Why not low dose clomiphene instead of HCG on TRT?

[Renholder]

I`m sorry guys, but I still do not feel any of you have provided an explanation that I can understand. I do not have fresh HCG at hand, so I will try 25 mg clomiphene EOD for a few weeks now and see what happens.

I asked the same question at Dr Johns forums and he does not seem to hold the same viewpoint as most here:

That's a great question.

THEORETICALLY clomiphene would be superior to HCG. However, it just does not work out well for many.

You will just have to try it to see.

[Vettester]

I`m sorry guys, but I still do not feel any of you have provided an explanation that I can understand. I do not have fresh HCG at hand, so I will try 25 mg clomiphene EOD for a few weeks now and see what happens.

I asked the same question at Dr Johns forums and he does not seem to hold the same viewpoint as most here:

I'll try to explain this differently ... The main thing you are looking to get is LH (luteinizing hormone), right? LH, will stimulate the testicles to produce testosterone, also known as endogenous production.

There's two (2) ways that the LH signal can get to the testicles to get them working ...

1) By the brain. This is achieved in the pituitary region of the brain, and is also referred to as the HPTA (hypothalamas pituitary thyroid axis). This is where you hear the term "axis" being used. When the axis is healthy, it will produce LH and signal the testes to produce endogenous testosterone. This will be regulated via a feedback loop to the "axis", which tells it when enough testosterone is in the body, or when more is needed. When serum levels drop, the axis gets the call to send more LH, then the testes go to work again ... The cycle repeats itself over, and over, and ...

2) When the HPTA does not function correctly, which can also be diagnosed as secondary hypogonadism, then a patient can look at HCG to signal the testes to produce endogenous testosterone. HCG, as explained by Oscar is an LH analogue, an exogenous method if you will to deliver that hormone to the testicles. Again, the testicles won't produce testosterone, or very little of it without the LH signal.

Clomid is compound, also known as a SERM, which is designed to stimulate the "axis" to produce LH & FSH. If your "axis" is shutdown, suppressed, not working, whatever you want to call it due to hypogonadism, then there's a good chance that clomid will have minimal effect, and it will probably not sustain gonadotropin production (LH/FSH) for very long. And as Oscar mentioned, using Clomid as method for a therapy solution isn't practical.

So, if there's a chance that your "axis" will function normally by running a clomid protocol, like a PCT, then by all means go for it. If your HPTA is anything like mine, then it's suppression is irreversible, thus Clomid would just be "spinning my wheels" if I took it. Therefore, I use HCG, which doesn't have anything to do with trying to get the brain to produce LH. It's just an exogenous (outside) source of the LH analogue, and my testicles don't care how they got it, they're just glad they got it.

Ren, that's about the best 10 year old, childlike explanation I can give you. Just keep reading up on it and stay involved with the forums, hopefully more time with our forum here. Any questions?

[Renholder]

Clomid is compound, also known as a SERM, which is designed to stimulate the "axis" to produce LH & FSH. If your "axis" is shutdown, suppressed, not working, whatever you want to call it due to hypogonadism, then there's a good chance that clomid will have minimal effect, and it will probably not sustain gonadotropin production (LH/FSH) for very long. And as Oscar mentioned, using Clomid as method for a therapy solution isn't practical.

So, if there's a chance that your "axis" will function normally by running a clomid protocol, like a PCT, then by all means go for it. If your HPTA is anything like mine, then it's suppression is irreversible, thus Clomid would just be "spinning my wheels" if I took it. Therefore, I use HCG, which doesn't have anything to do with trying to get the brain to produce LH. It's just an exogenous (outside) source of the LH analogue, and my testicles don't care how they got it, they're just glad they got it.

Ren, that's about the best 10 year old, childlike explanation I can give you. Just keep reading up on it and stay involved with the forums, hopefully more time with our forum here. Any questions?

Thank you for taking the time to explain like you would to a 10 year old.

I do believe I follow you and if I can be frank, I do believe I already knew what you told me. When you say clomiphene would be spinning your wheels, I assume you mean that it does not successfully stimulate your pituitary to produce LH?

For me personally, I know that clomiphene treatment did increase my LH levels in the past (without too much of an increase in free testosterone sadly) and I know with a 99% certainty that I`m secondary. If I understand you correctly with regards to irreversible suppression, that is the case for me as well, since my levels do drop back after stopping clomiphene treatment. Or does it not work for you at all? Is that what you mean by irreversible?

Regards,

Renholder