Ulcerative Colitis Causes
Basically, the immune systems of a person with ulcerative colitis continually attacks the lining of their colon. With repeated inflammation, the lining of the colon thickens and sores can develop. The sores further aggravate the lining and cause the symptoms of ulcerative colitis.
The Crohn’s & Colitis Foundation of America (CCFA) describes the immune systems of those with ulcerative colitis as having originally “switched on” to combat a pathogen, but then continues to mistake food, bacteria or other normal intestinal materials as pathogens themselves and seeks to rid them from the body. Additionally, the body sends additional white blood cells into the intestinal lining which accounts for the chronic inflammation.1 The immune response is understood to be the culprit for the symptoms of ulcerative colitis , even if the root cause of the disease itself is still unknown.
The cause, or "etiology," of Ulcerative Colitis is still unknown. Our medical model has long attributed disease to an external infectious pathogen as was true of many diseases in the early 1900s: polio, cholera, malaria, measles etc. So it is no surprise that science searched for years for the infectious agent responsible for ulcerative colitis. But when many potential pathogens (causes) were found (viruses, bacteria, yeast etc.) research seeking to find the cause of colitis turned to the individual immune response of each affected person.
According to a recent article in the Israel Medical Association Journal; "The association between infection and autoimmunity, the first leading to the latter by the mechanism of molecular mimicry… is well established. The role of infection may be primary, the infection being a prerequisite for disease initiation in a genetically susceptible host, or secondary, where the causation is vague and is suggested by an excess of positive serology for a certain pathogen…" 1
This simply means that antigens in the environment might either directly cause the inflammatory response exhibited in Ulcerative Colitis or that the immune system is overreacting to what might be an insignificant pathogen in another individual’s body. Additionally, the authors state “…the paradigm has shifted from infectious agents to loss of immune tolerance to commensal enteric bacteria.” The term “commensal enteric bacteria” refers to normal microorganisms that make up the natural gut flora. Persons with ulcerative colitis are often found to have an increased number of aggressive bacteria, such as Bacteroides and E. Coli in the gut while having fewer of the “good” or protective bacteria such as lactobacilli and bifidobacteria.1 (Prebiotics and probiotics can play a role in helping to restore the gut flora and are further mentioned in the “Nutrition and Supplements” section.)
This is similar in concept to Stephen Paget’s “seed and soil hypothesis,” where the medical community debated whether the cause of disease was the “seed” (environmental pathogen) or the “soil” (the individual’s own genetic makeup rendering their ability to or not to adequately combat the invading pathogen). Most doctors seem to believe the cause of ulcerative colitis to be a combination of both the seed and the soil; both an outside agent and the individual’s overactive immune response cause the body to attack the colon’s innermost lining.
An additional hypothetical contributor to the rise in Inflammatory Bowel Disease in western cultures in particular, is increased antibiotic use which kills many “indigenous” bacteria, beneficial or not. Ultimately, it seems a combination of factors contributes to the disease.
On the one hand, infection with a pathogenic organism could serve as an environmental trigger to initiate an inflammatory response, a response that may be perpetuated in a susceptible host by commensal microbial antigens. On the other hand, host genetic susceptibility, in the form of a defective mucosal barrier function, can lead to enhanced exposure to luminal bacteria. Either process can lead to an overly aggressive T cell response to normal bacteria, culminating in tissue damage. It seems, therefore, that it is the combined effect of genetic susceptibility with microbial exposure, in addition to increased antibiotic use and improved hygiene, that alters the balance of beneficial versus aggressive microbial species, that perpetuates the pathophysiology of inflammatory bowl disease.1
The Crohn’s & Colitis Foundation of America (CCFA) describes the immune systems of those with ulcerative colitis as having originally “switched on” to combat a true pathogen, but then continues to mistake food, bacteria or other normal intestinal materials as pathogens themselves and seeks to rid them from the body. Additionally, the body sends additional white blood cells into the intestinal lining which accounts for the chronic inflammation (CCFA, 2009). The immune response is understood to be the culprit for the symptoms of ulcerative colitis , even if the root cause of the disease itself is still unknown. Patients can learn what causes their individual immune system to overreact and in doing so, lessen their symptoms (sometimes having permanent remission from these symptoms) even if the disease is never "cured." By understanding what causes each individual's inflammatory process, practitioners can work to lessen the symptoms of the disease in a patient-specific manner.
- Crohn’s & Colitis Foundation of America. (2009) Diet and Nutrition. Retrieved April 1, 2010 from http://www.ccfa.org/info/diet?LMI=4.2
- Lidar, M. MD, Langevitz, P. MD, & Shoenfeld, Y.MD. (2009, September). The Role of Infection in Inflammatory Bowel Disease; Initiation, Exacerbation and Protection. IMAJ 11. Retrieved on March 30, 2010 from http://www.ima.org.il/imaj/ar09sep-10.pdf