Budwig Protocol

Η Dr. Johana Budwig (1908-2003), Γερμανίδα χημικός, φαρμακολόγος και φυσικός εξέλιξε τη δίαιτα Budwig ή αλλιώς Budwig protocol , το οποίο στηρίζεται στην κατανάλωση τροφών πλούσιων σε λινολεϊκό και λινολενικό οξύ, πρακτικά την ανάμειξη λινελαίου ή λιναρόσπορου με τυρί cottage. Το πρωτόκολλο αυτό θεωρείται από πολλούς εναλλακτικούς ως ευεργετικό (να μην πούμε θεραπεία και μας κυνηγήσουν) σχεδόν όλων των μορφών καρκίνου, κυρίως αυτών του μαστού και του προστάτη (των ορμονοεξαρτώμενων δηλαδή). Αξίζει να το ψάξετε περισσότερο. Ένα βίντεο μπορείτε να δείτε εδώ.

Viewing the Budwig Protocol

As usual, when I discover something extremely beneficial, I try to touch every life I can with the information. In this case, I find myself repeating this “news” so much I am writing my interpretation of the information to pass out along with the websites I gleaned it from. Please correct me if you disagree with (or have additional information to consider) this summary of the websites I’ll list later. Certainly, I cannot say this is a cure-all for cancer since diet, emotional lifestyles, etc. figure into the mix; but so many have been helped that the joy has been spreading. Thus, it must be stated that the information provided needs to be scientifically substantiated despite numerous testimonies from people who seem to have benefitted from Dr. Budwig’s work. Statements herein have not been evaluated by the FDA, are provided for information purposes only, and are not intended for medical claims or to take the place of a physician. These products and/or statements are not intended to diagnose, treat, cure or prevent any disease.
This past summer we noticed my mother’s minister (diagnosed with cancer) improving in energy over a period of four Sundays, even while the debilitating, weakening process of chemotherapy continued on and on. He explained that he was on the Budwig Protocol and a diet similar to the one Bill is using to (as of 4/15/2000) reverse his heart disease. To digress with a little bit of history here, first: Dr. Otto Warburg (1931 and 1944 Nobel Prize winner) stated, “...the cause of cancer is no longer a mystery, we know it occurs whenever any cell is denied 60% of its oxygen requirements.” Then, about twenty years later a (seven-time Nobel Prize nominee) German medical doctor and PhD scientist, Dr. Johanna Budwig, studied 1000’s of blood samples and discovered healthy people had a higher content of omega 3 oils in their blood than those who are ill. Dr. Budwig proclaims, "It is amazing how quickly the tumor, for instance with colon cancer, is being eliminated. Even with an old patient of 84 years who was scheduled for an operation because of his colon threatening to become blocked, I was able to achieve the complete elimination of the tumor and the patient’s restoration to health within a few days. These are not isolated cases, in fact 99% of the sick that come to see me to use the biological method of cancer therapy, are cancer patients who have had operations and radiation sessions, and who were diagnosed as being too far advanced for another operation to be of any help. Even in these cases health can be restored, usually within a few months, I would say in 90% of cases."
Also, “a Purdue University study showed that kids low in Omega-3 essential fatty acidsare significantly more likely to be hyperactive, have learning disorders, and to display behavioral problems. Omega-3 deficiencies have also been tied to dyslexia, violence, depression, memory problems, weight gain, cancer, heart disease, eczema, allergies, inflammatory diseases, arthritis, diabetes, and many other conditions. Over 2,000 scientific studies have demonstrated the wide range of problems associated with Omega-3 deficiencies.” Pertaining to Dr. Budwig’s method, Dr. Dan C. Roehm was quoted as saying, “cancer is easily curable” and “...this diet is far and away the most successful anti-cancer diet in the world.” He added, “I only wish that all my patients had a PhD in Biochemistry and Quantum Physics to enable them to see how with such consummate skill this diet was put together.” This is the simple formula by Dr. Budwig that can be created in a homemaker’s kitchen: she simply combined omega 3 fatty acids with sulfuric protein to produce a new food that was “different from either of its components”6 and which brought oxygen to the cells. “...By combining the protein with the oil, the oil becomes water soluble in the body and can be absorbed more readily. It can enter the smallest capillaries, dissolving any of the undesirable fats and cleaning out the veins and arteries.” What did she use? Flaxseed oil and the German quark - or organic, non-fat (if possible) cottage cheese in America. Is there an American company that provides quality flaxseed oil? Bruce Barlean (from the Barlean Company) traveled to Germany to meet Dr. Budwig. “At first Dr. Budwig seemed a bit suspicious of the fresh taste she experienced with the Barlean's product,’ says Bruce. Dr. Budwig (who we understand died in 2003 at the age of 96 -R.H.) soon endorsed the product... Barlean’s presses the flax seed on the same day orders are received, then ships them out the next morning via 3-day air to refrigerated shelves in retail stores. Consumers receive oils that are as fresh as those produced by small seed oil pressers a century ago.” Some competitors also, we understand, overpress the flax, resulting in “damaged seed oil, increased temperature, induced deterioration...” These higher temperatures are a concern because “the substance that is so important for respiration is very heat sensitive. It will be destroyed at approximately 42/ C (orapproximately 108/ F).”10 Allen (information on him later) cautions, “If you purchase flaxseed oil in a bottle from a store, make sure it has been stored in a refrigerator or freezer. Flaxseed oil is ultra-sensitive to light, air, and heat (in that order). Barlean’s provides a press date and a four-month expiration date (some marketers are using 6 – 9 month expirations). Also, it helps to know that one ounce of Barlean (company) flax oil equals two tablespoons.”

To repeat, the omega 3’s in the flax oil (FO) and the sulfuric protein in the cottage cheese (CC) combine to make a “new” water-soluble food that brings respiration to the cells. The body also converts it to EPA/DHA,11 as well (which are reportedly good for the heart). Check the websites at the end for a list of diseases that this combination seems to help. In a session where questions are answered on a German website (you have to get past a lot of strange beliefs and ideas unrelated to Dr. Budwig’s Protocol)12 frequently by direct translations of Dr. Budwig’s books into English (only two of her many books are in English), much truth can be found. For example, read this answer to questions 3 and 4: Dr. Budwig’s interpreter explains, “We take in too many ‘electron thieves’ because we eat foods and poisons which block cell respiration. Known ‘electron thieves’ are, for example, margarine, butter, animal fats, nitrates, radiation, and zycostatics (chemotherapy). They all prevent the uptake of electrons. Interestingly, belonging to this also are anti-oxidants like, for example, vitamins from a certain level on…” Dr. Budwig was very protective over her work and would take on anyone who would change it, according to two men I have met who had personal contact with her, Allen Wenzel and Cliff Beckwith. These two have been of immense help to me in my research. Allen (www.allensclub.com) got involved with this 13 years ago because of his caring heart which is manifested in his much-discounted flax oil prices. He warns to be careful – some companies try to make it look like they have kept the original lignans in the oil by adding ground flax seed afterward. He also can explain the details of the Barlean Company’s cautions concerning the flax oil’s heat, light, and oxygen
exposure. He is such a knowledgeable resource and so willing to answer questions. He also has important information about the original formula of Essiac tea, which has been praised by thousands as being significantly beneficial too.
Clifford Beckwith ended up making a tape to help people in 1998 (which he has continued to update). He has given away 5500 copies since he produced it, and Dr. Budwig herself liked it so much she invited him to her 88th birthday party in Germany. This was quite a compliment since she was very particular about how her research was represented. To obtain a tape (or CD), you can find him at www.BeckwithFamily.com. He was diagnosed with prostate cancer at age 69 simultaneously with another man having the same kind; but that man died 6 months later. Mr. Beckwith is now 83. His tape (or CD) explains how much to take of the FO/CC and gives multitudinous testimonies of survivors. Mr. Beckwith has crucial information on his tape that space does not permit discussing here. He says the following on a portion of his tape/CD transcript that you can find in its totality online at www.BeckwithFamily.com/Flax1.html: “Depending on the severity of the condition she had her patients use 3 to 6 tablespoons of flaxseed oil a day, with at least 4 oz or 1/2 cup of cottage cheese per day. “I would use at least 1/4 cup cottage cheese per tablespoons of oil. If 4 or less tablespoons were used per day and I'd split that up so that I took them at 4 different times, although there are no specific guidelines. I have learned recently that Dr. Budwig recommends that the oil and the cottage cheese be thoroughly mixed before eating it. I have realized that an excellent approach would be to mix however many tablespoons of flax oil one plans to use each day in a bowl with at least a half cup of cottage cheese and some fruit (such as crushed pineapple or frozen strawberries), put it in the refrigerator, and eat a portion of it at different times during the day. For two and a half years I put a half cup of cottage cheese in a bowl, added 2 tablespoons of flaxseed oil, mixed in some crushed pineapple or frozen strawberries or honey and took it to school for lunch - that tasted good. An excellent method of mixing is with the use of a small hand-held blender. Milk or juice may need to be added to make the mixture thin enough so that the little motor may be able to handle it. “After 3 months of treatment, the blood would be bright red, the tumors disappearing, and the amount of oil reduced to 1 Tbs. per day per hundred pounds body weight for maintenance. Yogurt will take the place of cottage cheese but more of it is needed; actually, about three times as much and if fruited yogurt is used it would need to be even more. “Flaxseed oil is increasingly available in health food stores though it must be kept fresh and cold. It will keep a year in a freezer, 4 months in a refrigerator, but only 3 weeks at room temperature.” It is also significant to note that in the book, How to Fight Cancer and Win, a menu was given using Dr. Budwig’s methods for a seriously ill patient named Jane D. If our calculations are correct in sorting out the tablespoons of flax oil from the rest of the diet that day, it appears that she was given up to approximately ten tablespoons of flax oil. Finally, for those concerned with weight gain or loss, a thought-provoking article by Jade Butler, “Weight Loss with Flaxseed Oil, the Non-Fat Fat,” can be found at http://www.barleans.com/literature/flax/61-weight-loss.html

Πηγή: http://www.barleans.com/

Mistletoe:Το γνωστό μας γκυ

Ένα ακόμη "θαυματουργό" δημιούργημα της φύσης είναι το γκυ. Διάφοροι μύθοι και παραδόσεις συνδέονται με αυτό, αυτό όμως που δεν είναι τόσο γνωστό είναι οι θεραπευτικές του ιδιότητες, ειδικά αυτές που συνδέονται με την καταπολέμηση του καρκίνου και τη συρρίκνωση των όγκων. Στις ΗΠΑ η χρήση του είναι απαγορευμένη, αλλά στην Ευρώπη και ιδιαίτερα στη Γερμανία χρησιμοποιείται ευρέως. Περισσότερα μπορείτε να βρείτε εδώ, εδώ και εδώ.

Φλεγμονή και Καρκίνος

Παρακάτω μπορείτε να διαβάσετε ένα αρθρο του Εθνικού Ινστιτούτου των ΗΠΑ για τον Καρκίνο (NCI, http://www.cancer.gov/) σχετικά με τη σύνδεση της χρόνιας φλεγμονής και την γέννεση και πολλαπλασιασμό των καρκινικών κυττάρων. Στο σύνδεσμο μετά το άρθρο μπορείτε να διαβάσετε για την ανακάλυψη των ερευνητών του Πανεπιστημίου της Καλιφόρνια στο San Diego, αναφορικά με τη μοριακή σχέση της φλεγμονής και του καρκίνου.

Executive Summary of Inflammation and Cancer Think Tank

Inflammation is a response to acute tissue damage, whether resulting from physical injury, ischemic injury, infection, exposure to toxins, or other types of trauma. It can play a role in tumor suppression by stimulating an antitumor immune response, but more often it appears to stimulate tumor development. Epidemiologic and clinical research indicates an increased risk of certain cancers in the setting of chronic inflammation. For example, two inflammatory bowel diseases, ulcerative colitis and Crohn’s disease, predispose to cancers of the intestinal tract. Basic research, in turn, has shown that many of the processes involved in inflammation (e.g., leukocyte migration, dilatation of local vasculature with increased permeability and blood flow, angiogenesis), when found in association with tumors, are more likely to contribute to tumor growth, progression, and metastasis than to elicit an effective host anti-tumor response.
Interestingly, inflammation functions at all three stages of tumor development: initiation, progression and metastasis. Inflammation contributes to initiation by inducing the release of a variety of cytokines and chemokines that alert the vasculature to release inflammatory cells and factors into the tissue milieu, thereby causing oxidative damage, DNA mutations, and other changes in the microenvironment, making it more conducive to cell transformation, increased survival and proliferation.
Chronic inflammation appears to contribute to tumor progression by establishing a milieu conducive to development of different cancers. However the precise mechanism by which it does so remains to be determined. Infection is a common cause of inflammation, and evidence indicates that the presence of microbes can be a cofactor in the tumor promoting effects of inflammation.
Tumor cells produce various substances that attract inflammatory cells, which then secrete an array of soluble mediators. These further stimulate proliferation of the initiated cell, tissue disruption in the stroma, and tumor growth. Leukocyte infiltration, and particularly macrophages, can lead to enhanced angiogenesis, which is associated with a poor prognosis in some tissues.
The role of inflammation in metastasis is less well defined than its roles in cancer initiation and progression. The soluble mediators secreted by tumor-associated leukocytes promote cell motility, and induce angiogenesis, vascular dilation and extravasation of tumor cells. Particularly interesting is the recent finding that metastatic cells leave the tumor as microcolonies, containing lymphocytes and platelets as well as the tumor cell. Inflammation continues to play a role at metastatic sites by creating a cytokine milieu conducive to tumor growth.
Although there is a strong association between chronic inflammation and cancer, investigators have not yet uncovered all the molecules, pathways, and mechanisms involved, and numerous questions remain to be resolved about the mechanisms and targets of pro-inflammatory mediators of tumor development. These are articulated in the body of the report and the recommendations that follow. Furthermore, to understand the role of inflammation in tumor formation and progression, we also need to understand its role in maintaining homeostasis and responding to damage in normal tissue. An appreciation of the importance of inflammation has already led to clinical trials of anti-inflammatory drugs (e.g., COX-2 inhibitors) for cancer prophylaxis and treatment. The results obtained will provide clues to the dominant mechanisms at work, and will help in the design of a new generation of interventions.

Introduction
Inflammation involves a complex set of interactions between soluble mediators and immunocytes, triggered in response to tissue injuries that include trauma, infection, toxic agents and autoimmune responses. Such injuries trigger a cascade of cellular infiltrations and cytokine releases that result in local cellular proliferation and repair of tissue damaged. While sustained proliferation alone is insufficient to initiate cancer, a functional relationship between inflammation and cancer has been recognized for a long time. The current discussions centered on our current understanding of the role of inflammation in cancer initiation, progression and metastasis and highlighted areas in which there are major, unresolved questions.

Discussion Themes
I. Inflammation and Cancer Initiation
Although inflammation is a necessary response to clear viral infections, to repair tissue insults - either chemical exposure or injury- and suppress tumor initiation/progression, chronic inflammation is also clearly correlated with increased risk of developing cancer. Inflammation may become chronic either because an inflammatory stimulus persists or because of dysregulation in the control mechanisms that normally turn the process off. Many of the cells, cytokines and systems (e.g., leukocyte migration, dilatation of the local vasculature and angiogenesis) involved in inflammation are also found in a variety of tumors. Chronic inflammation caused by intestinal flora leading to the inflammatory bowel diseases, ulcerative colitis and Crohn’s disease, is clearly linked with a higher incidence of colon cancer. The use of mouse models has furthered our understanding of the contributing cellular and molecular factors in colon cancer. Similarly, dietary intake of proinflammatory carcinogens has been associated with prostate cancer. Chronic inflammation resulting from esophageal reflux gives rise to gastroesophageal reflux disease (GERD) and Barrett’s esophagus, also linked with a higher incidence of cancer. In the case of Barrett’s, chronic inflammation leads to the production of TNF". This, in turn, induces the nuclear translocation of $-catenin and transcriptional activation of proliferative signals.
The molecular basis for the increased risk is thought to be two-fold: 1) generation by inflammatory macrophages of reactive oxygen (ROS) and nitrogen (RNS) species leads to DNA damage in the surrounding epithelial cells and 2) enhanced proliferative signals mediated by cytokines released by inflammatory cells increase the number of cells at risk for mutations. In combination, DNA damage and proliferative signals create a circumstance conducive to the development of cancer. ROS and RNS can cause extensive damage to essential proteins (e.g., DNA repair enzymes), to DNA and to the mitochondria through a series or cascade of reactions. Among the many possible mutations that may result from oxidative DNA damage are the formation of single- and/or double-stranded breaks and the stimulation of recombination events. Free-radical damage can be caused by the pro-inflammatory prostaglandin enzyme, cyclooxygenase 2 (COX-2), which leads to the production of highly reactive peroxide intermediates at high levels in a local tissue environment. Drugs that selectively inhibit the COX-2 enzyme, including NSAIDs, are being studied to determine their impact on local tumor biology and development, and in clinical trials. Recent studies have suggested protective effects of COX-2 inhibitors in colorectal cancer and breast cancer. Several small studies of colorectal, non-small cell lung cancer, breast, cervical and esophageal tumors have shown that increased COX-2 levels are associated with poor clinical prognosis. Animal models for colorectal cancer show similar patterns of COX-2 expression and response to COX-2 inhibitors as human neoplasias.
Inflammation results in the recruitment of leukocytes secreting a variety of proliferative cytokines and angiogenic factors to the site of tissue insult. These cytokines, necessary for proper wound healing, stimulate epithelial proliferation, which if unchecked could lead to dysplasias and ultimately cancer. Paradoxically, cytokine deficiency (e.g., GM-CSF, IL-2 and IFN() can also lead to tumor development. Immune homeostasis consists of a succession of pro- and anti-inflammatory signals. Loss of the anti-inflammatory signals leads to chronic inflammation and proliferative signaling. The mechanisms involved in the interplay of microbes and defective immune homeostasis is an area that requires further delineation. Future steps will involve clinical studies to determine whether individuals have polymorphisms or genetic variations that affect specific cytokine pathways.
The discussion highlighted the duality of inflammation in controlling and promoting tumor development. While chronic inflammation can establish conditions conducive to tumor initiation and progression, compelling data also suggest that the presence of lymphocytic infiltrates in a variety of tumors is associated with a good clinical outcome. The major challenge in this area is to understand the balance between inflammatory tumor suppression and promotion and how to control it.

II. Inflammation and Cancer Progression
It is generally accepted that chronic inflammation – triggered by toxins, microbes or autoimmune reactions – plays a major role as a tumor promoter. However, the precise function of inflammation in tumor progression remains to be elucidated. Tumor cells produce various cytokines and chemokines that attract leukocytes, which in turn produce cytokines and chemokines that stimulate further tumor cell proliferation; the inflammatory tumor microenvironment is characterized by the presence of host leukocytes both in the stroma and around the tumor. A developing neoplasm can contain a diverse leukocyte population, including neutrophils, dendritic cells, macrophages, eosinophils, mast cells and lymphocytes. These inflammatory cells secrete an array of cytokines, interleukins, interferons and other soluble mediators and further induce secretion of cytokines by resident stromal cells.
Interestingly, both cytokines that promote and suppress proliferation of the tumor cells are produced. As in the case of cancer initiation, it is the imbalance between the effects of these two classes of activity that results in tumor promotion. For example, in the presence of GM-CSF and IL-4, monocytes differentiate into immature dendritic cells, which migrate into inflamed peripheral tissue, capture antigens and then migrate to lymph nodes to stimulate T lymphocyte activation. Deletion of GM-CSF from Polyoma T transgenic mice reduces cancer progression. This is correlated with reduced macrophage infiltrates, which play a major role in the transition from adenoma to carcinoma. GM-CSF vaccines that stimulate dendritic cell and T cell responses are being combined with anti-CTLA4 treatment in clinical trials to potentiate the anti-tumor response.
In contrast, IL-6 and CSF-1 secreted by tumor cells can skew monocyte differentiation towards the macrophage lineage. Although tumor associated macrophages can kill tumor cells when activated by IL-2, IL-12 or interferon, they also produce a host of compounds – angiogenic factors, growth factors, proteases and cytokines – that either contribute to cancer progression or blunt the anti-tumor response. Macrophages generate a variety of proteases, including cathepsin B, which contribute to tumor growth. Stromal fibroblasts and monocytes enhance this proteolysis. During tumor progression, the degradation of the matrix and stromal fibroblasts appears to be focal, suggesting that widespread degradation may not be necessary for tumor growth. In mammary cancer models, a variety of leukocytes are found at the tumor-stroma interface. A complex interaction between tumor, stroma and inflammatory cells results in the secretion of protease and matrix degradation and the entrapment and degradation of fibroblasts by the tumor.
Other studies have indicated that hypoxia signaling pathways are engaged very early in cancer development. Hypoxia stabilizes HIF-1" which in turn induces VEGF secretion by epithelial cells that stimulates microvascularization and angiogenesis.
The spatial relationship between inflammatory cells and tumors is now being investigated by imaging of a range of live human tumor and associated cells. Examination of the interaction reveals that although T cells will home to the tumor, they stay on the periphery and do not enter. Real-time images of mammary tumors in mice show that the tumor regions are metabolically active, compared with surrounding stroma and fat cells. These regions also have a much greater inflammatory response; associated immune cells, particulary T cells, are very active and mobile. In mammary cancer models, imaging reveals that tumor associated macrophages preferentially line up along the lumenal side of the tumor-associated vessels. Macrophages in this region are relatively static, whereas those at the stromal interface are very active and motile, suggesting differential behavior within the tumor. The functional significance of this remains to be determined.
Although the role of inflammatory cells and soluble mediators in tumor progression is now well documented, the details of the cellular and molecular interplay between stroma and tumor progression remain to be elucidated.

III. Inflammation and Metastasis
Unlike tumor progression, where the role of inflammation in promoting cancer cell proliferation and stromal/matrix degradation is reasonably well understood, the role of inflammation in metastasis is less well defined, although appears to be important. The cytokines and chemokines secreted by tumor associated macrophages and leukocytes promote cell motility and induce angiogenesis and the growth of tumor-associated vessels, providing an egress route for metastatic tumor cells. The leukocytes also promote vessel dilation and extravasation of tumor cells. Particularly intriguing is the observation that metastatic cells leave the tumor as microcolonies, containing lymphocytes and platelets, the latter allowing attachment to distal organ sites. Tumors that are unable to form such microcolonies are not malignant.
At the distal, metastatic sites, evidence suggests that inflammation continues to play a role in the establishment of metastases. At the sites of prostate cancer metastases in the bone, inflammation triggers the secretion of TGF-β by osteoclasts. TGF-β in turn induces the cancer cells to secrete PDGF which further stimulates the osteoclasts, leading to bone degradation and stimulation of cancer cell growth. PDGFR on tumor-associated endothelial cells increases their levels of bcl-2 and bcl-xl, rendering them resistant to apoptosis and chemotherapy. Similarly, in brain metastases of melanoma, astrocytic infiltrates upregulate MDR (multiple drug resistance) in the tumor cells, making them more resistant to chemotherapy.

Next Steps and Important Questions
Despite the evidence for the role of inflammation in cancer intiation, progression and metastases, other evidence suggests that cancer proceeds through inflammation-dependent and independent stages. These stages need to be defined and characterized.
To better understand the critical role of inflammation in initiating and modulating tumor behavior, host-pathogen interactions need to be defined at a molecular level, the phenotypes of hematopoeitic cells (leukocytes, monocytes, platelets, etc) involved in wound repair and tumor initiation need to be characterized and the roles of endocrinological mediators on inflammation need to be examined.
To better understand the role of inflammation in tumor progression, tumor stage should be correlated with intensity and repertoire of hematopoietic infiltrates and with the levels of cytokines and proteases present; biomarkers for pre-malignant and malignant lesions need to be identified and validated.
To better understand the role of inflammation in metastasis, better pre-clinical models need to be developed, the molecular relationship between primary and metastatic tumor cells needs to be resolved, the nature of the inflammatory responses that influence primary versus metastatic tumor need to be determined, and the role of the hematopoietic network in tumor extravasation and migration needs to be elucidated.
Real-time imaging models need to be refined and extended to allow better definition of the relationship between inflammatory and tumor cells that influence the cancer initiation, progression and metastasis process.
Tumor immunotherapy approaches should include targeted intervention of inflammation-mediated growth, pairing molecular information of inflammatory infiltrates with that of specific tumors. Therapy should be specifically directed to both the organ microenvironment and the tumor.

Specific Recommendations for the NCI:
-Continue to support basic research aimed at characterizing the role of inflammation at all stages of cancer and specifically at determining the role of hematopoeitic cells in both metastasis and normal development.
-Encourage collaborative studies between basic and clinical investigators.

-Support studies that characterize inflammatory cells in the tumor microenvironment and correlate these with clinical outcomes and prognosis
-Consider mechanisms to stimulate multi-agency, multi-institutional and transdisciplinary collaborations to more rigorously define critical interactions that occur between tumor cells and their inflammatory microenvironment.
-Sponsor a series of workshops and/or interactive fora on inflammation and cancer that interface experts from different disciplines (i.e., toxicologists, cellular and tumor immunologists, systems biologists, cancer biologists).
-Develop and standardize reagents and protocols for analysis of archived tissues. -Establish a uniform database of existing reagents and well-defined and catalogued tumor types that are or are not associated with inflammation.
-Establish and make available conditional tissue- or cell-specific pre-clinical models to study the biology of inflammation-dependent cancers and to stimulate novel prevention, diagnostic and therapeutic strategies.
-Consider mechanisms to provide investigators with

1. access to imaging tools for in vitro and in vivo analysis to characterize immunocyte/tumor interactions.
2. more sophisticated and cheaper imaging modalities, perhaps by encouraging development in the private sector through the SBIR mechanism
3. training in the use and application of imaging techniques

"Molecular Link Between Inflammation And Cancer Discovered"

http://www.sciencedaily.com/releases/2007/01/070125122719.htm

Μεταβολική θεραπεία (2)

Η συνέχεια του προηγούμενου ποστ. Περισσότερες πληροφορίες για το θέμα στους συνδέσμους στο τέλος του άρθρου.

The use of Amygdalin (Vitamin B-17) in Metabolic Cancer Therapy. Francisco Contreras, M.D.Oasis of Hope Hospital

Amygdalin's Mode of Action

Metabolism is the total function of our body. In order for our body to function properly, all its attributes (physical, mental, and spiritual) must work in harmony. Total care is the goal of metabolic therapy. Metabolic therapy elements are utilised in order to provide our human organism the best environment to combat disease and regain health.
Metabolic therapy is a non-toxic cancer treatment based on the use of Vitamin B- 17, proteolytic pancreatic enzymes, immuno-stimulants, and vitamin and mineral supplements (see Phase I and II on page 28). Laetrile (B-17) is the chief anti-tumour agent. It is a natural chemotherapeutic agent found in over 1,200 plants, particularly in the seeds of common fruits such as apricots, peaches, plums, and apples. It is also a diglucoside with cyanide radical that is highly "bio-accessible." This means that it penetrates through the cellular membrane reaching high intra-cellular concentrations easily. This cyanide radical is what once made the vitamin controversial, but over the years, it has been proven that amygdalin is completely safe and non-toxic. The normal cells in our organism contain an enzyme called Rhodanese which "neutralises" the amygdalin. This enzyme does not allow the amygdalin to release the cyanide. In this way, amygdalin only serves as glucose to healthy cells providing energy. Malignant cells do not contain this enzyme. In the absence of Rhodanese, the amygdalin is activated liberating the cyanide radical inside the malignant cell causing its destruction. This is the way God creates things: Only cancer cells are destroyed but normal ones are not affected. As the amygdalin attacks unhealthy cells, it transforms into a silicate, which is much like aspirin. It contributes greatly to pain control. The hundreds of clinical studies conducted by many competent physicians around the world, including those directed by Dr. Emesto Contreras Rodriguez at the Oasis of Hope Hospital hospital in Mexico, give us complete confidence that there is no danger.

http://www.worldwithoutcancer.org.uk/index.html

http://home.bluegrass.net/~jclark/b17_dosage.htm

http://home.bluegrass.net/~jclark/b17_dosage.htm

Amygdalin, Laetrile ή βιταμίνη B-17

Δυστυχώς αδυνατώ να μεταφράζω τα κείμενα, γι'αυτό ελπίζω στις δικές σας γνώσεις αγγλικών.

AMYGDALIN (LAETRILE) B-17
MONOGRAPHIC SUMMARY

Edited by Dr. Jose Ernesto Contreras Pulido
Clinical Research of the Hospital Ernesto Contreras In Collaboration
with: KEM S.A. Laboratories and Hospital Oasis

In spite of the great advances in the diagnosis and treatment of malignant tumors, cancer continues be one of the principal causes of death in the highly industrialized countries. It is calculated that one out of four persons will eventually die from some form of cancer. Since it is true that surgery and radiotherapy are capable of curing some patients with localized tumors and that chemotherapy has achieved cures in some ten types of malignant tumors, the general mortality rate from cancer has not improved substantially in the last 25 years and nearly 60 percent of the patients, upon being diagnosed, find that their disease is so widespread that the chemotherapy drugs currently being used, due to their high toxicity, cannot be given in dosages sufficient to destroy the large tumoral mass present in patients. Many cannot be exposed to therapy, surgery or radiotherapy because of the undesirable effects. There are several types of tumors for which there is no effective treatment yet known.

All this justifies, and even makes imperative, the search for new substances with anti-tumor effect and ideally, with little or no toxicity in therapeutic doses. In the last ten years, several vegetable and hormonal substances have been discovered with such characteristics and, therefore, many patients who formerly could not be benefited or alleviated medicinally may now be exposed to useful , antineoplastic treatments.

KEM S.A. Laboratories, with great satisfaction, is able to present a vegetable agent whose anti-tumor action was known empirically for many years, but in the last twenty years has been scientifically proven, primarily through the clinical studies directed by Dr. Ernesto Contreras Rodriguez and carried out in the Centro Medico y Hospital Del Mar at Playas de Tijuana, B.C.N. Mexico.

This anti-tumor agent is AMYGDALIN (commonly known as Laetrile).

AMYGDALIN is a natural substance that can be found in a variety of species in the vegetable kingdom. The greatest concentration is found in the seeds of the rosaceous fruits, such as the apricot pits and other biter nuts. There are many seeds, cereals and vegetables that contain minimal quantities of Amygdalin and form part of our daily diet.

Various documents from the oldest civilizations such as Egypt at the time of the Pharaohs and from China 2,500 years before Christ mention the therapeutic use of derivatives of bitter almonds. Egyptian papyri from 5,000 years ago mention the use of "aqua amigdalorum" for the treatment of some tumors of the skin. The Greeks and Romans also attributed therapeutic properties to that extract in low doses. But the systematized study of AMYGDALIN really did not begin until the first half of the past century, when the chemist Bohn discovered in 1802 that during the distillation of the water from bitter almonds hydrocyanic acid was released.

Soon many researchers became interested in analyzing this extract and so Robiquet and Boutron isolated, for the first time, a white crystalline substance which they called AMYGDALIN (from amygdala = almond)

Leiberg and Wholler in 1937 isolated an enzymatic compound from sweet almonds, also present in the biter ones, which they called emulsin. They later reported that emulsin broke AMYGDALIN down into three compounds: glucose, hydrocyanic acid, and benzaldehyde.

Studies from that time, performed by several authors, can summarize the declaration made by Otto Jacobsen in his book "Die Glucoside" in 1887: "AMYGDALIN is not toxic," and gives 99 references from studies made within the 20 years prior to his publication.

Πηγή: http://www.worldwithoutcancer.org.uk