Irritable Bowel Syndrome (IBS)

Irritable Bowel Syndrome (IBS) is the most enigmatic gastrointestinal condition to deal with. In addition to being misunderstood it is usually mistreated as therapy is almost universally aimed at the symptoms and not the underlying pathophysiology. The blame for this can be partly directed at the pharmaceutical industry which needs to sell chemicals and partly at the alternative health movement which dictates a mystical high fruit and vegetable diet, and the avoidance of wheat. The latter is supported by legions of health shops, alternative practitioners, nutritionists and popular magazines

We, the traditional scientific medical practitioners, have spent too much effort on defining the condition. The Rome Criteria are regularly refined in an attempt to encapsulate the clinical presentation of these patients. This misses the point that this is a syndrome of disturbed intestinal physiology with deranged processes that lead to the clinical symptoms. The clinical approach is therefore to identify the disturbed physiology, exclude other pathology and manipulate the physiology back towards normal. To achieve this, the most important investigation is the clinical history. The aim is not to check the boxes of diagnostic criteria but understand where and how the symptoms originate.

The pillars of IBS pathophysiology are

  1. Disturbed feedback between brain and gut
  2. Hypersensitivity of the intestinal tract to distension.
  3. Deranged non propulsive bowel motility
  4. Intestinal stress and small hard stools

Numerous studies have addressed the above problems, and a logical all-encompassing model has not yet been formed or accepted by the scientific community. Based on the above factors, traditional treatment consists of tranquillizers/anti-depressants, antispasmodics, pro kinetics and laxatives. Which of these approaches is used is often arbitrary and fails to address the patient’s particular dysfunction.

The associated symptoms of IBS are

  1. Bloating due to relaxation of abdominal muscles and downward movement of the diaphragm. Although most bloated patients produce excessive flatus, the mechanism is completely different. Bloating is therefore a posture unrelated to the amount of gas in the colon.
  2. Cramping abdominal pain usually related to bowel function. This is most common prior to defaecation but also during and after defaecation. The pain can be very severe. Protalgia fugax is a related severe, searing and stabbing rectal pain which characteristically wakes the patient at night
  3. Constipation is the inevitable consequence of non propulsive motility. This leads to a colon full of stool and an associated increase in gas production.
  4. The intestinal confusion associated with small stools and excessive mucous production is well recognised by patients who often revert to intestinal stimulants to improve bowel function. Fruit and other laxatives are used which increases the hypersensitivity of the intestinal tract and completes the vicious circle which makes up the chronic irritable bowel syndrome.

The treatment of the disturbed physiology that is IBS is difficult as we have little in the way of intestinally active agents. Laxatives increase the spasm in a the bowel and therefore actually aggravate the situation. A much better approach is to try to manipulate our physiology.

  1. Bloating is a product of a cerebral reaction to perceived abdominal cramp. Stress management is central.Fortunately, an explanation of the physiology is often helpful.
  2. The hypersensitive cramping intestine needs to be relaxed. The options are twofold. Stress management is again central but aggravating stimulants such as laxatives and stimulatory fruits need to be avoided. There is no difference between a senna product and a bowl of prunes on bowel motility. Both increase intestinal contractions and can produce discomfort.
  3. The key pathophysiological disturbance of non- propulsive bowel motility leads to disturbed movement of intestinal gas as well as stool. Prokinetics which increase peristalsis would be useful but no powerful enough agents are now available after the withdrawal of Prepulsid (cisapride) and Zelnorm (tegaserod). We can however reduce the gas load by avoiding the gas producing leaves such as cabbage, broccoli and cauliflower. A seldom recognised but useful dietary stimulant of propulsive peristalsis is hard items such as corn/mielie kernels. We have all seen the rapid movement of yellow kernels from stew to loo without cramps or increased gas.
  4. Consistency of stools is entirely dependent on the number of bacteria present in the stool. Therefore, the only effective way to increase the stool volume is to increase the fibre intake to increase the bacterial numbers. In some patients a high fibre diet and the larger stool produced may exacerbate the discomfort due to the hypersensitivity of the intestine. It is therefore critical that propulsive motility needs to be encouraged with the hard items together with the increased fibre. A muesli with high fibre, sunflower seeds and nuts together with a reduction in consumption of laxatives/stimulatory fruit is the ideal combination.

The irritable bowel syndrome needs to be treated as a disturbance of intestinal physiology. Other factors such as psychological factors, intestinal infections, intestinal inflammation and bacterial disturbances will need further investigation until the conundrum of cause or effect is unpacked.

Pending better pharmaceutical agents, dietary manipulation remains the mainstay of therapy. This takes time in explanation and discussion with the patient. This is perhaps why it is so poorly treated by the profession.