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  • May 5, 2017
  • 03:55 AM

Trends in ADHD medication use in the US and Europe: is this a bad thing?

by Paul Whiteley in Questioning Answers

I don't want to dwell too much on the findings reported by Christian Bachmann and colleagues [1] observing that in five Western countries - Denmark, Germany, the Netherlands, the United Kingdom (UK) and the United States (US) - ADHD (attention-deficit hyperactivity disorder) medication use between 2005/2006-2012 was on the increase. But I do think it is important to mention some of the implications from such figures and some of the positives and negatives associated with such generated data.OK, first things first. The general consensus is that the prevalence of ADHD in many parts of the world is on the up compared with say a decade or two ago. We can um-and-ah about whether this is a true increase in cases or whether through changes to the way ADHD is diagnosed for example, the figures are artificially inflated (see here). Indeed, whether for some - not by any means all - a diagnosis of ADHD is merely a means to an end (see here). Suffice to say that many studies either looking directly at rates of ADHD or via analysis of medication prescribing patterns suggest that more cases are being diagnosed these days. And that includes the use of ADHD as a comorbid diagnosis in relation to labels such as autism for example (see here) on the back of the important discussions about autism not typically presenting in some sort of diagnostic vacuum (see here).The use of medication prescribing patterns to track estimated ADHD prevalence is the preferred method employed by Bachmann et al who concluded that: "ADHD medication use prevalence increased from 1.8% to 3.9% in the Netherlands cohort (relative increase: +111.9%), from 3.3% to 3.7% in the US cohort (+10.7%), from 1.3% to 2.2% in the German cohort (+62.4%), from 0.4% to 1.5% in the Danish cohort (+302.7%), and from 0.3% to 0.5% in the UK cohort (+56.6%)."So, the positives from the Bachmann data. Well, accepting that ADHD is a label that, in the longer term, has been associated with heightened risk for all-manner of adverse life events (see here and see here for examples) I don't think anyone would argue that with the availability of good, safe, reliable treatment options (see here) and that such management avenues should be properly utilised. I know some people might be a little reluctant to want to medicate children for example, but the data from the various collected studies on something like methylphenidate use (typically indicated for ADHD or the presentation of ADHD-type behaviours) generally regards the medicine as safe and well tolerated albeit with monitoring and good medicines management implied. And by saying that I'm not suggesting that medication is/should be the only management option when it comes to ADHD (see here and see here for other examples). My reading of the Bachmann data is that prescribing clinicians are doling out more prescriptions for managing ADHD but this is a reflection of (a) greater recognition of ADHD and ADHD behaviours and/or (b) the value of prescribing such medicines to things like quality of life of recipients and their families.The negatives... well, it wouldn't be difficult to suggest that with the realisation that quite a few ADHD medications have a good overall safety/response profile, clinicians perhaps become a little more 'comfortable' with their prescription over a wider range of presenting behaviours without necessarily looking at other options first. The fact for example, that Bachmann et al observed: "ADHD medication use was highest in 10-14-year olds", a special time when quite a few biological changes are on-going, could be interpreted as such medication use being a pharmacological 'crutch' during such a period. I don't know enough about ADHD to comment on whether its presentation is 'enhanced' as and when puberty hits but if it's anything like other labels [2]...Reiterating that medication is not the only intervention option when it comes to ADHD and that one still needs to be cautious about the use of psychoactive substances typically being part of ADHD pharmacotherapy, I am airing on the more positive implications of the Bachmann findings rather than the negatives. Like many other discussions about medication use under various different circumstances (see here for example) it's easy to say that such medicines use is growing because of inappropriate or over-zealous use and should be curbed. But such medications often afford a real increase in quality of life when it comes to ADHD and, bearing in mind those enhanced risks typically associated with the label of ADHD, I can't in all honesty say that greater medication use is specifically detrimental to individuals personally or in a wider context...----------[1] Bachmann CJ. et al. Trends in ADHD medication use in children and adolescents in five western countries, 2005-2012. Eur Neuropsychopharmacol. 2017 Mar 20. pii: S0924-977X(17)30184-0.[2] Gillberg C. & Schaumann H. Infantile autism and puberty. J Autism Dev Disord. 1981 Dec;11(4):365-71.----------Bachmann CJ, Wijlaars LP, Kalverdijk LJ, Burcu M, Glaeske G, Schuiling-Veninga CC, Hoffmann F, Aagaard L, & Zito JM (2017). Trends in ADHD medication use in children and adolescents in five western countries, 2005-2012. European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology PMID: 28336088... Read more »

Bachmann CJ, Wijlaars LP, Kalverdijk LJ, Burcu M, Glaeske G, Schuiling-Veninga CC, Hoffmann F, Aagaard L, & Zito JM. (2017) Trends in ADHD medication use in children and adolescents in five western countries, 2005-2012. European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology. PMID: 28336088  

  • May 4, 2017
  • 04:15 AM

Self-reported sexual attraction and autism

by Paul Whiteley in Questioning Answers

The findings reported by Tamara May and colleagues [1] are discussed today, looking at self-reported sexual attraction and past sexual relationships among adolescents diagnosed with an autism spectrum disorder (ASD) compared with not-autism controls.Asking 14-15 year olds who took part in The Longitudinal Study of Australian Children (94 diagnosed with autism and some 3400 controls) some rather personal questions, researchers reported that: "ASD males reported fewer prior boyfriends/girlfriends" and "female adolescents with ASD have differences in sexual attraction compared with non-ASD females." Those female 'differences' included things like greater "uncertainty in attraction" and "lower rates of heterosexual preference."Minus sweeping generalisations, the use of self-report in this study is a bit of a bonus in this context. Quite a few times on this blog I've been a little critical when self-report is used in the context of autism research (i.e. not necessarily as objective as some of the schedules out there administered by trained professionals) but when it comes to aspects of sexuality and relationships, it is the person who most definitely knows best [2]. If I did have one slight issue with this work it would be to ask the question: how representative of the autism spectrum were the participant group included for study? Y'know, self-report implies language use and all that...This work does continue a theme in autism research. Although perhaps seemingly obvious, it confirms a few important things; primarily that young adults on the autism spectrum are in the most part, interested in sex and relationships [3] (accepting that 'sex' and 'relationships' are not necessarily one and the same). I know for some this is not new news (see here) but such a finding can sometimes get lost in all the chatter about presenting symptoms, challenges and the like when it comes to the autism spectrum.Insofar as the finding that females with ASD included in the May cohort were more likely to report lower rates of heterosexual preference and higher rates of bisexuality, this is not a new finding. Bejerot & Eriksson [4] previously reported that "tomboyism and bisexuality were overrepresented amongst women with autism spectrum disorder" (not that tomboyism is necessarily a measure of bisexuality). Other groups have also mentioned this finding too [6]. This could have implications for things like sex education and ensuring that sex education covers 'all the bases' in terms of the spectrum of sexuality. I also draw back from making too many links with the literature for example, on gender dysphoria and autism / autistic traits (see here) but I daresay this might also show also some importance, at least for some.Sex and relationships are an integral part of growing up. Children on the autism spectrum [typically] grow up to be adults on the autism spectrum, and sex - thoughts, feelings, actions - will figure as part of that maturation process, the same as it does for everyone else. Providing comprehensive and tailored sex education [5] should be an important part of discussions; parents as well as educators, need to be in on those important discussions...Noting the date today (May the 4th), a customary link is required.----------[1] May T. et al. Brief Report: Sexual Attraction and Relationships in Adolescents with Autism. J Autism Dev Disord. 2017 Mar 24.[2] Dewinter J. et al. Parental Awareness of Sexual Experience in Adolescent Boys With Autism Spectrum Disorder. J Autism Dev Disord. 2016 Feb;46(2):713-9.[3] Fernandes LC. et al. Aspects of Sexuality in Adolescents and Adults Diagnosed with Autism Spectrum Disorders in Childhood. J Autism Dev Disord. 2016 Sep;46(9):3155-65.[4] Bejerot S. & Eriksson JM. Sexuality and gender role in autism spectrum disorder: a case control study. PLoS One. 2014 Jan 31;9(1):e87961.[5] Ingudomnukul E. et al. Elevated rates of testosterone-related disorders in women with autism spectrum conditions. Horm Behav. 2007 May;51(5):597-604.[6] Hannah LA. & Stagg SD. Experiences of Sex Education and Sexual Awareness in Young Adults with Autism Spectrum Disorder. J Autism Dev Disord. 2016 Dec;46(12):3678-3687.----------May T, Pang KC, & Williams K (2017). Brief Report: Sexual Attraction and Relationships in Adolescents with Autism. Journal of autism and developmental disorders PMID: 28342163... Read more »

  • May 3, 2017
  • 06:30 PM

Gimme Your Lunch Money!: Feeding Behaviors in Hummingbirds

by Melissa Chernick in Science Storiented

Ubatuba, São Paulo, Brazil; 9 October 2014 © Almir Cândido de AlmeidaI just put out my hummingbird feeder this season. It didn’t take those little guys long to find it either. Now I’ve got their cute little bodies whizzing about all over the place. They need Yackety Sax to play as their soundtrack. But it got me to thinking about hummingbirds and to looking through recent papers for a good study. I came across one in Zoologia about the feeding behavior of hummingbirds in artificial food patches. Perfect.First, a little background on hummingbirds. They belong to the family Trochilidae and are closely related to swifts. Males are typically more colorful that females, having highly reflective feathers on their chest and heads. Perhaps these birds are best known for their unique flying. They are able to produce power with both the down- and up-beat of their wing flap, getting 75 percent of their lift from their wings’ downstroke and the remaining 25 percent from the upstroke. This allows for both increased agility and sustained hovering ability. They are the only birds that truly hover and fly backwards. They also move those wings really fast: 60 times per second! So it is little wonder that they have among the highest metabolic rate among vertebrate animals.Hummingbirds are specialized and consume predominately nectar. To collect enough nectar to maintain that high metabolism, they forage many flowers each day. But not all flowers are created equally. Their sugar concentration can vary between 20-25 percent. In order to get the most sugar-bang for their hover-buck, hummingbirds must select and protect the richest food patches in their area. Three behavioral strategies have been observed for foraging:1) Dominance/territoriality – a bird will defend its flowers2) Intruder/subordinance – a bird sneaks into other patches until it is kicked out3) Trapline foraging – repeatedly visiting a set of plants in different patches without being territorial.Often, a bird will perch near a good food source and let others know that it is theirs. But defending a territory can be up to three times more energetically expensive, so those flowers need to be really good.The researchers conducted their study in Itacolomi State Park in the city of Ouro Preto, Minas Gerais, southwestern Brazil, in the Atlantic forest remnant. They created four artificial food patches, each patch containing a single sugar-water solution concentration of 5, 15, 25, or 35 percent. They observed the birds (using binoculars) for 3 hour stretches in the early mornings and late afternoon, recording all behaviors during that time. They looked at the time spent in each food patch and the behaviors of the birds (feeding, alert, vocalizing, expelling, fighting, frightening, expel attempt) in each patch. In this way, they could identify the birds’ strategies.They found that the most-visited feeders were those containing the highest concentration of sugar. Five of the seven species observed fed more on the 25-35 percent sucrose feeders. But there was a difference in the frequency of visitations for different species. The Brazilian ruby (Clytolaema rubricauda, pictured above), Scale-throated hermit (Phaethornis eurynome), and Phaethornis spp. visited the 35 percent feeder more often. And the Brazilian ruby won most of the aggressive encounters with other hummingbirds, both total and in individual patches. This species often stood alert and fought more often, and even “stood impassive” when faced down by the Violet-capped woodnymph (Thalurania glaucopis). I wonder if they looked down their long little beaks at the other birds with a f*ck off attitude? What a badass...hmm, or a bully. The Violet-capped woodnymph visited the 25 percent patch more often, the White-throated hummingbird (Leucochloris albicollis) and Versicoloured emerald (Amazilia versicolor) visited the 15 percent patch more often, and the Glittering-bellied emerald (Chlorostilbon lucidus) was the one that less frequently visited the food patches. Interestingly, the Phaetornithinae applied a hide-and-wait strategy, where they would be chased away by the territorial bird only to hide in the shrubs, remain quiet, and return to the feeder after the dominant bird left the area. Sneaky sneaky. The time spent feeding was found to be correlated with aggressive behaviors and also with body size. Big birds, big appetites, big aggression. The subordinate species chose resources depending on the presence or absence of the dominant species, preferring patches that were not guarded. This may be why they were seen in lower concentration sugar patches more often. Those itty bitty birds can pack some serious aggression. I guess it isn’t really surprising after seeing all of the chasing that goes on around my feeder. Yackety Sax remains appropriate.Lanna, L., de Azevedo, C., Claudino, R., Oliveira, R., & Antonini, Y. (2017). Feeding behavior by hummingbirds (Aves: Trochilidae) in artificial food patches in an Atlantic Forest remnant in southeastern Brazil Zoologia, 34, 1-9 DOI: 10.3897/zoologia.34.e13228If you would like to put out your own hummingbird feeder, I recommend this kind because it is simple, inexpensive and does a great job.The important part is the big red flowers with yellow centers. Hummingbirds really hone in on those color ques. Do NOT use honey in your feeder! And forget the red dye, if your feeder has red color on it then that is plenty to attract the hummingbirds.Here is a nice and simple recipe to make your own hummingbird food:¼ cup granulated sugar2 cups waterMix the ingredients in a small saucepan. Bring to a boil. Boil for a few minutes or until all of the sugar is dissolved. Let cool to room temperature. Whatever doesn’t fit in the feeder can be stored in the refrigerator. Increase the recipe as needed, it's a 1:4 ratio of sugar:waterChange the solution in the feeder every 3 days, sooner if it is really hot outside. Make sure to rinse the feeder each time it is refilled. Scrub away any growths (fungi, etc.) as needed. Brazilian Ruby picture via The Cornell Lab of OrnithologyFeeder image via World of Hummingbirds... Read more »

  • May 3, 2017
  • 03:42 PM

How Can We Measure Human Oxytocin Levels?

by Neuroskeptic in Neuroskeptic_Discover

Is oxytocin really the love and trust chemical? Or is it just the hype hormone? A new paper suggests that many studies of the relationship between oxytocin and behaviors such as trust have been flawed.

The paper is a meta-analysis just published by Norwegian researchers Mathias Valstad and colleagues. Valstad et al. found that the level of oxytocin in human blood, often used as a proxy measure of brain oxytocin, has no relation to central nervous system oxytocin levels under normal co... Read more »

Valstad M, Alvares GA, Egknud M, Matziorinis AM, Andreassen OA, Westlye LT, & Quintana DS. (2017) The correlation between central and peripheral oxytocin concentrations: a systematic review and meta-analysis. Neuroscience and biobehavioral reviews. PMID: 28442403  

  • May 3, 2017
  • 03:53 AM

ADHD and suicide

by Paul Whiteley in Questioning Answers

"There is a positive association between ADHD [attention-deficit hyperactivity disorder] and suicidality in both sexes and in all age groups."So said the results of the systematic review published by Balazs & Kereszteny [1] (open-access available here) who surveyed the recent peer-reviewed literature on the topic between 2011 and 2015. Reporting results based on findings included in 26 papers, authors concluded that suicidality - ideation, behavior, attempts, and suicide - seems to be an over-represented facet following receipt of a diagnosis of ADHD and that "early recognition and treatment of ADHD - either as a comorbid condition or as a main diagnosis- and the co-occurring psychiatric disorders, can play an important role in the secondary prevention of suicide."These are important findings. Alongside the various research results suggesting that ADHD may set someone up for a variety of 'future adverse outcomes' (see here) there are potential lessons to be learned for a whole host of labels/conditions where ADHD is part and parcel of the clinical picture. Given the core blogging material included on this site and the realisation that autism and ADHD can very much co-occur (see here) I'm inclined to suggest that the Balazs/Kereszteny findings are particularly pertinent to the autism spectrum and the issue of suicidality being over-represented when it comes to the diagnosis (see here for example). Indeed, when one talks about suicidality in the context of the autism spectrum and how one might mitigate any enhanced risk (see here), ADHD as one of several over-represented labels following autism may represent another important consideration. And that also goes for another over-represented but perhaps 'atypically presented' condition potentially following a diagnosis of autism [2].To close, although suicide (ideation and/or attempt) is a complicated and often very individual process, that's not to say that general intervention(s) might not be useful [3]...----------[1] Balazs J. & Kereszteny A. Attention-deficit/hyperactivity disorder and suicide: A systematic review. World J Psychiatry. 2017 Mar 22;7(1):44-59.[2] das Neves Peixoto FS. et al. Bipolarity and suicidal ideation in children and adolescents: a systematic review with meta-analysis. Ann Gen Psychiatry. 2017 Apr 21;16:22.[3] Riblet NBV. et al. Strategies to prevent death by suicide: meta-analysis of randomised controlled trials. Br J Psychiatr. 2017. April 20.----------Balazs J, & Kereszteny A (2017). Attention-deficit/hyperactivity disorder and suicide: A systematic review. World journal of psychiatry, 7 (1), 44-59 PMID: 28401048... Read more »

  • May 2, 2017
  • 04:00 AM

Mitochondrial mutations are not common in chronic fatigue syndrome but...

by Paul Whiteley in Questioning Answers

"We report the complete mtDNA [mitochondrial DNA] sequence of 93 CFS [chronic fatigue syndrome] patients from the UK and RSA, without finding evidence of clinically proven mtDNA mutations."So said the results reported by Elizna Schoeman and colleagues [1] (open-access available here) who drew on other research previously covered on this blog (see here) suggesting that "symptoms of mitochondrial diseases and CFS frequently overlap and can easily be mistaken" to look-see whether issues with mitochondrial DNA might be important to at least some cases of CFS. Their investigation found no evidence that within this cohort at least, undiagnosed mtDNA disease was apparent. They do caution however that their findings do not "exclude a role for mtDNA population variation in the susceptibility to CFS", neither also did they provide any functional biological analysis of the presentation of mitochondrial function/disease in cases on this research occasion. I might add that the lack of an association between mitochondrial genomes and CFS is not a new finding [2].Mitochondria represent the so-called 'powerhouse' of cells as a result of their link with compounds such as ATP (adenosine triphosphate) among other things. Functional issues with mitochondria are known to manifest as 'fatigue' on some occasions and so it stands to reason that they should be explored in conditions where fatigue is a primary symptom such as in CFS. Indeed, other authors have looked at 'targeting' mitochondria onward to tackling some of those fatigue-related symptoms present in cases of CFS (see here).The Schoeman results are a bit of a blow to the idea that genetically speaking, issues with mitochondria are a core part of CFS such that "CFS does not fall within the spectrum of inherited mtDNA disorders." But I would perhaps draw your attention to some of the 'interventions' that have been talked about in relation to CFS that have a 'mitochondrial' edge to them (see here) and have 'helped' under experimental conditions. Further, how just because CFS is not an inherited genetic condition as a result of underlying [genetic] mitochondrial disease does not necessarily rule out the targeting of mitochondrial functions in at least some cases of CFS. This bearing in mind the typical onset age of something like CFS (see here) and that various 'trigger' factors have been implicated with onset in mind (see here).To close, I also note that the Cochrane guidance on the use of exercise therapy in relation to CFS has been updated (again) recently [3]. Personally, I'm minded to be a little cautious about quite sweeping statements like: "We think the evidence suggests that exercise therapy might be an effective and safe intervention for patients able to attend clinics as outpatients" made by the authors, particularly when accompanying statements like: "Serious side effects were rare in all groups, but limited information makes it difficult to draw firm conclusions about the safety of exercise therapy" are made. 'First do no harm' and all that and then perhaps focus a little more on important concepts like PEM in light of other meta-analysed findings [4]...----------[1] Schoeman EM. et al. Clinically proven mtDNA mutations are not common in those with chronic fatigue syndrome. BMC Med Genet. 2017 Mar 16;18(1):29.[2] Billing-Ross P. et al. Mitochondrial DNA variants correlate with symptoms in myalgic encephalomyelitis/chronic fatigue syndrome. J Transl Med. 2016 Jan 20;14:19.[3] Larun L. et al. Exercise therapy for chronic fatigue syndrome. Cochrane Database Syst Rev. 2017 Apr 25;4:CD003200.[4] Loy BD. et al. Effect of Acute Exercise on Fatigue in People with ME/CFS/SEID: A Meta-analysis. Med Sci Sports Exerc. 2016 Oct;48(10):2003-12.----------Schoeman EM, Van Der Westhuizen FH, Erasmus E, van Dyk E, Knowles CV, Al-Ali S, Ng WF, Taylor RW, Newton JL, & Elson JL (2017). Clinically proven mtDNA mutations are not common in those with chronic fatigue syndrome. BMC medical genetics, 18 (1) PMID: 28302057... Read more »

Schoeman EM, Van Der Westhuizen FH, Erasmus E, van Dyk E, Knowles CV, Al-Ali S, Ng WF, Taylor RW, Newton JL, & Elson JL. (2017) Clinically proven mtDNA mutations are not common in those with chronic fatigue syndrome. BMC medical genetics, 18(1), 29. PMID: 28302057  

  • May 1, 2017
  • 06:22 AM

On abuse exposure and mate selection

by Paul Whiteley in Questioning Answers

The paper by Andrea Roberts and colleagues [1] is offered up for brief discussion today, and a slightly uncomfortable but nonetheless potentially important set of results that "provide evidence that childhood abuse affects mate selection, with implications for offspring health."I tread very carefully with this topic but was intrigued by the findings looking at whether 'offspring health' in the context of the presence of autism or autism spectrum disorder (ASD) might be at least sometimes mediated by the mate selection decisions made by women who "experienced childhood abuse." I might add that sweeping generalisations from this and related work from this authorship group (see here) are not required.Some of the data for this study, I believe, once again comes from the Nurses’ Health Study II where initially autistic traits were measured using the Social Responsiveness Scale (SRS) for men and women. These results were stratified for various types and levels of abuse reported to be encountered during childhood. Using some statistical modelling, researchers observed that: "Maternal childhood abuse was strongly associated with high paternal autistic traits." In other words, it seemed like the experience of childhood abuse - particularly severe childhood abuse - encountered by women, seemed to correlate with later selection of partners who scored high when it came to the presence of autistic traits (as measured by the SRS). Results also took into account various potential confounding variables including socio-economic status (SES).Bearing in mind previous discussions on assortative mating and autism [2] where "people who have certain “autistic” traits are increasingly meeting and marrying each other and having offspring who are more likely to be on the spectrum" the Roberts results potentially add an additional dimension. They suggest that early life experiences (particularly adverse experiences) may have quite a powerful effect when it comes to choices of mating partner. Whether this is driven by an active preference for the presence of autistic traits in a partner or is down to other factors such as 'availability' and/or 'accessibility' cannot be deduced from the current data. It is also important to add that looking at autistic traits alone does not necessarily mean that autistic traits drive any mating selection being undertaken. As I've mentioned before on this blog, various screens for autistic traits seem to have a generalisability issue (see here for example). I might also add that: "Maternal and paternal autistic traits accounted for 21% of the association between maternal abuse and offspring autism" so one has to be careful not to make too much of any single connection.But still there is something rather interesting from these latest results from Roberts et al [with appropriate cautions] that requires further research inspection...----------[1] Roberts AL. et al. Maternal Exposure to Childhood Abuse is Associated with Mate Selection: Implications for Autism in Offspring. J Autism Dev Disord. 2017 Apr 9.[2] Baron‐Cohen S. Two new theories of autism: hyper‐systemising and assortative mating. Archives of Disease in Childhood. 2006;91(1):2-5.----------Roberts AL, Lyall K, & Weisskopf MG (2017). Maternal Exposure to Childhood Abuse is Associated with Mate Selection: Implications for Autism in Offspring. Journal of autism and developmental disorders PMID: 28393290... Read more »

  • April 29, 2017
  • 06:18 AM

When grandmothers smoked during pregnancy...

by Paul Whiteley in Questioning Answers

Please, do not smoke during pregnancyALSPAC - the Avon Longitudinal Study of Parents and Children - continues to give in research terms as today I want to mention the findings reported by Jean Golding and colleagues [1] (open-access) observing "an association between maternal grandmother smoking in pregnancy and grand daughters having adverse scores in Social Communication and Repetitive Behaviour measures that are independently predictive of diagnosed autism."The study results have garnered quite a bit of media interest (see here for example) with calls for quite a bit more research to be carried out on this important topic. I might also give a hat-tip to Jill Escher and the Escher Fund for Autism who were instrumental in this study. Indeed, her analysis of the Golding results (see here) will no doubt trump my contribution.The Golding paper is open-access but a few details are worth mentioning:As I noted, ALSPAC provided the source data for the study (as it has on quite a few autism research occasions). This time around researchers looked at autistic traits among some of their 14,000 strong cohort comprising "a social communication score, a speech coherence score, a sociability temperament scale, and a repetitive behaviour score." Mothers and fathers of children involved in ALSPAC also provided information about pregnancy including answering questions on whether mothers themselves were/had smoked during pregnancy and also whether their mother (the child's grandmothers on both sides) smoked during pregnancy.The data obtained from the autistic traits measures (delivered at various times of the child's development) and the smoking histories were analysed. Data on some 170 participating children actually diagnosed with an autism spectrum disorder (ASD) were also thrown into the statistical mix.Results: "We found that two of the four autistic traits in the grandchild (F2) were increased in prevalence if the maternal grandmother (F0) smoked in pregnancy especially if the mother herself (F1) did not herself smoke." Researchers also noted a particular association between grandmother pregnancy smoking and grand-daughters over grandsons, and several potentially important confounding variables were also taken into account. They also concluded that "diagnosed autism was also associated with the maternal grandmother smoking in pregnancy" but express some caution in light of the smaller numbers included in this part of the analysis."These results are intriguing" say the authors. Indeed they are. Accepting the reliance on parental report, acceptance of the myriad of other factors that might affect any relationship and the fact that "sets of trait questions were not designed as measures of autistic traits but rather to identify the child’s performance in regard to a large number of attributes at different ages" as a consequence of researchers not originally expecting the prevalence of autism to be anything like it is today(!), further research is indicated. I say this in the context that research looking at any link between maternal pregnancy smoking and offspring autism risk has not consistently found any correlation (see here).Then to the question of mechanism of effect. Well, researchers talk about "two plausible candidate mechanisms" to account for results. First is "transmission of damage to mitochondrial DNA (mtDNA)" where mitochondria DNA is subject to 'mutation' as a result of exposure to tobacco smoke. The researchers noted that: "Mitochondrial transmission across the generations is exclusively via the mother, so is compatible with our observed associations between maternal prenatal tobacco exposure and adverse scores on Social Communication and Repetitive Behaviour measures in her granddaughters." The second possible mechanism is that of "epigenetic inheritance from one generation to the next." This builds upon something of a continuing debate where structural DNA issues (i.e. mutations) are put to one side in favour of chemical alterations to genes (e.g. the addition of methyl groups) affecting gene expression. It's a topic that has been talked about quite a bit on this blog with reference to autism (see here for example) but still needs a lot more science done on it specifically on transgenerational epigenetic inheritance. Smoking is known to have effects on DNA methylation (see here) but the suggestion is that these or other epigenetic effects could continue down into future generations.The potential effects of tobacco smoking during pregnancy in relation to second (or even third generation) autism or autistic traits risk requires quite a bit more study. Importantly, if such results are confirmed in future investigations, it opens up a whole myriad of possibilities in terms of how other previous generational exposures outside of just tobacco smoking during pregnancy might have affected future generations. This research area could get very, very complicated indeed.----------[1] Golding J. et al. Grand-maternal smoking in pregnancy and grandchild's autistic traits and diagnosed autism. Sci Rep. 2017 Apr 27;7:46179.----------Golding J, Ellis G, Gregory S, Birmingham K, Iles-Caven Y, Rai D, & Pembrey M (2017). Grand-maternal smoking in pregnancy and grandchild's autistic traits and diagnosed autism. Scientific reports, 7 PMID: 28448061... Read more »

Golding J, Ellis G, Gregory S, Birmingham K, Iles-Caven Y, Rai D, & Pembrey M. (2017) Grand-maternal smoking in pregnancy and grandchild's autistic traits and diagnosed autism. Scientific reports, 46179. PMID: 28448061  

  • April 28, 2017
  • 08:00 AM

Friday Fellow: Hooker’s Lips

by Piter Boll in Earthling Nature

by Piter Kehoma Boll We are always fascinated by plants that have some peculiar shape that resemble something else. And certainly one of them is the species I’m introducing today, Psychotria elata, also known as hooker’s lips or hot lips. Found … Continue reading →... Read more »

  • April 28, 2017
  • 04:04 AM

Autism, pregnancy maternal immune activation and vitamin D?

by Paul Whiteley in Questioning Answers

Today's post is a bit of a mash-up, drawing on two articles quite recently published in the peer-reviewed science domain.The first is by Stephanie Vuillermot and colleagues [1] (open-access) suggesting that "early dietary supplementation with vitamin D may open new avenues for a successful attenuation or even prevention of neurodevelopmental disorders following maternal inflammation during pregnancy." These findings have also received some media attention (see here for example) and continues a research theme focused on vitamin D (the sunshine vitamin/hormone) and [some] autism (see here for example).The second paper is by Michael Lombardo and colleagues [2] (open-access) and also covers the topic of maternal immune activation (MIA) and its potential effects on offspring outcomes, concluding that: "MIA may confer increased risk for ASD [autism spectrum disorder] by dysregulating key aspects of fetal brain gene expression that are highly relevant to pathophysiology affecting ASD."What are the connections between these papers? Well, obviously both deal with the concept of maternal immune activation (MIA) where infection, or possibly/rather 'inflammatory' responses to infection, during critical periods of pregnancy seem to be able to affect offspring developmental and other outcomes. This bearing in mind that pregnancy represents a time of 'reprogrammed immune function' such that the maternal immune system does not mount a response to the genetically dissimilar organism growing inside the body. Both papers model MIA in rodents (mice and rats respectively) given the ethics of undertaking such experimental studies in humans. Both studies concluded that (a) there is evidence that MIA is a real phenomenon and (b) bearing in mind rodents are not necessarily the same as humans (see here) (a shocker I know), MIA seems to invoke specific biochemical changes pertinent to the expression of genes *linked* to autism that are also potentially amenable to intervention.The Vuillermot findings in particular, offer some rather intriguing prospects for further study as a function of their conclusion that: "maternal VitD co-administration blocked the emergence of the ASD-relevant deficits in social interaction, stereotyped behavior, and emotional learning and memory." I appreciate that 'blocking the emergence' of autistic behaviours is not something that everyone is going to unanimously welcome (the implication being that every single autistic trait is somehow something to be eradicated). The idea however that aspects of even something like certain stereotyped behaviours under certain conditions and with certain intensity might 'set someone up' for the presentation of truly disabling conditions such as anxiety [3] (see here too) offers a degree of support for the idea of intervention targeting such behaviours in particular circumstances.But there is a potential research spanner in the works when it comes the idea that vitamin D might 'offset' some of the changes associated with exposure to MIA. The authors note: "VitD does not alter maternal or fetal inflammatory cytokine production." This statement was made on the basis that "prenatal administration of vitamin D had no effect on pro-inflammatory cytokine levels in dams or in fetal brains." Cytokines are those chemical messengers of the immune system. How then, you might ask? Well, back to the Lombardo paper and the possibility that vitamin D is not necessarily an 'anti-inflammatory' of choice under such circumstances but might - MIGHT - act on some of the mechanisms related to those genes expressed under MIA conditions. It's pretty well-known for example, that vitamin D does influence gene expression (see here for example) as our knowledge of the biological duties of the sunshine vitamin/hormone expand (see here). It is logical to assume that the next research step would be to see whether vitamin D administration *might* at certain times and under certain circumstances, affect the expression of those genes 'highly relevant to pathophysiology affecting ASD' under MIA conditions. This, in the context that maternal vitamin D levels during pregnancy again *might* have an important impact on the presentation of offspring autistic traits (see here).And since we're on the topic of vitamin D and autism (yet again), how about reading a new hypothesis paper on some potentially important connections [4]?----------[1] Vuillermot S. et al. Vitamin D treatment during pregnancy prevents autism-related phenotypes in a mouse model of maternal immune activation. Molecular Autism. 2017; 8: 9.[2] Lombardo MV. et al. Maternal immune activation dysregulation of the fetal brain transcriptome and relevance to the pathophysiology of autism spectrum disorder. Mol Psychiatr. 2017. Mar 21.[3] Bitsika V. & Sharpley CF. The association between parents' ratings of ASD symptoms and anxiety in a sample of high-functioning boys and adolescents with Autism Spectrum Disorder. Res Dev Disabil. 2017 Mar 1;63:38-45.[4] Gillberg C. et al. The role of cholesterol metabolism and various steroid abnormalities in autism spectrum disorders: A hypothesis paper. Autism Res. 2017. April 12.----------Vuillermot, S., Luan, W., Meyer, U., & Eyles, D. (2017). Vitamin D treatment during pregnancy prevents autism-related phenotypes in a mouse model of maternal immune activation Molecular Autism, 8 (1) DOI: 10.1186/s13229-017-0125-0Lombardo, M., Moon, H., Su, J., Palmer, T., Courchesne, E., & Pramparo, T. (2017). Maternal immune activation dysregulation of the fetal brain tran... Read more »

  • April 27, 2017
  • 09:49 AM

Code Orange for the Bengal Tiger!

by Jente Ottenburghs in Evolutionary Stories

Genetic study highlights challenging conservation of the Bengal Tiger in India.... Read more »

  • April 27, 2017
  • 03:57 AM

Is screen time a risk factor for ADHD?

by Paul Whiteley in Questioning Answers

The findings reported by Vivien Suchert and colleagues [1] observing that "screen time, but not other non-screen-based sedentary activities should be considered as being a risk factor for ADHD [attention-deficit hyperactivity disorder]" taps into long-running debates on whether our societal obsession with watching, clicking and swiping might not be 'a totally positive thing' when it comes to psychological development, health and wellbeing.Yes, I know this is a complicated area full of big personalities, sweeping generalisations, half-truths and soundbites (see here for example). But I talk about peer-reviewed science on this blog, and am dealing with presented evidence specifically looking at the issue of screen time and ADHD on this particular occasion.So, taking a not insignificant sample number of over 900 young adults aged 13-17 years old, researchers assessed various parameters in relation to "screen-based and non-screen-based sedentary behavior and ADHD symptoms." When I say 'assessed', immediately one potentially big issue stands out when it comes to measures of sedentary behaviour used in the study and the inclusion of the questionnaire method over and above the use of more objective measures such as physical activity monitors (see here). No mind, researchers analysed the collected data and determined a few key observations not least that: "Screen time was related to the total ADHD score (p < 0.001) as well as to the subscales inattention (p ≤ 0.016) and hyperactivity/impulsivity (p ≤ 0.008)." Further: "Sedentary time without screens was virtually not associated with ADHD."OK, to reiterate sweeping generalisations are not required on the basis of these results alone. There are a myriad of other methodological issues outside of just objective measures of sedentary behaviour that could skew the Suchert results and these should be taken into consideration. But set in the context that this is not the first time that screen use has been *corrrelated* with something like ADHD or ADHD-type behaviours [2] (or indeed the second time [3]) I'm minded to suggest that quite a more investigation is indicated. Of course, there are other factors to include in the research mix. The findings reported by Tong and colleagues [4] are potentially pertinent: "children with ADHD symptoms were likely to spend more time using a computer during school days; they were also more likely to eat while using a computer." This implies that ADHD or ADHD-type behaviours might predispose to increased screen time rather than the other way around. The relationship is likely to be complex.In terms of the potential 'hows and whys' of any connection between screen time and ADHD-type behaviours, well, there are already some clues. I'd perhaps suggest that the effects of screen time on sleep could be a good place to start given other peer-reviewed research clues [5]. The relationship between sleep and ADHD is a complicated one, but it is known that sleep interventions can [modestly] affect the presentation of some ADHD behaviours (see here). There are no doubt other research avenues worth looking into also.Should anyone act on the Suchert findings as they stand? Well, I don't do medical or clinical advice on this blog but I'm minded to suggest that some sensible advice provided by others might come into play: "No screens in the child’s bedroom. Pay attention to the content of the games, especially to violence. Set limits on screen time, and look for other ways to manage family interactions." With my 'what if' research hat on, I am also wondering whether the rise and rise of screens and screen time in the context of autism might also need some particular research examination, in light of the idea that autism and ADHD is not an unfamiliar diagnostic combination (see here)...To close, although perhaps most famous as a 'rat tickler', the passing away of Jaak Panksepp a few days back deserves mention given his notable ideas about autism and the influence they had and continue to have...----------[1] Suchert V. et al. Relationship between attention-deficit/hyperactivity disorder and sedentary behavior in adolescence: a cross-sectional study. Atten Defic Hyperact Disord. 2017 Apr 4.[2] Chan PA. & Rabinowitz T. A cross-sectional analysis of video games and attention deficit hyperactivity disorder symptoms in adolescents. Ann Gen Psychiatry. 2006 Oct 24;5:16.[3] Montagni I. et al. Association of screen time with self-perceived attention problems and hyperactivity levels in French students: a cross-sectional study. BMJ Open. 2016 Feb 26;6(2):e009089.[4] Tong L. et al. Attention-Deficit/Hyperactivity Disorder and Lifestyle-Related Behaviors in Children. PLoS One. 2016 Sep 22;11(9):e0163434.[5] Engelhardt CR. et al. Media use and sleep among boys with autism spectrum disorder, ADHD, or typical development. Pediatrics. 2013 Dec;132(6):1081-9.----------Suchert V, Pedersen A, Hanewinkel R, & Isensee B (2017). Relationship between attention-deficit/hyperactivity disorder and sedentary behavior in adolescence: a cross-sectional study. Attention deficit and hyperactivity disorders PMID: 28378132... Read more »

  • April 26, 2017
  • 04:02 AM

Hornig, Lipkin and chronic fatigue syndrome again

by Paul Whiteley in Questioning Answers

Drs Mady Hornig and Ian Lipkin once again provide some fodder for this blog, continuing one of their important research themes on how chronic fatigue syndrome (CFS) (sometimes also referred to as myalgic encephalomyelitis, ME) might show some important immune-related issues [1].This research tag-team and the teams of dedicated scientists who surround them are making some real progress with regards to the idea that ME/CFS is a physical condition (not psychosomatic and not 'biopsychosocial') with some readily identifiable biological features potentially accompanying cases. Of course we're not there just yet when it comes to a biological test for ME/CFS but science has at least started down that particular research path...With accompanying media attention in tow (see here), the focus of the most recent results were on how disease sub-types might be important to CFS and specifically, how: "Immune signatures in the central nervous system of ME/CFS patients with atypical features may be distinct from those with more typical clinical presentations."Authors described how cerebrospinal fluid (CSF) samples from "32 ME/CFS cases with classical features and presentations and 27 ME/CFS cases with atypical features or clinical presentations" were included for analysis. On what basis was 'typical' and 'atypical' described? Well: "The ‘classical’ (C-ME/CFS) group had acute onset of disease marked by a prodrome consistent with infection; ‘atypical’ (A-ME/CFS) ME/CFS patients met full diagnostic criteria for ME/CFS at onset of their illness, but had a less standard onset of ME/CFS and/or developed other disorders after illness onset of ME/CFS." Interestingly one person included in the A-ME/CFS group was described as having Gulf-War Illness (another important condition talked about on this blog).The results: various cytokines (chemical messengers of the immune system) were assayed for and with some nifty statistical 'corrections' authors reported some potentially important differences between the groups. So: "We found discrete differences in immune signatures of the CNS in ME/CFS subjects with atypical presentations that included sparse inter-cytokine networks and lower levels of two inflammatory mediators, the Th17 cytokine, IL17A, and the IFNγ- and TLR4-induced chemokine, CXCL9." All-in-all results suggested a "less robust CNS immune activation in A-ME/CFS."Much more research is required in this area for sure. But these results are interesting and pertinent to the idea that within the heterogeneity (where have a I heard that before?) of CFS/ME, there may be quite a few phenotypes and subgroups that might be readily separable with a little biological research effort. Does this therefore mean when we talk about the pluralisation of lots of labels (the autisms, the schizophrenias, the depressions, etc), we might also one day called it 'the chronic fatigue syndromes'? Well, I've kinda speculated about this before in the peer-reviewed domain...----------[1] Hornig M. et al. Immune network analysis of cerebrospinal fluid in myalgic encephalomyelitis/chronic fatigue syndrome with atypical and classical presentations. Transl Psychiatry. 2017 Apr 4;7(4):e1080.----------Hornig M, Gottschalk CG, Eddy ML, Che X, Ukaigwe JE, Peterson DL, & Lipkin WI (2017). Immune network analysis of cerebrospinal fluid in myalgic encephalomyelitis/chronic fatigue syndrome with atypical and classical presentations. Translational psychiatry, 7 (4) PMID: 28375204... Read more »

  • April 25, 2017
  • 04:15 AM

Who'd have thunk it: physical activity inversely associated with BMI and body fat percentage

by Paul Whiteley in Questioning Answers

"In this sample of middle-aged adults, drawn from the general population, physical activity was inversely associated with BMI [body mass index] and body fat percentage. For people with the same BMI, those who were more active had a lower body fat percentage."Those were the conclusions made by Kathryn Bradbury and colleagues [1] (open-access) drawing on data derived from "cross-sectional analysis of participants recruited into UK Biobank in 2006–2010." Said results continue a research theme where physical activity figures in the aforementioned dataset.So: "119 230 men and 140 578 women aged 40–69 years, with complete physical activity information, and without a self-reported long-term illness, disability or infirmity" were included for study - not an under-powered study by any means. Height and weight of participants were measured by trained staff "using standardised techniques." Physical activity estimates were gathered via self-report; specifically the use of 'touchscreens' as information gatherers regarding "walking, moderate physical activity and vigorous physical activity" and how often in a typical week participants "did each of the activities for 10 min or more" then onward for how many minutes during a day. Such data was number-crunched to provide something called "excess metabolic equivalent (MET)-hours/week of physical activity during work and leisure time." The authors also report on some efforts to off-set the potential unreliability of self-reported physical activity and several other variables (whether occupation involved primarily sitting or standing, tobacco smoking status, alcohol consumption, etc) were also thrown into the statistical mixer.Results: well, who'd have thunk it? Those reporting higher levels of physical activity (via questionnaire responses) tended to have a lower BMI and a lower body fat percentage. They were also likely to eat more fruit and vegetables that those with low levels of physical activity. Diet, occupation type and education level did not however seem to affect the primary findings.Accepting again that self-reported physical activity is not a great substitute for more objective measures and that BMI, whilst a good rough-and-ready indication of weight status, tends not to differentiate between fat and muscle, these are important results. They imply that far from not being able to outrun a bad diet (see here) physical activity still has an important place in maintaining a sensible weight and thus reducing the risk of a myriad of adverse health outcomes. Added to other findings indicating that we all really need to move quite a bit more (see here), the message seems to be that the human body was made for moving so move it. And the latest figures on obesity and physical activity highlight the challenges being faced in this area.And so to close,  a song to help with that 'move it' sentiment...----------[1] Bradbury KE. et al. Association between physical activity and body fat percentage, with adjustment for BMI: a large cross-sectional analysis of UK Biobank. BMJ Open 2017; 7: e011843.----------Bradbury, K., Guo, W., Cairns, B., Armstrong, M., & Key, T. (2017). Association between physical activity and body fat percentage, with adjustment for BMI: a large cross-sectional analysis of UK Biobank BMJ Open, 7 (3) DOI: 10.1136/bmjopen-2016-011843... Read more »

  • April 24, 2017
  • 05:22 AM

Promising mouse model for Ngly1 deficiency

by adam phillips in It Ain't Magic

A recent study of Ngly1 deficient mice used a secondary knockout to create double knockouts with symptoms similar to human NGLY1 deficiency.... Read more »

  • April 24, 2017
  • 04:05 AM

Sensory issues in adult ADHD controlling for autistic symptoms...

by Paul Whiteley in Questioning Answers

I was intrigued to read the paper by Bijlenga and colleagues [1] reporting on "the prevalence of sensory hyper- and hyposensitivity among adults with ADHD [attention-deficit hyperactivity disorder], controlling for autistic symptoms."The authors concluded that among their cohort of over 100 adults diagnosed with ADHD, both sensory hyper- and hyposensitivity symptoms as described by response to the Adolescent/Adult Sensory Profile-NL (AASP-NL), were over-represented compared with population norm data. Interestingly, authors also took a snapshot of 'autistic symptoms' based on responses to the Autism-spectrum Quotient (AQ) and reported that: "Adults with ADHD had more autistic symptoms" but: "Sensory hypo- and hypersensitivity were both related to an increased ADHD score, even showing a dose-response relationship, but not to any autistic symptom or comorbid disorder."My intrigue stems from a few implications of such findings, with the requirement for much more study. First is the quite important overlap between autism and ADHD (see here) confirmed symptom-wise in the Bijlenga paper. Second is the idea that, within this cohort at least, adults with ADHD may variably present with sensory issues. Third, assuming that the AQ 'does what it says on the tin' with regards to screening for autistic symptoms (see here), the lack of a notable connection between autistic symptoms and sensory sensitivities in the context of adult ADHD might have some important implications related to my first point when autism and ADHD appear simultaneously. Indeed it poses the question: are sensory issues, now noted in specific relation to autism via at least one diagnostic schedule (see here) actually 'a core part of all autism' or perhaps a feature of something else for some?Reiterating that more research is required (not least more formal screening for autism over and above the use of AQ or related screening schedules) that last point/question might actually make more sense than many people might first realise. If, for example, we take the view that autism rarely exists in some sort of diagnostic vacuum (see here and see here) and that science and clinical practice really needs to be more proactive when it comes to an autism diagnosis being a starting point not the finishing line (see here), it's not beyond the realms of possibility that sensory issues for some might have been spuriously linked to autism when in fact other comorbid labels/symptoms better account for their presentation. This not only has implications for screening/diagnosis but also management of said sensory symptoms, as per other reports talking about the use of stimulant medication indicated for ADHD 'affecting' aspects of odour sensitivities for example [2]. By saying that I'm not making any sweeping judgements about pharmacotherapy for ADHD treating sensory issues present alongside autism, merely that new avenues might open up.A final quick glance at some of the other peer-reviewed literature on the topic of sensory issues and ADHD reveals that there is some history in this area [3]. Said sensory issues have also been *linked* to some of the other behavioural facets noted in cases of ADHD [4]. Perhaps, in light of such data, it is time for ADHD - whether in symptoms or in label - to be taken into account when sensory issues are discussed in the context of autism in the science literature and in clinical practice?----------[1] Bijlenga D. et al. Atypical sensory profiles as core features of adult ADHD, irrespective of autistic symptoms. Eur Psychiatry. 2017 Feb 21;43:51-57.[2] Romanos M. et al. Improved odor sensitivity in attention-deficit/hyperactivity disorder. Biol Psychiatry. 2008 Dec 1;64(11):938-40.[3] Clince M. et al. Comparing and Exploring the Sensory Processing Patterns of Higher Education Students With Attention Deficit Hyperactivity Disorder and Autism Spectrum Disorder. Am J Occup Ther. 2016 Mar-Apr;70(2):7002250010p1-9.[4] Shimizu VT. et al. Sensory processing abilities of children with ADHD. Braz J Phys Ther. 2014 Jul-Aug;18(4):343-52.----------Bijlenga D, Tjon-Ka-Jie JY, Schuijers F, & Kooij JJ (2017). Atypical sensory profiles as core features of adult ADHD, irrespective of autistic symptoms. European psychiatry : the journal of the Association of European Psychiatrists, 43, 51-57 PMID: 28371743... Read more »

Bijlenga D, Tjon-Ka-Jie JY, Schuijers F, & Kooij JJ. (2017) Atypical sensory profiles as core features of adult ADHD, irrespective of autistic symptoms. European psychiatry : the journal of the Association of European Psychiatrists, 51-57. PMID: 28371743  

  • April 22, 2017
  • 07:14 AM

Autistic adults as critical autism experts (with research caveats)

by Paul Whiteley in Questioning Answers

"Findings suggest that autistic adults should be considered autism experts and involved as partners in autism research."That was the conclusion reached in the paper by Kristen Gillespie-Lynch and colleagues [1] (open-access) reporting on the results of an online survey assessing "autism knowledge and stigma among 636 adults with varied relationships to autism, including autistic people and nuclear family members." Among the various groups of people who contributed to the survey, several viewpoints emerged. The message primarily however was that: "autistic people are autism experts through their lived experiences." I don't think many people would quibble with such findings.A few other details emerged from the Gillespie-Lynch study that merit discussion. Many participants showed a "reduced tendency to view autism through a deficit-defined medical model compared with non-autistic people." This is perhaps not an unexpected finding given the history of applying the medical model to autism and the rise and rise of the neurodiversity movement that "challenges the medical model" in particular respect over the question of deficit vs. difference and implications thereof. Although the medical model provides the means to identify and diagnose autism or autism spectrum disorder (ASD) (on the basis of deficits), it's not unexpected that for some, once those tasks have been completed, the 'treatment' side of the model is not necessarily a top priority; or at least not as important as addressing the various inequalities that seem to stem from a diagnosis. That being said, I do agree with the authors sentiments that: "the neurodiversity movement and the medical model overlap in recognizing that supports are needed to ameliorate challenges associated with autism." Those challenges are variable and person-dependent but include the effects of both core and peripheral signs and symptoms and the various over-represented comorbidities that seem to follow a diagnosis of autism (see here). I would, at this point, also caution on using the words 'biopsychosocial model' in the context of autism as the authors have included in their discussions, given what it has meant for other labels (see here) and the potential 'psychologising' of some important medical symptoms.I added the words 'with research caveats' to the title of this post to ensure that such a positive message about autism and the autism spectrum is not just given a 'free pass' when it comes to scrutiny of the scientific method, the way the study was carried out and the applicability of the results to the entire autism spectrum. This was an online survey not a face-to-face piece of research (other related research has similarly used such a method and on more than one occasion) and the authors acknowledge that they: "did not verify diagnosis of participants who self-identified as autistic" for example. Given what we are beginning to see when it comes to some of the 'self-screening' instruments out there regarding possible autism or not (see here), I'm always a little cautious that self-diagnosis / self-identification does not necessarily mean [eventual] clinician-diagnosed autism and how important this is when it comes to correctly ascertaining the wants and wishes of those diagnosed as being on the spectrum.On the point about the representativeness of this research, the authors also note: "Findings may not generalize to autistic participants who lack the verbal and computer skills needed to complete the survey." Yet another example it seems of this important issue.I have to say that I'm also a little disheartened that yet again an important group that was once very firmly on the autism spectrum aren't really given the credit they deserve according to the Gillespie-Lynch findings: "Autistic participants were more likely to recognize that most children cannot outgrow autism." The 'optimal outcome' children and adults it seems, still represent one of the most maligned groups associated with the autism spectrum (assuming that optimal outcome occurring in up to 9% of the autism population is not an insignificant figure). This despite the fact that even the diagnostic stability of the most 'high-functioning' cases of autism can wobble it seems (see here) even into adulthood. One of the premier experts on autism also seems to agree according to some recent media (see here). I often wonder if the seeming lack of acceptance of this group/feature might have something to do with the 'identity' side of autism and the idea that within the vast heterogeneity of autism (or the plural autisms if you prefer) the use of 'them and us descriptions' like 'neurotypical' are perhaps not as binary or long-lasting as many would believe or want to believe?Within the context of [approximate] phrases such as 'if you've met one person with autism, you've met one autistic person' there is caution in over-generalising these latest results but they are nonetheless important. I think it would be rather fitting to end with a few choice phrases from the Gillespe-Lynch paper: "As many of our survey respondents indicated, each person, regardless of whether or not they are autistic, is unique" and: "Some autistic people seek out factual knowledge about autism while others believe that they can only be experts in their own particular form of autism." Either way, the insights provided by people on the autism spectrum (all parts of the autism spectrum and indeed, across the age ranges) should be valued, and where possible, incorporated into research and practice.And one voice from the autism spectrum carries some rather sensible messages...----------[1] Gillespie-Lynch K. et al. Whose Expertise Is It? Evidence for Autistic Adults as Critical Autism Experts. Front. Psychol. 2017. March 28.----------Gillespie-Lynch, K., Kapp, S., Brooks, P., Pickens, J., & Schwartzman, B. (2017). Whose Expertise Is It? Evidence for Autistic Adults as Critical Autism Experts Frontiers in Psychology, 8 DOI: 10.3389/fpsyg.2017.00438... Read more »

Gillespie-Lynch, K., Kapp, S., Brooks, P., Pickens, J., & Schwartzman, B. (2017) Whose Expertise Is It? Evidence for Autistic Adults as Critical Autism Experts. Frontiers in Psychology. DOI: 10.3389/fpsyg.2017.00438  

  • April 21, 2017
  • 08:00 AM

Friday Fellow: Crystalline crestfoot

by Piter Boll in Earthling Nature

by Piter Kehoma Boll Even in the smallest pools or ponds of freshwater lost in a field, the diversity of lifeforms is amazing. Sadly, these environments are one of the most damaged of all ecosystems on earth and we probably … Continue reading →... Read more »

  • April 21, 2017
  • 05:32 AM

Parental exposures and risk of offspring autism: some curious details

by Paul Whiteley in Questioning Answers

"Overall, our results were consistent with no positive association between parental asthmagen exposure and ASD [autism spectrum disorder] in the children."So said the findings reported by Alison Singer and colleagues [1] (open-access) continuing a research theme from this group [2] looking at whether "parental workplace exposures to risk factors for asthma (“asthmagens”)" might have relevance to offspring risk for autism.Based on data derived from some of those oh-so-important Scandinavian research registries (this one based in Denmark), researchers initially looked at some 12,000 cases (where autism was mentioned in medical records) compared with over 48,000 controls (not autism) to ascertain whether parental work exposures might play some role in autism risk. This numbers were eventually boiled down somewhat.Despite the opening line to the post, there were some curious details to emerge from the collected analyses. So: "We observed an inverse association between any maternal occupational asthmagen exposure and ASD in the children." Researchers reported that maternal occupational exposure actually seemed to be protective against the development of offspring autism according to their findings. They note that this finding was "largely explained by latex exposures" on the basis of linking occupational codes "to an asthma-specific job exposure matrix (JEM)." In other words, they didn't specifically look at latex exposure in every single case but rather relied on the probability that a particular occupation would entail this or other exposure.A few other curious details also emerged: "Some paternal occupational asthmagen categories were positively associated with ASD, including bioaerosols..., pharmaceutical drugs (manufacturing or extensive handling)..., and metals." The authors tend to talk down these findings as per the suggestion that: "Some of these associations could be chance findings resulting from multiple comparisons or could reflect bias, such as unmeasured confounding" but I would perhaps be a little more cautious about rejecting them outright. Indeed the authors note on one point in relation to maternal exposures: "While adjustment for unmeasured confounding could bring the association to the null, the confounding would need to be implausibly strong to mask a positive association."I've covered the topic of parental (occupational) exposures and offspring autism risk before on this blog (see here) alongside associated research (see here). The current take-away message from quite a bit of this research is that there may be target classes of compounds to 'look out for' when it comes to offspring autism risk, but as of yet there is no smoking gun. One also needs to read such research in the context of the myriad of 'associations' that have been made with offspring autism risk down the years (see here for example) and how genes and environment might mix in relation to the plural autisms. Cumulative effects are more likely over single factors.Insofar as the current Singer results, I do feel that the authors might have been a little premature in making the sweeping claims that they have on the basis of their findings: "this large population-based case-control study does not suggest a positive measurable association between parental occupational asthmagen exposure and ASD." I say this in the context that 'asthmagen' exposure could be incurred via several routes (see here). I don't doubt that the correlations/findings reported by Singer could be 'due to chance', but until such claims can be independently verified in direct study (see here for one idea) and perhaps tested in animal models for example, they should really just report what they found without fear, favour or complication...----------[1] Singer AB. et al. Parental exposures to occupational asthmagens and risk of autism spectrum disorder in a Danish population-based case-control study. Environmental Health. 2017 16: 31.[2] Singer AB. et al. Maternal Exposure to Occupational Asthmagens During Pregnancy and Autism Spectrum Disorder in the Study to Explore Early Development. J Autism Dev Disord. 2016 Nov;46(11):3458-3468.----------Singer, A., Burstyn, I., Thygesen, M., Mortensen, P., Fallin, M., & Schendel, D. (2017). Parental exposures to occupational asthmagens and risk of autism spectrum disorder in a Danish population-based case-control study Environmental Health, 16 (1) DOI: 10.1186/s12940-017-0230-8... Read more »

  • April 20, 2017
  • 06:19 AM

DHM attenuates obesity-induced slow-twitch-fiber decrease via FLCN/FNIP1/AMPK pathway

by Joana Guedes in BHD Research Blog

Obesity is often associated with decreases in the proportion of skeletal muscle slow-twitch fibers and insulin sensitivity. Slow-twitch fibers are rich in mitochondria and utilize fatty acid oxidative phosphorylation for energy production. In their new study, Zhou et al. (2017) explore the role of the FLCN/FNIP1/AMPK signalling pathway in obesity-induced reductions in slow-twitch fibers and insulin sensitivity in skeletal muscle using high-fat-diet-induced (HFD) obese mice, ob/ob mutant mice, and palmitate-treated C2C12 myotubes. The authors also assess the effects of dihydromyricetin (DHM) on the obesity-induced decrease in slow-twitch fibers, and the molecular mechanisms responsible for this effect.... Read more »

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