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Clomid and Nolvadex cause high estrogen.

blackrock

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Why does, clomid and nolvadex taken while on PCT raise your testosterone level to mid normal in 700's but the estrogen goes all the way up to 40's. which is high normal.

I know when I stop SERMS the estrogen will smack the LH and FSH back down... I can take an AI but thats just prolonging the inevitable, eventually I will have to get off the AI as well..
 
serms are completely different from AIs such as dex, letro et. al.

serms do not actually act on aromatase or the creation of estrogen, they keep the estrogen from attaching to estrogen receptors; rendering estrogen, whether it's 60 or 600, nearly useless. It will raise your testosterone, as well, as you can see.

When your testosterone is high, and aromatase is normal, your serum estrogen levels will be high as well.
 
Serms will also read as estrogen on a test giving you a higher than actual reading.
 
This is my problem with most PCT. Stimulating the HPGA with a SERM will lead to artificially high T and E2. E2 is ultimately what is shutting down the HPGA, and all E2 comes from T. SERMs are great for transitioning during periods of estrogen dominance while coming off, but anything beyond that short period is just going to further keep you shut down.

Clomid and it's active metabolites are EXTREMELY long lasting in the body, and I believe that bloodwork done 4-6 weeks after stopping clomid still gives artificially high T levels. I have seen this literally dozens of times and it fits with the research on clomid. I believe this is the main reason people think PCT "works."
 
This is my problem with most PCT. Stimulating the HPGA with a SERM will lead to artificially high T and E2. E2 is ultimately what is shutting down the HPGA, and all E2 comes from T. SERMs are great for transitioning during periods of estrogen dominance while coming off, but anything beyond that short period is just going to further keep you shut down.

Clomid and it's active metabolites are EXTREMELY long lasting in the body, and I believe that bloodwork done 4-6 weeks after stopping clomid still gives artificially high T levels. I have seen this literally dozens of times and it fits with the research on clomid. I believe this is the main reason people think PCT "works."

Are you suggesting not running pct and just keeping estrogen under control with the use of an ai on cycle? On cycle meaning until exogenous T has cleared as wel as any other compounds
 
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Yea the boost in LH -> testosterone results in testosterone aromatizing to estrodiol. Aromasin is brilliant to add to pct for this reason as well as because of the high E2 caused by HCG used in PCT. Other AI's have estrogen rebound but aromasin you can just stop.
 
They are supposed to cause high estrogen. Do you realize they are estrogen pills?
 
Is that a false reading?

Yes when I did clomid therapy (25mg per day for almost a year) I was in the 60-80 range.

doc told me not to worry at least half of the reading was the clomid.
 
This is my problem with most PCT. Stimulating the HPGA with a SERM will lead to artificially high T and E2. E2 is ultimately what is shutting down the HPGA, and all E2 comes from T. SERMs are great for transitioning during periods of estrogen dominance while coming off, but anything beyond that short period is just going to further keep you shut down.

Clomid and it's active metabolites are EXTREMELY long lasting in the body, and I believe that bloodwork done 4-6 weeks after stopping clomid still gives artificially high T levels. I have seen this literally dozens of times and it fits with the research on clomid. I believe this is the main reason people think PCT "works."

Clomids half life is 5 -7 days. it takes 5 half lifes to reach steady state and 5 half lifes to get out of the system generically speaking.


So when do you think would be an appropriate blood test after stopping clomid
 
Are you suggesting not running pct and just keeping estrogen under control with the use of an ai on cycle? On cycle meaning until exogenous T has cleared as wel as any other compounds

PCT has it's place in keeping the effects of E2 at bay while coming off or going into a cruise, but if you really want to stimulate natrual production, you need to reach a state low estradiol ASAP. If testosterone levels are low also, then you can safely remove SERMs and/or AIs without estradiol rebound.

All AIs naturally have rebound, it's a myth that aromasin doesn't.
 
Aromasin has no noticeable rebound when used for a a short period of time like 4 weeks. You can not compare the estradiol rebound of aromasin with letro and adex. If you use it throughout your cycle to lower E2 there is a very mild adjustment period when you come off compared to other AIs. If you haven't tried it in PCT you should.
 
Aromasin has no noticeable rebound when used for a a short period of time like 4 weeks. You can not compare the estradiol rebound of aromasin with letro and adex. If you use it throughout your cycle to lower E2 there is a very mild adjustment period when you come off compared to other AIs. If you haven't tried it in PCT you should.

There wouldn't be a rebound affect if you keep your estrogen in check while administering exogenous testosterone as you finish there wouldn't be extra to aromatize but if you still have high testosterone levels after you discontinue aromasin you will surely have a lot of t aromatizing afterwords. Kal thank you for the response I really think that makes a lot of sense as we know high estrogen levels will continue to keep us suppressed
 
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All AIs naturally have rebound, it's a myth that aromasin doesn't.

Perhaps there is a misunderstanding that comes into play here? Aromasin is a suicide inhibitor, but there are probably other factors that come into play. Is it a safe assumption to say that aromasin has less rebound?

Are there any other tools for transitioning off aromasin during PCT that will minimize the rebound effect?
 
would there be any significant benefits to utilizing Tamoxifen during a heavy cycle of Test Cyp to maximize Testosterone?

This is what I understand of it:
-prevention of gynocomastia
-properly functioning immune system
-lipid profile (both HDL and LDL) improvement
-possibly reduce IGF
 
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would there be any significant benefits to utilizing Tamoxifen during a heavy cycle of Test Cyp to maximize Testosterone?

This is what I understand of it:
-prevention of gynocomastia
-properly functioning immune system
-lipid profile (both HDL and LDL) improvement
-possibly reduce IGF

Nolvadex is not going to lower circulating estrogen but will compete for the receptor stopping gyno. I wouldnt run it during your cycle unless gyno becomes an issue. Just run your ai and have tamox on hand if needed.
 
This is my problem with most PCT. Stimulating the HPGA with a SERM will lead to artificially high T and E2. E2 is ultimately what is shutting down the HPGA, and all E2 comes from T. SERMs are great for transitioning during periods of estrogen dominance while coming off, but anything beyond that short period is just going to further keep you shut down.

Clomid and it's active metabolites are EXTREMELY long lasting in the body, and I believe that bloodwork done 4-6 weeks after stopping clomid still gives artificially high T levels. I have seen this literally dozens of times and it fits with the research on clomid. I believe this is the main reason people think PCT "works."

Not all, there are other extra-gondular sites of estrogen in males.

Have you got evidence Clomid's metabolites still cause ER inhibition after 4-6 weeks? I just done think thats possible.
 
Nolvadex is not going to lower circulating estrogen but will compete for the receptor stopping gyno. I wouldnt run it during your cycle unless gyno becomes an issue. Just run your ai and have tamox on hand if needed.

My two concerns are gyno and cholesterol issue which I have a propensity for both which is why I am running it with.
thoughts? any reason not too?
 
My two concerns are gyno and cholesterol issue which I have a propensity for both which is why I am running it with.
thoughts? any reason not too?

Are you running an AI alongside?
 

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