Diet and cancer

This advertisement suggests a healthy diet helps to prevent cancer.

Dietary factors are recognized as having a significant effect on the risk of cancers, with different dietary elements both increasing and reducing risk. Diet, physical inactivity, and obesity may be related to up to 30–35% of cancer deaths.[1] One review in 2011 suggested that total caloric intake influences cancer incidence and possibly progression.[2]

While many dietary recommendations have been proposed to reduce the risk of cancer, few have significant supporting scientific evidence.[2] Obesity and drinking alcohol are confirmed causes of cancer.[2] Lowering the drinking of beverages sweetened with sugar is recommended as a measure to address obesity.[3] A diet low in fruits and vegetables and high in red meat has been implicated but not confirmed,[4] and the effect may be small for well-nourished people who maintain a healthy weight.[2]

Some specific foods are linked to specific cancers. Studies have linked eating red or processed meat to an increased risk of breast cancer, colon cancer,[3] prostate cancer,[5] and pancreatic cancer, which may be partially explained by the presence of carcinogens in foods cooked at high temperatures.[6][7] Aflatoxin B1, a frequent food contaminate, causes liver cancer,[8] but drinking coffee is associated with a reduced risk.[9] Betel nut chewing causes oral cancer.[8] The differences in dietary practices may partly explain differences in cancer incidence in different countries. For example, stomach cancer is more common in Japan due to its high-salt diet[8][10] and colon cancer is more common in the United States. Immigrant communities tend to develop the risk of their new country, often within one generation, suggesting a substantial link between diet and cancer.[11]

Dietary recommendations for cancer prevention typically include weight management and eating "mainly vegetables, fruit, whole grains and fish, and a reduced intake of red meat, animal fat, and refined sugar."[2]

Types of diet

Restrictive diets

A number of diets and diet-based regimes are claimed to be useful against cancer. Popular types of "anti-cancer" diet include the Breuss diet, Gerson therapy, the Budwig protocol and the macrobiotic diet. None of these diets has been found to be effective, and some of them have been found to be harmful.[12]

There is insufficient evidence to support the use of the ketogenic diet as a standard treatment for cancer.[13]

Dietary patterns

Nutritional epidemiologists use multivariate statistics, such as principal components analysis and factor analysis, to measure how patterns of dietary behavior influence the risk of developing cancer.[14] (The most well-studied dietary pattern is the mediterranean diet.) Based on their dietary pattern score, epidemiologists categorize people into quantiles. To estimate the influence of dietary behavior on risk of cancer, they measure the association between quantiles and the distribution of cancer prevalence (in case-control studies) and cancer incidence (in longitudinal studies). They usually include other variables in their statistical model to account for the other differences between people with and without cancer (confounders). For breast cancer, there is a replicated trend for women with a more "prudent or healthy" diet, i.e. higher in fruits and vegetables, to have a lower risk of cancer.[15] A "drinker dietary pattern" is also associated with higher breast cancer risk, while the association is inconsistent between a more westernized diet and elevated risk of breast cancer.

Dietary components

Alcohol

Alcohol is associated with an increased risk of a number of cancers.[16] 3.6% of all cancer cases and 3.5% of cancer deaths worldwide are attributable to drinking of alcohol.[17] Breast cancer in women is linked with alcohol intake.[2][18] Alcohol also increases the risk of cancers of the mouth, esophagus, pharynx and larynx,[19] colorectal cancer,[20][21] liver cancer,[22] stomach[23] and ovaries.[24] The International Agency for Research on Cancer (Centre International de Recherche sur le Cancer) of the World Health Organization has classified alcohol as a Group 1 carcinogen. Its evaluation states, "There is sufficient evidence for the carcinogenicity of alcoholic beverages in humans. …Alcoholic beverages are carcinogenic to humans (Group 1)."[25]

Processed and red meat

On October 26, 2015, the International Agency for Research on Cancer of the World Health Organization reported that eating processed meat (e.g., bacon, ham, hot dogs, sausages) or red meat was linked to some cancers.[26][27][28]

Fiber, fruits and vegetables

The evidence on the effect of dietary fiber on the risk of colon cancer is mixed with some types of evidence showing a benefit and others not.[3] Eating fruit and vegetables while it has a benefit, has less benefit on reducing cancer than once thought.[3]

A 2014 study found fruit but not vegetables protected against upper gastrointestinal tract cancer.[29] While fruit, vegetable and fiber protected against colorectal cancer and fiber protected against liver cancer.[29]

Flavonoids

Flavonoids (specifically flavonoids such as the catechins) are "the most common group of polyphenolic compounds in the human diet and are found ubiquitously in plants."[30] While some studies have suggested flavonoids may have a role in cancer prevention, others have been inconclusive or suggested they may be harmful.[31][32]

Mushrooms

According to Cancer Research UK, "there is currently no evidence that any type of mushroom or mushroom extract can prevent or cure cancer", although research into some species continues.[33]

Nutrient bioactives

According to the American Cancer Society, although laboratory research has shown the possibility of some connection between soybeans and cancer, as yet there is no conclusive evidence about the anti-cancer effect of soy on human beings.[34]

Laboratory experiments have found that turmeric might have an anti-cancer effect.[35] Although trials are ongoing, large doses would need to be taken for any effect. It is not known what, in any, positive effect turmeric has for human beings with cancer.[36]

Although green tea has been promoted for its anti-cancer effect, research into it has produced mixed results; it is not known if it helps people prevent or treat cancer.[37][38] A review of all published studies by the US Food and Drug Administration in 2011 concluded it is very unlikely that green tea prevents any kind of cancer in humans.[38]

Resveratrol has shown anti-cancer activity in laboratory experiments, but as of 2009, there is no evidence of an effect on cancer in humans.[39][40]

Vitamin D supplements have been widely marketed on the internet and elsewhere for their claimed anti-cancer properties.[41] There is however insufficient evidence to recommend that vitamin D be prescribed for people with cancer, although there is some evidence that hypovitaminosis D may be associated with a worse outcome for some cancers.[42] A 2014 systematic review by the Cochrane Collaboration found, "no firm evidence that vitamin D supplementation decreases or increases cancer occurrence in predominantly elderly community-dwelling women."[43]

Mechanisms of action

Methionine metabolism

The methionine metabolism pathway. DHF, dihydrofolate; dSAM, decarboxylated S-adenosylmethionine; hCys, homocysteine; ME, methyl group; MetTR-1-P, 5-methylthioribose-1-phosphate; MT, methyltransferase; MTA, methylthioadenosine; MTHF, methylenetetrahydrofolate; SAH, S-adenosyl-L-homocysteine; SAM, S-adenosyl methionine; SUB, substrate.

Although numerous cellular mechanisms are involved in food intake, many investigations over the past decades have pointed out defects in the methionine metabolic pathway as cause of carcinogenesis.[44][45] For instance, deficiencies of the main dietary sources of methyl donors, methionine and choline, lead to the formation of liver cancer in rodents.[46][47] Methionine is an essential amino acid that must be provided by dietary intake of proteins or methyl donors (choline and betaine found in beef, eggs and some vegetables). Assimilated methionine is transformed in S-adenosyl methionine (SAM) which is a key metabolite for polyamine synthesis, e.g. spermidine, and cysteine formation (see the figure on the right). Methionine breakdown products are also recycled back into methionine by homocysteine remethylation and methylthioadenosine (MTA) conversion (see the figure on the right). Vitamins B6, B12, folic acid and choline are essential cofactors for these reactions. SAM is the substrate for methylation reactions catalyzed by DNA, RNA and protein methyltransferases.

Growth factor (GF) and steroid/retinoid activation of PRMT4.

The products of these reactions are methylated DNA, RNA or proteins and S-adenosylhomocysteine (SAH). SAH has a negative feedback on its own production as an inhibitor of methyltransferase enzymes. Therefore, SAM:SAH ratio directly regulates cellular methylation, whereas levels of vitamins B6, B12, folic acid and choline regulates indirectly the methylation state via the methionine metabolism cycle.[48][49] A near ubiquitous feature of cancer is a maladaption of the methionine metabolic pathway in response to genetic or environmental conditions resulting in depletion of SAM and/or SAM-dependent methylation. Whether it is deficiency in enzymes such as methylthioadenosine phosphorylase, methionine-dependency of cancer cells, high levels of polyamine synthesis in cancer, or induction of cancer through a diet deprived of extrinsic methyl donors or enhanced in methylation inhibitors, tumor formation is strongly correlated with a decrease in levels of SAM in mice, rats and humans.[50][51]

According to a 2012 review, the effect of methionine restriction on cancer has yet to be studied directly in humans and "there is still insufficient knowledge to give reliable nutritional advice".[52]

Signaling pathways

Multiple oncogenic signaling pathways have been involved in the processes of cancer cell invasion and metastasis. Among these signaling pathways, Wnt and Hedgehog signaling pathways are involved in the embryonic development, in the biology of cancer stem cells (CSCs) and in the acquisition of epithelial to mesenchymal transition (EMT).[35]

See also

References

  1. ↑ Anand, P; Kunnumakkara, AB; Sundaram, C; Harikumar, KB; et al. (September 2008). "Cancer is a preventable disease that requires major lifestyle changes". Pharmaceutical Research. 25 (9): 2097–116. doi:10.1007/s11095-008-9661-9. PMC 2515569Freely accessible. PMID 18626751.
  2. 1 2 3 4 5 6 Wicki, A; Hagmann, J (9 September 2011). "Diet and cancer". Swiss Medical Weekly. 141: w13250. doi:10.4414/smw.2011.13250. PMID 21904992.
  3. 1 2 3 4 Stewart, Bernard W.; Wild, Christopher P., eds. (2014). "Ch. 2: Cancer Etiology § 6 Diet, obesity and physical activity". World Cancer Report 2014. World Health Organization. pp. 124–33. ISBN 9789283204299.
  4. ↑ Key, TJ (4 January 2011). "Fruit and vegetables and cancer risk". British Journal of Cancer. 104 (1): 6–11. doi:10.1038/sj.bjc.6606032. PMC 3039795Freely accessible. PMID 21119663.
  5. ↑ Joshi, AD; Corral, R; Catsburg, C; Lewinger, JP; et al. (2012). "Red meat and poultry, cooking practices, genetic susceptibility and risk of prostate cancer: Results from a multiethnic case-control study". Carcinogenesis. 33 (11): 2108–18. doi:10.1093/carcin/bgs242. PMC 3584966Freely accessible. PMID 22822096.
  6. ↑ Zheng, W; Lee, SA (2009). "Well-done meat intake, heterocyclic amine exposure, and cancer risk". Nutrition and Cancer. 61 (4): 437–46. doi:10.1080/01635580802710741. PMC 2769029Freely accessible. PMID 19838915.
  7. ↑ Ferguson, LR (February 2010). "Meat and cancer". Meat Science. 84 (2): 308–13. doi:10.1016/j.meatsci.2009.06.032. PMID 20374790.
  8. 1 2 3 Park, S; Bae, J; Nam, BH; Yoo, KY (2008). "Aetiology of cancer in Asia" (PDF). Asian Pacific Journal of Cancer Prevention. 9 (3): 371–80. PMID 18990005.
  9. ↑ Larsson, SC; Wolk, A (2007). "Coffee consumption and risk of liver cancer: A meta-analysis". Gastroenterology. 132 (5): 1740–5. doi:10.1053/j.gastro.2007.03.044. PMID 17484871.
  10. ↑ Brenner, H; Rothenbacher, D; Arndt, V (2009). "Epidemiology of Stomach Cancer". In Verma, Mukesh. Cancer Epidemiology: Volume 2: Modifiable Factors. Methods in Molecular Biology. 472. pp. 467–77. doi:10.1007/978-1-60327-492-0_23. ISBN 9781603274913. PMID 19107449.
  11. ↑ Buell, P; Dunn, JE (May 1965). "Cancer mortality among Japanese Issei and Nisei of California". Cancer. 18 (5): 656–64. doi:10.1002/1097-0142(196505)18:5<656::AID-CNCR2820180515>3.0.CO;2-3. PMID 14278899.
  12. ↑ Hübner, J; Marienfeld, S; Abbenhardt, C; Ulrich, CM; et al. (2012). "How useful are diets against cancer?". Deutsche Medizinische Wochenschrift. 137 (47): 2417–22. doi:10.1055/s-0032-1327276. PMID 23152069.
  13. ↑ Kossoff, EH; Zupec-Kania, BA; Amark, PE; Ballaban-Gil, KR; et al. (February 2009). "Optimal clinical management of children receiving the ketogenic diet: Recommendations of the International Ketogenic Diet Study Group". Epilepsia. 50 (2): 304–17. doi:10.1111/j.1528-1167.2008.01765.x. PMID 18823325.
  14. ↑ Edefonti, V; Randi, G; La Vecchia, C; Ferraroni, M; et al. "Dietary patterns and breast cancer: A review with focus on methodological issues". Nutrition Reviews. 67 (6): 297–314. doi:10.1111/j.1753-4887.2009.00203.x.
  15. ↑ Brennan, SF; Cantwell, MM; Cardwell, CR; Velentzis, LS; et al. (May 2010). "Dietary patterns and breast cancer risk: A systematic review and meta-analysis". The American Journal of Clinical Nutrition. 91 (5): 1294–302. doi:10.3945/ajcn.2009.28796. PMID 20219961.
  16. ↑ National Institute on Alcohol Abuse and Alcoholism (NIAAA) (July 1993). "Alcohol and Cancer". Alcohol Alert. NIAAA: National Institutes of Health: US Dept. of Health and Human Services. 21: PH 345. Archived from the original on 2005-12-23.
  17. ↑ Boffetta, P; Hashibe, M; La Vecchia, C; Zatonski, W; et al. (August 2006). "The burden of cancer attributable to alcohol drinking". International Journal of Cancer. 119 (4): 884–7. doi:10.1002/ijc.21903. PMID 16557583.
  18. ↑ Seitz, HK; Pelucchi, C; Bagnardi, V; La Vecchia, C (May–June 2012). "Epidemiology and pathophysiology of alcohol and breast cancer: Update 2012". Alcohol and Alcoholism. 47 (3): 204–12. doi:10.1093/alcalc/ags011. PMID 22459019.
  19. ↑ Marmot, M; Atinmo, T; Byers, T; Chen, J; et al. (2007). "Ch. 4: Food and Drinks §8: Alcoholic drinks" (PDF). Food, Nutrition, Physical Activity, and the Prevention of Cancer: A Global Perspective (PDF). World Cancer Research Fund / American Institute for Cancer Research (AICR) Expert Reports. 2. Washington, DC: AICR. pp. 157–71. ISBN 9780972252225.
  20. ↑ Su, LJ; Arab, L (2004). "Alcohol consumption and risk of colon cancer: Evidence from the National Health and Nutrition Examination Survey I Epidemiologic Follow-up Study". Nutrition and Cancer. 50 (2): 111–9. doi:10.1207/s15327914nc5002_1. PMID 15623458.
  21. ↑ Cho, E; Smith-Warner, SA; Ritz, J; van den Brandt, PA; et al. (20 April 2004). "Alcohol intake and colorectal cancer: A pooled analysis of 8 cohort studies". Annals of Internal Medicine. 140 (8): 603–13. doi:10.7326/0003-4819-140-8-200404200-00007. PMID 15096331.
  22. ↑ Voigt, MD (February 2005). "Alcohol in hepatocellular cancer". Clinics in Liver Disease. 9 (1): 151–69. doi:10.1016/j.cld.2004.10.003. PMID 15763234.
  23. ↑ Benedetti, A; Parent, ME; Siemiatycki, J (2009). "Lifetime consumption of alcoholic beverages and risk of 13 types of cancer in men: Results from a case-control study in Montreal". Cancer Detection and Prevention. 32 (5): 352–62. doi:10.1016/j.canep.2009.03.001. PMID 19588541.
  24. ↑ Bagnardi, V; Blangiardo, M; La Vecchia, C; Corrao, G (2001). "Alcohol consumption and the risk of cancer: A meta-analysis". Alcohol Research & Health. 25 (4): 263–70. PMID 11910703.
  25. ↑ IARC Working Group on the Evaluation of Carcinogenic Risks to Humans: Alcohol Drinking; Berrino, F; Grant, M; Griciute, L; et al. (1988). "Ch. 6: Summary of Data Reported and Evaluation §5: Evaluation" (PDF). Alcohol Drinking (PDF). IARC Monographs on the Evaluation of Carcinogenic Risks to Humans. 44. Lyon: International Agency for Research on Cancer (IARC): World Health Organization. pp. 258–9. ISBN 9283212444.
  26. ↑ Staff (October 26, 2015). "World Health Organization - IARC Monographs evaluate consumption of red meat and processed meat" (PDF). International Agency for Research on Cancer. Retrieved October 26, 2015.
  27. ↑ Hauser, Christine (October 26, 2015). "W.H.O. Report Links Some Cancers With Processed or Red Meat". New York Times. Retrieved October 26, 2015.
  28. ↑ Staff (October 26, 2015). "Processed meats do cause cancer - WHO". BBC News. Retrieved October 26, 2015.
  29. 1 2 Bradbury, KE; Appleby, PN; Key, TJ (July 2014). "Fruit, vegetable, and fiber intake in relation to cancer risk: findings from the European Prospective Investigation into Cancer and Nutrition (EPIC).". The American Journal of Clinical Nutrition. 100 Suppl 1: 394S–8S. doi:10.3945/ajcn.113.071357. PMID 24920034.
  30. ↑ Spencer, JP (May 2008). "Flavonoids: Modulators of brain function?". British Journal of Nutrition. 99 (E Suppl 1): ES60–ES77. doi:10.1017/S0007114508965776. PMID 18503736.
  31. ↑ Romagnolo, DF; Selmin, OI (2012). "Flavonoids and cancer prevention: A review of the evidence". Journal of Nutrition in Gerontology and Geriatrics. 31 (3): 206–38. doi:10.1080/21551197.2012.702534. PMID 22888839.
  32. ↑ Jin, H; Leng, Q; Li, C (15 August 2012). "Dietary flavonoid for preventing colorectal neoplasms". Colorectal Cancer Group. Cochrane Database of Systematic Reviews. 8 (8): Art. No. CD009350. doi:10.1002/14651858.CD009350.pub2. PMID 22895989.
  33. ↑ "Mushrooms in cancer treatment § Mushrooms and cancer". www.cancerresearchuk.org. Cancer Research UK. 30 January 2013. Archived from the original on 2014-07-08.
  34. ↑ "Soybean". www.cancer.org. American Cancer Society. 17 January 2013. Archived from the original on 2014-08-26.
  35. 1 2 Sarkar, FH; Li, Y; Wang, Z; Kong, D (2010). "The role of nutraceuticals in the regulation of Wnt and Hedgehog signaling in cancer". Cancer and Metastasis Reviews. 29 (3): 383–94. doi:10.1007/s10555-010-9233-4. PMC 2974632Freely accessible. PMID 20711635.
  36. ↑ "Turmeric". www.cancer.org. American Cancer Society. 7 December 2012. Archived from the original on 2014-08-06.
  37. ↑ Boehm, K; Borrelli, F; Ernst, E; Habacher, G; et al. (8 July 2009). "Green tea (Camellia sinensis) for the prevention of cancer". Gynaecological Cancer Group. Cochrane Database of Systematic Reviews (3): Art. No. CD005004. doi:10.1002/14651858.CD005004.pub2. PMID 19588362.
  38. 1 2 "Green Tea". www.cancer.org. American Cancer Society. 4 May 2012. Archived from the original on 2014-08-26.
  39. ↑ Athar, M; Back, JH; Tang, X; Kim, KH; et al. (November 2007). "Resveratrol: A review of preclinical studies for human cancer prevention". Toxicology and Applied Pharmacology. 224 (3): 274–83. doi:10.1016/j.taap.2006.12.025. PMC 2083123Freely accessible. PMID 17306316.
  40. ↑ Bishayee, A (May 2009). "Cancer prevention and treatment with resveratrol: From rodent studies to clinical trials". Cancer Prevention Research. 2 (5): 409–18. doi:10.1158/1940-6207.CAPR-08-0160. PMID 19401532.
  41. ↑ Byers, T (July 2010). "Anticancer vitamins du Jour--The ABCED's so far". American Journal of Epidemiology. 172 (1): 1–3. doi:10.1093/aje/kwq112. PMC 2892535Freely accessible. PMID 20562190.
  42. ↑ Buttigliero, C; Monagheddu, C; Petroni, P; Saini, A; et al. (2011). "Prognostic role of vitamin D status and efficacy of vitamin D supplementation in cancer patients: A systematic review". The Oncologist. 16 (9): 1215–27. doi:10.1634/theoncologist.2011-0098. PMC 3228169Freely accessible. PMID 21835895.
  43. ↑ Bjelakovic, G; Gluud, LL; Nikolova, D; Whitfield, K; et al. (23 June 2014). "Vitamin D supplementation for prevention of cancer in adults". Metabolic and Endocrine Disorders Group. Cochrane Database of Systematic Reviews. 6 (6): Art. No. CD007469. doi:10.1002/14651858.CD007469.pub2. PMID 24953955.
  44. ↑ Mikol, YB; Hoover, KL; Creasia, D; Poirier, L (December 1983). "Hepatocarcinogenesis in rats fed methyl-deficient, amino acid-defined diets". Carcinogenesis. 4 (12): 1619–29. doi:10.1093/carcin/4.12.1619. PMID 6317218.
  45. ↑ Ghoshal, AK; Farber, E (1984). "The induction of liver cancer by dietary deficiency of choline and methionine without added carcinogens". Carcinogenesis. 5 (10): 1367–70. doi:10.1093/carcin/5.10.1367. PMID 6488458.
  46. ↑ Newmark, HL; Yang, K; Lipkin, M; Kopelovich, L; et al. (2001). "A Western-style diet induces benign and malignant neoplasms in the colon of normal C57Bl/6 mice". Carcinogenesis. 22 (11): 1871–5. doi:10.1093/carcin/22.11.1871. PMID 11698351.
  47. ↑ Henning, SM; Swendseid, ME; Coulson, WF (1997). "Male rats fed methyl- and folate-deficient diets with or without niacin develop hepatic carcinomas associated with decreased tissue NAD concentrations and altered poly(ADP-ribose) polymerase activity". Journal of Nutrition. 127 (1): 30–6. PMID 9040540.
  48. ↑ Caudill, MA; Wang, JC; Melnyk, S; Pogribny, IP; et al. (2001). "Intracellular S-adenosylhomocysteine concentrations predict global DNA hypomethylation in tissues of methyl-deficient cystathionine ß-synthase heterozygous mice". Journal of Nutrition. 131 (11): 2811–8. PMID 11694601.
  49. ↑ Poirier, LA; Wise, CK; Delongchamp, RR; Sinha, R (June 2001). "Blood determinations of S-adenosylmethionine, S-adenosylhomocysteine, and homocysteine: Correlations with diet". Cancer Epidemiology, Biomarkers & Prevention. 10 (6): 649–55. PMID 11401915.
  50. ↑ Prinz-Langenohl, R; Fohr, I; Pietrzik, K (2001). "Beneficial role for folate in the prevention of colorectal and breast cancer". European Journal of Nutrition. 40 (3): 98–105. doi:10.1007/PL00007387. PMID 11697447.
  51. ↑ Van den Veyver, IB (2002). "Genetic effects of methylation diets". Annual Review of Nutrition. 22: 255–82. doi:10.1146/annurev.nutr.22.010402.102932. PMID 12055346.
  52. ↑ Cavuoto, PI; Fenech, MF (October 2012). "A review of methionine dependency and the role of methionine restriction in cancer growth control and life-span extension". Cancer Treatment Reviews. 38 (6): 726–36. doi:10.1016/j.ctrv.2012.01.004. PMID 22342103.

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