Recent scientific investigations have identified the small intestine as the site of disruption in IBS.
The older thinking in the healthcare community was that IBS was primarily a psychosomatic condition. Later, this thinking evolved to the belief that the site of the disturbance in IBS was primarily in the colon. This understanding was based on the colon’s association with disrupted bowel movements and visceral sensitivity.
Recent thinking in IBS has been enabled by new tools such as confocal laser endomicroscopy1,2 staining of immune cells3, targeted biopsies4 and genotypic/phenotypic correlations. With the use of these new tools, it has been shown that, in addition to complex psychological and pain perception cascades in IBS, gut barrier disruption and reversible, localized, often temporary, low-grade immune activation and gut microbiota dysbiosis – all occurring in the small intestine - are now also clearly associated with IBS.
The typical epicenter of the disturbance in IBS is now seen to be the small intestine, while the visceral sensitivity involves the entire GI tract.5 In addition, it is now known that the dysmotility6 and abnormal permeability (intestinal malabsorption)7 observed in IBS is localized in the small intestine. This also involves irritated nerve endings (abdominal pain, discomfort, and cramping), and motility dysfunction (diarrhea, constipation, or both).8
IBgard® utilizes breakthrough targeted-delivery science via SST® (Site-Specific Targeting) technology to enable more distal delivery. Never before has peppermint oil been formulated into individually enteric-coated, sustained-release microspheres. These are first delivered where they are needed most in IBS –in the small intestine- and then later spread out in a broad brush manner to complete more distal delivery in the entire small intestine, over 3 to 4 hours. The American College of Gastroenterology IBS 2018 Monograph mentions more distal delivery as being preferred for peppermint oil since it reduces chances of heartburn.
Peppermint oil and its primary component, l-Menthol, have been shown in multiple studies to be effective for people with IBS.9 The l-Menthol in peppermint oil works locally on the disrupted gut mucosal barrier and the associated reversible, localized, often temporary, low-grade inflammation8 seen with IBS. It delivers its calming properties to the site where the digestion and absorption of food nutrients is disturbed and where visceral sensitivity, (especially abdominal pain and cramping), originates. Also, peppermint oil, via its antibacterial property, provides support in those cases where IBS is worsened by small intestinal bacterial overgrowth (SIBO).
New science is leading to new thinking in IBS.
The following three megatrends are characterizing the new thinking in IBS science:
- The growing appreciation of the complex, variable and multifactorial nature of IBS, and the clear centrality of abdominal pain as the signature symptom, along with varying bowel-related clinical subtypes i.e. IBS-D, IBS-M, IBS-C, and IBS-Ua.
- The growing importance of good gut health in IBS as a way to gain homeostasis in both the dietary intake and the dietary uptake via digestion and absorption of nutrients.
- The rapid acceptance of daily and proactive biopsychosocial practices, including nutritional support, to help facilitate management of acute symptoms, and to then fortify gut health to attenuate the frequency or magnitude of future IBS flares.
Around the world, regulatory science is striving to catch up with fast-advancing IBS science. The different stages of the journey of food through the GI tract are now better understood and is now leading to research on precision targeting at intervention points in this tract. The science of GI cascades, the science of targeted molecule delivery, and the science around more specific and potent molecules all are now becoming better understood in helping drive IBS innovation.
New Science, New Thinking on IBS
1 Fritscher-Ravens, A. et al. Conofocal Endomicroscopy Shows Food-Associates Changes in the Intestinal Mucosa of Patients with Irritable Bowel Syndrome. Gastroenterology. 2014;147:1012-1020.
2 Holtmann, Gerald J et al. Pathophysiology of irritable bowel syndrome. The Lancet Gastroenterology & Hepatology, Volume 1 , Issue 2 , 133 – 146.
3 Vanheel, Hanne, Maria Vicario, Tim Vanuytsel, Lukas Van Oudenhove, Cristina Martinez, Åsa V Keita, Nicolas Pardon, et al. 2014. “Impaired Duodenal Mucosal Integrity and Low-Grade Inflammation in Functional Dyspepsia.” Gut 63 (2): 262–71. doi:10.1136/gutjnl-2012-303857.
4 Yantiss, Rhonda K. et al. Optimal approach to obtaining mucosal biopsies for assessment of inflammatory disorders of the gastrointestinal tract. The American Journal of Gastroenterology. 2009;104:774-783.
5 Trimble, K C, R Farouk, A Pryde, S Douglas, and R C Heading. 1995. Digestive Diseases and Sciences 40 (8). Springer: 1607–13.
6 Kellow, John E, and Sidney F Phillips. 1987Gastroenterology 92 (6). Elsevier: 1885–93.
7 Dunlop, Simon P., John Hebden, Eugene Campbell, Jorgen Naesdal, Lars Olbe, Alan C. Perkins, and Robin C. Spiller. 2006. American Journal of Gastroenterology 101 (6): 1288–94. doi:10.1111/j.1572-0241.2006.00672.x.
8 González-Castro, Ana M, Cristina Martínez, Eloísa Salvo-Romero, Marina Fortea, Cristina Pardo-Camacho, Teresa Pérez-Berezo, Carmen Alonso-Cotoner, Javier Santos, and María Vicario. 2017. “Mucosal Pathobiology and Molecular Signature of Epithelial Barrier Dysfunction in the Small Intestine in Irritable Bowel Syndrome.” Journal of Gastroenterology and Hepatology 32: 53–63. doi:10.1111/jgh.13417.
9 Khanna R, MD, MacDonald, J.K. MA and Levesque, B.G. MD, MS. July 2014. Clin Gastroenterol, Vol 48, Num 6, pg 505.