For many years, psychological stress has been assumed to contribute to the development of peptic ulcer disease (which involves ulcerating lesions in the stomach or duodenum). Researchers and health care providers have proposed more recently that stress might also be related to other gastrointestinal disorders such as non-ulcer dyspepsia (associated with symptoms of upper abdominal pain, discomfort and nausea persisting in the absence of any identifiable organic cause) and irritable bowel syndrome (defined as altered bowel habits plus abdominal pain in the absence of abnormal physical findings). In this article, the question is examined whether there is strong empirical evidence to suggest that psychological stress is a predisposing factor in the aetiology or exacerbation of these three gastrointestinal disorders.
Gastric and Duodenal Ulcer
There is clear evidence that humans who are exposed to acute stress in the context of severe physical trauma are prone to the development of ulcers. It is less obvious, however, whether life stressors per se (such as job demotion or the death of a close relative) precipitate or exacerbate ulcers. Lay people and health care practitioners alike commonly associate ulcers and stress, perhaps as a consequence of Alexander’s (1950) early psychoanalytic perspective on the topic. Alexander proposed that ulcer-prone persons suffered dependency conflicts in their relationships with others; coupled with a constitutional tendency toward chronic hypersecretion of gastric acid, dependency conflicts were believed to lead to ulcer formation. The psychoanalytic perspective has not received strong empirical support. Ulcer patients do not appear to display greater dependency conflicts than comparison groups, though ulcer patients do exhibit higher levels of anxiety, submissiveness and depression (Whitehead and Schuster 1985). The level of neuroticism characterizing some ulcer patients tends to be slight, however, and few could be considered as exhibiting psychopathological signs. In any case, studies of emotional disorder in ulcer patients have generally involved those persons who seek medical attention for their disorder; these individuals may not be representative of all ulcer patients.
The association between stress and ulcers follows from the assumption that certain persons are genetically predisposed to hypersecrete gastric acid, especially during stressful episodes. Indeed, about two thirds of duodenal ulcer patients show elevated pepsinogen levels; elevated levels of pepsinogen are also associated with peptic ulcer disease. Brady and associates’ (1958) studies of “executive” monkeys lent initial support to the idea that a stressful lifestyle or vocation may contribute to the pathogenesis of gastrointestinal disease. They found that monkeys required to perform a lever press task to avoid painful electric shocks (the presumed “executives”, which controlled the stressor) developed more gastric ulcers than comparison monkeys that passively received the same number and intensity of shocks. The analogy to the hard-driving businessman was very cogent for a time. Unfortunately, their results were confounded with anxiety; anxious monkeys were more likely to be assigned to the “executive” role in Brady’s laboratory because they learned the lever press task quickly. Efforts to replicate their results, using random assignment of subjects to conditions, have failed. Indeed, evidence shows that animals who lack control over environmental stressors develop ulcers (Weiss 1971). Human ulcer patients also tend to be shy and inhibited, which runs counter to the stereotype of the ulcer-prone hard-driving businessman. Finally, animal models are of limited utility because they focus on the development of gastric ulcers, while most ulcers in humans occur in the duodenum. Laboratory animals rarely develop duodenal ulcers in response to stress.
Experimental studies of the physiological reactions of ulcer patients versus normal subjects to laboratory stressors do not uniformly show excessive reactions in the patients. The premise that stress leads to increased acid secretion which, in turn, leads to ulceration, is problematic when one realizes that psychological stress usually produces a response from the sympathetic nervous system. The sympathetic nervous system inhibits, rather than enhances, the gastric secretion that is mediated via the splanchnic nerve. Besides hypersecretion other factors in the aetiology of ulcer have been proposed, namely, rapid gastric emptying, inadequate secretion of bicarbonate and mucus, and infection. Stress could potentially affect these processes though evidence is lacking.
Ulcers have been reported to be more common during wartime, but methodological problems in these studies necessitate caution. A study of air traffic controllers is sometimes cited as evidence supporting the role of psychological stress for the development of ulcers (Cobb and Rose 1973). Although air traffic controllers were significantly more likely than a control group of pilots to report symptoms typical of ulcer, the incidence of confirmed ulcer among the air traffic controllers was not elevated above the base rate of ulcer occurrence in the general population.
Studies of acute life events also present a confusing picture of the relationship between stress and ulcer (Piper and Tennant 1993). Many investigations have been conducted, though most of these studies employed small samples and were cross-sectional or retrospective in design. The majority of studies did not find that ulcer patients incurred more acute life events than community controls or patients with conditions in which stress is not implicated, such as gallstones or renal stones. However, ulcer patients reported more chronic stressors involving personal threat or goal frustration prior to the onset or recrudescence of ulcer. In two prospective studies, reports of subjects being under stress or having family problems at baseline levels predicted subsequent development of ulcers. Unfortunately, both prospective studies used single-item scales to measure stress. Other research has shown that slow healing of ulcers or relapse was associated with higher stress levels, but the stress indices used in these studies were unvalidated and may have been confounded with personality factors.
In summary, evidence for the role of stress in ulcer causation and exacerbation is limited. Large-scale population-based prospective studies of the occurrence of life events are needed which use validated measures of acute and chronic stress and objective indicators of ulcer. At this point, evidence for an association between psychological stress and ulcer is weak.
Irritable Bowel Syndrome
Irritable bowel syndrome (IBS) has been considered a stress- related disorder in the past, in part because the physiological mechanism of the syndrome is unknown and because a large proportion of IBS sufferers report that stress caused a change in their bowel habits. As in the ulcer literature, it is difficult to evaluate the value of retrospective accounts of stressors and symptoms among IBS patients. In an effort to explain their discomfort, ill persons may mistakenly associate symptoms with stressful life events. Two recent prospective studies shed more light on the subject, and both found a limited role for stressful events in the occurrence of IBS symptoms. Whitehead et al. (1992) had a sample of community residents suffering from IBS symptoms report life events and IBS symptoms at three-month intervals. Only about 10% of the variance in bowel symptoms among these residents could be attributed to stress. Suls, Wan and Blanchard (1994) had IBS patients keep diary records of stressors and symptoms for 21 successive days. They found no consistent evidence that daily stressors increased the incidence or severity of IBS symptomatology. Life stress appears to have little effect on acute changes in IBS.
The symptoms of non-ulcer dyspepsia (NUD) include bloating and fullness, belching, borborygmi, nausea and heartburn. In one retrospective study, NUD patients reported more acute life events and more highly threatening chronic difficulties compared to healthy community members, but other investigations failed to find a relationship between life stress and functional dyspepsia. NUD cases also show high levels of psychopathology, notably anxiety disorders. In the absence of prospective studies of life stress, few conclusions can be made (Bass 1986; Whitehead 1992).
Despite considerable empirical attention, no verdict has yet been reached on the relationship between stress and the development of ulcers. Contemporary gastroenterologists have focused mainly on heritable pepsinogen levels, inadequate secretion of bicarbonate and mucus, and Heliobacter pylori infection as causes of ulcer. If life stress plays a role in these processes, its contribution is probably weak. Though fewer studies address the role of stress in IBS and NUD, evidence for a connection to stress is also weak here. For all three disorders, there is evidence that anxiety is higher among patients compared to the general population, at least among those persons who refer themselves for medical care (Whitehead 1992). Whether this is a precursor or a consequence of gastrointestinal disease has not been definitively determined, although the latter opinion seems to be more likely to be true. In current practice, ulcer patients receive pharmacological treatment, and psychotherapy is rarely recommended. Anti-anxiety drugs are commonly prescribed to IBS and NUD patients, probably because the physiological origins of these disorders are still unknown. Stress management has been employed with IBS patients with some success (Blanchard et al. 1992) although this patient group also responds to placebo treatments quite readily. Finally, patients experiencing ulcer, IBS or NUD may well be frustrated by assumptions from family members, friends and practitioners alike that their condition was produced by stress.