Letrozole good for Tren Prolactin?

[macrophage69alpha]

Actually, it also has an effect on ER negative cells:

http://www.nature.com/onc/journal/v18/n29/abs/1202755a.html

(among many others)

That would also explain why Nolva works for many people with tren gyno. Not saying and never did say it was the best. Since you have not provided any studies to show it there is a particular danger in increasing prolactin, there is no good reason not to use it.

see this is what happens when you let children play on medline. Just because tamoxifen has non-genomic effects or secondary effects in non ER positive cells does not mean anything.

that study has nothing to do with prolactin.

you want a study.. here.. since tren is the topic here and progestins the issue...

1: J Steroid Biochem Mol Biol. 2005 May;95(1-5):83-9. Links
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.

 

[Harleymarleybone]

see this is what happens when you let children play on medline. Just because tamoxifen has non-genomic effects or secondary effects in non ER positive cells does not mean anything.

that study has nothing to do with prolactin.

you want a study.. here.. since tren is the topic here and progestins the issue...

1: J Steroid Biochem Mol Biol. 2005 May;95(1-5):83-9. Links
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.

Or when childen play on google?

But, oops, you made a mistake. Progersterone is not the issue with Tren gyno, so your study here about an increase in PGR expression is not relevant. Prolactin is the issue. Here is a nice little summary which shows that progesterone isactually be beneficial in inhibiting prolactin, and that lactation begins when progesterone clears:


"Progesterone interferes with prolactin action at the alveolar cell's prolactin receptor level. While estrogen and progesterone are required to get full activity of the prolactin receptor,progesterone antagonizes the positive action of prolactin on its receptor by (1) inhibiting up regulation of the prolactin receptor, (2) reducing estrogen binding (lactogenic activity), and (3)competing for binding at the glucocorticoid receptor.

Actual lactation occurs after birth by allowing prolonged prolactin elevation without progesterone inhibition because of the more rapid clearance of progesterone in contrast to prolactin. It takes approximately seven days for prolactin to reach non-pregnant levels, while estrogen and progesterone elevations are cleared in three to four days postpartum."

http://library.med.utah.edu/kw/human_reprod/lectures/prolactin/

This would once again explain why Nolva can help Tren gyno.

 

[jacshelb]

All I know is that I got my worst gyno (only gyno really) when I was using tren and nolva together for the first time. I've done the same cycle since a few times, sans nolva and not had any gyno symptoms.


Jacob

 

[macrophage69alpha]

But, oops, you made a mistake. Progersterone is not the issue with Tren gyno, so your study here about an increase in PGR expression is not relevant. Prolactin is the issue.

prolactin is a secondary effect of trenbolones action at the PgR. trenbolone is a PgR agonist, it directly initiates issues with respect to gynecomastia while ALSO raising prolactin (though not necessarily).

treating the prolactin issue is treating a secondary problem with tren.

 

[macrophage69alpha]

Here is a nice little summary which shows that progesterone isactually be beneficial in inhibiting prolactin, and that lactation begins when progesterone clears:

since when did progestins become progesterone? remember last week in class when mrs. hinkledumper explained that humans are mammals but not all mammals are humans. progesterone is a progestin, but not all progestins are progesterone.

progestins are compounds that bind to the PgR, they can have vastly different activity. Trenbolone has both agonist and antagonistic activity. Progesterone on the other hand is a pure agonist.

even other agonist compounds can have VASTLY different transcriptive effects.

you might also want to consider carefully before relating post natal hormonal fluctuations in women to men.

 

[macrophage69alpha]

All I know is that I got my worst gyno (only gyno really) when I was using tren and nolva together for the first time. I've done the same cycle since a few times, sans nolva and not had any gyno symptoms.


Jacob

case in point.

 

[bigrand]

My gyno and tit fat is greatly reduced on tren/nolva/letro. Just the drugs with no cardio seen to have a great effect.

 

[caliboy]

I wasn't referring to you or anybody in particular, big caliboy. Dostinex works fine, for many people. Nolva works for some people. It suppresses prolactin in the same way. Yes, the scientific experts can and do get it wrong, sometimes, but they are still the best source of knowledge we have about these issues. And non-experts get it wrong even more. So, I'll go with the scientists when it comes to my health. I just find it odd and a little reckless when people so non-chalantly reject the actual science and go with the hearsay, which is often myth.

No biggie...just enjoying this thread.

 

[ricorico]

i dunno, this is the 1st thread ive ever seen someone reccommend nolva for tren gyno, until now i thought it was common knowlege not to use nolva with tren

 

[medrep]

My gyno and tit fat is greatly reduced on tren/nolva/letro. Just the drugs with no cardio seen to have a great effect.

I'm curious, reduced TEMPORARILY or reduced PERMANENTYL? I'm about to start my first tren run and have a little chest fat thinking of letro