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Research

The Michigan Dry Bean Industry has a unique agreement between growers and shippers to fund research to develop new bean varieties and improve dry bean quality. New bean varieties are tested for yield and quality characteristics in the field. Further testing for processing and canning quality is conducted in cooperation with Michigan State University.

Much of the Michigan Bean Commission's research is done at the Saginaw Valley Dry Bean and Sugar Beet Research Farm, a 250-acre Tuscola County field station. Current research is being conducted in development and testing, cropping systems research, tillage management, weed control, soil fertility and general crop management. For more information, please visit the Saginaw Valley site.

New Health Research Findings:

"Beans and Inhibition of Cancer" is the first in a series of four papers on
the health and nutritional aspects of dry beans. The papers are researched
and edited by Dr. Maurice R. Bennink and Elizabeth A. Rondini, MS, RD of Michigan State University. Dr. Bennink is well known for his own research on the reduced incidence and multiplicity of colon cancer with a dry bean diet (Hangen + Bennink 2002. The paper actually came out in 2003).

Eat Beans to Improve your health Part 1 of 5(Cancer)
Eat Beans to Improve your health Part 2 of 5(Obesity)
Eat Beans to Improve your health Part 3 of 5(Heart Disease)
Eat Beans to Improve your health Part 4 of 5(Diabetes Management)
Eat Beans to Improve your health Part 5 of 5(Antioxidant)

 

 

Part 1 of 5
by
Maurice R. Bennink and Elizabeth A. Rondini
Food Science and Human Nutrition
Michigan State University

Introduction
It is becoming increasingly apparent that many people could reduce their risk of developing a chronic disease simply by eating more beans. Chronic diseases are conditions that typically take many years (10 to 30 years) to develop and include certain types of cancer, type 2 diabetes mellitus, heart disease, and other diseases of the blood system. These diseases are the most common causes of death in the U.S. and they significantly lower the quality of life for millions. Beans are often overlooked in the diet of Western societies even though they are all naturally low in fat and are a significant source of both soluble and insoluble fibers, protein, essential vitamins and minerals, and phytochemicals (1). The beans referred to here are the dry beans such as navy, black, red, brown, pinto, kidney, etc. Soybeans are not included in this category. In a four part series, we will review 25 years of research that relates bean consumption and various aspects of health.

Beans and Inhibition of Cancer
Most epidemiological studies examining relationships between diet and cancer put little emphasis on legume/pulse (peas, lentils, soy beans, peanuts) consumption. The primary emphasis has been on intakes of total fat, animal fat vs plant fat, animal protein vs plant protein, minerals, vitamins and fiber. Even when legume intake is assessed most studies do not distinguish amongst the various legumes. Thus, it is impossible from these studies to determine the effect of dry beans on cancer versus the effect of any legume on cancer. In the Adventist Health Study, food intake patterns and colon cancer incidence were studied for 20 years. This study detected a significant inverse relationship between frequency of legume intake and colon cancer incidence (2,3). Singh and Fraser (2) noted that individuals consuming legumes more than 2 times per week were 47% less likely to develop colon cancer than individuals that consumed legumes less than once per week. Kolonel et al. (4) differentiated between soy and non-soy legumes and found an inverse relationship between non-soy legume consumption and prostate cancer. Dry beans are generally the most commonly consumed non-soy legume, so this study suggests that beans inhibit prostate cancer. Soy consumption was not related to prostate cancer incidence. Correa (5) was the only one to specifically examine bean consumption and cancer mortality. Data from 41 countries revealed that countries with the greatest consumption of beans had the lowest death rates due to breast, prostate, and colon cancer. Although limited in number, these epidemiological studies suggest that eating beans will help reduce breast, prostate, and colon cancer.

Inter country comparisons and prospective, long-term human studies are extremely important. In such studies, researchers attempt to control parameters that are known to influence cancer. But the precise importance of these known factors and the strong possibility that other cancer modifying factors are in the diet compel researchers to use additional approaches to measure food contribution to cancer risk. Animal studies are often used when dietary factors need to be carefully controlled for long periods and to provide additional support for epidemiological findings.

Two animal studies specifically demonstrated that bean consumption reduces colon cancer (6,7). Hughes et al. (6) fed rats either pinto beans or casein (milk protein) and found that feeding pinto beans reduced the number of rats with colon cancer by 50% compared to casein-fed rats. Moreover, in rats that did develop tumors, rats fed pinto beans had only 1 tumor while rats fed milk protein had 2.5 tumors. In a similar study, Hangen and Bennink (7) fed rats a casein-based diet, a diet containing black beans, or a diet containing navy beans. They reported that feeding either black beans or navy beans reduced the number of animals that had colon cancer by over 50%. Similar to Hughes et al. (6), the number of tumors per rat was 50% less in bean fed rats. Hangen and Bennink (7) noted that rats fed beans were significantly leaner compared to control animals. These two animal studies provide confidence that the epidemiological studies are detecting a true effect of bean consumption and reduction of colon cancer.

How beans slow cancer growth and which component(s) of beans have anticarcinogenic properties are not yet known. One potential mechanism whereby beans could inhibit cancer is related to regulation of blood glucose and insulin. Even though foods containing equal amounts of carbohydrate are consumed, some foods cause a much greater increase in blood sugar (glucose) and insulin concentrations than other foods. The glycemic index measures the rise in blood glucose after eating a test food compared to eating an equal amount of carbohydrate from either glucose or white bread. Foods with a high glycemic index cause a more rapid and greater rise in blood glucose and insulin than foods with a low glycemic index. Eating foods that have a high glycemic index for a long period of time can lead to hyperinsulinemia, insulin resistance and type 2 diabetes mellitus. Recent research findings suggest that high levels of blood insulin (8,9) and/or high levels of blood glucose (10) promote colon cancer. The Cancer Prevention Study by the American Cancer Society found that subjects with type 2 diabetes have a higher propensity of developing colon cancer than individuals without diabetes (11). Type 2 diabetics typically have elevated blood glucose and insulin concentrations. Data from other large prospective studies also suggest that subjects with type 2 diabetes have an increased risk of colon cancer (12,13). Additional evidence supporting the relationship between hyperinsulinemia and promotion of colon cancer was provided by two studies that utilized animals exposed to a colon carcinogen and subsequent injections with insulin. Insulin injections promoted both the early stages of colon cancer (14) and growth of colon tumors (15). It is well documented that eating beans produce low blood glucose and insulin concentrations compared to most other sources of dietary carbohydrates (16-25). Taken together, these studies suggest that eating beans to keep blood insulin and glucose low may be one mechanism that slows colon carcinogenesis.

The second issue of this series will discuss the relationship between high glycemic foods and the onset of obesity. Excess body fat increases the risk of developing cancers of the breast, colon, prostrate, endometrium, kidney, and gall bladder (26). It is likely that hyperinsulinemia and excess body fat are acting in synergy to enhance a variety of cancers. Future studies are expected to show that excess insulin and body fat alter metabolic pathways that enhance cancer.

Beans contain phytonutrients such as flavonoids, tannins, anthocyanins, protease inhibitors, phytic acid, and saponins. Phytonutrients are not considered to be essential nutrients. However, research over the past 15 years clearly demonstrate that some phytonutrients do provide health benefits. Purified protease inhibitors, phytic acid, and saponins inhibit various aspects of carcinogenesis (27-29). But direct evidence that these phytonutrients in foods inhibit cancer is lacking. Therefore, how much of the anticancer activity associated with beans is due to phytonutrients remains to be determined.

It is estimated that appropriate diet choices, weight control, and exercise could reduce cancer incidence by 30-40% (30-32). This translates to 3 - 4 million fewer cancer cases annually for the world and to about 700,000 - 900,000 fewer cases for the USA. The World Cancer Fund/American Institute for Cancer Research (32) recommend that diets be rich in fruits, vegetables, legumes and whole grains to reduce cancer risk. We suggest that dry beans should be a major component of the legume category. Slowing the rate of cancer development even slightly will dramatically increase the number of cancer free years, increase quality of life, and lower medical costs. Eating beans could be an extremely cost effective approach for improving health.

References
1. Geil, P. B., and Anderson, J. W. (1994) Nutrition and health implications of dry beans - a review. Journal of the American College of Nutrition 13, 549-558
2. Singh, P. N., and Fraser, G. E. (1998) Dietary risk factors for colon cancer in a low-risk population. American Journal of Epidemiology 148, 761-774
3. Fraser, G. E. (1999) Associations between diet and cancer, ischemic heart disease, and all-cause mortality in non-Hispanic white California Seventh-day Adventists. American Journal of Clinical Nutrition 70, 532S-538S
4. Kolonel, L. N., Hankin, J. H., Whittemore, A. S., Wu, A. H., Gallagher, R. P., Wilkens, L. R., John, E. M., Howe, G. R., Dreon, D. M., West, D. W., and Paffenbarger, R. S. (2000) Vegetables, fruits, legumes and prostate cancer: A multiethnic case-control study. Cancer Epidemiology Biomarkers & Prevention 9, 795-804
5. Correa, P. (1981) Epidemiological correlations between diet and cancer frequency. Cancer Research 41, 3685-3689
6. Hughes, J. S., Ganthavorn, C., and Wilson-Sanders, S. (1997) Dry beans inhibit azoxymethane-induced colon carcinogenesis in F344 rats. Journal of Nutrition 127, 2328-2333
7. Hangen, L. A., and Bennink, M. R. (2003) Consumption of black beans and navy beans (Phaseolus vulgaris) reduced axozymethane-induced colon cancer in rats. Nutrition and Cancer 44, 60-65
8. Giovannucci, E. (1995) Insulin and colon-cancer. Cancer Causes & Control 6, 164-179
9. Sandhu, M. S., Dunger, D. B., and Giovannucci, E. L. (2002) Insulin, insulin-like growth factor-I (IGF-I), IGF binding proteins, their biologic interactions, and colorectal cancer. Journal of the National Cancer Institute 94, 972-980
10. McKeown -Eyssen, G. (1994) Epidemiology of colorectal-cancer revisited - are serum triglycerides and/or plasma-glucose associated with risk. Cancer Epidemiology Biomarkers & Prevention 3, 687-695
11. Will, J. C., Galuska, D. A., Vinicor, F., and Calle, E. E. (1998) Colorectal cancer: Another complication of diabetes mellitus? American Journal of Epidemiology 147, 816-825
12. Hu, F. B., Manson, J. E., Liu, S. M., Hunter, D., Colditz, G. A., Michels, K. B., Speizer, F. E., and Giovannucci, E. (1999) Prospective study of adult onset diabetes mellitus (type 2) and risk of colorectal cancer in women. Journal of the National Cancer Institute 91, 542-547
13. Fung, T., Hu, F. B., Fuchs, C., Giovannucci, E., Hunter, D. J., Stampfer, M. J., Colditz, G. A., and Willett, W. C. (2003) Major dietary patterns and the risk of colorectal cancer in women. Archives of Internal Medicine 163, 309-314
14. Corpet, D. E., Peiffer, G., and Tache, S. (1998) Glycemic index, nutrient density, and promotion of aberrant crypt foci in rat colon. Nutrition and Cancer-an International Journal 32, 29-36
15. Tran, T. T., Medline, A., and Bruce, W. R. (1996) Insulin promotion of colon tumors in rats. Cancer Epidemiology Biomarkers & Prevention 5, 1013-1015
16. Foster-Powell, K., and Miller, J. B. (1995) International tables of glycemic index. American Journal of Clinical Nutrition 62, S871-S890
17. Miller, J. C. B. (1994) Importance of glycemic index in diabetes. American Journal of Clinical Nutrition 59, S747-S752
18. Viswanathan, M., Ramachandran, A., Indira, P., John, S., Snehalatha, C., Mohan, V., and Kymal, P. K. (1989) Responses to legumes in NIDDM subjects - lower plasma-glucose and higher insulin levels. Nutrition Reports International 40, 803-812
19. Wolever, T. M. S., Chiasson, J. L., Hunt, J. A., Palmason, C., Ross, S. A., and Ryan, E. A. (1998) Similarity of relative glycaemic but not relative insulinaemic responses in normal, IGT and diabetic subjects. Nutrition Research 18, 1667-1676
20. Riccardi, G., and Rivellese, A. A. (1991) Effects of dietary fiber and carbohydrate on glucose and lipoprotein metabolism in diabetic-patients. Diabetes Care 14, 1115-1125
21. Brand, J. C., Colagiuri, S., Crossman, S., Allen, A., Roberts, D. C. K., and Truswell, A. S. (1991) Low-glycemic index foods improve long-term glycemic control in NIDDM. Diabetes Care 14, 95-101
22. Jenkins, D. J. A., Wolever, T. M. S., Jenkins, A. L., Thorne, M. J., Lee, R., Kalmusky, J., Reichert, R., and Wong, G. S. (1983) The glycemic index of foods tested in diabetic-patients - a new basis for carbohydrate exchange favoring the use of legumes. Diabetologia 24, 257-264
23. Jenkins, D. J. A., Wolever, T. M. S., Buckley, G., Lam, K. Y., Giudici, S., Kalmusky, J., Jenkins, A. L., Patten, R. L., Bird, J., Wong, G. S., and Josse, R. G. (1988) Low-glycemic-index starchy foods in the diabetic diet. American Journal of Clinical Nutrition 48, 248-254
24. Coulston, A., Greenfield, M., Kraemer, F., Tobey, T., and Reaven, G. (1980) Effect of source of dietary carbohydrate on plasma-glucose and insulin responses to test meals in normal subjects. American Journal of Clinical Nutrition 33, 1279-1282
25. Jarvi, A. E., Karlstrom, B. E., Granfeldt, Y. E., Bjorck, I. E., Asp, N. G. L., and Vessby, B. O. H. (1999) Improved glycemic control and lipid profile and normalized fibrinolytic activity on a low-glycemic index diet in type 2 diabetic patients. Diabetes Care 22, 10-18
26. World Health Organization. (2002) The world health report: 2002: Reducing risk, promoting healthy life. Geneva, Switzerland
27. Kennedy, A. R. (1994) Prevention of carcinogenesis by protease inhibitors. Cancer Research 54, S1999-S2005
28. Harland, B. F., and Morris, E. R. (1995) Phytate - a good or a bad food component. Nutrition Research 15, 733-754
29. Koratkar, R., and Rao, A. V. (1997) Effect of soya bean saponins on azoxymethane-induced preneoplastic lesions in the colon of mice. Nutrition and Cancer-an International Journal 27, 206-209
30. Doll, R., and Peto, R. (1981) The causes of cancer - quantitative estimates of avoidable risks of cancer in the United-States today. Journal of the National Cancer Institute 66, 1191-&
31. Willett, W.C. (1995) Diet, nutrition, and avoidable cancer. Environmental Health Perspectives 103(Suppl 8), 165-170
32. World Cancer Research Fund/American Institute for Cancer Research (1997) Food, nutrition and the prevention of cancer: a global perspective. WCRF/AICR, Washington, D.C.

Part 2 of 5
by
Maurice R. Bennink and Elizabeth A. Rondini
Food Science and Human Nutrition
Michigan State University

Introduction

The adverse health effects associated with chronic elevation of blood glucose and blood insulin are very apparent in people that suffer from diabetes mellitus. Hyperinsulinemia (elevated blood insulin) and hyperglycemia (elevated blood glucose) often occur when excess body fat accumulates. Research now links excess body fat, hyperglycemia, and hyperinsulinemia to development of heart disease, strokes, and some types of cancer.

Dietary Carbohydrate and Control of Caloric Intake

Ludwig in an article in the Journal of the American Medical Association (1) presents a scientific explanation as to why the type of carbohydrate we eat has such a strong influence on food intake, maintenance of normal blood glucose and insulin concentrations, and the occurrence of chronic diseases. Eating high glycemic index foods (see issue 1 for an explanation of glycemic index) cause people to desire to eat sooner after their last meal than if they ate low glycemic index foods (2, 3). In addition, eating a high glycemic index meal produces the tendency to select high glycemic foods for a snack or for the next meal. This sets up a vicious cycle that leads to a greater caloric intake and greater blood glucose and insulin concentrations (1). With time, obesity and type 2 diabetes develop. On the other hand when low glycemic foods are consumed, there is greater satiety and people don't feel hungry as quickly. Also the tendency to select high glycemic index foods for snacks or the next meal is reduced. Therefore, the likelihood of excessive calorie consumption is reduced and so is the likelihood of becoming obese and a type 2 diabetic.

Excess body fat increases the risk of developing heart disease, strokes, type 2 diabetes, and some types of cancer (4). There has been a steady increase in the percentage of overweight and obese individuals in North America and Western Europe. The increase in obesity is considered to be of epidemic proportions in the U.S. (5) and in most industrialized countries (4-8). For example, on a worldwide basis, more than one billion adults are overweight and more than 300 million are obese (4, 6). In the U.S. more than 60% of the adult population is overweight or obese (7). Obesity and overweight account for approximately 300,000 deaths per year in North America (9, 10) and the cost associated with excess body fat is estimated to be greater than 117 billion dollars per year (11). Most of the costs associated with excess body fat are related to type 2 diabetes, heart disease, and high blood pressure (12). Perhaps even more disturbing is the great increase in overweight and obese children and adolescents (8). Accompanying the rise in excess body fat is an increased incidence of type 2 diabetes in children and adolescents.

While many factors contribute to being overweight and obese, over consumption of food and/or inadequate physical activity are the main factors causing excess body fat for most individuals. Nearly all people struggle to maintain appropriate caloric balance. Thus, it is important to select low glycemic index foods to help reduce the struggle rather than select high glycemic index foods that accentuate the struggle. Compared to other carbohydrate sources, beans have a low glycemic index, varying from 26-42 % relative to glucose (13). Beans are also high in fiber (typically 18% dietary fiber) and low in fat. Thus, beans have a low caloric density. While eating beans will not magically make you thin or make you loose weight, substituting beans for foods that have a high glycemic index will help curb excessive caloric intake and help maintain a leaner physique. Foster-Powell and Miller (13) provide a comprehensive list of foods and their glycemic indices.

References
1. Ludwig, D. D. S. (2002) The glycemic index - Physiological mechanisms relating to obesity, diabetes, and cardiovascular disease. Jama-Journal of the American Medical Association 287, 2414-2423
2. Leathwood, P., and Pollet, P. (1988) Effects of slow release carbohydrates in the form of bean flakes on the evolution of hunger and satiety in man. Appetite 10, 1-11
3. Ludwig, D. S., Majzoub, J. A., Al-Zahrani, A., Dallal, G. E., Blanco, I., and Roberts, S. B. (1999) High glycemic index foods, overeating, and obesity. Pediatrics 103, art. no.-e26 (available at: http://www.pediatrics.org/cgi/content/full/103/3/e26)
4. WHO. (2002) The world health report: 2002: Reducing risk, promoting healthy life, World Health Organization, Geneva
5. U.S. Department of Health and Human Services. (2001) The Surgeon General's call to action to prevent and decrease overweight and obesity, Rockville, MD
6. WHO. (2000) Obesity: Preventing and managing the global epidemic. World Health Organization, WHO Technical Report Series, No. 894, Geneva
7. Flegal, K. M., Carroll, M. D., Ogden, C. L., and Johnson, C. L. (2002) Prevalence and trends in obesity among US adults, 1999-2000. Jama-Journal of the American Medical Association 288, 1723-1727
8. Ogden, C. L., Flegal, K. M., Carroll, M. D., and Johnson, C. L. (2002) Prevalence and trends in overweight among US children and adolescents, 1999-2000. Jama-Journal of the American Medical Association 288, 1728-1732
9. McGinnis, J. M., and Foege, W. H. (1993) Actual causes of death in the United-States. Jama-Journal of the American Medical Association 270, 2207-2212
10. Allison, D. B., Fontaine, K. R., Manson, J. E., Stevens, J., and VanItallie, T. B. (1999) Annual deaths attributable to obesity in the United States. Jama-Journal of the American Medical Association 282, 1530-1538
11. Wolf, A. M. (1998) Impact of obesity on healthcare delivery costs. American Journal of Managed Care 4, S141-S145
12. Wolf, A. M., and Colditz, G. A. (1998) Current estimates of the economic cost of obesity in the United States. Obesity Research 6, 97-106
13. Foster-Powell, K., and Miller, J. B. (1995) International tables of glycemic index. American Journal of Clinical Nutrition 62, S871-S890

 

Part 3 of 5
by
Elizabeth A. Rondini and Maurice R. Bennink
Food Science and Human Nutrition
Michigan State University

Introduction
Heart disease remains the leading cause of death in the United States (1). Factors that increase one's risk of developing heart disease include high levels of total cholesterol and LDL cholesterol ("bad cholesterol"), low levels of HDL cholesterol ("good cholesterol"), obesity, diabetes, smoking, and high blood pressure. Both what you eat and how you live can alter one's risk of heart disease (2-4).

The Association Between Bean Consumption and Heart Disease
Only one epidemiological study has directly examined the frequency of legume consumption and risk of coronary heart disease in US men and women. After adjusting for confounding risk factors, individuals consuming legumes at least 4 times per week were found to have a 22% lower risk of heart disease than individuals consuming legumes less than once per week (4). In epidemiological studies where legumes are consumed as part of a healthier diet plan, consistent reductions in heart disease risk have also been observed. In the Health Professionals Follow-up Study, men that adhered to a more "prudent diet" which included greater consumption of whole grains, legumes, fish, and poultry had a 30% lower risk of having heart disease. Conversely, individuals following a more "Western" diet, characterized by increased consumption of red meat, refined grains, sweets, French fries, and high fat desserts had a higher risk of heart disease (3). Similar trends were seen in the Nurses Health Study (5). The relative risk of coronary heart disease in the 20% of women that followed the "prudent" dietary pattern more closely was 0.76 compared to 1.46 for women eating a "Western" type pattern (5). Thus, those that most consistently ate the "prudent" type of diet had one half the risk of developing heart disease compared to those that most often ate the "Western" type of diet.

How Beans Can Help Reduce the Risk of Heart Disease
A 1% reduction in total cholesterol corresponds to about a 2% decrease in the risk of developing heart disease (6). Beans are a good source of soluble dietary fiber, containing approximately 4 g per cup of cooked beans (7). Soluble fiber has been shown to reduce blood cholesterol in epidemiological (8), clinical (9-12), and animal (13, 14) studies. Data from several human intervention trials indicate that consumption of canned (11, 15, 16) and dry beans (11, 12, 17-19) reduce serum cholesterol. Differences in experimental design, the control diet used, and heterogeneity in the intervention groups make direct comparisons among the studies difficult. Only two studies (20, 21) did not find favorable changes in serum lipoproteins when beans were consumed. Generally, in carefully controlled clinical studies where the macronutrient intake was matched and the fiber content in the bean fed group was at least twice that of the control diet, significant reductions in both total and LDL cholesterol occurred (9, 11). Changes in HDL cholesterol and triglyceride concentrations are inconsistent (9,11,12,16,22). The consumption of dietary fiber in the US is only 12-13 g/day, well below the recommended 25-35 g/day. Incorporating one cup of cooked beans into the diet would add 12 g of total fiber and 4 g of soluble fiber per day. This increase in fiber intake would be expected to modestly lower serum cholesterol and risk of heart disease, especially in hyperlipidemic individuals.
In addition to cholesterol, recent attention has focused on high levels of plasma homocysteine as an independent risk factor for vascular disease (23, 24). Using meta-analysis, Boushey et al. (23) determined that individuals with elevated homocysteine had 1.7 to 2.5 times greater risk for developing cardiovascular disease. The prevelance of elevated homocysteine (>14 umol/L) in the U.S. is 29.3% based on the Framingham Heart Study. Within this group, plasma homocysteine was inversely related to plasma folate levels and with intake of dietary folate and vitamin B6 (24). Cleophas (25) suggests that increasing the consumption of folate-containing foods may lower the prevalence of vascular disease in people with elevated homocysteine. Controlled studies examining the potential of folate-containing foods to reduce homocysteine and therefore vascular disease need to be conducted (25). The current RDA for folate is 400 g/day for adult men and women, and beans provide a significant amount of folate (approximately 110 g per cup of cooked beans), ranging from 140 g in blackeyed peas to 87 g in red kidney beans (calculated from (26)).
Beans also contain compounds called phytonutrients. Phytonutrients are non-essential compounds in foods that can provide health benefits and some of the phytonutrients found in beans have been reported to reduce risk factors associated with cardiovascular disease. Eating beans can help maintain desired weight, can help reduce blood glucose, insulin, and cholesterol concentrations, and can help reduce the incidence and adverse consequences of diabetes. Thus, eating beans will help reduce your risk of premature atherosclerosis (heart attacks, strokes, and peripheral vascular disease). Of course other dietary factors, lifestyle and genetic background all strongly influence cardiovascular risk. Eating beans is just one practice that you can do to help reduce cardiovascular disease.

References

1. American Heart Association. (2002) Heart Disease and Stroke Statistics - 2003 Update. Dallas
2. Fraser, G. E. (1999) Associations between diet and cancer, ischemic heart disease, and all-cause mortality in non-Hispanic white California Seventh-day Adventists. American Journal of Clinical Nutrition 70, 532S-538S
3. Hu, F. B., Rimm, E. B., Stampfer, M. J., Ascherio, A., Spiegelman, D., and Willett, W. C. (2000) Prospective study of major dietary patterns and risk of coronary heart disease in men. American Journal of Clinical Nutrition 72, 912-921
4. Bazzano, L. A., He, J., Ogden, L. G., Loria, C., Vupputuri, S., Myers, L., and Whelton, P. K. (2001) Legume consumption and risk of coronary heart disease in US men and women. Archives of Internal Medicine 161, 2573-2578
5. Fung, T. T., Willett, W. C., Stampfer, M. J., Manson, J. E., and Hu, F. B. (2001) Dietary patterns and the risk of coronary heart disease in women. Archives of Internal Medicine 161, 1857-1862
6. Rifkind, B. M. (1984) The Lipid Research Clinics coronary primary prevention trial results .2. The relationship of reduction in incidence of coronary heart-disease to cholesterol lowering. Jama-Journal of the American Medical Association 251, 365-374
7. Anderson, J. W., Smith, B. M., and Gustafson, N. J. (1994) Health benefits and practical aspects of high-fiber diets. American Journal of Clinical Nutrition 59, S1242-S1247
8. Brown, L., Rosner, B., Willett, W. W., and Sacks, F. M. (1999) Cholesterol-lowering effects of dietary fiber: a meta-analysis. American Journal of Clinical Nutrition 69, 30-42
9. Anderson, J. W., Story, L., Sieling, B., Chen, W. J. L., Petro, M. S., and Story, J. (1984) Hypocholesterolemic effects of oat-bran or bean intake for hypercholesterolemic men. American Journal of Clinical Nutrition 40, 1146-1155
10. Anderson, J. W., and Tietyenclark, J. (1986) Dietary fiber - hyperlipidemia, hypertension, and coronary heart-disease. American Journal of Gastroenterology 81, 907-919
11. Anderson, J. W. (1987) Dietary fiber, lipids and atherosclerosis. American Journal of Cardiology 60, G17-G22
12. Anderson, J. W., Gustafson, N. J., Spencer, D. B., Tietyen, J., and Bryant, C. A. (1990) Serum-lipid response of hypercholesterolemic men to single and divided doses of canned beans. American Journal of Clinical Nutrition 51, 1013-1019
13. Rosa, C. O. B., Costa, N. M. B., Leal, P. F. G., and Oliveira, T. T. (1998) The cholesterol-lowering effect of black beans (Phaseolus vulgaris, L.) without hulls in hypercholesterolemic rats. Archivos Latinoamericanos De Nutricion 48, 299-305
14. Rosa, C. O. B., Costa, N. M. B., Nunes, R. M., and Leal, P. F. G. (1998) The cholesterol-lowering effect of black, carioquinha and red beans (Phaseolus vulgaris, L.) in hypercholesterolemic rats. Archivos Latinoamericanos De Nutricion 48, 306-310
15. Anderson, J. W., Smith, B. M., and Washnock, C. S. (1999) Cardiovascular and renal benefits of dry bean and soybean intake. American Journal of Clinical Nutrition 70, 464S-474S
16. Shutler, S. M., Bircher, G. M., Tredger, J. A., Morgan, L. M., Walker, A. F., and Low, A. G. (1989) The effect of daily baked bean (Phaseolus-Vulgaris) consumption on the plasma-lipid levels of young, normo-cholesterolemic men. British Journal of Nutrition 61, 257-265
17. Jenkins, D. J. A., Wolever, T. M. S., Jenkins, A. L., Thorne, M. J., Lee, R., Kalmusky, J., Reichert, R., and Wong, G. S. (1983) The glycemic index of foods tested in diabetic-patients - a new basis for carbohydrate exchange favoring the use of legumes. Diabetologia 24, 257-264
18. Simpson, H. C. R., Lousley, S., Geekie, M., Simpson, R. W., Carter, R. D., Hockaday, T. D. R., and Mann, J. I. (1981) A high-carbohydrate leguminous fiber diet improves all Aspects of diabetic control. Lancet 1, 1-4
19. Bingwen, L., Zhaofeng, W., Wanzhen, L., and Rongjue, Z. (1981) Effects of bean meal on serum cholesterol and triglycerides. Chinese Medical Journal 94, 455-458
20. Oosthuizen, W., Scholtz, C. S., Vorster, H. H., Jerling, J. C., and Vermaak, W. J. H. (2000) Extruded dry beans and serum lipoprotein and plasma haemostatic factors in hyperlipidaemic men. European Journal of Clinical Nutrition 54, 373-379
21. Mackay, S., and Ball, M. J. (1992) Do beans and oat bran add to the effectiveness of a low-fat diet. European Journal of Clinical Nutrition 46, 641-648
22. Jenkins, D. J. A., Wolever, T. M. S., Buckley, G., Lam, K. Y., Giudici, S., Kalmusky, J., Jenkins, A. L., Patten, R. L., Bird, J., Wong, G. S., and Josse, R. G. (1988) Low-glycemic-index starchy foods in the diabetic diet. American Journal of Clinical Nutrition 48, 248-254
23. Boushey, C. J., Beresford, S. A. A., Omenn, G. S., and Motulsky, A. G. (1995) A quantitative assessment of plasma homocysteine as a risk factor for vascular-disease - probable benefits of increasing folic-acid intakes. Jama-Journal of the American Medical Association 274, 1049-1057
24. Selhub, J., Jacques, P. F., Bostom, A. G., Dagostino, R. B., Wilson, P. W. F., Belanger, A. J., Oleary, D. H., Wolf, P. A., Rush, D., Schaefer, E. J., and Rosenberg, I. H. (1996) Relationship between plasma homocysteine, vitamin status and extracranial carotid-artery stenosis in the Framingham study population. Journal of Nutrition 126, S1258-S1265
25. Cleophas, T. J., Hornstra, N., van Hoogstraten, B., and van der Meulen, J. (2000) Homocysteine, a risk factor for coronary artery disease or not? A meta-analysis. American Journal of Cardiology 86, 1005-1009
26. U.S. Department of Agriculture, Agricultural Research Service. 2002. USDA National Nutrient Database for Standard Reference, Release 15. Nutrient Data Laboratory Home Page, http://www.nal.usda.gov/fnic/foodcomp

Part 4 of 5
by
Maurice R. Bennink and Elizabeth A. Rondini
Food Science and Human Nutrition
Michigan State University

Introduction

In the first three parts of this series we reviewed the relationship between bean intake to cancer, obesity, and cardiovascular disease. The potential adverse consequences of hyperglycemia and hyperinsulinemia to regulation of food consumption as well as cancer risk were also discussed. In this review, evidence linking low glycemic index diets to improvements in diabetes management as well as diabetes risk will be addressed. As in previous sections, few studies have looked directly at bean consumption. However because beans have a low glycemic index relative to other carbohydrate starches they will be discussed in this context.

Low glycemic index diets for diabetes management

It has long been recognized that components present in food, particularly soluble dietary fiber and the nature of the starch can influence the rate by which glucose is absorbed from the small intestine (reviewed in 1& 2). In the mid-1970's, research began to focus on manipulating dietary fiber and carbohydrates to help individuals with diabetes manage their blood glucose. In several clinical trials, it was shown that incorporation of very high amounts of fiber in the diet improved parameters associated with hyperglycemia and even lowered exogenous insulin requirements in some diabetics (3-8). However, it is very difficult for most individuals to consume such a high level of dietary fiber on a regular basis. Around the same time, several groups began to focus their attention on glycemic and insulin responses to different carbohydrate sources (9-13). Jenkins et al. later introduced the concept of glycemic index to characterize these differences (11). The glycemic index, defined in a previous section, is the ability of different sources of carbohydrates to increase blood glucose over a period of time compared to either glucose or white bread. Legumes in particular were found to produce relatively low glycemic responses in both healthy individuals (11) and in diabetics (12-13).

Eating low glycemic index diets may be one mechanism to minimize the normal rise in blood glucose that occurs following meals and therefore aid in the management of diabetes. Diabetes is a chronic condition associated with many metabolic abnormalities including elevated blood glucose and triglycerides. Individuals are instructed to lower blood glucose levels to help reduce the potential for complications associated with the disease. Many of these complications, including vascular disease and death are related to the long-term effects of hyperglycemia (14). Several feeding studies have shown improvements in glycemic control in both type 1 and type 2 diabetics when low compared to high glycemic index diets are consumed (summarized in 15-16; 17-26). In a recent study with type 1 diabetic children, dietary advice about how to consume a low glycemic index diet was reported to be more beneficial and less of a burden than utilization of the traditional carbohydrate exchange diet (18). In this study, improvements in glycosylated HbA1C and a reduced number of excessive hyperglycemic episodes were reported in children instructed to consume low glycemic index foods. Glycosylated proteins reflect blood glucose levels over long periods of time. Chronic elevations of blood glucose increase the amount of glycosylated blood proteins in blood and vice versa. In feeding studies with type 2 diabetics (adult-onset), lower fasting blood glucose (17), glycosylated proteins (17,20-22,25), insulin secretion (17,22), and lipoproteins (14,21,22,25) have been reported by lowering dietary glycemic index. Although still relatively few in number, these studies provide evidence that simply substituting low glycemic index carbohydrates such as beans for more processed starches can modestly improve glycemic control in diabetics. We acknowledge that some health scientists prefer to not use the concept of glycemic index, but instead emphasize high fiber foods with low caloric density. Regardless of the approach, beans are a highly desirable food since they have a low glycemic index and at the same time they are a high fiber, low caloric dense food.

High glycemic index diets and risk of type 2 diabetes

Consumption of complex carbohydrates and increasing soluble dietary fiber intake was originally advocated for individuals with diabetes and hyperlipidemia. However, two large epidemiological studies have now indicated that long-term consumption of high glycemic index, starchy foods may also increase the risk of developing type 2 diabetes (27-28). In these studies, individuals were followed for a period of time (6 years) and dietary comparisons were made between individuals diagnosed with diabetes and non-diabetics. In both studies, the researchers found a 37% increase in diabetes in individuals with the highest glycemic index intake compared to those having the lowest glycemic index intake after adjustment for known risk factors and cereal fiber. Foods most associated with diabetes risk included French fries, carbonated beverages, white bread, and white rice (27-28).

The exact reason why consumption of high glycemic index foods leads to an increased risk for type 2 diabetes is not known but may be due to an increase in insulin demand (2,15-16,29). High glycemic index foods are known to cause rapid elevations in blood glucose and insulin following a meal. Chronic consumption of high glycemic index diets may in turn lead to down-regulation or desensitization of receptors for insulin, eventually contributing to insulin resistance (2). The body initially adjusts to higher circulating glucose by increasing insulin secretion from the pancreas. However, in susceptible individuals over time insulin resistance combined with exhaustion of insulin producing cells will eventually lead to type 2 diabetes (15-16). Current research (30-31) also suggests that hyperglycemia and hyperinsulinemia stimulate fat cells and possibly cells that line blood vessels (endothelial cells) to secrete pro-inflammatory cytokines called tumor necrosis factor alpha (TNF-a) and interleukin-6 (IL-6). These cytokines promote insulin resistance and other clinical and biochemical symptoms associated with type 2 diabetes. In addition, these cytokines are predictive of risk for cardiovascular disease.

In conclusion, eating a diet rich in low glycemic index foods may help prevent development of diabetes. For diabetics and individuals with impaired glucose tolerance, a low glycemic index diet is important to help control hyperglycemia and hyperinsulinemia and reduce complications of diabetes such as atherosclerosis and kidney failure.

References

1. Jenkins DJA, Taylor RH and Wolever TMS. (1982) The Diabetic Diet, Dietary Carbohydrate and Differences in Digestibility. Diabetologia. 23 (6): 477-484.
2. Jenkins DJA, Axelsen M, Kendall CWC, Augustin LSA, Vuksan V and Smith U. (2000) Dietary fibre, lente carbohydrates and the insulin-resistant diseases. British Journal of Nutrition. 83:S157-S163.
3. Kiehm TG, Anderson JW and Ward K. (1976) Beneficial Effects of a High Carbohydrate, High Fiber Diet on Hyperglycemic Diabetic Men. American Journal of Clinical Nutrition. 29: 895-99.
4. Anderson JW. (1978) Improved Glucose and Lipid-Metabolism in Diabetic Men Treated with High Carbohydrate, High-Fiber Diets. Clinical Research. 26 (3): A526-A526.
5. Anderson JW and Ward K. (1979) High-Carbohydrate, High-Fiber Diets for Insulin-Treated Men with Diabetes-Mellitus. American Journal of Clinical Nutrition. 32 (11): 2312-2321.
6. Anderson JW and Ratliff P. (1987) High-Carbohydrate, High-Fiber Diets Decrease Insulin Requirements of Type-I Diabetic Individuals. Clinical Research. 35 (6): A898-A898.
7. Anderson JW, Zeigler JA, Deakins DA, Floore TL, Dillon DW, Wood CL, Oeltgen PR and Whitley RJ. (1991) Metabolic Effects of High-Carbohydrate, High-Fiber Diets for Insulin-Dependent Diabetic Individuals. American Journal of Clinical Nutrition. 54 (5): 936-943.
8. Simpson HCR, Lousley S, Geekie M, Simpson RW, Carter RD, Hockaday TDR and Mann JI. (1981) A High-Carbohydrate Leguminous Fiber Diet Improves All Aspects of Diabetic Control. Lancet. 1 (8210): 1-4.
9. Crapo PA, Kolterman OG, Waldeck N, Reaven GM, and Olefsky JM. (1980) Postprandial hormonal responses to different types of complex carbohydrate in individuals with impaired glucose tolerance. American Journal of Clinical Nutrition. 33:1723-28.
10. Coulston A, Greenfield M, Kraemer F, Tobey T and Reaven G. (1980) Effect of Source of Dietary Carbohydrate on Plasma-Glucose and Insulin Responses to Test Meals in Normal Subjects. American Journal of Clinical Nutrition. 33 (6): 1279-1282.
11. Jenkins DJA, Wolever TMS, Taylor RH, Barker H, Fielden H, Baldwin JM, Bowling AC, Newman HC, Jenkins AL, and Goff DV. (1981) Glycemic index of foods: a physiological basis for carbohydrate exchange. American Journal of Clinical Nutrition. 34: 362-66.
12. Jenkins DJA, Wolever TMS, Jenkins AL, Thorne MJ, Lee R, Kalmusky J, Reichert R and Wong GS. (1983) The Glycemic Index of Foods Tested in Diabetic-Patients - a New Basis for Carbohydrate Exchange Favoring the Use of Legumes. Diabetologia. 24 (4): 257-264.
13. Viswanathan M, Ramachandran A, Indira P, John S, Snehalatha C, Mohan V and Kymal PK. (1989) Responses to Legumes in Niddm Subjects - Lower Plasma-Glucose and Higher Insulin Levels. Nutrition Reports International. 40 (4): 803-812.
14. Stratton IM, Adler AI, Neil HAW, Matthews DR, Manley SE, Cull CA, Hadden D, Turner RC and Holman RR. (2000) Association of glycaemia with macrovascular and microvascular complications of type 2 diabetes (UKPDS 35): prospective observational study. British Medical Journal. 321 (7258): 405-412.
15. Ludwig DDS. (2002) The glycemic index - Physiological mechanisms relating to obesity, diabetes, and cardiovascular disease. Journal of the American Medical Association. 287 (18): 2414-2423.
16. Augustin LS, Franceschi S, Jenkins DJA, Kendall CWC and La Vecchia C. (2002) Glycemic index in chronic disease: a review. European Journal of Clinical Nutrition. 56 (11): 1049-1071.
17. Jenkins DJA, Wolever TMS, Buckley G, Lam KY, Giudici S, Kalmusky J, Jenkins AL, Patten RL, Bird J, Wong GS and Josse RG. (1988) Low-Glycemic-Index Starchy Foods in the Diabetic Diet. American Journal of Clinical Nutrition. 48 (2): 248-254.
18. Gilbertson HR, Brand-Miller JC, Thorburn AW, Evans S, Chondros P and Werther GA. (2001) The effect of flexible low glycemic index dietary advice versus measured carbohydrate exchange diets on glycemic control in children with type 1 diabetes. Diabetes Care. 24 (7): 1137-1143.
19. Buyken AE, Toeller M, Heitkamp G, Karamanos B, Rottiers R, Muggeo M and Fuller JH. (2001) Glycemic index in the diet of European outpatients with type 1 diabetes: relations to glycated hemoglobin and serum lipids. American Journal of Clinical Nutrition. 73 (3): 574-581.
20. Brand JC, Colagiuri S, Crossman S, Allen A, Roberts DCK and Truswell AS. (1991) Low-Glycemic Index Foods Improve Long-Term Glycemic Control in NIDDM. Diabetes Care. 14 (2): 95-101.
21. Wolever TMS, Jenkins DJA, Vuksan V, Jenkins AL, Wong GS and Josse RG. (1992) Beneficial Effect of Low-Glycemic Index Diet in Overweight NIDDM Subjects. Diabetes Care. 15 (4): 562-564.
22. Wolever TMS, Jenkins DJA, Vuksan V, Jenkins AL, Buckley GC, Wong GS and Josse RG. (1992) Beneficial effect of a low glycemic index diet in type 2 diabetes. Diabetes Medicine. 9: 451-58.
23. Fontvieille AM, Rizkalla SW, Penfornis A, Acosta M, Bornet FRJ and Slama G. (1992) The Use of Low Glycemic Index Foods Improves Metabolic Control of Diabetic-Patients over 5 Weeks. Diabetic Medicine. 9 (5): 444-450.
24. Miller JCB. (1994) Importance of Glycemic Index in Diabetes. American Journal of Clinical Nutrition. 59 (3): S747-S752.
25. Jarvi AE, Karlstrom BE, Granfeldt YE, Bjorck IE, Asp NGL and Vessby BOH. (1999) Improved glycemic control and lipid profile and normalized fibrinolytic activity on a low-glycemic index diet in type 2 diabetic patients. Diabetes Care. 22 (1): 10-18.
26. Giacco R, Parillo M, Rivellese AA, Lasorella G, Giacco A, D'Episcopo L and Riccardi G. (2000) Long-term dietary treatment with increased amounts at fiber- rich low-glycemic index natural foods improves blood glucose control and reduces the number of hypoglycemic events in type 1 diabetic patients. Diabetes Care. 23 (10): 1461-1466.
27. Salmeron J, Ascherio A, Rimm EB, Colditz GA, Spiegelman D, Jenkins DJ, Stampfer MJ, Wing AL and Willett WC. (1997) Dietary fiber, glycemic load, and risk of NIDDM in men. Diabetes Care. 20 (4): 545-550.
28. Salmeron J, Manson JE, Stampfer MJ, Colditz GA, Wing AL and Willett WC. (1997) Dietary fiber, glycemic load, and risk of non-insulin-dependent diabetes mellitus in women. Journal of the American Medical Association. 277 (6): 472-477.
29. Jenkins DJA, Wolever TMS, Collier GR, Ocana A, Rao AV, Buckley G, Lam Y, Mayer A, and Thompson LU. (1987) Metabolic effects of a low-glycemic index diet. American Journal of Clinical Nutrition. 46: 968-75.
30. Esposito K, Nappo F, Marfella R, Giugliano G, Giugliano F, Ciotola M, Quagliaro L, Ceriello A and Giugliano D. (2002) Inflammatory cytokine concentrations are acutely increased by hyperglycemia in humans - Role of oxidative stress. Circulation. 106 (16): 2067-2072.
31. Soop M, Duxbury H, Agwunobi AO, Gibson JM, Hopkins SJ, Childs C, Cooper RG, Maycock P, Little RA and Carlson GL. (2002) Euglycemic hyperinsulinemia augments the cytokine and endocrine responses to endotoxin in humans. American Journal of Physiology-Endocrinology and Metabolism. 282 (6): E1276-E1285.

 

Part 5 of 5
by
George Hosfield
ARS - Michigan State University

Potential Health Benefits from Antioxidant Compounds in Dry Beans

INTRODUCTION: Much has been written over the past 15 years regarding the potential "health benefits" associated with beans if they are included as a significant component of the diet. In the late 1980's, dry beans were touted as the "heart healthy" food for the 1990's. Although the "beans are good for the heart" campaigns of the 1990's have subsided a bit in the new millennium, beans should not be overlooked as an important food that can lower the risk of heart and other debilitating diseases and improve health and well being. Beans are a good source of several nutrient and nonnutrient plant compounds that have health promoting effects.1,2

Scientific studies have shown that beans, because of their high soluble dietary fiber content, can help reduce serum cholesterol and, thus, decrease the risk of developing heart disease 1,3,4 Beans are also a food with a low glycemic index.5 Such foods can help curb excessive caloric intake, and, consequently, help one to manage body fat.6 A low glycemic index food also may help in the management of diabetes.6 For more information on the dietary importance of the glycemic index and other health benefits associated with bean consumption see the papers in this series by M.R. Bennink and E.A. Rondini (Michigan Beans and Health, the health benefits of eating dry beans, Part 1,2,3, and 4).

Over the past decade, many consumers have been making dietary choices based on the natural chemicals present in foods. These natural plant chemicals are generally referred to as "phytochemicals". There are hundreds of phytochemicals in fruits and vegetables seen as beneficial to health because of their attributes as antioxidants. Nowadays, much attention is given to the effects of antioxidants in diets.

The health benefits of plant derived antioxidants are touted in articles found in health and nutrition magazines. Sometimes food manufacturers include on product labels the fact that the particular food is known to be a rich source of these compounds. A common example of an antioxidant is vitamin C (ascorbic acid) found abundantly in citrus fruits. Vitamin E and the carotenoids-pigments that give carrots, tomatoes, and yellow fleshed fruits and vegetables their color-are effective antioxidants.7 Antioxidants protect cells and tissues from the damaging effects of certain highly reactive atoms or molecules called free radicals. A free radical is an atomic species with a unpaired electron. How free radicals form in the body and how antioxidants work to inhibit their effects will be discussed in depth later in the article.

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Seed coats of colored dry beans are a rich source of a particular group of compounds with antioxidant activity. How are seed coat color and antioxidants related in beans? The color of beans is determined by the presence and amounts of pigments belonging to a group of phytochemicals known as flavonoids. The generalized structure of a flavonoid molecule is shown in Fig. 1. Flavonoids are simple and complex phenolic compounds that are found in a wide range of plants and, which perform a wide range of functions in plant tissues.8 The specific flavonoids found in bean seed coats are flavonols, anthocyanins, and condensed tannins (proanthocyanidins).9

While much has been published on the negative effects of phenolic compounds on nutrient digestibility in foods, very little has been reported on the beneficial effects of the array of phenolic compounds (flavonoids) found in bean seed coats.10-20 Recently, scientists at the USDA-ARS Dry Bean Genetics Laboratory located on the campus of Michigan State University isolated and identified the particular flavonoids associated with colors in gray, brown, yellow, red, and black beans.15-20 These colors were chosen because they distinguish several important market classes of beans recognized in the U.S. (e.g., the red, black, and brown seed coat colors of the kidney bean, small red, black, and pinto market classes). The various flavonoid compounds identified in seed coats of the different colored beans are presented in Table 1. After the flavonoids were identified, they were purified from seed coat extracts and tested for their antioxidant efficacy.2

The antioxidant assay consisted of adding individual flavonoid compounds to liquid suspensions of very tiny fat bodies called liposomes.2 Intact liposomes fluoresce and the amount of fluorescence was recorded with an instrument called a fluorometer. Oxidation of the liposome suspension caused the liposomes to break apart, which in turn, caused them to lose their fluorescing ability. The loss of fluorescence was compared to the commercial antioxidant, BHT (butylated hydroxytoluene), used as the control in the experiments.

BHT almost completely inhibited oxidation in the tests (Fig.2). The anthocyanins, delphinidin 3-O-glucoside and petunidin 3-O-glucoside and the flavonol, quercitin
3-O-glucoside were the most active of the pure compounds tested (Fig. 2) The third anthocyanins-malvidin 3-O-glucoside-showed antioxidant activity but was significantly less effective than BHT, delphinidin 3-O-glucoside, petunidin 3-O-glucoside, and quercitin 3-O-glucoside in preventing liposome destruction. Kaempferol 3-O-glucoside had the least antioxidant activity. Its activity was less than 20% relative to BHT. Tannins (phenolic polymers) also were found to have potent antioxidant activity.2 This was not surprising because of the reactive

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hydroxyl groups characteristic of the flavonoid skeleton from which tannins are formed through polymerization.

Other research also has shown condensed and hydrolysable tannins to be powerful antioxidants. For example, tannins from sorghum were found to be 15-30 times more effective than simple phenols at quenching free radicals.21 Similarly, tannins isolated from adzuki bean were found to have antioxidant properties.22 Tannin containing extracts from a variety of dry beans inhibited iron-catalyzed oxidation of soybean oil.23

Since tannin chemistry is complicated and separation techniques to purify tannins are difficult and often give unreliable results, the antioxidant activity of tannins was restricted to those present in methanol extracts-the solvent used to dissolve the pigments in the seed coats. In addition to the tannins, the methanol extracts also contained simple flavonoids (flavonoid monomers like quercitin). Tannins were found to have a higher antioxidant activity than the simple flavonoid compounds: delphinidin, petunidin, malvidin, quercitin, and kaempferol.2

Free Radicals. The cells of one's body are in a constant state of flux. Biochemical reactions are constantly occurring. The body uses its energy-yielding nutrients to fuel its metabolic and physical activities.7 Oxygen is a key element in the body's metabolism. Oxygen has an atomic number of eight, meaning that it has eight protons (positively charged particles) in its nucleus and eight electrons (negatively charged particles) that travel in paths about the nucleus. The eight positive and eight negative charges of elemental oxygen cancel each other, thus, leaving the atom electrically neutral to its surroundings. Oxygen's eight electrons are arranged in two orbitals or shells. The innermost shell contains two electrons, and the second and outermost shell contains six electrons. As the body uses oxygen for metabolic reactions, oxygen sometimes gains an extra electron (there are always free electrons floating about a cell seeking to match up with another electron). The extra electron gives oxygen a negative charge because it now has more electrons than protons. This oxygen species with the extra electron is highly unstable and highly reactive. Such molecules or atoms are known as free radicals.7 Free radicals characteristically have an unpaired electron or electrons in the outer shell (orbital). A free radical always wants to match its unpaired electron(s) by pulling an electron from another atomic species, because electrons like to pair up to form stable two electron bonds.24 Free radicals are known to be powerful cancer causing agents and can be especially damaging to body tissues and cause degenerative diseases especially in cases where they take an electron from lipid molecules in cell membranes.7 Hydroxyl radicals (another kind of

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free radical) are especially damaging to cell membranes because they can initiate a process called lipid peroxidation. Lipid peroxidation occurs by radical chain reaction. Once started, the chain reaction spreads rapidly and affects a great number of lipid molecules.24

Antioxidants Stop Free Radicals. Antioxidants can be viewed as biological scavengers. They seek out and quench free radicals generated by the body's
process of metabolism. An antioxidant neutralizes a free radical by donating one of its electrons, and in the case of lipid peroxidation, stopping the chain reaction.7,24 When antioxidants lose electrons, they do not become free radicals themselves because they are biologically stable in either the charged (when they donate an electron) or uncharged form.7

Flavonoid Structure-Activity Relationships. The relative antioxidant activity of flavonoids in bean seed coats (Fig. 2) may be explained by their structures and free radical generation in the body. In the body oxygen can gain an extra electron during the cellular process that reduces it to water. This sequence of events occurs via the electron transport chain in specialized cellular structures called mitochondria. The addition of an extra electron to oxygen generates the free radical called superoxide radical [O2]. Superoxide radical is also known as reactive oxygen species or ROS. The superoxide radical can gain another electron and react with two hydrogen ions to form hydrogen peroxide, and In the presence of iron or copper atoms, the peroxide can form the highly damaging hydroxyl radical [OH].25 Therefore, the ability of flavonoids to complex with metals plays a part in their role as antioxidants. As a general rule, the greater the number of hydroxy groups on the flavonoid nucleus, the higher the antioxidant activity.26 (Cao, et al., 1997)

The most important structural feature of flavonoids for antioxidant activity is the B-ring ortho 3',4' dihydroxy orientation (refer to Fig. 1). 27-29 The two most active flavonoids in the study, delphinidin and petunidin, are anthocyanins. Anthocyanins along with tannins are the flavonoids that give black and purple beans their color. Delphinidin and quercitin have a hydroxy group at the 3',4' positions and petunidin has a 4',5' dihydroxy group. Malvidin, the third anthocyanin found in black beans, has both the 3', and 5' hydroxy groups methylated (OCH3). The methyl group (CH3) essentially blocks the hydroxy group (OH), thus, rendering malvidin less effective as an antioxidant than the other flavonoids. Kaempferol,which has only a single B-ring 4'-hydroxyl substitution, has the least antioxidant activity of the flavonoid compounds found in beans.

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CONCLUSIONS. Research is providing solid evidence that consumption of a variety of phenolic compounds present in natural foods can lower the risk of serious health disorders because of the antioxidant activity of these compounds.
30-31 Dry beans are an integral part of the diets of people in many countries of the developing world. Statistics show that citizens of developing countries in which legumes are dietary staples have fewer diet related health problems than citizens in developed countries. In view of the positive contribution legume consumption makes to human health and well being, the question may be asked, "Shouldn't diets in the U.S. comprise a larger component of beans than is currently the case?"

The potential "health benefits" from eating beans has been addressed from several points of view; however, the beneficial effects on human health from the wide array of phenolic compounds found in seed coats of colored dry beans largely have been overlooked. It has been demonstrated that pure flavonoid compounds such as anthocyanins, quercitin glycosides, and proanthocyanidins (condensed tannins), the pigments that give bean seed coats their color, are potent antioxidants relative to BHT, a commercial antioxidant added to foods.2 The antioxidants in beans may have their greatest benefit on human health by reducing the risk of some types of cancer-colon cancer being one type-by scavenging lipid peroxyl radicals. Epidemiological studies have reported that people with high intakes of vegetables and fruits rich in antioxidant compounds have low rates of cancer.31 Also, positive benefits of bean antioxidants on heart health should not be considered trivial. Results of a long-term study of the diet and lifestyle of individuals in the Netherlands, showed that a regular intake of several dietary flavonoids, such as quercitin and kaempferol from black tea, onions and apples, reduced the risk of coronary heart disease in elderly men.31

Although there is no guarantee that eating beans will prevent cancer because of their antioxidant content, there is compelling scientific evidence regarding the free radical quenching effects of bean phenolics, to make it worthwhile to include beans as a major component of the diet. A decision to increase the amount of beans in the diet solely because of the ability of flavonoids to neutralize the effects of free radicals takes on added significance when one considers that under normal metabolic conditions, each cell in one's body is exposed to about ten billion molecules of superoxide per day.24 This amount of daily superoxide exposure extrapolated to an annual basis, amounts to about four pounds of free radicals for a person weighing 150 pounds. This is a substantial amount of highly reactive free radicals that can bombard cell membranes (lipids), DNA, and
proteins and cause severe cell and tissue damage resulting in debilitating diseases.

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To maximize health benefits from eating beans, go for the market classes with the darker seed coats-the brown and black colored beans. Black beans contain
Anthocyanins-the most efficacious monomeric antioxidant compounds found in the antioxidant experiment-while brown colored ones contain a goodly amount of tannins which have potent antioxidant effects.2 Black beans are robust in flavor, and combine nicely with many other ingredients in recipes. Indeed, black beans are not only appealing for their culinary qualities, but they also have tremendous potential for conferring health benefits to those who eat them on a regular basis. So! "Turn up the crock pot and bring on the feijoada!"

REFERENCES.

1. Geil, P.B., and Anderson,J.W. (1994) Nutrition and health implications of dry beans-a review. J. Am. Coll. Nutr. 13, 549-558

2. Beninger, C.W., and Hosfield, G.L. (2003) Antioxidant activity of extracts, condensed tannin fractions, and pure flavonoids from Phaseolus vulgaris L. seed coat color genotypes. J. Agric. Food Chem. 51, 7879-7883

3. Anderson, J.W. (1995) Dietary fibre, complex carbohydrate and coronary artery disease. Can. J. Cardiol.11, suppl.G, 55G-62G

4. Anderson, J.W., Smith, B.M., and Washnock,C.S. (1999) Cardiovascular and renal benefits of dry bean and soy intake. Am. J. Clin. Nutr.70, 464S-474

5. Jenkins, D.J.A., Wolever, T.M.S., Taylor,R.H. (1981) Glycemic index of foods: A physiological basis for carbohydrate exchange. Am. J. Clin. Nutr. 34, 362-366

6. Anderson,J.W., and Bryant, C.A. (1986) Dietary fiber: Diabetes and obesity. Am. J. Gastroenterol. 81, 898-906

7. Whitney, E.N., and Rolfes, S.R. (1999) Understanding Nutrition, 8th ed. West/Wadsworth, Belmont, Ca., 649, pp

8. Buchanan, B.B., Gruissem, W., and Jones, R.L. (2000) Biochemistry and molecular biology of plants. Am. Soc. Plant Physiol., Rockville, MD,1367, pp

9. Feenstra, W.J.L. (1960) Biochemical aspects of seedcoat colour inheritance in Phaseolus vulgaris L. Med. Landbouwhogeschool Wegeningen. 60,1-53

10. Kakade, M.L., and Evans, R.J. (1965) Toxic factors in beans: Growth inhibition of rats fed navy bean fractions. Agric. Food Chem. 13, 450-452

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11. Lindgren,E. (1975) The nutritive value of peas and field beans for hens. Swed. J. Agric. Res. 5, 159-161

12. Rannenkamp, R.R. (1977) The effect of tannins on nutritional quality of dry beans Phaseolus vulgaris L. Ph.D. thesis, Purdue Univ., West Lafayette, IN

13. Elias, L.G., Fernandez, D.G., and Bressani, R. (1995) Possible effects of seed coat polyphenolics on the nutritional quality of bean protein. J. food Sci. 44, 524-527

14.Beninger, C.W., and Hosfield, G.L. (1997) A natural products approach to understanding the value of beans. Mich. Dry Bean Dig. 22, 5-7

15. Beninger,C.W.,Hosfield, G.L., and Nair, M.G.(1997) Phytochemical methods for the extraction and analysis of seed coat flavonoids from common bean (Phaseolus vulgaris L.) 1997 Annu. Rep.Bean Improv. Coop. 40, 17-18.

16. Beninger,C.W.,Hosfield,G.L., and Nair, M.G. (1998) Flavonol glycosides from
the seedcoat of a new Manteca type dry bean (Phaseolus vulgaris L.).J. Agric. Food Chem 46, 2906-2910

17. Beninger,C.W., and Hosfield,G.L. (1999) Astragalin (kaempferol 3-O-glucoside) and proanthocyanidins are the main flavonoids compounds of four Phaseolus vulgaris L. seed coat color genotypes. Annu. Rep. Bean Improv. Coop.42, 119-120

18. Beninger, C.W.,and Hosfield, G.L. (1999) Flavonol glycosides from Montcalm dark red kidney bean: implications for the genetics of seed coat color in Phaseolus vulgaris L. J. Agric. Food Chem. 47, 4079-4082.

19. Beninger, C.W., Hosfield, G.L., and Bassett, M.J. (1999) Flavonoid composition of three genotypes of dry bean (Phaseolus vulgaris L.) differing in seed coat color. J.Am. Soc. Hortic. Sci. 124, 514-518.

20. Beninger,C.W., Hosfield, G.L., Bassett, M.J., and Owens,S. (1999) Chemical and morphological expression of the B and Asp seedcoat genes in Phaseolus vulgaris L. J. Am. Soc. Hortic. Sci. 125, 52-58

21. Hagerman, A.E., Riedl, K.M., Jones, G.A., Sovik, K.N., Ritchard, N.T., Hartzfeld, P.W., and Riechel, T.L. (1998) High molecular weight plant phenolics (tannins) as biological antioxidants. J. Agric. Food Chem. 46, 1887-1892

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