Poll: Have you been tested for leaky gut?

[Thinktank]

CD14 acts as a co-receptor (along with the Toll-like receptor TLR 4 and MD-2) for the detection of bacterial lipopolysaccharide (LPS).[7][8] CD14 can bind LPS only in the presence of lipopolysaccharide-binding protein (LBP). Although LPS is considered its main ligand, CD14 also recognizes other pathogen-associated molecular patterns such as lipoteichoic acid.[9]

https://en.wikipedia.org/wiki/CD14

 

[Biarritz13]

"To further examine whether the level of sCD14 is mainly related to bacteria exposure, the concentrations of sCD14 were determined in SF from five patients with septic arthritis and compared with those found in other rheumatic diseases. No significant difference was found between the SF concentrations of sCD14 in patients with septic arthritis (median, 3.0 g/ml; IQR, 2.7–3.3), and in those with RA."

http://www.jimmunol.org/content/172/7/4470.full.pdf

 

[Hip]

To quote your post though it seems pointless to talk about 'leaky gut' then as all anyone is interested in is if it causes symptoms or plays a role in triggering disease, at which point it would be leaky gut syndrome, if it exists but does not cause symptoms then what interest is it to anyone ?

Good point (and a nice bit sharp logic!).

I think in summary we can conclude that leaky gut (intestinal hyperpermeability) certainly exists, and is associated with a number of diseases, but whether leaky gut actually plays a causal role in those diseases is in unknown and unproven, but it is a possibility.

Since it is a possibility, ME/CFS patients looking to explore possibly useful treatments might consider trying some supplements and diets that have been shown to reduce intestinal hyperpermeability.

Dr Michael Maes found that a leaky gut diet and leaky gut supplements does bring clinical improvements in ME/CFS after around 1 year (and in one instance, he found treating leaky gut brought full remission from ME/CFS, but this was just in one patient).

So a leaky gut diet and leaky gut supplements may be useful for ME/CFS, but judging by Dr Michael Maes's studies, you'd need to commit to this for around a year in order to get results. It's unlikely to cure you, but it might possibly bring some improvements in symptoms.

More info on Maes's studies: Fixing Leaky Gut Helps ME/CFS, and Sometimes Achieves Full Remission

 

[Hip]

The lactulose/mannitol test only measures the permeability of the small intestine so cannot rule out increased permeability of the colon.

Although the colon (large intestine) can also be leaky, I think leaky gut studies and research generally examine leakiness in the small intestine.

I have been PubMed searching for studies that specifically looked at leakiness in the colon, and there are relatively very few studies that focus on the colon. Here are some:

This study found in a murine model of Parkison's, there is increased colonic permeability.
This study found that chronic psychological stress in rats is associated with increased colonic permeability.

Searching Google I could not find any information about the specific issues, specific clinical symptoms or clinical consequences that the colonic form of intestinal hyperpermeability produces. Perhaps there should be more research on this. Sucralose is used to measure colonic permeability, by the way.

The small intestine is found to be sterile in around one half of North American subjects, and in the other half contains bacteria. Ref: 1 The colon of course always contains large populations of bacteria.

So when you are talking about the inflammatory issues connected to the translocation of bacterial LPS across the intestinal lining, I guess this can happen in the small intestine (in the cases where the small intestine is not sterile) as well as the colon.



The distinction you are making between small intestine hyperpermeability and colonic hyperpermeability is interesting, but I think most of the time when researchers refer to leaky gut or intestinal permeability, the implication is small intestine permeability.

 

[Cheesus]

The distinction you are making between small intestine hyperpermeability and colonic hyperpermeability is interesting, but I think most of the time when researchers refer to leaky gut or intestinal permeability, the implication is small intestine permeability.

I always assumed that many (but not all) were talking about colonic permeability, simply because that is where, as you rightly say, you find the microbiome. There is quite a lot of research of the impact of the gut microbiome on epithelial permeability, and I assumed those studies could only be referring to the colon specifically as I do not know how the microbiome could influence the permeability of the small intestine unless you had SIBO. I imagined the colon was the target of existing hypotheses in ME for this same reason - how could bacterial translocation seen in the study investigating the impact of exercise on leaky gut and PEM arise otherwise?

I am going to have to have to look at this all again to recalibrate my understanding.

This review article seems to talk at length about factors that influence both colonic and small intestine permeability. It does not seem to favour one or the other.

 

[Cheesus]

This study found in a murine model of Parkison's, there is increased colonic permeability.
This study found that chronic psychological stress in rats is associated with increased colonic permeability.

Those studies are very interesting and both could have pertinence to ME.

 

[Hip]

I am going to have to have to look at this all again to recalibrate my understanding.

Please post any interesting findings you come across, because I would also like to understand this more.

I am guessing that in terms of undigested food proteins leaking across the intestinal lining and provoking an inflammatory immune response, that is going to be more of an issue in the small intestine, since food protein is broken down and digested in the small intestine, and so this protein will probably not be found once you reach the colon.

 

[Cheesus]

I am guessing that in terms of undigested food proteins leaking across the intestinal lining and provoking an inflammatory immune response, that is going to be more of an issue in the small intestine, since food protein is broken down and digested in the small intestine, and so this protein will probably not be found once you reach the colon.

Yes that certainly makes sense.

 

[Richard7]

a) done (I have responded no to the poll)

b) I have also been looking into this and found this article
https://www.researchgate.net/public...NDc3MTAwMDcyOTZAMTQ2NjU3MjgwMTA1NQ==&el=1_x_2
and this video

useful

 

[Cheesus]

You will be interested in this, @Hip

As I mentioned previously, I answered inconclusive on the above poll because the lactulose/mannitol I did was negative but only tests for the small intestine. I have just received the results of a PEG test - which looks at the entire gut - and my results seem to be outside of the normal range. The abnormality isn't dramatic, but it is sufficiently high that I will make an effort to treat it.

The two tests were done so far apart (around a year) that it is not possible to say whether or not this represents purely colonic permeability, as it is possible that my small intestine has since become more permeable. However it is fairly interesting nevertheless. If money was no object I would run both tests again in quick succession.

 

[ChrisD]

I would love to see this data on a much wider scale as it seems fairly conclusive that all CFS patients have some level of Leaky Gut syndrome. But I know that in this country (UK), the NHS doesn't acknowledge Leaky Gut