IBD: Inflammatory Bowel Disease
Most people wake up each morning and go to the washroom without much thought about it. However, when you start getting severe pain in your stomach, and looser and looser stool, especially when there is blood in the toilet bowl, waking up and going to the washroom can be an intensely stressful experience. People who have inflammatory bowel disease (IBD), including Crohn’s Disease and Ulcerative Colitis, often go through this experience on a daily basis.
Inflammatory Bowel disease is an umbrella term referring to chronic diseases (crohn’s and ulcerative colitis) causing inflammation of the intestines. It is often confused for’ IBS’ which stands for Irritable bowel syndrome.
Crohn’s disease is characterized by inflammation and sometimes ulcers in the gut lining that can affect anywhere from the esophagus to the anus. Ulcerative colitis on the contrary affects the large intestine alone. In ulcerative colitis, there can be healthy tissue amongst the inflamed and diseased.
What causes IBD?
Although the precise cause for IBD remains elusive, our current understanding is that IBD is caused by an interaction between immune, genetic, and environmental factors.
1. Both the conditions involve activation of the immune system and production of antibodies suggesting that they have an autoimmune component. Similar to any autoimmune disease, IBD is characterized by chronic inflammation, marked TH1 dominance and inflammatory cytokines.
2. It is thought that that GI inflammation is preceded by increased intestinal permeability, disrupted intestinal flora or infections that can subsequently disrupt mucosal immunity. There is evidence that IBD have one or more genetic predispositions to mount an inappropriate inflammatory response towards commensal microflora (imbalanced flora) which can result in a disruption to the physical and chemical barriers that protect from further penetration and adherence of unwanted microbes.
3. Antibodies to the commensal sacromyces cerevsiae for eg, are strongly associated with Crohn’s disease. 6
4. A variety of patterns of dysbiosis has been observed in patients with IBD further evidence that the composition of intestinal bacteria or fungus may play an important role in the in the disease process of IBD. 3
1. Genetic mutations in The NOD2 gene (which coordinates response to bacterial pathogens) increase succeptiblity to Crohn’s disease. 8
2. Increased expression of CEACAM6 mediates adhesion of pathogenic E.coli to lesions on the surface of ileum in patients with crohn’s disease. 2
3. Polymorphisms in CARD15, a gene that activates Th17 response to fungi, predispose to both Crohn’s and ulcerative colitis. 7
Environmental factors Influence intestinal microflora and the integrity of barrier function.
1. PPI (proton pump inhibitors) are implicated in the development of microscopic colitis by altering the microbial flora by decreasing gastric acid. 5
2. NSAIDS can induce colitis by increasing intestinal permeability and promoting inflammation. 4
3. Stress modulates the protective barrier function of the Gut via activation of the HPA axis (hypothalamic- pituitary- adrenal axis). Elevated cortisol from stress change intestinal permeability and increase the reactivity of T cells in the intestinal mucosa thereby increase the inflammatory responses. 1
How is IBD managed with conventional protocols and how an integrative Functional approach differs?
The goal of any treatment for IBD is to control Gastro intestinal inflammation. Anti inflammatory medications like aminosalycylates and corticosteroids are first line drugs used which generally offer some control over mild disease. The other categories used are Immune suppressive agents (azathioprinem methotrexate etc). These stronger medications are not without consequences. They may be absolutely required in severe condition where they can provide remission but they do not cure the disease. A last resort is surgery can be a radical curative step for ulcerative colitis but not for crohns.
The goal of functional and integrative therapies is to achieve remission without dependency on stronger medications. A functional (Naturopathic approach) has the ability to manage symptoms, control disease progression and prevent long term complications of IBD. In my experience, there is a lot of hope for improvement in patients facing inflammatory bowel disease from an integrative naturopathic perspective. Considering that it’s effecting younger children these days, it is important to even prevent its development in the first place.
Related Published Research:
1. Bai A, Chen J, Liao W, Lu N, Guo Y. Catecholamine Mediates Psychological Stress-Induced Colitis Through a2-Adrenoreceptor. J Interferon Cytokine Res. 2015;35(7):580-584. [abstract]
2. Barnich N, Darfeuille-Michaud A. Abnormal CEACAM6 expression in Crohn disease patients favors gut colonization and inflammation by adherent-invasive E. coli. Virulence. 2010;1(4):281-282. [abstract]
3. Bringiotti R, Ierardi E, Lovero R, Losurdo G, Di Leo A, Principi M. Intestinal microbiota: The explosive mixture at the origin of inflammatory bowel disease. World J Gastrointest Pathophysiol. 2014;5(4):550-559. [abstract]
4. Faucheron JL, Parc R. Non-steroidal anti-inflammatory drug-induced colitis. Int J Colorectal Dis. 1996;11(2):99-101. [abstract]
5. Keszthelyi D, Jansen SV, Schouten GA, et al. Proton pump inhibitor use is associated with an increased risk for microscopic colitis: a case-control study. Aliment Pharmacol Ther. 2010;32(9):1124-1128. [abstract]
6. Giaffer M HClark A, Antibodies to Saccharomyces cerevisiae in patients with Crohn’s disease and their possible pathogenic importance. Gut BMJ 1992 Aug; 33(8): 1071–1075.
7 . Hugot JP, Ann N Y Acad Sci. 2006 Aug;1072:9-18 CARD15/NOD2 mutations in Crohn’s disease.
8. zhernakova A1, Festen EM, 2008 May;82(5):1202-10. doi: 10.1016/j.ajhg.2008.03.016. Epub 2008 Apr 2. Genetic analysis of innate immunity in Crohn’s disease and ulcerative colitis identifies two susceptibility loci harboring CARD9 and IL18RAP