1 in 10 kids: the estimated prevalence of ADHD in the United States in 2016

Credit: Xu et al (2018) JAMA Network Open

"In a nationally representative population, we estimated that the prevalence of diagnosed ADHD [attention-deficit hyperactivity disorder] among US [United States] children and adolescents was 10.2% in 2016."

So said the findings published by Guifeng Xu and colleagues [1] who relied on data derived from the National Health Interview Survey (NHIS) in the United States over the course of two decades (1997-2016). As per an accompanying editorial [2] with the smart title "Paying Attention to Attention-Deficit/Hyperactivity Disorder", the Xu findings "fills an important need" insofar as their plotting a significant increase in the estimated prevalence rate of ADHD. The stats: "the estimated prevalence of ADHD significantly increased during the past 20 years—from 6.1% in 1997-1998 to 10.2% in 2015-2016." The year-on-year percentage figures considered by Xu et al showed a rise almost every year when it came to the [estimated] ADHD prevalence. Such figures are quite distinct from other (point) estimates in other parts of the world (see here).

Of course there are upsides and downsides to the authors' reliance on the NHIS dataset. So: the reliance on "parental reports about psychopathology rather than actual standardized assessments administered face-to-face with parents and/or children by trained evaluators" is one of the main limitations talked about across many different labels (see here). This has to be balanced with the large sample size included in the NHIS initiative and the "high response rate (child response rate of 85.6%-93.3%)." Personally I'm not inclined to believe that significant numbers of parents would provide 'false' answers to questions like: “Has a doctor or health professional ever told you that [the sample child] had attention-deficit/hyperactivity disorder (ADHD) or attention-deficit disorder (ADD)?” or “Does [the sample child] currently have attention-deficit/hyperactivity disorder (ADHD) or attention-deficit disorder (ADD)?” but ho-hum.

Then to the million dollar question: why has the estimated ADHD prevalence rate increased so dramatically across a relatively short period of time? Well, some well-worn explanations also seen with regards to the autism prevalence statistics (see here) have been banded around. So: "Nonetiologic factors may partly explain the apparent increase in the prevalence of diagnosed ADHD in this study" such as physician "sensitivity" to a diagnosis of ADHD, alongside the changes in ADHD diagnostic criteria already talked about in the peer-reviewed domain (see here). The issue of screening and diagnosis among non-white groups and their accessibility to said screening/diagnostic services is also discussed (something else that cropped up with the recent autism stats in mind too). And since I've just mentioned autism, it's also likely that the increasing recognition that ADHD is part of the clinical picture for quite a few on the autism spectrum (see here) probably contributes to the increase too.

But then there is the idea that the increase may also be - in part - reflective of a real increase too (see here). There are lots of possible candidates that may be contributory (see here and see here for examples) covering a multitude of genetic and non-genetic factors appearing during the nine months that makes us and beyond. As with any other developmental label and the reason(s) it comes about, there are going to be a multitude of potentially important factors to consider that may be quite individual. One thing is evident however, for whatever reason(s), the numbers are only heading in one direction...

A final question: what can be done to improve the life outcomes of those diagnosed with ADHD in ever-increasing numbers? I mention that question in the context that ADHD seems to elevate the risk of various adverse life events occurring (see here and see here and see here for examples) as well as being a potential 'driver' for other psychopathology appearing too (see here). In this context, we are already beginning to appreciate the benefits of certain types of intervention (see here) as well as the potential value of various other intervention options that are not yet considered 'mainstream' (see here and see here for examples). Further research is required to understand the societal and biological factors linked to a diagnosis of ADHD, and whether further advances in intervention and management can be made as a result, and onward lives (hopefully) enhanced...

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[1] Xu G. et al. Twenty-Year Trends in Diagnosed Attention-Deficit/Hyperactivity Disorder Among US Children and Adolescents, 1997-2016. JAMA Network Open. 2018; 1: e181471.

[2] Dickstein DP. Paying Attention to Attention-Deficit/Hyperactivity Disorder. JAMA Newtork Open. 2018; 1: e181504.

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Immune endophenotypes in paediatric autism

Today I'm serving up the paper by Milo Careaga and colleagues [1] for your blogging delight, who concluded that: "Children with ASD [autism spectrum disorder] may be phenotypically characterized based upon their immune profile." Further that there may be: "several possible immune subphenotypes within the ASD population that correlate with more severe behavioral impairments."

With many thanks to Natasa for the paper, participants - 50 boys with a median age of 3.2 years diagnosed with an ASD and enrolled "through the Autism Phenome Project (APP) study" and who were free of any "major immune modifying medications" - provided a blood sample. A similar process was employed for a smaller group of typically developing (asymptomatic) control group (n=16). Said blood sample went through various processes to harvest peripheral blood mononuclear cells (PBMC) which were then 'stimulated' to provoke an immune reaction via "either lipopolysaccharide (LPS) or phytohaemagglutinin (PHA)." Various cytokines were then assayed for in the stimulated PBMC and results analysed according to immune responses and behavioural outcomes.

Results: as per the opening paragraph, there was potentially something to see in the findings added to a more general role for cytokines in relation to autism [2]. Those children with ASD who presented with a more 'pro-inflammatory' cytokine profile in their stimulated blood results "showed more impaired developmental and behavioral scores, as well as increased problems with sleep and aggression." That pro-inflammatory cluster by the way (n=22) tended to show significantly increased production of cytokines such as IL-6 for example, than those children with autism (n=28) "who displayed a less robust response to LPS." Ergo, perhaps more to see and certainly more investigations required in these days of plural autisms.

I was taken by one particular sentence included in the conclusion of the Careaga paper: "Although immune abnormalities were first described in ASD over forty years ago, no consensus has been reached as to what constitutes clinically significant immune dysfunction in ASD." As per quite a bit of autism research, sweeping generalisations about this, that or t'other 'causing' autism or being part and parcel of autism have been a big contributor to the noticeable lack of progress on knowledge about autism and where required and wanted, what can be done to ameliorate the more disabling aspects including that related to comorbidity (see here). Realisation that 'autism' is probably better described as providing an umbrella term for various different conditions on a genetic and molecular level is making some headway these days (see here) including that linked to immune function (see here for example). This might have important implications for intervention (see here) as per other recent results that I'll be musing over soon.

As part of a broader realisation that immune function and psychiatry probably show a lot more connections than many people first realised (see here), I think we are seeing a shift in knowledge here. As per the Careaga results, the idea that there may be distinct clusters within the presentation of autism linked to immune function, opens up a whole new world of more 'targeted' inspection and intervention which, added to other similar phenotype work (see here), is probably an important direction for autism research...

Music: Duran Duran - Pressure Off feat. Janelle Monáe and Nile Rodgers.

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[1] Careaga M. et al. Immune endophenotypes in children with autism spectrum disorder. Biological Psychiatry. 2015. 10 Sept.

[2] Krakowiak P. et al. Neonatal Cytokine Profiles Associated with Autism Spectrum Disorder. Biol Psychiatry. 2015 Aug 14. pii: S0006-3223(15)00655-1.

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Milo Careaga, Sally Rogers, Robin L. Hansen, David G. Amaral, Judy Van de Water, & Paul Ashwood (2015). Immune endophenotypes in children with autism spectrum disorder Biological Psychiatry : 10.1016/j.biopsych.2015.08.036

Illogical garbage and ill-informed speculation

A short post this one. And I am almost in Hulk mode "Mr McGee, don't make me angry.." (almost).

Normally a fairly quiet and placid character, I am a little bit irritate right now. Irritate because of some comments raised on this post about the effect of social media and the Internet on autism. Don't get me wrong, I am not in anyway adverse to the main message of the post, "don't talk about things where you have very little evidence of effect or association" but I am disheartened about some of the comments about autism and what may or may not be involved in causation(s).

To quote from the post (not my words): "You may not realise just how much illogical garbage and ill-formed speculation parents of children with these conditions are exposed to. Over the years, they’ve been told that their children’s problems are caused by their cold style of interaction, inoculations, dental amalgams, faulty diets, allergies, drinking in pregnancy - the list is endless".

What do I disagree with? Well a few things. First, autism is not autism but rather autisms. To my mind, it is not beyond the realms of possibility that there may be more than one reason why people have autism, although not necessarily caused by any of the above. Second, parents of children with autism, from my experience, get pretty good at sniffing out BS. To say that they are 'told' what caused their child's autism implies passivity. On the contrary, most parents I know or have talked to are quite the opposite; mostly because they have had to be on behalf of their child. Finally, whilst there is still some degree of speculation about 'faulty diets' and their connection or not to autism, I would probably suggest that diet and autism is not yet ready for the 'illogical garbage and ill-informed speculation' bin just yet. Certainly putting diet in the same category as Bettelheim is rather too much I think. Coeliac disease and autism? Hyperpermeability of the gut and autism? Allergy and autism? Apparently none of these matter.

OK, so now I have to change my torn clothes as my transformation from Green monster back to quiet and placid me starts. Deep breaths Paul... deep breaths (cue the sombre Hulk piano music).