Thursday, 8 December 2016

Prescription medication use and autism: good medicines management required

"Prescription drug use and polypharmacy rates among adults with ASD [autism spectrum disorder] are substantially higher than those in an age-, sex-, and race-matched cohort of adults without ASD."

That sentence taken from the paper by Rini Vohra and colleagues [1] (open-access available here) is probably not likely to win any 'novel findings of the year' awards given the already quite voluminous data published on the medication use and autism (see here for example). What gives the Vohra data a bit of an edge is that: (a) they included data for some 1700 adults with autism "matched 1:3 with adults without autism", (b) data were derived from administrative health insurance claims databases in the United States ("Medicaid programs"), and (c) they examined "the rates of prescription drug use, general polypharmacy, and psychotropic polypharmacy among adults" thus were able to detail not just psychotropic medication use but also that for other, more general conditions too.

Their findings were stark. Accompanying that opening sentence on medication use and autism, authors reported that: "Annually, almost 75% of adults with ASD had >20 prescription drug claims compared with 33% of adults without ASD." That's more than 20 prescription medication claims per year.

Further: "Other than psychotropics, many adults with ASD used medical prescription drugs such as antimicrobials (47%), dermatologic agents (48%), respiratory agents (38%), gastrointestinal agents (31%), alternative medications (25%), antiparkinsonian agents (22.6%), antihyperlipidemics/statins (7.3%), and immunologics (2.0%)." So when we start talking about the label of autism not appearing in some sort of diagnostic vacuum, and particularly that various medical comorbidity seem to be 'over-represented' when it comes to autism (see here), this is reflected in the large burden of medication being dispensed. If readers trawl through the adjusted odds ratios (AORs) generated when those with autism were compared with controls (Table 1), you'll note that many classes of medicine were more frequently prescribed to those with autism.  And where medicines were less frequently prescribed to the autism group, there were some potentially telling signs too: analgesics (used for pain relief), antidiabetics and antimicrobials. One could argue that maybe those diagnosed with autism have less need of things like pain relief or antibiotics or less likely to need antidiabetic medicines. One might however similarly argue that their medical and healthcare screening services could perhaps be 'less rigorous' than those not diagnosed with autism too, potentially as a result of various factors (see here).

Onwards: "Adults with ASD and a psychiatric comorbidity such as an adjustment disorder (26%), mood disorder (31%), or schizophrenia (32%) had significantly high rates of psychotropic polypharmacy." I probably don't need to say much more about this sentence aside from the fact that mood disorder including things like depression are not uncommon diagnoses alongside autism (see here). The links with the schizophrenia spectrum are also not to be underestimated (see here).

Finally: "Older age, female gender, White race, and presence of three or more comorbid conditions among adults with ASD is significantly associated with using six or more prescription drug classes per year." This sentence is not a roadmap to predicting who will need what medicines when it comes to autism but does provide some important information. There is for example, a woeful lack of research on autism in a longitudinal sense (see here) despite the topic of ageing and autism being debated time and time again. Inevitably as people age, their medication requirements are likely to change (increase?); this is as true for autism as it is for the not-autism population.

I included the words 'good medicines management required' in the title of this post because, as you can see, the level of prescription medicines use when it comes to autism can be high and one needs to be careful that medicines are appropriate, monitored regularly and don't interact with one and another. Given what is also known about psychotropic medicines in particular in terms of potential side-effects (see here and see here for examples), the onus is surely on prescribers to keep an even closer eye on those with autism who are being medicated under their care.

Medication is a part of life when it comes to autism. I base that last sentence on the wealth of data, peer-reviewed and otherwise, that has been published on this topic. I'm sure nobody particularly likes the idea of medication particularly when it comes to autism and certainly nobody should like the idea that some people on the autism spectrum are receiving quite a lot of prescription medicine concurrently and over quite long periods of time. But here's the thing, medication (generally) serves an important purpose. In the case of the antiepileptics/anticonvulsants it can be life-saving. Where mood disorders such as depression are being pharmacologically treated, it can be life-saving. Until, science is able to get a better idea of why some many conditions/labels seem to be over-represented when it comes to autism, medication is often all that it can offer at the moment...


[1] Vohra R. et al. Prescription Drug Use and Polypharmacy Among Medicaid-Enrolled Adults with Autism: A Retrospective Cross-Sectional Analysis. Drugs Real World Outcomes. 2016 Nov 21.

---------- Vohra R, Madhavan S, Sambamoorthi U, StPeter C, Poe S, Dwibedi N, & Ajmera M (2016). Prescription Drug Use and Polypharmacy Among Medicaid-Enrolled Adults with Autism: A Retrospective Cross-Sectional Analysis. Drugs - real world outcomes PMID: 27873285

Wednesday, 7 December 2016

Pregnancy folic acid and offspring autism systematically reviewed

"A total of 22 original papers that examined the association between folic acid supplementation in human pregnancy and neurodevelopment/autism were identified after the screening, with 15 studies showing a beneficial effect of folic acid supplementation on neurodevelopment/autism, 6 studies showed no statistically significant difference, while one study showed a harmful effect in > 5 mg folic acid supplementation/day during pregnancy."

That rather long quote taken from the paper published by Yunfei Gao and colleagues [1] (open-access) opens today's post and provides a welcome [peer-reviewed] overview of where science is up to when it comes to the effects (or not) of pregnancy folic acid supplementation on 'risk' of offspring autism. I say 'where the science is up to' but at the same time note that the various searches of databases for material relevant to this topic/review was carried out up to the end of 2014. There have been other reports since that date including other reviews [2]...

Folic acid or folate in the context of autism has been a recurrent research theme down the years. Outside of the protective effects of pregnancy folate use with regards to reducing the risk of offspring neural tube defects (NTDs), the suggestion that pregnancy folic acid may confer a protective effect against offspring autism has been highlighted in several studies (see here).

Gao et al trawled the research literature and "included randomized controlled trials (RCTs), cohort studies, and case control studies that examined the association between folic acid supplementation during pregnancy and neurodevelopment/autism in the offspring children." As per that lengthy opening sentence from their paper, the authors found data that on the whole suggested that folate supplementation was protective rather than harmful when it came to offspring developmental outcomes. Given that most/many pregnant women are already taking folic acid during pregnancy to counter the risk of NTDs, this is good news indeed.

Without giving any undue weight to those studies that have perhaps not been so enthusiastic about the link between pregnancy folate use and offspring autism risk (see here) I do think there are words of caution in this area too. We're still for example, waiting for research to be published that was raised at this years IMFAR event in relation to folic acid and autism (see here). Indeed, in my discussion of that so-far-unpublished work, I mentioned that the genetics of folic acid metabolism also needs to be further inspected when it comes to autism (see here) and that screening for particular issues linked to folate might be something to consider for people on the autism spectrum and their significant others (see here). Both these areas are potentially relevant to that recent chatter on how folinic acid might be useful for some aspects of some autism (see here).

"Large scale RCTs with validated diagnosis and high follow up rate are needed in order to produce robust evidence regarding the effects of folic acid supplementation in pregnancy on fetal neurodevelopment" conclude the authors. Yes, we need more investigation of this area - including what effect certain medicines used during pregnancy might have had on folate levels -  but for now, the data seems to side with a protective effect of folate supplementation in pregnancy when it comes to offspring risk of autism or related neurodevelopmental issues.


[1] Gao Y. et al. New Perspective on Impact of Folic Acid Supplementation during Pregnancy on Neurodevelopment/Autism in the Offspring Children – A Systematic Review. PLoS ONE. 2016; 11(11): e0165626.

[2] DeVilbiss EA. et al. Maternal folate status as a risk factor for autism spectrum disorders: a review of existing evidence. Br J Nutr. 2015 Sep 14;114(5):663-72.

---------- Gao Y, Sheng C, Xie RH, Sun W, Asztalos E, Moddemann D, Zwaigenbaum L, Walker M, & Wen SW (2016). New Perspective on Impact of Folic Acid Supplementation during Pregnancy on Neurodevelopment/Autism in the Offspring Children - A Systematic Review. PloS one, 11 (11) PMID: 27875541

Tuesday, 6 December 2016

Infections treated with anti-infective agents linked to schizophrenia?

Identify everyone born in Denmark between 1985-2002. Identify those treated "in the primary care setting" for an infection. Identify those diagnosed with schizophrenia and affective disorders. Look-see whether there is an overlap between infection or treated infection and schizophrenia / affective disorders. Report results.

That's basically the study published by Köhler and colleagues [1] (a name that has appeared on this blog before) who concluded that: "Infections treated with anti-infective agents and particularly infections requiring hospitalizations were associated with increased risks of schizophrenia and affective disorders, which may be mediated by effects of infections/inflammation on the brain, alterations of the microbiome, genetics, or other environmental factors."

Mention of Denmark as being the source material for such a discovery means, yet again, that those various Scandinavian population registries are proving their 'big data' scientific worth. Indeed, such resources really do put countries such as Blighty to shame insofar as tracking the health of the Nation and at the same, providing science with lots and lots of research nuggets.

Taking into account various "confounders", authors report that alongside a possible connection between infection or treatment for infection being 'associated' with schizophrenia / affective disorders there was "a dose-response and temporal relationship" further substantiating their findings. Indeed, those who had to be hospitalised for infection (a serious infection then) were at much greater risk of subsequently being diagnosed with schizophrenia or affective disorders. This tallies with other research on this topic (see here).

One more thing: "The excess risk was primarily driven by infections treated with antibiotics, whereas infections treated with antivirals, antimycotics, and antiparasitic agents were not significant after mutual adjustment." Interesting. This suggests that bacterial infections or their treatments, e.g. antibiotics seem to be important factors in relation to the subsequent risk of schizophrenia and/or affective disorders. Again, this is not the first time that this point has been raised (see here and see here) and provides some corroborative evidence as to why the microbiome was mentioned by authors in relation to possible mechanisms to account for their findings.

I could start talking about how this research is further evidence for a role for the immune system and/or inflammatory processes in relation to psychiatric labels (see here for example) but you've probably heard it all before I'm sure. What we are also starting to understand with some confidence, is that infection and the effects of it's treatment might go way beyond just the somatic...


[1] Köhler O. et al. Infections and exposure to anti-infective agents and the risk of severe mental disorders: a nationwide study. Acta Psychiatr Scand. 2016 Nov 21.

---------- Köhler O, Petersen L, Mors O, Mortensen PB, Yolken RH, Gasse C, & Benros ME (2016). Infections and exposure to anti-infective agents and the risk of severe mental disorders: a nationwide study. Acta psychiatrica Scandinavica PMID: 27870529

Monday, 5 December 2016

Double-blind randomised, placebo-controlled trial of vitamin D in autism

It was inevitable ("it is your destiny") that I would formulate a post about the paper published by Khaled Saad and colleagues [1] reporting results based on "a double-blinded, randomized clinical trial (RCT)" looking at the potential usefulness of a vitamin D supplement on "the core symptoms of autism in children." Inevitable because the peer-reviewed research literature looking at the sunshine vitamin/hormone in relation to autism is getting rather voluminous (see here and see here for examples) with the promise of lots more to come (see here). The fact that the name Saad in relation to this area of autism research has appeared before on this blog (see here) indicates that this researcher/research group are no strangers to this area of autism science.

First, thanks to Alex for the Saad paper. And so... utilising the premier research design, where 109 children* (aged 3-10 years old) diagnosed with an autism spectrum disorder (ASD) were randomly allocated to receive vitamin D drops - "300 IU [international units] vitamin D3/kg/day, not to exceed 5,000 IU/day" - or a placebo drops over 4 months and then tested blind "by the Childhood Autism Rating Scale (CARS), Aberrant Behavior Checklist (ABC), Social Responsiveness Scale (SRS), and the Autism Treatment Evaluation Checklist (ATEC)" before and after their vitamin D or placebo, some interesting results emerged. Their trial and protocol, by the way, was also registered. [*Actually, 120 children were initially allocated to vitamin D or placebo but 11 were lost to follow-up or discontinued participation in the study.]

Results: well first and foremost the tenet 'do no harm' seemed to be adhered to as we are told that "vitamin D was well tolerated by the ASD children" at least for the study duration. This is particularly important in light of that case report a few weeks back talking about vitamin D toxicity in the context of autism (see here). Indeed: "The serum levels of 25-hydroxycholecalciferol (25 (OH)D) were measured at the beginning and at the end of the study" kinda shows that authors were probably mindful of possible toxicity issues [2] alongside wanting to get a little more information about baseline vs. endpoint levels of the stuff. Having said all that the use of vitamin D was not completely side-effect free as 5 children taking the vitamin D drops reported symptoms such as "skin rashes, itching, and diarrhea."

Further: "The autism symptoms of the children improved significantly, following 4-month vitamin D3 supplementation, but not in the placebo group." Scores on the CARS (Total scores) showed a "significant decrease" in the vitamin D group compared with the group taking the placebo drops. This was in the direction of vitamin D supplementation positively impacting on the presentation of autistic symptoms. Scores on the ATEC also showed something akin to improvement for those taking the vitamin D drops. As one might expect, measured levels of vitamin D - "serum levels of 25 (OH)D" - rose in the vitamin D supplemented group compared to those in the placebo group.

These are interesting results providing some of the first double-blind RCT findings in relation to vitamin D supplementation and autism. I particularly like the fact that alongside well-validated instruments such as the CARS for 'measuring autism', the authors also included the ATEC, an instrument that I have growing fondness for (see here). They also measured functional vitamin D levels (albeit via an ELISA assay - I'd prefer via mass spec!) so it's not difficult to see that minus any unknown variables, the behavioural changes seem to match the biological changes to vitamin D status.

There is more to do and indeed, more research in this area is already underway. Larger groups of participants still following that gold standard research methodology will give a more accurate picture and perhaps provide some details about potential best responders to such an intervention (something already hinted at in the Saad data). And then there is the question of 'how' vitamin D might be affecting the presentation of [some] autism. Well, far be it from me to speculate too much, and also taking into account what Saad et al have to say on this matter, I suggest that we might learn a thing or two from looking at vitamin D use in other areas of medicine (see here) and taking things from there...

For now, here is what the UK Government says about vitamin D and the population at large although not everyone is convinced...

Music: Kate Bush and This Woman's Work....


[1] Saad K. et al. Randomized controlled trial of vitamin D supplementation in children with autism spectrum disorder. J Child Psychol Psychiatry. 2016 Nov 21.

[2] Vogiatzi MG. et al. Vitamin D supplementation and risk of toxicity in pediatrics: a review of current literature. J Clin Endocrinol Metab. 2014 Apr;99(4):1132-41.

---------- Saad K, Abdel-Rahman AA, Elserogy YM, Al-Atram AA, El-Houfey AA, Othman HA, Bjørklund G, Jia F, Urbina MA, Abo-Elela MG, Ahmad FA, Abd El-Baseer KA, Ahmed AE, & Abdel-Salam AM (2016). Randomized controlled trial of vitamin D supplementation in children with autism spectrum disorder. Journal of child psychology and psychiatry, and allied disciplines PMID: 27868194

Saturday, 3 December 2016

Parent-mediated interventions for young children with autism meta-analysed

Do not mess with  Lois.
Today I'm posting on the topic of the paper by Rose Nevill and colleagues [1] concluding: "that while most outcome domains of parent-delivered intervention are associated with small effects, the quality of research is improving."

Parent-mediated interventions in relation to autism have been covered on this blog quite recently (see here) accompanied by that 'super-parenting' headline fail. Such approaches work on the idea that helping parents to "develop strategies for interaction and management of behaviour" [2] might be one route of early intervention when it comes to autism. The research road has however not been smooth when it comes to this class of intervention (see here) and despite some positives (see here) has perhaps not been the overwhelming success that many had hoped for.

Nevill and colleagues reviewed 19 trials of parent-mediated interventions for autism ("randomized clinical trials") looking at various outcomes in relation to core symptoms of autism and aspects such as communication and cognitive functions. The results kinda reiterate what we already know that so far, parent-mediated interventions aren't really cutting the statistical mustard when it comes to outcomes and important statistics related to effect sizes. Indeed, the [weighted] Hedge's g statistics produced by the authors on the cumulative data in this area can, at best, be described as 'modest' (and I mean at best). As a comparison, have a look at the Hedge's g stats produced by a meta-analysis of the placebo response when it came to autism [3]: "a moderate effect size for overall placebo response (Hedges' g=0.45, 95% confidence interval (0.34-0.56), P<0.001)" (based on "25 data sets (1315 participants)"). This bearing in mind that the parent-mediated intervention trials don't usually include a placebo condition (and indeed, typically don't even blind - how could you?)

I don't want to poo-poo all of this area of autism science because it may still be pretty important. A few things do however worry me about the attention here based on the ideas that parent-child interactions are somehow the be-all-and-end-all of autism (also harking back to the bad 'ole days) and that in these times of continued cost-savings and austerity, parents are being expected to carry out the same services as other professionals. On that first point focused on parent-child interactions, I've always been a little cautious about what this means. Certainly in light of the primary focus on this blog, looking at genetics, epigenetics and biochemistry when it comes to autism, parent-mediated interventions are to be seen as a reactive strategy attempting to deal with 'symptoms' not necessarily causes. Yes, I know 'symptoms' are what parents and other family members see and deal with day in day out, but I'm wondering how successful parent-mediated intervention would be if used in the context of autism secondary to an inborn error of metabolism for example? Surely it makes more sense to spend a little more time ruling out some of the potential reasons why autism or particular autistic features might come about (i.e. screening - see here and see here for some other examples) rather than universally providing a parent-mediated intervention manual and hoping for the best? I might also add that a greater recognition that among 'the autisms' (see here) there may be some important waxing and waning of presentation(s) (see here) potentially influenced by things like the presence of comorbidity too reiterates that every person is an individual and set manuals on parent-child interactions don't necessarily cover all that heterogeneity. And there's also the suggestion that some parent-mediated intervention options are also seemingly failing when it comes to important comorbidities such as anxiety (knowing how disabling these can be) as being something else that needs to be kept in mind.

We'll have to see how this area develops further but for now, I don't think anyone can seriously say the existing research on this topic has shown anything like the successes that everyone hoped for. And whilst we should celebrate the fact that "the quality of research is improving" I'm not sure one can blame the limited success of such an approach on previous poor quality research.

To close, today is a really, really big day for some of my brood who have their 1st Dan black belt grading. After several years of training, hard work and effort pertinent to their voyages through Shotokan karate it all comes down to examination this evening. Thanks and credit need to go to their Sensei for all their efforts in getting them this far, as well as a certain practitioner who is Shotokan YouTube royalty. Whoever you are, thank you.


[1] Nevill RE. et al. Meta-analysis of parent-mediated interventions for young children with autism spectrum disorder. Autism. 2016. Nov 14.

[2] Oono IP. et al. Parent-mediated early intervention for young children with autism spectrum disorders (ASD). Cochrane Database Syst Rev. 2013 Apr 30;(4):CD009774.

[3] Masi A. et al. Predictors of placebo response in pharmacological and dietary supplement treatment trials in pediatric autism spectrum disorder: a meta-analysis. Transl Psychiatry. 2015 Sep 22;5:e640.

---------- Nevill, R., Lecavalier, L., & Stratis, E. (2016). Meta-analysis of parent-mediated interventions for young children with autism spectrum disorder Autism DOI: 10.1177/1362361316677838

Friday, 2 December 2016

The prebiotic galactooligosaccharide (B-GOS) and autism: just add to poo(p)

Yes, it is childish but...
With all the continued chatter on a possible role for the collected gut microbiota - those wee beasties that inhabit our deepest, darkest recesses - in relation to some autism (see here for example), the paper by Roberta Grimaldi and colleagues [1] (open-access available here) provides yet more potentially important information.

So, poo(p) samples were the starring material in the paper - "obtained from three non-autistic children and three autistic child donors"- and specifically what happened when something called B-GOS "a prebiotic galactooligosaccharide" was added to samples following their journey through a "Three stage continuous culture gut model system" otherwise known as an artificial gut. Said gut model based at Reading University has already been the topic of other news (see here).

As well as looking at the initial bacterial profile of those stool samples, researchers plotted the changes to the stool's inhabitants (or what was left of the stool) over the course of B-GOS addition, as well as looking at things like the "production of SCFAs [short-chain fatty acids] in the fermentations" and other metabolites via the gold-standard chemical analytical technique called 1H-NMR (see here for more details).

Results: "Consistent with previous studies, the microbiota of ASD [autism spectrum disorder] children contained a higher number of Clostridium spp. and a lower number of bifidobacteria compared to non-autistic children." With the addition of B-GOS to the 'mixture', researchers reported on a significant increase in bifidobacterial populations at the different stages of their gut model and in samples from both those with autism and those without autism. Such "bifidogenic properties of B-GOS" are not unheard of.

As to the metabolites of those bacteria present in the poo(p) samples, there were some interesting knock-on effects noted in both raw and B-GOS supplemented samples. "Our data show a lower concentration of butyrate and propionate in autistic models, compared to non-autistic models, but no
differences in acetate before adding B-GOS into the system." Propionic acid (propionate) has some research history with autism in mind (see here). Butyric acid (butyrate) is something of a rising star in quite a few domains, having also been mentioned in the context of autism too (see here). Indeed it's interesting to note that B-GOS administration "mediated significant production of... butyrate... simulating the transverse and distal colon respectively. There was no effect on propionate." The findings of lower starting levels of butyrate in samples from children with autism were also substantiated by the NMR analyses undertaken. Increases in butyrate and changes to various other metabolites ("increasing ethanol, lactate, acetate and butyrate and decreasing propionate and trimethylamine") were also noted via this analytical method for this group.

A long quote coming up: "This in vitro study showed promising and positive results in that supplementing the microbiota of ASD children with 65%B-GOS may manipulate the gut bacterial population and alter metabolic activity towards a configuration that might represent a health benefit to the host. However, further work will be required to assess such changes in an in vivo human intervention study."

Just before anyone makes a run on B-GOS or any similar product however, I do need to stress a few important points. First, this was a study of poo(p) samples from 3 autistic children compared with samples from 3 non-autistic children. Aside from the small participant numbers, we don't know anything about participants' various comorbidities (although we know they were "free of any metabolic and gastrointestinal diseases") and only limited information on their dietary habits and medication history. Second, poo(p) was the target material included for analysis and what happened when B-GOS was supplemented during the journey through the artificial gut model. This study said nothing about what happens when real people with autism take B-GOS orally for example, and how it might affect gut bacterial populations and metabolites as it progresses down a real gastrointestinal (GI) tract. This also includes a lack of information on any potential side-effects in a real-world situation. We are also assuming that any supplement survives the stomach. There is quite a bit more to do in this area.

But for now, I stick to the idea that the Grimaldi paper provides some potentially important information and certainly, some new routes/methods for further study of the link between prebiotics, probiotics and synbiotics in the context of the gut microbiota and autism...


[1] Grimaldi R. et al. In vitro fermentation of B-GOS: Impact on faecal bacterial populations and metabolic activity in autistic and non-autistic children. FEMS Microbiol Ecol. 2016 Nov 16. pii: fiw233.

---------- Grimaldi R, Cela D, Swann JR, Vulevic J, Gibson GR, Tzortzis G, & Costabile A (2016). In vitro fermentation of B-GOS: Impact on faecal bacterial populations and metabolic activity in autistic and non-autistic children. FEMS microbiology ecology PMID: 27856622

Thursday, 1 December 2016

Dietary fibre deficiency and gut barrier integrity

"Dietary fiber deprivation, together with a fiber-deprived, mucus-eroding microbiota, promotes greater epithelial access and lethal colitis by the mucosal pathogen, Citrobacter rodentium."

So said the findings reported by Mahesh Desai and colleagues [1] meriting an editorial in the publishing journal [2] as the sentiments of 'eating your greens' applies to some rather interesting [mouse] findings.

Fibre (UK spelling) comes in various different forms typically categorised as soluble and insoluble depending on their relationship with water. Using a "gnotobiotic mouse model" - where mice were "colonized with a synthetic human gut microbiota composed of fully sequenced commensal bacteria" - Desai et al reported on the effects of different diets with different fibre content. Their results make for important reading as a fibre-deprived gut was associated with the rise of some rather potent bacteria that seemed to enjoy dining out on the "colonic mucus barrier, which serves as a primary defense against enteric pathogens." Yes, mice gut barriers - or some of their components at least - were being eaten by the very bacteria they contain. Enjoy your lunch.

I'm not dwelling too much on the Desai findings, bearing in mind their focus on mice not humans, but I do want to raise a couple of potentially relevant points. First is the focus on the intestinal barrier and how that so-called 'leaky gut' seems to show a connection to dietary fibre intake. Yet more research bringing this woo-like term in from the scientific cold (see here). Next is the idea that if the Desai results are transferable from mouse to humans, they could be relevant to quite a lot of people who perhaps don't enjoy as much dietary fibre as they should. Further, there may be particular groups of people who might be particularly prone to a poor diet [3] (see here too) where the already discussed term 'leaky gut' is also relevant (see here); also bringing in the idea of a role for those trillions of wee beasties (the gut microbiota) that call us home.

I'll be watching for how this research area pans out...


[1] Desai MS. et al. A Dietary Fiber-Deprived Gut Microbiota Degrades the Colonic Mucus Barrier and Enhances Pathogen Susceptibility. Cell. 2016 Nov 17;167(5):1339-1353.e21.

[2] Gazzaniga FS. & Kasper DL. Veggies and Intact Grains a Day Keep the Pathogens Away. Cell. 2016 Nov 17;167(5):1161-1162.

[3] Bandini LG. et al. Changes in Food Selectivity in Children with Autism Spectrum Disorder. J Autism Dev Disord. 2016 Nov 19.

---------- Desai MS, Seekatz AM, Koropatkin NM, Kamada N, Hickey CA, Wolter M, Pudlo NA, Kitamoto S, Terrapon N, Muller A, Young VB, Henrissat B, Wilmes P, Stappenbeck TS, Núñez G, & Martens EC (2016). A Dietary Fiber-Deprived Gut Microbiota Degrades the Colonic Mucus Barrier and Enhances Pathogen Susceptibility. Cell, 167 (5), 1339-2147483647 PMID: 27863247