Thursday, 18 January 2018

On coeliac disease and schizophrenia

"This systematic review and meta-analysis found a significantly higher risk of schizophrenia among patients with celiac disease."

So said the findings reported by Karn Wijarnpreecha and colleagues [1] examining whether "patients with celiac disease might be at an increased risk of schizophrenia" using everyone's favourite 'top of the methodological tree' analyses: the systematic review and meta-analysis.

Celiac (coeliac) disease (CD) represents the archetypal 'dietary gluten is baddie' autoimmune condition, where a certain type of immune system meets with everyone's 'love to hate' food group and biological and histological sparks begin to fly.

Authors identified a few studies (four studies that "compared the risk of schizophrenia among patients with celiac disease versus individuals without celiac disease") and came down on the side suggesting that yes, there is a higher risk of schizophrenia among those diagnosed with CD based on the currently available data. That all being said, there is quite a bit more to do in this research area.

Personally, I'm not too surprised by the Wijarnpreecha results. Enough times on this blog I've talked about the possibility of a *connection* between dietary gluten and various behavioural / psychiatric disorders including the possibility of a 'gluten-related subgroup of schizophrenia' (see here). I know not everyone is completely persuaded by the ideas espoused about by people such as the late Curt Dohan (see here) and the late Karl 'Tiny' Reichelt (see here) implicating gluten in the rise of [some] schizophrenia for example, but I've read enough on this topic to appreciate that an association is more than likely for some at least (see here).

With diagnosed CD in mind and not just the often nebulous term 'non-coeliac gluten sensitivity', the data is not however universally clear in relation to risk of schizophrenia. I say that on the basis that risk of various autoimmune conditions seemed to be elevated in relation to schizophrenia [2] of which CD is just one (see here). I could be really speculative and suggest that there may be some common mechanisms implicated in autoimmune conditions (gut barrier function, gut microbiota, HERVs, etc.) that could also be relevant to some schizophrenia too (see here for example). But at the moment, we just don't know enough, hence the need to screen and investigate further...


[1] Wijarnpreecha K. et al. Association between celiac disease and schizophrenia: a meta-analysis. Eur J Gastroenterol Hepatol. 2017 Dec 26.

[2] Chen SJ. et al. Prevalence of autoimmune diseases in in-patients with schizophrenia: nationwide population-based study. Br J Psychiatry. 2012 May;200(5):374-80.


Wednesday, 17 January 2018

Sleep duration and ADHD: a correlation across the years?

"Longer sleep duration (>10 hours per day) was associated with a lower ADHD [attention-deficit hyperactivity disorder] symptom score" was one of the findings reported by Gabriela Peralta and colleagues [1].

They sought to examine whether a particular set of activities (sleeping, physical activity, television watching, etc) might show some *correlation* to "(1) attention-deficit/hyperactivity disorder (ADHD) symptoms and (2) behavior problems, both assessed at 7 years, in ADHD-free children at baseline."

Drawing on a not-insignificant number of children participants (N=817) who were part of a research birth cohort previously discussed on this blog (see here and see here), authors relied on parental report via the Conners' Parent Rating Scales and the Strengths and Difficulties Questionnaire to ascertain ADHD and 'behaviour problem' scores respectively. This was carried out when the child was aged around 7 years old. A few years earlier - when the child was around 4 years old - parents had previously reported on a few other variables: "the time that their children spent sleeping, watching TV, engaging in cognitively stimulating activities, and engaging in physical activity." The two sets of data were married together for analysis.

Results: it's probably not escaped your notice that (a) parental report is a mainstay of the Peralta data and (b) data for a child at 4 years old and then again at 7 years old represents quite a large time frame during which lots can (and does) happen. With those factors firmly in mind, researchers provided some frequency data on activities at 4 years old. They then added in the data taken at 7 years old where that finding on longer sleep duration (at 4 years) seemed to be linked to lower ADHD scores (at 7 years) came from. Further: "Longer time spent in cognitively stimulating activities (>1 hours per day) was associated with lower scores of both ADHD symptoms... and behavior problems" and also rather interestingly: "Time spent watching TV and engaging in physical activity were not associated with either outcomes."

The quite fuzzy picture emerging from this data - with appropriate caveats - is that sleep and 'keeping the mind active' might be important factors when it comes to the presentation of something like ADHD (symptoms) and other 'behaviour problems' in childhood. The sleep side of things is particularly topical at the moment, given some research chatter about how a sleep intervention might be something to consider for at least some (diagnosed) cases of ADHD (see here). There are also seemingly lots of benefits from ensuring a regular bedtime routine for young children; assuming that is, that poor sleeping patterns are not an early marker for possible ADHD?

The whole 'cognitively stimulating activities' bit is slightly more fluffy in terms of what constitutes such activities and any relationship with ADHD or behavioural issues. I say this on the basis that whilst reading and writing for a 4-year old is likely to be cognitively stimulating, so are lots of other activities such as exploring nature for example or even spending time on the dreaded computer/tablet devices (depending on what activities are being done). Even time spent in front of the gogglebox could be considered cognitively stimulating if they're watching Blue Planet for example, and not just a re-run of Peppa Pig (sorry Peppa). And on the topic of television viewing or at least screen time in the context of ADHD risk, other data have suggested something *correlatively* different from the Peralta findings (see here) just to complicate matters further.

To close, it's been a while but here is some music... Elvin Bishop and a track brought back to life by the Guardians...


[1] Peralta GP. et al. Sleeping, TV, Cognitively Stimulating Activities, Physical Activity, and ADHD Symptom Incidence in Children: A Prospective Study. J Dev Behav Pediatr. 2017 Dec 18.


Tuesday, 16 January 2018

Vitamin D and autism... another double-take?

A quick-ish post today as I bring the results published by Dong and colleagues [1] to your attention and the [translated] observation that: "Serum 25-hydroxyvitamin D level in children with ASD [autism spectrum disorder] is obviously lower than that in the healthy control group, and there are negative correlations between vitamin D levels and core symptoms of ASD." 'Obviously' eh?

It's another study from China (see here) and yet again I find myself correcting language as per the authors' use of the term 'healthy control group' when describing not-autism. In much the same way that the word 'neurotypical' is a bit of a nonsense, so the insinuation that a diagnosis of of autism automatically means 'not healthy' is far too broad a sweeping generalisation.

Anyhow, vitamin D and autism was the name of the research game for these authors; something not altogether new and novel for at least some of the authorship group (see here and see here for examples). Indeed, my use of the term 'another double-take' in the title of this post refers to the observation that this group have really gone to town with their clinical trial registered research project in this area (see here for example).

"Serum vitamin D level in ASD children was significantly lower than that of the control group... and the between-group percentage difference of normal, insufficient and deficient levels of vitamin D was statistically significant." Bearing in mind that vitamin D levels were checked using a gold-standard technique (liquid chromatography-mass spectrometry, LC-MS), I'm inclined to accept these results as they stand. I'm not saying that other methods of vitamin D analysis are all bunk, but rather that LC-MS is a mighty powerful method for sample analysis with vitamin D in mind.

Further: "There were negative correlations between serum vitamin D level in ASD children and total ABC [Autism Behavior Checklistscore or ABC subscale scores (body behavior, self-care, language and social interaction). There were negative correlations between serum vitamin D level in ASD children and total CARS [Childhood Autism Rating Scalescore and CARS subscale scores (imitation, nonverbal communication and general impression). There were negative correlations between serum vitamin D level in ASD children and SRS [Social Responsiveness Scale] behavior subscale or ATEC [Autism Treatment Evaluation Checklistsocial interaction subscale." In short, vitamin D  levels seemed to *correlate* with quite a few behavioural results, although I'm slightly less inclined to read too much into such findings given the relatively small participant group included for study and the 'snaphot' study methodology.

But yet again, this is another example illustrating that vitamin D metabolism should very much be a part of any assessment when it comes to autism (see here and see here)...


[1] Dong HY. et al. Correlation between serum 25-hydroxyvitamin D level and core symptoms of autism spectrum disorder in children. Zhonghua Er Ke Za Zhi. 2017 Dec 2;55(12):916-919.


Monday, 15 January 2018

"Meningitis is a significant risk factor for developing ADHD later in childhood"

The quote heading this post comes from the results published by Hadžić and colleagues [1] who sought to "examine the frequency of ADHD [attention-deficit hyperactivity disorderin children who had had bacterial meningitis."

Bacterial meningitis by the way, reflects meningitis brought about by one of a number of bacteria (e.g. meningococcal, pneumococcal, TB, Group B Streptococcal, Hib) with treatment via timely use of antibiotics.

Comparing 60 children who "had had meningitis in the first year of their lives" with 60 control children who did not have meningitis, researchers looked at the frequency of ADHD - "assessed through the structural clinical interviews with parents according to the criteria set in DSM-IV." They observed that over 60% (37/60) of those with a history of meningitis had reported behaviours consistent with a diagnosis of ADHD compared with only 5% (3/60) of controls.

I might question the use of parental interviews outside that of the actual assessment of children as being one variable that puts the Hadžić results at something of a disadvantage. But, and it is an important 'but', this is not the first time that ADHD or behaviours that characterise ADHD have been talked about in the context of meningitis. Indeed, tuberculous meningitis (TBM) has been mentioned in the context of ADHD before [2] and on more than one research occasion [3] (albeit by the same research group).

The mechanisms / modes of action? Well, we're still left to speculate. Meningitis involves inflammation of the membranes (meninges) that protect the brain and spinal cord. The after-effects for some can involve brain damage but also a variety of other adverse outcomes have also been noted including issues such as epilepsy and/or seizure disorder. It's not inconceivable that one or more of these adverse effects *could* impact on the presentation of something like ADHD or at least, ADHD-related behaviours. Further research needs to be conducted on what follows from something like bacterial (and viral) meningitis in terms of 'brain symptoms' and onward what this might mean for risk of ADHD.

What this latest research does illustrate quite well is that, much like the debates in autism circles, not every single person diagnosed with ADHD or those presenting with clinically-relevant ADHD symptoms does so through some inborn process. Infection - or response/after-effects of infection - can seemingly play quite a big role for some; bearing in mind also that other, various types of infection, have been previously implicated in relation to ADHD (see here and see here) outside of just meningitis.

And whilst on the topic of infection potentially being related to *some* neurodevelopmental diagnoses, I note some conversations on social media have tried to (once again) poo-poo the idea that autism, or a diagnosis of autism, might not be a lifelong issue for some people. 'Masking' of autism is the new, universal idea emerging, which whilst important, probably doesn't cover every case of autism symptoms dissipating [4] (see here for my take)...


[1] Hadzic E. et al. Is Bacterial Meningitis a Risk Factor for Developing Attention Deficit Hyperactivity Disorder. Isr J Psychiatry Relat Sci. 2017;54(2):54-57.

[2] Wait JW. & Schoeman JF. Behaviour profiles after tuberculous meningitis. J Trop Pediatr. 2010 Jun;56(3):166-71.

[3] Wait JW. et al. Tuberculosis meningitis and attention deficit hyperactivity disorder in children. J Trop Pediatr. 2002 Oct;48(5):294-9.

[4] Hacohen Y. et al. N-methyl-d-aspartate (NMDA) receptor antibodies encephalitis mimicking an autistic regression. Developmental Medicine & Child Neurology. 2016; 58: 1092-1094.


Saturday, 13 January 2018

Bowel issues over-represented in autism (and perhaps linked to some behaviours)

"Make it so Mr WORF"
Once again(!) more evidence emerges from the peer-reviewed science domain highlighting how functional gastrointestinal (GI) issues such as constipation and diarrhoea are very much over-represented when it comes to a diagnosis of autism (see here). The study providing the data this time was by Zhu and colleagues [1] and was carried out in China; thus illustrating how such bowel issues cross countries and ethnicity when it comes to autism.

There's little novelty in their findings that all-manner of functional bowel condition were more frequently present in their cohort of over 320 children diagnosed with an autism spectrum disorder (ASD) compared with some 200 not-autism controls. The authors' observation that almost 50% of their sample of children diagnosed with autism presented with at least one bowel issue is not as surprising in research-terms as it perhaps once might have been.

What is perhaps interesting is the growing focus on how such bowel issues may *correlate* with behaviour noted in children with autism, as per the results of other independent findings (see here). To quote from Zhu et al: "Compared with ASD children without GID [gastrointestinal disorders] (n=166), the ASD children with GID (n=162) got higher scores in the "Body and Object Use" of ABC [Autism Behavior Checklistscale... and had more emotional problems. Moreover, the score of behavior problems questionnaire was higher in the ASD children with GID." This is not necessarily new news to many people (particularly to parents and caregivers) but should be a topic that is given more research and clinical consideration among professionals.

More needs to be done in this area, not least on:

  • improving the ways of detecting and reporting on functional bowel issues in the context of autism (see here),
  • ensuring that questions about bowel function are asked during autism assessments and exams,
  • moving away from over-simple 'psychological' assumptions/explanations to potentially account for bowel issues in relation to autism (see here) without appropriate gastroenterological referral (also including ridding ourselves of the old-saying 'it's part of their autism'),
  • ensuring that appropriate gastroenterological resources are available and timely referral is present (particularly for paediatric resources),
  • following guidance that is out there in the peer-reviewed domain on screening and treating bowel issues in the context of autism (see here),
  • not being afraid to look for signs of more serious bowel pathology as and when functional bowel symptoms are present (see here) and,
  • embracing the idea that gut and brain might not be completely separate and independent in the context of autism and beyond (see here). 

'Nuff said I think.

But just before you go, some other study results [2] for you to mull over with regards to the question: what is the 'normal range' of bowel movements? Answer: anything from 3 a day to 3 a week apparently.


[1] Zhu J. et al. Association between behavioral problems and gastrointestinal disorders among children with autism spectrum disorder. Zhonghua Er Ke Za Zhi. 2017 Dec 2;55(12):905-910.

[2] Mitsuhashi S. et al. Characterizing Normal Bowel Frequency and Consistency in a Representative Sample of Adults in the United States (NHANES). Am J Gastroenterol. 2018 Jan;113(1):115-123.


Friday, 12 January 2018

Allergic disease and ADHD yet again...

Although words like 'first' and 'largest' were used in the paper by Chia-Feng Yang and colleagues [1] (open-access available here) observing that "AD [atopic dermatitis] and asthma with allergic sensitization are associated with ADHD [attention-deficit hyperactivity disorder] in children", I'm minded to be a little cautious with such 'we're the first/best' assertions.

Cautious because, on quite a few peer-reviewed research occasions (see here for example), a possible *link* between various allergic disease and ADHD has already been noted; even potentially extending to studies talking about how treatment for allergic disease might on some occasions also impact on presented ADHD symptoms (see here) (with no medical advice given or intended).

Yang et al relied on data from a research favourite country, Taiwan, derived from an initiative called the Childhood Environment and Allergic diseases Study (CEAS). The clue is in the name of the initiative in terms of what they were looking for/at, as per other publications derived from the initiative [2]. From the 3200-odd participants eligible for participation, researchers relied on data from over 2700 children. Questions about allergic disease history were asked to parents of said participants, alongside other 'environmental' factors such as family income, tobacco exposure and breastfeeding history. I note also a question about 'incensing at home' is also included relating to the use of burning incense typically linked to religious practices in certain cultures.

When it came to a diagnosis of ADHD, it's not entirely clear about how this was ascertained but it looks like diagnosis was given by a clinician: "The conditions of disease in children were confirmed by board-certified child psychiatrists or pediatric neurologists, according to the clinical evaluation." I should also mention that participants also received skin prick tests (SPTs) covering a range of potential allergens: "house dust mites (HDMs mix, including Der p, Der f, Der m, and Blot allergens), cockroaches, dog dander, milk, egg, and crab allergens" as way of defining allergic sensitisation.

Results: there was a "strong positive association between ADHD and allergic sensitization as diagnosed by positive SPTs." In other words, despite finding a fairly low level of ADHD in their sample (1%), those who 'reacted' to one or more of the allergens tested for via the skin prick test seemed to be at some increased risk of ADHD. Such an enhanced risk spanned both those presenting with "AD with allergic sensitization and asthma with allergic sensitization."

The authors provide some further results and details on the possible hows-and-whys of their results. Obviously the immune system figures quite strongly given what for example, they were testing for with the SPT and their focus on AD and asthma. The word 'inflammation' also figures quite heavily. I note too that the authors reiterate previous suggestions that: "Control of allergens exposure might be a critical factor influencing the development of ADHD."

There is a further scheme of work to follow in this area, not just dealing with mechanisms but also in relation to 'treating' allergies also potentially 'treating' [some] ADHD. I say this on the basis that other independent research has observed that before reaching for the antihistamine as a potential ADHD-modifier, there may actually be a connection between early antihistamine exposure and the development of ADHD [3] (albeit with potential confounders) to keep in mind. Other work also supporting a link between ADHD and atopic disease [4] provides some other 'clues' that may require further investigation; not least "cow's milk intolerance", which ties into similar findings (see here) and could also be one route from which ADHD heightens the risk of subsequent future psychiatric disorder (see here) in light of other 'milk' associations (see here).


[1] Yang CF. et al. Association between allergic diseases, allergic sensitization and attention-deficit/hyperactivity disorder in children: A large-scale, population-based study. J Chin Med Assoc. 2017 Nov 24. pii: S1726-4901(17)30304-0.

[2] Wang IJ. et al. Allergens, air pollutants, and childhood allergic diseases. Int J Hyg Environ Health. 2016 Jan;219(1):66-71.

[3] Schmitt J. et al. Increased attention-deficit/hyperactivity symptoms in atopic dermatitis are associated with history of antihistamine use. Allergy. 2017 Oct 4.

[4] Hak E. et al. Association of childhood attention-deficit/hyperactivity disorder with atopic diseases and skin infections? A matched case-control study using the General Practice Research Database. Ann Allergy Asthma Immunol. 2013 Aug;111(2):102-106.e2.


Thursday, 11 January 2018

ICF core sets for autism: "third in a series of four empirical studies"

Peer-reviewed discussions on the International Classification of Functioning, Disability and Health (ICF) core sets for autism have appeared a couple of times before on this blog (see here and see here). The idea behind developing the ICF core sets - a World Health Organisation (WHO) initiative - is to build up a kind of framework for describing and organising information on functioning and disability across various diagnoses.

Autism has been in the ICF sights for a few years now. The hope is that science and clinical practice can start to get closer to the many abilities and disabilities that seem to derive from a diagnosis and offer more evidence-based 'clues' of where and when support needs to be targeted. Also perhaps potentially providing some good evidence for just how heterogeneous the autism spectrum really is...

Bearing in mind the previous research occasions where the development of the ICF core sets for autism have been discussed from a systematic review and 'experts' perspective, the paper by Soheil Mahdi and colleagues [1] adds a third tier to proceedings: "to describe functioning in ASD (as operationalized by the ICF) derived from the perspectives of diagnosed individuals, family members, and professionals." This is an important part of the ICF development schedule, in that it gave an important voice to those people who are themselves autistic and their family members. All of this set in light of a growing 'debate' on who speaks for who(m) in the context of autism (see here) and how talking more to those on the autism spectrum about their experience of autism might be a rather good idea (see here) (bearing in mind that not everyone can or does make their voice heard in such conversations - see here).

So, drawing on discussions - "focus groups and semi-structured interviews" - with some 19 stakeholder groups, the authors report how 'meaningful concepts' talked about by stakeholders were linked to the draft ICF categories already present. Various talking points emerged; some mirroring what has been previously observed: "Positive aspects of ASD [autism spectrum disorder] included honesty, attention to detail, and memory". Others, not exactly aligning with other discussions by other groups: "Body structures were sparsely mentioned by the participants."

The outcome was however pretty much the same as the other ICF development occasions: "The experiences provided by international stakeholders support the need to understand individuals with ASD in a broader perspective, extending beyond diagnostic criteria into many areas of functioning and environmental domains." The core triad/dyad of symptoms it seems, is only the starting point when it comes to what autism looks like and means. A shocker indeed!

I await more on this topic, and perhaps, mentioning how the ICF core sets for autism might also *correlate* with other important research streams such as that related to quality of life [2].


[1] Mahdi S. et al. An international qualitative study of functioning in autism spectrum disorder using the World Health Organization international classification of functioning, disability and health framework. Autism Res. 2017 Dec 11.

[2] Lin LY. & Huang PC. Quality of life and its related factors for adults with autism spectrum disorder. Disabil Rehabil. 2017 Dec 11:1-8.


Wednesday, 10 January 2018

Probiotics are "a good choice in remission of inflammatory bowel diseases" (says review)

The systematic review and meta-analysis published by Mahboube Ganji-Arjenaki & Mahmoud Rafieian-Kopaei [1] provides the blogging fodder today, on the topic of  "the efficacy of probiotics in attaining clinical response on patients with various types of IBD [inflammatory bowel disease]."

Probiotics, in case you've not heard, include a range of bacterial and yeast species thought to have some sort of health benefit by acting on the multitude of microorganisms that call us (predominantly our digestive tract) home. Inflammatory bowel disease (IBD) typically means one of two conditions: ulcerative colitis (UC) and/or Crohn's disease (CD). Both IBD conditions involve inflammation of parts of the gastrointestinal (GI) tract, in which many of those previously discussed microorganisms reside in. Putting the two concepts together - probiotics and IBD - and it stands to reason that they might have some [variable] interaction with one and another.

The authors surveyed the current peer-reviewed science literature on the topic of probiotics 'for' IBD, grouped the results together and set about trying to come up with some summary statements based on the statistical results obtained. Bearing in mind that the term 'probiotic' includes quite a few different bacterial/yeast species, both alone and in combination, they came up with a few take-home messages.

First: "Probiotics are beneficial in IBD, especially the combination ones in UC." Given what traditional treatment options are currently available for UC (see here), the idea that popping a few pills, most of which are readily available without a doctor's prescription, containing bacteria and/or yeasts must represent a rather good deal for those diagnosed with UC. I say this minus any medical or clinical advice from me: please, consult you medical physician before making any such changes.

Second: I note that two particular 'preparations' are mentioned in the review text: Saccharomyces boulardii and VSL#3. Both of these products (yes, I know S. boulardii is a strain of yeast) have had previous airtime on this blog for various different reasons (see here and see here for examples). Both of them also have some pretty good evidence when it comes to other bowel-related conditions and states as told again by the all-powerful meta-analysis/systematic review (see here).

Finally I note that the safety profile of these preparations seemed to be pretty good based on the trial data included for study. That's not to say that they are completely side-effect free [2] (particularly in the context of the use of immunosuppressants for potentially treating UC for example) but their risk profile seems at least to be on a par with more traditional pharmacotherapies.

What's more to say? Well, just before I finish I do want to try and relate some of the Ganji-Arjenaki - Rafieian-Kopaei findings back to the core material of this blog: autism. I say this with some cautions but: (a) science has told us a few times that inflammatory bowel disease does seem to be over-represented when it comes to a diagnosis of autism (see here), and (b) discussions should be turning to 'what can we do to help' when it comes to IBD accompanying autism, given that presentation might be slightly less 'mainstream' in such cases [2] (see here for my take on this study). I've also already touched upon the study by Grossi et al [3] (see here) talking about how a probiotic formulation seemed to affect both gut and behaviour in a case report and what that could mean for [some] others diagnosed with an autism spectrum disorder (ASD). Such findings asks science to do a lot more to see if a dual diagnoses of autism and IBD represents an important target for probiotics as an extension to work on autism and more 'functional' bowel complaints either already completed or still underway (see here and see here).

And bear in mind that outside of any gut-brain notions specifically with IBD and autism in mind (see here), there is evidence to suggest that effective medical treatment of IBD might generally extend to quite a few domains [4] which I daresay are just an important in the context of autism as they are to not-autism...


[1] Ganji-Arjenaki M. & Rafieian-Kopaei M. Probiotics are a good choice in remission of inflammatory bowel diseases: A meta analysis and systematic review. J Cell Physiol. 2018 Mar;233(3):2091-2103.

[2] Lee M. et al. Association of Autism Spectrum Disorders and Inflammatory Bowel Disease. J Autism Dev Disord. 2017 Nov 23.

[3] Grossi E. et al. Unexpected improvement in core autism spectrum disorder symptoms after long-term treatment with probiotics. SAGE Open Medical Case Reports. 2016;4:2050313X16666231.

[4] Mählmann L. et al. Psychological wellbeing and physical activity in children and adolescents with inflammatory bowel disease compared to healthy controls. BMC Gastroenterology 2017; 17: 160.


Tuesday, 9 January 2018

An exercise intervention for autism

"Our results provide support for exercise and physical activity, including basic coordination and strength exercises, as important therapeutic interventions for children with ASD [autism spectrum disorder]."

So said the results published by Chrystiane Toscano and colleagues [1] looking at an important, and sometimes easily overlooked, avenue of intervention with autism in mind: physical activity. I say 'intervention' but as with quite a few other programs/activities described in such terms, it's often more about offering equal access to things that most children (and adults) take for granted. Indeed, to 'intervention-ise' something like exercise in the context of autism kinda follows a pattern where even playing with some well-known connecting blocks is sometimes talked about in 'therapeutic' terms when mentioned alongside autism rather than just being play (see here). One has to be quite careful about the language used...

Anyhow, various parameters were monitored and measured as "a 48-week exercise-based intervention" was put into place looking at the presentation of autism as well as various physical-metabolic variables: "high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, and total cholesterol."

Bearing in mind potentially problematic issues such as a lack of blinding - double-blinding - and of course the idea that exercise really needs to make you feel happy in order to keep doing it, researchers reported that many aspects seemed to improve over the quite long study period, more so for the group in receipt of exercise intervention. Not only did physical indicators show improvements, so did autistic features and also "parent-perceived quality of life" too.

Allowing for the fact that there could be 101 different variables impacting on the Toscano results outside of the increase in physical activity, I am happy to see that exercise is a continued focus when it comes to the autism spectrum [2]. There is literally oodles and oodles of research out there talking about how sedentary behaviour(s) do seem to be over-represented in relation to autism (see here for example) and where they could (in part) lead (see here); bearing in mind the sentiment: you can't outrun a bad diet. Anything that gets kids (and adults) up and active has to be a good thing.

Once again, I'm going to draw your attention to one potential exercise option that ticks many boxes when it comes to the autism spectrum and beyond: the martial arts (see here and see here). Physical activity... check. Focus on "basic coordination and strength"... check. Focus on predefined and (sometimes very) repetitive patterns of movement... check. Focus on individual performance set within a social context... check. Regular accomplishment levels - gradings - to boost confidence, pride and self-esteem... check. Something that will make any would-be bullies perhaps think twice or thrice... check.

And of additional importance to any discussions on exercise and physical activity, the data from Flygare Wallén and colleagues [3] highlight the important physiological reason(s) why getting those on the autism spectrum moving more is so damn important...


[1] Toscano CVA. et al. Exercise Effects for Children With Autism Spectrum Disorder: Metabolic Health, Autistic Traits, and Quality of Life. Percept Mot Skills. 2017 Jan 1:31512517743823.

[2] Najafabadi MG. et al. The Effect of SPARK on Social and Motor Skills of Children with Autism. Pediatrics & Neonatology. 2018. Jan 6.

[3] Flygare Wallén E. et al. High prevalence of diabetes mellitus, hypertension and obesity among persons with a recorded diagnosis of intellectual disability or autism spectrum disorder. J Intellect Disabil Res. 2017 Dec 26.


Monday, 8 January 2018

On unintentional drowning deaths in children with autism

Sometimes science seems to be science for the sake of science. Y'know, findings are reported and published and are met with either 'so what' or 'what does this mean for me?' sentiments, particularly when dealing with potentially abstract concepts.

The findings published by Joseph Guan and Guohua Li [1] most definitely DO NOT fall into such a category. Their covering of a topic which has potential life-limiting implications - unintentional drowning deaths - in the context of autism is worthwhile repeating again and again and again until everyone sits up and takes note. I might add that other previous research from this authorship team similarly evoke such sit-up-and-listen sentiments (see here).

What did the authors do? Well, simply put, they scanned the Lexis-Nexis® Academic database looking for all newspaper entries covering the terms autism, drowning and boy/girl from the beginning of January 2000 until May 2017 in the United States. They analysed the collected data; retrieving specific details such as "time of day and distance from residence" when it came to such reports.

Results: "During January 2000 through May 2017, US newspapers reported a total of 23 fatal unintentional drowning incidents involving children under 15 years of age with ASD [autism spectrum disorder]." Let's just reflect on that a moment. Twenty-three children / young adults with autism who drowned. Twenty-three lives tragically cut short. Twenty-three families left grieving.

Also: "Data about proximity of the water body to the victim’s residence were available for 11 (47.8%) of the incidents, with all of them within 1000 m of the victim’s residence (mean = 290.7 ± 231.5 m)." And also: "The time of day at which victims were reported missing was available for 15 (65.2%) of 23 incidents, with 2 (13.3%) being in the morning (0:00–11:59), 11 (73.3%) being in the afternoon (12:00–17:59), and 2 (13.3%) being in the evening (18:00 PM – 23:59)." And finally: "Wandering was the most commonly reported activity that led to drowning, accounting for 73.9% of the incidents."

I could go on about the limitations of this study as highlighted by the authors - "small sample size and the availability of information reported in newspaper articles" - but really I have to ask 'does it matter?' The answer: no, such study limitation don't really make too much difference to the final - very final - outcomes reported on.

The fact that wandering (elopement if you will) was a feature of many of the cases found is not new news (see here). It reiterates once again that resources aplenty need to be put into reducing incidences of wandering or at least allowing parents and law enforcement and other agencies every opportunity to locate wandering children/adults as quickly as possible. Some might worry about things like civil liberties when it comes to monitoring someones movements. But in current times, when someone can be tracked by their mobile/cell phone use for example, I'd respectively disagree with such 'civil rights are being impinged' sentiments. Imagine if you will, if one of the various 'tracking' devices currently aimed at those on the autism spectrum was given to every child / every family free of charge at the point of diagnosis? A good use of money methinks...

Water safety is another important part of the current findings. There is science out there talking about how learning to swim might have quite a lot of positives when it comes to autism [2]; perhaps the most important being learning water safety skills. Who would argue with that? And if one wanted to be proactive in this area, how about making water safety and swimming lessons a compulsory part of the learning curriculum for everyone diagnosed with an autism spectrum disorder? Again, a very good use of money methinks and you never know, there may be other benefits too.

I'm not saying that there aren't individual circumstances around every one of those drowning deaths discussed by Guan & Li. I'm not saying that every death could have been avoided. What however I do believe is that armed with the knowledge that drowning is a significant cause of premature death in the context of autism, and knowing a little more about the general circumstances around some of those deaths, there are things that can potentially be done to mitigate future risks to the autistic population and potentially save lives.


[1] Guan J. & Li G. Characteristics of unintentional drowning deaths in children with autism spectrum disorder. Injury Epidemiology 2017; 4: 32.

[2] Alaniz ML. et al. The Effectiveness of Aquatic Group Therapy for Improving Water Safety and Social Interactions in Children with Autism Spectrum Disorder: A Pilot Program. J Autism Dev Disord. 2017 Dec;47(12):4006-4017.


Saturday, 6 January 2018

Challenging behaviour and autism: how do parents manage it?

I'm not going to dwell too much on the findings reported by Elizabeth O’Nions and colleagues [1] discussing some of the ways-and-means used "to manage problem behaviour" in the context of autism, but I did want to bring it to your attention.

It's an important summary because (a) it highlights how a diagnosis of autism or autism spectrum disorder (ASD) does seem to increase the risk of various 'challenging behaviours' appearing above and beyond what would typically be expected (see here), (b) it illustrates how said behaviours have an important impact both on the person themselves and significant others around them (see here), and (c) it details 'what might help' in terms of parents or significant others managing such behaviour(s) as well as providing a road map for further study and potentially, further guidance.

The O'Nions paper is open-access so you can read for yourself what the findings were. The main points as I saw them were:

  • Challenging behaviours covers a lot of ground.
  • Said behaviours can and do affect quality of life for all concerned.
  • Various strategies are employed by parents to cope with such behaviours including "accommodating the child... modifying the environment... providing structure, routine and occupation... managing non-compliance with everyday tasks and activities... [and] managing distress."
  • Strategies for 'dealing' with such behaviour(s) often take into account their effects not only on the person/child concerned but also the family unit.

What's missing from this review? Well, accepting that the focus was "to identify how parents and caregivers spontaneously manage problem behaviour in ASD" I found the O'Nions paper to be rather light on anything not related to behaviour and/or psychology. Take for example, the growing realisation that challenging behaviour(s) seem to show some connection to sleep patterns in the context of autism [2] and what that could mean for intervention(s) to manage sleep issues for example (see here). Similarly, the idea that challenging behaviours can, on some occasions, seem to be linked to the experience of pain (see here) and/or fatigue (see here) is perhaps something else important to reiterate, as part of a suite of potential factors to consider (see here). I might also add that a certain type of pain/discomfort (e.g. gastrointestinal) together with sleep issues in the context of autism have been a source of some joint inquiry (see here). There is also a case for further research looking at targeted pharmacotherapy in the context of some challenging behaviours too (see here) with appropriate concerns and caveats noted.

There is another aspect raised by the O'Nions review that also needs to be mentioned: "This analysis shows that many of the strategies used by parents of children with ASD are specifically targeted to manage particular vulnerabilities (e.g., sensory sensitivities, rigidity, insistence on sameness), or accomplish particular behavioural goals, and may be relatively unique to this population." I stress of course, the idea that the core features of autism / ASD seem to be 'targets' of intervention in this area illustrating the link between core behaviours and challenging behaviours. Although I've made quite a big thing on this blog about how 'comorbidity' appearing alongside autism is probably not just comorbidity (see here), I'm taking a slightly opposite view on this occasion, and suggesting that one also needs to be mindful that issues such as anxiety and depression may very well exert an effect on the presentation of challenging behaviour(s) and perhaps need to be looked at separately?

And whilst we're on the topic of challenging behaviours in the context of autism, the review of social outcomes for a sample of adults with autism published by Megan Farley and colleagues [3] provides some further interesting discussions on this topic. Specifically that: "most participants were only aggressive in response to frustrating situations or when experiencing problems with medical conditions." There's [seemingly] always a reason...


[1] O'Nions E. et al. How do Parents Manage Irritability, Challenging Behaviour, Non-Compliance and Anxiety in Children with Autism Spectrum Disorders? A Meta-Synthesis. J Autism Dev Disord. 2017. Dec 8.

[2] Cohen S. et al. Sleep patterns predictive of daytime challenging behavior in individuals with low-functioning autism. Autism Res. 2017 Dec 1.

[3] Farley M. et al. Mid-life social outcomes for a population-based sample of adults with ASD. Autism Res. 2017 Dec 20.


Friday, 5 January 2018

"illness course subtypes can account for significant differences in the experiences of patients with CFS and ME"

The quote titling this post - "illness course subtypes can account for significant differences in the experiences of patients with CFS [Chronic Fatigue Syndrome] and ME [Myalgic Encephalomlyelitis]" - comes from the findings reported by Jamie Stoothoff and colleagues [1] (open-access available here).

Including one Leonard Jason on the authorship list, someone who has quite a pronounced peer-reviewed research history when it comes to ME/CFS (see here and see here for examples), researchers looked at over 500 people from various research cohorts who were "at least 18 years of age with a current diagnosis of CFS or ME." Participants from one of the cohorts, we are told, included those "who self-identified as having a CFS or ME diagnosis" so one perhaps has to be little careful when interpreting results; especially given prior 'mix-ups' between notions of  'chronic fatigue' and a diagnosis of CFS (see here)...

Participants completed a few assessment instruments including the Medical Outcomes Study 36-item short-form health survey (SF-36) and the DePaul Symptom Questionnaire (DSQ), providing a snapshot in relation to "current physical and mental functioning" and "CFS-related symptomatology." Researchers also calculated "energy quotients" which, although sounding like something a bit 'new age' actually involved asking participants to "rate their available and expended energy yesterday and last week" based on items included in the DSQ. The main aim was to explore the 'feasibility' of "classifying differing experiences of CFS and ME symptomology."

Results: a few 'generalisations' were derived from the collected results, which translated into 'illness course sub-types' such as: "Fluctuating (59.7%), with 15.9% Constantly Getting Worse, 14.1% Persisting, 8.5% Relapsing and Remitting, and 1.9% Constantly Getting Better." Authors also reported that "no significant relationship was found between illness course groups and gender, race, ethnicity, marital status, education, or work status."

Outside of other pretty obvious results - "The Constantly Getting Worse group generally reported higher levels of symptom severity and frequency when compared to the other groups, while the Constantly Improving group reported lower levels of symptom severity and frequency compared to the other groups" - authors also reported findings in relation to those energy quotients previously mentioned. So: "the Constantly Getting Worse group reported overextending their personal energy envelopes to significantly higher degree compared to the average patient" with the need for a lot more research in this area.

I know some people might be shrugging their shoulders about these results with 'so what' sentiments but I'm not one of them. The reason: quite a lot of things in relation to ME/CFS have been taken 'as read' down the years. Be that something like discussions on what recovery looks like in relation to ME/CFS (see here) through to questions about whether ME/CFS in the UK for example, is the same as ME/CFS in other parts of the world (see here), [previous] research seems to have 'skipped' quite a few important steps along the way; only now being corrected. The ideas derived from this latest research on how ME/CFS is not necessarily a 'static condition' in terms of symptom profiles (albeit based on a snapshot) adds to that basic research on the label(s).

With the requirement for quite a bit more replicative work needed, I also wondered whether this research from Stoothoff et al might overlap with other, more biologically-orientated results too. So, those talking about typical/atypical ME/CFS presentation impacting on immune system markers (see here) or even the effects of duration/staging of the condition(s) when it comes to biochemistry (see here) might represent important inclusions in further drafts of work on illness subtypes?

Oh, and whilst on the topic of ME/CFS, the recent findings by Nilsson and colleagues [2] inform us that use of a monoaminergic stabiliser - (-)-OSU6162 - previously thought to show "promise for treating a variety of neuropsychiatric disorders such as Huntington’s disease, schizophrenia, and mental fatigue following stroke or head trauma" probably isn't going to be great for ME/CFS. Yet more evidence for the idea that mental fatigue, accompanying physical fatigue and PEM as a characteristic feature of ME/CFS, is probably not just some sort of stand-alone 'psychiatric' manifestation...


[1] Stoothoff J. et al. Subtyping Patients with Myalgic Encephalomyelitis (ME) and Chronic Fatigue Syndrome (CFS) By Course of Illness. J Biosens Biomark Diagn. 2017;2(1).

[2] Nilsson MKL. et al. A randomised controlled trial of the monoaminergic stabiliser (-)-OSU6162 in treatment of myalgic encephalomyelitis/chronic fatigue syndrome. Acta Neuropsychiatr. 2017 Dec 7:1-10.


Thursday, 4 January 2018

"Minor physical anomalies" and autism: hypermobility very much included

'Minor physical anomalies' (MPAs) are defined as "subtle, abnormal morphological features, such as deviations in morphology of the head, eyes, ears, mouth, hands, and feet." I appreciate that such a term is probably not going to everyone's cup of tea, but given the embryological links between organs such as the brain and skin, it's assumed that "MPAs may mirror altered brain development."

That was the starting point for the study results published by Lynnea Myers and colleagues [1] looking for the presence of MPAs in a cohort of over 110 twins, around half of whom had received a concordant or discordant neurodevelopmental disorder diagnosis such as "intellectual disability (ID), communication disorders, autism spectrum disorder (ASD), attention-deficit/hyperactivity disorder (ADHD), specific learning disorders, and motor disorders." Alongside various behavioural and diagnostic assessments, researchers also used a special MPA checklist "containing a total of 179 anomalies for males (24 body regions) and 171 for females (23 body regions)" with their cohort. This checklist also included various other 'issues' that are "commonly assessed for in physical exams."

Various results were produced bearing in mind the quite complicated participant mix included for study (i.e. presence or not of a neurodevelopmental disorder, concordance among twins, zygosity, specific neurodevelopmental diagnosis, etc). Autism was the only neurodevelopmental diagnosis that was "significantly associated with the extent of MPAs." If twins were concordant for autism or autism spectrum disorder (ASD), researchers observed that they "had descriptively the highest median (Md) number of MPAs." Where twins were discordant - one had autism, the other not - researchers still observed MPAs, albeit to a slightly lesser degree (number). Further: "The most common MPAs in participants with ASD included overweight (39%), hypermobility (36%), pes planus (29%), straight eyebrows (29%), vision impairment (25%; 29% of these with corrective lenses), arachnodactyly/long toes (25%), long eyelashes (21%), and microtia (21%)."

Putting to one side the important findings that almost 40% of those with ASD were described as overweight (see here) or that vision issues were present in a quarter (see here), I was drawn to the suggestion that quite a percentage of those with autism (36%) were described as having hypermobility. Hypermobility, where joints are more flexible than usual, in the context of autism is something of an interest of mine (see here and see here). Not least because it is an area of the autism research landscape crying out for a lot more investigation, both as part of a wider 'psychiatric picture' (see here) and also in the 'ESSENCE' context that autism rarely exists in some sort of diagnostic vacuum (see here).

Minus any sweeping generalisations, there are a few potentially important implications either linked to or arising from hypermobility in the context of autism. Poor balance and/or coordination is one possible outcome from hypermobility that would perhaps tie into what has been discussed in the autism research literature for years and years now [2] (even Kanner mentioned it). The observation that functional gastrointestinal (GI) issues such as constipation and diarrhoea also seem to be over-represented in relation to hypermobility [3] also potentially accords with findings pertinent to quite a lot of autism (see here) (bearing in mind that I'm not saying that all bowel issues noted in autism are necessarily hypermobility-connected). If however one was to stretch things further, one might be looking at something like joint hypermobility in the context of connective tissue disorder and what that could mean for something like intestinal permeability issues associated with 'some' autism (see here). I know this is speculative, but at least it provides a research plan of action to include in future investigations in this area.


[1] Myers L. et al. Minor physical anomalies in neurodevelopmental disorders: a twin study. Child and Adolescent Psychiatry and Mental Health. 2017; 11: 57.

[2] Cassidy S. et al. Dyspraxia and autistic traits in adults with and without autism spectrum conditions. Mol Autism. 2016 Nov 25;7:48.

[3] Fikree A. et al. Functional gastrointestinal disorders are associated with the joint hypermobility syndrome in secondary care: a case-control study. Neurogastroenterol Motil. 2015 Apr;27(4):569-79.


Wednesday, 3 January 2018

On the recent report suggesting that US autism rates "appear to be stabilizing"

The research letter by Guifeng Xu and colleagues [1] is making some New Year's headlines following their finding that: "In a large, nationwide population based study, the estimated ASD [autism spectrum disorder] prevalence was 2.41% among US children and adolescents in 2014-2016, with no statistically significant increase over the 3 years."

Based on data derived from the National Health Interview Survey (NHIS), researchers have kinda repeated what was reported in a recent NCHS data brief [2] that provided some blogging fodder here a few weeks ago (see here). On that occasion as this, the data reported an increasing percentage of families positively responding to the question: "Has a doctor or health professional ever told you that [sample child] had Autism, Asperger’s disorder, pervasive developmental disorder, or autism spectrum disorder?" year on year, but nothing to say that the percentage increase is statistically significant.

Unlike the Xu data, the previous data brief by Zablotsky and colleagues [2] also asked some questions about diagnoses 'around the edges of autism'  such as 'other developmental delay' alongside a composite measure called 'developmental disability' that included ASD, intellectual disability and other developmental delay. The stats for that composite measures were deemed statistically significant in terms of the increase in percentages of children/young adults being diagnosed year on year.

Whilst there may be some optimism that the rates of autism/ASD might be 'stabilising' based on the NHIS research format, I'd like to see a lot more data before anyone calls an end to the quite phenomenal increase in the numbers of children/young adults being diagnosed over the past few decades. I believe we should be due some updated CDC figures later this year (2018) on the basis of other data reported on a once-every-2-years basis with autism in mind (see here). And hopefully, the moves to "estimate ASD case status on the basis of both DSM-5 and DSM-IV-TR" in the next CDC figures, should provide some additional talking points too (see here)...


[1] Xu G. et al. Prevalence of Autism Spectrum Disorder Among US Children and Adolescents, 2014-2016. JAMA. 2018; 319: 81-82.

[2] Zablotsky B. et al. Estimated prevalence of children with diagnosed developmental disabilities in the United States, 2014–2016. NCHS Data Brief, no 291. Hyattsville, MD: National Center for Health Statistics. 2017


Tuesday, 2 January 2018

"Social cognitive deficits are present in a wide range of clinical conditions"

Happy New Year!

Welcome to Questioning Answers 2018-style. Let's continue...

Today I'm bringing to your attention the findings reported by Jack Cotter and colleagues [1] who concluded that: "social cognitive deficits appear to be a core cognitive phenotype of many clinical conditions."

Social cognitive issues defined as "mental operations that underlie social interactions" and "includes a range of cognitive processes that help individuals to understand how others think and feel" are something not unknown to the core subject of this blog: autism. Indeed, Cotter et al mention how the "most heavily researched aspects of social cognition are emotion recognition and theory of mind (ToM)." Right or wrong, ToM in particular, has had quite a significant influence on autism research and thought down the years (see here).

Cotter and colleagues "sought to collate existing meta-analytic data on social cognitive performance among individuals with a range of clinical conditions" on the basis that whilst the label of autism has received the lion's share of research interest, social cognitive issues perhaps span a far wider range of labels/conditions. They scoured the peer-reviewed literature and identified some 31 meta-analyses published that "examined performance on facial emotion recognition (24 papers) and/or ToM tasks (24 papers) among 30 different clinical populations relative to controls." The sorts of clinical populations identified ranged from psychiatric disorders such as psychosis and schizophrenia, to neurological disorders such as epilepsy and traumatic brain injury to developmental disorders such as attention-deficit hyperactivity disorder (ADHD) and intellectual (learning) disability.

Their conclusions: "Though these results do not provide directly comparable estimates between clinical conditions, they provide a robust indication that social cognitive deficits appear to be a core cognitive phenotype of many developmental, neurological and psychiatric disorders." The authors go on to discuss how, on the basis of their findings, social cognitive issues (impairment) might be "a general biomarker indicative of neurological abnormality" more generally; also, in some contexts, providing information on the 'progression' of a particular condition.

In these days of ever-blurring labels and conditions, where comorbidity is proving to be the rule rather than the exception [2] (see here also), there is common sense in the Cotter findings. Sense, insofar as the idea that no one diagnostic label has generally got a monopoly on a particular behaviour and/or symptom and that social cognitive issues might be 'core' to quite a few conditions. A greater appreciation of such an idea could potentially impact, in many different ways, on what we think about many seemingly different psychiatric, developmental and neurological labels. A few stand-out points include: (a) a reiteration of how nonsensical the term 'neurotypical' is from a social cognitive perspective when describing 'not-autism' (see here); (b) a further illustration of the value of a professional assessment as and when something like autism is suspected, rather than just a reliance on brief 'are you autistic?' questionnaires that tend to rely heavily on social cognition as a 'symptom' (see here); and (c) investigation into whether or not important biological 'issues' thought to accompany social cognitive 'issues' could also be quite wide-ranging among many conditions/labels (see here for some discussion on the concept of inflammation for example).

And since we're on the topic of grand, sweeping psychological concepts spanning different conditions, how about the idea that executive function issues might also cross labels [3] too...

Stay tuned for more in 2018.


[1] Cotter J. et al. Social cognitive dysfunction as a clinical marker: A systematic review of meta-analyses across 30 clinical conditions. Neuroscience & Biobehavioral Reviews. 2018; 84: 92-99.

[2] Posserud M. et al. Autism traits: The importance of “co-morbid” problems for impairment and contact with services. Data from the Bergen Child Study. Research in Developmental Disabilities. 2018; 72: 275-283.

[3] Carter Leno V. et al. Testing the specificity of executive functioning impairments in adolescents with ADHD, ODD/CD and ASD. Eur Child Adolesc Psychiatry. 2017 Dec 9.