Ours is one of the first population based prospective studies in the H pylori era which has examined the impact of several risk factors for PUD, including H pylori. The most important findings were that H pylori infection, tobacco smoking, and use of minor tranquillisers were the main risk factors for PUD in this population of Danish adults. Leisure time energy expenditure reduced the likelihood of PUD. When analyses were confined to H pylori positive individuals, wine drinking showed a possible protective effect against PUD whereas intake of spirits increased ulcer risk. Use of NSAIDs did not affect GU or DU rates. A significant effect modification was demonstrated between tobacco smoking and H pylori infection, suggesting that tobacco smoking only increases PU risk in those who harbour H pylori.
Approximately 25% of all incident ulcers were found in those with no serological signs of H pylori
infection. Serology usually overestimates the prevalence of active H pylori
infection. The serology used in this study measures low molecular weight H pylori
antigens that are less strongly expressed in patients with gastric atrophy. The prevalence of infection may therefore be slightly underestimated in older people. The low specificity of the serology implies a high number of anti-Hp
false positive results. This misclassification weakens the impact of H pylori
infection on ulcer incidence. As the prevalence of H pylori
infection is low in Denmark,19
the proportion of ulcers that can be attributed to H pylori
infection is likely to be higher in countries where H pylori
infection is more common.
In contrast with data from the USA,7
tobacco smoking seems to be a more important risk factor for PUD than H pylori
infection in Denmark.20,21
Recent studies have suggested that tobacco smoking causes PU only if H pylori
infection is present.22–24
Our findings support this notion but tobacco smoking remained an independent risk factor for PUD despite control for H pylori
infection status. For that reason, we believe that ulcer patients should be advised to cease smoking irrespective of H pylori
The association between coffee drinking and PUD is controversial.26
The prospective nature of this study should prevent bias resulting from changes in coffee drinking habits due to medical advice.27,28
Still, it is possible that ulcer patients may have reduced their coffee intake prior to ulcer diagnosis because of abdominal discomfort.
Recent studies have shown a significant reduction in duodenal ulcer risk in American men who exercise regularly.29
Older studies suggest that physical inactivity increases the likelihood of ulcer disease.30,31
Moderate energy expenditure was shown to reduce the overall likelihood of ulcer disease in this study. Possible mechanisms could include a decrease in gastric acid secretion, lower levels of stress, and differences in dietary factors.32
infection rates in DU disease are declining.33,34
The seroprevalence of H pylori
infection was 87.2% in DU patients when those with borderline increased anti-Hp
IgG were considered infected. This value overestimates the true prevalence as some patients with borderline increased IgG antibodies are uninfected. When this subgroup was excluded, the seroprevalence of H pylori
infection was 56.4% in DU patients and even lower in GU patients. The present data therefore support the notion that the prevalence of H pylori
infection in DU patients is lower than previously thought and emphasises that eradication therapy should not be initiated without prior verification of the infection.35
The absence of an association between the use of NSAIDs and PUD incidence is surprising. The link between PUD and NSAID consumption is most pronounced in elderly patients who present with bleeding GUs. Possible explanations for our findings may be limited statistical power due to a low number of first time diagnosed GUs, few complicated ulcers, a relatively young cohort whose maximum age was 70 years, or invalid data on the use of NSAIDs at study entry. It is also possible that the impact of NSAIDs could be less marked in the general population who primarily suffers from uncomplicated ulcers.
Although the present analyses were adjusted for psychological vulnerability, the relationship between minor tranquillisers and ulcer incidence could simply be explained by differences in personality traits between ulcer patients and other subjects.36
PUD was previously considered a psychosomatic disease and tranquillisers may have been used to treat ulcer patients. As more effective treatments have become available within the last 20 years, this approach is unlikely to explain the present findings.
In this study, inferences were made between baseline exposure to possible risk factors and the subsequent development of a peptic ulcer. No data were available on whether the participant was exposed to the risk factor in question at the time of ulcer formation. Although most patients retain their lifestyle habits until disease develops, it is likely that some may have ceased risk factor behaviour during the observation period while others may have been exposed to a possible risk factor not reported at study entry. This non-differential misclassification will weaken possible relationships.
Moderate alcohol intake may reduce the likelihood of ulcer disease3,32,37,38
but large scale population based studies have failed to confirm this association.4,5
Intake of spirits increased the risk of PU in patients with increased anti-Hp
IgG in this study. Excessive alcohol consumption has been shown to increase the risk of PUD.39
Wine and beer drinking is associated with lower rates of H pylori
Biological mechanisms that could explain a possible beneficial effect of wine drinking on H pylori
infection and ulcer formation have been reported.42,43
Wine drinking could also be a marker for an overall healthier lifestyle.44
In conclusion, the aetiology of PUD is multifactorial. Tobacco smoking, H pylori infection, and use of minor tranquillisers but not NSAIDs are the main determinants to PUD in this cohort of Danish adults. Alcohol containing beverages in general did not relate to PUD incidence but intake of spirits was shown to increase the risk of PU in patients with increased anti-Hp IgG. Physical activity on the other hand reduced the risk of PUD in this subgroup.