Recent scientific investigations have identified the small intestine as the site of disruption in IBS.
The older thinking in the healthcare community was that the site of 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 confocal1 laser endomicroscopy, staining of immune cells,2 targeted biopsies3 and genotypic/phenotypic correlations. With the use of these new tools it has been shown that gut barrier disruption and localized immune activation are associated with IBS.
The more recent scientific investigations reveal that the typical epicenter of the disturbance in IBS is the small intestine, while the visceral sensitivity involves the entire GI tract.4 In addition, it is now known that the dysmotility5 and abnormal permeability (intestinal malabsorption)6 observed in IBS is localized in the small intestine.
IBgard® utilizes breakthrough targeted delivery science via SST® (Site Specific Targeting) technology. Never before has peppermint oil been formulated into individually enteric-coated, sustained-release microspheres, delivered where they are needed most in IBS–in the small intestine.
Peppermint oil and its primary component l-Menthol have been shown in multiple studies to be effective for people with IBS.7 The l-Menthol in peppermint oil works locally on the disrupted gut mucosal barrier and associated localized and reversible low grade inflammation,8 seen with IBS, to deliver 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.
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 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.
4 Trimble, K C, R Farouk, A Pryde, S Douglas, and R C Heading. 1995. Digestive Diseases and Sciences 40 (8). Springer: 1607–13.
5 Kellow, John E, and Sidney F Phillips. 1987Gastroenterology 92 (6). Elsevier: 1885–93.
6 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.
7 Khanna R, MD, MacDonald, J.K. MA and Levesque, B.G. MD, MS. July 2014. Clin Gastroenterol, Vol 48, Num 6, pg 505.
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. 2016. Journal of Gastroenterology and Hepatology, 53–63. doi:10.1111/jgh.13417.