Propecia breasts starting to enlarge already?

triton2

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were did you hear this? Is this fact or conjecture? I have some red wine, how much do you need to drink for it to have any impact?

It's well known, both from a theorical point of view (1,2,3) and from a practical (4) and empirical (gynecomastia anecdotal reports) point of view, that using a 5AR blocker such as finasteride or dutasteride can lead to problems related to a highly estrogenic environment, such as gynecomastia.
In order to avoid this nasty side effect there have been some discussions about which is the best anti-estrogen to use. On the one hand we have SERMs and phytoestrogens, the former being quite dangerous for long term use, due to ocular damage issues, the latter lacking research to show clearly whether they are proestrogenic or antiestrogenic in males, on the other we have aromatase inhibitors, which are VERY expensive and difficult to obtain legally. While there's a lack in general consensus I think that the best option would be that of using an AI (Aromatase Blocker) provided we don't take too much (so that we don't risk our estrogen levels going below the physiological line) and money and availability are not a problem.
However, nature is very smart and red grapes might provide us with a solution, so that we don't have to spend a lot of money or risking buying fake anastrozole. Several studies have demonstrated that procyanidin B dimers in grape seeds have strong supressive properties on aromatase enzyme:

http://www.cbcrp.org/research/PageGrant ... ant_id=281

Some quotes:

"Grape juice has been found to suppress breast cancer cell growth by preventing the synthesis of the female hormone estrogen"

"Like the known specific aromatase inhibitor, Letrozole, the active B dimer fraction from red wine (administered by gavage) is a potent blocker of estrogen biosynthesis."

"These in vitro and in vivo studies demonstrated that procyanidin B dimers in red wine and grape seeds could be used as chemopreventive agents against breast cancer by suppressing in situ estrogen biosynthesis."

"The tumors of mice treated with an extract enriched with procyanidin B dimers showed a minimal increase in apoptotic cells compared with tumors of control mice, suggesting that the reduction in tumor growth in the treated mice was due to inhibition of aromatase and not due to a non-specific cytotoxic effect. Further, results from the feeding experiments indicate that these procyanidin B dimers are orally active and maintain their activity after ingestion. "

"A Phase I chemoprevention trial to evaluate the anti-aromatase activity of grape seed extract in postmenopausal women has been initiated at the City of Hope. The design and progress of this clinical trial will be discussed."

1: J Clin Invest. 1984 Dec;74(6):2272-8.
Antiestrogenic action of dihydrotestosterone in mouse breast. Competition with estradiol for binding to the estrogen receptor.

2:Attenuation of Estrogenic Effects by Dihydrotestosterone in the Pig Uterus Is Associated with Downregulation of the Estrogen Receptors1
Horacio Cárdenas2 and William F. Pope

3:Testosterone inhibits estrogen-induced mammary epithelial proliferation and suppresses estrogen receptor expression
JIAN ZHOU, SIU NG, O. ADESANYA-FAMUIYA, KRISTIN ANDERSON and CAROLYN A. BONDY1

4:Gynecomastia: effect of prolonged treatment with dihydrotestosterone by the percutaneous route


I dont know where you grew up wang, but for me, I only knew ONE kid who had gyno during puberty.

Turk J Pediatr. 1989 Apr-Jun;31(2):123-6.
The incidence of pubertal gynecomastia in boys living in the Ankara region.
Guvenc H, Yurdakok M, Kinik E, Buyukgebiz A.

The incidence of pubertal gynecomastia was determined in 646 Turkish boys in Ankara. A marked increase in the incidence was observed at Pubertal Stage 4 (60.2%) and age 14 years (61.1%). The incidence of gynecomastia during puberty at various pubertal stages and ages was 34.6%. Although the incidence of unilateral gynecomastia was 19.6%; there was no difference between right or left involvement.
 

rkim

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I need some advice.

I'm at the 2.5 month period on 1mg finasteride. I've had some sexual sides that seem to be getting a little better. New issue: gyno/breast swelling. It's the whole breast/peck, not just the nipple. Very soft as though there's water in there. On the left (why does it seem a lot of people get it on the left?). It's not just the burning, soreness and discomfort, but it IS bigger than the right side. No doubt. Will this subside? Some people seem to stop before restarting on .5mgs. Should I do the same or just cut down directly? Will this ruin any progress?

Thanks.
 

jeffsss

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rkim said:
I need some advice.

I'm at the 2.5 month period on 1mg finasteride. I've had some sexual sides that seem to be getting a little better. New issue: gyno/breast swelling. It's the whole breast/peck, not just the nipple. Very soft as though there's water in there. On the left (why does it seem a lot of people get it on the left?). It's not just the burning, soreness and discomfort, but it IS bigger than the right side. No doubt. Will this subside? Some people seem to stop before restarting on .5mgs. Should I do the same or just cut down directly? Will this ruin any progress?

Thanks.

well, what kind of progress have you made in 2.5 months?

yes there will be less side effects if you take .5 mg of finasteride.. but you wont see as good of results..

think of it this way..

your thirsty.. you drink a liter of water.. Your good!!!

or

your thirsty... you drink 1/2 a liter of water... your fine, but could be better.


if you have gyno you can get tamoxifen (anti-estrogen) it'll KO any gyno.
 

rkim

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Not much progress. Some shedding which seems to be lessening (I think).

I don't want to start taking something to counter the gyno. That's too far for me. I'd rather cut down or stop. I'm just not sure if it's something that'll get better or if it's even worth the risk. It might end up being too late.

Has anyone here experienced the sensitivity AND swelling, continued use and it subsided?

Thanks.
 

BiGi

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Rkim you should get tamoxifen asap or at least stop taking finasteride. The gyno problem will NOT go away by itself particularly if you continue to take finasteride.

Today the endocrinologist prescribed me tamofixen 10 mg pills. It should help the gyno problem... I've been off propecia for 4 days now but I still feel some pain :(
 

rkim

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Thanks for the responses.

At this point I think I should get to a doctor (he'll obviously say stop taking it).

One question: if the answer is either stopping, or getting on tamoxifen, and I can't get to a Doctor for a week, should I stop for now (ruining any progress), cut down (hopefully maintaining some kind of progress), or just continue using assuming another week couldn't hurt too bad? I've read that there could be respiratory problems. Are there any REALLY serious sides to be worried about?
 

HairlossTalk

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We should swamp the anti propecia web site with honest, legitimate, positive posts about Propecia. Give them a taste of their own medicine :)

HairLossTalk.com
 

michael barry

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Ive been on propecia since 97'. No tits yet........my temples receeded on it, but vertex and top are strong and thick (think Jude Law's hair).


Dutasteride may have a little more gynochomateic effects, but who knows? I really doubt propecia will turn men into women guys, unless their hormones were stacked with estrogens beforehand. Proscar is propeciaX5. There are benefits to propecia, it may keep you from prostate cancer later. Relax, and enjoy your hair.
 

Dave001

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triton2 said:
I don't see why it wouldn't be. I think that, even if there's no gyno, everybody should be taking an aromatase blocker along with their 5AR blocker as a measure of prevention.

That would be quite foolish for indefinite use.

triton2 said:
I mean what if you get sides from the other drug? Take another?

It's a little bit more complicated than that...

It's a LOT more complicated than that.

Estrogen is extremely important and an aromatase inhibitor won't restore one's original "balance". Endocrine tests could guide one in restoring estrogen levels to their original values, but that won't account for the complex interactions between estrogen receptors and androgens, of which DHT is a key mediator through its apparent antagonism of estrogen (whether acting directly at the ER, indirectly, or both).

Search PubMed for finasteride AND gynecomastia. 29 hits.
 

Dave001

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Why don't some of you spend time researching *topical* antiandrogenic options and drug delivery technology. Surely it's more productive than discussing celebrity hair lines?

Laziness causes b**ch tits and Zix.
 

triton2

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Dave001 said:
triton2 said:
I don't see why it wouldn't be. I think that, even if there's no gyno, everybody should be taking an aromatase blocker along with their 5AR blocker as a measure of prevention.

That would be quite foolish for indefinite use.

Why do you think it would be foolish? Which would be the reason? And wouldn't it be even more foolish to allow your estrogen/androgen ratio remain elevated indefinitely?

Estrogen is extremely important and an aromatase inhibitor won't restore one's original "balance".

In a hormonal environment in which E is too high, an aromatase inhibitor will lower E levels and you will be definately closer to balance than you'd be otherwise. Estrogen is extremely important, as you say, and not having too much estrogen is also extremely important, for it might lead to problems such as gyno and prostate cancer.
Endocrine tests could guide one in restoring estrogen levels to their original values, but that won't account for the complex interactions between estrogen receptors and androgens, of which DHT is a key mediator through its apparent antagonism of estrogen (whether acting directly at the ER, indirectly, or both).

That's precisely why even if you got blood tests and they showed normal E levels that wouldn't mean your estrogen agonism isn't being supraphysiological. Estrogen agonism will definately be too high in most, if not all, of the people who are inhibiting DHT. That's why an antiestrogen is so important, so that E/(T+DHT) ratio is closer to normal.
 

Dave001

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triton2 said:
Why do you think it would be foolish? Which would be the reason? And wouldn't it be even more foolish to allow your estrogen/androgen ratio remain elevated indefinitely?

No, because we have a good bit of data concerning the long-term effects of 5 alpha-reductase inhibitors and deficiency of the enzyme in males. Compare that to aromatase deficiency. Estrogen is especially critical for brain development. But speculating about this type of thing from a biochemical standpoint is futile. Human biology is at this point very poorly understood on the whole. Observation is a far safer guide.

triton2 said:
In a hormonal environment in which E is too high, an aromatase inhibitor will lower E levels and you will be definately closer to balance than you'd be otherwise. Estrogen is extremely important, as you say, and not having too much estrogen is also extremely important, for it might lead to problems such as gyno and prostate cancer.

[...]

That's precisely why even if you got blood tests and they showed normal E levels that wouldn't mean your estrogen agonism isn't being supraphysiological. Estrogen agonism will definately be too high in most, if not all, of the people who are inhibiting DHT. That's why an antiestrogen is so important, so that E/(T+DHT) ratio is closer to normal.

Why would it be closer to normal? There's a problem with trying to adjust something to a value for which the original and target are unknown: it isn't possible, unless you guess lucky. To me it makes sense to use finasteride either by itself (i.e., without an aromatase or ER antagonist) or not at all. I chose the latter, although not because of estrogen, but because I do not want to systemically reduce my androgen activity for cosmetic reasons. I'd rather target the hair follicle specifically and leave the rest of my hormones alone. It's a personal decision. Whether you or anyone else want to experiment with all sorts of radical systemic hormonal pharmacotherapies is not my concern.
 

triton2

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Dave,

blocking DHT production WILL undoubtetly increase estrogen agonism in the male body, sometimes to such an extent as to promote gynecomastia. I cannot see why reducing such estrogen agonism (which is SUPRAPHYSIOLOGICAL due to the reasons above mentioned) down to a PHYSIOLOGICAL level would be something to avoid. Oh, you can say "yeah, but how can you know you won't take too much anti-e and reduce it down to an INFRAphysiological level thus creating a dangerous situation?"; well, let's look at it this way: even if you took 1mg of anastrozole everyday, your E levels would only be reduced by around 50%, which I don't think it's that much... specially in a system with an E agonism rate which is clearly above normal... well, if you just take 0.1-0.25mg anastrozole daily, you'll most likely have less E reduction than with the 1mg dose... that's definately below what I consider reducing E to dangerous levels.
In a male system with above normal E agonism, if you take just A LITTLE of anti-e, you can be pretty sure, if not 100% sure, that your E agonism isn't going to go infraphysiological... with that little anti-e dose you won't be able to assure that you can avoid gyno, that would be the main concern: that you don't lower your E levels enough, but I think that, as long as you take a LITTLE, you can know almost for sure that you're not gonna lower them too much. And if you don't lower them enough that's not a problem either, because anyway your E levels will be lower than if you didn't take your SMALL anti-e dosage.
I think it's very good to be aware of the inherent risks driving E levels too low would have; however, I think we should also be aware of the dangers of having too much E agonism, such as increased breast cancer risk. Certainly, someone who already has preexisting gyno from adolescence should take some amount of anti-e along his 5AR blocker because, if not, he would have high chances of growing more gyno than he already has.
 

Dave001

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Do what you will, but be warned that you're going to drive yourself nuts with that sort of thinking.
 

triton2

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Dave001 said:
Do what you will, but be warned that you're going to drive yourself nuts with that sort of thinking.

What kind of thinking? Analytical thinking? Well, anyway, I'd prefer driving myself nuts rather than driving my gyno worse. :)
 

Dave001

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triton2 said:
Dave001 said:
Do what you will, but be warned that you're going to drive yourself nuts with that sort of thinking.

What kind of thinking? Analytical thinking? Well, anyway, I'd prefer driving myself nuts rather than driving my gyno worse. :)

I wasn't aware that you had already developed gyno. Propensity for gyno seems to vary quite a bit from person to person.

Have you considered using finasteride topically? I think its activity could be substantially localized with the proper vehicle. Two small controlled trials of topical finasteride in hirsutism showed a local effect from finasteride in a cream vehicle.
 

triton2

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I have considered it, but since topical finasteride's effectiveness, being optimist, wouldn't be able to even compare to oral dutas' effectiveness I have chosen taking dutas orally. I want to use the most effective protocol, I cannot allow myself to use less than that if I want to have the hair I wish. Besides, I already use spironolactone and folligen topically, so the topical route is pretty 'complete' (I'm considering using RU instead of spironolactone).
As far as gyno goes I haven't developed it as a result of dutasteride usage, but developed it in my teenage years and it became permanent. Given the fact that I couldn't allow it to grow bigger without looking quite ridiculous and the fact that it seems like I'm very prone to gyno I think it's best not to risk it and take an anti-e.
However, as I already said, I think that everyone, even if they're not closely as prone to gyno as I am, should be taking a small amount of anti-e if they are taking dutas/finas, for it's a fact that their estrogen environment will be supraphysiological (whether or not their E levels are higher than normal, for having a higher than normal E/(T+DHT) ratio is enough to promote estrogenic side effects. I think prevention of increased breast cancer risk can and should be properly addressed with an anti-e which lowers our estrogen agonism down to a physiological level.
I cannot understand why everybody seems to be so wary when it comes to anastrozole usage and yet they wouldn't show that wariness if it was about drinking a little glass of red wine or red grapeseed juice everyday; why? because red grapeseed juice MIGHT be almost as effective as taking 1mg of anastrozole daily.
 

Mako88

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Wow, I always wondered why I had developed a small amount of gyno in my 30s...No one can see it, and I just assumed they were fatty deposits. Now all the senstive nipple stuff and that being the only area on my body that's squishy makes sense. Damn propecia!!! :lol:

I've taken finasteride for around five years now, and now triton I'm curious about your tamoxifen suggestion. Is that the compound being sold here as "Tamoxifen Citrate"? http://www.innovative-research.net/aqs.htm

If so, I have two questions for you:

1. What sort of daily dosage do you recommend for the 3-week period?

2. If you stay on finasteride, won't the gyno return due to the estrogen imbalance the second the tamoxifen cycle is over? I assume that either a daily hit of anastrozole or your red wine/flax oil would be necessary to prevent it from recurring correct?

That's for your great posts, funny that for so long I've know what tamoxifen is as an post-cycle-recovery agent in bodybuilding (the steroid guys use it to knock out gyno), and here it shows up as something to offset a similar estrogen imbalance caused by finasteride. Small world. ;)
 

Dave001

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Mako88 said:
Wow, I always wondered why I had developed a small amount of gyno in my 30s...No one can see it, and I just assumed they were fatty deposits. Now all the senstive nipple stuff and that being the only area on my body that's squishy makes sense. Damn propecia!!! :lol:

I've taken finasteride for around five years now, and now triton I'm curious about your tamoxifen suggestion. Is that the compound being sold here as "Tamoxifen Citrate"? http://www.innovative-research.net/aqs.htm

If so, I have two questions for you:

1. What sort of daily dosage do you recommend for the 3-week period?

Tamoxifen will not correct existing gynecomastia, which is composed of fibrous tissue and must be surgicially removed.
 

Mako88

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Dave001 said:
Mako88 said:
Wow, I always wondered why I had developed a small amount of gyno in my 30s...No one can see it, and I just assumed they were fatty deposits. Now all the senstive nipple stuff and that being the only area on my body that's squishy makes sense. Damn propecia!!! :lol:

I've taken finasteride for around five years now, and now triton I'm curious about your tamoxifen suggestion. Is that the compound being sold here as "Tamoxifen Citrate"? http://www.innovative-research.net/aqs.htm

If so, I have two questions for you:

1. What sort of daily dosage do you recommend for the 3-week period?

Tamoxifen will not correct existing gynecomastia, which is composed of fibrous tissue and must be surgicially removed.

Actually there have been studies done that do indicate that Tamoxifen has a positive impact on pre-existing gyno, including fibrous mass. It's hit or miss, not everyone reacts to it, but it's worth a shot.

Same goes for Raloxifene. Bottom line: ALL possible avenues should be explored to reduce/eliminate gyno prior to surgery. It's worth a try.
 
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