Tuesday, 3 May 2016

Machine learning applied to autism screening going big time?

Machine learning, when machines, er.. learn, is of growing interest to the autism research field. The names Wall and Duda have filled quite a few posts on this blog (see here and see here for example) on this topic and their suggesting that applying machine learning algorithms to something like autism screening and detection could cut down on time taken and resources used.

As per the publication of the paper by Daniel Bone and colleagues [1] it appears that others working in autism research are also waking up to the idea that this might be a useful area to investigate. So: "In this work, we fastidiously utilize ML [machine learning] to derive autism spectrum disorder (ASD) instrument algorithms in an attempt to improve upon widely used ASD screening and diagnostic tools." Fastidiously is such a lovely word (particularly in the context of science).

The tools in question were the Autism Diagnostic Interview-Revised (ADI-R) and Social Responsiveness Scale (SRS) (both of which have already been machine learning 'applied') and their scores "for 1,264 verbal individuals with ASD [autism spectrum disorder] and 462 verbal individuals with non-ASD developmental or psychiatric disorders, split at age 10." And the results... well, let's just say that the authors were not disappointed - or at least less disappointed than on previous research occasions [2] - as they reported on created algorithms that "were more effective (higher performing) than the current algorithms, were tunable (sensitivity and specificity can be differentially weighted), and were more efficient (achieving near-peak performance with five or fewer codes)." Indeed: "We present a screener algorithm for below (above) age 10 that reached 89.2% (86.7%) sensitivity and 59.0% (53.4%) specificity with only five behavioral codes.Sensitivity and specificity are important concepts when it comes to something like screening instruments in terms of identifying 'all' those with a specific condition and making sure that no 'not-cases' aren't mistakenly identified as 'cases'. The nearly 90% sensitivity rate presented by Bone et al on the basis of 5 behavioural codes is not to be sniffed at.

The addition of one Cathy Lord to the authorship of the Bone paper also adds an air of inevitability that applying machine learning to autism research (and practice) is going to continue and increase. Not only because of her historical connection to the ADI-R [3] (which is a hefty document in anyone's book) but also given her very prominent role in autism research history. Who knows, I might one day be blogging about more big autism research names talking about Wall/Duda things including autism screening triage by YouTube? The final question is: outside of just behavioural variables, who would be brave enough to talk genetics/epigenetics/biology machine learning as the next step in autism screening and/or assessment?


[1] Bone D. et al. Use of machine learning to improve autism screening and diagnostic instruments: effectiveness, efficiency, and multi-instrument fusion. J Child Psychol Psychiatry. 2016 Apr 19.

[2] Bone D. et al. Applying machine learning to facilitate autism diagnostics: pitfalls and promises. J Autism Dev Disord. 2015 May;45(5):1121-36.

[3] Lord C. et al. Autism Diagnostic Interview-Revised: a revised version of a diagnostic interview for caregivers of individuals with possible pervasive developmental disorders. J Autism Dev Disord. 1994 Oct;24(5):659-85.


ResearchBlogging.org Bone D, Bishop S, Black MP, Goodwin MS, Lord C, & Narayanan SS (2016). Use of machine learning to improve autism screening and diagnostic instruments: effectiveness, efficiency, and multi-instrument fusion. Journal of child psychology and psychiatry, and allied disciplines PMID: 27090613

Monday, 2 May 2016

On defining chronic fatigue syndrome / myalgic encephalomyelitis (CFS/ME)

Most people who know a little bit about chronic fatigue syndrome / myalgic encephalomyelitis (CFS/ME) will probably understand the potential importance of the findings reported by Leonard Jason and colleagues [1] (open-access available here). Suggesting that there may be "four groupings of patients" when it comes to how we "name and define the illnesses", this research group who surveyed over 500 people "in the United States, Great Britain, and Norway" report on one of the biggest challenges facing ME/CFS... how do we accurately define it?

The problem of defining CFS/ME stems from the fact that there are currently several clinical presentations where CFS/ME might figure (or at least where patients fulfil ME/CFS criteria) and several different ways of clinically defining the condition(s) (see here and see here). That list of definitions may indeed also be growing (see here). With all that confusion about clinical overlap and what criteria are defining what patient group, it's little wonder that research is just starting to come to grips with some of the potential underlying biology of [some] CFS/ME (see here) after so many years in the scientific wilderness. Indeed, as with many conditions resting in that 'unexplained symptoms' category, not knowing can sometimes be fertile ground for various [unfounded] theorising...

Jason et al (whose research has graced this blog before) set about categorising their participant group based on various case definitions and symptom presentations. They reported four groupings; by far the largest group of their participants (n=346) fell into a categorisation that "involves more specific criteria" defining CFS/ME including use of the relative new term SEID (Systemic Exertion Intolerance Disease). Further: "efforts have specified domains of substantial reductions of activity, post-exertional malaise, neurocognitive impairment, and sleep dysfunction" and "Patients with these characteristics were more functionally impaired than those meeting just chronic fatigue criteria." The term used by authors for this group was Neuroendocrineimmune Dysfunction Syndrome (NDS) following on from previous work [2]. Smaller numbers of people included on their study did meet criteria for chronic fatigue (greater than 6 months) with (n=47) or without (n=62) explanation "by medical or psychiatric conditions." Jason and colleagues also defined a smaller group who met the Ramsay ME criteria and who were described as an "even more impaired group." I wonder if this might include the 'housebound' group described in other research?

The authors accept that there are 'limitations' to their research including issues around how they chose their sample(s) and some of the tools used relying on self-report; further work is indicated. But as a start trying to disentangle both the heterogeneity and issues with clinical classification when it comes to CFS/ME, their paper represents a good attempt to further focus minds on the spectrum of various overlapping fatigue conditions present and how we go about teasing apart phenotypes with a focus on core symptoms [2]. Minus the psychiatry focus, perhaps it is time to also looking at applying something like the principles of RDoC to the issue of ME/CFS?


[1] Jason LA. et al. Case definitions integrating empiric and consensus perspectives. Fatigue. 2016;4(1):1-23.

[2] Jason LA. et al. Factor Analysis of the DePaul Symptom Questionnaire: Identifying Core Domains. J Neurol Neurobiol. 2015 Sep;1(4).


ResearchBlogging.org Jason LA, McManimen S, Sunnquist M, Brown A, Furst J, Newton JL, & Strand EB (2016). Case definitions integrating empiric and consensus perspectives. Fatigue : biomedicine, health & behavior, 4 (1), 1-23 PMID: 27088059

Saturday, 30 April 2016

The 'anti-neuroinflammatory activity' of oxytocin

Whilst the package inserts of the various drugs that modern medicine has at its disposal provides important information on potential mode of action, there is a growing realisation that drugs generally have quite a few more molecular targets than are perhaps listed. Take for example the quite commonly used (in some parts of the world anyway) compound called melatonin  that in some instances can provide almost miraculous relief when it comes to sleeping issues under certain circumstances. A derivative of the amino acid tryptophan, melatonin might however be quite the molecular handy-person when it comes to its biological targets including its actions on something called leaky gut for example...

The paper by Lin Yuan and colleagues [1] similarly suggests that everyone's favourite 'cuddle hormone' (oxytocin) might also have a wider range of biological effects than has hitherto been fully appreciated.  Drawing on cell line results and intra-nasal administration of oxytocin (OT) to [artificially] immune-stimulated mice, authors reported that "OT possesses anti-neuroinflammatory activity and might serve as a potential therapeutic agent for treating neuroinflammatory diseases."

One of the primary analytical targets of the Yuan study were microglia, those 'constant gardeners' according to one description, and how administration of OT might have some interesting effects on the activation of microglia under certain circumstances. "BV-2 cells and primary microglia were pre-treated with OT (0.1, 1, and 10 μM) for 2 h followed by LPS [lipopolysaccharides] treatment" we are told, and microglia activation and "pro-inflammatory mediators" subsequently monitored. The results tallied with those 'anti-neuroinflammatory' sentiments previously expressed as authors report on various possible reasons for such an effect: "OT suppressed the expression of TNF-α, IL-1β, COX-2, and iNOS at the mRNA and proteins levels and reduced the elevation of [Ca2+]i in LPS-stimulated microglia cells." If that wasn't enough, researchers also looked at what happened following OT pre-treatment when a certain strain of mouse was 'immune stimulated' again in terms of microglia activation and those pro-inflammatory mediators. We are similarly told that: "pre-treatment with OT showed marked attenuation of microglial activation and pro-inflammatory factor levels." So we have something of a match in the lab and in an animal model.

These are interesting results. Yet again, one has to be a little cautious about the use of mouse models or indeed, cell lines (humans are so much more than a group of cells in a petri dish) and further, independent investigations are indicated. But: "These data suggested that OT would be a potential therapeutic agent for alleviating neuroinflammatory processes in neurodegenerative diseases."

I was inclined to talk about the Yuan paper because of the various 'connections' that have been made between oxytocin and autism (see here). With a growing interest in the oxytocin-autism connection in the peer-reviewed literature, this nonapeptide (9 amino acids long) has attracted quite a few researchers to its cause [2] as a function of the idea that: "Oxytocin increases the salience of social stimuli and promotes parental nurturing and social bonds" [3]. As per my interpretation of the current state of the oxytocin-autism research base, there are some interesting results available but once again, universal 'effects' are nowhere to be seen - Autisms, people. Autisms. The Yuan and other results focusing on the 'anti-neuroinflammatory' activity of oxytocin perhaps add another dimension to the possible hows and whys of efficacy when it comes to a label like autism. That also a growing number of people are coming around to the idea that neuroinflammation might be a facet of 'some' autism (see here) and including some mention of microglia (see here) offers an additional correlate to add into the future research mix. Could those with autism who have more prominent signs of neuroinflammatory issues potentially be 'best responders' to oxytocin for example? I did also wonder whether the idea that inflammation or inflammatory issues might feature in complex behaviours like social cognitive processing (see here) could provide another explanation for some of the reported results observed following use of oxytocin in [some] autism?

Much more research is indicated but again the message is... don't be too dogmatic when it comes to pharmacological targets and actions of medicines indicated for conditions such as autism. You might just end up being surprised...


[1] Yuan L. et al. Oxytocin inhibits lipopolysaccharide-induced inflammation in microglial cells and attenuates microglial activation in lipopolysaccharide-treated mice. Journal of Neuroinflammation. 2016; 13:77.

[2] Okamoto Y. et al. The Potential of Nasal Oxytocin Administration for Remediation of Autism Spectrum Disorders. CNS Neurol Disord Drug Targets. 2016 Apr 13.

[3] Young LJ. & Barrett CE. Neuroscience. Can oxytocin treat autism? Science. 2015 Feb 20;347(6224):825-6.


ResearchBlogging.org Yuan L, Liu S, Bai X, Gao Y, Liu G, Wang X, Liu D, Li T, Hao A, & Wang Z (2016). Oxytocin inhibits lipopolysaccharide-induced inflammation in microglial cells and attenuates microglial activation in lipopolysaccharide-treated mice. Journal of neuroinflammation, 13 (1) PMID: 27075756

Friday, 29 April 2016

Organophosphate exposure and ADHD?

"Children with higher urinary DMP [dimethylphosphate] concentrations may have a twofold to threefold increased risk of being diagnosed with ADHD [attention-deficit hyperactivity disorder]."

So said the results presented in the paper by Yu and colleagues [1] who looking at "97 doctor-diagnosed ADHD cases and 110 non-ADHD controls who were 4-15 years of age" examined urine and blood samples for various factors including "biomarkers of OP [organophosphate] pesticide exposure." They concluded that, adjusting for creatinine, urine levels of DMP but not other dialkylphosphate (DAP) metabolites were higher in the ADHD group compared with the non-ADHD group. Further: "Organophosphate pesticide exposure may have deleterious effects on children's neurodevelopment, particularly the development of ADHD." At the same time, Yu et al also reported nothing very much to see when it came to blood lead levels (BLLs) between the groups.

This is not the first time that examination of urinary metabolites of OPs have turned up something of a potential relationship with behavioural outcomes related to ADHD. The paper by Bouchard and colleagues [2] also reported a possible connection supporting a "hypothesis that organophosphate exposure, at levels common among US children, may contribute to ADHD prevalence." There too urine was the analytical medium and dialkylphosphate concentrations the target compounds. This and other research looking at this issue have led to statements [3] to the effect that: "Children's exposures to pesticides should be limited as much as possible." I don't think many people would disagree with that sentiment.

I've talked about OPs quite a bit on this blog (see here and see here) and how various conditions/labels might be 'associated' with this class of compounds either when used as insecticides or as something rather more ominous. I've tried not to be too alarmist about the possibility of a connection with health because OPs do serve an important purpose (as an insecticide) and have probably saved quite a few lives as a result. But it is getting increasingly difficult to ignore the possibility that this and other classes of pesticides either alone or in combination with other factors, seem to be implicated in various conditions/labels and more needs to be done looking at the hows and whys. This can however be done without scaremongering.

The Yu results whilst interesting are not however without some cautions. DAP metabolites as markers for OP exposure still requires further investigations [4], not least from which specific OP they are derived from. That other factors such as exposure to second-hand tobacco smoke might also link into the presentation of specific metabolites such as DMP [5] is another consideration. Continuing the theme that combinatorial exposures might also exert an effect [6] other research illustrates how difficult it might be to pin one specific type of exposure to specific behavioural outcomes. And then also we have the added layer of complexity that is the genetics of xenobiotic metabolism with specific focus on OPs. Relationships are likely to be pretty complicated as a result.

Having said all that does not however mean that results like the ones from Yu et al can be just brushed under the carpet...

Music to close, and having watched Guardians of the Galaxy for the Nth time last evening, all I can say is the film soundtrack is kinda cool...


[1] Yu CJ. et al. Increased risk of attention-deficit/hyperactivity disorder associated with exposure to organophosphate pesticide in Taiwanese children. Andrology. 2016 Apr 12.

[2] Bouchard MF. et al. Attention-deficit/hyperactivity disorder and urinary metabolites of organophosphate pesticides. Pediatrics. 2010 Jun;125(6):e1270-7.

[3] Roberts JR. et al. Pesticide exposure in children. Pediatrics. 2012 Dec;130(6):e1765-88.

[4] Sudakin DL. & Stone DL. Dialkyl phosphates as biomarkers of organophosphates: the current divide between epidemiology and clinical toxicology. Clin Toxicol (Phila). 2011 Nov;49(9):771-81.

[5] Jain RB. Levels of dialkylphosphate metabolites in urine among general U.S. population. Environ Toxicol Pharmacol. 2016 Feb 26;43:74-82.

[6] Osaka A. et al. Exposure characterization of three major insecticide lines in urine of young children in Japan-neonicotinoids, organophosphates, and pyrethroids. Environ Res. 2016 May;147:89-96.


ResearchBlogging.org Yu CJ, Du JC, Chiou HC, Chung MY, Yang W, Chen YS, Fuh MR, Chien LC, Hwang B, & Chen ML (2016). Increased risk of attention-deficit/hyperactivity disorder associated with exposure to organophosphate pesticide in Taiwanese children. Andrology PMID: 27070915

Thursday, 28 April 2016

What parents of children with autism expect from their child's therapists

"Parents ultimately wanted therapists to produce positive outcomes for their children and were willing to sacrifice other desired qualities, as long as the therapy program was effective."


"The SLPs [Speech-Language Pathologists] expressed strong support for evidence-based practice (EBP) and indicated that they thought parents expected their children would be provided with evidence-based interventions."

Those quotes come from two papers recently published in the same journal; the first by Amelia Edwards and colleagues [1] attempting to identify "the qualities parents seek in therapists who work with their children with ASD [autism spectrum disorder]" and the second from David Trembath and colleagues [2] titled: 'What do speech-language pathologists think parents expect when treating their children with autism spectrum disorder?'

Providing what is a quite fascinating (albeit small scale) insight into the expectations of therapists and parents who use therapists for their children when it comes to autism, these papers put some science to what many people might already have suspected. The Edwards paper also carried an important sentence in the paper title - "More than blowing bubbles" - implying how positive real world outcomes are always going to be the most important elements of any intervention program when it comes to autism or indeed, any other label. The idea that avenues towards those positive outcomes should be 'evidence-based' is perhaps a sentiment noted in the views and opinions of [many of] those professionals delivering intervention but might not necessarily be first and foremost for parents whose natural instinct is to want the best for 'their child'.

The link between the concept of 'evidence-based' and autism is particularly interesting. A few years back I covered a paper by Gary Mesibov & Victoria Shea [3] (see here) carrying the idea that there may be both "benefits and limitations" when it came to the application of evidence-based policy and autism intervention. The sorts of variables that made evidence-based policy difficult when applied to autism ranged from the vast heterogeneity present under the label (or labels) to the idea that the gold-standard 'randomised controlled trial' (RCT) might not be all that suitable when assessing comprehensive intervention programs that for example, contain multiple elements. In subsequent years we've also learned that autism rarely appears in some sort of diagnostic vacuum (see here), something that might also impact on evidence-based policy with regards to intervention (see here). For scientific puritans, the Mesibov-Shea discussions could be construed as heresy. For me, there was some substance in their arguments and some lessons on how autism research in particular, needs to adapt and change away from the notion that 'autism' universally covers everyone with autism in terms of similar aetiology and pathology. Endophenotypes and 'snowflakes' people...

It should of course be recognised that quite a lot of the 'not-knowing' when it comes to the autism spectrum has set the field of autism intervention up for a variety of 'unusual' proposals for interventions, many of which have not been suitably scientifically tested (see here). Some are even downright unsafe but are still pursued for one reason or another, probably pertinent to that opening sentence on 'effectiveness' and no doubt playing into other emotions as and when a child presents with autism [4]. Feelings run high on this topic as I once again refer you to the post by Tom Insel on the 'kingdoms of autism' (see here) with a suggestion that different views be respected but at the same time, safety should be paramount.

Acknowledging that there is no 'one-size-fits-all- approach when it comes to autism intervention and that for some, mention of the words 'therapy' and 'intervention' are not necessarily high on their list of priorities, the Edwards and Trembath papers invite quite a bit more investigation. The possibility of a 'disconnect' between what parents want for their children and what therapists are currently able to deliver for their children represents something that could potentially impact on the delivery of intervention and the importance of the parent-professional relationship in this context. I'm also going to throw the paper by Paynter and colleagues [5] into this mix too...

To close, I feel old. Jossy's Giants is 30 years old (although I'm more inclined to the Red and White)...


[1] Edwards A. et al. "More than blowing bubbles": What parents want from therapists working with children with autism spectrum disorder. Int J Speech Lang Pathol. 2016 Apr 4:1-13.

[2] Trembath D. et al. What do speech-language pathologists think parents expect when treating their children with autism spectrum disorder? Int J Speech Lang Pathol. 2016 Mar 10:1-9.

[3] Mesibov GB. & Shea V. Evidence-based practices and autism. Autism. 2011 Jan;15(1):114-33.

[4] Ooi KL. et al. A meta-synthesis on parenting a child with autism. Neuropsychiatric Disease and Treatment. 2016; 12: 745-762.

[5] Paynter JM. et al. Utilisation of evidence-based practices by ASD early intervention service providers. Autism. 2016. April 18.


ResearchBlogging.org Edwards, A., Brebner, C., Mccormack, P., & Macdougall, C. (2016). “More than blowing bubbles”: What parents want from therapists working with children with autism spectrum disorder International Journal of Speech-Language Pathology, 1-13 DOI: 10.3109/17549507.2015.1112835

ResearchBlogging.org Trembath, D., Hawtree, R., Arciuli, J., & Caithness, T. (2016). What do speech-language pathologists think parents expect when treating their children with autism spectrum disorder? International Journal of Speech-Language Pathology, 1-9 DOI: 10.3109/17549507.2016.1139625

Wednesday, 27 April 2016

The A Word: the science behind...

The A Word
I'm not typically inclined to talk about TV programmes on this blog (well, not usually) but today I'm making an exception based on the conclusion of the BBC drama series 'The A Word' last evening.

For those who might not know, this [fictional] series charts the ups and downs of a family living in the Lake District whose lives are in one way or another touched by autism as a function of a 5-year old boy diagnosed with the condition. The show had a notable addition to the cast with a very straight-talking Christopher Eccleston appearing (yes, one manifestation of Dr Who) but all the actors provided some pretty sterling performances including the child actor Max Vento, who plays Joe 'the 5-year old boy with autism'.

I don't want to go into all the ins-and-outs that the series covered (bearing in mind it was a fictional drama series and not 'real life autism' as per series such as the one by Louis Theroux) but there were a number of themes included that do fall into the peer-reviewed science domain typically covered on this blog. I'd like to briefly cover some of those themes and perhaps provide some short discussion on what they might mean without trying to over-analyse or over-generalise things. I might add that this is my interpretation of the series and readers are also advised to see what others also thought about it.


Every episode of the series opens with Joe happily strolling down a deserted road set against the backdrop of the beautiful Lake District. You'll already note that Joe is a boy and so already we have our first 'stereotype' when it comes to autism. Joe has a 'thing' for music (and some mighty good taste in music I might add) as per his almost constant earphone-wearing, and seems happy on his trails on his own. During most episodes of his wanderings he's met by a friendly couple who know Joe and are happy to return him home. I personally was in two minds about this depiction. As throughout the series, it's obvious that the writers know something about some of the themes in autism (research and practice) and I daresay that this reference is a nod to the idea that autism and wandering has received some much needed research attention. In real-life however, any 5-year old child discovered walking on their own on any road would in all likelihood trigger safeguarding mechanisms should authorities become aware... see episodes 5 & 6.

Parental concerns and diagnosis
The process of going from parental concerns about Joe's behaviour to getting a diagnosis is covered in the series. Again keeping in mind that this is fiction, I think many people (certainly on Twitter) saw the most disconnect in this part of the story given (a) the reluctance of the parents - particularly the mother - to 'accept' something might be 'out of place' with Joe's behaviour and (b) the extremely quick time taken for a diagnosis of autism or autism spectrum disorder (ASD) to be given. Without generalising, diagnosis here in the UK is very rarely a quick thing and many parents can and do feel some relief as and when the 'hurdle' of diagnosis has been eventually overcome. Certainly here in the UK, receipt of a diagnosis normally triggers access to important future plans.

Mainstream schooling vs. home schooling is an important issue covered during the series. We for example, see Alison - Joe's mum - worried about how Joe will cope in his village primary school where his social interaction with other children for example, looks to be minimal at best. The storyline in this area was perhaps one of the most powerful parts of the series as parental worries of 'how will my child cope?' intermixed with the variety of emotions viewers watch the family go through. Interestingly, the series did offer something important to this story as Joe himself voices an opinion about his desire to go to school. Granted things might not always be so easily communicated in real-life but the idea of taking into account the child's wants and wishes when it comes to schooling options is perhaps an important one. Later in the series we also see how Joe does make friends at school. Viewers who've seen the series might have also noticed the opening and closing of school doors during these school segments by Joe reflective of what might be considered a ritual or routine - a core feature of autism.

Speech and language therapy
Again, outside of the dramatic plot line that follows the introduction of a speech and language therapist (SALT) to the series (who it turns out was bullied by the mother of Joe during her school days), it was indeed useful to see how much impact a good SALT can have on a child with autism. As well as emphasising the 'stopping and starting' of developmental progress that accompanies any child irrespective of the presence of autism or not, the series does well to highlight how a range of professionals can make a real difference to the lives of children on the autism spectrum. Personally, I would have liked to have see the archetypal all-rounder that is the occupational therapist (OT) also included in the storyline but there you go...

Joe is seen in pretty much every episode asleep with his night light on followed by a soothing kiss good night from his mother. Again, not one to try and generalise but not every autistic child and their family look forward to such peaceful nights...

Parent and family relationships
Throughout the series, viewers watch how the ups and downs of family life manifest in the relationships between family members. We see for example, how Alison devotes almost her entire existence to Joe in terms of getting a diagnosis and arranging suitable schooling for example, whilst also running a busy household and a business. The stresses and strains tug and pull on important relationships manifesting in various different ways and impacting on various decisions. There are sexual scenes during the series and I know from what some people have written, these were thought of as a distraction to the main storyline. I however think it was important for the writers to include all aspects of parent and family relationships including more intimate moments (bearing in mind the program aired after the watershed). The idea also that autism in the family has the ability to impact on siblings was another important feature of the series. The experiences of Joe's older (half) sister, Rebecca, illustrate how siblings might require additional support when a diagnosis of autism is received in the family but also how they can be very vocal advocates for their brother(s) or sister(s) with autism.

Fever and autism (oh and broccoli...)
Episode 4 of the series introduced some interesting research-based concepts into the storyline. We see Joe develop an illness and 'fever' following a planned sleepover with some school friends resulting in some 'changes' to his behaviour. Joe seems more responsive as words like 'empathy' are banded about (bearing in mind no sweeping generalisation are required on this point). Changes to the presentation of autism in 'some' children following fever have been documented in the peer-reviewed literature [1]. It's not by any means a universal phenomenon and so one has to be a little bit cautious about generalisation. It is however something that requires quite a bit more study (allied to related research areas) about how certain 'types' of autism might be sensitive to such physiological changes. In the same episode we also hear mention of the words 'broccoli' and 'research' pointing to another issue that has surfaced on the peer-reviewed autism research radar [2] (see here for even more discussion). Although you might not know it, the commonality between fever and autism and broccoli and autism (aside from autism) is one Andrew Zimmerman and as if to prove a point [3]...

A hat-tip to gluten and casein
I also had to cast a wry smile as the series did include some reference to a topic close to my research heart: diet and autism, and specifically the involvement of gluten and casein. Granted, the reference to gluten and casein (although lactose is mention over casein) comes from one of the other boys sleeping over at Joe's house who has various 'allergies', but again, I think this highlights how the writers had some good insight into the varied autism research scene.

Final thoughts
There is always the risk that films or programmes 'about autism' can present a stereotype of autism and thereby fail to show just how wide and heterogeneous the autism spectrum is. I don't doubt that similar sentiments will be expressed about The A Word paralleling previous artistic presentations such as Rainman. That also important issues such as anxiety and sensory-perceptual issues were only paid lip service during the series is worthwhile mentioning as were the various often life-changing comorbidities that can accompany a diagnosis such as epilepsy or seizure disorders or learning disability. No programme will ever be perfect.

But I do think that quite a few of the important elements that surround childhood autism were included in the series albeit with the hint of drama required for such fictional storytelling. The struggles and strains were balanced with lighter moments and the idea that 'Joe is still Joe' even after receipt of an autism diagnosis came across on multiple occasions particularly from his on-screen sister. I think the writer Peter Bowker probably said it best about The A Word: 'You won't understand autism after watching The A Word – but it will make you want to learn more'. That sounds about as good a sentiment as any when it comes to the series and further expanding the public view about the very heterogeneous autism spectrum...


[1] Curran LK. et al. Behaviors associated with fever in children with autism spectrum disorders. Pediatrics. 2007 Dec;120(6):e1386-92.

[2] Singh K. et al. Sulforaphane treatment of autism spectrum disorder (ASD). Proc Natl Acad Sci U S A. 2014 Oct 28;111(43):15550-5.

[3] Singh K. & Zimmerman AW. Sulforaphane treatment of young men with Autism Spectrum Disorder. CNS Neurol Disord Drug Targets. 2016 Apr 13.


ResearchBlogging.org Singh K, & Zimmerman AW (2016). Sulforaphane treatment of young men with Autism Spectrum Disorder. CNS & neurological disorders drug targets PMID: 27071786

Tuesday, 26 April 2016

Bacterial origin and transferability of depression?

The paper by Zheng and colleagues [1] caught my eye recently and the interesting ideas that "dysbiosis of the gut microbiome may have a causal role in the development of depressive-like behaviors" and "transplantation of GF [germ-free] mice with ‘depression microbiota’ derived from MDD [major depressive disorder] patients resulted in depression-like behaviors compared with colonization with ‘healthy microbiota’ derived from healthy control individuals."

Bearing in mind the focus on mice not people in these results, it's not necessarily new news that the trillions of bacteria that call our gut home might be doing so much more than just helping to digest food and producing the odd vitamin or two. I've covered the concept a few times on this blog (see here for example) and how the so-called gut-microbiota-brain axis is gaining some scientific ground [2].

Whilst there are still quite a few more investigations to do in this area, this is not the first time that elements of the gut microbiome have been implicated in a complex condition like depression (see here) including how certain routinely available medicines might also show some involvement (see here). Zheng et al elaborate on some of the types of bacteria that might play a role in their results - "the gut microbiotic compositions of MDD patients and healthy controls were significantly different with MDD patients characterized by significant changes in the relative abundance of Firmicutes, Actinobacteria and Bacteroidetes" - but I think we have to be a little cautious about casting 'blame' just yet. The gut houses quite a lot more than just bacteria y'know and it's not outside the realms of possibility that elements of the gut virome for example, might also be able to exert some effect.

The idea of potential 'transferability' or transmission of depression [3] as a function of gut bacteria or other elements also gathers ground based on the Zheng findings. Accepting that familial transmission of depression is not an entirely new concept, the idea that genetic and other non-genetic factors might be complimented by sharing a similar gut microbial profile is a tantalising idea. Not least also because there is the prospect of 'changing' the gut microbiome [4] and potentially impacting on the the presentation of at least some 'types' of depression [5] alongside various other conditions. I say this also with the understanding that depression is a complicated condition and that various other 'biological' factors might also play an important role in presentation (see here and see here)...

But this is interesting work.

Music - and yet again, The Gimme Gimmes with I will survive...


[1] Zheng P. et al. Gut microbiome remodeling induces depressive-like behaviors through a pathway mediated by the host’s metabolism. Molecular Psychiatry. 2016. April 12.

[2] Rogers GB. et al. From gut dysbiosis to altered brain function and mental illness: mechanisms and pathways. Molecular Psychiatry. 2016. April 19.

[3] Canli T. Reconceptualizing major depressive disorder as an infectious disease. Biology of Mood & Anxiety Disorders. 2014;4:10.

[4] Evrensel A, Ceylan ME. The Gut-Brain Axis: The Missing Link in Depression. Clinical Psychopharmacology and Neuroscience. 2015;13(3):239-244.

[5] Dinan TG. et al. Psychobiotics: a novel class of psychotropic. Biol Psychiatry. 2013 Nov 15;74(10):720-6.


ResearchBlogging.org Zheng, P., Zeng, B., Zhou, C., Liu, M., Fang, Z., Xu, X., Zeng, L., Chen, J., Fan, S., Du, X., Zhang, X., Yang, D., Yang, Y., Meng, H., Li, W., Melgiri, N., Licinio, J., Wei, H., & Xie, P. (2016). Gut microbiome remodeling induces depressive-like behaviors through a pathway mediated by the host’s metabolism Molecular Psychiatry DOI: 10.1038/mp.2016.44