Consider this something of a micro blog post as I offer up your scientific TV dinner today in the form of the paper by White and colleagues* (open-access) on the numbers game when it comes to coeliac disease (even celiac disease if you prefer) in children.
On the understanding that not everyone knows about the currently known hows and whys of coeliac disease (CD) - the premier autoimmune condition linked to the protein gluten - readers might want to check out my CD mega-post over on a sister blog (see here).
Self-promotion over and done with, the paper from White et al looking at the incidence (that's incidence not prevalence) of CD is an important one, because as the authors conclude: "The significant increase in classic cases is strongly suggestive of a true rise in CD incidence". In other words, it's not just about better case ascertainment, at least when it comes to CD in Scotland.
So to the next question: 'why the increase?' We've been given a few areas that might require some further investigation (see here and here and here) but I'm not going to make any sweeping generalisations at this time.
Thursday, 12 September 2013
Friday, 12 July 2013
Probiotic mix effective for IBS?
We are already starting to appreciate just how (a) complex and (b) important our gut microbiota are to health and wellbeing outside of the more traditional duties of food digestion and making the odd nutrient or two. Those trillions of beasties which call us home seem to be cropping up everywhere these days in research terms, based on investigations as diverse as obesity (see here) and autoimmunity (see here) even to the point of speculation about involvement in psychological development (see here) (mice, not humans, mice... so far). That and the fact that stability seems to be a good word to describe their bacterial lives* (assuming that you don't swallow a grenade).
That being said, the involvement of gut bacteria whether alone or as part of the triad of gut involvement - gut bacteria, gut permeability and mucosal / systemtic immunity** - in relation to gastrointestinal (GI) illness and/or dysfunction should not get too lost in the dialogue. Indeed, how modification of gut bacteria, whether through diet, medicine or other means (yes, yuck factor 10) remains a real point of interest when it comes to GI conditions.
With that in mind I turn today to the paper by Yoon and colleagues*** who following quite a rigourous trial (double-blind, placebo-controlled) suggested that a mix of probiotics given over 4 weeks might be able to do some positive things to the symptoms of formally diagnosed irritable bowel syndrome (IBS). The "multi-species" mix included various species and strains: Bifidobacterium longum, Bifidobacterium bifidum, Bifidobacterium lactis, Lactobacillus acidophilus, Lactobacillus rhamnosus, and Streptococcus thermophilus. The authors reported that more of those in receipt of the probiotic mix reported greater relief from their IBS symptoms over and above placebo, and when looking at fecal microflora, there were accompanying changes too as a result of the mix. Interestingly even in the placebo group there were some bacterial changes to be had (mind over matter?).
I know that the Yoon paper is not necessarily new news when it comes to probiotics and IBS (see here) but what this paper does add is its suggestion that rather than thinking too narrow about specific bacteria and species affecting specific conditions, we should perhaps be taking a more broad perspective and realising that the whole is greater than the sum of its parts when it comes to the intricate connections between our various passengers residing in the gut.
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* Faith JJ. et al. The long-term stability of the human gut microbiota. Science. 2013 Jul 5;341(6141):1237439. doi: 10.1126/science.1237439.
** Groeger D. et al. Bifidobacterium infantis 35624 modulates host inflammatory processes beyond the gut. Gut Microbes. 2013 Jun 21;4(4).
*** Yoon JS. et al. Effect of multi-species probiotics on irritable bowel syndrome: a randomized, double-blind, placebo-controlled trial. J Gastroenterol Hepatol. 2013 Jul 5. doi: 10.1111/jgh.12322.
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That being said, the involvement of gut bacteria whether alone or as part of the triad of gut involvement - gut bacteria, gut permeability and mucosal / systemtic immunity** - in relation to gastrointestinal (GI) illness and/or dysfunction should not get too lost in the dialogue. Indeed, how modification of gut bacteria, whether through diet, medicine or other means (yes, yuck factor 10) remains a real point of interest when it comes to GI conditions.
With that in mind I turn today to the paper by Yoon and colleagues*** who following quite a rigourous trial (double-blind, placebo-controlled) suggested that a mix of probiotics given over 4 weeks might be able to do some positive things to the symptoms of formally diagnosed irritable bowel syndrome (IBS). The "multi-species" mix included various species and strains: Bifidobacterium longum, Bifidobacterium bifidum, Bifidobacterium lactis, Lactobacillus acidophilus, Lactobacillus rhamnosus, and Streptococcus thermophilus. The authors reported that more of those in receipt of the probiotic mix reported greater relief from their IBS symptoms over and above placebo, and when looking at fecal microflora, there were accompanying changes too as a result of the mix. Interestingly even in the placebo group there were some bacterial changes to be had (mind over matter?).
I know that the Yoon paper is not necessarily new news when it comes to probiotics and IBS (see here) but what this paper does add is its suggestion that rather than thinking too narrow about specific bacteria and species affecting specific conditions, we should perhaps be taking a more broad perspective and realising that the whole is greater than the sum of its parts when it comes to the intricate connections between our various passengers residing in the gut.
----------
* Faith JJ. et al. The long-term stability of the human gut microbiota. Science. 2013 Jul 5;341(6141):1237439. doi: 10.1126/science.1237439.
** Groeger D. et al. Bifidobacterium infantis 35624 modulates host inflammatory processes beyond the gut. Gut Microbes. 2013 Jun 21;4(4).
*** Yoon JS. et al. Effect of multi-species probiotics on irritable bowel syndrome: a randomized, double-blind, placebo-controlled trial. J Gastroenterol Hepatol. 2013 Jul 5. doi: 10.1111/jgh.12322.
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Tuesday, 21 May 2013
Gut bacteria determines social development? Psychobacteriomics?
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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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...
----------
* Desbonnet L. et al. Microbiota is essential for social development in the mouse. Molecular Psychiatry. May 2013.
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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?
----------
* 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.
----------
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.
----------
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.
----------
Thursday, 28 March 2013
Gut bacteria - obesity and coeliac disease - stem cells
Another very quick post to bring to your attention two very interesting papers which caught my attention recently.
The first is by Ciccocioppo and colleagues* and how, quote: "allogeneic HSCT may lead to induction of gluten tolerance in patients with CD [coeliac disease]." HSCT = hematopoietic stem cell transplantation, which is indeed as controversial as it sounds. Two patients, both with CD and β-thalassemia major who at 5 year follow-up after HSCT did not appear to show a reappearance of the some of the serological and histological markers of CD following gluten consumption. I'm not making any recommendations from this (or anything else) aside from stressing the need for quite a bit more research in this area.
The second paper by Liou and colleagues** suggested that based on a mouse model, changes to the gastrointestinal (GI) bacterial population following a gastric bypass might play some role in the weight loss above and beyond the surgery itself. This paper has received gallons of media coverage from places such as the BBC (see here) to Scientific American (see here) to Nature (see here). It's an interesting idea, that our gut bacteria might actually influence our body shape and particularly pertinent to our modern day obsession with weight and its health implications. That's not to say that this is the first time such a suggestion has been made (see this and this post from a sister blog) but at least now it is in the public consciousness and potentially opens the door to lots of possibilities not least the dreaded fecal bacterial transplant...
----------
* Ciccocioppo R. et al. Allogeneic Hematopoietic Stem Cell Transplantation May Restore Gluten Tolerance in Patients With Celiac Disease. J Pediatr Gastroenterol Nutr. 2013; 56: 422-427.
** Liou AP. et al. Conserved Shifts in the Gut Microbiota Due to Gastric Bypass Reduce Host Weight and Adiposity. Sci Transl Med 2013; 5: 178ra41.
The first is by Ciccocioppo and colleagues* and how, quote: "allogeneic HSCT may lead to induction of gluten tolerance in patients with CD [coeliac disease]." HSCT = hematopoietic stem cell transplantation, which is indeed as controversial as it sounds. Two patients, both with CD and β-thalassemia major who at 5 year follow-up after HSCT did not appear to show a reappearance of the some of the serological and histological markers of CD following gluten consumption. I'm not making any recommendations from this (or anything else) aside from stressing the need for quite a bit more research in this area.
The second paper by Liou and colleagues** suggested that based on a mouse model, changes to the gastrointestinal (GI) bacterial population following a gastric bypass might play some role in the weight loss above and beyond the surgery itself. This paper has received gallons of media coverage from places such as the BBC (see here) to Scientific American (see here) to Nature (see here). It's an interesting idea, that our gut bacteria might actually influence our body shape and particularly pertinent to our modern day obsession with weight and its health implications. That's not to say that this is the first time such a suggestion has been made (see this and this post from a sister blog) but at least now it is in the public consciousness and potentially opens the door to lots of possibilities not least the dreaded fecal bacterial transplant...
----------
* Ciccocioppo R. et al. Allogeneic Hematopoietic Stem Cell Transplantation May Restore Gluten Tolerance in Patients With Celiac Disease. J Pediatr Gastroenterol Nutr. 2013; 56: 422-427.
** Liou AP. et al. Conserved Shifts in the Gut Microbiota Due to Gastric Bypass Reduce Host Weight and Adiposity. Sci Transl Med 2013; 5: 178ra41.
Tuesday, 26 February 2013
The science of microbiomics
A very short post to plug... well, to plug me really, and my very, very small contribution to an article featuring in the Pharmaceutical Journal titled: Microbiomics: its growing significance in the world of medicines testing. The article is only open-access for a short period of time, so if you happen to have stumbled across this post years and years into the future (today is Tuesday 26th February 2013 according to my flux-capacitated DeLorean) sorry.
But just so you don't feel to left out, a few article highlights: yoghurt and C.diff infection, the human microbiome project (HMP), gut bacteria and immune function, dysbiosis, the microbiota-gut-brain axis, fecal transplants (yuck factor 10) and pharmacometabonomics.
But just so you don't feel to left out, a few article highlights: yoghurt and C.diff infection, the human microbiome project (HMP), gut bacteria and immune function, dysbiosis, the microbiota-gut-brain axis, fecal transplants (yuck factor 10) and pharmacometabonomics.
Sunday, 24 February 2013
Gluten, guts and glory
Yep, I know. First post for several months - indeed first post for 2013 - and more apologies to readers about not keeping up with this blog. A short post on this occasion focused on an interesting opinion piece by Moises Velasquez-Manoff titled: Who has the guts for gluten?
I'll admit to being pretty entertained by the work of Velasquez-Manoff given his previous articles crossing over into topics like autism spectrum disorders (see here and also covered here). This latest piece is equally thought-provoking and alongside the opinions of people like Alessio Fasano, he of the [General] zonulin (see here), asks some potentially important questions about our relationship with gluten.
One quote in particular caught my attention from Dr Fasano: “Keep the lactobacilli high enough in the guts of these kids, and you prevent autoimmunity.” following some observations based on the onset of type 1 diabetes and coeliac (celiac) disease.
I'm intrigued and am waiting for that confirmatory peer-reviewed evidence.
I'll admit to being pretty entertained by the work of Velasquez-Manoff given his previous articles crossing over into topics like autism spectrum disorders (see here and also covered here). This latest piece is equally thought-provoking and alongside the opinions of people like Alessio Fasano, he of the [General] zonulin (see here), asks some potentially important questions about our relationship with gluten.
One quote in particular caught my attention from Dr Fasano: “Keep the lactobacilli high enough in the guts of these kids, and you prevent autoimmunity.” following some observations based on the onset of type 1 diabetes and coeliac (celiac) disease.
I'm intrigued and am waiting for that confirmatory peer-reviewed evidence.
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