leaky nips

[bruno]

hey! bro's need some serious help. tonight after working chest I noticed my right nipple leaking, a very small amount but none the less scary, I have nolvadex but It was for my pct, If I take it now will that cure the problem or do I need something else. any help is appreciated.

[atomicone]

Definitely doesn't sound good. Are your nips tender or do you get any burning sensations in them (those are classic gyno symptoms)? I just want to make sure we're talking about gyno here and not possibly a different problem. If you indeed are already experiencing symptoms of gyno you better start hitting the Nolvadex at about 60+mg ED or 1mg Armidex until it's under controll.

Originally Posted by bruno

hey! bro's need some serious help. tonight after working chest I noticed my right nipple leaking, a very small amount but none the less scary, I have nolvadex but It was for my pct, If I take it now will that cure the problem or do I need something else. any help is appreciated.

[spound]

Originally Posted by bruno

hey! bro's need some serious help. tonight after working chest I noticed my right nipple leaking, a very small amount but none the less scary, I have nolvadex but It was for my pct, If I take it now will that cure the problem or do I need something else. any help is appreciated.

It depends oin what gear you are taking. If you are not tkaing any prog based drungs like tren or deca then yes nolva should help, but if you are then that is probably what the leakage is coming from (happened to me on deca once), if this is the case, you need dostinex or bromocriptine

[atomicone]

Originally Posted by spound

It depends oin what gear you are taking. If you are not tkaing any prog based drungs like tren or deca then yes nolva should help, but if you are then that is probably what the leakage is coming from (happened to me on deca once), if this is the case, you need dostinex or bromocriptine

If you're taking Deca switch to EQ. Much better option.

[Jergo]

Nolva is your best bet for ANY kind of gyno. AI's won't do hardly anything here fellas. You have to rid ALL estrogen in the RECEPTORS. No matter what the cause is from, prog, prol, etc.....all these kinds CANNOT survive as long as estrogen is not present. Taking an AI won't even rid all estrogen, just some.

Again, nolva is your best bet for any gyno.....if you say otherwise, I'll need to see some studies that conflict mine...

[Massive690]

you're not pregnant are you?

[MaxRep]

Originally Posted by Jergo

Nolva is your best bet for ANY kind of gyno. AI's won't do hardly anything here fellas. You have to rid ALL estrogen in the RECEPTORS. No matter what the cause is from, prog, prol, etc.....all these kinds CANNOT survive as long as estrogen is not present. Taking an AI won't even rid all estrogen, just some.

Again, nolva is your best bet for any gyno.....if you say otherwise, I'll need to see some studies that conflict mine...

Holy Smokes guy! I hardly know where to start. I will say that you're right in that estrogen is generally required to be present for progesterone to exert it's effects.

Let's start with a few abstracts of the most recent studies so you can update yourself on how superior AI's are over nolvadex on estrogen suppression.
__________________________________________________ ___________
1: Breast Cancer Res. 2004;6(6):269-74. Epub 2004 Oct 06.

Endocrinology and hormone therapy in breast cancer: aromatase inhibitors versus antioestrogens.

Howell A, Dowsett M.

CRUK Department of Medical Oncology, University of Manchester, Christie Hospital, Manchester, UK. maria.parker@christie-tr.nwest.nhs.uk

Endocrine therapies act by either blocking or downregulating the oestrogen receptor or by reducing oestrogen concentrations around and within the cancer cell. In postmenopausal women, oestrogen suppression is achieved by inhibition of the enzyme aromatase by aromatase inhibitors (AIs). Modern AIs (anastrozole, letrozole and exemestane) are more potent than earlier ones and suppress oestradiol levels in plasma to virtually undetectable concentrations.

Recent comparisons of AIs with the most widely used oestrogen receptor blocking drug tamoxifen indicate that, in general, AIs result in increased response rates and greater durations of response. Here, we summarize data supporting the difference between the two types of treatment and attempt to account for the underlying mechanisms that favour AIs.
PMID: 15535858 [PubMed - in process]
__________________________________________________ ___________
1: Oncologist. 2004;9(5):489-96.
Superiority of letrozole to tamoxifen in the first-line treatment of advanced breast cancer: evidence from metastatic subgroups and a test of functional ability.

Mouridsen H, Sun Y, Gershanovich M, Perez-Carrion R, Becquart D, Chaudri-Ross HA, Lang R.

Novartis Pharma AG, WKL-490.1.04, CH-4057 Basel, Switzerland.

PURPOSE: The letrozole study 025 is a large (n = 907), international, double-blind, randomized, phase III trial in postmenopausal women with advanced breast cancer. This subanalysis compares the efficacies of letrozole and tamoxifen as first-line therapy in postmenopausual women with advanced breast cancer according to site of metastatic lesions and Karnofsky Performance Status (KPS).
MATERIALS AND METHODS: Nine hundred seven patients with advanced breast cancer were randomly assigned to once-daily oral letrozole (2.5 mg; Femara; Novartis Pharma AG; Basel, Switzerland) or tamoxifen (20 mg; Tamofen; Leiras OY; Turku, Finland). Time to progression (TTP) was estimated using the Kaplan-Meier product-limit method. Treatments were compared by Cox proportional hazards regression models.
RESULTS: Letrozole treatment significantly prolonged TTP in all subsets of patients: those with nonvisceral metastases, those with visceral metastases without liver involvement, and those with liver metastases. The reduction in risk of progression ranged from 25%, for patients with nonvisceral metastases, to 36%, for patients with liver metastases. The distributions of baseline KPS scores for both treatment groups were similar (57% had KPS scores >/=90). Time to worsening of 20 points or more in KPS score was significantly longer with letrozole than with tamoxifen, but modest numbers of patients experienced such deterioration (letrozole, 20%, tamoxifen, 22%, in patients without visceral metastases; 23%-24% in patients with liver metastases; and letrozole, 14%, tamoxifen, 30%, in patients with visceral metastases without liver involvement).
CONCLUSION: These data demonstrate the consistent superiority of letrozole over tamoxifen and support the use of letrozole as a new standard of endocrine therapy in postmenopausal women with advanced breast cancer.

PMID: 15477633 [PubMed - in process]
__________________________________________________ ____________

So now you know that while nolvadex does not lower estrogen levels at all... it only blocks the estrogen receptors in breast tissue... you also know that AI's actually lower estrogen levels to virtually undetectable levels.

Considering the estrogen molecule only exists within an estrogen receptor for a matter of minutes, I wouldn't worry too much about "You have to rid ALL estrogen in the RECEPTORS." At least as long as the AI's have reduced estrogen levels far enough. Now if you use nolvadex, all the circulating estrogen is still there and you have to hope the nolvadex is blocking all receptors.

But wait, we can see from the second study above, nolvadex isn't effective at blocking all estrogen receptors. If it were, it would do a better job than Letro of slowing the progression of breast cancer... and unfortunately, it does a poorer job than an AI (Letrozole) of slowing breast cancer. Note: the speed of progression of breast cancer is largely mediated by the amount of estrogen able to bind to the estrogen receptors. Ergo: block or reduce estrogen to lowest possible levels in breast cancer patients. What does this most effectively? AI's do.

So, to Mr. Leaky Nips, above, take a high dose of Letro or Arimidex to reduce estrogen to virtually nothing, and supplement that with B6 at 200mg 3x/day to reduce your progestins.

Good luck,
MaxRep

P.S. Here's one more for the files...

1: Oncologist. 2004;9(4):378-84.
Tamoxifen--what next?

Gradishar WJ.

Division of Hematology/Oncology, Feinberg School of Medicine, Robert H. Lurie Comprehensive Cancer Center, Northwestern University, 676 North St. Clair, Suite 850, Chicago, Illinois 60611, USA. w-gradishar@northwestern.edu

Most patients with advanced breast cancer (ABC) ultimately die due to disease progression. Consequently, treatments for ABC are predominantly palliative in nature and, therefore, the tolerability profile of a given treatment is particularly relevant in these patients. While cytotoxic chemotherapy and endocrine therapy exhibit efficacy in hormone-sensitive, advanced disease, it is endocrine therapy that combines efficacy with minimal acute toxicity. Tamoxifen has been the chosen endocrine therapy for postmenopausal, hormone-sensitive, ABC for over 20 years.

More recently, new endocrine agents with different mechanisms of action from tamoxifen have been introduced. Evidence indicates that the aromatase inhibitors anastrozole (Arimidex; AstraZeneca; Wilmington, DE), letrozole (Femara; Novartis Pharmaceuticals Corp.; East Hanover, NJ) and exemestane (Aromasin; Pharmacia Corp.; Peapack, NJ) offer superior efficacy and tolerability to tamoxifen in the first-line treatment of postmenopausal, hormone-sensitive ABC.

Similarly, after tamoxifen failure, fulvestrant (Faslodex; AstraZeneca), a new estrogen receptor (ER) antagonist that downregulates the ER, is at least as effective as anastrozole, is well tolerated, and is not cross-resistant with tamoxifen. Unlike tamoxifen, fulvestrant has no known agonist effects. The sequential use of such agents may prolong the time during which endocrine therapies can be used, thereby avoiding the more acute toxicities associated with cytotoxic chemotherapy. Indeed, a series of studies has shown that this sequential use is a relevant, active, and well-tolerated option. Establishing the comparative efficacies and optimal sequences that incorporate the newer endocrine agents will be central in determining the future role of hormonal therapy in ABC; the results of this work will determine the relative place of tamoxifen in what is a rapidly changing therapeutic environment. Copyright AlphaMed Press

PMID: 15266091 [PubMed - indexed for MEDLINE]
__________________________________________________ __________

So we also see new estrogen receptor blockers that are on the horizon which may both block estrogen and downgrade the ER. Exciting times!

[Jergo]

Originally Posted by MaxRep

Holy Smokes guy! I hardly know where to start. I will say that you're right in that estrogen is generally required to be present for progesterone to exert it's effects.

Let's start with a few abstracts of the most recent studies so you can update yourself on how superior AI's are over nolvadex on estrogen suppression.
__________________________________________________ ___________
1: Breast Cancer Res. 2004;6(6):269-74. Epub 2004 Oct 06.

Endocrinology and hormone therapy in breast cancer: aromatase inhibitors versus antioestrogens.

Howell A, Dowsett M.

CRUK Department of Medical Oncology, University of Manchester, Christie Hospital, Manchester, UK. maria.parker@christie-tr.nwest.nhs.uk

Endocrine therapies act by either blocking or downregulating the oestrogen receptor or by reducing oestrogen concentrations around and within the cancer cell. In postmenopausal women, oestrogen suppression is achieved by inhibition of the enzyme aromatase by aromatase inhibitors (AIs). Modern AIs (anastrozole, letrozole and exemestane) are more potent than earlier ones and suppress oestradiol levels in plasma to virtually undetectable concentrations.

Recent comparisons of AIs with the most widely used oestrogen receptor blocking drug tamoxifen indicate that, in general, AIs result in increased response rates and greater durations of response. Here, we summarize data supporting the difference between the two types of treatment and attempt to account for the underlying mechanisms that favour AIs.
PMID: 15535858 [PubMed - in process]
__________________________________________________ ___________
1: Oncologist. 2004;9(5):489-96.
Superiority of letrozole to tamoxifen in the first-line treatment of advanced breast cancer: evidence from metastatic subgroups and a test of functional ability.

Mouridsen H, Sun Y, Gershanovich M, Perez-Carrion R, Becquart D, Chaudri-Ross HA, Lang R.

Novartis Pharma AG, WKL-490.1.04, CH-4057 Basel, Switzerland.

PURPOSE: The letrozole study 025 is a large (n = 907), international, double-blind, randomized, phase III trial in postmenopausal women with advanced breast cancer. This subanalysis compares the efficacies of letrozole and tamoxifen as first-line therapy in postmenopausual women with advanced breast cancer according to site of metastatic lesions and Karnofsky Performance Status (KPS).
MATERIALS AND METHODS: Nine hundred seven patients with advanced breast cancer were randomly assigned to once-daily oral letrozole (2.5 mg; Femara; Novartis Pharma AG; Basel, Switzerland) or tamoxifen (20 mg; Tamofen; Leiras OY; Turku, Finland). Time to progression (TTP) was estimated using the Kaplan-Meier product-limit method. Treatments were compared by Cox proportional hazards regression models.
RESULTS: Letrozole treatment significantly prolonged TTP in all subsets of patients: those with nonvisceral metastases, those with visceral metastases without liver involvement, and those with liver metastases. The reduction in risk of progression ranged from 25%, for patients with nonvisceral metastases, to 36%, for patients with liver metastases. The distributions of baseline KPS scores for both treatment groups were similar (57% had KPS scores >/=90). Time to worsening of 20 points or more in KPS score was significantly longer with letrozole than with tamoxifen, but modest numbers of patients experienced such deterioration (letrozole, 20%, tamoxifen, 22%, in patients without visceral metastases; 23%-24% in patients with liver metastases; and letrozole, 14%, tamoxifen, 30%, in patients with visceral metastases without liver involvement).
CONCLUSION: These data demonstrate the consistent superiority of letrozole over tamoxifen and support the use of letrozole as a new standard of endocrine therapy in postmenopausal women with advanced breast cancer.

PMID: 15477633 [PubMed - in process]
__________________________________________________ ____________

So now you know that while nolvadex does not lower estrogen levels at all... it only blocks the estrogen receptors in breast tissue... you also know that AI's actually lower estrogen levels to virtually undetectable levels.

Considering the estrogen molecule only exists within an estrogen receptor for a matter of minutes, I wouldn't worry too much about "You have to rid ALL estrogen in the RECEPTORS." At least as long as the AI's have reduced estrogen levels far enough. Now if you use nolvadex, all the circulating estrogen is still there and you have to hope the nolvadex is blocking all receptors.

But wait, we can see from the second study above, nolvadex isn't effective at blocking all estrogen receptors. If it were, it would do a better job than Letro of slowing the progression of breast cancer... and unfortunately, it does a poorer job than an AI (Letrozole) of slowing breast cancer. Note: the speed of progression of breast cancer is largely mediated by the amount of estrogen able to bind to the estrogen receptors. Ergo: block or reduce estrogen to lowest possible levels in breast cancer patients. What does this most effectively? AI's do.

So, to Mr. Leaky Nips, above, take a high dose of Letro or Arimidex to reduce estrogen to virtually nothing, and supplement that with B6 at 200mg 3x/day to reduce your progestins.

Good luck,
MaxRep

P.S. Here's one more for the files...

1: Oncologist. 2004;9(4):378-84.
Tamoxifen--what next?

Gradishar WJ.

Division of Hematology/Oncology, Feinberg School of Medicine, Robert H. Lurie Comprehensive Cancer Center, Northwestern University, 676 North St. Clair, Suite 850, Chicago, Illinois 60611, USA. w-gradishar@northwestern.edu

Most patients with advanced breast cancer (ABC) ultimately die due to disease progression. Consequently, treatments for ABC are predominantly palliative in nature and, therefore, the tolerability profile of a given treatment is particularly relevant in these patients. While cytotoxic chemotherapy and endocrine therapy exhibit efficacy in hormone-sensitive, advanced disease, it is endocrine therapy that combines efficacy with minimal acute toxicity. Tamoxifen has been the chosen endocrine therapy for postmenopausal, hormone-sensitive, ABC for over 20 years.

More recently, new endocrine agents with different mechanisms of action from tamoxifen have been introduced. Evidence indicates that the aromatase inhibitors anastrozole (Arimidex; AstraZeneca; Wilmington, DE), letrozole (Femara; Novartis Pharmaceuticals Corp.; East Hanover, NJ) and exemestane (Aromasin; Pharmacia Corp.; Peapack, NJ) offer superior efficacy and tolerability to tamoxifen in the first-line treatment of postmenopausal, hormone-sensitive ABC.

Similarly, after tamoxifen failure, fulvestrant (Faslodex; AstraZeneca), a new estrogen receptor (ER) antagonist that downregulates the ER, is at least as effective as anastrozole, is well tolerated, and is not cross-resistant with tamoxifen. Unlike tamoxifen, fulvestrant has no known agonist effects. The sequential use of such agents may prolong the time during which endocrine therapies can be used, thereby avoiding the more acute toxicities associated with cytotoxic chemotherapy. Indeed, a series of studies has shown that this sequential use is a relevant, active, and well-tolerated option. Establishing the comparative efficacies and optimal sequences that incorporate the newer endocrine agents will be central in determining the future role of hormonal therapy in ABC; the results of this work will determine the relative place of tamoxifen in what is a rapidly changing therapeutic environment. Copyright AlphaMed Press

PMID: 15266091 [PubMed - indexed for MEDLINE]
__________________________________________________ __________

So we also see new estrogen receptor blockers that are on the horizon which may both block estrogen and downgrade the ER. Exciting times!

YEah, when I posted last time, I was running late for work..lol...what I meant to say is that AI's do not reduce total E levels, they only reduce a small percentage...varying on doseages used of course. They still reduce total E levels throughout the whole body more than nolva does, yes.

But with the use of Tamoxifen, TOTAL or rather ALL E levels can and will be inhibited in the receptors...this is what needs to be accomplished in order to treat gyno symptoms succesfully.

IF you reduce TOTAL E levels in the receptors, then prog, prol, etc. cannot and will not survive. SO again using nolva for ANY type of gyno is still the best bet here.


Bkarch, thanks for those studies man, thats all I was asking before...its just that I never seen any ones like yours and was asking for some...will have to read up some more when I have some more time...gotta go to work again now...looking forward to reading up some more...later.