why am i seeing everyone saying dont use nolvadex for pct after a tren a or deca cycle?

[HAYEZ]

anyone got any links or articles ?
i keep seeing people mention dont use nolvadex for pct after a deca or tren cycle....why is this? this has been the norm for the last few years why all of a sudden are people against it?

for the last 5 years i have always used nolva for pct and recovered just fine on test e ,p, mast,eq ,dbol cycles,var....

 

[-Ariel-]

I asked the same question earlier bro, can't use nolvadex with nandralones, makes sides worse, someone sent me a link of a pubmed study and it confirmed this... I used nolvadex and had no problems at all with my pct after trenbolone ace and e, I wouldn't recommend it though...

 

[HAYEZ]

what would useing it for pct though have to do with any side if the aas are no longer active in the body?

 

[-Ariel-]

Re: why am i seeing everyone saying dont use nolvadex for pct after a tren a or deca

what would useing it for PCT - post cycle therapy - though have to do with any side if the anabolic androgenic steroids are no longer active in the body?

I wish I could find the link... but the aggravation of progestin related sides, increased body fat, gynocomastia were related to use of nolvadex, I'm unsure of the mechanism, but would love to read the pubmed study again to confirm this...

 

[eddymerckx]

now, if both of you guys had a plat membership the answer is seconds away--that said--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

 

[HAYEZ]

do you have a link that explains it? just wondering why it was never mentioned until recently

 

[-Ariel-]

Re: why am i seeing everyone saying dont use nolvadex for pct after a tren a or deca

now, if both of you guys had a plat membership the answer is seconds away--that said--when you are on PCT - post cycle therapy - 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 - post cycle therapy - is over

See, I knew one of the wise would answer this, thats what I love about this site , I keep learning, but yeah I'm should have the funds to get lifetime platinum by wednesday, I really hate myself for not being platinum...

 

[-Ariel-]

Thank eddy for this gift of wisdom...
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.

 

[eddymerckx]

Thank eddy for this gift of wisdom...
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.

you are welcome. i think i use the search function at least once a day just to find an answer i know is on here someplace.

 

[slat1]

Just use Clomid and your problem is solved.