"Having accessed treatment was associated with reporting lower levels of work/school attendance"

I have to admit that I did a bit of a double-take when I came across the quote titling this post - "Having accessed treatment was associated with reporting lower levels of work/school attendance" - in the paper published by Sheila Ali and colleagues [1] (open-access available here).

The findings came from a study that set out to investigate the "factors associated with fatigue, disability and school attendance in young people with severe CFS/ME [chronic fatigue syndrome/myalgic encephalomyelitis]." Part of the study also looked (in a preliminary manner) at whether some of the therapeutic options offered 'for ME/CFS' were up to scratch based on participants' responses and views.

"Questionnaire data were collected in two waves: at baseline (T1), and at follow-up (T2), which was 3–9 months later" as such data were collected from 51 young people "required to have a self-reported diagnosis of CFS/ME." Researchers mention how they focused on participants with "severe CFS" as measured by a self-report 'functional ability scale'. That being said, recruitment phases for the Ali study were not uniform, as two different thresholds for severity were eventually used in different recruitment phases.

No mind, Ali et al asked participants to complete various questionnaires around things like mobility, meaningful education and/or work (including attendance), and level of fatigue. Bearing in mind the use of words like 'fear avoidance' in the Ali paper (possibly denoting the biopsychosocial (BPS) 'sway' of some of the authors), various 'psychological' concepts were also included for study. The data were collated and analysed.

Results: although data for 51 participants were eventually analysed, nearly 400 young people were sent a letter inviting them to participate in the Ali study. Only 56 responses (consent forms and questionnaires) were eventually received which, even taking into account the 'severe CFS' inclusion criteria, represents a pretty low study turnout. This seems to follow a trend among certain types of study of ME/CFS (see here) which is starting to become quite noticeable.

"Thirty-seven (72.5%) participants reported using assistive equipment such as crutches, walking frames, ramps, stair-lifts and shower chairs. Thirty-three participants (64.7%) reported that they used a wheelchair. Nine participants (17.6%) reported that they were bed-bound." Contained within those sentences is the real cost of ME/CFS to something like mobility. On top of all that, researchers also observed that approaching 90% of their cohort were also taking some form of medication (I assume pertinent to things like mobility issues and beyond). In terms of how things like mobility issues impacted on participation in 'meaningful' education and/or work, we are told that only a quarter of participants "had been able to attend school, college or work in the past year." That's 'in the past year'.

Then back to those 'treatments' and their effects. So: "Although this was a naturalistic study and not an evaluation of treatment, it is notable that the majority of participants reported that they had accessed some form of treatment, and yet the mean scores for fatigue and social functioning had not changed considerably by T2." What sorts of treatments had they tried I hear you ask? Well, table 1 (see here) provides some details. The most popular treatment 'accessed' was "CBT, GET or both with at least one other treatment" closely followed by "CBT, GET or both." Allied to other independent data suggesting that cognitive behavioural therapy (CBT) and graded exercise therapy (GET) are failing many patients with ME/CFS (see here and see here and see here), and the case grows ever stronger for new treatment directions to be pursued. Such research directions should perhaps also be minus words like 'fear avoidance' or other psychobabble inclinations that have pervaded ME/CFS thought down the years. Indeed, one has to ask who would advocate for treatments that are seemingly at best ineffective and at worst downright detrimental to the patient group who are 'accessing' them?

There are some other points noted in the Ali paper including things like how "low mood is a consequence of having CFS/ME" and how "symptoms of CFS/ME and levels of functioning can fluctuate over time." These follow similar sentiments expressed in other research (see here and see here) along the lines of CFS/ME being very much a real physical illness with both physical and psychological effects.

There are some obvious caveats to mention about the Ali study, specifically around the sole use of questionnaires without any other 'actigraphic' form of inquiry (to measure something like activity levels), the representativeness of results, and the reliance on self-report when it came to diagnoses. Although I've also been pretty harsh on the effectiveness of the treatment options accessed, I will direct you to some author comments on this issue and how "the effects of treatment would not be seen within such a short period of time." I'm not too sure about such sentiments but, in the interests of balance, give them airtime in this study write-up.

Despite all that, the Ali findings add further to our knowledge about ME/CFS in young adults. They demonstrate how 'life-destroying' the illness is (are) and can be, and what that means to those who suffer with it (them). They also add to the multiple voices - research and patient voices - demanding a greater clinical focus on ME/CFS, and how objective, biological science in particular, needs to be front-and-centre of any new direction. But I'll also reiterate that any new focus and new direction needs to be minus the psychobabble; indeed it may be unethical not to [2]...

----------

[1] Ali S. et al. Psychological and demographic factors associated with fatigue and social adjustment in young people with severe chronic fatigue syndrome/myalgic encephalomyelitis: a preliminary mixed-methods study. J Behav Med. 2019 Jan 25.

[2] O'Leary D. et al. Ethical classification of ME/CFS in the United Kingdom. Bioethics. 2019 Feb 8.

----------

A puppet portrays the character of Laurence, who is described as “autistic, non-verbal and occasionally violent”

The title heading this non-sciencey post - "A puppet portrays the character of Laurence, who is described as “autistic, non-verbal and occasionally violent”" - comes from a news report discussing a play opening soon at a London theatre. The play is called 'All In A Row' and I believe centres on a family struggling to care for their son who is autistic. I believe the play specifically focuses on "the night before social services finally intervenes"...

That news item centres on the use of a puppet to depict Laurence and how writers arrived at such a decision on the reported basis that "We don’t think we could get informed consent from a non-verbal autistic actor aged 11 to play the role." Needless to say that the old tenet about not pleasing all of the people all of the time came into play, as "a backlash online" developed. Despite some initial input from the National Autistic Society (NAS) around "accuracy" and "representation" of autism in the play, they eventually decided that they couldn't support the play "particularly the use of a puppet to depict the autistic character alone."

I was a little surprised by the NAS stance on this. Surprised because when another puppet character came into being depicting autism, the NAS was a little more 'positive' on its introduction. That character was Julia "a little girl who also has autism" who appears on Sesame Street. And at the time of her introduction, the head of the NAS was reported as saying "his organisation hopes it will "inspire" other creators to include characters with autism in their work." Well it might have done, but what's the difference between Laurence and Julia, and why the different response?

I don't have any divine insight as to why the different response, but let's have a look at a few 'possibilities'.

Both puppets appear in productions that also include real-life actors, so this is not about the setting in a character-sense. The look of the puppets? Well, Julia has the typical muppet features: warm skin tone, big eyes, mouth inclined to a smile. A typical 'Anything Muppet'. Laurence is quite a bit different. More human in features, a much less warm skin tone, and eyes that can only be described as piercing. There's quite a physical difference between them. So could this be about that physical difference between the puppets?

Depiction is another factor to potentially consider. Outside of the 'autistic, non-verbal and occasionally violent' description, we are also told that "Laurence likes pizza. Laurence is about to go to school. Laurence thinks it’s okay to wee on mummy’s pillow." Allowing for the age difference in intended audiences between Sesame Street and All In A Row, I think you can see some potential differences between how autism is being depicted by Julia and Laurence. Indeed this perhaps ties into another part of the the NAS response about the use of Laurence: "we could not support the play overall due to its portrayal of autism." The question therefore is whether the depiction of autism including physical violence for example (something that has recently been enshrined in English educational law with autism in mind) is a reason for the 'backlash'? Is this more about PR than anything else?

I think what many people forget (or don't want to remember!) is that autism is a very, very heterogeneous spectrum. It describes so much human experience under one banner. There are no doubt many children who fit the Julia description of autism. Fairly quiet, wouldn't hurt a fly, thriving in some areas yet struggling in others. On the other hand, there are also children who probably better fit the Laurence description of autism: 99% of the time like Julia but also prone to aggressive outbursts (against themselves and also others) and sometimes challenging in their behaviour. The trend to show the world the Julia children over the Laurence children is quite pronounced in some quarter these days. It's also accompanied by online 'abuse' of parents and guardians who dare to show / talk about their 'challenging' children and their reality (see here). Indeed, social media is full of parents showing the good and not-so-good side of their kids, but if your child has autism / is autistic it seems some people think you're not entitled to do the same? Sounds like discrimination to me. Such sentiments have also probably partly contributed to the formation of a society that focuses on "the burgeoning population of children and adults affected by severe forms of autism or related disorders." Even that society attracted criticism (see here) despite, as far as I can see, some noble goals around healthcare and vocational options which may well benefit everyone on the autism spectrum. Like I said "not pleasing all of the people all of the time."

Finally, the word 'dehumanising' is used quite a bit in that news report: "a negative narrative of dehumanising" and "literally dehumanised the identity you sought to represent." My question: does Julia, as a puppet, also dehumanise autism? Because surely if the charge is levied against Laurence as a puppet, then Julia as a puppet also fits the bill too? And if so, perhaps the media need to come up with other ways and means of getting more characters with autism on the screen (see here) to depict the wide range of behaviour covered under the [currently] singular term of autism...

----------

Psychiatric and seizure medicines for autism: what 'works' best

The paper by Devon Coleman and colleagues [1] represents pretty good scientific value for money by my reckoning. Describing the results of a 'survey' called the "National Survey on Treatment Effectiveness for Autism" created by the researchers, the aim was to provide "separated... scales for overall benefits and overall AEs [adverse effects]" for a wide range of interventions used in the context of autism.

The focus this time around was on "Psychiatric and Seizure medications data" but it looks like there may be quite a bit more to see from this group in future with regards to data on "supplements, diets, therapies, and educational interventions" also collected during this initiative. Before continuing on with this paper I have to hat-tip the authors for mentioning a great and much under-valued resource in autism circles: "the Parent Ratings of Behavioral Effects of Biomedical Interventions Survey,... conducted by the Autism Research Institute (ARI) and published in 2008." Indeed, in other posts talking about the medicines cabinet and autism (see here) I've expressed my positive views of the ARI resource albeit with caveats.

Anyhow: "we report ratings of 26 psychiatric and seizure medications by 505 participants." Researchers actually noted that nearly 900 people completed their survey; most of whom were described as the "Primary caregiver of an individual with autism." Some people might um-and-ah about the lack of 'authentic autistic representation' in this study, but one needs to bear in mind that most participants - about three-quarters - were under 18 years of age, most diagnosed with autism and not autism spectrum disorder (described as "less severe than a diagnosis of autism") and most were currently described as having mild, moderate or severe autism. I know this won't be enough for some people, but there you have it.

Then to the medicines that were 'graded', which fell into "five general categories: stimulants (four medications), SSRIs [selective serotonin reuptake inhibitors] (five medications), antipsychotics (four medications), seizure (nine medications), and other (four medications)." There's a lot of data included in the Coleman paper which really is too much for a blog post. I'll direct you to Figure 8 of the Coleman paper which provides a handy 'net benefit score' taking into account an 'overall benefit score' and an 'overall adverse score' for each medicine. When it came to SSRI medicines - typically indicated for treating depression - sertraline came top. When it came to antiepileptic medicines - primarily used to manage epilepsy and/or seizures - lamotrigine came top. When it came to antipsychotic medicines, aripiprazole came top. I was also interested to see that buspirone, a medicine typically indicated for anxiety, also did pretty well according to the Coleman results, which kinda ties in with some continuing research interest in this medicine with autism in mind (see here). Researchers also provide a handy 'medications for symptoms' overview as a consequence of their results (see Table 7) covering various symptoms from aggression/agitation to tics/abnormal movements. I can see this being particularly useful when it comes to physicians having to make big medication decisions (which should never be entered into lightly).

There's a couple of other details that are also mentioned in the Coleman paper outside of those 'how was medicine rated?' sentiments. Some details are not likely to make many friends in some quarters. So, around 2% of participants were described as follows: "No current diagnosis, but he/she was on the autism spectrum previously." Yes folks, such data once again harks back to the idea that for some people at least, autism is not a lifelong diagnosis (see here and see here). And also: "Thirty-four percent of participants had early onset of symptoms, but 56% had normal development followed by a plateau or regression." Regression accompanying autism is not the 'dirty' concept that it used to be (see here). Indeed, in the few years that I've been blogging about autism research, I've seen it become a lot more commonplace to talk about regression and autism (see here) even to the point that some now talk about it being 'the rule rather than the exception' (see here). Interesting.

And then there's something even more controversial in the Coleman paper: "The perceptions of possible causes of the regression are listed in Table 2." So we have things like high fever, illness, seizure and then... vaccination. I know this takes us into some uncomfortable territory, but the authors report that 51% of respondents to their survey who cited regression as part of the clinical picture mentioned vaccination as the 'perceived cause' whether singly or in conjunction with other factors. Of course I'm going to provide a link to what the population-based science says on this matter (see here) with the caveat that such 'perceived cause' data perhaps needs objective and dispassionate follow-up (see here and see here).

The Coleman results are not without their limitations as per author comments such as: "The survey is retrospective and based on respondent memory which reduces the accuracy" and "The results are subject to “placebo effect” since it represents clinical data without a placebo control, so the real benefit is likely less than the perceived benefit." But let's not take too much away from the findings and how they may, as well as informing clinical practice, also hopefully lead to further inquiry to make medicines safer and more reliable for those on the autism spectrum who access them.

----------

[1] Coleman DM. et al. Rating of the Effectiveness of 26 Psychiatric and Seizure Medications for Autism Spectrum Disorder: Results of a National Survey. J Child Adolesc Psychopharmacol. 2019 Feb 6.

----------

"A genius. A saviour. But he was also autistic and gay. So we betrayed him." Autistic?

The legacy

The quote titling this post - "A genius. A saviour. But he was also autistic and gay. So we betrayed him" - came from the impassioned speech given by the naturalist and broadcaster Chris Packham. The speech probably contributed greatly to his Icon being crowned "the 20th century's most important and influential figure" as part of the BBC Two series called Icons. That icon was Alan Turing, the "Father of the computer and WW2 code-breaker."

I don't think many people would argue that Alan Turing was a worthy winner. To get to the finals of the Icons series, the public voted for him above other great scientists in his category such as Marie Curie and Albert Einstein (my brood and I actually thought Einstein was going to walk this category given his life, the universe and everything theories). Turing eventually saw off competition in the final from the likes of Pablo Picasso and Nelson Mandela. Even the 'greatest' couldn't match the impressive contribution that Turing made to the 20th Century and beyond. A worthy British winner voted for by a (predominantly) British audience 😉.

That all being said, I was a little disappointed by the reference to Alan Turing being 'autistic' made by Chris Packham (himself diagnosed with autism). Disappointed because, as a scientist who I assume sought truth or at least a significant degree of probability of truth, even Turing would perhaps raise an eyebrow at the notion that he was autistic without, as far as I am aware, ever being assessed or diagnosed as such. It might seem like a paltry point to focus on. After all, there were certainly clues throughout Turing's life that had he been alive and working today, someone, somewhere might have considered a diagnostic assessment for autism. But he wasn't diagnosed with autism. That's the 'truth' of the matter. And trying to rewrite history to say that he was autistic without any authoritative evidence (i.e. a diagnostic assessment of the man himself) is, well, unscientific.

Other writers have already discussed the Turing diagnosis issue in some depth (see here and see here). Although not necessarily sharing the politics of all those writers, I do share the sentiments that the rush to (armchair) diagnose historical figures of some importance to have autism or some other diagnosis serves no-one well. And believe me, there have been enough attempts at this down the years (see here); all speculative and many evidence-free. Any attempts to insinuate that the achievements of Alan Turing were 'down to his autism' pathologises his life and important works to a diagnostic label that he didn't even possess.

I know some people want that to be the case. They want the 'autistic identity' to reflect the achievements of people like Alan Turing; a sort of poster boy for autism, alongside the likes of Einstein and Newton according to some people. They'll say something along the lines of that autism wasn't recognised back then as much as it is nowadays. They might also say that autism is just a label, and that the current way of diagnosing is too restrictive or something like that. I don't disagree with some of those arguments (as long as you don't tell me self-diagnosis is as valid as formal diagnosis), but the simple fact of the matter is that Turing was never, as far as we know, assessed or diagnosed with autism. Period.

By saying that Turing was autistic would no doubt help the thousands of children (and adults) who have been labelled with autism / as autistic. It would convey a message that autism is not always exclusively about 'deficit' and that some of the greatest achievements of humankind might have had 'a pinch of autism' added. I admire such attempts to convey such a message; kids of all shapes and sizes should have role models and people to look up to. But such a message should not be made at the expense of facts. It shouldn't be made at the expense of rewriting history as one might prefer it to look, no matter your strength of feeling on a matter. Indeed if you want a good role model, look to Chris Packham and his 'Really Wild' influence over the past few decades. Fond memories for many including me.

If one follows the guidance on diagnosis, as in a diagnosis only being made when autistic signs and traits 'significantly impact on facets of life', one could similarly argue that Turing might not have even hit such a diagnostic threshold anyway. Did any of his 'autistic traits' impair his important work during World War 2? Obviously they did not. Did such a presentation deter him from coming up with the designs for the Automatic Computing Engine? No, they did not. And the idea that autistic traits are "present over time and have a noticeable effect on daily life" is an important part of the diagnosis of autism.

What did have a noticeable effect on Turing was his sexuality; his sexuality at a time when anti-homosexuality laws were active here in Blighty. A shameful set of laws eventually meant Turin accepting chemical castration rather than going to prison. This is the betrayal that Chris Packham rightly asserts in his speech, as Turing was barred from working at GCHQ. He was credited with saving millions of lives during the war, but archaic laws meant that counted for nothing during his lifetime. I don't know how much this affected Turing personally. Yes, he died by cyanide poisoning and the coroner at the time reported death by suicide. But even his death by suicide is now being questioning in some quarters (see here); to quote: "Turing had cyanide in his house for chemical experiments he conducted in his tiny spare room... And he was known for tasting chemicals to identify them." We don't know.

Alan Turing is a worthy winner of the BBC Icons series. His endeavours and achievements are very much still with us today in just about every corner of our lives. He was a genius, and certainly during World War 2 he was also a saviour. Labelling him however as autistic without even any hint of a diagnostic assessment being undertaken or diagnosis received represents a gross 'evidence-free' injustice to him and his memory. And the words 'evidence-free' is a particular slur on the memory of one of our greatest scientists...

----------

Autism and the measurement of urinary amino acids

Today's post concerns the findings reported by Aiping Liu and colleagues [1] who, following the analysis of urine samples from a group of children diagnosed with an autism spectrum disorder (ASD) and a not-autism control group, concluded that there may be something to see with regards to the urinary excretion of amino acids.

First things first, amino acids are the building blocks of proteins. Long chains of amino acids form different proteins (and peptides) that serve multiple biological functions. But making up proteins is but one of the roles of amino acids, as a variety of other functions are also included in their repertoire; notably also being the raw material for the formation of some neurotransmitters and related compounds (see here for example).

Liu et al approached their analysis of amino acids in relation to autism from the point of view of their measurement being "potential novel metabolic biomarkers for ASD." This follows something of a trend in autism research circles whereby patterns of certain amino acids and their associated chemistry in certain biofluids might have such 'potential' for some types of autism (see here and see here and see here for some other examples) albeit with certain caveats. Researchers utilised some quite well known methods when it came to their analysis - "liquid chromatography-tandem mass spectrometry (LC-MS/MS)-based analysis" - and set to work using a tried-and-tested method (see here): "a two-step discovery–validation approach."

Analysing urine samples from nearly 60 children with autism and over 80 not-autism controls ("28 ASD and 41 TD  [typically developing] children for the discovery stage and from an additional cohort of 29 ASD and 41 TD children for the validation stage"), researchers reported detecting and identifying "63 UAA [urinary amino acid] indicators." Twenty-one of these amino acids and/or amino acid metabolites were observed to be "present at significantly different levels in the urine of ASD children compared with TD children" in both participant sets. These compounds were fairly evenly either higher or lower in the kids with autism group (10 higher and 11 lower). I was particularly interested to see that creatinine was observed to be in the significantly higher category associated with the autism group given some other results that were counter to this finding (see here and see here) including some of my own published data [2] from a few years back. Authors also mention how they "identified a panel of 7 UAA indicators that [most effectively] discriminated between the samples from ASD and TD children (lysine, 2-aminoisobutyric acid, 5-hydroxytryptamine, proline, aspartate, arginine/ornithine, and 4-hydroxyproline)."

From those compounds, a few themes emerged with regards to the biochemistry that *might* show some involvement with autism. So: "Abnormalities in the Methionine Cycle in Children With ASD", "Evidence of High Oxidative Stress Levels in Children With ASD" and "Abnormalities in 5HT Metabolism in Children With ASD" are some of the systems potentially implicated by Liu et al. Needless to say that such biological systems are by no means strangers to autism research (see here and see here for examples) albeit not necessarily always in the same direction as the Liu findings.

Caveats? Well yes, a few, such as a reliance solely on single spot urine samples rather than multiple samples from the same person, no other measures of amino acid content in blood for example, and the focus on participants diagnosed with autism excluding things like "attention-deficit hyperactivity disorder, obsessive compulsive disorder" where 'real-life autism' rarely exists in some sort of diagnostic vacuum (see here). But, the findings are interesting and once again highlight how metabolomics is something particularly valuable to autism research (see here) and complementary to genetic studies for example, when trying to decipher the very heterogeneous autisms (plural). Issues with certain amino acids when identified in the context of autism *might* also point to a wider issue (see here) that could also indicate intervention too...

----------

[1] Liu A. et al. Altered urinary amino acids in children with autism spectrum disorders. Front. Cell. Neurosci. 2019. Jan 10.

[2] Whiteley P. et al. Spot urinary creatinine excretion in pervasive developmental disorders. Pediatr Int. 2006 Jun;48(3):292-7.

----------

Suicide risk and autism: data from "Utah over a 20-year period"

The findings reported by Anne Kirby and colleagues [1] are not for the faint-hearted but continue a vitally important theme in autism research and practice circles looking at suicide risk and autism (see here and see here). The 'value-added' bit to the Kirby results to distinguish them from other study in this area was the reliance on data across a 20-year period from a place that has some important autism research history: Utah in the United States (see here).

So: "Four sources of existing data were utilized for this study: URADD statewide autism surveillance data, statewide suicide surveillance data collected by the Utah Office of the Medical Examiner (OME), the UPDB, and Utah's Indicator‐Based Information System for Public Health (IBIS‐PH)." From such data sources, researchers accessed information for nearly 17,000 people diagnosed with an autism spectrum disorder (ASD) "alive at the beginning of 1998 and at least 5 years of age in 2013." Most were male and most were white. They similarly determined that nearly 9,000 people in their total population - not just those diagnosed with ASD - died by suicide between 1998 and 2017. Again, most were male and most were white. The data were combined and interrogated "to calculate the incidence (in 5‐year intervals) of suicide deaths in people with ASD over a 20‐year period (1998 to 2017) in total, as well as by sex, and compared suicide risk in people with versus without ASD." Researchers also looked at other important variables such as "sex, race, death age, occupational status, marital status, and manner of death" across the groups.

Results: "In the first 15 years of the study (1998–2012), we did not observe differences in suicide cumulative incidences between the ASD and non‐ASD populations." This means that when the groups were compared as a function of death by suicide, the figures for those with autism were not significantly different from those without autism for this time period. By saying that I don't want to belittle the fact that between 1998 and 2012 for example, 2 people out of 5,202 autistic people died by suicide or that 1,671 out of 1,928,484 non-autistic people died. Each of these figures was a person with a life and with a family, and that's something that should never ever be forgotten.

The pattern however changed when researchers looked at the period between 2013 and 2017: "For the most recent time interval (2013–2017), the cumulative incidence of suicide death in the ASD population was 0.17%, which is significantly higher than the non‐ASD population cumulative incidence of 0.11%." This percentage (0.17%) represented 28 deaths from an autistic population of 16,907 and 2,791 deaths from a non-autistic population of 2,630,221. Although a sideline point, I'll also bring to your attention how the autistic population numbers changed over the 5-year blocks of study in the Kirby paper: 1998-2002: 5,202 people; 2003-2007: 8,722 people; 2008-2012: 13,890 people; 2013-2017: 16,907 people.

A few other details were observed by Kirby et al: "In comparison with non‐ASD + suicide cases, ASD + suicide cases had significantly younger average death ages (32.4 years vs. 41.8 years; t = −3.8, P < 0.001)." Also: "Combined, 73% of the ASD + suicide cases used methods for suicide considered to be violent; the remaining 26% used nonviolent methods." This again, is important information.

Researchers also mention how across the 2013-2017 period, another important trend was observed: "suicide risk in females with ASD was over three times higher than in females without ASD (relative risk (RR): 3.42; P < 0.01)." They contrast this with the finding that "there were no documented cases of suicide death among females with ASD during the first 15 years of the surveillance period" and what this could mean when it comes to possible explanations of suicide risk in relation to autism.

There's quite a bit to learn from the Kirby findings. Although there are limitations attached to the study design - "inadequate data on intellectual ability was available to examine the influence ID may have on suicide risk in individuals with ASD" - the study was a good one because of its population-wide focus and the pretty good autism-related resources that Utah has (and has had for many years). It demonstrates once again that the difficult topic of suicide and autism should remain a research priority in order to identify who might be most at risk and why, alongside the ways and means that such risk *might* be mitigated (see here for one example).

And for those who might need someone to text / email / talk to, there are always options (see here for services in the UK or see here for those elsewhere).

----------

[1] Kirby AV. et al. A 20-year study of suicide death in a statewide autism population. Autism Res. 2019 Jan 21.

----------