New study below [1]. Earlier (2021) results [2] - full text.
The study was on men with non-metastatic biochemically relapsed PCa. There was no placebo arm.
Dr. Isaac Eliaz created PectaSol - Modified Citrus Pectin [P-MCP] thirty years ago. There are 110 PubMed references to it - Eliaz claims over 70 actual published studies. He has been co-author on 13. There are 13 PCa studies - 4 with Eliaz as co-author. He leads an Israeli team on [1] / [2].
"In an early report of the present phase 2 study {[2]}, P-MCP treatment for 6 months led to prostate-specific antigen doubling time (PSADT) improvement in 75% of patients with BRPC-M0.
"Herein, we report the second long-term treatment phase of an additional 12 months of P-MCP therapy (4.8 g × 3/day orally) in patients without disease progression after the initial 6 months of therapy. Of the 46 patients that entered the second treatment phase, 7 patients withdrew consent and decided to continue therapy out of pocket, and 39 initiated the second treatment phase. After a total of 18 months of P-MCP treatment, 85% (n = 33) had a durable long-term response, with 62% (n = 24) showing decreased/stable PSA, 90% (n = 35) PSADT improvement, and all with negative scans."
Has anyone with mets experienced an increased PSADT while using PectaSol?
I have used MCP for a number of years now. It’s quite expensive. I take a lot of other supplements . I can’t say whether it extended the doubling time. My doubling time was quite good for an extended period then decreased before I had CyberKnife treatment to lymph node and bicalutamide. Doubling time then went back to quite low levels and is now increasing. So I still take it but can’t “prove” anything.
Another actionable article about a non SOC product that has a better than average chance of keeping the beast at bay. I have had a jar on my future use shelf since Nal mentioned it. My intent is to start using it once my ADT vacation starts.
I would think that if someone was going to spend the $$ to help stop/slow BCR, it would be with BROQ (sulforaphane) which in my opinion, seems to do a better job than MCP. Am I wrong. I actually take both, but MCP at a maintenance dose of 5g/day.
Watched the videos. The link I provided was the study she cites or getting that great results. And the other doc who is involved with the family supplement business references the product also used in the study. The results obviously speak for themselves in the study. And it used to be only available in Europe as it was made in France. They finally moved to the US and the product here is called BROQ. Sticking with that as it is simple and has the data behind it. I think I am going to go back to 60mg/day since that is what they recommend in these videos, was the study dosage, and the docs mention results are dose dependent. Glad you sent those links.
There is no magic bullet of course, so I take supplements that I view as having "possible benefit". Turns out that, unlike other cancers, there are a lot of supplements with possible benefit. I assume that these supplements may have additive benefit, or even synergy - unless specific antagonisms have been reported.
Looking closely at PCa/supplement studies in PubMed, one can identify a subset with "probable benefit". Human studies add weight. We are told not to confuse "association" with "causality", but when one has metastatic disease, a rational theory can readily be taken as "evidence".
In the case of MCP, we have the words of its creator (Isaac Eliaz) [1]:
"Most biomedical reports of MCP focus specifically on its antagonism of galectin-3 (Gal-3). ...
"Galectin-3 is a unique chimeric galectin containing a single carbohydrate recognition domain (CRD) ..."
"... the damaging effects of Gal-3 are due to its ability to accelerate the rate-limiting steps of metastasis ..."
{So, what if we were to introduce carbohydrate into the blood stream to attach to Gal-3? The carbohydrate would have to escape digestion - as does pectin. But pectin molecules are long. They would need to be chopped up - small enough to pass from the gut into the blood, and attach to Gal-3.}
"Most of the morbidity and mortality associated with cancer is caused by metastasis, which is the migration of cancer from the site of primary tumor growth to distant organs and tissues. The metastatic cascade contains several rate-limiting steps that are modulated by Gal-3 and, in turn, by MCP as well [53]. The first step for neoplastic cells is to survive apoptosis that is associated with the loss of anchorage (anoikis) following escape from the primary tumor and intravasation. Galectin-3 protects cancer cells from anoikis [56,57] by causing a cell cycle arrest at the late G1 phase, which is an anoikis-insensitive point [56]. MCP has been shown to downregulate cyclin B and cdc2 in human prostatic JCA-1 cells [58], which may cause an accumulation of cancer cells in G2/M, thereby inducing apoptosis.
"The next rate-limiting step in metastasis involves tumor cell arrest in distant organ microvasculature. Galectin-3 has been shown to mediate metastatic cell adhesion to the endothelium [59,60,61,62,63]. MCP was demonstrated to inhibit tumor cell adhesion to the endothelium as well as cancer cell homotypic aggregation involved in metastatic cell arrest in distant organs and the formation of intravascular metastatic deposits [59,64,65,66,67,68].
"The third rate-limiting step in metastasis involves a forking point where tumor cells can either proliferate inside organ microvessels until the metastatic tumor outgrows the blood vessel and invades distant organ parenchyma [69], or extravasate before starting secondary tumor growth. Invasive propensity involves a series of tumor cell interactions with ECM proteins associated with the basement membrane and target organ stroma. MCP has been shown to reduce Gal-3-mediated tumor cell interactions with ECM proteins such as laminin [66]. Also, citrus pectin polysaccharides dose-dependently decreased the invasion through matrigel of human endothelial cells [67], of MDA-MB-231 human metastatic breast carcinoma cells [70], and human buccal metastatic cells [70].
"After the initial parking in distant organs and extravasation, the overwhelming majority of cancer cells undergo apoptosis caused by various factors, and only ~2% survive and lead to micrometastasis [71]. Clonogenicity survival of early metastatic colonies is, therefore, the fourth rate-limiting step in metastasis. Galectin-3 protects cancer cells from different types of apoptosis by acting on mitochondrial pathways [72,73,74]. Some have suggested that MCP could undo Gal-3 anti-apoptotic function, thereby reducing the clonogenicity survival of cancer cells [74]. MCP dose-dependently inhibited the clonogenicity survival of hemangiosarcoma cells, and this was associated with increased tumor cell apoptosis [75].
"Micrometastasis that transforms into clinically relevant secondary tumors eventually comes to depend on the development of new blood vessels via angiogenesis, the fifth and final rate-limiting step in metastasis. Galectin-3 promotes angiogenesis by serving as a chemoattractant for endothelial cells and inducing endothelial cell motility, invasion through matrigel, and capillary tube formation [67,76]. MCP was found to thwart chemotaxis of human endothelial cells toward Gal-3 dose-dependently, and inhibit in vitro capillary tube formation by endothelial cells dose-dependently [76]. The administration of MCP also reduced angiogenesis and spontaneous metastasis in vivo in tumor-bearing mice [76].
"MCP can also modulate cancer cell resistance to chemotherapy. Most anti-neoplastic drugs work by inducing tumor cell apoptosis via the mitochondrial apoptosis pathway. As mentioned above, Galectin-3 dampens this pathway [77,78,79,80,81]. It also directly affects the sensitivity of cancer cells to chemotherapeutic drugs such as cisplatin [79,81,82], staurosporine [79], etoposide [81], bortezomib [83], dexamethasone [83], and doxorubicin (Dox) [75]. MCP has been demonstrated to reduce Gal-3 anti-apoptotic function and thereby reverse multiple myeloma cell resistance to bortezomib and enhance the response to apoptosis induced by dexamethasone [83]. Also, MCP substantially increased sensitivity to Dox-induced apoptosis in hemangiosarcoma cells [75].
"Beyond this, MCP has been shown to induce apoptosis in cancer cells by itself through a caspase-8-to caspase-3 signaling cascade in the absence of change to mitochondrial membrane potential [83]."
etc, etc, [1].
Eliaz knows his stuff. After reading the entire paper, I have to rate MCP as having "probable benefit". How can one not be enthusiastic?
On the other hand:
1] The product has been around for ~ thirty years.
2] There are over three million men living in the US, who once had a PCa diagnosis. Why is there no "buzz" surrounding MCP? In almost twenty years, I have never witnessed "buzz".
3] The pricing of P-MPC is predatory imo.
In my case, having had DVTs a dozen years ago, I now use nattokinase to eliminate even micro-clots, and D-dimer tests to monitor dosage. I have zero tolerance for a D-dimer result that is not <20 (the lowest value that LabCorp reports.) Consequently, I take 6 caps before bed & 6 caps in the morning, an hour before breakfast. Crazy, but I am using DES [diethylstilbestrol], a synthetic estrogen used before Lupron was approved & known for inducing abnormal coagulation.
I believe that metastasis cannot occur without micro-clots. Therefore, I do not worry about circulating PCa cells. I may be wrong, of course. And there may be a case for using MCP too.
I do have some P-MCP in the house, but I no longer use it.
Thanks for that detail. I also think there is enough evidence to use MCP, Broq, pomegranate juice, etc. No real downside other than $$ IMHO, and possible many upsides even outside of PC. Good to hear from you.
In my case, having had DVTs a dozen years ago, I now use nattokinase to eliminate even micro-clots, and D-dimer tests to monitor dosage. I have zero tolerance for a D-dimer result that is not <20 (the lowest value that LabCorp reports.) Consequently, I take 6 caps before bed & 6 caps in the morning, an hour before breakfast. Crazy, but I am using DES [diethylstilbestrol], a synthetic estrogen used before Lupron was approved & known for inducing abnormal coagulation.
I believe that metastasis cannot occur without micro-clots. Therefore, I do not worry about circulating PCa cells. I may be wrong, of course. And there may be a case for using MCP too
This is very interesting, As we are all looking to prevent metastasis.
What form of DES do you take? What are the side effects?
Hi PatrickWould you say that taking Apixaban (Eliquis) twice a day for my recurring DVTs is a good thing then? Trying to get my head around things but reading your comments, but is stopping the micro clots using an anticoagulant a good thing then?
The idea behind anticoagulants is that they delay coagulation and give plasmin time to dissolve unwanted fibrin clots. In theory, any anticoagulant will allow the body to quickly eliminate micro-clots.
Removing a DVT will take a lot longer, of course.
Plasmin is structurally similar to nattokinase. i.e. nattokinase can speed things up.
D-dimer is a protein structure that is formed when fibrin is broken down. Thus, a D-dimer test is a measure of breakdown activity, and therefore of clot magnitude. If D-dimer is elevated, plasmin could use a little help - regardless of anticoagulation meds. If D-dimer is near zero, there is no serious active clot.
D-dimer may be elevated for other reasons, but that has never been the case with me - & I have been testing for a very long time. Also, men with PCa should always assume that an elevated D-dimer = a significant clot, imo.
So you decided P-MCP does not meet your criteria of "there are a lot of supplements with possible benefit. I assume that these supplements may have additive benefit, or even synergy - unless specific antagonisms have been reported." What changed your mind for P-MCP--I would love to shorten my supplements list. Was it just your above list of three "on the other hand"?
Looking closely at PCa/supplement studies in PubMed, one can identify a subset with "probable benefit". Human studies add weight.
Soon after diagnosis in 2004, I came across a 2003 paper on MCP where Stephen Strum was one of the authors. He was quite famous at that time - in the same way that Myers later became, so I paid more attention.
"A total of 13 men were evaluated for tolerability and 10 for efficacy. Changes in the prostate-specific antigen doubling time (PSADT) of the 10 men were the primary end point in the study. We found that the PSADT increased (P-value<0.05) in seven (70%) of 10 men after taking MCP for 12 months compared to before taking MCP. This study suggests that MCP may lengthen the PSADT in men with recurrent prostate cancer." [1]
(A co-author was Mark Scholz, with whom Strum wrote ten other papers.)
Strum was responsible for Life Extension material on PCa.
Anyway, 20 years have gone by since that paper & I don't think that MCP studies have delivered regarding its ability to prevent metastasis.
Meanwhile, the PCa literature on Warfarin supports the theory that micro-clots are essential for metastasis. Hence my Nattolinase/D-dimer protocol.
MCP might well be a good add-on. (And perhaps I'd do that if I didn't feel that Eliaz was price-gouging.)
Thanks. Amongst other things I take P-MCP, Pomi T, I have now started taking BROQ having previously taken BroccoMax from Jarrow formulas, I take 3 caps of Natto daily and, every 3 days a baby aspirin. I regard a lot of these as having predatory pricing and BROQ seems very expensive in the UK does anyone think it is more effective than BroccoMax? The only supplement that I have taken that showed a direct correlation to a PSA decline was when I first started taking Vit D3. My PSA was at 0.06 for about 6 months consistently post RP. Then I added D3 to my supplement regime and for many months my PSA went down to 0.03. Like you I think it is about taking intelligent punts without doing harm but as Teufel says is does cost $$ or in my case £££ ! But I am still here after 8 years Lol
UK here as well. I take pomi-t. I take Prostaphane, rather than BROQ. Again, expensive but this is the French version and it is claimed to be the best version, used in the sulforaphane clinical trials. I take 2 a day. The trials were based on 6 per day but the manufacturer now states to do 2 or 3 max. Good luck my friend.
Hi yes I have started Prostaphane too I just labelled it as BROQ because I thought most of the readers would be from US. Prostaphane is , as you say, expensive in U.K. but I think still cheaper than BROQ in U.K. and as you say the basis of the trial. I have just worked my way up to 6 per day. Good luck and best wishes to you too
For those interested in Sulforaphane in its various plant and supplement forms, turn off Netflix for a night and take 2 3/4 hours to watch these two videos from Sulforaphane super-advocate Dr. Ronda Patrick (FoundMyFitness.com). The first is her enthusiastic overview of the possible health benefits of sulforaphane. The second longer video, hosted by Dr. Patrick, is a Q&A session with noted and recently-retired Johns Hopkins Researcher, Dr. Jed Fahey.(Embedded in each is specific information related to prostate cancer and other related health conditions.)
1. Sulforaphane and Its Effects on Cancer, Mortality, Aging, Brain and Behavior, Heart Disease & More, FoundMyFitness
2. Q&A with Dr. Jed Fahey on Sulforaphane, Moringa and Chemoprotection [An authoritative discussion!], FoundMyFitness (Those taking supplements will want to pay attention to the discussion at 1:22:44. Being in the UK, you have the good fortune to have what Dr. Fahey says is the only stabilized sulforaphane product - not relying on your own or dietary myrosinase for its conversion from glucoraphanin - that is currently available world-wide.)
Note the heating process Dr. Patrick describes at the end of video #1. I'm currently doing something similar to what she described in the short video #3 below to increase the sulforaphane (+/- 3.5 x) and reduce the need to eat + 100 grams to get an effective dose. I also sprinkle some powdered mustard in the heated water and on any raw sprouts to help insure the formation of sulforaphane.
3. How To Increase Sulforaphane in Broccoli Sprouts by ~3.5-fold, FoundMyFitness
Hi Cujoe thanks very much for these. I am working my way through them. Very interesting. Was Prostophane the supplement that you were referring too as being available in the UK albeit made in France?
GS - Yes. Dr. Fahey refers to it specifically - and seems to indicate that more Sulforaphane-specific products may be under development. If I remember correctly, he indicated that these are synthesized products and not biologicals. Either way, it would be very beneficial to have the sort of consistent control over dosage that a Sulforaphane product like your Prostophane provides. As with PSMA diagnostics/theranostics our most-most-expensive-health-care-system-in-the-world here in the US lags behind that of other countries.
Cujoe current daily cost of 6 capsules of Prostophane is c 5.79 dollars if you buy 90 capsules. If you buy 360 capsules it works out at c 5.23 dollars (£4.14). It may be possible to reduce by c 5% via a longer term subscription. I don't think I should work out my total daily costs of supplements LoL
Daily Cost ~ Guess I could skip a dirt-cheap lunch and take a BROQ cap instead? You are correct, sometimes it is better not to know daily costs. Stay S&W, cujoe
Rather than pay a premium for the golden ratio, I bought the individual powders from Source Natural. Interestingly, The inositol tub weighed 16 oz, while the IP-6 tub weighed 400 grams - probably to avoid accusations that the two products were aimed at the IP-6 Gold market.
I used the stuff for years & I see that the remains that I have expired in 2014/15. I seem to have managed without, but I recommend the powder approach - the tubs last forever.
IP(6) - Inositol Hexaphosphate - phytic acid - is found in bran, seeds, legumes & nuts to varying degrees. In supplement form, it probably comes from rice bran.
IP(6) is a store of phosphorus in plants. Ruminants produce the enzyme phytase, which releases the phosphorus. Elsewhere, I write about the importance of limiting phosphorus intake, which inhibits conversion of hormonally active vitamin D. We do not want to liberate the phosphorus of IP(6), but gut bacteria may produce some phytase - perhaps more so in vegetarians.
Phytic acid is classed as an antinutrient. This is because it binds to minerals. When used as a supplement, IP(6) should not be taken with food, as it will bind to minerals in the meal & they will not be absorbed.
[2] PCa Cell & Mice Studies (oldest first).
[2a] Shamsuddin is the man behind "IP-6 Gold". He patented a ratio of (Inositol Hexaphosphate):(Inositol) = 22:80. [2a1] Competing supplements have to avoid combining the two in anything like that ratio.
Source Natural sells IP-6 powder (400 g) with a dose of 1.5 tsp = 3.7g [2a2], & they also sell Inositol powder (16 oz) with a dose of 0.25 tsp = 845 mg [2a3]. It's cute that one is packaged in grams & the other in ounces, & doses are given in g & mg, but I think the intent is clear. If they had used an IP-6 dose of 1.25 tsp, rather than 1.5 tsp, the ratio would be almost identical to Shamsuddin's.
(Look in Amazon for cheaper options.)
At those weights, the powder lasts forever. I measure, mix in water, & swallow while my 5 a.m. coffee is brewing. It has no taste to speak of. Wait at least an hour before eating.
gets 35 hits on PubMed, for those interested in his non-PCa IP(6) papers. The studies span ten years & stopped ten years ago.
[2a4] (1995 - U.S. - Shamsuddin)
"Inositol hexaphosphate inhibits growth and induces differentiation of PC-3 human prostate cancer cells."
[2b] Agarwal (Colorado) has done most of the research on IP(6) & PCa. Twelve PubMed papers (2000-2013). Some are too technical to comment on here, but links are provided for [2b1] through [2b12], below signature. Some extracts follow.
[2b4] "Our results suggest that IP6 could be a potent dietary agent in controlling the growth of advanced PCA cells and inducing their apoptotic death, in part, by its inhibitory effect on constitutively active NF-kappa B signaling pathway."
[2b5] (Mouse study) "IP6 suppresses hormone-refractory PCA growth accompanied by inhibition of tumor cell proliferation and angiogenesis and increased apoptosis. IP6-caused increase in IGFBP-3 and decrease in VEGF might have a role in PCA growth control."
IGFBP-3 is the major binding protein for IGF-I (insulin-like growth factor I) & is down-regulated by PCa. It reduces free IGF-I (a good thing). VEGF is the growth factor for new blood vessels, so a decrease is a good thing too.
[2b7] A full-text review paper.
[2b12] "Constitutive activation of ... (PI3K)-Akt pathway transmits growth-regulatory signals that play a central role in promoting survival, proliferation, and angiogenesis in human prostate cancer cells. Here, we assessed the efficacy of inositol hexaphosphate (IP6) against invasive human prostate cancer PC-3 and C4-2B cells and regulation of PI3K-Akt pathway. IP6 treatment of cells suppressed proliferation, induced apoptosis along with caspase-3 and poly(ADP-ribose) polymerase (PARP) cleavage, and inhibited constitutive activation of Akt and its upstream regulators PI3K ... "
"These findings suggest that, by targeting the PI3K-ILK1-Akt pathway, IP6 suppresses cell survival, proliferation, and angiogenesis but induces death in prostate cancer cells, which might have translational potential in preventing and controlling the growth of advanced and aggressive prostate cancer for which conventional chemotherapy is not effective."
[2c] Other PCa studies.
[2c1] "Inositol hexaphosphate represses telomerase activity and translocates TERT from the nucleus in mouse and human prostate cancer cells via the deactivation of Akt and PKCalpha."
"Since the activation of telomerase is crucial for cells to gain immortality and proliferation ability, we examined the role of IP6 in the regulation of telomerase activity in prostate cancer cells. Here, we show that IP6 represses telomerase activity in mouse and human prostate cancer cells dose-dependently."
The telomere is a primitive counter. It shortens with each cell division. This limits the number of times a cell can divide (Hayflick limit). PCa restores telomerase, which prevents the shortening of the telomere. IP(6) inhibits telomerase.
[2c2] (2014 - China) Seems to verify upregulation of IGFBP-3.
Interesting. Patrick I know that you do not take PMCP but it should be taken on an empty stomach too. Does anyone know whether it is desirable to take IP-6 at the same time or would PMCP need to be taken at a different time?
Regarding MCP, one wonders about bioavailability, & whether MCP binds to anything important (other than galactic-3).
A study looked at urinary excretion after "15 g of MCP ... each day for 5 days and 20 g on day 6. Twenty-four hour urine samples were collected on day 1 and day 6 for comparison with baseline."
"In the first 24 h of MCP administration the urinary excretion of arsenic increased significantly (130% ...). On day 6, urinary excretion was increased significantly for cadmium (150%, ...). In addition, lead showed a dramatic increase in excretion (560% ...)"
Do I see somewhere someone mentioning multiple studies on citrus pectin and cancer? Because they must not either be Modified Citrus Pectin or not specific to Prostae Cancer as I don't see a wide body of pubished evidence on MCP and Prostate Cancer.
I just have 2 points to make other than the above.
(1) There's always been a question of substances "masking" PSA versus actually having an affect on PCa cells.
(2) The most referenced study specifically states brand "Pectasol". Now that's good that they say what formulation they used, but anytime a study references a specific name brand supplement, I'm highly skeptical of potential bias ESPECIALLY if the study was funded by the maker!
"The authors acknowledge ecoNugenics, Inc. (Santa Rosa, CA, USA) for providing P-MCP and funding support."
PectaSol is professionally formulated in the USA by leading authority of integrative medicine & cellular health, Dr. Isaac Eliaz (M.D., L.Ac.), founder of ecoNugenics.
It sounds to me (and from my own reading a couple years ago) that the consensus of this thread is Sulforaphane has a larger more scientifically robust body of evidence for benefit than MCP. You could be spending hundreds a month on supplements and have no idea what is doing what. Could the KISS (Keep It Simple Stupid) premise apply? Diet, Exercise, and pick one or two things to supplement?
Diet, Exercise, Sulforaphane + Vitamin D+K would be my choice and spend the money saved on all the other supplements on a nice vacation once a year.
Since adding Sulforophane my 3 monthly PSA tests have shown one PSA reading at level in other words I have two successive level results without an increase. Prior to that successive small but steady increases. Too early to say obviously and a sample of 1. But if it helps buy a bit of time I would be very happy with that. The only time I got a decline post RP was when I loaded up on Vit D3 and that seemed to buy a year until presumably the cancer finds a work around. I take K2 too and diet/exercise.
What brand and dosage regimen are you using for Sulforphane? I know BROQ is the most well-known as the "stabilized' SFN they used is supposed to be the most bioavailable but they sure seem to be price gouging based on that reputation as I'd question if Jarrow's BroccoMax at 2 caps twice a day may be equally effective. Their lab results of their competitors are suspect as to the methodology and confusion as to did they test one dose or one cap in some products that one does = 2 caps.
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Metastasis Directed Therapy (MDT) is here to stay for Oligometastatic Patients !!! Part(1) SABR/SBRT