Newbie, puffy nipples on test cycle, plz help

[CleanedAndPressed]

Hey everyone, I am on my first cycle of test and have puffy nipples and need some honest opinions/answers if you all would be so kind.

About me: athlete(not a body builder), 30yr male, did one cycle of var only previous to this(and loved it). I have been perusing these forums and others for years, reading all of the great insight, though clearly a lot of it didn't sink in, because now I'm having estrogen related issues on my cycle. I bought Bill Llewelyn's 10th edition of Anabolics from mesoRx, and read it, cover to cover. I liked var because of the great recovery I had on it, which is really all I ever wanted in an AAS.

I decided to take the plunge and inject 500mg of test C because it bypasses the liver for the most part, and supposedly is just a safer, and more effective way to go about it. I started with no estrogen support, waiting to see how my body would respond to just the test(which clearly was a horrible idea). As soon as I started to gain water weight, I started talking 20mg of nolva a day, which cut the water weight right out. I didn't realize though, that my nipples were now puffy, as I think I was expecting them to become sensitive or itch or something first, which they never have.

My nipple puffiness has gone down quite a bit after I upped my dosage of nolva to 40mg ed, but now it's been about a week of being on this dosage, and my nipples are still fairly puffy. I didn't even really think too much about it, till I started researching puffy nipples, and now I'm really scared I screwed everything up. I am now in the process of switching over to letro from my nolva as prescribed here, and I have discontinued all aas usage after only 2.5 weeks on cycle. The letro administration I'm following is shown below as suggested somewhere else on the internet:
Day 1: .25mg Letro + anti-e*
Day 2: .50mg Letro
Day 3: 1.0mg Letro
Day 4: 1.5mg Letro
Day 5: 2.0mg Letro
Day 6: 2.5mg Letro (continue at this dose till symptoms subside)

So, my questions are:
1. Is the letro the right thing to be going to next, and is the regimen above correct?
2. Is the cessation of all AAS the proper thing to do while going the letro route? I am worried that I'm going to just torch every last ounce of estrogen in my body, then become wildly more susceptible to injury as a result. Should I stay on a maintenance dosage of test just so I don't have such a lack of estrogen while I'm building up the letro?
3. Will I most likely be able to completely eradicate these puffy nipples, or is surgery the only hope at this point?

Anyway, I know I messed this one up fairly bad, but was just hoping that some more experienced/wiser folks on this forum could help me out. Thanks in advance.

 

[REK]

How long have you been using the Nolva at 40 mg ED? Nolva IMO is great for gyno, Letro is too strong and not really needed, but thats also why I asked how long on Nolva. We are all different.
Also there are much better ways to control estrogen such as Adex, or Aromasin during a cycle.

Please advise on the Nolva and we can go from there.

Cheers REK

 

[CleanedAndPressed]

Thanks, for the help, this whole thing is really upsetting to me so far, so any help is much appreciated. I have been on the nolva for about 1 week, though the first 2 days of it were only at 20mg/day, and the next 5 were 40mg/day. I'm now completely switched over to the letro. I also have Adex to use as well, but some people really are against AIs because they ruin the positive estrogen effects in the body, which is why I didn't use it... I now am of the belief I should've just run adex from day one at .5mg eod, but hindsight is 20/20.

As a side note, I've gained considerable mass while on this very short cycle, but my recovery has not been anything out of the norm, so for me the test was not what I was looking for in the first place(what a great mass builder though).

 

[REK]

Thanks, for the help, this whole thing is really upsetting to me so far, so any help is much appreciated. I have been on the nolva for about 1 week, though the first 2 days of it were only at 20mg/day, and the next 5 were 40mg/day. I'm now completely switched over to the letro. I also have Adex to use as well, but some people really are against AIs because they ruin the positive estrogen effects in the body, which is why I didn't use it... I now am of the belief I should've just run adex from day one at .5mg eod, but hindsight is 20/20.

As a side note, I've gained considerable mass while on this very short cycle, but my recovery has not been anything out of the norm, so for me the test was not what I was looking for in the first place(what a great mass builder though).

Ok well, you have switched to Letro, that will help with gyno, but it's very harsh, and can affect your ability to get hard as well. Hind sight is always 20/20, but adex or aromasin would have kept estrogen down at a low dose, but not taken it out completely, thats why we use it on cycle, and the gyno would never have happened in the first place. Am I also to understand that you have stopped your test altogether as well? If so, IMO you should begin your PCT with Nolva or Clomid or both depending on what you had planned.

For the future, test IMO is the best way to go, but your experience with VAR was good to. If you go with Test please use Adex or aromasin at a small dose as now you are prone to gyno and it will probably come back. I will post an older article for you to read about gyno, now the article relates to progesterone and prolactin from substances such as Deca and Tren, but the messages is the same, control estrogen and all will be fine. You can use Nolva for gyno as it is best IMO ans still continue your cycle, but as mentioned above the adex or aromasin would have been the way to go. I will just dig out the article and post it for you.

Cheers REK

 

[REK]

Progesterone and prolactin induced gynecomastia
More from Nandi....

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
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Endocrinology 1972 May;90(5):1396-8

(14) Ferrando AA, Sheffield-Moore M, Yeckel CW, Gilkison C, Jiang J, Achacosa A, Lieberman SA, Tipton K, Wolfe RR, Urban RJ.
Am J Physiol Endocrinol Metab 2002 Mar;282(3):E601-7

(15) Sheffield-Moore M, Urban RJ, Wolf SE, Jiang J, Catlin DH, Herndon DN, Wolfe RR,
Ferrando AA
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(16) Doumit ME, Cook DR, Merkel RA..Endocrinology 1996 Apr;137(4):1385-94

(17) Bricout VA, Germain PS, Serrurier BD, Guezennec CY.Cell Mol Biol (Noisy-le-grand) 1994 May;40(3):291-4

(18) Ferrando AA, Sheffield-Moore M, Yeckel CW, Gilkison C, Jiang J, Achacosa A, Lieberman SA, Tipton K, Wolfe RR, Urban RJ.
Am J Physiol Endocrinol Metab 2002 Mar;282(3):E601-7

(19) Nicoletti I, Filipponi P, Fedeli L, Ambrosi F, Gregorini G, Santeusanio F
Acta Endocrinol (Copenh) 1984 Feb;105(2):167-72

(20) Ismail AA, Barth JH.Ann Clin Biochem 2001 Nov;38(Pt 6):596-607

(21) Grunberg SM, Weiss MH, Spitz IM, Ahmadi J, Sadun A, Russell CA, Lucci L, Stevenson LL J Neurosurg 1991 Jun;74(6):861-6

(22) Nomura K, Suzuki H, Saji M, Horiba N, Ujihara M, Tsushima T, Demura H, Shizume K
J Clin Endocrinol Metab 1988 Jan;66(1):230-2

(23) Perel E, Stolee KH, Kharlip L, Blackstein ME, Killinger DW
J Clin Endocrinol Metab 1984 Mar;58(3):467-72

(24) Casey RW, Wilson JD.

 

[CleanedAndPressed]

Thanks so much for the info. I've been on the letro for 3 days and already the puffiness has subsided substantially! Man, that stuff is magic, I'm feeling a lot better about the whole situation. So I have decided to kill this cycle before I even got 4 weeks in. Should I just switch over to var again from here and start my pct after the far, or should I just quit all gear, then wait the allotted time for my htpa to come back to normal before I try the var again? Also, if I do quit everything, I'll still be on the letro for the 2 weeks past my last injection, is there a way to use letro as a pct being that it causes the negative feedback loop like nolva/clomid would, or is that just madness?

 

[REK]

Thanks so much for the info. I've been on the letro for 3 days and already the puffiness has subsided substantially! Man, that stuff is magic, I'm feeling a lot better about the whole situation. So I have decided to kill this cycle before I even got 4 weeks in. Should I just switch over to var again from here and start my pct after the far, or should I just quit all gear, then wait the allotted time for my htpa to come back to normal before I try the var again? Also, if I do quit everything, I'll still be on the letro for the 2 weeks past my last injection, is there a way to use letro as a pct being that it causes the negative feedback loop like nolva/clomid would, or is that just madness?

Yes, Letro is very strong, but it will also remove estrogen to the point where it is not detectable, which is too strong for my liking. I would use clomid/nolva for my PCT. There is some good info on Letro in the profiles, also please remember estrogen is also a great substance to have in our bodies, we just don't want too much, or even worse too little.
This is only my thoughts, but I would stop and wait the allotted time, but you have used var on its own in the past, so I feel you should know best how you will react.

Best of luck

REK

 

[CleanedAndPressed]

Well, I laddered up to a 2.5mg/d dosage of letro over the course of a week. I've now been on that 2.5mg/d dosage for 5 days(today's the 5th day at full dosage). Wednesday will mark the 2 week period from my last test injection, so I'll want to start pct then. I feel like my nipples are slightly less puffy, but they are still definitely puffy, nearly like there's just some water behind them that makes the whole areola puff out a little. I have not lost any sex drive whatsoever on this high dose of letro. I'm taking an oral/liquid form of letro, do you think that the letro I'm taking isn't working? I'm thinking I need to get a blood test tomorrow to see where my estrogen levels are at just to be sure. Should I be in full panic mode now? Any suggestions/advice would be very appreciated, thanks.

 

[REK]

The best way always is to get labs done, and tell your doctor why as there are other tests you should have done. I wouldn't go into panic mode as it accomplishes nothing. Get your labs and go from there.

Best of luck bro.

REK

 

[Gear_Addict]

The best way always is to get labs done, and tell your doctor why as there are other tests you should have done. I wouldn't go into panic mode as it accomplishes nothing. Get your labs and go from there.

Best of luck bro.

REK

Agree ^^^ it's always best to get labs done & evaluate your situation from there