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As posted by myself at AF:
(Hope Cockedzl sees this as I want
to debate it)
Well, we all know that taking anti-estrogens
while taking meds that increase natural
test levels(Clomid and ***) is an effective
way of bringing nat. test levels up to
pre-cycle levels fast.
This system targets estrogen & testosterone.
But what about Prolactin?????
Well guess what? Prolactin is also involved
in male hypogonadism.
Is there a compound that blocks prolactin secretion.
L-Dopamine does, but its not particularly
effective and its effectiveness also wanes
over time thus increasing side-effects.
Bromocriptine is the answer to the riddle.
It nukes prolactin secretion. If you were
to use an analogy, it is the arimidex of
prolactin. Yes, it is THAT EFFECTIVE.
This study looks at the effect of chronic
alcohol treatment that increases estrogen
levels etc.... which is very similiar
to what happens post-cycle.
Possible role of prolactin in the induction of hypogonadism by chronic alcohol treatment in the male rat.
Fermoso J, Esquifino AI, Mateos A, Agrasal C, Martin I.
Departamento de Medicina Interna, Hospital Clinico, Facultad de Medicina, Salamanca, Spain.
Treatment of adult male rats with ethanol for a period of six weeks resulted in a numerical but not significant increase in plasma prolactin levels together with a reduction in plasma luteinizing hormone (LH) levels. Although basal plasma testosterone (T) levels were not affected in ethanol-treated animals, testicular weight was reduced and seminiferous tubules exhibited signs of atrophy. The responses of LH to luteinizing hormone releasing hormone (LHRH) and T to *** were significantly impaired in ethanol-treated rats (p less than 0.01). Treatment with bromocriptine (1 mg/kg body weight/day), resulted in the expected decrease in plasma levels of prolactin and an increase in basal plasma LH levels to the levels found in control groups. Basal plasma T levels were not affected by bromocriptine. However, both plasma LH responses to LHRH and plasma T responses to *** were significantly improved by bromocriptine treatment in alcoholic rats and became similar to the responses measured in control animals. The results suggest that bromocriptine-induced suppression of prolactin release has a beneficial effect on ethanol-induced hypogonadism.
High levels of prolactin DIRECTLY inhibited
the Gonads from up-regulating. So, its not
just the estrogen.(If only it were that simple
sigh...)
Another study that demonstrates that high
serum prolactin is involved im testicular
dysfunction:
Hypogonadism of male prolactinomas: relation to pulsatile secretion of LH.
Saitoh Y, Arita N, Hayakawa T, Onishi T, Koga M, Mori S, Mogami H.
Department of Neurosurgery, Osaka University Medical School, Japan.
In order to investigate whether a hypothalamic disorder cause hypogonadism in male prolactinomas, LH pulsatile secretion was studied in 13 male patients. Serum PRL levels ranged from 186 to 45,000 ng ml-1 before treatment, and all the tumors were macroadenomas. Reduced LH secretion was revealed in 5 of 13 patients, and FSH was reduced in 1 of 13. Serum testosterone (T) levels were lower than the normal limit in all the patients. *** tests in 3 patients showed good responses, but the peak values of T were lower than those of normal men. LH pulsatilities were examined in 5 hyperprolactinemic patients before treatment, in 4 hyperprolactinemic patients after operation, and in 8 normoprolactinemic patients after operation and/or bromocriptine treatment. There was no significant difference of the mean LH values, the frequencies of LH pulses, and amplitudes among the hyperprolactinemic patients before operation (n = 5), the normoprolactinemic patients after operation (n = 8), and normal men (n = 7). From these results, it was evident that the hypothalamus and pituitary function of male prolactinomas were well preserved, in spite of higher serum PRL levels and larger tumor size than those reported in females. It is suggested that the main cause of hypogonadism in these patients is due to testicular dysfunction resulting from excessive serum PRL.
And yet another that shows Bromocriptine
can be used for male hypogonadism:
Further acquisitions on gonadal function in bromocriptine treated hyperprolactinemic male patients.
Zini D, Carani C, Baldini A, Cavicchioli C, Piccinini D, Marrama P.
The diurnal variation of plasma total and free testosterone (tT and fT) and the gonadotropinemic response to LH-RH were evaluated in a group of hyperprolactinemic impotent males with pituitary microprolactinoma before and during therapy with bromocriptine, a well known dopamine agonist drug. Before treatment, basal levels not only of tT but also of fT were decreased and the diurnal variation of both tT and fT was absent. Moreover, the LH-RH test showed a delay in the LH response peak, together with normal basal levels of LH. Bromocriptine therapy caused normalization of both the secretion response of LH to LH-RH and of the secretion pattern of tT and of fT (basal levels and diurnal variation) besides a significant decrease in PRL levels and an improvement in sexual function. The possible effects of high plasma levels of PRL at various levels of the hypothalamus-pituitary-testicular axis are discussed.
PMID: 3532137 [PubMed - indexed for MEDLINE]
--------------------------------------------------------------------------------
How do we use Bromocriptine then?
Using by itself it is not particularly effective
as it doesn't combat the estrogen problem
associated with post-cycle metabolism bio-chem.
However, using it with test.elevating compounds
gives you an AMPLIFIED EFFECT. It is SYNERGISTIC
if used with Clomid and ***.
Here is one study that looks at this:
Effects of in vivo and in vitro exposure to bromocriptine on testicular LH receptors and in vitro testosterone production in Syrian hamsters.
Amador AG, Bartke A.
Department of Physiology, SIU School of Medicine, Carbondale, IL 62901-6512.
The effects of in vivo and in vitro exposure to bromocriptine (CB-154) were studied in testes of Syrian hamsters. In animals treated for two days with CB-154, a decrease in LH receptors (LH-R) was observed, with a greater decrease being measured in hamsters treated for 14 days, when compared with controls.
Here is the IMPORTANT SECTION:
Injection of *** caused, in hamsters treated with CB-154 for 14 days, up-regulation of LH-R and increased testosterone synthesis in response to *** administration in vitro. These changes were not observed in the two other groups of animals. When testis fragments were incubated with CB-154, those incubated with a large dose (10 micrograms/ml) had a normal pattern of response to ***, and those incubated with a small dose (1 ng/ml) had a smaller maximum response. These actions are similar to those observed in men treated with CB-154. It can be therefore concluded that: a) CB-154 has a direct effect on the testes; b) it probably is through modulation of LH-R synthesis; c) Syrian hamsters probably represent the best model for the study of the effects of CB-154 on the testes; and d) the possibility of using CB-154 as an adjuvant of gonadotropin treatment in hypogonadism has to be considered.
Damn cool, Bromocriptine+*** caused a HIGHER
testosterone spike than *** alone while
bromocriptine actually lowered LH levels.
An explanation to this is while you raise
Testosterone levels with *** and Clomid
you also get an increase in the levels of
estrogen AND PROLACTIN.
ESTROGEN AND PROLACTIN ARE DIRECT INHIBITORS
OF THE TESTES up-regulation post-cycle!!!
We all know arimidex will eliminate the
estrogen quite nicely, but I have no idea
why somebody has never given a second thought
to prolactin.
Bromocriptine at 2.5-5mg/day will inhibit prolactin
quite nicely, therefore decreasing the
amount of time your testes need to up-regulate.
Here is a study on the safety of Bromocriptine:
Long-term follow-up of hyperprolactinemic women treated with bromocriptine.
Corenblum B, Taylor PJ.
Seventy-five women with hyperprolactinemia and demonstrable or suspected prolactinomas were treated with bromocriptine only and followed for 5 to 9 years. Biochemical, radiologic, and clinical responses were generally maintained in the long term, once established in the short term. Underlying mass effects on neurologic and pituitary function tended to improve, and no tumor progression was noted. Hypogonadal symptoms normalized in 68 of 75 women. Bromocriptine responses in long-term follow-up do not demonstrate any cumulative problems not seen in short-term therapy.
Here would be a re-vamped Gainskeeper formula:
In theory, this latter Post-cycle structure should restore
the HPT axis faster than the old gainskeeper formula.
Clomid Day 1: 300mg/day
Clomid Days 2-14: 100mgs/day
Clomid Days 15-21: 50mgs/day
H C G: 2500 IU's 2X/week Weeks 1,2,3
Bromocriptine: 2.5mgs 2X/day Days 1-21
Arimidex: 1mg ED or 1/2mg ED Days 1-21
Fonz tuning out now....
Godspeed
As posted by myself at AF:
(Hope Cockedzl sees this as I want
to debate it)
Well, we all know that taking anti-estrogens
while taking meds that increase natural
test levels(Clomid and ***) is an effective
way of bringing nat. test levels up to
pre-cycle levels fast.
This system targets estrogen & testosterone.
But what about Prolactin?????
Well guess what? Prolactin is also involved
in male hypogonadism.
Is there a compound that blocks prolactin secretion.
L-Dopamine does, but its not particularly
effective and its effectiveness also wanes
over time thus increasing side-effects.
Bromocriptine is the answer to the riddle.
It nukes prolactin secretion. If you were
to use an analogy, it is the arimidex of
prolactin. Yes, it is THAT EFFECTIVE.
This study looks at the effect of chronic
alcohol treatment that increases estrogen
levels etc.... which is very similiar
to what happens post-cycle.
Possible role of prolactin in the induction of hypogonadism by chronic alcohol treatment in the male rat.
Fermoso J, Esquifino AI, Mateos A, Agrasal C, Martin I.
Departamento de Medicina Interna, Hospital Clinico, Facultad de Medicina, Salamanca, Spain.
Treatment of adult male rats with ethanol for a period of six weeks resulted in a numerical but not significant increase in plasma prolactin levels together with a reduction in plasma luteinizing hormone (LH) levels. Although basal plasma testosterone (T) levels were not affected in ethanol-treated animals, testicular weight was reduced and seminiferous tubules exhibited signs of atrophy. The responses of LH to luteinizing hormone releasing hormone (LHRH) and T to *** were significantly impaired in ethanol-treated rats (p less than 0.01). Treatment with bromocriptine (1 mg/kg body weight/day), resulted in the expected decrease in plasma levels of prolactin and an increase in basal plasma LH levels to the levels found in control groups. Basal plasma T levels were not affected by bromocriptine. However, both plasma LH responses to LHRH and plasma T responses to *** were significantly improved by bromocriptine treatment in alcoholic rats and became similar to the responses measured in control animals. The results suggest that bromocriptine-induced suppression of prolactin release has a beneficial effect on ethanol-induced hypogonadism.
High levels of prolactin DIRECTLY inhibited
the Gonads from up-regulating. So, its not
just the estrogen.(If only it were that simple
sigh...)
Another study that demonstrates that high
serum prolactin is involved im testicular
dysfunction:
Hypogonadism of male prolactinomas: relation to pulsatile secretion of LH.
Saitoh Y, Arita N, Hayakawa T, Onishi T, Koga M, Mori S, Mogami H.
Department of Neurosurgery, Osaka University Medical School, Japan.
In order to investigate whether a hypothalamic disorder cause hypogonadism in male prolactinomas, LH pulsatile secretion was studied in 13 male patients. Serum PRL levels ranged from 186 to 45,000 ng ml-1 before treatment, and all the tumors were macroadenomas. Reduced LH secretion was revealed in 5 of 13 patients, and FSH was reduced in 1 of 13. Serum testosterone (T) levels were lower than the normal limit in all the patients. *** tests in 3 patients showed good responses, but the peak values of T were lower than those of normal men. LH pulsatilities were examined in 5 hyperprolactinemic patients before treatment, in 4 hyperprolactinemic patients after operation, and in 8 normoprolactinemic patients after operation and/or bromocriptine treatment. There was no significant difference of the mean LH values, the frequencies of LH pulses, and amplitudes among the hyperprolactinemic patients before operation (n = 5), the normoprolactinemic patients after operation (n = 8), and normal men (n = 7). From these results, it was evident that the hypothalamus and pituitary function of male prolactinomas were well preserved, in spite of higher serum PRL levels and larger tumor size than those reported in females. It is suggested that the main cause of hypogonadism in these patients is due to testicular dysfunction resulting from excessive serum PRL.
And yet another that shows Bromocriptine
can be used for male hypogonadism:
Further acquisitions on gonadal function in bromocriptine treated hyperprolactinemic male patients.
Zini D, Carani C, Baldini A, Cavicchioli C, Piccinini D, Marrama P.
The diurnal variation of plasma total and free testosterone (tT and fT) and the gonadotropinemic response to LH-RH were evaluated in a group of hyperprolactinemic impotent males with pituitary microprolactinoma before and during therapy with bromocriptine, a well known dopamine agonist drug. Before treatment, basal levels not only of tT but also of fT were decreased and the diurnal variation of both tT and fT was absent. Moreover, the LH-RH test showed a delay in the LH response peak, together with normal basal levels of LH. Bromocriptine therapy caused normalization of both the secretion response of LH to LH-RH and of the secretion pattern of tT and of fT (basal levels and diurnal variation) besides a significant decrease in PRL levels and an improvement in sexual function. The possible effects of high plasma levels of PRL at various levels of the hypothalamus-pituitary-testicular axis are discussed.
PMID: 3532137 [PubMed - indexed for MEDLINE]
--------------------------------------------------------------------------------
How do we use Bromocriptine then?
Using by itself it is not particularly effective
as it doesn't combat the estrogen problem
associated with post-cycle metabolism bio-chem.
However, using it with test.elevating compounds
gives you an AMPLIFIED EFFECT. It is SYNERGISTIC
if used with Clomid and ***.
Here is one study that looks at this:
Effects of in vivo and in vitro exposure to bromocriptine on testicular LH receptors and in vitro testosterone production in Syrian hamsters.
Amador AG, Bartke A.
Department of Physiology, SIU School of Medicine, Carbondale, IL 62901-6512.
The effects of in vivo and in vitro exposure to bromocriptine (CB-154) were studied in testes of Syrian hamsters. In animals treated for two days with CB-154, a decrease in LH receptors (LH-R) was observed, with a greater decrease being measured in hamsters treated for 14 days, when compared with controls.
Here is the IMPORTANT SECTION:
Injection of *** caused, in hamsters treated with CB-154 for 14 days, up-regulation of LH-R and increased testosterone synthesis in response to *** administration in vitro. These changes were not observed in the two other groups of animals. When testis fragments were incubated with CB-154, those incubated with a large dose (10 micrograms/ml) had a normal pattern of response to ***, and those incubated with a small dose (1 ng/ml) had a smaller maximum response. These actions are similar to those observed in men treated with CB-154. It can be therefore concluded that: a) CB-154 has a direct effect on the testes; b) it probably is through modulation of LH-R synthesis; c) Syrian hamsters probably represent the best model for the study of the effects of CB-154 on the testes; and d) the possibility of using CB-154 as an adjuvant of gonadotropin treatment in hypogonadism has to be considered.
Damn cool, Bromocriptine+*** caused a HIGHER
testosterone spike than *** alone while
bromocriptine actually lowered LH levels.
An explanation to this is while you raise
Testosterone levels with *** and Clomid
you also get an increase in the levels of
estrogen AND PROLACTIN.
ESTROGEN AND PROLACTIN ARE DIRECT INHIBITORS
OF THE TESTES up-regulation post-cycle!!!
We all know arimidex will eliminate the
estrogen quite nicely, but I have no idea
why somebody has never given a second thought
to prolactin.
Bromocriptine at 2.5-5mg/day will inhibit prolactin
quite nicely, therefore decreasing the
amount of time your testes need to up-regulate.
Here is a study on the safety of Bromocriptine:
Long-term follow-up of hyperprolactinemic women treated with bromocriptine.
Corenblum B, Taylor PJ.
Seventy-five women with hyperprolactinemia and demonstrable or suspected prolactinomas were treated with bromocriptine only and followed for 5 to 9 years. Biochemical, radiologic, and clinical responses were generally maintained in the long term, once established in the short term. Underlying mass effects on neurologic and pituitary function tended to improve, and no tumor progression was noted. Hypogonadal symptoms normalized in 68 of 75 women. Bromocriptine responses in long-term follow-up do not demonstrate any cumulative problems not seen in short-term therapy.
Here would be a re-vamped Gainskeeper formula:
In theory, this latter Post-cycle structure should restore
the HPT axis faster than the old gainskeeper formula.
Clomid Day 1: 300mg/day
Clomid Days 2-14: 100mgs/day
Clomid Days 15-21: 50mgs/day
H C G: 2500 IU's 2X/week Weeks 1,2,3
Bromocriptine: 2.5mgs 2X/day Days 1-21
Arimidex: 1mg ED or 1/2mg ED Days 1-21
Fonz tuning out now....
Godspeed
