Lifestyle, Stress, and Genes in Peptic Ulcer Disease

cordance for disease was significantly higher in MZ than in DZ twin pairs; the probandwise concordance rate was 23.6% (95% confidence interval (CI), 20.9%-26.3%) in MZ twins and 14.8% (95% CI, 13.3%-16.3%) in DZ twins. In the model-fitting analysis, a model with both addi- tive genetic and unshared environmental effects had the best goodness-of-fit. Thirty-nine percent (95% CI, 32%- 47%) of the liability to peptic ulcer disease was ex- plained by genetic factors and 61% (95% CI, 53%-68%) by individual environmental factors. In the incidence study (logistic regression analysis of the entire cohort initially free of peptic ulcer disease, with subjects diagnosed as having peptic ulcer after 1975 as cases), current smok- ing (relative risk, 2.2; 95% CI, 1.5-3.2) and high stress levels (relative risk, 3.2; 95% CI, 1.4-7.6) in men and regu- lar use of analgesics (relative risk, 3.3; 95% CI, 1.3-8.1) in women predicted peptic ulcer disease during the fol- low-up from 1976 to 1991. In the analysis of discordant pairs, smoking in men and regular use of analgesics in both sexes were predictors of peptic ulcer disease. Conclusions: The questionnaire and hospital usage data on peptic ulcer disease in the population-based twin co- hort suggest that the familial aggregation of the disease is modest, and attributable almost solely to genetic fac- tors. Environmental effects not shared by family mem- bers were significant predictors of disease, and they were attributable to smoking and stress in men and the use of analgesics in women. The minor effects of shared envi- ronment to disease liability do not support the concept that the clustering of risk factors, such as H pylori infec- tion, would explain the familial accumulation of peptic ulcer disease. Arch Intern Med. 1998;158:698-704