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.
Introduction 2
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
Amygdalin - Vitamin B-17 (Laetrile).
BackgroundAmygdalin is a natural substance which contains a cyanogenradical - a nitriloside - and which can be found in apricot and peach stones, as well as in cherry pips, bitter almonds and other stones and pips of the amygdalus genus. Therapeutic amygdalin isknown as laetrile. Properly speaking the words laetrile and amygdalin are not synonyms. The chemical formulation of amygdalin, which as we have already said is a natural substance,with the chemical formula D-1-mandelonitrile gentiobioside (1) or D-mandelonitrile linked to the disaccharide gentiobiosis (2),formed by two D-glucose molecules. The natural cyanohydrins ofthis group are known as cyanogenic glycoside (3). The empiricalformula of amygdalin is written C20H27N11. Laetrile on the otherhand is a D-1 mandelonitrile-beta-glucuronide and is the result ofbreaking amygdalin into mandelonitrile and linking with gluconicacid. Laetrile's empirical formula is C4H15NO7.
Fruits of the amydalus genus have long been prized for theirhealing properties. They appear in the herbals of virtually allgreat civilizations. For example, the oldest known known herbal, the "Pen Tsao Kang-Mu", attributed to the Chinese Emperor Shennung, and dating from 2700 BC, mentions their properties. The same fruits are mentioned in works by Aulus Cornelius Celsus and Scribonius Largus, dating from the early first century AD. Scribonius in particular mentions that bitter almond is effective against cancer of the bladder. The elder Pliny discusses the therapeutic effect of oil of bitter almonds on condylomatoma. Subsequently the all too influential Galen recommended almonds for liver cirrhosis. While Priscian and Empiricus used almonds to treat tumors.
The great Persian apothecary and medical practitioner Avicenna used bitter almond oil to treat tumors of the uterus, spleen, stomach and liver. While Maimonides, the renowned Jewish legal thinker and physician stressed the importance of bitter almonds and beetroot as therapeutically valuable remedies. In the 13th century Harpestaeng, a Danish physician, used almond mixed with honey to treat hardening of the spleen, while his contemporary, Myreposos, a Byzantine physician, used almonds to treat cancers of the oral cavity. In the same century too Ibn-Al-Baitar was using almonds to treat breast cancers. Later on, in the 16th century, we find a Swiss biologist called Gesner using almonds to treat cancer.
John Gerard, who published his famous herbal in the mid-17th century in London, discusses the therapeutic properties of almonds and was the first to report their pain-killing effects. The great Flemish herbal of the same period, compiled by R. Dodoens, recommends the use of bitter almonds for "rotting tumors".By the 19th century bitter almonds were an accepted treatment for cancer both on the Old Continent and in the New World. In 1845, for example, the Parisian Gazette Medicale published an article by the Russian physician, Dr T. INOSEMTOFF, Professor at the Imperial University of Moscow, who claimed to have successfully halted the further development of two cases of metastased cancers using amygdaline.
Studies carried out by Sir Robert McCARRISON, Senior Physician to the King of England at the turn of the century, indicated that the Hunza tribe of Karakorum of north-western Pakistan hardly ever suffered from cancer. Similarly findings by the polar explorer, STEFANSSON, showed that the Eskimo tribes are also almost entirely untroubled by cancer as long as they live in their native habitat. Unlike most other populations these two groups include large amounts of nitrilosides in their diet, the Hunza, for example, by their habit of eating apricot stones, and the Eskimo by eating certain polar cherries and the partially digested contents of the stomachs of animals killed by them. Indeed certain animals - largely herbivores - do not suffer from cancer. A good example is the sheep (4). And remarkably enough grass contains 40 g of nitriloside per kg. It was really only in 1920 though that, as a result of the work of Ernst T. KREBS and his son and successor Ernst T. KREBS jr., that amygdalin became established in the USA, even though a request by KREBS jr. for FDA certification was turned down in 1962. Ever since then a war has been waged in the courts and the legislatures between those who support amygdalin therapy and those who oppose it. So far the latter have had the best of it and have succeeded in having amygdalin declared illegal.
The entire US medical establishment in the shape of the AMA, the American Cancer Society (ACS), the National Cancer Institute (NCI), and the Sloan-Kettering Institute for Cancer Research did everything in its power to prevent amygdalin therapy gaining a foothold in the US, and when this failed, redirected its efforts to stamping out all attempts at applying the therapy.
Dr Alexander M. SCHMIDT, Director of the all-powerful FDA, told the press on March 25, 1974, "Every study to date has not found any evidence of efficacy with Laetrile and, if there was one shred of evidence from animal or cell systems, I would issue an IND" (IND = Investigation of New Drug Status, which permits clinical trials in humans).
Mr Robert C. WETHERELL and Mr Gerald F. MEYER, Directors of the FDA's office of Legislative Services, declared that for their part "no evidence of antitumor activity has been found in any of the tests".
Dr Frank RAUSCHER, Director of the NCI, speaking in a CBS programme broadcast on March 31, 1974, said, "I would certainly not turn off Laetrile, if it had an iota of activity that we could pinpoint. Unfortunately there's no evidence at all".
Dr Robert M. HADSELL, an official of the NCI's cancer communication department distributed a nationwide circular inwhich it was stated, "All testing by NCI has found no evidence of activity against by cancer by Laetrile".
Dr Jesse L. STEINFIELD, head operating surgeon of the USPHS stated in a circular dated January 1974 to departmental heads of the respected Mayo clinic, "Laetrile has repeatedly been tested in animal tumor systems. There is no basis for the use of Laetrile in man based on data derived from experiments in animals".
Similarly Dr Charles MOERTEL, also of the Mayo Clinic, sent a letter to the Rochester (Minn.) Post Bulletin on January 21, 1974, in which he said "Extensive animal tumor studies conducted independently at two outstanding cancer research centres, New York Memorial Sloan-Kettering Institute and the Southern Research Institute, have shown this drug to be totally without evidence of anti-cancer activity".
To round off, we can refer to a statement made by Lane ADAMS, Chairman of the American Cancer Society, who said in an interview on May 6, 1974 that the Sloan-Kettering Institute had no trace whatsoever of the anti-tumor effect of Laetrile. To quote Mr Gerald F. MEYER again, "The NCI, Memorial Sloan-Kettering Institute, and others equally reputable have tested Laetrile and have found it to have no anti-tumor activity".
The above quotations from leading figures of the US "medicracy" show that the American medical establishment have mobilized their most powerful weapons in the war on Laetrile.
All the effects of Laetrile have been swept under the carpet. Even the mildest positive statement about Laetrile incurs the wrath of the powers that be, even though, as we shall see below, tests with amygdalin in animals have clearly and irrefutably demonstrated the activity of Laetrile.A memorandum dated June 14, 1974 from the FDA and sent to all FDA departments mades a fierce attack on Laetrile using the regrettable procedure we have seen at work elsewhere (see Chapter ).
Under the sub-title "Famous Supporters of Laetrile", the FDA memorandum refers to E.T. KREBS jr and his father, without, however, mentioning their qualifications and numerous honorary titles. Moreover this memorandum fails to mention that the younger KREBS was responsible for giving the name vitamin B17 to amygdalin and that it was he who introduced the name nitriloside for all cyanophoroglycoside of dietary significance (5).
The next figure to receive this treatment in the FDA memorandum is Dr Hans NIEPER a highly respected German onco logist (6). While the memorandum does manage to admit that he is the author of a large number of papers, it forgets to add that these have been published in highly respectable scientific journals. What the memorandum does say is that these papers produce no adequate support for the laetrile thesis. The FDA apparently considers this refutation by fiat to be adequate. The inquisition could not have done it better.
The last figure to be honoured in this way was Dr Dean BURK. This biochemist worked for the NCI for close to 45 years and became head of the Cytochemical Section of the NCI. The FDAmemorandum acknowledges that he is a proponent of Laetrile, but adds that his opinion is not shared by NCI's administrators, nor by the Public Health department of HEW, of which the FDA is an offshoot, nor by the "Academic Community" as a whole. It goes on to say that there is not a single trustworthy scientific study in support of BURK's thesis.
This memorable memorandum closes with the following advice to its sub-sections, "Examine the newspapers for announcements of forthcoming meetings of the IACVA, CCS, and the Committee for Freedom of Choice in Cancer Therapy. Try to be present at the meeting. If Laetrile is discussed and it appears to be possible to obtain Laetrile other than by going abroad try to obtain all the details. Take a copy of all proffered literature. Take down the names of companies whose products are mentioned at these meetings. Listen carefully to the speakers, summarize their speeches and pass them onto us.
One cannot help but wonder why officialdom goes to such great lengths to suppress laetrile. Apparently no avenue has been left unexplored in order to sink the laetrile therapy, attacks have been launched in the courts, and the police and even undercover agents have been deployed in an effort to stop people using laetrile. Such measures seem to be excessive, especially as the therapy has been demonstrated to be non-toxic, leaving aside the problem of whether it is effective against cancer or not.
To date, however, the medical establishment has not dared to maintain that Laetrile is toxic, if only for the fact that such a statement would be quite untenable.
The non-toxicity of amygdalin has been well-established ever since the appearance in 1887 of the book "Die Glycosides" by Otto JACOBSEN, in which the author states "Das Amygdaline ist nicht giftig". In support of this statement he provides a hundred odd references drawn from 20 years of practice prior to 1887.
Similarly DAVIDSON (7) writing in 1944 also maintains that amygdalin has no side-effects when injected (8).In 1948 HIMWICH and SAUNDERS calculated that the liver of a dog can convert 4015 mg of cyanide into non-toxic thiocyanate in the space of just 15 minutes. The skeletal muscles can detoxify a further 1763 mg of cyanide in the same period, making the dog's total detoxification capacity 5778 mg every 15 minutes.
Since then a number of acute, sub-acute, and chronic toxicity tests have been carried out with the oral, intra-muscular, intra-peritoneal and intravenous administration of amygdalin to mice, rats and dogs, which
Acute or cumulative toxicity was not found in any type of animal even with doses of 100 times the maximum intravenous dose used in human therapy (9). The tests also revealed that pure amygdalin is less toxic than ordinary sugar (glucose). Pure amygdalin was moreover found to be non-antigenic and therefore incapable of provoking reactions to a foreign protein.
The organs of the experimental animals were also examined for possible toxic damage, without any relevant damage ever being discovered. These animal experiments were repeated by MANNER in 1977 (10). MANNER also found incontrover-tible experimental proof of the absolute non-toxicity of amygdalin.
A comparison of the supposed toxicity of amygdalin to that of the more accepted (but often carcinogenic) cancer drugs and even such everyday drugs such as aspirin highlights the extent of the hypocrisy of the American medical establishment.
Toxicity trials in animals of a number of FDA approved chemo(toxico)therapeutica resulted in figures that were compared to the "toxicity" of laetrile
Further evidence of the non-toxicity of amygdalin is the fact that it does not appear in the FDA's authoritative Registry of Toxic Effects of Chemical Substances.
In sharp contrast is that all FDA recognized chemotherapeutica which are effective against neoplasms are listed as highly toxic and carcinogenic (11).
The bitter war of the US medical world against Laetrile, recognized as non-toxic by the FDA, and waged despite the many successful (even with the most unfavourable interpretation) and promising animal trials detailed below, can only be understood when considered in the light of chapter .... (12).
Animal Trials with Amygdalin
1. Toxicity Tests
We have already referred to MANNER's toxicity tests. MANNER (13) first of all carried toxicity tests out to determine the LD 50, that is the lethal dose for 50 % of the animals. From this it appeared that daily doses of 2500 mg/kg per day caused absolutely no harm to animals, indicating that parenteral use of amygdalin appeared to be wholly non-toxic.
Opponents of amygdalin therapy have responded to this by saying that the drug is non-toxic because it is passed in the urine without change. For this reason MANNER carried out tests on the intermediate metabolism of amygdalin. The test comprised a colometric measurement of the metabolic waste products of cyanides and benzaldehyde in the urine, i.e. thiocyanate and hippuric acid. The greater the quantity of amygdalin injected, the greater should be the quantity of decay products measured in the urine using colorimetric methods. These expectations were confirmed indicating that the organism does in fact react to the administration of amygdalin and is capable of breaking it down. MANNER then measured the toxic effects of amydalin on mouse embryos. From this it appeared that amygdalin had no toxic effects on the foetus or that the substance is incapable of traversing the placenta. Whatever the case may be it is not harmful during pregnancy.
2. Animal Trials on the Anticarcinogenic Effects of Amygdalin
a. Scind Laboratories
In 1968 the Scind Laboratories of the University of San Francisco (USA) carried out amygdalin trials on 400 rats with WALKER's carcinoma (200 treated and 200 controls). The dose was 500 mg/kg per day. The results indicated a significantly longer life for 80 % of the animals receiving amygdalin. NCI Director Carl BAKER wrote to Congressman Edwin E. Edwards in 1971 about these results, "The results ... undoubtedly indicate some effectiveness against animal tumors.
b. Pasteur Institute
Dr T. METIANU of the Pasteur Institute of Paris, France, conducted trials in association with the French Ministry of Agriculture on human cancers transplanted in mice. The researchers administered daily doses of 500 mg per kg body weight of amygdalin and were able to achieve a 100 % increase in life expectancy and the total inhibition of tumor growth.
c. The
The East German VON ARDENNE Institute (13) of Dresden investigated the effects of bitter almonds amygdalin taken ad libitum in a chow diet in mice with implanted EHRLICH ascites carcinoma. The implantation took place 15 days prior to the administration of treatment. The researchers observed significant increases in life expectancy as well as the inhibition of tumor growth (14).
In further trials in rats which were injected with both amygdalin and beta-glucosidase, M. VON ARDENNE and associates were able to obtain "results in growth inhibition and regression which appeared to most effective abd which could be favourably compared to (conventional) chemotherapeutica".
VON ARDENNE ascribes the effectiveness of the therapy to the lyosomal cytolytic chain reactions (15), to various well understood mechanisms of amygdalin (16), and to the stimulation of the body's defenses (17)(18).
d. Southern Research Institute
These were the first animal trials to be carried out by the US medical establishment, namely on behalf of the NCI. They were performed in December 1973 on 280 mice with Lewis lung carcinoma in the Southern Research Institute (SRI) in Birmingham, Alabama.
The SRI experimenters came to the conclusion that amygdalin had "no proven effect in Lewis lung carcinomas".These conclusions came in for considerable criticism by Dean BURK, NCI associate and Head of the NCI's Cytochemical Section. He contested the NCI conclusion most forcefully and began his own trials, aided by his own thorough knowledge of statistical theory (19). In doing so he sought the advice of numerous biologists and other scientists such as Dr Harris H. LLOYD and Dr J.G. MAYO, both of the SRI, Dr. Lawrence MUENZ, Dr John GART and Dr James L. MURRAY, all three of the NCI, Dr John HEARON of the National Institute for Health, Dr Peter STACPOOLE of the University of Tennessee's medical school, Dr Vincent LISANTI of the Council of Tobacco Research N.Y., and finally the advice of the authority on statistics already referred to, Dr W. Edward DEMING. It is interesting to add that for the last 30 years or so Japanese scientists have awarded a annual medal known as the Japanese Deming Medal.
BURK succeeded in refuting the SRI report first of all by demonstrating that the statistical method used, the Median Life Span Analysis method, was not suitable for this application and could be unreliable. Even so the results for ILS (increased life span) of 41 %, 51 % and 30 % (an average of 41 %) using this method lay above the accepted minimum significance level of 25 % for mouse carcinoma.
BURK furthermore delved into the NCI archives to produce reports on earlier tests with Lewis carcinoma, from which it appears that this sort of cancer barely reacts at all to conventional chemotherapeutica. Considered in this light the extension of survival time for 41 % of Lewis lung carcinomas becomes very significant indeed. If the more suitable Median Longevity Index Analysis method had been used the effectiveness of amygdalin in extending survival times would have shown up better. The following illustration highlights the difference between the two statistical methods: in the SRI method a mouse which survives 30 days is equivalent to a mouse which survives 20 and 10 days. It is thus not difficult to see why the 41 % increase in survival obtained by the SRI scientists is a low estimate of the reality.
A last argument in favour of BURK's interpretation of the SRI experiments, is that when the results are reinterpreted they broadly agree with the findings of the Pasteur Institute, the VON ARDENNE Institute, and the SCIND Institute.
e. Sloan Kettering Institute
A major step was the permission obtained by the Sloan Kettering Institute for Cancer Research to carry out trials of amygdalin in animals. Trials were then carried out in 1973 and 1974 under the leadership of Dr Kanematsu SUGIURA. The decision of the Institute to proceed to trials was not spontaneous and was the result of official pressure, itself a consequence of public pressure (20).
Whatever the case may be, SUGIURA submitted his findings in a Sloan Kettering Institute report on two series of trials in mice.
In both series of trials in mice, amygdalin prevented the phenomenon, observed in the controls, of metastasis in the lungs of natural breast cancers (CD8FI) in mice. Only 17.4 % of the mice treated with amygdalin showed secondary cancers or lung metastases, while among the controls this figure was 78.2 %.
These results were, however, not repeated in the second trial. The explanation lay in the fact that amygdalin of a different origin was used. A third series of tests using the original amygdalin preparation was thus carried out.
In the third series SUGIURA succeeded in confirming the original results. Lung metastases were observed in 11 % of the mice compared with 78 % in the controls.
A report on a fourth series of trials carried out in CD8F1 mice was made on September 30, 1974. The spontaneous breast cancers developed in both groups but with different incidences. Only 48 % of the amygdalin mice developed breast cancers compared with 70 % of the controls. Lung metastases were observed in 22 % of the amygdalin mice compared to 75 % of the controls.
A report on a fifth trial with spontaneous breast cancers in Swiss albino mice was leaked on February 8, 1975. The growth of small tumors (less than 1.5 cm across) could be inhibited in 51 % of the amygdalin mice, compared to 29 % in the controls. The effectiveness of amygdalin on lung metastases was again confirmed: no lung metastases in 77 % of cases in the amygdalin group compared to only 7 % in the control group.
All in all these were very promising results for the amygdalin cancer therapy. Nevertheless (or perhaps because they were so favourable (21)) the Sloan Kettering Institute failed to publish them and it was only thanks to a nameless employee that the information became known publicly. Copies of the report were sent to the press accompanied by an unsigned letter on the Sloan Kettering letterhead requesting the publication of these promising results (22).
f. Trials in animals by MANNER and associates
MANNER and associates (23) investigated the possible synergetic effects of amygdalin, emulsified vitamin A, and WOBE MUGOS enzyme preparation (24) on female C3H/HeJ mice with primary C3HBA tumors of the breast.
As soon as the tumors grew to about 4 to 6 mm across the mice were involved in the experiment and were given a daily dose of 500 mg per kg of body weight of amygdalin, 500 IE A-MULSIN® administered orally, and intra-tumoral injections of 25 mg WOBE MUGOS ® every two days.
The results were spectacular. In the controls the tumor mass continued to grow unimpeded, while in the mice receiving treatment the tumor mass regressed completely in 89.3 %, and partial regression was observed in the remaining 10.7 %.
3. Clinical Trials
The refusal of the US Food and Drug Administration to issue an IND has meant that all trials on humans are forbidden in the US. Therapeutical use, even in terminal cancers, is forbidden as well, and opens the user to prosecution. The FDA, need we add, has not hesitated to start criminal proceedings against offenders.
Even so the number of laetrile patients in the US is estimated at 70,000 and a thousand or so therapists are thought to be using it. Outside the USA amygdalin is used in about 20 countries. Among non-US practitioners who warmly recommend the use of amygdalin are Dr Hans NIEPER, Director of the Medical Department of the Silbersee Hospital in Hanover (FRG), Dr N.R. BOUZIANE, Director of the Research Laboratory of the Ste. Jeanne d'Arc Hospital of Montreal (Canada), Dr Ernesto CONTRERAS of the Good Samaritan Cancer Clinic in Tijuana (Mexico), Dr Manuel NAVARRO, Professor in Medicine and Surgery at the Santo Tomas University in Manila (Philippines), Dr David RUBIN of Jerusalem (Israel), Dr G. MAISIN of the Catholic University of Leuven (Belgium), Dr Ellore GUIDETTI of Turin University (Italy), and Dr Shigeaki SAKAI of Tokyo (Japan).
The numerous therapeutic successes which these physicians claim to have experienced with amygdalin in daily practice must be worth following up with the best clinical tests.
How does Amygdalin work?
The first stage is the hydrolysis or splitting of amygdalin (D-1-mandelonitrile-B-D-glucoside-6 B-D-glucoside or D-1-mande-lonitrile gentiobioside) under the influence of B-glucosidase, in a reaction which leaves this enzyme unaltered. The hydrolysis of amygdalin by certain enzymes such as B-glucosidase (or D-emulsine in plants) or by acids is an established fact and is reported in the literature by KRIEBLE (25), VIEHOEVER and MACK (26) and HALSMAN and KNIGHT (27). The distribution through the body of B-glucosidase, however, is still a matter of discussion.
Some workers such as MELLOR and associates (28), VON ARDENNE and associates (29), and HAWKSWORTH and associates (30) are of the opinion that it is only found in the liver and intestines (31). Others think that it is more likely to be found in nerve tissue. Traces of B-glucosidase have indeed been found in the blood but it is still not clear if this plays a role in the hydrolysis of amygdalin (32).
Whatever the details of the process the net result is that the original amygdalin is transformed into D-1-mandelonitrile-B-D-glucoside + glucose by the splitting off of a glucoside.
The original mandelonitrileglucoside is stereoisometric. The d-isomer is known as prunasine and the l-isomer as sambuni-grine, while the d+l-g stereisomer is called prulaurasine. The release of cyanide and benzaldehyde in a later stage thus depends on one of these three isomers. A discussion of the stereochemical properties of the three isomers and their reactions would go beyond the scope of this book. The interested reader is referred to BRADFORD and ALLEN (33). For our purposes it is enough to know that the l-isomer prunasine is formed. There are three hypothetical routes for the further dissociation of prunaside-glycoside.
Path I
Again under the influence of the B-glucosidase enzyme the prunasineglycoside enzyme hydrolyzes to D-d-mandelonitrile + glycose with the second glycoside being released.
In this hypothesis (unstable) D-d-mandelonitrile + glycoside spontaneously decays into poisonous cyanic acid (HCN) and benzaldehyde.Path II
This path assumes the intervention of another enzyme in the further decay of the prunasineglycoside. Called prunasinelase it leads to the creation of glucose and D-1-mandelonitrile, which is in turn converted by hydroxynitrileyase into benzaldehyde and HCN.
Path III
Prunasineglycoside is catalyzed in a two-stage oxidation process into laetrile-glucuronide (D-1-mandelonitrile-B-glucu-ronide) by the successive action of B-glucosidase with the formation of D-d-mandelonitrile + glucose and subsequent transformation into laetrile-glucuronide by the intervention of the UDP-glucuronosyltransferase enzyme. According to LEVVY and CONCHIE (34), MIETTINEN and LESKINEN (35), WHITE, HANDLER and SMITH (36) UDP-glucurono-syltransferase is found in the liver and kidneys. The laetrile-glucuronide is then further broken down by the lyosomal enzyme B-glucuronidase into D-1-mandelonitrile and glucuronic acid and decays yet further under the influence of hydroxinitrilease into HCN and benzaldehyde (37).
According to FISHMAN and ANLYAN (38) the activity of B-glucuronidase, present throughout the body, is more active in cancer cells because of leaks in the lyosomal membrane, characteristic of cancer, and is also present in the serum as a result of leakage through the plasma cell membrane (39).
THE KREBS HYPOTHESIS
The three (hypothetical) routes describe all eventually lead to the formation of HCN and benzaldehyde. The last link in the selective action against cancer of both substances was described by KREBS jr. and is known as the KREBS hypothesis. First of all, however, an understanding is necessary of the ability of healthy cells to withstand the toxic effects of free cyanide, in contrast to cancer cells. A mechanism of this sort would explain the selective effect of amygdalin. Indeed any non-selective action would be fatal, with cyanide and benzaldehyde attracting normal as well as cancer cells. This was why a possible cyanide therapy of cancer was discarded as impracticable and why KARCZAG abandoned his efforts in this direction in 1927.
The body has three lines of defence against free cyanide. In empirical terms there is no doubt at all about the fact that we regularly consume foodstuffs containing small quantities of cyanide without suffering any ill effects. In 1966 OKE, followed in 1968 and 1969 by OSUNTOKUN, provided experimental proof of these empirical observations. In 1970 OSUNTOKUN confirmed themwith experiments in rats (40).
1) It is known that HCN in a Na2SO3 milieu is converted into non-toxic thiocyanate (SCN) under the influence of rhodanese (also known as thiosulphate sulphurtransferase or transulpherase), an enzyme first investigated in 1933 by LANG (41).
According to DE DUVE (42) and HIMWICH (43) rhodanese is a mitochondrial enzyme with a molecular weight of 37000 possessing a disulphide bridge. This bridge can be broken down by the thiosulphate ion, with the release of non-toxic Na2SO3 and SCN, which is collected by the thymus and eventually secreted into the urine. Rhodanese is present in all (healthy) tissue, and particularly in the liver. The question then remains of why cyanide is so toxic to humans, if the body has such an effective way of dealing with it. The answer is that large-scale detoxification breaks down because of limitations on the available sulphur. Cyanide penetrates the cell very rapidly, while the sulphur-rich thiosulphate, essential for cyanide detoxification, enters the cell only very slowly. The result is that the greater part of the thiosulphate leaves the body in the urine before it has had the chance to react with the cyanide. In 1934 CHEN showed that by administering thiosulphate the minimum lethal dose could be raised by a factor of 3 or 4, depending on the dose of thiosulphate administered. Another of the body's sources of sulphur is 3-B-mercaptopyruvate, which is formed when cystine and the sulphur-rich amino acid cysteine are transformed into pyruvic acid, which is part of the aerobic metabolic process.
In 1953 WOOD and FIELDER (44) established that mercaptopyruvic acid also contains sulphur and transform HCN to non-toxic thiocyanate just as quickly as thiosulphate.2) The second detoxification process of the human body bonds the cyanide to hydroxycobolamine in the liver, where cyanocobolamine or vitamin B-12 is created under the influence of rhodanese. In 1952 MUSHETT (45) and others showed experimentally that by administering hydroxy-cobolamine to rats their resistance to cyanide poisoning could be raised. The double detoxification process in which rhodanese plays a central role is thus well established and was again confirmed by AURIGAS and KOJ (46) in 1975.
3) The third and last detoxification process has to do with the role of CO2. IN 1952 BOXER and RIKARDS (47) used 14CN as a radioactive tracer in dogs to demonstrate that the marked product was present in the exhaled CO2.
The KREBS hypothesis on the last link in the decay of amygdalin and the selective neo-plastic action thus developed as follows.
In 1946 MENDEL, RUDNEY and BOWMAN (48) and GIORDANO et al. in 1956 (49) stressed the high content of rhodanese and low concentration of B-glucuronidase in normal tissue in contrast to cancer cells where high concentrations of B-glucuronidase and low concentrations of rhodanese are found (50).
BRAUNSTEIN et al. observed that (51) cancer cells (carcinoma, melanoma and multiple myeloma) produce HCG hormone (52). According to SANCHEZ and BELTRAN (53) this hormone tends to block rhodanese synthesis and consequently the conversion of cyanide into non-toxic thiocyanate in the cancer cell.
The HCN, or better the cyanide ion (CN-), released in the cancer cell by the higher level of B-glucuronidase in the pathological cell is thus not rendered harmless by the normal protection mechanisms present in the healthy cells. The protective rhodanese is not present in the cancer cell and the CN-ion kills the cancer cells by reducing the enzymatic activity of the cell. The mechanism by which cyanide cripples enzyme function is as follows. The cyanide attaches itself to those enzymes with a metallic component and which are responsible for aerobic cell metabolism.
When the cyanide bonds with the copper components of cytochromoxidase the oxidizing function of the enzyme is blocked (54).
OKE (55) found that this resulted in a classic example of histotoxic anoxine (i.e. cell intoxication by reducing the oxygen supply) as described in 1931 by PETERS and VAN SLYKE (56).
When cyanogenic substances (including cyanogenic fruit and plants) are consumed the cellular detoxification mechanism converts the free cyanide into non-toxic thiocyanate.
In the human body thiocyanate is apparently stored in the thyroid gland (57). If the thiocyanate level is high the iodine content of the gland falls and reduces the synthesis of thyroxin (a natural blood pressure controller) (58). If the iodine level drops below a certain critical value, and sometimes even with mild iodine deficiencies, a rising thiocyanate level (caused by cyanide detoxification) will magnify the effects of iodine deficiency and its pathological effects (such as endemic goitre, LBT, etc.). By increasing the iodine content of the diet, the loss of iodine can be compensated and the iodine content of the gland can be kept at desirable levels.
This explains why iodine is so important in amygdalin cancer therapy. In this connection, furthermore, it is interesting to recall the high iodine P.S. therapy of SOLOMIDES (59).
Benzaldehyde, the second toxic product released by the decay of amygdalin also has a specific and selective effect on cancer cells (60). Normal cells have a high oxygen content and according to JOHNS (61) the benzaldehyde will be quickly oxidized to benzoic acid under the influence of aldehydeoxidase. By combining with glycine (one of the 20 alpha-amino acids) from the cell protein it forms hippuric acid, which is then secreted in the urine. This will in contrast not occur in cancer cells. The presence of cyanide inhibits the action of aldehydeoxidase (62), with the result that the benzaldehyde is not converted to benzoic acid. Moreover the benzaldehyde attracts the cell cholesterol and affects other cell lipids with the result that the vital membrane of the cancer cell is destroyed.
As like all cells, cancer cells depend on a double sugar metabolism, the aerobic (respiratory) and anaerobic (fermentative) metabolisms, the influence of cyanide on the aerobic metabolism (by inhibiting the cytochro-moxidase) is only of limited use. The alternative anaerobic cell metabolism can not be directly attacked by cyanide and the cancer cell can fall back on its anaerobic metabolism in order to survive, and HARROW and MAZUR (63) have shown that this is indeed so.Benzaldehyde, though, is capable of attacking the alternative metabolism. Recent studies have revealed that benzaldehyde inhibits the mitochondrial enzyme sodium, potassium and magnesium adenosinetri-phosphatase (ATPase), in turn inhibiting the conversion of the ATP into ADP (adenosinediphosphate) under the influence of ATPase (64).
This results in the inhibition of the aerobic glycolysis and brings about a fall in the glucose consumption of the tumor cell (65). The energy source for anaerobic glycolysis is thus blocked, demonstrating the synergy between cyanide (which blocks aerobic glycolysis) and benzaldehyde (which blocks anaerobic glycolysis). The general synergetic effects of the decay products of amygdalin has been stressed by BURK, McNAUGHTON and VON ARDENNE (66).
Pain-relieving Effects
This synergetic effect also applies to the empirically observed pain-relieving effect of amygdalin.
We know from work carried out by BARKER and LEVITAN (67) that benzaldehyde brings about a change in the permeability to sodium and potassium of the nerve membranes. Benzaldehyde and its metabolite benzoic acid produces an increase in membrane permeability for potassium (K+) and a corresponding reduction in permeability for sodium (Na-) so that nerve activity is diminished. This helps to explain the clinically observed pain-relieving effect of amygdalin.
Extended contact of benzaldehyde with blood results in the formation of methemoglobin, which has a local anaesthetic effect.Apart from the twin pain-relieving action of benzaldehyde, JACQUIER's theory (68) suggests that it has the power to produce peroxides in the cancer cell. This would mean that not only the cyanide ion but the peroxides produced by the benzaldehyde as well can destroy the cancer cell by lysis (particularly on the membrane). Once again this brings us very close to the theory and therapy of SOLOMIDES (69).
How does Amygdalin work?
The Hypothesis of PASSWATER AND BREWERAccording to PASSWATER and BREWER laetrile works essentially as follows. The attachment of carcinogens to cell membranes suppresses the transport of oxygen by the membranes. The conversion of dextrose into lactose as a result of the elimination of oxygen gives rise to a drop in the hydrogen-ion count (pH) from 7.35 to 6.0. Lysosome enzymes are released, while nucleic and amino acids ferment in the cell as a consequence of the above process. A reaction of lactic acid and lysome enzymes with DNA is the result, which in turn leads to the normal DNA-RNA (hereditary) reaction and the control mechanism of the cell being destroyed.
The therapy indicated is to raise the pH to 9, which can theoretically be achieved in persons with tumors with a low pH, by administering a suitable nitrile (Laetrile), causing the enzymatic release of cyan groups (C-N) in the cell itself.
The effect of the absorption of a cyan group on and in the cell membrane is that it will bring about a marked increase in the permeability of the membrane for cations (by the inclusion of potassium in the electromotive series - something wrong here) and will inhibit the expulsion of electrons by the phosphor groups (P=O) in the membrane (71).
The presence of CN groups on the cell membrane will considerably increase the transport of potassium ions in the cell. As under normal circumstances only a small proportion of these ions are related to dextrose, the final result is that the increased accumulation of very large numbers of electro-positive cations in the cell will tend to raise the pH of the cytoplasma.
In fact it is possible that, when there are enough cyan groups on the surface of the membrane, the cell will become moderately basic, on condition that enough potassium, or, more importantly, enough rubidium ions in the connecting fluid. This fact may be of very great importance to cancer therapy. Laetrile is perhaps part of the control mechanism, while potassium or rubidium may be necessary for another part. Laetrile on its own is never as effective as when combined with other therapies (72).
How does Amygdalin work?
The Hypothesis of BREKHMAN and DARDYMOVThis hypothesis was developed chiefly by scientists in the Soviet Union. In this hypothesis adaptogens (73) increase the non-specific resistance of the body.
Certain glycosides and other substances with a very low level of toxicity, have been shown to be capable of bringing about a significant increase in the capacity of the general immune mechanism to deal with cancer, arteriosclerosis, and other chronic degenerative disease.
Such adaptogenic glycosides, present in a wide range of plants, have proved to be effective in both trials in animals and human therapeutic applications in producing a non-specific normalizing effect in the immunological mechanism.
Probably these substances increase the production of antibodies, and are involved in the biosynthesis of proteins and in turn influence the nucleic acid mechanism.
Moreover general anabolic and anti-oxidizing effects which can counter free radial pathology are attributed to these adaptogenic glycosides.
Members of this group of adaptogenic glycoside include PANAX ginseng and ELEUTEROCOCCUS. The exact mechanism of these multiple influences still has to be uncovered and explained (74).
________________________________________________________________________________Foot-notes
(1) "D" stands for dextro(right)-rotatory isomer and "L" for levo(left)rota-tory isomer. This refers to the direction in which the isomers rotate the plane of polarized light passing through the complete compound in solution under certain specific conditions.
(2) A gentiobiosis is made up of two D-glucose units linked by a beta bond. See the Merck Index, 9th ed. page 81, Merck and Co., Rahway N.J. (1976);
(3) see Journal of Agriculture and Food Chemistry, 17, page 519. (1969).
(4) see chapter.... , page ....
(5) Journal of Applied Nutrition, page 74-88 (1970)
(6) See the chapter on the NIEPER Cure , page .
(7) DAVIDSON F.R., Synopis of Materia Medica, Toxicology and Pharmacology, 3rd ed. C.V. Mosby and Co. (1944)
(8) Oral administration is nevertheless 39 to 44 times more toxic than parenteral administration. This supports the consensus among laetrile therapists that parenteral administration (im, ip, and iv) is the most suitable. Certain authors are, like RUBIN*, of the opinion that by combining oral administration with an overall metabolic treatment, whereby certain substances such as emulsin (which contains certain enzymes such as B-prunase) are administered, the oral toxicity of amydalin can be avoided.
(*) RUBIN D., B-17 Breakthrough in ....
(9)
(10) MANNER H.W., The non-toxicity of Amydalin to laboratory mice, in Sc. Biol. J., May-June 347-349 (1977) see also
(11) See also the Report of the Southern Research Institute dated 13.4.1972 carried out on behalf of the NCI (under contract no. PH-43-68-998) which examines the possible carcinogenicity of classical chemotherapeutica. Most conventional antineoplastic drugs appear to be highly carcinogenic in trials in rats and mice, and in a surprisingly large number and variety of their organs.
(12) see chap. page...
(13) see the chapter on Manfred VON ARDENNE, page ...
(14)
(15) VON ARDENNE M. en REITNAUER P.G., Versuche zur lyosomalen Zytolyse-Kettenreaktion der Krebszellingschadigung, Z. Naturforsch., 29c, no 143 (1947)
(16) REITNAUER P.G., Mandelsaurenitril-Glykoside in Krebsforschung und Krebstherapie, Arzneimittel-Forschung, 22, no 122, page 1347 (1972)
(17) VON ARDENNE M. en REITNAUER P.G., Verstaurkung der mit Glukoseinfusion erzielbaren Tumorubersaurung in vivo durch Amygdalin und Beta-Glukosidase, Arch. Geschwulstfrsch., 43, no 157 (1974)
(18) This is similar to the Russian adaptogen theory of amygdalin's action, see below page ...
(19) In 1924 BURK completed his formal statistical studies, in 1927 he published a first article on statistical analysis and in 1934 he co-authored an innovative paper with Hans LINEWEAVER and Dr W. Edwards DEMING in the J. of the Amer. Chemical Society, 56, pps 225-230 (1934). In 1950 he published a mathematical biological article jointly with J. CORNFIELD in Scientific Monthly, 73,
(20) At my instigation, the Memorial Sloan Kettering Center is running a series of very serious tests with Laetrile. I hope this will give us some really useful evidence as to whether Laetrile does or does not have a truly useful role. I am not satisfied with simply repeating that claims about Laetrile have not been substantiated. I want to find out one way or the other, if we possibly can."
These lines were written by Benno C. SCHMIDT, who was appointed under the 1971 National Cancer Act by the President as head of the Cancer Board in order to supervise the distribution of Federal Cancer Funds (which in fiscal 1972-73 came to $ 432,000,000). In the US Mr SCHMIDT is regarded as Mr Cancer.
(21) When pressed to explain why the results of the SUGIURA tests were not published Chester STOCK, Vice-President of Chemotherapy Research at Sloan Kettering, said that if the earlier positive results had been made generally known at that time, all sorts of chaotic situations would have resulted. Robert GOOD, Head of the Sloan Kettering Institute added that the methods natural to science were simply not suited to that sort of pressure cooker atmosphere.
(22) An anonymous letter dated August 23, 1975 written on the "Memorial Sloan Kettering Cancer Center" letterhead received by M.L. CULBERT, a journalist, contained the following sentence,"Here are some of the results of Sloan Kettering's continuing experiments with Laetrile. Due to political pressures these results are being suppressed. Please do your best to bring these important findings to the attention of the people.
KREB's theory is very promising, and Laetrile should tested clinically to see if it really holds water".(23) MANNER H.W., DISANTI S.J., MAGGIO M.I., MICHAELSEN T.L., and ROWE V., How Laetrile, Vitamin A, Enzymes achieved 100 % response in mammary cancer in mice, in BRADFORD R.W. and CULBERT M.L., The Metabolic Management of Cancer, Ed. The Robert W. Bradford Foundation, Calif. (1979)
(24) see the chapter on proteolytic enzymes, page...
(25) KRIEBLE V.K., The Amygdalins and their inter-reactions with emulsin, J. Americ. Chem. Soc. 34, pps 716-735 (1912)
(26) VIEHOVER A. and MACK H., Biochemistry of Amygdalin, Am. J. of Pharm., 107, pps 397-450 (1935)
(27) HAILSMAN D.R. and KNIGHT D.J., The Enzymic Hydrolysis of Amygdalin, Biochem, J., 103, pps. 528-534 (1967)
(28) MELLOR J.D. and others, Intracellular Distribution of Steroid Glycosidase of Rabbit Liver, in the Canadian Journal of Biochemistry, 51, page 1292 (1973)
(29) VON ARDENNE M. and REITNAUER P.G. Tumor Hyperacidulation through Intravenous Glucose Infusion enhanced by Amygdalin and B-Glucosidase Application, in Arch. Geschwulstfrsch., 45 page 135 (1975). Chem Abstr., 83 94690 p. (1975)
(30) HAWKSWORTH G. and others, Intestinal Bacteria and the Hydrolysis of Glycosidic Bonds in J. of Med Microbiology, 4, page 451 (1971)
(31) in this view the production of B-glucosidase is dependent on the intestinal flora, and is thus influence by diet.
(32) BOSMANN H.B., Red Cell Hydrolases, Journal of Membrane Biology, 4, page 113 (1971)
(33) BRADFORD R.W. and ALLEN H.W., The Focal Action of Amygdalin in the Metabolic Therapy of Cancer, in BRADFORD R.W. and CULBERT M.L. op cit. page 27.
(34) LEVVY G.A. and CONCHIE J., B-glucuronidase and the hydrolysis of glucuronides in Glucuronic Acid - free and combined (G.J. DUTTON, ed.), Academic Press N.Y., page 301-357 (1966)
(35) MIETTINEN T.A. and LESKINEN E., Glucuronic acid pathway, in FISHMAN W.H. (ed.) Metabolic conjugation and metabolic hydrolysis, Academic Press, N.Y. page 157-237 (1970)
(36) WHITE A., HANDLER P. and SMITH E.L. Principles of Biochemistry, 5th Ed., McGraw Hill Book Co., N.Y. page 1296 (1973)
(37) According to RIEDERS this is not the result of an enzymatic process but a spontaneous occurrence in mildly alkaline milieu, and is thus pH dependent.
RIEDERS F. Formation of inorganic Cyanide from aliphatic nitriles in rabbits, in Federation Proceedings, 11 page 386 (1952).(38) FISHMAN W.H. and ANLYAN A.J., A comparison of the B-glucuronidase activity of normal, tumor, and lymph node tissues of surgical patients, in Science, 106, page 66-67 (1947)
(39) According to CZARNECK and others The simultaneous administration of 500,000 I.E. emulsified vitamin A can increase the leakage of B-glucuronidase from a lyosomal milieu by a factor of 400.
CZARNECKI M. and others Physiopathological Role of Lyosomes, in Polskie Arhiwum Medycyny Wewnetrznej (Polish Archives of Internal Medicine). Chem Abstr. 71. 457v. (1969).(40) OSUNTOKUN
(41) OKE O.L. The role of hydrocyanic acid in nutrition, Wld. Rev. Nutr. Diet, II, pps 170-198 (1969)
(42) DE DUVE C. et al., Tissue Fractionation Studies, in Biochemical Journal, 60, page 606 (1955)
(43) HIMWICH W.A. et al., Enyzmatic conversion of cyanide to thiocyanate, in the American Journal of Physiology, 153, page 348 (1948).
(44) WOOD & FIEDLER, J. Biol. Chem., 205, page 231 (1953)
(45) MUSHETT et al. Por. Soc. Exp. Biol., N.Y., 81, p. 234 (1952)
(46) AURIGA M. and KOJ. A., Protective effect of rhodanese on the respiration of isolated mitochondria intoxicated with cyanide, Bull. Polish Sci. Ser. Biol. 23(5), pps. 305-310 (1975).
(47) BOXER and RIKARDS, Arch. Biochem., 39, p. 7 (1952)
(48) MENDEL B., RUDNEY H. and BOWMAN M.C. Rhodanese and the Pasteur Effect, Cancer Research, 6, page 495 (Abstract) (1946)
(49) GIORDANO, G., VIOLANTE A., LERENZETTI G. and SAPLO U., Rhodanese activity on the neoplastic and hemopoetic tissue of rats with myeloma in leukemic phase, Biochem. Appll., 3, page 84 (1956).
(50) FISHMAN and ANLYAN (op cit) were able to show that the B-glucuronidase had incidences from 100 to 3600 times higher in cancer tissues from the breast, uterus and stomach than in the corresponding healthy tissue.
(51) BRAUNSTEIN G.D., VAITUKAITIS J.L., CARBONE P.P., and ROSS G.T., Ectopic production of chorionic gonadotrophin by neoplasms, Ann. Int. Med. 78 page 39-45 (1973).
(52) see the ...... test on page ..... which uses the presence of the HCG hormone to detect cancer.
(53) SANCHEZ F.S., and BELTRAN E.C., Variations in the rhodanese activity induced by injection of chorionic gonadotrophin, Ann. Fac. Vet. Univ., Madrid Inst. Invest. Vet., 3 pps. 78-82 (1951).
(54) SCHUBERT J. and BRILL W.A. Antagonism of experimental cyanide toxicity in relation to the in vivo activity of cytochrome oxydase, the Journal of Pharmacology and Experimental Therapeutics, 162, p. 352 (1968)
ALBAUM J.T. et al. A spectophotometric study of the competition of methemoglobin and cytochrome oxidase for cyanide in vitro, Journal of Biol. Chemistry, 163, page 641 (1946)(55) OKE O.L. op cit.
(56) PETERS J.P. and VAN SLYKE D.D. Quantitative clinical chemistry, Williams Co., Baltimore, 2 Vols. (1931)
(57) BRADFORD R.W. and ALLEN W.A. op cit
LAGARDE P. Cancers. Lumière sur les therapatiques rejet·Ç·es, p. 108 (1980)(58) N.N. Drill's Pharmacology in Medicine, McGraw Hill Book Co. Inc., N.Y. page 1447 (1977)
(59) See the chapter on the SOLOMIDES therapy, page...
(60) This is a reference to an experimental benzaldehyde cancer remedy developed by Dr Mutsuyuki KOCHI and which is under clinical trial in Japanese hospitals. Trials in animals yielded very encouraging results particularly on EHRLICH carcinoma and adenocarcinoma 755. KOCHI and YANO will soon be publishing their results in human therapy.
(61) JOHNS D.G. Human liver aldehyde oxydase: differential inhibition of oxidation of charged and uncharged substrates, J. Clin. INvest., 46(9), pps 1492-1505 (1967).
(62) SCHUBERT J. and BRILL W.A., op cit.
(63) RACKER E., Bioenergetics and the Problem of Tumor Growth, Amer. Scientist, 60, page 56, (1972). According to VIANNA the thiocyanate ion resulting from the detoxification of cyanide also inhibits TPAase.
(64) VIANNA A.L., Effects of anions and urea on the ATPase and calcium uptake activities of fragmented sarcoplasmic reticulum. Physiological Chemistry and Physics, 3, page 536 (1971).
(65) ERWIN V.G., KIM J. and ANDERSON A.D., Effects of aldehydes on sodium-plus- potassium ion-simulated ATP of mouse brain, Biochem. Pharmacol., 24 (22) page 2089-2095 (1975)
(66) BURK D., McNAUGHTON A.R.L. and VON ARDENNE M. National Cancer Institute, Bethesda M.D., Hyperthermia of cancer cells with amygdalin-glucosidase and synergistic action of derived cyanide and benzaldehyde. Panminerva Medica 13, page 520 (1971), Chem Abstracts, 77, 15036e, (1972)
(67) BARKER J.L. and LEVITAN H., Mitochondrial uncoupling agents. Effects on membrane permeability of molluscan neurons, J. Membr. Biol., 25 (3-4) pps 361-380 (1976)
(68) JACQUIER, ...
see also page ...(69) see the chapter on SOLOMIDES, page ...
(70) PASSWATER R.A., Cancer and its nutritional therapies, Keats Publishing Inc., Connecticut. (1978)
PASSWATER R.A. In defense of Laetrile. Let's Live, page 50 - 55 (June) (1977)(71) Here benzaldehyde may play an important role, as explained earlier in the "pain-relieving" part of this chapter (page ...)
(72) Of course the nutritional therapies and therapies which alter cell pH, such a as GELUM ORAL, (see page ...).
(73) The term 'adaptogen' refers to substance which possesses the property of exerting an 'adaptive' or 'normalizing' effect within the general immune mechanism. The term 'adaptogen' is due to Soviet scientists and corresponds broadly to our word 'normalization'.
(74) BREKHMAN I.I. and DARDYMOV I.D., New substances of plant origin which increases non-specific resistance, Ann. Rev. Pharm., 9, page 419-430 (1969).
PRACTICAL INFORMATION
I. MANUFACTURERS
1. AMYGATRILE® :
American Biologics
111 Ellis St. at Powell, Suite 300
San Francisco, Calif. 94102Phone : Calif. residents : (415) 981-8384
Toll free 800 / 227-4473
2. KEMDALYN® :
Laboratorios Kem S.A.
Av. Madrid y Calle Oslo, n° 422-B
Fraccionamiento Costa Azul
Playas de Tijuana
Tijuana, Baja California
MexicoPhone : (903) 38- -1850/5
Mailing address :
P.O.B. 4877
San Ysidro, Calif. 92073
3. LAEVALIN® :
Vitachem International
241 Hazel Ave.
Redwood City, Calif. 94061Phone : (415) 365-6692
Toll free 800 / 227-4473
4. Metalbolic Products
Mr. Art Usner
P.O.B. 3336
Albuquerque, New Mexico 87190
call collect : (505) 296-7300
5. C.R.W. Rahlstedt G.m.b.h. (Ltd)
Chemische und pharmazeutische Warenhandelsgesellschaft m.b.H.
P.O.B. 73 05 27
Buchwaldstraße, 67
D-2000 Hamburg 73
Federal Reuplic of GermanyPhone : (040) 647.41.43
direct from U.S.A. & Canada :
011-49-40-647.41.43Telex : 2173821 cpwr d.
II. FOR MORE INFORMATION ON LAETRILE, ON ECAN APPLY TO FOLLOWING ORGANIZATIONS :
1. Committee for Freedom of Choice in Cancer Therapy, Inc.
(a non-profit organization)
146 Main St., Suite 408
Los Altos, Calif. 94022
Phone : (415) 948-9475
2. Contreras Amigros International
519 E. San Ysidro Blvd.
San Ysidro, Calif. 92073
3. Nutrisearch Foundation
Redwood City, Calif. 94061
4. Cancer Control Society
(a non-profit educational Society)
2043 N. Berendo
Los Angeles, Calif. 90027
Phone : (213) 663-7801
Delaware Chapter
201 Hitching Post Drive
Wilmington, Delaware 19803
Phone : (302) 478-4426
Kalamazoo Chapter
2016 N. Westnedge Ave.
Kalamazoo, Michigan 49007
Phone : (616) 343-1100
Kansas City Chapter
533 S. Hardesty
Kansas City, Missouri 64124
Phone : (816) 231-8237
Mobile Chapter
3915 21st Court East
New Port Richey, Florida 33552
Phone : (813) 848-5675
Orange County Chapter
P.O.B. 933
Anaheim, Calif. 92805
Sunflower Chapter
R.R. 1
Grantville, Kansas 66429
Phone : (913) 289-3607
5. Robert W. Bradford Research Institute
111 Ellis St., Suite 300
San Francisco, Calif. 94102.
6. Dr. Harold Manner
Metabolic Research Foundation
8001 N. Milwaukee
Niles, Illinois 60648
7. C.R.W. Rahlstedt G.m.b.h.
Chemische und pharmazeutische Warenhandelsgesellschaft m.b.H.
above-mentioned
8. Mountainview Medical Association, P.C.
Mountainview Medical Bldg.
Mountainview Ave.
Nyack, New York 10960
Phone : (914) 358-6800
III. CLINICS AND MEDICAL CENTERS :
1. American Biologics-Mexico Hospital
Baja California, Mexico
Administration & Admission Headquarters :
111 Ellis St., Suite 300
San Francisco, Calif. 94102
Phone : Calif. Residents : (415) 981-8384
Toll free : (800) 227-4473
International telex : 171791
2. Centro Médico del Mar
Paseo Playas de Tijuana, n° 19
Playas de Tijuana
Tijuana, Baja California
México
Phone : (903) 38-7-1203/4
1222Hospital del Mar
Risco 57
Costa Hermosa
Playas de Tijuana
Tijuana, Baja California
México
mailing address :
P.O.B. 1561
Chula Vista, Calif. 92012
message phone : (714) 428-6438
3. Health and Wellness Center
of Minnesota, Inc.
8054 Morgan Circle
Bloomington Ave.
Phone : (612) 888-5002
4. Mountainview Medical Association, P.C.
Mountainview Medical Bldg.
Mountainview Ave.
Nyack, New York 10960
Phone : (914) 358-6800
5. Joseph L. Kaplowe, M.D.
195 Sherman Ave.
New Haven, Conn. 06511
6. "Auchenkyle"-Clinic
Southwoods Road
Troon, Ayrshire
Scotland
Phone : (0292) 311.414
Jan De Vries, Dr. H. Med. Ph.D., D.Ac., D.O.N.D.
IV. PHYSICIANS FAMILIAR WITH LAETRILE-THERAPEUTICS :
1. ask for leaflet "Nutritional-minded doctors in the U.S.
and Canada" published by :
Public Relation Service
Alacer Corp.
Buena Park, Calif. 90622
2. contact above-mentioned (under II ) organizations which
will provide you with some lists of physicians.
V. PUBLICATIONS :
1. "The Choice - The International Newsmagazine of Metabolic
Therapy and Freedom of Choice in Medicine".
Official publication of the Committee for Freedom of
Choice in Cancer Therapy, Inc.
146 Main Street, Suite 408
Los Altos, Calif. 94022
Phone : (415) 948-9475
2. Cancer Control Journal
Official publication of the Cancer Control Society
2043 N. Berendo
Los Angeles, Calif. 90027
Phone : (213) 663-7801
3. Cancer Book House
2043 N. Berendo
Los Angeles, Calif. 90027
distributes books and reprints on nutrition, cancer and other
nutritionally related diseases.
Also :
MANUFACTURER :
Cyto Pharma de Mexico, S.A.
Juan Carrasco, n° 13
Fracc. Soler
Appartado Postal 3437
Tijuana, Baja California
Mexico
Phone : (903) 38-7-15.85 and 15.96
mailing address :
P.O.B. 4290
San Ysidro, Calif. 92073
CLINIC :
Halstead Preventive Medical Clinix
11155 Mt. View Avenua, Suite A
Loma Linda, Calif. 92354
Phone : (714)796-8305
824-1750
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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