"Social cognitive deficits are present in a wide range of clinical conditions"

Happy New Year!

Welcome to Questioning Answers 2018-style. Let's continue...

Today I'm bringing to your attention the findings reported by Jack Cotter and colleagues [1] who concluded that: "social cognitive deficits appear to be a core cognitive phenotype of many clinical conditions."

Social cognitive issues defined as "mental operations that underlie social interactions" and "includes a range of cognitive processes that help individuals to understand how others think and feel" are something not unknown to the core subject of this blog: autism. Indeed, Cotter et al mention how the "most heavily researched aspects of social cognition are emotion recognition and theory of mind (ToM)." Right or wrong, ToM in particular, has had quite a significant influence on autism research and thought down the years (see here).

Cotter and colleagues "sought to collate existing meta-analytic data on social cognitive performance among individuals with a range of clinical conditions" on the basis that whilst the label of autism has received the lion's share of research interest, social cognitive issues perhaps span a far wider range of labels/conditions. They scoured the peer-reviewed literature and identified some 31 meta-analyses published that "examined performance on facial emotion recognition (24 papers) and/or ToM tasks (24 papers) among 30 different clinical populations relative to controls." The sorts of clinical populations identified ranged from psychiatric disorders such as psychosis and schizophrenia, to neurological disorders such as epilepsy and traumatic brain injury to developmental disorders such as attention-deficit hyperactivity disorder (ADHD) and intellectual (learning) disability.

Their conclusions: "Though these results do not provide directly comparable estimates between clinical conditions, they provide a robust indication that social cognitive deficits appear to be a core cognitive phenotype of many developmental, neurological and psychiatric disorders." The authors go on to discuss how, on the basis of their findings, social cognitive issues (impairment) might be "a general biomarker indicative of neurological abnormality" more generally; also, in some contexts, providing information on the 'progression' of a particular condition.

In these days of ever-blurring labels and conditions, where comorbidity is proving to be the rule rather than the exception [2] (see here also), there is common sense in the Cotter findings. Sense, insofar as the idea that no one diagnostic label has generally got a monopoly on a particular behaviour and/or symptom and that social cognitive issues might be 'core' to quite a few conditions. A greater appreciation of such an idea could potentially impact, in many different ways, on what we think about many seemingly different psychiatric, developmental and neurological labels. A few stand-out points include: (a) a reiteration of how nonsensical the term 'neurotypical' is from a social cognitive perspective when describing 'not-autism' (see here); (b) a further illustration of the value of a professional assessment as and when something like autism is suspected, rather than just a reliance on brief 'are you autistic?' questionnaires that tend to rely heavily on social cognition as a 'symptom' (see here); and (c) investigation into whether or not important biological 'issues' thought to accompany social cognitive 'issues' could also be quite wide-ranging among many conditions/labels (see here for some discussion on the concept of inflammation for example).

And since we're on the topic of grand, sweeping psychological concepts spanning different conditions, how about the idea that executive function issues might also cross labels [3] too...

Stay tuned for more in 2018.

----------

[1] Cotter J. et al. Social cognitive dysfunction as a clinical marker: A systematic review of meta-analyses across 30 clinical conditions. Neuroscience & Biobehavioral Reviews. 2018; 84: 92-99.

[2] Posserud M. et al. Autism traits: The importance of “co-morbid” problems for impairment and contact with services. Data from the Bergen Child Study. Research in Developmental Disabilities. 2018; 72: 275-283.

[3] Carter Leno V. et al. Testing the specificity of executive functioning impairments in adolescents with ADHD, ODD/CD and ASD. Eur Child Adolesc Psychiatry. 2017 Dec 9.

----------

"the importance of considering how autism acceptance could contribute to mental health in autism"

The quote heading this post comes from the findings reported by Eilidh Cage and colleagues [1] (open-access) who sought to examine how "experiences and perceptions of autism acceptance could impact on the mental health of autistic adults."

Using an on-line survey "to test the relationship between perceived autism acceptance and mental health (specifically, depression, anxiety and stress)" findings are reported based on responses from over 110 people diagnosed as on the autism spectrum. I say 'diagnosed as on the autism spectrum' but as with any internet survey, there is always a degree of 'trust' that autism diagnoses are being reported faithfully just as it is with other labels that were under study: "a high proportion of participants reported additional diagnoses." Indeed, I also note that "11 participants reported that they did not currently have a formal diagnosis of autism" and were still included in some of the analyses...

No mind, the authors sought to 'quantify' autism acceptance given no measure currently exists by asking various questions including "whether they felt that society (specified as the general public, made up of people who did not personally know them) generally accepted them, with “yes”, “no”, “sometimes” and “prefer not to say” as response options." Responses were also sought to statements such as "over the past week, I have felt accepted by society as an autistic person/person with autism" and onward "perceptions of autism acceptance from different sources." This was complemented by responses to the Depression, Anxiety and Stress Scale (DASS-21).

Results: "depression was predicted by autism acceptance from external sources (society, family and friends) and personal acceptance" but anxiety was not seemingly *linked* to autism acceptance. Drilling down further into their results, researchers observed that "greater personal autism acceptance predicted lower depressive symptoms" indicating that variables such as self-esteem might mediate any risk of presenting with depressive signs and symptoms [2] (see here for my take). This is something that perhaps tallies with other research talking about autistic traits and wellbeing [3].

The author has also written a piece for The Conversation on her research study (see here).

I'm not quite sure why the ever-fluffy psychological concept of 'Theory of Mind' (ToM) needed to be introduced into the Cage paper given that no measure of ToM was actually included in the study. A quick search of other published research from these authors reveals that ToM is a feature there too [4]. The authors talk about how "Theory of Mind ability may impact on perceptions of autism acceptance" but I'm not so sure that this is particularly important. It's kinda like suggesting that society is completely autism aware and accepting/accommodating but those on the spectrum 'don't seem to understand it' as a result of any ToM issues, which is of course, a nonsense. ToM also still requires a bit more investigation into what it actually means and covers (see here) including the idea that issues with ToM might themselves be 'impaired' as a result of something like depression (see here). I'd also point out that quite a few other over-represented diagnoses potentially appearing alongside autism also seem to present with ToM issues [5] too...

"There is still a long way to go in understanding and tackling the high prevalence of mental health difficulties in autism, but we believe that the social model approach is a useful and positive lens through which mental health outcomes could be improved." That was the conclusion reached by authors on the basis of their findings. I would agree that there is still a long way to go on the topic of mental health and autism and the social model approach - "disability is caused by the way society is organised, rather than by a person’s impairment or difference" - is an option for further research of this kind. But I would also caution that one needs to balance such a perspective with others too (see here), and accept that the organisation of society is not always the most disabling aspect of a person's disability, particularly when it comes to something like depressive symptoms. Indeed, to say that depressive symptoms accompanying autism might merely be a facet of a 'lack of acceptance' or a lack of understanding from society or the individual themselves, risks plunging autism back into some pretty dark times (see here) and is likely to conflict with various other views. From a clinical point of view, it ignores some very serious research on the wide spectrum that is depression potentially present for all-manner of different reasons, being relevant to the equally wide spectrum that is autism (see here for a discussion on how depression might actually be something rather more fundamental to some autism over just being 'comorbidity'). At worst, it may even delay or put people off from seeking timely recognised treatments when depression becomes 'clinical', which could be a rather dangerous path to start down (see here).

Having said all that, I don't however think too many people would argue with the idea that personal perception(s) whether positive or negative are likely to impact on a person's mental (and physical?) health and wellbeing. If one is constantly feeling like an 'outsider' or excluded or feels that ones needs are not being met, added to a possible history of being bullied or loneliness or indeed, with other clinical labels also potentially being present for example, one is likely to build up a mindset appropriate to such a situation which probably includes some advanced risk for depressive signs and symptoms. From that point of view, much more needs to be done to look at the ways and means of impacting those personal perceptions; possibly taking into account other relevant research which has some [evidence-based] suggestions on things like societal inclusion and increasing access to it (see here) for those who want this option, alongside other complementary strategies where some [peer-reviewed] evidence is present (see here) and continues to be produced (Google the 'HUNT Cohort Study' to see what I mean). I say all this reiterating that something like chronic loneliness can very much be a major contributor to issues like depression.

I also understand the calls to make society more autism-accepting which I think most people would support as being pertinent across the ENTIRE autism spectrum (see here). I'm however, a little unsure of the real-life plan and details of the plan attempting to achieve this goal; particularly in the current climate when even getting a timely diagnosis seems to be an uphill struggle and when also many on the autism spectrum are seemingly left to fend for themselves post-diagnosis. Society it seems, is getting much more autism aware (for good or bad based on current media portrayals for example) but not necessarily getting more autism accommodating nor necessarily putting important words into actions. Indeed, one could argue that other societal factors like unemployment and financial hardship readily experience by those with autism are probably as, if not more, important to their experiences of something like depression yet little appears to be done to improve such issues for the vast majority...

As for the "experiences of “camouflaging” [that] could relate to higher rates of depression" also mentioned in the Cage article, I have quite a lot of time for this area of autism research (see here). Particularly the idea that camouflaging is not necessarily an all-female pursuit in the context of autism (see here) and how truly energy-sapping it can be for many, many people on the spectrum...

----------

[1] Cage E. et al. Experiences of Autism Acceptance and Mental Health in Autistic Adults. J Autism Dev Disord. 2017. Oct 25.

[2] McCauley JB. et al. Self-Esteem, Internalizing Symptoms, and Theory of Mind in Youth With Autism Spectrum Disorder. J Clin Child Adolesc Psychol. 2017 Oct 19:1-12.

[3] Rodgers JD. et al. Brief Report: Personality Mediates the Relationship between Autism Quotient and Well-Being: A Conceptual Replication using Self-Report. J Autism Dev Disord. 2017 Sep 16.

[4] Cage E. et al. Reputation management: evidence for ability but reduced propensity in autism. Autism Res. 2013 Oct;6(5):433-42.

[5] Wang Y-Y. et al. Theory of mind impairment and its clinical correlates in patients with schizophrenia, major depressive disorder and bipolar disorder. Schizophrenia Res. 2017. Nov 7.

----------

"Are we expecting too much from the extreme male brain theory of autism?"

The title of this post reflects the commentary published by Andrew Whitehouse [1] (open-access) discussing the meaning of the findings reported by Kung and colleagues [2] who quite categorically stated that there was: "No relationship between prenatal androgen exposure and autistic traits" in their study.

OK, androgen exposure and psychology basically refers to the extreme male brain theory and autism which suggests that the so-called over-representation of autism in males is potentially down to hormone exposure (testosterone). The theory implies that androgen exposure at critical points in early development are skewing brain development towards a more 'male brain'. The definition of a male brain: well, apparently men are better systemisers than empathisers (better engineers that priests, I assume). The extreme male brain (EMB) hypothesis is an extension of the 'Theory of Mind' (ToM) stuff, which quite a few years back suggested that those diagnosed as being on the autism spectrum have greater difficulties in decoding mental states such as intents and desires. Grand psychological theories at their very finest you might say.

The problem is that whilst ToM and the EMB theory made great psychological textbook reading (certainly in their heyday between the mid-1980s up to the late 1990s) and have spawned a whole industry around testing and teaching ToM for example, the scientific evidence for these concepts being exclusively and universally attributable to the great heterogeneity that is autism is not actually all that great. A shocker I know; and don't even ask about how comorbidity around autism might also be pretty important to such psychological concepts (see here and see here for example).

Whitehouse - who himself has done some research in this area - talks quite a bit about the hows and whys of quite a few negative findings when it comes to the EMB theory (yes, there are quite a few) and what perhaps needs to be done to "advance beyond this stalemate" in relation to the EMB theory and autism.  His suggestion: "future research must first understand how the prenatal hormone environment relates to individual behavioural dimensions, and then incorporate this knowledge into the investigation of links with the more aetiologically and phenotypically complex profile of ASD [autism spectrum disorder]."

These are wise words indeed but I'd suggest this perhaps applies to any 'theory' in relation to autism, psychological, biological or genetic. Indeed, I believe that other authors (see here) have already staked their claim on how using the word 'autism' as a starting point for anything other than a descriptive label probably isn't going to move autism research along any time soon; autisms people, autisms. The challenge is also one of moving away from generalisations; so talking about male and female brains is probably about as useful as talking about left and right-sided brains. Indeed, I'll refer you to some discussions about 'gender brains' between the main proponent of the EMB theory and a psychologist a few years back (see here and see here) that kicked up some scientific dust.

I personally do think there is something in the findings looking at androgen levels and cognitive styles in the same way that there is something in most (replicated) peer-reviewed research when it comes to autism. But as Prof. Whitehouse indicates, it's probably going to be more relevant to some on the autism spectrum than others, and even then, disentangling the 'cognitive' structure of autism is going to be important [3]. The days of grand over-arching psychological theories about autism do seem to be riding off into the scientific sunset as the huge diversity and 'burden' of over-represented comorbidity start to come into plain sight. And certainly I don't think it's too rude to end with the words 'about time too'.

To close, I hark back to simpler days or should that be to a simpler future when Buck Rogers showed the 25th Century how to boogie. Tell him what you think Twiki.

----------

[1] Whitehouse AJO. Commentary: Are we expecting too much from the extreme male brain theory of autism? A reflection on Kung et al. (2016). J Child Psychol Psychiatry. 2016 Dec;57(12):1463-1464.

[2] Kung KT. et al. No relationship between prenatal androgen exposure and autistic traits: convergent evidence from studies of children with congenital adrenal hyperplasia and of amniotic testosterone concentrations in typically developing children. J Child Psychol Psychiatry. 2016 Dec;57(12):1455-1462.

[3] Happé F. et al. Time to give up on a single explanation for autism. Nat Neurosci. 2006 Oct;9(10):1218-20.

----------

Whitehouse AJ (2016). Commentary: Are we expecting too much from the extreme male brain theory of autism? A reflection on Kung et al. (2016). Journal of child psychology and psychiatry, and allied disciplines, 57 (12), 1463-1464 PMID: 27859346

Humour training for autism - is it needed and is it useful?

Can we and should we formally 'teach' humour to people diagnosed on the autism spectrum? Indeed, do we actually need to?

Yes said the results of the study published by Ching-Lin Wu and colleagues [1] although I personally am not so impressed.

Discussing how their results "supported the effectiveness of the 15-hour training" regime, Wu et al report that for a small group of adolescents diagnosed with an autism spectrum disorder (ASD) "and average intelligence" moves to implement "a humor-knowledge and humor-skill training workshop" seemed to impact on responses to a questionnaire covering joke appreciation and comprehension. They conclude by saying that "the appreciation of humor can be learned." This is not the first time that this group have looked at humour with autism in mind [2].

I don't disagree with the idea that humour is at least in part, a learned concept. How else does one come to appreciate the blunders of Alan Partridge ('raining cows') or the delivery of the Two Ronnies ('folk handles or four candles')? But the suggestion that humour needs to be specifically taught to those on the autism spectrum makes a number of sweeping assumptions.

First, it assumes that humour is 'missing' or somehow 'incomplete' when it comes to autism, all autism. As per historical sweeping generalisations on the now 'not typically discussed' issue of Theory of Mind (ToM), the 'mentalising' issues are for example, assumed to curb aspects of understanding behaviour including humour. As we've come to recognise however, issues with ToM are not universally present in autism and indeed, may not be specifically linked to the word 'autism' at all (see here). Insofar as the notion of 'missing humour' when it comes to autism, both peer-reviewed science [2] and quite a lot of anecdote suggest that this may not be typical. Indeed, even those who are quite profoundly autistic and with varying degrees of related learning disability, are not devoid of humour or an appreciation of humour (or mischief!).

Second, can you teach humour? This is a rather nebulous question because humour comes in many different forms. Yes, you can teach someone about the use of words and how words can be humorous ('velcro: what a rip off'), you can even teach someone how to appreciate a particular joke or set of jokes. But can you actual teach someone to think/believe that something is humorous or not or is this just some sort of artificial learned response? I always thought humour was something fairly individual; one person's humour is another person's 'not so funny'. The added question of how one goes about measuring a person's 'humour rating' is something else that I might throw in the mix in these days of evidence-based practice (something that I doubt is going to measured just by a questionnaire).

As you can see, I'm not overly impressed with the ideas that humour is missing or needs to be taught when it comes to autism. I'm not adverse the idea that teaching/training can help with some aspects of humour when it comes to language for example, but I'd like to think there are much easier and more 'natural' ways of picking up humour as per the focus on friendships and peer group involvement when it comes to autism. Indeed, in the age of the internet where humour/comedy is just a click away, the idea of spending 15 hours in 'humour-skill training' would probably be better spent scouring the internet comedy vaults for something a little more specific to the wants and wishes of that person...

To close, I've already linked to one of my favourite comedians, Tim Vine, but here is a little more...

----------

[1] Wu C-L. et al. Effectiveness of humor training among adolescents with autism. Psychiatry Research. 2016. Sept 13.

[2] Wu C-L. et al. Do individuals with autism lack a sense of humor? A study of humor comprehension, appreciation, and styles among high school students with autism. Research in Autism Spectrum Disorders. 2014; 8: 1386-1393.

----------

Wu, C., Liu, Y., Kuo, C., Chen, H., & Chang, Y. (2016). Effectiveness of humor training among adolescents with autism Psychiatry Research DOI: 10.1016/j.psychres.2016.09.016

"Theory of mind is not theory of emotion"

A rather interesting paper by Beth Oakley and colleagues [1] (open-access might be available here) appeared recently providing a "cautionary note on the Reading the Mind in the Eyes Test" [2], one of the premier assessments thought to offer a performance-based measure "involving mental state attribution and complex facial emotion recognition from photographs where only the eye region of the face is available."

Most people with some knowledge about autism research history will have heard about the proposal that Theory of Mind (ToM) - a term often used to cover that "mental state attribution" - might be affected in cases of autism (see here) and indeed, how careers and reputations have been made on such a generalisation. These days ToM is less and less being talked about as the heterogeneity of the autism spectrum becomes better understood and how specificity in particular, has proved to be an Achilles' heel for the concept (see here).

One of the emerging ideas to account for some of the results obtained using the Reading the Mind in the Eyes test (RMET) in cases of autism is that alexithymia - a construct characterised by an inability to describe or understand emotions - might actually be the more important issue than autism per se. The idea being that alexithymia can co-occur alongside some autism and that for those presenting with that combination, ToM and assessments like RMET might be problematic.

So Oakley et al delved a little deeper into some of the hows and whys of some of the RMET results obtained with autism in mind and whether "the RMET indexes emotion recognition, associated with alexithymia, or ToM, associated with ASD [autism spectrum disorder]." They did it on the basis of examining a small group of participants diagnosed with an ASD (n=19) alongside 24 participants without autism. Alexithymia was assessed using "the 20-item Toronto Alexithymia Scale (TAS–20)." Autism symptoms severity was measured using the Autism Spectrum Quotient (50) (oh dear..) and "current functioning" in the autism group was assessed using the gold-standard that is the Autism Diagnostic Observation Schedule (ADOS) (more like it).

Results: well bearing in mind the small participant numbers and the need for further independent replication of the findings, "Reading the Mind in the Eyes Test (RMET) performance was unaffected by autism spectrum disorder... but was negatively impacted by alexithymia." Indeed, we are told that: "Six ASD and eight control participants met the criterion for severe alexithymia, with a score of 61 or above on the 20-item Toronto Alexithymia Scale (TAS–20)." Further: "in individuals with ASD and comorbid alexithymia, it is alexithymia, rather than ASD per se, that impairs emotion recognition performance."

I probably don't need to say too much more about this line of research and its important implications outside of perhaps the requirement to screen for alexithymia as and when autism is diagnosed. Insofar as the idea of an "alexithymia hypothesis of emotion-related deficits in ASD", this does sound like a tantalising option but again, I'd be slightly reluctant to go all-in with yet another grand theory for autism given the trials and tribulations that psychological theories in particular have faced over the years with autism in mind. As to other potential impacts from work such as this, well, assertions that a lack of empathy might the root of all evil (see here) also made by proponents of ToM might do well to take on board a role for alexithymia in any future judgements...

Minus any charges of plagiarism, I leave you with the general summary from Oakley and colleagues:

"This study suggests that a highly popular test of the ability to detect what someone else is thinking—the Reading the Mind in the Eyes Test—is instead a test of the ability to recognize another person’s emotional expression. This is important because it suggests that patients who perform badly on this test may still be able to understand another person’s mental state and that, conversely, patients who perform well on this test may still have difficulties in mental state understanding."

----------

[1] Oakley BF. et al. Theory of mind is not theory of emotion: A cautionary note on the Reading the Mind in the Eyes Test. J Abnorm Psychol. 2016 Aug;125(6):818-23.

[2] Baron-Cohen S. et al. The “Reading the Mind in the Eyes” Test: Complete Absence of Typical Sex Difference in ~400 Men and Women with Autism. PLoS ONE. 2015; 10(8).

----------

Oakley BF, Brewer R, Bird G, & Catmur C (2016). Theory of mind is not theory of emotion: A cautionary note on the Reading the Mind in the Eyes Test. Journal of abnormal psychology, 125 (6), 818-23 PMID: 27505409

Big names coming around to 'neuroinflammation' and autism?

I won't keep you too long today as I bring the paper by Adam Young and colleagues [1] (open-access available here) to your attention and some discussions around the concept of inflammation and autism. To quote: "An emerging focus of research into the aetiology of ASC [autism spectrum condition] has suggested neuroinflammation as one candidate underlying [the] biological model."

Including one Simon Baron-Cohen on the authorship list, I have to say that I was impressed to see this quite comprehensive review of the peer-reviewed literature covering "the mechanisms that may underlie neuroinflammation and the evidence at genetic and protein levels for each of these mechanisms." The authors concluded that whilst there are some important gaps to be filled in the research literature in this area - "the greatest area of weakness in the field is that in general, the findings tend to be from individual studies and rarely are these replicated" - to mention 'inflammation' and 'autism' in the same sentence is no longer 'crazy talk'.

I've discussed quite a bit about inflammation and autism on this blog down the years. Personally, I've seen and read enough (peer-reviewed) papers on the topic to form an opinion that for at least some on the autism spectrum ('autisms' people, autisms) there is an overwhelming case for much more detailed investigation in this area. If you don't believe me, well, take a look at some of the science and form your own opinion (see here and see here for example). And when I say that some of the genetics of 'some' autism might also implicate inflammation and inflammatory processes too (see here), there appears to be something for everyone in the field.

One area that I would like to see more study on (aside from what science can potentially do when inflammation runs amok) is inspection of the interplay between genetic and biological factors pertinent to inflammation/inflammatory processes and behaviour and psychology. We've already had some hints down the years about how inflammation might 'affect' things like social cognitive processing (see here) including mention of a concept not unfamiliar to Prof. Baron-Cohen - Theory of Mind (ToM) - and potentially pertinent to autism. I'd like to see much more investigation on whether for example, cyclical patterns of inflammation might correspond to some of the cyclical patterns of behaviour noted in some on the spectrum. This set against the idea that some of the contents of the medicine cabinet already applied to some cases of autism might have some relevant actions on facets of immune function overlapping with inflammation and inflammatory processes (see here). Much more research is indicated.

Oh, and since we are on the topic of neuroinflammation and autism, I'd also suggest you having a look at the recent review from Janet Kern and colleagues [2] (open-access) too. They've also included some important mention of anti-NMDA-receptor encephalitis and autism (see here) which I'm particularly interested in...

Music: Me First and the Gimme Gimmes - My Heart Will Go On. Please, give the song a chance...

----------

[1] Young AM. et al. From molecules to neural morphology: understanding neuroinflammation in autism spectrum condition. Mol Autism. 2016 Jan 20;7:9.

[2] Kern J. et al. Relevance of Neuroinflammation and Encephalitis in Autism. Front Cell Neurosci. 2016 Jan 19;9:519.

----------

Young AM, Chakrabarti B, Roberts D, Lai MC, Suckling J, & Baron-Cohen S (2016). From molecules to neural morphology: understanding neuroinflammation in autism spectrum condition. Molecular autism, 7 PMID: 26793298

Theory of mind and major depressive disorder

Today I'm briefly serving up the paper by Emre Bora & Michael Berk [1] for your daily reading and the results of their meta-analysis stating that: "Theory of mind abilities are impaired during depression."

Based on data derived from 18 studies covering over 600 participants diagnosed with major depressive disorder (MDD) and over 500 asymptomatic controls, the Bora/Berk paper suggests that there may be much more to see when it comes to the psychological processes of attributing mental states and the myriad of presentations covered under the banner of depression.

Whilst I am interested in the label of depression on this blog (see here and see here for example) my reasoning for discussing this specific paper is slightly broader; namely in the context of how theory of mind (ToM) has waxed and waned specifically with autism in mind (see here). If one considers that depression shows more than a passing connection to quite a lot of autism (see here) or indeed, some of the somatic comorbidity talked about with autism in mind (see here), one might see a way whereby some of the historical scientific discussions about ToM and autism may have neglected the role of some quite important comorbidity. I say all this in the context that the label of autism rarely appears in some sort of diagnostic vacuum (see here) as per discussions on [its] ESSENCE (see here).

One other area of interest that I'd like to bring to your attention that might 'unite' some of the findings regarding ToM and autism and depression, is the idea that biological processes may play an important role in any relationship. Take for example the interesting data coming out in the peer-reviewed domain suggesting that inflammation or inflammatory process may affect important psychological processes such as social cognition as per the findings from Moieni and colleagues [2] (see here for my take). Inflammation and [some] autism y'say? Inflammation and [some] depression? Well, let's just to say that I don't think anyone is in a position to rule anything out at the moment (see here and see here respectively).

Music: Grace - You Don't Own Me.

----------

[1] Bora E. & Berk M. Theory of mind in Major Depressive Disorder: A meta-analysis. Journal of Affective Disorders. 2015. Nov 23.

[2] Moieni M. et al. Inflammation impairs social cognitive processing: A randomized controlled trial of endotoxin. Brain, Behavior, and Immunity. 2015. May 10.

----------

Bora, E., & Berk, M. (2015). Theory of mind in Major Depressive Disorder: A meta-analysis Journal of Affective Disorders DOI: 10.1016/j.jad.2015.11.023

Stalking and 'unexpected subthreshold autism spectrum'

I deliberated for quite a while as to whether or not I should write this post on the back of the findings reported by Liliana Dell’Osso and colleagues [1] detailing the experiences of a "25-year-old man with a diagnosis of delusional disorder, erotomanic type" who was hospitalised when presenting with psychotic symptoms "in the framework of a repeated stalking behavior towards his ex girlfriend." Said man was assessed for "adult autism spectrum symptoms" via the Ritvo Autism and Asperger Diagnostic Scale (RAADS-14) and came out with something approaching autism spectrum symptoms.

My blogging hesitancy was in the most part due to the risk of stigmatising and generalising on the basis of the words 'stalking' and 'autism' appearing in the same sentence even in the context of a case report and not necessarily including a formal diagnosis of autism. I'd like to make it very clear that this is/was not my intention at all. As in previous occasions when science has been covered on this blog that falls into a slightly uncomfortable area (see here and see here) I did however eventually choose to cover this topic on the basis that [peer-reviewed] science is science irrespective of particular emotions around topics.

Stalking - the unwanted or obsessive attention by an individual or group toward another person - is a life-changing experience that has profound effects on its victims. The precise hows and whys of stalking behaviour are still the topic of discussion, although thought to be variably mediated by social and personal factors potentially combining with other, more neurobiological processes [2]. As per the description provided in that last sentence and the use of the word 'obsessive' one might be able to see how such fixative behaviours might 'overlap' with some of the clinical description of autism or 'nearly autism' and particularly the idea that obsessions and compulsions might not be totally unfamiliar to the spectrum [3] including those around certain people.

I first came across discussions about stalking and the autism spectrum following my reading of the excellent overview by Tom Berney [4] (open-access). Describing the possible forensic presentation of Asperger syndrome, Dr Berney talked about "Overriding obsessions [that] can lead to offences such as stalking... Admonition can increase anxiety and consequently a ruminative thinking of the unthinkable that increases the likelihood of action." Anxiety and rumination, I might add, are areas crying out for more focused research with autism in mind (see here).

Other more experimental work looking at stalking in the context of autism has pointed to the possibility of an increased risk of such behaviours as per the findings reported by Stokes and colleagues [5]. They reported that individuals with autism were "more likely to engage in inappropriate courting behaviours... and were more likely to focus their attention upon celebrities, strangers, colleagues, and ex-partners... and to pursue their target longer than controls." All this is set in the context of researcher reporting on a small participant group and being based on parental reports.

Insofar as the possible basis for stalking behaviours and the autism spectrum, the paper from Haskins & Silva [6] offers several opinions external to the involvement of obsessionality centred around the idea that empathy and perspective-taking abilities may also play a role. I'm not exactly a great fan of the exclusivity of concepts such as a lack of Theory of Mind (ToM) when applied to the autism spectrum (see here) but can see the logic in this assumption linked to stalking behaviours. Indeed, with such ideas in mind, the paper from Post et al [7] on possible strategies to prevent and overcome stalking when coincidental to autism make some sense.

Just before I bring this post to a close I'd also like to comment on the idea that psychosis or psychotic behaviour might also be an important part of any link between stalking behaviour and autism. Regular readers of this blog might already know that whilst not necessarily a mainstream opinion, I do perhaps think that autism research was historically a little hasty in burning all the bridges between autism and schizophrenia (see here) particularly when it came to the work of people such as Mildred Creak and colleagues. Science is beginning to recognise that a diagnosis of autism is in no way protective against the development of psychosis (see here) and preferential regular screening might be indicated.

Analysing the possibility of a relationship between stalking behaviour, autistic traits and psychosis sounds like something that might provide some important answers particularly in the context of the recent findings from Ho and colleagues [8] talking about ToM potentially being a trait marker of schizophrenia. Again treading carefully not to stigmatise or generalise, any moves to decreasing the likelihood and impact of stalking behaviour and the often devastating consequences that it can bring should be welcomed.

----------

[1] Dell'Osso L. et al. Unexpected subthreshold autism spectrum in a 25-year-old male stalker hospitalized for delusional disorder: a case report. Compr Psychiatry. 2015 Apr 14. pii: S0010-440X(15)00054-1.

[2] Marazziti D. et al. Stalking: a neurobiological perspective. Riv Psichiatr. 2015 Jan-Feb;50(1):12-8.

[3] Russell AJ. et al. Obsessions and compulsions in Asperger syndrome and high-functioning autism. Br J Psychiatry. 2005 Jun;186:525-8.

[4] Berney T. Asperger syndrome from childhood into adulthood. Advances in Psychiatric Treatment. Aug 2004, 10 (5) 341-351.

[5] Stokes M. et al. Stalking, and social and romantic functioning among adolescents and adults with autism spectrum disorder. J Autism Dev Disord. 2007 Nov;37(10):1969-86.

[6] Haskins BG. & Silva JA. Asperger's disorder and criminal behavior: forensic-psychiatric considerations. J Am Acad Psychiatry Law. 2006;34(3):374-84.

[7] Post M. et al. Understanding stalking behaviors by individuals with Autism Spectrum Disorders and recommended prevention strategies for school settings. J Autism Dev Disord. 2014 Nov;44(11):2698-706.

[8] Ho KKY. et al. Theory of mind impairments in patients with first-episode schizophrenia and their unaffected siblings. Schizophrenia Res. 2015. June 3.

----------

Dell’Osso, L., Dalle Luche, R., Cerliani, C., Bertelloni, C., Gesi, C., & Carmassi, C. (2015). Unexpected subthreshold autism spectrum in a 25-year-old male stalker hospitalized for delusional disorder: a case report Comprehensive Psychiatry DOI: 10.1016/j.comppsych.2015.04.003

Inflammation impairs social cognitive processing

A quote to begin: "acute inflammation can lead to decreases in the ability to accurately and reliably comprehend emotional information from others."

It comes from the article published by Mona Moieni and colleagues [1] who examined a concept familiar to many people with a connection to autism either personally or professionally: Theory of Mind (ToM). Rather interestingly, Moieni et al "examined whether exposure to an experimental inflammatory challenge led to changes in ToM." Inflammatory challenge refers to the artificial induction of a state of inflammation via the use of something called endotoxin, something I've covered under another name previously on this blog (see here).

As part of a larger research project on inflammation-induced depressed mood (see here) researchers set about looking at social cognition under inflammatory-inducing and placebo conditions specifically based on the "Reading the Mind in the Eyes (RME) test". The RME test has quite a firm foundation in autism research [2]. Their results indicated that using the RME test as a sort of measure of ToM "endotoxin (vs. placebo) led to decreases in performance on the RME test from baseline to the peak of inflammatory response, indicating that acute inflammation can lead to decreases in the ability to accurately and reliably comprehend emotional information from others."

With the caveats that (a) this wasn't a study of people with autism (or at least not those diagnosed with autism) and (b) acute inflammation may not be the same as chronic inflammation, these are intriguing results potentially overlaying onto several other research areas. Autism and inflammation is something that I'm quite interested in on this blog as per the idea that physiology and psychology might not be some far apart in certain cases/types of autism (see here). That other somatic manifestations might also be linked to inflammatory processes with autism in mind (see here) is something else to mention.

I hold back from saying that all those with autism who 'fail' ToM tasks are somehow in a state of inflammation given that this is a complicated area (see here). As per my previous ramblings, I'm also not necessarily the greatest fan of the sweeping generalisations made about ToM when it comes to autism (see here). Particularly when one looks at the way that ToM is examined in relation to autism [3] and how ToM issues cross quite a few different labels [4] some of which might overlap with autism (see here).

Still, if there is the remotest possibility that the physiological state of acute inflammation might correlate with issues with mentalising or completing mentalising tasks, I'd be minded to suggest that future work on ToM might be minded to take this into account. Likewise, in all those studies looking at inflammatory processes linked to something like autism, measuring ToM before and after could represent an interesting parameter when looking at potential interventions...

Some music then... The Wedding Present and My Favourite Dress.

----------

[1] Moieni M. et al. Inflammation impairs social cognitive processing: A randomized controlled trial of endotoxin. Brain, Behavior, and Immunity. 2015. May 10.

[2] Baron-Cohen S. et al. The "Reading the Mind in the Eyes" Test revised version: a study with normal adults, and adults with Asperger syndrome or high-functioning autism. J Child Psychol Psychiatry. 2001 Feb;42(2):241-51.

[3] Iao LS. & Leekam SR. Nonspecificity and theory of mind: new evidence from a nonverbal false-sign task and children with autism spectrum disorders. J Exp Child Psychol. 2014 Jun;122:1-20.

[4] Chung YS. et al. A meta-analysis of mentalizing impairments in adults with schizophrenia and autism spectrum disorder. Schizophr Bull. 2014 May;40(3):602-16.

----------

Moieni M, Irwin MR, Jevtic I, Breen EC, & Eisenberger NI (2015). Inflammation impairs social cognitive processing: a randomized controlled trial of endotoxin. Brain, behavior, and immunity PMID: 25770082

Cord blood testosterone and autistic-like traits: no link?

Prof. Andrew Whitehouse has featured quite a bit on this blog. The most recent occasion (aside from this post) was a piece of research on maternal vitamin D status and early adult offspring scores on the Autism Spectrum Quotient (AQ) which concluded no overall link despite some interesting details. Indeed quite a bit of his work derived from the Raine study focuses on recording factors during pregnancy and the very earliest days in the big, wide world and seeing how they might relate to results like those derived from the AQ some years later. Not wholly dissimilar from the ethos behind looking at archive dried blood spots it has to be said.

Cord clamping @ Wikipedia  

In a similar vein, I want to talk about another of his papers* (open-access), this time on perinatal testosterone exposure and once again, early adult offspring AQ scores. And in particular a lack of association between the two variables and some potentially important implications for one of the more widely cited theories of how autism might come about.

I've kinda covered testosterone and autism before on this blog with reference to the finger length ratio (2D:4D), apparently quite an interesting correlate of how much testosterone we might have been swimming around in in-utero, and also more speculatively on a post on PCOS.

Most people thinking testosterone and autism are brought back to the theory posited by Prof. Simon Baron-Cohen - see one of the papers here** - extending the so-called extreme male brain (EMB) theory of autism*** itself extending the systemising/empathising sex differences**** again extending good old Theory of Mind (ToM). It's quite a logical train of thought I must admit, and probably why so many people truly do believe testosterone may show some primary connection to cases.

That being said, regular readers perhaps know that I'm not really one for sweeping generalisations when it comes to autism (see pages 949-951), no matter how much the science of psychology loves to try and compartmentalise conditions like autism. And take my word for it, psychology has been pretty fanatical about compartmentalising autism, its core cognitive features, down the years, almost it seems searching for some kind of scientific closure.

Anyhow, the paper in question is open-access but here are a few bullet points:

• The study is part of the Raine initiative again, whereby out of 861 children where BioT (free testosterone & albumin-bound testosterone) taken from umbilical cord blood at delivery was available, 707 provided diagnostic data at any of the specified follow-up points through infancy and early adulthood.
• Testosterone analysis was made by mass spectrometry, so one can't really fault accuracy, and DNA analysis from a small sample of the cohort ensured that cord blood samples were not contaminated by maternal blood so as to rule out reading maternal testosterone levels over offspring.
• Five of those 707 offspring were eventually diagnosed with an autism spectrum disorder (ASD).
• Results: "no significant correlations between TT levels and scores on any AQ scale among males (rho range: -.01 to .06) or females (rho value range: -.07 to .01)". TT = total testosterone.
• Indeed, "no significant association between BioT or TT concentrations and AQ scores among males (rho value range: -.07 to .08) or females (rho value range: -.06 to .12)".
• When looking at those 5 who were diagnosed with ASD, four "had TT and BioT levels lower than the sex-specific BioT means of the broader cohort, and all cases were within one standard deviation of these means".
• Not surprisingly the authors conclude that "testosterone concentrations from umbilical cord blood are unrelated to autistic-like traits in the general population".

There have been a few murmurs about this study in cyberspace, its results and implications for the EMB theory; partly genuine scientific interest, partly prejudice it has to be said. I'm going to try and remain objective. Assuming there was no significant sample degradation given that cord samples were taken at parturition and then thawed out apparently some years later for analysis, there are a few other factors to take into account which might have more general implications of the EMB-autism work.

Fair-do to Prof. Whitehouse for not totally poo-pooing the other research literature built up on testosterone and autism based on his findings. Indeed an even more recent study again by Bonnie Auyeung and colleagues***** (including Prof. Baron-Cohen) looking at amniotic fluid foetal testosterone and Q-CHAT results in 18-24 months old found a more positive relationship; bearing in mind a much smaller sample size and the focus on infancy not adulthood.

Back to the Whitehouse study: he for example talks about concentrations of cord testosterone not necessarily being the sole factor of any relationship but rather "individual differences in biological sensitivity to testosterone". That and the fact that the AQ is not a comprehensive autism assessment but rather a screen, and quite a subjective screen by all accounts. Other authors have talked about testosterone within a wider context of other biological markers as per this study by Geier and Geier****** who bring in words like glutathione, cysteine and homocysteine. I think you can see where I'm going with this; similar to the increasingly distant prospect of an autism gene, so an individual biomarker for autism is also looking less and less likely. Then there's heterogeneity (autisms not autism), comorbidity, etc. Indeed comorbidity is something that really needs a lot more study with testosterone-autism in mind.

Finally, I was interested to see that poverty might have been an influence on the AQ scores reported in the recent trial, to quote: "Total AQ scores were significantly higher for those adults whose mother was 
living below the poverty line during pregnancy". Assuming that you share the same enthusiasm for epigenetics and things like the Barker hypothesis as I do, you can perhaps see that this might be an area ripe for some further investigation.

To finish, a bad moon rising... oh yeah, I see it now.

----------

* Whitehouse AJ. et al. Perinatal testosterone exposure and autistic-like traits in the general population: a longitudinal pregnancy-cohort study. J Neurodev Disord. 2012; 4: 25.

** Auyeung B. et al. Fetal testosterone and autistic traits. Br J Psychol. 2009; 100: 1-22.

*** Baron-Cohen S. The extreme male brain theory of autism. Trends Cogn Sci. 2002; 6: 248-254.

**** Baron-Cohen S. et al.  Is there a link between engineering and autism? Autism. 1997; 1: 101-109.

***** Auyeung B. et al. Prenatal versus postnatal sex steroid hormone effects on autistic traits in children at 18 to 24 months of age. Molecular Autism. 2012; 3: 17.

****** Geier DA. & Geier MR. A clinical and laboratory evaluation of methionine cycle-transsulfuration and androgen pathway markers in children with autistic disorders. Horm Res. 2006; 66: 182-188.

----------

Whitehouse AJ, Mattes E, Maybery MT, Dissanayake C, Sawyer M, Jones RM, Pennell CE, Keelan JA, & Hickey M (2012). Perinatal testosterone exposure and autistic-like traits in the general population: a longitudinal pregnancy-cohort study. Journal of neurodevelopmental disorders, 4 (1) PMID: 23110806

Pets win (prosocial) prizes?

Miss Ellie Dog @Wikipedia

Pets have never really been a great part of my childhood it has to be said. Aside from a cat allergy which sort of ruled out any would-be Top Cat staying at ours, the family home just wasn't graced with enough space to accommodate other animal companions.

I did have a goldfish called George for a short period of time; that is until he/she(?) passed away and went to the great WC in the sky. Sad memories indeed.

This lack of animal contact during my childhood is probably why I am a little ambivalent towards children keeping pets at home (that and a very unfounded phobia of T.gondii) whilst, at the same time, being thankful for school pets who undoubtedly 'earn their keep' in the petting stakes.

Where autism is in mind however some recent research by Grandgeorge and colleagues* (full-text) suggests that pet arrival might very well have prosocial prizes.

The study is open-access so only a brief summary needed:

• From quite a large bank of participants (N=260), two studies were carried out on two very much smaller groups: study 1: arrival of a pet at age 5 years (n=12) vs. never owned a pet (n=12); study 2: owned a pet since birth (n=8) vs. never owned a pet (n=8).
• Alongside a questionnaire on human-pet relationships, parents of participants undertook questioning based on the ADI-R (see recent post) across two time periods (T0 and T1) primarily unaware of the reason for study participation.
• Results: based on study 1, pet arrival between the ages of 4-5 years was associated with significant changes to 2 algorithm items on the ADI-R (53) offering to share and (55) offers comfort which "reflect prosocial behaviors". Having a pet from birth (study 2) did not seem to bestow the same changes.

There are a few obvious caveats to these findings based on the sample size and sole reliance on ADI-R to assess change at the same time of pet arrival. As with all studies of association, people don't generally live in a vacuum outside of real life, so one has to be slightly cautious about linking just pet arrival to the reported changes in behaviour particularly over quite a long period of time.

All that being said, I am really quite interested in these findings. I know some have talked about the whole theory of mind (ToM) issue as accounting for the results (see here). Whilst this remains a possibility, I have to say that I still remain unconvinced of a major link between animal associated prosocial behaviours and perspective-taking or vice-versa in this particular instance. Such cold hard psychology fails to take into account the concept of 'enjoyment' in having a pet and also the responsibility that comes with ownership outside of trying to understand the mental state or what their pet might be thinking.

On the other hand, I do rather like the idea that stress, and importantly a reduction/moderation in stress and anxiety responses following the introduction of a pet might be part and parcel of the results seen as per suggestions like this one from Virués-Ortega & Buela-Casal**. If there's one thing we know about autism, it's that stress and anxiety are very often in the background.

This study also reminds me of an earlier blog post concerning some research on animal magic and the amygdala which suggested that the amygdala might the place to be when it comes to animal identification and recognition. Exactly what role the amygdala might play is still unclear in autism but one can speculate that neuronal functioning may have potentially been affected by pet companionship in a sort of 'pet brain training scenario'. Let's wait for more evidence of this first though.

Whilst perhaps being a more outlandish link, my post on the appeal behind Thomas the Tank Engine to some cases of autism might also be relevant. Think about it: cats, dogs, hamsters, guinea pigs, etc. are fairly uncomplicated creatures by human standards. They don't talk (aside from the odd 'sausages' here and there), they don't use a wide variety of facial or other gestures, and in most cases, they pretty much like, and are responsive to, interaction without other complications. Just a thought.

I would like to see more investigation on this topic with autism in mind; a call echoed by an even more recent review of the use of assistance and therapy dogs for autism***. I hold back from suggesting that every child with autism should be automatically handed a pet at aged 4 or 5 years given that not every child probably wants a pet, but for some it might be a useful aid to their development. Dare I even suggest that the introduction of a pet to the family home might also have some knock-on effects to immune functioning as per articles like this one by Tse and Horner**** (full-text) in light of autism and the immune system research or am I just being a little bit silly?

----------

* Grandgeorge M. et al. Does pet arrival trigger prosocial behaviors in individuals with autism? PLoS ONE. 2012; 7: e41739.

** Virués-Ortega J & Buela-Casal G. Psychophysiological effects of human-animal interaction: theoretical issues and long-term interaction effects. Journal of Nervous & Mental Disease. 2006; 194: 52-57.

*** Berry A. et al. Use of assistance and therapy dogs for children with autism spectrum disorders: a critical review of the current evidence. Journal of Alternative & Complementary Medicine. September 2012.

**** Tse H. & Horner AA. Allergen tolerance versus the allergic march: the hygiene hypothesis revisited. Current Allery & Asthma Reports. 2008; 8: 475-463.

----------

Grandgeorge M, Tordjman S, Lazartigues A, Lemonnier E, Deleau M, & Hausberger M (2012). Does pet arrival trigger prosocial behaviors in individuals with autism? PloS one, 7 (8) PMID: 22870246

Pretend play and autism

A lightsaber in production @ Wikipedia

I'm leaving the heavy biochemistry of late behind in this post with a link to an interesting paper recently posted on Twitter by Prof. Graham Davey (Twitter: @GrahamCLDavey) reviewing the current evidence on the impact of pretend play on child development*.

To quote: "...existing evidence does not support strong causal claims about the unique importance of pretend play for development".

Whoa there... pretend play over just play might not be such a vital component to child development? Y'mean all those hours honing my Vader-like lightsaber skills with those stuck together toilet roll tubes were wasted?

On reading such a paper my mind almost immediately wanders back to autism and publications like this one from Christopher Jarrold** reviewing the pretend play research base in autism alongside quite a few hours learning about play - imaginative and/or pretend play - through schedules like the ADOS. Indeed, isn't a problem with imagination and, by inference, imaginative/pretend play supposed to be a key hallmark of an autism diagnosis separating autism from not-autism? That was one of the findings from the artificial intelligence boiling down ADI-R paper published recently. So logically, does this mean that an absence/limitation of pretend play in cases of autism might not necessarily have such dire consequences for future development?

OK, I don't want to get too carried away here on the basis of one review. Indeed even the lead author, Prof. Angeline Lillard in this media piece admits that whilst pretend play probably doesn't have the final say in aspects such as creativity and problem-solving, it might very well aid in skills like language and social development - both key points to diagnosing autism; indeed social affect rolled into one according to the DSM-V suggestion. She also notes the very fuzzy issue in linking how specifically pretend play contributes to child development independently and outside of all the other factors which combine in that process called growing up.

It does however make me wonder whether the rigidity with which psychology has seemingly applied the importance of pretend play both in the context of autism and more generally in child development has been 'overstated'. Indeed, if we go back to the pretend play -- perspective-taking link as described by articles like this one by Doris Bergen*** for example, which makes mention of Theory of Mind (ToM), it makes me also wonder whether one could also question the global importance of ToM for 'proper' development too?

Individual differences? Compensation strategies? Have I said too much? Should I perhaps also not mention the recent paper by Sachse and colleagues on executive dysfunction and (adult) autism****?

---------

* Lillard AS. et al. The impact of pretend play on children's development: a review of the evidence. Psychological Bulletin. August 2012.

** Jarrold C. A review of research into pretend play in autism. Autism. 2003; 7: 379-390.

*** Bergen D. The role of pretend play in children's cognitive development. Early Childhood Research & Practice. 2002; 4.

**** Sachse M. et al. Executive and visuo-motor function in adolescents and adults with autism spectrum disorder. JADD. September 2012: PMID: 23011252

----------

Lillard AS, Lerner MD, Hopkins EJ, Dore RA, Smith ED, & Palmquist CM (2012). The Impact of Pretend Play on Children's Development: A Review of the Evidence. Psychological bulletin PMID: 22905949