Nitrilosides (B-17) - A Dietary Deficiency? (Cancer, Hypertension, Arthritis, etc)

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Nitrilosides (B-17) - A Dietary Deficiency? (Cancer, Hypertension, Arthritis, etc.)

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Significance (Antineoplastic Vitamin B-17) Ernst T. Krebs, Jr.

Reprinted from the Journal of Applied Nutrition, Volume 22, Numbers 3

and 4, 1970

 

http://www.navi.net/~rsc/krebs3.htm

 

 

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 natural 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 cause.

 

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.

 

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.

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 vitamin.

 

-------------------------- -----------

*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

 

-----

 

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 toxicity alone?

 

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 separate effects.

 

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 such material.

 

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 nitriloside-bearing plants.

 

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).

 

 

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A partial bibiliography is printed here. A complete listing of

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