Saturday, 22 July 2017

"medical disorders in children with ASD and ADHD appear to be widespread"

The quote titling this brief post is taken from the results of the systematic review undertaken by Jet Muskens and colleagues [1] (open-access) who surveyed the peer-reviewed science literature "on medical comorbidity in the two major developmental disorders autism spectrum disorder (ASD) and attention deficit hyperactivity disorder (ADHD)."

Continuing an important theme (see here), the authors concluded that various categories of conditions - "immunology, neurology and gastroenterology" - are over-represented in relation to autism and ADHD and that "future studies should not only focus on psychiatric symptoms, but provide a broader evaluation of medical disorders" when it comes to those labels.

Minus too much chatter, I was impressed to see that many of the research articles covered on this blog down the years had made it into the Muskens review. So, the likes of Harumi Jyonouchi gets a well-deserved mention (see here and see here) and the focus on how the immune system might be doing so much more than just protecting us from the odd pathogen or two. The authors also bring in some of the very convincing scientific evidence that various gastrointestinal (GI) issues are over-represented in relation to autism (see here). There's even mention of how useful that Taiwanese research database has been down the years to autism and ADHD research (see here).

What's more to say? Well, preferential screening for various medical conditions in the context of an autism diagnosis yet again, receives more support. As does the idea that when a medical diagnosis is received by a person diagnosed on the autism spectrum, that medical diagnosis deserves the same healthcare management and/or treatment as it does in the context of not-autism save any further health inequalities potentially appearing (see here). The days for example of 'blaming autism' for every single physical complaint are also to be consigned to the historical dustbin. And with it, recognition that concepts such as ESSENCE or 'autism plus' (see here and see here) really need to include the somatic as well as the behavioural/psychiatric...

Whilst welcoming the Muskens review, it's important to note that others have already 'primed' for the importance of medical comorbidity in relation to a diagnosis of autism...

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[1] Muskens JB. et al. Medical comorbidities in children and adolescents with autism spectrum disorders and attention deficit hyperactivity disorders: a systematic review. European Child & Adolescent Psychiatry. 2017. July 3.

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Friday, 21 July 2017

Antidepressants during pregnancy and autism in offspring (with care)

There are a few topic areas in the quite vast autism research landscape that consistently seem to keep cropping up. The possibility of some kind of *association* between pregnancy antidepressant use and risk of offspring autism is one of those areas (see here) as the results published by Dheeraj Rai and colleagues [1] (open-access) are presented for your attention. I would also draw your attention to an accompanying editorial discussing the Rai findings (see here).

So: "To help to improve the understanding of the association between antidepressant use during pregnancy and autism in offspring, we applied a range of... causal analytical methods on data from a large total population cohort in Stockholm County" was the starting point, as once again one of those very useful Scandinavian registries provided the source study material (indeed, Rai et al are seemingly experts in their analysis of such resources). The added bonus to the Rai study was their attempt to 'unravel' any association between gestational antidepressant exposure and autism from the reason why such medication was being taken in the first place: maternal psychiatric health issues (and whether this variable may in fact account, at least in part, for any association that has previously been identified).

From a starting population approaching three-quarters of a million people, researchers eventually settled on looking at over 250,000 children under 17 years of age (but over 4 years of age "in whom a diagnosis of autism might be less reliable") who were born to over 150,000 mothers. The vast majority of children (239,943 of 254,610) had no history of exposure to antidepressants during pregnancy. The remaining participants were divided up into two groups: one where there was documentation leading to the assumption of exposure to pregnancy antidepressants (n=3342) and one where there was an indication for such exposure ("mothers with a psychiatric disorder") but no recorded use of antidepressants during pregnancy (n=12,325). Researchers summed up how many children were diagnosed with an autism spectrum disorder (ASD) in each group and applied some statistical modelling.

Results: I think it's important to first highlight a statistic that seems to have been missed by many covering the Rai findings: "Of the 238 943 cohort children for whom there was no record of maternal history of psychiatric disorder or antidepressant use during pregnancy, 4889 had autism (2.1%)." That's 2.1% with a diagnosis of autism or ASD; quite a far cry from the 1% [estimate] statistic from just a few years back (at least here in Blighty).

Then: "Exposure to antidepressants during pregnancy was associated with a higher odds of a diagnosis of autism in offspring than exposure to a maternal psychiatric disorder without antidepressants." The authors caution that: "the absolute risk was small, and 4.1% of children exposed to antidepressants in utero had autism compared with 2.9% of those with a maternal history of psychiatric disorder." Further when looking at those children diagnosed with ASD in the groups, authors observed that "autism without intellectual disability" seemed to be over-represented; something also picked up in previous findings from authors on this current paper [2].

Alongside various opinions on these findings (see here for example), the authors caution about the possible meaning of their results. One obviously has to be quite careful when discussing such data to ensure that an important class of medicines is not unduly vilified. No medicine is however without potential side-effects and appropriate clinical decisions and good medicines management [2] is key, particularly when pregnancy is included as variable. The authors talk, for example, about how "if a causal link were robustly established, and if no pregnant women took antidepressants during pregnancy, only 2% of autism cases in this population would be prevented." Alongside they [importantly] mention that antidepressant use during pregnancy is not typically just a 'choice' but rather being clinically indicated: depression does not simply disappear when a woman is pregnant. Interestingly too, they mention about how their data "suggest that there is an increased background risk of autism in children of women with psychiatric conditions, regardless of antidepressant treatment." This follows a trend in other areas of psychiatry (see here for example).

Yet again, the call is further research in this area and, quite a few more investigations into the possible hows-and-whys of any association (with medication use and/or maternal psychiatric presentation) is made. I might also suggest that taking into account other childhood conditions such as attention-deficit hyperactivity disorder (ADHD), potentially over-represented when it comes to a diagnosis of autism or ASD, could be another important step forward in light of other preliminary *associations* being made with pregnancy medication history in mind (see here). This also includes looking at any issues associated with timing of potential exposure and/or dose ("Because of small numbers, we were not able to assess trimester specific or dose response effects.").

Insofar as the suggestion that autism without intellectual (learning) disability might be an important phenotype when it comes to any association, subsequent research in this area seemingly fits in well with increasingly vocal calls [4] to stop using the generic label of autism as a research starting point (see here). Allied to suggestions for more 'bottom-up' research with autism in mind (see here), also coincidentally mentioning "maternal SSRI use during pregnancy" in the context of autism [5], a future research agenda is seemingly emerging. I might also point out that certain sensitivities need to be kept in mind on the basis of suggestions that an 'environmental exposure' might, in whole or part, be *associated* with a particular type(s) of autism.

All such work - present and future - however needs to be done/presented with care, understanding and minus scaremongering, so as not to unduly alarm pregnant mothers, their families or indeed, the physicians providing their care at such a critical time...

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[1] Rai D. et al. Antidepressants during pregnancy and autism in offspring: population based cohort study. BMJ. 2017; 358: j2811.

[2] Rai D. et al. Parental depression, maternal antidepressant use during pregnancy, and risk of autism spectrum disorders: population based case-control study. BMJ. 2013 Apr 19;346:f2059.

[3] Angelotta C. & Wisner KL. Treating Depression during Pregnancy: Are We Asking the Right Questions? Birth Defects Res. 2017 Jul 17;109(12):879-887.

[4] Waterhouse L. et al. The ASD diagnosis has blocked the discovery of valid biological variation in neurodevelopmental social impairment. Autism Res. 2017 Jul;10(7):1182.

[5] Unwin LM. et al. A "bottom-up" approach to aetiological research in autism spectrum disorders. Front Hum Neurosci. 2013 Sep 19;7:606.

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Thursday, 20 July 2017

Is gluten avoidance linked to a lower risk for depression?

I've talked a few times on this blog about how avoiding dietary gluten both within (see here) and outside of (see here) the context of coeliac (celiac) disease, the archetypal 'gluten is baddie' autoimmune condition, might have some pretty interesting effects on some aspects of a person's psychology. Today's post reflects yet more peer-reviewed science suggesting that there may indeed be something to see in this potentially important area; particularly pertinent to the presentation of depression or depressive symptoms.

So, the findings reported by Haley Zylberberg and colleagues [1] based on data from some 22,000 participants taking part in the US 2009-2014 National Health and Nutrition Examination Survey are the source material today. Some background material related to this cohort can be found here. They specifically looked at the "prevalence of depression, insomnia, quality-of-life variables, and psychotropic medication use in CD [coeliac disease] participants and PWAGs [people who avoid gluten] to controls." People who avoid gluten - PWAG - represent a group who don't have a diagnosis of CD but nonetheless similar to those who were diagnosed with CD, reported avoiding dietary gluten.

Results: "Depression was present in 8.2% of controls compared with 3.9% of participants with CD... and 2.9% of PWAGs." Even after adjustment for various confounding variables ("age, sex, race, income, and access to healthcare") those gluten avoiders (without CD) less frequently presented with depression compared with data from controls.

Added to the previous occasions where gluten consumption seems either to be linked to [some] depression or removal of gluten seems to positively impact on depressive symptoms at least for some, this is interesting work. Yes, quite a few more controlled trials are required to examine such relationships between food and mood. Although we can speculate on possible mechanisms [2] we don't really know why there may be an effect from gluten removal, but this is an emerging area of science; particularly in the context of how disruptive/disabling/damaging depression can be to someone.

Bearing in mind the caveats of this blog - no medical or clinical advice is given or intended - please don't assume that I'm advocating gluten removal for anything (unless clinically indicated) on the basis of this or other posts. If in doubt, consult your medical physician.

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[1] Zylberberg HM. et al. Depression and insomnia among individuals with celiac disease or on a gluten-free diet in the USA: results from a national survey. Eur J Gastroenterol Hepatol. 2017 Jun 27.

[2] Pruimboom L. & de Punder K. The opioid effects of gluten exorphins: asymptomatic celiac disease. J Health Popul Nutr. 2015 Nov 24;33:24.

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Wednesday, 19 July 2017

"Medical history was associated with increased risk of CFS/ME"

The paper by Berit Feiring and colleagues [1] (open-access) is the source blogging material today covering an area that I was previously unaware of: "to study the association between HPV [human papillomavirus] vaccination and risk of CFS/ME [chronic fatigue syndrome/myalgic encephalomyelitis] among girls eligible for HPV vaccination in the national immunisation programme in Norway."

A quick trawl of PubMed to look-see whether there was any previous peer-reviewed science in this area revealed some inklings about a possible *association* between use of the HPV vaccine and some symptoms that may follow a diagnosis of ME/CFS [2] but not much to say that risk of an actual diagnosis of CFS/ME was significantly heightened [3] following HPV immunisation. On the topic of postural tachycardia syndrome (PoTS) and HPV vaccination, I had been aware of some, limited peer-reviewed discussions (see here).

As it happens, Feiring et al did not observe any population-wide links between HPV vaccination and increased risk of CFS/ME based on their analysis of "176,453 girls born 1997–2002 [who] were eligible for HPV vaccination." They tempered their conclusions slightly given that they "did not have access to patient records for verification of the CFS/ME diagnoses" derived from the Norwegian Patient Registry (NPR) but for all intents and purposes, their data is compelling based on sample size and how well Scandinavian countries tend to treat their population data.

A few other, rather interesting aspects to the Feiring data are also apparent: "we observed an increase in the incidence of CFS/ME among adolescents aged 10–17 in Norway, during 2009–2014" and: "Medical history was associated with both increased risk of CFS/ME and lower uptake of HPV vaccine." The idea that numbers of cases of CFS/ME is on the up in Norway is an interesting one and perhaps contrasts with other data from here in Blighty for example (see here) bearing in mind the age groups analysed. I was however specifically drawn to the idea that: "The risk of CFS/ME increased with increasing number of previous hospital contacts."

Looking at hazard ratios (HRs) for a diagnosis of CFS/ME based on how many times a girl had had hospital contact, a rather interesting dose-dependent pattern emerged. So, examining the entire follow-up period, the (adjusted) HR for CFS/ME diagnosis for those with only one hospital contact was 1.64 (1.22–2.19). For those with seven or more hospital contacts, the HR jumped to 5.23 (3.66–7.49). Also potentially important were the possible reason(s) for hospital contact and risk of CFS/ME: "According to ICD-10 diagnoses, the highest risk of CFS/ME was found among girls with diagnoses in chapters I00-I99 (Diseases of the circulatory system)..., A00-B99 (Certain infectious and parasitic diseases)... and R00-R99 (Symptoms, signs and abnormal clinical and laboratory findings, not elsewhere classified)."

Other discussions on data also from Norway (indeed, from some of the same authors) has talked about medical history around CFS/ME and what conditions seem to be 'over-represented' (see here). On that research occasion [3] they concluded that: "Children with CFS/ME were frequently diagnosed with infections, supporting the hypothesis that infections may be involved in the causal pathway." Said previous findings are not so dissimilar from the current ones reported by Feiring and colleagues.

Insofar as the next steps on from the Feiring data, well one might - assuming independent replication and the like - see a way forward where a potential early warning system for possible CFS/ME screening might be put in place on the basis of patterns of hospital visits and the types/patterns of diagnosis that are given. I appreciate that there is quite a lot of heterogeneity when it comes to CFS/ME (possibly even another label ripe for pluralisation or spectrum-ing?) so I don't want to get too ahead of myself here but there is potential. Whilst HPV vaccination did not seem to be connected to later CFS/ME diagnosis in the Feiring cohort, the question about what factors could be driving the increase in cases remains open: "The reasons for the increase in CFS/ME in Norway are unknown."

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[1] Feiring B. et al. HPV vaccination and risk of chronic fatigue syndrome/myalgic encephalomyelitis: A nationwide register-based study from Norway. Vaccine. 2017. June 23.

[2] Brinth LS. et al. Orthostatic intolerance and postural tachycardia syndrome as suspected adverse effects of vaccination against human papilloma virus. Vaccine. 2015 May 21;33(22):2602-5.

[3] Donegan K. et al. Bivalent human papillomavirus vaccine and the risk of fatigue syndromes in girls in the UK. Vaccine. 2013 Oct 9;31(43):4961-7.

[4] Bakken IJ. et al. Comorbidities treated in primary care in children with chronic fatigue syndrome / myalgic encephalomyelitis: A nationwide registry linkage study from Norway. BMC Family Practice. 2016; 17: 128.

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Tuesday, 18 July 2017

Anxiety disorder is rife in 'high-functioning' autism

"Lifetime prevalence rates of 53.5% for depressive disorder 73.5% for anxiety disorders and 37.5% for ADHD [attention-deficit hyperactivity disorder] were found."

Those were the figures arrived at by Alexandru Gaman and colleagues [1] who set about investigating the "prevalence rates of psychiatric co-morbidities" among other things in a cohort of over a hundred adults diagnosed with "high-functioning" autism via the quite recently revised DSM-5 criteria. I've stressed the words 'high-functioning' to denote this being the authors' words not mine (personally, I'm not so sure that general level of functioning is all that good as a descriptor).

Various other observations were made by authors such as the finding that: "Subjects with psychotic co-morbid symptoms had a more severe social deficit" which might tap into some other discussions being had on how some of the screening instruments talked about with autism in mind are seemingly not adverse from potentially picking up other labels with a psychosis element to them (see here). I say that also with the understanding that at least for some, autism and psychosis are not diagnostically unstrange bedfellows (see here).

I've zoomed in on the anxiety disorder(s) bit to the Gaman findings because of their very high lifetime prevalence and because, day-to-day, anxiety disorders can be absolutely disabling for many people on the autism spectrum (see here). Indeed, with all the very positive talk about things like employment and further education opportunities [slowly] increasing for autistic young people and adults, one of the details that does not seem to be talked about as much is how issues like anxiety can significantly hinder not only efforts to get a job/student place but also keeping that job/student place in the longer term (see here). Talent is being outshone by crushing anxiety in some cases.

Gaman and colleagues concluded by talking about how identification of something like anxiety disorder is "a crucial clinical issue." I would very definitely agree with this viewpoint but more than that, efforts now need to go into what can be done about treating/managing such anxiety to make people's lives easier (see here); accepting that we still have some distance to go in this process [2]. I'd also like to see some kind of research parity being arrived at specifically with regards to the question: how prevalent and what effects does anxiety have for those NOT described as having 'high-functioning' autism?

To close, having recently been party to some interesting debate on social media about the ins-and-outs, rights-and-wrongs and positives-and-negatives of [exclusive] self-diagnosis with autism in mind, I'd like to link to a paper by Ashwood and colleagues [3] on how one of the premier 'are you autistic?' self-report schedules is not necessarily fit for purpose when it comes to a self-diagnosis of autism. Indeed pertinent to today's post, how "generalized anxiety disorder may ‘mimic’ ASD [autism spectrum disorder] and inflate AQ [Autism-Spectrum Quotient] scores, leading to false positives" echos a viewpoint that I championed: identity, emotions and politics aside, there is no substitute for a thorough professional assessment when autism is suspected. Outside of such an assessment being potentially pertinent to the idea that autism rarely appears in some sort of diagnostic vacuum (see here), it is perhaps even more important as the DSM-5 criteria for ASD and SCD [social (pragmatic) communication disorder] start to become even more mainstream and what it means/will mean to the concept of autistic identity too...

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[1] Gaman A. et al. Psychiatric co-morbidities in a French cohort of adults with high-functioning autism (HFA). European Psychiatry. 2017; 41: S136.

[2] Lorenc T. et al. Support for adults with autism spectrum disorder without intellectual impairment: Systematic review. Autism. 2017 Jun 1:1362361317698939.

[3] Ashwood KL. et al. Predicting the diagnosis of autism in adults using the Autism-Spectrum Quotient (AQ) questionnaire. Psychological Medicine. 2016;46(12):2595-2604.

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Monday, 17 July 2017

Second seizure risk and "idiopathic autism"

Idiopathic autism refers to instances where autism is the primary diagnosis and not something secondary to another - usually genetic - condition. The paper by Asad Qadir and colleagues [1] reviewed the files of some 150 people diagnosed with an autism spectrum disorder (ASD), idiopathic ASD, and a history of at least one seizure in connection to an important issue: recurrence risk of seizure. They concluded that the average age of first seizure in their cohort was around about 7 years old and many, over 90% of participants included for review, were at serious risk of a second seizure on average just over 6 months later.

This is an important finding. We already know that epilepsy and seizure disorder(s) are not uncommon bedfellows to parts of the autism spectrum (see here) (indeed, many parts of the autism spectrum seem to be prone to unusual EEG - electroencephalographic or electroencephalogram - findings). We know that non-febrile seizures (seizures not attached to fever) are quite a bit more common in relation to autism when compared with non-autistic siblings for example (see here). And on top of all that, we know that seizures can in some instances be life-threatening (see here).

The Qadir data highlights the "short time to second seizure" as a window to appropriate management of seizure when coincidental to autism. The data suggest that even after one seemingly isolated incidence of seizure, clinicians might consider being proactive in (i) screening for signs of EEG anomalies for example, and (b) be pretty assured that initiation of appropriate treatment/management of seizure is very likely applicable insofar as the risk of recurrence in those diagnosed with an ASD. I say all that with my blogging caveat of no medical or clinical advice given or intended, in full working order.

I'd also like to think that as our knowledge about the autism spectrum increases, in particular the idea that there may be many different routes to many different types of autism (see here) so science will start to put some further flesh on the bones that what we call idiopathic autism with epilepsy at the moment, does not necessarily mean things will stay 'idiopathic' in future times. Then, other questions need answering, such as whether certain 'epileptic encephalopathy syndromes' might actually be the cause of some autism [2]...

As I've said many times before on this blog, don't mess with seizures and/or epilepsy...

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[1] Qadir AA. et al. Risk of Second Seizure in Pediatric Patients With Idiopathic Autism. J Child Neurol. 2017 Jan 1:883073817713906.

[2] Srivastava S. & Sahin M. Autism spectrum disorder and epileptic encephalopathy: common causes, many questions. J Neurodev Disord. 2017 Jun 23;9:23.

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Saturday, 15 July 2017

Should anyone be concerned about pathological video game use in relation to autism?

"... the risk for pathological game use appears larger in adults with ASD [autism spectrum disorder] compared with TD [typically developing] adults. These findings point to pathological game use as a potentially important focus of clinical attention in adults with ASD."

So concluded the paper by Christopher Engelhardt and colleagues [1] (open-access) looking at an interesting issue - "whether adults with autism spectrum disorder (ASD) are at higher risk for pathological game use than typically developing (TD) adults" - based on reports from some 120 participants with and without a diagnosis of autism. Including one Micah Mazurek on the authorship list (who has previously talked about the effects of screen time and autism), researchers delved into self-reported time spent playing video games based on data collected from a cohort "participating in a larger study on violent video game effects" [2]. The average age of participants (with and without a diagnosis of autism) was round about the 20 years old mark.

Results: both on weekdays and weekends, the typical hours of game play were different between the groups of those with autism and those without. Interestingly, authors used a slightly different statistical approach to the traditional "null hypothesis significance tests and 95% confidence intervals" via their use of "Bayes factors to state evidence for or against our predictions" to analyse their data. Bayes and Bayesian teachings provide an alternative to the 'frequentist' considerations in treating data. Alongside asking about game play time, researchers also asked participants to complete a questionnaire on "pathological video game use" that was based on "another behavioral addiction (pathological gambling)" and covered various aspects: "salience, euphoria or relief, tolerance, withdrawal, conflict, relapse and reinstatement."

"The results indicated that adults with ASD endorsed more symptoms of video game pathology than did TD adults. This relationship was strong, enjoying 300,000-to-1 odds in Bayesian model comparison." Such sentences kinda say it all. Risk of pathological video game use was quite a bit more likely in those with autism than those without, and 'escapism' was also reported to be an important reason for such extended use.

I do want to be a little careful in this post not to (a) demonise - pathologise - video game playing and/or (b) isolate those on the autism spectrum as being 'unique' in their video gaming habits. Personally, I don't see an issue if people want to spend large sections of their days playing video games as opposed to watching television or sitting down reading a book (reading in particular, is another fine example of escapism) or doing anything else. This was a study of adults doing what many millions of people do every day, so they should have the right to do as they please in this context. With the wonders of modern technology, gaming today is also not necessarily a socially-isolated pastime so one has to be quite careful about making any sweeping generalisations in that respect too.

I have however, always been a little worried about this and other research on screen time use in the context of autism and what detrimental effects it might have for a person's physical health. Everyone is prone to a degree of 'couch-potatoing' (i.e. loafing of the sofa for hours on end) but when people are talking about nearly 3 hours every day gaming, presumably sat on a couch/sofa, this really can't be doing anyone any good in terms of their long-term physical health. We're all being told to move more (see here) and given the data emerging when it comes to the physical activity patterns of rather a lot of people on the autism spectrum (see here), there are some good grounds for encouraging more movement and more physical activity minus any nanny-stating. I appreciate that sports and exercise is not everyone's cup of tea and in particular, more needs to be done in making physical activity more attractive to many groups of people including those on the autism spectrum (see here). Efforts should continue to ensure a balance is struck between times of sedentary behaviours typically associated with gaming and times of engaging in physical activity; as far as I can see, Engelhardt et al did not ask about physical activities or other related pastimes on this research occasion. Indeed, although I am still a little apprehensive about the use of exergaming, I do wonder if this could be a good bridging point on the road to balance...

Music to close: Shape of You by Ed for one of my brood who seems to be looking forward to becoming a kumite specialist (when she graduates from Ippon kumite).

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[1] Engelhardt CR. et al. Pathological game use in adults with and without Autism Spectrum Disorder. PeerJ. 2017. e3393.

[2] Engelhardt CR. et al. Effects of Violent-Video-Game Exposure on Aggressive Behavior, Aggressive-Thought Accessibility, and Aggressive Affect Among Adults With and Without Autism Spectrum Disorder. Psychol Sci. 2015 Aug;26(8):1187-200.

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Friday, 14 July 2017

Antidepressant use in pregnancy and risk of offspring ADHD?

Here we go again. Antidepressant use during pregnancy comes under the spotlight yet again (see here) as per the findings reported by Takoua Boukhris and colleagues [1], this time in connection to risk of offspring diagnosis of attention-deficit hyperactivity disorder (ADHD) following gestational exposure to this class of medicines.

Drawing on data derived from the Quebec Pregnancy/Children Cohort (QPC), researchers set out to examine the "risk of ADHD associated with overall and class-specific antidepressant exposure in utero." I might add that previous data from some of the authors of the Boukhris paper on the QPC has suggested that it is "an excellent tool for the study of the risk and benefit of drug use during the perinatal period" [2].

Following nearly 150,000 live births between 1998 and 2009, researchers looked at the rates of subsequent diagnosis of ADHD alongside the pattern of medication use during pregnancy and other important variables such as "maternal history of depression/anxiety and ADHD." They concluded that: "AD [antidepressant] use during the 2nd and 3rd trimester of pregnancy, specifically tricyclics, is an independent risk factor for ADHD in children above and beyond the risk associated with maternal depression/anxiety or ADHD." Further: "SSRI [Selective serotonin reuptake inhibitors] and SNRI [Serotonin–norepinephrine reuptake inhibitors] use were not associated with increased ADHD risk."

As per the convoluted research history talking about pregnancy antidepressant 'exposure' and possible risk of offspring autism, there are certain caveats and issues worth mentioning. Antidepressant use during pregnancy is not something to be taken lightly as per any calls to 'restrict use' during the special nine months that make us. Such medicines serve an important purpose in controlling some potentially important clinical symptoms; said symptoms do not just dissipate during the special time called pregnancy as per other clinical examples with other labels (see here).  It's also worth pointing out that such observational studies looking at medication use and offspring outcomes are just that - observational. As per the tenet 'correlation is not the same as causation', one has to be a little careful with such data...

That all being said, I do find the Boukhris results to be intriguing on the basis that this is not the first time that an *association* has been talked about in the peer-reviewed science domain [3] and on more than one occasion [4]. Further investigations are perhaps required into the possible mechanism(s) involved in any such relationship between medicine and offspring development, and indeed, whether such connections could potentially invite new intervention options for labels like ADHD? I'm also more than a little interested in the 'medication type' angle to the Boukhris observations not necessarily being the same as that put forward in relation to offspring risk of autism.

And just before you go, it's worth highlighting the findings reported by Viktorin and colleagues [5] looking at pregnancy antidepressant use and intellectual (learning) disability: "After adjustment for confounding factors... the current study did not find evidence of an association between ID and maternal antidepressant medication use during pregnancy."

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[1] Boukhris T. et al. Antidepressant Use in Pregnancy and the Risk of Attention Deficit with or without Hyperactivity Disorder in Children. Paediatr Perinat Epidemiol. 2017 Jun 22.

[2] Bérard A. & Sheehy O. The Quebec Pregnancy Cohort – Prevalence of Medication Use during Gestation and Pregnancy Outcomes. Croy A, ed. PLoS ONE. 2014;9(4):e93870.

[3] Man KKC. et al. Prenatal antidepressant use and risk of attention-deficit/hyperactivity disorder in offspring: population based cohort study. BMJ. 2017 May 31;357:j2350.

[4] Clements CC. et al. Prenatal antidepressant exposure is associated with risk for attention-deficit hyperactivity disorder but not autism spectrum disorder in a large health system. Mol Psychiatry. 2015 Jun;20(6):727-34.

[5] Viktorin A. et al. Association of Antidepressant Medication Use During Pregnancy With Intellectual Disability in Offspring. JAMA Psychiatry. 2017 Jul 12.

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Thursday, 13 July 2017

"a potential link between serious delinquency and later schizophrenia"

I was rather intrigued by the results reported by Nina Lindberg and colleagues [1] in their study designed to "investigate if serious delinquency was associated with future diagnoses of schizophrenia or schizoaffective disorder (here, broadly defined schizophrenia) among a nationwide consecutive sample of 15- to 19-year-old Finnish delinquents sent for a forensic psychiatric examination in 1989-2010."

I hadn't previously come across research directly linking delinquency - serious delinquency - with later schizophrenia diagnosis despite noting other research talking about other labels being potentially related to the extreme results of delinquency (see here) and onward some of those labels being potential risk factors for something like schizophrenia (see here).

Looking at the records of "313 delinquents with no past or current psychotic disorder" and around 1200 age- and sex-matched non-delinquents whose details were also held on a central population registry, researchers followed them all "[un]till death, emigration or the end of 2015, whichever occurred first." The results put delinquents as a group at quite a bit more risk of subsequently being diagnosed with schizophrenia than non-delinquents (12% vs. ~1% respectively). The authors conclude that their results "supports the previous research indicating a potential link between serious delinquency and later schizophrenia" and that more investigation is needed into the hows-and-whys of such a relationship.

Having already mentioned the slightly more indirect link between attention-deficit hyperactivity disorder (ADHD) and risk of offending behaviour (minus any sweeping generalisations) and ADHD and risk of schizophrenia, there could be lessons to be learned about the link between serious delinquency and schizophrenia. Also, minus further generalisations, I'm also wondering if some of the 'habits' perhaps more readily observed in delinquents (e.g. illicit drug use) could potentially be additional risk factors for a diagnosis of schizophrenia [2]. Minus any psycho-babble explanations, the rise and rise of scientific evidence pointing to various psychosocial factors as also being risk factors for schizophrenia [3] may additionally come into play, together with an understanding that elements of the parental home also may play a key role in cases of delinquency [4]. In short, there are several potentially important areas that could provide key research directions in this intriguing area.

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[1] Lindberg N. et al. Serious delinquency and later schizophrenia: A nationwide register-based follow-up study of Finnish pretrial 15- to 19-year-old offenders sent for a forensic psychiatric examination. Eur Psychiatry. 2017 May 15;44:173-178.

[2] Marconi A. et al. Meta-analysis of the Association Between the Level of Cannabis Use and Risk of Psychosis. Schizophr Bull. 2016 Sep;42(5):1262-9

[3] Larsson S. et al. High prevalence of childhood trauma in patients with schizophrenia spectrum and affective disorder. Compr Psychiatry. 2013 Feb;54(2):123-7.

[4] Fernández-Suárez A. et al. Risk Factors for School Dropout in a Sample of Juvenile Offenders. Front Psychol. 2016 Dec 26;7:1993.

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Wednesday, 12 July 2017

Analysing police involvement in the context of autism

"About 1 in 6 people with autism interacted with police over 18 months" went one of the media headlines covering the study published by Ami Tint and colleagues [1] looking at the hows-and-whys of police involvement in a cohort of nearly 300 young people and adults diagnosed with an autism spectrum disorder (ASD).

Researchers observed that some 16% of their cohort had some contact with law enforcement agencies but only a very small proportion actually resulted in any criminal charges being brought. Perhaps reassuringly, and despite 'aggressive behaviours' being cited as "the primary concern necessitating police involvement", most interactions between person and law enforcement were not especially adverse or particularly unpleasant for those on the spectrum. To quote: "Most parents reported being satisfied to very satisfied with their children’s police encounters."

But that's not to say that such encounters ended well for everyone, as talk about 1 in 5 police interactions involving physical restraint are also detailed and highlight the need for further research in this area. I might also add that symptom severity (I assume also referring to the presence of learning or intellectual disability alongside autism) was not a great indicator of police interaction or not according to the study.

Trawling through the quite small peer-reviewed research base in this area, there are some interesting points raised when it comes to awareness and training of police and other first responders [2] in respect of autism. Research here in Blighty has similarly highlighted gaps in police training [3] that may have been contributory to less positive satisfaction ratings when it came to interaction with people with autism. I draw back however from blanket blaming police for such statistics; they often have a very difficult job to do already, irrespective of whether diagnostic labels or other factor(s) are part and parcel of the situation(s) they are faced with.

So aside from greater training for law enforcement agencies and other first responders, what can be done to ensure that interactions with those on the autism spectrum are more positive? Some people have talked about setting up registries to guide police and related services where autism might be a factor in encounters. I can see the logic in such discussions, particularly in the context of another important issue to the autism spectrum - wandering or elopement - and ensuring that police have important knowledge about such an issue (see here). But with such registries come risks; risks of stigmatisation and also to personal liberties too. Some of the same issues relevant to the use of disclosure cards and autism come to the forefront (see here).

Perhaps a better arrangement would be a greater focus on community policing for example, where community Bobbies know their neighbourhood and it's residents and are able to apply that local knowledge as and when required. Appreciating that in these days of continued austerity, community policing numbers have suffered, perhaps a move back to neighbourhood policing is an important way of making police contact with those on the autism spectrum and no doubt various other groups that little more easier for all concerned?

Music to close, and the Beastie Boys meet Sesame Street?

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[1] Tint A. et al. Correlates of Police Involvement Among Adolescents and Adults with Autism Spectrum Disorder. J Autism Dev Disord. 2017. June 13.

[2] Kelly E. & Hassett-Walker C. The training of New Jersey emergency service first responders in autism awareness. Police Pract Res. 2016;17(6):543-554.

[3] Crane L. et al. Experiences of Autism Spectrum Disorder and Policing in England and Wales: Surveying Police and the Autism Community. J Autism Dev Disord. 2016 Jun;46(6):2028-41.

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Tuesday, 11 July 2017

Dementia risk in adult ADHD

"Adults with ADHD [attention-deficit hyperactivity disorderhave a 3.4-fold risk of developing dementia."

That was the conclusion reached by Nian-Sheng Tzeng and colleagues [1] who applied the 'big data' power of the Taiwanese National Health Insurance Research Database (NHIRD) to the question of whether yet more enhanced risk of adversity might be associated with a diagnosis of ADHD. Dementia by the way, reflects various symptoms/conditions pertinent to the decline of cognitive and other abilities.

Drawing on participant numbers in the hundreds, researchers determined that the risk of receipt of a dementia diagnosis in cases of adult ADHD was marginally higher compared with an asymptomatic (asymptomatic for ADHD) control group (5.4% vs. 4%). An association between ADHD diagnosis and risk of subsequent dementia remained after various, potentially interfering variables, were also taken into consideration ("age, gender, comorbidities, geographical area of residence, urbanization level of residence, and monthly income").

This is not the first time that enhanced risk of dementia in ADHD has been discussed in the peer-reviewed domain [2]. As per that previous report from Golimstok and colleagues - "there is no clear explanation for the association found" - science still does not have many clues as to why ADHD might preferentially predispose to certain types of dementia. I say this on the basis that we don't really know that much about the biology of either condition/diagnosis. That's not however to say that science is not getting closer to some important clues, as the report from Zhang and colleagues [3] talking about an animal model of Alzheimer's disease that also had "a high frequency of antecedent ADHD symptoms" is detailed. More studies are indicated.

To close, a link to an article marking the recent passing of the father of the ADHD diagnosis: Keith Conners together with a warning...

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[1] Tzeng NS. et al. Risk of Dementia in Adults With ADHD: A Nationwide, Population-Based Cohort Study in Taiwan. J Atten Disord. 2017 Jun 1:1087054717714057.

[2] Golimstok A. et al. Previous adult attention-deficit and hyperactivity disorder symptoms and risk of dementia with Lewy bodies: a case-control study. Eur J Neurol. 2011 Jan;18(1):78-84.

[3] Zhang Q. et al. Alzheimer's Model Develops Early ADHD Syndrome. J Neurol Neurophysiol. 2015;6(6):1-6.

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Monday, 10 July 2017

Rare genetic condition manifesting as autism and its management

"We report the case of a young boy with nonverbal autism and intellectual disability, with a rare de novo 1q21.3 microdeletion."

That was the starting point of the article published by Cora Cravero and colleagues [1] (open-access available here). Researchers describe in some detail how a diagnosis of autism spectrum disorder (ASD) was made "on communication and social interaction impairments and restricted, repetitive patterns of behaviour and interests" and what followed: "The patient had early and extreme self-injurious behaviours that led to blindness, complicated by severe developmental regression."

Detailing how "comparative genomic hybridization array identified a de novo 1.4 Mb microdeletion of chromosome 1q21.3" and various associated physiological findings, the Cravero report provides some rather intriguing evidence that the sentence 'science does not know what causes autism' might not necessarily ring true for everyone (see here for other examples). As the authors note: "The 1q21.3 microdeletion seems associated with ID [intellectual disability], dysmorphic features, and early SIB [self-injurious behaviour] and can be a cause of syndromic autism."

One or two particular details are noteworthy in the Cravero findings outside of the idea that the N=1 might be an important concept in relation to the autism spectrum.

First, is the quite extreme effects that self-injurious behaviour (SIB) in the context of autism can have on a person. This child was blinded by their extreme SIB: "intense and repeated mutilations of cheekbones and eyes, culminating in a bilateral blindness at the age of 4 years by intumescent white cataract after numerous surgical complications." As I've mentioned before on this blog, SIB can in some cases lead to some very complicated adverse health outcomes (see here) that are not uncommon to the autism spectrum (see here). There is however a brighter note to add to the SIB experienced by this child as the authors noted that a range of interventions seemed to help alleviate some of the challenging behaviours linked to such actions. I note for example that naltrexone - the opiate antagonist - was utilised to "decrease the endorphin sensation seeking procured by SIB and diminish SIB." This follows something of a resurgence in interest in this medicine (see here) and is music to my own research ears (see here).

Second, is a little detail mentioned about the eating habits of this child: "a diet almost exclusively made up of dairy products." Alongside some accompanying details on how "intestinal transit was altered, with episodes of diarrhoea (false constipation), encopresis, and coprophagia" and I'll just say that this is something I've heard quite a bit down my years of autism research. Alongside the use of lactulose to aid the bowel issues and the anti-opioid effect of naltrexone (yes, the protein in dairy products does break down into opioid-like compounds), I'm wondering whether some of the research I've been involved with down the years looking at casein-free diets might also be relevant too (see here)?

Finally, I need to draw your attention to the increasingly popular idea that regression is a part of quite a few cases of autism (see here). Indeed the pattern of autism + ID particularly being over-represented when it comes to regression in the context of autism (see here) seems to be borne out by the case report detailed by Cravero et al.

It is good to hear that after "a year of hospitalization" the outcomes reported on this child were quite a bit more favourable than where he began. So: "His mood was stable, without tantrums or irritability, and he felt pleasure without crippling stereotypes. The SIB were limited to small low intensity fists against his helmet or his cheekbone, occurring from time to time." Further: "During the best of times he wandered half-days without helmet, smiling and exploring his environment using tactile gestures."

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[1] Cravero C. et al. Management of Severe Developmental Regression in an Autistic Child with a 1q21.3 Microdeletion and Self-Injurious Blindness. Case Rep Psychiatry. 2017;2017:7582780.

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Saturday, 8 July 2017

Self-reported sexual attraction and autism continued

"Attention to gender identity and sexual diversity in education and clinical work with people with ASD [autism spectrum disorder] is advised."

So said the findings reported by Jeroen Dewinter and colleagues [1] (open-access) adding to something of an important theme in autism research circles in recent times (see here). Drawing on self-reported responses for some 675 people diagnosed (self-reported diagnosis) with an autism spectrum disorder (ASD) compared with over 8000 not-autism (self-reported?) controls on 9 questions, some interesting trends were observed. Those questions asked about information in relation to "assigned gender at birth, gender identity, sexual orientation (sexual attraction and sex of the partner), relationship status and evaluation of relationship status, duration of the relationship, living situation, and whether the partner has (or is suspected of having) ASD."

I mentioned that participants "self-reported a diagnosis on the autism spectrum" but to be fair, authors did also employ the Autism Spectrum Quotient—Short Version (AQ) "to assess autistic traits" of their ASD group. I've been a little critical of the AQ on other occasions on this blog (see here) but am willing to concede that as a rough-and-ready measure, it's about as good as we have at the moment.

Results: "Most men and women in the ASD group identified conforming their assigned gender at birth." Bearing in mind data on gender identity were not actually available for the control group, authors did note that about a quarter of women with ASD in their cohort and just short of 10% of men "reported some gender non-conforming feelings."

In terms of sexual orientation, researchers noted that: "Sexual orientation was more varied in ASD compared to controls in both men... and women." So: "Compared to general population peers, more people with ASD, especially women, reported sexual attraction to both same- and opposite-sex partners."

Relationship status was also something asked about during the study. Fewer participants with ASD reported being in a relationship at the time of inquiry compared with controls (50% vs. 70%) but for those in a relationship, most were living with their partner and most were pretty satisfied with their relationship. Yet also: "Of the singles, 29% regretted their relationship status" so one has to careful about sweeping generalisations.

There is quite a bit of important information included in this article but there are also caveats. Aside from the self-report angle to autism diagnoses, the question in my mind is: how representative is this sample in terms of the very heterogeneous autism spectrum? Y'know, self-report typically implies insight from the more 'able' end of the autism spectrum, or at least those able to self-report, and onward whether sweeping generalisations are necessarily warranted to covering the entire autism spectrum (see here). Bearing in mind also the gaps in some of the responses for the control group, I also wonder whether honesty could be a key variable when it comes to comparisons with the ASD group. I say this on the basis that very personal information about sexual identity and/or thoughts and feelings might be more honestly described by those with autism than those without autism. As the authors put it: "autistic participants being less influenced by societal views or stereotypes on attraction and gender." Such a suggestion could accord with other work looking at context effects in relation to autism [2].

The specific point about more women with ASD in the Dewinter study reporting greater levels of "sexual attraction to both same- and opposite-sex partners" and more "gender non-conforming feelings" adds to other independent findings in the peer-reviewed domain (see here). Again, such observations highlight how sex education in the context of autism (as indeed, in the context of the general population) needs to be inclusive of the spectrum of sexuality.

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[1] Dewinter J. et al. Sexual Orientation, Gender Identity, and Romantic Relationships in Adolescents and Adults with Autism Spectrum Disorder. J Autism Dev Disord. 2017. June 9.

[2] Farmer GD. et al. People With Autism Spectrum Conditions Make More Consistent Decisions. Psychol Sci. 2017 Jun 1:956797617694867.

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Friday, 7 July 2017

On preventing the deleterious effects of CMV: implications for some autism?

"Anxiety drug may prevent common virus that causes birth defects" went one of the headlines covering the study results published by Sara Ornaghi and colleagues [1].

Continuing a research theme from this group (see here) on how use of some mood stabilising medicines at critical periods might have some important impact on the deleterious effects of cytomegalovirus (CMV) infection, there is quiet optimism that this new research could have big implications for a range of different labels including some autism (see here).

So: "Valnoctamide (VCD), a neuroactive mood stabilizer with no known teratogenic activity, was recently demonstrated to have anti-CMV potential" was the starting premise for the Ornaghi study. Using mouse models - that's MOUSE models - of CMV infection and whether the anti-CMV potential of VCD could be "translated into an efficacious therapeutic effect to improve CMV-induced adverse neurological outcomes", researchers first looked at survival rates when injected 'low-dose' VCD was used. They reported that compared with those receiving a control substance (not VCD), the mice in receipt of VCD were more likely to survive. As per the media chatter about this study: "They lived longer, their body weight was greater – everything about them looked better" on the basis that congenital CMV infection can, in some cases, prove fatal.

Researchers also assessed whether various 'adverse neurological outcomes' associated with congenital CMV infection might be potentially offset by the use of VCD. They observed that: "VCD during the first 3 weeks of life restored timely acquisition of neurological milestones in neonatal male and female mice and rescued long-term motor and behavioral outcomes in juvenile male mice."

Then to the possible mechanism of effect, and based on the use of "CMV-infected human fetal astrocytes" they observed that "VCD reduced both viral infectivity and replication by blocking viral particle attachment to the cell." In other words, VCD, a medicine typically indicated as a sedative, seemed to possess some quite potent activity in relation to how CMV takes hold in important cells in the brain.

I've already mentioned about how at least some cases of autism might benefit from this work. I say this on the basis that there is a robust evidence base suggesting that congenital CMV infection could very well result in autism (see here). There is a need for quite a bit more investigation in this area in terms of translating mouse findings into human findings (see here) but the promises of this area of work are not to be under-estimated...

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[1] Ornaghi S. et al. Valnoctamide inhibits cytomegalovirus infection in developing brain and attenuates neurobehavioral dysfunctions and brain abnormalities. J Neurosci. 2017. June 19.

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Thursday, 6 July 2017

Another double-blind, placebo-controlled trial of vitamin D in autism. But...

The findings reported by Conor Kerley and colleagues [1] continue a theme in autism research circles of 'one study reporting one thing, and another study reporting something different'.

The name of the research game this time around was vitamin D supplementation in relation to autism spectrum disorder (ASD) and yet another gold-standard double-blind, placebo-controlled trial of the sunshine vitamin/hormone to look-see what happens to autistic signs and symptoms following supplementation. This continues on from a previous trial - again with gold-standard metholodgy - suggesting that there might be some benefit when it comes to supplementation (see here).

The Kerley study had been previously listed on ClinicalTrials.gov (see here). In short, supplementation with "2000 IU [international units] vitamin D3 supplementation or placebo daily for 20 weeks" were the intervention options for some 40 children diagnosed with ASD. The Aberrant Behaviour Checklist (ABC) was the primary outcome but other, more autism-specific measures (e.g. Social Responsiveness Scale) were also included in the scientific mix. Importantly in the context that vitamin D overdose is not unheard of in the context of autism (see here), researchers also probed vitamin D status in study participants.

Results: well, vitamin D supplementation did affect measures of vitamin D status as would be expected: "Following vitamin D3 supplementation, there was a significant increase in 25(OH)D to 83.8 nmol/L (p=0.0016)." When however it came to the behaviour side of things, scores on the primary outcome measure did not show any significant changes. The authors did find that "an improvement in self-care" in the supplemented group based on another scheduled used over the course of the study but that was about it.

Despite the lack of any significant effect, the authors seem to be still up-beat about the need for further study on vitamin D in relation to autism. They note: "Considering the other promising data as well as the relative safety and cheapness of vitamin D supplementation, further trials are warranted."

I would tend to agree that one study does not a scientific conclusion make. I can't say that there was a specific issue with the amount of vitamin D supplemented in the Kerley study compared to that used by Saad and colleagues [2] nor that the study timescale was too short. I might however draw your attention to the schedules used by the different studies and how perhaps the Saad study - using CARS and ATEC as well as the ABC and SRS - was perhaps better suited to detecting specific changes related to presenting autism symptoms than the Kerley study. But that is by no means an excuse for the Kerley results. There may also be other factors to consider [3].

Vitamin D deficiency/insufficiency is seemingly over-represented in relation to autism (see here for example) as it is in quite a few other behavioural/psychiatric labels (see here and see here). I do think this is an area that requires a lot more study; not least when one considers that (a) there may be groups on the autism spectrum who are genetically predisposed to lower vitamin D levels (see here) and (b) there may be potential 'best-responders' and 'non-responders' to this type of intervention (as there seems to be with many different intervention approaches with autism in mind). All this in the context that the label of autism is a great descriptor of symptoms but rather less splendid when it comes to research validity (see here).

So, just before anyone goes and touts vitamin D as 'not relevant to autism', think on...

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[1] Kerley CP. et al. Lack of effect of vitamin D3 supplementation in autism: a 20-week, placebo-controlled RCT. Arch Dis Child. 2017 Jun 16. pii: archdischild-2017-312783.

[2] Saad K. et al. Randomized controlled trial of vitamin D supplementation in children with autism spectrum disorder. J Child Psychol Psychiatry. 2016 Nov 21.

[3] Scragg R. Limitations of vitamin D supplementation trials: why observational studies will continue to help determine the role of vitamin D in health. J Steroid Biochem Mol Biol. 2017 Jun 13. pii: S0960-0760(17)30157-7.

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Wednesday, 5 July 2017

1 in 8 kids diagnosed with ADHD also diagnosed with autism

"Approximately one in eight children currently diagnosed with ADHD [attention-deficit hyperactivity disorder] was also diagnosed with ASD [autism spectrum disorder]."

So said the findings reported by Benjamin Zablotsky and colleagues [1] derived from results obtained from the US 2014 National Survey of the Diagnosis and Treatment of ADHD and Tourette Syndrome covering some 2500 participants. Based on parental responses via telephone interviews, researchers compared "children diagnosed with ADHD and ASD with children with ADHD, but not ASD" to arrive at their headline figure. They further observed that: "Children diagnosed with both disorders had greater treatment needs, more co-occurring conditions, and were more likely to have a combined hyperactive/impulsive and inattentive ADHD subtype."

It's not necessarily new news that autism and ADHD have more than a passing connection to one and another (see here). Indeed, the idea that those diagnosed with ADHD might also need to be preferentially assessed for autism too has been suggested before (see here and see here) and under more controlled scientific conditions. All very ESSENCE like if you ask me (see here).

I'm also struck by the suggestion that those with ADHD plus autism might also be more likely to have 'greater treatment needs' and 'more co-occurring conditions'. This rings particularly true when it comes to adulthood and the enhanced risks facing those with such dual diagnoses (see here). I might also add that 'co-occurring conditions' does not necessarily imply just the behavioural or psychiatric as per other findings [2]. Indeed, the observations reported by Anna Lamanna and colleagues on allergic disease potentially being something to consider when it comes to the comorbidity of ADHD and autism ties in with other findings covered on this blog (see here). The immune system might be doing so much more than just defending the body against the odd pathogen...

And to close, in keeping with today's subject matter, it appears that medications indicated for ADHD might also have some added value alongside the management of core ADHD symptoms [3].

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[1] Zablotsky B. et al. The Co-Occurrence of Autism Spectrum Disorder in Children With ADHD. J Atten Disord. 2017 Jun 1:1087054717713638.

[2] Lamanna AL. et al. Risk factors for the existence of attention deficit hyperactivity disorder symptoms in children with autism spectrum disorders. Neuropsychiatr Dis Treat. 2017 Jun 15;13:1559-1567.

[3] Lu Y. et al. Association Between Medication Use and Performance on Higher Education Entrance Tests in Individuals With Attention-Deficit/Hyperactivity Disorder. JAMA Psychiatry. 2017 Jun 28.

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Tuesday, 4 July 2017

Caring for the carers continued

Consider this post a brief extension to a previous one talking about how greater efforts need to be put into supporting those raising and caring for a person diagnosed as being on the autism spectrum (see here).

The science accompanying this post is that published by Cécile Rattaz and colleagues [1] who drew on data derived from the EpiTED cohort (see here), an initiative designed to "understand the heterogeneity of developmental trajectories among children with a diagnosis of PDD [pervasive developmental disorder] and the role of clinical, biological and environmental factors in their adaptive outcome." Researchers concluded that certain aspects associated with a diagnosis of autism in offspring - "young adults' level of adaptive skills... symptom severity and the presence of challenging behaviors" - can very much impact on parental quality of life (QoL). They argue for "the importance to propose specific interventions to target associated challenging behaviors in ASD [autism spectrum disorder]."

Quality of life when it comes to parents or primary caregivers of those young people on the autism spectrum is an often overlooked area when it comes to research and practice. Yes, the focus should quite rightly be on the person who lives with and experiences autism (in it's many different forms) but QoL for children/offspring is often inter-connected with QoL of parents and other family members. I appreciate that some might construe this work as autism presenting a 'burden' to the family and that is not something that anyone really wants to perpetuate. It is however important to realise that issues like challenging behaviours for example (bearing in mind what this covers) can affect many aspects of parenting behaviours, including those related to fatigue (see here) and perhaps further over the longer term [2]. When added to the dwindling resources available to parents (see here for example) there can be real strains placed on parents; more so bearing in mind other factors such as one-parent families and the demands placed on parents also potentially caring for siblings or even other family members.

There are no easy answers to the question of what to do to improve parental (and child) QoL in the context of autism. As mentioned, the sentiments of 'doing more with less' in these days of continued austerity for example, do not readily lend themselves to improving the situation in terms of the availability of something like respite care for example. The onus therefore continues to fall on parents and primary caregivers...

Music to close: The Saw Doctors - I Useta Lover.

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[1] Rattaz C. et al. Quality of Life in Parents of Young Adults with ASD: EpiTED Cohort. J Autism Dev Disord. 2017 Jun 17.

[2] Benson PR. The impact of child and family stressors on the self-rated health of mothers of children with autism spectrum disorder: Associations with depressed mood over a 12-year period. Autism. 2017 Jun 1:1362361317697656.

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Monday, 3 July 2017

Youth with autism talking about death and/or suicide

"Per parent report, 22% of youth with ASD [autism spectrum disorder] had several day periods when they talked about death or suicide "often," or "very often"."

That was one of the main conclusions reached in the study published by Lisa Horowitz and colleagues [1] drawing on data looking at "the prevalence of thoughts about death and suicide in 107 verbal youth with ASD with non-verbal IQ >55, assessed during inpatient psychiatric admission." Such results continue an important theme where risk of suicide (ideation, attempted or completed) seems to be quite a bit higher for those with autism compared with the non-autistic population (see here) (also including some worrying data on autism and assisted suicide).

The cohort for this study came from the Autism Inpatient Collection (AIC) [2] which set out to address an important disparity in autism research; the under-representation of those "severely affected by autism spectrum disorder (ASD), including those with intellectual disability, expressive language impairment, and/or self-injurious behavior (SIB)." This is an important theme being picked up on in many areas of the autism research landscape recently (see here for example). Having said all that, the focus on those 'verbal youth' with 'non-verbal IQ >55' (above 55) in the Horowitz paper did not seem to be keeping with the ethos of the AIC and the under-studied portions of the autism spectrum. Indeed, other independent data [3] on suicide attempts among those with learning (intellectual) disability may be quite relevant at this point

No mind, it is an important detail that over a fifth of this cohort of youth diagnosed with autism had death and suicide seemingly in mind so frequently. Researchers also highlighted how: "Clinical correlates included the presence of a comorbid mood... or anxiety disorder" also seemed to show connection to such results.

The implications of such work? Well, minus any sweeping generalisations or premature generation of formulae about what brings someone to talk/think about suicide so much and actual risk of suicide, the focus once again goes back to comorbidity over-represented in relation to the autism spectrum and the need for appropriate diagnosis and management. I've said it before on this blog, that some of the comorbidity accompanying autism (yes, I'm talking about you anxiety and depression) can sometimes be absolutely disabling for a person. One of the many important focuses needs to be how to manage such comorbidity and whether this impacts on aspects like death or suicide ideation and indeed, whether there may be other potential benefits accompanying such efforts (see here).

I cannot over-emphasise how important an area of autism research this and related work is. Although perhaps not great PR for the public perception of autism, lives are being lost in the autistic community to suicide. These are people, not statistics, people. Suicide is very much a complicated process and, despite some seemingly big headlines, not something that can reliably be predicted as we currently speak. Discussions however, about how suicide ideation/thoughts manifest in the context of autism and what drives the jump from ideation to attempt/completion need to be had, and need to be had soon. And that also includes how social factors (unemployment, poverty, social participation, contagion) as well as personal factors (e.g. self-harm) may play in role in driving any excess risk...

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[1] Horowitz LM. et al. Talking About Death or Suicide: Prevalence and Clinical Correlates in Youth with Autism Spectrum Disorder in the Psychiatric Inpatient Setting. J Autism Dev Disord. 2017 Jun 17.

[2] Siegel M. et al. The autism inpatient collection: methods and preliminary sample description. Mol Autism. 2015 Nov 10;6:61.

[3] Fuller-Thomson E. et al. Suicide Attempts Among Individuals With Specific Learning Disorders: An Underrecognized Issue. J Learning Disorders. 2017. June 21.

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