Modified Citrus Pectin as a Heavy Metal Chelator
Heavy metal toxicity is known to be an important factor in declining general health. Adult case reports, one short study in healthy people and one small clinical study in young children have shown tremendous effectiveness for MCP in reducing heavy metal toxicity including lead, mercury, arsenic and cadmium. Larger clinical trials are required for greater conclusiveness, but results like heavy metal reductions by up to 560% are mind-blowing.
Why Citrus Pectin Needs to be Modified
Pectin from citrus fruits contains a significant number of residues of the sugar galactose. This pectin is present in the form of long, complex chains whose galactose residues are hidden deep within their intricate molecular branchings. To solve this problem, the carbohydrate chains can be split into shorter fragments under pH-controlled conditions, exposing more galactose residues and simplifying the complicated branchings of the molecule. Working with the fibers of lemons, grapefruits, or tangerines in this way creates pH-modified citrus pectin (MCP). This modification process maximizes the opportunities for the pectin’s galactose residues to interact with galectin-3, unleashing the potential of citrus pectin.
Lectins & Glycoconjugates: A Lock & Key Mechanism for the Spread of Unhealthy Cells
Galactose is the same kind of sugar residue to which galectin-3 binds. Galectin-3 is a type of lectin. Lectins are cellular communication molecules that allow similar types of cells to bind together (these are called glycoconjugates) and to remain attached to their appropriate tissues. Lectin-glycoconjugate interactions also play a key role in immunity, allowing immune cells to distinguish “self” from “non-self” (foreign) cells, and in other cell-to-cell interactions.
An Unfortunate Match
Its been shown that many unhealthy cells exploit the lectin recognition system by covering themselves with “keys” that match the “locks” in distant, healthy tissues. Either the abnormal cell causes its surface to bristle with a lectin, which then binds to that lectin’s glycoconjugate on a healthy cell type, or vice-versa. Additionally, some unhealthy cells can coat themselves with lectins to allow them to bind to one another, ganging up into clumpings called emboli. This allows abnormal cells that are spreading to more easily escape from your immunological defenses, since the cells on the innermost layers of the emboli may survive even if the immune system destroys cells on the outer layer. By exploiting the match between lectin and glycoconjugate, unhealthy cells are more likely to launch an effective attack.
One lectin “lock” which many abnormal cells learn to “pick” is called galectin-3. Galectin-3 recognizes glycoconjugates, which have the sugar galactose as a key part of its structure (hence gal- (galactose) lectin). By sprouting galectin-3 – or its glycoconjugate – on their surfaces, these cells increase their ability to spread, to take root, and to grow new masses of deadly unhealthy cells. Manipulative abuse of galectin-3 has been implicated in the spread of abnormal cells in the pancreas, colon, lung, ovaries, breast, and especially the prostate. By churning out galectin-3, abnormal prostate cells can easily bind to healthy lung tissue, which is vulnerable to this attack because of its high amount of the lectin’s glycoconjugate; alternatively, by creating more galectin-3 glycoconjugates, abnormal prostate cells find it easier to metastasize to bone tissue.
MCP: A Molecular Decoy Against Metastasis
The idea of using MCP is that the galactose residues on the pectin molecules can provide alternate binding sites for abnormal cells rather than other cells. Animal and clinical studies have certainly found that this is an effective means to reduce the spread of abnormal cells. By delaying abnormal cell growth, MCP provides a larger window of opportunity for other interventions to be more effective.
Other Mechanisms that Promote Normal Cell Growth
MCP can inhibit certain steps of galectin-3-induced angiogenesis (the growth of new blood vessels to feed abnormal cell masses). Galectin-3 can also inhibit abnormal cell anoikis (a defensive mechanism in which abnormal cells are forced to detach from the healthy tissue’s extracellular matrix, leading them to commit cellular “suicide” (apoptosis)), and MCP can block the anti-anoikis action of galectin-3.