A member asked me to post the reply I was to get from Dr Isaac Eliaz on MCP, Modified Citrus Pectin / Pectasol and I do this.
Below is my communication with dr Eliaz, generously facilitated by AnnieAppleseed, followed by excerpts from two studies.
Dr. Eliaz writes that 80 % of patients with BRPC, biochemically recurrent prostate cancer, have shortening of PSADT, PSA doubling time, over time. This is contrary to the study provided by TA that I linked to him, which indicates lengthened PSADT. Both are contradictory to a second study, which indicates that most patients have no consistent shortening or lengthening of PSADT.
If the assumption is made that the second, to MCP more favorable study, is valid, the results from MCP use according to the phase II pilot study MCP trial are superior. His case would be stronger with a reference to the 80% statement, or if a placebo had been used in the trial.
My letter:
Dear Dr. Eliaz,
As a user of your Modified Citrus Pectin, Pectasol, may I ask a couple of questions?
The phase II pilot study shows a statistically significant and impressive increase in PSA doubling time when using Pectasol. However, I understand that PSA doubling time normally increases even in the absence of any intervention for men with biochemically recurrent prostate cancer, according to this study: ncbi.nlm.nih.gov/pmc/articl...
If possible, it would be great to get a comment from you!
The study states that ADT and other cancer treatmeants were discontinued at least six months before the start of the trial. Is it known whether any of the 59 patients may have started ADT or other cancer treatments during the trial? My high-risk cancer is currently senescent, but if my PSA was increasing, I doubt if I would dare trust MCP as my only treatment no matter how much I believe in it!
Reply from dr Isaac Eliaz
Quite the timing. We just presented our 18 months multi center follow up with 90% benefits.
Patients were not on ADT during the study.
They had no ADT for a few months before the beginning of the study. I assume that if we excluded anyone who had ADT we would have gotten even better results.
80% of patients with BRPC have increased PSA velocity/shortening of PSADT over time. We slowed it down in almost 90% of patients after 18 months, compared to baseline, as the only treatment.
What is interesting is results that we are getting from the community- real life cases. It will have a major impact when finally published.
There is no issue in combining MCP (Pectasol) with other supplements and therapies.
All the best,
Isaac
Excerpt from the study posted to dr Eliaz that indicates lengthened PSADT over time ncbi.nlm.nih.gov/pmc/articl...
Methods
In retrospective analyses of two BRPC cohorts: Johns Hopkins Hospital (JHH) patients who deferred therapy and placebo patients on a randomized clinical trial (RCT), we calculated changes in PSADT from early measurements to later measurements using subsets of available PSAs for patients with ≥6 and ≥9 PSAs. We simulated hypothetical single-arm trials using randomly selected, 50-patient subsets and simulated two-arm RCTs. (Note: “placebo patients”were prostate cancer patients who were randomized to the placebo arm of a phase II RCT of an experimental targeted non-hormonal agent conducted in 41 sites in the United States and Canada).
Results
JHH cohort (n=205) had median follow-up 58 months, median age 61 years, and median Gleason 7. PSA variability changed with duration of PSA measurement as median within-patient PSADT increases for men with >6 PSAs ranged from 1.0 to 1.4 months by PSA subset while increases for men with ≥9 PSAs ranged from 3.9 to 4.1 months. Frequency of measurement did not change PSA variability as PSADT increase was unchanged when odd values were used instead of all values. Approximately 30% of JHH men experienced >200% increases in PSADT. Up to 62% of 50-patient single-arm simulations detected significant PSADT change, whereas simulated RCTs did not. Results were supported in the RCT placebo cohort; 46% of patients experienced PSADT increases >200%.
Conclusion
These data suggest that calculated PSADT in BRPC may naturally increase over time in the absence of therapy and may be influenced by duration of PSA follow-up. As a result, single arm trials could show false significant increases despite the lack of active treatment of these patients. Placebo-controlled RCTs including clinical endpoints are recommended to screen novel agents in men with BRPC to mitigate bias because of natural PSADT variability.
Excerpt from the one other relevant study, from 2021, that I could find in a quick search, which indicates no consistent pattern in change of PSADT.
auajournals.org/doi/10.1097...
INTRODUCTION AND OBJECTIVE:
Among men with hormone naïve biochemically recurrent (BCR) prostate cancer (PCa) after primary therapy, a shorter prostate specific antigen (PSA) doubling time (PSADT) predicts a greater risk of PCa specific mortality (PCSM). However, whether PSADT values stay consistent over time and the corresponding impact on prognostication for PCSM is currently unknown.
METHODS:
There were 1,652 patients treated with radical prostatectomy (RP) between 1982 and 2019 at 8 Veterans Affairs hospitals who had a biochemical recurrence included. For all patients, PSADT values were calculated using all the PSA values within each 12-month block after BCR up to 3 years. All patients had PSADT values for year one, 705 patients had PSADT values for year two, and 379 patients had PSADT values for year three. All PSA values were prior to adjuvant therapy and therefore had no impact on PSADT calculation. Statistical analyses included a Wilcoxon signed-rank test to evaluate changes in PSADT between years and univariable and multivariable cox regression models to evaluate associations with PCSM.
RESULTS:
There was no significant change in PSADT between years 1 and 2 or between years 2 and 3 (both p<0.05). Of the 379 patients with year three PSADT data available, 289 (76%) of them showed no consistent pattern of shortening or lengthening of the PSADT over the first 3 years after BCR (Figure 1). Change in PSADT was not associated with PCSM in univariable or multivariable analysis (both p<0.05), whereas the year 2 PSADT [HR (95%CI)=0.62 (0.48-0.82), p<0.001] and year 3 PSADT [HR (95%CI)=0.61 (0.46-0.82), p<0.001] significantly predicted PCSM after adjusting for pathological Gleason sum, seminal vesicle invasion, and lymph node metastasis.
CONCLUSIONS:
For the majority of patients having BCR after RP, PSADT did not change over time. However, while PSADT does not change consistently over time, the PSADT in year 2 and year 3 were strongly predictive of PCSM. This information may serve to guide patients and physicians regarding timing of adjuvant treatment among those at higher risk for PCSM following BCR after RP.