" Kind hearts are the gardens, Kind thoughts are the roots, Kind words are the flowers, Kind deeds are the fruits. Take care of your garden, And keep out the weeds. Fill it with sunshine, Kind words and kind deeds. Henry Wadsworth Longfellow
WHICH FOOD STRATEGY TO CHOOSE? Organic? Vegetarian? Raw Foods? Blood Type Diet? Gerson? Budwig? Paleo? Dr. Hulda Clark? Keto? The Editors share different approaches to food strategies..
OCTOBER 2018 STUDY: HOW ABOUT A MEDITERRANEAN DIET? (Please scroll down for further information on different diets.)
MEDITERRANEAN VERSUS WESTERN DIET DIFFERENCES IN BACTERIA POPULATIONS IN BREAST CANCER HIGHLIGHTS FROM THE SHIVELY CA ET AL. 2018 STUDY
• "Diet modulates mammary gland microbiota populations in a non-human primate model
• Consumption of Mediterranean diet elevates mammary gland Lactobacillus abundance
• Mediterranean diet increases breast bile acid and bacterial-modified metabolites
• Consumption of Mediterranean diet decreases reactive oxygen species metabolites."
What is a Mediterranean diet? "Mediterranean dietary patterns are characterized by consumption of cereals (preferably as whole grains), legumes, nuts, vegetables and fruits, fish or seafood, white meat and eggs, and moderate to small amounts of poultry and dairy products. The principal source of dietary lipids in the Mediterranean diet is olive oil."
The objective of the Shively CA et al. study was to elucidate what microbiome populations were found in benign breast tumors and malignant breast tumors.
Conclusion: "Malignant breast tumors have lower Lactobacillus abundance compared with benign lesions, implicating Lactobacillus as a negative regulator of breast cancer."
(See Shively CA et al.m Consumption of Mediterranean Versus Western Diet Leads to Distinct Mammary Gland Microbiome Populations, Cell Rep, 2018.)
ONE OF THE EDITORS FOLLOWS A PETER D'ADAMO, ND FOOD STRATEGY
One of the Editors, Marilyn Lloyd, follows the genomic diet plan of Dr. Peter J. D’adamo. His first book, Eat Right for Your Type, was written 20 years ago and is being released with a 20th anniversary update. The basic blood type eating plan has been augmented with Dr. D'adamo's computer generated diet program, called Swami, which takes into account genomic risk factors. http://www.datapunk.net/swamiintro/.
Based on the Editor’s type A blood, first and foremost, this is essentially a plant-based diet that allows for turkey, chicken, and fish. She judiciously follows this dietary plan, because she truly believes in the lectin (surface proteins) philosophy, espousing that lectins may be either beneficial or damaging to one's health. The Editor's father had many stomach/gut issues, which she has thus far avoided by following this diet plan.
Every food type has a beneficial, neutral, or avoid label. (Based on a variety of health factors.) After 19 years of doing this diet, she has most of it memorized. She hardly ever eats adverse lectins, especially in the bean family that are harmful to her gut. She never ate tofu until the diagnosis of breast cancer. But she has eaten it ever since, predicated upon research showing the beneficial aspects of soy (organic), and soy's ability to seek out breast cancer cells in type A blood.
Where she diverges from her Swami program is with the dairy issue. Although her personal Swami results list some beneficial dairy, she abstains from dairy due to Jane Plant’s scientific writings and others on dairy’s adverse effects with breast cancer.
The Editor eats organic fruits and vegetables and meat in her home, and has encouraged her children to do the same. (NO GMOs and NO pesticides, if possible) Eating out brings challenges, but nothing is life is perfect. And that is when she sometimes diverges on some of the proteins she consumes. She has eliminated sugar from her life, except for dark chocolate, occasional cookies, family birthday cakes, and a once or twice a year indulgence in ice cream. We all do the best we can. See the Editor’s BLOG for more information. And see dadamo.com for all the scientific back up and food lists on Dr. D’Adamo’s website. There is a lot of support for newcomers.
A SECOND APPROACH ....
ONE OF THE EDITORS FOLLOWS A HULDA CLARK, PHD FOOD STRATEGY
One of the Editors strives to follow a Dr. Hulda Clark diet, eating mostly organic food, no processed food, no GMOs (no modified corn, soy, and canola), and she avoids wheat (sprayed with glyphosate in Roundup).
The Editor doesn't eat any onions, garlic, or mustard. Why? According to Dr. Clark, the parasite, Fasciolopsis buski, which has the same frequency as polonium (which initiates the cancer complex), subsists on ONION chemicals.
Dr. Clark wrote, "Onions belong to the lily family. ... Onions, garlic, leek, chives, and asparagus.... Certain non-lily plants: Cilantro, beans, peas, lentils (after cooking once), peanuts (after roasting), even aloe vera have onion chemicals. Fortunately, boiling destroys the onion factors. The solution for these vegetables is to cook them thoroughly. Unfortunately, canned and processed food escapes being cooked enough. Our plan will be to say away from these foods until the cancer is conquered, however long that might be. In one week, the Fasciolopsis population will be decimated."
In addition, the Editor avoids all soy products and is wary of apiol. Why? Dr. Clark wrote,"A food allergen, apiol, is the breast's 'enemy'. Apiol inflames the breast. What is apiol? "Apiol comes from soybeans but contaminates essentially all other oils on the market. Do not use oils unless tested for apiol." For more food tips, see Dr. Hulda Clark, The Cure and Prevention of All Cancers, New Century Press, 2009.
We just learned here in our FOODS' - ORGANIC FOOD - section of the importance, the absolute necessity, of eating organic food. But organic food is not always available. To reiterate, from the Environmental Working Group (EWG), here is their list of the "Dirty Dozen: Apples, Celery, Cherry Tomatoes, Cucumbers, Grapes, Nectarines, Peaches, Potatoes Snap peas, Spinach, Sweet Bell Peppers + Hot Peppers and Kale/Collard Greens. The Clean Fifteen include Asparagus, Avocados, Cabbage, Cantaloupe, Cauliflower, Eggplant, Grapefruit, Kiwis, mangoes, Onions, Papayas, Pineapple, Sweet Corn, Sweet Peas, and Sweet Potatoes. Note: A small amount of sweet corn, papayas, and summer squash old in the US is produced from GE seed stock." (See ewg.org)
We also just learned in our FOODS' section that there may be a potential for humans, just like plants and worms, to make energy upon eating a light-capturing metabolite of chlorophyll derived from greens and subsequent sun exposure.
Plus, we just learned that eating greens (chlorophyll) plus sunlight may help us to regenerate our antioxidants. Amazingly, once Co Q10 (ubiquinol) destroys a free radical and is oxidized to ubiquinone, it may be able to become an antioxidant again if you eat your greens and get some sun! As Michael Greger, MD, commented, "Poof ...Co Q10 is reborn."
And there is a bonus in eating cruciferous vegetables. Sulforaphane, which is an antioxidant found in cruciferous vegetables, has been found to inhibit breast cancer stem cells dangerously nurturing self-renewal.
In Yanyan Li et al.'s 2010 study, researchers discovered that the sulforaphane in broccoli/broccoli sprouts "inhibited breast cancer stem cells and downregulates the Wnt/B-catenin self-renewal pathway." Actually,"Sulforaphane eliminated breast CSCs (cancer stem cells) in vivo, thereby abrogating tumor growth after the reimplantation of primary tumor cells into the secondary mice." (See Yantan Li et al, Sulforaphane, a Dietary Compoent of Broccoli/Broccoli Sprouts, Inhibits Breast Cancer Stem Cells, Clin Cancer Res, 2010.)
*EAT NO SUGAR!
DIETARY SUGAR - OVER 100 POUNDS PER PERSON - WESTERN DIETS 2015 STUDY - COMPARABLE SUCROSE INTAKE IN MICE LED TO INCREASED BREAST CANCER TUMOR GROWTH AND METASTASIS AS COMPARED TO NON-SUGAR STARCH DIET. (WHY? INCREASED INFLAMMATORY EXPRESSION - 12-LOX AND RELATED FATTY ACID, 12-HETE.)
What is the impact of dietary sugar (sucrose) and fructose on the development of breast cancer?
The Jiang Y et al. 2015 study stated, "One proposed mechanism for the role of sugar in cancer development involves inflammation."
COXs (cyclooxygenases) and LOXs (lipoxygenases), metabolites of arachidonic acid, are involved in inflammation.
The researchers "examined the effect of sucrose enriched diets in the development of primary and metastatic breast tumor and relevant molecular mechanism primarily focusing on the 12-LOX pathway". Multiple mouse model studies were conducted to see the impact of sugar on breast cancer development and metastasis.
From the MD Anderson Press Release: "At six months of age, 30 percent of mice on a starch-control diet had measurable tumors, whereas 50 to 58 percent of the mice on sucrose-enriched diets had developed mammary tumors. The study also showed that the numbers of lung metastases were significantly higher in mice on a sucrose- or a fructose-enriched diet, versus mice on a starch-control diet."
Researcher Lorenzo Cohen, PHD, stated, “We determined that it was specifically fructose, in table sugar and high-fructose corn syrup, ubiquitous within our food system, which was responsible for facilitating lung metastasis and 12-HETE (a related fatty acid) production in breast tumors."
Conclusion from the Study: "Our data provides a strong evidence that added sugar (sucrose) accelerates the development of breast cancer partially through up-regulating expression of 12-LOX and production of 12-HETE. Therefore, dietary sugar induced 12-LOX signaling may play an important role in increased incidence for breast cancer that is associated with a high-carbohydrate diet and could be a promising target for intervention and risk-reducing strategies for breast cancer." (For the MD Anderson Press Release, see http://www.mdanderson.org/newsroom/news-releases/2015/sugar-diets-increases-risk-breast-cancer-tumors-metastasis.html, 2015 ... For the Study, see Jiang Y et al., Dietary Sugar Induces Tumorigenesis in Mammary Gland Partially Through 12 Lipoxygenase Pathway, 2915.)
*ANOTHER SUGAR AND BREAST CANCER STUDY: CAN SUGAR INTAKE, BY ITSELF, LEAD TO BREAST CANCER?
One of the researchers, Dr. Mina Bissell, of the 2014 study on sugar and cancer commented, "A dramatic increase in sugar uptake could be a cause of oncogenesis. Furthermore, through a series of painstaking analysis, we have discovered two new pathways through which increased uptake of glucose could itself activate other oncogenic pathways. This discovery provides possible new targets for diagnosis and therapeutics." (See www.sciencedaily.com/releases/2013/12/131218171230.htm.)
The researchers used a "3D assay and a breast cancer progression series as well as other breast cancer cell lines." ...."The researchers showed that overexpression of a glucose transporter in a nonmalignant human breast epithelial cell disrupted polarity and formation of organized tissue-like acini in 3D cultures and upregulated canonical oncogenic signaling." (See Onodera Y et al., Increased Sugar Uptake Promotes Oncogenesis Via EPAC/RAP1 and 0-GlcNAc Pathways, JClin Invest, 2014.)
The researchers focused on one particular glucose transporter protein in breast cells, namely GLUT3. The concentration of GLUT3 in malignant breast cancer cells was "400 times greater in malignant than in non-malignant breast cells. .... We found that overexpression of GLUT3 in the non-malignant human breast cells activated known oncogenic signaling pathways and led to the loss of tissue polarity and the onset of cancerous growth," Bissell says. "Conversely, the reduction of GLUT3 in the malignant cells led to a phenotypic reversion, in which the oncogenic signaling pathways were suppressed and the cells behaved as if they were non-malignant even though they still contained the malignant genome." (See www.sciencedaily.com/releases/2013/12/131218171230.htm.)
Avoid sugar! (The Study -See Onodera Y et al., Increased Sugar Uptake Promotes Oncogenesis Via EPAC/RAP1 and 0-GlcNAc Pathways, JClin Invest, 2014.)
(Editors' Note: But see how sugar deprivation in some people with a deficient protein may propel the tumor cells to utilize glutamine and become more aggressive. SEE THE KETOGENIC SECTION BELOW.)
*EAT A PLANT-BASED DIET?
In the Catsburg C et al. 2015 study, the dietary patterns of two cohorts of women were studied. Upon identifying three such dietary patterns as either healthy, ethnic, or meat and potatoes, the researchers found that, "The healthy dietary pattern was associated with reduced risk of breast cancer. ..... And the meat and potatoes dietary pattern was associated with increased risk in postmenopausal women only."
"Adherence to a plant-based diet that limits red meat intake may be associated with reduced risk of breast cancer, particularly in postmenopausal women." (See Carsburg C et al., Dietary Patterns and Breast Cancer Risk: A Study in 2 Cohorts, Am J Clin Nutr, 2015.)
"Recent studies evaluating natural products against cancer stem cells (failing to eradicate cancer stem cells may be the driving force behind recurrence and metastasis.) support the epidemiological evidence linking plant-based diets with reduced malignancy rates." Moselhy J et al., 2015. SEE THERAPY - RADIATION -MITIGATING DAMAGES' section.
*EATING TOO MUCH BEEF, DRINKING TOO MUCH COW'S MILK?
*TWO INTRIGUING 2015 VIRUS STUDIES
FIRST STUDY: The zur Hausen et al. 2015 study investigated whether eating too much beef and drinking too much cow's milk factor into cancer.
Commentary on the study: "The large number of breast and colon cancer cases might be due to viruses that are taken up with beef and dairy products. This is the provocative thesis of Nobel Laureate Harald zur Hausen who previously linked HPV with cervical cancer. In addition to epidemiological evidence, zur Hausen and his team have also provided experimental evidence to substantiate his thesis."
Specifically, zur Hausen "believes that the development of two of the most frequent cancers (colorectal carcinoma and breast cancer) can best be explained by infectious factors such as viruses. His thesis that the agents transferred to humans on consumption of beef and dairy products are viruses caused quite a stir. ... Zur Haussen calls viruses causative factors for human cancers; he does not like to use the word 'cause' because the development of cancer is down to many rather than just one cause. Moreover, the infectious agents can have a direct or indirect effect on the transformation of healthy cells into cancer cells."
From the zur Hausen H et al. study: "Uptake of dairy products of Bos taurus-derived milk cattle, particularly consumed at early age, is suggested to represent one of the main risk factors for the development of breast cancer." And, further, " A recent (2014) demonstration of reduced breast cancer rates in individuals with lactose intolerance seems to be in line with this interpretation."
Intriguingly "The recent isolation of a larger number of novel presumably viral DNAs from serum, meat and dairy products of healthy dairy cows, at least part of them infectious for human cells, deserves further investigation. Systemic infections early in life, resulting in latency and prevention of subsequent infections with the same agent by neutralizing antibodies, would require reconsideration of ongoing prospective studies conducted in the adult population." (For the commentary, see gesundheitsindustriebw. de/en/article/news/does-too-much-beef-and-cows-milkcause- cancer/... For the study, See zur Hausen H et al., Dairy Cattle Serum and Milk Factors Contributing to the Risk of Colon and Breast Cancers, Int J Cancer, 2015.)
*SECOND 2015 VIRUS STUDY
SECOND STUDY: Previously, the Buehring G et al team had "detected bovine leukemia virus (BLV), a common oncogenic virus of cattle, in the breast epithelium of humans". While 100% of cows in the US are infected with BLV, fewer than 5% develop leukosis, excluding them from the market place. "BLV-infected lymphocytes circulate through the blood of infected cattle. BLV also infects the mammary epithelial cells of cows, and infected cells may be found in cow’s milk, although pasteurization renders BLV noninfectious." How about in breast cancer tumors?
The Buehring G et al. 2015 study found: * 59% of breast cancer tumors have been exposed to the virus, BLV * 29% of healthy tissue was exposed to BLV * 38% of pre-malignant tissue was exposed to BLV. * Note: "The finding of BLV-related DNA in breast tissues from 29% of normal women is not surprising considering the long latency period of breast cancer, an estimated 20–30 years from the initiating carcinogenic event(s) to appearance of a clinically detectable tumor, and the life cycle of delta retroviruses (human, simian, and bovine leukemia viruses)." Sarah Yang, in Medicine and Health-Cancer, 2015, interviewed researcher Gertrude Buehring, PHD. " 'Studies done in the 1970s failed to detect evidence of human infection with BLV. The tests we have now are more sensitive, but it was still hard to overturn the established dogma that BLV was not transmissible to humans. As a result, there has been little incentive for the cattle industry to set up procedures to contain the spread of the virus.' " Note that the odds of having breast cancer are greater than 3:1 than if BLV was absent. " 'This odds ratio is higher than any of the frequently publicized risk factors for breast cancer, such as obesity, alcohol consumption and use of post-menopausal hormones,' " said Buehring. "Buehring emphasized that this study does not identify how the virus infected the breast tissue samples in their study. The virus could have come through the consumption of unpasteurized milk or undercooked meat, or it could have been transmitted by other humans." Conclusion: "Among the specimens in this study, the presence of amplified BLV DNA was significantly associated with breast cancer." (For the article, see Sarah Yang, Virus in Cattle Linked to Human Breast Cancer, Medicine and Health- Cancer, September 15, 2015. .... For the study, see Buehring G et al., Exposure to Bovine Leukemia Virus is Associated with Breast Cancer: A Case-Control Study, PLOS, 2015.)
*EAT A LOWER ESTROGEN DIETARY PATTERN?
In the Harris HR et al. 2015 study, the researchers stated that, "high endogenous hormone levels have been associated with breast cancer and dietary factors have the potential to influence breast cancer risk through effect on hormone levels."
The researchers "investigated whether a dietary pattern previously correlated with estradiol and estrone sulfate (such as red meat, legumes, and pizza) was associated with breast cancer in the prospective Swedish Mammography Cohort. After assessing the primarily postmenopausal women with dietary questionnaires, and following them for fifteen years, "A higher estrogen dietary pattern score was associated with an increased risk of breast cancer."
Specifically, "Women in the highest quartile of estrogen pattern score had a 29% increased risk of breast cancer compared to women in the lowest quartile." "Our findings suggest that a dietary pattern associated with higher estrogen levels may increase breast cancer risk. However, whether or not the influence of this dietary pattern is through a direct effect on estrogen levels deserves further study." (See Harris RR, An Estrogen Associated Dietary Pattern and Breast Cancer Risk in the Swedish Mammography Cohort, Int J Cancer, 2015.)
*EAT A KETOGENIC DIET?
WHAT IS A KETOGENIC DIET?
SUMMARY: "A ketogenic diet is one in which carbohydrates, and to a lesser extent, protein, are restricted in the diet and replaced with fat. This treatment has been effective for seizure control in epileptic children for over a century, and more recently for the treatment of obesity-related disorders. It may also provide a benefit in cancer subtypes with outcomes closely related to obesity and metabolic risk factors, such as breast cancer. It generally implements a ratio of 4:1 fat to protein and carbohydrates. However, many people will reach significant ketosis when their carbohydrates are limited to less than 50g per day, and others at around 20-30g." (See http://www.cavemandoctor.com/2013/01/01/an-introduction-a-ketogenic-diet-for-cancer/.)
The late wonderful doctor, Nicholas Gonzalez, MD, no fan of ketogenic diets, explained:
"On a low carb or no carb diet, our billions of cells in all our tissues and organs switch their energy mechanics from a process driven by glucose to one propelled by fatty acids and ketone bodies. The term 'ketosis' simply means the state in which, in the absence of sufficient glucose, our liver synthesizes ketones from acetyl coenzyme A. However, even on a no carb, all meat high-fat diet, we will still be consuming some glucose in the form of glycogen stored in muscle and organ meats, and our livers will continue to convert some dietary amino acids into glucose, so blood sugar levels never hit zero on such a diet . But in such cases, the amounts produced will be minimal. Though our normal cells do just fine in the absence of carbohydrates, cancer cells, Dr. Thomas Seyfried claims, do not. These cells, he says can never use fatty acids of ketone bodies for any significant energy production, since the citric acid cycle and electron transport in them remain basically inactive. So, he proposes, as the culmination of his exegesis, that on a high fat, moderate protein no carb diet, a cancer patient will deprive his or her deadly abnormal cells of their only useful source of energy, blood glucose, leading to apoptosis, or cell death. It's that simple. No dietary sugar, no cancer" (See http://www.chrisbeatcancer.com/dr-gonzalez-dismantles-ketogenic-diet-for-cancer/.)
*WHY KETOGENIC DIETS MAY NOT WORK?
KETOGENIC DIETS MAY NOT WORK IF TUMOR CELLS ARE DEFICIENT IN THE PROTEIN, PKCζ. EXCLUDING SUGAR MAY TRIGGER - "KICK-START" - ANOTHER PATHWAY TO USE GLUTAMINE, RESULTING IN MORE GROWTH, WORSE PROGNOSIS!
The thrust of the ketogenic diet is that excluding sugar from sugar-addicted tumor cells will starve them.
For some tumors, sugar starvation may result in "enhanced tumorigenesis".
There is a protein,PKCζ, that helps to keep the tumor cells happy and robust by lapping up sugar.
But when sugar is excluded from the diet, and there is a deficiency in PKCζ, the Ma L et al. 2013 study found that these sugar-starved tumor cells low in PKCζ may become more aggressive.
From Science Daily: "Although most cancer cells love glucose (sugar), tumors lacking PKCζ grow even better in the absence of this nutrient. Using human tumor samples and a mouse model of colon cancer, Jorge Moscat, PHD, and his team determined this growth-without-glucose paradox is because PKCζ-deficient tumors are able to reprogram their metabolism to use glutamine, another nutrient, instead. Without PKCζ around to keep them addicted to glucose, these tumors kick-start a new metabolic pathway. This altered metabolism helps PKCζ-deficient cancer cells survive in conditions that would otherwise be lethal. 'If we can find an effective way to add PKCζ back to tumors that lack it, we'd make them less suited for survival and more sensitive to current therapies,' Moscat said."
From the study: Thus, the researchers believe that PKCζ repletion - restoring the level of PKCζ - will help with sugar-depriving strategies, like the ketogenic diet. The results shown here have "important implications for the metabolic cancer therapeutics aimed at curtailing the supply or utilization of glucose. Such treatments could trigger reprogramming of the metabolic homeostasis of cancer cells, allowing for the efficient utilization of alternative nutrients and metabolic pathways for growth, thus increasing tumor aggressiveness. In this regard, our data demonstrate that PKCζ is a determinant of metabolic plasticity and suggest that attacking the Warburg effect would actually be effective in cancer therapy as long as PKCζ is activated". (EDITORS' NOTE: The late wonderful doctor, Nicholas Gonzalez, stated that he had some patients who had not done well on the ketogenic diet. While the ketogenic diet may be good for many people, perhaps this Ma L et al. study helps explain why this diet may not always work.) (For the study, see Ma L et al., Control of Nutrient Stress-Induced Metabolic Reprogramming by PKCζ in Tumorigenesis, Cell, 2013.... For the Science Daily article, see http://www.sciencedaily.com/releases/2013/01/130131144427.htm.)
* EAT KETONES TO INHIBIT METASTASIS EVEN WITH GLUCOSE?
In the 2014 Poff AM et al. study, among which one of researchers, Dr. Thomas Seyfried, elaborated a role for ketones in a cancer diet, there has now been a finding that ketone supplementation may help inhibit metastatic cancer in mice.
What are ketones? "Ketones are energy sources provided by our liver that can freely cross our blood brain barrier to provide a source of energy for our neurons (brain cells). These ketones replace glucose when it is not available, such as during fasting, during the winter months in traditional societies, and all the time in modern hunter-gathering societies like the Inuit Eskimos or Maasai tribesmen, who consume very little carbohydrate sources. Frankly, many readers of this blog likely have a significant amount of ketones floating around in their blood some mornings, and the low-carb followers even more often." (See http://www.cavemandoctor.com/2013/01/01/an-introduction-a-ketogenic-diet-for-cancer/.)
From the study: "Mitochondrial dysfunction underlies many aspects of cancer metabolic deficiency and prevents cancer cells from effectively using ketone bodies for energy. In our study, ketone supplementation decreased VM-M3 cell proliferation and viability, confirming similar results demonstrated in other cancer types in vitro.: The researchers "hypothesized that dietary administration of ketone body precursors would inhibit disease progression in vivo. Indeed, dietary administration of ketone precursors, BD and KE, increased mean survival time by 51% and 69%, respectively, in VM-M3 mice with metastatic cancer."
Supplementing with ketones "decreased proliferation and viability" of the cancer cells, "even in the presence of high glucose".
"Dietary ketone supplementation elicited anticancer effects in vitro and in vivo independent of glucose levels or calorie restriction." (See Poff et al., Ketone Supplementation Decreases Tumor Cell Viability and Prolongs Survival of Mice with Metastatic Cancer, International Journal of Cancer, 2014.)