hongkongguy
New member
can dostinex or bromo prevent deca gyno?i mean,has anyone taken one of these with deca?or...anyone had trouble with deca?
how to prevent deca gyno
- Thread starter hongkongguy
- Start date
midwtchamp
Banana
Deca aggravated my gyno, but didnt make it worse. As for the bromo I would stay away from it, kinda dangerous you dont wanna fug with
V
viper10139
Guest
bromo fucked with my sinus and I had a hard time breathing on it.....it's wild!!
BLEED GREEN
New member
Tried bromo 1x myself-Not on the to use list any longer
midwtchamp
Banana
way to prevent deca gyno=dont use it! lol sorry
learner202
Banana
So you might be doing squates and all the sudden ur a-hole just starts bleeding all over the place? sick!
hongkongguy
New member
did i mention dostinex??what about it??
tenn0titan
New member
Deca gyno? Where did that come from? Is that a real side effect or did you make that up. JK. Never had that problem. I would guess you could treat/stop it like you do with test gyno.
TT
TT
SkullKrusher
New member
Progesterone induced gyno comes from estrogen. therefor if you think that deca may cause you gyno start nolva before it even starts, to counter the estrogen that the progesterone comes from.
learner202
Banana
Good advice. I am not sure if you can prevent deca gyno in any waySkullKrusher said:
LA
New member
Yep, I remember back when Palumbo started his 1g a week deca thread and was taking RU486. Said it was working great (but I admit that I was surprized that Palumbo never had gyno surgery).Skip said:
Then a certain Chinese guy, let's call him EyePee was going to produce RU486. Then he tried it first. Bleeding of the a-hole! A few other people I remember from various boards (and by a few I mean a few, not many people tried it) reported the same condition.
hongkongguy
New member
bump
S
scorpio
Guest
Dostinex Clinical Pharmacology
Mechanism of Action
The secretion of prolactin by the anterior pituitary is mainly under hypothalmic inhibitory control, likely exerted through release of dopamine by tuberoinfundibular neurons. Cabergoline is a long-acting dopamine receptor agonist with a high affinity for D2 receptors. Results of in vitro studies demonstrate that cabergoline exerts a direct inhibitory effect on the secretion of prolactin by rat pituitary lactotrophs. Cabergoline decreased serum prolactin levels in reserpinized rats. Receptor-binding studies indicate that cabergoline has low affinity for dopamine D1,a1,- and a2- adrenergic, and 5-HT1- and 5-HT2-serotonin receptors.
Clinical Studies
The prolactin-lowering efficacy of DOSTINEX was demonstrated in hyperprolactinemic women in two randomized, double-blind, comparative studies, one with placebo and the other with bromocriptine. In the placebo-controlled study (placebo n=20; cabergoline n=168), DOSTINEX produced a dose-related decrease in serum prolactin levels with prolactin normalized after 4 weeks of treatment in 29%, 76%, 74% and 95% of the patients receiving 0.125, 0.5, 0.75, and 1.0 mg twice weekly respectively.
In the 8-week, double-blind period of the comparative trial with bromocriptine (cabergoline n=223; bromocriptine n=236 in the intent-to-treat analysis), prolactin was normalized in 77% of the patients treated with DOSTINEX at 0.5 mg twice weekly compared with 59% of those treated with bromocriptine at 2.5 mg twice daily. Restoration of menses occurred in 77% of the women treated with DOSTINEX, compared with 70% of those treated with bromocriptine. Among patients with galactorrhea, this symptom disappeared in 73% of those treated with DOSTINEX compared with 56% of those treated with bromocriptine.
Pharmacokinetics
Absorption: Following single oral doses of 0.5 mg to 1.5 mg given to 12 healthy adult volunteers, mean peak plasma levels of 30 to 70 picograms (pg)/mL of cabergoline were observed within 2 to 3 hours. Over the 0.5- to- 7 mg dose range, cabergoline plasma levels appeared to be dose-proportional in 12 healthy adult volunteers and nine adult parkinsonian patients. A repeatdose study in 12 healthy volunteers suggests that steady-state levels following a once-weekly dosing schedule are expected to be twofold to threefold higher than after a single dose. The absolute bioavailability of cabergoline is unknown. A significant fraction of the administered dose undergoes a first-pass effect. The elimination half-life of cabergoline estimated from urinary data of 12 healthy subjects ranged between 63 to 69 hours. The prolonged prolactin-lowering effect of cabergoline may be related to its slow elimination and long half-life.
Distribution: In animals, based on total radioactivity, cabergoline (and/or its metabolites) has shown extensive tissue distribution. Radioactivity in the pituitary exceeded that in plasma by >100-fold and was eliminated with a half-life of approximately 60 hours. This finding is consistent with the long-lasting prolactin-lowering effect of the drug. Whole body autoradiography studies in pregnant rats showed no fetal uptake but high levels in the uterine wall. Significant radioactivity (parent plus metabolites) detected in the milk of lactating rats suggests a potential for exposure to nursing infants. The drug is extensively distributed throughout the body. Cabergoline is moderately bound (40% to 42%) to human plasma proteins in a concentration-independent manner. Concomitant dosing of highly protein-bound drugs is unlikely to affect its disposition.
Metabolism: In both animals and humans, cabergoline is extensively metabolized, predominately via hydrolysis of the acylurea bond or the urea moiety. Cytochrome P-450 mediated metabolism appears to be minimal. Cabergoline does not cause enzyme induction and/or inhibition in the rat. Hydrolysis of the acylurea or urea moiety abolishes the prolactin-lowering effect of cabergoline, and major metabolites identified thus far do not contribute to the therapeutic effect.
Excretion: After oral dosing of radioactive cabergoline to five healthy volunteers, approximately 22% and 60% of the dose was excreted within 20 days in the urine and feces, respectively. Less than 4% of the dose was excreted unchanged in the urine. Nonrenal and renal clearances for cabergoline are about 3.2 L/min and 0.08 L/min, respectively. Urinary excretion in hyperprolactinemic patients was similar.
Special Populations
Renal Insufficiency: The pharmacokinetics of cabergoline were not altered in 12 patients with moderate-to-severe renal insufficiency as assessed by creatinine clearance.
Hepatic Insufficiency: In 12 patients with mild-to-moderate hepatic dysfunction (Child-Pugh score £10), no effect on mean cabergoline Cmax or area under the plasma concentration curve (AUC) was observed. However, patients with severe insufficiency (Child-Pugh score >10) show a substantial increase in the mean cabergoline Cmax and AUC, and thus necessitate caution.
Elderly: Effect of age on the pharmacokinetics of cabergoline has not been studied.
Food-Drug Interaction
In 12 healthy adult volunteers, food did not alter cabergoline kinetics.
Pharmacodynamics
Dose response with inhibition of plasma prolactin, onset of maximal effect, and duration of effect has been documented following single cabergoline doses to healthy volunteers (0.05 to 1.5 mg) and hyperprolactinemic patients (0.3 to 1 mg). In volunteers, prolactin inhibition was evident at doses >0.2 mg, while doses ³0.5 mg caused maximal suppression in most subjects. Higher doses produce prolactin suppression in a greater proportion of subjects and with an earlier onset and longer duration of action. In 12 healthy volunteers, 0.5, 1, and 1.5 mg doses resulted in complete prolactin inhibition, with a maximum effect within 3 hours in 92% to 100% of subjects after the 1 and 1.5 mg doses compared with 50% of subjects after the 0.5 mg dose.
In hyperprolactinemic patients (N=51), the maximal prolactin decrease after a 0.6 mg single dose of cabergoline was comparable to 2.5 mg bromocriptine; however, the duration of effect was markedly longer (14 days vs 24 hours). The time to maximal effect was shorter for bromocriptine than cabergoline (6 hours vs 48 hours).
In 72 healthy volunteers, single or multiple doses (up to 2 mg) of cabergoline resulted in selective inhibition of prolactin with no apparent effect on other anterior pituitary hormones (GH, FSH, LH, ACTH, and TSH) or cortisol.
__________________
Mechanism of Action
The secretion of prolactin by the anterior pituitary is mainly under hypothalmic inhibitory control, likely exerted through release of dopamine by tuberoinfundibular neurons. Cabergoline is a long-acting dopamine receptor agonist with a high affinity for D2 receptors. Results of in vitro studies demonstrate that cabergoline exerts a direct inhibitory effect on the secretion of prolactin by rat pituitary lactotrophs. Cabergoline decreased serum prolactin levels in reserpinized rats. Receptor-binding studies indicate that cabergoline has low affinity for dopamine D1,a1,- and a2- adrenergic, and 5-HT1- and 5-HT2-serotonin receptors.
Clinical Studies
The prolactin-lowering efficacy of DOSTINEX was demonstrated in hyperprolactinemic women in two randomized, double-blind, comparative studies, one with placebo and the other with bromocriptine. In the placebo-controlled study (placebo n=20; cabergoline n=168), DOSTINEX produced a dose-related decrease in serum prolactin levels with prolactin normalized after 4 weeks of treatment in 29%, 76%, 74% and 95% of the patients receiving 0.125, 0.5, 0.75, and 1.0 mg twice weekly respectively.
In the 8-week, double-blind period of the comparative trial with bromocriptine (cabergoline n=223; bromocriptine n=236 in the intent-to-treat analysis), prolactin was normalized in 77% of the patients treated with DOSTINEX at 0.5 mg twice weekly compared with 59% of those treated with bromocriptine at 2.5 mg twice daily. Restoration of menses occurred in 77% of the women treated with DOSTINEX, compared with 70% of those treated with bromocriptine. Among patients with galactorrhea, this symptom disappeared in 73% of those treated with DOSTINEX compared with 56% of those treated with bromocriptine.
Pharmacokinetics
Absorption: Following single oral doses of 0.5 mg to 1.5 mg given to 12 healthy adult volunteers, mean peak plasma levels of 30 to 70 picograms (pg)/mL of cabergoline were observed within 2 to 3 hours. Over the 0.5- to- 7 mg dose range, cabergoline plasma levels appeared to be dose-proportional in 12 healthy adult volunteers and nine adult parkinsonian patients. A repeatdose study in 12 healthy volunteers suggests that steady-state levels following a once-weekly dosing schedule are expected to be twofold to threefold higher than after a single dose. The absolute bioavailability of cabergoline is unknown. A significant fraction of the administered dose undergoes a first-pass effect. The elimination half-life of cabergoline estimated from urinary data of 12 healthy subjects ranged between 63 to 69 hours. The prolonged prolactin-lowering effect of cabergoline may be related to its slow elimination and long half-life.
Distribution: In animals, based on total radioactivity, cabergoline (and/or its metabolites) has shown extensive tissue distribution. Radioactivity in the pituitary exceeded that in plasma by >100-fold and was eliminated with a half-life of approximately 60 hours. This finding is consistent with the long-lasting prolactin-lowering effect of the drug. Whole body autoradiography studies in pregnant rats showed no fetal uptake but high levels in the uterine wall. Significant radioactivity (parent plus metabolites) detected in the milk of lactating rats suggests a potential for exposure to nursing infants. The drug is extensively distributed throughout the body. Cabergoline is moderately bound (40% to 42%) to human plasma proteins in a concentration-independent manner. Concomitant dosing of highly protein-bound drugs is unlikely to affect its disposition.
Metabolism: In both animals and humans, cabergoline is extensively metabolized, predominately via hydrolysis of the acylurea bond or the urea moiety. Cytochrome P-450 mediated metabolism appears to be minimal. Cabergoline does not cause enzyme induction and/or inhibition in the rat. Hydrolysis of the acylurea or urea moiety abolishes the prolactin-lowering effect of cabergoline, and major metabolites identified thus far do not contribute to the therapeutic effect.
Excretion: After oral dosing of radioactive cabergoline to five healthy volunteers, approximately 22% and 60% of the dose was excreted within 20 days in the urine and feces, respectively. Less than 4% of the dose was excreted unchanged in the urine. Nonrenal and renal clearances for cabergoline are about 3.2 L/min and 0.08 L/min, respectively. Urinary excretion in hyperprolactinemic patients was similar.
Special Populations
Renal Insufficiency: The pharmacokinetics of cabergoline were not altered in 12 patients with moderate-to-severe renal insufficiency as assessed by creatinine clearance.
Hepatic Insufficiency: In 12 patients with mild-to-moderate hepatic dysfunction (Child-Pugh score £10), no effect on mean cabergoline Cmax or area under the plasma concentration curve (AUC) was observed. However, patients with severe insufficiency (Child-Pugh score >10) show a substantial increase in the mean cabergoline Cmax and AUC, and thus necessitate caution.
Elderly: Effect of age on the pharmacokinetics of cabergoline has not been studied.
Food-Drug Interaction
In 12 healthy adult volunteers, food did not alter cabergoline kinetics.
Pharmacodynamics
Dose response with inhibition of plasma prolactin, onset of maximal effect, and duration of effect has been documented following single cabergoline doses to healthy volunteers (0.05 to 1.5 mg) and hyperprolactinemic patients (0.3 to 1 mg). In volunteers, prolactin inhibition was evident at doses >0.2 mg, while doses ³0.5 mg caused maximal suppression in most subjects. Higher doses produce prolactin suppression in a greater proportion of subjects and with an earlier onset and longer duration of action. In 12 healthy volunteers, 0.5, 1, and 1.5 mg doses resulted in complete prolactin inhibition, with a maximum effect within 3 hours in 92% to 100% of subjects after the 1 and 1.5 mg doses compared with 50% of subjects after the 0.5 mg dose.
In hyperprolactinemic patients (N=51), the maximal prolactin decrease after a 0.6 mg single dose of cabergoline was comparable to 2.5 mg bromocriptine; however, the duration of effect was markedly longer (14 days vs 24 hours). The time to maximal effect was shorter for bromocriptine than cabergoline (6 hours vs 48 hours).
In 72 healthy volunteers, single or multiple doses (up to 2 mg) of cabergoline resulted in selective inhibition of prolactin with no apparent effect on other anterior pituitary hormones (GH, FSH, LH, ACTH, and TSH) or cortisol.
__________________
hongkongguy
New member
thanks a LOT
S
scorpio
Guest
bump
LA
New member
Ok, someone clear this up for me.
There seems to be 3 things that cause gyno, estrogen, prolactin and progestrone.
We know that test and dbol are estrogen.
I always thought that deca, eq and drol were progrestrone and that tren was prolactin? (Notice the question mark!)
Can someone clear this up?
There seems to be 3 things that cause gyno, estrogen, prolactin and progestrone.
We know that test and dbol are estrogen.
I always thought that deca, eq and drol were progrestrone and that tren was prolactin? (Notice the question mark!)
Can someone clear this up?
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