Gyno from using Pharma Labs Tren Bomb?

seventy1

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Hi guys,

I took a 2 week course of Pharma labs, Tren-bomb and had good results.

Just before I came off it I woke up one night with a slightly itchy chest area, predominantly my left pec.

It's been about a week and a half since I've been off it and I've been taking Androbolix (6-oxo and trib etc) as a pct.

In the past few days my left nipple especially is very sensitive and I have a burning sensation.

I have a bad feeling I'm developing Gyno. I do have some clomid which I started taking last night as a precaution, but my understanding is that this isn't that effective.

I've never taken any anabolic steroids before I did do a week of M1t about a year ago, but stopped because I didn't like the sides.

Can anyone help? I'm pretty worried about it.
 

seventy1

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Nightmare.

I can't stop worring about it. Getting rid of it before it develops is all I can think about.

Would Nolvadex get rid of it at this early stage?
 
bb4life

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letro do some searching around on it.... very good stuff.
 

seventy1

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Thank you for the replies.

I'm pretty sure I can only get Nolvadex from my source, which isn't great since everything I've read makes me think Letro is the best option.

Would Nolvadex have any impact at all?

Thank you for this.
 
mooch2321

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nolva would be fine ran along with the 6-oxo you are already running....
 
mooch2321

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wait tho...whats in that tren bomb? most of the tren products are progestins....you might have to get caber
 

abuleh

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There are quite some discussions ongoing about what Tren Bomb actually is. I don't have a final answer but it looks very simular ti M1T (Not saying thats what it is).

Just read a discussion about it over at BB dot com (calling out PA......, for those that are interested in following)

For sure it does not look like any of those other Nor or Estra Tren designers and I doubt you really have to worry about adding caber or so...... might be wrong though bc nobody 100% knows what it is.......

~abuleh
 

seventy1

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Thanks Abuleh,

That more i research the more I think it could be prolactin related.

I have also read that if it is prolactin related then Nolva could make it worst. Is this correct?
 
HardTrainer

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Taken from a uk webstore FAQ on tren bomb:

Question

Tren Bomb: I heard that Tren Bomb is only Methyl 1 Testosteron Is this true?

Answer

Max, this is not true. M1T is no longer manufactured. Tren Bomb is a keto modified version of M1T, with a resulting modified chemical structure - making the compound unable to aromatise to estrogen. This makes Tren Bomb a truly designer and unqiue little compound, with little data on its usage or side effects. Although this may bear some similarities to Methyl 1 Testosterone, it simply is not.

Basically, nobody really seems to know what it is. It might be worth emailing the manufacturer.
 

seventy1

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I can't seem to find the pharma labs site. I'm so confused about what to do now.

I need to resolve the problem before it actually develops into something I can't get rid of without surgery.

I'm really unsure on what to do. I've ordered some Vitex Agnus Castus

as I have read that people have has success with it from prolactin related gyno.

I'm keeping my fingers crossed.
 

Knowbull

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I think you might be safe. are you getting lactation? When you look at yourself sideways, in a mirror, do your pectorals have the sloping grace and beauty of a playboy centerfold? I wouldnt worry about it.
 
sethroberts

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Adv Exp Med Biol. 2008;630:19-34.Related Articles, Links
Adaptation to estradiol deprivation causes up-regulation of growth factor pathways and hypersensitivity to estradiol in breast cancer cells.

Santen RJ, Song RX, Masamura S, Yue W, Fan P, Sogon T, Hayashi S, Nakachi K, Eguchi H.

Division of Endocrinology and Metabolism, University of Virginia Health Sciences Center, Charlottesville, Virginia, USA. [email protected]

Deprivation of estrogen causes breast tumors in women to adapt and develop enhanced sensitivity to this steroid. Accordingly, women relapsing after treatment with oophorectomy, which substantially lowers estradiol for a prolonged period, respond secondarily to aromatase inhibitors with tumor regression. We have utilized in vitro and in vivo model systems to examine the biologic processes whereby Long Term Estradiol Deprivation (LTED) causes cells to adapt and develop hypersensitivity to estradiol. Several mechanisms are associated with this response including up-regulation of ERalpha and the MAP kinase, PI-3-kinase and mTOR growth factor pathways. ERalpha is 4-10 fold up-regulated as a result of demethylation of its C promoter, This nuclear receptor then co-opts a classical growth factor pathway using SHC, Grb-2 and Sos. This induces rapid nongenomic effects which are enhanced in LTED cells. The molecules involved in the nongenomic signaling process have been identified. Estradiol binds to cell membrane-associated ERalpha which physically associates with the adaptor protein SHC and induces its phosphorylation. In turn, SHC binds Grb-2 and Sos which results in the rapid activation of MAP kinase. These nongenomic effects ofestradiol produce biologic effects as evidenced by Elk-1 activation and by morphologic changes in cell membranes. Additional effects include activation of the PI-3-kinase and mTOR pathways through estradiol-induced binding of ERalpha to the IGF-1 and EGF receptors. A major question is how ERalpha locates in the plasma membrane since it does not contain an inherent membrane localization signal. We have provided evidence that the IGF-1 receptor serves as an anchor for ERalpha in the plasma membrane. Estradiol causes phosphorylation of the adaptor protein, SHC and the IGF-1 receptor itself. SHC, after binding to ERalpha, serves as the "glue" which tethers ERalpha to SHC binding sites on the activated IFG-1 receptors. Use of siRNA methodology to knock down SHC allows the conclusion that SHC is needed for ERalpha to localize in the plasma membrane. In order to abrogate growth factor induced hypersensitivity, we have utilized a drug, farnesylthiosalicylic acid, which blocks the binding of GTP-Ras to its membrane acceptor protein, galectin 1 and reduces the activation of MAP kinase. We have shown that this drug is a potent inhibitor of mTOR and this provides the major means for inhibition of cell proliferation. The concept of "adaptive hypersensitivity" and the mechanisms responsible for this phenomenon have important clinical implications. The efficacy ofaromatase inhibitors in patients relapsing on tamoxifen could be explained by this mechanism and inhibitors of growth factor pathways should reverse the hypersensitivity phenomenon and result in prolongation of the efficacy of hormonal therapy for breast cancer.

Publication Types:
Research Support, N.I.H., Extramural
Research Support, U.S. Gov't, Non-P.H.S.
Review

PMID: 18637482 [PubMed - indexed for MEDLINE]

J Steroid Biochem Mol Biol. 2001 Dec;79(1-5):35-40.Related Articles, Links
Modulation of aromatase expression in human breast tissue.

Chen S, Zhou D, Yang C, Okubo T, Kinoshita Y, Yu B, Kao YC, Itoh T.

Division of Immunology, Beckman Research Institute of the City of Hope, Duarte, CA 91010, USA. [email protected]

Aromatase plays an important role in breast cancer development through its role in the synthesis of estrogen. Aromatase expression in breast tissue can be regulated by several mechanisms. The major promoter usage for aromatase expression in breast tumors (i.e. cAMP-stimulated promoters I.3 and II) is different from that in normal breast tissue (i.e. glucocorticoid-stimulated promoter I.4). Recent characterization of transcription factors that interact with the two important regulatory elements near promoters I.3 and II, i.e. S1 and CREaro, helps us better understand the mechanism of the switch of promoter usage between normal breast tissue and cancer tissue. It is thought that in normal breast tissue, the function of promoters I.3 and II is suppressed through the binding of EAR-2, COUP-TFI, and EARgamma to S1, and through the binding of Snail/Slug proteins to their binding site that quenchs the CREaro activity. In cancer tissue, the expression levels of EAR-2, COUP-TFI, EARgamma, Snail, and Slug decrease, and aromatase expression is then up regulated through the binding of ERRalpha-1 to S1 and the binding of CREB or related factors to CREaro. Results from this and other laboratories reveal that aromatase activity in aromatase expressing cells can also be modified by treatment with aromatase inhibitors and the antiestrogen ICI 182, 780. While aromatase inhibitors are used to treat breast cancer, the treatment has been found to increase the level of aromatase in the breast tissue of some patients. The enhancement of aromatase activity by aromatase inhibitors is thought to be due to a decrease of aromatase protein degradation by enzyme-inhibitor complex formation, up-regulation of the aromatase gene transcription through a cAMP-mediated mechanism, and an induction of aromatase expression by gonadtropins that are released from the pituitary in response to a reduction of estrogen levels in circulation in premenopausal women. Antiestrogen ICI 182, 780 has been found to suppress aromatase expression, but the mechanism has not yet been determined. In addition, aromatase activity and expression can be affected by environmental chemicals. A detailed structure-function study has revealed that flavones, but not isoflavones, are inhibitors of aromatase. It was found that flavones bind to the active site of aromatase in an orientation in which their rings-A and -C mimic rings-D and -C of the androgen substrate. The modulation of aromatase expression by endocrine disrupting chemicals is exemplified by two organochlorine pesticides (i.e. toxaphene and chlordane) that have been found to be antagonists of ERRalpha-1 orphan receptor. These compounds reduce ERRalpha-1 activity, resulting in a suppression of aromatase expression.

Publication Types:
Research Support, U.S. Gov't, P.H.S.

PMID: 11850205 [PubMed - indexed for MEDLINE]
 
GotTest

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Great research articles.
This is the first time I've actually seen research that backs the "rebound" theory. I've heard it discussed over and over but never really read the research.
 
GotTest

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Hi guys,

I took a 2 week course of Pharma labs, Tren-bomb and had good results.

Just before I came off it I woke up one night with a slightly itchy chest area, predominantly my left pec.

It's been about a week and a half since I've been off it and I've been taking Androbolix (6-oxo and trib etc) as a pct.

In the past few days my left nipple especially is very sensitive and I have a burning sensation.

I have a bad feeling I'm developing Gyno. I do have some clomid which I started taking last night as a precaution, but my understanding is that this isn't that effective.

I've never taken any anabolic steroids before I did do a week of M1t about a year ago, but stopped because I didn't like the sides.

Can anyone help? I'm pretty worried about it.
First thing you need to due is RELAX. :)

Gyno is the development of breast tissue so I wouldn't just go with the "itch/burn" as being gyno. Maybe it's an "indicator" of something happening but I wouldn't say gyno YET.

Press against your nipple and around the area, and see if you are developing sensitive lumps...sometimes it will feel like a "ballbearing" that is tender to the touch. The sensitivity will be the lump NOT the skin.

Post back.
 

seventy1

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GotTest thanks :) I feel a bit better.

I have no obvious lump yet, however its tender/sore just on my left pec and my nipple on the side feels quite tender.
 
GotTest

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GotTest thanks :) I feel a bit better.

I have no obvious lump yet, however its tender/sore just on my left pec and my nipple on the side feels quite tender.
If there is no real lump it may not be gyno.
I am speaking from experience...unfortunately. :rolleyes:

I have gyno from years past (15 or so) and I thought I had aggravated some it on one cycle and it ended up just being sore muscle. Your mind can play tricks for sure.

I would continue with the Clomid, and DON'T dose this over 100mg like some do, I actually go 50mg EOD taper down. Clomid has a 1/2 life of about 5days and will help block estrogen in breast tissue.

I taper UP then back DOWN with the 6-oxo as you taper DOWN the Clomid.

SIMILAR to this (EVERY cycle is different):
Clomid
EOD dosing
50/50/25/25

6-oxo
200/300/400/300/200

If things get worse don't hesitate to see a DR. That way you can have some bloodwork run and then the DR can see EXACTLY what is going on.
 

seventy1

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If there is no real lump it may not be gyno.
I am speaking from experience...unfortunately. :rolleyes:

I have gyno from years past (15 or so) and I thought I had aggravated some it on one cycle and it ended up just being sore muscle. Your mind can play tricks for sure.

I would continue with the Clomid, and DON'T dose this over 100mg like some do, I actually go 50mg EOD taper down. Clomid has a 1/2 life of about 5days and will help block estrogen in breast tissue.

I taper UP then back DOWN with the 6-oxo as you taper DOWN the Clomid.

SIMILAR to this (EVERY cycle is different):
Clomid
EOD dosing
50/50/25/25

6-oxo
200/300/400/300/200

If things get worse don't hesitate to see a DR. That way you can have some bloodwork run and then the DR can see EXACTLY what is going on.

Thank you for this. I feel a hell of a lot better.

:)
 

VantheMan

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ok im new to these forums but have been taking 2 tren a day for over 3 weeks now, and have had massive gains but i have tht crazy tingling thing all the time! and i look like i have small tits when im not tensing my pecks, im extremly worried about gyno, and what to do? HELP!
 

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