Table of Contents Author Guidelines Submit a Manuscript
Gastroenterology Research and Practice
Volume 2014 (2014), Article ID 826910, 5 pages
http://dx.doi.org/10.1155/2014/826910
Research Article

Dietary Factors in Relation to Helicobacter pylori Infection

1Physiology Research Center (PRC) and Department of Physiology, Research Institute for Infectious Diseases of Digestive System, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz 61357-15794, Iran
2Department of Nutrition, Research Institute for Infectious Diseases of Digestive System, School of Paramedical, Ahvaz Jundishapur University of Medical Sciences, Ahvaz 61357-15794, Iran
3Research Institute for Infectious Diseases of Digestive System, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz 61357-15794, Iran
4Research Institute for Infectious Diseases of Digestive System, School of Medicine, Kerman University of Medical Sciences, Kerman 7618747653, Iran

Received 6 September 2014; Revised 9 November 2014; Accepted 9 November 2014; Published 2 December 2014

Academic Editor: Sergio Morini

Copyright © 2014 Seyyed Ali Mard et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Background and Aim. Helicobacter pylori (HP) and diet are both risk factors for gastric cancer. The aim of this study was to evaluate the Helicobacter pylori infection and dietary habits common in Khuzestan province. Methods. This cross-sectional study was conducted in 2011–2013 on 374 patients. Participants were interviewed using a food frequency questionnaire and tissue sample of the antrum was sent for pathology lab. The histopathological major variables were graded on a scale of 3 (mild, moderate, and severe) and data analyzed using nonparametric tests. Results. In this study, of 160 patients (43%) that were determined, 8.1 percent had severe contamination. Among dietary patterns, relationship between energy intake and carbohydrate with H. pylori was significant. A direct association was found between mean daily intakes of sausage and burgers with HP infection. Low intake of fresh vegetables and fruits was the most significant risk factors . Conclusion. There is a possibility that some dietary factors such as consumption of fast foods and low intake of fresh vegetables may increase the chance of HP and severity of this infection.

1. Introduction

Helicobacter pylori is a spiral, gram negative, acid tolerant, microaerophilic bacterium that lives in the stomach and duodenum [1, 2]. In Iran, H. pylori infection is present in nearly 90% of adult population [3] and appears to occur early in life, with >50% of children infected before age of 15 [4]. Despite the fact that the incidence of and mortality from gastric cancer have declined markedly worldwide over the past decades, gastric cancer is still the second most common cause of cancer-related death in the world [5]. Epidemiological data suggest that environmental factors are the predominant cause of this disease. The most important factors thought to be responsible for GC development are diet and Helicobacter pylori infection [6].

Besides the fact that H. pylori was introduced as a class I carcinogen [7], the infection is difficult to cure and requires various combination therapies [8]. Previous epidemiological studies have suggested that not only H. pylori infection but also varieties of environmental factors are important risk factors for GC [912]. It is believed that dietary factors may contribute to the H. pylori infection [13]. Adequate nutritional status, especially high consumption of fruits, vegetables, and vitamins, appears to protect against the pathological consequences of H. pylori infection [14]. Knoops et al. stressed the role of vitamin C as a chemopreventive factor in H. pylori gastric disorders [15, 16].

Furthermore, which environmental factor is involved in the development of GC among persons infected with H. pylori has rarely been investigated [17]. Therefore, we also investigated this point among H. pylori-infected subjects. The aim of this study was to evaluate whether there are differences in dietary habits between patients who were infected and subjects who were not infected.

2. Materials and Methods

The study was carried out in 2011–2013 in a group of patients from the Gastroenterological Unit of the Emam Khomeini Hospital in Ahvaz who had functional dyspepsia and had been referred for endoscopic examination of the upper digestive tract. To minimize any known confounding effects, the subjects with the following conditions have been excluded from the study: subjects with habits such as smoking, tobacco chewing, and alcohol consumption; on corticosteroid therapy at pharmacological levels for duration of more than 6 months; diabetes mellitus (except for easily controlled, non-insulin-dependent diabetes mellitus).

For all patients, energy and nutrient intakes were measured using a 3-day 24 h recall (two week days and one weekend day). Three-day food diary form contains foods at every meal, snack, and the amount consumed per person. A validated food frequency questionnaire [18] was also used to determine dietary habits during the previous year. The information was obtained through face to-face interviews, with standard food models, and a variety of measuring tools to evaluate intake. To help people to recall precise quantities of food eaten homemade dishes and cups were accounted. The participants were asked to indicate consumption of specified food in daily, weekly, monthly, and yearly bases. The selected frequency choice, given by the subjects for each food item from the food groups, was then converted to a weekly intake. All subjects were asked about the average frequency of intake and portion size of 125 items over the past year. The frequency of other food items was classified into 9 categories (never, 1–3/month, 1-2, 3-4, or 5-6/week, almost once/day, or 2-3, 4–6, or 7+ times/day).

Values of each food were converted to grams by using household measures. An interview on dietary habits was performed by a dietician. Nutrients were analyzed by Nutritionist IV software (N-Squared computing, Salem, OR, USA), which was modified for Iranian foods.

After upper GI endoscopy a tissue sample from antrum, body, and fundus in plate containing formalin buffer was sent to the pathology lab. All samples were examined by a pathologist. Contamination detection was performed with hematoxylin eosin (H&E). Semiquantitative method of scoring according to the Updated Sydney Classification System was undertaken. Statistical analysis was done using SPSS software (version 13). To correlate variables with normal and nonnormal distribution, Pearson’s and Spearman’s correlations, respectively, were used. All tests were two-tailed, and was the significance threshold.

3. Result

In this study, 374 patients were evaluated, 182 patients (48%) of them were females and 192 (52%) were males. Based on pathological studies on H. pylori infection, 214 healthy subjects (57%) and 160 patients (43%) were diagnosed that 8% of them had severe contamination and 37.5% and 54.4% had moderate and mild contamination, respectively.

As it is shown in Table 1, there was a significant correlation between energy and carbohydrate intake with H. pylori infection. (, 0.02) There was also a negative and significant correlation between daily intake of fish (), olive oil () and honey (), and peas and beans () with H. pylori infection.

tab1
Table 1: Nutrient intakes of healthy group and patient group per day.

Table 2 shows that there was positive relation between sausages (), hamburgers (), fat mayonnaise (), and soft drinks () with H. pylori infection.

tab2
Table 2: Food frequency data on meat samples from healthy group and patient group (per a week).

Taking weekly tomatoes (), onions (), green pepper (), apple (), and citrus fruits () was significantly lower than in healthy individuals (Table 3).

tab3
Table 3: Food frequency data of Fruits and vegetables intakes of Healthy group and Patient group (per a week).

Among the micronutrients reported, there were significant differences in intake of vitamin C and folate between the healthy subjects and patient groups (Table 4).

tab4
Table 4: Nutrient intakes of healthy group and patient group per day.

Subjects with H. pylori infection were categorized into 3 groups: severe, moderate, and mild contamination (on Revised Sydney System).

As it is shown in Table 5, there were negative and significant correlation and significant difference in tomatoes, onions, green pepper, apple, citrus fruits, fish, olive oil, and honey and peas intake with severity of H. pylori infection.

tab5
Table 5: Nutrient intakes of subject without infection and patients with different infection.

4. Discussion

Epidemiological studies have shown that H. pylori is probably one of the most common bacterial infections throughout the world, involving 30% of the population living in developed countries and up to 80%–90% of the population in developing countries [19].

The treatment of H. pylori is difficult, requires a two-week application of at least three medicines (proton pump inhibitors and two antibiotics) simultaneously, proves successful in only 80%–90% of cases, and is connected with the risk of adverse effects of therapy with antibiotics (15%–30% of the treated) [20, 21].

A synergistic interaction between H. pylori infection and diet has been suggested [22]. In this research, the dietary factors were evaluated. The aim of this retrospective study was to investigate potential differences in the dietary habits of patients with H. pylori infection (group I) and in the control not-infected group (group II). We demonstrated a significantly higher consumption of fruit, vegetables, and vitamin C among persons who were not infected. Vitamin C is highly concentrated in stomach mucosa and gastric juice and probably lowers the risk of gastric cancer and influences the course of H. pylori infection through a number of mechanisms [23, 24]. It has a positive impact on the stimulation and activity of granulocytes, macrophages, and lymphocytes and the production of immunoglobulin. The direct inhibitory impact of this vitamin on the growth of H. pylori is now being examined. Jarosz et al. [13] showed that four-week treatment of H. pylori infected patients with chronic gastritis with a high dose of vitamin C caused H. pylori eradication in 30% of cases. In those patients, a highly significant rise in gastric juice total vitamin C concentration was demonstrated, which persisted for at least four weeks after treatment. Ruiz et al. [25] found a causal association between H. pylori infection and low ascorbic acid levels in the gastric juice. Their findings supported two hypotheses that explain this phenomenon: increased oxidation and decreased secretion of ascorbic acid.

Also diet may provide noxious agents that contribute to H. pylori pathogenicity or protective agents that hamper its activity as related to the appearance of cancer diseases. Production of nitrosylating species plays a fundamental role in this regard. Observational cohort studies should ideally provide much more reliable evidence. Analysis of the data substantially confirmed the significant increased risk of developing GC due to high intake of total carbohydrates, processed meat, refined grains, and saturated fat [26, 27]. Prospective Investigation into Cancer and Nutrition study reported a significant increase of noncardiac cancer risk associated with intake of total meat, red meat, and processed meat [28].

Previous studies have reported the protection role of allium vegetables (onion) in gastric cancer [2729]. In this study, we also observed negative significant relation between onion consumption and H. pylori infection.

In this study there was positive relation between carbohydrate, sausages (), hamburgers (), fat mayonnaise (), and soft drinks intake () with H. pylori infection.

A high salt concentration in the stomach destroys the mucosal barrier, favors colonization by H. pylori, and leads to inflammation and damage-causing gastritis and diffuse erosion [30]. Processed meats have high salt concentration that contributes to H. pylori pathogenicity.

We observed a significant difference in intake of unsaturated fatty acid between two groups. It is thought that unsaturated fatty acid may inhibit gastric carcinogenesis. This inhibitory role was experimentally shown in mice [31]. An inverse association was reported between consumption of unsaturated fat and H. pylori with a significant dose dependency [32].

Although information on a potentially protective effect of vegetable oil consumption (unsaturated fat) or regarding specific types of unsaturated fatty acids and gastric cancer is very limited, but, in some studies, protective effect of vegetable oil consumption in gastric cancer has been reported [33].

Some studies of healthy adults demonstrated subclinical deficiency of some B vitamins and high prevalence of H. pylori infection [34].

H. pylori stimulates the macrophage system through the l-arginine/nitric oxide (NO) pathway [35]. As a consequence, chronic H. pylori infection of the human stomach may increase endogenous NO formation, yielding, after oxidation, the nitrosating agents N2O3 and N2O4, which can produce nitrosamines or cause other types of DNA damage [36]. Nitrosating organisms are capable of catalysing a reaction between nitrite and other organic nitrogen compounds present in the gastric juice to form potent genotoxic N-nitroso compounds (NOC) [37]. Nitrite levels in the gastric juice are increased during hypochlorhydria, which typically occurs during H. pylori-induced atrophic gastritis. This may result from bacteria within the stomach generating nitrite from dietary nitrate [38].

In present study among the micronutrients reported, there were significant differences in intake of folate between the healthy subjects and patient groups.

It has been established that chronic H. pylori infection causes atrophic gastritis and decreased absorption of vitamin folic acid in patients with this condition. Because methylation of homocysteine to methionine requires folate, an increased plasma homocysteine level is found in H. pylori-infected patients [14]. Our study has several potential limitations. First, we did not collect information about lifestyle. Second, our results could also be affected by measurement error in dietary intake, a common limitation of cross-sectional studies. However, prospective cohorts study is required, which evaluates the interaction between dietary habits and H. pylori infection. Third limitation was that level of education, socioeconomic, and race of subjects are not considered.

5. Conclusion

In summary, the present study on food interaction and H. pylori-infection displayed that a diet rich in fruit and vegetables and poor in meat, fat, and salt has a good prophylactic potential for cancer. Fruits and vegetables are sources (among other protective agents) of ascorbic acid, which were associated with a high effect against the progression of gastric carcinogenesis.

Thus, “diet for cancer prevention” can be recommended as a general role of well-being and can represent the basis for a rational health policy.

Conflict of Interests

None of the authors have any conflict of interests associated with this study.

References

  1. M. J. Blaser and J. C. Atherton, “Helicobacter pylori persistence: biology and disease,” The Journal of Clinical Investigation, vol. 113, no. 3, pp. 321–333, 2004. View at Publisher · View at Google Scholar · View at Scopus
  2. C. Montecucco and R. Rappuoli, “Living dangerously: how Helicobacter pylori survives in the human stomach,” Nature Reviews Molecular Cell Biology, vol. 2, no. 6, pp. 457–466, 2001. View at Publisher · View at Google Scholar · View at Scopus
  3. R. Malekzadeh, M. Sotoudeh, M. H. Derakhshan et al., “Prevalence of gastric precancerous lesions in Ardabil, a high incidence province for gastric adenocarcinoma in the northwest of Iran,” Journal of Clinical Pathology, vol. 57, no. 1, pp. 37–42, 2004. View at Publisher · View at Google Scholar · View at Scopus
  4. J. Mikaeili, R. Malekzadeh, A. Z. B. Ziad et al., “Prevalence of Helicobacter pylori in two Iranian provinces with high and low incidence of gastric carcinoma,” Archives of Iranian Medicine, vol. 3, no. 1, 2000. View at Google Scholar
  5. D. M. Parkin, F. Bray, J. Ferlay, and P. Pisani, “Global cancer statistics, 2002,” A Cancer Journal for Clinicians, vol. 55, no. 2, pp. 74–108, 2005. View at Publisher · View at Google Scholar · View at Scopus
  6. A. Rocco and G. Nardone, “Diet, H. pylori infection and gastric cancer: evidence and controversies,” World Journal of Gastroenterology, vol. 13, no. 21, pp. 2901–2912, 2007. View at Google Scholar · View at Scopus
  7. Working Group Report on Schistosomes, Liver Flukes and Helicobacter pylori, Lyon, France, 1994.
  8. N. E. Daryani, M. Taher, and S. Shirzad, “Helicobacter pylori infection: a review,” Iranian Journal of Clinical Infectious Diseases, vol. 6, no. 1, pp. 56–64, 2011. View at Google Scholar · View at Scopus
  9. Y. Watanabe, J. H. Kurata, S. Mizuno et al., “Helicobacter pylori infection and gastric cancer (A nested case-control study in a rural area of Japan),” Digestive Diseases and Sciences, vol. 42, no. 7, pp. 1383–1387, 1997. View at Publisher · View at Google Scholar · View at Scopus
  10. K. Ozasa, J. H. Kurata, A. Higashi et al., “Helicobacter pylori infection and atrophic gastritis: a nested case-control study in a rural town in Japan,” Digestive Diseases and Sciences, vol. 44, no. 2, pp. 253–256, 1999. View at Google Scholar
  11. K. Shibata, M. Moriyama, T. Fukushima, H. Une, M. Miyazaki, and N. Yamaguchi, “Relation of Helicobacter pylori infection and lifestyle to the risk of chronic atrophic gastritis: a cross-sectional study in Japan,” Journal of Epidemiology, vol. 12, no. 2, pp. 105–111, 2002. View at Publisher · View at Google Scholar · View at Scopus
  12. Y. Kuwahara, S. Kono, H. Eguchi, H. Hamada, K. Shinchi, and K. Imanishi, “Relationship between serologically diagnosed chronic atrophic gastritis, Helicobacter pylori, and environmental factors in Japanese men,” Scandinavian Journal of Gastroenterology, vol. 35, no. 5, pp. 476–481, 2000. View at Google Scholar · View at Scopus
  13. M. Jarosz, E. Rychlik, H. Siuba et al., “Dietary and socio-economic factors in relation to Helicobacter pylori re-infection,” World Journal of Gastroenterology, vol. 15, no. 9, pp. 1119–1125, 2009. View at Publisher · View at Google Scholar · View at Scopus
  14. A. Izzotti, P. Durando, F. Ansaldi, F. Gianiorio, and A. Pulliero, “Interaction between Helicobacter pylori, diet, and genetic polymorphisms as related to non-cancer diseases,” Mutation Research: Fundamental and Molecular Mechanisms of Mutagenesis, vol. 667, no. 1-2, pp. 142–157, 2009. View at Publisher · View at Google Scholar · View at Scopus
  15. K. T. B. Knoops, L. C. P. G. M. De Groot, D. Kromhout et al., “Mediterranean diet, lifestyle factors, and 10-year mortality in elderly European men and women: the HALE project,” Journal of the American Medical Association, vol. 292, no. 12, pp. 1433–1439, 2004. View at Publisher · View at Google Scholar · View at Scopus
  16. E. Riboli, N. Slimani, and R. Kaaks, “Identifiability of food components for cancer chemoprevention,” IARC Scientific Publications, no. 139, pp. 23–31, 1996. View at Google Scholar · View at Scopus
  17. A. Montani, S. Sasazuki, M. Inoue, K. Higuchi, T. Arakawa, and S. Tsugane, “Food/nutrient intake and risk of atrophic gastritis among the Helicobacter pylori-infected population of northeastern Japan,” Cancer Science, vol. 94, no. 4, pp. 372–377, 2003. View at Publisher · View at Google Scholar · View at Scopus
  18. A. F. Malekshah, M. Kimiagar, M. Saadatian-Elahi et al., “Validity and reliability of a new food frequency questionnaire compared to 24h recalls and biochemical measurements: pilot phase of Golestan cohort study of esophageal cancer,” European Journal of Clinical Nutrition, vol. 60, no. 8, pp. 971–977, 2006. View at Publisher · View at Google Scholar · View at Scopus
  19. J. Salgueiro, M. Zubillaga, C. Goldman et al., “Review article: is there a link between micronutrient malnutrition and Helicobacter pylori infection?” Alimentary Pharmacology and Therapeutics, vol. 20, no. 10, pp. 1029–1034, 2004. View at Publisher · View at Google Scholar · View at Scopus
  20. P. Malfertheiner, F. Megraud, C. O'Morain et al., “Current concepts in the management of Helicobacter pylori infection: the Maastricht III Consensus Report,” Gut, vol. 56, no. 6, pp. 772–781, 2007. View at Publisher · View at Google Scholar · View at Scopus
  21. J. Dzieniszewski and M. Jarosz, “Guidelines in the medical treatment of Helicobacter pylori infection,” Journal of Physiology and Pharmacology, vol. 57, no. 3, pp. 143–154, 2006. View at Google Scholar · View at Scopus
  22. N. Yamaguchi and T. Kakizoe, “Synergistic interaction between Helicobacter pylori gastritis and diet in gastric cancer,” The Lancet Oncology, vol. 2, no. 2, pp. 88–94, 2001. View at Publisher · View at Google Scholar · View at Scopus
  23. M. Jarosz, J. Dzieniszewski, E. Dabrowska-Ufniarz, M. Wartanowicz, S. Ziemlanski, and P. Reed I, “Effects of high dose vitamin C treatment on Helicobacter pylori infection and total vitamin C concentration in gastric juice,” European Journal of Cancer Prevention, vol. 7, no. 6, pp. 449–454, 1998. View at Publisher · View at Google Scholar · View at Scopus
  24. L.-Q. Shi and R.-L. Zheng, “DNA damage and oxidative stress induced by Helicobacter pylori in gastric epithelial cells: protection by vitamin C and sodium selenite,” Pharmazie, vol. 61, no. 7, pp. 631–637, 2006. View at Google Scholar · View at Scopus
  25. B. Ruiz, J. C. Rood, E. T. H. Fontham et al., “Vitamin C concentration in gastric juice before and after anti-Helicobacter pylori treatment,” The American Journal of Gastroenterology, vol. 89, no. 4, pp. 533–539, 1994. View at Google Scholar · View at Scopus
  26. R. W. Kneller, J. K. McLaughlin, E. Bjelke et al., “A cohort study of stomach cancer in a high-risk American population,” Cancer, vol. 68, no. 3, pp. 672–678, 1991. View at Publisher · View at Google Scholar · View at Scopus
  27. M. C. J. F. Jansen, H. B. Bueno-de-Mesquita, L. Räsänen et al., “Consumption of plant foods and stomach cancer mortality in the seven countries study. Is grain consumption a risk factor?” Nutrition and Cancer, vol. 34, no. 1, pp. 49–55, 1999. View at Publisher · View at Google Scholar · View at Scopus
  28. C. A. González, P. Jakszyn, G. Pera et al., “Meat intake and risk of stomach and esophageal adenocarcinoma within the European Prospective Investigation Into Cancer and Nutrition (EPIC),” Journal of the National Cancer Institute, vol. 98, no. 5, pp. 345–354, 2006. View at Publisher · View at Google Scholar · View at Scopus
  29. N. Muñoz, M. Plummer, J. Vivas et al., “A case-control study of gastric cancer in venezuela,” International Journal of Cancer, vol. 93, no. 3, pp. 417–423, 2001. View at Publisher · View at Google Scholar · View at Scopus
  30. M. L. Caruso and L. Fucci, “Histological identification of Helicobacter pylori in early and advanced gastric cancer,” Journal of Clinical Gastroenterology, vol. 12, no. 5, pp. 601–602, 1990. View at Google Scholar · View at Scopus
  31. R. A. Karmali, J. Marsh, and C. Fuchs, “Effect of omega-3 fatty acids on growth of a rat mammary tumor,” Journal of the National Cancer Institute, vol. 73, no. 2, pp. 457–461, 1984. View at Google Scholar · View at Scopus
  32. L. López-Carrillo, M. López-Cervantes, M. H. Ward, J. Bravo-Alvarado, and A. Ramírez-Espitia, “Nutrient intake and gastric cancer in Mexico,” International Journal of Cancer, vol. 83, no. 5, pp. 601–605, 1999. View at Google Scholar
  33. E. Buiatti, D. Palli, A. Decarli et al., “A case-control study of gastric cancer and diet in Italy,” International Journal of Cancer, vol. 44, no. 4, pp. 611–616, 1989. View at Publisher · View at Google Scholar · View at Scopus
  34. Y. L. Domínguez, M. Hernández, C. M. Matos, and D. Zhou, “Is B vitamins deficiency associated with prevalence of Alzheimer's disease in Cuban elderly?” Nutrition and Health, vol. 18, no. 2, pp. 103–118, 2006. View at Publisher · View at Google Scholar · View at Scopus
  35. K. B. Shapiro and J. H. Hotchkiss, “Induction of nitric oxide synthesis in murine macrophages by Helicobacter pylori,” Cancer Letters, vol. 102, no. 1-2, pp. 49–56, 1996. View at Publisher · View at Google Scholar · View at Scopus
  36. R. H. Liu and J. H. Hotchkiss, “Potential genotoxicity of chronically elevated nitric oxide: a review,” Mutation Research/Reviews in Genetic Toxicology, vol. 339, no. 2, pp. 73–89, 1995. View at Publisher · View at Google Scholar · View at Scopus
  37. D. Ziebarth, B. Spiegelhalder, and H. Bartsch, “N-nitrosation of medicinal drugs catalysed by bacteria from human saliva and gastro-intestinal tract, including Helicobacter pylori,” Carcinogenesis, vol. 18, no. 2, pp. 383–389, 1997. View at Publisher · View at Google Scholar · View at Scopus
  38. C. Mowat, A. Carswell, A. Wirz, and K. E. L. McColl, “Omeprazole and dietary nitrate independently affect levels of vitamin C and nitrite in gastric juice,” Gastroenterology, vol. 116, no. 4, pp. 813–822, 1999. View at Publisher · View at Google Scholar · View at Scopus