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PectaSol Modified Citrus Pectin Powder Super-Nutrient to Support Cellular & Immune Health, Joint Support - 454 Grams - Formulated by Dr. Isaac Eliaz of ecoNugenics

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The original and only proven effective form of MCP is prepared with a proprietary, non-GMO enzymatic process controlled by pH and heat, which breaks the long chain molecules of the native pectin to produce the correct molecular size and structure of <13 kilodaltons and <5% esterification. An erythrocyte hemolysis assay was used to determine the cytotoxicity of pectin cerium oxide nanoparticles (Pe-CeO 2NPs), finding for the first time that when Pe-CeO 2NPs are detected in their natural habitat, they are biocompatible with living creatures [ 99]. Conversely, when the dosage of Pe-CeO2NPs was increased from 0.05 to 8.00 mg/mL, both the amount (0.55–8.31%) and rate (0.55–8.31%) of hemolysis increased. A 4 mg/mL concentration of Pe-CeO 2NPs was found to cause 4.55% hemolysis and was determined to be the appropriate concentration for human consumption based on the permitted hemolysis limit established for biocompatibility studies of materials and biomaterials [ 99]. It was found that a zebrafish toxicity model was effective in this study. A randomized controlled trial involving 87 patients with IBS and diarrhea symptoms showed that those who took daily pectin had significantly fewer symptoms, more formed stools, and better quality of life than those who took placebo. What’s more, MCP also lowered the rate of acute kidney injury, which went from 89% in the control group to 44% in both groups taking the modified pectin [ 14]. Improving Cognition R. Di, et al., “Pectic Oligosaccharide Structure-Function Relationships: Prebiotics, Inhibitors of Escherichia coli O157:H7 Adhesion and Reduction of Shiga Toxin Cytotoxicity in HT29 Cells,” Food Chem. 227, 245–254 (2017).

Optimal therapy of biochemically relapsed prostate cancer (BRPC) after local treatment is elusive. An established modified citrus pectin (PectaSol ®, P-MCP), a dietary polysaccharide, is an established antagonist of galectin-3, a carbohydrate-binding protein involved in cancer pathogenesis. Based on PSA dynamics, we report on the safety and the primary outcome analysis of a prospective phase II study of P-MCP in non-metastatic BRPC based. Sixty patients were enrolled, and one patient withdrew after a month. Patients ( n = 59) were given P-MCP, 4.8 grams X 3/day, for six months. The primary endpoint was the rate without PSA progression and improved PSA doubling time (PSADT). Secondary endpoints were the rate without radiologic progression and toxicity. 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), and PSA and radiologic progression in 5% (n = 3). No patients developed grade 3 or 4 toxicity. When taken at the active dose of 15 grams per day, many people report feeling a significant difference in the following areas: Keating N.L., O’Malley A.J., Smith M.R. Diabetes and Cardiovascular Disease During Androgen Deprivation Therapy for Prostate Cancer. J. Clin. Oncol. 2006;24:4448–4456. doi: 10.1200/JCO.2006.06.2497.Cancer cell proliferation, migration and colony formation, induced pancreatic cancer cells apoptosis, suppressed autophagy The American Cancer Society states that ’Severalanimal studies found that MCP helped reduce the spread of prostate, breast, and skin cancer. Animals with these types of cancer that were fed MCP had a much lower risk of the tumor spreading to the lungs’. A further study used Wistar DMH-treated rats to explore how AP formulations affect neoplastic damage and proliferative marker dysregulation, finding a substantial beneficial effect on colon carcinogenesis through the regulation of physiological indicators, oxidative stress, inflammatory markers, and hemodynamic alterations [ 26]. The anti-cancer activities of phenolics from apple trash have also been studied in HT29, HT115, and CaCo-2 cell lines as in vitro models of colon carcinogenesis. They found a significant decrease in HT115 cell invasion when apple phenolics were used to prevent DNA damage, a process associated with tumor initiation. In addition, hydrogen peroxide (H 2O 2)-induced damage was significantly reduced in HT29 cells, and CaCo-2 cell barrier function was increased, a process associated with reduced tumor promotion and metastatic potential [ 27]. In May 2011, data from the Prevention of REnal and Vascular ENd-stage Disease (PREVEND) study, a 10-year all-cause mortality investigation involving close to 8000 people, demonstrated that elevated serum Gal-3 increased all-cause mortality three-fold in the general population. 7 Another compelling large-scale study showed lower levels of Gal-3 in centenarians compared with those in their sixties and seventies who didn’t live as long. 8 Liu G, Chen YH, Kolesar J, Huang W, Dipaola R, Pins M, Carducci M, Stein M, Bubley GJ, Wilding G. Liu G, et al. Urol Oncol. 2013 Feb;31(2):211-8. doi: 10.1016/j.urolonc.2011.01.002. Epub 2011 Jul 23. Urol Oncol. 2013. PMID: 21784672 Free PMC article. Clinical Trial.

Research in cancer: With powerful antiadhesive, apoptosis-promoting properties, this researched MCP is shown in more than 15 published studies, including three clinical studies, to target numerous rate-limiting steps in cancer, primarily via its ability to inhibit Gal-3. 10–12 The natural history of men with biochemically relapsed, non-castrate prostate cancer is quite mixed. They may remain asymptomatic and free of clinical evidence of disease for many years [ 4]. Extensive data on patients’ natural history of relapsing after surgery and after curative radiotherapy indicate that the PSA doubling time (PSADT) predicts the probability of metastasis-free and prostate cancer-specific survival [ 5, 6, 7, 8, 9, 10, 11]. PSADT of <3 months, 3.00-8.99 months, and ≥nine months may be associated with poor, intermediate, and good prognosis in disease progression and development of overt metastatic disease. Furthermore, the Prostate-Specific Antigen Working Group’s guidelines on PSADT determined that clinical evidence supports PSADT as a predictive marker of cancer progression among post-local therapy prostate cancer patients experiencing biochemical recurrence [ 12]. Thus, PSADT has been used in our study design to define endpoints. Lau ES, Liu E, Paniagua SM, Sarma AA, Zampierollo G, López B, et al. Galectin-3 Inhibition With Modified Citrus Pectin in Hypertension. JACC Basic Transl Sci. 2021 Jan 6;6(1):12–21. DOI: 10.1016/j.jacbts.2020.10.006. PMID: 33532663. PMCID: PMC7838053. Brouns F, Theuwissen E, Adam A, Bell M, Berger A, Mensink RP. Cholesterol-lowering properties of different pectin types in mildly hyper-cholesterolemic men and women. Eur J Clin Nutr. 2012 May;66(5):591–9. DOI: 10.1038/ejcn.2011.208. PMID: 22190137. Unmodified citrus pectin does not have the same short, systemically available polysaccharide chains as MCP … and thus remains in the gastrointestinal (GI) tract. And other “modified” pectins may simply indicate that the pectin has been altered in some way, but doesn’t contain the shorter polysaccharide chains and molecular structure required for efficacy.expression level of its downstream target Bim, a pro-apoptotic protein, and induced the cleavage of Caspase-3 in PC3 and CASP1, ↓ cell proliferation and apoptosis

Azémar M, Hildenbrand B, Haering B, Heim ME, Unger C. Clinical Benefit in Patients with Advanced Solid Tumors Treated with Modified Citrus Pectin: A Prospective Pilot Study. Clin Med Oncol. 2007 Jan;1:CMO.S285. DOI: 10.4137/CMO.S285. Guess BW, Scholz MC, Strum SB, Lam RY, Johnson HJ, Jennrich RI. Guess BW, et al. Prostate Cancer Prostatic Dis. 2003;6(4):301-4. doi: 10.1038/sj.pcan.4500679. Prostate Cancer Prostatic Dis. 2003. PMID: 14663471 Clinical Trial. American Complementary and Integrative Medicine experts recommend different levels of consumption - one suggests5 grams, 3 times a day on an empty stomach for use with cancer patients and after cancer surgery and biopsies; another suggests just 6 grams a day. There is no research on this with humans. Pound C., Partin A., Eisenberger M., Chan D.W., Pearson J.D., Walsh P.C. Natural history of progression after PSA elevation following radical prostatectomy. JAMA. 1999;281:1591–1597. doi: 10.1001/jama.281.17.1591.I. Eliaz, et al., “The Effect of Modified Citrus Pectin on Urinary Excretion of Toxic Elements,” Phytother. Res. 20(10), 859–864 (2006). This was actually a large dose, so the fact that it was tolerated well by children is encouraging. The dose of MCP used in this study was equivalent to one scoop of Pectasol-C modified citrus pectin three-times daily for three months. (In our practice, we treat adults with one scoop twice daily for between 45 and 90 days, which we have found effective at lowering serum lead levels.) Slowing Heart Disease Importantly, there’s a direct relationship between elevated galectin-3 levels and poor outcomes for cancer patients. A number of scientific studies show that MCP can work synergistically with certain chemotherapy agents such as doxorubicin and paclitaxel . From this extensive body of published literature, only one available natural agent has emerged to demonstrate the singular ability to halt and reverse the harmful effects of Gal-3: a specific form of the nutraceutical ingredient modified citrus pectin (MCP) that’s derived from citrus peel pith and enzymatically modified to precise low molecular specifications for efficacy and bioactivity (PectaSol-C).

Hopefully, this dietary supplement will ultimately be one that lives up to its promise. In the meantime, we will continue to keep an eye on all this has to offer. Another significant study investigated the role of Gal-3 as a driver of oxidative stress in human cardiac fibroblasts, spontaneously hypertensive animal models and human aortic stenosis tissue. Results showed Gal-3 downregulates the antioxidant peroxiredoxin-4 (Prx-4) in cardiac fibroblasts, uncovering a new pathway whereby Gal-3 fuels cardiac damage. Importantly, MCP treatment restored cardiac Prx-4 and improved oxidative status. 3 Pedrosa LF, Nascimento KR, Soares CG, Oliveira DP, de Vos P, Fabi JP. Pedrosa LF, et al. Plants (Basel). 2023 Jul 24;12(14):2750. doi: 10.3390/plants12142750. Plants (Basel). 2023. PMID: 37514364 Free PMC article. Review.Z.Y. Zhao, et al., “The Role of Modified Citrus Pectin as an Effective Chelator of Lead in Children Hospitalized with Toxic Lead Levels,” Altern. Ther. Health Med. 14(4), 34–38 (2008). Nearly 1.7 million new cases of breast cancer arise annually worldwide, accounting for 25.2% of all cancer cases (WHO). Approximately 15% of breast cancer patients die following diagnosis, second only to lung cancer [ 10, 11]. Complex, molecular breast cancer occurs when gene mutations cause abnormal cell growth and proliferation [ 12]. In vitro and in vivo studies have shown that pectin-derived chemicals slow cell development and promote apoptosis [ 13]. The synergistic and additive effects of MCP have been studied in human breast cancer cells. Polybotanical compounds BreastDefend (BD) or ProstaCaid (PC) used in combination with MCP reduced the invasive potential of highly metastatic human breast cancer MDA-MB-231 cells. MCP may also prevent the development of human breast cancer in mice by reducing angiogenesis, a crucial mechanism for tumor growth. The α-galactosidase binding protein Gal-3 is one potential mediator of MCP’s inhibition of breast and prostate cancer cell adhesion, migration, and invasion [ 7]. MCP inhibits urokinase-type plasminogen activator (uPA) synthesis in breast and prostate cancer cells, and the uPA receptor (uPAR) regulates cell adhesion, migration, and invasion [ 14]. In addition to activating macrophages, CP decreased activator protein 1 (AP-1) and NF-κB signaling but increased LPS/Toll-like receptor 4 (TLR-4) signaling [ 15]. In another study, CP and apple pectin (AP) inhibited MDA-MB-231, MCF-7, and T47D breast cancer cells, finding that CP and AP inhibited cancer cells in the S and G1 or G2/M phases of the cell cycle. Similarly, the expression of Gal-3, a lectin implicated in cell adhesion, cell cycle, and death, was reduced by CP and AP. In addition, oxidative and strand-break DNA damage was observed in MDA-MB-231 cells, slowing proliferation [ 16]. Another randomized control trial concluded that at least 6 grams a day of pectin benefited cholesterol levels [ 6]. This trial also showed that citrus pectin was more effective than pectin derived from apples.

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