Trenbolones active metabolite (17beta-trenbolone) has a binding affinity to the progesterone receptor that is actually greater than progesterone itself.
Nolavadex makes potentiates/ makes the progesterone receptors sensitive
= no 19nors (trenbolone/Deca-Durabolin - nandrolone decanoate - /etc) w/nolavadex
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.
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....
when you are on PCT the 19 nors are still active in your body as remember that half lives mean half, then half, then half, so you will still have some receptor upregulation long after PCT is over
"there's 2 phases, on cycle vs PCT.
when on a cycle which includes nandrolones, use of nolva is contraindicated for gyno symtoms because nolva (also clomid) upregulate progesterone receptors. iow, you increase the liklihood of progesterone sides and sequalae (gyno and hyperprolactinemia)
when in PCT, as long as most of the active nandrolones have cleared your system (2-3 weeks), use of SERMs nolva/clomid is fine. the p-receptor upregulation is transient and wont affect a subsequent cycle. "
Dorland's Medical Dictionary for Health Consumers. © 2007 by Saunders, an imprint of Elsevier, Inc. All rights reserved
outta one of my books....
I think that what it comes down to is what works for your body... One study says one thing and one says another.... I have searched for the ast 2 days and when i try to find more info, the next thread says use it...
Good luck... Tamoxifen and prolactin dont mix at all....