Disease Proof : Disease Proof : Health & Nutrition News & Commentary : Dr. Joel Fuhrman

What are the foods you think of when you hear the word “fiber”? Although most people probably think of whole grains, all plant foods are rich in fiber. In fact, beans contain more fiber than whole grains, and vegetables and fruits (and some seeds) contain comparable amounts – here are a few examples:

• 1 cup cooked quinoa – 5 grams fiber
• 1 cup cooked brown rice – 4 grams fiber
• 1 cup cooked kidney beans – 11 grams fiber
• 1 cup cooked broccoli – 6 grams fiber
• 1 cup blueberries – 4 grams fiber
• 1 tablespoon chia seeds – 6 grams fiber

Fiber, by definition, is resistant to digestion in the human small intestine. This means that during the digestive process, fiber arrives at the large intestine still intact. Fiber takes up space in the stomach but does not provide absorbable calories, which makes meals feel more satiating and promotes weight loss. In the colon, fiber adds bulk and accelerates movement, factors that are beneficial for colon health. Soluble fiber (primarily from legumes and oats) is effective at removing cholesterol via the digestive tract, resulting in lower blood cholesterol levels. Some types of fiber are fermented by intestinal bacteria. The fermentation products, such as butyrate, have anti-cancer effects in the colon and also serve as energy sources for colonic cells. Fermentable fiber also acts as a prebiotic in the colon, promoting the growth of beneficial bacteria. Fiber intake is associated with a multitude of health benefits, including healthy blood pressure levels and reduced risk of diabetes, heart disease and some cancers.^{1, 2}

Fiber and breast cancer

A recent analysis of 10 scientific studies found that higher fiber intake is associated with lower risk of breast cancer.³  How does fiber impact one’s risk of breast cancer?

First and foremost, since animal products, refined grains, sugars and oils contain little or no fiber, fiber intake is a marker for greater intake of natural plant foods, many of which are known to have a variety of anti-cancer phytochemicals. Some breast cancer protective substances that have already been discovered include isothiocyanates from cruciferous vegetables⁴, organosulfur compounds from onions and garlic, aromatase inhibitors from mushrooms, flavonoids from berries, lignans from flax, chia and sesame seeds, and inositol pentakisphosphate (an angiogenesis inhibitor) from beans.

Does fiber itself have some potentially breast cancer protective actions?

High-fiber foods help to slow emptying of the stomach and absorption of sugars, which decreases the after-meal elevation in glucose. This is meaningful because elevated glucose levels lead to elevated insulin levels, which can send pro-cancer growth signals in the body, for example via insulin-like growth factor 1 (IGF-1). As such, high dietary glycemic index and glycemic load (characteristic of refined grains and processed foods) are associated with an increase in breast cancer risk.^5-7  Accordingly, a study on Korean women found that higher white rice intake was associated with higher breast cancer risk.⁸

Increased exposure to estrogen is known to increase breast cancer risk.^9-11 A woman may be exposed to estrogen via her ovaries’ own production, estrogen production by excess fat tissue, or environmental sources such as endocrine-disrupting chemicals (like BPA). Fiber can reduce circulating estrogen levels, thereby reducing breast cancer risk, because it helps to remove excess estrogen from the body via the digestive tract. Fiber binds up estrogen in the digestive tract, accelerates its removal, and prevents it from being reabsorbed into the body.^12-14 In addition, soluble fiber (as shown with prunes and flaxseed) seems to alter estrogen metabolism such that a less dangerous form of estrogen is produced, whereas insoluble fiber (wheat bran) did not have the same effect.^15,16  For this reason, beans, oats, chia seeds and flaxseeds may provide some extra protection due to their high soluble fiber content.

One notable case-control study looked specifically at different sources of fiber to determine the associations between vegetable fiber, fruit fiber, and grain fiber with breast cancer. Interestingly, when fiber was split up by source, only fruit fiber and vegetable fiber decreased risk; there was a 52% risk reduction for high intake of vegetable fiber, and a 46% risk reduction for fruit fiber. In contrast, there was no association between grain fiber and breast cancer risk.¹⁷ A new study, published in February 2013 came to a similar conclusion when analyzing the association between fiber subtypes and breast cancer risk. This study was part of the larger European Prospective Investigation into Cancer and Nutrition (EPIC) study of over 300,000 women; they found that among the fiber subtypes, only vegetable fiber was linked to decreased risk.¹⁸

Fiber itself has some breast cancer-protective properties, like limiting glycemic effects of foods and assisting in estrogen removal, but we get optimal protection when we focus on foods that are both rich in fiber and rich in phytochemicals. G-BOMBS contain numerous anti-cancer phytochemicals, and and greens, mushrooms, and flax and chia seeds in particular contain anti-estrogenic substances in addition to fiber, making them more effective breast cancer fighters than whole grains. 

Image credit: Flickr - Muffet

References:

1. Higdon J, Drake VJ: Fiber. In An Evidence-based Approach to Phytochemicals and Other Dietary Factors New York: Thieme; 2013: 133-148
2. Carbohydrates. In Nutritional Sciences: From Fundamentals to Food. Edited by McGuire M, Beerman KA; 2013
3. Dong JY, He K, Wang P, et al: Dietary fiber intake and risk of breast cancer: a meta-analysis of prospective cohort studies. Am J Clin Nutr 2011.
4. Liu X, Lv K: Cruciferous vegetables intake is inversely associated with risk of breast cancer: A meta-analysis. Breast 2012.
5. Dong JY, Qin LQ: Dietary glycemic index, glycemic load, and risk of breast cancer: meta-analysis of prospective cohort studies. Breast Cancer Res Treat 2011, 126:287-294.
6. Romieu I, Ferrari P, Rinaldi S, et al: Dietary glycemic index and glycemic load and breast cancer risk in the European Prospective Investigation into Cancer and Nutrition (EPIC). Am J Clin Nutr 2012, 96:345-355.
7. Sieri S, Pala V, Brighenti F, et al: High glycemic diet and breast cancer occurrence in the Italian EPIC cohort. Nutrition, metabolism, and cardiovascular diseases : NMCD 2012.
8. Yun SH, Kim K, Nam SJ, et al: The association of carbohydrate intake, glycemic load, glycemic index, and selected rice foods with breast cancer risk: a case-control study in South Korea. Asia Pac J Clin Nutr 2010, 19:383-392.
9. Hankinson SE, Eliassen AH: Endogenous estrogen, testosterone and progesterone levels in relation to breast cancer risk. J Steroid Biochem Mol Biol 2007, 106:24-30.
10. Pike MC, Pearce CL, Wu AH: Prevention of cancers of the breast, endometrium and ovary. Oncogene 2004, 23:6379-6391.
11. Bernstein L, Ross RK: Endogenous hormones and breast cancer risk. Epidemiol Rev 1993, 15:48-65.
12. Aubertin-Leheudre M, Gorbach S, Woods M, et al: Fat/fiber intakes and sex hormones in healthy premenopausal women in USA. J Steroid Biochem Mol Biol 2008, 112:32-39.
13. Aubertin-Leheudre M, Hamalainen E, Adlercreutz H: Diets and hormonal levels in postmenopausal women with or without breast cancer. Nutr Cancer 2011, 63:514-524.
14. Goldin BR, Adlercreutz H, Gorbach SL, et al: Estrogen excretion patterns and plasma levels in vegetarian and omnivorous women. N Engl J Med 1982, 307:1542-1547.
15. Haggans CJ, Travelli EJ, Thomas W, et al: The effect of flaxseed and wheat bran consumption on urinary estrogen metabolites in premenopausal women. Cancer Epidemiol Biomarkers Prev 2000, 9:719-725.
16. Kasim-Karakas SE, Almario RU, Gregory L, et al: Effects of prune consumption on the ratio of 2-hydroxyestrone to 16alpha-hydroxyestrone. Am J Clin Nutr 2002, 76:1422-1427.
17. Zhang CX, Ho SC, Cheng SZ, et al: Effect of dietary fiber intake on breast cancer risk according to estrogen and progesterone receptor status. Eur J Clin Nutr 2011, 65:929-936.
18. Ferrari P, Rinaldi S, Jenab M, et al: Dietary fiber intake and risk of hormonal receptor-defined breast cancer in the European Prospective Investigation into Cancer and Nutrition study1,2. Am J Clin Nutr 2013, 97:344-353.

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I first got to know Carrie and follow her health and weight loss progress through Dr. Fuhrman’s Member Center when she joined the first Holiday Challenge back in 2010. Then this past summer I met her in person at Dr. Fuhrman’s Health Getaway on Amelia Island. Carrie’s skin just glowed, and she was the epitome of vibrant health and fitness! One would never have known that just two years prior she was overweight and suffering from multiple ailments. Welcome to Disease Proof, Carrie.

What was your life like before discovering Dr. Fuhrman’s nutritarian eating-style?

I remember being a sick child, always getting colds which forced me to stay home from school a lot, and I wasn’t any healthier as an adolescent or young adult. By the time I turned 35, I was a mess: overweight and suffering from chronic migraines, allergies and anxiety, not to mention that I would get sick anytime I went on an airplane.

The last straw for me was when my migraines got so bad that I was taking prescription medication and over-the-counter painkillers every afternoon and living in fear of the pain. I could not keep up with my husband or friends nor could I make plans for my future because I was so debilitated by headaches. When I asked my doctor about my options, his only suggestion was for me to consider taking an anti-seizure medication that had been shown to help people with migraines; he never said anything about improving my diet. Fortunately, I discovered Dr. Fuhrman before I began taking them.

How did you find out about Dr. Fuhrman and Eat to Live?

I had already switched to a vegan diet prior to discovering Dr. Fuhrman because I was concerned about animal welfare. I listened to a podcast by Colleen Patrick-Goudreau who mentioned Dr. Fuhrman and his book. I was intrigued by his nutrition-based approach to health issues so I asked a friend to give me the book for my upcoming birthday. Little did I realize that reading Eat to Live would be the turning point in my life. I felt so inspired by the section on recovering from headaches that I joined the Holiday Challenge 2010 that was about to begin.

Those first 6 weeks were tough. Although I thought I was eating a healthy diet because I was vegan, I still had tons of changes to make. I cut out caffeine, quadrupled my intake of greens and other vegetables, ate more fresh fruits, got rid of salt and cut way back on added sugars. My husband joined me and ended up experiencing his own health transformation, losing 40 pounds and getting off of two blood pressure medications.

How do you feel now?

 I feel better now than I have in my entire life. All my unhealthy eating for all those years, and perhaps combined with environmental exposures, resulted in my being diagnosed with thyroid cancer last year; a slow growing cancer that I could’ve had for more than ten years. I don’t know if I would’ve pulled through so easily if it wasn’t for my new eating habits. I came though that experience with flying colors, and the cancer was small and completely removed. My doctors could not believe how quickly I recovered from surgery. My migraines, allergies and anxiety are distant memories, but I will never forget how far I'e come, and I am so grateful to Dr. Fuhrman for giving me my life back.

Do you have any success tips to share?

Preparation is an absolute. I know that the time I spend on the front end will benefit me on the back end, so I often wake up early to cook beans, prep vegetables or make a salad dressing. I also make sure to freeze leftovers so I don’t get caught without foods during those inevitable busy times when I don’t have time to cook.

My husband wanted me to share his tip for getting rid of the salt shaker and that is to use balsamic vinegar or fresh lemon juice on meals; it is amazing how the acidity brightens up the flavor of natural foods.

In a nutshell, what has nutritarian eating done for you?

My life now revolves around promoting a whole foods, high-nutrient eating style. I am almost finished with a master’s degree in public health nutrition and I write a blog called Carrie on Vegan where I discuss my journey.

While the numbers speak for themselves, they can’t begin to capture the extent of my personal transformation. I feel like I am living my life to the fullest because I have the energy and freedom from pain to do so.

Thank you for sharing your story with us Carrie, and all the best of continual health to you!

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October is Breast Cancer Awareness Month; this October, what women need to be aware of is that they are not powerless against breast cancer.  Mammograms for ‘early detection’ are not the only defense and do not even offer significant benefits. The scientific evidence shows that women do have the power to protect themselves against breast cancer with powerful preventive lifestyle measures. Staying slim and active, focusing on healthful natural foods, and avoiding the disease-causing foods of the Standard American diet are strategies women can use to win the war on breast cancer.

Most importantly, we must unleash the immune system’s special forces: G-BOMBS!

As I describe in my book Super Immunity, G-BOMBS (Greens, Beans, Onions, Mushrooms, Berries and Seeds) are the foods with the most powerful immune-boosting and anti-cancer effects.  These foods help to prevent the cancerous transformation of normal cells, and keep the body armed and ready to attack any pre-cancerous or cancerous cells that may arise.

 G – Greens

Green vegetables (the cruciferous family in particular) contain compounds with anti-cancer compounds and substances that protect blood vessels; they also promote healthy vision and reduce diabetes risk.^1-3 Cruciferous vegetable phytochemicals inhibit a wide range of cancer-promoting cellular processes, including angiogenesis; the angiogenesis inhibitors found in in cruciferous vegetables prevent new blood vessel growth, which is needed for tumor growth and fat tissue growth.^4-7 Eating cruciferous vegetables regularly is associated with decreased risk of breast cancer and has even been shown to increase survival in women after being diagnosed with breast cancer. 

B - Beans

Beans are unique foods because of their very high levels of fiber and resistant starch; carbohydrates that are not broken down by digestive enzymes. The fiber and resistant starch in beans reduce total the number of calories absorbed from beans,^8,9 reduce cholesterol levels, and are converted by healthy gut bacteria into many substances that protect against colon cancer. Eating fiber-rich beans regularly dramatically lowers colon cancer risk, and a recent analysis of 10 scientific studies has shown that the higher your fiber intake, the lower your risk of breast cancer.^10-15

O – Onions

Onions, leeks, garlic, shallots, chives, and scallions not only lend great flavor to meals, they have beneficial effects on the cardiovascular and immune systems, as well as anti-diabetic and anti-cancer effects.^16-19  These vegetables are known for their characteristic (and eye-irritating) organosulfur compounds, which slow tumor growth and kill cancer cells – eating onions and garlic frequently is associated with reduced risk of digestive cancers.^20,21  These vegetables also  contain high concentrations of anti-inflammatory flavonoid antioxidants that contribute to their anti-cancer properties.^16,22-24

M - Mushrooms

In one recent Chinese study, women who ate at least 10 grams of fresh mushrooms each day (which equates to about one button mushroom per day) had a 64% decreased risk of breast cancer!²⁵ All types of mushrooms all have anti-cancer properties.^26-32 Plus, mushrooms are unique in that they contain aromatase inhibitors – compounds that can block the production of estrogen. Aromatase inhibitors are thought to be largely responsible for the preventive effects of mushrooms against breast cancer. Even the most commonly eaten mushrooms (white, cremini, and Portobello) have high anti-aromatase activity.^25,33,34  Mushrooms also contain powerful angiogenesis inhibitors.^31,35,36 Keep in mind that mushrooms should only be eaten cooked:  several raw culinary mushrooms contain a potentially carcinogenic substance called agaritine, and cooking mushrooms significantly reduces their agaritine content.^37,38

B – Berries (and Pomegranate)

Berries’ plentiful antioxidant content helps to reduce blood pressure and inflammation, prevent DNA damage that leads to cancer, protect the brain against oxidative damage and stimulate the body’s own antioxidant enzymes.^39-44  Berries and pomegranate are anti-angiogenic foods, and have anti-inflammatory effects that may protect against cancer and other chronic diseases.^45-51 Pomegranate (similar to mushrooms) is one of the few foods that contain natural aromatase inhibitors – substances that inhibit the production of estrogen, which can reduce breast cancer risk.⁵²

S - Seeds 

Nuts and seeds are healthy fat sources that increase the absorption of nutrients in vegetables in addition to supplying their own spectrum of micronutrients including plant sterols (which help to reduce cholesterol), minerals, and antioxidants. Some seeds – sesame and flax in particular – are rich in lignans, plant estrogens that protect against breast cancer; in one fascinating study, women were given flaxseeds daily after being diagnosed with breast cancer, and reduced growth and increased death of their tumor cells was found after just 4-5 weeks.⁵³

Instead of Breast Cancer Awareness Month, make it Breast Cancer Prevention Month! Eat your G-BOMBS every day!

Image credit: Building Blocks Show (Flickr)

References:

1. Carter P, Gray LJ, Troughton J, et al. Fruit and vegetable intake and incidence of type 2 diabetes mellitus: systematic review and meta-analysis. BMJ 2010;341:c4229.
2. Higdon J, Delage B, Williams D, et al. Cruciferous vegetables and human cancer risk: epidemiologic evidence and mechanistic basis. Pharmacol Res 2007;55:224-236.
3. Stringham JM, Bovier ER, Wong JC, et al. The influence of dietary lutein and zeaxanthin on visual performance. J Food Sci 2010;75:R24-29.
4. Cavell BE, Syed Alwi SS, Donlevy A, et al. Anti-angiogenic effects of dietary isothiocyanates: mechanisms of action and implications for human health. Biochem Pharmacol 2011;81:327-336.
5. Kunimasa K, Kobayashi T, Kaji K, et al. Antiangiogenic effects of indole-3-carbinol and 3,3'-diindolylmethane are associated with their differential regulation of ERK1/2 and Akt in tube-forming HUVEC. The Journal of nutrition 2010;140:1-6.
6. Davis R, Singh KP, Kurzrock R, et al. Sulforaphane inhibits angiogenesis through activation of FOXO transcription factors. Oncol Rep 2009;22:1473-1478.
7. Kumar A, D'Souza SS, Tickoo S, et al. Antiangiogenic and proapoptotic activities of allyl isothiocyanate inhibit ascites tumor growth in vivo. Integrative cancer therapies 2009;8:75-87.
8. Bednar GE, Patil AR, Murray SM, et al. Starch and fiber fractions in selected food and feed ingredients affect their small intestinal digestibility and fermentability and their large bowel fermentability in vitro in a canine model. J Nutr 2001;131:276-286.
9. Muir JG, O'Dea K. Measurement of resistant starch: factors affecting the amount of starch escaping digestion in vitro. Am J Clin Nutr 1992;56:123-127.
10. Hamer HM, Jonkers D, Venema K, et al. Review article: the role of butyrate on colonic function. Aliment Pharmacol Ther 2008;27:104-119.
11. O'Keefe SJ, Ou J, Aufreiter S, et al. Products of the colonic microbiota mediate the effects of diet on colon cancer risk. J Nutr 2009;139:2044-2048.
12. Bazzano LA, Thompson AM, Tees MT, et al. Non-soy legume consumption lowers cholesterol levels: a meta-analysis of randomized controlled trials. Nutrition, metabolism, and cardiovascular diseases : NMCD 2011;21:94-103.
13. Aune D, De Stefani E, Ronco A, et al. Legume intake and the risk of cancer: a multisite case-control study in Uruguay. Cancer Causes Control 2009;20:1605-1615.
14. Singh PN, Fraser GE. Dietary risk factors for colon cancer in a low-risk population. Am J Epidemiol 1998;148:761-774.
15. Dong JY, He K, Wang P, et al. Dietary fiber intake and risk of breast cancer: a meta-analysis of prospective cohort studies. Am J Clin Nutr 2011.
16. Powolny A, Singh S. Multitargeted prevention and therapy of cancer by diallyl trisulfide and related Allium vegetable-derived organosulfur compounds. Cancer Lett 2008;269:305-314.
17. Ginter E, Simko V. Garlic (Allium sativum L.) and cardiovascular diseases. Bratisl Lek Listy 2010;111:452-456.
18. Taj Eldin IM, Ahmed EM, Elwahab HMA. Preliminary Study of the Clinical Hypoglycemic Effects of Allium cepa (Red Onion) in Type 1 and Type 2 Diabetic Patients. Environ Health Insights 2010;4:71-77.
19. Galeone C, Pelucchi C, Levi F, et al. Onion and garlic use and human cancer. The American journal of clinical nutrition 2006;84:1027-1032.
20. Zhou Y, Zhuang W, Hu W, et al. Consumption of large amounts of Allium vegetables reduces risk for gastric cancer in a meta-analysis. Gastroenterology 2011;141:80-89.
21. Pierini R, Gee JM, Belshaw NJ, et al. Flavonoids and intestinal cancers. Br J Nutr 2008;99 E Suppl 1:ES53-59.
22. Slimestad R, Fossen T, Vagen IM. Onions: a source of unique dietary flavonoids. J Agric Food Chem 2007;55:10067-10080.
23. Miyamoto S, Yasui Y, Ohigashi H, et al. Dietary flavonoids suppress azoxymethane-induced colonic preneoplastic lesions in male C57BL/KsJ-db/db mice. Chem Biol Interact 2010;183:276-283.
24. Shan BE, Wang MX, Li RQ. Quercetin inhibit human SW480 colon cancer growth in association with inhibition of cyclin D1 and survivin expression through Wnt/beta-catenin signaling pathway. Cancer Invest 2009;27:604-612.
25. Zhang M, Huang J, Xie X, et al. Dietary intakes of mushrooms and green tea combine to reduce the risk of breast cancer in Chinese women. Int J Cancer 2009;124:1404-1408.
26. Martin KR, Brophy SK. Commonly consumed and specialty dietary mushrooms reduce cellular proliferation in MCF-7 human breast cancer cells. Exp Biol Med 2010;235:1306-1314.
27. Fang N, Li Q, Yu S, et al. Inhibition of growth and induction of apoptosis in human cancer cell lines by an ethyl acetate fraction from shiitake mushrooms. J Altern Complement Med 2006;12:125-132.
28. Ng ML, Yap AT. Inhibition of human colon carcinoma development by lentinan from shiitake mushrooms (Lentinus edodes). J Altern Complement Med 2002;8:581-589.
29. Adams LS, Phung S, Wu X, et al. White button mushroom (Agaricus bisporus) exhibits antiproliferative and proapoptotic properties and inhibits prostate tumor growth in athymic mice. Nutr Cancer 2008;60:744-756.
30. Lakshmi B, Ajith TA, Sheena N, et al. Antiperoxidative, anti-inflammatory, and antimutagenic activities of ethanol extract of the mycelium of Ganoderma lucidum occurring in South India. Teratog Carcinog Mutagen 2003;Suppl 1:85-97.
31. Cao QZ, Lin ZB. Antitumor and anti-angiogenic activity of Ganoderma lucidum polysaccharides peptide. Acta pharmacologica Sinica 2004;25:833-838.
32. Lin ZB, Zhang HN. Anti-tumor and immunoregulatory activities of Ganoderma lucidum and its possible mechanisms. Acta pharmacologica Sinica 2004;25:1387-1395.
33. Hong SA, Kim K, Nam SJ, et al. A case-control study on the dietary intake of mushrooms and breast cancer risk among Korean women. Int J Cancer 2008;122:919-923.
34. Shin A, Kim J, Lim SY, et al. Dietary mushroom intake and the risk of breast cancer based on hormone receptor status. Nutr Cancer 2010;62:476-483.
35. Lee JS, Park BC, Ko YJ, et al. Grifola frondosa (maitake mushroom) water extract inhibits vascular endothelial growth factor-induced angiogenesis through inhibition of reactive oxygen species and extracellular signal-regulated kinase phosphorylation. J Med Food 2008;11:643-651.
36. Chang HH, Hsieh KY, Yeh CH, et al. Oral administration of an Enoki mushroom protein FVE activates innate and adaptive immunity and induces anti-tumor activity against murine hepatocellular carcinoma. International immunopharmacology 2010;10:239-246.
37. Toth B, Erickson J. Cancer induction in mice by feeding of the uncooked cultivated mushroom of commerce Agaricus bisporus. Cancer Res 1986;46:4007-4011.
38. Schulzova V, Hajslova J, Peroutka R, et al. Influence of storage and household processing on the agaritine content of the cultivated Agaricus mushroom. Food Addit Contam 2002;19:853-862.
39. Stoner GD, Wang LS, Casto BC. Laboratory and clinical studies of cancer chemoprevention by antioxidants in berries. Carcinogenesis 2008;29:1665-1674.
40. Bazzano LA, Li TY, Joshipura KJ, et al. Intake of Fruit, Vegetables, and Fruit Juices and Risk of Diabetes in Women. Diabetes Care 2008;31:1311-1317.
41. Hannum SM. Potential impact of strawberries on human health: a review of the science. Crit Rev Food Sci Nutr 2004;44:1-17.
42. Joseph JA, Shukitt-Hale B, Willis LM. Grape juice, berries, and walnuts affect brain aging and behavior. J Nutr 2009;139:1813S-1817S.
43. Cassidy A, O'Reilly EJ, Kay C, et al. Habitual intake of flavonoid subclasses and incident hypertension in adults. The American journal of clinical nutrition 2011;93:338-347.
44. Devore EE, Kang JH, Breteler MM, et al. Dietary intakes of berries and flavonoids in relation to cognitive decline. Ann Neurol 2012.
45. Roy S, Khanna S, Alessio HM, et al. Anti-angiogenic property of edible berries. Free Radic Res 2002;36:1023-1031.
46. Khan N, Afaq F, Kweon MH, et al. Oral consumption of pomegranate fruit extract inhibits growth and progression of primary lung tumors in mice. Cancer Res 2007;67:3475-3482.
47. Toi M, Bando H, Ramachandran C, et al. Preliminary studies on the anti-angiogenic potential of pomegranate fractions in vitro and in vivo. Angiogenesis 2003;6:121-128.
48. Sartippour MR, Seeram NP, Rao JY, et al. Ellagitannin-rich pomegranate extract inhibits angiogenesis in prostate cancer in vitro and in vivo. Int J Oncol 2008;32:475-480.
49. Panchal SK, Ward L, Brown L. Ellagic acid attenuates high-carbohydrate, high-fat diet-induced metabolic syndrome in rats. Eur J Nutr 2012.
50. Edirisinghe I, Banaszewski K, Cappozzo J, et al. Strawberry anthocyanin and its association with postprandial inflammation and insulin. Br J Nutr 2011;106:913-922.
51. Adams LS, Seeram NP, Aggarwal BB, et al. Pomegranate juice, total pomegranate ellagitannins, and punicalagin suppress inflammatory cell signaling in colon cancer cells. Journal of Agricultural and Food Chemis ry 2006;54:980-985.
52. Adams LS, Zhang Y, Seeram NP, et al. Pomegranate ellagitannin-derived compounds exhibit antiproliferative and antiaromatase activity in breast cancer cells in vitro. Cancer Prev Res (Phila) 2010;3:108-113.
53. Thompson LU, Chen JM, Li T, et al. Dietary flaxseed alters tumor biological markers in postmenopausal breast cancer. Clin Cancer Res 2005;11:3828-3835.

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Bisphenol-A (BPA) is its name and disrupting the our hormone function is its game. We should all be aware of what BPA is, the health conditions it’s associated with and where it’s lurking in our environment because this chemical is dangerous and it is found in many of the products we use each and every day. 

The health problems linked to BPA are astounding.  A mounting body of research shows that BPA is an endocrine disruptor that mimics our hormones, therefore interrupting their normal functioning.  This is serious given how much our delicate hormone balance influences our health.  Disruption of hormone levels due to BPA have been linked to breast cancer¹, prostate cancer², cardiovascular disease³, diabetes⁴, obesity⁵, infertility⁶, birth defects⁷, miscarriages⁸, developmental disorders in children⁹, premature puberty in young girls¹⁰, severe attention deficit disorder¹¹, cognitive and brain development problems, deformations of the body (like our limbs), sexual development problems^12-14, and feminizing of males or masculine effects on females.^15-17 It seems like a lovely substance, doesn’t it? No doubt the evil Queen from Snow White and the Seven Dwarfs would have loved to douse that poisonous apple with a nice shiny layer of BPA.  She might have permanently poisoned Snow White if she had.

A new study even shows that BPA negatively affects not just those who eat and touch BPA laden items, but it also affects multiple generations of their children.¹⁸  This study, published by the journal Endocrinology, studied trans-generational effects of BPA on mice.  One group of mice was fed BPA laden food and another group was fed their regular diets. Behavior was monitored and so was the behavior of three subsequent generations. Genetic testing was also conducted on all of the animals.

Remarkably, the mice that were exposed to BPA in the womb were less social and more isolated than the other group, as was the case for their children and their children’s children.  These mice spent less time exploring, playing and engaging in friendly behavior with the other mice. This is not the normal behavior of mice and shows that BPA can influence brain activity for generations.  Notably and frighteningly, the BPA exposed mice were exposed to levels of BPA that humans would normally be exposed to via our diets. While mice behavior and human behavior are obviously not the same, mice are a good laboratory model for what could happen to humans. The researchers even likened the behavioral issues they found in the BPA-exposed mice to autistic children and children with attention-deficit hyperactivity disorder.

To make matters worse, the same study found that 90 percent of Americans have BPA in their blood. Forget watching a horror movie, all we need to do to get a good scare is learn about the health effects of BPA and its ubiquity in our environment. That is, if we do not educate ourselves on which materials contain it and don’t make efforts to avoid it. 

Thankfully, with a bit of education we can steer clear of BPA as easily as a graceful decline of a receipt or the simple renouncement of tin can usage. BPA is found in quite a few unsuspecting places, which is why doing one’s homework really pays off.  Your jaw just may drop when you learn how many places BPA can be found, but thankfully there are plenty of alternatives.  Education really is power and this has never been truer than in the case of the malicious, microscopic villain that is BPA.

So which products are likely to contain BPA?

1. Receipts- these pieces of paper are coated with a BPA-based coating that rubs off onto our fingers and whatever else it comes in contact with.
2. Canned food- cans are lined with an epoxy resin that’s made of BPA, so watch out for soups, canned tomato sauces, fruits and vegetables.  Glass jars, frozen foods and paper cartons are our best alternatives.  One exception: the company Eden Organics produces a line of canned beans that are BPA free. They use oleoresin, which is a natural mixture of an oil and a resin extracted from plants. The can maker, Ball Corporation, says that Eden is the only company to date that makes BPA free cans. More information on their cans is available on the Eden Organics website.
3. Avoid contact with plastic- use glass appliances and storage containers rather than plastic tubs to store leftovers. Stainless steel containers are wonderful substitutes for plastic lunch bags and takeout clamshells.
4. “BPA-free” plastics are not safe- a study in the journal Environmental Health Perspectives found that those plastics purported to be safer that those containing BPA were lined with BPA alternatives that could be  just as noxious.
5. Dental sealants are a BPA warehouse- BPA is the most frequently used dental sealant material and it’s used in composite fillings used to treat cavities.  Dental treatments have been linked to social problems in children, leading a slew of pediatricians to advocate the use of other materials. However, this change has yet to manifest itself in safer dental care so our best bet is to brush regularly, floss and visit our dentists for regular cleanings.
6. Alcoholic beverages- wine and beer are fermented in BPA-resin lined vats.  If you enjoy your fair share of alcoholic drinks, this may just be the motivation you need to eschew that glass of wine or beer. Your hormones will thank you.
7. Infant formula and baby bottles- if you thought BPA in alcohol was sad, this one may be even sadder; I believe the worst is when helpless infants are exposed to BPA. We already knew breastfeeding was best for the little ones, but this news provides even more of an incentive to do so. If breastfeeding isn’t possible, glass bottles and un-canned, powdered formula is second best.
8. Plastic utensils- alas, BPA is found in almost all plastics, plastic utensils included. Although not possible all the time, bring your own utensils when as much as you can.
9. Aluminum soda cans- as if Coca Cola and Pepsi weren’t bad enough on their own, now we know they contain BPA as well as over the top amounts of high fructose corn syrup and artificial sweeteners.  Stay away, just stay away.
10. It’s in your dollar bills- yup, BPA makes its residency on our money because the ink it’s printed on is pure BPA. Other than avoiding touching money, which is impossible for most, our best option is to wash our hands after we exchange the moolah.  

There you have it. While completely avoiding BPA is likely impossible, knowing which products contain BPA will help us greatly reduce our exposure.  Maybe you and I, and all those we share this article with, can make ourselves part of the ten percent of Americans with undetectable blood BPA levels and help that percentage grow. 

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Vitamin D insufficiency is common among Americans overall but more prevalent among African Americans. A recent review of the literature suggests that vitamin D insufficiency is a key contributor to cancer survival disparities that exist between African Americans and white Americans (darker skin is less efficient at producing vitamin D in response to UV rays).¹ A striking part of this literature review is the comprehensive summary of the existing data on vitamin D status and cancer survival: the authors present a long list of studies reporting that vitamin D adequacy is associated with reduced risk of death in all cancers combined, breast, colorectal, lung, and prostate cancer, leukemia and lymphomas.¹

A protective effect of vitamin D against cancers was first proposed in 1980, based on an earlier observation that colon cancer mortality was the highest in geographical areas exposed to the least amounts of sunlight.^2,3

Several more studies of geographical variations in cancers have found the same result: inverse relationships exist between sun exposure and 24 types of cancer, including the most common cancers – those of the breast, colon, rectum, and prostate.^{4, 5}

Since 1980, evidence for the involvement of vitamin D in the relationship between sun exposure and decreased cancer risk has progressively accumulated, as associations were found between blood vitamin D levels and reduced risk of cancers.^{6, 7} Further support for the importance of vitamin D in cancer prevention was provided by randomized controlled trials of vitamin D supplementation that showed reduced cancer risk compared to placebo.  There have also been many reports that vitamin D receptor gene mutations, which interfere with the normal biological actions of vitamin D, were associated with increased cancer risk.^8-10

Additional studies confirmed that vitamin D has growth-inhibitory effects on cells derived from breast, colon, prostate, and skin cancers.¹¹ Vitamin D can block cancer cell growth in a number of ways: Vitamin D alters the expression of genes that regulate inflammation, cell death and cell proliferation, and also interferes with the growth-promoting actions of IGF-1 and other growth factors. Additional anti-cancer effects of vitamin D include enhanced DNA repair and immune defenses, and angiogenesis inhibition.¹²

Today, over 800 scientific papers have been published on the relationship between vitamin D and cancers. We now have ample evidence that maintaining adequate vitamin D levels is an effective strategy for protection against cancer.

Considering all of this evidence, achieving vitamin D sufficiency is so very important. Unfortunately, the Institute of Medicine is hesitant to significantly raise its vitamin D recommendations, so most multivitamins still do not contain nearly enough vitamin D (only 400 IU) to offer the security that a normal Vitamin D level will be achieved. This is an important reason why I designed my new Men’s and Women’s Daily Formula + D multivitamins to include 2000 IU of vitamin D3.  In my experience, 2000 IU has been an appropriate dose to bring most people into the favorable blood 25(OH)D range of 30-50 ng/ml (I also recommend getting a blood test to confirm adequate levels). These are the only multivitamin supplements with a 2000 IU dose of D3 plus no folic acid, beta-carotene, copper, and vitamin A. This enables most people to get everything they need without needing to take multiple different products.  For extra assurance, I’ve also utilized Vitamin D3 because of its highest biological value thus offering the most protection, which also is most effective for raising 25(OH)D levels.¹³ My goal is to make it as easy as possible to maintain healthy vitamin D levels, with plenty of D3 in a multivitamin which also gives you everything else that is worthy of supplementing, and carefully avoiding those supplemental ingredients that are potentially harmful; so additional supplements aren’t necessary to obtain the anti-cancer and bone-protective benefits of vitamin D and the other recommended nutrients. 

References:

1. Grant WB, Peris AN. Differences in vitamin D status may account for unexplained disparities in cancer survival rates between African and White Americans. DermatoEndocrinology 2012;4.
2. Garland CF, Garland FC. Do sunlight and vitamin D reduce the likelihood of colon cancer? Int J Epidemiol 1980;9:227-231.
3. Apperly FL. The Relation of Solar Radiation to Cancer Mortality in North America. Cancer Res 1941;1:191-195.
4. Grant WB, Garland CF. The association of solar ultraviolet B (UVB) with reducing risk of cancer: multifactorial ecologic analysis of geographic variation in age-adjusted cancer mortality rates. Anticancer Res 2006;26:2687-2699.
5. Grant WB. Ecological studies of the UVB-vitamin D-cancer hypothesis. Anticancer Res 2012;32:223-236.
6. Gandini S, Boniol M, Haukka J, et al. Meta-analysis of observational studies of serum 25-hydroxyvitamin D levels and colorectal, breast and prostate cancer and colorectal adenoma. Int J Cancer 2011;128:1414-1424.
7. Grant WB. Relation between prediagnostic serum 25-hydroxyvitamin D level and incidence of breast, colorectal, and other cancers. J Photochem Photobiol B 2010;101:130-136.
8. Kostner K, Denzer N, Muller CS, et al. The relevance of vitamin D receptor (VDR) gene polymorphisms for cancer: a review of the literature. Anticancer Res 2009;29:3511-3536.
9. Lappe JM, Travers-Gustafson D, Davies KM, et al. Vitamin D and calcium supplementation reduces cancer risk: results of a randomized trial. Am J Clin Nutr 2007;85:1586-1591.
10. Bolland MJ, Grey A, Gamble GD, et al. Calcium and vitamin D supplements and health outcomes: a reanalysis of the Women's Health Initiative (WHI) limited-access data set. Am J Clin Nutr 2011;94:1144-1149.
11. Fleet JC. Molecular actions of vitamin D contributing to cancer prevention. Mol Aspects Med 2008;29:388-396.
12. Fleet JC, DeSmet M, Johnson R, et al. Vitamin D and cancer: a review of molecular mechanisms. Biochem J 2012;441:61-76.
13. Tripkovic L, Lambert H, Hart K, et al. Comparison of vitamin D2 and vitamin D3 supplementation in raising serum 25-hydroxyvitamin D status: a systematic review and meta-analysis. Am J Clin Nutr 2012.

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In preparation for my recent appearance on The Dr. Oz Show (you can watch online here), I was asked to share a recipe for a healthful drink that would support weight loss efforts and promote detoxification – something satisfying and delicious while low in calories; most important to me was that this drink would be packed with disease-fighting nutrients.

I chose a simple blended frozen drink of whole strawberries and pomegranate juice with ice plus a squeeze of lemon for a tangy flavor. Why strawberries and pomegranate juice? I did not make those choices arbitrarily – these are powerful foods with several human studies to substantiate their profound benefits.

Antioxidant phytochemicals:

• Anthocyanins (the most abundant antioxidants in berries) provide antioxidant protection on their own, plus they increase the production of cells’ own antioxidant enzymes.¹ A 1.5 cup serving of strawberries increased antioxidant capacity in the blood of human subjects, building protection against oxidative damage.²
• Pomegranate contains a unique antioxidant called punicalagin; it is the most abundant antioxidant in pomegranate, responsible for more than half of the antioxidant activity of pomegranate juice.³ Pomegranate juice has been found to reduce oxidative stress markers in healthy humans.⁴

Detoxification:

• Ellagic acid, an antioxidant derived from berries and pomegranate interacts with a protein called Nrf-2 to increase expression of the body’s natural detoxification enzymes.⁵

Anti-cancer effects:

• Strawberry and pomegranate extracts slowed cell growth and induced cell death in human cancer cells from several cancer types.^6-9
• Pomegranate and strawberries are both anti-angiogenic – strawberry extracts help to prevent growing tumors from acquiring a blood supply – preventing those tumors from receiving the nutrients that would allow them to grow larger.^10-13
• Pomegranate is one of the few foods (mushrooms are another) that contain natural aromatase inhibitors – this means that they inhibit the production of estrogen, which can reduce breast cancer risk.¹⁴
• Strawberries and pomegranate have anti-inflammatory effects that may protect against cancer and other chronic diseases.^5,15,16
• Patients with precancerous esophageal lesions ate strawberries each day for six months.  The results were amazing – 29 out of the 36 patients in the study experienced a decrease in the histological grade of their lesion – this means that the progression toward cancer began to reverse, and the risk of the lesions becoming cancerous had decreased.¹⁷ 

Cardioprotective effects:

• Higher strawberry intake is associated with reduced risk of death from cardiovascular disease.¹⁸
• Human trials have found that daily consumption of strawberries decreases total and LDL cholesterol, and pomegranate phytochemicals reduce LDL oxidation (a contributor to atherosclerotic plaque development).^19-22
• Strawberry and pomegranate phytochemicals have blood pressure-reducing properties.^23-25
• In a study of patients with severe carotid artery blockages, after one ounce of pomegranate juice daily for one year, there was a 30 percent reduction in atherosclerotic plaque. In striking contrast, in the participants who did not take the pomegranate juice atherosclerotic plaque increased by 9 percent.²²

Anti-diabetes effects:

• Strawberry and pomegranate phytochemicals have actions on certain digestive enzymes that can result in reduced glucose levels following a meal.²⁶
• Ellagic acid, which can be derived from berries or pomegranate, reduced secretion by fat cells of an inflammatory molecule that is thought to contribute to insulin resistance.²⁷
• Adding strawberries to a meal was shown to reduce the insulin response in overweight adults.¹⁵

Looking at these effects all together, it is astounding what these foods can do for our health. The “Skinny Shake” has much more to offer than taste and satisfaction with minimal calories. Berries (and pomegranate) make up the second ‘B’ in G-BOMBS, my list of super foods with good reason!

Dr. Fuhrman’s Skinny Shake

Ingredients:

4 ounces pomegranate juice

1 cup frozen strawberries

1 cup of ice

Squeeze of lemon

Directions: Blend all ingredients in a high-powered blender.

References:

1. Shih PH, Yeh CT, Yen GC. Anthocyanins induce the activation of phase II enzymes through the antioxidant response element pathway against oxidative stress-induced apoptosis. Journal of Agricultural and Food Chemis ry 2007;55:9427-9435.
2. Cao G, Russell RM, Lischner N, et al. Serum antioxidant capacity is increased by consumption of strawberries, spinach, red wine or vitamin C in elderly women. J Nutr 1998;128:2383-2390.
3. Heber D: Pomegranate Ellagitannins. In Herbal Medicine: Biomolecular and Clinical Aspects 2nd Edition. Edited by Benzie IFF, Wachtel-Galor, S.: CRC Press; 2011
4. Aviram M, Dornfeld L, Rosenblat M, et al. Pomegranate juice consumption reduces oxidative stress, atherogenic modifications to LDL, and platelet aggregation: studies in humans and in atherosclerotic apolipoprotein E-deficient mice. Am J Clin Nutr 2000;71:1062-1076.
5. Panchal SK, Ward L, Brown L. Ellagic acid attenuates high-carbohydrate, high-fat diet-induced metabolic syndrome in rats. Eur J Nutr 2012.
6. Stoner GD, Wang LS, Casto BC. Laboratory and clinical studies of cancer chemoprevention by antioxidants in berries. Carcinogenesis 2008;29:1665-1674.
7. Kim ND, Mehta R, Yu W, et al. Chemopreventive and adjuvant therapeutic potential of pomegranate (Punica granatum) for human breast cancer. Breast Cancer Res Treat 2002;71:203-217.
8. Kohno H, Suzuki R, Yasui Y, et al. Pomegranate seed oil rich in conjugated linolenic acid suppresses chemically induced colon carcinogenesis in rats. Cancer Sci 2004;95:481-486.
9. Kawaii S, Lansky EP. Differentiation-promoting activity of pomegranate (Punica granatum) fruit extracts in HL-60 human promyelocytic leukemia cells. J Med Food 2004;7:13-18.
10. Roy S, Khanna S, Alessio HM, et al. Anti-angiogenic property of edible berries. Free Radic Res 2002;36:1023-1031.
11. Khan N, Afaq F, Kweon MH, et al. Oral consumption of pomegranate fruit extract inhibits growth and progression of primary lung tumors in mice. Cancer Res 2007;67:3475-3482.
12. Toi M, Bando H, Ramachandran C, et al. Preliminary studies on the anti-angiogenic potential of pomegranate fractions in vitro and in vivo. Angiogenesis 2003;6:121-128.
13. Sartippour MR, Seeram NP, Rao JY, et al. Ellagitannin-rich pomegranate extract inhibits angiogenesis in prostate cancer in vitro and in vivo. Int J Oncol 2008;32:475-480.
14. Adams LS, Zhang Y, Seeram NP, et al. Pomegranate ellagitannin-derived compounds exhibit antiproliferative and antiaromatase activity in breast cancer cells in vitro. Cancer Prev Res (Phila) 2010;3:108-113.
15. Edirisinghe I, Banaszewski K, Cappozzo J, et al. Strawberry anthocyanin and its association with postprandial inflammation and insulin. Br J Nutr 2011;106:913-922.
16. Adams LS, Seeram NP, Aggarwal BB, et al. Pomegranate juice, total pomegranate ellagitannins, and punicalagin suppress inflammatory cell signaling in colon cancer cells. Journal of Agricultural and Food Chemis ry 2006;54:980-985.
17. American Association for Cancer Research. Strawberries May Slow Precancerous Growth in Esophagus. 2011. http://aacrnews.wordpress.com/2011/04/06/strawberries-may-slow-precancerous-growth-in-esophagus/. Accessed
18. Mink PJ, Scrafford CG, Barraj LM, et al. Flavonoid intake and cardiovascular disease mortality: a prospective study in postmenopausal women. Am J Clin Nutr 2007;85:895-909.
19. Basu A, Lyons TJ. Strawberries, Blueberries, and Cranberries in the Metabolic Syndrome: Clinical Perspectives. Journal of Agricultural and Food Chemis ry 2011.
20. Zunino SJ, Parelman MA, Freytag TL, et al. Effects of dietary strawberry powder on blood lipids and inflammatory markers in obese human subjects. Br J Nutr 2011:1-10.
21. Basu A, Wilkinson M, Penugonda K, et al. Freeze-dried strawberry powder improves lipid profile and lipid peroxidation in women with metabolic syndrome: baseline and post intervention effects. Nutr J 2009;8:43.
22. Aviram M, Rosenblat M, Gaitini D, et al. Pomegranate juice consumption for 3 years by patients with carotid artery stenosis reduces common carotid intima-media thickness, blood pressure and LDL oxidation. Clin Nutr 2004;23:423-433.
23. Cassidy A, O'Reilly EJ, Kay C, et al. Habitual intake of flavonoid subclasses and incident hypertension in adults. Am J Clin Nutr 2011;93:338-347.
24. Aviram M, Dornfeld L. Pomegranate juice consumption inhibits serum angiotensin converting enzyme activity and reduces systolic blood pressure. Atherosclerosis 2001;158:195-198.
25. Aviram M, Volkova N, Coleman R, et al. Pomegranate phenolics from the peels, arils, and flowers are antiatherogenic: studies in vivo in atherosclerotic apolipoprotein e-deficient (E 0) mice and in vitro in cultured macrophages and lipoproteins. Journal of Agricultural and Food Chemis ry 2008;56:1148-1157.
26. McDougall GJ, Stewart D. The inhibitory effects of berry polyphenols on digestive enzymes. Biofactors 2005;23:189-195.
27. Makino-Wakagi Y, Yoshimura Y, Uzawa Y, et al. Ellagic acid in pomegranate suppresses resistin secretion by a novel regulatory mechanism involving the degradation of intracellular resistin protein in adipocytes. Biochem Biophys Res Commun 2012;417:880-885.

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If you are reading this blog, you probably already recognize what I am about to report and have read about why it is so important that we make wise eating choices.  However, most Americans are not like the average DiseaseProof reader and I’m willing to bet many people believe still believe that whether or not we get cancer depends on the genes we are dealt or even luck.  Most will agree that smoking is a cause of cancer, but what about what we eat? Will most people agree that our food choice make a difference in whether or not we get cancer down the road? Well, interestingly nutritional research scientists are now coming to the same conclusion as my father, indicating that, yes, our diets can be just as disease-promoting as smoking cigarettes. 

These findings were published by the World Cancer Research Fund in an article entitled, “Food, Nutrition and the Prevention of Cancer: A Global Perspective.” The report was the most comprehensive and systematic of its kind and involved 286 specialists who went through 500,000 scientific articles concerning 17 different types of cancer. The uncontestable findings were that 40 percent of all forms of cancer can be prevented by eating a well balanced diet, maintaining a normal body weight and participating in a moderate amount of physical activity. Head researcher, Jan Erik Paulsen, noted that the evidence shows that a bad diet is more likely to be a cause of cancer than smoking tobacco. 

The specialists on Paulsen’s team found that low carbohydrate diets that recommend red meat such as beef, pork, lamb and game, were particularly disease-promoting.  People who consume large quantities of red meat in order to keep their weight in check can end up getting cancer instead. 

What properties of red meat make it so dangerous? The researchers believe it is the combination of nitrates, heme iron and other substances found in red meats.  Nitrate reacts with heme iron to form a compound called nitrosyl hemoglobin, which can trigger certain types of cancer.  

Paulsen declared, “My theory is that heme iron is so stable that it survives the digestion of meat in the small intestine and goes on undamaged to reach the colon. Here it reacts with the metabolites (intermediate and end-products of metabolism), which are produced by the bacterial flora and forms nitrosamines, which are known to cause cancer.”

However, it is not just red meat that we should be wary of.  Unprocessed meats can be just as dangerous because they can use nitrite already in the stomach (produced from other foods) and form nitrosyl hemoglobin. Combine our diets of processed foods with animal products and limited quantities of vegetables and we’ve created the perfect cancer forming stew. 

Of course my father, Dr. Fuhrman disagrees, because he does not recommend a “balanced diet” to reduce cancer rates by 40 percent.  He recommends a nutritarian diet specifically designed with a portfolio of the world’s most powerful anti-cancer foods.  Dr. Fuhrman suggests that superior nutrition can decrease cancer death rates by 90 percent, not merely 40 percent.   This is because the dietary intervention he suggests is more rigorous and effective at preventing cancer and it is supported by tremendous evidence and clinical experience.  There are multiple studies on optimal consumption of super foods and cancer (his G-BOMBS list), and the statistics on very low rates of cancer in parts of the world that ate better more than 50 years ago before fast food and processed food became ubiquitous.  These populations had less than 10 percent of the cancer we see today. 

Cancer rates are now predicted to climb in the next few decades and the numbers aren’t pretty.  Globally, cancer rates are projected to rise by as much as 75 percent by the year 2030, while cancer rates in the poorest countries are predicted to double as more people are consuming a Western diet style.  These numbers are sad, yet what is even sadder is that many of them would have been prevented with changes in lifestyle. I think we need to begin to take responsibility as a country and begin accepting that our junk food lifestyle can no longer be acceptable.  We can make healthy eating taste great and we have the knowledge now to know which foods promote cancer and which foods prevent it.  It’s up to all of us to take care of our own bodies, but also to spread the word about eating healthfully to those we care about.  Until our nation declares that the salad should be the main dish or that we can reduce our risks of cancer by eating foods like mushrooms, cruciferous greens, and onions, we need to take this matter into our own hands and do our part. Every little bit counts.  

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At the recent American Association for Cancer Research annual meeting, new evidence highlighted the importance of cruciferous vegetables for breast cancer protection

The cruciferous vegetable family:

The cruciferous family is unique among vegetables because of their glucosinolate content – glucosinolates give cruciferous vegetables their characteristic spicy or bitter tastes; when the plant cell walls are broken by blending, chopping, or chewing, an enzyme called myrosinase converts glucosinolates to isothiocyanates (ITCs) – compounds with potent anti-cancer effects, including:¹

• Anti-inflammatory effects – ITCs have been found to decrease the secretion of inflammatory molecules.
•  Anti-angiogenic effects – isothiocyanates can inhibit the development of new blood vessels to limit tumor growth.
• Detoxification of carcinogens – Some carcinogens must be converted to their active form before they can bind DNA to cause carcinogenic changes – isothiocyanates can block this transformation.
• Preventing DNA damage – Isothiocyanates also increase the production of our body’s natural detoxification enzymes, which protect DNA against damage from carcinogens and free radicals.
• Stopping cell division in cells whose DNA has been damaged
• Promoting programmed cell death in cancerous cells
• Anti-estrogenic activity – Exposure to estrogen is known to increase breast cancer risk; estrogens can alter gene expression, promoting cell proliferation breast tissue. ITCs have been shown to inhibit the expression of estrogen-responsive genes.
• Shifting hormone metabolism – Eating cruciferous vegetables regularly helps the body to shift hormone metabolism, reducing the cancer-promoting potency of estrogen and other hormones.

Eating cruciferous vegetables produces measurable isothiocyanates in breast tissue², and observational studies show that women who eat more cruciferous vegetables are less likely to be diagnosed with breast cancer: In a recent Chinese study, women who regularly ate one serving per day of cruciferous vegetables had a 50% reduced risk of breast cancer.³ A 17% decrease in breast cancer risk was found in a European study for consuming cruciferous vegetables at least once a week.⁴

What about women who already have cancer? Is it too late for cruciferous vegetables to improve their prognosis?

We know that childhood and adolescence are the most crucial timesfor environmental stimuli to affect breast cancer risk, but changes made during adulthood and even after diagnosis still have the potential to create positive changes in the body.

The new study kept track of cruciferous vegetable intake in Chinese women with breast cancer for the first 3 years after diagnosis, and followed the women for a total of 5 years. They found dose-response effects – this means that the more cruciferous vegetables women ate, the less likely they were to experience breast cancer recurrence or die from breast cancer. When the women were grouped into four quartiles of cruciferous vegetable consumption, in the highest quartile had a 62% decrease in risk of death and 35% reduced risk of recurrence compared to the lowest quartile.⁵

This new data supports a previous report from the Women’s Healthy Eating and Living (WHEL) study. Breast cancer survivors who reported higher than median cruciferous vegetable intake and were in the top third of total vegetable intake had a 52% reduced risk of recurrence – especially powerful since the average intakes were quite low – 3.1 and 0.5 servings/day of total and cruciferous vegetables, respectively.⁶

Don’t forget: cruciferous vegetables must be chopped, crushed, or chewed well for maximum benefit!

The myrosinase enzyme is physically separated from the glucosinolates in the intact vegetables, but when the plant cells are broken, the chemical reaction can occur and ITCs can be formed. The more you chop before cooking (or chew if you are eating the vegetables raw), the better. Some ITC benefit may be lost with boiling or steaming, so we get the maximum benefit from eating cruciferous vegetables raw – however, gut bacteria also have the myrosinase enzyme, so additional ITC production may occur in cooked cruciferous vegetables after we eat them. Also, we can increase ITC production from cooked cruciferous vegetables by having some shredded raw cruciferous vegetables such as cabbage, kale, collards or arugula in a salad in the same meal to supply the myrosinase enzyme, which the body can use during the digestive process.

Read more about breast cancer prevention.

References:

1. Higdon J, Delage B, Williams D, et al. Cruciferous vegetables and human cancer risk: epidemiologic evidence and mechanistic basis. Pharmacol Res 2007;55:224-236.

2. Cornblatt BS, Ye L, Dinkova-Kostova AT, et al. Preclinical and clinical evaluation of sulforaphane for chemoprevention in the breast. Carcinogenesis 2007;28:1485-1490.

3. Zhang CX, Ho SC, Chen YM, et al. Greater vegetable and fruit intake is associated with a lower risk of breast cancer among Chinese women. Int J Cancer 2009;125:181-188.

4. Bosetti C, Filomeno M, Riso P, et al. Cruciferous vegetables and cancer risk in a network of case-control studies. Ann Oncol 2012.

5. Nechuta SJ, Lu W, Cai H, et al: Cruciferous Vegetable Intake After Diagnosis of Breast Cancer and Survival: a Report From the Shanghai Breast Cancer Survival Study. Abstract #LB-322. In Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4. Chicago, Il; 2012.

6. Thomson CA, Rock CL, Thompson PA, et al. Vegetable intake is associated with reduced breast cancer recurrence in tamoxifen users: a secondary analysis from the Women's Healthy Eating and Living Study. Breast Cancer Res Treat 2011;125:519-527.

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Colon cancer is the third most common cancer type, and the second leading cause of cancer death in the U.S.¹ These cancers are the ones most closely linked to lifestyle; the good news is, that means that colon and rectal cancers are also highly preventable by following healthful lifestyle habits – including avoiding disease-causing foods.

Scientists believe that elevated insulin levels contribute to cancer development; insulin in high concentrations may promote growth and division of cancer cells, and cancerous cells often have elevated levels of insulin receptors.² Foods with a high glycemic load (GL) such as white bread, white rice, sugar, and white potatoes, produce dangerous spikes in blood glucose, and consequently insulin levels. Diets including large quantities of high GL foods increase the risk of several chronic diseases, and a recent meta-analysis of several studies found a 26% increase in colorectal cancer risk in people who consumed the most high glycemic load foods in their diets.^3,4

Examples of high, medium and low GL carbohydrate sources:^5,6

According to the American Institute for Cancer Research, there is suggestive evidence that cheese and foods containing animal fats increase the risk of colon and rectal cancers. Cheese, the fattiest food in the American diet, is particularly high in saturated fat, which is known to impair insulin sensitivity.^7,8

New research suggests that over time, these dietary factors – excess, low-nutrient carbohydrate and fat – may disturb carbohydrate and fat metabolism in the colon by altering DNA methylation in colon cells.

DNA methylation acts essentially as an on/off switch for a gene, usually decreasing (but sometimes increasing) the amount of protein made from that genetic code. Dietary factors are known to affect DNA methylation, and too much or too little methylation can contribute to the development of cancer.⁹

A recent study compared methylation patterns of thousands of genes in the colon mucosa of control subjects without colon cancer to normal mucosa of colon cancer patients; the researchers found hundreds of genes whose methylation patterns differed in the two sets of subjects. When they looked at those genes with the greatest differences in methylation, they made an interesting observation: a common theme among many of these genes was that they are involved in carbohydrate and lipid metabolism – one of these was the insulin gene. In short, “normal” colon cells in colon cancer patients were making more insulin than normal colon cells from healthy subjects – and we know that excess insulin promotes cancer.

The authors hypothesize that an unhealthy diet full of refined carbohydrate and excess fat may cause this metabolic change – and once excess insulin is being produced by colon cells, it then feeds the growth of cancerous cells.¹⁰

Though the research may be complex, the message is simple: refined foods like sugar and white bread, and low-nutrient fats like oils and cheeses are harmful to the health of your colon. Colon cancer is a preventable disease – whole, natural foods provide the fiber, resistant starch, and phytochemicals that will keep the cells of the colon healthy and expressing the proper genes in the proper amounts.

References:

1. American Cancer Society. What are the key statistics about colorectal cancer? [http://www.cancer.org/Cancer/ColonandRectumCancer/DetailedGuide/colorectal-cancer-key-statistics ]
2. Vigneri P, Frasca F, Sciacca L, et al: Diabetes and cancer. Endocr Relat Cancer 2009;16:1103-1123.
3. Gnagnarella P, Gandini S, La Vecchia C, et al: Glycemic index, glycemic load, and cancer risk: a meta-analysis. Am J Clin Nutr 2008;87:1793-1801.
4. Barclay AW, Petocz P, McMillan-Price J, et al: Glycemic index, glycemic load, and chronic disease risk--a meta-analysis of observational studies. Am J Clin Nutr 2008;87:627-637.
5. Carbohydrates and the Glycemic Load. Harvard School of Public Health: The Nutrition Source. http://www.hsph.harvard.edu/nutritionsource/what-should-you-eat/carbohydrates-and-the-glycemic-load/. 
6. Atkinson FS, Foster-Powell K, Brand-Miller JC: International tables of glycemic index and glycemic load values: 2008. Diabetes Care 2008;31:2281-2283.
7. WCRF/AICR Expert Report, Food, Nutrition, Physical Activity and the Prevention of Cancer: a Global Perspective.: World Cancer Research Fund; 2007.
8. Vessby B, Uusitupa M, Hermansen K, et al: Substituting dietary saturated for monounsaturated fat impairs insulin sensitivity in healthy men and women: The KANWU Study. Diab tologia 2001;44:312-319.
9. Kulis M, Esteller M: DNA methylation and cancer. Adv Genet 2010;70:27-56.
10. Study shows how high-fat diets increase colon cancer risk. 2012. EurekAlert! http://www.eurekalert.org/pub_releases/2012-03/tu-ssh030712.php. Accessed March 28, 2012.

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Prostate cancer is exceedingly common, especially with age. It estimated from autopsy studies that one-third of men in their forties have prostate cancer, and by age 85, that figure increases to as high as 75%.1,2 However, most of these cases of prostate cancer are not actually life-threatening. U.S. The lifetime risk of a diagnosis is 15.9%, but the lifetime risk of death from prostate cancer is only 2.8%. Even without treatment, most prostate cancers are not deadly.2 Most men with prostate cancer die from other causes, not from prostate cancer.

Because of the low risk of death from prostate cancer, there is controversy regarding population-wide PSA screening of men without symptoms suggesting prostate cancer. There is no distinction by the PSA between disease that is likely or unlikely to progress to a life-threatening disease. So should all men be screened?

The most important question is this: Does screening reduce the risk of dying from prostate cancer?
The U.S. Preventive Services Task Force, an impartial agency that assesses scientific evidence on prevention and primary care, issued a statement in 2008 saying that they had found “insufficient evidence that screening for prostate cancer improved health outcomes” in men younger than 75. In men 75 or older, the USPSTF found that “the harms of screening and treatment outweigh any potential benefits.”3

New evidence that screening does not reduce death rates
A long-term study published in January 2012 has not found any decrease in prostate cancer deaths in men undergoing annual screening compared to a control group. The Prostate, Lung, Colorectal, and Ovarian cancer screening trial (PLCO trial) of over 76,000 men had published intermediate results after 10 years of follow up, and were not updating that study, extending to 13 years of follow up. The results were similar after 13 years: about 12% more cancers were diagnosed in the screening group, but death rates were not different between the two groups, suggesting that population-wide screening does not reduce the number of prostate cancer deaths.4

This report comes on the heels of a meta-analysis of PSA screening trials performed for the USPSTF in October 2011, which reported information from 5 trials (including the 10-year data from the PLCO trial). Collectively analyzing data from these trials, the authors concluded that PSA screening “results in small or no reduction in prostate cancer-specific mortality.”5

Could PSA screening be harmful?
Despite the above evidence, the idea of screening is still attractive – if you had prostate cancer, wouldn’t it be better to know it? Maybe not.

PSA screening is known to produce many false-positive results - about 70% of men who have elevated PSA levels do not actually have cancer.6 Certainly, psychological harms are inherent in false-positive results, although there is insufficient research to estimate the extent of this harm.5

Healthy men who undergo annual screening may expose themselves to unnecessary and potentially harmful treatments:

• Prostate biopsy complications include fever, infection, bleeding, pain, and urinary difficulty in some men.
• If an abnormal PSA followed by prostate biopsy does indeed detect cancer, 90% of men will be treated with surgery, radiation, or androgen deprivation therapy.
  
  • Up to 0.5% of men die within 1 month of prostate cancer surgery, and 0.6-3% have cardiovascular events. One to seven percent will have serious complications. Radiation and surgery have adverse effects including urinary continence and erectile dysfunction in 20-30% of men. Radiation is also associated with bowel dysfunction.2, 3
  • Androgen deprivation therapy for localized prostate cancer is associated with erectile dysfunction in about 40% of men. Additional serious harms have been reported in patients receiving androgen deprivation therapy for advanced prostate cancers, including increased risk of heart disease, diabetes and bone fractures.2,3,7

Since most cases of prostate cancer are not life-threatening, these procedures are often unnecessary.

The U.S. Preventive Services Task Force (USPSTF) is currently revising their screening recommendations.
As of now, a draft version of the new recommendations is available. In short:

“…the USPSTF now recommends against PSA-based screening for prostate cancer in all age groups.”2

For real protection against cancer, we must focus on prevention rather than relying on early detection. A diet based on beneficial plant foods with documented anti-cancer properties is much more reliable than PSA screening, and protects against heart disease, diabetes, and all cancers, not just prostate cancer. A healthful, plant-based diet is also effective at halting the progression of prostate cancer.8-11

To learn more about protecting yourself from prostate cancer, read my 10 strategies for preventing prostate cancer. Also, in my most recent book, Super Immunity, I discuss the latest scientific research on super foods that supercharge the immune system and fight cancer, and I explain how to put this knowledge into practice by following an anti-cancer eating style.

References:

1. Sakr WA, Haas GP, Cassin BF, et al: The frequency of carcinoma and intraepithelial neoplasia of the prostate in young male patients. J Urol 1993;150:379-385.
2. Screening for Prostate Cancer: U.S. Preventive Services Task Force Recommendation Statement DRAFT. U.S. Preventive Services Task Force; 2011.
3. Screening for Prostate Cancer: U.S. Preventive Services Task Force Recommendation Statement. 2008.
4. Andriole GL, Crawford ED, Grubb RL, 3rd, et al: Prostate Cancer Screening in the Randomized Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial: Mortality Results after 13 Years of Follow-up. J Natl Cancer Inst 2012;104:125-132.
5. Chou R, Croswell JM, Dana T, et al: Screening for prostate cancer: a review of the evidence for the U.S. Preventive Services Task Force. Ann Intern Med 2011;155:762-771.
6. Esserman L, Shieh Y, Thompson I: Rethinking Screening for Breast Cancer and Prostate Cancer. JAMA: The Journal of the American Medical Association 2009;302:1685-1692.
7. Robinson D, Garmo H, Lindahl B, et al: Ischemic heart disease and stroke before and during endocrine treatment for prostate cancer in PCBaSe Sweden. Int J Cancer 2012;130:478-487.
8. Frattaroli J, Weidner G, Dnistrian AM, et al: Clinical events in prostate cancer lifestyle trial: results from two years of follow-up. Urology 2008;72:1319-1323.
9. Fuhrman J: Dr. Joel Fuhrman Case Study Series: Prostate Cancer.
10. Ornish D, Magbanua MJ, Weidner G, et al: Changes in prostate gene expression in men undergoing an intensive nutrition and lifestyle intervention. Proc Natl Acad Sci U S A 2008;105:8369-8374.
11. Ornish D, Weidner G, Fair WR, et al: Intensive lifestyle changes may affect the progression of prostate cancer. J Urol 2005;174:1065-1069; discussion 1069-1070.

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