Controling Prolactin Gyno from HGH + T4?
- 01-14-2007, 01:51 AM
Controling Prolactin Gyno from HGH + T4?
getting the same sort of little hard lump under the left pec as when I ran tren.
blasting it with 80-100mg Nolva, Vitex and B6. and a topical anti-e.
what else can i do..? I don't want to drop the GH.
i read that fullybuilt dropped the t4 and the symptoms went away...
- 01-14-2007, 08:48 AM
basic research tells me...
(from superior, but not GH/IGF specific)
I'm using IGF for my injured knee, perhaps that is the main culprit.
"Gyno is the result of at least 4 different hormones working in concert; estrogen, progesterone, prolactin, and IGF-1. If you eliminate ANY of the four, gyno can't develop.
Bromo is a very harsh drug and it makes many nausous. If you MUST use a prolactin suppressing drug, dostinex is much more potent and has fewer sides. Any of the anti aromatase drugs (l-dex, arimidex, letrazole, aromasin) WILL work to prevent gyno as they prevent estrogen, a necessary hormone for gyno to develop. After you already have gyno, nolvadex is the best choice IMO.
There really isn't any difference in the gyno caused by deca or tren and that caused by aromatizing AAS. They ALL need estrogen to develop and grow. Without estrogen, you could inject pure progesterone and you wouldn't develop gyno.
Large doses of vitamin B6 has been shown to lower prolactin and would also help prevent or reduce gyno. Unlike bromo or even dostinex, B6 doesn't have ANY sides."
WHile it is true that deca is a progestin, it is also an aromatizable AAS. To make it worse, it is likely aromatized via a liver CYP enzyme and not aromatase. It may not even be a substrate for aromatase. This would render antiaromatases like letrazole or arimidex useless. Estrogen blockers like SERMS (nolva) would definitly be a better choice, HOWEVER, they are not 100% efficient; far from it in fact.
Look at it like this: a normal guy produces something like 50 to 100mg test a week (I think). Natural test production is not completely shut down when on a cycle, just suppressed. Let's say for the sake of argument, it is decreased by 75%. Let's also say that you are taking 300 mg ew deca (many take higher doses). Deca aromatizes to estradiol at around half the rate as test so now you have the estrogen production equivalent to 12.5 to 25 mg test (25% natural production) plus 150mg test (from aromatization of deca). This adds up to the equivalent of 162.5 to 175 mg test or a 62.5% to 75% INCREASE in estrogen over normal levels. An antiaromatase would only marginally affect the estrogen levels since deca is aromatized by a different enzyme than aromatase. All an antiaromatase would affect is that 25% residiual test being aromatized. Letrazole inhibits aromatase to the tune of something like 80% so instead of 12.5 to 25 mg test being aromatized at the normal rate, it would only be equivalent to 2.5 to 5 mg being aromatized. BIG DEAL, you still have 152.5 to 155 mg or 52.5% to 55% OVER normal levels. Taking a SERM like nolva blocks something like 40% of the estrogen at normal doses so by taking nolva alone, your estrogen goes down to that which would be obtained from aromatizing 97.5 to 105 mg test at normal rates. THAT IS EQUIVALENT TO THE AMOUNT OF ESTROGEN A NORMAL GUY PRODUCES ANYWAY AND IS TWICE AS MUCH AS NORMAL FOR SOME GUYS. And you wonder why deca causes gyno????
Throw into that mix that prolactin is produced by a progesterone mediated pathway and deca is a progestin. Now you have estrogen, progestin, and prolactin all at elevated levels. Most AAS. if not all of them, increase IGF-1 levels. Now you have all four necessary ingredients for gyno all at elevated levels. Unless you are gyno resistant, I'd say it is almost a sure thing.
Tren is a little different since it is not aromatized by any mechanism I know about. Stonecold - were you taking anything else besides the tren when it caused gyno? A test/tren cycle (very common cycle) will have similar problems as the deca cycle but antiaromatases should help in the tren/test case. Keep in mind though that antiaromatases do not completely inhibit aromatase so some estrogen is still being produced. If you are sensitive, the increased progestin/prolactin/IGF-1 along with even the decreased estrogen levels may still cause a problem.
I stand by my statements that all four of those hormones are needed for gyno to develop and the elimination of ANY of them will prevent gyno. If estrogen reduction alone doesn't work, perhaps a stratagy whereby estrogen AND prolactin are reduced may work better. LArge doses of vitamin B6 are known to reduce prolactin and dostinex can virtually eliminate it. Bromo is not even FDA approved for prolactemia anymore since it is so harsh and is less effective and less tolerated than dostinex.
- 01-14-2007, 08:57 AM
Bobo yelling at somebody, then posts a good study:
You do know that there has neve been a case of gyno that was directly caused by prolactin so why SHOULD he believe you? All the research on the subject indicates that prolactin can aggravate an already exsisting condition and that prolactin itself cannot cause gyno. Prolactin can be responsible for lactation but gyno is not caused by prolactin, ut is caused by estrogen. Prolactin and progesteron can aggravate this condition even though estrogen levels are low.
"Increased circulating levels of progesterone and prolactin alone do not explain the development of gynaecomastia in patients with liver disease, but progesterone may be an additional factor acting in association with the known disturbances of other sex steroids. (1)
(1) Gut. 1982 Apr;23(4):276-9.
Progesterone, prolactin, and gynaecomastia in men with liver disease.
Farthing MJ, Green JR, Edwards CR, Dawson AM.
Prolactin secretion in the human male is increased by endogenous oestrogens and decreased by exogenous/endogenous androgens.
Gooren LJ, van der Veen EA, van Kessel H, Harmsen-Louman W, Wiegel AR.
There is evidence that prolactin may be involved in testicular steroidogenesis, and we have therefore investigated whether there is feedback regulation of androgens/oestrogens on prolactin secretion in the human male. To assess this we have measured basal and TRH-stimulated prolactin levels in: Six eugonadal men before and after 2 weeks' administration of the aromatase inhibitor delta'-testolactone, which led to a fall in oestradiol levels with unchanged levels of testosterone. In these patients, prolactin levels decreased. Six eugonadal subjects before and after 6 weeks' administration of dihydrotestosterone undecanoate. In these subjects, prolactin levels decreased. Six agonadal subjects, tested after 12 weeks' treatment with dihydrotestosterone undecanoate and compared to: Six agonadal subjects who received no sex steroid treatment. Again, it was found that dihydrotestosterone treatment decreased prolactin levels in patients from Group C. Six eugonadal subjects were also studied before and after 6 weeks' administration of the androgen receptor antagonist, spironolactone, and this treatment increased Prl secretion. It is concluded that in the human male, endogenous oestrogens increase prolactin secretion whilst exogenous/endogenous androgens decrease prolactin secretion.
So even if you reduce the lactation with Bromo you won't eleviate the cause. Tamoxifen is still your best bet at reducing gyno. Bromo will only reduce the the after effects.
Management of physiological gynaecomastia with tamoxifen.
Khan HN, Rampaul R, Blamey RW.
Professorial Unit of Surgery, Department of Surgery, Nottingham City Hospital, Nottingham NG5 1PB, UK. firstname.lastname@example.org
AIMS: We aimed to confirm suggestions that tamoxifen therapy alone may resolve physiological gynaecomastia. METHODS: A prospective audit of the outcome of tamoxifen routinely given to men with physiological gynaecomastia was carried out at Nottingham. Men referred with gynaecomastia had clinical signs recorded, e.g., type (diffuse 'fatty' or retro-areolar 'lump'), size and possible aetiology. They were offered oral tamoxifen 20mg once daily for 6-12 weeks. On follow-up patients were assessed for complete resolution (CR), partial resolution where patient is satisfied with outcome (PR) or no resolution (NR). Success was either CR or PR. RESULTS: Thirty-six men accepted tamoxifen for physiological gynaecomastia. Median age was 31 (range 18-64). Tenderness was present in 25 (71%) cases. Sixteen men (45%) had 'fatty' gynaecomastia and 20 had 'lump' gynaecomastia. Tamoxifen resolved the mass in 30 patients (83.3%; CR=22, PR=8) and tenderness in 21 cases (84%; CR=0, PR=0). Lump gynaecomastia was more responsive to tamoxifen than the fatty type (100% vs. 62.5%; P=0.0041). CONCLUSIONS: Oral tamoxifen is an effective treatment for physiological gynaecomastia, especially for the lump type.
SOURCE: Breast. 2004 Feb; 13(1): 61-5
INTERNATIONAL STANDARD SERIAL NUMBER: 0960-9776 Scotland
01-14-2007, 11:19 AM
I personally would drop the T4 and change the Nolva to Letro at a decent dose, i.e. 1mg/day and up. Even with the Vitex and B6 I'm still very leery of using a SERM coupled with a progestin. I had a bad experience with that
That's just my opinion. If that didn't work then I might try something like Restore from ALRI. I've used it before but never for Prolactin or Estrogen control. That would be something of a last-ditch-effort.
I'm hoping you figure it out. I know this stuff sucks.
01-14-2007, 01:38 PM
- 5'10" 180 lbs.
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You could consider Ralox instead of Nolva (since Nolva is so hard on the liver).
01-14-2007, 07:46 PM
You left one thing out. Guess what it is in deca that takes the pain away from your joints.Originally Posted by CEDeoudes59
If we take any substance that eliminates or reduces the amount of progestins, we have just eliminated the ability for deca to heal joints.
02-19-2007, 02:17 AM
- 6'3" 231 lbs.
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Ced, I'm experiencing the same thing. You and I had the same thing happen week 5 from Tren, and now we're getting this from GH? You need to stop being like me, and do you.
02-21-2007, 11:05 AM
i did some thinking and some experimenting with this...we know that GH release often accompanies prolactin release, especially during sleep....also, GH and the GH-releasing compounds (peptides, l-dopa, GABA) make me hella drowsy after administering. well, this may not be grounded in science, but the prolactin surge after sex is part of the reason we get drowsy and feel compelled to just roll over and sleep.
anybody think there's a connection?
i have been using 500mg B6 20 minutes before GHRP-6 administration and the sleepy effect is blunted significantly. i read that B6 attentuates prolactin release (and potentiates the GH release) during exercise - i figured there's at least a chance it could do the same when GH is spiked exogenously.
well, i didnt sleep nearly as soundly the last 2 nights with B6...in fact, quite the opposite.
i'll try gaba and melatonin tonight with my GHRP-6/B6/arginine/lysine cocktail and see what happens. maybe i can hit it from some more angles.
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