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Whole grains, fiber, and colon cancer: some grains are more whole than others

The vast majority of the grain products eaten in the U.S. are refined. When whole grains are refined, they are stripped of fiber and micronutrients, leaving behind a calorie-rich and nutrient-poor food. A new meta-analysis pooling the data from 6 previous studies has concluded that eating three servings (about 90 grams) of whole grains daily provides a 17% decrease in risk of colorectal cancers. Also, taking into account 19 studies, they concluded that every 10 grams of fiber consumed daily provided a 12% reduction in colon cancer risk.1

So does this mean we should eat a whole grain cold cereal for lunch, a sandwich on whole wheat bread for lunch, and whole wheat pasta for dinner every day? Not so fast. Compared to the white flour, white pasta, and white rice of the standard American diet, certainly these products are a step up. However, the phrase “whole grain” on a packaged food label does not mean “health-promoting food”. Cooking intact grains in water is far more nutritious than eating cold cereals or other processed whole grain foods like pastas, crackers, and breads. When the whole grain is ground down into flour, there is a decrease in nutrient content and an increase in glycemic index (GI) compared to the original intact grain. Foods with a high glycemic index (or glycemic load, GL) produce dangerous spikes in blood glucose. Many studies have linked high GL foods to increased risk of colorectal cancers.2

Also, high temperature cooking of grains and starches (as in making breads, crackers, and cold cereals) produces dietary toxins called acrylamides, and acrylamide intake is associated with several cancers.3-5

Among carbohydrate sources, beans are superior to whole grains with respect to their micronutrient density, glycemic effects, and fiber and resistant starch content. For example, brown rice has a GI of 75, and a fiber + resistant starch content of 20.5%; black beans have a GI of 30 and fiber + resistant starch content of 69.5%.6,7 Fiber helps to prevent colon cancer by reducing the contact between dietary carcinogens and intestinal cells via increasing stool bulk and accelerating transit time.8,9 Resistant starch, similar to fiber, is a carbohydrate that is not broken down by human digestive enzymes. Fiber and and resistant starch act as prebiotics, fueling the growth of healthy bacteria (probiotics); healthy bacteria in the ferment fiber and resistant starch, forming short chain fatty acids that have a number of anti-cancer effects.10-13 Eating beans, peas, or lentils at least twice a week has been found to decrease colon cancer risk by 50%.14,15

Whole grains are the least nutrient-dense of the unrefined plant foods. They are more calorie-dense and not as powerfully protective as vegetables, fruits, beans, or raw nuts and seeds. However, intact whole grains are still healthful natural foods that contain beneficial phytochemicals. Some of the more nutrient-dense whole grains are steel cut oats, black and wild rice, barley, brown rice, and quinoa. Cooking these grains in water is the most healthful way to prepare them. The USDA recommends eating only half of grains whole. For optimal disease protection, I recommend eating beans every day, avoiding refined grains, and primarily eating whole grains intact and cooked in water (rather than as breads or pastas).

Dr. Fuhrman is a best-selling author and board certified family physician specializing in lifestyle and nutritional medicine. His new book Super Immunity, (released September 20, 2011) discusses in depth the connections between diet and cancer. Visit his informative website at DrFuhrman.com.


References:

  1. Aune D, Chan DS, Lau R, et al:Dietary fibre, whole grains, and risk of colorectal cancer: systematic review and dose-response meta-analysis of prospective studies.BMJ 2011;343:d6617.
  2. Gnagnarella P, Gandini S, La Vecchia C, et al: Glycemic index, glycemic load, and cancer risk: a meta-analysis. Am J Clin Nutr 2008;87:1793-1801.
  3. Hogervorst JG, Schouten LJ, Konings EJ, et al:A prospective study of dietary acrylamide intake and the risk of endometrial, ovarian, and breast cancer.Cancer Epidemiol Biomarkers Prev 2007;16:2304-2313.
  4. Hogervorst JG, Schouten LJ, Konings EJ, et al: Dietary acrylamide intake and the risk of renal cell, bladder, and prostate cancer.Am J Clin Nutr 2008;87:1428-1438.
  5. Center for Science in the Public Interest: Acrylamide Product Charts [http://www.cspinet.org/new/pdf/acrylamide_product_charts.pdf]
  6. Bednar GE, Patil AR, Murray SM, et al: Starch and fiber fractions in selected food and feed ingredients affect their small intestinal digestibility and fermentability and their large bowel fermentability in vitro in a canine model. J Nutr 2001;131:276-286.
  7. Foster-Powell K, Holt SH, Brand-Miller JC: International table of glycemic index and glycemic load values: 2002.Am J Clin Nutr 2002;76:5-56.
  8. Jacobs LR: Modification of experimental colon carcinogenesis by dietary fibers. Adv Exp Med Biol 1986;206:105-118.
  9. Gear JS, Brodribb AJ, Ware A, et al: Fibre and bowel transit times. Br J Nutr 1981;45:77-82.
  10. O'Keefe SJ, Ou J, Aufreiter S, et al: Products of the colonic microbiota mediate the effects of diet on colon cancer risk. J Nutr 2009;139:2044-2048.
  11. Dronamraju SS, Coxhead JM, Kelly SB, et al: Cell kinetics and gene expression changes in colorectal cancer patients given resistant starch: a randomised controlled trial. Gut 2009;58:413-420.
  12. Williams EA, Coxhead JM, Mathers JC:Anti-cancer effects of butyrate: use of micro-array technology to investigate mechanisms. The Proceedings of the Nutrition Society 2003;62:107-115.
  13. Hamer HM, Jonkers D, Venema K, et al:Review article: the role of butyrate on colonic function.Aliment Pharmacol Ther 2008;27:104-119.
  14. Aune D, De Stefani E, Ronco A, et al: Legume intake and the risk of cancer: a multisite case-control study in Uruguay. Cancer Causes Control 2009;20:1605-1615.
  15. Singh PN, Fraser GE: Dietary risk factors for colon cancer in a low-risk population.Am J Epidemiol 1998;148:761-774.
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