No, this is not a trick question & it’s certainly not a silly one. IBS, as many of us know, has a very loose diagnostic criteria: visceral hypersensitivity coupled with altered motility in the absence of organic disease. Hence it tends to ‘loosely’ fit a vast number of patients struggling with GIT issues. The differential diagnostic algorithm all health professionals are encouraged to use for patients presenting with GIT issues leads us to this IBS label, just as soon as we’ve excluded the red flags. But this ‘early opt out’ according to many experts, including Schiller et al in the American Journal of Gastroenterology, tends to propagate the illusion we’ve reached our diagnostic destination: practitioners stop thinking about the ‘why’ & stop looking for the real drivers & causes, which is the key to shifting the refractory patient into remission.
For those presenting with chronic diarrhoea, Bile Acid Diarrhoea (BAD) is in the diagnostic algorithm & there is strong evidence it’s at play in almost half of these patients!
It’s just that BAD, is the next station along the line after IBS-D, which means most clinicians have sadly disembarked already 🙁
Bile acids, as key biological agents, in both the behaviour & health of the gut & metabolic dx, are getting a lot of attention right now. While Bile acid malabsorption (BAM) in disorders of the small intestine such as Crohn’s & undiagnosed or refractory Coeliac dx, as well as other miscellaneous GIT disorders that clearly disrupt the bile acid balancing act of the gut-liver axis, have been known for a long time, there’s a new kid on the gut block, previously only known as the idiot, I mean, idiopathic BAD. But us idiots have finally worked it out! This is not about malabsorption but about excess production of bile acids and this pathophysiology is drastically over-represented in IBS-D patients.
And knowing if your IBS-D patient has a ‘BAD-thing’ going on, every researcher wants you to know, is game-changing. Explaining the strong heritability of this particular IBS subtype and the reason so many patients are refractory to standard IBS approaches.
We need to use distinctly different dietary strategies when IBS is BAD. Once again patients are our greatest teachers & I’ve relished the excuse one practitioner and her patient gave me to deep dive into the enormous body of BAD research, that is ‘so hot right now’! The way I look at, ask questions about and assess patients with chronic diarrhoea, especially IBS-D, is forever changed 💪🙏