Thursday, 24 May 2018

"Lonely young adults in modern Britain"

"Lonelier young adults were more likely to experience mental health problems, to engage in physical health risk behaviours, and to use more negative strategies to cope with stress."

Those were some of the conclusions reached in the study published by Timothy Matthews and colleagues [1] who relied on data from the "Environmental Risk (E-Risk) Longitudinal Twin Study, which tracks the development of a birth cohort of 2232 British children" to "examine the profile of loneliness in a prospective, contemporary, nationally representative cohort of 18 year-olds living in the UK." The specific focus was on how loneliness might impact on various domains: "mental health, physical health and health risks, coping and functioning, and career prospects."

Results: first and foremost, when it came to the question(s) of loneliness, and the prevalence of loneliness as measured by the UCLA Loneliness Scale, Version 3, "23–31% of participants reported experiencing any of these feelings ‘some of the time’, and 5–7% reported feeling them ‘often’." Sex/gender and socio-economic status did not seem to show any statistically significant relationship to reports on loneliness.

In terms of possible or actual psychopathology, we are told that: "Lonelier 18 year-olds were more likely to meet diagnostic criteria for depression, anxiety, ADHD [attention-deficit hyperactivity disorder], conduct disorder, alcohol and cannabis dependence, to have self-harmed, and to have attempted suicide." Depression and anxiety came out with the strongest *association* in relation to loneliness, and insofar as the 'attempted suicide' bit, I'm wondering whether it may tie into other recent quite shocking findings (see here). Researchers also noted that: "lonelier individuals engaged in less day-to-day physical activity and were more likely to be daily smokers."

Whilst realising that the various associations mentioned in the context of loneliness do not necessarily tie directly into loneliness (e.g. loneliness does not necessarily 'cause' anxiety and depression or indeed, vice-verse), these are important results. They add to a bank of peer-reviewed research which suggests that loneliness - chronic loneliness - is probably not great for anyone (see here). They also observe that increasing social contact with others, whilst not without benefits, is not necessarily all that can be done to combat this state and it's rather negative correlations.

And it is perhaps timely that at the time of writing this post, loneliness is highlighted as being over-represented when it comes to certain diagnostic labels as part of a package of issues affecting quality of life (see here)...

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[1] Matthews T. et al. Lonely young adults in modern Britain: findings from an epidemiological cohort study. Psychological Medicine. 2018. April 24.

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Wednesday, 23 May 2018

Pregnancy exposure to paracetamol and offspring developmental outcomes meta-analysed

Yes, I'm yet again talking about pregnancy paracetamol (acetaminophen) use and offspring developmental outcomes on this blog (see here and see here for other discussions on this topic). As I mentioned on another recent blogging occasion, the news regarding pregnancy paracetamol use and offspring outcomes seems to be getting worse and worse, as associations galore keep appearing in the peer-reviewed science arena. Of course one has to be a little cautious about the nature of the studies that are emerging (i.e. observational, not readily designed to look at 'cause-and-effect') but the volume of research is growing at a significant pace potentially suggestive of something to see.

Now we have the results of a "Systematic Review, Meta-Analysis, and Meta-Regression Analysis of Cohort Studies" published by Reem Masarwa and colleagues [1] on the topic of pregnancy paracetamol use and "the risk for attention deficit hyperactivity disorder (ADHD) and autistic spectrum disorder (ASD) in the offspring of women exposed to acetaminophen during pregnancy." All that meta-analysis stuff means that authors boiled down the current, existing peer-reviewed research into some sort of coherent whole. Their paper also comes complete with some lay media attention too (see here).

The findings? Well, taking into account various studies published "up to January 2017" and including some "132,738 mother and child pairs and with a follow-up period of 3-11 years", you probably won't be surprised to here that prolonged paracetamol use during pregnancy did seem to increase the risk of ADHD and/or autism in offspring to the tune of about 20-30% compared with those who did not take such medicine during pregnancy. That's not an unimportant percentage in anyone's book.

Reiterating the observational nature of the studies reviewed and boiled down (in a statistical sense) by Masarwa et al and the need for further investigations on things like possible mechanisms and indeed, whether the conditions for which paracetamol as pain relief was being taken *might* exert an effect on offspring risk, the results add to the concern. Much like other areas where various pregnancy medications are seemingly being implicated in relation to offspring outcome (see here and see here) such findings reiterate the importance of the nine months that made us and the need for much more sound research on this topic...

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[1] Masarwa R. et al. Prenatal Exposure to Acetaminophen and Risk for Attention Deficit Hyperactivity Disorder and Autistic Spectrum Disorder: A Systematic Review, Meta-Analysis, and Meta-Regression Analysis of Cohort Studies. American Journal of Epidemiology. 2018. April 24.

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Tuesday, 22 May 2018

A poo(p) transplant for depression and anxiety?

Contrary to the title of this post - "A poo(p) transplant for depression and anxiety?" - I don't think we are yet in a position to say that Fecal Microbiota Transplantation (FMT) is ready to go 'mainstream' as an approved treatment for depression and/or anxiety. I do however, think that the findings reported by Shunya Kurokawa and colleagues [1] provide evidence for a further, more controlled, scheme of research on this topic.

Based on their following a small-ish group of patients diagnosed with "either Irritable Bowel Syndrome (IBS), Functional Diarrhea (FDr) or Functional Constipation (FC) who underwent FMT for the treatment of gastrointestinal symptoms and observation of psychiatric symptoms" authors report results before said poo(p) transplant and after 4 weeks based on ratings on various instruments pertinent to the presentation of depression and anxiety. Alongside "intestinal microbiota were measured" with a particular focus on the level of diversity of species that were present in pre- and post-FMT samples. I might also mention at this point, how something like IBS is not without it's own 'psychological' correlates as per other research (see here and see here).

Following an 'open-trial' methodology and including only a "small sample size with no control group", researchers reported some significant improvements in relation to those depression and anxiety symptom scores for some. Importantly too, they noted that potential FMT effects on mood seemed to be independent of effects on "gastrointestinal symptom change." Similarly: "There was a significant correlation between baseline Shannon index and HAM-D [Hamilton Rating Scale for Depression] score, and a correlation between Shannon index change and HAM-D improvement after FMT." This suggests that bacterial diversity might be something to look at as potentially explaining the psychological effects of FMT.

Reiterating that the Kurokawa findings are preliminary and hence, require quite a lot more further (independent) study, I find this topic to be an interesting one. Although there may be some 'consumer resistance' to the idea of FMT, for some people, this type of intervention is nothing short of life-saving (see here). The idea that a similar type of transplant *might* also hold some benefits for conditions/labels outside of something like Clostridium difficile (C. difficile) infection has already been noted in the peer-reviewed science literature (see here and see here for examples), including conditions characterised by behaviour and psychology. This alongside a growing interest in how mood and temperament might have some important connection to those trillions of wee beasties (the gut microbiome) that call us all home (see here). We'll see where this goes...

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[1] Kurokawa S. et al. The effect of fecal microbiota transplantation on psychiatric symptoms among patients with irritable bowel syndrome, functional diarrhea and functional constipation: An open-label observational study. J Affect Disord. 2018 Apr 12;235:506-512.

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Monday, 21 May 2018

The "experiences and perspectives of people who have severe autism and are minimally verbal"

I'm not going to formulate some sort of mammoth, long-read post on the paper by Christie Welch and colleagues [1] but I did want to bring their findings to your attention. My reasoning: the authors include a quite 'under-represented' group (see here) when it comes to the public view of the autism spectrum: those who "have severe autism and are minimally verbal."

Presenting the results of a qualitative study whereby "three memoirs written by youths who have severe autism and are minimally verbal were examined using inductive thematic analysis", authors observed several important themes emerging. Principal among them: "regarding the youths' concern that the way they are perceived from the outside does not match the people they are on the inside."

"These youths emphasize concepts of embodiment and physical control as central to their experiences of autism" said Welch et al, as the message seems to be that more should be done to 'tackle' these experiences and ensuring that sweeping generalisations about language use or non-use for example, are not seen as a proxy for cognitive and intellectual abilities. Just because someone cannot speak verbally, does not mean that they have nothing to say, and vice-verse.

I'm careful not to fall into the trap of 'autism severity' on the basis of the Welch findings, where terms like 'high' and 'low' functioning unduly simplify people in a binary fashion and seemingly without regard for the complexity of how autism affects various aspects of a person's life. I do however like the idea that more effort needs to go into things like the development of communication systems for those who are minimally verbal; both for clinical and research purposes but perhaps more importantly, day-to-day purposes, given also some catastrophic examples where communication issues have severely impacted on autistic lives (see here and see here).

And to the question of 'how common is 'minimally verbal' in the context of autism', well, another recent paper [2] has come up with an estimate: about a third...

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[1] Welch C. et al. Autism inside out: lessons from the memoirs of three minimally verbal youths. Disabil Rehabil. 2018 Apr 23:1-9.

[2] Bacon EC. et al. Naturalistic language sampling to characterize the language abilities of 3-year-olds with autism spectrum disorder. Autism. 2018 May 1:1362361318766241.

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Saturday, 19 May 2018

Temporal armchair diagnosing taken to the max: 'How Do We Explain ‛Autistic Traits’ in European Upper Palaeolithic Art?'

Headlines aplenty...
I'm not a great fan of 'armchair diagnosing' also known as 'diagnosing at a distance'. It's speculative, often inaccurate and runs the real risk of ruining lives.

The remote diagnosing of psychiatric and behavioural disorders is a particular bugbear of mine. It's something that autism research and practice in particular has had to endure for quite a few years, as a volley of historical figures for example, were revealed to be supposedly autistic. Such musings also add a temporal aspect to proceedings.

The paper published by Penny Spikins and colleagues [1] takes such temporal armchair diagnosing to the absolute max, with their contribution to the "long standing debate about the existence of ‘autistic traits’ in European Upper Palaeolithic art." Some of the media that followed these findings really went to town, as per headlines such as 'Ice Age cave artists were AUTISTIC' (capital letters were already included in the headline, not added by me - see above) and 'Autism shaped the art of survival'. Wow. All of that information from a few paintings and carvings...

So how did the the authors and the lay media arrive at such a conclusion?

Well, first and foremost Spikins et al did not say that the makers of such early art were 'autistic'. They focused on autistic traits, and in particular the idea of an "extreme local processing bias" or attention to detail trait that seems to accompany the diagnosis of autism (for some). Importantly, they note that: "Local processing bias is common in autism but also seen in individuals without autism" and "‘Autistic traits’ in Upper Palaeolithic art do not necessarily signify the work of an individual with autism." So, from the outset, we can probably do away with that rather sweeping [diagnostic evidence-free] media headline on Ice Age cave artists being autistic.

Quite a lot of the Spikins paper focuses on what's been observed - directly observed - in some of those diagnosed as being on the autism spectrum when it comes to artistic talent, which is then 'extrapolated' to such prehistoric artists. This includes some rather nice pictures drawn by individuals with autism who expressed a "marked local processing bias" compared with age-matched drawings from non-autistic individuals. We're also told that the use of the (very) famous 'are you autistic?' self-report screener that is the Autism Spectrum Quotient (AQ) by the authors, revealed that "individuals with a very high autism quotient (AQ) of 32 or above, which is taken as indicative of an autism spectrum condition within a population sample were statistically much more likely than neurotypical individuals (i.e. those with a lower AQ score) to have an interest in and experience of art outside of any school curriculum." 'Indicative of an autism spectrum condition'? Well, we'll see. And I still have some problems with what comes under the term 'neurotypical' too (see here).

Of course you can perhaps see the issue here. Take one block of 'evidence', some of it based on individual case reports and some of it based on an 'autism' screener that probably picks up an awful lot more than 'just autism' (see here and see here and see here for examples), correlate and correlate some more and hey presto, we reach the conclusion that the art must have been drawn by someone expressing an autistic trait or even someone who was autistic.

A testable hypothesis? No, it's not. We don't know who drew those paintings or made those carvings. We don't know anything about them personally and we certainly don't have any evidence about whether they expressed any significant autistic or any other kind of trait. For all we know, the paintings or carvings could also have been made by more than one person; a family or group effort if you like. We just don't know because, well, those artistic depictions were made thousands and thousands of years ago before the tools that help us record history were even a twinkle in the cosmic eye.

I don't want to come across as poo-pooing such 'observations' stressing how autistic traits are not necessarily a new thing because, in essence, I do think that some autistic traits have probably been with us from our earliest evolutionary times (see here). I say that on the basis that the traits of autism are not some 'magical' behaviours that are completely distant from the human experience; more likely they represent the extremes of what is typically seen in the general population at particular ages and stages and environments. Taking such logic back in an evolutionary sense, one can for example see how something like an 'attention to detail' could be a good survival skill if your life depended on it.

But I do think one has to be very, very cautious about such research and any 'feelgood' factor it might attempt to generate or put forward. Autism, as a clinical definition, only really came about in the last hundred years or so, and for many, any benefits derived from a 'marked local processing bias' have to be balanced with the possible downsides to such directed focus (e.g. increased rumination and anxiety). I'd also add in that the idea that Palaeolithic Art (or indeed, any kind of art) merely comes about as a result of traits that are noted in the context of psychopathology is a pretty dangerous path to take. It risks boiling down human efforts such as creativity and artistic skill to nothing more than diagnostic characteristics and feeds into narratives such as the "creativity is akin to insanity" headlines of not so long ago (see here). As I've said before, people are so much more than the labels they've received or the diagnostic term they identify with.

In short, Palaeolithic art is interesting and adds to our understanding of how we evolved. But it simply cannot provide an accurate window on any states and traits of those who created it...

To close, there's a wedding on today apparently. Best wishes to the happy couple. And not to make light of our Royal Family, but The Windsors TV show is absolute comedy gold (particularly Harry Enfield)...

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[1] Spikins P. et al. How Do We Explain ‛Autistic Traits’ in European Upper Palaeolithic Art? Open Archaeology. 2018; 4: 262-279.

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Friday, 18 May 2018

ALSPAC does... prenatal mercury exposure and autism or autistic traits

The ALSPAC - Avon Longitudinal Study of Parents and Children - mentioned in the title of this post is something of quite a regular feature on this blog (see here and see here for examples).

On this particular blogging occasion I'm heading into the findings reported by Jean Golding and colleagues [1] who utilised this fabulous research resource to examine whether "prenatal exposure from total maternal blood Hg [mercury] in the first half of pregnancy is associated with the risk of autism or of extreme levels of autistic traits." They concluded that there were "no adverse effect of prenatal total blood Hg on autism or autistic traits provided the mother ate fish."

OK, mention of the heavy metal mercury in the context of autism and/or autistic traits can be a touchy subject for some. I'm talking about the various 'discussions' that have taken place both in the lay and peer-reviewed science arenas concerned with the exposure patterns relevant to mercury in the context of autism (see here and see here). This, on the basis that mercury exists in several 'forms', and those different forms have different potential exposure routes.

Golding et al relied on some of the gold-standard analytical methods for the analysis of whole blood Hg collected in the most part "at < 18 weeks gestation": "inductively coupled plasma dynamic reaction cell mass spectrometry (ICP-DRC-MS)." Variations on this method - ICP mass spectrometry - have been previously reported on in the context of mercury and autism research (see here and see here). Alongside, they looked at measured levels of mercury in relation to various behavioural and other variable groupings: "(1) direct comparison of 45 pregnancies resulting in children with diagnosed autism from a population of 3840, (2) comparison of high scores on each of the four autistic traits within the population at risk (n~2800), and (3) indirect measures of association of these outcomes with proxies for increased Hg levels such as frequency of fish consumption and exposure to dental amalgam (n > 8000)." They however cautioned that: "Although we accounted for several important confounders which are relevant to Hg levels and autism, the possibility of unmeasured confounding cannot be ruled out." I can think of one potential confounder that was not seemingly included in their list outside of fish consumption and dental amalgams but ho-hum...

Alongside their overall 'no relationship' results, a few other details are noteworthy. First: "all correlations indicated that with increasing levels of [maternal] mercury, the signs of autism [in offspring] were slightly less, but none were statistically significant." Interesting idea - higher maternal levels of mercury during pregnancy 'correlates' with 'less' autistic traits in offspring in childhood - but to reiterate, not statistically significant. Second was that 'provided the mother ate fish' detail attached to the main findings. So: "we have shown a differential relationship between the social cognition trait and prenatal Hg exposure, such that there was a significant difference in apparently protective effects contingent upon whether the mother ate fish." The authors opine as to what it is about fish consumption that might "counteract any possible adverse cognitive and behavioral differences that may be caused by prenatal exposure to Hg" including "the beneficial components of fish such as the omega-3 fatty acids, iodine, and vitamins D and B2." This in the context that omega-3 fatty acids have some research form in relation to autism (see here) as does the sunshine vitamin/hormone that is vitamin D (see here).

One has to be slightly careful with the Golding results given the focus on prenatal exposure, and prenatal exposure at only one early point in pregnancy, as well as also not actually looking at mercury levels in the children themselves. The current results say nothing for example, about any possible direct or acquired role for mercury in relation to autism as per other findings published during the same period [2]. Neither do they offer any additional information on the idea that exposure issues to such heavy metals may be only one part of the story, and that the biological processes involved in removing such heavy metals may be somehow perturbed in relation to some autism (see here).

But... set within the idea that prenatal mercury exposure may be linked to the 'etiology' of at least some autism, the Golding findings represent pretty strong evidence suggestive of no connection.

Music to close, and could I recommend the soundtrack to Sonic 3 while you work?

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[1] Golding J. et al. Prenatal mercury exposure and features of autism: a prospective population study. Molecular Autism. 2018; 9: 30.

[2] Qin YY. et al. A comparison of blood metal levels in autism spectrum disorder and unaffected children in Shenzhen of China and factors involved in bioaccumulation of metals. Environ Sci Pollut Res Int. 2018 Apr 22.

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Thursday, 17 May 2018

KPAX002 for Chronic Fatigue Syndrome part 2: controlled study says no

KPAX002 mentioned in the title of this post refers to "a mitochondrial modulator technology platform" according to the manufacturer that includes a low dose of methylphenidate combined with various nutrients designed to impact on mitochondrial function. Within the context of chronic fatigue syndrome (CFS) also known as myalgic encephalomyelitis (ME) (but not necessarily accurately so!), there is some preliminary research history suggesting that KPAX002 might be something to look at for intervening in some of the disabling characteristics of CFS/ME (see here). This, on the basis that mitochondria in particular, might be something quite important to at least some cases (see here and see here).

The fly in the scientific ointment?

Well the results of the "phase 2 randomized, double-blinded, placebo-controlled trial" on KPAX002 published by Jose Montoya and colleagues [1] that, from an intention-to-treat point of view, reported no significant statistical difference in self-reported group scores of fatigue and other measures between active treatment and a placebo. In keeping with the phase 2 label attached to the trial - looking at both initial clinical results and also any side- or adverse effects - authors reported no statistically significant difference in the frequency of reported adverse effects between KPAX002 and a placebo over the 12 weeks of study. First, do no harm and all that.

The Montoya paper is open-access so readers can see for themselves how things were done and the details of the results. I however, want to highlight a few points that I thought were important:

First, the authors acknowledge the "unexpectedly positive results" observed the last time around [2] that led to this more rigorous trial. Personally, I don't think there was anything too unexpected about those pilot study results, given the methodological issues typically associated with a pilot study. Y'know, a small un-blinded participant group taking part in a trial using a preparation that they probably will have been told *might* affect various symptoms they experience or themselves possibly 'exposed' to other anecdotal reports of good effects. That and no control group, no placebo included and importantly, no objective measure of fatigue (a real issue when it comes to quite a bit ME/CFS research) and well, I'd be surprised if something significant didn't come up during the initial findings. And just in case you think I'm being all 'high-and-mighty' about this, I've published using the same type of pilot study methodology before, including some of the same inherent issues (see here).

Second, I'm a little bit disappointed that the authors weren't more forthright in how the results weren't statistically significant on any and all measures included for study. I say this on the basis of both the commercial take on the results (see here) and also sentences like: "The two groups demonstrating the most robust response to KPAX002 were subjects with more severe ME/CFS symptoms at baseline (P=0.086) and subjects suffering from both fatigue and pain (P=0.057)." Both those p-values (p being a measure of statistical significance) are above the [currently] recognised threshold for p equal to or less than 0.05, yet are listed as a 'robust response'. Even more, throughout the paper I note the words 'trend in favor of' being used, which some people might translate as being 'well, they were nearly statistically significant results'. I say this also bearing in mind that the final participant numbers - KPAX002 use = 48 and placebo = 57 - are not exactly facets of what one would call an under-powered study. I'm probably being a nit-picker here but like it or not, the [current] rules of science are the [current] rules of science.

Finally, once again, I note that under the heading 'Disclosure of conflict of interest', the word 'none' appears as per the last research occasion [2]. Personally, and with no malice intended, I would have listed the detail that at least one of the authors is an employee of the manufacturer of KPXA002 given the affiliation details and email address for further correspondence provided on the paper. Again, it's a small detail but one that should nevertheless be acknowledged. I would have also like to have seen a little more on who funded the trial too and especially who funded the provision of the KPAX002 supplement for trial purposes. I reiterate that there is no malice is intended in saying that, but readers require such details.

I don't want to come down too hard on these results because it's obvious that quite a bit of work has gone into their production. I'm also not closing the door on the idea that future research with a more targeted group with ME/CFS might not produce something a little more statistically significant with regards to KPAX002. But for now, the answer must be that controlled study of the formulation did not meet clinical endpoints in a statistical sense, and hence KPAX002 cannot be said to be superior to placebo for CFS/ME. With all the setbacks that the label(s) ME/CFS has had to endure down the years with regards to the 'psychobabble' explanations (see here) and other 'eureka' moments (see here), the Montoya findings are bad news for patients yet again. But, they also should represent a further call to re-double research efforts; particularly when it comes to the biology of the condition(s) and onward the acceleration of research for interventions for this quality of life draining condition (see here).

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[1] Montoya JG. et al. KPAX002 as a treatment for Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS): a prospective, randomized trial. Int J Clin Exp Med 2018;11(3):2890-2900

[2] Kaiser JD. A prospective, proof-of-concept investigation of KPAX002 in chronic fatigue syndrome. Int J Clin Exp Med. 2015 Jul 15;8(7):11064-74.

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Wednesday, 16 May 2018

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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Tuesday, 15 May 2018

Higher autistic traits in those attending transgender health services don't necessarily mean autism

There are some key messages to take from the findings reported by Anna Nobili and colleagues [1] following their examination of "self-reported autism spectrum quotient-short (AQ-short) [scores] in a transgender clinical population." Not least that when compared with a control group - "cisgender individuals" - there "were no significant differences in the number of people who presented with scores suggesting a possible diagnosis of ASC [autism spectrum condition(s)]."

OK, before heading further into the Nobili findings I think it might be worthwhile setting the scene a little. So, for quite a while now there has been some increasing interest in how autism or at least some of the traits of autism, *might* be over-represented among those presenting with gender dysphoria (see here). Gender dysphoria, according to the UK NHS Choices website is "a condition where a person experiences discomfort or distress because there's a mismatch between their biological sex and gender identity." Allied to other peer-reviewed research looking at gender identity [2], sexual preferences in the context of [some] autism (see here), and combined with quite a sweeping *theory* talking about an 'extreme male brain' in the context of autism (see here), and well, let's just say some speculation about a link between some autism / autistic traits and elements of gender and sexuality has been noted. And indeed, continues to be noted [3]...

Nobili et al - including one author who is rather central in autism research circles to the promotion of that extreme male brain theory - examined AQ responses in some 650 matched pairs (transgender matched with cisgender). Among the transgender participants: "A total of 260 people (39.6%) in each group were assigned female at birth whilst 396 (60.4%) were assigned male." It's worthwhile noting that AQ is a self-report questionnaire, and whilst heralded in several quarters as a good 'are you autistic?' screener, there are some people - including me - who have some reservations about it's 'universal' usefulness to just autism (see here and see here for examples). I'll come back to this shortly...

As per the opening paragraph to this post, the numbers of participants "indicating possible ASC caseness" did not differ significantly between the groups. So, around 33% of the cisgender control group hit a score of 70 or more on their self-report responses to the AQ compared with 36% in the transgender group. The authors did detect a statistically significant difference in possible caseness when looking at those assigned female at birth in the transgender group but not for males. A similar finding has been noted in other independent studies [4]. Nobili and colleagues however concluded that their findings were in line with other observations in adults in that: "there is no evidence of increased rates of autism in transgender populations as a whole."

Going back to my reservations around the AQ as an exclusive autism screener, I also noted something important reported by Nobili and colleagues: "High AQ scores may not be indicative of the presence of an autism spectrum condition as the difference between groups mainly related to social behaviours; such scores may be a reflection of transgender people’s high social anxiety levels due to negative past experiences." I was really intrigued by this finding and interpretation, particularly in light of other recent peer-reviewed speculation by Jack Turban [5] who suggested that: "ASD [autism spectrum disorder] symptoms [in transgender youth] may represent social deficits that are secondary to social stress and deprivation, as transgender youth suffer high rates of peer and family rejection." On a previous blogging occasion, I've also discussed research suggesting that something like a generalised anxiety disorder (GAD) may 'inflate' responses/scores on the AQ (see here). Given that anxiety is an all-too-often bedfellow accompanying a diagnosis of autism, I'd be interested to see quite a bit more study on this topic in the context of AQ use. Y'know, perhaps alongside some more formal measures of anxiety both in relation to autism and also more readily pertinent to the subject matter analysed by Nobili et al. And, outside of just anxiety, other clinical features/conditions might also be thrown into the research mix [6]. Insofar as the idea that mental health may also be a topic requiring more focus in respect of the transgender population, I'll bring to your attention some other recent research by Becerra-Culqui and colleagues [7] on this point.

There is a further scheme of work to follow in this area, and I'll be interested to see what further results turn up, particularly with regards to females assigned at birth with gender dysphoria. And since I've mentioned the AQ and (once again) my reservations, I'll direct you to another paper published in the same journal at roughly the same time as the Nobili findings, where the AQ was again 'implied' as being equal to the presence of autistic traits [8]. And yet again, another example where one has to be very, very careful about making that 'exclusively autistic traits' link...

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[1] Nobili A. et al. Autistic Traits in Treatment-Seeking Transgender Adults. J Autism Dev Disord. 2018. April 13.

[2] Cooper K. et al. Gender Identity in Autism: Sex Differences in Social Affiliation with Gender Groups. J Autism Dev Disord. 2018. April 28.

[3] van der Miesen AIR. et al. Prevalence of the Wish to be of the Opposite Gender in Adolescents and Adults with Autism Spectrum Disorder. Archives of Sexual Behavior. 2018. May 7.

[4] Vermaat LEW. et al. Self-Reported Autism Spectrum Disorder Symptoms Among Adults Referred to a Gender Identity Clinic. LGBT Health. 2018 May 9.

[5] Turban JL. Potentially Reversible Social Deficits Among Transgender Youth. J Autism Development Disord. 2018. May 12.

[6] Lugnegård T. et al. Asperger syndrome and schizophrenia: Overlap of self-reported autistic traits using the Autism-spectrum Quotient (AQ). Nord J Psychiatry. 2015 May;69(4):268-74.

[7] Becerra-Culqui TA. et al. Mental Health of Transgender and Gender Nonconforming Youth Compared With Their Peers. Pediatrics. 2018. April 16.

[8] Loureiro D. et al. Higher Autistic Traits Among Criminals, But No Link to Psychopathy: Findings from a High-Security Prison in Portugal. J Autism Dev Disord. 2018. April 12.

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Monday, 14 May 2018

How much does it cost to assess a child for autism?

In answer to the question titling this post - 'How much does it cost to assess a child for autism?' - the results published by Mark Galliver and colleagues [1] provide some important findings, at least pertinent to the diagnostic experience here in Blighty.

Authors concluded that assessment for autism "typically takes 13 hours of professional time" and costs somewhere in the region of "£650–£1000 ($975–$1500) per child." Importantly too, the staff costs of around £800 per assessment do not cover "costs of intervention, parent psychological education, investigation and assessment and management of comorbidities."

I appreciate that talking about 'financial costs' associated with autism (assessment) is not a topic everyone will enjoy discussing. Much like other 'bean counter' discussions (see here and see here), everyone [rightly] aspires to providing this, that and t'other to improve facilities with regards to diagnosis and indeed, post-diagnostic services. The financial reality however, particularly in these days of continued austerity, is that such services are often under-funded, under-resourced and headlines including words like 'two year wait' for diagnostic assessment (see here) are not uncommon. People rightly get angry about this but the services themselves and the people delivering them are not to blame.

Galliver et al started out with some important premises. First, there are a growing number of referrals for assessment for autism. Second, such an 'increase in demand' naturally puts greater pressure on diagnostic services resulting in longer waiting times. Third, there are recognised pathways for referral and assessment for autism, but the resourcing of such pathways might not always be optimal either in form or amount. All of this is set in the context of the National Health Service (NHS) providing clinical and medical services here in the UK, free at the point of need and all that.

Researchers therefore decided to ask various local child development centres (CDC) in England about their diagnostic experiences in terms of resources and costs. Various questions were asked pertinent to the pathway used to deliver assessments and professional time typically allocated to said assessments. They report on responses from 60% of the CDC - no, not that CDC - initially questioned, covering a range of services in different geographic locations.

I don't need to rehash the financial findings again. I will however mention a couple of associated points that might be relevant. First, autism rarely exists in some sort of diagnostic vacuum (see here). The authors make the point that their figures did not cover the "investigation and assessment and management of comorbidities" something important in these days of greater realisation of 'autism plus' and ESSENCE (see here). In this respect, the figures provided by Galliver are likely to be an underestimate of the true financial cost of assessment.

Second, the issue of growing numbers of referrals and "increasing demand" for diagnostic services is highlighted in various parts of the reported findings. I have my own opinions as to why this is happening (see here and see here) but the one thing that is becoming increasingly clear is that such an increase is probably not just due to better recognition of autism or issues such as diagnostic switching (see here and see here). Yes, these points were probably relevant about 10-20 years ago, but now, I'd have to say not as much as [clinical] awareness must have peaked by now. At some point the question of 'why the increase' is going to have to be properly faced up to if it's not going to be all about just assessing and diagnosing in a catch-up sense.

Finally, although more funding would help, such demands on assessment services are probably not going to be met by just 'throwing a few quid' at them. The NHS is moving with the times in other areas; and the rise and rise of technology to potentially assist with autism assessments is becoming increasingly important. I'm thinking about work such as that being done at the Duda-Wall laboratory (see here and see here) where technology such as machine learning is being used in the context of autism screening. And things like autism screening triage via YouTube (see here) *might* also [eventually] become more commonplace. Technology can potentially ease the burden on assessment services.

Whatever does or does not happen as a result of findings such as those by Galliver and colleagues, the underlying messages are that autism assessment is (a) not an inexpensive process and (b) either significant funds need to be poured into the service or services need a revamp on the basis of current funding schedules and as national finances allow. Either way, I don't see assessment waiting times improving much in the near future despite the important work provided by our fantastic NHS and the desperate need for timely autism assessment.

And I've not even mentioned about adult diagnostic services...

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[1] Galliver M. et al. Cost of assessing a child for possible autism spectrum disorder? An observational study of current practice in child development centres in the UK. BMJ Paediatr Open. 2017 Nov 30;1(1):e000052

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Saturday, 12 May 2018

"Due to the definitions of ME and CFS, “ME/CFS” does not exist..."


Today, May 12th, is ME/CFS and Fibromyalgia International Awareness Day, a day to designed to "bring awareness to ME/CFS patients, families, caregivers, and researchers." Keep that terminology in mind...

The quote heading the title of this post - "Due to the definitions of ME and CFS, “ME/CFS” does not exist..." - comes from the viewpoint paper published by Frank Twisk [1]. The report covers an important topic in the realms of chronic fatigue syndrome (CFS) also known as myalgic encephalomyelitis (ME) also known as systemic exertion intolerance disease (SEID) in terms of whether it is appropriate to use such terms of defining the illness in a mixed or interchangeable fashion. Indeed, whether the connections between all those 'also known as' words I just used are actually accurately reflective of current diagnostic descriptions...

It's no secret that science and clinical practice is still coming to grips with some of the fundamentals of CFS, ME and SEID (see here and see here for examples) in terms of what to call it, how to define it and how to test for some of the fundamental diagnostic characteristics (see here). It's also still dealing with things like the definition of recovery (see here), which might seem like common sense (a complete and sustained remission of symptoms) but hasn't been particularly straightforward in this area for quite a few reasons.

Twisk takes the reader through some of the history of the terminology used and, how, whilst there is overlap in the way that ME, CFS and SEID are defined (chronic and long-lasting weakness or fatigue is a commonality), there are also some important differences. Take for example the authors description of the Ramsay criteria for ME and specifically onset: "Illness commonly initiated by respiratory and/or gastrointestinal infection, but an insidious or more dramatic onset following neurological, cardiac, or endocrine disability occurs." This contrasts with the onset criteria for CFS and SEID which basically says little about how symptoms start or come about.

Twisk concludes that: "ME is a neuromuscular disease" and should typically not to be viewed as 'equivalent' to CFS. CFS, he argues, tends to rely heavily on a single mandatory 'chronic fatigue' symptom, something that might intersect with ME but does not go far enough to evoke a full diagnosis of ME. As for SEID, well, trumpeted as being the solution to all the diagnostic confusion, SEID has it's own issues according to Twisk. Not least that it can't serve both masters (ME and CFS) in diagnostic terms. Also important: "SEID case criteria are also applicable to subsets of people with other diseases, for example, Multiple Sclerosis (MS) and lupus; and psychological conditions, for example, major depression." There is the propensity for diagnostic confusion.

I do think that Twisk is on to something with his observations. I know quite a few people who don't like the confusion caused by combination terminology like 'ME/CFS'; often seeing it as conflating two (or even more!) quite different conditions. Add in yet another potentially important variable to such an argument - the addition of chronic disabling fatigue (CDF) as "a proxy for clinically diagnosed CFS/ME" as some authors have (see here) - and things get even more muddled. I daresay a lot of this confusion might also intersect with discussions/debates/arguments as to how far something like the biopsychosical (BPS) model should or rather shouldn't be applied to such fatigue related conditions (see here)...

You want to do something for ME/CFS and Fibromyalgia International Awareness Day? Well, first thing you could do is watch 'Unrest', then follow the #millionsmissing hashtag and then push for more research, biological research...

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[1] Twisk FNM. Myalgic Encephalomyelitis, Chronic Fatigue Syndrome, and Systemic Exertion Intolerance Disease: Three Distinct Clinical Entities. Challenges. 2018; 9(1): 19.

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Friday, 11 May 2018

Estimated autism prevalence in Northern Ireland: 2.9% for 2017-2018

Consider this post discussing the publication: "The Prevalence of Autism (including Aspergers Syndrome) in School age Children in Northern Ireland 2018" an extension of other musings on previous figures to come out of Northern Ireland (see here).

On my last blogging occasion on this topic, the report (see here) covered the period 2015/2016 and detailed an estimated prevalence rate of autism spectrum disorder ("including Asperger syndrome") in Northern Ireland of 2.3%. I actually missed a report that covered the period 2016/2017 (see here) that detailed an estimated rate of 2.5%. This latest report covering 2017/2018 sets the rate at 2.9%. You can perhaps see the direction of the trend, mirroring other population estimated data (see here)...

The report(s) are open-access for anyone to see, but I'm going to pick out a few choice snippets of information.

So: the last blogging time I talked about the Northern Ireland (NI) report, I mentioned that the [estimated] prevalence rate for boys was approaching 4% based on those 2015/2016 figures. Well, that's been well and truly surpassed and is now heading towards 5% of boys in NI "identified with autism." How are they identified I hear you ask? Well, school data is the answer, "from the ‘Northern Ireland School Census’" where schools are legally obliged by the Department of Education in NI to provide information about registered pupils. Further: "The data only captures those children identified with autism, at any time there may be additional children who may be progressing through the full assessment process and it is possible that a number of children may be identified as having autism at a later date." That last point is important in the context that NI has a bit of a history of 'long-waiting lists' for autism assessments (see here). Oh, I should also mention that the National Health Service (NHS) functions in Northern Ireland just as it does in other parts of the United Kingdom (UK) meaning that healthcare (including autism assessment and diagnosis) is free at the point of need. This does not mean that things are going to be 'fast or rapid' temporally, but does mean that people don't have to typically pay extra for such clinical services.

Next: the 4:1 male:female ratio for diagnosis seems to be holding true (as it did in the latest CDC report on 'estimated' autism prevalence in the United States). I know that quite a few people talk about this ratio figure being 'inaccurate' in view of how autism may/may not present slightly 'differently' in females (see here for example), but, at the moment at least, that's what the statistics are telling us. One thing I perhaps am slightly cautious about in the latest report with regards to the sex/gender ratio thing is the phrase: "Autism could therefore be considered to be an extreme of the normal male profile." Hmm...

Also: autism prevalence by school year shows some interesting patterns. Take a look at the screen grab I've added observing that 3.4% of children in Year 9 were "identified with autism." Just in case you're not up to speed with what Year 9 translates as in age terms, have a look at this link which covers England. I think things are slightly different in NI (see here) but generally speaking, Year 9 covers somewhere between 12-14 years of age.

Finally, something else potentially quite important: "The Northern Ireland urban population has a statistically significant higher prevalence rate than the rural population." Note those words 'statistically significant', inferring that chance alone, is probably not the driver of such disparity. It's been a while since I've blogged about 'urban vs. rural' in the context of autism (see here) and I'm sure there are 101 different explanations for the mismatch. Combined however with some other observations on a possible influence of deprivation and poverty on the recent figures ("In 2017/18, the rate of autism in the most deprived MDM [Multiple Deprivation Measure] decile was 31% higher than the Northern Ireland average") one could argue that any explanation is going to be multi-factorial.

I look at these most recent figures and cannot help but think that 'increased awareness' and/or other 'artificial' explanations are (yet again) unable to entirely account for the sorts of increase in diagnosed autism being noted (see here). Were schools and other professionals 'so bad at recognising and/or recording autism' just a few years ago? No, they weren't. And to infer they were is bit a slur on the professionalism of many teachers and other associated professionals, many of whom have seen literally generations of schoolchildren pass through their educational doors.

There's also another important question to attend to on the basis of the recent figures: are the resources currently and in the future, in place to cope with the rising demands on things like education, health and social care following the increase in the numbers of children being diagnosed with autism? I say this in the context that if there are already insufficient resources to cope with the numbers requiring assessment for autism (assessments that are typically not inexpensive [1]), how can we hope that there will be sufficient resources in place over a lifetime of potential need?

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[1] Galliver M. et al. Cost of assessing a child for possible autism spectrum disorder? An observational study of current practice in child development centres in the UK. BMJ Paediatr Open. 2017 Nov 30;1(1):e000052.

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"psychiatric diagnoses, psychiatric care and psychotropic medication" in older age adults with autism

Is 55 years old still considered older age?

Well, according to the findings reported by Lena Nylander and colleagues [1] it represents the lower end cut-off point for their study looking at "the pattern of coexistent psychiatric diagnoses and the utilisation of psychiatric care and psychotropic medication among any individuals found to have ASD [autism spectrum disorder] diagnoses." Said individuals were aged between 55 and 96 in 2012 and "had a registered diagnosis of any ASD—defined as an ICD-10 code."

Those individuals 'found to have ASD' were located via some of those very useful Scandinavian population registries, this time based in Sweden. As a function of their registration for 'municipal services' researchers were also able to access other collected records and subsequently mined data on "gender, other psychiatric diagnoses, psychiatric care utilisation and psychotropic medication [use]" for a group of increasing research and clinical importance in the context of autism (see here).

The results proved interesting. Of the 600 people included for study, most had received a diagnosis of childhood autism (~40%), most had not received a concomitant intellectual disability (ID) diagnosis (~60%) and quite a few had received more than one 'type' of autism diagnosis (~15%).

When it came to the receipt of other psychiatric diagnoses such as affective disorder, personality disorder, anxiety or psychotic disorder, several notable observations were made. As a function of the total group, including everyone whether diagnosed with an ID or not, around 50% of participants had received at least one psychiatric diagnosis. A nebulous category defined as "other psychiatric diagnosis" was most frequently mentioned, but when it came to a named class of condition(s), affective disorders led the way in terms of frequency irrespective of the presence of ID or not. Affective disorders covers quite a bit of diagnostic ground but typically includes labels/conditions such as depression and/or bipolar disorder; conditions that are no stranger to autism (see here and see here respectively). Anxiety and psychotic disorders were also mentioned as being present among this cohort too; again not for the first time (see here and see here).

With regards to 'psychiatric care utilisation', it was more typical to see psychiatric care used than not used as nearly two-thirds of the cohort had used some kind of psychiatric care over the period included for study examination. Most were categorised as "general adult psychiatric care" and: "The group with Asperger’s syndrome had the highest number of people who had spent time as psychiatric inpatients" reflected in the odds ratio (OR) generated from the study for this group (OR: 6.87, 95% CI 3.80–12.43).

Finally, on the topic of psychotropic medication use, researchers observed that "63% of patients without registered ID diagnosis and as many as 84% of those with ID in combination with ASD had been prescribed antipsychotic medication." Antipsychotics were the most frequent medication mentioned in records, closely followed by anxiolytics (to manage anxiety) and antidepressants. Around 1 in 5 participants received more than one type of medication (irrespective of the presence of ID or not).

An important picture emerges from the Nylander findings. A picture suggesting that psychiatric diagnoses feature fairly prominently in the clinical profile of many older age adults with autism, and their identification and intervention need to be more clearly recognised. Nylander also pointed out that certain sub-groups within the autism spectrum should perhaps be more closely followed in relation to their achieving and maintaining good mental health. So, without trying to focus too much attention on one label: "It seems that the group with Asperger’s syndrome, or ASD without ID, is especially vulnerable to psychiatric disorders" on the basis that: "Only 15 individuals, or 11%, of the group with Asperger’s syndrome had not been in contact with psychiatric care, and 43% had been psychiatric in-patients, which may be interpreted as a sign of vulnerability in these individuals." That word again  - vulnerability - arises in the context of autism (see here and see here for other examples). And here is yet another example (see here) illustrating that phrases like 'high-functioning' in the context of the autism spectrum, really don't do justice to the lived experience of autism and the effects of it's important add-ons.

And on the topic of ageing and autism, and specifically ageing well, there are the findings reported by Ye In Hwang and colleagues [2] to consider, and specifically: "A very small proportion (3.3%) of autistic adults were found to be aging well."

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[1] Nylander L. et al. Older Adults with Autism Spectrum Disorders in Sweden: A Register Study of Diagnoses, Psychiatric Care Utilization and Psychotropic Medication of 601 Individuals. J Autism Dev Disord. 2018. April 16.

[2] 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.

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Thursday, 10 May 2018

"To Be Quite Honest, If It Wasn't for Videogames I Wouldn't Have a Social Life at All"

The quote heading this post - "To Be Quite Honest, If It Wasn't for Videogames I Wouldn't Have a Social Life at All" - comes from the findings reported by Erinn Finke and colleagues [1]. They looked at "the perceptions of individuals with autism spectrum disorder (ASD) who play videogames as their primary leisure activity regarding the role of videogames in their lives and their motivations for playing videogames."

I've kinda touched on this topic before on this blog (see here) and some of the ins-and-outs of 'pathological' videogame use in the context of autism. On that blogging occasion, I mentioned how one has to be a little careful about 'demonising' an activity that (a) is enjoyed by millions of people, some of whom are and some aren't diagnosed with an autism spectrum disorder, and (b) could, through the wonders of online gaming, provide a valuable 'social' outlet to a population who either might prefer limited face-to-face contact or are in many ways, discriminated against when it comes to more traditional forms of social inclusion and participation (see here). Apparently this area is also something that has been mentioned at the INSAR conference this year too. The downsides to gaming: well, every moment sat in front of a screen is a moment that could have been used in other more physically active pursuits (something that is quite a big issue when it comes to quite a proportion of the autism spectrum). I might also add that mention of the word 'online' can sometimes mean opening up a whole can of worms...

Finke et al relied on a qualitative study methodology that involved asking young adults about their experiences of videogame playing. Bearing in mind the small number of participants under study, authors observed that "participants perceived playing videogames to have a positive impact on their lives and their development." Aside from the enjoyment angle (an important angle by all accounts), participants mentioned about the 'social' element to their videogame playing. Interesting too was another comment from Finke: "The motivations for playing videogames described are similar to those reported by typically developing populations." Why would they be any different?

The authors see the potential value of videogaming when it comes to "teaching" in the context of autism but I'm slightly reluctant to take up this idea for a few reasons. Foremost is the idea that not every activity where autism is mentioned really needs to be 'medicalised' or indeed, 'interventionised' (if there is such a word). I think back to all the discussions about Lego 'therapy' (see here) for example, and how it would be really easy to turn a pastime that is really enjoyable into something more like schooling, and then onward potentially make it less enjoyable. I would also mention that the types of videogames likely to be enjoyed by those on the autism spectrum are probably the same types of videogames that everyone else likes to play. So developing new 'autism-specific' games with intervention(s) in mind are not likely to go down too well in the context of gaming choice and their applicability to larger audiences. Indeed, it could be seen as discriminatory. And yes, then there is also the notion that 'interventionising' videogames will probably also promote yet more sedentary behaviours, something which we should all be keen to discourage (and I have my views about which physical activities might be considered favourable for many young people both on and off the spectrum).

Music to close and Céline Dion with a special guest... Deadpool? Although, his heart probably will go on given his renowned healing abilities...

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[1] Finke EH. et al. "To Be Quite Honest, If It Wasn't for Videogames I Wouldn't Have a Social Life at All": Motivations of Young Adults With Autism Spectrum Disorder for Playing Videogames as Leisure. Am J Speech Lang Pathol. 2018 Apr 2:1-18.

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Wednesday, 9 May 2018

What factors potentially predict quality of life in adults with autism?

"The study findings are that autistic people on average have lower QoL [quality of life] than the general population in the UK." Further: "Three main characteristics were predictive of lower QoL in almost all domains: being female, having a current mental health diagnosis and higher severity of autism symptoms." By contrast: "Significant positive predictors of QoL were: being employed (physical QoL), receiving support (social and environment QoL), and being in a relationship (social QoL)."

So said the findings reported by David Mason and colleagues [1] describing the results of a study that examined "quality of life (QoL) of a large sample of autistic adults in the UK and investigates characteristics that may be predictive of QoL." This is a vitally important topic because perceived quality of life IS important and has been discussed before in the peer-reviewed research arena with autism in mind (see here).

This time around the focus was on 'self-reported' quality of life for autistic adults who submitted data as part of a research initiative "into the life experiences of autistic adults, the Adult Autism Spectrum Cohort‐UK." Some 370 people (mostly) formally diagnosed with an autism spectrum disorder (ASD) completed the WHOQoL‐BREF, a quality of life assessment schedule developed by the World Health Organisation, as well as the Social Responsiveness Scale (SRS) and a initiative-specific questionnaire that collected various information including that about "everyday life including relationship status; home life including living alone or with family members (family of origin or spouse/partner); employment including paid employment, volunteering, or retired; education including type of school and qualifications achieved; support including who supports the adult and how often support is needed; mental health/neurological conditions including current diagnoses and type of medication/therapy; physical health conditions; and autism spectrum in other family members." Acquired data was put into the statistical 'measuring' machine and trends were reported.

So, a large proportion of participants were aged between 41 and 60 years old (~40%). The sex/gender ratios were fairly evenly split (males: 54% vs. females: 43% vs. 'prefer not to say' ~3%). The vast majority of respondents reported either a mental health issue as being concurrent to their autism diagnosis/status (~70%) or a physical health issue as being present (70%). I don't think we were actually told all the specific diagnostic categories that were included under 'a mental health issue' or 'a physical health issue' but some clues are provided in the text: "most commonly depression and/or anxiety" and "sleep problems, or hypertension." The WHOQoL‐BREF, by the way, provides information on QoL in various domains: physical, psychological, social and environment. Authors therefore report that: "Reported QoL for autistic adults was lower across all four domains than UK norms."

Then to those potential predictors of 'poorer' or 'better' quality of life, as some further statistical analysis was actioned on the collected data. Quite consistently - in the physical, psychological and environment domains - the same three elements cropped up as potentially predicting poorer quality of life: being female, having a comorbid mental health diagnosis and total scores on the SRS (an instrument that "measures autism characteristics" with a focus on social aspects). Looking at the statistical strength of the various factors observed, I'd have to say that the SRS score (total) - that measure of 'autism characteristics' - was the one that seemed to be most strongly related to QoL. Yes, the implications are that the [social] manifestation of autism itself *could* be an important driver of poorer QoL. Insofar as the factors potentially related to a more positive (better) quality of life, being employed, receiving support and being in a relationship were all mentioned, but certainly not as consistently across all the various WHOQoL‐BREF domains as noted in those negative predictors.

The authors highlight a few positives and negatives in relation to their study: use of a "robust measure of QoL is a strength", pretty large sample size and the collection of some good quality 'complete' results. That being said, they also note that a general QoL questionnaire might not gather all the important information relevant to QoL in the context of autism (I do wonder if all that ICF core sets of autism work might help matters on future research occasions). And then there's the issue of representativeness to consider, when it comes to the applicability of Mason results to the (very) wide autism spectrum (see here)...

Recommendations - 'implications' - aplenty spring from the Mason results. Focus in on better screening and treatment/management of mental health (and physical health) issues when concurrent to an autism diagnosis (see here and see here for examples). Make employment - long-term employment - work better for those on the autism spectrum (see here). Devote greater resources to discovering what factors surrounding female autism might lead to poorer quality of life. All noble sentiments worth pursuing. Alongside, are those results about autism severity also seemingly impacting on QoL. Does this perhaps also imply that moves to 'intervene' on core autistic symptoms might also be a target too? Y'know, on the understanding that 'core autism features' have also been *correlated* to some other, rather extreme endpoints also significantly affecting quality of life (see here)?

Addition: 10 May 2018. Y'know I mentioned that SRS scores - "measures autism characteristics" - might be an important variable when it comes to quality of life? Well, it seems another cohort came to similar conclusions [2] (click here for a larger view of figure b and those self SRS scores)...

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[1] Mason D. et al. Predictors of quality of life for autistic adults.  Autism Res. 2018. May 7.

[2] Oakley B. et al. Why Is Quality of Life Reduced in Individuals with Autism Spectrum Conditions? Investigating the Impact of Core Symptoms and Psychiatric Comorbidities on Quality of Life in the EU-AIMS LEAP Cohort. INSAR 2018.

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