Cancer
: Enzyme Treatments
by
Roger Cathey
see also
Trophoblast Cancer
Theory
see also
World Without
Cancer
(Video)
This paper is written for the lay person. If you are a
specialist or a doctor, there is a more technical article
written about Trophoblastic Explanation of Cancer
The primary basis of the enzyme treatment of cancer emanates
from a recognition that cancer cells share properties with
placental cells found in pregnancy. These placental cells are
completely rejected by both fetus and mother by the time of
delivery. Therefore it was reasoned that whatever factor or
factors which underlay the rejection of the placenta could
play a similar role in the body's rejection or remission of
cancer cells. Other observations lead the earliest thinker
along these lines, Embryologist John Beard (1857-1924), to
believe that the pancreatic enzymes of fetus and mother
combine to bring about this event. Thus the basis of enzyme
therapy for cancer was first derived from the idea that
enzymes play a role in causing birth.
These placental cells are called trophoblasts and are the
first cells to differentiate from the fertilized egg. In this
creation of trophoblasts it is important to note that they
are a fully parasitic and a distinct feature surrounding the
fetal cells that will form the living individual. In their
role, trophoblasts mediate the implantation of the
individual, but they are never incorporated into the body of
the individual or fetus. Thus it is incorrect to call them
"fetal" cells. They will eventually be either destroyed or
rendered completely inert as far as the mother and fetus are
concerned. These cells are often seen as a thin membrane
covering the fetus at birth, the so-called "caul." Again,
they never form an integral part of the formative individual.
This fact is important to keep in mind, psychologically,
because the same holds true of the cancer cell which does not
in its incursion form an integral part of the individual. It
has been observed that after some time of enzyme treatment
tumors often "shell out," and they can be more readily
removed surgically, or they may extrude and drop out by
themselves if partially exposed on the outside of the body.
Somatic "tumors" or lumps or calluses consist of normal cells
that sometimes grow up around the cancer growth in an attempt
to mechanically limit their incursion. These types of growths
are not affected by enzyme treatment, but are reduced by a
morphogenic process of apoptosis or programmed cell death, or
they may need to be removed surgically. It is believed that
in many cases of radiation therapy, it is these normal cells
that are destroyed leaving the hardier cancerous cells with a
higher concentration in mass. In enzyme therapy, the cancer
cells alone are attacked.
The source cells of these trophoblasts in pregnancy are the
most potent cells in the life cycle, i.e., the united sperm
and egg result in the original "stem cell," or cell capable
of becoming any and every cell in the completed form. Other
tissues formed or differentiated from this primal cell may
have various powers of expression, but they do not possess
the power to become any other cell in the whole system. Most
cells of the body are therefore "derived" cells and they are
all observed to be of limited potential.
As noted above, in the course of gestation these trophoblasts
are rendered completely inert and finally rejected from the
host representing the event of birth and probably is also a
major cause of birth. This happens despite the fact that the
cells seem not to induce any immunological reaction. A prime
reason for this was discovered in this century by Currie and
Bhagshawe who showed that the trophoblast was surrounded by a
coating (sialo-glycoprotein) including a molecule that gave
it a negative charge. The molecule can be likened to mucilage
and has been termed the sialo-mucinous coat. A negative
charge is also found on the white blood cells responsible for
immune reactivity. Since two like charges repell we have
delineated the primary reason for lack of rejection based on
immune responses. This same type of coating is found on the
cancer cell. And in fact, it is one of the chief reasons for
classifying all cancer cells as "trophoblastic."
It bears repeating that although the first trophoblast cell
in the life cycle goes on to become the entire placenta, it
does not become any part of the oncoming fetus, but is
strictly a parasitic mediating and terminal cell or tissue
type. Because the cellular trophoblast (cytotrophoblast) can
differentiate further, it is said to be pleuripotent, but it
is still of limited potential compared to the stem or
totipotent cell.
John Beard was the first to organize a theory around the
cause of birth and the destruction of cancer cells. First he
observed that the invading and eroding trophoblast component
of the fertilized unit was remarkably similar to metastatic
cancer cells, and other observations lead him to believe
there was some intimate relationship between these
trophoblasts and cancer cells. Another observation was that
the placental trophoblasts seem to take a downturn in
activity around the time of the activation of the fetal
pancreas, which occurs around the 56th day. Modern research
has shown that these trophoblast cells secrete a hormone
called human chorionic gonadotropin (hCG), and the quantities
of this hormone rise until around the 56th day and then begin
to taper off. It is this very hormone that coats the
trophoblast and cancer cell to make them both immulogically
inert. This hormone of pregnancy is expressed in all types of
cancers.
Seeing this change in trophoblast behavior and the onset of
activity of the fetal pancreas has more than mere
coincidence, Beard began to speculate in his correspondence
with physicians about the possibility that the function of
both the mother's and the fetus' pancreases were somehow
involved in the resolution or destruction of the trophoblast.
If that is so, he asked, then might the same be said of
cancer cells in the cancer patient? In time Beard's
speculations were put to the test by several physicians using
pancreatic enzymes. At first they used only the proteolytic
enzyme trypsin, but when the reactions of patients to this
tended to be severe they then turned to combining trypsin
with amylase, the carbohydrate digesting enzyme, and found
that the reactions of the patients were much better. (For
details on this historic finding go to:
http://www.navi.net/~rsc/beard066.htm)
This accentuation of the protein digesting enzymes in many
versions of this therapy explains the oft reported periods of
nausea and other symptoms resembling pre-eclampsia or morning
sickness. Beard and his associates' final form of therapy
always accentuated amylase, sometimes completely eliminating
trypsin and other protein digesting enzymes after a certain
length of application or during so-called "rest periods" of
treatment.
This is logical, because the glycoprotein surrounding the
cancer cell, and the circulating hormone form of this
glycoprotein (often mistakenly called a "protein" or "fibrin"
coat), are fundamentally presenting to the system as
carbohydrate complexes. That is, the body sees the
carbohydrate side of the molecule, not the protein side, and
amylase attacks this before the proteinases can do a thing.
There is then the question of how the cancer/trophoblast
comes into being in the non-pregnant individual. Since all
stem cells have all potentialities within them, it has been
assumed by some researchers that cancer must arise from a
residual complement of stem cells in the body. There are a
number of observations recorded in the medical literature
attesting to the presence of these stem or totipotent cells
in the adult body. Others contend that since all cells have
the complete genome within them, if they can divide at all,
there is the possibility of them re-acquiring totipotency, or
simply to directly express the trophoblastic suite of
characteristics. That is something for research to definitely
establish, and we need not concern ourselves too much on this
point. It would appear that anything that can disturb the
genome sufficiently, presumably factors not normal to the
animal economy, whether parasitic, cytotoxins, or
carcinogenic or chronic injury of any kind, is sufficient to
bring these properties into expression. After all, the
trophoblast has proven to be the hardiest of expressions of
the differentiating zygote as it goes through a gamut of
harsh environs of low oxygen, then establishing a place in
the uterus and a reliable blood supply. In injury, something
of the same harshness exists.
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