Stomach cancer risk factors

75% (78% in males and 69% in females) of stomach cancer cases each year in the UK are linked to major lifestyle and other risk factors.[1]

Stomach cancer is associated with a number of risk factors.[2,3]

Stomach Cancer Risk Factors

Increases risk ('sufficient' or 'convincing' evidence) May increase risk ('limited' or 'probable' evidence) Decreases risk ('sufficient' or 'convincing' evidence) May decrease risk ('limited' or 'probable' evidence)
  • Helicobacter pylori (H Pylori
  • Working in rubber production
  • Tobacco smoking
  • X-radiation, gamma-radiation
  • Asbestos (all forms
  • Epstein-Barr virus
  • Inorganic lead compounds
  • Nitrate or nitritea
  • Pickled vegetables (traditional Asian)
  • Salted fish, Chinese-style
  • Salt
  • Salted/salty foods
 
  • Non-starchy vegetablesb
  • Allium vegetablesb
  • Fruitsb

International Agency for Research on Cancer (IARC) and The World Cancer Research Fund/American Institute for Cancer Research (WCRF/AICR) classifications.

a Ingested under conditions that result in endogenous nitrosation. b Not salted or pickled.

Use our interactive tool to explore risk factors for stomach cancer.

More information about cancer risk factors evidence

References

  1. Parkin DM, Boyd L, Walker LC. 16. The fraction of cancer attributable to lifestyle and environmental factors in the UK in 2010. BJC 2011;105 Suppl 2:S77-81.
  2. Cogliano VJ, Baan R, Straif K, et al. Preventable exposures associated with human cancers. JNCI 2011;103:1827-39.
  3. Helicobacter and Cancer Collaborative Group. Gastric cancer and Helicobacter pylori: a combined analysis of 12 case control studies nested within prospective cohorts. Gut 2001;49:347-53.
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Helicobacter Pylori (H Pylori) infection is classified by the International Agency for Research on Cancer (IARC)as a cause of stomach cancer.[1] An estimated 32% of stomach cancers in the UK are linked to H Pylori infection.[2]

Stomach (non-cardia) cancer risk is 6 times higher in people with H Pylori infection, a pooled analysis showed.[3] This relates to H Pylori status 10+ years prior to stomach cancer diagnosis, which is the most appropriate measure: negative H Pylori status shortly before stomach cancer diagnosis may reflect infection clearance due to the cancer itself, as H Pylori does not colonise cancer/pre-cancer cells.[3]

Stomach cancer risk is higher in CagA-positive H Pylori than in CagA-negative H Pylori.[4,5] Stomach cancer risk among H Pylori-infected people is lower in those who receive H pylori eradication treatment, versus those who do not, a meta-analysis showed.[6]

Stomach (non-cardia) cancer risk is higher in people with H pylori infection probably because H Pylori can cause gastric atrophy, in a minority of infected people.[4,7]

H Pylori prevalence is falling in the UK, but it remains a problem in developing countries.[8,9,2]

References

  1. Cogliano VJ, Baan R, Straif K, et al. Preventable exposures associated with human cancers. JNCI 2011;103:1827-39.
  2. Parkin DM. 11. Cancers attributable to infection in the UK in 2010. BJC 2011;105 Suppl 2:S49-56.
  3. Helicobacter and Cancer Collaborative Group. Gastric cancer and Helicobacter pylori: a combined analysis of 12 case control studies nested within prospective cohorts. Gut 2001;49:347-53.
  4. Palli D, Masala G, Del Giudice G, et al. CagA+ Helicobacter pylori infection and gastric cancer risk in the EPIC-EURGAST study. IJC 2007;120:859-67.
  5. Huang JQ, Zheng GF, Sumanac K, et al. Meta-analysis of the relationship between cagA seropositivity and gastric cancer. Gastroenterology 2003;125:1636-44.
  6. Ford AC, Forman D, Hunt RH, Yuan Y, Moayyedi P. Helicobacter pylori eradication therapy to prevent gastric cancer in healthy asymptomatic infected individuals: systematic review and meta-analysis of randomised controlled trials. BMJ 2014;348:g3174.
  7. Helicobacter and Cancer Collaborative Group. Gastric cancer and Helicobacter pylori: a combined analysis of 12 case control studies nested within prospective cohorts. Gut 2001;49:347-53.
  8. Parkin DM. The global health burden of infection-associated cancers in the year 2002. IJC 2006;118:3030-44.
  9. Vyse AJ, Gay NJ, Hesketh LM, et al. The burden of Helicobacter pylori infection in England and Wales. Epidemiol Infect 2002;128:411-7.
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Tobacco smoking is classified by the International Agency for Research on Cancer (IARC) as a cause of stomach cancer.[1] An estimated 22% of stomach cancers in the UK are linked to smoking.[2]

Stomach cancer risk is 62% higher in male smokers compared with male never-smokers, meta-analyses have shown.[3-5] Stomach cancer risk is 20% higher in female smokers compared with female never-smokers, meta-analyses have shown.[3-5] Risk is higher in smokers for both cardia and non-cardia stomach cancer,[4] and increases with number of cigarettes smoked per day.[5] Stomach cancer risk is not higher in ex-smokers compared with never-smokers.[5] Smokeless tobacco is not associated with stomach cancer risk.[6,7]

References

  1. Cogliano VJ, Baan R, Straif K, et al. Preventable exposures associated with human cancers. JNCI 2011;103:1827-39.
  2. Parkin DM, Boyd L, Walker LC. 16. The fraction of cancer attributable to lifestyle and environmental factors in the UK in 2010. BJC 2011;105 Suppl 2:S77-81.
  3. La Torre G, Chiaradia G, Gianfagna F, et al. Smoking status and gastric cancer risk: an updated meta-analysis of case-control studies published in the past ten years. Tumori 2009;95:13-22.
  4. Ladeiras-Lopes R, Pereira AK, Nogueira A, et al. Smoking and gastric cancer: systematic review and meta-analysis of cohort studies. Cancer Causes Control 2008;19:689-701.
  5. Tredaniel J, Boffetta P, Buiatti E, et al. Tobacco smoking and gastric cancer: review and meta-analysis. IJC 1997;72:565-73.Lee PN, Hamling J. Systematic review of the relation between smokeless tobacco and cancer in Europe and North America. BMC Med 2009;7:36.Boffetta P, Aagnes B, Weiderpass E, et al. Smokeless tobacco use and risk of cancer of the pancreas and other organs. IJC 2005;114:992-5.
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Pickled vegetables (traditional Asian style) are classified by the International Agency for Research on Cancer (IARC) as a cause of stomach cancer, based on limited evidence.[1]

Stomach cancer risk is 28-56% higher in people with the highest intake of pickled foods, compared with those with the lowest, meta-analyses have shown.[2,3]

References

  1. Cogliano VJ, Baan R, Straif K, et al. Preventable exposures associated with human cancers. JNCI 2011;103:1827-39.
  2. Kim HJ, Lim SY, Lee JS, et al. Fresh and pickled vegetable consumption and gastric cancer in Japanese and Korean populations: a meta-analysis of observational studies. Cancer Sci 2010;101:508-16.
  3. Ren JS, Kamangar F, Forman D, et al. Pickled Food and Risk of Gastric Cancer--a Systematic Review and Meta-analysis of English and Chinese Literature. Cancer Epidemiol Biomarkers Prev 2012.
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Salt and salty foods are classified by the World Cancer Research Fund/American Institute for Cancer Research (WCRF/AICR) as a probable cause of stomach cancer,[1] and Chinese-style salted fish is classified by the International Agency for Research on Cancer (IARC) as a probable cause of stomach cancer, based on limited evidence.[2] An estimated 24% of stomach cancers in the UK (31% in males and 12% in females) are linked to eating more than 6g of salt per day.[3]

Stomach cancer risk is 68% higher in people with high salt intake compared with those with low salt intake, a meta-analysis showed.[4] Salt intake may increase the extent of H Pylori infection (the association between salt and stomach cancer risk may be limited to people with H Pylori infection[5]) and/or inflame/damage stomach tissue directly.[6] Variability between studies may reflect differences in salt intake assessment or confounding by other components of high-salt foods/diets.[7,8]

References

  1. World Cancer Research Fund, American Institute for Cancer Research. Food, nutrition, physical activity and the prevention of cancer: A global perspective. Washington: American Institute for Cancer Research; 2007.
  2. Cogliano VJ, Baan R, Straif K, et al. Preventable exposures associated with human cancers. JNCI 2011;103:1827-39.
  3. Parkin DM. 7. Cancers attributable to dietary factors in the UK in 2010. IV. Salt. BJC 2011;105 Suppl 2:S31-3.
  4. D'Elia L, Rossi G, Ippolito R, et al. Habitual salt intake and risk of gastric cancer: a meta-analysis of prospective studies. Clin Nutr. 2012 Aug;31(4):489-98.
  5. Shikata K, Kiyohara Y, Kubo M, et al. A prospective study of dietary salt intake and gastric cancer incidence in a defined Japanese population: the Hisayama study. IJC 2006;119:196-201.
  6. Peleteiro B, Lopes C, Figueiredo C, et al. Salt intake and gastric cancer risk according to Helicobacter pylori infection, smoking, tumour site and histological type. BJC 2011;104:198-207.
  7. Ge S, Feng X, Shen L, et al. Association between Habitual Dietary Salt Intake and Risk of Gastric Cancer: A Systematic Review of Observational Studies. Gastroenterol Res Pract 2012;2012:808120.
  8. Wang XQ, Terry PD, Yan H. Review of salt consumption and stomach cancer risk: epidemiological and biological evidence. World J Gastroenterol 2009;15:2204-13.
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Processed, smoked, grilled or barbecued meat is classified by the World Cancer Research Fund/American Institute for Cancer Research (WCRF/AICR) as a possible cause of stomach cancer, based on limited-suggestive evidence.[1] Nitrate or nitrite ingested under conditions that result in endogenous nitrosation (the production of nitrosamines in the stomach) is classified by the International Agency for Research on Cancer (IARC) as a probable cause of stomach cancer, based on limited evidence;[2] some processed meats contain nitrites.

Stomach cancer risk is not associated with processed meat intake, a meta-analysis of cohort studies showed; though there was some evidence of risk increase in case-control studies.[3,4]

Stomach cancer risk is lower in vegetarians compared with meat-eaters, a cohort study showed.[5]

Variability between studies may reflect differences by stomach cancer subsite or H Pylori status.[6]

References

  1. Rugge M, Correa P, Di Mario F, et al. OLGA staging for gastritis: a tutorial. Dig Liver Dis 2008;40:650-8.
  2. Cogliano VJ, Baan R, Straif K, et al. Preventable exposures associated with human cancers. JNCI 2011;103:1827-39.
  3. Zhu H1, Yang X, Zhang C, et al. Red and processed meat intake is associated with higher gastric cancer risk: a meta-analysis of epidemiological observational studies. PLoS One. 2013 Aug 14;8(8):e70955.
  4. Rugge M, Correa P, Di Mario F, et al. OLGA staging for gastritis: a tutorial. Dig Liver Dis 2008;40:650-8.
  5. Key TJ, Appleby PN, Crowe FL, et al. Cancer in British vegetarians: updated analyses of 4998 incident cancers in a cohort of 32,491 meat eaters, 8612 fish eaters, 18,298 vegetarians, and 2246 vegans. Am J Clin Nutr 2014 Jun;100(Supplement 1):378S-385S. [Epub ahead of print]
  6. Gonzalez CA, Jakszyn P, Pera G, et al. Meat intake and risk of stomach and esophageal adenocarcinoma within the European Prospective Investigation Into Cancer and Nutrition (EPIC). JNCI 2006;98:345-54.
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Working in rubber production is classified by the International Agency for Research on Cancer (IARC) as a cause of stomach cancer. [1] Asbestos and inorganic lead compounds are classified by IARC as probable causes of stomach cancer, based on limited evidence.[1] An estimated 3% of stomach cancers in men in the UK, and 0.3% in women in the UK, are linked to occupational exposures (including working as a painter, as well as the IARC-classified factors).[2]

References

  1. Cogliano VJ, Baan R, Straif K, et al. Preventable exposures associated with human cancers. JNCI 2011;103:1827-39.
  2. Bevan R, Young C, Holmes P, et al. Occupational cancer in Britain. Gastrointestinal cancers: liver, oesophagus, pancreas and stomach. Br J Cancer. 2012;107 Suppl 1:S33-40.
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Stomach cancer risk is higher in male survivors of head and neck, oesophageal and larynx cancers, with no association with previous cancer in females, a cohort study in France showed.[1]

Stomach cancer risk is higher in female survivors of breast cancer, with no association with previous cancer in males, a cohort study in Australia showed.[2]

Stomach cancer risk is higher in testicular, cervical, or thyroid cancer survivors, which probably reflects the effects of radiotherapy treatment.[3-6]

References

  1. Jégu J, Colonna M, Daubisse-Marliac L, et al. The effect of patient characteristics on second primary cancer risk in France. BMC Cancer. 2014 Feb 15;14:94.
  2. Youlden DR, Baade PD. The relative risk of second primary cancers in Queensland, Australia: a retrospective cohort study. BMC Cancer. 2011 Feb 23;11:83.
  3. Richiardi L, Scelo G, Boffetta P, et al. Second malignancies among survivors of germ-cell testicular cancer: A pooled analysis between 13 cancer registries. IJC 2007;120:623-31.
  4. Travis LB, Fossa SD, Schonfeld SJ, et al. Second cancers among 40,576 testicular cancer patients: focus on long-term survivors. JNCI 2005;97:1354-65.
  5. Chaturvedi AK, Engels EA, Gilbert ES, et al. Second cancers among 104,760 survivors of cervical cancer: evaluation of long-term risk. JNCI 2007;99:1634-43.
  6. Subramanian S, Goldstein DP, Parlea L, et al. Second primary malignancy risk in thyroid cancer survivors: a systematic review and meta-analysis. Thyroid 2007;17:1277-88.
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X radiation and gamma radiation are classified by the International Agency for Research on Cancer (IARC) as causes of stomach cancer.[1] An estimated 1% of stomach cancers in the UK are linked to radiation (radiotherapy for a previous cancer, or diagnostic radiology).[2]

References

  1. Cogliano VJ, Baan R, Straif K, et al. Preventable exposures associated with human cancers. JNCI 2011;103:1827-39.
  2. Parkin DM, Boyd L, Walker LC. 16. The fraction of cancer attributable to lifestyle and environmental factors in the UK in 2010. BJC 2011;105 Suppl 2:S77-81.
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Stomach cancer risk is 2-10 times higher in people with a family history of the disease, a review of case-control studies showed.[1]

References

  1. Yaghoobi M, Bijarchi R, Narod SA. Family history and the risk of gastric cancer. BJC 2010;102:237-42.
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1-3% of stomach cancers are linked to inherited stomach cancer predisposition syndromes, it is estimated.[1]

Stomach cancer risk is higher in people with BRCA2 Open a glossary item mutation in their family.[2] Stomach cancer risk is not associated with BRCA1  mutation.[3]

Stomach cancer occurs in around 70-80% of people with mutations in the E-cadherin (CDH1) gene, a cohort study showed.[4]

Stomach cancer risk is higher in people with hereditary non-polyposis colorectal cancer (HNPCC), Li-Fraumeni syndrome Open a glossary item, familial adenomatous polyposis (FAP), or Peutz-Jeghers syndrome.[5]

References

  1. Fitzgerald RC, Hardwick R, Huntsman D, et al. Hereditary diffuse gastric cancer: updated consensus guidelines for clinical management and directions for future research. J Med Genet 2010;47:436-44.
  2. Cancer risks in BRCA2 mutation carriers. The Breast Cancer Linkage Consortium. JNCI 1999;91:1310-6.
  3. Thompson D, Easton DF. Cancer Incidence in BRCA1 mutation carriers. JNCI 2002;94:1358-65.
  4. Pharoah PD, Guilford P, Caldas C. Incidence of gastric cancer and breast cancer in CDH1 (E-cadherin) mutation carriers from hereditary diffuse gastric cancer families. Gastroenterology 2001;121:1348-53.
  5. Caldas C, Carneiro F, Lynch HT, et al. Familial gastric cancer: overview and guidelines for management. J Med Genet 1999;36:873-80.
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Stomach cancer risk is 20% higher per 50g+ (6+ units) per day of alcohol consumed, compared with non- or occasional drinking, a meta-analysis showed.[1] Stomach cancer risk is not associated with moderate alcohol consumption, cohort studies have shown.[2-5]

References

  1. Tramacere I, Negri E, Pelucchi C, et al. A meta-analysis on alcohol drinking and gastric cancer risk. Ann Oncol 2012;23:28-36.
  2. Steevens J, Schouten LJ, Goldbohm RA, et al. Alcohol consumption, cigarette smoking and risk of subtypes of oesophageal and gastric cancer: a prospective cohort study. Gut 2010;59:39-48.
  3. Freedman ND, Abnet CC, Leitzmann MF, et al. A prospective study of tobacco, alcohol, and the risk of esophageal and gastric cancer subtypes. Am J Epidemiol 2007;165:1424-33.
  4. Larsson SC, Giovannucci E, Wolk A. Alcoholic beverage consumption and gastric cancer risk: A prospective population-based study in women. IJC 2007;120:373-7.
  5. Duell EJ, Travier N, Lujan-Barroso L, et al. Alcohol consumption and gastric cancer risk in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort. Am J Clin Nutr 2011;94:1266-75.
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Stomach cancer risk is higher in people with gastric atrophy Open a glossary item, and risk increases with the extent of the atrophy.[1] Not all gastric cardia cancers are associated with gastric atrophy (and therefore H Pylori infection) – for those which resemble oesophageal adenocarcinomas, gastric atrophy may even be protective.[2,3]

References

  1. Rugge M, Correa P, Di Mario F, et al. OLGA staging for gastritis: a tutorial. Dig Liver Dis 2008;40:650-8.
  2. Islami F, Sheikhattari P, Ren JS, et al. Gastric atrophy and risk of oesophageal cancer and gastric cardia adenocarcinoma--a systematic review and meta-analysis. Ann Oncol 2011;22:754-60.
  3. Hansen S, Vollset SE, Derakhshan MH, et al. Two distinct aetiologies of cardia cancer; evidence from premorbid serological markers of gastric atrophy and Helicobacter pylori status. Gut 2007;56:918-25.
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Stomach (cardia) cancer risk is more than doubled in people with reflux or excess acid, case-control studies have shown;[1,2] though some studies show no association.[3]

References

  1. Wu AH, Tseng CC, Bernstein L. Hiatal hernia, reflux symptoms, body size, and risk of esophageal and gastric adenocarcinoma. Cancer 2003;98:940-8.
  2. Lagergren J, Bergstrom R, Lindgren A, et al. Symptomatic gastroesophageal reflux as a risk factor for esophageal adenocarcinoma. NEJM 1999;340:825-31.
  3. Farrow DC, Vaughan TL, Sweeney C, et al. Gastroesophageal reflux disease, use of H2 receptor antagonists, and risk of esophageal and gastric cancer. Cancer Causes Control 2000;11:231-8.
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Stomach cancer risk is 24% higher in diabetic males compared with non-diabetic males, and 90% higher in diabetic females compared with non-diabetic females, a meta-analysis showed; the association may be limited to populations in east Asia.[1]

Stomach cancer risk among diabetics may be lower in metformin users compared with non-users, a meta-analysis of cohort studies showed; however meta-analysis of randomised control trials (RCTs) showed no association.[2]

References

  1. Shimoyama S. Diabetes mellitus carries a risk of gastric cancer: A meta-analysis. World J Gastroenterol. 2013 October 28; 19(40): 6902–6910.
  2. Franciosi M, Lucisano G, Lapice E, et al. Metformin therapy and risk of cancer in patients with type 2 diabetes: systematic review. PLoS One. 2013;8(8):e71583.
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Stomach cancer risk is more than doubled in people who had gastrectomy for stomach ulcer 20-30 years ago, a cohort study showed.[1]

Stomach acid levels may be lower after surgery, increasing H Pylori susceptibility.[1,2]

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Stomach cancer risk is 20% higher in people with blood group A versus those with blood group O, a cohort study showed.[1] The association may be limited to diffuse type stomach cancer.[2]

H Pylori susceptibility and response may vary by blood group.[1]

References

  1. Edgren G, Hjalgrim H, Rostgaard K, et al. Risk of gastric cancer and peptic ulcers in relation to ABO blood type: a cohort study. Am J Epidemiol 2010;172:1280-5.
  2. Song HR, Shin MH, Kim HN, et al. Sex-specific differences in the association between ABO genotype and gastric cancer risk in a Korean population. Gastric Cancer 2012.
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Stomach cancer risk is higher in people who have been prescribed proton pump inhibitors (PPIs) for stomach ulcer treatment, a cohort study showed.[1] This probably reflects H Pylori infection (which causes stomach ulcers) rather than a direct effect of PPIs.

References

  1. Poulsen AH, Christensen S, McLaughlin JK, et al. Proton pump inhibitors and risk of gastric cancer: a population-based cohort study. BJC 2009;100:1503-7.
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Epstein-Barr virus (EBV) infection is classified by the International Agency for Research on Cancer (IARC) as a probable cause of stomach cancer, based on limited evidence.[1] Around 9% of stomach cancers are EBV-positive, meta-analyses have shown.[2]

It is unclear how EBV infection is associated with increased stomach cancer risk.[3,4]

References

  1. Cogliano VJ, Baan R, Straif K, et al. Preventable exposures associated with human cancers. JNCI 2011;103:1827-39.
  2. Murphy G, Pfeiffer R, Camargo MC, et al. Meta-analysis shows that prevalence of Epstein-Barr virus-positive gastric cancer differs based on sex and anatomic location. Gastroenterology 2009;137:824-33.
  3. Camargo MC, Murphy G, Koriyama C, et al. Determinants of Epstein-Barr virus-positive gastric cancer: an international pooled analysis. BJC 2011;105:38-43.
  4. Boysen T, Friborg J, Stribolt K, et al. Epstein-Barr virus-associated gastric 
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Stomach (cardia) cancer risk is 21-22% higher in people who are overweight (body mass index [BMI] 25-30), and 61-82% higher in people who are obese (BMI 30+), meta-analyses have shown.[1,2] Non-cardia stomach cancer risk is not associated with overweight and obesity, meta-analyses have shown.[1,2]

References

  1. Chen Y, Liu L, Wang X, et al. Body mass index and risk of gastric cancer: a meta-analysis of a population with more than ten million from 24 prospective studies. Cancer Epidemiol Biomarkers Prev 2013;22(8):1395-408.
  2. Lin XJ, Wang CP, Liu XD, et al. Body mass index and risk of gastric cancer: a meta-analysis. Jpn J Clin Oncol 2014;44(9):783-91.
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Stomach cancer death risk is 5% lower per 6.5cm height increment, a meta-analysis showed;[1] the association may be limited to males.[2]

References

  1. Wormser D, Angelantonio ED, Kaptoge S, et al. Adult height and the risk of cause-specific death and vascular morbidity in 1 million people: individual participant meta-analysis. Int J Epidemiol. 2012 Oct;41(5):1419-33.
  2. Wiren S, Häggstrom C, Ulmer H, et al. Pooled cohort study on height and risk of cancer and cancer death. Cancer Causes Control. 2013 Oct 31.
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Stomach cancer risk is not associated with age at menarche (first menstrual period), age at menopause, parity, age at first birth, or oral contraceptive use, a meta-analysis showed.[1]

References

  1. Camargo MC, Goto Y, Zabaleta J, et al. Sex hormones, hormonal interventions, and gastric cancer risk: a meta-analysis. Cancer Epidemiol Biomarkers Prev 2012;21:20-38.
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Stomach cancer risk in women is 22-23% lower in those who have ever taken hormone replacement therapy (HRT) compared with HRT never-users, meta-analyses have shown.[1,2]

References

  1. Camargo MC, Goto Y, Zabaleta J, et al. Sex hormones, hormonal interventions, and gastric cancer risk: a meta-analysis. Cancer Epidemiol Biomarkers Prev 2012;21:20-38.
  2. Green J, Czanner G, Reeves G, et al. Menopausal hormone therapy and risk of gastrointestinal cancer: nested case-control study within a prospective cohort, and meta-analysis. IJC 2012;130:2387-96.
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Stomach cancer risk is 13-28% lower in the most physically active people compared with the least, meta-analyses have shown.[1-4]

References

  1. Chen Y, Yu C, Li Y. Physical activity and risks of esophageal and gastric cancers: a meta-analysis. RPLoS One. 2014 Feb 6;9(2):e88082.
  2. Behrens G, Jochem C, Keimling M, et al. The association between physical activity and gastroesophageal cancer: systematic review and meta-analysis. Eur J Epidemiol. 2014 Apr 6.
  3. Singh S, Varayil JE, Devanna S, et al. Physical Activity is associated with reduced risk of gastric cancer: a systematic review and meta-analysis. Cancer Prev Res (Phila). 2014 Jan;7(1):12-22.
  4. Behrens G, Jochem C, Keimling M, et al. The association between physical activity and gastroesophageal cancer: systematic review and meta-analysis. Eur J Epidemiol. 2014;29(3):151-70.
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Non-starchy vegetables, allium vegetables, and fruits are classified by the World Cancer Research Fund/American Institute for Cancer Research (WCRF/AICR) as probably protective against stomach cancer.[1] Pulses and dietary selenium are classified by WCRF/AICR as possibly protective against stomach cancer, based on limited-suggestive evidence.[1]

Stomach cancer risk is lower in people with the highest intake of the following foods versus those with the lowest, meta- and pooled analyses or systematic reviews have shown (note that associations for fruit and vegetables may be limited to case-control studies, not cohort studies, and may be limited to smokers[2-7]):

  • Fruit overall – 10-51% lower risk.[8,9]
  • Cruciferous vegetables – 19% lower risk.[10]
  • Citrus fruits – 28% lower risk.[11]
  • Tomato products – 27% lower risk.[12]
  • Selenium measured in blood or toenails – around 50% lower gastric cardia cancer risk[13] (no association for stomach cancer risk overall[14]).
  • Dietary fibre – 42% lower risk[15] (though may be limited to cereal fibre[16]).
  • Vitamin A – 34% lower risk.[17]

References

  1. World Cancer Research Fund, American Institute for Cancer Research. Food, nutrition, physical activity and the prevention of cancer: A global perspective. Washington: American Institute for Cancer Research; 2007.
  2. Steevens J, Schouten LJ, Goldbohm RA, et al. Vegetables and fruits consumption and risk of esophageal and gastric cancer subtypes in the Netherlands Cohort Study. IJC 2011;129:2681-93.
  3. Gonzalez CA, Pera G, Agudo A, et al. Fruit and vegetable intake and the risk of stomach and oesophagus adenocarcinoma in the European Prospective Investigation into Cancer and Nutrition (EPIC-EURGAST). IJC 2006;118:2559-66.
  4. Larsson SC, Bergkvist L, Wolk A. Fruit and vegetable consumption and incidence of gastric cancer: a prospective study. Cancer Epidemiol Biomarkers Prev 2006;15:1998-2001.
  5. Freedman ND, Subar AF, Hollenbeck AR, et al. Fruit and vegetable intake and gastric cancer risk in a large United States prospective cohort study. Cancer Causes Control 2008;19:459-67.
  6. Gonzalez CA, Lujan-Barroso L, de Mesquita HB, et al. Fruit and vegetable intake and the risk of gastric adenocarcinoma: A reanalysis of the european prospective investigation into cancer and nutrition (EPIC-EURGAST) study after a longer follow-up. IJC 2012; 131(12):2910-9.
  7. Serafini M, Jakszyn P, Lujan-Barroso L, et al. Dietary total antioxidant capacity and gastric cancer risk in the European prospective investigation into cancer and nutrition study. IJC 2012;131:E544-54.
  8. Wang Q, Chen Y, Wang X, et al. Consumption of fruit, but not vegetables, may reduce risk of gastric cancer: Results from a meta-analysis of cohort studies. Eur J Cancer. 2014 May;50(8):1498-509.
  9. Lunet N, Valbuena C, Vieira AL, et al. Fruit and vegetable consumption and gastric cancer by location and histological type: case-control and meta-analysis. Eur J Cancer Prev. 2007 Aug;16(4):312-27.
  10. Wu QJ, Yang Y, Wang J, et al. Cruciferous vegetable consumption and gastric cancer risk: a meta-analysis of epidemiological studies. Cancer Sci. 2013 Aug;104(8):1067-73.
  11. Bae JM, Lee EJ, Guyatt G. Citrus fruit intake and stomach cancer risk: a quantitative systematic review. Gastric Cancer 2008;11:23-32.
  12. Yang T, Yang X, Wang X, et al. The role of tomato products and lycopene in the prevention of gastric cancer: a meta-analysis of epidemiologic studies. Med Hypotheses. 2013 Apr;80(4):383-8.
  13. Steevens J, van den Brandt PA, Goldbohm RA, et al. Selenium status and the risk of esophageal and gastric cancer subtypes: the Netherlands cohort study. Gastroenterology 2010;138:1704-13.
  14. Vinceti M, Dennert G, Crespi CM, et al. Selenium for preventing cancer. Cochrane Database Syst Rev. 2014 Mar 30;3:CD005195.
  15. Mendez MA, Pera G, Agudo A, et al. Cereal fiber intake may reduce risk of gastric adenocarcinomas: the EPIC-EURGAST study. IJC 2007;121:1618-23.
  16. Zhang Z, Xu G, Ma M, et al. Dietary fiber intake reduces risk for gastric cancer: a meta-analysis. Gastroenterology. 2013 Jul;145(1):113-120.e3.
  17. Wu Y, Ye Y, Shi Y, et al. Association between vitamin A, retinol intake and blood retinol level and gastric cancer risk: A meta-analysis. Clin Nutr 2014. pii: S0261-5614(14)00171-X.
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Stomach cancer risk is lower people who use the following medications or have the following medical conditions, versus those who do not, meta- and pooled analyses, systematic reviews or large cohort studies have shown:

  • Aspirin – 29% lower risk with use 4.5 times per week (no further benefit with more frequent use), 28% lower risk with use for 12 years (greater protective effect with longer-term use); association limited to non-cardia stomach cancer.[1]
  • Statins - 16% lower risk.[2]

References

  1. Bosetti C, Rosato V, Gallus S, et al. Aspirin and cancer risk: a quantitative review to 2011. Ann Oncol 2012;23:1403-15.
  2. Chiu HF, Ho SC, Chang CC, et al. Statins are associated with a reduced risk of gastric cancer: a population-based case-control study. Am J Gastroenterol 2011;106:2098-103.
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The World Cancer Research Fund/American Institute for Cancer Research (WCRF/AICR) make no judgement on the association between stomach cancer risk and intake of cereals, dietary fibre, potatoes, nuts and seeds, herbs and spices, condiments, poultry, eggs, milk and dairy, fats and oils, sugars,fruit juice, coffee, tea, alcohol, dietary nitrate and nitrite, N-nitrosodimethylamine (note the International Agency for Research on Cancer (IARC) classifies ingested nitrate or nitrite under conditions that result in endogenous nitrosation as a possible cause of cancer based on limited evidence[1]), thiamine, riboflavin, vitamin C, vitamin D, multivitamin/mineral supplements, calcium, iron, selenium supplements, and carotenoids, due to limited evidence.[2]

Stomach cancer risk is not associated with the following factors, meta- and pooled analyses or systematic reviews have shown:

  • Vegetables overall[3] (although some evidence of lower risk[4]).
  • Dairy.[5]
  • Allium vegetables e.g. onions and garlic (though some evidence of lower risk in case-control studies).[6]
  • Fish.[7]
  • Tea (though some evidence of lower risk for women).[8]
  • Coffee.[9]
  • Vitamin D supplements.[10]
  • Beta-carotene supplements (though some evidence of higher risk with high doses and in smokers and asbestos-exposed workers).[11]

References

  1. Cogliano VJ, Baan R, Straif K, et al. Preventable exposures associated with human cancers. JNCI 2011;103:1827-39.
  2. World Cancer Research Fund, American Institute for Cancer Research. Food, nutrition, physical activity and the prevention of cancer: A global perspective. Washington: American Institute for Cancer Research; 2007.
  3. Wang Q, Chen Y, Wang X, et al. Consumption of fruit, but not vegetables, may reduce risk of gastric cancer: Results from a meta-analysis of cohort studies. Eur J Cancer. 2014 May;50(8):1498-509.
  4. Lunet N, Valbuena C, Vieira AL, et al. Fruit and vegetable consumption and gastric cancer by location and histological type: case-control and meta-analysis. Eur J Cancer Prev. 2007 Aug;16(4):312-27.
  5. Sun Y, Lin LJ, Sang LX, et al. Dairy product consumption and gastric cancer risk: a meta-analysis.. World J Gastroenterol 2014;20(42):15879-98.
  6. Turati F, Pelucchi C, Guercio V, et al. Allium vegetable intake and gastric cancer: A case-control study and meta-analysis.. Mol Nutr Food Res 2015;59(1):171-9.
  7. Yu XF, Zou J, Dong J. Fish consumption and risk of gastrointestinal cancers: a meta-analysis of cohort studies. World J Gastroenterol 2014;20(41):15398-412.
  8. Yu F, Jin Z, Jiang H, et al. Tea consumption and the risk of five major cancers: a dose-response meta-analysis of prospective studies. BMC Cancer. 2014;14:197.
  9. Xie F, Wang D, Huang Z, Guo Y. Coffee consumption and risk of gastric cancer: a large updated meta-analysis of prospective studies. Nutrients. 2014;6(9):3734-46.
  10. Bjelakovic G, Gluud LL, Nikolova D, et al. Vitamin D supplementation for prevention of cancer in adults. Cochrane Database Syst Rev 2014;6:CD007469.
  11. Druesne-Pecollo N, Latino-Martel P, Norat T, et al. Beta-carotene supplementation and cancer risk: a systematic review and metaanalysis of randomized controlled trials. IJC 2010;127:172-84.
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  • Age at menarche.[1]
  • Parity.[1]
  • Age at first birth.[1]
  • Use of oral contraceptives.[1]
  • Age at menopause[1] (though some evidence of higher risk with younger age at menopause, and with being post-menopausal versus pre-menopausal/menopausal[2]).

References

  1. Camargo MC, Goto Y, Zabaleta J, et al. Sex hormones, hormonal interventions, and gastric cancer risk: a meta-analysis. Cancer Epidemiol Biomarkers Prev 2012;21:20-38.
  2. Green J, Roddam A, Pirie K, et al. Reproductive factors and risk of oesophageal and gastric cancer in the Million Women Study cohort. BJC 2012;106:210-6.
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