Cerebral palsy and autism continued

"Our findings support the need for a multidisciplinary approach to management of children with CP [cerebral palsy] to adequately identify and address all facets of presentation, including ASD [autism spectrum disorder]."So said the results of the study published by Malika Delobel-Ayoub and colleagues [1] who looked at the "prevalence of co-occurring autism spectrum disorders (ASDs) among children with cerebral palsy (CP)" among other things. Continuing a research theme (see here), researchers reported that around 9% of their 1200+ cohort of children diagnosed with CP had an "associated diagnosis of ASD". Said participant data coming from various European registries including one here in the bracing North-East of England.What's more to say other than yet again, preferential screening for autism might be indicated? One might also advance the idea that clues about the origins of at least some autism may be forthcoming when the label is comorbid to CP. The particular finding that 'co-occurring epilepsy' might be something important for example, is as good a research starting point as any given what other independent datasets have similarly observed [2] combined with the ever-growing [bidirectional] links being discussed between epilepsy and autism / autistic traits (see here).----------[1] Delobel-Ayoub M. et al. Prevalence and characteristics of autism spectrum disorders in children with cerebral palsy. Dev Med Child Neurol. 2017 Apr 25.[2] Christensen D. et al. Prevalence of cerebral palsy, co-occurring autism spectrum disorders, and motor functioning - Autism and Developmental Disabilities Monitoring Network, USA, 2008. Dev Med Child Neurol. 2014 Jan;56(1):59-65.----------Delobel-Ayoub M, Klapouszczak D, van Bakel MME, Horridge K, Sigurdardottir S, Himmelmann K, & Arnaud C (2017). Prevalence and characteristics of autism spectrum disorders in children with cerebral palsy. Developmental medicine and child neurology PMID: 28439889...

Delobel-Ayoub M, Klapouszczak D, van Bakel MME, Horridge K, Sigurdardottir S, Himmelmann K, & Arnaud C. (2017) Prevalence and characteristics of autism spectrum disorders in children with cerebral palsy. Developmental medicine and child neurology. PMID: 28439889  

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Adenotonsillectomy for obstructive sleep apnea and autistic behaviours?

Adenotonsillectomy refers to the surgical removal of the tonsils and adenoids and is typically indicated for a variety of reasons, not least in cases of obstructive sleep apnoea (OSA) (where breathing is interrupted during sleep). It's not an unfamiliar operation and is generally categorised as low-risk surgery. The positive outcomes following surgery have been described as 'dramatic' both in clinical terms and also related to quality of life [1].A recent study published by Emi Murata and colleagues [2] (open-access available here) adds a further dimension to the use of adenotonsillectomy (AT) for obstructive sleep apnoea specifically with the autism spectrum in mind. They concluded that: "Behavioral problems were significantly improved following AT in ASD [autism spectrum disorder] children with OSA."First off, I'll direct you to a previous post that I wrote about sleep apnoea and autism (see here) based on the findings reported by Hirata and colleagues [3]. They concluded that within their research cohort: "sleep problems, especially obstructive sleep apnea, are more common in ASD preschoolers than in community preschoolers." Then there are the study results by Malow and colleagues [4] who detailed a case report of treating sleep apnoea in a child with autism via use of AT. Bearing in mind this was an N=1, they observed that treatment coincided with "improvements in sleep, social communication, attention, repetitive behaviors, and hypersensitivity" based on use of the ADOS among other measures.Set within this context, the Murata paper detailed the results of a study including some 54 children diagnosed with ASD. Their aims were two-fold: "to determine whether AT for the treatment of OSA improves the behavior of Japanese children with ASD using the Child Behavior Checklist (CBCL)" and "to identify characteristics for behavioral improvement following the treatment of OSA in these children with ASD." Thirty of the study participants were diagnosed with OSA and all underwent surgery for AT. I must also stress that said surgery was a clinical decision: "Because hypertrophy of the adenoids and/or palatine tonsils was observed." The rest of the cohort served as a control group used "to establish whether observed changes in CBCL scores were due to the natural course or a result of the experimental intervention."The results are pretty interesting: "After AT, T-scores of the CBCL scales were significantly improved in the OSA group, but no change was observed in the control." This was based on before and after inspection at 0 months (before surgery) and 6 months after surgery. The sorts of things seemingly improved in the AT group were aspects of behaviour and functioning linked to being withdrawn, social problems. attention issues and aggressive behaviour. Authors noted that: "The domain of “thought problems” showed the largest decrease... in the OSA group."When it came to the 'characteristics for behavioural improvement' side of their study, authors noted that: "the improved group show[ed] significantly higher scores on the CBCL at pre-AT than the unchanged/deteriorated group in ASD children with OSA after OSA treatment". This implies that baseline presentation might be important when it comes to behavioural outcomes following the use of AT and also that not every child with ASD and sleep apnoea undergoing AT will show the same pattern of behavioural changes.I find these results to be fascinating. Not least because they offer a roadmap for (a) screening for sleep apnoea in cases of autism and (b) details of how a treatment for one cause of sleep apnoea in such cases might have effects well beyond just related to breathing patterns. Then also, there is the question of why such surgery might impact on presented behaviour? I'm afraid I don't know enough about such issues to offer any definitive explanations. I might refer you back to some other discussions on this blog about middle ear infections and autism (see here) in the context of ear, nose and throat being linked on several levels but further investigations are very much required on the biological parameters potentially important to findings such as those described by Murata et al. That being said [5] there may already be some clues in the peer-reviewed science literature...----------[1] Mitchell RB. Adenotonsillectomy for obstructive sleep apnea in children: outcome evaluated by pre- and postoperative polysomnography. Laryngoscope. 2007 Oct;117(10):1844-54.[2] Murata E. et al. Evaluation of behavioral change after adenotonsillectomy for obstructive sleep apnea in children with autism spectrum disorder. Res Dev Disabil. 2017 May 14;65:127-139.[3] Hirata I. et al. Sleep problems are more frequent and associated with problematic behaviors in preschoolers with autism spectrum disorder. Research in Developmental Disabilities. 2016; 49-50: 86-99.[4] Malow BA. et al. Impact of treating sleep apnea in a child with autism spectrum disorder. Pediatr Neurol. 2006 Apr;34(4):325-8.[5] Mitchell RB. & Kelly J. Behavioral changes in children with mild sleep-disordered breathing or obstructive sleep apnea after adenotonsillectomy. Laryngoscope. 2007 Sep;117(9):1685-8.----------Murata E, Mohri I, Kato-Nishimura K, Iimura J, Ogawa M, Tachibana M, Ohno Y, & Taniike M (2017). Evaluation of behavioral change after adenotonsillectomy for obstructive sleep apnea in children with autism spectrum disorder. Research in developmental disabilities, 65, 127-139 PMID: 28514706...

Murata E, Mohri I, Kato-Nishimura K, Iimura J, Ogawa M, Tachibana M, Ohno Y, & Taniike M. (2017) Evaluation of behavioral change after adenotonsillectomy for obstructive sleep apnea in children with autism spectrum disorder. Research in developmental disabilities, 127-139. PMID: 28514706  

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The many ways your smartphone is trying to control you….

While you may think most of the things we write about here are on litigation advocacy (and you would be correct) we also care about you, dear reader. We have written often about smartphones and their ubiquitous presence in our lives. This is a post to update you on the increasingly cruel reality of the […]...

Barque-Duran, A., Pothos, E., Hampton, J., & Yearsley, J. (2017) Contemporary morality: Moral judgments in digital contexts. Computers in Human Behavior, 184-193. DOI: 10.1016/j.chb.2017.05.020  

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Risperidone administration affects homocysteine levels in first episode schizophrenia

Of the many themes that seem to quite consistently surface on this blog looking at the peer-reviewed science in relation to various behavioural/psychiatric labels, the idea that various pharmacological interventions might do quite a bit more than 'what they say on the tin' is a recurring one. Take one case in point (see here)...Today's offering adds to that theme as the results reported by Ning Fan and colleagues [1] are presented for your reading pleasure and the particular finding that: "Serum Hcy [homocysteine] levels were significantly decreased in schizophrenia patients after risperidone treatment."OK, a few points need explaining first. Homocysteine is a compound that has also received considerable attention on this blog as per it's involvement in a particular group of intersecting biological cycles with relevance to various diagnostic labels including schizophrenia (see here for example). Alongside other independent pieces of research (see here), the diagnosis of schizophrenia seems to have some important connections to homocysteine although the precise details still need to be properly elucidated.High levels of homocysteine are generally not thought to be a good thing for quite a few reasons [2] and that goes as much for persons diagnosed with schizophrenia as it does for everyone else. So when elevated plasma levels of homocysteine are recorded, medicine really does need to do something to (a) identify why and (b) try and bring levels back to within a more typical range.Fan et al reported a few important things in their study of 56 participants "first-episode and drug-naïve inpatients with schizophrenia" compared with a similar number of sex- and age-matched asymptomatic controls. First, plasma homocysteine levels were elevated in those with schizophrenia. Nothing new there. They also reported on some potentially interesting *associations* between elevated homocysteine levels and specific symptoms relevant to schizophrenia: "a significant positive correlation between Hcy levels and PANSS negative sub-score was observed." Finally, they reported that risperidone use seemed to affect homocysteine levels in their clinical group. Interesting.That last point is rather intriguing. Risperidone is a treatment of choice as per its second generation antipsychotic label and accompanying properties. Despite quite a lot of focus on the side-effects associated with such a medicine (see here for example) it does serve an important purpose for many people. It's mode of action is still under debate but it is generally thought to have some action in relation to effects on one or more neurotransmitter receptors. But... other potential effects have also been noted in the peer-reviewed research literature pertinent to mode of action including some in relation to immune function (see here) and how schizophrenia (some schizophrenia?) *might* have a significant immune component attached to it (see here for example). The Fan results add another potential mode of action to risperidone use and why it may impact on symptom presentation for some diagnosed with schizophrenia and related conditions. I'm not by any means saying that homocysteine is 'causative' of schizophrenia but the Fan results do suggest that quite a few more investigations may be warranted on the connection between schizophrenia, homocysteine and risperidone. Indeed, whether also other homocysteine-lowering compounds may provide some novel intervention options for some diagnosed with schizophrenia (see here) (with no medical or clinical advice given or intended).----------[1] Fan N. et al. Effect of Risperidone on Serum Homocysteine Levels in First-episode, Drug-naïve Patients with Schizophrenia. Neurosci Lett. 2017 Apr 15. pii: S0304-3940(17)30326-9.[2] Zhang D. et al. Elevated Homocysteine Level and Folate Deficiency Associated with Increased Overall Risk of Carcinogenesis: Meta-Analysis of 83 Case-Control Studies Involving 35,758 Individuals. PLoS ONE. 2015; 10(5): e0123423. ----------Fan N, Tan Y, Yang F, Tian L, Chen S, Li J, Wang Z, & Zhang X (2017). Effect of Risperidone on Serum Homocysteine Levels in First-episode, Drug-naïve Patients with Schizophrenia. Neuroscience letters PMID: 28419824...

Fan N, Tan Y, Yang F, Tian L, Chen S, Li J, Wang Z, & Zhang X. (2017) Effect of Risperidone on Serum Homocysteine Levels in First-episode, Drug-naïve Patients with Schizophrenia. Neuroscience letters. PMID: 28419824  

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Differentiating between autism and ADHD the machine learning way (again)

So: "These results support the potential of creating a quick, accurate and widely accessible method for differentiating risks between ASD [autism spectrum disorder] and ADHD [attention-deficit hyperactivity disorder]."That was a conclusion reached in the paper by Marlena Duda and colleagues [1] (open-access) building on their previous foray into this important research area (see here). Last time around [2] this research group - the Duda/Wall et al research combination - set the scene for boiling down the Social Responsiveness Scale (SRS) from 65 items to something considerably smaller when it came to distinguishing autism from ADHD. This based on the idea that autism and ADHD are not unstrange diagnostic bedfellows (see here).This time around, researchers set out to "expand upon our prior work by including a novel crowdsourced data set of responses to our predefined top 15 SRS-derived questions from parents of children with ASD (n=248) or ADHD (n=174) to improve our model’s capability to generalize to new, ‘real-world’ data." Mention of the term 'crowdsourced' means that authors utilised various online social media platforms to "to inform the community of the study" and gather responses. Importantly, they note that "diagnoses of ASD or ADHD were provided as parent report."Results: once again applying various machine learning algorithms to their recently captured data and "mixing these novel survey data with our initial archival sample (n=3417)" authors reported some interesting findings. Taking the two samples - the archival samples and the recent crowdsourced data  - together they reported on the creation of "a classification algorithm that can generalize well to unseen data (AUC=0.89±0.01), even when those data have more natural variablity like the kind seen in our survey sample." This was based on the use of 15 items from the SRS.But... things were not all smooth sailing in this latest research effort. Bearing in mind the use of those 'parent reported' autism and ADHD participants in this latest study, authors noted that 'real-world' data is not necessarily the same as the very clinical data relied upon on the last research occasion. So: "In the archival sample, the responses for ADHD subjects were more uniform and on average less severe than the ADHD responses in the survey sample."Still, these are important results albeit requiring 'continued evaluation' as further crowdsourced and other data filter through. Indeed 'adaption' to new data seems to be something that the authors are particularly keen on to "further improve the generalizability of the classifier." I continue to applaud their research in this area as a function of their efforts (see here) to make autism and/or ADHD screening quicker, easier and more cost-effective.And on that last point. it is timely that such research continues given what is being proposed in certain parts of England when it comes to autism diagnoses (see here). Indeed, the suggestion of "restricting an autism diagnosis to only the most severe cases" as a function of some quite spectacular increasing demand - "The team is supposed to carry out 750 assessments a year. But it is getting almost double that level of demand, with about 25 referrals a week" - reiterates a need to streamline diagnostic services to make screening/diagnosis quicker, easier and more cost-effective.For those also who have said 'so what' to the increase in cases of autism (yes, someone actually did albeit with caveats), such proposals to potentially restrict autism diagnoses, I would say, are a direct result of such a mindset to 're-think' autism. Although well meaning, if enough people talk about difference over disability for example, purse string holders in the NHS (National Health Service) were eventually bound to ask 'why diagnose?' and 'why offer services?' (services that can cost quite a lot and even for those with 'severe autism' are often not there). As other authors have eloquently argued (see here) and indeed, foretold, mixed in with the current economic situation being put forward all in the name of austerity, low-hanging NHS services fruit like autism screening/assessment were certain to be eventually targeted and the 'difference over disability' framing unfortunately provides ample ammunition for such proposals...----------[1] Duda M. et al. Crowdsourced validation of a machine-learning classification system for autism and ADHD. Transl Psychiatry. 2017 May 16;7(5):e1133.[2] Duda M. et al. Use of machine learning for behavioral distinction of autism and ADHD. Transl Psychiatry. 2016 Feb 9;6:e732.----------Duda M, Haber N, Daniels J, & Wall DP (2017). Crowdsourced validation of a machine-learning classification system for autism and ADHD. Translational psychiatry, 7 (5) PMID: 28509905...

Duda M, Haber N, Daniels J, & Wall DP. (2017) Crowdsourced validation of a machine-learning classification system for autism and ADHD. Translational psychiatry, 7(5). PMID: 28509905  

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Your best bet for an expert witness is a friendly nerd rather than an attractive scientist

And it doesn’t really matter if the expert is male or female, if they are young or old, and they can be any ethnicity! In other words, said the researchers—the variables we have read so much about (i.e., gender, age, ethnicity) are not as notable as whether someone “looks like” our stereotype of a “good […]...

Gheorghiu, A., Callan, M., & Skylark, W. (2017) Facial appearance affects science communication. Proceedings of the National Academy of Sciences (PNAS)., 201620542. DOI: 10.1073/pnas.1620542114  

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On migration status and offspring autism severity

"Black women from East Africa had more than 3.5 times the odds of autism spectrum disorder with intellectual disability in their children than Caucasian nonimmigrant women."So said the study results reported by Jenny Fairthorn and colleagues [1] (open-access available here) providing yet more evidence for the need for much greater scrutiny as to why children of immigrant parents from East Africa are seemingly at higher risk of 'more severe' autism than other groups (see here and see here).Based on data from "Western Australian state registries" (yet again), researchers set about comparing autism prevalence with and without intellectual (learning) disability as a function of various variables: race (ethnicity), immigrant status and region of birth of mothers of children. The authors really drilled down into the details on immigrants according to their birth region in this study.Results: from a study sample of over 130,000 mothers, some 1000 had a child diagnosed with an autism spectrum disorder (ASD) together with intellectual disability (ID) and nearly 350 with a child with autism without ID. The figures equated to something like 0.7% of the total cohort with a child with autism and ID and 0.2% of the cohort with a child diagnosed with autism but not with ID. Authors also indicated that: "mothers of children with autism spectrum disorder with intellectual disability were more likely to be 40 years or more."Then to some important data: "After adjustment for demographic factors and compared to nonimmigrant women, immigrant women were less likely to have a child diagnosed with either autism spectrum disorder with intellectual disability or autism spectrum disorder without intellectual disability." This finding covered various geographic locations from which migrant mums came together with their race/ethnicity. That is however, aside from mothers from East Africa, and that "three-fold higher odds of having a child identified with autism spectrum disorder with intellectual disability." Authors added that "all autism spectrum disorder diagnoses in the children of Black mothers were of autism spectrum disorder with intellectual disability" and that all cases "were from mothers born in East Africa, with four born in Ethiopia and one each from Eritrea, Kenya, and Somalia."The authors acknowledge that their categorisations based on race/ethnicity and migration status led to some quite small group numbers being analysed (including not including any participants from other parts of Africa outside of East Africa). They also drew attention to the fact that their participant group of children with autism but without ID was quite a bit smaller than would be typically expected in comparison to the group with autism and ID (see here).But the results do paint an interesting picture and particularly with regards to those from East Africa, where they are in line with what has been previously discussed in the peer-reviewed and lay literature. The question of 'why' is probably going to be a complicated one as the authors suggested that "at least some of this difference could be the result of various factors leading to higher ascertainment of autism spectrum disorder in this group of children." They also qualify that statement by saying that they "cannot rule out the possibility of some biological risk factor, such as nutrition or stress" being involved which opens up a role for variables such as vitamin D exposure for example (see here).Personally, I think there are a few additional research directions that might need to be considered, primary among them is to have a little more detail on what autism prevalence might specifically look like in various areas of East Africa and Africa in general. I know this is a bit of a difficult ask in places where resources are really quite scarce, cultures are different (see here) and practical efforts for population screening are hindered by politics and the like. Until however we have such data, alongside some other important social and biological information, science doesn't have any 'baseline' measures on which to compare and contrast when it comes to families emigrating from such places and the possible reasons/changes that could be involved in this process and pertinent to offspring autism risk.----------[1] Fairthorne J. et al. Maternal Race-Ethnicity, Immigrant Status, Country of Birth, and the Odds of a Child With Autism. Child Neurol Open. 2017 Jan 12;4:2329048X16688125.----------Fairthorne J, de Klerk N, Leonard HM, Schieve LA, & Yeargin-Allsopp M (2017). Maternal Race-Ethnicity, Immigrant Status, Country of Birth, and the Odds of a Child With Autism. Child neurology open, 4 PMID: 28503625...

Fairthorne J, de Klerk N, Leonard HM, Schieve LA, & Yeargin-Allsopp M. (2017) Maternal Race-Ethnicity, Immigrant Status, Country of Birth, and the Odds of a Child With Autism. Child neurology open. PMID: 28503625  

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Healthcare use before, during and after a diagnosis of CFS/ME

"Adults and children with CFS/ME [chronic fatigue syndrome / myalgic encephalomyelitis] have greater health care needs than the rest of the population for at least ten years before their diagnosis, and these higher levels of health care resource use continue for at least ten years after diagnosis."So concluded the study published by Simon Collin and colleagues [1] (open-access available here) who once again (see here) relied on data derived from the "Clinical Practice Research Datalink (CPRD) GP practices in the UK" to further explore aspects of the debilitating condition(s) headed under the banner of CFS/ME.Using a case-control design, researchers set out to "investigate long-term patterns in health care resource use before and after a diagnosis of CFS/ME." They had a hypothesis in mind before any study results were produced in that "health care resource use would increase from around the time of patient-reported onset of illness... until diagnosis" but "did not have a prior hypothesis about post-diagnosis health care resource use, although this might be expected to fall if diagnosis led to referral and effective treatment."Their results based on "916 child (age <18 years) and 6710 adult patients" suggested a few things: (i) "a steep drop in resource use immediately after diagnosis was followed by sustained higher levels of health care resource use for at least ten years after diagnosis", (ii) adults and children with CFS/ME tended to have greater healthcare resource use "for at least ten years before the diagnosis", and (iii) allied to that last point: "there were steep increases in use of health care resources 2–4 years before diagnosis in adults and 1–2 years before diagnosis in children." Healthcare resource use, by the way, was defined as including several things including: "GP [general practitioner] consultations, tests, prescriptions, and referrals" (with certain caveats).Although carrying an important message that elevated healthcare resource use is associated with a diagnosis of CFS/ME (bearing in mind the limitations of the CPRD when it comes to CFS/ME), one has to be quite careful with how facets of the Collin data are handled. I say this specifically on the basis that healthcare use 'at least ten years before diagnosis' was found to be elevated for those with CFS/ME and how authors talk about this conflicting with "patients reporting that they were fit and well prior to the onset of their illness." You can perhaps see how this data *could* be used by some to 'challenge' patients with reference to their reliability in reporting their illness onset for example and/or the idea that "behaviour traits such as disease conviction and somatic concern could not be discounted as aetiological factors." This in the context that the biopsychosocial model of CFS/ME is still prevalent in some quarters (see here) particularly those linked to healthcare interactions.Thankfully the authors offer a couple of other potentially important reasons to account for their results based on (a) "people may simply have had CFS/ME for a very long time" and/or (b) "it is possible that people who develop CFS/ME have pre-existing risk factors which lead to higher rates of health care resource use." Indeed, on that second point, one might even argue that specific pre-existing medical complaints could/would/might predispose someone to developing CFS/ME (see here) particularly with all the talk about immune function potentially being a facet of some CFS/ME for example (see here). In this context, we perhaps need to know a little more about the genetics potentially important to CFS/ME, bearing in mind the emerging theme that condition-specific genes are not just genes specific to any one condition (see here for example).Accepting also that authors were "unable to determine from our data whether the type of health care resource use by patients changes following diagnosis" the finding that healthcare use continues to be fairly high after diagnosis is a worrying sign. It suggests that modern medicine might not be particularly good at treating/managing those with CFS/ME (and their associated conditions) in the longer term based on current best practice. I could be a little bit cynical on this point in relation to how current 'best practice' for managing/treating CFS/ME involves some rather controversial techniques which could be construed as 'failing' in the context of these results. Indeed, I will refer you to a quote by Jonathan Edwards [2] talking about the on-going controversy in CFS/ME circles in relation to how current best practice might not be as successful as many might think: "If they are still ill, presumably these approaches have failed and the priority is to find something more effective." Indeed.----------[1] Collin SM. et al. Health care resource use by patients before and after a diagnosis of chronic fatigue syndrome (CFS/ME): a clinical practice research datalink study. BMC Fam Pract. 2017 May 5;18(1):60.[2] Edwards J. PACE team response shows a disregard for the principles of science. 2017. J Health Psychology. March 28.----------Collin, S., Bakken, I., Nazareth, I., Crawley, E., & White, P. (2017). Health care resource use by patients before and after a diagnosis of chronic fatigue syndrome (CFS/ME): a clinical practice research datalink study BMC Family Practice, 18 (1) DOI: 10.1186/s12875-017-0635-z...

Collin, S., Bakken, I., Nazareth, I., Crawley, E., & White, P. (2017) Health care resource use by patients before and after a diagnosis of chronic fatigue syndrome (CFS/ME): a clinical practice research datalink study. BMC Family Practice, 18(1). DOI: 10.1186/s12875-017-0635-z  

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Witness preparation: To vocal fry or not to vocal fry?

If you are young(er) you likely know precisely what vocal fry means and if you are old(er)—probably not so much. It is a cultural phenomenon seen primarily (but not only) in young(er) women as described at the Mental Floss website: “Vocal fry describes a specific sound quality caused by the movement of the vocal folds. […]...

Anderson RC, Klofstad CA, Mayew WJ, & Venkatachalam M. (2014) Vocal fry may undermine the success of young women in the labor market. PLoS ONE, 9(5). PMID: 24870387  

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Assisted reproductive technology and risk of offspring autism meta-analysed

"Our study indicated that the use of ART [assisted reproductive technology] may [be] associated with higher risk of ASD [autism spectrum disorder] in the offspring. However, further prospective, large, and high-quality studies are still required."So said the results of the meta-analysis published by Liang Lui and colleagues [1] (open-access) surveying the peer-reviewed research literature - "11 records (3 cohort studies and 8 case-control studies)" - between 2006 and 2015. ART covers a variety of techniques "to achieve pregnancy and live birth" most notably including IVF (in vitro fertilisation) and artificial insemination. Some, but not all, of the studies included for review suggested an *association* between ART use and enhanced risk of offspring autism particularly in "European and Asian populations." The authors were however unable to tease apart which specific ART(s) might be associated with a higher risk than others.This is not the first time that this topic has been covered on this blog (see here). On that previous occasion I intimated that the source of any risk from ART on offspring autism was not yet identified and, in some cases, other birth factors might exert some effect. In short, it's more complicated than paper titles can transmit.Does my opinion change as a result of these meta-analysed findings? Well, not really. I appreciate the findings reported by Lui and colleagues but I still think other birth factors might come into play outside of just ART exerting a primary effect. Not least is the possibility that issues affecting fertility in the first place might be particularly relevant among other confounders. I echo the sentiments of the authors that more research might be required in this area but with the various stresses and strains being placed on autism research resources these days, I'm not inclined to suggest that this area should necessarily be top of this list of priorities. Sorry.----------[1] Liu L. et al. Association between assisted reproductive technology and the risk of autism spectrum disorders in the offspring: a meta-analysis. Sci Rep. 2017 Apr 7;7:46207.----------Liu L, Gao J, He X, Cai Y, Wang L, & Fan X (2017). Association between assisted reproductive technology and the risk of autism spectrum disorders in the offspring: a meta-analysis. Scientific reports, 7 PMID: 28387368...

Liu L, Gao J, He X, Cai Y, Wang L, & Fan X. (2017) Association between assisted reproductive technology and the risk of autism spectrum disorders in the offspring: a meta-analysis. Scientific reports, 46207. PMID: 28387368  

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Unattractive People Are Seen As Better Scientists

Good looking, sociable people don't make good scientists, according to popular stereotypes. This is one of the findings of an interesting new study of how scientists are perceived, from British researchers Ana I. Gheorghiu and colleagues. Gheorghiu et al. took 616 pictures of scientists, which they downloaded from the faculty pages at various universities. They gave the portraits to two sets of raters. The first group were asked to rate the attractiveness of the portraits and to say whet...

Gheorghiu AI, Callan MJ, & Skylark WJ. (2017) Facial appearance affects science communication. Proceedings of the National Academy of Sciences of the United States of America. PMID: 28533389  

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How Men Age, a book review

Nothing would be more interesting than reading a book on men aging by the author who is an expert on comparative male life histories. Richard G. Bribiescas is a Professor of Anthropology, Ecology and Evolutionary Biology at Yale University, and has conducted research in evolutionary biology and endocrinology of human, as well as comparative studies […]...

Pazhoohi, F. (2017) Book Review: How Men Age: What Evolution Reveals about Male Health and Mortality. Frontiers in Psychology. info:/10.3389/fpsyg.2017.00894

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Low dose suramin and autism: a small RCT with potentially big results

'Low dose' has been a feature of my autism research reading this week; first starting with the results from Dan Quintana and colleagues [1] talking about some important effects following intranasal delivery of low dose oxytocin and then moving on to the primary reason for this entry with results from Robert Naviaux and colleagues [2] (open-access) continuing a research theme looking at suramin and autism (see here for some background).For those interested in the oxytocin-autism research base, I can recommend following Dr Quintana on Twitter (find him here).In relation to the Naviaux findings  - the "Suramin Autism Treatment-1 (SAT-1) trial" - well, they are open-access but I want to provide some overview and then a little bit of discussion. I might add that this research team are making research waves in several areas of medical science as per their research foray into chronic fatigue syndrome (CFS) recently (see here). Such 'metabolomic' research is pertinent to their autism research too.This time around as on previous research occasions, the focus was on suramin - the "century-old sleeping sickness drug" - and, as far as I can see, the first time said drug has been tested experimentally with children diagnosed with an autism spectrum disorder (ASD). The accompanying ClinicalTrials.gov trial entry is here.As per the title to this blog entry, this was a small trial including only 10 participants, all male, aged between 5-14 years old. This was a randomised-controlled trial (RCT) with a placebo element to it too, so half of the participants got suramin - "a single, intravenous infusion of suramin (20 mg/kg)" - and half got saline as a control. Alongside looking at behaviour and functioning, researchers also took blood and urine samples "for safety and toxicity monitoring at 5 times throughout the study." This was accompanied by quite a bit of effort to look at the possibility of adverse events related to suramin or placebo administration.Results: "A single intravenous dose of suramin was associated with improved scores for language, social interaction, and decreased restricted or repetitive behaviors measured by ADOS, ABC, ATEC, and CGI scores. None of these improvements occurred in the five children who received placebo." The authors also do the right thing by stating: "The generalizability of these findings is unknown." I'm particularly impressed that the ATEC gets a showing given the rise and rise of this autism research tool (see here) in various placebo-controlled contexts (see here).In relation to the safety aspect to suramin, well, it seemed to do alright. We are told that: "Extensive monitoring revealed no serious toxicities" so one can assume that the 'first, do no harm' tenet was upheld in this trial. But there was one important side-effect noted: "Five children who received suramin developed a self-limited, evanescent, asymptomatic, fine macular, patchy, morbilliform rash over 1–20% of their body." The rash was short-lived and did not require specific attention/intervention but it's worthwhile noting it especially when nothing similar was reported in the placebo group.Going back to the mention of this research group delving into CFS with metabolomics in mind, so similar results are reported on the basis of examination of plasma samples from participants. Various biological pathways seemed to be affected by the infusion of suramin, not least "the importance of the cell danger response (CDR) [3]... and purinergic signaling." Interestingly, authors also noted effects in relation to "1-carbon, folate, methionine, and cysteine metabolism" too, potentially linked to other findings independently reported in relation to autism (see here for example).Reiterating again that this was a small study (albeit using the gold-standard in scientific methodologies) these results are rather interesting and potentially quite important. They most definitely point to the requirement for further large-scale studies to look at any effects in a larger participant group and to 'zoom in' on potential best-responders to this type of intervention. I end with an important conclusion from the authors who again, have not over-stated their findings:"Suramin is not approved for the treatment of autism. Like many intravenous drugs, when administered improperly by untrained personnel, at the wrong dose and schedule, without careful measurement of drug levels and monitoring for toxicity, suramin can cause harm. Careful clinical trials will be needed over several years at several sites to learn how to use low-dose suramin safely in autism, and to identify drug–drug interactions and rare side effects that cannot currently be predicted. We strongly caution against the unauthorized use of suramin."----------[1] Quintana DS. et al. Dose-dependent social-cognitive effects of intranasal oxytocin delivered with novel Breath Powered device in adults with autism spectrum disorder: a randomized placebo-controlled double-blind crossover trial. Transl Psychiatry. 2017 May 23;7(5):e1136.[2] Naviaux RK. et al. Low-dose suramin in autism spectrum disorder: a small, phase I/II, randomized clinical trial. Annals of Clinical & Translational Neurology. 2017. 26 May.[3] Naviaux RK. Metabolic features of the cell danger response. Mitochondrion. 2014; 16: 7-17.----------Naviaux, R., Curtis, B., Li, K., Naviaux, J., Bright, A., Reiner, G., Westerfield, M., Goh, S., Alaynick, W., Wang, L., Capparelli, E., Adams, C., Sun, J., Jain, S., He, F., Arellano, D., Mash, L., Chukoskie, L., Lincoln, A., & Townsend, J. (2017). Low-dose suramin in autism spectrum disorder: a small, phase I/II, randomized clinical trial Annals of Clinical and Translational Neurology DOI: 10.1002/acn3.424...

Naviaux, R., Curtis, B., Li, K., Naviaux, J., Bright, A., Reiner, G., Westerfield, M., Goh, S., Alaynick, W., Wang, L.... (2017) Low-dose suramin in autism spectrum disorder: a small, phase I/II, randomized clinical trial. Annals of Clinical and Translational Neurology. DOI: 10.1002/acn3.424  

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Cassandra’s Regret: The Psychology of Not Wanting to Know

Do you want to know the future? You may want to say it all depends on which aspects of your future. Typically, while we seek information routinely to make decisions in our day-to-day lives, we don’t always want to know for sure what will happen in our futures. These researchers remind us about the story […]...

Gigerenzer G, & Garcia-Retamero R. (2017) Cassandra's regret: The psychology of not wanting to know. Psychological Review, 124(2), 179-196. PMID: 28221086  

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The Ugliness Penalty: Does It Literally Pay to Be Pretty?

There are economic studies that show that attractive people earn more money and, conversely, unattractive earn less money. I’m pretty sure that I’ve heard something along those lines before, but I had no idea they were called the “beauty premium” and the “ugliness penalty.” How wonderful and sad at the same time. But while these seem like pretty commonplace ideas, there is no real evidence as to why they exist. A new paper published in the Journal of Business and Psychology tested three of the leading explanations of the existence or the beauty premium and ugliness penalty: discrimination, self-election, and individual differences. To do this, the researchers used data from the National Longitudinal Survey of Adolescent Health. This is a nationally representative sample that includes measurements of physical attractiveness (5-point scale) at four time points to the age of 29. People were placed into 5 categories based on physical attractiveness, from very attractive to very unattractive. They statistically compared every combination they could think of and came up with many tables full of tiny numbers, as well as some interesting results.DiscriminationIt is what it sounds like: ugly people are discriminated against and paid less. And it isn’t just from employers, it can also be from co-workers, customers, or clients that prefer to work with or do business with pretty people. Or it could be a combination, like an employer that hires someone pretty because they know that others will respond to them better. Because there is a monotonically positive association between attractiveness and earnings (an overly academic way of saying that one is linked to the other), it can be tested.The results painted a somewhat different picture than you might expect. There was some evidence of a beauty premium in that pretty people earned more than average looking people. However, the researchers found that attractiveness and earnings were not at all monotonic. In fact, ugly people earned more than both average and attractive people, with “very unattractive” people winning out in most cases. So no ugliness penalty and no discrimination there. Good, we don’t like discrimination. Rather, the underlying productivity of workers as measured by their intelligence and education accounted for the associations observed. Basically, ugly people were smarter (and yes, IQ was a variable).Self-ElectionThis occurs in the absence of discrimination. A person self-sorts themselves into an attractiveness group based on how attractive they perceive themselves to be and may choose their occupation accordingly. If a pretty person chooses an occupation that has higher earnings (or vice versa), then there is a positive association between attractiveness and earnings both across and within occupations.Once again, the results were unexpected. The self-selection hypothesis was refuted. Ugly people earned more than pretty people. In fact, very unattractive people earned more than both regular unattractive and average looking people. This is where the researchers start calling this effect “the ugliness premium.” Good term. Individual DifferencesThis one posits that a pretty and ugly people are genuinely different. Try looking at it in the context of evolutionary biology. Physical attractiveness is based on facial symmetry, averageness, and secondary sexual characteristics, which all signal genetic and developmental health. Many traits can be quantified very accurately with today’s computers. There are standards of beauty both within a single culture and across all cultures. Studies have also shown that attractive children receive more positive feedback from interpersonal interactions, making them more likely to develop an extraverted personality. If health, intelligence, and personality, along with other measures of productivity, are statistically controlled then attractiveness should be able to be compared to earnings.Again, there was absolutely no evidence for either the beauty premium or the ugliness penalty. Rather, there was some support for the ugliness premium. Now keep in mind, this was not as much a this-higher-than-that, but more of a this-different-from-that type of hypothesis. So there actually is strong support that there are differences. There was a significantly positive effect of health and intelligence on earnings. Also, the “Big Five” personality factors – Openness, Conscientiousness, Extroversion, Agreeableness, and Neuroticism (or OCEAN…cute) – were significantly correlated with physical attractiveness. Pretty people were more OCEA and less N. This may be why looks appear to have an effect on earnings.Overall, not what you thought it would be, huh? Me either. The importance of intelligence and education as it correlates with attractiveness would be an interesting next step. I wonder if it reflects the time at which these data were taken. We are seeing the Rise of the Nerds, where intelligence is outpacing beauty in terms of success. Had they analyzed data from another decade, would the ugliness penalty find support?Kanazawa, S., & Still, M. (2017). Is There Really a Beauty Premium or an Ugliness Penalty on Earnings? Journal of Business and Psychology DOI: 10.1007/s10869-017-9489-6image via Linked4Success...

Kanazawa, S., & Still, M. (2017) Is There Really a Beauty Premium or an Ugliness Penalty on Earnings?. Journal of Business and Psychology. DOI: 10.1007/s10869-017-9489-6  

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On ADHD medication and motor vehicle crashes

"Among patients with ADHD [attention-deficit hyperactivity disorder], rates of MVCs [motor vehicle crashes] were lower during periods when they received ADHD medication."That was the research bottom-line discussed by Zheng Chang and colleagues [1] who continue a theme on how managing/treating the symptoms of ADHD can often have some profound effects on those diagnosed with ADHD and also the wider population.The outcome measure on this occasion was MVCs; in particular: "Emergency department visits for MVCs" as assessed from data from the "Truven Health Analytics MarketScan Commercial Claims and Encounters databases." I've talked about the application of this resource in a research context before on this blog (see here). Such Emergency Room (ER) (also known as Accident & Emergency (A&E) here in Blighty) visits were assessed for those with and without a diagnosis of ADHD or those in receipt of  "ADHD medication between January 1, 2005, and December 31, 2014." Authors compared the "risk of at least one MVC between patients with ADHD and matched controls."The results, based on quite a large number of people (2 million+) diagnosed with ADHD, suggested that: "Patients with ADHD had a significantly higher risk of an MVC than their matched controls." Medication for ADHD - of which over 80% of the cohort with ADHD were taking - seemed to affect the risk of MVCs as per the sentence introducing this post. Indeed authors noted: "months with ADHD medication were associated with a 12%... lower risk of MVCs in male patients with ADHD relative to unmedicated months and a 14%... lower risk of MVCs in female patients with ADHD." The figures actually got even better for risk reduction of MVCs when analysed at the "within-individual" level: "men with ADHD were 38% less likely to have MVC events during medicated months relative to unmedicated months" and for women, this figure went up to 42% less likely to have an MVC during medicated months. All-in-all, treating ADHD with medication meant less visits to the ER for motor vehicle crashes.Accepting that the use of medication for ADHD (or anything else) is not something that should ever be entered into lightly, there is quite a large body of evidence emerging suggesting that specific preparations at least, are both safe and reliable in terms of tackling the symptoms of ADHD (see here). Indeed, clinicians are seemingly becoming a lot more comfortable with employing pharmacotherapeutic strategies for ADHD (see here) probably in part, due to the effectiveness of available medications and their pretty good safety profile. I say all that noting that medication is not necessarily the only tool in the arsenal (see here and see here for examples).Of course there are caveats to this latest set of results; not least that this was a study looking at two variables (MVCs leading to ER attendance and ADHD medication(s)) and so might potentially have missed other data/factors (e.g. MVCs not requiring ER attendance). One also assumes that ADHD medication prescriptions were also being taken uniformly every day as indicated...Still, there is good reason to think that ADHD medication might be 'doing what it says on the tin' in terms of tackling issues such as inattention and impulsivity and how this had knock-on effects for MVCs requiring hospitalisation. Indeed, thinking also about the safety of other motorists who might have potentially benefited from the behaviour of those drivers with ADHD under medication, one can only see the life-changing potential of these informative results...----------[1] Chang Z. et al. Association Between Medication Use for Attention-Deficit/Hyperactivity Disorder and Risk of Motor Vehicle Crashes. JAMA Psychiatry. 2017. May 10.----------Chang Z, Quinn PD, Hur K, Gibbons RD, Sjolander A, Larsson H, & D'Onofrio BM (2017). Association Between Medication Use for Attention-Deficit/Hyperactivity Disorder and Risk of Motor Vehicle Crashes. JAMA psychiatry PMID: 28492937...

Chang Z, Quinn PD, Hur K, Gibbons RD, Sjolander A, Larsson H, & D'Onofrio BM. (2017) Association Between Medication Use for Attention-Deficit/Hyperactivity Disorder and Risk of Motor Vehicle Crashes. JAMA psychiatry. PMID: 28492937  

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Gaslighting in the Medical Literature

Have you felt that your sense of reality has been challenged lately? That the word “truth” has no meaning any more? Does the existence of alternative facts make you question your own sanity? In modern usage, the term gaslighting refers to “a form of psychological abuse in which false information is presented to the victim with the intent of making him/her doubt his/her own memory and perception”.Gaslighting is a form of manipulation that seeks to sow seeds of doubt in a targeted individual or members of a group, hoping to make targets question their own memory, perception, and sanity. Using persistent denial, misdirection, contradiction, and lying, it attempts to destabilize the target and delegitimize the target's belief.In December 2016, the amazing Lauren Duca1 wrote a widely shared piece for Teen Vogue, Donald Trump Is Gaslighting America. In it, she argued that Trump won the election by normalizing deception. Duca noted that the term gaslighting originated from the 1938 play Gas Light by Patrick Hamilton, and explained it in this way:"Gas lighting" is a buzzy name for a terrifying strategy currently being used to weaken and blind the American electorate. We are collectively being treated like Bella Manningham in the 1938 Victorian thriller from which the term "gas light" takes its name. In the play, Jack terrorizes his wife Bella into questioning her reality by blaming her for mischievously misplacing household items which he systematically hides. Doubting whether her perspective can be trusted, Bella clings to a single shred of evidence: the dimming of the gas lights that accompanies the late night execution of Jack’s trickery. The wavering flame is the one thing that holds her conviction in place as she wriggles free of her captor’s control.Gaslighting in the Medical LiteratureBarton and Whitehead (1969) were the first to report cases where a patient's mental state was manipulated for material (or situational) gain, calling it the “Gas-Light Phenomenon”. If these incidents sound like something straight out of domestic noir or a TV crime drama, you'd be right.Case 1 – 48 year old mechanic, married for 10 years, with three childrenMr. A. was admitted one evening to a psychiatric hospital as an emergency. His general practitioner, when asking for his admission, had said he was mentally ill and had attacked his wife. ...On admission the patient said he had felt tense and depressed for about six months and related this to his wife’s changed attitude towards him. He said she had become "cold", and he thought she might have been seeing another man. He denied he had been violent and thought he had been sent into hospital because of his "nerves".His wife had concocted an elaborate tale of abuse, saying he had become “irritable, bad-tempered, and liable to unprovoked violent outbursts in which he sometimes hit her and once struck her with a hatchet.” She also claimed his memory was deteriorating, and she categorically denied having an affair. Mr. A was hospitalized for 12 days with no obvious physical or psychiatric disorder and left feeling more relaxed.However, he returned to hospital two weeks later: “He said his wife had started taunting him, saying he was mad and should be in a mental hospital. His wife said that his mental condition had considerably worsened and that he had attacked her twice.”Fortunately for Mr. A, his boss overheard a conversation between two men in the local tavern. One of the men was Mrs. A's lover, discussing how the two of them had plotted to get rid of Mr. A using the false claims of mental illness and abuse. The hospital staff confronted Mrs. A with her lies:She finally agreed that she had plotted with her boy-friend to get rid of her husband, but claimed she had been led on by him and now very much regretted her behaviour. Following some family counselling Mr. and Mrs. A. became reconciled and five years later were still living happily together.Case 2 – 45 year old pub owner married for 14 yearsMr. B was admitted based on his wife's story about her husband’s “heavy drinking, erratic behaviour, and aggressive outbursts.”On admission to the unit Mr. B. gave a history of domestic difficulties and described mild symptoms of anxiety and depression. ...  He agreed that he was irritable but said that he had never been aggressive and did not acknowledge any of the common symptoms of alcoholism. ... recently ... his wife had lost interest in him and had started associating with younger men. She often stayed out all night, and when he asked her about this behaviour she told him not to be silly and accused him of being a drunk who should be put away.A member of the staff eventually found out about Mrs. B's fabrication and her intent to get rid of her husband, keep the pub, and “then really start living.” Unlike the outcome of Case 1, Mr. B left his wife and was quite happy without her five years later.Case 3 – 72 year old widowThis case is unique, because it goes beyond mere mental manipulation. Mrs. C. was referred to a psychiatric hospital because of a "confusional state" and "fecal incontinence" that made her unfit for the old persons' home where she resided. She had moderate Parkinson's disease and slight dementia, but she was fairly well oriented and pleasant in demeanor. She stayed in the hospital for six weeks and showed no signs of fecal incontinence while there. And indeed it turned out that her incontinence had been cruelly induced by large doses of laxatives:The lady running the home had been unable to develop a good relationship with Mrs. C. and considered "she was a naughty old thing making life difficult for me, my staff, and other folk on purpose".For some weeks before admission to hospital Mrs. C. had been receiving ’Dulcolax’ tablets one three times a day. This had produced the expected effect with occasional "accidents" due to Mrs. C.’s mobility difficulties. The evidence suggested that Mrs. C. was not wanted in the home and induced incontinence was used as a method of getting her removed to hospital.Case 4 – Another example is an incident reported by Lund and Gardiner (1977), where the staff of the mental hospital conspired to keep a patient there so that one of them could live in her flat. The elderly woman had suffered from paranoid episodes in the past that were successfully treated with medication. But this time “they” were really out to get her:Miss A., an 80-year-old retired professional lady, was first admitted to a mental hospital in connection with this incident under Section 31 of the Mental Health (Scotland) Act 1960, from her pleasant flat in a residential establishment. The admission notes stated that she had complained that there were people on the premises who had no business there, that they had spoken outside her door saying that they were going to throw her into the river and that she further believed that these people were 'after my flat'...Miss A was shuttled in and out of hospital several times until the evil plot was finally foiled:She was admitted for the third time some four months later with a depressingly similar story. Her general practitioner had been called to the home where the patient had allegedly ' barricaded her room'; she had simply put a chair against the door. She was again admitted under an Emergency Order and once more settled down very rapidly, showing no sign of disturbed behaviour. She was generally pleasant and witty, showing some evidence of valuing her independence and mildly resenting the help of the nursing staff, which she regarded as unnecessary interference. At this point, suspicion about the motives of the staff at the institution were aroused. Discreet inquiries revealed that the rooms which Miss A occupied had...

Barton R, & Whitehead JA. (1969) The gas-light phenomenon. Lancet (London, England), 1(7608), 1258-60. PMID: 4182427  

Kutcher SP. (1982) The gaslight syndrome. Canadian journal of psychiatry. Revue canadienne de psychiatrie, 27(3), 224-7. PMID: 7093877  

Lund CA, & Gardiner AQ. (1977) The gaslight phenomenon--an institutional variant. The British journal of psychiatry : the journal of mental science, 533-4. PMID: 588872  

Smith CG, & Sinanan K. (1972) The "gaslight phenomenon" reappears. A modification of the Ganser syndrome. The British journal of psychiatry : the journal of mental science, 120(559), 685-6. PMID: 5043219  

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Blood heavy metal levels and autism (yet again)

"Data showed that the children with ASD [autism spectrum disorder] had significantly (p < 0.001) higher levels of mercury and arsenic and a lower level of cadmium."And... "It is desirable to continue future research into the relationship between ASD and heavy metal exposure."Those sentences come from the study by Huamei Li and colleagues [1] continuing a research theme regarding (generally) elevated levels of heavy metals being detected in those on the autism spectrum (see here). Yes, I know that this kind of research is not always met with great appreciation (see here) but the suggestion that the heavy metal burden seems to be quite a bit higher in the autistic population is not something that can just be ignored. More so when it might actually be treatable (with no medical or clinical advice given or intended)...There are numerous other examples in the peer-reviewed science literature that I could give where the heavy metal burden has been found to be elevated in relation to autism. Indeed, if someone is looking for yet another systematic review and meta-analysis topic, there you go - you're welcome. Personally, I think we've reached the point where the questioning needs to move on to (a) the possible sources of those heavy metals and (b) whether 'exposure amount' is the sole reason for the elevations in relation to autism over and above issues with the biology around 'detoxifying' said metals. Answers are not likely to be simple but questioning has to continue...To close, he was always my favourite James Bond...----------[1] Li H. et al. Blood Mercury, Arsenic, Cadmium, and Lead in Children with Autism Spectrum Disorder. Biol Trace Elem Res. 2017 May 8.---------- Li H, Li H, Li Y, Liu Y, & Zhao Z (2017). Blood Mercury, Arsenic, Cadmium, and Lead in Children with Autism Spectrum Disorder. Biological trace element research PMID: 28480499...

Li H, Li H, Li Y, Liu Y, & Zhao Z. (2017) Blood Mercury, Arsenic, Cadmium, and Lead in Children with Autism Spectrum Disorder. Biological trace element research. PMID: 28480499  

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The Invisibility Cloak Illusion: We are more observant (and yet, less observed) than all others

This is the sort of article that can either amuse or terrify you. It will amuse you if you are charmed by all the ways in which we see ourselves as superior to others. And it will terrify you if you do not want to know that you are always being observed closely by everyone […]...

Boothby EJ, Clark MS, & Bargh JA. (2017) The invisibility cloak illusion: People (incorrectly) believe they observe others more than others observe them. Journal of Personality and Social Psychology, 112(4), 589-606. PMID: 27977221  

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Irritable bowel syndrome (IBS) as a risk factor for bipolar disorder

"Only irritable bowel syndrome (IBS) emerged as a risk factor for BD [bipolar disorder] supported by convincing evidence."So said the results of the umbrella review of systematic reviews and meta-analyses by Beatrice Bortolato and colleagues [1] looking at the various environmental risk factors potentially linked to the diagnosis of bipolar disorder. I might add that this is a topic that has been discussed before on this blog (see here and see here for examples).If the systematic review / meta-analysis represents the top of the research methodology hierarchy, a review including a number of systematic reviews and meta-analyses represents the cherry on top. Indeed, there is a growing trend of this kind of research (see here).The authorship names included on the Bortolato paper are not unfamiliar to this type of study methodology (see here) and specifically, the focus on psychiatric and somatic variables often being intertwined. This time around attentions turned to bipolar disorder, previously called manic depression, and a survey of 16 research publications identified listing over 50 "unique environmental risk factors for BD." The report of a possible link (with 'convincing evidence') between IBS and BD consolidates the idea of a gut-brain axis. Authors also detailed a few other factors as showing weaker but not necessarily less important connections to BD including childhood adversity, obesity and asthma. Focusing in on asthma in particular - a condition again previously talked about in the context of BD - I am wondering whether there are quite a few more generalisations connected to this diagnosis within the context of psychiatric labels (see here and see here)?Of course, more science is indicated on the hows-and-whys of connections such as the one between IBS and BD and the tantalising prospect of new intervention avenues if such a relationship is further confirmed. Minus any medical or clinical advice, I'm specifically thinking about how alterations to the gut microbiome accompanying cases of IBS might mean that talk of things like probiotics affecting the symptoms of IBS (see here) could be applicable to the presentation of [some] BD too. That and the idea that certain dietary elements might also be important to cases (see here and see here)...To close, I know that the past few days have not exactly been ones for smiling, but if some smiles and laughter are what you need, then the animal kingdom can provide them...----------[1] Bortolato B. et al. Systematic assessment of environmental risk factors for bipolar disorder: an umbrella review of systematic reviews and meta-analyses. Bipolar Disord. 2017; 00: 1–13.----------Bortolato, B., Köhler, C., Evangelou, E., León-Caballero, J., Solmi, M., Stubbs, B., Belbasis, L., Pacchiarotti, I., Kessing, L., Berk, M., Vieta, E., & Carvalho, A. (2017). Systematic assessment of environmental risk factors for bipolar disorder: an umbrella review of systematic reviews and meta-analyses Bipolar Disorders DOI: 10.1111/bdi.12490...

Bortolato, B., Köhler, C., Evangelou, E., León-Caballero, J., Solmi, M., Stubbs, B., Belbasis, L., Pacchiarotti, I., Kessing, L., Berk, M.... (2017) Systematic assessment of environmental risk factors for bipolar disorder: an umbrella review of systematic reviews and meta-analyses. Bipolar Disorders. DOI: 10.1111/bdi.12490  

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