Saturday, 6 April 2019

"Anti-vaccination arguments are varied" (and not all about autism)

I tread very carefully with my slightly long discussions of the paper by Beth Hoffman and colleagues [1] (open-access available here). The Hoffman paper talks about the role of social media in an important issue: "anti-vaccination rhetoric". Specifically how an analysis of anti-vaccination sentiment on one particular social media platform suggests that "It's not all about autism" when it comes to such views being very publicly espoused. Some people might already know why autism was mentioned by Hoffman, but for others here is some discussion of the previous (peer-reviewed) science on that topic (see here and see here).

I know that there are some significant emotions surrounding this topic. I know it's a subject area that crosses lots of different issues ranging from individual and public health to personal choice and lots more in-between. It's also a topic which in some cases is literally the difference between life and death. And for those reasons it's why papers such as the one from Hoffman et al are so important: to understand why, in the age of social media where the world is literally your audience, such sentiments might occur and how any misgivings about vaccination could be suitably addressed. How much also, the anti-vaccination messages that are being promulgated on social media, actually do impact on people's actual vaccination behaviour is another point of more general study, and specifically why this might happen more for some but not for others [2] (a 'vaccine for anti-vaccination sentiment' perhaps?).

Hoffman continued a growing theme in various research circles where social media footprints represent data (see here and see here). They specifically zoomed in on "197 individuals on Facebook who posted anti-vaccination comments on a local paediatric clinic’s Facebook page" in response to a video about "the human papillomavirus (HPV) vaccine as an anti-cancer vaccine." And before you ask, yes, the HPV vaccine does indeed seem to be an anti-cancer vaccine [3]. The sorts of comments received were sometimes pretty extreme as per "being either (1) threatening (e.g. “you’ll burn in hell for killing babies”) and/or (2) extremist (e.g. “you have been brainwashed”)." That being said, I don't want to tarnish all commentators on the basis of the posting of such extreme comments by some.

Researchers went through the posts - "all publicly available information" - of their nearly 200 selected Facebook accounts, covering material published over a 2 year period. Various codes (N=26) were used to classify the posted content, alongside "8 variables related to sociodemographic information: age, gender, location, political affiliation, marital status (yes/no), parental status (yes/no), whether employment was listed (yes/no), and whether post-secondary education was listed (yes/no)." Results were collated.

"Posts on these individuals’ Facebook profile pages suggest that many are highly mistrustful of the medical and scientific community." That was one of the primary findings. Other observations included: "Of the 116 individuals with at least one public anti-vaccination post from 2015 to 2017, posts about “educational material” (73%), “media, censorship, and ‘cover up’” (71%), and “vaccines cause idiopathic illness” (69%) were the most common topics." 'Educational material' implying "content that claims to provide scientific evidence for the negative impact of vaccines" is perhaps slightly counter-intuitive to the 'mistrust' that Hoffman initially concluded. Indeed, it implies that this isn't necessarily about a general 'mistrust' of science per se that they noticed, but rather more of a selective mistrust of some of the science and/or 'guardians' of that science. This perhaps coincides with their focus on some key weakness of science including that: (a) science is more about probability than it is about absolutes, and (b) science is not produced uniformly; such that peer-reviewed science can still be published as peer-reviewed science irrespective of how well or badly it was designed and conducted. So for example, you can provide someone with a 100 or a 1000 well-designed studies showing 'no connection' between variable X and variable Y in a statistical sense, but it only takes one study *linking* variable X and variable Y appearing in the science literature for someone to be able to say that there is some science behind a possible link between variable X and variable Y (or at least that a link can't be definitively ruled out). That's the way science works for better or worse.

Insofar as the sentiments of 'media, censorship and cover-up' this is another key issue with some overlap with the other details observed. The cries of 'cover-up' and 'censorship' "suggesting that the government, pharmaceutical companies, and/or physicians consciously and wilfully fail to disclose adverse vaccine reactions" play into lots of different themes allied to the previous discussion about science and beyond. Whilst not wishing to stray too far from the Hoffman findings, I'll bring in some quite recent discussions about the whole Cochrane-Gøtzsche saga (see here) as one relevant example. I don't want to rehash that post in its entirety but the Jørgensen paper [4] including Peter Gøtzsche as an author which concluded that "The Cochrane human papillomavirus (HPV) vaccine review missed nearly half of the eligible trials" provides an example of how science again isn't necessarily always as uniform as it appears. On that basis, and with other medical commentators also concerned about clinical trial data not seemingly appearing in a timely fashion for example (see here) alongside some recent quite high-profile judgements (see here), the gaps left provide fertile ground for social media speculation and onward the stoking of potential anti-vaccination comments.

Hoffman et al also talk about various strategies that might be employed to "increase the level of community protection against the propagation of anti-vaccination messaging on social media." Personally I'm not sure whether things like increasing media literacy, the use of entertainment narratives and/or "for medical professionals to be more active on social media" and more [5] are really going to make any significant inroads into changing (often entrenched) hearts and minds. I'm even more doubtful that blanket 'censorship' is an entirely appropriate course of action, despite that being on the cards (see here) precisely because it may play directly into the hands of those cries of censorship.

There is however one thing that I think could be worth looking further into: dialogue. Minus any sweeping generalisations about equating anti-vaccination sentiments with anything else, most people here in Blighty will know about the history of Northern Ireland. Years and years of arguments, fighting, murders and more weren't solved by censorship (I remember the days when the voice of Gerry Adams was banned) but rather by talking and having constructive discussions. It was an unpalatable process for some people, particularly those who were personally touched by the violence in Northern Ireland, but dialogue happened and lives were probably saved as a result. I know some people would find the idea of talking to prominent people with anti-vaccination views likewise to be a difficult prospect. But the truth of the matter is that we're never going to get to the core of why people believe what they believe and say what they say without asking them about what motivates their view(s). It's kinda been done a little bit before in the peer-reviewed science arena and beyond but lots more data is required. And it appears that such 'dialogue' has been suggested by others too...

I'm also minded to mention that part of that dialogue needs to include discussions about 'experience'; something that could also be an important variable when it comes to vaccine hesitancy and its propagation among specific groups (see here and see here). Indeed, a realisation that those who express anti-vaccination views or opinions probably include many different people who arrived at their position for lots of different reasons is an important point. Probably not all of them having some inherent disposition to being anti-vaccination or indeed necessarily "in favour of magical or superstitious thinking" [6] as others have previously opined. Opening dialogue is a difficult prospect but if it saves one life from a vaccine-preventable disease, it's got to be worth a try.

Vaccination is a cornerstone of public health, a life-saving cornerstone of public health, something that should never, ever be forgotten. Indeed it's probably because people forget what measles for example and other childhood disease did to some children and adults that some complacency about vaccination has set in. If you need to see some of the effects of vaccine-preventable diseases in action, read about what measles did to the author Roald Dahl's daughter (see here). Anti-vaccination sentiment is a significant issue that has been with us since vaccination began. It needs to be approached head on to counter mis-information and calm and allay any fears. The way to tackle this issue is however going to be as complicated as the issue itself is. Yes, it needs to realise that social media is often an 'echo chamber' [7] giving people an opportunity to literally speak their mind and adapt accordingly. But another part of that strategy - an important part of that strategy - needs to be an understanding of why people think the way they do. In that respect, dialogue, however unappealing that might be to some people, is eventually going to be key...

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[1] Hoffman BL. et al. It's not all about autism: The emerging landscape of anti-vaccination sentiment on Facebook. Vaccine. 2019 Mar 14. pii: S0264-410X(19)30303-2.

[2] Zhang EJ. et al. Influence of political and medical leaders on parental perception of vaccination: a cross-sectional survey in Australia. BMJ Open. 2019 Mar 26;9(3):e025866.

[3] Palmer T. et al. Prevalence of cervical disease at age 20 after immunisation with bivalent HPV vaccine at age 12-13 in Scotland: retrospective population study. BMJ 2019; 365.

[4] Jørgensen L. et al. The Cochrane HPV vaccine review was incomplete and ignored important evidence of bias. BMJ Evid Based Med. 2018 Oct;23(5):165-168.

[5] Gesualdo F. et al. To talk better about vaccines, we should talk less about vaccines. Vaccine. 2018; 36: 5107-5108.

[6] Bryden GM. et al. Anti-vaccination and pro-CAM attitudes both reflect magical beliefs about health. Vaccine. 2018 Feb 21;36(9):1227-1234.

[7] Schmidt AL. et al. Polarization of the vaccination debate on Facebook. Vaccine. 2018 Jun 14;36(25):3606-3612.

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Friday, 5 April 2019

CBT for anxiety in kids with autism meta-analysed

A short post today to bring the findings reported by Celal Perihan and colleagues [1] to your attention with regards to the use of cognitive behavioural therapy (CBT) for anxiety in the context of paediatric autism.

It was yet another case of authors meta-analysing (boiling down) the data from the existing research literature and coming to a conclusion. Twenty-odd studies reported on the use of CBT - talking therapy - for an important quality-of-life draining issue for many diagnosed on the autism spectrum: anxiety (see here and see here). Researchers concluded that CBT did seem to be associated with a reduction in some anxiety-linked symptoms/behaviours but things weren't altogether cut-and-dried on the usefulness of CBT in this context.

I wasn't surprised by these results. I've blogged before about how CBT for anxiety in the context of autism might be a useful option for some (see here). That being said, I'm not 100% in favour of CBT being used in this context. I say that because, as things stand, we don't know enough about why anxiety seems to be over-represented in relation to autism (see here). I've opined on various occasions that anxiety is probably a lot more than 'just a comorbidity' when it comes to some autism (see here). In that context, the use of CBT 'for anxiety' is a little bit like saying that CBT is being used 'for autism'. And the evidence for that is pretty unconvincing (see here).

If you really want to convince me that CBT is good for anxiety in the context of autism, try pitting CBT against some of the other non-psychology interventions that have been talked about for anxiety in relation to autism (see here). See what comes out on top rather than just looking at CBT vs. treatment-as-usual (whatever that means). Oh, and bear in mind that we still don't know enough about the presentation of anxiety in those on the autism spectrum who are perhaps not able to participate in CBT (see here)...

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[1] Perihan C. et al. Effects of Cognitive Behavioral Therapy for Reducing Anxiety in Children with High Functioning ASD: A Systematic Review and Meta-Analysis. J Autism Dev Disord. 2019. Feb 27.

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Thursday, 4 April 2019

Magnesium and ADHD meta-analysed

The study results published by Mohammad Effatpanah and colleagues [1] provided some food for thought recently on the topic of whether there may be an *association* between "serum magnesium levels and the diagnosis of attention deficit hyperactivity disorder (ADHD)."

The name of the research game was meta-analysis, that well used 'boiling down' of the published (hopefully peer-reviewed) science literature into something like a coherent 'conclusion'. The starting point for Effatpanah was that: "Current research suggests conflicting evidence surrounding the association between serum magnesium levels and the diagnosis of attention deficit hyperactivity disorder (ADHD)." It's interesting that this isn't the first time that magnesium and ADHD has been put under the meta-analysis microscope [2] and that particular meta-analysis didn't suggest such conflict.

Never mind. Seven studies made the grade for Effatpanah, together revealing that "subjects with ADHD had 0.105 mmol/l (95% CI: -0.188, -0.022; P < 0.013) lower serum magnesium levels compared with to their healthy controls." Researchers did also talk about 'high heterogeneity' across the studies analysed. This indicates that whilst there may well be "an inverse relationship between serum magnesium deficiency and ADHD" overall, the individual studies included in their meta-analysis weren't always in agreement with one and another.

So what conclusions can we take from the Effatpanah and other (meta-analysis) studies in this area? Well, more investigation is required on the suggestion of a *link* between magnesium and ADHD. We need to know more about the biology of why reduced biological levels of magnesium might be important to ADHD or ADHD-type behaviours [3] and whether something as simple as supplementing with magnesium *might* make a difference for some people [4] (minus any medical or clinical advice from me on this or any other topic). Indeed, on that last issue, I might refer you back to some other occasions where magnesium has been mentioned in the context of nutritional intervention for ADHD (see here). I'm also inclined to mention that there may be other 'labels' where magnesium might require a little more study (see here), some of which might 'overlap' with a diagnosis of ADHD. And of course, we should remember that magnesium 'issues' in the context of autism might not be the end of the story when it comes to trace metals and ADHD (see here)...

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[1] Effatpanah M. et al. Magnesium status and attention deficit hyperactivity disorder (ADHD): A meta-analysis. Psychiatry Res. 2019 Feb 19;274:228-234.

[2] Huang YH. et al. Significantly lower serum and hair magnesium levels in children with attention deficit hyperactivity disorder than controls: A systematic review and meta-analysis. Prog Neuropsychopharmacol Biol Psychiatry. 2019 Mar 2;90:134-141.

[3] Black LJ. et al. Low dietary intake of magnesium is associated with increased externalising behaviours in adolescents. Public Health Nutr. 2015 Jul;18(10):1824-30.

[4] Ghanizadeh A. A systematic review of magnesium therapy for treating attention deficit hyperactivity disorder. Arch Iran Med. 2013 Jul;16(7):412-7.

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Wednesday, 3 April 2019

"This study provides important information about psychiatric comorbidity in adult ASD" (again)

The quote titling this post - "This study provides important information about psychiatric comorbidity in adult ASD [autism spectrum disorder]" - comes from the findings published by Jack Underwood and colleagues [1] (open-access available here).

The Underwood study is a bit of a mash-up paper because, alongside examining things like psychiatric comorbidity and other features accompanying or allied to 'adult autism', it also ventures into the possible genetics of autism. Unfortunately, the relatively small sample size - "105 eligible individuals were matched to 76 healthy controls" (authors words not mine) - means that the genetic results in particular need to be treated with some caution. With this in mind, I'm not going to go further into this side of the Underwood report.

So: "105 individuals were all confirmed to have an ASD diagnosis consistent with ICD-10 criteria by case-note review" were the cohort included for study, all derived from the National Centre for Mental Health institution based in Wales. Interviews and questionnaires were disseminated, covering topics like marriage and employment status alongside questions on 'biological offspring' (children, to you and me). Participants were questioned about psychiatric comorbidity (as in, did they have any diagnoses) as well as medication use and substance use/abuse. We are told that: "By definition, control participants did not have psychiatric morbidity and were not using any psychotropic medication."

"Comorbid psychiatric diagnosis was reported by 89.5% (n = 94) of individuals with ASD." If you would have told me that statistic about 10 or 15 years ago I might have been shocked. These days such figures, high figures, on psychiatric comorbidity accompanying autism seem to be reported on almost a weekly basis. I don't say that to downplay the effects of such high comorbidity; just that there is little novelty in their discovery (see here and see here) particularly the high rates of depression and anxiety that were picked up (see here). Oh, and once again I'll question whether the word 'comorbidity' is entirely accurate in the context of various issues appearing alongside autism (see here).

Medication use? Yes, as probably expected, there was quite a bit of that, particularly antidepressants, anxiolitics (for anxiety) and antipsychotics in the autistic group. Again, there's little novelty in those findings (see here) but they do reiterate the need for regular monitoring and good medicines management (see here).

Onward: "Adults with ASD were significantly less likely to be currently working..., to be married or cohabiting..., to be currently off work because of sickness or disablement... and to have alcohol-related problem." Yes, there was more overlap with other independent findings in some of those areas (see here and see here for examples) but also some quite important details. Take for example the category termed 'problems due to alcohol use' which was reported by 36% of the autistic group compared with 8% of controls. Although not exactly great PR for the label of autism, there is an emerging understanding that alcohol use and abuse does seem to be over-represented alongside a diagnosis of autism (see here). The authors opine that this "could be usage to self-medicate for the aforementioned anxiety as suggested by other authors, or to facilitate social interactions" but really we need lots more data about this and the long-term effects of such 'self-medication' if that's what it truly is.

Another details also stuck out for me: "Forty-one (42.7%) individuals with ASD reported lifetime history of migraine headaches compared with 15 (20.5%) control participants." Migraine headaches (or even just headaches) have been talked about before on this blog in the context of autism (see here). With such a large percentage of participants with autism talking about this issue, I'm minded to suggest that a lot more investigation is needed in this area.

There is little in the way of new, novel findings in the Underwood paper but I don't want readers to think that this is a not a valuable addition to the peer-reviewed science literature. It is, simply because it continues important conversations about (a) the presentation of autism into adulthood (see here), (b) the idea that autism rarely appears in some sort of diagnostic vacuum (see here), and (c) the various inequalities - health and social - faced by those on the autism spectrum. What however I would like to see more of is research on 'what helps' to iron out some of these important issues and how services can be effectively delivered. Alongside we need some debates about funding too.

And just before I go, the focus on autism "and no self-report comorbid intellectual disability" in the Underwood paper did not go unnoticed. Autism science also needs to make sure that all voices on the autism spectrum are equally heard (see here). Indeed, another recent paper [2] makes the point very eloquently: "We found selection bias against ID [intellectual disability] throughout all fields of autism research. We recommend transparent reporting about ID and strategies for inclusion for this much marginalised group." I wouldn't disagree...

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[1] Underwood JFG. et al. Autism spectrum disorder diagnosis in adults: phenotype and genotype findings from a clinically derived cohort. Br J Psychiatry. 2019 Feb 26:1-7.

[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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Tuesday, 2 April 2019

"Rates of death are higher for autistic individuals compared to the general population"

It's world autism awareness day today (2 April). The theme this year (2019), according to the United Nations, is "Assistive Technologies, Active Participation", something rather timely given the recent realisation that quite a few people diagnosed with autism are not properly represented [1] in various fields. Indeed, it continues a theme on the under-represented and under-studied populations within the autism spectrum being highlighted today of all days (see here)...

To mark this years autism awareness day, I'm turning to a topic that is probably about as important as it gets with regards to autism or any label: premature death. Specifically, highlighting how premature premature death can actually be when autism is diagnosed. I appreciate that this is not great PR for autism. But it's real-life for too many; and needs to be talked about as much as possible so people sit up and (hopefully) do something about it...

So...

The quote heading up this post - "Rates of death are higher for autistic individuals compared to the general population" - taken from the findings reported by Ye In (Jane) Hwang and colleagues [2] is perhaps not altogether accurate. A more precise meaning is required: as a group, those diagnosed with autism or autism spectrum disorder (ASD) are at some elevated risk for a premature (untimely) death than the non-autistic population (see here). Not exactly great dinner party conversation but vitally important nonetheless.

This is a topic that has cropped up time and time again in the peer-reviewed research literature and beyond (see here and see here). The grim trend crosses geographical boundaries and seems to cover the entirety of the autism spectrum. This time around New South Wales in Australia provided the source data with the aim "to report the rates and risk factors for mortality and cause of death in individuals on the autism spectrum (n = 35,929 age range 5-64) with and without concurrent intellectual disability (ID)."

The results: "Mortality rates for those on the autism spectrum were 2.06 times that of the general population." In line with other data (see here), those who also presented with intellectual (learning) disability alongside autism were at a higher risk of death. Epilepsy is also reported as being an important issue too (see here). A few other details are highlighted in the Hwang paper including the observations that "injury and poisoning" were some of the top-ranked causes of death as per other data (see here and see here).

What's more to say on this topic? Another call to action (see here)? Some more big news headlines (see here)? Another 'long-term plan' (see here)? All well-and-good, but what's actually being done to tackle such frightening statistics here and now and actually improve and extend lives in the here and now? What's currently helping autistic people to 'age well' [3]? And just in case you're of the inclination that epilepsy and intellectual (learning) disability are some how not a 'core' part of some autism, you're probably wrong in many cases (see here and see here)...

If the Hwang and other data aren't enough to satisfy you on this topic, another research paper with another (similar) set of grim findings has also recently been published [4]. Faced with such data, discussions about a puppet depicting one face of autism (see here) for example, don't seem all that important do they? Indeed, if half as much time was dedicated to highlighting the mortality stats associated with autism and making sure this makes headlines - over a 20 year period "6.4% of individuals died at an average age of 39 years" - may be more would be done to tackle them, including providing "adequate access to health care for individuals with autism spectrum disorder."

Food for thought, and hopefully important fuel for action...

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

[2] Hwang YIJ. et al. Mortality and cause of death of Australians on the autism spectrum. Autism Res. 2019 Feb 25.

[3] Hwang YI. et al. Aging Well on the Autism Spectrum: An Examination of the Dominant Model of Successful Aging. J Autism Dev Disord. 2018 May 2.

[4] Smith DaWalt L. et al. Mortality in individuals with autism spectrum disorder: Predictors over a 20-year period. Autism. 2019. Feb 28.

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Monday, 1 April 2019

"to [try and] advance the understanding of potential mechanisms underlying insomnia in adults with ASD"

The paper by Vanessa Hohn and colleagues [1] (open-access available here) provides the blogging fodder today and their findings in relation to the presence of insomnia as a "common source of distress in adults with autism spectrum disorder (ASD)."

Insomnia is essentially a regular problem in getting to sleep. It has a myriad of 'causes' ranging from uncomfortable sleeping conditions (bed, noise, temperature) to the influence of things like stress, depression and anxiety. Insomnia is no joke. Outside of the potential wide-ranging effects on physical and mental health [2] it puts a person at some heightened risk of all-manner of adverse outcomes [3].

As part of a suite of sleeping-related problems, insomnia is also no stranger to diagnostic labels like autism. With autism in mind, sleep problems that begin in childhood are pretty likely to carry over to adulthood. Nobody knows the precise reason(s) why those on the autism spectrum are more likely to experience sleep problems including insomnia. Some have speculated that the presence of autistic traits may be a risk factor for such sleeping issues (see here) but there is currently little detail regarding the bridge from core autism features to sleep problems. Others have observed an *association* between the presence of other somatic issues occurring alongside autism and sleep problems (see here and see here) but again, further clarity is needed on the hows-and-whys of any relationship and, importantly, what can be done to alleviate such issues.

Hohn et al started with the premise that: "Two characteristics of ASD could be relevant to insomnia complaints by hampering the entrainment of a circadian sleep-wake rhythm." They specifically talk about examining the link between sensory responsiveness and social skills in the context of insomnia in adults with ASD.

"Data were obtained from the Netherlands Autism Register (NAR), which is a longitudinal register including approximately 2000 individuals with ASD." Some 630 participants with autism were included for study, where "individual responses given to three measures of interest during an online survey in 2015 were analyzed." Those 'measures' were the Insomnia Severity Index (ISI), the Sensory Perception Quotient and the Autism Spectrum Quotient-28. The combined data were analysed.

Results: bearing in mind that this was a study exclusively including self-report from participants with autism - with no non-autistic control group - and one that relied on a single temporal snapshot of insomnia symptoms, one has to be a little careful with the findings. So: "The mean ISI score in the present sample was 9.50 (SD = 6.01), which is indicative of subthreshold insomnia and higher than means reported for the general population ranging between 1 and 7... but lower than values obtained from insomnia patients ranging between 17 and 20." Further, about half of participants scored in the "absence of insomnia" category with only around 20% of the group recording either moderate or severe insomnia. This tells us that, again according to self-report (and not using actigraphy for example), insomnia was not necessarily a widespread issue in this cohort but present in a not-significant number: about 1 in 5 people.

Next: "Primary analyses revealed that each of the covariates had a significant impact on the ISI total score." What this means is that biological sex, gender and medication use potentially played a role in insomnia. Women participating in the study tended to score higher on the ISI than men, and those aged 45-65 also seemingly showed more of a tendency towards insomnia. I don't think anyone would be really surprised with the idea that age and insomnia might be connected [4].

Some further statistical analysis of their results led researchers to opine on: "positive associations of insomnia severity with general and visual sensory hyper-reactivity and with impairment of social skills." I'm not too au fait with the specifics of the statistical modelling technique used by the authors - hierarchical multiple linear regression analyses (HMLR) - but can see what they did and how they did it, including "controlling for confounding effects of covariates" such as "medication, biological sex, intelligence, and age" (as previously mentioned). That being said, I'll draw your attention to some other conclusions reached by the authors: "The rather small effect sizes reported in the present study suggest that other factors not assessed in this study contribute to the emergence and persistence of sleep problems in adults with ASD."

The Hohn study does add something to the literature on sleep difficulties being experienced by quite a few people (children and adults) on the autism spectrum. I'm not overly convinced that they've stumbled upon evidence that core autistic features such as social skills problems and sensory issues are necessarily central to insomnia in their cohort but am willing to concede that they might play a role. Personally, I'd be inclined to go back to that data on 'comorbid' issues like gastrointestinal (GI) problems (see here) or breathing issues like apnoea (see here) as being something to explore further; also with the assumption that such issues are potentially 'treatable' and could have an important knock-on effect for something like insomnia and other sleep issues with autism in mind...

Oh, and don't forget the molecular handyperson that is melatonin and it's potential role in all of this (see here and see here). That and other potential avenues of research/clinical interest (see here)...

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[1] Hohn VD. et al. Insomnia Severity in Adults with Autism Spectrum Disorder is Associated with sensory Hyper-Reactivity and Social Skill Impairment. J Autism Dev Disord. 2019 Feb 9.

[2] Fernandez-Mendoza J. & Vgontzas AN. Insomnia and its impact on physical and mental health. Curr Psychiatry Rep. 2013;15(12):418.

[3] Garbarino S. et al. Insomnia is associated with road accidents. Further evidence from a study on truck drivers. PLoS One. 2017;12(10):e0187256.

[4] Foley DJ. et al. Sleep complaints among elderly persons: an epidemiologic study of three communities. Sleep. 1995 Jul;18(6):425-32.

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