Causes of irritable bowel syndrome
During the Internist Congress in Wiesbaden in spring this year, Prof. Dr. Hubert Mönnikes, Chief Physician of the Department of Internal Medicine at Martin Luther Hospital made a presentation on the causes of irritable bowel syndrome.
A reading version of his lecture was published in the colloquiums magazine "Gastroenterology", which was distributed as a supplement of the MEDICAL TRIBUNE. This is a translation of the text.
Dysmotility and inflammation as causes of irritable bowel syndrome
Patients with irritable bowel syndrome quite quickly have been declared as having a psychological problem not that long ago. That's because functional disorders were synonymous with imaginary problems. Today we know it better. Professor Dr. Hubert Mönnikes explains what organic changes cause the irritable bowel syndrome.
Today numerous factors are known, that are responsible for the development of irritable bowel syndrome. They range from a change of social conditions up to changes in the nervous processing of pain and sensory or immunological reactions and genetic predisposition.
Numerous studies have shown that patients with irritable bowel syndrome have a dysmotility. For diarrhea-predominant irritable bowel syndrome patients, both the motoric activity, especially of the colon, as well as the tonus of the colon are increased. In patients suffering mainly of constipation, however, one finds a decrease in bowel activity, the gastrocolic reflex is reduced.
Patients with irritable bowel syndrome feel pain much stronger
In addition, patients with irritable bowel syndrome, perception in the meaning of hypersensitivity and hypervigilance is changed. With an identical intensity of stimulus, an irritable bowel syndrome patient feels pain much more often than a healthy person. This can be caused by changes in sensory nerve cells in the colon as well as by changes in the area of the spinal cord or the central nervous system.
It has been demonstrated that healthy persons respond to a stimulus of the colon with increased activation of brain regions, that inhibit pain and perception. Stimulus to irritable bowel patients increasingly activates regions in the brain that play a role in processing emotions and controlling the amount of attention being payed. Even when affected only expect a stimulus to the colon they show such reactions. This suggests that they have a hypervigilance that, together with higher pain sensitivity, increased attention and greater pain, leads them to experience more pain.
Too much or too little serotonin – being followed by diarrhea or constipation
For many IBS patients changes in terms of micro-inflammation could be measured e.g. a higher rate of sensory nerve fibers in the colon, which – amongst other things - responded to capsaicin. Why the inflammatory activity occurs is largely unknown. Exceptions are patients who, after a gastroenteritis, develop a post-infectious irritable bowel syndrome.
An important neurotransmitter in the gastrointestinal tract is serotonin. It plays a role in the regulation of motor activity and secretion, but also in mediating sensory information from the periphery to the CNS. It is especially released from the enterochromaffin cells and inactivated by the resumption into the enterocyte via the 5-HT-transporter.
In IBS patients the serotonin system appears to be disturbed. Patients with diarrhea-predominant IBS show postprandial increased serotonin levels. The platelet 5-HT concentration in their thrombocytes is lowered.
Exactly the opposite it is with patients with constipation-predominant IBS. This leads to the conclusion that There is a transportation problem of serotonin in the digestive tract and possibly also in the CNS.
Stress slows the stomach and drives the large intestine to a sprint
But also the genetic predisposition plays an important Role. Certain genetic factors are responsible for changes in the serotonin metabolism. One knows from studies that there are functional polymorphisms of the serotonin receptor that increase the risk for IBS by a factor of 10 to 30.
60% of women and 40% of men reported about a correlation between their problems and stress. Even for healthy persons stress has direct effects on motility and sensitivity in the digestive tract. The gastric emptying is inhibited, stool frequency and colon sensitivity increase. These effects are mediated via serotonin and the mast cell product histamine.
It is assumed that the stress-induced release of the messengers lead to a defect in the intestinal barrier. Because of this more immunogenic substances from the lumen are added which leads to micro-inflammation. This is called a neuro-immune CNS-mast cell axis. But an IBS-patient must not necessarily have increased stress. His colon just reacts easier to exposure, for example because there are more mast cells in his colon.