Enclomiphene (androxal), any experiences?

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Forty2

Active Member
Have not heard of a drop from enclomiphene. And what would be the reason you want to add in clomid? Estrogen too low?
It's common for guys to experience either a slight reduction or no change in libido when taking enclomiphene. Enclomiphene antagonizes the estrogen receptors in the hypothalamus, which can negatively impact libido. The zuclomiphene isomer in clomid, on the other hand, is an estrogen receptor agonist. If the dose of clomd is low enough, it may be possible to achieve enough estrogenic activity in the brain to offset enclomiphene's antagonist effect without experiencing the well known emotional side effects of clomid.
 

mcs

Member
It's common for guys to experience either a slight reduction or no change in libido when taking enclomiphene. Enclomiphene antagonizes the estrogen receptors in the hypothalamus, which can negatively impact libido. The zuclomiphene isomer in clomid, on the other hand, is an estrogen receptor agonist. If the dose of clomd is low enough, it may be possible to achieve enough estrogenic activity in the brain to offset enclomiphene's antagonist effect without experiencing the well known emotional side effects of clomid.
Wouldn't it be more prudent to use something like preg or DHEA to optimize E2 levels and help restore libido? The zuclomiphene isomer has so many other drawbacks I would be concerned about (ocular issues, blood coagulation, etc.).
 

FunkOdyssey

Seeker of Wisdom
It's common for guys to experience either a slight reduction or no change in libido when taking enclomiphene. Enclomiphene antagonizes the estrogen receptors in the hypothalamus, which can negatively impact libido. The zuclomiphene isomer in clomid, on the other hand, is an estrogen receptor agonist. If the dose of clomd is low enough, it may be possible to achieve enough estrogenic activity in the brain to offset enclomiphene's antagonist effect without experiencing the well known emotional side effects of clomid.
I would rather deal with this by taking less enclomiphene, less often, rather than add zuclomiphene to the mix.

I'm going to be experimenting with 6.25 mg EOD, E3D, maybe even more, to see how far the dose interval can be pushed apart while maintaining T above baseline. I think if you have a functional HPTA, it doesn't take much, and you certainly don't need to take it every day. Give those antagonized estrogen receptors a break.

In my opinion, if there is a common theme with how people misuse enclomiphene, it is too much, too often.
 

Forty2

Active Member
I would rather deal with this by taking less enclomiphene, less often, rather than add zuclomiphene to the mix.

I'm going to be experimenting with 6.25 mg EOD, E3D, maybe even more, to see how far the dose interval can be pushed apart while maintaining T above baseline. I think if you have a functional HPTA, it doesn't take much, and you certainly don't need to take it every day. Give those antagonized estrogen receptors a break.

In my opinion, if there is a common theme with how people misuse enclomiphene, it is too much, too often.
I experimented with 12.5mg eod at first and it barely increased my levels and I didn't feel anything from it.
I felt better when I switched to 12.5mg daily and even better when I tried 25mg daily. That dose took my T slightly above the top of the lab reference range. I felt good in all respects apart from a lack of libido.
Clomid gave me a good libido at 12.5mg eod for the first month. After that, the estrogen side effects kicked in. It's hard to find anyone who got any kind of libido boost from enclomiphene monotherapy.
 

mcs

Member
I experimented with 12.5mg eod at first and it barely increased my levels and I didn't feel anything from it.
I felt better when I switched to 12.5mg daily and even better when I tried 25mg daily. That dose took my T slightly above the top of the lab reference range. I felt good in all respects apart from a lack of libido.
Clomid gave me a good libido at 12.5mg eod for the first month. After that, the estrogen side effects kicked in. It's hard to find anyone who got any kind of libido boost from enclomiphene monotherapy.
What were your E2 levels before and after taking both clomid and enclomiphene?
 

FunkOdyssey

Seeker of Wisdom
It's hard to find anyone who got any kind of libido boost from enclomiphene monotherapy.
It's possible some of the reason people are disappointed with enclomiphene is they've been sold a bill of goods about what high testosterone levels are supposed to do to libido. When used as monotherapy for the purpose of increasing testosterone (not PCT), people who are TRT-naive are usually trying it as a first step. Some of those same people will grow disenchanted with enclomiphene when it doesn't fix their libido, hop on TRT, and find that when the honeymoon is over, TRT didn't fix their libido either. They won't discover that until long after they've posted their negative comments about enclomiphene on social media though.

Having testicles in basic working order and having dispelled any illusions about high T turning me into a pornstar, I think I am a good candidate for a real, long-term, honest-to-goodness trial of enclomiphene at this point. I started 6.25 mg daily five days ago.
 

zakindi

New Member
It's possible some of the reason people are disappointed with enclomiphene is they've been sold a bill of goods about what high testosterone levels are supposed to do to libido. When used as monotherapy for the purpose of increasing testosterone (not PCT), people who are TRT-naive are usually trying it as a first step. Some of those same people will grow disenchanted with enclomiphene when it doesn't fix their libido, hop on TRT, and find that when the honeymoon is over, TRT didn't fix their libido either. They won't discover that until long after they've posted their negative comments about enclomiphene on social media though.

Having testicles in basic working order and having dispelled any illusions about high T turning me into a pornstar, I think I am a good candidate for a real, long-term, honest-to-goodness trial of enclomiphene at this point. I started 6.25 mg daily five days ago.
FunkOdyssey, really keen to hear how you are getting on with your low dose enclomiphene trial with a less frequent than a daily schedule. I am looking to do similar and wondering how it's affecting your energy levels and libido. Also if you had an test results that would be interesting.
 

FunkOdyssey

Seeker of Wisdom
FunkOdyssey, really keen to hear how you are getting on with your low dose enclomiphene trial with a less frequent than a daily schedule. I am looking to do similar and wondering how it's affecting your energy levels and libido. Also if you had an test results that would be interesting.
I stopped taking it shortly after that post. I think I was getting headaches or something, not sure. I might restart again later.
 

Soalian

New Member
Dont forget the "H" part of the HPTA. The hypothalamus must also be at least partly functioning. You need to produce both kisspeptin and GnRH for enclomiphene to work as monotherapy.

Kiss->GnRH->LH->T->E2
In the case you have "normal" T levels naturally (well-functioning HPTA) but want to get more intratesticular testosterone production through higher LH synthesis in the pituitary from using enclomiphene in order to block the pituitary estrogen => LH negative feedback,

you'll still be running into the problem of your natural T inhibiting Kisspeptin expression, hence less gnrh synthesized at the hypothalamus, so that the estrogen-blocking activity of the enclomiphene at the pituitary won't matter much, because there will still be not enough gnrh released left to stimulate pituitary LH expression?
 

mcs

Member
I guess my HPTA is functioning after all...

 

Cataceous

Super Moderator
In the case you have "normal" T levels naturally (well-functioning HPTA) but want to get more intratesticular testosterone production through higher LH synthesis in the pituitary from using enclomiphene in order to block the pituitary estrogen => LH negative feedback,

you'll still be running into the problem of your natural T inhibiting Kisspeptin expression, hence less gnrh synthesized at the hypothalamus, so that the estrogen-blocking activity of the enclomiphene at the pituitary won't matter much, because there will still be not enough gnrh released left to stimulate pituitary LH expression?
It's true that negative feedback from testosterone at the hypothalamus can be a new limiting factor for HPTA function after enclomiphene blocks negative feedback from estrogen. However, there are still likely to be decent gains in hormonal production. The usual caveats apply with respect to enclomiphene: it's not a perfectly selective SERM, so there can be unwanted effects.
 

Soalian

New Member
It's true that negative feedback from testosterone at the hypothalamus can be a new limiting factor for HPTA function after enclomiphene blocks negative feedback from estrogen. However, there are still likely to be decent gains in hormonal production. The usual caveats apply with respect to enclomiphene: it's not a perfectly selective SERM, so there can be unwanted effects.
he question I also ponder about Kisspeptin and exogenous test, is at what level do androgens exert negative feedback on hypothalamus gnrh secretion;

if it occurs right at the level of Kisspeptin signaling, then administering exogenous kisspeptin would still lead to gnrh being secreted in the presence of exogenous test.

But I don't really know whether or not that's the case.
 

Cataceous

Super Moderator
he question I also ponder about Kisspeptin and exogenous test, is at what level do androgens exert negative feedback on hypothalamus gnrh secretion;

if it occurs right at the level of Kisspeptin signaling, then administering exogenous kisspeptin would still lead to gnrh being secreted in the presence of exogenous test.

But I don't really know whether or not that's the case.
Based on what I've read I believe this is the case. That is, the negative feedback from androgens and estrogens at the hypothalamus reduces kisspeptin production directly, leading to an indirect effect on GnRH; androgens and estrogens do not directly affect GnRH neurons.
 
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