Wednesday 28 February 2018

Considerable vitamin D deficiency in a specialist secure unit for those with intellectual and developmental disability

The results published by Ian McKinnon and colleagues [1] (open-access available here) reporting that over 80% of patients in "secure care facilities for people with intellectual and developmental disabilities (IDD) who offend, as well as providing specialised services for people with severe autism spectrum disorders" presented with "suboptimal vitamin D levels" came as little surprise to me.

Having already discussed other research on vitamin D levels in another in-patient unit here in Blighty (see here) and more generally how autism seems to be particularly interesting to vitamin D research (see here), the messages seem to be that: (a) those presenting with a behavioural / developmental / psychiatric diagnosis are, in the most part, lacking in vitamin D biologically-speaking for whatever reason(s), and (b) screening for vitamin D levels should be commonplace in such facilities. Current guidance from the UK Government on population vitamin D supplementation also come into play (see here).

McKinnon et al discuss their findings based on a facility not a million miles away from where I currently write this post. They begin: "It is estimated that approximately 50% of the population of Northern England have insufficient or deficient vitamin D levels" which is something that I can vouch for in terms of our sunlight exposure 'ere up North. Further: "It was hypothesised that patients in secure services would have suboptimal levels of 25OHD due to less exposure to sunlight, and as a possible consequence of medications prescribed for mental disorders."

So, looking at two cohorts - existing patients who regularly provided blood samples "as part of their annual health checks" and new admissions to the facility - conveniently adding up to 100 participants, vitamin D was assayed for. Unfortunately, I can't actually find the technique used to test for vitamin D in the McKinnon paper so I can't really comment on whether the gold-standard technique that is mass spectrometry was used. I would assume so but...

Results: taking into account season of testing and various medication use history - "regression analysis demonstrated no effect of season or level of security on the vitamin D status of the patient at baseline" - the results are quite stark. At baseline, only 17 patients (17%!) had results that fell into the 'sufficient' or 'optimal' groupings (above 50 and 70 nmol/L respectively). Forty-two participants had results in the 'insufficient' grouping and even worse, forty-one were deficient.

Based on such results, and with guidance from the National Health Service Specialist Pharmacy Service, a supplementation protocol was put in place for those found to be lacking in vitamin D. Lo and behold, a year later at retesting things looked rather better from a vitamin D perspective: "The numbers of patients with sufficient and optimal 25OHD had improved substantially."

"We recommend further research in this area, including prospective studies of the longer-term health sequelae." I'd second that call from the authors for more research in this area. Not only on vitamin D status and any somatic health-related parameters, but also on what supplementation may or may not mean for some in terms of behavioural presentation too (see here and see here)...


[1] McKinnon I. et al. Vitamin D in patients with intellectual and developmental disability in secure in-patient services in the North of England, UK. BJPsych Bull. 2018 Feb;42(1):24-29.


Tuesday 27 February 2018

FITNET-NHS (Fatigue In Teenagers on the interNET in the NHS) - a trial protocol and some questions...

FITNET-NHS (Fatigue In Teenagers on the interNET in the NHS) is an initiative discussed in a recent study protocol paper published by Sarah Baos and colleagues [1]. It continues a research interest based on previous published results from a trial undertaken in the Netherlands by Sanne Nijhof and colleagues [2] looking at a possible intervention option for adolescents with chronic fatigue syndrome (CFS) (also referred to as myalgic encephalomyelitis, ME by some).

Said intervention option - Fatigue In Teenagers on the interNET (FITNET) - is "a web-based cognitive-behavioural treatment accessible to patients and both parents, based on the existing face-to-face CBT [cognitive behaviour therapy] protocol for adolescents developed by the ECCF [Expert Centre for Chronic Fatigue (Radboud University Nijmegen Medical Centre, ECCF)]." The previous Nijhof findings concluded that: "FITNET offers a readily accessible and highly effective treatment for adolescents with chronic fatigue syndrome" on the basis of previous (registered) trial results.

The recent Baos paper detailing 'what researchers are going to do' is looking to build on the previous Nijhof findings to determine whether "it is effective in the National Health Service (NHS) or if it is cost-effective." Alongside the descriptions offered by Baos et al, trial authors have also prospectively registered their intention to undertake this study (see here).

I don't want to recite all the study details described by Baos et al (the paper is open-access) but I do think a few points are worth noting and a few questions perhaps need to be asked. I say this on the basis that mention of the letters/words CBT in the context of CFS/ME has some 'history' (see here and see here for a part of that history). Also, at the time of writing this post, some of the premises for implementing the FITNET-NHS trial are also subject to 're-inspection' (see here) in light of fairly recent changes to official CFS/ME management guidance in countries outside of the UK (see here)...

Anyhow, point 1: "This is an RCT comparing FITNET-NHS with Activity Management for paediatric CFS/ME." RCT means randomised-controlled trial and means participants (planned 700+ aged 11-17 years old) will be randomly placed in either the treatment arm of the study or the 'activity management' control group. Actually, the authors mention another important detail in respect of the study progression: "An internal pilot study will be conducted with continuation of the trial based on achieving defined criteria." What this means is that certain criteria need to be met before the trial progresses, following a sort of pseudo-adaptive design. The stop criteria we are told are: "(1) the recruitment rate is substantially below target during the last 6 months of the internal pilot study and if the qualitative data suggests that we cannot improve recruitment by changing recruitment methods or (2) the qualitative data suggests that the interventions are not acceptable to participants." I've talked about recruitment rates in relation to trials run by some of the Baos authors before on this blog (see here). In terms of 'acceptability' of the interventions, well, the findings from Geraghty and colleagues [3] perhaps need airing in line with some of the history around the use of CBT in the context of CFS/ME. Will all of this affect recruitment rates? We'll see.

Point 2: Activity management (the comparator). There are various elements - mandatory, flexible, prohibited - that such activity management will include. Prohibited elements, I think, mean that specialist therapists cannot discuss in detail things like "feelings, beliefs and how they change" nor "feelings and their relationship with behaviour." Mandatory elements by contrast include finding a baseline level of activity, "to record time spent each day doing high-energy cognitive activities" and importantly: "Increasing activity by 10–20% each week." Yes, this is an active comparator that looks like it is expecting quite an increase in activity over the duration of the study. I think they call this graded exercise therapy (GET). All of this will be delivered on-line and participants will "receive treatment for 3 to 6 months." As you can see, things like recording activity levels (the ActiveME app is mentioned) is going to be predominantly (exclusively?) done via "paper/electronic diaries." I'm a little cautious of this method, and once again (see here) need to question why more objective activity trackers such as the wonderful technologies headed under the title of actigraphy are not being fully utilised with CFS/ME research in mind (see here for another example). Given also that the primary outcome measure is: "Disability measured using the Physical Function Scale (SF-36-PFS) at 6 months after randomisation", surely such actigraphic data would provide a really sound comparator to such subjective scoring?

Point 3: There are a range of secondary outcomes listed by Boas and colleagues in relation to measuring any effects from intervention and/or comparator. I am happy to see that quality of life (QoL) will be measured via use of the EQ-5D-Y (EuroQoL health-related quality of life questionnaire, Youth version) given some chatter about this previously (see here and see here). But there are some things missing from such an outcome line-up; a primary one seems to be that although fatigue and physical function is kinda (see above) mentioned in an analysis sense, more specific facets of CFS/ME are not seemingly being addressed such as PEM (post-exertional malaise). I note from the study website for example, the authors talk about how "fatigue and other symptoms get worse after exertion" suggesting that they know all about PEM. The question then: why not try and test for it and importantly, assess it before and after intervention? OK, I know that measuring PEM is still more of an art rather than a science [4], but I wonder if it would have been helpful for researchers to also potentially think about examining biochemistry for example, as well as psychology and behaviour throughout their study to aid some further investigation in this important area. Y'know things like immune function for example [5] which seems to be an area of research rising (see here) and could add something extra when it comes to sub-grouping among the CFS/ME population? Oh, and just in case you were thinking 'eh?' when it comes to me talking about CBT potentially affecting immune function, have a look at another trial protocol from Schakel and colleagues [6] and the measures they want to use/are using as part of their study "to investigate the effects of a psychological intervention on self-reported and physiological health outcomes in response to immune and psychophysiological challenges."

Point 4: Safety. I am happy to see that safety of the intervention(s) is also discussed in the Boas paper. To quote for example: "We will define a serious deterioration in health as: (1) clinician-reported serious deterioration in health, (2) a decrease of ≥ 20 in SF-36-PFS between baseline and 3, 6 or 12 months or scores of ‘much’ or ‘very much’ worse on the Clinical Global Impression Scale or (3) withdrawal from treatment because of feeling worse." Good news indeed, and I assume this covers the comparator arm of the study too. What is perhaps missing from such study safety features however, is a little more detail on what screening will be carried out before participants are allowed on to the study in order to reduce/minimise any potential adverse events or even worse, include those who really shouldn't be included in such a study ('first, do no harm'). So: "Young people will be excluded if any of the following apply: (1) they are not disabled by fatigue (defined in eligibility screening), (2) their fatigue is due to another cause, (3) they are unable to complete video calls or FITNET-NHS online chapters or (4) they report pregnancy at assessment." Under 'their fatigue is due to another cause' I'm a little unsure about what this might mean. Does this for example, infer that all potential participants will be screened for mitochondrial disease in light of other data suggesting overlap with cases of CFS/ME (see here) and a possible/probably connection with some fatigue-related symptoms? How is one able to rule out so many potential causes of fatigue other than CFS? As to the idea that there may be those 'unable to complete video calls or FITNET-NHS chapters', well, I imagine that excludes those who might be at a more severe presentation stage of their illness? This then introduces the issue of representativeness of any trial results subsequently obtained...

I applaud the authors for communicating as much as they did about their intentions to conduct this trial. More research groups need to do this both inside and outside the realms of CFS/ME to make replication easier and allow old farts like me to scrutinise and comment from on high. Relying solely on the cold, objective science in this often contentious area, I can also see the rationale behind their running this trial and the urgent need to improve quality of life for many, many young (and older) people diagnosed with CFS/ME.

But... as things stand with the protocol, particularly the distinct lack of using widely available objective measures to provide data on activity levels, I can't also see how this study is going to significantly add to the existing research base nor wider discussions about the use of something like CBT in the context of CFS/ME. I say that also acknowledging that the original FITNET trial is not without criticism [7], including a section that was titled 'The Actometer Results' that perhaps should be renamed 'What happened to the Actometer Results' given "the results were not reported and the reason for this was not given." One also needs look at the masses of discussions on the PACE trial (see here for example) that included CBT as part of an intervention package, to see how the biopsychosocial (BPS) model on which such research rest is, at best, disliked by many suffering with CFS/ME (see here). Said discussions now even reaching the House of elected officials here in Blighty (see here). The glaring lack of any biochemical measures also accompanying this new study adds to the feeling that despite recognition from the authors that "common symptoms in children and young people are unrefreshing sleep, problems with memory and concentration, headaches, nausea (feeling sick), dizziness, muscle and joint pain, and sore throats" psychosomatic ideas still prevail regarding the nature of such symptoms and the continuing rationale for studying CBT in the context of CFS/ME.

I'll hopefully come back to this topic as and when any study results are forthcoming ("Overall trial end date 30/10/2021").


[1] Baos S. et al. Investigating the effectiveness and cost-effectiveness of FITNET-NHS (Fatigue In Teenagers on the interNET in the NHS) compared to Activity Management to treat paediatric chronic fatigue syndrome (CFS)/myalgic encephalomyelitis (ME): protocol for a randomised controlled trial. Trials. 2018; 19: 136.

[2] Nijhof SL. et al. Effectiveness of internet-based cognitive behavioural treatment for adolescents with chronic fatigue syndrome (FITNET): a randomised controlled trial. Lancet. 2012 Apr 14;379(9824):1412-8.

[3] Geraghty K. et al. Myalgic encephalomyelitis/chronic fatigue syndrome patients' reports of symptom changes following cognitive behavioural therapy, graded exercise therapy and pacing treatments: Analysis of a primary survey compared with secondary surveys. J Health Psychol. 2017 Aug 1:1359105317726152.

[4] McManimen SL. & Jason LA. Differences in ME and CFS Symptomology in Patients with Normal and Abnormal Exercise Test Results. International journal of neurology and neurotherapy. 2017; 4(1): 066.

[5] Nijs J. et al. Unravelling the nature of postexertional malaise in myalgic encephalomyelitis⁄chronic fatigue syndrome: the role of elastase, complement C4a and interleukin-1b. J Intern Med. 2010 Apr;267(4):418-35.

[6] Schakel L. et al. The effects of a psychological intervention directed at optimizing immune function: study protocol for a randomized controlled trial. Trials. 2017 May 26;18(1):243.

[7] Ghatineh S. & Vink M. FITNET's Internet-Based Cognitive Behavioural Therapy Is Ineffective and May Impede Natural Recovery in Adolescents with Myalgic Encephalomyelitis/Chronic Fatigue Syndrome. A Review. Behav Sci (Basel). 2017 Aug 11;7(3). pii: E52.


Monday 26 February 2018

Scurvy and autism yet again...

"Here, we report a case of pediatric scurvy in an 11-year-old autistic child with a restricted diet who presented with refusal to walk, fatigue, a purpuric rash, and gingival bleeding."

Yep, the topic is scurvy and autism surfaces again on this blog (see here and see here and see here for other blogging entries), and yet another case report [1] illustrating how a disease that should really have been banished at least a century ago very much remains a part of modern medicine in some circumstances.

In case you didn't already know, scurvy is a disease of nutrition. A chronic lack of vitamin C (ascorbic acid), pretty vital for the synthesis and upkeep of collagen for example, leads to a variety of symptoms including weakness, fatigue, joint pain and perhaps most famously, bleeding gums (gingival bleeding). Vitamin C is present in many fruits and vegetables or can even be delivered as a supplement. Indeed, some pretty famous people have extolled the virtues of regular vitamin C consumption (see here) albeit with varying degrees of successful results outside of scurvy prevention or treatment.

As I mentioned, scurvy appearing alongside autism is not a novel finding. Restricted feeding patterns exemplified by the inclusion of a small repertoire of foods seems to be THE primary risk factor when it comes to scurvy following a diagnosis of autism. As far as I am aware, once the hurdle of actually diagnosing scurvy has been overcome, treatment with vitamin C supplementation seems to be able to resolve many symptoms pretty quickly both inside and outside the context of autism.

What's more to do in this area? Well, as I've mentioned before, screening for scurvy should perhaps be a lot more commonplace following a diagnosis of autism. Given that restricted feeding patterns - not necessarily including any special diets that are put in place for clinical reasons - are pretty frequent in relation to autism, there's a big case for further examinations for scurvy to be more widespread. Minus any clinical or medical advice being given or intended, use of nutritional supplements in the context of restricted feeding habits and autism might also be a sensible option given potential issues outside of just those linked to vitamin C (see here). Obviously this requires some clinical input to ensure that the right dose and preparation is given, but given the quite painful effects of something like scurvy, the question is: why should a diagnosis of autism be a barrier to sound health and wellbeing?

And as I write, there is yet more [2] appearing on this topic, and yet again treatment with vitamin C led to "rapid improvement"...


[1] Burhop J. et al. Do You C What I C: Emergency Department Evaluation and Diagnosis of Pediatric Scurvy in an Autistic Child With a Restricted Diet. Pediatr Emerg Care. 2018 Jan 23.

[2] Kinlin LM. et al. Scurvy as a mimicker of osteomyelitis in a child with autism spectrum disorder. International Journal of Infectious Diseases. 2018. Feb 6.


Saturday 24 February 2018

Endogenous Retroviruses (ERVs) and autism continued

It's been a while since I last mentioned Human Endogenous Retroviruses (HERVs) in the context of autism (see here) on this blog. I still however retain an interest in how these 'fossil viruses' - remnants of our ancient battle with various viruses down the ages that are still present in the genome - *might* impact on our health and well-being for all-manner of reasons.

One name in particular has been at the forefront of the work on HERVs with particular reference to autism (and ADHD and beyond) - Emanuela Balestrieri - and alongside, quite a significant peer-reviewed research record has been built up (see here). A new paper from the Balestrieri 'research group' (if I can call it that) continues their research journey in this area, from Chiara Cipriani and colleagues [1]. The aim of the research game this time around was to look at two popular mouse models of autism - "inbred BTBR T+tf/J mice and CD-1 outbred mice prenatally exposed to valproic acid (VPA)" - and examine the transcriptional activity of various ERVs (that's ERVs not HERVs 'cos these were mice) compared with control mouse strains ("C57BL/J and CD-1 untreated mice").

From what I gather, there were two main elements to the Cipriani study: (1) assessing intracisternal A-particle elements (IAPs) and Type II early transposons (ETns) in blood and brain samples of those autism-related mouse models, and (2) evaluating "the transcriptional activity of proinflammatory cytokines (IL-1β, IL-6, TNF-α) and Toll-like receptors (TLR3 and 4)... in whole embryos and, from the offspring at different time after birth, in blood and brain samples to investigate on the hypothesised link between the ERVs transcriptional activity and the immune system." If much of that sounds like a foreign language to you, well, you're not alone. From what I gather, intracisternal A-particle elements (IAPs) are "endogenous retroviral sequences" that can "induce genomic mutations and cell transformation by disrupting gene expression." Type II early transposons (ETns) are "mobile members of the repetitive early transposon family of mouse long terminal repeat (LTR) retroelements and have caused a number of mutations by inserting into genes" [2]. Clear as mud right?

Results: "In the two distinct mouse models analysed, the transcriptional activity of the ERV families was significant higher in comparison with corresponding controls, in whole embryos, blood and brain samples." Taking the BTBR mice first, in comparison to control mice (C57BL6/J), pretty much all of the expression levels of the ERV genes looked at were higher in embryos. In both blood and brain, over the course of 120 days post-natally, ERV expression was also higher than that in control mice. I say all this acknowledging that absolute number of 'mouse participants' in this study was relatively small.

Also, compared with 'vehicle treated' control mice, those offspring embryos exposed to maternal VPA ("VPA mice were produced by treating outbred pregnant CD-1 female mice with a single dose of VPA (500 mg/kg, sc) at gestational day (GD) 10.5") also saw higher transcriptional activity of 'most' ERVs. The data from blood and brain samples were similarly interesting; in brain samples in particular, those exposed to VPA always showed higher ERV transcriptional activity than non-exposed controls, and notably so. Insofar as the inflammatory cytokine look-see side of things, well in both autism-related mouse models, "the expression levels of the proinflammatory cytokines and TLRs [Toll-like receptorswere significantly higher than controls."

What does this all mean? Well, bearing in mind that mice are mice and not humans (see here), researchers conclude that "results are in agreement with our previous data showing a distinctive expression profile of some human HERV families in blood samples from two different cohorts of young autistic patients and support the hypothesis that ERVs could be implicated in ASD." The fact that authors used not one but two mouse models of autism - including something akin to an 'acquired' autism phenotype in that VPA mouse model - and found similar things adds something a little extra to their findings. The possibility of a tie-up between ERV expression and immune system 'activation' requires more investigation save any sweeping generalisations about linkage. I am wondering if autism research in this area might however benefit from looking at some initial research on myalgic encephalomyelitis (ME) (see here) and onward some chatter about a possible link between HERV proteins acting as 'superantigens' in immune system terms.

Hopefully further research will be forthcoming sooner rather than later...


[1] Cipriani C. et al. High expression of Endogenous Retroviruses from intrauterine life to adulthood in two mouse models of Autism Spectrum Disorders. Sci Reports. 2018; 8: 629.

[2] Baust C. et al. Structure and Expression of Mobile ETnII Retroelements and Their Coding-Competent MusD Relatives in the Mouse. Journal of Virology. 2003; 77: 11448-11458.


Friday 23 February 2018

ADHD and chronic tic disorder

"Compared with controls, children with ADHD [attention-deficit hyperactivity disorderwere 4.1 (95% CI 1.1 to 14.1) times more likely to have CTD [chronic tic disorderat age 7, and 5.9 (95% CI 1.6 to 17.9) times more likely at age 10."

That was one of the results observed by William Poh and colleagues [1] who set out to look at both the prevalence of chronic tic disorder (CTD) in their cohort of children diagnosed with ADHD (n=179) compared with asymptomatic (no ADHD) controls (n=212), and also any "additional psychiatric and functional burden of CTD in children with ADHD."

Chronic tic disorder (CTD) includes quite a bit under the label: "chronic motor tic disorder, chronic vocal tic disorder or Tourette syndrome" but the primary linking behaviours are quick, involuntary movements or sounds displayed/vocalised with seemingly no reason or goal. I've talked about tic disorder before on this blog (see here and see here); discussions that have also mentioned ADHD occurring alongside tic disorder so this isn't necessarily a new area of investigation [2].

Alongside finding that kids with ADHD are quite a bit more likely to present with CTD, researchers also found that ADHD + CTD seemed to be associated with other issues as per their experiencing "higher rates of internalising disorders and peer problems, and poorer quality of life than those with ADHD alone." I suppose, given the quite overt life-changing effects that a tic disorder can have, such observations are perhaps not unexpected.

"Clinicians need to consider CTD in both the initial assessment and ongoing management of children with ADHD, and address both the symptoms and the associated impairments." I don't think anyone would disagree with the concluding sentiments discussed by Poh et al. One area in particular that should not be neglected is the possibility that for some at least, tic disorder both inside and outside the context of ADHD might potentially have a bacterial origin (see here) and as such is testable and possibly treatable...


[1] Poh W. et al. Chronic tic disorders in children with ADHD. Arch Dis Child. 2018 Jan 9. pii: archdischild-2017-314139.

[2] Martino D. et al. Tourette Syndrome and Chronic Tic Disorders: The Clinical Spectrum Beyond Tics. Int Rev Neurobiol. 2017;134:1461-1490.


Thursday 22 February 2018

Pre-eclampsia increased the risk of ASD in offspring: meta-analysed

"The finding suggests a need for early screening for ASD [autism spectrum disorder] in offspring of women with pre-eclampsia."

That was the conclusion reached in the meta-analysis published by Berihun Assefa Dachew and colleagues [1] covering the literature on pre-clampsia and offspring risk of autism or ASD.

Pre-eclampsia refers to a condition/state typically occurring after about 20 weeks of pregnancy. It is characterised by a combination of symptoms including hypertension (raised blood pressure) and the presence of protein in the urine (proteinuria).

On the basis that pre-eclampsia has been mentioned as a *possible* risk factor for subsequent offspring autism diagnosis (see here), the authors set about meta-analysing the peer-reviewed research in this area covering the period up to the middle of March 2017. They eventually settled on 10 studies that suitably covered the topic; of which 5 were rated as 'good in methodological quality' and the rest, somewhere between fair and poor.

Results: most studies (7/10) reported a positive association between the presence of pre-eclampsia and offspring autism. Most studies included for meta-analysis had taken into account some potentially important confounding variables such as child gender, "maternal age and substance use during pregnancy." The overall enhanced risk of offspring autism - "pooled relative risk (RR)" - associated with intrauterine exposure to pre-eclampsia was 32% compared with non-exposed children. And with that, you can perhaps see why the authors make that call for preferential screening for autism in children exposed to pregnancy pre-eclampsia.

But one must also be a little careful with such results. Careful because studies were usually looking at one pregnancy variable and one offspring outcome. To quote the authors, studies typically "did not consistently adjust for important confounding factors such as maternal obesity, parity, gestational diabetes and infection during pregnancy" all of which have been mentioned with offspring autism risk in mind (see here and see here and see here and see here respectively). Lots of things go on during pregnancy (and indeed, before pregnancy) that *could* have a sizeable impact - alone or in combination with each other - on various offspring outcomes including risk of a diagnosis of autism.

Still the results are what they are. They invite further investigations in this area, including those relevant to the possible hows-and-whys of pre-eclampsia exposure potentially contributing to a developmental/behavioural diagnosis and what strategies might be useful to consider [2] more generally...


[1] Dachew BA. et al. Pre-eclampsia and the risk of autism-spectrum disorder in offspring: meta-analysis. British Journal of Psychiatry. 2018. Jan 24.

[2] Nordqvist M. et al. Timing of probiotic milk consumption during pregnancy and effects on the incidence of preeclampsia and preterm delivery: a prospective observational cohort study in Norway. BMJ Open. 2018; 8: e018021.


Wednesday 21 February 2018

" a parental history of T1D was associated with a 29% increased risk of being diagnosed with ADHD"

T1D mentioned in the title of this post - "a parental history of T1D was associated with a 29% increased risk of being diagnosed with ADHD [attention-deficit hyperactivity disorder]" - refers to type 1 diabetes. This is an autoimmune condition where the body's own immune system attacks 'self' and, in this case, leads to serious problems with the production of insulin with onward effects on blood sugar (glucose) levels.

The findings reported by Jianguang Ji and colleagues [1] observed something of a *correlation* between parental history of type 1 diabetes and offspring risk for ADHD. Based on the analysis of one of some of those splendid Scandinavian population registries - this time based in Sweden - researchers found upwards of 15,000 children "born after their parents were diagnosed with T1D." Bearing in mind previous research had hinted that a parental medical history of various autoimmune conditions might elevate the risk of offspring ADHD (see here), they looked-see whether "a family history of type 1 diabetes (T1D) is associated with an increased incidence of attention deficit hyperactivity disorder (ADHD) in offspring." It appeared to be so.

When taking into account various other potentially confounding variables, authors noted an overall increased risk (hazard ratio) to offspring which also appeared to fluctuate depending on whether mum or dad was diagnosed with T1D, albeit not statistically significantly so. Having said all that, this study is still one of correlation and not necessarily causation...

'Why?' is the question still to be answered. Why would an autoimmune condition with seemingly little neurodevelopmental 'connection' in terms of behavioural symptoms, raise the risk of something like ADHD in offspring? I might add that a similar question is being asked across quite a few other developmental diagnoses (see here for example). I have some ideas (see here) outside the obvious focus on blood glucose, but some solid research and science really needs to follow.


[1] Ji J. et al. Type 1 Diabetes in Parents and Risk of Attention Deficit Hyperactivity Disorder in Offspring: A Population-Based Study in Sweden. Diabetes Care. 2018 Jan 26. pii: dc170592.


Tuesday 20 February 2018

One percent of Chinese middle school students "met the definition of CFS"

CFS mentioned in the title of this post refers to chronic fatigue syndrome otherwise known as myalgic encephalomyelitis (ME). The question of how prevalent CFS/ME might be in various groups - particularly young people - was tackled in the paper published by Jieyao Shi and colleagues [1] (open-access available here). This continues some previous research chatter on this topic (see here) including the important differentiation of chronic fatigue syndrome from just 'chronic fatigue' (see here)...

So, what was done? "This cross-sectional survey enrolled 18,420 middle-school students aged 10 to 18 years (mean 14.9 ± 1.68) who were selected randomly between September 2010 and January 2011 from 25 junior- and senior-middle schools in Suzhou, China at a ratio of 1:1 with respect to the gender and grade." That's quite a big starting participant group in anyone's book; although eventually whittled down ever so slightly to 18,190 after dropping those who did not complete the study instruments properly for example.

As to the question of defining CFS (a *real issue* down the years), we are told that two schedules were used: "the US CDC-94 definition of CFS" otherwise known as the Fukuda criteria, and the "Chaldea fatigue scale (CFQ)" which is an error;  it should read the Chalder Fatigue Scale. A diagnosis of CFS was decided on the basis of both schedules yielding a positive result and "at the same time the school health workers excluded the fatigue symptoms that may be associated with other medical conditions after reviewing their yearly routine physical examination records." Where CFS criteria were not fully met, a diagnosis of chronic fatigue (CF) was given.

Results: "The prevalence of CFS and CF in this study was 0.9% and 12.0%, respectively." Nothing particularly novel there given other data that has discussed similar CFS frequency figures present in similar age-groups (see here). The idea that chronic fatigue not CFS is present in around 1 in 10 young adults is rather startling...

I was also quite interested in another observation made by Shi et al: "Other than fatigue, muscle pain, joint pain, difficulty in concentration, headache, and sore throat as specified in the CDC-94, despondency, irritability and being afraid of going to school were the most important symptoms of CFS in the middle-school students investigated in this study." Despondency, irritability and being afraid to go to school are again, probably not unexpected when it comes to CFS/ME in this age-group. I'm minded to suggest that such characteristics are likely 'reactive' symptoms to the presence of CFS/ME over and above having any significant aetiological input. If for example, you've been bed-bound, struck down by months or years of not being able to do all the things that teenagers and young adults like and want to do, it's very possible that you probably wouldn't feel your best and could, in the longer-term, be prone to developing something approaching depressive symptoms. That doesn't mean that depressive symptoms or actual depression caused your CFS/ME or even that depression is a core part of your CFS/ME; merely that depression joins the clinical presentation as per other instances in medicine [2]. As for the observation about being afraid to go to school, well, one only needs to look at other conditions where school refusal has been noted (see here) to perhaps understand some important hows-and-whys.

"Our study shows that CFS is prevalent among Chinese teenagers, and requiring proper intervention and treatment." That was the conclusion reached by Shi and colleagues, and with it the next obstacle to face: what is 'proper intervention and treatment'? Importantly too, will this manage to leave out the psychobabble explanations that have pervaded Western ideas on CFS/ME? Will it instead concentrate on the idea that CFS/ME is a multi-faceted organic illness - with probably more than one aetiology [3] - displaying both physiological and psychological side-effects?


[1] Shi J. et al. Chronic fatigue syndrome in Chinese middle-school students. Medicine (Baltimore). 2018 Jan;97(4):e9716

[2] Tang PL. et al. A Systematic Review and Meta-Analysis of Demoralization and Depression in Patients With Cancer. Psychosomatics. 2015 Nov-Dec;56(6):634-43.

[3] Mørch K. et al. Chronic fatigue syndrome 5 years after giardiasis: differential diagnoses, characteristics and natural course. BMC Gastroenterology. 2013;13:28.


Monday 19 February 2018

Behind the headline: "Autism: Scientists take 'first steps' towards biological test"

Monday 19th February 2018. I opened my computer up early in the morning and lo and behold, headlines about autism appeared, as exemplified by the BBC article titling this post: "Autism: Scientists take 'first steps' towards biological test." A cold shudder ran down my body as memories of previous 'Super-parenting' improves children's autism and similar headlines sprung to mind and with it, the question of whether big claims were being made...

The paper behind the headlines this time around was from Attia Anwar and colleagues [1] (open-access) and I have to say at first sight I was really rather interested in the specific topic under investigation. Namely: "to explore the diagnostic utility of proteotoxic biomarkers in plasma and urine, plasma protein glycation, oxidation, and nitration adducts, and related glycated, oxidized, and nitrated amino acids (free adducts), for the clinical diagnosis of ASD [autism spectrum disorder]." Interested because the words 'amino acids' (an area of interest to this blog) were mentioned and also that their description of using "stable isotopic dilution analysis liquid chromatography-tandem mass spectrometry" plays to the analytical chemistry nerd that I've seemingly become down the years.

So, bearing in mind the Anwar paper is open-access, what were the hows-and-whys of this 'first steps' research? Well, the initial premise was a sensible one as words like '3-nitrotyrosine (3-NT)' are mentioned following other research noting this compound with some autism in mind (see here). It all ties into the process of oxidative stress and neuroinflammation that are becoming more readily accepted to be part-and-parcel of at least some autism (see here and see here). Researchers set out to see if they could detect some important compounds involved in the process of protein homeostasis (amino acids are the building blocks of protein) and whether, by using the process of machine learning on the derived data (see here for another example of this being applied to autism), the possibility of a diagnostic test for autism might be forthcoming from such work. Yes, this was another example of metabolomics being applied to autism research (see here and see here) and seems to continue a research journey from members of this authorship group [2].

Urine and plasma samples were the chosen analytical media, as authors report on the recruitment of 38 children diagnosed with an ASD and 31 not-autism controls. Yet again, the words 'healthy controls' are used to denote not-autism; something that we really shouldn't be seeing in this day and age. I'd also, by the way, say the same things about the term 'neurotypical' too (see here). The autism group did seem to have quite an extensive diagnostic work-up as both ADOS and CARS scores are presented. Spot blood and urine samples were provided by all and metabolomic analysis was begun...

Results: bearing in mind the significant complexity of both urine and plasma samples when it comes to the presence of small molecules and metabolites, the use of that mass spec method made short work of detecting the glycation markers indicated for study. I note also authors also provide some results on various amino acids in both urine and plasma that is, I think, rather important.

The first thing that struck me was the authors use of a compound called creatinine to correct for sample strength and dilution. I'd like to think I know a thing or two about creatinine (urinary) in relation to some autism on the back of a bit of published research a decade or so back [3]. Our conclusion then and also in some other independent work since (see here) is that caution is required when using creatinine as a corrector with autism in mind...

Having said that, a few findings are noteworthy: "we identified changes in plasma protein AGE [advanced glycation endproductsand oxidation adducts, increased CML [Nε-carboxymethyl-lysine], CMA [Nω-carboxymethylarginine], and DT [dityrosine] and decreased 3DG-H [3-deoxyglucosone] in ASD." I'm not all too familiar with all of those compounds listed but going back to my observation on oxidative stress being something pertinent to some autism [4], I think there are some important connections to be seen. I note also that at least one of the findings - increased DT residue content of plasma proteins - might also provide a role for those trillions of wee beasties that call us home, the gut microbiota. Mention of the gastrointestinal (GI) tract in the context of autism is likely not to sit well with some people, despite multiple evidence of involvement for some in both a functional sense (see here) and also at a more biological level (see here).

Then to the headline maker: "Algorithms to discriminate between ASD and healthy controls gave strong diagnostic performance with features: plasma protein AGEs—CML, CMA—and 3-deoxyglucosone-derived hydroimidazolone, and oxidative damage marker, DT. The sensitivity, specificity, and receiver operating characteristic area-under-the-curve were 92%, 84%, and 0.94, respectively." Those sensitivity and specificity stats aren't bad at all. They are certainly on a par with other 'classification' attempts with autism in mind, such as when cortisol and a suite of cytokines got the same analytical treatment for example (see here). The trouble is that such stats are based on a relatively small sample size and indeed, children aged between 5-12 years old. Given that many children (but not all) are diagnosed quite a bit earlier than 5 years of age, one has to wonder how relevant any biological test might be at such a later age. One is left feeling that perhaps the discrimination analysis part of the Anwar paper should have perhaps been left until replication on an independent cohort with a larger sample size was carried out, and perhaps relying on more than one testing occasion.

I was also a little bit 'put out' that I couldn't find any 'limitation' discussions in the paper by Anwar et al. There was lots of chatter about how this, that and t'other might relate to biological processes pertinent to some autism but in the discussion section there was very little about what could be wrong with the results as they stand (e.g, small sample sizes). In the current age also when autism is more and more being talked about as NOT being a stand-alone diagnosis (see here) and indeed, probably is a more plural diagnosis ("the autisms"), it is always worthwhile mentioning how any obtained results might have to be framed in those contexts. Yes, authors did have exclusion criteria for study entrance: "Subjects with ascertained medical and neurological comorbidity were excluded, through a medical work up including electroencephalography (recorded during awake and sleep), cerebral magnetic resonance imaging, standard clinical and neurological examination, neurometabolic, and genetic investigations (including comparative genomic hybridization array, molecular assay for Fragile X and MECP2)" but autism pure might not be so typical in the real world [5].

Although some people have reacted quite strongly to the Anwar results, I do think this is quite a good study. No, as it stands, I don't think it can say that autism might be diagnosed on the basis of a urine and/or blood sample. Indeed, we've been here before (see here for example). But it does provide some welcome insight into some of the potential biology associated with at least some autism, and once again, champions the use of some really, really advanced metabolomic technology to provide potential systems biology insights into at least some autism...


[1] Anwar A. et al. Advanced glycation endproducts, dityrosine and arginine transporter dysfunction in autism - a source of biomarkers for clinical diagnosis. Molecular Autism. 2018; 9: 3.

[2] Anwar A. et al. Quantitation of plasma thiamine, related metabolites and plasma protein oxidative damage markers in children with autism spectrum disorder and healthy controls. Free Radic Res. 2016 Nov;50(sup1):S85-S90.

[3] Whiteley P. et al. Spot urinary creatinine excretion in pervasive developmental disorders. Pediatr Int. 2006 Jun;48(3):292-7.

[4] Rossignol DA. & Frye RE. Evidence linking oxidative stress, mitochondrial dysfunction, and inflammation in the brain of individuals with autism. Front Physiol. 2014 Apr 22;5:150.

[5] Gillberg C. & Fernell E. Autism plus versus autism pure. J Autism Dev Disord. 2014 Dec;44(12):3274-6.


"A greater understanding of ASD-related violence risk is needed to combat stigma"

This is another one of my long posts, so please, bear with me.

The topic of violence is always an emotional one. I know that even to mention the word 'violence' in the context of any label/diagnosis/condition/group carries the risk of making some people believe that there is some sort of generalisable connection. No smoke without fire eh? And one only needs to look at another label to see how a link with violence and by inference, 'dangerousness' has left a deep and long-lasting mark (see here) that continues today. So we're stuck between a rock and hard place: to talk about something and the risks attached in doing so, or just leave it, let people make their own judgements...

I've discussed quite a few uncomfortable topics on this blog down the years in light of various peer-reviewed research publications. I'm not one for shying away from calm and proportionate discussion where science - peer-reviewed science - has some vitally important input. In that context, I continue my discussions on the topic of violence and autism (see here). By doing so, I'm not making any sweeping generalisations. I'm not making any wild claims. I don't offer any brilliant insights into this topic. I'm just following the science and keeping emotions as far away from such cold, objective science as possible.

But there is a message before I continue. A message to those who might, in light of various media headlines, make some snap judgements about some of the people in your community. The message is simple: violence, in all it's forms, is not inherent to any one group. No-one is violent because of generalisations about who they are, whether on the basis of age, race, socio-economic circumstances or anything else. There are typically reasons for violence, and in many cases they're complicated. By saying all that, I'm not trying to talk down the very real effects that violence can have on individuals, families and society in general and the strong need for justice and more importantly, prevention. Just that seemingly apparent correlations and simple answers rarely provide an accurate insight into the particular hows-and-whys of violence and violent acts...

So today I'm talking about the paper published by Jill Del Pozzo and colleagues [1] who "provide a comprehensive review of the literature bearing on the relationship between ASD [autism spectrum disorder] and violent behavior." This is a timely publication because I'm sure many people have seen the word 'autism' being used among the coverage of a quite horrendous act recently. Indeed, even Del Pozzo et al allude to other similar attention: "Over the last decade, there has been increased media attention focused on the relationship between ASD [autism spectrum disorder] and violent behavior due to a number of school shootings and high-profile criminal cases involving offenders with alleged ASD diagnoses."

Perhaps I need to mention that the word/description 'violence' covers a lot of ground. It of course covers violence against others, whether on an individual or collective basis, but importantly, also covers violence in many other forms including against oneself in the form of self-injury and/or self-abuse. Most media coverage of violence covers violence against others. But I'd wager that violence against oneself is the predominant form of violence in many circumstances minus any big headlines...

Del Pozzo et al set about providing a "comprehensive review of the literature" on autism and violence. Following their surveying of the current peer-reviewed research literature in this area, the authors concluded that whilst a diagnosis of autism is by no means protective of someone committing a violent act, there is generally more peer-reviewed scientific support for the idea that "ASD does not cause violence" over and above the sometimes negative media portrayals of the label in this context (see here). A welcome conclusion it has to be said, and one that needs to be circulated widely; but again, minus any sweeping generalisations and bearing in mind that science is all about probability not absolutes.

There are caveats to the statement that 'ASD does not cause violence' insofar as the multiple observations that autism typically does not exist in a diagnostic or social vacuum (see here), and how various factors (environment, psychiatric comorbidity, criminality) can potentially elevate the risk of violence for some people. All of this is not about passing the diagnostic buck (see here) as some people quite unceremoniously have decided to do, but needs to be mentioned; particularly in light of these days where 'autism plus' [2] is more typically the norm (see here) over and above the label of autism existing as some sort of stand-alone diagnosis. The pertinent question therefore may not necessarily be one of 'does autism cause violence?' but rather what role autism may or may not play [3] when it comes to violence, taking into account an often very complicated, very individual clinical picture. I say this also acknowledging that a diagnosis of autism is not some 'magical status' automatically reserved only for 'good people' (see here); just as any other behavioural/psychiatric label does not similarly distinguish between 'good' and 'bad' people.

As per the title of this post utilising a quote from Del Pozzo and colleagues - "A greater understanding of ASD-related violence risk is needed to combat stigma" - there is a pressing need to further understand how and why violence can/does occur for some alongside the label of autism or rather autism plus. Whether as part of the often nebulous term that is 'challenging behaviours' (see here) or in other related contexts (importantly also including that self-aggression angle), trying to answer such how/why questions can only be of benefit to all concerned. Indeed, alongside another quite sweeping generalisation made by Del Pozzo et al that: "Violence results from undetected or untreated third variables (e.g. psychosis)" and "Individuals with ASD have an elevated risk of psychosis", various lessons continue to be learned [4] (see here also) albeit stressing how complicated any relationship is likely to be [5]. As I mentioned before, easy answers are not likely to forthcoming.

Finally, I want end by again introducing the concept of 'vulnerability' in the context of autism into proceedings. I'm not specifically talking about vulnerability to various comorbidity that 'probably' influence the presentation of violence in the context of autism, but rather vulnerability in more general terms (see here). The writings of Tom Berney [6] provide some particularly insightful details on such vulnerability in relation to violent and other offending acts within the context of some autism or rather some 'autism plus'. Such vulnerability issues stress how, minus hype or sensationalism or indeed any calls for censorship in this most delicate area, investigations need to continue and sensitively continue without stigmatising and without further disadvantaging an already quite disadvantaged community...


[1] Del Pozzo J. et al. Violent behavior in autism spectrum disorders: Who's at risk? Aggression and Violent Behavior. 2018. Jan 31.

[2] Gillberg C. & Fernell E. Autism plus versus autism pure. J Autism Dev Disord. 2014 Dec;44(12):3274-6.

[3] Allely CS. et al. Violence is Rare in Autism: When It Does Occur, Is It Sometimes Extreme? J Psychol. 2017 Jan 2;151(1):49-68.

[4] Långström N. et al. Risk factors for violent offending in autism spectrum disorder: a national study of hospitalized individuals. J Interpers Violence. 2009 Aug;24(8):1358-70.

[5] Bell V. et al. A symptom-based approach to treatment of psychosis in autism spectrum disorder in October 2017. BJPsych Open. 2018 Jan;4(1):1-4.

[6] Berney T. Asperger syndrome from childhood into adulthood. Brit Journal Psych Advances. 2044; 10: 341-351.


Saturday 17 February 2018

The 'oral microbiota' and autism: the power of a spit sample

Although not everyone's cup of tea there's a lot that can be learned from a humble spit (saliva) sample. Buccal epithelial cells from saliva samples provide a medium for the collection and analysis of DNA for example, and alongside, make for a much less invasive collection method than DNA capture from blood samples for example. Saliva also has it's own metabolome, meaning that one can potentially get quite a bit of information on quite an extensive library of small molecules linked to various genetic and biological processes.

Now add the oral microbiota to the list and, as per the findings reported by Yanan Qiao and colleagues [1], how the oral cavity (i.e. the mouth) is home to a complex network of bacteria and relations that might provide some important clues pertinent to various diagnoses.

Autism was the particular diagnosis in the research spotlight this time around, as authors "collected samples from two distinct intraoral habitats, including saliva and dental plaques, in children with and without ASD [autism spectrum disorder]." Analysing over 100 samples provided by 32 children with ASD and 27 not-autism controls, a few interesting things were noted in the results published by Qiao et al.

Bearing in mind this was a cross-sectional study which relied on a 'snapshot' sample over only one testing occasion, authors reported that: (a) data on bacterial richness and diversity showed no significant differences in salivary samples across the groups, but a difference was reported based on examination of those dental plaque samples; (b) "the phylum Proteobacteria was more abundant in ASD patients (both in salivary and dental samples) compared to controls" whilst other phyla predominated in controls; (c) "increased amounts of potential pathogens, including Haemophilus, Corynebacterium, Cardiobacterium, Kingella, Streptococcus and Rothia, were observed in ASD patients" some of which correlated with the measurement of the severity of autism (via parental report on the Aberrant Behavior Checklist (ABC) questionnaire); and (d) "diagnostic models based on key microbes were constructed, with 96.3% accuracy in saliva."

Of course, there is still some way to go in this research area, not least starting with independent replication of the Qiao results perhaps also relying on multiple samples provided across a range of times and situations. Y'know, assuming that medication for example, could be part and parcel of the profile with autism in mind and indeed remembering that autism as a stand-alone label is probably less like 'real-life autism' than many people realise (see here). I'm also a little unsure as to why the Aberrant Behavior Checklist (ABC) was employed "to preliminarily evaluate the severity of ASD" when both so many controls were employed for inclusion/exclusion on the study and so many other more 'autism-specific' instruments are quite freely available (see here for one example). There are things that could have been done differently for sure...

But, this is a good first attempt. It puts the oral microbiome on the research map with autism in mind, added to the more well-known relation: the gut microbiome (see here). It also provides us with a more generalised view of how the bacteria and various other miniature beasties around us, are probably more intricately involved in our lives than we ever previously thought possible...


[1] Qiao Y. et al. Alterations of oral microbiota distinguish children with autism spectrum disorders from healthy controls. Scientific Reports; 8: 1597.


Friday 16 February 2018

Autism, mental health and 'sexual and gender minority' status

The findings reported by Rita George & Mark Stokes [1] piqued my interest recently, and their conclusion that various mental health issues over-represented in autism (see here and see here for examples) might not be just solely connected to the presence of a diagnosis of autism.

Yes, I know this sounds like common sense (see here), but as I've come to realise in relation to lots of diagnostic labels, assumptions very often precede actual (peer-reviewed) evidence.

Based on responses on the DASS-21 (which is fast becoming the go-to measure for the self-report of things like stress, depression and anxiety-like behaviours with autism in mind [2]), researchers compared depression, anxiety and stress scores for over 300 people with autism compared with over 250 "typically-developing individuals." Alongside, membership of a minority grouping in terms of sex and gender, e.g. non-heterosexual, was also thrown into the statistical mix. Results suggested that along with differences in DASS scores being more generally observed between the groups: "As membership to a minority group became more restrictive, mental health symptoms worsened... suggesting stressors added."

Such an investigation follows a scheme of work by this authorship group who, quite recently, also reported that within the same participant group(?), some 70% of those with autism "reported being non-heterosexual" [3]. I was quite taken aback by the high rate of non-heterosexuality reported in this study, bearing in mind that this data was derived from an on-line sample and may not be entirely representative of the full autism spectrum as a function of the use of self-report for example (see here). I might also add that focusing just on autism to the exclusion of some other potentially important comorbid labels [4] could be something that needs to be looked at in future investigations in light of other results on gender variance for example [5].

Minus however, any 'I told you so' sentiments, I have previously mentioned about how gender and sexual identity in relation to autism is both a research-rising area and can often have some quite profound implications for the person concerned (see here). We can um-and-ah about whether there is a 'connection' between autistic traits and sexual orientation (see here) or whether something like gender dysphoria is more or less likely in the context of autism (see here), but there is no denying that gender and sexual identity are variables that can and do potentially impact on mental health. In support of the George/Stokes findings, one need only look to the non-autistic focused research literature to see how various aspects of health-related quality of life for example, are seemingly influenced by variables such as sexual orientation [6] and how this potentially plays out over both childhood and into adulthood [7].

So when George & Stokes talk about: "Specialized care is recommended for this vulnerable cohort" there could be some pretty profound implications associated with timely and appropriate education and support taking into account sexual and gender identity in the context of autism...


[1] George R. & Stokes MA. A Quantitative Analysis of Mental Health Among Sexual and Gender Minority Groups in ASD. J Autism Dev Disord. 2018 Jan 23.

[2] Nah YH. et al. Brief Report: Screening Adults with Autism Spectrum Disorder for Anxiety and Depression. J Autism Dev Disord. 2017 Dec 2.

[3] George R. & Stokes MA. Sexual Orientation in Autism Spectrum Disorder. Autism Res. 2018 Jan;11(1):133-141.

[4] May T. et al. Trends in the Overlap of Autism Spectrum Disorder and Attention Deficit Hyperactivity Disorder: Prevalence, Clinical Management, Language and Genetics. Current Developmental Disorders Reports. 2018. Jan 17.

[5] Strang JF. et al. Increased gender variance in autism spectrum disorders and attention deficit hyperactivity disorder. Arch Sex Behav. 2014 Nov;43(8):1525-33.

[6] Marti-Pastor M. et al. Health-related quality of life inequalities by sexual orientation: Results from the Barcelona Health Interview Survey. PLoS One. 2018 Jan 24;13(1):e0191334.

[7] Petterson LJ. et al. Sex, Sexual Orientation, Gender Atypicality, and Indicators of Depression and Anxiety in Childhood and Adulthood. Arch Sex Behav. 2017 Jul;46(5):1383-1392.


Thursday 15 February 2018

Walking as an intervention for good psychological health: number of steps or just enjoyment?

I'm once again returning to the topic of walking for health on this blog (see here) and some rather intriguing findings reported by Karen Hallam and colleagues [1] suggesting that adoption of a 100-day 10,000 steps a day program might have some bearing on aspects of mental and psychological health and wellbeing. But there's a bit of a twist...

The activity program in question was something called Stepathlon which, from what I gather, is a corporate initiative to promote health and fitness among employees. I might add that some employees in some occupations probably don't need such initiatives (see here). Various steps (pardon the pun!) are listed on the Stepathlon website including 'forming a team of 5 with your colleagues', getting yourself a pedometer or other fitness tracker that measures steps and then uploading your daily data on to their platform where it is compared with other groups across the world.

Hallam et al report results for nearly 2000 participants based on 'de-identified' data; also including participant reports based on the completion of the "short form of the Depression, Anxiety Stress Scales (DASS)" and the "Warwick-Edinburgh Mental Wellbeing Scale (WEMWBS)." The various strands of data were analysed, correlated and the like.

Results: "The results of this study highlight some psychological and wellbeing benefits of being engaged in work based 10,000 step programs." The authors talk about observing a nearly 9% reduction in stress levels, 8% reduction in 'signs of depression' and a 5% reduction in anxiety when comparing pre-program with post-program data. They add: "This reinforces the benefits of this type of exercise regimen as playing a small yet significant role in improving mental as well as physical health."


Things were not however completely straight-forward as the authors also talk about a "lack of a dose response" in terms of the number of steps completed and those psychological health and well being parameters being assessed. This could denote a few things: (a) participation in a program that encourages walking - walking in a group setting - may be beneficial irrespective of the number of steps that are actually taken, and/or (b) the wide variability in the number of daily steps taken over the course of the program - remember it lasted 100 days - scuppers any chance of getting meaningful correlation data between walking and psychological health. Indeed on that last point, authors mention that future work should really take into account things like the self-report nature of uploading daily activity levels and also the fact that within the sample there were "clearly individuals who were more active before commencing the program" and for whom such an intervention might not be all that effective given their already raised starting activity levels.

Still, I do think that this is a good piece of research that should encourage further investigation. Aside from the significant physical health benefits associated with getting more active, I'd also like to think that such a program could be further adapted for various groups, particularly when things like stress, depression and anxiety are considered a part of the clinical picture. Autism springs to mind as one such avenue for further study, based on various evidence [2] including result similarly using the DASS-21 tool. Indeed, on another blogging occasion where I critically discussed the suggestion that "
autism acceptance could contribute to mental health in autism" (see here) again based on DASS scores, I wonder if a group walking 'intervention' (although I'm not so sure about medicalising such an activity) could also be the topic of more study too, added to other research?

And finally... bearing in mind that exercise might have some nootropic value for some (see here and see this recent study [3]), it seems that much of the chatter about sitting around video game playing fostering "a broad range of cognitive abilities such as visual processing, attention, spatial ability, and cognitive control" is not readily supported by the current peer-reviewed evidence...


[1] Hallam K. et al. “Happy feet”: evaluating the benefits of a 100-day 10,000 step challenge on mental health and wellbeing. BMC Psychiatry. 2018; 18: 19.

[2] Nah YH. et al. Brief Report: Screening Adults with Autism Spectrum Disorder for Anxiety and Depression. J Autism Dev Disord. 2017 Dec 2.

[3] Gmiąt A. et al. Improvement of cognitive functions in response to a regular Nordic walking training in elderly women - A change dependent on the training experience. Exp Gerontol. 2018 Feb 9. pii: S0531-5565(17)30663-0.