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Thread: polyphenois

  1. #1

    polyphenois

    I have not seen polyphenols discussed. Was at PC support group today and an oncology nurse says their docs are advocating it in pill form.

    http://www.ascopost.com/issues/janua...ncer-patients/

    Any opinions/research? Denis
    65 YO healthy man
    PSA has been 4.1/2 for a couple years,
    PSA 5/1/17 4.6,
    Multiparametric MRI, 5/15/17 showed lesion
    13 core needle biopsy 3 cores positive 3+3 and one positive in the lesion, may be overlap
    All cores less than 30%
    8/22/17 - second opinion pathology shows a small amount of (3+4) in one core, < 5%, ordered decipher to inform next steps
    9/27/17 -Decipher test shows intermediate risk so now exploring treatment options.
    2/6/18 - completed HDR BT
    5/3/18 Post HDR BT PSA 1.3
    9/18/18 PSA 1.2
    Thanks, Denis
    "One day at a time"

  2. #2
    Denis, if you have a look at Topic (S) in the Subforum, you'll find a number of studies on polyphenols from plant sources. It is one of the most studied and promising group of supplements. See also Chuck's new thread Food for Thought.
    Last edited by DjinTonic; 12-06-2018 at 03:13 AM.
    69 yr at Dx, BPH x 20 yr, 9 (!) negative biopsies, PCA3 -
    2013 TURP (90→30 g) then PSA 2x/yr, DRE yearly
    6-06-17 DRE nodule R, last PSA rise, on finasteride: 3.6→4.3
    6-28-17 Biopsy #10: 2/14 cores: G10 (5+5) 50% RB, G9 (4+5) 5% RLM
    Bone scan, CTs, X-rays: negative
    8-7-17 Open RP, neg. frozen sections, Duke Regional, my Uro, 8-20 RPs/mo. x 25 yr.
    SM EPE LVI SVI LNI(16): negative, PNI +, nerves spared
    pT2c pN0, bilat. adenocarcinoma G9 (4+5) 5% of prostate (4.5 x 5 x 4 cm, 64 g)
    11-10-17 Decipher 0.37 Low Risk: 5-yr met risk 2.4%; 10-yr PCa-specific mortality 3.3%
    Dry; ED OK with sildenafil
    9-16-17 (5 weeks) PSA <0.1; Pomi-T (2 capsules/day)
    LabCorp uPSA (Roche ECLIA):
    11-28-17 (3 mo. ) 0.010
    02-26-18 (6 mo. ) 0.009
    05-30-18 (9 mo. ) 0.007
    08-27-18 (1 year) 0.018
    09-26-18 (13 mo) 0.013 (checking rise)
    11-26-18 (15 mo) 0.012

  3. #3
    Thanks Dijon
    65 YO healthy man
    PSA has been 4.1/2 for a couple years,
    PSA 5/1/17 4.6,
    Multiparametric MRI, 5/15/17 showed lesion
    13 core needle biopsy 3 cores positive 3+3 and one positive in the lesion, may be overlap
    All cores less than 30%
    8/22/17 - second opinion pathology shows a small amount of (3+4) in one core, < 5%, ordered decipher to inform next steps
    9/27/17 -Decipher test shows intermediate risk so now exploring treatment options.
    2/6/18 - completed HDR BT
    5/3/18 Post HDR BT PSA 1.3
    9/18/18 PSA 1.2
    Thanks, Denis
    "One day at a time"

  4. #4
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    Join Date
    Aug 2016
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    So here is my question. We use measurement of PSA to signal the activity of cancer. In studies such as these, how do we distinguish from the effect on PSA and the effect on the cancer?

    While I was able to manipulate my PSA with an anti-inflammatory diet and supplements what assures me it is having an impact on the cancer?

    For example, I can reduce a low grade fever to near normal with pain relievers yet the underlying cause goes untreated.

    Does a supplement reduced PSA give the cancer more time by delaying treatment?

    Here is my experience, I wasted a year or more denying and delaying treatment suppressing my PSA. Did I prolong my need for treatment, kick the can down the road so to speak, or did I give the cancer more time to do it's thing even if accepting it may have slowed, i.e. a stunted G4 throws off 2 metastic cells instead of 4.

    Prolonging treatment seems a risky business when you know, or don't know, you have G4 or 5.

    We use cranberry juice for UTIs. It can help, marginally, but a UTI is not cancer.

    I'll repeat, 20% of all liver and kidney damage is now the result of supplement use. Be careful.

    Delayed treatment, like death, seems a poor measure for success in these studies.
    Last edited by Another; 12-06-2018 at 01:27 PM.

  5. #5
    Quote Originally Posted by Another View Post
    So here is my question. We use measurement of PSA to signal the activity of cancer. In studies such as these, how do we distinguish from the effect on PSA and the effect on the cancer?

    While I was able to manipulate my PSA with an anti-inflammatory diet and supplements what assures me it is having an impact on the cancer?

    For example, I can reduce a low grade fever to near normal with pain relievers yet the underlying cause goes untreated.
    This is a good question, and here is my understanding.

    The impetus to try a plant-derived (or other natural compound) often can come from(1) anecdotal evidence that something helps another condition or disease, and (2) its chemical structure or family is similar to another compound that has demonstrated a desired effect. Studies are then done in vitro, where the compound is put in contact with tissue cultures of a PCa line. Researchers are looking for apoptosis, or the ability of the substance to cause the malignant cells to undergo the normal programmed death of healthy prostate cells (cancer cells are zombies they live on and on, grow, replace healthy tissue and don't function properly); healthy cells of most organs die at a certain point in their lives and are replaced). I see studies about new natural substances inducing apoptosis in PCa cells every month--which only means that they warrant being studied.

    If the substance is extracted and integrated in a diet as a supplement, it's reasonable to think that a lowering of PSA is from a direct effect on the tumor cells. The British Pomi-T study was formulated specifically for a study (capsules of green tea, broccoli, tumeric, and pomegranate); see Subforum (S) #9. The study was double-blind, randomized and placebo controlled. There was a lowering of PSA and another commentary I've put there states that this lowering was accompanied by a reduction of lesion size on imaging. That's the best kind of evidence, which, unfortunately, we don't usually have. I believe further studies are underway on Pomi-T, which was commercialized. I've been taking it.

    I think if you read the research studies you'll find discussion about various proposed mechanisms of action that substances have on PCa cells. But getting back to your point, there is current thinking that inflammation itself plays a role in the carcinogenesis of PCa, so the picture is complex!
    69 yr at Dx, BPH x 20 yr, 9 (!) negative biopsies, PCA3 -
    2013 TURP (90→30 g) then PSA 2x/yr, DRE yearly
    6-06-17 DRE nodule R, last PSA rise, on finasteride: 3.6→4.3
    6-28-17 Biopsy #10: 2/14 cores: G10 (5+5) 50% RB, G9 (4+5) 5% RLM
    Bone scan, CTs, X-rays: negative
    8-7-17 Open RP, neg. frozen sections, Duke Regional, my Uro, 8-20 RPs/mo. x 25 yr.
    SM EPE LVI SVI LNI(16): negative, PNI +, nerves spared
    pT2c pN0, bilat. adenocarcinoma G9 (4+5) 5% of prostate (4.5 x 5 x 4 cm, 64 g)
    11-10-17 Decipher 0.37 Low Risk: 5-yr met risk 2.4%; 10-yr PCa-specific mortality 3.3%
    Dry; ED OK with sildenafil
    9-16-17 (5 weeks) PSA <0.1; Pomi-T (2 capsules/day)
    LabCorp uPSA (Roche ECLIA):
    11-28-17 (3 mo. ) 0.010
    02-26-18 (6 mo. ) 0.009
    05-30-18 (9 mo. ) 0.007
    08-27-18 (1 year) 0.018
    09-26-18 (13 mo) 0.013 (checking rise)
    11-26-18 (15 mo) 0.012

  6. #6
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    Join Date
    Aug 2016
    Posts
    1,123
    Quote Originally Posted by DjinTonic View Post
    This is a good question, and here is my understanding.

    The impetus to try a plant-derived (or other natural compound) often can come from(1) anecdotal evidence that something helps another condition or disease, and (2) its chemical structure or family is similar to another compound that has demonstrated a desired effect. Studies are then done in vitro, where the compound is put in contact with tissue cultures of a PCa line. Researchers are looking for apoptosis, or the ability of the substance to cause the malignant cells to undergo the normal programmed death of healthy prostate cells (cancer cells are zombies they live on and on, grow, replace healthy tissue and don't function properly); healthy cells of most organs die at a certain point in their lives and are replaced). I see studies about new natural substances inducing apoptosis in PCa cells every month--which only means that they warrant being studied.

    If the substance is extracted and integrated in a diet as a supplement, it's reasonable to think that a lowering of PSA is from a direct effect on the tumor cells. The British Pomi-T study was formulated specifically for a study (capsules of green tea, broccoli, tumeric, and pomegranate); see Subforum (S) #9. The study was double-blind, randomized and placebo controlled. There was a lowering of PSA and another commentary I've put there states that this lowering was accompanied by a reduction of lesion size on imaging. That's the best kind of evidence, which, unfortunately, we don't usually have. I believe further studies are underway on Pomi-T, which was commercialized. I've been taking it.

    I think if you read the research studies you'll find discussion about various proposed mechanisms of action that substances have on PCa cells. But getting back to your point, there is current thinking that inflammation itself plays a role in the carcinogenesis of PCa, so the picture is complex!
    Good answer if you don't have cancer. Meaning, once you have cancer the cancer rules the context. The horse is out of the barn and avoiding cancer or delaying treatment is not the issue. If it is untreatable, then by all means.

  7. #7
    Quote Originally Posted by Another View Post
    Good answer if you don't have cancer.
    I'm not sure I'm following you. The Pomi-T subjects had had primary treatment for PCa and the study was looking at BCR.

  8. #8
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    We look for BCR to guide us in treatment, not delay. If I am ultimately going to need a second round of treatment I'd rather know sooner than later and treat it sooner than later. the only thing that alters that view is if the study reports the supplement cures cancer, not just slow it. A "slower" growing G4 still has a risk the longer it is alive and in my body.

    As long as these reports only report a drop or slowing of PSA and no actual regression of G4 and 5, I'm a skeptic.
    Last edited by Another; 12-06-2018 at 06:54 PM.

  9. #9
    great discussion. I have not been a supplement guy. The issue is the double edge sword. Does the supplement actually help or just delay? Depending on age delay may be a good thing. Also does the supplement cause other damage has to be considered. It seems logical that how we fuel our bodies has an impact on health and healing. And research into PC always takes a very long time. For those of us in our sixties and seventies, the timeline for proving research may be too late to help us, so do we gamble a bit and try promising ideas?

    Thanks, guys for the thoughts. Denis
    65 YO healthy man
    PSA has been 4.1/2 for a couple years,
    PSA 5/1/17 4.6,
    Multiparametric MRI, 5/15/17 showed lesion
    13 core needle biopsy 3 cores positive 3+3 and one positive in the lesion, may be overlap
    All cores less than 30%
    8/22/17 - second opinion pathology shows a small amount of (3+4) in one core, < 5%, ordered decipher to inform next steps
    9/27/17 -Decipher test shows intermediate risk so now exploring treatment options.
    2/6/18 - completed HDR BT
    5/3/18 Post HDR BT PSA 1.3
    9/18/18 PSA 1.2
    Thanks, Denis
    "One day at a time"

  10. #10
    Quote Originally Posted by SubDenis View Post
    great discussion. I have not been a supplement guy. The issue is the double edge sword. Does the supplement actually help or just delay? Depending on age delay may be a good thing. Also does the supplement cause other damage has to be considered. It seems logical that how we fuel our bodies has an impact on health and healing. And research into PC always takes a very long time. For those of us in our sixties and seventies, the timeline for proving research may be too late to help us, so do we gamble a bit and try promising ideas?

    Thanks, guys for the thoughts. Denis
    Lumping all supplements together is like asking "can medication help me?", as if either were monolithic. Some of the most important medications have come from nature. I would suggest anyone interested in supplements look at the research, ask your docs, and decide for yourself. The PDQ publication I've referenced is a good place to start. Benefit can probably be had by simply introducing or increasing some foods. Eating healthy isn't a bad idea.

    Perhaps the situation after primary treatment is like starting afresh, with few remaing, perhaps healthy, prostate cells. If I have some chance of delaying or even preventing PCa from taking hold before I die...why not do it?
    Last edited by DjinTonic; 12-08-2018 at 12:12 PM.

 

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