RIFE AND CANCER
CAUSES
APPENDIX
G BY PHYSICIST GARY
WADE
(THE
POSSIBLE GENETIC CAUSE OF A MAJORITY OF CANCER CASES THAT ARE MICROBE INDUCED--For A Less Technical Introductory Article Please see
"Vibratory Energy Medicine" )
In 1931, after seven years of
attempting to isolate a microbe cause of cancer from over 20,000 cancer tissue
samples, Dr. Royal Raymond Rife did just that. Rife's 1931 discovery of a
cancer microbe finally reached general public notice in 1944. That year an
article entitled THE NEW MICROSCOPES was published both in the February issue
of THE JOURNAL OF THE FRANKLIN INSTITUTE and in the 1944 ANNUAL REPORT OF THE
BOARD OF DIRECTORS OF THE SMITHSONIAN INSTITUTION. Rife's work was not then and
has not yet been appreciated by microbiology, because microbiology has a large
blind spot, both in its physical visual view of the living microworld and in
its conceptual view of the structure and life cycles of the living microworld.
If you wish to look at living cells, the best research optical microscopes
generally available throughout the world only reach about three thousand power.
These microscopes in general can not detect viruses, unless a fluorescence
technique like Rife's fluorescence technique is used. These microscopes give
very limited structural detail about living cell organelles. If the biologist
wants detailed structural information about some cell structure they use an
electron microscope. However, now the electron microscope picture is the
picture of a dead, often highly degraded and distorted structure. This is
because the sample preparation process, which produces a sample that can
withstand the conditions of high vacuum and bombardment by a high-energy
electron beam has degraded and distorted the original living structure. So at
best you end up with a distorted snap shot of a non-living structure. I do not
mean to denigrate the great and marvelous contributions made by the electron
microscope. I have considerable personal experience with the use and operation
of scanning electron microscopes and I hold them and transmission electron
microscopes with high regard. I particularly appreciate the immense
contributions made to the understanding of micro cell structure by the massive
ultra high resolution transmission electron microscopes such as can be found at
the University of Colorado at Boulder,CO.
However, all this not withstanding,
I also know the electron microscopes' limitations, both physically and in its
actual use by researchers. If you have a interest in understanding biological
microstructure, go to the trouble of going to a good research library and look
up the Feb. 1944 issue of THE JOURNAL OF THE FRANKLIN INSTITUTE or the 1944
ANNUAL REPORT OF THE BOARD OF DIRECTORS OF THE SMITHSONIAN INSTITUTION. In the
R.E. Seidel and M. Elizabeth Winter article, THE NEW MICROSCOPES, look at the
photographic plates. Note the high quality resolution comparable to that of
current electron microscope photographs. The photograph of the typhoid bacillus
was taken with the Rife Universal Microscope at 23,000 power and then
photographically enlarged to 300,000 power. Note that this photograph has the
resolution commonly found in today’s high-resolution electron microscope
pictures of bacteria. Further note that the resolution in this print is not as
good as the resolution on the negative it came from do to the limitations in
printing pictures in 1944 and even today. As was explained in technical detail
in Appendix A, Rife had discovered an optical assembly configuration that
effectively suppressed all Fraunhofer diffraction phenomenon, while at the same
time he made the organism light itself by a natural fluorescence phenomenon.
This fluorescence phenomenon was achieved by illuminating the specimen with an
intense narrow wavelength band of light. The particular band of light was
unique to each microbe. Also note that this is a photograph of an intact living
bacterium. If you are familiar with current microbiology, you know that little
if any time is spent by the great majority of researchers watching and studying
live microbes. Except for spot optical microscope checks to make sure live cultures
are as they should be or are as assumed they should be, research is carried out
by biochemical techniques the results of which are interpreted in the light of
past perceived research results. In short actually very little live observation
on microbe life cycles are carried out by researchers anywhere on the entire
planet.
This brings us to the other blind
spot in biology. Its name is pleomorphism or the ability of a microbe to change
its physical form. During the later half of the 19 th century and into the
early part of this century a sharply fought battle over whether or not some
microbes could change their physical form was waged. Those in favor of
monomorphism won out and it became "heresy" to advocate pleomorphism.
After two years of reviewing the research for and against pleomorphism it is
clear that the monomorphists were wrong. The monomorphists won the argument
because they had political prestige and economic positions of leverage. The
monomorphists used optical microscopes and lab techniques not adequate to
determine the issue due to inadequate magnification power, lack of non lethal
staining methods, sheer ignorance, and sloppy to lazy research work. If you go
to the trouble of looking up the Feb. 1944 issue of the Franklin Journal, note
that the Rife microscope photograph of the typhoid bacillus clearly shows the
formation of a filter passing form ( the original operational meaning of the
word virus) of the typhoid bacillus, in the top end of the bacillus. Rife found
that when this bacillus virus was released by the bacillus, it had a bacterium
flagella and was motile. Now all of this is just plain crazy, if you are a
currently trained microbiologist. However, no currently trained microbiologist
owns or uses a Rife type optical microscope which could easily view this and
the similar BX cancer virus, which is also a motile virus (ovoid body with
bacterium flagella). The oviod body dimensions of the BX cancer virus are 750
angstroms long by 500 angstroms thick. It is propelled by a proton transport
flagella the same as the parent bacterium. This "virus" will easily
fit inside the so-called AIDS virus (HIV) outer capsid and is comparable in
size to the inner (HIV) capsid. I now ask you microbiologists reading this:
Will this BX cancer "virus" be recognized in a high power electron
microscope photograph for what it is or will it just be considered another
piece of degraded cellular debris in the prepared cancer cell section sample?
Much of what you see is what you are trained to see. How are microbiologists
trained to see?
Rife using his Rife type microscope
had for seven years been able to observe and isolate a microbe from carcinoma
cancer tissue. However, upon injection of concentrations of this microbe into
test animals no cancer was produced. In 1931 Rife got the idea to expose a
sample of carcinoma breast cancer tissue to 24 hours of broad band violet to
ultraviolet light exposure from a argon gas discharge tube ( see Journal of the
Franklin Institute article). A one half centimeter on a side cube of carcinoma
breast cancer tissue was placed into a test tube containing
When concentrations of this BX
cancer virus were injected into 426 albino rats, all rats developed cancer
tumors at the injection release site in the animal tissue. Further experiments
with the BX cancer virus demonstrated that it can be easily changed from one
microbe form to another by means of altering the media upon which it is grown.
Rife found more than six forms, which the BX cancer virus could be transformed
into. These included: 1) BY cancer virus, which caused sarcoma cancer tumors,
2) Cryptomyces plemorphia fungi, which Rife found implicated in rheumatoid
arthritis, 3) Progenitor cryptocides, 4) Bacillus coli, 5) Bacillus typhus’s,
and 6) Virus of the bacillus typhus’s, which can be clearly seen in the
photograph of the typhoid bacillus appearing in the article THE NEW MICROSCOPES
of Feb. 1944.
Rife was not the only researcher to
find a microbial cause for cancer. Many others have also. Nor was Rife the only
one to build an optical microscope that could see the BX cancer virus.
Currently in
As for the other researchers who
have found the same microbial cause for cancer as Rife, they have all been
persecuted, while their work has been maligned and discredited by the corrupt
higher ruling circles of what currently passes for legitimate medicine and
microbiology. Perhaps a brief review of the work of one victim is in order.
Dr. Virginia Livingston-Wheeler in
1947 while studying tumors found the same organism in all of them. Her findings
were published in August 1948 by the New York Microscopical Society Bulletin.
Later in Dec. 1950 Wheeler had an article published in the American Journal of
Medical Sciences on microbes cultures taken from both human and animal tumors.
On
The San Diego Union of
In 1950 Dr. James Hillman of RCA
Labs in
For an in-depth documented overview
of the massive suppression by allopathic medicine of real cancer treatment
breakthroughs that worked, I recommend you read: 1) THE CANCER CURE THAT
WORKED, by Barry Lynes, and 2) THE HEALING OF CANCER, by Barry Lynes. Both
books are available through Marcus Books, P.O. Box 327, Queensville,
I will now share with you some
observations about cancer cells and a classic experiment in which they are
coverted to normal cells, which suggests a simple answer to how cells infected
with the BX cancer virus become cancerous. It has long been noted that cancer
cells act and appear somewhat like undifferentiated embryonic cells.
Furthermore, cancer cells apparently have mostly an anaerobic (without oxygen)
metabolism. Note that the only time in the normal life cycle of mammalian cells
in which they are of a undifferentiated embryonic nature and also have an
apparent appreciable anaerobic metabolism is the period between the time the
female egg, the ovum, has been fertilized in the fallopian tube and just before
a viable placenta has developed in the uterus. Geneticists and embryologists
have shown that the entire development of the fetus from just-fertilized ovum
to the fully developed fetus is governed completely by sequentially read and
expressed genetic information. There is an exceedingly complex genetic
interchange and feedback control system in operation. Some of this genetic code
is used only for a short period of time and is then sealed away not to be read
or opened up again in the individual's existence, except during chromosome
copying prior to cell division. Cancer cells act as though they have had some
set of embryonic gene sequences reactivated. However, in the now mature
differentiated mammalian cells from which this cancer cell has been derived,
the control system that normally would have deactivated this embryonic gene
sequence(s) is itself long since deactivated. The cancer cell is in a run away
catch 22 situation.
It has been found that many genes
occur in sequenced sets in which none of the genes in the sequence can be read
and expressed unless the first gene in the sequence has been opened to be read.
Just in front of that first gene there is a DNA code sequence which has to have
a promoter protein bound to it so that the DNA code sequence reading enzyme can
temporarily attach to this promoter protein and then begin reading/translating
the DNA code of the gene sequences into messenger RNA for protein synthesis by ribosomes.
For this promoter protein to attach to its DNA coupling sequence at the
beginning of the gene sequence, this sequence must be in the normal B-DNA right
handed double helix form ( see Figures 1 and 3 ) . If the coupling site code
sequence or the DNA code sequence immediately in front of it has a blocking
protein attached or is in the form of the left handed Z-DNA double helix ( see
Figure 2 ), the promoter protein can not bind / couple with its DNA code
sequence and therefor the entire sequence of genes will not be read and
expressed. The Z-DNA double helix form is a very compact form of the double
helix. It has no major grove structure like the B-DNA double helix which allows
a promoter protein to physically match up with a specific DNA code sequence
which will manifest itself in the unique molecular structure of the surface of
the major grove for that unique DNA code sequence. The Z-DNA double helix
structure gives very little information about what the DNA code sequence is in
its core. For a left handed Z-DNA double helix associated with a specific DNA
code sequence to convert itself into a right handed B-DNA double helix,so that
the promoter protein can attach, the concentrations of various ions in the cell
nucleus must be in certain specific ranges for that specific Z-DNA sequence.
The specific concentrations and ratios of ions in the nucleus is determined by
the actions of ion gates and pumps in the cell outer membrane. These ion gates
and pumps are controlled by messenger proteins and compounds from both inside
and outside the cell membrane. What this means is that the cell genetic
expression can be greatly influenced and controlled by the genetic expression
of other cells and cell sets (organs). And of coarse during embryonic
development this external cell influence is in dominant control of the whole
cell system of membrane ion gates and pumps.
Now that some of the basic genetic
control process has been stated, several questions need to be asked. Can one or
more microbe proteins or chemical compounds be generated and released inside a
mammalian cell by a parasitic microbe? Can these proteins or compounds act as a
messenger to open up or close down cell membrane ion gates or pumps? Can this
opening or closing of ion gates and or pumps cause a gene sequence which is
normally only open during early embryonic development to open up again and
thereby cause the cell to go cancerous? I believe the answer to all these
questions is yes. Of course there are many other possibilities i.e. some of
these protein fragments may act as promoter proteins or combine with and remove
blocker proteins, thereby allowing a promoter protein to attach to a DNA
sequence and thereby initiate DNA transcription.
Dr. Robert O. Becker, M.D. has
written a book THE BODY ELECTRIC in which he goes into great detail about
tissue regeneration processes and their electrical and ionic connection to
genetic expression. I will now use information distilled from Becker's book
which supports my above suppositions. In 1948 Dr. Meryl S. Rose performed a
mile stone experiment on salamanders. Rose transplanted frog kidney cancer
tumor tissue onto a salamander's hind limb. These frog tumors were virus
induced. The results of his experiment, however are the same even if the tumor
is carcinogen induced, which was done later. The transplanted tumors would grow
and spread, leading to the salamander's death, if no intervention was taken.
However, if Rose amputated the limb below or through the middle of the tumor,
the salamander would regrow the limb and in the process the tumor(s) would
disappear, even if the tumor had already spread to other body locations. Tissue
biopsies of the wound region during regeneration showed that both salamander
cells as well as cancerous frog kidney cells dedifferentiated into embryonic
cell forms during the blastema formation process as the wound healed. Even more
amazing, as the blastema propagated forward, regenerating the limb, both
embryonic frog and embryonic salamander cells of the blastema multiplied (divided).
They differentiated into the cell types needed to form the new limb tissue,
i.e. muscle cells, cartilage cells, capillary cells, etc. In later years
researchers such as Becker demonstrated that it was the near unique ability of
the salamander's nervous system to drastically change the ionic environment
around blastema cells, along with hormone secretions from nerve dendrites,
which allowed blastema cells to dedifferentiate into embryonic cells and then
to dedifferentiate into the new cell types of the regenerating limb. Becker and
other researchers were able to get rats to regrow most of, or all of an
amputated limb. They implanted a negative current source that produced a
negative electric potential distribution inside the limb directly behind the
amputation site. This closely mimicked what a salamander would have at that
site if it were scaled up to the rat’s size. To understand what is happening
here, you need to know that in a rat just as in a salamander the myelin sheath
cells coating the motor nerve fibers carry an electron current through collagen
fibers, which are N-type semi-conductors. This current is deposited mostly into
the body's electrolytic solution surrounding the cells near where the nerve
fiber ends. The myelin sheath cells coating the sensor nerve fibers carry an
electron current on their collagen fibers away from where the sensor nerve
fiber ends. The motor nerve fibers are essentially all in the body interior and
the sensor nerve fibers are essentially all on the body surface. As an
amputation wound heals over with skin ,surface sensor nerve fibers cover over
what is normally a motor nerve fiber region. In a short period of time the
cells under the new forming skin layer can be converted into dedifferentiated
embryonic cells under the influence or control of the external cell membrane
ionic environment at the wound site as determined by the electric
current/potential of the combined sensor and motor nerve sheaths activity in
the wound area (blastema formation zone). I can not here go into all of the
wonderful detail of Becker's book. However, I hope I have given the reader at
least an understanding of how cancer can possibly come about by a simple change
in the ion environment in the cell nucleus. If you are interested in tissue
regeneration or are a serious biologist, I can not recommend Becker's book
enough. Particularly the last chapter, PostScript: Political Science. This
chapter with great clarity and skill clearly shows why we as a nation need to
dismantle all centralized cesspools of corruption as exemplified by the
National Institutes Of Health. The NIH needs to be replaced by regional
institutes which are government funded, but ran and controlled by
democratically elected administrators elected by the research community.
Before ending this appendix, a
warning and an explanation of why X-ray radiation should never be used to treat
cancer. Rife was able to isolate the BX cancer virus from cancer tumor tissue
samples. He then exposed these viruses to 24 hours of ultra violet light
exposure. This virus obtained in this manner was 100% effective in inducing
cancer in lab animals. His form of the BX cancer virus was exceedingly
virulent. Other researchers who apparently isolated the same BX cancer virus or
a form of it and inoculated test animals by similar methods only had
approximately 25% cancer induction rates. A possible simple answer for the
discrepancy is that the ultraviolet light from the argon discharge caused some
of the adjacent thiamin DNA base codes to dimerize (chemically bond together).
When the DNA reader enzyme which translates the DNA base code into messenger
RNA for protein synthesis comes across a dimerized thimine base code pair, it
stops RNA synthesis. The reader enzyme then breaks into two fragments. One
fragment stays at the dimerization site to mark it and the other fragment
initiates a complex set of enzyme reactions to remove the dimerized pair and
replace them with a new undimerized pair. During this repair process the
messenger RNA generated fragment is released. If this messenger RNA fragment
contains the genetic RNA base code sequence for ribosome attachment, it will be
read by the ribosomes and a protein fragment will be generated and released. In
particular, if the RNA fragment is fed into a cluster of ribosomes (polyribosomes
) which are located on or associated with the intercellular matrix web
intersections, we can expect many copies of the coded protein fragment to be
generated and released. Furthermore, since the RNA fragment does not contain
the normal stop synthesis code and message RNA end sequence base code, the RNA
fragment is not likely to be immediately dismantled after polyribosome reading
and protein synthesis like regular messenger RNA is. This fragment is likely to
be read over again and again. Now, if the generated protein fragment happens to
be an activator or suppressor of a cell membrane ion channel or ion pump you
have the potential beginnings of a cancer-producing situation as discussed
above. This protein fragment(s) might also act as a promoter protein that
enables the DNA reader enzyme to attach to and read a gene sequence. Or this
protein fragment may combine with a blocker protein on a repressor gene at the
front of a DNA gene sequence and remove it, thereby allowing a promoter protein
to combine with a DNA sequence and then facilitating attachment of the DNA
reader enzyme(RNA polymerase). All of this is not the normal "plan"
of the normal cell metabolism. An excellent example of this sort of defective
protein production and its cancerous consequences is the genetic disease
xeroderma pigmentosum. In it the individual has an inherited defect in their
ability to repair the aforementioned DNA base code dimerization damage. They
are hypersensitive to sun light exposure and develop pre-cancerous and cancerous
skin conditions. They usually die of skin cancer before their twentieth
birthday.
Now what does this have to do with
massive cellular tissue damage suffered by cancer patients while under going
standard allopathic medical X-ray treatment for cancer? As stated in Appendix
B, Rife's normal treatment for cancer patients was three minutes of exposure
once every three days to his frequency instrument. This frequency instrument,
when treating cancer, probably produced repeating packets of 11,780,000 or 23,560,000
light pulses per second. These light pulses in turn produced ultra low
intensity ultra sound in the patient's body of a frequency of 11,780,000 or
23,560,000 cycles per second, which is the approximate mechanical structural
resonance frequency of the BX cancer viruses. The BX viruses disintegrated. In
the normal carcinoma cancer cell there are thousands of BX cancer viruses. When
these BX cancer viruses all disintegrate together at the same time, they
release their gnome, digestive enzymes, ribosomes, assorted proteins/enzymes,
etc. into the cell. The cancer cell is overwhelmed, dies, and promptly
disintegrates. When using Rife's cancer treatment method on a cancer patient
that has undergone extensive allopathic medical X-ray damage, there is the high
possibility of an encounter with a new kind of cancer cell which Rife's
treatment method won't work on. Allopathic medical X-ray treatment causes
significant ultraviolet light, ionization, and free radical production both in
tumor tissue and adjacent normal tissue. With this ultraviolet light,
ionization, and free radical production there is the associated dimerization of
adjacent DNA base code molecular pairs. Both cancer cells and adjacent
non-cancer cells suffer significant cell membrane integrity damage from the
X-ray radiation. All of this culminates in the possibility of a heavily
radiation damaged BX cancer virus penetrating the cell membrane of a non
cancerous cell and instigating production of cancer causing protein fragments
as discussed above. But its own gnome so badly damaged that it can not
propagate itself. If this were to occur, then a cancer cell could be created
which was not infested with the BX cancer virus and therefore not treatable by
Rife's frequency instrument or ultra sound of 11,789,000 or 23,560,000 cycles
per second. Of coarse the X-ray radiation alone could generate a cancer cell
that the original Rife's treatment method would not cure.
Well we have skimmed over a lot of
technical data in this appendix, however, I hope the reader now has a
conceptual frame work in which to begin questioning the current allopathic
medicine approach to cancer causes, treatments, and cures. Only by honest
researchers going back and looking at the suppressed results of past honest
cancer researchers can we hope to find honest valid answers about cancer causes
and cures.
"An important scientific
innovation rarely makes its way by gradually winning over and converting its
opponents: it rarely happens that Saul becomes Paul. What does happen is that
its opponents gradually die out and that the growing generation is familiarized
with the idea from the beginning." Max Planck
IF YOU FOUND THIS ARTICLE OF REAL VALUE, PLEASE MAKE A HARD COPY WHILE STILL AVAILABLE.
Taken from: DR. RIFE AND THE
DEATH OF THE CANCER INDUSTRY, a paper by physicist Gary Wade
Contact Gary Wade: RifeTech@FastMail.com
Phone:
P.S. - It is now imprecisely
known that many types of cancer can be easily and quickly killed by exposure to
pressure square waves of a frequency of approximately 2127 cycles per second.
It appears that one or more of the higher frequency hidden Fourier sine wave
components, i.e. 3(2127) ,5(2127), 7(2127), 9(2127), etc. opens up ion gates on
the cancer cells' membrane and radically changes the ionic conditions inside
the cancer cell such that it drops the bi-lipid layer potential difference
below some critical value below which the cancer cell can not recover and it
dies. (See other lectures on this site such as the
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