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Clomid and Nolvadex cause high estrogen.

kubes

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at the moment no...but I have Arimidex on hand
are you saying run them together?

Its important to keep estrogen under control on cycle. tamox is not going to do that so i would run your ai during your cycle and only add in the novadex if needed to fight the gyno.
 

Kaladryn

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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?

You can't assume aromasin would have less rebound, that makes zero sense. We already know that aromatase is replaced very rapidly. Aromasin has a peak activity at 12 hours of 62% E2 blockage and then only 38% after 24 hours. There is no "lingering effect" from destroying aromatase, the body just makes more.

In fact, since hyperactive aromatase is one of the main side effects of AAS, causing the body to upregulate aromatase expression may be the last thing you would want.

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.

You are talking about estrone to estradiol by HSD17B in females? If this occurs in males I was unaware of it. Even estradiol produced by aromatase in fat tissues is from testosterone.

I posted several studies recently on clomid half-life.

http://www.professionalmuscle.com/f...ng-dr-gs-pct-protocol-test-2.html#post1695293
 

Muscleaddict69

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I can speak from my experience which is not just a few cycles. PubMed is not going to give you the answers on this one. I always struggle with fighting off gyno. I get terrible estrogen rebound from letro. But nothing from aromasin, which I've used for pct for quite a while. This is on advice of a doc who has specialised in sports medicine with a master's thesis on steroid use in national level bodybuilding. He himself competed in BB and is an IFBB medical advisor. So that's all I need to know. I'm not the expert. Welcome to PM me if you think I'm talking bull.
 

rutger177

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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."


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.


Utter nonsense! This "estrogen rebound" is nothing more than some 'bro science" term that is meaningless within the scientific literature. It infers what? After removal of an AI, estrogen levels will begin to return dependent on the AI PK/PD.

Your understanding of how SERM"s aid in the restoration of the HPTA during pct is also lacking but that's another topic.
 
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Kaladryn

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Utter nonsense! This "estrogen rebound" is nothing more than some 'bro science" term that is meaningless within the scientific literature. It infers what? After removal of an AI, estrogen levels will begin to return dependent on the AI PK/PD.

Exactly, I only used the term "rebound" because it was being used, the only form of rebound AIs could have is increased aromatase activity, which does happen with long term AI use.

Your understanding of how SERM"s aid in the restoration of the HPTA during pct is also lacking but that's another topic.

Please elaborate, it seems very simple and straight forward to me.
 
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Matsuo Munefusa

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The "rebound" Kaladryn is speaking of is up-regulation of the production of the enzyme aromatase (the enzyme that converts testosterone to estrogen). The body is seeking to stabilize at a homeostasis with testosterone/estrogen, so if you start blocking aromatase, then the body will produce more aromatase to stabilize itself. The problem then becomes that AI dosages must be titrated over years because of this (ask specialized HRT doctors) and also for bodybuilding purposes when the AI therapy is cessated then with the increased levels of aromatase the bodybuilder is very likely to fall into an estrogen dominant environment.

It is one reason why Dr John Crisler tries to keep his patients off of AIs and seeks to stabilize their estrogen levels by controlling their testosterone levels (by more or less testosterone per injection).

This is my basic understanding - correct me if I am wrong.
 

chinaboy

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So what is better to take during cycle, aromasin or arimidex? Mimimal dose of either i take it. And then for pct, clomid 50/50/25? And then nolvadex on hand if needed. But does nolvadex help for pct?

I always did arimidex during cycle. Yet sometimes tapered off during cycle. And then clomid for pct. I may have added some nolvadex in pct a few times. This always worked for me.
 

Matsuo Munefusa

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Hard to say what is "better" since we do not know your goals, stats, plans, etc.

"Better" for me is taking enough testosterone and HCG (150mg/week test and 100ug/day HCG) that puts my test/estrogen levels in a range I like without having to use an aromatase inhibitor at all.

"Better" is too subjective without going in depth on your personal background.
 

rutger177

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Exactly, I only used the term "rebound" because it was being used, the only form of rebound AIs could have is increased aromatase activity, which does happen with long term AI use.



You are translating the reversible AI feedback on aromatase protein levels to be present after withdrawal of the AI, thus leading to more enzyme leading to more E2. That idea is only accepted in the bro lore - the scientific evidence has NOT shown it occurs.

[Note: For the irreversible AI's, there appears to be NO positive feedback on enzyme levels.]

Below is a table from a study done to determine the effect AI's have on bone mineral density, however, estrogen levels were deemed necessary because of the influence estrogen has on bone density. Changes in the concentrations of estrogens were assessed after daily administration of exemestane (25 mg), letrozole (2.5 mg), anastrozole (1 mg), or placebo for 24 weeks It shows NO "estrogen rebound" after AI withdrawal.


I appologize for the confusing nature of the table. I cut & pasted from a pdf. I only highlighted the results for exemestane in red (for E1 and E2) to make it easier to read but you'll get the idea.


Effects of steroidal and nonsteroidal arom... [Breast Cancer Res. 2007] - PubMed - NCBI


Table 4
Median values and median percentage change from baseline for plasma concentrations of estrogens (mITT population)
Estrogen Exemestane (n = 20) Letrozole (n = 20) Anastrozole (n = 18) Placebo (n = 20)
E1
Baseline, median (min., max.) 31 (11, 72) 28 (13, 51) 29 (14, 61) 26 (9.9, 61)
Week 12, median (min., max.) 2.0 (1.8, 10) 1.8 (1.8, 20) 1.8 (1.8, 84) 31 (8.4, 58)
% baseline, median (95% CI*) 7.8 (6.9, 9.3) 6.6 (5.5, 8.1) 7.6 (6.4, 11) 101 (89, 110)
Week 24, median (min., max.) 1.8 (1.8, 63) 1.8 (1.8, 33) 1.8 (1.8, 44) 26 (7.2, 56)
% baseline, median (95% CI) 6.7 (5.3, 8.6) 6.6 (5.1, 8.1) 7.9 (7.1, 11) 94 (76, 108)
Week 36, median (min., max.) 23 (10, 62) 19 (10, 44) 25 (8.4, 158) 22 (13, 46)
% baseline, median (95% CI) 72 (63, 86) 76 (61, 93) 70 (66, 121) 89 (72, 95)
E2
Baseline, median (min., max.) 4.4 (1.1, 13) 4.2 (1.8, 8.6) 3.8 (1.9, 32) 3.9 (1.9, 8.8)
Week 12, median (min., max.) 0.70 (0.70, 2.5) 0.70 (0.70, 2.7) 0.70 (0.70, 104) 3.8 (1.6, 15)
% baseline, median (95% CI) 18 (14, 22) 19 (14, 24) 20 (18, 31) 102 (87, 115)
Week 24, median (min., max.) 0.70 (0.70, 29) 0.70 (0.70, 7.3) 0.72 (0.70, 84) 4.4 (1.9, 12)
% baseline, median (95% CI) 19 (13, 22) 18 (13, 24) 22 (19, 31) 128 (95, 139)
Week 36, median (min., max.) 4.5 (1.6, 36) 4.2 (1.9, 15) 4.2 (1.4, 136) 4.0 (1.6, 11)
% baseline, median (95% CI) 103 (89, 134) 109 (81, 119) 106 (92, 130) 105 (90, 130)
E1S
Baseline, median (min., max.) 192 (58, 757) 193 (79, 1075) 202 (64, 896) 200 (62, 1156)
Week 12, median (min., max.) 13 (8.7, 246) 8.7 (6.0, 62) 15 (6.6, 3260) 209 (58, 876)
% baseline, median (95% CI) 9.1 (6.1, 11) 4.5 (3.3, 6.0) 11 (6.7, 13) 110 (91, 146)
Week 24, median (min., max.) 16 (6.1, 839) 10 (6.0, 254) 18 (8.8, 1440) 195 (64, 802)
% baseline, median (95% CI) 11 (7.2, 13) 4.7 (3.0, 7.2) 10 (8.6, 20) 105 (69, 123)
Week 36, median (min., max.) 223 (7.4, 2100) 222 (115, 932) 296 (58, 4890) 205 (68, 864)
% baseline, median (95% CI) 114 (90, 152) 121 (105, 135) 131 (109, 147) 125 (91, 143)
*95% CI, bias-corrected and adjusted 95% bootstrap CI for median.
CI, confidence interval; E1, estrone; E1S, estrone sulfate; E2, estradiol; max; min; mITT, modified intent to treat.
 
Last edited:

Kaladryn

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You are translating the reversible AI feedback on aromatase protein levels to be present after withdrawal of the AI, thus leading to more enzyme leading to more E2. That idea is only accepted in the bro lore - the scientific evidence has NOT shown it occurs.

[Note: For the irreversible AI's, there appears to be NO positive feedback on enzyme levels.]

Below is a table from a study done to determine the effect AI's have on bone mineral density, however, estrogen levels were deemed necessary because of the influence estrogen has on bone density. Changes in the concentrations of estrogens were assessed after daily administration of exemestane (25 mg), letrozole (2.5 mg), anastrozole (1 mg), or placebo for 24 weeks It shows NO "estrogen rebound" after AI withdrawal.


I appologize for the confusing nature of the table. I cut & pasted from a pdf. I only highlighted the results for exemestane in red (for E1 and E2) to make it easier to read but you'll get the idea.


Effects of steroidal and nonsteroidal arom... [Breast Cancer Res. 2007] - PubMed - NCBI


Table 4
Median values and median percentage change from baseline for plasma concentrations of estrogens (mITT population)
Estrogen Exemestane (n = 20) Letrozole (n = 20) Anastrozole (n = 18) Placebo (n = 20)
E1
Baseline, median (min., max.) 31 (11, 72) 28 (13, 51) 29 (14, 61) 26 (9.9, 61)
Week 12, median (min., max.) 2.0 (1.8, 10) 1.8 (1.8, 20) 1.8 (1.8, 84) 31 (8.4, 58)
% baseline, median (95% CI*) 7.8 (6.9, 9.3) 6.6 (5.5, 8.1) 7.6 (6.4, 11) 101 (89, 110)
Week 24, median (min., max.) 1.8 (1.8, 63) 1.8 (1.8, 33) 1.8 (1.8, 44) 26 (7.2, 56)
% baseline, median (95% CI) 6.7 (5.3, 8.6) 6.6 (5.1, 8.1) 7.9 (7.1, 11) 94 (76, 108)
Week 36, median (min., max.) 23 (10, 62) 19 (10, 44) 25 (8.4, 158) 22 (13, 46)
% baseline, median (95% CI) 72 (63, 86) 76 (61, 93) 70 (66, 121) 89 (72, 95)
E2
Baseline, median (min., max.) 4.4 (1.1, 13) 4.2 (1.8, 8.6) 3.8 (1.9, 32) 3.9 (1.9, 8.8)
Week 12, median (min., max.) 0.70 (0.70, 2.5) 0.70 (0.70, 2.7) 0.70 (0.70, 104) 3.8 (1.6, 15)
% baseline, median (95% CI) 18 (14, 22) 19 (14, 24) 20 (18, 31) 102 (87, 115)
Week 24, median (min., max.) 0.70 (0.70, 29) 0.70 (0.70, 7.3) 0.72 (0.70, 84) 4.4 (1.9, 12)
% baseline, median (95% CI) 19 (13, 22) 18 (13, 24) 22 (19, 31) 128 (95, 139)
Week 36, median (min., max.) 4.5 (1.6, 36) 4.2 (1.9, 15) 4.2 (1.4, 136) 4.0 (1.6, 11)
% baseline, median (95% CI) 103 (89, 134) 109 (81, 119) 106 (92, 130) 105 (90, 130)
E1S
Baseline, median (min., max.) 192 (58, 757) 193 (79, 1075) 202 (64, 896) 200 (62, 1156)
Week 12, median (min., max.) 13 (8.7, 246) 8.7 (6.0, 62) 15 (6.6, 3260) 209 (58, 876)
% baseline, median (95% CI) 9.1 (6.1, 11) 4.5 (3.3, 6.0) 11 (6.7, 13) 110 (91, 146)
Week 24, median (min., max.) 16 (6.1, 839) 10 (6.0, 254) 18 (8.8, 1440) 195 (64, 802)
% baseline, median (95% CI) 11 (7.2, 13) 4.7 (3.0, 7.2) 10 (8.6, 20) 105 (69, 123)
Week 36, median (min., max.) 223 (7.4, 2100) 222 (115, 932) 296 (58, 4890) 205 (68, 864)
% baseline, median (95% CI) 114 (90, 152) 121 (105, 135) 131 (109, 147) 125 (91, 143)
*95% CI, bias-corrected and adjusted 95% bootstrap CI for median.
CI, confidence interval; E1, estrone; E1S, estrone sulfate; E2, estradiol; max; min; mITT, modified intent to treat.

The study above is done on post-menopausal women who have extremely low amounts of aromatase (ovarian aromatase makes up the majority of aromatase activity in pre-menopausal women). But more importantly, E2 is not a negative feedback mechanism for testosterone in women. In men, taking an AI stimulates testosterone production, which then leads to high estradiol levels, even if aromatase activity remains the same.

In the clinical setting, patients on HRT and using an AI require increasing amounts of AI over time. This could be because of other factors, such as metabolism of the AI, etc, but it does happen.

There is also no doubt that long term AAS use causes an increase in aromatase activity...
 

rutger177

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T

In the clinical setting, patients on HRT and using an AI require increasing amounts of AI over time. This could be because of other factors, such as metabolism of the AI, etc, but it does happen.

Let's see your evidence.
 
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