Transcript Men's Cancer: Naturopathic Prevention & Adjunctive Support

Functional Medicine
Forum
2008
Men’s Health:
Cancer Prevention Strategies
&
Adjunctive Naturopathic Treatment Support
David B. Wood, BSc, ND
Cofounder, President, CEO:
Trinity Family Health Clinic, PS (1984 - )
Cofounder, Vice President, CMO:
BioGenesis Nutraceuticals, Inc.(2000 - )
Statistics
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CAFF2006PWSecured.pdf (Cancer Facts
and Figures 2006, American Cancer
Society)
Earlier detection + New Improved
Treatments
Estimated 5 year survival
(cured, relapsed or continuing treatment):
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1974-1976
1995-2001
50%
65%
1998-2002
Incidence & Death per 100K
180
160
140
120
Male I
Male Death
Female I
Female Death
100
80
60
40
20
0
Colon
Lung
Prostate
Breast
Cancer Facts and Figures 2006
American Cancer Society Surveillance Research 2006
Prevention Strategies
Screening exams/labs
 Diet
 Lifestyle
 Nutriceutical Support
 Genomic Issues (dealt with in Dr Veltman’s lecture)
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Screening Exams/Labs
Colorectal Cancer
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Colorectal cancer is extremely common.
Symptoms include blood in the stool or
change in bowel habits.
Screening –
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fecal occult blood testing (hemoccult)
In addition to the Hemoccult - Comprehensive
Digestive Stool Analysis (CDSA) - screen for nbutyrate levels as part of a overall digestive,
fatty acid, flora, inflammatory marker screen.
Diagnosis – Colonoscopy/biopsy
Standard Treatment – surgical resection +
chemotx for nodal involvement
Colorectal Cancer
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Surgery for cure can be attempted in the 70% of patients
presenting w/o metastatic disease.
Prognosis: 10 year survival
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Adjuvant Chemotherapy:
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Typically 5-fluorouracil and leucovorin
Improves survival by 10-30% in colon cancer patients with + lymph
nodes.
Follow up:
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Limited to the mucosa: approaches 90%
Extension through bowel wall: 70-80%
Positive lymph nodes: 30-50%
Metastatic disease: < 20%
Colonoscopy annually for 5 years and every 3 years thereafter if no
polyps or tumors are found.
Palliation:
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When curative surgery is not possible
Surgical debulking (endoscopic laser treatment, electrocoagulation or
held open by stents. Chemotherapy
Prognosis: median survival 7 months
Colorectal Cancer Staging
Stage
Tumor
(Maximum
Penetration)
Regional
Lymph Node
Metastasis
Distant
Metastasis
0
Tis
N0
M0
l
T1 or T2
N0
M0
ll
T3
N0
M0
lll
Any T or
T4
lV
Any T
Any N
N0
Any N
M0
M0
M1
Lung Cancer
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Lung carcinoma is a malignant lung tumor usually categorized as
small cell or non-small cell.
Risk factor:
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Symptoms include:
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Suspected:
Confirmed:
Treatment:
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cough, chest discomfort, and, less commonly hemoptysis, but many
patients are asymptomatic and some present with metastatic disease.
Diagnosis:
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Cigarette smoking is the major risk factor for most types.
Radon gas exposure
Asbestos, silica, arsenic, chromates, nickel, chloromethyl esthers,
beryllium and coke oven emissions.
Surgery, Chemotherapy, and/or radiation therapy
Prognosis:
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Chest X-ray or CT scan
Biopsy
Poor: despite advances in treatment
Focus is on early detection and prevention
Non -
Feature
Small Cell
Adenocarcinoma
Small
Cell
Squamous
Cell
Large
Cell
% of lung
cancers
15%
25-35%
30-35%
10-15%
Location
Submucosa of
airways, perihilar
mass
Peripheral
nodule or
mass
Central,
endobronchial
Peripheral
nodule or mass
Risks
Smoking
(100%)
Etoposide or
irinotecan or
topotecan +
carboplatin or
cisplatin;
Treatment
concurrent
radiation tx in
limited-stage
disease; no role
for surgery
Smoking, occupational exposure (asbestos,
radon)
Stage l/ll: Surgery with or without adjuvant
chemotherapy
Stage lllA: Surgery with or without adjuvant
therapy or concurrent chemoradiation
Stage lllB: Radiation with or without
chemotherapy
Stage lV: Chemotherapy with or without
palliative radiation
Feature
Small Cell
Non – Small Cell
Adenocarcinoma Squamous Cell Large Cell
Complications
Common cause of
SVC syndrome,
paraneoplastic
syndromes
Limited
Stage l: 57-67%
Stage ll: 39-55%
Extensive
Stage lll: 5-25%
Stage lV: <1%
Involvement:20%
5-year
survival
with
treatment
Hemoptysis, airway obstruction,
pneumonia, pleuritic involvement w/pain,
pleural effusion, SVC syndrome,
Pancoast’s tumor (shoulder or arm pain),
hoarseness (laryngeal nerve
involvement), neurologic sx from brain
mets, pathologic fracture from bone
mets, jaundice from liver mets
Involvement:< 5%
SVC = superior vena cava
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Superior vena cava (SVC)
syndrome/obstruction is a relatively rare
condition.
Most often it is caused by cancer in the
mediastinum (the area of the chest under
the breastbone and between the lungs).
The types of cancer that can lead to this
condition include lymphoma, cancer of the
lung that spreads, breast cancer, testicular
cancer, thyroid cancer, and thymic tumors.
Lung Cancer Staging
International Staging System For Lung Cancer
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Primary tumor (T)
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Tis Carcinoma in situ
T1 Tumor ≤3cm w/o invasion more proximal than
the lobar bronchus (ie, not in the main bronchus)
T2 Tumor with any one of the following features:
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T3
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T4
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> 3 cm
Involves main bronchus ≥ 2 cm distal to carina
Invades the visceral pleura
Atelectasis or obstructive pneumonitis that extends to the hilar region but
does not involve the entire lung
Tumor of any size with any one of the following features:
Invades chest wall (incl superior sulcus tumors), diaphram, mediastinal
pleura, or parietal pericardium
Involves main bronchus < 2cm distal to carina but w/o carinal involvement
Atelectasis or obstructive pneumonitis of the entire lung
Tumor of any size with any of the following features:
Invades mediastinum, heart, great vessels, trachea, esophagus, vertebral
body, carina
Malignant pleural or pericardial effusion
Satellite tumor nodule(s) within the same lobe as primary tumor
Lung Cancer Staging
International Staging System For Lung Cancer
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Regional lymph nodes (N)
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N0
N1
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N2
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N3
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No regional lymph node metastasis
Mets to ipsilateral peribronchial and/or ipsilateral hilar
lymph nodes, and intrapulmonary nodes involved by direct
extension of the primary tumor
Mets to ipsilateral mediastinal and/or subcarinal lymph
nodes(s)
Mets to contralateral mediastinal, contralateral hilar,
ipsilateral or contralateral scalene, or supraclavicular
lymph node(s)
Distant metastasis (M)
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M0
M1
No distant mets
Distant mets present [includes metastatic tumor nodule(s)
in a lobe(s) ipsilateral to but diffferent from the primary
tumor]
Stage 0 Tis
Stage IIB T2N1M0 or T3N0M0
Stage IAT1N0M0
Stage IIIA T3N1M0 or T1-3N2M0
Stage IIB T2N0M0
Stage IIIB any TN3M0 or T4 Any NM0
Stage IIA T1N1M0
Stage IV Any T Any N M1
Screening Exams/Labs
Prostate Cancer
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DRE, serum PSA (annual > 50 yo), Men’s health
questionnaires
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TRUS (transrectal ultrasound) may include needle biopsy
(“guided biopsy”)
Biopsy:
If (+) for Cancer – staging (define extent of tumor)
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PSA – PSA velocity important.
T1, T1a, b or c, T2, T2a, b or c, T3, T3a, b or c, T4
Define based on resemblance of tumor architecture to
normal glandular structure:
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Gleason score: grading of histologic heterogenicity of tumor.
Well differentiated 2-4, to mod differentiated 5-7, to
undifferentiated 8-10. Scores are based on the most
prevalent pattern and the next most prevalent pattern. The
lower the score, the less aggressive and invasive is the
tumor and the better is the prognosis.
PC staging
T1
Clinically inapparent by palpation or imaging
T1a
Incidentally found in ≤5% of resected tissue
T1b
Incidentally found in >5% of resected tissue
T1c
Identified by needle biopsy done for elevated PSA level
T2
Is Palpable or reliably visible by imaging; confined to
prostate
T2a
Involves ½ of one lobe or less
T2b
Involves > ½ of one lobe but not both lobes
T2c
Involves both lobes
T3
Extends through the prostatic capsule
T3a
Extends through the prostatic capsule unilaterally or
bilaterally
T3b
Invades seminal vesicles
T4
Is fixed or invades adjacent structures other than seminal
vesicles
PC con’t
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Prognosis (standard allopathic)
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Depends on stage and grade
Generally very good for localized
High grade (T score), poorly differentiated (Gleason score) =
poor prognosis.
Metastatic cancer has no cure; median life expectancy is 1-3
years, although some patients live for many years
Treatment:
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Varies (watchful waiting, hormonal ablation Tx, cryotherapy,
surgery, chemotx, brachytherapy (radio seed implants), radiotx
(external beam))
Cytotoxic and biologic drugs (eg, genetically designed vaccines,
antisense therapy, monoclonal antibodies), angiogenesis
inhibitors (eg, thalidomide, endostatin), and matrix
metalloproteinase inhibitors are being studied and may provide
palliation and prolong survival, but their superiority over
corticosteroids alone has not been proved.
Reference for Cancer Staging: The Merck Manual 18th Ed. 2006
Cancer Prevention Diet
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Avoid or minimize exposure to carcinogens (trans fatty acids,
hydrogenated oils, rancid fats, deep fried, grilled meats, + reduce
exposure to high glycemic foods, white sugar, white flour, artificial colors,
dyes, etc.)
Eat a well balanced organic whole food unprocessed/minimally
processed low glycemic diet with many colors for best food based
antioxidant/flavonoid exposure. Eat from the rainbow.
Balance protein, fat and carbohydrates from organic whole foods.
Eat cold water ocean fish. Increase Omega 3 fatty acid foods and reduce
Omega 6 fatty acid foods.
Drink clean water. Don’t overlook the importance of being well
hydrated with clean water. It makes everything function better. Many
people suffer from dehydration.
Work towards 40-50 grams of fiber intake per day. Fiber reduces
the risk of colon cancer, but also does so many other things (bowel
movement regulation, toxin clearance, flora and fatty acid regulation,
hormone and cholesterol clearance (minimize enterohepatic recirculation)
Get some unprocessed “raw” foods everyday. Fresh fruit, vegies,
sprouts are good candidates.
Eat Lycopenes/Carotenoids (tomatoes and other ‘red’ fruits/vegies)
Eat Cruciferous vegetables (broccoli, cauliflower, brussels sprouts,
cabbage)
Eat fermented foods (cabbage, kefir, yogurt, low fat/skim cheese, miso,
tempeh, pickles, vinegar)
Lifestyle
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Exercise moderately on a regular basis. Vary the exercise from
aerobic to weights to walk/run, cycle, etc. Have fun with it and
make it part of your lifestyle.
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Use your morning on waking pulse to determine tolerance and recovery
time.
Get regular exposure to sun to enhance Vitamin D and
melatonin production. Protect skin with antioxidant sunscreen
after 15 minutes of unprotected exposure.
Wear sunglasses that protect eyes from UVA/B/C induced
solar damage. Expose eyes indirectly (unprotected) to sunrise
and sunset rays to enhance circadian rhythm regulation and allow
beneficial full spectrum exposure
Decompress. Let go of emotional garbage. Forgive. Use of
prayer and/or meditation can be helpful.
Get a pet! Animals give love unconditionally and can be a great
loyal companion. Many studies show that people with pets tend to
be happier, healthier and live longer.
Don’t dwell on yourself. “Give and it shall be given unto you” is
so true. Bless others! It is great fun and makes life a much more
rewarding experience.
Standing on the Shoulders of
Giants
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Max Gerson
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William Donald Kelly
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Oxidative phosphorylation
Keith Brewer
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Enzymes
Otto Warburg
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Raw foods, juicing, Na/K ratio, thyroid
High alkaline pH
Angelo P. John, Sr.
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Molecular biologist and cancer scientist,
controlled amino acid therapy (CAAT), glycolysis
vs. oxidative phosphorylation strategies
Otto Warburg
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Nobel Prize in Medicine 1931: discovery of
oxygen transferring enzyme of cell
respiration
Nobel Prize in Medicine 1944: discovery of
the active groups of hydrogen transferring
enzymes
His main interests: Chemistry and Physics
of Life
No scientists have been more successful
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“Cancer, above all other diseases, has countless
secondary causes. But, even for cancer, there is only
one prime cause. Summarized in a few words, the
prime cause of cancer is the replacement of the
respiration of oxygen in the normal body cells by a
fermentation of sugar. All normal body cells meet their
energy needs by respiration of oxygen, whereas cancer
cells meet their energy needs in great part by
fermentation. All normal body cells are thus obligate
aerobes, whereas all cancer cells are partial anaerobes.
From the standpoint of the physics and chemistry of life
this difference between normal and cancer cells is so
great that one can scarcely picture a greater difference.
Oxygen gas, the donor of energy in plants and animals
is dethroned in the cancer cells and replaced by an
energy yielding reaction of the lowest living forms,
namely, a fermentation of glucose.”
Otto Warburg in “The Prime Cause and Prevention of Cancer”
Lecture Lindau, Germany 1966. English Ed. Published by Dean
Burk, National Cancer Institute, Bethesda, Maryland.
Otto Warburg
Director, Max Planck Institute for Cell Physiology,
Berlin-Dahlem
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“To prevent cancer it is therefore proposed first to
keep the speed of the blood stream so high that
the venous blood still contains sufficient oxygen;
second, to keep high the concentration of
hemoglobin in the blood; third to add always to
food, even in healthy people, the active groups of
the respiratory enzymes; and to increase the
doses of these groups, if a precancerous state has
already developed. If at the same time exogenous
carcinogens are excluded rigorously, then most
cancers may be prevented today.”
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Otto Warburg Wiesenhof, August 1966 in:
 “The Prime Cause and Prevention of Cancer”
Naturopathic Adjunctive
Support Options
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Cancer Cell Physiology
Specialized Diets
Individualized:
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Foundational nutrition
Digestion/elimination
Cytochrome P450/Phase I/II conjugation support
Pulsed antioxidants
Antimetastatics
Antiangiogenesis
Matrix metalloprotease Inhibition
Immune enhancement
Enhanced phagocytosis & macrophage debris field
cleanup
“Recently, The Journal of Clinical Oncology reported that an increasing number of
cancer patients are using complementary therapies as part of their treatment regimen
such as Controlled Amino Acid Therapy (CAAT). Also, The Journal of the American
Medical Association dedicated an entire issue to integrative and complementary cancer
Treatments. The effects of biological targeted therapies like CAAT which interfere with
specific functions in cancer cells, causing them to die, has also been reported in The
New England Journal of Medicine, The Journal of the National Cancer Institute, Clinical
Cancer Research and The Journal Of Cellular Biochemistry. It is now evident that not
only drugs, but specific biological compounds, such as those employed by CAAT, can
attack such sites on cancer cells.
•
Dr Albert B. Lorincz of the University of Chicago conducted several trials with
cancer patients, reducing tumor size in most of them who were fed a formula
reduced in certain amino acids, the treatment employed by CAAT.
•
Dr. Chi Van Dang, of the Johns Hopkins School of Medicine, and Dr. Douglas Spitz
of the University of Iowa report how carbohydrate deprivation, a part of the CAAT
protocol, kills cancer cells while having no effect on normal cells.
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Dr. Pascal J. Goldschmidt of the Johns Hopkins Medical School reports that
scientifically supported dietary supplements, such as those included in CAAT, may
be helpful in treating certain cancers.
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Dr. Marco Rabinowitz of the National Cancer Institute reports that amino acid
deprivation, such as Controlled Amino Acid Therapy (CAAT), inhibits
phosphofructokinase, shuts down energy supply to cancer cells and thereby
enhances the benefits of chemotherapy.
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Dr. Joel Evans, Honorary Co-Chairman of the Physicians Advisory Board to the U.S.
Congress, lectured at Yale’s Cancer Center on cancer and nutrition, discussing
Controlled Amino Acid Therapy and citing the notable recovery his patient
experienced since using CAAT….”
Angelo P. John, Sr.
Underline emphasis mine
Cancer Cell Physiology
Cancer cell
Healthy cell
Krebs Cycle Defective
Krebs Cycle Normal
Energy Almost all from Glycolysis
(80+ %) fermentation
Energy from Krebs Cycle
(70%)
Energy in Absence of Oxygen
Energy Most from Oxygen
(oxidative phosphorylation)
Growth & Reproduction Requires
certain amino acids (glycine,
serine, glutaminc acid and
aspartic acid) phosphorus and
Vitamin B6
Growth & Reproduction not
glycine dependent
Glycine not an essential amino
acid for healthy cells
Angiogenesis (regulated by Matrix Uses existing circulation
Metalloprotease) Stimulation of
rather than stimulating feeder
requires these same amino acids
vessels
Further information at: www.apjohncancerinstitute.org
Cancer Cell Physiology
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Diet/Nutriceutical intervention should:
Inhibit:
Glycolysis
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CHO restriction
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Angiogenesis as well as growth and reproduction of cancer cells
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Essential Fatty Acids from Fish, Perilla and Olive (squalene, oleic)
Epithelial Growth Factors
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Limonene (Citrus Fruits) inhibition of Ras cancer gene (Avoid Grapefruit)
Prostaglandin E2
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Diet Low in Glycine (key amino acid to restrict), Phosphorus and Vitamin B6
Ras cancer gene (overactive in 90% of all cancers)
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20% restriction to inhibit cell growth and reproduction
40% restriction to see cancer cell apoptosis (cancer cell death)
Parsley extract
Support:
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Oxidative Phosphorylation (Krebs Cycle)
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Increase Citric Acid and Acetic Acid intake
Citrus Fruits (lemon, esp.) and Vinegar (2 T with lunch, dinner)
Supports healthy cell function and promotes apoptosis of cancer cells
DCA
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Dichloroacetic Acid
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New synthetic analog of natural acetic acid
IUPAC name
Dichloroacetic acid
(all vinegars)
Other names
Dichloroethanoic acid
Cancer trials
Dichloroacetate
Potential cancer
Molecular formula CHCl2COOH
applications
Cancer cells generally use glycolysis rather than
oxidation for energy (the Warburg effect), as a
result of hypoxia in tumors and damaged
mitochondria.The body often kills damaged cells
by apoptosis, a mechanism of self-destruction
that involves mitochondria, but this mechanism
fails in cancer cells.
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A study published in January 2007 by researchers at the
University of Alberta, testing DCA on in vitro cancer cell lines
and a rat model, found that DCA restored mitochondrial
function, thus restoring apoptosis, killing cancer cells in vitro,
and shrinking the tumors in the rats.
These results received extensive media attention, beginning
with an article in New Scientist titled "Cheap, Safe Drug Kills
Most Cancers". Subsequently, the American Cancer Society and
other medical organizations have received a large volume of
public interest and questions regarding DCA. Reports have since
pointed out that although the study results are promising, no
formal clinical trials in humans with cancer have yet been
conducted, emphasizing the need for caution in interpreting the
preliminary results, though some doctors are treating patients
with DCA "off-label," and under a cloud of controversy.
The New Scientist later editorialized, "The drug may yet live up
to its promise as an anti-cancer agent - clinical trials are
expected to start soon. It may even spawn an entirely new
class of anti-cancer drugs. For now, however, it remains
experimental, never yet properly tested in a person with cancer.
People who self-administer the drug are taking a very long shot
and, unlikely as it may sound, could even make their health
worse."
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The historical likelihood that a promising agent in preclinical (i.e., cell-line killing) experiments will become an
effective human cancer drug is 5%,and the likelihood of
an FDA approval for any given drug entering Phase I
testing is reportedly 8-11%. DCA has been used
historically to treat patients with lactic acidosis, and
therefore, could arguably enter phase 2 trials in patients
with cancer.
DCA is non-patentable as a compound, though a patent
has been filed for its use in cancer treatment. Concerns
have been raised that without strong intellectual property
protection, the financial incentive for pharmaceutical
industry interest is reduced, and therefore clinical trials of
DCA may not be funded. However, other sources of
funding exist; previous studies of DCA have been funded
by government organizations such as the National
Institutes of Health, the Food and Drug Administration,
the Canadian Institutes of Health Research and by private
charities (e.g. the Muscular Dystrophy Association). Drs
Michelakis and Archer have applied for a patent on the
use of DCA in the treatment of cancer.
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Side effects of DCA:
Reports in the lay press after the 2007 University of Alberta announcement
claim that dichloroacetate "has actually been used safely in humans for
decades", but the limited scholarly literature suggests side effects of pain,
numbness and gait disturbances in some patients. A clinical trial where DCA
was given to patients of MELAS (a form of genetically inherited lactic
acidosis) at 25 mg/kg/day was ended prematurely due to excessive
peripheral nerve toxicity. Dichloroacetate can also have anxiolytic or
sedative effects.
Animal studies suggest that the neuropathy and neurotoxicity during
chronic dichloroacetate treatment may be partly due to depletion of
thiamine, and thiamine supplementation in rats reduced these effects.
However, more recent studies in humans suggest that peripheral
neuropathy is a common side effect during chronic DCA treatment, even
with coadministration of oral thiamine. An additional study reported that 50
mg/kg/day DCA treatment resulted in unsteady gait and lethargy in two
patients, with symptoms occurring after one month for one patient and two
months for the second. Gait disturbance and consciousness were recovered
with cessation of DCA, however sensory nerve action potentials did not
recover in one month.
Studies of the trichloroethylene (TCE) metabolites dichloroacetic acid (DCA),
trichloroacetic acid (TCA), and chloral hydrate suggest that both DCA and
TCA are involved in TCE-induced liver tumorigenesis and that many DCA
effects are consistent with conditions that increase the risk of liver cancer in
humans.
Acetic Acid
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Cancer Cell, Vol 11, 37-51, January 2007
A Mitochondria-K+ Channel Axis Is
Suppressed in Cancer and Its Normalization
Promotes Apoptosis and Inhibits Cancer
Growth
Sébastien Bonnet,1 Stephen L. Archer,1,2 Joan AllalunisTurner,3 Alois Haromy,1 Christian Beaulieu,4
Richard Thompson,4 Christopher T. Lee,5 Gary
D. Lopaschuk,5,6 Lakshmi Puttagunta,7 Sandra Bonnet,1
Gwyneth Harry,1 Kyoko Hashimoto,1 Christopher J. Porter,8
Miguel A. Andrade,8 Bernard Thebaud,1,6 and Evangelos
D. Michelakis1,
1 Pulmonary Hypertension Program and Vascular Biology Group, University of Alberta, Edmonton, AB
T6G 2B7, Canada
2 Department of Physiology, University of Alberta, Edmonton, AB T6G 2B7, Canada
3 Department of Oncology, University of Alberta, Edmonton, AB T6G 2B7, Canada
4 Department of Biomedical Engineering, University of Alberta, Edmonton, AB T6G 2B7, Canada
5 Department of Pharmacology, University of Alberta, Edmonton, AB T6G 2B7, Canada
6 Department of Pediatrics, University of Alberta, Edmonton, AB T6G 2B7, Canada
7 Department of Laboratory Medicine and Pathology, University of Alberta, Edmonton, AB T6G 2B7,
Canada
8 Ontario Genomics Innovation Centre, Ottawa Health Research Institute, and Department of Cellular
and Molecular Medicine, University of Ottawa, Ottawa, ON K1N 6N5, Canada
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The unique metabolic profile of cancer (aerobic glycolysis)
might confer apoptosis resistance and be therapeutically
targeted. Compared to normal cells, several human
cancers have high mitochondrial membrane potential
(ΔΨm) and low expression of the K+ channel Kv1.5, both
contributing to apoptosis resistance. Dichloroacetate
(DCA) inhibits mitochondrial pyruvate dehydrogenase
kinase (PDK), shifts metabolism from glycolysis to
glucose oxidation, decreases ΔΨm, increases
mitochondrial H2O2, and activates Kv channels in all
cancer, but not normal, cells; DCA upregulates Kv1.5 by
an NFAT1-dependent mechanism. DCA induces
apoptosis, decreases proliferation, and inhibits tumor
growth, without apparent toxicity. Molecular inhibition of
PDK2 by siRNA mimics DCA. The mitochondria-NFAT-Kv
axis and PDK are important therapeutic targets in cancer;
the orally available DCA is a promising selective
anticancer agent.
Cheap, safe drug kills most cancers
20 January 2007
NewScientist.com news service
Remember Acetic Acid
from Vinegar!
Andy Coghlan
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References to DCA
(taken from www.wikipedia.org)
Lide, D. R. (Ed.) (1990). CRC Handbook of Chemistry and Physics (70th Edn.).
Boca Raton (FL):CRC Press.
Stacpoole P, Henderson G, Yan Z, James M (1998). "Clinical pharmacology and
toxicology of dichloroacetate". Environ Health Perspect 106 Suppl 4: 989–94.
PMID 9703483. Free full text
Stacpoole P (1989). "The pharmacology of dichloroacetate". Metabolism 38 (11):
1124-44. PMID 2554095.
Stacpoole P, Lorenz A, Thomas R, Harman E (1988). "Dichloroacetate in the
treatment of lactic acidosis". Ann Intern Med 108 (1): 58-63. PMID 3337517.
Stacpoole P, Kerr D, Barnes C, Bunch S, Carney P, Fennell E, Felitsyn N, Gilmore R,
Greer M, Henderson G, Hutson A, Neiberger R, O'Brien R, Perkins L, Quisling R,
Shroads A, Shuster J, Silverstein J, Theriaque D, Valenstein E (2006). "Controlled
clinical trial of dichloroacetate for treatment of congenital lactic acidosis in
children". Pediatrics 117 (5): 1519-31. PMID 16651305.
Kaufmann P, Engelstad K, Wei Y, Jhung S, Sano M, Shungu D, Millar W, Hong X,
Gooch C, Mao X, Pascual J, Hirano M, Stacpoole P, DiMauro S, De Vivo D (2006).
"Dichloroacetate causes toxic neuropathy in MELAS: a randomized, controlled
clinical trial". Neurology 66 (3): 324-30. PMID 16476929.
Stacpoole P, Wright E, Baumgartner T, Bersin R, Buchalter S, Curry S, Duncan C,
Harman E, Henderson G, Jenkinson S (1992). "A controlled clinical trial of
dichloroacetate for treatment of lactic acidosis in adults. The Dichloroacetate-Lactic
Acidosis Study Group". N Engl J Med 327 (22): 1564-9. PMID 1435883.
3:20 PM
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
Xu R, Pelicano H, Zhou Y, Carew J, Feng L, Bhalla K, Keating M,
Huang P (2005). "Inhibition of glycolysis in cancer cells: a novel
strategy to overcome drug resistance associated with mitochondrial
respiratory defect and hypoxia". Cancer Res 65 (2): 613-21. PMID
15695406.
Bonnet S, Archer S, Allalunis-Turner J, Haromy A, Beaulieu C,
Thompson R, Lee C, Lopaschuk G, Puttagunta L, Bonnet S, Harry G,
Hashimoto K, Porter C, Andrade M, Thebaud B, Michelakis E (2007).
"A mitochondria-K+ channel axis is suppressed in cancer and its
normalization promotes apoptosis and inhibits cancer growth".
Cancer Cell 11 (1): 37-51. PMID 17222789.
Cheap, safe drug kills most cancers. New Scientist (2007-01-17).
Retrieved on 2007-01-17.
"DCA: Cancer Breakthrough or Urban Legend?". From ABC News, 5
February 2007. Accessed 15 Feb 2007.
"No Wonder Drug", letter to New Scientist from Ralph Moss
Lemont. Published February 3, 2007. Accessed 16 Feb 2007.
http://www.nationalreviewofmedicine.com/issue/poll/featured_artic
le.html
"Editorial: Gambling with your life", New Scientist, 31 March 2007
Food&Drug Packaging, August, 2004
Nature Reviews Drug Development, August 2004
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
A Letter from Dr. Evangelos Michelakis
http://www.ctv.ca/servlet/ArticleNews/story/CTVNews/20070120/DCA_feature_070
121/20070122?hub=Health
"Small molecule offers big hope against cancer", by Ryan Smith. From
ExpressNews, a University of Alberta publication. Published January 16, 2007.
Accessed 15 Feb 2007.
Researchers launch website on new cancer research, CTV.ca, 22 January 2007
A Method of Treating Cancer Using Dichloroacetate, Application to the European
Patent Office, 19 October 2006
"Long-used drug shows new promise for cancer", The Globe and Mail, 2007-01-17.
Retrieved on 2007-01-17.
Kaufmann P, Engelstad K, Wei Y et al. (2006). "Dichloroacetate causes toxic
neuropathy in MELAS: a randomized, controlled clinical trial". Neurology 66 (3):
324–30. PMID 16476929.
Stacpoole P, Harwood H, Cameron D, Curry S, Samuelson D, Cornwell P, Sauberlich
H (1990). "Chronic toxicity of dichloroacetate: possible relation to thiamine
deficiency in rats". Fundam Appl Toxicol 14 (2): 327–37. PMID 2318357.
Kurlemann G, Paetzke I, Moller H, Masur H, Schuierer G, Weglage J, Koch HG
(1995). "Therapy of complex I deficiency: peripheral neuropathy during
dichloroacetate therapy". Eur J Pediatr 154 (11): 928–32. PMID 8582409.
Spruijt L, Naviaux RK, McGowan KA, Nyhan WL, Sheean G, Haas RH, Barshop BA
(2001). "Nerve conduction changes in patients with mitochondrial diseases treated
with dichloroacetate". Muscle Nerve 24 (7): 916–24. PMID 11410919.
Oishi K, Yoshioka M, Ozawa R, Yamamoto T, Oya Y, Ogawa M, Kawai M (2003).
"Dichloroacetate treatment for adult patients with mitochondrial disease". Rinsho
Shinkeigaku 43 (4): 154–61. PMID 12892050.
Environ Health Perspect. 2006 Sep;114(9):1457-63 PMID 16966105 (free full text)
Andrea Sands. "Experts caution against patients compiling own data on unapproved
cancer drug", Edmonton Journal, March 18, 2007.
Cancer therapy: When all else fails, Linda Geddes. New Scientist (28 March 2007).
Design Custom Diet
You can easily design a custom diet:
 Make it:

CHO restricted


20% reduction decreases cancer cell reproduction
40% reduction increases cancer cell death via
apoptosis (inhibits glycolysis)
Glycine restricted
 Phosphorus and Vitamin B6 reduced
 Essential Fatty Acid enhanced
 Citrus enhanced
 Parsley approved
 Vinegar approved (natural source of acetic acid)
Via www.foodpharmacy.com

Eat
high fiber low glycemic
foods
high alkaline foods, esp.
foods high in
potassium
foods high in Selenium
foods high in Niacin
foods high in Vitamin D
foods high in Oleic acid,
Alpha Linolenic acid
(ALA) and foods high
in omega 3 fatty
acids
foods high in Phytosterols
Restrict
Carbohydrates
(20-40%)
High, medium glycemic
foods
L-Glycine
high Phosphorus foods
foods high in Vitamin
B6
•Meat/Poultry - beef, buffalo, lamb, venison, chicken (dark meat), cornish hen, elk,
pork (bacon), duck, turkey (dark meat)
•Seafood – abalone, catfish, caviar, grouper, lobster, oysters, rockfish, scallop, shark,
shrimp, tuna, cod, crayfish
•Legumes – azuki beans, black beans, fava beans, great northern beans, green beans,
green peas, lentils, lima beans, mung beans, red beans, tofu
•Beverages – vegetable juices, water (carbonated, distilled, pure bottled or tap filtered),
almond milk, beer, coffee (caffeinated, decaf steam), liquor, oat milk,
tea (green, black, herbal), wine (red, white)
•Dairy and Eggs – camembert, cheddar, edam, eggs (chicken – yolk), milk (whole),
roquefort, swiss, whey, blue cheese, brie, buttermilk, colby, cottage cheese (reg or lite),
cream (half and half), cream cheese, eggs (chicken – white), eggs (duck – whole), feta,
goat cheese, gouda, gruyere, ice cream, milk (skim), monterey jack, mozzarella,
muenster, neufchatel, parmesan, provolone, ricotta, romano sour cream, yogurt
•Nuts and Seeds – almonds, brazil nuts, cashews, chestnuts, filberts, hickory nuts,
macadamia nuts, peanuts, pecans, pine nuts, walnuts, poppy seeds, sesame seeds
•Grains – Ø (no ideal or neutral)
•Greens – Beet greens, kale, lettuce (bibb, iceberg,
loose-leaf, romaine), sprouts (alfalfa), swiss chard,
watercress, arugula, cilantro, collard greens, dandelion
greens, endive, mustard greens, radicchio, spinach,
sprouts (bean), turnip greens





Vegetables – artichokes, asparagus, avocado, bamboo shoots, broccoli, brussels
sprouts, cabbage, carrot, cauliflower, celery, cucumber, daikon, kohlrabi, mushroom
(all edible varieties), olive (all varieties), onion, parsnip, radish, rutabaga, tomato,
bok choy, eggplant, fennel, garlic, ginger root, jerusalem, artichoke, jicama, leek,
okra, pepper (bell, all colors), pepper (hot, all colors), pumpkin, shallot, turnip,
water chestnuts, zucchini
Sea Vegetables – Kelp, agar, irish moss, laver, wakame
Fruits – apples, blackberries, blueberries, cherries, coconut, elderberries, grapes,
guava, kumquat, lemons, limes, oranges, peaches, plums, pomegranates, raspberries
strawberries, tangerines, boysenberries, cranberries, gooseberries, kiwi,
loganberries, mango, nectarines, papaya, rhubarb
Oils and Fats – almond oil, black currant oil, butter (salted), canola oil, coconut oil,
corn oil, fish oil, flax oil, hemp oil, olive oil, peanut oil, safflower oil, sesame oil,
sunflower oil, wheat germ oil, borage oil, butter (unsalted), evening primrose oil,
ghee (clarified butter)
Herbs, Spices and Seasonings – chili powder, cinnamon, curry powder, ginger, salt
(sea salt, unrefined), vinegar (apple cidar, balsamic, rice, wine), anise, basil, bay
leaf, caraway, cardamom, carob, cayenne, chervil, chive, cloves, coriander, cumin,
dill weed, fennel seed, fenugreek, garlic powder, horseradish, ketchup, mace,
marjoram, mayonnaise, molasses (black unsulphured, small quantities) mustard,
mustard seed, nutmeg, oregano, paprika, parsley, pepper (black), peppermint,
rosemary, saffron, sage, salt (iodized or low sodium types), savory, soy sauce,
spearmint, tarragon, thyme, turmeric, vanilla (extract), wasabi





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






Meat/Poultry - beef (heart), pork (ham, chops), kidney (beef), liver (beef), rabbit,
chicken (white meat), goose, pheasant, quail, turkey (white meat)
Seafood – anchovy, bass (freshwater), clams, crab,
halibut, herring, mussels, perch, pompano, roughy, sardine,
squid, swordfish, trout, whitefish, bass (sea), mackerel, mahi mahi, octopus,
salmon, snapper
Legumes – black-eyed peas, garbanzo beans, navy beans, pink beans, pinto
beans, soy beans, white beans
Beverages – fruit juices, rice milk, soft drinks, soy milk
Dairy and Eggs – goats milk, milk (2%), sherbet
Nuts and Seeds – sunflower seeds, pistachios, pumpkin seeds
Grains – oats, wheat, wild rice, amaranth, barley, buckwheat, kamut, millet,
quinoa, rice (basmati, brown, white), rye, spelt, triticale
Greens – Ø (no restrictions)
Vegetables – beet, squash (summer, winter), sweet potato, yam, corn, potato (all
varieties)
Sea Vegetables - dulse
Fruits – cantaloupe, pineapple, apricots, banana, casaba melon, currents, dates,
figs, grapefruit, honeydew melon, pears, persimmon, prunes, raisins,
watermelon
Oils and Fats - cottonseed oil, margarine, palm kernel oil
Herbs, Spices and Seasonings – chocolate, honey, sugar (brown, brown
unrefined, turbinado, white)

Suggested Meal Plan:

Three meals per day + one snack
a meal = 2 servings from each group
a snack = 1 serving from each group
Avoid fried foods and foods high in sugar. Eat foods raw, steamed,
baked or broiled, juiced or sprouted. Eat organic whenever possible
CHO (carbohydrates: beverages, grains, greens, vegetables, sea vegetables,
fruits): 1 cup (note: greens and all “ideal” vegetables can be eaten in
unlimited quantities. Vegetable juice is allowed at 3 glasses per day in
addition to your










Alcohol should be limited to 1 glass (wine) twice weekly.
Grains (oats, wheat, wild rice) are only allowed once weekly and only in whole
unprocessed forms.)
PRO (proteins: meats, poultry, seafood, legumes, dairy, eggs): 4 ounces
FAT (fats: nuts/seeds, oils & fats): 2 tablespoons
Herbs, Spices & Seasonings: are allowed in unlimited quantities except for
salt which should be used minimally to taste.
Water/Tea allowance. It is also recommended that you drink 4 glasses of
pure water daily and 3 cups of green tea daily.
Make Sure You
Cover These Basics






Foundational Nutrition
Digestion/Elimination
Cytochrome p450/phase l/ll conjugation
support
Pulsed antioxidants
Antimetastatics
Matrix metalloprotease Inhibition



(MMP up-regulate angiogenesis)
Glycine is needed for angiogenesis!
Immune Enhancement
Adjunctive Nutraceuticals




Calcium D-Glucurate
 Use in hormone mediated cancers to enhance glucuronidation
Inhibit Isoprenylation with:
 D-Limonene
 Block Isoprenylation which is necessary for tumor cell
growth (RAS gene, Epithelial Growth Factor, Tyrosine Kinase,
Insulin-Like-Growth-Factor)
 Tocotrienols
 Inhibit isoprenylation via inhibition of HMG-2, assists DLimonene
 Niacin
 Also inhibits RAS gene
 Depletion of L-Glycine (Cancer cells need to synthesize DNA)
Choline
 Assist Liver metabolism of Niacin
Selenium
 Interfere with Cancer promoter genes and support cancer cell
apoptosis

DIM


Melatonin



Inhibit Leukotriene (Boswellia also) stimulation of cancer cells
Enhance Thymic hormonal maturation of T cells
Vitamin D and Curcumin


In hormone mediated cancers - Inhibit hormone stimulation of
cancer cell growth and reproduction (Aromatase Inhibition)
Inhibit Kinases (critical to cancer cell growth and reproduction)
via phosphatase activation
Green Tea, Curcumin, White Willow Bark

Cox2 inhibition, Phospholipase A2 inhibition – inhibition of
Matrix Metaloprotease induced angiogenesis. Inhibition of VEGF
(vascular endothelial growth factor)
A Word About…

Prenylation or isoprenylation is the addition
of hydrophobic molecules to a protein to
facilitate its attachment to the cell
membrane. The result is similar to that of
all lipid anchored proteins (e.g. the GPI
anchor). All isoprenylation chains are
products of the HMG-CoA reductase
pathway: geranylgeraniol (GG), farnesol
and dolichol.
en.wikipedia.org/wiki/Isoprenylation
Case History Colon Cancer





63 y.o. male. Dx primary Colon Cancer ~ 12/05. Positive
Colonoscopy with abnormal cells (6 cm pelvic mass with
several small ~ 1cm perirectal masses) just inside rectum.
CT scan positive for tiny spots on liver and lungs. Ø night
sweats or weight loss.
Hx: smoker x 23 years 1 pack/day, quit 20 y ago, Dx
emphysema x 3-4 years, Dx Hypertension controlled with
Benzapril)
Tx: Initially Ø surgery. 1/06 – 6/06 Chemo Tx
(5FU,leucovorin). Ø Radiation Tx. Chemo decreased tumor
bulk by 67%. Surgery scheduled for 8/06. Nat. Tx started
12/05. 8/06 f/u CT lungs unchanged, may not be Ca. Could
be nodule or lymph node enlargment due to Hx of particle
board exposure.
Lungs: doing better. Hiking. Less SOB.
Bowels: increased BMs due to chem. At worst was up to
15x/day. Alternating diarrhea/constipation. Much better
now.
Colon Cancer Case


Surgery 8/06: removed ~ 1 foot of colon. Reconnected. Spot
on Liver: scar tissue.
ROC f/u 10/06:




Bowel movements now 3-4x/day
Working on increased fiber in diet. Helps
Emphysema. Not sure if accurate dx. No inhalers since 7/06.
Breathing fine. Nose clearer, breathing better since Nasal Polyps
removed. Particle board exposure X 33 years (10 years longer
than hx of smoking)
ROC f/u 1/07:





CT scan good. Spot on liver smaller. ? Cyst.
Ø nausea or bloating. Some intestinal gas. Stools 3 per day nl
color and consistency.
Breathing: no need for combivent/flovent since 7/06. Hikes in
Mtns w/o problem. No SOB. Walks 3-4x/wk. Snowmobiling with
no cold air problems.
Gained 8-10 lbs. Current 70 inches and 175 lbs.
No recent infections.

ROC f/u 7/07:





Recent Colonoscopy (7/09/07) – normal. (no sign of Ca. “Even
areas where incision done in past are hard to tell. Looks very
good”)
Weight stable at 175
Nocturia 1x/night occ 2x.
Stools remain normal with frequency of 3/day.
Hiking 4-6x/wk 4-6 miles each occurrence. Ø SOB.
Case History Lung Cancer

Significant labs that needed support:









ESR: ranged from 56 to 20. Trended down with adjunctive support
even while prednisone was being tapered. 6/02 CRP 777 (50-300)
9/02 0.16 (<0.80)
Macrocytic anemia. Corrected with nutritional support
Occ Leukocytosis, elevated TC, granulocytosis dealt with
nutritionally
By 5/98 program reduced to ½ and patient continues to
improve.
Melatonin 20 mg PO QD before bed added 8/98
Side of effects of Radiation to lungs has been Radiation
pneumonia. MD have had patient on Rx prednisone. Dose now
has been lowered to 10 mg per day. By 11/98 prednisone
lowered to 5 mg QD
CT scan 5/98. Tumor almost gone!
8/00: No sign of tumor or metastatic spread.
10/05: No sign of return. Patient in excellent overall health.
Ongoing Asthma continues but minimal and does not interfere
with full activity. Mild DJD in hips, shoulder and knees.
Case History Prostate Cancer
#1






66 yo retired Engineer
CC: Prostate cancer (Dx 6/98, PSA 5.58), High Blood
Pressure.
HPI: History palpable ‘spot’ on prostate 1995 w/PSA of 3.19)
Ultrasound guided biopsy 6/98. Gleason score 7. No
regional lymph node evaluation despite CT scan showing 1
enlarged node near prostate
Tx: External beam radiation (11/12 – 12/14/98), followed by
radio seed implants (1/14/99) and Hormonal ablation with
Lupron shots q 3 months
Naturopathic Tx: FOC 12/2/98. Program included dietary
modification (glycemic balancing, etc.) + prostate support
nutrients, immune support, enzyme tx, MCPectin tx,
antiangiogenesis tx (S cartilage), EFA (EPA/DHA),
Hypertension support (garlic, Mg, EPA/DHA, kidney
botanicals)











Patient tolerating Tx well. Added Phytosterol support, Soy
Isoflavones and Yeast extract to support Krebs cycle oxidative
phosphorylation.
PSA (2/9/99) <0.1 Slt increase in nocturia after seed implants (~
3x per night)
BP improving now at 146/68. O: noted slt pansystolic murmur.
By 3/99 blood pressure down to 124-136/68-74.
Lupron tx completed 12/98. PSA 4/14/99 < 0.1. PSA 7/6/99
<0.1. PSA 10/99 <0.1. 4/00 < 0.1
Notes: high dose phytosterols creating a flush around eyes.
Decreased dose well tolerated
4/00 Health great. No infections, weight stable, energy good
9/00 Decreasing dosages on Nat Tx protocol to minimum support
12/01 PSA <0.1. Health remains good.
8/03 PSA <0.1 nocturia ~ 1x/night BP well controlled with Rx
med and Nat. Tx (Cardio HTN). Bare minimum Prostate support
3/05 PSA <0.1. (age 73) recent dx of NIDDM. Fasting BS 121,
Hgb A1C 6.3. Rx Diabetone.
9/06 PSA <0.1 (age 74) Hgb A1C 5.9%, BS 95. BP well
controlled. Mild knee arthritis (Rx ArthroGenx + Vit D1000)
PSA summary
1995
3.19
6/98 (Dx, tx begins, ext beam +
5.58
2/99 (seed implants 1/14/99)
<0.1
4/99
<0.1
7/99
<0.1
10/99
<0.1
4/2000
<0.1
12/01
<0.1
8/03
<0.1
3/05
<0.1
9/06
<0.1
Lupron) (Nat Tx starts 12/98)



Comments: Tx effective. PC cured
Nat Tx: adjunctive. Sharp decline in PSA probably
from Radiation (beam + seeds) and 3 shots of
Lupron.
Was Nat Tx needed or helpful?


Perhaps – recovered quickly from radio Tx side effects.
No infections during or after treatment for several years!
Strength and energy good. Weight stable. Patient felt ‘in
control and participating in his tx’. Don’t discount the
importance of this!
This is a case where the benefit of our tx is less obvious
but intuitively I believe that it was complementary.
Case History Prostate Cancer
#2

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



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


61 y.o. male law enforcement
April 2005 DRE exam positive for 2 hard nodules. PSA 3.55. Biopsy (+)
for PC. CT scan/Bone Scan Ø mets. Gleason score 7.
Overall health good. Exercises regularly. Dietary habits good.
Started Naturopathic Adjunctive Support 5/05
Patient elected to have local beam radiation followed by seed implants.
Started radio Tx 7/05. Staging T2b. Adjusted Gleason 5a. Seed implants
8/05.
11/05 Overall health remains good. Appetite good. Weight stable.
Experiencing some fatigue, urethritis and prostatitis sx as would be
expected following radio Tx. Vitals signs (ht, wt, bp, HEENT, Lymph,
Heart (slt irreg rhythm). Lungs Neuro, Spine, Abd are normal
1/06, 3/06 PSA 0.8 Overall health good. Urethritis and Prostatitis
resolving
2/07 Patient not seen in 11 months. Returns for f/u. Rx’d Food Pharm
Custom diet for PC. PSA 8/06 0.3, 11/06 0.39 (oncologists goal <0.5)
Bone/CT scan remain (-), Lymph nodes (-). Overall health good. Energy
good. Playing golf, racketball, cross-country skiing, and doing weight
training.. Prostatitis (-).
4/07 PSA checked in 3/07 down to 0.22. No physical health complaints
7/07 health remains good. PSA 6/07 0.20, 11/07 PSA 0.067!

PSA summary: 4/05 – 11/07


3.55 – 1.8 – 0.53 – 0.3 – 0.39 – 0.22 – 0.20 – 0.067
Additional Laboratory:





Leukopenia (specifically lymphocytopenia),
anemia (macrocytic) – near resolution
mild hyperlipidemia (215 – 222 range with HDL 70’s)
improved to ~200 TC
mild hyperglycemia (~102 fasting) improved to fasting 89
TSH (4.49, high nl with low oral/axillary temps) improved
to 1.07
Vit D (25 OH) 39 improved to 69-99 range. (excellent!)
Overall adjunctive Naturopathic care:
Lycopenes (Tomato extract), Vitamin D, EPA/DHA, DIM Pro Plus,
Melatonin 20 mg, BioInflammatory caps, TriZinc, MycoPotent
Immune drops, BioAlkalizer, Methylcobalamin/Folinic acid
(sublingual), Thyroid 60 mg, CholeLVR, UltraHematinic, UltaPure
Whey Protein. Custom Cancer Diet.
How BioGenesis Products Fit In

Primary Support: (Announcing New Support Products!)



Aromatase Inhibition (hormone mediated cancers of the breast, prostate,
ovaries, cervix, uterus):



BioCleanse powder/caps, BioInflammatory powder/caps
Additional COX 2 inhibition(if needed):


BioProstate, Intestinal Repair Complex
Additional Liver Detox Support (if needed):


MycoPotent Immune, Sterol 117, ImmunoGalactans, Liposomal Melatonin
Targeted Tissues:


Fractionated/Modified Citrus Pectin powder (5-6 grams per day total)
Secondary Support:
Immune Support:


EPA/DHA, Flax Oil
Anti-adhesion support:


DIM Pro Plus
Anti-inflammatory essential fatty acids:


Onco-X
Onco-Zymes
PainX
Pulsed Antioxidants:

OxyATP (supports Krebs Cycle)
Onco-X











Onco-X provides maximum adjunctive nutraceutical support for oncology
patients.
Onco-X functions as a multivitamin and multimineral.
Supplies amino acids, antioxidants and specialty ingredients for enhanced
cellular/cardiac energy (ATP) production and fatty acid metabolism
Antioxidant level compatible with allopathic chemotherapy and
radiotherapy treatments
Botanicals for adaptogenic support, cellular membrane support and antiinflammatory benefit
Methyl donor support via B vitamins to reduce dangerous byproducts of
protein metabolism.
Blood sugar regulatory support to aide in maintenance of healthy insulincortisol balance.
Able to individualize dosage support from light-moderate- high levels
easily.
Supports Healthy Liver Phase l and ll detoxification pathways including
Glucuronidation
Supports a healthy immune response with vitamins, minerals, botanicals,
IP-6 and Arabinogalactans.
Addresses multiple differences in normal vs. abnormal cell
physiology simultaneously.
Folinc Acid (5 formyl tetrahydrofolic acid)
Supports Oxidative
Phosphorylation to enhance
healthy cell metabolism while
simultaneously promoting
apoptosis of abnormal cell lines
with fully reacted mineral chelates
using Krebs cycle organic acids
(Citrate) and Acetic Acid.
Inhibits Isoprenylation with:
D-Limonene:
Block Isoprenylation which is
necessary for tumor cell growth
(RAS gene, Epithelial Growth
Factor, Tyrosine Kinase, InsulinLike-Growth-Factor)
Tocotrienols:
Inhibit isoprenylation via inhibition
of HMG-2, assists D-Limonene
Niacin:
Also inhibits RAS gene
Depletion of L-Glycine (Abnormal
cells need L-Glycine to synthesize
DNA)
Note: L-Glycine is essential for
abnormal cell growth and
reproduction but is a non-essential
amino acid for healthy cell
metabolism
Inhibits abnormal cell growth
and reproduction by restricting LGlycine and Vitamin B6. Pyridoxine
is a cofactor for L-Glycine
metabolism.
Inhibits abnormal cell glycolytic
energy pathways
Inhibits metastasis (spread) of
abnormal cells with anti-adhesion
properties of modified citrus pectin
and curcumin
Inhibits Angiogenesis (MMPs) to
reduce nutrient delivery to abnormal
cells and cell populations
Inhibits Kinases (critical to cancer
cell growth and reproduction) via
phosphatase activation with Vitamin
D and Curcumin
Continued
Onco-Zyme provides
enzymes for:
•anti-inflammatory
•fibrinolytic (antiencapsulation)
• circulation support
• enhanced
phagocytosis and
debris field clean up
and
• immune support
•
Activate
Mitochondrial
oxidative
phosphorylation to
induce apoptosis
(Citric and
Acetic Acids)
Inhibits Kinases
(critical to cancer
cell growth and
reproduction) via
phosphatase
activation with
Vitamin D and
Curcumin
Activate the Immune
system and
phagocytosis
Inhibit
Isoprenylation
with:
D-Limonene,
Tocotrienols,
Niacin
Additional References
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Lorincz AB, Kuttner RE. Tumor inhibition limiting amino acid diets
(Abstr.) J Am Med Assoc 1967; 200:211
Rabinowitz M. Consequences of amino acid deprivation in
combination chemotherapy. J Natl Cancer Inst 1995;87:142
John AP. Dysfunctional mitochondria, not oxygen insufficiency,
cause of cancer cells to produce inordinate amounts of lactic acid:
the impact of this on the treatment of cancer. Med Hypothesis
2001;57:429-431
Adjei Alex A. Blocking Oncogenic Ras Signaling for Cancer Therapy.
J Natl Cancer Inst 2001;93:1062-1072
Ruey Long Hong, William Spohn, Hien-Chie Hung. Curcumin
Inhibits Tyrosine Kinase Activity of p185neu and Also Depletes
p185neu1. Clin Cancer Res 1999;5:1884-1891
Khafif A Schantz SP. Quantification of chemopreventive synergism
between (-) epigallocatechin-3-gallate and curcumin in normal,
premalignant human oral epithelial cells. Carcinogenesis
1998;19:419-424.
Spitz DR. Glucose Deprivation-induced Oxidative Stress In Human
Tumor Cells. Annals of the New York Academy of Sciences.
2000;899:349-362.
•
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Warburg O., "On the Origin of Cancer Cells," Science, 1956;123: 309-14.
Broder S., Karp J., "Oncology and Hematology," JAMA, 1994;271: 1694.
Kaikobad I., Yong X., Zweier J., "Mitogaenic Signaling Mediated by Oxidants in Ras-Transformed Fibroblasts," Science, 1997; 275:14.
Folkman J., "What is the Evidence that Tumors are Angiogenesis-Dependant?" Journal of
National Cancer Institute, 1990; 82: 4-6.
Zbigniew W., Hanausek M., Sherman U., Adam A. K., "Antiproliferative Effect of Dietary
Glucarate on the Sprague-Dawley Rat Mammary Gland," Cancer Letters, 1990; 49: 51-57.
Chandrahar D., Wendy J., Heck B., Downie A. A., Sarroya L.,Webb T. E., "The Effect of
Calcium Glucarate on Glucuronidase Activity and Glucarate Content of Certain Vegetables
and Fruits,“ Biochemical Medicine and Metabolic Biology, 1990; 43: 83-92.
Ellis E. M., "Quest for New and Better Colon Cancer Treatments Picks Up Steam," Journal of
the National Cancer Institute, 1998; 90: 1858.
Niederhumber J., Brenan M. .F., Menck H., "The National Cancer Data Base Report on
Pancreatic Cancer," Cancer, 1995; 76: 1671-7.
Burk D., "Symposium on Respiratory Enzymes," Madison, WI: University of Wisconsin
Press, 1942; 235. Also - Kidd J. G., Winzler R. J., Burk D., Cancer Research,1944;4: 547.
Rabinobitz, M., "Consequences of Amino Acid Deprivation in Combination Chemo therapy,"
Journal of the National Cancer Institute, 1995; 87:142.
Brewer K. “Cancer: Its Nature and A Proposed Treatment”
http://www.mwt.net/~drbrewer/brew_art.htm
Gerson M. “A Cancer Therapy: Results of 50 Cases”, The Gerson Institute, San Diego, CA,
1990.
Kelly WD. “One Answer to Cancer”, 1999.
Kritchevsky D., "Can Reducing Caloric Intake Also Help Reduce Cancer?" Journal of the
National Cancer Institute, 1998; 90: 1766.
The End

Contact Information for Dr. David Wood:


[email protected]
[email protected]
“May your practices and your patients
be blessed by your care”