Search

Objective: To examine whether mental vulnerability, an enduring personality characteristic, predicts incident hospital-diagnosed ulcer over three decades., Materials and Methods: A population-based cohort study enrolled 3365 subjects with no ulcer history, ages 30-60, in 1982-3. Mental vulnerability, Helicobacter pylori IgG antibodies, socioeconomic status, and sleep duration were determined at baseline; non-steroidal antiinflammatory drug use, smoking, leisure time physical activity, and alcohol consumption both at baseline and in 1993-4. Hospital diagnoses of incident ulcer through 2011 were detected using the Danish National Patient Registry., Results: Ulcers were diagnosed in 166 subjects, including 83 complicated by bleeding or perforation. Age-, gender-, and socioeconomic status-adjusted associations were significant for mental vulnerability (Hazard Ratio (HR) 2.0, 95% Confidence Interval 1.4-2.8), Helicobacter pylori (HR 1.7, CI 1.2-2.3), smoking (HR 2.0, CI 1.3-3.1), heavy drinking (HR 1.6, CI 1.1-2.4), abstinence (HR 1.6, CI 1.1-2.5), non-steroidal antiinflammatory drugs (HR 2.1, CI 1.5-3.0), and sedentary lifestyle (HR 1.9, CI 1.4-2.7). Adjusted for all behavioral mediators, the HR for mental vulnerability was 1.5 (CI 1.0-2.2, p = .04). Mental vulnerability raised risk in Helicobacter pylori seropositive subjects and those exposed to neither Helicobacter pylori nor non-steroidal antiinflammatory drugs; its impact was virtually unchanged when analysis was limited to complicated ulcers., Conclusions: A vulnerable personality raises risk for hospital-diagnosed peptic ulcer, in part because of an association with health risk behaviors. Its impact is seen in 'idiopathic' and Helicobacter pylori-associated ulcers, and in acute surgical cases.

Objective: Research on ulcer psychosomatics has plummeted since the early 1970s, to the applause of many who argue that ulcer is simply an infectious disease. The purpose of this article is to discuss the relevance of ulcer psychogenesis in the age of Helicobacter pylori., Methods: A critical literature review was conducted., Results: There is a substantial and methodologically sound body of prospective studies linking stress with the onset and course of peptic ulcer. Psychosocial factors can be estimated to contribute to 30% to 65% of ulcers, whether related to nonsteroidal antiinflammatory drugs, H. pylori, or neither. The observed association between stress and ulcer is accounted for, in part, by recall bias, misreported diagnoses, and confounding by low socioeconomic status (a source of stress and of ulcer risk factors, such as H. pylori and on-the-job exertion) and by distressing medical conditions (which lead to use of nonsteroidal antiinflammatory drugs). Of the residual, true association, a substantial proportion is accounted for by mediation by health risk behaviors, such as smoking, sleeplessness, irregular meals, heavy drinking, and, again, nonsteroidal antiinflammatory drugs. The remainder results from psychophysiologic mechanisms that probably include increased duodenal acid load, the effects of hypothalamic-pituitary-adrenal axis activation on healing, altered blood flow, and impairment of gastroduodenal mucosal defenses., Conclusions: Peptic ulcer is a valuable model for understanding the interactions among psychosocial, socioeconomic, behavioral, and infectious factors in causing disease. The discovery of H. pylori may serve, paradoxically, as a stimulus to researchers for whom the concepts of psychology and infection are not necessarily a contradiction in terms.

The prevailing concept of peptic ulcer etiology has swung over entirely in just a few years from the psychological to the infectious, yet the rich literature documenting an association between psychosocial factors and ulcer is not invalidated by the discovery of Helicobacter pylori. Physical and psychological stressors interact to induce ulcers in animal models, concrete life difficulties and subjective distress predict the development of ulcers in prospective cohorts, shared catastrophes such as war and earthquakes lead to surges in hospitalizations for complicated ulcers, and stress or anxiety can worsen ulcer course. Many known ulcer risk factors, including smoking, nonsteroidal anti-inflammatory drug use, heavy drinking, loss of sleep and skipping breakfast, can increase under stress; the association of low socioeconomic status with ulcer is also accounted for in part by psychosocial factors. Among possible physiological mechanisms, stress may induce gastric hypersecretion, reduce acid buffering in the stomach and the duodenum, impair gastroduodenal blood flow, and affect healing or inflammation through psychoneuroimmunological mechanisms. Psychosocial factors seem to be particularly prominent among idiopathic or complicated ulcers, but they are probably operative in run of the mill H pylori disease as well, either through additive effects or by facilitating the spread of the organism across the pylorus, while gastrointestinal damage by nonsteroidal anti-inflammatory drugs can also be potentiated by stress. Although the clinical importance of peptic ulcer is fading along with the millennium, due to secular trends and new therapies, it remains worthy of study as a splendid example of the biopsychosocial model.