oct 2012 intergrative medicine isaac eliaz
TRANSCRIPT
Principles of Integrative Oncology
Isaac Eliaz, M.D., L.Ac., M.S. Medical Director Amitabha Medical Clinic & Healing Center
Santa Rosa, CA(707) 829-5900
www.facebook.com/dreliazwww.dreliaz.org
Why Practice Integrative Oncology:An Introspective Reflection
What is Integrative Medicine?
• Integrative Medicine is a patient-driven medicine
• Integrative Medicine requires no bias, preconceived ideas or judgment
• Integrative Medicine is individualized
Integrative Medicine
Integrative Medicine
Hands on Healing
AsianMedicine
Western Medicine
Acupuncture
Nutrition
Integrating Different Points of View
Path of Knowledge & Wisdom
Asian Medicine: Time-Medicine-Life-Patterns as Roads
Diagram 1
Health and Disease
Diagram 2 Diagram 3
Health and Disease
Diagram 4
Health and Disease
Integrative Medical Oncology
From Normal Tissue to Cancer
Four
Cancer
ThreeDysplasia
TwoHyperplasia
OneNormal Tissue
History & Physical Examination
• Big Picture• Details• Flow• Timing &
Rhythms
History
• Traditional• Temperature
Distribution• Excess & Deficiencies• Relationships• Pulse Diagnosis• Tongue Diagnosis
Physical Exam
• General• Cancer Specific
Labs
• General• Circulation• Inflammation• Hormonal• Metabolic• Immune• Cancer Markers
Labs Continued
• LP(a)• CRP• Fibrinogen• Galectin-3• Homocysteine • PT/PTT• IL-8, IL-6
Circulation & Inflammation
• The more you test, the better
Cancer Markers
Testing for Prostate Cacner
• CBC• Comp Metabolic Panel• Lipid Panel• Lipo (a)• PSA Free/Total• PCA-3• PAP• Fibrinogen• Testosterone Free/Total• Dihydrotestosterone (DHT)• Estrone Sulfate• Estradiol• Total Estrogens• Progesterone
Laboratory Testing forProstate Cancer
• Prolactin• Thyroid - TSA, Others• HgA1-C• IgF-1• Fasting insulin• C-reactive protein (CRP)• Homocysteine• Urine Deoxypyridinoline (DpD)• Urine Pyridinium Crosslinks• Carcinoembryonic Antigen (CEA)• Luteinizing hormone (LH)• Galectin-3• Other testing:
• 24 hour urine hormone evaluation with estrogen metabolites
• Heavy metal urine challenge test
• Patterns of Prostate Cancer
• Physiological vs. Pathological
• Maintenance vs. Cure
• Supplements & Adjuvant Therapy
Prostate Cancer
• Grade of the Disease• Stage of the Disease• PSA• Therapeutic Surgery, Radiation,
Hormonal• Hormonal Refractory Disease• Grade & State of the Person
Prostate Cancer General Guidelines
• Biopsy• Watchful Waiting• Local Therapy• Hormonal Therapy• Androgen Independent• Advanced Disease
Prostate Cancer-Stages
• History: Risk Factors, Family History, Age, Ethnicity
• Physical Exam - Digital Rectal Exam
• PSA - Discussion• Laboratory Testing
Prostate Cancer Evaluation
• MRI• MRI-S• PET vs CT• Color Doppler
Ultrasound• Prostascint Scan• Bone Scan
Imaging General & Cancer Specific
• CBC with Differential
• IL-2• IL-6• IL-8• NK Cells
Immune
• IGF-1• Insulin• HBA1C• Cortisol• Thyroid Panel• Urine DpD• Melatonin• Others
Metabolic
• Prevention of Metastasis & Angiogenesis
• Immune Enhancement
• Hormonal & Metabolic Modulation
• Direct Cytotoxicity
• Antioxidants, Anti Inflammatory & Anti Microbial
• Detoxification
• Circulation & Hyper Viscosity Improvement
• Redifferentiation
Approaches & Strategies
Prevention of Metastasis and Angiogenesis
• A unique member of the soluble β galactoside-binding lectins
• 30 kDa chimeric protein with three domains• NH2—terminal with serine-6 phosphorylation site• A collagen like pro/gly rich domain• COOH—terminal carbohydrate recognition domain
(CRD)• CRD has strong binding affinity for galacto-
oligosaccharides
• Regulatory roles in cancer tumorigenisis and metastasis, inflammation, fibrosis, and immunologic response
• Expressed in the nucleus, cytoplasm, cell surface, and extracellular microenvironment
What is Galectin-3?
• Biologically active marker for high risk
• Unlike CRP which represents the result or “bystander” biomarker, Galectin-3 is a “culprit” biomarker
• Promotes metastasis, inflammation & fibrosis
• Predicts outcome
Galectin-3 Plays Regulatory Role in Inflammation
• Elevated Galectin-3 is directly involved in the progression of:• Cancer• Cardiovascular Disease• Chronic Hepatitis• Kidney Disease• Diabetes• Inflammation & Fibrosis• Others
Galectin-3 & Disease
Sta
rt
Year-
1
Year-
2
Year-
3
Year-
4
Year-
5
Year-
6
Year-
7
Year-
8
Year-
9
Year-
10
Year-
11
85%
90%
95%
100%
Quintile-17.7Quintile-29.4Quintile-310.9Quintile-412.6Quintile-515.6
Number of Subjects n = 7,968
Cu
mu
lati
ve S
urv
ival R
ate
(%
) Median Galectin-3
Levels
OverallAverage11.9
Galectin-3 Levels & Mortality from All Causes in the General Population: PREVEND
• In Cancer, Galectin-3 plays a role in:• Cell to Cell Adhesion• Aggregation of Cancer Cells• Tumor Growth• Metastasis• Angiogenesis• Inhibition of Apoptosis
Galectin-3 & Cancer
Blood Vessel
Blood Vessel
Modified Citrus Pectin and Galectin-3
• MCP is derived from the pith of citrus fruit peels• Complex polysaccharide fiber of repeating galacturonic acid
groups with neutral sugar side chains• Unmodified citrus pectin molecular weight 50 to 300
kiloDaltons (kDa) with esterification ~70%• Optimal biological activity: molecular weight <13 kDa with
esterification <10%, and specific structure
What is Modified Citrus Pectin (MCP) ?
• Binds to Galectin-3 molecules• Blocks aggregation of cancer cells• Blocks docking of cancer cells• Blocks interactions with
endothelium necessary for angiogenesis
Modified Citrus Pectin is a Galectin-3 Blocker
Modified Citrus PectinCancer Research
• Anti-Cancer and Anti-Metastasis• Blocking of Galectin-3 Effects• Synergistic Effect with
Chemotherapy• Protection Against Post-Radiation
Damage• Improved Quality of Life
Benefits of MCP in Cancer Treatment
• Method: MCP’s inhibition of prostate cell adhesion to endothelial cells.
0.1% and 1.0% MCP in rats’ drinking water; controls had plain water
• Results: Significant reduction in lung metastases -- 50% reduction in 0.1% group; 56% reduction in 1.0% group (P<0.03 & P<0.001).
• Conclusion: MCP acted as potent inhibitor of spontaneous prostate carcinoma metastasis.
Inhibition of Spontaneous Metastasis in a Rat Prostate Model by Oral Administration of Modified Citrus Pectin
• Pienta KJ, Naik H, Akhtar A, Yamazaki K, Replogle, TS, Lehr J, Donat TL, Tait L, Hogan V, Raz A Wayne State University School of Medicine, Detroit, MI, USAJ Natl Cancer Inst 1995 87(5):348-53.
• Method: MCP’s inhibition of breast & colon cancer progression; MCP’s interaction with Galectin-3
• Results: 70.2% Reduction in Breast Tumor Growth• Breast Angiogenesis: 66% Reduction• Breast to Lung Metastasis: 0% MCP v. 100% Control• Colon to Liver Metastasis: 0% MCP v. 60% Control• Colon to Lymph Metastasis: 25% MCP v. 100% Control
• Conclusion: MCP inhibits carbohydrate mediated tumor growth, angiogenesis & metastasis via effects on Galectin-3 function
Inhibition of Human Cancer Cell Growth & Metastasis in Nude Mice by Oral Intake of Modified Citrus Pectin
Nangia-Makker P, Hogan V, Honjo Y, Baccarini S, Tait L, Bresalier R, Raz A Wayne State University, School of Medicine, Detroit, MI, USA J Natl Cancer Inst. 2002 94(24): 1854-62.
• Method: Human vascular endothelial cell layer & PC-3 prostate cancer cells.
• Results: Strong tumor cell death response with MCP, compared to controls.
Modified Citrus Pectin Induces Cytotoxicity of Prostate Cancer Cells in Co-Culture with Human Endothelial Monolayers
Control 0.1% 1.0%0%
10%
20%
30%
40%
50%
60%
70%
80%
90%
3.8%
76.9%80.7%
% C
yto
toxi
city
Weiss T, McCulloch M, Eliaz I Amitabha Medical Clinic & Healing Center, Sebastopol, CA, USAEcoNugenics, Santa Rosa, CA, USA Intl Conference on Diet & The Prevention of Cancer 1999, Tampere, Finland.
No Response Stable Disease Response0%
10%
20%
30%
40%
50%
60%
70%
80%
14% 14%
71%
% In
cre
as
e in
PS
AD
T
• Method: MCP 15 g/day to patients with biochemical relapse post local therapy. PSA Doubling Time (PSADT) evaluated at intervals.
• Results: MCP significantly increased PSADT in prostate cancer patients.
Effect of Modified Citrus Pectin on PSA Doubling Time in Prostate Cancer Patients: A Pilot Clinical Trial
Strum S, Scholz M, McDermed J, McCulloch M, Eliaz, IProstate Oncology Specialist, Marina del Rey, CA, USAAmitabha Medical Clinic & Healing Center, Sebastopol, CA, USAEcoNugenics, Santa Rosa, CA, USA. International Conference on Diet & The Prevention of Cancer 1999, Tampere, Finland.
Patient MCP Use (Months)
PSADT Change Status
Patient 1
5 193% Response
Patient 2
6 193% Response
Patient 3
3 80% Response
Patient 4
>15 55% Response
Patient 5
6 6% P. Response
Patient 6
6 -7% Stable Disease
Patient 7
5 -69% No Response
Pilot Clinical Results: MCP’s Effect on PSA Doubling Time
• Method: 10 men with biochemical prostate cancer relapse used MCP: 15g daily for 1 year.
• Results: MCP significantly increased PSADT in 7 out of the 10 participants (p<0.01).
Modified Citrus Pectin Increases the Prostate-Specific Antigen Doubling Time in Men with Prostate Cancer: A Phase II Pilot StudyGuess BW, Scholz MC, Strum SB, Lam RY, Johnson HJ, Jennrich RI Healing Touch Oncology, Marina del Rey, CA, USA Prostate Cancer & Prostatic Disease 2003;6(4):301-4.
Pati
e..
.
Pati
e..
.
Pati
e..
.
Pati
e..
.
Pati
e..
.
Pati
e..
.
Pati
e..
.
Pati
e..
.
Pati
e..
.
Pati
en
...0%
50%
100%
150%
200%
250%
300%
350%
400%
450%
500% Post-MCP Pre-MCP
PS
AD
T a
s %
of
Pre
MC
P
*
*
*
*
* P<0.01*
968 %
*
*
Phase II Study: PSADT Results After 1 Year
Using Splines to Detect Changes in PSA Doubling TimesGuess B, Jennrich R, Johnson H, Redheffer R, Scholz M, Healing Touch
Oncology, Marin del Ray, CA, Department of Statistics, UCLA, CA, The Prostate 2003 54:88-95.
MCP
Typical Patient Results
• Method: MCP 15g daily.• Results: 49 patients with advanced solid
tumors. 29 evaluated after 2 months -- 21% showed stabilization & improvements in quality of life. • One patient w/ metastasized prostate carcinoma
showed 50% decrease in PSA, with significant increase in quality of life & decrease in pain.
• Conclusion: MCP shows clinical benefits & improvements in quality of life in advanced cancer patients.
Clinical Benefit in Patients with Advanced Solid Tumors Treated with Modified Citrus Pectin
•Azémar M, Hildenbrand B, Haering B, Heim ME, Unger C •Albert-Ludwigs-University in Freiburg, Germany•Sonnenberg-Klinik, Bad Sooden-Allendorf, Germany•Clinical Medicine: Oncology 2007 1:73–80.
• Method: 5 groups of 15 mice. MCP: 0.0%, 1.0%, 2.5% and 5.0%; and negative control. • Colon cancer cells injected into spleen except negative
control -- liver metastasis observed after 3 wks. ELISA used to detect Galectin-3.
• Results: MCP groups: Metastasis 80%, 73.3% & 60%. MCP 0.0%: Metastasis100%.
• Conclusion: MCP significantly reduced liver metastasis.
Inhibitory Effect of Modified Citrus Pectin on Liver Metastasis in a Mouse Colon Cancer ModelLiu HY, Huang ZL, Yang GH, Lu WQ, Yu NRGuangzhou Medical College, Guangzhou, ChinaWorld J Gastroenterol 2008 14(48): 7386-7391.
• Method: 1% MCP treatment of human prostate cancer cell lines (LNCaP & PC3) and mouse prostate cancer cell lines (CASP2-1 & CASP1-1)
• Results: Confirmed apoptosis and inhibition of cancer cell proliferation
4 day MCP treatment showed cytotoxicity:• 52.28% in LNCaP • 48.16% in PC3• 23.03% in CASP2-1• 49.01% in CASP1-1
PectaSol-C Modified Citrus Pectin Induces Apoptosis & Inhibition of Proliferation in Human & Mouse Androgen Dependent & Independent Prostate Cancer CellsYan J, Katz A Columbia University Medical Center, New York, NY, USA Integrative Cancer Therapies 2010 9:197-203.
• Method: 48 hour effects of PectaSol on Doxorubicin (Dox) cytotoxicity, apoptosis and cell cycle in prostate cancer cell lines.
Combination Effect of PectaSol and Doxorubicin on Viability, Cell Cycle Arrest and Apoptosis in DU-145 and LNCaP Prostate Cancer Cell Lines
Najmeh T, Houri S, Parvin M, Firouzeh B, Arash HN, Abdolfattah S, Ebrahim HTehran University, Tehran, IranCell Biology International (2012) doi:10.1042/CBI20110309.
0
60
% Viability LNCaP
0
60
% Viability DU-145
Conclusion: Lower, less toxic doses Dox needed when combined with PectaSol.
IC50 Decrease: 1.5 fold IC50 Decrease: 1.3 fold
• MCP can enhance therapeutic effect of chemotherapy drugs and treatment of chemo resistant cancers• Cisplatin (Platinol), Bortezomib
(Velcade), Dexamethasone (Decadron), Doxorubicin
• MCP use very important in preventing post chemotherapy & radiation damage• Specifically post radiation induced
inflammation and fibrosis
MCP During Chemotherapy & Radiation
• MCP Reduces:• Primary Tumor• Angiogenesis• Metastatic Process
• MCP Provides:• Blocking of Galectin-3 Effects• Synergistic Effect with Chemotherapy• Protection Against Post-Radiation
Damage• Improved Quality of Life
Summary: MCP in Cancer Treatment
Modified Citrus PectinImmune Research
• Method (Part I): Healthy human blood samples incubated with increasing doses of MCP and antibodies.
• At 24 hours samples lyzed and run on a flow cytometer. Analyzed % of activated T-cytotoxic cell, B-cells, and NK-cells; and % increase over untreated control.
Activation of Human T-Cytotoxic Cell, B-Cell, and Natural Killer (NK)-Cells and Induction of NK-Cell Activity Against K562 Chronic Myeloid Leukemia Cells with Modified Citrus Pectin
• Ramachandran C, Wilk, B, Hotchkiss, A, Eliaz, I & Melnick SJ• Dharma Biomedical, Miami, FL, USA, EcoNugenics, Santa Rosa, CA, USA
Eastern Regional Research Center, ARS, USDA, Wyndmoor, PA, USA• Department of Pathology, Miami Children's Hospital, Miami, FL, USA • BMC Complementary and Alternative Medicine 2011, 11:59.
MCP50
ug/ml
MCP100
ug/ml
MCP200
ug/ml
MCP400
ug/ml
MCP800
ug/ml
CD2/CD2R20
ul/ml
PMA10
ng/ml
0%
20%
40%
60%
80%
100%
120%
140%
160%
Incr
ease
in
T-C
yto
toxic
Cell A
cti-
vati
on
(%)
**
* *
* p < 0.05** p < 0.01
Results Part I: MCP Activates T-Cytotoxic Cells
MCP10
ug/ml
MCP20
ug/ml
MCP50
ug/ml
MCP100
ug/ml
MCP200
ug/ml
MCP400
ug/ml
MCP800
ug/ml
PWM10
ug/ml
PWM25
ug/ml
0%
200%
400%
600%
800%
1000%
1200%
Incre
ased
B-C
ell A
cti
vati
on
(%
)
** p<0.010*** p<0.001 **
***
Results Part I: MCP Increases B-Cell Activation
MCP10
ug/ml
MCP20
ug/ml
MCP50
ug/ml
MCP100
ug/ml
MCP200
ug/ml
MCP400
ug/ml
MCP800
ug/ml
IL-23.3
ng/ml
IL-26.6
ng/ml
0%
100%
200%
300%
400%
500%
600%
700%
800%
900%
1000%
Incre
ased
NK
-Cell A
cti
vati
on
(%
)
* p < 0.05** p < 0.01
**
**
* *
Results Part I: MCP Increases NK Cell Activation
• Method (Part II): NK cell ability to induce leukemia cell death analyzed by co-incubating MCP-treated lymphocytes with K562 T-cell leukemia cells.
•
• Healthy human lymphocyte samples treated with increasing doses of MCP. After 24 hours, K562 labeled. Plates returned to incubator (for 4 hrs) to induce leukemia cell death.
MCP: Induction of NK-Cell Activity Against K562 Chronic Myeloid Leukemia Cells
MCP10
ug/ml
MCP20
ug/ml
MCP50
ug/ml
MCP100
ug/ml
MCP200
ug/ml
MCP400
ug/ml
MCP800
ug/ml
0%
10%
20%
30%
40%
50%
60%
Incre
ase in
NK
Cell A
cti
vit
y
(% K
56
2 c
ell d
eath
over
un
treate
d W
BC
)
Results Part II: MCP Induces NK Cell Activity
• Induces NK Cell Activation
• Induces NK Cell Activity
• Activates T Cytotoxic Cells
• Increases B Cell Activation
MCP Immune System Benefits
Modified Citrus Pectin:Chelation & Detoxification Research
MCP Heavy Metal Elimination
• Forms stacked “egg box” structure
• Each pocket negatively charged
• Negative charge binds heavy metals
• Toxic metal trapped in the “egg box”
• Safely excreted from the body
• Methods: MCP administered for 6 days. Baseline 24 hr urine collection before MCP, and on days 1 and 6. Days 1 - 5: MCP 15 g/day & Day 6: MCP 20 g/day.
• Results: Urinary excretion of lead, mercury, cadmium & arsenic increased. Essential minerals not changed. No side effects reported.
The Effect of Modified Citrus Pectin on Urinary Excretion of Toxic ElementsEliaz I, Hotchkiss AT, Fishman ML, Rode D; Amitabha Medical Clinic & Healing Center, Sebastopol, CA, USA; Eastern Regional Research Center, ARS, USDA, Wyndmoor, PA, USA; Univer. of CA, Davis, CA, USA Phytother Res 2006 20(10):859-64.
AlAluminum
SbAntimony
AsArsenic
CDCadmium
PbLead
HgMercury
SnTin
0%
50%
100%
150%
200%
250%
300%
350%
400%
450%Day-1 Day-6
% C
han
ge f
rom
Day Z
ero
*
#
#*
#
#*
* p < .05# p < .10
The Effect of Modified Citrus Pectin on Urinary Excretion of Toxic Elements
MCP Chelation:• Increased urinary excretion of toxic
metals• Demonstrated heavy metal chelation due
to reduced molecular size & esterification• 10% rhamnogalacturonan II -- known for
binding affinity and immune enhancement
• Does not affect essential minerals• No side effects reported
MCP & Urinary Excretion of Toxins
• Method: 5g MCP 3x/day; 4-10 months. Baseline and final total mercury body burden measured using IV DMPS challenge.
• Results: All subjects showed significant decrease in mercury levels. Avg decrease: 62.17% (p=0.03). No side effects reported.
Modified Citrus Pectin Decreases Total Mercury Body Burden: Pilot Human Clinical Trial
Eliaz I, Amitabha Medical Clinic & Healing Center, Sebastopol, CA,USAEcoNugenics, Santa Rosa, CA, USA 228th ACS National Meeting, Philadelphia PA, USA. 2004.
ug Mercury /g Creatinine
Patient Number
Baseline PostIntervention Difference
Percent Change in
Mercury Burden
Duration of
Intervention(months)
Patient 1 14 4.5 9.5 67.86% 10.0
Patient 2 180 49.0 131 72.78% 4.5
Patient 3 16 9.9 6.1 38.13% 4.0
Patient 4 29 7.3 21.7 74.83% 6.5
Patient 5 22 9.4 12.6 57.27% 6.5
Mercury Body Burden Results
Patient1
10 mo
Patient2
4.5 mo
Patient3
4 mo
Patient4
6 mo
Patient5
6.5 mo
Avg0%
10%
20%
30%
40%
50%
60%
70%
80%67.90%
72.80%
38.10%
74.80%
57.30%62.17%
% Mercury Reduction from Baseline
• Results: MCP decreased total body burden in all subjects • Average decrease
62.17% (p=0.03)
• MCP is a promising systemic chelator of heavy metals that can be used on an ongoing basis
Mercury Body Burden Study
The Role of Modified Citrus Pectin as an Effective Chelator of Lead in Children Hospitalized with Toxic Lead Levels
Zhao ZY, Liang L, Fan X, Yu Z, Hotchkiss AT, Wilk BJ, Eliaz I Children’s Hospital, Zhejiang University, School of Medicine, Hangzhou, Republic of ChinaCentrax International, Inc, San Francisco, CA, USAEastern Regional Research Center, ARS, USDA, Wyndmoor, PA, USAEcoNugenics, Santa Rosa, CA, USAAltern Ther Health Med. 2008 14(4):34-8.
Patient-1
Patient-2
Patient-3
Patient-4
Patient-5
Patient-6
Patient-7
0
10
20
30
40
50
60BeforeMCP
AfterMCP
(MCP 5 grams, 3 times daily)
Blo
od
Seru
m L
ead
Con
cen-
trati
on
(u
g/d
L)
P Value = 0.0016
Lead in Blood Serum
Patient-1
Patient-2
Patient-3
Patient-4
Patient-5
Patient-6
Patient-7
0
20
40
60
80
100
120
140BeforeMCP
AfterMCP
(MCP 5 grams, 3 times daily)
Lead
Levels
(m
cg
/dL)
P Value = 0.0007
Lead in 24 Hour Urine Excretion
• Galectin-3 Blocker• Anti-Cancer• Immunity• Chelation and Detox
Summary: Benefits of Modified Citrus Pectin
Research: Synergistic Benefits of MCP
Integrative blend of33 ingredients: Vitamins, Minerals, Botanically Enhanced Medicinal Mushrooms, and Botanical Extracts
Prostate Poly Botanical Formula
ProstaCaid Induces G2/M Cell Cycle Arrest & Apoptosis in Human & Mouse Androgen-Dependent & -Independent Prostate Cancer Cells
Effects on long-term cell viability by colony formation
Effects on cell viability on androgen-dependent, LNCaP (A) & CASP 2.1 (C), & androgen-independent PC3 (B) & CASP 1.1 (D)
Yan J & Katz AE; Department of Urology, Columbia University Medical Center, New York, NY, USA. Integr Cancer Ther 2010 9:186-196.
24 hours 48 hours 72 hours
Pro
lifer
atio
n In
dex
(%
)
0
20
40
60
80
100
120 0 g/ml10 g/ml20 g/ml40 g/ml80 g/ml*
**
**
*
**
* **
Jiang, J, Eliaz, I, and Sliva, DCancer Research Laboratory Methodist Research Institute, Indianapolis, IN, USA Amitabha Medical Clinic & Healing Center, Sebastopol, CA, USA Indiana Univer. Cancer Center, Indiana Univer. School of Med., Indianapolis, IN, USA , Int J Oncol 2011 Jun;38(6):1675-82.
Suppression of Growth and Invasive Behavior of Human Prostate Cancer Cells by ProstaCaid: Mechanism of Activity
Effect of ProstaCaid on Invasive Behavior of Prostate Cancer Cells
0
20
40
60
80
100
120
0 20 40 80
Ce
ll in
vas
ion
[%
]
ProstaCaid [g/ml]
*
*
0
20
40
60
80
100
120
0 20 40 80
Cel
l mig
rati
on
[%
]
ProstaCaid [g/ml]
*
*
0
20
40
60
80
100
120
0 20 40 80
Cel
l ad
hes
ion
[%
]
ProstaCaid (g/ml)
*
*
A B
C D
uPA
0 20 40 80
ProstaCaid ( mg/ml)
1.00 0.61 0.38 0.16
uPA Density
(A) Cell adhesion. PC-3 cells were treated with ProstaCaid for 24 hours and cell adhesion to fibronectin determined.
(B) Cell migration. Cell migration was determined after 24 hours of incubation with ProstaCaid in Boyden Chambers.
(C) Cell invasion. Cell invasion was determined after 24 hours of incubation with ProstaCaid in Boyden Chambers coated with Matrigel.
(D) uPA secretion. PC-3 cells were treated for 24 hours and the expression of uPA detected in conditioned media with anti-uPA antibody by Western blot. * p<0.05
• Method: ProstaCaid in xenograft model of human hormone refractory PC3 prostate cancer - (100, 200 and 400 mg/kg).
ProstaCaid Inhibits Tumor Growth in a Xenograft Model of Human Prostate Cancer
Jiang J, Loganathan J, Eliaz I, Terry C, Sandusky GE, Sliva D; Cancer Research Laboratory, MRI, Indiana University Health, Indianapolis, IN, USA; Amitabha Medical Clinic and Healing Center, Sebastopol, CA, USA; Intern J of Oncol 2012; Doi:10.3892/ijo.2012.1344.
ProstaCaid Inhibits Tumor Growth in a Xenograft Model of Human Prostate Cancer
• Results: No effect on body weight or activity of liver enzymes (ALT, AST).• No sign of toxicity in liver, spleen, kidney,
lung and heart Inhibition of tumor volumes (1024.6±378.6 vs. 749.3±234.3, P<0.001)
• qRT-PCR analysis showed significant up regulation of expression of CDKN1A (p21) and inhibition of expression of IGF2, NR2F2 and PLAU (uPA)
• Conclusion: ProstaCaid has significant anticancer activity in vivo with no signs of toxicity.
ProstaCaid
Contains botanicals, purified biologically active nutritional compounds and botanically enhanced medicinal mushrooms
Breast Poly Botanical Formula
24 hours 48 hours 72 hours
Pro
lifer
atio
n In
dex
[%]
0
20
40
60
80
100
120 0g/ml10 g/ml20 g/ml30 g/ml40 g/ml
*
*
*
***
*
* *
*
Suppression of Proliferation & Invasive Behavior of Human Metastatic Breast Cancer Cells by Dietary Supplement BreastDefend
Jiang J, Wojnowski R, Jedinak A, Sliva D; Cancer Research Laboratory, Methodist Research Institute, Indianapolis, IN, USA Department of Medicine, Indiana University. Cancer Center, School of Med., Indiana University, Indianapolis, IN, USA. Integr Cancer Ther 2011; Jun 10 (2):192 – 200.
• Method: Highly aggressive triple negative human breast cancer cells (MDA-MB-231) implanted into the mammary gland in mice then given the formula orally (100 mg/kg of body weight for 4 weeks) for four weeks.
• Results: The formula significantly decreased tumor growth and breast to lung metastasis, and did not affect body weight or activity of liver enzymes or show any sign of toxicity in liver spleen, kidney, lung and heart tissues in mice. • The cancer metastasized to the lungs in 67 percent of controls
but only 20 percent of treated mice. The number of metastases per animal was also significantly affected by the formula.
• Down-regulation of primary tumor genes PLAU (urokinase plasminogen activator, uPA) and CXCR4 (C-X-C chemokine receptor-4).
BreastDefend Suppresses MDA-MB-231 Growth and Breast-to-Lung Metastasis in a Orthotopic Tumor Model (poster at AACR April 2012)
Jiang J, Thyagarajan-Sahu A, Loganathan J, Eliaz I, Terry C,Sandusky GE, Sliva D. Oncol Rep. 2012; 28: 1139-1145.
BreastDefend
Synergistic and Additive Effects of Modified Citrus Pectin with Two Novel Poly Botanical Compounds, in the Suppression of Invasive Behavior of Human Breast and Prostate Cancer CellsJiang J, Eliaz I, and Sliva DCancer Research Laboratory, MRI, Indiana University Health, Indianapolis, IN, USA Amitabha Med. Clinic & Healing Center, Sebastopol, CA, USADepart. of Med., and Indiana Univer. Cancer Center, Indiana Univer. School of Med., Indianapolis, IN, USA.Integr Cancer Ther. 2012 Apr 24. [Epub ahead of print]
0 10 20 40 800
20
40
60
80
100
120
Pro
life
ratio
n I
nd
ex
(%
) .
*
*
*
PC3 growth measured using MTT assay. Cells incubated for 24 hrs with ProstaCaid (ug/ml). *P < .05
ProstaCaidEffect on Proliferation of Human Prostate Cancer Cells
% M
igra
tio
n
0
20
40
60
80
100
120
P<0.01
P<0.01
P<0.01
MCP 0 0.25 0.5 1.0 0 0.25 0.5 1.0 mg/ml
ProstaCaid 10 10 10 10 g/ml
BA
The invasive behavior of PC3 evaluated using migration assay in the presence of (A) MCP (mg/mL) & (B) MCP (mg/mL) plus Prostacaid
(10 ug/mL).
ProstaCaid & MCPEffect on Migration of Human Prostate Cancer Cells
0 5 10 20 400
20
40
60
80
100
120
Pro
life
ratio
n I
nd
ex
(%)
*
*
*
BreastDefendEffect on Proliferation of Human Breast Cancer Cells
Growth of MDA-MB-231 measured using MTT assay. MDA-MB-231 cells incubated for 24 hrs with BreastDefend(ug/mL) at the indicated concentrations. *P < .05
MCP 0 0.25 0.5 1.0 0 0.25 0.5 1.0 mg/ml
BreastDefend 20 20 20 20 g/ml
% M
igra
tio
n
0
20
40
60
80
100
120
P<0.01
P<0.01
P<0.01
BA
Invasive behavior of MDA-MB-231 evaluated using migration assay in the presence of (A) MCP (mg/mL) & (B) MCP (mg/mL) plus BreastDefend (20 ug/mL).
BreastDefend & MCP
• Honokiol is a small-molecule polyphenol isolated from the genus Magnolia officinalis (Hou Po)
• Properties• Anti-Tumor• Anti-Angiogenic• Anti-Inflammatory• Anti-Anxiety• Antioxidant• Selective Pro-Oxidant• Differentiation Agent• No Appreciable Toxicity• Synergistic Anticancer Effect w/ Multiple
Chemotherapy Drugs
HonoPure (98% Honokiol)
Mechanisms of Action• Modulation of GABA receptors
• Blocks signaling in tumors with defective p53 function and activated ras by blocking activation of phospholipase D
• Induces cyclophilin D, potentiating mitochondrial permeability transition pore and causing death in cells with wild-type p53
• MTOR-1 Inhibitor
Honokiol
• Honokiol traverses the blood-brain barrier and induces apoptosis of neuroblastoma cells via an intrinsic bax-mitochondrion-cytochrome c-caspase protease pathway. Lin JW, Chen JT, Hong CY, et al. Neuro Oncol. 2012 Jan 18.
• Antimetastatic activity of honokiol in osteosarcoma. Steinmann P, Walters DK, E Arlt MJ, et al. Cancer. 2011 Sep 20. doi: 10.1002/cncr.26434.
• Honokiol arrests cell cycle, induces apoptosis, and potentiates the cytotoxic effect of gemcitabine in human pancreatic cancer cells. Arora S, Bhardwaj A, Srivastava SK, et al. PLoS One. 2011;6(6):e21573.
Selected Honokiol Cancer Research
• Honokiol produces anti-neoplastic effects on melanoma cells in vitro. Mannal PW, Schneider J, Tangada A, et al. J Surg Oncol. 2011 Sep 1;104(3):260-4.
• Honokiol radiosensitizes colorectal cancer cells: enhanced activity in cells with mismatch repair defects. He Z, Subramaniam D, Ramalingam S, Dhar A, et al. Am J Physiol Gastrointest Liver Physiol. 2011 Nov;301(5):G929-37.
• Honokiol: a promising small molecular weight natural agent for the growth inhibition of oral squamous cell carcinoma cells. Chen XR, Lu R, Dan HX, et al. Int J Oral Sci. 2011 Jan;3(1):34-42.
Selected Honokiol Cancer Research
• Apoptosis induced by Magnolia Grandiflora extract in chlorambucil-resistant B-chronic lymphocytic leukemia cells. Marin GH, Mansilla E. J Cancer Res Ther. 2010 Oct-Dec;6(4):463-5.
• Modulation of multidrug resistance p-glycoprotein activity by flavonoids and honokiol in human doxorubicin- resistant sarcoma cells (MES-SA/DX-5): implications for natural sedatives as chemosensitizing agents in cancer therapy. Angelini A, Di Ilio C, Castellani ML, et al. J Biol Regul Homeost Agents. 2010 Apr-Jun;24(2):197-205.
• Honokiol induces paraptosis and apoptosis and exhibits schedule-dependent synergy in combination with imatinib in human leukemia cells. Wang Y, Yang Z, Zhao X. Toxicol Mech Methods. 2010 Jun;20(5):234-41.
Selected Honokiol Cancer Research
Control MCP 1 mg/ml
MCP 2 mg/ml
MCP 4 mg/ml
%98 Honokiol
20um
MCP 1 mg/ml +
%98 Honokiol
20um
0102030405060708090
100%Migration of PC3 Cells
Synergistic Effect of PectaSol-C MCP & HonoPure (98% Honokiol) on PC3 Cell line Migration (Pre-Published Data)
Galectin-3 Breakthrough Research
Modified Citrus Pectin Reduces Galectin-3 Expression and Disease Severity in Experimental Acute Kidney InjuryKolatsi-Joannou M, Price KL, Winyard PJ, Long DA. Nephro-Urology Unit, UCL Institute of Child Health, London, UK PLoS ONE 2011 April 6(4): e18683.
• Background: Folic acid (FA)-induced acute kidney injury model
• Method: Mice given 1% MCP-supplemented water, or plain water, 1 week before FA injection
• Results: During initial injury phase, all FA treated mice lost weight while their kidneys enlarged secondary to renal insult• Gross changes significantly lessened in MCP group
• MCP clearly reduced renal cell proliferation
• Recovery phase:
MCP group showed decreased Galectin-3 expression with decreased renal fibrosis, macrophages, pro-inflammatory cytokine expression, and apoptosis
MCP & Kidney Injury Study
The PREVEND Study (Prevention of Renal and Vascular End-stage Disease) Presented at the European Society of Cardiology (ESC)
Congress (Aug) 2011, in Paris, France. “Galectin-3, Cardiovascular Risk Factors and Outcome in the General Population,” presented by Rudolf de Boer, MD, PhD, Associate Professor in Cardiology, University Medical Center Groningen, University of Groningen, The Netherlands.
Sta
rt
Year-
1
Year-
2
Year-
3
Year-
4
Year-
5
Year-
6
Year-
7
Year-
8
Year-
9
Year-
10
Year-
11
85%
90%
95%
100%
Quintile-17.7Quintile-29.4Quintile-310.9Quintile-412.6Quintile-515.6
Number of Subjects n = 7,968
Cu
mu
lati
ve S
urv
ival R
ate
(%
) Median Galectin-3
Levels
OverallAverage11.9
Galectin-3 Levels & Mortality from All Causes in the General Population: PREVEND
Galectin-3 in General Population: PREVEND (number of subjects = 7,968)
CHARACTERISTICMedian Gal3
TOTAL11.9
QUINTILE-17.7
QUINTILE-29.4
QUINTILE-310.9
QUINTILE-412.6
QUINTILE-515.6
P
DM% 3.6 2.3 2.3 3.1 4.3 6.1 0.000
MI 3.7 1.8 2.4 2.7 4.2 7.4 0.000
Hypertension 33.4 22.2 26.6 31.1 39.7 47.9 0.000
Stroke % 0.9 0.8 0.6 0.6 1.3 1.6 0.004
Systolic BP 129.2±20.2 125.0±18.1 126.6±19.0 128.6±19.6 131.3±20.6 134.9±22.5 0.000
Diastolic BP 74.0±9.7 72.1 ±9.4 73.3±9.8 74.1±9.6 75.2±9.8 75.4±9.8 0.000
CHARACTERISTICMedian Gal3
TOTAL11.9
QUINTILE-17.7
QUINTILE-29.4
QUINTILE-310.9
QUINTILE-412.6
QUINTILE-515.6
P
CRP1.29
[0.56-3.00]0.89
[0.39-2.16]1.04
[0.49-2.40]1.33
[0.58-2.92]1.53
[0.71-3.42]1.98
[0.85-4.28]0.000
Cholesterol 5.66±1.12 5.41±1.05 5.56±1.10 5.68±1.11 5.79±1.11 5.91±1.17 0.000
LDL 3.69±1.05 3.47±1.00 3.60±1.01 3.71±1.04 3.77±1.05 3.90±1.06 0.000
HDL1.27
[1.03+1.56]1.32
[1.07-1.62]1.28
[1.04-1.57]1.25
[1.03+1.55]1.24
[1.03-1.53]1.24
[0.99-1.52]0.000
Triglycerides1.16
[0.85-1.68]1.02
[0.75-1.43]1.11
[0.82-1.59]1.17
[0.86-1.69]1.23
[0.89-1.78]1.31
[0.95-1.92]0.000
Galectin-3 in General Population: PREVEND (number of subjects = 7,968)
Sta
rt
Year-
1
Year-
2
Year-
3
Year-
4
Year-
5
Year-
6
Year-
7
Year-
8
Year-
9
Year-
10
Year-
11
85%
90%
95%
100%
Quintile-17.7Quintile-29.4Quintile-310.9Quintile-412.6Quintile-515.6
Number of Subjects n = 7,968
Cu
mu
lati
ve S
urv
ival R
ate
(%
) Median Galectin-3
Levels
OverallAverage11.9
Galectin-3 Levels & Mortality from All Causes in the General Population: PREVEND
The COACH (Coordinating Study on Outcomes of Advising and Counseling in Heart Failure)
Multicenter, randomized, controlled trial conducted in The Netherlands. A prospective sub-study was designed to evaluate Galectin-3 in patients with chronic heart failure and define cut-off levels for subsequent validation studies.
Galectin-3 levels were measured in 582 banked EDTA-plasma samples.
COACH Galectin-3 Sub-Study Mortality from All Causes at 1 Year in Patients with CHF
< 17.8 17.8 - 25.9 > 25.90%
5%
10%
15%
20%
25%
30%
35%
40%
12.57%
19.69%
36.51%
Galectin-3 Levels (n...
% D
ied
wit
hin
36
5 D
ays
COACH Galectin-3 Sub-Study Cardiovascular Mortality or Heart Failure-Related Hospitalization at 1 Year in Patients with CHF
< 17.8 17.8 - 25.9 > 25.90%
10%
20%
30%
40%
50%
60%
18.85%
33.51%
52.38%
Galectin-3 Levels (n...% D
ea
th o
r H
F H
osp
ita
liza
tion
wit
hin
3
65
Da
ys
• DeFillipi et al, U.S. Cardiology, 7,1, 3–6 (2010) clearly indicate that circulating Galectin-3 is an important factor in fibrosis of many organs and organ systems, and that reducing circulating Galectin-3 may have an important role in remediating cardiac injury and progression to heart failure (HF).
• Similarly, Psarras et al, Eur. Heart J., April 26 (2011) demonstrate that reduction in Galectin-3 levels in the myocardium may reduce fibrosis in the heart and improve outlook.
• De Boer et al, Ann. Med., 43,1, 60–68 (2011) identify Galectin-3 as a key indicator in cardiac health.
• Shash et al, Eur J. Heart Fail., 12,8, 826–32 (2011) identify Galectin-3 levels as a key agent in heart failure through fibrosis.
• De Boer et al. Eur. J. Heart Fail., 11, 9, 811-817 (2009) link an increase in Galectin-3 expression and presence to heightened fibrosis, and heart failure. The same article links Galectin-3 to inflammation. Inflammation is the hallmark of arteriosclerosis, therefore Galectin-3 levels also contribute to coronary artery disease, peripheral artery disease, strokes, and vascular dementia.
Galectin-3 and Cardiovascular Health
• Liver disease: Associated with extensive fibrosis of the liver linked with elevated Galectin-3 levels. Reduction of Galectin-3 levels resulted in a general improvement in hepatic health, including reducing inflammation, hepatocyte injury and fibrosis. (Honsawek et al, Eur. J. Pediatr. Surg., April, 2011; Federici, J. Hepatol. 54,5,975–83, 2011).
• Gastrointestinal conditions: Reducing Galectin-3 by binding may reduce inflammation in the gut mucosa, making MCP an important agent for treatment of ulcerative colitis, non-specific colitis and ileitis, Crohn’s disease, Celiac disease, and gluten sensitivity. (Fowler et al, Cell Microbiol., 81,1,44–54, 2006).
• Type 2 Diabetes, and similar metabolic diseases: The reduction in circulating Galectin-3 levels reduced inflammation associated with these conditions. (Weigert et al, J. Endocrinol. Metab. 95, 3,1404–1411, 2010).
Research: Galectin-3 Implicated in a Wide Variety of Biological Conditions
• Test for Galectin-3 levels• Address general inflammation &
hyperviscosity• Use MCP at appropriate dosages
by:• Condition• Galectin-3 levels• Therapeutic goal
Elevated Galectin-3:What can we do?
Serum Galectin-3
TestingUSFDA approved blood test that measures Galectin-3 for Cardiovascular Disease
• Screening• Prevention• Cardiovascular • Cancer• Inflammation & Fibrosis of Various
Organs
Importance of Routine Galectin-3 Testing
Galectin-3 Levels: Reference Ranges
• Galectin-3 levels > 17.8 ng/ml are considered to be an extreme risk factor of mortality.
• Ideal levels are < 14 ng/ml in the general population.
• For cancer and cardiac patients, ideal levels are < 12 ng/ml.
• Galectin-3 levels change in 20% of population every 3 months.
• Repeated testing is important.
• Desired levels: <14.0 ng/ml
Galectin-3 Levels: General Population
• Desired levels: <12.0 ng/ml
• In progressive heart failure follow Galectin-3 levels routinely
Galectin-3 Levels: Cardiovascular Disease
• Desired levels <12.0 ng/ml
• Follow up on Galectin-3 levels routinely every 3-6 months
Galectin-3 Levels: Cancer
• Levels <14.0 ng/mlMCP 5g daily
• Levels = 14.0 - 17.8 ng/ml
MCP 10g daily• Levels >17.8 ng/ml
MCP 15g daily
No Known Medical Conditions
• Levels < 12.0 ng/mlMCP 5g daily
• Levels = 12.0 – 17.8 ng/mlMCP 10g daily
• Levels >17.8 ng/mlMCP 15g daily
Cardiovascular, Hepatitis, Fibrosis & Inflammatory Diseases:
• Levels <17.8 MCP 15g daily
• Levels >17.8MCP 20 - 25g daily
Active Cancer
• Levels < 12.0 ng/mlMCP 5g daily
• Levels = 12.0 – 14.0 ng/mlMCP 10g daily
• Levels = 14.0 – 17.8 ng/mlMCP 15g daily
• Levels >17.8 ng/mlMCP 20 – 25g daily
Cancer Long Term Maintenance(3 years post therapy)
Galectin-3 Levels: MCP Dosage (grams)
Galectin-3 Test
Results(ng/ml)
No Known Medical
Conditions
Cardiovascular,
Inflammation, Fibrosis, Hepatitis
Active Cancer
PostCancer
(3 years)
<12 5 5 15 5
12.0 – 14.0 5 10 15 10
14.0 – 17.8 10 15 15 15
> 17.8 15 20 20 - 25 20 - 25
Not Tested 5 15 15 5 -10
• Galectin-3 is a novel, active biomarker that is both a cause of multiple diseases and a diagnostic and prognostic biomarker.
• Modified Citrus Pectin is the only proven natural Galectin-3 blocker.
In Conclusion: Galectin-3 and Modified Citrus Pectin
Immune Enhancement
• Medicinal Mushrooms
• Modified Citrus Pectin
• Honokiol
• Botanicals - Astragulus, Eleutherococcus, Others
• BCG (Bacillus Calmette-Guérin) Vaccine
Immune Enhancement
Immune Modulation with Medicinal Mushrooms
How do Medicinal Mushrooms Work?
• Multicolored polypore found in USA, Europe and China
• Active constituents include PSK, PSP, Beta-1, 4-Glucans, Sterols
• Uses: anti-cancer, genital herpes, HIV, hepatitis B, respiratory infections
Coriolus versicolor (Turkey Tails)
• Polypore with a hard, woody, shiny, varnished appearance. Found worldwide
• Active constituents include alkaloids, polysaccharides, Beta-D glucans, sterols, others
• Uses: Adaptogenic, anti-cancer, immune support, post radiation fibrosis
Ganoderma lucidum(Reishi)
Ten Mushroom Formula®
MycoPhyto Complex: Botanically Enhanced Mushroom Complex
Novel Medicinal Mushroom Blend Suppresses Growth & Invasiveness for Human Breast Cancer Cells
Jiang J, Sliva D.Cancer Research Laboratory, Methodist Research Institute, Indianapolis, IN, USA, Department of Medicine, Indiana University Cancer Center, School of Medicine, Indiana University, Indianapolis, IN, USA. Int J Oncol. 2010 Dec;37(6):1529-36.
Effect of MycoPhyto Complex on the growth of breast cancer cells. MDA-MB-231 cells were treated with MycoPhyto Complex (0 - 0.5 mg/ml) for 24, 48 and 72 hours. (A) Cell proliferation. Data are the means ± SD of triplicate determinations. * p<0.05
(A) Cell adhesion. MDA-MB-231 cells were treated with MC (0-0.5 mg/ml) for 24 hours and cell adhesion to vitronectin. (B) Cell migration. Cell migration was determined after 5 hours of incubation in the presence of MC (0-0.5 mg/ml) in Boyden Chambers. (C) Cell invasion. Cell invasion was determined after 24 hours of incubation in the presence of MC (0-0.5 mg/ml) in Boyden Chambers coated with Matrigel.
Effect of MycoPhyto Complex (MC) on the secretion of uPA and expression of CXCR4 and COX-2 in breast cancer cells. (A) MDA-MB-231 cells were treated with MC (0-0.5 mg/ml) for 24 h, and the secretion of uPA detected in conditioned media with anti-uPA antibody by Western blot analysis. The results are representative of three separate experiments. (B) MDA-MB-231 cells were treated as described in (A), and the expression of CXCR4, COX2 and ß-actin was determined. The results are representative of three separate experiments.
• MycoPhyto Complex (MC) demonstrated inhibition of cell proliferation & cell cycle arrest at G2/M phase of highly invasive human breast cancer cells MDA-MB-231.
• DNA-microarray analysis revealed that MC inhibits expression of cycle regulatory genes (ANAPC2, ANAPC2, BIRC5, Cyclin B1, Cyclin H, CDC20, CDK2, CKS1B, Culin 1, E2F1, KPNA2, PKMYT1 and TFDP1).
• MC suppressed metastatic behavior by the suppression of cell adhesion, cell migration & cell invasion.
• The potency of MC to inhibit invasiveness of breast cancer cells is linked to the suppression of secretion of the urokinase plasminogen activator (uPA).
Summary
Hormonal & Metabolic Modulation
• Botanicals• Curcumin (Turmeric Root Extract),
Ellagic Acid (Pomegranate Extract), Indoles (DIM), Others
• Honokiol (Magnolia Bark Extract)• Metformin• Dicloroacetate (DCA)• pH Manipulation• 3BP, 2DG
Hormonal & Metabolic Modulation
Krebs Cycle
Regulation of Cancer Cell Metabolism
Tumor Suppressor Genes
Direct Cytotoxicity
• Curcumin
• Green Tea Extracts
• Ban Zhi Lian (Scutellariae barbatae)
• Artemisinin
• MCP
• Honokiol
• MCP + Honokiol
• Others
Direct Cytotoxicity
Antioxidants, Anti Microbials, Anti Inflammatory
• Herbs• Pygeum, Curcumin (Turmeric Root Extract), Others
• Zinc
• Selenium
• Lycopene
• Quercetin
• Resveratrol
• Padma Basic (Tibetan Herbal Formula)
• Honokiol, Others
Antioxidants, Anti Microbials, Anti Inflammatory
Circulation andHyperviscosity Improvement
• Aspirin
• Clopidogrel
• LMW Heparin
• Nattokinase
• Lumbrokinase
• Botanicals
• Exercise
Medications & Supplements
Detoxification& Cancer
• What are You Detoxifying and Why?
What is Detoxification?
• Primary Gentle Safe Chelation• Modified Citrus Pectin• Alginates (from Kelp Seaweed)
• Secondary Herbal and Sulfur Containing Agents • Cilantro leaf extract (Coriandrum sativum)• Garlic bulb extract (Allium sativum)• Milk thistle seed extract (Silybum marianum)• N-Acetyl Cysteine (NAC)• Methylsulfonylmethane (MSM)• Alpha-Lipoic Acid
Detoxification
• Heavy metals such as lead, mercury, arsenic, cadmium, tin & aluminum propagate free-radical reactions and as a result suppress the immune system, and DNA adducts that result in mutations which can lead to cancer.
• The removal of toxins can allow the body to self-repair & to respond more favorably to traditional therapies when fighting the progression of chronic disease.
How Can Safe Natural Chelation and Detoxification Treat Cancer & Chronic Disease?
• Understand the difference between drainage and elimination and how to support both
• Initial preparation - assessment, strategy & planning with emphasis on seasonal timing
• Utilize appropriate support structure and tools
• Construct realistic goals and proceed slowly
• Follow up program:• Maximize benefits of detoxification• Smooth transition after detoxification
• Freedom - the concept of loosening our grip:• Mentally/Emotionally/Spiritually: supports overall detox• Physiologically: releasing the toxins from organs & tissues• Grasping & letting go• Expanding while detoxifying
Detox Principles & Philosophy
• Start by chelating from the blood & GI Tract using targeted nutrients and therapies
• Once “total body burden” has decreased, enhance chelation & add organ specific detoxification
• Avoid fasting and radical low protein diets
• Support body’s vitality and energy
• Minimize side effects & aggravations
• Gentle & gradual chelation is almost always preferable
Chelation GuidelinesA Multi-Step Graduated Program
• Drainage vs. Elimination
• Drainage- from the organ/matrix to the circulation system
• Elimination- From the circulation system out via the GI Tract, urination, breathing (lungs), skin, & other excretions
Detoxification Pathways
• Liver as the Starting Point
• Follow Circulation
• Lungs
• Heart / Brain
• Gastrointestinal Tract
• Systemic - Joints, etc.
• Elimination or… back to the Liver or Other Tissues
The Detoxification Cycle
• Diet
• Nutritional Supplements
• Botanicals
• Acupuncture & Moxibustion
• Heat therapies - Infra Red Saunas
• Purging - Colonics, Enemas, Washes
• Intra venous Therapies
• Lymph Drainage
Tools in Detoxification
Safe Natural Chelation
• Modified Citrus Pectin / Alginate Complex
• Medicinal Mushrooms - Balanced, Multi-Nutrient Type Formulations
• Alpha Lipoic Acid, Sulfured Amino Acids, Selenium, Vitamin C, Others
• Digestive Support - Herbs, Enzymes, Probiotics
Detoxification-Supplements
• Define your Goals - Patient & Practitioner
• Proper Timing
• Multi Faceted Program
• Post Detoxification Follow Up
• Repeat Cleanse During Spring & Fall
• Evaluate Success - Physical, Emotional & Mental / Psychological / Spiritual
Detoxification Summary
Redifferentiation
• Vitamin D3• Sodium Phenyl Butyrate (SPB)• Honokiol
Redifferentiation
• Key Principles• Integrating patient wellness with
fighting and preventing cancer• Keep treatment dynamic & changing• Things forever change - there are
always choices
Summary
