We are just about done with content for the new, very comprehensive website on Irritable Bowel Syndrome (IBS). IBS can be triggered by an incident of foodpoisoning, and we commonly see post infectious IBS in many clients involved in Salmonella, E. coli, and Campylobacter outbreaks. We hope the new website helps; here is the content:
What is Irritable Bowel Syndrome (IBS)?
Irritable bowel syndrome (IBS) is one disorder in a spectrum of common functional gastrointestinal disorders. Symptoms of IBS can include constipation, diarrhea, alternating diarrhea and constipation, abdominal pain, urgency, bloating, straining at stools, and a sense of incomplete evacuation. The Rome III definition for IBS, which is widely accepted in the medical community, is recurrent abdominal pain or discomfort at least three days per month for at least three months, with at least two of the following symptoms also present: improvement of the pain or discomfort with defecation, a change in frequency of stools, or a change also in the form or appearance of stool.
The symptoms of IBS are usually long term, and, although they can cause daily gastrointestinal symptoms, are frequently episodic, meaning that they may not occur on a daily or regular basis. Symptoms may be triggered by specific foods or by stress. Often, however, no specific triggers can be identified
IBS is much more common in women than men; and the onset of idiopathic IBS symptoms is usually in the teens or young adulthood. Symptoms of IBS can occur as a result of intestinal infection or can be precipitated by major life events.
It is estimated that 10-20 % of the Western population has symptoms consistent with IBS, although most (75-80%) never seek medical care. IBS symptoms do account for about 10% of visits to primary care providers, and for 25-50% of referrals to gastroenterologists.
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 hard to pass. Frequently patients 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 food-borne 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 pre-disposition
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.
What is Post Infectious IBS?
The observation that the onset of IBS symptoms can be precipitated by gastrointestinal infection dates to the 1950s. Different studies have shown that 7-31% of individuals, who have experienced an episode of infectious gastroenteritis, whether bacterial or viral, may develop symptoms of IBS.
One recent meta-analysis (a study that combines results from previously published research studies and analyzes the larger number) of 8 studies published between 1950 and 2005 found a positive association between gastrointestinal infection and the onset of IBS in 6 of the studies. In this meta-analysis alone, the average occurrence of post-infectious IBS was 9.8%, compared to 1.2% in the control group. This equates to a sevenfold increase in the odds of developing IBS after gastrointestinal infection.
There appear to be several risk factors associated with the development of post-infectious IBS, including female sex, severity and duration of the acute infectious illness, whether the person suffered from bloody stools, and psychological profile. As with non-post-infectious IBS, the precise mechanism that produces the symptoms is not specifically known. The pathogens known to precipitate post-infectious IBS symptoms include specifically, though not necessarily exclusively, Enterotoxigenic E. coli strains, Shiga toxin-producing E. coli strains (including E. coli O157:H7), Campylobacter, Shigella, and Salmonella.
What is Dyspepsia?
Dyspepsia is the name of another functional gastrointestinal disorder that may occur in the wake of a severe gastrointestinal infection. Symptoms of dyspepsia, which typically occur during or after eating, include nausea, vomiting, bloating, burning pain in the upper mid-abdomen (epigastrium), and filling up quickly while eating (early satiety). Symptoms of dyspepsia have recently been classified into two subgroups by the Rome III group: epigastric pain syndrome (EPS) (burning epigastric pain after eating) and postprandial distress syndrome (PDS) (nausea and bloating after eating). It is estimated that as much as 25% of the world’s population suffers from dyspepsia.
The specific cause of dyspepsia is not known, but individuals who suffer from the condition frequently exhibit any of several abnormalities that may play a role. These include a decreased ability of the stomach to expand with food, delayed gastric emptying, abnormal motility of the small bowel, and infection by Helicobacter pylori (though, in this latter group, dyspeptic symptoms rarely resolve even after eradication of H. pylori infection).
Recent studies have also demonstrated that, like post-infectious IBS, gastrointestinal infection may also act as a trigger for symptoms of functional dyspepsia. In one study of individuals who had been infected by Salmonella, one in seven had symptoms of dyspepsia, and one in ten had symptoms of IBS. In another, more comprehensive study, physicians following thousands of individuals infected by E. coli O157:H7 in a drinking water outbreak found that functional dyspepsia was twice as common in those who had suffered gastrointestinal infection than in those who had not. Risk factors for functional dyspepsia were female sex, smoking, pre-existing IBS, anxiety, depression, and having an acute gastrointestinal illness longer than 7 days.
What is gastroparesis?
Gastroparesis is a condition in which stomach emptying is delayed, resulting in symptoms of nausea, vomiting, early satiety and weight loss. It is most commonly associated with diabetes, but sporadic cases can occur. There appears to be a relationship with viral gastroenteritis, as studies have shown development after rotavirus infection in children. There are no studies linking gastroparesis to bacterial infection, but a link may exist. Studies of such a possible link are sorely needed.
How is IBS diagnosed?
Clinicians diagnose IBS by identifying typical symptoms, taking a thorough history and doing a complete physical examination, and testing blood samples for other potential causes of symptoms. Stool tests are also indicated as a means of testing for minute amounts of blood in the stools (occult blood), and sometimes to exclude active infection as the cause of symptoms. In some patients, examining the colon with colonoscopy may be indicated, particularly for anyone 50 or over. The most important organic diseases that can have similar symptoms are inflammatory bowel disease, colon cancer, celiac disease, and in women, ovarian cancer, which can initially present simply as abdominal bloating.
Signs and symptoms that suggest organic disease, rather than IBS, are onset of symptoms over age 50, short duration of symptoms, blood in the stools, symptoms waking one at night, unintentional weight loss, anemia, fever, mass on rectal or abdominal exam, symptoms associated with recent antibiotics, and a family history of organic GI disease (such as colon cancer, inflammatory bowel disease and celiac disease). If one or more of these features is present, further clinical investigation is indicated.
Treatment of IBS
Treatment of IBS varies from person to person, and case to case. They include, where appropriate, changes in lifestyle, such as eating regular meals; changes in diet, such as increasing fiber in those with constipation; and eliminating trigger foods such as fructose and non-absorbable sugars, which can cause diarrhea and bloating. Over the counter medications can be used to decrease diarrhea (loperamide), or improve constipation (soluble or insoluble fiber, laxatives).
Antispasmodics can help with pain, but narcotics are not a good therapy for IBS symptoms because they can alter gastrointestinal tract motility, affect mental function, and cause dependency. For a small number of patients with severe and refractory symptoms, especially pain, low dose antidepressants can be very effective. Probiotics have been helpful for some, though studies on probiotics in the setting of IBS are limited. In certain trials, benefits have also been seen with hypnotherapy, acupuncture, and psychotherapy.