Nolvidex and deca

[Jimmyinkedup]

Also I know many bodybuilders that use nolvadex during prep while using deca, npp, and tren... And some have problems and some don't...

Since nolva increases free test, which in turns increases estrogen, this upregulates prolactin causing lactation...

Prolactin comes from massive spikes in estrogen while having high estrogen levels...

This is true- to a degree as well. In most cases properly managing e2 also manages prolactin BUT not always. Sometimes even when you properly manage e2 there is still an increase in prolactin that needs to be managed, thats when the need for prami (a dopamine agonist) comes into the picture.
Managing e2 is always your first priority and will help to offset other hormonal issues, however if it does not I always have prami on hand just in case.

 

[trt newbie]

This really is not true. Nolva temporarily upregulates progesterone receptors, and deca is a progestin. That being said after 2 weeks time nolva actually causes a down-regulation in the very same progesterone receptors, which is a good thing!
There is absolutely no issue with running nolva with a 19nor or running nolva in your pct post 19 nor.
This has been blown way out of proportion on the boards and unfortunately has taken off and been accepted as true when in fact it is not.

Ya I read up on it and found that it was a rumor. I had some on hand and took one 10 mg tab and the itchiness went away I'll probably take one a week

 

[bigorse]

This really is not true. Nolva temporarily upregulates progesterone receptors, and deca is a progestin. That being said after 2 weeks time nolva actually causes a down-regulation in the very same progesterone receptors, which is a good thing!
There is absolutely no issue with running nolva with a 19nor or running nolva in your pct post 19 nor.
This has been blown way out of proportion on the boards and unfortunately has taken off and been accepted as true when in fact it is not.

i stay away just incase. you shouldn't need serms on cycle if your AI and caber/prami protocol is good. unless using the serm in the last few weeks before a show

 

[trt newbie]

I try and stay away from serms all together that one Nolva is the only kind of anti e that I've used in all my cycles, and so far I've been fine.. Knock on wood

 

[Jimmyinkedup]

i stay away just incase. you shouldn't need serms on cycle if your AI and caber/prami protocol is good. unless using the serm in the last few weeks before a show

For the most part I agree that most of the time a serm should not be needed on cycle but once again I am always prepared and have raloxifene on hand just in case for some reason gyno starts to rear its ugly head. For some a serm and ai is a must. Some that run very high doses can even use letro and still they find that they have gyno issues. For them a serm/ai protocol has become standard operating procedure. Granted this is the exception, not the rule, but it does occur.
I just think it is very important for people to realie that it is far more prudent to take nolva if you get gyno on cycle than to not take it because of this deca/nolva nonsense. Treat the damn gyno right away, dont no treat it because of some inaccurate broscience myth. If you dont catch gyno early, well thats when you end up in the position that surgery is your only option. The earlier you recognize and treat it the better off you are.

 

[bigorse]

For the most part I agree that most of the time a serm should not be needed on cycle but once again I am always prepared and have raloxifene on hand just in case for some reason gyno starts to rear its ugly head. For some a serm and ai is a must. Some that run very high doses can even use letro and still they find that they have gyno issues. For them a serm/ai protocol has become standard operating procedure. Granted this is the exception, not the rule, but it does occur.
I just think it is very important for people to realie that it is far more prudent to take nolva if you get gyno on cycle than to not take it because of this deca/nolva nonsense. Treat the damn gyno right away, dont no treat it because of some inaccurate broscience myth. If you dont catch gyno early, well thats when you end up in the position that surgery is your only option. The earlier you recognize and treat it the better off you are.

agreed on the gyno part. just as long as its estrogen related gyno and not prolactin/progesterone gyno.

 

[trt newbie]

Nolva will help estrogen and progesterone gyno it was some broscience myth that it would make it worse

 

[Jimmyinkedup]

agreed on the gyno part. just as long as its estrogen related gyno and not prolactin/progesterone gyno.

trt newb is correct, a serm will help gyno regardless of what seemingly caused it. It is impossible for gyno to form or grow in the absence of estrogen. Taking a serm will block e2 causing apoptosis and cell death regardless of the cause. The following write up by the late Nandi explains this perfectly. He was a very intelligent man and is sorely missed on these forums. Check this one out buddy I think you will like it!


PROGESTERONE AND PROLACTIN INDUCED GYNECOMASTIA


Before delving into this subject, I’d like to say first and foremost, that in users of anabolic /androgenic steroids (AAS) the first step in combating the development of gynecomastia, or male breast enlargement, is to eliminate the causative agent: the anabolic steroid . Drug-induced gynecomastia almost invariably resolves on its own when a person quits taking the drugs responsible for it, if caught before permanent fibrosis develops. Unfortunately, most AAS users don’t want to employ this simple approach, for obvious reasons, so the foregoing will all be under the assumption that a person wants to prevent or treat gyno and still continue steroid use .

In the belief that certain anabolic steroids increase prolactin levels as well as act as agonists at the progesterone receptor, some have advocated the use of antiprolactin agents, like bromocriptine, or progesterone receptor blockers like RU-486 to treat AAS related gynecomastia, in lieu of more traditional drugs like tamoxifen .

In truth, the etiology of gynecomastia is unknown and a number of agents including estrogens, progestins, GH, IGF -1, and prolactin may be involved. However, most authorities believe that a decreased (T+DHT)/E ratio is central to the development of gyno, and that blocking the effects of estrogen, or increasing T + DHT levels, is central to ameliorating the problem.

Regarding prolactin, androgens decrease prolactin levels whereas estrogens increase prolactin. Non-aromatizing androgens have never been shown to elevate prolactin levels in humans, but testosterone has, due to its aromatization to estradiol (19). Prolactin secreting tumors, or prolactinomas, are often associated with gyno. But in these cases the prolactin is believed to induce gyno by suppressing testosterone production: “Prolactinomas that are sufficiently large to cause gynecomastia do so as a result of impairment of gonadotropin secretion and secondary hypogonadism”. (20). However, this is a moot issue in AAS users whose gonadotropin secretion is already blunted.

According to research cited in (20), prolactin may have a direct stimulatory effect on mammary tissue development, but only in the presence of high estrogen levels:


The presence of mild hyperprolactinaemia is therefore not uncommon in patients with estrogen excess. Significant primary hyperprolactinaemia, on the other hand, may directly stimulate epithelial cell proliferation in an estrogen-primed breast, causing epithelial cell proliferation and gynaecomastia.

So rather than focusing solely on lowering prolactin levels which may be elevated in users of aromatizing androgens, attacking estrogen should be the first line of action.

GH and IGF-1 are considered critical to the proliferation of mammary tissue. An excellent review of the role played by these hormones, as well as a general overview of gynecomastia can be found here:




Since elevated GH and IGF-1 are considered important to the anabolic effect of AAS, it would be impractical and counterproductive to attempt to prevent gynecomastia by blocking GH/IGF.

Progesterone acts in concert with estrogen to promote breast development, and at least part of any role played by synthetic progestins may be to stimulate IGF-1 production in the breast. But again, blocking the action of progesterone or synthetic progestins is not practical. Specific progesterone receptor antagonists like RU-486 block not only the progesterone receptor, but the androgen receptor as well, and have actually been associated with the development of gynecomastia (21). In any case, progesterone is thought to act on the breast to enhance the effects of estrogen (22) so once again, attacking estrogen is the easiest and most logical approach.

DHT gel (Andractim) or a generic knockoff might help as well. DHT is thought to act as an aromatase inhibitor (23) and perhaps compete directly with estrogen for binding at the estrogen receptor (24). DHT has been used in several case reports and controlled trials to successfully treat gynecomastia. So perhaps a viable strategy would be to combine DHT gel with tamoxifen. I would recommend tamoxifen rather than an aromatase inhibitor due to the simple fact that tamoxifen has been widely used in numerous controlled studies to succesfully treat gynecomastia, whereas the evidence to support the efficacy of aromatase inhibitors is scanty at best.

References:

(1) Price TM, O'Brien SN, Welter BH, George R, Anandjiwala J, Kilgore M. Am J Obstet Gynecol 1998 Jan;178(1 Pt 1):101-7

(2) Bjorntorp P. Hum Reprod 1997 Oct;12 Suppl 1:21-5

(3) Ramirez ME, McMurry MP, Wiebke GA, Felten KJ, Ren K, Meikle AW, Iverius PH Metabolism 1997 Feb;46(2):179-85

(4) Zmuda JM, Fahrenbach MC, Younkin BT, Bausserman LL, Terry RB, Catlin DH, Thompson PD. Metabolism 1993 Apr;42(4):446-50

(5) Tomita T, Yonekura I, Okada T, Hayashi E
Horm Metab Res 1984 Oct;16(10):525-8

(6) Mystkowski P, Seeley RJ, Hahn TM, Baskin DG, Havel PJ, Matsumoto AM, Wilkinson CW, Peacock-Kinzig K, Blake KA, Schwartz MW. J Neurosci 2000 Nov 15;20(22):8637-42

(7) Greer,M. N Engl J Med 244:385, 1951

(8) Vagenakis AG, Braverman LE, Azizi F, Portinay GI, Ingbar SH. N Engl J Med 1975 Oct 2;293(14):681-4

(9) Krugman LG, Hershman JM, Chopra IJ, Levine GA, Pekary E, Geffner DL, Chua Teco GN J Clin Endocrinol Metab 1975 Jul;41(1):70-80

(10) Liva SM, Voskuhl RR J Immunol 2001 Aug 15;167(4):2060-7

(11) Ulloa-Aguirre A, Blizzard RM, Garcia-Rubi E, Rogol AD, Link K, Christie CM, Johnson ML, Veldhuis J Clin Endocrinol Metab 1990 Oct;71(4):846-54

(12) Hochman IH, Laron Z Horm Metab Res 1970 Sep;2(5):260-4

 

[bigorse]

well you learn something new everyday! what is your serm or choice jimmy? raloxifen? nolva can lower igf output, may not be massive but esp. with guys on low doses gh or igf it can be a concern. i have also read nolva can have a positive effect on lipid profiles

 

[Jimmyinkedup]

well you learn something new everyday! what is your serm or choice jimmy? raloxifen? nolva can lower igf output, may not be massive but esp. with guys on low doses gh or igf it can be a concern. i have also read nolva can have a positive effect on lipid profiles

Yes what is really amazing is that Nandi wrote that what 15 years or so ago! The man was years ahead of his time.
When it comes to gyno, prevention or treatment, Raloxifene is def my serm of choice. It has the highest binding affinity of any serm to the estrogen receptor in breast tissue making it the most effective serm when it comes to this area. It also doesnt appear to adversely impact igf as significantly as tamoxifen while it improves lipid profile even more significantly than tomox. Raloxifene has even been proven effective at treating pubertal and pre-pubertal gyno, the most stubborn forms of gyno to treat.
I always have raloxifene on hand just in case (for gyno treatment and prevention purposes).
The one thing to keep in mind about raloxifene is that while it is a serm and is the most beneficial serm when it comes to gyno as well as safety profile, it is just about the least effective serm when it comes to inducing the production of LH and thus restoring HPTA function. This makes ralox a poor PCT choice unless combined with another serm like say clomiphene.