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The Scotland Census 2011 and autism again: focus on children and young adults Consider this post an extension of some previous chatter on this blog (see here). That previous chatter was based on the work published by Ewelina Rydzewska and colleagues [1] talking about how (a) Scotland seems to be pretty unique insofar as 'asking about autism' in their population Census, and (b) how examination of such a query, alongside asking a few other questions, represents an important research resource particularly pertinent to the idea that autism rarely appears in some sort of diagnostic vacuum (see here).

Now there's more from Rydzewska and colleagues [2] and their analysis of the Scotland 2011 Census. This time the specific focus was on under 25 year olds (their previous research was dedicated to looking at "the prevalence of comorbid mental health conditions and physical disabilities in a whole country population of adults aged 25+ with and without reported autism").

Researchers report that 1.6% of their population (25,063/1,548,819) were reported to have (or someone on their behalf) ticked the box to the question 'have any of the following conditions' that was labelled 'Developmental disorder (for example, Autistic Spectrum Disorder or Asperger's Syndrome)'. This was quite a bit higher than the 0.2% of adults (over 25 years old) that was previously reported on. They also reported that the traditional 4:1 male:female ratio regarding autism was intact as other recent population (estimated) prevalence studies have also indicated (see here and see here).

Then to the main event: "Autism had an odds ratio of 5.4 (5.1–5.6) for predicting deafness/partial hearing loss, odds ratio of 8.9 (8.1–9.7) for blindness/partial sight loss, odds ratio of 49.7 (38.1–64.9) for intellectual disabilities, odds ratio of 15.7 (13.4–18.5) for mental health conditions, odds ratio of 15.8 (14.1–17.8) for physical disability and odds ratio of 3.9 (3.8–4.0) for other conditions."

It's worthwhile reiterating some of those observations made by Rydzewska et al: the chances (odds ratio) of intellectual or learning disability appearing alongside autism in under 25 year olds was about 50 times more likely than in those not ticking that 'Developmental disorder' option. In terms of specific percentage frequencies, the figures for learning disability in the age groups 0-15 years (children) and 16-24 years (young adults) where autism was mentioned were 13-14% and 18% respectively. This was contrasted against percentages of 0.3% and 0.4% in similar non-autistic age groupings. I'm also minded to include the observation that girls with autism across both age groups seemed to be at some elevated risk of learning disability when compared to boys. The next highest risk values came in for the presence of a mental health condition where again girls with autism seemed to shoulder the highest risk (a divide that seemingly grew as children aged into young adults). The conclusion yet again is that for quite a few people, autism is not a stand-alone condition/label and that such "conditions are disabling and have a significant impact on long-term quality of life; their coexistence with autism adds extra complexity."

On the last blogging occasion when the first research paper from Rydzewska using the Scotland Census 2011 data was discussed, I held back from commenting too much on the adult prevalence figure picked up by authors. This time I'm not going to, because the difference between children/young adults with autism (or a developmental disorder) (1.6%) and autistic adults (0.2%) is too stark not to mention. I appreciate that there may be many variables/factors contributory to such figures, and that such figures are perhaps prone to some degree of error (bearing in mind the legal requirements behind completing a Census), but the disparity between them cannot be just brushed under the scientific carpet. They show that for the year 2011 in Scotland, autism - all forms of autism - was quite significantly over-represented in children and young adults compared with autism in over 25 year old adults. They show that arguments about the prevalence of adult autism potentially being on a par with childhood autism were/are wrong. They show that autism is disproportionately affecting children/young adults and by inference, the trend in autism being diagnosed is an upward one primarily stemming from childhood/young adulthood diagnoses and not from the late diagnosis of adults.

By saying that I'm not ruling out the idea that there may be adults in Scotland in 2011 who had slipped through the diagnostic net with autism in mind. I'm not saying that some 7 years later, things haven't moved on with regards to autism awareness and the like. But I do find it extremely unlikely that there were literally thousands and thousands of 'hidden' people 'undiagnosed' in Scotland in 2011 however much some people have inferred, and continue to infer, that this is true. The peer-reviewed evidence for this phenomenon is just not there, and certainly nowhere near there when it comes to those with 'very visible' autism who for example, require significant day-to-day social and health care support (see here and see here for examples).

I am hoping that when the next Scottish Census (2021) results eventually come in we might see more from this fabulous research opportunity with autism in mind. Even better would be for other countries to follow the Scottish lead in their questioning of their nation and perhaps provide a more accurate picture of the rates of autism across the age groupings.


[1] Rydzewska E. et al. Prevalence of long-term health conditions in adults with autism: observational study of a whole country population. BMJ Open. 2018 Sep 1;8(8):e023945.

[2] Rydzewska E. et al. Prevalence of sensory impairments, physical and intellectual disabilities, and mental health in children and young people with self/proxy-reported autism: Observational study of a whole country population. Autism. 2018 Oct 17:1362361318791279.


Posted by Paul Whiteley at 09:00 No comments: Labels: adults, autism, census, children, comorbidity, intellectual disability (ID), prevalence, report, sex differences
 


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Prevalence of autism in preterm infants meta-analysed 


Regressive vs. non-regressive autism: limited chemical differences noted 


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Pervasive refusal syndrome and autism: autistic traits 'speeding up the recovery process'? Before reading the case report paper by Emily Bond & Rosalind Oliphant [1], I have to admit that I knew next to nothing about the label known as pervasive refusal syndrome (PRS). PRS, a condition manifesting as 'refusal to eat, weight loss, social withdrawal and school refusal', is not currently recognised in any of the major diagnostic manuals (DSM, ICD) but does seem to have a following in certain circles [2].

Bond & Oliphant detail a case report of a 9-year old boy who came to clinical attention "due to concerns regarding minimal dietary intake." He had previously been diagnosed with an autism spectrum disorder (ASD) as well as attention-deficit hyperactivity disorder (ADHD) following a trend these days (see here). He was subsequently detained under the Mental Health Act as a consequence of "his resistance of treatment in the community" and also him "lacking Gillick competence." The authors detail his clinical journey, and how, with the right support and accommodations, he was eventually discharged from hospital care with the expectation for him to "make a full recovery to his premorbid functioning with support in the community."

Among the various issues raised in the Bond/Oliphant paper, one of the most striking points made by the authors was in the sentence: "It is possible that the ASD [autism spectrum disorder] symptoms such as literal thinking and concrete processing have actually aided in speeding up the recovery process." The idea that certain autistic traits might actually have had a positive benefit to getting someone through treatment for PRS...

I'm slightly careful here not to go off on the 'autism is a superpower' tangent that some people have previously spoken about (particularly on social media). For this young man, autism for him included communication issues ("His sole method of communication was typing on an iPad to his mother")  and various other traits (e.g. "struggling with understanding abstract questions, complex reasoning, and problem solving skills") which probably didn't impart any superpower for him. He did have an interest in superheros and dressing up in costumes however...

Authors mention how his recovery from PRS - he was discharged after 4 months - was significantly quicker than is typically expected (around 12 months "from previous literature"). They noted that: "The clinical team working with our case quickly found that he responded very well to rules, boundaries, and clear consequences of behaviour." This is perhaps even more notable in the context of his autism-ADHD diagnostic combination.

It did get me wondering whether further research might be revealing into how autism or specific autistic traits might positively impact on other treatment/management scenarios. I'm specifically thinking about more psychologically-inclined interventions, for example, dealing with something like anxiety (see here) where talking therapy is something that is being particularly pushed forward. Whether or not I agree that such therapy is going to be all that useful in the longer-term if for example, one considers that anxiety might be intricately related to some core functions in relation to autism (see here) is irrelevant. Whether certain autistic traits might be a critical variable in intervention success however requires much further study...


[1] Bond EC. & Oliphant RYK. Pervasive Refusal Syndrome in Autistic Spectrum Disorder. Case Rep Psychiatry. 2018 Jun 7;2018:5049818.

[2] Nunn KP. et al. Pervasive refusal syndrome (PRS) 21 years on: a re-conceptualisation and a renaming. Eur Child Adolesc Psychiatry. 2014 Mar;23(3):163-72.

 Labels: ADHD, anxiety, autism, CBT, intervention, pervasive refusal syndrome (PRS), traits


Depressive symptoms in ADHD: "comparing child and parent reports" I was drawn to blogging about the results published by Annie Fraser and colleagues [1] for a few reasons. Their observation that: "Young people with ADHD [attention-deficit hyperactivity disorder] are at high risk of experiencing symptoms of depression but may under‐report the severity of their symptoms" was interesting. It potentially ties into some other important observations about 'happiness' in the context of ADHD (see here) and also how there is an elevated risk of suicidality when ADHD is part of the clinical picture (see here). Similarly, it fits the narrative that various developmental and/or behavioural labels/conditions/disorders are typically never really stand-alone diagnoses...

So: "This study used a subsample of children originally recruited as part of the Cardiff University Study of ADHD Genes and Environment (SAGE)." As per the 'comparing child and parent reports' part of the Fraser paper, both parents and children completed the Mood and Feelings Questionnaire (MFQ) to measures depressive signs and symptoms in participating children/young adults ("mean age was 14.6 years (range 8–20 years)"). The MFQ "is a widely used depression screening instrument" according to the authors, and has some pretty good backing. Results from the MFQ were compared with a non-ADHD (I assume?) general population sample from a similar part of the United Kingdom (UK) and statistics were applied.

Having already alluded to the observation that depression scores on the MFQ were higher (indicative of more depressive symptoms) in the ADHD group than the population control group (N=1460), there are some further details to mention. Both parent- and child-rated MFQs showed the trend of more depressive symptoms in participants with ADHD. And when it came to clinical cut-off points for suspected depression, quite a few more of those diagnosed with ADHD reached them compared with controls (parent‐report 54.5% vs. 10.6%... child‐report 32.4% vs. 10.5%).

"Amongst the most common depression symptoms found in our ADHD sample were difficulty concentrating, restlessness and feeling grumpy with parents. These symptoms overlap with those of ADHD, so it is unsurprising that they were common in our sample." Think of those last sentences in one particular context: the rise and rise of the term 'ESSENCE' (Early Symptomatic Syndromes Eliciting Neurodevelopmental Clinical Examinations) and all the chatter about how behavioural symptoms across various different labels seem to 'overlap' with one and another. How also, developmental and behavioural labels rarely exist alone or in some sort of diagnostic vacuum (see here for example). And add them to another sentence from the authors: "This could suggest that depression scores in this sample are artificially elevated by symptoms which overlap with ADHD symptoms." Indeed.

"Suicidal thoughts and symptoms of psychomotor and cognitive retardation (i.e. talking more slowly than usual, moving and walking more slowly than usual, and sleeping more than usual) were the lowest scoring symptoms on both parent‐ and child‐report." Having already mentioned those quite worrying statistics on how a diagnosis of ADHD seems to elevate the risk of suicidality, this might initially seem like better news from the Fraser paper. Items such as "S/he thought about death or dying.... S/he thought his/her family would be better off without him/her... S/he thought about killing him/herself" were not, in the majority, reported on with great fervour. But one needs to be cautious. I say that because the authors also added: "symptoms of suicidality (‘I thought about killing myself’) were present in 20%–25% of the ADHD sample, according to both parent‐report and child‐report, compared to 2%–7% of the population sample." This is a more worrying way of looking at the findings.

So to conclude: depression or depressive symptoms are no stranger to ADHD, the symptoms of ADHD probably overlap with some of the symptoms of depression (at least according to the MFQ), and an enhanced risk of suicidality seems to be confirmed as and when ADHD is diagnosed. There's more than enough further investigations to be done on those topics; perhaps also drawing on a few other important observations too (see here and see here and see here).


[1] Fraser A. et al. The presentation of depression symptoms in attention‐deficit/hyperactivity disorder: comparing child and parent reports. Child and Adolescent Mental Health. 2018;23(3):243-250.

 Labels: ADHD, depression, diagnosis, ESSENCE, parents, reporting practices, risk, self report, suicide


"the friendships and social experiences of autistic girls are similar to those of neurotypical girls" The quote heading this post - "the friendships and social experiences of autistic girls are similar to those of neurotypical girls" - comes from the findings reported by Felicity Sedgewick and colleagues [1] (open-access available here) continuing a growing research theme looking at the presentation of autism across the sexes/genders. The results however perhaps challenge the idea that "being autistic ‘overrides’ being female in some way."

OK, first things first, by mentioning the word 'neurotypical' the authors refer to a not-autistic control group. As I've said on many, many occasions, the word 'neurotypical' from a research/clinical point of view is however meaningless (see here): there is no way for a living brain, with all its complex structures, connections and functions, some of which are changing second to second, to ever be described as 'typical'. And autism research in particular really shouldn't be using such a misnomer, no matter how [social media] fashionable it might seem.

Rant over. Despite using the term, the Sedgewick paper covers an important real-world part of the whole 'gender differences in autism' area looking at "gender differences in the friendships and conflict experiences of autistic girls and boys relative to their neurotypical [non-autistic] peers." Over 100 adolescents (aged 11-18 years) were included for study; about half diagnosed with autism with an "independent clinical diagnosis of an autism spectrum condition." Said autism diagnoses were also complemented by assessment via the gold-standard ADOS which actually revealed that: "Two boys and four girls failed to meet the ADOS-2 threshold (score = 7) for autism." Data from these children were still included in the study given the "pre-existing clinical diagnosis" and other supporting information. I'm wondering however if perhaps some of these children were examples that an autism diagnosis (or reaching the cut-off points on one of the gold standard autism assessment instruments) is not necessarily for life (see here)? Further, all participants "completed the Friendship Qualities Scale, the Revised Peer Experiences Questionnaire and were interviewed about their friendships" and results were analysed...

Results: "Autistic and non-autistic girls’ conflict and friendships were more like each other than autistic and non-autistic boys, and vice versa." The authors frame this in the context that their findings "provide compelling support for the possibility that gender may be more important than diagnosis in determining young autistic people’s social experiences." That's not to say that there weren't some important group differences in relation to social challenges, conflict and conflict resolution - "autistic girls described an ‘all-or-nothing’ approach, either taking sole responsibility for what had happened... or ending the friendship entirely, seeing the other person as the wrong-doer..., or feeling it could not be resolved" - just that there was more to align girls than to divide them when it came to comparisons with non-autistic peers.

Authors also report results from their interviews with adolescents which again revealed that gender over a diagnosis of autism seemed to a key aspect. So: "Having a few good friends was key, with all girls talking about having a small number of close friends that they considered to be ‘best’ friends. These close friends were those who they spent the most time with and talked to most." Also: "Both autistic and neurotypical girls emphasised that friends supported them." And finally: "Both autistic and neurotypical girls alluded to wanting to fit in, but in different ways." It should also be noted that Sedgewick et al mention how 'camouflaging' (a term being increasingly used in autism circles) is not a specific strategy reserved for autism: "Few girls reporting having boyfriends, but most said people dated to fit in with the popular crowd. These behaviours could be seen as a form of ‘camouflaging’, as teenagers described seeking peer acceptance, even if they were not personally motivated to date."

As to the boys of this particular cohort, well again, there didn't appear to be any really prominent stand-out separation points between autism and not-autism. As the authors report: "autistic and non-autistic adolescent boys reported their friendship and conflict experiences as highly similar – activity-focused, practically supportive friendships combined with a laissez-faire attitude to conflict. The exception to this pattern was that neurotypical boys described more intimate friendship experiences than their autistic male counterparts."

Cumulatively the Sedgewick findings reinforce the idea that there may be some subtle but important differences between boys and girls, women and men diagnosed with autism (see here). In this light, the suggestion that "autistic girls (and possibly women) need different strategies and supports to understand and effectively navigate the social expectations placed upon them" is correct when compared to males diagnosed with autism. The results suggesting however, little significant differences in friendships and social experiences between autistic girls and non-autistic girls (and autistic boys and non-autistic boys) kinda grates against some of the narratives that have emerged in recent years. It implies that rather than viewing someone as an 'autistic girl' one should perhaps first focus on that person as a girl when it comes to social experiences and friendships rather than subscribing to the idea that autism is wholly 'behind' any issues as some 'identity' discussions have intimated. The findings also imply that camouflaging and masking are not necessarily exclusive features of autism but, perhaps in some contexts, are rather more representative of a general effect specifically across gender.

I would like to see a lot more research done in this area. I'd like to see more longitudinal work done looking at friendships and social experiences into adulthood with autism in mind, where other environments replace the school playground (including the online and social media environments). I'd like to know about how friendships develop, persist or 'fall to one side' and whether other 'comorbidity' (see here), that more likely than not will 'follow' a diagnosis of autism (see here), play any role in such social experiences. I'd also like to see further work on societal inclusion (see here) in the context of the Sedgewick research too. There is a scheme of work to do.

And let us also not forget that learning the intricacies of things like friendships and social experiences or challenges such as conflict are also influenced by other important variables, such as a role for siblings [2] (for better or for worse)...


[1] Sedgewick F. et al. 'It's different for girls': Gender differences in the friendships and conflict of autistic and neurotypical adolescents. Autism. 2018 Oct 3:1362361318794930.

[2] Ben-Itzchak E. et al. Having Siblings is Associated with Better Social Functioning in Autism Spectrum Disorder. J Abnorm Child Psychol. 2018 Oct 3.

 Labels: ADOS, autism, camouflage effect, conflict, diagnosis, experience, friendships, gender, masking, neurotypical, sex differences, social


MDMA-assisted psychotherapy for the "reduction of social fear and avoidance that are common in the autistic population" I approach the findings reported by Alicia Danforth and colleagues [1] (open-access available here) very, very carefully. Their preliminary observations on the use of 3,4-methylenedioxymethamphetamine (MDMA)-assisted psychotherapy in the context of adult autism, specifically "to reduce social anxiety" require a lot more follow-up work before anyone gets too carried away. Not least because MDMA or "chemical entities represented as containing MDMA" is categorised as a drug of abuse.

OK, first things first: what is "MDMA-assisted psychotherapy for reduction of social fear and avoidance"? Well, MDMA is  more commonly known as Ecstasy or Molly/Mandy in drug circles. Its effects include "producing feelings of increased energy, pleasure, emotional warmth, and distorted sensory and time perception" thought to be due to its chemical activity on various neurotransmitters (and related biology) such as dopamine and serotonin. Here in Blighty it's currently listed as a Class A drug of abuse alongside things like cocaine and heroin.

MDMA-assisted psychotherapy aims to utilise some of those, and other, behavioural effects associated with recreational MDMA drug use to help further the aims of psychotherapy (talking therapy). Danforth et al have previously published on some of the background behind such a notion [2] specifically in the context of 'treating' social anxiety comorbid to autism. And just before you say/think anything, anxiety and autism is most definitively a 'happening topic' at the moment (see here and see here for examples).

Their most recent publication discusses the results of a small clinical trial of MDMA-assisted psychotherapy with 12 adults with autism. The study details were held on ClinicalTrials.gov (see here) albeit with the published paper listing the wrong trial entry. Authors used a "randomized, placebo-controlled, double-blind methodology for this exploratory phase 2 single-site study conducted from February 2014 through April 2017." MDMA was 'synthesised' and compounded into capsules alongside placebo (dummy) capsules containing lactose (I'm assuming that none of the participants were lactose intolerant given the emerging data on lactose issues and autism [3]). Then: "After three 60- to 90-min non-drug preparatory psychotherapy sessions, participants received two blinded experimental sessions with MDMA or placebo, spaced approximately 1 month apart." Said psychotherapy sessions were described as "standardized mindfulness-based therapy adapted from dialectical behavioral therapy (DBT)." Various assessments of behaviour and physiology were used during the study to ascertain any effect. Importantly too, authors describe their use of various instruments to pick up any adverse side-effects including that related to suicidality.

Results: this was a small study. Although 12 participants were enrolled and entered the study, only data for 11 were available as the authors remarked that a participant "enrolled with hypertension and pre-study substance use disorder within exclusion window for enrollment." Researchers reported however that scores on their primary outcome measure - The Liebowitz Social Anxiety Scale (LSAS) - showed evidence of "rapid and durable improvement in social anxiety symptoms in autistic adults following MDMA-assisted psychotherapy." They also commented that: "Reductions were retained for the MDMA group at 6-month follow-up compared to primary endpoint, supporting durability of improvements." And participants themselves in their subjective reporting also communicated similar sentiments regarding the use of MDMA-assisted psychotherapy as per accounts of "reduced barriers to successful social interactions and increased confidence in school, at work, in friendships, and in romantic relationships."

Then: "No SAEs [serious adverse events] were reported on this study." That's good but doesn't mean that no adverse events were reported following the use of MDMA-assisted psychotherapy, as anxiety and 'depressed mood' were listed as "treatment-emergent psychiatric adverse events" and not specifically seen in the placebo group. Also: "Suicidal ideation was the most commonly reported AE; however, prevalence was similar across groups (25.0% both groups) and was pre-existing in medical history." In other words, one needs to be a little cautious about using MDMA in this context as in other contexts.

Caveats? I've already mentioned the small participant group included for study, which kinda 'down-grades' the levels of positive effects noted by Danforth and colleagues. I was also drawn to another sentence in their paper - "Both groups in this study received the same type of psychotherapy with encouragement toward self-directed healing and meaning-making" - and a niggling question I have about how one is able to ensure that both experimental and control groups received the same type/magnitude/experience of psychotherapy. I say this in the context that DBT seems to have a lot of different 'elements' to it (see here) which are perhaps not easily tested/compared under controlled conditions. Perhaps next time authors could think about including a cross-over portion to their trial too?

That all being said, I'm still [cautiously] interested in the findings presented by Danforth and what research is yet to come on this topic. I've said it a few times on this blog about how anxiety is a real quality-of-life-drainer in many contexts but specifically with autism in mind, the evidence is pretty strong for an important effect. Anything that could safely and reliably help those who are confronted with such issues (and perhaps other issues too?) should be explored objectively and dispassionately.

And on the topic of MDMA, whoever thought it would be a good idea to give to an octopus in the name of science?


[1] Danforth A. et al. "Reduction in social anxiety after MDMA-assisted psychotherapy with autistic adults: a randomized, double-blind, placebo-controlled pilot study". Psychopharmacology. 2018. Sept 8.

[2] Danforth AL. et al. MDMA-assisted therapy: A new treatment model for social anxiety in autistic adults. Progress in Neuro-Psychopharmacology and Biological Psychiatry. 2016; 64: 237-249.

[3] Kushak RI. et al. Intestinal disaccharidase activity in patients with autism: effect of age, gender, and intestinal inflammation. Autism. 2011 May;15(3):285-94.

 Labels: 3, 4-methylenedioxymethamphetamine (MDMA), anxiety, autism, clinical trial, drugs of abuse, placebo, psychotherapy


On autism symptom trajectories and diagnosing autism late... It's another one of my mash-up posts today, as two paper are brought to the blogging table. The first paper is from So Hyun Kim and colleagues [1] and looked at the rather interesting topic of differing symptom trajectories in the context of diagnosing autism. The second paper by Sally Ozonoff and colleagues [2] follows in a similar vein in terms of their analysis of children "who had undergone multiple comprehensive assessments in preschool and were determined to be ASD [autism spectrum disorder]-negative, only to meet criteria for ASD when tested in middle childhood."

Both these paper originate from well-respected autism research groups and appear in the same respected journal (Journal of the American Academy of Child & Adolescent Psychiatry). The common theme between them is that within the significant heterogeneity seen under the label of 'autism', there are various different developmental and presented symptoms trajectories, some of which (a) are not as stable as one might imagine, and (b) do not seemingly follow the oft-used assertion that 'autism is present and manifests from birth'. Indeed, on that last point, the implications are that autism is sometimes very much associated with regression (see here) and onward, that genetic and/or non-genetic post-natal factors may very well influence some children reaching clinical cut-off thresholds for a diagnosis of autism (see here for example).

So, to the Kim paper first: authors looked at over 900 "observations of the Autism Diagnostic Observation Schedule (ADOS)" from nearly 150 young children. They were specifically looking at symptoms trajectories based on those ADOS scores and whether or not 'clusters' of similar symptom trajectories were evident. The answer: yes, yes there were some different clusters of symptom trajectories noted. Not six developmental trajectories as per other research (see here) but four clusters: "Nonspectrum ∼25%; Worsening ∼27%; Moderately-Improving ∼25%; Severe-Persistent ∼23%)." Authors also report how: "Trajectory clusters varied significantly in the proportions of confirmatory ASD diagnosis, the level of baseline and final verbal/nonverbal abilities, and symptom severity."

Then to the Ozonoff paper: "Fourteen children met inclusion criteria for the Late Diagnosed group and were compared to a large sample of high- and low-risk siblings from the same sites who had ASD or typical development (TD) outcomes at age 3." Authors focused in on these 14 children and concluded that: "Seven showed very little evidence of ASD in preschool, while seven demonstrated subtle, subthreshold symptomatology." They also suggest that their results identifying a small but important group of children who seemingly first present with 'typical' behaviour but then 'grow into' the presentation of autism "shed light on reasons why the mean age of ASD diagnosis remains over 4 years." Indeed (see here).

I don't really need to say much more than I have already on these studies. Aside that is, from reiterating that the autism spectrum is truly wide and heterogeneous in both symptom presentation and also it seems, with regards to symptom onset and stability too. Alongside other research (see here) talking about how the presentation of autistic signs and symptoms wax and wane for some, I'm wondering when autism research is going to start looking beyond just presented behaviour, at whether for example, genetic and biological 'changes' might accompany such fluidity in behaviour and 'cluster' differences. Y'know, the same way that another group seemingly heading in the opposite direction - those who 'lose their diagnosis' (see here and see here) - also need to be closely investigated from a biological point of view too. It's only when we have such biological data that we can then start meaningfully probing the possible hows-and-whys...


[1] Kim SH. et al. Variability in Autism Symptom Trajectories Using Repeated Observations from 14 to 36 Months of Age. Journal of the American Academy of Child & Adolescent Psychiatry. 2018. Sept 5.

[2] Ozonoff S. et al. Diagnosis of Autism Spectrum Disorder After Age 5 in Children Evaluated Longitudinally Since Infancy. Journal of the American Academy of Child & Adolescent Psychiatry. 2018. Sept 3.


Posted by Paul Whiteley at 10:00 No comments: Labels: ADOS, autism, biology, delay, diagnosis, genetics, onset, optimal outcome, symptoms, trajectory


"C-Reactive Protein as a Peripheral Biomarker in Schizophrenia" The results of the 'updated systematic review' published by Guillaume Fond and colleagues [1] looking at the "relationships between elevated blood C-reactive protein (CRP) levels and schizophrenia (SZ) onset risk, illness characteristics and treatments, cognition and physical health" provides the blogging fodder today.

Fond (a name not unfamiliar to all-things schizophrenia) et al dip into a topic with more than its fair share of research 'uncertainty' (see here and see here for examples) on whether or not C-reactive protein (CRP), a marker of systemic inflammation, shows a connection to schizophrenia. On this particular research occasion, no new data is added to the debate, but rather authors looked at the collected peer-reviewed data (up to November 2017) to see if any 'general opinions' could be discerned from the collected works.

Results: based on over 50 studies included in their review, authors concluded that it was 'reasonable' to assume that high-sensitivity CRP (hs-CRP) may be a marker for 'schizophrenia onset risk'. The caveat to that statement is that CRP is probably not something 'schizophrenia-specific' in terms of elevations of CRP being indicative of a inflammatory state. So increased hs-CRP may well be a risk factor for "increased positive symptoms, cognitive impairment, hypovitaminosis D, microbiota disturbances, cardiovascular and metabolic syndrome risk in SZ subjects, and increased nicotine dependence in SZ smokers."

I'm pretty happy with the Fond results and interpretation as they stand. They suggest that CRP probably does show some sort of connection to schizophrenia and onward, points to an immune system connection to at least some cases (see here and see here). At the same time, they also imply that certain other observations around schizophrenia - such as a link with certain physical health issues (see here) and/or vitamin D deficiency (see here) - probably also contribute to the elevations of CRP noted in relation to cases of schizophrenia. They also imply that moves to reduce levels of CRP in relation to schizophrenia may well have various other 'knock-on' effects on those other risk factors associated with the condition/diagnosis. This 'double hit' effect could be quite useful.

And with that last sentence in mind, and accepting that consistently high levels of CRP are probably good for no-one, the next question: what can we do about elevated CRP levels in relation to schizophrenia and further, the immune system issues also being co-expressed? Lots, is my impression; perhaps also learning from other labels where immune function (and dysfunction) has been noted [2] and intervention is similarly indicated.

And there's more to come from this authorship group on this blog soon...


[1] Fond G. et al. C-Reactive Protein as a Peripheral Biomarker in Schizophrenia. An Updated Systematic Review. Front. Psychiatry. 2018. Aug 23.

[2] Marchezan J. et al. Immunological Dysfunction in Autism Spectrum Disorder: A Potential Target for Therapy. Neuroimmunomodulation. 2018 Sep 5:1-20.


Posted by Paul Whiteley at 09:10 No comments: Labels: biomarker, C-reactive protein (CRP), immune system, inflammation, schizophrenia, systematic review, vitamin D
