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How Vitamin B17 Works

 


This page presents a paper by Charles Gurchot, MD, that shows how the components of B17 (laetrile) operate to destroy cancer cells.

This is my complete list of links regarding the research behind B17 and laetrile for treating cancer. READ them. Ernst Krebs is the world's leading authority on the relationship between cancer and nitrilosides, and the inventor of laetrile.


Suggested Mechanisms of Action of Vitamin B-17

by Charles Gurchot, Ph.D.

Oral doses of Vitamin B-17 seem not to much affected by the action of the acid medium of the stomach, but pass into the intestine where the substance is acted upon by bacterial enzymes.

In the intestine the enzyme complex Emulsin containing the enzymes Beta-glucosidase, Benzocyanase, and others, degrades the Amygdalin into four components: Hydrocyanic acid, Benzaldehyde, Prunasin, and Mandelonitrile, which are absorbed into the lymph and portal circulations.

Cyanide is converted to thiocyanate probably in the blood circulation, and certainly in the liver by the enzyme rhodanese in the presence of sulfur-bearing compounds.1,2 The circulating thiocyanate exerts certain physiological effects on blood pressure and thyroid action, and is not excreted rapidly. (In the absence of the enzyme or sulfur, the cyanide may form cyano-hemoglobin.)

In cancer patients some thiocyanate finds its way to the site of the cancer lesion.

The benzaldehyde formed in the intestine probably has no important function, but in the circulation forms benzoic acid and is excreted as benzaldehyde hippurate.

Prunasin (the mono-glucoside of Mandelonitrile) can circulate in the body and reach the malignant lesion, and as such hydrolyse to liberate hydrocyanic acid, benzaldehyde, and one glucose molecule.

Prunasin may also be changed in the liver to Mandelonitrile glucuronoside. This conversion to the glucuoronoside may take place in two different ways: 1) by combining with glucuronic acid, which would remove one sugar molecule; 2) by oxidation of the terminal alcohol group of the prunasin glucose molecule.

The mandelonitrile is absorbed from the intestine, going directly to the liver where it is converted by the detoxification mechanism of joining it to glucuronic acid. It may then be excreted as the glucuronide or find its way to the site of a malignant lesion.

Glucosidic enzymes at the lesion may hydrolyse prunasin into its components cyanide, benzaldehyde, and a glucose molecule, to interfere with tissue respiration. In the process of enzyme hydrolysis pure mandelonitrile, as an intermediate step, may be released.

Mandelonitrile of itself may undergo spontaneous hydrolysis to HCN and benzaldehyde or enzymatic decomposition by benzocyanase present in the emulsin complex.

Mandelonitrile glucuronide may be hydrolysed at the tumor site by Beta-glucuronidase to yield HCN, benzaldehyde and glucuronic acid.

Benzaldehyde released through these processes at the site of the malignant lesion may be reduced to benzyl alcohol, and combine with the thiocyanate to form benzo thiocyanate. This compound is further reduced to a thio-alcohol, benzo mercaptain, and hydrocyanic acid. In this manner HCN reappears and may continue to do so in a cyclic manner until the intracellular conditions that permit the reaction involved in the cycle are no longer operative.

These phenomena would explain the synergistic effect of benzaldehyde and cyanide in depressing the metabolism of mouse tumor slices in the Warburg apparatus (Dean Burk3).

In the absense of rhodanese the cyanide probably exerts its lethal effects on cell respiration, which is relatively small in cancer cells, by interferance with the cytochrome oxidase enzymes.

Cyanide, either as such, or as mandelonitrile, may combine with glucose to form cyanoglucose, which, on hydrolysis, forms a glucuronide heptose analogous to gluconic acid, which would be excreted, or dehydrogenated to heptose, which also would be excreted. The conditions for this transformation exist in cancer tissue and would constitute anti-gluconeogenesis.

[From Physicians Handbook of Vitamin B-17 Therapy, McNaughton Foundation, Published by: Science Press International, 1973]

References:

  1. Sorbo, Acta Chem.Scand. 5,1951,(724-34);1953 (1129-1136);1953 (1137-1145).
  2. Clemedson et al, Acta Physiol.Scand. 32, 1954, 245.
  3. Burk, McNaughton, Von Ardenne, PanMinerva Med.13,#12,Dec.1971.

 


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