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-   -   Resveratrol by Biotivia (https://her2support.org/vbulletin/showthread.php?t=38649)

Vic 03-27-2009 08:55 AM

Resveratrol by Biotivia
 
Are any of you taking Resveratrol in your vitamin regimen? I don't often watch Oprah, but caught the last 15 minutes this week when Dr. Oz was on and he had green capsules of Resveratrol and said this is an important part of good health. I quickly read the credits (do this in the theatre, too!) and noticed the name Biotivia, so I called the company and he was sending me some info. on it and suggested I take Resveratrol TransMax (500 mg.), which is really expensive.

Yes, red wine is so much more fun to consume. But, as Lani shows, alcohol is alcohol.

Your thoughts on Resveratrol?

Cheers,

Vicki

Joe 03-27-2009 09:00 AM

Vickie,
You may wish to research olive oil and the HER2 gene. Studies show that it is beneficial.

Regards
Joe

hutchibk 03-27-2009 09:54 AM

I asked my cancer nutritionist, and she told me that the jury is still out/it is still not known on how much resveratrol supplements one must consume to have impact on cancer. She said that I should drink grape juice everyday (a couple of glasses). Yes it is caloric, but it tastes good and is much less expensive than the supplement pills.

ElaineM 03-27-2009 10:35 AM

Resveratrol by Biotivia
 
Yes. Good quality grape juice has the same good stuff as red wine does. If anyone wants to check out what Dr. Oz said I posted a link to the show on Life Extension with Dr. Oz in the articles section. Some very cool ideas and suggestion where discussed on the show.

Vic 03-28-2009 10:34 AM

Grape juice and olive oil works!
 
Just had breakfast and put olive oil on my nine-grain toast. As for the grape juice, Hutch, I'm 110# and the extra calories should be okay. (Nice photo! You're workin' it.)

Elaine, when I clicked on your links, there's a lot of info. and I couldn't find the Oz/Resveratrol/cool ideas part. Also, after seeing Joe's note, when I clicked on the olive oil link, all I got as a classmates.com ad and an error message for a website.

I'll "google it."

Thanks to all,

Vic

Laurel 03-28-2009 06:07 PM

Vic,

I seem to recall reading an article on E.R. + bc needing to avoid resveratrol if they were E.R.a or E.R. b; I'm sorry I cannot recall which one is not to be in the presence of resveratrol. I'll google it! Just a moment!

Okay, this seems to speak to what I was remembering:

Estrogenic and Anti-estrogenic Activities Endogenous estrogens are steroid hormones synthesized by humans and other mammals; these hormones bind to estrogen receptors within cells. The estrogen-receptor complex interacts with unique sequences in DNA (estrogen response elements; EREs) to modulate the expression of estrogen-responsive genes (17). A compound that binds to estrogen receptors and elicits similar responses to endogenous estrogens is considered an estrogen agonist, while a compound that binds estrogen receptors but prevents or inhibits the response elicited by endogenous estrogens is considered an estrogen antagonist. The chemical structure of resveratrol is very similar to that of the synthetic estrogen agonist, diethylstilbestrol (see figure 2), suggesting that resveratrol might also function as an estrogen agonist. However, in cell culture experiments resveratrol acts as an estrogen agonist under some conditions and an estrogen antagonist under other conditions (18, 19). In estrogen receptor-positive breast cancer cells, resveratrol acted as an estrogen agonist in the absence of the endogenous estrogen, 17beta-estradiol, but acted as an estrogen antagonist in the presence of 17beta-estradiol (20, 21). At present, it appears that resveratrol has the potential to act as an estrogen agonist or antagonist depending on such factors as cell type, estrogen receptor isoform (ER alpha or ER beta), and the presence of endogenous estrogens (17).


Here is the link to the entire page:


http://lpi.oregonstate.edu/infocente...ol/#estrogenic


I post this because triple pos folks like me must be careful about estrogen mimickers. I see you are not ER/PR positive, but others reading this thread may be and should exercise caution with resveratrol

Jackie07 03-28-2009 10:18 PM

I am ER positive. Thanks for the caution.

caya 03-29-2009 08:34 AM

Thanks Laurel for the clarification info, I'm triple +.

all the best
caya

Vic 03-29-2009 10:36 AM

Good work, Laurel
 
Glad you posted this, Laurel, as attention to the fine details is crucial. Even though I'm ER-, maybe I'll save my money on this expensive supplement and just drink grape juice or when the organic red grapes come back to the market, buy those. Then, I wash and freeze them and eat them as frozen treats.

Have a grapeful day,

Vic

Vic 03-31-2009 11:28 AM

Sent by Biotivia, makers of Resveratrol, read accordingly, for science types, not me
 
Anticarcinogenicity Studies of Resveratrol


Test System or Species,
Strain, and Age, Number,
and Sex of Animals
Chemical Form
and Purity
Route, Dose, Duration, and
Observation Period
Results/Comments
Reference
In Vitro Assays
Mammary glands of mice, BALB/c, 3- to 4-wk-old,number n.p., F

resveratrol, purity n.p.

incubation with 1, 2.5, 5, and 10 µM (0.2, 0.57, 1, and 2.3 µg/mL) for the first 10 days of 14-day culture (Ductal lesions were induced with 2 µg/mL DMBA on day 3 for 24 h.)

The incidence of hyperplastic and aggressive ductal lesions
induced by DMBA was reduced by resveratrol in a dose dependent manner (IC50 ~3 µM).

Bhat et al. (2001)

Human breast cancer cell
lines: ER-positive KPL-1
and MCF-7 and ERnegative MKL-F

trans-resveratrol,
99.8% pure

incubation with 0.01-40 µg/mL (0.04-180 µM) for 24, 48, 72, and 96 h At 44 µM, the growth of all cell lines was inhibited in time- and
dose-dependent manners.
The IC50 for the 72-h treatment ranged from 105 to 149 µM. At lower concentrations of resveratrol,moderate inhibition of the growth of MKL-F and stimulation of
KPL-1 and MCF-7 in a time-dependent manner were seen. At 72 h, the cells were stimulated by up to 132 and 115% of control level, respectively.

Nakagawa et al. (2001)

Human breast cancer cell
lines: hormone-sensitive
MCF-7 and T47-D and
hormone-resistant MDAMB-
231

(+)-resveratrol,
>99% pure

incubation with 10-12 – 10-6 M
(1 pM-1 µM [2 x 10-7 -0.2 µg/mL]) for a total of 6 days;applied on day 2 (one cell cycle) and day 5 (three cell
cycles)

Cell proliferation was inhibited in a dose-dependent manner in all cell lines; the effect after day 5 was more apparent than at day 2. The IC50 and maximum inhibition of resveratrol were as follows:
IC50 (pM) Inhibition
MCF-7 13.7±8.3 0.42
T47-D 0.1±1.2 0.56
MDA-MB-231 5.2±9.1 0.30

Damianaki et al. (2000)


Prostate cancer cell lines:
hormone-sensitive LNCaP,PC3, and DU145

(+)-resveratrol,
>99% pure

incubation with 10-12 – 10-6 M
(1 pM-1 µM [2 x 10-7 -0.2 µg/mL]) given one day after seeding (day 0) and cultured for 6 days

Resveratrol had no effect in LNCaP cells (IC50 = >10-6 M). At >10-7 M, resveratrol produced partial inhibition of growth in the PC3 cell line (IC50 = 0.11±1.23 x 10-6 M; maximum inhibition at 0.48). In DU145 cells, it was a potent inhibitor of cell growth, which was time- and dose-dependent (IC50 = 0.57±0.58 x 10-12 M; maximum inhibition at 0.82). In LNCaP cells, resveratrol was a very weak competitor of androgen binding.

Kampa et al. (2000)

Prostate cancer cell line
LNCaP

resveratrol, purity
n.p.

incubation with up to 200 µM (45.7 µg/mL) for 24 or 32 h with or without Mib 2 days after cells were seeded

At 100 µM, Mib-stimulated cell growth was inhibited and very little apoptosis was observed. At 200 µM, massive apoptotic cell death was seen.

Mitchell et al.
(1999)

In Vivo Assays
Mice, C57B16/J
(implanted s.c. with a
murine T241 fibrosarcoma
in the middle dorsum
[tumors visible after 72 h]), 5- to 6-wk-old, 6-7M/group

resveratrol, >99% pure

oral; 5.7 µg/mL (25 µM) or 1 mg/kg/day in absolute ethanol added to drinking water for 25 days

Resveratrol significantly inhibited the growth of T241
fibrosarcomas in the animals.

Bråkenhielm et al. (2001)

Rats, F344, 2-mo-old,
10M/group

resveratrol, purity
n.p.

oral; 200 µg/kg (0.876 µmol/kg) bw/day in drinking water for 100 days beginning 10 days before s.c. injection of 2 doses of 15 mg/kg AOM 1 wk apart

The number of ACF in the colorectal mucosa (25.7±3.6 vs.
39.4±3.3 in controls) and mean multiplicity (2.7±0.3 vs. 4.9±0.6 in controls) were significantly reduced. Resveratrol also reduced the number of small and medium ACF and stopped the development of large ACF. Compared to controls, bax was significantly expressed in ACF of
treated rats (53±1.3% and 57±1.3%, respectively) but not in the surrounding mucosa. In addition, p21 was expressed in ACF of treated rats but to a lower degree compared to controls (1.5±0.1% and 2.2±0.1%, respectively) but not in the normal mucosa.

Tessitore et al. (2000)

Rats, Sprague-Dawley, 42-days-old, 20F/group

resveratrol, purity n.p.

intragastric; 10 and 100 mg/kg (0.044 and 0.438 mmol/kg) bw 5 days/wk starting 7 days before NMU administration and terminating 120 days after administration of NMU

By day 21, tumors were palpable in the control group after NMU administration. By day 111, 100% incidence was reached. The high dose of resveratrol delayed tumorigenesis: on day 40, 0% incidence was observed versus 42% incidence in the control group; the median time for appearance of the first tumor was 79.5 days in the treated group versus 51.5 days in the control group; at
termination, the multiplicity of tumors was 3.9 versus 6.0 in
control animals. There was also a decrease in the total number of tumors. Morphologically, there was an increase in differentiated alveolar structures among tumor parenchyma, focal reduction of cell layers and numerous luminal openings within alveolar structures, and necrosis and apoptotic cells in small areas of some tumors.

Bhat et al. (2001)



hutchibk 03-31-2009 07:54 PM

As my doctor used to tell me, "...last time I looked, you were not a mouse..." - whenever I brought mouse model research to him. LOL

I think the reason that my nutritionist steered me clear of the supplement - is because all there is for proof so far is mouse model research, and as I have learned, that doesn't mean it directly corresponds to humans. (though sometimes it does...)

Thanks for the info though...

Rich66 04-19-2009 10:49 AM

1: Clin Exp Metastasis. 2009 Mar 18. [Epub ahead of print]http://www.ncbi.nlm.nih.gov/corehtml...ringerlink.gif Links
Inhibition of mammary tumor growth and metastases to bone and liver by dietary grape polyphenols.

Castillo-Pichardo L, MartÃ*nez-Montemayor MM, MartÃ*nez JE, Wall KM, Cubano LA, Dharmawardhane S.
Department of Biochemistry, School of Medicine, University of Puerto Rico, Medical Sciences Campus, San Juan, PR, USA.
The cancer preventive properties of grape products such as red wine have been attributed to polyphenols enriched in red wine. However, much of the studies on cancer preventive mechanisms of grape polyphenols have been conducted with individual compounds at concentrations too high to be achieved via dietary consumption. We recently reported that combined grape polyphenols at physiologically relevant concentrations are more effective than individual compounds at inhibition of ERalpha(-), ERbeta(+) MDA-MB-231 breast cancer cell proliferation,resveratrol, quercetin, or catechin cell cycle progression, and primary mammary tumor growth (Schlachterman et al., Transl Oncol 1:19-27, 2008). Herein, we show that combined grape polyphenols induce apoptosis and are more effective than individual at inhibition of cell proliferation, cell cycle progression, and cell migration in the highly metastatic ER (-) MDA-MB-435 cell line. The combined effect of dietary grape polyphenols (5 mg/kg each resveratrol, quercetin, and catechin) was tested on progression of mammary tumors in nude mice created from green fluorescent protein-tagged MDA-MB-435 bone metastatic variant. Fluorescence image analysis of primary tumor growth demonstrated a statistically significant decrease in tumor area by dietary grape polyphenols. Molecular analysis of excised tumors demonstrated that reduced mammary tumor growth may be due to upregulation of FOXO1 (forkhead box O1) and NFKBIA (IkappaBalpha), thus activating apoptosis and potentially inhibiting NfkappaB (nuclear factor kappaB) activity. Image analysis of distant organs for metastases demonstrated that grape polyphenols reduced metastasis especially to liver and bone. Overall, these results indicate that combined dietary grape polyphenols are effective at inhibition of mammary tumor growth and site-specific metastasis.

Vic 04-20-2009 07:04 AM

Fascinating, Rich. Thanks!! I'll print this out and take it to my onc. visiti today along with Lani's post on the "IMPORTANT discovery" post on MUC4.

That's what this board is all about. Appreciate everyone's knowledge, curiosity and research capabilities.

Vicki Z

PetuniaJan 04-20-2009 08:23 AM

1 Attachment(s)
here is what my onc nurse sent me when I inquired about resveratrol.
Have a great day!
Love Jan

Vic 04-21-2009 04:28 PM

Here's what my onc. said about Resveratrol
 
After I saw my oncologist yesterday, she said she would speak with one of her colleagues who has been doing some studies on Resveratrol and here is what she wrote me in her email today:

"he told me he tells breast cancer patients to avoid Resveratrol because of data showing that it can stimulate some breast cancer cell types."

So, there you have it. That's one opinion, but it seems to go along with what others have also posted.

Vicki Z



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