The positives of ADHD?

I tread carefully with my discussions of the paper by Jane Ann Sedgwick and colleagues [1] talking about "insights into positive human qualities, attributes or aspects of ADHD [attention-deficit hyperactivity disorder] that can support and sustain high functioning and flourishing in ADHD life." Carefully because, just like discussions over another label closely associated with this blog, there are a myriad of different views and opinions about the way neurodevelopmental disorders / conditions / labels are presented and viewed by those who have been diagnosed with them. Who am I to tell someone what they should or shouldn't be thinking?

Sedgwick et al started from the idea that although 'disorder' is a defining part of ADHD, the subsequent focus on 'deficit' does not perhaps do justice to all that is included under the diagnostic term. They reference 'positive psychology' and its moves "away from a deficit-focused view of mental health, towards approaches that were more enabling, strength-based and emphasised positive aspects of human functioning and flourishing (i.e. positive emotions, engagement, relationships, meaning and accomplishment)." They then move to the aim of their study: "to explore ability and disability in ADHD from the participants own perspective using the WHO International Classification of Functioning, Disability and Health (ICF) framework." Mention of the WHO ICF framework also brings me back to similar discussions with autism in mind (see here).

"We recruited six successful (i.e. HF[high-functioning]-ADHD and flourishing) adult males aged between 30 and 65 years from an NHS tertiary service in London." Said participants were interviewed with questions such as: "(1) What do you think are the advantages and disadvantages of having ADHD? (2) Please describe a time when you felt that your ADHD helped to achieve something? (3) What aspects of your ADHD would you miss if it went away?" Following some content analysis of results, certain themes emerged.

"The main findings of this study are characterised by six core themes (cognitive dynamism, courage, energy, humanity, resilience and transcendence)." Alongside, a number of sub-themes were also reported including "divergent thinking, hyper-focus, nonconformist, adventurousness, self-acceptance and sublimation." Researchers concluded that because these themes and sub-themes were not listed as "sanities in positive psychology" (i.e. "relevant to people in general, with or without ADHD") they *might* be specifically linked to ADHD.

OK, a few steps back. You'll no doubt recognise that this was research based on interviewing six men with ADHD (and 'flourishing' with their ADHD at that). It's not difficult to see how the issue of 'representativeness' might be a particular problem with the Sedgwick results. If for example, they had presented data from their six participants compared with another six who perhaps weren't described as 'flourishing' (see here for one possible example), I'd be a lot more confident in their findings. Better than that would have also been the views of a few other participants representing other labels where ADHD is part-and-parcel of a more complicated clinical picture (see here and see here for examples). And don't forget their focus on one gender/sex too...

I can see how something like 'cognitive dynamism' conceptualising "ceaseless mental activity" could be seen as a double-edged sword when it comes to ADHD. Yes, it can be utterly disabling for some (many) in terms of being "scattered, chaotic and a bit random." But in some scenarios and with the right environment and encouragement, such an issue could be a lot more positive a trait to have. Likewise the concept of 'energy' whilst quite synonymous with ADHD, probably also has an upside as well as a downside, particularly when harnessed to the benefit of the person concerned and their strengths.

But... I have some difficulty with the ideas that courage, humanity and resilience for example, are somehow to be viewed as 'the positive side of ADHD'. There are plenty of people out there who demonstrate such strengths without a diagnosis of ADHD or indeed, a diagnosis of anything. The fact that Freud and Nietzsche are also referenced in relation to some of those terms suggests to me that the authors have perhaps moved slightly outside of the evidence-based arena in some of their interpretations of their findings. Similarly, the use of the term 'divergent thinking' isn't exactly what I would call science-based either, as my 'neurotypical' brow starts to furrow (see here).

I appreciate what the authors have tried to do with this paper: reaching out "to people with lived experience of ADHD: service users, patients, family members, carers, partners, to say that not all symptoms of ADHD are maleficent." It's admirable that such thinking is there, particularly when a diagnosis of ADHD can seem such a daunting prospect both in the short- and long-term (see here). I'm slightly concerned however that this paper seems to be insinuating that a clinical diagnosis of something like ADHD should be used as a framework to 'psychologise' someones life. The inference being that because ADHD undoubtedly affects many aspects of a person's life, it is something that defines them and all their behaviour(s) and attitude(s) on many aspects of life. I've seen it before in other labels too as diagnosis morphs into identity.

Personally, I don't think anyone should be defined by their clinical or related label in the same way that sex/gender, skin colour, religion or politics shouldn't define a person. It's OK to say yep, I have ADHD and it affects my life in this way or that way, and this is what I need to help overcome such issues. But I'm not convinced that adopting an 'ADHD identity' and seeing all the positives and negatives of life as part of that diagnostic identity is particularly good for anyone. A person is defined by their actions not their [diagnostic] label...

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[1] Sedgwick JA. et al. The positive aspects of attention deficit hyperactivity disorder: a qualitative investigation of successful adults with ADHD. ADHD Attention Deficit and Hyperactivity Disorders. 2018. Oct 29.

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"Vitamin D and omega-3 reduced irritability symptoms in children with ASD"

The title heading this post - "Vitamin D and omega-3 reduced irritability symptoms in children with ASD [autism spectrum disorder]" - comes from the findings reported by Hajar Mazahery and colleagues [1] discussing the results of their clinical trial. I have already mentioned the Mazahery trial before on this blog (see here) as a 'study to watch' based on the publication of their study protocol [2]. It looks like the wait is finally over...

So, as researchers previously reported, there were four arms to this clinical trial: supplementation with vitamin D alone ("2000 IU/day, VID"), supplementation with an omega-3 fatty acid ("722 mg/day DHA, OM"), vitamin D plus fatty acid supplementation together ("2000 IU/day vitamin D + 722 mg/day DHA, VIDOM") and a placebo group (olive oil). Results are reported for over 70 children diagnosed with an autism spectrum disorder (ASD) - "VID = 19, OM = 23, VIDOM = 15, placebo = 16" - over a 12-month period, with the primary outcome being "the Aberrant Behaviour Checklist (ABC) domains of irritability and hyperactivity."

Aside from the main finding - "vitamin D and omega-3 LCPUFA [long chain polyunsaturated fatty acid] reduced irritability symptoms in children with ASD" (compared against placebo) - a few other observations are noteworthy: "Compared to placebo, children on VID [vitamin D] also had greater reduction in hyperactivity." All this bearing in mind that the biological testing to examine for vitamin D and fatty levels reported "a good compliance rate" indicating that supplements were routinely being taken as required by the study.

Implications? Well, strike up more peer-reviewed evidence that nutrition is important not just for physiological health but also for psychological/behavioural health and wellbeing too (see here). Add this research also to other peer-reviewed science that suggests that at least 'some autism' might be particularly 'sensitive' to elements of such nutritional medicine (see here).

I could go on about how vitamin D in particular seems to be something important to autism (see here and see here for examples). I could also go on about how fatty acids have some important evidence-based history with autism in mind (see here). But do I really need to? Minus any medical or clinical advice given or intended, the Mazahery results really speak for themselves.

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[1] Mazahery H. et al. A randomised controlled trial of vitamin D and omega-3 long chain polyunsaturated fatty acids in the treatment of irritability and hyperactivity among children with Autism Spectrum Disorder. The Journal of Steroid Biochemistry and Molecular Biology. 2018. Oct 26.

[2] Mazahery H. et al. Vitamin D and omega-3 fatty acid supplements in children with autism spectrum disorder: a study protocol for a factorial randomised, double-blind, placebo-controlled trial. Trials 2016; 17:295.

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1 in 40 children with parent-reported autism in the US

Consider this post an extension of another entry published some years ago (see here) talking about the parent-reported (estimated) autism prevalence rate in the United States.

On that last blogging occasion, the paper by Stephen Blumberg and colleagues [1] was the discussion piece, and the observation that: "Based on parent reports, the prevalence of diagnosed ASD [autism spectrum disorder] in 2011–2012 was estimated to be 2.00%" or 1 in 50. That finding was based on the examination of "the 2007 and 2011–2012 National Survey of Children’s Health (NSCH), which are independent nationally representative telephone surveys of households with children."

Enter then a more recent publication from Michael Kogan and colleagues [2] who, also using data from the NSCH, this time the 2016 NSCH, extrapolated that: "Parents of an estimated 1.5 million US children aged 3 to 17 years (2.50%) reported that their child had ever received an ASD diagnosis and currently had the condition." Their calculated estimate increased from 1 in 50 children in 2011-2012 with parent-reported autism in the United States to 1 in 40 children in 2016...

Based on an Internet survey (see here), where over 50,000 responses "focused on the health and well-being of children aged 0 to 17 years" were received, researchers examined data from well over 40,000 children aged 3-17 years old. Analysing the findings from the NSCH sample with regards to affirmative answers to questions on "whether children ever received an ASD diagnosis by a care provider, current ASD status, health care use, access and challenges, and methods of treatment", they concluded that around 1 in 40 children had parent-reported autism in their cohort.

What's more to say? Well, there's always going to be the old 'they've relied on parent report' issue to contend with, despite the fact that most parents aren't 'making it up' when they talk about autism being present in their children. Indeed, the lead author of the study, Michael Kogan, when talking to the lay media about his results (see here) put it better than I ever could: "We know that in terms of having a major condition like autism, parents are usually pretty good reporters compared to medical records." Indeed.

Then, despite arguments such as "changes in the survey make it difficult to compare the findings to data from previous years" [3] and increasingly worn out soundbites like better awareness, expanded diagnostic criteria and diagnostic substitution (see here) as potentially accounting for the increase in prevalence (estimates), I do think it's about time that we started to have some real-world conversations about the figures being presented and what could be behind them. And yes, this probably means mentioning the words 'real increase' at some point (see here) and not being ashamed to say so. Bearing in mind that this is seemingly an increase that is going on around many parts of the world (see here) and seems to be driven by new diagnoses in younger cohorts and not for example, the diagnosis of 'missed adults' (see here), science and clinical practice really needs to get to the bottom of this. Not least because resources and money need to be put in place to ensure that the growing numbers of people being diagnosed are provided with the care and support they need and require over a lifetime.

I've watched a lot of 'burying heads in the sand' around the autism prevalence figures over the past few decades (see here) similar to what's been seen with various other developmental and behavioural labels (see here and see here). It's perhaps time to wake up, pull heads out of the sand and start organising more research about what is potentially driving the ever increasing autism prevalence figures...

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[1] Blumberg SJ. et al. Changes in Prevalence of Parent-reported Autism Spectrum Disorder in School-aged U.S. Children: 2007 to 2011–2012. National Health Statistics Report. 2013; 65: March 20.

[2] Kogan MD. et al. The Prevalence of Parent-Reported Autism Spectrum Disorder Among US Children. Pediatrics. 2018. Nov 26.

[3] AAP News. Study: 1 in 40 children diagnosed with autism. 2018. Nov 26.

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Project TENDR and chemical exposures part 2: organophosphate pesticides aren't great for child health

So, without striking too many chords on the old 'we've been here before' piano, consider this post an extension of some other discussions a while back suggesting that exposure to some classes of 'chemicals' might not be particularly great for child health (see here).

The findings reported by Irva Hertz-Picciotto and colleagues [1] continue the Project TENDR theme with their assertion that there is "compelling evidence" that prenatal exposure to organophosphate (OP) pesticides "is putting children at risk for cognitive and behavioral deficits and for neurodevelopmental disorders." Their observations have also been picked up by the lay media with some striking headlines like 'Ban entire pesticide class to protect children's health, experts say' complete with the required stock photo of crops being sprayed from the air.

Organophosphate (OP) compounds such as OP pesticides have a very mixed history. As well as being the insecticide of choice in many countries as a result of their excellent pest control profile, the organophosphate chemistry has also been utilised for less desirable purposes as per its classification as a component of nerve agents. Remember all the quite recent chatter about a nerve agent called Novichok? Well, the chemistry behind Novichok apparently has a very distinctive OP "structural backbone" [2]. That's not to say that every OP pesticide is Novichok. But rather that the activity of OPs specifically targeting the action of acetylcholinesterase (AChE) enzymes, important enzymes that are required for proper nerve function, is also an important biological action of various nerve agents. This in itself would suggest caution in the use of OPs.

The Hertz-Picciotto paper (policy forum) is pretty data heavy in terms of how much OP pesticides are used across the globe, the slew of mostly observational research studies that have looked at pesticide exposure and various neurodevelopmental variables and the concerns voiced at both high and low levels of OP pesticide exposure. They make a few recommendations: better training for health professionals on the potential risks attached to OP pesticide exposure, greater moves to switching to "nontoxic approaches to pest control" and perhaps most controversially: "Governments phase out chlorpyrifos and other OP pesticides."

The caveats? Well I might mention a few, minus any charges of me somehow 'standing up for OPs'. First, I don't think it's unreasonable to suggest that children in particular, do need to be more strongly protected against pesticides that are (chemically-speaking) not a million miles away from nerve agents. As the authors mention, there is quite a bit of evidence in the peer-reviewed literature to suggest a possible *association* between pesticide exposure and diagnoses such as autism (see here and see here) or beyond (see here). The thing is that like many other non-genetic environmental factors (e.g. air pollution) *linked* to a heightened risk of autism or other neurodevelopmental labels, it's more about environment + genetics when it comes to risk (see here) rather than environment just working on its own. We need for example, to know more about the ways and means that OPs are metabolised in the body and whether there could be some interesting biochemistry potentially linked to labels like autism (see here).

Second, some thought needs to go into the possible replacements if OP pesticides were to be banned outright. Thinking back to a post not-so-long-ago talking about DDT exposure and offspring autism (see here) I was struck by how short some memories are in terms of why such products were developed in the first place. I don't think anyone would seriously contemplate that the development of OP pesticides was anything more than to stop pests attacking crops and to maintain yields that can feed the population. These compounds were developed with good intentions. Obviously, as the research literature has grown, we have come to realise that such products are not side-effect free and more stringent controls have been put into place regarding safety. But to ban them outright is not something that can be done overnight. What do we replace them with? Do we just accept that crop yields will be lower and less food will be produced? Do we instead start thinking about other ways to make crops more resistant to the pests that blight them? That last question has already had its own 'issues'.

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[1] Hertz-Picciotto I. et al. Organophosphate exposures during pregnancy and child neurodevelopment: Recommendations for essential policy reforms. PLoS Med 15(10): e1002671.

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Child maltreatment and autism continued

As per other occasions when the topic of child maltreatment and autism has been discussed on this blog (see here), this is a subject that is never going to make for great dinner party conversation. It's important however that, minus any sweeping generalisations, such issues are not just swept under the research or clinical carpet...

So it is then that the paper by Christina McDonnell and colleagues [1] is offered up for discussion, and once again minus any sweeping generalisations, how a diagnosis of autism spectrum disorder (ASD) with or without accompanying intellectual (learning) disability (ID) seems to increase the risk of maltreatment compared with not-autistic, not learning disabled population controls.

McDonnell et al discuss their cross-analysis of the records held at "the Department of Social Services (DSS) and the Autism and Developmental Disabilities Monitoring (ADDM) network" in parts of the United States (US). The ADDM has appeared before on this blog as part of those very important discussions about the (estimated) prevalence rate of autism in the US alongside related matters (see here). Researchers included quite a decent sized participant number - "ASD-only (n = 316), ASD and comorbid ID (ASD+ID; n = 291), ID-only (n = 1,280), and controls (n = 3,101)" - and set to work looking at the prevalence of maltreatment based on reported and substantiated cases.

So: "Controlling for demographic factors, this study found significantly higher odds of reported and substantiated maltreatment among children with ASD-only (odds ratio = 1.86 for reported, 1.51 for substantiated), ASD+ID (odds ratio = 2.35 for reported, 1.97 for substantiated), and ID-only (odds ratio = 2.45 for reported, 2.49 for substantiated) relative to a population control group." Specific maltreatment falling into the category 'physical neglect' was notable among the groups, but various other forms of abuse were also detailed as appearing. Researchers also observed that: "Maltreatment was associated with higher likelihood of aggression, hyperactivity, and tantrums for children with ASD."

In light of other independent evidence in this area [2] I don't think anyone should be too surprised by the McDonnell findings. I don't say that in a blasé manner; maltreatment is not something that any child should have to tolerate. I merely point out that the evidence is accumulating suggesting that a diagnosis of autism or learning disability does seem to increase the risk of such an issue occurring.

On the previous blogging occasion where this topic was discussed (see here) I went through some of the possible hows-and-whys of such behaviour(s). I'm not going to repeat myself here, aside from stressing that maltreatment probably has many different 'causes' or routes towards it and the more successful ways to tackle such issues are probably going to be multi-factorial.

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[1] McDonnell CG. et al. Child maltreatment in autism spectrum disorder and intellectual disability: results from a population-based sample. J Child Psychol Psychiatry. 2018 Oct 19.

[2] Duan G. et al. Physical maltreatment of children with autism in Henan province in China: A cross-sectional study. Child Abuse Negl. 2015 Oct;48:140-7.

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Childhood ADHD and vitamin D meta-analysed again

Consider this short post about the findings reported by Evangelia Kotsi and colleagues [1] an extension of some previous discussions on the topic of vitamin D levels and attention-deficit hyperactivity disorder (ADHD) (see here and see here).

The conclusion reached by Kotsi et al - "The systematic review and meta-analysis of observational studies demonstrated an inverse association between serum 25(OH)D and young patients with ADHD" - was not entirely unexpected given the results of other independent meta-analyses [2]. They do however reiterate that in amongst the tons of research linking vitamin D deficiency / insufficiency to various labels (see here and see here for other examples), ADHD should perhaps be part of any future research strategy. Specifically, as the authors mention, the question is: "whether vitamin D-deficient infants are more likely to develop ADHD in the future?" (Perhaps.)

A couple of next research steps should also include: (a) a focus on the reason(s) for vitamin D deficiency / insufficiency in relation to ADHD (including the genetics angle) and (b) whether supplementation *might* be something that 'affects' the behavioural presentation of ADHD [3] as well as just physiological levels of the sunshine vitamin/hormone and hence should be considered an intervention? We'll see what happens.

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[1] Kotsi E. et al. Vitamin D levels in children and adolescents with attention-deficit hyperactivity disorder (ADHD): a meta-analysis. Atten Defic Hyperact Disord. 2018 Oct 26.

[2] Khoshbakht Y. et al. Vitamin D Status and Attention Deficit Hyperactivity Disorder: A Systematic Review and Meta-Analysis of Observational Studies. Adv Nutr. 2018 Jan 1;9(1):9-20.

[3] Dehbokri N. et al. Effect of vitamin D treatment in children with attention-deficit hyperactivity disorder. World J Pediatr. 2018 Nov 19.

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"A fast reduction in HERV-H activity in ADHD patients undergoing MPH therapy"

Just in case the title of this post is not readily translatable, here's a key to help. HERV-H refers to human endogenous retrovirus H. ADHD means attention-deficit hyperactivity disorder. MPH therapy refers to the therapeutic use of methylphenidate, "widely used in the treatment of attention deficit hyperactivity disorder."

Putting all these concepts together are the findings reported by Cipriani Chiara and colleagues [1] following a research trend in recent years (see here). The general idea is that those fossil viruses, that we all carry in our genome as a result of our ancestral exposure to various viruses down the ages, might not be as dormant or 'junk' as many would believe. Being 'transcriptionally active', meaning that they could code for viral proteins, such HERVs have been *associated* with quite a few conditions and labels (see here and see here for examples). ADHD has also been mentioned with HERVs in mind (see here).

The Chiara results observing a "fast reduction in HERV-H activity in ADHD patients undergoing MPH therapy" were based on the examination of HERV-H expression in peripheral blood mononuclear cells (PBMCs) from those diagnosed with ADHD (N=7) first under drug-naïve conditions (without use of MPH) and then at intervals of 1 week, 8 weeks and 24 weeks of MPH use. Results were also compared with a small cohort of not-ADHD controls (I hate the use of the term 'healthy controls' (HC) despite the fact that: "None of them had a history of neurological or psychiatric disorders, learning disability, or infectious diseases"). Researchers observed a rapidly decreasing HERV-H 'relative' expression at all intervals of MPH use in their participant group with ADHD. The concluded that: "after 24 weeks of MPH therapy, HERV-H levels were comparable to those found in PBMCs from HC."

Alongside, although quite notably not reported in the study abstract, authors also looked at some of the clinical signs and symptoms of their participants with ADHD over the course of the study. Based on the use of the "long version of the Conners’ Parents Rating Scale-Revised questionnaire (CPRS-R)" they observed a corresponding trend of a reduction in scores (indicative of improvement) specifically focused on "the Conners’ parent oppositional (CP-O), the Conners’ parent inattention (CP-I), the parent hyperactivity/impulsivity (CP-H), and the Conners’ parent ADHD-Index (CP-AI)."

Putting the two findings together, the authors conclude that methylphenidate use *might* be something important to HERV-H expression in ADHD and *could* potentially explain part of the therapeutic action of the drug on ADHD.

Obviously one has to bear in mind issues such as correlation not being the same as causation alongside the relatively small participant numbers and the lack of any comparative data (say, from other interventions being used in the context of ADHD or following the use of MPH in non-ADHD populations). But the Chiara findings are interesting, and suggest some follow-up studies could be equally enlightening...

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[1] Chiara C. et al. The Decrease in Human Endogenous Retrovirus-H Activity Runs in Parallel with Improvement in ADHD Symptoms in Patients Undergoing Methylphenidate Therapy. Int J Mol Sci. 2018 Oct 23;19(11). pii: E3286.

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"The Camouflaging Autistic Traits Questionnaire (CAT-Q)"

There are quite a few reasons why the findings from Laura Hull and colleagues [1] are to be welcomed. Their report detailing the development and validation of the The Camouflaging Autistic Traits Questionnaire (CAT-Q) covers an important area of autism research and practice that has hitherto been quite extensively discussed in lay circles but not readily quantified in scientific ones.

So: "Social camouflaging is defined as the use of strategies by autistic people to minimise the visibility of their autism during social situations." Further: "Camouflaging is driven by the desire to ‘fit in’ so as to appear non-autistic, and to form relationships with others, which may be harder to achieve when the person presents autistic behaviour." Discussions about camouflaging/masking in the context of autism have figured in some peer-reviewed research already; stretching from some worrying data on the risk of suicidality (see here) to discussions about friendship experiences (see here) to potentially hindering assessment and diagnostic outcomes (see here). The difficulty so far however, is a lack of instruments able to accurately quantify camouflaging...

Hull et al set out to develop their questionnaire to fill the gap between lay reports and science, and perhaps eventually provide some data pertinent to questions like: "Who, among the many different autistic people, camouflages their autism? Do autistic girls and women camouflage more than boys and men, and does this partly account for gender disparities in the rate and timing of diagnosis? What is the relationship between camouflaging and mental health outcomes?"

I won't bore you with psychometric details of how the CAT-Q was developed and validated. Suffice to say that it was developed from "autistic adults’ experiences of camouflaging" combined with initial testing results from several hundred people both on and off the autism spectrum. That's not to say there aren't issues to consider with for example, the use of an on-line survey or that "the self-report CAT-Q only measures individuals’ own reflections/perceptions of their camouflaging behaviours, and is thus limited in its use to those who are able to reflect on their own behaviours and provide insight to their motivations." But it does represent a good first effort to look into this important area. I'd also hat-tip the researchers for another part of their study protocol: "Those who reported being self-diagnosed were automatically excluded from the study and did not complete any further questions." I support this on the basis that self-diagnosis does not necessarily mean accurate diagnosis (see here and see here) no matter how many people would wish it to be so.

I was also interested to read about the authors' findings breaking down camouflaging into some smaller units. So: "Compensation (strategies used to actively compensate for difficulties in social situations), Masking (strategies used to hide autistic characteristics or portray a non-autistic persona), and Assimilation (strategies that reflect trying fit in with others in social situations)." Such descriptions are important insofar as putting some scientific flesh onto the bones of social camouflaging and the possible processes/motivations behind it.

What else? Well, there is a need for more investigation in this area. The authors have already highlighted some of the areas that need more study (who, males vs females, mental health outcomes). Minus any sweeping generalisations and without trying to furrow any brows, I'd also add that study on camouflaging might also be something to consider in another autism-related context: those presenting with so-called 'optimal outcome' where some people who were previously diagnosed and presented as autistic, no longer do so (see here and see here). I'm not saying this to somehow imply that all those who have experienced a 'loss of diagnosis' are somehow all camouflaging their symptoms. But it would be interesting to look-see whether this could explain a proportion of cases and indeed whether some camouflaging might not be as negative as some people might think (see here)...

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[1] Hull L. et al. Development and Validation of the Camouflaging Autistic Traits Questionnaire (CAT-Q). J Autism Dev Disord. 2018. Oct 25.

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Psychosis in depression linked to an increased risk of completed suicide

The results of the systematic review and meta-analysis published by Rossetos Gournellis and colleagues [1] provide the blogging fodder today, discussing an important topic on "whether psychotic features increase the risk of completed suicides in unipolar depression." The authors' conclusion was that yes: "The presence of psychosis in major depression should alert clinicians for the increased risk of completed suicide", something that may potentially have implications for various different 'scenarios' where psychosis (psychotic features), depression and suicide risk intersect. I'll come back to this shortly.

So, the name of the research games was systematic review and meta-analysis focused on both the peer-reviewed and 'gray' literature for studies "providing data on completed suicides in PMD [unipolar psychotic major depression] compared to non-PMD." Psychotic major depression by the way, is pretty much what the name suggests: depression or a depressive episode with the addition of psychotic symptoms such as hallucinations or delusions. Boiling down the pertinent research literature from thousands of articles to just nine articles covering "33,873 patients, among them 828 suicides", authors began their analyses.

Results: As already mentioned, the data pointed to the idea that psychosis might be an important part of suicide risk: "PMD patients manifest elevated risk of suicide even when they are compared with non-PMD patients who suffer from severe depression." Authors also concluded that: "This [suicide] risk is elevated in both the acute phase of the disorder and lifetime" and: "The data are inconclusive on the contribution of age, mood congruence, comorbidity, and suicide method on PMD’s suicide risk." The bottom line is that psychosis or the presence of symptoms of psychosis could be an important screening variable for risk of suicide in depression and also a target for intervention/prevention...

Before I go, I just want to head back to that previous sentence about these results perhaps having significance for 'different scenarios' where depression, psychosis and risk of suicide mix. I speak of course about the core topic of this blog - autism - and the on-going efforts to understand the complicated hows-and-whys of suicide risk in relation to autism (see here and see here). Acknowledging that the paths that take someone towards suicidality are often complex (see here), there is already some recognition in the peer-reviewed science domain that psychosis alongside autism might be a risk factor for suicide (see here). This, on the basis that psychosis and conditions manifesting psychosis might be 'over-represented' in relation to the autism spectrum (see here and see here) and depression is also not something unfamiliar (see here). It strikes me as eminently sensible that psychosis as well as depression could perhaps be screened more routinely as and when a diagnosis of autism is received. Both conditions/states are manageable...

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[1] Gournellis R. et al. Psychotic (delusional) depression and completed suicide: a systematic review and meta-analysis. Annals of General Psychiatry. 2018;17, 39.

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"a Brief Parent-Report Screen for Common Gastrointestinal Disorders in Autism"

I wanted to bring the findings reported by Kara Margolis and colleagues [1] to your attention today. Their observations pertinent to the "development of a brief, parent-report screen that relies minimally upon the child’s ability to report or localize pain for identifying children with ASD [autism spectrum disorder] at risk for one of three common gastrointestinal disorders (functional constipation, functional diarrhea, and gastroesophageal reflux disease)" represent something that 'fills a gap' in autism research and practice. Their authorship group including some of the great and the good looking gastrointestinal (GI) issues being over-represented in autism (see here and see here) was also an attraction to blogging about these results.

So, GI or gut problems are no stranger to autism. I don't think anyone (anymore) would seriously question such a finding given the multitude of times it has been recorded in the peer-reviewed science domain and beyond. Indeed, it's now even becoming more readily accepted that outside of functional bowel issues such as constipation and diarrhoea being over-represented in autism (see here), so other more pathological bowel states are also present for some too (see here and see here). And be in no doubt that such issues can be truly life-altering in their effects (see here and see here)...

It should also be acknowledged that when it came to starting the conversation about bowel issues and autism, it was parents and caregivers that led the way with their very astute observations of their nearest and dearest. Yes, there have always been 'professionals' who've shown an interest (and concern) in such observations, but parents and caregivers were there first. And despite many parents not (initially) being 'gastrointestinal experts', their observations, in the most part, were/are typically considered pretty accurate ones (see here).

So, Margolis et al talk about how the development of a screening instrument is the next logical step to ensure that parent reports of their children with autism potentially presenting with bowel issues are accurately recorded, onward to eventually leading to more specialised screening, evaluation and hopefully, appropriate intervention. Over 130 parents of children diagnosed with autism registered with the Autism Treatment Network (ATN) initiative agreed to take part in the study. Initially, parents were given a 35-item questionnaire looking at 3 particular functional bowel issues: "functional constipation, functional diarrhea, and gastroesophageal reflux disease" and asked to respond on behalf of their children. Gastroenterologists were also asked to evaluate the children; said professional were blinded to the parental responses to the questionnaire. When looking at these combined data sources, researchers were able to whittle down the 35-item questionnaire to 17 questions that seemed most important to the lay identification of potential bowel issues. Some further nifty statistics led authors to conclude that: "this 17-item screen identified children having one or more of these disorders with a sensitivity of 84%, specificity of 43%, and a positive predictive value of 67%." Ergo, the authors have 'the makings of' a potentially important parent/caregiver-based questionnaire to assess for the possible presence of bowel issues in autism. The makings of...

Obviously more work is required in this area. This instrument is labelled a 'screen' for such bowel issues so there is still the requirement for professional involvement when it comes to diagnosis and intervention. But one should never forget the very important perspective that parents/caregivers can have with regards to the presence of bowel issues in their children...

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[1] Margolis KG. et al. Development of a Brief Parent-Report Screen for Common Gastrointestinal Disorders in Autism Spectrum Disorder. J Autism Dev Disord. 2018. Oct 22.

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"Hypovitaminosis D is frequent and associated with depressive symptoms and anxiety disorders in schizophrenia"

The paper published by Guillaume Fond and colleagues [1] concluding that: "Hypovitaminosis D is frequent and associated with depressive symptoms and anxiety disorders in schizophrenia" provides the blogging fodder today. Hypovitaminosis D is just another way of saying vitamin D deficiency (or perhaps insufficiency) and follows a number of previous research findings (see here) concluding that schizophrenia seems to be one of a number of conditions/diagnosis/labels where tested vitamin D levels show sub-optimality.

Fond report results based on their examination of the "national FondaMental Expert Center (FACE-SZ) Cohort", something that has been talked about on this blog before (see here). So: "A comprehensive 2 daylong clinical and neuropsychological battery was administered in 140 SZ subjects included between 2015 and 2017" including vitamin D testing and analyses looking for the signs and symptoms of depression and anxiety.

Results: about one in five of the study participants were in a state of hypovitaminosis D. Looking at the accumulated behavioural data - "Depressive symptoms were assessed by the Positive and Negative Syndrome Scale depressive subscore and current anxiety disorder by the Structured Clinical Interview for Mental Disorders" - I was particularly struck by the *link* between vitamin D deficiency and 'current anxiety disorder' ("aOR = 6.18 [2.15-17.75], p = 0.001"). Further: "Vitamin D supplementation has been administered during the previous 12 months in only 8.5% of the subjects but was associated with lower depressive symptoms... and lower rate of current anxiety disorder... compared to patients with hypovitaminosis D."

These are interesting results. They reiterate that a diagnosis of schizophrenia does not seem to be protective against the development of vitamin D deficiency/insufficiency. They also highlight that schizophrenia perhaps should not be considered as a stand-alone diagnosis; something that is beginning to be realised across various different behavioural labels (see here). The suggestion of an *association* between anxiety and/or depression in the context of vitamin D is also important (perhaps even relevant to other studies that have suggested a direct link between vitamin D and schizophrenia). And then there is the 'already supplemented' finding that seems to fly in the face of quite a lot of other evidence suggesting that correcting vitamin D deficiency in the context of something like depression might not be directly applicable to improvement in depressive symptoms (see here). Research questions remain but the Fond results look interesting...

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[1] Fond G. et al. Hypovitaminosis D is associated with depression and anxiety in schizophrenia: Results from the national FACE-SZ cohort. Psychiatry Res. 2018 Sep 13;270:104-110.

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"Children are getting weaker, study finds"

The title of this post - "Children are getting weaker, study finds" - comes from one of the media headlines covering the study findings presented by Gavin Sandercock & Daniel Cohen [1]. In their study, the authors detail results derived from the Chelmsford Children's Fitness and Activity Survey, an initiative that has been monitoring the fitness of local children (local to Chelmsford) for about 20 years. Their results for the most recent cohort (2014) compared with previous study cohorts (2008, 1998) make for worrying reading: children are getting weaker alongside "a decrease in self-reported physical activity concurrent with the accelerated declines in fitness from 2008 to 2014."

So: "We measured; height, weight, standing broad-jump, handgrip, sit-ups and bent-arm hang in 10-year-old boys and girls from Chelmsford, England in: 2014 (n = 306), 2008 (n = 304) and 1998 (n = 310)." Researchers also asked about recent physical activity among their cohort using the Physical Activity Questionnaire for Children/Adolescents (PAQ-C), a self-report questionnaire. The collected results were analysed and among other analyses, authors "compared percentage change per year 1998–2008 with 2008–2014" across the variables being studied.

As per the headline, the results were worrying: "Pairwise comparisons showed muscular fitness of both sexes was significantly lower in 2014 than in 1998." They also observed that self-reported physical activity was lower in the later cohort. Obviously, I need to stress that this was self-reported physical activity information, so not exactly objective actigraphic data for example. Out of the several results reported relating to specific aspects of fitness across the cohorts, the issue of handgrip strength stuck out for me in light of some still emerging research suggesting that handgrip strength might have "prognostic value for mortality" according to some studies. Without wishing to make connection when none might exist, I do wonder whether such data might one day eventually tally with some other quite worrying statistics on longevity recently published?

Another detail discussed by Sandercock & Cohen is their finding that "Ten-year-olds in 2014 were taller and heavier than in 2008 and 1998 but there were no differences in BMI [body mass index]." They authors talk about this more in their media interviews: "As today's ten-year-olds are taller and heavier than the children measured six and 16 years ago we expect them to be stronger and more powerful, but this was not the case." Worrying. And it also appears that the declines in strength were increasing more rapidly in the later cohort than compared with the earlier ones, as the authors mention that from 1998 to 2008, strength (group strength) fell by just over half a percent per year, whereas from 2008 to 2014 this decline increased to 1.6% per year.

So what does this all mean for the health and well being of the next generation, and what can be done to reverse such trends? Well, health in childhood is often a good indicator of what health will look like in adulthood. I say this not only from a physiological point of view but also bearing in mind that habits bred in childhood tend to persist into adulthood. Low levels of physical activity probably also follow that pattern.

The possible reasons to account for the cohort disparities? Minus any sweeping generalisations I don't think it would be out of place to mention that things have changed quite a bit when it comes to hobbies and pastimes for at least some parts of the paediatric population. More time spent playing video games or on the Internet have perhaps replaced previous scenarios when kids would meet (in person), play out, run around, climb trees, play football and the like. I don't say that to demonise such digital pastimes (see here) but rather to point out a shifting pattern in activities that also have been noted in other relevant studies [2]. It's perhaps also worthwhile pointing out that opportunities for physical activity have also perhaps changed as a function of the environment we now live in. Why else would schools have had to implement strategies such as the daily mile for example?

Possible solutions? When I first tweeted about the publication of the Sandercock & Cohen article I added in the idea that physical activity specifically along the lines of strength and conditioning could perhaps be added to the learning curriculum. So, alongside maths and English (here in Blighty), there is also a focus on physical education too. Yes, I know physical ed(ucation) is part of the school agenda, but I actually meant something like getting kids into a gym and doing something akin to circuit training at least a few times a week. I know this is ambitious and I know that not every kid is going to be able to do this. But surely in these days of adaption and flexibility in teaching and learning, there are also ways to make such exercise open to all. And you never know, start children young with the mindset that exercise is fun and good for physical (and mental) health, and it might just serve them for a lifetime...

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[1] Sandercock GRH. & Cohen DD. Temporal trends in muscular fitness of English 10-year-olds 1998–2014: An allometric approach. Journal of Science and Medicine in Sport. 2018. Aug 1.

[2] Walsh JJ. et al. Associations between 24 hour movement behaviours and global cognition in US children: a cross-sectional observational study. The Lancet Child & Adolescent Health. 2018. Set 26.

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"Children with DDs [developmental disabilities] had higher chronic school absenteeism"

The findings reported by Lindsey Black & Benjamin Zablotsky [1] were not unexpected. Utilising data derived from the 2014–2016 National Health Interview Survey (NHIS) based in the United States, researchers concluded that: "In this nationally representative sample of children aged 5–17 years, children with ADHD [attention-deficit hyperactivity disorder], autism spectrum disorder, and intellectual disability were more likely to have had chronic school absenteeism compared with children who did not have these conditions even after controlling for demographic and selected physical health conditions." The reason I say that such findings were not unexpected is because such observations add to other independent literature on this topic (see here) suggesting that school isn't always a great environment for children with such diagnoses and attendance figures perhaps reflect that.

This isn't the first time that the NHIS has cropped up on this blog (see here and see here). On those previous occasions, the NHIS has provided important evidence that the rates of various developmental disabilities are continuing to increase (autism, developmental delay) whilst some diagnoses are a little more static (intellectual disability) in line with other data (see here). This time around, researchers looked at what role developmental disabilities (DDs) might play in the finding that "14% of all public school students are chronically absent from school, missing 15 or more days per year" in the United States.

Based on the NHIS methodology that involved sampling households with said households completing "a brief questionnaire to collect selected demographics and broad health measures", researchers first ascertained whether "the parent had ever been told by a doctor or health professional
that the child had attention-deficit/hyperactivity disorder (ADHD), autism spectrum disorder, intellectual disability, or other developmental delay." They also asked about school absenteeism using the question: "During the past 12 months, about how many days did (sample child) miss school because of illness or injury?" Findings were collated and analysed.

Results: covering nearly 27,000 children, of which about 1 in 10 were diagnosed with ADHD and 2.5% reported to be diagnosed with an autism spectrum disorder (ASD), a few important results emerged. Those diagnosed with an intellectual disability (sometimes called a learning disability here in Blighty) "had the highest prevalence of chronic school absenteeism (14.0%)." Chronic school absenteeism by the way, was defined as 15 or more days missing from school throughout the school year. The percentage rates for school absenteeism for autism, developmental delay and ADHD were 9%, 7.2% and 5.2% respectively. Compared against data from children without any reported developmental disability diagnosis, those with DDs were quite a bit more likely to be chronically missing from school even when adjusted for various other co-occurring physical health conditions such as "asthma, allergies, and headaches" or for other demographic differences ("age, sex, race and ethnicity, poverty status, family structure (categorized as two parent, single parent, or other), and geographical region of residence").

Even taking into account possible research caveats such as the fact that "data are based on a parent or guardian report" the Black/Zablotsky findings represent some important data. 'Every school day counts' is an oft-heard about phrase in educational circles, drawing attention to the idea that not only is educational attendance a legal requirement in many countries, but also that as chronic absenteeism creeps in, so educational chances and opportunities start to slip by and where this can potentially lead (see here). This is bad for the kids, bad for the teachers (who often have to 'go over' missed work) and not particularly great for the rest of the class either.

Bearing in mind all that, the next question should really be 'why?' Why are children with DDs more prone to school absenteeism and what can be done to remedy the situation? Well I don't doubt that it's going to be complicated and so doesn't need any sweeping generalisations from me or anyone else. I'm first drawn to mention that whilst Black & Zablotsky controlled for various physical health conditions that might affect school attendance, they probably did not control for all of them (including bouts of illness due to infections for example) and so one needs to look more closely to see if these exerted any effect on their results (see here for another example). My second preference for further study would be to see whether education is actually meeting the child's individual requirements as another area associated with chronic absenteeism. Y'know, the idea that school can be a source of significant stress and strain for children (see here); even in those educational environments that have a more specialised ethos (see here). Finally, and again minus any sweeping generalisations, more research is needed on family circumstances and child's school absenteeism. I know it's a little uncomfortable to mention but irrespective of a child's diagnostic status or not, some parents are not always 'on message' when it comes to the 'every school day counts' idea. Coupled with a child who might not be particularly interested in school, and well, it's not difficult to see how this could play out with regards to the onset and perpetuation of chronic absenteeism. I would add that this is not a universal 'blame the parents' observation.

There are no easy fixes to this issue. But identifying potentially vulnerable groups, asking appropriate questions and providing targeted support, would seem to me to be a step in the right direction.

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[1] Black LI. &  Zablotsky B. Chronic School Absenteeism Among Children With Selected Developmental Disabilities: National Health Interview Survey, 2014–2016. National Health Statistics Reports. 2018; 118.

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Big data does... the extreme male brain theory of autism and the Empathizing–Systemizing theory

"Two long-standing psychological theories – the empathising-systemising theory of sex differences and the extreme male brain theory of autism – have been confirmed by our new study, the largest of its kind to date."

That was the opening sentence to a write-up (see here) of a recent research paper published by David Greenberg and colleagues [1] which sought to "test 10 predictions from the Empathizing–Systemizing (E-S) theory of sex differences and the Extreme Male Brain (EMB) theory of autism." The 'big data' words included in the title of this post refer to the collection of data from hundreds of thousands of people as part of a TV documentary that aired here in Blighty called 'Are you autistic?' whose data were included for study. This follows a similar format from some of the co-authors on the Greenberg paper on previous research occasions (see here).

Minus any charges of plagiarism, a few descriptors might be useful. First: "The first theory, known as the empathising-systemising theory of typical sex differences, posits that, on average, females will score higher on tests of empathy than males, and that, on average, males will score higher on tests of systemising than females." Second: "The second theory, known as the extreme male brain theory of autism, extends the empathising-systemising theory. It posits that autistic people will, on average, show a shift towards “masculinised” scores on measures of empathy and systemising." Researchers also talked about something called a 'd score': "the difference between each person’s score on the systemising and empathy tests" in their research, alongside mention of the words 'brain type'.

As part of the interactivity of that TV documentary, some 670,000 people "who indicated they were males or females" completed various measures: "the Autism Spectrum Quotient-10 (AQ-10)... the Empathy Quotient (EQ)..., Systemizing Quotient-Revised (SQ-R)..., and the Sensory Perception Quotient (SPQ)" via an on-line questionnaire portal. About 36,000 people who took part "indicated that they had been diagnosed with an “Autism Spectrum Condition”." Data from responses to the questionnaires were crunched pertinent to those 10 predictions from both theories (said predictions concerned sex differences based on responses to the questionnaires, those various 'brain types' and how responses might look with reference to the presentation of autistic traits). For good measure, researchers also describe carrying out an 'independent replication' of their findings on a separate cohort of adults ("14,354 participants (226 autistic individuals, and 14,119 controls)"). Although there were some minor differences from the larger main trial, to all intents and purposes the same procedures were employed "for calculating brain types and performing statistical analysis."

Results: well "all 10 predictions from the E-S and EMB theories" were confirmed. So for example, men taking part in the study "had a shift towards a high d score" suggestive of being more likely to be systemisers than empathisers, whilst "typical females had a shift towards a low d score" (i.e. more likely to empathetic than systemiser). The previous STEM (science, technology, engineering, and mathematics) findings [2] were also supported, in that: "STEM professionals on average scored significantly higher on the AQ" suggesting a link between the choice of STEM career and autistic traits. And for those reporting a diagnosis of autism or autism spectrum disorder (ASD): "autistic people, regardless of their sex, had a shift towards an even higher d score than typical males" (systemisers) but "were not more likely to work in STEM occupations, compared with controls."

There is a lot to take in from the Greenberg research and related commentary. The study has a number of things going for it insofar as the huge participant size and the use of an independent replication set to confirm findings. These factors should not be underestimated. The limitations? Well, self-report is still one of them, and the fact that at least one of the questionnaires used is probably picking up a lot more than just 'autistic traits' (see here). I'm also inclined to point out once again that the *correlation* between autistic traits and STEM career choice did not seemingly extend to those with autism being "more likely to work in STEM occupations, compared with controls." Going back to that 'what is being tested' issue, the AQ for example, might also be picking up something linked to "loneliness, social anxiety, depression, and anxiety" [3] or even something approaching the schizophrenia spectrum (see here) or personality disorder (see here). Indeed, one might have to entertain the idea that the definition 'autistic traits' may not tell the whole story in this study.

I have to admit to being still a little sceptical of big psychological theories such as the EMB or the E-S theory of sex differences. The reason? Whilst attractive in their compartmentalising nature, real life is often far from being so clear-cut and linear. The fact also that an important part of the evidence behind such theories remains a little 'fluffy' (see here for example) cannot be readily brushed under the scientific carpet. As for the use of the term 'brain types', well, I can see what the authors were getting at, but I'm not convinced such terminology is particularly useful. 'Brain types' kinda sits in the same category as 'neurotypical' (see here). I was also drawn to the fact that the authors have to explicitly say that their results don't mean that "autistic people lack empathy" and that "autistic people are not hyper-male in general." It kinda tells you how some of the history behind these theories shows that they have not exactly been received with open arms by many.

But even with all that, the Greenberg results cannot be just discounted, and more research on this topic is indicated.

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[1] Greenberg DM. et al. Testing the Empathizing-Systemizing theory of sex differences and the Extreme Male Brain theory of autism in half a million people. Proc Natl Acad Sci U S A. 2018 Nov 12. pii: 201811032.

[2] Ruzich E. et al. Sex and STEM Occupation Predict Autism-Spectrum Quotient (AQ) Scores in Half a Million People. PLoS One. 2015 Oct 21;10(10):e0141229.

[3] Reed P. et al. Loneliness and Social Anxiety Mediate the Relationship between Autism Quotient and Quality of Life in University Students. Journal of Developmental and Physical Disabilities. 2016; 28: 723-733.

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Vitamin D supplementation and autism: more work needed on the biochemistry of vitamin D metabolism

The findings reported by Conor Kerley and colleagues [1] provide the brief blogging fodder today. Researchers, who are no stranger to the research area that is vitamin D and autism (see here), decided to conduct a 'post-hoc analysis' of data from two controlled trials where vitamin D supplementation was experimentally tested for children with autism and children with asthma. They were specifically looking at the "serum response to vitamin D supplementation" rather that the amount of vitamin D supplemented as potentially being important to the clinical results obtained. They concluded that "children with ASD [autism spectrum disorder] had a lower increase in 25(OH)D levels with supplementation." Further: "Potential mechanisms include altered absorption/metabolism as well as well genetic factors."

Bearing in mind the relatively small participant group numbers used and comparisons between kids with autism and kids with asthma without any other 'asymptomatic' group involvement, I was really rather interested in the Kerley findings. This was a research group who previously concluded that vitamin D supplementation did little for their cohort of autistic children under experimental conditions [2]. Now they're perhaps suggesting that there may have been valid biological reasons behind such results with respect to the biochemistry/metabolism behind vitamin D with such issues potentially affecting how much vitamin D supplementation is required to suitably raise vitamin D levels.

Of course this is not necessarily a new finding. Science has already started to look at the genetics/biology of vitamin D metabolism in relation to autism (see here and see here) and continues to do so [3]. It also converges with the idea that a deficiency/insufficiency of vitamin D is an important clinical finding but does not necessarily mean that a universal dose of vitamin D supplementation will 'fix anything' (see here for another example in another label).

"Clinical and research work relating to vitamin D is ASD should measure 25(OHO)D response to supplementation to assess therapeutic doses." I can't argue with such sentiments on the basis of the results observed. Working back from sayings such as 'the dose makes the poison', it appears that for some on the autism spectrum, that dose may not be the same as everyone else...

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[1] Kerley CP. et al. Blunted serum 25(OH)D response to vitamin D3 supplementation in children with autism. Nutr Neurosci. 2018 Oct 10:1-6.

[2] Kerley CP. et al. Lack of effect of vitamin D3 supplementation in autism: a 20-week, placebo-controlled RCT. Arch Dis Child. 2017 Nov;102(11):1030-1036.

[3] Biswas S. et al. Fok-I, Bsm-I, and Taq-I Variants of Vitamin D Receptor Polymorphism in the Development of Autism Spectrum Disorder: A Literature Review. Cureus. 2018 Aug 29;10(8):e3228.

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SEED says... risk of overweight/obesity in autism is heightened

SEED - The Study to Explore Early Development - provides yet more discussion fodder today as I bring the findings reported by Susan Levy and colleagues [1] to the blogging table. This time around the focus was on the risk of being overweight and/or obese in relation to a diagnosis of autism and the conclusion that: "Prevention of excess weight gain in children with ASD [autism spectrum disorder], especially those with severe symptoms, and in children with developmental delays/disorders represents an important target for intervention" on the basis of results observed.

It's not exactly a new thing to observe that those diagnosed with autism are perhaps at a greater risk of being overweight and/or obese (see here). There are a multitude of possible reasons behind such statistics covering everything from research showing those on the autism spectrum to typically be more sedentary than peers (see here) (bearing in mind the idea that 'you can't outrun a bad diet'), to a heightened risk of receiving medicines that list weight issues as a side-effect (see here) to a possible role for over-represented comorbidity (see here) with regard to weight issues. The net results however is the same: being diagnosed with an autism spectrum disorder places someone at a heightened risk of being overweight or obese.

Levy et al compared three groups of young children - "2-5 years of age" - classified by a diagnosis of autism spectrum disorder (ASD) or developmental delay/disorder or classed as a general population controls (i.e. asymptomatic). Importantly they describe how height and weight were "measured during a clinical visit" thus removing the reliance on 'at home' or routine records measurements [2] and the risk of bias that they can sometimes bring. Researchers also gathered background information on various co-occurring conditions/diagnoses.

Results: "The odds of overweight/obesity were 1.57 times... higher in children with ASD than general population controls and 1.38 times... higher in children with developmental delays/disorders than general population controls." One needs to be bear in mind the quite young age of participants when putting that last sentence into some context. Also: "Among children with ASD, those with severe ASD symptoms were 1.7 times... more likely to be classified as overweight/obese compared with children with mild ASD symptoms."

There's little more to say about such findings other than autism or autistic traits, yet again, seems to place someone as a quite significant disadvantage when it comes to their physical health and wellbeing. Now, the important question: what can be done about it?

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[1] Levy SE. et al. Relationship of Weight Outcomes, Co-Occurring Conditions, and Severity of Autism Spectrum Disorder in the Study to Explore Early Development. The Journal of Pediatrics. 2018. 9 Oct.

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Quality of life and autism continued

"In this study it was found that psychiatric comorbidity, sleeping difficulty, intellectual disability, maladaptive behavior, adaptive functioning, autism symptomatology, main daytime activity and residence were associated with QoL [quality of life], independent of respondent type."

So concluded the findings reported by Ane Knüppel and colleagues [1] continuing an important research theme looking at quality of life with autism in mind (see here and see here and see here). There's nothing specifically novel about the factors reported on as affecting quality of life (QoL) where a diagnosis of autism is mentioned (mental health issues, autism severity, comorbidity, activities, social inclusion) but the fact that authors drew on data from both self-reports and proxy-reports is important and perhaps provides an important dual perspective. Indeed as the authors noted: "Proxy-reported QoL is different from self-reported QoL and should be considered as an alternative source of information." Similar sentiments have been expressed recently (see here).

Having previously talked [2] about the properties of the specific instrument used to gauge QoL with autism in mind, the authors relied on responses on the INICO-FEAPS scale in their investigation. More than 1700 participants with autism completed the scale where: "For 165 individuals with ASD [autism spectrum disorder], self-reports only were available, and for 863 individuals with ASD, only parental proxy-reports were available." The scale itself is pretty comprehensive, consisting of "72 items divided into the following eight subdomains: self-determination, rights, emotional wellbeing, social inclusion, personal development, interpersonal relationships, material wellbeing, and physical wellbeing." A higher score on the INICO-FEAPS scale denotes a higher QoL 'level'. Various other measures were also included for study; some of them based on the setting of the study in Denmark and the fact that Scandinavian countries are particularly 'geared up' for collecting all-manner of details on the basis of various national registries held on the population.

Alongside the results suggesting that various factors seemed to be important to QoL, there were some details to consider. So: "Across all respondent groups, the lowest rated QoL domains were emotional wellbeing (range of means = 71.10–74.05) and interpersonal relationships (range of means = 65.07–71.88), and the highest rated QoL domains were rights (range of means = 83.79–86.21) and material wellbeing." Further, researchers also observed that being employed or in education also correlated with a higher QoL score "compared to individuals without any regular daytime activity" and "significant associations were found for all respondent groups, with lower levels of QoL among individuals living with their parents... and among individuals with ASD living outside the family home with support... compared to individuals living independently without support."

I was also interested in the idea discussed by the authors that: "treating psychiatric comorbidity, reducing maladaptive behavior, raising the level of independence, and offering individuals with ASD an opportunity to be involved in any job-related occupation or to receive education may raise the level of QoL." 'Treating psychiatric comorbidity' is already a research and clinical priority when it comes to autism (see here and see here). Yes, science needs to do a lot better in terms of establishing the 'hows-and-whys' of such comorbidity being over-represented alongside autism but there are some important themes starting to emerge (see here) including that looking at core autism symptoms as being potential risk factors for the appearance of such issues. And once again we can look to an important group of people for further clues as to how such psychiatric issues are indeed perhaps more 'core' than comorbidity (see here).

Although 'reducing maladaptive behaviour' potentially covers a lot of 'challenging' ground - "Behavior classified as self-destructive, breaking belongings, defiant, disruptive, hurtful to others and/or socially offensive" - I don't think anyone would seriously argue against the idea that such behaviours are neither good for the individual nor good for those around them. I'm minded to suggest that the reason(s) for such behaviour are likely to be complex (see here and see here), but one thing that could be useful would be to look at some of the research on particular 'profiles' being present and connected to autism and beyond (see here) as a starting point.

And then there is also the suggestion of a possible effect for society more generally, as in ensuring that education and employment opportunities are available to all and making 'an inclusive society' a priority...

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[1] Knüppel A. et al. Quality of life in adolescents and adults with autism spectrum disorder: Results from a nationwide Danish survey using self-reports and parental proxy-reports. Research in Developmental Disabilities. 2018; 83: 247-259.

[2] Knüppel A. et al. Psychometric properties of the INICO-FEAPS scale in a Danish sample with autism spectrum disorders. Research in Developmental Disabilities. 2018; 75: 11-21.

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