Roger Moore's eyebrows, ADHD and coeliac disease part 2

Consider this post an extension of some previous blogging chatter (see here) about how behaviourally defined diagnostic labels such as attention-deficit hyperactivity disorder (ADHD) seem to rarely exist in some sort of clinical vacuum. Part of that vacuum also potentially encompasses a range of somatic symptoms and/or diagnostic labels.

The findings reported by Vendel Kristensen and colleagues [1] set out to "assess self-reported symptoms of impaired concentration in coeliac disease before and after treatment with gluten-free diet, compared with healthy controls and patient controls." Coeliac (celiac) disease, in case you didn't know, refers to the archetypal 'gluten can affect biology' condition, where a certain genetic predisposition (or two) adds to gluten exposure to start a whole cascade of biological actions that impact on physical health and well being. Alongside things like bowel symptoms, there is an increasing recognition that coeliac disease (CD) also potentially brings with it certain psychological symptoms, particularly when it is not properly treated/managed (see here).

Kristensen et al asked some 30 people - "newly diagnosed coeliac patients" - to complete various questionnaires pertinent to the presentation of ADHD type symptoms, depression and anxiety and gut issues. These were compared with responses from those diagnosed with an inflammatory bowel disease (IBD) and controls (healthcare professionals).

They reported that those diagnosed with CD before implementation of a gluten-free diet had "significantly higher scores than healthy controls" in relation to the presence of self-reported ADHD and depression/anxiety symptoms. Further: "After a gluten-free diet, their scores improved and were not significantly different from healthy controls." That gluten-free diet by the way, was in place for a minimum of 12 months.

One has to be careful not to make too many sweeping generalisations from the Kristensen data. The data do not, for example, mean that all cases of ADHD are somehow the product of undiagnosed coeliac disease. Not even close. What do they do (cautiously) suggest, is that preferential screening for something like coeliac disease *might* be a good idea as and when ADHD is diagnosed or significant ADHD-like symptoms present. Such findings also resonate with the idea that certain dietary interventions to manage *some* ADHD could be a research area to consider (see here) and bring into play an interesting concept: the gut-brain axis.

Oh, and in case you were wondering about the 'Roger Moore's eyebrows' bit, well, he was the best James Bond wasn't he?

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[1] Kristensen VA. et al. Attention deficit and hyperactivity disorder symptoms respond to gluten-free diet in patients with coeliac disease. Scand J Gastroenterol. 2019 May 3:1-6.

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On gut bacteria and depression

I'm kinda standing on the shoulders of giants with this post talking about the findings reported by Mireia Valles-Colomer and colleagues [1]. An editorial published in Nature [2] to coincide with the publication of the Valles-Colomer paper says just about everything that needs to be said on this research, which observed that: "Gut–brain module analysis of faecal metagenomes identified the microbial synthesis potential of the dopamine metabolite 3,4-dihydroxyphenylacetic acid as correlating positively with mental quality of life and indicated a potential role of microbial γ-aminobutyric acid production in depression." Yes folks, the idea that "microorganisms in the human gut could influence the brain" is moving from 'wild idea' to "wise pursuit".

The sequencing of DNA from donor stool samples as part of the Flemish Gut Flora Project ('You too are a walking bacteria colony' is the strap line) was the starting point for the Valles-Colomer study; stool samples provided by over 1000 participants. Researchers also accessed data on both self-reported and "physician-diagnosed depression" and set to work looking for any potentially important correlates between bacteria and psychology. The words "with validation in independent data sets (ntotal = 1,070)" are also (importantly) mentioned in the Valles-Colomer paper. Oh, and they also "mined the data to generate a catalogue describing the microbiota’s capacity to produce or degrade molecules that can interact with the human nervous system."

Results: "Butyrate-producing Faecalibacterium and Coprococcus bacteria were consistently associated with higher quality of life indicators." There's that word again: butyrate and yet more positive publicity for this compound (see here) and it's standing reaching almost 'bacterial sainthood'. Researchers also observed that two groups of bacteria were also reduced in those with depression: Coprococcus and Dialister alongside observing that this finding held "even after correcting for the confounding effects of antidepressants [use]." And then there was that 3,4-dihydroxyphenylacetic acid, also called DOPAC, finding, a metabolite of the neurotransmitter dopamine. I have actually mentioned DOPAC before on this blog (see here) in relation to what happens when rats are subjected to 'early immune stimulation' [2]. I don't think there is much overlap between that rat study and the Valles-Colomer paper (that rat paper was looking at DOPAC levels in brain tissue for example) but the suggestion from the authors that DOPAC levels were "correlating positively with mental quality of life" requires quite a bit more investigation.

Caveats? Well, out of their initial 1054 participant cohort, only 121 participants had "GP-reported depression." About half of these participants were taking antidepressants for their depression, the others weren't. The participant numbers aren't exactly tremendous for this portion of the study. Similar to something mentioned in other research (see here), I'm also minded to suggest that future research might perhaps consider looking at multiple stool samples taken over different occasions for the same person. This would perhaps establish whether gut bacterial populations are stable and whether that stability translates into stability of something like depressive symptoms too. I am likewise cautious that we don't jump ahead of ourselves here in terms of important issues like cause-and-effect and for example; whether there may be other important 'influencers' of gut bacteria when it comes to depression (see here and see here).

Lots more study is required on the suggestion of a gut bacterial *link* to depression [3], including that focused on the mechanics of any relationship (e.g. any involvement of the vagus nerve). If the link is further established, there are a number of potentially important implications: the possibility of a 'bacterial transferability hypothesis of [some] depression' (see here), intervention options focused on redressing balance in bacterial colonies (see here) and what such findings might do for the whole 'gut-brain axis' idea.

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[1] Valles-Colomer M. et al. The neuroactive potential of the human gut microbiota in quality of life and depression. Nature Microbiology. 2019. Feb 4.

[2] Editorial. Links between gut microbes and depression strengthened. Nature. 2019. Feb 4.

[3] Cheung SG. et al. Systematic Review of Gut Microbiota and Major Depression. Front Psychiatry. 2019;10:34.

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Pigeons, meet cat: "The Hans Eysenck affair: Time to correct the scientific record"

I'm heading off-piste with my musings today, drawing your attention to a paper by Anthony Pelosi [1] and an accompanying editorial by David Marks [2] (both open-access) that are likely to 'put the cat among the pigeons' in some quarters (with thanks to Matthew Dalby for bringing the Pelosi study to my Twitter attention). Indeed, the publishing journal - The Journal of Health Psychology - is no stranger to 'cat among the pigeons' discussions, as per their 2017 special edition [3] on the PACE trial "for patients with myalgic encephalomyelitis (ME)/chronic fatigue syndrome (CFS)." Perhaps interestingly, there is a 'psychosomatic' connection between the topic covered in the Pelosi paper and those critical musings on how to (or perhaps how not to) treat ME/CFS...

The person at the centre of the Pelosi paper is the late Prof. Hans Eysenck; a figure who anyone with the slightest interest in the discipline called psychology would probably have heard of. Personality was one of the major research interests for Eysenck, and in particular, the proposal of dimensions to personality: extroversion/introversion, neuroticism/stability, psychoticism/socialisation. Perhaps not as famously known about, but still influential, were Eysenck's views relating to "his persistent denial of the carcinogenic effects of tobacco." Indeed, his 'alternative view' that "certain personality traits that lead to smoking also increase the risk of developing cancer" is starting to look decidedly 'shaky' in modern times. More so when there is talk of 'funding' and 'sources of funding' potentially complicating the issue.

Pelosi (and Marks) make a case that the time is right for psychology and various other interconnected disciplines to start looking more critically at the collected published work of Eysenck and some of his colleagues. They argue that claims "about the alleged effectiveness of psychotherapy in preventing cancer" or that "behaviour therapy may be useful in prolonging life, as well as in preventing disease" have little place in modern, evidence-based, science and medicine. Pelosi - who has some important history of being slightly critical of some of Eysenck's findings alongside other notable names - also goes one stage further in suggesting that some of the "widely cited studies" published with Eysenck's name attached "have had direct and indirect influences on some people’s smoking and lifestyle choices." Further: "This means that for an unknown and unknowable number of individual men and women, this programme of research has been a contributory factor in premature illness and death." Strong words indeed.

Marks ends his editorial with open letters to the President and Principal of King's College London and the Chief Executive of the British Psychological Society (BPS) calling for further investigation of the points highlighted in the Pelosi paper. Pelosi has seemingly approached the BPS previously on this matter but apparently did not receive a particularly warm reception to his then request for further investigation of some of the science and conclusions made in this area (see here). Whether such a second request - made in the era of social media - will be acted upon differently this time is a 'wait and see' question. All of this taking into account the moves being made to make psychology a more credible science these days...

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[1] Pelosi AJ. Personality and fatal diseases: Revisiting a scientific scandal. Journal of Health Psychology. 2019. Feb 23.

[2] Marks DF. The Hans Eysenck affair: Time to correct the scientific record. Journal of Health Psychology. 2019. Feb 23.

[3] Marks DF. Special issue on the PACE Trial. Journal of Health Psychology. 2017. July 31..

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"Bowel perforation in chronic idiopathic megarectum and megacolon" and autism: 15 years on...

There was something all-too familiar about the case report detailed by Chukwuebuka Anyaegbuna and colleagues [1]. The description of a young man in his mid-twenties "with autism spectrum disorder" and a "history of chronic constipation" (going back years with "multiple previous admissions") eventually being admitted to intensive care on the basis of a potentially life-threatening bowel state is, unfortunately, nothing new to science and clinical practice (see here).

Bowel issues - both functional and more pathological - are over-represented when it comes to a diagnosis of autism (see here and see here for examples). The specific diagnosis of 'megarectum' detailed in the Anyaegbuna paper in relation to autism had also been noted some 15 years previously [2] in the peer-reviewed science literature. Indeed, the paper by Nadeem Afazal and colleagues [2] looking at over 100 children with autism "who were referred for gastroenterological assessment" showed that constipation was not an infrequent finding for this group. They also reported that many autistic children in their cohort "had moderate/severe loading or acquired megarectum." Their observation that "consumption of milk [was found] to be the strongest predictor of constipation in the autistic group" also chimed with me, as an interested researcher of diet as being a potentially important variable for 'some autism' [3]. And indeed, such an observation also seemingly intersects with other more recent dietary-bowel findings too (see here)...

The Anyaegbuna findings represent the continued failure of autism research and practice to take seriously the issue of bowel problems associated with autism. Stretching back over a period of about twenty years or so, I've noted the various comments from various (typically ill-informed) people protesting that various gastrointestinal (GI) investigations are 'not medically indicated' when it comes to some cases of autism. Some even made jokes about it. It's probably not unreasonable for me to say that set within this atmosphere, there has been a general reluctance to look at such issues for fear of castigation or shaming. There have been some brave research souls (see here and see here) who've kept on looking at bowel issues and autism, but not half as many as there should be. And it is those suffering with such bowel problems who have been let down: please do make sure that you take a good look at the X-rays accompanying the Anyaegbuna report to see what I mean.

Having said all that, I would like to think that things are slowly changing. It's no longer taboo to talk about bowel issues being over-represented in relation to autism. Indeed, we've had study after study all pointing in the same direction: bowel issues are seemingly related to autism, covering both childhood and adulthood. And such bowel issues might have some important effects on behaviour (see here). What we are sadly lacking at the current time however, is a concerted research effort asking 'why'? and 'what can we do to prevent (yes, prevent) such bowel issues occurring rather than just treating them when they occur?'

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[1] Anyaegbuna C. et al. Bowel perforation in chronic idiopathic megarectum and megacolon. BMJ Case Rep. 2018 Aug 20;2018. pii: bcr-2018-225406.

[2] Afzal N. et al. Constipation with acquired megarectum in children with autism. Pediatrics. 2003 Oct;112(4):939-42.

[3] Whiteley P. et al. Nutritional management of (some) autism: a case for gluten- and casein-free diets? Proc Nutr Soc. 2015 Aug;74(3):202-7.

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On 'negative first impressions' and autism: even those on the autism spectrum are prone to them

The findings reported by Ruth Grossman and colleagues [1] talking about 'perceptions of self and others' in the context of autism are really quite intriguing. Researchers reported that when adolescents, either diagnosed with or without autism, were shown brief video clips of adolescents with and without autism (and not explicitly being told about whether actors were autistic or not), "all participants provided more negative judgments of autistic than neurotypical adolescents in the videos." I've hyperlinked that mention of the word 'neurotypical' to some previous discussions on this blog about how this term really is a misnomer...

OK, let's rewind a little. Grossman et al mention that: "Neurotypical adults often form negative first impressions of individuals with autism spectrum disorder and are less interested in engaging with them socially." Such sweeping sentiments are based on other research that she has been involved in (see here) observing that "the social presentations of individuals with ASD, particularly their non-verbal cues, including prosody, facial expressions, and body posture, are perceived less favorably and are associated with reluctance on the part of observers to pursue social engagement" [2]. I should add that 'undergraduates' were the "rating participants" on that research occasion; a participant group who may not be as representative of the general population [3] as many people might think.

Further study in this area [4] revealed that diagnostic disclosure and "increased autism understanding" seemed to improve such first impressions. They also revealed that once again, the diagnosis known as schizophrenia was viewed even less favourably; heaping yet more stigma and misery on to this label and those diagnosed with it.

The most recent Grossman findings added a new dimension to such 'first impression' research by including young adults with autism into their study. They specifically started out by mentioning that: "individuals with autism spectrum disorder actively seek out the company of others who share their diagnosis", I assume, on the basis that 'like attracts like' across various types of relationship, and 'shared' characteristics might be more likely to provide shared viewpoints and shared understanding. That's the [sweeping] theory anyway. The fact however that those on the autism spectrum were seemingly not immune to those initial negative judgements "without being explicitly informed of a shared diagnosis" kinda implies that at least when it comes to first impressions, those on the autism spectrum aren't so dissimilar from those results from the not-autism cohort.

Should anyone be surprised by these findings? Well, I was initially taken aback by them, particularly when so much was (and still is) made of the idea that society and it's 'reactions' to autism is part of the reason why some of those on the autism spectrum feel disabled. I don't want to get into any ideological debates or discussions about the application of the social model of disability to autism ("disability is caused by the way society is organised, rather than by a person’s impairment or difference") but I can think of some occasions where those original 'first impression' findings were suggested to be supportive of such a model. The Grossman findings also don't discount the social model of disability; indeed they're supportive of it from a first-impressions point of view. But they do blur the distinction between autism and 'neurotypical' in terms of who makes those first impression responses. In short, a diagnosis of autism does not seemingly mean prejudice-free nor does it necessarily mean that everyone on the autism spectrum probably wants to, or necessarily seeks out, the company of like-minded spectrum people. Yet again, sweeping generalisations about autism falls...

I would like to see more investigations done in this area. I've talked about the use of the student population in this post already, so the next step would be talking to your average Joe or Josephine who doesn't rely on getting a 'class credit' for their study participation to gauge their views. It's also important to see whether variables like baseline 'familiarity' with autism (if there is such a thing!) or chronological age of raters are also consistent with such findings: are older folk for example, who've lived a little longer and experienced a bit more in their lives, more or less likely to hold a particular 'first impression' view of autism? Does it also vary according to the 'severity' of autism presentation?

Assuming also that it is rather difficult to significantly impact on one persons first impression of another, I'd like to know further details about why those negative judgments were formed. 'Social skills' were part-and-parcel of the Grossman analyses but this covers quite a lot of ground. We are also told that: "Both participant groups spent less time gazing at videos of autistic adolescents" implying that poise, posture and other physical features/characteristics might similarly be important in grabbing and keeping someones (positive) attention. Going back to the previous research where the (mis)label of schizophrenia was mentioned, I'd also like to see the inclusion of autistic voices when it comes to this area too. So, do the same prejudices about something like schizophrenia hold for those on the autism spectrum? What about other mental issues and illnesses such as depression and/or anxiety? I say this also bearing in mind that labels like schizophrenia, depression and anxiety are sometimes not unfamiliar facets of the autism spectrum (see here and see here), in a world where autism typically does not exist in a diagnostic vacuum (see here)...

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[1] Grossman RB. et al. Perceptions of self and other: Social judgments and gaze patterns to videos of adolescents with and without autism spectrum disorder. Autism. 2017. July 17.

[2] Sasson N. et al. Neurotypical Peers are Less Willing to Interact with Those with Autism based on Thin Slice Judgments. Scientific Reports. 2017; 7: 40700.

[3] Hanel PHP. & Vione KC. Do Student Samples Provide an Accurate Estimate of the General Public? PLoS ONE. 2016;11(12):e0168354.

[4] Sasson NJ. & Morrison KE. First impressions of adults with autism improve with diagnostic disclosure and increased autism knowledge of peers. Autism. 2017 Oct 1:1362361317729526.

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ALSPAC says... "Social communication impairments had the strongest association with a depression diagnosis at age 18 years"

ALSPAC mentioned in the title of this post refers to The Avon Longitudinal Study of Parents and Children, one of the premier research initiatives here in Blighty, that has provided all-manner of interesting and important research associations. With autism in mind, ALSPAC has opined on various different research questions (see here and see here for examples) including the issue of a possible 'real' increase in the numbers of children presenting with autistic traits (see here).

On this particular research occasion, ALSPAC was the source data for the findings reported by Dheeraj Rai and colleagues [1] who set out to "compare trajectories of depressive symptoms from ages 10 to 18 years for children with or without ASD [autism spectrum disorder] and autistic traits, to assess associations between ASD and autistic traits and an International Statistical Classification of Diseases, 10th Revision (ICD-10) depression diagnosis at age 18 years, and to explore the importance of genetic confounding and bullying." I might add that some of this authorship group are making some real research waves when it comes to investigations using population registries with autism in mind (see here).

The starting point this time around was the notion that a diagnosis of autism is in no way protective when it comes to a diagnosis of depression and/or the expression of depressive signs and symptoms. Again, it's a topic that has cropped up before on this blog (see here) and is perhaps one of the longer term associations that have been made down the years. The idea that depression or depressive symptoms *might* be something much more than just 'comorbid' in the context of at least 'some' autism is something else that has been banded around the peer-reviewed research literature before (see here) but the evidence base is not particularly big or strong in this area at the moment.

There were a few different research questions asked by Rai et al, including looking at children "with or without ASD or high scores on autistic trait measures" and any relationship(s) with depression and depressive traits. They report findings for over 6000 children ("maximum sample with complete data") where questionnaire items on bullying were also included ("Relational and overt bullying was assessed as separate yes or no items at ages 8, 10, and 13 years using the modified Bullying and Friendship Interview Schedule") alongside various other potentially confounding variables.

Results: "children with ASD and those with higher scores on all autistic trait measures had more depressive symptoms at age 10 years than the general population, and these remained elevated in an upward trajectory until age 18 years." I don't think there's anything too novel in such findings, aside from the observation that depression / depressive symptoms may start quite early on in childhood. I can remember when I started out in autism research a couple of decades ago hearing about depression being typically linked to the onset of adulthood in the context of autism. This current data suggests otherwise.

Next: "Social communication impairments had the strongest association with a depression diagnosis at age 18 years. Findings were robust to adjustment for a range of confounders, including maternal depression and anxiety and the child’s polygenic risk for autism." This is important. What it suggests is that there may something 'more than just comorbid' about depression or depressive symptoms appearing alongside autism or at least in connection to certain autistic traits. I know some people have already taken exception to this possibility alongside the use of the word 'impairment' by the authors. But much like other research on an important bedfellow to depression - anxiety - one may have to entertain the possibility that there may be some enhanced 'predisposition' to something like depression alongside the presentation of autistic traits (see here and see here) perhaps mediated by factors such as rumination and perseveration for example [2]. This doesn't mean that depression is solely a product of autistic traits; merely that certain traits may potentially form an important vulnerability factor. I'm similarly minded to bring in other work from the ALSPAC initiative [3] (including Rai and colleagues as authors) where related findings were mentioned: "Social communication impairments are an important autistic trait in relation to suicidality." This on the basis that depression and suicidality show an important association.

Also: "We found evidence of a substantial role of bullying in contributing to and explaining a higher risk of depression in individuals with ASD and autistic symptoms." Bullying in the context of autism is another long-standing topic (see here). Bullying covers a lot of ground in terms of behaviour and also source (see here). The authors opine that: "Previous work has shown strong links between the experience of bullying and later depression... although confounding could have a role, the association is considered to be at least partially causal." It's also important to note that social-communication 'issues' were reported to be potentially predictive of being bullied according to the authors. The model that then appears hints that the appearance of depression *might* be linked to "reduced self-esteem or social isolation after the bullying" accepting that causality is not established and also not accounting for other variables: "other relevant characteristics, including comorbidities with neurodevelopmental conditions (eg, attention-deficit/hyperactivity disorder) and classroom placement could be important in this association within or outside the context of bullying." That last point is important in the context that autism rarely exists in some sort of diagnostic vacuum (see here).

There are a few caveats attached to the Rai findings that need to be kept in mind outside of any 'correlation does not necessarily equal causation' sentiments. So: "atypical presentations of depression are common in ASD, and our study has the potential for outcome measurement error because we used scales... that have not been adapted for autism." Indeed. I've previously talked about how bipolar disorder for example, might not follow a typical pattern when present in the context of autism (see here). I daresay that this could also hold for other types/forms of depression too. I'm also minded to reiterate that depression, as well as being a heterogeneous condition, also seemingly has many pathways to it. Some of those pathways will include psychological and social variables such as bullying and perhaps even more extremes of 'trauma'; where a diagnosis of PTSD is for example, no stranger to autism (see here). 'Happiness' and perceived quality of life (see here) are also likely to exert an important effect too.

Other pathways to depression seem to be more biologically defined as per depression in the context of physical ailments (see here) that may have a *link* to some autism (see here) or following the use of seemingly common medicines according to recent news reports (see here). I'll also mention that things like physical activity and exercise *seem* to show an important relationship with depression (see here). This could also be pertinent to the data suggesting that physical activity levels are typically not optimal where and when autism is diagnosed (see here). Other factors (fatigue, sleep, etc) also need to be mentioned in the context of depression. In short, there are lots and lots of potential variables to consider [4].

Outside of the important messages from the Rai findings on how depression is over-represented in relation to autism and how social factors like bullying seem to be linked  to it and thus are subsequently 'modifiable', there is another important point to consider: depression is typically treatable. Minus any medical or clinical advice being given or intended, the first step in managing/treating depression is identifying it. Perhaps the Rai findings might serve as a further call to action for preferential screening in the context of autism...

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[1] Rai D. et al. Association of Autistic Traits With Depression From Childhood to Age 18 Years. JAMA Psychiatry. 2018 Jun 13.

[2] Patel S. et al. Association between anger rumination and autism symptom severity, depression symptoms, aggression, and general dysregulation in adolescents with autism spectrum disorder. Autism. 2017 Feb;21(2):181-189.

[3] Culpin I. et al. Autistic Traits and Suicidal Thoughts, Plans, and Self-Harm in Late Adolescence: Population-Based Cohort Study. J Am Acad Child Adolesc Psychiatry. 2018 May;57(5):313-320.e6.

[4] Köhler CA. et al. Mapping risk factors for depression across the lifespan: An umbrella review of evidence from meta-analyses and Mendelian randomization studies. J Psychiatr Res. 2018 May 25;103:189-207.

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A poo(p) transplant for depression and anxiety?

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

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

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

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

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

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

Headlines aplenty...

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

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

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

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

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

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

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

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

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

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

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

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

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

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Bullying and autism: not always originating from where you might expect...

There is something rather uncomfortable about the findings reported by Imar Toseeb and colleagues [1] but, at the same time, they do raise an important issue that needs to be openly discussed. Specifically their findings on: "sibling bullying, and the associated psychopathological adversities, in children with and without ASD [autism spectrum disorder]" deserve some airtime.

Bullying and autism is quite a regular talking point in the peer-reviewed research literature (see here) and beyond. Although a diagnosis of autism is by no means protective of someone becoming a bully or being involved in what could be considered bullying behaviour, it is far more typical that those with autism are going to be a victim of bullying rather than perpetrator (see here). Indeed, I reluctantly use the word 'vulnerable' yet again on this occasion but...

When one thinks about bullying in any context including that with autism in mind I would imagine that the school bully who name calls or becomes physical aggressive towards someone - usually smaller and quieter than them - probably first springs to mind. Siblings by contrast, conjure up an image of being caring, supportive and again, with autism in mind, often very protective of their brother(s) and/or sister(s) given their important role, present and probably future. And indeed, many, many siblings are just that (see here).

But real life is rarely so clear-cut or 'homogeneous' as many parents, whether with children diagnosed with autism or not, will attest. Siblings argue, fight and probably because of how well they 'know each other', often know all the right buttons to press to get their required reaction. And yes, behaviour sometimes can spill over to what would be considered bullying under any other circumstance...

Toseeb et al started with the hypothesis that: "children with ASD (child has ASD but their sibling does not) would experience higher levels of sibling bullying compared to those without ASD (child and sibling do not have ASD)." They arrived at this hypothesis on the basis of various factors such as a role for the social-communicative issues that follow autism, the possible effect of the 'broader autism phenotype' (BAP) on siblings, and issues such as a greater frequency of aggression - "reactive aggression" - accompanying particularly boys with autism.

They relied on data from the Millennium Cohort Study (MCS) (a resource that has been mentioned before on this blog) and eventually included data from nearly 500 children with autism alongside over 13,000 not-autism controls. The question(s) on sibling bullying were asked at 11 years of age and went: "he/she was asked to respond to two questions on a six-point scale (never, less often, every few months, approximately once a month, approximately once a week, most days): “how often do your brothers or sisters hurt you or pick on you on purpose?” (victimization) and “how often do you hurt or pick on your brothers or sisters on purpose?” (perpetration)." Responses were coded according to who did what and how often. Various other measures were also examined as part of the MCS and used in the Toseeb paper: socio-demographic data (single parent status, birth order, number of siblings, household incomes), parenting style, psychopathology and cognition.

Results: children diagnosed with autism or ASD were more likely to be bullied by their non-autistic sibling compared with those who did not have autism. This finding held "even after controlling for socio-demographic and family level variables" and "was associated with adverse psychopathologies." Further: "having ASD, being a girl, of White ethnicity, having more siblings, and experiencing harsher parenting were all associated with increased odds of being bullied by a sibling." Whilst we're on the topic of 'adverse psychopathologies, it's perhaps pertinent to mention the findings reported by Dantchev and colleagues [2] observing a possible connection between sibling bullying receipt and psychotic disorder. Yes, it is quite an extreme example, but nonetheless demonstrates the effects bullying can have long-term. I might also refer you back to some discussion arising from the ICF core sets development with autism in mind too (see here).

I digress. I note also that authors discuss sibling bullying as a two-way street: "Our findings indicate that children with ASD are specifically at increased risk of sibling victimization as a bully-victim."

As I said at the beginning of this post, this all makes for uncomfortable reading. If it's not bad enough that a child may be being bullied at school to also then potentially learn that there is little respite from such behaviour at home, makes for an uncomfortable (intolerable?) situation all-round. The question then arises minus any sweeping generalisations: what can be done about sibling bullying for the good of all concerned? And please, don't just solely suggest 'coping strategies' for the bullying victim either.

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[1] Toseeb U. et al. The Prevalence and Psychopathological Correlates of Sibling Bullying in Children with and without Autism Spectrum Disorder. J Autism Dev Disord. 2018 Feb 8.

[2] Dantchev S. et al. Sibling bullying in middle childhood and psychotic disorder at 18 years: a prospective cohort study. Psychological Medicine. 2018. Feb 12.

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Anxiety prevention meta-analysed and some implications...

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

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

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

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

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

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

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

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

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

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

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

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"What Happens When I Can No Longer Support My Autistic Relative?"

I've kinda touched upon the subject matter examined in the paper by Renske Herrema and colleagues [1] before on this blog (see here). Detailing important results on views and concerns about the future and specifically what will happen to loved ones with autism when families are no longer able to care for or support them, the findings approach a difficult but important question. Part of that questioning surrounds the perception that social and other supports for example, are pertinent and in place to keep loved ones safe, cared for and able to deliver suitable services onward to ensuring a nurturing environment that caters to the individual's needs, wants and wishes.

Drawing on data from "120 family members of autistic adults" (or adults with autism if you prefer), authors asked about "concerns about the future for their relative" via an online survey. Several key themes emerged from their inquiry on things like concerns for individual needs not being met, the happiness of their loved one and the question of who will care for them as and when primary caregivers are not able to or are not around to care for them. These concerns were things that quite regularly featured in the minds of family members according to their online reporting.

The authors talk about the need for planning to start early - 'timely' - when it comes to ensuring that support is both available now and in the future for family members with autism. I would definitely agree with such early planning given the history of almost Herculean efforts that parents/caregivers have had to go through to ensure that their loved ones are provided the same rights as anyone else. Indeed, legacies have already evolved from such planning (see here). I do worry however that there are factors that parents and other family members seem to have to overcome in modern times; where austerity is pushing social care to breaking point (at least here in Blighty) and the availability of social support being more and more reserved for those who cannot live independently potentially at the expense of the 'look like they're managing' masses...

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[1] Herrema R. et al. Brief Report: What Happens When I Can No Longer Support My Autistic Relative? Worries About the Future for Family Members of Autistic Adults. J Autism Dev Disord. 2017 Jul 28.

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"a potential link between serious delinquency and later schizophrenia"

I was rather intrigued by the results reported by Nina Lindberg and colleagues [1] in their study designed to "investigate if serious delinquency was associated with future diagnoses of schizophrenia or schizoaffective disorder (here, broadly defined schizophrenia) among a nationwide consecutive sample of 15- to 19-year-old Finnish delinquents sent for a forensic psychiatric examination in 1989-2010."

I hadn't previously come across research directly linking delinquency - serious delinquency - with later schizophrenia diagnosis despite noting other research talking about other labels being potentially related to the extreme results of delinquency (see here) and onward some of those labels being potential risk factors for something like schizophrenia (see here).

Looking at the records of "313 delinquents with no past or current psychotic disorder" and around 1200 age- and sex-matched non-delinquents whose details were also held on a central population registry, researchers followed them all "[un]till death, emigration or the end of 2015, whichever occurred first." The results put delinquents as a group at quite a bit more risk of subsequently being diagnosed with schizophrenia than non-delinquents (12% vs. ~1% respectively). The authors conclude that their results "supports the previous research indicating a potential link between serious delinquency and later schizophrenia" and that more investigation is needed into the hows-and-whys of such a relationship.

Having already mentioned the slightly more indirect link between attention-deficit hyperactivity disorder (ADHD) and risk of offending behaviour (minus any sweeping generalisations) and ADHD and risk of schizophrenia, there could be lessons to be learned about the link between serious delinquency and schizophrenia. Also, minus further generalisations, I'm also wondering if some of the 'habits' perhaps more readily observed in delinquents (e.g. illicit drug use) could potentially be additional risk factors for a diagnosis of schizophrenia [2]. Minus any psycho-babble explanations, the rise and rise of scientific evidence pointing to various psychosocial factors as also being risk factors for schizophrenia [3] may additionally come into play, together with an understanding that elements of the parental home also may play a key role in cases of delinquency [4]. In short, there are several potentially important areas that could provide key research directions in this intriguing area.

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[1] Lindberg N. et al. Serious delinquency and later schizophrenia: A nationwide register-based follow-up study of Finnish pretrial 15- to 19-year-old offenders sent for a forensic psychiatric examination. Eur Psychiatry. 2017 May 15;44:173-178.

[2] Marconi A. et al. Meta-analysis of the Association Between the Level of Cannabis Use and Risk of Psychosis. Schizophr Bull. 2016 Sep;42(5):1262-9

[3] Larsson S. et al. High prevalence of childhood trauma in patients with schizophrenia spectrum and affective disorder. Compr Psychiatry. 2013 Feb;54(2):123-7.

[4] Fernández-Suárez A. et al. Risk Factors for School Dropout in a Sample of Juvenile Offenders. Front Psychol. 2016 Dec 26;7:1993.

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Reducing depression scores (in IBS) using a probiotic?

"Probiotics can reduce symptoms of irritable bowel syndrome (IBS), but little is known about their effects on psychiatric comorbidities."

OK, go on...

"In a placebo-controlled trial, we found that the probiotic BL [Bifidobacterium longum NCC3001] reduces depression but not anxiety scores and increases quality of life in patients with IBS."

So said the findings reported by Maria Ines Pinto-Sanchez and colleagues [1] extending their research interest in all-things 'anxiety and depression related to functional bowel issues' (see here). Just in case you were wondering whether probiotics might be an effective intervention for at least some cases of IBS, yes, there is some meta-analysed evidence of positive effects (see here) albeit with more work to do.

This time around the name of the research game was to see whether various psychological issues that can very much accompany cases of IBS (see here) might also be affected by administration of a particular probiotic under gold-standard - "double-blind, placebo-controlled" - experimental conditions. Based on data from "44 adults with IBS and diarrhea or a mixed-stool pattern (based on Rome III criteria) and mild to moderate anxiety and/or depression (based on the Hospital Anxiety and Depression scale)" researchers followed participants taking either BL or a placebo capsule for 6 weeks. Alongside looking at bowel and behavioural signs and symptoms, they also collected blood and urine specimens and assessed using functional magnetic resonance imaging (fMRI).

As per the sentences above, use of the probiotic seemed to have some effect on scores of depression in the supplemented group when compared to the placebo-receiving participants. Indeed: "At week 6, 14/22 patients in the BL group had reduction in depression scores of 2 points or more on the Hospital Anxiety and Depression scale, vs 7/22 patients in the placebo group." Such an effect also seemed to carry forward when it came to another important measure: quality of life.

The authors also talk about seeing some changes on the imaging side of their study alongside: "reduced urine levels of methylamines and aromatic amino acids metabolites" in the probiotic supplemented group. All-in-all there was quite a bit to see from this study; certainly enough to provoke further investigations.

Of course, one needs to be a little careful based on the idea that not all probiotics are the same and further questioning is required on the specific mode of action. But, given the pretty good safety profile of various probiotics alongside an increasing volume of peer-reviewed research suggesting positive effects for some using such preparations when it comes to things like [some kinds of] depression (see here), I'm minded to suggest that the future is looking pretty bright when it comes to the use of probiotics for various conditions/labels/states...

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[1] Pinto-Sanchez MI. et al. Probiotic Bifidobacterium longum NCC3001 Reduces Depression Scores and Alters Brain Activity: a Pilot Study in Patients With Irritable Bowel Syndrome. Gastroenterology. 2017 May 5. pii: S0016-5085(17)35557-9.

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Pinto-Sanchez MI, Hall GB, Ghajar K, Nardelli A, Bolino C, Lau JT, Martin FP, Cominetti O, Welsh C, Rieder A, Traynor J, Gregory C, De Palma G, Pigrau M, Ford AC, Macri J, Berner B, Bergonzelli G, Surette MG, Collins SM, Moayyedi P, & Bercik P (2017). Probiotic Bifidobacterium longum NCC3001 Reduces Depression Scores and Alters Brain Activity: a Pilot Study in Patients With Irritable Bowel Syndrome. Gastroenterology PMID: 28483500

Social interaction and autism: it takes two to tango

Psychology experiments are not generally fodder for this blog when it comes to autism. The main reason being that quite a few appearing in the peer-reviewed literature tend to look at quite abstract features perhaps somewhat removed from the daily lives of autistic people and their significant others. A few also seem to struggle with the idea that grand over-arching psychological theories (that seem to inevitably follow psychological findings in particular) are not required when it comes to autism in these days of heterogeneity and plurality.

I am making an exception today however with the paper by Noah Sasson and colleagues [1] (open-access) and their findings suggesting advocating "for a broader perspective of social difficulties in ASD [autism spectrum disorder] that considers both the individual’s impairments and the biases of potential social partners." In other words, it takes two to [socially, interactively] tango. I might add that a doctoral thesis by one of the co-authors on the Sasson paper (Daniel Faso) is also available for further inspection too (see here).

Based on the idea that issues with social interaction "quantity and quality" might not be something exclusively under the control of those diagnosed with autism, Sasson et al devised a series of experiments to test their hypothesis: "three studies conceived and conducted independently by three research groups assessing observers’ first impressions of—and intentions to socially engage with— children and adults with ASD based upon “thin slices” of their real-world social behavior." I'm not going to go into too much detail about the experiments because the paper is open-access and you can read about them for yourselves. 'Thin slices' in the context of the experiments carried out referred to media that were rated pertinent to "observers’ first impressions of individuals with ASD engaging in real-world social behavior."

The results make for some important reading as across the different experiments undertaken the key messages were that: "first impressions of individuals with ASD are significantly less favorable than those of matched TD [typically developing] controls, and are associated with greater reluctance on the part of observers to pursue social engagement." Further: "social interaction difficulties in ASD are not solely an individual impairment but also a relational one, and consideration of both of these factors is necessary for a full understanding of social impairment in ASD." I relay all of that bearing in mind that these were experiments carried out under controlled conditions (I don't know about you, but I don't generally rate people at first contact using a "0-3" Likert scale or a "non-graduated slider" on 'how approachable' they were or the likelihood of a friendship developing).

Although important, I don't think anyone should be too surprised by the results reported in the context of how first impressions count and how people are generally quick to judge from "personality and character traits" whether social engagement with a person or group of people is going to be a short or longer-term thing. I say this also bearing in mind that minus any psychobabble, people generally take into account things like context, familiarity and similarity when it comes to their social interaction decisions too [if for example, you happen to be a fan of Star Wars or a Shotokan karateka, I might be more inclined to chat with you than say if you talked about the goings-on on various reality TV shows]. Indeed, the authors note: "these studies present only group-wise comparisons and do not address individual differences among those with ASD, nor whether individual characteristics of the raters (e.g., gender, personality, etc.) affect the results reported here." I'd also forward the idea that they might also include important concepts such as self-monitoring for example when it comes to future studies in this area. Similarly, it would also be handy to see if 'comorbidity counts' when it comes to further investigations on this topic in light of expanding links between different labels and traits (see here).

The question of what to do about the Sasson findings similarly provide some food for thought. The authors suggest that: "intervention and education approaches that target both those with ASD as well as their TD [typically developing] peers may offer a more comprehensive approach for improving social and functional outcomes in autism." In the context of other studies looking at social interaction and autism particularly in the school setting (see here) I can see how this might work in terms of raising awareness of how people are not always the same when it comes to the presentation of their social persona. Intervening with a wider group (i.e. peers) and taking the onus off 'just the person with autism' is a win-win situation and will no doubt have other positive knock-on effects in terms of self-esteem and helping to remove barriers around the 'disability' framing of autism. I might add that in these days of the potential virality of personality traits, it makes sense to include everyone.

In a wider context - outside of school - and in the big, wide [adult] world however, I'm slightly less sure of how such intervention is going to be achieved. Yes, we would all love people to be more understanding and less 'judgemental' in their first (and subsequent) impressions, but when it comes to influencing aspects such as views on "awkwardness, attractiveness, [and] likability" I'm not so sure that this can be universally achieved. Indeed, facets such as attractiveness and likability are probably going to be influenced by lots of variables outside of those just linked to an autism diagnosis and its presentation (frank or not). By saying all that, I'm not suggesting that we shouldn't try to educate and perhaps even move people away from the whole 'first impressions last' [2] thing, but rather am looking at the realistic prospect of achieving such a societal goal, mindful that it takes two to tango...

And on the topic of first impressions, at least get the handshake right (i.e. let go)...

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[1] Sasson NJ. et al. Neurotypical Peers are Less Willing to Interact with Those with Autism based on Thin Slice Judgments. Sci Rep. 2017 Feb 1;7:40700.

[2] Gunaydin G. et al. Impressions Based on a Portrait Predict, 1-Month Later, Impressions Following a Live Interaction. Social Psychological and Personality Science. 2017. 8: 36-44.

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Sasson NJ, Faso DJ, Nugent J, Lovell S, Kennedy DP, & Grossman RB (2017). Neurotypical Peers are Less Willing to Interact with Those with Autism based on Thin Slice Judgments. Scientific reports, 7 PMID: 28145411