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]

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 [13-17] 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 [10,13,18-20] 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]

The second theory states that cancer cells contain more beta-glucosidase activity than normal cells and, as in the first theory, that they are deficient in rhodanese. Reviewed in [1,5,13,15,18,23,24] Evidence from laboratory studies demonstrates that this theory cannot be supported. As noted previously, normal cells and cancer cells contain similar amounts of rhodanese.[21] Furthermore, most types of mammalian cells contain only small traces of beta-glucosidase,[22] and this enzyme has not been detected in tumor samples [8,25] or in human blood.[5] Without sufficient levels of beta-glucosidase, it is difficult for intravenously administered amygdalin to be broken down into cyanide and other products.

The third theory states that cancer is the result of a metabolic disorder caused by a vitamin deficiency. It states further that laetrile, or “vitamin B-17,” is the missing vitamin needed by the body to restore health. Reviewed in [18,26-28] Experimental evidence indicates that the level of intake of individual vitamins and/or the vitamin status of an organism can influence the development of cancer, but there is no evidence that laetrile is needed for normal metabolism or that it can function as a vitamin in animals or humans. Reviewed in [29,30]

The fourth theory suggests that the cyanide released by laetrile has a toxic effect beyond its interference with oxygen utilization by cells. According to this theory, cyanide increases the acid content of tumors and leads to the destruction of lysosomes (compartments inside cells that contain enzymes capable of breaking down other cellular molecules). The injured lysosomes release their contents, thereby killing the cancer cells and arresting tumor growth. Reviewed in [15] According to this theory, another consequence of lysosome disruption is stimulation of the immune system.

References

1. Dorr RT, Paxinos J: The current status of laetrile. Ann Intern Med 89 (3): 389-97, 1978.  [PUBMED Abstract]
   
   
2. Viehoever A, Mack H: Bio-chemistry of amygdalin (bitter, cyanogenetic principle from bitter almonds). Am J Pharm 107(Oct): 397-450, 1935. 
   
   
3. The laetrile controversy. In: Moss RW: The Cancer Industry: The Classic Expose on the Cancer Establishment. Brooklyn, NY: First Equinox Press, 1996, pp 131-52. 
   
   
4. Laetrile at Sloan-Kettering: a case study. In: Moss RW: The Cancer Industry: The Classic Expose on the Cancer Establishment. Brooklyn, NY: First Equinox Press, 1996, pp 153-86. 
   
   
5. Curt GA: Unsound methods of cancer treatment. Princ Pract Oncol Updates 4 (12): 1-10, 1990. 
   
   
6. Fenselau C, Pallante S, Batzinger RP, et al.: Mandelonitrile beta-glucuronide: synthesis and characterization. Science 198 (4317): 625-7, 1977.  [PUBMED Abstract]
   
   
7. Chandler RF, Anderson LA, Phillipson JD: Laetrile in perspective. Can Pharm J 117 (11): 517-20, 1984. 
   
   
8. Newmark J, Brady RO, Grimley PM, et al.: Amygdalin (Laetrile) and prunasin beta-glucosidases: distribution in germ-free rat and in human tumor tissue. Proc Natl Acad Sci U S A 78 (10): 6513-6, 1981.  [PUBMED Abstract]
   
   
9. Rauws AG, Olling M, Timmerman A: The pharmacokinetics of prunasin, a metabolite of amygdalin. J Toxicol Clin Toxicol 19 (8): 851-6, 1982.  [PUBMED Abstract]
   
   
10. Ross WE: Unconventional cancer therapy. Compr Ther 11 (9): 37-43, 1985.  [PUBMED Abstract]
    
    
11. Ames MM, Moyer TP, Kovach JS, et al.: Pharmacology of amygdalin (laetrile) in cancer patients. Cancer Chemother Pharmacol 6 (1): 51-7, 1981.  [PUBMED Abstract]
    
    
12. Krebs ET Jr, Krebs ET Sr, Beard HH: The unitarian or trophoblastic thesis of cancer. Med Rec 163 (7): 149-74, 1950. 
    
    
13. Ellison NM: Unproven methods of cancer therapy. Drug Ther (NY) 10(July): 73-82, 1980. 
    
    
14. Navarro MD: The Philippine experience in the early detection and chemotherapy of cancer. St Tomas J Med 25 (3): 125-33, 1970. 
    
    
15. Greenberg DM: The case against laetrile: the fraudulent cancer remedy. Cancer 45 (4): 799-807, 1980.  [PUBMED Abstract]
    
    
16. Levi L, French WN, Bickis IJ, et al.: Laetrile: a study of its physicochemical and biochemical properties. Can Med Assoc J 92: 1057-61, 1965. 
    
    
17. Cancer Commission of the California Medical Association.: The treatment of cancer with "laetriles". Calif Med 78 (4): 320-26, 1953. 
    
    
18. Unproven methods of cancer management. Laetrile. CA Cancer J Clin 22 (4): 245-50, 1972 Jul-Aug.  [PUBMED Abstract]
    
    
19. Navarro MD: Five years experience with laetrile therapy in advanced cancer. Acta Unio Int Contr Cancrum 15(suppl 1): 209-21, 1959. 
    
    
20. Morrone JA: Chemotherapy of inoperable cancer: preliminary report of 10 cases treated with laetrile. Exp Med Surg 20: 299-308, 1962. 
    
    
21. Gal EM, Fung FH, Greenberg DM: Studies on the biological action of malononitriles, II: distribution of rhodanese (transulfurase) in the tissues of normal and tumor-bearing animals and the effect of malononitriles thereon. Cancer Res 12: 574-79, 1952. 
    
    
22. Conchie J, Findlay J, Levvy GA: Mammalian glycosidases: distribution in the body. Biochem J 71: 318-25, 1959. 
    
    
23. Herbert V: Laetrile: the cult of cyanide. Promoting poison for profit. Am J Clin Nutr 32 (5): 1121-58, 1979.  [PUBMED Abstract]
    
    
24. Scott PJ: Laetrile and cancer quackery problems. Cancer Forum 5 (2): 93-97, 1981. 
    
    
25. Biaglow JE, Durand RE: The enhanced radiation response of an in vitro tumour model by cyanide released from hydrolysed amygdalin. Int J Radiat Biol Relat Stud Phys Chem Med 33 (4): 397-401, 1978.  [PUBMED Abstract]
    
    
26. Lerner IJ: Laetrile: a lesson in cancer quackery. CA Cancer J Clin 31 (2): 91-5, 1981 Mar-Apr.  [PUBMED Abstract]
    
    
27. Lerner IJ: The whys of cancer quackery. Cancer 53 (3 Suppl): 815-9, 1984.  [PUBMED Abstract]
    
    
28. Shils ME, Hermann MG: Unproved dietary claims in the treatment of patients with cancer. Bull N Y Acad Med 58 (3): 323-40, 1982.  [PUBMED Abstract]
    
    
29. Young VR, Newberne PM: Vitamins and cancer prevention: issues and dilemmas. Cancer 47 (5 Suppl): 1226-40, 1981.  [PUBMED Abstract]
    
    
30. Jukes TH: Laetrile struggles. Nature 263 (5578): 543, 1976. 
    
    

Back to Top

< Previous Section  |  Next Section >