nose and ears every time they dive. 6. Platypuses don’t use their tails like beavers do. Whereas beavers use their large, flat, leathery tails for swimming and slapping the water to send signals, platypuses don’t use their tails for any of that. Platypuses have large, flat tails for storing fat in case of a food shortage. Unlike beaver tails, platypus tails are covered in fur, which the mothers use to snuggle with their incubating eggs.A platypus ankle spur. Photo by E.Lonnon at Wikimedia Commons.7. Male platypuses have venomous ankle spurs. Their venom is strong enough to kill small animals and to create excruciating pain in humans. Since only males have it and they produce more venom during the breeding season, we think its main function may be to compete for mates and breeding territories.8. Platypuses are knuckle-walkers with a reptilian gait. Although they are well-built for swimming with their webbed feet and legs on the sides of their bodies, these traits make it quite awkward to get around on dry land. To walk, they pull in their webbing and walk on their knuckles, exposing their claws. Like reptiles and salamanders, platypuses flex their spines from side-to-side, supported by their sprawling legs. 9. Platypuses have unusually low body temperatures. As unusual as they are, platypuses are still mammals, which are defined, in part, by their ability to generate most of their own body heat with their metabolism. Platypuses do this as well, but whereas most mammals maintain body temperatures between 37-40 degrees C (99-104 degrees F), platypuses are happy with a body temperature of 32 degrees C (90 degrees F). This lower metabolism reduces the amount of calories they need to eat.10. They have no stomach. Stomachs are specialized protein-digesting chambers of digestive tracts that contain protein-digesting enzymes and acids to activate them. Not all animals have them, but most carnivores do. The most common exceptions to this rule are fish… and platypuses. Why? We don’t know for sure, but many of these animals consume diets high in calcium carbonate, which is a natural antacid. If their own diet would constantly neutralize their stomach acid, then the stomach really isn’t going to do them any good anyway.11. They have 10 sex chromosomes! Most mammals have two sex chromosomes, one from each parent. An individual that has two X chromosomes is usually female and an individual that has one X and one Y chromosome is usually male. Thus, female mammals pass along an X chromosome to each offspring and males can pass along an X or a Y. But platypuses are not content to be normal in any way…They have 10 sex chromosomes: 5 from mom and 5 from dad. All 5 chromosomes from mom are Xs, whereas a male sperm either contains 5 Xs or 5 Ys. Birds also have two sex chromosomes, but in birds, individuals with two of the same type are usually male and individuals with different chromosomes are usually female. Their system is called ZW, where the mammalian system is XY. The platypus X chromosome is more similar than the X chromosome of other mammals to the bird Z chromosome.12. The platypus genome is as much of a hodgepodge as its body. Only 80% of the platypus’ genes are like other mammals. Some of their genes have only previously been found in birds, reptiles, fish, or amphibians.To learn about more weird animals, go here.References: ... Read more »

Scheich, H., Langner, G., Tidemann, C., Coles, R., & Guppy, A. (1986) Electroreception and electrolocation in platypus. Nature, 319(6052), 401-402. DOI: 10.1038/319401a0  

Warren, W., Hillier, L., Marshall Graves, J., Birney, E., Ponting, C., Grützner, F., Belov, K., Miller, W., Clarke, L., Chinwalla, A.... (2008) Genome analysis of the platypus reveals unique signatures of evolution. Nature, 453(7192), 175-183. DOI: 10.1038/nature06936  

  • March 21, 2017
  • 03:57 AM
  • 51 views

PACE trial recovery data and chronic fatigue syndrome - a reply

by Paul Whiteley in Questioning Answers

I'd encourage readers interested in the background to the response paper by Michael Sharpe and colleagues [1] to have a look at a previous blogging occasion when the topic of the PACE trial, chronic fatigue syndrome (CFS) and 'recovery' were discussed (see here).Suffice to say that this latest paper is a reply to one published by Carolyn Wilshire and colleagues [2] who concluded that: "The claim that patients [with CFS] can recover as a result of CBT [cognitive behaviour therapy] and GET [graded exercise therapy] is not justified by the data, and is highly misleading to clinicians and patients considering these treatments." Said discussions linking back to some quite extensive debates on how one should (and shouldn't) treat/manage conditions like CFS (see here).I wanted to highlight the latest Sharpe paper because (a) I anticipated a reply from these authors following the Wilshire paper criticism of their recovery paper [3], and (b) although the debates in this area have been quite extensive already, the use of the scientific peer-reviewed medium to discuss and even argue is an important avenue. The authors have a right to scientific reply.So how did Sharpe et al respond? Well the words 'recovery', 'threshold' and ''no generally agreed measure of recovery" when it comes to CFS form the crux of the response to the Wilshire paper. They address the issue of recovery thresholds that have been a real source of discussion in relation to the PACE trial secondary analysis concluding that: "No participant met our full criteria for recovery at baseline." They point out that whilst "13% of participants met the recovery criterion of being within the normal range... for physical functioning when entering the trial" physical functioning was but one measure they used to determine recovery.They also approach the topic of 'changing thresholds' when it came to the definition of recovery in the PACE trial. To quote: "We changed these thresholds for our detailed analysis plan because after careful consideration and consultation, we concluded that they were simply too stringent to capture clinically meaningful recovery." They also report that elements of their assessment - the PACE walking test - are "not comparable with data collected in other studies" as a function of their reliance on personal motivation/ability over and above the use of encouragement as in other studies.Finally, authors also talk about 'what other studies have found regarding recovery' when it comes to CFS. They note that their findings in relation to the use of standard medical care (SMC) for CFS in the PACE trial were similar to other reports [4]. They also point to research suggesting that the use of CBT in independent study for CFS show similar rates of recovery [5] to theirs originally reported. In other words, they make a case for their findings fitting in with some of the other literature on this topic.A quick trawl of PubMed with the terms 'chronic fatigue syndrome' and 'recovery' reveals that there is indeed quite a bit more to do in this area of science. To quote from one paper (a critical review) [4]: "Estimates of recovery ranged from 0 to 66 % in intervention studies and 2.6 to 62 % in naturalistic studies." What this tells us is that (a) how recovery is reported in relation to CFS is still in need of some clarification [6] and perhaps more importantly, agreed uniformity is still required in its assessment; (b) some of the measures used to form judgements of recovery when it comes to CFS are not necessarily fit for purpose [7] (bearing in mind not everyone agrees with this); and (c) further efforts need to go into looking at many more aspects of CFS recovery outside of just a reliance on the fatigue parameter (see here and see here for examples). In short, science does not really know what recovery looks like in relation to CFS [8] despite it seemingly happening for all manner of reasons...Where do we go from here? This is a difficult question to answer. It is doubtful that the response from Sharpe and colleagues is going to change too many opinions about PACE given the strength of feeling on the topic and the various goings-on that have occurred around debate in this area (see here). Still today, other comments on the PACE trial continue to emerge in the peer-reviewed domain [9] from notable CFS researchers and there are even calls to retract the original recovery paper (see here). Yes, there are lessons to be learned from the PACE trial (e.g. stick to your "original protocol thresholds", make your data 'open-access' and think about how to do this in the planning/recruitment stages of your trial, be mindful that short-term gains don't necessarily translate into long-term ones, work with the ME/CFS community (rather than labelling elements of them 'vexatious' or worse when they ask questions or request data) but I can't see how these factors will immediately and positively affect the lives of people living with CFS/ME here and now. That recommendations on the use of CBT for CFS have already altered in some parts of the world (see here) - "The strength of evidence on global improvement is downgraded from moderate to low when considering CBT separately from other counseling and behavioral interventions" - and are potentially likely to change here in Blighty perhaps signifies that science and medicine is moving on when it comes to this topic. Science should be doubling its efforts to expand its research boundaries when it comes to managing CFS outside of just a reliance on the [outdated?] psychosomatic model and indeed, it is...And on the topic of other CFS research avenues, I've already talked about a few interesting avenues on this blog (see here and see here and see here) mindful that when we talk about CFS/ME, we're probably not talking about just one entity (see here). Also alongside, that there seems to be an awful lot of 'over-represented' comorbidity accompanying quite a lot of CFS/ME (see here for example) to also contend with...Music: Lush Life (even if you don't know the song title, you might rec... Read more »

M Sharpe, T Chalder, AL Johnson, KA Goldsmith, & PD White. (2017) Do more people recover from chronic fatigue syndrome with cognitive behaviour therapy or graded exercise therapy than with other treatments?. Fatigue: Biomedicine, Health , 1-5. info:/10.1080/21641846.2017.1288629

  • March 20, 2017
  • 11:25 AM
  • 52 views

Opioids, Benzos and Risk for Overdose

by William Yates, M.D. in Brain Posts

The evolving epidemic of opioid overdose and overdose deaths is receiving increased public and research attention.Opioids overdoses and overdose deaths are often unintentional or accidental. It has been known that concurrent use of opioids with alcohol or benzodiazepines (i.e. Valium or Xanax) increases risk for overdose toxicity.A recent study published in the British Medical Journal confirmed the association of concurrent benzodiazepine prescription with opioid overdose.This research team examined confidential medical database records from over 500,000 patients in the U.S.Those that were enrolled in a medical plan including pharmaceutical benefits between 2001 and 2013 were included in the analysis.The key findings from the study included the following:The percentage of opioid users concurrently using a benzodiazepine rose from 9% of opioid users in 2001 to 17% of opioid users in 2013Chronic users of opioids nearly doubled their risk of opioid overdose if they took a concurrent benzodiazepine medication (4/100 persons/year to 7-8/100 person years)If the association is causal, the authors estimate emergency room visits and inpatient admissions could be reduced by 15% by stopping concurrent prescriptionsThis association of risk seems reasonable given the toxicities of opioids and benzodiazepines. Both at higher doses decrease respiratory drive potentially contributing to hypoxia and death.The authors note several take home messages for clinicians. Chronic users of benzodiazepines should be prescribed opioids cautiously if at all. Opioid prescriptions should be for short periods of time and low doses for chronic benzodiazepine patients.Likewise, if chronic opioids are necessary they should rarely be combined with intermittent or long-term benzodiazepine prescriptions.Readers with more interest in this topic can access the free full-text manuscript by clicking on the PMID link in the citation below.Photo of NCAA men's basketball tournament in Tulsa, OK is from my files.Follow me on Twitter WRY999Sun EC, Dixit A, Humphreys K, Darnall BD, Baker LC, & Mackey S (2017). Association between concurrent use of prescription opioids and benzodiazepines and overdose: retrospective analysis. BMJ (Clinical research ed.), 356 PMID: 28292769... Read more »

  • March 20, 2017
  • 04:13 AM
  • 61 views

ALSPAC says no to cat ownership - psychosis risk hypothesis but...

by Paul Whiteley in Questioning Answers

"While pregnant women should continue to avoid handling soiled cat litter, given possible T. gondii exposure, our study strongly indicates that cat ownership in pregnancy or early childhood does not confer an increased risk of later adolescent PEs [psychotic experiences]."So said the findings reported by Francesca Solmi and colleagues [1] (open-access) who brought a smile to any reader of the title of their paper: "Curiosity killed the cat: no evidence of an association between cat ownership and psychotic symptoms at ages 13 and 18 years in a UK general population cohort." For those who might not be aware of the hypothesis, cat ownership has been previously linked to 'adverse' psychological outcomes (see here) tied into some peer-reviewed evidence on one possible environmental factor linked to psychosis and conditions manifesting psychosis: Toxoplasma gondii.ALSPAC - Avon Longitudinal Study of Parents and Children - brought it's quite significant scientific prowess to bear on the question of whether "cat ownership in pregnancy and childhood (ages 4 and 10 years) was associated with psychotic experiences (PEs) in early (age 13, N = 6705) and late (age 18, N = 4676) adolescence, rated from semi-structured interviews." Having a cat in the house was not the only question asked by Solmi et al as the presence of other pets were also investigated: "dogs, rabbits, rodents, birds (all waves), and tortoises and fish (from 21 months)." PEs were assessed at approximate ages of 13 and 18 years old via responses to the "psychotic-like symptoms interview (PLIKSi), a semi-structured interviewer-rated screening assessment for PEs." Various other variables were also factored into the examination of any effect or not.Results: well, as per the opening sentence to this post, cat ownership did not seem to be related to later PEs. The potential caveat being that in some of their analyses there did seem to be a possible association - "Owning a cat at age 4 years was associated with higher odds of having PEs at age 13 years in univariable models" - but the significance of this association disappeared when adjustments for other potentially confounding variables were made. Obviously this kind of study can't control for every single potentially confounding variable but they did at least try.Why the disparity between these results and the previous ones suggestive of a possible connection between childhood cat ownership and later adverse psychological health? Well, an important point is made by Solmi and colleagues: "Our study was based on PEs in early and late adolescence, unlike other studies which were based on a clinical diagnosis of schizophrenia." In other words. psychotic experiences might be part and parcel of schizophrenia but not necessarily all that schizophrenia encompasses and not necessarily just enough to merit a diagnosis of schizophrenia. They do also go on to highlight how the previous report on the association may also not have included the range of potentially confounding variables that were included and controlled for in the current study as another possibility for the differences reported. Having said that [2]...Does the T. gondii - schizophrenia hypothesis fall as a result of the Solmi results? Probably not. Solmi et al hint that even though cat ownership probably isn't related to PEs, they do not totally debunk the idea that there may be a connection. They did not for example, look for the presence of contact with T. gondii in this particular study (others have) as per serological examination of participants. I say this bearing in mind that not every moggy is necessarily infected with T. gondii or anything else. Sweeping generalisations on all cats are not required.Music to close, and containing the lyric 'Caringosity killed the Kerouac cat', a chirpy little number from a band with quite a contentious name...----------[1] Solmi F. et al. Curiosity killed the cat: no evidence of an association between cat ownership and psychotic symptoms at ages 13 and 18 years in a UK general population cohort. Psychol Med. 2017 Feb 22:1-9.[2] Fuller Torrey E. et al. The antecedents of psychoses: a case-control study of selected risk factors. Schizophr Res. 2000 Nov 30;46(1):17-23.----------Solmi F, Hayes JF, Lewis G, & Kirkbride JB (2017). Curiosity killed the cat: no evidence of an association between cat ownership and psychotic symptoms at ages 13 and 18 years in a UK general population cohort. Psychological medicine, 1-9 PMID: 28222824... Read more »

  • March 18, 2017
  • 04:58 AM
  • 84 views

HSV-2 gestational infection and offspring autism risk

by Paul Whiteley in Questioning Answers

"In our cohort, high levels of antibodies to herpes simplex virus 2 at midpregnancy were associated with an elevated risk of autism spectrum disorder in male offspring. These findings provide support for the hypothesis that gestational infection may contribute to the pathogenesis of autism spectrum disorder and have the potential to drive new efforts to monitor women more closely for cryptic gestational infection and to implement suppressive therapy during pregnancy."That was the conclusion reached in the paper published by Milada Mahic and colleagues [1] including the research tag-team that is Mady Hornig and Ian 'virus hunter' Lipkin in the list of contributing authors. Having already received some media attention (see here), it doesn't need much more from me but I do want to include a few details and relevant points in this blog entry.So, the Autism Birth Cohort was the starting point, and "442 mothers of children with ASD... and 464 frequency-matched controls" who all provided plasma samples "(903 samples acquired at midpregnancy and 878 acquired after delivery)." Said samples were analysed for IgG antibodies to ToRCH agents: "Toxoplasma gondii, rubella virus, cytomegalovirus (CMV), and herpes simplex viruses 1 (HSV-1) and 2 (HSV-2)." Some of those viruses and parasites have previously been mentioned with [some] autism in mind (see here and see here and see here).Results: well, an important detail first: "Because rubella vaccination is part of the routine child vaccination schedule in Norway, almost all individuals had IgG antibodies to rubella virus." Indeed, other authors have speculated that rubella vaccination has actually "prevented substantial numbers" of autism as a knock-on effect of reducing the numbers of cases of congenital rubella syndrome [2]. Vaccination doing more than just saving lives eh?Next: "Our data suggest that the presence of high levels of anti-HSV-2 antibodies at midpregnancy increases the risk of ASD [autism spectrum disorder] in boys." The authors complemented this finding by some rather neat statistical wizardry whereby odds ratios were calculated based on "four different anti-HSV-2 reference levels (60, 120, 180, and 240 arbitrary units [AU]/ml)." Having said that: "High levels of antibodies, which are typically indicative of recent infection, were found in only a small number of subjects." They also reported "no statistically significant association with risk was found with high levels of HSV-2 antibodies at delivery" and saw nothing significant when it came to the other infections examined. These important points have been picked up in the NHS Choices entry on this study (see here).These are interesting findings and, as far as I can see, represent something quite novel to the quite vast autism research landscape (assuming you count maternal HSV-2 levels and not antibody levels in actual people diagnosed with autism). The reliance on data from an initiative like the Autism Birth Cohort ensured some rigour in terms of the diagnosis of autism [3] and with the reputations following Drs Hornig and Lipkin, one would have to be pretty brave to question their virus-hunting credentials also with autism in mind [4].Then to the million-dollar question: how might elevated HSV-2 antibodies during pregnancy affect offspring risk of autism? There is a familiar theme offered by the authors to this question as per statements like: "ASD risk associated with high levels of antibodies to HSV-2 is not specific to HSV-2 but instead reflects the impact of immune activation and inflammation on a vulnerable developing nervous system." I know some people still have a bit of a problem with the idea that something like maternal immune activation (MIA) might up the risk for various offspring outcomes [hint: if an article contains the word 'truth' in the title, step away] but please, stop with the 'it can never happen' generalisations and instead look to the existing peer-reviewed evidence on the topic [5]. Yes, science needs to do more on the topic of MIA and autism but clues are emerging all the time...Oh, and I'll be coming to research talking about another member of the herpesviruses in relation to autism quite soon on this blog.To close, operation hardtack and other videos (best viewed in full-screen mode).----------[1] Mahic M. et al. Maternal Immunoreactivity to Herpes Simplex Virus 2 and Risk of Autism Spectrum Disorder in Male Offspring. mSphere. 2017. Feb 22.[2] Berger BE. et al. Congenital rubella syndrome and autism spectrum disorder prevented by rubella vaccination - United States, 2001-2010. BMC Public Health. 2011; 11: 340.[3] Stoltenberg C. et al. The Autism Birth Cohort (ABC): A Paradigm For Gene-Environment-Timing Research. Molecular Psychiatry. 2010;15(7):676-680.[4] Hornig M. et al. Lack of association between measles virus vaccine and autism with enteropathy: a case-control study. PLoS One. 2008 Sep 4;3(9):e3140.[5] Careaga M. et al.  Maternal Immune Activation and Autism Spectrum Disorder: From Rodents to Nonhuman and Human Primates. Biol Psychiatry. 2017 Mar 1;81(5):391-401.----------Milada Mahic, Siri Mjaaland, Hege Marie Bøvelstad, Nina Gunnes, Ezra Susser, Michaeline Bresnahan, Anne-Siri Øyen, Bruce Levin, Xiaoyu Che, Deborah Hirtz, Ted Reichborn-Kjennerud, Synnve Schjølberg, Christine Roth, Per Magnus, Camilla Stoltenberg, Pål Surén, Mady Hornig, & W. Ian Lipkin (2017). Maternal Immunoreactivity to Herpes Simplex Virus 2 and Risk of Autism Spectrum Disorder in Male Offspring. mSphere : ... Read more »

Milada Mahic, Siri Mjaaland, Hege Marie Bøvelstad, Nina Gunnes, Ezra Susser, Michaeline Bresnahan, Anne-Siri Øyen, Bruce Levin, Xiaoyu Che, Deborah Hirtz.... (2017) Maternal Immunoreactivity to Herpes Simplex Virus 2 and Risk of Autism Spectrum Disorder in Male Offspring. mSphere. info:/10.1128/mSphere.00016-17

  • March 17, 2017
  • 05:29 PM
  • 88 views

Unethical "Stem Cell" Therapy for Autism In India?

by Neuroskeptic in Neuroskeptic_Discover

I just read a concerning paper about an experimental stem cell treatment for children with autism.





The authors are Himanshu Bansal and colleagues of India. The senior author, Prasad S Koka, is the Editor-in-Chief of the Journal of Stem Cells where the paper appeared, which raises questions about whether the manuscript received a thorough peer review. Koka is actually an author on all five of the research papers published in that issue of the journal. But that's a minor issue compared ... Read more »

Bansal H, Verma P, Agrawal A, Leon J, Sundell IB, Koka PS. (2016) A Short Study Report on Bone Marrow Aspirate Concentrate Cell Therapy in Ten South Asian Indian Patients with Autism. Journal of Stem Cells, 11(1). info:/

  • March 17, 2017
  • 03:39 AM
  • 87 views

Fatty acids and autism meta-analysed yet again (with a different result?)

by Paul Whiteley in Questioning Answers

OK I'm a little confused right now.Not so long ago I talked about the paper from Horvath and colleagues [1] (see here) concluding that "the limited data currently available suggest that ω-3 FA [omega-3 fatty acid] supplementation does not enhance the performance of children with ASD [autism spectrum disorder]." Such a conclusion was based on the application of a systematic review and meta-analysis of the available peer-reviewed literature up to August 2016.Now however, another systematic review and meta-analysis on the topic has emerged from Mazahery and colleagues [2] and reported something a little bit different: "Populations with ASD have lower n-3 LCPUFA status and n-3 LCPUFA supplementation can potentially improve some ASD symptoms." Don't you just love science!OK, so what could be the reason(s) for the differing conclusions reached by the reviews on this topic? Well, Mazahery and colleagues (the most recent review) actually conducted two meta-analyses: "meta-analysis 1 compared blood levels of LCPUFA and their ratios arachidonic acid (ARA) to docosahexaenoic acid (DHA), ARA to eicosapentaenoic acid (EPA), or total n-6 to total n-3 LCPUFA in ASD to those of typically developing individuals (with no neurodevelopmental disorders), and meta-analysis 2 compared the effects of n-3 LCPUFA supplementation to placebo on symptoms of ASD." Horvath et al only conducted one meta-analysis in their study roughly equivalent to meta-analysis 2 presented by Mazahery looking at the effects of fatty acid supplementation on the presentation of autism. Mazahery and colleagues also surveyed the literature up to May 2016 and found four randomised-controlled trials (RCTs) (N=107) whereas Horvath et al (who published earlier!) surveyed the literature up to August 2016 and found five RCTs (N=183). Indeed, it appears that based on that last 'difference' one might see how the grand 'top of the scientific hierarchy' meta-analysis is yet again, only as good as the data it contains. And a certain celebrity in science circles seems to agree...Where next I hear you ask? Well, I'd be tempted to follow the recommendations of Mazahery and colleagues when they suggest that: "Further research with large sample size and adequate study duration is warranted to confirm the efficacy of n-3 LCPUFA." Indeed, there are already studies to watch in this area. That and recognising that within the vast plurality that is the autisms it is not totally outside the realms of possibility that specific parts of the autism spectrum might be more vulnerable to fatty acid issues than others. Oh, and don't forget that outside of impacting autistic 'performance' (or not), fatty acid supplementation does seem to have other health-related properties too...----------[1] Horvath A. et al. ω-3 Fatty Acid Supplementation Does Not Affect Autism Spectrum Disorder in Children: A Systematic Review and Meta-Analysis. J Nutr. 2017 Jan 11. pii: jn242354.[2] Mazahery H. et al. Relationship between Long Chain n-3 Polyunsaturated Fatty Acids and Autism Spectrum Disorder: Systematic Review and Meta-Analysis of Case-Control and Randomised Controlled Trials. Nutrients. 2017 Feb 19;9(2). pii: E155.----------Mazahery H, Stonehouse W, Delshad M, Kruger MC, Conlon CA, Beck KL, & von Hurst PR (2017). Relationship between Long Chain n-3 Polyunsaturated Fatty Acids and Autism Spectrum Disorder: Systematic Review and Meta-Analysis of Case-Control and Randomised Controlled Trials. Nutrients, 9 (2) PMID: 28218722... Read more »

  • March 16, 2017
  • 03:44 AM
  • 130 views

Autoimmune disease(s) and ADHD: birds of a feather?

by Paul Whiteley in Questioning Answers

"A personal history and a maternal history of autoimmune disease were associated with an increased risk of ADHD [attention-deficit hyperactivity disorder]. The previously reported association between type 1 diabetes and ADHD was confirmed. In addition, specific parental autoimmune diseases were associated with ADHD in offspring."So said the study results published by Nielsen and colleagues [1] including "a study population of 983,680 individuals followed from 1995 to 2012." Reliant once again on one/some of those marvellous Scandinavian population registries (every country should have them), researchers "investigated the association between a personal history and a family history of autoimmune disease and the risk of developing attention-deficit/hyperactivity disorder (ADHD)." Autoimmune disease refers to the development of symptoms when the body's own immune system fails to recognise 'self' as 'self' and starts attacking its own tissue(s). I might add that the authors on the Neilsen paper have some research history when it comes to the behavioural correlates of autoimmune disease (see here).Drawing on data for around 23,000 children diagnosed with ADHD, researchers reported a modest but significant 'risk' of ADHD being diagnosed where an autoimmune condition was reported. The presence of an autoimmune condition being diagnosed in mums also elevated the risk of offspring being diagnosed with ADHD (again modestly but significantly). Further: "a paternal history of autoimmune diseases was not significantly associated with ADHD in the offspring." Various types of autoimmune disease in the immediate family were potentially associated with offspring ADHD diagnosis: "a family history of thyrotoxicosis, type 1 diabetes, autoimmune hepatitis, psoriasis, and ankylosing spondylitis." This follows other population registry studies in this area [2].Based on the Nielsen and other data, I don't yet think we're in the realm of calling something as diverse as ADHD an autoimmune condition on the basis that autoimmune conditions tend to 'flock together' [3]. But I do think this adds to a growing body of literature talking about immune function and ADHD (see here for example) and some quite 'strong' data (see here). Hopefully without being too speculative, I'd also draw your attention to some interesting work talking about some possible reasons why autoimmunity might be over-represented when it comes to [some] ADHD on the basis of the expression of those fossil viruses that we all have and their 'super-antigen' and 'molecular mimicry' properties. Just one possibility among many...Music: Nana Mouskouri sings Hey Jude...----------[1] Nielsen PR. et al. Associations Between Autoimmune Diseases and Attention-Deficit/Hyperactivity Disorder: A Nationwide Study. J Am Acad Child Adolesc Psychiatry. 2017 Mar;56(3):234-240.e1.[2] Instanes JT. et al. Attention-Deficit/Hyperactivity Disorder in Offspring of Mothers With Inflammatory and Immune System Diseases. Biol Psychiatry. 2017 Mar 1;81(5):452-459.[3] Assa A. et al. Large population study shows that adolescents with celiac disease have an increased risk of multiple autoimmune and non-autoimmune comorbidities. Acta Paediatr. 2017 Mar 1.----------Nielsen PR, Benros ME, & Dalsgaard S (2017). Associations Between Autoimmune Diseases and Attention-Deficit/Hyperactivity Disorder: A Nationwide Study. Journal of the American Academy of Child and Adolescent Psychiatry, 56 (3), 234-2400 PMID: 28219489... Read more »

  • March 15, 2017
  • 12:57 PM
  • 126 views

Emotional Intelligence and the Physician

by William Yates, M.D. in Brain Posts

Emotional intelligence (EI) is characterized by the ability to recognize emotional states in self and in others.This emotional recognition may be helpful in guiding behavior and in improving interpersonal relationships.It seems logical on a face validity level to assume that higher levels of EI would be good in the selection of students for medical school.However, there are few studies assessing EI in physicians. There are fewer studies that examine whether EI influences physician behavior, patient satisfaction and ultimately patient outcomes.Rhamzan Shahid and colleagues at the Stritch School of Medicine at Loyola University Medical examined levels of EI in a group of resident physicians in training in the specialties of pediatrics and combined internal medicine-pediatrics.This was a cross-sectional study design that included comparison of residents in the first two years of training versus those in years 3 and 4. The main findings included the following:Residents tended to score high on EI overall with the highest scores on impulse control and the interpersonal composite subscaleResidents scored relatively lower on assertiveness and independence subscalesAssertiveness subscale scores were higher in the more senior residentsEmpathy scores were lower in the the more senior residentsIncreased assertiveness sub-scale scores in more senior residents might be a good thing, possibly indicating a growth in confidence and skill level. This cannot be stated definitely as this study was not longitudinally designed.The lower empathy sub-scale scores in senior residents is an interesting finding. Some might argue it is a negative consequence of training and reflects an increasing disenchantment with being a physician. The authors of the study encourage interventions to "ensure they (resident physicians) do not lose empathy".However, it may be that in a group selected for high empathy, a reduction may also represent a normal maturational process. Maybe high empathy contributes to higher physician distress in the clinical setting and potentially more burnout and depression. Maybe empathy levels that are too high produce emotional states that actually impair physician behavior and reduce effectiveness of clinical decision making.These possibilities should prompt studies correlating EI with patient satisfaction, patient outcome, physician satisfaction with medicine and their specialty and risk for physician burnout.The manuscript reviewed and commented on today is available in free full-text format by clicking on the link in the citation below.Follow me on Twitter @WRY999Photo of the lesser scaup duck is from my personal photography files.Shahid, R., Stirling, J., & Adams, W. (2016). Assessment of Emotional Intelligence in Pediatric and Med-Peds Residents Journal of Contemporary Medical Education, 4 (4) DOI: 10.5455/jcme.20170116015415... Read more »

  • March 15, 2017
  • 04:30 AM
  • 124 views

Balance Assessments Unable to Predict ACL Injury in Elite Female Athletes

by Nicole Cattano in Sports Medicine Research (SMR): In the Lab & In the Field

Balance assessments were not associated with anterior cruciate ligament injury risk among elite female handball and soccer athletes.
... Read more »

  • March 15, 2017
  • 04:08 AM
  • 116 views

The extra-intestinal effects of coeliac disease autoimmunity?

by Paul Whiteley in Questioning Answers

"In 3.5-year-old children, CDA [coeliac disease autoimmunity] is associated with increased reports of child depression and anxiety, aggressive behavior, and sleep problems when mothers are unaware of their child’s CDA status."So said the findings reported by Laura Smith and colleagues [1] (open-access available here) adding to an emerging body of peer-reviewed research suggesting that the archetypal 'gluten is the baddie' autoimmune condition known as coeliac disease might, when not managed, have effects well beyond the classical somatic presentations. Real gut-brain axis stuff in action, as also agreed in an editorial by the 'godfather' of coeliac disease research Prof. Alessio Fasano [2].Smith et al focused on data derived from the TEDDY study (no, really it was called TEDDY), an initiative "looking for the causes of type 1 diabetes mellitus (T1DM)." T1DM is also categorised as an autoimmune condition, where the body's defences fail to recognise 'self' as 'self' and attack it's own tissues. Researchers were able to access biological samples taken as part of the TEDDY study and screen for something called tissue transglutaminase autoantibodies (tTGA), part and parcel of the typical screening protocol for coeliac disease (CD). Where values were "persistently positive" for tTGA, the authors used the term 'celiac disease autoimmunity (CDA)' to illustrate not necessarily a diagnosis of CD but something potentially very close. The Achenbach Child Behavior Checklist (CBCL) was the questionnaire of choice for assessing child "behavioral and emotional functioning" between 3 and 5 years of age.Results: "At 3.5 years, 66 mothers unaware their child had CDA reported more child anxiety and depression, aggressive behavior, and sleep problems than 3651 mothers of children without CDA." The 'unaware' bit refers to the fact that some participants falling into the CDA grouping "were unaware their child was developing CDA" This number (n=66) was quite a bit smaller than the "already aware their child had CDA" grouping (n=440). For those aware of CDA: "The CBCL responses of mothers in the aware-CDA group were not significantly different from those of mothers in the no-CDA group."The authors also looked at whether instigation of a gluten-free diet (the treatment of choice when it comes to coeliac disease) had any effect on those who were already aware of CDA presence. The answer: "No differences were found in CBCL scores for aware-CDA mothers based on whether the child was on a gluten-free diet."These are important findings. As the authors note: "These results support previous studies documenting depression, anxiety, and sleep problems as possible manifestations of celiac disease." They also try and put their results into some context in terms of how "knowledge of the child’s CDA increases a parent’s sensitivity to physical discomforts of their child while providing an alternative explanation for any psychological symptoms the child exhibits." In other words, maybe there is an unwritten rule that young children with coeliac disease might be more prone to behavioural issues? They even go as far as suggesting that: "pediatricians may want to recommend tTGA testing in children <4 years of age with a family history of celiac disease if parents report child psychological symptoms."  More research is definitely indicated and I'll be coming to related studies soon enough...Music, and a catchy track that always seems to be playing outside my dojo (not great for the concentration I might add)...----------[1] Smith LB. et al. Psychological Manifestations of Celiac Disease Autoimmunity in Young Children. Pediatrics. 2017 Feb 20. pii: e20162848.[2] Fasano A. Celiac Disease, Gut-Brain Axis, and Behavior: Cause, Consequence, or Merely Epiphenomenon? Pediatrics. 2017. Feb 20.[3] Butwicka A. et al. Celiac Disease Is Associated with Childhood Psychiatric Disorders: A Population-Based Study. J Pediatr. 2017 Mar 7. pii: S0022-3476(17)30153-1.----------Smith LB, Lynch KF, Kurppa K, Koletzko S, Krischer J, Liu E, Johnson SB, Agardh D, & TEDDY study group. (2017). Psychological Manifestations of Celiac Disease Autoimmunity in Young Children. Pediatrics PMID: 28219962... Read more »

Smith LB, Lynch KF, Kurppa K, Koletzko S, Krischer J, Liu E, Johnson SB, Agardh D, & TEDDY study group. (2017) Psychological Manifestations of Celiac Disease Autoimmunity in Young Children. Pediatrics. PMID: 28219962  

  • March 14, 2017
  • 03:56 AM
  • 120 views

Depression in parents of children with autism

by Paul Whiteley in Questioning Answers

"Mothers (OR 2.95, 95% CI 2.81-3.09) and fathers (OR 2.41, 95% CI 2.25-2.58) of children with ASD [autism spectrum disorder] were more likely to have a diagnosis of depression than parents of children without ASD."The paper by Cohrs and Leslie [1] is probably not going to win any awards for novelty when it comes to their findings that: "Autism Spectrum Disorder (ASD) in children can have secondary effects on the child's parents." It does however represent another important piece of evidence pertinent to the idea that 'caring for the carers' should be a mainstay of the support and services offered when a diagnosis of autism is received in the family.I did say in a post not so long ago that I would talk about the Cohrs/Leslie paper and there, I [briefly] have. Added to the body of literature talking about parental stress (and what we can do about it) in the context of autism, resources aplenty should be poured into this area. That and the fact that we already have some clues as to what areas of child rearing might be primary targets for intervention and support....----------[1] Cohrs AC. & Leslie DL. Depression in Parents of Children Diagnosed with Autism Spectrum Disorder: A Claims-Based Analysis. J Autism Dev Disord. 2017 Feb 18.----------Cohrs AC, & Leslie DL (2017). Depression in Parents of Children Diagnosed with Autism Spectrum Disorder: A Claims-Based Analysis. Journal of autism and developmental disorders PMID: 28214978... Read more »

  • March 13, 2017
  • 11:38 AM
  • 127 views

Earliest Brain Changes in Alzheimer's Disease

by William Yates, M.D. in Brain Posts

Amyloid brain plaques are well-known pathological changes associated with Alzheimer's disease. Changes preceding amyloid plaque build up are less well studied and understood. Some of this relates to limitations to current imaging technology.Klementieva and colleagues from Sweden and Spain recently published an important reserach topic in this area.Their studied used a rat model of Alzheimer's disease and imaging techniques that included infrared microspectroscopy and gel electrophoresis.The main findings of their study included the following:Conformation changes of beta amyloid and it's amyloid precursor protein (APP) start before the development of amyloid plaquesThe early changes in beta amyloid localize to the synaptic terminalsThese early changes may provide novel targets for drug developmentThese findings suggest current strategies to alter beta amyloid plaques after development may be too late to alter the course of the disease.Identification and reversal of earlier mechanisms may be a more productive drug development strategy.Readers with more interest in this topic can access the free full-text manuscript by clicking on the citation link below.Follow be on Twitter WRY999Photo of robin in back yard waterer is from my photography files.Klementieva, O., Willén, K., Martinsson, I., Israelsson, B., Engdahl, A., Cladera, J., Uvdal, P., & Gouras, G. (2017). Pre-plaque conformational changes in Alzheimer’s disease-linked Aβ and APP Nature Communications, 8 DOI: 10.1038/ncomms14726... Read more »

Klementieva, O., Willén, K., Martinsson, I., Israelsson, B., Engdahl, A., Cladera, J., Uvdal, P., & Gouras, G. (2017) Pre-plaque conformational changes in Alzheimer’s disease-linked Aβ and APP. Nature Communications, 14726. DOI: 10.1038/ncomms14726  

  • March 13, 2017
  • 03:29 AM
  • 135 views

Mitochondria support for mitochondrial activity in [some] autism

by Paul Whiteley in Questioning Answers

"This study examined the effect of common mitochondrial treatments on specific mitochondrial components in a group of children diagnosed with ASD [autism spectrum disorder], some of which also were diagnosed with co-morbid mitochondrial disease."That was the premise of the study results published by Leanna Delhey and colleagues [1] (open-access available here) and follows previous discussions suggesting that mitochondrial disease might not be totally unfamiliar to at least some autism (see here). Including some notable names on the authorship list previously linked to the area of mitochondrial functions in relation to autism (see here), the authors provide some important information about how specific mitochondrial function might be 'supported' by various interventions.I'm not on this occasion going to venture into all the details discussed by Delhey but I do want to pick out some interesting titbits. First, of the 127 children diagnosed with an autism spectrum disorder (ASD), we are told that "15% of the sample was clinically diagnosed with mitochondrial disease." Bearing in mind this particular cohort might not be totally representative of the autistic population at large, 15% is not an insignificant figure. What this tells us is that as and when a diagnosis of autism is received, screening for a possible mitochondrial disorder should be initiated (yes, an autism diagnosis is a starting point not the finishing line and the diagnosis rarely exists in a diagnostic vacuum).Next, various supplements were taken by participants, some of which have recognised effects on mitochondrial functions. Of particular note was the use of coenzyme Q10 (CoQ10) and carnitine; both of which have been discussed on this blog previously (see here and see here respectively) with the word 'mitochondrial' also being mentioned. Interestingly, a couple of other supplements are also included in the Delhey paper including fatty acids and folate; some of which I have to say, didn't immediately pop into my mind as being primarily mitochondrial-related (folate is though, still a hot topic when it comes to autism). The authors head into how said supplements might affect specific facets of mitochondrial function. It also reminded me that I really need to brush up on my knowledge of mitochondrial functions..."This study provides empirical support for common mitochondrial treatments and demonstrates that the relationship between activities of mitochondrial components might be a marker to follow in addition to absolute activities." I'd agree that there is the beginnings of a roadmap for further study based on the Delhey results. That and including important parameters related to the presentation of autism and how it may/may not be affected by treating underlying mitochondrial disorder, and the scene is set for further recognition of how indeed, autism rarely exists in a diagnostic vacuum...----------[1] Delhey LM. et al. The Effect of Mitochondrial Supplements on Mitochondrial Activity in Children with Autism Spectrum Disorder. J Clin Med. 2017 Feb 13;6(2). pii: E18.----------Delhey LM, Nur Kilinc E, Yin L, Slattery JC, Tippett ML, Rose S, Bennuri SC, Kahler SG, Damle S, Legido A, Goldenthal MJ, & Frye RE (2017). The Effect of Mitochondrial Supplements on Mitochondrial Activity in Children with Autism Spectrum Disorder. Journal of clinical medicine, 6 (2) PMID: 28208802... Read more »

Delhey LM, Nur Kilinc E, Yin L, Slattery JC, Tippett ML, Rose S, Bennuri SC, Kahler SG, Damle S, Legido A.... (2017) The Effect of Mitochondrial Supplements on Mitochondrial Activity in Children with Autism Spectrum Disorder. Journal of clinical medicine, 6(2). PMID: 28208802  

  • March 11, 2017
  • 04:19 AM
  • 152 views

B vitamins for schizophrenia?

by Paul Whiteley in Questioning Answers

I'd like to briefly draw your attention to the results - systematic review and meta-analysis results - published by Joseph Firth and colleagues [1] observing that "certain vitamin and mineral supplements may reduce psychiatric symptoms in some people with schizophrenia" and specifically that certain B vitamins might be something to consider.Such results come from a research team who are making significant waves in the field of meta-analyses and systematic reviews for all manner of different [important] topics. The additional inclusion of one Jerome Sarris to the authorship team adds a 'nutritional medicine as mainstream in psychiatry' touch to proceedings.Drawing on data from 18 clinical trials - randomized controlled trials (RCTs) - cumulatively including over 800 participants, researchers reported that: "vitamin B supplementation (including B6, B8 and B12) reduced psychiatric symptoms significantly more than control conditions." Dose seemed to be important (higher doses appeared to be more effective than lower doses) as did timing of vitamin 'intervention'. Authors also indicated that subgroups of people with schizophrenia might be 'better responders' to this type of intervention, suggesting that either individual genetic differences or possibly nutritional deficiency before intervention might count in terms of effectiveness of B vitamin use. I was wondering whether those last points might tie into other discussions on this blog referencing genotype, B vitamins and [some] schizophrenia (see here).In the context of the rise and rise of plurality in psychiatry ('the schizophrenias' and 'schizophrenia does not exist: discuss') there are some important research directions to be followed on the basis of the Firth findings. Identifying those people on the schizophrenia spectrum who might be potential best responders to this type of nutritional intervention is a research priority. Closely followed by further investigations on the hows-and-whys of such intervention potentially being useful. In that final respect, the peer-reviewed literature has already provided a few ideas for starters (see here and see here for examples).To close, "I've got a good idea..."----------[1] Firth J. et al. The effects of vitamin and mineral supplementation on symptoms of schizophrenia: a systematic review and meta-analysis. Psychological Medicine. 2017. Feb 16.----------Firth J, Stubbs B, Sarris J, Rosenbaum S, Teasdale S, Berk M, & Yung AR (2017). The effects of vitamin and mineral supplementation on symptoms of schizophrenia: a systematic review and meta-analysis. Psychological medicine, 1-13 PMID: 28202095... Read more »

  • March 10, 2017
  • 06:05 AM
  • 132 views

Spontaneous Pneumothorax and air travel in BHD Syndrome

by Joana Guedes in BHD Research Blog

Previous studies show that BHD syndrome causes spontaneous pneumothorax (SP) in 24-38% of patients, with a recurrence rate of up to 75% (Toro et al., 2007; Toro et al., 2008; Houweling et al., 2011). A common preventative strategy used following an initial SP in patients with BHD is pleurodesis, however, its efficacy in preventing recurrent episodes is not well known. Due to the pressure changes during air travel, cystic air spaces expand and compress in the thorax possibly leading to cyst rupture and pneumothorax. In their new study, Gupta et al. (2017) evaluate the risk of pneumothorax, the efficacy of pleurodesis, and the safety of air travel in patients with BHD.... Read more »

Gupta N, Kopras EJ, Henske EP, James LE, El-Chemaly S, Veeraraghavan S, Drake MG, & McCormack FX. (2017) Spontaneous Pneumothoraces in Patients with Birt-Hogg-Dubé Syndrome. Annals of the American Thoracic Society. PMID: 28248571  

  • March 10, 2017
  • 05:00 AM
  • 115 views

Running Shoes and the Preferred Motion Pathway

by Craig Payne in Running Research Junkie

Running Shoes and the Preferred Motion Pathway... Read more »

Nigg BM, Vienneau J, Smith AC, Trudeau MB, Mohr M, & Nigg SR. (2017) The Preferred Movement Path Paradigm: Influence of Running Shoes on Joint Movement. Medicine and science in sports and exercise. PMID: 28277405  

  • March 10, 2017
  • 02:37 AM
  • 136 views

I would walk 500 miles... or maybe just 8 miles (a day).

by Paul Whiteley in Questioning Answers

"Desk-bound workers should ‘walk EIGHT miles a day’ to slash risk of heart attacks or stroke" went one headline talking about the findings reported by William Tigbe and colleagues [1]. Drawing on data from over 110 postal workers - "(55 office-workers, 5 women, and 56 walking/delivery-workers, 10 women)" - who wore "activPAL physical activity monitors for seven days", researchers observed some potentially important trends.Alongside wearing their activity monitors, participants were also assessed on the basis of weight, height, and blood pressure; also providing blood samples pertinent to analyses for cholesterol and triglycerides. Such collected data were used to assess cardiovascular risk based on the PROCAM risk calculator.Results: those who were described as office workers and had a 'desk job' were generally larger at the waist and showed a slightly larger body mass index (BMI) score. They were also deemed to have an elevated risk of cardiovascular disease (over 10 years) compared with the walking/delivery workers. These observations were discussed in terms of the sedentary behaviours associated with their desk job. By contrast, those who delivered post (i.e. were active for large parts of the day) fared quite a bit better than their desk-bound colleagues, bearing in mind that all study participants were fairly healthy to begin with in terms of being non-smokers for example and not being in current receipt of blood pressure or glucose lowering medicines at time of study.The 'walk 8 miles a day' headline that followed the Tigbe study was derived from the observation(s) that: "Those with no metabolic syndrome features walked >15 000 steps/day, or spent >7 h/day upright." Metabolic syndrome refers to a collection of symptoms - "a combination of diabetes, high blood pressure and obesity" - that increases the risk of adverse events associated with cardiovascular (dys)function. It seems that being active, or at least not being sedentary, is important for our health - a shocker indeed!I've covered some of the other research in this area before (see here and see here for examples) and so the Tigbe results really don't come as a surprise. The strengths of the study are multiple in terms of objective measuring of activity (not reliant on the 'how much activity/exercise did you do today' type questionnaires) and all those biochemical measurements taken for participants to complement such findings. Yes, the sample size is OK but not particularly large and yes, these were pretty healthy participants to start with, but the results are nonetheless important.Obviously one has to be a little careful so as not to imply that being active is the only thing that leads to good health and wellbeing. Science has already heard about how 'you can't outrun a bad diet' [2] and for some people, walking 15,000 steps every day or even standing up for 7 hours a day is going to be a big ask. But as part of a package of 'interventions' to potentially ward off metabolic syndrome or related issues [3], the idea that we should all be quite a bit more active is one that really should be given a lot more consideration...Music to close, and with the title to this post, what else could I offer?----------[1] Tigbe WW. et al. Time spent in sedentary posture is associated with waist circumference and cardiovascular risk. Int J Obes (Lond). 2017 Jan 31.[2] Malhotra A. et al. It is time to bust the myth of physical inactivity and obesity: you cannot outrun a bad diet. Br J Sports Med. 2015 Aug;49(15):967-8.[3] Alexander DD. et al. A Meta-Analysis of Randomized Controlled Trials and Prospective Cohort Studies of Eicosapentaenoic and Docosahexaenoic Long-Chain Omega-3 Fatty Acids and Coronary Heart Disease Risk. Mayo Clinic Proceedings. 2017; 92: 15-29.----------Tigbe WW, Granat MH, Sattar N, & Lean ME (2017). Time spent in sedentary posture is associated with waist circumference and cardiovascular risk. International journal of obesity (2005) PMID: 28138134... Read more »

  • March 9, 2017
  • 03:06 AM
  • 152 views

"Relatives of individuals with ASD were at higher risk of ADHD"

by Paul Whiteley in Questioning Answers

"Individuals with ASD [autism spectrum disorder] and their relatives are at increased risk of ADHD [attention-deficit hyperactivity disorder]."So said the paper published by Laura Ghirardi and colleagues [1] (open-access) who studied "1 899 654 individuals born in Sweden between 1987 and 2006" and identified some 28,000 cases of ASD and 82,000 cases of ADHD "with 13 793 individuals... being comorbid cases."Results: "Individuals with ASD were at higher risk of having ADHD, compared with those who did not have ASD (OR=22.33, 95% CI: 21.77–22.92)." This is not a particularly surprising finding given what is already emerging in peer-reviewed science and clinical circles about autism rarely appearing in some sort of diagnostic vacuum (see here). The authors also report that: "the prevalence of ASD–ADHD comorbidity was higher in males (1.01%) than in females (0.43%)."Looking further at various degrees of familial relationship starting with monozygotic (MZ) twins - twins sharing the same genome - outwards to full- and half-cousins, authors reported a sort of sliding scale of risk on the association between autism and ADHD. So: "monozygotic twins of ASD cases had an increased risk of having ADHD" which was a higher risk than that noted for dizygotic (non-identical twins). Next on the list of heightened risk of ADHD where another family member was diagnosed with autism was a full sibling (actually, the calculated risk was slightly higher for full siblings over dizygotic twins) and then maternal and paternal half siblings respectively. The authors note that: "The pattern of within-family associations between ASD and ADHD across different types of relatives reflected the decreasing genetic resemblance among them." This potentially signifies quite a substantial role for genetics when it comes to the co-occurrence of autism and ADHD as per other important data [2] (assuming that environmental - non-genetics - factors don't impact on pregnancy or before pregnancy processes related to sperm and egg for example).Where next? Well, the pathway(s) potentially linking autism and ADHD still requite a lot more investigation. With my continued interest in how autism and ADHD might 'set someone up' for later mental health issues (see here and see here for examples) I'd be inclined to widen the range of diagnoses/labels that might also need examination pertinent to processes involved. Assuming also that genes for autism or ADHD might not necessarily be just genes for autism and ADHD (see here), an open mind needs to be kept of what could be potentially involved, as per the whole immune system link for example (see here). I'd also be inclined to suggest that the Ghirardi findings suggest greater examination a possible new dimension when it comes to concepts like the broader autism phenotype (BAP) (see here) too (including signs and symptoms based around sensory profiles [3]).Music to close: The Flaming Lips - She Don't Use Jelly.----------[1] Ghirardi L. et al. The familial co-aggregation of ASD and ADHD: a register-based cohort study. Mol Psychiatry. 2017 Feb 28.[2] Sokolova E. et al. A Causal and Mediation Analysis of the Comorbidity Between Attention Deficit Hyperactivity Disorder (ADHD) and Autism Spectrum Disorder (ASD). J Autism Dev Disord. 2017 Mar 2.[3] Bijlenga D. et al. Atypical sensory profiles as core features of adult ADHD, irrespective of autistic symptoms. European Psychiatry. 2017. Feb 21.----------Ghirardi L, Brikell I, Kuja-Halkola R, Freitag CM, Franke B, Asherson P, Lichtenstein P, & Larsson H (2017). The familial co-aggregation of ASD and ADHD: a register-based cohort study. Molecular psychiatry PMID: 28242872... Read more »

Ghirardi L, Brikell I, Kuja-Halkola R, Freitag CM, Franke B, Asherson P, Lichtenstein P, & Larsson H. (2017) The familial co-aggregation of ASD and ADHD: a register-based cohort study. Molecular psychiatry. PMID: 28242872  

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