Autism and optimal outcome: the continuing saga

I think it's fair to say that the paper published by Deborah Fein and colleagues* (discussed in this post and this post) was a bit of a game-changer when it comes to how we view the autism spectrum conditions.

Describing a group of children originally diagnosed as being on the autism spectrum and then "losing all symptoms of ASD in addition to the diagnosis, and functioning within the nonautistic range of social interaction and communication", there was plenty of comment on this optimal outcome study at publication. Some commentators at the time seemed to go out of their way to try and shred this bit of science and reinforce the "autism is always lifelong" line. Even now an expression of doubt remains of any notion of 'autism recovery'. Note my use of the singular - autism - when it comes to describing the condition in those previous sentences.

Is it draughty in here? @ Wikipedia 

In some respects, I can see why the Fein paper was treated the way it was in some quarters. With all the due respects to our thriving media, to say that autism (or at least the diagnosis and diagnostic elements making up the diagnosis) might not in some cases be as set in stone as we all might have first thought, carries a significant risk that autism - all autism - might be just viewed as some passing developmental phase. It's not by the way.

It all boils down to generalisation and, as we've witnessed in recent weeks when it comes to the depiction of mental health (see this headline), how generalisation can often be so very damaging.

To reiterate from the original Fein paper and quote from the accompanying journal editorial** "They conclude, rather modestly, that these results ‘‘substantiate the possibility of optimal outcome,’’ demonstrating that some children with a clear early history and accurate diagnosis of ASD do indeed move into the entirely normal range of social and communication development later in childhood." I've underlined the word 'some' to stress that they weren't generalising to everyone with autism. Some.

After that very long-winded introduction, I'm talking today about some of the follow-up work that has been published on these optimal outcomers in relation to their wider presentation including academic ability. The paper by Troyb and colleagues*** adds to the interest in this group suggesting that when it came to "measures of decoding, reading comprehension, mathematical problem solving, and written expression" the optimal outcomers were more similar to 'typically developing' peers than those with a diagnosis of autism which puts them under the 'high-functioning' description of presentation.

The paper by Eigsti & Fein**** likewise reported that when it came to pitch discrimination (see here for more details) "Unlike an ASD group, which shows heightened pitch discrimination, the Optimal Outcome group's abilities do not differ from those of typically developing controls". This based on the suggestion that pitch sensitivity might be enhanced among (some of) those with high-functioning autism*****.

If one were to base the judgement of optimal outcome on these studies alone, you may very well get the impression that autism was just a passing phase for these children, and seemingly left little or no mark on their subsequent development and performance skills.

But things are never so straight forward. And to think that autism - defined as a disorder of early development - with its heightened risk of a range of other comorbidities, even if now removed from the developmental equation would not have some bearing on future development is perhaps a little too narrow a view to take.

Take for example another paper by Troyb and colleagues***** looking at executive functioning (EF) in those optimal outcomers. Another rather long quote I'm afraid: "Despite their average performance, however, the OO [optimal outcome] and TD [typically developing] groups differed on measures of impulsivity, set-shifting, problem-solving, working memory, and planning, suggesting that the OO group does not have the above-average EF scores of the TD group despite their high-average IQs". In other words, allowing for the still quite small numbers of participants in these studies and their cognitive functions, issues seem to remain, at least in childhood.

If I were to get even more 'psychological' with this topic, I might also show you the paper from Naigles and colleagues****** whose title - 'Residual difficulties with categorical induction in children with a history of autism' - sums up my argument that the more visible aspects of autism might indeed have vanished into the diagnostic ether, but that does not mean that typical developmental service has just resumed. Likewise based on the data from the paper by Kelley and colleagues******* on residual language issues (in areas of pragmatic and semantic language comprehension) and that from Tyson and colleagues******** on language and verbal memory in optimal outcomers.

I'm not trying to reverse my original assertion that the Fein paper was a game-changer based on these evidence. I still see the work of Fein and colleagues as being potentially, some of the most important work ever done on autism; big words I know. I still also see those optimal outcomers as carrying some of the most important data about autism. And harking back to my highlighting the singular term 'autism', how the optimal outcomers are some of the strongest evidence yet for the concept of 'the autisms' which I seemingly keep going on about in every post.

But alongside, there is the realisation that autism is potentially much more than just the triad (or dyad) of symptoms that we've diagnostically boiled it down to. Optimal outcome? The mum in this newspaper article talks about "shadows left behind from his autism". I was also, for example, going to do a separate post based on the paper by Leonard and colleagues********* in relation to motor development and autism. Something along the lines of how even Kanner in his original writings about autism, hinted that autism might be so much more than just a triad of symptoms. But since I'm here already with this rather long blog post, let's just say autism, sorry the autisms, might be so much more than what we currently call it.

I'm going to close this post with a few things I'd still like to see from the optimal outcome data. The obvious question is: who are the optimal outcomers and indeed, what makes them different from other children on the autism spectrum? I'm not necessarily just talking about overt clinical presentation or scores on some psychometric tool but rather biologically, genetically, epi-genetically, microbiomic-ally(?) who are they and what makes them optimal outcomers?

I'd like to know more about the ways and means they went towards their path of optimal outcome. Are we talking about some spontaneous arrest of autistic traits similar to what might be expected in an infection-based model of presentation or something rather more gradual? Are we talking about the effects of early behavioural intervention, pharmacotherapeutic intervention and/or all those myriad of so-called complementary 'biomedical' interventions?

Perhaps more in the long-term, I'd like to know how does optimal outcome translate into the 'real world' when it comes to transitioning from child to adult. Does it mean a better shot at good educational achievement, a decent job, a living wage, independent living, the option of a family, a healthy life relatively free of medication or ill-health? And what happens to the various comorbidities?

Questions still remain about optimal outcome in relation to autism. But I'm not taking anything away from the pretty comprehensive picture that is already being drawn about optimal outcome occurring in cases of autism.

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* Fein D. et al. Optimal outcome in individuals with a history of autism. J Child Psychol Psychiatry. 2013 Feb;54(2):195-205.

** Ozonoff S. Editorial: Recovery from autism spectrum disorder (ASD) and the science of hope. J Child Psychol Psychiatry. 2013 Feb;54(2):113-114.

*** Troyb E. et al. Academic abilities in children and adolescents with a history of autism spectrum disorders who have achieved optimal outcomes. Autism. 2013 Oct 4.

**** Eigsti IM. & Fein DA. More Is Less: Pitch Discrimination and Language Delays in Children with Optimal Outcomes from Autism. Autism Res. 2013 Aug 8. doi: 10.1002/aur.1324.

***** Troyb E. et al. Executive functioning in individuals with a history of ASDs who have achieved optimal outcomes. Child Neuropsychol. 2013 Jun 3.

****** Naigles LR. et al. Residual difficulties with categorical induction in children with a history of autism. J Autism Dev Disord. 2013 Sep;43(9):2048-61.

******* Kelley E. et al. Residual language deficits in optimal outcome children with a history of autism. J Autism Dev Disord. 2006 Aug;36(6):807-28.

******** Tyson K. et al. Language and Verbal Memory in Individuals with a History of Autism Spectrum Disorders Who Have Achieved Optimal Outcomes. J Autism Dev Disord. 2013 Aug 28.

********* Leonard HC. et al. Motor development in children at risk of autism: A follow-up study of infant siblings. Autism. 2013 Oct 7.

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Troyb E, Rosenthal M, Eigsti IM, Kelley E, Tyson K, Orinstein A, Barton M, & Fein D (2013). Executive functioning in individuals with a history of ASDs who have achieved optimal outcomes. Child neuropsychology : a journal on normal and abnormal development in childhood and adolescence PMID: 23731181

Anti-phospholipid antibodies and autism

Regular readers are probably quite tired of hearing me go on about autoimmunity and autism. It's a research topic which seems to come up pretty regularly these days for all manner of reasons and in all manner of places (see here). Indeed, now even being linked to the new kid on the block that is MAR autism (see here).

As I've mentioned before, I don't think we can quite say that all autism (all of the autisms sorry) 'are autoimmunity' because immune function is a pretty varied thing when it comes to autism. But there is a growing evidence base to suggest that we should be looking into this issue with much greater assiduity for at least some on the autism spectrum and whether markers of autoimmunity might be related to presented symptoms or at the very least, affecting aspects of quality of life.

A further addition to the area of autoimmunity and autism is that of the paper by Careaga and colleagues* who quite recently reported on the presence of increased anti-phospholipid antibodies** in a cohort of children diagnosed with an autism spectrum condition as part of the CHARGE study.

As per the very informative description by Misita and Moll**, anti-phospholipid antibodies (APLAs) reflect activity by the immune system against a class of substances called phospholipids which are a vitally important part of cell membranes. Some of the main issues associated with the presence of APLAs relates to blood clots and pregnancy loss as per the description of anti-phospholipid syndrome (APS) or Hughes syndrome.

Careaga et al (carrying quite an impressive authorship list it has to be said) looked at the presentation of various APLAs across three groups: children diagnosed with an autism spectrum disorder (ASD) (n=54), children diagnosed with a developmental delay (but not autism) (n=22) and typically developing controls (n=33). They looked at antibodies to anticardiolipin, antiphosphoserine, and anti-β2-glycoprotein 1 across each of the groups and further whether levels of these APLAs correlated with specific behaviours or impairments in behaviours.

The results: well, comparing the autism group vs. the typically developing group, levels of each of the APLAs were higher in autism (and significantly so). Aside from the cardiolipin antibodies, the other APLAs were also significantly higher in the autism group compared with the developmental delay group too. Ergo, another study finding "increased presence of autoantibodies in children with ASD". When examined alongside various behavioural functions derived from schedules such as the VABS, there were also some significant correlations noted (see here) but "no significant differences found when analyzing within the individual groups based on diagnosis".

It is worth pointing out that although these APLAs were detected in higher concentrations in the autism group (a) not every child with autism had significant elevations in these antibodies and (b) "the levels are below what is considered clinically significant levels for APS". Importantly too that even if levels of APLAs were getting into the APS diagnostic range, the study results in themselves probably wouldn't be able to diagnose APS given the need for two separate testing occasions (see here) and other criteria.

Looking at some of the published research literature around APLAs, I stumbled across a few potentially important connections. Abisror and colleagues*** reported on some preliminary observations of offspring autism in children born to mums with APS. This following similar preliminary reporting (see here) bearing in mind that a chance association cannot at this point, be ruled out. That being said, all that recent chatter about MAR autism (see here) and maternal immune activation and behavioural issues (see here) must also be thrown into the research mix too. When looking also at a condition like attention-deficit hyperactivity disorder (ADHD) however, which has more than once been linked to cases of autism (see here), other investigations have not found any relationship between APLAs and behavioural presentation****. So one needs to remain a little guarded about how the Careaga results will eventually pan out.

I do think there is more to do in the area of APLAs and autism. The link between APLAs during pregnancy and adverse birth outcomes such as preterm birth (see here) and low birth weight (see here) must be seen as important confounding variables given the complicated links made in these areas with offspring autism risk (see here). The findings that at least some people with APLAs will eventually go on to be diagnosed with autoimmune conditions such as systemic lupus erythematosus (SLE) or related mixed connective tissue disorder is also worthy of greater investigation; indeed whether conditions like SLE are likely to be more prevalent among mums and dads of children with autism (as per the recent suggestion) particularly those with elevated APLAs (oh, we're back to MAR autism again).

I'm gonna stop there for now. On purpose I've not headed too far into the mechanism of how elevated levels of APLAs detected in cases of autism might work, simply because I'd rather see some independent replication of these results first before heading down the path of speculation. But still I remain very interested in the Careaga findings....

Some music to close, and in memory of Lou Reed, a Velvet Underground special: I'm Waiting for the Man.

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* Careaga M. et al. Increased Anti-Phospholipid Antibodies in Autism Spectrum Disorders. Mediators of Inflammation. 2013: 935608.

** Misita CP. & Moll S. Antiphospholipid Antibodies. Circulation. 2005; 112: e39-e44.

*** Abisror N. et al. Autism spectrum disorders in babies born to mothers with antiphospholipid syndrome. Semin Arthritis Rheum. 2013 Jul 30. pii: S0049-0172(13)00149-2. doi: 10.1016/j.semarthrit.2013.07.001.

**** Bujanover S. et al. Lack of association between anti-phospholipid antibodies (APLA) and Attention Deficit/Hyperactivity Disorder (ADHD) in children. Clin Dev Immunol. 2003 Jun-Dec;10(2-4):105-9.

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Milo Careaga,Robin L. Hansen,Irva Hertz-Piccotto,Judy Van de Water,Paul Ashwood (2013). Increased Anti-Phospholipid Antibodies in Autism Spectrum Disorders Mediators of Inflammation DOI: 10.1155/2013/935608

MAR autism and maternal autoimmune conditions: speculations

The term MAR autism - maternal autoantibody-related autism - whilst still a relatively new addition to the autism research vocabulary, has nevertheless already courted some controversy. This follows a decision to try and commercialise the growing research base in this area (see here) which raised a few eyebrows in various quarters.

Speculating on a dead cat bounce?  @ Wikipedia 

As I indicated on my previous post about said commercialisation, there are a few questions which perhaps need answering before this work starts down the path of becoming any sort of reliable 'autism test'. Some of these questions being particularly important if one is to learn the lessons from another proposed autism test which came across a few problems in replication recently (see here).

Away from such discussions, the notion that a proportion of mums of children with autism spectrum disorder (ASD) "have antibodies in their bloodstream that react with proteins in the brain of their babies" is potentially a very important finding. The evidence for such a process is actually becoming quite consistent (see here) following on from other investigations pointing at some role for the maternal immune system when it comes to at least some cases of autism (see here).

The paper by Lior Brimberg and colleagues* adds to the autism - maternal anti-brain antibodies story with their findings suggesting that "Mothers of an ASD child were four times more likely to harbor anti-brain antibodies than unselected women of child-bearing age (10.5 vs 2.6%)" based on the analysis of collected data from one or two quite large autism study initiatives (Simons Simplex Collection and Autism Genetic Exchange Resource). This in itself would be a worthy confirmatory research finding bearing in mind the number of plasma samples that were analysed as part of the study.

But of perhaps equal importance was the observation that "The analysis of ASD mothers with brain-reactive antibodies also revealed an increased prevalence of autoimmune diseases, especially rheumatoid arthritis and systemic lupus erythematosus". This point was covered by other commentary of this study (see here) including findings related to the detection of anti-nuclear antibodies (ANAs) (53% vs 13.4%) in autism mums with and without the anti-brain antibodies respectively.

Those who regularly visit this blog might know about my interest in all things autoimmunity with autism in mind (see here). The suggestion that the presence of brain reactive antibodies seemed to correlate with an increased frequency of maternal autoimmune conditions or their biological links represents yet another possible connection between autoimmunity and autism, at least some cases of autism.

With my speculating hat firmly in place, I wondered about a couple of things as a result of these findings. I wondered for example, whether the anti-nuclear antibodies were also present in offspring of those mums who tested positive for both brain reactive antibodies and ANAs. I note that ANAs have been previously reported in cases of autism as per the findings of Mostafa and Kitchener** who observed: "Children with autism had a significantly higher percent seropositivity of anti-nuclear antibodies (20%) than healthy children (2.5%; P < 0.01)". That and their suggestion: "Anti-nuclear antibody seropositivity was significantly higher in autistic children with a family history of autoimmunity than those without such history (36.8% and 5%, respectively; P < 0.001)" makes for some interesting connections.

Harking back to the ScienceDaily piece on the Brimberg study (see here) I was also intrigued by the suggestion that a 'leaky' blood-brain barrier may "allow the "anti-brain" antibodies to pass through to the babies' brains, possibly causing autism".

Now just before I get too carried away with this, there has been a bit of debate down the years about just when the blood-brain barrier (BBB) actually becomes effective in the foetus and infant. The more recent discussions suggest that there is a "well developed barrier mechanisms in the developing brain". This contrasts with other reports such as the study by Volodin and colleagues*** suggesting that the final establishment of the foetal BBB, under typical circumstances, is carried out in the latter stages of gestation. I'll leave readers to draw their own conclusions on which is the correct position.

This barrier however, partly physical and partly biochemical, is susceptible to 'damage' under certain circumstances as reported in an older post on this topic (see here). That alongside some of the gatekeeper molecules such as P-glycoprotein which help transport things through the BBB (see here) being potentially susceptible to 'alteration' as a function of various factors, means that BBB permeability is influenced by quite a few fluidic variables.

If one assumes that, as in the example of a potential link between maternal SSRI use during the first trimester of pregnancy and offspring autism risk (see here**** and here for my post), early stage pre-completed formation of the infant BBB is a 'risk' time for the developing foetus and its susceptibility to things like anti-brain antibodies and/or ANAs, one might get a sense of how and when such a process "possibly causing autism" may come about. I hasten to add that I'm still speculating at this point.

With leaky membranes in mind and the still-awaited peer-review publication of some conference proceedings from the lab of Paul Patterson (see here) on the suggestion of leaky gut present in their maternal immune activation offspring mouse model, I'm also wondering whether there may be another connection to be had here too. Various autoimmune conditions have been talked about with gut hyperpermeability in mind; ranging from gastrointestinal conditions such as coeliac disease (see here*****) to type 1 diabetes (see here******). It's not necessarily an all-or-nothing relationship but leaky gut and autoimmunity (with other factors such as gut bacteria also in the mix) is certainly on the scientific map.

In a similar vein to the ANA story, I'm wondering whether there may be merit in looking at whether there is any tie-up between gut permeability issues and (a) those mums where brain reactive antibodies have been reported, and (b) children of those mums with reported brain reactive antibodies and/or ANAs. Indeed, if (and it is still a very speculative 'if') there is some association to be found, whether as per the collected de Magistris work, one might envisage a role for dietary intervention to act on the permeability issue and any knock-on effects that might have with regards to autoimmune processes and presented symptoms? The other potential factor in this relationship being the link between gluten (or rather gliadin) and another barrier gatekeeper molecule called zonulin (see here******* open-access and here for a previous post) which is also deserving of some study with autism in mind.

I know that there's been speculation-a-go-go on this entry and I'm very much exceeding the remit of the paper by Brimberg and colleagues. I apologise. It's an easy thing to do when it comes to a blog, open-access, with no peer-review and full editorial control to the owner (i.e. me). I'd like to think however, that this area of immune activation and autoimmunity potentially opens up a whole range of further research questions ripe for scientific inquiry outside of just the formulation of a test for autism risk or not. In these days of autisms over autism and "autism as fractionable into different, largely independent sets of clinical features" new frontiers for autism research abound, and that's just as true for MAR autism and autoimmunity.

And for those interested in the attached picture included with this post and what a 'dead cat bounce' is, it's not as harrowing as you might think... (see here). Meow.

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* Brimberg L. et al. Brain-reactive IgG correlates with autoimmunity in mothers of a child with an autism spectrum disorder. Molecular Psychiatry. 2013; 18: 1171-1177.

** Mostafa GA. & Kitchener N. Serum anti-nuclear antibodies as a marker of autoimmunity in Egyptian autistic children. Pediatr Neurol. 2009 Feb;40(2):107-12.

*** Volodin NN. et al. Status of the blood-brain barrier in newborn infants of various gestational ages in the normal state and in pathology. Pediatriia. 1989;(3):10-4.

**** Croen LA. et al. Antidepressant use during pregnancy and childhood autism spectrum disorders. Arch Gen Psychiatry. 2011 Nov;68(11):1104-12.

***** Drago S. et al. Gliadin, zonulin and gut permeability: Effects on celiac and non-celiac intestinal mucosa and intestinal cell lines. Scand J Gastroenterol. 2006 Apr;41(4):408-19.

****** Bosi E. et al. Increased intestinal permeability precedes clinical onset of type 1 diabetes. Diabetologia. 2006 Dec;49(12):2824-7.

******* Fasano A. Zonulin and its regulation of intestinal barrier function: the biological door to inflammation, autoimmunity, and cancer. Physiol Rev. 2011 Jan;91(1):151-75.

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Brimberg L, Sadiq A, Gregersen PK, & Diamond B (2013). Brain-reactive IgG correlates with autoimmunity in mothers of a child with an autism spectrum disorder. Molecular psychiatry PMID: 23958959

Put it in the (autism science) replicator

Replication is one of the most important processes in those things we call science and the scientific method. Outside of conjuring up images of a certain 'Make it so' Captain with his "Earl Grey, Hot", scientific replication provides the community at large with some degree of reassurance that a research finding was not just a fluke or an artefact of a particular sample of people or a method used or an interpretation of results. As per the recent BBC article on vitamin use: "Looking at any one individual study won't be very revealing to answer the question of whether vitamin supplementation is good for you."

Uncanny likeness @ Wikipedia 

With the issue of replication in mind, I was interested to read the Letter to the Editor from Robinson and colleagues* (open-access) who set about trying to replicate the findings from Skafidas and colleagues** (open-access) and their notion that science might be making some in-roads into the detection of "genetic biomarkers [that] can correctly classify ASD from non-ASD individuals". I posted about the Skafidas study at the time also (see here) and their analysis of single-nucleotide polymorphisms (SNPs) in relation to autism spectrum disorder (ASD).

The Robinson letter reports an attempt to replicate the Skafidas findings based on an independent analysis of data from the Psychiatric Genomics Consortium (PGC) "which includes ~5400 cases, more than three times the number used in the original [Skafidas] report". I'm not on this occasions going to get the fine-toothed comb out on both papers because they're open-access so free for anyone to read.

The conclusions from Robinson et al are pretty clear: "We find no evidence that the implicated SNPs, the classifier or the pathways named in Skafidas et al.1 are associated with ASDs. We therefore conclude that the classifier, as presented, cannot be used in a general way to predict ASDs, and consequently is unlikely to have any translational value."

Obviously such findings are both a blow to autism research and also the original authors who first proposed the classifier model, who I don't doubt probably invested quite a lot of time, effort and funds into getting their experiments done and results published (and published in a Nature journal). The ego also takes a bit of a knock under such circumstances, believe me (see here and here and here).

The Robinson data however re-emphasize the importance of replication in autism research. Perhaps just as important, they also reaffirm that autism is a tremendously difficult set of conditions to study. As is often the case when it comes to a heterogeneous condition like autism (or should that be the autisms) often carrying more than its fair share of comorbidity (see here) including risk of certain somatic conditions (see here), consistent findings are often few and far between. Indeed, that the use of the label autism, whilst providing a way of classifying certain types of behaviour and their impact on a person's life, is not necessarily the best thing for research purposes, as was vocalised through the grudge match that was DSM V vs. RDoC (see here).

The added realisation that outside of no one single SNP being linked to all autism (see here) there may be a significant degree of overlap when it comes to the genetics of the autisms with other developmental and psychiatrically defined conditions (see here) implies that it's going to be some time yet before any genetic biomarkers or test is going to be able to accurately classify autism, sorry the autisms with any great accuracy. Then there is the question of what such a test would accomplish. I've not even mentioned the fact that autism, whilst having a genetic component, is probably not without it's [variable] partner in crime, environment (however you want to define this) when it comes to aetiology. And don't even mention that other area of increasing interest, epigenomics (see here)... which in recent days has seen some interesting papers published (see here and see here).

I suppose in the spirit of all this talk on replication, the last question should be: who next is going to try and replicate the Robinson results? Indeed, does science any longer need the 'Letter to the Editor' in light of the rolling out of PubMed Commons?

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* Robinson EB. et al. Response to ‘Predicting the diagnosis of autism spectrum disorder using gene pathway analysis’. Molecular Pyschiatry. 2013: Oct 22. doi: 10.1038/mp.2013.125

** Skafidas E. et al. Predicting the diagnosis of autism spectrum disorder using gene pathway analysis. Molecular Psychiatry. 2013; Sep 11. doi: 10.1038/mp.2012.126

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E B Robinson, D Howrigan, J Yang, S Ripke, V Anttila, L E Duncan, L Jostins, J C Barrett, S E Medland, D G MacArthur, G Breen, M C O'Donovan, N R Wray, B Devlin, M J Daly, P M Visscher, P F Sullivan, B M Neale (2013). Response to ‘Predicting the diagnosis of autism spectrum disorder using gene pathway analysis’ Molecular Psychiatry DOI: 10.1038/mp.2013.125

Suicidal behaviour in autism

The paper by Hannon and Taylor* was the starting point for today's post looking at suicidal behaviour among people diagnosed as being on the autism spectrum. Granted such a topic is hardly great dinner table conversation, but as per their suggestion on the prevalence of "suicidal behaviour among young people with ASD ranges from 7-42%", this is nevertheless a potentially important subject to cover. Even more so if one considers the age range included in the Hannon/Taylor review (< 25 years) allied to the numbers of children on the autism spectrum who are turning into young adults and the various challenges they face.

As I've indicated on previous posts, suicide either completed or ideation, is a very complicated process. It is neither uniform in the reasons which bring a person to such a state nor is it necessarily biomarker-able (despite some good research attempts - see here). I should also add that whilst there is some quite lively research interest looking into the role of certain agents or organisms being somehow correlated with suicide risk - think T.gondii and 'cat ladies' - issues remain in teasing out such variables as being the most important 'causative' ones in that relationship.

The Hannon/Taylor paper does provide one or two suggestions about how suicide might be a risk issue for some on the autism spectrum. To quote again: "Depression and abuse are risk factors for suicidal behaviour in this population". Indeed this issue of depression being a potentially important aspect was something that has been picked up by other authors, in particular the paper by everyone's favourite 'historical character has autism' author, Prof. Michael Fitzgerald in his paper on suicide and Asperger syndrome**. Depression as autism research sort of already knows, is no stranger to autism as comorbidity (see here) although there is still discussion about the hows and whys of depression onset in cases of autism. I'd hazard a guess that it's probably going to be a complicated, and yet again, non-uniform relationship.

The suggestion that abuse might be a risk factor for suicide ideation/completion in relation to cases of autism is also a very relevant topic these days. More than one campaigner (see here and here) here in the UK is bringing the issue of bullying in relation to autism for example, into the public consciousness. If one assumes that bullying (whether person-to-person or online) is a form of abuse, you can see how it might affect anyone; but perhaps more so someone who might already be quite anxious, sometimes quite socially-isolated and perhaps prone to a heightened degree of mental 'regurgitation' (i.e. going over the same thoughts again and again and again). The term also includes other forms of more readily recognised abuse such as physical or sexual abuse, which have also, unfortunately, been reported to be part and parcel of the history of some on the spectrum***.

Outside of depression and abuse being linked to suicide in autism, I was also drawn to the paper by Raja and colleagues**** (open-access here) and their suggestion that "Most patients with suicidal behavior or ideation presented psychotic symptoms". Again, this is a most interesting area of research when it comes to autism, albeit still quite an emerging area. I've talked before about the paper by Davidson and colleagues (see here) for example, reporting on the prevalence of Asperger syndrome in cases of first episode psychosis (3.6%). This combined with the growing interest in the overlap between the autism spectrum and the schizophrenia spectrum (see here) adds a further degree of complexity to the question of how suicide might be linked to cases of autism. And then there is the gender issue to consider when it comes to suicide...

Outside of the issue of awareness that as Kato and colleagues***** put it: "ASDs should always be a consideration when dealing with suicide attempts in adults at the emergency room", the combined research in this area offers some potentially important ways that professionals and families might be able to intervene if suicide ideation starts to become an issue for some on the spectrum. I've listed a few points below but please, don't see this as some sort of definitive list by any means. Also keep in mind my caveat on this blog about not giving medical or clinical advice being particularly important when it comes to something like suicide.

(i). Social circles and support. In the same way that having a social network might be one of the tools in the arsenal to relive parenting stress (see here) so I'm minded to point out that it might also serve some positive function when it comes to affecting risk of suicide in cases of autism. Extrapolating from research on the periphery of autism such as the paper by Szanto and colleagues****** some degree of social support or having a social network might be seen as a protective factor against suicide risk. How this translates practically is another issue, particularly in these austere times, but one could argue that social support could mean face-to-face contact or even something like an online group outside of just family contact. The issue of religious belief and affiliations impacting on suicide risk is perhaps a related issue and not necessarily something that should be discounted despite the sweeping generalisations made about autism and a belief in God.

(ii). Medication. I'm by no means qualified to talk about medication and who should be prescribed what, so please don't take this as any kind of advice. Drawing on research again outside or on the periphery of autism however, there does appear to be a case for certain medicines being used where suicide ideation comes about. Reutfors and colleagues******* for example, looking at suicide risk in schizophrenia and the use of preventative medication suggested that: "Lower suicide risk was found in patients who had been prescribed a second generation antipsychotic (clozapine, olanzapine, risperidone, or ziprasidone)". As I've mentioned, the Fitzgerald paper on suicide and Asperger syndrome also talked about depression as being potentially linked, so perhaps there may be merit in looking at medication to combat this aspect as also potentially affecting suicide risk. That being said, one has to mindful of the results by Björkenstam and colleagues******** (open-access) "linking initiation of SSRI to increased short-term suicide risk". The take-home message is to speak to someone in medical authority about this option.

(iii) The talking therapies. I'm not going to get too hung up on the use of things like cognitive behavioural therapy (CBT) as another option when it comes to suicide ideation and autism but it is something that could perhaps be considered for some. Based on the published literature on CBT for suicide ideation, the picture is still a little bit tentative for (a) effects and (b) why it may have some positive effect for some people. To quote from the paper by Handley and colleagues********* "CBT appears to be associated with reductions in hopelessness.... Less consistent results were observed for suicidal ideation". In short, it's again complicated.

There are various other strategies which have been suggested more generally with regards to suicide prevention (see here) but as of yet, there's little in the way of published evidence as to whether suicide ideation in cases of autism is more or less likely to be affected by such options.

From a cold, hard research point of view, I do think there is quite a bit more to do on this topic and not necessarily just with purely social or psychological factors in mind. I'm for example intrigued by the idea that gut and brain might be involved in depression, one of the risk factors for suicide ideation and autism (see here).  I'm also taken back to the collected work on suicide and vitamin D and suicide and lithium (see here) as other potentially important factors, especially given the emerging results on some of these areas with autism in mind (see here). Of course, harking back to my opening statement, the path towards suicide and suicide ideation is a complex one and likely to be a very individual one too.

To close, just in case you need someone to talk to, the Samaritans here in the UK (see here) and in the US (see here) are only a phone call or email away...

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* Hannon G. & Taylor EP. Suicidal behaviour in adolescents and young adults with ASD: Findings from a systematic review. Clinical Psychology Review. 2013: October 15 [in press].

** Fitzgerald M. Suicide and Asperger's syndrome. Crisis: The Journal of Crisis Intervention and Suicide Prevention. 2007; 28: 1-3.

*** Mandell DS. et al. The prevalence and correlates of abuse among children with autism served in comprehensive community-based mental health settings. Child Abuse Negl. 2005 Dec;29(12):1359-72.

**** Raja M. et al. Autism Spectrum Disorders and Suicidality. Clin Pract Epidemiol Ment Health. 2011 Mar 30;7:97-105.

***** Kato K. et al. Clinical features of suicide attempts in adults with autism spectrum disorders. Gen Hosp Psychiatry. 2013 Jan-Feb;35(1):50-3.

****** Szanto K. et al. Social emotion recognition, social functioning, and attempted suicide in late-life depression. Am J Geriatr Psychiatry. 2012 Mar;20(3):257-65.

******* Reutfors J. et al. Medication and suicide risk in schizophrenia: A nested case-control study. Schizophr Res. 2013 Oct 1. pii: S0920-9964(13)00500-8.

******** Björkenstam C. et al. An Association between Initiation of Selective Serotonin Reuptake Inhibitors and Suicide - A Nationwide Register-Based Case-Crossover Study. PLoS One. 2013 Sep 9;8(9):e73973.

********* Handley TE. et al. Incidental treatment effects of CBT on suicidal ideation and hopelessness. J Affect Disord. 2013 Oct;151(1):275-83.

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Geraldine Hannon, Emily P. Taylor (2013). Suicidal behaviour in adolescents and young adults with ASD: Findings from a systematic review Clinical Psychology Review DOI: 10.1016/j.cpr.2013.10.003

Not metabolomics and autism again...

I don't mind admitting that I am a bit of a nerd when it comes to certain things.

Yes I still thrill at watching the films of the 1970s / 1980s; in particular a certain trilogy of films almost known word for word ("delusions of grandeur..."). And yes, despite my very restricted competence on the issue, I do like looking through the odd study with the words 'metabolomics' or 'mass spectrometry' in the title as per the findings of Stein and colleagues* following up the limited research findings on phthalate metabolism and autism (see here).

Time of Flight? About 3 hours if you're lucky. @ Wikipedia 

Indeed on that last point of mass spectrometry, I was always going to be interested in the paper by Kuwabara and colleagues** (open-access) detailing their efforts of screening the plasma of a small group of adults diagnosed with an autism spectrum disorder compared to asymptomatic controls with a view to identifying "novel candidate metabolites as potential biomarkers".

I've talked about these types of studies before (see here and here) and how the technology is absolutely fantastic in what it enables science to do these days. The Kuwabara paper is a little bit different in terms of their chosen method being based on something called capillary electrophoresis (CE) or to put it more completely CE-ToF MS (CE Time of Flight Mass Spectrometry). You can find out more about CE here.

My memories of second supervising a PhD on this chosen method with autism biomarker research in mind, reminds me that CE was a particularly inviting technique when applied to biological samples in comparison to other more industry-standard methods such as HPLC (see here). So much so that other groups have also looked at CE with autism in mind as per the study by Soria and colleagues*** although I don't think things really progressed any further in this area despite the allure of CE.

Anyhow, the Kuwabara paper reported that based on a two-step identification and validation study using CE-ToF MS, a number of metabolites came up as being potentially important to autism cases including high plasma levels of the amino acids arginine and taurine and "significantly low levels of 5-oxoproline (p<0.001) and lactic acid (p = 0.031) compared with the controls".

I've mentioned before how amino acids, the building blocks of peptides and proteins, have been the source of quite a bit of study with regards to autism (and lots of other conditions). I should really formulate a mega-post on what the various studies of the amino acids have found so far with regards to autism, but at this point in time, the task is just a little too daunting. That being said, the Kuwabara results show some passing connection to other data in this area specifically with regards to taurine (see here) but as with everything seemingly linked to autism, there is nothing universal about this finding****. Indeed on that lactic acid finding (yes, I know it's not an amino acid) and in particular, the lower levels of lactic acid reported, one might say this was slightly at odds with other research (see here).

It is perhaps one of the downsides to the whole metabolomics and proteomics disciplines that whilst the technology is astounding in terms of findings and accuracy (accurate mass anyone?), when applied to a heterogeneous condition like autism, grouped and consistent results are often few and far between. Yes it very much depends on factors such as what medium you are sampling (blood, urine), when you sample (age of participants) and under what circumstances you sample (diet, medication, etc.). But as with the very complicated genetics (and epigenetics) of autism (see here), so the proteome and metabolome in relation seem to be also going the same way in terms of a lack of consistent and verifiable markers.

As I've indicated before, the whole concept of biomarkers 'for autism' is perhaps a moot point given issues like the rise of the autisms (see here) and all that comorbidity which can, and does, seem to follow a diagnosis (see here) interfering with any results. That's not however to say that there may be some benefit in continuing this line of investigation with some subtle alterations such as focusing on sub-groups (see here) or using the technology to explore intervention response for example (see here). Indeed with this in mind, I should also tip my hat to the study by Ramsey and colleagues***** (open-access) and their age-related "molecular trajectories" work in relation to autism which mimics where metabolomics seems to be going in other areas of medical research.

Oh and how about marrying up metabolomics with another very interesting -omic, the gut microbiome******?

To close, and especially for a very sensitive member of my brood who shed a tear at this part of the movie, the redemption of Anakin Skywalker. Bless you darling, don't ever change.

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* Stein TP. et al. Autism and Phthalate Metabolite Glucuronidation. JADD. 2013; 43: 2677-2685.

** Kuwabara H. et al. Altered Metabolites in the Plasma of Autism Spectrum Disorder: A Capillary Electrophoresis Time-of-Flight Mass Spectroscopy Study. PLoS One. 2013 Sep 18;8(9):e73814. doi: 10.1371/journal.pone.0073814.

*** Soria AC. et al. Data processing in metabolic fingerprinting by CE-UV: application to urine samples from autistic children. Electrophoresis. 2007 Mar;28(6):950-64.

**** Geier DA. et al. A prospective study of transsulfuration biomarkers in autistic disorders. Neurochem Res. 2009 Feb;34(2):386-93.

***** Ramsey JM. et al. Identification of an age-dependent biomarker signature in children and adolescents with autism spectrum disorders. Mol Autism. 2013 Aug 6;4(1):27. doi: 10.1186/2040-2392-4-27.

****** De Angelis M. et al. Fecal Microbiota and Metabolome of Children with Autism and Pervasive Developmental Disorder Not Otherwise Specified. PLoS ONE 8(10): e76993.

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Kuwabara H, Yamasue H, Koike S, Inoue H, Kawakubo Y, Kuroda M, Takano Y, Iwashiro N, Natsubori T, Aoki Y, Kano Y, & Kasai K (2013). Altered Metabolites in the Plasma of Autism Spectrum Disorder: A Capillary Electrophoresis Time-of-Flight Mass Spectroscopy Study. PloS one, 8 (9) PMID: 24058493

Autism in the UK: levelling off?

A short post today based on the paper by Brent Taylor and colleagues* (open-access) adding to the considerable literature on the autism numbers game. The headlines generated from this study are no better encapsulated than that of the BBC: "UK autism cases have 'levelled off'".

Reaching the summit? @ Wikipedia

The crux of the paper is that based on an analysis of the UK General Practice Research Database (GPRD) which carries details of several million patient records following patient contact with what's known as a General Physician (GP) here in the UK, cases of autism spectrum disorder included in those records were counted and annual prevalence and incidence rates based on 8-year olds were generated.

The results: cases of autism recorded on the GPRD suggested that "the annual prevalence of autistic spectrum disorders was estimated at 3.8 per 1,000 boys and 0.8 per 1,000 for girls".

Importantly, from the BBC: "The study concluded there was "compelling evidence that a major rise in incidence rates of autism, recorded in general practice, occurred in the decade of the 1990s but reached a plateau shortly after 2000 and has remained steady through 2010"".

There are also a few interesting nuggets of information to take from the Taylor paper such as the reason(s) put forward for the dramatic increase in cases witnessed during the 1990s. Another quote I'm afraid on whether greater awareness or broadening diagnostic criteria or diagnostic substitution were the sole causes of the increase: "it seems unlikely that these factors materially explain the extraordinary increase in the number of children diagnosed in the 1990s; nor the steady state that followed thereafter in 2004 through 2010". This is in line with what other commentators have talked about (see here).

The Taylor paper is an interesting one and no doubt will generate some discussion about the numbers of cases of autism. I note that the figures reported by Taylor and colleagues are somewhat at odds with other studies using different data collection methods based in other parts of the world such as that 1 in 50 figure in the US discussed quite recently (see here) or other incidence data (see here). Whether this is down to how the data are collected and verified or truly representative of differing rates of autism in different geographical populations is yet more substance for discussion.

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* Taylor B. et al. Prevalence and incidence rates of autism in the UK: time trend from 2004–2010 in children aged 8-years. BMJ Open. 2013; 3: e003219

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Brent Taylor, Hershel Jick, Dean MacLaughlin (2013). Prevalence and incidence rates of autism in the UK: time trend from 2004–2010 in children aged 8-years BMJ Open DOI: 10.1136/bmjopen-2013-003219

Maternal diabetes and offspring autism risk

The systematic review and meta-analysis reported by Xu and colleagues* caught my eye recently. Concluding that: "maternal diabetes was significantly associated with a greater risk of ASD in the offspring" my interest was truly piqued.

Insulin @ Wikipedia  

Diabetes in relation to autism has cropped up a few times on this blog. I've talked about the possibility of a more general connection (see here) and also more specific as part of some of the CHARGE results (see here).

Indeed those CHARGE results, based on the study by Paula Krakowiak and colleagues** (open-access) I remember generated quite a bit of discussion at the time of their publication given the suggested link with various facets making up metabolic syndrome in mums.

I'm not really surprised by the Xu results when you think that the association between gestational diabetes and offspring autism risk has been talked about before based on some pretty strong association data. I note for example, that the study by Lyall and colleagues*** (open-access) flagged up this association - "gestational diabetes was associated with a significantly increased risk of ASD" - based on quite a nice sample size. That and the paper by Hannah Gardener and colleagues**** (open-access) who suggested that gestational diabetes was perhaps one of several factors which might elevate offspring risk as per the Krakowiak results.

The question of mechanism of effect is slightly less clear it has to be said. In my first post on autism and diabetes, quite a lot was made of the connection between type 1 diabetes and autism as per the familial autoimmune connection (have a look at my Money post for example). Granted this doesn't really add anything more specific than to say that autoimmune conditions can 'club together' (see here) which might take us down some other avenues particularly when talking about at least some autism comorbidity (see here). That and the implication that autism might also be an autoimmune condition***** as some have implied.

As to any mechanism of gestational diabetes being linked to the aetiology of autism, well I'm afraid I can't offer anything too concrete at this point. There is some speculation that gestational diabetes might be linked to other cognitive and developmental issues as per the research on ADHD (Attention-deficit hyperactivity disorder)****** and schizophrenia*******. Indeed, that paper by Van Lieshout & Voruganti (open-access) on gestational diabetes and risk of offspring schizophrenia suggests: "at least 3 prenatal mechanisms: hypoxia, oxidative stress and increased inflammation" of potential effect. Suffice to say that all of them have also been banded around as being involved with cases of autism at various times (particularly the roles of inflammation and oxidative stress). I might also draw reader's attention to the paper by Nousen and colleagues******** too.

The take-home message whilst still one of caution in singling out one particular factors as being linked to autism (or should that be the autisms?) is that maternal diabetes should be registering on the various investigations into pregnancy and birth factors linked to offspring autism risk to further explore mechanisms. Whether altering the presentation of maternal diabetes (lifestyle changes or even reviewing medication*********) might also impact on offspring outcome is another question which should be on the lips of autism research...

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* Xu G. et al. Maternal Diabetes and the Risk of Autism Spectrum Disorders in the Offspring: A Systematic Review and Meta-Analysis. J Autism Dev Disord. 2013 Sep 22.

** Krakowiak P. et al. Maternal metabolic conditions and risk for autism and other neurodevelopmental disorders. Pediatrics. 2012 May;129(5):e1121-8. doi: 10.1542/peds.2011-2583.

*** Lyall K. et al. Pregnancy complications and obstetric suboptimality in association with autism spectrum disorders in children of the Nurses' Health Study II. Autism Res. 2012 Feb;5(1):21-30. doi: 10.1002/aur.228.

**** Gardener H. et al. Prenatal risk factors for autism: comprehensive meta-analysis. Br J Psychiatry. 2009 Jul;195(1):7-14. doi: 10.1192/bjp.bp.108.051672.

***** Ashwood P. & Van de Water J. Is autism an autoimmune disease? Autoimmun Rev. 2004 Nov;3(7-8):557-62.

****** Nomura Y. et al. Exposure to gestational diabetes mellitus and low socioeconomic status: effects on neurocognitive development and risk of attention-deficit/hyperactivity disorder in offspring. Arch Pediatr Adolesc Med. 2012 Apr;166(4):337-43. doi: 10.1001/archpediatrics.2011.784.

******* Van Lieshout RJ. & Voruganti LP. Diabetes mellitus during pregnancy and increased risk of schizophrenia in offspring: a review of the evidence and putative mechanisms. J Psychiatry Neurosci. 2008 Sep;33(5):395-404.

******** Nousen EK. et al. Unraveling the Mechanisms Responsible for the Comorbidity between Metabolic Syndrome and Mental Health Disorders. Neuroendocrinology. 2013. Sept 21.

********* Barnard KB. et al. Antidepressant Medication as a Risk Factor for Type 2 Diabetes and Impaired Glucose Regulation. Systematic review. Diabetes Care. 2013; 36: 3337-3345.

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Xu G, Jing J, Bowers K, Liu B, & Bao W (2013). Maternal Diabetes and the Risk of Autism Spectrum Disorders in the Offspring: A Systematic Review and Meta-Analysis. Journal of autism and developmental disorders PMID: 24057131

Parental stress and autism: what's effective at reducing it?

Raising children is an extremely rewarding experience. That's not to say however that every minute of every day is spent with smiles and adoration of your offspring and their various endeavours: "Was that family heirloom that I just dropped on the floor really, really important Daddy?" Generally speaking the majority of parents I imagine though, would look favourably at the experience of going the family-way.

Gathering the light @ Wikipedia  

The rosy picture of having a family is however never truly complete without realising that having children can be quite a stressful experience. Whether as a result of those earliest days of sleep deprivation and almost constant nappy changing duties, through to some of the growing pains as puberty beckons and even onwards into the adult years, stress is a pretty constant companion to the family journey. And the amount of stress parents face in the child rearing odyssey is very much influenced by lots of other external variables such as money, job, relationships et al. Oh and also how many kids you're parenting (see here).

To have a child with additional needs, whether a physical disability or intellectual / developmental disorder, has been suggested to carry it's own unique challenges which can also impact on parental stress levels. I'm not saying that to somehow blame or stigmatise or anything like that, but merely to reflect the quite extensive body of research which has concentrated on that point (see here for example).

There is also quite a large evidence base to suggest that parents report greater levels of stress associated with raising a child with an autism spectrum disorder as per the example article by Koegel and colleagues*. Indeed it is with this area in mind that I stumbled across the paper by Dykens & Lambert** who noted: "Stress-reducing interventions are needed for parents of children with autism" as part of their analysis of cortisol levels in mums raising children, including those raising children with autism.

I've talked about stress and cortisol before on this blog (see here) as per the collected findings in relation to people with autism. The net result of that post was to say that yes, quite a few people on the autism spectrum present with an unusual stress profile (although not necessarily beyond the range seen in not-autism) but importantly, stress - as monitored via cortisol levels - seems to be a rather more continual process for many. Such results have obvious implications in relation to things like the anxiety issues often reported to follow autism.

The highlighted sentence from the Dykens paper on the need for stress reduction interventions for caregivers pinpoints a fairly obvious issue which I'm sure many people would take as read. Indeed with the suggestion from Osborne and colleagues*** that parenting stress might also potentially impact on the effectiveness of early intervention for autism, the questions are: what kinds of stress-reducing interventions are available and importantly, which ones work?

I don't claim to have some special insight into these questions, but a quick trawl of the research literature offers a few potentially important pointers.

(i) Social support. "With a little help from my friends" was a song by the Beatles but also the title of a rather interesting paper by Brian Lovell and colleagues**** on one potential route for tackling caregiver stress. Appreciating that to many this is not new news, it is perhaps little surprise that through the wonders of social media and the Internet, on-line social support groups for parents of children with autism are numerous and easily accessible in our digital age. With all the talk about how such resources might be 'changing our brains' (erm, or not), I'm minded to say that in this example, it might actually be a change for the better.

(ii) Mindfulness. I know, I know. It sounds like psycho-babble mumbo-jumbo to the nth degree when you first hear it. But actually I'm becoming a bit of a fan of mindfulness as per my previous post making mention of the BBC Horizon program 'The Truth About Personality' featuring the ever-intrepid Dr Michael Mosley. The basic idea is to think about the present, nay focus on the present, and manage the thoughts and feelings that are linked to stress. The evidence base for mindfulness for relieving caregiver stress is what might be described as emerging as per the study by Neece***** although with some potential bonuses for offspring too. It's also worth pointing out that mindfulness techniques are seemingly also finding a role in helping some people on the autism spectrum too (see Spek and colleagues******). Relations to mindfulness such as the use of relaxation techniques for caregivers have also been put forward as potentially useful*******. I wonder if something like blogging might also come under the description of 'managing thoughts and feelings'?

(iii) Parent training. I must point out that I am in no way trying to say that anyone is in need of "training" just in case anyone thinks I'm harking back to the bad old 'Bettelheim' days or casting aspersions about parenting style. I merely refer to the body of literature which 'suggests'******** that there may be some merit in looking into this option with stress relief in mind. Whether parent training might also fit under the banner of other programs such as RDI or more generic programs like Stepping Stones Triple P and any knock on effects this might have to parent stress levels is something perhaps requiring a little bit more study in order to define things like potential best responder characteristics.

(iv) Respite. I don't think this option really needs much explanation. Harper and colleagues********* said it best: "More respite care was associated with increased uplifts and reduced stress". Indeed, part of that reduction in stress was seemingly getting a little more quality time with your spouse or significant other... break out the Marvin Gaye. Seriously though, I can't stress enough how important respite care can be to some families. And if you happen to live here in Blighty (that's the UK), there are quite a few resources about respite and how to access the care: see here and here.

(v) A hobby or external interest. Although this is supposed to be an evidence-based post, there are a few other stress-relieving options that have been mentioned in a more anecdotal fashion. An interest involving physical exercise as a stress reducer seems to be a common theme. Indeed as I write this post, I'm just watching the preparations for the Great North Run on this slightly soggy Sunday morning and one parent of a child with Asperger syndrome running for the charity Ambitious About Autism. Using her running preparations as a way of getting some down time was mentioned in her interview. Other parents have talked about the use of activities like martial arts as being a stress reducing tool, which did make think back to some other work on the use of martial arts as a self-esteem builder for children with autism (see here). I'm not necessarily saying that every parent has to immediately join their local Jui-jitsu class or anything like that, but one can perhaps see how the process of physical activity might serve more than just a physical purpose.

I've only really scratched the surface with this post on parental stress and autism and how one might go about tackling / reducing it. If you want a perspective from a parent with autism who is also a medical doctor, look no further than these insights (see here) from a physician who's research has previously appeared on this blog (see here).

One might also argue that tackling some of the more 'disruptive' issues associated with autism which have been reported to be linked to greater parental stress (see here) might also be another route to reducing stress. The very interesting paper from McStay and colleagues********** reporting that "child hyperactivity was the only factor significantly related to parenting stress in parents of children with autism" might even tie into some of the observations we've made recently on the use of a GFCF diet (see here) and even explain some of the popularity of this approach. Indeed, I've not really approached the question of whether comorbidity (including ESSENCE) appearing alongside autism might also be a significant source of parental stress, as one might expect from something like epilepsy or seizure-related disorders for example. And then there is the increasingly common scenario of parents (one or both) with autism bringing up children with autism and how that situation might present additional unique parental stresses. Let us also not forget other siblings of the family unit too and how stress can affect them.

What remains apparent is that (a) parenting, as well as very rewarding, can be a stressful activity, (b) parenting a child with additional needs can carry some of its own unique stresses and (c) tackling or reducing that stress has got to be a win-win situation for everyone concerned; importantly not just for the child, but also for parents too (see here) including in relation to related aspects like fatigue.

To close, some music to dance to (dancing is also a very good stress-relieving activity I'm led to believe).... Wham and Wake Me Up Before You Go-Go. And for all you fathers out there who partake of a bit of 'dad dancing', a hypothesis for you to consider...

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* Koegel RL. et al. Consistent stress profiles in mothers of children with autism. J Autism Dev Disord. 1992 Jun;22(2):205-16.

** Dykens EM. & Lambert W. Trajectories of Diurnal Cortisol in Mothers of Children with Autism and Other Developmental Disabilities: Relations to Health and Mental Health. J Autism Dev Disord. 2013; 43: 2426-2434.

*** Osborne LA. et al. Parenting stress reduces the effectiveness of early teaching interventions for autistic spectrum disorders. J Autism Dev Disord. 2008 Jul;38(6):1092-103.

**** Lovell B. et al. With a little help from my friends: psychological, endocrine and health corollaries of social support in parental caregivers of children with autism or ADHD. Res Dev Disabil. 2012 Mar-Apr;33(2):682-7. doi: 10.1016/j.ridd.2011.11.014.

***** Neece CL. Mindfulness-Based Stress Reduction for Parents of Young Children with Developmental Delays: Implications for Parental Mental Health and Child Behavior Problems. J Appl Res Intellect Disabil. 2013 Jul 1. doi: 10.1111/jar.12064.

****** Spek AA. et al. Mindfulness-based therapy in adults with an autism spectrum disorder: a randomized controlled trial. Res Dev Disabil. 2013 Jan;34(1):246-53. doi: 10.1016/j.ridd.2012.08.009.

******* Gika DM. et al. Use of a relaxation technique by mothers of children with autism: a case-series study. Psychol Rep. 2012 Dec;111(3):797-804.

******** Bendixen RM. et al. Effects of a father-based in-home intervention on perceived stress and family dynamics in parents of children with autism. Am J Occup Ther. 2011 Nov-Dec;65(6):679-87.

********* Harper A. et al. Respite Care, Marital Quality, and Stress in Parents of Children with Autism Spectrum Disorders. J Autism Dev Disord. 2013 Mar 26.

********** McStay RL. et al. Parenting stress and autism: The role of age, autism severity, quality of life and problem behaviour of children and adolescents with autism. Autism. 2013. 8 October.

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Dykens EM, & Lambert W (2013). Trajectories of Diurnal Cortisol in Mothers of Children with Autism and Other Developmental Disabilities: Relations to Health and Mental Health. Journal of autism and developmental disorders PMID: 23468069