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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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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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.
5. Esserman, L., Y. Shieh, and I. Thompson, Rethinking Screening for Breast Cancer and Prostate Cancer. JAMA, 2009. 302(15): p. 1685-1692.

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October is National Breast Cancer Awareness month, and I want to raise awareness that childhood diets are the major cause of adult cancers, including breast cancer. [1] I also want to raise awareness that women are not powerless against breast cancer – mammograms for ‘early detection’ are not the only defense and do not even offer significant benefits. The most important thing to be aware of is that women can achieve meaningful risk reduction with powerful preventive lifestyle measures.

The American Institute for Cancer Research estimates that 40% of breast cancers are preventable through diet and lifestyle measures. I propose that we could prevent much more than 40% of breast cancers in the future, if we can ingrain healthy habits in our children at a young age.

Early studies found wide international variations in breast cancer rates, originally generating the hypothesis that nutrition is a major determinant of breast cancer risk. Obesity is a significant risk factor for breast cancer:

• Gaining one pound per year during adulthood can double breast cancer risk after menopause.
• Obesity alone is thought to be responsible for 17% of breast cancers.
• Obesity is associated with greater tumor burden and poorer prognosis in breast cancer patients. [2, 3]
• Production of inflammatory molecules and estrogen by body fat, as well as elevated insulin and insulin-like growth factor (IGF-1) levels are thought to contribute to obesity-related breast cancer risk. [2]

Plenty of experts have predicted that the explosion of childhood obesity we have seen in recent years will result in crisis proportions of heart disease and diabetes in the future, but cancer seems to be ignored. Today, over 30% of children are overweight or obese. [4] Clearly, with all the research demonstrating that obesity is a major risk factor for breast cancer, our young girls are in danger.

The prevalence of early puberty, another established risk factor for breast cancer, has been consistently increasing over the past 100 years. Today, by the age of 8, 18.3% of Caucasian girls, 42.9% of African-American girls, and 30.9% of Hispanic girls have already entered puberty. Obesity, soft drinks, and excessive animal protein are the likely culprits (Read more).

This is a grim indication of things to come – when these girls reach adulthood, tragically we will see an upsurge in breast cancer cases. With the increases in fast food and processed food consumption in America in the last 20 years, I predict a tragic explosion in pre-menopausal breast cancers in our country in the next 20 years.

Breast tissue is most vulnerable to carcinogenic influences when it is growing and developing – during childhood and adolescence. Children are also especially susceptible to weight gain during adolescence. [5] Thus, this window of time is when a healthy diet is absolutely crucial. Animal studies have demonstrated that a high-fat diet or a body fat promoting diet during puberty promotes abnormal development of breast tissue and production of inflammatory molecules, which in turn may promote tumor growth.[6, 7] Adolescent diet was examined in the Nurses’ Health Study – greater consumption of vegetables during high school was associated with a decreased risk of breast cancer, and high glycemic index foods were associated with an increased risk. [8]

The typical American childhood diet of chicken fingers, French fries, and mac and cheese is not harmless – it is creating a cancer-friendly environment in children’s bodies.

As parents, we must feed our children healthful foods from an early age. This is the most effective protection from future chronic disease that we can provide for them. Healthy eating is a lifetime commitment, and we can give our children a head start. Our goal should be to instill healthy habits in our children so that they grow up at a healthy weight, appreciating healthy food and exercise, and hold on to those habits as adults. In order to do this, we must set a positive example, focusing on nutrient-dense, health-promoting foods.

New research is revealing the protective effects of natural foods against breast cancer. For example, mushrooms have anti-estrogenic activity, and regular mushroom consumption is associated with a 60% decrease in cancer risk. [9] Cruciferous vegetables such as watercress, other leafy greens, and broccoli contain compounds known to inhibit cancer cell growth. [10, 11]

Instead of wearing a pink ribbon, eat vegetables, onions and mushrooms – and make sure to feed some to your kids.

References:

1. Maynard, M., et al., Fruit, vegetables, and antioxidants in childhood and risk of adult cancer: the Boyd Orr cohort. J Epidemiol Community Health, 2003. 57(3): p. 218-25.
2. Cleary, M.P. and M.E. Grossmann, Minireview: Obesity and breast cancer: the estrogen connection. Endocrinology, 2009. 150(6): p. 2537-42.
3. Abrahamson, P.E., et al., General and abdominal obesity and survival among young women with breast cancer. Cancer Epidemiol Biomarkers Prev, 2006. 15(10): p. 1871-7.
4. Ogden, C.L., et al., Prevalence of high body mass index in US children and adolescents, 2007-2008. JAMA, 2010. 303(3): p. 242-9.
5. Jasik, C.B. and R.H. Lustig, Adolescent obesity and puberty: the "perfect storm". Ann N Y Acad Sci, 2008. 1135: p. 265-79.
6. Olson, L.K., et al., Pubertal exposure to high fat diet causes mouse strain-dependent alterations in mammary gland development and estrogen responsiveness. Int J Obes (Lond), 2010. 34(9): p. 1415-26.
7. Michigan State University: High-fat diet during puberty linked to breast cancer risk later in life. 2010; Available from: http://news.msu.edu/story/8233/.
8. Frazier, A.L., et al., Adolescent diet and risk of breast cancer. Cancer Causes Control, 2004. 15(1): p. 73-82.
9. Zhang, M., et al., Dietary intakes of mushrooms and green tea combine to reduce the risk of breast cancer in Chinese women. Int J Cancer, 2009. 124(6): p. 1404-8.
10. Clarke, J., R. Dashwood, and E. Ho, Multi-targeted prevention of cancer by sulforaphane. Cancer Letters, 2008. 269(2): p. 291-304.
11. Higdon, J., et al., Cruciferous vegetables and human cancer risk: epidemiologic evidence and mechanistic basis. Pharmacological Research, 2007. 55(3): p. 224-236.

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Watercress is a super-duper food. Along with kale, collards, mustard greens, and turnip greens, watercress is one of the most nutrient-dense foods in the world. Most importantly, watercress is a specialist at preventing cancer.

Watercress belongs to the family of cruciferous vegetables, uniquely high in glucosinolates, which are precursors to cancer-fighting molecules called isothiocyanates (ITCs). Watercress is rich in a specific glucosinolate called gluconasturtiin, which is a precursor to the ITC phenethyl isothiocyanate (PEITC).[1] Epidemiologic associations between cruciferous vegetable intake and reduced cancer risk have sparked a surge in studies on the anti-cancer effects of specific cruciferous vegetables and their constituent isothiocyanates.

Anti-cancer properties of watercress had previously been established in cell culture experiments: In human breast cancer cells, watercress extract blocked the degradation of structural proteins, an early step in preparation for migration and subsequent invasion, which eventually leads to metastasis. [2] PEITC in watercress was also found to reduce tumor cell survival and decrease the action of hypoxia-inducible factor (HIF), which is a molecule that stimulates angiogenesis (blood vessel development), allowing a tumor to obtain a blood supply. [3]

A new study has investigated the effects of watercress on HIF activity in human subjects. Hypoxia (low oxygen levels) is a key stimulus for tumor growth – as a tumor grows, its oxygen and nutrient needs exceed those that it can receive by diffusion from adjacent healthy tissue. When tumor cells sense hypoxia, they send angiogenic signals to surrounding normal tissue in order to obtain a direct blood supply. HIF is an essential part of this process, activating the production of angiogenic proteins, consequently promoting tumor growth. [4]

Since the current study tested the effects of ingesting watercress on HIF activity in cells of human subjects, the data provided is more physiologically relevant, and strengthens the earlier cell culture results. Four breast cancer survivors ingested 80 grams of watercress (about 2 cups). Six and eight hours later, blood was drawn; PEITC levels were found to be elevated, and the effects of the watercress on white blood cells were measured. HIF activity was indeed reduced in these cells, confirming in humans the anti-cancer effects of watercress previously observed in cultured cells. [3, 5]

In short, PEITC from watercress prevents tumors from sending the signal to the body that requests a blood supply. Without a blood supply, the tumor cannot continue to grow. Watercress is a potent anti-cancer food!

For more information on the anti-cancer effects of cruciferous vegetables, read Dr. Fuhrman’s Newsletter #32.

References:
1. Higdon, J., et al., Cruciferous vegetables and human cancer risk: epidemiologic evidence and mechanistic basis. Pharmacological Research, 2007. 55(3): p. 224-236.
2. Rose, P., et al., Broccoli and watercress suppress matrix metalloproteinase-9 activity and invasiveness of human MDA-MB-231 breast cancer cells. Toxicol Appl Pharmacol, 2005. 209(2): p. 105-13.
3. Syed Alwi, S.S., et al., In vivo modulation of 4E binding protein 1 (4E-BP1) phosphorylation by watercress: a pilot study. Br J Nutr, 2010: p. 1-9.
4. Chen, L., A. Endler, and F. Shibasaki, Hypoxia and angiogenesis: regulation of hypoxia-inducible factors via novel binding factors. Exp Mol Med, 2009. 41(12): p. 849-57.
5. Watercress may 'turn off' breast cancer signal. 9/14/2010 9/30/2010]; Available from: http://www.soton.ac.uk/mediacentre/news/2010/sep/10_94.shtml.

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In his book Disease Proof Your Child, Dr. Fuhrman states that the biggest contributor to adult cancers is an unhealthy childhood diet.¹

Cancer takes years and years to develop. In fact,  a woman's diet during pregnancy is known to influence the risk of childhood cancers in her children.² A woman’s risk of breast cancer similarly is influenced during fetal development by her mother’s dietary habits.³ But breast cancer risk may begin even earlier than this.

A recent animal study suggests that breast cancer risk may be transmitted even from previous generations – that a grandmother’s unhealthy diet may translate into increased breast cancer risk for her granddaughters. 

The researchers conducted their study as follows:  A generation of female rats (grandmothers) was fed either a normal or high-fat diet during pregnancy - the high-fat diet provided an excess amount of omega-6 fat, attempting to partially mimic the standard American diet, with its abundance omega-6-rich animal products and oils.  Mother and granddaughter rats were fed a normal diet, and granddaughter rats either had two normal diet grandmothers, two high-fat diet grandmothers, or one of each. “Granddaughter” rats were given a chemical carcinogen to initiate breast cancer, and researchers recorded whether or not they developed tumors.⁴

These were their findings:

• 50% of the rats with two normal diet grandmothers developed breast tumors
• 68% of the rats with one high-fat diet grandmother developed breast tumors
• 80% of the rats with two high-fat diet grandmothers developed breast tumors⁵

Based on these results, an unhealthy diet may cause inheritable changes in gene expression, causing subsequent generations to be more susceptible to breast cancer-initiating factors such as chemical carcinogens. Family-related risk of breast cancer is usually thought to be related only to specific genes, such as BRCA1 and BRCA2, which are known to increase breast cancer risk. However, this study points to non-genetic, but family-related transmission of risk via dietary habits.

These findings imply that what mothers eat during pregnancy not only affects their children, but their children’s children as well.

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Overweight/obesity is a significant risk factor for breast cancer.¹ The American Institute for Cancer Research estimates that 17% of breast cancers (this equates to 33,000 new cases per year) are due to excess weight alone, and women who are obese when diagnosed are more likely to die from breast cancer after diagnosis.²

A study of 72,000 postmenopausal women presented at this year’s American Association for Cancer Research annual meeting took into account body mass index (BMI) at age 20 and at their current age (55-74), and compared breast cancer risk between those who gained weight and those who did not. They found that a 5 point increase in BMI during these years doubled the likelihood of postmenopausal breast cancer compared to women whose BMI remained stable.³

Although excess weight has been consistently associated with breast cancer risk, the scientists undertook this study because previous studies investigating BMI or body weight during early adulthood were not conclusive. Rather than look simply at BMI at age 20, they looked at the change in BMI over time. Their results clearly indicate that weight gain puts women at risk for breast cancer, and confirms the importance of maintaining a healthy weight for cancer protection.

How much weight gain is risky?

Weight gain of 30 lbs. in a 5’4” woman would produce a 5 point increase. This may seem like a large amount of weight, but over thirty years, it would be a barely noticeable amount – a steady weight gain of 1 pound per year. This study suggests that even 1 pound per year is a dangerous amount of weight gain. And it turns out that this dangerous amount of weight gain is quite common - 60% of the women in the study had increased their BMI by at least 5 points since age 20.⁴  This tells us that most American women likely do gain this much weight during adulthood, doubling their risk of breast cancer.

Read more about Dr. Fuhrman’s strategy for breast cancer prevention.

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 Two new studies have examined the effects of certain dietary factors on recurrence of breast cancer in survivors. Soy had protective effects, and alcohol had detrimental effects.  Read the full article on DrFuhrman.com.

Soy and breast cancer recurrence

Some individuals suspected and even promoted the idea that soy was potentially dangerous with regard to breast cancer risk, because of the phyto-estrogenic compounds it contains. However, in Asian countries where soy is a staple food, rates of breast cancer were much lower than those in the U.S. This paradox launched much debate and hundreds of studies on the relationship between soy and breast cancer.

A review of the most recent clinical studies on this subject supports a protective effect of soy:

•  2006: A meta-analysis in the Journal of the National Cancer Institute examining data from 18 studies on soy and breast cancer that were published between 1978 and 2004 concluded that soy overall has a protective effect.¹

• 2008: A meta-analysis in the British Journal of Nutrition compiling data from 8 different studies (not included in the 2006 meta-analysis) also concluded that soy consumption decreases breast cancer risk. These effects were dose-dependent – a 16% reduced risk for each 10 mg of soy isoflavones consumed daily.²

In spite of these clear documented results, the myth that soy contributes to breast cancer has persisted. Plus, many scientists and physicians continue to doubt the safety of soy for current or previous breast cancer patients, because of soy’s phytoestrogen content.

A new study of breast cancer survivors has shown that these doubts are unwarranted too. Premenopausal breast cancer survivors who consumed more soy had a 23% reduced risk of recurrence.³

Which soy products are most beneficial?

Cruciferous vegetables are the most powerful anti-cancer foods. In addition, Dr. Fuhrman also recommends consuming a variety of beans, including soybeans, as components of an anti-cancer diet. Soybeans may be consumed as edamame (whole soybeans), or in minimally processed forms such as unsweetened soymilk, tofu, and tempeh. As little as 10 mg of soy isoflavones consumed per day has a protective effect with regard to breast cancer – this equates to approximately 1 ounce of one of these soy foods.

Alcohol and breast cancer recurrence

In contrast to the mainstream assumption that alcohol is heart healthy, even moderate amounts of alcohol are associated with increased risk for breast cancer.⁴

The current study of breast cancer survivors showed that women who consumed 3-4 alcoholic drinks per week were 34% more likely to experience a recurrence than the women who had less than 1 drink per week. This study was presented last week at the San Antonio Breast Cancer Symposium.⁵

Alcohol has no beneficial effect on the cardiovascular system, it only inhibits the blood’s clotting mechanisms. Since breast cancer is the second leading cause of death in women (second to cardiovascular disease), Dr. Fuhrman recommends minimizing alcohol consumption in order to reduce this risk.

Read the full article here.

Read “Dr. Fuhrman on Breast Cancer” to learn more diet and lifestyle strategies for breast cancer prevention.

References:

1. Trock BJ et al. Meta-analysis of soy intake and breast cancer risk. J Natl Cancer Inst. 2006 Apr 5;98(7):459-71.

2. Wu AH et al. Epidemiology of soy exposures and breast cancer risk. British Journal of Cancer (2008) 98, 9– 14

4. Lew JQ et al. Alcohol and risk of breast cancer by histologic type and hormone receptor status in postmenopausal women: the NIH-AARP Diet and Health Study. Am J Epidemiol. 2009 Aug 1;170(3):308-17. Epub 2009 Jun 18.

5. http://www.medpagetoday.com/MeetingCoverage/SABCS/17444

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