Please Scroll Down to See Forums Below Fukkenshredded
New member
For use in conjunction with GHB, perhaps? Huck, did you ever find a cheap route for this or a generic equivalent? Let us know, bro...we're awaitin.
Permax for prolactin...Huck??
- Thread starter Fukkenshredded
- Start date
I'm working feverishly on it FS...If I can locate us a cost effective route,this stuff will be a godsend to fina/E/GHB users,as well as ALL steroids(which ALL have the ability to regulate prolactin secretion to some degree,although some more than others).Hopefully I should have word within the next couple of weeks.Would you like to be a tester of the prototype(IF it becomes available)?
monkeyballs
New member
Some studies have shown Permax to decrease LH levels. But it also is shown to raise GH levels. Not sure what that would mean for gains exactly.
Also, Huck, where would you put Ox and Halo on the prolactin scale. The research provided by the pharm companies on both products doesn't mention anything about prolactin. Would it be reasonable to assume that its because these AS's really have no effect on prolactin levels, or should I just chalk it up to useless research that was conducted with low doses (up to 10mgs ED for both products was the dose used in the studies).
Also, Huck, where would you put Ox and Halo on the prolactin scale. The research provided by the pharm companies on both products doesn't mention anything about prolactin. Would it be reasonable to assume that its because these AS's really have no effect on prolactin levels, or should I just chalk it up to useless research that was conducted with low doses (up to 10mgs ED for both products was the dose used in the studies).
Actually,my above comment is a typo MB,I should've said ALL AROMITIZABLE androgens.There appears to be some link between aromitization and prolactin secretion,as well as progestin activation of prolactin(which appears to be much more pronounced).The non-aromatic compounds don't seem to exhibit these tendencies.
naturally anabolic
New member
i'll guinea pig it for ya.
*squeak squeak, runs and hides under woodshavings*
*squeak squeak, runs and hides under woodshavings*
monkeyballs
New member
Thanks for the clarification. If possible, I'd like to avoid all dopamine agonsits as they all seem to have some grizly sides.
A common side of Permax is Dyskensia.
Spastic movements of my limbs wouldn't help my sports specific training one bit.
Dostinex looks to have the fewest sides, but the price is off the charts (i'm guessing this is what your working on getting cheap rather than Permax).
A common side of Permax is Dyskensia.
Spastic movements of my limbs wouldn't help my sports specific training one bit.
Dostinex looks to have the fewest sides, but the price is off the charts (i'm guessing this is what your working on getting cheap rather than Permax).
Cabergoline is the ticket.Imparts less sides,and is superior to bromo for prolactinemic inhibition.But like you said,cost/availability up to this point has made it one of those RU-486-type meds.Hopefully this will change,as I believe this is going to be a very potent ancillary weapon in the future.
If there is any ability of androgens to elevate prolactin (there seems to be a distinct lack of research to support it), the increased ability of aromatizable androgens is probably related to their ability to elevate IGF-1 levels more effectively than nonaromatizable androgens. IGF-1 seems to elevate prolactin:
Comp Biochem Physiol B Biochem Mol Biol 2001 Jun;129(2-3):237-42
Insulin-like growth factor-I augments prolactin and inhibits growth hormone release through distinct as well as overlapping cellular signaling pathways.
Fruchtman S, Gift B, Howes B, Borski R.
Department of Zoology, North Carolina State University, Box 7617, Raleigh, NC 27695-7617, USA.
We recently discovered a new role for insulin-like growth factor-I (IGF-I) as a specific and direct stimulator of prolactin (PRL) release in addition to its recognized function as an inhibitor of growth hormone (GH) release and synthesis. Little is known of the mechanisms that transduce the actions of IGF-I on PRL and GH release in vertebrates. The present study was undertaken to determine the cellular pathways that mediate the disparate actions of IGF-I on PRL and GH release in hybrid striped bass (Morone saxatilis X M. chrysops). When regulating cellular function, IGF-I may activate two primary pathways, phosphatidylinositol 3-kinase (PI 3-K) and mitogen-activated protein kinase (MAPK). The specific MAPK inhibitor, PD98059, blocked IGF-I-evoked PRL release as well as GH release inhibition over an 18-20-h incubation. LY294002, a specific PI 3-K inhibitor, overcame IGF-I's inhibition of GH release but was ineffective in blocking PRL release stimulated by IGF-I. These studies suggest IGF-I disparately alters PRL and GH by activating distinct as well as overlapping signaling pathways central for mediating actions of growth factors on secretory activity as well as cell proliferation. These results further support a role for IGF-I as a physiological regulator of PRL and GH.
Comp Biochem Physiol B Biochem Mol Biol 2001 Jun;129(2-3):237-42
Insulin-like growth factor-I augments prolactin and inhibits growth hormone release through distinct as well as overlapping cellular signaling pathways.
Fruchtman S, Gift B, Howes B, Borski R.
Department of Zoology, North Carolina State University, Box 7617, Raleigh, NC 27695-7617, USA.
We recently discovered a new role for insulin-like growth factor-I (IGF-I) as a specific and direct stimulator of prolactin (PRL) release in addition to its recognized function as an inhibitor of growth hormone (GH) release and synthesis. Little is known of the mechanisms that transduce the actions of IGF-I on PRL and GH release in vertebrates. The present study was undertaken to determine the cellular pathways that mediate the disparate actions of IGF-I on PRL and GH release in hybrid striped bass (Morone saxatilis X M. chrysops). When regulating cellular function, IGF-I may activate two primary pathways, phosphatidylinositol 3-kinase (PI 3-K) and mitogen-activated protein kinase (MAPK). The specific MAPK inhibitor, PD98059, blocked IGF-I-evoked PRL release as well as GH release inhibition over an 18-20-h incubation. LY294002, a specific PI 3-K inhibitor, overcame IGF-I's inhibition of GH release but was ineffective in blocking PRL release stimulated by IGF-I. These studies suggest IGF-I disparately alters PRL and GH by activating distinct as well as overlapping signaling pathways central for mediating actions of growth factors on secretory activity as well as cell proliferation. These results further support a role for IGF-I as a physiological regulator of PRL and GH.
monkeyballs
New member
Are there any studies that show the IGF-1 increase that is associated with tren? Probably not since its vet. But if there were you could compare the IGF-1 response from tren with other aromatiziable AS's and see if tren stands out. This would be consistent with the research linking prolactin with IGF-1.
If IGF-1/Prolactin is the cause of tren gyno, then maybe Nolvadex would be as effective as any dopamine agonist for treatment.
Gotta cite nandi on this one...
If IGF-1/Prolactin is the cause of tren gyno, then maybe Nolvadex would be as effective as any dopamine agonist for treatment.
Gotta cite nandi on this one...
I responded to your post over at my home site. I just have never seen studies where exogenous HGH raises prolactin. The ability of GH to induce lactation has always been attributed to its ability to bind to the prolactin receptor. I don't understand the disparity in results of the studies involving GH and IGF administered directly unless it is a feedback inhibition of GH on prolactin secretion as we discussed. One study in animals showed that GH administration actually decreased prolactin:
Andrologia 1998 Feb-Mar;30(1):37-42
Effects of very high doses of human growth hormone (hGH) on the male reproductive system in the dog.
Sjogren I, Jonsson M, Madej A, Johansson HE, Ploen L.
Toxicology, Pharmacia & Upjohn AB, Stockholm, Sweden.
The effects of very high doses of human growth hormone (hGH), pituitary derived or recombinant methionyl-hGH, on the morphology of reproductive organs and on some hormones in the male dog are described. The studies were part of a toxicological documentation of hGH. A total of 18 male dogs aged 7.5-20.5 months, from four studies were treated subcutaneously with hGH for 20-28 days at dose levels of 3, 10 or 25 IU kg-1 day-1 or 1 IU kg-1 three times weekly. Plasma levels of luteinizing hormone (LH), testosterone and prolactin were determined in one study. Organ weighing, macroscopic and histopathologic examinations of male reproductive organs at the end of the treatment period were included in all studies. Treatment with 25 IU kg-1 day-1 resulted in reduction of testis and prostate weights, degeneration of germ cells and epithelial atrophy in the testis, degenerative changes in epididymis and reduced height of the prostatic epithelium. Similar, although less severe morphological changes were observed after treatment with 10 IU kg-1 day-1. .Treatment with 25 IU kg-1 day-1 also caused a marked reduction of plasma prolactin, LH and testosterone levels. . These results suggest that repeated administration of very high doses of hGH interferes with the hormonal regulation of the testis in the dog.
Andrologia 1998 Feb-Mar;30(1):37-42
Effects of very high doses of human growth hormone (hGH) on the male reproductive system in the dog.
Sjogren I, Jonsson M, Madej A, Johansson HE, Ploen L.
Toxicology, Pharmacia & Upjohn AB, Stockholm, Sweden.
The effects of very high doses of human growth hormone (hGH), pituitary derived or recombinant methionyl-hGH, on the morphology of reproductive organs and on some hormones in the male dog are described. The studies were part of a toxicological documentation of hGH. A total of 18 male dogs aged 7.5-20.5 months, from four studies were treated subcutaneously with hGH for 20-28 days at dose levels of 3, 10 or 25 IU kg-1 day-1 or 1 IU kg-1 three times weekly. Plasma levels of luteinizing hormone (LH), testosterone and prolactin were determined in one study. Organ weighing, macroscopic and histopathologic examinations of male reproductive organs at the end of the treatment period were included in all studies. Treatment with 25 IU kg-1 day-1 resulted in reduction of testis and prostate weights, degeneration of germ cells and epithelial atrophy in the testis, degenerative changes in epididymis and reduced height of the prostatic epithelium. Similar, although less severe morphological changes were observed after treatment with 10 IU kg-1 day-1. .Treatment with 25 IU kg-1 day-1 also caused a marked reduction of plasma prolactin, LH and testosterone levels. . These results suggest that repeated administration of very high doses of hGH interferes with the hormonal regulation of the testis in the dog.
I have always believed Nolvadex (or Raloxifene) is the drug of choice for gyno, period. No matter what other things might be contributing to gyno, estrogen is essential. Estrogen levels do not have to be elevated. Hypogonadal individuals have very low testosterone AND estrogen levels and gyno is a hallmark symptom of that disorder.
Estrogen receptor knockout mice do not develop breasts no matter how much progesterone or IGF-1 they are esposed to. Those things contribute for sure in the presence of estrogen, but without estrogen they can do nothing.
Estrogen receptor knockout mice do not develop breasts no matter how much progesterone or IGF-1 they are esposed to. Those things contribute for sure in the presence of estrogen, but without estrogen they can do nothing.
Yes. Prolactin, progesterone, and IGF-1 are all stimulatory in the presence of estrogen, but estrogen is the key ingredient. Endocrinologists don't know how gyno develops. It is either due to an excess of estrogen of a deficiency in the testosterone that normally puts the brakes on estrogen's ability to promote mammary development.
Androgens don't have to aromatize to cause gyno. The countless stories on this board of people getting gyno from tren are a testimonial to this. Why don't these other androgens act as if they were testosterone and also put the brakes on gyno? That is the mystery.
Maybe they don't bind as strongly to the androgen receptor. Maybe their progestigenic properties stimulate mammary epithelial development in the presence of estrogen. Or maybe low DHT due to suppression of endogenous test is a factor. The latter is interesting since the incidence rate of gyno in finasteride users is aroud 0.4%, although studies have shown no change in estradiol levels in finasteride users. Moreover, several studies have demonstrated success treating gyno with DHT.
Why some people get gyno and others don't is also a mystery. One very interesting study showed a higher rate of aromatase activity in gyno sufferers than in normal patients (1). Maybe those steroid users who are prone to gyno have higher aromatase activity.
Obviously the use of aromatase inhibitors, and probably the use of dopaminergic agonists to reduce prolactin can help prevent gyno, but Nolvadex or Raloxifene are the only drugs consistently able to prevent and treat it, as long as it has not become fibrous.
(1) J Clin Endocrinol Metab 1987 Mar;64(3):618-23
Increased aromatase activity in pubic skin fibroblasts from patients with isolated gynecomastia.
Bulard J, Mowszowicz I, Schaison G.
Androgens don't have to aromatize to cause gyno. The countless stories on this board of people getting gyno from tren are a testimonial to this. Why don't these other androgens act as if they were testosterone and also put the brakes on gyno? That is the mystery.
Maybe they don't bind as strongly to the androgen receptor. Maybe their progestigenic properties stimulate mammary epithelial development in the presence of estrogen. Or maybe low DHT due to suppression of endogenous test is a factor. The latter is interesting since the incidence rate of gyno in finasteride users is aroud 0.4%, although studies have shown no change in estradiol levels in finasteride users. Moreover, several studies have demonstrated success treating gyno with DHT.
Why some people get gyno and others don't is also a mystery. One very interesting study showed a higher rate of aromatase activity in gyno sufferers than in normal patients (1). Maybe those steroid users who are prone to gyno have higher aromatase activity.
Obviously the use of aromatase inhibitors, and probably the use of dopaminergic agonists to reduce prolactin can help prevent gyno, but Nolvadex or Raloxifene are the only drugs consistently able to prevent and treat it, as long as it has not become fibrous.
(1) J Clin Endocrinol Metab 1987 Mar;64(3):618-23
Increased aromatase activity in pubic skin fibroblasts from patients with isolated gynecomastia.
Bulard J, Mowszowicz I, Schaison G.
I think that is a very good idea. The nolvadex will also reduce IGF-1 levels so there is less potential for the IGF-1 to stimulate breast development. Some believe though that running nolva during a cycle reduces gains somewhat due to the lowered IGF-1, but others say they notice no difference. It will be interesting to see how it works for you. I guess there is no free lunch. If I were prone to gyno, I'd rather my gains suffered a bit than grow breasts.
ultragainz
New member
ok i didnt read all the post above but it sounds like it stops gyno....and is that all it stops??it sounds good for people who use fina like siad above but what if you dont get gyno at all,still good to take?sorry iam a little lost,lol.
Similar threads
