I'm about to receive my first batch of HCG. I will be doing the Swale Protocol from now on but Im wondering if I should run some extra HCG to get the boys back to their pre-HRT condition, since Ive had some shrinkage. Currently Im doing 125 mg enanthate every 6 days plus Arimidex 0.125 mg ED. Would it be prudent to run HCG at say 100-200 iu ED or EOD for a couple of weeks and back off the enanthate entirely for the period or just forget about all that and start straight in the with SP?
MESO-Rx
Anabolic Steroids
Testicular tune-up advice
- Thread starter bcachot
- Start date
Weatherlite
New Member
Go straight into the SWALE protocol. If you drop the Enthanate you will screw things up big time and you'll start feeling like shit. Just like diagnosing a computer or car problem, you only make one change at a time or else you won't know what caused a change in symptoms. If you add HCG but drop T and then you experience a change you won't know if it was from dropping T or adding HCG.
Also, if you are wanting to increase the size of the "boys" quickly you may want to consider a slightly higher dose of HCG for a couple of weeks and then drop down to the regular 250. I only say this because I recently found out that I inadvertantly did this. I was running 500iu instead of 250 for three weeks due to an error in my reconstitution of the HCG. My boys started hurting a bittle bit (felt like a case of blue balls) and they were a bit larger than normal. I accredit this to the higher HCG--high HCG=high production of sperm which means larger balls...and the ache which was essentiall blue balls!
Once I went back down to 250 the ache went away and the size went back to normal. Anyway, my hypothesis is that a slightly higher dose may bring them up to size quicker. If anyone can say for sure that this is wrong please correct me.
Also, if you are wanting to increase the size of the "boys" quickly you may want to consider a slightly higher dose of HCG for a couple of weeks and then drop down to the regular 250. I only say this because I recently found out that I inadvertantly did this. I was running 500iu instead of 250 for three weeks due to an error in my reconstitution of the HCG. My boys started hurting a bittle bit (felt like a case of blue balls) and they were a bit larger than normal. I accredit this to the higher HCG--high HCG=high production of sperm which means larger balls...and the ache which was essentiall blue balls!
Once I went back down to 250 the ache went away and the size went back to normal. Anyway, my hypothesis is that a slightly higher dose may bring them up to size quicker. If anyone can say for sure that this is wrong please correct me.
I would have thought that keeping the T going at my current rate and adding in higher than normal doses of HCG might get my T up too high. I have already backed off on the T somewhat in anticipation of starting the HCG. I've eased it down slowly to about 85 mg every 7 days and still feel fine. I figure now if I slowly add in the HCG and bring it up to 250 iu 3-4 times I week that might stimulate rapid recovery without overcooking T levels.
I got my Dr. to give me Hcg he read SWALE's protocol but started me on 500 IU's 3 times a week and I am doing 150 mgs. of Depo T. shots every week. After the 15th. shot of Hcg my Dr. had me do a blood test. My T levels went from 686 to 1135 range for a young man is 262 to 1593. So my Testis brought the levels up from 686 to 1135. My next test is in 2 weeks still doing 500 IU's of Hcg 3 times a week. I feel like my testis are a lot bigger and if my levels go higher my Dr. will be making some changes what they will be I don't know. I am primary and using Hcg has got my testis making T why I don't know.
Phil
Phil
Take this with a grain of salt as I am not qualified to render any type of scientific opinion (poli sci major!):
Hmmm....HCG does not, in an of itself, create sperm. HCG mimics LH. LH binds to Leydig cells and increases cAMP which increases protein secretion and the side-chain cleavage of cholesterol, as well as other likely steps, to increase steroidogenesis and the production of testosterone and other androgens. Regulated by steroid feedback. The Leydig cells produce the testicular steroids, lie between the seminiferous tubules, and assist in the transportation of steroids in the blood, lymph and seminiferous tubules. In other words, HCG mimics LH which then creates Test in the leydig cells.
FSH binds to the Sertoli cells of the seminiferous tubules, increases cAMP and protein synthesis, androgen binding in the tubules, etc. Regulated by inhibin produced by the Sertoli cells. Sertoli cells secrete proteins that are important to spermatogenesis and have been called the director cells of spermatogenesis. They comprise the blood-testis barrier. Sperm are released into the lumen through spermiogenesis which involves a gradual release of sperm from the Sertoli cells into the tubule lumen.
However, there is some cross-over between Testosterone and FSH, and their effect on spermogenesis. I have read some articles where testosterone is needed for the proper delivery of Sperm (although comes from the Sertoli cells which are stimulated by FSH). Here is a quote from a endo text book "The processes by which the Sertoli cells are involved in the expression of hormone action are more readily apparent for FSH than testosterone, since in the latter, the molecular mechanisms are still obscure."
Here is everything you need to know (and then some):
http://www.endotext.org/male/male1/male1_2.htm
So, I am not sure why you are feeling pain, maybe overstimulation of the Leydig Cells? High dose HCG has been used effectively to lower retractile testes. (getting testicles to drop).
Hmmm....HCG does not, in an of itself, create sperm. HCG mimics LH. LH binds to Leydig cells and increases cAMP which increases protein secretion and the side-chain cleavage of cholesterol, as well as other likely steps, to increase steroidogenesis and the production of testosterone and other androgens. Regulated by steroid feedback. The Leydig cells produce the testicular steroids, lie between the seminiferous tubules, and assist in the transportation of steroids in the blood, lymph and seminiferous tubules. In other words, HCG mimics LH which then creates Test in the leydig cells.
FSH binds to the Sertoli cells of the seminiferous tubules, increases cAMP and protein synthesis, androgen binding in the tubules, etc. Regulated by inhibin produced by the Sertoli cells. Sertoli cells secrete proteins that are important to spermatogenesis and have been called the director cells of spermatogenesis. They comprise the blood-testis barrier. Sperm are released into the lumen through spermiogenesis which involves a gradual release of sperm from the Sertoli cells into the tubule lumen.
However, there is some cross-over between Testosterone and FSH, and their effect on spermogenesis. I have read some articles where testosterone is needed for the proper delivery of Sperm (although comes from the Sertoli cells which are stimulated by FSH). Here is a quote from a endo text book "The processes by which the Sertoli cells are involved in the expression of hormone action are more readily apparent for FSH than testosterone, since in the latter, the molecular mechanisms are still obscure."
Here is everything you need to know (and then some):
http://www.endotext.org/male/male1/male1_2.htm
So, I am not sure why you are feeling pain, maybe overstimulation of the Leydig Cells? High dose HCG has been used effectively to lower retractile testes. (getting testicles to drop).
Weatherlite said:
Wow! Perhaps your doc will use you in a study? Is there any other drug/treatment you followed to stimulate the testes? Especially since you have been on TRT for 21 yrs that is highly unusual. ALthough it would probably mess up the way you feel, it would be interesting to go off treatment for a little bit to see where you are "au naturel".
pmgamer18 said:
Weatherlite
New Member
Yes, HCG does mimic LH. It also, in a roundabout way, stimulate production of sperm. In fact, that is the primary prescription reason for HCG-infertility. I didn't state that in my post assuming that folks around here already knew that. Sorry....you know what you get when you ASS-U-ME something!!!! 
Yep, but the $64,000 question is how? HCG is the first step to fertilty treatment because it is much much cheaper than HMG. Although theoretically HCG only leads to the production of Test in the leydig cells, while sperm is produced in the Sertoli cells. However, test is somehow necessary for spermogenesis. But on the other hand some folks have experimenting with using T as a form of male birth control
I would like to get these articles:
FSH and testosterone signaling in Sertoli cells.
Walker WH, Cheng J.
Department of Cell Biology and Physiology, University of Pittsburgh, Pittsburgh, PA 15261, USA. walkerw@pitt.edu
Testosterone and follicle-stimulating hormone (FSH) are required to obtain full reproductive potential. In the testis, somatic Sertoli cells transduce signals from testosterone and FSH into the production of factors that are required by germ cells as they mature into spermatozoa. Recent advances in identifying new signaling pathways that are regulated by FSH and testosterone have allowed for refinement in the understanding of the independent, overlapping and synergistic actions of these hormones. In this review, we discuss the signaling pathways that are regulated by FSH and testosterone as well as the resulting metabolic and gene expression changes that occur as related to Sertoli cell proliferation, differentiation and the support of spermatogenesis.
J Androl. 2005 May-Jun;26(3):343-8. Related Articles, Links
Click here to read
Bioactivity of androgens within the testes and serum of normal men.
Jarow JP, Wright WW, Brown TR, Yan X, Zirkin BR.
Department of Urology, Johns Hopkins University School of Medicine, Baltimore, MD, USA. jjarow@jhmi.edu
Little is known about how human spermatogenesis is regulated, so it is not surprising that there have been few breakthroughs in the treatment of male infertility resulting from abnormalities of spermatogenesis. Testosterone is the predominant intratesticular steroid in both the rat and man. Previous studies have shown that the testosterone concentration within the rat testis that is required for the quantitative maintenance of spermatogenesis is far higher than the total testosterone concentration in rat blood, indicating that much of the testosterone within the testis might be biologically inactive. In contrast to the rat, little is known about the androgen requirements for human spermatogenesis, in part because, until recently, a minimally invasive method suitable for obtaining intratesticular fluids from the human testis has not been available. Percutaneous aspiration now makes it feasible to do so. A major objective of the present study was to assay the bioactive androgen concentration within the testes of normal, fertile men. Percutaneous aspiration was used to obtain intratesticular fluid from such men, and we adapted a highly sensitive recombinant protein mammalian cell-based bioassay to measure androgen bioactivity. Total intratesticular testosterone concentration, which we define as immunoreactive testosterone as measured by radioimmunoassay, was well in excess of that in serum (1236 +/- 86 nM vs 11.7 +/- 0.7 nM). The concentration of bioactive androgens within the normal human testis was found to be about two thirds that of the total testosterone concentration. Interestingly, the concentration of the major, known binding proteins for testosterone within the testis, serum hormone-binding globulin (SHBG)/ABP (52.4 +/- 9.7 nM), was insufficient to account for the difference between total testosterone and bioactive androgens. This indicates that, in addition to its binding to SHBG/ABP, androgens may also be bound by unknown molecules, and that this contributes to reducing androgen bioactivity. These observations could have relevance for understanding the relationship between spermatogenesis and intratesticular androgens in normal men and in men diagnosed with infertility.
PMID: 15867001 [PubMed - in process]
I would like to get these articles:
FSH and testosterone signaling in Sertoli cells.
Walker WH, Cheng J.
Department of Cell Biology and Physiology, University of Pittsburgh, Pittsburgh, PA 15261, USA. walkerw@pitt.edu
Testosterone and follicle-stimulating hormone (FSH) are required to obtain full reproductive potential. In the testis, somatic Sertoli cells transduce signals from testosterone and FSH into the production of factors that are required by germ cells as they mature into spermatozoa. Recent advances in identifying new signaling pathways that are regulated by FSH and testosterone have allowed for refinement in the understanding of the independent, overlapping and synergistic actions of these hormones. In this review, we discuss the signaling pathways that are regulated by FSH and testosterone as well as the resulting metabolic and gene expression changes that occur as related to Sertoli cell proliferation, differentiation and the support of spermatogenesis.
J Androl. 2005 May-Jun;26(3):343-8. Related Articles, Links
Click here to read
Bioactivity of androgens within the testes and serum of normal men.
Jarow JP, Wright WW, Brown TR, Yan X, Zirkin BR.
Department of Urology, Johns Hopkins University School of Medicine, Baltimore, MD, USA. jjarow@jhmi.edu
Little is known about how human spermatogenesis is regulated, so it is not surprising that there have been few breakthroughs in the treatment of male infertility resulting from abnormalities of spermatogenesis. Testosterone is the predominant intratesticular steroid in both the rat and man. Previous studies have shown that the testosterone concentration within the rat testis that is required for the quantitative maintenance of spermatogenesis is far higher than the total testosterone concentration in rat blood, indicating that much of the testosterone within the testis might be biologically inactive. In contrast to the rat, little is known about the androgen requirements for human spermatogenesis, in part because, until recently, a minimally invasive method suitable for obtaining intratesticular fluids from the human testis has not been available. Percutaneous aspiration now makes it feasible to do so. A major objective of the present study was to assay the bioactive androgen concentration within the testes of normal, fertile men. Percutaneous aspiration was used to obtain intratesticular fluid from such men, and we adapted a highly sensitive recombinant protein mammalian cell-based bioassay to measure androgen bioactivity. Total intratesticular testosterone concentration, which we define as immunoreactive testosterone as measured by radioimmunoassay, was well in excess of that in serum (1236 +/- 86 nM vs 11.7 +/- 0.7 nM). The concentration of bioactive androgens within the normal human testis was found to be about two thirds that of the total testosterone concentration. Interestingly, the concentration of the major, known binding proteins for testosterone within the testis, serum hormone-binding globulin (SHBG)/ABP (52.4 +/- 9.7 nM), was insufficient to account for the difference between total testosterone and bioactive androgens. This indicates that, in addition to its binding to SHBG/ABP, androgens may also be bound by unknown molecules, and that this contributes to reducing androgen bioactivity. These observations could have relevance for understanding the relationship between spermatogenesis and intratesticular androgens in normal men and in men diagnosed with infertility.
PMID: 15867001 [PubMed - in process]
Weatherlite said:Yes, HCG does mimic LH. It also, in a roundabout way, stimulate production of sperm. In fact, that is the primary prescription reason for HCG-infertility. I didn't state that in my post assuming that folks around here already knew that. Sorry....you know what you get when you ASS-U-ME something!!!!
Here is another:
Int J Androl. 2004 Dec;27(6):335-42.
Hormonal regulation of spermatogenesis.
Holdcraft RW, Braun RE.
University of Washington, School of Medicine, Department of Genome Sciences, 1959 NE Pacific Street, Seattle, WA 98195-7730, USA.
Proper functioning of the mammalian testis is dependent upon an array of hormonal messengers acting through endocrine, paracrine, and autocrine pathways. Within the testis, the primary messengers are the gonadotrophins, follicle stimulating hormone and luteinizing hormone, and the androgens. Abundant evidence indicates that the role of the gonadotrophins is to maintain proper functioning of testicular somatic cells. It is the androgens, primarily testosterone, which act through the somatic cells to regulate germ cell differentiation. Despite extensive research in this area, little is known about the cell-specific requirements for androgens and even less is understood about the downstream effectors of androgen signalling. However, recent work using cell-specific ablation of androgen receptor function has demonstrated a clear requirement for androgen signalling at multiple, discrete time points during spermatogenesis. These models also provide useful tools for identifying the targets of androgen receptor activity. The purpose of this review is to provide a brief overview of recent advances in our understanding of hormonal regulation of spermatogenesis, with an emphasis on the role of testosterone within the testis, and to pose important questions for future research in this field.
Publication Types:
* Review
* Review, Tutorial
PMID: 15595952 [PubMed - indexed for MEDLINE]
Int J Androl. 2004 Dec;27(6):335-42.
Hormonal regulation of spermatogenesis.
Holdcraft RW, Braun RE.
University of Washington, School of Medicine, Department of Genome Sciences, 1959 NE Pacific Street, Seattle, WA 98195-7730, USA.
Proper functioning of the mammalian testis is dependent upon an array of hormonal messengers acting through endocrine, paracrine, and autocrine pathways. Within the testis, the primary messengers are the gonadotrophins, follicle stimulating hormone and luteinizing hormone, and the androgens. Abundant evidence indicates that the role of the gonadotrophins is to maintain proper functioning of testicular somatic cells. It is the androgens, primarily testosterone, which act through the somatic cells to regulate germ cell differentiation. Despite extensive research in this area, little is known about the cell-specific requirements for androgens and even less is understood about the downstream effectors of androgen signalling. However, recent work using cell-specific ablation of androgen receptor function has demonstrated a clear requirement for androgen signalling at multiple, discrete time points during spermatogenesis. These models also provide useful tools for identifying the targets of androgen receptor activity. The purpose of this review is to provide a brief overview of recent advances in our understanding of hormonal regulation of spermatogenesis, with an emphasis on the role of testosterone within the testis, and to pose important questions for future research in this field.
Publication Types:
* Review
* Review, Tutorial
PMID: 15595952 [PubMed - indexed for MEDLINE]
I don't under stand it ether and I think my levels are still going up. My E2 is giving me trouble now more so the before. Last night I had a bad panic attack and this only happens when my E2 is going to high last test it was 50 to high for me so been taking more Indlolpelx/DIM and .5 arimidex every 5 days to keep it down. My next test is in 2 weeks.Random987 said:
Phil
