RIFE RAY CANCER TREATMENT AND MYCOPLASMAS IN CANCER AND AIDS

draft  paper by  Alan Blood

P.O. Box 128 Nathan 4111
Brisbane Australia

email:s1080313@student.gu.edu.au Dec

to end Feb email:  mgates@powerup.com.au
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ABSTRACT

This article reviews the theory that mycoplasma and other bacterial
organisms may be involved in masking of surface antigens and a number of
other immunosuppressive and carcinogenic effects in cancer and in AIDS.
The second section  discusses the theory of  Rife- type electric field
oscillators as a medical  treatment. We discuss the possibility that
modulated induced high frequency oscillating microcurrents on membrane
surfaces may remove or disrupt the masking (eg by hCG) of tumour antigens
and also of white blood cells.  Simultaneously there may be proliferation
and hyperactivity of white blood cells caused by cytokine stimulation
response. The synergy of these two effects may enhance the restoration of
anti- tumour antigen immune recognition and attack in cancer, and possibly
other immunosuppressive pathways could also be disrupted. If the bacterial
forms associated with cancer or pre- cancer pathology can be successfully
attacked in this type of treatment, their immunosuppressive effects could
be eliminated as well, although this has not been demonstrated in vivo. It
is believed that these hypotheses may account for unconfirmed reports of
rapid clinical remissions by Johnson et al  prior to WW2, and later by
Hamer *22, as well as claims for other types of modulated or pulsed
oscillator devices. An appendix section discusses some uncertainties of
interpretation of forms observed in live blood,and suggestions for new
investigations.
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BACKGROUND FACTS ON MYCOPLASMAS

Mycoplasmas have several features which are different from other bacteria.
They have no true cell wall. They have a very small number of genes
(genome), around 10 times smaller than typical bacteria such as e. coli,
and about the same size as the more complex types of virus. There are many
classes and species of mycoplasma. They are believed to have had a common
ancestor with the Gram- positive Orders of bacteria. Evolutionary studies
on rRNA suggest that mycoplasmas may be degenerate forms whose origins may
be the hybridization of L-forms of early gram- positive types of bacteria.
Mycoplasmas show a large degree of genetic diversity and it seems that they
also have a high rate of mutation, possibly because of the loss of
protection of a true cell wall. The most researched species is the one
which causes atypical pneumonia in humans.  Mycoplasmas are also known by
the name Pleuro- pneumonia like organisms (PPLO).  They can divide like
typical bacteria, or alternatively they can assume adult forms where nuclei
continue to divide inside a single growing cell enclosed by a sheath.
Sometimes multiple adult forms develop partly  fused together to give a
variety of shapes. At maturity the “adult” form can burst to release viable
elementary bodies or “seed forms”. These can be extremely small, (viable
free forms around  0.3 micron), and they can pass through fine filters
which do not allow bacterial forms through. For this reason they have been
called filterable bacteria. Because of this characteristic, A.Kendall in
1931 incorrectly proposed a theory of a pleomorphic cancer virus, since
filterability is a characteristic of virus. Despite the differences from
other bacteria, today none of the many types of filterable bacteria are
classed as virus, because they all have true cell phases which virus do not
have. Some mycoplasmas are harmless commensal populations of mouth or
genitals. Others can also be pathogens which can live inside white and red
blood cells, especially in AIDS.  Sometimes in AIDS the flask- shaped
species including newly observed M.Fermentans Incognitus strain can grow
fine threads which can bud from the ends.
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IMMUNOSUPPRESSION

Since 1920, a number of researchers have isolated and cultured filterable
pleomorphic (many- shaped) bacterial forms from a variety of neoplastic
tissue *1. Various forms may often be observed in fresh blood in cancer and
in AIDS in dark- field microscopy *2. A pin- prick test can guage cancer
risk even before tumour formation (*3), by looking for these forms, as well
as spots within red blood cells. Though often dismissed as an opportunistic
infection, it may be that micro-organisms play a causative and contributing
role in cancer *4,7. The link between pleomorphic bacterial forms and
cancer was first indicated by research showing tumour formation in
innoculated animals, as well as their presence in microscopic observations
of cancer tissue (*1,4).

Some of the observations of cell- like or spore- like forms have been
claimed not to be bacteria, but rather membrane fragments, and researchers
interested in the Rife approach ought to be aware that in some observations
this may well be the case. On the other hand, some forms isolated from
cancer, or observed in cancer or AIDS blood are undoubtedly bacterial.
Kendall and Rife announced a pleomorphic cancer virus, a theory still
supported by Rife “true believers”.  This article points out that their
early observations of the filterable bacterial forms were not in fact
virus, but rather of mycoplasmas or of cell- wall deficient bacteria.

Over the years a variety of names and phylogeny have been suggested for the
cancer isolates. Recent film demonstrations by various independent
researchers were shown at the World Cancer Congress, including high
resolution Somatoscope footage by G. Naessens. The phases of the organisms
suggest that at least some of them may be mycoplasmas, but the distinction
between these and the cell- wall deficient forms (cwdf) of other bacterial
species is still not entirely clear. Other interpretations, ie of host
membrane fragments (Url), and of Endobiont forms (Enderlein) need to be
acknowledged. (See appendix discussion).  Note also the probability of
sexual and blood transfusion transmission of the more pathogenic species eg
M. Fermentans, M. Penetrans, and M. Pirum and their putative role in AIDS
and/ or cancer.
  
Kleineberger- Nobel noted that mycoplasma (PPLO) could proliferate in a
stressed host *6.  Observations suggest that a lowering of immune
competence as a  result of  an episode of grief can lead to cancer in an 18
month timeframe *3. We can reasonably postulate that mycoplasma or other
bacterial proliferation subsequent to immune depression may induce cancer.
Evidence of carcinogenic effects and a variety of immunosuppressive effects
from mycoplasmas have been presented in the literature, and hCG secretion
by other species isolated from cancer have been reported by Acevedo et al

Naessens has postulated that in a healthy host the so- called  “Somatid”
organisms are found as a commensal population of underdeveloped coccoid and
sometimes rod forms whose growth factor secretions are controlled by
humoral response. He claims that where immune function becomes sub-
optimal, an increase in the concentration of the secretions may stimulate
development of the advanced multinuclear adult  forms, and may also
stimulate host cell growth *7. Naessens claims that his observations lead
him to the conclusion that once a tumour acheives a "critical mass", nearby
white blood cells appear to become paralyzed, and thus the immune system
cannot recognize or challenge the abnormal cells. He attributes this effect
to the secretion of  "Co-carcinogenic K-factor" by the tumour mass. This
interpretation is echoed in findings that NK activity is suppressed via
hexosamine formation via deacetylase from N-acetyl aminosugars in tumour
cells.

It has been reported that human growth factors can stimulate kinase release
within human cells leading to oncogenic expression. Some mammal and
prokaryote growth factors are quite similar, and it has been suspected that
“mimic” bacterial growth factors may induce cancer subsequent to local
chronic infection.  Indeed mycoplasma secretions have induced nuclear
transformations in animal fibroblast cell lines in vitro  (*4,20), although
the mechanism is unknown. In one such study viral infection and DNA
transfection had been ruled out *9, The question of whether mycoplasma
growth factors can be oncogenic must be considered, however there is no
conclusive evidence to verify this theory.

Transformed (cancer) cells should normally be attacked by white blood cell
mediated immune response, but we assume that they may proliferate where
antigenicity is masked. A healthy immune system can recognise and attack
transformed cells, but on the other hand most  human tumours tend to
attract only weak immune response. This paradox has been one of the central
unsolved mysteries of cancer research. Recently research has islated a
cancer cell protein antigen which has been named malignin. Also an antibody
level test was developed *16. Other reviews confirm some antigen expression
of  antigens on cancer cells coded by genes which are normally dormant. It
was noted however that the malignin antigen could often be covered over by
polysaccharide substances, thus reducing the antibody contact or white cell
recognition site contact with the malignin antigen. This observation raises
the questions a) to what extent are mycoplasma polysaccharide secretions,
eg galactan, involved in the masking phenomena, especially prior to tumour
formation; and b) to what extent are hCG secreting bacteria or their cell-
wall deficient forms responsible for antigen masking and local immune
suppression.

Cancer cells secrete their own growth factor but require a certain critical
level of factor concentration in the interstitial fluid to trigger
division. It has been demonstrated that cultured cancer cells need a
critical mass of neighbours (in culture tests) before they can build up
sufficient concentration to trigger cell division*9. Therefore it is not
unreasonable to postulate that in some circumstances a single transformed
cell may not proliferate alone without a boost from bacterial secretions
which mimic host growth factors.

In 1972 V Livingstone- Wheeler discussed the discovery of
“Choriogonadotropin”- like secretions from cultured human cancer
pleomorphic bacterial isolates.  Human Chorionic Gonadotropin (hCG) is
secreted by the trophoblast and chorion in pregnancy. It is also secreted
by human cancer cells. Cancer research has pondered two important questions
in regard to this and other similarities between zygote cells and cancer
cells. One question is in relation to the mechanism of  how the zygote
brings about maternal immune tolerance; herein may lie the secret of  the
apparent non- immunogenicity of cancer tissues. The other question relates
to how the chorion induces blood vessel growth, and whether this can help
us understand angiogenesis.

CG- like secretions from bacteria may play some role in immune suppression.
H F Acevedo reported a direct correllation between hCG titer in normal
pregnancy, chorionic carcinoma and hydatit mole versus Immunoglobin levels
and a number of other immune cell standards. He has also demonstrated a
correlation of human cancer cell lines to metastasize in nude mice models
to the degree of hCG expression of the cell line.  Later we discuss
Acevedo’s isolation of CG secreting ”abnormal” bacteria from cancer.

At the point of tumorogenesis, before there is any significant tumour cell
secretion, we may postulate that bacterial secretions are involved in the
prevention of  immune response against newly transformed cancer cells *7.
According to a review by Macomber, Chorionic Gonadotropin- like substances
(*19) contain sialic acid residues which may increase membrane negative
charge by adhesion to cell surfaces of cancer, trophoblast, sperm and T-
cells. This results in reduced immunogenicity of the above cells and of the
mycoplasmas. CG adhesion to white blood cells may interfere with receptor
binding in immune recognition. A role of electrostatic repulsion has been
postulated as inhibiting white blood cell response against transformed
cells*4. Other immunosuppressive pathways are briefly discussed.

At this point I would remind the reader that  the dominant research finding
is that cancer cells secrete hCG. Therefore much of the relevant reseach on
hCG in cancer will have been investigating this connection.  However the
possibility of a similar model of immunosuppression arising from CG
secretion of  bacterial origin has generally not been considered.

Bogoch recently completed research which developed a useful malignin
antibody test. Malignin is a tumour antigen which seems to be universal to
most cancer types. The protein antigen is part of the cell membrane.
Bogoch notes that this protein antigen is often covered over by
polysaccharide substances, implying antigen masking. High titers of
antibody correlated well with survival. Conversely, low titers correlated
with progressive disease and mortality. In some cases the marker was
subsequently shown to be present before clinical observation of cancer. It
is not clear whether general immunosuppression causes a failure to mount an
immune response against tumour antigens, or whether antigen masking is to
blame. It seems likely that both play some role in the pathology of cancer,
and that they are interrelated.

Instead of a covering cell wall, mycoplasmas can protect themselves by
making a slime covering. They can secrete considerable quantities of
polysaccharide substances. Some reviews have noted what appears to be the
ability of mycoplasmas to alter their secretion products. Also some lipid-
associated membrane proteins can change the expression and size of  the
antigen molecule with high frequency. A variable expression genetic system
has been elucidated for this type of control of membrane antigens. It is
possible that  because these antigen molecular patterns are not constant,
they can to some degree elude immune response. Other workers have reported
that some mycoplasma galactan polysaccharide secretions bind antibodies,
and inhibit phagocytosis.  Other research notes the detection of unusual
products in mycoplasma infected helper T-cells. It is probable that if the
helper cells fail to secrete IL-2, (a required “second message”) that there
can be no T- cell activation against tumour antigens. Some mycoplasma
species can cause membrane damage via cytadsorbtion by localised peroxide
and N-O secretion. Some “flask- shaped” species can live inside white blood
cells to escape immune attack *9. Naessens has also filmed the migration of
small rod forms between red cells. Note that epithelial basal membrane
degradation has been suggested as a likely first step in angiogenesis,
followed by growth factor- like chemotactic signals from the tumour
inducing blood vessel capilliary growth. A question arises regarding a
possible contributing role of local damage and / or growth promotion by
mycoplasmas in angiogenesis. The outgrowth of threads from the flask-
shaped species may also be pertinant to this question.

Once established, many types of cancer cells create their own
immunosuppressive effects, eg secretion of substances similar to p15-E
retroviral proteins, which have anti-immune effects probably including
blocking macrophage chemotaxis pathways *4, 24. In addition, tumour
secretion of histamines has been shown to be immunosuppressive, and more
importantly, angiogenic. (This is now treated with Cimetidine in bowel
cancer at Sydney's St George hospital) *17. Tumour lactic acid metabolism
also creates gross effects and liver load. The immunosuppresive effects of
tumour secretion make it difficult to acheive a healing response, and are
the target of various approaches in immunotherapy.  But even before tumour
formation, we can postulate that mycoplasma proliferation may have
triggered and supported the initiation of cancer.  Therefore methods to
improve immune strength, eg  nutrition, should be considered as a
preventative approach *3.

Livingstone- Wheeler used autologous vaccines against the patient’s own
pleomorphic bacterial isolates along with BCG (an anti- TB serum) as cancer
therapy *11. In 1982 success in cancer control was reported in animal
vaccination with CG-beta subunit with tetanus toxoid and adjuvants *9.  It
may also be possible to develop vaccines with isolates from sarcoid tissue
and in Kaposi’s sarcoma in AIDS *27. Cantwell has reported acid - fast
bacteria in KS.  Recent studies have been in conflict as to whether
mycoplasmas can be isolated from KS tissue. Various other means could be
considered to therapeutically attack mycoplasmas, eg specific antibiotics
or drugs. Naessens developed a method to inhibit some cancer cell
secretions by lymphatic injections of  714X camphoramine *7.  Mycoplasmas
are inhibited by anionic detergents *18, and therefore saponific plants may
be useful. Perhaps this is why yucca, a cactus, has become a traditional
remedy. Natural substances which stimulate NK activity have been reported,
as well as substances which stimulate T- cell activity against tumour cells
probably by IL-2 stimulation.

THE USE OF ELECTRIC FIELD OSCILLATORS IN MEDICINE

In the 1920's Royal R.Rife of San Diego (*21, 22) developed an audio-
pulsed radio frequency electric field oscillator which produced an audio
intermittent or square wave modulated r.f. oscillating electric field set
up in an electrode gap within a large spherical gas plasma tube output
fired by an overmodulated a.m. signal *12. In the area near the tube, the
so- called “Rife Ray” was claimed to be able to kill or affect motility of
various pathogens at modulations of audio frequencies specific to each
species. It could be that this claim may in fact only apply to wall- less
or abnormal- walled organisms.  Rife made visual and film observation
through a special high magnification micropolariscope of his own design.
In some cases Rife claimed to have observed membrane rupture of bacteria.
In 1995 Bare produced film showing  the process of rupture of some
Paramecia in a sample using a variant design of the Rife device over 45
seconds *13. However this film should not be interpreted as fully verifying
Rife’s claims, since it was necessary to visually track forms of abnormal
morpholgy to capture the rupture event, and other cells in the sample did
not rupture. Modified Phanotron gas tubes are now available which have been
driven by conventional 100W transmitter/ linear amp/ tuner * 13. The most
powerful c 1935 Rife design was reported to be driven by a 500 W
transmitter with a 8000 V signal. Whether this Voltage was an r.f.  peak
value or power supply value is not clear.

A suitable variation to this type of device for experimental cell research
would be the adaptation of an electrophoresis unit  by driving it with
audio- pulsed r.f., and using a non conductive sucrose medium.
Alternatively an air gap between 2 electrodes could be employed. Bare’s
design employs a straight gas tube which is externally wrapped by cable
from a transmitter. Each cable end is tied off into circle or loop ends,
and a gap remains between each of these loops, creating a dipole.

We could assume that an electron or negatively charged particle in the body
of the patient experiences an attraction to the anode. The amplitude of the
force of attraction varies at r. F. Hydrogen ions and other positive ions
will experience forces in the opposite direction. Therefore we assume that
in the area near the tube, all charges will experience some induction due
to local electric field perturbation at r.f. We also assume that most
induced current flow will occur on membrane outer surfaces, just like r.f.
current concentrated on the outside surface of a cable. Because the audio
modulated intensity falls away to a low or zero amplitude for about half
the audio cycle, membranes experience a switching from surface current or
excited state to relaxed state at audio freqeuncy. This may equate to an
audio oscillation of charges from interior to exterior of the local
membrane. Various speculations as to the mode of biological effect follow,
but note that testing of various claims has not been undertaken.

Recent research has suggested that at least some ion pumps utilizing ATP
run at fixed frequencies from 1kHz to 1 Mhz *19. The claimed Rife mortal
oscillatory rate effect on bacteria (m.o.r. effect) may conceivably be
caused by ion pump failure by electrical resonance when subject to
synchronized oscillator output.  On the other hand such a phenomenon could
in theory adversely affect animal cells, but the treatment was claimed to
be safe for humans. However claims have been made by Crane of parasite
killing (ie worms at 20 Hz modulation). Post- treatment effects of weakness
or illness have been reported, but have been attributed to toxin release,
or may be a symptom of fever- like immune hyperactivity.

An alternative explanation may be that postulated by Pappas, ie that the
plasma membrane exhibits different electrical resistance depending on the
direction of current flow, and that the efficaciousness of pulsed h.f.
magnetic or electric field oscillators lies in generating ion dispersion in
tumour cells such that there is an increment of one- way charge movement at
each modulation pulse.  Thus cells revert to normal type membrane
potentials, and thus lose the mitotic condition at low potential, as well
as becoming immunogenic *28. Pappas also claims that weak- walled and wall-
less bacterial samples have been killed by his coil magnet device. This
latter recent observation seems to be in agreement with Rife’s claims of
success in killing pleomorphic forms. (These were of major interest to
A.Kendall and E. Rosenow). It may be that other claims by Rife that a whole
library of bacteria and virus could succumb to his treatment at individual
mortal oscillatory rates may simply not be true.  On the other hand models
of immune stimulation may be plausible.

Rife claims effective modulation values at 1927 Hz for carcinoma and 2008
Hz for sarcoma. I was interested to read Giannni Dotto (who developed the
patented Dotto Ring in 1975 in USA) mention 2000 Hz frequency as a sort of
cell self- tuning frequency, but no explaination was expounded. Recently I
studied nerve impulse action potentials in unmyelinated nerve cell axons.
Na channels open quickly, followed more slowly by K channels which counter
the Na flow- induced potential change. (These types of channels are
Voltage- gated). It just so happens that peak depolarization occurs 0.5 ms
after the initiation of the action potential. Therefore a 2000 Hz modulated
excitation would trigger Na flow like a diode current, but K flow would not
get a chance to “kick in”.

In addition to the concept of an antibiotic effect, it has been noted that
various electrical oscillatory applications can cause the stimulation (*13)
of white blood cells, probably by causing cytokine secretion, similar to
what the blood does near the site of a wound. This effect may be of
particular importance to encouraging immune recovery by recognition and
response to cancer cells. It has been claimed that after electrotherapy
white blood cells are observed to undergo rapid multiplication and to
become hyperactive for about 18 hours until dying off.

It may be that binding sites or electrostatic bonds of CG- like secretions
and possibly other polysaccharide substances may be broken by induced or
transduced electric oscillating currents. If this is the case, then the
combined effect of white cell hyperactivity and their access to newly
exposed tumour antigens may engender an immune recovery.

In trying to develop a theory to explain the claimed anti-cancer effects of
oscillators of quite different designs and outputs developed independently
by various different innovators, it has seemed to me most likely that in
all cases an immune recovery is engendered somehow by means of induced
microcurrents. The role of hCG secreted by tumour cells, and the possible
role of other bacterial secretions, must be prime suspects in
immunosuppressive mechanisms. The dispersion of these slimy coatings by
modulated h.f. local membrane microcurrents would firstly expose tumour
antigens, and secondly the coatings on T- cells would also be dispersed.
Activation of the helper T-cells would be necessary to provide IL-2 “second
message”. This may occur naturally, or alternatively IL-2 therapy may prove
a useful adjunct. Also IL-2+ genetically engineered anti-tumour activated
autologous CD8+ T-cell therapy as outlined by D M Pardoll may be useful.
Wheeler’s vaccine method may be of use, but her clinic was closed down by
an ever- vigilant FDA. Modern research is also investigating vaccine
therapy against cancer.

In searching for a means to kill Kendall’s pleomorphs, Rife learned to
force the aggregation of viable filtrates isolated from cancer tissue by an
r.f.  stressing technique, using a corkscrew or helical plasma tube as a
test tube holder, and driven with unmodulated r.f. Thus a sample of
filtrate in a test tube could be positioned so that one electrode was above
and the other below the sample. The aggregation or clumping occurs because
cells stick together under r.f. fields eg in r.f. electrophoresis.  In the
case of filtrates of wall- less organisms it is likely that the elementary
bodies will completely fuse. The motile aggregates could then be imaged,
and a mortal audio resonant frequency was determined by tests with the Rife
Ray. Tumour formation after innoculation was claimed to have been prevented
by Rife Ray treatment. In hindsight the latter conclusion may be open to
criticism. It is true that innoculation of cancer bacterial isolates will
induce tumours, and that effective antibacterial treatment post-
innoculation may prevent the tumour growth. However the link between the
cancer microbes and human cancer is not universal as Rife and Kendall were
tempted to believe. Kendall’s culture technique required a pork gut medium,
and we could suspect that his culture organisms were contaminants.  However
their capacity to induce tumours by innoculation is still significant.
Modern research has verified that pure cultures of mycoplasma isolates do
indeed cause tumours by innoculation.

AIDS DISCUSSION

A significant number of AIDS patients are infected with mycoplasmas, and it
was thought that these were opportunistic infections after HIV
immunosuppression. A new strain named M. Fermentans Incognitus has been
discovered in some 17 % of cases. CD-4 binding sites on the membrane of M.
Incognitans have been discovered, which means that the virus can be
transported by Incognitans, and it has been argued that the AIDS syndrome
may in at least some cases be a co-infection based on the sexual
transmission of mycoplasmas. A revealing series of experiments with monkeys
shows that innoculation with HIV-1 alone will not kill monkeys, probably
because this virus is human specific. However when injected with M.
Incognitus alone, monkeys showed wasting syndrome, and death within 7 to 9
months. One in vitro experiment showed that a cell line infected with both
M. Arginini and HIV-1 showed HIV-1 expression at a rate 40 times greater
than a control with HIV-1 only. If this is the case in vivo in AIDS, the
mycoplasma co-factor link should not be ignored.We may postulate mycoplasma
pathogenicity and various immunosuppressive effects as contributing to the
disease process. Therefore the therapeutic treatment of  mycoplasmas in
AIDS eg by specific antibiotics may be useful.

Interestingly, Beck claims that transduction electrotherapy prevents the
capacity of the HIV virus to attach to the CD-4 surface receptors of helper
T-cells * 14. An interesting article appeared in an Australian newspaper
describing how a farmer suffering the long term effects of Ross River virus
was pushed into an electric fence by a playful calf only to discover that
his symptoms were relieved. A neighbour with the same affliction thought
he’d try his luck, and was also rewarded with respite of symptoms!
Unfortunately it is unlikely that any  “anecdotal “ claims of this kind
will attract any follow- up research.

The mycoplasma- cancer link may be disputed on the grounds that less than
half of cancer or AIDS cases have yielded mycoplasma isolates.  However we
contend that the question of a link in some cancer pathways is is still
open. Even if the Mycoplasma infections in AIDS are indeed late-comers to
the disease, their contribution to the disease may be significant.

CLINICAL NOTES

In his cancer treatment Rife set a protocol of 3 minute exposures with 3
day rests in order to allow toxin elimination. There may be some danger of
kidney failure or lesion haemmorrage in cases of breakdown of tumour
masses, *23 . In many cases surgury or the other tumour destructive
therapies may be indicated prior to Rife treatment. For bleeding it may be
appropriate to administer Tributyrate *26. Like other forms of
electrotherapy, there is a danger of induced heart attacks as well as
epilepsy. Electrotherapy may therefore be generally be considered
contra-indicated for patients with a history of these conditions. Rife
claimed that he detected no harmful effect from his oscillator to humans.
However there may be unknown hazards, and there have been reports of
frequencies which affect intestinal flora. Possible effects on early
pregnancy should also be considered. Where live blood observation indicates
pre-cancer pathology, Rife treatment may similarly unmask the bacterial
forms and T- cells, thus engendering anti-mycoplasma immune response. A
reduction of mycoplasma population, particularly of the advanced phases,
could eliminate the source of immunosuppression, which would be considered
a major cancer risk factor.

Because the emphasis is on immune response, various natural therapies,
exercise, vegetable juices, anti-oxidant vitamin and mineral supplements,
herbs, nutritional protocol, substitution of refined salt for sea salt,
etc, medical immunotherapies and even psychotherapy are considered
necessary adjuncts to the Rife therapy. Conventional immunosuppressive
therapies (ie X ray and chemotherapy) may counteract the desired immune
response in the short to medium term, but could be considered
nonconcurrently. Surgery, on the other hand, may be indicated as an early
treatment, and would be expected to assist the process of immune recovery.
Critics may suggest that these comments constitute a danger to the public
should they be tempted to avoid seeking qualified treatment. Such debate is
dealt with by other commentators. However there is no excuse for the
ongoing failure of the “establishment” to grant funding to undertake
impartial investigation, eg for the Wheeler vaccine, nor for the many “snow
jobs” that have recently been exposed, eg on Sheridan’s Entelev.

A number of products using skin- contact electrodes (transduction devices)
go by the name of Rife devices, but in fact use only audio currents. These
have been reported to be of use in pain relief in arthritis at 5000 Hz, and
would be expected to stimulate white blood cells, but have not been
demonstrated to be of use against cancer. “Hulda Clark Zappers” use high
frequency unmodulated currents, supposedly against a pathogenic fluke
parasite. Although her theory is most likely flawed by misinterpretation of
radionic signatures, it may nevertheless come to be shown as a useful
therapy. I have thought she may be reading “slime” rather than liver flukes
(or reading AIDS, which has often mistakenly been the case).  Various other
designs have been produced including magnetic field oscillators, some of
which are legal to use and have demonstrated physiological effects. Because
of the prevalent prejudice in the scientific establishment, there appears
to be no peer reviewed literature to prove or disprove the various claims,
and no doubt no adequate funding for such research. Inevitably this boils
down to “assignment of priorities”, and the prejudice becomes invisible. If
anyone has relevent literature or data, please let me know!

The public are often warned to avoid unproven therapies, and perhaps
rightly so. However in view of the acknowledged poor results of orhtodox
treatments, it must be in the public interest to properly investigate new
alternatives. Other authors have pointed out that this logic conflicts with
corporate and professional interests. While this unfortunately may have
tended to be the case at certain times in many countries, it is to be hoped
that compassion and common sense will prevail in the future.

APPENDIX TO DISCUSSION ON BACTERIAL FORMS IN CANCER

A good deal of controversy and misinterpretation has dogged this study,
from as far back as Bechamp over 100 years ago, and is still unresolved.
Research collated in V. Livingstone- Wheeler’s “Microbiology of cancer”
contains various speculations as to the classification of these organisms,
including mycobacteria, mycoplasma, Actinomycetales, as well as the then
mysterious L-forms or cell- wall deficient forms (cwdf).  Wheeler’s “folly”
was to declare a new species called Progenitor Cryptocides, What appeared
to be a definitive elucidation was later presented by Acevedo et al, who
reported the isolation and identification of a number of non-mycoplasma
bacterial species from cancer *29. The American Cancer Society publication
CA in its criticism of Wheeler made an unreferenced comment to the effect
that Wheeler’s organism was not a new species, but a collection of common
and rare known types.

A closer reading of the abstact of Acevedo’s paper is warranted. The paper
reports the expression of hCG- like material, or fragments thereof, from 7
bacterial species isolated from cancer, and cwd forms of 2 bacterial
species from non- cancer patients. (I might add at this point that
mycoplasmas, had they been present, would not have been isolated by
standard culturing techniques.) From Acevedo: “ Electron microscopy of
these 9 strains” (including comparison of CG negative controls of these
strains (sic)) “revealed morphological alterations in the bacterial cell
walls and cytoplasmic material and/ or bizzarre forms of reproduction in 6
of the 9 strains expressing hCG- like material including the 2 cwd
variants.”

Majnarich and Wheeler reported the transmission of CG+ characteristic
between bacterial species which suggested the transmission of a CG+
plasmid. While this suggestion may be verified in future work, we may
speculate on a role of mycoplasmas as a possible CG+ plasmid vector.
Acevedo’s description of morphological and reproductive alterations in his
CG+ isolates begs the question of the mechanism of this manifestation. Is
this an effect of CG on the cell? The latter question could be reasonably
simply tested by adding CG+ extracts to CG-neg strains in vitro. For the
purposes of the current discussion we shall assume that this is not the
case.  I have found no literature to suggest CG production in mycoplasma
studies. However I would like to point out that mycoplasmas have been shown
to cause  nuclear transformations of hamster fibroblast cells. Also
persistant mycoplasma infection showed multi- stage malignant
transformation in animal embryo cells which was reversible up to a certain
point upon disinfection. Hemolytic activity has been described, including a
role of  H2O2 and NO. Intracellular mycoplasmas have been shown to take up
a position near the nucleus. Plasmid transfection studies in mycoplasmas
has shown “co-integrate structures”. Perhaps mycoplasma supernatants and
sonicates could be adde to Acevedo’s CG neg strains to determine any
effects. Other studies could probe for CG plasmids or gene amplification in
the CG+ strains, as well as in mycoplasma isolates from cancer. Here we
note a reported capacity of mycoplasmas to “take” entire sequences in
plasmid transfection in”co-integrate structures” (with the genome),
implying their capacity as vectors for a whole range of genetic material of
host origin, and possibly indirectly as infective vectors for cancer.

It is also relevent to point out that critics have stressed that any
isolates from cancer may merely be opportunistic infections, and this may
also be the case for Acevedo’s isolates. This argument is countered by the
induction of tumours by innoculation, and claims by some oncologists that
the blood forms are to be found before any sign of tumour. Of the 7 strains
isolated from cancer by Acevedo, none were reported to be cwdf.  How can we
reconcile this finding with the extensive list of reports of extremely
pleomorphic forms by other workers? This conundrum has been neatly side-
stepped by critics who imply that all such observations are the result of
“contaminations”. This thinking may have some justification due to the
infamous ability of mycoplasmas to contaminate bacterial and cell cultures.
Also the early special serum supplemented media developed by Wheeler’s
associates cannot be considered as contaminant free. However the live blood
observations and innoculation experiments are overlooked by the critics,
and therfore the whole issue should again be thrown open to debate and
research. The divide between proponents of the bacterial link to cancer
versus a powerful orthodoxy in denial are extreme.  The ACS critic claimed
that he had never encountered the presence of bacteria as described by
Wheeler in cancer tissue, and that they simply “do not exist”.

Mycoplasma research has isolated various strains from some cancer tissue,
and from blood in AIDS, but not in a majority of cases. I would very much
like to see Naessens’ organism genotyped. To ensure that any putative
mycoplasmas are not discounted yet again as suspected contaminants, it may
be appropriate to employ a micromanipulator to individually select the
pleomorphs in blood. Also I would like to see Acevedo’s work repeated with
an emphasis on the culturing requirements of mycoplasmas.

SOMATID CYCLE

Under high resolution light microscopy, Naessens has defined a 16 stage
life- cycle for the Somatid, much of which appears similar to mycoplasma
phases.  However there are controversial differences to Kleineberger-
Nobel’s PPLO cycle. Dancing dots are shown in Naessens’ films which he
assigns as Phase 1.  These were said to contain no DNA and were stable when
heated, whereas chylomicrons (lipid micelles) were not. If these particles
are membrane fragments, their composition would be a mix including proteins
which may be stable under the heat test. In orthodoxy, the smallest viable
elementary bodies are around 0.2 micron, around the size of Naessens’ Phase
2. The phase 1 would seem unlikely to be a bacterial precursor.

The Somatid cycle as observed in in vitro culture were reported to go from
the “spore” (phase 2, normally kept underdeveloped in vivo by antibody
attack against its growth factors) through to rod form (pathological in
vivo) which grows out to a mycobacteria- like form with which goes on to
develop a bubbled cytoplasm and later bursts. The released substance was
said to form “levurid” or yeast like forms which grow out to 4 to 7 micron
spherical forms. (In vivo films showed forms like this attached to red
cells or free in the plasma in cancer pathology). These grew out in culture
to larger long bulbous forms which peristaltically ejected the cytoplasmic
content at maturity, and left the sheath or thallus behind.  These thalli
could be observed in blood in advanced cancer. Kleineberger- Nobel’s work
focussed on M. Pneumoniae. She describes only one bursting stage at
maturity, and therein lies an apparent discrepancy.  It is possible that
Naessens has isolated more than one species, or grown contaminants. The
larger adult phase resembles the flask-shaped species of mycoplasmas, and
it may have grown out more slowly. Alternatively, changes in culture
conditions over time may have given rise to altered morphology of later
maturing forms. The observed thalli in pathology may arise from either
bursting form. Naessens commented on different in vitro morpholgy; a snake-
like long thin form was filmed in vitro. It may be that Naessens cycle is
indeed basically accurate. Since mycoplasma research has been far from
comprehensive, this is not entirely unlikely.

Demonstrations of hypotonically stressed or heat stressed healthy red blood
cells showed the outgrowth of chains, which could coalesce into more
spherical forms, and both forms could break away. Similar outgrowths were
also demonstrated by W J Clifford by the addition of minute dilutions of
toxic metals to blood in isotonic solution. It was claimed that similar
phenomena could be observed in cancer, and Naessens assigned the chain
shapes as bacterial phase Somatids. W Url argues that these outgrowths
consist of the cell membrane, but not any bacterial form. Naessens’ film
also clearly shows spots in red cells and these were assigned as cancer or
pre- cancer indicators.  These have also been noted as “sclerotic
inclusions” in the work of Enderlein.

ENDERLEIN’S ENDOBIONTS

The Enderlein school describes various forms observed by dark- field
microscopy in cancer blood, but I have not studied this material in detail.
Endobiont lifeforms are purportedly symbioses of Aspergilla and Mucor,
which can “copulate” from assigned lower forms to a series of higher forms
(Beilin). A system of medical therapy including Homoeopathics have been
developed to treat cancer via the treatment of the Endobionts.  Enderlein
developed innoculations of lower forms to induce devolution of native
forms. In common with Naessens, Enderlein also ascribes a very small
precursor; the protit. The tiny dancing forms would seem to have lively
motion, which Naesens attributes to electrostatic repulsion.  Perhaps this
characteristic caused Enderlein in the 1950’s to believe them to be cell
precursors. However the weight of modern orthodox opinion would go against
such an interpretation. Some blood pictures show these dancing dots, and
others, even in advanced cancer, do not. In some cases such forms are seen
only after treatment with 714X. I have heard naturopaths ascribe these
forms to a result of leaky gut syndrome.

Although the pioneering work of many early researchers may have led them to
advance theories which we may veiw as uninformed or even arcane, we must
acknowledge the detail of their observation and consider the general thrust
of their findings. The history of science shows many “rediscoveries” of the
research of scientists which had fallen into obscurity. The approaches of
Livingstone- Wheeler, Rife, and many others may well set the stage for a
new wave of therapeutic approaches. As ever, a self- annointed hierarchical
preisthood stands in the way of progress. I would like to end this paper
with a salient quote from Fleming.  “Pennicillin sat on the shelf for ten
years while I was called a quack”.

REFERENCES

*1  T.J. Glover,  M. J Scott, 1925; Wuerthle- Caspe et al 1953 etc;
    See Refs in *4 von Bremer  1938, Enderlein 1954 etc; See Refs in *7

*2  Enby, Url;  World Cancer Congress 1994. Naessens; WCC 1995

*3  Kostler, Url; WCC 1995

*4  P. B. Macomber, 'Cancer and cell wall deficient bacteria', Medical
    Hypothesis, U.K. 1990 32, 1-9

*6  E. Kleineberger- Nobel ,  'PPLO'

*7  G. Naessens, COSE, Film,'Somatidian Orthobiology' ref
    http://www.cose.com/enhome.htm

*8  Torture et al, 'Introduction to Microbiology'

*9  'Recent Advances in Mycoplasmology', 1988 QR 201.M97 I57 1988
    pp 145   pp 202-212

*11 V. Livingstone-Wheeler,'Conquest of Cancer' also,
    'Microbiology of Cancer'.... a compendium of papers.

*12 A. Blood  'The Rife Ray Cancer Treatment',
    http://www.navi.net/~rsc/ablood1.htm [note: deleted at author's
    request.rsc] also correspondence on Rife microscope:
    http://www.navi.net/~rsc/tech.htm

*13 J. Bare: http://www.rt66.com/~rifetech.htm
    http://www.rt66.com/~rifetech/kaboom.avi rifetech@Rt66.com

*14 Beck, ref links http://www.navi.net/~rsc/[?]

*15 W. Barnes,  WCC 1995

*16 Bogoch, San Francisco Medical Research Foundation. "An accurate
    test for cancer"
    http://www.newagenet.com/LightParty/ProjectHealth/DETECT.html

*17 ABC TV Australia, "Quantum" program Nov 1996

*18 Biology of Mycoplasma, Smith  p. 195  QR352.S65 1971

*19 Acevedo et al. "Immunodetection of CG-like antigens in bacteria
    isolated from cancer patients"

*20 Diller I.C. Diller W.F.  "Intracellular acid fast organisms
    isolated from malignant tissue" Trans Am Microscop Soc 84:138
    1965 also in *11b.

*21 Barry Lynes "The Cancer cure that worked"

*22 Mark Simpson "The Rife Way III"

*23 Wilhelm Reich "The Cancer Biopathy"

*24 Cianciolo G.J. "Antiinflammatory proteins asssociated with human
    and murine neoplasms." Biochem Biophys Acta 865:69, 1986.

*25 Rios A, Simmons R.L. "Immunosuppressive regression of various
    syngeneic mouse tumours in response to neuraminidase-treated tumor
    cells."  JNCI 51:637, 1973.

*26 Tributyrate by Swedish Pharmaceuticals, US.  H.Cederberg, WCC 1994.

*27 Cantwell A, “The Cancer Microbe”.

*28 Pappas P.T and Wallach C, “Effects of pulsed magnetic field
    oscillations in cancer therapy”.

*29 Acevedo H F et al,   J. Gen. Microbiol. 133: 783-791 (1978).