Crohn's and Genetics

Last year, I took a class on human genetic variation. As the final project for the class, we had to write a 10-15 page paper on a topic regarding genetic variation in humans. I decided to focus my paper on Crohn's disease. Because Crohn's is an autoimmune disease, I figured there had to be some kind of genetic connection. If there is a mutation in a gene that codes for a cell receptor on digestive cells, then the body could identify it as foreign and thus attack the cells. 


So, I'd like to share with you my research. This paper is called a "review of the literature." I perused the research of others, compiling and synthesizing it to create a somewhat comprehensive view of the studies that have been done over the years. 


Enjoy this first installment!

It is estimated that 60 to 70 million people are affected by some sort of digestive disease in the United States alone. One to two million of these cases of digestive disease are inflammatory bowel disease, which can be separated into two categories: Crohn’s disease and colitis (Head and Jurenka 2004). Both are defined as a chronic inflammation of the digestive tract. Crohn’s disease can occur anywhere in the digestive system, but is typically found in the ileum or colon (Shoenstadt 2004).  Colitis is essentially the same thing, but is only found in the colon. This review will be focusing on Crohn’s disease, which is a complex interplay of environmental and genetic risk factors. While the evidence is inconclusive as to the exact cause of Crohn’s disease, Western style treatments focus on using drugs. However, the literature suggests that changes in diet can treat the disease much more effectively. Therefore, more research needs to be done on diets that are helpful to people with Crohn’s disease.


While Crohn’s disease is less prevalent than colitis (according to National Digestive Disease Information Clearinghouse (NDDIC 2010) statistics in 1998, Crohn’s affected only 359,000 people, whereas colitis affected 619,000) in 2004 it accounted for 1.1 million ambulatory care visits and 141,000 hospitalizations in the US. Furthermore, 1.8 million prescriptions were made in 2004 for the treatment of the disease (NDDIC 2010). Clearly, the disease has resounding effects. It is typically diagnosed between the ages of 15 and 35 and is the result of inflammatory T helper cells that cause lesions in the digestive tract (Cariappa et al. 1998, Forcione et al. 1996).

Many studies have been done on the demographics of people that Crohn’s affects. It is generally thought of as a primarily “white” disease, in that is rarely found in people not of Caucasian descent. Jeshion et al. (1998) found in a study of 337 children with Crohn’s that 92.9% of their subjects were white, 4.4% were black, 1.2% were Hispanic and 1.5% were other, unspecified races. In contrast, Shapira and Tamir (1994) note that in the United States, the United Kingdom and Sweden, Crohn’s has been predominant in Jewish patients. Shapira and Tamir’s study examined the prevalence of Crohn’s in the Euro-American, African-Asian and Israeli populations of the Kinnaret sub-district of north Israel. They found that the prevalence of the disease in the European-American born population was twice that of the other two populations. This suggests that susceptibility to the disease correlates more with country of origin rather than just their race. This conclusion supports Ghosh and Rona’s (2003) statement that a Western diet is one of the most prominent risk factors of Crohn’s disease.