Prop + Tren + PCT Critique Please

[lolfb]

Clomid with no Nolva is a bad idea IMO.

Never had a problem with clomid alone. Not to mention that no one should even consider using nolva for a tren cycle. Unless that is you like big lumps behind your tits that leak fluid.

[Lunk1]

Never had a problem with clomid alone. Not to mention that no one should even consider using nolva for a tren cycle. Unless that is you like big lumps behind your tits that leak fluid.

LOL. Nolva is by far a superior SERM to Clomid. If I had to choose one of the 2 it would be Nolva hands down. Whoever told you that no Nolva on a tren cycle is regurgitating shit they keep hearing on from other ppl who have no clue.

Besides we are talking about a PCT not gyno reversal on cycle anyhow.

[lolfb]

LOL. Nolva is by far a superior SERM to Clomid. If I had to choose one of the 2 it would be Nolva hands down. Whoever told you that no Nolva on a tren cycle is regurgitating shit they keep hearing on from other ppl who have no clue.

Besides we are talking about a PCT not gyno reversal on cycle anyhow.

I don't know where you're getting your information from but nolva is not superior to clomid in any way. Clomid triggers test production at a higher rate then nolva could ever do. It binds to the hypothalamus at a high rate, whereas nolva binds more to the breast tissue.
If you're wanting to combat gyno then go ahead and use nolva, but if you want a faster response by your body and start producing test, clomid beats out nolva in every way. There were a few studies done that proved clomid as being the only SERM that can bring back HPTA functions. But beyond that, nolva can trigger prolactin and progrestorone sides, which tren already has elevated on cycle. Tossing nolva after that will cause prolactin induced gyno
And i know we're talking about pct, that was my exact reason for saying it.

[Lunk1]

I don't know where you're getting your information from but nolva is not superior to clomid in any way. Clomid triggers test production at a higher rate then nolva could ever do. It binds to the hypothalamus at a high rate, whereas nolva binds more to the breast tissue.
If you're wanting to combat gyno then go ahead and use nolva, but if you want a faster response by your body and start producing test, clomid beats out nolva in every way. There were a few studies done that proved clomid as being the only SERM that can bring back HPTA functions. But beyond that, nolva can trigger prolactin and progrestorone sides, which tren already has elevated on cycle. Tossing nolva after that will cause prolactin induced gyno
And i know we're talking about pct, that was my exact reason for saying it.

Not sure what forum you are parroting from but please read this thread to get started. There is a reason Nolva AND Clomid are suggested routinely here. I'm saying that IF I chose only one for PCT Nolva is superior!!
http://forums.steroid.com/pct-post-c...lomid-pct.html

[lolfb]

Not sure what forum you are parroting from but please read this thread to get started. There is a reason Nolva AND Clomid are suggested routinely here. I'm saying that IF I chose only one for PCT Nolva is superior!!
http://forums.steroid.com/pct-post-c...lomid-pct.html

And here is a study to show that clomid has actually been tested on steroid users and has been shown to kickstart hpta functions.

And as I stated before, nolva is a great anti-oestrogen. It is however not as good as clomid when it comes to recovery. Clomid binds to the hypothalamus and blocks estrogen there, thus starting up your test production. Nolva works by blocking estrogen in similar ways but it doesn't focus on the hypothalamus. Nolva mainly targets the breast tissue

Fertil Steril 2003 Jan;79(1):203-5

Use of Clomiphene citrate to reverse premature andropause secondary to steroid abuse.

Tan RS, Vasudevan D.

Department of Family and Community Medicine, University of Texas Health Sciences Center, Houston, Texas 77030, USA. [email protected]

OBJECTIVE: To report a case of symptomatic hypogonadism induced by the abuse of multiple steroid preparations that was subsequently reversed by Clomiphene. DESIGN: Case report. SETTING: University-affiliated andrology practice within family practice clinic. PATIENT(S): A 30-year-old male. INTERVENTION(S): Clomiphene citrate, 100-mg challenge for 5 days, followed by treatment at same dose for 2 months. MAIN OUTCOME MEASURE(S): Clinical symptoms, androgen decline in aging male questionnaire, total T, FSH - follicle stimulating hormone - , lh - leutenizing hormone - . RESULT(S): Reversal of symptoms, normalization of T levels with lh - leutenizing hormone - surge, restoration of pituitary-gonadal axis. CONCLUSION(S): Clomiphene citrate is used typically in helping to restore fertility in females. This represents the first case report of the successful use of Clomiphene to restore T levels and the pituitary-gonadal axis in a male patient. The axis was previously shut off with multiple anabolic steroid abuse.

[Lunk1]

And here is a study to show that clomid has actually been tested on steroid users and has been shown to kickstart hpta functions.

And as I stated before, nolva is a great anti-oestrogen. It is however not as good as clomid when it comes to recovery. Clomid binds to the hypothalamus and blocks estrogen there, thus starting up your test production. Nolva works by blocking estrogen in similar ways but it doesn't focus on the hypothalamus. Nolva mainly targets the breast tissue

Nolva works at both the hypothalamus and the pituitary just like Clomid. You have no idea what you are posting after you google it!
Do you really feel confident enough to continue this?

[lolfb]

Nolva works at both the hypothalamus and the pituitary just like Clomid. You have no idea what you are posting after you google it!
Do you really feel confident enough to continue this?

I suggwst re-reading my post. Both SERMs are effectve at targeting estrogen receptors. I never stated they weren't. I stated that clomid targets the hypothalamus more than it does breast tissue. Nolva targets the breast tissue more than it does the hypothalamus. The breast tissue isn't what causes hpta kickstart, the hypothalamus plays a way bigger role. I'm more than confident sense I have posted a study that makes clomid the only SERM that has been PROVEN to be effective on steroid users. Nolva doesn't have such study. And I have read that post you linked a million times on a million different steroid boards for the past 10 years. Studies linked to it are as old as I am, whereas studies on clomid are newer and more accurate and nolva has been used as PCT for a lot longer than clomid. Hence why more people tend to use it even now. It "works". So people jst continue to use it as they did in the past. But that doesn't mean that it's more effectice than clomid. My initial post on this subject was telling OP not to use nolva as it will trigger prolactin gyno since his prolactin will already be high as it is from tren. I never argued that a person shouldn't use both Serms as two of them will be more effective than one, but in the case of tren and deca, it's different. I prefer clomid in every way, I've recovered and kept my gains on clomid alone pct and have never had a problem with it. You can go ahead and use whatever you want.

[ChiveOn]

Never had a problem with clomid alone. Not to mention that no one should even consider using nolva for a tren cycle. Unless that is you like big lumps behind your tits that leak fluid.

I would absolutely love to see something factual supporting this instead of parroted bro science. That's such a sweeping generalized misconception... Completely antiquated and irrelevant knowledge

[lolfb]

I would absolutely love to see something factual supporting this instead of parroted bro science. That's such a sweeping generalized misconception... Completely antiquated and irrelevant knowledge

Took less than 30 seconds of googling to find factual evidence to support my claim, so here you go. If you need any more studies, I'll be happy to dig up more when I get on my computer

Tamoxifen citrate increases expression of progesterone receptor.
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.