Nitrilosides (B-17) - A Dietary Deficiency?

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

Hypertension,

Arthritis, etc.) JoAnn Guest Oct 24, 2005 17:17

PDT

THE ROBERT CATHEY RESEARCH SOURCE

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

-

 

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).

 

 

BIBLIOGRAPHY

A partial bibiliography is printed here. A complete

listing of

references will follow in a subsequent issue.

 

 

REFERENCES

 

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--

 

 

 

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