Peptic ulcer disease (PUD) was first described centuries ago, and its pathogenesis and management have always been themes of discussion. Long ago physicians emphasised the importance of food and environmental factors in the aetiology and management of PUD. In 30 BC, Celsus recognised that certain foods were acidic and recommended that “if the stomach is infested with an ulcer…., light and gelatinous food must be used…. and everything acrid and acid is to be avoided.”(1) It is possible that food ingested may cause mechanical injury, mucosal breach and ulcer formation. Although the relationship between ulceration and diet remains unsettled, a number of theories exist explaining ulcer formation and its remedy. Modern physicians like Benjamin Sippy were the early advocators of bland diet and antacids.(2) The only cure of PUD held in high favour in earlier days was surgery and vagotomy. However the invention of H2 blockers and proton pump inhibitors in the 70’s and 80’s proved a phenomenal breakthrough in treatment; they dramatically reduced the number of surgeries performed, augmented ulcer healing and evinced the major role of acid in PUD. Subsequently with the recognition of the bacterial role (Helicobacter pylori) in the pathogenesis of this disease in the late 80’s, experts seemingly went the other extreme, in discarding altogether, the roles of diet and stress in the aetiology of peptic ulcer.(3)

Is H.pylori the primary and only cause of PUD? Is that the ultimate answer? Inspite of a prevalence as high as 80% of H.pylori infection in developing countries,(4) the occurrence of PUD is not excessive.  Moreover, about 40% patients with duodenal ulcer (DU) may be H.pylori negative in areas with low prevalence of H.pylori. Even after complete H. pylori eradication, recurrence of DU within 6 months in some reports has been up to 20%.(5) Hence H.pylori remains a silent spectator, perhaps somewhat like Mycobacterium tuberculosis, waiting for the right opportunity to cause injury. But what are the contributing factors that may create this opportunity?

Most of the dietary advice is more often based on mere impression and prejudice rather than fact. This is mainly because obtaining a clear idea of the part played by diet in the causation of peptic ulcer is often difficult to ascertain. It is even harder to determine the mechanisms by which any postulated dietary factor operates. Nevertheless, we cannot ignore the dual and contrary effects of diet, even if diet modification does not lead to curing or healing of the ulcer, small manipulations in the patient’s diet may always help in relieving the symptoms.(6)

In this issue of the journal, Singh et al found no association between diet and lifestyle factors, and ulcer healing and H.pylori eradication.(7) However, they reported an association between body mass index (BMI) and per capita income with H.pylori eradication and ulcer healing, respectively. The medical literature focuses on diet and lifestyle as risk factors for DU. There are very few studies which have examined ulcer healing and H.pylori eradication in relation to diet.

Most of the studies on BMI with respect to DU have reported that higher BMI is a risk factor for developing DU. BMI is indirectly related to physical activity. Cheng et al(8)found that both moderately active and active men had a 45% to 60% reduced risk of DU. On the contrary Katschinski et al(9) showed that even after adjusting for age, sex, smoking and social class, physical work was associated with duodenal ulcer, with a relative risk for moderate and high activity compared with sedentary work being 1.3 (95% CI, 0.6-3.0) and 3.6 (95% CI, 1.3-7.8), respectively. Cross-sectional data from the British Regional Heart Study indicated that BMI and the proportion of obese people tend to fall with increasing exercise, and so the effect of BMI on the risk of developing DU would likely be similar to the effect of physical activity.(10)Increased BMI was also associated with abnormal upper endoscopic findings such as erosive gastritis, gastric ulcer, duodenal ulcer and reflux oesophagitis.(11)

Kamada et al(12) reported a significant increase in BMI after eradication of H.pylori and increase in the incidence of obesity in patients with peptic ulcer. The probable reason for increased obesity after H.pylori eradication may be the increased ghrelin expression following eradication therapy leading to increase in appetite and fat storage.(13) However in the present study the authors associated a higher BMI with eradication of H.pylori.(7)

The socioeconomic status (SES) has always been associated with H.pylori infection, along with morbidity and mortality due to PUD. Higher death rate was associated with lower socioeconomic class.(14) H.pylori infection increases with deprived socioeconomic conditions while it declines with improved hygiene, smaller families and better socioeconomic conditions.(15) In the literature not much information is available on the association between SES and ulcer healing. Mason et al,(16) reported that both Indian and black DU patients experienced greater stress including low income and dissatisfaction when compared with controls. Poor SES has also been reported to work independently of Helicobacter pylori infection as an important risk factor for PUD.(17)

In the present study the reason for the association between a high BMI and increased eradication of H.pylori is not clear. In fact a better socioeconomic status should rather have been associated with greater H.pylori eradication and BMI with ulcer healing. Moreover ulcer healing and H.pylori eradication are interlinked, as higher eradication should be accompanied with a higher healing rate. In this regard the observation does not have a plausible explanation.

Tovey et al(4) suggested that reduced mucosal resistance results in duodenal gastric metaplasia which permits colonisation of the duodenum with H.pylori. Evidence suggests that this mucosal resistance may be related to the diet. This theory would explain the mystery of regional variations in DU prevalence unrelated to H.pylori prevalence.

Till date the exact pathogenesis and healing of the duodenal ulcer remain an enigma. But have we taken it too far by making H. pylori the sole culprit? Are all the other factors including diet simply bystanders?  Well planned and more conclusive studies are required before we discard the role of diet and other factors completely.

REFERENCES

1.     Modlin IM, Sachs G. The discovery of acid In: Acid related diseases: Biology and treatment. Schetztor-Verlag GmbH, Konstanz, Milano. 1998;3–7.

2.     Modlin IM, Sachs G. Gastric and duodenal ulcer disease In: Acid related diseases: Biology and treatment. Schetztor-Verlag GmbH, Konstanz, Milano. 1998;199–216

3.     Spiro HM. About this issue. J Clin Gastroenterol. 1995;21:175

4.     Megraud F. Epidemiology of Helicobacter pylori infection: where are we in 1995? Eur J Gastroenterol Hepatol. 1995;7:292–5

5.     Tovey FI, Hobsley M. Is Helicobacter pylori the primary cause of duodenal ulceration? J.Gastroenterol Hepatol. 1999;14:1053–6

6.     No authors listed. Eating and ulcers. Br Med J. 1980; 280:205–6

7.     Singh N, Deb R, Kashyap PC, Bhatia V, Ahuja V, Sharma MP. Body mass index and per capita income influence duodenal ulcer healing and H. pylori eradication whilst dietary factors play no part. Trop Gastroenterol. 2008;29:26–31

8.     Cheng Y, Macera CA, Davis DR, Blair SN. Physical activity and peptic ulcer. Does physical activity reduce the risk of developing peptic ulcer? West J Med. 2000;173:101–7

9.     Katschinski BD, Logan RF, Edmond M, Langman MJ. Physical activity at work and duodenal ulcer risk. Gut. 1991;32:983–6

10.   Weatherall R, Shaper AG. Overweight and obesity in middle-aged British men. Eur J Clin Nutr. 1988;42:221–31

11.   Kim HJ, Yoo TW, Park DI, Park JH, Cho YK, Sohn CI, et al. Influence of overweight and obesity on upper endoscopic findings. J Gastroenterol Hepatol. 2007;22:477–81

12.   Kamada T, Hata J, Kusuvoki H, Ito M, Tanaka S, Kawamura Y, et al. Eradication of Helicobacter pylori increases the incidence of hyperlipidaemia and obestiy in peptic ulcer patients. Dig Liver Dis. 2005;37:39–43

13.   Tatsuguchi A, Miyake K, Gudis K, Futagami S, Tsukui T, Wada K, et al. Effect of Helicobacter pylori infection on ghrelin expression in human gastric mucosa. Am J Gastroenterol. 2004;99:2121–7

14.   Susser M, Stein Z. Civilization and peptic ulcer. 1962. Int J Epidemiol. 2002;31:13–7.

15.   Susser M, Stein Z. Commentary: civilization and peptic ulcer 40 years on. Int J Epidemiol. 2002;31:18–21.

16.   Mason JB, Clark PM, Schlemmer L, Spitaels JM. Stressful life situations and perception of stress in black and Indian duodenal ulcer patients. S Afr Med J.1986;70:24–6

17.   Rosenstock SJ, Iorgensen T, Bonnevie O, Andersen LP. Does Helicobacter pylori infection explain all socio-economic differences in peptic ulcer incidence? Genetic and psychological markers for incident peptic ulcer disease in a large cohort of Danishadults. Scand J Gastroenterol. 2004;39:823–9