-IBIS-1.7.6-
tx
reproductive system
breast cancer
Nutrition

dietary guidelines

» eating principles:
• several 7-10 day alkaline fasts interspersed with eating for 3 weeks (see Fasting in materia medica)

» therapeutic foods:
• foods rich in Vitamin A
• liver-cleansing foods: beets, carrots, artichokes, lemons, parsnips, dandelion greens, watercress, burdock root
• Rats with chemically-induced breast cancer that received a series of injections of tomato extract rich in the carotenoid lycopene developed significantly fewer tumors and the tumor size was smaller compared to placebo. Rats injected with beta-carotene did not experience the benefits against breast cancer.
(Sharoni Y, et al. Cancer Detect Prev 1997,21(2): 118-123.)

» fresh juices:
• carrot (Walker, 129.)
• carrot and spinach (Walker, 129.)
• apple (Shefi)
Note: Carrots and apples are considered estrogenic foods to be avoided by some sources, but recommended in concentrated in juice therapy by other sources.

» recommendations for all cancers:
• seaweeds, mushrooms - Chinese black, Maitake and Shiitake, figs, beets, beet tops, papaya, mung beans, licorice, sea cucumbers, carrot, garlic, walnut, lychee fruit, mulberries, asparagus, pumpkin, burdock, dandelion greens, white fungus, taro roots, pearl barley, grains, fresh fruits and vegetables (Ni, 108-109.)

» specific remedies:
• soup of black or ling zhi mushrooms and white fungus, three times daily (Ni, 108-109.)
• boil together mung beans, pearl barley, adzuki beans, and figs (Ni, 108-109.)
• dandelion, burdock, and chrysanthemum flower tea (Ni, 108-109.)
• tea from asparagus and dandelion, apply externally as compress to breast
• charcoal the pumpkin cap into powder, take l tsp. of powder in l shot of rice wine twice daily (Ni, 108-109.)

» avoid:
• meat, alcohol, hot sauces, spicy foods, fried foods, fatty foods, rich foods, salty foods, caffeine, coffee
• estrogenic foods: animal products, apples, cherries, olives, plums, carrots, yams, nightshade family, peanuts, soy products, coconut, brown rice, barley, oats, wheat
• Foods that contain estrogen-like sterols (see materia medica)


supplements

• Beta-Carotene: 25,000 IU per day for cancer prevention and 100,000 IU per day for secondary prevention of breast cancer
(Austin S, Hitchcock C, 218-223.)
• Vitamin A: 350,000-500,000 IU per day, a potentially toxic dose, was used in a controlled French trial involving postmenopausal late-stage breast cancer patients, along with chemotherapy; remission rates were significantly higher than when the chemotherapy was used without the vitamin A. However, similar outcomes did not appear in premenopausal women. (Israel L, et al. Ann Med Interne (Paris) 1985;136(7):551-554.)
• Vitamin C: 1,000 mg per day for cancer prevention and 10,000 mg per day for secondary prevention of breast cancer (Austin and Hitchcock, p. 216-218)
• Vitamin E (Wald, 1984)
• Iodine (Eskin, 1983)
• Selenium: 200 mcg per day for cancer prevention and for secondary prevention of breast cancer (Austin S, Hitchcock C, 220-222.)
• Shark cartilage: 2 g per kg body weight, per day, to inhibit angiogenesis (growth of new blood vessels) in and to tumors. While anecdotal claims of efficacy are widespread no large scale, well-designed clinical research on the efficacy of cartilage for the treatment of cancer have been conducted so no conclusive evidence is available. (Lane IW, 1992.)
• Omega-3 fatty acids
• Progesterone: The use of hormones post breast cancer is controversial. Many physicians feel that natural progesterone may indeed be protective to breast tissue, and have published data in support. There are numerous studies that address the effects of both synthetic progestins and natural progesterone on the breast. Research involving natural progesterone has suggested a protective role via numerous separate biochemical pathways, although there is some evidence that synthetic progestins do not share this relationship. No studies have been found that find natural progesterone poses a risk for women with a history of breast cancer. Several clinical trials following women using estrogen with progesterone showed progesterone adequately opposed the increased risk for breast cancer imposed by estrogen. Progesterone can act as an estrogen antagonist in the breast and uterus, decreasing cell division, increasing cellular maturity, and inhibiting the replenishment of estrogen receptors. Progesterone has also been shown to stimulate 17 beta-dehydrogenase, which allows for the conversion of estradiol to a less active metabolite. One clinical study showed that infertile women with endogenous progesterone deficiencies have a five-fold increased risk of pre-menopausal breast cancer compared to women with normal hormone levels. Another study demonstrated protective effects of progesterone similar to that of Tamoxifen in treating breast cancers. While there is encouraging data to infer that progesterone has a protective effect on the breast, there is at this time still considerable debate over the use of any hormone with women who have had a history of breast cancer.
• Soy: In a double-blind clinical trial involving breast cancer survivors with histories of substantial hot flashes, Quella et al found no suggestion that soy was more effective in reducing hot flashes than placebo.
(Quella SK, et al. J Clin Oncol. 2000 Mar;18(5):1068.)

» drug interactions:
• Vitamins C and E for patients using adriamycin: antioxidants, specifically reduces cardiac toxicity of adriamycin (Doxorubicin)
(Fujita, et al., 1982:42:309-316; Ellison, 1985;37(3):112-113; Am Heart J, 1986;111:95.)
• Vitamins B1, B2, B3, Vitamin K and folic acid can become deficient in patients using chemotherapy due to consequent anorexia, damage to the digestive tract, and malabsorption (Dreizen, et al., 1990; 87 (1): 163-170.)
• Vitamin K has been found to potentiate various chemotherapeutic drugs in animals. (Taper, et al., 1987; 40: 575-579)
• Vitamin A and cancer chemotherapy, esp. fluorouracil (5-FU): vitamin A enhances antitumor effect in animals
(Nakagawa, et al., 1985;76: 887-894.)


footnotes

Austin S, Hitchcock C. Breast Cancer: What You Should Know (But May Not Have Been Told) About Prevention, Diagnosis, and Treatment. Rocklin, CA: Prima Publishing, 1994.

Brooks PG. The relationship of estrogen and progesterone to breast disease. J Reprod Med, 1984, 29(7): supp.

Buzdar AU. Progestins in cancer treatment. In: Stoll BA, ed. Endocrine management of cancer. New York: Karger, 1-15, 1988.

Chang KJ, et al. Influences of percutaneous administration of estradiol and progesterone on human breast epithelial cell cycle in vivo. Fertility and Sterility, April 1995;63(4).
Abstract: The effect of transdermal estradiol (1.5 mg), transdermal progesterone (25 mg), and combined transdermal estradiol and progesterone (1.5 mg and 25 mg) on human breast epithelial cell cycles was evaluated in vivo. Results demonstrated that estradiol significantly increases cell proliferation, while progesterone significantly decreases cell replication below that observed with placebo. Transdermal progesterone was also shown to reduce estradiol-induced proliferation.

Cowan LD, Gordis L, Tonascia JA, et al: Breast cancer incidence in women with a history of progesterone deficiency. Am J Epid, 1981;114:;209-217.
Abstract: 1,083 infertile women were followed for 14-34 years. Those who were deficient in progesterone showed a five-fold greater incidence of premenopausal breast cancer.

Gambrell RD Jr: Use of progestogen therapy. Am J Obstet Gyn, 1987;156:1304-1313.
Abstract: In a study of over 5,000 postmenopausal women, data indicated that when progesterone was added to estrogen therapy, there was a significant drop in breast cancer occurrence.

Gambrell RD Jr: Editorial: Hormone replacement therapy in patients with previous breast cancer. Menopause, 1995; 2( 2);55-57, 1995.

Hargrove JT, Maxson WS, Wentz AC, Burnett LS: Menopausal hormone replacement therapy with continuous daily oral micronized estradiol and progesterone. Obstetr Gynec, Apr 1989; 73(4), 606-612.

Inoh A, Kamiya K, Fuji Y, Yokoro K: Protective effects of progesterone and tamoxifen in estrogen-induced mammary carcinogenesis in ovariectomized W/FU rats. Jpn J Cancer Res, August 1995;76, 699-704.

Israel L, Hajji O, Grefft-Alami A, Desmoulins D, Succari M, Cals MJ, Miocque M, Breau JL, Morere JF [Vitamin A augmentation of the effects of chemotherapy in metastatic breast cancers after menopause. Randomized trial in 100 patients]. Ann Med Interne (Paris) 1985;136(7):551-554. [Article in French]
Abstract: Vitamin A was administered to randomly allocated patients in a group of 100 patients with metastatic breast carcinoma treated by chemotherapy. The daily doses (given indefinitely) ranged from 350,000 to 500,000 IU according to body weight. A significant increase in the complete response rate was observed. When subgroups determined by menopausal status were considered, it was observed that serum retinol levels were only significantly increased in the post-menopausal group on high dose Vitamin A. Response rates, duration of response and projected survival were only significantly increased in this subgroup. The therapeutic and biological implications of these findings are discussed.

Laidlaw IJ, Clarke RB: The proliferation of normal breast tissue implanted into athymic nude mice is stimulated by estrogen, but not by progesterone. Endocrinology, 136(1):164-71, January 1995.
Abstract: Normal human breast tissue was implanted subcutaneously into athymic nude mice. The mice were then treated with estradiol or progesterone such that serum levels approximated those seen in normal menstruating women. Immunocytochemical measures were made of proliferative activity and steroid receptor expression of the tissue implants. It was found that physiologic levels of estradiol significantly stimulated the proliferation of human breast epithelial cells and increased progesterone receptor expression 10-20-fold. Progesterone failed to effect proliferation alone or after estradiol priming.

Lane AW, Contreras E Jr. High rate of bioactivity (reduction in gross tumor size) observed in advanced cancer patients treated with shark cartilage material. J Naturopathic Med 1992;3:86-88.

Lane IW, Comac L. Sharks Don't Get Cancer: How Sharks Cartilage Could Save Your Life. Avery, 1992.

Lane IW. 60 Minutes. July 11, 1993 transcript.

Lee J, Hopkins V. What Your Doctor May Not Tell You About Menopause. Warner Books, NY: 1996.

Leis HP: Endocrine prophylaxis of breast cancer with cyclic estrogen and progesterone. Intern Surg, 1996;45: 496-503.

Mathews J. Media feeds frenzy over shark cartilage as cancer treatment. J National Cancer Institute 1993 Aug 4;85(15):1190-1191.

Mathews J. Sharks still intrigue cancer researchers. J National Cancer Institute 1992 July 1;84(13):1000-1002.

McGuire TR, Kazakoff PW, Hoie EB, Fienhold MA. Antiproliferative activity of shark cartilage with and without tumor necrosis factor-alpha in human umbilical vein endothelium. Pharmacotherapy. 1996 Mar-Apr;16(2):237-244.

McGuire TR, et al. Tamoxifen and shark cartilage: potential anti-angiogenic combination. (Abstract from American College of Clinical Pharmacy Annual Meeting St. Louis, 1994) Pharmacotherapy 1994;14(3):362.

Miller DR, Anderson GT, Stark JJ, Granick JL, Richardson D. Phase I/II trial of the safety and efficacy of shark cartilage in the treatment of advanced cancer. J Clin Oncol 1998 Nov;16(11):3649-3655.
Abstract: PURPOSE: Patients with cancer and chronic inflammatory disorders have used shark cartilage (SC) preparations for many years. Preclinical studies that support their beneficial effects are scanty, and reports of clinical trials have been anecdotal. The proposed mechanisms of antitumor action include direct or indirect inhibition of angiogenesis. Because of the emerging use of SC as an alternative to conventional cancer therapy, this trial was launched to evaluate the safety and efficacy of SC. PATIENTS AND METHODS: Sixty adult patients with advanced previously treated cancer (breast, 16 patients; colorectal, 16 patients; lung, 14 patients; prostate, eight patients; non-Hodgkin lymphoma, three patients; brain, one patient; and unknown primary tumor, two patients) were enrolled. Eligibility criteria included confirmation of diagnosis, resistance to conventional therapy, objective measurable disease, life expectancy of 12 weeks or greater, Eastern Cooperative Oncology Group (ECOG) performance status of 0 to 2, no recent or concomitant anticancer therapy, no prior SC, and informed consent. Patients underwent evaluation of the extent of disease, quality-of-life score (Functional Assessment of Cancer Therapy-General [FACT-G] scale), and hematologic, biochemical, and selected immune function studies at baseline and after 6 and 12 weeks of SC therapy. The dose of SC was 1 g/kg daily orally in three divided doses. Standard criteria were used to evaluate adverse events and response. RESULTS: Ten of 60 patients were lost to follow-up(LTFU) or refused further treatment (RFT) before the 6-week evaluation and were not assessable for toxicity and response. Three patients with stable disease at 6 weeks were LTFU or RFT thereafter. Of the 47 fully assessable patients, five were taken off study because of gastrointestinal toxicity or intolerance to SC. Progressive disease (PD) at 6 or 12 weeks occurred in 22 and five patients, respectively. Five patients died of PD while undergoing SC therapy. No complete (CRs) or partial responses (PRs) were noted. Median time to tumor progression in the entire study population was 7+/-9.7 weeks (mean, 11.4 weeks; range, 3.7 to 45.7 weeks). Ten (20%) of 50 assessable patients, or 16.7% of the 60 intent-to-treat patients, had stable disease (SD) for 12 weeks or more. The median time to tumor progression was 27 weeks, the mean was 28.8+/-9.9 weeks, and the range was 18.6 to 45.7 weeks. In this subset, FACT-G scores improved in four patients, were unchanged in four patients, and declined in two patients. Twenty-one adverse events (grade 1, eight events; grade 2, seven events; and grade 3, six events) were recorded, 14 of which were gastroenterologic (nausea, vomiting, constipation). CONCLUSION: Under the specific conditions of this study, SC as a single agent was inactive in patients with advanced-stage cancer and had no salutary effect on quality of life. The 16.7% rate of SD was similar to results in patients with advanced cancer treated with supportive care alone.

Mohr PE, Wang DY, Gregory WM, Richards MA, Fentiman IS: Serum progesterone and prognosis in operable breast cancer. Br J Cancer, 1996;73: 1532-1533.
Abstract: Higher blood levels of progesterone measured during surgical treatment of breast cancers were associated with significantly better survival, especially in women who were node-positive (P<0.01). There was no significant relationship between E2 levels and survival. This study demonstrated that a higher level of progesterone at time of excision is associated with improved prognosis in women with operable breast cancer.

Newman V, Rock CL, Faerber S, Flatt SW, Wright FA, Pierce JP. Dietary supplement use by women at risk for breast cancer recurrence. The Women's Healthy Eating and Living Study Group. J Am Diet Assoc. 1998 Mar;98(3):285-292.

Nicholson A. Diet and the prevention and treatment of breast cancer. Altern Ther Health Med 1996 Nov;2(6):32-38. (Review)
Abstract: The role of diet in breast cancer has been considered since the 1940s. However, most epidemiological studies on the incidence of the disease have been limited by their focus on one dietary component-fat-at the expense of a balanced consideration of the effect of the total diet. Further, only the intercultural comparison studies examine a wide range of fat intakes. These studies indicate a dearth of breast cancer in populations with diets in which less than 10% of calories are from fat. Although dietary fat, estrogenic food additives, and alcohol increase the risk of breast cancer, fiber, indoles, flavonols, vitamins C and E, beta carotene, and selenium are associated with a decreased risk. Except for alcohol, factors that increase risk predominate in animal products, whereas those that decrease risk abound in plant products. These factors have similar effects on progression and prognosis in breast cancer. Mechanistically, higher serum levels of estrogen have been linked with risk of breast cancer. Dietary fat, insecticide residues, and alcohol result in higher estrogen activity. A variety of plant nutrients have estrogen-blocking activity. Current evidence justifies recommending that women of all ages follow a plant-based diet in which fat provides no more than 10% of calories, with the goals of preventing breast cancer and improving its prognosis in a low-cost, safe manner.

Pelton R, et al. How to Prevent Breast Cancer.

Quella SK, Loprinzi CL, Barton DL, Knost JA, Sloan JA, LaVasseur BI, Swan D, Krupp KR, Miller KD, Novotny PJ. Evaluation of Soy Phytoestrogens for the Treatment of Hot Flashes in Breast Cancer Survivors: A North Central Cancer Treatment Group Trial. J Clin Oncol. 2000 Mar;18(5):1068.
Abstract: PURPOSE: Hot flashes represent a significant clinical problem for some breast cancer survivors. Safe, effective treatment is needed for this prominent clinical problem. Although it has been shown that estrogen or progesterone replacement therapy can alleviate this problem, there are continued safety concerns regarding the use of hormonal therapies in these women. Based on anecdotal information, we hypothesized that soy-derived phytoestrogens, weak estrogen-like substances in the soybean that demonstrate estrogen agonist and/or antagonist effects when they bind to estrogen receptors, could alleviate hot flashes. This current trial was designed to investigate this hypothesis. PATIENTS AND METHODS: This double-blind clinical trial involved breast cancer survivors with substantial hot flashes. After randomization, patients underwent a 1-week baseline period with no therapy. This was followed by 4 weeks of either soy tablets or placebo. The patients then crossed over to the opposite arm in a double-blind manner for the last 4 weeks. Patients completed a daily questionnaire documenting hot flash frequency, intensity, and perceived side effects. RESULTS: Of the 177 women who were randomized and started the study substance, 155 (88%) provided useable data over the first 5 weeks; 149 provided usable data over the entire 9 weeks. There was no suggestion that the soy product was more effective in reducing hot flashes than the placebo. At study completion, patients preferred the soy product 33% of the time, the placebo 37% of the time, and neither substance 31% of the time. No toxicity was observed. CONCLUSION: The soy product did not alleviate hot flashes in breast cancer survivors.

Sharoni Y, Giron E, Rise M, Levy J. Effects of lycopene-enriched tomato oleoresin on 7,12-dimethyl-benz[a]anthracene-induced rat mammary tumors. Cancer Detect Prev 1997;21(2):118-123.
Abstract: Consumption of carotenoids has frequently been inversely correlated with cancer incidence. In this report we used the 7,12-dimethyl-benz[a]anthracene (DMBA)-induced rat mammary tumor model to compare the effect of lycopene-enriched tomato oleoresin on the initiation and progression of these tumors with that of beta-carotene. Rats were injected i.p. with lycopene-enriched tomato oleoresin or beta-carotene (10 mg/kg, twice per week) for 2 weeks prior to tumor induction by DMBA and for an additional 16 weeks after carcinogen administration. HPLC analysis of carotenoids extracted from several tissues showed that both carotenoids were absorbed into blood, liver, mammary gland, and mammary tumors. The tomato oleoresin-treated rats developed significantly fewer tumors, and the tumor area was smaller than that of the unsupplemented rats. Rats receiving beta-carotene showed no protection against the development of mammary cancer.

Simone, Charles. Breast Health: What You Need to Know About Disease Prevention, Diagnosis, Treatment, and Guidelines for Healthy Breast Care.

Sitruk-Ware R, Seradour, B, and Lafaye, C. Treatment of Benign Breast Diseases by Progesterone Applied Topically. Percutaneous Absorption of Steroids. Ed. Mauvais-Jarvis P, C Vickers FH, Wepierre J. Academic Press, 1980.

Smith-Warner S, et al. Alcohol and Breast Cancer in Women A Pooled Analysis of Cohort Studies. JAMA. 1998;279:535-540.
Abstract: Combining analyses from 6 prospective studies that included a total of 322,647 women evaluated for up to 11 years, cconcluded that alcohol consumption is associated with a linear increase in breast cancer incidence in women over the range of consumption reported by most women. For alcohol intakes less than 60 g/d (reported by >99% of participants), risk increased linearly with increasing intake. Limited data suggested that alcohol intakes of at least 60 g/d were not associated with further increased risk. The specific type of alcoholic beverage did not strongly influence risk estimates. The association between alcohol intake and breast cancer was not modified by other factors. Among women who consume alcohol regularly, reducing alcohol consumption is a potential means to reduce breast cancer risk.

Veronesi U, et al: Effect of menstrual phase on surgical treatment of breast cancer. Lancet, Vol. 343, June 18, 1994.