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Dry Beans and Human Health

http://beaninstitute.com/health-benefits/dry-beans-and-human-health/

An Overview of the Status of the Science on Dry Beans and Human Health

The nutritional values of dry beans are many, but the relationship between consumption of dry beans and health outcomes is one that has been taken for granted for too long! The last several years have seen a resurgence of interest in unraveling those many possible health paths and a growing body of evidence is pointing to the remarkable value of beans to the maintenance, if not potential for improvement, of human wellness.

The Northarvest Bean Growers Association recently commissioned a review of the scientific literature on beans and human health by well-known nutrition researcher Dr. Maurice Bennink (http://fshn.msu.edu/directory/facultyBennink.html) of Michigan State University. Dr. Bennink and colleague Dr. Elizabeth Rondini have produced Beans and Health: A Comprehensive Review © including literature on the relationship between dry beans and health, examining studies available through early 2008. You may download a copy for your use here: Bennink and Rondini article.

TABLE OF CONTENTS

INTRODUCTION

NUTRIENT PROFILE OF DRY BEANS

Nutrient density

Digestibility considerations

NON-NUTRITIVE BIOACTIVE COMPOUNDS

Saponins

Phytic acid

Plant sterols

Phenolic compounds

α-Amylase inhibitors

Lectins (phytohemagglutins)

Trypsin/chymotrypsin

LONGEVITY

RELATIONSHIP OF CHRONIC DISEASES TO GLYCEMIC INDEX AND GLYCEMIC LOAD

Blood glucose

Insulin

Body weight

Beans, glycemic index, and glycemic load

LOW GLYCEMIC CARBOHYDRATES AND DIABETES

BEAN CONSUMPTION AND CARDIOVASCULAR DISEASE (CVD)

BEAN CONSUMPTION AND CANCER

Colorectal Cancer

A. Epidemiological Studies

B. Experimental Studies

Breast cancer

Prostate cancer

ADDITIONAL DATA RELATING BEANS TO CANCER PREVENTION

Fiber and cancer

Folate and cancer

INTRODUCTION return to top

Dry beans are an economical source of concentrated vegetable protein, and are also an excellent source of fiber (both soluble and insoluble), and an excellent source of several minerals and vitamins. Despite their nutritional value, bean consumption by the average adult in the United States remains low, especially as compared with nutritional value. Numerous studies indicate that incorporating beans into the diet could aid in the prevention and/or management of chronic diseases such as diabetes, obesity, and cancer.

The leading causes of death in the USA are: (1) heart disease, (2) cancer, (3) stroke, (4) chronic lower respiratory diseases, (5) accidents, and (6) diabetes (1). It is widely accepted that environmental (i.e., non-genetic) factors, including inappropriate food choices, are major causative factors in the development of chronic diseases. Dietary guidelines to prevent and/or manage chronic diseases are made independently by professional and/or governmental agencies at national, regional, and international levels. The similarities and harmonious nature of the recommendations are quite amazing. Almost all agencies emphasize the importance of consuming legumes (pulses). Eating more beans could potentially reduce the number of premature deaths due to 4 of the top 6 leading causes of death in the USA – heart disease, cancers at certain locations in the body, stroke, and diabetes.

The purpose of this monograph is to encapsulate the recent literature on dry beans and human health. The authors begin by providing an overview of the nutrients found in dry beans, and then also address the range of bio-active compounds they are known to contain. Then, the relationship between dry bean consumption and health is reviewed, including associations with longevity, the links between chronic disease and glycemic index/load, with special attention to diabetes.

Studies of bean consumption and cardiovascular disease, as well as the association between bean use and cancer are next examined. The authors complete their review by briefly discussing research on fiber and cancer, and folate and cancer.

NUTRIENT PROFILE OF DRY BEANS return to top

Nutrient density

Dry beans are a nutrient-dense food. Nutrient density is defined here as the amount of a nutrient in beans divided by nutrient requirement per unit of energy (i.e., 2,000 kcal). In Table 1 the right column shows the nutrient density of beans for adults. As seen in Table 1, beans are an excellent source of protein. Typically beans contain 20 – 30% protein on a dry weight basis which is greater than most plant foods. Bean protein, similar to most plant protein sources, are incomplete (i.e., one or more of the essential amino acids is(are) present in less than optimal amounts). Methionine and tryptophan are the limiting amino acids for bean protein. Consuming beans with cereal grains in proper proportions improves the nutritional value of the protein consumed and most healthy adults can consume all the amino acids they need from such a mixture. Amino acid composition is of little consequence for most North Americans unless they do not eat meat or drink milk

Dry beans are about 70% carbohydrate. Starch (43 – 45%), non-starch polysaccharides or fiber (18 – 20%), α-galactosides (starchyose, verbascose, and raffinose; 3 – 5%), and sucrose (3 – 5%) are the major types of carbohydrate. Beans are an excellent source of fiber as can be seen in Table 1. Bean fiber is roughly one-third soluble and two-thirds insoluble. Since North Americans consume less than one-half of the recommended amount of fiber, adding one serving of beans per day would increase fiber intake by 6g which is 20 – 25% of the recommended intake.

Beans are naturally low in fat with little saturated fat. The neutral lipid content is only 1.5% of the dry bean and unsaturated fatty acids make up 75% of the lipid material. As with all plant foods, beans do not contain any cholesterol.

Beans are a significant dietary source of several essential minerals. Beans are particularly rich in magnesium, phosphorus, copper, and manganese (Table 1). Beans are a good source of potassium, a fair source of calcium and selenium, and are naturally low in sodium. Although beans contain significant amounts of iron and zinc, they do not provide as much iron and zinc as it appears in Table 1 due to low bioavailability (addressed later).

Dry beans are an excellent source of the water-soluble vitamins thiamin and folate. Adequate intakes of folate are associated with a lower risk of cardiovascular disease in some individuals (2) and with a lower risk of cancer at some sites in the body (3). One serving (½ cup) of cooked beans provides approximately 20% of the recommended daily intake (RDI) for folate (400 μg, Table 1). Beans are also a good source of riboflavin and vitamin B6.

Digestibility considerations

Both bean protein and starch are less well digested than protein and starch from cereal grains. One reason for poorer digestion is due to the physical form of the protein and starch when it enters the stomach and small intestine. Beans are generally consumed as cooked or canned beans as opposed to grinding and heat processing that occurs with cereal grains. Bean protein and starch are contained within cell walls that remain primarily intact during cooking and canning. Chewing and mixing in the stomach breaks open only a few of the cells. As a result, bean protein and starch enter the small intestine encased within fibrous cell walls. This impedes proteolysis and amylolysis. We have noted that when beans are cooked in boiling water longer than 10 min, crystalline material starts to form in the cell walls. We feel that the crystalline structures further impede the digestive process.

The digestibility of bean protein is rather low compared to animal protein and most cereal grains. True protein digestibility averages about 73%, but digestibilities range from 65 – 85% depending upon seed coat color. Digestibility of protein from white and light colored beans is in the 80 – 85% range while protein digestibility for black, dark brown, and dark red varieties ranges from 65 – 75%. In addition to the colored seed coat pigments, some fractions of bean protein are inherently less digestible. About 61% of bean protein is in the albumin and globulin GI fractions, which are highly digestible. The globulin GII fraction (lectin fraction) comprises 10% of the bean protein and is only 60% digestible. Glutelins (18% of the protein) and protease inhibitors (0.3% of the protein) are only 40% digestible. The digestibility coefficient for the non-extractable proteins found primarily in the seed coat and cell walls (11%,) is not known but it is likely to be less than 50% based on the digestibility of protein associated with a variety of similar fiber sources. Less than optimal digestion of bean protein may be important in some countries, but it is probably of little concern for North Americans that tend to eat 1.5 – 2.5 times more protein than needed.

Bean starch is digested much slower (a positive feature) and less completely (both a negative and positive feature) than cereal starch. The slow rate of starch digestion contributes to the low glycemic index noted for beans and is a compelling reason to consume beans. The importance of low glycemic foods is discussed in a later section. Incomplete digestion of bean starch contributes to the flatulence problems associated with eating beans but it may also help protect against colon cancer.

As bean starch enters the small intestine, it is entrapped within cell walls, which partially explains the slower starch digestion. Other important aspects affecting starch digestion include extent of gelatinization and retrogradation of starch. Cooking beans in an open kettle does not provide sufficient thermal energy to cause complete gelatinization of bean starch. Canning, because of the higher temperature attained, allows nearly complete gelatinization of the starch. As would be expected, the glycemic index of canned beans is greater than the glycemic index of cooked beans. Retrograded starch is not digested within the small intestine and does not raise blood glucose. There are several factors that affect extent of starch retrogradation, but amylose content and degree of polymerization within amylose are important factors. Bean starch contains more amylose than most other sources of starch and the average degree of polymerization is 1000 – 1200, which is highly conducive to forming retrograded starch. We have utilized in vitro methods to estimate resistant starch (non-gelatinized and retrograded) in canned beans from 30 bean lines and we estimate that about 10% of bean starch in canned beans is not digestible. We predict that the amount of indigestible starch in cooked beans is 20% of the total starch content. Additional research on bean starch is warranted.

Table 1: Nutrient compostion of dry beans

The α-galactosides (oligosaccharides) are not digested in the upper part of the small intestine due to a lack of the enzyme, α-galactosidase. The α-galactosides, resistant starch (starch not digested and absorbed in the small intestine), and fiber pass into the colon where they are fermented by colonic bacteria to produce short chain fatty acids, carbon dioxide, hydrogen, and in some individuals, methane. Soaking beans and then discarding the water reduces oligosaccharide content and may help reduce some of the abdominal discomfort associated with bean consumption. While oligosaccharides receive the blame for causing flatulence, resistant starch and fiber contribute more fermentable material (and thus more gas) than oligosaccharides. Presumably, it is the rapid fermentation of the oligosaccharides that is more bothersome to people than the slower, more consistent fermentation of the insoluble fiber. It is not known how much of the initial, rapid increase in flatulence is due to fermentation of resistant starch and soluble fiber.

Poor bioavailability of iron and zinc from plant foods is due to the presence of phytate, fiber, and phenolic compounds. Poor absorption of iron and zinc may be of little concern for North Americans (except for vegetarians), but is of particular concern in developing countries where cereal grain products and dry beans are consumed in large quantities and consumption of animal products is limited. Improving the amount of iron and zinc absorbed from beans is a major effort by “HarvestPlus”, CIAT, and several Agricultural Experiment Stations.

NON-NUTRITIVE BIOACTIVE COMPOUNDS return to top

Legumes contain a number of compounds that have potential health benefits as well as some that can reduce the bioavailability of nutrients. These compounds include saponins, phytic acid, plant sterols, phenolic compounds, enzyme inhibitors, and lectins. Much interest has been generated in examining some of these compounds with respect to chronic disease prevention.

Saponins

Saponins are amphiphilic compounds present in a wide variety of plants and herbs. Structurally, saponins in food exist as glycosides, with a hydrophobic triterpenoid or steroid (sapogenin) group linked to water-soluble sugar residues (4). The main types of steroid aglycones include the spirostan, furostan, and nautigenin derivatives whereas oleanan derivatives comprise the more common triterpenoid aglycones (5). The amount and type of sugar residues vary between saponin species, the most common being glucose, glucuronic acid, arabinose, rhamnose, xylose, and fucose attached at either the C-3 position (monodesmoside saponins) or on both the C-3 and C-22 position (bidesmoside saponins) (5). The major saponins present in Phaseolous vulgarus were identified as soyasaponin I, V, and phaseoleamide (6, 7).

Saponins are surfactants, and were initially thought to be harmful due to their strong hemolytic activity in vitro. Gestetner et al. (8) found that after feeding mice, rats, and chicks a 20% soy flour diet, neither saponins nor sapogenins were detectable in blood. Saponins were the major form present in the small intestine and sapogenins were primarily detected in the cecum and colon after hydrolysis by microflora. Since the saponins found in dry beans are the same triterpenoid type of saponins found in soy, it is unlikely that dry bean saponins would be absorbed.

Saponins have been shown to have anticarcinogenic and antimutagenic properties in a variety of in vitro approaches (cell culture). The saponins used in these studies were from soy beans. Since dry bean saponins are similar to soy saponins, it would be expected that dry bean saponins would produce similar results. Soyasaponins reduced the growth of HCT-15 and HT-29 colon carcinoma cells and also significantly decreased TPA-associated protein kinase C activation. Because saponegins are presumably the major form of saponins present in the colon, Gurfinkel and Rao (9) looked at the effect of the chemical structure of soyasaponins on anticarcinogenic activity. Soyasaponins (I, II, III) were found to be ineffective up to 50 ppm in inhibiting cell growth, whereas soyasapogenols A and B (aglycones) effectively suppressed growth in a dose-dependent manner (6-50 ppm). These levels could easily be achieved after consumption of 10 g soy flour. Complete conversion of soyasaponins to their aglycone forms by microflora would produce approximately 25 ppm soyasapogenol A and 75 ppm soyasapogenol B (10). Only one study with saponins on carcinogenesis has been conducted in vivo. Koratkar and Rao (11) found that incorporation of soyasaponins into the diet of mice (3%) reduced the incidence of mice with ACF, and significantly decreased the number of ACF/colon and the number of AC/foci.

We did not find any research that dealt directly with dry bean saponins and health. A number of publications extol the health benefits of the steroid type of saponins. Steriod saponins are absorbable and apparently elicit numerous biological responses following systemic distribution of the saponin. However, the triterpenoid saponins are not absorbed and presumably provide benefits only in the intestine.

Phytic Acid

Phytic acid (IP6, myo-inositol hexaphosphate) is the main storage form of phosphorous in dry beans (12, 13). Different forms of phytic acid exist depending on the pH and metal ions present – phytate is the calcium salt and phytin is the calcium-magnesium salt (13). The amount of phytic acid in legumes is between 0.4% to 2.06% but can vary with genetics, environmental conditions, type of soil, and fertilizer (12-14). Consumption of foods high in phytate, mainly IP4-IP6 derivatives are known to influence zinc, calcium, and iron bioavailability by forming insoluble mineral-phytate complexes in the intestine. These effects would likely be of most concern for vegetarians and in developing countries where cereal and grain products are consumed in large quantities (15).

The suggestion that phytic acid and/or its derivatives have anti-cancer properties was first derived from epidemiological data in two Scandinavian populations (16). The incidence of colon cancer is much lower in Finland (11.9%) than in Denmark (17.9%) despite similar dietary fiber intakes (16). However, upon further analysis, the Finnish consume 20-40% more phytate than Danish populations, owing to a greater intake of rye and wheat bran products. This led to the proposal that phytic acid contributed to the lower colon cancer incidence in this group. Several experimental studies have now demonstrated that phytic acid (IP6) inhibits colon cancer development (16-19). The effect of phytic acid on colon cancer was found to be dose-dependent and adding inositol improved IP6 efficacy. IP6 is most effective if provided after carcinogen administration (i.e., during cancer promotion). IP6 was effective even when given 5 months after carcinogen administration. Phytic acid has also been demonstrated to inhibit cancer at other sites including mammary, lung, liver, skin and prostate (20-26).

The mechanisms through which IP6 and inositol derivatives inhibit tumorigenesis have not been entirely defined. Vucenik and Shamsuddin (27) suggested that IP6 can be internalized and inhibit tumor growth by affecting cellular signaling through lower inositol derivatives. In support of this, there is some evidence that IP6 interacts with the Akt-NFκB cell survival pathway, by reducing insulin and TNF-induced Akt translocation to the cell membrane (28). Phytic acid also appears to influence the cell cycle. Treatment of cells with IP6 has been shown to cause G1 cell cycle arrest and a reduction of cells in S phase in breast (29), colon (29), and prostate cancer cell lines (30). Additionally, IP6 and inositol derivatives containing at least 3 phosphates (IP5, IP4, and IP3) can bind divalent metals, reducing iron catalyzed lipid peroxidation and high iron-induced promotion of colon tumorigenesis in rats.

Plant sterols

β-sitosterol, campesterol, and stigmasterol are the most common types of phytosterols found in food, including beans, and are structurally similar to cholesterol. The absorption of phytosterols by humans is low relative to that of cholesterol (20-50%) with only about 5% of ingested phytosterols being absorbed and the remaining 95% excreted from the colon (31). Phytosterols have been documented to decrease plasma cholesterol in humans (32) and animals (33, 34). The cholesterol reducing activity of bean sterols should help reduce cardiovascular diseases. The cholesterol lowering effect is likely due to a reduction in cholesterol solubilization into bile salt micelles resulting in a reduction in cholesterol absorption (34).

The relatively low absorption of ingested phytosterols from the intestine suggests that they can potentially affect colon carcinogenesis either directly or indirectly. Only a few animal studies, however, have been conducted to date. Phytosterols have been shown to reduce the rate of colonic epithelial proliferation and the proliferation zone in animals either induced with a carcinogen or administered 0.1-0.2% cholic acid. Addition of phytosterols (0.2-0.3%) to the diet also caused a reduction in both preneoplastic colon lesions and colon tumorigenesis in rodents (35). Lastly, although phytosterols were not examined specifically in this study, wheat bran oil (2%) decreased colon tumor incidence, multiplicity, and tumor size and reduced tumor expression of iNOS and COX-2 in rats injected with azoxymethane (AOM) (36). The mechanisms of chemoprevention by phytosterols have been suggested to include (a) alterations in membrane phospholipid composition (37), (b) decreased formation of secondary bile acids (38), and (c) an increase in apoptosis.

Phenolic Compounds

Over the past 15 years there has been an exponential increase in publications related to plant phenolics. The great interest in this class of non-nutritive compounds is largely due to: 1) epidemiologic studies showing that plant based diets lead to less chronic diseases; 2) fruits, vegetables, and whole grains are rich in phenolic compounds; 3) many of the phenolic compounds in fruits, vegetables, and whole grains are excellent antioxidants in vitro; and 4) researchers began to suggest oxidative stress was a strong contributing factor in the development of cancer, cardiovascular diseases, and neurodegenerative diseases.

Relatively little is known about the phenolic compounds in dry beans compared to fruit, vegetables, chocolate, wine, and tea. More recently, several groups (39-41) have identified phenolic compounds in dry beans. Anthocyanins are present in black and blue-violet colored beans (39-41). A black colored Italian bean contained 170 mg of anthocyanins/kg of flour which is equivalent to 6.5 mg/serving (41). Beninger et al. (42) reported the only flavonol present in 2 lines of pinto beans was glycosides of kaempferol. The amount of kaempferol that would be consumed in one serving was 26.6 mg and 64 mg for the 2 lines. Romani et al. (40) reported the only significant flavonol in yellow, brown, and black colored beans was kaempferol glycosides, although a trace of quercetin was detected in the brown and black variety. The amounts of kaempferol glycosides that would be consumed per serving were 23.5 and 20 mg for the 2 yellow varieties, 25.2 mg for the brown variety and 4.2 mg for the black bean. Aparicio-Fernandez et al. (41) identified glycosides of kaempferol, quercetin, and myriceten in a black bean as well as oligomers containing (epi)catechin, (epi)afzelechin and (epi)gallocatechin in the proanthocyanidin fraction (i.e., condensed tannins). No quantitative data was available from this report, but estimates based on other published studies indicate that one serving of beans would provide 300 – 1300 mg of proanthocyanidins depending on seed coat color, storage time, etc. Luthria and Pastor-Corrales (43) identified ferulic acid, p-coumaric acid, and sinapic acid in 15 varieties of raw dry beans. Caffeic acid was found only in 2 black bean varieties. The average phenolic acid that would be consumed was 11.1 mg/serving with a range of 6.8 to 17.2 mg/serving. For comparative purposes, dark blue-black berries and grapes provide 100 – 1500 mg of anthycyanins/serving. One serving of fruit provides 10 – 200 mg of phenolic acids and the amount of procyanidins from beans is equal or greater than that per serving of chocolate or green tea (44).

The studies reported above for phenolics all used raw beans which is not what we eat. Therefore, we cooked navy beans, black beans, pinto beans and small red beans and extracted the phenolic compounds. We identified protocatechuric acid, p-hydroxybenzoic acid, (+)-catechin, vanillic acid, caffeic acid, syringic acid, p-coumaric acid, ferulic acid, sinapic acid and isovanillic acid in all 4 types of beans. Ferulic acid was the predominant phenolic compound present in all beans. The flavonol, quercetin was detected in the black and red beans, while kaempherol was identified in pinto and red beans. We have not attempted to identify anthocyanins that have been identified in raw black beans and we do not have quantitative data for phenolic content at this time.

In general, polyphenolics are poorly absorbed. Of the phenolic compounds in beans, the phenolic acids would be absorbed the best and maximum plasma concentrations should occur one to three hours after beans are consumed (based on data reviewed by Manach (45)). One would not expect plasma concentrations to ever be greater than 0.5 umol/l and clearance from the blood is rapid (half-life for clearance in urine is < 2 hours). We can predict the amount of quercetin and kaempherol that would absorbed would be 1 – 2% of what is in beans (45). Blood concentrations would not exceed 0.5 umol/l. Even though the blood concentrations would be low, the clearance of quercetin (and maybe kaempherol) from the blood is slow compared to the other phenolic compounds (clearance half-life 15- 20 hr). Therefore, what little reaches the blood would be there for a longer period. Very little anthocyanins and essentially no proanthocyanidins would be absorbed (45).

Part of the poor absorption is due to the very active glucuronidation system in intestinal cells which results in the export of the glucuronidated phenolic compound back into the gut (45, 46). Even if the phenolic compound escapes glucuronidation in the enterocytes, much of the absorbed phenolic compound is glucuronidated and/or sulfated in the liver. Following glucuronidation and/or sulfation, much of the absorbed polyphenolic compound may be excreted into the bile and never appear in the blood. Rarely are glucuronidated and/or sulfated polyphenolic compounds in the blood in more than 1 umol/l concentrations when polyphenolic containing foods are consumed (45). The steady-state concentrations of polyphenolics in blood are often in the 100 – 900 nanomolar range and the concentration of unesterified polyphenolics in blood rarely exceeds picomolar concentrations.

Almost all of the research that demonstrates anti-cancer activity and biological end points that are purported to indicate a reduction in cardiovascular diseases, cancer, or untoward consequences of diabetes are done with concentrations that are 1,000 to 10,000 or more times greater than the concentrations of unesterified polyphenolics found in humans or laboratory animals. To have physiological relevance, the experiments need to be conducted with no more than 1 or 2 μmol/l concentrations of the glucuronidated and or sulphated polyphenolic compound.

Even though polyphenolics are poorly absorbed, have low concentrations in blood, are present as conjugates with greatly reduced bioactivity, and are eliminated fairly quickly, beneficial effects have been attributed to the consumption of plant phenolics by humans (47-51) and laboratory animals (52-55). Much additional research is required to determine if the phenolic compounds found in beans are protective against chronic diseases.

The one tissue that may be exposed to the high concentrations of phenolics utilized in the in vitro studies is the gut (46, 56, 57). However, in the colon, the polyphenolics are rapidly converted into monophenolics by the colonic microflora and the biological activity of the monophenolic metabolites are unknown. Much work remains here also.

a-Amylase inhibitors

α-Amylase inhibitors are naturally present in a variety of plants, but are particularly high in common beans (58). They are large glycoprotein molecules (38-60 kDa) that are inhibitory towards mammalian α-amylases. Lajolo et al. (58) screened 150 common beans and isolated two types of inhibitors, I-1 and I-2. The α-amylase inhibitors varied to some degree in thermal stability, subunit composition, molecular weight, and ratios of I-1:I-2 between bean varieties. Inhibitor activity was not correlated with seed color. Normal cooking methods destroy most if not all of the α-amylase inhibitor activity (59). However, there are occasional public health problems resulting from consuming active α-amylase inhibitors. For example, a raw white bean preparation was sold in Japan to promote weight loss. Many people became sick and some required hospitalization due to dehydration.

Lectins (phytohemagglutins)

Lectins are large glycoprotein molecules that bind to glycoconjugates on cell membranes and can agglutinate red blood cells in vitro (60). Following ingestion, they can survive passage through the acid environment of the stomach and proteolytic activity in the duodenum. Lectins bind to epithelial cells in the small intestine thereby affecting nutrient absorption. Binding of lectins cause jejunal villi hypoplasia and crypt cell hyperplasia resulting in shorter, thicker microvilli and a reduction in brush border enzymatic activity. In the 1980s, there were several reported outbreaks of lectin poisoning in Britain as the result of consumption of incompletely cooked beans, causing severe nausea, vomiting, and diarrhea. Growth depression has also been observed in animals fed either purified lectins or raw beans. Proper cooking methods are therefore important to reduce the possibility of illness. Moist heat is more effective in eliminating lectin activity than dry heat (61).

Trypsin/chymotrypsin inhibitors

Trypsin and chymotrypsin (protease) inhibitors are present in many legumes including dry beans (62, 63). Protease inhibitors, in particular trypsin inhibitors, have generally been considered as anti-nutritional due to the long-standing observations that feeding animals raw beans causes growth depression and reduces nitrogen retention. Additionally, in rats, chickens, and growing guinea pigs, long-term feeding of raw legume flour or purified trypsin inhibitor stimulated pancreatic hypertrophy and, in rats, pancreatic adenoma development. This has raised some concern whether chronic consumption of legumes and other foods containing protease inhibitors may also produce adverse effects in humans. However, commonly employed cooking methods reduce the trypsin inhibitor activity in beans by 80-95%. Based on animal feeding studies, only 55-69% of the trypsin inhibitor activity needs to be destroyed to reduce pancreatic hypertrophy in susceptible animals and 79-87% destruction issufficient to allow maximum weight gain (64).

Protease inhibitors have been examined in several different model systems for the ability to suppress carcinogenesis. The most effective are those that inhibit chymotrypsin, and within this group, the Bowman-Birk inhibitor (BBI) from soybeans has been most extensively studied (reviewed in (65, 66)). Purified BBI or a concentrate enriched in BBI (BBIC) incorporated into the diet at 0.5-1% has been repeatedly shown to reduce colon carcinogenesis in both mice and rats without producing adverse effects on pancreatic lesions or body weight gain. The effects on colon carcinogenesis are most pronounced when low doses of carcinogen are administered. BBI has also been demonstrated to inhibit DMBA-induced oral carcinogenesis in hamsters, dimethylhydrazidine (DMH)-induced liver angiosarcomas and 3-methylcholanthrene (MC) induced lung tumorigenesis in mice, and in vitro, suppress radiation or chemically induced malignant transformation. More recently, the efficacy of BBIC as a potential chemopreventitive agent has been extended to phase I clinical trials in humans with some suggestion of a protective effect on benign prostate hyperplasia and oral leukoplakia (67, 68).

The exact cellular target of BBI in tissues and the mechanism of chemoprevention are not known with certainty. BBI can distribute among most tissues, except the brain, within three hours following oral ingestion. The highest concentrations are found in urine and that remaining in intestinal contents (69). Because the catalytic activity of BBI remains intact within tissue, Kennedy proposed that BBI may be inhibiting one or more enzymes involved in inducing the transformed phenotype (66, 70). In support of this, BBI has been associated with reversing the up-regulation of a proteolytic activity (Boc-Val-Pro-Arg-MCA) in the oral epithelium following carcinogen treatment and suppressing radiation-induced expression of proto-oncogenes (c-myc) in colon tissue and cancer cell lines.

We did not find any research related to the protease inhibitors in dry beans and health. The potential for dietary protease inhibitors to be beneficial to human health is controversial and the research interest in this area appears to have declined during the past 8 years.

LONGEVITYreturn to top

What one eats affects disease susceptibility and survival. Comparing dietary patterns of elderly is one approach to discovering if there is a common denominator that promotes longevity. When food intake patterns of people 70 yr and older were examined in a cross-cultural study for a 5 to 7 yr period in 5 cohorts, the only statistically significant, consistent indicator of longevity was legume intake (71). For every 20g of legume consumption, there was a 7-8% reduction in mortality hazard ratio. The predominant legume consumed by the Swedish cohort was brown beans and peas and for the Greek cohorts in Australia and Greece, the predominant legumes consumed were white beans, lentils, and chickpeas. While this study doesn’t provide overwhelming evidence that eating beans increases longevity, the data are intriguing!

RELATIONSHIP OF CHRONIC DISEASES TO GLYCEMIC INDEX AND GLYCEMIC LOADreturn to top

Dietary factors that promote excess glucose in the blood (hyperglycemia), excess insulin in the blood (hyperinsulinemia), and excess body fat also promote development of several chronic diseases including Type 2 diabetes, cardiovascular diseases, and cancer at several sites in the body. Hyperglycemia, hyperinsulinemia, and excess body fat are simply markers for a milieu of changes – hormones, growth factors, inflammatory products, oxidative stress, to name a few – that contribute to development of chronic diseases.

The extent to which different foods or meals raise blood glucose depends on the glycemic index of the consumed foods and the quantity of carbohydrate. The glycemic index of a food is a ratio of how much the blood glucose rises after consuming a standard amount of available carbohydrate compared to a standard. The glycemic load is calculated by multiplying the glycemic index of a food by the quantity of available carbohydrate eaten. The glycemic load of a meal is computed by summing the glycemic loads of all foods consumed. The following will discuss how the type of carbohydrate and the amount of the carbohydrate consumed impacts hyperglycemia, hyperinsulinemia, and body weight and thus indirectly to the development of chronic diseases.

A considerable amount of research has been devoted to studying the impact of consuming foods with a low glycemic index in contrast to high glycemic index foods. However, when one component of the diet is modified, invariably other aspects of the diet are altered also. This has led to inconsistent results. A key study (72) used meta-analysis and meta-regression to control for confounding variables that occur when prospective studies are conducted to determine the outcome of substituting low glycemic food for high glycemic foods. Since the total amount of carbohydrate consumed is important, the effect of both glycemic index and glycemic load were studied. Dietary factors considered as covariates were intakes of energy, fat, protein, and unavailable carbohydrates. The data from 45 studies were analyzed for the impact of glycemic index and glycemic load on fasting concentrations of blood glucose and insulin, blood glucose control, and body weight.

Blood glucose

Thirty-six studies provided data regarding fasting blood glucose concentrations. The studies utilized subjects that were: normal healthy, glucose intolerant, type 1 and 2 diabetics, and those at risk for heart disease. These studies reported a range in the reduction of glycemic index and glycemic load. Eating a diet with a low glycemic index significantly (p < 0.05) reduces fasting blood glucose in proportion to the reduction in glycemic index. Almost all low glycemic index foods are good sources of unavailable carbohydrate and therefore as the glycemic index of the diet was reduced, the amount of unavailable carbohydrate was increased. It was determined that both a reduction in glycemic load as well as an increase in unavailable carbohydrate intake was important in causing a reduced fasting blood glucose concentration. A reduced glycemic load can be achieved by simply reducing the amount of carbohydrate containing foods that are consumed. It was further determined that a reduction in fasting blood glucose was better achieved by including low glycemic index foods and increasing unavailable carbohdrate rather than decreasing glycemic load by simply reducing the amount of available carbohydrate consumed.

Blood concentrations of glycated proteins (fructosamine and HbA1c) reflect overall control of blood glucose. Fifteen of the 36 studies provided information about fructosamine and/or HbA1c concentrations. These studies showed that overall control of blood glucose is strongly related to the glycemic index and glycemic load of the diet and the amount of unavailable carbohydrate consumed. It was suggested that optimum control of blood glucose is achieved when the diet has a glycemic index < 45, a glycemic load < 100g per day and a fiber intake of ≥ 25g per day.

Insulin

A reduction in insulin concentrations in fasting blood samples by switching from a high to a low glycemic index diet was achieved only when subjects had hyperinsulinemia (insulin > 100 pmol/l) initially. Non-diabetics with insulin > 100 pmol/l reduced their fasting insulin concentrations by an average of 73 pmol/l (p<0.001) when a low glycemic index diet intervention was implemented (2 studies). Likewise, fasting insulin was decreased by 73 pmol/l in overweight or obese, non-diabetics upon implementation of a low glycemic index diet only if their initial insulin was > 100 pmol/l (2 studies).

The amount of insulin required to promote glucose uptake by tissues (insulin sensitivity) is an important aspect of blood glucose control. Eighteen of the 45 studies reported measurements of insulin sensitivity. There was an average of 20% improvement (p< 0.004) in insulin sensitivity for the 18 studies when low glycemic index foods were substituted for high glycemic index foods. Non-diabetics (12 studies) improved (p<0.014) their insulin sensitivity by 25% and type 2 diabetics (5 studies) improved (p<0.014) their insulin sensitivity by 12%. Normal weight individuals (4 studies) did not achieve a significant improvement in insulin sensitivity while overweight and obese individuals (14 studies) had a 14% improvement (p<0.001) in insulin sensitivity. Taken together, people other than type 1 diabetics can expect an improvement in insulin sensitivity by switching from a high glycemic index diet to a low glycemic index diet.

Body Weight

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. (73) and in most industrialized countries (73-76). For example, on a worldwide basis, more than one billion adults are overweight and more than 300 million are obese (74, 75). In the U.S. more than 60% of the adult population is overweight or obese (76). Obesity and overweight account for approximately 300,000 deaths per year in North America (77, 78) and the cost associated with excess body fat is estimated to be greater than 117 billion dollars per year (79). Most of the costs associated with excess body fat are related to type 2 diabetes, heart disease, and high blood pressure (80).

Twenty-three studies examined changes in body weight that occurred when subjects changed from a high to a low glycemic index diet. It goes without saying that a reduction body weight can occur only if there is a reduction in metabolizable energy intake. On the average, the glycemic load needed to be decreased by 17g/day before weight loss would occur. Consistent weight loss was not reported until the glycemic load was reduced by > 42g/day. If a reduction in glycemic load by substituting low glycemic index foods for high glycemic index foods resulted in less available carbohydrate (therefore a lower energy intake), weight loss occurred. The only significant factor related to weight loss was a reduced glycemic load and caloric intake; changes in fat, protein, and fiber intake that occur by substituting low glycemic index foods for high glycemic index foods could not explain the weight loss.

Clearly, if bean consumption could be increased and if there was a concomitant decrease in body weight, the public health benefit would be enormous! Since increasing bean consumption would not increase the cost of the diet, it is hard to imagine a more cost effective intervention.

Beans, glycemic index, and glycemic load

The study by Livesey et al. (72) provides very strong evidence that eating diets with a low glycemic index (< 45), a low glycemic load (<100 g equivalents per day), and more than 25g per day of unavailable carbohydrate will help normalize blood glucose, blood insulin and body weight. Controlling blood glucose, blood insulin, and body weight in turn will reduce the incidence of type 2 diabetes, cardiovascular diseases and cancer in certain parts of the body.

Beans are the perfect food to improve glycemic control. Beans have a low glycemic index, varying from 27-42% relative to glucose and 40-59% that of white bread (Table 2; (81)). Beans are also high in non-starch polysaccharides (typically 18-20%), 5% resistant starch, and 4% oligosaccharides to give a dietary fiber value of 27 – 29%. Substituting beans for foods prepared from white flour (on an equal dry weight basis) will reduce the glycemic index of the diet by about two-thirds and glycemic load by about 80%. Furthermore, consuming beans will significantly increase your intake of dietary fiber and that is particularly important for controlling blood glucose concentrations.

LOW GLYCEMICGLYCEMIC CARBOHYDRATES AND DIABETESreturn to top

Consumption of low glycemic index carbohydrates and soluble dietary fiber aids in managing some of the metabolic abnormalities associated with insulin resistance, diabetes, and hyperlipidemia.

Epidemiological evidence also suggests that long-term consumption of high glycemic index/load diets may increase the risk of developing NIDDM (82-85). Six prospective studies have reported on the relationship of glycemic index or glycemic load to risk of NIDDM. Only two studies further evaluated dietary intake among different food categories, and included an analysis on legumes (84, 86). Collectively, these studies indicate a protective role for low glycemic index diets on risk of incident NIDDM.

In the Health Professionals Study and Nurses Health Study, a 37-40% increase in diabetes was found in individuals with the highest glycemic 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 (82, 83). In a cohort from the Nurses Health study II, an increased risk of incident NIDDM was also found in young and middle aged women (24-44 years of age at baseline), when comparing highest vs lowest quintiles for glycemic index (adjusted relative risk 1.62, 95% CI 1.28-2.03) (87). Krishnan et al. (85) examined differences in glycemic indices and risk of NIDDM among a cohort of US black women. After 8 years of follow-up, they found a positive association for diabetes in women consuming higher glycemic index diets, which was surprisingly stronger in women with a BMI <25. The incidence relative risk was 1.91 (1.16-3.16, P=0.002) for women in the highest quintile (glycemic index (GI); 60.7 ± 6.8) compared to those in the lowest quintile (GI 41.9 ± 2.8). In a cohort of older Australians, Barclay et al. (84) reported a 1.75-fold increased risk of NIDDM in women < 70 years of age consuming higher GI carbohydrates, after multiple adjustments for other known risk factors (HR 1.75, 95% CI 1.05-2.92, P=0.031). Lastly, in a cohort of middle-aged Chinese women (88), individuals in the highest quintile for glycemic index and glycemic load and with a BMI > 25 had a relative risk for NIDDM of 1.30 (95% CI 1.06-1.6) and 1.52 (95% CI 1.22-1.89), respectively, after adjustment for other known risk factors.

Two epidemiologic studies specifically related legume intake to risk of NIDDM. In a cohort of middle-aged Chinese women, Villegas et al. (86) reported a 38% reduced risk in the incidence of NIDDM for women in the highest quintile (65 g/day) of total legume intake (soybeans, peanuts, and other legumes) compared to those in the lowest quintile (12.3 g/day). This trend persisted when analyzed for “other legumes” (excluding soybeans and peanuts), with an adjusted relative risk in the highest quintile (37.1 g/day) of intake 0.76 (95% CI 0.64-0.90) compared to the lowest quintile of intake (5.6 g/day). One case-control study conducted in Europe found individuals consuming higher amounts of legumes were linked to a dietary pattern score associated with higher diabetes risk (89). The authors further acknowledged, however, that most of the legume intake in this group was attributable to a stew that also contains bacon, sausages, beef, or pork.

The ability of low GI carbohydrates to decrease risk of NIDDM may be related to lower post-prandial excursions in glucose and insulin coupled to improvements in insulin sensitivity (reviewed in (90)). High glycemic index foods are known to cause rapid elevations in blood glucose and insulin following a meal (discussed above). 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 (91). 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 (91, 92). Short-term studies in humans (93-99) indicate a role for low GI carbohydrates on improving insulin sensitivity. The accepted mechanism appears to be related to a decrease in counter-regulatory hormones (cortisol, and growth hormone) and non-esterified fatty acid release when low vs high GI foods are consumed (90). Current interest is also focusing on the role of hyperglycemia to inflammation, oxidative stress, and risk of diabetes. Increased circulating levels of the pro-inflammatory cytokines TNF α and IL-6 have been reported in insulin resistant individuals and diabetics (100-102) and serum IL-6 and C-reactive protein predict risk of diabetes in women (103). Higher plasma cytokine levels (IL-6, TNF α, and IL-18) have been reported in both normal and glucose intolerant individuals during acute hyperglycemic conditions, which were attenuated when the antioxidant, glutathione was co-administered (104). Although premature, these data suggest an intimate relationship of hyperglycemia to inflammation, and that reductions in hyperglycemia may mitigate risk of and vascular complications associated with diabetes.

It has been estimated that for every 1% reduction in HbA1c, there is a 21% reduction in risk in any end point examined for diabetes: 21% reduction for deaths, 14% for myocardial infarctions, and 37% for microvascular complications (105). Thus, the potential for low GI carbohydrates, especially beans, in the management, treatment, and delay in onset of NIDDM has profound implications for reducing morbidity and mortality associated with the disease.

BEAN CONSUMPTION AND CARDIOVASCULAR DISEASES (CVD)return to top

Only one epidemiological study has directly examined the relationship between bean consumption and occurrence of CVD. Kabagambe et al. (106) reported that 1 serving per day of beans was associated with a 38% lower risk of myocardial infarction. More than one serving per day did not elicit a further decrease in risk for myocardial infarction. Only one study examined the relationship between legume consumption and risk of CVD. All other studies were even less precise concerning bean consumption since they examined the relationship between a “healthy eating pattern” that includes legumes and risk of CVD.

Bazzano et al. (107) reported that individuals consuming legumes at least 4 times per week had a 22% lower risk of heart disease than individuals consuming legumes less than once per week. In the 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 (108) . Similar trends were seen in the Nurses Health Study (109). 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 (109). 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. Lastly, a prospective study (110) utilizing the Nurses Health Study cohort found an inverse, but not significant (p = 0.13) trend between eating the prudent diet and a lower the risk of stroke.

Data from several human intervention trials indicate that consumption of canned (111-114) and cooked beans (111, 115-121) reduce serum cholesterol. All 11 studies found small, but statistically significant reductions in total and LDL cholesterol by eating beans. Only two studies (122, 123) 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. Changes in HDL cholesterol and triglyceride concentrations are inconsistent (111-121, 124).

Reductions in blood cholesterol due to consuming beans is modest at best (typically in the 6 – 10% range) and not likely to attract much interest by the medical profession. The study by Kabagambe et al. (106) suggests that eating beans provides protection from CVD beyond what can be explained by a small depression in blood cholesterol. It is quite possible that the wide variety of phytochemicals in beans provide protection against developing CVD. For example, publications reporting “anti-oxidant phytochemicals” protect the heart from adverse conditions in various animal models are starting to appear (125).

BEAN CONSUMPTION AND CANCERreturn to top

The World Cancer Research Fund/American Institute for Cancer (3) recently published a comprehensive review that linked diet to cancer at 19 different locations in the body. Considering the etiology of cancer at many of the sites, one would expect that diet would have little impact except for excess body fat possibly increasing the risk. Beans were not considered as a separate entity, but as a group of foods labeled “pulses (legumes)”. If a food, group of foods, and individual nutrients were found to be related to cancer incidence at one of the 19 sites, the relationship was classified as “decreased the risk” or “increased the risk”. The strength of the evidence was classified as “convincing”, “probable”, “limited – suggestive”, or “limited – no conclusion”. To be classified as “probable”, there had to be considerable data demonstrating a relationship existed.

The panel of experts did not feel that the evidence relating legume consumption to a decreased risk of developing cancer was “convincing” or even “probable” for cancer located at any of the 19 sites in the body. However, fiber containing foods were considered “probable” for reducing the risk of cancer in the colon and rectum. Since beans are rich in fiber, it can be inferred that eating beans will probably reduce one’s risk of developing colon and rectal cancer. The data relating legume consumption to a reduction of stomach and prostate cancer was considered “limited, but suggestive”. It should be noted that the link between stomach cancer and legume intake is most likely based on soy and not on legumes other than soy. The study panel concluded that the data suggest that eating non-soy legumes would result in a reduction in prostate cancer (the specifics are discussed below). The panel also felt that the data relating foods rich in folate (naturally occurring or fortified) to a reduction in colon and rectal cancer was suggestive, but limited. The data relating legume consumption to cancers of the mouth, pharynx, larynx, esophagus, lung, pancreas, breast, ovary, and endometrium was too limited and no conclusion could be reached. There was no mention about dietary intake of legumes and the incidence of cancer in the nasopharynx, gallbladder, liver, cervix, kidney, bladder, or skin.

The expert panel did not include animal studies nor did they include human studies unless RR or OR with 95% CI were reported for their analyses. We feel that there are data to support that eating beans will reduce cancers of the colon, prostate, and breast, and possibly pancreas and esophageal.

The studies supporting our contention are discussed below.

BEANS and COLORECTAL CANCERreturn to top

A. Epidemiological Studies.

Despite the strong relationship of dietary habits to risk of colorectal cancer (CRC), epidemiologic studies are generally insufficient to conclude dry beans decrease CRC risk, although there is some suggestion of a protective effect. One cross-sectional study specifically related bean consumption to cancer mortality (126). Per capita data compiled from 41 countries (15 when beans were analyzed alone), revealed that countries with the greatest consumption of beans had the lowest mortality rates due to colon cancer (R=-0.68) (126). Nine case control studies have been conducted where legume intake on CRC risk was evaluated. Five case-control studies have reported a protective effect of legume consumption on some aspect of CRC risk (127-131), three reported no association (132-134), and one reported increased risk (135). Another case-control study in Majorca reported on fiber from pulses, rather than pulse intake (136). The authors found a significant protective effect (P < 0.01) for individuals in the highest quartile of legume fiber intake, with an OR of 0.4.

In a prospective study examining dietary patterns and disease risk as part of the Adventist Health Study in the US, significant inverse associations between legume (beans, peas, lentils) consumption and colon cancer were found (137). After 6 years of follow-up, Singh and Fraser (137) reported that overall, individuals consuming legumes > 2 times/week were 47% less likely of developing colon cancer when compared to individuals consuming legumes never to < 1 time/week (RR=0.53, 95% CI 0.33-0.86). Upon further analysis, a complex relationship was detected between legume and red meat intake and body mass index (BMI). They found that individuals consuming legumes < 1 time/week and red meat ≥ 1 time/week and with a BMI ≥ 25 kg/m2 had a RR of colon cancer development of 3.19 (95% CI 1.62-6.26) compared to individuals with a BMI ≤ 25 kg/m2 and consuming legumes > 1 time/week and red meat ≤ 1 time/week. This association was stronger in men (RR = 5.10, 95% CI 1.48-17.5) than in women (RR = 2.00, 95% CI 0.78-5.11). Other large cohort studies published since this have found no association between legume intake and CRC risk (138), however two studies reported a protective effect of legumes against adenoma recurrence. Lanza et al. (139) studied changes in specific subcategories of fruit and vegetable intake to risk of adenoma recurrence as part of the Polyp Prevention Trail in the US. The authors reported a 65% reduced risk of advanced adenoma recurrence (OR=0.35, 95% CI 0.18-0.69) for subjects in the highest quartile of change in dry bean intake from baseline levels (median change in intake from baseline = 370%) compared to individuals in the lowest quartile. There was no effect of change in bean intake on non-advanced adenoma recurrence (OR=1.01, 95% CI 0.76-1.34). In a cohort of the Nurses Health Study, women consuming four or more servings of legumes per week had a 33% lower risk of adenoma recurrence than those consuming less than one serving/week (OR=0.67, 95% CI 0.51-0.90; (140)).

B. Experimental Studies.

Three experimental studies have been conducted specifically examining the relationship of dry bean consumption to chemically-induced colon cancer in rats. Hughes et al. (141) fed rats diets containing either pinto beans (59% wt/wt) or casein as the protein source. They found that feeding pinto beans inhibited colon tumor incidence by 52% (50% in casein-fed animals vs 24% in bean-fed animals) and significantly reduced the number of tumors that developed (1.0 ± 0.0 vs 2.5 ± 0.6 tumors/ tumor bearing animal). In a similar design, Hangen and Bennink (142) also reported a protective effect of dry beans on experimental colon cancer. They found that feeding either black beans or navy beans (75% wt/wt) inhibited colon cancer by ~57%, and similar to Hughes et al. (141), bean-fed rats also developed fewer tumors (1.0 ± .17 vs 2.2 ± 1.2 tumors/tumor bearing animal). In this study, the chemoprevention of beans was associated with significantly more resistant starch reaching the colon, resulting in higher colonic acetate and butyrate production, and a decrease in body fat (142).

In the last study, Rondini and Bennink (unpublished data) corroborated chemically-induced tumor inhibition by black beans in rats. They found that black beans (74% wt/wt of diet) reduced the number of animals with colon tumors at both early (18 weeks after carcinogen administration, 8% vs 38%) and late (31 weeks post-carcinogen administration, 33% vs 75%) time points. Because the effect of beans on carcinogenesis appeared to be due to a delay in the development of tumors from normal-appearing colonic mucosa, they further profiled gene changes in non-involved (ie, “normal appearing”) distal colonic tissue from black bean- and casein-fed animals, either administered the carcinogen azoxymethane (AOM) or saline-injected controls, using microarrays. They anticipated that genes most important to black bean-induced suppression of tumorigenesis would have altered expression (increased or decreased) that paralleled tumor incidence. They identified 145 genes (90 up-regulated, 55 down-regulated) differentially expressed by beans compared to casein-fed animals. Bean-feeding induced changes in genes consistent with reduced cell proliferation and inflammation and enhanced energy metabolism. Specific molecular targets of beans that appear to corroborate reduced tumorigenesis included suppression of the pro-inflammatory gene secretory phospholipase A2 (sPLA2), the innate immune gene NP defensin 3α, as well as alterations in extracellular matrix components (collagen 1α1, fibronectin 1). These genes were induced by carcinogen (AOM) injection in both diets, but much less so in black bean-fed animals. These data provided preliminary evidence that inclusion of beans into the diet differentially affects molecular pathways in the colon important in carcinogenesis.

Breast cancer

In the Nurses Health Study, Adebamowo et al. (143) reported on intake of flavonols and flavonol-rich foods and risk of breast cancer in women who were premenopausal at baseline. A majority of breast cancer cases (89.7%) were premenopausal, 5.5% postmenopausal, and 4.8% of unknown menopausal status. They found a significant (P = 0.03) inverse association with bean and lentil intake, but not other flavonol-rich foods, and risk of breast cancer. The multivariate relative risk for highest (2 or more times/week) compared to lowest (<1 time/month) cumulative average intake was 0.76 (95% CI 0.57-1.00) and 0.67 (95% CI 0.48-0.94) when compared to baseline intake (p = 0.02). In the same cohort, however, Fung et al. (144) reported on dietary patterns and risk of postmenopausal breast cancer and found no association (P = 0.16) between legume intake (4-6 servings/week vs < 1 serving/week) and risk of estrogen receptor negative breast cancer (multivariate RR = 0.79, 95% CI 0.51-1.22).

Three case-control studies have been conducted where bean intake was assessed. Silva et al. (145) conducted a case-control study on vegetarianism and risk of breast cancer in South Asian immigrants living in England. They reported significant, inverse associations between the highest (>107.4 g/day) and the lowest (<35 g/day) quartiles of pulse, lentil, and dhal consumption (OR=0.54, 95% CI 0.31-0.94, P = 0.007) and risk of breast cancer in middle-aged women (median age cases (51.5), controls (51.9)). A non-significant inverse association was also found for intake of non-starch polysaccharides from pulses (adjusted OR=0.66, 95% CI 0.38-1.15) when comparing highest (>2.6 g/day) to lowest (<0.9 g/day) quartile of intake. In a case-control study in Shanghai, China, Shannon et al. (146) found no association between non-soy legumes and breast cancer risk (OR=0.76, 95% CI 0.48-1.21) when comparing highest (> 3.9 servings/week) to lowest (<1.9 serving/week) quartile after adjusting for age and total energy intake. The last case-control study, conducted in Argentina, found an increased risk (OR=3.3) in individuals consuming higher intakes of pulses (147). One study reported on fiber from beans (148). Potischman (148) examined food group and micronutrient associations with risk of early-stage breast cancer in women in the US. They found an insignificant, inverse association between cases and controls for intake of fiber from beans (OR=0.88, 95% CI 0.7-1.2) when comparing the highest (>1.89g/day) to lowest quartile (<0.72 g/day) of intake. After adjustment for energy, the same trend existed, although this did not reach statistical significance.

Three ecological studies found a negative association between legume consumption and breast cancer mortality (149-151). One cross-sectional study specifically related bean consumption to breast cancer mortality (126). Per capita data from 15 countries, revealed that countries with the greatest consumption of beans had the lowest mortality rates due to breast (R=-0.70) cancer.

Prostate cancer

One case-control and one cohort study specifically identified beans and risk of prostate cancer. The case-control study reported a reduced risk for prostate cancer with increasing consumption of baked beans (152). An odds ratio of 0.844 (95% CI; 0.709 – 1.00) was determined per increase in serving of baked beans per week. The cohort study conducted in the Netherlands (153) found an inverse relationship between consumption of broad bean and risk of prostate cancer (OR 0.956 (95% CI; 0.823 – 1.11)). Both studies reported that consuming beans reduced the risk of prostate cancer, but the results from the cohort study were not statistically significant.

Four studies compared the frequency of bean and lentil consumption to risk for prostate cancer. A prospective cohort study (154) found that eating beans and lentils significantly reduced the risk of prostate cancer (OR of 0.817 (95% CI; 0.714 – 0.934)). Meta analysis of the three case-control studies (152, 155, 156) showed a statistically non-significant protective relationship between bean and lentil consumption and risk of prostate cancer OR of 0.956 (95% CI; 0.884 – 1.03). One cohort study (157) did not report quantified data but they did indicate that the association between prostate cancer mortality and bean and lentil consumption was not statistically significant. One case-control study (152) reported a non-significant increase in prostate cancer was associated with eating beans, lentils, and peas.

Kolonel et al. (158) studied dietary patterns and risk of prostate cancer in the USA and Canada. When they differentiated between soy and non-soy legumes, an inverse relationship between non-soy legume consumption and prostate cancer was determined (OR of 0.966 (95% CI; 0.941 – 0.991). Dry beans are the most commonly consumed non-soy legume in the US and Canada, so this study suggests that eating beans helps to inhibit prostate cancer. Soy consumption was not related to prostate cancer incidence.

There were five case-control studies (152, 158-161) when the food category was broadened to include all pulses (studies cited in the above 3 paragraphs are included as part of the pulse category). These studies produced an overall OR of 0.966 (95% CI; 0.951 – 0.981) per increase in pulse serving/week. Four ecological studies reported a protective effect of legume consumption on prostate cancer risk (149, 162-164). One cross-sectional study specifically examined bean consumption and mortality rates from prostate cancer (126). Data from 15 countries revealed that countries with the greatest consumption of beans had the lowest death rates due to prostate cancer (r = -0.66).

It is important to note that the expert committee (3) concluded that the cohort study and the case-control studies showed that consuming pulses reduced the risk of prostate cancer.

ADDITIONAL DATA RELATING BEANS TO CANCER PREVENTIONreturn to top

Fiber and cancer

A large number of studies have examined the relationship between fiber intake and colorectal cancer with mixed results. The WCRF/AICR study panel (3) summarized 19 cohort studies. Ninety-one case-control studies have been conducted, but because of the large number of cohort studies, the case-control studies were not summarized. It was possible to conduct a meta-analysis on 8 of the cohort studies. The OR from the meta-analysis was 0.90 with a 95% CI (0.84 – 0.97) per 10g of fiber intake per day and a dose-response relationship was apparent. The expert panel concluded that foods containing fiber (naturally occurring, not added fiber) are probably protective against colon cancer based on generally consistent cohort studies, a clear dose-response, and plausible mechanisms. High

Page 19intakes of fiber have been associated with a reduced risk of esophageal cancer and cardiovascular diseases also. Pulses (legumes) and minimally processed cereals are the most concentrated sources of fiber.

Folate and cancer

Foods that are good sources of folate were identified as protecting against cancer at several sites (3). The strongest protective association for folate containing foods was noted for pancreatic cancer. The data for cancers of the colon and esophagus was strong, but not as strong as for protection against pancreatic cancer.

LITERATURE CITED

1. Minino AM, Heron MP, Murphy SL, Kochanek KD. National Vital Statistics Reports. 2007:55(19).

2. Cleophas TJ, Hornstra N, van Hoogstraten B, van der Meulen J. Homocysteine, a risk factor for coronary artery disease or not? A meta-analysis. American Journal of Cardiology. 2000;86(9):1005-1009.

3. World Cancer Research Fund/American Institute for Cancer Research. Food, Nutrition, Physical Activity, and the Prevention of Cancer: a Global Perspective. Washington DC: AICR, 2007

4. Oakenfull D. Saponins in Food – a Review. Food Chemistry. 1981;7(1):19-40.

5. Lasztity R, Hidevegi M, Bata A. Saponins in food. Food Reviews International. 1998;14(4):371-390.

6. Curl CL, Price KR, Fenwick GR. Isolation And Structural Elucidation Of A New Saponin (Soyasaponin-V) From Haricot Bean (Phaseolus-Vulgaris L). Journal Of The Science Of Food And Agriculture. 1988;43(1):101-107.

7. Kinjo J, Hatakeyama M, Udayama M, et al. HPLC profile analysis of oleanene-glucuronides in several edible beans. Bioscience Biotechnology And Biochemistry. 1998;62(3):429-433.

8. Gestetner B, Birk Y, Tencer Y. Soybean Saponins – Fate Of Ingested Soybean Saponins And Physiological Aspect Of Their Hemolytic Activity. Journal Of Agricultural And Food Chemistry.1968;16(6):1031-1035.

9. Gurfinkel DM, Rao AV. Soyasaponins: The relationship between chemical structure and colon anticarcinogenic activity. Nutrition and Cancer-an International Journal. 2003;47(1):24-33.

10. Gurfinkel DM, Rao AV. Determination of saponins in legumes by direct densitometry. Journal of Agricultural and Food Chemistry. 2002;50(3):426-430.

11. Koratkar R, Rao AV. Effect of soya bean saponins on azoxymethane-induced preneoplastic lesions in the colon of mice. Nutrition and Cancer-an International Journal. 1997;27(2):206-209.

12. Reddy NR, Sathe SK, Salunkhe DK. Phytates in Legumes and Cereals. Advances in Food Research.

13. Oatway L, Vasanthan T, Helm JH. Phytic acid. Food Reviews International. 2001;17(4):419-431.

14. Urbano G, Lopez-Jurado M, Aranda P, Vidai-Valverde C, Tenorio E, Porres J. The role of phytic acid in legumes: antinutrient or beneficial function? Journal of Physiology and Biochemistry. 2000;56(3):283-294.

15. Plaami S. Myoinositol phosphates: Analysis, content in foods and effects in nutrition. Food Science and Technology-Lebensmittel-Wissenschaft & Technologie. 1997;30(7):633-647.

16. Graf E, Eaton JW. Suppression of Colonic-Cancer by Dietary Phytic Acid. Nutrition and Cancer-an International Journal. 1993;19(1):11-19.

17. Shamsuddin AM, Elsayed AM, Ullah A. Suppression of Large Intestinal Cancer in F344 Rats by Inositol Hexaphosphate. Carcinogenesis. 1988;9(4):577-580.

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Bennink – Rondini 2008

18. Shamsuddin AM, Ullah A. Inositol Hexaphosphate Inhibits Large Intestinal Cancer in F344 Rats 5 Months after Induction by Azoxymethane. Carcinogenesis. 1989;10(3):625-626.

19. Ullah A, Shamsuddin AM. Dose-Dependent Inhibition of Large Intestinal Cancer by Inositol Hexaphosphate in F344 Rats. Carcinogenesis. 1990;11(12):2219-2222.

20. Vucenik I, Tomazic VJ, Fabian D, Shamsuddin AM. Antitumor-Activity of Phytic Acid (Inositol Hexaphosphate) in Murine Transplanted and Metastatic Fibrosarcoma, a Pilot-Study. Cancer Letters. 1992;65(1):9-13.

21. Vucenik I, Sakamoto K, Bansal M, Shamsuddin AM. Inhibition of Rat Mammary Carcinogenesis by Inositol Hexaphosphate (Phytic Acid) – a Pilot-Study. Cancer Letters. 1993;75(2):95-102.

22. Estensen RD, Wattenberg LW. Studies of Chemopreventive Effects of Myoinositol on Benzo[a]Pyrene- Induced Neoplasia of the Lung and Forestomach of Female a/J Mice. Carcinogenesis. 1993;14(9):1975-1977.

23. Vucenik I, Yang GY, Shamsuddin AM. Inositol Hexaphosphate and Inositol Inhibit Dmba-Induced Rat Mammary-Cancer. Carcinogenesis. 1995;16(5):1055-1058.

24. Vucenik I, Yang G, Shamsuddin AM. Comparison of pure inositol hexaphosphate and high-bran diet in the prevention of DMBA-induced rat mammary carcinogenesis. Nutrition and Cancer-an International Journal. 1997;28(1):7-13.

25. Vucenik I, Kalebic T, Tantivejkul K, Shamsuddin AM. Novel anticancer function of inositol hexaphosphate: Inhibition of human rhabdomyosarcoma in vitro and in vivo. Anticancer Research. 1998;18(3A):1377-1384.

26. Gupta KP, Singh J, Bharathi R. Suppression of DMBA-induced mouse skin tumor development by inositol hexaphosphate and its mode of action. Nutrition and Cancer-an International Journal. 2003;46(1):66-72.

27. Vucenik I, Shamsuddin AM. Cancer inhibition by inositol hexaphosphate (IP6) and inositol: From laboratory to clinic. Journal of Nutrition. 2003;133(11):3778S-3784S.

28. Sandra F, Matsuda M, Yoshida H, Hirata M. Inositol hexakisphosphate blocks tumor cell growth by activating apoptotic machinery as well as by inhibiting the Akt/NF kappa B-mediated cell survival pathway (vol 23, pg 2031, 2003). Carcinogenesis. 2003;24(1):149-149.

29. El-Sherbiny YM, Cox MC, Ismail ZA, Shamsuddin AM, Vucenik I. G(0)/G(1) arrest and S phase inhibition of human cancer cell lines by inositol hexaphosphate (IP6). Anticancer Research. 2001;21(4A):2393-2403.

30. Singh RP, Agarwal C, Agarwal R. Inositol hexaphosphate inhibits growth, and induces G1 arrest and apoptotic death of prostate carcinoma DU145 cells: modulation of CDKI-CDK-cyclin and pRb-related protein-E2F complexes. Carcinogenesis. 2003;24(3):555-563.

31. Salen G, Shore V, Tint GS, et al. Increased Sitosterol Absorption, Decreased Removal, And Expanded Body Pools Compensate For Reduced Cholesterol-Synthesis In Sitosterolemia With Xanthomatosis. Journal Of Lipid Research. 1989;30(9):1319-1330.

Page 21

Bennink – Rondini 2008

32. Normen L, Dutta P, Lia A, Andersson H. Soy sterol esters and beta-sitostanol ester as inhibitors of cholesterol absorption in human small bowel. American Journal of Clinical Nutrition. 2000;71(4):908-913.

33. Vahouny GV, Connor WE, Subramaniam S, Lin DS, Gallo LL. Comparative Lymphatic Absorption Of Sitosterol, Stigmasterol, And Fucosterol And Differential Inhibition Of Cholesterol Absorption. American Journal Of Clinical Nutrition. 1983;37(5):805-809.

34. Ikeda I, Sugano M. Inhibition of cholesterol absorption by plant sterols for mass intervention. Current Opinion in Lipidology. 1998;9(6):527-531.

35. Raicht RF, Cohen BI, Fazzini EP, Sarwal AN, Takahashi M. Protective Effect of Plant Sterols against Chemically-Induced Colon Tumors in Rats. Cancer Research. 1980;40(2):403-405.

36. Reddy BS, Hirose Y, Cohen LA, Simi B, Cooma I, Rao CV. Preventive potential of wheat bran fractions against experimental colon carcinogenesis: Implications for human colon cancer prevention. Cancer Research. 2000;60(17):4792-4797.

37. Awad AB, Hernandez AYT, Fink CS, Mendel SL. Effect of dietary phytosterols on cell proliferation and protein kinase C activity in rat colonic mucosa. Nutrition and Cancer-an International Journal. 1997;27(2):210-215.

38. Rao AV, Koratkar R. Anticarcinogenic effects of saponins and phytosterols. Antinutrients and Phytochemicals in Food. 1997;662:313-324.

39. Beninger CW, Hosfield GL. Antioxidant activity of extracts, condensed tannin fractions, and pure flavonoids from Phaseolus vulgaris L. seed coat color genotypes. Journal Of Agricultural And Food Chemistry. 2003;51(27):7879-7883.

40. Romani A, Vignolini P, Galardi CR, Mulinacci N, Benedettelli S, Heimler D. Germplasm characterization of zolfino landraces (Phaseolus vulgaris L.) by flavonoid content. Journal Of Agricultural And Food Chemistry. 2004;52(12):3838-3842.

41. Aparicio-Fernandez X, Yousef GG, Loarca-Pina G, de Mejia E, Lila MA. Characterization of polyphenolics in the seed coat of Black Jamapa bean (Phaseolus vulgaris L.). Journal Of Agricultural And Food Chemistry. 2005;53(11):4615-4622.

42. Beninger CW, Gu LW, Prior RL, Junk DC, Vandenberg A, Bett KE. Changes in polyphenols of the seed coat during the after-darkening process in pinto beans (Phaseolus vulgaris L.). Journal Of Agricultural And Food Chemistry. 2005;53(20):7777-7782.

43. Luthria DL, Pastor-Corrales MA. Phenolic acids content of fifteen dry edible bean (Phaseolus vulgaris L.) varieties. Journal Of Food Composition And Analysis. 2006;19(2-3):205-211.

44. Manach C, Scalbert A, Morand C, Remesy C, Jimenez L. Polyphenols: food sources and bioavailability. American Journal Of Clinical Nutrition. 2004;79(5):727-747.

Page 22

Bennink – Rondini 2008

45. Manach C, Williamson G, Morand C, Scalbert A, Remesy C. Bioavailability and bioefficacy of polyphenols in humans. I. Review of 97 bioavailability studies. American Journal Of Clinical Nutrition. 2005;81(1):230S- 242S.

46. Stevenson DE, Hurst RD. Polyphenolic phytochemicals – just antioxidants or much more? Cellular And Molecular Life Sciences. 2007;64(22):2900-2916.

47. Aggarwal BB, Bhardwaj A, Aggarwal RS, Seeram NP, Shishodia S, Takada Y. Role of resveratrol in prevention and therapy of cancer: Preclinical and clinical studies. Anticancer Research. 2004;24(5A):2783- 2840.

48. Neuhouser ML. Dietary flavonoids and cancer risk: Evidence from human population studies. Nutrition And Cancer-An International Journal. 2004;50(1):1-7.

49. Manach C, Mazur A, Scalbert A. Polyphenols and prevention of cardiovascular diseases. Current Opinion In Lipidology. 2005;16(1):77-84.

50. Zern TL, Wood RJ, Greene C, et al. Grape polyphenols exert a cardioprotective effect in pre- and postmenopausal women by lowering plasma lipids and reducing oxidative stress. Journal Of Nutrition. 2005;135(8):1911-1917.

51. Hodgson JM, Croft KD. Dietary flavonoids: effects on endothelial function and blood pressure. Journal Of The Science Of Food And Agriculture. 2006;86(15):2492-2498.

52. Tsuda T, Horio F, Uchida K, Aoki H, Osawa T. Dietary cyanidin 3-O-beta-D-glucoside-rich purple corn color prevents obesity and ameliorates hyperglycemia in mice. Journal Of Nutrition. 2003;133(7):2125-2130.

53. Fuhrman B, Volkova N, Coleman R, Aviram M. Grape powder polyphenols attenuate atherosclerosis development in apolipoprotein E deficient (E-O) mice and reduce macrophage atherogenicity. Journal Of Nutrition. 2005;135(4):722-728.

54. Wang Q, Simonyi A, Li WL, et al. Dietary grape supplement ameliorates cerebral ischemia-induced neuronal death in gerbils. Molecular Nutrition & Food Research. 2005;49(5):443-451.

55. Zunino SJ, Storms DH, Stephensen CB. Diets rich in polyphenols and vitamin A inhibit the development of type I autoimmune diabetes in nonobese diabetic mice. Journal Of Nutrition. 2007;137(5):1216-1221.

56. Williamson G, Manach C. Bioavailability and bioefficacy of polyphenols in humans. II. Review of 93 intervention studies. American Journal Of Clinical Nutrition. 2005;81(1):243S-255S.

57. Halliwell B. Dietary polyphenols: Good, bad, or indifferent for your health? Cardiovascular Research. 2007;73(2):341-347.

58. Lajolo FM, Finardi F, Menezes EW. Amylase Inhibitors in Phaseolus-Vulgaris Beans. Food Technology. 1991;45(9):119-121.

59. Lajolo FM, Genovese MI. Nutritional significance of lectins and enzyme inhibitors from legumes. Journal of Agricultural and Food Chemistry. 2002;50(22):6592-6598.

Page 23

Bennink – Rondini 2008

60. Liener IE. Implications of Antinutritional Components in Soybean Foods. Critical Reviews in Food Science and Nutrition. 1994;34(1):31-67.

61. Gatel F. Protein-Quality of Legume Seeds for Non-Ruminant Animals – a Literature-Review. Animal Feed Science and Technology. 1994;45(3-4):317-348.

62. Weder J, Belitz HD. Trypsin And Chymotrypsin Inhibitors In Foodstuffs. Angewandte Chemie-International Edition. 1968;7(12):957-&.

63. Weder JKP, Telek L, Vozari-Hampe M, Saini HS. Antinutritional factors in anasazi and other pinto beans (Phaseolus vulgaris L.). Plant Foods for Human Nutrition. 1997;51(2):85-98.

64. Deshpande SS. Food Legumes in Human-Nutrition – a Personal Perspective. Critical Reviews in Food Science and Nutrition. 1992;32(4):333-363.

65. Kennedy AR. The Bowman-Birk inhibitor from soybeans as an anticarcinogenic agent. American Journal of Clinical Nutrition. 1998;68(6):1406S-1412S.

66. Kennedy AR. Chemopreventive agents: Protease inhibitors. Pharmacology & Therapeutics. 1998;78(3):167- 209.

67. Armstrong WB, Kennedy AR, Wan XS, Atiba J, McLaren E, Meyskens FL. Single-dose administration of Bowman-Birk inhibitor concentrate in patients with oral leukoplakia. Cancer Epidemiology Biomarkers & Prevention. 2000;9(1):43-47.

68. Armstrong WB, Kennedy AR, Wan XS, et al. Clinical modulation of oral leukoplakia and protease activity by Bowman-Birk inhibitor concentrate in a phase IIa chemoprevention trial. Clinical Cancer Research. 2000;6(12):4684-4691.

69. Billings PC, Stclair WH, Maki PA, Kennedy AR. Distribution of the Bowman Birk Protease Inhibitor in Mice Following Oral-Administration. Cancer Letters. 1992;62(3):191-197.

70. Billings PC, Habres JM. A Growth-Regulated Protease Activity That Is Inhibited by the Anticarcinogenic Bowman-Birk Protease Inhibitor. Proceedings of the National Academy of Sciences of the United States of America. 1992;89(7):3120-3124.

71. Darmadi-Blackberry I, Wahqvist ML, Kouris-Blazos A, et al. Legumes: the most important dietary predictor of survival in older people of different ethnicities. Asia Pacific Journal Of Clinical Nutrition. 2004;13(2):217- 220.

72. Livesey G, Taylor R, Hulshof T, Howlett J. Glycemic response and health – a systematic review and meta- analysis: relations between dietary glycemic properties and health outcomes. American Journal Of Clinical Nutrition. 2008;87(1):258S-268S.

73. U.S. Department of Health and Human Services. The Surgeon General’s call to action to prevent and decrease overweight and obesity, Rockville, MD: 2001.

Page 24

Bennink – Rondini 2008

74. WHO. The world health report: Reducing risk, promoting healthy life, World Health Organization, Geneva: 2002.

75. WHO. Obesity: Preventing and managing the global epidemic. World Health Organization, WHO Technical Report Series, No. 894, Geneva: 2000.

76. Ogden CL, Yanovski SZ, Carroll MD, Flegal KM. The epidemiology of obesity. Gastroenterology. 2007;132(6):2087-2102.

77. McGinnis JM, Foege WH. Actual Causes Of Death In The United-States. Jama-Journal Of The American Medical Association. 1993;270(18):2207-2212.

78. Allison DB, Fontaine KR, Manson JE, Stevens J, VanItallie TB. Annual deaths attributable to obesity in the United States. Jama-Journal Of The American Medical Association. 1999;282(16):1530-1538.

79. Wolf AM. Impact of obesity on healthcare delivery costs. American Journal Of Managed Care. 1998;4(3):S141-S145.

80. Wolf AM, Colditz GA. Current estimates of the economic cost of obesity in the United States. Obesity Research. 1998;6(2):97-106.

81. Foster-Powell K, Miller JB. International Tables of Glycemic Index. American Journal of Clinical Nutrition. 1995;62(4):S871-S890.

82. Salmeron J, Ascherio A, Rimm EB, et al. Dietary fiber, glycemic load, and risk of NIDDM in men. Diabetes Care. 1997;20(4):545-550.

83. Salmeron J, Manson JE, Stampfer MJ, Colditz GA, Wing AL, Willett WC. Dietary fiber, glycemic load, and risk of non-insulin-dependent diabetes mellitus in women. Jama-Journal of the American Medical Association. 1997;277(6):472-477.

84. Barclay AW, Brand-Miller JC, Mitchell P. Macronutrient intake, glycaemic index and glycaemic load of older Australian subjects with and without diabetes: baseline data from the Blue Mountains Eye Study. British Journal Of Nutrition. 2006;96(1):117-123.

85. Krishnan S, Rosenberg L, Singer M, et al. Glycemie index, glycemie load, and cereal fiber intake and risk of type 2 diabetes in US black women. Archives Of Internal Medicine. 2007;167(21):2304-2309.

86. Villegas R, Gao YT, Yang G, et al. Legume and soy food intake and the incidence of type 2 diabetes in the Shanghai Women’s Health Study. American Journal Of Clinical Nutrition. 2008;87(1):162-167.

87. Schulze MB, Liu SM, Rimm EB, Manson JE, Willett WC, Hu FB. Glycemic index, glycemic load, and dietary fiber intake and incidence of type 2 diabetes in younger and middle-aged women. American Journal Of Clinical Nutrition. 2004;80(2):348-356.

88. Villegas R, Liu SM, Gao YT, et al. Prospective study of dietary carbohydrates, glycemic index, glycemic load, and incidence of type 2, diabetes mellitus in middle-aged Chinese women. Archives Of Internal Medicine. 2007;167(21):2310-2316.

Page 25

Bennink – Rondini 2008

89. Heidemann C, Hoffmann K, Spranger J, et al. A dietary pattern protective against type 2 diabetes in the European Prospective Investigation into Cancer and Nutrition (EPIC) – Potsdam Study cohort. Diabetologia. 2005;48(6):1126-1134.

90. Willett W, Manson J, Liu SM. Glycemic index, glycemic load, and risk of type 2 diabetes. American Journal of Clinical Nutrition. 2002;76(1):274S-280S.

91. Augustin LS, Franceschi S, Jenkins DJA, Kendall CWC, La Vecchia C. Glycemic index in chronic disease: a review. European Journal of Clinical Nutrition. 2002;56(11):1049-1071.

92. Ludwig DDS. The glycemic index – Physiological mechanisms relating to obesity, diabetes, and cardiovascular disease. Jama-Journal of the American Medical Association. 2002;287(18):2414-2423.

93. Jenkins DJA, Taylor RH, Wolever TMS. The Diabetic Diet, Dietary Carbohydrate and Differences in Digestibility. Diabetologia. 1982;23(6):477-484.

94. Wolever TMS, Jenkins DJA, Ocana AM, Rao VA, Collier GR. 2nd-Meal Effect – Low-Glycemic-Index Foods Eaten At Dinner Improve Subsequent Breakfast Glycemic Response. American Journal Of Clinical Nutrition. 1988;48(4):1041-1047.

95. Jenkins DJA, Jenkins AL. Nutrition Principles and Diabetes – a Role for Lente Carbohydrate. Diabetes Care. 1995;18(11):1491-1498.

96. Frost G, Leeds A, Trew G, Margara R, Dornhorst A. Insulin sensitivity in women at risk of coronary heart disease and the effect of a low glycemic diet. Metabolism-Clinical And Experimental. 1998;47(10):1245- 1251.

97. Jarvi AE, Karlstrom BE, Granfeldt YE, Bjorck IE, Asp NGL, Vessby BOH. Improved glycemic control and lipid profile and normalized fibrinolytic activity on a low-glycemic index diet in type 2 diabetic patients. Diabetes Care. 1999;22(1):10-18.

98. Liljeberg HGM, Akerberg AKE, Bjorck IME. Effect of the glycemic index and content of indigestible carbohydrates of cereal-based breakfast meals on glucose tolerance at lunch in healthy subjects. American Journal Of Clinical Nutrition. 1999;69(4):647-655.

99. Liljeberg H, Bjorck I. Effects of a low-glycaemic index spaghetti meal on glucose tolerance and lipaemia at a subsequent meal in healthy subjects. European Journal Of Clinical Nutrition. 2000;54(1):24-28.

100. Zinman B, Hanley AJG, Harris SB, Kwan J, Fantus IG. Circulating tumor necrosis factor-alpha concentrations in a native Canadian population with hgh rates of type 2 diabetes mellitus. Journal Of Clinical Endocrinology And Metabolism. 1999;84(1):272-278.

101. Rodriguez-Moran M, Guerrero-Romero F. Increased levels of C-reactive protein in noncontrolled type II diabetic subjects. Journal Of Diabetes And Its Complications. 1999;13(4):211-215.

102. Pickup JC, Chusney GD, Thomas SM, Burt D. Plasma interleukin-6, tumour necrosis factor alpha and blood cytokine production in type 2 diabetes. Life Sciences. 2000;67(3):291-300.

Page 26

Bennink – Rondini 2008

103. Pradhan AD, Manson JE, Rifai N, Buring JE, Ridker PM. C-reactive protein, interleukin 6, and risk of developing type 2 diabetes mellitus. Jama-Journal Of The American Medical Association. 2001;286(3):327- 334.

104. Esposito K, Nappo F, Marfella R, et al. Inflammatory cytokine concentrations are acutely increased by hyperglycemia in humans – Role of oxidative stress. Circulation. 2002;106(16):2067-2072.

105. Stratton IM, Adler AI, Neil HAW, et al. Association of glycaemia with macrovascular and microvascular complications of type 2 diabetes (UKPDS 35): prospective observational study. British Medical Journal. 2000;321(7258):405-412.

106. Kabagambe EK, Baylin A, Ruiz-Narvarez E, Siles X, Campos H. Decreased consumption of dried mature beans is positively associated with urbanization and nonfatal acute myocardial infarction. Journal Of Nutrition. 2005;135(7):1770-1775.

107. Bazzano LA, He J, Ogden LG, et al. Legume consumption and risk of coronary heart disease in US men and women. Archives of Internal Medicine. 2001;161(21):2573-2578.

108. Hu FB, Rimm EB, Stampfer MJ, Ascherio A, Spiegelman D, Willett WC. Prospective study of major dietary patterns and risk of coronary heart disease in men. American Journal of Clinical Nutrition. 2000;72(4):912- 921.

109. Fung TT, Willett WC, Stampfer MJ, Manson JE, Hu FB. Dietary patterns and the risk of coronary heart disease in women. Archives of Internal Medicine. 2001;161(15):1857-1862.

110. Fung TT, Stampfer MJ, Manson JE, Rexrode KM, Willett WC, Hu FB. Prospective study of major dietary patterns and stroke risk in women. Stroke. 2004;35(9):2014-2019.

111. Anderson JW, Ratliff P. High-Carbohydrate, High-Fiber Diets Decrease Insulin Requirements of Type-I Diabetic Individuals. Clinical Research. 1987;35(6):A898-A898.

112. Shutler SM, Bircher GM, Tredger JA, Morgan LM, Walker AF, Low AG. The Effect of Daily Baked Bean (Phaseolus-Vulgaris) Consumption on the Plasma-Lipid Levels of Young, Normo-Cholesterolemic Men. British Journal of Nutrition. 1989;61(2):257-265.

113. Anderson JW, Smith BM, Washnock CS. Cardiovascular and renal benefits of dry bean and soybean intake. American Journal of Clinical Nutrition. 1999;70(3):464S-474S.

114. Winham DM, Hutchins AM, Johnston CS. Pinto bean consumption reduces biomarkers for heart disease risk. Journal Of The American College Of Nutrition. 2007;26(3):243-249.

115. Simpson HCR, Lousley S, Geekie M, et al. A High-Carbohydrate Leguminous Fiber Diet Improves All Aspects of Diabetic Control. Lancet. 1981;1(8210):1-4.

116. Jenkins DJA, Wolever TMS, Jenkins AL, et al. The Glycemic Index of Foods Tested in Diabetic-Patients – a New Basis for Carbohydrate Exchange Favoring the Use of Legumes. Diabetologia. 1983;24(4):257-264.

Page 27

Bennink – Rondini 2008

117. Anderson JW, Gustafson NJ, Spencer DB, Tietyen J, Bryant CA. Serum-Lipid Response of Hypercholesterolemic Men to Single and Divided Doses of Canned Beans. American Journal of Clinical Nutrition. 1990;51(6):1013-1019.

118. Bingwen, L., Zhaofeng, W., Wanzhen, L., and Rongjue, Z. Effects of bean meal on serum cholesterol and triglycerides. Chinese Medical Journal 1981: 94:455-458.

119. Jimenez-Cruz A, Turnbull WH, Bacardi-Gascon M, Rosales-Garay P. A high-fiber, moderate-glycemic-index, Mexican style diet improves dyslipidemia in individuals with type 2 diabetes. NutritionResearch. 2004;24(1):19-27.

120. Winham DM, Hutchins AM. Baked bean consumption reduces serum cholesterol in hypercholesterolemic adults. Nutrition Research. 2007;27(7):380-386.

121. Finley JW, Burrell JB, Reeves PG. Pinto bean consumption changes SCFA profiles in fecal fermentations, bacterial populations of the lower bowel, and lipid profiles in blood of humans. Journal Of Nutrition. 2007;137(11):2391-2398.

122. Mackay S, Ball MJ. Do Beans and Oat Bran Add to the Effectiveness of a Low-Fat Diet. European Journal of Clinical Nutrition. 1992;46(9):641-648.

123. Oosthuizen W, Scholtz CS, Vorster HH, Jerling JC, Vermaak WJH. Extruded dry beans and serum lipoprotein and plasma haemostatic factors in hyperlipidaemic men. European Journal of Clinical Nutrition. 2000;54(5):373-379.

124. Anderson JW, Story L, Sieling B, Chen WJL, Petro MS, Story J. Hypocholesterolemic Effects of Oat-Bran or Bean Intake for Hypercholesterolemic Men. American Journal of Clinical Nutrition. 1984;40(6):1146-1155.

125. Most MM. Estimated phytochemical content of the dietary approaches to stop hypertension (DASH) diet is higher than in the control study diet. Journal Of The American Dietetic Association. 2004;104(11):1725-1727.

126. Correa P. Epidemiological Correlations between Diet and Cancer Frequency. Cancer Research. 1981;41(9):3685-3689.

127. Iscovich JM, Labbe KA, Castelleto R, et al. Colon Cancer In Argentina.2. Risk From Fiber, Fat And Nutrients. International Journal Of Cancer. 1992;51(6):858-861.

128. Steinmetz KA, Potter JD. Food-Group Consumption And Colon Cancer In The Adelaide Case-Control Study.1. Vegetables And Fruit. International Journal Of Cancer. 1993;53(5):711-719.

129. LeMarchand L, Hankin JH, Wilkens LR, Kolonel LN, Englyst HN, Lyu LC. Dietary fiber and colorectal cancer risk. Epidemiology. 1997;8(6):658-665.

130. Deneo-Pellegrini H, Boffetta P, De Stefani E, Ronco A, Brennan P, Mendilaharsu M. Plant foods and differences between colon and rectal cancers. European Journal Of Cancer Prevention. 2002;11(4):369-375.

Page 28

Bennink – Rondini 2008

131. Agurs-Collins T, Makambi K, Palmer JR, Rosenberg L, Adams-Campbell LL. Dietary patterns and breast cancer risk in women participating in the Black Womens Health Study. Cancer Epidemiology Biomarkers & Prevention. 2005;14(11):2697S-2698S.

132. Lavecchia C, Negri E, Decarli A, et al. A Case-Control Study Of Diet And Colo-Rectal Cancer In Northern Italy. International Journal Of Cancer. 1988;41(4):492-498.

133. Bidoli E, Franceschi S, Talamini R, Barra S, Lavecchia C. Food-Consumption And Cancer Of The Colon And Rectum In North-Eastern Italy. International Journal Of Cancer. 1992;50(2):223-229.

134. Kampman E, Verhoeven D, Sloots L, Vantveer P. Vegetable And Animal Products As Determinants Of Colon- Cancer Risk In Dutch Men And Women. Cancer Causes & Control. 1995;6(3):225-234.

135. Haenszel W, Berg JW, Segi M, Kurihara M, Locke FB. Large-Bowel Cancer in Hawaiian-Japanese. Journal of the National Cancer Institute. 1973;51(6):1765-1779.

136. Benito E, Stiggelbout A, Bosch FX, et al. Nutritional Factors In Colorectal-Cancer Risk – A Case-Control Study In Majorca. International Journal Of Cancer. 1991;49(2):161-167.

137. Singh PN, Fraser GE. Dietary risk factors for colon cancer in a low-risk population. American Journal of Epidemiology. 1998;148(8):761-774.

138. Michels KB, Giovannucci E, Joshipura KJ, et al. Prospective study of fruit and vegetable consumption and incidence of colon and rectal cancers. Journal Of The National Cancer Institute. 2000;92(21):1740-1752.

139. Lanza E, Hartman TJ, Albert PS, R. Shields, M. Slattery, B. Caan, E. Paskett, F. Iber, J. W. Kikendall, P. Lance, C. Daston, and A. Schatzkin. High dry bean intake and reduced risk of advanced colorectal adenoma recurrence among participants in the polyp prevention trial. Journal Of Nutrition 136: 1896-1903, 2006.

140. Michels KB, Giovannucci E, Chan AT, Singhania R, Fuchs CS, Willett WC. Fruit and vegetable consumption and colorectal adenomas in the nurses’ health study. Cancer Research. 2006;66(7):3942-3953.

141. Hughes JS, Ganthavorn C, Wilson-Sanders S. Dry beans inhibit azoxymethane-induced colon carcinogenesis in F344 rats. Journal of Nutrition. 1997;127(12):2328-2333.

142. Hangen L, Bennink MR. Consumption of black beans and, navy beans (Phaseolus vulgaris) reduced azoxymethane-induced colon cancer in rats. Nutrition and Cancer-an International Journal. 2002;44(1):60-65.

143. Adebamowo CA, Cho E, Sampson L, et al. Dietary flavonols and flavonol-rich foods intake and the risk of breast cancer. International Journal Of Cancer. 2005;114(4):628-633.

144. Fung TT, Hu FB, Holmes MD, et al. Dietary patterns and the risk of postmenopausal breast cancer. International Journal Of Cancer. 2005;116(1):116-121.

145. Silva ID, Mangtani P, McCormack V, Bhakta D, Sevak L, McMichael AJ. Lifelong vegetarianism and risk of breast cancer: A population-based case-control study among South Asian migrant women living in England. International Journal Of Cancer. 2002;99(2):238-244.

Page 29

Bennink – Rondini 2008

146. Shannon J, Ray R, Wu CY, et al. Food and botanical groupings and risk of breast cancer: A case-control study in Shanghai, China. Cancer Epidemiology Biomarkers & Prevention. 2005;14(1):81-90.

147. Iscovich JM, Iscovich RB, Howe G, Shiboski S, Kaldor JM. A Case-Control Study Of Diet And Breast- Cancer In Argentina. International Journal Of Cancer. 1989;44(5):770-776.

148. Potischman N, Swanson CA, Coates RJ, et al. Intake of food groups and associated micronutrients in relation to risk of early-stage breast cancer. International Journal Of Cancer. 1999;82(3):315-321.

149. Armstrong B, Doll R. Environmental Factors And Cancer Incidence And Mortality In Different Countries, With Special Reference To Dietary Practices. International Journal Of Cancer. 1975;15(4):617-631.

150. Ishimoto HN Epidemiological study on relationship betweeen bbreast cancer mortality and dietary factors. Tokushima Journal of Experimental Medicine. 41:(3/4):103-114.

151. Lagiou P, Trichopoulou A, H. K. Henderickx, C. Kelleher, I. U. Leonhauser, O. Moreiras, M. Nelson, A. Schmitt, W. Sekula, K. Trygg, and G. Zajkas. Household budget survey nutritional data in relation to mortality from coronary heart disease, colorectal cancer and female breast cancer in European countries. European Journal Of Clinical Nutrition 1999:53: 328-332.

152. Key TJA, Silcocks PB, Davey GK, Appleby PN, Bishop DT. A case-control study of diet and prostate cancer. British Journal Of Cancer. 1997;76(5):678-687.

153. Schuurman AG, Goldbohm RA, Dorant E, van den Brandt PA. Vegetable and fruit consumption and prostate cancer risk: A cohort study in the Netherlands. Cancer Epidemiology Biomarkers & Prevention. 1998;7(8):673-680.

154. Mills PK, Beeson WL, Phillips RL, Fraser GE. Cohort Study Of Diet, Lifestyle, And Prostate-Cancer In Adventist Men. Cancer. 1989;64(3):598-604.

155. Villeneuve PJ, Johnson KC, Kreiger N, Mao Y. Risk factors for prostate cancer: Results from the Canadian National Enhanced Cancer Surveillance System. Cancer Causes & Control. 1999;10(5):355-367.

156. Cohen JH, Kristal AR, Stanford JL. Fruit and vegetable intakes and prostate cancer risk. Journal Of The National Cancer Institute. 2000;92(1):61-68.

157. Hsing AW, McLaughlin JK, Schuman LM, et al. Diet, Tobacco Use, And Fatal Prostate-Cancer – Results From The Lutheran Brotherhood Cohort Study. Cancer Research. 1990;50(21):6836-6840.

158. Kolonel LN, Hankin JH, Whittemore AS, et al. Vegetables, fruits, legumes and prostate cancer: A multiethnic case-control study. Cancer Epidemiology Biomarkers & Prevention. 2000;9(8):795-804.

159. Lee MM, Wang RT, Hsing AW, Gu FL, Wang T, Spitz M. Case-control study of diet and prostate cancer in China. Cancer Causes & Control. 1998;9(6):545-552.

160. Jain MG, Hislop GT, Howe GR, Ghadirian P. Plant foods, antioxidants, and prostate cancer risk: Findings from case-control studies in Canada. Nutrition And Cancer-An International Journal. 1999;34(2):173-184.

Page 30

Bennink – Rondini 2008

161. Hodge AM, English DR, McCredie MRE, et al. Foods, nutrients and prostate cancer. Cancer Causes & Control. 2004;15(1):11-20.

162. Howell MA. Factor-Analysis Of International Cancer Mortality Data And Per-Capita Food- Consumption. British Journal Of Cancer. 1974;29(4):328-336.

163. Hebert JR, Hurley TG, Olendzki BC, Teas J, Ma YS, Hampl JS. Nutritional and socioeconomic factors in relation to prostate cancer mortality: a cross-national study. Journal Of The National Cancer Institute. 1998;90(21):1637-1647.

164. Ganmaa D, Li XM, Wang J, Qin LQ, Wang PY, Sato A. Incidence and mortality of testicular and prostatic cancers in relation to world dietary practices. International Journal Of Cancer. 2002;98(2):262-267.

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Living With Phytic Acid

http://www.westonaprice.org/health-topics/living-with-phytic-acid/

Living With Phytic Acid

Preparing Grains, Nuts, Seeds and Beans for Maximum Nutrition

Phytic acid in grains, nuts, seeds and beans represents a serious problem in our diets. This problem exists because we have lost touch with our ancestral heritage of food preparation. Instead we listen to food gurus and ivory tower theorists who promote the consumption of raw and unprocessed “whole foods;” or, we eat a lot of high-phytate foods like commercial whole wheat bread and all-bran breakfast cereals. But raw is definitely not Nature’s way for grains, nuts, seeds and beans. . . and even some tubers, like yams; nor are quick cooking or rapid heat processes like extrusion.


Phytic acid is the principal storage form of phosphorus in many plant tissues, especially the bran portion of grains and other seeds. It contains the mineral phosphorus tightly bound in a snowflake-like molecule. In humans and animals with one stomach, the phosphorus is not readily bioavailable. In addition to blocking phosphorus availability, the “arms” of the phytic acid molecule readily bind with other minerals, such as calcium, magnesium, iron and zinc, making them unavailable as well. In this form, the compound is referred to as phytate.

Phytic acid not only grabs on to or chelates important minerals, but also inhibits enzymes that we need to digest our food, including pepsin,1 needed for the breakdown of proteins in the stomach, and amylase,2 needed for the breakdown of starch into sugar. Trypsin, needed for protein digestion in the small intestine, is also inhibited by phytates.3

Through observation I have witnessed the powerful anti-nutritional effects of a diet high in phytate-rich grains on my family members, with many health problems as a result, including tooth decay, nutrient deficiencies, lack of appetite and digestive problems.

The presence of phytic acid in so many enjoyable foods we regularly consume makes it imperative that we know how to prepare these foods to neutralize phytic acid content as much as possible, and also to consume them in the context of a diet containing factors that mitigate the harmful effects of phytic acid.

spring2010-phyticacid
Six-sided phytic acid molecule with a phosphorus atom in each arm.

PHYTATES IN FOOD

Phytic acid is present in beans, seeds, nuts, grains—especially in the bran or outer hull; phytates are also found in tubers, and trace amounts occur in certain fruits and vegetables like berries and green beans. Up to 80 percent of the phosphorus—a vital mineral for bones and health—present in grains is locked into an unusable form as phytate.4 When a diet including more than small amounts of phytate is consumed, the body will bind calcium to phytic acid and form insoluble phytate complexes. The net result is you lose calcium, and don’t absorb phosphorus. Further, research suggests that we will absorb approximately 20 percent more zinc and 60 percent magnesium from our food when phytate is absent.5

The amount of phytate in grains, nuts, legumes and seeds is highly variable; the levels that researchers find when they analyze a specific food probably depends on growing conditions, harvesting techniques, processing methods, testing methods and even the age of the food being tested. Phytic acid will be much higher in foods grown using modern high-phosphate fertilizers than those grown in natural compost.6

Seeds and bran are the highest sources of phytates, containing as much as two to five times more phytate than even some varieties of soybeans, which we know are highly indigestible unless fermented for long periods. Remember the oat bran fad? The advice to eat bran, or high fiber foods containing different types of bran, is a recipe for severe bone loss and intestinal problems due to the high phytic acid content. Raw unfermented cocoa beans and normal cocoa powder are extremely high in phytates. Processed chocolates may also contain phytates. White chocolate or cocoa butter probably does not contain phytates. More evidence is needed as to phytate content of prepared chocolates and white chocolate. Coffee beans also contain phytic acid. The chart in Figure 1 shows the variability of phytate levels in various common foods as a percentage of dry weight. Phytate levels in terms of milligrams per hundred grams are shown in Figure 2.

DETRIMENTAL EFFECTS

High-phytate diets result in mineral deficiencies. In populations where cereal grains provide a major source of calories, rickets and osteoporosis are common.10

Interestingly, the body has some ability to adapt to the effects of phytates in the diet. Several studies show that subjects given high levels of whole wheat at first excrete more calcium than they take in, but after several weeks on this diet, they reach a balance and do not excrete excess calcium.11 However, no studies of this phenomenon have been carried out over a long period; nor have researchers looked at whether human beings can adjust to the phytate-reducing effects of other important minerals, such as iron, magnesium and zinc.

The zinc- and iron-blocking effects of phytic acid can be just as serious as the calcium-blocking effects. For example, one study showed that a wheat roll containing 2 mg phytic acid inhibited zinc absorption by 18 percent; 25 mg phytic acid in the roll inhibited zinc absorption by 64 percent; and 250 mg inhibited zinc absorption by 82 percent.12 Nuts have a marked inhibitory action on the absorption of iron due to their phytic acid content.13

Over the long term, when the diet lacks minerals or contains high levels of phytates or both, the metabolism goes down, and the body goes into mineral-starvation mode. The body then sets itself up to use as little of these minerals as possible. Adults may get by for decades on a high-phytate diet, but growing children run into severe problems. In a phytate-rich diet, their bodies will suffer from the lack of calcium and phosphorus with poor bone growth, short stature, rickets, narrow jaws and tooth decay; and for the lack of zinc and iron with anemia and mental retardation.

THE EXPERIMENTS OF EDWARD MELLANBY

As early as 1949, the researcher Edward Mellanby demonstrated the demineralizing effects of phytic acid. By studying how grains with and without phytic acid affect dogs, Mellanby discovered that consumption of high-phytate cereal grain interferes with bone growth and interrupts vitamin D metabolism. High levels of phytic acid in the context of a diet low in calcium and vitamin D resulted in rickets and a severe lack of bone formation.

His studies showed that excessive phytate consumption uses up vitamin D. Vitamin D can mitigate the harmful effects of phytates, but according to Mellanby, “When the diet is rich in phytate, perfect bone formation can only be procured if sufficient calcium is added to a diet containing vitamin D.”20

Mellanby’s studies showed that the rickets-producing effect of oatmeal is limited by calcium.21 Calcium salts such as calcium carbonate or calcium phosphate prevent oatmeal from exerting rickets-producing effect. According to this view, the degree of active interference with calcification produced by a given cereal will depend on how much phytic acid and how little calcium it contains, or how little calcium the diet contains. Phosphorus in the diet (at least from grains) needs some type of calcium to bind to. This explains the synergistic combination of sourdough bread with cheese. Historically, the cultivation of grains usually accompanies the raising of dairy animals; high levels of calcium in the diet mitigates the mineral-depleting effects of phytic acid.

In Mellanby’s experiments with dogs, increasing vitamin D made stronger bones regardless of the diet, but this increase did not have a significant impact on the amount of calcium excreted. Those on diets high in phytate excreted lots of calcium; those on diets high in phosphorus from meat or released from phytic acid through proper preparation excreted small amounts of calcium.

Based on Mellanby’s thorough experiments, one can conclude that the growth of healthy bones requires a diet high in vitamin D, absorbable calcium and absorbable phosphorus, and a diet low in unabsorbable calcium (supplements, pasteurized dairy) and unabsorbable phosphorus (phytates). Interestingly, his experiments showed that unbleached flour and white rice were less anti-calcifying than whole grains that contain more minerals but also were higher in phytic acid. Other experiments have shown that while whole grains contain more minerals, in the end equal or lower amounts of minerals are absorbed compared to polished rice and white flour. This outcome is primarily a result of the blocking mechanism of phytic acid, but may be secondarily the result of other anti-nutrients in grains.

Thus, absorbable calcium from bone broths and raw dairy products, and vitamin D from certain animal fats, can reduce the adverse effects of phytic acid.

Other studies show that adding ascorbic acid can significantly counteract inhibition of iron assimilation by phytic acid.22Adding ascorbic acid significantly counteracted phytate inhibition from phytic acid in wheat.23 One study showed that anti-iron phytate levels in rice were disabled by vitamin C in collard greens.24

Research published in 2000 indicates that both vitamin A and beta-carotene form a complex with iron, keeping it soluble and preventing the inhibitory effect of phytates on iron absorption.25 Here we have another reason to consume phytate-rich foods in the context of a diet containing organ meat and animal fats rich in vitamin A, and fruits and vegetables rich in carotenes.

PHYTASE

Phytase is the enzyme that neutralizes phytic acid and liberates the phosphorus. This enzyme co-exists in plant foods that contain phytic acid.

Ruminant animals such as cows, sheep and goats have no trouble with phytic acid because phytase is produced by rumen microorganisms; monogastric animals also produce phytase, although far less. Mice produce thirty times more phytase than humans,26 so they can be quite happy eating a raw whole grain. Data from experiments on phytic acid using mice and other rodents cannot be applied to humans.

In general, humans do not produce enough phytase to safely consume large quantities of high-phytate foods on a regular basis. However, probiotic lactobacilli, and other species of the endogenous digestive microflora can produce phytase.27Thus, humans who have good intestinal flora will have an easier time with foods containing phytic acid. Increased production of phytase by the gut microflora explains why some volunteers can adjust to a high-phytate diet. Sprouting activates phytase, thus reducing phytic acid.28 The use of sprouted grains will reduce the quantity of phytic acids in animal feed, with no significant reduction of nutritional value.29

Soaking grains and flour in an acid medium at very warm temperatures, as in the sourdough process, also activates phytase and reduces or even eliminates phytic acid.

Before the advent of industrial agriculture, farmers typically soaked crushed grain in hot water before feeding it to poultry and hogs. Today, feed manufacturers add phytase to grain mixes to get better growth in animals. Commercial phytases are typically produced using recombinant DNA technology. For example, a bacterial phytase gene has recently been inserted into yeast for commercial production.

Not all grains contain enough phytase to eliminate the phytate, even when properly prepared. For example, corn, millet, oats and brown rice do not contain sufficient phytase to eliminate all the phytic acid they contain. On the other hand, wheat and rye contain high levels of phytase—wheat contains fourteen times more phytase than rice and rye contains over twice as much phytase as wheat.30 Soaking or souring these grains, when freshly ground, in a warm environment will destroy all phytic acid. The high levels of phytase in rye explain why this grain is preferred as a starter for sourdough breads.

Phytase is destroyed by steam heat at about 176 degrees Fahrenheit in ten minutes or less. In a wet solution, phytase is destroyed at 131-149 degrees Fahrenheit.31 Thus heat processing, as in extrusion, will completely destroy phytase—think of extruded all-bran cereal, very high in phytic acid and all of its phytase destroyed by processing. Extruded cereals made of bran and whole grains are a recipe for digestive problems and mineral deficiencies!

Phytase is present in small amounts in oats, but heat treating to produce commercial oatmeal renders it inactive. Even grinding a grain too quickly or at too high a temperature will destroy phytase, as will freezing and long storage times. Fresh flour has a higher content of phytase than does flour that has been stored.32 Traditional cultures generally grind their grain fresh before preparation. Weston Price found that mice fed whole grain flours that were not freshly ground did not grow properly.33

Cooking is not enough to reduce phytic acid—acid soaking before cooking is needed to activate phytase and let it do its work. For example, the elimination of phytic acid in quinoa requires fermenting or germinating plus cooking (see Figure 3). In general, a combination of acidic soaking for considerable time and then cooking will reduce a significant portion of phytate in grains and legumes.

THE PHYTATE THRESHOLD

It appears that once the phytate level has been reduced, such that there is more available phosphorus than phytate in the grain, we have passed a critical point and the food becomes more beneficial than harmful. Retention of phosphorus decreases when phytate in the diet is 30-40 percent or more of the total phosphorus.35

For best health, phytates should be lowered as much as possible, ideally to 25 milligrams or less per 100 grams or to about .03 percent of the phytate-containing food eaten. At this level, micronutrient losses are minimized. (For phytate content of common foods as a percentage of dry weight, see Figures 4 and 5.)

White rice and white bread are low-phytate foods because their bran and germ have been removed; of course, they are also devitalized and empty of vitamins and minerals. But the low phytate content of refined carbohydrate foods may explain why someone whose family eats white flour or white rice food products may seem to be relatively healthy and immune to tooth cavities while those eating whole wheat bread and brown rice could suffer from cavities, bone loss and other health problems.

PHYTATES AND GERMINATION

Beer home brewers know that in order to make beer, they need malted (sprouted) grains. Soaking and germinating grains is a good idea, but it does not eliminate phytic acid completely. Significant amounts of phytic acid will remain in most sprouted grain products. For example, malting reduces wheat, barley or green gram phytic acid by 57 percent. However, malting reduces anti-nutrients more than roasting.36 In another experiment, malting millet also resulted in a decrease of 23.9 percent phytic acid after 72 hours and 45.3 percent after 96 hours.37

In legumes, sprouting is the most effective way to reduce phytic acid, but this process does not get rid of all of it. Germinating peanuts led to a 25 percent reduction in phytates. After five days of sprouting, chick peas maintained about 60 percent of their phytate content and lentils retained about 50 percent of their original phytic acid content. Sprouting and boiling pigeon pea and bambara groudnut reduced phytic acid by 56 percent.38 Germinating black eyed beans resulted in 75 percent removal of phytate after five days sprouting.

Germination is more effective at higher temperatures, probably because the heat encourages a fermentation-like condition. For pearled millet, sprouting at 92 degrees F for a minimum of 48 hours removed 92 percent of the phytate. At 82 degrees F, even after 60 hours, only 50 percent of phytic acid was removed. Higher temperatures above 86 degrees F seem less ideal for phytate removal, at least for millet.39

Sprouting releases vitamins and makes grains and beans and seeds more digestible. However it is a pre-fermentation step, not a complete process for neutralizing phytic acid. Consuming grains regularly that are only sprouted will lead to excess intake of phytic acid. Sprouted grains should also be soaked and cooked.

ROASTING AND PHYTIC ACID

Roasting wheat, barley or green gram reduces phytic acid by about 40 percent.40 If you subsequently soak roasted grains, you should do so with a culture that supplies additional phytase, as phytase will be destroyed by the roasting process.

ACIDIC SOAKING AND PHYTIC ACID

For grains and legumes that are low in phytase, soaking does not usually sufficiently eliminate phytic acid. Soaking of millet, soya bean, maize, sorghum, and mung bean at 92 degrees F for 24 hours decreased the contents of phytic acid by 4–51 percent.43 With these same grains and beans, soaking at room temperature for 24 hours reduced phytic acid levels by 16–21 percent.44 However, soaking of pounded maize for one hour at room temperature already led to a reduction of phytic acid by 51 percent.45

Sourdough fermentation of grains containing high levels of phytase—such as wheat and rye—is the process that works best for phytate reduction. Sourdough fermentation of whole wheat flour for just four hours at 92 degrees F led to a 60 percent reduction in phytic acid. Phytic acid content of the bran samples was reduced to 44.9 percent after eight hours at 92 degrees F.46 The addition of malted grains and bakers yeast increased this reduction to 92-98 percent. Another study showed almost complete elimination of phytic acid in whole wheat bread after eight hours of sourdough fermentation (See Figure 6).47

A study of phytates in recipes used typically by home bread bakers found that leavening with commercial yeast was much less effective at removing phytates. Yeasted whole wheat breads lost only 22-58 percent of their phytic acid content from the start of the bread making process to the complete loaf.48

PHYTIC ACID AND YOU

The purpose of this article is not to make you afraid of foods containing phytic acid, only to urge caution in including grains, nuts and legumes into your diet. It is not necessary to completely eliminate phytic acid from the diet, only to keep it to acceptable levels.

An excess of 800 mg phytic acid per day is probably not a good idea. The average phytate intake in the U.S. and the U.K. ranges between 631 and 746 mg per day; the average in Finland is 370 mg; in Italy it is 219 mg; and in Sweden a mere 180 mg per day.49

In the context of a diet rich in calcium, vitamin D, vitamin A, vitamin C, good fats and lacto-fermented foods, most people will do fine on an estimated 400-800 mg per day. For those suffering from tooth decay, bone loss or mineral deficiencies, total estimated phytate content of 150-400 mg would be advised. For children under age six, pregnant women or those with serious illnesses, it is best to consume a diet as low in phytic acid as possible.

In practical terms, this means properly preparing phytate-rich foods to reduce at least a portion of the phytate content, and restricting their consumption to two or three servings per day. Daily consumption of one or two slices of genuine sourdough bread, a handful of nuts, and one serving of properly prepared oatmeal, pancakes, brown rice or beans should not pose any problems in the context of a nutrient-dense diet. Problems arise when whole grains and beans become the major dietary sources of calories— when every meal contains more than one whole grain product or when over-reliance is placed on nuts or legumes. Unfermented soy products, extruded whole grain cereals, rice cakes, baked granola, raw muesli and other high-phytate foods should be strictly avoided.

RICE

Brown rice is high in phytates. One reference puts phytate content at 1.6 percent of dry weight, another at 1250 mg per 100 grams dry weight (probably about 400 mg per 100 grams cooked rice). Soaking brown rice will not effectively eliminate phytates because brown rice lacks the enzyme phytase; it thus requires a starter. Nevertheless, even an eight-hour soak will eliminate some of the phytic acid, reducing the amount in a serving to something like 300 mg or less.

The ideal preparation of rice would start with home-milling, to remove a portion of the bran, and then would involve souring at a very warm temperature (90 degrees F) at least sixteen hours, preferably twenty-four hours. Using a starter would be ideal (see sidebar recipe). For those with less time, purchase brown rice in air-tight packages. Soak rice for at least eight hours in hot water plus a little fresh whey, lemon juice or vinegar. If you soak in a tightly closed mason jar, the rice will stay warm as it generates heat. Drain, rinse and cook in broth and butter.

NUTS

In general, nuts contain levels of phytic acid equal to or higher than those of grains. Therefore those consuming peanut butter, nut butters or nut flours, will take in phytate levels similar to those in unsoaked grains. Unfortunately, we have very little information on phytate reduction in nuts. Soaking for seven hours likely eliminates some phytate. Based on the accumulation of evidence, soaking nuts for eighteen hours, dehydrating at very low temperatures—a warm oven—and then roasting or cooking the nuts would likely eliminate a large portion of phytates.

Nut consumption becomes problematic in situations where people on the GAPS diet and similar regimes are consuming lots of almonds and other nuts as a replacement for bread, potatoes and rice. The eighteen-hour soaking is highly recommended in these circumstances.

It is best to avoid nut butters unless they have been made with soaked nuts—these are now available commercially. Likewise, it is best not to use nut flours—and also coconut flour—for cooking unless they have been soured by the soaking process.

It is instructive to look at Native American preparation techniques for the hickory nut, which they used for oils. To extract the oil they parched the nuts until they cracked to pieces and then pounded them until they were as fine as coffee grounds. They were then put into boiling water and boiled for an hour or longer, until they cooked down to a kind of soup from which the oil was strained out through a cloth. The rest was thrown away. The oil could be used at once or poured into a vessel where it would keep a long time.50

By contrast, the Indians of California consumed acorn meal after a long period of soaking and rinsing, then pounding and cooking. Nuts and seeds in Central America were prepared by salt water soaking and dehydration in the sun, after which they were ground and cooked.

BEANS

All beans contain phytic acid and traditional cultures usually subjected legumes to a long preparation process. For example, according to one source, “Lima beans in Nigeria involve several painstaking processes to be consumed as a staple.”51 In central America, beans are made into a sour porridge called chugo, which ferments for several days.

The best way of reducing phytates in beans is sprouting for several days, followed by cooking. An eighteen-hour fermention of beans without a starter at 95 degrees F resulted in 50 percent phytate reduction.52 Lentils fermented for 96 hours at 108 degrees F resulted in 70-75 percent phytate destruction.53 Lentils soaked for 12 hours, germinated 3-4 days and then soured will likely completely eliminate phytates.

Soaking beans at moderate temperatures, such as for 12 hours at 78 degrees F results in an 8-20 percent reduction in phytates.54

When legumes comprise a large portion of the diet, one needs to go to extra steps to make beans healthy to eat. Beans should usually have hull and bran removed. Adding a phytase-rich medium to beans would help eliminate the phytic acid in beans. Adding yeast, or effective micororganisms, or kombu seaweed may greatly enhance the predigestive process of the beans. One website suggests using a starter containing effective microorganisms and cultured molasses for soaking beans.55

At a minimum, beans should be soaked for twelve hours, drained and rinsed several times before cooking, for a total of thirty-six hours. Cooking with a handful of green weed leaves, such as dandelion or chickweed, can improve mineral assimilation.

TUBERS

Sweet potatoes and potatoes contain little phytic acid but yams and other starchy staples contain levels of phytate that we cannot ignore. The phytic acid content of arrowroot is unknown, but it may contain a significant amount.56 These foods should be fermented—as they usually are in traditional cultures—if they are a staple in the diet. For occasional eating, cooking well and consuming with plenty of butter and vitamin C-rich foods should suffice.

BREAD

Bread can only be called the staff of life if it has undergone careful preparation; otherwise bread can be the road to an early grave. For starters, the flour used in bread should be stone ground. Wheat and rye contain high levels of phytase, but this is destroyed by the heat of industrial grinding, and also lessens over time. Fresh grinding of wheat or rye berries before use will ensure that the original amount of phytase remains in the flour.

Rye has the highest level of phytase in relation to phytates of any grain, so rye is the perfect grain to use as a sourdough starter. Phytates in wheat are greatly reduced during sourdough preparation, as wheat is also high in phytase. Yeast rising bread may not fully reduce phytic acid levels.57 Phytate breakdown is significantly higher in sourdough bread than in yeasted bread.58

Yet even with the highly fermentable rye, a traditional ancient recipe from the French calls for removal of 25 percent of the bran and coarse substances.59 As an example of this practice, one small bakery in Canada sifts the coarse bran out of the flour before making it into bread.62

OATS

Oats contain very little phytase, especially after commercial heat treatment, and require a very long preparation period to completely reduce phytic acid levels. Soaking oats at 77 degrees F for 16 hours resulted in no reduction of phytic acid, nor did germination for up to three days at this temperature.63 However, malting (sprouting) oats for five days at 52 degrees F and then soaking for 17 hours at 120 degrees F removes 98 percent of phytates. Adding malted rye further enhances oat phytate reduction.64 Without initial germination, even a five-day soaking at a warm temperature in acidic liquid may result in an insignificant reduction in phytate due to the low phytase content of oats. On the plus side, the process of rolling oats removes a at least part of the bran, where a large portion of the phytic acid resides.

How do we square what we know about oats with the fact that oats were a staple in the diet of the Scots and Gaelic islanders, a people known for their robust good health and freedom from tooth decay? For one thing, high amounts of vitamin D from cod’s liver and other sources, helps prevent calcium losses from the high oat diet. Absorbable calcium from raw dairy products, consumed in abundance on mainland Scotland, provides additional protection.

In addition, it is likely that a good part of the phytase remained in the oats of yore, which partially germinated in stacks left for a period in the field, were not heat treated and were hand rolled immediately prior to preparation. And some Scottish and Gaelic recipes do call for a long fermentation of oats before and even after they are cooked.

Unprocessed Irish or Scottish oats, which have not been heated to high temperatures, are availabile in some health food stores and on the internet. One study found that unheated oats had the same phytase activity as wheat.65 They should be soaked in acidulated water for as long as twenty-four hours on top of a hot plate to keep them at about 100 degrees F. This will reduce a part of the phytic acid as well as the levels of other anti-nutrients, and result in a more digestible product. Overnight fermenting of rolled oats using a rye starter—or even with the addition of a small amount of fresh rye flour—may result in a fairly decent reduction of phytate levels. It is unclear whether heat-treated oats are healthy to eat regularly.

SEEDS

Seeds—such as pumpkin seeds—are extremely high in phytic acid and require thorough processing to remove it. Some may be removed by soaking and roasting. It is best to avoid consuming or snacking on raw seeds. By the way, cacao is a seed. Cacao contains irritating tannins and is said to be extremely high in phytic acid, although studies verifying phytic acid levels in cacao could not be located. Some brands of raw cocoa and cocoa powder may be fermented, others may not be. Check with the manufacturer before indulging!

CORN

Corn is high in phytic acid and low in phytase. The Native Americans fermented cooked corn meal for two weeks, wrapped in corn husks, before preparing it as a flat bread or tortilla. In Africa, corn is fermented for long periods of time using a lactobacillis culture to produce foods like kishk, banku, or mawe. No such care is given to corn products in the western world! But you can prepare healthy corn products at home. As with oatmeal, the addition of a rye starter or rye flour to the soaking water may be particularly helpful in reducing phytate content—think of the colonial “Ryn‘n’Injun” bread made from rye and corn. In one research project, soaking ground corn with 10 percent whole rye flour resulted in a complete reduction of phytate in six hours.66 Again, more research—and more experimenting in the kitchen—is needed!

RYE TO THE RESCUE

For those who need to reduce phytic acid to minimum levels—those suffering from tooth decay, bone loss and nutrient deficiencies—the magic ingredient is rye. To bring the phytate content of your diet to the absolute minimum, add freshly ground rye flour or a sourdough rye culture to rolled or cut oats, cornmeal, rice and other low-phytase grains, then soak in an acidic medium—preferably water with whey, yogurt or sour milk added—on a hot plate to bring the temperature up to about 100 degrees F. This is a better solution than consuming white rice and white flour, which are relative low in phytate but have a greatly reduced mineral content (see Figure 7).

The intention of the article is not to impose a decision about whether or not to consume grains, nuts, seeds and beans; rather it is to clarify how to consume them with awareness. This way you can maximize your health by making grain-based foods more digestible and absorbable. Now it is very clear which foods contain phytic acid and how much they contain, what the health effects of phytic acid are and how to mitigate phytic acid in your diet with complementary foods rich in vitamin C, vitamin D and calcium. Methods for preparation of grains, seeds, and beans have been clarified, so that you can estimate how much phytic acid you are consuming. One meal high in phytic acid won’t cause a healthy person any harm. But high phytic acid levels over weeks and months can be very problematic.

Fortunately, not only are properly prepared foods better for you, they also taste great. Now you can enjoy some well fermented sourdough bread, together with a piece of raw milk cheese, lots of butter and a slice of meat of your choice and taste the essence of life.

Note to readers: This article is a work in progress. Please send additional information or comments to phytates@curetoothdecay.com


SIDEBARS

FIGURE 1: FOOD SOURCES OF PHYTIC ACID7
As a percentage of dry weight

FOOD MINIMUM MAXIMUM
Sesame seed flour 5.36 5.36
Brazil nuts 1.97 6.34
Almonds 1.35 3.22
Tofu 1.46 2.90
Linseed 2.15 2.78
Oat meal 0.89 2.40
Beans, pinto 2.38 2.38
Soy protein concentrate 1.24 2.17
Soybeans 1.00 2.22
Corn 0.75 2.22
Peanuts 1.05 1.76
Wheat flour 0.25 1.37
Wheat 0.39 1.35
Soy beverage 1.24 1.24
Oats 0.42 1.16
Wheat germ 0.08 1.14
Whole wheat bread 0.43 1.05
Brown rice 0.84 0.99
Polished rice 0.14 0.60
Chickpeas 0.56 0.56
Lentils 0.44 0.50

FIGURE 2: PHYTIC ACID LEVELS8
In milligrams per 100 grams of dry weight

Brazil nuts 1719
Cocoa powder 1684-1796
Brown rice 12509
Oat flakes 1174
Almond 1138 – 1400
Walnut 982
Peanut roasted 952
Peanut ungerminated 821
Lentils 779
Peanut germinated 610
Hazel nuts 648 – 1000
Wild rice flour 634 – 752.5
Yam meal 637
Refried beans 622
Corn tortillas 448
Coconut 357
Corn 367
Entire coconut meat 270
White flour 258
White flour tortillas 123
Polished rice 11.5 – 66
Strawberries 12

PHYTATES: A BENEFICIAL ROLE?

As evidence of the detrimental effects of phytates accumulates, reports on alleged beneficial effects have also emerged. In fact, a whole book, Food Phytates, published in 2001 by CRC press, attempts to build a case for “phytates’ potential ability to lower blood glucose, reduce cholesterol and triacylglycerols, and reduce the risks of cancer and heart disease.”14

One argument for the beneficial effects of phytates is based on the premise that they act as anti-oxidants in the body. But recent studies indicate that an overabundance of anti-oxidants is not necessarily a good thing as these compounds will inhibit the vital process of oxidation, not only in our cells but also in the process of digestion.

Another theory holds that phytates bind to extra iron or toxic minerals and remove them from the body, thus acting as chelators and promoting detoxification. As with all anti-nutrients, phytates may play a therapeutic role in certain cases.

For example, researchers claim that phytic acid may help prevent colon cancer and other cancers.15 Phytic acid is one of few chelating therapies used for uranium removal.16

Phytic acid’s chelating effect may serve to prevent, inhibit, or even cure some cancers by depriving those cells of the minerals (especially iron) they need to reproduce.17 The deprivation of essential minerals like iron would, much like other broad treatments for cancer, also have negative effects on non-cancerous cells. For example, prolonged use of phytic acid to clear excess iron may deprive other cells in the body that require iron (such as red blood cells).

One theory is that phytates can help patients with kidney stones by removing excess minerals from the body. However, a long-term study involving over forty-five thousand men found no correlation between kidney stone risk and dietary intake of phytic acid.18

Phytates also have the potential for use in soil remediation, to immobilize uranium, nickel and other inorganic contaminants.19

OTHER ANTI-NUTRIENTS

Phytates represent just one of many anti-nutrients in grains, nuts, tubers, seeds and beans. These include oxalates, tannins, trypsin inhibitors, enzyme inhibitors, lectins (hemagglutinins), protease inhibitors, gluten, alpha-amylase inhibitors and alkylresorcinols .

Anti-nutrients exist in these plant foods because they are part of the process of life. The natural world requires them in order to perform many important tasks, including protection against insects, maintaining freshness of seeds for germination, and protection against mold and fungus. In order to consume these foods on a regular basis we must remove the phytates and other anti-nutrients through processing in harmonious ways. Many people in the health field assure us that if something is from nature, then it doesn’t require processing. Phytates act as the seed’s system of preservatives, like the impossible-to-open plastic packaging of many consumer goods. To get to the item we need—namely, phosphorus—we need to unwrap the phytate-phosphorus package.

FIGURE 3: QUINOA PHYTATE REDUCTION34

PROCESS PHYTATE REDUCTION
Cooked for 25 minutes at 212 degrees F 15-20 percent
Soaked for 12-14 hours at 68 degrees F, then cooked 60-77 percent
Fermented with whey 16-18 hours at 86 degrees F, then cooked 82-88 percent
Soaked 12-14 hours, germinated 30 hours, lacto-fermented 16-18 hours, then cooked at 212 degrees F for 25 minutes 97-98 percent

FIGURE 4: PHYTATE41
As Percentage of Dry Weight

Sesame seeds dehulled 5.36
100% Wheat bran cereal 3.29
Soy beans 1.00 – 2.22
Pinto beans 0.60 – 2.38
Navy beans 0.74 – 1.78
Parboiled brown rice 1.60
Oats 1.37
Peanuts 1.05 – 1.76
Barley 1.19
Coconut meal 1.17
Whole corn 1.05
Rye 1.01
Wheat flour 0.96
Brown rice 0.84 – 0.94
Chickpeas 0.28 – 1.26
Lentils 0.27 – 1.05
Milled (white) rice 0.2

FIGURE 5: BREAD PHYTATES42
As Percentage of Weight

Cornbread 1.36
Whole wheat bread 0.43-1.05
Wheat bran muffin 0.77-1.27
Popped corn 0.6
Rye 0.41
Pumpernickel 0.16
White bread 0.03- .23
French bread 0.03
Sourdough rye 0.03
Soured buckwheat 0.03

FIGURE 6: REDUCTION OF PHYTIC ACID IN WHOLE WHEAT SOURDOUGH BREAD47

Percentage of Phytic Acid

spring2010-phyticacid-fig6Time
—- Yeast Fermentation
___ Sourdough Fermentation

PREPARATION OF BROWN RICE

1. Soak brown rice in dechlorinated water for 24 hours at room temperature without changing the water. Reserve 10% of the soaking liquid (should keep for a long time in the fridge). Discard the rest of the soaking liquid; cook the rice in fresh water.

2. The next time you make brown rice, use the same procedure as above, but add the soaking liquid you reserved from the last batch to the rest of the soaking water.

3. Repeat the cycle. The process will gradually improve until 96% or more of the phytic acid is degraded at 24 hours.

Source: Stephan Guyenet http://wholehealthsource.blogspot.com/2009/04/new-way-to-soak-brown-rice.html.

PHYTATES IN BRAN

A survey of indigenous dishes shows that the bran is consistently removed from a variety of grains. The only exception seems to be beer. Traditional beer production—involving soaking, germination, cooking and fermentation—removes phytic acid and releases the vitamins from the bran and germ of grains.

The traditional method for preparing brown rice is to pound it in a mortar and pestle in order to remove the bran. The pounding process results in milled rice, which contains a reduced amount of the bran and germ. Experiments have verified the fact that milled rice, rather than whole brown rice, results in the highest mineral absorption from rice.

The idea we should eat bran is based on the idea of “not enough.” We somehow believe that grains without the bran do not provide enough nutrients. But solving the problem of a lack of bioavailable minerals in the diet may be more a question of soil fertility than of consuming every single part of the grain. A study of the famous Deaf Smith County Texas, the “town without a toothache”—because of their mineral-rich soil producing fabulous butter fat—found that its wheat contained six times the amount of phosphorus as normal wheat.60 In this case, wheat minus the bran grown in rich soils will have significant amounts or even more phosphorus compared to wheat with the bran grown in poor soil. Low nutrient content in food seems to be better solved by focusing on soil fertility, rather than trying to force something not digestible into a digestible form.

There are many studies in which researchers have tried to find out how to make the bran of different grains digestible and to provide additional nutrition. But small additions of phosphorus- and calcium-rich dairy products, such as milk and cheese, or phosphorous-rich meat will make up for the moderate reductions in mineral intakes from grains without the bran. In one study, the calcium, magnesium, phosphorous and potassium in diets made up with 92 percent flour (almost whole wheat) were less completely absorbed than the same minerals in diets made up with 69 percent flour (with a significant amount of bran and germ removed).61 This study involved yeasted bread. With sourdough bread, the phytate content of bran will be largely reduced if a phytase-rich starter is used and the flour is fermented at least twenty-four hours.

FIGURE 7: NUTRIENTS IN GRAINS AND OTHER FOODS67
In milligrams per 100 grams.

Calcium Phosphorus Iron Calories
Whole grain wheat flour 34 346 3.9 339
Unenriched white flour 15 108 1.2 364
White rice 9 108 0.4 366
Milled rice 10-30 80-150 .2-2.8 349-373
Brown rice 10-50 170-430 .2-5.2 363-385
Blue corn mush (Navajo) 96 39 2.9 54
Acorn stew 62 14 1 95
Milk 169 117 0.1 97
Free range buffalo steak 4 246 3.8 146
Cheese, mozarella 505 354 0.4 300

SOME FERMENTED GRAIN FOODS FROM AFRICA

KISHK, a fermented product prepared from parboiled wheat and milk, is consumed in Egypt and many Arabian countries. During the preparation of kishk, wheat grains are boiled until soft, dried, milled and sieved in order to remove the bran. Milk is separately soured in earthenware containers, concentrated and mixed with the moistened wheat flour thus prepared, resulting in the preparation of a paste called a hamma. The hamma is allowed to ferment for about 24 hours, following which it is kneaded. Soured salted milk is added prior to dilution with water. Fermentation is allowed to proceed for a further 24 hours. The mass is thoroughly mixed, formed into balls and dried.

BANKU is a popular staple consumed in Ghana. It is prepared from maize or a mixture of maize and cassava. The preparation involves steeping the raw material in water for 24 hours followed by wet milling and fermentation for three days. The dough is then mixed with water at a ratio of 4 parts dough to 2 parts water; or 4 parts dough to 1 part cassava and 2 parts water. Continuous stirring and kneading of the fermented dough is required to attain an appropriate consistency during subsequent cooking. Microbiological studies of the fermentation process revealed that the predominant microorganisms involved are lactic acid bacteria and moulds.

MAWE is a sour dough prepared from partially dehulled maize meal which has undergone natural fermentation for a one- to three-day period. Traditional mawe production involves cleaning maize by winnowing, washing in water and crushing in a plate disc mill. The crushed maize is screened by sieving whereby grits and hulls are separated by gravity and the fine endosperm fraction collected in a bowl. The grits are not washed but home dehulled, following which they are mixed with the fine fraction, moistened over a 2- to 4-hour period and milled to a dough. The kneaded dough is then covered with a polyethylene sheet and allowed to ferment naturally to a sour dough in a fermentation bowl, or wrapped in paper or polyethylene. In the commercial process which takes place entirely in a milling shop, the grits are washed by rubbing in water, following which the germ and remaining hulls are floated off and discarded along with the water. The sedimented endosperm grits are subsequently blended with the fine endosperm fraction. The dominant microorganisms in mawe preparation include lactic acid bacteria and yeasts.

INJERA is the most popular baked product in Ethiopia. It is a fermented sorghum bread with a very sour taste. The sorghum grains are dehulled manually or mechanically and milled to flour which is subsequently used in the preparation of injera. On the basis of production procedures three types of injera are distinguishable: thin injera which results from mixing a portion of fermented sorghum paste with three parts of water and boiling to yield a product known as absit, which is, in turn, mixed with a portion of the original fermented flour; thick injera, which is reddish in color with a sweet taste, consisting of a paste that has undergone only minimal fermentation for 12-24 hours; and komtata-type injera, which is produced from over-fermented paste, and has a sour taste. The paste is baked or grilled to give a bread-like product. Yeasts are the major microorganisms involved in the fermentation of the sweet type of injera. Source:http://www.fao.org/docrep/x2184e/x2184e07.htm#pre

IRISH AND SCOTTISH OATMEAL

Commercial oats in the U.S. are heat treated to about 200o F for four or five hours, to prevent rancidity—oats are rich in polyunsaturated oils that can go rancid within three months, especially at warm temperatures, and oats are harvested only once a year. Heat treatment kills enzymes that accelerate oxidation and helps prevent a bitter taste, although it surely damages the fragile polyunsaturated oils as well.

While Irish and Scottish oatmeal is said to be “unheated,” this is not exactly true; these oats are also heat treated —for the same reasons, to minimize rancidity—but usually at lower temperatures. McCann’s Irish steel cut oats are heated to 113-118o F but Hamlyn’s heats to 212o F. Truly raw rolled oats are available from www.rawguru.com.

The Alford brand, available only in the U.K., is kiln dried for four hours according to their websitewww.oatmealofalford.com; they do not provide temperatures.

Hulless oats that have not been heat treated are available from www.sproutpeople.com; these can be ground or rolled at home before soaking and preparation as oat meal.

UPDATE ON PHYTIC ACID by Rami Nagel

The article on phytic acid (Spring, 2010) was written in response to reports of dental decay, especially in children, even though the family was following the principles of traditional diets. Phytates become a problem when grains make up a large portion of the diet and calcium, vitamin C and fat-soluble vitamins, specifically fat-soluble vitamin D, are low. In the diet advocated by WAPF, occasional higher phytate meals will not cause any noticeable health effects for people in good health. Significantly more care is needed with whole grains when the diet is low in fat-soluble vitamins and in diets where two or more meals per day rely significantly on grains as a food source. Vitamin C reduces the iron and perhaps other mineral losses from phytic acid. Vitamin D can mitigate the harmful effects of phytates. Calcium (think raw milk, raw cheese, yogurt, and kefir) balances out the negative effects of phytates. The best indicator of whether dietary phytic acid is causing problems can be seen in the dental health of the family. If dental decay is a recurrent problem, then more care with grain preparation and higher levels of animal foods will be needed. Article Correction , Brown Rice Preparation The article stated: “Soak brown rice in dechlorinated water for 24 hours at room temperature, without changing the water. Reserve 10 percent of the soaking liquid (which should keep for a long time in the fridge). Cook the rice in the remaining soaking liquid and eat. This will break down about 50 percent of the phytic acid.” The soaking water is to be discarded and the rice should be cooked in fresh water. Readers have noted that after the fourth cycle using the brown rice starter the brown rice becomes significantly softer and more digestible.

PHYTIC ACID IN potatoes , YAMS AND SWEET POTATOES

White potatoes have 0.111-0.269 percent of dry weight of phytic acid, a level approximately equivalent to the amount in white rice. Cooking does not significantly remove phytates in potatoes, but consumption of potatoes with plenty of butter or other animal fat in the context of a nutrient dense diet should be enough to mitigate the effects of phytate. Yams contain an amount of phytate equal to or less than that in white potatoes, and sweet potatoes contain no phytate at all. One idea for corn would be to soak/sour it with wheat such as in the process of making corn bread. Corn generally is prepared without the whole kernel, removing the kernel will reduce the phytate content a little bit. I don’t have further details on corn preparation, an entire article could be written on corn and traditional preparation.

PREPARATION OF OATS AND CORN

When preparing these grains according to traditional methods, such as those provided in Nourishing Traditions, the best idea is to add one or more tablespoons of freshly ground rye flour. Rye flour contains high levels of phytase that will be activated during the soaking process. This method reflects new information obtained since the publication of Nourishing Traditions. Even without the rye flour, overnight soaking of oats and other low-phytase grains greatly improves digestibility but won’t eliminate too much phytic acid. Another grain that benefits from added rye flour during soaking is sorghum, which is lower in phytic acid than wheat but lacking in phytase. (Buckwheat contains high levels of phytase and would not need added rye flour.) You can keep whole rye grains and grind a small amount in a mini grinder for adding to these grains during the soaking process.

PREPARATION OF BEANS

If beans are a staple of your diet, extra care is needed in their preparation, including soaking for twenty-four hours (changing the soaking water at least once) and very long cooking. In general, soaking beans and then cooking removes about 50 percent of phytic acid. One report with peas and lentils shows that close to 80 percent of phytic acid can be removed by soaking and boiling. Boiling beans that haven’t been soaked may remove much less phytic acid. Germinating and soaking, or germinating and souring is the best way to deal with beans; dosas made from soaked and fermented lentils and rice is a good example from India. In Latin America, beans are often fermented after the cooking process to make a sour porridge, such as chugo.

PREPARATION OF NUTS

We still do not have adequate information on nut preparation to say with any certainty how much phytic acid is reduced by various preparation techniques. Soaking in salt water and then dehydrating to make “crispy nuts” makes the nuts more digestible and less likely to cause intestinal discomfort, but we don’t know whether this process significantly reduces phytic acid, although it is likely to reduce at least a portion of the phytic acid.

Roasting probably removes a significant portion of phytic acid. Roasting removes 32-68 percent of phytic acid in chick peas and roasting grains removes about 40 percent of phytic acid. Germinated peanuts have 25 percent less phytic acid then ungerminated peanuts. Several indigenous groups cooked and or roasted their nuts or seeds. I notice that I like the taste and smell of roasted nuts.

The real problem with nuts comes when they are consumed in large amounts, such as almond flour as a replacement for grains in the GAPS diet. For example, an almond flour muffin contains almost seven hundred milligrams of phytic acid, so consumption should be limited to one per day. Eating peanut butter every day would also be problematic.

PREPARATION OF COCONUT FLOUR

We do not have enough information about the preparation of coconut flour to say whether soaking reduces phytic acid, but as with other phytic-acid containing foods, the likelihood is that it is at least partially reduced.

MORE UPDATES

COCONUT AND PHYTIC ACID
I’m writing in regard to the article written by Ramiel Nagel titled “Living with Phytic Acid” (Spring 2010). In the article there are references to the phytic acid content of coconut. Since the publication of this article people have been asking me whether they should soak coconut or coconut flour to reduce the phytic acid.
Phytic acid occurs in nuts and seeds in two forms—phytic acid and phytic acid salts [Reddy, NR and Sathe, SK (Eds.) Food Phytates. CRC Press, 2001]. Both are generally referred to as “phytates.” Together, these two compounds make up the total percentage of phytates reported in various foods. However, they do not possess the same chelating power. So the chelating effect of the phytates in corn, wheat, or soy are not the same as those in coconut. You cannot predict the chelating effect based on total phytate content alone.
The mineral-binding effect of the phytates in coconut is essentially nonexistent. It is as if coconut has no phytic acid at all. In a study published in 2002, researchers tested the mineral binding capacity of a variety of bakery products made with coconut f lour. Mineral availability was determined by simulating conditions that prevail in the small intestine and colon. The researchers concluded that “coconut flour has little or no effect on mineral availability.” (Trinidad, TP and others. The effect of coconut flour on mineral availability from coconut flour supplemented foods. Philippine Journal of Nutrition2002;49:48-57). In other words, coconut flour did not bind to the minerals. Therefore, soaking or other phytic acid-neutralizing processes are completely unnecessary.
Soaking has been suggested as a means to reduce the phytic acid content in grains and nuts. Some suggest coconut flour should also be soaked. To soak coconut flour doesn’t make any sense. The coconut meat from which the flour is made, is naturally soaked in water its entire life (12 months) as it is growing on the tree. To remove the meat from the coconut and soak it again is totally redundant. After the coconut meat has been dried and ground into flour, soaking it would ruin the flour and make it unusable. You should never soak coconut flour.
In the tropics coconut has been consumed as a traditional food for thousands of years. Those people who use it as a food staple and regard it as “sacred food,” do not soak it or process it in any way to remove phytates. It is usually eaten raw. This is the traditional method of consumption. They apparently have not suffered any detrimental effects from it even though in some populations it served as their primary source of food.

Bruce Fife, ND
Colorado Springs, Colorado


REFERENCES

1. Tannenbaum and others. Vitamins and Minerals, in Food Chemistry, 2nd edition. OR Fennema, ed. Marcel Dekker, Inc., New York, 1985, p 445.

2. Ibid.

3. Singh M and Krikorian D. Inhibition of trypsin activity in vitro by phytate. Journal of Agricultural and Food Chemistry1982 30(4):799-800.

4. Johansen K and others. Degradation of phytate in soaked diets for pigs. Department of Animal Health, Welfare and Nutrition, Danish Institute of Agricultural Sciences, Research Centre Foulum, Tjele, Denmark.

5. Navert B and Sandstrom B. Reduction of the phytate content of bran by leavening in bread and its effect on zinc absorption in man. British Journal of Nutrition 1985 53:47-53; Phytic acid added to white-wheat bread inhibits fractional apparent magnesium absorption in humans1–3. Bohn T and others. American Journal of Clinical Nutrition. 2004 79:418 –23.

6. Srivastava BN and others. Influence of Fertilizers and Manures on the Content of Phytin and Other Forms of Phosphorus in Wheat and Their Relation to Soil Phosphorus. Journal of the Indian Society of Soil Science. 1955 III:33-40.

7. Reddy NR and others. Food Phytates, CRC Press, 2001.

8. Figures collected from various sources. Inhibitory effect of nuts on iron absoprtion. American Journal of Clinical Nutrition1988 47:270-4; J Anal At Spectrum. 2004 19,1330 –1334; Journal of Agriculture and Food Chemistry 1994, 42:2204-2209.

9. Effects of soaking, germination and fermentation on phytic acid, total and in vitro soluble zinc in brown rice. Food Chemistry 2008 110:821–828.

10. Wills MR and others. Phytic Acid and Nutritional Rickets in Immigrants. The Lancet, April 8, 1972, 771-773.

11. Walker ARP and others. The Effect of Bread Rich in Phytate Phosphorus on the metabolism of Certain Mineral Salts with Special Reference to Calcium. The Biochemical Journal 1948 42(1):452-461.

12. Iron absorption in man: ascorbic acid and dose-depended inhibition. American Journal of Clinical Nutrition. Jan 1989 49(1):140-144

13. Inhibitory effect of nuts on iron absorption. American Journal of Clinical Nutrition 1988 47:270-4.

14. Reddy NR and others. Food Phytates, CRC Press, 2001.

15. Vucenik I and Shamsuddin AM. Cancer inhibition by inositol hexaphosphate (IP6) and inositol: from laboratory to clinic. The Journal of Nutrition 2003 Nov 133(11 Suppl 1); Jenab M and Thompson LU (August 2000). Phytic acid in wheat bran affects colon morphology, cell differentiation and apoptosis. Carcinogenesis 2000 Aug 21(8):1547–52.

16. Cebrian D and others. Inositol hexaphosphate: a potential chelating agent for uranium. Radiation Protection Dosimetry 2007 127(1-4):477–9.

17. http://www.phytochemicals.info/phytochemicals/phytic-acid.php.

18. Critical Reviews in Food Science and Nutrition, 1995 35(6):495- 508.

19 Seaman JC and others. In situ treatment of metals in contaminated soils with phytate. Journal of Environmental Quality 2003 32(1):153–61.

20. Mellanby E. The Rickets-producing and anti-calcifying action of phytate. Journal of Physiology I949 I09:488-533.

21. Creese DH and Mellanby E. Phytic acid and the rickets-producig action of cereals. Field Laboratory, University of Sheffield, and the Department of Biochemistry, Queen’s University, Belfast (Received 11 August 1939)

22. Iron absoprtion in man: ascrobic acid and dose-depended inhibition. American Journal of Clinical Nutrition. Jan 1989. 49(1):140-144.

23. Ibid.

24. Rice and iron absorption in man. European Journal of Clinical Nutrition. July 1990. 44(7):489-497.

25. Layrisse M and others. New property of vitamin A and Bcarotene on human iron absorption: effect on phytate and polyphenols as inhibitors of iron absorption. Archivos Latinoamericanos de Nutricion Sept 2000 50(3).

26. Iqbal TH and others. Phytase activity in the human and rat small intestine. Gut. 1994 September 35(9):1233–1236.

27. Famularo G and others. Probiotic lactobacilli: an innovative tool to correct the malabsorption syndrome of vegetarians?Medical Hypotheses 2005 65(6):1132–5.

28. Malleshi NG. Nutritive value of malted millet flours. Plant Foods for Human Nutrition 1986 36:191–6.

29. Malleshi NG. Nutritive value of malted millet flours. Plant Foods for Human Nutrition 1986 36:191–6.

30. Egli I and others. The Influence of Soaking and Germination on the Phytase Activity and Phytic Acid Content of Grains and Seeds Potentially Useful for Complementary Feeding. Journal of Food Science 2002 Vol. 67, Nr. 9.

31. Peers FG. Phytase of Wheat. The Biochemical Journal 1953 53(1):102-110.

32. Campbell J and others. Nutritional Characteristics of Organic, Freshly stone-ground sourdough and conventional breads. http://eap.mcgill.ca/publications/EAP35.htm.

33. Price WA. Nutrition and Physical Degeneration. Price-Pottenger Nutrition Foundation. 8th edition, page 249.

34. Reddy NR and others. Food Phytates, CRC Press, 2001.

35. Gontzea I and Sutzescu P. Natural Antinutritive Substances in Foodstuffs and Forages. Karger AG, Basel, Switzerland, 1968.

36. Antinutritional content of developed weaning foods as affected by domestic processing. Food Chemistry. 1993 47(4):333-336.

37. Effect of traditional fermentation and malting on phytic acid and mineral availability from sorghum (Sorghum bicolor) and finger millet (Eleusine coracana) grain varieties grown in Kenya. Food and Nutrition Bulletin 2002 23(3 supplement).

38. Effects of processing methods on phytic acid level and some constituents in bambara groundnut and pigeon pea. Food Chemistry 1994 50(2):147-151.

39. Reddy NR and others. Food Phytates, CRC Press, 2001, p 118.

40. Food Chemistry 1993. 47(4)333-336.

41. Reddy NR and others. Food Phytates, 1st edition, CRC Press, 2001, pages 30-32

42. Ibid.

43. Lestienne I and others. Relative contribution of phytates, fibers and tannins to low iron and zinc in vitro solubility in pearl millet. Journal of Agricultural Food Chemistry 2005 Oct 53(21):8342-8.

44. Mahgoub SEO and Elhag SA. Effect of milling, soaking, malting, heat-treatment and fermentation on phytate level of four Sudanese sorghum cultivars. Food Chemistry January 1998 61 (1-2):77-80.

45. Hotz C and others. A home-based method to reduce phytate content and increase zinc bioavailability in maize based complementary diets. International Journal of Food Science and Nutrition 2001 52:133–42.

46. Dephytinization of wheat bran by fermentation with bakers’ yeast, incubation with barley malt flour and autoclaving at different pH levels. Journal of Cereal Science 2008 48(2):471-476.

47. Hauspy R. Fabrication du pain au levain naturel. Nature et Progres. Paris 1983, 1:26-28.

48. McKenzie-Parnell JM and Davies NT. Destruction of Phytic Acid During Home Breadmaking. Food Chemistry 1986 22:181−192.

49. Ellis R and others. Phytate:zinc and phytate X calcium: zinc millimolar rations in self-selected diets of American, Asian Indians, and Nepalese. Journal of the American Dietetic Association 1987 Aug 87(8):1043-7; Ready NR and others. Food Phytates, CRC Press, 2001

50. http://www.marciesalaskaweb.com/choctawFood.htm

51. Ologhobo AD and Fetuga BL. Distribution of Phosphorus and Phytate in Some Nigerian Varieties of Legumes and some Effects of Processing. Journal of Food Science 1984 Volume 49.

52. Indigenous legume fermentation: effect on some anti-nutrients and in-vitro digestibility of starch and protein. Food Chemistry 1994. 50(4):403-406.

53. Journal of the Science of Food and Agriculture 1996 71(3).

54. Proximate Composition and Mineral and Phytate Contents of Legumes Grown in Sudan. Journal of Food Composition and Analysis 1989 2:69-78.

55. www.gobeyondorganics.com.

56. Analysis of phytate in raw and cooked potatoes. Journal of Food Composition and Analysis 2004 17:217-226; Ion Chromatography of Phytate in Roots and Tubers. Journal of Agriculture and Food Chemistry 2003 51:350-353.

57. Journal of Agriculture and Food Chemistry 2001, 49 (5), pp 2657–2662 DOI: 10.1021/jf001255z Publication Date (Web): May 4, 2001 Copyright © 2001 American Chemical Society.

58. Journal of Agriculture and Food Science 2001 49(5):2657–2662.

59. http://www.williamrubel.com/artisanbread/examples/ryebread/rye-bread-from-france-painbouilli.

60. Taylor, Edward. Preliminary Studies on Caries Immunity in the Deaf Smith County (Texas) Area. Journal of the American Dental Association. March, 1942.

61. Mineral Metabolism of Healthy Adults on White and Brown Bread Dietaries. Journal of Physiology 1942 101:44-8.

62. http://www.littlestream.com/.

63. Egli and others. The Influence of Soaking and Germination on the Phytase Activity and Phytic Acid Content of Grains and Seeds Potentially Useful for Complementary Feeding. Journal of Food Science 2002 67(9):3484-3488.

64. Phytate reduction in oats during malting. Journal of Food Science. July/Aug 1992 57(4):994-997.

65. Frolich W and others. Studies on phytase activity in oats and wheat using 31P-NMR spectroscopy. Journal of Cereal Science July 1988 8(1):47-54.

66. Egli and others. Phytic Acid Degradation in Complementary Foods Using Phytase Naturally Occurring in Whole Grain Cereals. Journal of Food Science 2003:68(5):1855-1859.

67. http://www.nutritiondata.com/facts/cereal-grains-and-pasta/5744/2.

This article appeared in Wise Traditions in Food, Farming and the Healing Arts, the quarterly journal of the Weston A. Price Foundation, Spring 2010.

Rami Nagel is a father who cares about the way we affect each other, our children and our planet through our lifestyle choices. His health background is in hands-on energy healing, Hatha and Bhaki yoga, and Pathwork. Rami is author of several health resources: http://www.healingourchildren.net, http://www.preconceptionhealth.org, http://www.curetoothdecay.com, and http://www.yourreturn.org.