PectaSol-C® is a natural product derived from the pith of citrus fruit, and modified to meet specific molecular chain and weight characteristics. This non-allergenic product is clinically recognized for its ability to support healthy cellular proliferation. *

• Supports cellular health*
• Promotes prostate and breast health*
• Supports healthy immune function*

*These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease.

Dietary Supplement

Supplement Facts
Serving Size: 6 capsules/1 scoop (5 grams)
 

Amount Per Serving:

Total Carbohydrates 4 g
Dietary Fiber 3 g
Sodium 170 mg
Potassium 410 mg
PectaSol-C? Modified Citrus Pectin 4.8 g

Other Ingredients: Vegetable capsule (natural vegetable cellulose, water), stearic acid, magnesium stearate, microcrystalline cellulose, silicon dioxide

Suggested Use:

As a dietary supplement, for maximum support, take 6 capsules or 1 scoop (5 grams), three times daily, in divided doses on an empty stomach. For long term maintenance, take 6 capsules or 1 scoop (5 grams) once daily on an empty stomach.

Does PectaSol Modified Citrus Pectin work on any specific health concerns?
Modified Citrus Pectin has been reported to inhibit metastasis in the published literature.

Do people experience adverse reactions?
There have a few reports of mild effects such as loose stools in some sensitive individuals.

Is PectaSol Modified Citrus Pectin safe for diabetics to use?
When introducing any new food product, diabetics should be cautious. Therefore, we recommend closely monitoring blood sugar levels under your doctor?s supervision while you begin to use this product, as you would when introducing any item in your diet.

How long can PectaSol Modified Citrus Pectin be safely used? Any toxicity?
The scientific research on modified citrus pectin lists no adverse affects or toxicity. PectaSol? Modified Citrus Pectin matches the specifications used in scientific research studies. Consumption can continue for as long as desired.

What is pectin and how does PectaSol Modified Citrus Pectin differ from ordinary pectin?
Ordinary pectin is a complex carbohydrate molecule found in almost all plants. It is recognized for its ability to gel (as in the making of jams), but is not absorbed into the bloodstream because of its long molecular chain. For modified citrus pectin, a special manufacturing process creates a shorter molecular chain. According to the scientific research, that modification enhances absorption and utilization of the crucial polysaccharide compounds. Pecta-Sol Modified Citrus Pectin is a trademarked version of modified citrus pectin which conforms to the published specifications used in scientific research.

PectaSol modified citrus pectin has been shown in clinical trials to help slow down the spread of cancer cells to additional sites in the body. PectaSol? is uniquely formulated in a way that allows it to penetrate into the bloodstream, where it binds to the surface of cancer cells. The bound citrus pectin prevents the cancer cells from sticking to each other, which may interfere with their growth cycle and block their ability to adhere to new sites in the body.

Cancer Metastasis
In vitro research has shown that certain cancer cell types (such as carcinoma of the prostate, breast, colon and larynx, as well as lymphoma, melanoma and glioblastoma) have specific carbohydrate-binding protein molecules on their cell surfaces, called galectins (or galactoside-binding lectins). It has been observed that metastatic cells express significantly more of a particular galectin, galectin-3, than the cells of the primary tumor from which they originated. Galectins are known for their carbohydrate-binding abilities. They play an important role in cellular interactions during the metastatic process, binding to the galactose molecules on neighboring cancer cells, as well as to other sugars called oligosaccharides on the surface of healthy cells.

Human studies of colon, stomach and thyroid cancers have also shown that the amount of galectin produced increases proportionally as the cancer progresses from its early to advanced stages. Higher galectin levels encourage greater adhesion of cancer cells to each other, and they also facilitate the process of binding to non-cancerous cells at distant sites.

A Proposed Role for Modified Citrus Pectin
It is felt that Modified Citrus Pectin works by blocking tumor cell surface galectins, so that the tumor cells cannot adhere to other cells. This appears to be accomplished by galactose, a monosaccharide (simple sugar) found on the branch chains of Modified Citrus Pectin that has a particular affinity for the galectin-3 proteins. The impact of this galectin blockage is twofold: (1) it inhibits the aggregation of cancer cells to each other, preventing them from forming colonies, and (2) it inhibits the adhesion of cancer cells to normal cells. If cancer cells are deprived of their own adhesive ability, they fail to thrive and can be more easily destroyed by the immune system.

Modified Citrus Pectin may also augment the immune response to cancer in additional ways. One of its components, rhamnogalacturonan, enhances the cytotoxicity of CD3+ T-cells and natural killer (NK) cells, while also mediating increased monocyte cytotoxicity. Attachment of activated T-cells to tumor cells is a necessary step in tumor cell destruction.

PectaSol is the only brand of modified citrus pectin that has been successfully tested in human clinical trials.

Human clinical trial results for PectaSol showed a significant slowing of Prostate Specific Antigen (PSA) doubling time. 86% of patients in the initial trial either stabilized or had a significant positive response.

PectaSol's proprietary manufacturing process creates a unique form of modified pectin that allows its absorption and utilization into the blood stream. Other modified pectins and ordinary pectins do not have the same unique characteristics to enable absorption into the bloodstream.

Journal Article: The Potential Role of Modified Citrus Pectin in the Prevention Of Cancer Metastasis
By: Issac Eliaz MD. L.Ac.
Clinical Practice of Alternative Medicine, Vol. 2 No. 3, Fall 2001

Abstract:
This paper reviews progress in the laboratory and clinical evaluation of Modified Citrus Pectin (MCP), a low molecular weight pectin that has shown promising results in the prevention of metastasis of prostate adenocarcinoma. Following the initial published in-vitro¹ and animal² studies, we designed two trials to investigate the benefits of MCP further:
1) a human prostate cancer pilot study,
2) an in vitro study that evaluated its cytotoxic effects on a prostate cancer cell line.
Encouraging results in these two studies has led to a larger phase II clinical trial that is underway at the present time. This substance may play an important role in the prevention of cancer metastasis.

Background
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?s 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.³

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:
1) to inhibit aggregation of cancer cells, whereby they bind to each other to form colonies, and
2) 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.² 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
1) the percentage of rats that developed metastatic disease, and
2) 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.⁵ 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 Peinta² 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^2,3 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^1,6 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 that1 the lower molecular weight of MCP allowed absorption into the bloodstream, and that² 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, CA⁷ 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.^8-11 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 study¹² 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.^{4, 13, 14}

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.^15-21

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.^22-25

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.

Conclusion
MCP may be a promising nutritional supplement. Its benefits can include the lowering of cholesterol, possible immune enhancement^25-28 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.

References:
1. Naik H, Kalemkerian G. Inhibition of in vitro tumor cell-endothelial adhesion by modified citrus pectin: a pH modified natural complex carbohydrate (Meeting abstract). Proc Annul Meet Am Assoc Cancer Res. 1995;36: 377.
2. Pienta KJ, Naik H, Akhtar 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(5):348-353.
3. Raz A, Lotan R. Endogenous galactoside-binding lectins: a new class of functional tumor cell surface molecules related to metastasis. Cancer Metastasis Rev. 1987; 6:433-452.
4. Robert S, Bresalier RS, Yan PS, et al. Expression of the endogenous galactose-binding protein galectin-3 correlates with the malignant potential of tumors in the central nervous system. Cancer. 1997; 80:776-787
5. Hayashi A, Gillen AC, Lott JR. Effects of daily oral administration of quercetin chalcone and modified citrus pectin. Altern Med Rev. 2000;5(6): 546-552.
6. Platt D. Modulation of the lung colonization of B16-F1 melanoma cells by [modified] citrus pectin. J Natl Cancer Inst. 1992;84(6):438-442.
7. Strum S, Scholz M, McDermed J, et al. Modified citrus pectin slows PSA doubling time: a pilot clinical trial. (Abstract) International Conference on Diet and Prevention of Cancer (Finland). May 1999. www.Econugenics.com
8. Roberts SG, Blutte ML, Bergstralh EJ, et al. PSA doubling time as a predictor of clinical progression after biochemical failure following radical prostatectomy for prostate cancer. Mayo Clin Proc. 2001;76(6):576-581.
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12. Weiss T, McCulloch M, Eliaz I. Modified citrus pectin induces cytotoxicity of prostate cancer cells in co-cultures with human endothelial monolayers. (Abstract) International Conference on Diet and Prevention of Cancer. (Finland); May 1999. WWW.Econugenics.COM
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17. Fernandez ML Sun DM; Tosca MA; McNamara DJ. Citrus pectin and cholesterol interact to regulate hepatic cholesterol homeostasis and lipoprotein metabolism: a dose-response study in guinea pigs. Am J Clin Nutr. 1994;59(4):869-878.
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19. Fernandez ML. Distinct mechanisms of plasma LDL lowering by dietary fiber in the guinea pig: specific effects of pectin, guar gum, and psyllium. J Lipid Res. 1995;36(11):2394-2404.
20. Garcia-Diez F, Garcia-Mediavilla V, Bayon JE, et al. Pectin feeding influences fecal bile acid excretion, hepatic bile acid and cholesterol synthesis and serum cholesterol in rats. J Nutr. 1996;126(7):1766-1771.
21. Tinker LF, Davis PA, Schneeman BO. Prune fiber or pectin compared with cellulose lowers plasma and liver lipids in rats with diet-induced hyperlipidemia. J Nutr. 1994;124(1):31-40.
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27. Zhu HG, Zoller TM, Klein-Franke A, et al. Enhancement of MHC-unrestricted cytotoxic activity of human CD56+ CD3- natural killer (NK) cells and CD3+ T cells by rhamnogalacturonan: target cell specificity and activity against NK-insensitive targets. J Cancer Res Clin Oncol. 1994; 120(7):383-388.
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