(DrEddyClinic News) The vast majority of the grain products eaten in the U.S. are refined. When whole grains are refined, for example into white flour or white rice http://www.dreddyclinic.com/forum/viewtopic.php?f=18&t=32823, they are stripped of fiber and micronutrients, leaving behind a calorie-rich, nutrient-poor food. A meta-analysis pooling the data from 6 previous studies has concluded that eating three servings (about 90 grams) of whole grains daily is associated with a 17% decrease in the risk of colorectal cancers http://www.dreddyclinic.com/findinformation/cc/colorectalcancer.php. Also, in review of 16 other studies, they concluded that every 10 grams of fiber consumed daily provided a 12% reduction in colon cancer risk.1 So it is the refined grains that could increase one’s risk of colon cancer.2,3 Studies have also linked refined grains with higher rates of breast cancer http://www.dreddyclinic.com/findinformation/cc/breastcancer.php as well.4,5
The most favorable way to consume grains is with the grain remaining intact. Examples of intact grains are brown and wild rice, wheat berries, barley, quinoa http://www.dreddyclinic.com/forum/viewtopic.php?f=18&t=33577, and steel cut oats. Cooking these grains in water is the most healthful way to prepare them, which also prevents the formation of acrylamide, a potentially toxic compound formed with dry cooking. Intact whole grains can be eaten for breakfast with fruit and seeds or with tomato sauce and onions with lunch or dinner. Whole wheat pasta also has a fairly favorable glycemic load, but bean and lentil pastas are even better, considering the resistant starch content and glycemic benefits of beans.
Also, too much grain, even whole grains can make your diet sub-optimal. The reason for this can be:
1. If you eat too many grains, you may not be eating enough beans and green and yellow vegetables, which are more micronutrient dense.
2. Most brown rice is contaminated with arsenic-containing agricultural chemicals, which can find their way on to your plate.
3. Many whole grain breads, cereals, and crackers are dry cooked and can be browned forming a toxin called acrylamide http://www.dreddyclinic.com/forum/viewtopic.php?f=11&t=33722, which is potentially harmful. High acrylamide intake is associated with several cancers.6-8
4. Whole grain pastry flour can still have an unfavorable glycemic load (GL) because it is ground so fine. Many studies have linked high GL foods to increased risk of colorectal cancers.9
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, barley has a GL of 12, and a fiber plus resistant starch content of 35.2%; black beans have a GL of 5 and fiber plus resistant starch content of 69.5%.10,11
Glycemic load (GL)
Fiber + Resistant Starch
Whole wheat bread
26
13.8%
Barley
12
35.2%
Black beans
5
69.5%
Fiber helps to prevent colon cancer by reducing the contact between dietary carcinogens and intestinal cells via increasing stool bulk and accelerating transit time.12,13 Resistant starch, similar to fiber, is a carbohydrate that is not broken down by human digestive enzymes. Fiber and resistant starch act as prebiotics, fueling the growth of healthy bacteria (probiotics); healthy bacteria in gut the ferment fiber and resistant starch, forming short-chain fatty acids that have a number of anti-cancer effects.14-17 Eating beans, peas or lentils, at least twice a week, has been found to decrease colon cancer risk by 50%.18,19
In summary, intact whole grains are healthful natural foods that contain beneficial phytochemicals. 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).
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. Higginbotham S, Zhang ZF, Lee IM, et al: Dietary glycemic load and risk of colorectal cancer in the Women's Health Study. J Natl Cancer Inst 2004;96:229-233.
3. Michaud DS, Fuchs CS, Liu S, et al: Dietary glycemic load, carbohydrate, sugar, and colorectal cancer risk in men and women. Cancer Epidemiol Biomarkers Prev 2005;14:138-147.
4. Romieu I, Ferrari P, Rinaldi S, et al: Dietary glycemic index and glycemic load and breast cancer risk in the European Prospective Investigation into Cancer and Nutrition (EPIC). Am J Clin Nutr 2012;96:345-355.
5. Dong JY, Qin LQ: Dietary glycemic index, glycemic load, and risk of breast cancer: meta-analysis of prospective cohort studies. Breast Cancer Res Treat 2011;126:287-294.
6. 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.
7. 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.
8. Center for Science in the Public Interest: Acrylamide Product Charts [http://www.cspinet.org/new/pdf/acrylamide_product_charts.pdf]
9. 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.
10. 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.
11. Atkinson FS, Foster-Powell K, Brand-Miller JC: International tables of glycemic index and glycemic load values: 2008. Diabetes Care 2008;31:2281-2283.
12. Jacobs LR: Modification of experimental colon carcinogenesis by dietary fibers. Adv Exp Med Biol 1986;206:105-118.
13. Gear JS, Brodribb AJ, Ware A, et al: Fibre and bowel transit times. Br J Nutr 1981;45:77-82.
14. 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.
15. 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.
16. 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.
17. Hamer HM, Jonkers D, Venema K, et al: Review article: the role of butyrate on colonic function. Aliment Pharmacol Ther 2008;27:104-119.
18. 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.
19. 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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