CITRUS PECTIN

Modified Citrus Pectin is a soluble fiber derived from white pulp or inner peel of citrus fruits. They do not contain furocoumarins, which lead grapefruit to interfere with oncology drugs. Evidence from cancer trials has been emerging in oncology, particularly for prostate cancer. Branded products such as Pectasol are reported successful at phase II. The slowing of prostate disease rates is less than class leading hormone targeting drugs, but with none of the side effects.

There are additional small trials with fascinating positive evidence in late stage breast, colorectal , lung and other cancers where around 20% of advanced stage patients see measurable improved outcomes following relapses of oncology treatments. Typical dosages can be up to 5g three times daily. Just like newer oncology drugs, citrus pectin needs targeting and will not work for all, but in comparative terms there no side-effects. These trials need broader replication to help understand which patients can benefit. The direct actions of citrus pectin are inhibiting galectin-3 protein signaling pathway. Gal-3 expression is elevated in tumor tissues both primary and at metastatic sites. Its strongly associated with cancers in the digestive system – gastric, pancreatic, colorectal. But also melanoma, breast, ovarian, prostate, lung, head and neck cancers. In kidney cancer too, most notably the metastatic phase.

Along with its need for extra sugars, proteins and lipids, cancers also use high amounts of metals to fuel their growth including copper and iron. Indeed, cancer activity includes upregulating the circulating levels of these metals, so it can store them in the tumor microenvironment. Citrus Pectin can reduce levels of heavy these metals including lead, mercury, copper. But it does so without removing essential minerals. Both alone and in combination with alginates from brown seaweeds for instance branded product PectaClear. These metals are shown increase progression in many cancers, often in combination with reduced selenium and zinc. Alginates can reduce zinc so be sure to maintain zinc with supplements too.

The inhibition of aberrant galectin-3 activity make it probable that citrus pectins benefits include reduced metastatic spread, in particular used in combination with oncology treatments. Further evidence is needed here for confirmaion.

TYPICAL ABSORPTION LEVELS

5 -20%

EXAMPLES OF IMPROVED OUTCOMES

YES
ANALYSIS

PRE-DIAGNOSIS OR PREVENTION

PENDING

Highlighted Studies

Herein, we report the second long-term treatment phase of an additional 12 months of P-MCP therapy (4.8 g × 3/day orally) in patients without disease progression after the initial 6 months of therapy. Of the 46 patients that entered the second treatment phase, 7 patients withdrew consent and decided to continue therapy out of pocket, and 39 initiated the second treatment phase. After a total of 18 months of P-MCP treatment, 85% (n = 33) had a durable long-term response, with 62% (n = 24) sho...

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However, in consideration of this background, it is remarkable that even 12 (10) out of 49 patients showed a stabilized disease over a period of at least 8 (16) weeks of oral MCP treatment. Moreover, 6 patients had a SD for a period longer than 24 weeks. Furthermore, the 50% decrease of the serum PSA level after 16 weeks of treatment associated with a significant increase of clinical benefit, quality of life and reduction in pain in one patient with far advanced hormone-refractory prostate ca...

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Patients that did not progress by PSA and radiologically at six months continued for an additional twelve months. After six months, 78% (n = 46) responded to therapy, with a decreased/stable PSA in 58% (n = 34), or improvement of PSADT in 75% (n = 44), and with negative scans, and entered the second twelve months treatment phase. Median PSADT improved significantly (p = 0.003). Disease progression during the first 6 months was noted in only 22% (n = 13), with PSA progression in 17% (n = 10), ...

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The progression of this promising anti-cancer agent into clinical practice, hampered by various factors, was rather slow. Nevertheless, limited clinical studies performed to date demonstrated that MCP significantly increased prostate specific antigen doubling time in patients with recurrent prostate cancer,38 thus confirming its potential usefulness in treating prostatic neoplasia. As the potential and the necessity of developing MCP-based pharmaceuticals and nutraceuticals is becoming more a...

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https://www.mdpi.com/2072-6643/15/16/35335Herein, we report the second long-term treatment phase of an additional 12 months of P-MCP therapy (4.8 g × 3/day orally) in patients without disease progression after the initial 6 months of therapy. Of the 46 patients that entered the second treatment phase, 7 patients withdrew consent and decided to continue therapy out of pocket, and 39 initiated the second treatment phase. After a total of 18 months of P-MCP treatment, 85% (n = 33) had a durable long-term response, with 62% (n = 24) showing decreased/stable PSA, 90% (n = 35) PSADT improvement, and all with negative scansLong-term outcome as determined by PSA level, PSADT, and disease progression: Out of the 39 patients that entered the second phase of the study (the additional 12 months of therapy, creating a total of 18 months), 85% (n = 33) demonstrated a decreased or stable PSA (Figure 2) and/or improvement of PSADT (54%, n = 21), with negative scans (90%, n = 35). Median PSADT improved significantly versus baseline (p = 0.003), from a median pre-treatment PSADT of 10.3 (median range = 1.4–54.6) months to a median post-treatment PSADT of 43.5 (median range = 3.5–981.0) months (Table 1 and Table 2).
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8706421/5Furthermore, P-MCP’s [Citrus Pectin] mechanisms of action suggest that this compound may be particularly interesting for delaying disease progression in a group of patients with relatively low disease burden states, such as in the non-metastatic biochemically relapsed prostate cancer. For more definitive conclusions regarding the efficacy of P-MCP in this patient population, further testing in prospective randomized studies evaluating more conventional disease endpoints is warranted.The extracellular galectin-3 protein participates in the tumorigenesis process by various mechanisms, including inflammation, cellular proliferation, angiogenesis, and progression to an overt metastatic state via cancer cell–endothelial adhesion in distant organs. Elevated galectin-3 serum level was reported in prostate cancer patients.... P-MCP is an oral competitive inhibitor of galectin-3, and preliminary preclinical and clinical data suggest that it is active in patients with prostate cancer..Screenshot from 2024-10-02 20-29-19
https://journals.sagepub.com/doi/pdf/10.4137/CMO.S2854.5After 2 cycles of oral intake of MCP, 6/29 patients (20.7%) had an overall clinical benefit response associated with a stabilization or improvement of life quality. On an intent to treat basis 11/49 patients (22,5%) showed a stable disease (SD) after 2 cycles and 6/49 patients (12,3%) had a SD for a period longer than 24 weeks. One patient suffering from metastasized prostate carcinoma showed a 50% decrease in serum PSA level after 16 weeks of treatment associated with a significant increase of clinical benefi t, quality of life and decrease in pain. it is remarkable that even 12 (10) out of 49 patients showed a stabilized disease over a period of at least 8 (16) weeks of oral MCP treatment. Moreover, 6 patients had a SD for a period longer than 24 weeks. Furthermore, the 50% decrease of the serum PSA level after 16 weeks of treatment associated with a signifi cant increase of clinical benefi t, quality of life and reduction in pain in one patient with far advanced hormone-refractory prostate cancer indicates antitumoral effi cacy even in patients with far advanced solid tumors
https://www.researchgate.net/publication/56329593The gradual decrease of total body heavymetal burden is believed to have played an importantrole in each patient’s recovery and health maintenance.This is the first known documentation of evidence ofsuch results in a clinical report of case studies with pos-sible correlation between clinical outcome and a reduc-tion in toxic heavy metal load in patients using MCPand/or an MCP/alginate complex.These five case studies demonstrate that the use of MCP alone and in combination with alginates, successfully reduced heavy metal burden over time. It has been previously demonstrated that MCP has the ability to increase the urinary excretion of toxic elements in subjects with ‘normal’ body loads of metals without increasing excretion of essential minerals [10]. De- crease in total body burden of mercury using MCP has also been previously demonstrated [11]. This is the first known documentation of evidence of such results in a report of case studies with possible correlation between clinical outcome and a reduction in toxic heavy metal load in patients with MCP and/or an MCP/alginate complex. No adverse side effects have been reported or documented. These compounds appear able to provide a measured, progressive detoxification
https://www.mdpi.com/2072-6643/11/11/26192.5Modified citrus pectin (MCP) has a low-molecular-weight degree of esterification to allow absorption from the small intestinal epithelium into the circulation. MCP produces pleiotropic effects, including but not limited to its antagonism of galectin-3, which have shown benefit in preclinical and clinical models. Regarding cancer, MCP modulates several rate-limiting steps of the metastatic cascade. MCP can also affect cancer cell resistance to chemotherapy. Regarding fibrotic diseases, MCP modulates many of the steps involved in the pathogenesis of aortic stenosis. MCP also reduces fibrosis to the kidney, liver, and adipose tissue. Other benefits of MCP include detoxification and improved immune functionHonokiol, a purified extract from magnolia bark used in traditional Asian medicine and MCP, has been shown to have synergistic antioxidant activity and anti-inflammatory effects [46]. There was an inhibition of toxin-producing Escherichia coli adhesion and reduced Shiga toxin cytotoxicity with MCP [45]. Furthermore, MCP co-administration with live probiotic L. acidophilus ATCC 4356 supplement helped maintain or improve the integrity and population of the intestinal microbiota [44]. Finally, MCP has an immunomodulatory effect on the levels of cytokine secretion in the spleen of mic
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2782490/2Due to its anti-adhesive, apoptosis-promoting, and apoptosis-inducing properties, it appears that MCP is capable of targeting multiple critical rate-limiting steps involved in cancer metastasis. In addition, by inhibiting Gal-3 anti-apoptotic function and enhancing apoptosis induced by cytotoxic drugs, it holds the potential to increase dramatically the efficiency of a conventional chemotherapyMCP significantly increased prostate specific antigen doubling time in patients with recurrent prostate cancer.. thus confirming its potential usefulness in treating prostatic neoplasia. As the potential and the necessity of developing MCP-based pharmaceuticals and nutraceuticals is becoming more and more commonly recognized..the addition of MCP to armamentarium of anti-cancer drugs holds the promise of improving treatment of multiple human malignancies.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2778124/1MCP can effectively inhibit the growth of colon cancer and liver metastasis by intercepting the adhesion and aggregation of cancer cells. MCP, as a natural polysaccharide derived from fruits and a nontoxic drug, may pave a new way in controlling the growth and metastasis of colon cancer and other cancers. The role of MCP and chemotherapy in controlling and curing liver metastatic colon cancer needs further study.Galectin-3 is a carbohydrate-binding protein closely related with cancer growth and metastasis. Studies have shown that galectin-3 is over-expressed in different types of cancer. Dietary components play an important role in cancer progression and metastasis, carbohydrate-mediated recognition processes participate in cancer progression. Modified citrus pectin (MCP), a non-digestible and water-soluble polysaccharide fiber derived from citrus fruits, can inhibit galectin-3-mediated function in vivo and in vitro.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9160294/1Results showed that MCP significantly inhibited tumor orthotopic growth and pulmonary metastases. To evaluate whether MCP affects circulating tumor cell seeding at metastatic sites, tumor lung metastasis mice models was also established. Results also showed that MCP inhibited pulmonary metastasis of breast cancer cells. In addition, MCP not only decreased the percentage of M2-like TAM in primary tumor tissues but also suppressed M2-like TAM at metastatic sites. Moreover, MCP decreased the angiogenesis of breast cancer cells by detecting CD31 expression in tumor tissues. These suggest that MCP prevents lung metastasis of breast cancer by inhibiting angiogenesis through targeting M2 macrophages.We showed that MCP (0.06%–1%) concentration-dependently suppressed the survival of TAM through inhibiting glucose uptake with a greater extent in hypoxia than in normoxia. Furthermore, MCP treatment decreased ROS level in TAM through its reducibility and inhibiting galectin-3 expression, leading to inhibition of glucose transporter-1 expression and glucose uptake. In addition, MCP suppressed M2-like polarization via inhibiting STAT3 phosphorylation. Moreover, the tumor-promoting effect of TAM could be restrained by MCP treatment as shown in human breast cancer MDA-MB-231 cells in vitro and in mouse breast cancer 4T1-luc orthotopic and metastasis models. In both tumor tissue and lung tissue of the mouse tumor models, the number of TAM was significantly decreased after MCP treatment. Taken together, MCP may be a promising agent for targeting TAM in tumor hypoxic microenvironment for breast cancer treatment.Screenshot from 2024-08-19 13-02-42
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9657392/1Modified pectin (MP), specifically modified citrus pectin (MCP), is gaining popularity as evidence accumulates of its high efficacy in reducing the development and spread of malignancies, such as colon and breast cancer. The modification of pectin as part of a newly discovered chemical process releases, or predisposes the release of, fragments of the pectin molecule during intestinal digestion [6]. During digestion, these fragments bind to and block the activity of the pro-metastatic regulatory protein galectin 3 (Gal-3), inducing tumor progression. This finding is supported by data from various settings, including cellular and animal studies and human clinical trials.The cytotoxic effects of pectin provide it with anti-cancer properties, which have been shown to inhibit tumor growth and proliferation. MCPs inhibit almost all cancer cells via inhibition of the MAPK signal pathway. The high monogalacturonic acid content of PectaSol-C may make it easier to absorb and disperse than other PectaSols. LRP3-S1 inhibited the MAPK and FAK/AKT/GSK-3 signaling pathways in pancreatic cancer cell lines BxPC-3, PANC-1, and AsPC-1. Colon cancer cells invade the liver through galectins, carbohydrate-based recognition proteins.
https://academic.oup.com/jnci/article/94/24/1854/2906798?login=false#559447121MCP, given orally, inhibits carbohydrate-mediated tumor growth, angiogenesis, and metastasis in vivo, presumably via its effects on galectin-3 function. These data stress the importance of dietary carbohydrate compounds as agents for the prevention and/or treatment of cancer.The data indicate that MCP might reduce mammary and colonic tumor growth and metastasis by inhibiting angiogenesis.. we observed a 70.2% reduction in the mean tumor volume by 7 weeks following the oral intake of MCP (Fig. 1). This was associated with a 66% reduction in blood vessels [mice] and a complete inhibition of metastasis to the lungs
https://www.tandfonline.com/doi/pdf/10.4161/cbt.259371To confirm the results obtained from genetic method, we employed a Gal-3 inhibitor, modified citrus prectin (MCP), and co-treated the RCC cells with ATO. The cells showed an increased apoptosis in the syngeneic application of Gal-3 inhibition and ATO compared with ATO application alone. Based on these results, we conclude that Gal-3 inhibition sensitizes human renal cell carcinoma cells to ATO treatment through increasing mitochondria-dependent apoptosis. Our studies implicate synergetic application of ATO [chemotherapy] and Gal-3 inhibition as a potential strategy for RCC treatmentTo directly confirm that Gal-3 is the key factor in RCC cells against ATO-induced apoptosis, we used shRNA technique to knockdown Gal-3 expression. According to Park et al.,10 Caki-1 cells were the primary cells, which have immunity to ATO treatment. To this end, we transferred the shRNA to knock down Gal-3 expression in Caki-3 cells. We found that Gal-3 inhibition by shRNA significantly induced Caki-1 cells apoptosis and proliferation inhibition.
https://pmc.ncbi.nlm.nih.gov/articles/PMC5980349/1Galectin-3 (Gal-3) is a lectin that contributes to TME immunosuppression and regulates diverse functions including cellular homeostasis and cancer biology. Increased Gal-3 expression during cancer progression augments tumor growth, invasiveness, metastatic potential, and immune suppression, which highlights the potential use of Gal-3 as a therapeutic target capable of modulating anti-tumor immunityGal-3 expression typically increases during cancer progression, and this expression results in both enhanced suppression of the immune response and other detrimental outcomes including increased tumor progression, invasiveness, and metastatic potential. Recent data suggests that inhibiting Gal-3 in combination with established immunotherapy has the potential to both alleviate immune suppression and decrease tumor growth. Given these promising preliminary results, additional studies are warranted to further investigate how Gal-3 contributes to tumor progression
https://pmc.ncbi.nlm.nih.gov/articles/PMC2782490/1The anti-adhesive properties of MCP as well as its potential for increasing apoptotic responses of tumor cells to chemotherapy by inhibiting galectin-3 anti-apoptotic function are discussed in the light of a potential use of this carbohydrate-based substance in the treatment of multiple human malignancies.Nevertheless, limited clinical studies performed to date demonstrated that MCP significantly increased prostate specific antigen doubling time in patients with recurrent prostate cancer,38 thus confirming its potential usefulness in treating prostatic neoplasia. As the potential and the necessity of developing MCP-based pharmaceuticals and nutraceuticals is becoming more and more commonly recognized,27,36,37 the addition of MCP to armamentarium of anti-cancer drugs holds the promise of improving treatment of multiple human malignancies.

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