Thursday 31 May 2018

Chronic kidney disease is over-represented in cases of serious mental illness

The findings reported by Masao Iwagami and colleagues [1] observing that "CKD [chronic kidney diseaseis identified more commonly among patients with SMI [serious mental illness] than in the general population" are not entirely novel. I've touched upon this topic before (see here), set within the broader perspective that physical / somatic ailments experienced by those with a psychiatric and/or behavioural diagnosis can sometimes be 'downplayed' in light of their receipt of a 'primary' psychiatric / behavioural label. It stretches across various different labels (see here for example) with sometimes catastrophic outcomes.

Iwagami et al started out with the premise that risk factors for CKD - "a long-term condition where the kidneys don't work as well as they should" - including tobacco smoking and diabetes, are more frequently reported in those diagnosed with an SMI, hence their risk of CKD may be greater. To see if there was any heightened association between SMI and CKD here in Blighty, they relied on data from a resource called the Clinical Practice Research Datalink (CPRD). CPRD allows researchers to access various details from patient records based on the accrual of primary healthcare data. Importantly, as well as containing read codes for SMI, the database also includes laboratory test results pertinent to CKD: "CKD was based on two measurements of estimated glomerular filtration rate <60 mL/min/1.73 m2 separated by 3 months or longer; calculated from serum creatinine." The combined data was analysed and 'adjusted' for various potentially confounding variables including lithium use (lithium can affect kidney function).

From a starting population of some 2.5 million people (records), authors identified a diagnosis of SMI in about 28,000 (~1%). Most of those 28,000 or so diagnosed with a SMI had no history of lithium use (24,101 / 28,396). The prevalence of CKD was 14.6% in those with a SMI and history of lithium use. The prevalence of CKD was 3.3% in those with a SMI and no history of lithium use. This compares with a CKD prevalence rate of 2.1% in the population not diagnosed with a SMI (N=2,387,988). Ergo: "patients with SMI had a greater prevalence of CKD compared to the general population." Authors also mention how risk of renal replacement therapy (RRT) was also increased in those with a SMI.

This is important data. It's not foolproof data insofar as "a greater prevalence of CKD among patients with SMI may, in part, be influenced by surveillance or ascertainment bias. Patients with SMI take medications, such as lithium and other psychotropic drugs, which need regular monitoring." It does however suggest that regular screening for CKD needs to be a priority for those diagnosed with a SMI particularly given that "CKD is strongly and independently associated with mortality and cardiovascular risk" (something else mentioned in the context of certain psychiatric diagnoses). But there is also something rather uncomfortable in the Iwagami results: that possibility of an advanced risk of CKD in cases of SMI with a history of lithium use.

Minus any clinical or medical advice given or intended on this blog, I can see why the authors haven't overplayed the potential effect of lithium use on their results. Lithium, in the context of various psychiatric disorders and beyond, is an important medication, particularly when it comes to its proposed properties as an 'anti-suicidal' agent (see here). It really does save lives. But as with just about every medicine available, there is an important cost-benefit ratio to take into account when prescribing this medication and ensuring regular monitoring is available to minimise any side-effects. I might also add that there are *possibilities* [2] when it comes to potentially reducing some of the effects that lithium use might have on kidney function but I'll leave such discussions to the experts.

For now, we have further evidence that for whatever reason(s), being diagnosed with a SMI has the potential to impact on many areas of health, both mental and physical.


[1] Iwagami M. et al. Severe mental illness and chronic kidney disease: a cross-sectional study in the United Kingdom. Clin Epidemiol. 2018 Apr 16;10:421-429.

[2] Lodin M. & Dwyer J. The role of amiloride in managing patients with lithium‐induced nephrogenic diabetes insipidus. J Pharmacy Practice & Research. 2017; 47(5): 389-392.


Wednesday 30 May 2018

Functional levels of vitamin D and autistic behaviours?

The paper by Feiyong Jia and colleagues [1] although following a 'case report' methodology provided some interesting reading recently. Based on the idea that maintaining an adequate supply of vitamin D might be rather important on a behavioural level, at least when it comes to 'some' autism, authors provide a route map for some further study.

Including a few notable names previously attached to research looking at a possible connection between vitamin D and autism (see here and see here), Jia et al reported findings for 3 children diagnosed with an autism spectrum disorder (ASD) who "were given vitamin D3 supplementation followed by a long interruption." Alongside looking at serum levels of vitamin D - the sunshine vitamin/hormone - researchers also discussed examination of autistic traits in their small case report population.

They noted that: "the core symptoms of ASD [autism spectrum disorder] fluctuated in severity with changes in serum 25(OH)D levels in children, indicating that maintaining a responsive 25(OH)D level is important for treating ASD." Authors concluded that: "Maintaining a serum 25(OH)D level between 40.0 and 100.0 ng/ml may be optimal for producing therapeutic effects in vitamin D-responsive individuals with ASD." I'll also direct you to an article about levels of vitamin D and what they might mean (see here) with no medical or clinical advice given or intended.

Keeping in mind that a case report methodology is very good at providing data on individuals but not necessarily great when it comes to information about a wider population, there are some potentially important points to take from the Jia findings. Not least is the idea that screening for something like vitamin D insufficiency or deficiency is something 'under-used' in the current context (and something that has been mentioned in previous peer-reviewed research occasions). More formal, rigorous study of how autistic and other behaviour(s) *might* fluctuate as a function of vitamin D status (indeed, among other potentially important variables) is indicated.


[1] Jia F. et al. Fluctuations in clinical symptoms with changes in serum 25(OH) vitamin D levels in autistic children: Three cases report. Nutr Neurosci. 2018 Apr 8:1-4.


Tuesday 29 May 2018

Treating anxiety and depression in the context of autism: is 'talk therapy' cutting the mustard?

The findings reported by Brenna Maddox and colleagues [1] caught my eye recently, talking about "community treatment" patterns for co-occurring anxiety or depression in the context of autism.

Researchers concluded that talking therapy such as cognitive behavioural therapy (CBT) typically indicated for such mental health issues, is utilised in the context of autism but perhaps not as frequently as experienced in a not-autistic group. That finding covered various types of talk therapy such as individual therapy for anxiety/depression and case management. Alongside: "Adults with ASD [autism spectrum disorder] are more likely to be prescribed multiple medications concurrently."

Drawing on "Pennsylvania Medicaid claims data", researchers were able to identify adults with ASD who also presented with defined depression and/or anxiety. They matched this group (numbering about 270) with other adults presenting with depression and/or anxiety but not diagnosed with autism (N=1072). They then compared psychiatric treatment experiences between the groups.

"Adults without ASD were more likely to receive talk therapy for anxiety/depression." I added the bolding to the text so that we are clear that the Maddox results suggested that talking therapies for co-occurring depression and/or anxiety were less likely to be used when autism was mentioned. The authors further explain that these results are consistent with the idea that "they [those diagnosed with autism] often experience difficulty accessing mental health services." That being said, when talk therapy was accessed by adults with autism, researchers reported that they "averaged more individual talk therapy visits per month than did adults without ASD." I'll come back to this point in a moment...

Going back to the experiences of pharmacotherapy for those with and without autism, Maddox et al observed that: "the ASD group had a significantly higher number of days per month prescribed for all medication classes" covering medicines such as antidepressants, antipsychotics, benzodiazepines (anxiolytic) and CNS stimulant. Polypharmacy - where more than one medicine is dispensed - was also a more frequent occurrence for autistic adults too (nearly half were taking two or more psychotropic medicines).

What could all this mean? Well, going back to the observation that when they were able to access talk therapy, more visits per month were noted for the adults with autism, there is one possibility entertained by the authors to account for this: "talk therapy in the community is less effective with adults with ASD, who therefore stay in therapy for a longer period in pursuit of greater symptom relief." That possibility alongside the higher rates of 'multiple medicine use' noted in that group, adds weight to the idea that whilst talking therapy is useful for some cases of anxiety and depression, in the context of autism it might not necessarily be 'cutting the mustard'. The words "having more “treatment refractory” or complex constellations of symptoms" are also mentioned by Maddox and, well, have been discussed before (see here for example).

Further research is required on this issue before any sweeping generalisations are made by me or anyone else. For the record, I'm not adverse to the idea that talking therapy could be useful for depression/anxiety in the context of autism, but am open to the idea that the presentation of such mental health issues alongside autism might not be the same in form or for the same reason(s) as that in other non-autistic contexts. Indeed, in these days of ESSENCE and 'autism plus', I'm fast coming around to the idea that anxiety and depression could well be a core part of [some] autism (see here) as per what other - often forgotten names - had previously suggested (see here). Contrary then to the idea being promulgated among some (mainly psychological) quarters of the autism research and practice scene, that anxiety and depression develop in the most part as a consequence of external sources (see here for some chatter on 'social acceptance'), such mental health issues could be more fundamental characteristics of autism [2]. By saying that, I'm not discounting *some* influences like the contributions of loneliness and self-esteem (see here) but would also look to more intrinsic (biological and genetic) variables as also exerting something of a powerful effect. Similar sentiments have also been voiced when it comes to some other extremes of behaviour and their possible 'core' link to autism (see here).

"Our results suggest the need both for more granular and sophisticated assessment of community treatment for adults with ASD and anxiety/depression, and for better training for clinicians working with this population." I don't think many people would disagree with such conclusions. What I would like to see, under scientifically controlled circumstances, is some further comparisons of talking therapy for anxiety/depression in autism vs. not autism. I'm not talking about CBT vs no CBT with autism in mind [3] but rather research comparisons taking into account whether a diagnosis of autism might mean rethinking particularly talking therapy strategies for managing such quality-of-life-draining issues such as depression and anxiety.

The implication is also, yet again, that to really positively impact on the presentation of such issues, one needs to consider 'targeting' the core symptoms of autism themselves, as per what other research has similarly hinted at (see here). I can see conflicts arising following such sentiments...


[1] Maddox BB. et al. Treatment utilization by adults with autism and co-occurring anxiety or depression. Research in Autism Spectrum Disorders. 2018; 51: 32-37.

[2] Spain D. et al. Social anxiety in autism spectrum disorder: A systematic review. Research in Autism Spectrum Disorders. 2018; 52: 51-68.

[3] Kilburn TR. et al. Rationale and design for cognitive behavioral therapy for anxiety disorders in children with autism spectrum disorder: a study protocol of a randomized controlled trial. Trials. 2018 Apr 2;19(1):210.


Monday 28 May 2018

'Artistic creativity' and risk of hospitalisation for schizophrenia, bipolar disorder and unipolar depression

"Students of artistic subjects at university are at increased risk of developing schizophrenia, bipolar disorder and unipolar depression in adulthood."

So concluded the findings reported by James MacCabe and colleagues [1] who set about examining whether studying a creative subject at high school or university placed someone at an enhanced risk of later hospitalisation for a mental disorder such as schizophrenia, bipolar disorder or depression. The rationale behind the research was the 'long-standing idea' that "mental disorders are associated with enhanced creativity, intelligence or artistic talent."

To test the hypothesis, researchers employed some of those fabulous Scandinavian population registries (yet again), this time covering the population of Sweden. Based on the "unique registration number carried by all Swedish residents" they were able to look at educational records, results of intelligence tests (via testing during military service) and details of any psychiatric hospitalisations for nearly 4.5 millions people. A creative subject studied at high school or University was defined in both a broad sense - "which included a wider variety of creative or artistic subjects corresponding to ‘Art and Media’... but excluding ‘Science and History of Art, Music, Dance, Film and Theatre’" and also following a narrower definition: "comprising visual arts, music, dance, theatre and drama, film, radio and TV production, and fashion design." As I said, a fabulous population resource.

Results: about 5% of the population studied (~194,000) were deemed to have studied an artistically creative subject by the broad definition, falling to just over 1% (50,000) when the narrow criteria were followed. As per that opening sentence of this post, there did seem to be something in the idea that studying an artistically creative subject was *associated* with hospitalisation for schizophrenia, bipolar disorder and unipolar depression. Authors also noted that: "The associations remain when the analyses are restricted to sibling pairs, indicating that family-level factors alone cannot explain the association."

The possible reasons for this association are also explored by MacCabe et al. The ‘balancing selection’ hypothesis is mentioned whereby "the genetic variants conferring risk for psychosis also carry a biological advantage, such as enhanced intelligence or creativity, and this translates into reproductive advantage in the relatives of those with psychoses; thus maintaining the frequency of risk alleles in the population." Similar to the idea that the genetics of autism are probably not just 'genes for autism' (see here) so the genetics potentially linked to psychiatric disorders such as schizophrenia, probably also affect other areas of functioning (positively and negatively). Authors also entertain more 'psychological theory' (here we go) where, for example: "certain cognitive styles may be associated with artistic creativity and psychosis." Personally, I'd be more inclined to believe the first explanation over the second on the basis that 'cognitive styles' tends to make rather sweeping generalisations (see here for an example) and are rather difficult to confirm/refute from a scientific perspective.

Despite the results obtained by MacCabe, I am not totally convinced of any universally general connection between artistic creativity (or any other kind of creativity) and psychiatric disorder. I say this on the basis of other, independent findings (see here) that have not been so kind to the hypothesis. I'm also a little cautious that making such sweeping generalisations could potentially detract from the often very significant effects that such psychiatric disorders have on a person's life; many of which can lead to issues such as 'hospitalisation' (where hospital records were an important data source for the authors in this study).

Still, these are interesting results and have grabbed some media attention...


[1] MacCabe JH. et al. Artistic creativity and risk for schizophrenia, bipolar disorder and unipolar depression: a Swedish population-based case–control study and sib-pair analysis. British Journal of Psychiatry. 2018. April 26.


Saturday 26 May 2018

"CFS symptoms resemble a hypothyroid state" but...

I am a little late getting to the paper published by Begoña Ruiz-Núñez and colleagues [1] observing that, at least for some diagnosed with chronic fatigue syndrome (CFS), clinical findings related to thyroid function might "resemble a mild form of “non-thyroidal illness syndrome” and “low T3 syndrome” experienced by a subgroup of hypothyroid patients receiving T4 monotherapy." But I did get here eventually. Before heading into this paper, I'm gonna link to one of the 'already prepared' discussions on the Ruiz-Núñez findings (see here). My analysis is pretty similar but not entirely the same...

So: "We studied 98 CFS patients (21–69 years, 21 males) and 99 age- and sex-matched controls (19–65 years, 23 males)" was the starting point, as participants provided blood samples and 24-hour urine samples onward to various analyses being carried out. This included: "the measurement of routine hematological parameters [Hb, hematocrit, WBC, red blood cells (RBC), and thrombocytes]" and more specifically: "parameters of thyroid function, low-grade inflammation and gut wall integrity..., together with secondary markers of inflammation." Those 'parameters of thyroid function' included various measures of free and total levels of T3 and T4 required to ascertain the presence of "low-T3 syndrome." I was impressed to see that a measure of gut wall integrity was also on the research menu in the form of plasma zonulin levels being included (albeit analysed via ELISA and bearing in mind the issues that have emerged with that particular method).

Results: "Chronic fatigue syndrome patients exhibited lower FT3, TT4, TT3, %TT3, SPINA-GD, and SPINA-GT, lower ratios of TT3/TT4, FT3/FT4, TT3/FT3, and TT4/FT4; and higher %rT3 and rT3/TT3 ratio." These findings were based on 'group' comparisons with those sex-matched not-CFS controls, and point to some 'issues' with thyroid function in general. Coupled to other thyroid related findings, the Ruiz-Núñez suggest that lower levels of thyroid hormones were detected but "distinct from thyroidal disease" typical levels of thyroid-stimulating hormone (TSH) were also reported. TSH is the stuff that tells the thyroid gland to make thyroid hormone (thyroxine (T4)), where T4 is, in effect, the starting material for T3 (triiodothyronine). Where there are suitable levels of TSH but lower levels of T4 and/or T3, one gets the impression that it's more about what's 'happening' to T3 and T4 over and above issues with their production. Indeed, the collected findings led authors to talk about that 'low T3 [triiodothyronine]syndrome' as being potentially pertinent to their findings in relation to CFS. Going back to those plasma zonulin findings, and there is just a sentence from Ruiz-Núñez and colleagues: "Zonulin, a parameter of intestinal permeability... was lower in CFS patients as compared to controls" but not much else.

I'm not particularly au fait with all the details of low T3 syndrome in the context of CFS or anything else so can't really add too much more. From what I gather, this is not a CFS-exclusive condition but does seemingly tap into talk about CFS being reflective of a "hypometabolic state" (see here). Questions about how to 'treat' such thyroid-related issues in the context of CFS remain unanswered, despite authors talking about "trials with, e.g., T3 and iodide supplements" being potentially indicated. I say this bearing in mind that the focus on biochemistry in the Ruiz-Núñez paper could perhaps, have been complemented by a little more on the presentation of clinical symptoms too.

In short, quite a bit more investigation in this area is indicated...


[1] Ruiz-Núñez B. et al. Higher Prevalence of “Low T3 Syndrome” in Patients With Chronic Fatigue Syndrome: A Case–Control Study. Front. Endocrinol. 2018. Mar 20.


Friday 25 May 2018

Exercise may protect against the development of depression

"Available evidence supports the notion that physical activity can confer protection against the emergence of depression regardless of age and geographical region."

So said the findings reported by Felipe Schuch and colleagues [1] who undertook a review of the existing peer-reviewed research literature looking at whether physical activity a.k.a exercise *might* provide some important protection against the development of depression. Such a review took place in the context that NHS Choices, the go-to place for health and medical information here in Blighty, already has an entry called 'exercise for depression'.

The authors - many of whom are quite recognisable names in the area of science looking at the physical and the mental coexisting together - located almost 50 studies labelled as prospective cohort studies including over a quarter of a million participants residing across the globe. They undertook a meta-analysis - combining all the data from the various studies together and coming up with a sort of consensus finding - and concluded that yes, physical activity does seem to have a positive effect on reducing the risk of depression. The level of the decrease in risk of depression from participation in physical activity seemed to vary slightly according to age, amount of exercise and geographical region, but the trend was most definitely in the protective direction across such variables and remained even after potentially important variables such as body mass index (BMI) and tobacco smoking were taken into account. The authors also reported that: "Although significant publication bias was found, adjusting for this did not change the magnitude of the associations" indicating that although there was a tendency for results 'friendly' to the 'physical activity might reduce depression' hypothesis to be published over less positive results, this did not seemingly affect the findings in any particularly meaningful way.

Accepting that there is a further scheme of work required on this topic in terms of things like what physical activities might be 'best' for depression or depressive symptoms (see here), how to measure physical activity more objectively (ahem, actigraphy) and what the mechanism(s) of effect might be, these are important results. I can think of many, many different areas that the Schuch results could be pertinent to; several already covered on this blog (see here and see here). Many of those areas / conditions / labels reflect states where either physical activity seems to be reduced by choice (see here) or through necessity (see here) but the net result could be the same in terms of elevated risk of depression.

Still, the general message emerging from the Schuch paper is: if you can, move more, and perhaps not just for the physical benefits that accompany physical activity.

And just in case you need some more reading material on this topic, you could do a lot worse than the paper by Brett Gordon and colleagues [2] who concluded that: "Resistance exercise training significantly reduced depressive symptoms among adults regardless of health status, total prescribed volume of RET, or significant improvements in strength."


[1] Schuch FB. et al. Physical Activity and Incident Depression: A Meta-Analysis of Prospective Cohort Studies. Am J Psychiatry. 2018 Apr 25:appiajp201817111194.

[2] Gordon BR. et al. Association of Efficacy of Resistance Exercise Training With Depressive Symptoms. JAMA Psychiatry. 2018. May 9.


Thursday 24 May 2018

"Lonely young adults in modern Britain"

"Lonelier young adults were more likely to experience mental health problems, to engage in physical health risk behaviours, and to use more negative strategies to cope with stress."

Those were some of the conclusions reached in the study published by Timothy Matthews and colleagues [1] who relied on data from the "Environmental Risk (E-Risk) Longitudinal Twin Study, which tracks the development of a birth cohort of 2232 British children" to "examine the profile of loneliness in a prospective, contemporary, nationally representative cohort of 18 year-olds living in the UK." The specific focus was on how loneliness might impact on various domains: "mental health, physical health and health risks, coping and functioning, and career prospects."

Results: first and foremost, when it came to the question(s) of loneliness, and the prevalence of loneliness as measured by the UCLA Loneliness Scale, Version 3, "23–31% of participants reported experiencing any of these feelings ‘some of the time’, and 5–7% reported feeling them ‘often’." Sex/gender and socio-economic status did not seem to show any statistically significant relationship to reports on loneliness.

In terms of possible or actual psychopathology, we are told that: "Lonelier 18 year-olds were more likely to meet diagnostic criteria for depression, anxiety, ADHD [attention-deficit hyperactivity disorder], conduct disorder, alcohol and cannabis dependence, to have self-harmed, and to have attempted suicide." Depression and anxiety came out with the strongest *association* in relation to loneliness, and insofar as the 'attempted suicide' bit, I'm wondering whether it may tie into other recent quite shocking findings (see here). Researchers also noted that: "lonelier individuals engaged in less day-to-day physical activity and were more likely to be daily smokers."

Whilst realising that the various associations mentioned in the context of loneliness do not necessarily tie directly into loneliness (e.g. loneliness does not necessarily 'cause' anxiety and depression or indeed, vice-verse), these are important results. They add to a bank of peer-reviewed research which suggests that loneliness - chronic loneliness - is probably not great for anyone (see here). They also observe that increasing social contact with others, whilst not without benefits, is not necessarily all that can be done to combat this state and it's rather negative correlations.

And it is perhaps timely that at the time of writing this post, loneliness is highlighted as being over-represented when it comes to certain diagnostic labels as part of a package of issues affecting quality of life (see here)...


[1] Matthews T. et al. Lonely young adults in modern Britain: findings from an epidemiological cohort study. Psychological Medicine. 2018. April 24.


Wednesday 23 May 2018

Pregnancy exposure to paracetamol and offspring developmental outcomes meta-analysed

Yes, I'm yet again talking about pregnancy paracetamol (acetaminophen) use and offspring developmental outcomes on this blog (see here and see here for other discussions on this topic). As I mentioned on another recent blogging occasion, the news regarding pregnancy paracetamol use and offspring outcomes seems to be getting worse and worse, as associations galore keep appearing in the peer-reviewed science arena. Of course one has to be a little cautious about the nature of the studies that are emerging (i.e. observational, not readily designed to look at 'cause-and-effect') but the volume of research is growing at a significant pace potentially suggestive of something to see.

Now we have the results of a "Systematic Review, Meta-Analysis, and Meta-Regression Analysis of Cohort Studies" published by Reem Masarwa and colleagues [1] on the topic of pregnancy paracetamol use and "the risk for attention deficit hyperactivity disorder (ADHD) and autistic spectrum disorder (ASD) in the offspring of women exposed to acetaminophen during pregnancy." All that meta-analysis stuff means that authors boiled down the current, existing peer-reviewed research into some sort of coherent whole. Their paper also comes complete with some lay media attention too (see here).

The findings? Well, taking into account various studies published "up to January 2017" and including some "132,738 mother and child pairs and with a follow-up period of 3-11 years", you probably won't be surprised to here that prolonged paracetamol use during pregnancy did seem to increase the risk of ADHD and/or autism in offspring to the tune of about 20-30% compared with those who did not take such medicine during pregnancy. That's not an unimportant percentage in anyone's book.

Reiterating the observational nature of the studies reviewed and boiled down (in a statistical sense) by Masarwa et al and the need for further investigations on things like possible mechanisms and indeed, whether the conditions for which paracetamol as pain relief was being taken *might* exert an effect on offspring risk, the results add to the concern. Much like other areas where various pregnancy medications are seemingly being implicated in relation to offspring outcome (see here and see here) such findings reiterate the importance of the nine months that made us and the need for much more sound research on this topic...


[1] Masarwa R. et al. Prenatal Exposure to Acetaminophen and Risk for Attention Deficit Hyperactivity Disorder and Autistic Spectrum Disorder: A Systematic Review, Meta-Analysis, and Meta-Regression Analysis of Cohort Studies. American Journal of Epidemiology. 2018. April 24.


Tuesday 22 May 2018

A poo(p) transplant for depression and anxiety?

Contrary to the title of this post - "A poo(p) transplant for depression and anxiety?" - I don't think we are yet in a position to say that Fecal Microbiota Transplantation (FMT) is ready to go 'mainstream' as an approved treatment for depression and/or anxiety. I do however, think that the findings reported by Shunya Kurokawa and colleagues [1] provide evidence for a further, more controlled, scheme of research on this topic.

Based on their following a small-ish group of patients diagnosed with "either Irritable Bowel Syndrome (IBS), Functional Diarrhea (FDr) or Functional Constipation (FC) who underwent FMT for the treatment of gastrointestinal symptoms and observation of psychiatric symptoms" authors report results before said poo(p) transplant and after 4 weeks based on ratings on various instruments pertinent to the presentation of depression and anxiety. Alongside "intestinal microbiota were measured" with a particular focus on the level of diversity of species that were present in pre- and post-FMT samples. I might also mention at this point, how something like IBS is not without it's own 'psychological' correlates as per other research (see here and see here).

Following an 'open-trial' methodology and including only a "small sample size with no control group", researchers reported some significant improvements in relation to those depression and anxiety symptom scores for some. Importantly too, they noted that potential FMT effects on mood seemed to be independent of effects on "gastrointestinal symptom change." Similarly: "There was a significant correlation between baseline Shannon index and HAM-D [Hamilton Rating Scale for Depression] score, and a correlation between Shannon index change and HAM-D improvement after FMT." This suggests that bacterial diversity might be something to look at as potentially explaining the psychological effects of FMT.

Reiterating that the Kurokawa findings are preliminary and hence, require quite a lot more further (independent) study, I find this topic to be an interesting one. Although there may be some 'consumer resistance' to the idea of FMT, for some people, this type of intervention is nothing short of life-saving (see here). The idea that a similar type of transplant *might* also hold some benefits for conditions/labels outside of something like Clostridium difficile (C. difficile) infection has already been noted in the peer-reviewed science literature (see here and see here for examples), including conditions characterised by behaviour and psychology. This alongside a growing interest in how mood and temperament might have some important connection to those trillions of wee beasties (the gut microbiome) that call us all home (see here). We'll see where this goes...


[1] Kurokawa S. et al. The effect of fecal microbiota transplantation on psychiatric symptoms among patients with irritable bowel syndrome, functional diarrhea and functional constipation: An open-label observational study. J Affect Disord. 2018 Apr 12;235:506-512.


Monday 21 May 2018

The "experiences and perspectives of people who have severe autism and are minimally verbal"

I'm not going to formulate some sort of mammoth, long-read post on the paper by Christie Welch and colleagues [1] but I did want to bring their findings to your attention. My reasoning: the authors include a quite 'under-represented' group (see here) when it comes to the public view of the autism spectrum: those who "have severe autism and are minimally verbal."

Presenting the results of a qualitative study whereby "three memoirs written by youths who have severe autism and are minimally verbal were examined using inductive thematic analysis", authors observed several important themes emerging. Principal among them: "regarding the youths' concern that the way they are perceived from the outside does not match the people they are on the inside."

"These youths emphasize concepts of embodiment and physical control as central to their experiences of autism" said Welch et al, as the message seems to be that more should be done to 'tackle' these experiences and ensuring that sweeping generalisations about language use or non-use for example, are not seen as a proxy for cognitive and intellectual abilities. Just because someone cannot speak verbally, does not mean that they have nothing to say, and vice-verse.

I'm careful not to fall into the trap of 'autism severity' on the basis of the Welch findings, where terms like 'high' and 'low' functioning unduly simplify people in a binary fashion and seemingly without regard for the complexity of how autism affects various aspects of a person's life. I do however like the idea that more effort needs to go into things like the development of communication systems for those who are minimally verbal; both for clinical and research purposes but perhaps more importantly, day-to-day purposes, given also some catastrophic examples where communication issues have severely impacted on autistic lives (see here and see here).

And to the question of 'how common is 'minimally verbal' in the context of autism', well, another recent paper [2] has come up with an estimate: about a third...


[1] Welch C. et al. Autism inside out: lessons from the memoirs of three minimally verbal youths. Disabil Rehabil. 2018 Apr 23:1-9.

[2] Bacon EC. et al. Naturalistic language sampling to characterize the language abilities of 3-year-olds with autism spectrum disorder. Autism. 2018 May 1:1362361318766241.


Saturday 19 May 2018

Temporal armchair diagnosing taken to the max: 'How Do We Explain ‛Autistic Traits’ in European Upper Palaeolithic Art?'

Headlines aplenty...
I'm not a great fan of 'armchair diagnosing' also known as 'diagnosing at a distance'. It's speculative, often inaccurate and runs the real risk of ruining lives.

The remote diagnosing of psychiatric and behavioural disorders is a particular bugbear of mine. It's something that autism research and practice in particular has had to endure for quite a few years, as a volley of historical figures for example, were revealed to be supposedly autistic. Such musings also add a temporal aspect to proceedings.

The paper published by Penny Spikins and colleagues [1] takes such temporal armchair diagnosing to the absolute max, with their contribution to the "long standing debate about the existence of ‘autistic traits’ in European Upper Palaeolithic art." Some of the media that followed these findings really went to town, as per headlines such as 'Ice Age cave artists were AUTISTIC' (capital letters were already included in the headline, not added by me - see above) and 'Autism shaped the art of survival'. Wow. All of that information from a few paintings and carvings...

So how did the the authors and the lay media arrive at such a conclusion?

Well, first and foremost Spikins et al did not say that the makers of such early art were 'autistic'. They focused on autistic traits, and in particular the idea of an "extreme local processing bias" or attention to detail trait that seems to accompany the diagnosis of autism (for some). Importantly, they note that: "Local processing bias is common in autism but also seen in individuals without autism" and "‘Autistic traits’ in Upper Palaeolithic art do not necessarily signify the work of an individual with autism." So, from the outset, we can probably do away with that rather sweeping [diagnostic evidence-free] media headline on Ice Age cave artists being autistic.

Quite a lot of the Spikins paper focuses on what's been observed - directly observed - in some of those diagnosed as being on the autism spectrum when it comes to artistic talent, which is then 'extrapolated' to such prehistoric artists. This includes some rather nice pictures drawn by individuals with autism who expressed a "marked local processing bias" compared with age-matched drawings from non-autistic individuals. We're also told that the use of the (very) famous 'are you autistic?' self-report screener that is the Autism Spectrum Quotient (AQ) by the authors, revealed that "individuals with a very high autism quotient (AQ) of 32 or above, which is taken as indicative of an autism spectrum condition within a population sample were statistically much more likely than neurotypical individuals (i.e. those with a lower AQ score) to have an interest in and experience of art outside of any school curriculum." 'Indicative of an autism spectrum condition'? Well, we'll see. And I still have some problems with what comes under the term 'neurotypical' too (see here).

Of course you can perhaps see the issue here. Take one block of 'evidence', some of it based on individual case reports and some of it based on an 'autism' screener that probably picks up an awful lot more than 'just autism' (see here and see here and see here for examples), correlate and correlate some more and hey presto, we reach the conclusion that the art must have been drawn by someone expressing an autistic trait or even someone who was autistic.

A testable hypothesis? No, it's not. We don't know who drew those paintings or made those carvings. We don't know anything about them personally and we certainly don't have any evidence about whether they expressed any significant autistic or any other kind of trait. For all we know, the paintings or carvings could also have been made by more than one person; a family or group effort if you like. We just don't know because, well, those artistic depictions were made thousands and thousands of years ago before the tools that help us record history were even a twinkle in the cosmic eye.

I don't want to come across as poo-pooing such 'observations' stressing how autistic traits are not necessarily a new thing because, in essence, I do think that some autistic traits have probably been with us from our earliest evolutionary times (see here). I say that on the basis that the traits of autism are not some 'magical' behaviours that are completely distant from the human experience; more likely they represent the extremes of what is typically seen in the general population at particular ages and stages and environments. Taking such logic back in an evolutionary sense, one can for example see how something like an 'attention to detail' could be a good survival skill if your life depended on it.

But I do think one has to be very, very cautious about such research and any 'feelgood' factor it might attempt to generate or put forward. Autism, as a clinical definition, only really came about in the last hundred years or so, and for many, any benefits derived from a 'marked local processing bias' have to be balanced with the possible downsides to such directed focus (e.g. increased rumination and anxiety). I'd also add in that the idea that Palaeolithic Art (or indeed, any kind of art) merely comes about as a result of traits that are noted in the context of psychopathology is a pretty dangerous path to take. It risks boiling down human efforts such as creativity and artistic skill to nothing more than diagnostic characteristics and feeds into narratives such as the "creativity is akin to insanity" headlines of not so long ago (see here). As I've said before, people are so much more than the labels they've received or the diagnostic term they identify with.

In short, Palaeolithic art is interesting and adds to our understanding of how we evolved. But it simply cannot provide an accurate window on any states and traits of those who created it...

To close, there's a wedding on today apparently. Best wishes to the happy couple. And not to make light of our Royal Family, but The Windsors TV show is absolute comedy gold (particularly Harry Enfield)...


[1] Spikins P. et al. How Do We Explain ‛Autistic Traits’ in European Upper Palaeolithic Art? Open Archaeology. 2018; 4: 262-279.


Friday 18 May 2018

ALSPAC does... prenatal mercury exposure and autism or autistic traits

The ALSPAC - Avon Longitudinal Study of Parents and Children - mentioned in the title of this post is something of quite a regular feature on this blog (see here and see here for examples).

On this particular blogging occasion I'm heading into the findings reported by Jean Golding and colleagues [1] who utilised this fabulous research resource to examine whether "prenatal exposure from total maternal blood Hg [mercury] in the first half of pregnancy is associated with the risk of autism or of extreme levels of autistic traits." They concluded that there were "no adverse effect of prenatal total blood Hg on autism or autistic traits provided the mother ate fish."

OK, mention of the heavy metal mercury in the context of autism and/or autistic traits can be a touchy subject for some. I'm talking about the various 'discussions' that have taken place both in the lay and peer-reviewed science arenas concerned with the exposure patterns relevant to mercury in the context of autism (see here and see here). This, on the basis that mercury exists in several 'forms', and those different forms have different potential exposure routes.

Golding et al relied on some of the gold-standard analytical methods for the analysis of whole blood Hg collected in the most part "at < 18 weeks gestation": "inductively coupled plasma dynamic reaction cell mass spectrometry (ICP-DRC-MS)." Variations on this method - ICP mass spectrometry - have been previously reported on in the context of mercury and autism research (see here and see here). Alongside, they looked at measured levels of mercury in relation to various behavioural and other variable groupings: "(1) direct comparison of 45 pregnancies resulting in children with diagnosed autism from a population of 3840, (2) comparison of high scores on each of the four autistic traits within the population at risk (n~2800), and (3) indirect measures of association of these outcomes with proxies for increased Hg levels such as frequency of fish consumption and exposure to dental amalgam (n > 8000)." They however cautioned that: "Although we accounted for several important confounders which are relevant to Hg levels and autism, the possibility of unmeasured confounding cannot be ruled out." I can think of one potential confounder that was not seemingly included in their list outside of fish consumption and dental amalgams but ho-hum...

Alongside their overall 'no relationship' results, a few other details are noteworthy. First: "all correlations indicated that with increasing levels of [maternal] mercury, the signs of autism [in offspring] were slightly less, but none were statistically significant." Interesting idea - higher maternal levels of mercury during pregnancy 'correlates' with 'less' autistic traits in offspring in childhood - but to reiterate, not statistically significant. Second was that 'provided the mother ate fish' detail attached to the main findings. So: "we have shown a differential relationship between the social cognition trait and prenatal Hg exposure, such that there was a significant difference in apparently protective effects contingent upon whether the mother ate fish." The authors opine as to what it is about fish consumption that might "counteract any possible adverse cognitive and behavioral differences that may be caused by prenatal exposure to Hg" including "the beneficial components of fish such as the omega-3 fatty acids, iodine, and vitamins D and B2." This in the context that omega-3 fatty acids have some research form in relation to autism (see here) as does the sunshine vitamin/hormone that is vitamin D (see here).

One has to be slightly careful with the Golding results given the focus on prenatal exposure, and prenatal exposure at only one early point in pregnancy, as well as also not actually looking at mercury levels in the children themselves. The current results say nothing for example, about any possible direct or acquired role for mercury in relation to autism as per other findings published during the same period [2]. Neither do they offer any additional information on the idea that exposure issues to such heavy metals may be only one part of the story, and that the biological processes involved in removing such heavy metals may be somehow perturbed in relation to some autism (see here).

But... set within the idea that prenatal mercury exposure may be linked to the 'etiology' of at least some autism, the Golding findings represent pretty strong evidence suggestive of no connection.

Music to close, and could I recommend the soundtrack to Sonic 3 while you work?


[1] Golding J. et al. Prenatal mercury exposure and features of autism: a prospective population study. Molecular Autism. 2018; 9: 30.

[2] Qin YY. et al. A comparison of blood metal levels in autism spectrum disorder and unaffected children in Shenzhen of China and factors involved in bioaccumulation of metals. Environ Sci Pollut Res Int. 2018 Apr 22.


Thursday 17 May 2018

KPAX002 for Chronic Fatigue Syndrome part 2: controlled study says no

KPAX002 mentioned in the title of this post refers to "a mitochondrial modulator technology platform" according to the manufacturer that includes a low dose of methylphenidate combined with various nutrients designed to impact on mitochondrial function. Within the context of chronic fatigue syndrome (CFS) also known as myalgic encephalomyelitis (ME) (but not necessarily accurately so!), there is some preliminary research history suggesting that KPAX002 might be something to look at for intervening in some of the disabling characteristics of CFS/ME (see here). This, on the basis that mitochondria in particular, might be something quite important to at least some cases (see here and see here).

The fly in the scientific ointment?

Well the results of the "phase 2 randomized, double-blinded, placebo-controlled trial" on KPAX002 published by Jose Montoya and colleagues [1] that, from an intention-to-treat point of view, reported no significant statistical difference in self-reported group scores of fatigue and other measures between active treatment and a placebo. In keeping with the phase 2 label attached to the trial - looking at both initial clinical results and also any side- or adverse effects - authors reported no statistically significant difference in the frequency of reported adverse effects between KPAX002 and a placebo over the 12 weeks of study. First, do no harm and all that.

The Montoya paper is open-access so readers can see for themselves how things were done and the details of the results. I however, want to highlight a few points that I thought were important:

First, the authors acknowledge the "unexpectedly positive results" observed the last time around [2] that led to this more rigorous trial. Personally, I don't think there was anything too unexpected about those pilot study results, given the methodological issues typically associated with a pilot study. Y'know, a small un-blinded participant group taking part in a trial using a preparation that they probably will have been told *might* affect various symptoms they experience or themselves possibly 'exposed' to other anecdotal reports of good effects. That and no control group, no placebo included and importantly, no objective measure of fatigue (a real issue when it comes to quite a bit ME/CFS research) and well, I'd be surprised if something significant didn't come up during the initial findings. And just in case you think I'm being all 'high-and-mighty' about this, I've published using the same type of pilot study methodology before, including some of the same inherent issues (see here).

Second, I'm a little bit disappointed that the authors weren't more forthright in how the results weren't statistically significant on any and all measures included for study. I say this on the basis of both the commercial take on the results (see here) and also sentences like: "The two groups demonstrating the most robust response to KPAX002 were subjects with more severe ME/CFS symptoms at baseline (P=0.086) and subjects suffering from both fatigue and pain (P=0.057)." Both those p-values (p being a measure of statistical significance) are above the [currently] recognised threshold for p equal to or less than 0.05, yet are listed as a 'robust response'. Even more, throughout the paper I note the words 'trend in favor of' being used, which some people might translate as being 'well, they were nearly statistically significant results'. I say this also bearing in mind that the final participant numbers - KPAX002 use = 48 and placebo = 57 - are not exactly facets of what one would call an under-powered study. I'm probably being a nit-picker here but like it or not, the [current] rules of science are the [current] rules of science.

Finally, once again, I note that under the heading 'Disclosure of conflict of interest', the word 'none' appears as per the last research occasion [2]. Personally, and with no malice intended, I would have listed the detail that at least one of the authors is an employee of the manufacturer of KPXA002 given the affiliation details and email address for further correspondence provided on the paper. Again, it's a small detail but one that should nevertheless be acknowledged. I would have also like to have seen a little more on who funded the trial too and especially who funded the provision of the KPAX002 supplement for trial purposes. I reiterate that there is no malice is intended in saying that, but readers require such details.

I don't want to come down too hard on these results because it's obvious that quite a bit of work has gone into their production. I'm also not closing the door on the idea that future research with a more targeted group with ME/CFS might not produce something a little more statistically significant with regards to KPAX002. But for now, the answer must be that controlled study of the formulation did not meet clinical endpoints in a statistical sense, and hence KPAX002 cannot be said to be superior to placebo for CFS/ME. With all the setbacks that the label(s) ME/CFS has had to endure down the years with regards to the 'psychobabble' explanations (see here) and other 'eureka' moments (see here), the Montoya findings are bad news for patients yet again. But, they also should represent a further call to re-double research efforts; particularly when it comes to the biology of the condition(s) and onward the acceleration of research for interventions for this quality of life draining condition (see here).


[1] Montoya JG. et al. KPAX002 as a treatment for Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS): a prospective, randomized trial. Int J Clin Exp Med 2018;11(3):2890-2900

[2] Kaiser JD. A prospective, proof-of-concept investigation of KPAX002 in chronic fatigue syndrome. Int J Clin Exp Med. 2015 Jul 15;8(7):11064-74.


Wednesday 16 May 2018

The headline: "One in nine young people in Scotland have attempted suicide"

I have to say that I drew a sharp intake of breath when I read the media headline titling this post - "One in nine young people in Scotland have attempted suicide" - based on the findings reported by Rory O'Connor and colleagues [1]. The idea that, from a sample of some 3500 young people in Scotland, some 10% and 15% of respondents to the questions: "Have you ever made an attempt to take your life, by taking an overdose of tablets or in some other way?’ and ‘Have you ever deliberately harmed yourself in any way but not with the intention of killing yourself? (i.e. self-harm)" answered in the affirmative, seemed pretty important. Not least with the question 'why?' in mind.

OK, media headlines aside, the O'Connor findings require some dissection. The reasoning behind studying this issue was not only to look at the very complicated topic of suicide in a part of the UK (Scotland) that authors write "has a higher suicide rate than England", but also to try and understand how non-suicidal self-injury (NSSI) or non-suicidal self-harm (NSSH) presents in young adults and whether there is something important linking NSSH and suicidal thoughts and/or attempts.

The participant group was drawn from "a representative sample of young people aged 18–34 years from across Scotland" who were recruited to the Scottish Wellbeing Study. Lots of measures were completed by participants as part of the wider study initiative but we are told that "only the prevalence of NSSH and suicide attempts information is reported" in the O'Connor article on this occasion. I might also add that participants were compensated to the tune of £25 (pounds sterling) for their time and participation.

Alongside those headline findings on self-reported attempted suicide and self-harm, a few other important trends were observed. So: "More than 20% reported lifetime suicidal thoughts, 2.4% reported that they last thought about suicide in the past week and 10.4% reported they last thought about suicide in the past 12 months." Around 6% of respondents reported that they had both attempted suicide and also engaged in self-injury suggesting that professionals should "routinely enquire about history of self-injurious behaviour, especially as past behaviour is such a strong predictor of suicide." Also: "Earlier age at NSSH or suicide attempt onset was associated with more frequent lifetime NSSH and suicide attempts." And finally: "The prevalence of NSSH and suicide attempts was significantly higher among those classified as unemployed... and economically inactive... compared with those who were employed." Age, societal and environmental factors seem to play some roles too.

Then to another important set of questions: (a) why? and (b) what can be done to reduce these headline-grabbing statistics? Well, there are no easy answers to such questions I'm afraid. The authors do note that: "From a public health perspective, the unemployment and economic inactivity findings are noteworthy" and perhaps suggest that there are some modifiable variables that could influence suicidal thoughts and/or actions focused on getting people into employment and the benefits that this brings (wide-ranging benefits by all accounts). But this probably only covers one side of the issue, as discussions inevitably turn to what role psychiatric and/or behavioural comorbidity might play in such reporting (see here and see here and see here) and whether there may be a need for (a) something like enhanced screening for suicidal thoughts or other 'risks' among selected populations and/or (b) the [careful] use of 'preventative' strategies in such cases (see here and see here). I say all that accepting that diagnoses around mental health probably play an important role in suicide-related behaviours but are not necessarily a pre-requisite...

As always, there is always someone to talk to if needed...


[1] O'Connor RC. et al. Suicide attempts and non-suicidal self-harm: national prevalence study of young adults. BJPsych Open. 2018; 4: 142-148.


Tuesday 15 May 2018

Higher autistic traits in those attending transgender health services don't necessarily mean autism

There are some key messages to take from the findings reported by Anna Nobili and colleagues [1] following their examination of "self-reported autism spectrum quotient-short (AQ-short) [scores] in a transgender clinical population." Not least that when compared with a control group - "cisgender individuals" - there "were no significant differences in the number of people who presented with scores suggesting a possible diagnosis of ASC [autism spectrum condition(s)]."

OK, before heading further into the Nobili findings I think it might be worthwhile setting the scene a little. So, for quite a while now there has been some increasing interest in how autism or at least some of the traits of autism, *might* be over-represented among those presenting with gender dysphoria (see here). Gender dysphoria, according to the UK NHS Choices website is "a condition where a person experiences discomfort or distress because there's a mismatch between their biological sex and gender identity." Allied to other peer-reviewed research looking at gender identity [2], sexual preferences in the context of [some] autism (see here), and combined with quite a sweeping *theory* talking about an 'extreme male brain' in the context of autism (see here), and well, let's just say some speculation about a link between some autism / autistic traits and elements of gender and sexuality has been noted. And indeed, continues to be noted [3]...

Nobili et al - including one author who is rather central in autism research circles to the promotion of that extreme male brain theory - examined AQ responses in some 650 matched pairs (transgender matched with cisgender). Among the transgender participants: "A total of 260 people (39.6%) in each group were assigned female at birth whilst 396 (60.4%) were assigned male." It's worthwhile noting that AQ is a self-report questionnaire, and whilst heralded in several quarters as a good 'are you autistic?' screener, there are some people - including me - who have some reservations about it's 'universal' usefulness to just autism (see here and see here for examples). I'll come back to this shortly...

As per the opening paragraph to this post, the numbers of participants "indicating possible ASC caseness" did not differ significantly between the groups. So, around 33% of the cisgender control group hit a score of 70 or more on their self-report responses to the AQ compared with 36% in the transgender group. The authors did detect a statistically significant difference in possible caseness when looking at those assigned female at birth in the transgender group but not for males. A similar finding has been noted in other independent studies [4]. Nobili and colleagues however concluded that their findings were in line with other observations in adults in that: "there is no evidence of increased rates of autism in transgender populations as a whole."

Going back to my reservations around the AQ as an exclusive autism screener, I also noted something important reported by Nobili and colleagues: "High AQ scores may not be indicative of the presence of an autism spectrum condition as the difference between groups mainly related to social behaviours; such scores may be a reflection of transgender people’s high social anxiety levels due to negative past experiences." I was really intrigued by this finding and interpretation, particularly in light of other recent peer-reviewed speculation by Jack Turban [5] who suggested that: "ASD [autism spectrum disorder] symptoms [in transgender youth] may represent social deficits that are secondary to social stress and deprivation, as transgender youth suffer high rates of peer and family rejection." On a previous blogging occasion, I've also discussed research suggesting that something like a generalised anxiety disorder (GAD) may 'inflate' responses/scores on the AQ (see here). Given that anxiety is an all-too-often bedfellow accompanying a diagnosis of autism, I'd be interested to see quite a bit more study on this topic in the context of AQ use. Y'know, perhaps alongside some more formal measures of anxiety both in relation to autism and also more readily pertinent to the subject matter analysed by Nobili et al. And, outside of just anxiety, other clinical features/conditions might also be thrown into the research mix [6]. Insofar as the idea that mental health may also be a topic requiring more focus in respect of the transgender population, I'll bring to your attention some other recent research by Becerra-Culqui and colleagues [7] on this point.

There is a further scheme of work to follow in this area, and I'll be interested to see what further results turn up, particularly with regards to females assigned at birth with gender dysphoria. And since I've mentioned the AQ and (once again) my reservations, I'll direct you to another paper published in the same journal at roughly the same time as the Nobili findings, where the AQ was again 'implied' as being equal to the presence of autistic traits [8]. And yet again, another example where one has to be very, very careful about making that 'exclusively autistic traits' link...


[1] Nobili A. et al. Autistic Traits in Treatment-Seeking Transgender Adults. J Autism Dev Disord. 2018. April 13.

[2] Cooper K. et al. Gender Identity in Autism: Sex Differences in Social Affiliation with Gender Groups. J Autism Dev Disord. 2018. April 28.

[3] van der Miesen AIR. et al. Prevalence of the Wish to be of the Opposite Gender in Adolescents and Adults with Autism Spectrum Disorder. Archives of Sexual Behavior. 2018. May 7.

[4] Vermaat LEW. et al. Self-Reported Autism Spectrum Disorder Symptoms Among Adults Referred to a Gender Identity Clinic. LGBT Health. 2018 May 9.

[5] Turban JL. Potentially Reversible Social Deficits Among Transgender Youth. J Autism Development Disord. 2018. May 12.

[6] Lugnegård T. et al. Asperger syndrome and schizophrenia: Overlap of self-reported autistic traits using the Autism-spectrum Quotient (AQ). Nord J Psychiatry. 2015 May;69(4):268-74.

[7] Becerra-Culqui TA. et al. Mental Health of Transgender and Gender Nonconforming Youth Compared With Their Peers. Pediatrics. 2018. April 16.

[8] Loureiro D. et al. Higher Autistic Traits Among Criminals, But No Link to Psychopathy: Findings from a High-Security Prison in Portugal. J Autism Dev Disord. 2018. April 12.


Monday 14 May 2018

How much does it cost to assess a child for autism?

In answer to the question titling this post - 'How much does it cost to assess a child for autism?' - the results published by Mark Galliver and colleagues [1] provide some important findings, at least pertinent to the diagnostic experience here in Blighty.

Authors concluded that assessment for autism "typically takes 13 hours of professional time" and costs somewhere in the region of "£650–£1000 ($975–$1500) per child." Importantly too, the staff costs of around £800 per assessment do not cover "costs of intervention, parent psychological education, investigation and assessment and management of comorbidities."

I appreciate that talking about 'financial costs' associated with autism (assessment) is not a topic everyone will enjoy discussing. Much like other 'bean counter' discussions (see here and see here), everyone [rightly] aspires to providing this, that and t'other to improve facilities with regards to diagnosis and indeed, post-diagnostic services. The financial reality however, particularly in these days of continued austerity, is that such services are often under-funded, under-resourced and headlines including words like 'two year wait' for diagnostic assessment (see here) are not uncommon. People rightly get angry about this but the services themselves and the people delivering them are not to blame.

Galliver et al started out with some important premises. First, there are a growing number of referrals for assessment for autism. Second, such an 'increase in demand' naturally puts greater pressure on diagnostic services resulting in longer waiting times. Third, there are recognised pathways for referral and assessment for autism, but the resourcing of such pathways might not always be optimal either in form or amount. All of this is set in the context of the National Health Service (NHS) providing clinical and medical services here in the UK, free at the point of need and all that.

Researchers therefore decided to ask various local child development centres (CDC) in England about their diagnostic experiences in terms of resources and costs. Various questions were asked pertinent to the pathway used to deliver assessments and professional time typically allocated to said assessments. They report on responses from 60% of the CDC - no, not that CDC - initially questioned, covering a range of services in different geographic locations.

I don't need to rehash the financial findings again. I will however mention a couple of associated points that might be relevant. First, autism rarely exists in some sort of diagnostic vacuum (see here). The authors make the point that their figures did not cover the "investigation and assessment and management of comorbidities" something important in these days of greater realisation of 'autism plus' and ESSENCE (see here). In this respect, the figures provided by Galliver are likely to be an underestimate of the true financial cost of assessment.

Second, the issue of growing numbers of referrals and "increasing demand" for diagnostic services is highlighted in various parts of the reported findings. I have my own opinions as to why this is happening (see here and see here) but the one thing that is becoming increasingly clear is that such an increase is probably not just due to better recognition of autism or issues such as diagnostic switching (see here and see here). Yes, these points were probably relevant about 10-20 years ago, but now, I'd have to say not as much as [clinical] awareness must have peaked by now. At some point the question of 'why the increase' is going to have to be properly faced up to if it's not going to be all about just assessing and diagnosing in a catch-up sense.

Finally, although more funding would help, such demands on assessment services are probably not going to be met by just 'throwing a few quid' at them. The NHS is moving with the times in other areas; and the rise and rise of technology to potentially assist with autism assessments is becoming increasingly important. I'm thinking about work such as that being done at the Duda-Wall laboratory (see here and see here) where technology such as machine learning is being used in the context of autism screening. And things like autism screening triage via YouTube (see here) *might* also [eventually] become more commonplace. Technology can potentially ease the burden on assessment services.

Whatever does or does not happen as a result of findings such as those by Galliver and colleagues, the underlying messages are that autism assessment is (a) not an inexpensive process and (b) either significant funds need to be poured into the service or services need a revamp on the basis of current funding schedules and as national finances allow. Either way, I don't see assessment waiting times improving much in the near future despite the important work provided by our fantastic NHS and the desperate need for timely autism assessment.

And I've not even mentioned about adult diagnostic services...


[1] Galliver M. et al. Cost of assessing a child for possible autism spectrum disorder? An observational study of current practice in child development centres in the UK. BMJ Paediatr Open. 2017 Nov 30;1(1):e000052