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

The Women’s Healthy Eating and Living (WHEL) Study was a randomized controlled trial that was designed to test whether adhering to a diet high in vegetables, fruits, and fiber would reduce the risk of recurrence in breast cancer survivors. The study was conducted from 1995-2006, and the subjects were 3,088 women who had been treated for early stage breast cancer. Women were either in a control group or an intervention group.

The daily dietary goals given for the intervention group in the WHEL study were as follows:

• 5 servings of vegetables
• 16 ounces of vegetable juice
• 3 servings of fruit
• 30 g of fiber
• 15-20% of calories from fat.¹

The overall results of the WHEL study were published in 2007 and were disappointing. Women in the intervention group on average increased their vegetable intake by 65%, their fruit intake by 25%, and their fiber intake by 30%; they also decreased their energy percentage from fat by 13%. However, there were no significant differences in the number of breast cancer recurrences or deaths between the control and intervention groups.²

Why did this intervention fail?

There were likely many contributing factors. This dietary intervention was started after the women had already been diagnosed and treated for breast cancer; after eating the Standard American Diet for decades and developing cancer; moderate dietary improvements at that point may be too late to prevent recurrence. The dietary advice was likely not specific enough or rigorous enough to have a significant effect. For example, vegetables with breast cancer preventive properties, such as cruciferous vegetables and mushrooms, were not emphasized over starchy vegetables – women were simply advised to eat 5 servings of vegetables daily. Plus, 75% of the women were already consuming 5 servings of vegetables daily before being randomized to control or intervention groups. ²

Women were not instructed to eat less of anything except fat or to decrease their caloric intake – so it is unsurprising that there was no significant change in body weight in the intervention group. ² This is an important issue, since excess weight is strongly linked to breast cancer risk.^3-7 Plus, these women were also consuming significant amounts of animal protein, which increases cancer risk by increasing IGF-1. ^8-11

Another potential issue was the advice to reduce percentage of calories from fat, but no advice on limiting refined carbohydrates. Advising women to decrease their calories from fat without direction on what to replace those calories with likely resulted in the women choosing more pasta, rice, white potatoes, bread, and low fat processed foods. These women received no guidance on limiting refined carbohydrates, which is an important point here. Refined carbohydrates are higher in glycemic index and contain less fiber and more starch compared to natural carbohydrate foods. High dietary glycemic index is known to be associated with increased breast cancer risk.¹² In contrast, consuming high-fiber foods increases the excretion of estrogen and decreases breast cancer risk.^13-15 Now, new research coming out of the original WHEL data suggests that starch intake may play a role in breast cancer risk as well.

Starch intake and breast cancer recurrence

In new research presented at the San Antonio Breast Cancer Symposium in December, data from the WHEL Study were re-analyzed with respect to changes in carbohydrate intake. Women from both the control and intervention groups were included in the analysis.

The subjects were arranged into four groups based on how much their starch intake changed over the first year of the study: in the group who had the greatest decreases in starch intake, the likelihood of recurrence was 9.7%; in the group with the greatest increases in starch intake the likelihood of recurrence was 14.2%.^16,17 The women who increased their starch intake were at greater risk of recurrence.

Although this particular study did not investigate specific foods, we know that white rice, white flour products, and white potatoes are some of the highest starch foods – these are also low nutrient, high glycemic foods and staples in the Standard American Diet. Breast cancer survivors and all women who want to prevent breast cancer must focus on protective foods (GOMBBS) such as mushrooms, green vegetables, beans, and onions; and avoid low-nutrient disease-causing foods, like refined starches and sugars, animal products, and oils. Too often, researchers do not study dietary patterns with the best anti-cancer potential.

References:

1. Pierce JP, Faerber S, Wright FA, et al: A randomized trial of the effect of a plant-based dietary pattern on additional breast cancer events and survival: the Women's Healthy Eating and Living (WHEL) Study. Control Clin Trials 2002;23:728-756.
2. Pierce JP, Natarajan L, Caan BJ, et al: Influence of a diet very high in vegetables, fruit, and fiber and low in fat on prognosis following treatment for breast cancer: the Women's Healthy Eating and Living (WHEL) randomized trial. JAMA 2007;298:289-298.
3. American Institute for Cancer Research. New Estimate: Excess Body Fat Alone Causes over 100,000 Cancers in US Each Year [http://www.aicr.org/site/News2/153571380?abbr=pr_&page=NewsArticle&id=17333&news_iv_ctrl=1102]
4. Trentham-Dietz A, Newcomb PA, Storer BE, et al: Body size and risk of breast cancer. Am J Epidemiol 1997;145:1011-1019.
5. Ballard-Barbash R, Schatzkin A, Taylor PR, et al: Association of change in body mass with breast cancer. Cancer Res 1990;50:2152-2155.
6. Vrieling A, Buck K, Kaaks R, et al: Adult weight gain in relation to breast cancer risk by estrogen and progesterone receptor status: a meta-analysis. Breast Cancer Res Treat 2010;123:641-649.
7. Parker ED, Folsom AR: Intentional weight loss and incidence of obesity-related cancers: the Iowa Women's Health Study. Int J Obes Relat Metab Disord 2003;27:1447-1452.
8. Rinaldi S, Peeters PH, Berrino F, et al: IGF-I, IGFBP-3 and breast cancer risk in women: The European Prospective Investigation into Cancer and Nutrition (EPIC). Endocr Relat Cancer 2006;13:593-605.
9. Hankinson SE, Willett WC, Colditz GA, et al: Circulating concentrations of insulin-like growth factor-I and risk of breast cancer. Lancet 1998;351:1393-1396.
10. Sugumar A, Liu YC, Xia Q, et al: Insulin-like growth factor (IGF)-I and IGF-binding protein 3 and the risk of premenopausal breast cancer: a meta-analysis of literature. Int J Cancer 2004;111:293-297.
11. Shi R, Yu H, McLarty J, et al: IGF-I and breast cancer: a meta-analysis. Int J Cancer 2004;111:418-423.
12. 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.
13. 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.
14. 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.
15. Park Y, Brinton LA, Subar AF, et al: Dietary fiber intake and risk of breast cancer in postmenopausal women: the National Institutes of Health-AARP Diet and Health Study. Am J Clin Nutr 2009;90:664-671.
16. Emond JA, Patterson RE, Pierce JP: Change in Carbohydrate Intake and Breast Cancer Prognosis. In San Antonio Breast Cancer Symposium, vol. Presentation #P3-09-01; 2011.
17. Starch Intake May Influence Risk for Breast Cancer Recurrence. 2011. AACR in the News. http://www.aacr.org/home/public--media/aacr-in-the-news.aspx?d=2654. Accessed December 29, 2011.

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What are lignans?

Plant lignans are one of the four classes of phytoestrogens (isoflavones, lignans, stilbenes, coumestans), phenolic compounds that are structurally similar to the main mammalian estrogen, estradiol.¹ Plant lignans are modified by bacteria in the human digestive tract into enteroligans. It is important to recognize the role of healthy bacteria in this process, because antibiotics can destroy beneficial bacteria in the gut resulting in long-term reduction in enteroligans.² Eating commercial meats exposes us to antibiotics, as does the overuse and inappropriate prescribing by physicians.

Which foods are good sources of plant lignans?

Flaxseeds are the richest source of plant lignans, having about 8 times the lignan content of sesame seeds [note that flaxseed oil does not contain lignans – they bind to the fiber]. The other plant foods on the list have about one-tenth or less the amount of lignans as sesame seeds per serving.^2,3 Chia seeds are also a rich source of lignans, however the exact amount is still debatable, so that number will be made available at a later date.

• Flaxseeds (85.5 mg/ounce)
• Sesame seeds (11.2 mg/ounce)⁴
• Kale (curly; 1.6 mg/cup)
• Broccoli (1.2 mg/cup)

Anti-cancer effects of lignans

Enterolignans are structurally similar to estrogen and can bind to estrogen receptors – this capability allows lignans to either have weak estrogenic activity or block the actions of estrogen in the body. For this reason, plant lignans are classified as phytoestrogens, and there has been much interest in the potential contribution of lignan-rich foods to reduced risk of hormone-related cancers.^2,5 Enterolignans inhibits aromatase⁶ and estradiol production in general, lowering serum estrogen levels.⁷ Plant lignans also increase concentration of sex hormone binding globulin, which blunts the effects of estrogens.^8-10 These benefits were documented when 48 postmenopausal women consumed 7.5 g/day of ground flax seeds for 6 weeks, then 15 g for 6 weeks – and significant decreases in estradiol, estrone, and testosterone were noted with a bigger decrease in overweight and obese women.¹¹

In a mouse model, a flaxseed diet (5%, 10%) shows dose-dependent inhibition of breast tumor growth.¹² Human trials also confirmed similar beneficial effects. A double-blinded, randomized controlled trial of dietary flaxseed demonstrated dramatic protection. Women ate either a control muffin with no flax seeds imbedded or 25g flax-containing muffin starting at time of diagnosis of breast cancer for just 32-39 days until surgery. Tumor tissue analyzed at diagnosis and surgery demonstrated surprising benefits even in this short timeframe. There was a significant apoptosis (tumor cell death) and reduced cell proliferation in the flaxseed group in just the one month.¹³ Likewise women eating more flaxseeds with a documented higher serum enterolactone were found to have a 42% reduced risk of death from postmenopausal breast cancer and a dramatic (40 percent) reduction in all causes of death.^14,15 Flaxseeds are clearly super foods; even with a mediocre diet they offer powerful protection against certain types of breast cancer. Another interesting study on flax followed women for up to 10 years and found a 51% reduced risk of all-cause mortality and a 71% reduced risk of breast cancer mortality. The intake of dried beans was also associated with a 39% reduced risk of all-cause mortality.¹⁶ Endometrial and ovarian cancer have not been as extensively studied, but the few studies that have been conducted suggest a protective effect.^2,17

Bottom line; don’t forget to take your ground flax seeds (or chia seeds) every day. I sometimes forget too, but reviewing the science encourages me to remember. When used in conjunction with dietary exposure to greens, onions, mushrooms and beans, dramatic reductions in the risk of breast cancer are possible.

My newest book, Super Immunity, addresses my full nutritional program to win the war against breast cancer.

References:
1. Mense SM, Hei TK, Ganju RK, et al: Phytoestrogens and breast cancer prevention: possible mechanisms of action. Environ Health Perspect 2008;116:426-433.
2. Higdon J: Lignans. In An Evidence-Based Approach to Dietary Phytochemicals. New York: Thieme; 2006: 155-161
3. Milder IE, Arts IC, van de Putte B, et al: Lignan contents of Dutch plant foods: a database including lariciresinol, pinoresinol, secoisolariciresinol and matairesinol. Br J Nutr 2005;93:393-402.
4. Coulman KD, Liu Z, Hum WQ, et al: Whole sesame seed is as rich a source of mammalian lignan precursors as whole flaxseed. Nutr Cancer 2005;52:156-165.
5. Adlercreutz H: Lignans and human health. Crit Rev Clin Lab Sci 2007;44:483-525.
6. Adlercreutz H, Bannwart C, Wahala K, et al: Inhibition of human aromatase by mammalian lignans and isoflavonoid phytoestrogens. J Steroid Biochem Mol Biol 1993;44:147-153.
7. Brooks JD, Thompson LU: Mammalian lignans and genistein decrease the activities of aromatase and 17beta-hydroxysteroid dehydrogenase in MCF-7 cells. J Steroid Biochem Mol Biol 2005;94:461-467.
8. Adlercreutz H, Mousavi Y, Clark J, et al: Dietary phytoestrogens and cancer: in vitro and in vivo studies. J Steroid Biochem Mol Biol 1992;41:331-337.
9. Adlercreutz H, Hockerstedt K, Bannwart C, et al: Effect of dietary components, including lignans and phytoestrogens, on enterohepatic circulation and liver metabolism of estrogens and on sex hormone binding globulin (SHBG). J Steroid Biochem 1987;27:1135-1144.
10. Low YL, Dunning AM, Dowsett M, et al: Phytoestrogen exposure is associated with circulating sex hormone levels in postmenopausal women and interact with ESR1 and NR1I2 gene variants. Cancer Epidemiol Biomarkers Prev 2007;16:1009-1016.
11. Sturgeon SR, Heersink JL, Volpe SL, et al: Effect of dietary flaxseed on serum levels of estrogens and androgens in postmenopausal women. Nutr Cancer 2008;60:612-618.
12. Chen J, Power KA, Mann J, et al: Flaxseed alone or in combination with tamoxifen inhibits MCF-7 breast tumor growth in ovariectomized athymic mice with high circulating levels of estrogen. Exp Biol Med (Maywood) 2007;232:1071-1080.
13. 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.
14. Buck K, Vrieling A, Zaineddin AK, et al: Serum enterolactone and prognosis of postmenopausal breast cancer. J Clin Oncol 2011;29:3730-3738.
15. Buck K, Zaineddin AK, Vrieling A, et al: Estimated enterolignans, lignan-rich foods, and fibre in relation to survival after postmenopausal breast cancer. Br J Cancer 2011;105:1151-1157.
16. 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.
17. Bandera EV, King M, Chandran U, et al: Phytoestrogen consumption from foods and supplements and epithelial ovarian cancer risk: a population-based case control study. BMC Womens Health 2011;11:40.

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Why Awareness? Is there anyone out there who has never heard of Breast Cancer? Do you want to know why it wasn’t called Breast Cancer Prevention Month? I’ll tell you why, because its purpose is not to help women by preventing breast cancer; it is all about money.

It is obvious this pink product promotion kick is all about promoting mammograms so radiologists can make more money. They need plenty of awareness to counter all the recent research from large studies showing that mammograms aren’t too effective.^1-3 It is clear that this was just another mammogram campaign and a fundraising effort designed to save money for the pharmaceutical companies so they don’t have to pay for the drug research to test expensive new chemotherapeutic agents.

If preventing human suffering and saving women's lives were the overriding purpose then promoting how to reduce the risk of developing breast cancer would be front and center as the main objective. Women should be getting notified of the scientific evidence that has accumulated in recent years that can enable women to avoid breast cancer. There are powerful protective steps women need to be aware of, such as:

• Exercise
• Stay slim
• Eat lots of green vegetables, onions, and mushrooms daily.
• Do not eat mass factory farmed dairy products, especially those given rBGH
• Stay away from fast foods and insulin promoting refined foods such as white flour and sweets.
• Do not eat mass factory farmed meats given antibiotics and growth promoting hormones.

Consider: these cancer non-profits are affiliated with drug companies and mammogram machine companies. They are also supported by companies such as Omaha Steaks, Pretzel Crisps, Boar’s Head Meats, General Mills, and ACH Foods (which makes margarine and cooking oils for fast food restaurants). They have no interest in preventing cancer, only treating it. The search for the magic “cure” for breast cancer is just another belief system with no reality behind it. I wish you a long life waiting for this to happen - that women can eat fast food, pasta, doughnuts, and bagels with cream cheese every day and then take a magic pill and not get cancer. Never gonna happen. The whole purpose of buying pink and raising money is to actually increase the amount of women with the diagnosis of cancer so they can be tested and treated, making more money for this billion dollar industry.

Hysterical wasn’t it that Southern Cancer Fried Chicken was selling pink buckets of the cancer-causing (junk food fried) chicken to raise money for breast cancer awareness? A skull and crossbones on the chicken bucket would have made more sense than a pink ribbon, but what do I know? I am sure next year we will see a pink Big Mac with a ribbon around it, and we will be encouraged to drink Pepsi for breast cancer awareness. I say let’s have some pink-ribboned cigarettes, and whiskey in pink bottles, too. I wonder if the cocaine pushers will get in on the act. Why not? Maybe even we can get the lawn service technicians that spray toxic weed killer on the neighbor’s lawn to dress in pink.

Let me tell you something, a cure is not coming soon. You’d better hedge your bets and eat right.

Acknowledgement of conflict of interest: Please note I (Dr. Fuhrman) have an interest in preventing women from getting breast cancer and as the research director of the Nutritional Research Project of the National Health Association am working on a research project on breast cancer prevention. If you are a woman who is willing to take a pledge to follow a nutritarian diet for prevention of cancer (for over 10 years) please put your name on the e-mail list at NutritionalResearch.org so we can contact you with the details as this research trial is fully established in the upcoming months. If you are interested in learning more about participation please enter your name where it says "Sign Up For Updates."

References:

1. Gotzsche PC, Nielsen M: Screening for breast cancer with mammography. Cochrane Database Syst Rev 2009:CD001877.
2. Wright CJ, Mueller CB: Screening mammography and public health policy: the need for perspective. Lancet 1995;346:29-32.
3. 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.

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It is estimated that there are more than 100,000 new cases of colon cancer diagnosed each year in the U.S. alone, and colon and rectal cancers are the third leading cause of cancer-related deaths.¹  The American Institute for Cancer Research estimates that forty-five percent of these new cases could be prevented by following a few simple lifestyle habits: avoiding processed and red meat, exercising regularly, maintaining a healthy weight, and limiting alcohol consumption.²  But we can do better – imagine the level of protection if we not only avoided carcinogenic foods, but also focused on eating the foods that work on a cellular level to prevent  colon cancer.

So which foods offer us the best protection?

Anti-cancer compounds have been identified in many plant foods: for example cruciferous vegetables, mushrooms, and the onion and garlic family are known to contain substances that can prevent cellular processes involved in cancer development. Certainly, a diet high in fruits and vegetables in general is protective^3-5, but many observational studies on diet have not investigated specific food groups, only broad categories like “fruits,” “vegetables,” etc.  But there is a wide range of anti-cancer activity in the wide range of plant foods – for example, kale is more protective than iceberg lettuce.  Identifying these protective plant foods helps us to construct an anti-colon cancer diet.

A recent study aimed to find some specific foods and food groups that protect against colon cancer. Twenty-six years after reporting information about their diets, subjects were asked whether they had undergone screening colonoscopy, and if so, whether they had physician-diagnosed polyps. The majority of colorectal cancers originate from polyps, so polyps are considered a precursor to the development of cancer. This study was part of the larger Adventist Health Study, which studies relationships between diet and chronic disease in members of the Seventh-day Adventist Church, which emphasizes healthy living in its teachings.

The researchers examined about 25 different foods and food groups. Those that were associated with reduced risk of polyps were cooked green vegetables, dried fruit, legumes (beans, lentils, etc.), and brown rice. All of these displayed dose-dependent effects, meaning that the more of these foods the subjects ate, the more protection they had from colon cancer.⁶

Green vegetables are rich in folate and isothiocyanates, nutrients with potent anti-cancer properties. Folate is a B vitamin that is involved in turning genes on and off – this is important in preventing the early cellular events that lead to cancer.  Adequate folate levels are protective against several cancers, including colon cancer. It is important to note, however, that synthetic folic acid from supplements is not protective.^7,8  Isothiocyanates are a group of nutrients found in cruciferous vegetables that have a wide variety of cancer preventive properties – they can detoxify or remove carcinogens from healthy cells, kill cancer cells, have anti-inflammatory and antioxidant effects, and prevent tumors from acquiring a blood supply.⁹ 

The protection from beans and other legumes was likely due to their soluble fiber and resistant starch, carbohydrates that are not broken down by digestive enzymes.  Intestinal bacteria ferment these carbohydrates, forming short chain fatty acids such as butyrate.  Butyrate has a number of anti-cancer effects including disrupting cancer cell growth, increasing levels of detoxification enzymes, limiting DNA damage, and preventing tumors from acquiring a blood supply.^10-13

 High fiber foods, including dried fruit and brown rice (as well as vegetables and beans) help to reduce transit time of gastrointestinal contents through the colon – this reduces the potential contact between dietary toxins or carcinogens and the cells that line the colon.  Reduced transit time is believed to be an important contribution of fiber to the prevention of colon cancer. ^14,15  Raisins, probably the most popular dried fruit, have been shown to increase short chain fatty acid production and decrease colon transit time.^16,17 In addition to fiber content, dried fruit likely also contributed antioxidant protection of colon cells from DNA damage, which is an early event in the development of cancer.¹⁸ 

Previous studies found a protective effect of berries, citrus fruits, and yellow-orange vegetables, which was likely due to their high concentration of flavonoid and carotenoid antioxidants, respectively.^10,19,20Additional studies on specific food groups have also found a reduced risk of colon polyps with high intake of green leafy vegetables (many of which are cruciferous), onions, and garlic.^12,19

All of these foods contain known anti-cancer compounds, and of course there are thousands of anti-cancer compounds in plant foods that scientists have not yet discovered.  Each of these colorful plant foods contains a spectrum of micronutrients and phytochemicals that work in concert to protect the body against carcinogenic influences. Future studies will continue to reveal these phytochemicals and their anti-cancer properties.

My new book Super Immunity, which will be released September 20, 2011, discusses in depth the connections between diet and cancer. 

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. American Institute for Cancer Research. What you need to know about preventing colorectal cancer. http://www.aicr.org/reduce-your-cancer-risk/cancer-site/cancersite_colon_rectum.html. Accessed September 2, 2011.

3. Reedy J, Krebs-Smith SM: A comparison of food-based recommendations and nutrient values of three food guides: USDA's MyPyramid, NHLBI's Dietary Approaches to Stop Hypertension Eating Plan, and Harvard's Healthy Eating Pyramid. J Am Diet Assoc 2008;108:522-528.

4. van Duijnhoven FJ, Bueno-De-Mesquita HB, Ferrari P, et al: Fruit, vegetables, and colorectal cancer risk: the European Prospective Investigation into Cancer and Nutrition. Am J Clin Nutr 2009;89:1441-1452.

5. Wirfalt E, Midthune D, Reedy J, et al: Associations between food patterns defined by cluster analysis and colorectal cancer incidence in the NIH-AARP diet and health study. Eur J Clin Nutr 2009;63:707-717.

6. Tantamango YM, Knutsen SF, Beeson WL, et al: Foods and food groups associated with the incidence of colorectal polyps: the Adventist Health Study. Nutr Cancer 2011;63:565-572.

7. Kim YI: Role of folate in colon cancer development and progression. The Journal of nutrition 2003;133:3731S-3739S.

8. Kim YI: Folate and colorectal cancer: an evidence-based critical review. Molecular nutrition & food research 2007;51:267-292.

9. 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.

10. 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.

11. Dronamraju SS, Coxhead JM, Kelly SB, et al: Cell kinetics and gene expression changes in colorectal cancer patients given resistant starch: a randomised controlled trial. Gut 2009;58:413-420.

12. Williams EA, Coxhead JM, Mathers JC: Anti-cancer effects of butyrate: use of micro-array technology to investigate mechanisms. The Proceedings of the Nutrition Society 2003;62:107-115.

13. Hamer HM, Jonkers D, Venema K, et al: Review article: the role of butyrate on colonic function. Aliment Pharmacol Ther 2008;27:104-119.

14. Jacobs LR: Modification of experimental colon carcinogenesis by dietary fibers. Adv Exp Med Biol 1986;206:105-118.

15. Gear JS, Brodribb AJ, Ware A, et al: Fibre and bowel transit times. Br J Nutr 1981;45:77-82.

16. Spiller GA, Story JA, Furumoto EJ, et al: Effect of tartaric acid and dietary fibre from sun-dried raisins on colonic function and on bile acid and volatile fatty acid excretion in healthy adults. The British journal of nutrition 2003;90:803-807.

17. Spiller GA, Story JA, Lodics TA, et al: Effect of sun-dried raisins on bile acid excretion, intestinal transit time, and fecal weight: a dose-response study. Journal of medicinal food 2003;6:87-91.

18. Federico A, Morgillo F, Tuccillo C, et al: Chronic inflammation and oxidative stress in human carcinogenesis. International journal of cancer Journal international du cancer 2007;121:2381-2386.

19. Wu H, Dai Q, Shrubsole MJ, et al: Fruit and vegetable intakes are associated with lower risk of colorectal adenomas. J Nutr 2009;139:340-344.

20. Michels KB, Giovannucci E, Chan AT, et al: Fruit and vegetable consumption and colorectal adenomas in the Nurses' Health Study. Cancer Res 2006;66:3942-3953.

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Eating a high-nutrient diet focused on whole plant foods allows us to avoid many of the common environmental toxins and carcinogens that humans come into contact with on a regular basis, like heterocyclic amines, acrylamides, dioxins, and mercury.  But there are other environmental carcinogens that do not come from the diet, and we need to be aware of these too.

The World Health Organization’s International Agency for Research on Cancer (IARC) recently issued a cautionary statement about the potential dangers of radiation from radiofrequency electromagnetic fields, the type of radiation emitted by mobile phones and other wireless communication devices, radar, microwaves, radio, and television.   A panel of scientists reviewed the existing research on the topic, and they decided to classify radiofrequency electromagnetic fields as “possibly carcinogenic to humans."¹

The research is not conclusive yet, but the IARC advises caution while we wait for further studies to be done.  Many of the studies so far have not found a connection between mobile phone use and cancer, but a few studies have found significant risk of brain tumors:

• The 13-country industry-funded Interphone study whose results were published last year did not find any increase in brain tumor risk associated with mobile phone use overall.  However, they did see an increased risk of one type of brain tumor (glioma) at the highest exposure levels to radiofrequency electromagnetic fields.²
• An Israeli study found that greater cell phone use was associated with the development of parotid gland (a salivary gland) tumors.³
• A series of studies in Sweden have found links between cell phone use and brain tumors, particularly with long-term cell phone use (10 years or more) and in those who began using cell phones before age 20.^4-6
• A review of 11 studies on cell phone use and brain tumors reported that most studies did not find associations, but 3 studies of long-term cell phone use did find that the risk of one type of brain tumor (acoustic neuroma) more than doubled in those who had used cell phones for 10 years or more.⁷
• A recent study found that an active cell phone against the ear increases glucose metabolism in the area of the brain closest to the antenna.  Whether this has any relevance to the brain tumor studies is unknown, but this result does confirm that cell phone radiation can affect biological processes in the brain.⁸

Avoiding mobile phones is simply not an option for most of us, so what can we do to reduce our exposure?

The Environmental Working Group provides these tips:

• Choose a phone that emits lower levels of radiation – check the guide to the best and worst phones to see where your current phone ranks.
• Use a headset or speakerphone – holding your phone away from the body reduces radiation exposure significantly.
• Send a text message instead of calling when possible.
• Keep your cell phone turned off until you need to use it.
• Don’t talk when your phone is “working” to acquire a signal: when signal is low, or when you are in a moving vehicle.
• Children’s cell phone use should be very limited. Remember that children’s smaller bodies and dividing cells are more susceptible to carcinogenic influences. 

Cell phones have only been in widespread use for a relatively short time, and it can take years or even decades for cancer to develop after exposure to a carcinogenic influence.  We simply don’t know how safe cell phones are, and how their radiation may affect our physiology in the long term.  In light of the data so far, cautious and conservative cell phone use is likely a valuable addition to an anti-cancer lifestyle.

References:

1. Cell Phones Possibly Carcinogenic, WHO Says. Medscape Family Medicine News. http://www.medscape.com/viewarticle/743673?sssdmh=dm1.691945&src=nl_newsalert. Accessed June 22, 2011.

2. Brain tumour risk in relation to mobile telephone use: results of the INTERPHONE international case-control study. Int J Epidemiol 2010;39:675-694.

3. Sadetzki S, Chetrit A, Jarus-Hakak A, et al: Cellular phone use and risk of benign and malignant parotid gland tumors--a nationwide case-control study. Am J Epidemiol 2008;167:457-467.

4. Hardell L, Carlberg M: Mobile phones, cordless phones and the risk for brain tumours. Int J Oncol 2009;35:5-17.

5. Hardell L, Carlberg M, Hansson Mild K: Pooled analysis of case-control studies on malignant brain tumours and the use of mobile and cordless phones including living and deceased subjects. Int J Oncol 2011;38:1465-1474.

6. Hardell L, Carlberg M, Soderqvist F, et al: Meta-analysis of long-term mobile phone use and the association with brain tumours. Int J Oncol 2008;32:1097-1103.

7. Han YY, Kano H, Davis DL, et al: Cell phone use and acoustic neuroma: the need for standardized questionnaires and access to industry data. Surg Neurol 2009;72:216-222; discussion 222.

8. Volkow ND, Tomasi D, Wang GJ, et al: Effects of cell phone radiofrequency signal exposure on brain glucose metabolism. JAMA 2011;305:808-813.

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A recent study produced confusing results.  It found that a higher blood concentration of omega-3 fatty acids was associated with increased risk of high-grade prostate cancer, and a higher concentration of trans-fats was associated with decreased risk.¹  These men were not supplementing with liquid fish oil, so it can be assumed that the blood levels represented fish intake.  So should men still take omega-3 supplements?  We know that DHA is good for the heart and the brain, but is it really bad for the prostate?  What about trans-fats – how could more of this unhealthy fat possibly be beneficial for the prostate? 

When we look more closely, we can see that this one study should not dictate major changes in our view of a cancer-preventive lifestyle. Read the entire article on DrFuhrman.com.

High fish consumption/blood omega-3s increase risk in some studies, decrease risk in others

• In a 2010 meta-analysis of 31 studies, the risks of prostate cancer diagnosis calculated for high fish consumption ranged from a 61% decrease in risk to a 77% increase in risk, and several showed no significant differences in risk at all. 
• In the same meta-analysis, pooled data from four studies on fish consumption and death from prostate cancer (rather than diagnosis of prostate cancer) found a 63% decrease in risk for high fish consumption. ² 
• A recent meta-analysis of studies on ALA intake (the omega-3 in plant foods like flax, hemp, chia, and walnuts, and small amounts in leafy greens) concluded that there was a small but significant decrease in risk (5%) for men consuming more than 1.5 grams of ALA per day.³  
• At least 15 studies (the current study included), have used blood concentrations of omega-3 fatty acids as a measure of omega-3 intake.  Some studies reported increased risk, some decreased risk, and some no effect.

Remember when looking at fish intake, we are not looking at omega-3 intake alone.  

Fish are rich in omega-3s, but they also contain a significant amount of animal protein and accumulated environmental pollutants, both of which have been linked to prostate cancer. ^4-7  Sufficient research has not been done on omega-3 supplements and prostate cancer to make any conclusions. 

If we were to conclude anything from all the studies available on this subject it would be that fish and omega-3 fats in general do not have a major impact on this disease, but the inconsistency and widely differing results suggest regional variation in pollutant levels in the fish consumed.

Trans-fats and blood levels; more confusion in the midst.  

Before you start eating Twinkies and French Fries fried in trans fat for their prostate cancer protection, let’s consider the possibility that after consuming trans fats (trans fats are man-made fat, already linked with cancer in multiple studies), those inflammatory fats are either burned, removed or stored in the body.  Their levels may fluctuate abnormally because of having cancer.  Therefore the high omega-3 and low trans fat blood levels in this study could be early signs of developing cancer, not the cause of it.  Also, three previous studies on either trans-fat intake or blood trans-fats have found increased risk of prostate cancer.^8-10

Should men still take omega-3 supplements?  

Remember that omega-3s are essential fatty acids – the body cannot make them if we don’t get them from our diet.  A deficiency of nutrients the body requires is never favorable for health, but more than needed may not be better when it comes to omega-3 fatty acids.   I still recommend omega-3 sufficiency, which can be achieved with 100-200 mg/day of DHA plus 1 tbsp. of ground flaxseed for ALA.  Almost all nutrients can be harmful in deficiency or excess.  

Read the entire article on DrFuhrman.com

References:

1. Brasky TM, Till C, White E, et al: Serum Phospholipid Fatty Acids and Prostate Cancer Risk: Results From the Prostate Cancer Prevention Trial. Am J Epidemiol 2011.

2. 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.

3. Carayol M, Grosclaude P, Delpierre C: Prospective studies of dietary alpha-linolenic acid intake and prostate cancer risk: a meta-analysis. Cancer Causes Control 2010;21:347-355.

4. Giovannucci E, Pollak M, Liu Y, et al: Nutritional predictors of insulin-like growth factor I and their relationships to cancer in men. Cancer Epidemiol Biomarkers Prev 2003;12:84-89.

5. Rowlands MA, Gunnell D, Harris R, et al: Circulating insulin-like growth factor peptides and prostate cancer risk: a systematic review and meta-analysis. Int J Cancer 2009;124:2416-2429.

6. Hardell L, Andersson SO, Carlberg M, et al: Adipose tissue concentrations of persistent organic pollutants and the risk of prostate cancer. J Occup Environ Med 2006;48:700-707.

7. Van Maele-Fabry G, Libotte V, Willems J, et al: Review and meta-analysis of risk estimates for prostate cancer in pesticide manufacturing workers. Cancer Causes Control 2006;17:353-373.

8. Hu J, La Vecchia C, Gibbons L, et al: Nutrients and risk of prostate cancer. Nutr Cancer 2010;62:710-718.

9. King IB, Kristal AR, Schaffer S, et al: Serum trans-fatty acids are associated with risk of prostate cancer in beta-Carotene and Retinol Efficacy Trial. Cancer Epidemiol Biomarkers Prev 2005;14:988-992.

10. Chavarro JE, Stampfer MJ, Campos H, et al: A prospective study of trans-fatty acid levels in blood and risk of prostate cancer. Cancer Epidemiol Biomarkers Prev 2008;17:95-101.

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Today in the U.S., about 16% of girls enter puberty by the age of 7, and about 30% by the age of 8 – A recent study determined that the number of girls entering puberty (defined by breast development) at these early ages has increased markedly between 1997 and 2010.¹ 

Trends in Age at Menarche

The average age at menarche in Western countries began declining during the early part of the 20^th century due to increased consumption of animal products and  increasing calorie intake; the decline slowed in the 1960s, and now in the U.S. there has been a more recent surge in early puberty starting in the mid-1990s.² In Europe, in 1830, the average age at menarche was 17.  Similarly in the 1980s in rural China, the average age at menarche was 17.³ In the U.S. in 1900, the average was 14.2.  By the 1920s, average age at menarche in the U.S. had fallen to 13.3  and by 2002, it had reached 12.34.⁴ Similar trends are occurring in other Western nations.^5,6 For example, age at menarche in Ireland has declined from 13.52 in 1986 to 12.53 in 2006.⁷ In Italy, a recent study showed that girls’ age at menarche was on average 3 months earlier than their mothers’.⁸  

Taking all this data together, we can estimate that the normal, healthy age at menarche under conditions of excellent nutrition without caloric excess, would probably fall somewhere between 15 and 18.  But today in the U.S., about half of girls begin developing breasts before age 10, and the average age at menarche is less than 12 ½ and still declining. 

Why is this happening? 

The neurological and hormonal systems that regulate pubertal timing are complex, but research has identified a number of environmental factors that may be contributing to the decline in age at puberty:

Increasing rates of childhood overweight and obesity

Several studies have found associations between higher childhood BMI and earlier puberty in girls.^{4, 9-11}

Excess body fat alters the levels of the hormones insulin, leptin, and estrogen, and these factors are believed to be responsible for the acceleration of pubertal timing by obesity.  Also, physical inactivity may decrease melatonin levels, which can also affect signals in the brain that trigger pubertal development.^{4, 12} 

Increased animal protein intake

Higher total protein, animal protein, and meat intake in children age 3-7 have been associated with earlier menarche in multiple studies.^13-15  In contrast, higher vegetable protein intake at age 5-6 is associated with later menarche.¹⁵  High protein intake elevates IGF-1 levels and promotes growth, which could accelerate the onset of puberty – IGF-1 contributes to pubertal development on its own and in part by its involvement in estradiol signaling.^4,16  Meat and dairy consumption in children may also reflect ingestion of environmental endocrine-disrupting chemicals (EDCs) that have accumulated in animal tissues (see EDCs below).

Other dietary factors: 

High dairy consumption is associated with earlier than average menarche.¹⁷  Soft drink consumption is associated with early menarche.¹⁸

Children with lower nutrient diets (based on analysis of macronutrients, vitamins, minerals, and certain whole foods) tend to enter puberty earlier.¹⁹  Overall our modern diet rich in processed foods, dairy, processed meats and fast food is disruptive to normal development and aging.  Early puberty is an early sign of premature aging.  

Exposure to endocrine-disrupting chemicals (EDCs)

EDCs are hormonally active synthetic chemicals that either mimic, inhibit, or alter the action of natural hormones.  These chemicals are ubiquitous in our environment, and are considered by scientists to be a significant public health concern. Although EDCs are thought to pose a threat to adults as well, children’s bodies are more sensitive to exposure to exogenous hormones.²⁰ Chemicals are not currently tested for their endocrine disruption potential before they are approved for use and enter our environment, and there are endocrine disruptors in a vast array of products we come into contact with every day, including organochlorine pesticides, plastics, fuels, and other industrial chemicals.²¹ 

The substances of most concern currently are BPA and phthalates. BPA is one of the highest volume chemicals produced in the world.  It is used in the manufacture of polycarbonate plastics, such as rigid cups, water bottles and food storage containers; BPA is also found in the linings of food cans and dental sealants.  BPA can leach from containers into food and beverages, especially during heating and washing.⁴  BPA exposure is associated with early puberty in girls.²²

Phthalates are chemicals used to make PVC plastics more flexible, and are found in a variety of products including toys, food packaging, hoses, raincoats, shower curtains, vinyl flooring, wall coverings, lubricants, adhesives, detergents, nail polish, hair spray, and shampoo. Phthalates are associated with early breast development in girls.^22,23 They are considered chemicals of concern to the EPA and may be phased out – some phthalates have already been removed from children’s toys and cosmetics.²⁴

Additional EDCs that have been associated with dysregulation of pubertal timing include industrial chemicals such as PCBs, pesticides such as DDT and endosulfan, the flame retardant PBB, and dioxins and furans, which are formed during incineration of waste, chlorine bleaching of paper, and chemical manufacturing. ^22,23,25,26

It is important to note that EDCs break down very slowly and accumulate in the fatty tissues of animals, so animal foods contain higher levels of these chemicals than plant foods.

Why is this troublesome?  

The most significant and alarming consequence of early maturation is an increased risk for breast cancer in adulthood.  Early menarche is an established risk factor for breast cancer, and this is believed to be due to the extended lifetime exposure to ovarian hormones.^10,27,28  Similarly, exposure to EDCs during childhood is associated with hormonal cancers, such as breast and testicular cancers.^29-31

Seven, eight and nine year old girls are not emotionally or psychologically equipped to handle puberty.  As such, earlier puberty is also associated with a higher risk of psychological problems during adolescence such as anxiety, depression, and eating disorders.  Girls who mature earlier are also more likely to take part in risky behaviors like smoking and alcohol use.^4,12 

What can parents do to protect their children?

• Children’s diets should focus on whole plant foods rather than animal foods – this will keep protein intake in a safe range and reduce their consumption of EDCs.  

• Minimize dairy products in children’s diets – use almond and hemp milks instead of cows’ milk
• Encourage children to exercise and exercise with them.
• Minimize processed foods – these are calorie-dense and nutrient-poor, and they promote obesity and other diseases.
• Children’s diets should include a wide variety of natural plant foods as possible including, green vegetables, squashes, corn, carrots, tomatoes, onions, mushrooms, nuts, seeds, avocados, beans, fruits and whole grains.  This means that healthy eating is a lifetime event.  
• Buy organic produce when possible to avoid synthetic pesticides.
• Minimize children’s exposure to BPA: 
  • Avoid using of rigid polycarbonate plastics (recycling label #7) whenever possible. 
  • Do not use plastic water bottles if they are old or scratched. 
  • Do not microwave in plastic containers.
  • Minimize the use of canned foods and avoid canned infant formulas.³²
• Minimize children’s exposure to phthalates
  • Avoid plastics marked with recycling label #3 (PVC) whenever possible.
  • Check ingredient lists on personal care products for phthalates. Also be aware that “fragrance” listed as an ingredient often means that the products contains phthalates. For more information, visit the Environmental Working Group’s guide to children’s personal care products.

To conclude, the earlier occurence of puberty is an ominous event that we can stop.  We can even win the war on breast cancer in America and prevent millions of young females from developing it.   The answer however, must begin in the way we feed ourselves and our children.  The most effective type of health care is vigilant and excellent self care.  

References:

1. Biro FM, Galvez MP, Greenspan LC, et al: Pubertal Assessment Method and Baseline Characteristics in a Mixed Longitudinal Study of Girls. Pediatrics 2010.

2. Biro FM, Khoury P, Morrison JA: Influence of obesity on timing of puberty. Int J Androl 2006;29:272-277; discussion 286-290.

3. Gates JR, Parpia B, Campbell TC, et al: Association of dietary factors and selected plasma variables with sex hormone-binding globulin in rural Chinese women. Am J Clin Nutr 1996;63:22-31.

4. Steingraber S: Tha Falling Age of Puberty in U.S. Girls: What We Know, What We Need To Know. In Breast Cancer Fund; 2007.

5. McDowell MA, Brody DJ, Hughes JP: Has age at menarche changed? Results from the National Health and Nutrition Examination Survey (NHANES) 1999-2004. J Adolesc Health 2007;40:227-231.

6. Anderson SE, Must A: Interpreting the continued decline in the average age at menarche: results from two nationally representative surveys of U.S. girls studied 10 years apart. J Pediatr 2005;147:753-760.

7. O'Connell A, Gavin A, Kelly C, et al: The mean age at menarche of Irish girls in 2006. Ir Med J 2009;102:76-79.

8. Rigon F, Bianchin L, Bernasconi S, et al: Update on age at menarche in Italy: toward the leveling off of the secular trend. J Adolesc Health 2010;46:238-244.

9. Aksglaede L, Juul A, Olsen LW, et al: Age at puberty and the emerging obesity epidemic. PloS one 2009;4:e8450.

10. Vandeloo MJ, Bruckers LM, Janssens JP: Effects of lifestyle on the onset of puberty as determinant for breast cancer. Eur J Cancer Prev 2007;16:17-25.

11. Kaplowitz PB: Link between body fat and the timing of puberty. Pediatrics 2008;121 Suppl 3:S208-217.

12. Burt Solorzano CM, McCartney CR: Obesity and the pubertal transition in girls and boys. Reproduction 2010;140:399-410.

13. Berkey CS, Gardner JD, Frazier AL, et al: Relation of childhood diet and body size to menarche and adolescent growth in girls. Am J Epidemiol 2000;152:446-452.

14. Rogers IS, Northstone K, Dunger DB, et al: Diet throughout childhood and age at menarche in a contemporary cohort of British girls. Public Health Nutr 2010:1-12.

15. Gunther AL, Karaolis-Danckert N, Kroke A, et al: Dietary protein intake throughout childhood is associated with the timing of puberty. J Nutr 2010;140:565-571.

16. Veldhuis JD, Roemmich JN, Richmond EJ, et al: Endocrine control of body composition in infancy, childhood, and puberty. Endocr Rev 2005;26:114-146.

17. Wiley AS: Milk intake and total dairy consumption: associations with early menarche in NHANES 1999-2004. PloS one 2011;6:e14685.

18. Vandeloo MJ, Bruckers LM, Janssens JP: Effects of lifestyle on the onset of puberty as determinant for breast cancer. Eur J Cancer Prev 2007;16:17-25.

19. Cheng G, Gerlach S, Libuda L, et al: Diet quality in childhood is prospectively associated with the timing of puberty but not with body composition at puberty onset. J Nutr 2010;140:95-102.

20. Aksglaede L, Juul A, Leffers H, et al: The sensitivity of the child to sex steroids: possible impact of exogenous estrogens. Hum Reprod Update 2006;12:341-349.

21. Diamanti-Kandarakis E, Bourguignon JP, Giudice LC, et al: Endocrine-disrupting chemicals: an Endocrine Society scientific statement. Endocr Rev 2009;30:293-342.

22. Roy JR, Chakraborty S, Chakraborty TR: Estrogen-like endocrine disrupting chemicals affecting puberty in humans--a review. Med Sci Monit 2009;15:RA137-145.

23. Den Hond E, Schoeters G: Endocrine disrupters and human puberty. Int J Androl 2006;29:264-271; discussion 286-290.

24. Chemical Families: Phthalates. In Environmental Working Group.

25. Schell LM, Gallo MV: Relationships of putative endocrine disruptors to human sexual maturation and thyroid activity in youth. Physiol Behav 2010;99:246-253.

26. Massart F, Parrino R, Seppia P, et al: How do environmental estrogen disruptors induce precocious puberty? Minerva Pediatr 2006;58:247-254.

27. Leung AW, Mak J, Cheung PS, et al: Evidence for a programming effect of early menarche on the rise of breast cancer incidence in Hong Kong. Cancer Detect Prev 2008;32:156-161.

28. Pike MC, Pearce CL, Wu AH: Prevention of cancers of the breast, endometrium and ovary. Oncogene 2004;23:6379-6391.

29. Cohn BA, Cirillo PM, Christianson RE: Prenatal DDT exposure and testicular cancer: a nested case-control study. Arch Environ Occup Health 2010;65:127-134.

30. Cohn BA, Wolff MS, Cirillo PM, et al: DDT and breast cancer in young women: new data on the significance of age at exposure. Environ Health Perspect 2007;115:1406-1414.

31. Maffini MV, Rubin BS, Sonnenschein C, et al: Endocrine disruptors and reproductive health: the case of bisphenol-A. Mol Cell Endocrinol 2006;254-255:179-186.

32. Consumer tips to avoid BPA exposure. In Environmental Working Group.

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There are a few different classifications of fiber, and their common characteristic is resistance to digestion in the human small intestine.   Eating fiber-rich foods is associated with a number of health benefits:

• Fiber promotes weight maintenance by slowing gastric emptying; and adding volume to food, promoting satiety
• Fiber helps to prevent diabetes by slowing entrance of glucose into the bloodstream, curbing glucose (and insulin) spikes after meals
• Soluble fiber (a type of fiber abundant in oats and beans) has cholesterol-lowering effects.
• Cardiovascular health – a pooled analysis of 10 prospective studies found that an increase of 10 grams of dietary fiber per day was associated with a 24% decrease in deaths from coronary heart disease.¹
• Digestive health – fiber adds bulk and acts as a stool softener, making bowel movements faster and easier, and preventing constipation and diverticular disease.
• Fermentation of fiber and resistant starch by bacteria in the large intestine helps to prevent colorectal cancers ²

Fiber vs. fiber-rich foods: Fiber can be isolated and taken as a supplement or added to a processed food, but these are not the recommended ways to get your fiber.  Although fiber itself has beneficial properties, fiber-rich whole foods come packaged with disease-fighting phytochemicals.  There have been inconsistencies in the results of studies on fiber and colorectal cancer, probably because it appears to be high-fiber foods, not fiber alone that reduces risk. ^3-8

The American Heart Association recommends consuming 25 grams of fiber each day –a nutritarian diet far exceeds that recommendation, providing about 60-80 grams of fiber each day, since the vast majority of my recommended food pyramid is made up of fiber-rich foods like vegetables, fruits, seeds and beans.  

A study relating dietary fiber intake to lifetime risk of cardiovascular disease was presented at the American Heart Association’s Nutrition, Physical Activity, and Metabolism conference last week. Data from the 2003-2008 U.S. National Health and Nutrition Examination Surveys were analyzed. The researchers used a mathematical algorithm to predict lifetime risk for cardiovascular disease, based on diet, blood pressure, cholesterol, smoking, and history of diabetes.  All of the participants were free of cardiovascular disease at the start.  

The algorithm placed participants in groups of either high or low lifetime risk of cardiovascular disease.  Then they were arranged into four groups according to the ratio of their intake of dietary fiber to calories - dietary fiber only, no fiber supplements were included.  The lowest fiber intake was 0.1g/1000 calories, and the highest was on par with a nutritarian diet, 49.1g/1000 calories.

Individuals aged 20-39 in the highest quartile of fiber intake were almost twice as likely to be in the low risk category than those in the lowest quartile. Middle aged individuals in the highest quartile were about 50% more likely to be in the low risk category. Interestingly though, a similar association was not seen in 60-79 year olds.  The researchers theorized that many older adults with high fiber intake may have already developed significant risk for heart disease before they added more high-fiber foods to their diet.   They concluded that starting to increase fiber intake at a younger age helps to decrease the risk of cardiovascular disease later in life.^9,10

It is important to eat healthfully your entire life to get maximum benefits, however once you have not eaten properly for the first 60 years, then to get the disease-protective benefits to dramatically reduce heart attack, stroke and cancer risk from a plant-based diet (vegan or flexitarian) later in life, it is not good enough to just be good, you have to be great.  In other words, a nutritarian diet with attention to the most nutritionally powerful and protective plant foods is necessary, not just the dietary mediocrity practiced by most vegans and vegetarians.

Eating to Live is a lifetime commitment – just like it takes years for heart disease to develop, it takes years to build up protection against heart disease.  No matter what your age, you can benefit from improving your diet – but the point is, the time to start is right now and the place to start is with a nutritarian diet that pays attention to the disease-fighting nutrients in foods. Once you are past middle age, the way to start is not with some wishy-washy low fat, high fiber diet.  That is not good enough, you have to do better than that and pay attention to the micronutrient-richness of your meals and achieve comprehensive nutritional adequacy, which is the core of my message.  

References:

1. Pereira MA, O'Reilly E, Augustsson K, et al: Dietary fiber and risk of coronary heart disease: a pooled analysis of cohort studies. Arch Intern Med 2004, 164:370-376.

2. 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.

3. Singh PN, Fraser GE: Dietary risk factors for colon cancer in a low-risk population. Am J Epidemiol 1998, 148:761-774.

4. Uchida K, Kono S, Yin G, et al: Dietary fiber, source foods and colorectal cancer risk: the Fukuoka Colorectal Cancer Study. Scand J Gastroenterol 2010, 45:1223-1231.

5. Park Y, Hunter DJ, Spiegelman D, et al: Dietary fiber intake and risk of colorectal cancer: a pooled analysis of prospective cohort studies. JAMA : the journal of the American Medical Association 2005, 294:2849-2857.

6. Michels KB, Fuchs CS, Giovannucci E, et al: Fiber intake and incidence of colorectal cancer among 76,947 women and 47,279 men. Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology 2005, 14:842-849.

7. Terry P, Giovannucci E, Michels KB, et al: Fruit, vegetables, dietary fiber, and risk of colorectal cancer. J Natl Cancer Inst 2001, 93:525-533.

8. Wakai K, Date C, Fukui M, et al: Dietary fiber and risk of colorectal cancer in the Japan collaborative cohort study. Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology 2007, 16:668-675.

9. Northwestern University (2011, March 23). Load up on fiber now, avoid heart disease later. . In ScienceDaily; 2011.

10. Ning H, Van Horn L, Shay CM, et al: Dietary Fiber Intake and Long Term Cardiovascular Risk: Findings from the National Health and Nutrition Examination Surveys (NHANES) 2003-2008. In American Heart Association: Nutrition, Physical Activity, and Metabolism 2011.

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The Allium family of vegetables, which includes onions, garlic, leeks, shallots, chives, and scallions add more than just flavor to your diet, they also add anti-cancer, anti-inflammatory, and antioxidant compounds.

Epidemiological studies have found that increased consumption of Allium vegetables is associated with lower risk of gastric and prostate cancers, and this is thought to be due to their organosulfur compounds, which are released when the vegetables are chopped, crushed, or chewed. These compounds prevent the development of cancers by detoxifying carcinogens, halting cancer cell growth, and preventing tumors from obtaining a blood supply.[1]

New research suggests that the organosulfur compounds in Allium family members may also have anti-inflammatory actions that protect against osteoarthritis. Osteoarthritis is characterized by painful degradation of the cartilage in the joints of the knees, hands, hips, back, and/or neck. Osteoarthritis is a common chronic condition among middle-aged and elderly persons, a progressive disease affecting nearly 27 million Americans. It is the most common cause of disability in the U.S. [2]

Excess weight is a risk factor for osteoarthritis (particularly in the knee), and scientists hypothesized that in addition to mechanical pressure on the joints in overweight individuals, a diet low in micronutrients may also contribute to the progression of osteoarthritis. Oxidative stress is known to contribute to osteoarthritis by damaging cartilage[3], and levels of endogenous antioxidants are suppressed in the fluid of arthritic joints compared to joints with intact cartilage. [4] Dietary antioxidants are thought to be protective against osteoarthritis, but other micronutrients have not yet been studied.

Dietary patterns and osteoarthritis were assessed in a study of 1086 women. After adjustment for age, body mass index, and physical activity, the ‘fruit and vegetable’ dietary pattern, which was characterized by frequent intake of fruit, Allium vegetables, and cruciferous vegetables and low intake of fried potatoes, was protective for hip osteoarthritis. Two specific food groups also had strong beneficial effects: non-citrus fruits and Allium vegetables.

To investigate a potential mechanism by which Allium vegetables might protect the joints from cartilage damage, researchers then tested diallyl disulphide (DADS; an organosulfur compound) for its effects on inflammation-induced cartilage damage in vitro. DADS suppressed the expression of matrix metalloproteinases (MMPs) – MMPs are elevated in response to inflammatory signals and contribute to the cartilage degradation characteristic of osteoarthritis.[5] These results suggest that organosulfur compounds in Allium vegetables can help to prevent or halt the progression of osteoarthritis.

DADS is just one of many phytochemicals present in Allium vegetables – when we eat these vegetables, thousands of organosulfur compounds, antioxidants, and other micronutrients work together to prevent disease. And when we use garlic and onion to flavor a dish of greens, beans, and mushrooms, the additive nutritional benefits that we receive are remarkable. A nutritarian dietary approach is designed to maximize anti-cancer and disease-protective benefits. If you choose otherwise, eat at your own risk.

References:

1. Powolny, A. and S. Singh, Multitargeted prevention and therapy of cancer by diallyl trisulfide and related Allium vegetable-derived organosulfur compounds. Cancer Letters, 2008. 269(2): p. 305-314.
2. Arthritis Foundation: Osteoarthritis Fact Sheet. 2008.
3. Henrotin, Y. and B. Kurz, Antioxidant to treat osteoarthritis: dream or reality? Curr Drug Targets, 2007. 8(2): p. 347-57.
4. Regan, E.A., R.P. Bowler, and J.D. Crapo, Joint fluid antioxidants are decreased in osteoarthritic joints compared to joints with macroscopically intact cartilage and subacute injury. Osteoarthritis Cartilage, 2008. 16(4): p. 515-21.
5. Williams, F.M., et al., Dietary garlic and hip osteoarthritis: evidence of a protective effect and putative mechanism of action. BMC Musculoskelet Disord, 2010. 11(1): p. 280.

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A recent study has revisited this issue, and the answer seems to be ‘very few’. Women must be given accurate information outlining the risks and benefits of mammography so that they can make an informed decision about whether to be screened.

A study of 40,000 women in Norway aged 50-69, recently published in the New England Journal of Medicine, investigated the effects of screening mammography on breast cancer mortality. Some counties in Norway conduct mammography screenings, while others do not. Four groups of women were studied: a screening counties group and a nonscreening counties group followed from 1996 to 2005; and also ‘historical’ screening and nonscreening groups, who had been followed from 1986 to 1995. The goal of the study was to find out how much of the reduction in breast cancer mortality that has been observed over time was due specifically to mammography screening. The reduction in breast cancer mortality over time was 10% greater in the screening groups than the nonscreening groups. [1]

What are the risks and benefits of screening mammography? The Nordic Cochrane Centre, an independent research group that conducts extensive and thorough reviews of the medical literature, assessed the potential benefits and harms of mammography in 2009. These were their conclusions: For every 2000 women that are screened regularly for ten years, one will have her life prolonged. However, 10 healthy women will be unnecessarily treated for breast cancer, either by having a lumpectomy, mastectomy, chemotherapy, or radiotherapy. Also, 200 healthy women will experience a false alarm, leading to substantial psychological and emotional strain. In their analysis, the Cochrane group stated that it is “not clear whether screening does more good than harm.”[2] In women under the age of 50, false positive results are very common. [3] In 2009, the U.S. Preventive Services Task Force began recommending against routine screening mammography in women between the ages of 40 and 49.[4]

Mammograms are not nearly as life-saving as we are led to believe. The main problem with mammograms is over-diagnosis. Eighty percent of biopsies initiated by a mammogram result are negative. Furthermore, many slow-growing, non-threatening tumors are being detected and treated; at the same time, the more dangerous and aggressive cancers may be missed because they can grow and become lethal in the time interval between screenings, and by then treatment will not work. [3, 5]

Whether or not to undergo mammography is a personal choice, but it is important to know the true risks and benefits of the screening in order to make a sound decision. Regardless of their decision on this matter, women should not rely solely on detection by mammography to protect them against breast cancer. The take home message is that mammograms can’t be counted on as the sole intervention to save women’s lives—they just don’t do enough. Taking steps to prevent breast cancer from developing in the first place – for example, exercising regularly, maintaining a slim, healthy weight, eating plenty of mushrooms, onions, and cruciferous vegetables, minimizing processed foods and animal products, maintaining adequate vitamin D levels, and limiting alcohol consumption – is a much more effective approach than detecting and treating breast cancer after it has begun to develop.

A pamphlet on the potential harms and benefits of mammography screening is available on the Cochrane group’s website.

Read more about diet and lifestyle methods for cancer prevention at DrFuhrman.com.

References:
1. Kalager, M., et al., Effect of screening mammography on breast-cancer mortality in Norway. N Engl J Med, 2010. 363(13): p. 1203-10.
2. Gotzsche, P.C. and M. Nielsen, Screening for breast cancer with mammography. Cochrane Database Syst Rev, 2009(4): p. CD001877.
3. Wright, C.J. and C.B. Mueller, Screening mammography and public health policy: the need for perspective. Lancet, 1995. 346(8966): p. 29-32.
4. Screening for breast cancer: U.S. Preventive Services Task Force recommendation statement. Ann Intern Med, 2009. 151(10): p. 716-26, W-236.
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