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Tren and Nolva
- Thread starter dosteov
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A
Anthony Roberts
Guest
Tren is a progestin and nolvadex increases progestin receptors.
anthony roberts said:
What's up Anthony. Looking forward to the book.
I actually had private messaged you recently regarding a friend of mine and his total lack of libido after a Tren cycle.
I'm on week 3 of a Test/Tren cycle and my right nipple is a little sore and there's a hard little rock under the nipple. I had this towards the end of my last cycle and uped my Adex dose to 1mg and took Nolva and stopped all gear (it was towards the end of my cycle so it wasn't a big deal). But now it's only week 3 and I'm seeing sick gains and really don't want to stop. So I've upped my dose of Adex to 1MG and am going to get some Femara from AGGuys on Monday (I'm obviouslly not going to take any Nolva now).
I found this link (see below) on steroids.com (basically the guy claims that lumps are estrogen gyno and enlarged nipple areas are progesterone gyno). Any truth to that? He basically recommends Femara for either case of gyno (claiming that Femara will also help progesterone gyno because without estrogen there is no gyno).
Anyway you think I can continue to take my TrenAce ED and TestEnanthate? I'm going to monitor the situation daily (like I said it really is only a tad sore, I was looking out for it so noticed it early I think). I've upped my Adex dose and am waiting on the Femara. I'll hopefully have it by Thursday.
Thanks man...
http://forums.steroid.com/showthread.php?t=236880
wootool
New member
anthony roberts said:
there is ONE single unitary study that I'm aware of done on (if I recall) post menopausal female breast cancer patients that made an incidental mention of increased Progesterone receptor expression using tamoxifin. and no followup of what that means, or to reproduce the results.
hardly a reason to throw away 10 or 20 years (or however long nolva's been around) of accepted protocol dealing with gyno treatment/prevention.
as you know the basic theory is that progesterone gyno, if such a thing exists (separate syndrome from prolactin related sides), requires a small amount of estrogen to manifest. block it and no gyno whether e based of pr based.
as far as I know, nolva is still the accepted protocol, E or PR based gyno. If thats changed, I'd like to see some studies/references etc. Always ready to admit I missed something, should that be the case.
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jacshelb
New member
wootool said:
I don't need studies for this myself. Though not everyone will react the same way, I didn't get gyno on my tren cycle till I added in nolva. Then, I got the worst case of my life, lactation etc etc. It sucked. When I removed the nolva, things started calming down after a while. Then, I thought it would be safe to add nolva in again(far enough away from my cycle end). Big mistake, more puffiness, lactation. Took it away, things calmed down again. So, that's my experience. I won't touch nolva again as I seem to be very prolactin sensitive.
Jacob
Mavafanculo
New member
jacshelb said:
my head is spinning. apples, oranges, coconuts, monkeys, pencils....
This is why science is good, anecdotal reports not so good.
Progesterone inhibits lactation. If the theory is nolva upregulates progesterone receptors (a single incidental mention in an unrelated study) nolva should reduce not cause your lactation.
get yourself some dostinex.
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Mavafanculo
New member
dosteov said:
If anyone has any on point reproducable studies to post, I'd love to examine them. Some guy saying it dont make it so. nor does a single incidental mention in an unrelated study make it so. you dont change established protocol on such flimsy possibilities.
this isnt directed at you btw.
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macrophage69alpha
New member
wootool said:
not really, its called receptor cross reactance.
there is a significant # of people on these forums alone that have gotten gyno while using tamoxifen with progestins (nandrolone/tren/etc) and where the addition of tamoxifen worsened or caused the onset (usually PCT) of gynecomastia.
the study that has been referenced was brought forward to explain why this was occuring, not the other way around.
macrophage69alpha
New member
Mavafanculo said:
progestins dont
and guess what else progestins do--- they suppress natural progesterone. Now there are a lot of compounds that can bind to that PR (its a bit promiscuous-- one of which is estrogen- you know the thing that tamox is displacing- but still present)....
just something to mull over
Silent Method
New member
____________________________________________
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. [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.
____________________________________________
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. [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.
____________________________________________
