Content Links Within "Biologics"
Mechanism of Vitamin B17
Occurrence in Nature
The Nitrilosides (Vitamin B-17)-Their Nature, Occurrence and Metabolic
Significance (Antineoplastic Vitamin B-17)
Ernst T. Krebs, Jr.
Vitamin B-17 (nitriloside) is a designation proposed to include a large group of
water-soluble, essentially non-toxic, sugary, compounds found in over 800 plants, many of
which are edible. These factors are collectively known as Beta-cyanophoric glycosides.
They comprise molecules made of sugar, hydrogen cyanide, a benzene ring or an acetone.
Though the intact molecule is for all practical purposes completely non-toxic, it may be
hydrolyzed by Beta-glycosidase to a sugar, free hydrogen cyanide, benzaldehyde or acetone.
We have proposed the collective generic term n-i-t-r-i-l-o-s-i-d-e for all such
cyanophoric glycosides of dietary significance.
One of the most common nitrilosides is amygdalin. This nitriloside occurs in the
kernels of seeds of practically all fruits. The seeds of apples, apricots, cherries,
peaches, plums, nectarines, and the like carry this factor; often in the extraordinary
concentration of 2 to 3 per cent. Since the seeds of fruits are possibly edible, it may be
proper to designate the non-toxic water soluble accessory food factor or nitriloside that
they contain as vitamin B-17. The presence of nitriloside in the diet produces specific
physiologic effects and leaves as metabolites specific chemical compounds of a
physiologically active nature. The production by a non-toxic, water-soluble accessory food
factor of specific physiological effects as well as identifiable metabolites suggests the
vitamin nature of the compound.
The ubiquity of the compound or its metabolites in plant and animal foods further
corroborates its vitamin status. And the development of specific deficiency states as a
result of its deficiency in or absence from the diet, and the correction of such
pathologic deficiency states by supplying the factor confirm its vitamin status.
The diet of primitive man and most fruit-eating animals was very rich in nitrilosides.
They regularly ate the seeds (and kernels) of all fruits, since these seeds are rich in
protein, polyunsaturated fats, and other nutrients. Seeds also contain as much as 2 per
cent or more nitriloside. There are scores of other major foods naturally, or normally,
very rich in nitriloside. Let's consider now what happens when one eats the
nitriloside-rich seeds of fruit.
In metabolism, nitriloside is hydrolyzed to free hydrogen cyanide, benzaldehyde or
acetone and sugar. This occurs largely through the enzyme Beta-glucosidase produced by
intestinal bacteria as well as by the body. The released HCN [hydrocyanide] is detoxified
by the enzyme rhodanese to the relatively non-toxic thiocyanate molecule. The sugar is
normally metabolized. The released benzaldehyde in the presence of oxygen is immediately
oxidized to benzoic acid which is non-toxic. Thus this newly designated vitamin B-17
(nitriloside) could account for:
- The thiocyanates in the body fluids--blood, urine, saliva, sweat, and tears;
- For part of the benzoic acid (and subsequently hippuric acid); salicylic acid isomers;
- For the HCN that goes to the production of cyanocobalamin from hydrocobalamin, or
production of vitamin B12 from provitamin B12.
These are the physiological properties of the common nitriloside amygdalin. Before
considering the possible antineoplastic activity of this vitamin B-17, let us recall that
the benzoic acid arising from it has certain antirheumatic and antiseptic properties. It
was rather widely used (in Germany and elsewhere) for rheumatic disease therapy prior to
the advent of the ortho-hydroxy addition product of benzoic acid known as
ortho-hydroxybenzoic acid or salicylic acid. It was originally obtained from beech-wood
bark. As a matter of interest, the para- hydroxy isomer of benzoic acid occurs in the para
hydroxybenzaldehyde aglycon (non-sugar) of the nitriloside found in the cereal millet.
Millet was once more widely used in human nutrition than wheat. Wheat seed contains little
or no nitriloside.
Recall now, that thiocyanate also was once widely used, in both Germany and American
medicine, as an effective agent for hypertension. Used as such, as the simple chemical,
the dosage was difficult to control. Obviously, this difficulty does not arise from the
thiocyanate usually produced in the body through metabolizing vitamin B-17 (nitriloside).
However, chronic hypotension has been reported in Nigerians who eat quantities of the
nitriloside-containing manioc (cassava)--especially that of the bitter variety.
Let us pause to reflect upon this question: Might not the rheumatic diseases as well as
certain aspects of hypertension be in some cases partially related to a dietary deficiency
in nitrilosides? One can hardly deny that the ingestion of a sufficient quantity of
nitriloside-containing foods will metabolically yield sufficient benzoic acid and/or
salicylic acid isomers to palliate rheumatic disease and certainly to decrease, however
temporarily, hypertension as well as to foster the nitrilosation of provitamin B-12 to
active vitamin B-12: cyanocobalamin.
Despite all this, are we justified in suggesting that cancer itself might be another
chronic metabolic disease that arises from a specific vitamin deficiency--a deficiency
specifically in vitamin B-17 (nitriloside)?
Again, let us reflect for a moment. There are many chronic or metabolic diseases that
challenge medicine. Many of these diseases have already been conquered. What proved to be
their solution? By solution we mean both prevention and cure. What really cures really
prevents. Let us think of some of these diseases that have found total prevention and
hence cure. We are speaking of metabolic or non-transmissible diseases. At one time the
metabolic disease known as scurvy killed hundreds of thousands of people, sometimes entire
populations. This disease found total prevention and cure in the ascorbic acid or vitamin
C component of fruits and vegetables. Similarly, the once fatal diseases so aptly called
pernicious anemia, pellagra, beri beri, countless neuropathies, and the like, found
complete cure and prevention in specific dietary factors, that is, essential nutrients in
an adequate diet.
I can hear an objection of course. But let me remind you that all the solved or conquered chronic or metabolic diseases were found to be simple specific dietary
diseases. Remember this: before these diseases were understood, before the means of total
prevention and cure were discovered, it was widely believed that these dietary deficiency
diseases were due to viruses, bacteria, bad air, "infection," or some such
Now I ask you to name a single chronic or metabolic disease that has ever found total
prevention and cure except by specific dietary factors and/or factors normal to adequate
animal economy. I have never found anyone who has been able to suggest a single chronic or
metabolic disease that has ever been totally prevented and cured except through a factor
essential to adequate diet and/or to the animal economy.
Let's go a step further, almost to the border of dogmatism, to advance an axiom in
medicine and biology:
No chronic or metabolic disease has ever found cure or prevention, that is, real cure
and real prevention--except through factors essential to an adequate diet and/or normal to
I would welcome a contradiction to this principle; but even an exception would
"prove the rule."
Does it seem likely, therefore, that cancer will be the first exception to this
generalization that to date has not had a single known exception? In my humble opinion,
certainly not. But does it follow from this that vitamin B-17 (nitriloside) is the
specific antineoplastic vitamin? Logically, by itself, alone, this conclusion that
nitriloside is the specific antineoplastic vitamin does not follow. However,
examine the brilliant laboratory studies of Dr. Dean Burk of the Department of
Cytochemistry of the National Cancer Institute in Washington. I believe that in light of
the experimental evidence that he has produced, you might agree that vitamin B-17
(nitriloside) is indeed the antineoplastic vitamin.*
One might ask, then, whether we suggest that vitamin B-17 (nitriloside) or Laetrile is
an effective cancer drug. Our reply must be: it is not a drug; it is a
*Author's footnote: Dr. Dean Burk's paper was in the same program, also a report on the
pharmacodynamics and clinical application of vitamin B-17 nitriloside (amygdalin) by Dr.
Hans Nieper, a brilliant young man who combines an excellent ability in biochemistry with
a genius in clinical medicine, in my opinion.
vitamin. We feel certain that it will never be possible to speak of a true or effective
"cancer drug," any more that it is possible to speak of a pellagra drug, a
scurvy drug, a pernicious anemia drug, or the like. The U.S. Food & Drug
Administration has just announced that the major drug (as contrasted to the normal
animal product insulin) used in the palliation of diabetes--Orinase--is "no
good." We know of no true drug that actually prevents or cures metabolic or chronic
diseases--or really does any genuine good. We mean by "drug," of course,
relatively toxic chemicals foreign to the body or foreign to the animal economy.
As already mentioned, vitamin B-17 (Laetrile) is totally non-toxic. Its lethal dose in
mice and rats, by injection, is about 25,000 milligrams per kilogram of body weight. It is
so nearly non-toxic that in some studies the water, used as a diluent, presents a greater
toxicity than the vitamin. This applies for acute, subacute and chronic toxicity. By mouth
in test animals it is less than 1/20 as toxic as aspirin. Speaking of aspirin, let us
recall that this great German discovery, the acetylation product of ortho-hydroxy benzoic
acid, and some salicylic acid isomers, as well as benzoic acid itself, are the normal
metabolites of dietary nitrilosides found in the seeds of nearly all fruits and some
cereals. For example, millet, mentioned above, once more widely used than wheat, yields
the salicylic acid isomer para-hydroxybenzoic acid, which arises as the metabolic product
of its nitriloside: p-hydroxymandelonitrile-B-glucoside. In this you can discern, however
dimly, the dietary-therapeutic profile of the salicylates as a means of satisfying a
dietary deficiency in benzoic acid and the related salicylic acid isomers.
Returning to the non-toxicity of nitriloside; it is no more toxic than dextrose or
ascorbic acid--and to the diabetic less toxic than the former.
I have noticed that newspapers are carrying wire dispatches reporting the studies of
Professor Roger Williams of the University of Texas. He is quoted on the
"toxicity" of commercial white bread as sold in the United States. You will
recall that Doctor Williams is the discoverer of vitamin B-1 or thiamine; and the first to
synthesize it. Doctor Williams, in effect, showed that commercial white bread as sold in
the United States is about 70 times more toxic than vitamin B-17. Doctor Williams fed four
strains of white rats (noted for their vigor), nothing but commercial American white bread
for three months. Seventy-five per cent of all the experimental animals so fed died of
malnutrition before the experiment was complete. Those fed on whole wheat all survived.
The commercial white bread was enriched by law with some crystalline vitamins, but not in
a sufficient quantity and variety to prevent these rats being killed by the bread. So how
about vitamin B-17 toxicity studies? White rats fed 70 times the normal human dose of
vitamin B-17 (nitriloside) used in the palliation of human cancer were completely normal
and healthy after 90 days. None of them died. There were some "physiological side
reactions" to vitamin B-17--greater weight and appetite. After all they were
receiving nourishment; a vitamin, not a vitamin-deficient ration or a drug.
The rats that died from eating commercial white bread--all 75 per cent of them--died as
a direct result of a deficiency in vitamins found in the whole grain of wheat. There was
the deficiency in vitamin E as a result of the missing germ or seed of the wheat, a
deficiency of choline, vitamin B-15 (pangamic acid), vitamin B-6, biotin and other factors
as a result of the missing bran taken from highly refined bleached white flour. Recall
that the natural whole grain of wheat is composed of the starchy endosperm or bulk of the
grain as well as the germ or the seed which carries the oils in which are dissolved the
tocopherols or vitamin E; and the bran which contains an abundance of the B vitamins.
Those rats died from a vitamin deficiency produced by eating less than the whole grain,
the whole food. When civilized man eats less than the whole fruit, for example, by
discarding the seed or kernel he experiences a specific and total deficiency not only in
oils and proteins but in minerals and such vitamins as vitamin B-17 (nitriloside) which is
found only in the seed, not in the flesh of the fruit. By discarding the seed or kernel,
man experiences a specific and total deficiency in vitamin B-17 so far as that fruit is
concerned. Let me remind you that were man by circumstance limited to no source of food
but apricots, peaches, plums, cherries and the like and ate only their fruit without their
seeds he would in a short time develop a fatal deficiency in proteins and fats not to
mention vitamins. He would die from this deficiency just as the white rats died from the
deficiency produced by eating only the starch of wheat without the seed germ and bran. But
if he ate the seeds or kernels with the fruit flesh, he would get proteins, fats
and other nutrients essential to health.
Vitamin B-17 (nitriloside) is also found in great abundance in a very wide variety of
vegetable foods once eaten in great abundance by man, and the natural fodder of animals is
similarly rich in the factor. In a paper which I hope to publish soon, I have listed over
62 plant foods eaten by man and over 70 common fodder plants that are very rich in vitamin
B-17 (nitriloside). Their concentration of this vitamin compares favorably with that of
vitamin C (ascorbic acid) so far as quantity and ubiquity are concerned. As in the case of
many other vegetables, sprouts may contain 10 to 30 times as much vitamin B-17 as mature
plants. It is not practicable to furnish here the several hundred references of the basic
research on nitrilosides nor to list extensive tables showing the occurrence of this new
vitamin in a wide range of foods. It would not be germane to explain the reasons why and
how "modern diet" has been almost totally stripped of nitrilosides. Suffice it
to say that the factors that made commercial white bread lethal to rats and gave the world
the empty calories of refined white sugar also have served to produce a fulminating
deficiency in vitamin B-17 (nitriloside) in the diet of so called civilized man.
So much for the specific nutritional aspect of vitamin B-17 (nitriloside). How can a
compound that is totally non-toxic be relevant to a disease as serious as cancer, a
disease perhaps as lethal as pernicious anemia once was? Would we not expect that very
powerful cytotoxic compounds would be required to destroy cancer cells? Would these not be
compounds like the nitrogen mustards, the antimetabolites, the cyclophosphoramides,
methotrexate, 5-fluoruracil, 6-chloropurine, 6-mercaptopurine, azaserine,
triethlyenphosphramide, the nitrosoguanidines, and countless other compounds so toxic that
some kill almost 25 per cent of the patients treated directly or indirectly through
It is true that neoplastic cells are destroyed by cytotoxins. The cytotoxins used so
far, the ones I have mentioned, are more toxic to body or somatic cells than specifically
to cancer cells. This is obvious. Otherwise we would be able to administer these
cytotoxins until they killed all cancer cells and left the host alive. But they almost always, if not always, kill the host before killing the neoplastic cells. In the problem
of neoplastic therapy we have in drugs an almost insoluble paradox. For an agent to be
effective it must be both non-toxic to somatic cells and yet present powerful cytotoxins
to neoplastic cells--cytotoxins like the cyanides and benzaldehyde.
Vitamin B-17 (nitriloside) releases a specific and powerful cytotoxin, probably the
most powerful one known. This is hydrogen cyanide. Our formulation of Laetrile also
releases an equimolar quantity of benzaldehyde which, before oxidation to benzoic acid, is
a very powerful cytotoxin. We have here two very powerful cytotoxins. Doctor Dean Burk of
the National Cancer Institutue has brilliantly demonstrated, largely through utilization
of the technics and manometer of Otto Warburg, that the benzaldehyde released by the
hydrolysis of nitriloside or Laetrile is not only in itself a powerful cytotoxin but that
it multiplies through a very powerful synergy the cytotoxic effects of both--cyanide
and benzaldehyde--to an extent many, many times greater than the arithmetic sum of their
These two compounds in synergy are more powerful cytotoxins than any of those that I
have already mentioned above.
Why isn't the equimolecular quantity of benzaldehyde oxidized immediately by the cancer
cells to harmless benzoic acid as occurs in body or somatic cells, and why isn't the
equimolecular quantity of cyanide converted immediately to thiocyanate as it is in body or
somatic cells? Recall that Otto Warburg himself received one Nobel Prize for proving the
suboxidative activity of cancer cells. They ferment--fermentative metabolism rather than
respiratory metabolism plays a large role in cancer. This metabolism utilizes less oxygen
(in the free state); therefore, oxidation of benzaldehyde occurs much more slowly.
Unoxidized benzaldehyde lags, as it were, in the neoplastic cell. This cell also lacks a
very important enzyme possessed by body or somatic cells. This enzyme is rhodanese or
thiosulfate transulfurase. It convert cyanide to the harmless thiocyanate. With the selective lag of both undetoxified cyanide as well as unoxidized benzaldehyde in the
neoplastic cell, and the multiplication of cytotoxicity that the combination affords, the
neoplastic cells suffer a lethal cytotoxicity while the hostal or somatic cells are
totally unaffected--except possibly in a beneficial or physiological manner. We are dealing
with a vitamin, remember.
Pause again to reflect. Is it possible that this described cytotoxic synergy arising
from the hydrolysis product of vitamin B-17 (nitriloside), is a coincidental or fortuitous
phenomenon--a synergy totally ungrounded in any other biological experience, a pure
accident? Or does this synergy represent the end product of the enduring effects of a
process of natural selection between plants and animals through which a specific
antineoplastic vitamin, vitamin B-17, has evolved in a natural environment once as
abundantly rich in nitrilosides as in ascorbic acid?
There is no controversy, of course, on the fact that equimolecular quantities of
benzaldehyde and cyanide resulting from the hydrolysis of vitamin B-17 will selectively
kill cancer cells. The cytotoxicity of these chemicals against neoplastic cells is known,
but the margin of safety for these raw chemicals is very little greater than the
most powerful cytotoxins--except that different from the latter there is no residual,
cumulative or chronic toxicity from them. Contrast this to the utter non-toxicity of these
same chemicals bound in the white sugary nitriloside molecule.
Wherein, then, is there a controversy over this vitamin in therapy? Though the major
and practically sole controversy is and has always been a political one, if we were to try
to pin-point a specific scientific criticism it would probably be this: what real or
experimental proof is there that the nitriloside molecule is selectively hydrolysed
or broken down to free cyanide, benzaldehyde and sugar at and by the neoplastic lesion? It
is, of course, a commonplace-now almost a century old--that the nitriloside is split to
its 3 major components by the enzyme Beta-glucosidase. It is also known that the malignant
lesion contains a high concentration of certain Beta-glycosidases (e.g., Beta
glucuronidase). The proponents of vitamin B-17 for the prevention and palliation of cancer
have long argued inferentially for the presence of specific Beta-glucosidase activity in
the malignant lesion, which would account or its selective lysis here with the release of
the admittedly highly cytotoxic HCN and benzaldehyde in synergy.
The opponents of vitamin B-17 in cancer therapy have rather myopically, (I believe),
argued that there is no proof that selective hydrolysis of the nitriloside occurs in the
neoplastic cell. They reject all existing clinical evidence, however impressive, for this
effect. Thus it is an extraordinarily important finding that Doctor Dean Burk reports on
his observation of the effect of the incubation of C3H mouse mammary cancer with vitamin
B-17 in the Warburg manometer. He reports that the malignant mammary tissue selectively
hydrolyzes the added nitriloside to free cyanide, benzaldehyde and sugar with a highly
effective cytotoxicity; and that this does not occur in benign or somatic control
mammary tissue! This experimental observation means, of course, that the neoplastic tissue
carries a specific Beta-glucosidase activity that normal or somatic tissue lacks, which
lack here is obvious in view of the total non-toxicity of the material toward normal
tissue. This very crucial experiment will, of course, be repeated and checked and
rechecked in many laboratories.
Let us in summary simplify all this in terms of vitamin action. When vitamin B-17
enters the body (in foods, for example), it is hydrolyzed only to a very slight degree by
body or somatic cells. This is obvious from the non-toxicity shown by B-17. But even if
some of the B-17 is hydrolyzed by body or somatic cells, the very high concentration of
the enzyme rhodanese in these cells converts the HCN immediately to relatively non-toxic
thiocyanate. (This accounts largely for the thiocyanate that you find in blood, urine,
saliva, etc., as stated above).
How different it is with the neoplastic cell! It contains great quantities of
Beta-glycosidase. Fischman and many others in America have independently shown this in the
case of Beta-glucuronidase. Sometimes there is over 1,000 times as much of this
Beta-glycosidase as in the contiguous normal or body cell. The neoplastic cell is almost
completely deficient in the enzyme rhodanese. Recalll that when B-17 reaches the cancer
cell the Beta-glycosidase there hydrolyzes it with the release of extremely large
quantities of cyanide (relative to the situation in normal body cells). This selective
effect occurs in a cell that is almost totally deficient in the enzyme rhodanese, which in
normal body cells is present to detoxify cyanide to thiocyanate. Thus the end result of
the presence of one enzyme that causes the selective release of hydrogen cyanide in cancer
cells, plus an oxidative deficiency (fermentative metabolism) that causes a lag in
benzaldehyde oxidation to benzoic acid, result in the selective persistence of free or
undetoxified cyanide plus free or unoxidized benzaldehyde which synergistically exert
their selective antineoplastic effect.
A discussion of the clinical details of vitamin B-17, nitriloside in animal and human
cancer is best left to our clinical students of the subject. They are faced with the fact
that today more people per 100,000 of the population are developing cancer and dying from
it at an earlier age than any other time in recorded history of the human race. At least
one in three of the population develops clinical cancer and probably all develop
subclinical neoplasms in the course of a lifetime. The situation, in our opinion, almost
identifies itself in terms of a fulminating deficiency disease a priori. As our
veterinary friends tell us, even our cats and dogs are showing an incidence of cancer
parallel to that of their "civilized" owners. Observe how quickly these animals
when released from an apartment or kennel will single out (and eat) such nitriloside-rich
grasses as Johnson grass, Tunis grass or Sudan grass as a supplement to their diet. Some
of these grasses contain as much as 17,000 mg of nitriloside per kilogram of dry weight!
In this presentation we have attempted to touch a vast and relatively unexplored area.
But before closing let me introduce a little Yankee humor. It may be sick humor: judge for
yourselves. We know of the white bread that will kill 75 per cent of hearty rats in 90
days, of calorie-free white sugar, of cola drinks, of fulminating vitamin deficiencies,
and the like. But in the United States there is one "school of nutritional
thought" that, despite all this, sought to append the following statement to the
labels of all bottles of vitamins:
"Vitamins and minerals are supplied in abundant amounts by the foods we eat. The
Food and Nutrition Board of the National Research Council recommends that dietary needs be
satisfied by foods. Except for persons with special needs, there is no scientific basis
for recommending routine use of dietary supplements."
The lethal commercial white bread is by law supplemented, but not supplemented enough
not to kill the rats. It is argued, of course, that this won't hurt man too much unless he
relies almost solely on this staff of life and is no tougher than the rats!
Lest this new vitamin B-17 or nitriloside still be a less concrete reality in your mind
than ascorbic acid, thiamine, niacin or the like, let me leave you with an example of a
daily ration or diet remarkably rich in nitriloside or vitamin B-17. For breakfast we
start with buckwheat, millet and flax-seed gruel; all three cereals are very rich in
nitriloside. On our millet bread toast we put some nitriloside rich elderberry jelly. The
stewed apricots we eat carry the nitriloside-rich seeds, which we detect through their
delicious almond-like flavor. At lunch we have nitriloside-rich lima beans or possibly a
succotash containing nitriloside-rich chick peas. Our millet rolls may be spread with plum
jam carrying the nitriloside-rich seeds that add so much to the flavor of the jam. We may
choose some nitriloside-rich elderberry wine. For dinner we may have a salad with some
nitriloside-rich bean sprouts and nitriloside-rich millet sprouts. Our dinner rolls may be
made of nitriloside-rich buckwheat and nitriloside-rich millet and sweetened with
nitriloside-rich sorghum molasses extracted from sorghum cane--almost all of the foregoing
are very rich in nitrilosides. For our meat course we may have rabbet that fed on
nitriloside-rich clover and as a result carries 5 to 10 times more thiocyanate and
nitriloside than animals not so fed. If the milk we drink came from cows that ate fodder
rich in nitrilosides this milk will contain as much as 7 times more nitriloside than a cow
living on nitriloside-deficient fodder. At the end of the dinner we may choose a
nitriloside-rich apricot, peach, cherry, or plum brandy originally prepared from crushing
the entire or whole fruit. We may also choose a number of wild berries very rich in
nitrilosides--all members of the raspberry family. We may nibble on some nitriloside-rich
macadamia nuts or chew nitriloside-rich bamboo sprouts.
In such a menu of three meals in the course of a day we should ingest over 300 mg of
nitriloside or vitamin B-17 in our foods--every one of which contained nitriloside. The
quantities of the vitamin B-17 in the described foods have been very carefully determined
by independent workers over the years. Because of our cultural antipathy to cyanide, our
food technology has made every conceivable effort through processing, hybridizing,
distilling, etc., to remove every trace of derivable cyanide from foods for man and
animals. It is good that this irrationality has not to date, at least, completely removed
the cyanide-containing vitamin B-12 or cyanocobalamin.
Finally, let me conclude with this. In nitriloside or vitamin B-17 we have a new
vitamin in which all of us are severely deficient. This fact is beyond question. As to the
clinical application of vitamin B-17 (nitriloside) in human and animal cancer, we feel
that every case is morally entitled to whatever vitamin B-17 can offer, just as every
being stricken with scurvy, pellagra, or pernicious anemia is morally entitled,
respectively, to vitamin C, niacin, vitamin B-12 and folic acid. Indeed, the matter goes
far beyond clinical cancer itself. Mankind can not afford any longer a human and animal
population deficient in vitamin C, vitamin B-12, vitamin B-15, vitamin B-17 or any
other vitamin essential to animal or human nutrition.
However, the capacity of political power for stupidity is truly infinite. We can not
predict how long the orderly clinical study of crystalline vitamin B-17 will be delayed.
But take some comfort in this. Were vitamin B-12 and folic acid completely proscribed
tomorrow, liver would still offer complete salvation in pernicious anemia. Similarly, one
gram of defatted apricot seed or kernel carries about 30 milligrams of nitriloside. Six or
seven teaspoonful will supply what our clinical investigators consider an adequate oral
dose--one gram. It is best that the B-glucosidase enzyme be completely heat inactivated in
So far as other parts of the world may be concerned, I fear no such described
obstruction. In Germany I was very happy to find from four to five proprietary and ethical
brands of vitamin B-15 (pangamic acid), or its DIPA analogue, and I look forward to seeing
a similar distribution of vitamin B-17 (nitriloside) very soon. In visiting the great
museum in Hanover I was pleased to find in a display of food-stuffs recovered from Stone
Age digging in Europe that of eight food plants shown, three of them are heavy
nitriloside-producers. One was Himbeere (Rubus idaeus), another Brombeere (Rubus
fruiticosus) and Schwarzer Hollunder (Sambucus niger) or the common elderberry (from which
the nitriloside sambunigrin was originally isolated). In the United States the Lovelock
Caves in Nevada have yielded petrified animal and human faeces (fecoliths) that through
carbon-dating have been found to go back many years. They showed numerous remnants of
Just as the German chemists Huber and Weidel in 1873 first synthesized niacin through
the oxidation of nicotine about forty years after Wohler and Liebig in your country first
isolated and identified the first nitriloside, amygdalin, and just as niacin was destined
half a century later to be identified and defined as the factor that prevents and cures
pellagra in man, so we find that the nitriloside isolated and identified over a century
ago in Germany likewise is now achieving the status of a vitamin--vitamin B-17. Let us
hope that like niacin it has at least left the chemical museum to serve the impelling
needs of improved nutrition.
Ernst Theodor Krebs, Jr.
A noted biochemist, Ernst Krebs, Jr. took his student work at Hahnemann Medical College
in Philadelphia 1938-41. He received his AB at the University of Illinois in 1942; he did
graduate work at the University of California during 1943-45, researching in pharmacology
during the periods of 1942-45. He is science director of the John Beard Memorial
Foundation, having held this position since 1946. He is the author of "Unitarian or
Trophoblastic Thesis of Cancer" (1950); co-discoverer of pangamic acid (1948), the
role of pancreatic enzymes in human cancer (1948-50), and the relevance of the
nitrilosides (Vitamin B-17) to animal and human nutrition.
This paper is a summary of remarks presented in German before a congress of the
International Medical Society for Blood and Tumor Disease, Nov. 7, 1970, in Baden-Baden,
West Germany. On this occasion, the author received an award honoring his discovery and
research on vitamin B-15 (pangamic acid) and vitamin B-17 (nitriloside).
A partial bibiliography is printed here. A complete listing of references will follow
in a subsequent issue.
Baker, J.E., Rainey, D.P., Norris, D.M., and Strong, F.N., p-Hydroxybenzaldehyde and
other Phenolics as Feeding Stimulants for the Smaller European Bark Bettle, Forest Sci.,
Blum, M.S., and Woodring, J.P., Secretion of Benzaldehyde and Hydrogen Cyanide by the Millipede
Pachydemus crassicutus (Wood), Science, 158: 512-513, 1962.
Briese, R.R., and Couch, J.F., Preservation of Cyanogenetic Plants for Chemical Analysis, J.Agr.Research,
57(2): 81-107, 1937.
Brown, W.E., Wood, C.D., and Smith, A.N., Sodium Cyanide as a Cancer Chemotherapeutic
Agent -- Laboratory and Clinical Studies, Am.J.Obst. & Gynec., 80: 907-918,
Browne, J.G., Progress Report on the Work Done on the Hydrocyanic Acid Content of
California Grown Lima Beans, Univ. Calif. Coll. of Agr., Agr. Exptl. Station,
Project No. 521, p. 770 et seq., June 17, 1932.
Brioux, and Jones, E., The Production of Cyanogenetic Glycosides by Linseed: Measurement
of HCN Production, Ann. Agron., 8(4): 468-480, 1932.
Chappel, C., Toxicity Studies on Amygdalin, McNaughton Foundation, Montreal, Canada, 1967,
Charlton, J., The Selection of Burma Beans for Low Hydrocyanic Acid Content, Memoirs
Dept. Agr. India Chemical Series, 9(1), 1926-1928.
Dedolph, R.R., and Hamilton, R.A., The Bitterness Problem in Some Seedling Macadamias (Due
to amygdalin -- ed.), Hawaii Farm. Sci., 8(1): 7-8, 1959.
Delga, J., Mizoula, J., Veverka, B., and Bon, R., Studies on the Treatment of Cyanide
Intoxication by Hydroxycobalamin (Provitamin B-12), Ann. Pharmaceut., 19(12):
Dillemann, G., Hydrocyanic Acid in Hybrids of the Pear with the Quince, Bull. Museum
Natl. Hist. Nat., 18: 465-467, 1946.
Doak, B.W., Cyanoglucosides in White Clover, New Zealand J.Agr., 51: 159-162, 1935.
Domingues, J.B., Hydrocyanic Acid in Shoots of Dendrocalamus giganteus (Bamboo), An.Fac.Farm.,
E. Odontal Univ., Sao Paulo, 13: 169-171, 1955-1956.
Dunstan, W.R., Henry, T.A., and Auld, S.J.M., Cyanogenesis
IV. Occurrence of Phaseolunatin in Common Flax
V. Occurrence of Phaseolunatin in Cassava,Proc.Roy.Soc., 1906, 78B, 145-158.
Dunstan, W.R., and Henry, T.A., and Auld, S.J.M., Cyanogenesis in Plants
II. The Great Millet, Sorghum vulgare, Phil.Trans.Roy.Soc.,199A: 399-410, 1902.
Dunstan, W.R., Henry, T.A., and Auld, S.J.M., Cyanogenesis
VI. Phaseolunatin and the Associated Enzymes in Flax, Cassava, and the Lima Bean, Proc.Roy.Soc.,
79B: 315-322, 1907.
Ekpechi, O.L., Dimitriadoo, A., and Fraser, R., Goitrogentic Activity of Cassava (A Staple
Nigerian Food), Nature, 5041: 1137, June 11, 1966.
Festenstein, G.U., Substrates for Rumen Beta-Glucosidase, Biochem. J., 70(1):
Flux, D.S., Butler, G.W., Johnson, J.M., Glenday, A.C., and Petersen, G.B., Goitrogenic
Effects of White Clover, New Zealand J.of Sci. and Tech., 38(A): 88-102, 1956.
Flux, D.S., Butler, G.W., Rae, A.L., and Brougham, R.W., Relationship between Levels of
Iodine and Cyanogenetic Glucoside in Pasture and the Performance of Sheep, J.Agric.Soc.,
55(2): 191-196, 1960.
Golse, J., New Method for the Determination of Hydrocyanic Acid and Benzaldehyde in Cherry
Brandy, J.Phar.Chim., 12:44-65, 1915.
Greshoff, M., The Distribution of Prussic Acid (HCN) in the Vegetable Kingdom, Report
Brit.Assn., 138-144, 1906.
Guignard, L., The Development of Cyanogenetic Glucosides During the Germination of Plants, Compt.rend., 147: 1023-1038, 1908.
Guignard, L., The Presence of Cyanide-Yielding Compounds in the Elderberry, Compt.rend.,
141: 16-20, 1905.
Herissey, H., The Cyanogenetic Glycoside Prulsurasin Crystallized from the Leaves of the
Cherry Laurel, Compt.rend., 141: 959-961, 1905.
James, M.B., Fleming, J.W., and Bailey, L.F., Cyanide as a Growth-Inhibiting Substance in
Extracts of Peach Leaves, Proc.Amer.Soc.Hort. Sci., 69: 152-157, 1957.
Jones, M.B., Seasonal Trend of Cyanide in Peach Leaves and Flower Buds and Its Possible
Relation to the Rest Period.Proc. amer.Soc.Hort.Sci., 77: 117-120, 1961.[nee
Liebig, J., and Wohler, F., The Composition of Bitter Almonds,Annalen, 22(1): 1-24,
Liebig, J., and Wohler, F., Formation of the Oil of Bitter Almonds, Ann.Chim.Phys.,
64: 185-209, 1837.
Luh, B.S., and Pinochet, M.F., Spectrophotometric Determination of Hydrogen Cyanide in
Canned Apricots, Cherries and Prunes, Food Research, 24: 423-427, 1950.
Martin, J.H., Couch, J.F., and Briese, R.R., Hydrocyanic Acid Content of Different Parts
of the Sorghum Plant, Jour.Amer.Soc.Agron., 30(9): 725-734, 1938.
Michajlovski, M., Stukovsky, R., and Nemeth, S., Effects of Feed Composition on the
Thiocyanate Content of Cow Milk, Biologica(Broteslavia), 16: 459-468, 1961.
Monekosso, G.L., and Wilson, J., Plasma Thyocyanate and Vitamin B-12 in Nigerian Patients
with Neurological Disease, Lancet, No. 7446: 1062-1064, 1966.
McIlroy, "The Plant Glycosides," Edward Arnold & Co., London, 1951,
Oke, O.L., Chemical Studies of Some Nigerian Vegetables, Exp.Agr., 1(2): 125-129,
Osborne, D., Solving the Riddle of Wetherhill Mesa, Natl.Geo.Mag., 125(2): 155-194,
Perry, I.H., The Effect of Prolonged Cyanide Treatment on Body and Tumor Growth in Rats, Am.J.Cancer,
Pobiondek-Eabini, R., The Hydrogen Cyanide Content of Millet, Arch.Tiernarh., 2/3,
Pjoan, M., Cyanide Poisoning from Choke Berry Seed, Am.J.Med.Sci., 204: 350-553,
Rabati, J., Biochical Study of the Peach Tree, The Presence of Amygdonitrile Glucoside, Bull.Soc.Chim.Biol.,
15: 385-395, 1933.
Schroder, J., and Damman, H., Studies of the Amount of Hydrocyanic Acid Obtained from
Different Millets, Chem.Ztg., 35: 1436-7 (Chem.Abst. 62 1327).
Stebbins, R.C., Lizards Killed by Millipede (Through HCN-benzaldehyde emission from
latter, ed.), Amer.Midland Nat., 32(3); 771-778, 1944.
Weiss, M., Hydrocyanic Acid in Apple Embryos, Flora, 149(3): 386-395, 1960.
Wokes, F., and Willimott, S.G., The Determination of Cyanide in Seeds, J.Pharm. &
Pharmacol., 3: 905-917, 1951.
Worth, F.J., A Note on the Hydrocyanic Acid Content in Burma Beans, Memoirs Dept. Agi.
India Chem.Series, 7(1), 1928 (cf paper by Browne, J.G.).