DSM V on autism or is that autism spectrum disorder?

It has been on the horizon for quite a while.

Last month the American Psychiatric Association (APA) detailed the proposed revisions to the Diagnostic & Statistical Manual (DSM) - DSM V. Details of the various documents are available here. There has already been quite a lot of chatter about this in the professional, peer-reviewed and lay domains. The main changes being put forward are:

1. Revision of the name to 'Autism Spectrum Disorder', 
2. Reducing the triad of impairments to a "pair" of impairments, merging current social and communication areas into a 'social/comunication' super-domain, 
3. Inclusion of a sensory aspect to the 'restricted repetitive patterns' domain, 
4. Replacing the 3 year cut-off period with presentation instead during 'early childhood', 
5. Detailing levels of severity based on the amount of support required, and 
6. Use of a single diagnostic category which does not include Asperger syndrome as an exclusive diagnosis.

Phew! Sit down... have a drink... and I will carry on. One has to remember that these are the clinical description guidelines for autism (autism spectrum disorder excuse me!) and hence form the criteria for diagnosis - that is all. Like past DSM revisions they make no reference to any other aspect of autism - medical, political or personal, nor do they detail any 'life course' of autism. All they specify is what a physician or team use to say 'autism or not-autism'.

The name change to autism spectrum disorder is perhaps a more welcome addition to the DSM. Thanks principally to the work of Lorna Wing and her book 'the autistic spectrum' first published in 1996, this terms has seen regular usage in the UK expanding outwards to other countries. It signifies two important things: (a) that autism is a heterogeneous spectrum in terms of presentation of symptoms, and (b) at what is often called the higher-functioning end of the spectrum, the condition overlaps with what is often called neurotypicality. I suppose the only issue here is the use of the word 'disorder' over 'condition'; noting that many organisations nowadays use one (e.g. the National Autistic Society) or the other (e.g. NICE).

Merging the current social and communication sub-domains into one is slightly more contentious. Far be it from me to say that this point has already been approved, but for a few years now there have been clues to this merger happening. The biggest clue came from one of the gold standard instruments used to assess autism, the Autism Diagnostic Observation Schedule (ADOS). Briefly, ADOS is a standardised tool that assesses the responses (and non-responses) of a child/adult to certain tasks and cues which vary according to age and degree of language the person has. The scores derived from the schedule are summed and put through an algorithm which determines whether autism or autism spectrum cut-off points are reached. The original algorithm used has received quite a lot of study. In recent times revised algorithms have however appeared; the first was by Gotham and colleagues in 2007, where separate social and communication domains were merged into one super-domain labelled 'social affect'. Coincidence?

The inclusion of a sensory aspect to autism (autism spectrum disorders!) is another welcome addition. Many people with autism report on various hypo- and hyper-sensitivities to all kinds of things (noise, light, touch, etc). I remember reading some of the books of Donna Williams where these are described; more recently also discussed in some detail by Olga Bogdashina (I am not plugging any of their books by the way!).
Replacing the cut-off periods is a slightly odd one so I am going to skirt over that issue.

A measure of 'severity' is probably going to be a mixed bag. On the one hand it will provide some information both to the person with autism / their parents where on the spectrum the diagnosis has been graded. I assume this means that where support is required (in one or both of the domains at the same level or variably), there will be clear instructions to education and social services to provide for the needs of that individual. From a research perspective (ah yes) it also gives the possibility (just a possibility) to examine/assess the natural progression of the condition, either as a result of maturation or possibly intervention based on the severity scale provided. The one downside that I could envisage is how to ensure that severity is accurately portrayed at diagnosis. What happens if it is queried after a diagnosis is received?

Finally, the use of a single diagnostic category. Mmm, this is where I could get myself in some hot water. The rise of 'Asperger syndrome' as a specific diagnostic entity is a notable one over the past few years. For many, the diagnosis is a valued one; as is evidenced by the number of blogs and websites dedicated to 'Aspie pride' (of which there are too many to list here). The questions are these: how would an individual (most probably an adult) who has a diagnosis of Asperger syndrome now react if their diagnosis 'disappears' from the diagnostic literature? How would an individual with Asperger syndrome feel about being 'reclassified' as having an autism spectrum disorder according to the new criteria?

These are not easy questions to answer. Remodelling autism in such a significant manner takes us into unknown territory. Will the changes increase or decrease the numbers of cases being diagnosed? If DSM takes the lead, will the alternative WHO diagnostic schedule (ICD) be forced to follow?

I am sure that many of these issues will come further to the front of discussions as the time approaches for transition and we eventually say thank you and good night to DSM-IV.

Gluten relations

As this blog develops you will see that I have a bit of a penchant for all things related to diet and particularly gluten. Don't get me wrong; I am not anti-gluten (or anti-casein for that matter); indeed quite the opposite, acknowledging the significant part gluten has had, and continues to play, in feeding our ever increasing populations. I do however believe in 'horses for courses' - what is suitable for one might not necessarily be suitable for another.

For many years I have been struck by the number of people, groups, studies outside of autism who have suggested a possible link between their symptoms (whatever they may be) and their diet - that is what they eat seemed to go hand-in-hand with how they felt or what illness/condition they developed. Diet mediating physical health is of course well-recognised; diet mediating mental health and development is perhaps another story. From the outset I will admit that I am a fan of the notion that correlation does not imply causation; that is just because 2 events occur close together does not necessarily mean that one causes the other. I also however believe that if two events do happen close together, it is the responsibility of science to investigate any possibility of a relationship, if nothing else just to disprove it.

I digress. One of the more interesting conditions where reports of a link between presented symptoms and diet have surfaced was with a group of people who had been diagnosed with myalgic encephalomyelitis (ME) or Chronic Fatigue Syndrome (CFS). First and foremost I will admit that I am not an expert on ME/CFS (add it to the list of my non-expertise). I know a little bit about the symptoms; a little bit about the various hypotheses on aetiology and pathology; and a little bit about the variability and heterogeneity involved (similar to autism). That's it. I have corresponded with a few people who have ME/CFS and got a flavour of how much it impacts on their lives.

My interest in ME/CFS and diet was perked after reading a newspaper article recently. The article described the daughter of quite a famous UK TV personality who has ME and a purported link to gluten. OK it is a newspaper and things tend to get a little sensationalised (to sell more newspapers perhaps?), but it was a very interesting read. The summary is that this young lady struggled with ME for many years, presented also with some other 'somatic' conditions and eventually was led through to the possibility that she could have a problem with gluten. The article mentions coeliac disease (quite extensively) but a connection between the two in this case has been queried. I have since done a little hunting around and found a couple articles suggesting that routine screening for coeliac disease should be carried out in cases of CFS given indications of about 2% of patients presenting with CFS also being endomysial antibody (EMA) positive, whether co-morbid or as an alternate diagnosis to explain fatigue. What I was unable to find was good scientific questioning of what happens to ME/CFS symptoms when those with positive EMAs went on a gluten-free diet, and whether the recent newspaper story suggestive of positive effects potentially outside of coeliac disease has been examined.
 
Set against the recent PACE study published in the Lancet and the various discussions around the trial design and results, it is perhaps timely that the UK Medical Research Council (MRC) have this week set aside funds to conduct further research into ME/CFS. I wonder if anyone will chose to look at the potential connection between diet and ME/CFS?

Food and ADHD: lessons for autism?

I admit that I am a little late in getting to this topic. Late because for quite a while now (years in fact) questions have been raised about a possible link between food, diet and some cases of ADHD (Attention Deficit Hyperactivity Disorder), late because the study published by Pelsser and colleagues which forms the bulk of this post has already been through the blog mill, and late because I had to really think about how to write this post - unlike my others!

First things first. For many years some parents of children diagnosed with ADHD (or ADHD-type symptoms also co-morbid to other things on some occasions) have reported a connection between what their child eats and their child's subsequent behaviour. It was the work of Dr Feingold and a few others who set out the stall that certain types of food preservatives, colours and flavours might be implicated in behaviours associated with ADHD. There has, since the early years of this work, been some significant to-ing and fro-ing about whether Feingold's assertions were correct.

In 2007-2008 two things happened: McCann and colleagues published the results of a tightly controlled study on the effects of food additives on hyperactivity, concluding that certain preservatives and artificial colourings did impact on behaviour. A review by Schonwald in the American Academy of Pediatrics Grand Rounds journal was accompanied by an editorial which all but admitted that following the McCann paper there may be a connection; to quote:  ".. that even we skeptics, who have long doubted parental claims of the effects of various foods on the behavior of their children, admit we might have been wrong".

OK so far? The next "stage" in this saga was the publication a few days back now, of a study from Lidy Pelsser and colleagues (like McCann et al, also published in the Lancet). Pelsser and the group based at the ADHD Research Centre in the Netherlands which includes Jan Buitelaar, have been very, very busy in the area of food and diet in connection to ADHD, publishing results from quite a few trials (see here and here). The result of their most recent study concluded that "a strictly supervised restricted elimination diet is a valuable instrument to assess whether ADHD is induced by food". I am not going to dissect the study here; feel free if you wish to.

So what we have is some good evidence that diet and food could affect some children who present with ADHD or ADHD-type behaviours - emphasis on the "some" children because as we know science is about probability not certainty and we would be hard pressed to say all children show a connection. You may ask then where autism comes into this?

Well, first off, we know that autism and ADHD can occur alongside each other and the association seems quite strong. We also know that some people with autism seem to be affected by diet; whether as a consequence of co-morbid conditions such as coeliac disease or through less well-defined connections. The types of diet most commonly linked with autism are those excluding gluten- and casein, but there are several more being quite widely discussed. I will stay with the GFCF diet because that's what I know ('a cobbler should stick to his last' and all that).

The most recent Pelsser study described their diet (at least in the first phase of their study) as consisting of a few foods; just rice, meat, vegetables, pears and water. Notice that a few things are missing from this diet including our old friends gluten and casein (although I believe small amounts of wheat were included on specific days for some participants for RDA reasons). When however you compare the Pelsser results on ADHD with some of the data from autism, a few "similarities" start to occur. For example, during our most recent 2-year ScanBrit trial of the GFCF diet for autism we included a few measures outside of autism aimed at examining ADHD-type behaviours (for those of you interested it was the ADHD-IV scale by DuPaul and Power) given the previous suggestions that such areas of functioning may be affected by diet. What we found and reported on was that hyperactivity and inattention sub-domains seemed to indicate some "group" reduction following intervention.

Fair enough I hear you say, a non-blinded study showing that ADHD-type behaviours presented by children with autism "seemed" to show a significant group reduction effect after diet? One study: it shows nothing. Well not quite. Another recent trial by Cynthia Johnson and colleagues also looked at the effects of a GFCF diet on children with autism. Similar to ScanBrit, the trial was randomised but not blinded and compared a GFCF diet to a healthy low sugar diet for autism over the course of 3 months. Their results: overall no significant gains on the GFCF diet vs. the healthy low sugar diet but reading the full-text to their paper, an interesting finding: a significant reduction in ADHD behaviours for the GFCF group (p = 0.043) (Table 5) which were also examined during their study.

The skeptic in me says OK possibly a fluke event in both cases; the reduction in ADHD-type behaviours could be down to the study design (non-blinded), other things the participants were doing at the time of study or merely because more attention was given to them as a consequence of being "studied". A small, little, tiny voice is however telling me: "mmm, this is interesting, does this need a little more study?" I will let you answer that question yourselves.

Should I mention gastrointestinal symptoms in autism?

There have been plenty of discussions, debates and controversies in autism research down the years. One of the first ones that I remember from a few years back was the issue of whether or not the hormone secretin could be a potential "treatment" for autism. Those who were around at the time of the secretin story will remember the hype, where newspapers, TV programmes and a young internet was awash with stories about this compound. I even remember our own research team doing a little bit of blue-sky thinking about secretin (and gastrin and CCK) at the time.

I am not going into the details of whether secretin was "right" or "wrong". Sure, there were quite a few studies suggesting that there was no universal effect from secretin but again, as per my mantra, science is about probability not absolutes; and autism is an extremely varied condition.

In the same year, the now widely discussed Lancet case series paper describing a specific pattern of bowel symptoms co-morbid to various presentations of autism and related conditions was also published and later retracted by the Lancet. The suggestion that a specific pattern of gastrointestinal histopathology may be present hit the world with a bang.

Both these areas of work have been, and in some cases, continue to be a major source of debate both within the autism community and also in the wider population. I am not getting into the nitty-gritty of such debates - there are plenty of other places on the Web to do that. What I would like to discuss further is the commonality between these two areas of research: the potential role of gastrointestinal symptoms / conditions being associated with some cases of autism.

A recent review article written by Chen and colleagues has been published reviewing the evidence for abnormal gastrointestinal histopathology in children with autism spectrum conditions down the years. Their conclusions after weighing up all the available evidence so far were: (a) GI findings in children with autism are inconsistent - aside from the finding of intestinal lymphonodular hyperplasia (LNH), (b) the present evidence does not support or refute a link between GI findings and autism, (c) the significance of LNH in this group is unknown.

Now, I am no Gastroenterologist - I can point to my gut (which seems to be growing as my years progress) but that is about the sum total of my expertise in this area so I can't claim to be an authority on the subject. What I can however offer is an opinion which is this: if the evidence is inconsistent and the significance of any gastrointestinal findings are not known, is it perhaps time to undertake a few more definitive studies to help try and answer these questions?

Some would say 'no' the book is closed - such invasive studies should not be done, the limited research money should be spent on other areas. Others might say we can still learn more about any connection between bowel symptoms (functional and histopathological) and autism, even if only for a proportion of people on the spectrum and perhaps just as important look at the various treatment measures to help alleviate any suffering as a result of any bowel problems irrespective of any autism connection (see here and my previous posts mentioning coeliac disease and autism).

In recent years it has become almost a dirty word to discuss the gut in relation to autism in some quarters. The title of this post is 'should I mention gastrointestinal symptoms in autism'. The question remains: should I?

Gluten sensitivity and coeliac disease

In previous posts I have discussed co-morbidity of autism and coeliac disease, and the fact that whilst such co-morbidity is comparatively rare (as far as we know!) it nevertheless exists. For those cases where a genuine diagnosis of coeliac disease has been made through serological testing (and biopsy), there is a scientifically justifiable reason to embark on a gluten-free diet with the hope of remediation of coeliac symptoms (abnormal functional bowel habits, weight loss, etc) and pathology (flattening of mucosal villi) and possibly autistic symptoms (see here).

For those cases where testing for coeliac disease shows a negative result, the problems in justifying use of a gluten-free diet (perhaps alongside a casein-free diet) increase. No coeliac disease, no problem with gluten - or is there?

A recent study published by Jessica Biesiekierski and colleagues reported on the potential effects of gluten to cause gastrointestinal symptoms without coeliac disease being involved. They reported on a so-called "non-celiac gluten intolerance" which seemed to hold for some of their patient group diagnosed with irritable bowel syndrome (IBS). This was a very well conducted trial, double-blind, randomised, placebo-controlled and including a re-challenge element (I only dream about such methodology as this!). The only problem is that they could not explain why the trial worked: not coeliac disease, not intestinal permeability, not inflammation - some speculation on the direct action of gluten peptides on humoral immune response, perhaps.

This is of course only one study. A study that does not mention autism in any way shape or form and looked principally at gastrointestinal problems (of which only a proportion of people with autism present). It would be a huge leap to infer similar results or mechanisms in some cases of autism, particularly where gut problems are co-morbid.

It does however gift us a possible idea for investigation and potentially another reason why some people with autism seem to show an effect from the introduction of a gluten-free diet in the absence of co-morbid coeliac disease. Slice of bread anyone?

Epidemiology of autism: contrasting differences

One of the more animated debates in autism research relates to the possible reasons behind the quite staggering increase in cases being diagnosed world-wide over the past 25 years or so. One of the benchmark studies used for prevalence of autism (note prevalence not incidence), at least in the UK, is the study published by Gillie Baird and colleagues back in 2006 suggesting a total prevalence of all autism spectrum conditions of 116.1 per 10,000.

Two recent reports caught my eye. The first was a comparison of autism prevalence rates in Denmark and Western Australia published by Parner and colleagues. As per the link they reported differences between Danish and Australian prevalence rates of total autism spectrum conditions (68 vs. 51 per 10,000 respectively). These rates are different. Not only between the two countries in question, but also compared with the Baird data. One could perhaps suggest that there were differences in the birth years covered or methodologies employed to "find" and "record" cases (whether it was actively searching for cases of merely reliant on database figures as much of the Danish data tends to be for example because of the way their healthcare records are set up). This could perhaps explain some difference; my question however would be how much can it explain? Does this mean that prevalence of autism spectrum conditions is higher in the UK, than in Denmark or Western Australia? If so, what are the factors influencing such a difference?

A second study that deserves some comment is a follow-up study from Barnevik-Olsson and colleagues on the prevalence of autism in Somali children living in Sweden born between 1999-2003. They reported prevalence of autism as a percentage comparing Somali children with non-Somali children (rates were 0.98% vs. 0.21% respectively). Their initial study published in 2008 showed rates of: 0.7% vs. 0.19% (Somali vs. non-Somali) for children born between 1988-1998. These data again show differences. Differences in the rates between Somali and non-Somali children with autism, differences between the birth years and also differences with the other studies listed in this post. The issue of whether autism rates are elevated in Somali children is the focus of some interest already so I am not going to speculate on any reasons why there may be a difference.

Going back to the Baird data, again with all the caveats regarding case ascertainment et al, are we actually saying that the prevalence of cases of autism spectrum conditions in Sweden (amongst non-Somali children) are so markedly different from the UK data? Questions, questions, questions.

Gluten- and casein-free diets for autism - absolutes?

For all of my research career so far (limited as it is), investigations into the potential effectiveness of a gluten-free and casein-free (GFCF) diet on some of the core and peripheral symptoms associated with autism has formed the vast majority of the work. It is true that the studies I have been involved with in this area have, on the whole, suggested that such a diet (in part or whole) might be a useful intervention for some people with autism (you can read about them here and here). It is also true that for some people with autism, such a diet has no effect whatsoever as described by other studies reporting no significant effect (here and here). Cumulatively these studies are also reflective of the 1000s of reports in books and posted on the web about the success / non-success of dietary intervention.

Taking into account the evidence base and all the methodological issues that have been discussed many times on such diet studies, I suppose the best position to take on whether a GFCF diet could help or not is to say, yes, potentially in some cases, but not universally and at the moment no-one really knows how or why (see the Research Autism opinion here).

I was therefore quite surprised to read a recent posting from the very prestigious Mayo Clinic on the topic of GFCF dietary intervention for autism; the headline reading: there is no evidence that special diets are an effective treatment for autism. More surprising was that the article included as references our recent ScanBrit study and also the most recent Cochrane Review of dietary intervention for autism from 2008 which concluded that more research is required.

Well, as per the information about this blog, science and real-life do not generally speaking deal in absolutes, but rather probability. For example, one could argue that if I jumped out of an aeroplane without a parachute or without my parachute opening, I would absolutely, without a doubt, die. The reality however is that a small number of people do survive such a "certainty" (see link to the Bonus Day Club) as a consequence of many different factors and effects; hence our use of probability over the absolute. It is indeed a shame that such a dead-cert line was adopted in the recent Mayo Clinic article; certainly from a group who should know a little about science, evidence-based practice and probability. I note that there has been some discussion about this on other blogs and websites; some people in agreement with the Mayo Clinic line, others slightly more hesitant to accept such an absolute account.

I think the bottom line is to remember the parachute.

NICE to see you, NICE

The headline and content to this post are probably more relevant to a UK audience so I apologise in advance.

In this era of evidence-based medicine (EBM), autism and its research has perhaps fallen down a few cracks. Autism being such a heterogeneous condition, sometimes accompanied by various co-morbidities has meant there is a real quandary in how to formulate good evidence-based guidance on intervention and management. Whilst there have been some valiant attempts to formulate such guidance on autism in the UK including that provided by Research Autism we are not quite there yet.

That is until, by direction from the Department of Health, the National Institute for Health and Clinical Excellence (NICE) have been asked to formulate some guidance on autism. NICE provide guidance on everything to do with health in the UK from medication prescribing patterns to the use of techniques and instruments for all manner of conditions. In autism, there are currently 3 strands of guidance being sought, all at various stages of development.

These are: (i) autism spectrum disorders in children and young adults, (ii) autistic spectrum conditions in adults, and (iii) autism - management of autism in children and young people. Producing universal guidance is going to be a challenge to all involved in these exercises but promises to provide some National standards. Good luck guys - we await the final outcomes.

'Leaky gut' and autism

OK, I'm on a bit of a roll; what with this being my first blog. The next topic that I want to discuss is one quite close to my own research, namely 'leaky gut' and autism. Leaky gut is a little bit of a misnomer. In reality from what I believe, we all have a leaky gut to some degree; the issue at hand is that permeability of the gut is perhaps increased (hyperpermeability) at least in some cases of autism.

I will admit that it has always been fascinating to think that what goes on in the gut could influence behaviour and possibly facets of development and that hyperpermeability might contribute to this. Coeliac disease - that exquisite sensitivity to gluten (celiac to the non-UK audience) has long been associated with gut permeability issues. Looking at the co-morbidity of coeliac disease and autism, it is clear that whilst there is probably no universal relationship, it does occur and perhaps at levels greater than expected in non-autism populations.

The study by Genuis reported a case where autism and coeliac disease was diagnosed and a gluten-free diet introduced. The diet positively affected presented gastrointestinal symptoms but also seemed to affect the presentation of autistic symptoms.  The trouble is that coeliac disease is not routinely checked for in autism (it involves taking a blood sample and possibly a biopsy, so there are ethical considerations).

Anyway back to hyperpermeability, for many years the only study suggestive of hyperpermeability of the gut in autism was that by D'Eufemia and colleagues. They found hyperpermeability in just over 40% of the people with autism involved in their study. That was back in 1996. It was a long time before anything else was done specifically with this issue in mind although there was the odd attempt. Fast forward to 2010 and Laura de Magistris and colleagues published their study suggesting that enhanced gastrointestinal permeability was present in just below 40% of their group. The added value to the de Magistris study was that they had a good size experimental group (90 children) who were well defined in terms of autism diagnosis (ADOS, CARS), a good size control group (64 children), they looked at first-degree relatives and they also looked at what happens to gastrointestinal permeability following use of a gluten- and casein-free (GFCF) diet. Their results were interesting: being on a GFCF diet seemed to reduce the level of permeability present. They even went as far as to suggest that intestinal permeability may be a marker for identifying the sub-group of people with autism who might benefit from such dietary intervention. Don't get me wrong, there is an awful lot of questions that still need to be answered on this whole approach. We have tried to deal with some of them in one of our peer-reviewed papers (read it here) including the negative results from Robertson and colleagues. Still, if there is a subset of people with autism who also may present with coeliac disease or hyperpermeability of the gut, science should be doing more to try and find them. After all, from all the data so far, we know that autism does not confer protection against other conditions, diseases or co-morbidities.

Gut microflora, urine and autism

OK, first proper posting.

The journal Biomarkers posted a new study today on the detection of p-cresol in urine samples from children with autism. A link to their abstract can be found here. I don't have the full article yet but the abstract is quite descriptive.

Basically they reported findings based on 59 children and matched controls, where analysis for para-cresol was by High-Performance Liquid Chromatography (HPLC) with ultra-violet detection. Levels of p-cresol were elevated in children with autism compared to controls and more specifically in younger and more severely affected children. p-cresol is an interesting compound (more details are available here) in that whilst derived from several environmental agents, it also potentially relates back to specific types of gut bacteria (as per the author report). The authors were able to exclude one environmental agent (exposure to tobacco smoke) as a significant factor relating to their findings by analysis of urinary cotinine.

There are a few comments to make about this. First such metabolites have been examined in relation to autism during previous studies. Yap and colleagues (2010) reported on levels of 4-cresol sulfate in their study of urine samples from people with autism. They found no overall difference in this related metabolite compared with controls and siblings in their samples (their methods were based on a superior analytical system, NMR). Yap and colleagues did however conclude on the basis of various other metabolites analysed during their study, some invovement for gut microbiota in some cases of autism.

Second, there is quite a body of evidence building up to suggest the involvement of gut bacteria in some cases of autism. A few choice links are here and here. It is still an area under investigation; one question that has not been answered is whether the various gastrointestinal co-morbidities reported in some cases of autism show involvement with cases where such bacterial species have been found and whether they are "causative", "resultant" or just coincidental.

Finally, assuming that there is an issue with gut bacteria and autism, what then is there to do about it and what potential effect will it have. On this issue I was reminded what I was told quite a while ago by a pretty eminent researcher on the connection between our gut bacteria, our immune system and good old homeostasis - can we actually change what we have?

There is some limited evidence that in the short-term at least eradication of certain types of gut bacteria could have knock-on effects for autism (see here). Note however the use of the words "short term". This kind of goes back to the whole issue of taking probiotics in an attempt to influence gut bacterial populations as is so evident nowadays and whether we are truly able to influence our bacterial colonies in a long-term and sustainable way to impact on our health. I don't have an answer unfortunately. Still, this study does present another potentially important marker requiring further study.

Post 001.1 v1.1 etc.

I should, I suppose, say something meaningful and thought provoking as an introduction to this blog. Truth of the matter is that I can't think of anything to start this blog in such a way, so I won't. I will reiterate that this blog is about science and research predominantly related to autism spectrum conditons but no doubt will include other things too. I will sometimes use terms interchangably; so instead of autism spectrum conditions, I might just write autism (to save my typing). Comments are welcome but please keep it civil (no swearing!). I know that many people have very different views of autism and in some cases there is genuine emotion about various issues related to the condition. I am not offering any specific viewpoint and even when presenting my own research on the topic will try and keep it as objective as possible.
God bless this blog and all that sail with it.