Healing after breast cancer treatment.
Breast cancer (Drug therapy)
Breast cancer (Development and progression)
Breast cancer (Patient outcomes)
|Publication:||Name: Townsend Letter Publisher: The Townsend Letter Group Audience: General; Professional Format: Magazine/Journal Subject: Health Copyright: COPYRIGHT 2012 The Townsend Letter Group ISSN: 1940-5464|
|Issue:||Date: Feb-March, 2012 Source Issue: 343-344|
|Geographic:||Geographic Scope: United States Geographic Code: 1USA United States|
Breast cancer is a "survivable disease" for most
women.(1) The relative survival rates are 89% at 5 years, 82% at 10
years, and 77% at 15 years. (2) Most are for postmenopausal women whose
tumors are node-negative, estrogen-receptor positive (ER + ), and
HER2/neu-negative. (3-6) After cancer patients have survived 5 years,
they are thought to be cancer free. However, breast cancer is a
late-recurring disease. Twenty percent of women who were disease-free 5
years posttreatment are still at risk of a recurrence at 10 years. (7)
Most of the late-recurring cases had estrogen-receptor positive tumors
and their oral hormone-modifying medication tenure is only 5 years. This
leaves a significant gap in the conventional treatment of breast cancer.
After conventional cancer treatment removes the manifestation of the body's underlying state of imbalance, the process of facilitating healing begins, in order to help restore health and hopefully remain cancer free. I propose that naturopathic medicine can play a role in reducing this late recurrence risk by treating patients with basic complementary and individually designed, constitutional methods. I review the roles that naturopathic physicians play in helping breast cancer survivors to heal.
Naturopathic Care After Conventional Treatment for Breast Cancer
To summarize the roles that naturopathic physicians play in support of those healing after breast cancer treatment, I describe three broad categories: complementary care, basic naturopathic care, and individualized constitutional care (Table1).
Supporting breast cancer patients recovering from surgery, chemotherapy and/or radiation is the first of role that we play after treatment ends. Next, manage lingering treatment-related side effects and potential toxicities. This is reviewed with Dr. Kelly Jennings in our textbook, The Breast Cancer Companion: A Complementary Care Manual. (8)
Next, support patients taking hormone-modifying medications. We have many tools for limiting symptoms related to menopause, arthralgia, myalgia, and so on. (9) Help monitor them for endometrial, osteoporotic, hepatic, clotting, lipid changes, and other possible signs of toxicity. (10) Help patients avoid taking contraindicated supplements and botanicals. In addition, offer agents found to be synergistic with selective estrogen-receptor modulator (SERM) and aromatase inhibitor (Al) medications. See Table 2 (p. 78) for a summary of contraindications and synergistic agents.
Basic Naturopathic Care
In addition to complementary care during conventional treatment, naturopathic physicians offer numerous methods for helping patients afterwards. What I am calling basic naturopathic care is a posttreatment naturopathic template.
First, educate patients on the evidence-based lifestyle modifications found to help prevent recurrence by up to 50%. Previously, we relied on primary prevention studies. Now we have a small body of data that can be used to empower patients to optimize their lifestyle in order to reduce risk of recurrence. Conflicting dietary intervention trials prove confusing. Some studies do, however, support recommending a diet that is high in fiber, vegetables, fruit, and soy and calories from fat as low as 15%. See Table 3 (p.80), for details and references. There seems to be consensus, however, about the therapeutic value of exercise, achieving optimal body mass index, limiting alcohol intake and drinking green tea. Studies on preventing recurrence with an empowering lifestyle are detailed in Table 3.
Many nutritional supplements and botanicals recommended in breast cancer treatment plans are based on primary prevention studies and warrant consideration such as turmeric, mushroom extracts, melatonin, higher dosages of CoQ 10. These agents are more thoroughly reviewed and are referenced in The Breast Cancer Companion as well as The Definitive Guide to Cancer. (11), (12)
There are several agents, however, that have prevention of recurrence data in animals and humans. Taking vitamin supplements, vitamin C and E, CoQ10 with antioxidants, drinking green tea all have inverse associations with breast cancer recurrence. Taking Coriolus versicolor mushroom extracts, melatonin, and black cohosh were also found to increase survivorship among specific subsets of breast cancer survivors. See Table 4 (p. 81) for studies, references, and an associated basic treatment plan.
In review, there are important roles that the naturopathic physicians offer patients after conventional breast cancer treatment. The aim of complementary care is to assist patients in recovery and healing after conventional oncologic therapies and to resolve residual side effects. In addition, basic naturopathic guidelines provide a template for helping patients to reduce recurrence risk with both lifestyle medications and evidence-based natural therapeutics.
Individualized, Constitutional Treatment of People Who Have Had Breast Cancer
Conventional approaches to treating breast cancer are like the Coast Guard arresting a speedboat. This is especially important in cases of aggressive or late-stage disease. Naturopathic approaches are like a sailboat harnessing the natural power of the wind to guide the boat to safety. Adding these approaches is recommended, especially for the majority of women who may develop late-recurring breast cancer. I propose that together, we may be able to arrest the manifestation of this disease and guide the patient toward healing.
Naturopathic foundational principles include treating the whole person, not treating cancer, treating the underlying cause of an illness, not the symptom, using the healing power of nature, and removing obstacles to a cure. To inspire transformational healing, first identify the patient's constitutional factors.
There are nonmodifiable risk factors that many patients share, such as being female and aging. (13) However, many patients have no other risk factors like obesity, smoking, DES exposure, excessive alcohol consumption, gene mutations, or family history. Other women who do have breast cancer risk factors never get it. (14) The cause in many cases is multifactorial. Consider a combination of factors like genomics, unfortunately timed toxic exposures, individual constitution and lifestyle factors.
Over the 14 years that I have treated women with breast cancer, I have noted that there are common constitutional factors that need to be treated in order for transformational healing to occur. For simplicity's sake, I have grouped them into three broad categories; detoxification, inflammation, and stress response.
To identify an individual's constitutional imbalance(s), take a thorough medical history, environmental exposure history, psychological/social history, and family history. (15) You may include a Chinese Medical history. Perform a traditional and nutritional physical examination, Chinese Medicine pulse, tongue, and energy evaluation if desired. From the clues presented, run appropriate tests. Then methodically treat each layer of dysfunction using naturopathic foundation principles (Table 1).
Detoxification refers to the risk of malignant transformation from breast tissue toxicity in an individual whose genome inhibits metabolism and elimination of toxins. (16) Exposure is most concerning at times of rapid cell division such as in utero or during puberty.
To evaluate the hypothesis that detoxification issues play at least a partial role in the etiology of a patient's breast cancer, perform single nucleotide polymorphism (SNP) testing. (17), (18) Evaluate: (1) hormone metabol ism; (2) detoxification of specific environmental toxins; (3) medication metabolism. Consider testing sufficiency of amino acids used in detoxification as wed as a urine organic acids test to evaluate hepatic stress.
Subsequent to identifying SNPs related to hormone metabolism, order an estrogen metabolism test of the ratio of 2-hydroxy estrone to 16-alpha hydroxyestrone. Higher ratios are associated with reduced risk of breast cancer, especially in those with ER-negative tumors and if premenopausal. (19-21) If patients are taking hormone-modifying medications, consider treating issues of estrogen metabolism with diet alone. Consider a diet low in animal protein, or vegan plus low-toxin fish, ground flaxseed meal (especially in those with catechol-O-methyltransferase polymorphism, or COMT SNP), organic whole soy foods, cruciferous vegetables, and green and white tea. (22-26) If they are not on hormone-modifying drugs, consider diindolylmethane (DIM) and test estrogen metabolism quarterly until therapeutic dose is achieved. (27)
if a patient has SNPs that affect detoxification of solvents or polyaromatic hydrocarbons and their history indicates, consider testing specific toxin load. (28) If they are deficient in amino acids of detoxification and/or have hepatic stress, consider replenishing amino acids during a six-week toxin-specific cleanse. Follow with quarterly 10-day cleansing.
If a patient has a null GSTM SNP and history indicates, cautiously consider oral or IV-chelated toxic metal test and treatment. It is theoretically possible that liberating carcinogens may increase vulnerability to mutation.
For some, the constitutional imbalance is related to inflammation. This refers to the risk of malignant cellular transformation of breast tissue resulting from states of systemic, tissue, and/or intracellular inflammation. Research supports the potential role of inflammation as a factor that may contribute to breast cancer occurrence. (29) In 2009, the Journal of Clinical Oncology reported "some of the most persuasive evidence yet that chronic inflammation might increase the risk of breast cancer recurrence." (30) Further evidence points to a negative immune shift from TH1 to TH2 dominance that contributes. (31)
When considering treatment for chronic inflammation, lookforathickly coated or scalloped tongue, slippery pulse, edema, overweight. Listen for a history of bloating, diarrhea, constipation, digestive infections, congestion, allergies, discharges, itching, phlegm, rash, pain, and so on. Research studies have identified blood markers of inflammation that have been correlated to breast cancer incidence, recurrence, and prognosis: CRP, circulating acute phase proteins, interleukin 6, VEGF, TH2 immune activation complexes, D-dimer, and so on. (32-38)
Evaluate and treat thyroid dysfunction. Autoimmune thyroid disorders account, to a large extent, for the increased prevalence of thyroid disorders among breast cancer patients. (39)
Test for food allergies/intolerances to eliminate food-based inflammation. Consider allergy elimination and an anti-inflammatory diet as a template for food-based treatment of inflammation.(40), (41)
I have observed that digestive infections/dysbiosis are common sources of inflammation in breast cancer patients, especially those who have deficiencies in the Earth element from a Chinese Medicine perspective. Test stool and/or urine organic acids to evaluate and guide treatment of dysbiosis. (42) Restore the integrity of the digestive mucosa.
In addition to treating the cause of the inflammation, consider natural anti-inflammatory agents that also inhibit breast cancer such as fish oil, curcumin, and so on. (43-45)
Cancer is not caused by stress alone. (46) The stress response constitutional factor refers to the theory that while the cause of breast cancer is often multifactorial, it may partially result from or progress due to a patient's neurochemical response to chronic stress. There is value in treatments that limit the impact that chronic negative stress response may have on the immune and endocrine systems.
Certain genotypes of the COMT SNP are correlated with breast cancer risk and prognosis. (47), (48) COMT SNPs result in 3- to 4-fold less COMT enzyme activity and therefore inhibition of catecholamine degradation. (49) Prolonged activation of either the sympathetic nervous system or the hypothalamic-pituitary-adrenal axis (stimulator of Cortisol production) may promote tumor growth. (50) One researcher of ovarian cancer stated that the evidence may be even stronger for stress's playing a role in cancer progression. (51) Others found elevations of catecholamines in tumor samples of patients under extreme stress compared with those who were less stressed. (52) In addition, cancer patients reporting higher stress levels have elevated levels of tumor angiogenic cytokines. (53)
Consider testing stress response as a constitutional factor by testing the COMT SNP, neurotransmitters, DHEA, diurnal Cortisol, and amino acids as they relate to neurotransmitters (Table 1).
I use a combination of lifestyle, mind-body-spirit treatment, energetic-balancing with acupuncture, and qi gong, as well as Western and Chinese botanicals, amino acids, and other nutritional supplements (Table 1). My goal is to support patients in experiencing longer periods of being in the moment. I have a theory: the more time spent being in the moment, the more time spent vibrating at the appropriate frequency for our cellular being. I like to think that this equates with slowing down those rapidly dividing cancer cells.
Individualized, constitutional treatment of people who have had breast cancer requires adherence to the foundational principles of naturopathic medicine. By identifying and treating the cause, treating the whole person, and inspiring the healing power within each patient by removing obstacles to her cure, we facilitate transformational healing. By combining this approach with evidence-based basic naturopathic care and complementary care methods, we are at the very least inspiring health.
(1.) Howlader N, Noone AM, Krapcho M, et al. SEER Cancer Statistics Review, 1975-2008 [Web page]. National Cancer Institute, http://seer.cancer.gov/csr/19752008. Based on November 2010 SEER data submission, posted to the SEER website 2011.
(3.) Lyman GH, Kuuderer NM, Lyman SL, et al. Menopausal status and the impact of early recurrence on breast cancer survival [online articfej. Moffit Cancer Center & Research Institute, http://www.moffitt.org/moffittapps/ccj/v4n4/article5.html. Accessed December 4, 2011.
(4.) Gloeckler, LA, Eisner MP. Cancer of the female breast. SEER Survival Monograph. 1998-2001;13:101-110. Available at: http://seer.cancer.gov/publications/survival/survbreast.pdf. Accessed December 4, 2011.
(5.) Dunnwald, LK, Rossing MA, Li CI. Hormone receptor status, tumor characteristics, and prognosis: a prospective cohort of breast cancer patients. Breast Cancer Res. 2007;9(1).
(6.) Attiqa N, M'uza MD, Nadeem Q, et al. Prognostic factors in node-negative breast cancer. Ann Surg. 2002;235(1):10-26.
(7.) Brewster AM, et al. Residual Risk of breast cancer recurrence 5 years after adjuvant therapy. J Natt Cancer Inst. 2008;100;DOI:10.1093/jnci/djn233.
(8.) MacDonald B, Jennings K. The Breast Cancer Companion: A Complementary Care Manual. Portland, OR: Brains and Braun Publications; 2010:95-192.
(9.) Ibid.; 200-201,207-208.
(10) Tamoxifen [Web page]. MedlinePlus. http://www.nim.nih.gov/medlineplus/druginfo/meds/a682414.html. Accessed November 27, 2011.
(11.) MacDonald BM, Jennings K. Breast Cancer Companion. 292-305.
(12.) Alschuler L, Gazella Karolyn. The Definitive Guide to Cancer. 3rd ed. Berkeley, CA: Celestial Arts; 2010.
(13.) American Cancer Society. Breast cancer and early detection [online document], http://www.cancer.org/acs/groups/cid/documents/webcontent/003165-pdf.pdf. Accessed December 4, 2011.
(15.) Marchese M. Environmental exposure history questionnaire-Permission granted by author. Available at: www.drmarchese.com/images/Exposure_Questionnaire.doc. Accessed December 6, 2011.
(16.) Marchese M. Environmental links to breast cancer and endometriosis. Naturopath Doctor News Rev. 2011;7(2):9-10.
(17.) Bugano DD, Conforti-Froes N, Yamaguchi NH, et al. Genetic polymorphisms, the metabolism of estrogens and breast cancer: a review. Eur) Gynaecol Oncol. 2008;29(4):313-20.
(18.) Consider the Genova Diagnostics Laboratory DetoxiGenomic Profile. Available at: http://www.gdx.net/product/10038. Accessed December 6, 2011.
(19.) Muti P, Bradlow HL, Micheli A, et al. Metabolism and risk of breast cancer: a prospective analysis of 2:16 hydroxyestrone ratio and risk of breast cancer in premenopausal and postmenopausal women. Cancer Epidemiol. 2000;11:635-640.
(20.) Eliassen AH, Missmer SA, Tworoger SS, et al. Circulating 2-hydroxy and 16-alph hydroxy! estrone levels and risk of breast cancer among postmenopausal women. Cancer Epidemiol Biomarkers Prev. 2008;17(8):2029-2035.
(21.) Muti P, Bradlow HL, Micheli A, et al. Metabolism and risk of breast cancer: a prospective analysis of 2:16 hydroxyestrone ratio and risk of breast cancer in premenopausal and postmenopausal women. Cancer Epidemiol. 2000;11:635-640.
(22.) Adlercreutz H, Fotsis T, Hockerstedt K, et al. Diet and urinary estrogen profile in premenopausal omnivorous and vegetarian women and in premenopausal women with breast cancer. J Steroid 6ioctiem;l989;34(1-6h527-530.
(23.) McCann SE, Wactawski-Wende J, Kufel K, et al. Changes in 2-hydroxyestrone and 16alpha-hydroxyestrone metabolism with flaxseed consumption: modification by COMT and CYP1B1 genotype. Cancer Epidemiol Biomarkers Prev. 2007;16(2):256-262.
(24.) Nettleton JA, Greany KA, Thomas W, et al. The effect of soy consumption on the urinary 2:16-hydroxyestrone ratio in postmenopausal women depends on equol production status but is not influenced by probiotic consumption. Nutr Cancer. 2005;135(3):603-608.
(25.) Fowke JH, Longcope C, and Hebert JR: Brassica vegetable consumption shifts estrogen metabolism in healthy postmenopausal women. Cancer Epidemiol Biomarkers Prev. 2000;9:773-779.
(26) Bradlow HL and Sepkovic D. Diet and Breast Cancer. Ann NYAcadSci. 2002;963, 247-267.
(27.) Dalessandri KM, Firestone CL, Ritch MD, et a!. Pilot study: effect of 3, 3Q-diindolyImethane supplements on urinary hormone metabolites in postmenopausal women with a history of early-stage breast cancer. Nulr Cancer. 50(2): 161-167.
(28.) Consider Metametrix Clinical Laboratory's Toxic Effects Profiles. Available at: http://www.metametrix.com/test-menu/profiles/categorized. Accessed on December 6, 2011.
(29.) Cole S. Chronic inflammation and breast cancer recurrence. J Clin Oncol. 2009;27(21):3418-3419.
(31.) DeNardo DG, Coussens LM. Inflammation and breast cancer: balancing immune response: crosstalk between adaptive and innate immune cells during breast cancer progression. Breast Cancer Res. 2007;9:2t2.
(32.) Pierce GL, Ballard-Barbash R, Bernstein L, et al. Elevated biomarkers of inflammation are associated with reduced survival among breast cancer patients. J Clin Oncol. 2009;27(21):3437-3444.
(33.) Han Y, Mao F, Wu Y et al. Prognostic role of C-reactive protein in breast cancer: a systematic review and meta-analysis. Int I Biol Markers. Epub 2011 Dec2:0:105301/JBM.2011.8872.
(34.) Cole, op. cit,
(35.) Bachelot T, Ray-Coquard I, Menetrier-Caux C, et al. Prognostic value oi serum levels of interleukin 6 and of serum and plasma levels of vascular endothelial growth factor in hormone-refractory metastatic breast cancer patients. Br J Cancer;2003;88:1721-1726.
(37.) DeNardo DG, Coussens LM. Inflammation and breast cancer, balancing immune response: crosstalk between adaptive and innate immune cells during breast cancer progression. Breast Cancer Res. 2007;9:212.
(38.) Dirix LY, Salgado R, Weytjens R, et al. Plasma fibrin D-dimer levels correlate with tumour volume, progression rate and survival in patients with metastatic breast cancer. Br I Cancer. 2002;86(3):389-95.
(39.) Giani C, Fierabracci P, Bonacci R et al. Relationship between breast cancer and thyroid disease: relevance of autoimmune thyroid disorders in breast malignancy. J Clin Endocrinol Metabl. 1996;81(3):990-4.
(40.) See Black J. The Anti-Inflammatory Diet and Recipe Book. Alameda, CA; 2006.
(41.) Consider anti-inflammatory resources such as those at drweil.com. Anti-inflammatory food pyramid chart available at http://www.drweil.eom/drw/u/ART02995/Dr-Weil-Anti-lnflammatory-Food-Pyramid.html. Accessed December 6, 2011.
(42.) Elena M. Health, probiotics, and inflammation. J Clin Gastroenterol. 2006;42:S177-S178.
(43.) Mandal CC, Ghosh-Choudhury T, Yoneda T, et al. Fish oil prevents breast cancer cell metastasis to bone. Biochem Biophys Res Commun. 2010;402(4):602-607.
(44.) Simopoulos A. Omega-3 fatty acids in inflammation and autoimmune diseases. J Am Coll Nutr. 2002 Dec;21 (6):495-505.
(45.) Altenburg JD, Bieberich AA, et al. A Synergistic antiproliferation effect of curcumin and docosahexaenoic acid in SK-BR-3 breast cancer cells: unique signaling not explained by the effects of either compound alone. BMC Cancer. 2011 Apr 21;11:149.
(46.) Nielsen NR, Gronbaek M. Stress and breast cancer: a systematic update on the current knowledge. Nat Clin Pract Oncol. 2006;3(11):612-620.
(47.) Onay UV, Aaltonen K, Briollais L, et al. Combined effect of CCND1 and COMT polymorphisms and increased breast cancer risk. BMC Cancer. 2008;8:6.
(48.) LonglR, Cai Q, Shu XO, et al. Genetic polymorphisms in estrogen-metabolizing genes and breast cancer survival. Pharmacogenet Genomics. 2007;(5):331-338.
(49.) Dauvilliers Y, Neidhart E, Lecendreux M, et al. MAO-A and COMT polymorphisms and gene effects in narcolepsy. Mol Psychiatry. 2001;64):369.
(50.) Ross, K. Mapping pathways from stress to cancer progression. J Natl Cancer Inst. 2008;100(13):914-917.
(52.) Lee JW, Shahzad MMK, Lin YG, et al. Surgical stress promotes tumor growth in ovarian carcinoma. Clin Cancer Res. 2009;15(8):2695-2701.
(53.) Lutgendorf SK, Lamkin DM, Jennings 1MB, et al. Biobehavioral influences on matrix metalloproteinase expression in ovarian carcinoma. Clin Cancer Res. 2008;14(21):6839-6846. (41.) Consider anti-inflammatory resources such as those at drweil.com. Anti-inflammatory food pyramid chart available at http://www.drweil.eom/drw/u/ART02995/Dr-Weil-Anti-lnflammatory-Food-Pyramid.html. Accessed December 6, 2011.
by Barbara MacDonald, ND, LAc, MSOM
Barbara MacDonald, ND, LAc, MSOM, coauthored The Breast Cancer Companion: A Complementary Care Manual, a practitioner's guide to support women through conventional cancer treatment (2010). Dr. MacDonald graduated from National College of Naturopathic Medicine (NCNM) with degrees in naturopathic medicine and Classical Chinese medicine (1997, 2003 respectively). She did women's health with a focus on breast cancer care at A Woman's Time in Portland, Oregon, for 14 years. After her residency, she was adjunct teaching faculty at NCNM, where she started the first dual-degree cancer teaching shift. She returned to New England in 2010. She currently practices at Camden Whole Health in midcoast Maine, where she continues to write and lecture on the subject of breast cancer care. Contact: www.thebreastcancercompanion.com or email@example.com.
Table 2: Substances Contraindicated and Synergistic with Hormone-Modifying Medication Tamoxifen (TAM) selective estrogen-receptor modulator Avoid Powerful inhibitors of CYP2D6 pathway such as SSRIs, moderate inhibitors such as OTC antihistamines, berberines, less concern with mild inhibitors like Panax ginseng. (1-5) Agents metabolized by the CYP3A4 pathway such as St. John's wort, especially in the elderly; moderate inhibitors (rhodiola, gaultheria, uva ursi), echinacea, and other mild 3A4 inhibitors appear to be safer. (6-9) Synergistic mdole-3-carbinole enhances TAM effect; may also increase toxic metabolites (caution: hepatotoxicity). (10) DIM has no effect on TAM metabolism. (11) Green tea, omega-6 (gamma linolenic acid), and melatonin may enhance effect of TAM in vitro. (12-15) Diet high in vegetables associated with reduced risk of recurrence among TAM users. (16) Flax seeds enhanced the tumor-inhibiting effect of TAM-resistant breast cancer cells in mice. (17) Quercetin enhances the effect of TAM in vitro and may reduce acquired TAM resistance. (18), (19) Black cohosh reduces hot flashes among TAM users, enhances the inhibition of proliferation of TAM in vitro; possible concern for 2D6 and 3A4 inhibition, caution; may increase hepatotoxicity of TAM. NB: Black cohosh may increase the risk of lung metastasis in those with HER2+breast cancer. (20-23) Vitamin E enhances the tumor inhibition of TAM in vitro and tocotrienols were found to increase survivorship by as much as 60% among TAM users; the result was not statistically significant. (24), (25) Dietary intake of soy isoflavones combined with TAM (in postmenopausal American women) resulted in 60% reduction in breast cancer recurrence comparing highest with lowest intake; "appears not to interfere with tamoxifen efficacy." (26) Silymarin, grapeseed extract, and curcumin reduced hepatotoxicity in TAM-intoxicated rats. (27) Taurine appears to do the same. (28) Notes Consider CYP2D6 and CYP 3A4 polymorphism testing to ensure proper drug metabolism. See notes below. Aromatase Inhibitors (Al) Avoid Inducers of the CYP3A4 drug metabolism pathway may lower plasma concentrations of Als (see notes) such as St. John's wort (especially in the elderly) and berberine-rich plants like goldenseal, which may interfere with efficacy of these medications. (29), (30) Caution is recommended when taking with other 3A4 substrates and inhibitors (such as SSRIs, antifungals, antibiotics, opiates, ginkgo, milk thistle, grapefruit juice, gaultheria, rhodiola, uva ursi) as plasma concentrations of Als may increase resulting in. toxicity For a list of substrates and inhibitors, consider; http:ctep.cancer.gov/protocolDevelopment/docs/cyp3a4.doc (31), (32) A study to evaluate the safety of flaxseed consumption by those taking anastrozole is under way. (33) Synergistic Women eating the most soy with anastrozole had 33% lower recurrence vs. those who ate the least. (34) Curcumin enhances the effect of letrozole in mice endometrial cancer model. (35) Vitamin D: Achieving a 40 ng/mL concentration of 250HD may prevent Al-induced arthralgia. Routine pre-AI vitamin D testing recommended due to risk of bone loss with Als. (36), (37) Notes Consider CYP3A4 polymorphism testing to identify errors in drug metabolism and inform selection. SERM; selective estrogen receptor modulator such as tamoxifen (TAM) commonly used in premenopausal survivors Al: aromatase inhibitor such as anastrozole (Arimidex), exemestane (Aromasin), and letrozole (Femara) used only in postmenopausal survivors to block the conversion of adrenal testosterone to estrogen SSRI: selective serotonin reuptake inhibitor Notes: Tamoxifen-treated patients carrying CYP2D6 variants that impaired formation of 4-hydroxytamoxifen, had more than double the risk of recurrence of breast cancer, shorter reiapse-free periods, and worse event-free survival rates compared with patients with functional CYP2D6. (38) Those with CYP3A41b variants are at higher risk of endometrial cancer. (39) Femara only mildly inhibits 3A4; Arimidex moderately inhibits 3A4; Aromasin is metabolized by 3A4 and has the greatest risk of interactions with other 3A4-metabolised drugs. (40) (1.) Wang L, Arnold K. Hot flash drug may hinder effectiveness of tamoxifen. J Natl Cancer Inst. 20O3;95(23): 1734-1735. Available at: http://jnci.oxfordjoumals.org/content/95/23/1734.short Accessed December 6.2011. (2.) Davis R. Perkins L. Brooks-DeWeese A. Trends in concomitant tamoxifen and SSRI use. 2008 Breast Cancer Symposium. American Society of Clinical Oncology. Available at. http://:www.asco.org/ascov2/Meetings/ Abstracts?&vmview=absLdetaitview&confiD=58&abstractlD=40387. Accessed November 27, 2011, (3.) Borges S et al. Quantitative effect of CYP2D6 genotype and inhibitors of tamoxifen metabolism: implications for optimization of breast cancer treatment Clin Pharm Ther. 2006;80(1):61-74. (4.) Guriey B. Swain A, Hubbard M et al. Clinical assessment of CYP2D6-mediated herb-drug interactions in humans: Effects of milk thistle, black cohosh, goldenseal, kava kava, St. John's wort and Echinacea. Mol Nutr Food Res. 2008 July;52(7):755-763. (5.) Gurtey. B, Gardner S, Hubbard M, et at. Clinical assessment of botanical supplementation on cytochrome p450 phenotypes in the elderly: St. John's wort, garlic oil. Panax Ginseng, and Gingko biloba. Drugs Aging. 2005;22(6):525-539. (6.) Caraci F, Crupi R, Drago F, et al. St John's Wort may reduce effect of tamoxifen due to CYP3A4 metabolic interference. Curr Drug Metab. July 2011; 12(16):570-577. (7.) Gurley. B. Gardner S. Hubbard M. el al. Op cit. (8.) Scolt IM, Leduc Rl. Burt AJ, et al. The inhibition of human cytochrome p450 by ethanol extracts of North American botanicals. Pharmac Biology. 2006; 44(5):315-327. (9.) Freeman C, Spelman K. A critical evaluation of drug interactions with Echinacea sop. Mof Hute Food Res. 20G8;52-.789-798. (10.) Malejka-Giganti D, Parken DR, Bennett K. et all. Suppression of mammary gland carcinogenesis by post-initiation treatment of rats with tamoxifen or indote-3-carbinot or their combination. Eur J Cancer Prev. 2007;16(2):130-141. (11.) Parkin DR, Malejka-Giganti D. Differences in the hepatic P450-dependenl metabolism of estrogen and tamoxifen in response to treatment of rats with 3.3'-diindolylmethane and its parent compound indole-3-carbinol. Cancer Detect Prev. 2004; 28(1):72-79. (12.) Sakata M, Ikeda T, Imoto S, et al. Prevention of mammary carcinogenesis in C3H/OuJ mice by green tea and tamoxifen. Asian Pac J Cancer Prev. 2011; 12(2):567-571. (13.) Suganuma M, Okabe S. Kai Y, et al. Synergistic effects of (-)-epigallocatechin gallate with (-)- epicatechin, sulindac. or tamoxifen on cancer- preventive activity in the human lung cancer cell line PC-9. Cancer Res. 1999; 59(1):44-47. (14.) Mendertdez JA. Colomer R, Lupu R. Omega-6 polyunsaturated fatty acid gamma-linolenic acid (18:3n-6) is a selective estrogen-response modulator in human breast cancer cells: gamma-linolenic acid antagonizes estrogen receptor-dependent transcriptional activity, transcriptionally represses estrogen receptor expression and synergistically enhances tamoxifen and IC1182, 780 (Faslodex) efficacy in human breast cancer cell. Int J Cancer. 2004;109(6):94[pounds sterling]-954. (15.) Kubatka P, Bojkova B, Cikova-Kalicka K. et a!. Effects of tamoxifen and melatonin on mammary gland cancer induced by N-methyl-n-nitrosourea and by 7(12-demethylbenz(a)anthracene, respectively, in female Sprague-Dawiey rats. Folia fiio. 2001;47(1):5-l0. (16.) Thomson CA, Rock CL, Thompson PA, et al. Vegetable intake is associated with reduced breast cancer recurrence in tamoxifen users; a secondary analysis from the Women's Healthy Eating and Living Study. Breast Cancer Res Treat. 2011;125(2):519-527. (17.) Thompson L, Chen J, Hui E, et al. Interactive effects of flaxseed and tamoxifen on human breast cancer. Clinical Cancer Research. 2004;10:7703-7711. (18.) Shin SC. Choi JS. Li X. Enhanced bioavailability of tamoxifen after oral administration of tamoxifen with quercetin in rats. Int J Pharm. 2006;26(1-2);144-149. (19.) Oh SJ, Kim O, Lee JS, eta!. Inhibition of angiogenesis by quercetin in tarnoxilen-reststant breast cancer ceils. Food Chem lox'tcoi. 2010;48(11):3227-3234. (20.) Kanadys WM. Leszczynska-Gorzeleak B. Oleszczuk J. Efficacy and safety of Black Cohosh (Actaea/Cimicifuga racemosa) in the treatment of vasomotor symptoms-review of clinical trials. Ginekol Pol. 2008;79(4):287-296. (21.) Bodinet C, Freudenstein J. Influence of Cimicifuga racemosa on the proliferation of estrogen receptor-positive human breast cancer celts. Breast Cancer Res Treat 2002;76(1);1-10. (22.) Li J. Godecke T, Chen SN. et al. In vitro metabolic interactions between black cohosh (Cimicifuga racemosa) and tamoxifen via inhibition of cytochrome P450 2D6 and 3A4. Xenobiotha. Epub 2011 Aug 9. Available at: http://www.ncbi.nlm.nih.gov/pubmed/21827327. Accessed Nov. 27. 2011. (23.) Davis, V. Jayo M, Ho, A. et al. Black cohosh increases metastatic mammary cancer in transgenic mice expressing c-erbB2- Cane Res. 2008;68;8337. (24.) Guthrie N, Gapor A. Chambers A, Carroll KK: Inhibition of proliferation of estrogen receptor negative MDA-MB-435 and positive MCF-7 human breast cancer cefts by patm tocotrienols and tamoxifen, alone or in combination. J Nutr. 1997;127:544S-548S. (25.) Nesaretnam K, Meganathan P, Veerasenan SD. et al. Tocotrienols and breast cancer: the evidence to date. Genes Nutr. Epub 2011 Apr 24. Available at http://breast-cancer-research.com /content/pdf/bcr2726.pdf. Accessed Nov 27,2011. (26.) Guha N, Kwan ML, Quesenberry CP Jr. et al. Soy isoflavones and risk of cancer recurrence in a cohort of breast cancer survivors: the Life After Cancer Epidemiology study Breast Cancer Res Treat. 2009;118(2):395-405. (27.) El-Beshbishhy HA, Mohamadin AM, Nagy AA, et al. Amelioration of tamoxifen-induced liver injury in rats by grape seed extract, black seed extract and curcumin. Indian J Exp Bioi 2010;48(3):280-288. (28.) Tabassum H, Rehman H, Banerjee BD, et al. Attenuation of tamoxifen-induced hepatotoxicity by taurine in mice. Clin ChimActa 2006:370(1-2): 129-36. (29.) List of drugs that may have potential CYP3A4 interactions. Available at: ctep.cancer. gov/protocolDevelopment/docs/cyp3a4.doc. Accessed November 27, 2011. Adapted from Cytochrome P450 enzymes: substrates, innibftors, and inducers, in: lacy CF, Armstrong It, Goldman MP, Lance LL, eds. Dnig Information Handbook. 15th ed. Hudson, OH; LexiComp Inc.; 2007:1899-1912. (30.) Gurley B, Swain A. Hubbard M et al. Clinical assessment of CYP206-mediated herb-drug interactions in humans: Effects of milk thistle, black cohosh, goldenseal, kava kava, St. John's wort and Echinacea. Mo/Nutr Food Res. 2008 Jury; 52(7);755-763. (31.) Scott IM, Leduc Rl, Burt AJ. et al. The inhibition of Human Cytochrome P450 by Ethanol Extracts of North American Botanicals. Pharmac Biology. 2006;44(5):315-327. (32.) List of drugs that may have potential CYP3A4 interactions. Op cit. (33.) Flaxseed, aromatase inhibitors and breast tumor characteristics (FABrC) [Web page]. http://clinicaltrials.gov/ct2/show/NCT00612560. Refer to ClinicaiTrials.gov identifier: NCT00612560. Accessed Nov. 27, 2011. (34.) Kang X, Zhang Q, Wang S. et al. Effect of soy isoflavones on breast cancer recurrence and death for patients receiving adjuvant endocrine therapy. CMAJ. 2010;182(17):1857-1862. (35.) Liang YJ, Zhang HM. Wu YZ, et al. Inhibiting effect of letrozole combined with cuTCumin on xenogiafted endometrial carcinoma growth in nude mice. Chin J Cancer. 2010;29(1) :9-14, (36.) Prieto-Alhambra 0, Javaid MK. Servitja S. et al. Vitamin D threshold to prevent aromatase inhibitor-induced arthralgia: a prospective cohort study. Breasr Cancer Res Treat. 2011; 125(3):869-878. (37.) Nogues X, Servitja S, Pena MJ, et al. Vitamin D deficiency and bone mineral density in postmenopausal women receiving aromatase inhibitors for early breast cancer. Mafuntes. 2010;66(3):291-297. (38.) Schroth W. Antoniadou L, Fritz P, et al. Breast cancer treatment outcome with adjuvant tamoxifen relative to patient CYP2D6 and CYP2C19 genotypes. J Clin Oncol. 2007;25(33): 5187-5193. (39.) Chu W, Fyles A, Sellers E, et al. Association between CYP3A4 genotype and risk of endometrial cancer following tamoxifen use. Carcinogenesis. 2007,28 (10): 2139-2142. (40.) Buzdar A. Pharmacology and pharmacokinetics of the newer generation aromatase inhibitors. Clinic Cancer Res. 2003;9:468s. Table 3: Lifestyle Modifications that Lower the Risk of Recurrence of Breast Cancer Fitness/Shape Exercise There was a 50% greater chance of WHEL trial: being a survivor in those who got 1490 women the equivalent of 30 minutes of diagnosed and exercise 6 days a week or 3 hours treated for weekly. (1) earty-stage breast cancer between 1991 and 2000. Not only does physical activity Prospective increase survivorship, but the observational amount matters. The women who study based on exercised 3-5 hours a week at an responses from average pace (2-2.9 mph) were 50% 2987 more likely to be long-term participants in survivors. The women who only the Nurses' exercised 1-3 hours a week were Health Study 30% less likely to survive. (2) who were diagnosed with stage I, II. or Ml breast cancer between 1984 and 1998. Women who increased their activity Prospective level after diagnosis and observational treatment had a 45% higher chance study of 933 of survival and\hose who reduced women; (Hearth. their posttreatment activity had a Eating. four-fold lower chance of Activity, and survival. Modest increase in Lifestyle posttreatment fitness improves Study) prognosis. (3) diagnosed with local or regional breast cancer (1995-1998); observed until death or 2004. Body mass index Those who had a body mass index of 1453 women with less than 25 or a waist-to-hip invasive breast ratio (WHR) of less than or equal cancer, to 0.85 were 38% more likely to be diagnosed a survivor than those whose BMI 1991-1994 were was greater than or equal to 30 or interviewed a WHR of O.80. (Low vegetable and during fruit consumption and current or follow-up; past smoking were also associated Italian with worse breast cancer multicenter survival.) (4) case-control study. Body fat Women with higher percentage of 2010 review of body fat had a 30% lower risk of epidemiologic surviving breast cancer. The most studies consistent finding was that conducted at adiposity was associated with a Moores UCSD 30% increased risk of mortality. Cancer Center. (5) Beveraqes/Diet Alcohol Drinking 3 to 4+ drinks per week Kaiser's Life is associated with a 1,3-foid After Cancer increased risk of breast cancer Epidemiology recurrence. (5) (LACE) prospective study of 189? early stage breast cancer survivors diagnosed between 1997 and 2000 Green tea One meta-analysis reported that 2010 more than 3 cups of green tea meta-analysis consumed daily reduces the risk of of other recurrence by 27% while 5+ cups studies, 5617 was required in the 2005 analysis. cases and 2005 (7), (8) systematic review and meta-analysis. Vegetables/fruits There was a 50% greater likelihood This & fitness of being a survivor among those prospective who consumed five or more servings study was of vegetables and fruits daily and performed of who accumulated 540+ metabolic 1490 women equivalent tasks-min/ wk diagnosed and (equivalent to walking 30 minutes treated for 6 d/wk); only the combination was early-stage associated with a significant breast cancer survival advantage. (9) between 1991 and 2000. Note: the Women's Healthy Eating and Living trial did not find high vegetable and fruit consumption to more benefit compared with controls in the general first analysis of the study However, a subgroup of women taking tamoxifen who ate the most servings of cruciferous vegetables daily had a 52% lower recurrence rate than those who ate the fewest servings. (10) Soy isoflavones Asian women who ate the most soy 5042 Chinese foods had the least recurrence and breast cancer the greatest survival. (11) survivors ages Another study found that among 20-75 diagnosed postmenopausal American women who between take tamoxifen, those who ate the 2002-2006 vs. equivalent of isoflavones in an California Asian diet had a 60% reduction in cohort of 1954 breast cancer recurrence. (12) survivors from Note: published warnings regarding 1997-2000 in a the differences in the epigenetics prospective of American breast cancer assessment of survivors (vs. Asian) caution the isoflavone consumption of soy foods equaling consumption. the equivalent of the Asian diet until more data are available. (13) Dietary intervention trials in review and support of limiting animal fat for breast cancer survivorship The Nurses' Health Study reported no evidence suggesting that lower intake of total fat or a specific type of fat was associated with death from breast cancer. 14 Higher levels of dietary intake of butter, margarine, lard, and beef were found to increase the risk of recurrence. There was also an increased risk associated with consumption of red meat, liver, and bacon, corresponding to a doubling of the risk for each time per day that foods in this category were consumed (p = 0.09). 15 During the Women's Intervention Nutrition Study (WINS), women counseled to reduce fat intake to 15% of calories had a 24% lower risk of recurrence compared with the control group counseled to eat between 20-35% calories from fat (p < 0.05). 16 Basic recommendations for therapeutic lifestyle modifications to reduce risk of recurrence of breast cancer: * Exercise 3-5 hours a week, at least more than you did before you were diagnosed. * Optimize BMI, waist/hip ratio, and body fat to meet study guidelines listed above. * Drink fewer than three alcoholic beverages weekly. * Drink 5-10 cups of green tea a day (or the equivalent in capsules). * Eat a diet high in fiber with a therapeutic dose (5-10 half-cup portions) of a variety of local, organic vegetables (particularly cruciferous) and fruits (particularly berries) daily, and limit or eliminate animal protein and, if eaten, use free-ranging, hormone-free sources. * Eat organic, whole soy foods if you are from Asia, were raised on an Asian equivalent of soy, and/or are on tamoxifen. (1.) Pierce JP. Stefanick ML. Flatt SW. et al. Greater survival after breast cancer in physically active women with high vegetable-fruit intake regardless of obesity. J Clin Oncol 2007;25(17):2345-2351. (2.) Holmes M. Chen W. Feskanich D. et al. Physical activity and survival after breast cancer diagnosis. JAMA. 2005;293:2479-2486. (3.) Irwin M, Smith A, McTiernan A, et al. Influence of pre-and postdiagnosis physical activity on mortality in breast cancer survivors; The health, eating activity, and lifestyle study. J of Cfift One. 2008;26(24).3958-3964. (4.) Dal Maso L, Zucchetto A, Talamini R. et at. Effect of obesity and other lifestyle factors on mortality in women with breast cancer. Int J Cancer. 2008;123(9):2188-2194. (5.) Patterson RE, Cadmus LA, Emond JA, et al. Physical activity, diet, adiposity and female breast cancer prognosis: a review of the epidemiologic literature. Maturitas. 2G10;66(1):5-15. (6.) Kwan ML. Kushi LH. Weltzien E, et al. Alcohol consumption and breast cancer recurrence and survival among women with early-stage breast cancer: the life after cancer epidemiology study. J Clin Oncol. 2010;28(29):4410-4416. (7.) Ogunleye AA, Xue F, Michels KB. Green tea consumption and breast cancer risk or recurrence: a meta-analysis. Breast Cancer Res Treat. 2010;119(2):477-484. (8.) Seely D, Mills EJ. Wu P, et at. The effects of green tea consumption on incidence of breast cancer and recurrence of breast cancer; a systematic review and meta-analysis. Integr Cancer Trier. 2005;4(2):144-155. (9.) Pierce JP, Stefanick ML, Flatt SW, et al. Greater survival after breast cancer in physically active women with high vegetable-fruit intake regardless of obesity. J Clin Oncol. 2007;25(17):2345-2351. (10.) Thomson CA, Rock CL, Thompson PA, et al. Vegetable intake is associated with reduced breast cancer recurrence in tamoxifen users: a secondary analysis from the Women's Healthy Eating and Living Study. Breast Cancer Res Treat. 2011 125(2):519-527. (11.) Ou Shu X, Zheng Y, Cai H. et al. Soy food intake and breast cancer survival. JAMA. 2009;302(22):2437-2433. (12.) Guha N, Kwan ML. Ouesenberry CP Jr. et al. Soy isoflavones and risk of cancer recurrence in a cohort of breast cancer survivors: the Life After Cancer Epidemiology study. Breast Cane Res Treat. 2009;118(2):395-405. (13.) Hilakivi-Clarke L, Andrade JE, Helferich W. Is soy consumption good or bad for the breast? J Nutr 2010;140(12):2326S-2334S. (14.) Holmes MD. Hunter DJt Colditz GA. et al. Association of dietary intake of fat and fatty acids with risk of breast cancer JAMA. 1999:281:914-920. (15.) Hetert JR. Huriey TG. Ma Y (19%) The effect of dietary exposures on recurrence and mortality in early stage breast cancer. Breasf Cancer Res Treat. 51:17-28. (16.) Chlebowski, R.. G. Blackburn, et at. Dietary fat reduction and breast cancer outcome: interim efficacy results from the Women's Intervention Diet Study. J Natl Cancer Inst. 2006;98:1767-1776. Table 4: Natural Therapeutic Interventions and Prevention of Recurrence of Breast Cancer Vitamin supplements taken the Breast cancer survivors with serum first six months after treatment vitamin D concentrations at 55 resulted in lower recurrence and nmol/L had a 1.55 times longer 18% reduced risk of mortality. disease-free survival than those The authors stated: "Our results with 35 nm/L concentration.2 do not support the current However, this was not seen in the recommendation that breast cancer WHEL trial where no relation patients should avoid use of between vitamin D and breast cancer vitamin supplements." (1) recurrence was found. (3) There is a (nonsignificant) lower Increased green tea consumption risk of recurrence and (more than three cups a day) was disease-related mortality among inversely associated with breast those who self-reported using cancer recurrence (pooled RR = vitamins C and E for three years 0.73, 95% CI: 0.56-0.96) in a posttreatment (vitamin E nearly meta-analysis of 5716 cases. (5) halved the risk.) (4) Black cohosh lengthened A pilot study evaluated the disease-free survival among survival of patients with various 18,861 patients observed for 3.6 types of end-stage cancer including years. After 2 years following breast. 76% of those who received initial diagnosis, 14% of the supplements of coenzyme Q10 and a control group had developed a mixture of other antioxidants recurrence, while the black (e.g., vitamin C, selenium, folic cohosh extract group didn't reach acid and beta-carotene) survived this proportion until after 6.5 longer than predicted among the years.6 However, black cohosh was treatment group; on average, found to increase the risk of surviving 5 more months than the lung metastasis in control group. (8) HER2-expressing transgenic mice. Caution in HER2+ patients is advised. (7) The disease-free survival was Daily administration of melatonin increased from 84% to 100% when significantly increased the PSK (extract from Coriolus survival time of tumor-bearing versicolor) was added to biannual animals. This is only recommended chemotherapy x 5 years. They for those with ER+ tumor history. studied 134 randomly selected (10) breast cancer survivors who were HLAB40+. The benefit was not apparent among those whose tumors were HLAB40-. (9) From these studies, I might recommend that a posttreatment patient with ER+ breast cancer consider: * whole-foods multivitamin/mineral complex without iron (such as Innate's Iron-free one daily) * selenium, 400 meg from food (100 mg per Brazil nut) and supplementation combined * vitamin D3 to achieve serum concentration of 50-60 ng/mL * green tea at 5+ cups a day or the equivalent in capsules (two 300 mg capsules of Vitanica's green tea, which include 50 mg of whole plant (95% polyphenols,80% catechins, 55% EGCg, 10% caffeine) * Coriolus versicolor mushroom extracts from JHS Natural Products (five 600 mg capsules daily in divided doses) n 6 months minimum and either add or put in quarterly rotation with therapeutic dosages ofcurcumin, artemisia, astragalus, AHCC, or arabinogalactan, etc. * melatonin, 20 mg at bed (1.) Nechuta S, Lew W, Chen 2, et al. Vitamin supplement use during breast cancer treatment and survival: a prospective cohort study. CancerEpidem Biomark Prev. 2011;20(2):262-271. (2.) Goodwin PJ, Ennis M. Pritchard, et al. Prognostic effects of 25-hydroxyvitamin D levels in early breast cancer J Clin Oncol. 2O09;27(23):3757-3763. (3.) Jacobs ET, Thomson CA( Flatt SW. et al. Vitamin D and breast cancer recurrence in the Women's Healthy Eating and Living (WHEL) Study. Am J Clin Nutr. 2001;93(1):108-117. (4.) Fleischauer AT, Simonsen N, Arab L. Antioxidant supplements and risk of breast cancer recurrence and breast cancer-related mortality among postmenopausal women. Nutr Cane. 2003:46(1): 15-22. (5.) Ogunleye AA, Xue F. Micheis KB. Green tea consumption and breast cancer risk of recurrence: a meta-analysis. Breast Cancer Res Treat 2010;119(2):477-484. (6.) Henneicke-von Zepelin HH, Meden H, Kostev K, Isopropanolic black cohosh extract and recurrence-free survival after breast cancer. Int J Clin Pharmacol Ther. 2007;45:143-154. (7.) Davis. V, Jayo MJ. Ho A. et al. Black cohosh increases metastatic mammary cancer in transgenic mice expressing c-erbB2. Cancer Res. 2008:68:8377. (8.) Hertz N, lister RE. Improved survival in patients with end-stage cancer treated with coenzyme Q(10) and other antioxidants: a pilot study. J Int Med Res. 2009:37(6): 1961-1971. (9.) Yokoe T. lino Y, Takei H, et al. HLA antigen as predictive index for the outcome of breast cancer patients with adjuvant immunochemotherapy with PSK. Anticancer Res. 1997;17(4A);2815-2818. (10.) Saez MC. Barriga C. Garcia JJ, et al. Melatonin increases the survival time of animals with untreated mammary tumours: neuroendocrine stabilization. Mol Cell Biochem. 2005;278(1-2):15-20.
Table 1: The Role of Naturopathic Care After Conventional Breast Cancer Treatment Complementary Care Help patients For those taking hormone-modifying medications, offer recover from natural treatments that reduce side effects and side effects potential drug toxicity. Educate patients about and and long-term avoid contraindications. Offer agents that act toxicities synergistically (see Table 2, p.78). that may result from surgery, chemotherapy, and/or radiation and accompanying oral medications. Basic Naturopathic Care Inspire Provide evidence-based supplements and patients with botanicals that have been found to research on reduce the risk of recurrence of lifestyle breast cancer (see Table 4, p. 81). changes found to dramatically reduce the risk of recurrence and help them implement these lifelong goals (see Table 3, p 80) Optimize Optimize Optimize immune Reduce Optimize function of antioxidant function and exposure to detoxification status reduce environmental pathways. primarily inflammation toxins through diet. Improve Manage metabolism response of to stress hormones. and encourage mindfulness. Individualized, Constitutional Treatment In addition to the above, use naturopathic foundational principles to evaluate and treat the individual. Consider the following constitutional categories, take a thorough history, do a physical examination, test your clinical hypotheses, and methodically treat each layer until a healthy constitution is restored. Detoxification Inflammation Stress Response Take a toxic Question and examine for Take a social exposure symptoms and signs of history, life history and inflammation. stressor, and listen for trauma history and other symptoms observe for signs that may relate of tension in face, to toxicity of muscles. posture, chemicals, and pulse. metals, hormones, etc. (1) Test: Test: Test: * single * appropriate conventional * methylation SNPs nucleotide markers of inflammation such as (12), (13) polymorphisms CRP7, (8) (2) * organic acids * food allergies * for hepatic Neurotransmitters: stress (3) (catecholamines, GABA, etc.) (14) * amino acids * digestive function, digestive * DHEA, diurnal related to infection, flora and dysbiosis Cortisol rhythm detoxification (9) (15), (18) (4) * specific * thyroid function and * serum amino acids toxin load (5) autoimmune antibodies (10), for precursors to (11) neurotransmitters and GABA (17) * estrogen metabolism (6) Educate/coach: Educate/coach: Educate/coach: * tools for * avoid pro-inflammatory foods * schedule avoidance of (20) modifications to xenoestrogens reduce rushing and other concerning toxins determined by above testing (18) * foods and * avoid persona! allergens * cultivate inner beverages for peace with detoxification mindfulness, qi (19) gong, yoga, tai chi, etc. * increase anti-inflammatory * optimize fitness foods (21) (22-25) Treatment: Treatment: Treatment: * replenish * treat dysbiosis; restore * botanicals for deficient amino proper balance of bowel flora calming the mind acids (28) and Shen (35) * safely timed * implement therapeutic * amino acids based toxin-specific anti-inflammatory/anti-allergic on deficiencies + cleansing until diet L-theanine (36) normal on retesting (26) * optimize * naturopathic and Chinese * adrenal tonics 2:16oh-estrone Medicine protocols to reduce based on (27) chronic inflammation such as test results curcumin, fish oil (29-32) * quarterly * Optimize thyroid function * body-mind-spirit 10-day cleanse (33), (34) therapies * energetic/meridian treatments (37) (1.) Marchese M. Environmental exposure history questionnaire. Permission granted by author Available at: www.drmarchese.com/images/Exposure.Questionnaire.doc. Accessed December 6, 2011. (2.) Consider the Genova Diagnostics Laboratory DetoxiGenomic Profile. Available at: http://www.gdx.net/product/10038. Accessed (3.) December 6. 2011 (4.) Consider Metametrix Clinical Laboratory's Urine Organic Acids Profiles. Available at: http://www.metametrix.com/test -menu/profiles/organic-acids/organix-comprehensive. Accessed December 6, 2011. (5.) Consider Metametrix Clinical Laboratory's Amino Acid 20 plasma profile. Available at: http://www.metametrix.com /test-menu/profiles/amino-acids/amino-acids-20-plasma. Accessed December 6, 2011. (6.) Consider Metametrix Clinical Laboratory's Toxic Effects Profiles. Available at: http://www.metametrix.com /test-menu/profiles/categorized. Accessed on December 6, 2011. (6.) Consider Genova Diagnostic Laboratory Estrogen Metabolism Assessment. Available at: http://www.gdx.net/ core/one-page-test-deschptions/Estrogen-Metabolism-Assess- Test-Descriptton.pdf. Accessed December 6, 2011. (7.) Pierce GL, Ballard-Barbash R, Bernstein L, et al. Elevated biomarkers of inflammation are associated with reduced survival among breast cancer patients. J Clin Oncol. 2009:27(21):3437-3444. (8.) Han Y. Mao F. Wu Y, et al. Prognostic roie of C-reactive protein in breast cancer: a systematic review and meta-analysis. Int J Biol Markers. Epub2011 Dec 2:0:105301/JBM.2011.8872. (9.) Elena M. Health, probiotics, and inflammation. J Clin Gastroent, 2008; 42:S177-S178. (10.) Giam C, Fierabracci P. Bonacci R. et al. Relationship between breast cancer and thyroid disease: relevance of autoimmune thyroid disorders in breast malignancy. J Clin Endocrinol Metab. l996; 81(3):990-994. (11.) Giustarini E. Pinchera A. Fierabracci R et al. Thyroid autoimmunity in patients with malignant and benign breast diseases before surgery. Eur J Endocrinol. 2006;154(5):645-649. (12.) Thompson PA, Shields PG, Freudenheim JL, et ai. Genetic polymorphisms in Catechoio-O-methyltransferase, menopausal status, and breast cancer, Cancer Res. 1998;58:2107-2110. (13.) Shrubsole MJ, Gao YT. Cai Q, et al. MTHFR polymorphisms, dietary folate intake, and breast cancer risk: results from the Shanghai Breast Cancer Study. Cancer Epidemiol Biomarkers Prev, 2004;13(2):190-196. (14.) Consider NeuroScience comprehensive Neuro- endo-immune profile or Neuroscreen. Available at: https://www.neuroreIief.com/index.php?p=testing. Accessed December 9, 2011. (15.) Lopez-Marure R, Contreras PG, Dillon JS. Effects of dehydroepiandrosterone on proliferation, migration, and death of breast cancer ceils. Eur J Pharmacol. 2011;660(2-3):268-274. (16.) Bower JE, Ganz PA, Dickerson SS, et al. Diurnal Cortisol rhythm and fatigue in breast cancer survivors. Psychoneuroendocrinology. 2005;30(1):92-100. (17.) Opolski A. Mazurkiewicz M, Wietrzyk J, et al. The role of GABA-ergic system in human mammary gland pathology and in growth of transplantable murine mammary cancer. J Exp Clin Cancer Res. 2000; 19(3):383-390. (18.) Consider Marchese M. 8 Weeks to Women's Wellness. Petaluma, CA; 2011; also Alschuler L, Gazella K. Five to Thrive: Your Cutting Edge Cancer Prevention Plan. E! Segundo, CA; 2011. (19.) Marchese. Op cit (20.) Consider Black J. The Anti-Inflammatory Diet and Recipe Book. Alameda, CA; 2006. (21.) Consider anti-inflammatory resources such as those at drweil.com. Anti-inflammatory food pyramid chart available at: http://www.drweil.com /drw/u/ART02995/Dr-Weil-Anti-inflammatory-Food-Pyramid.html. Accessed December 6, 2011. (22.) Matattm Y, Arcnev M, Stewart BR. EKecte of mindMness-based stress reduction (MBSR) on health among breast cancer survivors. West J Nurs Res. 2011; 33(8):996-1016. (23.) Ulger O, Yali NV. Effects of yoga on the quality of life in cancer patients. Complement Ther Clin Pract. 2010; 16(2):60-63. (24.) Janelsins MC, Davis PG, Wideman L, et al. Effects of Tai Chi Chuan on insulin and cytokine levels in a randomized controlled pilot study on breast cancer survivors. CJin Breast Cancer. 2011/11(3):161-170. (25.) Saxton JM, Daley A, Woodroofe N, et ai. Study protocol to investigate the effect of a lifestyle intervention on body weight, psychological health status and risk factors associated with disease recurrence in women recovering from breast cancer treatment. BMC Cancer. 2006;6:35. (26.) Marchese. Opcft.:125-151. (27.) Marchese. Op cit.:138-139. (28.) Plummer, S, Garaiova I, Pevac-Djukic M. Probiotics and gastrointestinal hearth [online article]. Naturopath Doctor News Rev. 2010. http://ndnr.com/web-articles/ gastrointestinai/probiotics-and-gastrointestinal- health.Accessed December 6, 2011. (29.) Dharmananda S. Reducing inflammation with diet and supplements: the story of eicosanoid inhibition (online article]. Institute for Traditional Medicine, http://www.itmonline.org /artstox.htm. Accessed December 6, 2011. (30.) Schaffer M, Schaffer PM, Zidan J, et al. Curcuma as a functional foods in the control of cancer and inflammation. Curr Opin Clin Nut Metab Care. 2011; 14(6):588-597. (31.) Jurenka JS. Anti-inflammatory properties of curcumin, a major constituent of Curcuma long; a review of preclinical and clinical research. Mem Med Rev. 2009;14(2):141-153. (32.) Berqum IM, Edwards IJ, Chen YQ. Multi- targeted therapy of cancer by omega-3 fatty acids. Cancer Lett. 2008;269(2):363-377. (33.) Turker 0. Kumanlioglu K, Karapolat I. et al. Selenium treatment in autoimmune thyroiditis: 9-month follow-up with variable doses. J Endocrinol. 2006;190(1):151-156, (34.) Brownstein D. Overcoming Thyroid Disorders. West Bioomfield, Ml: Medical Alternatives Press; 2002. (35.) Koetter U, Barrett M, Lacher S, et al. Interactions of Magnolia and Ziziphus extracts with selected central nervous system receptors. J Ethnopharmacol. 2009; 124(3):421-425. (36.) Nathan PJ, Lu K, Gray M, et al. The neuropharmacology of Uheanine(N-ethyl- L-glutamine); a possible neuroprotective and cognitive enhancing agent. J Hert) Pharmacother. 2006; 6(2):21-30. (37.) Errington-Evans N. Acupuncture for anxiety. CNS Neurosd Ther. 2011 Jun 7. doi:10.1111/j.1755-5949.2011.00254.x.
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