Saturday, 22 April 2017

Autistic adults as critical autism experts (with research caveats)

"Findings suggest that autistic adults should be considered autism experts and involved as partners in autism research."

That was the conclusion reached in the paper by Kristen Gillespie-Lynch and colleagues [1] (open-access) reporting on the results of an online survey assessing "autism knowledge and stigma among 636 adults with varied relationships to autism, including autistic people and nuclear family members." Among the various groups of people who contributed to the survey, several viewpoints emerged. The message primarily however was that: "autistic people are autism experts through their lived experiences." I don't think many people would quibble with such findings.

A few other details emerged from the Gillespie-Lynch study that merit discussion. Many participants showed a "reduced tendency to view autism through a deficit-defined medical model compared with non-autistic people." This is perhaps not an unexpected finding given the history of applying the medical model to autism and the rise and rise of the neurodiversity movement that "challenges the medical model" in particular respect over the question of deficit vs. difference and implications thereof. Although the medical model provides the means to identify and diagnose autism or autism spectrum disorder (ASD) (on the basis of deficits), it's not unexpected that for some, once those tasks have been completed, the 'treatment' side of the model is not necessarily a top priority; or at least not as important as addressing the various inequalities that seem to stem from a diagnosis. That being said, I do agree with the authors sentiments that: "the neurodiversity movement and the medical model overlap in recognizing that supports are needed to ameliorate challenges associated with autism." Those challenges are variable and person-dependent but include the effects of both core and peripheral signs and symptoms and the various over-represented comorbidities that seem to follow a diagnosis of autism (see here). I would, at this point, also caution on using the words 'biopsychosocial model' in the context of autism as the authors have included in their discussions, given what it has meant for other labels (see here) and the potential 'psychologising' of some important medical symptoms.

I added the words 'with research caveats' to the title of this post to ensure that such a positive message about autism and the autism spectrum is not just given a 'free pass' when it comes to scrutiny of the scientific method, the way the study was carried out and the applicability of the results to the entire autism spectrum. This was an online survey not a face-to-face piece of research (other related research has similarly used such a method and on more than one occasion) and the authors acknowledge that they: "did not verify diagnosis of participants who self-identified as autistic" for example. Given what we are beginning to see when it comes to some of the 'self-screening' instruments out there regarding possible autism or not (see here), I'm always a little cautious that self-diagnosis / self-identification does not necessarily mean [eventual] clinician-diagnosed autism and how important this is when it comes to correctly ascertaining the wants and wishes of those diagnosed as being on the spectrum.

On the point about the representativeness of this research, the authors also note: "Findings may not generalize to autistic participants who lack the verbal and computer skills needed to complete the survey." Yet another example it seems of this important issue.

I have to say that I'm also a little disheartened that yet again an important group that was once very firmly on the autism spectrum aren't really given the credit they deserve according to the Gillespie-Lynch findings: "Autistic participants were more likely to recognize that most children cannot outgrow autism." The 'optimal outcome' children and adults it seems, still represent one of the most maligned groups associated with the autism spectrum (assuming that optimal outcome occurring in up to 9% of the autism population is not an insignificant figure). This despite the fact that even the diagnostic stability of the most 'high-functioning' cases of autism can wobble it seems (see here) even into adulthood. One of the premier experts on autism also seems to agree according to some recent media (see here). I often wonder if the seeming lack of acceptance of this group/feature might have something to do with the 'identity' side of autism and the idea that within the vast heterogeneity of autism (or the plural autisms if you prefer) the use of 'them and us descriptions' like 'neurotypical' are perhaps not as binary or long-lasting as many would believe or want to believe?

Within the context of [approximate] phrases such as 'if you've met one person with autism, you've met one autistic person' there is caution in over-generalising these latest results but they are nonetheless important. I think it would be rather fitting to end with a few choice phrases from the Gillespe-Lynch paper: "As many of our survey respondents indicated, each person, regardless of whether or not they are autistic, is unique" and: "Some autistic people seek out factual knowledge about autism while others believe that they can only be experts in their own particular form of autism." Either way, the insights provided by people on the autism spectrum (all parts of the autism spectrum and indeed, across the age ranges) should be valued, and where possible, incorporated into research and practice.

And one voice from the autism spectrum carries some rather sensible messages...


[1] Gillespie-Lynch K. et al. Whose Expertise Is It? Evidence for Autistic Adults as Critical Autism Experts. Front. Psychol. 2017. March 28.

---------- Gillespie-Lynch, K., Kapp, S., Brooks, P., Pickens, J., & Schwartzman, B. (2017). Whose Expertise Is It? Evidence for Autistic Adults as Critical Autism Experts Frontiers in Psychology, 8 DOI: 10.3389/fpsyg.2017.00438

Friday, 21 April 2017

Parental exposures and risk of offspring autism: some curious details

"Overall, our results were consistent with no positive association between parental asthmagen exposure and ASD [autism spectrum disorder] in the children."

So said the findings reported by Alison Singer and colleagues [1] (open-access) continuing a research theme from this group [2] looking at whether "parental workplace exposures to risk factors for asthma (“asthmagens”)" might have relevance to offspring risk for autism.

Based on data derived from some of those oh-so-important Scandinavian research registries (this one based in Denmark), researchers initially looked at some 12,000 cases (where autism was mentioned in medical records) compared with over 48,000 controls (not autism) to ascertain whether parental work exposures might play some role in autism risk. This numbers were eventually boiled down somewhat.

Despite the opening line to the post, there were some curious details to emerge from the collected analyses. So: "We observed an inverse association between any maternal occupational asthmagen exposure and ASD in the children." Researchers reported that maternal occupational exposure actually seemed to be protective against the development of offspring autism according to their findings. They note that this finding was "largely explained by latex exposures" on the basis of linking occupational codes "to an asthma-specific job exposure matrix (JEM)." In other words, they didn't specifically look at latex exposure in every single case but rather relied on the probability that a particular occupation would entail this or other exposure.

A few other curious details also emerged: "Some paternal occupational asthmagen categories were positively associated with ASD, including bioaerosols..., pharmaceutical drugs (manufacturing or extensive handling)..., and metals." The authors tend to talk down these findings as per the suggestion that: "Some of these associations could be chance findings resulting from multiple comparisons or could reflect bias, such as unmeasured confounding" but I would perhaps be a little more cautious about rejecting them outright. Indeed the authors note on one point in relation to maternal exposures: "While adjustment for unmeasured confounding could bring the association to the null, the confounding would need to be implausibly strong to mask a positive association."

I've covered the topic of parental (occupational) exposures and offspring autism risk before on this blog (see here) alongside associated research (see here). The current take-away message from quite a bit of this research is that there may be target classes of compounds to 'look out for' when it comes to offspring autism risk, but as of yet there is no smoking gun. One also needs to read such research in the context of the myriad of 'associations' that have been made with offspring autism risk down the years (see here for example) and how genes and environment might mix in relation to the plural autisms. Cumulative effects are more likely over single factors.

Insofar as the current Singer results, I do feel that the authors might have been a little premature in making the sweeping claims that they have on the basis of their findings: "this large population-based case-control study does not suggest a positive measurable association between parental occupational asthmagen exposure and ASD." I say this in the context that 'asthmagen' exposure could be incurred via several routes (see here). I don't doubt that the correlations/findings reported by Singer could be 'due to chance', but until such claims can be independently verified in direct study (see here for one idea) and perhaps tested in animal models for example, they should really just report what they found without fear, favour or complication...


[1] Singer AB. et al. Parental exposures to occupational asthmagens and risk of autism spectrum disorder in a Danish population-based case-control study. Environmental Health. 2017 16: 31.

[2] Singer AB. et al. Maternal Exposure to Occupational Asthmagens During Pregnancy and Autism Spectrum Disorder in the Study to Explore Early Development. J Autism Dev Disord. 2016 Nov;46(11):3458-3468.

---------- Singer, A., Burstyn, I., Thygesen, M., Mortensen, P., Fallin, M., & Schendel, D. (2017). Parental exposures to occupational asthmagens and risk of autism spectrum disorder in a Danish population-based case-control study Environmental Health, 16 (1) DOI: 10.1186/s12940-017-0230-8

Thursday, 20 April 2017

"a gradual decline in recorded diagnoses of CFS/ME since 2001"?

The quote forming the title of today's post comes from the paper by Simon Collin and colleagues [1] (open-access available here) who, based on analysis of the UK "Clinical Practice Research Datalink (CPRD), formerly known as the General Practice Research Database (GPRD)" set out to look at the "Incidence of CFS/ME [chronic fatigue syndrome/ myalgic encephalomyelitis], FM [fibromyalgia], post-viral fatigue syndrome (PVFS), and asthenia/debility." I say incidence but that last sentence should really read as  'recorded incidence'.

Searching the research database between January 2001 and December 2013, researchers looked at the [recorded] incidence (that's incidence not prevalence) of the various fatigue-related conditions/labels recorded by participating GP (general practice) surgeries.

Recorded diagnoses of CFS/ME showed a soft but noticeable decline over the period of study: "Annual incidence of CFS/ME decreased from 17.5 [per 100,000 people] in 2001 to 12.6 in 2013." A similar decline was also noted in respect of PVFS and asthenia/debility. When however it came to FM, there was an overall increase in cases between 2001 and 2013 (albeit characterised by peaks and troughs in recorded diagnoses across specific years).

Some other important data were also reported on. So: "All diagnoses showed strong evidence of variation by age and sex" and estimated socio-economic status (SES). Further: "Incidence rates of CFS/ME were 2.4-fold higher among women... with peak incidence in the 40–49 years age group." Women were also more likely to be over-represented in relation to a diagnosis of FM too.

This is potentially important data. It suggests that at least among participating GP practices in the CPRD, recorded diagnoses of CFS/ME seem to be going down. The caveats however mentioned by the researchers do need to be highlighted, not least that they "examined recorded data rather than actual incidence, i.e. we are describing incidence rates of GPs’ recording of diagnostic codes" and "diagnoses were not independently validated." In other words, this is data based on "GPs enter[ing] medical diagnoses and symptoms as Read codes." I might also add in another quote from the authors too: "In 2005, 48% of GPs in one English region did not feel confident about making a diagnosis of CFS/ME, and 28% did not recognise CFS/ME as a legitimate illness." A bit of an issue by all accounts if one would like to get accurate data on incidence or prevalence.

I also have a to raise a point in relation to this latest data and how it compares with other data produced by the same research group (see here). Keeping in mind that incidence is not the same as prevalence, I bring back to your attention the findings reported by Collin and colleagues [2] on another occasion suggesting that nearly 2% of 16-year olds in the ALSPAC cohort were affected by CFS. More work needs to be done when it comes to official monitoring of the numbers of cases of CFS/ME (and FM) outside of just reliance on GP practice recordings in order to get a true picture of numbers of cases. Of course, there is another possible explanation for the fall in recorded diagnoses: GPs are increasingly understanding that some of the symptoms included under the banner of CFS/ME overlap with various other conditions/labels too...


[1] Collin SM. et al. Trends in the incidence of chronic fatigue syndrome and fibromyalgia in the UK, 2001-2013: a Clinical Practice Research Datalink study. J R Soc Med. 2017 Jan 1:141076817702530.

[2] Collin SM. et al. Chronic Fatigue Syndrome at Age 16 Years. Pediatrics. 2016 Feb;137(2):e20153434.

---------- Collin SM, Bakken IJ, Nazareth I, Crawley E, & White PD (2017). Trends in the incidence of chronic fatigue syndrome and fibromyalgia in the UK, 2001-2013: a Clinical Practice Research Datalink study. Journal of the Royal Society of Medicine PMID: 28358988

Wednesday, 19 April 2017

Allergy and ADHD meta-analysed and guess what...

"Reports of frequent manifestation of allergic diseases in children with attention deficit hyperactivity disorder (ADHD) have been the subject of mounting clinical interest."

OK, go on.

"The objective of this study was to compile and assess available studies on the association between ADHD and allergic diseases in children."

And your findings... "children with ADHD are more likely to have asthma, allergic rhinitis, atopic dermatitis, and allergic conjunctivitis than their counterparts. Interventions including strategies for managing allergies in children with ADHD would be beneficial."

So said the systematic review and meta-analysis published by Celine Miyazaki and colleagues [1] (open-access) who provide quite a good 'where we're at' update when it comes to a potentially important intersection between a developmental condition (ADHD) and a series of somatic, immune-based conditions (allergy).

Regular readers of this blog might already know that I have a blogging interest in all-things immune system and behaviour (see here for example). Indeed, acknowledging that the immune system may be doing so much more than protecting us from the multitude of viral, bacterial and other insults we face each day is gaining some real [peer-reviewed] scientific momentum.

Boiling down the peer-reviewed literature to five studies meeting the meta-analysis criteria laid out by authors, cumulatively including some 60,000 research participants (including data derived from that wonderful Taiwanese research registry that I keep going on about), researchers set to work on the examining the various findings. Nearly 8,000 of the 61,811 children included for study were diagnosed with ADHD and various allergic diseases were 'examined' in the context of the ADHD label or without the label. The results were as mentioned in the first paragraph.

When it came to looking at which specific allergic disease diagnoses were most strongly linked to ADHD a familiar theme emerged: "children with ADHD have an 80% increased odds of asthma compared with children without ADHD." I'm beginning to lose track of the number of times I've covered this association down the blogging years (see here and see here and see here). Indeed, these results add to other reviews on this topic [2] previously covered on this blog (see here).

The nature of the association? Well, more studies are still required. The authors talk about some work looking at possible overlapping genetic issues with autoimmunity in mind, and that is probably going to be quite important. More than that however is the idea that other less-genetic factors might also play a role. Y'know how social factors such as poverty might figure (see here) for example. I'm also minded to bring in the possibility of an 'association' between food allergy and behavioural symptoms (see here) in light of other work. Such a connection might also implicate all-manner of other bodily systems including the [hyped-up] field of microbiomics for example. Suffice to say that connections are likely to be complex and potentially numerous.

The other implication from the Miyazaki results is another thing I've been going on about for some years on this blog: preferential screening. Y'know, when a diagnosis of asthma for example, is received, how about screening for ADHD and related developmental issues? Or, the other way around, screen for allergic diseases when a diagnosis of ADHD is received? And then there's the intervention angle, and some potentially useful data from both other developmental/behavioural diagnoses and allergy symptoms (see here) and some rather more direct evidence (see here)?

To close, my brood have just discovered Little Britain and the laughter has gone on and on and on...


[1] Miyazaki C. et al. Allergic diseases in children with attention deficit hyperactivity disorder: a systematic review and meta-analysis. BMC Psychiatry. 2017; 17: 120.

[2] Schans JV. et al. Association of atopic diseases and attention-deficit/hyperactivity disorder: A systematic review and meta-analyses. Neurosci Biobehav Rev. 2017 Mar;74(Pt A):139-148.

---------- Miyazaki, C., Koyama, M., Ota, E., Swa, T., Mlunde, L., Amiya, R., Tachibana, Y., Yamamoto-Hanada, K., & Mori, R. (2017). Allergic diseases in children with attention deficit hyperactivity disorder: a systematic review and meta-analysis BMC Psychiatry, 17 (1) DOI: 10.1186/s12888-017-1281-7

Tuesday, 18 April 2017

"Asthma was associated with increased risk for schizophrenia"

'Big data' Taiwan is once again the topic of a post on this blog as the results published by Wei-Chen Wang and colleagues [1] (open-access available here) receive an airing, specifically that: "Asthma was associated with increased risk for schizophrenia."

There are some common themes attached to these findings. Taiwan is already a research-favourite place on this blog as a result of their use of the National Health Insurance Research Database (NHIRD) for various research purposes. I can't name all the occasions I've talked about research from Taiwan based on the NHIRD but a few of them can be seen here and here. Another commonality of this latest research from Wang et al is the idea that physical illness with a substantial immune system component to it *might* show an important connection to a behavioural/psychiatric disorder. Asthma and related atopic diseases has been mentioned on a few other occasions (see here and see here). Hold those thoughts for now...

This time around Wang and colleagues "aimed to investigate the association between asthma, corticosteroid use, and schizophrenia." Comparing 'measures of schizophrenia' in some 25,000 participants diagnosed with asthma and 50,000 without asthma over 7 years, and adjusting for various potentially confounding variables - "sex, age, residence, socioeconomic status, corticosteroid use, outpatient and emergency room visit frequency, Charlson comorbidity index, and total length of hospital stays days for any disorder" - the results were interesting. Not least that "asthma was associated with significantly greater hazard ratio for incident schizophrenia." Researchers also noted that various other confounding variables also showed a relationship with schizophrenia such as rural residence, poor general health and lower economic status. "Corticosteroid use was not associated with increased risk for schizophrenia" we are also told.

Whilst interesting, the results do not say that everyone with asthma is at risk of developing schizophrenia. Not even close. The rates of schizophrenia identified in the Wang study were also quite low overall despite the large starting populations studied: "Of the total 75,069 subjects, 238 were diagnosed with schizophrenia during the study period: 100 (0.40%) of subjects were in the asthma cohort and 138 (0.28%) in the non-asthma cohort."

But, set within the context of other independent datasets [2] observing "the existence of an association between atopic disorders in general and asthma in particular and the risk of developing schizophrenia" there is cause for further investigation into any association. Not least that Wang et al describe their results in the context that: "a convergent disturbance in the immune-inflammatory system may contribute to the pathoetiology of asthma and schizophrenia." Y'know, all that talk that among the [plural] schizophrenias, one or two phenotypes might, to some quite large extent, be linked to immune function or dysfunction. Well, it's not as if we haven't got some quite reliable research clues already (see here). There may also be some subsequent discussions on the requirement for enhanced screening for something like schizophrenia as and when a diagnosis of asthma (or other atopic disease) is diagnosed as per other data (see here).

Finally, going back to the previous research occasions when asthma has been *correlated* with labels such as attention-deficit hyperactivity disorder (ADHD) and even autism, I'm wondering whether there could be wider links present when it comes to immune-related conditions and behavioural presentations. It's pretty well known that various behavioural/developmental/psychiatric labels tend to 'club together' (see here and see here for examples). There is also a growing realisation that alongside overlapping genetics and biology when it comes to such labels, the days of autism genes for example, just being genes for autism are beginning to drift off (see here); something probably relevant to conditions such as ADHD and schizophrenia too. So, could it be that immune system related conditions such as asthma and atopic disease, might have lots and lots of implications in relation to many developmental/behavioural/psychiatric labels? Even more intriguing, are there clues to possible intervention avenues too? (with no medical or clinical advice given or intended).

We await further investigations...


[1] Wang WC. et al. Asthma, corticosteroid use and schizophrenia: A nationwide population-based study in Taiwan. PLoS One. 2017 Mar 28;12(3):e0173063.

[2] Pedersen MS. et al. Schizophrenia in patients with atopic disorders with particular emphasis on asthma: a Danish population-based study. Schizophr Res. 2012 Jun;138(1):58-62.

---------- Wang WC, Lu ML, Chen VC, Ng MH, Huang KY, Hsieh MH, Hsieh MJ, McIntyre RS, Lee Y, & Lee CT (2017). Asthma, corticosteroid use and schizophrenia: A nationwide population-based study in Taiwan. PloS one, 12 (3) PMID: 28350822

Monday, 17 April 2017

The continuing trials and tribulations of PACE

I honestly hadn't intended talking about the PACE trial - "pacing, graded activity, and cognitive behaviour therapy: a randomised evaluation" in relation to chronic fatigue syndrome (CFS) - quite so much on this blog. Others have done it so much better than I ever could.

My interest however keeps being piqued in relation to the results originally produced suggesting that: "CBT [cognitive behaviour therapy] and GET [graded exercise therapy] can safely be added to SMC to moderately improve outcomes for chronic fatigue syndrome" and the subsequent myriad of voices quite unanimously suggesting that one perhaps needs to be a little careful with such sweeping generalisations (see here).

OK, for anyone new to this topic, below are a few of the previous occasions that it has been discussed on this blog in chronological order:

  • Chronic Fatigue Syndrome and various factors (2014) (see here)
  • Chronic fatigue syndrome and the detrimental application of the 'biopsychosocial model' (2016) (see here)
  • PACE-gate! (2016) (see here)
  • PACE trial recovery data and chronic fatigue syndrome (2017) (see here)
  • PACE trial recovery data and chronic fatigue syndrome - a reply (2017) (see here)

I want to add a few more 'science references' to this issue because some important things are being discussed in the peer-reviewed domain, in the context that CBT and GET at the moment, are considered 'best practice' here in the UK and beyond when it comes to CFS. That may change in future times (see here) as it has in other parts of the world (see here) but that's where we are at the time of writing. I might add that the addition of new references to this post is a rather more descriptive thing minus too much additional commentary from me, and that the views represented are those of the authors. I wrote this post on 9 April 2017 so it is accurate up to that point.

OK, starting with the editorial from Keith Geraghty [1] mentioned in that PACE-gate! post, we have an authors reply to some of the points raised [2]. The main crux of the reply is to correct "misunderstandings and misrepresentations of the PACE trial." Next up was a paper by Leonard Jason [3] (someone with quite an impressive research track record when it comes to CFS) and some comments on the pacing intervention (adaptive pacing therapy, APT) used and "patient selection ambiguity." This is a particularly interesting paper because APT - "based on the envelope theory of chronic fatigue syndrome" where the symptoms of CFS are "not reversible by changes in behaviour" - did not hit the 'research spot' according to the original PACE trial results.

I want to next include the paper by Luis Nacul and colleagues [4] into proceedings, and a role for "selection bias and disease misclassification" when it comes to studies on CFS (and myalgic encephalomyelitis, ME). To quote from them: "When studies using the broad Oxford criteria... were excluded, a virtual disappearance of effect for graded exercise therapy (GET), cognitive behaviour therapy (CBT) and other psychological therapies recommended by the NICE guidelines (National Institute for Health and Care Excellence.. was revealed." Guess which criteria (among the many available) were used in the original trial?

Onward. The paper by Steven Lubet [5] titled: 'Investigator bias and the PACE trial' sets out quite an 'accusation' in that: "the PACE investigators “impartiality might reasonably be questioned”." This is a theme that crops up again shortly. The paper by Tom Kindlon [6] asked whether graded exercise in particular, could be thought of as 'safe and risk-free'? I set this question within the context that the original PACE trial did find that: "Non-serious adverse events were common" and GET did seem to produce the largest number of 'serious adverse effects' in number if not in participants.

Nearly there. Next up is the paper from Carolyn Wishire [7] who, when talking about "lively discussion", reports on various potential forms of bias in behavioural intervention studies using the PACE study as a kind of template. This author was the lead on the recent peer-reviewed commentary (open-access) re-analysing the 'recovery' data subsequently published in relation to the PACE trial. Then, we have the paper by Jonathan Edwards [8] who notes that the PACE trial represents a lesson in how research design needs to develop further when it comes to science in general. To quote: "The failure of the academic community to recognise the weakness of trials of this type suggests that a major overhaul of quality control is needed." And finally Charles Shepherd [9] provides further commentary on the PACE trial and a call for independent review.

And rest.

There is quite a lot to take in from those various publications and I don't doubt that this is not the last we are going to hear about the PACE trial. Allied to articles such as this one describing how: "Physicians used to dismiss the disease as psychosomatic" (past tense) it certainly would not out of place to suggest that there are still questions that need to be answered about the design and results obtained from the PACE trial and their applicability to the (very) wide CFS/ME population. To quote again from the paper by Edwards [8]: "If they are still ill [those diagnosed with CFS/ME], presumably these approaches have failed and the priority is to find something more effective." Wise words indeed.

To close, it's here... the first glimpse of The Last Jedi.


[1] Geraghty KJ. ‘PACE-Gate’: When clinical trial evidence meets open data access. J Health Psychology. 2016. Nov 1.

[2] White PD. et al. Response to the editorial by Dr Geraghty. J Health Psychology. 2017. Jan 24.

[3] Jason LA. The PACE trial missteps on pacing and patient selection. J Health Psychology. 2017. Feb 1.

[4] Nacul L. et al. How have selection bias and disease misclassification undermined the validity of myalgic encephalomyelitis/chronic fatigue syndrome studies? J Health Psychology. 2017. March 1.

[5] Lubet S. Investigator bias and the PACE trial. J Health Psychology. 2017. March 7.

[6] Kindlon T. Do graded activity therapies cause harm in chronic fatigue syndrome? J Health Psychology. 2017. March 20.

[7] Wilshire C. The problem of bias in behavioural intervention studies: Lessons from the PACE trial 2017. J Health Psychology. March 23.

[8] Edwards J. PACE team response shows a disregard for the principles of science. 2017. J Health Psychology. March 28.

[9] Shepherd CB. PACE trial claims for recovery in myalgic encephalomyelitis/chronic fatigue syndrome – true or false? It’s time for an independent review of the methodology and results. J Health Psychology. April 9.

---------- Edwards, J. (2017). PACE team response shows a disregard for the principles of science Journal of Health Psychology DOI: 10.1177/1359105317700886 White, P., Chalder, T., Sharpe, M., Angus, B., Baber, H., Bavinton, J., Burgess, M., Clark, L., Cox, D., DeCesare, J., Goldsmith, K., Johnson, A., McCrone, P., Murphy, G., Murphy, M., O’Dowd, H., Potts, L., Walwyn, R., & Wilks, D. (2017). Response to the editorial by Dr Geraghty Journal of Health Psychology DOI: 10.1177/1359105316688953

Thursday, 13 April 2017

Video Interaction for Promoting Positive Parenting in autism: yes but not quite...

"Video feedback may help babies ‘at risk of autism’" went one write-up of the study results published by Jonathan Green and colleagues [1] (open-access available here). Continuing a theme of kids at risk of autism potentially 'avoiding' an autism diagnosis (see here) following the use of "a 12-session parent-mediated social communication intervention delivered between 9 and 14 months of age (Intervention in the British Autism Study of Infant Siblings-Video Interaction for Promoting Positive Parenting)" there is some degree of optimism from these latest results together with a pinch of 'not-so-fast'...

Including data from some 54 families - "28 intervention, 26 nonintervention" - researchers reported on the effects of interventions vs. no intervention on various aspects of functioning primarily the "severity of autism prodromal symptoms." Prodromal means early symptoms and is more readily associated with other labels/conditions. The authors reported that results were not completely cut-and-dried in terms of effect(s) of intervention on diagnostic outcome for example (i.e. there were "no intervention effects on diagnostic outcome") but potentially something to see when it comes to the 'severity' of autism prodromal symptoms and "parent-dyad social communication." The authors also noted that measures of communication and language did show something of a trend towards some benefit observed in the intervention group, but did not yield any significant difference when comparing intervention with no intervention over the quite long study period (39 months). This contrasts with their previous results [2] possibly indicating something rather more adverse when it came to intervention and aspects of language/communication. I might also draw your attention to the fact that from a bank of some 84 families invited to join the study, just over half actually agreed or fulfilled the criteria for joining.

I know this is an area of research that people really want to see work. Alongside other early intervention research in relation to autism (see here for example), the idea that some small adjustments to early interactions might affect the presentation of autism still enjoys quite a lot of support in various quarters. The thing is that these and other results whilst suggesting that things like 'parental responsiveness' can improve as a result of intervention(s), have so far shown that important outcomes for young children are far less impressive. This is something evident across quite a lot of the research literature in this area even when meta-analysed (see here including some chatter about effect sizes).

I'm not suggesting that we everyone just 'gives up' when it comes to early interventions like the one described by Green and colleagues. I do however think science and clinical practice needs to be a little more focused on things like potential best-responders to such interventions (as it does for many other aspects of autism science) and not so focused on creating grand media headlines. I might also throw in the idea that study design is something that needs to be improved particularly in light of other recent findings [3] talking about how "placebo-like effects represent substantial challenges for randomized controlled trials (RCTs) that use treatment as usual" (guess what many studies in this area use as their comparator?) Accepting that variables such as the plural autisms (see here) are inevitably going to affect results from such studies, I'm minded to suggest that quite a few more resources need to be committed to looking at the possible 'hows and whys' of autism coming about before any talk about early parent-mediated intervention becoming widespread. So, questions like whether screening for inborn errors of metabolism in relation to autism (see here) could be a good first step as part of the mantra 'diagnosis is a starting point not the finishing line' and then taking things from there...


[1] Green J. et al. Randomised trial of a parent-mediated intervention for infants at high risk for autism: longitudinal outcomes to age 3 years. J Child Psychol Psychiatry. 2017 Apr 10.

[2] Green J. et al. Parent-mediated intervention versus no intervention for infants at high risk of autism: a parallel, single-blind, randomised trial. Lancet Psychiatry. 2015. Jan 22.

[3] Jones RM. et al. Placebo-like response in absence of treatment in children with Autism. Autism Res. 2017. 12 April.

---------- Green J, Pickles A, Pasco G, Bedford R, Wan MW, Elsabbagh M, Slonims V, Gliga T, Jones EJ, Cheung CH, Charman T, Johnson MH, & British Autism Study of Infant Siblings (BASIS) Team. (2017). Randomised trial of a parent-mediated intervention for infants at high risk for autism: longitudinal outcomes to age 3 years. Journal of child psychology and psychiatry, and allied disciplines PMID: 28393350