For Informed People Using Alternative Treatments

Melissa - there are many cases, my own included, where the GLUTEN contributed to inflammation and extreme joint pain while taking an aromatase inhibitor, as soon as I stopped having any wheat products, no rye, my joint pain stopped. Completely. Stopped needing the pain medication I was taking. Several studies are going on now, showing that the wheat used today has much more gluten, and a higher protein content than what was just grown about 25 years ago. I didn't need the studies to learn how it was effecting me, such an amazing difference when I stopped eating all wheat products, and I do not have celiac disease.

Kay, I sometimes have teff, but my mainstay grain/carb is Quinoa. Organic in large bag is at most Costcos.

My hubby and I tried to go Gluten free for several months last year to see if it impacted our allergies or energy but for us we noticed no difference except that it cost a lot more money and the bread just really tasted bad IMHO. I rarely eat anything with whole grains but when I want a sandwich I do use 100% whole wheat bread. I guess since I rarely eat bread or grains I figure it is like anything else in life - moderation is the key.

Anywho, on another note I think I goofed up! I rec'd my iodine supplements in the mail yesterday and put a whole dropper in my tea because I saw on the reviews people used 1-2 drops at first (there are NO instructions on the bottle!). My husband saw me before I used the dropper today and said he was fairly certain I was supposed to only put 1 "drop" not one whole dropper's worth in there! Good thing he caught me the second day before I did it again! I need instructions! hahahaha

hjpz, sounds like you've been hitting the iodine hard! Good thing your husband was there to keep you from overdosing. Does the iodine taste funny in tea?

hjpz, Google "Iodine Protocol" It's on several websites.

Fallleaves, are you the one that's moving near Bastyr? I'd like to find out more about their work w/ Stage IV pts.

Abigail, thanks for the mushroom tip. My granny foraged for mushrooms but it's skipped a generation. Some do it locally here.

Falleaves, as far as I can understand it is important to get enough fibre, and among the reasons why is that lots of fibre helps to maintain a healthy gut flora. Basically it is important to keep the gut working hard and moving things along rather swiftly, ahem. This is, of course, not a new idea at all, but we are now beginning to find out some of the reasons why this has always been tied to health in folk and other medicine.

When you eat a lot of refined carbs and not enough fibre you basically clog up your bowel with a sludge that promotes unhealthy gut flora.

The thing that impressed me when I went about changing my diet and analyzing what I ate (which was never too terrible to begin with) was that in order to get enough fibre, veggies and nutrients from my diet, there really was hardly any room left (in my stomach, I mean, and I have a very healthy appetite) for any crap. So considering how much crap food is sold and consumed, I have to conclude that most people do not get enough fibre etc.

oatmeal to make now: ground organic raw flaxseed, coconut shreds, walnut,cranberry,pecan ground up mixture, black rasberry powder, blueberries, organic scottish oatmeal, cooked together. probably forgot something, always do

forgot ground indonesian cinnamon & ground organic turmeric in oatmeal but can't have breakfast yet: gotta do the castor oil pack, weekly 45 minutes. not fun but getting used to it. does it help? who knows

Selena, agree. I feel grateful that when I was a kid (and beyond), both my mom and grandma were good cooks and concerned with the provenance and quality of the food they cooked. My mother would find farms where she could get organic meat, for example, long before it was mainstream or trendy. When she moved to the city as a middle-aged lady, she would hop on her bike and go out to Christania - a large hippie enclave not usually frequented by middle-aged, middle class ladies with good shoes - because there she could get organic veggies. The last many years she has been baking her own sourdough, traditional, Danish rye bread (she and my bro have a running competition about who makes it better) and has become a pretty devoted locavore.

Of course, I got stupid BC anyway, but at least I know how to cook

On another note, I asked nutritionist about the NAC issue:

My question: I've also heard that N-acetyle cystine might not be good for cancer patients: http://denvernaturopathic.com/NAC2011.htm

Her response: You are taking it in a moderate dose to protect healthy cells during treatment. It is not contraindicated. You will not continue once treatment (radiation) is completed.

I also asked her about taking evening primrose oil because I'm on perception, and it is supposed to enhance effectiveness

Fatty acid protocol AFTER radiation, see rationale at the bottom. No evening primrose oil, too low dose- CLA (1) with food http://www.amazon.com/Natrol-Tonalin-CLA-1200mg-Softgels/dp/B00005317T GLA (2) with food http://www.amazon.com/Source-Naturals-Mega-GLA-Hexane-Softgels/dp/B000GFPD1U Fish oil to equal 5,000 mg combine EPA and DHA more than you take now Dark extra virgin olive oil on everything. Make sure it is FRESH. Costco has the Sicilian. About 2 tablespoons of flax seed (buy organic and keep in the freezer) ground (use small coffee grinder) and mixed into some food or drink. Do not buy the oil. If you like you may get the softgels and keep in the freezer. As the studies show it is the omega-3/omega-6 ratio than makes the difference, just as explained in the workbook. EPO does not contain enough fatty acid to be effective. You need the real deal if you are going to use it. Studies below.

(sorry, the spacing didn't come through when I copied.)

1. Nutr Cancer. 2013;65(3):451-9. doi: 10.1080/01635581.2013.756921. Dietary flaxseed-trastuzumab interactive effects on the growth of HER2-overexpressing human breast tumors (BT-474). Mason JK, Fu MH, Chen J, Yu Z, Thompson LU. Department of Nutritional Sciences, Faculty of Medicine, Toronto, Ontario, Canada. Flaxseed (FS) reduces breast tumorigenesis and human epidermal growth factor receptor 2 (HER2) expression in postmenopausal patients and animal models. The primary treatment for HER2-overexpressing tumors is trastuzumab (TRAS). FS oil enhances TRAS effectiveness in athymic mice but the FS effect is unknown and was therefore determined. Athymic mice with established BT-474 tumors were fed the basal diet (control), or 10% FS diet, with or without TRAS (2.5mg/kg) treatment for 5 wk. After 2 wk, TRAS and FS reduced tumor size with a trend for an FS × TRAS interaction; however, after 5 wk, only TRAS reduced tumor size and increased tumor apoptosis. FS did not further improve TRAS effect but increased overall survival. TRAS reduced signaling biomarkers [phosphorylated HER2 and mitogen-activated protein kinase (MAPK) proteins; Akt1, Akt2, MAPK, and estrogen receptor-a mRNA], FS reduced phosphorylated-Akt1 protein, and FS × TRAS interactions were seen for HER2 mRNA and phosphorylated-Akt1 protein. FS, with and without TRAS, increased tumor n-3 PUFA levels and serum lignans indicating potential roles in the observed effect. In conclusion, TRAS reduces tumor growth by influencing HER2 signaling. Dietary FS has minimal tumor-reducing effect, does not interfere with TRAS action, but improves overall survival in athymic mice. PMID: 23530645 [PubMed - indexed for MEDLINE] 2. PLoS One. 2009;4(4):e5342. doi: 10.1371/journal.pone.0005342. Epub 2009 Apr 28. t10c12 conjugated linoleic acid suppresses HER2 protein and enhances apoptosis in SKBr3 breast cancer cells: possible role of COX2. Flowers M, Thompson PA. Department of Nutritional Sciences, University of Arizona, Tucson, AZ, USA. mflowers@email.arizona.edu BACKGROUND: HER2-targeted therapy with the monoclonal antibody trastuzumab (Herceptin) has improved disease-free survival for women diagnosed with HER2-positive breast cancers; however, treatment resistance and disease progression are not uncommon. Current data suggest that resistance to treatment in HER2 cancers may be a consequence of NF-kappaB overexpression and increased COX2-derived prostaglandin E2 (PGE(2)). Conjugated linoleic acid (CLA) has been shown to have anti-tumor properties and to inhibit NF-kappaB activity and COX2. METHODS: In this study, HER2-overexpressing SKBr3 breast cancer cells were treated with t10c12 CLA. Protein expression of the HER2 receptor, nuclear NF-kappaB p65, and total and phosphorylated IkappaB were examined by western blot and immunofluorescence. PGE(2) levels were determined by ELISA. Proliferation was measured by metabolism of 3-(4, 5-Dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT), and apoptosis was measured by FITC-conjugated Annexin V staining and flow cytometry. RESULTS/CONCLUSIONS: We observed a significant decrease in HER2 protein expression on western blot following treatment with 40 and 80 microM t10c12 CLA (p<0.01 and 0.001, respectively) and loss of HER2 protein in cells using immunoflourescence that was most pronounced at 80 microM. Protein levels of nuclear NF-kappaB p65 were also significantly reduced at the 80 microM dose. This was accompanied by a significant decrease in PGE(2) levels (p = 0.05). Pretreatment with t10c12 CLA significantly enhanced TNFalpha-induced apoptosis and the anti-proliferative action of trastuzumab (p = 0.05 and 0.001, respectively). These data add to previous reports of an anti-tumor effect of t10c12 CLA and suggest an effect on the HER2 oncogene that may be through CLA mediated downregulation of COX2-derived PGE(2). PMCID: PMC2671134 PMID: 19399184 [PubMed - indexed for MEDLINE] 3. Int J Mol Med. 2008 Oct;22(4):433-9. Analyzing effects of extra-virgin olive oil polyphenols on breast cancer-associated fatty acid synthase protein expression using reverse-phase protein microarrays. Menendez JA, Vazquez-Martin A, Oliveras-Ferraros C, Garcia-Villalba R, Carrasco-Pancorbo A, Fernandez-Gutierrez A, Segura-Carretero A. Girona Biomedical Research Institute, Medical Oncology, Dr. Josep Trueta University Hospital of Girona, E-17007 Girona, Catalonia, Spain. jmenendez@ico.scs.es Inhibitors of fatty acid synthase (FASN), a key enzyme involved in the anabolic conversion of dietary carbohydrates to fat in mammals, are receiving increasingly more attention as they may provide therapeutic moieties for the treatment of human malignancies. Natural compounds, such as the green tea polyphenol epigallocatechin-3-gallate, have been shown to induce anti-cancer effects by suppressing FASN, which may account for the epidemiologically observed inverse correlation between green-tea drinking and cancer risk in Oriental populations. Since extra-virgin olive oil (EVOO)-derived phenolics have been suggested to possess biological activities that may explain the health-promoting effects of the 'Mediterranean diet', we evaluated their effects on the expression of FASN protein in human breast epithelial cell lines. First, we developed a reverse phase protein microspot array (RPPA) capable of rapidly assessing the relative amount of FASN protein in whole lysates from cultured human cells. Then we tested the effects of phenolic fractions from EVOO and its main constituents including single phenols (i.e. tyrosol, hydroxytyrosol, vanillin), phenolic acids (i.e. caffeic acid, p-coumaric acid, vanillic acid, ferulic acid, elenolic acid), lignans (i.e. 1-[+]-pinoresinol, 1-[+]-acetoxy-pinoresinol), flavonoids (i.e. apigenin, luteolin), or secoiridoids (i.e. deacetoxyoleuropein aglycone, ligstroside aglycone, oleuropein glycoside, oleuropein aglycone) on FASN protein expression. EVOO polyphenols lignans, flavonoids and secoiridoids were found to drastically suppress FASN protein expression in HER2 gene-amplified SKBR3 breast cancer cells. Equivalent results were observed in MCF-7 cells engineered to overexpress the HER2 tyrosine kinase receptor, a well-characterized up-regulator of FASN expression in aggressive sub-types of cancer cells. EVOO-derived lignans, flavonoids and secoiridoids were significantly more effective than the mono-HER2 inhibitor trastuzumab ( approximately 50% reduction) and as effective as the dual HER1/HER2 tyrosine kinase inhibitor lapatinib (> or =95% reduction) at suppressing high-levels of FASN protein in HER2-overexpressing SKBR3 and MCF-7/HER2 cells. EVOO single phenols and phenolic acids failed to modulate FASN expression in SKBR3 and MCF-7/HER2 cells. These findings reveal for the first time that phenolic fractions, directly extracted from EVOO, may induce anti-cancer effects by suppressing the expression of the lipogenic enzyme FASN in HER2-overexpressing breast carcinoma cells, thus offering a previously unrecognized mechanism for EVOO-related cancer preventive effects. PMID: 18813848 [PubMed - indexed for MEDLINE] 4. Clin Transl Oncol. 2006 Nov;8(11):812-20. HER2 (erbB-2)-targeted effects of the omega-3 polyunsaturated fatty acid, alpha-linolenic acid (ALA; 18:3n-3), in breast cancer cells: the "fat features" of the "Mediterranean diet" as an "anti-HER2 cocktail". Menéndez JA, Vázquez-Martín A, Ropero S, Colomer R, Lupu R. Fundació d'Investigació Biomédica de Girona Dr. Josep Trueta (IdIBGi), Girona, Catalonia. Spain. javiermenendez72@yahoo.com BACKGROUND: Data derived from epidemiological and experimental studies suggest that alphalinolenic acid (ALA; 18:3n-3), the main omega-3 polyunsaturated fatty acid (PUFA) present in the Western diet, may have protective effects in breast cancer risk and metastatic progression. A recent pilot clinical trial assessing the effects of ALA-rich dietary flaxseed on tumor biological markers in postmenopausal patients with primary breast cancer demonstrated significant reductions in tumor growth and in HER2 (erbB-2) oncogene expression. HYPOTHESIS: The molecular mechanism by which ALA inhibits breast cancer cell growth and metastasis formation may involve a direct regulation of HER2, a well-characterized oncogene playing a key role in the etiology, progression and response to some chemo- and endocrine therapies in approximately 20% of breast carcinomas. METHODS: Using HER2-specific ELISA, flow cytometry, immunofluorescence microscopy, Western blotting, RT-PCR and HER2 promoter-reporter analyses, we characterized the effects of exogenous supplementation with ALA on the expression of HER2 oncogene, a master key player in the onset and metastasis formation of breast cancer disease. Metabolic status (MTT) assays were performed to evaluate the nature of the cytotoxic interaction between ALA and the humanized anti-HER2 monoclonal antibody trastuzumab (Herceptin). To study these issues we used BT-474 and SKBr-3 breast cancer cells, which naturally exhibit amplification of the HER2 oncogene. RESULTS: ALA treatment dramatically suppressed the expression of HER2-coded p185Her-2/neu oncoprotein as determined by ELISA, flow cytometry, immunofluorescence microscopy and immunoblotting techniques. Interestingly, ALA-induced down-regulation of p185Her-2/neu correlated with a transcriptional response as no HER2 mRNA signal could be detected by RT-PCR upon treatment with optimal concentrations of ALA (up to 20 microM). Consistent with these findings, ALA exposure was found to dramatically repress the activity of a Luciferase reporter gene driven by the HER2 promoter. Moreover, the nature of the cytotoxic interaction between ALA and trastuzumab (Herceptin) revealed a significant synergism as assessed by MTT-based cell viability assays. CONCLUSIONS: i) These findings reveal that the omega-3 PUFA ALA suppresses overexpression of HER2 oncogene at the transcriptional level, which, in turn, interacts synergistically with anti-HER2 trastuzumab- based immunotherapy. ii) Our results molecularly support a recent randomized double-blind placebo-controlled clinical trial suggesting that ALA may be a potential dietary alternative or adjunct to currently used drugs in the management of HER2-positive breast carcinomas. iii) Considering our previous findings demonstrating the <> of the omega-6 PUFA linolenic acid (LA; 18:2n-6) and the <> of the omega-3 PUFA docosahexaenoic acid (DHA; 22:6n-3) and of the omega-9 monounsaturated fatty acid oleic acid (OA; 18:1n-9), it is reasonable to suggest that a low omega-6/omega-3 PUFA ratio and elevated MUFA levels, the two prominent <> of the <>, should be extremely efficient at blocking HER2 expression in breast cancer cells. PMID: 17134970 [PubMed - indexed for MEDLINE] 5. Clin Transl Oncol. 2006 Jan;8(1):15-21. Mediterranean diet, olive oil and cancer. Colomer R, Menéndez JA. Medical Oncology, Institut Catala d'Oncologia, Hospital de Girona Dr. Josep Trueta, Girona, Spain. rcolomer@ico.scs.es Olive oil is an integral ingredient of the "Mediterranean diet" and accumulating evidence suggests that it may have a potential role in lowering the risk of several types of cancers. The mechanisms by which the cancer-preventing effects of olive oil can be performed, however, are not known. We recently hypothesized that a novel molecular explanation concerning the anti-cancer actions of olive oil may relate to the ability of its monounsaturated fatty acid (MUFA) oleic acid (OA; 18:1n-9) to specifically regulate cancer-related oncogenes. Supporting our hypothesis, exogenous supplementation of cultured breast cancer cells with physiological concentrations of OA was found to suppress the overexpression of HER2 (Her-2/neu, erbB-2), a well-characterized oncogene playing a key role in the etiology, progression and response to chemotherapy and endocrine therapy in approximately 20% of breast carcinomas. OA treatment was also found to synergistically enhance the efficacy of trastuzumab, a humanized monoclonal antibody binding with high affinity to the ectodomain (ECD) of the Her2-coded p185(HER2) oncoprotein. Moreover, OA exposure significantly diminished the proteolytic cleavage of the ECD of HER2 and, consequently, its activation status, a crucial molecular event that determines both the aggressive behavior and the response to trastuzumab of Her2-overexpressing breast carcinomas. Our most recent findings further reveal that OA exposure may suppresses HER2 at the transcriptional level by up-regulating the expression of the Ets protein PEA3 -a DNA-binding protein that specifically blocks HER2 promoter activity- in breast, ovarian and stomach cancer cell lines. This anti-HER2 property of OA offers a previously unrecognized molecular mechanism by which olive oil may regulate the malignant behavior of cancer cells. From a clinical perspective, it could provide an effective means of influencing the outcome of Her-2/neu-overexpressing human carcinomas with poor prognosis. Indeed, OA-induced transcriptional repression of HER2 oncogene may represent a novel genomic explanation linking "Mediterranean diet", olive oil and cancer as it seems to equally operate in various types of Her-2/neu-related carcinomas. PMID: 16632435 [PubMed - indexed for MEDLINE] 6. J Natl Cancer Inst. 2005 Nov 2;97(21):1611-5. Effect of gamma-linolenic acid on the transcriptional activity of the Her-2/neu (erbB-2) oncogene. Menendez JA, Vellon L, Colomer R, Lupu R. Department of Medicine, Evanston Northwestern Healthcare Research Institute, Evanston, IL 60201, USA. jmenendez@enh.org Comment in J Natl Cancer Inst. 2006 May 17;98(10):718; author reply 718-20. The omega-6 polyunsaturated fatty acid gamma-linolenic acid (GLA; 18:3n-6), which is found in several plant oils and is used as an herbal medicine, has antitumor activity in vitro. We examined the effect of GLA on the expression of the Her-2/neu (erbB-2) oncogene, which is involved in development of numerous types of human cancer. Flow cytometric and immunoblotting analyses demonstrated that GLA treatment substantially reduced Her-2/neu protein levels in the Her-2/neu-overexpressing cell lines BT-474, SK-Br3, and MDA-MB-453 (breast cancer), SK-OV3 (ovarian cancer), and NCI-N87 (gastrointestinal tumor derived). GLA exposure led to a dramatic decrease in Her-2/neu promoter activity and a concomitant increase in the levels of polyomavirus enhancer activator 3 (PEA3), a transcriptional repressor of Her-2/neu, in these cell lines. In transient transfection experiments, a Her-2/neu promoter bearing a PEA3 site-mutated sequence was not subject to negative regulation by GLA in Her-2/neu-overexpressing cell lines. Concurrent treatments of Her-2/neu-overexpressing cancer cells with GLA and the anti-Her-2/neu antibody trastuzumab led to synergistic increases in apoptosis and reduced growth and colony formation. PMID: 16264182 [PubMed - indexed for MEDLINE] 7. Ann Oncol. 2005 Mar;16(3):359-71. Epub 2005 Jan 10. Oleic acid, the main monounsaturated fatty acid of olive oil, suppresses Her-2/neu (erbB-2) expression and synergistically enhances the growth inhibitory effects of trastuzumab (Herceptin) in breast cancer cells with Her-2/neu oncogene amplification. Menendez JA, Vellon L, Colomer R, Lupu R. Department of Medicine, Breast Cancer Translational Research Laboratory, Evanston Northwestern Healthcare Research Institute, 1001 University Place, Evanston, IL 60201, USA. Comment in Ann Oncol. 2005 Mar;16(3):339-40. BACKGROUND: The relationship between the intake of olive oil, the richest dietary source of the monounsaturated fatty acid oleic acid (OA; 18:1n-9), and breast cancer risk and progression has become a controversial issue. Moreover, it has been suggested that the protective effects of olive oil against breast cancer may be due to some other components of the oil rather than to a direct effect of OA. METHODS: Using flow cytometry, western blotting, immunofluorescence microscopy, metabolic status (MTT), soft-agar colony formation, enzymatic in situ labeling of apoptosis-induced DNA double-strand breaks (TUNEL assay analyses), and caspase-3-dependent poly-ADP ribose polymerase (PARP) cleavage assays, we characterized the effects of exogenous supplementation with OA on the expression of Her-2/neu oncogene, which plays an active role in breast cancer etiology and progression. In addition, we investigated the effects of OA on the efficacy of trastuzumab (Herceptin), a humanized monoclonal antibody binding with high affinity to the ectodomain of the Her-2/neu-coded p185(Her-2/neu) oncoprotein. To study these issues we used BT-474 and SKBr-3 breast cancer cells, which naturally exhibit amplification of the Her-2/neu oncogene. RESULTS: Flow cytometric analyses demonstrated a dramatic (up to 46%) reduction of cell surface-associated p185(Her-2/neu) following treatment of the Her-2/neu-overexpressors BT-474 and SK-Br3 with OA. Indeed, this effect was comparable to that found following exposure to optimal concentrations of trastuzumab (up to 48% reduction with 20 microg/ml trastuzumab). Remarkably, the concurrent exposure to OA and suboptimal concentrations of trastuzumab (5 microg/ml) synergistically down-regulated Her-2/neu expression, as determined by flow cytometry (up to 70% reduction), immunoblotting, and immunofluorescence microscopy studies. The nature of the cytotoxic interaction between OA and trastuzumab revealed a strong synergism, as assessed by MTT-based cell viability and anchorage-independent soft-agar colony formation assays. Moreover, OA co-exposure synergistically enhanced trastuzumab efficacy towards Her-2/neu overexpressors by promoting DNA fragmentation associated with apoptotic cell death, as confirmed by TUNEL and caspase-3-dependent PARP cleavage. In addition, treatment with OA and trastuzumab dramatically increased both the expression and the nuclear accumulation of p27(Kip1), a cyclin-dependent kinase inhibitor playing a key role in the onset and progression of Her-2/neu-related breast cancer. Finally, OA co-exposure significantly enhanced the ability of trastuzumab to inhibit signaling pathways downstream of Her-2/neu, including phosphoproteins such as AKT and MAPK. CONCLUSIONS: These findings demonstrate that OA, the main monounsaturated fatty acid of olive oil, suppresses Her-2/neu overexpression, which, in turn, interacts synergistically with anti-Her-2/neu immunotherapy by promoting apoptotic cell death of breast cancer cells with Her-2/neu oncogene amplification. This previously unrecognized property of OA offers a novel molecular mechanism by which individual fatty acids may regulate the malignant behavior of breast cancer cells and therefore be helpful in the design of future epidemiological studies and, eventually, dietary counseling. PMID: 15642702 [PubMed - indexed for MEDLINE]

Kay, I hear you, lol. But, happy eating!

Kayb and Momine, I am so jealous! I was raised on white bread, iceberg lettuce and t.v. dinners. I learned to cook on my own, but my mom is still eating from boxes. Of course, I have BC and she doesn't! Go figure. I honestly don't know how she doesn't at least have diabetes. She puts chocolate syrup in her morning coffee, doesn't eat vegetables (maybe peas on occasion), loves cream sauces, frequently has dessert for breakfast and dessert for dessert, and generally eats on the white end of the food color spectrum. Also she's 30 pounds overweight, doesn't exercise, and smokes (all opposite of me).

Falleaves, wow! But as you say, your mom is fine, so who the heck knows. My childhood was pretty dysfunctional in many ways, but at least we ate well and I am grateful for that.