Peptides and women??

[s2h]

So in terms of female system receiving peptides to stimulate and lengthen gh pulses, would same dose protical be applicable?

its no diff then in men..dosing is going to be depend on age and wieght...its still just a Gh pulse..thats not gonna differ between a man and a women too much...

[BiggTexx]

its no diff then in men..dosing is going to be depend on age and wieght...its still just a Gh pulse..thats not gonna differ between a man and a women too much...

How about the higher estrogen levels in women. You think that might effect the GHRH? Could it possibly have a negating effect on the benefits of GH pulsing?

[Bryan Hildebrand]

in my opinion, no, because they are two independent endo systems.

[Bencher]

Are we going to have any women post on rather they have thought of using peptides or if they have tried?

[Bencher]

Bryan, could you adjust the title to something that would catch the girls eyes? Asking if they have given it a thought?

[Bryan Hildebrand]

actually, why dont I move this to fem chem???

[Bencher]

actually, why dont I move this to fem chem???

Thanks biggen!

[Dre23]

How about the higher estrogen levels in women. You think that might effect the GHRH? Could it possibly have a negating effect on the benefits of GH pulsing?

in my opinion, no, because they are two independent endo systems.

Agreed with Bryan.

Estrogen release and gh release, while both hormonal, have different negative feedback systems with which one has nothing to do with the other.

[tankygirl]

I have used GHRP6 & CJC1295 at the same time as my husband... sorry "I" is the female lab rat and "husband" is her male cage friend. They are both 50 yr old rats and have both also cycled with steriods. I was using only Winny by pin. The only difference I and her Husband found was that the Peptides gave him a great sleep but I woke up every hour on the hour wide a wake for about 15 mins then back into a deep sleep. Also had severe night sweats but then as a 50 yr old female rat that may have just been a coincidence.... except as soon as I stopped the peptides the broken sleep and night sweats also stopped... Although both were on them for 3 months there was not a noticeable fat reduction in either rat, saying that husband rat is about to try peptides again. I is currently on a winny/var stack which is giving great muscle growth and strength gains but seems to be causing a lot of bloating/water retnetion in lower abs.
I is looking at adding Osterine to the stack as well.
I am very interested in the keto cycling that was mentioned above. I have basically been on the same low carb diet now for 2 years and apart from being totally bored with it I have hit a plateau at 12% BF and can't get below it.
Is the keto diet listed on here somewhere.

[tankygirl]

Also forgot to mention... when I was on the GHRP6 and CJC1295 hunger was a major issue... especially after dosing....

[s2h]

Also forgot to mention... when I was on the GHRP6 and CJC1295 hunger was a major issue... especially after dosing....

give ipamorelin a try..its the most recent generation of the GHRP's...it causes a release of your natural GH...it is also long acting and doesnt effect your hunger..i have found in my research that it is very effective...

[BiggTexx]

So whats the word on women and peptides for leaning out?

Bencher, my wife and I have been using peptides for almost 3 years now. I have a very long log on PM that has been abandoned and continued on DAT's board

BigTex Log PM
http://www.professionalmuscle.com/fo...xperience.html

BigTex Log DATs'
[ame="http://datbtrue.co.uk/forums/showthread.php?t=411"]Datbtrue[/ame]

[BiggTexx]

in my opinion, no, because they are two independent endo systems.

Kin-Chuen Leung, Gudmundur Johannsson, Gary M. Leong and Ken K. Y. Ho. Estrogen Regulation of Growth Hormone Action. Endocrine Reviews October 1, 2004 vol. 25 no. 5 693-721Abstract

GH plays a pivotal role in regulating body growth and development, which is modulated by sex steroids. A close interplay between estrogen and GH leads to attainment of genderspecific body composition during puberty. The physiological basis of the interaction is not well understood. Most previous studies have focused on the effects of estrogen on GH secretion. There is also strong evidence that estrogen modulates GH action independent of secretion. Oral but not transdermal administration of estrogen impairs the metabolic action of GH in the liver, causing a fall in IGF-I production and fat oxidation. This results in a loss of lean tissue and a gain of body fat in postmenopausal women and an impairment of GH effect in hypopituitary women on GH replacement. The negative metabolic sequelae are potentially important because of the widespread use of oral estrogen and estrogen-related compounds.
Estrogen affects GH action at the level of receptor expression and signaling. More recently, estrogen has been shown to inhibit Janus kinase/signal transducer and activator of transcription signaling by GH via the induction of suppressor of cytokine signaling-2, a protein inhibitor for cytokine signaling. This represents a novel paradigm of steroid regulation of cytokine receptors and is likely to have significance for a diverse range of cytokine function.



K. C. Leung, N. Doyle, M. Ballesteros, K. Sjogren, C. K. W. Watts, T. H. Low, G. M. Leong, R. J. M. Ross, and K. K. Y. Ho. Estrogen inhibits GH signaling by suppressing GH-induced JAK2 phosphorylation, an effect mediated by SOCS-2. PNAS February 4, 2003 vol. 100 no. 3 1016-1021
Abstract

Oral estrogen administration attenuates the metabolic action of growth hormone (GH) in humans. To investigate the mechanism involved, we studied the effects of estrogen on GH signaling through Janus kinase (JAK)2 and the signal transducers and activators of transcription (STATs) in HEK293 cells stably expressing the GH receptor (293GHR), HuH7 (hepatoma) and T-47D (breast cancer) cells. 293GHR cells were transiently transfected with an estrogen receptor-α expression plasmid and luciferase reporters with binding elements for STAT3 and STAT5 or the β-casein promoter. GH stimulated the reporter activities by four- to sixfold. Cotreatment with 17β-estradiol (E2) resulted in a dose-dependent reduction in the response of all three reporters to GH to a maximum of 49–66% of control at 100 nM (P < 0.05). No reduction was seen when E2 was added 1–2 h after GH treatment. Similar inhibitory effects were observed in HuH7 and T-47D cells. E2 suppressed GH-induced JAK2 phosphorylation, an effect attenuated by actinomycin D, suggesting a requirement for gene expression. Next, we investigated the role of the suppressors of cytokine signaling (SOCS) in E2 inhibition. E2 increased the mRNA abundance of SOCS-2 but not SOCS-1 and SOCS-3 in HEK293 cells. The inhibitory effect of E2 was absent in cells lacking SOCS-2 but not in those lacking SOCS-1 and SOCS-3. In conclusion, estrogen inhibits GH signaling, an action mediated by SOCS-2. This paper provides evidence for regulatory interaction between a sex steroid and the GH/JAK/STAT pathway, in which SOCS-2 plays a central mechanistic role.



Bryan, there is literally tons of data showing how estrogen slows the benefits of GH in women. Therefore any GHRH will not be near as effective in women ad GHRPs. I would strongly suggest that women use smaller then saturation levels of GHRH and saturation levels of GHRP if they want to over come the effects of estrogen and get good results from peptides. Stoping the production of estrogen by either drugs or low body fat will also take care of this issue which is why women with very low body fat levels get great results with GH or peptides.

[BiggTexx]

Also forgot to mention... when I was on the GHRP6 and CJC1295 hunger was a major issue... especially after dosing....

I might suggest to you to use less of the modified GRF 1-29(CJC) next time and switch to ipamorelin. The GHRP6 increases ghrelin levels. Why is that an issue? Well ghrelin is a hormone produced mainly the human stomach and epsilon cells of the pancreas. Any increase in ghrelin production is what stimulates hunger. Since GHRP-2, GHRP-2, and hexarelin all increase ghrelin production most of us are going to have hunger issues. Ipamorelin does not stimulate ghrelin production so you won't have the huger you would with the GHRP's.

[Bryan Hildebrand]

I love science! thanks for posting these.

the one thing to take away from this is that the women were studied who were taking exogenic estrogen. not the other way around. but, i stand corrected about them being two different systems. obviously at some level there is an interaction.

Kin-Chuen Leung, Gudmundur Johannsson, Gary M. Leong and Ken K. Y. Ho. Estrogen Regulation of Growth Hormone Action. Endocrine Reviews October 1, 2004 vol. 25 no. 5 693-721Abstract

GH plays a pivotal role in regulating body growth and development, which is modulated by sex steroids. A close interplay between estrogen and GH leads to attainment of genderspecific body composition during puberty. The physiological basis of the interaction is not well understood. Most previous studies have focused on the effects of estrogen on GH secretion. There is also strong evidence that estrogen modulates GH action independent of secretion. Oral but not transdermal administration of estrogen impairs the metabolic action of GH in the liver, causing a fall in IGF-I production and fat oxidation. This results in a loss of lean tissue and a gain of body fat in postmenopausal women and an impairment of GH effect in hypopituitary women on GH replacement. The negative metabolic sequelae are potentially important because of the widespread use of oral estrogen and estrogen-related compounds.
Estrogen affects GH action at the level of receptor expression and signaling. More recently, estrogen has been shown to inhibit Janus kinase/signal transducer and activator of transcription signaling by GH via the induction of suppressor of cytokine signaling-2, a protein inhibitor for cytokine signaling. This represents a novel paradigm of steroid regulation of cytokine receptors and is likely to have significance for a diverse range of cytokine function.



K. C. Leung, N. Doyle, M. Ballesteros, K. Sjogren, C. K. W. Watts, T. H. Low, G. M. Leong, R. J. M. Ross, and K. K. Y. Ho. Estrogen inhibits GH signaling by suppressing GH-induced JAK2 phosphorylation, an effect mediated by SOCS-2. PNAS February 4, 2003 vol. 100 no. 3 1016-1021
Abstract

Oral estrogen administration attenuates the metabolic action of growth hormone (GH) in humans. To investigate the mechanism involved, we studied the effects of estrogen on GH signaling through Janus kinase (JAK)2 and the signal transducers and activators of transcription (STATs) in HEK293 cells stably expressing the GH receptor (293GHR), HuH7 (hepatoma) and T-47D (breast cancer) cells. 293GHR cells were transiently transfected with an estrogen receptor-α expression plasmid and luciferase reporters with binding elements for STAT3 and STAT5 or the β-casein promoter. GH stimulated the reporter activities by four- to sixfold. Cotreatment with 17β-estradiol (E2) resulted in a dose-dependent reduction in the response of all three reporters to GH to a maximum of 49–66% of control at 100 nM (P < 0.05). No reduction was seen when E2 was added 1–2 h after GH treatment. Similar inhibitory effects were observed in HuH7 and T-47D cells. E2 suppressed GH-induced JAK2 phosphorylation, an effect attenuated by actinomycin D, suggesting a requirement for gene expression. Next, we investigated the role of the suppressors of cytokine signaling (SOCS) in E2 inhibition. E2 increased the mRNA abundance of SOCS-2 but not SOCS-1 and SOCS-3 in HEK293 cells. The inhibitory effect of E2 was absent in cells lacking SOCS-2 but not in those lacking SOCS-1 and SOCS-3. In conclusion, estrogen inhibits GH signaling, an action mediated by SOCS-2. This paper provides evidence for regulatory interaction between a sex steroid and the GH/JAK/STAT pathway, in which SOCS-2 plays a central mechanistic role.



Bryan, there is literally tons of data showing how estrogen slows the benefits of GH in women. Therefore any GHRH will not be near as effective in women ad GHRPs. I would strongly suggest that women use smaller then saturation levels of GHRH and saturation levels of GHRP if they want to over come the effects of estrogen and get good results from peptides. Stoping the production of estrogen by either drugs or low body fat will also take care of this issue which is why women with very low body fat levels get great results with GH or peptides.