When the Body Says No: The Cost of Hidden Stress (23 page)

Irritable bowel syndrome is said to affect up to 17 per cent of the population in the industrialized world and is the most frequent reason for which patients are referred to gastroenterologists. Interestingly, most people with symptoms that would qualify them for the diagnosis do not consult physicians.

The medical profession’s reflexive discomfort with uncertainty immensely complicates life for patients like Patricia and Fiona. We expect people to present us with diseases that fit neatly into symptom categories and bear unequivocal pathological findings. As the gastroenterologist Douglas Drossman points out, “Forty years ago, Renee Fox, a medical sociologist, noted that one of the most difficult transitions for medical students is to accept the uncertainty that is intrinsic to medical practice. But the biomedical model creates uncertainty for these common conditions that are not explained by underlying disease.”
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That uncertainty follows from our innate distrust of the patient’s story when we cannot match it with the hard data of physical examination techniques or scans, X-rays, blood tests, scopes, biopsies or electrodiagnostic tools. In such cases, the complainant finds her symptoms dismissed by doctors. Worse, she may be accused of drug-seeking behaviour, of being neurotic, manipulative, of “just looking for attention.” IBS patients, as well as people with chronic fatigue syndrome and fibromyalgia, often find themselves in that situation.

Magda, a physician herself, knew better than to go the emergency wards with her debilitating abdominal pains. She, too, was diagnosed with irritable bowel syndrome. “Mostly I had pain and distension. Nobody could find anything wrong with me, so we called it IBS. I had a colonoscopy and everything done. There was just nothing else to find. I guess you could call it a diagnosis of exclusion.

“There was hardly a day that I didn’t have a bellyache. Sometimes I was lying on the floor of my office, with heating pads, wondering how I would get through the afternoon and how I would drive myself home. It was extremely severe pain and frequent. I had abdominal pain 80 or 90 per cent of the time. There was not a day that, by mid-afternoon, I didn’t have abdominal pain—for years! I’m sure I would have been in emergency many times, too, with the severity of my pain—it’s just that I stay away from places like that because I know what happens there. I didn’t think anything helpful would happen. I didn’t go, but not because of the lack of severity.”

When not seen as the patient’s neurotic imaginings, the pain of IBS—and of undiagnosed abdominal pain in general—has been, until recently, thought to be caused purely by uncoordinated contractions of the intestines. Hence phrases like
spastic colon. Now
it has been confirmed that dysfunction in these disorders does not lie solely in the gut itself. A key issue is the way that the nervous system senses, evaluates and interprets pain.

Several observations have led to this new understanding of abdominal problems. Of particular interest are new findings on electrical and scan studies of the brain. When parts of the intestine are artificially distended, the response pattern in the brains of persons with functional abdominal pain characteristically varies from the brain activity of subjects who have no complaints of pain.
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Pain from distension of the colon or other parts of the intestine can also be studied by inserting an endoscope into the bowel and then inflating a balloon attached to the scope. In such studies, the functional patient groups repeatedly exhibit a hypersensitivity to distension. They report that the pain from this procedure is similar to the pain they usually experience. One study compared the effects of balloon inflation in IBS sufferers and controls. “Balloon inflation to 60 ml caused pain in 6 per cent of control subjects and 55 per cent of IBS patients…. Estimated gut wall tension at different volumes was similar in the two groups.
However, the incidence of pain in relation to wall tension was increased by nearly ten-fold in the IBS group.”
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Parallel observations have been made elsewhere in the digestive tract, from the esophagus to the small intestine. It appears, then, that in functional abdominal pain, physiological messages from the gut are
transmitted by the nervous system and received by the brain in an altered fashion. “There is a new area of investigation for patients with these disorders,” Dr. Drossman writes. “After decades of studying how IBS patients are distinguished from normals with regard to their gastrointestinal physiology, we are beginning to see differences in brain physiology.”

A type of scan known as positron emission tomography, or PET, measures the activity of brain regions by recording variations in blood flow. When study subjects experience distension of their rectums, a PET scan will indicate which part of the brain registers a response. With rectal distension, or even the anticipation of rectal distension, IBS patients activated the prefrontal cortex, an area not activated in normals.
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The prefrontal cortex is where the brain stores emotional memories. It interprets present stimuli, whether physical or psychological, in light of past experiences, which can date as far back as infancy. Activation in this part of the brain means that some event of emotional significance is occurring. In people who have experienced chronic stress, the prefrontal cortex and related structures remain in a state of hypervigilance, on the lookout for danger. Prefrontal activation is not a conscious decision by the individual; rather, it is the result of the automatic triggering of nerve pathways programmed long ago.

In another investigation, the electrical amplitudes of brainwaves evoked by sound stimuli were greater in IBS patients than in controls, again indicating a physiological hypervigilance.
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What accounts for these altered nervous-system responses? The answer emerges when we look not only at human organs but at human lives. There is a high incidence of abuse in the histories of patients with intestinal diseases and especially in those patients with IBS and other functional disorders.

In a 1990 study of women patients conducted at the gastroenterology clinic of the North Carolina School of Medicine, 44 per cent of the women reported some type of sexual and/or physical abuse. “Those with abuse history had a four-fold greater risk of pelvic pain, two to three times more non-abdominal symptoms (e.g., headaches, backaches, fatigue), as well as more lifetime surgeries.”
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In a more recent investigation at the same centre, fully two-thirds of the women interviewed had experienced abuse of a physical or sexual nature, or both. Again, abused patients were more likely to undergo various surgeries, such as
gallbladder operations, hysterectomies, and laparotomies. They also had “more pain, non-gastrointestinal somatic symptoms, bed disability days, psychological distress, and functional disability compared to those without sexual abuse.”
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It is self-evident that direct physical trauma—a severe brain contusion or the cutting or bruising of a nerve—could physiologically disrupt the nervous system. But how does psychological trauma exert its effect on the perception of pain?

The nervous system of the gut contains about one hundred million nerve cells—we have as many in the small intestine alone as there are in our entire spine!
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These nerves do more than coordinate the digestion and absorption of food and the elimination of waste—they also form part of our sensory apparatus. The gut responds to emotional stimuli by muscle contractions, blood flow changes and the secretion of a multitude of biologically active substances. Such brain-gut integration is essential for survival. Large volumes of blood, for example, may need to be diverted from the intestines to the heart and to the muscles of the limbs at a moment’s notice.

In turn, the gut is abundantly supplied with sensory nerves that carry information to the brain. Quite to the contrary of what was believed until recently, nerve fibres ascending from the intestines to the brain greatly outnumber ones descending from brain to gut.
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The brain relays to the gut data from sensory organs such as the eyes, the skin or the ears—or more correctly, relayed to the gut is the
interpretation
of such data by the brain’s emotional centres. The resulting physiological events in the gut then reinforce that emotional interpretation. The signals sent back to the brain give rise to gut feelings that we can apprehend consciously. If we lose touch with gut feelings, the world becomes less safe.

Obviously, life would not be livable if we felt every micro-event in our bodies. Digestion, breathing, blood flow to organs or limbs and myriad other functions must take place without intruding on consciousness. There has to be a threshold below which the brain does not register sensation, below which stimuli are accepted as unremarkable but above which the brain will be alerted to potential danger from within or without. There needs to be, in other words, a well-calibrated thermostat for pain and other sensations.

When there are too many “gut-wrenching” experiences, the neurological apparatus can become oversensitized. Thus, in the spinal cord the conduction of pain from gut to brain is adjusted as a result of psychological trauma. The nerves involved are set off by weaker stimuli. The greater the trauma, the lower becomes the sensory threshold. A normal amount of gas in the intestinal lumen and a normal level of tension in the intestinal wall will trigger pain in the sensitized person.

At the same time, the prefrontal areas of the cortex will be in a heightened state of vigilance, responding with distress to normal physiological processes. Along with increased pain, IBS patients report higher levels of anxiety, arousal and fatigue during rectal distension than do healthy people. During emotional stress, activity of the cortical regions amplifies the perception of distress.

Dr. Lin Chang is associate professor at the UCLA Medical School and co-director of the UCLA/CURE Neuroenteric Disease Program. He has summarized the current understanding of irritable bowel syndrome this way: “Both external and internal stressors contribute to the development of IBS. External stressors include abuse during childhood and other pathological stresses, which alter stress responsiveness and make a predisposed individual more vulnerable to developing IBS. Later in life, infections, surgery, antibiotics and psychosocial stressors can all contribute to IBS onset and exacerbation.”
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Stress can definitely induce contractions of the intestines. Women who have been sexually abused, for example, are prone to constipation when the muscles in their pelvic floor are chronically tight, incapable of relaxing with defecation. Alternatively, as people who have been terribly frightened have experienced, stress can set off uncontrollable movements in the colon. That was graphically illustrated in a young doctor-to-be who became an unwitting guinea pig in an experiment: “The investigators produced an elaborate hoax by suggesting to a fourth-year medical student undergoing a voluntary sigmoidoscopic examination that they were seeing a cancer. This led to increased contractility or ‘spasm’ of the bowel, which persisted until the hoax was explained. These type of studies confirmed that stress affects colonic function in normal persons and patients.”
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What has been discovered about IBS applies to other diseases of the gut. Patricia, in addition to her IBS, suffers heartburn that has seemed
to defy medical explanation. She speaks of it with bitterness. “I have this mysterious gastrointestinal problem that has never been diagnosed. I get acid from eating things that are completely bland. I’ve had to cut out anything with any flavour from my diet.

“I keep having tests, and they keep telling me I’m fine … or, I should say, one test did show a tiny bit of upset, but they tell me it’s totally out of proportion to what I actually feel. They put that thing up your nose and down into your esophagus, and they measure the amount of acid. There was, they said, a tiny bit of acid, but not enough to cause the degree of pain I’m having.

“I’ve been on Pantoloc for about three or four years. It’s supposed to wipe out acid completely, and I was only supposed to take it for six weeks. I also take Diovol or Gaviscon every day. I still have symptoms of acid, but they can’t find anything.”

The medical name for the distressing chronic experience of stomach acid flowing upward into the esophagus is gastroesophageal reflux disease (GERD). Researchers in 1992 studied the relationship of reflux symptoms to stress in subjects diagnosed with GERD. While the perception of reflux-associated heartburn by these patients was markedly increased during the stressful stimuli, the objective measures of acid levels were unchanged from one stimulus to another. Stress, in other words, lowered the pain threshold.
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An intestinal specialist unfamiliar with the neurophysiology or psychology of pain who looked at Patricia’s lower esophagus through an endoscope could, in good conscience, tell her that the acid reflux he observed was inadequate to explain the degree of her pain. And Patricia, in equally good conscience, would be incensed by what she perceived as the callous dismissal of a symptom that is a source of intense daily discomfort in her life.

This is not to say that people with GERD do not experience more frequent reflux than other people. They probably do, and, once more, it is a brain-gut problem. Investigators comparing healthy controls with reflux patients found that the resting pressure of the esophageal sphincter was more frequently low in the GERD subjects. The decreased efficiency of the sphincter muscles permitted more episodes of reflux.
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How can the mind and the brain contribute to reflux? It happens by means of the vagus nerve, which is responsible for the tone of the
muscles of the lower esophageal sphincter. In turn, the activity of the vagus is influenced by the hypothalamus. The hypothalamus, as we have seen, receives input from the emotional centres in the cortex that are susceptible to stress. Thus, in GERD, a lower pain threshold is combined with excessive relaxation of the sphincter—both phenomena that can be related to stress.