Diet and cancer

From Wikipedia, the free encyclopedia
Jump to: navigation, search
this advertisement advises a healthy diet to prevent cancer

Almost all cancers (80–90%) are caused by environmental factors,[1] and of these, 30–40% of cancers are directly linked to the diet.[2] While many dietary recommendations have been proposed to reduce the risk of cancer, few have significant supporting scientific evidence.[3] The primary dietary factors that increase risk are obesity and alcohol consumption, with a diet low in fruits and vegetables and high in red meat being implicated but not confirmed.[4][5] Consumption of coffee is associated with a reduced risk of liver cancer.[6] Studies have linked consumption of red or processed meat to an increased risk of breast cancer, colon cancer, prostate cancer,[7] and pancreatic cancer, a phenomenon which may be partially explained by the presence of carcinogens in foods cooked at high temperatures.[8][9] Dietary recommendations for cancer prevention typically consist promoting consumption of legumes (pulses),[10] and eating "mainly vegetables, fruit, whole grains and fish, and a reduced intake of red meat, animal fat, and refined sugar."[3]

Types of diet[edit]

Restrictive diets[edit]

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.[11]

There is insufficient evidence to support the use of the ketogenic diet as a standard treatment for cancer.[12]

Dietary patterns[edit]

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.[13] (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.[14] 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[edit]

Alcohol[edit]

Alcohol is associated with an increased risk of a number of cancers.[15] 3.6% of all cancer cases and 3.5% of cancer deaths worldwide are attributable to consumption of alcohol.[16] Breast cancer in women is linked with alcohol intake.[17] Alcohol also increases the risk of cancers of the mouth, esophagus, pharynx and larynx,[18] colorectal cancer,[19][20] liver cancer,[21] stomach[22] and ovaries.[23] 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)."[24]

Fiber, fruits and vegetables[edit]

Recent studies have cast doubt on the claim that dietary fiber reduces the risk of colon cancer.[25][26] In April 2010, the results of a major study involving 500,000 people in Europe suggested that consumption of fruit and vegetables had little impact on reducing cancer.[27][28]

The Cornell China Study concluded that plant-based diets dramatically and rapidly reduce heart disease, diabetes, cancer and obesity.[29][30][31]

Flavonoids[edit]

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."[32] While some studies have suggested flavonoids may have a role in cancer prevention, others have been inconclusive or suggested they may be harmful.[33]

Mushrooms[edit]

According to Cancer Research UK, "there is currently no evidence that any type of mushroom or mushroom extract can prevent or cure cancer".[34]

Nutrient bioactives[edit]

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.[35]

Laboratory experiments have found that turmeric might have an anti-cancer effect.[36] 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.[37]

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.[38]

Resveratrol has shown anti-cancer activity in laboratory experiments, but as of 2007, there is no evidence of an effect on cancer in humans.[39]

Vitamin D supplements have been widely marketed on the internet and elsewhere for their claimed anti-cancer properties.[40] 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.[41]

Mechanisms of action[edit]

Methionine metabolism[edit]

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.[42][43] For instance, deficiencies of the main dietary sources of methyl donors, methionine and choline, lead to the formation of liver cancer in rodents.[44][45] 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.[46][47] 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.[48][49]

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".[50]

Signaling pathways[edit]

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).[36]

See also[edit]

References[edit]

  1. ^ Abdulla, M. et al. (2000). "Role of diet modification in cancer prevention". BioFactors 12 (1–4): 45–51. doi:10.1002/biof.5520120108. PMID 11216504. 
  2. ^ "Food, nutrition, physical activity, and the prevention of cancer:a global perspective.". World Cancer Research Fund & American Institute for Cancer Research. August 19, 2009. 
  3. ^ a b Wicki, A; Hagmann, J (Sep 9, 2011). "Diet and cancer". Swiss medical weekly 141: w13250. doi:10.4414/smw.2011.13250. PMID 21904992. 
  4. ^ Cappellani, A; Di Vita, M, Zanghi, A, Cavallaro, A, Piccolo, G, Veroux, M, Berretta, M, Malaguarnera, M, Canzonieri, V, Lo Menzo, E (Jan 1, 2012). "Diet, obesity and breast cancer: an update". Frontiers in bioscience (Scholar edition) 4: 90–108. PMID 22202045. 
  5. ^ Key, TJ (Jan 4, 2011). "Fruit and vegetables and cancer risk". British journal of cancer 104 (1): 6–11. doi:10.1038/sj.bjc.6606032. PMC 3039795. PMID 21119663. 
  6. ^ 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. 
  7. ^ Joshi, AD; Corral, R.; Catsburg, C.; Lewinger, J. P.; Koo, J.; John, E. M.; Ingles, S. A.; Stern, M. C. (2012). "Red meat and poultry, cooking practices, genetic susceptibility and risk of prostate cancer: results from a multiethnic case-control study". Carcinogenesis 33 (11): 2108–2118. doi:10.1093/carcin/bgs242. PMC 3584966. PMID 22822096. 
  8. ^ 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 2769029. PMID 19838915. 
  9. ^ Ferguson, LR (February 2010). "Meat and cancer". Meat science 84 (2): 308–13. doi:10.1016/j.meatsci.2009.06.032. PMID 20374790. 
  10. ^ Singh, Jagdish; Partha Sarathi Basu (Dec 2012). "Non-Nutritive Bioactive Compounds in Pulses and TheirImpact on Human Health: An Overview". Food and Nutrition Sciences 03 (12): 1664–1672. doi:10.4236/fns.2012.312218. Retrieved 24 March 2014. 
  11. ^ Hübner, J; Marienfeld, S; Abbenhardt, C; Ulrich, CM; Löser, C (2012). "How useful are diets against cancer?". Deutsche medizinische Wochenschrift (1946) 137 (47): 2417–22. doi:10.1055/s-0032-1327276. PMID 23152069. 
  12. ^ Kossoff EH, Zupec-Kania BA, Amark PE, 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. 
  13. ^ Edefonti, Valeria; Randi, Giorgia; La Vecchia, Carlo; Ferraroni, Monica; Decarli, Adriano. "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. 
  14. ^ Brennan, SF; Cantwell, MM; Cardwell, CR; Velentzis, LS; Woodside, JV (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. 
  15. ^ "Alcohol and Cancer". Alcohol Alert (National Institute on Alcohol Abuse and Alcoholism) 21. 1993. 
  16. ^ Boffetta P, Hashibe M, La Vecchia C, Zatonski W, Rehm J (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. 
  17. ^ Review of Alcohol: Association with Breast Cancer
  18. ^ World Cancer Research Fund, American Institute for Cancer Research (2007). Food, Nutrition, Physical Activity, and the Prevention of Cancer: a Global Perspective. Washington, D.C.: American Institute for Cancer Research. ISBN 978-0-9722522-2-5. Retrieved 29 June 2009. [page needed]
  19. ^ 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. 
  20. ^ Cho E, Smith-Warner SA, Ritz J, 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. 
  21. ^ 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. 
  22. ^ 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 Detect. Prev. 32 (5–6): 352–62. doi:10.1016/j.canep.2009.03.001. PMID 19588541. 
  23. ^ 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. 
  24. ^ International Agency for Rescarch on Cancer, World Health Organization. (1988). Alcohol drinking. Lyon: World Health Organization, International Agency for Research on Cancer. ISBN 92-832-1244-4.  p8
  25. ^ [unreliable medical source?]Liz Kowalczyk (December 14, 2005). "Doubts cast on fiber's effect on cancer". The Boston Globe. 
  26. ^ [unreliable medical source?]"Study: Fiber Doesn't Prevent Cancer". Associated Press. October 13, 2000. 
  27. ^ [unreliable medical source?]Murphy, Clare (2010-04-07). "Five-a-day has little impact on cancer, study finds". bbc.co.uk. Retrieved 2011-03-03. 
  28. ^ [non-primary source needed]Boffetta, P. et al.; Couto, E.; Wichmann, J.; Ferrari, P.; Trichopoulos, D.; Bueno-De-Mesquita, H. B.; Van Duijnhoven, F. J. B.; Buchner, F. L.; Key, T.; Boeing, H.; Nothlings, U.; Linseisen, J.; Gonzalez, C. A.; Overvad, K.; Nielsen, M. R. S.; Tjonneland, A.; Olsen, A.; Clavel-Chapelon, F.; Boutron-Ruault, M. C.; Morois, S.; Lagiou, P.; Naska, A.; Benetou, V.; Kaaks, R.; Rohrmann, S.; Panico, S.; Sieri, S.; Vineis, P.; Palli, D.; Van Gils, C. H. (2010-02-18). "Fruit and Vegetable Intake and Overall Cancer Risk in the European Prospective Investigation Into Cancer and Nutrition (EPIC)". J Natl Cancer Inst (oxfordjournals.org) 102 (8): 529–537. doi:10.1093/jnci/djq072. PMID 20371762. Retrieved 2011-03-02. 
  29. ^ [unreliable medical source?]Campbell TC, Parpia B, Chen J (November 1998). "Diet, lifestyle, and the etiology of coronary artery disease: the Cornell China study". Am. J. Cardiol. 82 (10B): 18T–21T. doi:10.1016/S0002-9149(98)00718-8. PMID 9860369. 
  30. ^ [unreliable medical source?]Alessandro Menotti,Daan Kromhout,Henry Blackburn,Flaminio Fidanza,Ratko Buzina,Aulikki Nissinen (1999). "Food intake patterns and 25-year mortality from coronary heart disease: Cross-cultural correlations in the Seven Countries Study". European Journal of Epidemiology 15 (6): 507–515. 
  31. ^ Cancer Manag Res. 2011; 3: 1–8. PMCID: PMC3048091, Reduced cancer risk in vegetarians: an analysis of recent reports Amy Joy Lanou1 and Barbara Svenson
  32. ^ Scott, Jeremy P.E (May 2008). "Flavonoids: modulators of brain function?". British Journal of Nutrition 99 (E-S1): ES60–ES77. doi:10.1017/S0007114508965776. PMID 18503736. Retrieved Nov 25, 2012. 
  33. ^ 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. 
  34. ^ "Mushrooms and cancer". Cancer Research UK. Retrieved September 2013. 
  35. ^ "Soybean". American Cancer Society. 17 January 2013. Retrieved 19 September 2013. 
  36. ^ a b Sarkar, F. H.; 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): 383–394. doi:10.1007/s10555-010-9233-4. PMC 2974632. PMID 20711635.  edit
  37. ^ "Turmeric". American Cancer Society. 7 December 2012. Retrieved 19 September 2013. 
  38. ^ "Green Tea". American Cancer Society. 2 April 2012. Retrieved 19 September 2013. 
  39. ^ Athar M, Back JH, Tang X, Kim KH, Kopelovich L, Bickers DR, Kim AL (November 2007). "Resveratrol: a review of preclinical studies for human cancer prevention". Toxicol. Appl. Pharmacol. 224 (3): 274–83. doi:10.1016/j.taap.2006.12.025. PMC 2083123. PMID 17306316. 
  40. ^ Byers T (July 2010). "Anticancer vitamins du Jour--The ABCED's so far". Am. J. Epidemiol. (Review) 172 (1): 1–3. doi:10.1093/aje/kwq112. PMC 2892535. PMID 20562190. 
  41. ^ Buttigliero C, Monagheddu, C, Petroni, P, Saini, A, Dogliotti, L, Ciccone, G, Berruti, A (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 3228169. PMID 21835895. 
  42. ^ Mikol, Y. B.; Hoover, K. L.; Creasia, D.; Poirier, L. A. (1983). "Hepatocarcinogenesis in rats fed methyl-deficient, amino acid-defined diets". Carcinogenesis 4 (12): 1619–1629. doi:10.1093/carcin/4.12.1619. PMID 6317218. 
  43. ^ Ghoshal, A. K.; Farber, E. (1984). "The induction of liver cancer by dietary deficiency of choline and methionine without added carcinogens". Carcinogenesis 5 (10): 1367–1370. doi:10.1093/carcin/5.10.1367. PMID 6488458. 
  44. ^ Newmark, H. L.; Yang,, K.; Lipkin, M.; Kopelovich, L.; Liu, Y.; Fan, K.; Shinozaki, H. (2001). "A Western-style diet induces benign and malignant neoplasms in the colon of normal C57Bl/6 mice". Carcinogenesis 22 (11): 1871–1875. doi:10.1093/carcin/22.11.1871. PMID 11698351. 
  45. ^ Henning, S. M.; Swendseid, M. E.; Coulson, W. F. (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): 30–36. PMID 9040540. 
  46. ^ Caudill, M. A.; Wang, J. C.; Melnyk, S.; Pogribny, I. P.; Jernigan, S.; Collins, M. D.; Santos-Guzman, J.; Swendseid, M. E. et al. (2001). "Intracellular S-Adenosylhomocysteine Concentrations Predict Global DNA Hypomethylation in Tissues of Methyl-Deficient Cystathionine ß-Synthase Heterozygous Mice". J. Nutr. 131 (11): 2811–2818. PMID 11694601. 
  47. ^ Poirier LA, Wise CK, Delongchamp RR, Sinha R (June 2001). "Blood determinations of S-adenosylmethionine, S-adenosylhomocysteine, and homocysteine: correlations with diet". Cancer Epidemiol. Biomarkers Prev. 10 (6): 649–55. PMID 11401915. 
  48. ^ 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. 
  49. ^ Van den Veyver IB (2002). "Genetic effects of methylation diets". Annu. Rev. Nutr. 22: 255–82. doi:10.1146/annurev.nutr.22.010402.102932. PMID 12055346. 
  50. ^ Cavuoto, PI; Fenech MF (Oct 2012). "A review of methionine dependency and the role of methionine restriction in cancer growth control and life-span extension.". Cancer Treat Rev. 38 (6): 726–36. doi:10.1016/j.ctrv.2012.01.004. PMID 22342103. 

External links[edit]