1. Modified Citrus Pectin & Galectin-3
The Role of Modified Citrus Pectin and Galectin-3 in the Prevention and Treatment of Metastatic Cancer

2. Galectin-3 & Disease
Elevated Galectin-3 in the body is directly involved in:
Cancer
Cardiovascular Disease
Chronic Hepatitis
Kidney Disease
Diabetes
Inflammation & Fibrosis
Others

3. Galectin-3 Levels & Mortality from All Causes in the General Population: PREVEND
Overall
Average
11.9

4. Galectin-3 & Cancer In Cancer, Galectin-3 plays a role in:
Cell to Cell Adhesion
Aggregation of Cancer Cells
Tumor Growth
Metastasis
Angiogenesis
Inhibition of Apoptosis

6. Blood Vessel

7. Blood Vessel

11. What is Modified Citrus Pectin (MCP) ?
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

12. Modified Citrus Pectin is a Galectin-3 Blocker
Binds to Galectin-3 molecules
Blocks aggregation of cancer cells
Blocks docking of cancer cells
Blocks interactions with endothelium necessary for angiogenesis

13. Modified Citrus Pectin Cancer Research

14. Benefits of MCP in Cancer Treatment
Anti-Cancer and Anti-Metastasis
Blocking of Galectin-3 Effects
Synergistic Effect with Chemotherapy
Protection Against Post-Radiation Damage
Improved Quality of Life

15. 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, USA J Natl Cancer Inst (5):
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).

16. 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, USA J Natl Cancer Inst (5):
Conclusion: MCP acted as potent inhibitor of spontaneous prostate carcinoma metastasis.

17. 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 (24):
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

18. 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 (24):
Conclusion: MCP inhibits carbohydrate mediated tumor growth, angiogenesis & metastasis via effects on Galectin-3 function

19. Modified Citrus Pectin Induces Cytotoxicity of Prostate Cancer Cells in Co-Culture with Human Endothelial Monolayers
Weiss T, McCulloch M, Eliaz I Amitabha Medical Clinic & Healing Center, Sebastopol, CA, USA EcoNugenics, Santa Rosa, CA, USA Intl Conference on Diet & The Prevention of Cancer 1999, Tampere, Finland.
Method: Human vascular endothelial cell layer & PC-3 prostate cancer cells.
Results: Strong tumor cell death response with MCP, compared to controls.

20. 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, I
Prostate Oncology Specialist, Marina del Rey, CA, USA
Amitabha Medical Clinic & Healing Center, Sebastopol, CA, USA
EcoNugenics, Santa Rosa, CA, USA. International Conference on Diet & The Prevention of Cancer 1999, Tampere, Finland.
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.

21. Pilot Clinical Results: MCP’s Effect on PSA Doubling Time
Patient
MCP Use (Months)
PSADT Change
Status
Patient 1 5
193%
Response
Patient 2 6
Patient 3 3
80%
Patient 4
>15
55%
Patient 5 6%
P. Response
Patient 6
-7%
Stable Disease
Patient 7
-69%
No Response

22. Modified Citrus Pectin Increases the Prostate-Specific Antigen Doubling Time in Men with Prostate Cancer: A Phase II Pilot Study
Guess 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.
Method: 10 men with biochemical prostate cancer relapse used MCP: 15g daily for 1 year.

23. Modified Citrus Pectin Increases the Prostate-Specific Antigen Doubling Time in Men with Prostate Cancer: A Phase II Pilot Study
Guess 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.
Results: MCP significantly increased PSADT in 7 out of the 10 participants (p<0.01).

24. Phase II Study: PSADT Results After 1 Year
968 % * *

25. Using Splines to Detect Changes in PSA Doubling Times
Guess B, Jennrich R, Johnson H, Redheffer R, Scholz M, Healing Touch Oncology, Marin del Ray, CA, Department of Statistics, UCLA, CA, The Prostate :88-95.

26. Typical Patient Results
MCP

27. 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 :73–80.
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.

28. 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 :73–80.
Conclusion: MCP shows clinical benefits & improvements in quality of life in advanced cancer patients.

29. Inhibitory Effect of Modified Citrus Pectin on Liver Metastasis in a Mouse Colon Cancer Model
Liu HY, Huang ZL, Yang GH, Lu WQ, Yu NR
Guangzhou Medical College, Guangzhou, China
World J Gastroenterol (48):
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%.

30. Conclusion: MCP significantly reduced liver metastasis.
Inhibitory Effect of Modified Citrus Pectin on Liver Metastasis in a Mouse Colon Cancer Model
Liu HY, Huang ZL, Yang GH, Lu WQ, Yu NR
Guangzhou Medical College, Guangzhou, China
World J Gastroenterol (48):
Conclusion: MCP significantly reduced liver metastasis.

31. PectaSol-C Modified Citrus Pectin Induces Apoptosis & Inhibition of Proliferation in Human & Mouse Androgen Dependent & Independent Prostate Cancer Cells
Yan J, Katz A
Columbia University Medical Center, New York, NY, USA
Integrative Cancer Therapies :
Method: 1% MCP treatment of human prostate cancer cell lines (LNCaP & PC3) and mouse prostate cancer cell lines (CASP2-1 & CASP1-1)

32. 4 day MCP treatment showed cytotoxicity:
PectaSol-C Modified Citrus Pectin Induces Apoptosis & Inhibition of Proliferation in Human & Mouse Androgen Dependent & Independent Prostate Cancer Cells
Yan J, Katz A
Columbia University Medical Center, New York, NY, USA
Integrative Cancer Therapies :
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

33. 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 H Tehran University, Tehran, Iran Cell Biology International (2012) doi: /CBI
Method: 48 hour effects of PectaSol on Doxorubicin (Dox) cytotoxicity, apoptosis and cell cycle in prostate cancer cell lines.
IC50 Decrease: 1.5 fold
IC50 Decrease: 1.3 fold

34. 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 H Tehran University, Tehran, Iran Cell Biology International (2012) doi: /CBI
Conclusion: Lower, less toxic doses Dox needed when combined with PectaSol.

35. MCP During Chemotherapy & Radiation
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

36. Summary: MCP in Cancer Treatment
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

37. Modified Citrus Pectin Immune Research

38. MCP Immune System Benefits
Modified Citrus Pectin:
Induces NK Cell Activation
Induces NK Cell Activity
Activates T Cytotoxic Cells
Increases B Cell Activation

39. 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.
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.

40. Results Part I: MCP Activates T-Cytotoxic Cells** * *

41. Results Part I: MCP Increases B-Cell Activation
*** **

42. Results Part I: MCP Increases NK Cell Activation** ** * *

43. MCP: Induction of NK-Cell Activity Against K562 Chronic Myeloid Leukemia Cells
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.

44. Results Part II: MCP Induces NK Cell Activity

45. Modified Citrus Pectin: Chelation & Detoxification Research

46. 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

47. The Effect of Modified Citrus Pectin on Urinary Excretion of Toxic Elements
Eliaz I, Hotchkiss AT, Fishman ML, Rode D; Amitabha Medical Clinic & Healing Center, Sebastopol, CA, USA; Eastern Regional Research Center, ARS, USDA, Wyndmoor, PA, USA; UC, Davis, CA, USA Phytother Res (10):
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.

48. The Effect of Modified Citrus Pectin on Urinary Excretion of Toxic Elements
Eliaz 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 (10):
Results: Urinary excretion of lead, mercury, cadmium & arsenic increased. Essential minerals not changed. No side effects reported.

49. The Effect of Modified Citrus Pectin on Urinary Excretion of Toxic Elements#
* p < .05
# p < .10 # # * * * #

50. MCP & Urinary Excretion of Toxins
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

51. Modified Citrus Pectin Decreases the Total Body Burden: A Pilot Human Clinical trial
Eliaz I. Amitabha Medical Clinic & Healing Center, Sebastopol, California, USA.
EcoNugenics, Santa Rosa, California, USA.
228th ACS National Meeting, Philadelphia, PA
Methods: Oral intake 5 g Modified Citrus Pectin/3x day for 4-10 months. Base line body burden and change measured with DMPS challenge (250mg i.v. followed by 6 hr. urine collection).
Results: All subjects showed significant decrease in Mercury levels. Average decrease was 62.17%, ranging between 38.13% & 74.83% (p=0.0313).
No significant side effects were noted.

52. Study Conclusion Percent Reduction in Mercury from Baseline
MCP was effective in decreasing the total body burden of Mercury in all subjects.
MCP is a promising systemic gentle chelator of heavy metals that can be used on an on going basis.
10 months
4.5 months
4 months
6 months
6.5 months
MCP Intervention Individual Results

53. 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 China
Centrax International, Inc, San Francisco, CA, USA
Eastern Regional Research Center, ARS, USDA, Wyndmoor, PA, USA
EcoNugenics, Santa Rosa, CA, USA
Altern Ther Health Med (4):34-8.

54. Lead in Blood Serum
P Value =

55. Lead in 24 Hour Urine Excretion
P Value =

56. Synergistic Benefits of MCP

57. Prostate Poly Botanical Formula
Integrative blend of 33 ingredients: Vitamins, Minerals, Botanically Enhanced Medicinal Mushrooms, and Botanical Extracts

58. ProstaCaid Induces G2/M Cell Cycle Arrest & Apoptosis in Human & Mouse Androgen-Dependent & -Independent Prostate Cancer Cells
Yan J & Katz AE; Department of Urology, Columbia University Medical Center, New York, NY, USA. Integr Cancer Ther :
Effects on cell viability on androgen-dependent, LNCaP (A) & CASP 2.1 (C), & androgen-independent PC3 (B) & CASP 1.1 (D)
Effects on long-term cell viability by colony formation

59. Effect of ProstaCaid on Invasive Behavior of Prostate Cancer Cells
(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 D
uPA Density
uPA
ProstaCaid ( mg/ml)
(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
(C) Cell invasion. Cell invasion was determined after 24 hours of incubation with ProstaCaid in Boyden Chambers coated with Matrigel.

60. 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 ±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.

61. Prostate Polybotanical Formula

62. Breast Polybotanical Formula
Contains botanicals, purified biologically active nutritional compounds and botanically enhanced medicinal mushrooms

63. 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.

64. BreastDefend Suppresses MDA-MB-231 Growth and Breast-to-Lung Metastasis in a Orthotopic Tumor Model
Jiang J, Thyagarajan-Sahu A, Loganathan J, Eliaz I, Terry C,
Sandusky GE, Sliva D. Oncol Rep. 2012; 28:
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 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% 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).

65. Breast Polybotanical Formula

66. Synergistic and Additive Effects of Modified Citrus Pectin with Two Novel Polybotanical Compounds, in the Suppression of Invasive Behavior of Human Breast and Prostate Cancer Cells
Jiang J, Eliaz I, and Sliva D. Cancer Research Laboratory, MRI, Indiana University Health, Indianapolis, IN, USA
Amitabha Med. Clinic & Healing Center, Sebastopol, CA, USA
Depart. of Med., and Indiana Univer. Cancer Center, Indiana Univer. School of Med., Indianapolis, IN, USA.
Integr Cancer Ther March 12 (2):

67. Prostate Polybotanical Formula*
Effect on Proliferation of Human Prostate Cancer Cells
PC3 growth measured using MTT assay. Cells incubated for 24 hrs with ProstaCaid (ug/ml). *P < .05

68. Effect on Migration of Human Prostate Cancer Cells
Prostate Formula & MCP
Effect on Migration of Human Prostate Cancer Cells
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). B A

69. Breast Polybotanical Formula
Effect 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

70. Breast Formula & MCP
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). B A

71. Modified Citrus Pectin Published Data Summary
Preclinical and Clinical Research Highlights on Modified Citrus Pectin

72. Preclinical Studies with MCP (17 Published Articles)
In vitro (Type of Cancer)
In vivo (Type of Cancer)
Ex vivo (Type of Cancer)
5 (Prostate*)
2 (Prostate) including 1 Lung Metastasis Study
1 (Immune; Leukemia)
2 (Breast*,**)
2 (Breast*,**) including 1 Lung Metastasis Study
1 (Angiosarcoma & Hemangiosarcom)
1 (Melanoma***)
1 (Melanoma***) including 1 Lung Metastasis Study
3 (Colon**) including 1 Lymph and 1 Liver Metastasis Study
 1 (Non Cancer; Small Intestine Permeability)
2 (Non Cancer; Kidney Injury, Arteriole Fibrosis)
9 Total
10 Total
2 Total
*One in vitro study reported on both prostate and breast cancer (Glinskii OV, Huxley VH, Glinsky GV. et al. Neoplasia. 2005;7(5): ). **One article reported two in vivo studies and one in vitro study (Nangia-Makker P, Hogan V, Honjo Y, et al. J Natl Cancer Inst Dec 18;94(24): ). ***One articles reported both an in vivo and an in vitro study (Platt D, Raz A. J Natl Cancer Inst Mar;84(6):438-42)

73. Seven Clinical Studies with MCP
Human Clinical Study (Number of Participants)
Type of Trial
Results
Zhoa, et al., Altern Ther Health Med (n = 7)
Pilot trial: Lead toxicity in hospitalized children ages 5-12
Very significant decrease in blood serum levels of lead (P = .0016) and very significant increase in 24-hour urine collection (P = .0007). No adverse effects.
Azémar, et al., Clinical Medicine: Oncology (n = 49)
Pilot trial: To assess the quality of life, clinical benefit and antitumoral efficacy in advanced stage solid tumors (colorectal, prostate, breast, kidney, cervix/uterine, liver, pharynx, pancreatic, melanoma, stomach, bile duct carcinoma and chondrosarcoma)
22.5% patients showed a stable disease (SD) and 12.3% patients had a SD for a period longer than 24 weeks. One patient with metastasized prostate carcinoma showed a 50% decrease in serum PSA level after 16 weeks of treatment associated with a significant increase of clinical benefit, quality of life and decrease in pain. 20.7% patients had an overall clinical benefit response associated with a stabilization or improvement of life quality. All patients tolerated the therapy well without any severe adverse events.
Eliaz, et al. Forsch Komplementmed (n = 5)
Case studies: Involving lowering of lead and mercury body burden
5 case studies presented show reduction in toxic heavy metals was achieved without side effects. Gradual decrease of total body burden is believed to have played an important role in recovery and health maintenance.

74. Human Clinical Study (Number of Participants) Type of Trial Results
Eliaz, et al. Phytother Res (n = 8)
Pilot trial: Toxic heavy metal removal in healthy population
In the first 24 hours the urinary excretion of arsenic increased significantly (p < 0.05). On day 6, urinary excretion was increased significantly for cadmium (p < 0.05). Lead showed a dramatic increase in excretion (p < 0.08), and mercury approached significance on day six. Other elements analyzed including essential elements did not show any significant change in excretion.
Eliaz. 228th Annual American Chemistry Meeting. August (n = 5)
Pilot trial: Decrease total body burden of mercury
A significant decrease in total body mercury burden was seen in all participants. The decrease was found more significant over time. The mercury burden for the group dropped 68.32% (p=0.0313). All individual completed the study, and there were no side effects reported.
Guess, et al. Prostate Cancer Prostatic Dis (n = 13)
Phase II pilot trial: Lengthening of PSA doubling time in biochemical relapsed prostate cancer patients.
There were no serious side effects in any patient, but three patients withdrew from the study due to abdominal cramping or diarrhea. MCP was well tolerated by the remaining 10 evaluable patients. Seven (70%) of these evaluable patients had a significantly increased doubling time of PSA compared with their times before the treatment.
Strum, et al. International Conference on Diet and Prevention of Cancer. May (n = 7)
Pilot Study: Lengthening of prostate-specific antigen doubling time in biochemical relapsed prostate cancer patients.
PSA doubling time was lengthened by more than 30% in 4/7 (57%) of patients. One patient had a partial response, one patient had stable disease, and one patient did not respond. No adverse effects were reported.

75. The role of active biomarker galectin-3 in chronic disease progression
Galectin-3 Research
The role of active biomarker galectin-3 in chronic disease progression

76. The PREVEND Study (Prevention of Renal and Vascular End-stage Disease)
de Boer RA, van Veldhuisen DJ, R. T. Gansevoort RT, et al. The fibrosis marker Galectin-3 and outcome in the general population. J Intern Med doi: /j x. University of Groningen, Groningen, The Netherlands

77. Galectin-3 Levels & Mortality from All Causes in the General Population: PREVEND
Overall
Average
11.9

78. Galectin-3 in General Population: PREVEND (number of subjects = 7,968)
CHARACTERISTIC
Median Gal3
TOTAL
11.9
QUINTILE-1
7.7
QUINTILE-2
9.4
QUINTILE-3
10.9
QUINTILE-4
12.6
QUINTILE-5
15.6 P
DM%
3.6
2.3
3.1
4.3
6.1
0.000 MI
3.7
1.8
2.4
2.7
4.2
7.4
Hypertension
33.4
22.2
26.6
31.1
39.7
47.9
Stroke %
0.9
0.8
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
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

79. Galectin-3 in General Population: PREVEND (number of subjects = 7,968)
CHARACTERISTIC
Median Gal3
TOTAL
11.9
QUINTILE-1
7.7
QUINTILE-2
9.4
QUINTILE-3
10.9
QUINTILE-4
12.6
QUINTILE-5
15.6 P
CRP
1.29
[ ]
0.89
[ ]
1.04
[ ]
1.33
[ ]
1.53
[ ]
1.98
[ ]
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
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
HDL
1.27
[ ]
1.32
[ ]
1.28
[ ]
1.25
[ ]
1.24
[ ]
[ ]
Triglycerides
1.16
[ ]
1.02
[ ]
1.11
[ ]
1.17
[ ]
1.23
[ ]
1.31
[ ]

80. 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.

81. COACH Galectin-3 Sub-Study Mortality from All Causes at 1 Year in Patients with CHF

82. COACH Galectin-3 Sub-Study Cardiovascular Mortality or Heart Failure-Related Hospitalization at 1 Year in Patients with CHF

83. Galectin-3 and Cardiovascular Health
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, (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.

84. Modified Citrus Pectin Reduces Galectin-3 Expression and Disease Severity in Experimental Acute Kidney Injury
Kolatsi-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.

85. MCP & Kidney Injury Study
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

86. Galectin-3 Mediates Aldosterone-Induced Vascular Fibrosis
Calvier L, Miana M, Reboul P, et al.
Arterioscler Thromb Vasc Biol Jan;33(1):67-75.

87. Aldosterone Galectin-3 MCP Vascular Fibrosis Study
Background: Aldosterone is involved in arterial stiffness and heart failure. Galectin-3 plays an important role in inflammation, fibrosis, and heart failure. MCP blocks Galectin-3
Methods and Results: Rats were treated with aldosterone combined with MCP for 3 weeks. Hypertensive aldosterone-treated rats presented vascular hypertrophy, inflammation, fibrosis, and increased aortic Gal-3 expression. Those also treated with MCP treatment abolished all the above effects.
Conclusion: Galectin-3 is required for inflammatory and fibrotic responses to aldosterone in vascular smooth muscle cells in vitro and in vivo. By inhibiting Galectin-3, MCP prevents vascular fibrosis.

88. Elevated Galectin-3: What can we do?
Test for Galectin-3 levels
Address general inflammation & hyperviscosity
Use MCP at appropriate dosages by:
Condition
Galectin-3 levels
Therapeutic goal

89. Serum Galectin-3 Testing USFDA approved blood test that measures Galectin-3 for Cardiovascular Disease

90. 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.

91. Galectin-3 Levels: Cancer
Desired levels <12.0 ng/ml
Follow up on Galectin-3 levels routinely every 3-6 months

92. Active Cancer Levels <17.8, or not tested MCP 15g daily
Levels >17.8 MCP g daily
Put MCP Table in

93. Cancer Long Term Maintenance (3 years post therapy)
Levels < 12.0 ng/ml MCP 5g daily
Levels = 12.0 – 14.0 ng/ml
MCP 10g daily
Levels = 14.0 – 17.8 ng/ml
MCP 15g daily
Levels >17.8 ng/ml
MCP 20 – 25g daily
Put MCP Table in

94. Galectin-3 Levels: MCP Dosage (grams)
Galectin-3 Test Results
(ng/ml)
No Known Medical Conditions
Cardiovascular, Inflammation, Fibrosis, Hepatitis
Active Cancer
Post Cancer (3 years)
<12 5 15
12.0 – 14.0 10
14.0 – 17.8
> 17.8 20
Not Tested
5 -10

95. In Conclusion: Galectin-3 and Modified Citrus Pectin
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 a proven natural Galectin-3 blocker.