Clomid for Low Test

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Mfri225

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Just got prescribed Clomid for 4 weeks. I am taking it to raise my test. Does anyone have experience with taking clomid alone and no prior history of anabolics?
 
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Does anyone have experience with taking clomid alone and no prior history of anabolics?
Clomid isn't a long term solution and can have some pretty bad side effects. It also may boost your hormones but you may not feel much different than pre-treatment. Clomid blocks estrogen in various tissues and organs throughout the body because the synthetic estrogen competes, binds to the estrogen receptor.

Clomid side effects:

  • Mood swings, psychological / emotional side effects
  • Hot flashes
  • Visual disturbances
  • Nausea
 
Clomid is a polarizing topic. It seems that there are haters and lovers. I'm a lover. Started out with clomid for eight weeks then switched to enclomiphene. This has been my protocol for a year now. note: I also take hcg. The exact protocol is in my signature. I'm doing great and feel great. No "other organ" issues as of yet and frankly I've not seen research on humans that indicate any significant risk.
All medications have side effect risks and each individual has individual responses to them. So, clomid or Test, it all comes with risk. Take labs at regular intervals.
 
There are countless anecdotes, scientific research, etc, stating clomid is safe an effective in some cases to raise testosterone. As with any medications, it may cause side effects in some people. I've never been on clomid but I have been on enclomiphene for more than 6 months. Testosterone raised to 1100 ng/dL, no side effects, subjectively symptoms did not improve to the level I expected. By that was me, there are other people who have been on clomid for years a love it. Other's complain of eye floaters, getting emotional, feeling bloated, etc.

The same happens with TRT regardless of the method. If you search this forum, you'll see people quitting TRT after 1 year, 2 years, 4 years, etc. Some people complain of high blood pressure, decreased orgasm, etc. Others are pretty dialed in and love it. There's no single solution for everyone. You won't know until you try it (under medical supervision).

I think it's irresponsible to issue one-size-fits-all answers, particularly when new members come asking for help. Maybe it's just me, but one of the benefits I get from this forum is education. One line ideological zingers do not contribute to that.

Regarding to whether enclomiphene binds to multiple receptors in different organs, I'm still waiting for evidence to be provided to backup this statement, which I'd love to see. So far the literature I've reviewed claims it binds to ER receptors in the hypothalamus and pituitary. Some suspect it binds antagonistically to ER receptors in the breast tissue, and some theorize it must bind to ER receptors in the liver because enclomiphene tends to decrease IGF-1, but as far as I understand, it's just a hypothesis.

Take my advice: don't take advice from me.
 
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Regarding to whether enclomiphene binds to multiple receptors in different organs, I'm still waiting for evidence to be provided to backup this statement, which I'd love to see. So far the literature I've reviewed claims it binds to ER receptors in the hypothalamus and pituitary. Some suspect it binds antagonistically to ER receptors in the breast tissue, and some theorize it must bind to ER receptors in the liver because enclomiphene tends to decrease IGF-1, but as far as I understand, it's just a hypothesis.
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The question here is, who has the burden of proof? Usually with drugs we're expecting the promoter to prove safety and efficacy. It's true that clomiphene has been around a long time, but long-term usage seems to be a more recent thing. We can hope that the lack of acute side effects is reflective of overall safety. Nonetheless, in taking enclomiphene I'd feel more comfortable if the interactions with the non-HPTA estrogen receptors were better characterized.
 
The question here is, who has the burden of proof? Usually with drugs we're expecting the promoter to prove safety and efficacy. It's true that clomiphene has been around a long time, but long-term usage seems to be a more recent thing. We can hope that the lack of acute side effects is reflective of overall safety. Nonetheless, in taking enclomiphene I'd feel more comfortable if the interactions with the non-HPTA estrogen receptors were better characterized.
Couldn't agree more. I've searched as more as I could and cannot find any serious references to binding to ER receptors outside HP, and I would definitely feel more comfortable if I knew what happens as that would help me predict potential side effects, and explain why in some people, even though enclomiphene significantly raises endogenous testosterone in a relatively normal way, (which I'd expect keep other hormones "proportional", as opposed to "shutting down" anything) fails to improve some of the symptoms people seek help for.
 
One thing I found with my short stint of Clomid is that taking 12.5 mg 3x a week gave me the same testosterone results as taking 25 mg per week with lower estrogen. I probably should have taken it longer to see if it worked but was eager to get on enanthate injections with hcg after a horrific experience enduring elevated E2.

it definetely raised by testosterone hugely when I started the therapy, remember feeling unstoppable, building mass, sudden morning erections, before it all unwinded and went to the pits due to estrogen spiking to unreal amounts along with lh/fsh.

Lower dosing Clomid (12.5 3x weekly) was clearly the right answer but my doctor had initially prescribed 50 mg per day if I remember.
 
I started on Clomid and did fairly well on it for the first year or so with no prior anabolic experience. I strongly suggest starting at a low dose, 12mg every other day, because due to the long half-life, you pretty much have to come off for a month or so and restart at a lower dose if you want to lower the dose.
 
A problem I see across forums regarding Clomid is people will say their “numbers were perfect, but got no symptom relief” but don’t post their lab results.

They might mention that their TT shot up to 700 but they don’t post their estradiol results, meaning their lack of symptom relief could have resulted from high E2 and not Clomid itself per se. I’m actually not sure how many posts I’ve seen where people have actually posted “perfect” numbers (ie: 600 TT and 30 E2 or something like that) but still report no symptom relief.

Have people actually seen cases where people have truly “perfect” labs and still have not reported symptom relief?

@Cataceous. Would love to know if you’ve seen such scenarios.
 
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Have people actually seen cases where people have truly “perfect” labs and still have not reported symptom relief?

@Cataceous. Would love to know if you’ve seen such scenarios.
There have been some pretty credible reports like this. The more I think about clomiphene in particular, the less surprised I am about its low success rate. With it one is taking a pretty strong estrogen—zuclomiphene—combined with a strong anti-estrogen—enclomiphene. These have different relative strengths at different estrogen receptors. In addition there's usually more estradiol created due to both the higher LH and the higher endogenous testosterone. With all this jumbled together, how likely is it to achieve a reasonable balance of androgenicity and estrogenicity in the tissues that matter?
 
Clomid is a polarizing topic. It seems that there are haters and lovers. I'm a lover. Started out with clomid for eight weeks then switched to enclomiphene. This has been my protocol for a year now. note: I also take hcg. The exact protocol is in my signature. I'm doing great and feel great. No "other organ" issues as of yet and frankly I've not seen research on humans that indicate any significant risk.
All medications have side effect risks and each individual has individual responses to them. So, clomid or Test, it all comes with risk. Take labs at regular intervals.
Would it be more accurate to say you are a lover of enclomiphene citrate, not clomiphene citrate? These are very different drugs. The OP has been prescribed Clomid which has the Zuclomiphene component that may cause many of the issues most men complain about.

I am curious to know if you have had recent labs done to see where your gonadotropin levels are, given you are also on hCG?
 
Would it be more accurate to say you are a lover of enclomiphene citrate, not clomiphene citrate? These are very different drugs. The OP has been prescribed Clomid which has the Zuclomiphene component that may cause many of the issues most men complain about.

I am curious to know if you have had recent labs done to see where your gonadotropin levels are, given you are also on hCG?
Half my labs are complete and I have more in the morning then I meet with my men's health clinic Friday. Last July I had requested the clinic switch me off clomid to enclomiphene. I'll post the complete labs after the all come in.

NOTE: correction - that was last April not July.
 
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Would it be more accurate to say you are a lover of enclomiphene citrate, not clomiphene citrate? These are very different drugs. The OP has been prescribed Clomid which has the Zuclomiphene component that may cause many of the issues most men complain about.

I am curious to know if you have had recent labs done to see where your gonadotropin levels are, given you are also on hCG?
I view enclomiphene as the lesser evil. Still, there may be a few cases where guys with low natural estrogenic activity would do better with clomiphene. The question is whether enclomiphene alone can be too antagonistic of the non-targeted estrogen receptors. I don't like this lack of understanding about something I'm taking long-term. If I didn't have good subjective results I would be looking harder for an alternative.

I phased out hCG early on when I found LH rising into the reference range. I haven't tested the gonadotropins recently, but I expect they are still hovering at the low ends of their ranges.
 
The question is whether enclomiphene alone can be too antagonistic of the non-targeted estrogen receptors. I don't like this lack of understanding about something I'm taking long-term.
I, too, would like some answers to these questions. I'm upon my annual review with labs and would like a better understanding of the mechanisms. At 64, I have a rapidly closing window for establishing vital mental and physical health. From there, it's living off the foundations until the end of life.
 
A problem I see across forums regarding Clomid is people will say their “numbers were perfect, but got no symptom relief” but don’t post their lab results.

They might mention that their TT shot up to 700 but they don’t post their estradiol results, meaning their lack of symptom relief could have resulted from high E2 and not Clomid itself per se. I’m actually not sure how many posts I’ve seen where people have actually posted “perfect” numbers (ie: 600 TT and 30 E2 or something like that) but still report no symptom relief.

Have people actually seen cases where people have truly “perfect” labs and still have not reported symptom relief?

@Cataceous. Would love to know if you’ve seen such scenarios.
There have been some pretty credible reports like this. The more I think about clomiphene in particular, the less surprised I am about its low success rate. With it one is taking a pretty strong estrogen—zuclomiphene—combined with a strong anti-estrogen—enclomiphene. These have different relative strengths at different estrogen receptors. In addition there's usually more estradiol created due to both the higher LH and the higher endogenous testosterone. With all this jumbled together, how likely is it to achieve a reasonable balance of androgenicity and estrogenicity in the tissues that matter?
You’ve seen cases where people had good numbers (and not just reported that they had good numbers) and they didn’t feel any better?
 
You’ve seen cases where people had good numbers (and not just reported that they had good numbers) and they didn’t feel any better?
Yes, at least with respect to testosterone and estradiol and their free levels. The situation with enclomiphene may not be so different. The FDA told Repros Therapeutics that their Phase 3 clinical trials didn't demonstrate clinical benefit, in spite of nice looking numbers. Repros gave up rather than try to demonstrate such benefit.
 
Yes, at least with respect to testosterone and estradiol and their free levels. The situation with enclomiphene may not be so different. The FDA told Repros Therapeutics that their Phase 3 clinical trials didn't demonstrate clinical benefit, in spite of nice looking numbers. Repros gave up rather than try to demonstrate such benefit.
Presumably because Repros wasn’t confident in their ability to show symptomatic benefit?

Do we know for sure that’s the reason Repros gave up?
 
Beyond Testosterone Book by Nelson Vergel
This is what I can tell based on a single anecdote (me) and 1 year of almost continuous enclomiphene citrate usage:
- Total Testosterone goes up like crazy (using 12.5mg 3 times a week it goes from 300 to 700)
- Estradiol doesn't go up if normal, goes down if high
- SHBG increases about 10 mol/L (57nmol/L)
- Free testosterone decreases to bottom of normal range
- LH and FSH goes to the top of the range, or higher
- T/E2 ratio = 27

If I take EC 7 days a week, the effects above are magnified.
- Total T goes to 1100,
- LH and FSH to 20.
- No values for SHBG.
- Estradiol remains in the 20s.
- T/E ratio = 35

Combining EC and HCG (250 IU) 3 times a week, the effects of EC are modulated
- Total testosterone goes up to 900
- Estradiol goes up to normal/high (high 40s low 50s)
- SHBG goes down to normal values (low 40s for me )
- Free testosterone increases to optimal levels
- Don't have data on LH and FSH but would assume it remain at the same level or lower than EC only.
- T/E2 ratio = 17

Subjectively, not much difference between the three options, though I seem to lean towards EC/HCG, don't ask me why (I don't know)

My next experiment is to maintain HCG at 250 IU 3 times a week and lower EC to twice a week.

For reference, never done TRT, PCT, steroids or PED, so I can't compare.

In all cases Albumin, HCT and HGB are all completely normal.
 
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