"Depression, dysthymia and symptoms of anxiety and post-traumatic stress are associated with extremist sympathies"

It's a particularly poignant time to be writing this post about the findings reported by Kamaldeep Bhui and colleagues [1] on the day that news broke about events in New Zealand (see here). An all-too-familiar story of hate leading to bloodshed helped along by access to weapons; communities are left scared, confused and broken following such acts of depravity.

Although snippets of information about the events leading to the New Zealand murders are still at the time of writing coming to light, the incident is being treated as a terrorist attack. News agencies have converged on the suspect; the life behind such crimes and any possible motives. Discussions will eventually lead to inevitable questions about what motivates someone to kill innocent people under such circumstances and on such a horrific scale, and could such an act have been foreseen and potentially avoided.

The Bhui findings hopefully represent a part of that inquiry as per their focus on trying to "better understand the drivers of radicalisation and extremist attitudes more generally, and the links with symptoms of psychological and mental illnesses." I say the Bhui findings might help, but also reiterate that at the time of writing, we don't know for example, whether 'psychological and mental illness' was part-and-parcel of the motivation for the New Zealand attacks.

The basics: a study based here in Blighty, researchers recruited over 600 adults (18-45 years of age) and asked various questions and for various bits of information. They asked for information about psychiatric variables such as depression (depressive symptoms), dysthymia "(i.e. persistent mild depression, or depressive personality)", personality disorder symptoms and symptoms related to post-traumatic stress disorder (PTSD). We're also told that: "Autism symptoms were measured by using a total score on the Autism Spectrum Quotient (AQ-10), which is reported as having high discriminant validity for those with and without a clinical diagnosis." I'll come back to that sentence shortly. Alongside, participants completed something called the "'SyfoR': Sympathies for Radicalisation" tool. As the name suggests, the instrument is used to gauge sympathies to "(a) committing minor crime, (b) committing violence… in political protests, (c) organising radical terrorist groups, (d) threatening to commit terrorist actions, (e) committing terrorist actions… as a form of political protest, (f) using bombs and (g) using suicide bombs to fight against injustices." Respondents are categorised as sympathisers, condemners or neutral. It appears that Bhui has played an integral part in developing the SyfoR tool.

Results: bearing in mind this was a study of extremist beliefs, not extremist actions, and mental health, researchers observed that: "SVPT [sympathies for violent protest and terrorism] were more common in those with major depression with dysthymia..., symptoms of anxiety... or post-traumatic stress." Perhaps just as important, we are told that: "Autism and personality disorder scores were not associated with SVPT" which kinda ties in with a judgement recently (see here). I say that bearing in mind that the AQ might be picking up quite a bit more than just a possible 'clinical diagnosis' of autism (see here) and reference to the growing research literature on how vulnerability is something to consider when autism is mentioned in several contexts (see here and see here). What else? Well, age played a factor (younger people were more likely to display SVPT) and SVPT was more commonly noted in those who drank, smoked and reported having a previous criminal conviction. Also of important note was the finding that: "SVPT were shown by 15.1% of the White British and 8.1% of the Pakistani groups" taking into account that half of participants were White British and half were of Pakistani heritage.

I don't want to get too carried away with sweeping generalisations stemming from the Bhui results but one can't help but wonder about the potential implications. As the authors opine: "in the absence of links with extremist groups or histories of extremist offending, the presence of mental illnesses may add risk" when it comes to SVPT. Onward: "A more general approach to improving population mental health alongside prevention in specific populations such as those experiencing post-traumatic symptoms and younger people may be helpful." I say all that being very careful not to stigmatise any individual or any group of people.

But there are concerns too. Concerns that for example, with the data suggesting that more and more young people are suffering with mental ill-health (see here) so this *might* potentially tie into some of the Bhui conclusions minus any sweeping generalisations...

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[1] Bhui K. et al. Extremism and common mental illness: cross-sectional community survey of White British and Pakistani men and women living in England. Br J Psychiatry. 2019 Mar 15:1-8.

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"...although their autistic traits were sometimes helpful, at other times they hindered their progress"

There's quite a lot of important information to be gleaned from the findings reported by Ginny Russell and colleagues [1] (open-access) following their questioning of autistic adults (or adults with autism if you prefer) about how they viewed themselves. How for example, said participants viewed their abilities and how "these abilities had helped them in their everyday lives: at work, in their relationships with other people, and at home" makes for interesting firsthand reading.

I have quite a lot of time for the primary author on this paper given other research she has produced (see here) and her recent involvement in an important paper that basically said what many people had been thinking for a while: autism research is typically biased against those who present with autism and intellectual (learning) disability [2]. That last research theme seems to have been something (partially) taken on board in this recent paper from Russell et al given their inclusion of voices from various 'parts' of the autism spectrum including those "receiving high-level support (living in full-time residential care)."

So: "All but one participant was able to describe their own traits and how these had benefited them, and the majority of participants could and did attribute these to autism." Various traits were discussed in the interviews (n=28) held with participants (n=24); key among them were "perceptual differences, memory, focus, and attention to detail, logic, and vivid imagination." Interview data / responses were also coded into various themes: "(1) experience of difference, (2) false dichotomies, and (3) moderating influences" which similarly provided further interesting data.

In relation to the 'experience of difference' we are told that this theme "encompassed how participants conceptualized the causes of their difference from “neurotypical” (NT) individuals." Although I am less than enamoured with the misnomer that is 'neurotypical' (see here for some discussions on how there is no single way for a brain to be 'normal') there is some important information contained in those accounts. Specifically how "most participants talked about autism as a set of qualities they possessed rather than an illness they had."

The theme of 'false dichotomies' was equally revealing as: "Participants gave accounts of traits as advantageous and simultaneously disadvantageous in the workplace, in relationships, and at home." The phrase 'double-edged sword' seems to be particularly apt when it came to the descriptions offered by participants in the Russell study; also denoting how: "There was no boundary between a strength and a weakness." This continues a theme from other research discussed recently (see here). Interestingly too under this category, some participants reported that: "there is no “autism—self” opposition... thus [they] saw their abilities and skills more holistically as generalized personality traits, which included autistic traits." Autistic traits as part of a wider picture eh?

The final theme - "Moderating influences" - also included some interesting data. Authors defined this as: "Factors that might determine whether a participant experienced a trait as advantageous or disadvantageous were classified as moderating influences." Perhaps unsurprisingly, social context was something mentioned in this theme, with examples like serving in the army or being incarcerated in prison being places where "a lack of empathy" and "sticking to routines" respectively, were seen as the right places to present such behaviours. Personally I'd quibble that a lack of empathy is a good place for the armed forces given that serving in active theatre is only part of the job but ho-hum. Another important part of the 'moderating influences' theme was the issue of 'controllability and extent'. As per my musings on the issue of 'stimming' and autism (see here again) this is probably the best example of that 'double-edged sword'. How things like focus, attention to detail and logic whilst all very positive traits, can sometimes become 'out of control' and cause all-manner of issues to a person.

There are of course caveats to the Russell findings, not least that their study reflected "a lack of severely intellectually and language-impaired participants" and so results cannot be generalised to everyone on the autism spectrum. Indeed they offer a solution: "Eliciting the opinions of these groups would require a different approach, perhaps observational" which really should be a research priority (see here). I'd also have been interested to see data on the comorbidity profile of the participant group too, bearing in mind that autism rarely appears in some sort of diagnostic vacuum (see here). And I'm also minded to mention that similar to other discussions on the 'positives' of other diagnostic labels (see here) one has to remember that autistic traits are not just something noted alongside a diagnosis of autism, and what this means when using emotive terms like "autistic advantage". This, particularly in the context that autism is diagnosed on the basis of traits significantly impinging on functioning and daily life (see here).

I suppose the bottom line from the Russell findings is summed up pretty well in their conclusions: "The findings make us wary of describing autistic advantages as fixed traits, rather their expression (and development) is context dependent." In other words, things like 'situation' influence whether a trait is seen as a deficit or an advantage. And just because a trait might initially be start out as an advantage or a deficit does not mean that it will necessarily stay that way across many different situations and various different time periods...

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[1] Russell G. et al. Mapping the Autistic Advantage from the Accounts of Adults Diagnosed with Autism: A Qualitative Study. Autism in Adulthood. 2019. Apr 3.

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

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"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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'Stimming' and autism: an insiders perspective

"Autistic adults highlighted the importance of stimming as an adaptive mechanism that helps them to soothe or communicate intense emotions or thoughts and thus objected to treatment that aims to eliminate the behaviour."

So said the findings reported by Steven Kapp and colleagues [1] (open-access available here) who analysed the viewpoints of around 30 autistic adults (or adults with autism if you prefer) on the topic of self-stimulatory behaviour 'reclaimed' as stimming. Said participants aged between 21 and 56 years old, were recruited "through residential homes specialising in housing autistic adults, a training centre for autistic adults and existing networks." All were formally diagnosed with autism; something that might be particularly important when it comes to the specific patterns of behaviour under study (see here).

Before proceeding, a question: What is stimming? Well, I found one particularly good article describing stimming (see here) as something that "somebody is doing... to give themselves sensory input." In clinical terms, stimming falls under the category of repetitive behaviours, and covers quite a wide array of presentations ranging from flicking fingers in front of the eyes, to more pronounced body movements such as rocking, jumping or walking on tiptoes (see here) and lots more in-between. The source website describing stimming that I just highlighted also lists "banging one’s head on the floor" as a stim; something I'll come on to shortly.

"Autistic people have become increasingly mobilised and vocal in defence of stimming" is an important starting point raised in the Kapp paper, as some "believe that stims may serve as coping mechanisms, thus opposing attempts to eliminate non-injurious forms of stimming." Not surprisingly accompanying such sentiments, Kapp et al identified a couple of primary themes garnered from their interviews of said study participants: "stimming as (1) a self-regulatory mechanism and (2) lacking in social acceptance, but can become accepted through understanding." Important stuff.

There are a couple of 'issues' that interrupt the important messages presented by Kapp, as 'psychobabble' seemingly creeps into some of the text. For example: "Several participants internalised the stigmatisation of stimming, with ambivalent attitudes despite recognising the utility of their stims." Internalised stigma? What exactly does that mean and how was it objectively tested for? As I said psychobabble. I also note that there is a hint of a socio-political side to the Kapp paper, as per quotes like the findings "suggest that many autistic adults agree with the neurodiversity movement’s opposition to eliminating all forms of stimming across all contexts (e.g. traditional uses of early intensive behavioural intervention) and desire for society to accept non-harmful forms of stimming." This in the context that some people on the autism spectrum have for example, voiced concerns about the use of techniques such as applied behavioural analysis (ABA) in the context of autism, and the accusation that "they basically condition them like Pavlov’s dogs to stop stimming." I'm not so sure that every single occasion when ABA or other intensive behavioural intervention is used in the context of autism is quite that forthright in their aims and objectives (i.e. stopping all stimming), but ho-hum. And whist I've mentioned the concept of neurodiversity, well, let's just say that such a movement is still seemingly very much in its infancy on lots of different matters (see here).

What else? Well in amongst the various good points raised in defence of stimming, another side to such behaviour is also discussed in the Kapp paper: harms. So: "Participants gave several examples of stimming behaviours that caused physical harm to themselves (with no evidence of intentional self-injury), which they did not find helpful, regardless of social context." It's important that this side of stimming is discussed as per my previous mention of head-banging. I say this also because stimming might not just solely be a self-stimulatory behaviour but rather also reflective of various other processes too [2] including "stimming caused by uncontrollable thoughts." If one for example assumes that stress and anxiety (something which may be a lot more 'core' to autism than hitherto reported) are part-and-parcel of some stimming behaviours used on some occasions, the logical next step is to ask what is being done to address something like anxiety as a possible trigger. Again minus any psychobabble, there are further studies that could be undertaken (see here). And as for the notion that there is "potential evidence of the spread of the movement through the report of teaching oneself how to stim via online resources" well, let's just say that someone, somewhere making such 'online resources' probably doesn't have a great understanding of the wide (wide!) complexity surrounding stimming...

The Kapp paper provides an important [autistic] perspective on stimming. It suggest that as part of a core feature of autism, stimming should not always be viewed as a 'negative thing' provided that it does not harm or significantly interfere with a person's quality of life or that of others. As per the possibility of an 'anxiety link' to some stimming, one also needs to recognise that the presence of stimming might be reflective of some unmet need and make any possible (reasonable) adjustments. And if you happen to see someone rocking or flapping their hands in a public place, don't stare, don't snigger, and as long as they don't seem to be in distress or causing any distress, just let them be...

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[1] Kapp SK. et al. 'People should be allowed to do what they like': Autistic adults' views and experiences of stimming. Autism. 2019 Feb 28:1362361319829628.

[2] Cunningham AB. & Schreibman L. Stereotypy in Autism: The Importance of Function. Res Autism Spectr Disord. 2008;2(3):469-479.

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"The most common peri-onset events reported by subjects were infection-related episodes (64%)"

The quote titling this post - "The most common peri-onset events reported by subjects were infection-related episodes (64%)" - comes from the (open-access) findings reported by Lily Chu and colleagues [1] continuing something of a research theme from this authorship group examining myalgic encephalomyelitis/ chronic fatigue syndrome (ME/CFS) (see here).

Indeed, it's probably no coincidence that the Chu cohort of "150 subjects fitting Fukuda 1994 CFS criteria" is the same as that used in their other research [2] when discussing another important issue: "post-exertional malaise in myalgic encephalomyelitis/ chronic fatigue syndrome."

On this most recent publishing occasion, Chu et al set out to: "Describe ME/CFS onset and course in one United States-based cohort." They did this via the use of "a detailed survey" that asked various questions about the first stages of participants' illness and what this eventually led to. The results obtained weren't exactly unexpected, but yet again stress how lots of things 'assumed' about ME/CFS really need to be properly verbalised in the peer-reviewed science literature (see here and see here for other examples). Of particular note in the Chu findings pertinent to inquiry on the 'course' of ME/CFS is this important snippet of information: "Based on available data, the median age of illness onset was 36.6 ± 12.3 years and median duration of illness was 12.5 ± 10.1 years." That's 'median duration of illness was 12.5± 10.1 years'.

Results: "The most common peri-onset events reported by subjects were infection-related episodes (64%), stressful incidents (39%), and exposure to environmental toxins (20%)." Infection or rather 'infection-related episodes' came out top of the pops with regards to possible onset events. I've said 'possible onset events' in that last sentence not to be belittle the first-hand reports obtained, but rather to emphasise how we're still in a bit of a 'not knowing' state when it comes to definite causative infective agents and ME/CFS onset. Yes, there is some quite strong evidence that infections caused as a result of Epstein–Barr virus (EBV) seem to be involved in some cases of ME/CFS (see here) but more often that not, people aren't screened for every possible viral or bacterial agent. At this point, I'd also hark back to the viral 'hit-and-run' hypothesis that has been talked about in some ME/CFS circles recently (see here and see here) and what this also means.

Onward: "For the overwhelming majority of patients (96%, n = 141), their illness did not improve with time although different patterns of illness were seen." That last sentence really speaks for itself in terms of what ME/CFS means in the long-term. That's not to say that symptoms did not 'fluctuate' - "59%, fluctuating (symptoms could change in severity but were always present)" - but participants on the whole did not 'shake off' their disability. And when it came to some details about how symptoms ebbed and flowed over the course of time, Chu et al have some data on that too: "Over time, flu-like symptoms, fatigue, unrefreshing sleep, and exertion-related items decreased the most, by between 12 and 25%... Cognitive symptoms present at the beginning of the illness tended to persist, declining by only 4–10%." Further focus on 'cognitive symptoms' is perhaps important [3].

Further: "Ninety-seven percent suffered from at least one other illness: anxiety (48%), depression (43%), fibromyalgia (39%), irritable bowel syndrome (38%), and migraine headaches (37%) were the most diagnosed conditions." The authors phrase this in the context that "patients with co-morbid medical or psychiatric conditions are the rule rather than the exception" when it comes to ME/CFS. But just before anyone starts making noises that anxiety and depression are so significantly present in this cohort and probably beyond, such findings does not open the door to any psychobabble 'biopsychosocial' (BPS) explanations about the cause/perpetuation of ME/CFS. I think many patients (and researchers) have had quite enough of all that (see here).

The Chu paper is a comprehensive one and adds to our knowledge about ME/CFS. It has its limitations - "reliance on subject self-report, recall bias, and relative superficiality of some survey items" - but no more or less than lots of other ME/CFS research. It hopefully will open the door to a lot more similar study; perhaps also including the odd biological measure also.

And just before you go, I'll draw your attention to the findings reported by Katherine Rowe [4] who also asked a cohort of participants with ME/CFS about their illness experiences. There's a few important matching details included in the paper - "Eighty percent reported a defined onset following an infection" - but also some other noteworthy information. One such observation was that: "Many indicated the need to be sensitive about when psychological assistance is offered... They were sensitive as to whether this was implying that psychological issues were the “cause.”." It's not difficult to see why patients with ME/CFS would think such [BPS] things.

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[1] Chu L. et al. Onset patterns and course of myalgic encephalomyelitis/ chronic fatigue syndrome. Front. Pediatr. 2019. Jan 16.

[2] Chu L. et al. Deconstructing post-exertional malaise in myalgic encephalomyelitis/ chronic fatigue syndrome: A patient-centered, cross-sectional survey. PLoS One. 2018;13(6):e0197811.

[3] Robinson LJ. et al. Impairments in cognitive performance in chronic fatigue syndrome are common, not related to co-morbid depression but do associate with autonomic dysfunction. PLoS One. 2019 Feb 5;14(2):e0210394.

[4] Rowe KS. Long Term Follow up of Young People With Chronic Fatigue Syndrome Attending a Pediatric Outpatient Service. Front Pediatr. 2019 Feb 21;7:21.

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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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"A high prevalence of disordered eating in individuals with ADHD was observed"

The quote heading this post - "A high prevalence of disordered eating in individuals with ADHD [attention-deficit hyperactivity disorder] was observed" - comes from the study results published by Louis Jacob and colleagues [1].

Drawing on information derived from the 2007 Adult Psychiatric Morbidity Survey (APMS) here in Blighty (an initiative that has been talked about previously on this blog), researchers looked at the data for 'screened for' ADHD signs and symptoms using the Adult ADHD Self-Report Scale (ASRS) Screener as well as data derived from "the five-item SCOFF screening instrument" relevant to eating disorders (ED) completed by over 7000 adults.

Researchers reported that: "The prevalence of possible eating disorder (ED) was much higher among those with ADHD symptoms (ASRS score ≥14) compared to those without ADHD symptoms (19.2 vs. 5.7%)." They also noted that issues such as anxiety and the presence of borderline personality disorder (BPD) also might have an important influence on disordered eating as measured by the SCOFF. ADHD plus anxiety linked to a heightened increased risk of another condition presenting? I've heard that before (see here).

Accepting the fact that use of the ASRS in initiatives such as the APMS is not without potential 'limitations' (see here), and the important word 'possible' when it comes to the presence of an eating disorder based on SCOFF results alone, these are potentially important results. I say that on the basis that a connection between food/diet and ADHD has a long history from many different perspectives (see here and see here and see here for examples). I should also add that this is not the first time that ADHD and eating disorders have been talked about in the peer-reviewed research literature (see here and see here).

Other implications aside from the potential need for preferential screening for eating disorders as and when ADHD or ADHD-type behaviours feature? Well, I'd be minded to suggest that including another label/diagnosis/constellation of symptoms into future research proceedings might be useful. I speak of autism or autistic traits and the ideas that: (i) autism and ADHD occurring together is not unheard of (see here) and (ii) there is some increasing interest regarding the presence of autistic traits in relation to those diagnosed with an eating disorder (see here and see here).

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[1] Jacob L. et al. Attention deficit hyperactivity disorder symptoms and disordered eating in the English general population. Int J Eat Disord. 2018 Sep 6.

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"Greater ADHD symptom severity was associated with higher odds for feeling less happy"

Of course correlation does not necessarily equal causation, but the *correlative* results published by Andrew Stickley and colleagues [1] observing that: "Greater ADHD [attention-deficit hyperactivity disorder] symptom severity was associated with higher odds for feeling less happy" were worthy of some blogging attention.

Drawing on data derived from the 2007 Adult Psychiatric Morbidity Survey based here in Blighty, researchers tackled quite an important question: how do ADHD signs and symptoms potentially impact on happiness?

So: "Information was collected on ADHD symptoms using the Adult ADHD Self-Report Scale (ASRS) Screener, while happiness was assessed with a single (3-point) measure." Including data for over 7000 people - adults aged 18 years and over - researchers observed that important negative relationship between ADHD symptoms and happiness. Alongside, they also noted that various other variables might also play a role in such a [correlative] relationship: "Mood instability (percentage mediated 37.1%), anxiety disorder (35.6%) and depression (29.9%) were all important mediators of the association between ADHD and happiness."

I'm a great believer that we need more of this kind of research asking relatively simple questions about whether someone is happy or not across various different labels and combinations of labels. I reiterate the whole 'correlation does not necessarily equal causation' mantra and the fact that happiness is not a 'setting' switched to the on position every moment of someones life. One also has to be slightly careful about extrapolating the Stickley results to diagnosed ADHD, and the various issues that come with such a diagnosis (including enhanced risk of comorbidity or 'symptoms' of other diagnostic labels).

But it strikes me as 'logical' that the manifestation of certain types of behaviour - hyperactivity, inattentiveness, impulsivity - might not be all that great for a person when it comes to perceived happiness at certain points in life. I say this in the context that a diagnosis of ADHD has already been *linked* to quite a few adverse life events (see here) including some enhanced risk for something like suicidality (see here). One has to wonder therefore, what role happiness might play in the context of such extremes of behaviour, and whether intervention 'for ADHD' (whatever form this might take) might have some important effects on subjective and objective markers of happiness alongside the manifestation of signs and symptoms...

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[1] Stickley A. et al. Attention-deficit/hyperactivity disorder symptoms and happiness among adults in the general population. Psychiatry Res. 2018 May 5;265:317-323.

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The headline: "One in nine young people in Scotland have attempted suicide"

I have to say that I drew a sharp intake of breath when I read the media headline titling this post - "One in nine young people in Scotland have attempted suicide" - based on the findings reported by Rory O'Connor and colleagues [1]. The idea that, from a sample of some 3500 young people in Scotland, some 10% and 15% of respondents to the questions: "Have you ever made an attempt to take your life, by taking an overdose of tablets or in some other way?’ and ‘Have you ever deliberately harmed yourself in any way but not with the intention of killing yourself? (i.e. self-harm)" answered in the affirmative, seemed pretty important. Not least with the question 'why?' in mind.

OK, media headlines aside, the O'Connor findings require some dissection. The reasoning behind studying this issue was not only to look at the very complicated topic of suicide in a part of the UK (Scotland) that authors write "has a higher suicide rate than England", but also to try and understand how non-suicidal self-injury (NSSI) or non-suicidal self-harm (NSSH) presents in young adults and whether there is something important linking NSSH and suicidal thoughts and/or attempts.

The participant group was drawn from "a representative sample of young people aged 18–34 years from across Scotland" who were recruited to the Scottish Wellbeing Study. Lots of measures were completed by participants as part of the wider study initiative but we are told that "only the prevalence of NSSH and suicide attempts information is reported" in the O'Connor article on this occasion. I might also add that participants were compensated to the tune of £25 (pounds sterling) for their time and participation.

Alongside those headline findings on self-reported attempted suicide and self-harm, a few other important trends were observed. So: "More than 20% reported lifetime suicidal thoughts, 2.4% reported that they last thought about suicide in the past week and 10.4% reported they last thought about suicide in the past 12 months." Around 6% of respondents reported that they had both attempted suicide and also engaged in self-injury suggesting that professionals should "routinely enquire about history of self-injurious behaviour, especially as past behaviour is such a strong predictor of suicide." Also: "Earlier age at NSSH or suicide attempt onset was associated with more frequent lifetime NSSH and suicide attempts." And finally: "The prevalence of NSSH and suicide attempts was significantly higher among those classified as unemployed... and economically inactive... compared with those who were employed." Age, societal and environmental factors seem to play some roles too.

Then to another important set of questions: (a) why? and (b) what can be done to reduce these headline-grabbing statistics? Well, there are no easy answers to such questions I'm afraid. The authors do note that: "From a public health perspective, the unemployment and economic inactivity findings are noteworthy" and perhaps suggest that there are some modifiable variables that could influence suicidal thoughts and/or actions focused on getting people into employment and the benefits that this brings (wide-ranging benefits by all accounts). But this probably only covers one side of the issue, as discussions inevitably turn to what role psychiatric and/or behavioural comorbidity might play in such reporting (see here and see here and see here) and whether there may be a need for (a) something like enhanced screening for suicidal thoughts or other 'risks' among selected populations and/or (b) the [careful] use of 'preventative' strategies in such cases (see here and see here). I say all that accepting that diagnoses around mental health probably play an important role in suicide-related behaviours but are not necessarily a pre-requisite...

As always, there is always someone to talk to if needed...

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[1] O'Connor RC. et al. Suicide attempts and non-suicidal self-harm: national prevalence study of young adults. BJPsych Open. 2018; 4: 142-148.

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Mood cognition, fatigue, musculoskeletal, gastrointestinal and dermatological symptoms make up Gulf War Syndrome

The results of the meta-analysis by Alexis Maule and colleagues [1] provide an important addition to the peer-reviewed literature on Gulf War Syndrome / Illness (GWS). Their detailing and combining of results from various studies looking at self-reported health symptoms among deployed troops during the Persian Gulf War of 1990 adds further credence to the range of symptoms reported by returning troops. Also, they provide further clues as to where science should continue to look and intervene to help our veterans.

I've talked about the Persian Gulf War and GWS a few times before on this blog (see here and see here and see here for examples). Described in some quarters as one of the most toxic wars in history, there are still many questions that require answering about why so many veterans returned from theatre in such poor health. Much like another quite nebulous condition very often confused with other diagnoses under the heading 'medically unexplained symptoms' (see here), the relative lack of knowledge about GWS has made the condition / constellation of symptoms fertile ground for various 'psychosomatic explanations'. This, I believe, has done, and continues to do, a real disservice to the veterans of this conflict and their loved ones.

Maule et al settled on some 21 published studies, including nearly 130,000 participants and covering almost 30 years of research (the war itself started in late 1990) where self-reported symptoms were compared "in GW-deployed veterans and GW-era control veterans." GW-deployed veterans were defined as "veterans who deployed to the Gulf area in support of the 1990–1991 GW." Their comparators were described as "non-deployed veterans or veterans serving in the military during the 1990–1991 GW period who deployed to areas other than the Gulf (eg, Germany, Bosnia)." Reported health symptoms were searched for and responses boiled down across the studies.

Results: "A total of 56 distinct health symptoms were reported in three or more studies and included in the meta-analysis." Of the various health symptoms reported, 'lacking energy' topped the frequency chart for deployed veterans, fairly closely followed by related issues such as 'fatigue' and 'unrefreshing sleep'. When classifying reported health symptoms together, the following categories emerged: mood-cognition, fatigue, musculoskeletal, gastrointestinal and dermatological symptoms. Further: "Results of the meta-analysis showed GW-deployed veterans had increased odds of reporting all of the analysed symptoms compared with GW-era controls, indicating that the health problems associated with GW deployment include widespread, multiple body symptoms."

The authors do caution that it is not possible to say that all of these symptoms are cardinal features of GWS insofar as their inability "to assess the effect of some covariates relevant to health symptom reporting (eg, post-traumatic stress disorder and specific deployment exposures)." They also talk about how their meta-analysis approach, similar to other occasions across various different topics, may also be liable to publication bias ("when studies with positive findings are more likely to be published than studies with null and/or negative findings"). They did try and 'correct' for this possible bias and still reported that "42 out of the 56 summary ORs [odds ratios] remained significant." That included all those 'fatigue-related' health items previously reported on.

The work from Maule and colleagues adds to a significant research base observing that poorer health outcomes seem to be an important part of deployment to the Persian Gulf during Operation Desert Storm [2]. It again reminds us that we owe a debt to those veterans and their families, to continue to pursue a research agenda that takes their health issues seriously, and provides them with answers and the relief that many still sorely need.

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[1] Maule AL. et al. Meta-analysis of self-reported health symptoms in 1990–1991 Gulf War and Gulf War-era veterans. BMJ Open. 2018; 8: e016086.

[2] Porter B. et al. Health Status of Gulf War and Era Veterans Serving in the US Military in 2000. J Occup Environ Med. 2018 Jan 24.

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More evidence for the 'anti-aggression' effect of fish oils?

"In conclusion, this experiment indicates that Omega-3 administration has beneficial effects in reducing aggression among the general population."

So concluded the study by Laurent Bègue and colleagues [1] potentially adding to other research suggesting that fish oils - omega 3 fatty acids including docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) - might have something of an interesting effect on aggression and violence in various contexts (see here).

Based on a "double-blind randomized trial" design, nearly 200 participants with seemingly no current clinical psychiatric issues were allocated to receive a daily omega-3 fish oil supplement or placebo ("copra oil") over a 6-week period. Self-reported aggression was measured before and after receipt of the active supplement or placebo. Bearing in mind that both researchers and participants were blinded to who was taking what, the self-reports for those taking the daily fish oil supplement suggested that they thought/reported themselves less aggressive at the end of the study compared with the beginning. Ergo, fish oils supplements might, in some part, *act* on self-reported aggression, bearing in mind that self-report may not be the only way to assess for something like aggression.

As per my previous blogging foray into this topic, there is a surprising amount of peer-reviewed research that has been done on the topic of fish oils and aggression [2]. Don't get me wrong, the science is not yet in any position to conclusively suggest that fish oils should be approved for reducing aggression and/or violence at a population level, but there are some glimmers that an effect may be present at least for some. Other, related investigations talking about a negative correlation between circulating blood omega-3 levels and various aspects of aggression [3] add to the 'correlative' evidence base in this area.

There are a myriad of reasons why people are aggressive that are probably going to be different in different occasions and in different environments. These range from the effect(s) of something like impulsiveness in reactive aggression to the often negative influence of things like drugs and/or alcohol or even as a possible manifestation of certain psychopathology. One also needs to understand that aggression is not always a negative thing as anyone who participates in combat sports for example, will testify.

There is likely no single 'quick fix' to such feelings and/or behaviours when undesirable, despite the strong need and want for such intervention(s) (although there are some glimmers of hope in the peer-reviewed domain). Bearing in mind however, that affecting aggression might be just one part of the fairly beneficial profile related to fatty acid supplement use, I'm fast approaching a position whereby the overall picture of fatty acid use is favouring 'beneficial' for many people over 'adverse'. If aggression is similarly [positively] affected, and given the relative in-expense and wide availability of such fatty acid supplements, the emphasis switches towards putting up logical arguments on why such supplements shouldn't be used rather than why they should...

To close, here's hoping...

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[1] Bègue L. et al. Omega-3 supplements reduce self-reported physical aggression in healthy adults. Psychiatry Research. 2018; 261: 307-311.

[2] Gajos JM. & Beaver KM. The effect of omega-3 fatty acids on aggression: A meta-analysis. Neurosci Biobehav Rev. 2016 Oct;69:147-58.

[3] Meyer BJ. et al. Baseline omega-3 index correlates with aggressive and attention deficit disorder behaviours in adult prisoners. PLoS One. 2015 Mar 20;10(3):e0120220.

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Maternal immune history and autism (social) symptom severity

"Pregnant mothers' asthma and allergies linked to more severe autism in their children" went one of the media headlines discussing the findings reported by Patel and colleagues [1]. Drawing on data derived from the "Western Australian Autism Biological Registry (WAABR)" researchers set out to examine whether "having an immune or autoimmune-driven MIA [maternal immune activation] is associated with increased severity of ASD [autism spectrum disorder] symptoms for the child."

The conclusions arrived at: "a positive immune history (allergies or asthma) was associated with increased severity of social symptoms in child." Said data derived from 220 families/children who were quizzed about "the medical history of the biological mother, where details regarding any diagnosed illnesses or chronic conditions were reported, along with age of any diagnosis" alongside the use of more direct measures to ascertain autistic traits in children: Autism Diagnostic Observation Schedule-Generic (ADOS-G) and the Social Responsiveness Scale (SRS).

One obviously has to be a little cautious about such results where the study was conducted 'retrospectively' and what this could mean in terms of recall [2] (although, I hasten to add, other studies of maternal recall vs. medical records in the context of autism are actually quite promising). That no objective confirmation of the presence of allergy or autoimmune disease via direct testing for example, were included in this publication is also something to be a little careful about (I'm pretty sure however, someone would know if they had received a diagnosis of coeliac disease or not for example).

So what do the results mean and what are the implications? Well, MIA - maternal immune activation - in the context of offspring autism risk is not something new (see here and see here for examples) as the authors mention in their paper. Added to work talking about how inflammation, a process that is part-and-parcel of immune function, might have the ability to 'affect' social cognitive processing (see here) one might see further evidence for how the immune system seems to be doing quite a bit more than just protecting us from the odd pathogen or two. This might be particularly relevant during pregnancy; a time when a reprogrammed immune system is in place to prevent mum's body from 'rejecting' the developing foetus and associated systems.

"Findings support the role of an immune system-mediated subtype in ASD, which may be driven by MIA and changes in levels immune markers. Identification of such a subtype in ASD will enable more streamlined diagnosis and management in clinical environments." Yes, alongside acknowledgement that there may be an 'immune phenotype' of autism (see here), the authors do mention the potential future use of "immune-modulating pharmacotherapies" in the context of the growing evidence base for MIA and risk of offspring autism. Such options are already being explored in the animal research domain as per those findings from Vuillermot and colleagues [3] and how "early dietary supplementation with vitamin D may open new avenues for a successful attenuation or even prevention of neurodevelopmental disorders following maternal inflammation during pregnancy." Vitamin D and autism is already quite a hot topic (see here for example). And things don't just stop at vitamin D neither (see here for another example) as further investigations are warranted with the hope that children with possible 'MIA autism' (if I can use that term) are "able to function and integrate into the world... [and] have a level of independence" required to do so successfully (and of course, happily).

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[1] Patel S. et al. Social impairments in autism spectrum disorder are related to maternal immune history profile. Molecular Psychiatry. 2017. Oct 10.

[2] Ozonoff S. et al. Reliability of parent recall of symptom onset and timing in autism spectrum disorder. Autism. 2017 Sep 1:1362361317710798.

[3] Vuillermot S. et al. Vitamin D treatment during pregnancy prevents autism-related phenotypes in a mouse model of maternal immune activation. Mol Autism. 2017 Mar 7;8:9.

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Self-reported sexual attraction and autism

The findings reported by Tamara May and colleagues [1] are discussed today, looking at self-reported sexual attraction and past sexual relationships among adolescents diagnosed with an autism spectrum disorder (ASD) compared with not-autism controls.

Asking 14-15 year olds who took part in The Longitudinal Study of Australian Children (94 diagnosed with autism and some 3400 controls) some rather personal questions, researchers reported that: "ASD males reported fewer prior boyfriends/girlfriends" and "female adolescents with ASD have differences in sexual attraction compared with non-ASD females." Those female 'differences' included things like greater "uncertainty in attraction" and "lower rates of heterosexual preference."

Minus sweeping generalisations, the use of self-report in this study is a bit of a bonus in this context. Quite a few times on this blog I've been a little critical when self-report is used in the context of autism research (i.e. not necessarily as objective as some of the schedules out there administered by trained professionals) but when it comes to aspects of sexuality and relationships, it is the person who most definitely knows best [2]. If I did have one slight issue with this work it would be to ask the question: how representative of the autism spectrum were the participant group included for study? Y'know, self-report implies language use and all that...

This work does continue a theme in autism research. Although perhaps seemingly obvious, it confirms a few important things; primarily that young adults on the autism spectrum are in the most part, interested in sex and relationships [3] (accepting that 'sex' and 'relationships' are not necessarily one and the same). I know for some this is not new news (see here) but such a finding can sometimes get lost in all the chatter about presenting symptoms, challenges and the like when it comes to the autism spectrum.

Insofar as the finding that females with ASD included in the May cohort were more likely to report lower rates of heterosexual preference and higher rates of bisexuality, this is not a new finding. Bejerot & Eriksson [4] previously reported that "tomboyism and bisexuality were overrepresented amongst women with autism spectrum disorder" (not that tomboyism is necessarily a measure of bisexuality). Other groups have also mentioned this finding too [6]. This could have implications for things like sex education and ensuring that sex education covers 'all the bases' in terms of the spectrum of sexuality. I also draw back from making too many links with the literature for example, on gender dysphoria and autism / autistic traits (see here) but I daresay this might also show also some importance, at least for some.

Sex and relationships are an integral part of growing up. Children on the autism spectrum [typically] grow up to be adults on the autism spectrum, and sex - thoughts, feelings, actions - will figure as part of that maturation process, the same as it does for everyone else. Providing comprehensive and tailored sex education [5] should be an important part of discussions; parents as well as educators, need to be in on those important discussions...

Noting the date today (May the 4th), a customary link is required.

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[1] May T. et al. Brief Report: Sexual Attraction and Relationships in Adolescents with Autism. J Autism Dev Disord. 2017 Mar 24.

[2] Dewinter J. et al. Parental Awareness of Sexual Experience in Adolescent Boys With Autism Spectrum Disorder. J Autism Dev Disord. 2016 Feb;46(2):713-9.

[3] Fernandes LC. et al. Aspects of Sexuality in Adolescents and Adults Diagnosed with Autism Spectrum Disorders in Childhood. J Autism Dev Disord. 2016 Sep;46(9):3155-65.

[4] Bejerot S. & Eriksson JM. Sexuality and gender role in autism spectrum disorder: a case control study. PLoS One. 2014 Jan 31;9(1):e87961.

[5] Ingudomnukul E. et al. Elevated rates of testosterone-related disorders in women with autism spectrum conditions. Horm Behav. 2007 May;51(5):597-604.

[6] Hannah LA. & Stagg SD. Experiences of Sex Education and Sexual Awareness in Young Adults with Autism Spectrum Disorder. J Autism Dev Disord. 2016 Dec;46(12):3678-3687.

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May T, Pang KC, & Williams K (2017). Brief Report: Sexual Attraction and Relationships in Adolescents with Autism. Journal of autism and developmental disorders PMID: 28342163

Is screen time a risk factor for ADHD?

The findings reported by Vivien Suchert and colleagues [1] observing that "screen time, but not other non-screen-based sedentary activities should be considered as being a risk factor for ADHD [attention-deficit hyperactivity disorder]" taps into long-running debates on whether our societal obsession with watching, clicking and swiping might not be 'a totally positive thing' when it comes to psychological development, health and wellbeing.

Yes, I know this is a complicated area full of big personalities, sweeping generalisations, half-truths and soundbites (see here for example). But I talk about peer-reviewed science on this blog, and am dealing with presented evidence specifically looking at the issue of screen time and ADHD on this particular occasion.

So, taking a not insignificant sample number of over 900 young adults aged 13-17 years old, researchers assessed various parameters in relation to "screen-based and non-screen-based sedentary behavior and ADHD symptoms." When I say 'assessed', immediately one potentially big issue stands out when it comes to measures of sedentary behaviour used in the study and the inclusion of the questionnaire method over and above the use of more objective measures such as physical activity monitors (see here). No mind, researchers analysed the collected data and determined a few key observations not least that: "Screen time was related to the total ADHD score (p < 0.001) as well as to the subscales inattention (p ≤ 0.016) and hyperactivity/impulsivity (p ≤ 0.008)." Further: "Sedentary time without screens was virtually not associated with ADHD."

OK, to reiterate sweeping generalisations are not required on the basis of these results alone. There are a myriad of other methodological issues outside of just objective measures of sedentary behaviour that could skew the Suchert results and these should be taken into consideration. But set in the context that this is not the first time that screen use has been *corrrelated* with something like ADHD or ADHD-type behaviours [2] (or indeed the second time [3]) I'm minded to suggest that quite a more investigation is indicated. Of course, there are other factors to include in the research mix. The findings reported by Tong and colleagues [4] are potentially pertinent: "children with ADHD symptoms were likely to spend more time using a computer during school days; they were also more likely to eat while using a computer." This implies that ADHD or ADHD-type behaviours might predispose to increased screen time rather than the other way around. The relationship is likely to be complex.

In terms of the potential 'hows and whys' of any connection between screen time and ADHD-type behaviours, well, there are already some clues. I'd perhaps suggest that the effects of screen time on sleep could be a good place to start given other peer-reviewed research clues [5]. The relationship between sleep and ADHD is a complicated one, but it is known that sleep interventions can [modestly] affect the presentation of some ADHD behaviours (see here). There are no doubt other research avenues worth looking into also.

Should anyone act on the Suchert findings as they stand? Well, I don't do medical or clinical advice on this blog but I'm minded to suggest that some sensible advice provided by others might come into play: "No screens in the child’s bedroom. Pay attention to the content of the games, especially to violence. Set limits on screen time, and look for other ways to manage family interactions." With my 'what if' research hat on, I am also wondering whether the rise and rise of screens and screen time in the context of autism might also need some particular research examination, in light of the idea that autism and ADHD is not an unfamiliar diagnostic combination (see here)...

To close, although perhaps most famous as a 'rat tickler', the passing away of Jaak Panksepp a few days back deserves mention given his notable ideas about autism and the influence they had and continue to have...

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[1] Suchert V. et al. Relationship between attention-deficit/hyperactivity disorder and sedentary behavior in adolescence: a cross-sectional study. Atten Defic Hyperact Disord. 2017 Apr 4.

[2] Chan PA. & Rabinowitz T. A cross-sectional analysis of video games and attention deficit hyperactivity disorder symptoms in adolescents. Ann Gen Psychiatry. 2006 Oct 24;5:16.

[3] Montagni I. et al. Association of screen time with self-perceived attention problems and hyperactivity levels in French students: a cross-sectional study. BMJ Open. 2016 Feb 26;6(2):e009089.

[4] Tong L. et al. Attention-Deficit/Hyperactivity Disorder and Lifestyle-Related Behaviors in Children. PLoS One. 2016 Sep 22;11(9):e0163434.

[5] Engelhardt CR. et al. Media use and sleep among boys with autism spectrum disorder, ADHD, or typical development. Pediatrics. 2013 Dec;132(6):1081-9.

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Suchert V, Pedersen A, Hanewinkel R, & Isensee B (2017). Relationship between attention-deficit/hyperactivity disorder and sedentary behavior in adolescence: a cross-sectional study. Attention deficit and hyperactivity disorders PMID: 28378132

Diagnosing ME/CFS the machine learning way?

In today's post I want to draw your attention to the findings reported by Diana Ohanian and colleagues [1] (open-access available here) talking about "the use of machine learning to further explore the unique nature"of various conditions/labels including those typically headed under the label of chronic fatigue syndrome / myalgic encephalomyelitis (CFS/ME).

Including one 'Jason LA' on the authorship list, researchers set about looking at "what key symptoms differentiate Myalgic Encephalomyelitis (ME) and Chronic Fatigue syndrome (CFS) from Multiple Sclerosis (MS)."You may be wondering why such a comparative study was undertaken but a quick trawl of the research literature reveals that these different clinical labels may well have some important commonalities [2].

This was an internet-based research project whereby "106 people with MS and 354 people with ME or CFS fully completed the [DePaul Symptom Questionnaire] questionnaire" and based on the responses received "decision trees were used to determine what symptoms differentiated those with MS from those with ME or CFS." Decision trees, as the name suggests, is a statistical technique where binary (0 or 1, no or yes) choices make branches and: "At each branch the computer decides what symptom would best predict classifications, in this case whether someone has MS or ME or CFS." This process continues and continues through the different levels of branches "until the tree reaches a balance between classification accuracy and generalizing to new data." Such a machine learning tool has been previously discussed quite recently on this blog (see here).

Results: "Five symptoms best differentiated the groups." These were: flu-like symptoms, tender lymph nodes, alcohol intolerance, inability to tolerate upright position and next day soreness after strenuous activity. The first two symptoms - flu-like symptoms and tender lymph nodes - were pretty good by themselves at correctly categorising MS or CFS/ME (~80% correct). Indeed, these seemed to be the core differentiators that were examined and as the authors note: "The most important two symptoms that differentiated MS versus ME or CFS existed within the immune domain."

Of course further investigations are warranted to potentially build on these findings. One has however to be slightly cautious about the use of the internet and social media when undertaking such research, especially when very little information about the formal diagnoses of participants is included in the current paper. This is a particular issue when it comes to CFS/ME and the various ways that it can be defined and diagnosed [3].

Still, I can't quibble with the continued rise and rise of machine learning being applied to many areas of medicine, and not before time that it starts to reach ME/CFS. And just before I go, it appears that the research team at DePaul University have been quite busy...

To close, on what retiring Presidents of the USA should do next. I think I would go with George Washington and his whisky business... 🍻

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[1] Ohanian D. et al. Identifying Key Symptoms Differentiating Myalgic Encephalomyelitis and Chronic Fatigue Syndrome from Multiple Sclerosis. Neurology (ECronicon). 2016;4(2):41-45.

[2] Morris G. & Maes M. Myalgic encephalomyelitis/chronic fatigue syndrome and encephalomyelitis disseminata/multiple sclerosis show remarkable levels of similarity in phenomenology and neuroimmune characteristics. BMC Medicine. 2013; 11: 205.

[3] Jason LA. et al. Case definitions integrating empiric and consensus perspectives. Fatigue. 2016;4(1):1-23.

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Ohanian D, Brown A, Sunnquist M, Furst J, Nicholson L, Klebek L, & Jason LA (2016). Identifying Key Symptoms Differentiating Myalgic Encephalomyelitis and Chronic Fatigue Syndrome from Multiple Sclerosis. Neurology (E-Cronicon), 4 (2), 41-45 PMID: 28066845