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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 C. Ramachandran, et al., “Activation of Human T-Helper/Inducer Cell, T-Cytotoxic Cell, B-Cell, and Natural Killer (NK)-Cells and Induction of Natural Killer Cell Activity Against K562 Chronic Myeloid Leukemia Cells with Modified Citrus Pectin,” BMC Complement Altern. Med. 11, 59 (2011). Both the green banana and the pectin significantly improved intestinal permeability and also reduced diarrhea [ 13]. Increasing Sepsis Survival S. Conti, et al., “Modified Citrus Pectin as a Potential Sensitizer for Radiotherapy in Prostate Cancer,” Integr. Cancer Ther. 17(4), 1225–1234 (2018). To overcome this limitation, control its renal clearance and improve its therapeutic efficacy, G3-C12 ( 27, Fig. 5) was conjugated to an N-(2-hydroxypropyl)methacrylamide polymeric carrier. This substitution increased its molecular size and generated a larger GAL3-targeted copolymer that was proposed as an anticancer agent 260, 261. Conjugation of HMPA–G3-C12 copolymer to 5-FU led to increased cytotoxicity, tumour cell apoptosis and inhibition of migration in vitro compared with 5-FU, as well as greater reductions in tumour volume in a PC-3 prostate cancer mouse model 262. Micellar nanoparticles assembled by poly(oligo(ethylene glycol)) monomethyl ether methacrylate (POEGMA) and poly(ε-caprolactone) (PCL) copolymers conjugated to G3-C12 peptide were designed to deliver G3-C12 ( 27, Fig. 5) to the tumour microenvironment. This copolymer formed nanoparticles that were loaded with the anticancer drug bufalin (BUF) and tested as a drug delivery system for castration-resistant prostate cancer (CRPC). Biodegradable BUF-G3-C12 nanoparticles exhibited controlled drug release and enhanced tumour reduction in mice bearing DU145 prostate cancer cells 263. Biological agents
In this pilot study, 15 grams of MCP (this study used PectaSol by EcoNugenics Inc.) taken orally did not increase the loss of calcium, magnesium, zinc, selenium or iron. But it did decrease toxic arsenic, cadmium, and lead levels [ 3]. Within the galectin family, Gal-3 has unique properties. It is a beta-galactoside-binding protein involved in a wide array of biological processes, mainly related to cell cycle, immunity and injury repair. Gal-3 is found in the nucleus, cytoplasm, mitochondrion, fibroblasts, cell surface and extracellular matrix. Circulating Gal-3 levels increase with age, injury and chronic illness. Meanwhile, animal studies have shown that MCP can reduce galectin-3 levels in rats [ 15]. Could the same be true for humans? And could MCP therefore help to lower galectin-3 levels and improve thinking? Possibly. But of course, further study is needed here. Side Effects of Modified Citrus PectinJ. Jiang, I. Eliaz and D. Sliva, “Synergistic and Additive Effects of Modified Citrus Pectin with Two Polybotanical Compounds in the Suppression of Invasive Behavior of Human Breast and Prostate Cancer Cells,” Integr. Cancer Ther. 12(2), 145–152 (2013). 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 We now understand that as a culprit biomarker, extracellular Gal-3 functions as a key driver behind the development and progression of metastatic cancer, cardiovascular disease, organ fibrosis, neurodegenerative disease, immune dysregulation, premature ageing and many other conditions. The most well-established pathogenic role of Gal-3 is in the development and migration of cancer. Gal-3 is over-expressed on the surface of cancer cells, acting as the primary adhesion molecule that allows cancers to proliferate, metastasize and evade the immune system. PectaSol® Metal Detox exerts a dual action in the body. Algimate® Modified Alginate Complex remains in the digestive tract where it works to bind and eliminate heavy metals and radioactive particles to be eliminated through the stools. PectaSol-C® MCP is absorbed into the circulation from the intestine and works systemically, binding heavy metals and environmental pollutants in the circulation for safe elimination through the urinary system.*
Pathological fibrosis is the consequence of abnormal mechanisms of tissue repair that are typically associated with cellular stress, chronic inflammation and/or severe tissue damage. It can lead to organ failure. Inadequate tissue regeneration has been described in several chronic fibroproliferative diseases such as IPF 24 and chronic inflammatory diseases such as NASH 19. The abnormal wound-healing process results in scar formation with excessive collagen deposition via mechanisms that involve fibroblasts, epithelial and endothelial cells, and immune cells, notably macrophages 19. Given the high prevalence of fibrotic diseases and the limitations of current drugs, which mainly limit the rate of organ dysfunction, the quest for effective therapies is clearly important. Suggested Use:As a dietary supplement, for maximum support, take one 5 gram scoop 3 times daily with liquid on any empty stomach. For long term maintenance, take one 5 gram scoop daily with liquid on an empty stomach. Other polysaccharides have also emerged as potential galectin inhibitors. For example, RN1 ( 20, Fig. 4), an arabinogalactan polysaccharide isolated from the flowers of the Chinese ginseng plant ( Panax notoginseng), was proposed as a GAL3 inhibitor. This compound showed antitumoural activity in pancreatic ductal adenocarcinoma both in vitro and in vivo 236. Other ginseng-derived pectins prevented GAL3-driven T cell apoptosis and reduced tumour growth in mouse models of sarcoma 237. Peptides and peptidomimetics Extracellular GAL1 and GAL3 directly modulate tumour cell fitness, migration, EMT and stemness through their interactions with glycosylated tumour-associated receptors, including epidermal growth factor (EGF), transforming growth factor β (TGFβ) receptors and cell surface integrins 68, 69, 70, 71, 72, 73, 74, that contribute to cancer progression and metastasis. GAL1 can trigger EMT in gastric cancer 75 and hepatocellular carcinoma 72, 76 via non-canonical activation of the Hedgehog pathway 75, downregulation of E-cadherins 72 and induction of α vβ 3 integrin-dependent AKT signalling 76. Collectively, these actions have an impact on clinical outcomes and therapeutic responses to both sorafenib and doxorubicin 77, 78. GAL1 also regulates events that promote the growth of pancreatic adenocarcinoma, including tumour cell proliferation, invasion and metastasis 78, and GAL1 silencing inhibits migration and invasion of metastatic castration-resistant prostate cancer cells via suppression of androgen receptor and AKT-mediated signalling 79. In turn, interactions between GAL3 and the glycosylated transmembrane protein mucin 1 (MUC1) enhance EGF receptor dimerization and activation (Fig. 2), and thus promote proliferation and motility of epithelial cancer cells by activating ERK1/2 and AKT signalling pathways 80, 81. Notably, complex N-glycans linked to EGF receptors on breast carcinoma cells control EMT, cell motility and tumour metastasis by facilitating the exposure of GAL3-specific glycoepitopes 68 (Fig. 2). Tumour-derived GAL3 also promotes invasion via its capacity to impair interactions between adhesion molecules expressed on the surface of malignant cells and N-glycosylated proteins within the extracellular matrix, such as laminin and fibronectin 74. Furthermore, GAL3 promotes the establishment of metastatic niches by binding to the Thomsen–Friedenreich antigen (Tf antigen) expressed by metastatic lung tumour cells 70 and facilitating homotypic and heterotypic aggregation and emboli formation 82. Similarly, overexpression of GAL3 promotes proliferation, migration and invasion of oral squamous cell carcinoma (OSCC) cells via enhanced WNT–β-catenin signalling and EMT 83. The interaction of GAL3 with α vβ 3 integrin promotes KRAS addiction 84; these findings identified GAL3 as a potential druggable target for ‘KRAS-addicted’ lung and pancreatic cancers (Fig. 2). GCS-100 ( 17, Fig. 4), developed by La Jolla Pharmaceutical Company, was initially developed as a potential inhibitor of GAL3. GCS-100 has broad antitumour activity, including inducing apoptosis of multiple myeloma cells 212, 224, 225, 226. Moreover, GCS-100 alone or in combination with BCL-2 homology domain 3 (BH3) mimetics induced apoptosis in acute myeloid leukaemia cells 227. A phase II clinical trial (NCT00514696) evaluated intravenous administration of GCS-100 in patients with chronic lymphocytic leukaemia. The inhibitor showed excellent tolerability and led to partial remission in 25% of patients and >50% shrinkage of lymph node lesions in 16% of patients.Extracellular Gal-3 acts as an adhesion surface protein, forming lattices with itself, binding glycoproteins and glycolipid membrane receptors and creating a gel-like biofilm that anchors other procancerous growth factors and inflammatory compounds within the extracellular matrix. The pectin found in many fruits cannot be absorbed into the bloodstream due to its large molecular size. Only PectaSol-C MCP is produced using a proprietary process that carefully controls the weight and structure of the pectin molecules. The result is Modified Citrus Pectin with a specific low molecular weight range less than 15 kilodaltons and a low degree of esterification. This means that it is readily and effectively absorbed into the bloodstream, where it can actively promote cellular wellness.
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