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Anabolic Steroids
What is wrong with daily low dose HCG with TRT?
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FWIW-- 'HIPPA' -- That is a typo on the banner, it is correct on their website.
foreveryoung
New Member
AI works against the aromatisation of testosterone into estrogen
isn`t the issue with hcg that the estrogen is produced directly, not by aromatisation?
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There is no other molecule like hCG. What about hCG makes sense to administer it every day. NOTHING. This is no more than BS from someone FOS. It is well established that the hormone hCG act on an hCG/luteinizing hormone (LH) receptor to evoke a response.
The different composition of these oligosaccharides affects bioactivity and speed of degradation. The biologic half-life of LH is 20 minutes, shorter than that of FSH (3–4 hours) and hCG (36 hours). hCG has 50 times the biological activity of LH per mole of hormone (sulfated hCG is less potent than regular hCG, which is 86-fold more potent than LH).
Birken S, Maydelman Y, Gawinowicz MA, Pound A, Liu Y, Hartree AS. Isolation and characterization of human pituitary chorionic gonadotropin. Endocrinology. 1996;137(4):1402-11. Isolation and characterization of human pituitary chorionic gonadotropin.
The different composition of these oligosaccharides affects bioactivity and speed of degradation. The biologic half-life of LH is 20 minutes, shorter than that of FSH (3–4 hours) and hCG (36 hours). hCG has 50 times the biological activity of LH per mole of hormone (sulfated hCG is less potent than regular hCG, which is 86-fold more potent than LH).
Birken S, Maydelman Y, Gawinowicz MA, Pound A, Liu Y, Hartree AS. Isolation and characterization of human pituitary chorionic gonadotropin. Endocrinology. 1996;137(4):1402-11. Isolation and characterization of human pituitary chorionic gonadotropin.
I think the docs who are recommending daily low dose HCG at 100iu are doing so to keep E2 levels lower and more stable. 2 x 350iu shots per week causes E2 to spike much higher than 100iu ED.
I see. Sorry, I seem to be misunderstanding your posts. Yes, it is unfortunate. It seems to be a never ending road with new discoveries that raise yet even more questions.
I believe that is the case? That being said, whether through aromatization or direct production, AI will decrease your overall Estrogen. At least to my understanding.
I believe people administer HCG everyday now, because it provides more consistent levels and a sense of well-being in people. How often do you suggest it be used?
What is 100 IU supposed to be doing? This comes back to what is the purpose of hCG.
Are you saying that doing this for a week is the equivalent of 2 350 IU injections, but without the E2? What do you think happens to daily hCG injections? Does anyone really believe that just because you inject daily that somehow the half-life changes!
Dr Crisler has said that he thinks the best TRT protocol is daily T gel application and 100iu HCG daily. For those that require HCG, do you think something like 250iu twice a week would be best?
I am not trying to avoid your question. And, I think it is important to understand what is the purpose of the hCG. The purposes are: (1) testosterone, (2) Spermatogenesis, (3) Testes volume (TV), (4) Extragonadal, (5) "Backfilling." IIRC, (4) & (5) are promoted by some, which is no more than BS. Are there other purposes?
And, this is separate from the idiotic idea of daily hCG use. And, it is as stupid as stupid gets. Can anyone point me to any clinical study where there is daily hCG use? There are 1000s of hCG studies. Point me to ONE (1). If someone wishes to inject themselves daily, go ahead, but know why it is done.
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Ok so rather than daily HCG, in your opinion (for those who require it during TRT), what is the best way of implementing it? 250iu twice a week perhaps?
Bump.
I'm curious as to what you suggest for HCG usage in a TRT protocol. How much, how often?
I am not being difficult, but first one must decide what is the purpose of the hCG. Following is some info on Extragonadal Luteinizing Hormone / Chorionic Gonadotropin Receptors [LH/hCG-R].
There have been some statements that there exists Extragonadal Luteinizing Hormone / Chorionic Gonadotropin Receptors [LH/hCG-R], particularly within the Central Nervous System (CNS), that are functionally significant. Moreover, they use these statements as reasoning for the use of human Chorionic Gonadotropin (hCG) within Testosterone Replacement Therapy (TRT). Not surprisingly, these practitioners provide no evidence foe these claims. [IIRC, they point to a possible short feedback loop as evidence, which is unproven. If this is the evidence for its use, then any drug is okay for just about anything! https://thinksteroids.com/community/posts/854916 ]
In a 2007 review, the authors’ concluded, “further evidence is needed before the extragonadal LH/hCG-R expression can be considered functionally significant.” In a recent communication a study author stated, “Further information is accumulating, but I would still stick to our old original conclusion. You can find recent publication on LHR expression in the uterus, but I am still not convinced about their functional significance.
There is NO, NADA, ZIP, ZERO evidence for functional Extragonadal Luteinizing Hormone / Chorionic Gonadotropin Receptors [LH/hCG-R] within the CNS and more especially in males.
Pakarainen T, Ahtiainen P, Zhang F-P, Rulli S, Poutanen M, Huhtaniemi I. Extragonadal LH/hCG action—Not yet time to rewrite textbooks. Molecular and Cellular Endocrinology 2007;269(1-2):9-16. ScienceDirect.com - Molecular and Cellular Endocrinology - Extragonadal LH/hCG action—Not yet time to rewrite textbooks
Gonadotropins are indispensable in both sexes in the regulation of gonadal sex steroid production and gametogenesis. In addition to their well-established classical actions, numerous recent publications have indicated the presence and function of luteinizing hormone/chorionic gonadotropin receptors (LH/hCG-R) in a variety of extragonadal tissues. However, the physiological significance of such effects has remained unclear. We have generated two genetically modified mouse models, one with excessive production of hCG and the other with targeted disruption of LH/hCG-R gene, and used them to address the functions of LH and hCG. Numerous gonadal and extragonadal phenotypes were found in the models with the two extremes of LH/hCG action. However, when the extragonadal effects were scrutinized in greater detail, they all appeared to arise through modification of gonadal function, either through enhanced or inhibited response to LH/hCG stimulation. Hence, further evidence is needed before the extragonadal LH/hCG-R expression can be considered functionally significant.
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Dr S as you are aware there is some disagreement about what type (primary or secondary) is best suited for those designated as having either a "mixed" or "compensated" causation.
Consequently until the classification becomes more practical, based on predetermined algorithms, utilizing a response to a specific drug (SERM, LH, GnRH, HCG, etc) challenge, confusion will remain and a unified categorization elusive.
Nevertheless I've enclosed the article used to support my assertion of 60% , although it's actually being closer to 50%. Admitedly it does include those with "compensated" hypogonadism since these patients are characterized by inappropriately high gonadotropin levels compared to their depressed TT values.
I also included an article which determined an ultrashort LH/HCG feedback loop does not exist in humans, ( yet this same feedback loop does seem to influence LH secretion some other animal studies such as; pig, monkey, rabbit)
As always your assistance in clarifying any of my posts is greatly appreciated.
Best regards
jim
Consequently until the classification becomes more practical, based on predetermined algorithms, utilizing a response to a specific drug (SERM, LH, GnRH, HCG, etc) challenge, confusion will remain and a unified categorization elusive.
Nevertheless I've enclosed the article used to support my assertion of 60% , although it's actually being closer to 50%. Admitedly it does include those with "compensated" hypogonadism since these patients are characterized by inappropriately high gonadotropin levels compared to their depressed TT values.
I also included an article which determined an ultrashort LH/HCG feedback loop does not exist in humans, ( yet this same feedback loop does seem to influence LH secretion some other animal studies such as; pig, monkey, rabbit)
As always your assistance in clarifying any of my posts is greatly appreciated.
Best regards
jim
hardasnails1973
New Member
In my cases hcg is not used to increase testosterone, but to stimulate LH receptors in the brain. I had several cases where there were guys on try with optimal levels but still had depression. Recommending to their doctor to add hcg 100 ius 3 times a week had a profound effect on their depression. The.doctors patients had no.clue since they did.not.research on line, but did what doctor said. The placebo effect was not an issue here. There should be a study about low dosages of hcg and its effect on depression non responsive to trt. I think the results be interesting ...
I go back and forth between IM T (about 20 mg every other day) with an intermittent substitution of HCG (250 IUs or sometimes 500 IUs) for an IM T shot about once a week or once every two weeks, and IM T ONLY, and occasional weekly to monthly runs of HCG (500 IUs M/W/Fri or 750 IUs twice a week) when I've gone a while (say 3 months) on IM T only.
I dont think HCG with a weekly IM T protocol works very well because: when would you take it?? You take it the 2 days before your IM T shot and now you've got three consecutive days of hormone shots that make your E2 go ballistic. Take it on the middle day and thats when your E2 is already high from the T shot. It makes more sense to squeeze it in weekly or bi-weekly as part of an every other day IM T protocol - IOW substitute an HCG shot for an IM T shot every now and then. You're taking a LOW dose of T and that helps keep the E2 response to exogenous T at a minimum and you're adding in HCG only occasionally to keep the Leydigs active. I've been doing this for the last year or so and it works.
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Have you started drinking again................................................:drooling:
It's all a helluva lot easier to do with a slin pin instead of that 25 G monstrosity everyone seems to start off with.
HANS
Why do you insist on presenting non-verifiable anecdotes as evidence to either diagnose or treat complex diseases such as depression where the etiology is multifactorial, hence placebo could have had the effect you describe?
This is akin to promoting "junk science" unless accompanied with a peer reviewed article supporting your less than conventional "therapies"!
Jim
Why do you insist on presenting non-verifiable anecdotes as evidence to either diagnose or treat complex diseases such as depression where the etiology is multifactorial, hence placebo could have had the effect you describe?
This is akin to promoting "junk science" unless accompanied with a peer reviewed article supporting your less than conventional "therapies"!
Jim
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