Action and Mechanism of
Occurence in Nature
Suggested Mechanisms of Action of Vitamin B-17
Charles Gurchot, Ph.D.
We at Christian Brothers believe that the seed is the most
effective remedy along with enzymes (Megazyme), Noni, herbs Cansema (Draw), Coral
water a good digestion rejuvenator (Ultra Lax), Liver stimulating
and blood cleaning tea (Organic Milk Thistle Tea). The Machines are
for high stage cancers but we do not sell the machines. They are about
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
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
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,
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
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
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
[From Physicians Handbook of Vitamin B-17 Therapy, McNaughton Foundation, Published by:
Science Press International, 1973]
- Sorbo, Acta Chem.Scand. 5,1951,(724-34);1953 (1129-1136);1953 (1137-1145).
- Clemedson et al, Acta Physiol.Scand. 32, 1954, 245.
- Burk, McNaughton, Von Ardenne,