Foods That Fight Cancer

Dry Beans and Peas (Legumes)


Dry Beans, Split Peas & Lentils

Kidney and black beans, yellow split peas and red lentils are among the thousands of colorful foods called pulses. Pulses - seeds of legumes that use nitrogen from the atmosphere to make protein - are an important protein source worldwide. So valuable in ancient Rome, prominent families derived their names from beans and peas; for example, Cicero is from the Latin word for chickpea.

What's in Beans and Peas?

legumes nutrition facts

Dry beans and peas are rich in fiber (20% of Daily Value) and a good source of protein (10% of Daily Value). They are also an excellent source of folate, a B vitamin.

Pulses contain other health-promoting substances that may also protect against cancer:

  • Lignans and saponins
  • Resistant starch, starch not digested in the small intestine, is used by healthful bacteria in the colon to produce short-chain fatty acids, which seem to protect colon cells.
  • Antioxidants from a variety of phytochemicals, including triterpenoids, flavonoids, inositol, protease inhibitors and sterols.

Full Glossary for Foods That Fight Cancer

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The Cancer Research

There are several ways in which legumes may act to prevent cancer.

A serving of legumes provide at least 20 percent of the recommended daily amount of folate and fiber. Dietary fiber can act in several ways to lower cancer risk, including helping with weight control. (Excess body fat increases the risk of eight cancers.) Gut bacteria feed on fiber, which produces compounds that may protect colon cells. And folate is essential for healthy DNA and maintaining control of cell growth.

Dry beans, split peas and other legumes also contain a variety of phytochemicals that scientists are studying for their anti-cancer effects.

Current Evidence: AICR/WCRF Expert Report and its Updates (CUP)

Dry beans and other legumes contain dietary fiber. After a systematic review of the global scientific literature, AICR/WCRF analyzed how these factors affect the risk of developing cancer. This comprehensive review concluded that there is strong – probable – evidence that:

- foods containing dietary fiber DECREASE the risk of colorectal cancer

Evidence categorized as "probable" means there is strong research showing a causal relationship to cancer – either decreasing or increasing the risk. The research must include quality human studies that meet specific criteria and biological explanations for the findings. A probable judgement is strong enough to justify recommendations.

”…Beans, rich in fiber and a variety of phytochemicals, can contribute to a diet that helps lower risk for cancer.”
- Karen Collins, MS, RD, CDN.

Open Areas of Investigation: Laboratory Research

In laboratory studies, flavonoids found in legumes have slowed the development of cancers during several stages of development. Current research suggests that protection may come as much from directly affecting cell growth as from antioxidant activity. Lab studies suggest many phytochemicals in legumes may decrease growth factors and chronic inflammation, risk factors for many cancers, and increase self-destruction of cancerous cells. Animal and human studies show that healthful bacteria in the colon use fiber (resistant starch) in legumes to produce substances that seem to protect colon cells.

Animal studies related to the whole legume have primarily focused on cancers of the breast and colon. Relatively few studies show decreased colon cancer in animals fed dry beans. Even fewer studies suggest a potential link between beans and lower risk of breast cancer.

Open Areas of Investigation: Human Studies

Human studies include case-control studies, which compare groups of people with and without cancer checking for a difference in legume consumption. It also includes cohort studies that follow people without cancer for several years and then look at how many dried beans participants generally consumed.

Several studies link higher consumption of legumes with lower risk of colon cancer or the benign adenomas (polyps) that are the beginning of most colon cancer. But overall, human studies focusing on legumes and cancer risk have resulted in inconsistent findings.  One reason may be that few Americans eat dry beans as a regular part of their diet, making comparison between groups that eat high and low amounts of beans difficult. Early data links regular bean consumption with a possible reduced risk of prostate and breast cancers, but more research is needed.

AICR-Supported Studies
Grant Number Title
09A020: Dietary Induced Sporadic Colon Cancer
08A083: Transcriptional Attenuation Induced by Sodium Butyrate and Vitamin D3 in Colon Cancer Cells
94A37: Dietary Influences on Reversal of Changes in DNA Methylation and Expression of Protooncogenes and Suppressor Genes Induced by Short Term Lipotrope Deficiency
95A106: Dietary and Environmental Estrogen Sulfation by Human Cytosolic Sulfotransferases
03B031: Soybean Consumption and Colon Cancer Prevention - Studies in a Mouse Model and in Human Colon Cells
89SG19: Effect of Soluble Fibers on Colonic Physiology
95B089: Reversal of Apoptosis Resistance in Malignant Rat Lymphoma Cells and Human B-Cell Chronic Lymphocytic Leukemia by Butyrate, a Diet-Derived Fatty Acid
08A084: Use of Secoisolariciresinol Diglucoside (SDG) in Radiation Pneumonopathy
08A127: Interaction Between Vitamin A and Phosphatidylinositol 3-kinase in Colorectal Tumor Metastasis
94A78: Retinoic Acid-Dependent Regulation of PDGF A Chain Expression
89B60: Retinoids: Mode of Action as Inhibitors of Human Carcinogenesis
93SG09: Increased Dietary Omega-3 Fatty Acids to Selectively Sensitize Cancer Cells to Chemotherapy
93A23: Non-invasive Detection of Colonic Cellular Markers: Modulation by Diet and Carcinogen
02A072: Iron Increases Breast and Prostate Cancer Cells Invasion
95B104: Dietary-Component Inhibition of Mutagenesis in Transgenic Mice
02A099: Anti-Angiogenesis Effects of IP6
92B18: Effect of Inositol Compounds on Mammary Carcinogenesis
MG92B02: Effect of Inositol Hexaphosphate on Mammary Carcinogenesis
98A051: Metabolism and Pharmacokinetics of IP6 In Vivo
MG92B01: Colon Cancer Inhibition by INSP6
98A075: Phytate Promotes Apoptosis in Coloncytes via Inhibition of the PI 3 Kinase/Akt Signaling Pathway
97B061: Folate Status and the Development of Chemically-Induced Mammary Tumors
97A028: Pharmocodynamic Effects of Perillyl Alcohol in Humans
94B02: Role of Dietary Carotenoids as Anti-Cancer Agents
00A046: Modulation of Fatty Acylation of Src Family Kinases by Dietary Fat
05A110: The Obesity-Cancer Link: Do Fatty Acids Promote the Tumorigenic Actions of IGF-1?
92B69: Therapy of Neuroblastoma with Retinoic Acid
98B018: Sensitizing Cancer for Chemotherapy
93A28: Metabolic, Dietary and Environmental Factors in Head and Neck Cancer
09A055: The Effect of a Lycopene-rich Tomato Extract on Gene Expression in Benign Prostate Tissue: Results from a Randomized Trial in Men with HGPIN
07B032: Effects of LLSO and LLHOSO on the Progression of Breast Cancer
93B34: Effect of Mevinolin and Limonene on CT-26 Hepatic "Metastasis" in BALB/c Mice
05B088: A Mouse Model to Understand Connections Between Dietary Folate Deficiency and Leukemogenesis
03B026: Iron, Hemochromatosis (HFE) and Estrogen in Breast Cancer
95A119: Induction of Iron-Metabolizing Enzymes by Dietary Chemopreventive Agents
92B56: Iron and the Risk of Cancer
93A65: Does Iron Deficiency and/or Iron Overload Play a Role in Breast Cancer?
98A110: The Molecular Mechanism of Iron Chelation in Neuroblastoma
91B23: Iron and Mammary Carcinogenesis
06A123: Inositol Pentakisphosphate, a Novel Bioactive Compound for the Prevention and Treatment of Human Cancer
91SG04: Effect of Inositol Hexaphosphate on the Growth of Transplantable Fibrosarcoma in Mice
95A111: Mechanism of Dietary Indoles in Prevention of Papillomavirus Induced Cancers
97A072: Role of Dietary Fats and Estrogens in the Etiology of Prostate Cancer: A Rat Model
93A63: Dietary Promotion of HBV-Induced Liver Tumors
09A056: The Role of Dietary Fiber and Gut Microflora in Prevention of Colorectal Cancer
90A47: Cancer Chemoprevention by Green Tea Polyphenols
99A097: Molecular Mechanisms of Human CYP1A Gene Regulation by Bioflavonoids
96A083: Folate Status: Modulation of Early and Late Molecular Events in Colonic Carcinogenesis
98A086: The Effects of Folate on Intestinal Carcinogenesis in Genetically Predisposed Murine Models
01A034: Effect of Folate and Methyl Deficiency on DNA Methyltransferases and Methylated DNA Binding Proteins
03A061: Folate, DNA Repair and Cancer
06A131: Effects of Folate and the Folate Receptor on Ovarian and Endometrial Cancer: an In Vitro Study
07A052: Dietary Folate Manipulation to Prevent Prostate Cancer Progression
07A103: Dietary Folate Manipulation: Impact on Prostate Tumor Biology, Genetics and Epigenetics
02A002: Effects of Folic Acid Metabolism on DNA Repair
97A159: The Role of Folate Deficiency in Leukemogenesis
94B80: The Role of Folate Deficiency in Leukemogenesis
05A081: Use of Novel Gentic Mouse Models to Investigate the Health Benefits of Folate in Colon Cancer
93A67: Effects of Dietary Folic Acid Modulation Upon Development of Bronchogenic Carcinoma
96B084: Mutators and Folate Deficiency in Colon Cancer
06A117: Folate and Related Micronutrients, Folate Metabolising Genes and Risk of Barrett's Esophasus and Esophageal Cancer
02A066: Folate Deficiency; 5, 10-Methylenetetrahydrofolate Reductase (MTHFR) Gene Polymorphism, and Molecular Pathways in Colorectal Carcinogenesis
91SG64: Localized Folate Status and Cancer
03A038: Use of Novel Genetic Mouse Models to Investigate the Health Benefits of Folate in Colon Cancer
06A043: Flaxseed/omega-3 Fatty Acid Chemoprevention for Ovarian Cancer
00B048: Mammary Cancer Protective Effects of Lactational Exposure to Flaxseed or Its Purified Lignan
96A033: Biologic Effects of Flaxseed in Patients with Breast Cancer
88A39: Effects of Dietary Fish Oil on Correlates of Human Colon Cancer
09A097: Adolescent Diet and Benign Breast Disease
95A24: Mechanism of Fatty Acid Effects
94A25: Fatty Acids, Mitochrondia and Molecular Genetics of Colon Cancer
95B025: Short Chain Fatty Acid Metabolism and APC Initiated Colon Cancer
91SG05: Azoxymethane-induced Colon Cancer in Rats Fed Varying Levels of Bean(Phaseolous vulgaris) Dietary Fiber
92A05: Fatty Acids, Mitochondria, and Molecular Genetics of Colon Cancer
95B029: Gene-Environment Interaction in Heterocyclic Amine Carcinogenesis
97B068: Decreased Retinoid Response in Peroxisome Proliferator Treated Keratinocytes
91A19: Fat-Fiber Interactions: Effect on Colonic Cytokinetics
89B48: Can Putative Preneoplastic Foci be Used to Evaluate Inhibitors of Colon Carcinogenesis
96A095: Dietary Inhibition of Cyclooxgenase as a Chemopreventive Strategy for Upper Aerodigestive System Cancer
04B072: Iron and the Chemopreventive Activity of Curcumin
85A05: Effect of Dietary Lipid on Transplantable Colon Carcinoma
83B07: Assays on Blood & Urine Specimens Obtained in a Human Subject Survey on Diet & Cancer Relationships in The Peoples Republic of China
89A25: Cellulose Structure and Inhibition of Colon Carcinogenesis
91SG21: Colon Carcinogenesis: Nutritional Modulation of Biomakers
90B73: Investigation of the Induction of Malignancy in Celiac Disease by Dietary Gluten
87A27: Prevention of Malignant Phenotype Generation by Diet-administered Retinoids
94A55: Modulation of Colon Cancer Phenotype by Short Chain Fatty Acids
96A078: Activation of a Tumor Suppressor Gene by Nutrient Derivatives
00A066: Mechanism of Cancer Prevention by Fiber
96A077: Regulation of Apoptosis in Human Colorectal Carcinoma Cells
95A17: Butyrate-mediated Signal Transduction in Colonocytes: Role of cAMP-dependent Protein Kinase
09A002: Factors Determining the Apoptotic Response of Colorectal Carcinoma Cells to Butyrate, a Fermentation Product Derived from Dietary Fiber
03A002: Role of Wnt Signaling in Butyrate-Induced Colon Carcinoma Cell Proliferation, Differentiation and Apoptosis
86A25: Dietary Fiber, Bile Acids and Colon Carcinogenesis
90BW65: Role of Dietary Cholesterol and Fat in the Promotion of Breast Cancer
09A066: Does Dietary Folate Intake Modify Treatment-related Toxicity or Disease Outcome Among Children with Acute Lymphoblastic Leukemia?
94B03: Fatty Acid Synthesis as a Novel Chemotherapeutic Target: Therapeutic Consequences of Dietary Fatty Acids
83B11: Type and Amount of Dietary Fiber in Experimental Colon Cancer
Legumes Tips

In the Kitchen


  • Choose either uncooked or canned beans; nutritional quality is equivalent.
  • Uncooked, dried beans are most economical, yet canned beans offer ready-to-eat convenience.
  • To reduce sodium, drain canned beans in a strainer and rinse well, or better yet, choose beans canned with no added salt.


  • Uncooked dry beans can be stored for a year or longer in the unopened plastic bag in which they are sold.
  • Once opened, store in an airtight container in a cool, dry place (not the refrigerator).


  • Before preparing, inspect and remove any debris or dirt.
  • Dry beans and whole peas need to soak before cooking. Soak in a big pot of cold water overnight, or in hot water for one to four hours.
  • To reduce gas-producing substances, soak longer, then discard the soaking water and use fresh water for cooking.
  • Cook dry beans more quickly with a pressure cooker - they’re ready in 15 minutes once the presoaking is complete.
  • Use beans in stews, soups, casseroles, combined with whole grains, in salads and pureed for dips.

Lentils and split peas are the “fast foods” in the pulses family; they need only about 30-40 minutes to cook, no pre-soaking required.

One cup of dry beans and peas equals about 2-1/2 to 3 cups cooked. When drained, one 15-ounce can equals about 1-1/2 cups of beans.

Three Bean Salad with Creamy Mustard Dill Dresing
Three Bean salad
  • 1 cup canned chickpeas, rinsed and drained
  • 1 cup canned Great Northern beans, rinsed and drained
  • 1 cup canned kidney or red beans, rinsed and drained
  • 1/2 cup finely chopped red onion
  • 1 small red bell pepper, diced (optional)
  • 1 small green bell pepper, diced (optional)
  • 2 Tbsp. fat-free or 2 percent Greek yogurt
  • 1 Tbsp. low-fat mayonnaise
  • 1 Tbsp. coarse seed mustard
  • 1 tsp. lemon juice
  • 2 dashes hot pepper sauce
  • 1/2 tsp. salt
  • 1/4 tsp. ground black pepper
  • 2 tsp. extra virgin olive oil
  • 1/2 cup chopped fresh dill
  • 1/4 cup chopped flat-leaf parsley

In mixing bowl, combine beans with onion and peppers, if using.

For dressing, place in mini food processor the yogurt, mayonnaise, mustard, lemon juice, hot sauce, salt and pepper and whirl to combine. With the motor running, drizzle in oil. Add dressing to beans and mix to combine. If serving immediately, mix in dill and parsley. Or, cover the dressed beans and refrigerate for up to 8 hours, adding herbs just before serving.

Makes 4 servings.

Per serving:230 calories, 5 g total fat (

More Recipes
Below are answers to some of the most frequently asked questions we get asked.


Which fruits and vegetables should I be eating?


Eat as many different vegetables and fruits as you can. Variety is the key to obtaining the many protective phytochemicals. Each vegetable and fruit has its own profile of health-promoting substances.

The phytochemicals found in cantaloupe are different from those in broccoli or leeks or cherries. Try to include a lot of colors on your plate. Aim to eat some bright red, green, orange, blue, purple and yellow vegetables and fruits each day.


Should I buy organic foods whenever possible?


There are many reasons to eat organic foods, but currently, there is no convincing evidence that shows a difference between organic and conventionally grown foods related to cancer risk. Studies show pesticide residues on conventionally grown foods are almost always within safety tolerance limits.

If you are concerned about pesticide residues and can afford to spend more, organic produce may be a choice for you. Eating generous servings of a large variety of veggies and fruits - whether organic or not will benefit your health. The advantages of including more vegetables and fruits in your diet outweigh the potential risks from pesticides.


Can grilled meats really cause cancer?


Lab studies show that exposing meats to direct flame, smoke and intense heat (like when you grill or broil) can cause the formation of carcinogens (cancer-causing substances). Cooking methods that involve less heat, such as microwaving, baking, steaming and poaching, do not promote the formation of these substances.

Several strategies you can use to cut carcinogen formation on meat include marinating, flipping frequently, removing excess fat from meat before cooking, and microwaving for part of the cooking time. So for delicious and healthful options, try grilling vegetables, veggie burgers and fruit slices and cut down on meat, fish and poultry.