In today's world, more than ever, we are exposed to a wide variety of toxins, and the toxins are expanding daily: They're in our air, food and water, in the workplace and at home. We even generate toxins within our own bodies. Our bodies are designed to be self-cleansing and self-healing. The internal detoxification process is an automatic daily procedure of the major detoxification organs. Toxins however produce irritation and inflammation, adding to the burden of our digestive system. When our digestive system becomes overwhelmed, it is no longer able to adequately perform detoxification functions. This is a condition called "toxic overload".

Exposure to toxins results in an increased production of free radicals which over time damage or age our body tissues. Long term "toxic overload" may result in metabolic and genetic alternations that can affect cell growth, behavior and immune response. This is because the molecular structures of toxins are carcinogenic as they interact with human DNA. The World Health Organization has implicated environmental toxic chemicals in over 60 to 80 per cent of all cancer cases.

Scientists estimate that over 50 percent of U.S. residents have too much heavy metal in their bodies. These metals, which include lead, mercury, aluminum, cadmium and arsenic, are found in industrial byproducts as well as in tainted drinking water, pesticides and even things as common as dental fillings and cooking utensils. Once these chemicals are inside us, we can never fully eliminate them unless we undergo a detoxification process. As a result, most of us need some form of detoxification.

In the past, detoxification was administered to reformed alcoholics and drugs addicts, cancer patients and people with severe allergies. Today it is adopted by healthy individuals to maintain their body systems in pristine condition. Detoxification can make a big difference in optimizing the bodily functions. In fact, it might even help prevent chronic opportunistic diseases such as cancer, diabetes, chronic fatigue and arthritis. Detoxification, coupled with a healthy diet, is an essential anti-aging tool. It is one of the best ways to remain healthy in a polluted and toxic environment.

LifeSource's Heavy Metal & Toxic Cleanse contains Modified Citrus Pectin (MCP) which contains PectaSol®, a patented, low molecular weight citrus pectin that can pass through the intestinal barrier so it can work systemically.  MCP can bind to and facilitate excretion of low levels of heavy metals that commonly come from mild environmental exposure.  A recent study indicates that modified citrus pectin promotes healthy urinary excretion of common, mild environmental exposures of heavy metals such as mercury, arsenic, cadmium, lead and tin without altering excretion of other nutritional minerals, including calcium, magnesium, iron, copper and selenium.  In addition, MCP has been shown to support healthy cellular growth and reproduction.*

A commercially available supplement has been shown to inhibit cancer cell metastasis, lower cholesterol, and remove toxic metals from the body!

Signs that Detoxification is Needed:

History that may indicate Detoxification is needed:

Benefits of Detoxification:

LifeSource's Heavy Metal & Toxic Cleanse unique formula makes for a very potent detoxification support product, designed to bind with and remove heavy metals and other toxins in the body.

Modified Citrus Pectin is recommended for:

Stop taking your medicine right away and talk to your doctor if you have any of the following side effects. Your medicine may be causing these symptoms which may mean you are allergic to it.

• Breathing problems or tightness in your throat or chest
• Chest pain
• Skin hives, rash, or itchy or swollen skin

Modified Citrus Pectin

•  MODIFIED CITRUS PECTIN SLOWS PSA DOUBLING TIME: A Pilot Clinical Trial
Stephen Strum MD, Mark Scholz MD, Jon McDermed Pharm D, Michael McCulloch BA, Isaac Eliaz MD
Presented at the International Conference on Diet and Prevention of Cancer
May 28 ­ June 2, 1999
Tampere, Finland

•  ABSTRACT
The purpose of this pilot clinical trial was to evaluate the ability of Modified Citrus Pectin to influence the PSA slope in men with prostate cancer. Patients who had either relapsed after or failed prior treatment for prostate cancer (PSA range 0.63 to 7.50) were given Modified Citrus Pectin (PectaSol ® , EcoNugenics, Inc., San Rafael, CA 94901) at a dosage of 15 grams per day in three divided oral doses. PSA doubling time was calculated. A response (more than 30% lengthening of PSA doubling time) was seen in 4/7 patients (57%). One patient (1/7) had a partial response, one patient (1/7) had stable disease, and one patient (1/7) did not respond. Modified Citrus Pectin appears to lengthen the PSA doubling time in prostate cancer patients with low levels of PSA. Study responses are additionally compelling, as all study participants are still alive and evaluable for long­term follow­up almost three years after completion of this study. More research involving larger numbers of patients is needed to full), define the role of MCP in prostate cancer treatment.

•  PURPOSE
The purpose of this pilot clinical trial was to evaluate the ability of Modified Citrus Pectin to influence the PSA slope in men with prostate cancer.

•  INTRODUCTION
For prostate cancer to spread, research indicates that a clump of cells may be required rather than a single cell or a few individual cells together. The ability for cancer cells to "clump" appears to be mediated, at least in part, by carbohydrate­binding, proteins (CBP's) located on the cell surface. One such CBP is a galactoside­binding lectin or "galectin" called galectin­3.

•  In human studies involving colon, stomach and thyroid cancers, the amounts of galectin produced increased proportionally as the cancers grew from their earliest to their most advanced stages. It is reasonable to hypothesize that the higher galectin levels permit greater adhesion and clumping of cancer cells at a "target site," i.e. the site of metastasis. Thus, these lectin binding "receptors" and their ability to bind cell surface carbohydrates and glycoproteins may serve as the cement that allows cancer cells to clump and possibly bind to metastatic target sites.

•  Plant fiber derived from citrus fruit contains "citrus pectin", a highly non­branched complex polysaccharide that is rich in galactosyl (sugar carbohydrate) residues. MCP is citrus pectin that has been pH­modified into smaller, less complex molecules that dissolve much better in water and are absorbed more completely by the body when taken by mouth. MCP appears to compete with the galectin­3 receptor sites thereby interfering with cancer cell­cancer cell and cancer cell-metastatic target site interactions.

•  In a study by Pienta et al, two groups of rats serving as an animal model for human prostate cancer were injected with MAT­LyLu Dunning, R3327 rat prostate adenocarcinorna cells. (MAT­LyLu cancer cells grow more rapidly and have a greater tendency to metastasize throughout the body). Half of the rats were "controls" and were given plain drinking water, while the others were given MCP in their water at a 0.1% concentration.

•  Results from this study showed 7/14 (50%) of 0.1% MCP-treated rats developed lung, metastases, which was significantly lower in 15/16 of control animals (93.75%). When 1% MCP was studied in the same manner, lung metastases occurred in 9/16 (56.3%) of MCP­treated animals. The number of metastatic colonies in the lungs of the 1.0% MCP group (1 +/- 1) was significantly lower than in the control group (9 +/- 4).

•  The same authors later showed that MCP also reduced the ability of rat prostate adenocareinoma cells to bind to rat endothelial cells (the type of cells that form the inside lining of blood vessels) in a dose­dependent manner. In other words, with higher doses of MCP, proportionately greater reductions in cancer cell binding to endothelial cells were observed. When human prostate cancer cells metastasize, they appear to bind to the same target receptor site, i.e. galectin­3, that MCP binds with (Pienta KJ et al, J Natl Cancer Inst. 87:348-353,1995).

•  MATERIALS & DOSAGE
Modified Citrus Pectin (PectaSol ® , EcoNugenics, Inc., San Rafael , CA 94901 ) was orally administered at a dosage of 15 grams per clay in three divided doses. The study material specifications had a molecular weight (MW) of 10,000-15,000 daltons and methylation (DM) less than 10%.

•  STUDY PROTOCOL
Eligibility Requirements
1) Prostate cancer patients failing first­line androgen deprivation therapy.
2) Patients in relapse after radical prostatectomy, external beam radiation therapy, brachytherapy or cryosurgery.
3) Untreated patients, or those off Intermittent Hormone Blockade (IHB), both having low levels of PSA and a defined PSA doubling time.

•  Baseline Studies
1) CBC, chemistry panel, PSA and other tumor markers as appropriate.
2) Radiological studies pertinent to the patient's clinical stage of disease.
3) Physical examination and complete review of systems.

•  RESPONSE EVALUATION
All patients were seen in office follow­ups at least once a month. Follow­up studies included a CBC, chemistry panel, PSA and/or other tumor markers, physical examination, and a review of systems. PSA doubling time was plotted using computer software. The PSA doubling time reflects the speed at which the cancer is growing. The faster the growth, the shorter the PSA doubling time. Lengthening of the PSA doubling time represents a decrease in the rate of growth of the cancer. PSA doubling time data was evaluated at 3, 6, and 12 months intervals. A minimum of 3 months on study was required for patients to be evaluable for this study.

•  CRITERIA FOR STUDY DISCONTINUATION
Patients were discontinued from the study when there was (1) a lack of response to MCP, (2) clinical findings of progressive disease unrelated to PSA, or (3) patient intolerance to MCP.

•  RESPONSE DEFINITION
Response = More than 30% lengthening of PSA doubling time
Partial response = Less than 30% lengthening of PSA doubling time
Stable disease = Less than 50% shortening of PSA doubling time
No response = More than 50% shortening in PSA doubling time
Progression = 50% PSA increase above baseline measured on two successive monitoring, intervals, or clinical evidence for disease progression unrelated to the PSA response.

•  RESULTS
Clinical Data: MCP Results In 7 Patients With Prostate Cancer

•  1 DT = PSA Doubling Time
2 Cryo = Cryosurgery

•  DATA ANALYSIS
Seven patients were enrolled into this study and considered evaluable. A response (more than 30% lengthening of PSA doubling time) was seen in 4/7 patients (57%). All of these were patients off IHB. In one patient there was a 5.7% lengthening in his PSA doubling time (PSADT). He was thus judged to have had a partial response. One patient had a 6.7% shortening in PSADT. He was judged to have stable disease. The remaining patient had a 69.4% shortening in PSADT, and so had no response.

•  CONCLUSIONS
Modified Citrus Pectin appears to slow the PSA doubling time in prostate cancer patients with low levels of PSA. More research involving larger numbers of patients is needed to fully define the role of MCP in prostate cancer treatment. Study responses are additionally compelling, as all study participants are still alive and evaluable for long­term followup almost three years after completion of this study.

•  REFERENCES
Inohara H, et al. Effects of natural complex carbohydrate ([modified] citrus pectin) on murine melanoma cell properties related to galectin­3 functions. Glycoconj J 1994 Dec; 11(6): 527­32

•  Naik H, et al. Inhibition of in vitro tumor cell­endothelial adhesion by modified citrus pectin: a pH modified natural complex carbohydrate (Meeting abstract). Proc Annu Meet Am Assoc. Cancer Res; 36:A377 1995

•  Pienta KJ, et al. Inhibition of spontaneous metastasis in a rat prostate cancer model by oral administration of modified citrus pectin [see comments]. JNatl. Cancer Inst 1995 Mar 1; 87(5): 348­53

•  Platt D. Modulation of the lung colonization of B 16­Fl melanoma cells by [modified] citrus pectin. J Natl Cancer Inst 1992 Mar 18; 84 (6): 438­42

•  Zhu HG, et al. Activation of human monocyte/macrophage cytotoxicity by IL­2/IFN gamma is linked to increased expression of an antitumor receptor with specificity for acetylated mannose. Immunol Lett 1993 Oct; 38 (2): 111­9

•  Zhu HG, et al. Enhancement of MHC­unrestricted cytotoxic activity of human CD56+ CD3­ natural killer (NK) cells and CD3+ T cells by rhamnogalacturonan: target cell specificity and activity against NK­insensitive targets. J Cancer Res Clin Oncol 1994, 120 (7): 383­8

•  Zollner TM, et al. Induction of NK­like activity in T cells by IL­2/anti­CD3 is linked to expression of a new antitumor receptor with specificity for acetylated mannose. Anticancer Res 1993 Jul­Aug; 13(4): 923­30

Modified citrus pectin (MCP), also known as fractionated pectin, is a complex polysaccharide obtained from the peel and pulp of citrus fruits. Modified citrus pectin is rich in galactoside residues, giving it an affinity for certain types of cancer cells. Metastasis is one of the most life-threatening aspects of cancer and the lack of effective anti-metastatic therapies has prompted research on MCP's effectiveness in blocking metastasis of certain types of cancers, including melanomas, prostate, and breast cancers.

Chemistry

Modified citrus pectin powder is produced from citrus pectin via pH and temperature modification that breaks it into shorter, non-branched, galactose-rich, carbohydrate chains. These shorter chains dissolve more readily in water and are better absorbed and utilized by the body than ordinary, long-chain pectins. It is believed the shorter polysaccharide units afford MCP its ability to access and bind tightly to galactose-binding lectins (galectins) on the surface of certain types of cancer cells.[1]

Mechanism of Action

Research indicates that in order for metastasis to occur, cancerous cells must first clump together; galectins on their surface are thought to be responsible for much of this metastatic potential. Galactose-rich, modified citrus pectin has a binding affinity for galectins on the surface of cancer cells, resulting in an inhibition, or blocking, of cancer cell aggregation, adhesion, and metastasis.[1,2] Due to the life-threatening nature of metastatic cancer, most research on anti-metastatic therapies has either been in in vitro cell cultures or in animal studies. Although it is still unclear exactly how these study results translate to humans, MCP studies are promising.[3]

Clinical Indications

Prostate Cancer

Pienta et al examined modified citrus pectin's effectiveness against prostate cancer metastasis in the Dunning rat model. Rats were injected with prostate adenocarcinoma cell lines and given drinking water containing various MCP concentrations. Oral MCP did not affect primary tumor growth, but significantly reduced metastases when compared to control animals.[4] In one human study, Strum et al examined the effect of MCP on prostate specific antigen (PSA) doubling time in seven prostate cancer patients. PSA is an enzymatic tumor marker, and its doubling time reflects the speed at which the cancer is growing. Modified citrus pectin was administered orally at a dosage of 15 grams per day in three divided doses. Four of seven patients exhibited more than 30-percent lengthening of PSA doubling time. Lengthening of the doubling time represents a decrease in the cancer growth rate.[1]

Breast Cancer

As with prostate adenocarcinoma, research demonstrates metastasis of breast cancer cell lines requires aggregation and adhesion of the cancerous cells to tissue endothelium in order for it to invade neighboring tissue.[5] The anti-adhesive properties of modified citrus pectin were studied in an in vitro model utilizing breast carcinoma cell lines MCF-7 and T-47D. MCP blocked the adhesion of malignant cells to blood vessel endothelia, thus inhibiting metastasis.[6] A more recent human study examined galectin expression in 27 patients with invasive breast cancer. The study revealed that increasing histologic grades of breast cancer exhibited a decrease in galectin-3 expression, possibly resulting in increased cancer cell motility and metastasis.[7]

Melanoma

One of the better animal models for studying metastasis is the highly metastatic mouse B16-F1 melanoma. Using this system Platt and Raz determined that MCP significantly decreased tumor metastasis to the lung by more than 90 percent. In comparison, regular citrus pectin administration resulted in a significant increase (up to three-fold) in tumor metastases. The researchers concluded MCP's interference in the metastatic process might lead to a reduced ability to form tumor cell aggregates and metastases.[8]

Safety and Side Effects

Because it is a soluble fiber, administration of modified citrus pectin is unlikely to result in gastric intolerance, even at high doses. No pattern of adverse reaction has been recorded in the scientific literature. As with any dietary fiber, MCP at high doses may result in mild cases of loose stool, but this is usually self-limiting and does not warrant discontinuing treatment.

References

[1.] Strum S, Scholz M, McDermed J, et al. Modified citrus pectin slows PSA doubling time: A pilot clinical trial. Presentation: International Conference on Diet and Prevention of Cancer, Tampere , Finland . May 28, 1999 - June 2, 1999 .

[2.] Raz A, Loton R. Endogenous galactoside-binding lectins: a new class of functional cell surface molecules related to metastasis. Cancer Metastasis Rev 1987;6:433-452.

[3.] Nicolson GL. Cancer metastasis: tumor cell and host organ properties important in metastasis to specific secondary sites. Biochim Biophys Acta 1988;948:175-224.

[4.] Pienta K J, Naik H, Akhtah A, et al. Inhibition of spontaneous metastasis in a rat prostate cancer model by oral administration of modified citrus pectin. J Natl Cancer Inst 1995;87:348-353.

[5.] Glinsky VV, Huflejt ME, Glinsky GV, et al. Effects of Thomsen-Friedenreich antigen-specific peptide P-30 on beta-galactoside-mediated homotypic aggregation and adhesion to the endothelium of MDA-MB-435 human breast carcinoma cells. Cancer Res 2000;60:2584-2588.

[6.] Naik H, Pilat MJ, Donat T, et al. Inhibition of in vitro tumor cell-endothelial adhesion by modified citrus pectin: a pH modified natural complex carbohydrate. Proc Am Assoc Cancer Res 1995:36:Abstract 377.

[7.] Idikio H. Galectin-3 expression in human breast carcinoma: correlation with cancer histologic grade. Int J Oncol 1998;12:1287-1290.

[8.] Platt D, Raz A. Modulation of the lung cell colonization of B16-F1 melanoma cells by citrus pectin. J Natl Cancer Inst 1992;18:438-442.

COPYRIGHT 2000 Thorne Research Inc.
This material is published under license from the publisher through the Gale Group, Farmington Hills , Michigan . All inquiries regarding rights should be directed to the Gale Group.