Friday, 22 June 2018

"results support HLA involvement in ASD"

HLA mentioned in the title of this post - "results support HLA involvement in ASD [autism spectrum disorder]" - refers to the human leukocyte antigen (HLA) system. This is an important part of our biology that "helps the immune system distinguish the body's own proteins from proteins made by foreign invaders such as viruses and bacteria." Y'know, making sure that our immune system is able to correctly distinguish between 'self' and 'not-self' in terms of its decision on who to 'attack'...

The findings reported by Meriem Bennabi and colleagues [1] provide further analysis of the HLA system in the context of autism with their study designed to "more precisely explore the polymorphisms of the HLA class II loci, at allele, genotype and haplotype levels." Before further journeying through the Bennabi paper, I'll direct you to some other discussions I've had on this blog in relation to the HLA system and autism (see here). Specifically, how certain HLA links with autoimmune conditions such as coeliac disease, *might* overlap with some autism (see here). I'd also like to take this opportunity to remember one of the first people to look at the HLA in relation to autism [2]: the late Reed Warren.

The starting point for the Bennabi study was the idea that immune 'dysfunction' is no stranger to autism research. Indeed, the authors list three important 'immune-related' areas as evidence: "(i) a deleterious effect of prenatal or perinatal infectious pathogen exposure; (ii) a pro-inflammatory state often concomitant with abnormal cell-mediated immunity or inflammatory-mediated gut dysbiosis; (iii) a frequent autoimmune component observed in mothers of ASD off-spring as well as in ASD patients, with circulating anti-brain autoantibodies sometimes correlating with disease severity and/or behavior impairments." And yes, they did actually mention 'gut dysbiosis' too...

The authors move further into speculating about a possible role for the HLA system in some of those 'immune-related issues', and specifically whether subtle genetic differences to the HLA system might be involved.

"HLA genotyping data was available only for 474 ASD and 350 HC subjects on which the statistical analysis were performed." HC refers to the pretty awful term 'healthy control' which I, personally, dislike in the context of autism and other behavioural labels. Bearing in mind that I've already mentioned the classic 'diet affects physiology' autoimmune condition that is coeliac disease (CD), I note some important findings observed by Bennabi et al: "the HLA-DRB1 *11-DQB1*07 haplotype was more prevalent in ASD patients, versus HC (Pc = 0.001), partially replicating previous data and possibly linking to gastro-intestinal (GI)-related pro-inflammatory processes, given that this haplotype associates with pediatric celiac disorders." They also note that there may be a potentially 'protective' HLA haplotype too: "the HLA-DRB1 *17-DQB1*02 haplotype was higher in HC, versus ASD patients (Pc = 0.002), indicating that this is a protective haplotype." The stuff about linking autism related scores (function and severity of autism) with haplotype also documented by the authors are interesting but perhaps fodder for another blogging occasion.

So what might this all mean? Well, y'know when people talk about dietary gluten potentially showing a *relationship* with some facets of autism? They could actually be on the something. Whether that be the 'over-representation' of a formal diagnosis of coeliac disease in relation to autism (see here) or the idea that something 'not quite coeliac disease but something close' might be present (see here and see here), there is a peer-reviewed evidence base to consider. I know this kind of 'diet' research can furrow brows in some quarters, but peer-reviewed science is peer-reviewed science and well, there's already enough physical health inequality in relation to autism.

Alongside mention of the 'gut-brain axis', authors also discuss another potentially important area that may link to their results: "the involvement of the HLA system in wider physiological processes, including synaptic pruning." Yes, it is true that the HLA system probably does more than just serve as a 'pattern-recognition' system for differentiating between 'self' and invading pathogens and this could also be important to a diagnosis like autism. And there's more, as per another quote from the authors talking about... "the presence of the human endogenous retrovirus K (HERV-K) and increased expression of C4A molecules, with both related to excessive synaptic pruning during specific developmental windows." C4A is part of the complement system related to immunity. Going back to my mention of Reed Warren, he and his research group looked at another aspect of the complement system with autism in mind: C4B [3]. Talk about HERVs - human endogenous retroviruses - by Bennabi et al, is also a subject quite close to my heart (see here). HERVs have been investigated in the context of labels such as autism before (see here and see here) and whilst 'activation' of elements of such fossil viruses probably has many different effects, there has been some chatter about them being possible 'superantigens'. This in the context that whilst parts of these fossil viruses have been 'incorporated' into our genetic being and so considered 'self', there's always the possibility that they might be recognised as 'foreign' under certain circumstances and thus setting off an autoimmune cascade. That's the theory anyway...

The HLA system is not an easy system to get your head around. It's particular link to autoimmune conditions - where self is not recognised as self by the immune system - fits well with other research-based observations with [some] autism in mind. It does still require quite a bit of further investigation; and, bearing in mind the significant heterogeneity present in autism on various different levels, is probably going to be more relevant to some people diagnosed on the autism spectrum, than for others. But where one sees potential overlaps between the HLA system in autism and other autoimmune conditions like coeliac disease, one would assume a lot more research should be really be forthcoming...


[1] Bennabi M. et al. HLA-class II haplotypes and Autism Spectrum Disorders. Scientific Reports. 2018; 8: 7639.

[2] Warren RP. et al. Immunogenetic studies in autism and related disorders. Mol Chem Neuropathol. 1996 May-Aug;28(1-3):77-81.

[3] Warren RP. et al. Increased frequency of the null allele at the complement C4b locus in autism. Clin Exp Immunol. 1991 Mar;83(3):438-40.


Thursday, 21 June 2018

Do childhood sleep issues "have a causal role" in 'chronic disabling fatigue' in adolescence?

There's those words again: 'chronic disabling fatigue' or CDF, being used as a proxy for chronic fatigue syndrome (CFS, also known as 'ME') as per the findings reported by Simon Collin and colleagues [1].

Elements of this authorship group seem to be using CDF quite a bit (see here and see here) in their various research studies, and I have to say it's starting to get a little confusing (see here). I'll come back to my thoughts on the term CDF in a moment...

On this research occasion, Collin et al set out to explore whether "sleep might be a causal risk factor for CFS/ME" (or should that just be CDF) on the basis that sleep issues have been reported in that context previously [2]. Once again, "data from the Avon Longitudinal Study of Parents and Children (ALSPAC) birth cohort" was the research source material, and researchers were specifically looking at: "sleep patterns of children aged 6 months to 11 years, who were subsequently classified as having (or not having) 'chronic disabling fatigue'... between the ages 13 and 18 years." Sleep duration was quite a big element to this study.

So yeah, shorter night-time sleep duration from 6 months to 11 years of age did seem to show some connection to CDF. To quote: "The odds of CDF at age 13 years were 39% lower... for each additional hour of night-time sleep at age nine years, and the odds of CDF at age 16 years were 51% lower... for each additional hour of night-time sleep at age 11 years." This and a few other observations led authors to conclude that sleep abnormalities might have a role to play in relation to CFS/ME (sorry, CDF).

I have to say however, that I'm not particularly impressed with these findings. I say that on the basis that one set of variables (sleep) are being *correlated* with another later variable (CDF) and well, correlation does not necessarily equal causation. As per other work from this authorship group [2], they've also previously suggested that level of physical activity *might* also correlate with CFS/ME (sorry CDF) albeit with a reduced timescale between the variables. This dual research based on the same cohort I assume, kinda disqualifies any one variable from being related to CDF. Assuming that is, that sleep and physical activity are not somehow connected...

And then there's the issue of how sleep duration was measured in the latest Collin paper: "The sleep durations in our study were obtained from parents’ (mostly mothers’) answers to questions about the child’s usual bedtime and waking time, rather than from data collected in a sleep/wake diary or by actigraphy." So, they basically asked what time children went to bed and what time they woke up. There's nothing wrong with asking such questions but likewise there is little to confirm that children actually closed their eyes and nodded off the minute they went to bed and/or woke up the minute of parental report on waking. Anyone who has children knows that this is 'optimistic' at best (and indeed, takes no account of things like duration of night waking or quality of sleep for examples). The lack of use of actigraphy - that fabulous wearable tech that allows us to objectively chart sleep and activity cycles - is a real problem for elements of CFS/ME research (see here), and is something that is getting harder and harder to overlook. This includes the lack of use in this particular research study too.

Then, back to CDF. CDF basically comes about because we are told that "children in [the] study were not examined by a physician" when it comes to CFS/ME. Further: "CDF at ages 13 and 16 years was defined as fatigue (feeling tired or lacking in energy) of >6 months’ duration that was associated with absence from full-time school or that had prevented the child from taking part in activities ‘quite a lot’ or ‘a great deal’, excluding fatigue possibly associated with sport, snoring, and other illnesses." So fatigue is a primary symptom. But how can you exclude fatigue associated 'other illnesses'? Did the authors for example, screen for something like fatigue due to mitochondrial issues or disorders (see here)? No, they didn't appear to. Similarly there is no mention as far as I can see of another primary symptom of CFS/ME: post-exertional malaise (PEM). Important too was another quote from the authors: "Our definition of CDF did not exclude children with comorbid depressive symptoms." I'll say little more on this topic.

So, again, unfortunately I have to say that I'm left unimpressed by these latest findings from Collin and colleagues. And once again, I have to point out that CDF whilst described as "a proxy for chronic fatigue syndrome/ME" is not necessarily CFS or ME (and indeed, neither it seems, could it be both).


[1] Collin SM. et al. Childhood sleep and adolescent chronic fatigue syndrome (CFS/ME): evidence of associations in a UK birth cohort. Sleep Med. 2018 Jun;46:26-36.

[2] Collin SM. et al. Physical activity at age 11 years and chronic disabling fatigue at ages 13 and 16 years in a UK birth cohort. Arch Dis Child. 2018 Jun;103(6):586-591.


Wednesday, 20 June 2018

The International Classification of Diseases version 11 (ICD-11) has arrived...

Although peer-reviewed science research is the typical fodder for this blog, I am inclined to post about other important papers and/or events as they emerge. Today is such an occasion, as I draw your attention to an important announcement from the World Health Organization (WHO) recently titled: "WHO releases new International Classification of Diseases (ICD 11)."

Yes, this announcement covers the release of the the much anticipated ICD-11 system "for identifying health trends and statistics worldwide" also including "around 55 000 unique codes for injuries, diseases and causes of death." The ICD-11 schedule as it currently stands can be accessed here.

I might add that the release of ICD-11 is not the same as the 'roll out' of ICD-11, which are we informed "will come into effect on 1 January 2022." This 'advance preview' is basically a way of introducing the new schedule to the world and helping to facilitate a smooth transition from the version currently in use to this new system.

The ICD-11 has not been without some controversy as for example, a new condition known as 'gaming disorder' has been picked up by some media outlets (see here). Others have opined about the inclusion of "Traditional Medicine conditions - Module I" (see here) (where "disorders and patterns which originated in ancient Chinese Medicine and are commonly used in China, Japan, Korea, and elsewhere around the world" have been added in).

Relevant also to this blog - being a blog predominantly about autism research - is the entry on autism, and how the term 'Asperger syndrome' doesn't seem to figure (same as in the DSM-5). Instead, there is the umbrella term 'Autism Spectrum Disorder', complete with various sub-categorisation of diagnosis on the basis of intellectual development 'level' and functional language 'level'. The waning of the term Asperger syndrome is seemingly coincidental to the recent revelations about Hans Asperger (see here) but perhaps reflects long-standing 'doubts' about it's inclusion in previous versions of the diagnostic manual used (see here). There are other changes noted in ICD-11 which are also pertinent to autism (see here) including those relevant to the idea that a diagnosis of autism rarely exists in some sort of diagnostic vacuum (see here).

It's still very early days for the ICD-11 and so we'll have to wait and see what else emerges as physicians and the like across the globe come to terms with the revised schedule. I don't doubt that the evolving diagnostic nature of autism will also create discussions (and arguments) aplenty...


Tuesday, 19 June 2018

"Greater ADHD symptom severity was associated with higher odds for feeling less happy"

Of course correlation does not necessarily equal causation, but the *correlative* results published by Andrew Stickley and colleagues [1] observing that: "Greater ADHD [attention-deficit hyperactivity disordersymptom severity was associated with higher odds for feeling less happy" were worthy of some blogging attention.

Drawing on data derived from the 2007 Adult Psychiatric Morbidity Survey based here in Blighty, researchers tackled quite an important question: how do ADHD signs and symptoms potentially impact on happiness?

So: "Information was collected on ADHD symptoms using the Adult ADHD Self-Report Scale (ASRS) Screener, while happiness was assessed with a single (3-point) measure." Including data for over 7000 people - adults aged 18 years and over - researchers observed that important negative relationship between ADHD symptoms and happiness. Alongside, they also noted that various other variables might also play a role in such a [correlative] relationship: "Mood instability (percentage mediated 37.1%), anxiety disorder (35.6%) and depression (29.9%) were all important mediators of the association between ADHD and happiness."

I'm a great believer that we need more of this kind of research asking relatively simple questions about whether someone is happy or not across various different labels and combinations of labels. I reiterate the whole 'correlation does not necessarily equal causation' mantra and the fact that happiness is not a 'setting' switched to the on position every moment of someones life. One also has to be slightly careful about extrapolating the Stickley results to diagnosed ADHD, and the various issues that come with such a diagnosis (including enhanced risk of comorbidity or 'symptoms' of other diagnostic labels).

But it strikes me as 'logical' that the manifestation of certain types of behaviour - hyperactivity, inattentiveness, impulsivity - might not be all that great for a person when it comes to perceived happiness at certain points in life. I say this in the context that a diagnosis of ADHD has already been *linked* to quite a few adverse life events (see here) including some enhanced risk for something like suicidality (see here). One has to wonder therefore, what role happiness might play in the context of such extremes of behaviour, and whether intervention 'for ADHD' (whatever form this might take) might have some important effects on subjective and objective markers of happiness alongside the manifestation of signs and symptoms...


[1] Stickley A. et al. Attention-deficit/hyperactivity disorder symptoms and happiness among adults in the general population. Psychiatry Res. 2018 May 5;265:317-323.


Monday, 18 June 2018

Selective mutism and autism

The findings reported by Hanna Steffenburg and colleagues [1] make for potentially important reading reporting: "In this study of a clinical group of children who were diagnosed with SM [selective mutismand assessed at a center for neurodevelopmental disorders, 63% also met criteria for ASD [autism spectrum disorder]."

Selective mutism (SM) refers to an anxiety disorder typically manifesting during early childhood that affects the use of spoken language in certain social situations such as at school. 'Literally being unable to speak' is a phrase that follows SM in certain contexts, where speech and language skills are not typically affected when and where family or close friends are around. It's not surprising that there is 'overlap' between SM and autism given the characterisation of SM in terms of being "nervous, uneasy or socially awkward" and "stiff, tense or poorly co-ordinated" (minus any sweeping generalisations). And just before you question it, 'poorly-coordinated' is perhaps an under-rated aspect for many people diagnosed as being on the autism spectrum (see here).

Steffenburg and colleagues - including the notable ESSENCE-related name of Christopher Gillberg - sought to examine the possible 'overlap' of SM and autism on the basis that various diagnoses/labels can occur alongside SM; quite a few of them also recognised in relation to autism (see here). Approaching 100 children/young adults diagnosed with selective mutism were assessed at the premier 'autism spectrum conditions' clinic in Gothenberg, Sweden. The clinical assessment undertaken of course covered the diagnosis of autism but also various cognitive functions too.

Almost two-thirds of those with SM who were assessed also met criteria for an autism spectrum disorder (ASD). Added to that: "A further 20% (n=19) had autistic features that were “subclinical”, but, nevertheless, sufficiently marked to have an impact on everyday life." Only 17% were described as having no ASD symptoms. Those are pretty interesting percentages.

Authors also mention how: "The level of cognitive function was average in more than half of the study group but more than one-third of the study group had a borderline IQ or an ID [intellectual disability]." They use such a finding in the context of the ESSENCE term - Early Symptomatic Syndromes Eliciting Neurodevelopmental Clinical Examinations - where overlapping diagnoses/labels is the rule not the exception.

The implications? Well, screen and keep a continual eye open for autism in cases of SM seems to be an important first implication. That also includes keeping in mind those 'subclinical' signs and symptoms, which could be relevant to discussions about the broader autism phenotype (BAP) (see here) and also that curious DSM-5 diagnostic category known as social communication disorder (SCD) (see here). The focus on 'anxiety' in relation to SM might also be important given the pretty well-established connection between autism and anxiety (see here for example) following in the footsteps of some often forgotten autism research history (take a bow Mildred Creak and colleagues for including the term "acute, excessive and seemingly illogical anxiety"). I'm also minded to mention that given the pretty high rate of autism described in SM by Steffenburg and other researchers, further investigations perhaps need to be directed towards shared biology/genetics as well as shared behavioural presentation? Y'know, along the lines of whether 'comorbidity' might be something more 'core' (see here)?


[1] Steffenburg H. et al. Children with autism spectrum disorders and selective mutism. Neuropsychiatr Dis Treat. 2018 May 7;14:1163-1169.


Saturday, 16 June 2018

ALSPAC says... "Social communication impairments had the strongest association with a depression diagnosis at age 18 years"

ALSPAC mentioned in the title of this post refers to The Avon Longitudinal Study of Parents and Children, one of the premier research initiatives here in Blighty, that has provided all-manner of interesting and important research associations. With autism in mind, ALSPAC has opined on various different research questions (see here and see here for examples) including the issue of a possible 'real' increase in the numbers of children presenting with autistic traits (see here).

On this particular research occasion, ALSPAC was the source data for the findings reported by Dheeraj Rai and colleagues [1] who set out to "compare trajectories of depressive symptoms from ages 10 to 18 years for children with or without ASD [autism spectrum disorder] and autistic traits, to assess associations between ASD and autistic traits and an International Statistical Classification of Diseases, 10th Revision (ICD-10) depression diagnosis at age 18 years, and to explore the importance of genetic confounding and bullying." I might add that some of this authorship group are making some real research waves when it comes to investigations using population registries with autism in mind (see here).

The starting point this time around was the notion that a diagnosis of autism is in no way protective when it comes to a diagnosis of depression and/or the expression of depressive signs and symptoms. Again, it's a topic that has cropped up before on this blog (see here) and is perhaps one of the longer term associations that have been made down the years. The idea that depression or depressive symptoms *might* be something much more than just 'comorbid' in the context of at least 'some' autism is something else that has been banded around the peer-reviewed research literature before (see here) but the evidence base is not particularly big or strong in this area at the moment.

There were a few different research questions asked by Rai et al, including looking at children "with or without ASD or high scores on autistic trait measures" and any relationship(s) with depression and depressive traits. They report findings for over 6000 children ("maximum sample with complete data") where questionnaire items on bullying were also included ("Relational and overt bullying was assessed as separate yes or no items at ages 8, 10, and 13 years using the modified Bullying and Friendship Interview Schedule") alongside various other potentially confounding variables.

Results: "children with ASD and those with higher scores on all autistic trait measures had more depressive symptoms at age 10 years than the general population, and these remained elevated in an upward trajectory until age 18 years." I don't think there's anything too novel in such findings, aside from the observation that depression / depressive symptoms may start quite early on in childhood. I can remember when I started out in autism research a couple of decades ago hearing about depression being typically linked to the onset of adulthood in the context of autism. This current data suggests otherwise.

Next: "Social communication impairments had the strongest association with a depression diagnosis at age 18 years. Findings were robust to adjustment for a range of confounders, including maternal depression and anxiety and the child’s polygenic risk for autism." This is important. What it suggests is that there may something 'more than just comorbid' about depression or depressive symptoms appearing alongside autism or at least in connection to certain autistic traits. I know some people have already taken exception to this possibility alongside the use of the word 'impairment' by the authors. But much like other research on an important bedfellow to depression - anxiety - one may have to entertain the possibility that there may be some enhanced 'predisposition' to something like depression alongside the presentation of autistic traits (see here and see here) perhaps mediated by factors such as rumination and perseveration for example [2]. This doesn't mean that depression is solely a product of autistic traits; merely that certain traits may potentially form an important vulnerability factor. I'm similarly minded to bring in other work from the ALSPAC initiative [3] (including Rai and colleagues as authors) where related findings were mentioned: "Social communication impairments are an important autistic trait in relation to suicidality." This on the basis that depression and suicidality show an important association.

Also: "We found evidence of a substantial role of bullying in contributing to and explaining a higher risk of depression in individuals with ASD and autistic symptoms." Bullying in the context of autism is another long-standing topic (see here). Bullying covers a lot of ground in terms of behaviour and also source (see here). The authors opine that: "Previous work has shown strong links between the experience of bullying and later depression... although confounding could have a role, the association is considered to be at least partially causal." It's also important to note that social-communication 'issues' were reported to be potentially predictive of being bullied according to the authors. The model that then appears hints that the appearance of depression *might* be linked to "reduced self-esteem or social isolation after the bullying" accepting that causality is not established and also not accounting for other variables: "other relevant characteristics, including comorbidities with neurodevelopmental conditions (eg, attention-deficit/hyperactivity disorder) and classroom placement could be important in this association within or outside the context of bullying." That last point is important in the context that autism rarely exists in some sort of diagnostic vacuum (see here).

There are a few caveats attached to the Rai findings that need to be kept in mind outside of any 'correlation does not necessarily equal causation' sentiments. So: "atypical presentations of depression are common in ASD, and our study has the potential for outcome measurement error because we used scales... that have not been adapted for autism." Indeed. I've previously talked about how bipolar disorder for example, might not follow a typical pattern when present in the context of autism (see here). I daresay that this could also hold for other types/forms of depression too. I'm also minded to reiterate that depression, as well as being a heterogeneous condition, also seemingly has many pathways to it. Some of those pathways will include psychological and social variables such as bullying and perhaps even more extremes of 'trauma'; where a diagnosis of PTSD is for example, no stranger to autism (see here). 'Happiness' and perceived quality of life (see here) are also likely to exert an important effect too.

Other pathways to depression seem to be more biologically defined as per depression in the context of physical ailments (see here) that may have a *link* to some autism (see here) or following the use of seemingly common medicines according to recent news reports (see here). I'll also mention that things like physical activity and exercise *seem* to show an important relationship with depression (see here). This could also be pertinent to the data suggesting that physical activity levels are typically not optimal where and when autism is diagnosed (see here). Other factors (fatigue, sleep, etc) also need to be mentioned in the context of depression. In short, there are lots and lots of potential variables to consider [4].

Outside of the important messages from the Rai findings on how depression is over-represented in relation to autism and how social factors like bullying seem to be linked  to it and thus are subsequently 'modifiable', there is another important point to consider: depression is typically treatable. Minus any medical or clinical advice being given or intended, the first step in managing/treating depression is identifying it. Perhaps the Rai findings might serve as a further call to action for preferential screening in the context of autism...


[1] Rai D. et al. Association of Autistic Traits With Depression From Childhood to Age 18 Years. JAMA Psychiatry. 2018 Jun 13.

[2] Patel S. et al. Association between anger rumination and autism symptom severity, depression symptoms, aggression, and general dysregulation in adolescents with autism spectrum disorder. Autism. 2017 Feb;21(2):181-189.

[3] Culpin I. et al. Autistic Traits and Suicidal Thoughts, Plans, and Self-Harm in Late Adolescence: Population-Based Cohort Study. J Am Acad Child Adolesc Psychiatry. 2018 May;57(5):313-320.e6.

[4] Köhler CA. et al. Mapping risk factors for depression across the lifespan: An umbrella review of evidence from meta-analyses and Mendelian randomization studies. J Psychiatr Res. 2018 May 25;103:189-207.


Friday, 15 June 2018

'What really grinds my gears': a "slight uptick' in the estimated prevalence of autism

For those who watch the sometimes 'cutting' TV show called Family Guy, the first part of the title of today's post - "what really grinds my gears" - will make sense. For those who don't, it represents a TV segment offered to one of the main characters of the series, Peter Griffin, during which he aired increasingly bizarre opinions of things that 'irk' him. At the close, he revealed that just about everything 'grinds his gears'.

Whilst I'm not typically a person that is easily irked (much of my early years irking has dissipated as a result of age and my hobby), I was a little put out by the opening sentence included in the news piece published by Bridget Kuehn [1] talking about the most recent autism estimated prevalence figures published by the US CDC [2] (see here for my take). To quote: "A slight uptick in US cases of autism spectrum disorders (ASDs) was detected in 2014 compared with the years between 2010 and 2012, according to a new CDC report."

It was the use of the word 'slight' that furrowed my brow. And how a 15% increase in the estimated autism prevalence rate in the US over 2 years - translating as a move from an estimated 1 in 66 8-years olds being diagnosed to 1 in 59 8-years olds being diagnosed - is somehow inferred to be less important than it actually was. Words matter.

I know prevalence (and incidence) rates (estimated or actual) when it comes to autism can invoke some often heated discussions. Such debates perhaps tie into wider views held about autism, and whether you're of the opinion that autism has always been with us, or autism is a relatively new 'condition'; whether autism is primarily explained by genetics or whether non-genetic environmental factors play a significant role; whether you view autism as a serious public health issue or are more inclined towards the idea of an 'autistic identity'. I'm sure there are other polar opinions to add, but the end result is that [peer-reviewed] data can sometimes become a secondary consideration when it comes to such views and opinions.

Personally, I go with the data. I go with the data that suggest that autism prevalence is still increasing, and not just in the United States (see here and see here for examples). I go with the associated idea that explanations such as 'increasing awareness' and 'diagnostic substitution' probably play some role in the increase, but don't provide a wholly intellectually satisfying explanation for the increasing numbers (see here and see here). I go with the idea that alongside increasing numbers of cases of autism being diagnosed, so more needs to be done in terms of the provision of educational and social support being offered for an often complicated clinical pictures (see here). I also go with the idea that research questions need to be asked (and answered) about what factors could be driving the remarkable increase in autism over the past couple of decades without fear or favour.

I also go with the idea that there needs to be a bit more urgency in the response to such figures. I'm not talking about the use of 'inflammatory' language or soundbites which are bound to make some people nervous or angry. Merely that behind the CDC statistics there are real children and there are families and other loved ones. And they deserve a lot more and a lot better than society is currently providing (see here)...


[1] Kuehn B. Uptick in Autism. JAMA. 2018 Jun 12;319(22):2264.

[2] Baio J. et al. Prevalence of Autism Spectrum Disorder Among Children Aged 8 Years — Autism and Developmental Disabilities Monitoring Network, 11 Sites, United States, 2014. Morbidity and Mortality Weekly Report (MMWR). 2018; 67(6): 1-23.