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  • December 17, 2016
  • 05:51 AM
  • 347 views

Pregnancy influenza infection not linked to offspring autism

by Paul Whiteley in Questioning Answers

"There was no association between maternal influenza [flu] infection anytime during pregnancy and increased ASD [autism spectrum disorder] risk."So said the findings reported by Ousseny Zerbo and colleagues [1] continuing a research theme from this author (see here for example) looking at how various infections 'encountered' during critical periods of pregnancy may / may not impact on offspring autism risk. This time around the focus was on viral infections and in particular "maternal influenza infection and vaccination from conception date to delivery date" as derived from either diagnosis using ICD-9 criteria or "a positive laboratory result for influenza based on the Prodesse ProFlu+ Assay (Hologic), a multiplex real-time polymerase chain reaction in vitro diagnostic test." Said participants numbering nearly 200,000 children were all born "at Kaiser Permanente Northern California from January 1, 2000 to December 31, 2010, at a gestational age of at least 24 weeks." The press release accompanying the publication can be seen here."Maternal influenza infection during pregnancy was not associated with increased ASD risk in this study, and the association did not vary by the timing of influenza infection." Importantly, authors also looked at whether maternal influenza vaccination during pregnancy was also related to offspring ASD risk based on the data contained in their patient databases. The results pertinent to pregnancy flu vaccination and offspring risk were not exactly cut-and-dried as "in an initial analysis unadjusted for multiple comparisons" the authors reported seeing a 'slightly increased' risk for offspring autism associated with maternal vaccination during the first few months of pregnancy. This was set against data indicating no significant association between maternal influenza vaccination covering 'anytime' during pregnancy. Indeed, after "adjusting for the multiplicity of hypotheses tested" they concluded that the first trimester vaccination - offspring autism risk was potentially a 'chance finding'. Minus any scaremongering and to be on the safe side the authors suggested that "additional studies are warranted to further evaluate any potential associations between first-trimester maternal influenza vaccination and autism."Aside from a few potential 'weakness' attached to the Zerbo results including the fact that "subclinical infections or illnesses for which women did not seek medical attention" were not counted in the data, these are interesting results. Quite a few times on this blog I've covered the so-called maternal immune activation (MIA) hypothesis - where mum's reprogrammed pregnancy immune system is 'challenged' and potentially has implications for offspring development - and this work kinda falls into that category of autism science. Indeed, I've talked about the possibility quite recently (see here). Drawing also on data looking at season of conception/birth as potentially being important to pregnancy viral/bacterial exposure and onward offspring outcomes (see here) there has been a steady stream of peer-reviewed publications hinting at a potentially important 'association' between infection exposure in-utero and developmental outcomes for the child. The current Zerbo data however put a bit of a research spanner in the works when it comes specifically to any pregnancy flu and offspring autism risk suggestion albeit with the continued requirement for further investigations in this area covering other infections.----------[1] Zerbo O. et al. Association Between Influenza Infection and Vaccination During Pregnancy and Risk of Autism Spectrum Disorder. JAMA Pediatr. 2016 Nov 28.----------Zerbo O, Qian Y, Yoshida C, Fireman BH, Klein NP, & Croen LA (2016). Association Between Influenza Infection and Vaccination During Pregnancy and Risk of Autism Spectrum Disorder. JAMA pediatrics PMID: 27893896... Read more »

  • December 16, 2016
  • 05:25 AM
  • 328 views

Patient participation in clinical trials

by Joana Guedes in BHD Research Blog

Clinical trials are crucial to help doctors and scientists understand how to safely treat a particular condition, to evaluate new treatments and to test drug safety and efficacy. They have an important role in every step of managing a condition with different clinical trials helping with prevention, diagnosis, treatments and follow-up support.... Read more »

  • December 16, 2016
  • 04:30 AM
  • 293 views

Frequency and Location of Head Impacts in Division 1 Men’s Lacrosse Players

by Patricia Kelshaw, MS, LAT, ATC in Sports Medicine Research (SMR): In the Lab & In the Field

Player position and session type such as practice or game are the main factors that influence head impact frequencies and magnitudes for lacrosse athletes.... Read more »

  • December 16, 2016
  • 03:16 AM
  • 340 views

Non-febrile seizures in children with autism vs unaffected siblings

by Paul Whiteley in Questioning Answers

"Children with idiopathic ASD [autism spectrum disorder] are significantly more likely to have non-febrile seizures than their unaffected siblings, suggesting that non-febrile seizures may be ASD-specific."So said the findings from Lena McCue and colleagues [1] (open-access) continuing a research theme looking at one of the important 'comorbidities' that seems to be over-represented when it comes to a diagnosis of autism (see here). Idiopathic autism or ASD refers to autism as the primary diagnosis and not something tied to an existing condition where autism can also present. Non-febrile seizures are seizures without fever (where fever can very much result in seizures).McCue et al "conducted a secondary analysis of data from a registry-based retrospective cohort study of 731 children with ASD and their 192 children unaffected siblings from the AGRE project for whom phenotypic data were collected." Data from around 320 families with at least one child diagnosed with an ASD (n=610) were compared with sibling data (n=160) in relation to the presence of non-febrile seizures. Siblings (not autism) were chosen as the control group because "siblings share, on average, fifty percent of genes as well as the same environment" so perhaps providing an alternative to just general population control groups.Results: "The prevalence of non-febrile seizures in the ASD group was 8.2% (50/610) and 2.5% in the unaffected siblings (4/160)." What this tells us, aside from the increased frequency of non-febrile seizures in those children diagnosed with autism, is that so-called 'unaffected' siblings are not completely immune to seizures or seizure-linked conditions minus fever. Further: "the odds of having non-febrile seizures increased with age..., presence of GI [gastrointestinal] dysfunction..., and those with a history of febrile seizures had five times the odds of reporting non-febrile seizures."I was particularly interested in the observations that: (a) gastrointestinal (GI) dysfunction, denoting functional bowel issues such as constipation or diarrhoea, were pretty well over-represented among the children with autism in this cohort, similar to other research (see here) and (b) said GI issues might itself/themselves 'up' the risk of non-febrile seizures in relation to autism. In these days of the 'gut-brain axis' where the grey/pinkish matter floating in the skull might not be totally separate and independent from the more mucus-y matter situated in the torso (see here for example), it strikes me as important that further investigations be carried out on how epilepsy might not just be a 'brain-thing'. We have for example, evidence pertinent to an autoimmune connection to some epilepsy (see here) that has implications for other autoimmune conditions affecting the gut too as per the notion that 'birds of an autoimmune feather may flock together'. That also one of the primary 'treatments' for epilepsy not responsive to the usual anti-epileptic medicines is the ketogenic diet (see here) is something else to consider when talking about gut and brain potentially being quite close neighbours."Our study found a five-fold higher lifetime prevalence of non-febrile seizures in children with idiopathic ASD from largely multiplex families compared to their unaffected siblings. These findings suggest that the reported non-febrile seizures may be ASD-specific and cannot be explained by genetic predisposition alone." With that conclusion from the study authors, one might similarly also suggest that the presence of autism in affected children vs. siblings also cannot be explained by genetic predisposition alone...----------[1] McCue LM. et al. Prevalence of non-febrile seizures in children with idiopathic autism spectrum disorder and their unaffected siblings: a retrospective cohort study. BMC Neurology. 2016; 16:245.----------McCue, L., Flick, L., Twyman, K., Xian, H., & Conturo, T. (2016). Prevalence of non-febrile seizures in children with idiopathic autism spectrum disorder and their unaffected siblings: a retrospective cohort study BMC Neurology, 16 (1) DOI: 10.1186/s12883-016-0764-3... Read more »

  • December 15, 2016
  • 04:30 AM
  • 317 views

Cortisol and Testosterone Levels Following Exhaustive Endurance Exercise: How Much Recovery Do Athletes Really Need?

by Jennifer Fields in Sports Medicine Research (SMR): In the Lab & In the Field

Following high-intensity endurance exercise, recovery may require 48-72 hours for cortisol and testosterone to return back to resting levels. ... Read more »

Anderson, T., Lane, A., & Hackney, A. (2016) Cortisol and testosterone dynamics following exhaustive endurance exercise. European Journal of Applied Physiology, 116(8), 1503-1509. DOI: 10.1007/s00421-016-3406-y  

  • December 15, 2016
  • 02:59 AM
  • 402 views

ADHD, not autism, might count when it comes to 'comorbid psychiatric symptomatology'

by Paul Whiteley in Questioning Answers

A quote to begin this fairly brief post: "Our study concluded that higher levels of ADHD [attention-deficit hyperactivity disorder] severity-not ASD [autism spectrum disorder] severity-were associated with a higher prevalence of comorbid psychiatric symptomatology in school-age children with ASD. These findings may encourage clinicians to thoroughly assess ADHD symptomatology in ASD children to better inform treatment planning."That was the research bottom line reported by Rosleen Mansour and colleagues [1] following their examination of how a pretty common comorbidity accompanying a diagnosis of autism (see here) might well play an important role in terms of other 'comorbid psychiatric symptomatology' among those with autism.I'm interested in these findings for several reasons. A diagnosis of autism does seem to elevate the risk of receipt of various other psychiatric diagnoses (see here for example). As I've just said, ADHD is a pretty common comorbidity when it comes to autism (see here). A diagnosis of ADHD (and not the medication commonly used to manage such symptoms) seems to elevate the risk of receipt of various other psychiatric diagnoses too (see here). It's not too difficult to suggest that autism per se might not be 'the most important variable' when it comes to at least some people's risk of other psychiatric diagnoses being received. Indeed, there is another potentially important strand of evidence to include in this proposal, in terms of the continued experiences of some of those who 'move off the autism spectrum ' (see here).More research is implied with one important question to answer about the nature of the synergy between autism and ADHD when it comes to any enhanced risk of psychiatric comorbidity...So, Rogue One finally sees the cinematic light of day...----------[1] Mansour R. et al. ADHD severity as it relates to comorbid psychiatric symptomatology in children with Autism Spectrum Disorders (ASD). Res Dev Disabil. 2016 Nov 24;60:52-64.----------Mansour R, Dovi AT, Lane DM, Loveland KA, & Pearson DA (2016). ADHD severity as it relates to comorbid psychiatric symptomatology in children with Autism Spectrum Disorders (ASD). Research in developmental disabilities, 60, 52-64 PMID: 27889487... Read more »

  • December 14, 2016
  • 04:30 AM
  • 308 views

Identifying Athletes at Risk for Chronic Ankle Instability

by Matt Prebble in Sports Medicine Research (SMR): In the Lab & In the Field

The jump-landing protocol was able to distinguish between healthy, ‘coper’, and unstable ankles. This protocol may be useful for identifying athletes at increased risk for injury, and as a return to play indicator following rehabilitation.... Read more »

  • December 14, 2016
  • 03:07 AM
  • 368 views

Urinary metabolomics in autism turns up tryptophan (again)

by Paul Whiteley in Questioning Answers

"The tryptophan metabolic pathway collectively displays the largest perturbations in ASD [autism spectrum disorder]."So said the findings reported by Federica Gevi and colleagues [1] (open-access) who provide yet more 'metabolomic' data when it comes to autism to add to the already quite voluminous peer-reviewed matter on this topic (see here for example).Just in case you aren't analytical chemistry-saavy, metabolomics is basically the study of the various chemical fingerprints that the multitude of cellular processes going on in the body leave behind. It's the technology available these days that makes metabolomics the discipline that it is, as words such as mass spectrometry and nuclear magnetic resonance (spectroscopy) fill the metabolomic airwaves coupled with some rather smart statistics and software to translate all that captured data into something meaningful.Gevi et al report results based on the analysis of urine samples from a small-ish group of children diagnosed with an ASD ("idiopathic ASD") compared with samples from a similar number of not autism controls. The aim was to focus on "autistic and unrelated typically developing children 2–8 years old, tightly matched by age, sex, Italian ancestry, and city of origin within the country" and look-see whether a particular HPLC-mass spec technique "hydrophilic interaction chromatography (HILIC)-LC-electrospray ionization (ESI)-MS" might provide some important data on autism vs. not autism.Results: well, it's always nice to get a research mention in such studies as per the line: "Data were normalized by urinary specific gravity, because creatinine excretion may be abnormally reduced in ASD children" with reference to some work published a few years back [2]. Indeed, this is not the first time creatinine has cropped up in autism metabolomic studies (see here) and is perhaps worthy of quite a bit more study itself (see here).The authors report that urine samples from those with autism vs. those with not-autism are "largely distinguishable" based on some nifty analysis of the compounds examined from those groups. They even provide a 'top 25 discriminating metabolites' summary to illustrate this fact. Before venturing further into this list, I would perhaps advise some caution however. Caution based on the fact that urine contains many hundreds/thousands of small molecules or chemical entities as a function of being a waste product and carrying waste products from a multitude of different biological processes. It's not outside the realms of possibility that with such a huge number of metabolites, any two groups could be separated out, not just those based on the appearance of autism or not...Anyhow: "The “metabolome overview” obtained through metabolic pathway analysis (MetPA) shows tryptophan metabolism, purine metabolism, vitamin B6 metabolism, and phenylalanine-tyrosine-tryptophan biosynthesis as the four most perturbed metabolic pathways in ASD." The reference to the aromatic amino acid called tryptophan (the stuff that eventually ends up as serotonin and melatonin) used in the title of this post kinda points to where the money might be when it came to these particular results. I've been interested in tryptophan metabolism and autism for quite a while now (see here for example) and how, outside of the whole serotonin/melatonin bit, there is quite a lot more to see besides. Mention of something called the kynurenine pathway by Gevi is interesting; not least because this pathway overlaps with other conditions/labels too (see here). This pathway might also have some important implications when it comes to epilepsy (see here) as a comorbidity to autism too.It's also interesting (to me at least!) to note that the authors found something related to the indoles in their analyses too. So: "we also detect a significant increase in indole derivatives of bacterial tryptophan including indolyl 3-acetic acid, indoxyl sulfate, and most prominently, indolyl lactate." Indoxyl sulfate, a uremic toxin - something that is not great for the kidneys - crops up yet again [3] and importantly, highlights how bacteria can also 'go to work' on tryptophan in the gut. Indole -3-acetic acid also brings back research memories in relation to an indole compound close to my research heart, indolyl-3-acrylolyglycine (IAG) [4] that has received a bit of a research bruising quite recently [5] (the authors of that study and another one [6] however, really need to rethink their paper titles insofar as them not actually testing whether dietary intervention actually 'affects' levels of IAG or related metabolites but nonetheless implying so).There are a range of other findings reported by Gevi and colleagues but I don't want to bore you with all the details. Suffice to say that metabolomics continues its research rise with autism in mind, and provides some rather interesting results. Of course there is more to do in this area; not least the focus on subgroups in these days of 'the autisms' and perhaps a little more metabolomic inquiry when it comes to the myriad of intervention options put forward 'for autism'. Who for example, wouldn't like to see metabolomic profiles pre- and post-folinic acid for example alongside the myriad of other interventions detailed in the peer-reviewed literature? Indeed, I might also advocate a little more investigation on whether specific patterns of urinary compounds might also be related to specific behavioural facets of autism. Given the move towards gut bacteria as potentially showing involvement in some of the results obtained by Gevi et al, it would also be interesting to see if 'altering' certain types of gut bacteria (see here for example) might also have some interesting knock-on effects when it comes to the metabolites detected too? There is quite a bit more to do.Music and more bad lip reading.... sick of blue milk?----------[1] Gevi F. et al. Urinary metabolomics of young Italian autistic children supports abnormal tryptophan and purine metabolism. Molecular Autism. 2016l 7: 47.[2] Whiteley P. et al. Spot urinary creatinine excretion in pervasive developmental disorders. Pediatr Int. 2006 Jun;48(3):292-7.[3] Diémé B. et al. Metabolomics Study of Urine in Autism Spectrum Disorders Using a Multiplatform Analytical Methodology. J Proteome Res. 2015 Dec 4;14(12):5273-82.[4] Bull G. et al. Indolyl-3-acryloylglycine (IAG) is a putative diagnostic urinary marker for autism sp... Read more »

  • December 13, 2016
  • 04:30 AM
  • 316 views

Can Using a Whole Body Vibration Warm-up Give Athletes Quicker Feet?

by Stuart McCrory in Sports Medicine Research (SMR): In the Lab & In the Field

Whole-body vibration improves performance on quick feet test when compared to a traditional warm-up.... Read more »

Donahue RB, Vingren JL, Duplanty AA, Levitt DE, Luk HY, & Kraemer WJ. (2016) Acute Effect of Whole-Body Vibration Warm-up on Footspeed Quickness. Journal of strength and conditioning research, 30(8), 2286-91. PMID: 27328378  

  • December 13, 2016
  • 04:25 AM
  • 367 views

'My child is not talking'. Online concerns and internet-based screening for autism?

by Paul Whiteley in Questioning Answers

"Online communities are used as platforms by parents to verify developmental and health concerns related to their child."That was the starting point for the study results reported by Ben-Sasson & Yom-Tov [1] (open-access available here) who approached an increasingly important issue related to how the Internet and social media in particular, is fast becoming one of the 'go-to' options when it comes to parental concerns about their child's development and the question: could it be autism?So: "we analyzed online queries posed by parents who were concerned that their child might have ASD and categorized the warning signs they mentioned according to ASD [autism spectrum disorder]-specific and non-ASD-specific domains." The online queries included for study came from "the Yahoo Answers platform" between June 2006 and December 2013. There's a lesson there to reiterate that the Internet is an open platform and what you post is typically in the public domain and hence fodder for many different purposes...Authors turned up quite a few thousand queries, determining that over 1000 were "posted by parents who suspected their child might have autism". They randomly selected 195 to be used as the basis for this study. I personally don't know why 195 were selected and not rounded up to say 200, but ho-hum. Content analysis - analysing the content of the post! - was undertaken first "to rate a child's risk of ASD as either low, medium, or high". High risk was defined "as concerns related to at least two types of ASD-specific sign, 1 from the RRBI domain and another from the Social and Communication domains" among other things. Then content analysis was used to "identify the types of warning signs noted by parents." From these analyses: "each query received an ASD global risk score and was coded for either presence or absence of each sign domain and its subdomains."Results: from the 195 queries selected, the vast majority were posted in relation to a boy and most concerned a boy who was aged under 3 years. Contrary to the title of this blog post - 'My child is not talking' - the majority of queries were actually in relation to repetitive and restricted behaviors and interests (RRBI) although concerns related to language were not too far behind in frequency. In relation to those categorisations of low, medium and high risk groups, over half of the queries were labelled as high risk. Interestingly, there were fewer language concerns noted in those allocated to the low risk group than the medium or high risk groups, so perhaps I wasn't so far off with using those 'my child is not talking' words in the title.But things didn't just stop there for the authors, as the words "test the efficacy of machine learning tools in classifying the child's risk of ASD based on the parent's narrative" are also noted in their paper. Machine learning as in, 'giving computers the ability to learn without being explicitly programmed' according to one definition, is something that has cropped up on the blog before with autism in mind (see here for example). This led to the production of a decision tree - yes or no - "for distinguishing low-risk queries from medium- and high-risk queries." This is interesting but I'd perhaps like to see it tested independently before I say too much more.In these days of continued austerity and seemingly evermore limited resources when it comes to things like autism assessment and screening for various reasons, this kind of work has an important place. Certainly I don't think posting symptoms on-line with ever replace autism screening, and one has to bear in mind that at least here in the UK, we might have (knowingly or unknowingly) already initiated population autism screening in children (see here) as a consequence of changes to the Healthy Child Program. But with the technological advances being made where machine learning and the connected artificial intelligence are starting to make strides in relation to science and medicine, I don't doubt that one day parents will be typing in their child's symptoms on-line and somehow and somewhere Dr Google or some related system(s) might be talking back...Music and more bad lip reading applied to Star Wars: No, it's not the future (and watch Chewie holler).----------[1] Ben-Sasson A. & Yom-Tov E. Online Concerns of Parents Suspecting Autism Spectrum Disorder in Their Child: Content Analysis of Signs and Automated Prediction of Risk. J Med Internet Res. 2016 Nov 22;18(11):e300.----------Ben-Sasson A, & Yom-Tov E (2016). Online Concerns of Parents Suspecting Autism Spectrum Disorder in Their Child: Content Analysis of Signs and Automated Prediction of Risk. Journal of medical Internet research, 18 (11) PMID: 27876688... Read more »

  • December 12, 2016
  • 04:37 AM
  • 348 views

Maternal immune activation (MIA) and Old World monkeys

by Paul Whiteley in Questioning Answers

Old World monkeys detailed in the title of this post, specifically refers to a type of animal called a rhesus macaque who were the 'participants' of choice as detailed in a recent study by Destanie Rose and colleagues [1] looking at a concept called maternal immune activation (MIA).Those who followed this blog down the years will no doubt have seen me discuss MIA before in the context of autism and/or schizophrenia (see here for example). The basic theory is that whilst in-utero and enjoying approximately nine months in a warm and comfortable environment with a reprogrammed maternal immune system to stop a mother's body from 'rejecting' a developing foetus, infections encountered by the mother at critical periods of pregnancy might themselves or through their effects on the maternal immune system, have the ability to 'affect' offspring outcomes in a variety of ways. The majority of work on the concept of MIA has been in smaller animals such as rodents, so the inclusion of rhesus macaques is an important step as it was in other work with the immune system and autism in mind (see here).So, take 21 pregnancy rhesus macaques and give them either "three injections over 72 hours of poly I:C-LC [an immune stimulant], a double stranded RNA analog (viral mimic), or saline as a control." Said injections were given either "near the end of the first trimester or near the end of the second trimester" to see whether timing of immune stimulation might be important. Macaque offspring were subsequently born and followed for about 4 years. Blood samples were collected from offspring "at the end of their first (year 1) and fourth (year 4) years to assess dynamic cellular immune function." At the same time, the behaviours of monkey offspring were also analysed to see if there were any effects from MIA exposure.Results: behaviour did seem to be affected by MIA exposure, particularly stereotyped behaviours, noted to be a core feature of autism. Similarly, researchers reported some important immune system 'changes' associated with MIA exposure: "elevated production of innate inflammatory cytokines including: interleukin (IL)-1β, IL-6, IL-12p40, and tumor necrosis factor (TNF)α" at 1 year of age. Immune system changes were also noted longer-term at 4-years: "the MIA exposed offspring continued to display elevated IL-1β, and there was also a pattern of an increased production of T-cell helper type (TH)-2 cytokines, IL-4 and IL-13." Although being careful not to generalise too much when it comes to immune system markers and what they mean for pro- or anti-inflammatory signals, the leaning towards the production of Th-2 cytokines is typically linked to atopy and 'the promotion of IgE and eosinophilic responses in atopy.' The authors - including some notable names from the MIND Institute - conclude by suggesting that: "Data from this study suggests long-term behavioral and immune activation was present in offspring following MIA."Accepting that animal models of something like MIA are not necessarily the same as human MIA and its responses, this is interesting work. If one however accepts the data on something like vaccine function being modelled in animals (see here for example) is akin to what happens in people, real people, there is some added strength to the information published by Rose and other groups on how MIA may indeed be a relevant factor when it comes to immune function potentially affecting offspring behaviour and development.This research also intersects with quite a lot of other peer-reviewed science talking about how (human) pregnancy infection does seem to be related to offspring risk for conditions such as autism (see here). That various immune-related conditions such as asthma in mothers might also 'prime' for offspring neurodevelopmental issues is another important strand of research potentially pertinent to this area (see here). And then also there is the idea of an 'inflammatory autism subtype' (see here) also previously suggested continuing the important theme of immune function and behaviour/development being linked. There are, as you can see, quite a few potentially important connections that can be made between the Rose results and other data on MIA and offspring development.Oh, and I'll be coming to the recent paper by Zerbo and colleagues all in good time...----------[1] Rose DR. et al. Long-term altered immune responses following fetal priming in a non-human primate model of maternal immune activation. Brain Behav Immun. 2016 Nov 19. pii: S0889-1591(16)30522-0.----------Rose, D., Careaga, M., Van de Water, J., McAllister, K., Bauman, M., & Ashwood, P. (2016). Long-term altered immune responses following fetal priming in a non-human primate model of maternal immune activation Brain, Behavior, and Immunity DOI: 10.1016/j.bbi.2016.11.020... Read more »

  • December 12, 2016
  • 04:30 AM
  • 317 views

Substance Use by Gender and Race Among Teenage Athletes

by Jessica Pope in Sports Medicine Research (SMR): In the Lab & In the Field

While general substance use patterns are seen in adolescent athletes, some gender and racial/ethnic groups are at more risk than others. Prevention and educational programs should be designed with this in mind.... Read more »

Parent, M., Bradstreet, T., Piper, M., Brace, T., & Parkman, T. (2016) Racial Disparities in Substance Use by Sport Participation Among High School Students. Journal of Studies on Alcohol and Drugs, 77(6), 980-985. DOI: 10.15288/jsad.2016.77.980  

  • December 10, 2016
  • 04:48 PM
  • 317 views

Yet again, more of the same …

by Craig Payne in Running Research Junkie

Yet again, more of the same …... Read more »

  • December 10, 2016
  • 04:28 AM
  • 416 views

"Are we expecting too much from the extreme male brain theory of autism?"

by Paul Whiteley in Questioning Answers

The title of this post reflects the commentary published by Andrew Whitehouse [1] (open-access) discussing the meaning of the findings reported by Kung and colleagues [2] who quite categorically stated that there was: "No relationship between prenatal androgen exposure and autistic traits" in their study.OK, androgen exposure and psychology basically refers to the extreme male brain theory and autism which suggests that the so-called over-representation of autism in males is potentially down to hormone exposure (testosterone). The theory implies that androgen exposure at critical points in early development are skewing brain development towards a more 'male brain'. The definition of a male brain: well, apparently men are better systemisers than empathisers (better engineers that priests, I assume). The extreme male brain (EMB) hypothesis is an extension of the 'Theory of Mind' (ToM) stuff, which quite a few years back suggested that those diagnosed as being on the autism spectrum have greater difficulties in decoding mental states such as intents and desires. Grand psychological theories at their very finest you might say.The problem is that whilst ToM and the EMB theory made great psychological textbook reading (certainly in their heyday between the mid-1980s up to the late 1990s) and have spawned a whole industry around testing and teaching ToM for example, the scientific evidence for these concepts being exclusively and universally attributable to the great heterogeneity that is autism is not actually all that great. A shocker I know; and don't even ask about how comorbidity around autism might also be pretty important to such psychological concepts (see here and see here for example).Whitehouse - who himself has done some research in this area - talks quite a bit about the hows and whys of quite a few negative findings when it comes to the EMB theory (yes, there are quite a few) and what perhaps needs to be done to "advance beyond this stalemate" in relation to the EMB theory and autism.  His suggestion: "future research must first understand how the prenatal hormone environment relates to individual behavioural dimensions, and then incorporate this knowledge into the investigation of links with the more aetiologically and phenotypically complex profile of ASD [autism spectrum disorder]."These are wise words indeed but I'd suggest this perhaps applies to any 'theory' in relation to autism, psychological, biological or genetic. Indeed, I believe that other authors (see here) have already staked their claim on how using the word 'autism' as a starting point for anything other than a descriptive label probably isn't going to move autism research along any time soon; autisms people, autisms. The challenge is also one of moving away from generalisations; so talking about male and female brains is probably about as useful as talking about left and right-sided brains. Indeed, I'll refer you to some discussions about 'gender brains' between the main proponent of the EMB theory and a psychologist a few years back (see here and see here) that kicked up some scientific dust.I personally do think there is something in the findings looking at androgen levels and cognitive styles in the same way that there is something in most (replicated) peer-reviewed research when it comes to autism. But as Prof. Whitehouse indicates, it's probably going to be more relevant to some on the autism spectrum than others, and even then, disentangling the 'cognitive' structure of autism is going to be important [3]. The days of grand over-arching psychological theories about autism do seem to be riding off into the scientific sunset as the huge diversity and 'burden' of over-represented comorbidity start to come into plain sight. And certainly I don't think it's too rude to end with the words 'about time too'.To close, I hark back to simpler days or should that be to a simpler future when Buck Rogers showed the 25th Century how to boogie. Tell him what you think Twiki.----------[1] Whitehouse AJO. Commentary: Are we expecting too much from the extreme male brain theory of autism? A reflection on Kung et al. (2016). J Child Psychol Psychiatry. 2016 Dec;57(12):1463-1464.[2] Kung KT. et al. No relationship between prenatal androgen exposure and autistic traits: convergent evidence from studies of children with congenital adrenal hyperplasia and of amniotic testosterone concentrations in typically developing children. J Child Psychol Psychiatry. 2016 Dec;57(12):1455-1462.[3] Happé F. et al. Time to give up on a single explanation for autism. Nat Neurosci. 2006 Oct;9(10):1218-20.----------Whitehouse AJ (2016). Commentary: Are we expecting too much from the extreme male brain theory of autism? A reflection on Kung et al. (2016). Journal of child psychology and psychiatry, and allied disciplines, 57 (12), 1463-1464 PMID: 27859346... Read more »

  • December 9, 2016
  • 04:53 AM
  • 380 views

'Big data' Taiwan and schizophrenia risk

by Paul Whiteley in Questioning Answers

Today I bring the findings reported by Chou and colleagues [1] (open-access available here) to the blogging table and how the research might of the Taiwan National Health Insurance Database (NHIRD) brought it's 'big data' ("n = 23 422 955") to bear on the question: what is the risk of developing schizophrenia where one or more first-degree or other relatives are affected?The answer: "Having an affected co-twin, first-degree relative, second-degree relative, or spouse was associated with an adjusted RR [relative risk] (95% CI) of 37.86 (30.55-46.92), 6.30 (6.09-6.53), 2.44 (1.91-3.12), and 1.88 (1.64-2.15), respectively. Compared with the general population, individuals with one affected first-degree relative had a RR (95% CI) of 6.00 (5.79-6.22) and those with 2 or more had a RR (95% CI) of 14.66 (13.00-16.53) for schizophrenia."To translate the science-talk: if one twin is diagnosed with schizophrenia, there is a hugely increased risk of the other twin also being affected. If a mother or father, sister or brother, or your child(ren) are diagnosed with schizophrenia, there is an enhanced risk but nothing like the risk to twins. As you move outwards to other outlying family members (uncles, aunts, grandparents, etc) affected, your risk continues to diminish albeit still noticeable. Interestingly, when it comes to spouses (husband or wife), there is a small but increased risk that if they are diagnosed with schizophrenia so the other partner is at some small, enhanced risk. This tallies with the concept of assortative mating [2] but does not necessarily rule out other shared non-genetic factors either.The final sentence in that quote provides some evidence for a cumulative effect too. So if one of your close family members is diagnosed with schizophrenia, so the risk to yourself might be heightened. If two or more close family members are diagnosed, the relative risk to yourself jumps quite a bit more."A family history of schizophrenia is therefore associated with a higher risk of developing schizophrenia, mood disorders, and delusional disorders. Heritability and environmental factors each account for half of the phenotypic variance of schizophrenia."To close, Yoda don't like seagulls...----------[1] Chou IJ. et al. Familial Aggregation and Heritability of Schizophrenia and Co-aggregation of Psychiatric Illnesses in Affected Families. Schizophr Bull. 2016 Nov 21. pii: sbw159.[2] Parnas J. Assortative mating in schizophrenia: results from the Copenhagen High-Risk Study. Psychiatry. 1988 Feb;51(1):58-64.----------Chou IJ, Kuo CF, Huang YS, Grainge MJ, Valdes AM, See LC, Yu KH, Luo SF, Huang LS, Tseng WY, Zhang W, & Doherty M (2016). Familial Aggregation and Heritability of Schizophrenia and Co-aggregation of Psychiatric Illnesses in Affected Families. Schizophrenia bulletin PMID: 27872260... Read more »

  • December 9, 2016
  • 04:30 AM
  • 333 views

Balancing on the BACK

by Abbis Haider Jaffri in Sports Medicine Research (SMR): In the Lab & In the Field

Patients who suffer from current or previous symptoms of lower back pain demonstrated lower reach distances in the posterior directions of the Y-Balance Test compared to healthy individuals.... Read more »

  • December 8, 2016
  • 03:14 PM
  • 196 views

ExAC presents a catalogue of human protein-coding genetic variation

by Kamil S. Jaron in genome ecology evolution etc

Exploration of variability of human genomes represents a key step in the holy grail of human genetics – to link genotypes with phenotypes, it also provides insights to human evolution and history. For this purpose Exome Aggregation Consortium (ExAC) have … Continue reading →... Read more »

Lek M, Karczewski KJ, Minikel EV, Samocha KE, Banks E, Fennell T, O'Donnell-Luria AH, Ware JS, Hill AJ, Cummings BB.... (2016) Analysis of protein-coding genetic variation in 60,706 humans. Nature, 536(7616), 285-91. PMID: 27535533  

  • December 8, 2016
  • 04:51 AM
  • 367 views

Prescription medication use and autism: good medicines management required

by Paul Whiteley in Questioning Answers

"Prescription drug use and polypharmacy rates among adults with ASD [autism spectrum disorder] are substantially higher than those in an age-, sex-, and race-matched cohort of adults without ASD."That sentence taken from the paper by Rini Vohra and colleagues [1] (open-access available here) is probably not likely to win any 'novel findings of the year' awards given the already quite voluminous data published on the medication use and autism (see here for example). What gives the Vohra data a bit of an edge is that: (a) they included data for some 1700 adults with autism "matched 1:3 with adults without autism", (b) data were derived from administrative health insurance claims databases in the United States ("Medicaid programs"), and (c) they examined "the rates of prescription drug use, general polypharmacy, and psychotropic polypharmacy among adults" thus were able to detail not just psychotropic medication use but also that for other, more general conditions too.Their findings were stark. Accompanying that opening sentence on medication use and autism, authors reported that: "Annually, almost 75% of adults with ASD had >20 prescription drug claims compared with 33% of adults without ASD." That's more than 20 prescription medication claims per year.Further: "Other than psychotropics, many adults with ASD used medical prescription drugs such as antimicrobials (47%), dermatologic agents (48%), respiratory agents (38%), gastrointestinal agents (31%), alternative medications (25%), antiparkinsonian agents (22.6%), antihyperlipidemics/statins (7.3%), and immunologics (2.0%)." So when we start talking about the label of autism not appearing in some sort of diagnostic vacuum, and particularly that various medical comorbidity seem to be 'over-represented' when it comes to autism (see here), this is reflected in the large burden of medication being dispensed. If readers trawl through the adjusted odds ratios (AORs) generated when those with autism were compared with controls (Table 1), you'll note that many classes of medicine were more frequently prescribed to those with autism.  And where medicines were less frequently prescribed to the autism group, there were some potentially telling signs too: analgesics (used for pain relief), antidiabetics and antimicrobials. One could argue that maybe those diagnosed with autism have less need of things like pain relief or antibiotics or less likely to need antidiabetic medicines. One might however similarly argue that their medical and healthcare screening services could perhaps be 'less rigorous' than those not diagnosed with autism too, potentially as a result of various factors (see here).Onwards: "Adults with ASD and a psychiatric comorbidity such as an adjustment disorder (26%), mood disorder (31%), or schizophrenia (32%) had significantly high rates of psychotropic polypharmacy." I probably don't need to say much more about this sentence aside from the fact that mood disorder including things like depression are not uncommon diagnoses alongside autism (see here). The links with the schizophrenia spectrum are also not to be underestimated (see here).Finally: "Older age, female gender, White race, and presence of three or more comorbid conditions among adults with ASD is significantly associated with using six or more prescription drug classes per year." This sentence is not a roadmap to predicting who will need what medicines when it comes to autism but does provide some important information. There is for example, a woeful lack of research on autism in a longitudinal sense (see here) despite the topic of ageing and autism being debated time and time again. Inevitably as people age, their medication requirements are likely to change (increase?); this is as true for autism as it is for the not-autism population.I included the words 'good medicines management required' in the title of this post because, as you can see, the level of prescription medicines use when it comes to autism can be high and one needs to be careful that medicines are appropriate, monitored regularly and don't interact with one and another. Given what is also known about psychotropic medicines in particular in terms of potential side-effects (see here and see here for examples), the onus is surely on prescribers to keep an even closer eye on those with autism who are being medicated under their care. Medication is a part of life when it comes to autism. I base that last sentence on the wealth of data, peer-reviewed and otherwise, that has been published on this topic. I'm sure nobody particularly likes the idea of medication particularly when it comes to autism and certainly nobody should like the idea that some people on the autism spectrum are receiving quite a lot of prescription medicine concurrently and over quite long periods of time. But here's the thing, medication (generally) serves an important purpose. In the case of the antiepileptics/anticonvulsants it can be life-saving. Where mood disorders such as depression are being pharmacologically treated, it can be life-saving. Until, science is able to get a better idea of why some many conditions/labels seem to be over-represented when it comes to autism, medication is often all that it can offer at the moment...----------[1] Vohra R. et al. Prescription Drug Use and Polypharmacy Among Medicaid-Enrolled Adults with Autism: A Retrospective Cross-Sectional Analysis. Drugs Real World Outcomes. 2016 Nov 21.----------Vohra R, Madhavan S, Sambamoorthi U, StPeter C, Poe S, Dwibedi N, & Ajmera M (2016). Prescription Drug Use and Polypharmacy Among Medicaid-Enrolled Adults with Autism: A Retrospective Cross-Sectional Analysis. Drugs - real world outcomes PMID: 27873285... Read more »

  • December 7, 2016
  • 12:36 PM
  • 358 views

Pregnancy folic acid and offspring autism systematically reviewed

by Paul Whiteley in Questioning Answers

"A total of 22 original papers that examined the association between folic acid supplementation in human pregnancy and neurodevelopment/autism were identified after the screening, with 15 studies showing a beneficial effect of folic acid supplementation on neurodevelopment/autism, 6 studies showed no statistically significant difference, while one study showed a harmful effect in > 5 mg folic acid supplementation/day during pregnancy."That rather long quote taken from the paper published by Yunfei Gao and colleagues [1] (open-access) opens today's post and provides a welcome [peer-reviewed] overview of where science is up to when it comes to the effects (or not) of pregnancy folic acid supplementation on 'risk' of offspring autism. I say 'where the science is up to' but at the same time note that the various searches of databases for material relevant to this topic/review was carried out up to the end of 2014. There have been other reports since that date including other reviews [2]...Folic acid or folate in the context of autism has been a recurrent research theme down the years. Outside of the protective effects of pregnancy folate use with regards to reducing the risk of offspring neural tube defects (NTDs), the suggestion that pregnancy folic acid may confer a protective effect against offspring autism has been highlighted in several studies (see here).Gao et al trawled the research literature and "included randomized controlled trials (RCTs), cohort studies, and case control studies that examined the association between folic acid supplementation during pregnancy and neurodevelopment/autism in the offspring children." As per that lengthy opening sentence from their paper, the authors found data that on the whole suggested that folate supplementation was protective rather than harmful when it came to offspring developmental outcomes. Given that most/many pregnant women are already taking folic acid during pregnancy to counter the risk of NTDs, this is good news indeed.Without giving any undue weight to those studies that have perhaps not been so enthusiastic about the link between pregnancy folate use and offspring autism risk (see here) I do think there are words of caution in this area too. We're still for example, waiting for research to be published that was raised at this years IMFAR event in relation to folic acid and autism (see here). Indeed, in my discussion of that so-far-unpublished work, I mentioned that the genetics of folic acid metabolism also needs to be further inspected when it comes to autism (see here) and that screening for particular issues linked to folate might be something to consider for people on the autism spectrum and their significant others (see here). Both these areas are potentially relevant to that recent chatter on how folinic acid might be useful for some aspects of some autism (see here)."Large scale RCTs with validated diagnosis and high follow up rate are needed in order to produce robust evidence regarding the effects of folic acid supplementation in pregnancy on fetal neurodevelopment" conclude the authors. Yes, we need more investigation of this area - including what effect certain medicines used during pregnancy might have had on folate levels -  but for now, the data seems to side with a protective effect of folate supplementation in pregnancy when it comes to offspring risk of autism or related neurodevelopmental issues.----------[1] Gao Y. et al. New Perspective on Impact of Folic Acid Supplementation during Pregnancy on Neurodevelopment/Autism in the Offspring Children – A Systematic Review. PLoS ONE. 2016; 11(11): e0165626.[2] DeVilbiss EA. et al. Maternal folate status as a risk factor for autism spectrum disorders: a review of existing evidence. Br J Nutr. 2015 Sep 14;114(5):663-72.----------Gao Y, Sheng C, Xie RH, Sun W, Asztalos E, Moddemann D, Zwaigenbaum L, Walker M, & Wen SW (2016). New Perspective on Impact of Folic Acid Supplementation during Pregnancy on Neurodevelopment/Autism in the Offspring Children - A Systematic Review. PloS one, 11 (11) PMID: 27875541... Read more »

  • December 7, 2016
  • 04:30 AM
  • 315 views

Thinking about high-dose vitamin D supplements for your athletes? Make sure the dose is right.

by Kyle Harris in Sports Medicine Research (SMR): In the Lab & In the Field

A Blanket high dose vitamin D supplement plan results in elevated levels of vitamin D metabolites after the supplementation is completed. This could result in lower than normal levels of vitamin D, which is the opposite effect of the intended supplementation.... Read more »

Owens DJ, Tang JC, Bradley WJ, Sparks SA, Fraser WD, Morton JP, & Close GL. (2016) Efficacy of High Dose Vitamin D Supplements for Elite Athletes. Medicine and science in sports and exercise. PMID: 27741217  

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