"Depression, dysthymia and symptoms of anxiety and post-traumatic stress are associated with extremist sympathies"

It's a particularly poignant time to be writing this post about the findings reported by Kamaldeep Bhui and colleagues [1] on the day that news broke about events in New Zealand (see here). An all-too-familiar story of hate leading to bloodshed helped along by access to weapons; communities are left scared, confused and broken following such acts of depravity.

Although snippets of information about the events leading to the New Zealand murders are still at the time of writing coming to light, the incident is being treated as a terrorist attack. News agencies have converged on the suspect; the life behind such crimes and any possible motives. Discussions will eventually lead to inevitable questions about what motivates someone to kill innocent people under such circumstances and on such a horrific scale, and could such an act have been foreseen and potentially avoided.

The Bhui findings hopefully represent a part of that inquiry as per their focus on trying to "better understand the drivers of radicalisation and extremist attitudes more generally, and the links with symptoms of psychological and mental illnesses." I say the Bhui findings might help, but also reiterate that at the time of writing, we don't know for example, whether 'psychological and mental illness' was part-and-parcel of the motivation for the New Zealand attacks.

The basics: a study based here in Blighty, researchers recruited over 600 adults (18-45 years of age) and asked various questions and for various bits of information. They asked for information about psychiatric variables such as depression (depressive symptoms), dysthymia "(i.e. persistent mild depression, or depressive personality)", personality disorder symptoms and symptoms related to post-traumatic stress disorder (PTSD). We're also told that: "Autism symptoms were measured by using a total score on the Autism Spectrum Quotient (AQ-10), which is reported as having high discriminant validity for those with and without a clinical diagnosis." I'll come back to that sentence shortly. Alongside, participants completed something called the "'SyfoR': Sympathies for Radicalisation" tool. As the name suggests, the instrument is used to gauge sympathies to "(a) committing minor crime, (b) committing violence… in political protests, (c) organising radical terrorist groups, (d) threatening to commit terrorist actions, (e) committing terrorist actions… as a form of political protest, (f) using bombs and (g) using suicide bombs to fight against injustices." Respondents are categorised as sympathisers, condemners or neutral. It appears that Bhui has played an integral part in developing the SyfoR tool.

Results: bearing in mind this was a study of extremist beliefs, not extremist actions, and mental health, researchers observed that: "SVPT [sympathies for violent protest and terrorism] were more common in those with major depression with dysthymia..., symptoms of anxiety... or post-traumatic stress." Perhaps just as important, we are told that: "Autism and personality disorder scores were not associated with SVPT" which kinda ties in with a judgement recently (see here). I say that bearing in mind that the AQ might be picking up quite a bit more than just a possible 'clinical diagnosis' of autism (see here) and reference to the growing research literature on how vulnerability is something to consider when autism is mentioned in several contexts (see here and see here). What else? Well, age played a factor (younger people were more likely to display SVPT) and SVPT was more commonly noted in those who drank, smoked and reported having a previous criminal conviction. Also of important note was the finding that: "SVPT were shown by 15.1% of the White British and 8.1% of the Pakistani groups" taking into account that half of participants were White British and half were of Pakistani heritage.

I don't want to get too carried away with sweeping generalisations stemming from the Bhui results but one can't help but wonder about the potential implications. As the authors opine: "in the absence of links with extremist groups or histories of extremist offending, the presence of mental illnesses may add risk" when it comes to SVPT. Onward: "A more general approach to improving population mental health alongside prevention in specific populations such as those experiencing post-traumatic symptoms and younger people may be helpful." I say all that being very careful not to stigmatise any individual or any group of people.

But there are concerns too. Concerns that for example, with the data suggesting that more and more young people are suffering with mental ill-health (see here) so this *might* potentially tie into some of the Bhui conclusions minus any sweeping generalisations...

----------

[1] Bhui K. et al. Extremism and common mental illness: cross-sectional community survey of White British and Pakistani men and women living in England. Br J Psychiatry. 2019 Mar 15:1-8.

----------

"Physical and mental health issues were highly prevalent among children with obesity..."

The quote titling this post - "Physical and mental health issues were highly prevalent among children with obesity" - comes from the findings reported by Stasia Hadjiyannakis and colleagues [1].

Researchers set out to "examine the association between BMI [body mass index] class and EOSS-P [Edmonton Obesity Staging System for Pediatrics] stage" on the basis that measures such as BMI "do not always accurately and reliably identify children and youth with obesity-related health risks or comorbidities" [2] and issues like obesity don't typically appear in a "metabolic, mechanical, mental health and social milieu" vacuum.

As you might have already noted, Hadjiyannakis and colleagues have some 'research form' in this area. This time around data on nearly 850 children "with obesity aged 5-17 years" attending one of a number of weight management clinics were the source material. They observed that most of their cohort - about two-thirds of them - were described as having severe obesity according to their BMI score. When it came to their EOSS-P staging scores, 80% fell into the categories of a 2 or 3 denoting moderate to severe issues with regards to health issues such as metabolic complications either requiring pharmacotherapy or being described as "uncontrolled".

Of particular note to this blog and the focus on the intersection between physical and mental health parameters, researchers describe how "mental health concerns were most common" among their participant group. By 'mental health concerns' they specifically talk about anxiety and attention-deficit hyperactivity disorder (ADHD) as being present and "equally distributed across BMI classes." I was particularly intrigued with the ADHD bit because despite the focus on hyperkinetic behaviours in ADHD, the emerging research picture is suggesting that ADHD and obesity *might* actually be connected (see here) under quite a few different circumstances (see here).

What's more to say? Well, the Hadjiyannakis results perhaps imply that preferential screening for various physical and mental / behavioural are indicated when obesity is present. Specifically, and bearing in mind that "mental health risks were high across BMI classes" the results suggest that the possibility of an elevated risk of mental / behavioural diagnoses is not something confined to those with more or less severe obesity but rather, potentially, a universal issue.

----------

[1] Hadjiyannakis S. et al. Obesity class versus the Edmonton Obesity Staging System for Pediatrics to define health risk in childhood obesity: results from the CANPWR cross-sectional study. Lancet Child Adolesc Health. 2019 Apr 2. pii: S2352-4642(19)30056-2.

[2] Hadjiyannakis S. et al. The Edmonton Obesity Staging System for Pediatrics: A proposed clinical staging system for paediatric obesity. Paediatr Child Health. 2016;21(1):21–26.

----------

A role for viral infection in the aetiology of coeliac disease?

"In this longitudinal study, we found that a higher frequency of enterovirus infections was associated with increased risk of coeliac disease."

So said the findings reported by Christian Kahrs and colleagues [1] (open-access available here) based on the results of their: "Case-control study nested within Norwegian birth cohort recruited between 2001 and 2007 and followed to September 2016."

Following the screening of some 47,000 infants for the 'genetics of coeliac disease' - HLA genotype DR4-DQ8/DR3-DQ2 - over 900 children were entered on to the study. This group were followed "with repeated blood and faecal samples from the age of 3 months" for quite a few years. Just over 500 participants who quite regularly donated blood samples, were asked if they wanted a screen for coeliac disease. Two hundred and twenty of them (or their parents/guardians) said 'yes please' and the study results were drawn from this group. Twenty seven of the 220 participants with those all-important coeliac risk genes were diagnosed with the condition. Twenty five of those 27 diagnosed with coeliac disease were matched against 50 of the no coeliac disease participants; matching was done "for duration of follow-up, date of birth, and county of residence." It was then just a case of looking at all the biological data that had been accrued from those blood and fecal samples to ascertain things like (a) "the time interval when cases seroconverted for coeliac disease markers" (i.e. when the antibodies diagnostic of coeliac disease began to be present) and (b) if and when enterovirus was detected in some of the samples (stool samples) via PCR (polymerase chain reaction).

Results: as shown in the supplementary material, the mean age at first presence of coeliac disease (CD) antibodies in the CD diagnosed sample (n=25) was around 42 months (when the first positive sample was recorded). Symptoms 'debut' was around an average age of 73 months and CD diagnosis was received on average at 87 months. Enterovirus was reported in both CD (n=25) and non-CD groups (n=49). Some 20% of the stool samples from the CD group were positive for some kind of enterovirus exposure compared with 16% of controls. Slightly more enterovirus positive stool samples were observed in the CD group (median 4 positive samples per child) than the control group (median 3 positive samples per child).

As per the opening quote to this post: "Enterovirus was found in 370 (17%) of 2135 samples and was significantly more frequent in samples collected before development of coeliac disease antibodies in cases than in controls." Further: "The association was restricted to infections after introduction of gluten." In other words, there seemed to be some evidence of a possible temporal connection between enterovirus and the development of CD, suggesting that enterovirus exposure and not gluten was the more important trigger for CD.

Mechanisms? Well, there's some speculation about that in the Kahrs paper and a: "plausible explanation is that enterovirus causes impaired barrier function, which in turn increases the risk of coeliac disease." Enterovirus causing impaired intestinal (gut) barrier function eh? Interesting, does that mean 'leaky gut' might have a viral origin in some cases? Mmm, that could have lots of implications...

Obviously more investigation is required in this area. The Kahrs study has some strengths in terms of the sample collection protocols and frequency and potentially establishing a temporal *link* between CD and enterovirus exposure. But there's still more to do: "unmeasured confounding factors or residual confounding can never be entirely ruled out in non-randomised studies." But don't let that take anything away from the potential importance of these findings.

And on the topic of prospectively following children who might be prone to develop coeliac disease, the study findings published by Lionetti and colleagues [2] are equally interesting. In particular, based on 23 of their 26 children who received a "potential diagnosis of CD" but nonetheless "continued a gluten-containing diet... 19 (83%) became antibodies negative at 1 year from the first biopsy and remained negative up to 10 years of follow-up." Could there be a tie-up with the Kahrs findings perhaps?

----------

[1] Kahrs CR. et al. Enterovirus as trigger of coeliac disease: nested case-control study within prospective birth cohort. BMJ. 2019 Feb 13;364:l231.

[2] Lionetti E. et al. Long-Term Outcome of Potential Celiac Disease in Genetically at-Risk Children: The Prospective CELIPREV Cohort Study. J Clin Med. 2019 Feb 5;8(2). pii: E186.

----------

Psychiatric symptoms in minimally verbal kids with autism: filling a gap

The findings reported by Daniela Plesa Skwerer and colleagues [1] (open-access available here) provide the blogging fodder today. They include some important information on an under-studied group on the autism spectrum (see here) with regards to the "overall burden of psychiatric comorbidities and emotion dysregulation" in those diagnosed with an autism spectrum disorder (ASD) "who had limited verbal abilities (i.e., few to no words used spontaneously)." Such work follows the recent publication of a paper by Ginny Russell and colleagues [2] who observed that those diagnosed with autism + intellectual (learning) disability were not exactly well-represented in the peer-reviewed autism research arena.

The Plesa Skwerer paper started with the observation that various psychiatric symptoms and conditions seem to be over-represented when it comes to a diagnosis of autism (see here for example). They noted that much of the research on this topic tended look at those who could be considered to be at the 'more able end' of the autism spectrum based on skills like self-report ability. They noted that "the population most severely affected, the ~30% of individuals with ASD who remain non- or minimally verbal beyond school-age" are not particularly well-represented in such comorbidity studies. The specific words they use are the "neglected “severe end of the spectrum”."

So: "Sixty-five participants diagnosed with ASD who had limited verbal abilities" were invited to participate in their study. They were already part of a larger research initiative. When I say 'invited' what I really meant is that: "Informed consent was obtained from the parents." All were diagnosed with an autism spectrum disorder (ASD) and the group was fairly equally split between children (5-11 years old) and young adults (12-18 years old). Parents/caregivers had a big role to play in the Plesa Skwerer study as we told that they were asked to complete various questionnaires about their children, including the Child and Adolescent Symptom Inventory (CASI-5) to "examine the frequency and severity of comorbid psychiatric symptoms." Completing the CASI-5 is no mean feat as per it having "173 items, which rate behaviors as occurring never, sometimes, often and very often."

Results: "All participants met cutoff criteria for at least one CASI-5 classification, and the number of categorical classifications parents endorsed ranged from 1 to 15, with a mode and a median of 6 classifications." This is an important detail. It tells us that, based on proxy reporting, every participant, child or young adult, presented with potentially clinically significant symptoms for one or more psychiatric/behavioural disorder. Some of the most popular labels that featured were things like vocal tics, phobia and the various types of attention-deficit hyperactivity disorder (ADHD). Further: "except oppositional defiant disorder and conduct disorder, more participants showed clinically concerning severity scores than expected based on general population norms." Authors concluded that: "The overall picture to emerge from this study is that minimally verbal children and adolescents present with extremely heterogeneous profiles of co-morbid psychopathology that are not easily predicted by autism symptom severity, intellectual disability, or limitations in communication."

There are some important caveats to the Plesa Skwerer findings, not least that proxy-reporting was the method used to ascertain the presence of not of such psychiatric comorbidity. This point tells us that a lot more needs to be done to help those who are minimally-verbal to be able to communicate much more readily. Yes, it's a tall order but where there's a will, there's a way. Also, researchers admit that they "excluded those with the most severe behavior problems including aggression, self-injury or non-compliance, and therefore our findings must be viewed in the context of whom our participants represent." Personally I see this is being a pretty issue across quite a lot of research on autism. Indeed, in light of legal rulings here in the UK (see here) talking about aggression 'not being a choice for children with autism' I daresay that by excluding those who present with such issues means that many, many children and adults on the autism spectrum are under-represented in autism research as it stands.

Still, the important message from Plesa Skwerer et al stands: those with autism who are described (defined?) as minimally-verbal seem to show a similar profile of psychiatric comorbidity and a "high degree of maladaptive behavior" as that identified in other parts/regions of the autism spectrum. Screening is implied and, so as to ensure that health inequalities are minimised, access to intervention is also indicated.

Bravo to the researchers who look at the under-studied parts of the autism spectrum.

----------

[1] Plesa Skwerer D. et al. Prevalence and Correlates of Psychiatric Symptoms in Minimally Verbal Children and Adolescents With ASD. Front Psychiatry. 2019 Feb 18;10:43.

[2] Russell G. et al. Selection bias on intellectual ability in autism research: a cross-sectional review and meta-analysis. Molecular Autism. 2019; 10: 9.

----------

"Autism prevalence in China is comparable to Western prevalence" But is it really?

I was intrigued by the findings reported by Xiang Sun and colleagues [1] whose paper is the source material for the quote heading this brief post: "Autism prevalence in China is comparable to Western prevalence."

Intrigued because the idea that the prevalence of autism - in school-aged children - hovers around 1 in 100 (1%) in the Western world is still being banded around, even when data is being produced suggesting that rates are actually increasing well beyond the 1% mark in recent times (see here and see here).

Don't get me wrong, I am impressed with the Sun paper and the significant efforts and work that went into their study to look at "autism prevalence (mainstream and special schools) in Jilin City, and mainstream school autism prevalence in Jiamusi and Shenzhen cities" in China. Impressed because of the numbers involved, the 3-stage process undertaken (screening, clinical assessment, research diagnostic assessment) as part of the study and also because the data adds to a growing volume of other studies looking at autism in China (see here and see here for examples) and nearby areas (see here).

I'm not going to bore you with any more of my musings on this paper and issue. Suffice to say that the 1% statistic is old and increasingly out of touch with the current reality of autism in many, many different nations...

----------

[1] Sun X. et al. Autism prevalence in China is comparable to Western prevalence. Molecular Autism. 2019; 10: 7.

----------

"An estimated 7.7 million children in the United States (16.5 percent) have at least one mental health disorder"

The press release carrying the quote titling this post - "An estimated 7.7 million children in the United States (16.5 percent) have at least one mental health disorder" - concerns the findings reported by Daniel Whitney & Mark Peterson [1]. Their research letter discussed findings (from the United States) "providing recent national and state-level estimates of the prevalence of treatable mental health disorders and mental health care use in children."

Based on data derived from the 2016 National Survey of Children’s Health (NCSH), a "nationally representative, parent-proxy survey of US children younger than 18 years" that has been mentioned more than once on this blog (see here and see here), researchers present some important data. Including information from over 46 million children (now that's what I call a decent sample size) various trends were observed, notably that almost one in seven children and young adults were reported to have a mental health condition. Such conditions covered "depression, anxiety problems, or attention-deficit/hyperactivity disorder" and by present, I mean that parents responded in the positive to the question: "Has a doctor or other health care provider EVER told you that this child has” a mental health disorder?"

Another detail was also mentioned in the Whitney & Peterson paper: "half of the estimated 7.7 million US children with a treatable mental health disorder did not receive needed treatment from a mental health professional." This was based on responses to the question: "DURING THE PAST 12 MONTHS, has this child received any treatment or counseling from a mental health professional? Mental health professionals include psychiatrists, psychologists, psychiatric nurses, and clinical social workers." Other media on the Whitney / Peterson paper have picked up on this trend (see here) and the possible whys-and-wherefores.

The primary weakness of the NCSH - "parent-proxy survey" - is more than compensated for by the huge participant numbers included for study. The figures arrived at also follow a trend seemingly present across many nations (see here and see here and see here) suggesting that significant numbers of young people are experiencing mental health disorder. We can quibble about the reasons for the increase but there is no mistaking the fact that something is going on. And it's seemingly affecting millions of children and young people around the world...

And as if to prove the point further [2] the startling findings from Gräf et al: "School performance was available for 1462 children (51% boys, mean age 7.3 years). Of these, 41% had signs of at least one MHP [mental health problem]."

----------

[1] Whitney DG. & Peterson MD. US National and State-Level Prevalence of Mental Health Disorders and Disparities of Mental Health Care Use in Children. JAMA Pediatrics. 2019. Feb 11.

[2] Gräf C. et al. Mental health problems and school performance in first graders: results of the prospective cohort study ikidS. European Child & Adolescent Psychiatry. 2019. Feb 26.

----------

"Ashleigh's vision problems were misdiagnosed as autism"

The quote titling this post - "Ashleigh's vision problems were misdiagnosed as autism" - comes from a TV programme that was picked up by the BBC news website recently.

It continues a theme in recent times showing examples where autism has been seemingly 'misdiagnosed' (see here and see here) at the cost of other recognised medical conditions being present. Such misdiagnoses have many potential implications; not least for the various trends in some quarters to 'self-diagnose' autism or self-identify as autistic without any formal assessment seemingly being undertaken (see here and see here).

So what was the misdiagnosed condition this time around? Well, it's potentially an important one because is covers a topic rather salient to autism: vision and the processing of visual (sensory) information (see here for example). To quote: "After being misdiagnosed with Asperger syndrome, Ashleigh later found out that her behavioural problems actually came from Cerebral Visual Impairment (CVI)." When describing CVI, the key point I get from the descriptive literature is that vision is not just about the eyes but also what the brain does to/with the visual information collected through the eyes.

Aside from the label 'Asperger syndrome' disappearing from diagnostic texts and discussions for various reasons (see here and see here), a quick glance at some of the information on CVI reveals that the potential misdiagnosis of autism when CVI was present is not something entirely new (see here). To quote from the RNIB (Royal National Institute for the Blind) website here in Blighty: "Many of the standard special needs assessments generally fail to identify children with CVI. If anything there is a danger that they may be misdiagnosed as possibly having autistic spectrum condition, due to some of the characteristics being shared. Not being able to maintain eye contact or respond to facial expressions, may be due to poor contrast sensitivity or to the part of the brain that recognises facial expressions being impaired." They don't however discount the idea that CVI and autism can co-occur - "Of course CVI and autism can co-exist" - something that an expert I mentioned this study to confirmed and something noted in the peer-reviewed science literature [1] too. But misdiagnosis is also a potential risk.

I'm not going to say too much more on this topic aside from reiterating an oft-mentioned phrase on this blog: the diagnosis of autism should be a starting point for further investigations and not the finishing line. I appreciate that to many people - individuals and their parents/caregivers - the time and effort spent actually getting and going through assessment and diagnosis of autism feels like it should be the finishing line (see here). But please, don't stop there. Keep questioning and importantly, keep screening, and screening for lots of different things. As per the example of Ashleigh, there may be lots more to see (pardon the pun) and in some cases, potentially novel and important 'intervention' avenues to consider to improve quality of life [2]...

----------

[1] Bosch DG. et al. Cerebral visual impairment, autism, and pancreatitis associated with a 9 Mbp deletion on 10p12. Clin Dysmorphol. 2015 Jan;24(1):34-7.

[2] Bartel T. Mystery solved: Our son's autism and extreme self-injury is genetic and treatable. Am J Med Genet A. 2017 May;173(5):1190-1193.

----------

Paediatric Acute-onset Neuropsychiatric Syndrome (PANDAS) misdiagnosed as autism: some implications

Credit: BBC Website 25 January 2019

The BBC website recently ran with an interesting story headed under the title: "Mother's appeal after boy diagnosed with autism when he just needed antibiotics." It was an interesting piece that drew attention once again to an increasingly important condition known as Paediatric Acute-onset Neuropsychiatric Syndrome (PANDAS) also called PANS.

Classically triggered by Streptococcal infections, PANDAS/PANS is typically characterised by quite an abrupt change in behaviour to include things like "clinically significant obsessions, compulsions and/or tics" alongside things like anxiety, sensory issues, aggression and a corresponding loss of academic abilities. Treatment is often multi-disciplinary; but in the most part intervention includes the use of various types of antibiotics clinically indicated to treat strep infections. This also follows a wider research-based thread suggesting that strep infections *might* have some important links to various neuropsychiatric conditions (see here).

The BBC piece specifically focused on how the young boy highlighted was "repeatedly diagnosed as having autism and severe anxiety" and how following a PANDAS diagnosis, and after just two days of antibiotic treatment, the mother of the young boy "felt like Jack was back." I'll also mention that the mum of Jack was herself a medic, a psychiatrist, and so was perhaps more attuned than most people about clinical diagnoses like autism and anxiety. It also emphasises how she kept on questioning...

Mention of the label autism in the BBC story got me thinking about quite a few things. Although still relatively sparse, there are some isolated reports in the peer-reviewed science literature observing that something like PANDAS/PANS can be "misdiagnosed as autism spectrum disorder" [1] in some circumstances. Such a notion complements some still emerging views that: (i) there may be many different routes to a diagnosis of autism (pertinent to the notion of 'the autisms'), (ii) autism is not universally an inborn genetic condition/state/diagnosis present from birth or early infancy, and (iii) autism for some people, is not necessarily a lifelong condition or label or state. Having discussed those views quite a bit on this blog (see here and see here and see here respectively) and noted some 'resistance' in some quarters to them, it is important that stories such as the one about Jack are continually highlighted. Not least because for him at least, his mother's determination and tenacity ultimately led to a new [accurate] diagnosis and subsequent treatment tailored to his particular circumstances. I daresay that other children (and even adults) who perhaps share Jack's clinical picture remain undiagnosed and untreated out there; something which represents a significant health inequality for them and their families. I might also add that the autism-anxiety diagnostic mix discussed in the BBC piece also complements the idea that the word 'comorbidity' may not be entirely accurate for the experience of [some] anxiety in the context of [some] autism (see here).

Jack's story begs the question: just how many people have been diagnosed with autism yet are 'suffering' with undiagnosed PANDAS/PANS? There's a research study there for someone brave enough there; alongside further study on whether elucidating the mechanisms of PANDAS/PANS when seemingly mimicking the signs and symptoms of autism & anxiety *could* be beneficial for at least some other parts of the wider autism spectrum...

Continue questioning and continue investigating seem to be the key lessons, as once again we are reminded that a diagnosis of autism should be a starting point and not 'the finishing line'.

----------

[1] Goncalves MVM. et al. Pediatric acute-onset neuropsychiatric syndrome (PANS) misdiagnosed as autism spectrum disorder. Immunol Lett. 2018 Nov;203:52-53.

----------

Are early "movement and sensory differences" prodromal signs of autism?

"These results highlight the importance of early surveillance of children who are at elevated risk for ASD [autism spectrum disorder], and early initiatives should focus on early signs of the phenotype, including both movement and sensory differences (prodromal signs) prior to the emergence of diagnostic characteristics."

It was that sentence from the findings reported by Lori-Ann Sacrey and colleagues [1] (open-access available here) that caught my eye, and the idea, once again, that movement 'issues' should perhaps be considered a core feature of autism (see here) or at least more of a core feature than they currently are. I might add that I've covered other important findings from Sacrey et al on this blog previously (see here).

Although open-access, a few details might be useful: "Infants were selected at random to comprise three groups of equal size: (1) 10 non-sibling controls (LR [low risk]-control; 7 boys); (2) 10 HR [high-risk] siblings without an ASD diagnosis (i.e., with an older sibling with ASD but did not receive an ASD diagnosis themselves at 36 months; HR-N; 3 boys); and (3) 10 HR siblings with an ASD diagnosis (i.e., with an older sibling with ASD and also received an ASD diagnosis at 36 months; HR-ASD; 6 boys)." As you can see the participant numbers were fairly small but to balance this, authors did report results based on testing "for differences in reaching-to-grasp" across quite a long period (6-36 months) and utilised quite an array of psychometric testing tools pertinent to their population and study aims.

Researchers found that: "Children who were later diagnosed with ASD showed higher (worse) total scores on the reach-to-grasp movement, as well as higher scores on the components of Orient, Lift, and Pronate compared to children in the LR and HR-N groups." They concluded that: "results suggest that such movement mechanics are relevant to monitoring motor development in children at risk for or diagnosed with ASD." Ergo, there may be quite a bit to see when it comes to early surveillance for autism in respect of movement and/or sensory differences.

Just before you leave I'll also bring the findings reported by Emilia Biffi and colleagues [2] to your attention. Theirs wasn't so much a study of the possible early 'prodromal' signs of autism with a focus on movement patterns but rather another finding suggesting that such movement issues may be persistent in relation to autism and can be readily tested for. Utilising some pretty nifty movement capture technology - "an immersive virtual environment using a 3-D motion analysis system with a dual-belt, instrumented treadmill" - Biffi et al reported that their findings "depicted gait peculiarities in children with ASD, including both kinetic and kinematic features." Movement and gait issues it seems, may very well be a vitally important part of autism...

----------

[1] Sacrey LR. et al. The reach-to-grasp movement in infants later diagnosed with autism spectrum disorder: a high-risk sibling cohort study. J Neurodev Disord. 2018 Dec 27;10(1):41.

[2] Biffi E. et al. Gait Pattern and Motor Performance During Discrete Gait Perturbation in Children With Autism Spectrum Disorders. Front Psychol. 2018;9:2530.

----------

"Hyperopia, astigmatism, and strabismus seem to be independently associated with ADHD"

The findings reported by Charlotte Reimelt and colleagues [1] provide the brief blogging fodder today and the observation that following their analysis: "all examined forms of refractive error and strabismus showed an association with ADHD [attention-deficit hyperactivity disorder]."

Refractive error (e.g. near and far sightedness) and strabismus (squint) are not uncommon eye/vision issues among the general population. I've previously talked on this blog about such issues being potentially over-represented among certain diagnostic labels (see here) but up until now I don't think I've talked about such issues with ADHD in mind. I have discussed visual impairment and ADHD (see here) but not these specific eye issues.

Drawing on data derived from "the German Health Interview and Examination Survey for Children and Adolescents (KiGGS) study (N = 13,488)", researchers observed "an increased risk for ADHD in children with hyperopia, astigmatism, and strabismus compared with the control group." They also make a case for further research in this area.

Obviously the oft-used tenet 'correlation is not the same as causation' comes into play here. It means that we have to be quite careful not to say that such eye/visions are a *cause* of ADHD or vice-verse because that has not been proven by such data. The Reimelt findings do however imply that preferential screening for such eye conditions when a diagnosis of ADHD is received might be a good idea. They also imply that preferential screening for ADHD and/or related behavioural issues, might also be a good idea as and when such eye/vision conditions are also detected.

So, Merry Christmas and as is typical, Kirsty MacColl and The Pogues. And just in case you thought 'drunk tanks' were a thing of the past, think again...

----------

[1] Reimelt C. et al. The Underestimated Role of Refractive Error (Hyperopia, Myopia, and Astigmatism) and Strabismus in Children With ADHD. J Atten Disord. 2018 Oct 29:1087054718808599.

----------

1 in 5 adults with autism diagnosed with non-affective psychotic disorder (NAPD) before the age of 35?

The quote heading this post - "1 in 5 adults with autism diagnosed with non-affective psychotic disorder (NAPD) before the age of 35?" - comes from the findings reported by Schalbroeck and colleagues [1] continuing a research theme from this authorship group [2] on how autism rarely appears in some sort of diagnostic vacuum.

Relying on longitudinal data from the Netherlands ("from Dutch psychiatric case registers"), authors sought to capitalise on their previous findings from Sweden to "to assess the risk of NAPD or BD [bipolar disorder] among individuals with ASD [autism spectrum disorder], and compared the results to those obtained for the Dutch population in earlier studies." NAPD in this case refers to a grouping of labels covering schizophrenia, delusional disorder and acute and transient psychotic disorder. Bipolar disorder was previously called manic depression, reflecting mood swings between depression and mania. Both labels have some research history when it comes to autism (see here and see here for examples).

Based on the longitudinal analysis of participant records in the thousands, over 17,000, all diagnosed with ASD, researchers set about calculating the risk of NAPD and BD in their cohort. They observed that: "Of the individuals with ASD, 23.50%... were diagnosed with NAPD and 3.79%... with BD before age 35 years." Such percentages contrasted with general population figures of 0.9% and 0.1% for NAPD and BD respectively. Further study based on around 8,000 people "diagnosed with ASD before age 16 years" also showed elevated levels of NAPD and BD being diagnosed before 25 years of age (1.8% and 0.5% respectively) compared with general population figures (0.6% and 0.1%); albeit to a lesser extent.

Aside from concluding that the risk of NAPD and BD in relation to autism "is likely not the result of diagnostic or selection bias", the Schalbroeck findings reiterate again that autism seemingly rarely exists in some sort of diagnostic vacuum (see here). They reiterate that psychiatric comorbidity, some of which can often be both serious and quality-of-life destroying, is not uncommon in the context of the label of autism. They also reiterate that timely screening, diagnosis and yes, treatment for such comorbidity, are basic human rights that are as relevant to someone with autism as they are to someone not on the autism spectrum.

Oh, and given the quite significant overlap between autism and such psychiatric comorbidity, it is perhaps all the more reason to keep on studying a group where autistic and psychiatric issues seemingly were but are no more (see here)...

----------

[1] Schalbroeck R. et al. Risk of non-affective psychotic disorder or bipolar disorder in autism spectrum disorder: a longitudinal register-based study in the Netherlands. Psychol Med. 2018 Nov 21:1-8.

[2] Selten JP. et al. Risks for nonaffective psychotic disorder and bipolar disorder in young people with autism spectrum disorder: a population-based study. JAMA Psychiatry. 2015 May;72(5):483-9.

----------

Scurvy in a child with autism following a ketogenic diet

"We report a case of a 5-year-old patient with autism, who presented with scurvy secondary to the dietary restrictions of a ketogenic diet."

That was the aim of the paper by Syed Amir Ahmad and colleagues [1] who continue an important theme in autism research and clinical practice circles pertinent to the seeming over-representation of illnesses of malnutrition in relation to autism (see here).

The 'value added' bit to the Ahmad findings is the observation that scurvy - a disease caused by insufficient vitamin C in the diet - was seemingly present as a result of "the dietary restrictions of a ketogenic diet" (where a ketogenic diet represents a high fat, low carbohydrate eating schedule). I assume said diet was put in place in light of some previous research suggesting that a ketogenic diet (KD) may be 'useful' for some children on the autism spectrum (see here and see here) from a behavioural perspective or where indicated following the detection of an inborn error of metabolism for example.

Scurvy is something of a pet topic on this blog (see here and see here). Described as a rare disease, the growing [research] literature on autism and scurvy indicates that it is perhaps not as rare as many people think or would like it to be. One of the big issues in this area is that more screening needs to be done for scurvy in relation to a diagnosis of autism, particularly when children (and adults) on the autism spectrum might have a limited or restricted diet (see here).

"This case emphasizes the importance of vitamin supplements in patients consuming a special diet." I wholeheartedly agree with that conclusion made by the authors. I say this in the context that supplementation with various vitamins, minerals and nutrients where autism is present and a 'special diet' is being followed is already a good idea (see here). The fact that some of those nutrients being supplemented might themselves have an 'effect' of on the behaviour of some children (see here and see here for examples) is also something important to mention.

the bottom line: screen and keep screening for health issues like scurvy when autism is diagnosed.

----------

[1] Ahmad SA. et al. Florid Scurvy in an Autistic Child on a Ketogenic Diet. Pediatr Emerg Care. 2018 Nov 19.

----------

Gut symptoms are important for 'psychiatric outcomes' in autism

"Individuals with autism spectrum disorder (ASD) are at heightened risk of psychiatric comorbidities across the lifespan, including elevated rates of internalizing, externalizing, and self-injurious behaviors." And: "Gastrointestinal (GI) conditions are of particular interest, as they are prevalent among those with ASD, may share genetic or neurobiological etiologies with the core features of ASD, and are linked with psychiatric difficulties in the general population."

Putting the issue of 'psychiatric comorbidities' and 'gastrointestinal (GI) conditions' together are the results of the findings reported by Emily Neuhaus and colleagues [1] who concluded that: "the presence and quantity of GI symptoms should be considered when evaluating psychiatric and behavioral concerns among children with ASD." Importantly too, they talk about how 'alleviating' accompanying bowel issues in the context of autism *might* also have some important influences on some of those psychiatric issues.

The starting point for Neuhaus and colleagues was a recognition that autism does not exist in some sort of diagnostic vacuum. This means that various 'comorbid' conditions/labels seem to be over-represented when it comes to autism, covering the behavioural/psychiatric (see here) and also the somatic (see here). The authors specifically zoomed in on GI symptoms because they've mentioned over and over and over again as being part-and-parcel of quite a few instances of autism (see here). Marrying the psychiatric and gastrointestinal together, they had two aims: "First, we sought to document the prevalence and variety of GI concerns within a large, well-characterized sample of children and adolescents with ASD. Second, we sought to understand relationships between ASD symptoms and GI concerns over and above the effects of psychosocial factors."

So, authors "draw on data from nearly 2,800 children and adolescents with ASD within the Simons Simplex Collection" pertinent to their aims and objectives. The Simons Simplex Collection (SSC) is no stranger to autism research for various reasons (see here and see here). Importantly too, the SSC is not stranger to specifically looking at GI issues in relation to autism (see here). They reported that: "Consistent with previous literature, families in the SSC frequently reported that their child with ASD had significant GI symptoms" to the tune of over one third of their sample experiencing at least one GI symptom.

Looking at their types of psychiatric symptoms - "internalizing, externalizing, and self-injurious behaviors" - they observed "evidence of unique variance associated with GI symptoms across all three measures of psychiatric symptoms we examined." This didn't mean that GI symptoms were 'the' [singular] cause of those psychiatric/behavioural issues; merely that the presence of such physical symptoms should be considered as one possible factor alongside things like "ASD symptoms, verbal IQ, adaptive behavior, family income." Given that something like self-injurious behaviour (SIB) can be pretty hard-hitting in terms of effects on the person and the people around them (see here), the idea that GI issues might be 'in the mix' alongside "more ASD symptoms, lower adaptive behavior, lower income" should not be ignored. To quote again: "levels of GI symptoms accounted for unique variance in psychiatric outcomes over and above these other factors, linking increased GI problems with increased psychiatric symptoms in children with ASD."

There is a further scheme of work to be followed in this important area.

----------

[1] Neuhaus E. et al. Gastrointestinal and Psychiatric Symptoms Among Children and Adolescents With Autism Spectrum Disorder. Front. Psychiatry. 2018. Oct 22.

----------

"Hypovitaminosis D is frequent and associated with depressive symptoms and anxiety disorders in schizophrenia"

The paper published by Guillaume Fond and colleagues [1] concluding that: "Hypovitaminosis D is frequent and associated with depressive symptoms and anxiety disorders in schizophrenia" provides the blogging fodder today. Hypovitaminosis D is just another way of saying vitamin D deficiency (or perhaps insufficiency) and follows a number of previous research findings (see here) concluding that schizophrenia seems to be one of a number of conditions/diagnosis/labels where tested vitamin D levels show sub-optimality.

Fond report results based on their examination of the "national FondaMental Expert Center (FACE-SZ) Cohort", something that has been talked about on this blog before (see here). So: "A comprehensive 2 daylong clinical and neuropsychological battery was administered in 140 SZ subjects included between 2015 and 2017" including vitamin D testing and analyses looking for the signs and symptoms of depression and anxiety.

Results: about one in five of the study participants were in a state of hypovitaminosis D. Looking at the accumulated behavioural data - "Depressive symptoms were assessed by the Positive and Negative Syndrome Scale depressive subscore and current anxiety disorder by the Structured Clinical Interview for Mental Disorders" - I was particularly struck by the *link* between vitamin D deficiency and 'current anxiety disorder' ("aOR = 6.18 [2.15-17.75], p = 0.001"). Further: "Vitamin D supplementation has been administered during the previous 12 months in only 8.5% of the subjects but was associated with lower depressive symptoms... and lower rate of current anxiety disorder... compared to patients with hypovitaminosis D."

These are interesting results. They reiterate that a diagnosis of schizophrenia does not seem to be protective against the development of vitamin D deficiency/insufficiency. They also highlight that schizophrenia perhaps should not be considered as a stand-alone diagnosis; something that is beginning to be realised across various different behavioural labels (see here). The suggestion of an *association* between anxiety and/or depression in the context of vitamin D is also important (perhaps even relevant to other studies that have suggested a direct link between vitamin D and schizophrenia). And then there is the 'already supplemented' finding that seems to fly in the face of quite a lot of other evidence suggesting that correcting vitamin D deficiency in the context of something like depression might not be directly applicable to improvement in depressive symptoms (see here). Research questions remain but the Fond results look interesting...

----------

[1] Fond G. et al. Hypovitaminosis D is associated with depression and anxiety in schizophrenia: Results from the national FACE-SZ cohort. Psychiatry Res. 2018 Sep 13;270:104-110.

----------

Relative age and ADHD: more data and a meta-analysis

So, relative age and ADHD. The observation that in amongst the various pathways that might lead someone to a diagnosis of attention-deficit hyperactivity disorder (ADHD), "the youngest children within a school class are at a disadvantage in many aspects compared with their older classmates" including increasing "the probability of having ADHD-related symptoms... or other psychopathology..., of receiving a diagnosis of ADHD... or being treated with stimulant medications."

I've talked about this issue a few times on this blog (see here and see here) and am blogging today about a couple of other studies that add to the literature in this area. The first investigation was undertaken by Janine Wendt and colleagues [1] and concluded that: "Using a prospective study design and comprehensive adjustment for confounding and baseline symptoms, we confirmed prior evidence of the association between young ASE [age at school entry] and teacher-reported ADHD symptoms in primary school." The second study was published by Josephine Holland & Kapil Sayal [2] who, following a systematic review of the peer-reviewed science literature on this topic, concluded that "the majority of studies show evidence of a relative age effect influencing both the diagnosis of and receipt of medication for ADHD."

Both studies are open-access so really don't require too much explanation from me. The Wendt study relied on data collected from over 120 "Rudolf Steiner Schools (Waldorf Schools) located within Germany" (Waldorf schools are based on the philosophy of producing "free, morally responsible, and integrated individuals equipped with a high degree of social competence") covering over 3000 children. We are told that this prospective study gathered data via parent- and teacher- reports: "ADHD-related symptoms were assessed at school entry and second and fourth grades by parent-reported and teacher-reported versions of the Strengths and Difficulties Questionnaire (Hyperactivity-Inattention Subscale)." Their results found a possible *association* between age and school entry (ASE) and teacher-reported ADHD symptoms using the SDQ: "ASE was negatively associated with ADHD-related symptoms in the second grade... and fourth grade. Associations remained after adjusting for potential confounders and pre-existing symptoms at baseline." Those 'potential confounders' included "gender, time of observation and source of information." I'm also inclined to point out that the prevalence of possible ADHD overall in the Wendt study was pretty high in some scenarios: "The frequency of ADHD indications ranged from 3.7% (girls, second grade, parent reports) to 25.0% (boys, second grade, teacher reports)."

Then to the Holland-Sayal study. This was a systematic review of the existing research literature pertinent to the questions: "Is there an association between younger relative age, defined as being in the second half of the academic year, and: (1) the presence of high levels of ADHD symptoms, (2) receiving a clinical diagnosis of ADHD and (3) receiving medication for ADHD?" Based on an examination of the literature "published from the 1st of January 2000 to the search date of the 7th September 2017" and including 20 papers for review, the answer: yes, generally-speaking, there is more evidence for a relative age effect in relation to ADHD symptoms, diagnosis or receipt of medication for ADHD than against it.

Holland & Sayal do caution that their findings were not totally unambiguous. They discuss how differences across the various studies included for analysis might be important to the final outcome determined. So: "studies differed by sample size, years studied, ages studied and methods of reporting and recording ADHD diagnosis and medication." They also noted that: "The culture of diagnostic practice within a country’s health system may have an influence on the relative age effects found" implying that the willingness to diagnose ADHD in a particular country or region could very well have had an effect on the main findings.

Overall however, these studies add to the existing research-based message observing that age and maturation may be important 'influencers' of reported ADHD symptoms, diagnosis and/or receipt of ADHD medicines.

The big question now is 'what is science and clinical practice going to do about it? bearing in mind that there may be 'redshirting' models to follow [3]...

----------

[1] Wendt J. et al. Young age at school entry and attention-deficit hyperactivity disorder-related symptoms during primary school: results of a prospective cohort study conducted at German Rudolf Steiner Schools. BMJ Open. 2018;8:e020820.

[2] Holland J. & Sayal K. Relative age and ADHD symptoms, diagnosis and medication: a systematic review. European Child & Adolescent Psychiatry. 2018. Oct 6.

[3] Whitely M. et al. Attention deficit hyperactivity disorder late birthdate effect common in both high and low prescribing international jurisdictions: systematic review. J Child Psychol Psychiatry. 2018 Oct 14.

----------

Autistic traits assessed between 5 and 8 years old are 'primarily stable'

The findings reported by Hideyuki Haraguchi and colleagues [1] (open-access available here) provide the [brief] blogging fodder today and their conclusion that: "total and two subdomain-related autistic trait scores remained primarily stable in males and females" in the general population. Further that "assessing autistic traits before school entrance may aid in predicting later autistic traits as well as other co-occurring social and emotional problems."

Autistic traits were measured "by a mother-reported quantitative measure, the Social Responsiveness Scale, at age 5 and 8 years." The Social Responsiveness Scale or SRS has some good history with autism in mind both from a research and clinical perspective. In this case the Japanese version of the SRS was used, and data from total scores and "Social Communication and Interaction (SCI)" and "restricted and repetitive behaviors (RRBs)" domains also reported on in approaching 170 "Japanese community-based children."

Results: "We found that although autistic traits assessed by the SRS decreased slightly from age 5 to 8, the extent of this change did not reach statistical significance in this sample, indicating that autistic traits are primarily stable during this transition period at the group level."

This is an important finding. Whilst one has to be careful of any sweeping generalisations that for example, the expression of autistic traits by individual children or smaller subgroups might not be as stable as you think (see here and see here), the results do have implications for various areas. Not least those areas connected to the idea that autistic traits might have some subsequent important 'influence' on later psychopathology (or indeed, a subsequent diagnosis of autism). I say this in several important contexts covering the presence of depression and anxiety (see here) and also in relation to other 'overlapping' spectrums (see here and see here) and what this *could* mean for some potentially life-threatening risks (see here and see here).

The next stage of such research? Look beyond the late childhood years and into adulthood with autistic traits in mind.


----------

[1] Haraguchi H. et al. Stability of Autistic Traits from 5 to 8 Years of Age Among Children in the General Population. J Autism Dev Disord. 2018 Oct 5.

----------

Colliding spectrums again: autism and schizophrenia meta-analysed (again)

"The systematic review and meta-analysis showed a significant association between schizophrenia and ASD [autism spectrum disorder]."

That was the conclusion made by Zhen Zheng and colleagues [1] following their trawl through the peer-reviewed science literature with a view to examining "the association between schizophrenia and ASD."

This is not the first time that Zheng et al have featured in the autism meta-analysis arena (see here and see here and see here) so one could perhaps see them as seasoned professionals when it comes to this type of science. It's also not the first time that the relationship between autism and schizophrenia has been subjected to such analyses either (see here) continuing quite a long relationship between the labels and/or spectrums [2] (see here also).

So: "The meta-analysis of the prevalence of schizophrenia in individuals with ASD encompassed 1,950,113 participants and 14,945 individuals with ASD." From such numbers/data, authors were quite confidently able to determine that schizophrenia was more frequent in cases of autism than in control participants. Indeed, this was described as a 'robust' finding and the magnitude of the risk was not to be sniffed at: "odds ratio = 3.55, 95% confidence interval: 2.08-6.05, P < .001."

In relation to the "prevalence of ASD in individuals with schizophrenia", the authors relied on a smaller number of participants but concluded that: "The prevalence of ASD in individuals with schizophrenia ranged from 3.4 to 52%." Ergo, schizophrenia occurring alongside autism and autism occurring alongside schizophrenia both show over-representation.

As I mentioned on a previous blogging occasion when these labels were discussed in an overlapping sense, there are many implications from such findings. There are implications related to the preferential screening for schizophrenia and/or autism (also including other related issues too) when one or other label is diagnosed and for timely and appropriate intervention for such issues when detected (see here). There are implications for the idea that, biologically-speaking, there may be some shared mechanisms at work covering both (heterogeneous) labels (see here and see here for examples). There are also implications in relation to the social impact of such an association; bearing in mind the often very negative image portrayed of schizophrenia in certain quarters of the media and the rise and rise of 'autistic identity' in other circles. There is lots to think about.

And finally and quite timely, the paper from Giacomo Deste and colleagues [3] talking about the PANSS Autism Severity Score (PAUSS) as a "simple, fast and reliable tool for the identification of autistic features in adult patients with schizophrenia" looks rather interesting...

----------

[1] Zheng Z. et al. Association Between Schizophrenia and Autism Spectrum Disorder: A Systematic Review and Meta-Analysis. Autism Res. 2018 Oct 3.

[2] Evans B. How autism became autism: The radical transformation of a central concept of child development in Britain. History of the human sciences. 2013;26(3):3-31.

[3] Deste G. et al. Looking through autistic features in schizophrenia using the PANSS autism severity score (PAUSS). Psychiatry Research. 2018. Oct 29.

----------

Unrecognised autism in epilepsy

"All children with epilepsy, particularly those with IQ ≤ [less than or equal to] 50, irrespective of age of onset of epilepsy, seizure type, frequency of seizures, or intractability of epilepsy, should be screened for ASD [autism spectrum disorder]."

So said the findings reported by Monica Juneja and colleagues [1] continuing an important research theme on how autism and epilepsy seem to be very, very closely linked (see here and see here).

Researchers "randomly selected" over 100 children with epilepsy "(defined as two or more epileptic seizures unprovoked by any immediate identifiable cause...)" who were first screened for using Social Communication Questionnaire (SCQ) for autism and then for some, given a more detailed diagnostic work-up. They reported that about 8% of their cohort (9/106) 'screened positive' on the SCQ - "had [a] SCQ score of ≥15" - and 8 of those 9 subsequently went on to meet the criteria for an ASD based on the DSM-IV. They conclude that: "The prevalence of unrecognized ASD was 7.5/100."

This is important work. It adds to an increasing body of peer-reviewed research literature that sees both autism as a risk factor for epilepsy (see here) and epilepsy as a risk factor for autism. The authors also make reference in their findings that they: "add to the growing body of evidence that epilepsy, autism, and ID [intellectual disability] are different clinical manifestations of neurological damage that disrupts the normal neuronal pathways in the developing brain." Accepting that 'neurological damage' is perhaps rather too sweeping a term to apply to the entire autism spectrum (see here), I do think such a conclusion by Juneja et al is worthy of further investigation. I say that from the point of view that the term 'epileptogenic brain lesions' is no stranger to the research literature [2] and that the use of the term 'comorbidity' referencing epilepsy appearing alongside autism, might not always be entirely accurate (see here)...

----------

[1] Juneja M. et al. Prevalence of Unrecognized Autism Spectrum Disorders in Epilepsy: A Clinic-Based Study. Journal of Pediatric Neurosciences. 2018;13(3):308-312.

[2] Kreilkamp BAK. et al. Neuroradiological findings in patients with "non-lesional" focal epilepsy revealed by research protocol. Clin Radiol. 2018 Sep 28. pii: S0009-9260(18)30519-1.

----------

"A high prevalence of disordered eating in individuals with ADHD was observed"

The quote heading this post - "A high prevalence of disordered eating in individuals with ADHD [attention-deficit hyperactivity disorder] was observed" - comes from the study results published by Louis Jacob and colleagues [1].

Drawing on information derived from the 2007 Adult Psychiatric Morbidity Survey (APMS) here in Blighty (an initiative that has been talked about previously on this blog), researchers looked at the data for 'screened for' ADHD signs and symptoms using the Adult ADHD Self-Report Scale (ASRS) Screener as well as data derived from "the five-item SCOFF screening instrument" relevant to eating disorders (ED) completed by over 7000 adults.

Researchers reported that: "The prevalence of possible eating disorder (ED) was much higher among those with ADHD symptoms (ASRS score ≥14) compared to those without ADHD symptoms (19.2 vs. 5.7%)." They also noted that issues such as anxiety and the presence of borderline personality disorder (BPD) also might have an important influence on disordered eating as measured by the SCOFF. ADHD plus anxiety linked to a heightened increased risk of another condition presenting? I've heard that before (see here).

Accepting the fact that use of the ASRS in initiatives such as the APMS is not without potential 'limitations' (see here), and the important word 'possible' when it comes to the presence of an eating disorder based on SCOFF results alone, these are potentially important results. I say that on the basis that a connection between food/diet and ADHD has a long history from many different perspectives (see here and see here and see here for examples). I should also add that this is not the first time that ADHD and eating disorders have been talked about in the peer-reviewed research literature (see here and see here).

Other implications aside from the potential need for preferential screening for eating disorders as and when ADHD or ADHD-type behaviours feature? Well, I'd be minded to suggest that including another label/diagnosis/constellation of symptoms into future research proceedings might be useful. I speak of autism or autistic traits and the ideas that: (i) autism and ADHD occurring together is not unheard of (see here) and (ii) there is some increasing interest regarding the presence of autistic traits in relation to those diagnosed with an eating disorder (see here and see here).

----------

[1] Jacob L. et al. Attention deficit hyperactivity disorder symptoms and disordered eating in the English general population. Int J Eat Disord. 2018 Sep 6.

----------

Autism research really needs to study the prevalence and treatment of scurvy in autism

The results published by Melinda Saavedra and colleagues [1] describing another case report where scurvy was [eventually] diagnosed as appearing alongside autism represents yet another 'call to action' on this topic.

I've covered this issue quite a few times before on this blog (see here and see here and see here), and quite frankly it's reached the point where autism research really needs to step up and formally study the prevalence of scurvy in relation to autism. Indeed given the almost universal reports of medical science not initially recognising that scurvy can be no stranger to autism, the time has also come to "announce [to] the pediatrician and other professionals dedicated to primary health care about scurvy as a potential consequence of restrictive diets in children with autism spectrum disorders."

This time around the clinical focus was on a 4 year old boy who was brought to clinical attention as a result of "hip pain and refusal to walk, associated with petechiae and bruising of the lower limbs." The clues were all there that scurvy could be a cause of such symptoms, but it was only when it was revealed that the child had "selective feeding habit" that the penny seemed to finally drop. Indeed: "Levels of Vitamin C in blood were measured and without waiting for results he started treatment with 300 mg per day of ascorbic acid." Lo and behold, his vitamin C results were found to be low, and vitamin C supplementation eventually did the trick. Of vital importance, the pain associated with scurvy also showed improvement and he was discharged from clinical care with a maintenance dose of vitamin C and some nutritional advice.

'Selective feeding patterns', 'picky eating' or whatever you want to call it, is an issue that is not stranger to autism (see here). It's reasonable to assume that where such feeding issues continue into the longer-term, and dependent on what foods are consumed as part of such a restrictive pattern, there are likely to be biological consequences for the person concerned as a function of what nutritional inadequacies follow. Indeed, I daresay that such a pattern follows what is being noticed in connection with other food-related conditions in the longer term (see here). Set in this context, a lot more research and importantly, clinical practice, needs to focus on the hows-and-whys of such behaviours and their remediation. There is no longer any excuse for allowing diseases of the past such as scurvy and also others like rickets, to plague the children of today, vulnerable children of today, where healthy food in most parts of the world, is not in short supply.

Oh, and bear in mind that 'picky eating' might not be the only reason why scurvy might appear alongside autism [2]. We need lots more data.

And also, as I write this [3]...

----------

[1] Saavedra MJ. et al. Scurvy due to restrictive diet in a child with autism spectrum disorder: case report. Arch Argent Pediatr. 2018 Oct 1;116(5):e684-e687

[2] Hasan Al-Breiki S. et al. Scurvy as the tip of the iceberg. Journal of Dermatology & Dermatologic Surgery. 2014; 18: 46-48.

[3] Caldwell KJ. et al. Child With Autism and a Limp. Ann Emerg Med. 2018 Oct;72(4):493-495.

----------