Saturday, 17 February 2018

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

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

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

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

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

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

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


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


Friday, 16 February 2018

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

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

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

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

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

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

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


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

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

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

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

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

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

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


Thursday, 15 February 2018

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

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

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

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

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


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

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

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


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

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

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


Wednesday, 14 February 2018

Low grade intestinal inflammation and autism

The suggestion that low grade intestinal inflammation might be related to some autism comes from the findings reported by Katarina Babinská and colleagues [1] (open-access available here).

Researchers set out to "assess the concentrations of fecal calprotectin in a sample of children with ASD [autism spectrum disorder] and to investigate the correlations of this inflammatory marker with the core behavioral symptoms of ASD."

Faecal calprotectin (FC) is a measure of the amount of calprotectin in a stool (poo) sample. It's typically released in response to the presence of inflammation and, here in Blighty at least, is indicated as "an option to support clinicians with the differential diagnosis of inflammatory bowel disease (IBD) or irritable bowel syndrome (IBS) in adults with recent onset lower gastrointestinal symptoms for whom specialist assessment is being considered." 

In terms of research history looking at autism and FC, there is some peer-reviewed science on the topic; also having been included as a parameter in the important paper by Laura de Magistris and colleagues [2] talking about 'leaky gut' in the context of some autism (see here) and how "FC was elevated in 24.4% of patients with autism and in 11.6% of their relatives." Such research is set in the more general context that bowel or gastrointestinal (GI) issues are absolutely no stranger to a diagnosis of autism (see here).

This time around Babinská et al measured FC (via ELISA) in some 87 children diagnosed with an autism spectrum disorder (ASD) aged between 2 and 17 years of age. The authors use the term 'low functioning' to describe this portion of their participant group but I'm rather less enamoured with such labels (see here) despite the well-deserved focus on a group very much under-represented in autism research and other areas. Alongside, over 50 age-matched controls (not-autism) and 29 siblings of children with ASD also provided samples for analysis and comparisons.

Results were not exactly as cut-and-dried as one might have expected. So: "In non-relatives significantly lower values of fecal calprotectin were observed than in both subjects with ASD and their siblings." What this means is that based on group results, those with autism and the siblings of those with autism seemed to manifest higher levels of FC than non-related controls. Based on individual results, where elevated levels of fecal calprotectin was set at 50 µg/g of feces or higher according to test producers guidance as being a level of concern, the frequency of such a finding was greater in those with autism (22%) and their siblings (20%) than in non-related controls (9%) but this difference was reported as 'non-significant'.

Authors also did a little work on another important area in relation to bowel symptoms/pathology and autism: how *might* something like intestinal inflammation 'interact' with the behavioural signs and symptoms of autism? Well, we are told that those diagnosed with autism "had to meet criteria for ASD" on two gold-standard diagnostic tools: the Autism Diagnostic Observation Schedule – second edition and the Autism Diagnostic Interview-Revised (ADI-R). Data from the ADI was examined in the context of the FC findings and lo and behold: "In the group with ASD significant correlations of fecal calprotectin with all domains of the ADI-R diagnostic tool were found: qualitative abnormalities in reciprocal social interaction and communication, restrictive and repetitive patterns of behavior." I say this bearing in mind that similar analyses between FC values and ADOS ratings do not seem to have been either done or reported on for some reason.

When the authors talk about low grade intestinal inflammation as potentially being relevant to some autism, they seem to be accurate insofar as the measured levels of FC in some participants and the *correlation* with autism scores on one of the gold-standard assessment instruments. That being said, there is quite a bit more to do in this area before anyone gets too carried away with the results as they stand. So for example, all that chatter about inflammatory bowel disease (IBD) being related to some autism (see here and see here) did not seem to register in this particular study insofar as the guidance on FC being a marker for possible IBD, albeit based on higher levels of FC being detected: "Active, symptomatic inflammatory bowel disease 200 – 40,000 mg/kg."

I also note that the authors report an important limitation when it came to their research: "Additional factors that might have been a cause of elevated FC levels, such as nutritional or gastrointestinal factors were not analysed." Nutritional factors eh? Y'mean like milk type for example [3] or other dietary and/or environmental factors such as the implementation of a gluten-free diet [4] positively affecting FC levels? Indeed, there are lots of potential factors that could cause a 'false-positive' when it comes to elevated FC such as infections like C. diff or gastrointestinal conditions such as coeliac disease, many of which have shown some important connections to autism (see here for example).

It looks like there is still much more research to do in this area but investigations should definitely continue.

To close, my brood have just discovered the brilliant film 'The Great Escape'. As well as setting up many, many discussions about war, bravery and captivity, they've also commented on the theme tune...


[1] Babinská K. et al. Fecal calprotectin levels correlate with main domains of the autism diagnostic interview-revised (ADI-R) in a sample of individuals with autism spectrum disorders from Slovakia. Physiol Res. 2017 Dec 30;66(Supplementum 4):S517-S522.

[2] de Magistris L. et al. Alterations of the intestinal barrier in patients with autism spectrum disorders and in their first-degree relatives. J Pediatr Gastroenterol Nutr. 2010 Oct;51(4):418-24.

[3] Ho S. et al. Comparative effects of A1 versus A2 beta-casein on gastrointestinal measures: a blinded randomised cross-over pilot study. Eur J Clin Nutr. 2014 Sep;68(9):994-1000.

[4] Balamtekın N. et al. Fecal calprotectin concentration is increased in children with celiac disease: relation with histopathological findings. Turk J Gastroenterol. 2012;23(5):503-8.


Tuesday, 13 February 2018

Once more... listen to parents: on the identification of the early behavioural signs of autism

"The results suggest that parents may detect some clinically informative behaviors based on their day-to-day observations more readily than do clinicians during brief clinical assessments."

So said the findings reported by Lori-Ann Sacrey and colleagues [1] who compared the views of parents "of children at high-risk of autism spectrum disorder (ASD; have an older sibling with ASD)" with clinicians opinions when it came to reporting on around 20 clinical signs that could indicate the presence of autism.

Clinicians relied on the Autism Observational Scale for Infants (AOSI) to make their judgements and parents used the Autism Parent Screen for Infants (APSI) (a sort of parent-version of the AOSI) for theirs when infants were between 12 and 18 months of age. Infants being 'observed' subsequently underwent "a blind independent diagnostic assessment for ASD at 36 months of age" to see how accurate those earlier parent and clinician observations were.

The old adage that 'parents generally know their children best' shines through in the Sacrey results with "parent-reported symptoms being better able to differentiate between children with and without ASD at both 12 and 18 months of age compared to clinician observations during a brief office visit." No, most parents aren't experts when it comes to child development and no, typically they aren't seeing lots of children on a day-to-day basis who may present with various developmental issues including autism. But... compared with an often "brief clinical assessment", all those day-in day-out observations that are made - particularly when autism is 'already a part of the family' - do seem to count for quite a bit. Once again, we would all do well to listen to parents (see here) and any concerns they have about their child's development. I might add that combined with the recording technology available to most people these days and the tendency for many parents to document their child's every developmental move, there is potentially plenty of data available for further analysis (see here).

There are a few other issues that could come into play as a result of the Sacrey and other, related but independent findings. I tend to go on quite a bit on this blog about how various 'comorbidities' (if I can still call them that) seem to be over-represented when it comes to a diagnosis of autism. One of the more prevalent ones is that of bowel / gastrointestinal (GI) issues (see here) which is becoming more readily accepted in various circles as being a part of the clinical picture for quite a few people on the autism spectrum. I've talked before about how parents were/are typically the first ones to pick up the bowel-side of things and how, their observations of their own child's bowel symptoms, can on many occasions, provide some important 'pointers' to the professionals (see here). I see the Sacrey work as an extension of this other research, as the message 'listen to parents' continues to be a consistent theme.


[1] Sacrey LR. et al. Parent and clinician agreement regarding early behavioral signs in 12- and 18-month-old infants at-risk of autism spectrum disorder. Autism Res. 2018 Jan 22.


Monday, 12 February 2018

Methylphenidate affecting academic performance meta-analysed

When first tweeting about the paper by Anne Fleur Kortekaas-Rijlaarsdam and colleagues [1] I kinda made a mistake. The text of the tweet read something like: "Does methylphenidate improve academic performance? A systematic review and meta-analysis... Pretty much so, but only in relatively small amounts."

Reading that tweet back to myself I realised that by saying 'but only in relatively small amounts' it's highly likely that any readers might have thought that I was talking about the dose of methylphenidate (MPH) rather than the [intended] effect on things like "math productivity (7.8% increase, p < .001); math accuracy (3.0% increase, p = .001); [and] increased reading speed (SMD .47, p < .001)." I apologise, and once again reiterate my blogging (and social media) caveat about not giving anything that looks, sounds or smells like medical or clinical advice.

I did think it worthwhile to write a short post about the Kortekaas-Rijlaarsdam findings given that (a) ADHD (attention-deficit hyperactivity disorder) is something that turns up quite a bit on this blog (see here for example), and (b) pharmacotherapy 'for ADHD' is an important intervention area which has also, unfortunately under some circumstances, been 'hijacked' for other purposes (see here). On that last point, I specifically refer to the idea that for some people, striving for a diagnosis of ADHD is merely a route to either better academic accommodations or perhaps more worryingly, to gain access to a class of medicines with some potentially significant 'cognitive-enhancing' qualities...

What sets the Kortekaas-Rijlaarsdam findings apart from other reviews of the potential nootropic (cognitive enhancing) abilities of something like MPH is their focus on resolving the issue of "whether there are improvements in core academic skills or just improvements in academic productivity" in the context of "the mediating or moderating effects of symptom improvements, demographic-, design- and disorder-related variables."

From a starting number of 148 full-text research articles, the collected texts were screened for eligibility and some 34 were eventually included for meta-analysis ("quantitative synthesis"). These articles were included because they "provided information about either accuracy or productivity scores for math, reading or spelling, or a combination of these" or could at least be calculated on the basis of their included data. Various mediating and moderating variables were also thrown into the statistical mix - "age, gender, percent diagnosed with ADHD-inattentive subtype, and study characteristics: release system, trial duration, and titration method" - and results reported.

As per previous sentences, various aspects of maths performance showed an improvement that correlated with MPH use, and reading speed but not accuracy also came out as potentially showing a relationship with medicine usage. Important too was the information that: "None of our mediators or moderators influenced MPH effects on math and reading accuracy or productivity."

So, following meta-analytic scrutiny of some 1700 children, it looks like there is a small but potentially relevant effect from MPH use of some academic abilities, at least in the short-term ("between 1 and 7 days"). The authors do well not to stray too much into speculating mode when it comes to the cause of any nootropic effect but instead to include the need for more research "to isolate groups of patients who may benefit more or less from MPH and to reveal its mechanism of action." Can't argue with that.

And going back to the topic of cognitive enahncers, an interesting article from a few years back on what they may or may not be doing to elements of our University student body...

Music to close... Sia and Chandelier. Seemingly always playing outside my dojo....


[1] Kortekaas-Rijlaarsdam AF. et al. Does methylphenidate improve academic performance? A systematic review and meta-analysis. Eur Child Adolesc Psychiatry. 2018 Jan 20.


Saturday, 10 February 2018

The latest CDC figures on ADHD medication trends among women aged 15-44

The report published by Kayla Anderson and colleagues [1] has made quite a few media headlines (see here for example) based on their observations that: "The percentage of privately insured reproductive-aged women who filled a prescription for an ADHD [attention-deficit hyperactivity disordermedication increased 344% from 2003 (0.9%) to 2015 (4.0%). Further: "ADHD medication prescriptions increased across all age groups and U.S. geographic regions, and the increase was confined to stimulant medications."

"The new report raises questions about the increasing use of a diagnosis that once was reserved for children and adolescents" was one of the issues discussed following the publication of the Anderson report. This continues a theme in psychiatric circles on whether the diagnosis of ADHD is being 'over-used' across many different age groups [2]. Another issue - that of the potential performance-enhancing abilities of certain medicines commonly indicated for managing ADHD (see here for a recent review [3]) - has also come into the media spotlight too as a result of these latest findings.

A further point of discussion has also been noted by Anderson et al: "ADHD medication prescriptions are increasingly common among privately insured, reproductive-aged women. Additional research on ADHD medication safety among this population, including safety before and during pregnancy, could help women and their health care providers make evidence-based decisions concerning the risks and benefits of pharmacologic and behavioral treatment options for common conditions, including ADHD." The question raised is whether use of something like "a prescription for mixed amphetamine salts... for lisdexamfetamine.. for methylphenidate" is 'safe' before and during pregnancy when it comes to offspring health, wellbeing and development?

The area of pregnancy medicine use is a particularly complicated issue. Not least because various medicines used before and during pregnancy have come under the spotlight in recent times, in terms of their potential effects on the unborn child. Ranging from the pretty convincing valproate story (and guidance) (see here) to the *possible* effects of various anti-depressants (see here) to that of over-the-counter pain relief medicines (see here), the research literature is quite 'lively' when it comes to pregnancy pharmacotherapy. Of course there are gaps in the literature as it stands, and one should never forget that many of the prescription medicines under the research spotlight are not typically prescribed and dispensed willy-nilly, but...

In relation to 'stimulant medication' indicated for ADHD and any effect(s) on the unborn child, we're not yet in any position to make any valued judgements just yet. There is some research out there [4] and it's not all positive [5] but a lot more investigations are indicated. I say that bearing in mind that: (a) ADHD might not be the only condition/label given to some mothers, which will likely affect their medication profile too (see here for example), and (b) much like other work looking at medicines and risk of 'adverse' childhood issues, there's always the possibility that the risk to offspring *might* be elevated as a result of the underlying condition being treated/managed (i.e. ADHD) or some related comorbidity irrespective of any medication influences.

I'm not coming out as any sort of 'champion' for ADHD medications (despite their quite impressive safety and efficacy profiles) but neither am I going to demonise a whole class of medicines based on a currently pretty scant evidence base. Understanding also how much of an effect a diagnosis of ADHD can have on a person (see here and see here for examples), further investigations are indicated before hype and sweeping generalisations take hold.

And this is not the first time that research has indicated that ADHD medication use is on the up (see here)...


[1] Anderson KN. et al. Attention-Deficit/Hyperactivity Disorder Medication Prescription Claims Among Privately Insured Women Aged 15-44 Years - United States, 2003-2015. MMWR Morb Mortal Wkly Rep. 2018 Jan 19;67(2):66-7

[2] Danielson ML. et al. Prevalence of Parent-Reported ADHD Diagnosis and Associated Treatment Among U.S. Children and Adolescents, 2016. J Clin Child Adolesc Psychol. 2018 Jan 24:1-14.

[3] Kortekaas-Rijlaarsdam AF. et al. Does methylphenidate improve academic performance? A systematic review and meta-analysis. Eur Child Adolesc Psychiatry. 2018 Jan 20.

[4] Nörby U. et al. Perinatal Outcomes After Treatment With ADHD Medication During Pregnancy. Pediatrics. 2017 Dec;140(6). pii: e20170747.

[5] Bro SP. et al. Adverse pregnancy outcomes after exposure to methylphenidate or atomoxetine during pregnancy. Clin Epidemiol. 2015 Jan 29;7:139-47.


Friday, 9 February 2018

"ASD characteristics in adulthood are differently perceived across age, sex, and informants"

The research tag-team that is Anne Lever and Hilde Geurts have provided peer-reviewed fodder for this blog before (see here and see here). Without wishing to cajole their research interests into a specific box, quite a bit of their time seems to be taken up by looking at autism in the context of ageing, alongside how the label of autism does not seem to have a monopoly on the presentation of certain autistic traits.

A recent paper published by this team [1] provides yet more blogging material, specifically focused on testing "the association between age and ASD [autism spectrum disorder] characteristics, including empathy and sensory sensitivity, in adults aged 19–79 years." A scientific hat-tip is offered to other research in this area [2] that previously observed that: "older age was associated with higher ratings of ASD traits and better cognitive performance."

Drawing on data derived from a participant group numbering above 400 (N=237 with autism and N=198 without autism) spanning the age ranges, a variety of self-report and informant-report (family members, friends, other significant others) were utilised. I should point out that the autism participant group seemed to be represented by the 'more able' part of the autism spectrum (I don't use the term 'functioning') insofar as most either being diagnosed with Asperger syndrome or PDD-NOS (pervasive developmental disorder - not otherwise specified), being predominantly independent or living with a partner or housemate in residential status terms and also with that reliance on self-report used throughout the study kept in mind. This is worth knowing given other discussions on under-represented groups when it comes to scientific study (see here) and how representative autism research may or may not be to the entire spectrum.

Among the measures included for analysis we have an old favourite - the Autism-Spectrum Quotient (AQ) - as well as the Interpersonal Reactivity Index (IRI) (measuring various aspects of empathy) and the Sensory Sensitivity Questionnaire (SSQ) (examining sensory hyper- or hyposensitivity). Obtained results were collated and subjected to quite a few statistical analyses.

Results: noted as a 'group difference' findings were reported observing that: "Adults with ASD reported higher scores on the SSQ and on all subscales of the AQ than adults without ASD." This is pretty much what would be expected, despite any qualms I might have about what the AQ actually measures (see here for more of them). Sensory issues being reported as being greater in those with a diagnosis of autism also ties in well with their inclusion in the DSM-5 schedule for diagnosing autism or ASD (see here).

Then: "Within the ASD group, age-related differences were observed in self-reported ASD traits and sensory sensitivity, with a peak among middle-aged adults." Alongside that previously 'hat-tipped' study, the authors conclude that "ASD characteristics are more heavily experienced in middle adulthood than in younger or older adults." This is interesting from quite a few perspectives; bearing in mind that such findings say nothing about the expression of autism in childhood and early adulthood. Appreciating that the self-report of autism or sensory traits may not be the same as everyday autism expression, such findings *might* have some relevance to various issues such as the rise and rise of adult autism diagnoses being given and indeed, how a diagnosis of autism for some (a few?) might not be a 'lifelong' issue (see here). I know that last point raises blood pressure in some quarters as words like 'masking' are banded around (with the need for far greater study), but there is good reason to think that like many other conditions/labels, autistic behaviours and/or traits ebb and flow according to environment and perhaps other factors, such as the presentation of comorbidity for example (as per the author's other work [3] already mentioned). In short, the presentation of autism is probably dynamic and fluidic, rather than just a static thing.

Onward: "we replicated earlier findings that females with ASD had more sensory issues and reported more ASD characteristics than males... whereas females without ASD manifested fewer ASD traits than non-ASD males.". Females with ASD (74 females vs. 163 males) 'reported more ASD characteristics than males'? Intriguing - "ASD females reported higher scores than ASD males on the AQ total score" - to say the least in light of other [childhood] findings [4] but not without cautions. I go back once again the question of what the AQ is actually measuring and whether for example, the typically higher rate of mood disorders generally noted in females could be a potential confounder when it comes to AQ scores in the context of that previous reference [3] from the authors. This area requires further investigation.

Finally: "Overall, the current results show poor to fair agreement between self- and other-reports of well-known proxies, even though the agreement of the overall group was similar to those previously reported for social responsiveness." Again, some potentially important lessons to be learned here insofar as the 'meaning of autism' to a person and those around them. Indeed I note the authors' offer one explanation: "the self may be more accurate about traits that describe unobservable thoughts and feelings due to privileged access (e.g. feelings of empathy and sensory sensitivity), whereas an informant would be more accurate about observable behavior (e.g., ASD traits)." Again, jumping back into 'hot potato' territory, such a finding may have implications for the whole 'self-diagnosed vs. formal diagnosis' debate that still continues at a pace (see here).

There is quite a bit more to take in from this latest paper from Lever & Geurts and definitely some food for thought. I'll leave you however with one final quote from the authors that is perhaps one of the more important take-away points from their study: "it is important to repeatedly assess self-reported ASD characteristics during adulthood." Who would argue with that in terms of getting wants, wishes, needs and requirements accurate and up-to-date?


[1] Lever AG. & Geurts HM. Is Older Age Associated with Higher Self- and Other-Rated ASD Characteristics? Journal of Autism & Developmental Disorders. 2018. Jan 18.

[2] Happé FG. et al. Demographic and Cognitive Profile of Individuals Seeking a Diagnosis of Autism Spectrum Disorder in Adulthood. J Autism Dev Disord. 2016 Nov;46(11):3469-3480.

[3] Geurts HM. et al. Autism Characteristics in Older Adults with Depressive Disorders. The American Journal of Geriatric Psychiatry. 2016; 24: 164-169.

[4] Øien RA. et al. Sex-Differences in Children Referred for Assessment: An Exploratory Analysis of the Autism Mental Status Exam (AMSE). J Autism Dev Disord. 2018. Feb 8.


Thursday, 8 February 2018

Maternal diabetes and offspring autism risk meta-analysed

"Maternal diabetes, especially gestational diabetes mellitus, is associated with ASDs [autism spectrum disorders] in offspring based on a limited number of convincing case-control studies. More large-scale population-based prospective studies are still needed to draw firm conclusions."

So concluded the systematic review and meta-analysis by Hongquan Wan and colleagues [1] taking on an important question: does maternal diabetes confer an enhanced risk of offspring autism? Diabetes by the way, covers quite a bit of diagnostic ground, but is typically characterised by elevations in blood sugar levels and the various ways that this can (and does) affect biology and risk of some important adverse conditions.

Yes, appears to the answer based on the peer-reviewed research literature so far (until June 2017) with regards to maternal diabetes affecting offspring autism risk; although with it, a greater need to confirm such findings and also elucidate possible genetic and biological pathways linking diabetes exposure and offspring autism risk is required. I might add that having covered this topic a few times on this blog (see here and see here), including discussing other meta-analysis results [2], I'm not all that surprised by the findings.

Wan et al report results based on 12 articles - "7 were case-control studies... and 5 were cohort study." Combining results in a meta-analytic fashion produced some important observations: "The overall analysis demonstrated that gestational diabetes increased the risk of ASD by 48%" and when reliant on "case-control studies with moderate... or high quality [standing]", the risk increased to over 60%. In short, maternal diabetes exposure does seem to have something of an important effect on offspring risk of autism.

Mechanism(s) of effect? Well, the authors do provide some summary of hypotheses previously put forward. Diabetes exposure causing "brain malformation and aberrant neurodevelopment" is one theory; with words such as "enhanced cell apoptosis and activated oxidative stress" also included. Even possible immune system effects gets some airtime; as the discussion also turns to "the presence of autoantibodies" as a potentially important variable. Autoantibodies, I might add, are part and parcel of at least one type of diabetes. I might also throw in the idea of foetal programming as an over-arching concept to perhaps keep in mind and with it, the implication that early and timely diagnosis and management of maternal diabetes both before and during pregnancy *could* potentially affect offspring autism risk. *Could* is the operative word there...

But... alongside all the 'we need more and better research in this area' sentiments, I'm also minded to highlight how maternal diabetes - in all it's forms - is not necessarily a stand-alone condition. Indeed, it's an important point to remember that when talking about pregnancy factors in the context of something like offspring autism risk, there could be a range of separate but overlapping issues to contend with (see here and see here for examples) which complicate any attempts to single out particular variables as being more or less important when it comes to offspring outcomes.

It's also unwise to assume that 'all autism' is somehow conception or pregnancy-associated either (see here and see here)...


[1] Wan H. et al. Association of maternal diabetes with autism spectrum disorders in offspring: A systemic review and meta-analysis. Medicine. 2018' 77: e9438.

[2] Xu G. et al. Maternal diabetes and the risk of autism spectrum disorders in the offspring: a systematic review and meta-analysis. J Autism Dev Disord. 2014 Apr;44(4):766-75.


Wednesday, 7 February 2018

More evidence for the 'anti-aggression' effect of fish oils?

"In conclusion, this experiment indicates that Omega-3 administration has beneficial effects in reducing aggression among the general population."

So concluded the study by Laurent Bègue and colleagues [1] potentially adding to other research suggesting that fish oils - omega 3 fatty acids including docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) - might have something of an interesting effect on aggression and violence in various contexts (see here).

Based on a "double-blind randomized trial" design, nearly 200 participants with seemingly no current clinical psychiatric issues were allocated to receive a daily omega-3 fish oil supplement or placebo ("copra oil") over a 6-week period. Self-reported aggression was measured before and after receipt of the active supplement or placebo. Bearing in mind that both researchers and participants were blinded to who was taking what, the self-reports for those taking the daily fish oil supplement suggested that they thought/reported themselves less aggressive at the end of the study compared with the beginning. Ergo, fish oils supplements might, in some part, *act* on self-reported aggression, bearing in mind that self-report may not be the only way to assess for something like aggression.

As per my previous blogging foray into this topic, there is a surprising amount of peer-reviewed research that has been done on the topic of fish oils and aggression [2]. Don't get me wrong, the science is not yet in any position to conclusively suggest that fish oils should be approved for reducing aggression and/or violence at a population level, but there are some glimmers that an effect may be present at least for some. Other, related investigations talking about a negative correlation between circulating blood omega-3 levels and various aspects of aggression [3] add to the 'correlative' evidence base in this area.

There are a myriad of reasons why people are aggressive that are probably going to be different in different occasions and in different environments. These range from the effect(s) of something like impulsiveness in reactive aggression to the often negative influence of things like drugs and/or alcohol or even as a possible manifestation of certain psychopathology. One also needs to understand that aggression is not always a negative thing as anyone who participates in combat sports for example, will testify.

There is likely no single 'quick fix' to such feelings and/or behaviours when undesirable, despite the strong need and want for such intervention(s) (although there are some glimmers of hope in the peer-reviewed domain). Bearing in mind however, that affecting aggression might be just one part of the fairly beneficial profile related to fatty acid supplement use, I'm fast approaching a position whereby the overall picture of fatty acid use is favouring 'beneficial' for many people over 'adverse'. If aggression is similarly [positively] affected, and given the relative in-expense and wide availability of such fatty acid supplements, the emphasis switches towards putting up logical arguments on why such supplements shouldn't be used rather than why they should...

To close, here's hoping...


[1] Bègue L. et al. Omega-3 supplements reduce self-reported physical aggression in healthy adults. Psychiatry Research. 2018; 261: 307-311.

[2] Gajos JM. & Beaver KM. The effect of omega-3 fatty acids on aggression: A meta-analysis. Neurosci Biobehav Rev. 2016 Oct;69:147-58.

[3] Meyer BJ. et al. Baseline omega-3 index correlates with aggressive and attention deficit disorder behaviours in adult prisoners. PLoS One. 2015 Mar 20;10(3):e0120220.


Tuesday, 6 February 2018

Could early sleep characteristics "constitute one clinical sign of ASD risk"?

Could problematic early sleep behaviours constitute one sign of autism?

That was the question asked and partially answered in the paper by A. K. Danny Nguyen and colleagues [1] who set out to "estimate prospective associations between infant sleep characteristics at 12 months and later ASD [autism spectrum disorder] screening scores at 24 months."

Based on data obtained for over a thousand children and their mothers enrolled on the "Conditions Affecting Neurocognitive Development and Learning in Early Childhood longitudinal birth cohort study" (CANDLE study), researchers measured several sleep characteristics in young infants at approximately a year old ("nighttime and daytime sleep, night wakings, and sleep onset latency") and then at 2 years of age, screened them for the signs and symptoms of autism.

Researchers reported that: "The number of night wakings was the only sleep characteristic at 12 months to be significantly associated with the development of early ASD symptoms at 24 months." Whilst an important finding, this suggests that despite the authors' claims that: "Infants with more sleep problems by 12 months, especially those waking more often during the night, showed an increased number of early ASD symptoms a year later", early sleep behaviours are perhaps not yet ready to go 'mainstream' as a clinical sign of autism. I say this also because once again (see here), we have two variables being measured at two different time periods in the Nguyen study...

But just before anyone thinks I'm poo-pooing sleep as a potentially important factor when it comes to autism, I'm not. I've for example, covered other (independent) research suggesting that infant sleep duration at 3-4 months objectively measured via actigraphy might be important for girls in particular when it comes to autism (see here). I've also talked about issues such as sleep apnoea as being important to some autism too (see here). Sleep (perhaps alongside other issues) is worthy of a lot more research and clinical attention in the context of autism.

But as a specific 'clinical sign of ASD risk'? I stand by initial reaction for now...


[1] Nguyen AKD. et al. Prospective Associations Between Infant Sleep at 12 Months and Autism Spectrum Disorder Screening Scores at 24 Months in a Community-Based Birth Cohort. J Clin Psychiatry. 2018 Jan 2;79(1). pii: 16m11127.


Monday, 5 February 2018

Edging ever closer to the ICF core sets for autism

Yet another post about the ICF core sets for autism is offered up today, and the findings reported by Sven Bölte and colleagues [1] (open-access available here) detailing some consensus...

OK, a quick reminder of what the ICF core sets for autism were designed for: "To capture this complex melange of functioning experiences beyond the diagnosis, the ICF offers a tool to describe the lived experience of a person with ASD [autism spectrum disorder] in a comprehensive and standardized way." Melange? More people should use the world melange methinks.

I've discussed the ICF core sets for autism a few times on this blog (see here and see here and see here) and the various developmental processes leading up to the consensus on the core sets. This has included talking to many different groups of people about what they felt was important when it comes to autism outside of just the presentation of the core diagnostic characteristics.

The Bölte paper seems to be heading towards the end-game of the ICF core sets for autism development and their use of "20 international autism spectrum disorder experts" who "applied an established iterative decision-making consensus process to select from the candidate categories the most relevant ones to constitute the autism spectrum disorder Core Sets." Alongside decisions on a Comprehensive and a Brief (Common) ICF Core Set for autism, authors also decided that it would be useful to have some age-appropriate brief sets too: "a preschool set (aged 0–5 years), a school-age set (aged 6–16 years), and an older adolescent and adult set for individuals 17 years old and older."

I'm not going to say too much more about the Bölte findings because there really isn't too much more to say. Readers are invited to peruse the various descriptions included and make their own decision on their relevance or not. I will however raise one point covered by the authors regarding their study limitations: "despite efforts to achieve a broad representation of disciplines, some professional groups may have been underrepresented." Sadly for example, I see little professional representation when it comes to important things like gastrointestinal (GI) issues that are very much over-represented when it comes to autism (see here) and can have a real impact on day-to-day functioning (see here). On the more positive side of things however, the all-rounder than is the occupational therapist (OT) seemed to have had quite a bit of representation and input, which is really rather good to see (see here).

It looks like a new dawn is approaching when it comes to how we characterise autism beyond just the core dyad/triad...


[1] Bölte S. et al. The Gestalt of functioning in autism spectrum disorder: Results of the international conference to develop final consensus International Classification of Functioning, Disability and Health core sets. Autism. 2018 Jan 1:1362361318755522.


Saturday, 3 February 2018

More bad news for pregnancy paracetamol use?

An article in Medical News Today titled: "Is acetaminophen really safe in pregnancy?" caught my attention recently. Highlighting various recent peer-reviewed research suggesting that pregnancy paracetamol (acetaminophen) use seems to carry some *elevated risk* for quite a few potential adverse events for offspring, the *correlation* news just seems to be getting worse for this go-to over-the-counter painkiller and fever-reducer (see here and see here).

The Medical News Today article highlights a few studies but I want to focus on one in particular, by Carl-Gustaf Bornehag and colleagues [1], which suggested that risk of language delay in female offspring *might* show some correlation with early pregnancy paracetamol use.

Based on data derived from the SELMA study (Swedish Environmental Longitudinal, Mother and child, Asthma and allergy [2]), an important initiative that has already produced quite a bit of data (see here), researchers looked at "prenatal APAP [acetyl-para-aminophenol a.k.a paracetamol] exposure in relation to language development in offspring at 30 months of age." Data from over 750 women were garnered; covering both maternal report on paracetamol usage between conception and enrolment on the study (between 8-13 weeks of pregnancy) and "APAP urinary concentration at enrollment." Yes, this study did actually test for paracetamol [metabolite] concentration(s) in urine during the early stages of pregnancy. Such data was analysed in the context of offspring language development around 30 months of age via a nurse's assessment and parental report on "the number of words the child used (<25, 25–50 and >50)."

Results: paracetamol usage during conception/early pregnancy was not uncommon (around 60% of mothers reported this). Nothing particularly shocking there. Also: "APAP was measurable in all urine samples and urinary APAP was correlated with the number of APAP taken during pregnancy (P < 0.01)." Some good news there that maternal reports of paracetamol usage seemed to correlate pretty well with the measured values of paracetamol metabolites in the urine samples analysed.

Then, although language delay - "parental report of use of fewer than 50 words, termed language delay (LD)" - was present in about 1 in 10 children with a characteristic male bias (see here), female offspring born to mothers reporting paracetamol usage more than six times during early pregnancy were approximately six times more likely to show such language delay than those reporting no paracetamol usage. In effect, the female advantage over males when it came to reported language delay disappeared when paracetamol use was put into the clinical picture. Further: "The OR [odds ratio] for LD in girls whose mothers’ urinary APAP was in the highest compared to the lowest quartile was 10.34 (95% CI 1.37–77.86)." Those girls born to mums with the highest urinary concentrations of paracetamol metabolites, compared with those born to those with some of the lowest levels, seemed also to be at greater risk of language delay.

The authors themselves note that independent replication of their results is required before any grand claims are made. Alongside more formal assessment for something like language delay, I'd also like to see how some of the other metabolites measured for [3] in the SELMA initiative (there we quite a few) might also impact on their conclusions too; particularly in the context of endocrine disrupting chemicals being noted in other studies of paracetamol - offspring development (see here). Further investigation is also required on the 'whys' of paracetamol use in the context of pregnancy: does higher use of something like paracetamol perhaps indicate that some underlying issue that is being 'treated' by such use might also/instead be correlated with offspring developmental outcomes? Pain, fever or something else?

As you can see, the Bornehag study is interesting but not without flaws. Still, set within the rising tide of peer-reviewed research talking about potential issues associated with pregnancy use (excessive use?) of paracetamol and offspring outcomes [4], it's not however something that can be easily ignored...

And whilst we're on the topic of paracetamol, I also recently came across the paper by Abdulaziz Saeedan and colleagues [5] talking about testing the hypothesis that "paracetamol (PCM) can precipitate autistic like features when used to counteract vaccine-induced fever using experimental rat pups." I know (a) this takes us into a 'hot potato' area and (b) this is a study on rats, but set against work from other authors discussing a potential role for post-vaccine paracetamol use in the context of 'risk' of autism [6], such findings also perhaps offer a few further ideas for experimental study.


[1] Bornehag C-G. et al. Prenatal exposure to acetaminophen and children's language development at 30 months. European Psychiatry. 2018. Jan 10.

[2] Bornehag C-G. et al. The SELMA study: a birth cohort study in Sweden following more than 2000 mother-child pairs. Paediatr Perinat Epidemiol. 2012 Sep;26(5):456-67.

[3] Bornehag C-G. The SELMA study, a longitudinal study following 2,000 mother-child pairs from early pregnancy over birth and up in school age. Environ Health Perspectives. 2013: 5824: S-2-35-05.

[4] Bauer AZ. et al. Prenatal paracetamol exposure and child neurodevelopment: A review. Horm Behav. 2018 Jan 13. pii: S0018-506X(17)30454-3.

[5] Saeedan AS. et al. Effect of early natal supplementation of paracetamol on attenuation of exotoxin/endotoxin induced pyrexia and precipitation of autistic like features in albino rats. Inflammopharmacol. 2018. Jan 11.

[6] Schultz ST. et al. Acetaminophen (paracetamol) use, measles-mumps-rubella vaccination, and autistic disorder: the results of a parent survey. Autism. 2008 May;12(3):293-307.


Friday, 2 February 2018

Intolerance of uncertainty (IU) is "directly related to features of ASD"

Time and time again an important issue keeps cropping up in relation to autism and the various *comorbidity* that seem to be over-represented alongside the diagnosis: the core features of autism seem to be intricately related to the presentation of such *comorbidity*. Indeed, I wonder if the word 'comorbidity' should, on some occasions, really be replaced with something a lot more 'core' à la Mildred Creak for example and their coverage of the topic of anxiety years back...

It's been noted in relation to depression (see here) and anxiety (see here) and even some other 'extremes' of behaviour (see here) and, to be frank, is starting to become a bit of an elephant in the room. I know not everyone is completely enamoured with either the notion that anxiety is a core part of autism [1] or with 'intervening' in relation to altering the presentation of the core features of autism, but the available data is starting to suggest that for some, this could be a primary option if one wants to effectively tackle certain, often very disabling, *comorbidity* (see here).

Another potential example is offered in the findings reported by Roma Vasa and colleagues [2] who, looking at nearly 60 children diagnosed with an autism spectrum disorder (ASD) compared with 30-odd not-autism controls, reported that various [core] aspects of autism seemed to be related to intolerance of uncertainty (IU); but specifically "emotion dysregulation was the only significant predictor of IU."

IU is a concept rising in importance when it comes to autism (see here). As the name suggests, it's all about the negative effect(s) following uncertainty (i.e. not knowing) (some have talked about 'threat' as being important), and how anxiety in particular, seems to be cardinal symptom following such uncertainty and onward, the often disabling effects that arise from it (see here).

"These findings suggest that IU is directly related to features of ASD possibly due to shared genetic, neurological, or psychological underpinnings." Well that just about covers all the bases(!) but really the conversation should be moving to 'what can be done to mitigate IU and its effects?' Vasa, in another study [3], provides some more basic options when it comes to tackling anxiety in the context of autism, but specifically with IU in mind, we must wait [4] and wonder...


[1] Montazeri F. et al. Network Analysis of Anxiety in the Autism Realm. J Autism Dev Disord. 2018. Jan 30.

[2] Vasa RA. et al. Relationships between autism spectrum disorder and intolerance of uncertainty. Autism Res. 2018 Jan 7.

[3] Vasa RA et al. Assessment and Treatment of Anxiety in Youth With Autism Spectrum Disorders. Pediatrics. 2016 Feb;137 Suppl 2:S115-23.

[4] Rodgers J. et al. Towards a Treatment for Intolerance of Uncertainty in Young People with Autism Spectrum Disorder: Development of the Coping with Uncertainty in Everyday Situations (CUES©) Programme. J Autism Dev Disord. 2017 Dec;47(12):3959-3966.


Thursday, 1 February 2018

Does a diagnosis of autism today mean the same as a diagnosis of autism decades ago?

I'm pretty sure that the findings reported by Olof Arvidsson and colleagues [1] are going to be a talking point for some time to come. Examining whether: "A decrease over time in the number of autism symptoms required for a clinical autism diagnosis would partly help explain" the increase in the prevalence of autism "reported to have increased worldwide", the authors relied on data from the parents of several thousand twins alongside other resources to look at this important issue.

There is no doubt that there has been a considerable increase in the numbers of people being diagnosed with autism (see here) stretching across nations (see here). People have previously used the term 'epidemic' to describe the increase but that's not strictly accurate given that autism is not an infectious disease like flu for example. And despite some very forthright assertions about 'knowing the causes' from various quarters, the reason(s) for the increase are likely complex and probably not always the same in different parts of the world (see here for example)...

The Child and Adolescent Twin Study in Sweden (CATSS) and the Swedish National Patient Register (NPR) were the data sources included for study by Arvidsson and colleagues. CATSS is a telephone-based study where parents of all twins born in Sweden are asked to participate. Those who responded to administration of the Autism-Tics, ADHD and other Comorbidities inventory (A-TAC) were included in the present study (N~28,000 between 1992 and 2007).  Alongside, participants diagnosed with autism or with an autism spectrum disorder (ASD) were identified in the NPR (N=430) and whittled down to some 270 children based on being born between 1992 and 2007.

The study aims were three-fold: "(a) detect whether the number of ASD symptoms in clinically diagnosed ASD cases had decreased over time, (b) analyze whether any changes might be associated with age at diagnosis and (c) investigate whether individuals diagnosed with ASD in childhood would show variation in the amount of coexisting non-ASD problems and of dysfunction and suffering over time."

Results: it looks like there were some important trends going through the years based on the presented data. Based on the A-TAC data defining an "autism symptom score", there was a steady decline in said mean autism symptom score over the years 1992-1993 to 2002. In every single year banding, the mean autism symptom score decreased, denoting fewer symptoms/features to be present. The authors concluded that: "Over time, considerably fewer autism symptoms seemed to be required for a clinical diagnosis of autism."

And there's more. When age at diagnosis was divided up to form two groups - those diagnosed between 1-6 years of age, and those diagnosed later, between 7-12 years of age - for those diagnosed between 7-12 years of age the "mean autism symptoms score in the A-TAC decreased for 8.96 in 2004-2005 to 4.63 in 2014." No such significant change was seen in the 1-6 years of age at diagnosis grouping. The authors conclude that it could be this 7-12 year old at diagnosis grouping that seem to be driving the 'fewer symptoms needed for a diagnosis' finding, given that their older age at diagnosis potentially implies a less obvious autistic presentation or "with impairments stemming from 'comorbid problems." All of this is set within the context that registered ASD diagnoses went up and up and up during the periods being analysed.

There's lots to take in from this research but I'll start with a quote from the authors: "the observed decrease in autism 'symptom load' in diagnosed individuals does not necessarily correspond to a decrease in the need for interventions and societal support." This was quite evident when authors looked at the data on comorbidity and "dysfunction/suffering scores" (yes, some people with autism do suffer as a result of their symptoms) that remained fairly constant throughout. Indeed, added to this, the authors talk about how there may be a "change in perception of what it is that is disabling" in terms of schools for example, requiring more "cooperation in groups and self-reflecting abilities." Overall symptom severity might be decreasing but the environment *might* be getting tougher in different ways?

But it's difficult to brush these findings under the carpet and how they relate to the question titling this post: Does a diagnosis of autism today mean the same as a diagnosis of autism decades ago? On the basis of these findings, one would have to say perhaps not (in the general quantitative sense). More study is required however including on how 'female autism' *might* influence some of the patterns (see here) discussed by Arvidsson et al, alongside the idea that age and maturation might influence the often quite fluid presentation of autism [2]. I'm also minded to reiterate that 'autism-related dimensions' are not always 'autism-specific dimensions' (see here) and the important studies suggesting that the presentation of autistic traits does not always merit a clinical diagnosis of autism (see here).

And bearing in mind the tweet snapshot picture accompanying this post, the paper by Sebastian Lundström and colleagues [3] is here and well worth a read...


[1] Arvidsson O. et al. Secular changes in the symptom level of clinically diagnosed autism. J Child Psychol Psychiatry. 2018 Jan 29.

[2] Lever AG. & Geurts HM. Is Older Age Associated with Higher Self- and Other-Rated ASD Characteristics? J Autism Dev Disord. 2018 Jan 18.

[3] Lundström S. et al. Autism phenotype versus registered diagnosis in Swedish children: prevalence trends over 10 years in general population samples. BMJ. 2015 Apr 28;350:h1961.