Saturday, 13 July 2019

"Suicidal spectrum behaviors" and ADHD meta-analysed

"Awareness of the association between ADHD [attention-deficit hyperactivity disorder] and SSBs [suicidal spectrum behaviors] should contribute to more effectively prevent SSBs."

That was the conclusion reached in the study published by Mathilde Septier and colleagues [1] and the results of their "first meta-analysis on the association between ADHD and SSBs taking possible confounders into account." Their systematic review and meta-analysis was preregistered (see here) so we knew it would be coming.

Starting with nearly 3000 references, the available data was whittled down to just over 50 studies. The data were analysed and boiled down to reveal "a significant association between ADHD and suicidal attempts..., suicidal ideations..., suicidal plans..., and completed suicide."

What's more to say? Well such results although stark are not completely unexpected given what has already been discussed on this blog on this topic (see here and see here and see here). They serve to confirm that a diagnosis of ADHD (or even the presentation of subclinical ADHD symptoms?) should really set in motion some preferential screening for suicidal spectrum behaviours and appropriate support offered as and when detected. Minus any sweeping generalisations, such results also invite further inquiry into how certain intervention options indicated for ADHD *might* also affect risk of suicidality in the context of ADHD (see here).

If you need someone to talk to, there are organisations out there...


[1] Septier M. et al. Association between suicidal spectrum behaviors and Attention-Deficit/Hyperactivity Disorder: A systematic review and meta-analysis. Neurosci Biobehav Rev. 2019 May 23. pii: S0149-7634(18)30941-2.


Monday, 8 July 2019

Asking about "growing up with a sibling with autism"

The findings reported by Philippa Moss and colleagues [1] provide the blogging fodder today, and another important research venture into asking siblings about their experiences of growing up with a brother / sister diagnosed with autism. Such work continues an important theme whereby a diagnosis of autism doesn't just impact on the person concerned, but also on significant others around them too (see here). It also reiterates that the 'nothing about us without us' phrase should really be extended to include siblings as well as parents/primary caregivers and of course, those diagnosed with autism (see here)...

Researchers talked to over 50 adult siblings with a brother and/or sister with autism. They asked them questions about growing up with their sibling and importantly "about their worries for the future." The results provided an important snapshot into the experiences of siblings. It was a mixed bag in terms of positive and negative experiences; where themes like tolerance and caring were discussed in relation to how their autistic sibling had positively impacted on their lives. The not-so-positive themes included things like "coping with behavioural difficulties (39%) and disruption to family relationships (32%) or social life (23%)."

There was another important observation to come from the Moss study too: "The main concerns for the future, expressed by the majority of participants, focussed on problems of finding appropriate care (77%) and the potential emotional impact on the autism siblings of loss of parents." Such sentiments take us into some difficulty territory as the issue of long-term care comes into the discussion, alongside other issues voiced by parents such as 'why I can never die' (see here).

Given that siblings will probably emerge as the primary caregiver or at least responsible person when it comes to their brother(s) / sister(s) with autism as parents age, one can see the logic in the suggestion from Moss to "involve siblings in care planning and decision-making." Support for siblings is also required to prepare them for the future and ensure that the sentiments of 'caring for the carers' extends to them too.


[1] Moss P. et al. Growing older with autism – The experiences of adult siblings of individuals with autism. Research in Autism Spectrum Disorders. 2019; 63: 42-51.


Wednesday, 3 July 2019

"being autistic does not always make someone bad at seeing the world from another's viewpoint"

The quote titling today's post - "being autistic does not always make someone bad at seeing the world from another's viewpoint" - comes from the findings reported by Shisei Tei and colleagues [1].

Their research paper observing that "more careful attention should be paid to the idea of egocentricity in individuals with ASCs [autism spectrum conditions]" is part of a research mash-up post today that also includes the findings reported by Hidetsugu Komeda and colleagues [2]. Both papers help to put a 'real-life perspective' on to sweeping generalisations that everyone on the autism spectrum is completely egocentric and lack the capacity to help others.

The Tei study was initially based on the idea that: "Individuals with autism spectrum conditions (ASCs) often experience difficulty and confusion in acknowledging others' perspectives and arguably exhibit egocentricity." Egocentrism can mean a few things, but all have in common that self is the be-all-and-end-all, and the interests, beliefs and attitudes of others are of secondary regard. It's a concept that we all engage in to some degree at certain times of development and maturation, and from an evolutionary perspective, probably served (and continues to serve) as an important survival mechanism. But: "whether this egocentricity necessarily results in selfish behavior during social situations remains a matter of debate." Tei et al examined the possibility of a link between egocentricity and selfish behaviour in the context of autism...

I'm not totally au fait with all the ins-and-outs of the Tei study techniques - "derived from cognitive psychology and behavioral economics" - but it looks like it was quite a bit to do with response times to a "computerized visuospatial perspective-taking task (VPT)" and the use of a task to measure altruism ("disinterested and selfless concern for the well-being of others"). Compared with a non-autistic control group, they observed some differences among their tested groups but, and it is an important 'but', "having ASCs does not always exhibit selfish behavior during interpersonal communication."

Then we have the findings reported by Komeda et al. The starting point was a sweeping one: "Individuals with Autism Spectrum Disorder (ASD) often lack cognitive empathy, so they experience difficulty in empathizing with others." Their study was perhaps less complicated than the Tei study as a group of adults with autism and control non-autistic adults were asked to read a number of stories - "(12 stories featured protagonists with characteristics of ASD and the other 12 featured TD protagonists)" - and answer questions about said stories. Questioning included "How did the protagonist feel?" and "Would you help if the protagonist were in trouble?"

Results again were interesting. So: "individuals with ASD empathize with other people who have ASD and are motivated to help other people with ASD." Based also on examination of autism spectrum quotient (AQ) scores and when "controlling for alexithymia" (marked dysfunction in emotional awareness, social attachment, and interpersonal relating), authors concluded that: "the reason why individuals with ASD are considered to have limited cognitive empathy and helping behaviors could be related to alexithymia and the lack of social skills and attention to detail, which are related to atypical perception."

OK, both the Tei and Komeda findings have to be put into some perspective. They don't for example, completely exonerate the social cognition or perspective-taking issues that are seen in autism. They can't do so either, because issues with social interaction for example, are a core facet of a diagnosis of autism. In effect, they define autism. I should also add that the reliance on participants who were very much cognitively able in both the Tei and Komeda studies means that one has to be quite careful of generalising such findings to all quarters of the autism spectrum, particularly the under-studied and under-represented (see here) parts.

But as I mentioned earlier in this post, the combined findings do help to put a 'real-life perspective' on things; specifically that such core issues that have defined autism for many, many years - empathy and perspective-taking - don't always manifest in a uniform fashion across people or situations. They also suggest that various other variables also might serve to promote issues with empathy and perspective-taking in relation to autism, as per mention of alexithymia; something that has been noted before by other independent study (see here).


[1] Tei S. et al. Egocentric biases and atypical generosity in autistic individuals. Autism Res. 2019 May 17.

[2] Komeda H. et al. Do individuals with autism spectrum disorders help other people with autism spectrum disorders?: An investigation of empathy and helping behaviors in adults with ASD. Front. Psychiatry. 2019. May 13.


Monday, 1 July 2019

Maternal polycystic ovary syndrome (PCOS) and autism yet again

Another mash-up post for you today as I bring two papers to the blogging table discussing a topic which has already had quite a bit of airtime on this blog: maternal diagnosis of polycystic ovary syndrome (PCOS) and risk of offspring diagnosis of autism (see here and see here). The papers in question are from Maria Katsigianni and colleagues [1] and Carolyn Cesta and colleagues [2] and, via different experimental means, both papers suggest that women with PCOS have a significantly greater risk of having a child diagnosed with autism or autism spectrum disorder (ASD).

PCOS, in case you didn't know, is a fairly common condition according to the NHS entry. It's characterised by three main features: irregular periods, the presence of high levels of androgens (male hormones) and polycystic ovaries ("ovaries become enlarged and contain many fluid-filled sacs (follicles) that surround the eggs"). Mention of (male) sex hormones in relation to PCOS have led quite a few researchers to suspect a connection between PCOS and autism but another important angle to the diagnosis is a link between PCOS and insulin (the hormone involved in blood sugar control)...

Anyhow, the Katsigianni paper first. This was a systematic review and meta-analysis of the existing peer-reviewed science on the topic of "whether women with PCOS have increased odds of having a child with ASD, while, secondarily, if these women themselves are at high risk of having the disease." Now just before anyone gets shirty with the use of the word 'disease', those are the authors words not mine. I fully go with the idea that autism is not a disease. Their 'boiling down the research literature' efforts yielded 10 studies which included over 30,000 children with autism and some 320,000 "non-ASD children." The results: "Diagnosed PCOS was associated with a 1.66 times increase in the odds of ASD in the offspring" and: "Women with PCOS were 1.78 times more likely to be diagnosed with ASD." Most data on which those findings were based were deemed to be of 'good quality'.

Then to the Cesta study. The primary aim was to "measure, in the general population, the association between maternal PCOS and offspring neuropsychiatric disorders where prenatal androgen levels and/or altered androgen function have been implicated in their etiology." That population was the Sweden, and yet another example of those fantastic Scandinavian population registries being put to good research use. Autism, by the way, wasn't the only label looked at by Cesta et al: "offspring attention-deficit/hyperactivity disorder (ADHD), autism spectrum disorders (ASD), and Tourette's disorder and chronic tic disorders (TD/CTD)."

Results: based on detecting some 20,000 PCOS-exposed offspring and 200,000 "unrelated PCOS-unexposed offspring" authors concluded that: "PCOS-exposed offspring had increased risk of being diagnosed with ADHD, ASD, and TD/CTD compared with unrelated PCOS-unexposed offspring." Interestingly Cesta observed that the association between maternal PCOS and autism and ADHD was stronger in girl offspring than boy offspring. They then go on to talk about prenatal androgen exposure "leading to ‘hyper-masculine’ behavioral and cognitive traits" in offspring as being one potential biological mechanism.

What's more to say? Well, despite the whole 'male sex hormone' *link* to autism I'd like to see a lot more investigation looking at biological mechanisms. Going back to the insulin link with PCOS, there is a requirement for further study in light of other findings (see here and see here). Insofar as implications for policy, well, preferential screening for autism in offspring when mum has a diagnosis of PCOS could be indicated. This adds to the growing number of other circumstances where such preferential screening seems to be indicated.

Oh, and there could be other areas of potential investigation to consider too (see here)...


[1] Katsigianni M. et al. Maternal polycystic ovarian syndrome in autism spectrum disorder: a systematic review and meta-analysis. Molecular Psychiatry. 2019. March 13.

[2] Cesta CE. et al. Maternal polycystic ovary syndrome and risk of neuropsychiatric disorders in offspring: prenatal androgen exposure or genetic confounding? Psychol Med. 2019 Mar 12:1-9.


Friday, 28 June 2019

Roger Moore's eyebrows, ADHD and coeliac disease part 2

Consider this post an extension of some previous blogging chatter (see here) about how behaviourally defined diagnostic labels such as attention-deficit hyperactivity disorder (ADHD) seem to rarely exist in some sort of clinical vacuum. Part of that vacuum also potentially encompasses a range of somatic symptoms and/or diagnostic labels.

The findings reported by Vendel Kristensen and colleagues [1] set out to "assess self-reported symptoms of impaired concentration in coeliac disease before and after treatment with gluten-free diet, compared with healthy controls and patient controls." Coeliac (celiac) disease, in case you didn't know, refers to the archetypal 'gluten can affect biology' condition, where a certain genetic predisposition (or two) adds to gluten exposure to start a whole cascade of biological actions that impact on physical health and well being. Alongside things like bowel symptoms, there is an increasing recognition that coeliac disease (CD) also potentially brings with it certain psychological symptoms, particularly when it is not properly treated/managed (see here).

Kristensen et al asked some 30 people - "newly diagnosed coeliac patients" - to complete various questionnaires pertinent to the presentation of ADHD type symptoms, depression and anxiety and gut issues. These were compared with responses from those diagnosed with an inflammatory bowel disease (IBD) and controls (healthcare professionals).

They reported that those diagnosed with CD before implementation of a gluten-free diet had "significantly higher scores than healthy controls" in relation to the presence of self-reported ADHD and depression/anxiety symptoms. Further: "After a gluten-free diet, their scores improved and were not significantly different from healthy controls." That gluten-free diet by the way, was in place for a minimum of 12 months.

One has to be careful not to make too many sweeping generalisations from the Kristensen data. The data do not, for example, mean that all cases of ADHD are somehow the product of undiagnosed coeliac disease. Not even close. What do they do (cautiously) suggest, is that preferential screening for something like coeliac disease *might* be a good idea as and when ADHD is diagnosed or significant ADHD-like symptoms present. Such findings also resonate with the idea that certain dietary interventions to manage *some* ADHD could be a research area to consider (see here) and bring into play an interesting concept: the gut-brain axis.

Oh, and in case you were wondering about the 'Roger Moore's eyebrows' bit, well, he was the best James Bond wasn't he?


[1] Kristensen VA. et al. Attention deficit and hyperactivity disorder symptoms respond to gluten-free diet in patients with coeliac disease. Scand J Gastroenterol. 2019 May 3:1-6.


Monday, 24 June 2019

ADHD and "criminogenic cognitions": is inattention a key issue?

"These results indicate that in community-recruited adults, inattention rather than hyperactivity is related to criminogenic cognitions."

That was a key conclusion reached in the paper by Paul Engelhardt and colleagues [1] who set out to put some further scientific flesh on the bones of the finding of a "strong link between ADHD [attention-deficit hyperactivity disorder] and criminal behaviour." They were specifically interested in some of the cognitive processes behind such a correlation, and whether specific facets of ADHD might be more strongly related to criminal behaviour.

OK, first things first, although there is more than a passing connection between ADHD and risk of incarceration for example (see here and see here) I do need to point out that not every person diagnosed with ADHD is a criminal or would-be criminal. Sweeping generalisations about the effects of behavioural and/or psychiatric labels have done more than enough damage down the years, and I don't want to add to any stigma. That being said, I don't think it's unfair to point out that there is a body of peer-reviewed research evidence out there observing that ADHD certainly seems to increase the risk of contact with law-makers and law enforcers alongside a host of other events (see here).

Engelhardt et al provided a sample of adults (N=198) aged between 18-65 years with a package of questionnaires designed to assess 'criminal thinking styles' and ADHD-related traits. Questionnaires were of the self-report kind. The results suggested that various variables/items on the ADHD questionnaire and more general demographic information *correlated* with criminogenic cognitions. So: "higher age and being female were negatively related to criminogenic cognitions" indicating that such variables were associated with lower criminogenic cognitions. Further, and as mentioned at the start of this post: "inattention/memory problems were more strongly associated with criminogenic cognitions than was impulsivity/emotional lability." In total, age, sex/gender and ADHD symptoms accounted for "between half and two-thirds of the variance in criminogenic cognitions."

The authors mention how their results differ from other data talking about hyperactivity as being linked to criminality, and whether their use of a non-criminal participant group and focus on criminogenic cognitions rather than criminality might be important. I'd agree that the Engelhardt results are important but require further investigations to be carried out to assess their validity. Having said that, the results as they stand do perhaps offer another avenue for intervention, based on the the idea that managing inattention (if that is possible) *could* be have some really important effects.


[1] Engelhardt PE. et al. The Relationship between Adult Symptoms of Attention-Deficit/Hyperactivity Disorder and Criminogenic Cognitions. Brain Sci. 2019 Jun 2;9(6). pii: E128.


Friday, 21 June 2019

The rise and rise of CM-AT for autism

Today's post surrounds a poster presentation delivered at INSAR 2019, the (still) premier international autism conference, albeit not without its battles. The poster was delivered by Heil and colleagues [1] and talks about a compound / preparation that has been discussed a few years back on this blog: CM-AT (see here).

CM-AT is described as a "pancreatic enzyme preparation" with chymotrypsin - a digestive enzyme - seemingly placed quite prominently in its list of ingredients. CM-AT is, from what I understand, something that is still going through the research processes with regards to its use in the context of autism. Heil and colleagues presented data on part of that research agenda, specifically pertinent to ascertaining "whether or not behavior (e.g., symptoms of irritability, hyperactivity) in preschoolers with autism could be improved with CM-AT."

Bearing in mind a conference poster presentation is not necessarily the same as a published peer-reviewed research article, the Heil data was based on the use of a "randomized, placebo-controlled, 12-week clinical trial" methodology where 92 children, aged between 3-5 years, diagnosed with an autism spectrum disorder (ASD) received CM-AT "as granules sprinkled on food" and almost a hundred boys with ASD received a placebo "which consisted of visually identical inert sprinkles." The 'Irritability' scale of the Aberrant Behavior Checklist (ABC) was the primary outcome measure.

Results: "children receiving CM-AT (relative to those receiving placebo) demonstrated significant reductions in Irritability... Hyperactivity... Inappropriate Speech... over the 12 weeks of the trial." Researchers further reported that those children with higher levels of irritability at baseline tended to show a greater positive response than when the participant sample as a whole was analysed.

I think you can perhaps see why these results - preliminary as they are - are worthy blogging material. Irritability, perhaps listed as a 'challenging behaviour' in the context of autism is something that many, many people would love to be able to effectively tackle; if not just because of the impact it can have on those with autism and those around them who have to 'cope' with such behaviours. Indeed, given the other options for managing such behaviour such as the antipsychotic risperidone (see here) and the issues which that drug and its similars can bring (see here), the idea that there may be other, less side-effect heavy options (see here) is definitely something to consider.

I'm hopeful that soon, very soon, I can talk more about CM-AT in the context of irritability and beyond in relation to autism...


[1] Heil MF. et al. Pancreatic Replacement Therapy with CM-at Is Associated with Reduction in Maladaptive Behaviors in Preschoolers with Autism. INSAR 2019.


Wednesday, 19 June 2019

Mindfulness for ADHD systematically reviewed

"According to presented descriptive results, all the studies (100%) showed improvement of ADHD [attention-deficit hyperactivity disorder] symptoms."

That was the standout sentence derived from the findings reported by Hélène Poissant and colleagues [1] who looked at "the available literature concerning MBIs [mindfulness-based interventions] in adult participants with ADHD." Mindfulness by the way, is described as a way of "reconnecting with our bodies and the sensations they experience" with a specific focus on "an awareness of our thoughts and feelings as they happen moment to moment." I'm no expert on mindfulness or mindfulness-based interventions but, from what I gather, the core of such intervention(s) is based around "somatically focused meditative techniques (body scan, sitting meditation, and mindful yoga) that are thought to help participants cultivate nonjudgmental, mindful awareness of present-moment experience." 'Focusing in on the present' seems to be the phrase that springs to mind.

Poissant et al examined the relevant peer-reviewed science on the application of the MBIs to ADHD upto June 2018. They specifically focused on adults with ADHD, and were able to track down "13 studies conducted with 753 adults (mean age of 35.1 years)" for inclusion in their systematic review. They observed that: "All the studies (100%) showed improvement of ADHD symptoms following an MBI." They also mentioned that: "mindfulness meditation training improves some aspects of executive function and emotion dysregulation" as per the findings of some of those studies.

Despite the '100% of studies showing improvement in ADHD symptoms' sentiments, I'm not falling hook, line and sinker for the value of MBIs in relation to ADHD. The main reason is the high risk of bias identified in quite a few of the studies reviewed by Poissant, related to things like performance bias ("blinding of participants and of personnel") and selection bias ("allocation concealment" and "selection bias"). One could argue that the examination of something like MBIs under research conditions is never going to be perfect. Unlike scientific investigation of a medicine, where a placebo can be formulated to look, smell and taste the same, it would be difficult to come up with something to approximate MBI and indeed, approximate what the 'active ingredient' of mindfulness actually is. Similar issues have been talked about on other occasions on this blog (see here).

That all being said, there is something appealing about MBIs both in terms of effect and also the fact that it can be learned by pretty much anyone, is cost-free and probably about as side-effect free as one could get. If such a simple technique helps with any one of the symptoms of ADHD and improves quality of life for those with ADHD, it's got to be something to be considered alongside the myriad of other possible interventions (see here and see here and see here) that *might* offset the risks that follow a diagnosis of ADHD (see here).

Oh, and it appears that mindfulness and ADHD is a topic in the ascendancy [2]...


[1] Poissant H. et al. Behavioral and Cognitive Impacts of Mindfulness-Based Interventions on Adults with Attention-Deficit Hyperactivity Disorder: A Systematic Review. Behav Neurol. 2019;2019:5682050.

[2] Xue J. et al. A meta-analytic investigation of the impact of mindfulness-based interventions on ADHD symptoms. Medicine (Baltimore). 2019 Jun;98(23):e15957.


Monday, 17 June 2019

Following ADHD long-term: "a persistence rate of 27.8%"

Studies such as the one published by Michel Lecendreux and colleagues [1] always catch my attention. Research that follows a group of people over a period of years makes for interesting reading; not least because one gets a flavour for what *could* happen when such findings are applied to a larger population.

The Lecendreux findings focused on a few important issues pertinent to a diagnosis of attention-deficit hyperactivity disorder (ADHD) specifically related to (a) the persistence of ADHD, and (b) the idea that signs and symptoms of ADHD not meeting the thresholds for a diagnosis of ADHD might be rather important. Indeed, that they may merit "a subthreshold diagnostic category" of their own.

So, based on a starting participant sample of just over a thousand families including a child in the "6-12 years age range", interviews were conducted covering various aspects of ADHD and beyond: "symptoms of ADHD, conduct disorder, and oppositional defiant disorder as well as family living situation, school performance, sleep disturbance, eating habits, use of supplemental iron, and history of ADHD treatment." Approaching half of the original sample (492 / 1012) were followed up some 9 years later where "the persistence of ADHD and its impairments and the emergence of new conditions were assessed."

Results: "At follow-up, 16.7% of the children diagnosed with ADHD at baseline met full criteria for ADHD and 11.1% met criteria for subthreshold ADHD, yielding a persistence rate of 27.8%." Diagnosis of ADHD was, by the way, based on DSM-5 criteria (see here). That figure of 27.8% in terms of ADHD persistence from childhood to early adulthood is potentially an important one. It tells us that for a majority of children diagnosed with ADHD in childhood, their symptoms of inattention, hyperactivity and impulsivity will reduce to such a degree that they are no longer considered clinically significant or at least not reaching thresholds for a diagnosis of ADHD. Whether such a reduction in symptoms is through processes such as maturation or the timely implementation of intervention/management strategies needs quite a bit more work. Whether also ADHD potentially 'morphs' into something else as people age also needs further exploration (see here).

Another important detail was also mentioned by Lecendreux et al: "Among children not diagnosed with ADHD at baseline, 1.1% met criteria for ADHD at follow-up." Such a figure is important in relation to the concept of adult-onset ADHD [2] and the question of whether ADHD is a diagnosis with foundations always rooted in infancy. The Lecendreux findings suggest that for some people, this might not be the case and opens the door to possible talk about acquired ADHD for examples. This also sounds very familiar (see here).

Insofar as the issue of a possible 'subthreshold diagnostic category' for ADHD, I find myself agreeing with the "dimensional conceptualization" mentioned by the authors. Several other conditions / states / diagnoses have recognised 'lite versions' of the label. In autism for example, one might see this as social communication disorder (SCD) or mention of the broader autism phenotype (BAP). I'm even minded to place the label known as pathological demand avoidance (PDA) in a similar bracket given recent opinions (see here). Such chatter about 'lite' does not and should not downplay the effects of such sub-threshold labels. It merely acknowledges that there may be a wider spectrum of issues / difficulties experienced outside of the receipt of a core diagnosis.

So it should perhaps be the same with ADHD too, given what is beginning to emerge on the long-term 'effects' that a diagnosis of ADHD and subthreshold ADHD might bring (see here and see here).


[1] Lecendreux M. et al. A 9-Year Follow-Up of Attention-Deficit/Hyperactivity Disorder in a Population Sample. J Clin Psychiatry. 2019 May 7;80(3). pii: 18m12642.

[2] Cooper M. et al. Investigating late-onset ADHD: a population cohort investigation. J Child Psychol Psychiatry. 2018 Oct;59(10):1105-1113.


Friday, 14 June 2019

Nighttime body movements and autism

I was rather interested in the findings reported by Nobushige Naito and colleagues [1] talking about how atypical body movements during the night seemed to be more frequently observed in children diagnosed with an autism spectrum disorder (ASD) compared to not-autism controls. Interested because, sleep is a long-running 'issue' in relation to autism (see here) and because, researchers relied on the use of actigraphy in their study: "a movement-based index measured by an accelerometer" rather than just second-hand observational questioning.

So: "Seventeen TD [typically developing] children and 17 children with ASD participated in this study (5 to 8 years old)." Importantly (see here) we are told that: "Considering the frequent co-occurrence of ASD and ADHD [attention-deficit hyperactivity disordersymptoms, we did not exclude ASD patients with ADHD symptoms." Authors relied on data from a waistband accelerometer worn by participants over at least 3 nights. Using a waistband was seen as preferable to the more typical wristband. Data was collected and analysed. It included something called a movement index (MI): "the ratio of the body movement period in 20 minutes was calculated continuously for 9 hours using the sliding window method."

Results: "a higher rate of body movement 2 to 3 hours after the first onset of body stillness was more prominent in children with ASD than in TD children." Importantly authors also mention how the objective data provided by the waistband accelerometer showed a different "time course of body movements during night in young children with ASD" despite parents/carers reporting no "apparent" problems with sleeping. They also talk some of the differences in body movements seen in those children with ASD potentially *related* to some awake behaviours - "a lower social ability and more frequent maladaptive behaviour."

The Naito results represent a good start at looking at these important behaviours. I'm a little bit hesitant to go all-in with the suggestion from the authors that "atypical nocturnal body movement could be an ASD state and trait marker in young children with ASD" but can see the importance of further investigations in this area.


[1] Naito N. et al. Atypical body movements during night in young children with autism spectrum disorder: a pilot study. Sci Rep. 2019 May 6;9(1):6999.


Wednesday, 12 June 2019

Childhood dietary patterns and ADHD?

The findings of the systematic review and meta-analysis published by Bianca Del-Ponte and colleagues [1] provide the blogging fodder today, and the suggestion that: "a diet high in refined sugar and saturated fat can increase the risk, whereas a healthy diet, characterized by high consumption of fruits and vegetables, would protect against ADHD [attention-deficit hyperactivity disorder] or hyperactivity."

The starting point: "The diet during childhood has been investigated as a factor potentially involved in the ADHD etiology." Yes it has, and Del-Ponte et al managed to find 14 studies looking at this issue published in the peer-reviewed literature. The data were boiled down and results obtained suggesting that "healthy dietary patterns were protective against ADHD (OR: 0.65; 95% CI: 044 – 0.97), while unhealthy dietary patterns were found as risk to ADHD (OR: 1.41; 95% CI: 1.15–1.74)."

The authors admit that the science upon which they made their observation is "weak" insofar as cause and effect not being proved. This is an important point (see here) that follows other research in this area too (see here and see here) together with an understanding that many different variables *might* influence the risk of something like ADHD as a diagnosis or in behaviour (see here and see here for examples).

Still, if there is even the remotest possibility that diet might be something to consider in respect of ADHD, adding it to the intervention arsenal that already exists (see here) can only be a good thing...


[1] Del-Ponte B. et al. Dietary patterns and attention deficit/hyperactivity disorder (ADHD): A systematic review and meta-analysis. Journal of Affective Disorders. 2019; 252: 160-173.


Tuesday, 11 June 2019

SHANK3, gut issues and (mouse) autism continued

"We conclude that apart from its well-known role in the CNS [central nervous system], SHANK3 plays a specific role in the GI [gastrointestinal] tract that may contribute to the ASD [autism spectrum disorder] phenotype by extracerebral mechanisms."

So said the findings reported by Ann Katrin Sauer and colleagues [1], and yet more evidence that issues with SHANK3 mentioned in relation to 'some' autism, may well (partly) explain much more than just behaviour (see here and see here).

The Sauer study was yet another mouse study. They specifically focused on the "Shank3αβ KO" mouse, where KO means knock-out, referring to the engineering of this mouse strain to mimic issues with the functioning and availability of SHANK3, "a known scaffolding protein of the postsynaptic density (PSD) of glutamatergic excitatory synapses." Said knock-out mice have been "reported to display ASD-like behavior with abnormal ultrasonic vocalization, repetitive self-grooming, and reduced interest in novel mice." I say this being careful to reiterate that we're talking about a mouse not human beings (see here).

On the basis of the observation that SHANK3 is expressed in the gut as well as brain and that GI issues are no stranger to autism (see here), researchers set about looking at how SHANK3 issues might also manifest as gut issues, and what this *could* mean for some autism. They observed some interesting things:

  • "analysis of the GI tract of Shank3αβ KO mice revealed significantly altered gut morphology" which included, among other things, increased levels of ZONULIN1 ("a modulator of tight junctions and alterations"). Zonulin is something that I'm particularly interested in on this blog (see here and see here) on the basis of its *connection* to intestinal barrier function and the misnomer that is 'leaky gut' (see here).
  • "The Microbiome of Shank3 KO Mice Is Altered." Bearing in mind the increasing importance of the gut microbiome to autism (see here), researchers reported some interesting difference between "Shank3αβ KO mice" and controls with regards to several different bacterial species. 
  • Researchers describe how those gut morphology and gut bacterial differences seemed to be linked to alterations in the "expression of inflammatory markers" too as they talked about "signs of increased immune activation in the periphery and the brain." A familiar cytokine is mentioned - IL-6 - and quite a few avenues for further investigation.

The net result of all this work is to say that, yes, the SHANK3 mouse model *potentially* mimicking some of the behavioural signs and symptoms of autism does also appear to show some significant gut-related issues. No, this does not directly translate into issues for 'all human autism', but it does add further credence to the idea that the gut-brain axis is likely important to at least 'some autism'. Where also SHANK3 issues are identified as coinciding with 'human autism', one might also entertain the idea that gut issues should be screened and treated/managed. And there might be lots of ways to manage them (see here for one example)...


[1] Sauer AK. et al. Altered Intestinal Morphology and Microbiota Composition in the Autism Spectrum Disorders Associated SHANK3 Mouse Model. Int. J. Mol. Sci. 2019; 20: 2134.


Monday, 10 June 2019

Constipation and autism is not an uncommon combination

For those who know (or think they know) anything about autism, the title of this post - "Constipation and autism is not an uncommon combination" - is unlikely to be new or novel. Indeed, I've talked again and again and again about how functional gastrointestinal (GI) symptoms are very well over-represented when it comes to a diagnosis of autism (see here for example).

Enter then two further recent articles - one from Bradley Ferguson and colleagues [1] and one from María José Penzol and colleagues [2] - which further add to the evidence base in this area. Both papers are open-access, so please peruse at your leisure. The long-and-short of them can be quickly summarised:

  • The Ferguson paper set out to examine the "relationships among GI [gastrointestinal] problems, problem behaviors, and internalizing symptoms in a sample of 340 children and adolescents with ASD [autism spectrum disorder]." Caregivers/parents reported on their child's GI issues. Bottom line: "The majority of the sample experienced constipation (65%)." Various other functional GI issues were also reported.
  • The Penzol paper "reviewed the medical records of all patients admitted to the Comprehensive Medical Program for ASD (AMITEA) at Gregorio Marañón University General Hospital from January 2012 to December 2015." They analysed records for nearly 850 patients diagnosed with ASD. Their data were collected and transcribed by physicians including the "presence of fGID [functional gastrointestinal disorders] (gastrointestinal reflux, aerophagia, functional diarrhea, functional constipation, functional abdominal pain, cyclic vomiting)." Bottom line: "At least one fGID was present in 30.5% of patients, constipation being the most prevalent (47.4% of fGID patients)." They also observed that GI issues *seemed* to be related to the presence of intellectual (learning) disability, sleep issues and behavioural problems. These are not novel associations (see here and see here).

Of course there are strengths and weaknesses to those studies. No-one would dispute the fact that these are not perfect data. But, set within the context of a mountain of peer-reviewed science suggesting that something like constipation is over-represented when it comes to a diagnosis of autism, the collected results add a further layer of evidence. They also ask the question 'why', why oh why have we not got a greater handle on how to successfully treat/manage such symptoms?


[1] Ferguson BJ. et al. The Relationship Among Gastrointestinal Symptoms, Problem Behaviors, and Internalizing Symptoms in Children and Adolescents With Autism Spectrum Disorder. Front Psychiatry. 2019 Apr 9;10:194.

[2] Penzol MJ. et al. Functional Gastrointestinal Disease in Autism Spectrum Disorder: A Retrospective Descriptive Study in a Clinical Sample. Front Psychiatry. 2019 Apr 10;10:179.


Friday, 7 June 2019

Preventing, yes preventing, elopement in kids with autism

I know the word 'prevention' is a dirty word for some in relation to some aspects of autism. When however 'prevention' is used in the context of elopement or wandering and autism, the word(s) take on an altogether different meaning...

The word prevention is used in the study findings reported by Silvia Pereira‐Smith and colleagues [1] and their focus on "the use of preventive measures that target elopement" in relation to autism. They add that "elopement can lead to dire consequences." Seldom have truer words been spoken in relation to this issue with autism in mind (see here).

For those of you who might know too much about this topic, wandering is an important issue in both autism research and practice (see here and see here). Figures suggest that around 1 in 4 children diagnosed with an autism spectrum disorder (ASD) will consistently wander from home or school or other place, but this issue does not seem to be as widely talked about or parents/caregivers consistently given as much information about it as they should.

Pereira-Smith and colleagues asked nearly 400 parent-caregivers of children and young people diagnosed with an autism spectrum disorder (ASD) about their [child's] experience of wandering/elopement. They asked questions about who did it, "preventive measure use, and sociodemographic characteristics" of their cohort.

Results: "Two hundred and sixty-seven caregivers (68%) reported elopement by their child." That figure is way over the 1 in 4 estimate that has been previously banded around. Researchers also found that wandering was not confined to any one "sociodemographic characteristics, nor with any specific comorbidity or neurobehavioral medication." Kids and young people across the autism spectrum wandered. That being said: "Children with limited communication skills were more likely to have a history of elopement." As for that word 'prevention', most families used "lock(s) at top of doors" with other families utilising "handicap permits, signs/visual markers, or tracking devices" albeit to a lesser degree than locks. Researchers conclude that "use of specific preventive measures can help guide recommendations for this dangerous comorbid symptom, and provide information needed for future studies to assess the efficacy of various preventive measures." Who would argue with that?

Oh, and just to let you know that there are some autism organisations who have really taken a lead in this area (see here)...


[1] Pereira-Smith S. et al. Preventing elopement in children with autism spectrum disorder. Autism Res. 2019 Apr 29.


Thursday, 6 June 2019

That 'gut bacteria transplant provokes autistic signs in mice' paper is not perfect but...

The paper by Gil Sharon and colleagues [1] has certainly created headlines and discussion in equal measure (see here and see here and see here and see here). Concluding that: "Mice harboring human ASD [autism spectrum disorder], but not TD [typically developing], microbiomes exhibit ASD-like behaviors", the idea of a gut-brain connection in relation to autism (see here) potentially gains some research traction.

The Sharon study involved transplanting gut bacteria - the gut microbiome - from a small number of participants - "from 5 control volunteers and 11 patients diagnosed with autism spectrum disorder" - into mice lacking a microbiome and breeding said mice. They then analysed the behaviour and other biological parameters of those offspring mice according to whether their mother mice had received a transplant from controls or participants with various 'degrees' of autism. They also looked at 'metabolite profiles' based on "analyses of colon contents from oTD [offspring typically developing] and oASD [offspring autism spectrum disorder] mice."

Results: "colonization with ASD microbiota is sufficient to induce hallmark autistic behaviors." By 'hallmark autistic behaviors' researchers observed that said mice showed "increased repetitive behavior, decreased locomotion, and decreased communication... compared to mice colonized with samples from TD controls (oTD), as tested by marble burying (MB), open-field testing (OFT), and ultrasonic vocalization (USV), respectively." Researchers also observed specific differences across the mouse group gut microbiomes, some of which were consistent with that noted in other independent studies.

Also: "Twenty-seven out of 313 detected metabolites were significantly different in the colon contents of oASD mice, compared to oTD mice." They specifically focused in on two metabolites - taurine and 5-aminovaleric acid (5-AV) - both of which were reported in lower levels in the oASD mice, and how these compounds show a *connection* to GABA, a compound potentially important to autism (see here). Further they showed that supplementation of 5-AV and taurine to another strain of mouse that serves as a 'mouse model of autism' (BTBR T+ tf/J (BTBR) mouse model) resulted in "improved repetitive and social behaviors." I should add the word 'mouse' into the sentence "improved repetitive and social behaviors."

Insofar as the limitations of the Sharon studies and paper, various people have been keen to point out that the results should be viewed cautiously and as preliminary. This on the basis of the number of animals included for study, the reliance on mouse models of autism (and the logical fallacies that can sometimes follow) and some of the generalisations made in the study write-up by the authors. I wouldn't disagree with such cautions, bearing in mind that some mouse models of autism - the valproic acid autism mouse model for example - actually seem to be pretty good at mimicking some facets of (induced) autism. I'd also point out that the metabolomics work undertaken by Sharon and colleagues looks to be pretty wide-ranging (GC-MS and NMR are discussed) and findings related to taurine have also been noted in other independent study (see here). I also observed that there was a research tie-up with Arizona State University in the Sharon study, as the name Dae-Wook Kang is mentioned and 'poo transplants for [some] autism' makes yet another appearance (see here and see here).

"While ours is a limited study, with 16 donor samples from a pediatric cohort, the results support a hypothesis that the human gut microbiota contributes to ASD phenotypes." I'd agree that the Sharon results add a further layer to the idea that the new triad - intestinal permeability, mucosal immunology and intestinal microbiota - could be important to at least some autism. The results offer a road map for further investigation in this area and perhaps eventually, yet another avenue for screening and intervention to complement other recent initiatives (see here); all set with the view of the (plural) 'autisms'.

Finally, I note that another study [2] mentioning the words 'mouse' and 'autism' has been published recently. With some media attention mentioning how: "Exercise reversed autistic behaviors in an animal model of the condition" there didn't seem to be the same 'keenness' to point out the flaws of the Andoh study, despite once again a reliance on 'mouse autism' and all which that entails. It makes me wonder whether the focus on the second brain (gut) and autism detailed in the Sharon study might still have the ability to raise hackles in some quarters?


[1] Sharon G. et al. Human Gut Microbiota from Autism Spectrum Disorder Promote Behavioral Symptoms in Mice. Cell. 2019 May 30;177(6):1600-1618.e17.

[2] Andoh M. et al. Exercise Reverses Behavioral and Synaptic Abnormalities after Maternal Inflammation. Cell Reports. 2019; 27: 10. June 4.


Wednesday, 5 June 2019

"specific clinical and neuropsychological dimensions might be related to suicidal behaviors in ASD"

The quote titling this post - "specific clinical and neuropsychological dimensions might be related to suicidal behaviors in ASD [autism spectrum disorder]" - comes from the findings reported by Luisa Weiner and colleagues [1] (open-access). It adds to other recent research talking about how elements of autism *might* associate with suicidality (see here). I should warn you that some of the Weiner findings make for difficult reading.

Authors described a case report of "a 21-year-old male [Mr A] with ASD who attempted suicide twice, in the absence of other psychiatric diagnoses." They detail how, following some quite comprehensive observations, a possible *connection* was noted between his suicidality and "some of the core clinical and neuropsychological features of ASD."

A few important points are highlighted in the Weiner study: "Mr. A. reported that his suicidal thoughts started when he was 18, following an unrequited infatuation with a classmate – the result of a rational decision: he had decided to “fall in love” with her." Things did not however go as he planned, as we are told that: "He started having “obsessive negative thoughts”, and attempted suicide by jumping from a window." He survived but "his suicidal thoughts lingered, characterized by a restrictive, rigid pattern."

Researchers relied on the Beck Depression Inventory (BDI) to rule out depression in this case: his score "was in the normal range (3/63)." This inventory is one of a few that have been described as being "robust in their measurement properties in the general population" [2] but with perhaps more to do in the context of its use in autism. In the absence of depression or rather elevated self-report scores indicative of depression, authors suggest this raises "the question of whether the persistence of suicidal thoughts was associated with ASD-related features."

The Weiner findings have to be placed in the context of other independent research looking at suicidality and autism. First, risk of suicidality is seemingly heightened when autism is diagnosed (see here). Second, although depression - an important variable *linked* to suicidality - is over-represented in relation to autism (see here), questions are still being asked about the impact of depression in relation to suicidality accompanying autism in the context of an often complicated clinical picture (see here). Third, the idea that the features/traits of autism might themselves be independent predictors of suicidality in autism has been discussed on several research occasions (see here and see here and see here).

The culmination of all this work is that quite a lot more research and clinical resources need to be ploughed into looking at suicidality and autism. And, importantly, translating said research into real-world actions to potentially save lives.

If you need someone to talk to, there are organisations out there...


[1] Weiner L. et al. A case study of suicidality presenting as a restricted interest in autism Spectrum disorder. BMC Psychiatry. 2019; 19: 126.

[2] Cassidy SA. et al. Measurement properties of tools used to assess depression in adults with and without autism spectrum conditions: A systematic review. Autism Res. 2018 May;11(5):738-754.


Tuesday, 4 June 2019

Barriers to recruitment in paediatric CFS research: "the focus of the study itself"

I want to mention the study results published by Maria Loades and colleagues [1] today. This piece of research focused on the issue of participant recruitment "in the context of an observational study of mental health problems in adolescents with paediatric Chronic Fatigue Syndrome (CFS/ME) presenting to a specialist paediatric CFS team" and the barriers faced when trying to recruit for such a study. Various obstacles to participation were noted, including an important variable: "the focus of the study itself."

The Loades article is open-access so doesn't need any long post from me. The main points: researchers asked researchers about their research experience specifically focused on "exploring healthcare professionals’ views of recruiting to studies, including the facilitators and barriers to recruitment to this study." 'This study', by the way was an "observational study of co-morbid mental health problems in adolescents with confirmed CFS/ME."

Results: based on interviews with six researchers, various qualitative results were provided. Some interesting points were raised. The ones that stood out for me were related to how researchers themselves talked about the research focus on mental health in relation to ME/CFS. A few choice quotes exemplify this: "…because it’s got depression in the title and um I think um you it just seems a little bit more explanation um by inviting them to take part I’m not suggesting that they are depressed…" and "because it is more objectively more obviously about the mental health side of things I have found it to be a different experience recruiting to this."

I'm sure that for those with some knowledge about the debates on-going in the context of ME/CFS you can perhaps see where I'm going with this. I speak of course about the 'application' of things like the biospychosocial (BPS) model to ME/CFS which has, I'm afraid to say, caused some significant distress down the years to patients, their loved ones and many researchers alike (see here and see here). Indeed, one could argue that the application of the BPS model to ME/CFS, where 'unhelpful thoughts' for example are deemed part-and-parcel of some peoples view of ME/CFS, has been so damaging to the concept of ME/CFS, that any study looking at mental health in the realm of CFS/ME is likely to be seen as 'tainted' by association.

And, as I write, still the BPS beat continues [2] although with scrutiny continuing to follow [3]...


[1] Loades ME. et al. Obstacles to recruitment in paediatric studies focusing on mental health in a physical health context: the experiences of clinical gatekeepers in an observational cohort study. BMC Med Res Methodol. 2019 Apr 27;19(1):89.

[2] Gregorowski A. et al. Child and adolescent chronic fatigue syndrome/myalgic encephalomyelitis: where are we now? Curr Opin Pediatr. 2019 Apr 30.

[3] Vink M. & Vink-Niese A. Cognitive behavioural therapy for myalgic encephalomyelitis/chronic fatigue syndrome is not effective. Re-analysis of a Cochrane review. Health Psychol Open. 2019;6(1):2055102919840614. 


Saturday, 1 June 2019

Parent stress and autism: an issue that needs a lot more discussion

Two paper are brought to the (brief) blogging table today: the first from Nik Aida Nik Adib and colleagues [1] and the second from Elena Pattini and colleagues [2], both focused on the topic of stress and parenting in the context of autism.

Yes, I know to mention the words 'parenting stress' and 'autism' in the same sentence requires some caution. I know some people don't like to talk about this and related topics (see here). But obscuring such important research from view for fear of upsetting people or impacting on any 'positive PR' does little to approach an issue that is seemingly so widespread (see here).

So what are the key points to take away from both papers on this topic?

1. "Caregivers of an ASD [autism spectrum disorder] child perceived significant stress while taking care of their children." Not exactly a novel results I grant you, but important to reiterate.
2. Autism plus learning disability seems to increase the 'perceived' stress.
3. Parental stress may well present as physiological stress. This is particularly important in relation to the measurement of something called cortisol.

OK, there's nothing earth-shattering about such findings. They again imply that as and when a child receives a diagnosis of autism or ASD, parents or primary caregivers might also benefit from some information on what they might expect and what they can do when it comes to coping with stress. Caring for the carers (see here) and offering things like respite care to those who need it (see here) sound like good initiatives. Bear also in mind, that parenting a child with autism is often done alongside parenting other children too, and what effect that can sometimes have on them (see here)...


[1] Nik Adib NA. et al. Perceived Stress among Caregivers of Children with Autism Spectrum Disorder: A State-Wide Study. Int J Environ Res Public Health. 2019 Apr 25;16(8). pii: E1468.

[2] Pattini E. et al. Psychological characteristics and physiological reactivity to acute stress in mothers of children with Autism Spectrum Disorder. Stress Health. 2019 Apr 26.


Friday, 31 May 2019

Baclofen is back: "Baclofen as an adjuvant therapy for autism"

"Our data support [the] safety and efficacy of baclofen as an adjuvant to risperidone for improvement of hyperactivity symptoms in children with ASD [autism spectrum disorder]."

So said the findings reported by Seyedeh-Mahsa Mahdavinasab and colleagues [1] talking about the use of baclofen as an add-on medicine in the context of risperidone use in relation to autism. Baclofen by the way, is typically known as "a gamma-aminobutyric acid (GABA) agonist" (binds to the GABA receptors and activates them) which accounts for its use as "a skeletal muscle relaxant" given the inhibitory function of GABA and GABA receptors.

Why the 'baclofen is back' sentiment expressed in the title of this post? Well, a few years back there was some excitement about a compound called STX209 otherwise known as arbaclofen in the context of a genetic condition manifesting autistic signs and symptoms (see here) and autism itself. Arbaclofen is an enantiomer (mirror image in a chemical sense) of baclofen, but unfortunately fell by the wayside after some less than impressive results emerged from clinical trials (see here). Arbaclofen might have been kicked into the long grass for now but baclofen it seems, is still on the autism research agenda...

Researchers report results based on a "10-week randomized-controlled study aimed at evaluating the potential of baclofen as an adjuvant therapy to enhance the effect of risperidone in children with ASD." Risperidone is an antipsychotic which is indicated for selective use with children with autism (see here) specifically to treat/manage aggressive and challenging behaviours. They reported that several outcome measures saw a change - a positive change - specifically in relation to hyperactivity behaviours which can often accompany aggression. Importantly, they also noted that during and after 10 weeks of add-on baclofen use, adverse events were reported to be at a minimum.

There is more to do in this area before any sweeping generalisations are made. I personally would like to see more data on potential best- and non-responders in the context that GABA is still a topic of interest to autism research (see here). I know also that some people might be a little put-out by the idea that more medication is added to the lives of young children with autism and worries about how this might impact them in later years. We need a lot more data.


[1] Mahdavinasab SM. et al. Baclofen as an adjuvant therapy for autism: a randomized, double-blind, placebo-controlled trial. Eur Child Adolesc Psychiatry. 2019 Apr 12.


Thursday, 30 May 2019

What's potentially behind self-injury coincidental to autism?

"Alexithymia, depression, anxiety and sensory differences may place some autistic individuals at especial risk of self-injury."

Those were some of the conclusions reached in the paper published by Rachel Moseley and colleagues [1] (open-access) following their investigation of an important topic - non-suicidal self-injury (NSSI) - in relation to autism "without intellectual disability." Self-injurious behaviour (SIB) is not a pleasant topic to talk about, but is important to quite a few people diagnosed as being on the autism spectrum (see here and see here).

Drawing on data provided by over one hundred adults with autism (autistic adults if you prefer), half of whom were categorised as 'current self-harmers', a quarter of whom were 'historic self-harmers' and a quarter of whom were 'non self-harmers', researchers set to work "to examine alexithymia, mentalising impairments, autistic traits and sensory differences" as possible important variables for NSSI. Alexithymia by the way, is described as "the subclinical inability to identify and describe emotions in the self." Researchers utilised several different questionnaires including a tool specifically designed to test for NSSI: The Non-Suicidal Self-Injury Assessment Tool (NSSI-AT), a "comprehensive instrument [that] documents the nature and bodily location of any self-injurious behaviours; their functional utility; their recency, frequency and likelihood of reoccurrence; the age of onset of self-injury; the severity of injuries" among other things. Results were collated and analysed.

Alongside the headline finding that was included in the opening sentence to this post, other interesting details also emerged from the data. So: "Of the 76 current and historic self-harmers, 60 could recall the onset of self-injury at an average age of 15.1 years." Bearing in mind that 15.1 years was an average age of onset, such a finding potentially provides a developmental window when self-harming could maybe be screened for and interventions put in place. Indeed, from what I understand, this is a fairly typical time of onset for self-injury in the general population minus any sweeping generalisations.

Also: "The most common function of NSSI was the regulation of low-energy affective states (depression, dissociation), followed by the regulation of high-energy states such as anger and anxiety." There's an important word in that last sentence - regulation - that needs a lot more inquiry. It implies that self-injury is not just mindless violence against self but might actually serve some sort of purpose. Indeed, other recent papers have also mentioned regulation in the context of self-injury [2] too. Allied to other research suggesting that 'challenging behvaiours' might for example, under some circumstances, also serve a purpose (see here) and how self-injury could present in a variety of ways (see here), and there are leads to follow. Indeed, it could imply that teaching regulatory processes such as those linked to exercise (see here) or the use of meditative techniques (see here) could be worthwhile for some at least.

And just before I leave this topic, I'm minded to bring in another issue that could be investigated in the context of self-injury: interoception and body awareness in the context of autism (see here). Minus any psychobabble, interoception represents "the sense of the physiological condition of the body." It strikes me as possible that a reduced capacity for interoception in relation to autism, as has been talked about in other independent study [3], could be another important variable in the cycle of self-injury and another point of intervention...


[1] Moseley RL. et al. A ‘choice’, an ‘addiction’, a way ‘out of the lost’: exploring self-injury in autistic people without intellectual disability. Molecular Autism. 2019; 10: 18.

[2] Weiner L. et al. A case study of suicidality presenting as a restricted interest in autism spectrum disorder. BMC Psychiatry. 2019; 19: 126.

[3] Fiene L. & Brownlow C. Investigating interoception and body awareness in adults with and without autism spectrum disorder. Autism Res. 2015 Dec;8(6):709-16.


Wednesday, 29 May 2019

Probiotics for autism systematically reviewed

"Our review includes two randomized controlled trials, which showed improvement of ASD [autism spectrum disorder] behaviors, and three open trials, all which exhibited a trend of improvement."

So said the findings reported by Jun Liu and colleagues [1] and the results of their "updated systematic review" on the topic of probiotic 'therapy' in the context of behaviour and gastrointestinal (GI) functioning in autism.

The current scientific outlook for probiotic use in the context of autism looked to be pretty good on the basis of the Liu findings. They corroborate quite a few individual study results that have been fodder for this blog (see here and see here) and fit in well with an emerging pattern of research suggesting that the trillions of wee beasties that inhabit the gastrointestinal (GI) tract might be doing a lot more than just helping us digest food (see here and see here).

What else is required? Well Liu et al talk about more "rigorous trials" to answer questions like who on the autism spectrum might be a best responder to this type of intervention and what bacterial species might be most important. I'd also like to see a little more research on the hows-and-whys of such intervention (see here for example) and whether probiotics are as harmless as many have made them out to be.



[1] Liu J. et al. Probiotic Therapy for Treating Behavioral and Gastrointestinal Symptoms in Autism Spectrum Disorder: A Systematic Review of Clinical Trials. Curr Med Sci. 2019 Apr;39(2):173-184.


Tuesday, 28 May 2019

Breastfeeding and autism continued

"We found that the percentage of mothers who started breastfeeding was similar between the two groups, but mothers of children with ASD [autism spectrum disorder] breastfed for a shorter amount of time compared to mothers of children without ASD."

So said the findings reported by Gnakub Soke and colleagues [1] continuing a research theme that I've had some professional interest in down the years (see here) on whether breastfeeding (use, duration, etc) *might* have some important *links* to risk of offspring autism and/or related conditions (see here). The same caveats mention in some of my other musings on this topic come into effect when talking (briefly) about the Soke findings (i.e. no-one is saying that a lack of breastfeeding 'causes' autism). That being said, there might still however be some important science to do on how breastfeeding and/or the constituents of breast milk might have some important biological effects for the developing child (minus any psychobabble explanations).

The Study to Explore Early Development or SEED was the starting point for the Soke study (continuing an autism research theme), and specifically investigation into the: "associations between ASD and breastfeeding initiation (yes/no) and duration (months categorized in tertiles)." The findings suggested that (a) breastfeeding rates (initiation rates) were high in mums of children with ASD compared to not-autism controls (85% vs. 90%), and (b) "mothers of children with ASD were less likely to report duration of breastfeeding in the high (≥12 months) versus low tertile (<6 months)... or the middle (6-<12 months) versus low tertile."

I don't want to dwell too much on the whys-and-wherefores of the Soke findings but there are some important questions that need answering. Not least the question of why breastfeeding seems to end quicker for those mums of children who were subsequently diagnosed as having an ASD. Were these infants more difficult to feed (something which Kanner might have picked up on in his seminal paper describing autism)? What role does the presentation of the 'broader autism phenotype' (BAP) in mothers mentioned by Soke et al play in such findings? That last point in particular, draws on the need for lots more research into the experience of pregnancy and motherhood with the BAP (see here) and/or autism in mind (see here).


[1] Soke GN. et al. Association Between Breastfeeding Initiation and Duration and Autism Spectrum Disorder in Preschool Children Enrolled in the Study to Explore Early Development. Autism Res. 2019 Mar 9.