Placental inflammation and autism?

The placenta. Quite an important part of the nine months that makes us; an organ exquisitely evolved to provide oxygen and nutrition to the developing embryo/foetus as well as removing various un-necessaries. Without it we wouldn't even be...

A recent paper by Jennifer Straughen and colleagues [1] suggests that when it comes to the placenta and it's important functions during gestation, there may be some interesting data pertinent to at least some cases of autism spectrum disorder (ASD). Indeed the authors note: "Histologic evidence of placental inflammation and maternal vascular malperfusion pathology are associated with ASD."

Based on identifying some 55 persons diagnosed with ASD and nearly 200 matched controls, researchers analysed findings based on placentas "reviewed as part of routine care." Although not particularly au-fait with the inner workings of the placenta, I understand that various 'issues' were screened for and some interesting observations made. Words like 'acute placental inflammation' and 'maternal vascular malperfusion pathology' are banded around; many of which seemed to be more frequently associated with a subsequent diagnosis of ASD. In short, there seemed to be quite a bit more going on with those placentas from mums of children with autism compared with the not-autism controls.

This is important work. I've talked about the placenta and offspring autism previously a few times on this blog (see here and see here for examples). Allied to the rather sweeping idea that autism 'begins in-utero' and there is a case to be made for further inspection of organs like the placenta [2] when it comes to at least some cases of offspring autism - some, but not all. Indeed, it is perhaps timely that other independent papers [3] remind us of the work of the late Paul Patterson et al and the concept of maternal immune activation (MIA) and how the required reprogramming of the maternal immune system during pregnancy might very much rely on optimal placental function to keep the developing child safe and sound...

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[1] Straughen JK. et al. The association between placental histopathology and autism spectrum disorder. Placenta. 2017. July 8.

[2] Schroeder DI. et al. Placental methylome analysis from a prospective autism study. Mol Autism. 2016 Dec 15;7:51.

[3] Bilbo SD. et al. Beyond infection - Maternal immune activation by environmental factors, microglial development, and relevance for autism spectrum disorders. Experimental Neurology. 2017. July 8.

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Various childhood psychiatric disorders may be risk factors for later substance abuse

"Childhood ADHD [attention-deficit hyperactivity disorder], ODD [oppositional defiant disorder], CD [conduct disorder], and depression increase the risk of developing substance-related disorders."

So concluded the results of the meta-analysis published by Annabeth Groenman and colleagues [1] surveying the peer-reviewed research literature between 1986 and 2016. Drawing on data from nearly 40 studies covering over three quarters of a million people that "included 22,029 participants with ADHD, 434 participants with ODD or CD, 1,433 participants with anxiety disorder, and 2,451 participants with depression" researchers looked at the risk in relation to "later alcohol-, nicotine-, or drug-related disorders or substance use disorders (SUDs)."

The level of risk identified concerning childhood psychiatric disorders and later substance abuse were not by any means borderline. Risk for SUD, substance use disorder, was particularly marked for all diagnoses and confirms the authors' conclusions about their findings that "emphasize the need for early detection and intervention to prevent debilitating substance-related disorders in later life." I say that, bearing in mind that one other diagnosis or set of diagnoses - anxiety disorder - did not seem to be related to later risk of substance-related disorder ("although the findings are highly heterogeneous").

As part of a growing pattern of research exploring the risk of future adversity associated with a diagnosis of something like ADHD or CD (see here) I share the author's sentiments that 'early detection' and 'intervention' are worthwhile ventures when it comes to such diagnoses. If one also assumes that ADHD and/or CD in particular, might also increase the risk for future psychopathology (see here), the case becomes even stronger to try and intervene early and improve future quality of life for both the individual and also on a more societal level. Guidance on this topic already exists [2].

But there are other factors to consider with such research. SUD reflects a complicated set of conditions in terms of how-and-why people arrive at such a diagnosis. Factors such as the role of peers and social issues such as poverty and homelessness [3] can all influence risk of SUD as can a variety of other variables that need to be taken on board. Whilst zooming in on individuals is a big part of the strategy to minimise any excess adverse risk of SUD in relation to ADHD, CD, ODD or depression, it should not be the only focus.

Finally, allied to the Groenman results, I might also draw your attention to those published by Clarissa Bauer-Staeb and colleagues [4] talking about how "substance misuse history conveys the greatest risk in all BBV [blood-borne viruses]" in relation to those diagnosed with a severe mental illness as a further undesirable outcome potentially stemming from certain substance abuses. And with it, yet more action is required...

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[1] Groenman AP. et al. Childhood Psychiatric Disorders as Risk Factor for Subsequent Substance Abuse: A Meta-Analysis. J Am Acad Child Adolesc Psychiatry. 2017 Jul;56(7):556-569.

[2] Harstad E. et al. Attention-Deficit/Hyperactivity Disorder and Substance Abuse. Pediatrics. 2014; 134:

[3] Tompsett CJ. et al. Peer Substance Use and Homelessness Predicting Substance Abuse from Adolescence Through Early Adulthood. American journal of community psychology. 2013;51(0):520-529.

[4] Bauer-Staeb C. et al. Prevalence and risk factors for HIV, hepatitis B, and hepatitis C in people with severe mental illness: a total population study of Sweden. Lancet Psychiatry. 2017 Jul 4. pii: S2215-0366(17)30253-5.

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'Somali autism': a phenotype?

"Results lend support to previous studies that found higher rates of ASD [autism spectrum disorder] intellectual disability in children of immigrants from low human resource index countries compared to other groups."

So said the findings reported by Amy Esler and colleagues [1] continuing an important research theme looking at how race/ethnicity might have some important 'effects' on the presentation of autism (see here). Although I've titled this post 'Somali autism' I don't necessarily want anyone to assume that I'm just zooming in on Somalia and that every Somali child who has been diagnosed with autism is somehow the same as each other either in autistic presentation terms or any of the comorbidity that inevitably surrounds autism. Autism is an extremely heterogeneous diagnosis with an often very individual and complicated clinical presentation.

I'm not going to dwell too much on this topic because I've covered it a few times before on this blog (see here and see here). Suffice to say that Esler et al follow the trend suggesting that "children from the Somali diaspora" seem more likely to present with autism + learning (intellectual) disability based on their study cohort. They also observed that: "Few differences were found in the presence of specific symptoms and behaviors across groups once IQ was controlled" meaning that the presence of intellectual/learning disability seemed to be the important variable.

There are some important extensions required to this area of study. Not least is the idea that genetic and/or biological variables could eventually be studied and compared with other racial/ethnic groupings with autism in mind. I'm minded also to mention that in amongst such 'where next' research, the potential role of something like vitamin D might be explored, given the [growing] interest in this vitamin/hormone with autism in mind (see here for example). As well as looking at differing sun exposure patterns (particularly mother and child exposure patterns) in those moving to less sunnier climates, the genetic machinery of making vitamin D might also figure in any future investigations too (see here).

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[1] Esler AN. et al. Phenotypic Characteristics of Autism Spectrum Disorder in a Diverse Sample of Somali and Other Children. J Autism Dev Disord. 2017 Jul 8.

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Early pregnancy vitamin D levels and later offspring 'behavioral difficulties'?

Drawing on data derived from the Rhea mother-child cohort based in Crete, Greece, the findings reported by Vasiliki Daraki and colleagues [1] provide some food for thought; specifically the observation that "high maternal vitamin D levels in early pregnancy may protect against [offspring] behavioral difficulties, especially ADHD [attention-deficit hyperactivity disorder]-like symptoms at preschool age."

Including nearly 500 mother-child pairs, researchers set about looking at whether pregnancy levels of vitamin D - "serum 25(OH) D concentrations were measured at the first prenatal visit (13 ± 2.4 weeks)" - correlated with cognitive functions and/or behavioural 'difficulties' in offspring at 4 years of age.

Results: as per the headline titling this post, there did seem to be some potentially important *associations* between maternal pregnancy levels of vitamin D and offspring outcomes. So: "children of women in the high 25(OH) D tertile (>50.7 nmol/l) had 37% decreased number of hyperactivity-impulsivity symptoms... and 40% decreased number of total ADHD-like symptoms... at 4 years of age, compared to children of women in the low 25(OH) D tertile (<38.4 nmol/l), after adjustment for several confounders." Investigations looking at pregnancy vitamin D levels and various cognitive functions of offspring children revealed nothing too significant.

Of course you would be right to point out that this was a study pitting one variable - pregnancy vitamin D levels - against a multitude of different offspring cognitive/behavioural outcomes some four years later. It's not entirely inconceivable that despite 'adjustment for several confounders' the authors might be in error in linking vitamin D to offspring outcomes and that some (more than one?) other variable(s) might account for the results. I should also point out that Greece is not exactly sunshine deficient; sunshine being a primary pathway pertinent to the biological synthesis of vitamin D.

But this is not the first time that pregnancy vitamin D levels have been *associated* with offspring ADHD or ADHD-like behaviours (see here) and I doubt it will be the last. Added to work looking at the possibility of an *association* between pregnancy vitamin D levels and offspring risk of autism (see here for example), bearing in mind autism and ADHD are not totally unconnected, there is an interesting theme developing on this topic. Perhaps Government (English at least) policy on recommending vitamin D supplementation for large swathes of the population (see here) may have a multitude of onward effects outside of just reducing the risk of bone manifestations of vitamin D deficiency/insufficiency?

And just before you go, even ALSPAC has something further to say on this matter [2]...

To close, 'Are you Tony Stank?'

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[1] Daraki V. et al. High maternal vitamin D levels in early pregnancy may protect against behavioral difficulties at preschool age: the Rhea mother-child cohort, Crete, Greece. Eur Child Adolesc Psychiatry. 2017 Jul 6.

[2] Darling AL. et al. Association between maternal vitamin D status in pregnancy and neurodevelopmental outcomes in childhood: results from the Avon Longitudinal Study of Parents and Children (ALSPAC). Br J Nutr. 2017 Jul 12:1-11.

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Open label study of probiotics and autism

"We concluded that probiotics have beneficial effects on both behavioral and GI [gastrointestinal] manifestations of ASD [autism spectrum disorder]."

So said the study results published by Sanaa Shaaban and colleagues [1] detailing observations from their "prospective, open-label study" following some 30 children diagnosed with an autism spectrum disorder (ASD) before and after 3 months of probiotic usage. The study details were posted in a clinical trials repository (see here) and note how various measurements were taken as participants took a preparation containing "100 × 106 colony forming units of three probiotic strains; Lactobacillus acidophilus, Lactobacillus rhamnosus and Bifidobacteria longum."

Including some notable authors on the paper who are seemingly not adverse to [scientifically] examining some of the more non-traditional interventions put forward with autism in mind (see here and see here), researchers caution about their latest findings. So: "this study is a single center with a small number of patients and a great deal of additional wide-scale randomized controlled trials are needed to critically confirm the efficacy of probiotics in ASD." Yes, indeed; blinding for example, is a rather important part of the scientific process and other studies 'in progress' have adopted such factors (see here). Set against a growing tide of research suggesting that those trillions of wee beasties that inhabit our deepest, darkest recesses (the gut microbiome) might have more than a passing connection to some autism - some aspects of autism - this area of study is crying out for quite a bit more attention (see here also) not least on hows-and-whys (see here). The way that someone might potentially 'impact' on the gut microbiome in a probiotic sense is also potentially important (see here).

I have only one further point to make about the Shaaban results in relation to the observations that behavioural signs and symptoms (as assessed by the ATEC) seemed to show a relationship with GI symptoms following probiotic use. I'm wondering whether this potential tie-up might learn something from work looking at probiotic use in something like irritable bowel syndrome (IBS) (see here) and onward what happens to psychiatric issues that are seemingly over-represented in cases of IBS (see here). I say that on the basis that bowel issues seem to be most definitely over-represented when it comes to a diagnosis of autism (see here) and the whole 'gut-brain axis' thing continues -across decades - to persist with autism in mind (see here)...

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[1] Shaaban SY. et al. The role of probiotics in children with autism spectrum disorder: A prospective, open-label study. Nutr Neurosci. 2017 Jul 7:1-6.

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"a leaky gut may play a critical role in the development of age-related inflammation and frailty"

The quote heading this post is taken from the findings reported by Yanfei Qi and colleagues [1] who set out to investigate whether "an aging-associated leaky gut is linked to the age-related inflammation and frailty."

'Leaky gut' is still something of a contentious claim in medical and scientific circles despite some increasing evidence to say that it is a real phenomenon and potentially relevant to several conditions (see here) including some parts of the autism spectrum (see here). Although leaky gut is perhaps a slight misnomer - we all have leaky guts to some degree - the more accurate term 'intestinal hyperpermeability' suggests that for several different reasons, parts of the gastrointestinal (GI) tract may, at times or more chronically, be slightly more permeable that they typically should be. This in turn means that the contents of the GI tract - food derivatives, gut bacteria, etc - might be more readily exposed to parts of the body that they really shouldn't be and onward, potentially pathogenic.

Qi et al carried out some important analysis on two cohorts of differing ages (18-30 years old vs. 70 years and over) with regards to serum samples provided by participants. Markers of immune function, specifically inflammatory related compounds (e.g. tumour necrosis factor (TNF)-α and interleukin (IL)-6)) were assayed for, alongside levels of zonulin "a marker for leaky gut". Zonulin is something that I've covered quite recently on this blog in relation to autism research (see here). This biological data gathered by Qi and colleagues was also complemented by physiological measures such as "strength of plantar flexor muscles and number of steps taken per day."

Results: serum concentrations of zonulin were quite a bit - 22% - higher in the older participants compared to younger ones. Researchers also reported that levels of "high-mobility group box protein (HMGB1, a nuclear protein triggering inflammation)" were elevated in the older participants group too. They observed that zonulin levels also seemed to tie into concentrations of TNF-α and IL-6 (albeit not necessarily impressively). Zonulin levels also showed a potentially important *relationship* with "habitual physical activity" (those 'steps per day' data that was collected). The conclusion: "Serum zonulin was associated with both systemic inflammation and 2 key indices of physical frailty. These data suggest that a leaky gut may play a critical role in the development of age-related inflammation and frailty."

This is interesting stuff. It kinda accords with other independent data suggesting that generally speaking, gut barrier function does not necessarily have to deteriorate with age, but under certain circumstances such as age + inflammation, there might be effects to had [2]. Certain classes of medication might also show some involvement in this process too [3]. Although by no means a universal connection, I was interested in these results in the context of autism. Specifically how those Esnafoglu et al findings [4] reporting on 'significantly higher' serum zonulin levels in their cohort with autism, might also tie into reports of inflammatory markers being elevated in at least a subgroup of those on the autism spectrum (see here for example). I'd like to see the Qi study replicated with quite a few different labels and subgroups within labels...

In relation to the suggestion that serum zonulin levels negatively correlated with habitual physical activity (steps per day), again, there is a whole other research agenda to be [cautiously] followed. It's already known that certain patterns of exercise can affect (increase) intestinal permeability [5] although the specifics still require quite a bit more investigation (hint: exercising for 2 hours plus at a time is probably not great for gut function). As with everything in life, there is a balance to be struck between too little and too much of a good thing...

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[1] Qi Y. et al. Intestinal Permeability Biomarker Zonulin is Elevated in Healthy Aging. J Am Med Dir Assoc. 2017 Jul 1. pii: S1525-8610(17)30297-9.

[2] Valentini L. et al. Small intestinal permeability in older adults. Physiol Rep. 2014 Apr 22;2(4):e00281.

[3] Meier J. & Sturm A. The intestinal epithelial barrier: does it become impaired with age? Dig Dis. 2009;27(3):240-5.

[4] Esnafoglu E. et al. Increased Serum Zonulin Levels as an Intestinal Permeability Marker in Autistic Subjects. J Pediatr. 2017 May 11. pii: S0022-3476(17)30487-0.

[5] Costa RJS. et al. Systematic review: exercise-induced gastrointestinal syndrome-implications for health and intestinal disease. Aliment Pharmacol Ther. 2017 Aug;46(3):246-265.

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On DSM-5, Asperger syndrome and 'level of support'

It wasn't so much the findings reported by Garrido and colleagues [1] that took my attention, but rather their use of a particular sentence: "We have equated diagnosis of Asperger syndrome with ASD-level 1 of support" in the context of the DSM-5 guidance for diagnosing an autism spectrum disorder.

For those who might not know, the two main documents for diagnosing autism or autism spectrum disorder (ASD) are the ICD and DSM schedules. Both are currently under/have recently been the subject of revision (ICD-11 and DSM-5 respectively) and both have played a significant role in relation to various aspects around autism (see here for example).

The quite recently revised DSM-5 description of autism (see here) has been the source of quite a lot of discussion. Not only that the latest description might have some quite important effects on the numbers of people potentially being diagnosed with autism or ASD (see here) but also that this revision did away with the diagnostic sub-categories included in previous DSM versions; notably the diagnosis of Asperger syndrome. There were mechanisms built into the DSM-5 such that those already diagnosed with Asperger syndrome (AS) would not lose out in terms of 'identity' but as the DSM-5 becomes more readily used (and also assuming ICD-11 allies with DSM-5 as anticipated), the specific diagnosis of AS is likely to be consumed by the broader ASD label in the longer term. Other authors have talked about the hows-and-whys of this issue in more informed detail than I ever could (see here although I think the authors needs to spellcheck 'Asperger' in some places).

With that rather long introduction in mind, I want to go back to that 'ASD-level 1 support' labelling of AS in the Garrido paper. DSM-5 criteria for autism, sorry ASD, does provide the diagnosing team with an option to place the recipient of a diagnosis on a scale of severity ranging from 'requiring support' to 'requiring very substantial support' shown as levels 1-3 respectively. The assumption is that money and resources will be attached at varying degrees based on the support level indicated. The level 1 support option applied to AS presumes that the dyad of symptoms - social affect and restricted, repetitive behaviours - does impact on day-to-day functioning but issues such as the consistent and complex use of language as a communicative strategy for example, puts their support requirements below say those with 'marked' or 'severe' deficits in verbal and nonverbal social communication skills. Fair enough. When however it comes to the repetitive behaviour side of things in terms of severity, level 1 support basically acknowledges that inflexible behaviour "causes significant interference with functioning in one or more contexts" but importantly, does not use words like 'distress' as it does in level 2 and 3 descriptions.

I may just be focusing too much on details here, but it strikes me that the sweeping assumption made by Garrido et al reveals a broader issue with level of support shown in DSM-5. Although there is not a great deal of peer-reviewed research out there on the severity/support level components to the DSM-5 ASD diagnosis, the work that is there tends to suggest a degree of 'fuzziness' both in the pattern of skills/deficits displayed in relation to autism and onward how clinicians might define decisions on support level [2]. What seems to be inferred with the level of support criteria offered in DSM-5 is that those with a current diagnosis of AS as a group - this diagnosis then changing to ASD - will seemingly never hit criteria for levels 2 or 3 on the basis of the language and communicative skills they possess. I say this with the understanding that I'm not precisely sure whether the individual components of the dyad - social affect and restricted, repetitive behaviours - are separately graded in terms of level of support needed in DSM-5 or just condensed into one severity level for all the diagnostic components combined. Garrido and colleagues imply that one severity level is likely going to be the rule.

There is another issue that needs comment, on whether at least some cases of AS actually meet the operational criteria of DSM-5 ASD over and above the new categorisation of social (pragmatic) communication disorder (SCD) (see here). I can see this being a contentious point. SCD as the name suggests, focuses on 'the social use of verbal and nonverbal communication' and how 'deficits result in functional limitations in effective communication, social participation, social relationships, academic achievement, or occupational performance, individually or in combination'. Previous data has suggested that something approaching 10% of cases of AS - redefined as ASD in DSM-5 - might not actually meet DSM-5 criteria for ASD but might hit diagnostic thresholds for SCD [3]. As I've asked before on this blog, what level of support are those with SCD likely to get? and what are the implications for 'membership' of the autism spectrum for those diagnosed with SCD? are questions that still need answering.

I have been a little pedantic in this post but do want to convey the message that even with the redefinition of AS into ASD, the DSM-5 severity/level of support descriptions are in need of a lot more experimental study to see how they work in real-life [4]. Indeed, further longitudinal studies on how DSM-5 diagnosis and severity 'grading' translate into money, resources and services offered and received and onward outcomes for those diagnosed, should really be in the planning stages as we speak...

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[1] Garrido D. et al. Communicative and social-adaptive profile in children with autism spectrum disorder: a new approach based on the DSM-5 criteria. Rev Neurol. 2017 Jul 16;65(2):49-56.

[2] Weitlauf AS. et al. Brief Report: DSM-5 “Levels of Support:” A Comment on Discrepant Conceptualizations of Severity in ASD. Journal of autism and developmental disorders. 2014;44(2):471-476.

[3] Kim YS. et al. A comparison of DSM-IV pervasive developmental disorder and DSM-5 autism spectrum disorder prevalence in an epidemiologic sample. J Am Acad Child Adolesc Psychiatry. 2014 May;53(5):500-8.

[4] Burns CO. & Matson JL. An evaluation of the clinical application of the DSM-5 for the diagnosis of Autism Spectrum Disorder. Expert Rev Neurother. 2017 Jul 5.

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"medical disorders in children with ASD and ADHD appear to be widespread"

The quote titling this brief post is taken from the results of the systematic review undertaken by Jet Muskens and colleagues [1] (open-access) who surveyed the peer-reviewed science literature "on medical comorbidity in the two major developmental disorders autism spectrum disorder (ASD) and attention deficit hyperactivity disorder (ADHD)."

Continuing an important theme (see here), the authors concluded that various categories of conditions - "immunology, neurology and gastroenterology" - are over-represented in relation to autism and ADHD and that "future studies should not only focus on psychiatric symptoms, but provide a broader evaluation of medical disorders" when it comes to those labels.

Minus too much chatter, I was impressed to see that many of the research articles covered on this blog down the years had made it into the Muskens review. So, the likes of Harumi Jyonouchi gets a well-deserved mention (see here and see here) and the focus on how the immune system might be doing so much more than just protecting us from the odd pathogen or two. The authors also bring in some of the very convincing scientific evidence that various gastrointestinal (GI) issues are over-represented in relation to autism (see here). There's even mention of how useful that Taiwanese research database has been down the years to autism and ADHD research (see here).

What's more to say? Well, preferential screening for various medical conditions in the context of an autism diagnosis yet again, receives more support. As does the idea that when a medical diagnosis is received by a person diagnosed on the autism spectrum, that medical diagnosis deserves the same healthcare management and/or treatment as it does in the context of not-autism save any further health inequalities potentially appearing (see here). The days for example of 'blaming autism' for every single physical complaint are also to be consigned to the historical dustbin. And with it, recognition that concepts such as ESSENCE or 'autism plus' (see here and see here) really need to include the somatic as well as the behavioural/psychiatric...

Whilst welcoming the Muskens review, it's important to note that others have already 'primed' for the importance of medical comorbidity in relation to a diagnosis of autism...

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[1] Muskens JB. et al. Medical comorbidities in children and adolescents with autism spectrum disorders and attention deficit hyperactivity disorders: a systematic review. European Child & Adolescent Psychiatry. 2017. July 3.

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Antidepressants during pregnancy and autism in offspring (with care)

There are a few topic areas in the quite vast autism research landscape that consistently seem to keep cropping up. The possibility of some kind of *association* between pregnancy antidepressant use and risk of offspring autism is one of those areas (see here) as the results published by Dheeraj Rai and colleagues [1] (open-access) are presented for your attention. I would also draw your attention to an accompanying editorial discussing the Rai findings (see here).

So: "To help to improve the understanding of the association between antidepressant use during pregnancy and autism in offspring, we applied a range of... causal analytical methods on data from a large total population cohort in Stockholm County" was the starting point, as once again one of those very useful Scandinavian registries provided the source study material (indeed, Rai et al are seemingly experts in their analysis of such resources). The added bonus to the Rai study was their attempt to 'unravel' any association between gestational antidepressant exposure and autism from the reason why such medication was being taken in the first place: maternal psychiatric health issues (and whether this variable may in fact account, at least in part, for any association that has previously been identified).

From a starting population approaching three-quarters of a million people, researchers eventually settled on looking at over 250,000 children under 17 years of age (but over 4 years of age "in whom a diagnosis of autism might be less reliable") who were born to over 150,000 mothers. The vast majority of children (239,943 of 254,610) had no history of exposure to antidepressants during pregnancy. The remaining participants were divided up into two groups: one where there was documentation leading to the assumption of exposure to pregnancy antidepressants (n=3342) and one where there was an indication for such exposure ("mothers with a psychiatric disorder") but no recorded use of antidepressants during pregnancy (n=12,325). Researchers summed up how many children were diagnosed with an autism spectrum disorder (ASD) in each group and applied some statistical modelling.

Results: I think it's important to first highlight a statistic that seems to have been missed by many covering the Rai findings: "Of the 238 943 cohort children for whom there was no record of maternal history of psychiatric disorder or antidepressant use during pregnancy, 4889 had autism (2.1%)." That's 2.1% with a diagnosis of autism or ASD; quite a far cry from the 1% [estimate] statistic from just a few years back (at least here in Blighty).

Then: "Exposure to antidepressants during pregnancy was associated with a higher odds of a diagnosis of autism in offspring than exposure to a maternal psychiatric disorder without antidepressants." The authors caution that: "the absolute risk was small, and 4.1% of children exposed to antidepressants in utero had autism compared with 2.9% of those with a maternal history of psychiatric disorder." Further when looking at those children diagnosed with ASD in the groups, authors observed that "autism without intellectual disability" seemed to be over-represented; something also picked up in previous findings from authors on this current paper [2].

Alongside various opinions on these findings (see here for example), the authors caution about the possible meaning of their results. One obviously has to be quite careful when discussing such data to ensure that an important class of medicines is not unduly vilified. No medicine is however without potential side-effects and appropriate clinical decisions and good medicines management [2] is key, particularly when pregnancy is included as variable. The authors talk, for example, about how "if a causal link were robustly established, and if no pregnant women took antidepressants during pregnancy, only 2% of autism cases in this population would be prevented." Alongside they [importantly] mention that antidepressant use during pregnancy is not typically just a 'choice' but rather being clinically indicated: depression does not simply disappear when a woman is pregnant. Interestingly too, they mention about how their data "suggest that there is an increased background risk of autism in children of women with psychiatric conditions, regardless of antidepressant treatment." This follows a trend in other areas of psychiatry (see here for example).

Yet again, the call is further research in this area and, quite a few more investigations into the possible hows-and-whys of any association (with medication use and/or maternal psychiatric presentation) is made. I might also suggest that taking into account other childhood conditions such as attention-deficit hyperactivity disorder (ADHD), potentially over-represented when it comes to a diagnosis of autism or ASD, could be another important step forward in light of other preliminary *associations* being made with pregnancy medication history in mind (see here). This also includes looking at any issues associated with timing of potential exposure and/or dose ("Because of small numbers, we were not able to assess trimester specific or dose response effects.").

Insofar as the suggestion that autism without intellectual (learning) disability might be an important phenotype when it comes to any association, subsequent research in this area seemingly fits in well with increasingly vocal calls [4] to stop using the generic label of autism as a research starting point (see here). Allied to suggestions for more 'bottom-up' research with autism in mind (see here), also coincidentally mentioning "maternal SSRI use during pregnancy" in the context of autism [5], a future research agenda is seemingly emerging. I might also point out that certain sensitivities need to be kept in mind on the basis of suggestions that an 'environmental exposure' might, in whole or part, be *associated* with a particular type(s) of autism.

All such work - present and future - however needs to be done/presented with care, understanding and minus scaremongering, so as not to unduly alarm pregnant mothers, their families or indeed, the physicians providing their care at such a critical time...

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

[2] Rai D. et al. Parental depression, maternal antidepressant use during pregnancy, and risk of autism spectrum disorders: population based case-control study. BMJ. 2013 Apr 19;346:f2059.

[3] Angelotta C. & Wisner KL. Treating Depression during Pregnancy: Are We Asking the Right Questions? Birth Defects Res. 2017 Jul 17;109(12):879-887.

[4] Waterhouse L. et al. The ASD diagnosis has blocked the discovery of valid biological variation in neurodevelopmental social impairment. Autism Res. 2017 Jul;10(7):1182.

[5] Unwin LM. et al. A "bottom-up" approach to aetiological research in autism spectrum disorders. Front Hum Neurosci. 2013 Sep 19;7:606.

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Is gluten avoidance linked to a lower risk for depression?

I've talked a few times on this blog about how avoiding dietary gluten both within (see here) and outside of (see here) the context of coeliac (celiac) disease, the archetypal 'gluten is baddie' autoimmune condition, might have some pretty interesting effects on some aspects of a person's psychology. Today's post reflects yet more peer-reviewed science suggesting that there may indeed be something to see in this potentially important area; particularly pertinent to the presentation of depression or depressive symptoms.

So, the findings reported by Haley Zylberberg and colleagues [1] based on data from some 22,000 participants taking part in the US 2009-2014 National Health and Nutrition Examination Survey are the source material today. Some background material related to this cohort can be found here. They specifically looked at the "prevalence of depression, insomnia, quality-of-life variables, and psychotropic medication use in CD [coeliac disease] participants and PWAGs [people who avoid gluten] to controls." People who avoid gluten - PWAG - represent a group who don't have a diagnosis of CD but nonetheless similar to those who were diagnosed with CD, reported avoiding dietary gluten.

Results: "Depression was present in 8.2% of controls compared with 3.9% of participants with CD... and 2.9% of PWAGs." Even after adjustment for various confounding variables ("age, sex, race, income, and access to healthcare") those gluten avoiders (without CD) less frequently presented with depression compared with data from controls.

Added to the previous occasions where gluten consumption seems either to be linked to [some] depression or removal of gluten seems to positively impact on depressive symptoms at least for some, this is interesting work. Yes, quite a few more controlled trials are required to examine such relationships between food and mood. Although we can speculate on possible mechanisms [2] we don't really know why there may be an effect from gluten removal, but this is an emerging area of science; particularly in the context of how disruptive/disabling/damaging depression can be to someone.

Bearing in mind the caveats of this blog - no medical or clinical advice is given or intended - please don't assume that I'm advocating gluten removal for anything (unless clinically indicated) on the basis of this or other posts. If in doubt, consult your medical physician.

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[1] Zylberberg HM. et al. Depression and insomnia among individuals with celiac disease or on a gluten-free diet in the USA: results from a national survey. Eur J Gastroenterol Hepatol. 2017 Jun 27.

[2] Pruimboom L. & de Punder K. The opioid effects of gluten exorphins: asymptomatic celiac disease. J Health Popul Nutr. 2015 Nov 24;33:24.

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"Medical history was associated with increased risk of CFS/ME"

The paper by Berit Feiring and colleagues [1] (open-access) is the source blogging material today covering an area that I was previously unaware of: "to study the association between HPV [human papillomavirus] vaccination and risk of CFS/ME [chronic fatigue syndrome/myalgic encephalomyelitis] among girls eligible for HPV vaccination in the national immunisation programme in Norway."

A quick trawl of PubMed to look-see whether there was any previous peer-reviewed science in this area revealed some inklings about a possible *association* between use of the HPV vaccine and some symptoms that may follow a diagnosis of ME/CFS [2] but not much to say that risk of an actual diagnosis of CFS/ME was significantly heightened [3] following HPV immunisation. On the topic of postural tachycardia syndrome (PoTS) and HPV vaccination, I had been aware of some, limited peer-reviewed discussions (see here).

As it happens, Feiring et al did not observe any population-wide links between HPV vaccination and increased risk of CFS/ME based on their analysis of "176,453 girls born 1997–2002 [who] were eligible for HPV vaccination." They tempered their conclusions slightly given that they "did not have access to patient records for verification of the CFS/ME diagnoses" derived from the Norwegian Patient Registry (NPR) but for all intents and purposes, their data is compelling based on sample size and how well Scandinavian countries tend to treat their population data.

A few other, rather interesting aspects to the Feiring data are also apparent: "we observed an increase in the incidence of CFS/ME among adolescents aged 10–17 in Norway, during 2009–2014" and: "Medical history was associated with both increased risk of CFS/ME and lower uptake of HPV vaccine." The idea that numbers of cases of CFS/ME is on the up in Norway is an interesting one and perhaps contrasts with other data from here in Blighty for example (see here) bearing in mind the age groups analysed. I was however specifically drawn to the idea that: "The risk of CFS/ME increased with increasing number of previous hospital contacts."

Looking at hazard ratios (HRs) for a diagnosis of CFS/ME based on how many times a girl had had hospital contact, a rather interesting dose-dependent pattern emerged. So, examining the entire follow-up period, the (adjusted) HR for CFS/ME diagnosis for those with only one hospital contact was 1.64 (1.22–2.19). For those with seven or more hospital contacts, the HR jumped to 5.23 (3.66–7.49). Also potentially important were the possible reason(s) for hospital contact and risk of CFS/ME: "According to ICD-10 diagnoses, the highest risk of CFS/ME was found among girls with diagnoses in chapters I00-I99 (Diseases of the circulatory system)..., A00-B99 (Certain infectious and parasitic diseases)... and R00-R99 (Symptoms, signs and abnormal clinical and laboratory findings, not elsewhere classified)."

Other discussions on data also from Norway (indeed, from some of the same authors) has talked about medical history around CFS/ME and what conditions seem to be 'over-represented' (see here). On that research occasion [3] they concluded that: "Children with CFS/ME were frequently diagnosed with infections, supporting the hypothesis that infections may be involved in the causal pathway." Said previous findings are not so dissimilar from the current ones reported by Feiring and colleagues.

Insofar as the next steps on from the Feiring data, well one might - assuming independent replication and the like - see a way forward where a potential early warning system for possible CFS/ME screening might be put in place on the basis of patterns of hospital visits and the types/patterns of diagnosis that are given. I appreciate that there is quite a lot of heterogeneity when it comes to CFS/ME (possibly even another label ripe for pluralisation or spectrum-ing?) so I don't want to get too ahead of myself here but there is potential. Whilst HPV vaccination did not seem to be connected to later CFS/ME diagnosis in the Feiring cohort, the question about what factors could be driving the increase in cases remains open: "The reasons for the increase in CFS/ME in Norway are unknown."

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[1] Feiring B. et al. HPV vaccination and risk of chronic fatigue syndrome/myalgic encephalomyelitis: A nationwide register-based study from Norway. Vaccine. 2017. June 23.

[2] Brinth LS. et al. Orthostatic intolerance and postural tachycardia syndrome as suspected adverse effects of vaccination against human papilloma virus. Vaccine. 2015 May 21;33(22):2602-5.

[3] Donegan K. et al. Bivalent human papillomavirus vaccine and the risk of fatigue syndromes in girls in the UK. Vaccine. 2013 Oct 9;31(43):4961-7.

[4] Bakken IJ. et al. Comorbidities treated in primary care in children with chronic fatigue syndrome / myalgic encephalomyelitis: A nationwide registry linkage study from Norway. BMC Family Practice. 2016; 17: 128.

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Anxiety disorder is rife in 'high-functioning' autism

"Lifetime prevalence rates of 53.5% for depressive disorder 73.5% for anxiety disorders and 37.5% for ADHD [attention-deficit hyperactivity disorder] were found."

Those were the figures arrived at by Alexandru Gaman and colleagues [1] who set about investigating the "prevalence rates of psychiatric co-morbidities" among other things in a cohort of over a hundred adults diagnosed with "high-functioning" autism via the quite recently revised DSM-5 criteria. I've stressed the words 'high-functioning' to denote this being the authors' words not mine (personally, I'm not so sure that general level of functioning is all that good as a descriptor).

Various other observations were made by authors such as the finding that: "Subjects with psychotic co-morbid symptoms had a more severe social deficit" which might tap into some other discussions being had on how some of the screening instruments talked about with autism in mind are seemingly not adverse from potentially picking up other labels with a psychosis element to them (see here). I say that also with the understanding that at least for some, autism and psychosis are not diagnostically unstrange bedfellows (see here).

I've zoomed in on the anxiety disorder(s) bit to the Gaman findings because of their very high lifetime prevalence and because, day-to-day, anxiety disorders can be absolutely disabling for many people on the autism spectrum (see here). Indeed, with all the very positive talk about things like employment and further education opportunities [slowly] increasing for autistic young people and adults, one of the details that does not seem to be talked about as much is how issues like anxiety can significantly hinder not only efforts to get a job/student place but also keeping that job/student place in the longer term (see here). Talent is being outshone by crushing anxiety in some cases.

Gaman and colleagues concluded by talking about how identification of something like anxiety disorder is "a crucial clinical issue." I would very definitely agree with this viewpoint but more than that, efforts now need to go into what can be done about treating/managing such anxiety to make people's lives easier (see here); accepting that we still have some distance to go in this process [2]. I'd also like to see some kind of research parity being arrived at specifically with regards to the question: how prevalent and what effects does anxiety have for those NOT described as having 'high-functioning' autism?

To close, having recently been party to some interesting debate on social media about the ins-and-outs, rights-and-wrongs and positives-and-negatives of [exclusive] self-diagnosis with autism in mind, I'd like to link to a paper by Ashwood and colleagues [3] on how one of the premier 'are you autistic?' self-report schedules is not necessarily fit for purpose when it comes to a self-diagnosis of autism. Indeed pertinent to today's post, how "generalized anxiety disorder may ‘mimic’ ASD [autism spectrum disorder] and inflate AQ [Autism-Spectrum Quotient] scores, leading to false positives" echos a viewpoint that I championed: identity, emotions and politics aside, there is no substitute for a thorough professional assessment when autism is suspected. Outside of such an assessment being potentially pertinent to the idea that autism rarely appears in some sort of diagnostic vacuum (see here), it is perhaps even more important as the DSM-5 criteria for ASD and SCD [social (pragmatic) communication disorder] start to become even more mainstream and what it means/will mean to the concept of autistic identity too...

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[1] Gaman A. et al. Psychiatric co-morbidities in a French cohort of adults with high-functioning autism (HFA). European Psychiatry. 2017; 41: S136.

[2] Lorenc T. et al. Support for adults with autism spectrum disorder without intellectual impairment: Systematic review. Autism. 2017 Jun 1:1362361317698939.

[3] Ashwood KL. et al. Predicting the diagnosis of autism in adults using the Autism-Spectrum Quotient (AQ) questionnaire. Psychological Medicine. 2016;46(12):2595-2604.

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Second seizure risk and "idiopathic autism"

Idiopathic autism refers to instances where autism is the primary diagnosis and not something secondary to another - usually genetic - condition. The paper by Asad Qadir and colleagues [1] reviewed the files of some 150 people diagnosed with an autism spectrum disorder (ASD), idiopathic ASD, and a history of at least one seizure in connection to an important issue: recurrence risk of seizure. They concluded that the average age of first seizure in their cohort was around about 7 years old and many, over 90% of participants included for review, were at serious risk of a second seizure on average just over 6 months later.

This is an important finding. We already know that epilepsy and seizure disorder(s) are not uncommon bedfellows to parts of the autism spectrum (see here) (indeed, many parts of the autism spectrum seem to be prone to unusual EEG - electroencephalographic or electroencephalogram - findings). We know that non-febrile seizures (seizures not attached to fever) are quite a bit more common in relation to autism when compared with non-autistic siblings for example (see here). And on top of all that, we know that seizures can in some instances be life-threatening (see here).

The Qadir data highlights the "short time to second seizure" as a window to appropriate management of seizure when coincidental to autism. The data suggest that even after one seemingly isolated incidence of seizure, clinicians might consider being proactive in (i) screening for signs of EEG anomalies for example, and (b) be pretty assured that initiation of appropriate treatment/management of seizure is very likely applicable insofar as the risk of recurrence in those diagnosed with an ASD. I say all that with my blogging caveat of no medical or clinical advice given or intended, in full working order.

I'd also like to think that as our knowledge about the autism spectrum increases, in particular the idea that there may be many different routes to many different types of autism (see here) so science will start to put some further flesh on the bones that what we call idiopathic autism with epilepsy at the moment, does not necessarily mean things will stay 'idiopathic' in future times. Then, other questions need answering, such as whether certain 'epileptic encephalopathy syndromes' might actually be the cause of some autism [2]...

As I've said many times before on this blog, don't mess with seizures and/or epilepsy...

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[1] Qadir AA. et al. Risk of Second Seizure in Pediatric Patients With Idiopathic Autism. J Child Neurol. 2017 Jan 1:883073817713906.

[2] Srivastava S. & Sahin M. Autism spectrum disorder and epileptic encephalopathy: common causes, many questions. J Neurodev Disord. 2017 Jun 23;9:23.

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Should anyone be concerned about pathological video game use in relation to autism?

"... the risk for pathological game use appears larger in adults with ASD [autism spectrum disorder] compared with TD [typically developing] adults. These findings point to pathological game use as a potentially important focus of clinical attention in adults with ASD."

So concluded the paper by Christopher Engelhardt and colleagues [1] (open-access) looking at an interesting issue - "whether adults with autism spectrum disorder (ASD) are at higher risk for pathological game use than typically developing (TD) adults" - based on reports from some 120 participants with and without a diagnosis of autism. Including one Micah Mazurek on the authorship list (who has previously talked about the effects of screen time and autism), researchers delved into self-reported time spent playing video games based on data collected from a cohort "participating in a larger study on violent video game effects" [2]. The average age of participants (with and without a diagnosis of autism) was round about the 20 years old mark.

Results: both on weekdays and weekends, the typical hours of game play were different between the groups of those with autism and those without. Interestingly, authors used a slightly different statistical approach to the traditional "null hypothesis significance tests and 95% confidence intervals" via their use of "Bayes factors to state evidence for or against our predictions" to analyse their data. Bayes and Bayesian teachings provide an alternative to the 'frequentist' considerations in treating data. Alongside asking about game play time, researchers also asked participants to complete a questionnaire on "pathological video game use" that was based on "another behavioral addiction (pathological gambling)" and covered various aspects: "salience, euphoria or relief, tolerance, withdrawal, conflict, relapse and reinstatement."

"The results indicated that adults with ASD endorsed more symptoms of video game pathology than did TD adults. This relationship was strong, enjoying 300,000-to-1 odds in Bayesian model comparison." Such sentences kinda say it all. Risk of pathological video game use was quite a bit more likely in those with autism than those without, and 'escapism' was also reported to be an important reason for such extended use.

I do want to be a little careful in this post not to (a) demonise - pathologise - video game playing and/or (b) isolate those on the autism spectrum as being 'unique' in their video gaming habits. Personally, I don't see an issue if people want to spend large sections of their days playing video games as opposed to watching television or sitting down reading a book (reading in particular, is another fine example of escapism) or doing anything else. This was a study of adults doing what many millions of people do every day, so they should have the right to do as they please in this context. With the wonders of modern technology, gaming today is also not necessarily a socially-isolated pastime so one has to be quite careful about making any sweeping generalisations in that respect too.

I have however, always been a little worried about this and other research on screen time use in the context of autism and what detrimental effects it might have for a person's physical health. Everyone is prone to a degree of 'couch-potatoing' (i.e. loafing of the sofa for hours on end) but when people are talking about nearly 3 hours every day gaming, presumably sat on a couch/sofa, this really can't be doing anyone any good in terms of their long-term physical health. We're all being told to move more (see here) and given the data emerging when it comes to the physical activity patterns of rather a lot of people on the autism spectrum (see here), there are some good grounds for encouraging more movement and more physical activity minus any nanny-stating. I appreciate that sports and exercise is not everyone's cup of tea and in particular, more needs to be done in making physical activity more attractive to many groups of people including those on the autism spectrum (see here). Efforts should continue to ensure a balance is struck between times of sedentary behaviours typically associated with gaming and times of engaging in physical activity; as far as I can see, Engelhardt et al did not ask about physical activities or other related pastimes on this research occasion. Indeed, although I am still a little apprehensive about the use of exergaming, I do wonder if this could be a good bridging point on the road to balance...

Music to close: Shape of You by Ed for one of my brood who seems to be looking forward to becoming a kumite specialist (when she graduates from Ippon kumite).

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[1] Engelhardt CR. et al. Pathological game use in adults with and without Autism Spectrum Disorder. PeerJ. 2017. e3393.

[2] Engelhardt CR. et al. Effects of Violent-Video-Game Exposure on Aggressive Behavior, Aggressive-Thought Accessibility, and Aggressive Affect Among Adults With and Without Autism Spectrum Disorder. Psychol Sci. 2015 Aug;26(8):1187-200.

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Antidepressant use in pregnancy and risk of offspring ADHD?

Here we go again. Antidepressant use during pregnancy comes under the spotlight yet again (see here) as per the findings reported by Takoua Boukhris and colleagues [1], this time in connection to risk of offspring diagnosis of attention-deficit hyperactivity disorder (ADHD) following gestational exposure to this class of medicines.

Drawing on data derived from the Quebec Pregnancy/Children Cohort (QPC), researchers set out to examine the "risk of ADHD associated with overall and class-specific antidepressant exposure in utero." I might add that previous data from some of the authors of the Boukhris paper on the QPC has suggested that it is "an excellent tool for the study of the risk and benefit of drug use during the perinatal period" [2].

Following nearly 150,000 live births between 1998 and 2009, researchers looked at the rates of subsequent diagnosis of ADHD alongside the pattern of medication use during pregnancy and other important variables such as "maternal history of depression/anxiety and ADHD." They concluded that: "AD [antidepressant] use during the 2nd and 3rd trimester of pregnancy, specifically tricyclics, is an independent risk factor for ADHD in children above and beyond the risk associated with maternal depression/anxiety or ADHD." Further: "SSRI [Selective serotonin reuptake inhibitors] and SNRI [Serotonin–norepinephrine reuptake inhibitors] use were not associated with increased ADHD risk."

As per the convoluted research history talking about pregnancy antidepressant 'exposure' and possible risk of offspring autism, there are certain caveats and issues worth mentioning. Antidepressant use during pregnancy is not something to be taken lightly as per any calls to 'restrict use' during the special nine months that make us. Such medicines serve an important purpose in controlling some potentially important clinical symptoms; said symptoms do not just dissipate during the special time called pregnancy as per other clinical examples with other labels (see here).  It's also worth pointing out that such observational studies looking at medication use and offspring outcomes are just that - observational. As per the tenet 'correlation is not the same as causation', one has to be a little careful with such data...

That all being said, I do find the Boukhris results to be intriguing on the basis that this is not the first time that an *association* has been talked about in the peer-reviewed science domain [3] and on more than one occasion [4]. Further investigations are perhaps required into the possible mechanism(s) involved in any such relationship between medicine and offspring development, and indeed, whether such connections could potentially invite new intervention options for labels like ADHD? I'm also more than a little interested in the 'medication type' angle to the Boukhris observations not necessarily being the same as that put forward in relation to offspring risk of autism.

And just before you go, it's worth highlighting the findings reported by Viktorin and colleagues [5] looking at pregnancy antidepressant use and intellectual (learning) disability: "After adjustment for confounding factors... the current study did not find evidence of an association between ID and maternal antidepressant medication use during pregnancy."

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[1] Boukhris T. et al. Antidepressant Use in Pregnancy and the Risk of Attention Deficit with or without Hyperactivity Disorder in Children. Paediatr Perinat Epidemiol. 2017 Jun 22.

[2] Bérard A. & Sheehy O. The Quebec Pregnancy Cohort – Prevalence of Medication Use during Gestation and Pregnancy Outcomes. Croy A, ed. PLoS ONE. 2014;9(4):e93870.

[3] Man KKC. et al. Prenatal antidepressant use and risk of attention-deficit/hyperactivity disorder in offspring: population based cohort study. BMJ. 2017 May 31;357:j2350.

[4] Clements CC. et al. Prenatal antidepressant exposure is associated with risk for attention-deficit hyperactivity disorder but not autism spectrum disorder in a large health system. Mol Psychiatry. 2015 Jun;20(6):727-34.

[5] Viktorin A. et al. Association of Antidepressant Medication Use During Pregnancy With Intellectual Disability in Offspring. JAMA Psychiatry. 2017 Jul 12.

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"a potential link between serious delinquency and later schizophrenia"

I was rather intrigued by the results reported by Nina Lindberg and colleagues [1] in their study designed to "investigate if serious delinquency was associated with future diagnoses of schizophrenia or schizoaffective disorder (here, broadly defined schizophrenia) among a nationwide consecutive sample of 15- to 19-year-old Finnish delinquents sent for a forensic psychiatric examination in 1989-2010."

I hadn't previously come across research directly linking delinquency - serious delinquency - with later schizophrenia diagnosis despite noting other research talking about other labels being potentially related to the extreme results of delinquency (see here) and onward some of those labels being potential risk factors for something like schizophrenia (see here).

Looking at the records of "313 delinquents with no past or current psychotic disorder" and around 1200 age- and sex-matched non-delinquents whose details were also held on a central population registry, researchers followed them all "[un]till death, emigration or the end of 2015, whichever occurred first." The results put delinquents as a group at quite a bit more risk of subsequently being diagnosed with schizophrenia than non-delinquents (12% vs. ~1% respectively). The authors conclude that their results "supports the previous research indicating a potential link between serious delinquency and later schizophrenia" and that more investigation is needed into the hows-and-whys of such a relationship.

Having already mentioned the slightly more indirect link between attention-deficit hyperactivity disorder (ADHD) and risk of offending behaviour (minus any sweeping generalisations) and ADHD and risk of schizophrenia, there could be lessons to be learned about the link between serious delinquency and schizophrenia. Also, minus further generalisations, I'm also wondering if some of the 'habits' perhaps more readily observed in delinquents (e.g. illicit drug use) could potentially be additional risk factors for a diagnosis of schizophrenia [2]. Minus any psycho-babble explanations, the rise and rise of scientific evidence pointing to various psychosocial factors as also being risk factors for schizophrenia [3] may additionally come into play, together with an understanding that elements of the parental home also may play a key role in cases of delinquency [4]. In short, there are several potentially important areas that could provide key research directions in this intriguing area.

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[1] Lindberg N. et al. Serious delinquency and later schizophrenia: A nationwide register-based follow-up study of Finnish pretrial 15- to 19-year-old offenders sent for a forensic psychiatric examination. Eur Psychiatry. 2017 May 15;44:173-178.

[2] Marconi A. et al. Meta-analysis of the Association Between the Level of Cannabis Use and Risk of Psychosis. Schizophr Bull. 2016 Sep;42(5):1262-9

[3] Larsson S. et al. High prevalence of childhood trauma in patients with schizophrenia spectrum and affective disorder. Compr Psychiatry. 2013 Feb;54(2):123-7.

[4] Fernández-Suárez A. et al. Risk Factors for School Dropout in a Sample of Juvenile Offenders. Front Psychol. 2016 Dec 26;7:1993.

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Analysing police involvement in the context of autism

"About 1 in 6 people with autism interacted with police over 18 months" went one of the media headlines covering the study published by Ami Tint and colleagues [1] looking at the hows-and-whys of police involvement in a cohort of nearly 300 young people and adults diagnosed with an autism spectrum disorder (ASD).

Researchers observed that some 16% of their cohort had some contact with law enforcement agencies but only a very small proportion actually resulted in any criminal charges being brought. Perhaps reassuringly, and despite 'aggressive behaviours' being cited as "the primary concern necessitating police involvement", most interactions between person and law enforcement were not especially adverse or particularly unpleasant for those on the spectrum. To quote: "Most parents reported being satisfied to very satisfied with their children’s police encounters."

But that's not to say that such encounters ended well for everyone, as talk about 1 in 5 police interactions involving physical restraint are also detailed and highlight the need for further research in this area. I might also add that symptom severity (I assume also referring to the presence of learning or intellectual disability alongside autism) was not a great indicator of police interaction or not according to the study.

Trawling through the quite small peer-reviewed research base in this area, there are some interesting points raised when it comes to awareness and training of police and other first responders [2] in respect of autism. Research here in Blighty has similarly highlighted gaps in police training [3] that may have been contributory to less positive satisfaction ratings when it came to interaction with people with autism. I draw back however from blanket blaming police for such statistics; they often have a very difficult job to do already, irrespective of whether diagnostic labels or other factor(s) are part and parcel of the situation(s) they are faced with.

So aside from greater training for law enforcement agencies and other first responders, what can be done to ensure that interactions with those on the autism spectrum are more positive? Some people have talked about setting up registries to guide police and related services where autism might be a factor in encounters. I can see the logic in such discussions, particularly in the context of another important issue to the autism spectrum - wandering or elopement - and ensuring that police have important knowledge about such an issue (see here). But with such registries come risks; risks of stigmatisation and also to personal liberties too. Some of the same issues relevant to the use of disclosure cards and autism come to the forefront (see here).

Perhaps a better arrangement would be a greater focus on community policing for example, where community Bobbies know their neighbourhood and it's residents and are able to apply that local knowledge as and when required. Appreciating that in these days of continued austerity, community policing numbers have suffered, perhaps a move back to neighbourhood policing is an important way of making police contact with those on the autism spectrum and no doubt various other groups that little more easier for all concerned?

Music to close, and the Beastie Boys meet Sesame Street?

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[1] Tint A. et al. Correlates of Police Involvement Among Adolescents and Adults with Autism Spectrum Disorder. J Autism Dev Disord. 2017. June 13.

[2] Kelly E. & Hassett-Walker C. The training of New Jersey emergency service first responders in autism awareness. Police Pract Res. 2016;17(6):543-554.

[3] Crane L. et al. Experiences of Autism Spectrum Disorder and Policing in England and Wales: Surveying Police and the Autism Community. J Autism Dev Disord. 2016 Jun;46(6):2028-41.

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