Irritable Bowel Syndrome (IBS) / Colitis and Crohn's Disease (IBD)

Paul L. Reller L.Ac. / Last Updated: August 03, 2017

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Ulcerative Colitis and Crohn's Disease

The subject of chronic inflammatory disease of the gastrointestinal tract is complex. The wide spectrum of contributing disorders that may lead to these chronic inflammatory states, and the large variance in patient presentations, as well as the often inexplicable episodic nature, has led to a confusion in allopathic medicine. Our standard allopathic approach has been to monitor the disease and try to control symptoms until a more drastic allopathic treatment is necessary, such as colon resection, or harsh medications. Patients, as well as medical doctors open to Complementary Medicine, have been increasingly utilizing a more conservative and holistic approach, which is proving successful for a large number of patients. Ulcerative colitis affects nearly 2 million patients in the U.S. and the exact cause remains undetermined. Medical experts agree that the condition appears to be related to a combination of genetic propensity and environmental factors, which is standard medical jargon for "we don't know." Recent studies have determined that NSAIDS (non-steroidal anti-inflammatory drugs) may be a causative factor in a significant percentage of cases. Studies on animals found that ibuprofen selectively inhibited oxidation of butyrate, leading to increased permeability of the colon membrane, and various studies have linked a number of NSAIDS to acute episodes of colitis.

If you routinely take NSAIDS or prescription medications that may contribute to inflammatory dysfunction you might want to discuss possible gastrointestinal side effects with the prescribing medical doctor, and reduce use when possible to avoid aggravation of inflammatory bowel disease. Onset of IBD occurs in childhood in greater than 20 percent of cases, and incidence is greater in industrialized countries such as the United States and the United Kingdom, implying that typical diets and environmental factors play a large role in the disease. What distinguishes Ulcerative Colitis from Crohn's Disease is the affected mucosal tissues. In Ulcerative Colitis, the rectum is the primary location of the disease, with variable degrees of inflammation up the large intestine. In Crohn's Disease, the entire gastrointestinal tract is affected, or any part of the GI tract from the oropharynx to the perianal area, with highly affected areas of the GI tract separated by areas of normal tissue. The affected areas may extend into the submucosa as well, while only the mucosa is affected in Ulcerative Colitis. The most affected areas with Crohn's Disease are the ileocecal region (connection between the small intestine and large intestine), a common site of diverticulae, the terminal ileum (the end of the small intestine), or diffuse areas of the small intestine. Fistulas, or abnormal connections between 2 parts of the bowel, occur in about 20 percent of cases with Crohn's Disease.

Diagnosis of inflammatory bowel disease primarily involves analysis of symptom history (frequent or episodic diarrhea, abdominal cramping or tenderness often relieved by the bowel movement, blood in the stool, weight loss or loss of appetite, recurrent low-grade fever, fatique or malaise), as well as stool cultures, fecal blood tests, complete blood labs, sigmoidoscopy or colonoscopy. Since hormonal imbalances have been linked to the pathological mechanisms, an active hormone metabolite panel may also be helpful in a full analysis to guide treatment. Allergy testing has become popular, but often the lab results are somewhat misleading. We all have antibodies to all foods, and so various problems could trigger the higher than normal antibody responses to common foods seen in allergy tests. A practical way to determine if food allergies are effecting your condition is to keep a food journal and systematically analyze worsening symptom episodes in relation to food intake, then eliminate these foods from the diet and see if improvement occurs. Often, the patient develops an intolerance and malabsorption of lactose and glutens. The symptoms are more dramatic in Ulcerative Colitis early in the disease, and often are mild enough in the progression of Crohn's Disease that the diagnosis is made late in the progression of the disease, and colonic resection is required. Early signs of these inflammatory bowel diseases are muscle pain and joint inflammation, apthous mouth ulcers, and recurrent low-grade fevers. In Ulcerative Colitis, inflammation of the bile ducts and sclerosing is often seen, but usually ignored, despite the difficulty in digesting fats in the diet. Often, a lab test revealing elevated alkaline phosphatase, and perhaps elevated GGT (gamma-glutamyltransferase), one of the common liver enzymes measured as a disease sign, lead to the diagnosis of bile duct inflammation and sclerosis, or cholangitis, and reveal the progression of Crohn's Disease. Serum antibody tests are often conducted, but have a relatively low sensitivity, with DNase-sensitive pANCA (antineutrophil cytoplasmic antibody), IgA and IgG antibodies ASCA (antibodies to Saccharomyces cervisiae), and antibodies to specific E. coli bacterial membrane porins tested. This antibody panel can be useful to contribute to diagnosis, and to distinguish between Ulcerative Colitis and Crohn's Disease early in the course of the disease, but may not be useful to fully confirm or rule out the disease.

Despite a century of scientific study we are still unclear as to the exact pathogenesis, or physiological cause, of inflammatory bowel disease. Standard medicine has long focused on finding a genetic cause to counter, but with the mapping of the human genome we have found that this genetic link is much more complex that we had imagined, and involves interaction of the epigenetic code that is closely tied to environmental stress with the full genetic code, not just 23 chromosomes, which compose basic inheritable traits. So far, more than 71 genes have been found that relate to symptoms in inflammatory bowel disease, and many epigenetic abnormalities, and such research is now being used to try to guide drug therapy and provide more accurate predictive markers of disease, not a cure. There is hope that such genetic and epigenetic markers may provide early identification of individuals with future inflammatory bowel disease, allowing them to utilized preventive medicine, and especially Complementary Medicine, to prevent or slow the onset of serious inflammatory bowel disease.

Research in the last decade has discovered a complex weave of interacting causes of IBD, including an unhealthy Biota in the intestine (symbiotic bacteria and other microbial life), unhealthy intestinal mucosa and mucosal immune function, and non-immune components involving dysfunction in the membrane epithelia, the mesenchymal tissues, and the endothelial cells of the intestinal lining. Reestablishing a healthy Biota, intestinal membrane health, immune balance, and support for cell adhesion molecule (CAM) blockade have been the foci of therapeutic protocols. In fact, there is much promise that a biotic fecal transplant therapy, with matched Biomes, may someday provide very effect therapy in IBD, at a very low cost. Integration of Complementary Medicine and a holistic approach is obviously important in this refining of a workable treatment protocol, and must involve a strong proactive role on the part of each patient. Presently, research has identified species of bacteria that when overgrown appear to contribute to these dysfunctions, and sulfa antibiotics are given to counter them, but since the overgrowth of pathogenic bacteria involves poor homeostatic control of a complex microbial balance, use of antibiotics will surely make this imbalance worse, even if temporary symptom relief is obtained. Since evidence points to a broad immune dysfunction, use of synthetic corticosteroids will surely worsen this imbalance as well. Nevertheless, this is the only current pharmaceutical approach in standard medicine. As patients with inflammatory bowel disease become more educated to their problem, a realization is occurring that the standard treatment protocol is problematic, and more and more patients are turning to integration of restorative protocols in Complementary Medicine.

To understand how the gastrointestinal mucosa could acquire an inflammatory problem that the body is not able to control, we need to take a look at the pathophysiology of inflammatory ulcers and the various known causes. The stomach lining, or mucosa, is a very protected type of tissue, since it is subjected to hydrochloric acid and other digestive chemicals that are able to break down and dissolve almost anything that we ingest. Gastritis, or inflammation of the stomach lining, can be caused by any of, or combination of, factors, including flora and fauna imbalance (primarily bacterial), medication (anti-inflammatory medication causes the most cases, but a wide variety of medications may lead to uncontrolled mucosal inflammation), excessive alcohol intake, autoimmune reactions, food allergies, and functional disorders of the GI tract. The bottom line, in pathophysiological terms, is a problem of excess gastric acids not countered by appropriate alkiline secretions, and insufficient or excess immune responses. The causes of these physiological dysfunctions is the chief concern in the holistic treatment, and these gastric dysfunctions and problems could elucidate the pathology of the inflammatory bowel disease.

In the small intestine, the mucosa is also protected by the alkilinity of pancreatic secretion, the bile, and the secretions of the Brunner's glands, all of which normally contain large quantities of sodium bicarbonate that neutralizes the gastric acids that enter the intestine. The small intestine also has feedback mechanisms that are meant to inhibit excess gastric acid from both being secreted inappropriately, and emptied into the intestine in excess. The hormone secretin is normally secreted to regulate these protective reflexes. When any of these mechanisms are dysfunctional, or inhibited by improper diet, hormonal imbalance, or medications, there is increased risk of stimulating the intestinal inflammatory disease. Malabsorption syndromes, such as celiac sprue, or malabsorption of glutens and gliadins, may also stimulate an allergic or autoimmune response. These inflammatory problems may be well controlled during periods of less stress on the body's immune system, but when a number of physiological stressors occur or increase, the immune capability is not up to the task of controlling the inflammatory disease, and episodes of intestinal inflammation will occur. Medical experts associate oxidative stress, imbalance of normal flora and fauna, abnormal glycosaminoglycen content of the mucosa, increased intestinal permeability, increased sulfide production, decreased oxidation of short chain fatty acids, and decreased methylation as common pathological finding with ulcerative colitis. While these appear highly technical to the patient, they do point Complementary Medicine in the right direction to discover effective treatment protocols.

Large studies have shown that there is a high incidence of inflammatory diseases outside of the intestines, as well as malabsorption syndromes, autoimmune disorders, gallstones and kidney stones, associated with ulcerative colitis and Crohn's disease. In 1976, a review of the records of 700 such patients in Baltimore hospitals found that 42 percent of patients with colon disease also has extra-intestinal inflammatory complications with their health, and the 23 percent of patients with upper intestinal disease had such complications. Some more recent studies reveal that even larger percentage of patients have these more systemic inflammatory, functional disorders, or immune health problems. Certain hormonal disorders, such as Vitamin D hormone deficiency, have been strongly linked, as well as specific nutritional deficiencies and problems with protein metabolism. All of this information points to the need for a holistic approach to care. As with all difficult diseases, the complexity of the pathological process is frustrating, but persistence and knowledge are the key to eventual success with treatment.

Both Crohn's disease and ulcerative colitis have been linked to immune dysfunction. Crohn's disease appears to be a T-cell autoimmune disease associated with T-helper 1 (Th1), while ulcerative colitis appears to be associated with Th2 dominance. These findings reflect evidence of high levels of IgG antibodies and autoantibodies. Crohn's disease usually shows high levels of inflammatory mediators associated with autoimmune reaction in the blood as well as in the intestinal mucosa, whereas ulcerative colitis usually shows these inflammatory mediators are high in the mucosa only. For this reason, Crohn's disease was called an autoimmune disease in the past while ulcerative colitis was not. The inflammatory mediators that are involved in both types of inflammatory bowel disease are the interleukins 1,2 6, 8, and TNFalpha (tumor necrosis factor). Interferon gamma is also usually high in the mucosa of Crohn's disease patients.

The lower intestine, or colon, may be reactive to these common problems of the upper GI, or may have problems of chronic inflammation that are unique to the colon itself. Research has found that the colon mucosa resected from patients had altered glycosaminoglycans (GAGs), which is related to inflammatory conditions, and these GAGs had a high amount of hyaluronic acid content. This could signify that the body is producing more of this protective acid in response to bowel inflammation, or it could signify an excess that could come from an overgrowth of certain bacteria that have capsules made of hyaluronic acid, such as streptococcus A. Since hyaluronic acid can inhibit our immune responses to inflammatory mediators, or cytokines, and stimulate excess of the various interleukins and lymphocytes involved in the autoimmune responses, this could be a key part of the disease process. An herbal course of treatment that utilizes formulas to counter excess bacterial growth, then restores normal flora and fauna could be a key strategy in treatment.

Studies of the fecal microflora in inflammatory bowel disease have produced no consistent culprit, with the execption of Clostridium difficile, which was specific to patients that had colitis induced by antibiotic use. Overuse of antibiotics leads to imbalances of normal flora and fauna, and some of these drugs have high rates of side effects and allergic reactions. Antibiotic resistant strains of Clostridium difficile and Streptococcus are becoming epidemic in recent years in the United States, and an herbal course may be a smart part of the overall therapy. In addition, the U.S. CDC states that pathogenic strains of Clostridium difficile now account for 15-25 percent of cases of antibiotic-associated diarrhea, with pseudomembranous colitis and toxic megacolon, perhaps a conservative estimate, and that testing for pathogenic Clostridium difficile infection is problematic and not routinely included in standard stool testing for patients. Since Clostridium difficile is a nonaerobic spore-forming bacteria, even eradication with a course of antibiotics does not stop the next growth cycle. Clearly, Complementary and Integrative Medicine is needed to enhance the thorough treatment of this problem, but is still discouraged in standard medicine. Quality probiotics have also been proven effective to counter the various overgrowths associated with ulcerative colitis, such as Clostridium difficile. While no specific culprits have been implicated, a number of pathogens with potential association have been found in the mucosal microflora of these patients. These include E. coli, diplostreptococcus, Clostridium difficile, Fusobacterium necrophorum, Shigella, Heliobacter hepaticus, Blastocystis hominus, RNA virus, Bacteroides vulgatus and Yersinia, and various strains of mycobacterium. Unlike antibiotics, herbal antibacterial and antiviral agents have a broad spectrum of application, since they protect the plant from a wide variety of these pathogens, and do not come with the alarming side effects and long-term adverse effects of antibiotics, or the problem with creation of antibiotic resistance. Integration of short course of clearing herbal formulas interspersed in a professional probiotic, prebiotic routine is both sensible and safe.

High sulfate levels in the diet and produced by the metabolism also play a potential role in unhealthy colon mucosal cells. High sulfates result in high amounts of sulfate-reducing bacteria, which produces hydrogen sulfides, which inhibit the metabolism of butyric acid and other metabolites, which starves cells in the colonic mucosa. High sulfate results from excessive meat eating, eating of preservative chemicals, eating of aged cheeses and meats, as well as wines, and possibly even use of shampoos that contain sodium laurel sulphate. Sulphites are highly related to allergic diseases, and many people suffer from intolerances. Migraines, hives, gastritis, water retention, lethargy, depression and rapid heart beat episodes have all been linked to sulfites. These should be avoided.

Increased cancer risk is associated with Ulcerative Colitis and Crohn's disease

Persons with ulcerative colitis (UC) have an increased risk for colon cancer. Standard therapy with resection and harsh medications, may not decrease this risk, and this is another important reason why the patient should engage in a more thorough, but complicated, holistic treatment regimen. Studies have shown that common medications used to treat inflammatory bowel disease actually increase the cancer risk, such as mitronidazole, sulfasalazine and low dose aspirin. Sulfasalazine also results in inhibition of folic acid absorption, a key aspect of inflammatory dysfunction explained below. A 2001 population-based study at the University of Manitoba, Winnipeg, Canada found that there was an increased incidence of colon cancer for both Crohn's disease and UC patients compared to a randomly selected portion of the general population without inflammatory bowel disease. UC patients had an increased risk of rectal carcinoma, and Crohn's disease patients had an increased risk of small intestinal cancer and lymphoma. Both Crohn's and UC patients had an increased risk of liver cancer. This is despite the therapy with steroidal anti-inflammatory and immunomodulating drugs. The study authors stated that these findings corroborated previous findings regarding increased cancer risk in the broad North American population.

Numerous studies have linked oxidant free radical stress in inflammatory bowel disease to the mechanisms of these cancers. Many experts now believe that decreasing oxidant stress will both aid in the treatment of inflammatory bowel disease and reduce cancer risks. A variety of oxidant free radicals and oxidant dysfunctions have been identified that contribute to both cancers and inflammatory bowel disease, and for this reason a number of key antioxidants are being heavily researched. In animal studies, treatment with N-acetyl cysteine reduced both the intestinal inflammation and tumor incidence (see study link below). The glutathione antioxidant and detoxification mechanism is perhaps the most important inherent intercellular defense. Studies with animals have shown that when this system is disrupted, incidence of inflammatory bowel disease and colon cancer increase dramatically. You may read my article on the glutathione mechanism on this website to gain a better understanding of maintenance of this system with herbal and nutrient medicine. Melatonin, resveratrol, methylselenocysteine, zinc monomethionine, B12, 5MTHF (active folate), and various Chinese herbs high in flavonoids, as well as electroacupuncture stimulation at key points, have all been proven to boost the function of the glutathione metabolism. Incorporating these therapeutic regimens into an individualized holistic protocol will not only help to treat inflammatory bowel disease, but will help prevent cancers, and unlike harsh pharmaceutical steroid and immunomodulating drugs, will actually benefit the overall health and will have no side effects.

Inflammatory intestinal disease may also be linked to esophageal cancer. Barrett's Esophagus is a poorly understood syndrome that occurs when inflammation of the esophagus near the gastric entry resolves and the normal squamous cells of the esophageal lining turn into columnar cells similar to those seen in the intestinal lining. It has been assumed that this is purely due to gastric reflux and irritation by stomach acids, but landmark studies by the Veterans Administration, the Mayo Clinic, and Stanford University School of Medicine have shown that the incidence of Barrett's Esophagus is about the same in a patient population with GERD and heartburn symptoms, and those without these gastric reflux problems, and autopsy studies have shown up to a 1 percent incidence in the aging population of Barrett's Esophagus, with about 70 percent undiagnosed and without a history of GERD or heartburn. Obviously, a tissue mechanism exists that would explain this dramatic tissue change in the throat, and it is not just a consequence of GERD, yet standard medicine is slow to change its assumptions. There is also a low incidence for advancement of Barrett's Esophagus to esophageal adenocarcinoma, contrary to standard advice in the past, which greatly alarmed patients with the diagnosis, as the survival rate is very poor, even when detected and treated. Some of the same adjunct protocols to treat intestinal inflammation and prevent cancer could be applied easily to prevention and treatment of Barrett's Esophagus and esophageal adenocarcinoma, and restoration of GI homeostasis may be important in overall prevention. The standard treatment consists of chronic use of acid inhibiting medications, which are now shown to be ineffective in treatment of Barrett's Esophagus, and in one study was shown to be associated with progression from Barrett's Esophagitis to Barrett's Esophagus Syndrome.

Currently, there is no effective treatment for Inflammatory Bowel Disease (IBD), and the expanding protocols in standard medicine are intended for managing symptoms only. For ulcerative colitis, standard medication still relies on a sulfa drug called Sulfasalazine, although for a large subset of patients, the chronic adverse effects of a metabolite of this drug have reduced its use, and another metabolite of the sulfa drug that is less problematic has been introduced into standard treatment called 5-ASA (5-aminosalicylic acid), as <em>mesalazine</em>. Since sulfa drugs are antibiotics, there may be a problem with sustaining a healthy balanced Biome with these drugs, which is very important in IBD. In recent years, corticosteroid injections were found to reduce the flare-ups of more severe bowel inflammation that eventually resulted in death for a high percentage of patients in the past, but this therapy comes with many adverse side effects, and the goal of reducing the corticosteroid use is now an important issue. Studies have shown that effective anti-inflammatory therapy allows a significant reduction in the periodic need for corticosteroid therapy. To reduce corticosteroid use and to finally find an effective and comprehensive therapeutic protocol, Complementary Medicine should be integrated into standard treatment protocol, providing an array of benefits in addition to effective and safe anti-inflammatory effects, such as immune modulation, repair of intestinal membrane tissues, and restoration of gastrointestinal function. Increasingly, an array of immune inhibiting and suppressing drugs are being prescribed for both Crohn&rsquo;s Disease and Ulcerative Colitis, which often overlap in comorbidity for a percentage of patients, including biologic tumor necrosis factor blockers (TNF-blockers). Such drugs do come with numerous adverse health effects and decreased quality of life, though, and for many patients, herbal chemicals that act at TNF-alpha inhibitors and immune modulators may achieve the goals of therapy without these adverse side effects. In addition, such immune suppressing drugs come with serious health risks with long-term use that can be countered with Complementary Medicine. No matter what course of therapy each individual patient chooses, integration of Complementary Medicine provides a number of advantages and can be effectively utilized in any treatment plan. For more information on Ulcerative Colitis, Crohn's disease, and other intestinal disease click on the links in the section entitled Additional Information.

Treatment strategies for Inflammatory Bowel Disease in Complementary Medicine

A focus on a proactive holistic treatment strategy for IBD that is individualized to the patient, and proceeds in a step-by-step manner, is essential in Integrative and Complementary Medicine. This begins with sensible changes in the diet and lifestyle. Short courses of acupuncture and electroacupuncture are proven effective to achieve a number of direct goals in improving gastrointestinal health as well as immune function and adaptation to stress. Herbal and nutrient medicines may accomplish a number of goals, and should be utilized in a sensible step-by-step protocol to achieve both relief of symptoms and elimination of underlying causes. We know that the intestinal Biota must be restored to a healthy symbiotic balance, that the intestinal mucosa must become healthier, that immune modulation and better balance between pro-inflammatory and anti-inflammatory activity must be achieved, and that improved liver, pancreatic and gastrointestinal function is important. While standard medicine is focused on relief of more severe flare-ups of threatening symptoms, the adverse effects of this therapy must be alleviated with Complementary Medicine, and restoration of health achieved each time the patient must resort to these harsh medications. The goal of individualized protocols for the wide variety of presentations in inflammatory bowel disease, utilizing more and more specific markers of disease and subsets of the patient population, as well as goal of periodically reducing medications to see if the patient does well without these problematic drugs, is now common in the treatment guidelines in standard medicine. By integrating professional Complementary Medicine, all of these goals can be better realized, and the least problematic individualized protocol can be achieved. The Licensed Acupuncturist and herbalist is the ideal choice in Integrative Medicine for Inflammatory Bowel Disease. Of course, treatment protocols started early in the course of the disease will be most effective, and patients should start treatment with Complementary Medicine even when these chronic inflammatory diseases are suspected. Waiting until the course of the disease is severe is not a sensible approach, and many of these IBD syndromes could be prevented with the integration of safe and inexpensive Complementary Medicine.

Besides genetic and epigenetic markers that can be utilized to identify the needs of subsets of patients with IBD, immune markers of the disease are also being found that identifies subsets of patients with specific therapeutic needs. While standard medicine is utilizing to better refine the drug therapies, these markers also reveal individualized therapeutic needs that can be met by Complementary Medicine. For example, the p-ANCA, or perinuclear anti-neutrophil cytoplasmic antibodies marker, is fairly specific, not unfortunately, not very sensitive, for ulcerative colitis, and is used with double ASCA, anti-saccharomyces cerivisiae antibodies, to identify subsets of patients with more aggressive forms of IBD. Double ASCA positive IgA and IgG markers are seen more often in younger patients with a high risk of developing an aggressive Crohn's Disease, while the pANCA marker is seen in older patients with ulcerative colitis. These markers imply that specific neutrophil proteins associated with high oxidative stress, iron toxicity and increased lactoferrin, and reactions against increased adhesion molecules, elastase, and cathepsin G, are present, or that vascular inflammation is a problem not being managed by the immune system. Such information points to a variety of treatment protocols that could be integrated in Complementary Medicine to help the body deal with these stressors. If standard medicine could someday work with, or integrate with, Complementary Medicine, much better treatment protocols, individualized and involving fewer adverse side effects, could obviously by devised. Only patient demand will achieve these integrative goals, though, and any effort by patients today may have profound benefits for future patients.