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Tren e and clomid vs nolvadex

-Ariel-

-Thandzilla-
Platinum
Starting tomorrow I'm starting a 12 week cycle 400 mg tren e with week 4-12 adding 290 test prop, I got some feedback that for pct I should use clomid 50 mg ed for 4 weeks in conjunction with hcg. My question is why clomid over nolva for the non arom tren e, and why not arimidex? Also I'm thinking about increasing cycle duration to 16 weeks with tren e, is that too risky? I'm 5 7 195 around 15% body fat and want to get shredded, so doing 60- 90 minutes of cardio 6 days a week, anyway, any help for a newbie would be appreciated much. You guys have been extremely informative.
 
ariel347 said:
Starting tomorrow I'm starting a 12 week cycle 400 mg tren e with week 4-12 adding 290 test prop, I got some feedback that for pct I should use clomid 50 mg ed for 4 weeks in conjunction with hcg. My question is why clomid over nolva for the non arom tren e, and why not arimidex? Also I'm thinking about increasing cycle duration to 16 weeks with tren e, is that too risky? I'm 5 7 195 around 15% body fat and want to get shredded, so doing 60- 90 minutes of cardio 6 days a week, anyway, any help for a newbie would be appreciated much. You guys have been extremely informative.


Tren is a nandrolone. Nolva will make nandrolone sides WORSE before making them better. Huge no-no to use nolva at all when using things like Deca, Tren etc. If you want a more "chemistry" detailed answer, ask Tatyana or Nelson although they may be tired of answering that...
 
thanks, this is only my second cycle did tren a 300 mg alone without test, for the first cycle... last year, I know how dumb was that, put on much size and only had to deal with sweats and a little difficulty sleeping... but is 16 weeks with tren e too long?
 
ryno9000 said:
Tren is a nandrolone. Nolva will make nandrolone sides WORSE before making them better. Huge no-no to use nolva at all when using things like Deca, Tren etc. If you want a more "chemistry" detailed answer, ask Tatyana or Nelson although they may be tired of answering that...

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 (tren/deca/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.
 
I know its stupid, I guess... I guess since my first cycle was 8 weeks, and I didn't lose much after pct, that 16 weeks I'm gonna be able to gain more and keep it... this is so cognitively dysfunctional I know, I'm not gonna go 16 weeks on tren e thats putting myself at way too much risk.
 
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