Eggs, a concentrated source of cholesterol, have been linked to a variety of diseases including, heart disease, diabetes, and different types of cancer. In this article, learn what diseases and types of cancer eggs are most strongly associated with and why you should avoid or limit eating eggs for better health
Those who eat more whole grains have a lower risk of colon cancer, and there are ways to eat your whole grains that are healthier than others. Read more at DrFuhrman.com.
Onions and garlic protect against cancer! Learn more about these super foods in this article.
All vegetables are nutrient rich and promote good health, but green cruciferous vegetables (like kale, broccoli, and bok choy) have the highest nutrient density scores and are associated with the most substantial health benefits. Why is that? In addition to vitamins, minerals and antioxidants, cruciferous vegetables contain an exclusive class of phytochemicals called glucosinolates (glu'ko-sin'o-lates), which are the precursors to powerful anti-cancer compounds. Learn about the cruciferous family of vegetables and how they fight cancer in this article.
One in four Americans takes blood pressure-lowering drugs, and some of these drugs may double a woman's risk for breast cancer when taken for many years.
Whether or not to undergo mammography is a personal choice, and women must be given accurate information about the risks and benefits of mammograms in order to make an informed decision.
I have reported on the inconsistent studies on omega-3 fatty acids and prostate cancer risk. More recently, a study has added to the confusion; the media has picked it up and scared men away from omega-3 supplements, meanwhile some experts have criticized the authors’ methodology and conclusions.
This study used data from a clinical trial on vitamin E and selenium supplementation for cancer prevention, and added on a blood test for omega-3 to determine whether there was an association between plasma levels of omega-3 fatty acids and incidence of prostate cancer. The authors found a statistically significant difference in the average total long-chain omega-3 blood level between men who did or did not develop prostate cancer throughout the study.1
I have serious concerns about the potential risks of taking lots of fish oil capsules. So much fish oil can have paradoxical effects, reducing immune function in later life. Plus eating lots of fish exposes you to risky amounts of chemical pollutants, and raises IGF-1, a hormone that is causative in prostate cancer, so it is not that this relationship has no potential to be true. However, this study does not tell us if these are valid concerns or not and we can’t make any meaningful conclusions from this new study. This study does NOT indicate that omega-3 supplementation or eating fish are a contributory factor in the prostate cancer equation for numerous reasons.
1. Plasma vs. erythrocyte fatty acid measurement, done only once
Although measuring omega-3 levels in the blood seems like it would be an objective and accurate indicator of fish oil intake compared to using the subjects’ reported dietary intake, this test does not accurately reflect long-term dietary intake. There are two methods for measuring blood fatty acids; in plasma or in erythrocyte (red blood cell) membranes. Erythrocyte omega-3 measurement has been reported to be a more accurate reflection of long-term blood levels, and to correlate more closely with dietary intake compared to plasma measurement.2 Regardless of which test was used, one blood test does not reflect one’s fish oil intake or fish exposure over a lifetime or even over a twenty year period. Cancer is caused by what you do for many, many years, not what you do for a few weeks or months. You would have to do multiple blood tests over many years to assure the results were indicative of a dietary pattern. Also, since there was only one blood test at baseline in this study (and they used plasma levels), it only reflects what they consumed a few days before the test was drawn. This is very important, since cancer takes many years to develop. Some men that did have higher levels may have started taking fish oils supplements only recently, and some may have simply eaten a large piece of fish the night before the blood test.
2. The tiny difference in blood omega-3s between the cases and controls.
The authors found a statistically significant difference in the average total omega-3 blood level between men who did or did not develop prostate cancer throughout the study. But is this a meaningful difference out in the real world? In men diagnosed with prostate cancer, the average was 4.66% of total fatty acids; in men without cancer, the average was 4.48%. This is a very small difference, and likely reflects an insignificant difference in omega-3 intake.
3. No information on fish, fish oil, or other omega-3 supplement intake of subjects.
Where did the slight difference in omega-3 blood levels come from? Were the men who were diagnosed with cancer more likely to be taking fish oil capsules? Were they eating more fish overall? More breaded and fried fish? More large, predator fish? The type of fish and how it is prepared would impact the level of environmental contaminants and dietary carcinogens. Could the early development of prostate cancer increase blood omega-3s, rather than vice versa? 3 These unanswered questions make it very difficult to extract any useful information from this study’s results. For it to have substantive impact they would have had to track dietary fish consumption, fish oil consumption and have confirm that was a true recall, with confirmatory blood tests taken episodically.
4. Rancid fish oil?
Industry experts have pointed to the potential role of rancid fish oil in the inconsistent results among omega-3 studies. Animal studies have shown that rancid fish oil could promote inflammation and even cancer, and the majority of fish oil capsules are indeed rancid. Omega-3s are highly unstable fats, very susceptible to oxidation, forming lipid peroxides and starting a chain of oxidation reactions leading to rancidity. Exposure of EPA and DHA to light, heat and oxygen increase the likelihood of oxidation.4
(Fresh, non-rancid fish oil does not have an unpleasant taste or smell. If you take omega-3 capsules, open one up and taste the oil to test whether it has gone rancid.)
5. Research on omega-3s and prostate cancer remains inconsistent.
The authors state, “It is unclear why high levels of long-chain omega-3 PUFA would increase prostate cancer risk, and further study will be needed…” As discussed in my previous article, the literature on omega-3 fatty acids and prostate cancer is indeed inconsistent.
A 2010 meta-analysis of 31 studies on fish consumption and prostate cancer risk found no significant effect overall, and noted the inconsistency between studies: the risks of prostate cancer diagnosis calculated for high fish consumption ranged from a 61% decrease to a 77% increase.5 A 2013 meta-analysis of studies on blood omega-3 levels and prostate cancer also found no effect overall on prostate cancer risk, and noted significant heterogeneity (inconsistency in results) between studies. Only after removing one study from their analysis did they see an increased risk of high-grade prostate cancer.6 Interestingly, Asian populations, such as in Japan, that consume high levels of fish tend to have lower rates of prostate cancer.7-9 The 2010 meta-analysis also found a 63% decrease in risk of death from prostate cancer with high fish consumption.5 Many studies have shown that DHA and EPA decrease proliferation and increase cell death in prostate cancer cells, and that omega-3-enriched diets slow prostate tumor growth in animals.10-20 A clinical trial published in 2011 gave patients about to undergo prostatectomy either a low-fat (15% of calories) diet plus fish oil supplementation or a Western diet with no supplements for 4-5 weeks prior to surgery. The fish oil supplemented group showed a 32.2% decrease in malignant cell proliferation when prostate tissue was analyzed after surgery.21 Though many people with biases want to jump on the results of one of these studies to claim fish or fish oil are good or bad, we simply cannot do so with scientific integrity. There are many different studies on this topic with widely varying results.
Omega-3 supplementation: the big picture
For optimal health (including cancer protection), we require the complete composition of the nutrient-dense (Nutritarian) diet that supplies us with optimal amounts of all valuable nutrients and phytochemicals. Avoiding deficiencies is critical, but it is important to avoid excesses too. Omega-3 fatty acids are essential nutrients that we must get from our diets because our bodies cannot make them; they are crucial for early brain development, and there is much evidence that they promote cardiovascular health and cognitive function.22,23 Note also, that higher omega-3 blood levels have been associated with reduced risk of death from all causes.24 Avoiding supplemental omega-3s is not the appropriate response to this new study. This is especially critical because we all convert short chain omega-3 (ALA) into long chain omega-3 (DHA) differently, and if you are one of those poor converters, the lack of DHA in your diet can turn out to be devastating to you in later life. Many vegans are gambling with their future cognitive health to uphold a philosophical viewpoint, because once you develop a neurological or cognitive deficit in later life, it will be too late to try to fix a deficiency that could have caused it.
Of course, too much of any potentially good thing turns it bad. For any needed nutrient, especially fat soluble nutrients, too much can be problematic. Since all fish oil capsules give a pretty high dose of EPA and DHA, and most of them are rancid too, they could be part of the problem. Plus, fish is an unfavorable omega-3 source, since animal protein and environmental contaminants are packaged with the DHA and EPA. I advise most people take a low dose of algae-derived EPA-DHA, or follow your omega-3 levels episodically to assure no deficiency exists. Maintaining adequate, but not excessively high DHA and EPA levels is the safest and most conservative and responsible strategy.
1. Brasky TM, Darke AK, Song X, et al: Plasma Phospholipid Fatty Acids and Prostate Cancer Risk in the SELECT Trial. J Natl Cancer Inst 2013.
2. Sun Q, Ma J, Campos H, et al: Comparison between plasma and erythrocyte fatty acid content as biomarkers of fatty acid intake in US women. Am J Clin Nutr 2007;86:74-81.
3. Liu Y: Fatty acid oxidation is a dominant bioenergetic pathway in prostate cancer. Prostate Cancer Prostatic Dis 2006;9:230-234.
4. Albert BB, Cameron-Smith D, Hofman PL, et al: Oxidation of marine omega-3 supplements and human health. Biomed Res Int 2013;2013:464921.
5. Szymanski KM, Wheeler DC, Mucci LA: Fish consumption and prostate cancer risk: a review and meta-analysis. Am J Clin Nutr 2010;92:1223-1233.
6. Sorongon-Legaspi MK, Chua M, Sio MC, et al: Blood level omega-3 Fatty acids as risk determinant molecular biomarker for prostate cancer. Prostate Cancer 2013;2013:875615.
7. Dewailly E, Mulvad G, Sloth Pedersen H, et al: Inuit are protected against prostate cancer. Cancer Epidemiol Biomarkers Prev 2003;12:926-927.
8. Kobayashi M, Sasaki S, Hamada GS, et al: Serum n-3 fatty acids, fish consumption and cancer mortality in six Japanese populations in Japan and Brazil. Jpn J Cancer Res 1999;90:914-921.
9. Hebert JR, Hurley TG, Olendzki BC, et al: Nutritional and socioeconomic factors in relation to prostate cancer mortality: a cross-national study. J Natl Cancer Inst 1998;90:1637-1647.
10. Cavazos DA, Price RS, Apte SS, et al: Docosahexaenoic acid selectively induces human prostate cancer cell sensitivity to oxidative stress through modulation of NF-kappaB. Prostate 2011.
11. Hu Y, Sun H, Owens RT, et al: Syndecan-1-dependent suppression of PDK1/Akt/bad signaling by docosahexaenoic acid induces apoptosis in prostate cancer. Neoplasia 2010;12:826-836.
12. Chung BH, Mitchell SH, Zhang JS, et al: Effects of docosahexaenoic acid and eicosapentaenoic acid on androgen-mediated cell growth and gene expression in LNCaP prostate cancer cells. Carcinogenesis 2001;22:1201-1206.
13. Rose DP, Connolly JM: Effects of fatty acids and eicosanoid synthesis inhibitors on the growth of two human prostate cancer cell lines. Prostate 1991;18:243-254.
14. Bureyko T, Hurdle H, Metcalfe JB, et al: Reduced growth and integrin expression of prostate cells cultured with lycopene, vitamin E and fish oil in vitro. Br J Nutr 2009;101:990-997.
15. Istfan NW, Person KS, Holick MF, et al: 1alpha,25-Dihydroxyvitamin D and fish oil synergistically inhibit G1/S-phase transition in prostate cancer cells. J Steroid Biochem Mol Biol 2007;103:726-730.
16. Yi L, Zhang QY, Mi MT: [Role of Rho GTPase in inhibiting metastatic ability of human prostate cancer cell line PC-3 by omega-3 polyunsaturated fatty acid]. Ai Zheng 2007;26:1281-1286.
17. Nakajima T, Kubota N, Tsutsumi T, et al: Eicosapentaenoic acid inhibits voltage-gated sodium channels and invasiveness in prostate cancer cells. Br J Pharmacol 2009;156:420-431.
18. Aronson WJ, Barnard RJ, Freedland SJ, et al: Growth inhibitory effect of low fat diet on prostate cancer cells: results of a prospective, randomized dietary intervention trial in men with prostate cancer. J Urol 2010;183:345-350.
19. Berquin IM, Min Y, Wu R, et al: Modulation of prostate cancer genetic risk by omega-3 and omega-6 fatty acids. J Clin Invest 2007;117:1866-1875.
20. Kelavkar UP, Hutzley J, Dhir R, et al: Prostate tumor growth and recurrence can be modulated by the omega-6:omega-3 ratio in diet: athymic mouse xenograft model simulating radical prostatectomy. Neoplasia 2006;8:112-124.
21. Aronson WJ, Kobayashi N, Barnard RJ, et al: Phase II prospective randomized trial of a low-fat diet with fish oil supplementation in men undergoing radical prostatectomy. Cancer Prev Res (Phila) 2011;4:2062-2071.
22. Simopoulos AP: The importance of the omega-6/omega-3 fatty acid ratio in cardiovascular disease and other chronic diseases. Exp Biol Med (Maywood) 2008;233:674-688.
23. Simopoulos AP: Evolutionary aspects of diet: the omega-6/omega-3 ratio and the brain. Mol Neurobiol 2011;44:203-215.
24. Mozaffarian D, Lemaitre RN, King IB, et al: Plasma Phospholipid Long-Chain omega-3 Fatty Acids and Total and Cause-Specific Mortality in Older Adults: A Cohort Study. Ann Intern Med 2013;158:515-525.
Despite the abundance of scientific evidence demonstrating the benefits of whole soy foods, many people have been scared off from healthful foods like edamame by the anti-soy propaganda (lacking responsible scientific integrity) that continues to float around the internet.
It is true that the nutrient-depleted isolated soy in protein powders and processed foods is likely problematic. And of course, I recommend steering clear of genetically modified soy, as its safety, phytochemical value, and environmental impact remain questionable.
However, research has shown overwhelmingly that whole and minimally processed soy foods (like edamame, tofu and tempeh) provide meaningful health benefits. The presence of isoflavones, a class of phytoestrogen, has sparked much of the controversy around soy. There were concerns that these plant estrogens could potentially promote hormonal cancers, such as breast and prostate cancers; however, those fears were unfounded. I have previously discussed the large body of evidence that convincingly suggests that whole and minimally processed soy foods protect against breast cancer. In addition, a 2009 meta-analysis of studies on soy and prostate cancer found that higher soy intake was associated with a 26% reduction in risk.1 In addition, it appears that isoflavones have a number of anti-cancer effects that are unrelated to their ability to bind the estrogen receptor. Accordingly, soy foods are not only associated with decreased risk of hormonal cancers, but also lung, stomach, and colorectal cancers.2-4 (For further discussion of soy foods and health, see the May 2012 member teleconference.)
An article posted by John Robbins seeks to finally put the soy misinformation to rest. He provides a balanced review of the available information, addressing all the common concerns about soy, from cancer and osteoporosis risk to protein digestibility and mineral absorption.
Soy is not a magic pill or a poison; it is simply a bean.
One can’t argue with the data – the associations between minimally processed soy intake and reduced risk of cancers has been reported over and over again. There is no real controversy here. However, one still should not eat lots of soy products, to the exclusion of other valuable foods. Variety is crucial for obtaining diversity in protective phytochemicals, and a variety of beans are health promoting, along with many other foods. So use good judgment, avoid processed foods, GMO foods and eat a variety of whole natural plant foods including beans such as black beans, chickpeas, lentils and enjoy some edamame, tofu and tempeh as well.
Image credit - Flickr: cl_03
1. Hwang YW, Kim SY, Jee SH, et al: Soy food consumption and risk of prostate cancer: a meta-analysis of observational studies. Nutr Cancer 2009;61:598-606.
2. Yang WS, Va P, Wong MY, et al: Soy intake is associated with lower lung cancer risk: results from a meta-analysis of epidemiologic studies. Am J Clin Nutr 2011;94:1575-1583.
3. Kim J, Kang M, Lee JS, et al: Fermented and non-fermented soy food consumption and gastric cancer in Japanese and Korean populations: a meta-analysis of observational studies. Cancer Sci 2011;102:231-244.
4. Yan L, Spitznagel EL, Bosland MC: Soy consumption and colorectal cancer risk in humans: a meta-analysis. Cancer Epidemiol Biomarkers Prev 2010;19:148-158.
Angelina Jolie’s choice to undergo a preventive double mastectomy because of a family history of breast cancer and a mutation in the BRCA1 gene made news and raised important questions. Complex medical decisions like these are personal and must be made on an individual basis. The appearance of this story and subsequent debate in the global media, however, brings up critical issues about the relative contributions of genetics and lifestyle to breast cancer risk. Also it begs the question, if you are indeed genetically susceptible to breast cancer, can you reduce this risk through nutrition?
The BRCA1 and BRCA2 genes are tumor suppressors.1 Having one of several known mutations in one of these genes is known to impair their function and produce a predisposition for breast cancer and several other cancers. There are mutations in other genes that also increase risk; however the majority of hereditary breast cancer cases are attributed to BRCA1 and BRCA2 mutations. These mutations produce a substantial increase in breast cancer risk. About 12 percent of women in the general population will develop breast cancer throughout their lifetimes, but about 60 percent of women who carry a BRCA mutation will develop breast cancer;2 women with a family history and a BRCA mutation could have a risk of breast cancer as high as 87 percent.3 This is frightening, but keep in mind that most breast cancers are not due to these mutations. The percentage of breast cancer cases that are due to BRCA1 mutations is estimated at 3.5-6.2 percent and 2.1-3.4 percent for BRCA2 mutations.3
Breast cancer is a complex disease with many contributing factors. Even those with a genetic issue can dramatically reduce their risk of breast cancer and other cancers through strong dietary decisions. Natural plant foods contain a huge quantity and variety of phytochemicals, micronutrients with a variety of anti-cancer effects: anti-estrogenic, anti-proliferative, pro-apoptotic, anti-angiogenic, antioxidant and anti-inflammatory effects. All of these different functions act synergistically to prevent the development of cancers, regardless of a person’s genotype.
For example, studies have demonstrated that vegetable and fruit consumption or an overall healthful diet is associated with decreased breast cancer risk, even in carriers of BRCA mutations.6,7 The fact that not every woman who has these mutations gets breast cancer suggests that environmental factors can have a preventive effect. An important study demonstrated that higher cruciferous vegetable intake cut risk in half for women with a breast cancer-associated genetic mutation.8,9 This significant reduction in risk was only from the green vegetables at modest intake, it was not the the entire Nutritarian diet – a diet consisting primarily of nutrient-rich foods - designed to maximize protection with all the anti-cancer foods present simultaneously. So even with heightened genetic risk, healthful foods are significantly protective. Since several populations around the world 25 years ago had only about one-tenth of the breast cancer rates that we had in the U.S.,10-12 it is clear that even in the context of increased genetic risk, diet and lifestyle trump genetics.
Regardless of family history, genetic mutation, or even double mastectomy, a Nutritarian diet is essential for reducing cancer risk.
A Nutritarian diet consists of the following key foods referred to as G-BOMBS (Greens, Beans, Onions, Mushrooms, Berries, Seeds). Unfortunately because every cancer prevention study focuses only on one variable, not the synergistic benefits that add up from the entire Nutritarian lifestyle: isothiocyanates from cruciferous vegetables13, organosulfur compounds from onions and garlic, aromatase inhibitors from mushrooms, flavonoids from berries, lignans from flax, chia and sesame seeds, angiogenesis inhibitors from beans, anti-estrogenic effects of fiber, plus the protective effects of exercise have yet to be calculated. That said, each of these factors has been shown to be powerfully protective; for example, one interesting study on lignans followed women for up to 10 years and found a 71 percent reduced risk of breast cancer mortality in women with the highest lignan intake.14 This demonstrates dramatic anti-cancer potential from the Nutritarian approach, because this study was performed on women late in life who already had a diagnosis of breast cancer, and their lignan intake was only minimal. In other words, even more significant protection can be assumed when these changes are much more significant and started earlier in life before breast cancer occurs.
An important point this news story brought up was empowerment, and I want to emphasize that when faced with simple, every day choices – what to have for breakfast, lunch and dinner – all women have the power to achieve substantial protection against breast cancer. Many women can’t afford to get genetic testing, or a preventive mastectomy if they are positive for a mutation, but all women can’t afford NOT to eat a Nutritarian diet for their hearts, their brains, their breasts and their peace of mind.
1. Fan S, Meng Q, Auborn K, et al: BRCA1 and BRCA2 as molecular targets for phytochemicals indole-3-carbinol and genistein in breast and prostate cancer cells. Br J Cancer 2006;94:407-426.
2. BRCA1 and BRCA2: Cancer Risk and Genetic Testing. National Cancer Institute. http://www.cancer.gov/cancertopics/factsheet/Risk/BRCA. Accessed
3. Robson ME: Clinical considerations in the management of individuals at risk for hereditary breast and ovarian cancer. Cancer Control 2002;9:457-465.
4. Bosviel R, Durif J, Dechelotte P, et al: Epigenetic modulation of BRCA1 and BRCA2 gene expression by equol in breast cancer cell lines. Br J Nutr 2012;108:1187-1193.
5. Fustier P, Le Corre L, Chalabi N, et al: Resveratrol increases BRCA1 and BRCA2 mRNA expression in breast tumour cell lines. Br J Cancer 2003;89:168-172.
6. Ghadirian P, Narod S, Fafard E, et al: Breast cancer risk in relation to the joint effect of BRCA mutations and diet diversity. Breast Cancer Res Treat 2009;117:417-422.
7. Nkondjock A, Ghadirian P: Diet quality and BRCA-associated breast cancer risk. Breast Cancer Res Treat 2007;103:361-369.
8. Lee SA, Fowke JH, Lu W, et al: Cruciferous vegetables, the GSTP1 Ile105Val genetic polymorphism, and breast cancer risk. Am J Clin Nutr 2008;87:753-760.
9. Huang MY, Wang YH, Chen FM, et al: Multiple Genetic Polymorphisms of GSTP1 313AG, MDR1 3435CC, and MTHFR 677CC highly correlated with early relapse of breast cancer patients in Taiwan. Ann Surg Oncol 2008;15:872-880.
10. International Agency for Research on Cancer, World Health Organization. CI5plus: Cancer Incidence in Five Continents Annual Dataset [http://ci5.iarc.fr/CI5plus/ci5plus.htm]
11. Ahn YO, Park BJ, Yoo KY, et al: Incidence estimation of female breast cancer among Koreans. J Korean Med Sci 1994;9:328-334.
12. Bah E, Hall AJ, Inskip HM: The first 2 years of the Gambian National Cancer Registry. Br J Cancer 1990;62:647-650.
13. Liu X, Lv K: Cruciferous vegetables intake is inversely associated with risk of breast cancer: A meta-analysis. Breast 2012.
14. McCann SE, Thompson LU, Nie J, et al: Dietary lignan intakes in relation to survival among women with breast cancer: the Western New York Exposures and Breast Cancer (WEB) Study. Breast Cancer Res Treat 2010;122:229-235.
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
An 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 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.
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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