Diet and cancer

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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] By far, the most significant dietary cause of cancer is overnutrition (eating too much).[3]

While many dietary recommendations have been proposed to reduce the risk of cancer, few have significant supporting scientific evidence.[3] Obesity and alcohol consumption are confirmed causes of cancer.[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.[3]

Some specific foods are associated with particular kinds of cancer. Consumption of coffee is associated with a reduced risk of liver cancer.[5] Studies have linked consumption of red or processed meat to an increased risk of breast cancer, colon cancer, prostate cancer,[6] and pancreatic cancer, a phenomenon which may be partially explained by the presence of carcinogens in foods cooked at high temperatures.[7][8] Alcohol consumption is associated with breast cancer and liver cancer.[9][3]

Dietary recommendations for cancer prevention typically include weight management and promoting the 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 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 (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]


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]


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