Monday, 10 December 2018

"the incidence of ADHD, ASD, and DD significantly increased after TBI events in early childhood"

TBI mentioned in the title of this post refers to traumatic brain injury, and represents the 'target variable' examined by Hsuan-Kan Chang and colleagues [1] in the context of rates of "attention-deficit/hyperactivity disorder (ADHD), autism spectrum disorder (ASD), and developmental delay (DD)."

Consistent with various other research published by this authorship group, the fantastic but sadly now defunct National Health Insurance Research Database (NHIRD) in Taiwan was the resource used by Chang et al in pursuit of their research goal. And the participant numbers under study reflected the use of the NHIRD: "A total of 7,801 and 31,204 children were enrolled in the TBI and control cohorts, respectively."

As well as instances of TBI being listed in the NHIRD "from 1998-2008", researchers also had access to "the incidence of subsequent ADHD, ASD, or DD (according to ICD-9 criteria)." They observed that: "The TBI cohort exhibited a higher incidence of subsequent ADHD, ASD, or DD than the controls" and that said developmental diagnoses tended to be made "at a younger age compared with the controls" (non-TBI controls). They concluded that TBI seemed to increase the risk of each developmental diagnosis and that "severe TBI, repeated TBI events, and TBI at a younger age" were all (variably) potentially important factors for the labels.

This is interesting and thought-provoking research. It does require some 'treading carefully' sentiments; not least with the idea that within the huge heterogeneity and variability of labels such as ADHD and autism (ASD), TBI *might* be a route or part of a possible route towards a diagnosis. Whilst not discounting the idea that sub-clinical signs and symptoms of developmental disorders could actually put someone at greater risk for TBI (see here for example), the possibility that TBI 'might lead to' a developmental diagnosis should not be shied away from. Indeed, other independent findings might also be important (see here). I say that mentioning that TBI is a general term that says nothing about the reason for the injury, the type of injury or what specific part of the brain may be affected. If one however takes autism as an example, it's not beyond the realms of possibility that certain TBIs could 'mimic' effects seen in other examples of 'acquired autism' where brain injury is part-and-parcel of the clinical picture (see here and see here). Indeed, similar sentiments have been expressed in relation to ADHD too (see here).

Whatever the relationship and mechanisms involved, the Chang findings imply that further investigations are needed in this area. Also, far greater efforts need to go into first preventing and then managing TBI...


[1] Chang HK. et al. Traumatic Brain Injury in Early Childhood and Risk of Attention-Deficit/Hyperactivity Disorder and Autism Spectrum Disorder: A Nationwide Longitudinal Study. J Clin Psychiatry. 2018 Oct 16;79(6). pii: 17m11857.


Saturday, 8 December 2018

"Anti-Candida albicans IgG antibodies in children with autism spectrum disorders"

The quote titling this post - "Anti-Candida albicans IgG antibodies in children with autism spectrum disorders" - reflects the title of the paper by Paul Ashwood & Heather Hughes [1] who set out to "determine if children with ASD [autism spectrum disorder] exhibit elevations in antibodies that target C. albicans, indicating current or previous overgrowth of this fungal species." Such work is based on the still developing idea that "individuals with ASD have significant aberrations in the composition of their gut microbiota, known as dysbiosis" and part of that dysbiosis might also stretch to fungal as well as bacterial species.

Candida albicans also known as C. albicans is described as a 'opportunistic pathogenic yeast' quite readily observed in quite a large proportion of 'healthy adults'. For most people, this yeast does not cause any issues. On occasion however, C. albicans can lead to problems, particularly among those who are described as 'immunocompromised'. This is not the first time that C. albicans has been examined in the context of autism. Granted, the studies so far have been relatively small scale [2] and in requirement of follow-up [3] but this topic is no stranger to the peer-reviewed science literature. The Ashwood & Hughes paper should also be viewed in the context of other science discussions from this authorship group [4]; indeed several [5].

So: "We measured anti-C. albicans immunoglobulin (IgG) in plasma from eighty children enrolled in the UC Davis MIND Institute CHARGE study." IgG antibodies, represent 'immune status' with regards to a history of encountering specific pathogens. So, being positive to "anti-C. albicans immunoglobulin (IgG)" means that someone has been exposed to C. albicans at some point in their lifetime and retained something of an 'immune memory' to it. This subsequently means that your immune system is 'primed' in case that specific pathogen is encountered once again.

Results: "Plasma anti-C. albicans antibody positivity was found in 36.5% (19/52) of children with ASD. Anti-C. albicans antibodies in typically developing controls was (14.3%; 4/28)." I'm sure that you can see the disparity between the groups, bearing in mind that this was not an 'all-or-nothing' finding in relation to the separation of the groups. I should also mention that researchers also reported that gastrointestinal (GI) symptoms, also examined in this cohort, did not seemingly play a role in C. albicans antibody positivity.

Where next for this area of investigation? Well, alongside perhaps taking these results into consideration with other findings from this research group (see here), the authors mention that "exploring fungal composition within the gut as well as metabolic byproducts of yeast species such as d-arabinitol and ethanol, and identifying associations these might have with behaviors in ASD" could be one direction. In light of other independent research (see here), I'd say that was a sensible next step to take.


[1] Ashwood P. & Hughes HK. Brief Report: Anti-Candida albicans IgG antibodies in children with autism spectrum disorders. Front. Psychiatry. 2018. Nov 26.

[2] Ekiel A. et al. Intestinal microflora of autistic children. Med Dosw Mikrobiol. 2010;62(3):237-43.

[3] Iovene MR. et al. Intestinal Dysbiosis and Yeast Isolation in Stool of Subjects with Autism Spectrum Disorders. Mycopathologia. 2017 Apr;182(3-4):349-363.

[4] Hughes HK. et al. The Gut Microbiota and Dysbiosis in Autism Spectrum Disorders. Curr Neurol Neurosci Rep. 2018 Sep 24;18(11):81.

[5] Hughes HK. et al. Immune Dysfunction and Autoimmunity as Pathological Mechanisms in Autism Spectrum Disorders. Front. Cell. Neurosci. 2018.


Friday, 7 December 2018

"hold promise as cross-cultural key indicators for autism"

The quote heading this post - "hold promise as cross-cultural key indicators for autism" - comes from the paper by Sophie Carruthers and colleagues [1] which "aimed to identify the items on the Autism Spectrum Quotient (AQ)-Child that are most predictive of an autism diagnosis among children aged 4–9 years across samples from India, Japan and the UK." Attempting to fill quite an important 'hole' in the use of the go-to 'are you autistic' screener, authors set out to look at the presentation of autistic traits across three different countries, all with some quite different cultural perspectives and contexts.

The Carruthers paper is open-access so doesn't need too many grand discussions from me. The basics: "parent-reported AQ-Child data from India (73 children with an autism diagnosis and 81 neurotypical children), Japan (116 children with autism and 190 neurotypical children) and the UK (488 children with autism and 532 neurotypical children)" was the source material. Once again I'll mention how the term neurotypical is a misnomer (see here); it's use in this paper is all the more surprising given that one of the authors wrote an editorial paper [2] mentioning how "there is no single way for a brain to be normal, as there are many ways for the brain to be wired up and reach adulthood." Oh well.

Results: from the collected data, researchers were able to undertake various statistical analyses. Pertinent to the quote titling this post were some important findings "identified to be universal key indicators" across the different countries and cultures. These were: "In a social group, s/he can easily keep track of several different people’s conversations; s/he enjoys social chit-chat; s/he knows how to tell if someone listening to him/her is getting bored; s/he is good at social chit-chat and s/he finds it difficult to work out people’s intentions." Alongside, various other indicators were rated as "performed excellently or acceptably" across the three different country groups.

The conclusion: "Cross-cultural overlap in the items most predictive of an autism diagnosis supports the general notion of universality in autistic traits whilst also highlighting that there can be cultural differences associated with certain autistic traits." I'd like to see more research done in this area. Quite a few years ago I posed the question 'Is autism the same all over the world?' (see here) and well, I don't have a good answer despite the Carruthers and other results. Obviously such a question needs also to be wrapped in the idea that the plural 'autisms' also exert an effect (see here) and take into account other factors such as comorbidity (if that is the right word). It should also perhaps appreciate that whilst the AQ is undoubtedly 'picking up' something, it might not just exclusively be autism or autistic traits (see here and see here)...


[1] Carruthers S. et al. A cross-cultural study of autistic traits across India, Japan and the UK. Molecular Autism 2018; 9:52.


Thursday, 6 December 2018

On autism and exposure to fragranced consumer products

The findings reported by Anne Steinemann [1] tap into an important issue seemingly relevant to many people diagnosed with autism or an autism spectrum disorder (ASD): exposure to various fragranced products such as air fresheners, deodorants and perfumes can seemingly cause various adverse physiological reactions. I know to some people this might not seem like particularly groundbreaking research, but when you read that almost 60% of autistic adults have been reporting "lost workdays or lost a job, in the past year, due to fragranced product exposure in the workplace" it kinda turns into something a lot more important.

Steinemann reports results across various different geographical cohorts pertinent to "the effects of fragranced products on autistic individuals ages 18–65 in the United States, Australia, and United Kingdom." This was a questionnaire-based study, a "web-based" survey, "part of the SSI [Survey Sampling Internationalweb-based panel." The numbers included for study are in the thousands, with some 4% reporting "medically diagnosed autism" upon which the Steinemann study is based.

The conclusion: "83.7% report adverse health effects from fragranced products." Said effects included "migraine headaches (42.9%), neurological problems (34.3%), respiratory problems (44.7%), and asthma attacks (35.9%)." Further: "Health problems can be severe, with 74.1% of these effects considered potentially disabling under legislation in each country."

As you can perhaps see, exposure to fragranced products is potentially an important issue for many people on the autism spectrum. The Steinemann results are based on discussions with adults (18-65 years) but I daresay there may be much to see with younger cohorts too. I'd also be interested to see whether issues like comorbidity potentially over-represented alongside autism might also exert something of an important effect too.

Solutions? Well, I don't think it's too much to ask if public and workplaces could perhaps look at some of their spaces with a view to reducing their use of fragranced products. If for example, this means cutting back on things like those automated air fresheners that periodically squirt out a cloud of smelly stuff, I'm pretty sure quite a few more people - more than just autistic people - would benefit. Indeed, with all the focus on 'autism hours' these days, I wonder if this could be something to add to the list of being 'autism-friendly'? As for personal scented products and the like, well, if you know that you're going to be interacting with autistic people who might be particularly sensitive to fragrances, how about giving those scented products a miss for that day? I promise that you will still smell OK. I don't think these are unreasonable requests.

Then the next question: why? Why do such symptoms come about and what are the biological mechanism through which such 'sensitivity' occurs? Well, it appears that Steinemann has some research history when it comes to fragrances and autism [2] albeit looking at "the neuromodifications of three selected fragrances on male and female human fetal brain neurons." Oxytocin and arginine vasopressin were the molecular targets in that study. Whether there may be more to see from these compounds in relation to fragrance sensitivity in adults is a question to ask. Such issues also perhaps overlap with other research talking about olfaction and autism (see here and see here). I'm also minded to point readers in the direction of another condition/set of symptoms that could be relevant: multiple chemical sensitivity (MCS). Yes, yes, I know that MCS is disputed in some quarters, even to the point of mentioning the word 'psychosomatic' on some occasions [3], but it strikes me that such high rates of 'fragrance intolerance' in relation to autism *could* also be tied into the presentation of MCS. And such high numbers reporting such an intolerance is probably not just 'all in the mind'.


[1] Steinemann A. Fragranced consumer products: effects on autistic adults in the United States, Australia, and United Kingdom. Air Quality, Atmosphere & Health. 2018; 10: 1137-1142.

[2] Sealey LA. et al. Environmental factors may contribute to autism development and male bias: Effects of fragrances on developing neurons. Environ Res. 2015 Oct;142:731-8.

[3] Jimenez XF. et al. Polyallergy (Multiple Chemical Sensitivity) is Associated with Excessive Healthcare Utilization, Greater Psychotropic Use, and Greater Mental Health/Functional Somatic Syndrome Disorder Diagnoses: A Large Cohort Retrospective Study. Psychosomatics. 2018 Aug 2. pii: S0033-3182(18)30418-3.


Wednesday, 5 December 2018

Cannabis treatment and autism

"This preliminary study supports [the] feasibility of CBD [cannabidiol]-based cannabis trials in children with ASD [autism spectrum disorder]."

That was the research bottom-line suggested by Adi Aran and colleagues [1] following their retrospective study of some "60 children with ASD and severe behavioral problems" who were given cannabidiol (CBD)-rich cannabis. They report that nearly two-thirds of parents/caregivers of those children in receipt of CBD-rich cannabis observed "much improved or very much improved" behaviour on the Caregiver Global Impression of Change scale, "a 7-point, caregiver rated scale, designed to assess how much the child's symptoms have improved (‘No change’, ‘Slightly improved’, ‘Much improved’, or ‘Very much improved’), or worsened (‘Slightly worse’, ‘Much worse’, or ‘Very much worse’) relative to the baseline state."

Cannabidol (CBD) is a component of cannabis. Distinct from tetrahydrocannabinol (THC) in terms of chemical arrangement, CBD is still thought to have some psychoactive properties, although perhaps not as 'detrimental' as THC [2]. Cannabis and CBD have been fairly big news lately as a consequence of the legalisation of such compounds for specific medicinal uses here in Blighty (see here).

Aran et al report findings suggesting that further controlled research is required in this area. They observed that among their 60 children (50 boys and 10 girls with an average age of 12 and 10 years respectively) taking on average between 4-5 "drugs for behavioral problems", quite a high proportion were still being treated with cannabis "≥ 6 months from treatment onset." Perhaps also importantly, a third of children received less medications or lower dosage of medication following their "cannabis treatment."

I will however add in a word or two of caution following the Aran observations. First, although there is a lot of discussion and hype around the use of medicinal cannabis and various diagnoses / conditions / labels, one still has to remember that this is a drug, and a drug of abuse at that. This mirrors the chatter about another substance of abuse being potentially indicated in the context of autism (see here). Aran et al also talked about some adverse effects noted in their cohort ("sleep disturbances (14%) irritability (9%) and loss of appetite (9%)") including: "One girl who used higher tetrahydrocannabinol [THC] had a transient serious psychotic event which required treatment with an antipsychotic." Others have also independently warned about medical cannabis use [3] citing ASD as one example. What this information imply is that alongside any potential studies of cannabis or specific compounds derived from cannabis with autism in mind, one needs to also keep a focus on the potential downsides to its use as well as any positives...


[1] Aran A. et al. Brief Report: Cannabidiol-Rich Cannabis in Children with Autism Spectrum Disorder and Severe Behavioral Problems-A Retrospective Feasibility Study. J Autism Dev Disord. 2018 Oct 31.

[2] Pierre JM. et al. Cannabis-induced psychosis associated with high potency "wax dabs". Schizophr Res. 2016 Apr;172(1-3):211-2.

[3] Bou Khalil R. Why Is It Important to Protect Children with Mental Disorders from Medical Cannabis? J Dev Behav Pediatr. 2015 Nov-Dec;36(9):766.


Tuesday, 4 December 2018

One more time... (roughly) 1 in 40 children with parent-reported autism in the US

Consider this short post an extension of another recent entry on this blog talking about new data observing that the estimated autism prevalence rate (parent-reported) is around 1 in 40 children in the United States (US) (see here). That entry was based on the paper by Michael Kogan and colleagues [1] and their examination of data "using the 2016 National Survey of Children's Health (NSCH)" initiative.

Enter then another piece of research published little over a week after the Kogan study from Guifeng Xu and colleagues [2] which concluded that: "In a large, nationwide, population-based study, the estimated prevalence of ever-diagnosed ASD [autism spectrum disorder] was 2.79% among US children in 2016." In case you were wondering, 2.79% or 2.8% roughly translates as 1 in 36 children. Xu and colleagues, I might add, are no strangers to prevalence studies on childhood neurodevelopmental disorders (see here and see here).

Both these studies have attracted some media attention (see here and see here) mainly because they show a prevalence rate quite a bit higher than the recent CDC (estimated) autism prevalence figures - 1 in 59 8-year olds - published earlier this year (2018) (see here). Those media reports also seem to make quite a big deal of the 'parent-reported' nature of the figures (both derived from the NSCH initiative). As I mentioned in my last discussion of the Kogan paper, a quote from the lead author Michael Kogan is important in the context of those parent-report 'issues' that some people seem to have: "We know that in terms of having a major condition like autism, parents are usually pretty good reporters compared to medical records." Indeed they are.

Other details to add? Well, the Xu paper also reported on "state-level prevalence of ASD in the United States." They observed variations in the reported prevalence of autism (ASD) across the different states: "The state-level prevalence varied from 1.54% (95% CI, 0.60-2.48) in Texas to 4.88% (95% CI, 2.72-7.05) in Florida." Little explanation is given about such a discrepancy in their paper and so further research is implied.

Also: "Among those who had ever been diagnosed as having ASD, 92.79% (95% CI, 90.19-95.39) reported currently having ASD." This is interesting. Allowing for the fact that the diagnosis of autism or ASD is often more of an art form than a scientific endeavour, I did wonder whether the loss of about 8% of children who were previously diagnosed with autism but did not report currently having autism might overlap with the 9% figure with regards to the term 'optimal outcome' (see here). Y'know, the ever-growing body of peer-reviewed research that seems to suggest that for some people, a diagnosis of autism is not necessarily 'lifelong' (see here) (even if 'optimal outcome' is not necessarily the best phrase to use). Again, further research is implied.

For now however, we can conclude that there is : "a relatively high prevalence of ASD among US children" mirroring that in other parts of the world (see here for example). We really need to be asking questions like 'why?' and also 'are the relevant mechanisms in place to ensure that money, resources and services are directed towards this growing population?'


[1] Kogan MD. et al. The Prevalence of Parent-Reported Autism Spectrum Disorder Among US Children. Pediatrics. 2018 Nov 26. pii: e20174161.

[2] Xu G. et al. Prevalence and Treatment Patterns of Autism Spectrum Disorder in the United States, 2016. JAMA Pediatrics. 2018. Dec 3.


Pregnancy depression (with or without antidepressant use) and offspring autism risk continued

"Women with depression during pregnancy have an increased risk of having a child with ASD [autism spectrum disorder], regardless of antidepressant use."

That was the conclusion reached by Katrina Wilcox Hagberg and colleagues [1] following their analysis of the UK Clinical Practice Research Datalink (CPRD). Their study was carried out as a result of the still-rumbling-on question of whether pregnancy depression or the pharmacological treatment of depression during pregnancy *might* be a risk factor for an offspring diagnosis of autism (see here and see here). As you might appreciate, it's difficult to pin down whether depression or the treatment of depression is the more important issue given that the two typically appear together.

The CPRD held here in Blighty is a mighty fine resource and has been used to examine all-manner of potentially important issues (see here and see here for some examples). Researchers looked at mums and offspring ("singleton infants") born between 1989 and 2011 totalling nearly 200,000 mother-baby pairs. They reported that: "Mothers were required to have at least 12 months of recorded history before the baby's delivery date, and the children were required to have at least 3 years follow-up after birth." Because antidepressants require a doctor's prescription in the UK, they were also able to identify those other important elements vital to this study: depression and it's antidepressant intervention or not, as well as "the timing of antidepressant use during the exposure period." Authors also report some additional analyses based on "a sibling case-control analysis of maternal pregnancy exposures in ASD cases compared to non-ASD siblings of the same mother."

Results: based on the examination of 'read codes', authors identified some 2100 children with a diagnosis of ASD. The old 4:1 male:female ratio yet again held true (see here). Taking into account being exposed to depression or not and whether exposure was treated or untreated, researchers formed their headline conclusion on pregnancy exposure to maternal depression being linked to an increased risk of offspring autism. Further: "The risk was slightly higher among women with treated depression... compared to untreated depression." The results of the sibling case-control part of their trial - "601 same-sex siblings who did not have an ASD diagnosis matched to 531 ASD cases" - also revealed that: "the risk of ASD in offspring of mothers with untreated depression was 1.18 (95% CI 0.64-2.20) and 1.53 (95% CI 0.89-2.62) for treated depression, compared to unexposed." Some further analysis looking at the timing of antidepressant exposure during pregnancy revealed that it didn't really matter when the exposure happened (i.e. which trimester).

Perhaps contrary to some of their findings, it's clear from some of the statements included in the Hagberg paper that the authors seem to have sided with the idea that "antidepressants are not themselves associated with the increased risk" of offspring autism. It's depression that is the important factor, and the "slight increase in risk with antidepressant use reflects differences in the underlying severity of depression." The other evidence they draw on to support their assertion is the "finding that the risk of ASD was not elevated in women who were prescribed antidepressants for other indications."

I'm not however so sure that we can be so certain about such a siding. I say that on the basis that researchers "did not evaluate the effect of antidepressant dose in this study" and: "Drug information in the CPRD covers written, but not dispensed prescriptions" so therefore they "cannot be sure that women used all the prescribed antidepressants." Their 'nested sibling case-control analysis' also revealed that: "the risk of ASD in offspring of mothers with untreated depression was 1.18 (95% CI 0.64-2.20) and 1.53 (95% CI 0.89-2.62) for treated depression, compared to unexposed." Not proof positive by any means, but interesting. I'm also inclined to direct you to other studies previously discussed on this blog, where the finger of suspicion has not rested entirely with maternal depression [2]. Indeed, where meta-analysed data [3] has been more partial to the idea that prenatal exposure to certain antidepressant formulations could still be on the menu with some offspring autism risk in mind.

Obviously one has to be very careful when talking about this area of autism research. Much like when another class of important medicines used during pregnancy are talked about with 'autism risk in mind' (see here), such medicines are not typically prescribed or dispensed willy-nilly without good reason. By saying that, I feel I must repeat my oft-said caveat on this blog: no medical or clinical advice is given or intended; if in doubt, talk to your prescribing physician.

But the weight of evidence produced so far has not let antidepressant use off the research hook just yet. And drawing on data suggesting that the frequency of depression during pregnancy might be on the increase (see here), one should perhaps also suspect that this could have something - a small part at least - to do with the ever-increasing rates of autism...


[1] Hagberg KW. et al. Maternal depression and antidepressant use during pregnancy and the risk of autism spectrum disorder in offspring. Clinical Epidemiology. 2018; 10: 1599-1612.

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

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


Monday, 3 December 2018

Disclosure of autism and juror perceptions

The paper by Katie Maras and colleagues [1] really interested me. It describes results based on examining "mock juror perceptions of credibility and culpability of a defendant who is described as displaying autistic-like characteristics and behaviours, and whether the provision of information about the defendant’s ASD [autism spectrum disorder] diagnosis alters these perceptions." Such investigations continue a theme in autism research circles and beyond on 'how autism is viewed' (see here and see here and see here) and how disclosure of an autism diagnosis might be important and influential in various circumstances.

Given the focus on the criminal justice system and autism in this post, I'm also going to pass some brief comment on the paper by Kamaldeep Bhui [2] too. That paper was more concerned with trying to "understand radicalisation, ethical and definitional issues, and how public health approaches may help." Minus any sweeping generalisations, the label of autism was also mentioned in the Bhui paper and could be relevant to the Maras findings too.

So, autism and the criminal justice system. This is not the first time that this topic has been discussed on this blog (see here and see here for examples) reflective of some ever-increasing research interest. It highlights how a diagnosis of autism is by no means protective of someone coming into contact with law enforcement services and/or the court system, and how various discussions are still needed on the hows-and-whys of such contact, as well as ensuring that those on the autism spectrum are treated justly and fairly in the eyes of the law.

In the Maras paper researchers report that: "One-hundred-and-sixty jury-eligible participants read a vignette describing a male who was brought to the attention of police for suspicious and aggressive behaviours and displayed atypical behaviours in court." The specific imaginary crime of this individual was "assault and battery of a police officer" where "the defendant was behaving aggressively at a train station and when police officers tried to restrain him with handcuffs, he became violent and struck an officer." Further details also included: "it reportedly emerged that the defendant was trainspotting and was upset because his train was cancelled."

Half of participants were randomly allocated to receive "Label+info" and the other half "no label". The 'no label' group received no further information about the defendant or any possible diagnosis. The 'label+info' group "were informed that the defendant had been assessed by a forensic psychiatrist and was diagnosed with ASD, and they were given further information defining ASD and how it impacted on his behaviours." Participants were then asked to make various judgements about the imaginary case and defendant.

Results: "The provision of a label and information led to higher ratings of the defendant's honesty and likeability, reduced blameworthiness, and resulted in fewer guilty verdicts, and more lenient sentencing." Various themes are detailed by the authors based on their findings: honest, inappropriate language, culpability and consequences.  Interestingly, on the topic of 'consequences', even some of those in the 'no label' group indicated that "they thought the defendant might have ASD" and how punishment would perhaps be less useful than "some form of rehabilitation to help the defendant." The net result is that jurors may be sympathetic to the presentation of autism in some contexts of involvement with the criminal justice system provided they are given the appropriate information about the individual concerned.

I take some comfort from the Maras findings that the law may not be blind to the circumstances around particular defendants and the crimes for which they are accused. Similar to the guidance here in Blighty when it comes to 'mentally disordered offenders' the law recognises that whilst crime is crime, sometimes things aren't always as straightforward as they seem (see here). By saying that I'm not trying to deflect away from why the law is there and the often serious effects that crime has on individuals (victims) and society; merely that 'context' is sometimes important too.

Going back to the Bhui findings and discussions pertinent to understanding radicalisation and particularly the idea that: "Common mental illnesses appear to be a risk factor at a population level for developing extremist beliefs, and psychoses and autism are reported as more common amongst some terrorist offenders" there are also implications. One has to be sensitive and avoid any sweeping generalisations when discussing this topic, but the issue of radicalisation and autism has been talked about before (see here). One of the primary themes to emerge from the growing data in this area is that a pattern of fairly unique vulnerabilities seems to follow autism that *might* make someone more susceptible to unscrupulous individuals intent on spreading their own agendas and getting someone else to do their dirty work.

Applying the Maras results to the Bhui discussions, one would hope that both mock and real jurors would apply the same logic as and when offences linked to radicalisation in the context of autism are presented to them. One would hope that a diagnosis of autism and everything that entails would be taken into account as and when such crimes are put to them. Indeed, perhaps that is the next round of study for Maras et al if they should wish to replicate their study: replace 'assault and battery' with something linked to radicalisation. I for one, would be interested in what results they observe and what we can potentially learn from them.


[1] Maras K. et al. Mock Juror Perceptions of Credibility and Culpability in an Autistic Defendant. J Autism Dev Disord. 2018 Oct 31.

[2] Bhui K. Radicalisation and mental health. Nord J Psychiatry. 2018 Nov 1:1-4.