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History

    Amygdalin was first isolated in 1830 by 2 French chemists. Reviewed in [1,2] It was used as an anticancer agent in Russia as early as 1845, with positive results reported for the first patient treated. Reviewed in [3,4] Its first recorded use in the United States as a treatment for cancer occurred in the early 1920s. Reviewed in [5] At that time, amygdalin was taken in pill form; however, the formulation was judged too toxic, and the work was abandoned. In the 1950s, a purportedly nontoxic intravenous form of amygdalin was patented as Laetrile. Reviewed in [1,6,7]

    Laetrile has been tested on cultured animal cells (cells grown in specialized containers in the laboratory), in whole animals, in xenograft models (tumor cells from one species transplanted onto another species), and in humans to determine whether it has specific anticancer properties (an ability to kill cancer cells more readily than normal cells). As noted previously (General Information), cyanide is believed to be the main cancer-killing ingredient in laetrile.[8,9] When amygdalin interacts with the enzyme beta-glucosidase or undergoes hydrolysis (breakdown in a reaction with water) in the absence of enzymes, hydrogen cyanide, benzaldehyde, and glucose (sugar) are produced. Reviewed in [1,7,8,10,11] Cyanide can also be produced from prunasin, which is a less-than-complete breakdown product of amygdalin. Reviewed in [1,8]

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    Four different theories have been advanced to explain the anticancer activity of laetrile. The first of these incorporates elements of the trophoblastic theory of cancer, a theory that is not widely accepted as an explanation for cancer formation. According to the trophoblastic theory, all cancers arise from primordial germ cells (cells that, under normal circumstances, would give rise to eggs or sperm), some of which become dispersed throughout the body during embryonic development and, therefore, are not confined to the testes or ovaries. The trophoblastic theory also suggests that transformation of primordial germ cells to a cancerous state is normally prevented by enzymes from the pancreas, and that cancers can be destroyed by pancreatic enzyme supplements and treatment with laetrile.[12] Reviewed in [13,14,15,16,17] The rationale for laetrile use is the suggestion that malignant cells have higher than normal levels of an enzyme called beta-glucuronidase (which is different from the aforementioned enzyme beta-glucosidase) and that they are deficient in another enzyme called rhodanese (thiosulfate sulfurtransferase). It has been suggested further that laetrile is modified in the liver and that beta-glucuronidase breaks down the modified compound, ultimately producing cyanide. Rhodanese can convert cyanide into the relatively harmless compound thiocyanate. Thus, it has been proposed that cancer cells are more susceptible to the toxic effects of laetrile than normal cells because of an imbalance in these 2 enzymes. Reviewed in [10,13,18,19,20] It is important to note that there is no experimental evidence to support the idea that normal tissues and malignant tissues differ substantially in their concentrations of beta-glucuronidase or rhodanese.[21,22]

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