Thread: Started my Prop/Tren Ace cutter

I would use a moderate dose AI instead of nolva. Nolva potentiates the progesterone receptors, so it may not be wise using it while on tren. What is your dosing schedule for this cycle?

Originally Posted by PirateFromHell

I would use a moderate dose AI instead of nolva. Nolva potentiates the progesterone receptors, so it may not be wise using it while on tren. What is your dosing schedule for this cycle?

I'm doing 2cc's prop/1cc tren EOD.

What problems might arise with the progesterone receptors?? I've heard that term before in relation to tren and I think deca, but am kinda in the dark...

The reason I was going to try the nolva at 10mgs a day is because I'm actually having a hard time getting a hold of an AI. I start a new job thursday...kinda hesitant about shelling out the extra money for that right now...but I shouldn't have a problem getting it in the next couple weeks ( I hope)

Originally Posted by PWGriffin

What problems might arise with the progesterone receptors?? I've heard that term before in relation to tren and I think deca, but am kinda in the dark...

Gyno, libido loss, emotional disturbances...Your prop dose is pretty high. I don't think 10 mg nolva is going to prevent gyno for long.

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

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. w.r.miller@ed.ac.uk

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.

agree with pirate, i wouldn't bother with the nolva