Peanuts are not recommended for breast cancer
Peanuts contain resveratrol and are an excellent source of monounsaturated fat. Consumption of peanuts is associated with lower levels of inflammatory markers, which may account for the inverse relationship between nut consumption and cardiovascular risk and diabetes risk. Peanuts have also been shown to promote weight management when consumed as part of a moderate fat diet because of its satiating effect. Frequent peanut consumption is associated with a reduced risk of gallstone disease in men. Peanut extracts have been shown to suppress the proliferation of human prostate cancer cells. Nevertheless, based on the available evidence concerning cancer, it makes sense for breast cancer patients, breast cancer survivors and those at high risk for breast cancer to avoid peanuts and peanut butter and limit their consumption of peanut oil.Cancer-related effects of eating peanuts
Peanuts typically are infected to some extent with molds which produce aflatoxins, which are mutagenic, carcinogenic and teratogenic and cause immuno-suppression in humans. Aflatoxin B1 has been shown to cause liver cancer, especially in hepatitis B-positive individuals. Peanuts have been shown in several studies to stimulate proliferation of colon cancer cells. However one large Taiwanese study found that peanut consumption was associated with lower colorectal cancer risk. Breathing the fumes of peanut oil used in frying has been shown to increase the risk of lung cancer. The case against peanut consumption for breast cancer patients and those at high risk is based on the fact that peanuts can cause cancer (albeit not breast cancer). Breast cancer patients have been shown to be at higher risk for other cancers and should avoid known mutagens. In addition, it is possible to get the potential health benefits of peanuts by consuming other nuts and foods.
Additional comments
Although the United States is a net exporter of peanuts, in 2007 the U.S. imported nearly $29.2 million worth of peanuts, mainly from Argentina, China and Mexico. The aflatoxin problem described in the section above is not related to the multistate outbreak of salmonella that occurred in January 2009. The outbreak was caused by salmonella-contaminated peanut butter and peanut paste produced by the Peanut Corporation of America. Peanut oil typically contains a small fraction of the aflatoxins contained in peanuts and peanut butter. Almond butter, found in health food stores and some supermarkets, can often be an acceptable substitute for peanut butter.
Selected studies
Natural Occurrence of Aflatoxins in Chinese Peanut Butter and Sesame Paste Journal of Agricultural and Food Chemistry, April 2009The present Chinese study was designed to determine the level of aflatoxins in 50 peanut butter and 100 sesame paste samples. The predominant toxin found was aflatoxin B1. Using liquid chromatography, aflatoxin B1 was detected at levels up to 68.51 μg/kg in 41 of the 50 peanut butter samples and up to 20.45 μg/kg in 37 of the 100 sesame paste samples. Regarding the Aflatoxin B1-contaminated samples, 15 (37%) and 1 (2%) peanut butter samples exceed European Union (EU) and Chinese regulations, respectively. Similarly, 19 and 32% of the sesame paste samples contained Aflatoxin B1 at levels higher than Chinese and EU regulations, respectively. The authors comment that seeking to balance health benefits with the potential trade disruptions that regulations can cause is an issue of concern.
Natural Occurrence of Aflatoxin B1 in Marketed Foods and Risk Estimates of Dietary Exposure in Koreans Journal of Food Protection, December 2007
The present study determined the natural occurrence of Aflatoxin B1 in food and estimated the excess risk for liver cancer through exposure to Aflatoxin B1 to Koreans posed by food consumption. 694 food samples from six different regions of South Korea were analyzed for their Aflatoxin B1 content. Thirty-two samples were found to be contaminated with Aflatoxin B1. The level of contamination in 28 of the 32 food products was below 10 μg kg−1, which is the upper legal limit in Korea. From data on typical daily food consumption, the exposure to Aflatoxin B1 was estimated. The major contributors to the dietary intake of Aflatoxin B1 were soybean paste and soy sauce, which composed 91% of the total exposure to Aflatoxin B1. The additional risk of liver cancer for those exposed to Aflatoxin B1 through food was estimated to be 5.78 × 10−6 for hepatitis B-negative individuals and 1.48 × 10−4 for hepatitis B-positive individuals.
Peanut lectin stimulates proliferation of colon cancer cells by interaction with glycosylated CD44v6 isoforms and consequential activation of c-Met and MAPK: functional implications for disease-associated glycosylation changes Glycobiology, July 2006
Peanut agglutinin lectin binds the Thomsen-Friedenreich oncofetal carbohydrate antigen (galactoseβ1-3N-acetylgalactosamineα) that shows increased expression in colon cancer, adenomas, and inflammatory bowel disease. Peanut agglutinin lectin is mitogenic for colon epithelial cells. In these cells, peanut agglutinin lectin binds predominantly to cell-surface Thomsen-Friedenreich antigen expressed by high molecular weight isoforms of the transmembrane glycoprotein CD44 that are generated in inflamed and neoplastic colonic epithelia by altered RNA splicing. The authors found that the expression of Thomsen-Friedenreich antigen by CD44 isoforms in colonic epithelial cells allows lectin-induced mitogenesis that is mediated by phosphorylation of c-Met and MAPK.
Peanut consumption and reduced risk of colorectal cancer in women: a prospective study in Taiwan World Journal of Gastroenterology, January 2006
12026 men and 11917 women aged 30 to 65 years in seven Taiwanese townships were interviewed during 1990-1992 and followed up annually for ten years. Colorectal cancer cases in this group were identified from cancer registry and death certificates. The dietary intake was assessed by means of weekly food frequency measures, including frequently consumed food groups such as sweet potato, bean products, peanut products, pickled foodstuffs, and nitrated or smoked foodstuffs. During the study period 107 new colorectal cancer cases occurred. The multivariate Cox's proportional hazard model showed that the relative risk (RR) of peanut consumption was 0.73 for men and 0.42 for women. However, frequent intake of pickled foods was harmful for women (RR = 2.15). The risk of colorectal cancer was also elevated among cigarette smokers but not significantly. The authors conclude that the results demonstrate the antiproliferative effect of peanut intake.
Fractions of cottonseed and peanut extracts suppress the proliferation of human LNCaP and DU145 prostate carcinoma cells The FASEB Journal, 2006 20:A565
Chloroform and methanol extracts of cottonseed and peanut have been shown to suppress the proliferation of human DU145 prostate cancer cells. In the present study, fractions of chloroform extract of peanut flour were found to be antiproliferative toward both DU145 cells and LNCaP (another line of cultured human prostate cancer cells) cells. The fractions of methanol extracts were found to contain phenolics including quercetin derivatives, p-coumaric acid, kaempferol, a ferulic acid derivative and t-cinnamic acid.
Mutagenicity and Identification of Mutagenic Compounds of Fumes Obtained from Heating Peanut Oil Journal of Food Protection, February 2001
The purpose of this study was to evaluate the mutagenicity of, and to isolate the mutagens in, the fumes of peanut oil heated to the smoke point. Peanut oil made from roasted peanuts has a lower smoke point, less unsaturated fatty acids, more fume formation, and stronger mutagenicity than that made from unroasted kernels. Among the 12 compounds identified from the neutral fraction of methanol extract, four compounds at a dose of 10 g per plate were found to be mutagenic.
