Thorne (heat treated) Fractionated Pectin Powder = Superior
Quote:
One Brand of Modified Citrus Pectin Kills Prostate Cancer Cells, Another Brand Has �Little Activity� Researchers Say
category: prostate, Pectin, Cancer, Vegetables, Fruits, Food News posted by jacquie @ 12:44 am
The Georgia researchers who announced that citrus pectin kills cancer cells actually discovered something more specific. They expected and showed that Thorne�s modified citrus pectin (heat-treated) is much more apoptosis-inducing than Pectasol (pH treated). The bombshell is dropped in the following sentences:
Commercially available fractionated pectin powder (FPP) [identified as the Thorne product] induced apoptosis (approximately 40-fold above nontreated cells) in both cell lines . . . . Conversely, citrus pectin (CP) [the standard umodified product] and the pH-modified CP, PectaSol, had little or no apoptotic activity.
And again when they go on to explain their aim, to see if they could turn plain citrus pectin into a potent anti-prostate cancer product by heat-treating it:
Since FPP had significant apoptotic activity, but PeS (Pectasol) or CP [standard unmodified citrus pectin] did not, intact and mild base treated FPP were compared with treated and untreated PeS and CP to identify any structural differences that correlated with FPP�s apoptotic activity.
I say bombshell because Pectasol, which failed the apoptosis test, is a brand of pH modified citrus pectin widely sold to prostate cancer patients, individually and through support groups.
Key to Pectasol�s popularity is one small clinical study conducted by Dr. Stephen Strum with and for Dr. Isaac Eliaz, who created and sells Pectasol (scroll down this German page for MODIFIED CITRUS PECTIN SLOWS PSA DOUBLING TIME: A Pilot Clinical Trial, Stephen Strum MD, Mark Scholz MD, Jon McDermed Pharm D, Michael McCulloch BA, Isaac Eliaz MD Presented at the International Conference on Diet and Prevention of Cancer, May 28 * June 2, 1999, Tampere, Finland); see also Strum et al, Prostate Cancer, 2003. Dr. Strum is on a medical advisory board at Life Extension Foundation. LEF markets the Pectasol brand. Dr. Eliaz sells it also, of course, through his company Econugenics.
Part of the theory behind Pectasol is that �The ability for cancer cells to �clump� appears to be mediated, at least in part, by carbohydrate-binding, proteins (CBP�s) located on the cell surface. One such CBP is a galactoside-binding lectin or �galectin� called galectin-3.� Now, a third type of citrus pectin, unmodified, called Pectin Plus is promoted and sold with claims that Pectasol is over-hyped and too costly. The same theory is repeated, that �cell-to-cell interaction is made possible by special protein molecules called galectins that sit on the outer surfaces of the cancer cells.� The claim is, unmodified pectin is effective at preventing cancer by interfering with this process.
To be clear, Dr. Eliaz does not claim that Pectasol induces apoptosis. He says (as in this press release) that his supplement �is recognized for its interaction with cellular adhesion.� He adds: �studies have demonstrated its effect on inhibiting cancer metastasis and reducing tumor growth. In prostate cancer, PectaSol� has been clinically shown to considerably slow the prostate specific antigen, PSA doubling time.� He continues: �The molecular weight and proper structure of the citrus pectin used in PectaSol� have been modified through several proprietary laboratory processes, making PectaSol� more readily absorbed into the bloodstream than regular pectin. PectaSol�s unique component, galactyosyl [sic; elsewhere, galactosyl], has an affinity for binding to certain cells of the prostate.
Everyone agrees that carbohydrate-binding, proteins (CBP�s) located on the cell surface, are involved in metastatic prostate cancer and are an appropriate target. Interaction between the galactosyl receptor on the cell surface and ligand on bone marrow cell surfaces, it�s believed, occurs in development of bone metastasis.CRD inhibitors are sought after. However, as the Georgia scientists point out, it has been known since 1999 that not all galectins sit on the surface of all prostate cancer cells.
The Georgia study states, prostate cancer cells of a common type (LNCaP), unlike those of other major cancers (lung, breast, colon, stomach, among others), �do not express galectin-3 (Ellerhorst et al. 1999, 2002; Califice et al. 2004; our unpublished observations).� Another recent article adds support to this negative view. Supposing pH modified citrus pectin is a small enough molecule to reach the surface of the cell, can it penetrate the cell wall? According to a Japanese team, in late stage cancer gallactin-3, no longer expressed to the cell surface, lurks in the cell nucleus or in the cytoplasm (Tomoharu Fukumori, 2006, full free text).)
Eating fruits and vegetables in plenty may prevent prostate cancer. And pH modified citrus pectin slows PSA rise (modifies log slope) in men with level 1 androgen-independence. That�s wonderful. Is it possioble that pH modified citrus pectin might do more for prostate cancer if combined with the heat-modified type?
The Georgia scientists say pectin appears to inhibit both primary tumors and metastatic progression, which is unusual:
Cancer therapy is aimed at either the primary tumor or metastatic cells. Because of the differences in the response of primary and metastatic cancers, most therapies do not address both cancer types. Pectin, a natural plant polysaccharide present in all higher plant cell walls, and thus in all fruits and vegetables and in most plant derived foods, is a compound that appears to be able to inhibit cancer metastasis and primary tumor growth in multiple types of cancer in animals.
They add that most of the published evidence for the anticancer effects of pectin used pH modified type, which is designed �to fragment pectin structure to facilitate biological effects in the systems under study. [e.g.to make a smaller molecule].� A possible downside to fragmenting the pectin is that this �may affect the structure of the pectin and thus its function.� FPP [the Thorne variety] �was not produced by pH treatment, but rather was produced by heating CP. We therefore utilized several methods to correlate the biological function of FPP with its structure and compared FPP structure with that of PeS and CP, which were not apoptotic.�
In seeing a problem in the rationale for selecting pH MCP for use against prostate cancer, namely, that LNCaP cells do not express galectin-3, they suggest that �the apoptotic effects of pectins reported here are due to mechanisms not mediated through galectin-3.� They set about to see if heating standard citrus pectin makes it more able to induce apoptosis in LNCaP cells.
And they succeeded: �Heat modification of the CP significantly increased its apoptotic response, making HTCP as apoptotically active as FPP.�
Finally, they ran a series of chemical tests on FPP (Thorne) in search of the structure that makes it able to kill cancer cells. �Taken together the results suggest that an ester-based (or related) cross-link in pectin is important for the apoptosis inducing activity of FPP.�
�Significantly, we have been successful in generating the apoptosis-inducing capability in CP by heat treatment, a critical step in the production of FPP from the mother pectin. This supports our conclusion that a specific pectin structure and/or pectin-containing linkage is responsible for inducing apoptosis.� If this is so, then fragmenting this structure by pH modification degrades the very quality of pectin which heat-treatment enhances. https://psa-rising.com/eatingwell/?p=28
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Thorne Research - Fractionated Pectin Powder - 5 oz
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Rebuttal from another forum:
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Commercially available fractionated pectin powder (FPP) [identified as the Thorne product] induced apoptosis (approximately 40-fold above nontreated cells) in both cell lines . . . . Conversely,
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Don't plan on getting excited just yet. This study was in the test tube with cells that were once part of a real live human prostate tumor, but were removed and are kept alive in artificial culture conditions. There are similarities and also substantial differences from how they functioned in the complex environment of a malignant tumor growing in its extremely complex human host.
I can't tell you how many studies with cultured cells have fallen flat on their face when the study moved from the test tube to a real live creature. The exciting test tube results vanished, and that was that.
sheila
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09-04-2007, 11:48 PM
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