What is Modified Citrus Pectin,MCP,an inhibitor of cancer metastasis and its wide uses?

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How MCP Works as a Gentle Chelator?.

Modified Citrus Pectin MCP photo picture image Pectins are natural gelling agents, binders, thickeners, and stabilizers in foods. They mostly consist of galacturonic acid and galacturonic-acid methyl esters with average molecular weights from 50,000 to 150,000 daltons. High-methoxy (HM) pectin has at least 50% DE (degree of esterification) or greater, while a low-methoxy (LM) pectin?s DE is 50% or less. For systemic chelation of heavy metals, pectin is modified to a low molecular weight, and low-methoxy content.

 My observation from using MCP as a detoxification agent in my clinic is that it works as a gentle chelator in the bloodstream and it is very useful for ongoing use. Because fish are still recommended as part of a healthy diet and an essential source of certain nutrients (essential fatty acids like DHA), mercury levels are also becoming a widespread health concern. It is a Catch-22 for dietary health. As the widespread environmental cleanup of mercury is unlikely in the short-term, the medical community should develop methods to treat toxicity or reduce high body levels of mercury body burden. One approach is the use of traditional and alternative medicine cleansing programs along with the use of dietary supplements such as MCP that may act as gentle chelators.

 For chelation purposes, 5-15 grams of MCP should be taken per day depending on mercury levels for one year. Maintenance at 2-5 grams per day thereafter is usually sufficient. In my practice, I use 15 grams per day or 15 grams per day in the first 3-5 days of the month and 5 grams per day for the remainder of the month. MCP is generally regarded as safe and is well tolerated. Reported side effects have been rare, but may include mild and transient gastrointestinal discomfort.

 Citrus pectin is a complex polysaccharide (long-chain carbohydrate) obtained from the peel and pulp of citrus fruits such as lemons, grapefruits, oranges and tangerines. This long chain of sugars has numerous branches with important binding capabilities that are related to pectin is unique anti-metastatic attributes. Both the molecular weight and the structure of the chain influence the binding properties of the pectin. First, low molecular weight is required in order for pectin to be absorbed into the bloodstream during digestion; secondly, a reduced number of side chains facilitate the ability of the pectin molecule to bind to its target sites.

 MCP is composed of citrus pectin that has been broken down into shorter chain molecules. In the laboratory, this is done by heat and pH modification. Industry progress in the production of low methoxy, low molecular weight pectins has resulted in the availability of material for both research work and public consumption.

 Proprietary processing of citrus pectin results in a substance with a shorter molecular chain and low degree of methoxy content, thus allowing the lower molecular weight compound to be absorbed into the bloodstream. This processing also enhances the absorption and utilization of the polysaccharide compounds. One of these compounds is galactose, a natural sugar found on the branches of the pectin molecule. Because galactose has an affinity for galectin-3 proteins on the cancer cell surface, this naturally occurring sugar is felt to play a role in the ability of MCP to inhibit cancer metastasis.

 Cancer Metastasis - The Role of Galectins:

 Certain cancer cell types, such as prostate cancer, breast cancer, colon cancer, lymphoma, melanoma, glioblastoma, and laryngeal epidermoid carcinoma, all have specific protein molecules on their cell surface, called galectins. It has also been observed that metastatic cells express significantly more galectin-3 than the original primary tumor cells from which they were derived. Galectins are known for their carbohydrate-binding abilities. These proteins on the cancer cell surface are involved in binding between cells. They play an important role in cellular interactions during the metastatic process, binding to galactose on neighboring cancer cells and oligosaccharides on the surface of normal cells.

 Human studies of colon, stomach and thyroid cancers showed that the amounts of galectin produced increased proportionally as the cancers progressed from their early to advanced stages.(4) Higher galectin levels permit greater adhesion of cancer cells and increases the ability of these cells to bind to non-cancerous cells at a distant site, where metastasis occurs. Thus, these lectin binding sites and their proclivity for binding to cancer cell surface carbohydrates appear to be the basis by which cancer cells aggregate together and bind to metastatic target sites.

 A Proposed Role for Modified Citrus Pectin:

 It is felt that MCP works by blocking tumor cell surface galectins, so that tumor cells cannot adhere to other cells. The galactose branch chains on the modified pectin molecule appear to be the part, which has an affinity for galectins on the tumor cell surface. The impact of this galectin blockage is twofold: to inhibit aggregation of cancer cells, whereby they bind to each other to form colonies, and to inhibit adhesion of cancer cells to host cell surfaces. Due to these affects, MCP may also prevent the formation of organized tumor emboli.

 Animal Studies:

 The first evaluation of the feasibility of oral use of MCP in living systems was conducted by the research team of Dr. Kenneth Pienta. In an animal study, it was introduced in drinking water to rats implanted with prostate cancer cells. Only 50% of the rats given MCP developed lung metastases, significantly lower than a control population of rats where lung metastases occurred in 93.75% of the control group. In addition, the group that received 1% MCP had only one colony in the lungs (+/-1) compared to nine colonies (+/-4) in the control group. Reductions in the percentage of rats that developed metastatic disease, and the number of metastatic colonies per diseased animal were both statistically significant. MCP did not affect their primary tumor growth at any concentration tested.

 A recent study evaluated the effect of daily oral administration of MCP on colon-25 tumors implanted in balb- c mice. In comparison to the control group the investigators observed a significant reduction in tumor size. There was a 38% reduction in size in the group fed 0.8mg/ml, and 70% reduction in the group fed 1.6mg/ml of MCP. There was no statistically significant difference in mean tumor weight between the group receiving MCP and the control group. The investigators suggest that this may be due to differences in the overall tissue constituents of the excised tumors The discrepancy between the decrease in tumor size observed and the lack of change in tumor mass puts into question the results of the study, especially in lieu of the fact that Peinta in his landmark animal study did not observe a change in the growth of the primary tumor. Based on the proposed mechanism of MCP in preventing tumor emboli formation we can anticipate that MCP may effect the formation of the primary tumor and thus potentially serve as a preventative agent, but not effect the growth of the primary tumor once it is implanted. Additional studies are required to determine the exact role of MCP in treatment of the primary tumor.

 Published studies demonstrated a time-and dose-dependent inhibition of tumor cell adhesion. This suggested that saturation of galectin cell surface sites on tumor cells by the galactose of MCP was a viable model on which to base further research. The animal research suggested that the lower molecular weight of MCP allowed absorption into the bloodstream, and that higher levels had a greater impact. Converting this information to a human model in a useful way led us to the design of the first human clinical trial.

 Human studies and additional in vitro studies:

 A human clinical trial designed by our group and conducted by Dr. Steven Strum and Dr. Mark Schultz of the Prostate Cancer Research Institute, Los Angeles, CA evaluated the changes in PSA level in patients with prostate cancer. The patients studied consumed 15 grams per day of MCP (PectaSol? EcoNugenics Inc., Santa Rosa, CA 95407). Seven patients were enrolled into the study. Cancer progression was evaluated based on the time that it takes for the PSA to double, a standard measurement of prostate cancer progression. Lengthening of this doubling time represents a slowing in the progression of the cancer. Full response was measured as a 30% lengthening in PSA doubling time and was seen in 4/7 patients. In all, 6/7 patients showed increased doubling times in PSA levels and were classified as full or partial responders. This pilot clinical trial showed that MCP significantly slowed the PSA doubling time in prostate cancer patients with low levels of PSA. It is especially significant in patients where the PSA increase is due to secondary tumors as it signifies inhibition or retardation of the progress of cancer metastasis.

 An in vitro study that assessed the cytotoxic effect of MCP on PC-3 prostate cancer cell lines demonstrated a very high cytotoxic effect as compared with control. Cytotoxicity was found to be 80.7% at 1.0% concentration of MCP, and 76.9% at 0.1% concentration, compared with 3.8% with the control group. The authors concluded that MCP may interfere with the adherence of PC-3 cells to an endothelial monolayer.

 Additional Benefits of Modified Citrus Pectin:

 MCP may have a beneficial effect on primary tumors in addition to the main effect of slowing metastasis. A possible mechanism that can explain such an effect is that it may inhibit the formation of organized tumor emboli.

 Because pectin can bind to cholesterol, a reduction of serum cholesterol has been observed. Regular pectin reduces cholesterol by binding to it in the intestines. MCP can bind to cholesterol in the bloodstream. Due to its binding effects it may have a more direct effect on preventing and reducing arteriosclerosis.

 Pectin can bind to various heavy metals and function as a chelating agent. MCP may specifically bind to heavy metals in the blood stream. At the present time we are studying the potential effects of modified citrus pectin as a single agent and in combination with modified alginate (low molecular weight alginate) as systemic chelating agents. These potential uses of pectin warrant additional research.

 Tolerance and recommended dosage:

 MCP is well tolerated. While, based on the human clinical trial and our clinical experience, the optimal dosage for slowing of metastasis may be 15 grams per day; the dosage that should be used for prevention is lower. Dosages as low as 3-5 grams per day can be beneficial as a preventative measure.

 Suggested Use: Start with 2 teaspoons (5 grams) daily. Gradually increase to 4-6 teaspoons daily, or as recommended by your health care professional. For daily maintenance, 1 to 2 teaspoons can be used. Mix in a blender with 8 oz. of water, juice, or other liquid and drink immediately. The powder's neutral taste mixes well with natural flavors in foods, beverages, and soups.

 Caution: Do not exceed suggested use. Take this product with large amounts of fluids. If you do not drink enough liquid, the product may cause constipation. Discontinue use if intestinal discomfort or constipation occurs. If you are pregnant or breast feeding, on medication, or have diabetes or an intestinal disorder, consult your health care professional before using this product.

 Conclusion:

 MCP may be a promising nutritional supplement. Its benefits can include the lowering of cholesterol, possible immune enhancement, but more significantly, the inhibition of cancer metastasis.This safe-to-use preparation is showing promising results, and will require more research in order to determine more accurately its role in the treatment and prevention of cancer.

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citations1.What is Modified Citrus Pectin,MCP,an inhibitor of cancer metastasis and its wide uses?

last edit date:22th,June.2009.