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How Irritable Bowel Syndrome Develops
For a complete website devoted to Irritable Bowel Syndrome go to www.IBSTreatmentCenter.com.
This page describes the mechanisms by which irritable bowed syndrome (IBS) can develop.
Altered Gastrointestinal Motion in Irritable Bowel Syndrome
IBS has historically been considered a disturbance of gastrointestinal movement. Studies have identified abnormal patterns of peristalsis and electrical activity throughout the gastrointestinal tract in patients with IBS. More recently it has become clear that these patterns are exaggerations of normal patterns. They are disturbances of gastrointestinal function that occur in everyone on occasion due to poor dietary habits or emotional upheaval. However, they occur with a greater frequency and severity in people with irritable bowel syndrome.
The alteration in motility is due to a hypersensitive gastrointestinal tract. This gastrointestinal sensitization may be regarded as an alarm signal that stops the normal unconscious processes of digestion and puts the gut on alert, ready to evacuate its contents at a moment’s notice, either downward by diarrhea or upward by vomiting. This does not, however, account for IBS patients who experience constipation.
Internal Organ Sensitivity in Irritable Bowel Syndrome
Irritable bowel syndrome is associated with a wide range of hyper-reactivity of the internal organs. There is evidence of exaggerated intestinal secretory responses, increased frequency of strong esophageal contractions, increased frequency of disturbances in gastric emptying, altered reactivity of the gallbladder, urinary tract contractile abnormalities, increased responsiveness of bronchiolar smooth muscle, and enhanced vasomotor reactivity in patients with IBS when compared with normal subjects.
Causes of Increased Gastrointestinal Sensitivity
Inflammatory disease of the colon such as ulcerative colitis is associated with heightened internal organ sensitivity and reactivity, similar to that seen in irritable bowel syndrome. Several studies have shown an increase in inflammatory cells, particularly mast cell, in the colon of IBS patients, as well as an increase in proinflammatory cytokines (chemicals) in patients with diarrhea type IBS. One common cause of inflammation is food allergies.
Inflammation is associated with the release of cytokines from damaged tissue, white blood cells (the immune system), and other cells in the vicinity. Cytokines orchestrate the inflammatory and immune processes and enhance sensitivity and reactivity by stimulating sensory nerve endings and by encouraging the proliferation and degranulation (breakdown and release of chemicals) of local mast cells. Once stimulated, a cycle of sensitization may be maintained.
The Link Between Emotion and Gastrointestinal (GI) Movement
An association between emotion and gut motility has long been recognized. Studies into the physiological of the GI tract have shown that anger is associated with exaggerated contractile activity in the colon, and the sadness and fear are associated a lack of motility. Anxiety is associated with rapid small bowel transit and increased frequency of bowl movements. And depression leads to delays in small bowel and whole gut transit. Incidentally, this delay is also seen in those who exercise great control over their anger, giving a scientific basis to the tight anal sphincter commonly associated with certain personality types exhibiting this type of behavior.
The effects of emotion on gastrointestinal function are mediated the autonomic nervous system (sympathetic and parasympathetic reactions). Eating and the presence of food in the gut activate the vagus nerve, which promotes digestive secretions and a pattern of smooth muscle activity that is digestion. With the body at rest the parasympathetic nervous system is primarily in control, leading a relaxed, normal digestive function. Any threat or stressor induces a state of arousal, interrupting gut function due to the stimulation of the sympathetic nervous system.
Measurements of autonomic nerve activity have shown that increased sympathetic activity is associated with diarrhea and that low vagal tone is associated with constipation. The use of experimental stressors to induce a state of tension and arousal has been associated with enhanced visceral sensitivity, irregular contractility in the small intestine, and accelerated small bowel and colonic transit times, thus diarrhea.
The brain can influence the transmission of information from the gut to the brain, as well as the influence the activation of visceral reflexes by means of descending inhibitory and excitatory nerve pathways. During relaxed normal digestion, the inhibitory signals dampen sensory transmission and ensure that normal gut events do not reach consciousness. Anxiety, anger and other causes of emotional arousal alter the balance of these descending neurological influences in the direction of excitation. More gastrointestinal events reach consciousness, and the events that normally cause slight discomfort may cause severe pain, and the pain is distributed over a wider area. Patients with irritable bowel syndrome often experience pain over a wide area, including the thigh, shoulder blade, and back.
Up-regulation of nerve traffic returning from the gut also reduces the stimulation required to induce gastrointestinal reflexes, leading to increased contractile responses. These result in diarrhea, vomiting, and disturbances in eating behavior.
Gastrointestinal sensitization induced by emotional arousal is also associated with increases in bronchiolar tone and reactivity (asthma-like), urinary frequency, and vasomotor instability (e.g. cold hands and/or feet, headaches, flushing).
Sensitization of the sympathetic nervous system relates to the sweaty palms, cardiac palpitation, increased tendon jerks, and nervousness common in patients with IBS. In fact, anxiety could be the consequence of gastrointestinal sensitization rather than its cause.
States of diminished emotional arousal, including fatigue and depression, may enhance descending inhibitory nerves from the brain and reduce intestinal sensitivity. This in turn can cause constipation.
All of this complicated neurological control of gastrointestinal function may help to explain why the symptoms of irritable bowel syndrome are not constant, but can change from day to day and at different times of day, why diarrhea may alternate with constipation, and why IBS sufferers can experience dramatic changes in mood. Even in normal subjects, GI sensitivity and motility can be increase by sleep deprivation, stress, focused attention, and anger and can be reduced by relaxation, sadness, and distraction.
Dr. Stephen Wangen
IBS Treatment Center and Center for Food Allergies
11300 Roosevelt Way NE Suite 100 Seattle, WA 98125 • 206-264-1111
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