Author Topic: Which med do you guys suggest for self-treating?  (Read 4934 times)

Offline laurier

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Tamoxifen or Raloxifene?

Thank you very much

Offline gynosucks1

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raloxifene, but i also suggest taking an AI with this medication.

ral will both spike ur test/est and cause bloat/moodiness most likely because of elevated est.

both are actually est antagonists in breast and very few other places.  other than that they act like estrogen

i would suggest a supplement version of an aromo inhib.. something like rebound xt.

using arimidex or letro is overkill.

Offline laurier

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I've already ordered Tamoxifen, so I was afraid that would be your answer.  Sigh.

Offline AngryPuppy

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Hi,

What do you mean with "overkill"?

Only that I will be going into Arimidex pretty soon.

Cheers!

Quote
raloxifene, but i also suggest taking an AI with this medication.

ral will both spike ur test/est and cause bloat/moodiness most likely because of elevated est.

both are actually est antagonists in breast and very few other places.  other than that they act like estrogen

i would suggest a supplement version of an aromo inhib.. something like rebound xt.

using arimidex or letro is overkill.


Offline Paa_Paw

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Generally speaking, I would have to say that I do not recommend self medication at all.  

Before you can treat a condition successfully, you need to know What your base line is and have a plan as to where you are going with the treatment.

Because there are so many different things that can cause gynecomastia, you would need to have a good set of base line lab tests before starting treatment.  Then you would need someone who has the expertise to interpret those tests.  Finally, since the treatment involves hormones capable of altering your reproductive physiology, your treatment should be monitored.  

This is simply not a good place for DIY.

Do it right and see an Endocrinologist.

DIY=Do It Yourself=a bad idea.
Grandpa Dan

Offline Hypo-is-here

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Echoing the words of Paw Paw.

You might have;

Hypergonadotropic hypogonadism, Klinefelters syndrome in particular accounts for around 1 in 500 male births
Hypogonadotropic hypogonadism, in particular pituitary insufficiency or from bith Kallman syndrome which accounts for 1 in every 1500 male births.

Metabolic hypogonadism,

1 in 10 gynecomastia sufferers have hypogonadism of one form or another.

Hyperthyroidism,
Hypothyroidism,

Accounts for about 1-2 percent of gynecomastia sufferers.

Hemochromatosis, 1-350 of born with this condition if it is not found and treated it can and does kill.
cirhhosis of the liver, or general hepatic problems,

Hepatic problems account for 8 percent of all gynecomastia sufferers.

renal insufficiency or general renal problems,

Accounts for around 2 percent of gynecomastia sufferers

A Prolactinoma

A benign brain tumor which reduces the gronadotrophin messenger hormones therby reducing testosterone and requires minor surgical intervention to correct

A testicluar malignancy- obviously they kill if left untreated.

accounts for around 1-2 percent of all gynecomastia sufferers.


YOU MIGHT HAVE NO PROBLEM AT ALL and the hormonal surge at puberty may well be responsible for your gynecomastia, if this is so how do you know if you are treating something that no longer exists without pathology investigations?

Using something like anti-estrogens if you have nomal estrogen levels can lower your estrogens too much and put your thyroid out of whack and give you metabolic problems, often doing this causes a man to completely lose his libido and erections- nice!

In short;

How can you treat a condition when you don't know what the condition is and even if one exists?


Perhaps I may suggest seeing a good endocrinologist who specializes in reproductive endocrinology?

Just a thought.

Offline Time_to_fix_it

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As usual Hypo has said put forward all the correct clinical arguments.  Might I just add a laymans opinion? ... Don't mess with your hormones, that is a job for an Endocrinologist.  A little (or no knowledge) is a very dangerous thing here.  Many people have regretted their initial panic which led them to self medication.  Use your brain to tackle Gyne .. seem an Endo.

Take care.
Surgery performed by Mr Levick at The Priory Hospital Bimingham (UK) 20th October 2006

Offline gynosucks1

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by overkill, i mean the only reason u would take an AI , like letro, armidex, or a supplement version, is to control the extra est that will be in your system from a SERM

it doesnt actually help... again i could be wrong because an ai will raise your test, but i dont know if test/dht actually plays a roll in reduction of breast tissue or just the intrinsic properties of combating EST.. like say dht has.

arimidex/letro is too powerful

however, rebound xt is good.. or any other supplement version

i didn't say this, i usually do.  GEt bloodwork, and see an endo first.  IF there's a problem.. honestly u can find better ways to treat it on the interent then ur endo.

but again, depends on yoru doc.. however ud be surprized about how many dont know about the newer stuff like femera, and raloxifene.. hell theres stuff out there now that is suppose to be more powerful/less toxic then these

Offline Hypo-is-here

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Quote

but i dont know if test/dht actually plays a roll in reduction of breast tissue or just the intrinsic properties of combating EST.. like say dht has.


Gynecomastia is at its heart a result of a hormone imbalance, either one of a temporary nature via puberty or the use of given medications or steroid abuse or a more permanent imbalance caused by an underlying condition.

The ratio/balance between Androgens and estrogens is very often crucial.

So yes an individuals testosterone and dihydrotestosterone levels are of the utmost importance and at the heart of the issue along with estradiol.



Offline gynosucks1

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Quote


Gynecomastia is at its heart a result of a hormone imbalance, either one of a temporary nature via puberty or the use of given medications or steroid abuse or a more permanent imbalance caused by an underlying condition.

The ratio/balance between Androgens and estrogens is very often crucial.

So yes an individuals testosterone and dihydrotestosterone levels are of the utmost importance and at the heart of the issue along with estradiol.




ya but do u know why >? lol I know DHT has specific properties of supressing estradiol.  I'm sure test has some kind of mechanisim at supressing expression of the various ests 2.  But does it in itself combat breast tissue?  

people with hypogandisim even dont nec have gyno.  Even low test lvls dont mean ur going to get gyno.  The way i understand it .. is it's all EST.

Offline Hypo-is-here

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ya but do u know why >? lol I know DHT has specific properties of supressing estradiol.  I'm sure test has some kind of mechanisim at supressing expression of the various ests 2.  But does it in itself combat breast tissue?  

people with hypogandisim even dont nec have gyno.  Even low test lvls dont mean ur going to get gyno.  The way i understand it .. is it's all EST.



It is is categorically NOT just to do with estrogens.

Starting with DHT

I'll explain DHT from the point of view of what happens if it increases- how it does is not so important from the point of view of the explanation.

DHT is a potent androgen in its own right.

Like all Androgens and estrogens  DHT is recognized by the Hypothalamus.  When DHT increases the Hypothalamus down regulates GnRH in doing so it instructs the pituitary to reduce gonadotrophins.  

With reduced  LH/Downregulated LH the testicles leydig cells hypertrophy.  

This results in lowered testosterone production.

When you have lowered testosterone via this mechanism you reduce the fuel for estradiol the most potent estrogen.

You see estradiol and DHT are the major metabolites of testosterone (a prohormone) .  It is what testosterone is most readily converted to.

Without oxygen you cannot have a fire, it is what fuels a fire, likewise testosterone is usually required to fuel estradiol.

So increasing the androgen DHT reduces testosterone, this as a result reduces (the fuel for estradiol) estradiol.

With reduced estradiol but with the increased androgen DHT (which itself cannot convert to estradiol) you have an increased androgen to estrogen balance and this can reduce gynecomastia if it is in its proliferation phase.

Which is why DHT Andractim has been shown to reduce gynecomastia in 75% of cases and resolve gynecomastia in 25% of cases in controlled studies as reported by Glen D Braunstein M.D endocrinologist in his white paper on gynecomastia.

Testosterone like DHT sits on one side of the balance with other androgens and all other estrogens the most potent of which estradiol sit on the other.  

Of course it is further complicated by intracrinology, given the fact that many hormones can change from one kind to another- testosterone being on the one side of the balance being able to convert to estrogens on the other side of the balance.  

As a man you need your Androgens to outbalance your estrogens by x amount, otherwise you have a good chance of developing gynecomastia.

The very reason that men who abuse steroids (such men account for 25% of all gynecomastia sufferers)  don't tend to develop gynecomastia on steroids is because despite having significantly elevated estrogens their Androgens out balance them in the androgen to estrogen balance/ratio.

When they stop abusing the steroids those who don't take PCT as these guys term it are left with the same high levels of estrogens, but now they are unopposed as they no longer have high androgen levels.

High estrogen that previously didn't cause gynecomastia now does.

It is all to do with the ratios/balance of androgens to estrogens and ancillary hormones.

The reason some men with hypogonadism do not have gynecomastia is because having low testosterone means that quite a few of them have little testosterone to convert into estrogen in the first place.  So these men have low testosterone and low estrogen.

For some unfortunate reason some men with low testosterone have additional complicating factors that result in low testosterone and high estrogen such as;

Chromosomal abnormalities that mean an altered expression of androgen and estrogen receptors and related effects, as in Klinefelter and Kallman syndromes.

Metabolic syndromes/problems also cause this situation such as hemochromatosis.

Poor liver function
Poor kidney function

As the above two can result in high levels of SHBG or in poor metabloization of estrogens.

Just to further illustrate the importance of the balance/ratios of androgens to estrogens;

You can develop gynecomastia with normal levels of estrogens if you testosterone is low, because in such a situation you can have a poor androgen to estrogen balance/ratio.

Lets say you had 10,000 dollars in the bank (think of that as androgens) and you have 3,000 dollars worth of bills (think of them as estrogens).

That might be thought to be ok.

Now lets say your bills (estrogen) are only 2,000 dollars, you might think no problem, but what if you only have 1,000 dollars (androgens).

As you can see, how much a pain in the ass your bills (estrogens) are is dependent upon your how much money (androgens) you have.

You can never really look at estrogens independently of androgens as the balance/ratio between the two is crucial.

Which is why testing and considering hormones in isolation is absurd and something that a good reproductive endocrinologist would not do.

I have waffled and the analogies were made up on the spot so are a bit daft, but hopefully you get the picture.

I could have explained all of this in exacting medical detail, but I thought that it was better in this form.




 

















 




Offline gynosucks1

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Quote



It is is categorically NOT just to do with estrogens.

Starting with DHT

I'll explain DHT from the point of view of what happens if it increases- how it does is not so important from the point of view of the explanation.

DHT is a potent androgen in its own right.

Like all Androgens and estrogens  DHT is recognized by the Hypothalamus.  When DHT increases the Hypothalamus down regulates GnRH in doing so it instructs the pituitary to reduce gonadotrophins.  

With reduced  LH/Downregulated LH the testicles leydig cells hypertrophy.  

This results in lowered testosterone production.

When you have lowered testosterone via this mechanism you reduce the fuel for estradiol the most potent estrogen.

You see estradiol and DHT are the major metabolites of testosterone (a prohormone) .  It is what testosterone is most readily converted to.

Without oxygen you cannot have a fire, it is what fuels a fire, likewise testosterone is usually required to fuel estradiol.

So increasing the androgen DHT reduces testosterone, this as a result reduces (the fuel for estradiol) estradiol.

With reduced estradiol but with the increased androgen DHT (which itself cannot convert to estradiol) you have an increased androgen to estrogen balance and this can reduce gynecomastia if it is in its proliferation phase.

Which is why DHT Andractim has been shown to reduce gynecomastia in 75% of cases and resolve gynecomastia in 25% of cases in controlled studies as reported by Glen D Braunstein M.D endocrinologist in his white paper on gynecomastia.

Testosterone like DHT sits on one side of the balance with other androgens and all other estrogens the most potent of which estradiol sit on the other.  

Of course it is further complicated by intracrinology, given the fact that many hormones can change from one kind to another- testosterone being on the one side of the balance being able to convert to estrogens on the other side of the balance.  

As a man you need your Androgens to outbalance your estrogens by x amount, otherwise you have a good chance of developing gynecomastia.

The very reason that men who abuse steroids (such men account for 25% of all gynecomastia sufferers)  don't tend to develop gynecomastia on steroids is because despite having significantly elevated estrogens their Androgens out balance them in the androgen to estrogen balance/ratio.

When they stop abusing the steroids those who don't take PCT as these guys term it are left with the same high levels of estrogens, but now they are unopposed as they no longer have high androgen levels.

High estrogen that previously didn't cause gynecomastia now does.

It is all to do with the ratios/balance of androgens to estrogens and ancillary hormones.

The reason some men with hypogonadism do not have gynecomastia is because having low testosterone means that quite a few of them have little testosterone to convert into estrogen in the first place.  So these men have low testosterone and low estrogen.

For some unfortunate reason some men with low testosterone have additional complicating factors that result in low testosterone and high estrogen such as;

Chromosomal abnormalities that mean an altered expression of androgen and estrogen receptors and related effects, as in Klinefelter and Kallman syndromes.

Metabolic syndromes/problems also cause this situation such as hemochromatosis.

Poor liver function
Poor kidney function

As the above two can result in high levels of SHBG or in poor metabloization of estrogens.

Just to further illustrate the importance of the balance/ratios of androgens to estrogens;

You can develop gynecomastia with normal levels of estrogens if you testosterone is low, because in such a situation you can have a poor androgen to estrogen balance/ratio.

Lets say you had 10,000 dollars in the bank (think of that as androgens) and you have 3,000 dollars worth of bills (think of them as estrogens).

That might be thought to be ok.

Now lets say your bills (estrogen) are only 2,000 dollars, you might think no problem, but what if you only have 1,000 dollars (androgens).

As you can see, how much a pain in the ass your bills (estrogens) are is dependent upon your how much money (androgens) you have.

You can never really look at estrogens independently of androgens as the balance/ratio between the two is crucial.

Which is why testing and considering hormones in isolation is absurd and something that a good reproductive endocrinologist would not do.

I have waffled and the analogies were made up on the spot so are a bit daft, but hopefully you get the picture.

I could have explained all of this in exacting medical detail, but I thought that it was better in this form.




 

















 





i know all of this in much simple rhetoric.. however.. i dont want to sound like a moron but i guess i have no opt left.. lol

test/dht doesnt actually attack the breast tissue and break it up?? again that's what i was refering to.  it acts really indriectly.. like u so elaborately explained



Offline Hypo-is-here

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i know all of this in much simple rhetoric.. however.. i dont want to sound like a moron but i guess i have no opt left.. lol

test/dht doesnt actually attack the breast tissue and break it up?? again that's what i was refering to.  it acts really indriectly.. like u so elaborately explained



Asking questions is not stupid, it seems perfectly reasonable to me.


Testosterone/DHT can and does attack breast tissue.

Dihydrotestosterone gel is used as a treatment for gynecomastia precisely because as well as having an indirect endocrine affect on breast tissue, it also has a localized topical affect.

According to Dr Glen D Braunstein in his 1993 white paper entitled Gynecomastia 74% of those treated with this DHT gel had significant reductions in breast tissue 25% of which had complete resolution.

Breast tissue has a developmental/proliferation phase where the maintenance and development of the breast tissue is dependent on an “estrogen dominant hormonal environment”.

If you remove that "hormonal environment" by favorable alteration of the androgen to estrogen ratio- bring about an environment that favors androgens, “a androgen dominant hormonal environment”, the breast tissue will no longer be supported.

And IF that happens;

The breast tissue hypertrophies- SHRINKS or resolves if you prefer that word.

Above I said that breast tissue has this developmental phase, after around a year and a half to two years, breast tissue becomes more fibrous, at this point it is far less likely to be positively affected by changes in the hormonal environment, so alterations in the androgen to estrogen ratios are less likely to make major in roads into the condition.

Unfortunately this does not mean to say that gynecomastia cannot develop further if at any point the "hormonal environment" should once again favor estrogens over androgens resulting in an estrogen dominant hormonal environment.



« Last Edit: November 10, 2005, 01:07:07 PM by Hypo-is-here »

Offline gynosucks1

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Asking questions is not stupid, it seems perfectly reasonable to me.


Testosterone/DHT can and does attack breast tissue.

Dihydrotestosterone gel is used as a treatment for gynecomastia precisely because as well as having an indirect endocrine affect on breast tissue, it also has a localized topical affect.

According to Dr Glen D Braunstein in his 1993 white paper entitled Gynecomastia 74% of those treated with this DHT gel had significant reductions in breast tissue 25% of which had complete resolution.

Breast tissue has a developmental/proliferation phase where the maintenance and development of the breast tissue is dependent on an “estrogen dominant hormonal environment”.

If you remove that "hormonal environment" by favorable alteration of the androgen to estrogen ratio- bring about an environment that favors androgens, “a androgen dominant hormonal environment”, the breast tissue will no longer be supported.

And IF that happens;

The breast tissue hypertrophies- SHRINKS or resolves if you prefer that word.

Above I said that breast tissue has this developmental phase, after around a year and a half to two years, breast tissue becomes more fibrous, at this point it is far less likely to be positively affected by changes in the hormonal environment, so alterations in the androgen to estrogen ratios are less likely to make major in roads into the condition.

Unfortunately this does not mean to say that gynecomastia cannot develop further if at any point the "hormonal environment" should once again favor estrogens over androgens resulting in an estrogen dominant hormonal environment.





good read mate thanks.  i never truely understood the point of the topical dht creams on the chest... just didn't know that dht actually had a localized effect.

Offline Hypo-is-here

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No problem.

Yes, not only the direct localized effect, but also the indirect and signifcant affect on breast tissue by alteration of the hormonal environment at a global/endocrine level.



 

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