Read an Excerpt from A New IBS Solution |
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Irritable bowel syndrome (IBS) is the most common chronic medical condition and is characterized by abdominal pain, bloating, and altered bowel habits. Although there is some variation from study to study and country to country, up to 20% of a given population appears to be affected by this condition. In addition, unlike other chronic conditions such as heart disease, IBS commonly affects all ages. In fact, studies have shown that patients with IBS have a lower quality of life than those with heart disease or other chronic medical conditions. Despite these facts, developments that may identify causes for IBS have happened only recently. The progress to find a cause for IBS can hardly be called a race. The nature of the illness has interfered with that progress; most patients with IBS find it difficult to discuss their bowel problems with others, and often suffer in silence. This may be in part because the media tends to ridicule patients with IBS or other digestive conditions such as lactose intolerance. All of these factors lead to social isolation and continued unwillingness to discuss the condition, further contributing to the patients’ lower quality of life and the public’s ignorance of IBS. One reason for our lack of knowledge about IBS is the lack of funding for research into its cause and treatment. Since IBS is not a fatal illness, it is not given priority for research funding. As a result, researchers who wish to unravel the IBS puzzle struggle to secure resources; fundraising takes up time those physicians would otherwise have for treating patients. Moreover, only a handful of researchers in the U.S. are working to identify a cause for IBS. The result is that most physicians continue to have a poor understanding about IBS. Often, when a disease is not clearly understood, the first inclination is to link the disease with the psychological condition of the patient. There are many historical examples of such thinking. In the 1970’s, there was much discussion about the cardiac risk posed by having a “type A” personality. We now understand heart disease in a completely different way and this reference is no longer part of the medical doctrine. In another example, stress was thought to be the main cause of stomach ulcers until the discovery of the bacteria Helicobacter pylori as the most common culprit. With the inability of scientists to pinpoint the causes of IBS, the patients have fallen victim to psychological scrutiny and are often stigmatized as a result. In some cases this stigma makes it difficult for IBS sufferers to obtain insurance policies, especially disability insurance. To be fair, it is well known that a history of severe psychological trauma can lead to changes in bowel function. It is also understood that stress can influence the degree of symptoms in some IBS sufferers. However, now it is known that in most cases stress and psychological problems neither cause nor are associated with IBS. While this conclusion should be a victory for those with IBS, the stigma remains since the misconceptions run deep in the grass-roots medical community. Many factors have contributed to the declarations of IBS as being more than psychological. For example, in non-university-based medical studies, the psychological profile of IBS patients is no different than the rest of the community. This discovery was paralleled by research contributing to the development of four new theories in IBS. The discovery of altered pain perception in the gut was the first of four key findings. In the 1990’s studies demonstrated that IBS patients experienced gut pain at much lower thresholds than the general population. In other words, what would not be considered painful to the gut in normal subjects was perceived as painful in IBS patients. This led to innovative studies looking at pain processing in the gut and its transmission to the brain, or the “Brain-Gut Axis.” Brain imaging has since shown that IBS patients respond differently to pain; locations of the brain not otherwise activated by pain were being turned on in IBS. This work had several limitations; the techniques for measuring brain imaging required a high level of expertise and yielded inconsistent results among studies. Also, for patients, this concept has not easily translated into a better understanding of the causes and treatment of IBS. One negative outcome of these findings was the initial marrying of these pain and brain findings to the older psychological theory of IBS. This union led investigators to consider antidepressant medications as a potential remedy. Since some antidepressants (especially tricyclic antidepressants such as amitryptyline) have also been shown to have numbing effects on the spine pain fibers (nerves), the fit was too tempting. While the ill effects of widespread antidepressant use had some in the scientific community concerned, studies showed that antidepressants could slow down bowel movements. Thus the concept that any antidepressant could work began to take hold. The ultimate consequence is that antidepressants have been a mainstay of IBS treatment. Shortly after the discovery of heightened sensation in the gut in IBS, others were taking a different scientific approach. One sentiment was that IBS was difficult to define because the disease was really a mixed group of conditions. The division of IBS into subcategories could in theory simplify its definition, making the causes more apparent. This approach led to the second theory of IBS, in which IBS is a group of disorders, with the dominant symptom defining each group. IBS with diarrhea as the main symptom would be labeled “diarrhea-predominant IBS”; and if constipation was the main feature, the label would read “constipation-predominant IBS.” Efforts were also made to provide a clear definition of IBS. From this thinking was born what is now referred to as the Rome Criteria. Studies then emerged showing that for IBS patients suffering from constipation, intestinal movements were slower compared with normal controls. In contrast, in IBS patients suffering from diarrhea, the gut appeared to propel its contents too fast. Based on this, drug companies began to search for the chemicals produced by the gut that control its movement. A key chemical is serotonin, secreted by cells that line the gut wall. When food enters the area, serotonin is released, causing the gut to contract in a special fashion called peristalsis. Peristalsis in this context is a forward movement or spreading of gut contents such as food down the gut. On a simplified level, if there is too much serotonin there is too much movement; not enough and the gut is slower. Some IBS studies demonstrated this connection between serotonin levels and gut movement, which became the basis for a new class of drugs that block (alosetron, cilansetron, granisetron) or augment (tegaserod) the sites of action of serotonin. The third theory of IBS stems from a pattern that investigators began to recognize among patients with IBS who had suffered attacks of acute diarrhea. Approximately 20% of IBS sufferers declare that their bowel habits were perfectly normal until such an attack. In most cases the patients recall the incident as a clear case of food poisoning, while in many other instances the acute diarrhea began on a trip abroad. Even after the acute episode of diarrhea subsides, the bowel habits never return to normal. In light of this history, clinicians aggressively investigated the stool for infective agents but found nothing, often years after the initial event. The recognition of this symptom complex has led researchers from Europe and Canada to study food poisoning cases. Now, most researchers agree that a certain proportion of food poisoning cases will lead to perpetual IBS-like symptoms. This idea of IBS being precipitated by an intestinal infection was termed “post-infectious IBS.” The final, most recent theory defines IBS as a bacterial disease. Patients with IBS inevitably complain of gas and bloating. While this was once considered a major hallmark of IBS, the failure to understand this component led investigators in the 1980’s to emphasize what was more easily grasped; hence the focus on diarrhea and constipation. Still, even as most members of the scientific community were distracted by the emphasis on bowel function, others investigated the bacterial component of IBS. In the 1990’s, research showed that IBS patients (over a given time) produced 5 times more gas than did people without IBS. Since the only source of those gases was bacterial, the initial presumption was that IBS patients had excessive bacteria in the colon, where bacteria were expected to be. Subsequent studies showed that IBS patients had excessive quantities of gas in the small bowel; these data were the catalyst for studying small bowel bacteria in IBS. Normally the small intestine contains a very small quantity of bacteria. In published studies, indirect measures of small bowel bacteria suggest that 84% of IBS sufferers have excessive quantities of bacteria typically found in the colon. Intuitively, higher bacterial levels in the small bowel, where absorption takes place, would ferment the nutrients from the food into gas. Further work in this area has determined that these bacteria could produce both constipation and diarrhea, depending on the types of bacteria that have moved into the small bowel. These results have led to studies showing that antibiotics can almost completely relieve IBS symptoms if successful in eliminating the intestinal bacteria. This is called the “bacterial overgrowth theory of IBS.” This book takes you through the evolution of thinking in IBS in a way that can be easily understood. The research is often complex even for those in the field; physicians and patients alike may get lost trying to understand the quagmire of opinions and research findings. In the desire for help, along with frustration with their physicians’ limited understanding of how to treat IBS, patients have turned to alternative therapies such as probiotics. While some of these therapies have positive results, others are not as helpful and in some rare cases may be detrimental. These too will be discussed. While the initial chapters focus on how the theories of IBS diverge, the final chapters will show how the theories converge into a unifying hypothesis, and will give an indication of where IBS developments are heading in the future. |