I’m proposing that MAP causes IBS by attaching itself to a human host's intestinal lining and, if a colony or colonies of MAP eventually become large enough, fermenting a wide-range of sugars to produce enough organic acid(s) at low ph to burn the gut lining, leading to various levels of low-grade intestinal inflammation which alters intestinal motility and increases gut sensitivity.

I’m further proposing that abnormal intestinal motility found in IBS sufferers (constipation, alternating constipation/diarrhoea, or diarrhoea) is directly related to the level of low-grade inflammation - as the inflammation varies so may the predominant bowel symptom. Consider the graph below.

Where N is normal bowel movement, C is constipation, A is alternating between constipation and diarrhoea, and D is diarrhoea.

Also, consider the three points below:

• Two studies have noted bowel-symptom instability in IBS sufferers.
• A significant number of studies have noted worsening symptoms in IBS patients after various quantities of sugar consumption. And, equally, numerous studies have noted symptom improvement in IBS patients after following assorted sugar-restricted diets.
• Various studies have observed low-grade intestinal inflammation in IBS patients; especially in D-IBS patients. In particular, elevated intraepithelial lymphocytes (IEL), lamina propria lymphocytes, and increased numbers of enteroendocrine cells have been found.

So, in view of my hypothesis above, decreased sugar consumption should reduce the level of low-grade inflammation and therefore affect the predominant bowel symptom.

I’m proposing a study that would test whether a low-carb diet would normalize low-grade intestinal inflammation found in a group of diarrhoea-predominant IBS patients, and consequently shift the predominant bowel symptom from diarrhoea to constipation or even return to normal.

The study would analyse intestinal mucosal biopsies from a group of severe diarrhoea-predominant IBS patients for inflammatory cells and inflammatory mediators. The group would then be advised eat a low-carbohydrate diet for 6-weeks or until their predominant-bowel symptom shifted to constipation or normal. After that, intestinal mucosal biopsies would be taken again and analysed for inflammatory cells and inflammatory mediators.

A small group of controls should be used without any history of IBS or recurrent bowel problems.

If my hypothesis is correct most, if not all, D-IBS patients should observe a shift from diarrhoea as the predominant bowel symptom to constipation or normal bowel movement, and results from the analysis and comparison of mucosal biopsies for inflammatory cells and inflammatory mediators should differ from their previous results and be similar to controls.

A complementary study to verify the opposite of this would involve a group of C-IBS patients consuming a high carbohydrate diet for six-weeks or until their predominant bowel symptom shifted to diarrhoea.

At the end of the complementary study, if my hypothesis is correct, results from the analysis and comparison of their mucosal biopsies for inflammatory mediators and inflammatory cells should differ from their original results at the start of the study, and the patients’ predominant bowel symptom should have shifted from constipation to diarrhoea.