Clomid & Testosterone: Why they don't work together - By Mike Gaiso

[JasonLu]

Very good explanation for us "lay" people.
Clear and concise.

Exactly!!!!! I agree

 

[Disco41]

SERMs work differently than hCG.During a PCT,they shouldnt be used simultaneously.SERMs lower E2 and trigger GnRH to produce LH.On the contrary,hCG peptide is a gonadotropin itself,thus it inhibits GnRH.It acts as LH analoge (LHRH) and supports testosterone production in Leyding cells.HCG supports testicular atrophy during TRT.

Does Clomid lower E2?

 

[Jame51]

ive read something about it causing nightblindness or something long term. sounds scary to use clomid long term.

 

[GEORGE TOULIATOS]

Does Clomid lower E2?

Yes,the anti-estrogenic half of it

 

[GEORGE TOULIATOS]

http://gtoul.com/pct-post-cycle-therapy/

http://gtoul.com/suppression-of-the-pituitary-hypothalamic-testicular-axis-as-a-result-of-aas-abuse/

These links will lighten up

 

[Jahshines]

Discovery, are you taking anything to help with estrogen levels or are you taking only testosterone?

Is it possible that the weak anti-E action of clomid simply brought E2 levels down enough to fire up your libido?

 

[Dakeri]

I need to see if I can find the studies again, but I *believe* the studies that showed long-term suppression with HCH were using doses much larger than what is normal with TRT. I could be incorrect, but that is what I recall, anyway.

Clomid can cause eyesight issues - floaters, etc...but I believe that is also with larger than usual dosages.

do you know for sure if the floaters is due to large doses andnot all doses?

 

[dooger]

I kept having hot flashes and learned that LH might be an important part to it. Since estrogen was fine. HCG did the trick. I take 100mg testosterone a week and my doctor suggested to just add Clomid. I asked do you think it will work? He said I don't see why it wouldn't. Starting out my LH was 0.2 IU/ml. After taking Clomid 25mg a day my LH is 1.4 IU/ml. The range is 1.7 to 8.6. So, I am not over the minimum, but I am sure higher than what I started at. My testicles haven't shrunk up and I don't get hot flashes or sweat anymore. I am thinking about trying 25mg every 3 days and seeing if I can get by with that.

 

[Ronnny]

Starting out my LH was 0.2 IU/ml. After taking Clomid 25mg a day my LH is 1.4 IU/ml.

Your LH is still low. How many days or weeks you had taken Clomid before doing the last test?

 

[dooger]

Your LH is still low. How many days or weeks you had taken Clomid before doing the last test?

Been taking the Clomid probably at least 6 months. Then did the blood test. So it probably won't get any higher. But it's enough to keep my side effects away.

 

[Ronnny]

Then did the blood test. So it probably won't get any higher. But it's enough to keep my side effects away.

are you taking only Clomid now or taking Testosterone also?

 

[dooger]

Then did the blood test. So it probably won't get any higher. But it's enough to keep my side effects away.

are you taking only Clomid now or taking Testosterone also?

Taking both. That 1.4 IU/ml is with testosterone and clomid combined

 

[Ronnny]

Taking both. That 1.4 IU/ml is with testosterone and clomid combined

Ok. That is why your LH is low since you are taking Testosterone. I thought you were on Clomid only.

 

[dooger]

Ok. That is why your LH is low since you are taking Testosterone. I thought you were on Clomid only.

Yeah, both. So, it does seem to work to a certain extent but won't get you way up there. I guess if you took a whole bunch of it. If you take more than 100mg of testosterone probably wouldn't help either. But for me, it stops shrinkage and the hot flashes. I just worry about the long-term effects of using a pill designed for a woman. But I like making my own LH.

 

[Vestpocket]

I hate to chime in on this, given that I respect many of the posters and knowledge they provide, but there is a great deal of misinformation presented here.

Thermostat clicks ON = When the hypothalamus (H) senses that estrogen (E) is too low, it releases Gonadotropin-releasing hormone (GnRH), which tells the pituitary (P) to release luteinizing hormone (LH), which in turn tells the testes to make Testosterone. Some of this Testosterone will be aroamatased into estrogen and dihydrotestosterone (DHT).

This is misleading. If the thermostat clicks on when estrogen (E) is too low, then men with an androgen deficiency would, from concomitant low estradiol, experience an elevated LH pulse. The mistake here is that the "thermostat clicks on" in eugonadal men only. With secondary hypogonadism, where clomiphene citrate is normally indicated, the level of E deficiency required to "click on the thermostat" is substantially reduced and irregular. The thermostat is NOT operating properly. If it were working properly, there wouldn't be secondary hypogonadism in the first place.

Thermostat clicks OFF = When Estrogen levels are adequate, the Hypothalamus stops releasing GnRH. This means that nothing is telling the pituitary to release LH. That in turn, means nothing is telling the testes to make Testosterone.

Except, with secondary hypogonadism, T and E2 levels are already inadequate and yet the thermostat is already "off." Again, the thermostat is broken. We have to virtually starve it of E2 to get it to work properly.

What happens when you take Clomid while on an APPROPRIATE AMOUNT of testosterone? Well, I left something very important out in my thermostat analogy. You see, the Hypothalamus senses androgen's as well as estrogen. So when you are on TRT, the exogenous testosterone shut the HTPA. So, properly-dosed TRT causes the thermostat to be stuck in the OFF position.

The action of testosterone on the hypothalamus is mostly indirect, versus direct AR stimulation, and vastly, vastly less than the inhibitory effect of E2. In fact, T mostly affects the pulse frequency of LH and does not significantly attenuate the pulse amplitude. E2, however, affects amplitude. Regardless, per studies, it requires BOTH E2 and T to be sufficient to cause feedback. E2 insufficiency will still amplify the LH pulse even when T is normalized. In fact, that's why men on Clomid can have normal LH along with normal T and E.

Take all the Clomid you want, the HTPA will not respond because it is suppressed by the exogenous testosterone. Sure Clomid will still blind the hypothalamus to your estrogen. However, in this case It won’t matter; HTPA is shutdown.

This is false. Normal testosterone levels alone will not suppress the HPTA when E2 is blocked from inhibiting the LH pulse hypothalamus. Clomid will succeed in convincing the hypothalamus of an imbalance and LH will increase.

It will only increase marginally, however, because the LH will cause T/E2 to increase to the point of actual hypothalamic suppression. You'll hit a wall.

So, what actually interrupts the MoA of of Clomid? Extremely elevated androgens (steroids/supraphysiological FT) or significantly elevated free estradiol.

Normal T will NOT suppress LH without E2 also being normal, and in such a case — Clomid will always falsify E2 to the hypothalamus and cause it to panic.

I have the labs to prove it, because I have used this combination myself. Apparently, so have other people in this thread. LH does return, but not fully.

I don't know why this myth persists. It requires a severely fundamental misunderstanding of the HPTA.

 

[Vince]

I hate to chime in on this, given that I respect many of the posters and knowledge they provide, but there is a great deal of misinformation presented here.



This is misleading. If the thermostat clicks on when estrogen (E) is too low, then men with an androgen deficiency would, from concomitant low estradiol, experience an elevated LH pulse. The mistake here is that the "thermostat clicks on" in eugonadal men only. With secondary hypogonadism, where clomiphene citrate is normally indicated, the level of E deficiency required to "click on the thermostat" is substantially reduced and irregular. The thermostat is NOT operating properly. If it were working properly, there wouldn't be secondary hypogonadism in the first place.



Except, with secondary hypogonadism, T and E2 levels are already inadequate and yet the thermostat is already "off." Again, the thermostat is broken. We have to virtually starve it of E2 to get it to work properly.



The action of testosterone on the hypothalamus is mostly indirect, versus direct AR stimulation, and vastly, vastly less than the inhibitory effect of E2. In fact, T mostly affects the pulse frequency of LH and does not significantly attenuate the pulse amplitude. E2, however, affects amplitude. Regardless, per studies, it requires BOTH E2 and T to be sufficient to cause feedback. E2 insufficiency will still amplify the LH pulse even when T is normalized. In fact, that's why men on Clomid can have normal LH along with normal T and E.



This is false. Normal testosterone levels alone will not suppress the HPTA when E2 is blocked from inhibiting the LH pulse hypothalamus. Clomid will succeed in convincing the hypothalamus of an imbalance and LH will increase.

It will only increase marginally, however, because the LH will cause T/E2 to increase to the point of actual hypothalamic suppression. You'll hit a wall.

So, what actually interrupts the MoA of of Clomid? Extremely elevated androgens (steroids/supraphysiological FT) or significantly elevated free estradiol.

Normal T will NOT suppress LH without E2 also being normal, and in such a case — Clomid will always falsify E2 to the hypothalamus and cause it to panic.

I have the labs to prove it, because I have used this combination myself. Apparently, so have other people in this thread. LH does return, but not fully.

I don't know why this myth persists. It requires a severely fundamental misunderstanding of the HPTA.

I would be very interested in seeing your protocol and labs. If you're not comfortable posting them, could you at least PM them to me.

 

[Woolnemis]

This is interesting, I have been on TRT for several years, and on Clomid for a year now. What I did see within a month or two was the return of normal size testes. I also noted when my Testosterone cycle is at it end I still have some remaining T. Pre Clomid I did not and would be less than 100 (I was on shots first one per two weeks, than Testopel 12 pellets every 3 months, now I am taking shots every 3 days, but when on Testopel I saw the levels hold in the 300 range. not good, but better than sub 100. I saw this as a sign my Testes were also working again. Again I am not a medical person, but I recognize the changes in my own body. Tire Reviews | TireReviews.co

Hi, I administered Clomid for some months but them quit. I have read much info about it so it has some side effects also. We were so desperate for our second baby, but now I don't use anything I just hope the God will help us. In case you can advise me with some other fertility drugs, please put down for me. Thank you

 

[xqfq]

I was reading about DHT’s effect on estrogen / estrogen receptors and I discovered something extremely interesting.

DHT has a metabolite, 3β-androstanediol, which may be how testosterone suppresses the hypothalamus. It does not look like testosterone itself suppresses the hypothalamus, but I am not sure:

A Role for the Androgen Metabolite, 5α-Androstane-3β,17β-Diol, in Modulating Oestrogen Receptor β-Mediated Regulation of Hormonal Stress Reactivity

An alternate pathway for androgen regulation of brain function: Activation of estrogen receptor beta by the metabolite of dihydrotestosterone, 5α-androstane 3β, 17β diol

So if this were true, some men may be able to use Clomid alongside TRT if their DHT was low.

It might also somehow be possible to fully suppress DHT using e.g. dutasteride to allow Clomid to work concurrently with TRT if this is true. Of course, I am not saying it’s a good idea for someone to take dutasteride; it’s just a hypothesis.

For me, I noticed Raloxifene concurrently with 154mg/week test-e made my testicles larger and improved my ejaculation. But I don’t have any data besides my own recollection / experience, which could be wrong. I also take finasteride and have for years.

 

[Cataceous]

I was reading about DHT’s effect on estrogen / estrogen receptors and I discovered something extremely interesting.

DHT has a metabolite, 3β-androstanediol, which may be how testosterone suppresses the hypothalamus. It does not look like testosterone itself suppresses the hypothalamus, but I am not sure:
...

Interesting information. If I'm remembering correctly, there is some evidence that testosterone has a suppressive effect independent of the conversion to estradiol. A little tangential, but I'm wondering if DHT derivatives, e.g. mesterolone (Proviron) or drostanolone (Masteron), produce this metabolite?

Some other tidbits from the Wiki article: 3β-androstanediol is described as an estrogen, which seems odd given that DHT itself is not considered estrogenic in any respect. 3β-androstanediol is also formed via 5α-reduction of DHEA, so if you're low in the 5α-reductase enzymes then there's a double-whammy reducing this metabolite. It has some nice effects: "Through the ERβ, 3β-diol positively regulates oxytocin neurons and signaling in the paraventricular nucleus of hypothalamus (PVN), and has been found to have antidepressant, anxiolytic, cognitive-enhancing, and stress-relieving effects via this action."

Normal levels in men are 239 ± 76 pg/ml, around ten times the level of estradiol. This seems significant because 3β-androstanediol "has approximately 3% and 7% of the affinity of estradiol at the ERα and ERβ, respectively." Would it be correct to say then that this metabolite has almost equal influence on ERβ compared to estradiol?

 

[xqfq]

Interesting information. If I'm remembering correctly, there is some evidence that testosterone has a suppressive effect independent of the conversion to estradiol. A little tangential, but I'm wondering if DHT derivatives, e.g. mesterolone (Proviron) or drostanolone (Masteron), produce this metabolite?

Some other tidbits from the Wiki article: 3β-androstanediol is described as an estrogen, which seems odd given that DHT itself is not considered estrogenic in any respect. 3β-androstanediol is also formed via 5α-reduction of DHEA, so if you're low in the 5α-reductase enzymes then there's a double-whammy reducing this metabolite. It has some nice effects: "Through the ERβ, 3β-diol positively regulates oxytocin neurons and signaling in the paraventricular nucleus of hypothalamus (PVN), and has been found to have antidepressant, anxiolytic, cognitive-enhancing, and stress-relieving effects via this action."

Normal levels in men are 239 ± 76 pg/ml, around ten times the level of estradiol. This seems significant because 3β-androstanediol "has approximately 3% and 7% of the affinity of estradiol at the ERα and ERβ, respectively." Would it be correct to say then that this metabolite has almost equal influence on ERβ compared to estradiol?

I think you’d need to know its binding affinity to SHBG to be able to guess at that. E.g. if it had very high SHBG affinity (much more than estradiol), then it’s less likely to have more free molecules. I wasn’t able to figure it out with a quick search.