Letro help

[Chev]

So ive ran many different cycles (test P,E) tren , winny, var.... i think thats it. Im currently on week 5 of a deca /test cycle, which i never ran deca. (had dbol first 4 weeks at 30 ED) I noticed for the first time a lump behind one of my nipples as well as both nipples are pretty sore. So i did some research and bought letro, but after doing MORE reading some people run other AI's. I recieved the letro today, should i start the letro now or try something else. Ive never had to use an AI so im a little cunfused on what to do and how much. Thanks for any help guys.


30 years old
245 pounds
6'4"
14bf
In the kitchen or in the gym!!

[ROBOCOP]

If it were me mate I would hold off using the letro. If this is the first time youve felt a lump then I would try using arimidex every day at .25mg and see how you go. If it doesnt feel any better then I would consider upping it to .50mg every day. If that fails then it may be time to use letro. Be careful though. You should be tapering its use both up and down.

[CHUCKYthentic]

letro will not be a good idea right now. its best for gyno reversal at end of cycle, it will whipe out too much estrogen right now, and we need some in our body

what you need to do right now is start with 40mg of nolvadex right away, take that for about a week until the nips arent sore anymore. after that run 10-20mg for the rest of your cycle. this will prevent the estrogen from binding to anymore of the receptors.

you could start adex too right now at .5mg EOD to start knocking out that estrogen and control it rest of the way out

DO NOT use the letro righ tnow, its ok that u bought it just in case u get full blown gyno. but if you follow what i said above you should be fine

[chuckt12345]

^ yup

Chev letro absolutely suks balls especially if you run the protocol to reduce gyno. Im sure it prb the most effecient method but id def try nolva first

[ROBOCOP]

Hey CHUCKY.

Whats your thoughts on running nolva when using deca ? Im just concerned it will exasserbate the gyno which is why adex would be better. Just my 2 cents mate

[CHUCKYthentic]

u know what ROBO you are 100% correct, i cant believe i overlooked that

ya only option is guess given that is adex or stop the deca and wait 3 weeks to start the nolva therapy

thanks ROBO

[chuckt12345]

think the board splits down the middle on that one

[CHUCKYthentic]

ya thats a really tough decision to make. i have never encountered the issue so i wouldnt be able to speak from experience on that

like you re damned if u do damned if u dont

[chuckt12345]

unless its prolactin issue,, so ill stay away from this one
i run nolva on all my cycles including the deca ones ive done and not had problems so im not really sure

[ROBOCOP]

u know what ROBO you are 100% correct, i cant believe i overlooked that

ya only option is guess given that is adex or stop the deca and wait 3 weeks to start the nolva therapy

thanks ROBO

Thought it was an oversight mate.

The reason Im an advocate of this regime chuck12345 is that I ran nolva during my first couple of cycles when signs of gyno appeared. It stopped the itching at first so I stayed with it. Problem was the gyno got worse. The adex works for me far better than nolva for my gyno issues and that too of many others. There is a split of sorts though mate, I just choose to sit this side of the fence

[ROBOCOP]

unless its prolactin issue,, so ill stay away from this one
i run nolva on all my cycles including the deca ones ive done and not had problems so im not really sure

I think the prolactin issue is the main protagonist but all opinions are worthwhile and individual experiences are as credible as the next

[CHUCKYthentic]

i run adex on all my cycles, if theres a 19nor i run caber

so i never experience the problems

i see Merc hovering down there, maybe he can shed some light

sorry to call u out buddy haha

[Merc.]

So ive ran many different cycles (test P,E) tren , winny, var.... i think thats it. Im currently on week 5 of a deca /test cycle, which i never ran deca. (had dbol first 4 weeks at 30 ED) I noticed for the first time a lump behind one of my nipples as well as both nipples are pretty sore. So i did some research and bought letro, but after doing MORE reading some people run other AI's. I recieved the letro today, should i start the letro now or try something else. Ive never had to use an AI so im a little cunfused on what to do and how much. Thanks for any help guys.


30 years old
245 pounds
6'4"
14bf
In the kitchen or in the gym!!

Letro has been shown to lower PGR... but it is really strong and can kill your sex drive..

Keep in mind estrogen is somewhat anabolic ( you dont want to destroy it .. or it can effect/ reduce your gains .. as well as kill your sex drive, and hard ons)..

Heres a link to my Estrogen and Ai article ( that was published in Muscular Development mag)...

The entire thread has a lot of good info in you wanna read through the post ...

Estrogen Will It Effect My Gains



Merc.

[chuckt12345]

Thought it was an oversight mate.

The reason Im an advocate of this regime chuck12345 is that I ran nolva during my first couple of cycles when signs of gyno appeared. It stopped the itching at first so I stayed with it. Problem was the gyno got worse. The adex works for me far better than nolva for my gyno issues and that too of many others. There is a split of sorts though mate, I just choose to sit this side of the fence

ill agree
he may need caber or somthing as well
i have alot of questions about the deca gyno so maybe merc can chime in or something?
If your running test/deca and you get gyno it can be caused by 2 diffrent types?

[Chev]

Thanks guys!!! Came through for me again! I love this board....

[FatalFunnel]

What will happen if you don't taper up on letro, and you start immediatley at 2.5mg (this is what I began about 7 days ago)?


And why does Letro suck so bad side-effect wise? It seems like people fear it sooo much. Besides a low-sex drive, what is to fear?

[FatalFunnel]

Also, when getting tapering off letro and running nolvadex , should I see a return of sex drive fast?

Will Nolvadex help return hormones and sex drive to normal, because Ive heard some people say that nolvadex decreases sex drive.

[chuckt12345]

Also, when getting tapering off letro and running nolvadex , should I see a return of sex drive fast?

Will Nolvadex help return hormones and sex drive to normal, because Ive heard some people say that nolvadex decreases sex drive.

why u runnin the letro at 2.5mg a day? Made my dk not work, felt like shit (cus pretty much zero estrogen in my body), got sick and gave me sores on my head.

[Merc.]

i run adex on all my cycles, if theres a 19nor i run caber

so i never experience the problems

i see Merc hovering down there, maybe he can shed some light

sorry to call u out buddy haha

The studies seem to go back and forth on this .. but I think that Nolva does increase PgR in breast tissue .. Which in turn can give more of the nasty deca / tren metabolites to bind too .. and could possibly increase the chance of getting gyno( but it is not a problem for all people )..

If you do a search you will see that there are peeps that report that they have problems when using 19 nor and nolva ( so we are sorta left with a shortage of info in the medical studies because they tend to go back and forth on this topic . But we do have an accumulation of independent anecdotal observations that can at least provide some idea how much of an issue it really is.

That said I will post some studies that show that nolva does increase PgR..

Here is one study showing nolva increases PgR . Like I said it gives more for the 19 nors metabolites to bind to and because of this it could possibly increase your chances of getting gyno..



Estrogen receptor (ER) and progesterone receptor (PgR), by ligand-binding assay compared with ER, PgR and pS2, by immuno-histochemistry in predicting response to tamoxifen in metastatic breast cancer: a Southwest Oncology Group Study.

Elledge RM, Green S, Pugh R, Allred DC, Clark GM, Hill J, Ravdin P, Martino S, Osborne CK.
Baylor College of Medicine, Houston, TX, USA. [email protected]
Results of estrogen receptor (ER) and progesterone receptor (PgR) ligand-binding assays (LBAs) are strongly correlated with ER and PgR by immuno-histochemistry (IHC). To investigate whether ER and PgR by IHC are also strongly correlated with tamoxifen response, time to treatment failure (TTF) and overall survival (OS), the results of the 2 methods were directly compared in 205 patients with ER(+) metastatic breast cancer treated with daily tamoxifen (Southwest Oncology Group protocol 8228) with 9 years median follow-up. pS2, another estrogen-regulated molecule, was also analyzed. Tumors were scored for IHC from 0 to 5, according to the proportion of positively stained cells. These IHC scores for both ER and PgR were significantly associated with LBA levels (p < 0.001). There was a significant direct relationship between higher IHC ER, PgR and pS2 and increasing response to tamoxifen. TTF and OS were also significantly longer for patients with higher ER or PgR, but not pS2, IHC scores. Low, intermediate and high ER or PgR categories showed similar differences in response rates whether defined by LBA or IHC. In logistic regression models which included ER, PgR and pS2 by IHC; ER and PgR by LBA; and menopausal status, only ER (IHC) and pS2 (IHC) retained significance for predicting tamoxifen response (p = 0. 02 and p = 0.005, respectively), along with menopausal status (for PgR by IHC, p = 0.09). Increasing ER and PgR by IHC, as by LBA, are thus significantly associated with a progressively better response and longer survival in ER(+) metastatic breast cancer. pS2 is also predictive in this setting. Copyright 2000 Wiley-Liss, Inc.
PMID: 10754487 [PubMed - indexed for MEDLINE]




And this one


The PgR gene is an estrogen-regulated gene (34) , so drugs with estrogenic activity will increase its expression. Accordingly, tamoxifen has been shown to increase PgR levels (35) , whereas initial work on primary breast tumors found that a short-acting formulation of ICI 182,*** reduced PgR levels (30) , suggesting that it is devoid of estrogen-agonist activity and may have a different mechanism of action to that of tamoxifen. Additional evidence that ICI 182,*** and tamoxifen have different underlying modes of action comes from studies showing that tamoxifen-resistant tumors remain sensitive to ICI 182,*** treatment in vitro (18 , 19) , in vivo (36 , 37) , and in the clinic (38, 39, 40) .


http://cancerres.aacrjournals.org/cg...ull/61/18/6739



Also


Aromatase inhibitors: cellular and molecular effects.

Miller WR, Anderson TJ, White S, Larionov A, Murray J, Evans D, Krause A, Dixon JM.
Breast Unit, Western General Hospital, Edinburgh, Scotland, UK. [email protected]

Marked cellular and molecular changes may occur in breast cancers following treatment of postmenopausal breast cancer patients with aromatase inhibitors. Neoadjuvant protocols, in which treatment is given with the primary tumour still within the breast, are particularly illuminating. In Edinburgh, we have shown that 3 months treatment with either anastrozole, exemestane or letrozole produces pathological responses in the majority of oestrogen receptor (ER)-rich tumours (39/59) as manifested by reduced cellularity/increased fibrosis. Changes in histological grading may also take place, most notably a reduction in mitotic figures. This probably reflects an influence on proliferation as most tumours (82%) show a marked decrease in the proliferation marker, Ki67. These effects are generally more dramatic than seen with tamoxifen given in the same setting. Differences between aromatase inhibitors and tamoxifen are also apparent in changes in steroid hormone expression. Thus, immuno-staining for progesterone receptor (PgR) is reduced in almost all cases by aromatase inhibitors, becoming undetectable in many. This contrasts with effects of tamoxifen in which the most common change on PgR is to increase expression. Changes in proliferation occur rapidly following the onset of exposure to aromatase inhibitors. Thus, neoadjuvant studies with letrozole in which tumour was sampled before and after 14 days and 3 months treatment show that decreased expression of Ki67 occur at 14 days and, in many cases, the effect is greater at 14 days than 3 months. These early changes precede evidence of clinical response but do not predict for it. However, this study design has allowed RNA analysis of sequential biopsies taken during the neoadjuvant therapy. Based on clustering techniques, it has been possible to subdivide tumours into groups showing distinct patterns of molecular changes. These changes in tumour gene expression may allow definition of tumour cohorts with differing sensitivity to aromatase inhibitors and permit early recognition of response and resistance.
PMID: 16002280 [PubMed - indexed for MEDLINE]


And this one is good also


Estrogen Receptor Downregulators

Dr. Tony Howell,[10] of the University of Manchester and the Christie Hospital, Manchester, UK, spoke concerning work with ER downregulators (formerly called "pure" antiestrogens). The prototype of these drugs is the steroidal compound fulvestrant, which induces ER downregulation[11] in animal and cell models. Dr. Robertson's group has shown that tamoxifen induces mild downregulation of ER but upregulation of PgR, whereas fulvestrant downregulates both ER and PgR. Aromatase inhibitors may produce similar effects to those produced by fulvestrant, but they do so by completely removing all estrogen.


http://www.medscape.com/viewarticle/440361



Merc.

[Swifto]

The studies seem to go back and forth on this .. but I think that Nolva does increase PgR in breast tissue .. Which in turn can give more of the nasty deca / tren metabolites to bind too .. and could possibly increase the chance of getting gyno( but it is not a problem for all people )..

If you do a search you will see that there are peeps that report that they have problems when using 19 nor and nolva ( so we are sorta left with a shortage of info in the medical studies because they tend to go back and forth on this topic . But we do have an accumulation of independent anecdotal observations that can at least provide some idea how much of an issue it really is.

That said I will post some studies that show that nolva does increase PgR..

Here is one study showing nolva increases PgR . Like I said it gives more for the 19 nors metabolites to bind to and because of this it could possibly increase your chances of getting gyno..



Estrogen receptor (ER) and progesterone receptor (PgR), by ligand-binding assay compared with ER, PgR and pS2, by immuno-histochemistry in predicting response to tamoxifen in metastatic breast cancer: a Southwest Oncology Group Study.

Elledge RM, Green S, Pugh R, Allred DC, Clark GM, Hill J, Ravdin P, Martino S, Osborne CK.
Baylor College of Medicine, Houston, TX, USA. [email protected]
Results of estrogen receptor (ER) and progesterone receptor (PgR) ligand-binding assays (LBAs) are strongly correlated with ER and PgR by immuno-histochemistry (IHC). To investigate whether ER and PgR by IHC are also strongly correlated with tamoxifen response, time to treatment failure (TTF) and overall survival (OS), the results of the 2 methods were directly compared in 205 patients with ER(+) metastatic breast cancer treated with daily tamoxifen (Southwest Oncology Group protocol 8228) with 9 years median follow-up. pS2, another estrogen-regulated molecule, was also analyzed. Tumors were scored for IHC from 0 to 5, according to the proportion of positively stained cells. These IHC scores for both ER and PgR were significantly associated with LBA levels (p < 0.001). There was a significant direct relationship between higher IHC ER, PgR and pS2 and increasing response to tamoxifen. TTF and OS were also significantly longer for patients with higher ER or PgR, but not pS2, IHC scores. Low, intermediate and high ER or PgR categories showed similar differences in response rates whether defined by LBA or IHC. In logistic regression models which included ER, PgR and pS2 by IHC; ER and PgR by LBA; and menopausal status, only ER (IHC) and pS2 (IHC) retained significance for predicting tamoxifen response (p = 0. 02 and p = 0.005, respectively), along with menopausal status (for PgR by IHC, p = 0.09). Increasing ER and PgR by IHC, as by LBA, are thus significantly associated with a progressively better response and longer survival in ER(+) metastatic breast cancer. pS2 is also predictive in this setting. Copyright 2000 Wiley-Liss, Inc.
PMID: 10754487 [PubMed - indexed for MEDLINE]




And this one


The PgR gene is an estrogen-regulated gene (34) , so drugs with estrogenic activity will increase its expression. Accordingly, tamoxifen has been shown to increase PgR levels (35) , whereas initial work on primary breast tumors found that a short-acting formulation of ICI 182,*** reduced PgR levels (30) , suggesting that it is devoid of estrogen-agonist activity and may have a different mechanism of action to that of tamoxifen. Additional evidence that ICI 182,*** and tamoxifen have different underlying modes of action comes from studies showing that tamoxifen-resistant tumors remain sensitive to ICI 182,*** treatment in vitro (18 , 19) , in vivo (36 , 37) , and in the clinic (38, 39, 40) .


http://cancerres.aacrjournals.org/cg...ull/61/18/6739



Also


Aromatase inhibitors: cellular and molecular effects.

Miller WR, Anderson TJ, White S, Larionov A, Murray J, Evans D, Krause A, Dixon JM.
Breast Unit, Western General Hospital, Edinburgh, Scotland, UK. [email protected]

Marked cellular and molecular changes may occur in breast cancers following treatment of postmenopausal breast cancer patients with aromatase inhibitors. Neoadjuvant protocols, in which treatment is given with the primary tumour still within the breast, are particularly illuminating. In Edinburgh, we have shown that 3 months treatment with either anastrozole, exemestane or letrozole produces pathological responses in the majority of oestrogen receptor (ER)-rich tumours (39/59) as manifested by reduced cellularity/increased fibrosis. Changes in histological grading may also take place, most notably a reduction in mitotic figures. This probably reflects an influence on proliferation as most tumours (82%) show a marked decrease in the proliferation marker, Ki67. These effects are generally more dramatic than seen with tamoxifen given in the same setting. Differences between aromatase inhibitors and tamoxifen are also apparent in changes in steroid hormone expression. Thus, immuno-staining for progesterone receptor (PgR) is reduced in almost all cases by aromatase inhibitors, becoming undetectable in many. This contrasts with effects of tamoxifen in which the most common change on PgR is to increase expression. Changes in proliferation occur rapidly following the onset of exposure to aromatase inhibitors. Thus, neoadjuvant studies with letrozole in which tumour was sampled before and after 14 days and 3 months treatment show that decreased expression of Ki67 occur at 14 days and, in many cases, the effect is greater at 14 days than 3 months. These early changes precede evidence of clinical response but do not predict for it. However, this study design has allowed RNA analysis of sequential biopsies taken during the neoadjuvant therapy. Based on clustering techniques, it has been possible to subdivide tumours into groups showing distinct patterns of molecular changes. These changes in tumour gene expression may allow definition of tumour cohorts with differing sensitivity to aromatase inhibitors and permit early recognition of response and resistance.
PMID: 16002280 [PubMed - indexed for MEDLINE]


And this one is good also


Estrogen Receptor Downregulators

Dr. Tony Howell,[10] of the University of Manchester and the Christie Hospital, Manchester, UK, spoke concerning work with ER downregulators (formerly called "pure" antiestrogens). The prototype of these drugs is the steroidal compound fulvestrant, which induces ER downregulation[11] in animal and cell models. Dr. Robertson's group has shown that tamoxifen induces mild downregulation of ER but upregulation of PgR, whereas fulvestrant downregulates both ER and PgR. Aromatase inhibitors may produce similar effects to those produced by fulvestrant, but they do so by completely removing all estrogen.


http://www.medscape.com/viewarticle/440361



Merc.

Intresting.

PgR is synthsized in response to the ER in breast tissue and Tamox causes downregulation of the ER.

I know these are breast cancer patients, so the results may not be able to compltely be transferred to the bodybuilder using AS. Breast cancer patients may show abnormal results, but I still think Tamox cen help with gyno from 19-Nor's. Although it will do nothing for PRL.

[chuckt12345]

Intresting.

PgR is synthsized in response to the ER in breast tissue and Tamox causes downregulation of the ER.

I know these are breast cancer patients, so the results may not be able to compltely be transferred to the bodybuilder using AS. Breast cancer patients may show abnormal results, but I still think Tamox cen help with gyno from 19-Nor's. Although it will do nothing for PRL.

im a little confused,, does prolactin just cause leaky nipples or does it create gyno as well?

[Swifto]

im a little confused,, does prolactin just cause leaky nipples or does it create gyno as well?

E has to be present I believe. PRL on its own cannot cause ductal/glandular tissue. It will though, cause a build up WITH estrogen.

"Leaky nipples" isnt just from PRL. But also when hypogondal (low natural testosterone ) an inbalance in the A:E ratio also. You can get "leaky nipples" from testosterone on its own, though rare. 19-Nors dont only cause this side effect. E is probably the main culprit, worsened by PRL.

[Swifto]

E = Estrogen
PRL = Prolactin
PgR = Progesterone

I stand by my opinoin of PgR meaning just about **** all in the build up of ductal/glandular tissue from androgen use. E and PRL can cause gyno, PgR...Not for me.

[chuckt12345]

E has to be present I believe. PRL on its own cannot cause ductal/glandular tissue. It will though, cause a build up WITH estrogen.

"Leaky nipples" isnt just from PRL. But also when hypogondal (low natural testosterone) an inbalance in the A:E ratio also. You can get "leaky nipples" from testosterone on its own, though rare. 19-Nors dont only cause this side effect. E is probably the main culprit, worsened by PRL.

so in theory tamox should stop the gyno even if PRL is high? And say people take it the gyno goes away,, but if they get off and then they may see a big rebound because PRL was always present and now a estrogen influx?

[Merc.]

Intresting.

PgR is synthsized in response to the ER in breast tissue and Tamox causes downregulation of the ER.

I know these are breast cancer patients, so the results may not be able to compltely be transferred to the bodybuilder using AS. Breast cancer patients may show abnormal results, but I still think Tamox cen help with gyno from 19-Nor's. Although it will do nothing for PRL.

Swifto I think the problem is that the studies dont really establish that progesterone activity is regulated by regulating the number of PgRs ....If so a good deductive connection would be made..




Merc.

[Merc.]

E has to be present I believe. PRL on its own cannot cause ductal/glandular tissue. It will though, cause a build up WITH estrogen.

"Leaky nipples" isnt just from PRL. But also when hypogondal (low natural testosterone) an inbalance in the A:E ratio also. You can get "leaky nipples" from testosterone on its own, though rare. 19-Nors dont only cause this side effect. E is probably the main culprit, worsened by PRL.

Yea gyno needs estrogen , progesterone as well as other mediators such as IGF and GH to form ..

Heres copy and past of a article I wrote about it ..


Gyno needs more than just estrogen
By Merc.


There has been a lot of post as of late concerning gyno .. I wanted to go over a few things that seem to be misunderstood ..

Lets start with talking about gyno .. What is it ? The medical term is gynecomastia .. It is the formation of breast tissue .. Here is the medical definition of gynecomastia..

Gynecomastia

Alternative Names
Breast development in a male
Definition
Gynecomastia is the development of abnormally large breasts in males.

Considerations
The condition may occur in one or both breasts and begins as a small lump beneath the nipple, which may be tender. The breasts often enlarge unevenly. Gynecomastia during puberty is not uncommon, and usually goes away over a period of months.
In newborns, breast development may be associated with milk flow (galactorrhea). This condition usually lasts for a couple of weeks, but in rare cases may last until the child is 2 years old.

Causes
The most common cause of gynecomastia is puberty.
Other causes include:
Chronic liver disease
Exposure to anabolic steroid hormones
Exposure to estrogen hormone
Genetic disorders
Kidney failure
Marijuana use
Side effects of some medications
Testosterone (male hormone) deficiency
Rare causes include:
Genetic defects
Overactive thyroid
Tumors

Home Care
Apply cold compresses and use analgesics as your health care provider recommends if swollen breasts are also tender.

When to Contact a Medical Professional
Call your health care provider if the breasts have developed abnormally or if there is swelling or pain in one or both breasts.
Note: Gynecomastia in children who have not yet reached puberty should always be checked by a health care provider.

What to Expect at Your Office Visit
Your health care provider will take a medical history and perform a physical examination.
Medical history questions may include:
Is one or both breasts involved?
What is the age and gender of the patient?
What medications is the person taking?
How long has gynecomastia been present?
Is the gynecomastia staying the same, getting better, or getting worse?
What other symptoms are present?
Testing may not be necessary, but the following tests may be done to rule out certain diseases:
Blood hormone level tests
Breast ultrasound
Liver and kidney function studies
Mammogram
Intervention:
If an underlying condition is found, it is treated. Gynecomastia during puberty usually goes away on its own; however, persistent, extreme, or uneven breast enlargement may be embarrassing for an adolescent boy. Breast reduction surgery may be recommended.
After seeing your health care provider:
If your health care provider made a diagnosis related to gynecomastia, you may want to note that diagnosis in your personal medical record.
Update Date: 12/6/2007



As you can see from the common causes ( listed above), gyno can occur during puberty .. There are many other known things that can cause gyno .. Steroids is not the only thing .. People seem to relate gyno mostly with steroid use , but they are surprised when I tell them all the other things that can contribute to having the dreaded bitch tits form..

I see a lot of post on the board about people asking about gyno and how estrogen's role is very important in it's formation ..

There is a misconception about this ( so it seems ) ... Yes, estrogen's role is a important one in the formation of gyno .. Gyno needs estrogen to form .. You see these post about it all the time .. " Take a AI's to try to knock out estrogen so gyno cant form " .. " If there isn't any estrogen you wont get gyno" blah blah blah ..

Well as we know estrogen is also important in the muscle building process ( I spoke about it in my estrogen and Ai post)... So trying to totally destroy it is not the best idea as it can reduce your gains .. As well as the health benefits estrogen provides in men ( I will do another post on that though in the future)..


As I have said .. and as you probably have heard (a bunch of times ) .. at least if you are an active member here .. Gyno needs estrogen to form , but what you dont hear a lot is that gyno actually requires estrogen , progesterone as well as other mediators such as IGF and GH to form ..

Gyno cant not form if the internal conditions are not right.. Estrogen or progesterone alone cant cause gyno ..

So like estrogen , progesterone will have minimal effects in breast development ( without anterior pituitary hormones ).. Development of breast tissue in men occurs in a similar manner as it does in females ( same hormones cause it)....

Males testes secrete 6 -10 mg of of estradiol per day .. The rest comes from the aromatization of testosterone , as well as androstenedione to estradiol and estrone.. So if you are taking steroids the test your body is converting to estrogen could possible create the proper environment for gyno to form , but I want to clear up the misinformation I keep seeing on the web so people can start to understand that is is not just estrogen that causes gyno ..

People using 19nors ( like deca , tren ) are concerned with progesterone ( and prolactin) issues .. Its is the samething .. Gyno requires progesterone , estrogen ( as well as other mediator's to form).. People using 19 nors could also consider using letro as it has been shown to lower PgR ( progesterone receptors)...

So yes controlling estrogen is a good way to avoid gyno , but I wanted to clear this up a little bit so more people understand it's not just estrogen that causes gyno .. There have been a lot of post about this so I thought is was worth discussing ..


Gyno needs more than just estrogen


Merc.

[Swifto]

Swifto I think the problem is that the studies dont really establish that progesterone activity is regulated by regulating the number of PgRs ....If so a good deductive connection would be made..




Merc.

How else would PgR be regulated without regulating the PgR's?

The fact is, Tamox is an antagonist in breast tissue (agonist in others tissues, yes) in healthy humans. So why wouldnt PgR follow suit with ER? In breast cancer this may be different.

When I, you, take Tamox it downregulates the ER.

[Merc.]

The number of PgRs may have little to do with modulating progesterone activity ( we really need more vaild studies on this though)... the PgRs may be far in excess of progesterone. the amount of progesterone would have far more to do with side effects than the number of receptors.




Merc.

[Hazard]

This has turned out to be one incredibly informative thread.....

~Haz~

[Merc.]

This has turned out to be one incredibly informative thread.....

~Haz~

Sup Haz

Yea I think it is a really interesting topic ... Nothing conclusive though because the studies just go back and forth ...




Merc.

[Chev]

This has turned out to be one incredibly informative thread.....

~Haz~

No dought!! i think my eyes hurt as well!! lol

[Merc.]

No dought!! i think my eyes hurt as well!! lol

LOL







Merc.

[Swifto]

The studies seem to go back and forth on this .. but I think that Nolva does increase PgR in breast tissue .. Which in turn can give more of the nasty deca / tren metabolites to bind too .. and could possibly increase the chance of getting gyno( but it is not a problem for all people )..

If you do a search you will see that there are peeps that report that they have problems when using 19 nor and nolva ( so we are sorta left with a shortage of info in the medical studies because they tend to go back and forth on this topic . But we do have an accumulation of independent anecdotal observations that can at least provide some idea how much of an issue it really is.

That said I will post some studies that show that nolva does increase PgR..

Here is one study showing nolva increases PgR . Like I said it gives more for the 19 nors metabolites to bind to and because of this it could possibly increase your chances of getting gyno..



Estrogen receptor (ER) and progesterone receptor (PgR), by ligand-binding assay compared with ER, PgR and pS2, by immuno-histochemistry in predicting response to tamoxifen in metastatic breast cancer: a Southwest Oncology Group Study.

Elledge RM, Green S, Pugh R, Allred DC, Clark GM, Hill J, Ravdin P, Martino S, Osborne CK.
Baylor College of Medicine, Houston, TX, USA. [email protected]
Results of estrogen receptor (ER) and progesterone receptor (PgR) ligand-binding assays (LBAs) are strongly correlated with ER and PgR by immuno-histochemistry (IHC). To investigate whether ER and PgR by IHC are also strongly correlated with tamoxifen response, time to treatment failure (TTF) and overall survival (OS), the results of the 2 methods were directly compared in 205 patients with ER(+) metastatic breast cancer treated with daily tamoxifen (Southwest Oncology Group protocol 8228) with 9 years median follow-up. pS2, another estrogen-regulated molecule, was also analyzed. Tumors were scored for IHC from 0 to 5, according to the proportion of positively stained cells. These IHC scores for both ER and PgR were significantly associated with LBA levels (p < 0.001). There was a significant direct relationship between higher IHC ER, PgR and pS2 and increasing response to tamoxifen. TTF and OS were also significantly longer for patients with higher ER or PgR, but not pS2, IHC scores. Low, intermediate and high ER or PgR categories showed similar differences in response rates whether defined by LBA or IHC. In logistic regression models which included ER, PgR and pS2 by IHC; ER and PgR by LBA; and menopausal status, only ER (IHC) and pS2 (IHC) retained significance for predicting tamoxifen response (p = 0. 02 and p = 0.005, respectively), along with menopausal status (for PgR by IHC, p = 0.09). Increasing ER and PgR by IHC, as by LBA, are thus significantly associated with a progressively better response and longer survival in ER(+) metastatic breast cancer. pS2 is also predictive in this setting. Copyright 2000 Wiley-Liss, Inc.
PMID: 10754487 [PubMed - indexed for MEDLINE]


You're misreading the abstract. The study did not find that nolva increases PgR. It found that PgR levels (along with ER levels, etc) were predictive of how well the tissue would respond to hormonal therapy (tamoxifen). Basically, if there are more steroid receptors in the tissue (e.g. ER+/PgR+), the tissue is going to be more responsive to hormonal therapy. They did not examine the effect of tamoxifen on PgR expression.



And this one


The PgR gene is an estrogen-regulated gene (34) , so drugs with estrogenic activity will increase its expression. Accordingly, tamoxifen has been shown to increase PgR levels (35) , whereas initial work on primary breast tumors found that a short-acting formulation of ICI 182,*** reduced PgR levels (30) , suggesting that it is devoid of estrogen-agonist activity and may have a different mechanism of action to that of tamoxifen. Additional evidence that ICI 182,*** and tamoxifen have different underlying modes of action comes from studies showing that tamoxifen-resistant tumors remain sensitive to ICI 182,*** treatment in vitro (18 , 19) , in vivo (36 , 37) , and in the clinic (38, 39, 40) .


http://cancerres.aacrjournals.org/cg...ull/61/18/6739


If you look at what reference 35 says, you'll see that when they administered tamoxifen, 40% (21/52) had an increase in PgR, 37%(19/52) has a decrease in PgR, and the remaining (12/52) were negative for the receptor. The overall increase in PgR was statistically significant, but as you can see, the results were far from uniform.




Also


Aromatase inhibitors: cellular and molecular effects.

Miller WR, Anderson TJ, White S, Larionov A, Murray J, Evans D, Krause A, Dixon JM.
Breast Unit, Western General Hospital, Edinburgh, Scotland, UK. [email protected]

Marked cellular and molecular changes may occur in breast cancers following treatment of postmenopausal breast cancer patients with aromatase inhibitors. Neoadjuvant protocols, in which treatment is given with the primary tumour still within the breast, are particularly illuminating. In Edinburgh, we have shown that 3 months treatment with either anastrozole, exemestane or letrozole produces pathological responses in the majority of oestrogen receptor (ER)-rich tumours (39/59) as manifested by reduced cellularity/increased fibrosis. Changes in histological grading may also take place, most notably a reduction in mitotic figures. This probably reflects an influence on proliferation as most tumours (82%) show a marked decrease in the proliferation marker, Ki67. These effects are generally more dramatic than seen with tamoxifen given in the same setting. Differences between aromatase inhibitors and tamoxifen are also apparent in changes in steroid hormone expression. Thus, immuno-staining for progesterone receptor (PgR) is reduced in almost all cases by aromatase inhibitors, becoming undetectable in many. This contrasts with effects of tamoxifen in which the most common change on PgR is to increase expression. Changes in proliferation occur rapidly following the onset of exposure to aromatase inhibitors. Thus, neoadjuvant studies with letrozole in which tumour was sampled before and after 14 days and 3 months treatment show that decreased expression of Ki67 occur at 14 days and, in many cases, the effect is greater at 14 days than 3 months. These early changes precede evidence of clinical response but do not predict for it. However, this study design has allowed RNA analysis of sequential biopsies taken during the neoadjuvant therapy. Based on clustering techniques, it has been possible to subdivide tumours into groups showing distinct patterns of molecular changes. These changes in tumour gene expression may allow definition of tumour cohorts with differing sensitivity to aromatase inhibitors and permit early recognition of response and resistance.
PMID: 16002280 [PubMed - indexed for MEDLINE]


The full text of this paper explains, "In a small series of PgR-positive cancers treated with tamoxifen, a different pattern of change was seen. Thus, only 17% of cases showed a decrease and the most common change was a paradoxical increase in staining." In table 2, we see that 24% the tamoxifen group had down-regulation of the PgR, 26% had no change, and 50% showed up-reguation.



And this one is good also


Estrogen Receptor Downregulators

Dr. Tony Howell,[10] of the University of Manchester and the Christie Hospital, Manchester, UK, spoke concerning work with ER downregulators (formerly called "pure" antiestrogens). The prototype of these drugs is the steroidal compound fulvestrant, which induces ER downregulation[11] in animal and cell models. Dr. Robertson's group has shown that tamoxifen induces mild downregulation of ER but upregulation of PgR, whereas fulvestrant downregulates both ER and PgR. Aromatase inhibitors may produce similar effects to those produced by fulvestrant, but they do so by completely removing all estrogen.


http://www.medscape.com/viewarticle/440361


It looks like this wasn't a peer-reviewed paper, but an article from medscape that's no longer there. If anyone can find it or find the references for it, I'd be interested in looking at them.



Merc.

Merc,

I put these studies to someone that really knows what there talking about. Not saying you dont, but I put his responses in bold.

Making assumptions from abstracts can be quite contradictory, as you'll see.

[Swifto]

In contrast to those papers, this study found what they described as "a modest decline" in PgR levels in all three histologies they tested with tamoxifen treatment, though it failed to achieve statistical significance (p values of .19, .82, and .15).

I know there were other places where I had seen down-regulation of PgR in breast tissue. I'll do a little more research when I have some free time. I want to thank Swifto for posting what he did. It definitely challenges my statement that nolva decreases PgR density, though it shows that the response to tamoxifen is far from consistent.

I'm especially interested in seeing any data in normal, healthy breast tissue, as opposed to tumors and cancerous tissue, which could respond differently. I doubt there's any data in males, which would be most relevant, so data in healthy females is probably would be the best available. I'll look for more data when I have some free time. Thanks again Swifto.

[amostofi1999]

too much technical data for me :S
can one of you guys tell us newbies what to take during tren /deca cycles to avoid gyno?(specially when stacked with test)

[Swifto]

too much technical data for me :S
can one of you guys tell us newbies what to take during tren/deca cycles to avoid gyno?(specially when stacked with test)

Control estrogen with an AI. Aromasin 10mg/ED.

Keep Cabergoline on hand and Tamoxifen .

[Merc.]

Merc,

I put these studies to someone that really knows what there talking about. Not saying you dont, but I put his responses in bold.

Making assumptions from abstracts can be quite contradictory, as you'll see.

I said in my post that the studies go back and forth on this ( i will post some links of ones that shows it decreases them as well ( so you can show him so he doesnt have to waste his time looking for them.. it can be such a pain digging through studies .. I will post link at the bottom of this post mate )..

That said my intent was just to say my opinion according to what some of the studies show , and with what some peeps report back in real life on the boards .. like I said in my other post above .. we do have an accumulation of independent anecdotal observations that can at least provide some idea how much of an issue it really is.

So from reading his responses I did what I was trying to accomplish( by posting those studies) .. which is showing that there is a possibility that it does increase PgR ( which he agrees with because he said he wanted to thank You for posting what You did. and that it definitely challenges His statement that nolva decreases PgR density, He also said that it shows that the response to tamoxifen is far from consistent( which I do agree with .. it is what I meant by saying the studies do go back and forth ).. It is hard sometimes over the internet to explain exactly what i want to ( i wish we had a s.com radio station or something .LOL).... I do work in a field that requires me to read a lot of studies ( not all the time ).... so I do know what I am talking about ..

Heres is some links that show a decrease .. EDIT ... MEANT it decreases ..

http://www.issoonline.com/content/3/1/29

I think this one does ( i have it in my "shows decreased " PgR folder , but dont have time to read through it right now..

http://jco.ascopubs.org/cgi/content/full/25/15/1957



Merc.

[Swifto]

I said in my post that the studies go back and forth on this ( i will post some links of ones that shows it decreases them as well ( so you can show him so he doesnt have to waste his time looking for them.. it can be such a pain digging through studies .. I will post link at the bottom of this post mate )..

That said my intent was just to say my opinion according to what some of the studies show , and with what some peeps report back in real life on the boards .. like I said in my other post above .. we do have an accumulation of independent anecdotal observations that can at least provide some idea how much of an issue it really is.

So from reading his responses I did what I was trying to accomplish( by posting those studies) .. which is showing that there is a possibility that it does increase PgR ( which he agrees with because he said he wanted to thank You for posting what You did. and that it definitely challenges His statement that nolva decreases PgR density, He also said that it shows that the response to tamoxifen is far from consistent( which I do agree with .. it is what I meant by saying the studies do go back and forth ).. It is hard sometimes over the internet to explain exactly what i want to ( i wish we had a s.com radio station or something .LOL).... I do work in a field that requires me to read a lot of studies ( not all the time ).... so I do know what I am talking about ..

Heres is some links that show a increase ..

http://www.issoonline.com/content/3/1/29

I think this one does ( i have it in my shows increses PgR folder , but dont have time to read through it right now..

http://jco.ascopubs.org/cgi/content/full/25/15/1957



Merc.

Thanks for your time as always Merc.

Good thread and discussion mate.

[Merc.]

Thanks for your time as always Merc.

Good thread and discussion mate.

Yea it is a GREAT topic ...

I edited my post above.. I got rushed by my girlfriend and posted increase by mistake .. The studies are ones that show a decrease in PgR.....





Merc.

[amostofi1999]

Control estrogen with an AI. Aromasin 10mg/ED.

Keep Cabergoline on hand and Tamoxifen.

thanks man! what about letro? i know letro will wipe out estrogen but i cant get aromasin or adex. what dosage of letro can i run and still not kill all the estrogen? maybe 0.25mg eod?