Saturday, 23 September 2017

Pregnancy antidepressant use and offspring outcomes beyond autism?

I'll say one thing for the British Medical Journal (BMJ), they don't seem to be afraid to cover important issues relating to the *possible* "reproductive safety of drugs" [1] as per their publication of yet another paper looking at antidepressant use during pregnancy and offspring outcomes published by Xiaoqin Liu and colleagues [2]. This follows another paper published in the BMJ and covered on this blog a few weeks back (see here).

The specific class of drugs being examined again are, as I mentioned, the antidepressants and based, yet again, on data from one or more of those wonderful Scandinavian population registries in relation to how pregnancy use of antidepressants *might* impact on risk of risk of various psychiatric disorders in offspring. A diagnosis of autism spectrum disorder (AD) has been a primary focus of previous research in this area; particularly the question of whether the medicines themselves or the condition(s) that the medicines are used for (i.e. maternal psychopathology) might be the more important variables related to enhanced offspring risk of autism. The last paper covered on this blog by Rai and colleagues [3] very cautiously suggested that: "The results of all these analyses, which used different assumptions, seemed to be consistent with each other, suggesting that the association between in utero exposure to antidepressants and autism might not be fully explained by confounding." Cautiously...

This time around the net was widened from just looking at autism as an offspring outcome to "overall risk of psychiatric disorders" including: "autism spectrum disorder... mood disorder... neurotic, stress related, and somatoform disorder... behavioural and emotional disorder... and mental retardation." I might add that these are the authors words not mine and diagnoses were based on ICD-10 criteria and codings.

Looking and following some 900,000 children born between 1998 and 2012 in Denmark until 2014, researchers categorised participants according to their pregnancy antidepressant exposure(s): "unexposed, antidepressant discontinuation (use before but not during pregnancy), antidepressant continuation (use both before and during pregnancy), and new user (use only during pregnancy)" and looked at the frequency of those conditions included for study.

Results: some 2% of children were born to mums who used an antidepressant during pregnancy (n=21,063). Various types of antidepressants were used but the majority were prescribed SSRIs (Selective Serotonin Reuptake Inhibitors) either alone (monotherapy) or in conjunction with other non-SSRI medication.

"We observed increased risks of psychiatric disorders in all three groups of antidepressant users (discontinuation, continuation, and new user groups), compared with the unexposed group." This itself is an important finding but does not yet disentangle whether medicine use or the reason(s) for medicine use might be the more important variable. Then: "we observed an increased risk of psychiatric disorders in children whose mothers continued antidepressant use during pregnancy, compared with mothers who discontinued." Such a statement potentially edges a little closer to some influence of pregnancy antidepressant use on offspring outcomes but, and it is an important but: "These associations could be attributable to the severity of the underlying maternal disorders in combination with in utero antidepressant exposure." In other words, those mums who needed to continue antidepressant use throughout pregnancy probably had to do so because their symptoms either returned or were not controlled properly when medication is not in place. This might imply that more serious maternal psychiatric disorder could be a variable in any enhanced risk of offspring psychiatric disorder.

When it came to looking at specific diagnostic labels for offspring, all but "mental retardation" (I prefer the term learning disability) seemed to be elevated alongside "in utero exposure to antidepressants." The conditions with the highest risk were the mood disorders including diagnoses such as clinical depression and bipolar disorder. Given that antidepressants are typically (but not exclusively) used to treat/manage mood disorders, such a finding of maternal mood disorder potentially transmitting down into offspring mood disorder receives further credence from such results.

The Liu paper and accompanying editorial grapple with the question of whether the *possible* risks from pregnancy use of antidepressants on offspring merit a change to guidance on their use at such a critical time. As I've mentioned on other occasions discussing this topic, antidepressants are not typically just dispensed willy-nilly without appropriate clinical indication. They provide an important service in controlling various types of symptoms; pertinent to the idea that uncontrolled depression during pregnancy for example, can have all-manner of negative outcomes. As all medicines do, yes they may have side-effects but these need to be weighed up against perceived benefits, taking into account any important influence on the developing child. Indeed, the authors note: "any final decision on antidepressant continuation should be individualised and made jointly by health professionals and patients."

And whilst I've mentioned pregnancy antidepressant use and offspring autism risk, yet another review paper enters the scientific fray [4]...

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[1] Nordeng H. et al. Prenatal exposure to antidepressants and increased risk of psychiatric disorders. BMJ. 2017; 358: j3950.

[2] Liu X. et al. Antidepressant use during pregnancy and psychiatric disorders in offspring: Danish nationwide register based cohort study. BMJ. 2017; 358: j3668.

[3] Rai. D. et al. Antidepressants during pregnancy and autism in offspring: population based cohort study. BMJ. 2017; 358: j2811.

[4] Andalib S. et al. Maternal SSRI exposure increases the risk of autistic offspring: A meta-analysis and systematic review. Eur Psychiatry. 2017 Jun 20;45:161-166.

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Friday, 22 September 2017

SMILE: On the Lightning Process + specialist medical care for chronic fatigue syndrome (CFS)

Even before the publication of the results by Esther Crawley and colleagues [1] I had already seen quite a few discussions on the use of the Lightning Process being applied to the label chronic fatigue syndrome (CFS) (see here for example).

A trial protocol [2] and some additional 'building work' [3] on this topic had already been published in the peer-reviewed domain, talking about how use of the "Phil Parker Lightning Process® (LP)" developed from "osteopathy, life coaching and neuro-linguistic programming" was already reported in the context of CFS (and CFS/ME - myalgic encephalomyelitis) and the requirement to study it given "no reported studies investigating the effectiveness or possible side effects (for example serious adverse events) of the LP."

The theory behind the LP is that of training individuals "to recognize when they are stimulating or triggering unhelpful physiological responses and to avoid these, using a set of standardized questions, new language patterns and physical movements with the aim of improving a more appropriate response to situations." In short, I don't think it's unreasonable to say that the biopsychosocial (BPS) view forms part of the methodological basis for the intervention. Alarm bells were already starting to ring (see here).

The Crawley results have been posted across the lay media, with headlines such as 'Controversial Lightning Process helps children with chronic fatigue syndrome' and 'Chronic fatigue therapy 'could help teenagers', study says.' Interestingly however, various counter viewpoints about the trial have also been included in such reports, as per quotes such as "The over-simplistic and largely psychological model of ME/CFS causation that is being put forward to patients by Lightning Process practitioners is totally out of step with emerging scientific evidence as to its cause." Even expert opinion has it's own worries about the trial and it's subject matter. I'll come back to all that shortly.

So what did the study actually do and find? Well, teens with mild/moderate CFS/ME were the target study group (100 of them): "Children were diagnosed with CFS/ME after a thorough assessment which included screening for other disorders associated with fatigue." The authors noted that recruitment was 'problematic' when it came to this trial as per the note: "Fewer than 30% of eligible children were randomised. We do not know why the majority did not want to take part in the trial but it may be because they did not want to take part in groups or travel for three consecutive days." Diagnosis by the way, I assume followed the NICE guidance on the topic; the same NICE guidance that has seen a U-turn in recent days on the potential need for some reconsideration (see here). Real 'patient power' was behind this decision by the way.

Fifty-one of the 100 participants were allocated to receive specialist medical care (SMC) plus a few days LP training and the remaining 49 just received SMC. SMC by the way, again follows those NICE guidance "focused on improving sleep and using activity management to establish a baseline level of activity (school, exercise and social activity) which is then gradually increased." CBT - cognitive behaviour therapy - is also offered to those with "significant anxiety or low mood" and: "Participants could choose to use physiotherapist-delivered graded exercise therapy, which provides detailed advice about exercise and focuses on an exercise programme rather than other activities." The primary outcome of the trial was scores on the "the 36-Item Short-Form Health Survey Physical Function Subscale (SF-36-PFS)" at baseline and again at 6 months. Various other measures were also included as secondary outcomes looking at "pain, anxiety, depression, school attendance and cost-effectiveness from a health service perspective at 3, 6 and 12 months."

Results: "It is the first trial that has demonstrated the effectiveness of an intervention other than CBT for paediatric CFS/ME." Although it is debatable whether CBT is as 'effective' an intervention for CFS/ME as many people might think (see here for a real world perspective on this from some of the authors on the current paper and see here for other findings), the results did seemingly show a difference between the groups when it came to mean SF-36 physical function scores in favour of the experimental group. The margin of the group difference was significant and authors noted that: "There was little evidence that the effect of LP+SMC compared with SMC on the primary outcome differed according to baseline age, anxiety or school attendance." The caveat to all this is the reliance on patient-reported outcomes and the unblinded nature on the trial that "may have been affected by participants’ knowledge of the group to which they were randomised." As other commentators have noted (see here again) 'positive expectations' seem to be part-and-parcel of the LP method and it's not inconceivable that these might have subsequently affected patient scores. Further comment from the authors that "it would be unethical to have a control group without treatment"as part of their study is to some extent justified but does not discount the idea that other, non-psychological interventions, could have been pitted against both SMC and the LP+SMC (see here for one double-blind, placebo-controlled example). Indeed, I'd like to see more of such comparisons in further study.

When it came to another important part of the study - adverse effects - authors specifically noted that: "Physical function at 6 months deteriorated in nine participants, of whom eight were in the SMC arm." They also reported on a few instances of adverse events but concluded that generally both study arms were considered safe over the course of study.

From a scientific point of view, the Crawley results provide some support for the use of the LP + SMC in the context of [some] teen CFS/ME. The authors noted that they don't know whether their results are likely to generalise to more severe cases of CFS/ME or indeed those younger than 12 years old, and offer little in the way of explanation as to why they got the results that they got (i.e. "Further research is needed to understand why LP improves outcomes at 6 and 12 months and which aspects of the LP contribute to its effectiveness.") I'm not however totally sold on the idea that the LP is "teaching people to use their brain to “stimulate health-promoting neural pathways”" as an explanation for the the findings, but would be willing to concede should the relevant (MRI?) scientific evidence ever emerge. As an aside, quite a lot of the research with a BPS slant to it with regards to CFS/ME could benefit from the odd physiological measures now and again just to see what may or may not be being affected...

Bearing in mind the [long] history of medical involvement in CFS/ME and the often detrimental focus on things like the BPS model [4] with regards to the condition, it's not a surprise that even despite 'positive' results, the SMILE trial has not been received with open arms by quite a few. Problems with trial recruitment? Well, one might opine that this could have had something to do with the subject matter and that BPS-type implication behind the trial potentially putting people off. Other more qualitative reports on the use of the LP in the context of CFS/ME [5] have hinted at issues with things like the "secrecy surrounding it, and feelings of being blamed if the treatment did not work" that hardly provide a great endorsement for getting involved. Yet again, the burden of CFS/ME is seemingly being placed on the person, with only little regard for the fact that there is a growing body of evidence to suggest that biology trumps psychology when it comes to the presentation and perpetuation of symptoms for many (see here). All the positive feelings, thinking and 'reprogramming' in the world are probably not going to fundamentally alter such biological (medical) issues as per other examples in the research literature (see here). Given also that science does not exist in a social or cultural vacuum, and past scientific experiences when it comes to treatment options for CFS/ME (see here) I wonder if perhaps a new direction needs to be taken - particularly here in Blighty - whereby as many resources and research interests are put into trying to understand the biology of the spectrum that is CFS/ME as are seemingly being dedicated to looking at and tackling the psychology of CFS/ME.

Parity in biological and psychological research is the real 'mind-body' stuff when it comes to CFS/ME...

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[1] Crawley EM. et al. Clinical and cost-effectiveness of the Lightning Process in addition to specialist medical care for paediatric chronic fatigue syndrome: randomised controlled trial. Archives of Disease in Childhood. 2017. 20 Sept.

[2] Crawley E. et al. Comparing specialist medical care with specialist medical care plus the Lightning Process for chronic fatigue syndrome or myalgic encephalomyelitis (CFS/ME): study protocol for a randomised controlled trial (SMILE Trial). Trials. 2013 Dec 26;14:444.

[3] Crawley E. et al. The feasibility and acceptability of conducting a trial of specialist medical care and the Lightning Process in children with chronic fatigue syndrome: feasibility randomized controlled trial (SMILE study). Trials. 2013 Dec 5;14:415.

[4] Geraghty KJ. & Esmail A. Chronic fatigue syndrome: is the biopsychosocial model responsible for patient dissatisfaction and harm? Br J Gen Pract. 2016 Aug;66(649):437-8.

[5] Reme SE. et al. Experiences of young people who have undergone the Lightning Process to treat chronic fatigue syndrome/myalgic encephalomyelitis – a qualitative study. Br J Health Psychology. 2012; 18: 508-525.

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Thursday, 21 September 2017

"the likely effects of autism spectrum disorder on adolescent driving abilities"

"The literature revealed that drivers with autism (particularly males) were less likely to identify social hazards (e.g., pedestrians), had slower reaction times, more tactical driving difficulties, reported more traffic crashes, citations and intentional driving violations, and had poorer situation awareness skills than drivers without autism."

So said the literature review published by Clara Silvi and colleagues [1] looking at how young people diagnosed with an autism spectrum disorder (ASD) manage the multiple tasks involved in driving and how various characteristics linked to autism *might* translate into "driving-related challenges."

I feel I must add a caveat or two before proceeding with this post. First up is the quite widely known about association between age and driving ability (or inability). Younger drivers are, for various reasons, already more likely to be "overrepresented in road crash statistics." Inexperience, more risk-taking driving behaviours combined with the 'overconfidence of youth' are likely to be important reasons for such adverse driving statistics. Second, a diagnosis of autism does not automatically make everyone with autism a poor driver. Granted, here in the Blighty at least, a diagnosis of autism or ASD is something that needs to be considered in the context of licencing for driving (see here) but unlike something like epilepsy - "epileptic attacks, seizures, fits or blackouts" - the condition/label does not automatically disqualify someone from being licensed to drive.

OK, the Silvi review initially took in quite a lot of the literature on this topic, eventually being boiled down to 9 articles. These collected research papers provided various viewpoints on autism and driving behaviours/outcomes including that from parents/caregivers, driving instructors and importantly, young novice drivers with autism. The endpoint reached suggested that "symptoms of autism spectrum disorder can negatively affect the driving abilities of young drivers with autism spectrum disorder, further impacting their ability to drive, and in this way increasing their risk of crashing."

The authors have zoomed in quite a bit on a possible role for situational awareness when it comes to adverse outcomes in the context of autism and driving. Situational awareness combines various elements whereby the 'here and now' of the driving environment is constantly changing and hence drivers require a high degree of perceptual and cognitive flexibility and adaptation to adjust their driving behaviour accordingly. Indeed the authors talk about how: "Poor/underdeveloped situation awareness can represent a lack of mental models and schemas (thought/behavioral patterns)."

I can kinda see how some of the ways that autism has been defined *might* overlap with the findings talking about how "situation awareness skills were less developed in drivers with autism spectrum disorder." This is something picked up in other research too [2]. I'm not so sure about the whole 'lacking in mental models' thing applied specifically to autism (seemingly harking back to the sweeping generalisation of a 'lack of theory of mind') but can perhaps see a way forward for how cognitive flexibility might be something important in the context of traits related to being rule-bound and highly perseverative.

There is a balance to be struck between the safety of autistic drivers (and indeed, the safety of other road users) and ensuring that personal liberties are not impinged on too much as a result of the Silvi findings. As many drivers will tell you, the freedom that comes with driving a car or other vehicle is something that adds considerably to quality of life; a topic that has already revealed some quite profound issues in relation to some autism [3] (see here for my take). Indeed, if accessibility is a factor in ensuring those on the autism spectrum can live a good quality of life, moves to make driving safer and more readily available to more people on the spectrum should be further [carefully] investigated.

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[1] Silvi C. et al. A Literature Review of the Likely Effects of Autism Spectrum Disorder on Adolescent Driving Abilities. Adolescent Research Review. 2017. Sept 2.

[2] Chee DYT. et al. Investigating the driving performance of drivers with and without autism spectrum disorders under complex driving conditions. Disabil Rehabil. 2017 Aug 28:1-8.

[3] Ayres M. et al. A systematic review of quality of life of adults on the autism spectrum. Autism. 2017 Aug 1:1362361317714988.

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Wednesday, 20 September 2017

Treating violence in schizophrenia with fish oils?

"Violent schizophrenia patients treated with fish oil (360mg DHA+540mg EPA) demonstrated a decrease in violence."

That was the primary conclusion arrived at in the study results by Yi Qiao and colleagues [1] suggesting that some aspects of nutrition may very well have implications for extremes of behaviour in the context of psychiatric diagnoses. The ClinicalTrials.gov entry for this study can be seen here.

DHA - Docosahexaenoic acid - and EPA - Eicosapentaenoic acid - are categorised as omega-3 fatty acids. In this research instance, Qiao et al divided up their "Fifty inpatients meeting ICD-10 criteria for schizophrenia" such that roughly half received a fish oil for 12 weeks and half received a placebo. I should add that this 'inpatient' group also scored significantly on the Modified Overt Aggression Scale (MOAS) at baseline.

Results: well, fish oil use did not seem to make any significant difference to some of the [positive and negative] signs and symptoms of schizophrenia compared with placebo use. But as per the opening sentence to this post, there did seem to be something significant to see when it came to follow-up of violent behaviour alongside the use of fish oils.

These are interesting findings. My first thoughts on reading the Qiao results harked back to previous work looking at the use of nutrition in the context of a prison population by Bernard Gesch and colleagues [2]. That research concluded that: "Antisocial behaviour in prisons, including violence, are reduced by vitamins, minerals and essential fatty acids" where EPA and DHA were part of the supplement provided under "double-blind, placebo-controlled, randomised trial" conditions; albeit in smaller doses that those used by Qiao and colleagues.

The Qiao results are also not the first time that fish oil use for violence in the context of schizophrenia have been talked about in the peer-reviewed science domain [3]. With the understanding that violence accompanying schizophrenia is probably going to be as complex as violence outside of schizophrenia, such promising results require some further replication and a little more data on possible hows-and-whys. The low cost, pretty favourable safety profile and reports of other potential health benefits associated with fish oil use however, suggest that such an intervention could easily be incorporated into treatment plan for many people fitting a similar profile to those described by Qiao and colleagues.

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[1] Qiao Y. et al. Effects of Omega-3 in the treatment of violent schizophrenia patients. Schizophr Res. 2017 Aug 19. pii: S0920-9964(17)30501-7.

[2] Gesch CB. et al. Influence of supplementary vitamins, minerals and essential fatty acids on the antisocial behaviour of young adult prisoners. Randomised, placebo-controlled trial. Br J Psychiatry. 2002 Jul;181:22-8.

[3] Légaré N. et al. Omega-3 and violence in schizophrenia. Schizophrenia Res. 2007; 96: 269.

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Tuesday, 19 September 2017

"a heightened co-occurrence rate of ASD [autism spectrum disorder] and GD [gender dysphoria]"

Gender dysphoria "where a person experiences discomfort or distress because there's a mismatch between their biological sex and gender identity" is something that has seemingly risen in research popularity in the context of autism (see here).

The findings reported by Janssen Aron and colleagues [1] (open-access available here) add to the body of research in this area where "endorsement of sex item 110, “wish to be opposite sex,” is 7.76 times more likely among participants with an ASD [autism spectrum disorder] diagnosis than in a nonreferred comparison group." 'Sex item 110' refers to a question item on the Child Behavior Checklist (CBCL) by the way.

Drawing on data derived from almost 500 participants diagnosed with an ASD and some 1600 responses to the CBCL from a 'normative sample', researchers inquired about possible gender variance. Importantly: "In the present study, all CBCL charts had been filled out by the patients' parents" so we need to bear in mind this was a study of proxy reporting albeit from those who probably know the participant pretty well. Researchers observed that some 5% of the ASD cohort "endorsed sex item 110" compared with about half a percent of the control group. Biological gender discussed in terms of 'natal gender' did not suggest that any one gender were more or less likely to endorse that CBCL question and age of participants similarly showed little impact on the endorsement of the questionnaire item.

The authors caution that response to one item on the CBCL does not a gender dysphoria diagnosis make. But they do suggest that further screening could be preferentially offered as and when either autism is diagnosed or indeed screening for autism/autistic traits when gender variance is encountered in the clinic minus any sweeping generalisations. One might also see a need for designing new questionnaires/schedules to specifically ascertain signs of gender dysphoria in cases of autism - indeed, as some have [2] - with a focus on both longitudinal research i.e. how might signs and symptoms change with age/maturation and also taking into account more direct reporting from participants themselves...

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[1] Janssen A. et al. Gender Variance Among Youth with Autism Spectrum Disorders: A Retrospective Chart Review. Transgend Health. 2016 Feb 1;1(1):63-68.

[2] George R. & Stokes MA. Gender identity and sexual orientation in autism spectrum disorder. Autism. 2017. Sept 15.

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Monday, 18 September 2017

Parent-mediated intervention for autism falls yet again

"We found minimal evidence for main effects of ART [Adapted Responsive Teaching] on child outcomes."

So said the study results reported by Linda Watson and colleagues [1] adding to a bank of studies (and meta-analyses) suggesting that parent delivered early behavioural interventions for autism or cases of 'at-risk for autism' in the most part are not seemingly cutting the scientific mustard (see here). I temper that last sentence with a number of caveats; not least that the methodological quality of the studies in this area still has some way to go and also that parent-mediated interventions covers quite a bit of ground in terms of techniques. The idea however that moves to make parents with children with autism some kind of 'super-parents' (yes, someone did use a term similar to that) to impact on their child's early presentation is not exactly borne out by the scientific data in this area. I would add that many parents of children with autism are already super-parents without any additional help, indications or guidance for the powers-that-be.

This time around nearly 90 young infants "at-risk of later ASD [autism spectrum disorder] diagnoses" were given either ART or REIM (referral to early intervention and monitoring) following other work from this authorship group on this topic [2]. ART by the way, focuses on 'relationships' over a 6 month period where aspects such as engagement, awareness and joint action between parent and child are some of the points of interest. Various facets of functioning were assessed and, assuming the equal use of other early intervention services between the groups, the time, effort and costs of ART did not seemingly provide some wildly significant gains when compared with REIM. In short, yes something like ART is a wonderful aid for things like increasing parental responsiveness to their kids but when it came to important child outcomes - including autism-related outcomes - the intervention did not seemingly fare so well.

What's more to say on this topic? Well, being careful not to hark back to the bad 'ole days where parenting behaviours were 'blamed' for the development of offspring autism, I'm not going to totally poo-poo this area of research and practice. There are some pretty good intervention strategies out there for helping parents to further *connect* with their children in the context of autism and potentially raising the potential and wellbeing of all parties concerned. My issue however is that moves to 'manualise' such interventions in the context of all autism (or rather all 'potential cases' of autism bearing in mind the use of the words 'at-risk') is not a great idea. As I've mentioned before in the context of the pluralised autisms, screening for things like inborn errors of metabolism potentially presenting with autism or autistic features seems a better first use of resources, assuming that underlying biological issues being associated with autism are probably not going to be that amenable to something like parent-mediated intervention or the like as per the example of something like phenylketonuria and autism (see here).

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[1] Watson LR. et al. Parent-Mediated Intervention for One-Year-Olds Screened as At-Risk for Autism Spectrum Disorder: A Randomized Controlled Trial. J Autism Dev Disord. 2017 Aug 31.

[2] Baranek GT. et al. Preliminary Efficacy of Adapted Responsive Teaching for Infants at Risk of Autism Spectrum Disorder in a Community Sample. Autism Research and Treatment. 2015: 386951.

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Saturday, 16 September 2017

Guess what? Gastrointestinal symptoms are prevalent in autism

The paper by Calliope Holingue and colleagues [1] provides brief blogging fodder today and a topic that has finally found its way into accepted peer-reviewed science when it comes to autism spectrum disorders (ASD): gastrointestinal (GI) issues are an often over-represented comorbidity when it comes to ASD.

Reviewing the peer-reviewed research literature on this topic, the authors concluded that there are some quite wide and sometimes disparate findings on the frequency of functional GI symptoms in the context of autism. Part of the reason for this is the lack of a standardised tool for looking at GI symptoms in relation to the label.

But: "The prevalence range for constipation was 4.3-45.5% (median 22%), for diarrhea was 2.3-75.6% (median 13.0%), and for any or more than one symptom was 4.2-96.8% (median 46.8%)." Median by the way, refers to the middle number (or in this case middle percentage) from the collected datasets and stresses that approaching half of all people on the autism spectrum may present with 'any or more than one' GI symptom of clinical relevance.

I've said it before and will say it again, there is guidance out there for the screening, diagnosis and management of bowel symptoms as and when they occur alongside a diagnosis of ASD [2]. We can um-and-ah about the cause(s) of such issues (stressing that the physiological is likely just as important as any psychological explanations) but at the end of the day, those diagnosed with autism and accompanying bowel issues - both functional and/or pathological - should receive the same care and management for their bowel issues as anyone else, save any further tragedies. Indeed, given the links being made between something like slow intestinal transit and autism for example (see here), preferential screening should perhaps be the order of the day before severe endpoints are reached (see here)...

To close, and not to make light of GI issues in relation to autism, a cautionary tale against 'throwing your poo(p) out of the window because it would not flush'???

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[1] Holingue C. et al. Gastrointestinal symptoms in autism spectrum disorder: A review of the literature on ascertainment and prevalence. Autism Res. 2017 Aug 30.

[2] Buie T. et al. Evaluation, diagnosis, and treatment of gastrointestinal disorders in individuals with ASDs: a consensus report. Pediatrics. 2010 Jan;125 Suppl 1:S1-18.

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