The IBS Within the IBD
In this article Dr. Weiner illuminates how IBS (Irritable Bowel Syndrome) is now appreciated for containing an inflammatory component and can be part of IBD (Inflammatory Bowel Disease). He explains the relationship between IBS and IBD to offer a deeper understanding of these conditions.
This original article was published on January 11, 2016 at ndnr.com. It is the third part of our new in depth series of posts exploring IBS, IBD, and SIBO, all still very relevant in 2019.
The previous posts in the series were about Treating IBD. Look forward to additional articles in this series on the differences between IBS, IBD, and SIBO, Use of Elemental Diets in IBS and IBD, and additional videos and summary articles including posts related to Chinese Medicine and Acupuncture as treatments for IBS, IBD, and SIBO.
Gary Weiner, ND, LAc
Read the full text of the original article here:
In the January 2014 issue of NDNR, I argued that naturopathic primary care for patients with inflammatory bowel disease (IBD) was where “the rubber meets the road” in our medicine.1 I made a plea for our treatment strategy to have enough “traction” to hold IBD patients securely in a healing process, lest they flee care due to IBD’s bumpy road of exacerbations and remissions. One strategy giving the treatment wheel its needed traction and to help guide decision-making is a clinical grasp of the overlapping nature of irritable bowel syndrome (IBS) and IBD. Understanding what (besides the patient) needs to be treated can help prevent the unnecessary escalations of conventional treatment that occur when clinicians so easily mistake IBS manifestations for those of IBD – or, when they fail, if you will, to get the IBS out of the IBD.
ONE, OR TWO DISEASES?
In general, we continue to see IBS and IBD represented as separate entities with no intrinsic relationship2: IBD is described as a heterogeneous group of disorders that feature various forms of mucosal and/or transmural intestinal inflammation, while IBS is characterized as a “functional,”3 if not an etiologically illusive, bowel disorder without detectable structural abnormalities or pathology. However, evidence has accumulated suggesting “shared pathophysiologic mechanisms” between IBS and IBD, including altered mucosal permeability, interaction between luminal flora and the mucosal immune system, persistent mucosal immune activation, alterations in gut motility, and the role of sustained life stressors in symptom modulation.4
Rather than being viewed as purely “functional,” or a diagnosis of “exclusion,” IBS is now appreciated for containing an inflammatory component that, like IBD, activates the immune system, albeit with a much milder intensity. The transition between mild immune activation and intense gut inflammation has been proposed to occur on a continuum, making the setting of an arbitrary threshold between IBS and IBD misleading.5 Moreover, it is no longer useful to think of IBS as a purely functional motility disorder, when it has become clear that inflammation-induced neuroplasticity contributes to disrupted motility in quiescent IBD and in functional gastrointestinal disorders.6
Supporting the continuum model is the fact that IBD patients often have a history of IBS symptoms. One study showed that the prodromal periods in Crohn’s disease (CD) and ulcerative colitis (UC) were 7.7 and 1.2 years, respectively, with IBD patients presenting with symptoms of abdominal bloating, diarrhea, excessive gas production, and stomach pain before the IBD manifested as acute symptoms.7 This would suggest that many IBD cases start out as IBS.
At the other end of the continuum, IBD cases in complete remission often present with IBS symptoms, including constipation and bloating.8 Persistent IBS-type symptoms are found in 1 in 3 patients with quiescent UC, ie, no evidence of disease activity.8 Some are now postulating that etiologies of both UC and IBS are related to enteric nervous system dysregulation, a disrupted microbiome, low-grade mucosal inflammation, and activation of the gut-brain axis that are common to both.9 CD displays similar IBS manifestations in clinical remission, estimated at 43% of those patients studied.10 These findings seem to suggest that, given genetic and environmental conditions, IBS may lead to IBD, which in turn can produce more IBS (functional bowel symptoms in the absence of a “lesion”), in a vicious cycle of coexistence.
A UNIFYING LINK – DYSBIOSIS
Not surprisingly, microbiome disturbance is one of the key links between IBS and IBD, and is the subject at the center of IBD discussions as we consider fecal transplants, helminthic therapy, colostrum, pre-, pro-, and anti-biotics as tools used to correct a microbiome gone awry. While naturopathic doctors have forever excelled in the multifactorial treatment of functional as well as lesional bowel problems, focusing on diet, stress, hormones, psycho-emotional patterns, lactose intolerance, parasitic, yeast, and bacterial dysbiosis, pancreatic insufficiency, and hypochlorhydria – or to put it succinctly, tolle totum – some clinicians and researchers have now focused us on small intestinal bowel overgrowth (SIBO), a particular variant of dysbiosis, with a focal impact on the development and treatment of IBS. Dr Mark Pimental, joined by Drs Steven Sandberg-Lewis and Allison Siebecker, are showing us that SIBO could likely be, as Pimental writes, the “primary cause of IBS.”11 Treating the SIBO in IBS patients seems consistent with the most basic principle of tolle causam when we observe these patients thrive after their microbiome gets tuned-up and toned-down with the appropriate antimicrobial strategy along with dietary and prokinetic support. It is remarkable how many IBS cases are resolved in this way, though controversy surrounds bold conclusions about its centricity to all cases of IBS.12
DOES SIBO PLAY A ROLE IN IBD?
If SIBO plays a central role in IBS, what about IBD? When I started testing for SIBO in 2013, I was startled by the impact that SIBO treatment had on my IBD patients. The improvement I observed in these IBD patients clarified just how much IBS there was in IBD. As a product of this realization, I was sensitized to the fact that even if SIBO was absent and we were looking at other causes of dysmotility in an IBD case besides the IBD itself, there might still be some IBS in those patients (ie, bowel dysfunction not caused directly by the IBD, or SIBO, that may be “within” the IBD and not of it). Notwithstanding the fact that there are other causes of IBS besides SIBO, the fact that IBD patients so often improved as a result of treating the SIBO prompted me to ask the following: If SIBO is responsible for so many cases of IBS, and IBS often precedes IBD, then could SIBO be related to the development of some of the IBD?
That may well be a grandiose notion, as it is not supported by studies. The CD research shows only that CD patients are predisposed to develop SIBO (due to the fistulae, strictures, and inherent motility disturbances in CD) and that SIBO symptoms (diarrhea, constipation, abdominal pain, bloating) may give an impression that CD symptoms are exacerbated. The conclusion in limited studies is not that SIBO causes CD, but rather that SIBO represents “a frequently ignored yet clinically relevant complication” of CD that can mimic symptoms of acute flare.”13 As a clinician, it is important to understand which symptoms are due to the CD, and which are due to other factors not directly associated with exacerbation of the disease.
With regard to UC, one study14 showed that, compared with controls, UC patients displayed elevated cytokines, lipid peroxidation, and low reduced glutathione, and that all of these findings were strongly correlated with delayed transit time and SIBO. However, the conclusion, as with the CD study, was not that SIBO causes UC, but rather that inflammatory activity – represented by increased cytokines and decreased antioxidants – resulted in oxidative stress that caused delayed motility and led to SIBO.14 Pimentel examined whether the different gas patterns on lactulose breath tests coincided with diarrhea and constipation symptoms in IBD.15 In a retroactive study, breath-tested IBS subjects were compared and contrasted to IBD patients. It was found that methane gas production was “almost non-existent” in predominantly diarrheal conditions of CD and UC, and that it was more prevalent in IBS than in either CD or UC.15
SIBO clearly exists in some IBD patients as part or all of what is causing their IBS, and treatment of the SIBO may favorably alter the expression of bowel symptoms in these cases. I have seen this enough times to conclude that selective treatment of SIBO in IBD has 1) contributed to breaking cycles of symptom expression by taking the IBS out of the IBD; and 2) at times appeared to affect the progression of the IBD itself, likely through the treatment’s alteration of the microbiome. It is not surprising to note, when reviewing research on the use of the antibiotic, rifaximin (the standard treatment for SIBO), that its use resulted in induction of remission in CD (up to 69% in open studies and significantly higher rates than placebo in double-blind trials) and UC (76% in open studies and significantly higher rates than placebo in controlled studies).16 There is even recent research showing rifaximin as “protective” in IBD via the mechanism of human pregnane X receptor activation.17
This is the first part of a multipart article by Dr. Gary Weiner. The remaining parts will be published soon. Full reference list available at the original source.
Dr. Gary Weiner, ND. L.Ac. is the medical director of Pearl Natural Health in Portland, Oregon, where he has developed an alternative and complementary care program for inflammatory bowel disease. He graduated from NCNM in 1997 and completed a 1-year residency in family medicine. He has served as adjunct faculty and clinical supervisor at NCNM, and is on the medical advisory board of the Northwest Crohn’s and Colitis Foundation of America. He is a sought after speaker and lecturer on IBD, IBS and SIBO, speaking to both naturopathic and conventional medical doctors. Dr Weiner lives with his wife and daughter.