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BY MAHESH KRISHNA<br />

Iam a first generation American, as<br />

both of my parents immigrated here<br />

from Myanmar, a third world country.<br />

There had been no occurrence of any<br />

Inflammatory Bowel Disease (IBD) in my<br />

family, yet I was diagnosed with Ulcerative<br />

Colitis at the beginning of my sophomore<br />

year of high school. Since IBD is known<br />

to be caused by a mix of genetic and<br />

environmental factors, 1, 2 what specifically<br />

triggered me to develop Ulcerative<br />

Colitis? Was it the food in America, the<br />

air I was exposed to, a combination of<br />

the two, or neither of them at all? Did<br />

the “environment” of the first world in<br />

the United States cause me to develop<br />

Ulcerative Colitis?<br />

IBD is a chronic autoimmune disease,<br />

characterized by persistent inflammation<br />

of the digestive tract and classified into<br />

two separate categories: Ulcerative Colitis<br />

and Crohn’s Disease. 3 Currently, there is no<br />

known cure for IBD, as its pathogenesis (i.e.<br />

the manner in which it develops) is not fully<br />

understood. 1 Interestingly, the incidence<br />

of IBD has increased dramatically over<br />

the past century. 1 A systematic review by<br />

Molodecky et al. showed that the incidence<br />

rate of IBD was significantly higher in<br />

Western nations. This may be due to better<br />

diagnostic techniques or the growth of<br />

environmental factors that promote its<br />

development. This could also suggest that<br />

there may be certain stimuli in first world<br />

countries that can trigger pathogenesis in<br />

individuals with a genetic predisposition to<br />

IBD.<br />

Environmental factors that are believed to<br />

affect IBD include smoking, diet, geographic<br />

location, social status, stress, and<br />

microbes. 1 Smoking has had varying effects<br />

on the development of IBD depending on<br />

the form; smoking is a key risk factor for<br />

Crohn’s Disease, while non-smokers and<br />

ex-smokers are usually diagnosed with<br />

Ulcerative Colitis. 4 There have not been<br />

many studies investigating the causal<br />

relationship between diet and IBD due to<br />

the diversity in diet composition. 1 However,<br />

since IBD affects the digestive system, diet<br />

has long been thought to have some impact<br />

on the pathogenesis of the disease. 1 In<br />

first world countries, there is access to a<br />

larger variety of food, which may impact the<br />

prevalence of IBD. People susceptible to the<br />

disease in developing countries may have a<br />

smaller chance of being exposed to “trigger”<br />

foods. In addition, IBD has been found in<br />

higher rates in urban areas versus rural<br />

areas. 1,4, 5 This makes sense, as cities have<br />

a multitude of potential disease-inducing<br />

environmental factors including pollution,<br />

poor sanitation, and microbial exposure.<br />

Higher socioeconomic status has also been<br />

linked to higher rates of IBD. 4 This may be<br />

partly due to the sedentary nature of white<br />

collar work, which has also been linked<br />

to increased rates of IBD. 1 Stress used<br />

The Hygiene Hypothesis<br />

states that the lack of<br />

infections in western<br />

countries is the reAson<br />

for an increasing<br />

amount of autoimmune<br />

and allergic diseases.<br />

The idea behind the theory<br />

is that some infectious<br />

agents guard against a<br />

wide variety of immunerelated<br />

disorders.<br />

to be viewed as a possible factor in the<br />

pathogenesis of IBD, but recent evidence<br />

has indicated that it only exacerbates the<br />

disease. 3 Recent research has focused on<br />

the microorganisms in the gut, called gut<br />

flora, as they seem to have a vital role in<br />

the instigation of IBD. 1 In animal models, it<br />

has even been observed that pathogenesis<br />

of IBD is not possible in a germ-free<br />

environment. 1 The idea of the importance<br />

of microorganisms in human health is also<br />

linked to the Hygiene Hypothesis.<br />

The Hygiene Hypothesis states that the<br />

lack of infections in western countries is<br />

the reason for an increasing amount of<br />

autoimmune and allergic diseases. 6 The idea<br />

behind the theory is that some infectious<br />

agents guard against a wide variety of<br />

immune-related disorders. 6 Animal models<br />

and clinical trials have provided some<br />

evidence backing the Hygiene Hypothesis,<br />

but it is hard to causally attribute the<br />

pathogenesis of autoimmune and allergic<br />

diseases to a decrease in infections, since<br />

first world countries have very different<br />

environmental factors than third world<br />

countries. 6<br />

The increasing incidence of IBD in<br />

developed countries is not yet fully<br />

understood, but recent research points<br />

towards a complex combination of<br />

environmental and genetic factors. The<br />

rise of autoimmune disease diagnoses<br />

may also be attributed to better medical<br />

equipment and facilities and the tendency<br />

of people in more developed countries to<br />

regularly get checked by a doctor. There<br />

are many difficulties in researching the<br />

pathogenesis of IBD including isolating<br />

certain environmental factors and obtaining<br />

tissue and data from third world countries.<br />

However, there is much promising research<br />

and it might not be long until we discover a<br />

cure for IBD.<br />

Works cited<br />

[1] Danese, S. et al. Autoimm Rev 2004, 3.5, 394-400.<br />

[2] Podolsky, Daniel K. N Engl J Med 2002, 347.6,<br />

417-29.<br />

[3] Mayo Clinic. “Inflammatory Bowel Disease (IBD).”<br />

http://www.mayoclinic.org/diseases-conditions/<br />

inflammatory-bowel-disease/basics/definition/con-<br />

20034908 (accessed Sep. 30, 2016).<br />

[4] CDC. “Epidemiology of the IBD.” https://www.<br />

cdc.gov/ibd/ibd-epidemiology.htm (accessed Oct.17,<br />

2016).<br />

[5] Molodecky, N. et al. Gastroenterol 2012, 142.1, n.<br />

pag.<br />

[6] Okada, H. et al. Clin Exp Immuno 2010, 160, 1–9.<br />

Design by Juliana Wang<br />

EDITED by Carolina Hatanpaa<br />

36 | CATALYST

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