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My thoughts on Pramipexole.

Terrymundo
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Terrymundo Senior member

Terrymundo

Posted
Posted

No go bros (so far). I have been running prami at 0.25mg then pumoped up to 0.5mg which I've been taking just before bed everyday.

A) Didnt not help with my gyno from 19-nors (deca @ 600 EW). My nips were still puffy and slightly less sore. Lump still present but reduced

B) Sides were noticable. Very broken sleep, I wake every few hours and find it tough to fall back asleep but I strangely feel like i'm rested the next day,

C) Slighly nausea after each meal (very tough when bulking)

D) Libido is very high, I have opened my parameters on tinder to the widest they will go and am consistently masturbating 2+ times a day

I will keep running it just to see if sides:benefits improve.

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Daz69 Senior member

Daz69

Posted
Posted

No go bros (so far). I have been running prami at 0.25mg then pumoped up to 0.5mg which I've been taking just before bed everyday.

A) Didnt not help with my gyno from 19-nors (deca @ 600 EW). My nips were still puffy and slightly less sore. Lump still present but reduced

I will keep running it just to see if sides:benefits improve.


Nolvadex for gyno removal...

D2 agonists for prolactinemia...

AI's won't work for estrogen issues caused by Nandrolone...

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rapz Senior member

rapz

Posted
Posted

How much test u taking with dat deca cock breath?

Are you serious??

why would i not be srs? (Not srs)

 

 

have u tired bromo? worked for me
not yet. How dis it go for you? sides? Dosage? cycle?

 

How much test u taking with dat deca cock breath?

bouta gram ya f*ck-tard

also you got slight gyno from 600 deca ? Not enough ai?

also running 0.5mg adex but switched to letro at 2.5mg ED till lumps are gone, will be back on adex after

 

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Daz69 Senior member

Daz69

Posted
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i used 2.5mg bromo ed only side i got was nausea but i just took it b4 bed.

Its highly likely you would do as Prami is a D2 agonist... D2 antagonists are given to combat motion sickness...

Using D2 agonists for gyno is a flawed concept based on dodgy science, or rather no science at all.... 

You cant combat Estrogen sides caused by Nandrolone as its believed to work via the AR, best action if you are prone to high E2 issues with Nandrolone is not to use it....

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Daz69 Senior member

Daz69

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best action if you are prone to high E2 issues with Nandrolone is not to use it....

same for trenbolone? Not sure if I can just take out tren of my toolbox just cause it aggrevates my gyno. I would rather run it and combat the sides, to me the end result is better regardless.

Also many people (if not most) on other forums complain about nausea on prami, even good ol' wikipedia lists nausea as side effect, is prami still a D2 agonist????? Yes: D2L, D2S, D3, D4.

 

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  • 2 weeks later...
Daz69 Senior member

Daz69

Posted
Posted

Further reason not to administer D2 agonists, Lowering Prolactin can potentially lead to among others: reduced testosterone, reduced sperm counts and reduced immunity. Quit messing with your endocrine system for no reason. Keep your prolactin at NORMAL levels and stop using things like Bromocriptine and L-Dopa just "because"


Clin Pharmacol Ther. 1995 Sep;58(3):354-9.
Restoration of normal sperm characteristics in hypoprolactinemic infertile men treated with metoclopramide and exogenous human prolactin.

Ufearo CS, Orisakwe OE.

Department of Physiology, Faculty of Medicine, Nnamdi Azikiwe University, Nigeria.

We investigated the effects of induced increase in prolactin levels on spermatogenesis in 20 infertile men with hypoprolactinemia using exogenous human prolactin (hPRL) and metoclopramide. The subjects were selected from a population of 175 infertile men in whom the prevalence of hypoprolactinemia was 33.14%. Mean basal plasma prolactin was 2.79 +/- 0.62 ng.ml-1 in the infertile men and 9.57 +/- 2.14 ng.ml-1 in the normal control subjects. At the sixteenth week, mean plasma prolactin was 9.41 +/- 1.3 ng.ml-1 in subjects treated with exogenous hPRL and 5.2 +/- 0.7 ng.ml-1 in subjects treated with metoclopramide. Mean basal sperm concentration was approximately 8.8 million per milliliter in the infertile men and 41.5 million per milliliter in the normal control subjects. Mean sperm concentration was approximately 37 million per milliliter in subjects treated with exogenous hPRL, whereas the peak mean value was 23 million per milliliter in subjects treated with metoclopramide for 16 weeks. At basal conditions, the mean percentages of abnormal sperm were 66.75% +/- 14.93% and 21.36% +/- 4.78% in infertile and normal subjects, respectively. In subjects treated with exogenous hPRL and metoclopramide, the mean percentage of abnormal sperm were 24.7% and 31%, respectively, at week 16. Mean plasma prolactin, mean sperm concentration and the mean percentage of abnormal sperm were 3.3 +/- 1.4 ng.ml-1, 7 million per milliliter, and 60.5, respectively, in the infertile subjects after drug withdrawal at week 14. In normal control subjects, there was no significant difference (p = 0.01) in the plecebo effect. We therefore conclude that the low prolactin levels in this group of infertile men may be one of the primary causes of their infertility.

J Androl. 1985 Jan-Feb;6(1):10-4.
Induced hypoprolactinemia and testicular steroidogenesis in man.

Suescun MO, Scorticati C, Chiauzzi VA, Chemes HE, Rivarola MA, Calandra RS.

The effects of short-term hypoprolactinemia on the pituitary-gonadal axis were evaluated in a group of patients with untreated prostatic carcinoma. Each patient was studied prior to and during 7-day oral administrations of bromocriptine (2.5 mg q.i.d.). Serum LH, prolactin (PRL), androst-4-ene-3,17 dione (androstenedione), testosterone, and 5 alpha-androstane-3 alpha, 17 beta-diol (5 alpha-Diol) levels, as well as intra-testicular testosterone, dihydrotestosterone (DHT), 5 alpha-Diol and zinc (Zn) concentrations, were determined. Daily administration of bromocriptine caused a marked suppression of serum PRL (mean +/- SEM, 23.8 +/- 2.5 vs. 6.4 +/- 1.0 ng/ml) without concomitant changes in serum LH levels (mean +/- SEM, 8.3 +/- 1.6 vs. 8.9 +/- 2.1 ng/ml). Hypoprolactinemia induced a significant decrease (P less than 0.05) in the mean peripheral testosterone levels; but 5 alpha-Diol and androstenedione remained unchanged. However, in testicular tissues, bromocriptine treatment resulted in significant increases in mean concentrations of total androgens (P less than 0.001), testosterone (P less than 0.001) and DHT (P less than 0.02). Testicular levels of 5 alpha-Diol were not significantly altered. There was no change in Zn levels in basal conditions and during bromocriptine administration. These results indicate that short-term suppression of serum PRL levels in man affects basal testicular function without altering serum LH. However, a direct action of bromocriptine on the human gonad cannot be excluded.

Andrologia. 1985 Mar-Apr;17(2):172-7.
Bromocriptine, a dopamine agonist, directly inhibits testosterone production by rat Leydig cells.

Chambon M, Grizard G, Boucher D.

We investigated the direct effects of bromocriptine (BR) on both basal and hCG-stimulated testosterone production by rat collagenase-dispersed Leydig cells. In a final volume of 2.2 ml, 2.10(6) Leydig cells were incubated at 33 degrees C for 3 h either alone or with various amounts of hCG (1. 10. 10(2). 10(3). 10(4) mUI/vial) and BR (1.5 10(-9), 1.5 10(-7), 1.5 10(-5) M); BR was dissolved in 20 microliters of ethanol. BR (1.5 10(-5) M) decreased significantly both basal and hCG-stimulated testosterone production whereas at lower doses, BR had no effect. These results suggest that the dopamine itself may regulate rat Leydig cell function and that there is room for criticism of BR-induced hypoprolactinemia as an experimental model to study the effect of prolactin on the androgenic function.

Fertil Steril. 1991 Feb;55(2):355-7.
Effects of chronic bromocriptine-induced hypoprolactinemia on plasma testosterone responses to human chorionic gonadotropin stimulation in normal men.

Oseko F, Nakano A, Morikawa K, Endo J, Taniguchi A, Usui T.

Department of Medicine, Shimane Medical University, Japan.

To study the role played by normal levels of plasma prolactin (PRL) in the secretion of testosterone (T) in the testes, we induced hypoprolactinemia with a daily dose of 5 mg bromocriptine administered orally in five normal men 20 to 35 years of age for 8 weeks. The basal PRL, T, luteinizing hormone, follicle-stimulating hormone, and maximum responses of plasma T to human chorionic gonadotropin (hCG) stimulation were measured every 2 weeks. Basal levels of plasma T were reduced in the 1st 2-week-long period of hypoprolactinemia. In the 4-week-long period of hypoprolactinemia, the maximal response of plasma T to hCG stimulation was significantly reduced. The findings suggest that normal levels of plasma PRL may play an important role in the secretion of T in the human testes in vivo.

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