Just this evening I happened upon a new paper published in the open-access journal BMC Gastroenterology on the potential link between autism and gastrointestinal (GI) symptoms. The paper (which is free to view - thank you!) published by Jim Adams and colleagues caught my eye for several different reasons.
The formalities first: autism group (n=58) vs. controls (n=39); age-matched (sort of); diagnosis based on 'already received' so not independently validated including a spread across the autism spectrum; gender splits were slightly unequal; control group criteria were no ADD/ADHD, no sibling with autism (I assume no autism diagnosis although this is not stated in the paper) and seemingly physically well; stool samples were the sole indicators.
I am not going to regurgitate all the paper's findings in their entirety, but several interesting points were raised including: (a) autism severity was linked to GI symptom severity, (b) a suggestion that levels of so-called 'beneficial bacteria' were different in autism vs. controls, (c) levels of so-called 'dysbiotic' bacteria showed no difference between autism and controls, (d) levels of cultured yeast were rare and not significantly different between groups, and (e) markers of inflammation were in general not significantly different between the groups aside from lower levels of lysozyme in the autism group. I have picked these particular findings out as being of interest but there were others relating to things like probiotic and fish oil use which might form later posts.
Why are these findings important? Well, first of all the authors suggest that reported gastrointestinal problems are more strongly associated with an autism diagnosis than a non-autism control. I am not going to disagree with this because other studies have showed the same thing and I have blogged about this in past posts. If I was to be a nit-picker I would perhaps argue that without any other control groups (e.g. learning disability), it is not possible to ascertain how far this finding is specific to autism (and not to learning disability) given also the lack of information on participant characteristics including the level of intellectual development.
The added value from the paper on GI disorders (bearing in mind this is functional GI disorder such as constipation, diarrhoea et al) is the connection proposed between increasing autism severity and increasing GI disorders. That is, the more severe the autism, the more severe the functional GI disorders.
I am not either going to quibble with their measure of autism severity by use of the ATEC given the recent revelations that ATEC is actually quite a good instrument, or at least as good as anything else we have. Again, the nit-picker would perhaps question the validity of the GI severity index used to probe GI symptoms (which seems to be a truncated version of the one used for this study) over other more robust measures. Additionally it is not altogether clear from the paper how the GI data was derived (interview, questionnaire, etc).
Gut bacteria is something which has been linked to autism in one form or another for many moons. It was interesting that this study seemed to suggest that whilst levels of beneficial bacteria were lower in the autism group, levels of so-called dysbiotic bacteria showed no significant difference. There is a caveat to this: the levels of dysbiotic bacteria only included 5 strains of bacteria and as mentioned in the paper discussion, they unfortunately did not look at one of the prime candidate bacteria, clostridia species which is indeed a shame.
Moving on, the lack of any significant detection of yeast in either autism or controls is slightly at odds with a lot of the discussions on autism and the gut particularly on the internet. Many times I have heard people suggest that an overgrowth of yeast such as Candida albicans is related to autism; indeed another recent study has suggested some difference in levels of this yeast in autism vs. controls. But Adams and colleagues reported no difference between their groups, and so nothing more to be said there.
Finally, markers of inflammation (GI inflammation). Interestingly there were no significant differences in white blood cells (WBC) or levels of lactoferrin. This suggests that there was no significant difference in immune activation in these particular participant groups. The lower levels of lysozyme in the autism group were the exception here and perhaps complement other older research by the late Reed Warren and colleagues looking at underlying genetic differences in the way the body handles things like bacterial infections.
So, an interesting paper, which whilst carrying some potential methodological issues provides a further insight into the complex interaction between autism and gastrointestinal symptoms. Yes, functional GI symptoms seem to be more present in cases of autism, and potentially there may be a connection with gut microflora. How this pans out in further replication studies remains to be seen.
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