By Michael Chiorean, MD **
Ulcerative colitis and Crohn’s disease are the most common forms of inflammatory bowel disease (IBD). While the cause of IBD is unknown, there are a number of hypotheses trying to explain an association between changes in the environment, genetics and immune dysregulation and the development of IBD. Although a definitive explanation is lacking, the environment is likely to play an important role since nothing else can have such a dynamic nature that explains the increased frequency of IBD over the last few decades. The human genes, in comparison, have not changed substantially in the last 25,000 years.
Diet, the Western kind in particular, is usually a primary suspect. Consumption of a diet rich in red meats, in contrast to a vegetarian diet, may be a risk factor. How diet can change the gut bacteria or the immune system in a way to promote IBD is unclear. Furthermore, despite false claims in social media, there is no diet that can improve or “cure” IBD, with the exception of artificial (elemental) diet in young children. Due to its poor taste, this often has to be given through feeding tubes directly in the stomach which is very poorly tolerated long term. It is advisable that patients with IBD follow a generally healthy diet, including a balanced intake of meats, fruits and vegetables. Favoring lean meats, such as fish or chicken, over red meat may be good advice. In contrast, other nonconventional diets such as the special carbohydrate diet or restrictive diets may be detrimental by leading to malnutrition, sometimes severe. Lactose (dairy)-free or gluten-free diets are generally better tolerated, without being necessarily safer or healthier for patients with IBD. There is also no harm in these diets, so patient preference may play a role in this choice.
Other possible risk factors that have been the subject of debate are certain drugs such as non-steroidal anti-inflammatory drugs (NSAIDs, like aspirin and ibuprofen) and oral contraceptives; the use of both has increased substantially in the last century. While the association of chronic NSAID use with flares of IBD appears certain, no such certainty exists in regards to contraceptive use and, therefore, no specific recommendations exist. I tend to reassure my patients in regards to contraceptives and let them choose the method that best fits their lifestyles. We have to remember that these are some of the most commonly used medications worldwide, while the number of IBD cases remains relatively small (approximately 1 in 500 people in the U.S.).
Smoking is a definite risk factor for Crohn’s disease, while it may be somewhat protective against ulcerative colitis. The harmful effects of smoking are evident not only in Crohn’s disease but also in an increased risk of almost every cancer, as well as heart disease, stroke and dementia. Smokers with inflammatory bowel disease, and Crohn’s patients in particular, should make every effort to quit.
Stress is ubiquitous as a consequence of our increasingly busy, productive and sometimes chaotic lives. It has been linked to a large number of diseases, called psychosomatic disorders, as well as IBD. Stress may cause disease exacerbations in certain predisposed individuals. There have been studies describing disease flares related to natural disasters, and I occasionally see patients who have predictable flares around stressful events, such as final exams. A stress-free world is not only unrealistic, but medications that help relieve stress, such as anti-anxiety drugs, have no effect on IBD flares – even in patients who experience high anxiety levels related to their diseases or lifestyles. That said, the majority of patients can learn to cope with stress with or without medical assistance, and this leads to an improved quality of life.
There is no human disease where genes have not been incriminated at least to some extent. In fact, we are the expression of a complicated genetic code which has been developed and perfected over millions of years. There are more than 25,000 genes in the human body and the genetic material present in every human cell, if stretched in a single string, is several miles long. So it comes as no surprise that certain genetic “accidents” happen and some of them may predispose a person to IBD. More than 100 genes have been associated with Crohn’s disease and almost 50 with ulcerative colitis, with some overlap between the two. This means genes alone are probably not the most important factor in IBD, otherwise we would have only one or two genes responsible, like with hemochromatosis or cystic fibrosis. There is probably more than one way for people to get IBD, which is a topic of intense research these days. The bottom line is that IBD as a whole is only weakly hereditary. In fact, less than 10 percent of first degree relatives of patients with IBD also carry the disease, a little more in Crohn’s than ulcerative colitis. Even in identical twins the concordance rate is only 30 percent for Crohn’s and about half that for ulcerative colitis.
In conclusion, we may not know what causes IBD or disease flares, but we are beginning to understand the complex interactions that exist between the human genes, the environment, normal and abnormal microbial flora, and the immune response in the gut. We are still far away from a unifying theory of IBD, and therefore a treatment that might provide a cure. Until then, we have good medications that can treat the disease and keep it in remission as long as people stay on them and new medications are constantly being developed, some with very promising results. So, stay tuned, there is a fair amount of light at the end of the IBD tunnel.
Michael Chiorean, MD, is a gastroenterologist with the Digestive Disease Institute at Virginia Mason. He specializes in inflammatory bowel disease, Crohn’s disease, ulcerative colitis, C Difficile, gastrointestinal bleeding and small bowel endoscopy.