Saturday, 18 November 2017

Probiotics degrading gluten peptides - part 4

Here we go again. Probiotics degrading gluten peptides part 4 adds to previous posts on this topic (see part 1 here, part 2 here and part 3 here).

The difference this time around? People. People actually eating a a test meal containing gluten - "a porridge containing 0.5 g gluten" - and being given a potential gluten-degrading preparation - "Aspergillus niger-derived prolyl endoprotease (AN-PEP)" - or a placebo whilst their gastric and duodenal content was sampled for gluten concentrations over a 3-hour period after. So described the results published by Julia König and colleagues [1] continuing a research theme from this group [2].

AN-PEP was the product under the research spotlight following some previous scientific findings [3] suggesting that unlike various other digestive enzyme supplements, this stuff showed some pretty good actions/effects on immunogenic gluten peptides. Following a "randomized placebo-controlled crossover study" design, researchers followed 16 participants "with self-reported gluten sensitivity" (but not coeliac disease or wheat allergy) across 3 test days when on each day either a high dose of AN-PEP was given, or a low dose of AN-PEP was given or a placebo was given. Details of the high and low doses included: "The low dose tablets provided 83300 Protease Picomol International (PPI), and the high dose 166700 PPI of AN-PEP enzyme (1 PPI is the amount of enzyme that releases one picomole of p-nitroaniline per second under defined assay conditions)."

This was quite an invasive study as researchers had to gain access to parts of the gastrointestinal (GI) tract of participants and so: "Subjects attended each test day after an overnight fast, and a multi-lumen nasoduodenal catheter was placed with one lumen tip in the gastric antrum and one lumen tip 15 cm lower in the duodenum." It was then a case of drawing off stomach and duodenal samples and analysing for gluten content. Further: "success of AN-PEP in degrading gluten was defined as at least 50% gluten degradation compared to placebo, calculated as area under the curve (AUC) over 180 min."

Results: "It actually works" was a quote from one of the authors of the paper in previous media attention of this study before peer-reviewed publication. "In the stomach, gluten levels were reduced from 176.9 to 22.0 in the high dose and to 25.4 μg × min/ml in the low dose. In the duodenum, gluten levels were reduced from 14.1 in the placebo to 6.3 in the high dose and to 7.4 μg × min/ml in the low dose." AN-PEP appeared to be doing its designated job. Importantly too: "No severe adverse events were reported" over the course of the study period.

Scientific replication is the name of the game following the König results. Replication with larger sample numbers and also potentially looking at whether such a preparation might be useful for those diagnosed with something like coeliac disease or other accepted immune-related pathology linked to gluten consumption. I say that acknowledging that a gluten-free diet is the best that science and medicine currently has for the management of coeliac disease. The authors also note that they "did not perform a double-blinded placebo-controlled gluten challenge as sometimes suggested to confirm the diagnosis of gluten sensitivity" in their participants. This kinda intersects with the continuing discussions about what non-coeliac gluten/wheat sensitivity actually is (see here).

"In conclusion, our study showed that the AN-PEP enzyme is effective in degrading small amounts of gluten as part of a complex meal in the stomach. Even though the use of AN-PEP is not intended to replace a gluten-free diet in gluten-related disorders, it appears to be effective as a digestive aid protecting against the unintentional intake of gluten." I can't argue with that and look forward to seeing more on this topic in future.


[1] König J. et al. Randomized clinical trial: Effective gluten degradation by Aspergillus niger-derived enzyme in a complex meal setting. Sci Rep. 2017 Oct 12;7(1):13100.

[2] Salden BN. et al. Randomised clinical study: Aspergillus niger-derived enzyme digests gluten in the stomach of healthy volunteers. Aliment Pharmacol Ther. 2015 Aug;42(3):273-85.

[3] Janssen G. et al. Ineffective degradation of immunogenic gluten epitopes by currently available digestive enzyme supplements. PLoS One. 2015 Jun 1;10(6):e0128065.


Friday, 17 November 2017

On iron and vitamin D and autism

"This study suggests that deficiency of iron and Vitamin D as well as anemia were more common in autistic compared to control children."

'This study' refers to the findings reported by Abdulbari Bener and colleagues [1] (open-access available here) who set out to "investigate iron deficiency anemia and Vitamin D deficiency among autism children" in Qatar, a part of the world not renowned for its 'lack of sunshine' (a source material for the production of vitamin D).

Looking at some 300 children diagnosed with an autism spectrum disorder (ASD) and an equal number of controls, not-autism controls "who visited the primary health-care centers", researchers concluded that as a group, those with autism were more likely to present with low serum iron levels (and various related measures) and further that: "Vitamin D deficiency was considerably more common among autistic children." The authors provide some background details on what constitutes vitamin D deficiency and other 'levels': "Participants were classified into four categories: (1) severe Vitamin D deficiency, 25OHD <10 ng/ml; (2) moderate deficiency, 25OHD 10–19 ng/ml; (3) mild deficiency, 25OHD 20–29 ng/ml; and normal/optimal level is between 30 and 80 ng/ml."

When attempting to ascertain what factors might be important to the autism vs. not-autism participants, researchers reported that: "serum iron deficiency, serum calcium levels, serum Vitamin D levels; ferritin, reduced physical activity; child order, body mass index percentiles, and parental consanguinity can all be considered strong predictors and major factors associated with autism spectrum disorders." I might add that consanguinity defined as "unions between couples who share at least one common ancestor" is perhaps something more 'culturally-relevant' to autism in certain countries and societies [2] but not necessarily widely applicable...

What's more to say about the Bener findings? Well, given that issues with iron (see here) and issues with vitamin D (see here) are no strangers to the autism research landscape, there is little novelty in the conclusions reached even if being "the first report on an establishing level of iron deficiency in children with autism in Qatar and in Arabian Gulf Countries." The implication is again that preferential screening and treatment of such issues should be offered when a diagnosis of autism is received, save any further health inequalities arising. Whether or not treating something like iron deficiency and/or vitamin D issues will impact on behavioural presentation (see here) is perhaps an issue for another day. I say this bearing in mind the sentiments expressed in the recent paper by Philippe Autier and colleagues [3] examining the collected data on vitamin D supplementation "on non-skeletal disorders" and results seemingly "strengthening the hypothesis that low vitamin D status is a consequence of ill health, rather than its cause."


[1] Bener A. et al. Iron and vitamin D levels among autism spectrum disorders children. Ann Afr Med. 2017 Oct-Dec;16(4):186-191.

[2] Mahajnah M. et al. Clinical characteristics of autism spectrum disorder in Israel: impact of ethnic and social diversities. Biomed Res Int. 2015;2015:962093.

[3] Autier P. et al. Effect of vitamin D supplementation on non-skeletal disorders: a systematic review of meta-analyses and randomised trials. Lancet Diabetes Endocrinol. 2017 Oct 25. pii: S2213-8587(17)30357-1.


Thursday, 16 November 2017

Sleep and gut issues in autism: a clinically relevant subtype?

"Autistic children with gastrointestinal or/and sleep problems may represent clinically relevant subtypes of ASD [autism spectrum disorder], for which targeted treatments may be needed."

That was one of the conclusions reached by Xiao-Lei Yang and colleagues [1] looking at an interesting combination of symptoms/conditions that have featured before on this blog (see here and see here): gastrointestinal (GI) and sleep issues with autism in mind.

Surveying around 170 children diagnosed with an autism spectrum disorder (ASD) and a similar number of "healthy children" (authors words, most definitely not mine), researchers sought to estimate the prevalence of GI and sleep issues among their cohort(s). Perhaps unsurprisingly "GI and sleep problems were prevalent in Chinese ASD children." Interestingly too: "ASD children with GI symptoms reported more severe ASD core symptoms than others." Those with sleeping issues also showed "lower performance in daily living skills, social cognition, social communication and intellectual development" than the children with ASD who did not present with sleeping issues.

The implications of such observations? Several. Not least that when one talks about GI issues  - whether functional or more pathological - being over-represented in relation to autism, one has some confidence that such 'over-representation' seems to cross different ethnicities and different countries and is not just derived from or based on Western research findings. This adds further weight to the notion that at least some types/phenotypes of autism may have a significant bowel-related component to them for whatever reason(s).

Next, the suggestion that children with autism who also present with GI symptoms might present with a more 'severe ASD core symptoms' profile provides some truly tantalising clinical and research opportunities. Not least that said bowel symptoms might be able to affect some aspects of behaviour and onward the question: what happens when bowel symptoms are effectively treated? I know such sentiments are not necessarily welcomed in some quarters ('autism symptoms are lifelong and immutable' so the saying goes) but for others, particularly those suffering with bowel symptoms (yes, I did say suffering), there are some potentially interesting consequences following intervention. Assuming also that pain and discomfort are key parts of 'suffering' from bowel issues in autism as they are when present in not-autism, we arrive at a situation whereby certain autistic traits may be at least 'heightened' when pain is present. Such a proposition is not necessarily new news to the peer-reviewed autism research (see here and see here). And if one was to assume that something like 'inflammation' might be part and parcel of said GI issues and pain in relation to autism, we arrive at yet another testable hypothesis (see here)...

Finally, sleep issues in relation to the autism spectrum. What's more to say? They are pretty prevalent throughout children and adults on the autism spectrum and probably contribute to the various 'quality of life' disparities that have been shown in relation to autism (see here). There are things that can be 'tried' in relation to intervention (see here and see here for examples) but by no means is there some 'magic wand' that helps every single sleep issue for every single person. The idea that sleep issues, like GI issues, might also impact on certain behavioural aspects linked to autism is probably not unexpected but I would like to see a lot more research done in this area before any grand sweeping generalisations are made. Not least recognising that certain over-represented behavioural comorbidity such as attention-deficit hyperactivity disorder (ADHD) is rising through the sleep research ranks (see here) and what that might mean for autistic traits in these ESSENCE-like times...


[1] Yang X-L. et al. Are Gastrointestinal and Sleep Problems Associated with Behavioral Symptoms of Autism Spectrum Disorder? Psychiatry Research. 2017. Oct 24.


Wednesday, 15 November 2017

Loneliness --> low self-esteem ---> depression?

It was the findings reported by James McCauley and colleagues [1] that prompted today's post. Working on the basis that "there have been few comprehensive investigations of self-esteem in children and adolescents with autism spectrum disorder (ASD)" researchers set out "to assess how youth with ASD rate their self-esteem compared to age-matched TYP [typically developing] youth." Further, how levels of self-esteem (or not) might onward influence "internalizing psychopathology", the fancy phrase for issues such as depression and anxiety.

I don't typically go for grand theories and sweeping generalisations on this blog, particularly when referencing the very large and very diverse autism spectrum. I've not moved over to the 'dark side' of generalisation in this post but am particularly interested in the some of the *associations* talked about my McCauley et al.

Specifically how: "youth with ASD rated their self-esteem significantly lower than did TYP youth" and how self-esteem was "strongly related to depression." Add in the findings reported by Micah Mazurek [2] who observed that "loneliness was associated with increased depression and anxiety and decreased life satisfaction and self-esteem" and some potentially important processes emerge as per the equation titling this post: Loneliness --> low self-esteem ---> depression?

McCauley and colleagues do also talk about how Theory of Mind (ToM) also showed some possible *associations* to elements of their results but I'm not really minded to go into this part of their findings with any great detail. It's not that I don't believe that ToM might not be an issue for some on the autism spectrum, but rather as other results have suggested [3], questions still remain about what ToM actually means and whether other issues (i.e. alexithymia) might predominate in relation to some autism [4] (where the stress is on 'some').

I don't doubt that there are several other important elements potentially influencing things like self-esteem in relation to autism and how it can lead to issues such as depression (see here). Further studies are needed on this topic, including drawing on the autism-not-specifically-mentioned research literature [5]. But insofar as the simplistic relationship set out in the post, there is an obvious area ripe for intervention: loneliness. And on that point, there are options available (see here) if and when desired; accepting that not everyone wants (or needs) lots of people around them all of the time. This perhaps is also where the online world (in moderation) can also come into it's own [6] (I repeat 'in moderation').

Finally, I'll be coming to the findings reported by Cage and colleagues [7] in the not-too-distant-future talking about how "personal acceptance significantly predicted depression" in the context of autism and what role self-esteem might play here too (minus too much psychological fluff and ToM chatter)...


[1] McCauley JB. et al. Self-Esteem, Internalizing Symptoms, and Theory of Mind in Youth With Autism Spectrum Disorder. J Clin Child Adolesc Psychol. 2017 Oct 19:1-12.

[2] Mazurek MO. Loneliness, friendship, and well-being in adults with autism spectrum disorders. Autism. 2014 Apr;18(3):223-32.

[3] Oakley BF. et al. Theory of mind is not theory of emotion: A cautionary note on the Reading the Mind in the Eyes Test. J Abnorm Psychol. 2016 Aug;125(6):818-23.

[4] Trevisan DA. et al. Alexithymia, but not autism spectrum disorder, may be related to the production of emotional facial expressions. Mol Autism. 2016 Nov 11;7:46.

[5] Sowislo JF. & Orth U. Does low self-esteem predict depression and anxiety? A meta-analysis of longitudinal studies. Psychol Bull. 2013 Jan;139(1):213-240.

[6] Sundberg M. Online gaming, loneliness and friendships among adolescents and adults with ASD. Computers in Human Behavior. 2017. Nov 1.

[7] Cage E. et al. Experiences of Autism Acceptance and Mental Health in Autistic Adults. J Autism Dev Disord. 2017 Oct 25.


Tuesday, 14 November 2017

Breastfeeding and autism meta-analysed

"This meta-analysis provides evidence that breastfeeding (exclusively or including additional supplements) may protect against ASD [autism spectrum disorder]. Prospective longitudinal research is required to disentangle the complex relationships and to explore potential pathophysiological mechanisms."

So said the systematic review and meta-analysis published by Ping-Tao Tseng and colleagues [1] covering a [complicated] topic that has been discussed on this blog before (see here). I should mention that I was part of the 'and colleagues' bit to this latest paper; something that will in no way interfere with my hopefully critical musings on this latest publication.

Bearing in mind "a controversial relationship between ASD and breastfeeding" that exists in the peer-reviewed literature and the strong requirement not to make new mums feel bad just because they don't want to or can't breastfeed, the aim of the meta-analysing game was to synthesise the collected research literature into something like a coherent 'where we're at' statement. Seven studies out of a possible 20 were included for review, together including nearly 1500 children diagnosed with ASD and nearly 1200 not-diagnosed-with-autism controls.

Results: "Cumulatively, children with ASD, either in the form of clinical diagnosis or self-report, were significantly less likely to have been breastfed than children without ASD." I should add that 'self-report' refers to parents reporting on their child receiving a diagnosis of autism but not necessarily being independently confirmed by researchers or medical records. The strength of the association/effect was not to be sniffed at; with results even holding up when taking into account those "who were breastfed with additional supplementation."

Another important quote: "one should note the observational nature of these preliminary findings, whereby causation can clearly not be determined." What this means is that whilst variable A (breastfeeding) and variable B (autism or ASD) might be *associated* it is nigh on impossible to definitively say whether variable A *causes* or *protects against* variable B on the basis of the studies analysed. I might also suggest that the call for 'prospective longitudinal research' is also not likely to provide a definitive answer any time soon either, when taking into account how many other variables might be associated with risk of offspring autism and indeed, the plurality of the label and some related discussions on that topic (see here and see here). It's also noteworthy that autism rarely exists in some sort of diagnostic vacuum (see here) and how breastfeeding trends might be important there too [2] thus complicating any 'causative' picture.

Still, the Tseng results do provide some further information about this issue and a reiteration of the value of breastfeeding for many different reasons. Other studies have arrived at a similar conclusion insofar as the impact that breastfeeding *might* have on 'autistic traits' [3]; again, with more research to do.

Mechanisms of effect? Well, once again we're faced with a 'we don't know yet' scenario. Tseng et al speculated on various possible factors linked to breastfeeding and breast milk 'ingredients' that may be important (neurotrophic factors, oxytocin, fatty acid constitution, casomorphins) and could conceivably impact on risk of offspring autism. I'm also minded to add in the idea that the early presentation of autism in the first months of life [for some] could also potentially affect breastfeeding patterns; perhaps making breastfeeding practices more difficult and/or contributing to the early cessation of breastfeeding in some cases. Relevant mechanisms are likely to be complicated.

I appreciate that not everyone is going to be enthralled with this study or topic - no, it doesn't say that a lack of breastfeeding causes all autism - particularly when words like "protect against ASD" are also included in the text. All I can say is that we faithfully looked at the existing peer-reviewed research available to us in this area and went where the data instructed us to do so without fear or favour...


[1] Tseng P-T. et al. Maternal breastfeeding and autism spectrum disorder in children: A systematic review and meta-analysis. Nutritional Neuroscience. 2017. Oct 18.

[2] Bar S. et al. Long-term neurodevelopmental benefits of breastfeeding. Curr Opin Pediatr. 2016 Aug;28(4):559-66.

[3] Boucher O. et al. Association between breastfeeding duration and cognitive development, autistic traits and ADHD symptoms: a multicenter study in Spain. Pediatr Res. 2017 Mar;81(3):434-442.


Monday, 13 November 2017

Who speaks for who in relation to autism?

I'm probably stirring up a hornet's nest by writing this post around the findings reported by Karin Jongsma and colleagues [1] touching on the subject of 'who speaks for who' in autism advocacy, but thought it an important topic to approach. Not least because in some quarters, there are some quite heated discussions being had (mainly, and unsurprisingly, across social media and related platforms) concerning representation across various organisations and initiatives with a focus on autism. The question at the heart of such debates is: 'Who should be the primary voice(s)?' when it comes to things like decision-making about research and policy in the context of autism, both at an individual and group level? It's not a new debate by any means and such discussions will likely be part of the autism landscape forever more...


"The inclusion of people with a 'neuro-psychiatric' condition poses a particular challenge for the organizational processes and political representation of such collectives" was the starting point for Jongsma et al. I'm not very philosophically literate so can't really tell you too much about the use of 'epistemic injustice' as a framework by Jongsma, outside of it being an idea that includes 'testimonial injustice' meaning "prejudices that cause one to "give a deflated level of credibility to a speaker's word".

The authors conducted interviews with a number of patient organisation (PO) representatives and concluded that: "persistent stereotypes hamper the inclusion of affected members both within POs and on the health political level." Further: "Being affected causes distrust in having the 'capacity to know' in a two-fold way; it is assumed that those who can represent themselves are "not affected enough" to present valuable insights into the condition and those who have difficulties to express themselves due to their condition are excluded because of their affectedness."

That last sentence kinda hits the nail slap-bang on the head when it comes to many of the discussions around 'who speaks for who' in the context of autism. Remembering that autism is about as heterogeneous as it comes with regards to the huge range of abilities and disabilities covered under the spectrum label, many, if not all, arguments about representation stem from perspectives on whether the so-called 'able' are able/allowed/qualified to speak for the so-called 'not so able' and the apparent lack of the 'not so able' to have an appropriate voice, thus relying on proxy voices such as their parents and/or primary caregivers. The bold emphasis was added by me just in case you ask. Such issues are also positioned in the context of tenets such as: 'if you've met one person with autism, you've met one autistic person' (or words to that effect) and older adages about 'mother (or father) knowing [their child] best'. The fact that Jongsma et al also included dementia in their study - another condition/label/state where ability and disability is pretty heterogeneous - is also worth noting.

I'd advance the idea that there is no right or wrong answer in the debate on who speaks for who when it comes to autism. Certainly, further grand sweeping generalisations in relation to autism are not required. The moves to encourage greater participation by #actuallyautistic people are to be welcomed and reflect many factors such as the rise and rise of numbers of people being diagnosed with autism (some rather late in life) and how again, social media in particular, is providing an important tool to voice wants, needs, hopes, fears, concerns, vision and lots more when it comes to the lives of those on the autism spectrum. Various different sorts of group identities are emerging/have emerged as many, particularly adults with autism / autistic adults (see here), have come together. Sometimes this is under the banner of neurodiversity and the principles which it includes; other times not, or with more specific issues in mind. Without getting too 'reflective' on the topic, the autism/autistic group identities emerging probably also help fill an important gap, taking into account all the chatter down the years about how loneliness and isolation are very much over-represented and onward how the desire to 'belong' has been too long neglected in the context of autism.

It's also fair to say that not everyone diagnosed on the autism spectrum is 'part of the conversation' bearing in mind the 'nothing about us without us' mantra. There are many children and adults with autism for whom such debates on advocacy are probably not as big a concern as overcoming various day-to-day issues; be they based on the effects of core autism presentation or other important comorbidities such as epilepsy or gastrointestinal (GI) issues. For many of this group, their voice is their parents and/or primary caregivers and will be for the rest of their lives. By saying all that I'm not falling into the whole 'high' and 'low' functioning narrative about 'who's the more disabled'. I'm simply acknowledging that some people on the autism spectrum can't and probably won't ever participate in discussions about 'who speaks for them' and therefore their own voices are heard only through their parents/caregivers, siblings or significant others. I know some people will say that we aren't trying hard enough to give this section of the autism spectrum a voice, but right or wrong, that's where we currently stand.

What can be done to improve the situation and perhaps bridge any gulf between voices from the spectrum and proxy voices from the spectrum? Well, there's no easy fix because yet again, heterogeneity rules. It would be unwise to assume that every actually autistic adult who can vocalise or communicate wants the same thing for themselves or any group they feel allied to, just as any sweeping generalisations that every non-communicating person with autism (I don't know how else to describe this group) or parent/primary caregiver wants the same thing are likely untrue. I think this is an important point to raise particularly when for example, the social model of disability - "disability is caused by the way society is organised, rather than by a person’s impairment or difference" - can too often be assumed to be a significant part of the vocal autism agenda, seemingly at the expense of acknowledging some very real disabilities. It's not, for example, difficult to imagine how such an extreme sentiment might sound to the parent or caregiver of a child/adult who requires significant day-to-day care and is very much disabled as a result of their autism and the issues it brings, irrespective of societal organisation. This also goes for those 'autism as a superpower' and related statement(s) which have been mentioned down the years. How such sweeping generalisations, seemingly contrary to the diagnostic tenets of autism, may well reflect individual perceptions and abilities of autism, but often do very little to forward the agenda of those severely impacted by their autism and their representation (including in the lay media).

There are substantial benefits to be had from listening to the many voices from the autism spectrum particularly when it comes to outcomes and events that will likely impact them as individuals and/or other groups on the spectrum. Similar sentiments are being discussed with other labels in mind too. I note for example, there are quite a few autistic voices that provide both informative and compassionate 'middle-ground' on many topics related to the details included in this post and the Jongsma paper. Importantly too that some are also not afraid to critique some of the tenets of neurodiversity (and by virtue, the misnomer of 'neurotypical' that has seemingly pervaded autism science and practice). These are important voices not just because of the accounts and experiences they provide, but also because theirs provides a hint of what challenges/successes might be 'more likely to occur' when a person is diagnosed with autism. Further, they do to some extent, provide an opportunity to positively act on such issues for the benefit of the person themselves and others who may not be in such a fortunate [communicative] position.

But also there is no reason why autistic voices cannot be complemented by hearing the equally important messages that parents and primary caregivers - the people who raise and mould children - can bring to the discussion table too. This also includes the 'teachings' of a rapidly emerging group who offer a really unique perspective: the rise and rise of autistic parents raising children with autism.

I suppose the bottom line is that everyone deserves to be heard no matter what section of the autism community they are allied to, and autism research and practice is all the richer for have such a diverse set of voices on the topic of autism. But this does not mean that conflict(s) are going to be so easily solved given the multitude of opinions, viewpoints and experiences included with autism in mind. How, the very individual nature of autism, is probably never going to lend itself particularly well to favouring one specific viewpoint over any others...


[1] Jongsma K. et al. Epistemic injustice in dementia and autism patient organizations - an empirical analysis. AJOB Empir Bioeth. 2017 Nov 8:0.


Saturday, 11 November 2017

Relative age and ADHD continued

"In a health service system with low prescribing rates for ADHD [attention-deficit hyperactivity disorder], a younger relative age is associated with an increased likelihood of receiving a clinical diagnosis of ADHD."

So said the findings published by Kapil Sayal and colleagues [1] (open-access available here) adding to an important body of peer-reviewed research evidence suggesting that younger relative age - relative age compared with other children in the same school year - does seem to be a factor in both receipt of a diagnosis of ADHD (see here) and use of medication purposed for ADHD (see here). I might also direct your attention to another paper also recently published by Sayal and colleagues [2] discussing ADHD in a more general sense.

The Sayal study represents yet another large population being used to analyse any such link; this time relying on "nationwide population-based registers to identify all Finnish children born between Jan 1, 1991, and Dec 31, 2004, who were diagnosed with ADHD from age 7 years onwards (age of starting school)." They found over 6000 children diagnosed with ADHD, and as well as looking at relative age compared to other children in the school year, also examined the important variable of year of diagnosis - "(1998-2003 vs 2004-11)" - to ascertain whether changes in diagnostic practices might be contributory to this issue.

As per the opening line, there was consistency in the Sayal findings with the other occasions that this issue has been examined. So: "Compared with the oldest children in the school year (ie, those born between January and April), the cumulative incidence of an ADHD diagnosis was greatest for the youngest children (ie, those born between September and December)." Sex/gender did not seem to show any differences in this trend. Also relevant: "This effect has increased in recent years."

If all that wasn't enough, the results published by Boland and colleagues [3] (open-access available here) also add to the data on relative age and ADHD by observing that: "Attention deficit hyperactivity disorder was the only identified relative age association" in their study utilising "electronic health record data from 6 sites representing 10.5 million individuals in 3 countries (United States, South Korea, and Taiwan)." The more general research brief for Boland et al to examine "Birth month and climate impact lifetime disease risk" took into account lots and lots of diagnoses not just ADHD concluding that: "children younger than their peers [are] experiencing greater ADHD risk."

Other coverage of the Sayal study (see here) caution about the 'applicability' of the results particularly in the context of school and ADHD here in Blighty. I agree that the study does not 'prove' relative age is directly linked to ADHD diagnosis (and/or medication use for ADHD) but in the context of this not being the first time that such a link has been made and the strength of the accumulating evidence, I find it difficult to suggest that any relationship is just a spurious one.

Finally, to quote from Sayal: "In terms of clinical and educational implications, these findings suggest that key adults (teachers and parents) might interpret behaviour differently of children who are younger than their classmates." Translation: one should be careful not to mis-classify 'developmental immaturity' with a diagnosis of ADHD [4] and that ideas discussing greater flexibility on school age start dates perhaps come into their own...

To close, lest we forget today of all days...


[1] Sayal K. et al. Relative age within the school year and diagnosis of attention-deficit hyperactivity disorder: a nationwide population-based study. Lancet Psychiatry. 2017 Oct 9. pii: S2215-0366(17)30394-2.

[2] Sayal K. et al. ADHD in children and young people: prevalence, care pathways, and service provision. Lancet Psychiatry. 2017 Oct 9. pii: S2215-0366(17)30167-0.

[3] Boland MR. et al. Uncovering exposures responsible for birth season - disease effects: a global study. J Am Med Inform Assoc. 2017 Sep 28.

[4] Efron D. The role of schools in the diagnosis of ADHD. Lancet Psychiatry. 2017 Oct 9. pii: S2215-0366(17)30406-6.