Do No Harm: 714X Defying A Hopeless Prognosis
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DOWNLOAD E-BOOK HERE NOW!
Want to know how to eliminate cancer with confidence, with NO side effects and inexpensively?
Want to avoid deadly side effects of chemotherapy and radiation?
Does it anger you, 714X was approved in Canada in 1989, and then blocked in the USA, after a Congressman testified in Congress, it saved his life in 1993?
Why is Big Pharma so threatened it caused the BAN this book in 1996?
Did you know over 30 Million Americans died from chemotherapy and radiation in the last 20 years at a cost in the TRILLIONS of dollars?
Do you approve of the medical industrial complex collecting over $3 TRILLIONS and have block cures for cancer for the last 100 years?
Since 1980 big medicine harvested, over 100 million lives worldwide, and reaped an est. $117 TRILLION, in cancer treatment alone.
Less than 3% survive past 5 years following standard treatment.
Will you fight, for your Right to Life, to avoid being a statistic?
Knowledge is the way - out of no way out.
Order and read this book today.
CANCER and IMMUNE PROFILE BLOOD TEST
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In order to establish a baseline of health and to track progress through the treatment process, a blood test is available which will indicate the presence of primary and metastatic cancer activity, liver function and immune function.
This blood test identifies and quantifies in a highly calibrated, manually conducted test five significant markers, the HCG (human chorionic gonadotropic hormone) by the HCG-beta- chain test, PHI (phosphohexose isomerase), the key enzyme in glycolysis which is greatly increased in cancer cell lines, GGTP for liver function, CEA (carcinoembryonic antigen) and DHEA-S.
The FDA requires an adequate means to monitor and track progression or regression during clinical use of an unapproved substance within the scope of the Institutional Review Board. Beyond these requirements the test allows the following:
- For Prevention of disease:
- Establish an individual's health baseline.
- Determine an individual's immune defense status.
- In established disease:
- Determine activity status, such as primary and secondary in malignant diseases not possible with status quo type scans or MRIs, thus allowing:
- Exact monitoring of response to whatever treatment chosen by treating physician and/or patron, conventional as well as unconventional.
- permits exact and scientific determination of remission in a patron.
- Establishes cures over longer period interval testing.
- Thus, preventing recurrence or relapse of disease.
- For Scientific Clinical Studies and Trials
- Eliminates double blind etc., studies with high degree of inaccuracies (certainly from a true epidemiological scrutiny).
- Eliminates randomized trials.
- Provides early risk factors for malignancies as a true prevention, therefore, complements cancer-search at too late a (clinical) stage with reduced survival chances (Mammography, Colonoscopy, etc.).
- Provides exact clinical-biochemical parameter results for effectiveness of new substances.
- In conjunction with unconventional medical practices.
- Complements Gaston Naessens’ Somatoscopic diagnosis
- Monitors effect of Cell-Milieu-Medicine, fetal tissue therapy, bio-electronic and homeopathic approaches.
Dr. Nieper compares the immune system with the army (which calls out the reserves when there is danger), and the anti-cancer surveillance system with the police whose strength is essentially fixed.
The latter system includes mechanisms for gene repair, and certain steroids such as tumosteron and DHEA. Approximately 60% of all people have sufficient DHEA in their blood to be protected from cancer. Of the remaining 40% about half will develop hidden cancer but not die from it while the rest (20%) will die of diagnosed cancer.
A lack of DHEA has been correlated with peculiarities of the person’s character -- non aggressive, amiable, easily depressed and indecisive.
DHEA-S is produced in the adrenal glands and circulates in the body as DHEA sulfate. A special activation factor, (which possibly is produced in the pineal gland or the thymus gland or the small intestines) changes DHEA-S into free DHEA.
DHEA paralyzes an enzyme (glucose-g-phosphate dehydrogenase) which is of primary importance to the action of cancer cells. This drastically reduces the vitality of the cancer cell and makes it possible for lymphocytes and other white blood cells to overcome the cancer cell.
Dr. Nieper found that during the course of disease, there is a tendency for the DHEA level to gradually decrease, sometimes to values less than 0.1 (100 nano-grams per milliliter). The cancer patient then does not have sufficient starting material to form free DHEA.
There are a number of drugs whose side effects are to cause the level of DHEA-S to drop. Most prominent are the clofibrates that are used to reduce lipid levels. A correlation has been found between higher cholesterol levels in the blood and lower frequency of cancer-if accompanied by higher values of DHEA.
DHEA was isolated by the German Nobelist Butenandt in 1934 and analyzed by the German chemist and Nobelist Windaus. However, the credit for having identified it as an important pillar of our anticancer surveillance system goes to Arthur Schwartz and his coworkers at Temple University in Philadelphia.
A summary of Dr. Hans Neiper's discussion of DHEA from "Revolution in Medicine and Health,"
(Human Chorionic Gonadotropic hormone)
Radioimmunoassay for the HCG-Beta-chain allows the quantitation of minute amounts of human choironic gonadotropic hormone even in the presence of LH, FSH and TSH. The obvious value is the detection of pregnancy within 2-3 days after conception, detection of micro abortion and detection and follow-up of HCG-secreting tumors.
Teratoma, hydatidiform mole and choriocarcinomas in the uterus, ovaries, testes, mediastinum, pineal and pituitary glands, stomach, lungs, esophagus and bladder have long been recognized as trophoblastic HCG-secreting tumors. However, HCG-B has been found in patients with practically all types of malignancies where trophoblasts were not expected:
- testicular, non-trophoblastic gastrointestinal: carcinoid, colonic/rectal, gastric, pancreatic, small intestinal
- hematopoietic: leukemia, all types of lymphomas, multiple myeloma, sarcomas: fibrosarcoma, leiomyosarcoma, osteogenic sarcoma.
- miscellaneous tumors: breast, thyroid, uterine, bladder, adrenal gland, insulinomia, pheochromocytoma
- lung carcinoma
Indeed, it seems that the HCG-secreting trophoblast may play an important role and it may be closely associated with not only embryogenesis but also carcinogenesis. As more data is becoming available, utilizing the sensitive and specific HCG-B test, it becomes evident that the frequency and types of tumors associated with HCG production are much greater than it has been suspected.
Due to the extreme sensitivity of the test (0.0025IU/ml or about 0.2 ng/ml) it is possible to detect, without localization, ongoing malignancies at a very early stage. Once a base level has been established, a patient’s response to therapy can be monitored. The probability of detecting HCG in cancers of all types is, according to the literature surveyed, 10-100%. The longest interval for elevated HCG-B before cancer diagnosis was 26 months.
(Phospho-Hexose Isomerase or glucose phosphate isomerase)
PHI is a key enzyme in glycolysis, i.e. the main anaerobic energy generating step of glucose metabolism. Glycolysis has been observed to become greatly increased in cancer cell lines, hence the measuring of PHI became accepted as a valuable too! in the appraisal of neoplasias.
Elevated PHI levels were found in localized and metastasized cancers of the: bladder, bone, brain, breast, intestines, liver, lungs, lymphosarcoma, melanoma, mouth, head, neck, esophagus, pancreas, prostate, ovary, stomach, colon, rectum and uterus.
PHI has been shown to be elevated in more patients with neoplasia than other enzymes. However, it may not be elevated in the serum of some patients in an early state of neoplasia and indeed, it is not elevated in the serum of some patients with active diseased state. The detection of the enzyme at elevated levels may warrant a more thorough evaluation of the patient.
Once a base level has been established, PHI is a promising enzyme in following the effectiveness of therapy. When, for instance, this enzyme was monitored during treatment of breast cancer, changes in activity followed progression or regression of tumor growth and antedated other laboratory evidence by days or weeks.
It was also found to be indicative of regressions induced by steroids, radio-therapy, oophorectomy, chemotherapy, and hypophysectomy. In cases of confirmed malignancy any elevation or drop, even within the normal ranges, may be significant.
PHI may be elevated in heart, liver and skeletal muscle diseases. Preliminary data indicates that PHI levels parallel CEA results (Personal communications, Miami Heart Institute and Worthington Biochemical Corporation), however, it does not seem to be affected by smoking and it seems to reflect upon a greater variety of diseases. (The performance cost of PHI is about one-half of that of CEA.)
PHI is very abundant in the red blood cells: therefore, it is imperative that the serum specimen is free from hemolysis.
References for HCG:
B.D. Weintraub and S.W. Rosen, Ectopic Production of HCS and HGB by Non-trophoblastic Cancers. J. Clin. Endocr., 13, 94,1971.
- Civantos and A.M. Rywlin, Carcinomas with Trophoblastic Differentiation and Secretion of Chorionic Gonadotropins. Cancer, 29, 789, 1972.
G.D. Braunstein, et al., Ectopic Production of'HCG by Neoplasms. Annals Int. Med., 78, 39, 1973.
A.S. Rabson et al., Production of HCG in vitro by a Cell Line Derived from a Carcinoma of the Lung. J. Natl. Cancer Inst., 50, 669, 1973.
W.S. Floyd and S.L. Cohn, Gonadotropin Producing Hepatoma. Obst. Gyn, 41, 665, 1973.
D.W. Gold et al., Gonadotropin-Secreting Renal Carcinoma. Cancer. 33, 1048,1974.
D.P. Goldstein et al., The clinical Application of Specific RIA for HCG in Trophoblastic and Nontrophoblastic tumors. Surg, Gvnec. Obst., 138. 747, 1974.
D.C. Torney etal., Biological Markers in Breast Carcinoma. Cancer, 35, 1095, 1975.
R.R. Williams et al., Tumor-Associated Antigen Levels Antedating the Diagnosis of Cancer in the Framingham Study. J, Natl. Cancer Inst., 58,1547, 1977.
References for PHI:
- Bodansky, Serum PHI in Cancer: II. As an Index of Tumor Growth in Metastatic Carcinoma of the Breast. Cancer, 7, 1191, 1954.0. Bodansky, Serum PHI in Cancer: III. As an Index of Tumor Growth in Metastatic Carcinoma of the Prostate. Cancer, 8, 1087, 1955.
M.M. Griffith and J.C. Beck, The Value of Serum PHI as an Index of Metastatic Breast Carcinoma Activity. Cancer, 16, 1032. 1963/
M.H. Gault et al., Serum Enzymes in Patients with Carcinoma of the Lung. Canada Med. Assoc. J96,87. 1967.
C.R. Ratliff et al., Serum LDH, PHI and Serological Evidence of Malignant Diseases. Clin. Chem., 16, 527. 1970.
C.R. Ratliff, Serum PHI: A glycolytic Enzyme for Appraising Neoplasia. 4th Ann. So. Calif. Lab. Conference, Anaheim, March 6, 1973.
Worthington Biochemical Corporation, In Case of Malignancy-PHI Monitors Therapy, 1974.