Could an "ill-state" associated with anorexia nervosa mimic the symptoms of autism?

The question posed in the title of this post 'Could an "ill-state" associated with anorexia nervosa mimic the symptoms of autism?' stems from the findings reported by Heather Westwood and colleagues [1] (open-access).

They continued a research theme looking at the potential 'overlap' when it comes to autism and eating disorders such as anorexia nervosa (AN) (see here). Notably, researchers questioned whether the finding that some 50% of their cohort "scored above the clinical cut-off on the ADOS-2" but "when developmental history was obtained, only 10% met diagnostic criteria for ASD [autism spectrum disorder]" could be due to "the ill-state associated with AN."

The Westwood paper is open-access so doesn't need any further grand explanations from me. The research caveats alongside relying on quite a small cohort - "40 females aged between 12 and 18" - were that this was a snapshot study not a longitudinal one and whilst relying on data other than that just linked to the presence of autism traits, they did not control for things like social anxiety "which could lead to high scores on the ADOS-2." Interesting.

On the question of whether 'active AN' (please pardon my lack of knowledge on this topic) might have the ability to 'provoke' autistic traits, I have to say that I'm quite intrigued. This might have a few, quite important, implications not least that (a) autistic traits can be 'acquired' as per what has been noted under other different circumstances (see here and see here for examples) and (b) the potential stability of said traits might not be particularly stable for everyone at every time (see here). On that last point, we do need a lot more data as to what happens/happened when AN is treated/managed or goes into remission for example and any subsequent impact on autistic traits.

It's too early to start talking mechanisms when it comes to AN and autistic traits in light of this data alone. I might also venture into the idea that other comorbidities than can appear alongside AN might also have some impact on clinical presentation (see here) and are also in need to further investigation in the context of any eating disorders - autism correlation. Indeed, there are potentially lots of variables that need to be kept in mind (see here and see here) before any sweeping generalisation are made...

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[1] Westwood H. et al. Assessing ASD in Adolescent Females with Anorexia Nervosa using Clinical and Developmental Measures: a Preliminary Investigation. J Abnorm Child Psychol. 2017 Apr 17.

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Westwood, H., Mandy, W., Simic, M., & Tchanturia, K. (2017). Assessing ASD in Adolescent Females with Anorexia Nervosa using Clinical and Developmental Measures: a Preliminary Investigation Journal of Abnormal Child Psychology DOI: 10.1007/s10802-017-0301-x

Neuropsychiatric disorder onset "temporally related to prior vaccinations"?

"Given the modest magnitude of these findings in contrast to the clear public health benefits of the timely administration of vaccines in preventing mortality and morbidity in childhood infectious diseases, we encourage families to maintain vaccination schedules according to CDC guidelines."

The quote opening this post comes from the paper published by Douglas Leslie and colleagues [1] (open-access) and offers not a conclusion from their study looking at the possibility that "the onset of some neuropsychiatric disorders may be temporally related to prior vaccinations in a subset of individuals" but a caution that cause-and-effect were not 'proven' in their study. Anyone with any knowledge about previous occasions where administration of vaccines have been correlated with specific psychiatric or behavioural outcomes (see here and see here for examples) will recognise how important such a caution is, bearing in mind that vaccines are medicines (albeit preventative) and are subject to similar monitoring for safety and the small possibility of adverse effects as other medicines.

Based on the examination of "the MarketScan® Commercial Claims and Encounters database", a US drug and medical insurance claims database, researchers looked at various diagnoses of interest including OCD (obsessive compulsive disorder), AN (anorexia nervosa), anxiety disorder, tic disorder, major depression, bipolar disorder and ADHD (attention-deficit hyperactivity disorder) in children/young adults aged 6-15 years old. This alongside several other classes of diagnosis including broken bones and 'open wounds'. Participants were matched one-to-one with controls without said neuropsychiatric diagnoses and exposure(s) to various vaccinations - "influenza, tetanus and diphtheria (TD), hepatitis A, hepatitis B, meningitis, and varicella" - were 'tracked'. Interestingly, this is not the lead authors' first foray into using the MarketScan database [2], where autism was the previous topic of analysis (specifically healthcare service use and costs).

Results: bearing in mind that samples sizes varied according to those diagnoses under investigation, the authors report: "Receipt of any vaccine in the previous 6 months was highest for children with AN (21.4%), followed by OCD (15.9%) and tic disorder (15.8%), and was lowest for children with open wounds (10.3%)." This information needs to be treated carefully because - again - it tells us nothing about any cause-and-effect relationship, just correlation and trend; trends that could be there for all-manner of different reasons outside of the variables looked at. Further: "HRs [hazard ratio] associated with receipt of any vaccine were highest for children with AN... followed by OCD."

The authors also looked at specific vaccinations in relation to those neuropsychiatric disorders included in their study. They report: "Influenza vaccinations during the prior 3, 6, and 12 months were... associated with incident diagnoses of AN, OCD, and an anxiety disorder." Conversely: "children with major depression were less likely to have received the influenza vaccine in the previous 3 months" and "children with bipolar disorder were also less likely to have received the influenza vaccine in the previous 3 or 6 months."

OK, it is worth reiterating - yet again - that this was a study looking at possible associations and not necessarily cause-and-effect. Indeed, judging by that last paragraph and the table of HRs produced by the authors (see here) one might easily claim that flu vaccination might potentially shield someone from developing major depression as much as 'cause' AN, OCD and/or anxiety disorder. Such is the nature of such studies and the findings being reported. And indeed someone has actually looked at depressive symptoms (symptoms that is, not depression as a clinical diagnosis) before and after an influenza vaccination and found very little...

I note that with specific regard to the influenza vaccine and the findings that "children with AN, OCD, or a tic disorder were more likely to have received the influenza vaccine in the preceding periods" the authors head into the research talking about narcolepsy and the "AS03-adjuvanted H1N1 vaccine" as a possible template for their findings. This despite not covering the diagnosis of narcolepsy in their study (they could have). I've touched upon this area of research before on this blog (see here) (something that continues to appear in media discussions) and whilst not disputing the findings, do for example, wonder why in the work of Szakács and colleagues [3] ADHD was picked up as a comorbidity present in their "post-H1N1 vaccination (PHV) narcolepsy group" but in the Leslie data the HRs showed little evidence of any relationship. Yes, H1N1 vaccination is not necessarily the same as influenza vaccination reported in the Leslie data (we don't actually know what specific influenza vaccines were administered), but surely if discussions turn to an 'autoimmune' element as a possible mechanistic feature potentially linking vaccination and [some] neuropsychiatric disorder(s), one would expect to see the same/similar pattern of conditions being represented and reported? For balance, I should also point out that other independent study has talked about eating disorders potentially having "immune-mediated mechanisms" connected, particularly those associated with autoimmunity [4] although I don't doubt such a connection is likely complicated and probably not universally applicable.

It's not difficult to find issues with the Leslie paper and no doubt these will be emphasised in any further discussions about the data reported even when the authors stress throughout that "findings do not demonstrate a causal role of vaccination in the pathoetiology of any of these conditions." The strengths of the data - e.g. the use of that administrative database for confirming diagnoses and vaccine exposure - are worth mentioning again in light of other debates on data sources from other 'disappearing' manuscripts in this area. I might also add that by focusing in on various diagnoses but not autism (which again, they could have done) and not a certain vaccine, the authors seem well aware of the history in this area - "the association of the measles, mumps, and rubella vaccine with autism spectrum disorder has been convincingly disproven" - and probably either thought nothing more of it or chose to steer well clear of it (or perhaps a combination of both).

Is there a 'where next' when it comes to the Leslie data? To quote again from the paper: "findings require replication in a larger population-based sample, possibly including assessments of various potentially important host factors, e.g., the individual’s genomic and epigenomic background, the individual’s microbiome, their history of antecedent psychosocial stress, infections, as well as other potentially simultaneously administered vaccinations, the differences in vaccine types, and the route of administration (e.g., intramuscular or intranasal administration of influenza vaccine)." The scientific literature also provides some other avenues for further study in this area [5]. But science does not happen in a social vacuum; any further research needs to be done with care and focus. Mindful of both the important reliance on vaccination in protecting both the individual and population at large and mindful that sweeping generalisations (often emanating from scientific study) need to be minimised.

And on the topic of the research of Douglas Leslie, I'll be coming to another recent paper he published on the important issue of depression in parents of children diagnosed with autism [6] quite soon...

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[1] Leslie DL. et al. Temporal Association of Certain Neuropsychiatric Disorders Following Vaccination of Children and Adolescents: A Pilot Case-Control Study. Front Psychiatry. 2017 Jan 19;8:3.

[2] Wang L. et al. Healthcare Service Use and Costs for Autism Spectrum Disorder: A Comparison Between Medicaid and Private Insurance. Journal of autism and developmental disorders. 2013;43(5):1057-1064.

[3] Szakács A. et al. Psychiatric comorbidity and cognitive profile in children with narcolepsy with or without association to the H1N1 influenza vaccination. Sleep. 2015 Apr 1;38(4):615-21.

[4] Raevuori A. et al. The increased risk for autoimmune diseases in patients with eating disorders. PLoS One. 2014 Aug 22;9(8):e104845.

[5] Sadarangani SP. et al. "Let there be light": the role of vitamin D in the immune response to vaccines. Expert Rev Vaccines. 2015;14(11):1427-40.

[6] Cohrs AC. & Leslie DL. Depression in Parents of Children Diagnosed with Autism Spectrum Disorder: A Claims-Based Analysis. J Autism Dev Disord. 2017 Feb 18.

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Leslie DL, Kobre RA, Richmand BJ, Aktan Guloksuz S, & Leckman JF (2017). Temporal Association of Certain Neuropsychiatric Disorders Following Vaccination of Children and Adolescents: A Pilot Case-Control Study. Frontiers in psychiatry, 8 PMID: 28154539

Gut dysbiosis in anorexia nervosa

"Collectively, these results clearly indicate the existence of dysbiosis in the gut of AN [anorexia nervosa] patients."

That opening sentence comes from the paper by Chihiro Morita and colleagues [1] (open-access available here) who "compared the fecal microbiota of female patients with AN (n = 25), including restrictive (ANR, n = 14) and binge-eating (ANBP, n = 11) subtypes, with those of age-matched healthy female controls (n = 21)." Stool and blood samples were analysed for various potentially important markers, and some interesting results were forthcoming.

So: "AN patients had significantly lower amounts of total bacteria, C. coccoides group, C. leptum subgroup, B. fragilis, and Streptococcus than age-matched healthy women." Although I am a little wary of zooming in on just one bacterial finding, the suggestion that this relatively small participant group diagnosed with AN showed something akin to a decrease in levels of B. fragilis (Bacteroides fragilis) caught my eye. My reasoning: well, lets just say that research on a certain mouse model applied to another diagnosis frequently discussed on this blog has mentioned B. fragilis before; particularly what happened when this stuff was offered as an oral treatment: "Bacteroides fragilis corrects gut permeability, alters microbial composition, and ameliorates defects in communicative, stereotypic, anxiety-like and sensorimotor behaviors." Now apply all that to the idea that there may be some 'overlap' when it comes to autistic traits and AN (see here) and hopefully I'm not getting too carried away.

One other detail from the Morita study also caught my eye specifically with C-reactive protein (CRP) in mind. We are told that: "The ANR group exhibited significantly lower serum levels of C-reactive protein than the control group." Again accepting the small participant numbers included for study, I was a little surprised that nothing too much was made of this finding in the paper discussion and conclusions. If one assumes that CRP levels might be a rough-and-ready response indicator to something like inflammation, the idea that there may be 'issues' with either systemtic inflammation or the response to inflammation is something than I'd like to see a little more investigation into.

There is a small but growing interest in the possible role of the gut microbiota in relation to AN. Accepting that the issues with food (restriction and in some cases "abnormal eating or purging behaviors") that define the condition are probably going to play some role in the make-up of the gut microbiome, I do think are some interesting routes for future study. That intestinal dysbiosis when present in cases of AN may have some possible psychological repercussions as per the findings reported by Kleiman and colleagues [2] for example, is one area of interest that could lead to some important discussion points.

Oh and whilst we're on the topic of gut bacteria, yes, we might have to redefine what 'the common knowledge' on numbers of bacteria that call us home vs. cells, but don't downplay what important role(s) they play (see here).

Music: Me First and the Gimme Gimmes - Sweet Caroline.

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[1] Morita C. et al. Gut Dysbiosis in Patients with Anorexia Nervosa. PLoS One. 2015 Dec 18;10(12):e0145274.

[2] Kleiman SC. et al. The Intestinal Microbiota in Acute Anorexia Nervosa and During Renourishment: Relationship to Depression, Anxiety, and Eating Disorder Psychopathology. Psychosom Med. 2015 Nov-Dec;77(9):969-81.

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Morita C, Tsuji H, Hata T, Gondo M, Takakura S, Kawai K, Yoshihara K, Ogata K, Nomoto K, Miyazaki K, & Sudo N (2015). Gut Dysbiosis in Patients with Anorexia Nervosa. PloS one, 10 (12) PMID: 26682545

The Autism-Spectrum Quotient (AQ) and the media: a few thoughts

"Are you on the autistic spectrum? Take the test" read a recent media headline.

Commenting on the findings reported by Emily Ruzich and colleagues [1], the headline is followed by some pretty bizarre text about how the study "has confirmed that men are more likely to be autistic than women."

I have to take some exception to this sentence, as I quote from the Ruzich findings: "In a sample of nearly half a million individuals, we found a moderate effect of sex on AQ [Autism-Spectrum Quotient], with males scoring higher than females by an average of 2.5 points." As per other discussions about the Ruzich research (see here) scores on the AQ reflect the presentation of autistic traits not the likelihood of 'being diagnosed autistic'. That and the fact that their findings were geared towards the idea that sex/gender and occupational path might be correlated with AQ scores and I'm not entirely sure that accuracy is at the forefront of that particular headline and media article.

Stepping back a little, some people might know that the AQ represents something of a potential 'screening' instrument when it comes to autism and Asperger syndrome (AS) [2]. I have emphasised the word 'screening' because screening is something quite independent from 'assessment' when it comes to autism and the often detailed investigation(s) needed to arrive at an accurate diagnosis of something like autism or an autism spectrum disorder (ASD). If you want a little more information about how assessment for autism might run here in the UK, take a look at the NICE guidance on the topic specifically with adults in mind (see here), paying particular attention to the sentence: "Comprehensive (diagnostic, needs and risks) assessment of suspected autism."

I've been interested in the AQ for a while on this blog and the large, and growing, peer-reviewed evidence base that has utilised the instrument (see here). Appreciating the strengths of the AQ, I am still a little wary about what is being measured by the AQ especially when one considers research such as that from Lugnegård and colleagues [3] (discussed in this post) and the idea that: "significant overlap of AQ scores... reduces the discriminating power of the AQ in the separation of schizophrenia from AS." In other words, with the requirement for further study, does a high score on the AQ denote something like Asperger syndrome or could it be also picking up people who might be more readily considered to be on the schizophrenia spectrum (to coin a phrase) bearing in mind how said spectrums might be colliding?

Hopefully without coming across as having a 'bee in my bonnet' I was similarly taken to comment on the findings reported by Heather Westwood and colleagues [4] (open-access) and their systematic review and meta-analysis of the available peer-reviewed literature when it came to AQ in cases of the eating disorder, anorexia nervosa (AN). As per previous research (see here), there is something of a growing recognition that some of the signs and symptoms of autism might also cross over into AN following a trend in looking at autistic traits crossing diagnostic labels (see here and see here). Westwood et al surveyed the literature and reported that those with AN may indeed present with: "significant difficulties with social skills, communication and flexibility that present in a manner characteristic of autistic traits." Importantly, and bearing in mind their acknowledgement of the Lugnegård findings, they conclude however that: "the results do not allow for conclusions to be drawn regarding whether a proportion of those with AN also have an underlying ASD [autism spectrum disorder]" as a function of the sole reliance on the AQ among other factors.

I appreciate that in these days of pop psychology and the increased use of 'Dr Google' people want to find out as much as they can about themselves and their behaviour and/or health. I'm no exception to that trend in some of my googling habits either. Media headlines however about how simple screening instruments can 'tell' if someone is on the autism spectrum can seriously undervalue what it means to be on the autism spectrum and to have a clinical label of autism, with all the strengths and struggles that includes. Of course there is cross-over when it comes to the presentation of autistic traits in the general population and the blurred boundaries that distinguish between clinically relevant (as in clinically affecting a person's life) and something a little less life-changing. I do think however that we all need to be a little more cautious using the term autism or autistic spectrum, save any charges of diluting its impact...

Music: Muppets and giant crumpets? "Mad for it!"

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[1] Ruzich E. et al. Sex and STEM Occupation Predict Autism-Spectrum Quotient (AQ) Scores in Half a Million People. PLoS One. 2015 Oct 21;10(10):e0141229.

[2] Baron-Cohen S. et al. The autism-spectrum quotient (AQ): evidence from Asperger syndrome/high-functioning autism, males and females, scientists and mathematicians. J Autism Dev Disord. 2001 Feb;31(1):5-17.

[3] 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.

[4] Westwood H. et al. Using the Autism-Spectrum Quotient to Measure Autistic Traits in Anorexia Nervosa: A Systematic Review and Meta-Analysis. Journal of Autism and Developmental Disorders. 2015; Nov 5.

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Westwood, H., Eisler, I., Mandy, W., Leppanen, J., Treasure, J., & Tchanturia, K. (2015). Using the Autism-Spectrum Quotient to Measure Autistic Traits in Anorexia Nervosa: A Systematic Review and Meta-Analysis Journal of Autism and Developmental Disorders DOI: 10.1007/s10803-015-2641-0

Autoimmune disease risk and eating disorders

"We were set up. The cops were waiting for us."

"We observed an association between eating disorders and several autoimmune diseases with different genetic backgrounds. Our findings support the link between immune-mediated mechanisms and development of eating disorders".

So said the paper by Anu Raevuori and colleagues [1] (open-access) based on an analysis of over 2300 people "treated at the Eating Disorder Unit of Helsinki University Central Hospital between 1995 and 2010" compared with nearly 10,000 control participants (so yes, this was quite a well-powered study).

The Raevuori paper is open-access but if you want a few choice details, here goes...

• Based on a body of research literature looking at a possible association between eating disorders and autoimmune conditions like type 1 diabetes [2], authors set about testing the hypothesis on a large scale on whether "the risk of autoimmune diseases would be increased in individuals with eating disorders both prior and after the onset of the treatment for an eating disorder".
• Having already mentioned how large a scale the authors' participants groups were, various eating disorder diagnoses were confirmed based on ICD-10 criteria [3] and both research and control populations were assessed for some 30 autoimmune conditions based on existing hospital discharge registry. "Period and lifetime prevalences" were calculated from the data. 
• Results: "Participants with BN [bulimia nervosa] made up the largest patient group (54.0%), followed by those with AN [anorexia nervosa] (38.8%), and those with BED [binge eating disorder] (7.3%)". Over 5% of those diagnosed with an eating disorder had been diagnosed with one or more autoimmune conditions compared with just under 3% of controls when it came to looking at period prevalence (at the onset of treatment). Long quote coming up... "The risk of prior diagnosis of endocrinological autoimmune diseases (OR 3.3, 95% CI 2.4–4.6, P<0.001), of gastroenterological immune-mediated diseases (OR 2.0, 95% CI 1.3–3.1, P = 0.002), and of autoimmune diseases combined (OR 2.1 95% CI 1.7–2.7, P<0.001) was significantly higher among patients than among matched controls".
• With regards to lifetime prevalence (over the whole study period) "8.9% (N = 209) of patients and 5.4% of control individuals (N = 509) had ever been diagnosed with one or more autoimmune disease". 

Whilst only looking like a relatively small percentage difference in the rates of autoimmune conditions between the groups, it is the scale of the Raevuori study in terms of participant numbers which gives the data some 'edge'. As the authors also note, their use of the category BED - binge eating disorder - is also another plus to their study given it's recent inclusion into DSM-5 (see here).

As I always seem to be about papers mentioned on this blog, I was really quite interested in the results presented by Raevuori et al and their potential implications for how we describe eating disorders and the potential mechanisms involved in onset. Research into autoimmune conditions has recently been producing some rather important associations as per my covering of things like a [possible] link between autoimmune disorders following trauma and PTSD (see here) and even a suggested connection with some epilepsy (see here).

Raevuori and colleagues discuss several pertinent mechanisms potentially linking their findings including the ever-present issue of inflammation and: "Pro-inflammatory cytokines and antibodies/autoantibodies against neuronal antigens". They also mention some possible role for "intestinal microflora contributing to the development of cross-reactive neuronal autoantibodies [providing] a link between gut and brain" and the growing fascination with all-things gut microbiome. Their finding of a greater frequency of the inflammatory bowel disease (IBD), Crohn's disease in their eating disorder cohort offers some evidence for this assertion as a function of the growing interest in gut bacteria and IBDs [4].

Without hopefully going too far off tangent from the Raevuori paper, I started to think about how these results might also fit in with some of the research done on autism and whether there may be a bigger picture here. Eating disorders have been mentioned alongside the label autism quite a few times in the research literature [5]. My previous discussions on signs of autism in cases of eating disorders (see here) is one example. Likewise, autoimmune conditions and autism also seem to have something of a connection (see here) alongside presented data on markers of autoimmunity in cases of autism (see here and see here). One can perhaps see how the various elements - immune function, inflammation, gut bacteria, gut permeability? - might be intertwined, albeit in a rather complex fashion...?

Music then, and Naive by The Kooks.

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[1] Raevuori A. et al. The increased risk for autoimmune diseases in patients with eating disorders. PLoS One. 2014 Aug 22;9(8):e104845.

[2] Young V. et al. Eating problems in adolescents with Type 1 diabetes: a systematic review with meta-analysis. Diabet Med. 2013 Feb;30(2):189-98.

[3] Herpetz S. et al. The Diagnosis and Treatment of Eating Disorders. Dtsch Arztebl Int. Oct 2011; 108(40): 678–685.

[4] Manichanh C. et al. The gut microbiota in IBD. Nat Rev Gastroenterol Hepatol. 2012 Oct;9(10):599-608.

[5] Huke V. et al. Autism spectrum disorders in eating disorder populations: a systematic review. Eur Eat Disord Rev. 2013 Sep;21(5):345-51.

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Raevuori A, Haukka J, Vaarala O, Suvisaari JM, Gissler M, Grainger M, Linna MS, & Suokas JT (2014). The increased risk for autoimmune diseases in patients with eating disorders. PloS one, 9 (8) PMID: 25147950

Signs of autism in eating disorders?

To mention 'food and autism' in the same sentence can conjure up images of quite a few associations made in the peer-reviewed research literature over the years. You have for example, the growing body of work talking about how certain dietary interventions might be useful for some people on the autism spectrum (see here) and all the accompanying science on potentially why which seems to follow (see here).

Your differential analyser or mine? @ Wikipedia 

In another vein, issues with food and feeding behaviours, present in quite a few cases of autism, represent a far more practical issue to contend with; something which I've talked about before on this blog (see here).

Outside of the various sensitivities to things like taste, texture and smell which can affect a person's relationship with food (see here for a great overview* with autism in mind), questions are being asked about whether there may be more pathological issues to contend with as a result (see here**). I refer readers to the question asked by Prof. Gillberg 30 years ago on whether autism and familial anorexia might be linked (see here).

With this in mind, and slightly reversing the nature of any relationship, I want to discuss the paper by Baron-Cohen and colleagues*** (open-access) which suggested that females diagnosed with anorexia nervosa (AN) might being more likely to present with a cognitive style reminiscent of that seen in autism. Quite a nice overview of the study and its findings can be found here and due credit should be given to the article by Clare Allely which recently appeared in The Psychologist.

In essence (no, not that ESSENCE) we are talking about a group of adolescent females diagnosed with AN (n=66) compared with a control group of similarly aged young women without AN (n=1609). Based on the previous work looking at empathising and systemising (see here) styles in autism, participants completed questionnaires (EQ --- SQ-R --- AQ) to report on these attributes.

The results: "As predicted, the patients with anorexia has a higher AQ and SQ". In other words, the distribution of AN cases scoring higher on the AQ (see here for some more chatter about this instrument) was greater than that seen in the non-AN controls (see Figure 1 of the paper here). Ergo, more autistic traits in the AN group as per earlier research****. That also the AN group seemed to be better systemisers was another finding.

Whilst I have had my doubts about some of the earlier manifestations of the whole empathising-systemising theory (think the sweeping generalisations of Theory of Mind and autism) I have to say I am really interested in these recent results. I note also that another review study looking at the presence of autism in eating disorder populations***** likewise suggests that this might be a relationship which requires much further investigation.

If I had to throw a few spanners into the works outside of the study limitations already talked about by the authors, it would have to be that we should be cautious of making too many over-generalisations from this work. The recent 'mixed' findings by Courty and colleagues****** need to be considered. Although I am not an expert on eating disorders, it's still possible that we might also consider some shared comorbidity outside of autism as potentially accounting for some of the results at least in a sub-group. So for example, are features such as anxiety or obsessionality potential links between AN and the autism spectrum disorders particularly when talking about being better systemisers? The paper by Morsanyi and colleagues******* might be relevant here: [the systemising quotient] "was correlated with statistics-related attitudes, self-efficacy, and anxiety". I tip my hat also to the findings reported by Coombs and colleagues********. I'd also like to see more data on whether the described relationship between eating disorders and autistic traits holds for other kinds of eating disorders such as bulimia too?

Without also wishing to cause any offence, I do wonder about these results potentially being extended following in the tracks of the Gillberg letter. Take for example the paper by Grove and colleagues********* who talked about the empathising-systemising results being extended to other family members where autism is present. Does this therefore imply that we should be thinking about eating disorders potentially being more prevalent in other family members where autism is present? Indeed should we consider the possibility that the presence of a maternal (or paternal) eating disorder could be [another] subsequent risk factor for offspring autism?

To close, an Elvis track for you... His Latest Flame. I'd also like to mark the passing of David Barker (see here for his obituary) and his insightful contribution to science discussed in an earlier post (see here) which in an odd sort of way might also be relevant to today's discussions.

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* Cermak SA. et al. Food selectivity and sensory sensitivity in children with autism spectrum disorders. J Am Diet Assoc. 2010 February; 110(2): 238–246.

** Råstam M. et al. Eating Problems and Overlap with ADHD and Autism Spectrum Disorders in a Nationwide Twin Study of 9- and 12-Year-Old Children. Scientific World Journal. 2013; 2013: 315429.

*** Baron-Cohen S. et al. Do girls with anorexia nervosa have elevated autistic traits? Mol Autism. 2013; 4: 24.

**** Hambrook D. et al. Empathy, systemizing, and autistic traits in anorexia nervosa: a pilot study. Br J Clin Psychol. 2008 Sep;47(Pt 3):335-9. doi: 10.1348/014466507X272475.

***** Huke V. et al. Autism spectrum disorders in eating disorder populations: a systematic review. Eur Eat Disord Rev. 2013 Sep;21(5):345-51.

****** Courty A. et al. Levels of autistic traits in anorexia nervosa: a comparative psychometric study. BMC Psychiatry. 2013 Sep 10;13(1):222.

******* Morsanyi K. et al. Are systemizing and autistic traits related to talent and interest in mathematics and engineering? Testing some of the central claims of the empathizing-systemizing theory. Br J Psychol. 2012 Nov;103(4):472-96.

******** Coombs E. et al. An investigation into the relationship between eating disorder psychopathology and autistic symptomatology in a non-clinical sample. Br J Clin Psychol. 2011 Sep;50(3):326-38.

********* Grove R. et al. Empathizing, systemizing, and autistic traits: latent structure in individuals with autism, their parents, and general population controls. J Abnorm Psychol. 2013 May;122(2):600-9.

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Baron-Cohen S, Jaffa T, Davies S, Auyeung B, Allison C, & Wheelwright S (2013). Do girls with anorexia nervosa have elevated autistic traits? Molecular autism, 4 (1) PMID: 23915495