Treading carefully: vaccination rates among younger siblings of kids with autism

'Treading carefully' is a requirement for any discussion about a research study that mentions 'vaccination' and 'autism' in the same breath. I say this on the basis that vaccine coverage is an important cornerstone of public health and now appears to be making significant in-roads with regards to public health, at least here in Blighty.

But much like [scientific] discussions covering other areas of the important public health topic of immunisation, one shouldn't be afraid to look, examine and yes, talk about this subject (see here) particularly where there may be a need for further study minus any hype, sweeping generalisations or logical fallacies...

The paper by Gena Glickman and colleagues [1] discussed an important topic in relation to vaccination behaviour - "whether or not and when parents choose to vaccinate a child" - in the context that parents who already have a child with autism may perhaps be slightly more hesitant to vaccinate their other children in light of "the perceived link between vaccines and autism spectrum disorder." This is a topic that has cropped up on this blog previously (see here). Far be it from me to question any parent about their own child, but I will refer you to some of the peer-reviewed science already done on this topic (see here and see here).

Based on a sample of over 200 families, Glickman et al looked at "vaccination behaviors" as a function of having a child with autism or not. From what I surmise from their report, the focus was specifically on "vaccination against measles–mumps–rubella (MMR)." They reported: "no significant difference between rates of vaccination among children with and those without autism" which is rather comforting. Minus too much politics or anything related, this data suggests that anti-vaccination sentiments are not naturally rife among parents/caregivers of children with autism, at least before a diagnosis of autism is given. Indeed with vaccination rates of 100% among children with autism vs. 98% in the slightly larger control group, one might argue that parents of children with autism are/were extremely vaccine compliant when it came to their first born child.

But then also: "Families with children who had autism spectrum disorder were less likely to vaccinate subsequent children." Authors observed that: "the rate of vaccination among full biologic infant siblings of children with autism spectrum disorder was 83.1%, as compared with 97.0% among low-risk infants."

One can speculate (and speculate) about the reason(s) why younger siblings of children with autism were seemingly less likely to be vaccinated but I'm sure the answers are going to be complex. The authors suggest that: "parents who had an older child with autism spectrum disorder retrospectively reported a higher rate of adverse reactions to vaccination among the older child than did those who did not have an older child with autism" and that this may have impacted on subsequent vaccination behaviour. The rates of adverse reactions reported - 22% in the autism group vs. ~4% in the control group - are not to be sniffed at and indeed, seemingly filtered down to observations of adverse reactions in younger siblings too (6.9% vs. 0.8%). Authors also noted that: "Reported reactions included fever, diarrhea, unusual crying or screaming, and general malaise."

This is a nice piece of research. It doesn't go overboard in it's interpretations of the findings and calmly suggests that "a better understanding of the relationship between perceived adverse reactions to vaccine and autism spectrum disorder is necessary in order to more effectively address concerns about vaccination." It is important to note that the authors don't mention 'onset of autism' or anything like that in their discussion of 'reported reactions' following vaccination, despite the seemingly 'once bitten, twice shy' sentiments portrayed in the findings.

Personally, I would have like to have seen more details about the hows-and-whys of this study insofar as what "available data on vaccination behaviors" were used and whether important information on the timescale(s) of adverse reactions were also available keeping in mind certain issues [2]. Some idea of the rate of autism recurrence among younger siblings might also have been useful too (something that at least one of the authors on the Glickman paper seems to be interested in [3]). Given also the quite apparent differences noted in the rates of reported adverse reactions among those with autism vs. controls, there is also a requirement for further careful investigation in this area. Specifically, whether aspects of the biology (or genetics [4]) of at least 'some' autism (or it's possible comorbidity [5]) might be something to consider when it comes to studies of adverse reactions [6] or indeed whether for example, other medications used at the same time of vaccination might have had an effect [7] onward to finding ways and means to minimise such issues.

To close, although some ten years old, the paper by Shona Hilton and colleagues [8] still stands the test of time in this often fractious area...

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[1] Glickman G. et al. Vaccination Rates among Younger Siblings of Children with Autism. N Engl J Med. 2017 Sep 14;377(11):1099-1101.

[2] Ozonoff S. et al. Reliability of parent recall of symptom onset and timing in autism spectrum disorder. Autism. 2017. Sept 13.

[3] Ozonoff S. et al. Recurrence risk for autism spectrum disorders: a Baby Siblings Research Consortium study. Pediatrics. 2011 Sep;128(3):e488-95.

[4] Verbeek NE. et al. Effect of vaccinations on seizure risk and disease course in Dravet syndrome. Neurology. 2015 Aug 18;85(7):596-603.

[5] Poling JS. et al. Developmental regression and mitochondrial dysfunction in a child with autism. J Child Neurol. 2006 Feb;21(2):170-2.

[6] McClenathan BM. et al. Metabolites as biomarkers of adverse reactions following vaccination: A pilot study using nuclear magnetic resonance metabolomics. Vaccine. 2017 Mar 1;35(9):1238-1245.

[7] 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.

[8] Hilton S. et al. MMR: marginalised, misrepresented and rejected? Autism: a focus group study. Archives of Disease in Childhood. 2007;92(4):322-327.

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"evidence to date is overwhelmingly in favour of lithium as an antisuicidal agent"

If the systematic review and/or meta-analysis sits at the top of the evidence-based pyramid then a systematic review of existing systematic reviews in a particular area should perhaps be the cherry on the top.

The paper published by Katharine Smith & Andrea Cipriani [1] is that cherry on top of the pyramid, looking at a topic of some interest to some of this authorship group [2] on how the "evidence to date is overwhelmingly in favour of lithium as an antisuicidal agent."

I've talked about lithium a few times on this blog (see here and see here) including research pertinent to the idea that the lithium content of public drinking water supplies might show an interesting *relationship* with suicide rates roundabout (see here). Such work stemming from the idea that lithium might have some rather important (positive) influences on suicide prevention [3] for whatever reason(s).

Smith & Cipriani searched the peer-reviewed literature for "systematic reviews and meta-analyses of RCTs [randomised controlled trials] of lithium and suicide and self harm." They found a handful of papers meeting their guidance and with them 'overwhelming' evidence that lithium does seem to impact on risk of suicide. They comment on the fact that there is more to do in this area; for example on: "the supporting evidence that observational and non-randomized studies can also provide" but present an important case that lithium use "should be incorporated more assertively into current guidelines" when it comes to suicide prevention.

Bearing in mind the cost-benefit profile of lithium [4] and that suicide - whether ideation, attempt or completion - stems from a complicated (and often individual) set of circumstances, this is one area where the term 'life-saving' is not to be under-emphasised. And I can think of at least one label where quite a bit more 'life-saving' is required (see here)...

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[1] Smith KA. & Cipriani A. Lithium and suicide in mood disorders: Updated meta-review of the scientific literature. Bipolar Disord. 2017 Sep 12.

[2] Cipriani A. et al. Lithium in the prevention of suicide in mood disorders: updated systematic review and meta-analysis. Database of Abstracts of Reviews of Effects (DARE). 2013.

[3] Lewitzka U. et al. The suicide prevention effect of lithium: more than 20 years of evidence—a narrative review. International Journal of Bipolar Disorders. 2015;3:15.

[4] Albert U. et al. Lithium treatment and potential long-term side effects: a systematic review of the literature. Riv Psichiatr. 2014 Jan-Feb;49(1):12-21.

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On housing and autism

The commentary published by David Mandell [1] provides some food for thought today pertinent to the on-going debate about "how and where to house adults with autism."

I've kinda touched upon this complicated subject in past blog posts (see here) but wouldn't dare think that any quick and easy solutions are going to be forthcoming on this important topic.

Housing for those on the autism spectrum (and beyond) has a patchy history across the globe. From the dark days of mass institutionalisation of those with psychiatric and developmental disabilities to moves towards 'care in the community', one can almost chart how society's views and attitudes to some of its most vulnerable people have seemingly advanced in a relatively short space of time. As Mandell points out: "institutions and the practices that occur within them were hidden from public view, which led to little accountability and serious abuses" reflecting how moves towards "greater observability and accountability" have probably been a primary driver in the switch in housing options.

But all has not been plain sailing in this transition. Many people here in Blighty remember those harrowing scenes filmed in places such as Winterbourne View, a place meant to be 'home' for many people, and with it, meant to provide all the trappings of home such as happiness, comfort and dignity; all sadly lacking in that case. There have, as Mandell also acknowledges, also been serious misgivings about how community services serve all those on the autism spectrum particularly when "caring for individuals with more profound impairments." A recent and relevant example of this can be read here. Balancing civil rights such as "inclusion and community participation" with basic needs such as actually finding suitable housing arrangements is a task still faced by far too many.

As I've said, there are no quick and easy solutions to ensuring that housing services meet everyone's needs. I do like the ideas that Mandell discusses in terms of a change of focus when it comes to housing arrangements in the context of autism, where "happiness and life satisfaction" and care quality are key over and above generic requirements such as inclusion and community participation. By saying that I'm not suggesting that inclusion and community participation aren't and shouldn't be important (see here for example) but rather that mandating them when it comes to residential options for those on the autism spectrum perhaps risks putting a 'one-size-fits-all' recommendation on what is supposed to be a personalised and tailored core issue. Living in the countryside or remote areas as quite a few people in the general population also do - "segregated farming communities" - should not for example, be viewed as 'a worse option' if and when someone is happy in such a setting and experiences a good quality of life. Even worse, that by housing people in "poor neighborhoods with few opportunities for community engagement" purely on the basis of concepts such as social inclusion, risks putting vulnerable adults in an even more vulnerable position (combining at a time when care resources and finances are already reaching breaking point).

And when it comes to residential placement for children when required [2] similar considerations also might apply... happiness, life satisfaction and good quality care and support. Simple.

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[1] Mandell DS. A house is not a home: The great residential divide in autism care. Autism. 2017 Oct;21(7):810-811.

[2] Benderix Y. et al. Parents' experience of having a child with autism and learning disabilities living in a group home: a case study. Autism. 2006 Nov;10(6):629-41.

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Zonulin (testing): "its clinical utility questionable"

The quote making up part of the the title of today's post is taken from the paper by Aristo Vojdani and colleagues [1] (open-access available here) providing some well needed analysis of a compound of some interest for various clinical areas: zonulin.

Just in case you weren't familiar with all-things zonulin, this is a compound that has found some scientific favour when it comes to the concept of intestinal barrier function being perturbed in several diagnoses [2]. I must admit to being pretty interested in some quite recent research talking about zonulin in the context of 'some' autism (see here) based on the idea that intestinal barrier function might not be 'optimal' for some people diagnosed with an autism spectrum disorder (ASD) and what implications that might have (see here and see here).

Vojdani - who is also no stranger to autism research - cautions that the inevitable testing 'free for all' that has ensued as zonulin has risen up the scientific ranks might not be all good, as they pitted the direct measurement of serum zonulin levels against "antibodies against zonulin" to see which measure might provide the most accurate results. Antibodies against zonulin by the way, meant IgA and IgG antibodies against zonulin and was carried out "using enzyme-linked immunosorbent assay methodology."

Results: based on the analysis of over 70 blood samples from "18 volunteers at intervals of 0, 6, 24, and 30 h[ours]" authors noted that a third of participants (6/18) had low levels of serum zonulin "very close to the detection limit of the assay." We are told over the course of the hours, levels of serum zonulin "did not significantly fluctuate" in their trace amounts in this group. For the other 12 participants, it was a slightly different story as "significant fluctuation in zonulin levels was observed in almost all 12 of these subjects at the 6-, 24- or 30-h blood draws." When it came to those antibodies against zonulin, the clinical picture appeared to be slightly more calm as data showed that "both IgG and IgA antibody levels from blood obtained at 0, 6, 24, and 30 h were highly stable with variations of less than 10%." On that basis, the authors recommend that a single measurement of zonulin itself may not be a suitable indicator "for assessment of intestinal barrier integrity."

There was also another part to the Vojdani study looking at serum zonulin levels in "30 healthy controls along with 30 patients with known celiac disease." Coeliac or celiac disease (CD) is the archetypal gluten-related autoimmune condition and has some connection to zonulin. Results for this part of the study indicated a significant group difference between CD and non-CD groups where serum zonulin levels were higher in those with CD. When comparing serum zonulin levels against those antibodies to zonulin in the CS vs no-CD groups, authors reported "detection of antibodies against zonulin in 67% of patients with CD while zonulin level elevations were detected in only 33%." They suggested that these results could be due to "zonulin fluctuation in the blood and its removal by the immune system."

These types of results are interesting and help to add some 'detail' to big, sometimes sweeping, scientific findings with an emphasis on the technology and techniques used to measure such compounds. In the context of the Esnafoglu paper [3] that was the source material for my blogpost on zonulin and autism, there may be lessons to be learned as per their use of an enzyme-linked immunosorbent assay to analyse for serum zonulin levels in that particular cohort. That being said, a comparison of the range of zonulin levels reported in their autism cohort "(ASD (122.3 ± 98.46 ng/mL) compared with the healthy controls (41.89 ± 45.83 ng/mL)" compared with the Vojdani results (CD mean = 8.5 ng/mL vs. controls mean = 3.7 ng/mL ) shows that there may be quite a bit more to see when it comes to zonulin and [some] autism outside of just testing factors.

Just before I go, I do have one possible suggestion which might help matters in the area of zonulin measurement. Being quite a big fan of techniques such as mass spectrometry over other analytical methods and bringing in other recent data suggesting that *some* immunoassay kits purposed for zonulin analysis might be missing the mark [4], I'm minded to suggest that a more direct analysis of something like serum zonulin in various groups could be warranted based on mass spec and related techniques including those diagnosed with CD and autism (or even both)...

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[1] Vojdani A. et al. Fluctuation of zonulin levels in blood vs stability of antibodies. World J Gastroenterol. 2017 Aug 21;23(31):5669-5679.

[2] Fasano A. Zonulin, regulation of tight junctions, and autoimmune diseases. Annals of the New York Academy of Sciences. 2012;1258(1):25-33.

[3] Esnafoglu E. et al. Increased Serum Zonulin Levels as an Intestinal Permeability Marker in Autistic Subjects. J Pediatrics. 2017. May 11.

[4] Scheffler L. et al. Widely used commercial ELISA for human Zonulin reacts with Complement C3 rather than preHaptoglobin2. bioRxiv preprint. 2017. Jun 30.

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Autism diagnosis as an "independent risk factor of attempted suicide"

The topic covered in the paper by Mu-Hong Chen and colleagues [1] is unfortunately, a familiar one to this blog examining the association between a diagnosis of autism or autism spectrum disorder (ASD) and suicidality.

Although various research and clinical efforts continue in this area, there remains a worrying association between autism and various aspects of suicidality covering ideation/discussion, attempts and unfortunately, completion in some cases. I might even add in the concept of assisted suicide to such as association (see here). Lives are being lost.

Chen et al once again drew on the 'big data' resource that is the Taiwan National Health Insurance Research Database to look at whether: "ASD independently increases the risk of attempted suicide" on the basis that comorbidity such as depression, has been suggested to exert an influence on suicidality - peripherally or directly - in the context of autism (see here).

Looking at over 5,500 adolescents (12-17 years) and young adults (18-29 years) with a diagnosis of ASD compared to over 22,000 sex- and aged-matched 'not autism' controls, researchers looked for catalogued instances of suicide attempt(s) alongside various other data on participants - "demographic data and psychiatric comorbidities." They observed that suicide attempts were significantly higher in the ASD cohort compared with controls (~4% vs. ~1%) and onward presented with elevated hazard ratios. Those elevated hazard ratios took into account those various demographic and psychiatric comorbidity data, leading the authors to conclude that the diagnosis of ASD was itself an independent risk factor for attempted suicide.

One might um-and-ah about how representative Taiwanese data might be to the rest of the world or indeed, whether with all the strengths of the Taiwanese dataset, there may be psychopathology such as depression that is not recorded in the insurance database on the basis of being sub-clinical for example. But with big participant numbers comes big(ger) confidence that the findings might be generalisable. Knowing also that various types of depression do seem to be over-represented in cases of autism (see here), so one might assume that it would be on the clinical radar no matter what country you come from or are currently living in.

Without trying to simplify the road(s) that lead someone to contemplate suicide (big data Taiwan has also already told us about some of them) I do find some hope in the findings of Chen and colleagues. Their suggestion that autism - the facets of autism - might be an independent risk factor for suicide suggest that if one is able to 'pin down' what specific parts of autism might be linked to a greater risk for suicide, then one could conceivably act upon them. I know some people don't like the idea of 'acting on' autism, but taking the example of another pretty disabling feature of quite a few instances of autism - anxiety - there are indications that acting on core symptoms *might* aid in reducing/dispensing with this quality-of-life-draining clinical feature also (see here). I might also add that even though facets of autism itself might be linked to an elevated risk of suicidality, one shouldn't necessarily assume that comorbid depression is completely off the hook; also keeping in mind that a variety of social factors might play a role in such behaviour(s) (see here)...

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[1] Chen MH. et al. Risk of Suicide Attempts Among Adolescents and Young Adults With Autism Spectrum Disorder: A Nationwide Longitudinal Follow-Up Study. J Clin Psychiatry. 2017 Aug 29. pii: 16m11100.

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Anxiety prevention meta-analysed and some implications...

"Psychological and/or educational interventions had a small but statistically significant benefit for anxiety prevention in all populations evaluated. Although more studies with larger samples and active comparators are needed, these findings suggest that anxiety prevention programs should be further developed and implemented."

That was the research bottom-line published by Patricia Moreno-Peral and colleagues [1] assessing the collected peer-reviewed literature pertinent to the question: "Are psychological and/or educational preventive interventions for anxiety effective in varied populations?" An accompanying editorial on the Moreno-Peral findings is also worthwhile reading [2].

The methodological name of the game was systematic review and meta-analysis followed by "meta-regression" to boil down data from some 29 studies examining whether "psychological and/or educational interventions are effective in the prevention of anxiety." Said interventions covered some ground but in the most part relied on the use of cognitive behavioral therapy (CBT).

I'm not going to say too much more about the Moreno-Peral findings because I think they speak for themselves. I do however want to make comment on the authors' use of the term 'varied populations' to highlight potential implications for a couple of populations pertinent to this blog: (a) the autism spectrum and (b) those diagnosed with chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME).

Starting with autism, there are two salient points to make: (i) anxiety is pretty rife in relation to autism (see here and see here) and (ii) treating anxiety in relation to autism already has some peer-reviewed science efforts (see here) but little so far has seemingly been done on the point of potentially heading-off clinically relevant anxiety before it takes hold. I say this mindful of the idea that core symptoms linked to autism might be potential 'anxiety-provokers' (see here). Quite a bit more research is needed to ensure that psychological and/or educational interventions for anxiety currently available are specifically tailored to the wants and needs of those on the autism spectrum (including all of the spectrum!) but this area promises quite a bit. It's also worth appreciating that there may be a place for other types of prevention/intervention when it comes to anxiety (see here for example) in the context of autism (see here).

I also mentioned the [careful] application of the Moreno-Peral findings to CFS/ME. Coincidentally at the time of writing this post, I stumbled across the paper by Sarah Stoll and colleagues [3] asking: 'What treatments work for anxiety in children with chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME)?' The answer, based on the available literature is 'we don't know yet' with the requirement for more investigations.

I tread very carefully in this area based on the fact that whilst anxiety does seem to be part and parcel of some CFS/ME (see here), suggestions about the possible usefulness of something like CBT to manage anxiety have to viewed in the context of CBT still courting controversy as part of the biopsychosocial 'view' of CFS/ME (see here) (something that is relevant to other recent discussions about CFS/ME). Indeed, one might see the Stoll findings in the context that the 'failure' of interventions like CBT in relation to treating core CFS/ME (see here for what I mean by 'failure') is moving some people along to still try and stick with CBT but re-do and re-apply it in the context of treating more peripheral signs and symptoms accompanying CFS/ME such as anxiety. I might be wrong but...

To close, but keeping the CFS/ME link in mind, I once again note a welcomed U-turn from NICE (National Institute for Health and Care Excellence) on the topic of CFS/ME: "The strong message from stakeholders was that the continuing debate about the causes of this condition and the best approach to treatment argued for a review of the current guideline." I've said it before and will say it again: patient-power has driven this reconsideration (see here)...

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[1] Moreno-Peral P. et al. Effectiveness of Psychological and/or Educational Interventions in the Prevention of Anxiety. JAMA Psychiatry. 2017. Sept 6.

[2] Hudson JL. Prevention of Anxiety Disorders Across the Lifespan. JAMA Psychiatry. 2017. Sept 6.

[3] Stoll SVE. et al. What treatments work for anxiety in children with chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME)? Systematic review. BMJ Open. 2017; 7: e015481.

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Pregnancy antidepressant use and offspring outcomes beyond autism?

I'll say one thing for the British Medical Journal (BMJ), they don't seem to be afraid to cover important issues relating to the *possible* "reproductive safety of drugs" [1] as per their publication of yet another paper looking at antidepressant use during pregnancy and offspring outcomes published by Xiaoqin Liu and colleagues [2]. This follows another paper published in the BMJ and covered on this blog a few weeks back (see here).

The specific class of drugs being examined again are, as I mentioned, the antidepressants and based, yet again, on data from one or more of those wonderful Scandinavian population registries in relation to how pregnancy use of antidepressants *might* impact on risk of risk of various psychiatric disorders in offspring. A diagnosis of autism spectrum disorder (AD) has been a primary focus of previous research in this area; particularly the question of whether the medicines themselves or the condition(s) that the medicines are used for (i.e. maternal psychopathology) might be the more important variables related to enhanced offspring risk of autism. The last paper covered on this blog by Rai and colleagues [3] very cautiously suggested that: "The results of all these analyses, which used different assumptions, seemed to be consistent with each other, suggesting that the association between in utero exposure to antidepressants and autism might not be fully explained by confounding." Cautiously...

This time around the net was widened from just looking at autism as an offspring outcome to "overall risk of psychiatric disorders" including: "autism spectrum disorder... mood disorder... neurotic, stress related, and somatoform disorder... behavioural and emotional disorder... and mental retardation." I might add that these are the authors words not mine and diagnoses were based on ICD-10 criteria and codings.

Looking and following some 900,000 children born between 1998 and 2012 in Denmark until 2014, researchers categorised participants according to their pregnancy antidepressant exposure(s): "unexposed, antidepressant discontinuation (use before but not during pregnancy), antidepressant continuation (use both before and during pregnancy), and new user (use only during pregnancy)" and looked at the frequency of those conditions included for study.

Results: some 2% of children were born to mums who used an antidepressant during pregnancy (n=21,063). Various types of antidepressants were used but the majority were prescribed SSRIs (Selective Serotonin Reuptake Inhibitors) either alone (monotherapy) or in conjunction with other non-SSRI medication.

"We observed increased risks of psychiatric disorders in all three groups of antidepressant users (discontinuation, continuation, and new user groups), compared with the unexposed group." This itself is an important finding but does not yet disentangle whether medicine use or the reason(s) for medicine use might be the more important variable. Then: "we observed an increased risk of psychiatric disorders in children whose mothers continued antidepressant use during pregnancy, compared with mothers who discontinued." Such a statement potentially edges a little closer to some influence of pregnancy antidepressant use on offspring outcomes but, and it is an important but: "These associations could be attributable to the severity of the underlying maternal disorders in combination with in utero antidepressant exposure." In other words, those mums who needed to continue antidepressant use throughout pregnancy probably had to do so because their symptoms either returned or were not controlled properly when medication is not in place. This might imply that more serious maternal psychiatric disorder could be a variable in any enhanced risk of offspring psychiatric disorder.

When it came to looking at specific diagnostic labels for offspring, all but "mental retardation" (I prefer the term learning disability) seemed to be elevated alongside "in utero exposure to antidepressants." The conditions with the highest risk were the mood disorders including diagnoses such as clinical depression and bipolar disorder. Given that antidepressants are typically (but not exclusively) used to treat/manage mood disorders, such a finding of maternal mood disorder potentially transmitting down into offspring mood disorder receives further credence from such results.

The Liu paper and accompanying editorial grapple with the question of whether the *possible* risks from pregnancy use of antidepressants on offspring merit a change to guidance on their use at such a critical time. As I've mentioned on other occasions discussing this topic, antidepressants are not typically just dispensed willy-nilly without appropriate clinical indication. They provide an important service in controlling various types of symptoms; pertinent to the idea that uncontrolled depression during pregnancy for example, can have all-manner of negative outcomes. As all medicines do, yes they may have side-effects but these need to be weighed up against perceived benefits, taking into account any important influence on the developing child. Indeed, the authors note: "any final decision on antidepressant continuation should be individualised and made jointly by health professionals and patients."

And whilst I've mentioned pregnancy antidepressant use and offspring autism risk, yet another review paper enters the scientific fray [4]...

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[1] Nordeng H. et al. Prenatal exposure to antidepressants and increased risk of psychiatric disorders. BMJ. 2017; 358: j3950.

[2] Liu X. et al. Antidepressant use during pregnancy and psychiatric disorders in offspring: Danish nationwide register based cohort study. BMJ. 2017; 358: j3668.

[3] Rai. D. et al. Antidepressants during pregnancy and autism in offspring: population based cohort study. BMJ. 2017; 358: j2811.

[4] Andalib S. et al. Maternal SSRI exposure increases the risk of autistic offspring: A meta-analysis and systematic review. Eur Psychiatry. 2017 Jun 20;45:161-166.

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SMILE: On the Lightning Process + specialist medical care for chronic fatigue syndrome (CFS)

Even before the publication of the results by Esther Crawley and colleagues [1] I had already seen quite a few discussions on the use of the Lightning Process being applied to the label chronic fatigue syndrome (CFS) (see here for example).

A trial protocol [2] and some additional 'building work' [3] on this topic had already been published in the peer-reviewed domain, talking about how use of the "Phil Parker Lightning Process® (LP)" developed from "osteopathy, life coaching and neuro-linguistic programming" was already reported in the context of CFS (and CFS/ME - myalgic encephalomyelitis) and the requirement to study it given "no reported studies investigating the effectiveness or possible side effects (for example serious adverse events) of the LP."

The theory behind the LP is that of training individuals "to recognize when they are stimulating or triggering unhelpful physiological responses and to avoid these, using a set of standardized questions, new language patterns and physical movements with the aim of improving a more appropriate response to situations." In short, I don't think it's unreasonable to say that the biopsychosocial (BPS) view forms part of the methodological basis for the intervention. Alarm bells were already starting to ring (see here).

The Crawley results have been posted across the lay media, with headlines such as 'Controversial Lightning Process helps children with chronic fatigue syndrome' and 'Chronic fatigue therapy 'could help teenagers', study says.' Interestingly however, various counter viewpoints about the trial have also been included in such reports, as per quotes such as "The over-simplistic and largely psychological model of ME/CFS causation that is being put forward to patients by Lightning Process practitioners is totally out of step with emerging scientific evidence as to its cause." Even expert opinion has it's own worries about the trial and it's subject matter. I'll come back to all that shortly.

So what did the study actually do and find? Well, teens with mild/moderate CFS/ME were the target study group (100 of them): "Children were diagnosed with CFS/ME after a thorough assessment which included screening for other disorders associated with fatigue." The authors noted that recruitment was 'problematic' when it came to this trial as per the note: "Fewer than 30% of eligible children were randomised. We do not know why the majority did not want to take part in the trial but it may be because they did not want to take part in groups or travel for three consecutive days." Diagnosis by the way, I assume followed the NICE guidance on the topic; the same NICE guidance that has seen a U-turn in recent days on the potential need for some reconsideration (see here). Real 'patient power' was behind this decision by the way.

Fifty-one of the 100 participants were allocated to receive specialist medical care (SMC) plus a few days LP training and the remaining 49 just received SMC. SMC by the way, again follows those NICE guidance "focused on improving sleep and using activity management to establish a baseline level of activity (school, exercise and social activity) which is then gradually increased." CBT - cognitive behaviour therapy - is also offered to those with "significant anxiety or low mood" and: "Participants could choose to use physiotherapist-delivered graded exercise therapy, which provides detailed advice about exercise and focuses on an exercise programme rather than other activities." The primary outcome of the trial was scores on the "the 36-Item Short-Form Health Survey Physical Function Subscale (SF-36-PFS)" at baseline and again at 6 months. Various other measures were also included as secondary outcomes looking at "pain, anxiety, depression, school attendance and cost-effectiveness from a health service perspective at 3, 6 and 12 months."

Results: "It is the first trial that has demonstrated the effectiveness of an intervention other than CBT for paediatric CFS/ME." Although it is debatable whether CBT is as 'effective' an intervention for CFS/ME as many people might think (see here for a real world perspective on this from some of the authors on the current paper and see here for other findings), the results did seemingly show a difference between the groups when it came to mean SF-36 physical function scores in favour of the experimental group. The margin of the group difference was significant and authors noted that: "There was little evidence that the effect of LP+SMC compared with SMC on the primary outcome differed according to baseline age, anxiety or school attendance." The caveat to all this is the reliance on patient-reported outcomes and the unblinded nature on the trial that "may have been affected by participants’ knowledge of the group to which they were randomised." As other commentators have noted (see here again) 'positive expectations' seem to be part-and-parcel of the LP method and it's not inconceivable that these might have subsequently affected patient scores. Further comment from the authors that "it would be unethical to have a control group without treatment"as part of their study is to some extent justified but does not discount the idea that other, non-psychological interventions, could have been pitted against both SMC and the LP+SMC (see here for one double-blind, placebo-controlled example). Indeed, I'd like to see more of such comparisons in further study.

When it came to another important part of the study - adverse effects - authors specifically noted that: "Physical function at 6 months deteriorated in nine participants, of whom eight were in the SMC arm." They also reported on a few instances of adverse events but concluded that generally both study arms were considered safe over the course of study.

From a scientific point of view, the Crawley results provide some support for the use of the LP + SMC in the context of [some] teen CFS/ME. The authors noted that they don't know whether their results are likely to generalise to more severe cases of CFS/ME or indeed those younger than 12 years old, and offer little in the way of explanation as to why they got the results that they got (i.e. "Further research is needed to understand why LP improves outcomes at 6 and 12 months and which aspects of the LP contribute to its effectiveness.") I'm not however totally sold on the idea that the LP is "teaching people to use their brain to “stimulate health-promoting neural pathways”" as an explanation for the the findings, but would be willing to concede should the relevant (MRI?) scientific evidence ever emerge. As an aside, quite a lot of the research with a BPS slant to it with regards to CFS/ME could benefit from the odd physiological measures now and again just to see what may or may not be being affected...

Bearing in mind the [long] history of medical involvement in CFS/ME and the often detrimental focus on things like the BPS model [4] with regards to the condition, it's not a surprise that even despite 'positive' results, the SMILE trial has not been received with open arms by quite a few. Problems with trial recruitment? Well, one might opine that this could have had something to do with the subject matter and that BPS-type implication behind the trial potentially putting people off. Other more qualitative reports on the use of the LP in the context of CFS/ME [5] have hinted at issues with things like the "secrecy surrounding it, and feelings of being blamed if the treatment did not work" that hardly provide a great endorsement for getting involved. Yet again, the burden of CFS/ME is seemingly being placed on the person, with only little regard for the fact that there is a growing body of evidence to suggest that biology trumps psychology when it comes to the presentation and perpetuation of symptoms for many (see here). All the positive feelings, thinking and 'reprogramming' in the world are probably not going to fundamentally alter such biological (medical) issues as per other examples in the research literature (see here). Given also that science does not exist in a social or cultural vacuum, and past scientific experiences when it comes to treatment options for CFS/ME (see here) I wonder if perhaps a new direction needs to be taken - particularly here in Blighty - whereby as many resources and research interests are put into trying to understand the biology of the spectrum that is CFS/ME as are seemingly being dedicated to looking at and tackling the psychology of CFS/ME.

Parity in biological and psychological research is the real 'mind-body' stuff when it comes to CFS/ME...

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[1] Crawley EM. et al. Clinical and cost-effectiveness of the Lightning Process in addition to specialist medical care for paediatric chronic fatigue syndrome: randomised controlled trial. Archives of Disease in Childhood. 2017. 20 Sept.

[2] Crawley E. et al. Comparing specialist medical care with specialist medical care plus the Lightning Process for chronic fatigue syndrome or myalgic encephalomyelitis (CFS/ME): study protocol for a randomised controlled trial (SMILE Trial). Trials. 2013 Dec 26;14:444.

[3] Crawley E. et al. The feasibility and acceptability of conducting a trial of specialist medical care and the Lightning Process in children with chronic fatigue syndrome: feasibility randomized controlled trial (SMILE study). Trials. 2013 Dec 5;14:415.

[4] Geraghty KJ. & Esmail A. Chronic fatigue syndrome: is the biopsychosocial model responsible for patient dissatisfaction and harm? Br J Gen Pract. 2016 Aug;66(649):437-8.

[5] Reme SE. et al. Experiences of young people who have undergone the Lightning Process to treat chronic fatigue syndrome/myalgic encephalomyelitis – a qualitative study. Br J Health Psychology. 2012; 18: 508-525.

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"the likely effects of autism spectrum disorder on adolescent driving abilities"

"The literature revealed that drivers with autism (particularly males) were less likely to identify social hazards (e.g., pedestrians), had slower reaction times, more tactical driving difficulties, reported more traffic crashes, citations and intentional driving violations, and had poorer situation awareness skills than drivers without autism."

So said the literature review published by Clara Silvi and colleagues [1] looking at how young people diagnosed with an autism spectrum disorder (ASD) manage the multiple tasks involved in driving and how various characteristics linked to autism *might* translate into "driving-related challenges."

I feel I must add a caveat or two before proceeding with this post. First up is the quite widely known about association between age and driving ability (or inability). Younger drivers are, for various reasons, already more likely to be "overrepresented in road crash statistics." Inexperience, more risk-taking driving behaviours combined with the 'overconfidence of youth' are likely to be important reasons for such adverse driving statistics. Second, a diagnosis of autism does not automatically make everyone with autism a poor driver. Granted, here in the Blighty at least, a diagnosis of autism or ASD is something that needs to be considered in the context of licencing for driving (see here) but unlike something like epilepsy - "epileptic attacks, seizures, fits or blackouts" - the condition/label does not automatically disqualify someone from being licensed to drive.

OK, the Silvi review initially took in quite a lot of the literature on this topic, eventually being boiled down to 9 articles. These collected research papers provided various viewpoints on autism and driving behaviours/outcomes including that from parents/caregivers, driving instructors and importantly, young novice drivers with autism. The endpoint reached suggested that "symptoms of autism spectrum disorder can negatively affect the driving abilities of young drivers with autism spectrum disorder, further impacting their ability to drive, and in this way increasing their risk of crashing."

The authors have zoomed in quite a bit on a possible role for situational awareness when it comes to adverse outcomes in the context of autism and driving. Situational awareness combines various elements whereby the 'here and now' of the driving environment is constantly changing and hence drivers require a high degree of perceptual and cognitive flexibility and adaptation to adjust their driving behaviour accordingly. Indeed the authors talk about how: "Poor/underdeveloped situation awareness can represent a lack of mental models and schemas (thought/behavioral patterns)."

I can kinda see how some of the ways that autism has been defined *might* overlap with the findings talking about how "situation awareness skills were less developed in drivers with autism spectrum disorder." This is something picked up in other research too [2]. I'm not so sure about the whole 'lacking in mental models' thing applied specifically to autism (seemingly harking back to the sweeping generalisation of a 'lack of theory of mind') but can perhaps see a way forward for how cognitive flexibility might be something important in the context of traits related to being rule-bound and highly perseverative.

There is a balance to be struck between the safety of autistic drivers (and indeed, the safety of other road users) and ensuring that personal liberties are not impinged on too much as a result of the Silvi findings. As many drivers will tell you, the freedom that comes with driving a car or other vehicle is something that adds considerably to quality of life; a topic that has already revealed some quite profound issues in relation to some autism [3] (see here for my take). Indeed, if accessibility is a factor in ensuring those on the autism spectrum can live a good quality of life, moves to make driving safer and more readily available to more people on the spectrum should be further [carefully] investigated.

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[1] Silvi C. et al. A Literature Review of the Likely Effects of Autism Spectrum Disorder on Adolescent Driving Abilities. Adolescent Research Review. 2017. Sept 2.

[2] Chee DYT. et al. Investigating the driving performance of drivers with and without autism spectrum disorders under complex driving conditions. Disabil Rehabil. 2017 Aug 28:1-8.

[3] Ayres M. et al. A systematic review of quality of life of adults on the autism spectrum. Autism. 2017 Aug 1:1362361317714988.

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Treating violence in schizophrenia with fish oils?

"Violent schizophrenia patients treated with fish oil (360mg DHA+540mg EPA) demonstrated a decrease in violence."

That was the primary conclusion arrived at in the study results by Yi Qiao and colleagues [1] suggesting that some aspects of nutrition may very well have implications for extremes of behaviour in the context of psychiatric diagnoses. The ClinicalTrials.gov entry for this study can be seen here.

DHA - Docosahexaenoic acid - and EPA - Eicosapentaenoic acid - are categorised as omega-3 fatty acids. In this research instance, Qiao et al divided up their "Fifty inpatients meeting ICD-10 criteria for schizophrenia" such that roughly half received a fish oil for 12 weeks and half received a placebo. I should add that this 'inpatient' group also scored significantly on the Modified Overt Aggression Scale (MOAS) at baseline.

Results: well, fish oil use did not seem to make any significant difference to some of the [positive and negative] signs and symptoms of schizophrenia compared with placebo use. But as per the opening sentence to this post, there did seem to be something significant to see when it came to follow-up of violent behaviour alongside the use of fish oils.

These are interesting findings. My first thoughts on reading the Qiao results harked back to previous work looking at the use of nutrition in the context of a prison population by Bernard Gesch and colleagues [2]. That research concluded that: "Antisocial behaviour in prisons, including violence, are reduced by vitamins, minerals and essential fatty acids" where EPA and DHA were part of the supplement provided under "double-blind, placebo-controlled, randomised trial" conditions; albeit in smaller doses that those used by Qiao and colleagues.

The Qiao results are also not the first time that fish oil use for violence in the context of schizophrenia have been talked about in the peer-reviewed science domain [3]. With the understanding that violence accompanying schizophrenia is probably going to be as complex as violence outside of schizophrenia, such promising results require some further replication and a little more data on possible hows-and-whys. The low cost, pretty favourable safety profile and reports of other potential health benefits associated with fish oil use however, suggest that such an intervention could easily be incorporated into treatment plan for many people fitting a similar profile to those described by Qiao and colleagues.

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[1] Qiao Y. et al. Effects of Omega-3 in the treatment of violent schizophrenia patients. Schizophr Res. 2017 Aug 19. pii: S0920-9964(17)30501-7.

[2] Gesch CB. et al. Influence of supplementary vitamins, minerals and essential fatty acids on the antisocial behaviour of young adult prisoners. Randomised, placebo-controlled trial. Br J Psychiatry. 2002 Jul;181:22-8.

[3] Légaré N. et al. Omega-3 and violence in schizophrenia. Schizophrenia Res. 2007; 96: 269.

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"a heightened co-occurrence rate of ASD [autism spectrum disorder] and GD [gender dysphoria]"

Gender dysphoria "where a person experiences discomfort or distress because there's a mismatch between their biological sex and gender identity" is something that has seemingly risen in research popularity in the context of autism (see here).

The findings reported by Janssen Aron and colleagues [1] (open-access available here) add to the body of research in this area where "endorsement of sex item 110, “wish to be opposite sex,” is 7.76 times more likely among participants with an ASD [autism spectrum disorder] diagnosis than in a nonreferred comparison group." 'Sex item 110' refers to a question item on the Child Behavior Checklist (CBCL) by the way.

Drawing on data derived from almost 500 participants diagnosed with an ASD and some 1600 responses to the CBCL from a 'normative sample', researchers inquired about possible gender variance. Importantly: "In the present study, all CBCL charts had been filled out by the patients' parents" so we need to bear in mind this was a study of proxy reporting albeit from those who probably know the participant pretty well. Researchers observed that some 5% of the ASD cohort "endorsed sex item 110" compared with about half a percent of the control group. Biological gender discussed in terms of 'natal gender' did not suggest that any one gender were more or less likely to endorse that CBCL question and age of participants similarly showed little impact on the endorsement of the questionnaire item.

The authors caution that response to one item on the CBCL does not a gender dysphoria diagnosis make. But they do suggest that further screening could be preferentially offered as and when either autism is diagnosed or indeed screening for autism/autistic traits when gender variance is encountered in the clinic minus any sweeping generalisations. One might also see a need for designing new questionnaires/schedules to specifically ascertain signs of gender dysphoria in cases of autism - indeed, as some have [2] - with a focus on both longitudinal research i.e. how might signs and symptoms change with age/maturation and also taking into account more direct reporting from participants themselves...

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[1] Janssen A. et al. Gender Variance Among Youth with Autism Spectrum Disorders: A Retrospective Chart Review. Transgend Health. 2016 Feb 1;1(1):63-68.

[2] George R. & Stokes MA. Gender identity and sexual orientation in autism spectrum disorder. Autism. 2017. Sept 15.

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Parent-mediated intervention for autism falls yet again

"We found minimal evidence for main effects of ART [Adapted Responsive Teaching] on child outcomes."

So said the study results reported by Linda Watson and colleagues [1] adding to a bank of studies (and meta-analyses) suggesting that parent delivered early behavioural interventions for autism or cases of 'at-risk for autism' in the most part are not seemingly cutting the scientific mustard (see here). I temper that last sentence with a number of caveats; not least that the methodological quality of the studies in this area still has some way to go and also that parent-mediated interventions covers quite a bit of ground in terms of techniques. The idea however that moves to make parents with children with autism some kind of 'super-parents' (yes, someone did use a term similar to that) to impact on their child's early presentation is not exactly borne out by the scientific data in this area. I would add that many parents of children with autism are already super-parents without any additional help, indications or guidance for the powers-that-be.

This time around nearly 90 young infants "at-risk of later ASD [autism spectrum disorder] diagnoses" were given either ART or REIM (referral to early intervention and monitoring) following other work from this authorship group on this topic [2]. ART by the way, focuses on 'relationships' over a 6 month period where aspects such as engagement, awareness and joint action between parent and child are some of the points of interest. Various facets of functioning were assessed and, assuming the equal use of other early intervention services between the groups, the time, effort and costs of ART did not seemingly provide some wildly significant gains when compared with REIM. In short, yes something like ART is a wonderful aid for things like increasing parental responsiveness to their kids but when it came to important child outcomes - including autism-related outcomes - the intervention did not seemingly fare so well.

What's more to say on this topic? Well, being careful not to hark back to the bad 'ole days where parenting behaviours were 'blamed' for the development of offspring autism, I'm not going to totally poo-poo this area of research and practice. There are some pretty good intervention strategies out there for helping parents to further *connect* with their children in the context of autism and potentially raising the potential and wellbeing of all parties concerned. My issue however is that moves to 'manualise' such interventions in the context of all autism (or rather all 'potential cases' of autism bearing in mind the use of the words 'at-risk') is not a great idea. As I've mentioned before in the context of the pluralised autisms, screening for things like inborn errors of metabolism potentially presenting with autism or autistic features seems a better first use of resources, assuming that underlying biological issues being associated with autism are probably not going to be that amenable to something like parent-mediated intervention or the like as per the example of something like phenylketonuria and autism (see here).

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[1] Watson LR. et al. Parent-Mediated Intervention for One-Year-Olds Screened as At-Risk for Autism Spectrum Disorder: A Randomized Controlled Trial. J Autism Dev Disord. 2017 Aug 31.

[2] Baranek GT. et al. Preliminary Efficacy of Adapted Responsive Teaching for Infants at Risk of Autism Spectrum Disorder in a Community Sample. Autism Research and Treatment. 2015: 386951.

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Guess what? Gastrointestinal symptoms are prevalent in autism

The paper by Calliope Holingue and colleagues [1] provides brief blogging fodder today and a topic that has finally found its way into accepted peer-reviewed science when it comes to autism spectrum disorders (ASD): gastrointestinal (GI) issues are an often over-represented comorbidity when it comes to ASD.

Reviewing the peer-reviewed research literature on this topic, the authors concluded that there are some quite wide and sometimes disparate findings on the frequency of functional GI symptoms in the context of autism. Part of the reason for this is the lack of a standardised tool for looking at GI symptoms in relation to the label.

But: "The prevalence range for constipation was 4.3-45.5% (median 22%), for diarrhea was 2.3-75.6% (median 13.0%), and for any or more than one symptom was 4.2-96.8% (median 46.8%)." Median by the way, refers to the middle number (or in this case middle percentage) from the collected datasets and stresses that approaching half of all people on the autism spectrum may present with 'any or more than one' GI symptom of clinical relevance.

I've said it before and will say it again, there is guidance out there for the screening, diagnosis and management of bowel symptoms as and when they occur alongside a diagnosis of ASD [2]. We can um-and-ah about the cause(s) of such issues (stressing that the physiological is likely just as important as any psychological explanations) but at the end of the day, those diagnosed with autism and accompanying bowel issues - both functional and/or pathological - should receive the same care and management for their bowel issues as anyone else, save any further tragedies. Indeed, given the links being made between something like slow intestinal transit and autism for example (see here), preferential screening should perhaps be the order of the day before severe endpoints are reached (see here)...

To close, and not to make light of GI issues in relation to autism, a cautionary tale against 'throwing your poo(p) out of the window because it would not flush'???

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[1] Holingue C. et al. Gastrointestinal symptoms in autism spectrum disorder: A review of the literature on ascertainment and prevalence. Autism Res. 2017 Aug 30.

[2] Buie T. et al. Evaluation, diagnosis, and treatment of gastrointestinal disorders in individuals with ASDs: a consensus report. Pediatrics. 2010 Jan;125 Suppl 1:S1-18.

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"Children with autism spectrum disorder who improve with fever"

The title of this post mirrors that published by Rebecca Grzadzinski and colleagues [1] looking at an intriguing phenomenon whereby "some children with ASD [autism spectrum disorder] may show behavioral improvements during fever."

I had expected these results to be published given their appearance at this years IMFAR conference (see here) as one of my 'ones to watch' picks. Indeed, the results do not disappoint as the words 'discovery sample' and 'replication sample' are used as per other instances in the peer-reviewed research literature of this methodology (see here for example).

Drawing on data from the Simons Simplex Collection where over 1500 parents with children with autism were asked "whether and in which areas their child improved during fever", researchers randomly assigned participants to either the discovery or replication sample. They took various information - "demographics, medical history, ASD symptoms, adaptive skills, and presence of de novo ASD-associated mutations" - for each child and compared 'fever improvers' with 'fever non-improvers' across those measures for the discovery set.

Results: "Parent reports of 17% of children indicated improvements during fever across a range of domains." Some people might quibble with the reliance on parent report in this study but not me as per other work indicating 'sensitivity to an issue if not necessarily expertise' (see here). That almost a fifth of children with ASD might potentially show some clinical improvement during a fever episode is not to be sniffed at (see here) and hints that previous chatter about 'hot baths and autism' (no really, see here) might not be just some odd idea (albeit with the requirement for further experimental study and certainly with no endorsement from me at this time).

Then: "Discovery and replication analyses revealed that the Improve Group had significantly lower non-verbal cognitive skills (NVIQ) and language levels and more repetitive behaviors." Such results, whilst requiring replication, hint at some interesting future studies to be done with certain parts of the autism spectrum. Lower NVIQ and language levels shouldn't however be just interpreted as just meaning those towards the more 'severe' end of the autism spectrum; even those with spoken language on the autism spectrum can be quite severely disabled by their autism.

"Understanding the profiles of children who improve during episodes of fever may provide insights into innovative treatments for ASD." I find myself in agreement with such sentiments, particularly when set in the context of possible "immunologic and neurobiological pathways, intracellular signaling, and synaptic plasticity" being potentially affected by fever onset [2] in the context of autism. I of course understand that for some people, the whole notion of fever being tied into behavioural presentation is gonna be met by the same old cynicism (of course, autism is lifelong and immutable!) but science is science...

Music to close: Hüsker Dü - Makes No Sense At All (no reflection of the current research I might add).

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[1] Grzadzinski R. et al. Children with autism spectrum disorder who improve with fever: Insights from the Simons Simplex Collection. Autism Res. 2017 Aug 31.

[2] Curran LK. et al. Behaviors Associated With Fever in Children With Autism Spectrum Disorders. Pediatrics. 2007; 120: e1386-92.

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What nearly 1500 patients with ME/CFS actually think about CBT, GET and pacing therapy

Today I'm discussing the findings reported by Keith Geraghty and colleagues [1] (open-access might be available here).

Looking at some interesting data derived from a rather large patient survey, authors examined what people diagnosed with myalgic encephalomyelitis / chronic fatigue syndrome (ME/CFS) actually thought about / experienced when it came to three intervention options: cognitive behavioural therapy (CBT), graded exercise therapy (GET) and pacing therapy (PT). A little bit of context about these interventions can be seen here including reference to some other peer-reviewed published work from members of this authorship group.

Based on the results of a survey offered by one of the premier UK organisations devoted to ME/CFS - certainly the one I tend to use when it comes to defining the spectrum that is ME/CFS - Geraghty et al add something to a body of research looking at the 'real world' impact (or not) of the various interventions currently advised for 'treating' CFS/ME (at least here in the UK). Their analyses suggested that: "While a small percentage of patients report some benefit from either CBT or GET, the majority experience no benefit." Even worse: "GET brings about a substantive deterioration in symptoms for almost half of patients"; something important to mention in the context of other, similar, intervention results being published earlier this year (see here).

At this point, I'll also refer you to other discussions of the Geraghty paper (see here).

Details are important to the Geraghty results. Including quite a sizeable cohort (N=1428) and asking over 200 questions "regarding treatment, particularly CBT, GET or PT", results were also compared against other patient survey results in the context of the intervention(s) being scrutinised. The combined results painted a similar sort of picture when it comes to experiences of the interventions insofar as "CBT brought about improvement in symptoms for approximately 35 per cent of respondents (65% unchanged/worse)" and "25 per cent of GET reported improvement in symptoms (17% unchanged/54% worse)." All this needs to be read in the context of the primary medical tenet: first, do not harm.

Geraghty et al acknowledge that there are limitations to their study results; not least that recall bias might be a potentially important issue and also that delivery of said interventions  might not have been carried out in "a uniform manner" (something also mentioned in the paper by Collin & Crawley [2]). With all due respect to the respondents, I might also add that independent confirmation of their diagnosis - knowing how important this - might also have provided some further methodological strength to the results too.

But in the context that patient surveys "offer a valuable insight into the ‘patient experience’" and how controversial some (all?) of these intervention options have been/continue to be in relation to CFS/ME (see here), these latest results represent an important research voice. They suggest yet again, that blanket recommendations for treating CFS/ME may have lots of potential effects (some positive but also quite a few negative) for many, many people diagnosed with such debilitating conditions. And once again, in the words of Jonathan Edwards [3] "If they [those diagnosed with ME/CFS] are still ill, presumably these approaches have failed and the priority is to find something more effective." Indeed (but don't hold your breath at least here in Blighty).

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[1] Geraghty K. et al. Myalgic encephalomyelitis/chronic fatigue syndrome patients' reports of symptom changes following cognitive behavioural therapy, graded exercise therapy and pacing treatments: Analysis of a primary survey compared with secondary surveys. J Health Psychol. 2017 Aug 1:1359105317726152.

[2] Collin SM. & Crawley E. Specialist treatment of chronic fatigue syndrome/ME: a cohort study among adult patients in England. BMC Health Serv Res. 2017 Jul 14;17(1):488.

[3] Edwards J. PACE team response shows a disregard for the principles of science. J Health Psychol. 2017 Aug;22(9):1155-1158.

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Autism portrayed in the movies: pleasing some of the people some of the time...

Things have come a long way since the first real mainstream appearance of autism on the silver screen (Rain Man). Nowadays, not a week seems to go by when autism doesn't feature in one form or another on a television show or new film/movie; even appearing in Sesame Street. I see this as a good thing when it comes to bringing autism further into the public psyche and hopefully preventing headlines such as 'Mother sent 'hurtful' letter about 'screechy' son with autism' from making many more appearances.

The downside however, is that with every representation of autism, there are typically comments galore about how autism is not being accurately portrayed or represented. A case in point is a new series called Atypical which has, according to one commentator, invited the same-old-same-old from some quarters (see here). Indeed, the old tenet: 'you can please some of the people some of the time, but not all of the people all of the time' seems to be tailor-made when it comes to views and opinions on the representation of autism on the screen.

It's timely that a new paper looking at the representation of autism in film and TV has also been published by Anders Nordahl-Hansen and colleagues [1]. Starting on the basis that: "Inaccurate portrayals [of autism] are a concern as they may lead to increased stereotypes toward the condition" authors concluded that many characters portraying autism seemed to "align unrealistically well with DSM-5 diagnostic criteria." They mention that those 'savant skills' (a.k.a 'a superpower') that every person with autism is supposed to have(!) were VERY well represented in the media content they surveyed. The authors go on to talk about the educational value of such portrayals and "the notion of authenticity in representing the autistic experience."

As I mentioned a few sentences back, I see autism appearing in more TV and films as a good thing. It makes an often invisible condition a lot more visible and helps to spread the idea that children/adults who were traditionally 'hidden away' deserve the same rights as anyone else. Insofar as the notion of 'authenticity' there have been quite a few, quite authentic portrayals of autism on TV shows. 'The A Word' was one of them (see here) (although I don't doubt some might disagree). Of course, there are always going to be creative processes acting on the fictional portrayal of autism; this goes for just about anything to do with creative media - soap operas do this all the time in the constant chase for viewer ratings. Indeed, one should never forget that TV shows and movies are in a constant state of chasing viewer ratings and not always necessarily produced with authenticity in mind.

In the context of autism also being an extremely heterogeneous condition (y'know, those 'autisms' that I keep going on about), I find it nigh on impossible that any single representation of autism is going to please all of the people all of the time. 'Authentic' is always going to be a matter of perspective...

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[1] Nordahl-Hansen A. et al. Mental health on screen: A DSM-5 dissection of portrayals of autism spectrum disorders in film and TV. Psychiatry Res. 2017. Aug 22.

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