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Cancer chemo(toxico)therapy revisited and alternative ways of healing.
A thesis presented to the Anglo-American Institute of Drugless Therapy and leading to the Degree of Doctor of Naturopathy (N.D.).
© 1990 by Dr. Henri Rosenberg.
TABLE OF CONTENTS
Chapter I : Chemo(toxico)therapy 3
Chapter II : Amygdalin - Vitamin B 99
Chapter III : The Synthetic Physiatrons 128
Chapter IV : Trypanosoma Therapy 140
Chapter V : Selenium Therapy 146
Chapter VI : The beer's yeast cure 156
Chapter VII : Tumor related indicators 164
Chapter VIII : The Thymus Therapy 188
Chapter IX : The H-11 Therapy 194
Chapter X : Antineoplaston 202
Chapter XI : Gelum Oral RD® 205
Chapter XII : Neoblastine® 212
Chapter XIII : The WIEDERMANN cure 219
Chapter XIV : Beetroot (juice) as cancer therapy 225
Chapter XV : Integral Fasting Therapy 229
Chapter XVI : The Iron Cancer Cure 235
The H-11 Therapy
This form of cancer therapy was first devised by the London Professor James H. Thompson who in the nineteen-thirties was engaged in a study of the parathyroid gland.
Thompson was looking for a substance he called a "growth inhibitor" secreted by the gland, quite apart from its function of controlling the body's calcium and phosphorus metabolism. This substance ensures that, once the body is fully grown, the growth rhythm is adapted to maintaining the status quo (1).
Thompson reasoned as follows, "growth inhibitor" injected into the human body would disperse throughout the whole organism and somewhere fulfil its growth inhibiting task. In a mature healthy body this substance would, after, as it were, its tour of inspection round the body, not be broken down but secreted. Thompson proceeded with his hypothesis by suggesting that in an unhealthy body, where growth is taking place despite maturity (e.g. cancer), the growth inhibitor would be drawn to that place and there fulfil its inhibiting function.
In order to test his theory Thompson and others with him started experiments in animals.
His first experiments were with parathyroid extracts which he injected into rats and mice with tumors. In all cases he noted that after a few days the tumor ceased to grow. After further injections with the parathyroid extract the volume of the tumor gradually decreased. Upon microscopic biopsy he noticed that the tumor seemed to be encapsulated and that as a result the malignant cells could not multiply or metastase. Further experiments on animals also pointed in this direction;
In numerous experiments on mice with Twort-carcinomas both OLLERENSHAW, THOMPSON e.a. (2), as well as WILLIAMS and WALTERS (3) noted independently of each other that growth was not only arrested but in certain cases there was a decrease in the tumor mass. THOMPSON, WILLIAMS, WALTERS with mice with 20-methylchlorantrene fibrosarcoma and BROWN and WALTERS (5) with sarcoma 37 and sarcoma 180 in rats and FLEMINGS, WALTERS and WILLIAMS (4) arrived at the same conclusions.
The H-11 preparation
THOMPSON's problem was now to isolate the "growth inhibitor". He decided to examine human secretions for "growth inhibitors" which as explained above should in his hypothesis be secreted unused from healthy bodies.
BARDOS, GORDON and CHMIELEWIECZ and others (6) had already examined 1500 animal secretions for their oncolyitic properties (on sarcoma, adeno-carcinoma and Ehrlich ascites tumor transplants) and had discovered only 14 organ extracts which had shown significant tumor retardation in their many experiments. These substances came from the red bone marrow, prostate and thymus gland, plasma and red blood cells. (7)
On the basis of his hypothesis THOMPSON suggested that these "growth inhibitors" ought to be found in urine.
Urine extracts have in fact turned out to be retardants of tumoral as well as normal tissue as numerous investigations have shown, including those by RHODENBURG and NAGY (8), TURNER (9), STEELE, KOCH and STEINER (10), MAGNELA, KAPLAN and HYSON (11), THOMPSON (12), MURLIN and others. (13), NORRIS and MAGNARICH (14), WOLLHEIM (15), HERBUT (16), TSALTAS and KRAEMER (17), COMPTON and PANNETT (18), PANNETT (19) and Nobel prize winner SZENT-GYORGI, HGYELI and McLAUGHLIN (20) which all point in the direction of the growth and tumor inhibiting property of urine extracts.
THOMPSON then isolated a polypeptide from urine taken from healthy adults using a step-by-step process with ethanol and methanol at pH 3. He took as starting point researchers who credited polypeptides with an important role in cell growth (21) and in so doing isolated his growth retardant, being further supported by other researchers who had proved that polpeptides inhibit the growth of cancer cells. (22)
Here it should be pointed out that polypeptides carry out a variety of conflicting biological activities. Certain polypeptides such as the epidermal growth factor (23) and the fibroblast growth factor (24) stimulate normal cell growth. Other peptide structures are attributed to a number of hormones (25), chalomes (26) and kinins (527), all of which have important biological functions. On the other hand certain urine peptides retard the growth of cancer cells as numerous researchers have shown (28).
This polypeptide obtained from urine is a dark brown substance with a molecular formula of C96H57N11SO46, a molecular weight of 2132.5 and contains sulphonic acid and phenol groups. Its sodium salt is water soluble and the polypeptide is also soluble in ethanol, aliphatic alcohol, formic acid at 90% and phenol.(29)
Chromotographic analyses after hydrolysis have revealed the amino acids glycine, lysine, valine, leucine, tyrosine, asparagine and glutamine as well as creatinine and polypeptide degradation products.
In the meantime H 11, a product extracted from human urine, had been put to clinical use.
In 1948 OLLERENSHAW and LOWE (30) and THOMPSON and LOWE (31), working independently, achieved subjective as well as objectives improvement with the prolonged use the H 11 preparation on cancer patients.
By 1950 THOMPSON had already treated 2277 patients suffering from an enormous range of non-operable tumors with the H 11 extract. In 70% of cases he achieved satisfactory results.
Other clinical applications of H 11 by CUNNINGHAM-JONES and others in 1950 (32), GARCIA and FERNANDEZ in 1954 (33) and BRADFIELD in 1961 (34) pointed in the same direction, i.e. the achievement of objective as well as subjective improvements. The subjective improvement was a decrease in pain and in other symptoms such as vomiting, coughing, ascites and jaundice plus a significant improvement in general well-being, with the result that certain bedridden patients became ambulant.
The objective results included the inhibition of growth in primary tumors and/or of the metastases whereby in many cases patients survived significantly longer.
In certain cases there was even tumor regression and on occasion even a recovery of the tissue from tumoral to normal tissue.
In 1962 KLOSE(36) and in 1967 and 1969 KLOSE and BELOW (37) reported on clinically observed tumor retarding properties of the H-11 therapy on bronchial carcinomas.
Other clinical experiments included studies of H 11 therapy for carcinomas of the alimentary tract (38) (carcinoma of the oesophagus, stomach, caecum and rectum, with or without liver metastases), breast carcinomas (39), tumor of the uterus, cervix and ovaries where the observed inhibition was 79%, 74% and 70% respectively (40).
Brain tumors, including neuroblastomas (41), meningoblastomas (42) and astrocytomas (43) reacted favourably to treatment with H-11. Cancers of the bladder with (44) or without (48) metastases, and kidney cancers (49) also reacted favourably. Lymphosarcomas (50) also produced good results. Oesteosarcomas, however, responded less favourably (50%). Malignant skin melanomas were improved with the H-11 therapy and neo-plastic relapses did not occur(48).
Action of H-11
FLEMING and PECZENIK (49) noticed during experiments with animals that the administration of H-11 to male mice with mammary carcinoma resulted in a significant decrease in the alkaline glycerophosphate contents of the tumor. At the same time they noted that this was inversely proportional to the degree of growth retardation.
WALTERS (50) showed that the polypeptide from H-11 retards alkaline phosphatase in vitro. Kinetic experiments have demonstrated that this is a real, competitive retardation.
Liver catalase in mice with tumors decreased considerably (51).
BROWN and WALTER (52) confirmed that the liver catalase in mice with sarcoma-37 was very low.
By administering H-11 ADAMS (53) was able to significantly arrest the decrease in liver catalase and inhibit tumor growth
KLOSE and BELOW are of the opinion that the activity of H-11 may well have a positive influence on the physiological defence mechanism, perhaps even within the context of the Antigen-Antibody-Reaction in the sense of SZENT-GYORGYI (55), DOMAGK (56) and others.
Polypeptide with sulphonic acid and phenol groups 0.1%
Amino acids, creatinine and phenol groups 0.9%
Sodium sulphate 0.1%
in ampoules, tablets, liquid, suppositories and salve
Orally (liquid or tablets) or deep subcutaneously, just above the muscle layer.
Suppositories and salve are for local application.
NB: In certain cases a test should be carried out (reaction to collodial vanadine) in order to determine the exact, optimal individual dosage.
For this, 3-5 ml serum without additives should be taken and sent for examination to the Hosa Research Laboratories, Sunbury-on-Thames, GB.
All tumors with their histological sub-groups and metastases except anaplastic tumors as less favourable results are obtained with these.
There is no evidence to justify the use of H-11 for leukemia.
In addition H-11 has a proven (58) synergetic effect with traditional medicine's threefold therapies as well as with hormone therapy (stilboestrol, androgens, methyltesto-sterone);
Standard Laboratories Ltd.,
Middlesex TW 16 7DT,
Bureau Central d'Information
19, rue de la Croix-d'Or
phone. (022) 28.37.33
(1) compare with R. Steiner's theory, p....
(2) OLLERENSHAW, G.J.W., Clinic Med...; June (1948)
(3) WILLIAMS, J.L. and WALTERS, C.L., Nature, 195. p. 503 (1947)
(4) FLEMING, R., WALTERS, C.L. and WILLIAMS, J.L., Acta Intern. Cancer, 7455. (1951)
(5) BROWN, C.B. and WALTERS, C.L., Science, 125, p. 1246 (1957)
(8) RHODENBURG, G.I. and NAGY, S.M., Am. J. Cancer, 29, p. 66 (1937)
(9) TURNER, F.C., U.S. Public Health Rep., 54, p. 1855 (1939)
(10) STEELE, R., KOCH, F.C. and STEINER, P.C., Cancer Res., 1, p. 614 (1941)
(11) MAGNELIA, A.L., KAPLAN, J.H. and HYSON, E., Illinois Med. J., 83, p. 43 (1943)
(12) THOMPSON, J.H., Proc. Physiol. Soc., Oct. (1930)
(13) MURLIN and others, Science, 110, p. 275 (1939)
(14) NORRIS, E.R. and MAGNARICH, J.J., Science, 109, p. 32 (1949)
(15) WOLLHEIM, E., Schweiz; Med. Woche, 78, 18, p. 428 (1948)
(16) HERBUT, P.A., TSALTAS, T.T. and KRAEMER, W.H., Journ. Amer. Med. Ass., 178, p. 732 (1961)
(18) COMPTON, A. and PANNETT, C.A., Nature, 191, p. 1101 (1961)
(19) PANNETT, C.A., Nature, 201, p. 404 (1964)
(20) SZENT-GYORGYI, A., HEGYELI, A. and McLAUGHLIN, J.A., Science, 140, p.1391 (1963)
(23) HOLLENBERG, M.D., Epidermal growth factor: Biological activity and receptor binding of 1-5 I-labelled peptide in cultures human fibroblasts and rabbit lens cells, Fed. Proc., 34, 731, 1975
(24) GOSPODAROWICZ, D., Localization of a fibroblast growth factor and its effect alone and with hydrocortisone on 3T3 cell growth, Nature, 249, 123, 1974.
(25) WOLLHEIM, E. and NAST, H.P., Ein humoraler Faktor in der Genese der essentielen Hypertonie Klin. Wochenschr., 49, 426, 1971
(26) VERLY, W.G., DESCHAMPS, Y., PUSHPATHADAM, J. and DESROSIERS, M., The hepatic Chalone, Cancer J. Biochem., 49, 1376, 1971
(27) MIWA, I., ERDOS, E.G. and SEKI, T., Presence of three Life Sci., 7, Part III, 1339, 1968
(28) KIVILAAKSO, E. and RYTOMAA, T., Erythrocyte chalone, a tissue-specific inhibitor of cell proliferation in the erytheon, Cell Tissue Kinet., 4, 19, 1971.
PAUKOVITS, W.R., Control of granulocyte production: Separation and chemical identification of a specific inhibitor (chalone), Cell Tissue Kinet., 4, 539, 1971.
DE BARBIERI, A., DI VITTORIO, P., GOLFERINI, A., MANGERI, M., MISTRETTA, A.P., PERRONE, F., TASSI, G.C., TEMELCOU, O. and ZAPELLI, P., Investigations on the effect of anti-tumor peptides and mixtures of same, Est. Bol. Chim. Farm., III, 216, 1972
(29) WALTERS, C.L., Enzymol., 20,1, p. 33 (1958)
(30) OLLERENSHAW, G.J.W. and LOWE, E.C., Med. Wld., June (1948)
OLLERENSHAW, G.J.W. and LOWE, E.C., Med. Wld., Sept. (1949)
(31) THOMPSON, J.H. and LOWE, E.C. Med. Wld., Dec. (1950)
(32) CUNNINGHAM-JONES, R., and co., Med. Wld., Apr. (1950)
(33) GARCIA, G. and FERNANDEZ, F., Journ. Philip. Fed. Med. Pract., 4,3, p. 99 (1954)
(34) BRADFIELD, P.A., M.D. Journ., 10, 6, p. 340 (1961)
(35) H-11 Review, 9.2 and 9.3 (1966)
(36) KLOSE, G., Schlesw.-Holst. Arztebl., p. 442, Dec. (1962)
(40) WILLIAMS, J.L. and WALTERS, C.L., Nature, 195, p. 503 (1947)
(41) H-11 Review 9.2. and 9.3 (1966)
(42) CUNNINGHAM-JONES, R. and associates. ditto
(43) H-11 Review 9.2 and 9.3 (1966)
(44) CUNNINGHAM-JONES, R. and associates. ditto
(45) H-11 Review, 3.3 (1959)
(46) OLLERENSHAW, G.J.W. and LOWE, E.C., Med. Wld., Dec. (1949)
(47) OLLERENSHAW and LOWE, ditto
(48) THOMPSON, J.H. and LOWE, E.C., Med. Wld. Dec. (1950) H-11 Review, 9.2. and 9.3 (1966)
(49) FLEMING, R.F. and PECZENIK, O., Nature, 162, p. 338 (1948)
(50) WALTERS, C.L., Enzymol., 20, 1, p. 33 (1958)
(51) BROWN, C.B. and WALTERS, C.L., Science, 125, p. 1246 (1957)
(52) ADAMS, D.H., Brit. J. Cancer, 4, p. 183 (1950)
(53) It is worth pointing out the findings of certain researchers which show that hypophysesectomy can combat depression of liver catalase.
(55) SZENTI-GYORGI, A., HEGYELI, A. and McLAUGHLIN, J.A., Science, 140, 1391, 1963
(56) DOMAGK, G., Krebsarzt, 15, 235, 1960
(57) BEGEMANN, H. and FELLMER, K.H., Med., 60, 1681, 1965
BOHNENKAMP, H., Krebsforschung u. Krebsbekampfung, IV, 148, published by Urban and Schwarzenberg, Munich, Berlin, 1961
KLEIN, G., Med. et Hyg., Geneva, 24, 1106, 1966. Composition
Dr. Henri ROSENBERG, LL.D., Ph.D., N.D.
Doctor of Naturopathy
Permanent Member of the British
Guild of Drugless Practitioners.
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