This post discusses the credibility of modified citrus pectin [MCP] as a concept & as a product for men with mets. Gus Gold prefers to defer to Dr. Myers, who saw no benefit in patients who used it, while Nalakrats cites an Israeli study (no link given).
A year ago, I reviewed the literature in:
"Foods/Supplements-Vitamins: Modified Citrus Pectin"
The first PCa study was published in 1995.
It is estimated that there are three million men in the U.S., living today, that once received a PCa diagnosis. With a product that has been around for over 20 years, I imagine that a large number of men have tried it or are currently using it. But so far, there hasn't been a lot of excitement generated.
As I mentioned in the earlier post, the only human study on PubMed is the 2003 paper (Dr. Strum was involved), where:
"We found that the PSADT increased ... in seven (70%) of 10 men after taking MCP for 12 months compared to before taking MCP."
Two months ago, I posted:
"ASCO Genitourinary Cancers Symposium (PectaSol-C modified citrus pectin)"
This is the study that Nalakrats mentions. It is not on PubMed & I doubt anything has been published yet.
"A stabilization or improvement (increase) of PSA doubling time was noted in 79% (n = 27) of" patients.
This appears to be the trial:
It is supposed to be completed by August.
"Study Director:Isaac Eliaz", who happens to be the MCP inventor.
Both studies are similar. In the more recent, the men had undetectable PSA after primary treatment, followed by biochemical relapse with negative scans.
MCP, the term coined by Eliaz, consists of short-chain nondigestible carbohydrate that can be taken up by the gut & into circulation. It just so happens that Gallectin 3, a protein that may be present on the surface of PCa cells, has an affinity for binding to carbohydrate. Gallectin may also be involved in the process by which circulating PCa cells dock, & also in the ability of distant cells to clump & form colonies.
So the idea is that MCP gums up the works & interferes with metastasis.
Neither study looked at metastasis - only PSA doubling time [PSADT].
Given the duration of the studies & the sustained increase in PSADT, there is presumably a direct effect on local tumors - not just on circulating tumor cells.
But, for men with advanced PCa, the question is whether MCP is able to have any effect on existing bone mets. We aren't likely to see a meaningful trial, IMO, so it requires a leap of faith.
How would we prove a benefit while on ADT, unless CRPC?
Of course, preventing new mets is always beneficial.
An account of the recent findings is below.
“With more than 60 percent of patients in the trial showing no evidence of disease progression, the results imply improvement over historical cohort data. No patient discontinued therapy because of side effects,” said Daniel Keizman, M.D., lead investigator of the multicenter trial study and head of the Genitourinary Oncology Service at Meir Medical Center in Kfar-Saba, Israel.
Of the first 34 patients completing six months of treatment, 27 (79%) showed lengthening of prostate specific antigen (PSA) doubling times, which is a measure of the progression of the disease. These results indicated that P-MCP may be controlling their cancer progression. Twenty-one patients (62%) showed improvement or stabilization of disease, without any progression. In 13 patients (38%), disease progression was seen, with 10 patients (29%) progressing only by PSA and only 3 patients (9%) progressing on bone or CT scans. In addition, P-MCP produced no significant side effects during the study period.
“Following surgery and/or radiation, about 30 percent of prostate cancer patients relapse biochemically with rising PSA levels. The benefit of androgen deprivation therapy, the typical treatment used in this situation, has not been demonstrated and may be offset by significant toxicities,” said Dr. Keizman.
The clinical trial is looking into the effects of P-MCP, which is a form of soluble, dietary fiber. Normal pectin contains long-branched carbohydrate molecules that cannot be absorbed by the gastrointestinal tract. P-MCP is a low molecular weight pectin with shorter fibers, providing greater bioavailability and therapeutic value. In addition, P-MCP has been shown to be active against galectin-3, an inflammatory protein overexpressed in cancer cells and linked to tumorigenesis and metastasis.
In the study, patients with biochemically relapsed prostate cancer, with progressively rising PSA levels in three or more tests, were enrolled in the prospective trial. Participants received 4.8 grams of P-MCP, three times a day, for six months. Since all patients demonstrated progression before the study on consecutive PSA tests, the reduction of PSA doubling time is a promising result.
This research builds on two previous clinical trials showing P-MCP consistently slows PSA level increases. A final analysis of this six-month study is planned for late 2018. Patients who did not progress clinically at six months are being treated for another 12 months. A full report, including 18-month data and correlative analysis, will be released once the data is complete.
“We are happy with the current results suggesting that P-MCP therapy may be active and safe in this setting. We are planning a future phase III randomized trial to assess the clinical benefit of P-MCP treatment in this setting,” says Dr. Keizman.
Source: Effect of PectaSol-C modified citrus pectin (P-MCP) treatment (tx) on PSA dynamics in patients (pts) with nonmetastatic, biochemically relapsed prostate cancer (BRPC): Results of the interim analysis of a prospective phase II study.
Daniel Keizman, Moshe A. Frenkel, Todd Michael Edwards, Eli Rosenbaum, David Margel, David Sarid, Victoria Neiman, Maya Gottfried, Natalie Maimon, Ilan Leibovitch, Hadas Dresler, and Isaac Eliaz. Journal of Clinical Oncology 2017 35:15_suppl, e16588-e16588