oxygen, and pantotropha
Majid Ali, M.D.
During my 29 years of work as a hospital
pathologist, I conservatively estimate I assumed the
responsibility for diagnosing over 75,000 malignant
neoplasms and followed the clinical course of many
of those cases. That experience was rewarding. It
gave me a clear sense of the biology of diverse
cancers, as well as the clinical outcomes achievable
with the mainstream therapies. During the last two
decades, my colleagues at the Institute and I
participated in the clinical management of over
2,000 cases of cancer. That experience has been
disconcerting, largely because it was not possible
to clearly delineate the long-term efficacy of our
integrative therapies. Most of those patients
concurrently received immunosuppressive
therapies--chemotherapy, radiotherapy and
others--that countered the integrative oxystatic
therapies which we prescribed. Another common
problem has been the financial burden of integrative
therapies on patients, since insurance carriers
nearly always refuse to cover such therapies,
seriously compromising the continuity of care.
Fortunately, there has also been a subgroup of about
60 self-selected, well-informed, highly-motivated,
and strong-willed individuals who assumed the
primary responsibility of the control of their own
cancers. They have been under our care for two to
twelve years. Though limited, my experience with
this small subgroup has been richly rewarding. I
write this article to share my views of the biology
of cancer and responses to integrative therapies
based on insights they gave me, as well as on
personal pathologic, clinical, and research
findings. In my effort, I have looked at the
problems of cancer through the prism of oxygen
homeostasis because, as I explain below, oxygen
drives all host defense responses to malignant
neoplasms. From that perspective, I succinctly state
my conclusion as follows:
The long-term outcome in unresectable cancer is
primarily determined by how well oxygen homeostasis
can be achieved and maintained. The benefits of soy
and other phytofactors, with or without therapies
that modify specific molecular and genetic pathways,
are often substantial in the sense that such
therapies can alter the behavior of cancer cells for
variable periods of time until oxystatic therapies
begin to take hold.
Oxidative Injury and Cancer
In 1995, I put forth my view that accelerated
oxidative injury is the common denominator in all
known factors implicated in carcinogenesis.
Furthermore, unrelenting oxidative stress from any
and all causes is the single most important
mechanism for sustaining and perpetuating the
malignant cellular replication. (1) In 2001, looking
through the prism of oxygen homeostasis, I extended
that hypothesis and offered the following definition
Cancer is destructive behavior of cells incited and
perpetuated by many factors that cumulatively lead
to anomalous oxygen signaling. It has six other
principal characteristics: (1)
respiratory-to-fermentative (RTF) shift in ATP
production; (2) production of prodigious quantities
of organic acids--lactic acid and others; (3)
creation of a cocoon of coagulated proteins around
malignant cells to exclude functioning host immune
cells and their soluble defense molecules; (4)
uncontrolled cellular replication that disrupts
local tissue architecture; (5) colonization of
distant tissues in which the destructive behavior of
neoplastic cells continues; and (6) under certain
conditions, a cancer cell can be coaxed to alter its
Coaxed to alter its behavior! From a clinical
standpoint, this last attribute of cancer, in my
view, should be accepted as the singular aspect of
cancer of interest, both for the patient and the
Except when early surgical excision can extirpate
the cancer in toto, the long-term outcome with
cancer therapies depends on how effectively oxygen
homeostasis is achieved and preserved. This
statement may raise some eyebrows. But this
conclusion seems inescapable to me in light of
personal pathologic, clinical, and research
There are three treatment approaches to cancer in
oncology today: (1) chemotherapy; (2) radiotherapy;
and (3) newer agents that target one or more of the
signaling pathways in host defenses. All three
approaches seek to remove or destroy every cancer
cell in the body of the patient. Notwithstanding
exuberance of the oncology community, the real story
of progress in cancer treatment has been--and
continues to be--dismal. Consider the following
quote from a 1997 report concerning national cancer
statistics in The New England Journal of Medicine:
"In 1986, we concluded that some 35 years of intense
effort focused largely on improving treatment must
be judged a qualified failure. Now, with 12 more
years of data and experience, we see little reason
to change that conclusion." (3)
The approach of altering the behavior of a cancer
cell by focusing on issues of oxygen homeostasis, by
contrast, has a different goal: to so alter the host
conditions in a person with cancer that the cancer
cells can be coaxed to behave in a nonmalignant
fashion and/or to facilitate destruction of cancer
cells by host defenses.
Thiosphaera pantotropha is a metabolic
two-timer--highly skillful in extraction of energy
from sewage when oxygen is essentially absent, as
well as when it is available. (4-6) First identified
in 1983 in sewage plants, T. pantotropha energizes
itself by robust metabolism of sulfides and
thiosulfate, using nitric oxides instead of oxygen.
When oxygen is available, it switches to aerobic
metabolism and efficiently extracts energy from a
wide array of inorganic substrates by aerobic
respiration. Evidently, the bug is wise in the ways
of managing its genetic pool to serve dual roles
under changing conditions of oxygen availability.
Indeed, in sewage plants, bursts of oxygen are
introduced periodically to invigorate this microbe
for enhanced sewage treatment. It is noteworthy in
this context that there are many other microbial
A cancer cell, like T. pantotropha, is also a
metabolic two-timer, but with a difference: it
survives in the presence of oxygen but thrives in
its absence. The singular challenge in the field of
cancer--in my view--is this: Can we create oxygen
conditions in the body that coax a cancer cell to
relinquish its infatuation with the
respiratory-to-fermentative (RTF) shift, and revert
back to its human respiratory mode of ATP generation
with a fermentative-to-respiratory (FTR) shift? In
other words, can the predominantly glycolytic
metabolism mode of a cancer cell be switched to the
physiologic respiratory ATP energetics of a healthy
cell, fundamentally altering its energetic behavior?
That is a tantalizing possibility. But, what may be
realistically hoped for here? I see limited value of
chemotherapeutic agents in this endeavor. By
contrast, in the future I see much potential in the
clinical benefits of antibodies directed against
signaling molecules that sustain and perpetuate
malignant cell replication. Some notable examples of
such drugs are: (1) imatinib (Gleevec, a
protein-tyrosine kinase inhibtor) Bcr-Ab1 tyrosine
kinase; (2) gefitinib (Iressa, an inhibitor of
intracellular phosphorylation of several tyrosine
kinases) which binds epidermal growth factor; (3)
trastuzumab (Herceptin, a DNA-derived humanized
monoclonal antibody) which binds with the
extracellular domain of the human epidermal growth
factor receptor 2 protein (HER2); (4) rituximab (Rituxin,
a chimeric murine/human monoclonal antibody) which
binds to CD20 antigens; (5) Avastin which targets
angiogenesis; and others.
Altering the Behavior of Cancer Cells:
Fermentative-to-Respiratory (FTR) Shift
Returning to the core issue of the possibility of
coaxing cancer cells to a
fermentative-to-respiratory (FTR) shift--return from
glycolytic metabolism back to physiological
respiratory ATP production--I cite the example of
well-differentiated adenocarcinoma of endometrium
that arises in severe atypical endometrial
hyperplasia in young anovulatory females. Pregnancy
in many such cases so alters the endometrial
microecology that no sign of endometrial malignancy
can be seen years later. Evidently, in such cases
conception does not physically eradicate every
single cancerous endometrial cell. Rather, gestation
alters the behavior of malignant cells.
The FTR shift, of course, is also seen in other
types of cancer. I have been most impressed by a
group of 28 patients with biopsy-proven
prostatic adenocarcinoma whom I managed with primary
focus on direct oxystatic therapies (described in
Part II of this article) for one to 14 years. Most
of them did not receive any synthetic hormonal
intervention. Some of them received such treatment
for short periods of time. Many of them used
soy-derived and other phytofactors intermittently.
They have shown no clinical (including direct rectal
palpation of tumor) or laboratory evidence of
progression of disease with therapies designed to
maintain oxygen homeostasis and redox equilibrium.
It has been clear to me that the prostatic lesions
diagnosed histologically as cancers did not
metabolically behave like malignant neoplasms. (I
might add here that some other patients did not fare
In 1974, I received a large basin full of resected
ovarian cancer involving large segments of omentum.
Histologically, the tumor was a poorly
differentiated, high-grade adenocarcinoma. In 1994,
I received smears prepared with a fine needle
aspiration (FNA) biopsy material obtained from a
pelvic mass in that patient for cytologic diagnosis.
The cellular morphology of 1994 tumor was found to
be identical to that of 1974 cancer. Later I learned
from the surgeon who had performed the 1974
procedure that a CAT scan done about four years
earlier had revealed the existence of the pelvic
tumor. He had elected to 'let the sleeping dogs lie'
since the patient had been clinically asymptomatic
for years. The FNA was performed by his younger
associate who was not fully aware of the
considerations of the older surgeon. All experienced
pathologists recall many such cases. What may we
make of such cases?
A very large number of cases of spontaneous
regression of histologically proven cancer have been
meticulously documented. (7) I believe that occurs
in most, if not all, cases because changes in
cellular microenvironment coax the cancer cells to
relinquish their two-timer habits, and stay faithful
to respiratory ATP production.
In 1949, the American Journal of Obstetrics and
Gynecology reported a highly negative charge on the
cancer cells of the uterine cervix. (8) Ten years
later, Science magazine reported control of cancer
by normalization of the surface charge of cancer
cells in mice. (9) Regrettably, those enormously
significant leads were not followed. Why? Because in
the United States, the pharmaceutical industry
determines which research leads are funded and which
ones are killed. And, of course, there are no drug
dollars to be made by controlling cancer by
normalizing cancer cell surface charges.
Can the cellular energetics in cancer also be
influenced and restored to normalcy with an
electromagnetic approach? Nicolas Tesla clearly
thought so, though, to my knowledge, he never
treated any cancer that way. Some other researchers
have employed it with variable results. I have
personally seen some cancers respond to Tesla
electrotherapeutics. However, I do not have
sufficient follow-up data to draw any definitive
conclusion about the long-term efficacy of that
Do Cancer Cells Induce Respiratory-to-Fermentative
Shift In Non-Cancer Cells?
The full impact on oxygen homeostasis of
non-cancerous cells in close vicinity of cancer
cells is seldom fully appreciated in discussions of
cancer biology. In my view, this is a crucial issue
when the goal is altering the behavior of malignant
cells. Cancer cells produce prodigious amounts of
organic acids that cause incremental oxidative-dysoxygenative
stress on non-malignant cells in their
microenvironment. It is to be entirely expected that
unrelenting oxidative-dysoxygenative will eventually
induce a RTF shift in non-cancerous cells as
well--in the process 'metabolically de-humanizing'
them, so to speak. Evidently, cancer cells thrive in
oxidative-dysoxygenative conditions, whereas host
cells attempting to cordon them off are suffocated
by those microecologic conditions. Thus, in the
battle between cancer and non-cancer cells, the
outcome does not merely depend on the genomic
characteristics of malignant cells but also on
metabolic resilience of the host cells. I believe
this explains a common observation in integrative
practices: Many patients with cancer who clinically
do well with vigorous adherence to integrative
management programs (that preserve oxygen
homeostasis and redox equilibrium) deteriorate
rapidly when they abandon such therapies.
Warburg Was Right, Warburg Was Off the Mark
The German chemist Otto Warburg clearly and
emphatically designated the fermentative metabolism
of a cancer cell as its fundamental metabolic
lesion. That, of course, was an enormous
contribution to our understanding of cellular
energetics of cancer. I begin my definition of
cancer with the fermentative aspect of the
metabolism of a cancer cell to recognize that
contribution, as well as to emphasize the crucial
clinical significance of Warburg's assertion.
Warburg took pains to underscore his notion of the
irreversibility of the metabolic (glycolytic) shift
in cancer. That notion--it seems to me--is open to
question. Warburg wrote: "For cancer formation there
is necessary not only an irreversible damaging of
respiration but also an increase in
fermentation--indeed, such an increase of the
fermentation that the failure of respiration is
compensated for energetically." (10)
Fully in awe of Warburg's contribution to the field,
here I express my opposition to his view of
irreversibility of cancer. My primary argument
against Warburg's view is the experience of many of
my patients who have lived--and are living--long
healthful lives with oxystatic therapies, and
without surgery, radiotherapy, or chemotherapy,
years after the initial diagnosis. Similar cases are
not unknown to integrative clinicians.
I now underscore my definition by clearly
identifying cancer as a "cellular behavioral
disorder." To underscore the core metabolic
derangement in cancer, I state that all dynamics of
a cancer--first and foremost--are driven by deranged
oxygen metabolism, designated as dysoxygenosis. This
view of cancer evidently, is at variance with a
multitude of others that hold as common denominators
the issues of genes and cascades of regulatory and
downstream effectors initiated by mutated genes.
Cancer, oxygen, and pantotropha�Part 1
by Majid Ali
Comments .Previous 12345678910Next ..In 1931,
Warburg was awarded the Nobel Prize in medicine for
his discovery of oxygen transferring enzymes.
Thirteen years later, he won a second Nobel Prize
for his delineation of hydrogen transferring enzyme.
(He was prevented from receiving that prize for
being Jewish by the Hitler regime.) During that
period he recognized the energetic shift in
malignant cells alluded to earlier. (16-18) The
following two quotes from his writings are
noteworthy for the succinctness of description of
his view of cancer: "Since the respiration of all
cancer cells is damaged, our first question is. How
can the respiration of body cells be injured? Of
this damage to respiration [of cancer cells], it can
be said that at the outset that it must be
irreversible, since the respiration of cancer cells
never returns to normal." (18)
Warburg went on designate the shift in the
oxygen-related energetics of a cancer cell as the
prime cause of cancer, to which all secondary causes
contribute. Consider the following quote from a
special lecture he delivered on June 30, 1966, at
the meeting of the Nobel laureates at Lindua,
Germany: "There are prime and secondary causes of
diseases.... Cancer, above all other diseases, has
countless secondary causes. Almost anything can
cause cancer. But even for cancer, there is only one
prime cause." (19)
Warburg, of course, was referring to oxygen in the
above quote. The implications of Warburg's notion of
the fundamental difference between the metabolism of
a cancer cell and a normal cell were both profound
and clear. It meant that oxygen-related issues must
be in the centerfield in all considerations for
treating cancer. Initially, Warburg's seminal
discovery sparked intense interest about the
potential of oxygen therapeutics for the treatment
of malignant neoplasms among a large number of
European and American clinicians. (20-22) Those
therapies included: (1) direct oxygenative (nasal
oxygen, oxygen baths, and others); and (2) indirect
bio-oxidative therapies (intravenous infusions of
ozone and hydrogen peroxide).
The Oxidative-Dysoxygenative Model of Cancer
In 1998, soon after I developed the core concept of
dysoxygenosis, (23) it became evident to me that one
cannot separate redox dynamics from oxygen
homeostasis in cancer any more than one can do so in
other disorders. In essence, the
respiratory-to-fermentative shift in cancer--the
core tenet of Warburg's theory of metabolism of
malignant tumors--is primarily triggered by
oxidative injury to cellular replication and
differentiation pathways. (2) That conclusion seemed
inescapable as I surveyed a large body of data
concerning redox dynamics of neoplastic cells. I
proposed that all known cancer risk factors and
existing theories of cancer can be brought together
by the simple notion that oxidative injury is the
common denominator. Furthermore, in chronic
disorders systemic and/or local oxidosis mediates
its most destructive effects through the systemic
and/or local dysoxygenosis it sets the stage for.
Thus, the oxidative-dysoxygenative (OD) model of
cancer evolved as an extension of my earlier
hypothesis of the primacy of oxidative injury in the
causation and perpetuation of cancer. (2)
There are five critical issues in this context:
1. A major strength of the OD model of
carcinogenesis--in my view--is that it is fully
consistent with the focus of Warburg on glycolysis;
of Pauling on antioxidants; and of others on
environmental, viral, and genetic factors in
considerations of etiology and treatment of cancer.
2. The OD model of cancer brings into sharp focus
how dysoxygenosis alters the milieu of host cells in
vicinity of malignant cells. (Cancer cells
metabolically dehumanize the surrounding cells, so
to speak, by inducing respiratory-to-fermentative
shift in them, further fanning the flames of
3. The OD model of cancer has a strong explanatory
power for several clinical phenomena concerning the
biologic behavior of malignant neoplasms, such as
long periods of quiescence of tumors, spontaneous
regression, and explosive growth of cancers after
severe oxidative-dysoxygenative stresses, such as
those associated with acute illnesses and
discontinuation of strong support.
4. In contrast to Warburg's notion of
irreversibility of the glycolytic metabolism of
cancer, the OD model of cancer recognizes the
possibility of restoration of oxygen homeostasis in
cancer cells with the resumption of predominantly
oxygenative respiratory mode of ATP energetics.
5. Most important, the OD model serves as a complete
model for designing rational and scientifically
sound integrative management plans for good
long-term clinical results with a sharp focus on
Genetic Modulation of the Behavior of Cancer Cells
A large number of genes have been implicated in
carcinogenesis. Oncogenes promote carcinogenesis
while suppressor genes prevent it. (24) Cancer
susceptibility genes have been divided into two
categories: gatekeepers and caretakers. Gatekeepers
control cell proliferation and demise, whereas
caretakers repair damaged DNA sequences and prevent
DNA strand breakage, translocation, and aneuploidy.
(25-27) Impaired gatekeeper function sets the stage
for uncontrolled cellular proliferation and
neoplastic transformation, while suppression of
caretakers results in genetic instability and
increased risk of carcinogenesis.
To cite two specific examples, the ras oncogene is
activated in about 30-40% of cancers, whereas the
p53 suppressor gene is nonfunctional in a variable
number of patients with cancers arising in various
body organs. Those findings led to simplistic
thinking--and irrational exuberance--about the
possibility of curing cancer either by switching off
the oncogenes or switching on the suppressor genes.
Biology seldom, if ever, yields to such enthusism.
Not unexpectedly, no results have been achieved in
the field to date. Genes form an enormous web in
which every change in one site brings forth broad
change in every other site. In 2000, in Oxygen and
Aging I offered the explanation why gene modulation
will never provide the full answer to the problem of
cancer with the following words: Genes are living
beings. They talk and listen to each other. Their
language is living and creative. They do not
recognize simplistic mechanical models of replacing
worn-out materials with spare parts. Genes read
their environment and adapt. But humans need a
living environment to flourish, hence the core
importance of optimal oxygen metabolism for their
Gene therapies in the future may yield some
short-term results but--in my view--not to the
degree that patients and practitioners will be able
to neglect the essential issue of oxygen homeostasis
without sacrificing the chances of good long-term
control of cancer.
Acetylation, Methylation, and Cancer Control
The structural and functional integrity of DNA is
profoundly influenced by enzymes involved with
acetylation, deacetylation, methylation, and
demethylation. Recent advances in those enzymatic
dynamics have brought forth a misguided enthusiasm
about curing cancer by controlling those dynamics,
reminiscent of earlier misguided enthusiasm
concerning oncogenes and suppressor genes.
Since deacetylase inhibitors do not add or delete
nucleotide sequences in DNA, theoretically histone
deacetylase inhibitors are capable of altering the
behavior of cancer cells by "normalizing DNA."
Indeed, one such inhibitor, FK228--a copy of a
peptide isolated from a soil bacterium, has shown
limited initial results in some patients with
cutaneous T-cell lymphomas. (29) It seems safe to
predict that additional experience will show such
results to be temporary. Such is the complementarity
and contrariety in genomics. (See Nature's
Preoccupation With Complementarity and Contrariety,
the first volume of The Principles and Practice of
Integrative Medicine (30) for detailed discussion of
As for methylation/demethylation reactions, it has
been claimed (with supportive data) that some
natural compounds in human blood and urine can
reverse abnormal methylation and mutation of
carcinogeneic genes. (31) It is likely that this
approach will also yield some clinical benefits.
Again, as in the case of acetylation/deacetylation
dynamics, it seems safe to predict that additional
experience will show such results to be temporary.
In closing, there are some promising leads in cancer
therapies which may yield variable clinical results.
Among those are empirically tested phytofactor
formulations, such as fermented soy concoctions,
which are likely to prove clinically more valuable
than therapies directed to modulation of cancer
genomics. However, the long-term health and survival
of persons with cancer--it seems to me--will
continue to depend on how well oxygen homeostasis
can be achieved and maintained.
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by Majid Ali, MD
Director, The Institute of Integrative Medicine
212-873-2444 * 973-586-4111
Dr. Ali is president and professor of medicine of
Capital University of Integrative Medicine,
Washington, DC, and Director of the Institute of
Integrative Medicine, New York. www.majidali.com.
This article is adapted from Dysoxygenosis and
Oxystatic Therapies, the third volume of The
Principles and Practice of Integrative Medicine.