Why the words "every one of us hovers somewhere along the autistic spectrum" are so dangerous

The Guardian, Friday 26th April 2019

Today I offer another post based on a newspaper report, as Greta Thunberg and her autism diagnosis continue to generate debate (see here).

This time around the report (letter) in question (see here) titled "Autism and Asperger’s are useless diagnostic labels" is the focus, and, in my opinion, quite a dangerous quote included in the text: "... every one of us hovers somewhere along the autistic spectrum."

Why is it so dangerous to imply that the general population is just a (hovering) footstep away from autism spectrum you might ask? Well, I don't think anyone would disagree with the idea that the behaviours noted in autism aren't something that's just magically present in those diagnosed. Such behaviours can be seen in various other states or conditions and/or across various different times of life and maturation. The thing that makes the presentation of such behaviours so distinct and worthy of a diagnosis of autism is the frequency and intensity of such behaviours and importantly, the way they significantly impinge on functioning and daily life. In that respect, yes, autistic behaviours are part of the complex and intricate tapestry of life. But the (sustained) frequency and impact of such behaviours distinguish autism from not-autism.

In such a context then, the idea that everyone hovers along the autism spectrum is a misnomer. It conflates the 'autistic behaviours are part of the complex and intricate tapestry of life' idea with the important reasons why an autism diagnosis is given. This is dangerous because it has the potential to belittle a diagnosis of autism and what it means to those in receipt of such a diagnosis; often a diagnosis that as taken months/years to finally receive. Indeed some people have suggested that the claim that 'everyone is on the autism spectrum' is an "absolute sin"...

It's also dangerous because such thinking opens the door to other things like the self-diagnosis of autism. I've talked about self-diagnosis quite a bit on this blog (see here and see here) and how, self-realisation is often an important (nay, crucial) step to getting an autism diagnosis for many. When however such self-realisation turns to self-identification and/or self-diagnosis on the basis of various 'are you autistic?' screens available on the Internet and beyond (see here), the side-stepping of formal assessments can lead to problems. Problems that can include potentially missing important conditions/states that seemingly overlap with autism or the presentation of autistic traits (see here and see here) as well as also skewing some important narratives from those who have been formally diagnosed with an autism spectrum disorder and their experiences.

I know some people disagree with such a position. Some people think that the diagnostic criteria for autism are too stringent, too medically focused, or access to formal assessment/diagnostic services is too restricted and costly. I don't disagree that we need to do more to 'fill a gap' and ensure that those who might fulfil the diagnostic criteria (including the "significantly impinge on functioning and daily life" bit) should have access to the relevant professional assessment services. But that doesn't mean that anyone and everyone can or should just publicly label themselves as autistic in the meantime.

And finally, as we're learning from the evolution of the neurodiversity movement, autism is still very much to be seen as a disability (see here). So another possible implication of the "every one of us hovers somewhere along the autistic spectrum" sentiment is that we are all somehow 'disabled' by our hovering along the autism spectrum. This is frankly a ridiculous suggestion and, continuing the theme of how dangerous such a sentiment is, could have some really serious consequences for the provision of resources and services for those who are genuinely disabled by facets of their autism. Words matter.

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"Gaps in current autism research". What the great and good think...

I would encourage readers to have a good look through the commentary paper by David Amaral and many, many colleagues [1] discussing the important question: what's missing from current autism research?

Published in "advance of the 2019 INSAR Conference in Montreal, Quebec, Canada", the annual autism conference (see here) which starts later this week (1st May 2019), the commentary provides some details on where the gaps seem to be when it comes to autism research. Various views are provided by some of the great-and-the-good of autism research,

Lots of 'gaps' are highlighted, many of which have been discussed on this blog down the years. Things like: "the failure to take into account the heterogeneity of the autism spectrum disorder (ASD) category", the relationship between autism and mental health conditions, intervention, aetiology, "novel, efficient diagnostic processes", longitudinal research studies, early biomarkers, the use of neural stem cell research, ageing and autism, parenting and autism, self-injury and autism, autism and the criminal justice system, "Minimally verbal autistic people and those with severe autism who are overlooked across all stages of development and inquiry", "Distinguishing autism in intellectually able adults from conditions, such as bipolar disorder, personality disorders, and schizophrenia" and lots more besides are considered. All represent gaps which require much more investment and study.

The Amaral paper got me thinking what my response to such a question would be. Based on my 'for what their worth' musings down the years, I could probably suggest two primary issues that stick out: (1) autism is a label that describes symptoms/behaviours/traits but says little about how these manifest at an individual level; we need to come up with some way of expanding how we describe autism and what it actually describes as a plural condition, and (2) we need much more focus on translating research findings into real-life improvements. It's all well and good getting some fantastic research results that make big newspaper headlines, but for the child who is facing yet another school exclusion or for the adult living a life of seclusion and poverty for examples, what do such research findings do for them? This also includes translations covering detection, diagnosis, intervention, and a whole host of other things pertinent to improving quality of life of those diagnosed and their family and significant others. One particularly pressing part of this translation issue are the shocking figures on early mortality in relation to autism (see here) and the question of how they can be reversed.

The hows-and-whys of achieving such goals are a little more difficult. I do think autism research could learn quite a bit more from people like Prof. Gillberg and others who've talked for sometime about the concept of ESSENCE (Early Symptomatic Syndromes Eliciting Neurodevelopmental Clinical Examinations) (see here) and how autism rarely appears in some sort of diagnostic vacuum (see here). It could also do with listening more to lots of groups of people with a connection to autism: those who are autistic themselves, their parents and caregivers and other significant others, including siblings, and how they can help with the autism research agenda. And by listening I don't mean just attending to selected groups of people or those with the loudest voices. I mean listening to voices from across the entire autism spectrum [2], bearing in mind the oft-cited phrase: 'if you've met one autistic person, you've met one person with autism'.

Just before I leave this topic, I must also mention one thing that I don't wholeheartedly agree with that is highlighted in the Amaral paper: the notion from someone that "the genesis of autism spectrum disorder (ASD) occurs prenatally." The prenatal period is definitely important to autism; but there is ample evidence that the 'genesis' of 'some autism' is rooted long, long after the nine months that makes us (see here for example) or in some cases quite a bit before conception, pregnancy and onward (see here). In that respect, sweeping generalisations about autism - aetiology, life course, etc - are also perhaps something else that needs to be far less *seen* when it comes to the autism research agenda and the gaps that they can sometimes generate...

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[1] Amaral DG. et al. Gaps in current autism research: The thoughts of the Autism Research Editorial Board and Associate Editors. Autism Res. 2019 Apr 26.

[2] Russell G. et al. Selection bias on intellectual ability in autism research: a cross-sectional review and meta-analysis. Mol Autism. 2019 Mar 1;10:9.

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"The burden of care of mothers as caregivers of ASD children leads to suicidal ideation among them"

I appreciate that the title heading this post - "The burden of care of mothers as caregivers of ASD [autism spectrum disorder] children leads to suicidal ideation among them" - derived from the findings reported by Bushra Akram and colleagues [1] is (a) a rather sweeping generalisation, and (b) not likely to be met with great enthusiasm by some/many people. I say that on the basis that words like 'burden of care' carry significant emotional meaning, even if only trying to describe "the psychological, emotional, social and economic challenges that are experienced by a caregiver of mentally or physically ill person."

Language aside, I did want to blog about the Akram findings because they represent another uncomfortable topic that needs to be talked about and further researched in relation to autism. They bring to our attention how parenting is not always about smiles, fluffy clouds and rainbows but sometimes can be bloody difficult. More so when something like autism is part and parcel of the family unit (see here and see here). Such recognition of reality is not meant to stigmatise anyone or devalue them as a person. It merely implies that burying heads in the sand for the sake of good PR or other reasons helps no-one in the long run. Least of all children. And in that respect, there seems a change recently (see here)...

I think you've kinda got the gist of what Akram et al were looking at in their study. They managed to recruit over 300 mums of children diagnosed with an autism spectrum disorder (ASD) from various cities in Pakistan. Diagnosis was apparently 'assessed' via DSM-5 criteria (see here). We're also told that: "Single mothers or those with more than 1 child with disability were excluded." Various questionnaires were delivered to participants - "the 19-item Burden Assessment [Scale]... (BAS), 12-item Multi-Dimensional Scale of Perceived Social Support...(MSPPS) and 5-item Suicidal Ideation Attributes Scale... (SIDAS)" - pertinent to the study aims. The quality of the translation of some of the instruments into Urdu was tested on a favourite cohort, psychology students.

Results: "The relationship between burden of care and suicidal ideation was positive, but perceived social support had a negative association with burden and with suicidal ideation." What this translates into is that if mums reported that a high score when it came to 'burden of care' so their scores regarding suicide ideation also seemed to be high. Also, if mums perceived themselves to have little or less social support, so they more more likely to experience a burden of care and/or suicidal ideation. This is important if not entirely unexpected.

Of course there are other potential explanations for the findings. Depression, something that seems to have some important links to something like suicidal ideation, was not looked at in the Akram study. Given some previous independent research on depression in parents/guardians of children with autism (see here), depression can't be discounted as playing an important role in suicidal ideation in this case. Likewise, factors such as money and employment would probably play some sort of role too. There are probably a myriad of other intrinsic and external variables to consider.

But let's not over-analyse this over-and-above the actual results obtained by Akram. They really do make a case of more 'caring for the carers' investigation and action (see here). Minus any psychobabble [2] it's the small things that can make a difference. Y'know, things like offering respite to parents/guardians (see here) and ensuring that in these days of a connected world, parents/guardians of children with autism are also connected too (see here). I know it's not politically correct in some quarters to mention it, but such data also make a good case for looking at what can be done to alleviate/reduce some of the more challenging behaviours that can make parenting a child with autism more difficult. Oh, and whilst on the topic of parenting, yes, there is a place for helping parents who are struggling to manage and cope via the teaching of various strategies, but please, leave off the 'super-parenting' stuff for now (see here). Many parents are already super-parents.

And whilst on the topic of caring for the carers, it's worthwhile mentioning that where an autistic child has siblings they also require 'parenting' attention too (see here)...

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[1] Akram B. et al. Burden of care and Suicidal Ideation among Mothers of Children with Autism Spectrum Disorder: Perceived Social Support as a Moderator. J Pak Med Assoc. 2019; 69: 504.

[2] Lee GK. et al. Needs, strain, coping, and mental health among caregivers of individuals with autism spectrum disorder: A moderated mediation analysis. Autism. 2019 Mar 20:1362361319833678.

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"the first nationwide population-based study to investigate the risk of CFS in patients with IBD"

The quote titling this post - "the first nationwide population-based study to investigate the risk of CFS [chronic fatigue syndrome] in patients with IBD [inflammatory bowel disease]" - comes from the research published by Shin-Yi Tsai and colleagues [1].

Inflammatory bowel disease (IBD) covers quite a bit of diagnostic ground, but typically refers to ulcerative colitis (UC) or Crohn's disease (CD). There are many similarities between the conditions, but also some important differences too (see here). Both conditions manifest in the bowel (inflammation) and have pathological effects; both also typically show functional bowel symptoms too.

Utilising that fabulous (but sadly now defunct) research resource that was the National Health Insurance Research Database (NHIRD) in Taiwan, researchers set out to "evaluate the subsequent risk of CFS in patients with IBD" on the basis of "possible common pathophysiology between IBD and CFS" among other things. One of those 'pathophysiological' mechanisms quite prominently featuring in the Tsai article is "a similarity to the impaired intestinal mucosa of IBD." Interesting (see here).

So, from a starting population of a million people (or medical insurance records of a million people), authors whittled the figures down to the thousands in two groups: an IBD group (n=2163) and a non-IBD group (n=8652). All were "newly diagnosed" with IBD apparently; and none had a previous diagnosis of CFS "before the index date." Then: "Both groups were followed from the index date until the diagnosis of CFS, withdrawal from the NHI program, or December 31, 2011" with said CFS diagnosis following the Fukuda/CDC criteria.

Results: before heading into the CFS frequency figures according to group, there was another important observation made, potentially pertinent to a gut-brain connection: "The prevalence of depression, anxiety, [and] sleep disorder... was higher in the IBD group than in the non-IBD group." Indeed, the increased frequency of sleep disorder in the IBD group *might* have some important 'connection' with another diagnosis where sleep and 'gut issues' has been mentioned (see here and see here). And I might as well also mention depression and anxiety in that context too (see here).

Continuing: "After adjustment for age, and comorbidities, the risk of CFS was higher in the IBD group than in the non-IBD group (adjusted HR, 2.25; confidence interval [CI], 1.70–2.99)." There was also a possible sex-linked relationship too: "we identified male sex, advanced age, absence of comorbidities, and CD as the predictors of increased CFS risk." There's a pretty little diagram to accompany the Tsai findings (see here) outlining what *could* be going on with regards to IBD and CFS. Terms like 'bacterial translocation' and 'immunoinflammatory pathways' are used, in line with some other research in this area [2]. There's no mention of any psychobabble 'biopsychosocial' or the like in the Tsai paper which is always a good thing.

What else is there to say? Well authors go on to mention about the possibility of "intrinsic defects in IBD patients that precipitates CFS" which could have some quite profound implications for at least some cases of CFS. They added that future work might want to have a look at what certain immunotherapies indicated for some IBDs * might* mean for CFS and it's potential *treatment* too. We'll have to wait and see.

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[1] Tsai S-Y. et al. Increased risk of chronic fatigue syndrome in patients with inflammatory bowel disease: a population-based retrospective cohort study. Journal of Translational Medicine. 2019; 17:55.

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"If you want to support Greta Thunberg, don’t do it by defending her autism – stand up for her beliefs instead"

The quote titling this post - "If you want to support Greta Thunberg, don’t do it by defending her autism – stand up for her beliefs instead" - comes from a recent newspaper report by James Sinclair on the noble actions of the 16-year old Greta Thunberg, the current poster person for student activism.

Many people will have heard of Greta and her school strike for climate which snowballed into an international movement demanding action on global warming and climate change. She's subsequently been named as "one of the 100 most influential people of 2019" and could even be in the running for a Nobel prize later this year (2019). Not many teenagers can add those sorts of credentials to their CV...

Alongside the important message that Greta has spread, the revelation that she has a diagnosis of autism - Asperger syndrome - has not escaped media and indeed, social media attention. Her autism diagnosis (Asperger syndrome is now pretty much defunct as a clinical diagnosis) has, in many ways, been placed front-and-centre of her story, but not always in the politest of terms.

The Sinclair feature on Greta caught my eye for several different reasons. Diagnosed himself with autism, Sinclair approaches an important part of the Greta Thunberg story: how autism is not necessarily relevant to the important climate change message that is being promulgated. Indeed, some stand-out quotes from his article are worthwhile circulating widely: "This is why many including myself struggle with sharing our diagnosis with people, as once we do everything is viewed through a person’s past experiences and expectations of autism" and "It suggests that autism is still perceived as something we must all scramble to protect at a moment’s notice."

Why is this relevant? Well, potentially for lots of different reasons, some of which have kinda been picked up in a recent paper by Lily Cresswell & Eilidh Cage [1] which was blogging fodder (see here) not so long ago. The message then - albeit a message derived from a small participant number - was that autism is not necessarily the 'identity' that some would like it to be represented as. For example, as reported in the Cresswell/Cage result: "less than half of participants mentioned autism in their identity descriptions", inferring that many young people potentially see themselves and their achievements/struggles as so much more than due to the receipt of a clinical diagnosis. And one can perhaps see that the continual pressure to make autism a part of any successful narrative, whilst noble in intent, seemingly does little for either the individual and their personal accomplishments nor the masses, on the basis of the significant heterogeneity of autism and how autism for some means things like early mortality (see here) and lots and lots more besides. It perhaps should also be noted that depression has also been mentioned by Greta too: "After learning about climate change when she was 8, Greta later developed depression when she was 11, which she links partly to the issue" but this point doesn't seem to have been widely picked up on even bearing in mind that autism / autistic traits and depression have some important links (see here for example).

I appreciate that my ramblings about autism not necessarily being an identity for all nor not always relevant to a person's socio-political messages aren't likely to be received well by everyone. That's fine. I'll end however with comments from Greta herself and her views of autism and other labels "not being a gift." The caveat she makes to that point being that with appropriate adjustments, support and resources, there are things that can make life easier for those on the autism spectrum and beyond. Bearing in mind that is, the need for 'personalisation' of such supports and a move away from any 'one-size-fits-all' philosophy.

And whilst I'm on the topic of Greta Thunberg, it seems as though her autism diagnosis is now being dragged into the 'autism wars' too (see here). Yet another example of her important climate message seemingly being overshadowed...

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[1] Cresswell L. & Cage E. ‘Who Am I?’: An Exploratory Study of the Relationships Between Identity, Acculturation and Mental Health in Autistic Adolescents. J Autism Dev Disord. 2019. April 19.

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"Maternal diabetes, especially GDM, is probably a risk factor for ADHD"

It's coincidental that as I write this post about the findings reported by Lifeng Zhao and colleagues [1] talking about how "Maternal diabetes, especially GDM [gestational diabetes mellitus], is probably a risk factor for ADHD [attention-deficit hyperactivity disorder]" so the BBC news website highlights how screening for gestational diabetes here in Blighty is still a bit of a hit-and-miss affair (see here).

That news report mentions how about a quarter of those mums-to-be who are most at risk of developing pregnancy diabetes - "having a high BMI [body mass index] or being of South Asian or Black Caribbean ethnicity" - did not get screened at all. Left untreated, gestational or pregnancy diabetes can increase the risk of various adverse events including "a baby that grows larger than usual, leading to problems in labour; premature birth; pre-eclampsia and stillbirth."

The Zhao findings - a meta-analysis - continue a theme suggesting that exposure to maternal diabetes, including pregnancy diabetes, seems to increase the risk of various other developmental and behavioural diagnoses also being present in offspring. The primary source material of this blog - autism - has been talked about on various occasions as being one of those developmental/behavioural diagnoses (see here and see here). That ADHD is quite often mentioned in the diagnostic mix when it comes to autism (see here) is another point to make.

The basics of the Zhao paper: a search of the peer-reviewed science literature was undertaken revealing nine studies that fitted the inclusion criteria including "7,218,903 participants." The quality of most studies was ranked as high. The results were interesting in that researchers "did not find significant association between maternal diabetes and ADHD risk (OR: 1.20, 95% CI: 0.96–1.49)." This observation is slightly at odds with the quote titling this post, which Zhao et al put down to the "high heterogeneity" detected among the included studies and their subgroup analysis of case-control studies (n=3).

Also... when it came to looking at another type of study - a cohort study (n=6) - "the meta-analysis demonstrated that maternal diabetes increased the risk of ADHD in offspring by 40%." Further, and bearing in mind the description 'diabetes' covers quite a bit of diagnostic ground, authors zoomed in on one particular 'type of diabetes', that called gestational diabetes (GDM) and looked at any effect. This is where things got a little more interesting as their results, based on four studies, indicated that "GDM exposure increased the risk of ADHD for children by 164%" in Caucasian children. Ergo, although a little mixed, the existing research literature at the time of analysis indicated that maternal diabetes during pregnancy, particularly GDM, *might* have some important effect on risk of offspring ADHD.

I'm not going to say much more at this point in time in terms of potential mechanisms that *might* elevate the risk of ADHD in offspring exposed to pregnancy diabetes. It's likely to be pretty complicated. Given also that GDM appears more often than not alongside other conditions (see here), it's not going to be easy to tease apart what might be the more important issues. Is it inflammation? Is something to do with blood sugar or insulin? At the moment, we just don't know enough...

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[1] Zhao L. et al. The association of maternal diabetes with attention deficit and hyperactivity disorder in offspring: a meta-analysis. Neuropsychiatr Dis Treat. 2019;15:675–684.
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A role for viral infection in the aetiology of coeliac disease?

"In this longitudinal study, we found that a higher frequency of enterovirus infections was associated with increased risk of coeliac disease."

So said the findings reported by Christian Kahrs and colleagues [1] (open-access available here) based on the results of their: "Case-control study nested within Norwegian birth cohort recruited between 2001 and 2007 and followed to September 2016."

Following the screening of some 47,000 infants for the 'genetics of coeliac disease' - HLA genotype DR4-DQ8/DR3-DQ2 - over 900 children were entered on to the study. This group were followed "with repeated blood and faecal samples from the age of 3 months" for quite a few years. Just over 500 participants who quite regularly donated blood samples, were asked if they wanted a screen for coeliac disease. Two hundred and twenty of them (or their parents/guardians) said 'yes please' and the study results were drawn from this group. Twenty seven of the 220 participants with those all-important coeliac risk genes were diagnosed with the condition. Twenty five of those 27 diagnosed with coeliac disease were matched against 50 of the no coeliac disease participants; matching was done "for duration of follow-up, date of birth, and county of residence." It was then just a case of looking at all the biological data that had been accrued from those blood and fecal samples to ascertain things like (a) "the time interval when cases seroconverted for coeliac disease markers" (i.e. when the antibodies diagnostic of coeliac disease began to be present) and (b) if and when enterovirus was detected in some of the samples (stool samples) via PCR (polymerase chain reaction).

Results: as shown in the supplementary material, the mean age at first presence of coeliac disease (CD) antibodies in the CD diagnosed sample (n=25) was around 42 months (when the first positive sample was recorded). Symptoms 'debut' was around an average age of 73 months and CD diagnosis was received on average at 87 months. Enterovirus was reported in both CD (n=25) and non-CD groups (n=49). Some 20% of the stool samples from the CD group were positive for some kind of enterovirus exposure compared with 16% of controls. Slightly more enterovirus positive stool samples were observed in the CD group (median 4 positive samples per child) than the control group (median 3 positive samples per child).

As per the opening quote to this post: "Enterovirus was found in 370 (17%) of 2135 samples and was significantly more frequent in samples collected before development of coeliac disease antibodies in cases than in controls." Further: "The association was restricted to infections after introduction of gluten." In other words, there seemed to be some evidence of a possible temporal connection between enterovirus and the development of CD, suggesting that enterovirus exposure and not gluten was the more important trigger for CD.

Mechanisms? Well, there's some speculation about that in the Kahrs paper and a: "plausible explanation is that enterovirus causes impaired barrier function, which in turn increases the risk of coeliac disease." Enterovirus causing impaired intestinal (gut) barrier function eh? Interesting, does that mean 'leaky gut' might have a viral origin in some cases? Mmm, that could have lots of implications...

Obviously more investigation is required in this area. The Kahrs study has some strengths in terms of the sample collection protocols and frequency and potentially establishing a temporal *link* between CD and enterovirus exposure. But there's still more to do: "unmeasured confounding factors or residual confounding can never be entirely ruled out in non-randomised studies." But don't let that take anything away from the potential importance of these findings.

And on the topic of prospectively following children who might be prone to develop coeliac disease, the study findings published by Lionetti and colleagues [2] are equally interesting. In particular, based on 23 of their 26 children who received a "potential diagnosis of CD" but nonetheless "continued a gluten-containing diet... 19 (83%) became antibodies negative at 1 year from the first biopsy and remained negative up to 10 years of follow-up." Could there be a tie-up with the Kahrs findings perhaps?

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[1] Kahrs CR. et al. Enterovirus as trigger of coeliac disease: nested case-control study within prospective birth cohort. BMJ. 2019 Feb 13;364:l231.

[2] Lionetti E. et al. Long-Term Outcome of Potential Celiac Disease in Genetically at-Risk Children: The Prospective CELIPREV Cohort Study. J Clin Med. 2019 Feb 5;8(2). pii: E186.

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"less than half of participants mentioned autism in their identity descriptions"

One important point to make about the findings reported by Lily Cresswell & Eilidh Cage [1] is the participant number. It was small; including only 24 young people "recruited through mainstream secondary schools in London, UK" who were diagnosed with an autism spectrum disorder (ASD) and who were asked to participate in a study examining "the relationships between identity, acculturation and mental health in autistic adolescents." Small participant numbers means one has to be quite careful about making sweeping generalisations.

If that study aim - identity, acculturation and mental health - sounds a little bit like psychobabble to you, the long-and-short of it was to look-see whether there was a possible link between how young autistic people / people with autism see themselves ("the way a person understands and views him or herself, and is often viewed by others") and their self-reported mental health; also including the concept of 'autistic culture' into the research mix.

OK, first things first: autistic culture. From what I read, it kinda sits somewhere around the idea of 'neurodiversity' (see here) with culture defined as "a system of meanings through which people organise and make sense of their lives." The addition of the word 'autistic' to culture therefore means "building a culture around the ways of speaking, thinking, and acting that come naturally to autistic people." The authors liken autistic culture to deaf culture "with both being supportive communities focused on the distinctive issues and experiences related to being autistic or deaf." Noble intentions on both counts.

Study participants were given the Twenty Statements Task (TST) - "a measure used to assess how individuals define themselves using their own words" - and the Autism Identity Scale (AIS) which "looks at whether an individual aligns more to an autistic or non-autistic culture." Responses to these instruments and to the Strengths and Difficulties Questionnaire (SDQ) were captured and analysed.

Results: I should point out that the AIS used in this study is not exactly what one would call a 'mainstream' instrument. Indeed, the reference for it's development and use comes from a doctoral thesis which, as far as I can see, is the only reference at the present time. The authors talk about responses on the AIS being use to rank participants into one of four groups: "Marginalised (alignment to non-autistic culture)... Bicultural (alignment to both cultures)... Assimilated (alignment to neither culture)... and Separated (alignment to autistic culture)." I'm not altogether sure but I think some of those groupings and their descriptions mentioned by Cresswell/Cage might not be exactly the same as that talked about in the thesis from Jarrett (see page 20 of the thesis). The AIS by the way, purports to measure both "autistic (AIS1) and non-autistic (AIS2) acculturation."

Cresswell/Cage observed that: "Average scores on the AIS2 were higher than the AIS1, indicating autistic adolescents typically felt more aligned to non-autistic, than autistic, culture." Minus any sweeping generalisations, this meant that participants as a group were typically more inclined towards statements like "I feel that I fit in with other people who do not have autism" and "I would prefer my education to be at a school with and without people with autism" over and above "Being autistic is an important part of who I am" and "I would prefer my closest friend(s) to have autism." Again, I reiterate that no sweeping generalisations are to be made from such findings on the basis of such a small participant group. Also added to those alignment findings, researchers observed some potentially important connections to SDQ scores used as a proxy for self-reported mental health and wellbeing. Specifically that the "lowest scores [on the SDQ] were found in those who aligned themselves only non-to autistic culture (assimilated; n = 7)." This *could* be translated to mean that self-reported mental health and wellbeing was marginally better for those who identified with a specific culture and, in particular, non-autistic culture.

I kinda get the impression that the results garnered during this study weren't exactly what the authors were expecting. Indeed, as I've mentioned before on this blog, there is 'slant' towards the whole neurodiversity angle in other research from some of the authors of this study (see here and see here) which would have probably benefited from different results being observed on this most recent research occasion. Credit is therefore due to the authors for publishing their findings. The inclusion of phrases such as: "These findings suggest autistic adolescents should be encouraged to explore autistic culture and supported in constructing their identity" included in the paper poses a bit of a quandary because that's not entirely what the resultant data implied. I've seen similar things particularly where neurodiversity has been mentioned in the context of autism before (see here). Indeed when we are also told that "less than half of participants mentioned autism in their identity descriptions", one interpretation is that many participants see/saw themselves as so much more than the sum of a clinical diagnosis they've received at some point. I daresay others will have alternative explanations for such findings.

More study is required on this topic. More study around the issue of 'belonging' in the context of autism, and the potential 'positives' that belonging brings (see here), is something that stands out from the Cresswell/Cage findings. Insofar as the concept of autistic culture, well, we'll have to see. Much like the term 'autistic community' (see here) used on more than one occasion, the inference is that there's some universal 'one-size-fits-all' ethos that everyone on the autism spectrum should be adhering too. The reality however, is some much more varied and complicated, bearing in mind the oft-used phrase: if you've met one autistic person, you've met one person with autism (or words to that effect). Yes, people should be proud of themselves. Everyone should have a sense of self-worth, achievement and that word again, belonging. But as per the small scale results from Cresswell/Cage, that pride and identity does not necessarily have to mean aligning oneself according to the receipt of a clinical diagnosis...

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[1] Cresswell L. & Cage E. ‘Who Am I?’: An Exploratory Study of the Relationships Between Identity, Acculturation and Mental Health in Autistic Adolescents. J Autism Dev Disord. 2019. April 19.

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Saffron for ADHD?

I'm very partial to a bit of 'left field' research on this blog. By 'left field' I mean research that is slightly unusual or atypical. I'd place the study findings by Sara Baziar and colleagues [1] in that 'left field' category because they reported results - randomised double-blind study results - suggesting that: "Short-term therapy with saffron capsule showed the same efficacy compared with methylphenidate" when it came to managing some of the symptoms of attention-deficit hyperactivity disorder (ADHD).

Saffron a.k.a Crocus sativus L is a herb commonly cultivated in places like India and Greece. As with many herbs/spices, cooking represents but one potential use of saffron. It contains a myriad of different chemical compounds, some of which seem to have a variety of potential medicinal uses. Real pharmacognosy in action.

The starting point for the Baziar study was that although methlyphenidate (ritalin) is indicated for treating / managing many cases of ADHD, not everyone is suited to such a medicine or the side-effects that it can sometimes produce. So "alternative medication, like herbal medicine, should be considered." Enter then saffron, and some evidence that it might be a useful herb for various psychiatric complaints [2], to be pitted against methylphenidate in a sort of scientific head-to-head contest with ADHD symptoms in mind.

For 6 weeks, fifty or so children and young adults with "a Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) diagnosis of ADHD" were randomly allocated to receive methylphenidate (MPH) "20-30 mg/d (20 mg/d for <30 kg and 30 mg/d for >30 kg)" or saffron capsules "20-30 mg/d saffron capsules depending on weight (20 mg/d for <30 kg and 30 mg/d for >30 kg)." At baseline, 3 weeks and 6 weeks researchers measured ADHD-related symptoms.

The results were unsurprisingly surprising. By that, I mean that there were no statistically significant differences between the two groups, bearing in mind the clinical effectiveness profile that methylphenidate use for ADHD has already established (see here). So: "General linear model repeated measures showed no significant difference between the two groups on Parent and Teacher Rating Scale scores." Importantly too we are told that: "The frequency of adverse effects was similar between saffron and MPH groups."

The Baziar results don't immediately open the floodgates to saffron being used to 'manage ADHD' instead of a clinically-proven molecule like methylphenidate. It doesn't work like that. As far as I can see this seems to be the first time that saffron has been put under the scientific spotlight with ADHD mind (taking into account other 'herbal medicines' have been explored with ADHD in mind). We therefore need more data and some all-important replication. We need more data comparing saffron against methylphenidate and other intervention options for ADHD. And we also need more data on why? Why might saffron be a useful therapeutic option for some ADHD? What are the pertinent biological mechanisms at work?

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[1] Baziar S. et al. Crocus sativus L. Versus Methylphenidate in Treatment of Children with Attention-Deficit/Hyperactivity Disorder: A Randomized, Double-Blind Pilot Study. J Child Adolesc Psychopharmacol. 2019 Feb 11.

[2] Shafiee M. et al. Saffron in the treatment of depression, anxiety and other mental disorders: Current evidence and potential mechanisms of action. J Affect Disord. 2018 Feb;227:330-337.

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Autistic traits in schizophrenia: meta-analysed

"Current findings support that individuals with schizophrenia spectrum disorders have higher autistic symptoms than healthy controls."

So said the meta-analysis findings reported by Franco De Crescenzo and colleagues [1] and their study which "systematically reviews and quantitatively synthetizes the current evidence on the presence of autistic symptoms in individuals with schizophrenia spectrum disorders." I might quibble (again) with the use of the term 'healthy controls' but the findings reiterate something quite important: autistic signs and symptoms are not necessarily exclusively linked to a diagnosis of autism (see here and see here).

The De Crescenzo paper represents a 'let's boil down the existing peer-reviewed science literature into a coherent statement' kinda study; as 13 studies including nearly 2000 participants were included for review and meta-analysis. The primary outcome "was the Autism Spectrum Quotient (AQ)" and its use on those diagnosed with schizophrenia or schizophrenia spectrum disorder (SSD) vs. those with autism or vs. those asymptomatic controls as a total score or scores on the various sub-domains. The results went something along the lines of "individuals with SSDs have significantly higher autistic symptoms than healthy controls and lower autistic symptoms than individuals with autism." That finding followed for the total AQ score and most of the sub-domain scores.

What else is there to say? Well, the De Crescenzo results relied on the AQ for their measurement of autistic signs and symptoms. I've mentioned more than once on this blog how the AQ might show an important connection to autism but is not necessarily the premier (exclusive) autism screener (see here and see here). Applying such logic to the current meta-analysis findings and one has to be a little bit careful about what is being measured by such a scale and whether such overlap is there on the basis of just autistic signs and symptoms.

That all being said I have talked about overlap between scores on the AQ in autism and schizophrenia before on this blog (see here) and the notion of potential 'fuzzy boundaries' between the two labels. Indeed, it makes you wonder whether science and clinical practice were too quick to dismiss the important findings from Mildred Creak and colleagues [2] and the seeming desire to move autism as far away from schizophrenia as possible...

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[1] De Crescenzo F. et al. Autistic Symptoms in Schizophrenia Spectrum Disorders: A Systematic Review and Meta-Analysis. Front Psychiatry. 2019;10:78.

[2] Evans B. How autism became autism: The radical transformation of a central concept of child development in Britain. Hist Human Sci. 2013;26(3):3-31.

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Post-Exertional Malaise (PEM) in ME/CFS: what do patients say about it?

"The findings of this survey suggest that there are key domains of this symptom, including triggers, symptom onset, and duration, which have often not been comprehensively assessed in a previous PEM [post-exertional malaise] instrument."

So said the findings reported by Carly Holtzman and colleagues [1] (open-access available here) examining (yet again and yet again) an important part of the clinical profile of the conditions known as myalgic encephalomyelitis (ME) / chronic fatigue syndrome (CFS): post-exertional malaise or PEM.

Although still the source of some debate (see here), PEM basically refers to "a worsening of ME/CFS symptoms after minimal physical or mental exertion." Some authors have used other words to describe PEM - "payback" is one of them - but the sentiments remain the same: a physiological (and psychological) 'cost' following exertion. And said exertion does not necessarily have to be over-exertion either.

In light of the 'confusion' around PEM, Holtzman et al decided on a rather sensible course of action: "to try to develop a comprehensive measure [of PEM] with active collaboration of the patient community." This follows other independent research that has reaped the rewards of asking patients suffering with ME/CFS (yes, suffering) about their experience of their illness (see here for example). To do this, one of the rather famous authors on the Holtzman paper - Leonard Jason - started some conversations with various other patients who were unhappy with some of the descriptions of PEM that were being bounced around. Joined by Holtzman, things took off with regards to a questionnaire that was developed with PEM in mind [2] as we are told that: "comments and items received helped shape each new revision of the questionnaire."

"A survey was ultimately developed and was subsequently completed by 1534 members of the patient community."

Findings? Well, first and foremost "94.4% reported being diagnosed by a medical doctor." Nearly three-quarters of participants reported 'symptom exacerbation' immediately following exertion. Nine out of ten participants "had experienced delayed onset after exertion." As to the triggers of PEM, well, "basic activities of daily living" was a big one, as was "emotional events (88.3%), noise (85.5%), and sensory overload (83.6%)." What sorts of symptoms were experienced? So: "reduced stamina and/or functional capacity (99.4%), physical fatigue (98.9%), cognitive exhaustion (97.4%), problems thinking (97.4%), unrefreshing sleep (95.0%), muscle pain (87.9%), insomnia (87.3%), muscle weakness/instability (87.3%), temperature dysregulation (86.9%), and flu-like symptoms (86.6%)." Quite a few. How long did PEM last for? An average of 3-6 days (that's days) and in some cases, an awful lot longer. Also: "67.1% of the sample had experienced a “crash” that never resolved." Most participants who answered the survey also felt that it pretty well reflected their experience of PEM.

There's quite a bit more to do in this area in terms of developing said questionnaire and hopefully putting more flesh on the descriptive bones of PEM. I'm also inclined to suggest that as well as describing PEM and how it is experienced by those diagnosed with ME/CFS, science needs to do a lot more on the biology of PEM and what could potentially help (yet again, minus the psychobabble). Still, 'asking patients' continues to be an important theme in ME/CFS research...

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[1] Holtzman CS. et al. Assessment of Post-Exertional Malaise (PEM) in Patients with Myalgic Encephalomyelitis (ME) and Chronic Fatigue Syndrome (CFS): A Patient-Driven Survey. Diagnostics (Basel). 2019 Mar 2;9(1). pii: E26.

[2] Jason LA. et al. The development of an instrument to assess post-exertional malaise in patients with myalgic encephalomyelitis and chronic fatigue syndrome. J Health Psychol. 2018 Oct 24:1359105318805819.

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Early Autism and Developmental Disabilities Monitoring says autism prevalence is still rising...

"The overall ASD [autism spectrum disorder] prevalence was 13.4 per 1,000 children aged 4 years in 2010, 15.3 in 2012, and 17.0 in 2014 for Early ADDM [Autism and Developmental Disabilities Monitoring] sites with data for the specific years."

So said the surveillance summary published by Deborah Christensen and colleagues [1]. Those of you who follow the US ADDM initiative (see here) will already know about the aims of this "group of programs funded by the CDC" looking at the (estimated) autism numbers, changes to the numbers and the impact of the numbers on various communities. Through initiatives like the ADDM, we already know that the estimated prevalence of autism in 8-year olds living in the United States is round about 1 in 59 (see here) and that the estimate continues to grow for pretty much every surveillance year examined. We are also starting to find out about how the change to DSM-5 from DSM-IV is likely to/not to impact on future figures (see here). And hopefully, at some point, we might have some further data on what happens to autism past childhood (see here) from such an initiative.

The Christensen paper adds another tier to the knowledge being acquired as per their analysis of the (estimated) prevalence rate of autism in 4 year olds "whose parents or guardians lived within designated sites." Those sites were: Arizona, Colorado, Missouri, New Jersey, North Carolina, Utah, and Wisconsin. The Early ADDM initiative does not cover the same area as its big brother/sister ADDM but "is conducted in two phases using the same methods and project staff members as the ADDM Network." Those phases include first "reviewing and abstracting data from children’s records, including comprehensive evaluations performed by community professionals" and then a second phase involving "a review of the abstracted evaluations by trained clinicians using a standardized case definition and method." DSM-IV criteria covers most of the time points examined but: "For 2014 only, prevalence estimates based on surveillance case definitions according to DSM-IV-TR and the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) were compared."

Results: as per the opening sentence of this post, the overall (estimated) autism prevalence across all sites for autism in 4 year olds was on the increase between 2010 and 2014. That's not to say that there weren't differences between the various sites - New Jersey, a favourite autism prevalence site (see here) showed the highest prevalence: 19.7, 22.1, and 28.4 per 1,000 for 2010, 2012 and 2014 respectively - but overall the prevalence rate was increasing not decreasing.

There were a number of other important points raised in the Christensen findings. So: "Among four sites with ≥60% data on cognitive test scores (Arizona, New Jersey, North Carolina, and Utah), the frequency of co-occurring intellectual disabilities was significantly higher among children aged 4 years than among those aged 8 years for each site in each surveillance year except Arizona in 2010." I don't think I need to say much more about that. Also: "The overall prevalence estimate using a DSM-IV-TR case definition was approximately 20% higher than the prevalence estimate based on DSM-5 criteria." Again, I don't think too much more discussion is needed on this point aside from saying that for 4-year olds, the switch to DSM-5 might have made more of a difference than for 8-year olds. Indeed in comparison to the Wiggins data [2] based on 8-year olds where "46.0% children met both DSM-IV-TR and DSM-5 surveillance status, 44.0% met neither the DSM-IV-TR nor DSM-5 surveillance status, 4.0% met DSM-IV-TR status, but not DSM-5 status, and 6.0% met DSM-5 status, but not DSM-IV-TR status of ASD" the Christensen data showed something a little different: "Among 1,237 children who met the surveillance case definition for either DSM-IV-TR or DSM-5, 974 (78.7%) met both case definitions, 234 (18.9%) met the DSM-IV-TR but not the DSM-5 case definition, and 29 (2.3%) met the DSM-5 but not the DSM-IV-TR case definition." Perhaps more study is required on the diagnostic changes?

What's more to say? Well, one of the authors - Walter Zahorodny - kinda said it all in a media comment: "There’s no letup. I really don’t understand why the rate is going up in this way." So maybe the next question, a question that really should have been examined a long, long time ago, needs to be 'Why?' rather than just a continual chain of studies saying autism prevalence is increasing...

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[1] Christensen DL. et al. Prevalence and Characteristics of Autism Spectrum Disorder Among Children Aged 4 Years - Early Autism and Developmental Disabilities Monitoring Network, Seven Sites, United States, 2010, 2012, and 2014. MMWR Surveill Summ. 2019 Apr 12;68(2):1-19.

[2] Wiggins L. et al. Comparison of autism spectrum disorder surveillance status based on two different diagnostic schemes: Findings from the Metropolitan Atlanta Developmental Disabilities Surveillance Program, 2012. PLoS ONE. 2018; 13(11): e0208079.

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A poo(p) transplant for [some] autism? 2 years on with caveats...

The results published by Dae-Wook Kang and colleagues [1] provide some important follow-up work to a study already discussed on this blog (see here) which suggested that: "MTT is safe and well-tolerated in children with ASD ages 7–16 years" and also "led to significant improvements in both GI- and ASD [autism spectrum disorder] -related symptoms" [2]. MTT by the way, refers to Microbiota Transfer Therapy, or in other words a poo(p) transplant. A press release accompanying the recent Kang paper is also available (see here).

The original Kang study included quite a bit more than just a poo(p) transplant as per their use of a 4-stage protocol: "(1) oral vancomycin, (2) MoviPrep, (3) SHGM [Standardized Human Gut Microbiota], and (4) Prilosec" with 18 participants diagnosed with an autism spectrum disorder (ASD). The results on that last occasion were promising insofar as (a) adverse effects being small and fairly limited and (b) some improvements noted in relation to behaviour and gastrointestinal (GI) symptoms. That all being said, one needs to remember that the previous study was an open trial and results were therefore preliminary.

On this latest research occasion, Kang et al followed up their 18 participants "two years after treatment was completed." The follow-up involved "the same GI and behavior tests that we employed previously" which involved the use of various parent- and professional-report questionnaires on behaviour, questionnaire analysis of GI issues and analysis of poo(p) samples: "16 out of 18 original ASD participants provided an additional fecal sample two years after the open-label trial."

Researchers reported that "most improvements in GI symptoms were maintained, and autism-related symptoms improved even more after the end of treatment." They observed something of a possible *relationship* between bowel and behavioural signs and symptoms whereby "GI relief provided by MTT may ameliorate behavioral severity in children with ASD, or vice versa, or that both may be similarly impacted by another factor" which is interesting (see here). They also noted that the bacterial composition of stools analysed at follow-up showed evidence of sustained change "including significant increases in bacterial diversity and relative abundances of Bifidobacteria and Prevotella." In short, things were still looking pretty good after 2 years.

"Despite steady and continuous improvement in behaviors over two years, we must underscore that the original clinical trial and current follow-up study are open-label trials without a control for placebo effect." The authors are frank about the limitations of their studies, and how behavioural and GI symptoms in particular can potentially be influenced by all-manner of different variables. Indeed, they noted that "12 of 18 participants made some changes to their medication, diet, or nutritional supplements" which allied to the waxing and waning of symptoms typically associated with autism (see here), means that one has to be careful about making too many sweeping statements about cause-and-effect.

But in the context that for these 18 participants, a poo(p) transplant was seemingly not associated with too many adverse side-effects and that their behavioural and GI data typically followed a course of improvement, one cannot easily discount the Kang results. The call for further research "with a placebo-control arm" made by the authors should echo throughout the autism research landscape. And with it, further focus on how gut bacterial make-up and the all-important metabolites that specific bacterial species produce seem to be something quite important to at least some autism (see here)...

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[1] Kang D-W. et al. Long-term benefit of Microbiota Transfer Therapy on autism symptoms and gut microbiota. Scientific Reports. 2019; 9: 5821.

[2] Kang D-W. et al. Microbiota Transfer Therapy alters gut ecosystem and improves gastrointestinal and autism symptoms: an open-label study. Microbiome. 2017; 5: 10.

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Psychiatric symptoms in minimally verbal kids with autism: filling a gap

The findings reported by Daniela Plesa Skwerer and colleagues [1] (open-access available here) provide the blogging fodder today. They include some important information on an under-studied group on the autism spectrum (see here) with regards to the "overall burden of psychiatric comorbidities and emotion dysregulation" in those diagnosed with an autism spectrum disorder (ASD) "who had limited verbal abilities (i.e., few to no words used spontaneously)." Such work follows the recent publication of a paper by Ginny Russell and colleagues [2] who observed that those diagnosed with autism + intellectual (learning) disability were not exactly well-represented in the peer-reviewed autism research arena.

The Plesa Skwerer paper started with the observation that various psychiatric symptoms and conditions seem to be over-represented when it comes to a diagnosis of autism (see here for example). They noted that much of the research on this topic tended look at those who could be considered to be at the 'more able end' of the autism spectrum based on skills like self-report ability. They noted that "the population most severely affected, the ~30% of individuals with ASD who remain non- or minimally verbal beyond school-age" are not particularly well-represented in such comorbidity studies. The specific words they use are the "neglected “severe end of the spectrum”."

So: "Sixty-five participants diagnosed with ASD who had limited verbal abilities" were invited to participate in their study. They were already part of a larger research initiative. When I say 'invited' what I really meant is that: "Informed consent was obtained from the parents." All were diagnosed with an autism spectrum disorder (ASD) and the group was fairly equally split between children (5-11 years old) and young adults (12-18 years old). Parents/caregivers had a big role to play in the Plesa Skwerer study as we told that they were asked to complete various questionnaires about their children, including the Child and Adolescent Symptom Inventory (CASI-5) to "examine the frequency and severity of comorbid psychiatric symptoms." Completing the CASI-5 is no mean feat as per it having "173 items, which rate behaviors as occurring never, sometimes, often and very often."

Results: "All participants met cutoff criteria for at least one CASI-5 classification, and the number of categorical classifications parents endorsed ranged from 1 to 15, with a mode and a median of 6 classifications." This is an important detail. It tells us that, based on proxy reporting, every participant, child or young adult, presented with potentially clinically significant symptoms for one or more psychiatric/behavioural disorder. Some of the most popular labels that featured were things like vocal tics, phobia and the various types of attention-deficit hyperactivity disorder (ADHD). Further: "except oppositional defiant disorder and conduct disorder, more participants showed clinically concerning severity scores than expected based on general population norms." Authors concluded that: "The overall picture to emerge from this study is that minimally verbal children and adolescents present with extremely heterogeneous profiles of co-morbid psychopathology that are not easily predicted by autism symptom severity, intellectual disability, or limitations in communication."

There are some important caveats to the Plesa Skwerer findings, not least that proxy-reporting was the method used to ascertain the presence of not of such psychiatric comorbidity. This point tells us that a lot more needs to be done to help those who are minimally-verbal to be able to communicate much more readily. Yes, it's a tall order but where there's a will, there's a way. Also, researchers admit that they "excluded those with the most severe behavior problems including aggression, self-injury or non-compliance, and therefore our findings must be viewed in the context of whom our participants represent." Personally I see this is being a pretty issue across quite a lot of research on autism. Indeed, in light of legal rulings here in the UK (see here) talking about aggression 'not being a choice for children with autism' I daresay that by excluding those who present with such issues means that many, many children and adults on the autism spectrum are under-represented in autism research as it stands.

Still, the important message from Plesa Skwerer et al stands: those with autism who are described (defined?) as minimally-verbal seem to show a similar profile of psychiatric comorbidity and a "high degree of maladaptive behavior" as that identified in other parts/regions of the autism spectrum. Screening is implied and, so as to ensure that health inequalities are minimised, access to intervention is also indicated.

Bravo to the researchers who look at the under-studied parts of the autism spectrum.

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[1] Plesa Skwerer D. et al. Prevalence and Correlates of Psychiatric Symptoms in Minimally Verbal Children and Adolescents With ASD. Front Psychiatry. 2019 Feb 18;10:43.

[2] Russell G. et al. Selection bias on intellectual ability in autism research: a cross-sectional review and meta-analysis. Molecular Autism. 2019; 10: 9.

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"Autism prevalence in China is comparable to Western prevalence" But is it really?

I was intrigued by the findings reported by Xiang Sun and colleagues [1] whose paper is the source material for the quote heading this brief post: "Autism prevalence in China is comparable to Western prevalence."

Intrigued because the idea that the prevalence of autism - in school-aged children - hovers around 1 in 100 (1%) in the Western world is still being banded around, even when data is being produced suggesting that rates are actually increasing well beyond the 1% mark in recent times (see here and see here).

Don't get me wrong, I am impressed with the Sun paper and the significant efforts and work that went into their study to look at "autism prevalence (mainstream and special schools) in Jilin City, and mainstream school autism prevalence in Jiamusi and Shenzhen cities" in China. Impressed because of the numbers involved, the 3-stage process undertaken (screening, clinical assessment, research diagnostic assessment) as part of the study and also because the data adds to a growing volume of other studies looking at autism in China (see here and see here for examples) and nearby areas (see here).

I'm not going to bore you with any more of my musings on this paper and issue. Suffice to say that the 1% statistic is old and increasingly out of touch with the current reality of autism in many, many different nations...

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[1] Sun X. et al. Autism prevalence in China is comparable to Western prevalence. Molecular Autism. 2019; 10: 7.

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DSM-IV vs DSM-5 criteria for autism continued

It's another 'DSM-5 autism' post (see here) from me today as the findings reported by W. Jason Peters & Johnny Matson [1] caught my attention on a topic that has been and remains pretty important: what happened to the rates of diagnosed autism when clinicians switched from the DSM-IV to DSM-5?

DSM-IV and DSM-5 represent versions of the Diagnostic and Statistical Manual of Mental Disorders, one of two manuals containing standardised criteria for diagnosing various behavioural and psychiatric labels. Autism is included in the DSM (and has been for a while). As with various other labels, the refinements to the diagnosis of autism that came with the introduction of the DSM-5 have the been the source of some speculation as to the potential impact on the rates of diagnosed autism.

The data produced so far have been a little bit mixed as to whether more, less or the same number of people would reach diagnostic cut-off points under DSM-5 compared with the application of the DSM-IV criteria (see here and see here) but perhaps with a slight inclination towards DSM-5 being more restrictive (also including a separate catch-all category called social (pragmatic) communication disorder (SCD) (see here)).

And so it was with the Peters/Matson findings, as we are told that: "Fewer individuals met criteria according to DSM-5" based on their cohort of infants and toddlers. The caveat? Well: "individuals with higher levels of symptoms were more likely to meet criteria for both versions [DSM-IV-TR and DSM-5] as compared to either alone" which kinda stands to reason. Indeed other papers recently published [2] pretty much said the same. The conclusion: "results suggest that there are meaningful differences in how DSM criteria may apply to individuals with an ASD [autism spectrum disorder]."

And, since I'm on the topic of what the DSM-5 did or did not do to autism diagnoses, a timely systematic review and meta-analysis from Kulage and colleagues [3] also adds something to the conversation: "Findings suggest smaller decreases in ASD diagnoses compared to earlier reviews."

End of line.

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[1] Peters WJ. & Matson JL. Comparing Rates of Diagnosis Using DSM-IV-TR Versus DSM-5 Criteria for Autism Spectrum Disorder. J Autism Dev Disord. 2019. Feb 27.

[2] Wiggins LD. et al. DSM-5 criteria for autism spectrum disorder maximizes diagnostic sensitivity and specificity in preschool children. Soc Psychiatry Psychiatr Epidemiol. 2019 Mar 8.

[3] Kulage KM. et al. How has DSM-5 Affected Autism Diagnosis? A 5-Year Follow-Up Systematic Literature Review and Meta-analysis. J Autism Dev Disord. 2019 Mar 9.

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(Subclinical) mania symptoms in kids with autism

Although published a few years ago, PubMed recently brought the paper by Yu Okada and colleagues [1] to my attention and the finding that: "school-aged ASD [autism spectrum disorder] children frequently present subclinical BP [bipolar disorder] symptoms."

As per the authors' idea that "there has been increasing interest in bipolar disorder (BP) in children" and specifically that bipolar disorder might be important to at least some autism (see here and see here), a study idea emerged. That idea merged into a hypothesis: "to identify [the] reliable prevalence of BP and to evaluate a variety of subclinical BP symptoms in children with ASD."

Okada report case-control study results based on "110 referred children aged 6-15 years: 46 with ASD (the case group), 64 without ASD (the control group)" who were first time outpatients at a clinic in Osaka in Japan. As well as the use of a quite comprehensive "diagnostic approach for ASD", researchers also measured various types of cognitive functioning, also looking for the possible presence of the signs and symptoms of a diagnosis of bipolar disorder (via something called the K-SADS-PL-J). Results were collated.

"None of the children were diagnosed with BP in the case [autism] group, although two children were diagnosed with BP in the control group." Various other diagnoses were also recorded in the control (not-autism) group including anxiety disorder (n=28) and depressive disorder (n=16). When however researchers looked at subclinical mania symptoms - "elation/expansive mood, increased goal-directed activity, racing thoughts" - there was something to see for the autism group: "Based on the subclinical BP symptoms, the prevalence of elation/expansive mood and racing thoughts was significantly higher in the case group than in the control group: 26.1% versus 3.1% (p<.001) and 32.6% versus 9.4% (p=0.002), respectively."

There are a couple of ways to take the Okada findings. You could say that bipolar disorder in children with autism, with an average age of about 12 years, is low to non-existent. That's a good thing. But you could also argue that the increased frequency of subclinical mania symptoms noted in those with autism compared to not-autism controls might not be such a good thing. Indeed it could foretell a future greater risk of bipolar disorder in that group or even more pronounced mania in times to come (see here). With specific regard to the possible future diagnosis of bipolar disorder, I'm thinking specifically of the word 'prodrome' to mean early signs and symptoms indicating the onset of future 'disease' (psychopathology). I'll leave you to make the decision as to which option is more important but perhaps further investigation [2] may be indicated...

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[1] Okada Y. et al. Subclinical Manic Symptoms in Children with Autism Spectrum Disorder. Osaka City Med J. 2016 Dec;62(2):103-110.

[2] Van Meter A. et al. Bipolar Prodrome Symptom Scale - Abbreviated Screen for Patients: Description and validation. J Affect Disord. 2019 Feb 12;249:357-365.

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