S100B protein and autism continued

"Our findings showing an increase in peripheral concentrations of S100B and TNF-α provide limited support to the hypothesis about the roles of altered immune function and S100B in autism spectrum disorder (ASD)."

So said the findings reported by Selin Aktan Guloksuz and colleagues [1] (open-access available here) continuing some discussions a few years back on a possible role for S100B in relation to at least some autism (see here).

S100B - S100 calcium-binding protein B - is a compound involved in quite a few biological reactions not least "as a biomarker of global glial activity." Elevations of the S100B have been reported in relation to several states including that of [traumatic] brain injury. Outside of some research suggesting that elevations of S100B might also be a feature of diagnoses such as schizophrenia (see here), it has also been the topic of investigations with [some] autism in mind [2] too. The name of the game is elevations in S100B in relation to autism and more.

Based on analyses of fasting blood samples from "40 unmedicated children with autism" (where autism diagnoses were confirmed by study researchers) and 35 asymptomatic control children, researchers measured levels of plasma S100B alongside various markers of immune function (cytokines). Among the suite of cytokines examined, levels of "tumor necrosis factor alpha (TNF-α), interferon gamma, interleukin (IL)-1β, IL-4, IL-6, IL-10, and IL-17A" were included. The idea of using unmedicated children with autism stems from the suggestion that at least one medication used for some autism might have the ability to elevate S100B [3].

Results: as per the opening sentence to this post, levels of S100B and TNF-α were 'different' between the groups (both elevated) and this finding remained "after controlling for age, sex, and BMI [body mass index]." Researchers also reported some results looking at whether ASD symptom presentation might show any 'association' with S100B levels. On this topic they reported that: "Plasma S100B concentrations in children with severe ASD symptoms were higher than in children with mild-moderate ASD symptoms" but when again controlling for age, sex and BMI this association did not hold (significantly). As for the other cytokines outside of TNF-α... nothing came up as significant between the groups. This is interesting in light of recent work (see here) and even Guloksuz et al talk about future "prospective longitudinal studies investigating a broad set of immune markers, both in serum and CSF [cerebrospinal fluid], in large samples" and the pros- and cons of looking in CFS.

Where next for this area of investigation? Well, taking into account the link between S100B and brain injury and what that could mean for cognitive processes for example, I'd be minded to suggest that more study is needed looking at the effect of S100B levels in relation to cognition and autism. Take for example the study results from Chen and colleagues [4] who reported that "serum S100B level was an independent contributor to the global cognitive dysfunctions, particularly for the speed of processing, attention/vigilance, visual learning and reasoning/problem solving subscores" in their cohort of participants with schizophrenia. Might similar correlations be present alongside S100B elevations in relation to autism? I'd also be minded to suggest looking at a possible role for comorbidities potentially accompanying a diagnosis of autism as being important for S100B elevations in light of other research on depression for example [5]. Depression (various types) and autism is very much an important area of overlap (see here for example) and might actually offer at least one way to target elevations in S100B.

There is more to do on this topic.

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[1] Guloksuz SA. et al. Elevated plasma concentrations of S100 calcium-binding protein B and tumor necrosis factor alpha in children with autism spectrum disorders. Rev Bras Psiquiatr. 2017 Jan 12:0.

[2] Al-Ayadhi LY. & Mostafa GA. A lack of association between elevated serum levels of S100B protein and autoimmunity in autistic children. J Neuroinflammation. 2012 Mar 16;9:54.

[3] Quincozes-Santos A. et al. Effect of the atypical neuroleptic risperidone on morphology and S100B secretion in C6 astroglial lineage cells. Mol Cell Biochem. 2008 Jul;314(1-2):59-63.

[4] Chen S. et al. Cognitive dysfunction correlates with elevated serum S100B concentration in drug-free acutely relapsed patients with schizophrenia. Psychiatry Res. 2017 Jan;247:6-11.

[5] Rajewska-Rager A. & Pawlaczyk M. The role of S100B protein as a potential marker in affective disorders. Psychiatr Pol. 2016;50(4):849-857.

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Guloksuz SA, Abali O, Aktas Cetin E, Bilgic Gazioglu S, Deniz G, Yildirim A, Kawikova I, Guloksuz S, & Leckman JF (2017). Elevated plasma concentrations of S100 calcium-binding protein B and tumor necrosis factor alpha in children with autism spectrum disorders. Revista brasileira de psiquiatria (Sao Paulo, Brazil : 1999) PMID: 28099628

High frequency of (self-reported) ADHD symptoms in eating disorders

"There is a high frequency of ADHD [attention-deficit hyperactivity disorder] symptoms in patients with binge eating/purging eating disorders that motivates further studies."

That was the conclusion reached in the study by Nils Erik Svedlund and colleagues [1] (open-access) who, among other things, set out to "explore the prevalence and types of self-reported ADHD symptoms in a large, unselected group of ED [eating disorder] patients assessed in a specialized ED clinic." Participants (over 1100 of them) were "seeking help at the Stockholm Centre for Eating Disorders (SCED) from 4 February 2013 through 18 September 2015" and as well as being confirmed to have an eating disorder were also screened for ADHD-type behaviours using the WHO ADHD Self-Rating Scale for Adults (ASRS-screener). Notice the 'self-rated' part of that last sentence...

Based on a ASRS screener score of 14 or above, researchers reported that some 30% of females (N=1094) self-reported 'issues' associated with a diagnosis of ADHD. Some 34% of men included for study (N=47) reported similar ADHD traits (31.3% of the total group including those diagnosed with 'Eating Disorder Not Otherwise Specified (EDNOS) type 5' were on or above the ASRS screener score of 14).

Bearing in mind the presence of various types of different eating disorders in their cohort, researchers also looked at how those self-reported ADHD traits might correlate with sub-groupings. They report that: "The highest frequency of possible ADHD was found in BN [Bulimia Nervosa] and in AN-BP [Anorexia Nervosa bingeing/purging subtype], respectively." They also noted that specific symptoms of ED correlated with the ASRS-screener scores: binge eating, purging, loss of control over the eating and BMI [body mass index] > 17.5. I might add that based on responses to another schedule - the Comprehensive Psychiatric [Psychopathological] Rating Scale (CPRS) - included as part of the study, authors noted something of a link between the ASRS trait scores and "the CPRS scales for depression..., anxiety... and obsession-compulsion." But: "Psychiatric comorbidity correlated to ADHD symptoms without explaining the differences between eating disorder diagnoses."

Keeping in mind that answering 6 questions on a screener questionnaire does not an ADHD diagnosis make, I am rather interested in these and other findings. I am by no means an expert on eating disorder but I have previously been interested in the suggestion that autistic traits may be 'over-represented' when it comes to ED (see here). Combined with the idea that autism and [diagnosed] ADHD might not also be unstrange diagnostic bedfellows (see here) and you can perhaps see that there is potentially more research to do in this area in these times of overlap and ESSENCE. And speaking of ESSENCE [2]...

With a word or two of caution, I note the authors also talked about potential 'treatment' options given the overlap between ADHD traits (self-reported) and ED. So: "This motivates further randomized trials with stimulant treatment for bingeing/purging ED-patients with and without a concomitant ADHD diagnosis." Certain stimulants have quite a good track record when it comes to ADHD (see here) but the authors rightly note that 'appetite suppression' is a potential side-effect of such pharmacotherapy and something perhaps not ideal if someone is already underweight. More studies are indicated to disentangle what is linked to what.

And while I'm on the topic, the link between autism traits and anorexia nervosa might actually be a little more tenuous that you perhaps think [3]...

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[1] Svedlund NE. et al. Symptoms of Attention Deficit Hyperactivity Disorder (ADHD) among adult eating disorder patients. BMC Psychiatry. 2017; 17: 19.

[2] Karjalainen L. et al. Eating disorders and eating pathology in young adult and adult patients with ESSENCE. Compr Psychiatry. 2016 Apr;66:79-86.

[3] Postorino V. et al. Investigation of Autism Spectrum Disorder and Autistic Traits in an Adolescent Sample with Anorexia Nervosa. J Autism Dev Disord. 2017. Jan 24.

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Svedlund, N., Norring, C., Ginsberg, Y., & von Hausswolff-Juhlin, Y. (2017). Symptoms of Attention Deficit Hyperactivity Disorder (ADHD) among adult eating disorder patients BMC Psychiatry, 17 (1) DOI: 10.1186/s12888-016-1093-1

"Should gluten-free foods be available on prescription?"

Continuing the theme of blogging outside of the core material typically included on this site, I couldn't resist a mention of the 'head-to-head' debate talked about in the article by Matthew Kurien and colleagues [1] published in the British Medical Journal (BMJ).

As per the title of this post, the name of the game was gluten-free products being available on prescription here in Blighty, and in particular, the prescribing of gluten-free products to patients diagnosed with coeliac disease. The head-to-headers were Matthew Kurien, Sarah Sleet & David Sanders* (*a name not unfamiliar to this blog) all in favour of keeping the status quo and James Cave presenting the opposing view and why prescriptions of gluten-free products to those with coeliac disease might not be the only way.

OK, first things first. A gluten-free diet is not some dietary 'fad' for people living with coeliac disease (CD); it is a clinically-indicated treatment tool for this autoimmune condition. As I've said a few times on this blog, not only are there are physiological effects linked to CD mostly 'solved' by use of a gluten-free diet, but there may be psychological effects too (see here). Gluten is most definitely the 'baddie' when it comes to CD and should not be in the diet of those with CD.

The head-to-head piece makes for interesting reading in terms of how in these days of focus on the finances of the National Health Service (NHS), the idea that removing food prescriptions as one way to "reduce costs in the short term" might have some important repercussions in the longer-term. Indeed I was taken by one quote in the 'keep gluten-free food prescriptions' camp: "Would clinical commissioning groups consider this if the treatment for coeliac disease was an immunosuppressive drug and not food?" Food as medicine? I like that sentiment (see here).

I have to say however that I did find the viewpoint from James Cave rather appealing in some aspects. Within his various facts and figures he shows how perverse it is that one can go into a supermarket and buy a gluten-free loaf of bread for one price and yet the same loaf is bought by the NHS for prescription for quite a bit more. Sorry to focus on cost and finances but this is salient point in these days of continued austerity and financial/political uncertainty. Cave also adds that gluten-free food prescriptions tend to be restricted to set items, come in bulk and generally need to be collected from a pharmacy. There are additional costs added to the supply of such goods.

The two viewpoints do however agree that slight changes could be made to the system to make it both run more efficiently and provide those with coeliac disease a little more 'opportunity' in what they select. As Cave notes: "A national voucher scheme or a personalised health budget could be provided to ensure that patients receive recompense for the extra expense of gluten-free products." As Kurien and colleagues note: "Alternative strategies to prescriptions, such as direct supply schemes from community pharmacies, or voucher allowances, may be a more efficient way of delivering NHS support." A voucher scheme for gluten-free products? Interesting.

In these days where areas of England are already seeing changes to gluten-free prescriptions (see here for example) I'm wondering if a voucher scheme might be the [inevitable] way forward, at least for the majority of patients. Not only does this offer more choice to the consumer in terms of what products they buy (and indeed, what they might prefer) but the whole process of the NHS ordering, buying and dispensing such products is also reduced. For those who perhaps do not have access to a full-range of gluten-free products as their local supermarket for example or have mobility issues, exceptions could be made but for the most part, patients are handed choice and a lot more buying power and freedom. A voucher scheme might also 'normalise' the idea of gluten-free products when it comes to CD. By 'normalise' I mean that a young adult diagnosed with CD for example, no longer has to go to their local pharmacy for their 'months supply' but rather can shop - pick and choose - from the growing range of gluten-free products that adorn supermarket shelves these days. Compliance to the gluten-free diet will no doubt benefit when there is more choice and a voucher scheme will bring choice.

Change is often difficult when it comes to the NHS and it's been over 50 years since gluten-free products were put on prescription for those with CD so this would be a big change. But gluten-free is everywhere these days and there is seemingly little to hold the NHS back from further empowering those diagnosed with CD in terms of their dietary choices...

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[1] Kurien M. et al. Should gluten-free foods be available on prescription? BMJ 2017: 356.

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Kurien M, Sleet S, Sanders DS, & Cave J (2017). Should gluten-free foods be available on prescription? BMJ (Clinical research ed.), 356 PMID: 28073799

Vitamin D deficiency and risk of dementia

"The results of this systematic review show that low vitamin D levels might contribute to the development of dementia."

Whilst slightly off-topic when it comes to the core research material typically included on this blog, I did want to bring to your attention the systematic review and meta-analysis results published by Isolde Sommer and colleagues [1] (open-access) for your perusal. Although unable to "identify a single study investigating the association between sunlight exposure and dementia risk" authors did manage to find "indirect evidence from studies using vitamin D status as a surrogate parameter" where five out of six studies identified ("18,639 participants") suggested a possible correlation. Sunlight by the way, is the primary route of synthesising vitamin D.

The sort of 'risk' determined in the Sommer calculations when it comes to vitamin D levels and dementia is not to be sniffed at: "Translated into absolute numbers, 28 (at least 10 but up to 50 more) out of 1000 people with serious vitamin D deficiency would develop dementia compared with 1000 people with sufficient D levels over 18.03 years" despite some cautions around the quality of the studies reviewed.

Caveats? Well, examining just one variable (vitamin D status) when it comes to a nebulous condition like dementia has to be kept in mind when interpreting such data and another pet topic of mine - how one assays for vitamin D - is also mentioned: "There is still an ongoing debate regarding the method of choice but a recent comparison between liquid chromatography– tandem mass spectrometry (LC-MS/MS) methods and immunoassays showed variable performance of immunoassays apart from the radioimmunoassay that achieved a performance similar to LC-MS/MS." Discussions on this topic should also mention the epimers of vitamin D too [2]. Then there is the rather important issue of how the genetics of vitamin D formation/metabolism might also be something to look at [3] if one assumes some connection between small genetic 'blips' and possible risk, bearing in mind gene expression over just gene mutation might be important [4].

Minus any medical or clinical advice given or intended (something not given on this blog), I do however find data such as that from Sommer et al potentially important and something that can seemingly be acted upon quite easily (at least in terms of correcting any vitamin D deficiency/insufficiency). There is for example, a growing body of evidence potentially linking vitamin D and cognitive functions (see here) and alongside more population-wide advice being handed out by Government (see here), there seems to be some common sense in ensuring adequate sunlight exposure or vitamin intake.

Finally, minus any scaremongering or making connections where none might exist, specific groups of people where vitamin D deficiency seems to be 'over-represented' (see here and see here for example) might also be eligible for some enhanced screening for dementia in later life if one assumes a possible longitudinal link...

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[1] Sommer I. et al. Vitamin D deficiency as a risk factor for dementia: a systematic review and meta-analysis. BMC Geriatrics. 2017; 17: 16.

[2] Aghajafari F. et al. Plasma 3-Epi-25-Hydroxycholecalciferol Can Alter the Assessment of Vitamin D Status Using the Current Reference Ranges for Pregnant Women and Their Newborns. J Nutr. 2016 Jan;146(1):70-5.

[3] Lee YH. et al. Vitamin D receptor polymorphisms and susceptibility to Parkinson's disease and Alzheimer's disease: a meta-analysis. Neurol Sci. 2014 Dec;35(12):1947-53.

[4] Delgado-Morales R. & Esteller M. Opening up the DNA methylome of dementia. Mol Psychiatry. 2017 Jan 3.

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Sommer I, Griebler U, Kien C, Auer S, Klerings I, Hammer R, Holzer P, & Gartlehner G (2017). Vitamin D deficiency as a risk factor for dementia: a systematic review and meta-analysis. BMC geriatrics, 17 (1) PMID: 28086755

Andrew Whitehouse on challenging yet another autism status quo: diagnosis before intervention

"This paper provides an overview of the benefits and drawbacks of the current clinical pathway that places primacy on a diagnostic assessment for triggering the commencement of therapy. The paper then presents an alternative clinical pathway - the identification and provision of therapy to infants at risk of ASD [autism spectrum disorder] - and provides a critical review of current evidence supporting this model."

So said the 'lecture paper' by Andrew Whitehouse [1] and, as per the title of this short post, another peer-reviewed critical look at an autism status quo from this author (see here) who does not seem to be afraid to rock the boat (NB. see Cordelia Fine's new book for further discussion on the idea that there probably is no 'male' and female' binary brain differentiation).

Bearing in mind this was a paper based on a lecture given at a speech and language conference in Australia, I'm once again intrigued with the sentiments expressed by Prof. Whitehouse, who really does seem to be quite clued into how (a) an autism / autism spectrum diagnosis is for many children, happening 'too late' in terms of the time between when symptoms start manifesting and them getting an 'official' label, and (b) how quite a few children are entering into early intervention programs (for autism) before formal diagnosis is given (see here). I'm not going to go into the possible reasons 'why' the diagnostic pathway seems to be such a long one for so many (although there are clues outside of 'we're just better at recognising autism') but it strikes me as eminently sensible that if a child presents with autistic traits/behaviours, why wait for formal assessment but rather set plans in motion to 'zoom in' on specific areas where intervention might be required. Yes, there will be cost implications - without sounding too conspiracy-like, I've often wondered whether the 'queues' of those waiting for diagnosis at least here in Blighty is partly because the powers-that-be know that there will be cost implications following a diagnosis - but if one assumes that early intervention might have some long-term positive effects (see here) even the bean counters might see some benefits. I might add that whilst behavioural intervention is probably important, this should not be at the expense of other 'types' of intervention for some 'types' of autism (see here) and the value of other screening programs outside of just asking 'is it autism' (see here)?

'Nuff said, for now at least but I will be coming to another Whitehouse paper quite soon on this blog...

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[1] Whitehouse AJ. Elizabeth Usher Memorial Lecture: Rethinking the clinical pathway for autism spectrum disorder and challenging the status quo. Int J Speech Lang Pathol. 2017 Jan 13:1-10.

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Whitehouse AJ (2017). Elizabeth Usher Memorial Lecture: Rethinking the clinical pathway for autism spectrum disorder and challenging the status quo. International journal of speech-language pathology, 1-10 PMID: 28084105

A poo transplant for [some] autism?

I've talked about 'fecal microbial transplants' a.k.a the poo(p) transplant before on this blog (see here). That previous entry was about the more typical (and potentially life-saving) use of a poo transplant - where stool from one person is extracted, 'repackaged' and transferred to another person - albeit with caveats in terms of possible long-term side-effects. Now it appears that poo transplants are being investigated with something rather more central to the typical contents of the blog...

The paper by Dae-Wook Kang and colleagues [1] (open-access) has already been picked up by some media (see here) and it seems, also has a following from likely proponents and detractors particularly on social media. Including one James Adams on the authorship list, someone who is quite well-known in autism research circles (see here and see here for examples) alongside some other notable inclusions (Alessio Fasano, Thomas Borody, etc), the authors describe the results of small open-label study - I repeat, a small open-label trial - of 18 participants diagnosed with an autism spectrum disorder (ASD) who underwent a 10-week program characterised by the use of antibiotics, a bowel cleanse and then regular poo transplants for approximately 8 weeks. Additional information about the study and its results can be found here or if you wish, you can see the ClinicalTrials.gov entry here.

Tapping into a growing interest in how the gut (and its contents) might be important for at least some autism (see here for example) the aims of the trial were to "follow gut microbiota in healthy and treated children with ASD longitudinally as well as to evaluate an investigational new treatment, MTT [Microbiota Transfer Therapy], for its effectiveness in children with ASD in treating both GI [gastrointestinal] symptoms (primary outcome) and ASD-related symptoms (secondary outcomes), and to determine the effect of MTT on the gut microbiome."

The study included children diagnosed on the autism spectrum - ADI-R diagnosed - aged between 7-16 years old. All presented with moderate to severe functional bowel issues alongside their autism (something not unusual it seems). The authors also report using a control group of "20 age- and gender-matched neurotypical children without GI disorders" who were monitored but not treated as part of their study design.

The study first involved the administration of the antibiotic vancomycin for 2 weeks (something that has, on its own, some peer-reviewed research history with autism in mind [2]) used to 'profoundly suppress' pathogenic bacteria. Prilosec, the brand name for omeprazole was also administered towards the end of the bacterial washout phase initiated by the use of vancomycin. Prilosec is a medicine traditionally used to suppress stomach acid secretions and was used to "remove most remaining gut bacteria and vancomycin" and aid the passage and survival of the donor stool to the wider gastrointestinal (GI) tract. I say all that knowing that such medicines can affect the composition of the gut microbiota. Then came the bowel cleanse (Moviprep) complete with a fasting from food day, followed by the main [research] event: oral or rectal administration of donor stool and an initial high dose followed by maintenance doses. I know some people might be slightly uncomfortable with the idea of the rectal administration of medicines but there are some common-sense reasons behind this form of medicines delivery particularly where oral dosage forms (tablets, capsules) might not be well tolerated. As for the initial oral dosage form: "the participants began either oral administration of SHGM [Standardized Human Gut Microbiota] (2.5 × 1012 cells/day) mixed in a chocolate milk, milk substitute, or juice for 2 days (divided into three daily doses)." I have to say that whilst I initially envisaged Austin Powers and his 'tastes a bit nutty' scene, this was very much NOT how things actually were.

Alongside the donor stool formulation being trialled predominantly with regards to safety and initial efficacy, researchers also surveyed participants in relation to (i) effects on their gut microbiota (diversity and species present), (ii) the presentation of bowel symptoms/habits and (iii) behavioural outcomes covering autism-specific issues (via the CARS) and more general adaptive behaviours (via the Vineland scales for example). I was also happy to see a section included in their paper labelled 'virome bioinformatics' hat-tipping the idea that gut bacteria are not the only passengers we carry in our deepest, darkest recesses.

Results: well something certainly seemed to happen when looking at before, during and after results of this case series trial. First and foremost adverse effects were small and limited (hyperactivity, irritability) meaning that in the short term at least, the poo transplants and pre-poo transplant protocols were tolerated quite well. This is also evident in the 0% study attrition rate (i.e. everyone who started the study stayed in the study).

So: "Substantial changes in GI and ASD symptoms were observed. GI symptoms, as assessed by the GSRS [Gastrointestinal Symptom Rating Scale], significantly improved for abdominal pain, indigestion, diarrhea, and constipation." The authors report some significant differences in scores over the course of the intervention period such that: "The average GSRS score dropped 82% from the beginning to end of the treatment and remained improved (77% decrease from baseline) even 8 weeks after treatment stopped." That is a helluva placebo effect! Indeed, only 2 participants from the cohort were classified as 'non-responders' on the basis of their GSRS scores over the course of the study.

Also: "Beyond these GI improvements, ASD-related behavior also improved following MTT." The sorts of changes to CARS scores being reported were in the region of a 20% reduction in 'core ASD' symptoms at 8 weeks compared to baseline reports. Further, 8 weeks after the intervention had been completed the behavioural gains ("relative to baseline") were still evident based on CARS scoring. These ratings also did not depend on whether the poo transplant was administered orally or rectally.

The authors also discuss some not unexpected changes to gut bacterial profiles in their cohort over the intervention period. At baseline: "gut bacteria were significantly less diverse in children with ASD than neurotypical controls." This finding is in line with other study results from the authors (see here). Bacterial diversity did (slowly) change over the intervention period to a point where at 18 weeks after baseline median richness "was statistically indistinguishable between the ASD and control groups." This was noted in 16 of the 18 participants with ASD.

Finally: "Specific genera that significantly changed in their relative abundances with treatment included Bifidobacterium, Prevotella, and Desulfovibrio." The authors have chosen to zoom in on Prevotella as a consequence of their results - "the increase in the relative abundance of Prevotella after MTT is consistent with their potentially beneficial role in the gut of children with ASD" - but I'd like to see a little more work done on this before any grand claims are made. As to the virome/phage side of things: "phage richness and evenness did not significantly change following MTT given the timeframe of this study" so again, there is more science needed in this area too as to hows and why (nots).

OK, I think it is worth stressing again that this was an open-label study not a gold-standard, double-blind, randomised-controlled trial or anything like that. What this means is that these results are preliminary - very preliminary - and although quite promising, need scientific follow-up for a longer period. Whilst such results are seemingly pretty good evidence for the whole 'gut-brain axis' thing with regards to autism (see here) there are still questions that need answering, not least with regards to possible mechanisms linking gut bacteria changes to behaviour changes. Do these results, for example, point to some role for intestinal permeability changes given what is already being said about 'leaky gut' in the context of [some] autism (see here) and the growing interest in a relationship between gut bacteria and gut barrier integrity? How do gut bacteria 'communicate' with the grey-pink matter floating in the skull? Questions aplenty there be. There is also a certain degree of 'yuck factor; to contend with as a result of the use of a poo transplant in this context and what this might mean for future trials and possible 'rolling out' of such an intervention assuming effectiveness is confirmed. I can just see the headlines now...

But I don't want to take anything away from these novel findings and [with caveats] the significance of the results. When one considers how many people on the autism spectrum are suffering (yes, suffering) with bowel complaints, whether functional or something rather more pathological (see here), efforts to reduce pain and any additional burden they bring should be welcomed from wherever they emerge...

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[1] Kang D-W. et al. Microbiota Transfer Therapy alters gut ecosystem and improves gastrointestinal and autism symptoms: an open-label study. Microbiome. 2017; 5: 10.

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Kang, D., Adams, J., Gregory, A., Borody, T., Chittick, L., Fasano, A., Khoruts, A., Geis, E., Maldonado, J., McDonough-Means, S., Pollard, E., Roux, S., Sadowsky, M., Lipson, K., Sullivan, M., Caporaso, J., & Krajmalnik-Brown, R. (2017). Microbiota Transfer Therapy alters gut ecosystem and improves gastrointestinal and autism symptoms: an open-label study Microbiome, 5 (1) DOI: 10.1186/s40168-016-0225-7

Autism and visual impairment reviewed

Of the various autism science journals out there in peer-reviewed (La-La!) land, one journal in particular is really starting to grow on me: [The] Review Journal of Autism and Developmental Disorders.

I like this journal because it is basically systematic review and meta-analysis heaven when it comes to the quite voluminous autism research literature and seems to publish some real gems (see here for example).

Another paper from this journal caught my eye recently by Maggie Butchart and colleagues [1] (open-access) synthesising the collected research on "the prevalence of visual impairments in children and adults with Autism Spectrum Disorder (ASD), and the similar behavioural traits associated with both visual impairment and autism." Affiliated with the RNIB - Royal National Institute of Blind People - Scotland among other groups, the authors trawled the research literature looking at reported visual impairments in relation to the autism spectrum and provide quite a nice overview of 'where we're at' with regards to "papers published from 2000-2015."

The paper is open-access but a few comments are required bearing in mind my relative lack of knowledge on the complexities of visual impairments.

First: "Collating the evidence from six of the seven prevalence studies suggests a refractive error rate in the childhood ASD population studied at 22.9–32.7%, which is comparable with general childhood refractive error rates in 6–7 year olds at 29%, and 32.3% in 12–13 year olds." What this means is that a diagnosis of autism does not protect against the presence of refractive errors ('when the shape of the eye prevents light from focusing directly on the retina').

Second: "Estimates of childhood strabismus in the UK is 1.5 to 5.3%... but in the evidence collated in this review, the incidence of strabismus amongst autistic participants is higher at 8.3%." Strabismus, where the eyes don't align properly, seems to be a little bit more prevalent when it comes to autism compared with general population statistics. This is a topic that I've talked about before on this blog in relation to correcting such an issue with autism in mind (see here).

Finally: "There were no studies examining ophthalmic conditions and adult autistic populations who are more at risk of age-related visual impairments." Bearing in mind the search parameters included in the Butchart paper, I'm kinda dismayed that this is the current state of affairs. You'd have thought with all the money and resources being thrown into autism research that someone, somewhere might have thought more about eye health in adults with autism? Eye-tracking, reading the mind in the eyes test... the word 'eye' or 'eyes' is prominent in autism research but just not in relation to eye health it seems. And bear in mind that issues with eye health probably will affect the results of some of those autism 'eye' studies.

Eye or vision issues related to autism have often been a topic of discussion on this blog (see here and see here for examples) and so I'm glad that someone has finally brought a review of this area into the peer-reviewed arena. Screening is important; even if some of those on the autism spectrum may not always be by first sight (pardon the pun) particularly amenable to taking part in an eye exam - adjustments can and should be made.

And finally consider this: "Undiagnosed visual impairment is likely to severely impact quality of life. There is a need therefore for education and training that equip autism support practitioners with the awareness and skills to identify potential visual impairment, to refer individuals to optometry professionals if necessary, and to make necessary adjustments to service environments and support practices for individuals identified as having a visual impairment." Not much more to say really is there aside from 'make it so'.

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[1] Butchart M. et al. Autism and Visual Impairment: a Review of the Literature. Review Journal of Autism and Developmental Disorders. 2017. Jan 5.

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Butchart, M., Long, J., Brown, M., McMillan, A., Bain, J., & Karatzias, T. (2017). Autism and Visual Impairment: a Review of the Literature Review Journal of Autism and Developmental Disorders DOI: 10.1007/s40489-016-0101-1

Fatty acids 'for autism'? Meta-analysis says probably not but...

"Because of the limited number of included studies and small sample sizes, no firm conclusions can be drawn. However, the limited data currently available suggest that ω-3 FA [fatty acid] supplementation does not enhance the performance of children with ASD [autism spectrum disorder]."

Those were the conclusions reached in the systematic review and meta-analysis paper published by Andrea Horvath and colleagues [1] looking at the collected peer-reviewed literature on the topic up to August 2016. Specifically focused on randomised-controlled trials (RCTs), where participants are randomly allocated to receive a treatment - in this case ω-3 (omega-3) FA supplementation - or no treatment/placebo, researchers identified 5 studies where ω-3 supplements had been delivered to children diagnosed as being on the autism spectrum. The authors add: "With 4 exceptions, there were no statistically significant differences in ASD symptoms between groups measured by validated scales."

I'm not too surprised by these findings given some previous discussion on this topic (see here). I would however point out a few relevant issues that should be considered when it comes to fatty acids and autism: (i) Despite core symptoms not necessarily showing any general 'improvement' following fatty acid supplementation, this does not mean that other non-core features might not be affected by such supplements. Take for example, the collected data on what fatty acid supplementation might do for [some] attention-deficit hyperactivity disorder (ADHD) for example (see here), allied to the idea that ADHD might be 'over-represented' when it comes to autism (see here). Same goes for fatty acids and reading ability (see here) and indeed, into adulthood, the possibility of a connection between fatty acids and conditions such as bipolar disorder (see here) or psychosis (see here) (bearing in mind some recent discussions on the psychosis 'association'). Both bipolar disorder and psychosis have cropped up in relation to autism (see here and see here respectively). (ii) Horvath and colleagues report that: "Adverse effects were similar in both groups" meaning that fatty acid supplementation is probably not any more 'dangerous' than the placebos or 'no supplementation' used in the reviewed studies when it comes to autism. Given the growing literature suggesting that everyone should be eating a little more fish for heart health for example, supplementing those who don't like fish or who don't seem to eat enough fish is not ruled out. This is particularly relevant when one talks about autism and some peculiar eating habits (see here). (iii) There is a sizeable peer-reviewed literature talking about alterations in the levels of essential fatty acids in cases of autism (see here). Allied to the idea that there is no 'one-size-fits-all' intervention for 'the autisms', it is conceivable that selected supplementation on the basis of those presenting with deficiency could be considered advantageous. Much like when another nutrient of the hour - vitamin D - is shown to be deficient in relation to autism (see here), the onus should surely be to correct the deficiency when found, albeit under appropriate medical supervision (see here).

I don't disagree with the findings reported by Horvath and colleagues and, as I've said a few times before, vitamins and other supplements should be treated in the same way as other 'medicines' in terms of their use and safety (even if they don't typically come as a prescription). But I'd hate to think that the message 'fish oils generally don't benefit autism' gets translated into those on the autism spectrum potentially ignoring what are some potentially important nutrients for general health and wellbeing [2]...

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[1] Horvath A. et al. ω-3 Fatty Acid Supplementation Does Not Affect Autism Spectrum Disorder in Children: A Systematic Review and Meta-Analysis. J Nutr. 2017 Jan 11. pii: jn242354.

[2] Alexander DD. et al. A Meta-Analysis of Randomized Controlled Trials and Prospective Cohort Studies of Eicosapentaenoic and Docosahexaenoic Long-Chain Omega-3 Fatty Acids and Coronary Heart Disease Risk. Mayo Clinic Proceedings. 2017; 92: 15-29.

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Horvath A, Łukasik J, & Szajewska H (2017). ω-3 Fatty Acid Supplementation Does Not Affect Autism Spectrum Disorder in Children: A Systematic Review and Meta-Analysis. The Journal of nutrition PMID: 28077731

Autism diagnoses (and diagnostic stability) in Germany

"From 2006 to 2012, the prevalence of autism spectrum disorder diagnoses in 0- to 24-year-olds increased from 0.22% to 0.38%."

That was one of the details included in the rather interesting paper by Christian Bachmann and colleagues [1] who provided some introductory information on the the trends in autism diagnoses in Germany. I say 'introductory information' because it appears that autism or autism spectrum disorder (ASD) has not exactly received the research attention in Germany that it perhaps has in other similarly developed nations such as the United States or here in Blighty. Indeed, as Bachmann et al note: "Due to the only available study to date, the prevalence of ASD in Germany is estimated to be about 0.25% in 0- to 24-year-olds in 2009" and even that was taken from another study by the author [2].

This time around, the authors listed two primary aims for their research: (a) "to establish the time trends in the administrative prevalence of autism spectrum disorder diagnoses" and (b) "to assess the stability of autism spectrum disorder diagnoses over time." I'm interested in both these areas on this blog (see here for example). Data for the time trends part of this research came from "the German statutory health insurance company Allgemeine Ortskrankenkassen (AOK) from the years 2006 to 2012" where a diagnosis of ASD was registered by ICD-10 definition. Data for the stability side of their research was via a "cohort with a first-time diagnosis of autism spectrum disorder in 2007 through 2012, investigating the percentage of retained autism spectrum disorder diagnoses."

Results: well as per the opening sentence to this post, the only way is up when it comes to the estimated prevalence of autism or ASD despite the figures being a tad lower than those for other countries. Those percentages were based on nearly 15,000 ASD diagnoses being recorded in 2006 out of 6.9 million insurees, and nearly 22,000 ASD diagnoses in 2012 out of 6.4 million insurees. Males were quite a bit more likely to be diagnosed with autism/ASD and prevalence peaked for the age group 6-11 year olds.

Then to that stability part of the study and from "3927 patients (mean age: 8.7 years, 68.9% males)" with a specific ASD diagnosis in 2007 only a third 'carried on' with a specific diagnosis by 2012. The authors note: "This figure is lower than the usual persistence for ASD diagnoses, which is about 73%–100%." Lower? Yes, I'd say. The reasons for this quite notable lack of diagnostic stability? Well, the authors note that there is probably going to be more than one (before anyone makes any sweeping generalisations). They talk about the lack of "specialised mental health services that are competent to diagnose ASD according to international standards and guidelines" as one factor. They talk about diagnoses "often made by paediatricians or occupational therapists, without employing diagnostic gold standards like Autism Diagnostic Observation Schedule (ADOS)." They even talk about diagnostic switching between ASD subgroups as potentially also being a factor to consider. And then another possibility: "Other reasons include improvement of symptoms because of successful therapeutic interventions" without any specific mention of what types of therapeutic intervention might be involved. Sounds very 'optimal outcome' to me (see here). In short, it's probably going to be complicated.

Bearing in mind those diagnostic stability figures and the authors reliance on a database that relied on those unstable figures for prevalence estimates, this is interesting research. It shows that even a social and economic powerhouse like Germany still has some way to go in many areas not least with that related to autism. Where next? Well, as per the authors suggestion: "one possible option could be to establish standardised diagnostic algorithms and certify ASD diagnostic centres who employ these standards." Sounds good but in amongst the chatter about autism 'misdiagnosis' and seemingly 'ill-trained' professionals diagnosing, I do wonder whether further, more detailed, investigations are needed on the autism diagnostic stability figures of Germany and whether it's all just due to administrative errors...

Music to close, and this guy was/is apparently quite big in Germany...  Permit denied!

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[1] Bachmann CJ. et al. Diagnoses of autism spectrum disorders in Germany: Time trends in administrative prevalence and diagnostic stability. Autism. 2016. Dec 20.

[2] Bachmann CJ. et al. Psychopharmacological treatment in children and adolescents with autism spectrum disorders in Germany. Res Dev Disabil. 2013 Sep;34(9):2551-63.

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Christian J Bachmann, Bettina Gerste, & Falk Hoffmann (2016). Diagnoses of autism spectrum disorders in Germany: Time trends in administrative prevalence and diagnostic stability Autism: International Journal of Research & Practice : 10.1177/1362361316673977

"no evidence that the probiotic formulation is effective in treating low mood"

I'm a great believer in balance when it comes to this blog and its content. As enthusiastic as I might be about a particular topic or topics, I don't want to lose sight of the fact that peer-reviewed science is a messy business and often filled with contrary findings.

With 'contrary' in mind, I want to talk today about a paper by Amy Romijn and colleagues [1] detailing the results of a double-blind, randomised, placebo-controlled trial of a probiotic mix which contained "freeze-dried L. helveticus R0052 (strain I-1722 in the French National Collection of Cultures of Microorganisms [CNCM], Institut Pasteur, Paris, France) and B. longum R0175 (CNCM strain I-3470) bacteria at a dosage of three billion colony-forming units (⩾3 × 109 CFU) per 1.5 g sachet" with a sample of participants selected for 'low mood'. Probiotics, just in case you don't know, are those various live bacteria and yeasts that are supposed to confer some health benefit.

The reason for this study? Well, as the authors note, the specific probiotics under study were "previously found to improve emotional behaviour in animals and psychological outcomes and humans" as per other findings [2]. So with [prospective] trial registration (see here) in hand, researchers set out to look at what 8 weeks worth of probiotics might do for 'low mood' and other psychological parameters when pitted against a placebo formulation (that contained only the excipients included in the probiotic formulation). Blood samples were also provided by participants at baseline (before intervention) and at 8 weeks post-intervention "to measure levels of high-sensitivity C-reactive protein (hsCRP), IL-1β, IL-6, TNF-α, vitamin D and BDNF."

Results: "Intent-to-treat analysis (n = 79) showed no significant group differences on any outcome measure." The scores for the groups - probiotic (n=40) & placebo (n=39) - did not seem to differ significantly on any of the measures used during the trial. Indeed, when taking into account individual scores on the primary outcome measures called the Montgomery–Åsberg Depression Rating Scale (MADRS) - something used to measure "the severity of depressive episodes" - the results actually (non-significantly) seemed to favour the placebo in terms of those who "showed a ⩾60% change on the MADRS (responders)."

Insofar as adverse effects, well taking this probiotic probably won't do any harm if we rely on the Romijn findings, as authors describe "three serious adverse events over the course of the trial, all of which were suicide attempts by one participant from the placebo group. There were no serious adverse events in the probiotic group."

But all was not completely negative when it came to the trial as a little gem was potentially uncovered: "Among those randomized to the probiotic group, those who had high vitamin D at baseline showed greater improvement in mood and functioning than those who had low vitamin D at baseline." Without trying to make mountains out of molehills, the authors speculate that: "the vitamin D status of the host could have an effect on the relationship between the gut microbiota and the immune system: low vitamin D could limit response to probiotic treatment as any changes to the microbiome composition would not necessarily be translated to the immune system." A rather interesting sentiment given the increasingly vocal link between vitamin D and depression for example in the research literature (see here).

These results do represent a bit of a set-back for the idea of psychobiotics [3] but I'm not ready to poo-poo the whole area just yet. Among the various caveats raised by the study authors (samples size, length of intervention, etc) it is possible that 'low mood' over and above something a little more clinically 'transforming', might not be a suitable target for such intervention (indeed, other research might also be relevant [4]) despite the fact that other research on subclinical psychological symptoms have been seemingly affected by probiotic administration (see here). The specific formulation used might also be a factor as the authors quite correctly suggest that: "It is important that the results of the current study are not generalized to all potential probiotic strains." Baby and bathwater eh?

But these results stand, and given some important names on the authorship list (see here), this is one study that cannot and should not be just swept under the scientific carpet...

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[1] Romijn AR. et al. A double-blind, randomized, placebo-controlled trial of Lactobacillus helveticus and Bifidobacterium longum for the symptoms of depression. Aust N Z J Psychiatry. 2017 Jan 1:4867416686694.

[2] Messaoudi M. et al. Assessment of psychotropic-like properties of a probiotic formulation (Lactobacillus helveticus R0052 and Bifidobacterium longum R0175) in rats and human subjects. Br J Nutr. 2011 Mar;105(5):755-64.

[3] Dinan TG. et al. Psychobiotics: a novel class of psychotropic. Biol Psychiatry. 2013 Nov 15;74(10):720-6.

[4] Kleiman SC. et al. The Gut-Brain Axis in Healthy Females: Lack of Significant Association between Microbial Composition and Diversity with Psychiatric Measures. PLoS One. 2017 Jan 19;12(1):e0170208.

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Romijn AR, Rucklidge JJ, Kuijer RG, & Frampton C (2017). A double-blind, randomized, placebo-controlled trial of Lactobacillus helveticus and Bifidobacterium longum for the symptoms of depression. The Australian and New Zealand journal of psychiatry PMID: 28068788

Diagnosing ME/CFS the machine learning way?

In today's post I want to draw your attention to the findings reported by Diana Ohanian and colleagues [1] (open-access available here) talking about "the use of machine learning to further explore the unique nature"of various conditions/labels including those typically headed under the label of chronic fatigue syndrome / myalgic encephalomyelitis (CFS/ME).

Including one 'Jason LA' on the authorship list, researchers set about looking at "what key symptoms differentiate Myalgic Encephalomyelitis (ME) and Chronic Fatigue syndrome (CFS) from Multiple Sclerosis (MS)."You may be wondering why such a comparative study was undertaken but a quick trawl of the research literature reveals that these different clinical labels may well have some important commonalities [2].

This was an internet-based research project whereby "106 people with MS and 354 people with ME or CFS fully completed the [DePaul Symptom Questionnaire] questionnaire" and based on the responses received "decision trees were used to determine what symptoms differentiated those with MS from those with ME or CFS." Decision trees, as the name suggests, is a statistical technique where binary (0 or 1, no or yes) choices make branches and: "At each branch the computer decides what symptom would best predict classifications, in this case whether someone has MS or ME or CFS." This process continues and continues through the different levels of branches "until the tree reaches a balance between classification accuracy and generalizing to new data." Such a machine learning tool has been previously discussed quite recently on this blog (see here).

Results: "Five symptoms best differentiated the groups." These were: flu-like symptoms, tender lymph nodes, alcohol intolerance, inability to tolerate upright position and next day soreness after strenuous activity. The first two symptoms - flu-like symptoms and tender lymph nodes - were pretty good by themselves at correctly categorising MS or CFS/ME (~80% correct). Indeed, these seemed to be the core differentiators that were examined and as the authors note: "The most important two symptoms that differentiated MS versus ME or CFS existed within the immune domain."

Of course further investigations are warranted to potentially build on these findings. One has however to be slightly cautious about the use of the internet and social media when undertaking such research, especially when very little information about the formal diagnoses of participants is included in the current paper. This is a particular issue when it comes to CFS/ME and the various ways that it can be defined and diagnosed [3].

Still, I can't quibble with the continued rise and rise of machine learning being applied to many areas of medicine, and not before time that it starts to reach ME/CFS. And just before I go, it appears that the research team at DePaul University have been quite busy...

To close, on what retiring Presidents of the USA should do next. I think I would go with George Washington and his whisky business... 🍻

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[1] Ohanian D. et al. Identifying Key Symptoms Differentiating Myalgic Encephalomyelitis and Chronic Fatigue Syndrome from Multiple Sclerosis. Neurology (ECronicon). 2016;4(2):41-45.

[2] Morris G. & Maes M. Myalgic encephalomyelitis/chronic fatigue syndrome and encephalomyelitis disseminata/multiple sclerosis show remarkable levels of similarity in phenomenology and neuroimmune characteristics. BMC Medicine. 2013; 11: 205.

[3] Jason LA. et al. Case definitions integrating empiric and consensus perspectives. Fatigue. 2016;4(1):1-23.

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Ohanian D, Brown A, Sunnquist M, Furst J, Nicholson L, Klebek L, & Jason LA (2016). Identifying Key Symptoms Differentiating Myalgic Encephalomyelitis and Chronic Fatigue Syndrome from Multiple Sclerosis. Neurology (E-Cronicon), 4 (2), 41-45 PMID: 28066845

The correlates of regressive autism

"A more homogeneous subgroup with regression between 18 and 36 months (n = 48) had higher rates of intellectual disability, epilepsy, and special education, more socially restrictive educational settings, and more severe ASD [autism spectrum disorder] communication deficits and schizophrenia spectrum symptoms than non-regressed youth (n = 136)."

So said the findings reported by Kenneth Gadow and colleagues [1] taking on one of the more important issues in relation to autism: developmental regression (see here). I say 'more important' in that last sentence because whilst it has taken autism research and science quite a while to accept that regression in skills/behaviour can occur in cases of autism, there is now a realisation that such regression can impact on various other areas of investigation, not least the discussions on the potential [very] early detection of autism (see here). And still researchers continue to talk about very early autism detection...

Gadow (a name not unfamiliar to this blog in terms of autism and schizophrenia spectrums potentially colliding) et al set out to examine "the psychiatric and clinical correlates of loss of previously acquired skills (regression) as reported by parents of youth with autism spectrum disorder (ASD)." They relied to quite a large extent on data derived from the Child and Adolescent Symptom Inventory partly created by Dr Gadow, that assesses for the presence of various behaviours linked to various developmental and psychiatric labels. Some 213 6- to 18-year old children and adolescents with ASD were included for study; 77 (36%) of them defined as showing some parent-reported regression in skills coincidental to the presentation of their autism.

As per that opening sentence, there did appear to be some differences in clinical presentation when using regression as a characterising feature. A few additional details: 37% of those "whom parents indicated had regressed (whether or not they indicated age of regression and type of skill)" fell into the intellectual/learning disability category vs. 18-19% of non-regressed participants. Significantly more participants who regressed were 'ever hospitalised' (48% vs 29%); a statistic that probably ties into the rates of epilepsy/seizure disorder also described in this cohort (18% vs 5-6%). Although the authors talk about 'a more severe ASD communication deficit' being linked to reports of regression, the data obtained from both parent and teacher ratings in relation to the presentation of autistic traits were mainly 'more severe' in the regression group when examined as a whole: social deficits, communication deficits and perseverative behaviours; albeit not significantly so.

Then to the suggestion that schizophrenia spectrum symptoms were more pronounced in the regression group. Appreciating that there is some history when it comes to autism and schizophrenia (think Mildred Creak for example) but also some controversy, this is something potentially quite important, not least when one considers the rise and rise of research interest into something like psychosis and [some] autism (see here and see here) and also how [some] regressive autism might not be a million miles away from a condition like anti-NMDA-receptor encephalitis (see here) typically encompassing a psychotic element to it. I also wonder whether the talk about regression accompanying autism might set the tone for further regression potentially accompanying the onset of something like schizophrenia for example. Could a life of 'regression in skills' be a feature of this group?

Of course further investigations are required to independently verify the findings reported by Gadow and colleagues; such work should really also include more professionally-derived ratings (bearing in mind parents are generally the experts on their own children). I wonder too if it's time to start including a few more 'biological' measures when it comes to looking at regression vs. no regression in the context of autism to see if genetics/epigenetics/biochemistry variables might also tie up with some of the behavioural findings. Indeed, this should really be a must.

Finally: "A brief parent report of developmental regression may be a useful clinical indicator of later general functioning." I agree that this might be a rather good idea based on the current data; perhaps allied to some further chatter about ESSENCE and autism also (see here).

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[1] Gadow KD. et al. Parent-Reported Developmental Regression in Autism: Epilepsy, IQ, Schizophrenia Spectrum Symptoms, and Special Education. J Autism Dev Disord. 2017 Jan 10.

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Gadow KD, Perlman G, & Weber RJ (2017). Parent-Reported Developmental Regression in Autism: Epilepsy, IQ, Schizophrenia Spectrum Symptoms, and Special Education. Journal of autism and developmental disorders PMID: 28074354

Physical activity levels and autism (again)

"Adolescents with ASD [autism spectrum disorder] spent less time in MVPA [moderate and vigorous physical activity] compared to TD [typically developing] adolescents (29 min/day vs. 50 min/day, p < 0.001) and fewer met the Physical Activity Guidelines for Americans (14 vs. 29%, p > 0.05)."

So said the study results published by Heidi Stanish and colleagues [1] adding yet more to another growth autism research area - physical activity and exercise - a topic also fast becoming a repetitive blogging issue for me.

It's not necessarily new news that physical activity and exercise levels are not what they could or should be for many people on the autism spectrum (see here) but rather that the use of objective measures such as accelerometers for data collection are starting to put some scientific flesh on previous 'what exercise did you do' type questionnaire studies. And the trend that is being revealed really is quite a disturbing one if one assumes that physical activity is a significant gateway to rude health and well-being, particularly in the context of ever-increasing waistlines and onward longitudinal effects. I might even point you in the direction of some new research hinting that MVPA in childhood might predict "fewer symptoms of major depressive disorders" later on; something that could be particularly relevant to autism in light of those over-represented comorbidities that I keep going on about (see here).

Stanish et al have been mentioned before on this blog in the context of physical activity / exercise and autism and particularly the ways that said activity could be made more attractive to teens diagnosed on the autism spectrum (see here). Small steps and finding the right activity were some of the routes offered in that previous paper [2].

Before I go I do want to briefly mention one point raised in the latest Stanish paper: "Walking/hiking and active video gaming were among the top activities for both groups." Both groups refers to adolescents with autism (n=35) and those described as typically developing (n=60) who were included for study (although much like the term 'neurotypical' I'm still at a loss as to the precise meaning of 'typically developing'). Walking/hiking... great, really worthwhile encouraging (see here) including exposing people to the great outdoors and that yellow thing usually high in the sky. 'Active videogaming' is something I'm a little less sure of at the moment and indeed, some people have talked about such 'exergaming' as being a poor substitute for the real thing [3]. I don't doubt that one can build up a sweat on something like those new-fangled 'watch my movement' games consoles that abound these days, but might such exergaming just further feed into the 'screen time' narrative that typically accompanies sedentary behaviours?

And of the multiple correlates potentially attached to low levels of physical activity, one might also count bone health [4] among them as being relevant to at least some autism...

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[1] Stanish HI. et al. Physical Activity Levels, Frequency, and Type Among Adolescents with and Without Autism Spectrum Disorder. J Autism Dev Disorders. 2017. Jan 9.

[2] Stanish H. et al. Enjoyment, Barriers, and Beliefs About Physical Activity in Adolescents With and Without Autism Spectrum Disorder. Adapt Phys Activ Q. 2015 Oct;32(4):302-17.

[3] Daley AJ. Can Exergaming Contribute to Improving Physical Activity Levels and Health Outcomes in Children? Pediatrics. 2009; 124: 2.

[4] Neumeyer AM. et al. Bone microarchitecture in adolescent boys with autism spectrum disorder. Bone. 2017 Jan 11. pii: S8756-3282(17)30009-1.

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Stanish, H., Curtin, C., Must, A., Phillips, S., Maslin, M., & Bandini, L. (2017). Physical Activity Levels, Frequency, and Type Among Adolescents with and Without Autism Spectrum Disorder Journal of Autism and Developmental Disorders DOI: 10.1007/s10803-016-3001-4