The paper by Desbonnet and colleagues* (open-access) asks some intriguing questions about how our gut bacteria - those trillions of passengers which we all carry in our deepest, darkest recesses - might have the propensity to affect the behavioural development of a mouse specifically focused on social development.
Whilst to some people this might not sound like a particularly exciting finding, to others such a suggestion might potentially signal the start of a whole new way of looking at how our (human) physiology might actually impact on our psychological development. Move over Piaget et al and make way for something rather more complex. Even possibly a new -omic..... psychobacteriomics (you heard here first folks).
OK let's not get ahead of ourselves here. This was only a small study of germ-free (GF) and conventionally colonised (with bacteria) mice measuring their mouse-like behaviours across various 'sociability tests'. Mice are mice not humans and this finding needs replication.
That being said I'm interested. I'm interested whether these findings could be crossed over to other animals and even humans. I'm interested whether different bacteria might be linked to various aspects of social development. I'm interested whether this means that taking lots of antimicrobials during early infancy could affect social development. Indeed, I'm interested if this might have implications for the arguments: breast vs. bottle, c-section vs. natural birth, even whether supplementation with probiotics during critical stages of development might show some relationship to a person social development bearing in mind I'm not making any recommendations by the way.
And then there's conditions like autism to consider...
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* Desbonnet L. et al. Microbiota is essential for social development in the mouse. Molecular Psychiatry. May 2013.
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Tuesday, 21 May 2013
Tuesday, 14 May 2013
Akkermansia muci... muciniphila and diet induced obesity
It just rolls off the tongue: Akkermansia muciniphila*.
As we speak A.muciniphila is making headlines across the world based on the study by Amandine Everard and colleagues** (open-access) on what happened to mice who had or were lacking in this stalwart of the gut microbiome.
No need for me to go into great detail about the Everard trial because (a) the paper is open-access and (b) it's already received plenty of coverage as per an entry in Nature (see here) and the National Geographic (see here).
The long-and-short of it (I should perhaps rename this blog with those words) was that A.muciniphila is, as it's name suggests, a bacteria with a connection to mucin; in particular it's love of the stuff. The finding: mice who were obese and diabetic (type 2 diabetes) seemed to have lower levels of A.muciniphila, and "that A. muciniphila treatment reversed high-fat diet-induced metabolic disorders, including fat-mass gain, metabolic endotoxemia, adipose tissue inflammation, and insulin resistance". The speculation is whether these mouse findings might, just might turn out to be something truly remarkable for humans presenting with similar symptoms.
But as with everything in life, things are rarely so simple. My first thought when I saw the name A.muciniphila were the intriguing findings reported by Lynne Wang and colleagues*** of lower numbers of A.muciniphila in fecal samples from children diagnosed with an autism spectrum disorder and their siblings. Just in case your interested, I talked about this paper on a post for a sibling blog. So unless we are talking about children with autism subsequently being a greater risk for obesity and type 2 diabetes, I would wager that there is more to A.muciniphila than just weight loss and insulin.
Leaky gut anyone?
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* Derrien M. et al. Akkermansia muciniphila gen. nov., sp. nov., a human intestinal mucin-degrading bacterium. IJSEM. 2004; 54: 1469-1476.
** Everard A. et al. Cross-talk between Akkermansia muciniphila and intestinal epithelium controls diet-induced obesity. PNAS. May 2013.
*** Wang L. et al. Low Relative Abundances of the Mucolytic Bacterium Akkermansia muciniphila and Bifidobacterium spp. in Feces of Children with Autism. Appl Environ Microbiol. 2011; 77: 6718–6721.
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As we speak A.muciniphila is making headlines across the world based on the study by Amandine Everard and colleagues** (open-access) on what happened to mice who had or were lacking in this stalwart of the gut microbiome.
No need for me to go into great detail about the Everard trial because (a) the paper is open-access and (b) it's already received plenty of coverage as per an entry in Nature (see here) and the National Geographic (see here).
The long-and-short of it (I should perhaps rename this blog with those words) was that A.muciniphila is, as it's name suggests, a bacteria with a connection to mucin; in particular it's love of the stuff. The finding: mice who were obese and diabetic (type 2 diabetes) seemed to have lower levels of A.muciniphila, and "that A. muciniphila treatment reversed high-fat diet-induced metabolic disorders, including fat-mass gain, metabolic endotoxemia, adipose tissue inflammation, and insulin resistance". The speculation is whether these mouse findings might, just might turn out to be something truly remarkable for humans presenting with similar symptoms.
But as with everything in life, things are rarely so simple. My first thought when I saw the name A.muciniphila were the intriguing findings reported by Lynne Wang and colleagues*** of lower numbers of A.muciniphila in fecal samples from children diagnosed with an autism spectrum disorder and their siblings. Just in case your interested, I talked about this paper on a post for a sibling blog. So unless we are talking about children with autism subsequently being a greater risk for obesity and type 2 diabetes, I would wager that there is more to A.muciniphila than just weight loss and insulin.
Leaky gut anyone?
----------
* Derrien M. et al. Akkermansia muciniphila gen. nov., sp. nov., a human intestinal mucin-degrading bacterium. IJSEM. 2004; 54: 1469-1476.
** Everard A. et al. Cross-talk between Akkermansia muciniphila and intestinal epithelium controls diet-induced obesity. PNAS. May 2013.
*** Wang L. et al. Low Relative Abundances of the Mucolytic Bacterium Akkermansia muciniphila and Bifidobacterium spp. in Feces of Children with Autism. Appl Environ Microbiol. 2011; 77: 6718–6721.
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Wednesday, 8 May 2013
Gluten exclusion for cases of diarrhoea predominant IBS
If I had the intellect I would try and deliver this very concise entry in the form of a witty poem or ditty just to try and make things a little more entertaining for readers rather than enduring yet another dry excuse for not making a proper "chatty" post. Unfortunately, I am to poetry what chocolate is to teapot material, so won't even try.
Instead I offer a link to a potentially very, very interesting trial by Maria Vazquez–Roque and colleagues* (open-access) reporting physiological results based on the use of a gluten-free diet for cases of irritable bowel syndrome (IBS) diarrhoea predominant type. The accompanying editorial by Lowe and Moseley** does a great job of summing up what Vazquez-Roque et al found, so leaves me very little to add.
Basically, under randomised-controlled conditions, "Patients on the gluten-containing diet exhibited greater small intestinal permeability than those on the gluten-free diet. The study was able to measure significant changes that provided physiologic support for a gluten-free diet in patients with IBS-D without celiac disease".
Whilst small intestinal permeability - also known as gut hyperpermeability or leaky gut - is already discussed in coeliac disease (CD) circles, the added-value from this recent trial is the suggestion that the effect of gluten on permeability might extend slightly outside of just diagnosed CD. I'm not getting into the nitty-gritty of the MHC and those CD-related serotypes at this point even though they were important to the findings. Also too were some interesting results based on those tight junction proteins including 'General' zonulin.
I do wonder how far outside of CD and indeed IBS-D we might venture with these findings. Y'know that very interesting paper from Laura de Magistris and colleagues*** (discussed here) with autism in mind; bearing in mind of course the experimental differences between the studies and that autism is not IBS....
Maybe also at this point I'll also introduce the latest study by Jessica Biesiekierski and colleagues**** on non-coeliac gluten sensitivity (see here) in relation to FODMAPs and gluten as further fodder for consumption.
Now, 'the boy stood on the burning deck....' (scroll down the link to see the Spike Milligan parody).
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* Vazquez–Roque MI. et al. A Controlled Trial of Gluten-Free Diet in Patients With Irritable Bowel Syndrome-Diarrhea: Effects on Bowel Frequency and Intestinal Function. Gastroenterology. 2013; 144: 903-911.
** Lowe AW. & Moseley RH. Covering the Cover. Gastroenterology. 2013; 144: 859-862.
*** de Magistris L. et al. Alterations of the intestinal barrier in patients with autism spectrum disorders and in their first-degree relatives. J Pediatr Gastroenterol Nutr. 2010; 51: 418-424.
**** Biesiekierski JR. et al. No Effects of Gluten in Patients with Self-Reported Non-Celiac Gluten Sensitivity Following Dietary Reduction of Low-Fermentable, Poorly-Absorbed, Short-Chain Carbohydrates. Gastroenterology. May 2013.
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Instead I offer a link to a potentially very, very interesting trial by Maria Vazquez–Roque and colleagues* (open-access) reporting physiological results based on the use of a gluten-free diet for cases of irritable bowel syndrome (IBS) diarrhoea predominant type. The accompanying editorial by Lowe and Moseley** does a great job of summing up what Vazquez-Roque et al found, so leaves me very little to add.
Basically, under randomised-controlled conditions, "Patients on the gluten-containing diet exhibited greater small intestinal permeability than those on the gluten-free diet. The study was able to measure significant changes that provided physiologic support for a gluten-free diet in patients with IBS-D without celiac disease".
Whilst small intestinal permeability - also known as gut hyperpermeability or leaky gut - is already discussed in coeliac disease (CD) circles, the added-value from this recent trial is the suggestion that the effect of gluten on permeability might extend slightly outside of just diagnosed CD. I'm not getting into the nitty-gritty of the MHC and those CD-related serotypes at this point even though they were important to the findings. Also too were some interesting results based on those tight junction proteins including 'General' zonulin.
I do wonder how far outside of CD and indeed IBS-D we might venture with these findings. Y'know that very interesting paper from Laura de Magistris and colleagues*** (discussed here) with autism in mind; bearing in mind of course the experimental differences between the studies and that autism is not IBS....
Maybe also at this point I'll also introduce the latest study by Jessica Biesiekierski and colleagues**** on non-coeliac gluten sensitivity (see here) in relation to FODMAPs and gluten as further fodder for consumption.
Now, 'the boy stood on the burning deck....' (scroll down the link to see the Spike Milligan parody).
---------
* Vazquez–Roque MI. et al. A Controlled Trial of Gluten-Free Diet in Patients With Irritable Bowel Syndrome-Diarrhea: Effects on Bowel Frequency and Intestinal Function. Gastroenterology. 2013; 144: 903-911.
** Lowe AW. & Moseley RH. Covering the Cover. Gastroenterology. 2013; 144: 859-862.
*** de Magistris L. et al. Alterations of the intestinal barrier in patients with autism spectrum disorders and in their first-degree relatives. J Pediatr Gastroenterol Nutr. 2010; 51: 418-424.
**** Biesiekierski JR. et al. No Effects of Gluten in Patients with Self-Reported Non-Celiac Gluten Sensitivity Following Dietary Reduction of Low-Fermentable, Poorly-Absorbed, Short-Chain Carbohydrates. Gastroenterology. May 2013.
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