Saturday 29 September 2018

1 in 10 kids: the estimated prevalence of ADHD in the United States in 2016

Credit: Xu et al (2018) JAMA Network Open
"In a nationally representative population, we estimated that the prevalence of diagnosed ADHD [attention-deficit hyperactivity disorder] among US [United States] children and adolescents was 10.2% in 2016."

So said the findings published by Guifeng Xu and colleagues [1] who relied on data derived from the National Health Interview Survey (NHIS) in the United States over the course of two decades (1997-2016). As per an accompanying editorial [2] with the smart title "Paying Attention to Attention-Deficit/Hyperactivity Disorder", the Xu findings "fills an important need" insofar as their plotting a significant increase in the estimated prevalence rate of ADHD. The stats: "the estimated prevalence of ADHD significantly increased during the past 20 years—from 6.1% in 1997-1998 to 10.2% in 2015-2016." The year-on-year percentage figures considered by Xu et al showed a rise almost every year when it came to the [estimated] ADHD prevalence. Such figures are quite distinct from other (point) estimates in other parts of the world (see here).

Of course there are upsides and downsides to the authors' reliance on the NHIS dataset. So: the reliance on "parental reports about psychopathology rather than actual standardized assessments administered face-to-face with parents and/or children by trained evaluators" is one of the main limitations talked about across many different labels (see here). This has to be balanced with the large sample size included in the NHIS initiative and the "high response rate (child response rate of 85.6%-93.3%)." Personally I'm not inclined to believe that significant numbers of parents would provide 'false' answers to questions like: “Has a doctor or health professional ever told you that [the sample child] had attention-deficit/hyperactivity disorder (ADHD) or attention-deficit disorder (ADD)?” or “Does [the sample child] currently have attention-deficit/hyperactivity disorder (ADHD) or attention-deficit disorder (ADD)?” but ho-hum.

Then to the million dollar question: why has the estimated ADHD prevalence rate increased so dramatically across a relatively short period of time? Well, some well-worn explanations also seen with regards to the autism prevalence statistics (see here) have been banded around. So: "Nonetiologic factors may partly explain the apparent increase in the prevalence of diagnosed ADHD in this study" such as physician "sensitivity" to a diagnosis of ADHD, alongside the changes in ADHD diagnostic criteria already talked about in the peer-reviewed domain (see here). The issue of screening and diagnosis among non-white groups and their accessibility to said screening/diagnostic services is also discussed (something else that cropped up with the recent autism stats in mind too). And since I've just mentioned autism, it's also likely that the increasing recognition that ADHD is part of the clinical picture for quite a few on the autism spectrum (see here) probably contributes to the increase too.

But then there is the idea that the increase may also be - in part - reflective of a real increase too (see here). There are lots of possible candidates that may be contributory (see here and see here for examples) covering a multitude of genetic and non-genetic factors appearing during the nine months that makes us and beyond. As with any other developmental label and the reason(s) it comes about, there are going to be a multitude of potentially important factors to consider that may be quite individual. One thing is evident however, for whatever reason(s), the numbers are only heading in one direction...

A final question: what can be done to improve the life outcomes of those diagnosed with ADHD in ever-increasing numbers? I mention that question in the context that ADHD seems to elevate the risk of various adverse life events occurring (see here and see here and see here for examples) as well as being a potential 'driver' for other psychopathology appearing too (see here). In this context, we are already beginning to appreciate the benefits of certain types of intervention (see here) as well as the potential value of various other intervention options that are not yet considered 'mainstream' (see here and see here for examples). Further research is required to understand the societal and biological factors linked to a diagnosis of ADHD, and whether further advances in intervention and management can be made as a result, and onward lives (hopefully) enhanced...


[1] Xu G. et al. Twenty-Year Trends in Diagnosed Attention-Deficit/Hyperactivity Disorder Among US Children and Adolescents, 1997-2016. JAMA Network Open. 2018; 1: e181471.

[2] Dickstein DP. Paying Attention to Attention-Deficit/Hyperactivity Disorder. JAMA Newtork Open. 2018; 1: e181504.


Friday 28 September 2018

Parental separation in the context of offspring autism or ADHD

It's been quite a few years since I've approached the topic of parental separation/divorce in the context of an offspring diagnosis of autism or attention-deficit hyperactivity disorder (ADHD) (see here). The net result of that discussion was that the (peer-reviewed) evidence base, at the time, was a little mixed when it came to whether parental separation was more or less likely in the context of offspring autism for example. Indeed, whilst family parenting pressures no doubt contribute to parental relationship 'anxiety', there are a myriad of other factors to take into consideration too...

Fast forward to recent times and the study results published by Sabrina Just Kousgaard and colleagues [1] make for the blogging fodder, with their conclusion that: "Parents of children diagnosed with ADHD or ASD [autism spectrum disorder] were more likely to separate than control parents."

From a cold, objective science view the Kousgaard study is a well-powered one, insofar as including "the parents of 12,916 children with ADHD, 7496 children with ASD and 18,423 controls." With those sorts of participant numbers, you probably won't be surprised to hear that the source country was Denmark and yet again, the use of one of those fabulous Scandinavian population registries. Indeed: "all children with ADHD or ASD born between 1990 and 1998 in Denmark" were studied and followed-up "until the child's 25th birthday, parental separation or December 31, 2015, whichever came first."

Authors acknowledge that although there was a higher rate of parental separation in those families with a child with autism or ADHD it wasn't as straight-forward as 'blaming' offspring diagnostic status or not. So: "Other factors associated with parental separation were parental imprisonment, parental psychopathology, low parental education level, low household income and living in a larger city." What this finding does is reiterate that family circumstances are universally 'weird and wonderful' and that just because there is a child or children in the family diagnosed with autism or ADHD (or both) does not mean that families are any more or less 'weird and wonderful'.

Then to the big questions: (i) why was the parental separation rate elevated when autism or ADHD is diagnosed in the family, and (ii) what can be done to help families 'stay together'? Well, without getting too high-and-mighty about this (acknowledging for example, that in some circumstances parental separation is actually a better option than a continued 'toxic' family environment) there are other clues in the research literature (see here).

So, first of all let's acknowledge that parenting is tough. That's a universal issue, irrespective of whether children are diagnosed with this, that or t'other. Having a child with a developmental disorder/label/diagnosis does seem to make things tougher insofar as the additional 'things' that need to be catered for, and the almost constant battles that follow trying to get those additional 'things' catered for. I say this not only from the perspective of the parent-child relationship but also the additional strains related to schooling and education and navigating often complicated social welfare systems for example. It's little wonder that some parents voice sentiments like 'why I can never die' in this context (see here). The research literature is also pretty much unanimous that quality of life for parents with a child with a developmental diagnosis is reduced compared with families without that diagnosis (see here). This also highlights how such pressures take their toll both psychologically and physically. There is no malice intended in that last sentence and no blame to be apportioned; I'm just guided by what the research in this area is telling us.

From the perspective of parents and their relationship with each other, it's not difficult to see how diverting energy into a family and their welfare often means diverting energy away from each other. The words 'emotional roller-coaster' have probably been used more than once to describe parenting a child with a behavioural and/or developmental diagnosis, and minus any psychobabble, such a roller-coaster can be emotionally draining. Yes, there are ups, but also there are downs; and in the context that various types of 'energy' (psychological and physical) are often finite in amount, so when such energies and time are focused on a child or children, there is logically, less for the other significant partner. Simple physics. Throw in the dwindling resources devoted to something like respite care for example (see here) and, well, you can see how this might quite severely affect the family dynamic. And results also tend to be cumulative...

I don't doubt that the issue of parental separation in the context of an offspring developmental and/or behavioural diagnosis is a complicated one. People split up all the time and, more often that not, it's more about the people (parents) themselves and their relationship than anything else. It would be foolish however to disregard data such as that generated by Kousgaard and colleagues showing how context and environment can also play a (variable) role when it comes to family break-up.

And on the back of the Kousgaard results, it's perhaps also time to start thinking about how parental break-up / separation might affect said offspring, particularly when a diagnosis of autism and/or ADHD is part of the clinical picture...


[1] Kousgaard SJ. et al. The effect of having a child with ADHD or ASD on family separation. Soc Psychiatry Psychiatr Epidemiol. 2018 Aug 28.


Thursday 27 September 2018

"Anxiety and depression in adults with autism spectrum disorder" research reviewed and meta-analysed

I'm only making a fairly brief post today around the paper published by Matthew Hollocks and colleagues [1] titled: "Anxiety and depression in adults with autism spectrum disorder: a systematic review and meta-analysis."

Brief, because their results - "The pooled estimation of current and lifetime prevalence for adults with ASD [autism spectrum disorder] were 27% and 42% for any anxiety disorder, and 23% and 37% for depressive disorder" - were not entirely unexpected (see here and see here for examples) despite the 'gathered together' literature suffering from "a high degree of heterogeneity in study method and an overreliance on clinical samples."

I've said it before and I'll say it again, the [research] conversation now needs to move in a different direction to answer a couple of key questions in this area: (1) why are anxiety and depression so over-represented when it comes to autism? and (2) what are the most effective strategies to combat such issues in the context of a diagnosis of autism?

My opinion? I'm inclined to suggest that anxiety and depression are going to be present for a myriad of different reasons. I know people talk about life experiences as being important to their presentation of such symptoms and I'm not disagreeing at all. I'm inclined however to also suspect that the use of the word 'comorbidity' in respect of anxiety and depression in the context of autism is not altogether accurate. There is ample evidence in the peer-reviewed domain to suggest for example, that some of the core features of autism may actually 'heighten' the risk of depression and anxiety occurring (see here and see here). The nature of any relationship between core symptoms and things like depression and/or anxiety are likely to be complex and probably include aspects such as self-attention and brooding [2] and other related concepts such an intolerance of uncertainty (see here) and perhaps even something more pathological (see here). As unpalatable as this might be to some, the accompanying data from those who 'lost their diagnosis' (see here) supports the need for further investigations into this area...

And whilst on the topic of 'comorbidity', the paper by Eric Rubenstein  & Lauren Bishop‐Fitzpatrick [3] is definitely timely...


[1] Hollocks MJ. et al. Anxiety and depression in adults with autism spectrum disorder: a systematic review and meta-analysis. Psychol Med. 2018 Sep 4:1-14.

[2] Burns A. et al. Self-Focused Attention and Depressive Symptoms in Adults with Autistic Spectrum Disorder (ASD). J Autism Dev Disord. 2018 Sep 14.

[3] Rubenstein E. & Bishop-Fitzpatrick L. A Matter of Time: The Necessity of Temporal Language in Research on Health Conditions that Present with Autism Spectrum Disorder. Autism Res. 2018 Sep 5.


Wednesday 26 September 2018

On transparency in science: lessons from the Pandemrix vaccine and 'partial' evidence-based practice

Minus any hype or sweeping generalisation, I want to draw your attention to a feature article recently published by Peter Doshi [1] titled: "Pandemrix vaccine: why was the public not told of early warning signs?" complete with some media interest (see here).

The feature is based around the vaccines developed to counter the 2009 flu pandemic that starred the H1N1 influenza virus which was sweeping across the globe at the time. The 2009 flu pandemic was potentially serious insofar as its infection pattern and fatalities linked to infection although in reality did not turn out to be quite the 'global killer' that was prophesied. The rush to bring to market a vaccine to protect lives and counter the rise of H1N1 also brought with it controversy from several perspectives [2]; some later talking points seemingly stemming from the inclusion of a specific adjuvant - AS03 - in some vaccine preparations, and data suggestive of a possible correlation between onset of narcolepsy and use of certain flu vaccines containing the AS03 adjuvant (see here). Narcolepsy - a sleep disorder - was one potential adverse side-effect talked about, but other labels/conditions were also the source of some inquiry too (see here). On the basis of the emerging published data, court cases ensued, some of which have apparently unearthed some "internal reports" suggesting that some manufacturers "were aware of other serious adverse events logged" in relation to certain H1N1 vaccines...

The Doshi feature goes through some of these 'revelations' that did not seem to have been made public at the time. He talks about an 'undisclosed problem' whereby one vaccine in particular, Pandemrix, seemed to have a greater frequency of various adverse events reported according to those internal company reports. Most worrying are the reports of 'fatal outcome' across different vaccine preparations, particularly Pandemrix. He also writes: "And the raw numbers of adverse events were not small" highlighting how in one of the latest internal reports dated March 2010 seen by himself (or at least, the British Medical Journal) over 5000 reports of "serious adverse events for Pandemrix" had been received by the company behind the vaccine.

It's timely that the Doshi feature appears now at the time of writing this post, just days after the Peter Gøtzsche - Cochrane drama (see here) and at the same time as other relevant pieces have been published (see here and see here [3]). The similarities around questions of transparency in science (particularly industry-derived science that has a public health aspect attached to it) are very noticeable. As is also the question of 'how much detail should the public be provided with?' when it comes to science in general and then specifically, science and science communication linked to the potential cost-benefit ratio of particular medicines or medical preparations. It's interesting too that Doshi also references some past debate in Germany [4] about the 2009 flu pandemic where it was apparently reported that "the German interior ministry rejected accusations that the ministry had ordered a less risky vaccine for top officials" in light of some newspaper headlines published at the time. 'All animals are equal, but some animals are more equal than others' perhaps springs to mind...

I don't think the issue of less than full transparency in science and the question 'how much detail should the public be provided with' are going to go away any time soon. Such issues strike to the heart of the matter of how peer-reviewed published science is seemingly only one part of a much bigger picture when it comes to the search for a complete truth. One wonders for example, how many other 'internal reports' lie in [research] file cabinets around the world that could conceivably influence evidence-based decisions on the effectiveness and safety of various medicines and other interventions indicated for various conditions? Without such documents ever seeing the cold light of day, how can science ever truly be said to be complete, transparent or indeed settled?

Such a 'transparency' situation also makes initiatives like OpenTrials - calling for all research to be more 'discover-able' and 'traceable' - all the more vital and important. Issues such as the requirement for pre-registration of all studies via databases such as and importantly, the timely release and publication of results (see here) are pressing features. Study pre-registration (especially prospective registration) in particular, should perhaps be pushed a lot more than it currently is, and shouldn't just be reserved for big studies of drugs and medicines either.

Science is great and is getting better all the time. But it still has lots of issues and problems to overcome. A lack of research transparency seems to be a particularly important issue that, whilst starting to receive some much required attention, will if present, always mean that evidence-based practice really should be re-branded as 'partial evidence-based practice'. And that has lots of implications...

To close, given the subject matter included in the Doshi paper, I want to end with a reminder about not making sweeping generalisations. At the same time I'd also champion the words included in another recent article by Jørgensen and colleagues [5] (yes, also including Peter Gøtzsche as an author) responding to the idea that public confidence in public health initiatives such as vaccination may be "undermined" by even having such discussions in public. To quote: "Debates over sources of evidence must take place in public, especially when public health interventions are at stake." This is again, with the idea that science needs transparency - even better in the peer-reviewed domain - and closed door discussions rarely aid such transparency.


[1] Doshi P. Pandemrix vaccine: why was the public not told of early warning signs? BMJ 2018;362:k3948

[2] Doshi P. Influenza: marketing vaccine by marketing disease. BMJ 2013;346:f3037.

[3] Jørgensen L. et al. Challenges of independent assessment of potential harms of HPV vaccines. BMJ 2018;362:k3694

[4] Stafford N. Only 12% of Germans say they will have H1N1 vaccine after row blows up over safety of adjuvants. BMJ 2009;339:b4335.

[5] Jørgensen L. et al. Response to Cochrane editors: Jørgensen, Gøtzsche and Jefferson. BMJ EBM Spotlight. 2018. Sept 23.


Tuesday 25 September 2018

More welcomed (and interesting) research on pathological demand avoidance (PDA)

Pathological demand avoidance (PDA) [syndrome] is a label that currently occupies an unusual place in psychiatric and developmental circles. Defined by "obsessive non-compliance, distress, and florid challenging and socially inappropriate behaviour", PDA has seemingly found a place (somewhere) on the autism spectrum, but at the time of writing, does not actually occupy any unique position in any of the current systems of diagnostic classification mentioning autism (e.g. DSM, ICD). The National Autistic Society (NAS) here in Blighty talk about PDA in the context of "a behaviour profile within the autistic spectrum" but that's just one description among others.

The rise and rise of the term PDA as a specific diagnosis is firmly rooted (geographically) here in Blighty. This is probably as a result of the first description of PDA emanating from the late Elizabeth Newson during her time at the Early Years Diagnostic Centre (now called the Elizabeth Newson centre). Not everyone however is totally convinced that PDA is an independent syndrome (see here) or indeed, whether it is deserving of its specific and exclusive link with the autism spectrum at the cost of other labels... I'll be touching on that last point again in this post.

After that long introduction, I bring the findings reported by Vincent Egan and colleagues [1] to the blogging table, and some more welcome research in this area. The name of the research game for Egan et al was to adapt the Extreme Demand Avoidance Questionnaire (EDA-Q) "an informant-rating instrument" into a self-report version - the Extreme Demand Avoidance Questionnaire—Adult version (EDA-QA). Two studies are reported on in this context: "In Study 1, we use this measure to examine the relationship between PDA traits, ASD [autism spectrum disorder] traits, and other psychopathology dimensions, in a community sample of adults reporting self-identified psychopathology" and: "The second study examined the EDA-QA in a community sample and measured ASD traits more thoroughly, using the full ASQ." Yes, that's ASQ as in AQ (the Autism Spectrum Quotient) "used to quantify cognitive and behavioural features associated with ASD" and all the baggage that goes with it (see here and see here).

Results: yes, the EDA-QA was "reliable, univariate, and correlated with negative affect, antagonism, disinhibition, psychoticism, and ASQ score." This bearing in mind that the nearly 350 people who took part in study 1 were all self-reporting on the various instruments used, were "recruited from a variety of specialist on-line blogs and community forums focusing on the needs and concerns of persons with ASD" and were described as "a highly educated group." I also note that the words 'self-identifying' were also used extensively during the study write-up, specifically: "29 individuals reporting self-identified ASD also reported having PDA, 44 persons claimed to have PDA alone, and a further 19 self-identified PDA alongside depression or anxiety; separately, 59 persons claimed to have formally diagnosed ASD." Even the authors acknowledge that "self-reported ASD is not without it’s difficulties." No arguments from me there (see here and see here) and others have similar opined.

When it came to study 2 results, we are told that: "A path analysis to fit the data indicated that ASQ and EDA-QA scores were positively related." Irrespective of my various musings on how the ASQ (AQ) is not seemingly 'specific' when it comes to traits being 'linked to autism', this is an encouraging result. But there was more too... "The EDA-QA measure was associated with lower agreeableness, lower emotional stability, and higher scores on the ASQ. The effects were stronger for personality traits than for ASQ scores, suggesting it may be personality that differentiates how ASD traits are expressed, with more emotionally unstable and antagonistic persons with ASD expressing PDA-type qualities." One of the thoughts I had about this finding - 'personality that differentiates how ASD traits are expressed' - is the 'tie up' between the expression of autistic traits in relation to something like borderline personality disorder (BPD) (see here and see here) that has become more frequent in the peer-reviewed science arena recently. Yet more evidence perhaps that 'self-identifying' or 'self-diagnosis' when it comes to autism is not necessarily the most accurate measure?

The authors conclude that their instrument has promise and "could be easily integrated into assessment packages currently used with prisoners, mentally disordered offenders, and homeless people, where PDA may be suspected." Minus any big headlines regarding those particular groups (see here for example), I think examination of PDA in some of those contexts could be rather revealing. The link, for example, between PDA and offending behaviour (see here) in the context that SRED (Self-Report Early Delinquency Scale) scores - indicating "higher overall self-reported delinquency" -  significantly positively correlated with EDA-QA is an intriguing finding. That also AQ scores showed no such association with SRED scores might also suggest that PDA is not as necessarily well suited to an all-encompassing link to autism (autistic traits) as many people might think...

Let's hope that there is more research to come on the topic of PDA.


[1] Egan V. et al. The Measurement of Adult Pathological Demand Avoidance Traits. J Autism Dev Disord. 2018 Aug 23.


Monday 24 September 2018

"This goal is basically to find out what’s happened to these kids since age 8."

Credit: Disability Scoop 23 August 2018
It's another news report that provides the blogging fodder today, rather than a peer-reviewed science paper. No, this does not signify a significant shift in the aims and objectives of this blog away from peer-reviewed science material; rather I'm just commenting on something that might turn out to be quite important to the autism spectrum and will probably appear in the peer-reviewed science domain at some point. The news report in question (see here) is titled: CDC Expands Autism Monitoring Efforts.

CDC refers to the US Centers for Disease Control and Prevention, and the report is pertinent to their continuing efforts to chart the estimated prevalence of autism in the United States (see here and see here for some examples). This is done to a large extent via the Autism and Developmental Disabilities Monitoring Network (ADDM), with statistics based on the number of eight year olds estimated to be diagnosed with autism or an autism spectrum disorder (ASD). Why 8 year olds? Well, I assume it's because this is an age where autism will (*should*) be diagnosed and avoids any earlier years diagnostic confusion and the like.

But it appears that this initiative does not want to just remain focused on 8 year olds as we are told that: "the agency wants researchers at up to two sites to look at 16-year-olds who were previously identified as having autism symptoms in the network’s tracking when they were age 8." Further: "This goal is basically to find out what’s happened to these kids since age 8."

The rationale behind such a decision is a noble one. It's about looking at whether children diagnosed with autism/ASD "have other health conditions and what types of services they are receiving at school and otherwise." 'Other health conditions'? Erm, I'd hazard a guess and say yes, yes they will typically have some other health conditions (see here) also presenting. It's an agenda that also fits in well with the partial shift in focus from children on the autism spectrum towards teens and adults with autism. As for the 'services they are receiving at school' angle, well, this could also be important in terms of best practice too. I say that mindful of the fact that over here on the other side of the Pond, there has been some significant legal movement on schooling in the context of autism recently (see here).

But there is another aspect to such a decision by the CDC that might also be interesting to look at: that pertinent to the stability of an autism diagnosis (see here and see here for examples).

I know some people don't like to talk about the observation that autism, for some, is not necessarily a lifelong diagnosis (see here). The idea that within the huge heterogeneity included under the label of autism not everyone has a stable presentation across the lifespan is a jarring concept, particularly in the context that some people see their autism as so much more than just a diagnostic label. I hear words like 'masking' and 'camouflaging' being used more often to potentially explain why some people don't meet the diagnostic cut-offs for autism/ASD having previously done so. This may well apply to some people, but I don't think this represents an intellectually satisfying universal explanation for such a phenomenon and denigrates a potentially important finding. That also, 'losing a diagnosis' might impact on other issues 'over-represented' in relation to autism (see here and see here) provides further evidence for something other than masking potentially going on (unless the act of masking is somehow 'protective against' the likelihood of psychiatric comorbidity occurring alongside autism?)

I don't want to pre-empt any decisions from the CDC about their shift in focus and what they will and won't look at. Guaranteed that if such a proposal comes to being, the data will reveal something interesting and important, moving forward from just the autism 'numbers game'. If however, diagnostic stability does crop up as part-and-parcel of the new CDC autism prevalence agenda, I daresay that more research resources will be put into looking at the hows-and-whys of this issue. And perhaps too important areas like whether there are genetic and/or biological 'changes' associated with not subsequent fulfilling the diagnostic criteria for autism will also start to figure.

To close, I'm going to link again to the recent-ish findings from Bal and colleagues [1] suggesting that "some older adolescents and adults with ASD may not exhibit the same difficulties observed in young children with ASD" as a template for further study in this area. This, as part of a recognition, that "some will be largely free from symptoms of the disorder by adulthood" [2] (see here for my take) observed by some authors. Feathers will no doubt be ruffled.


[1] Bal VH. et al. Autism spectrum disorder symptoms from ages 2 to 19 years: Implications for diagnosing adolescents and young adults. Autism Res. 2018 Aug 12.

[2] Lord C. et al. Autism spectrum disorder. Lancet. 2018 Aug 11;392(10146):508-520.


Saturday 22 September 2018

SEED says... opioid prescription before or in early pregnancy may impact on 'child neurodevelopment'

One has to be a little careful with a few things associated with the findings reported by Eric Rubenstein and colleagues [1] but they are interesting.

In it, researchers talk about analysing for various opioid based medicines prescribed over the period 3 months before conception up to the point of childbirth and onward any subsequent correlation with "child’s risk of ASD [autism spectrum disorder], developmental delay/disorder (DD) with no ASD features, or ASD/DD with autism features." Readers may have already heard about this study as a function of its inclusion in the 2018 INSAR (IMFAR) meeting (see here).

Outside of the old tenet 'correlation is not the same as causation', the authors specific focus was on 'opioid prescription', referring to a range of opiate-based medicines that are typically indicated for pain relief and supplied under medical consultation/supervision. This was not a study looking at other types of opioid 'drug' use that seem to be making a lot of news headlines in recent times (see here), despite the inclusion of methadone and buprenorphine in their list of watched-for prescriptions in maternal medical records. Authors do however mention that opioid use among pregnant women is increasing for various different reasons...

The use of the SEED - Study to Explore Early Development - initiative was the starting point for the Rubenstein study. As per the title of this post - 'SEED says' - it's yet another research venture (see here and see here for other examples) that seems to be producing some important data covering various aspects of autism and related developmental disorders (see here). At first glance, I was a little confused about the categorisation of 'ASD/DD with autism features' included in the study but readily accepted that this was a grouping distinct from another categorisation: 'developmental delay/disorder without features of ASD'. The authors were specifically looking at autistic features with such a division of the groups.

Taking into account the various medicines that are listed as opiates (including medicines containing codeine and fentanyl), authors scoured maternal medical records looking for opioid prescriptions. The also looked at time of use covering pregnancy trimesters, their use 3 months prior to conception and 'peri-pregnancy', all as a function of those diagnostic bandings.

Results: "Preconception opioid prescription was associated with 2.43 times the odds of ASD [95% confidence interval (CI) 0.99, 6.02] and 2.64 times the odds of ASD/DD with autism features (95% CI 1.10, 6.31) compared to mothers without prescriptions." CI refers to confidence interval and although I'm no statistics expert, I noted that the first finding on preconceptual opioid prescription being *associated with* an increased odds of offspring ASD (as in a diagnosis of ASD) did cross the magical '1' number: "95% confidence interval (CI) 0.99, 6.02." Combined with quite a large CI interval, and some might say that the 'precision' of that finding was less than convincing in a statistical sense. The other 'autistic traits' finding is a little more robust but there's still a need for further investigations in this area, including the use of some biological testing parameters perhaps?

I'm not saying that medicines taken during pregnancy can't have a possible impact on offspring neurodevelopment. The still-emerging data for example, on paracetamol (see here) or valproate (see here) seem to underline that point; albeit with a scheme of work to follow in those areas too. I'm also not saying that opioid-based medicines might not have some effect on offspring development [2], quite a few effects by all accounts [3], bearing in mind the pressing need to look at this issue in the context of the opioid crisis seemingly affecting many nations these days. But, at the present time, we have to be a little careful with the still-emerging-picture in this area so as not to make big claims or unduly tarnish what is an important class of prescription medicines when it comes to pain relief and beyond. And I say that as someone who has done his fair share of using the words 'opioid' and 'autism' down the [research] years [4]...


[1] Rubenstein E. et al. Brief Report: Maternal Opioid Prescription from Preconception Through Pregnancy and the Odds of Autism Spectrum Disorder and Autism Features in Children. J Autism Dev Disord. 2018. Aug 21.

[2] Hans SL. & Jeremy RJ. Postneonatal mental and motor development of infants exposed in utero to opioid drugs. Infant Mental Health Journal. 2001. May 9.

[3] Fill M-MA. et al. Educational Disabilities Among Children Born With Neonatal Abstinence Syndrome. Pediatrics. 2018. Aug 30.

[4] Shattock P. & Whiteley P. Biochemical aspects in autism spectrum disorders: updating the opioid-excess theory and presenting new opportunities for biomedical intervention. Expert Opin Ther Targets. 2002 Apr;6(2):175-83.


Friday 21 September 2018

"risperidone is efficacious in the treatment of symptoms in children and adolescents with ASD"

The heading titling this post - "risperidone is efficacious in the treatment of symptoms in children and adolescents with ASD [autism spectrum disorder]" - comes from the systematic review published by Narong Maneeton and colleagues [1]. These researchers scoured the existing peer-reviewed research literature - "from January 1988 to February 2017" - to "systematically review the efficacy, acceptability and tolerability of risperidone in children and adolescents with ASD." They concluded that, on balance, around "one in every three ASD children and adolescents has benefits from treatment with risperidone." They also cautioned that there is a further scheme of work to follow, looking at the use of risperidone in this particular patient group as per the findings of previous reviews. The continued examination of potential adverse side-effects associated with risperidone use is one such important area to be investigated (see here and see here for examples).

Risperidone is categorised as an antipsychotic medicine. It's typically used to treat psychosis and mania. It's also sometimes used in the context of certain 'challenging behaviours' being presented as a function of a diagnosis of autism or autism spectrum disorder (ASD): "explosive and aggressive behavior" according to one source. Importantly however, the use of risperidone as a tool to intervene on the 'core features' of autism is not, at the time of writing, currently indicated.

Maneeton et al looked specifically for studies classified as a randomised controlled trials (RCTs) in the context of risperidone use with children and adolescents aged up to 18 years of age and diagnosed with autism or ASD. They found seven RCTs including some 370 participants. All of the trials relied on the DSM-IV description of autism or ASD and, aside from two trials, most lasted for between 6 and 8 weeks. The Aberrant Behaviour Checklist (ABC) was a commonly used tool in the studies included for review, with response criteria on such an instrument anticipating between a 25% and 50% reduction in scores (specifically on the irritability subscale) as a result of risperidone use.

Results: as per the opening sentence of this post, a positive behavioural response typically favoured risperidone use over the placebo used as a comparator when it came to certain challenging behaviours. This was noted across those short-term studies ("acute response") and also longer-term intervention (6 months). The authors also reported that a variety of side-effects - adverse side-effects - were noted alongside the use of risperidone. These included things like an increase in appetite, "drowsiness, somnolence, fatigue, anxiety, hypersalivation and elevation of prolactin level." The prolactin bit has been discussed before on this blog (see here) specifically in the context that: "There is no known normal function for prolactin in men."

Bearing in mind that Maneeton and colleagues were discussing risperidone use in 'children and adolescents' with autism, and the requirement for particular caution when using such a powerful medicine on the [still] developing body and brain, these are useful findings. Of course in an ideal world, no-one would want children and young people to have to take risperidone. But like other medicines indicated for other behavioural labels (see here), with regular and appropriate monitoring and medicines management, such pharmacotherapy can be transformative in its effects for some.

The situation however does need improving; particularly in the context of those side-effects and the worry they carry especially into the longer-term. I'm also minded to suggest that science needs to delve a little further into the proposed mechanism of effect when using medicines like risperidone in terms of immune system effects (see here) and other important biological pathways (see here) outside of the known "dopamine D2, 5-HT2A, alpha1-adrenoceptor, and histamine-1 receptor antagonist" biological action. By doing so, one *could* perhaps foresee future medicines with the 'anti-irritability' action but perhaps minus the considerable risk of side-effects?

And without any comment or opinion from me, the recent ruling here in Blighty that 'aggressive behaviour is not a choice for children with autism' (see here for my take) needs to be very carefully managed from a pharmacotherapy point of view. I say this so as not to make medicines such as risperidone, the first line of intervention or worse still, a 'chemical cosh'...


[1] Maneeton N. et al. Risperidone for children and adolescents with autism spectrum disorder: a systematic review. Neuropsychiatr Dis Treat. 2018 Jul 11;14:1811-1820.


Thursday 20 September 2018

ADHD in a 'detention setting': meta-analysed

"Our results confirmed the high prevalence rate of ADHD [attention deficit hyperactivity disorderamong PLD [people living in detention], corresponding to a five-fold increase compared to the general population."

So said the meta-analysis findings reported by Stéphanie Baggio and colleagues [1] pulling together the current peer-reviewed research literature - "between January 1, 1966 and January 2, 2018" - on the estimated rate of ADHD in the prison/incarcerated population. The intention to undertake this meta-analysis had already been previously published (see here).

This is a topic that has been covered before on this blog (see here and see here for examples). It strikes to the heart of the idea that a diagnosis of ADHD (or the presence of significant ADHD-linked behaviours) confers an elevated risk for various adverse outcomes (see here and see here for another couple of such outcomes). It also implies that we need to know more about the 'hows-and-whys' of such elevated risks and what can be done to reduce or minimise them as and when ADHD is diagnosed...

Baggio et al describe how they boiled down the available research literature to just over 100 studies including data on nearly 70,000 participants. The studies covered various geographical locations and looked across various ages. We are told that: "The ADHD adolescent/adult meta-analytic prevalence estimate was 26.2%." So about 1 in 4 of the total incarcerated population included for study met the diagnostic criteria for ADHD. When looking at the 'retrospective assessment of ADHD in childhood' this figure climbed to over 40%. When researchers looked for any differences across the diagnostic criteria used (including DSM-5), they found no significant differences. They conclude that the rate of ADHD in PLD is quite a bit higher than that reported in the population at large.

"These results suggest that PLD bear a heavy mental health burden on secure services as around one-third may require treatment for ADHD." This is important. It reiterates that alongside the personal effects that ADHD has, there are also societal implications too. I know this is not exactly great PR when it comes to ADHD, but lives are needlessly being wasted when spent in captivity; lives that could be so much more productive in other circumstances.

Other important questions are asked by Baggio and colleagues too; questions around whether suitable "treatment, monitoring, and care for ADHD during and after detention" could aid in cutting re-offending rates and offering those who were detained a better life. I'd have to say that 'yes' is the most likely answer to this question; bearing in mind that offending behaviour is multi-faceted in terms of individual and other more socially and environmentally driven factors. But we have to, as a society, at least try...


[1] Baggio S. et al. Prevalence of Attention Deficit Hyperactivity Disorder in Detention Settings: A Systematic Review and Meta-Analysis. Front Psychiatry. 2018 Aug 2;9:331.


Tuesday 18 September 2018

On Cochrane and 'facts' and 'politics' in evidence-based medicine

The controversy surrounding the reported expulsion of Peter Gøtzsche from the Cochrane Collaboration (or should that just be Cochrane?) is something that I've been following for a few days now (see here). Cochrane, under the heading "Trusted evidence. Informed decisions. Better health", represents one of the premier go-to sources for evidence-based healthcare advice on a range of topics. Some of those topics have been previous fodder for this blog too (see here and see here for examples).

I don't profess to have any unique insight into the various goings-on leading to the reported expulsion of Gøtzsche and resignations of fellow members beyond that which has been discussed in various sections of the science media (see here and see here and see here). From what I gather, things look like they've been 'brewing' for a while with regards to Cochrane and the views and opinions expressed by some of those who are seemingly departing. Such a public spat however, is unlikely to be good for science or evidence-based medicine, and indeed may have some wider implications for some fundamentals of science and science communication...

One of the possible [late] precipitating events mentioned around the Gøtzsche saga was the publication of a quite scathing article by Lars Jørgensen and colleagues [1] (including Gøtzsche as an author) questioning the published results of a recent Cochrane review [2] titled: "Prophylactic vaccination against human papillomaviruses [HPV] to prevent cervical cancer and its precursors". The original review by Marc Arbyn et al garnered media headlines when published (see here) as per conclusions such as: "There is high‐certainty evidence that HPV vaccines protect against cervical precancer in adolescent girls and young women aged 15 to 26." A comforting finding by all accounts. Accompanying such efficacy data were other statements made by the authors on the basis of the evidence reviewed that: "The vaccines do not increase the risk of serious adverse events, miscarriage or pregnancy termination."

Jørgensen and colleagues however put forward their [peer-reviewed] view that the Arbyn paper fell short of the expected standards from Cochrane: "We do not find the Cochrane HPV vaccine review to be ‘Trusted evidence’, as it was influenced by reporting bias [3] and biased trial designs." They highlighted several 'issues' with the original review stretching from trial selection for the review, to the assessment of "serious and systemic adverse events" to potential "conflicts of interest." Similar sentiments had been voiced about other Cochrane reviews too that were subsequently pulled from the scientific literature. Feathers were inevitably ruffled (see here) by the Jørgensen paper, even as far as prompting a response from the journal that published the paper [4] about the peer-review process leading to publication of the critique. Things are getting serious when a journal has to defend its publication of a paper.

Without wishing to reduce this saga to any one event, I don't think it would be unreasonable to assume that the Jørgensen paper might have influenced matters quite considerably; perhaps even bringing them to a head. As per involvement on the Boesen paper [5] Gøtzsche is no stranger to calling out Cochrane reviews that seemingly don't make the grade, alongside also voicing opinions on various other matters down the years. To quote: "... in another book, [he] likened the pharmaceutical industry to "organized crime""; such forthright statements stretching back some years are unlikely to have made too many friends in certain circles.

As per the title of this post mentioning the words 'facts' and 'politics', one particular write-up of this saga I think hits the nail on the head. The opinion piece from Trish Greenhalgh [6] presents the two sides to this 'dispute': on the one hand is that the “crisis” is "philosophical (relating to the nature of facts)" and on the other, "political (relating to organisational governance)." The philosophical side of things is pretty evident as per the publication of the Jørgensen paper as a counter to the Arbyn paper. Greenhalgh mentions about how "Gøtzsche might be classified as an evidence-based medicine purist" given his views and sizeable contribution to various "statements on how to undertake and publish research." In this respect, his published views on the original Arbyn paper (and similarly in other reviews) seem to detail scientific standards not being met, or at least not being met to his and his co-authors standards. And certainly on points such as access to trial results and data, he's seemingly not alone in his concern (see here).

On the political side of things, well, at the time of writing we just don't know enough to reasonably comment. Greenhalgh mentions that: "The political explanation for Cochrane’s crisis relates to the tension between governing an organisation and respecting individual members’ academic freedom to express dissent." The fact that such dissent has over the years covered various important public health topics - "cast doubts about the safety of a vaccine against human papillomavirus (HPV), a cause of cervical cancer, and says psychiatry has “gone astray” by coercing patients into taking medication, such as antidepressants, they don’t want to use and that cause “brain damage” over the long run" - is likely to have really stretched those organisational relationships with Gøtzsche. Not least because immunisation and antidepressant use reflect important pillars of modern public healthcare and, historically, uptake of such medicines is very, very susceptible to differences in scientific views, opinions and beyond.

As to the idea mentioned by Greenhalgh that: "We should cut it [Cochrane] some slack while it gets its house in order", I'm not exactly sure how it's going to approach this 'house in order' requirement and what this means for the future credibility of Cochrane. Based solely on the 'facts' side of this saga, it strikes me that organisations like Cochrane actually need people like Peter Gøtzsche and their "evidence-based medicine purist" beliefs. They need them in order to critically (really critically) boil down the ever-growing research literature into scientifically sound statements for public and policy consumption without fear or favour. Minus such voices, it's more likely that evidence-based messages originating from such initiatives are perhaps going to be weakened, which in turn means that population healthcare is potentially going to suffer. Moreover, I assume also that just because Gøtzsche is reportedly not part of Cochrane any more does not mean that he won't be heard from again in the peer-reviewed domain...


[1] Jørgensen L. et al. The Cochrane HPV vaccine review was incomplete and ignored important evidence of bias. BMJ Evidence-Based Medicine. 2018. July 27.

[2] Arbyn M. et al. Prophylactic vaccination against human papillomaviruses to prevent cervical cancer and its precursors. Cochrane Database Syst Rev. 2018 May 9;5:CD009069.

[3] Jørgensen L. et al. Index of the human papillomavirus (HPV) vaccine industry clinical study programmes and non-industry funded studies: a necessary basis to address reporting bias in a systematic review. Syst Rev. 2018 Jan 18;7(1):8.

[4] Heneghan C. & Onakpoya I. Editors’ response to concerns over the publication of the Cochrane HPV vaccine review was incomplete and ignored important evidence of bias. BMJ Evidence-Based Medicine. 2018. Sept 12.

[5] Boesen K. et al. The Cochrane Collaboration withdraws a review on methylphenidate for adults with attention deficit hyperactivity disorder. Evid Based Med. 2017 Aug;22(4):143-147.

[6] Greenhalgh T. The Cochrane Collaboration—what crisis? BMJ. 2018. Sept 17.


Thirty fold future risk of bipolar disorder if ADHD and anxiety are diagnosed together

"The combination of ADHD [attention-deficit hyperactivity disorder] and anxiety increased the risk of bipolar disorder 30-fold... compared with those with no prior ADHD or anxiety."

That was the conclusion reached in the study results published by Sandra Meier and colleagues [1] following their examination of one of those oh-so-useful Scandinavian population registries.

Drawing on data for over 2.4 million people born in Denmark between 1955 and 1991 and followed "from their sixteenth birthday or from January 1995 to their first clinical contact for bipolar disorder or until December 2012", researchers came to a attention-grabbing observation with some potentially profound implications when it comes to 'risk' and screening. The magnitude of the risk - "30-fold" - when ADHD and anxiety were joined in terms of bipolar disorder being diagnosed represents something that is difficult to brush under the scientific carpet.

Am I surprised by these latest findings? Well, no. For quite a while now, it's been 'known' that a diagnosis of ADHD alongside other developmental labels might be a risk factor for all-manner of psychiatric disorders (see here for example). This added to other literature indicating an *association* between ADHD and other, potentially life-limiting behaviours (see here) that compliments evidence discussing suicide attempts in relation to bipolar disorder [2] for example. All set in an age of increasing realisation that behavioural and psychiatric conditions rarely exist in a diagnostic vacuum (see here).

I'm also minded to point out that ADHD and anxiety are pretty common 'comorbidities' when it comes to a label/condition of specific interest to this blog: autism or autism spectrum disorder (ASD) (see here and see here for examples). Following this logically, the implication is that alongside a diagnostic combination of autism, ADHD and anxiety, there may be implications for the identification of a heightened risk of bipolar disorder there too. Indeed, it's been mentioned before in the peer-reviewed research literature that bipolar disorder *might* be a feature of some autism (see here) albeit not necessarily presenting in a 'classical' fashion (which could be a significant factor in under-diagnosis).

There is another implication from such shared, overlapping diagnostic sentiments: successfully tackle one or other element (ADHD or anxiety) and perhaps modify the subsequent risk of bipolar disorder being diagnosed... Some food for thought.


[1] Meier SM. et al. Attention-deficit hyperactivity disorder and anxiety disorders as precursors of bipolar disorder onset in adulthood. Br J Psychiatry. 2018 Jun 21:1-6.

[2] Novick DM. et al. Suicide attempts in bipolar I and bipolar II disorder: a review and meta-analysis of the evidence. Bipolar Disord. 2010 Feb;12(1):1-9.


Monday 17 September 2018

Maternal tobacco smoking and offspring ADHD risk again

"ADHD [attention-deficit hyperactivity disorderand movement disorders were found to be more common in hospitalized children of smoking mothers."

That was one of the details recorded in the research findings published by Gil Gutvirtz and colleagues [1] adding to a growing research 'trend' suggesting that maternal tobacco smoking during pregnancy seemingly does little for mum's health and also probably not a great deal for her offspring's health and wellbeing either (see here).

Based on results analysing "all deliveries of mothers who reported smoking during pregnancy and non-smoking mothers between 1991 and 2014 at a single tertiary medical center" researchers included almost 250,000 children in their study. Quite a small proportion - "2861 (1.2%)" - were children of mothers who smoked during pregnancy. When researchers looked at these children they noted "higher rates of movement, eating and developmental disorders as well as attention deficit hyperactive disorder" as compared with the larger non-smoking group. "Maternal smoking during pregnancy is an independent risk factor for long-term neurological morbidity of the offspring" was the conclusion.

Allowing for the fact that observational studies, even population-based ones, aren't great for 'proving' cause-and-effect, the volume of such studies independently reaching the conclusion that maternal smoking during pregnancy *might* have an important connection to risk of offspring ADHD is growing. Indeed, alongside all the other adverse outcomes seemingly connected to smoking during pregnancy (see here) I don't think it would be out of place for regulators and health-related agencies to start informing the population at large that ADHD or ADHD-related behaviours as an outcome is at least possible; as some agencies seem to be doing (see here)...

Another research step could be some further investigations actually looking at something like cotinine levels (and important marker of tobacco smoke exposure) in both mums and offspring to see whether 'the dose makes the poison' as other recent studies have hinted at [2].

Tobacco smoking ain't good for anyone it seems, and children seem to be particularly vulnerable to its effects.


[1] Gutvirtz G. et al. Maternal smoking during pregnancy and long-term neurological morbidity of the offspring. Addictive Behaviors. 2018. Aug 16.

[2] Kim KM. et al. Associations between urinary cotinine and symptoms of attention deficit/hyperactivity disorder and autism spectrum disorder. Environ Res. 2018 Jun 26;166:481-486.


Friday 14 September 2018

Statistically significant group differences in self-reported repetitive movements between diagnosed and self-identifying autism

One needs to remember that, at the time of writing this post, the article posted by Joost Wiskerke and colleagues [1] suggesting that "camouflaging of RMs [repetitive movements] may contribute to under diagnosis of autism, at least in females and transgender people" is just a preprint ("a version of a scholarly or scientific paper that precedes publication in a peer-reviewed scholarly or scientific journal"). It has not been through formal peer-review yet, but rather the authors have bravely 'put it out there' for old farts like me to pore over.

Having glanced through the abstract first and discovered the use of the words "self-identified as autistic" my brow furrowed somewhat. Upon further reading of the paper in its entirety, the furrowing brow furrowed a little less as I understood why the authors mentioned use of a cohort that was "56% formally diagnosed participants and 44% who self-identified as autistic." But that's not to say that I was completely enamoured with the study write-up as it currently stands...

Before continuing and in order to repel any accusations that come my way, I'll mention that I don't have any particular issue with people without a formal diagnosis of autism thinking/believing they are on the autism spectrum. It's their right to do so and indeed, such self-realisation is often an important step towards getting a professional assessment for autism. For some people, their hunch about being autistic eventually turns out to be correct as per them reaching defined clinical cut-off points for autism on the various instruments of assessment that are available during said professional assessment. But that's not to say that every person who self-identifies as being autistic/having autism is always going to be right. As we are starting to realise from the wealth of peer-reviewed science on this topic, the label autism does not seemingly have any exclusive rights to the presentation of autistic traits (see here and see here for examples). And it is for that reason why we have so many good and knowledgeable diagnosticians when it comes to such professional assessments, combined with an important focus on: "Symptoms caus[ing] clinically significant impairment in social, occupational, or other important areas of current functioning" in order to receive a diagnosis. Access to such autism assessments is another issue, but shouldn't be used as an excuse...


Wiskerke et al started from the premise that repetitive movements (RMs) are common in autism but there are some potentially important differences in the expression of such issues between the genders. This follows other independent findings in this area (see here) detailing how stereotyped and repetitive behaviours may be less frequently observed in females [2] minus any sweeping generalisations. Researchers then moved on to suggesting that one of the reasons why such RMs may be less frequently observed is because they are actively being masked or camouflaged, and this could eventually lead to an under-diagnosis of autism among certain groups. 'Masking' or camouflaging in the context of autism is a bit of a hot [social media] topic at the moment (see here and see here).

"In this exploratory study, we took a first step... by using self-report measures from a large number of female and transgender adults, using recruitment on social media to an on line questionnaire." Ah yes, the on line questionnaire, which seems to becoming more and more popular in certain autism research circles [3] (see here also for another example). There's nothing wrong with using such tools for asking about opinions and the like, but they are typically open to anyone and everyone (who has access to the internet!), and not exactly great for authenticating complicated things like clinical diagnoses, behaviours and comorbidity for example. As for the incorporation of data from transgender adults, well, again this follows a theme in autism research recently (see here) where 'autistic identity' and sexual identity seem to be converging for some people/groups (see here).

"We assessed current RMs using a combination of visual analog scales for specific behaviors and textboxes for free-text responses." There's mention of using some of the DSM-5 criteria for autism in this section. Authors also talk about testing for camouflaging "using the matrix multiple-choice question “Did/do you hide these behaviors from others…” 1) “…as a child?”, 2) “…as an adolescent?”, 3) “…as an adult?”" Yet again (see here) a research priority needs to be the formulation of a valid and reliable questionnaire pertinent to 'measuring' masking/camouflaging with autism in mind. And finally there was the use of an old favourite  - the autism spectrum quotient (AQ) - by the authors, but with some added caveats...

Results:  "We found high rates of RMs in both diagnosed and self-identifying participants, and a striking prevalence of camouflaging" was one of the headlines. But... there were also some other important details observed too. So: "Higher scores in the diagnosed group were found for object fidgeting, repetitive hand movements, rocking, object spinning and hand flapping." I think most people would agree that such behaviours represent some of the more 'classical' manifestations included in the RM categorisation of autism. By contrast, other RMs such as scratching/rubbing skin, walking in circles and 'banging head' were not different between the diagnosed and self-identifying groups.

Based also on the strength of the camouflaging data presented by Wiskerke et al I have to say that I'm not yet altogether convinced by the evidence presented. It's not that I don't believe that 'self-inhibition' plays a role in such masking, nor that: "There were many references (47 participants) to having been bullied or disciplined for childhood RMs." It's just that methodologically speaking, offering up one question on such a complicated issue does not make for a scientifically compelling argument. As I previously said, autism science needs to invest in some high quality research on how to assess masking in the context of autism; perhaps including some important measure of self-monitoring for example. And one also needs to control for things like intellectual ability too and perhaps be open to other reasons why the presentation of autism between the genders/sexes might be subtly different.

I was also a little dismayed that the discussion of results by the authors did not seem to fully 'tally' with their findings. So: "The striking similarities between diagnosed and undiagnosed participants are consistent with a clinically relevant prevalence of autism in the undiagnosed group." As I've mentioned, the picture of 'striking similarities' was far from consistent when comparing RMs across the groups and those statistically significant differences reported on between diagnosed and self-identifying autism. Added to the fact that authors zoomed in on RMs without too much clinical focus on the other elements to autism, and the 'clinically relevant' picture is also far from complete based on this study alone. Indeed, other text in the discussion provide further clues as to the probable inclination of the authors: "We believe that this study in part reached the “lost generation” of autistic adults... many of whom appear to have turned to social media for support and kinship, sometimes after many disappointing encounters with clinicians and scientists." Emotive language such as 'Lost generation' really shouldn't be in a science paper without [strong] corresponding evidence.

What else? Well the authors did acknowledge some shortcomings in their study: "the on line format limited our ability to ascertain that robust diagnostic procedures had been used in all cases" and: "The self-report format also makes it possible that some participants erroneously reported an official diagnosis" (erroneously?) but perhaps more is needed to be said about participants ("the vast majority were indeed very cognitively able") and onward the applicability of results to other parts of the autism spectrum. It would also have been useful to include a few other (self-report) measures of other conditions/labels where autistic characteristics overlap, just to see...

I do think Wiskerke et al have tapped into a increasingly important research 'need' for some of those on the autism spectrum - masking - and how such behaviour does seem to impact on quality of life for quite a few people. We need a lot more research on this topic, and yes, there also needs to be some further analysis of what social accommodations could be made too, bearing in mind such understanding needs to come from lots of different quarters of society (see here). I'd also like to acknowledge the fact that one of the authors on the Wiskerke took the time to converse (on Twitter) with me about their paper, which was rather encouraging.

But still, I can't shake the idea that the methodological shortcomings of this study and the sweeping interpretations imply caution before any generalisations are made as a result. The fact also remains that self-identifying as being autistic/having autism is not the same as receiving a formal diagnosis of autism, however much people might want this to be true or find 'kinship' with the autism spectrum...


[1] Wiskerke J. et al. Camouflaging of repetitive movements in autistic female and transgender adults. bioRxiv. 2018. Sept 10.

[2] Mandy W. et al. Sex differences in autism spectrum disorder: evidence from a large sample of children and adolescents. J Autism Dev Disord. 2012 Jul;42(7):1304-13.

[3] Kupferstein H. Evidence of increased PTSD symptoms in autistics exposed to applied behavior analysis. Advances in Autism. 2018; 4: 19-29.