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 lit
erature documenting an association between psychosocial factors and ulcer i
s not invalidated by the discovery of Helicobacter pylori. Physical and psy
chological stressors interact to induce ulcers in animal models, concrete l
ife difficulties and subjective distress predict the development of ulcers
in prospective cohorts, shared catastrophes such as war and earthquakes lea
d to surges in hospitalizations for complicated ulcers, and stress or anxie
ty can worsen ulcer course. Many known ulcer risk factors, including smokin
g, nonsteroidal anti-inflammatory drug use, heavy drinking, loss of sleep a
nd skipping breakfast, can increase under stress; the association of low so
cioeconomic status with ulcer is also accounted for in part by psychosocial
factors. Among possible physiological mechanisms, stress may induce gastri
c hypersecretion, reduce acid buffering in the stomach and the duodenum, im
pair gastroduodenal blood flow, and affect healing or inflammation through
psychoneuroim-munological mechanisms. Psychosocial factors seem to be parti
cularly prominent among idiopathic or complicated ulcers, but they are prob
ably 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 p
ylorus, while gastrointestinal damage by nonsteroidal anti-inflammatory dru
gs can also be potentiated by stress. Although the clinical importance of p
eptic ulcer is fading along with the millenium, due to secular trends and n
ew therapies, it remains worthy of study as a splendid example of the biops
ychosocial model.