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What is Laetrile and Amygdaline?

(In short, Laetrile is the extract from apricot seeds)


An intelligent discussion of a chemical substance such as Laetrile (amygdaline) demands an accurate scientific definition of all chemical terminology relating to the topic. In the past both pro-Laetrilists and anti-Laetrilists have created an enormous amount of confusion because both sides have refused to deal with the primary issues of technical semantics and definitions of terminology. Great pains have been taken to avoid that pitfall in the present publication.

The terms Laetrile and amygdalin are used interchangeably and according to the Merk Index (1989) they are chemically synonymous. To make it emphatically clear this reading is dealing with amygdalin and nothing else but the cacogenic glycoside known as amygdalin unless clearly designated to the contrary when the subject of Laetrile metabolic cancer therapy which will be discussed shortly.

Krebs and company have done much to completely confuse the issue as the precise chemical formula of Laetrile by introducing a potpourri of chemical terms such as Laetrile, laetrile, mandelonitrile, sarcomas, nitriloside. Vitamin B17, and betacyanogenic glycosides. All of these compounds are not chemically the same. Most of these issues are discussed in the FDA publication, Laetrile, The Comms1isioner’s Decision (HEW, 1977).

There are two spellings of the term Laetrile and laetrile. The capitalized Laetrile is synonymous with amygdalin and will be used as such throughout the book, unless otherwise noted. According to the FDA the term laetrile with a lower case “I” is a generic term that includes Laetrile, Laetrile ï½®, laetrile, amygdalin, nitriloside, and vitamin B17. It is also used to include a number of other compounds, in which case it may appear as “laetrile.” The entire subject of amygdalin therapy is plagued with a cloud of technical semantics, most of which can be credited to Krebs and company and many of their proponents. The following chemical compounds have all been involved at one time or another in the amygdalin scenario:

Some of the following comments on the chemical structure and genesis of the laetriles were takes directly from a series of letters that I (BWH) received in the 1980’s from Ernst Krebs, Jr.

According to Krebs, Jr. “laetrile” spelled with the small “l” was simply a crude extract of amygdalin. However, this is a worthless chemical definition that is of no practical value.

The compound which Krebs, Jr. extracted from apricot kernels (prunes armaeniaca Linnaeus), known as Laetrile was chemically pure natural amygdalin. Ernst T. Krebs, and Ernst T. Krebs Jr. registered the term Laetrile with the U.S. Patent Office June 30, 1953. This product is pure amygdalin and that is the form that historically had been used for medicinal purposes. Pure Amygdalin is the form that is being discussed throughout this book.

The uncertainty of the chemical identity of laetrile, Laetrile, and amygdalyn is the major legal problem that has confronted the pro-laetrilsts, which they have largely ignored. The FDA has attempted to define the chemical nature of Laetrile and amygdalin. (Kennedy, FDA Docket No 77N-0048, 1977). The issue of chemical semantics has been the Achilles heel of the entire Laetrile movement. Clarification of the chemical identity of commercial Laetrile is imperative. It should be kept in mind that commercial Laetrile is not a crude extract of apricot kernels, but is a “purified” chemical agent that has been extracted with the use if ethyl alcohol. This requires the use of the correct chemical terminology, which is not always palatable to the no chemist, but is vital to any legal, therapeutic, or pharmaceutical discussion of Laetrile. The definition as given herein may not meet with complete acceptance by all pro-literalists, but follows the Merck Index, which is acceptable to chemists, and the FDA. It is a basic fact of pharmacology that you must have consistency in the chemical structure of the drug you are administering, if you are to determine the proper dosage of the drug, it’s toxicity and consistent efficacy in therapeutic results. We will be adhering to the Merck Index (1976).

The Chemical Nature of Amygdalin

Amygdalin is the first discovered and best known of the cyanogenic glycosides. Crystalline Amygdalin was first isolated in 1930 by two French chemists, Robiquet and Boutron-Charlard, from the bitter almond, Amygdalus communis Linnaeus, now known as Prunus amygdalus Batsch, of the rose family Rosaceae. Hence, the term amygdalin is appropriately named after the scientific name of the bitter almond. However, in modern times amygdalin is commercially extracted form the kernels of apricots (Prunus armeniaca Linnaeus). The generic tem amygdalus is derived from the Greek amygdale, amygdalin that is eaten throughout the world as a nutritional supplement. Apricot kernels are eaten in moderation, but should not be eaten with almonds.

The chemical structure of amygdalin is well established and is clearly recorded in the Merck Index, (9th Ed., p. 81, 1976) as D(1)-mandelonitrile-b -D-glucosido-6-b -D-glucoside (other synonyms: (R-a-[(6-O-b -D-Glocopyranosyl-b -D-glucopyranosyl)] oxy benzeneacetronitrile; amygdaloidal; mandelanitrile-b -gentiobioside). The empirical formula is C20 H27 NO11. The molecular weight is 457.22. The element composition is C 52.51%, H 5.959%, N 3.06%, O 38.47%. For further information on the biochemistry of amygdalin see Vie hover and Mack (1935) and Oke (1969).

The Chemical Nature of Laetrile

The term laetrile was first proposed by Ernest T. Krebs, Jr., about 1949. The word is derived from a contraction of the chemical term laevo-mandelonitrile. Unfortunately derived from a technical viewpoint, the introduction of the term laetrile has not helped to clarify the issue, but if anything, has muddied up the water still further. Krebs has also used the term laetrile to broadly designate the beta-cyanogenic glycosides, which includes amygdalin and any of its chemical relatives as previously noted. Krebs has also designated laetrile as Vitamin B17 and has further proposed the term nitrilosides which is more or less a generic name for these same glucosides. The vitamin status of Laetrile is generally not accepted by most biochemists.

Synthetic Laetrileï½® is a decomposition product resulting from the hydrolysis of amygdalin. Synthetic laetrile apparently has never been commercially available in the United States to any great extent. One of the confusing issues is the chemical structure of one of Krebs’s “laetrile” components, which contains one less glucose molecule than amygdalin, but does contain cyanide ion. The FDA feels that the confusion in the laetrile semantics was purposely perpetrated by Krebs and company for the express purpose to continue to use drugs containing amygdalin while justifying the use of drugs by theories associated with the Laetrile of Krebs, Jr., and they are probably correct. The explanation upon which Krebs believed that Laetrile functioned was known as the trophoblast theory. This theory which has never been proven has been discussed at length in Gurchot’s book, Biology. Key to the riddle of cancer, 1943).

Laetrile (amygdalin) does not contain unbound free toxic cyanide, which is contrary to what the anti-literalists would like the public to believe. True cyanides will be discussed shortly.

Regardless of how one might feel about the use of the term laetrile, the word is here to stay and all one can hope to do is to define its usage. In the interest of clarification, the use of the term Laetrile (amygdalin) will be restricted in this publication to that defined by the Merck Index (9th ed., 1976), which has been discussed in the previous paragraph.

Optical Isomers of Amygdalin

Optical isomers are two or more compounds which have the same chemical composition and the same two-dimensional structural formulas, but differ in the spatial arrangement of the atoms or groups about one or more asymmetric atoms or bonds that are present, so that the plane of polarized light is rotated in a different direction, either (left, levo or right, dextro). Amygdalin is either in a dextro or a levo form. Ordinary amygdalin is D(l)-mandelonitrile-β-D-glucosido-6-D-glucoside (Merck, 1976). However, when racemization (Production of mixture in which a dextro-and levorotatory optically active isomers in equal amounts) takes place, the amygdalin molecule can be transformed into its tow optical isomers of the dextro-and lavo- forms. Chemical analyses have shown that racemic amygdalin is 56.25% of the dextro and 43.75% of the levo form. This matter is believed to be of biological and therapeutic importance because the Dextro form is considered to be therapeutically inactive in cancer therapy, whereas the leve form is reputedly the therapeutically is the active form. It is therefore imperative that the highest level of quality control be employed in the production of amygdalin. Failure to recognized these points may result in inadequate dosage levels and poor therapeutic results (Krieble, 1912; Levi, et al, 1965; Rubin and Issahary, 1976)


Linamarin is a canogenic glycoside, chemically related to amygdalin, which is derived from various plant species. Linamarin has been known since 1891. It does not contain free cyanide. The cyanide ion (CN-) only becomes free when it undergoes hydrolysis. One of the most common plant sources of linamarin is the cassava, also known as manioc or tapioca (Manihot esculenta Crantz).

The cassava is a major starch food for millions of people throughout the tropical world, and provides a valuable source of carbohydrate, protein, calcium, iron, thiamine, riboflavin and niacin. Cassava is commonly used by anti-laetrilists as an example of the poisonous properties of “laetrile” because tropical ataxic neuropathy and endemic goiter appear to be associated with malnutrition. It is believed that there are multiple factors involved in the causation of ataxic neuropathy. Attributing ataxic neuropathy solely to linamarin is of questionable scientific validity and has even less pertinence to amygdalin (laetrile) since linamarin has never been used in cancer metabolic therapy in the United States, but has been used elsewhere in the world. The toxicity of linamarin has been discussed in great detail by Nestel & MacIntyre (1973). Those that have used linamarin claim to have good results similar to laetrile, but was less costly (Navarroto laetrile at less cost). It should also be noted that none of the physicians using linamarin has ever reported their patients developing ataxic neuropathy as claimed by Victor Herbert in the Chad Green trial.

It should be noted that linamarin has a different chemical structure than amygdalin. Linamarin is 2-(-D-glucopyranoslyloxy)-2-methylprpanenitrile, or phaseolunatin. The empirical formula is C10H17NO6. The molecular weight is 247.24. The elemental composition is c 48.58%, H 6.93%, N 5.67%, O 38.83%.


Benzaldehyde is also known as benzoic aldehyde and commercially as an artificial essential oil of almonds. The chemical formula is C7H6O. It has a molecular weight of 106.12. The elemental composition is C 79.22%, H 5.70%, O 15.08%. Benzaldehyde occurs in the kernels of bitter almonds and apricots. Benzaldehyde can be synthetically produced from benzyl chloride and lime of by oxidation of toluene. It is used commercially in dyes, perfumes and flavorings. It is a normal metabolic byproduct of amygdalin (laetrile) and has been demonstrated to have anticancer activity in laboratory animals (Takeuchi, er al, 1978) and acts as a analgesic (Barker & Levitan, 1976; Contreras, 1982).


This compound is also known as sulfocyanate of rhodanate. The chemical formula is SCN. The molecular weight is 58.07. The elemental composition is S 55.2%, C 20.6%, N 14.0%. The sodium and potassium salts of thicyanate have been used extensively in the past in the United States in the treatment of hypertension. Thiocyanate was first studied by Claude Bernard in 1857, but despite this long history of usage the mechanism of action is still unknown. Thiocyanate is normal metabolic byproduct resulting from ingestion of cyanide-containing foods (nitrilosides) such as maize, sorghum, millet, beans, cassava, lettuce, cabbages, cruciferous vegetables, apricot kernels, almonds, etc. (Osol and Farrar, 1947). The National Research Council.


The FDA and other agencies frequently refer to pyrogens and pyrogenic reactions due to improperly manufactured laetrile. Pyrogens are toxic substances produced by certain types of microorganisms that have contaminated a solution, medicines, or glassware during the process of manufacturing. Pyrogens are sometimes referred to as bacterial pyrogens or endotoxins. Bacteriologists have recognized them since 1875. Pyrogens are derived from the cell walls of gram-negative bacteria and have been identified biochemically as lipo-polysaccharides of high molecular weight. However, in addition to these end toxins, various other types of gram-positive bacteria, viruses and fungi are also capable of producing pyrogenic substances known, and may produce adverse effects at even submicrogram amounts. Pyrogens are not limited to laetrile and may be found in any contaminated solution, water, or medicine. They must be injected to produce their effects. Pyrogenic reactions consist of fever, chills, changes in the white blood count, and in rare instances may adversely affect various other organ systems. Pyrogen reactions are usually of short duration, self-limiting, and are treated symptomatically.


The purpose of this recital on the subject of cyanide is to clarify the continual misconception that laetrile contains chemical cyanide. It does not contain chemical cyanide, but it does contain cyanide ion (-CN). When laetrile is metabolized in the body it is converted to thiocyanate, a relatively non-toxic product that has inhibitory effect against cancer (Contreras, 1982).

The term “cyanide” is used to designate hydrogen cyanide (also known as hydrocyanic acid, prussic acid, or formonitrile), or cyanide salts (sodium cyanide (NaCN), potassium cyanide (KCN), or calcium cyanide (Ca(CN)2). The word “cyanide” or the symbol “CN” are commonly used to designate both hydrogen cyanide as well as the salts of cyanide. These cyanide substances are also referred to as “free cyanide.” When the term “cyanide” is used, it refers to one of the above substances. This is an important fundamental point of chemistry and toxicology because on this point hinges most of the deceptions and fraudulent claims of anti-laetrilists. Most of the information provided in this presentation is taken directly from the publication of the National Institute for Occupational Safety and Health (NIOSH), U.S. Department of Health, Education, and Welfare (DHEW), entitled Occupational Exposure to Hydrogen Cyanide and Cyanide Salts (NIOSH, 1976), and the Merck Index, 9th edition, 1976 and the 11th edition, 1989.

Hydrogen Cyanide (hydrocyanic acid, prussic acid, or formonitrile): Hydrogen cyanide is prepared on a large scale by the catalytic oxidation of ammonia-methane mixtures, or by the catalytic decomposition of form amide. The chemical formula is HCN. The molecular weight is 27.03. The elemental composition is C 44.44%, H 3.73%, N 51.83%. It is a colorless gas or liquid, having a penetrating characteristic odor of bitter almonds.

Sodium Cyanide: The commercial form of this compound form of this compound is 95-98% pure, and is known as cyanogran. Mixtures of sodium cyanide with sodium chloride or carbonate are marketed for various purposes. NaCN is a white crystalline solid at room temperature. The chemical formula is NaCN. The molecular weight is 49.02. The elemental composition is C 24.50%, N 28.58%, Na 48.92%. NaCN consists of either white granules or fused pieces. It is odorless when dry but emits an odor of HCN when moist. The aqueous solution is strongly alkaline. It is commercially produced from coke-oven gas by the reaction of HCN and sodium hydroxide.

Potassium Cyanide: The chemical formula is KCN. The molecular weight is 65.11. The elemental composition is C 18.440%, K 60.05%, N 21.51%. The article of commerce contains about 95% KCN. Strong solutions are can be absorbed through the skin. KCN is in the form of white granules or fused pieces which, when exposed to the air, may emit an odor of HCN. An aqueous solution is strongly alkaline. KCN is commercially produced by methods similar to NaCN.

Calcium Cyanide: The chemical formula is Ca(CN)2, commercially known as black cyanide. The molecular weight is 92.12. The elemental composition is C 26.0%, Ca 43.52%, N 30.41%. The commercial product of this compound contains 40-50% of Ca (CN)2. Ca(CN)2 consists of crystals or a powder. When moist it emits an odor of HCN. Ca(CN)2 is commercially made by heating calcium cyanamide in a electric furnace at high temperatures in the presence of sodium chloride, and then rapidly cooling it. Ca(CN)2 is used in a variety of manufacturing procedures.

Other chemical agents used in the laetrile scenario

Beta-cyanogenic glucosidesThere are two terms that have been used interchangeably, they are beta-cyanorphoric glucoside and beta– cyanogenetic glucoside. These two chemical terms are used interchangeably. They are two compounds that can be broken down to yield a cyanogenic glycoside, which contain cyanide ion and glucose which are similar to amygdallin.

Enzyme: These are specialized proteins produced by living organisms that act as catalysts to speed up a chemical reaction. They generally act only on a specific substrate.

Beta-glucosidase: An enzyme present in plants that participates in the metabolism of glucosides. This enzyme has been identified in apricot, peach, and related fruit kernels and catalyzes the breakdown of amygdalin to free two molecules of glucose and a molecule of mandelonitrile. The enzyme is found only in trace amounts in animal tissue.

Beta-glucoronidase: acid derivatives, also called glucuronides. The enzyme reportedly catalyzes the breakdown product of Laetrile (1-mandelonitrile-beta-glucuronic acid) to free aleuronic and mandelonitrile

Mandelonitrile: Is a specific chemical entity. The dextro form is derived from the hydrolysis of amygdalin.

Nitriloside: A term proposed by Ernest T. Krebs, Jr. that includes all cyanophoriouglyconsides of dietary significance.

Prunasin: A monosaccharide derivative of mandelonitrile consisting of benzaldehyde cyanohydrin coupled to a dextro-glucose residue.

Sarcarcinase: The term given to an enzyme preparation, as a mixture of the following Krebs, Sr. and described by him a 1933 patent application, as a mixture of the following enzymes: amylase, prunase, oxynitrilase, catalase, peroxydase, and a proteoloytic enzyme. He also suggested the presence isomaltase, lipase and perhaps other enzymes.

Vitamin B17: Described Krebs, Jr. as a group of compounds which include water souluble essentially nontoxic glucosides found in over 800 plants. A term which Krebs, Jr. used interchangeably with nitrilosides, Laetrile, amygdalin, beta-cyanogenic glucosides. This is an example of the confusion that Krebs perpetrated in his Laetrile operations. Vitamin B17 has never been accepted as a true vitamin by most biochemist.

How Does Laetrile Work?

An attempt will be made to explain the scientific rationale for the use of Laetrile in cancer metabolic therapy. It should be pointed out that there are hundreds of drugs that are currently in use in medicine throughout the world in which the precise mechanism of therapeutic action is not completely known. Aspirin is one such drug. The precise mechanism of action for Laetrile is not known but there are a number of hypotheses that have been presented. See Viehoever and Mack (1935).

Metabolic cancer physicians are convinced that nutrition plays a major role in cancer therapy and some of the reasons for their belief have been expressed in Chapter Two. Laetrile therapy has largely been developed and used on the basis of this nutritional approach.

One of the theories on the action of Laetrile in the body is based on the work of Ernest Krebs, Jr., and is sometimes referred to as the cyanide theory. However, this theory is not entirely of Krebs’ making, but is based on biochemical facts derived from several different sources. In order to follow the development of this cyanide theory it will be helpful to examine the biochemical pathway of amygdalin tin the body and its chemical relationship to Laetrile and the final degradation products.

It will be noted that there are two separate pathways which have been designated as I and II. Pathway I is well established in the chemical literature dealing with amygdalin, and results from the hydrolysis of amygdalin by the enzymes β-glucocidase, emulsin, etc., and acids (Krieble, 1912; Viehoever & Mack, 1935; Haisman & Knight, 1967; Oke, 1969). There does not appear to be any question concerning the scientific validity of pathway, I of the resulting end products hydrogen cyanide, the final end product which ends up as thiocyanate, a nontoxic cancer inhibitor.

Pathway II is a second degradation pathway that has been proposed by Krebs and is an essential component in his theory as to how Laetrile acts in the cancer cell. Although the scientific validity of this process has been questioned (Greenberg, 1975), there is a growing amount of biochemical evidence that this process does take place in the liver of persons ingesting amygdalin. It is theorized that the prunasen glucoside can be catalyzed in the Laetrile glucuronide, but this takes a two-step oxidative and the exact process has not been experimentally demonstrated. However, it has been established that glucuronide formation occurs in the liver and to a lesser extent in the intestines and kidneys (White, Handler & Smith, 1973). In order for the laetrile glucuronide to produce the HCN and benxaldehyde given in Pathway II, it requires β-glucuronidase enzyme, and it has been demonstrate that this enzyme be present in cancerous tissue of the breast, intestine, uterus, stomach, mesentery, abdominal wall, and esophagus, about 100 to 3,600 times higher than is present in non-cancerous tissue (Fishman and Anlyan, 1947).

In order to proceed with the Krebs hypothesis as to how amygdalin (Laetrile) works against cancer, there is one additional point that must be explained which relates to the occurrence of the enzyme rhodanase or transulferase (transulferase) in the liver cells. Rhondanase was discovered by Lang in 1933, and is now known to be concerned with the conversion of toxic hydrocyanic acid to thiocyanate, a nontoxic cancer inhibitor (Oke, 6, NRC, 1982). Rhodanse also appears to be actively involved in the formation of cyanocobalmin or vitamin B12. Rhodanase is now known to be part of the detoxification process of the body (Auriiga &Koj, 1975). However, it was found that normal cells contain a relatively high concentration of rhodanase and a low concentration of rhodanase is now known to be part of the detoxification process of the body (Auriga & Koj, 1975). However, it was found that normal cells contain a relatively high concentration of rhodanase and a low concentration of the enzyme β-glucuronidase, whereas some cancer cells are high in β-glucuronidase and low in rhodanase. Tumor cells (carcinoma, melanoma, multiple myeloma) produce human chrionic gonadotropin (HCG) (Braunstein, et al, 1973). HCG present in the tumor cell inhibits rhodanase, and thereby blocks the conversation of hydrogen cyanide to thiocyanate (Sanchez & Beltran, 1951). Thus, the normal cellular protective mechanism is decreased in tumor cells and becomes more sensitive to the effects of the cyanide. According to Krebs, the purpose to designing the Laetrile glucuronide molecule was to provide a molecule that would concentrate its toxic effects against the cancer cell and not the host. Krebs postulated that since cancer cells contained high levels of β-glucuronidase, this enzyme would act upon the Laetrile glucuronide and thereby release the cyanide ion against the cancer cell. It would depress the activity of the protective enzymes of the cancer cell, and thereby destroy it.

The mechanism by which cyanide enzyme functions is well established in the scientific literature. Cyanide combines with cytochrome oxidase and thereby inhibits its function as an oxidative enzyme in electron transfer and provides historic anoxic which was described by Peters and Van Slyke in 1931 (Oke, 1969; Sakai, 1963). Since normal cells contain large quantities of rhodanase and relatively low quantities of β-glucuronidase, the available rhodonase would detoxify the cyanide ion, forming the non-toxic thiocyanate cancer inhibitor. Brown, Wood, and Smith (1960) found that experimental studies in animals’ tumor systems in dogs and mice responded to treatment with parenteral injections of sodium cyanide. The animals lived longer. The administration of cyanide in human terminal uterine cancer cases that were too far advanced to use any other form of treatment failed to respond to sodium cyanide. Nevertheless, the investigators concluded that there were no accumulative toxic effects from the cyanide and there were inhibitory effects against the tumor cells. There was no follow-up on this work.

Krebs further reported that additional benefits were to be obtained by the cancer patients from the use of laetrile because of the well-known analgesic effects of the benzaldehyde. Benzaldehyde is believed to produce its action by decreasing neuron membrane permeability to sodium and potassium ions (Barker & Levitan, 1976). This analgesic effect has now been observed and documented in hundreds of patients (Contreras, 1982). There appears to be a synergistic action of some type because benzaldehyde by itself does not seem to provide the remarkably high analgesia as that obtained from the mandelonitrile-bezaldehyde complex. Recent studies have shown that benzadehyde inhibits the enzyme adenosine triphoshpatase (ATPase), an enzyme concerned with the production of cellular energy from biological processes, which thereby blocks aerobic glycolysis. The inhibition of ATPase decreases the utilization of glucose as an energy source for the tumor cell (Racker,1972; Erwin, Kim & Anderson, 1975). Benzadehyde is converted to benzoic acid by the enzyme aldehyde oxidase. This enzyme is inhibited by cyanide, which in laetrile therapy, prevents the conversion to benzoic acid (Johns, 1967). The toxic effects of laetrile on cancer cells is believed to be due to synergistic effect of cyanide and benzaldehyde (Burke, McNaughton &Van Ardene, 1971).

Pass water (1977) explains the mechanism of Laetrile on the basis that carcinogens tend to decrease oxygen transport through the intracellular membranes of the cell. The decrease in oxygen transport causes a drop in the hydrogen ion concentration (pH) from 7.35 to 6.0 due to the conversion of glucose into lactic acid as a result of the oxygen loss. With the liberation of lysosomal enzymes the cellular metabolism reverts to a fermentation process, which in turn alters the DNA-RNA metabolism and the basic genetic regulatory mechanisms of the cell are impaired. Passwater believes that the cyanide ion tends to restore intracellular permeability, the pH of the cell, and basic genetic regulatory machinery of the cell. See also Szent-Gyorgi (1957,1976).

What is Laetrile (Amygdalin) Therapy?

Laetrile (amygdalin) therapy is a form of therapy which uses as a part of metabolic cancer therapy, the cyanogenic glycoside amygdalin, or one of its by-products, together with a broad-based nutritional program for use in the control of cancer. This therapy includes the use of vitamins, minerals, adaptogenic hers, pschoneuroimmunolgy, and electromagnetic energy. Cancer is controlled by employing the use of biochemical symphony of non-toxic natural measures.

Laetrile (amygdalin) does not meet the specifications of an anticancer agent as generally designated by orthodox clinical oncologists. This aspect will be discussed in greater detail later in this book.

How effective is Laetrile in Cancer metabolic Therapy?

Laetrile is not a magic bullet. There are a number of factors that enter into the cancer treatment complex. The type of cancer involved is an important one. Some types of cancer tend to be more sensitive than others. Laetrile is not equally effective in all types of cancers. In their clinical investigations in Israel where they were using laetrile, Rubin and Issahary (1976) found that it was most effective against Aden carcinomas and Hodgkin’s disease. It was somewhat less effective in sarcomas and the leukemia’s. Similar results have been achieved in Mexico, the U.S. and elsewhere (Navarro, 1957a,b; Contreras, 1982). Navarro (1955, 1957a,b) and Navarro and Lagman (1956) reported excellent results using laetrile and the enzyme chemotropism in a five year study in 83 cancer patients. The types of cancers treated included adenocarinoma of the breast, stomach, lungs, tongue, larynx, nasopharynx, rectum, colon, liver, esophagus, thyroid, uterus, Hodgkin’s, lymphorcomas, fibro sarcomas, etc. At no time did they encounter any evidence of toxicity from the use of laetrile. They obtained the following results: Twenty percent of the patients receive a decrease in the size of the tumor or complete regression. They found that most of the patients suffered much less pain except in those who had taken deep radiotherapy. Some of the patients were able to relieve the feted odor of superficial cancerous lesions by topical applications of laetrile. They were able to relieve the feted odor of internal cancers by using parenteral injections of laetrile. The appetite improved in anorexic patients with a resulting gain weight. Hypertensive cancer patients developed a reduction in blood pressure. A few patients developed a low fever. The reader should see the original articles for further details.

One of the things that they have found is that they get better tumor regression when Laetrile is used in conjunction with Vitamin A and enzymes. They conducted a laboratory study in mice working with murine Aden carcinoma and found that they got up to 89.3% tumor regression depending upon the size of the tumors (Contreras, 1982). This is one of the reasons why the Greens were using vitamin A and enzymes in Chad’s diet, but the Court made them discontinue these nutrients.

Importance of the Chemical Quality of Laetrile

In the early days of the manufacture of Laetrile, one of the primary issues in the FDA Commissioner’s Report (USFDA, 1977). One was never certain about the quality control from one manufacturer to the next. Laetrile was being manufacturer to the next. Laetrile was being manufactured in the U.S., Mexico, Israel, Switzerland, West Germany, and elsewhere. Only the laevo isomer was found to be therapeutically the most effective. For a period of time the highest quality was believed to be produced in Switzerland and West Germany, but even that was not certain. Kem, S.A.a Labs in Tijuana, Mexico, in recent years has also produced a high quality Laetrile using FDA good manufacturing practices.

Updated on May 30, 2023

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