From the nation’s leading law firm representing victims of IBS and other foodborne illness outbreaks.

Chapter 2

Causes of IBS

What causes IBS?

IBS is a functional gastrointestinal disorder. This means that there are no structural abnormalities or other objective findings. Thus, organic diseases with similar symptoms like celiac disease or inflammatory bowel disease must be excluded. The specific etiology is not known but there are many possible factors involved. Traditionally, the focus was on changes in gut motility and on visceral hypersensitivity. Lately researchers are looking at changes in the gut microbiome (previously called gut flora) and mucosal inflammation.

1. Altered gastrointestinal motility

Although researchers and clinicians have not yet identified any actual anatomic changes, it is likely that some people with IBS have 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 fluid reabsorption, diarrhea results. Alternatively, if transit is slowed, the result may be constipation with hard stools that are difficult to pass. The most common stool pattern in IBS is alternating between constipation and diarrhea.

Another common symptom is urgency, or an uncontrollable urge to defecate. This may be related to diarrhea—when the distended rectum sends a signal to the brain to empty the gut. The normal increase in motility of the lower intestinal tract following a meal is called the “gastrocolic reflex”—i.e. the signal sent to the colon to empty when the stomach fills with food. This may be heightened in patients with IBS, who may experience this reflex urgently 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.

Newer drugs that affect gut motility can improve IBS symptoms, supporting the role of dysmotility in this syndrome.

2. Visceral Hypersensitivity and the Brain Gut Connection

In addition to the central nervous system (CNS), there is 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 CNS. 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 that stimulate smooth muscle contraction, increase intestinal secretions, and prompt the release of enteric hormones and dilation of blood vessels.

Visceral hypersensitivity is an increased sensation in response to stimuli. 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 at a smaller volume than that experienced in people without IBS.

Evidence also suggests that some IBS patients may suffer from faulty communication between the gut and the CNS—interference that may be brought on by psychological stressors, hormones, the immune system, or infection. Since the CNS is where stress and coping mechanisms are found, it is felt that these and other psychological factors may play a role in the development of IBS symptoms.

Stress is also implicated in IBS because it has physiologic consequences, including increased heart rate, delayed stomach emptying, and increased colon contractions; as a result, it may contribute to symptoms such as diarrhea in IBS.

3. Effect of the gut microbiome

Recent evidence suggests that changes in the normal gut microbiome (including intestinal bacteria) may play a role in the development of IBS. There are ten times more resident bacteria in the gut than elsewhere in the human body. These resident bacteria and other microorganisms comprise the fecal microbiome, which performs multiple functions important to health, such as the digestion of carbohydrates. 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.

Moreover, it is well documented that IBS can occur after an enteric infection (see discussion on post-infectious IBS below).

4. Intestinal inflammation

After an enteric infection, it is theorized that there may be 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.

5. Genetic predisposition

Studies of twins 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 addition, individuals with IBS are 33% more likely to have a family history of IBS.

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Irritable Bowel Syndrome

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Post-Infectious IBS

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