It is definitely good form to get an OK from your doctors- the guys you are paying big $ to for them to give you treatments- to make sure you are not taking any substance- prescript
ion or non- that will fight against your treatment. Maybe even more so for the RT guys. You would not want to take a bunch of anti oxidants( also makes me wonder about
certain foods supposedly loaded with anti-ox?) that might well fight against the ROS approach of your treatment. Be careful!
But, an interesting take on that whole anti-oxidant thing is: apparently- at least some have claimed- certain vitamins and nutrients can act in the role of either anti OR pro ox, according to the bodies need. After my diagnosis, just prior to joining here, while I waited for my scheduled RP, with my doc's permission I did some supplemental changes. One was a combination of Vitamin C and Vitamin K in a specific ratio. Someone was trying to patent this combo as a prescript
ion drug, so it got some sort of FDA "orphan drug" status and a small human trial ensued. But in this trial, as well as another from Uraguay that I read, and multiple in vitro and in vivo studies, they all seemed to be saying the same thing:
this combo caused PC cell apoptosis via ROS production, IOW production of hydrogen peroxide at the PC cell level, or something like that.
Based on this and advice from some other sources that I have had good luck with, I decided to try it. Of course I could not take the
drug that had been tested, but I could easily enough mix the vitamins in the ratio and dose used in the tests, and I did so during the month or two prior to my RP. Now I well realize that decreasing PSAs mean nothing, even though we often call a regular medical treatment good(surgery,RT,HT) if PSAs drop as hoped for. And, in my case I had never, over a 12 year period, had a PSA that did anything but go up. Including a significant rise after antibiotic treatment while waiting to get in to see my URO. Plus, PSAs are more likely to go up after a Bx than go down, right? And surely it would have been just as easy for my PSA to have gone up or stayed the same during the 2 months after Bx? But my PSA dropped 25% during the 2 months before surgery. Whatever.
Probably means nothing. But the point is that there are some science types out there who are of the opinion that some nutrients or vitamins have the ability to act as either anti or pro oxidants, which I personally find interesting. Still, everyone should clear anything they take with their doctors. I do that myself, so far my docs have told me to just keep on doing whatever I am doing, so I do.
Here is the study of the
drug Apatone(VitC/VitK3) that put me onto that.
Very low level evidence no doubt, but interesting(to me) none the less. This is the lower dose trial where PSAs did not actually go down, but simply stopped rising or at least slowed down until treatment was discontinued. The other study, from Uruguay, used a higher dose and homocystein(sp?) and PSA(after an initial PSA rise such as is supposedly seen when PC cells start dying?) dropped steadily during the entire treatment period. Also, these guys can not be accused of designing a study to help sell a supplement, but can possibly be accused of designing a study in hopes of selling a drug. But wouldn't that be the purpose of all drug studies?
Caution: I am NOT presenting these studies because I want someone to go out and try to mimic this drug! It is to make the point that some scientists appear to think that some vitamins- known mainly for their anti-oxidant roles, can also function in a pro-oxidant manner, just the opposite of the way we think they normally operate /www.ncbi.nlm.nih.gov/pmc/articles/PMC2288789/Somebody said...
A 12 Week, open Label, Phase I/IIa Study Using Apatone® for the Treatment of Prostate Cancer Patients Who Have Failed Standard Therapy
Basir Tareen,1 Jack L. Summers,1 James M. Jamison,1 Deborah R. Neal,1 Karen McGuire,1 Lowell Gerson,1 and Ananias Diokno2
1. Summa Health System, Department of Urology, Akron, Ohio, USA
2. William Beaumont Hospital, Department of Urology, Royal Oak, Michigan, USA
Correspondence to: Basir Tareen, M.D., Department of Urology, New York University, 550 First Avenue, New York, NY 10016. ude.kadon.enicidem@neerat
Conflict of interest: The authors have declared that no conflict of interest exists.
Author information ▼ Article notes ► Copyright and License information ►
This article has been cited by other articles in PMC.
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Abstract
Purpose: To evaluate the safety and efficacy of oral Apatone® (Vitamin C and Vitamin K3) administration in the treatment of prostate cancer in patients who failed standard therapy.
Materials and Methods: Seventeen patients with 2 successive rises in PSA after failure of standard local therapy were treated with (5,000 mg of VC and 50 mg of VK3 each day) for a period of 12 weeks. Prostate Specific Antigen (PSA) levels, PSA velocity (PSAV) and PSA doubling times (PSADT) were calculated before and during treatment at 6 week intervals. Following the initial 12 week trial, 15 of 17 patients opted to continue treatment for an additional period ranging from 6 to 24 months. PSA values were followed for these patients.
Results: At the conclusion of the 12 week treatment period, PSAV decreased and PSADT increased in 13 of 17 patients (p ≤ 0.05). There were no dose-limiting adverse effects. Of the 15 patients who continued on Apatone after 12 weeks, only 1 death occurred after 14 months of treatment.
Conclusion: Apatone showed promise in delaying biochemical progression in this group of end stage prostate cancer patients.
Keywords: Prostate, Prostate neoplasms, ascorbic acid, menadione, Vitamin K3, Apatone, Cancer
Go to:
Introduction
The PSA era has led to a stage migration in the clinical course of prostate cancer. While this success has dramatically lowered the death rate from prostate cancer, it remains the most common cancer in men with 234,460 new cases and 27,350 deaths in the US in 2007....................................Treatment
All patients were treated with Vitamin C: K3 (5,000 mg. of VC and 50 mg. of VK3 each day, Apatone) for a total of 12 weeks. Apatone in capsular form (500 mg VC as ascorbate and 5mg VK3 as bisulfite) at a dose of 2 capsules on arising, then 1 capsule every two hours for six doses followed by two capsules at bedtime for a total of ten capsules per day. Following the 12 week study, two of the three “non-responders” in the study who had large body mass index values were given double the dose of Apatone by doubling the number of capsules in the previous regimen.........................
Pre-treatment PSAV ranged from 1.05 to 696 ng/ml/year (median 21.6 ng/ml/yr), while in-trial PSAV ranged from -12 to 256 ng/ml/year (median 6.39 ng/ml/yr). Conversely, pre-treatment PSADT values ranged from 2.0 to 54.4 months (median 3.12 months), while in-trial PSADT values ranged from -39 to 57.1 months (median 7.88 months)........................................
Table 2
Table 2
PSA Velocity and Doubling Time in Months
Following the 12 week trial, 15 of 17 patients opted to continue Apatone therapy. Any decision to remain on Apatone therapy was left entirely to the patient. Anecdotally, most patients reported feeling “better” and more “energetic.” This coupled with stabilization of rising PSA along with no significant side effects led the men to continue therapy. Four continued therapy for 6 months and 11 continued for at least 1 year with one patient continuing for more than 2 years. Therapy was not discontinued in any patient due to vitamin toxicity or for other safety reasons. The PSA values of these patients were checked at various intervals while on treatment and remained stable. Patients terminating Apatone therapy experienced sharp increases in PSA levels as seen in the linear spline fit analysis (Figure (Figure1).1). Of the 11 patients on therapy for greater than 1 year, only one (initial PSA 256, PSADT= 3 months, and PSAV 157ng/ml/yr) passed away after 14 months.
No noteworthy changes were observed in the patient's complete blood counts, biochemistry panels or coagulation studies. No dose limiting toxicity or adverse events were experienced................
Discussion
In a previously published, prospective, randomized trial, patients with pathologically proven prostate cancer in advanced stages (M1), osseous metastasis and resistance to hormone therapy were given two, 7 day courses of oral Apatone (VC at 5 g/m2/day and VK3 at 50 mg/m2/day), VC alone, VK3 alone, or a placebo.14 The 7day courses of treatment occurred during the first and fourth week of the study with two weeks of follow up after each treatment period. For the vitamin combination, homocysteine (a marker of tumor cell death induced by Apatone) assays showed an immediate and statistically significant drop (p<<0.01) in tumor cell numbers, while PSA serum levels rose in the two initial weeks and then fell to levels that were significantly different (p << 0.01) from the control group. For VC and VK3 alone, a non-significant difference was observed between the serum levels of homocysteine and PSA compared to the control group which suggested that the decreased PSA levels were due to tumor cell death.14In this study, Apatone was administered daily in a single oral dose which was 2.5 to 3 times higher than the dose employed during the initial 12 weeks of our study. This dose resulted in a significant decrease in patient PSA levels which was ascribed to Apatone- induced tumor cell death by autoschizis. Conversely, the lower Apatone doses employed in the current study, led to increased PSADT without decreasing patient PSA levels......................................
/www.ncbi.nlm.nih.gov/pubmed/8476199/Somebody said...
Abstract
The growth inhibitory effects of a combined application of sodium ascorbate (Vitamin C) and 2-methyl-1,4-naphthoquinone (Vitamin K3) together with various chemotherapeutic agents has been examined on in vitro cultured human endometrial adenocarcinoma (AN3CA) cells. Combined vitamin treatment and chemotherapy in well defined conditions of cell confluence and at the dose levels applied result in a synergistic effect on growth inhibition. The combined vitamins when reaching their own synergistic cytotoxicity levels frequently obscure the additional synergistic effects attributable to the chemotherapeutic agents. Apart from the specific cytotoxic characteristics of the chemotherapeutic drugs examined, the formation of reactive oxygen radicals during treatment, possibly accentuated by less defined secondary mechanisms, appears essentially responsible for the observed stimulated cytotoxicity.
/www.euro-med.us/content/uploads/2016/06/dr-lasalvia-publications.pdf (scroll down to page 19 to find this study and look at charts)
Somebody said...
Introduction
A high dose of ascorbic acid has an antitumoral effect in some individual cases of human solid
tumors (1), but the statistical significance of these results has been controversial (2).
Menadione has also inhibited the growth of human solid tumors in preclinical studies (3–5)
and it was also reported that it has a clinical antitumoral effect acting as a radiosensitizer (6).
When technological advances in plasma determination of menadione were available(7),
the difficulty of achieving in patients the plasma concentration/time of in vitro cell exposure to mena-
dione in order to reproduce the effect of this drug as a single antitumoral agent at the clinical level was evidenced (8).
Serum Markers Variation Consistent with Autoschizis Induced
by Ascorbic Acid–Menadione in Patients with Prostate Cancer
Eduardo Lasalvia-Prisco,1,2,3,4,*Silvia Cucchi,3,4 Jesús Vázquez, 2,3 Eduardo Lasalvia-Galante, 2,3
Wilson Golomar, 2,3 and William Gordon4 1 School of Medicine, University of Uruguay, Montevideo, Uruguay;
2 National Cancer Institute, Montevideo, Uruguay; 3 Interdoctors, Montevideo, Uruguay; and
4 PharmaBlood, Inc, North Miami Beach, FL
Abstract
In vitro exposure of malignant prostate cell lines to ascorbic acid–menadione showed that tumor cells were
killed through a mechanism named autoschizis.
Experimental animal studies showed that autoschizis is also evident when ascorbic acid–menadione is administered to nude mice with implanted human prostate tumors.
Prostate-specific antigen (PSA) is a known serum marker of prostate tumor cells specific activity. Recently,
total serum homocysteine has been identified as a marker of tumor cell numbers with sensitivity for early detection of tumor cell death induced by treatments. A clinical trial with prostate cancer patients submitted to the association of ascorbic acid–menadione was performed and PSA/homocysteine was assessed in the follow-up. The early response in serum PSA and homocysteine levels was reported. The results showed that ascorbic acid–menadione produced an immediate drop in tumor cell numbers as assessed by homocysteine levels. Serum PSA levels showed an early rise and later dropped. These results suggest that autoschizis can also be induced by this pharmacological association at the clinical level in prostate cancer patients. Further studies are being performed in order to research if these results can be found with other primary tumors as it was shown in in vitro and experimental models. Ascorbic acid–menadione could be emerging as a new anti-tumoral chemotherapy.
Key Words:
Menadione; ascorbic acid; chemotherapy; tumor cell death; prostate cancer.........................
All patients fulfilled the following eligibility cri-
teria:
pathologically proven prostate cancer,
advanced stages (M1), osseous metastasis; resistant
to hormonotherapy, performance status (PS) accord-
ing to the Eastern Cooperative Oncology Group
(ECOG) .......................................
The patients were randomly distributed in four groups of five patients each. Group 1 was submitted
to the described two courses of ascorbic acid–mena- dione treatment. In group 2, ascorbic acid was omit-
ted. In group 3, menadione was omitted. A placebo was administered to patients of group 4. The homo-
cysteine and PSA assays were performed in the four groups as was described.................Results
Table 1 shows that the four groups of patients were comparable in most relevant parameters. Figure 1
shows the results registered in the 42-d follow-up of this clinical trial. The two courses of treatment were
administered the first and fourth week of the study. Serum homocysteine and PSA were measured the
first day of each week (d 1, 8, 15, 22, 29, 36, and 42 of the study). In group 1, treated with ascorbic
acid–menadione, the pretreatment serum level of HCY (d 1) fell in all posttreatment samples (d 8, 15,
22, 29, 36, and 42). Also in the group 1, the PSA serum levels rose in the two initial weeks (d 8 and 15)
and, afterward, it fell at d 36 and 42. Variations that were not relevant were observed in homocysteine and
PSA serum levels in groups 2 and 3, which were treated with a single agent—menadione and ascorbic
acid, respectively..............................
In vitro studies have shown that dead prostate tumor cells can release their PSA within
hours or days (19). An early increase of PSA after the induction of tumor cells death by treatments can
be observed as a consequence of the release of cell contents into the blood. As a consequence, PSA is
not recommendable as a measure of early tumor cell death induced by treatments. In this trial, PSA
increases in the initial serum specimens taken immediately after treatment with ascorbic acid–menadione
and it drops slowly afterward. In the frame of this short treatment, PSA reaches a significant drop at
the end of the follow-up. The variations of serum homocysteine and PSA suggest that malignant cell
death is induced in prostate cancer patients by the administration of ascorbic acid–menadione. Pre-
clinical studies have shown that this drug association induces prostate tumor cell death by autoschizis
in vitro and in experimental animal models
(11,14,15).
Our results suggest that ascorbic
acid–menadione also produces autoschizis in vivo
in human prostate cancer patients. ..................................................
The membrane and cell injury produced by oxidative radicals generated by H2O2
has been proposed as the mechanism of action involved in the autoschizis induced by ascorbic acid–menadione. It is well known that the ascor-
bic acid–menadione association generates H2O2..........................
Post Edited (BillyBob@388) : 6/29/2017 12:24:35 PM (GMT-6)