Causes of IBS
What causes IBS?
IBS is often described as a “functional” gastrointestinal disorder. This means that there is no structural abnormality or other objective findings to explain it. The specific cause (or causes) of IBS is not known; but for all IBS patients, there are likely several factors that contribute to both onset and continuation of the problem.
A. Altered gastrointestinal motility
Although researchers and clinicians have not yet identified any actual anatomic changes, it is likely that people suffering from IBS have experienced dysregulation in the motor function (also called “motility” or “peristalsis”) of their gastrointestinal tracts. Peristalsis is the process by which the intestinal wall contracts and forces material through the small intestine and colon. In IBS patients, the bowel transit can be irregular. If material is forced through too fast for water reabsorption, diarrhea results. Alternatively, if transit is slowed, the result may be constipation with hard stools that are difficult to pass. IBS patients frequently alternate between constipation and diarrhea.
In addition, the gastrocolic reflex—i.e., the signal sent to the colon to empty when the stomach fills with food—may be heightened in patients with IBS, who may feel the urgent need to relieve themselves after eating, especially in the morning. As a result of this, many feel that food is “going right through them,” but this is not the case.
B. The brain-gut connection
Evidence also suggests that some IBS patients may suffer from faulty communication between the gut and central nervous system—interference that may be brought on by psychological stressors, hormones, the immune system, or infection.
In addition to the central nervous system, IBS also implicates a parallel nervous system within the digestive tract itself—i.e., the enteric nervous system, which is so large and complex that it has been dubbed “the second brain.” The enteric nervous system is embedded in the wall of the digestive tract and functions semi-autonomously from the central nervous system. Extending from the esophagus to the anus, it regulates digestive tract motility and gastrointestinal blood flow, and also generally senses the environment within the digestive tract.
The enteric nervous system emits a wide array of neurotransmitters, such as acetylcholine, which stimulates smooth muscle contraction, increases intestinal secretions, and prompts the release of enteric hormones and dilation of blood vessels.
Many researchers and clinicians believe that the central nervous system and the enteric nervous system both play a role in causing IBS symptoms. Since the central nervous system is where stress and coping mechanisms are found, it is felt that these and other psychological factors that are frequently associated with the development of IBS symptoms play a major role. Some people with IBS have hypersensitive intestines, giving them increased sensory sensation and input—i.e., an increased perception of feeling in the gastrointestinal tract. For example, persons with IBS will experience pain with distension of a balloon in the rectum when the balloon has a smaller volume than in people without IBS. This is called visceral hypersensitivity.
Stress is also implicated in IBS because it has physiologic consequences, including increased heart rate, delayed stomach emptying, and increased colon contractions. Stress results in the release of various substances, one of which, corticotropin releasing factor (CRF) is found in both the gut and the brain. CRF increases water and mucus secretion in the colon and, as a result, may contribute to symptoms such as diarrhea in IBS.
The close, interrelated nature of communication between the digestive tract and the brain is underscored by the neurotransmitter serotonin, which is found in both organs. Indeed, the vast majority, 95%, of serotonin is contained in the gut. When the gut releases serotonin, which binds to a variety of receptors in nerves, it simulates intrinsic nerves that initiate secretion and peristalsis, as well as extrinsic nerves that modulate sensation.
Normally, after serotonin is released into the gut, it is removed from the bowel by a molecule known as the serotonin transporter (SERT), which is found in the cells that line the gut wall. It is theorized, however, that some people with IBS do not have enough SERT, and thus have too much serotonin in the colon, causing diarrhea. Two recently developed drugs were introduced that target these receptors and thus alter serotonin in the gut. One, called alosetron, slows transit and has the resulting effect of decreasing diarrhea. The other, tegaserod, increases transit, which improves constipation. Alosetron and tegaserod are no longer readily available, however, due to their potential to cause serious side effects, but their efficacy in treating IBS supports the role of serotonin in generating IBS symptoms.
Moreover, serotonin selective reuptake inhibitors (SSRIs—a class of antidepressants) are sometimes prescribed to decrease symptoms in severe cases of IBS, but are used at lower doses than those employed to treat depression.
Recent preliminary evidence also suggests that, in some cases, an enteric infection (see discussion on post infectious IBS) may cause chronic, low-grade inflammation of the gastrointestinal tract, which can disrupt normal gastrointestinal motility. This may involve mast cells, which are important in fighting pathogens in the gut wall. The mast cells secrete histamine, prostaglandin, and other chemicals to fight infection and produce inflammation, but their effect may persist after the infection has cleared, with chronic low-grade inflammation at levels too low to be seen visually.
C. Effect of the normal gut flora, including bacteria
Increasing evidence suggests that changes in normal gut bacteria may play a role in the development of IBS. There are ten times more resident bacteria in the gut—i.e., intrinsic fecal (or colonic) flora—than elsewhere in the human body. These resident bacteria comprise the fecal microbiome that performs multiple functions important to health, such as the digestion of carbohydrates. These bacteria are distinct from common foodborne pathogens like Salmonella, Shigella, and E. coli O157:H7, which can act as the precipitating cause of IBS symptoms in cases of post-infectious IBS (see discussion on post infectious IBS).
Recent studies suggest that some individuals suffering from IBS may have experienced changes in their levels of normal gut bacteria. In certain cases, treatment with antibiotics or probiotics (living organisms that, when ingested, have a beneficial effect on the host), have helped reduce IBS symptoms, supporting the notion of the importance of the gut flora.
D. Genetic predisposition
Finally, studies suggest that a certain percentage of those suffering from IBS are genetically predisposed to the condition, though many individuals included in this group experience an inciting or precipitating event (e.g. gastrointestinal infection, discussed below) that initiates symptoms. In fact, individuals with IBS are 33% more likely to have a family history of IBS.