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SURVIVAL FACTOR IN NEOPLASTIC AND
VIRAL DISEASES
By
WILLIAM FREDERICK KOCH, Ph.D., M.D.
Chapter 6
ENERGY PRODUCTION
In order to explain the therapeutic procedure and reasons for
certain features controlling the care of the patient, a
consideration of the energy producing mechanism will be helpful.
We do not know what energy is, but we can differentiate several
forms, and measure them in various ways. It is the consensus
that all energy produced in the cell, whether by oxidation —
namely the Krebs tricarboxylic acid process — or by
fermentation, is the same and is stored as ATP (Adenosin
triphosphate) high-energy bonds, before it is transferred to the
working elements of the cell to be transformed into the energy
of work. No other mechanisms of energy production are
recognized, simply because no intermediaries identifiable with
any other processes have been encountered. However,
there is plenty of room for the operation of a far more
efficient process than the Krebs Cycle, which indeed is a
decarboxylation process nicely adapted to the lower forms of
life. The clinical data show that the Krebs system does not
fulfill the requirements of the oxidations that maintain
health and that some other process of higher efficiency is
present that provides the Survival Factor we have identified
and reproduced for four decades for clinical use. The
intermediaries of this High Efficiency Process are not to be
trapped. They constitute the “smokeless flame” that supplies
the energy as a preferred process. This is our Postulate
that will be supported by practical proof later.
Ochoa and others have calculated that the combustion of a gram
mol. of glucose in the tissues yields 450,000 calories of energy
as the total from the various steps of the Krebs Cycle. This
gives 36 (38) high-energy phosphate bonds with a P/O
ratio of three. The free energy ^ F of glucose is, however, —
691,000 calories, and the energy of combustion ^ H is — 673,000
calories. Thus, 18,100 calories are consumed in the process. The
energy calculated as — 450,000 calories from the Krebs process
of oxidations is therefore — 220,000 calories shy of the —
673,000 calories available for work, and that are not accounted
for in anyway. Therefore, some other process of higher
efficiency than the Krebs Cycle has plenty of room to operate.
Further, the highly inefficient Krebs process (65%) offers no
protection against pathogens as it provides no O/R potentials
high enough to start their combustions, but supports viral and
neoplastic processes instead. It thus does not account for the
survival oxidations that are clinically demonstrated. This
process we identify with the FCG dehydrogenations that start a
chain of oxidations via the free radical formed and its addition
of oxygen to produce a peroxide free radical as carrier of the
process. In free circulating toxins the reaction may be pictured
thus:
Where TH is the toxin, and RCO the Survival Reagent
Carbonyl Group.
In combined or integrated toxins, the most mobile hydrogen atom
is alpha to a double bond in the most activated region which
would be adjacent to the position of integration with the FCG or
its activating double bond. Free radical production where this
hydrogen is removed and addition of molecular oxygen to form a
peroxide free radical causes cleavage into two parts with
Carbonyl terminals. The azomethine double bond is broken, and
the nitrogen oxidized away. The double bond of the new Carbonyl
groups formed by the cleavage activate alpha positioned hydrogen
atoms where further dehydrogenations repeat the process forming
more peroxide free radicals that are the best dehydrogenators
and carriers of the oxidation chains to new molecules of fuel or
toxin that enter the field. All of the peroxide free
radicals serve destructively to toxins therefore and
constitute what we referred to as the antitoxic state of
structure of the toxin after the Synthetic Antitoxic Reagent
worked on it. Koch, “Cancer Journal,” October
1924; Philadelphia; “Koch, Investigations,” 1924. Here
the process was described as converting toxin into antitoxin.
Our Postulate required that the FCG is activated by
conjugation with the double bonds of an ethylene linkage from
which it receives electrons.These two atomic groups are the
center of romance in the maintenance of function and in the
protection against toxins that enter the field. They are also
the centers of attack of pathogens in viral, neoplastic and
degenerative diseases. Whether or not a pathogenic
response is to be had will depend upon:
(a)the presence or absence of a normal quota of molecular
oxygen, and
(b) upon the firmness of condensation of an amine
with the FCG, that guarantees or destroys its potency.
In case the normal range of energy production cannot cleave the
bond, FCG function is destroyed and disease results.
Then a superiorly efficient dehydrogenator Carbonyl group must
be supplied to burn off the pathogen as previously stated. This
restores the FCG for normal function. This super
dehydrogenator is our Therapeutic Synthetic Survival Factor,
(SSR).
The adequate oxygen supply plays two parts:
(1) it is the ultimate electron acceptor when the hydrogen
atom removed from fuel or toxins by FCG is transferred to some
oxidase system so the FCG is free to start new oxidations, and
(2) after the fuel or toxin is dehydrogenated to become
a free radical, molecular oxygen must be at hand to convert
it into a peroxide free radical to continue the oxidation
process.
Otherwise the free radical would under hypoxia add to the
closest reactive group that would accept it, and this is the
double bond of the ethylene linkage that activates the FCG. The
pathogen would thus integrate with the host cell’s energy
producing mechanism where it would draw off energy for its own
vegetation or to transfer ectopically, and produce disease, and
at the same time block the activation of the FCG and stop
further FCG dehydrogenations. Thus oxidation is blocked and the
consequent colloidal degenerations would follow to produce
further anoxia. Thus anoxia is essential to the integration of
the pathogen with the grana when the FCG is still operating.
However, the moment the pathogen is added to its ethylenic
activating double bond, electrons are no longer contributed to
it, so the FCG is no longer able to dehydrogenate, and the grana
appears to be out of commission, destroyed and lost. Ectopic
uncontrolled transfer of energy to various secreting and
contractile or conducting functional systems referred to above
we hold to be the cause of allergy.
Since creatine did not interfere with FCG function as did
guanidine, and since it is the only amine possibly that forms
high-energy phosphate bonds, it was easy to assume that it
played a role in the transfer of energy produced from the
oxidation of fuel to high-energy phosphate bonds as of ATP. It
would accommodate this transfer by condensing with the FCG to
form an azomethine bond until enough energy had been generated
to admit phosphoric acid into the bond and unite it with the
amine group of creatine sending the creatine phosphate off as a
high-energy carrier. The FCG is thus free to start further
dehydrogenations physiologically. However, if the amine
condensed with the FCG forms a tight bond not separable under
normal ranges of energy production, as did guanidine in the
parathyroid experiments, the whole train of pathological events
must follow. For this reason it is well to inquire into the
sources of such pathogenic amines. One is the production of
toxic amines in the acid colon by various bacteria that
decarboxylate amino acids. In many people, the intestinal
flora is firmly entrenched and converts the food into one’s
poisons that serve as the vanguard of disease. Animal proteins
are the main sources of these toxic amines, and sulfides, while
vegetables, cereals, and fruits supply plenty of protein and at
the same time do not support decarboxylating germs. The
intestine must be kept at a range of pH above 7, since the
decarboxylations progress best at a pH of 3.5 to 6 when mediated
by the Streptococcus fecalis and so many others.
The fungus found always in cancer is an amine producer that
could initiate the pathogenesis as explained above, with its
whole train of symptoms. And the modern antibiotic amine
poisons, especially those that attack the liver and cause
suspensions of consciousness like the sulfa drugs, and any in
fact, are to be scrutinized with great suspicion as the cancer
death rate his increased so greatly since they have become so
widely used. Sulfides and sulfhydryl derived from food add to
the double bonds that activate the FCG and thus block its
activation powers. The intestinal flora again is to be
considered with the diet if one is to maintain a normal function
of the FCG as an energy producer and protector against
pathogens. Especially during the Treatment period, when
a dehydrogenator Carbonyl group of highest efficiency has been
administered, one must protect the oxidation progression that
follows from being blocked, as can take place through permanent
free radicals as the oxides of nitrogen. Gas anesthesia should
never be used in connection with this Therapy. Highly polar
double bonds can also add to and quench the free radicals of the
recovery process and block it, so certain terpenoids and even
perfumes, and especially acrolein and polymerizing acrylic
aldehydes from frying pans, are to be avoided in this regime.The
proofs of our Postulate are serious practical facts.
Some medications absorbed into the tissue colloids may alter
the steric set-up so that the remedial Carbonyl group which
ordinarily could attack the hydrogen atom to be removed
perpendicularly to the plane of the conjugation of its carrier
carbon atom with the double bond that activates it, now finds a
distortion that hinders this line of attack. Opiates and coal
tar drugs, and especially aspirin, appear to interfere in this
way.
The atomic set-up of the Reagent itself that carries the
Super-high-efficiency Carbonyl group must offer a steric
advantage in each disease where it is applied. For example: in
Hog Cholera, diphenoquinone proved 100% efficient in several
epidemics, while it proved 100% worthless in Rabies, and the
serial system of Carbonyl groups used in Hog Cholera proved 100%
worthless, while it was 86% efficient in Rabies in terminal
cases. Both diseases kill 100%, within 3 to 5 days. Rabies is
neurotropic always and Hog Cholera rarely before the terminal
hours. Our search has been for a molecule carrier of the
Survival Efficient Carbonyl group that is equally applicable in
all diseases where drug interference has not modified the steric
set-up. This will be discussed later on. It will be seen,
however, that to identify the high efficiency oxidation system,
we consider normal to the cell, as of the same order as the
therapeutic substitute used to rescue the FCG and restore normal
function and structure, a few comparisons will have to be made.
For example: that they are of the same order is seen in being
blocked by the same agencies as anoxia, sulfhydryl, and that
their processes are blocked by permanent free radicals, highly
polar double bonds, etc. Likewise, the restitution program, that
follows the freeing of the FCG system of its pathogen by the
Synthetic Reagent, is the normal process. So the Synthetic
Reagent fits into the mechanism with equal grace, as did the
FCG before it was attacked by the pathogen. Likewise,
since recoveries from viral and neoplastic diseases that could
never be combated successfully before are accomplished by the
natural resources of the body after the Synthetic Survival
Reagent is used, they both fit the cell chemistry, but each in
its respective capacity for survival. Since the recovery
mechanism includes cyclic reactions at definite periods never
seen in medicine before, just as the cure of the pathologies
involved were never seen before, a deeper grasp on tissue
physiology is made possible and a wider range of expertness can
be acquired. Any successful clinician will recognize that
expertness in this Therapy depends upon study and experience,
and some new viewpoints must be adopted. To illustrate let us
review a few toxic cases.
These cases show the characteristics of the recovery process,
which itself gives evidence as to the nature of the etiological
factor. Only the most pertinent data is used. It will be seen
that each case presents a long pretreatment control period that
definitely established the downward trend of health with the
steady and often rapid advance of the diseases. Thus the best
possible control for comparison of pretreatment and
post-treatment progress was followed, and no confusing variables
were permitted, as for example, other medications or treatment
measures. Likewise factors that interfere with recovery were
eliminated, so that the contest lay plainly between the Therapy,
the patient’s cooperation, and physical advantage on the one
hand, and the disease forces on the other. The Remedy is
named the Synthetic Survival Reagent (SSR). There are two
forms, the Quinone form which when used is so named, and the
Carbonyl group chain form with free radical terminals. This is
simply called the Synthetic Survival Reagent (SSR) or given a
similar appellation. The quinone dose is two micrograms,
and the SSR, two micrograms, millimicrograms and micro
micrograms in water, given intramuscularly or under the skin.
With few exceptions, the case records are taken from Federal
Court and Federal Trade Commission Testimony, where they were
proven factually uncontradictable. Some of the exhibits
have been reproduced for use in this book. This policy was
adopted to give the student full confidence in the proofs of a
Thesis as unusual as this one.
A case of toxic nodular goiter illustrates some of the main
features of the oxidation mechanism of our Postulate.