Tamoxifen is not necessary for PCT

CatSnake

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[SIZE=3

Question: Do you know if you have shut down and if you are still in the "normal" range does it make a difference?

Fact: Testosterone levels in the "normal" range don't seem to make a difference unless you are going by "feeling". Boosting to 1200 ng/dl did nothing for muscle gain. The body has many many fail safes to lowered androgen levels and will likely upregulate the AR's in response to the change in T. Conversely it probably reduces AR sensitivity when you have high levels.

Thus you only get a major response to "testosterone" when you go well above the "high normal greater than 1200ng/dl" levels with prohormones or steroids and push past the natural defenses.


[/SIZE]
eh.

I know in this study the levels are a bit above 1200 ng/dl, but there is a very significant difference in LBM gains, strength gains, etc. between the 125 group and the 300 group.

http://ajpendo.physiology.org/content/ajpendo/283/1/E154.full.pdf

http://ajpendo.physiology.org/content/ajpendo/281/6/E1172.full.pdf
 
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Nah, I actually take the advice of Dr Rand McClain who actually refutes the entire idea of prolactin induced gyno and also agrees with Eric on Nolva for PCT. He's only one of the most experienced TRT docs in the country that works with bodybuilders.
 

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Nah, I actually take the advice of Dr Rand McClain who actually refutes the entire idea of prolactin induced gyno and also agrees with Eric on Clomid/Nolva for PCT. He's only one of the most experienced TRT docs in the country that works with bodybuilders.
care to post some of that data that disproves those theories?
 
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care to post some of that data that disproves those theories?
Sure, go listen to him on Muscle Insider on Youtube as he talks about in depth over about 12 hours of video. Have at it. And unlike the forum bro's, he has blood work to back it up.
 

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some data on DAA and prolactin, for later:


1. D’ Aniello A, et al. Involvement of D-aspartic acid in the synthesis of testosterone in rat testes. Life Sci. 1996;59(2):97-104

2. Topo E, et al. The role and molecular mechanism of D-aspartic acid in the release and synthesis of LH and testosterone in humans and rats. Reprod Biol Endocrinol. 2009 Oct 27;7:120

3. D’ Aniello A. D-aspartic acid: an endogenous amino acid with an important neuroendocrine role. Brain Res Rev. 2007 Feb;53(2):215-234

4. Pampillo M, et al. The effect of D-asparate on luteinizing hormone-releasing hormone, alpha-melanocyte-stimulating hormone, GABA and dopamine release. Neuroreport. 2002 Dec 3;13(17):2341-2344

5. Nagy GM, et al. Control of prolactin secretion by excitatory amino acids. Endocrine. 2005 Dec;28(3):303-308

6. Shibli-Rahhal A and Schlechte J. The effects of hyperprolactinemia on bone and fat. Pituitary. 2009;12(2):96-104

7. Brandebourg TD, Brown JL and Ben-Jonathan N. Prolactin upregulates its receptors and inhibits lipolysis and leptin release in male rate adipose tissue. Biochem Biophys Res Commun. 2007 Jun 1;357(2):408-413

8. Ben-Jonathan N, et al. Focus on prolactin as a metabolic hormone. Trends Endocrinol Metab. 2006 Apr;17(3):110-116

9. Ribeiro RS and Abucham J. Recovery of persistent hypogonadism by clomiphene in males with prolactinomas under dopamine agonist treatment. Eur J Endocrinol. 2009 Jul;161(1):163-169

10. Gillam MP, et al. Advances in the treatment of prolactinomas. Endocr Rev. 2006 Aug;27(5):485-534
 
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some data on DAA and prolactin, for later:


1. D’ Aniello A, et al. Involvement of D-aspartic acid in the synthesis of testosterone in rat testes. Life Sci. 1996;59(2):97-104

2. Topo E, et al. The role and molecular mechanism of D-aspartic acid in the release and synthesis of LH and testosterone in humans and rats. Reprod Biol Endocrinol. 2009 Oct 27;7:120

3. D’ Aniello A. D-aspartic acid: an endogenous amino acid with an important neuroendocrine role. Brain Res Rev. 2007 Feb;53(2):215-234

4. Pampillo M, et al. The effect of D-asparate on luteinizing hormone-releasing hormone, alpha-melanocyte-stimulating hormone, GABA and dopamine release. Neuroreport. 2002 Dec 3;13(17):2341-2344

5. Nagy GM, et al. Control of prolactin secretion by excitatory amino acids. Endocrine. 2005 Dec;28(3):303-308

6. Shibli-Rahhal A and Schlechte J. The effects of hyperprolactinemia on bone and fat. Pituitary. 2009;12(2):96-104

7. Brandebourg TD, Brown JL and Ben-Jonathan N. Prolactin upregulates its receptors and inhibits lipolysis and leptin release in male rate adipose tissue. Biochem Biophys Res Commun. 2007 Jun 1;357(2):408-413

8. Ben-Jonathan N, et al. Focus on prolactin as a metabolic hormone. Trends Endocrinol Metab. 2006 Apr;17(3):110-116

9. Ribeiro RS and Abucham J. Recovery of persistent hypogonadism by clomiphene in males with prolactinomas under dopamine agonist treatment. Eur J Endocrinol. 2009 Jul;161(1):163-169

10. Gillam MP, et al. Advances in the treatment of prolactinomas. Endocr Rev. 2006 Aug;27(5):485-534
To date, he's never seen one instance of prolactin induced gyno that was not estrogen related.

You can post all the studies you want. I've read most, if not all of them in the past 15 yrs.
 
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Actually it was the 300-600mg group.
there's a significant difference between all 3 groups.

but, the 125 group was closer to :normal" the 300 group was closest to higher normal (although a bit higher than 1200 ng)
 
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there's a significant difference between all 3 groups.

but, the 125 group was closer to :normal" the 300 group was closest to higher normal (although a bit higher than 1200 ng)
1. The first study is was 300-600mg in healthy individuals.

2. The second study they saw 125mg and anything higher than that...you know why? They are hypogonadal and eugonadal men. Its like giving a women 5mg of Anavar. Of COURSE they are all going to see an increase...they are starting from literally nothing. It has zero basis for a healthy person with normal HTPA function.
 

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To date, he's never seen one instance of prolactin induced gyno that was not estrogen related.

You can post all the studies you want. I've read most, if not all of them in the past 15 yrs.
right on.

I'm not saying the Doc is wrong.... but I don't think high prolacitn is good. and allowing prolactin to be high without controlling E2 is also not good. an easy solution to me would be not raising prolactin while raising testosterone/LH.

hard for me to ignore all the guys that use DAA products in PCT and have issues, tho.
 
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right on.

I'm not saying the Doc is wrong.... but I don't think high prolacitn is good. and allowing prolactin to be high without controlling E2 is also not good. an easy solution to me would be not raising prolactin while raising testosterone/LH.

hard for me to ignore all the guys that use DAA products in PCT and have issues, tho.
Its not high..its actually relative to Test and Estrogen increases...which is should be. Remove the estrogen component, no gyno....and you don't do that with Tamoxifen, you do with an AI.
 

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1. The first study is was 300-600mg in healthy individuals.

2. The second study they saw 125mg and anything higher than that...you know why? They are hypogonadal and eugonadal men. Its like giving a women 5mg of Anavar. Of COURSE they are all going to see an increase...they are starting from literally nothing. It has zero basis for a healthy person with normal HTPA function.

1. both studies used 25, 50, 125, 300 and 600 mg doses.

2. in the second study which was in healthy eugonadal men (which were given a GnRH suppressant, by the way, which was to assess the doses used and not their own production), 125 mg resulted in nearly the same total testosterone levels as their baseline. hence me using that as a metric for a "normal" man. and the 300 dose resulted in 1345, which was what I compared to the OP's comment of 1200 ng not resulting in greater gains. it clearly does, both in loss in bodyfat, but gains in LBM, strength and power.

http://ajpendo.physiology.org/content/ajpendo/281/6/E1172.full.pdf
 

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Its not high..its actually relative to Test and Estrogen increases...which is should be. Remove the estrogen component, no gyno....and you don't do that with Tamoxifen, you do with an AI.
right, I get that. I've explained how to address gyno in detail in numerous thread here.

I'll stop arguing about DAA, as I see where this road is taking me.
 
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1. both studies used 25, 50, 125, 300 and 600 mg doses.

2. in the second study which was in healthy eugonadal men (which were given a GnRH suppressant, by the way, which was to assess the doses used and not their own production), 125 mg resulted in nearly the same total testosterone levels as their baseline. hence me using that as a metric for a "normal" man. and the 300 dose resulted in 1345, which was what I compared to the OP's comment of 1200 ng not resulting in greater gains. it clearly does, both in loss in bodyfat, but gains in LBM, strength and power.

http://ajpendo.physiology.org/content/ajpendo/281/6/E1172.full.pdf
1. Yes but and the major results were in the 300mg and 600mg conentrations. It literally states that.

2. The one study had both hypogonadal and eugonadal. Only the hypogonadal men showed LBM increases of any significance at 125mg and that was because of the reason I stated above.

Also, if you actually read the second study they actually talk about the dose dependent curve and the differences between physiological levels, which downgrades androgen receptors, and those results seen at supraphysiological levels (which is anything over 200mg per week). They clearly state there are two different dose respondent curves. Its the same with insulin....Higher levels from a normal man compared to injecting has a completely different effect even if the amounts were the same.

In other words, this really has nothing to do with a normal men and normal testosterone levels. Its only showing there is a dose dependent curve. Low testosterone, less gains. More testosterone, more gains. Its that simple.
 

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So after all that, here's my final thoughts:

1. I can get real clomid and nolva cheaper than the OP's product. (research chems for prolly 1/4 of the regular price, too)

2. I know that there's clinical evidence that nolva and clomid are more effective at raising testosterone and LH than DAA, etc.

3. I've seen thread after thread of guys having side effects from DAA.

4. personally, I can't use anything with yohimbine, as it's the only thing I've every taken that triggers panic attacks in me, and it does it quick.

5. there's plenty of clinical evidence that higher than normal testosterone levels result in greater gains.
 
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So after all that, here's my final thoughts:

1. I can get real clomid and nolva cheaper than the OP's product. (research chems for prolly 1/4 of the regular price, too)
I don't care. Just because its cheap, doesn't mean its necessary or even good and there is also the legal factor.

2. I know that there's clinical evidence that nolva and clomid are more effective at raising testosterone and LH than DAA, etc.
There really has never been a comparison in any of them in men coming off steroid cycles. In fact, I've seen bloodwork in all of them and there reason isn't much of a difference in recovery time when its a mild cycle. Heavy longer cycles its unknown and where you get into trouble that even Clomid and Tamoxifen won't even help.

3. I've seen thread after thread of guys having side effects from DAA.
Same with Clomid and Tamox.

4. personally, I can't use anything with yohimbine, as it's the only thing I've every taken that triggers panic attacks in me, and it does it quick.
Its one of my favorite supplements.

5. there's plenty of clinical evidence that higher than normal testosterone levels result in greater gains.
As compared to what? Lower? Of course. Your lower post cycle with anything you take. Its not a switch that gets turned on overnight. It takes weeks..with anything..and nothing.
 

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1. Yes but and the major results were in the 300mg and 600mg conentrations. It literally states that.

2. The one study had both hypogonadal and eugonadal. Only the hypogonadal men showed LBM increases of any significance at 125mg and that was because of the reason I stated above.

Also, if you actually read the second study they actually talk about the dose dependent curve and the differences between physiological levels, which downgrades androgen receptors, and those results seen at supraphysiological levels (which is anything over 200mg per week). They clearly state there are two different dose respondent curves. Its the same with insulin....Higher levels from a normal man compared to injecting has a completely different effect even if the amounts were the same.

In other words, this really has nothing to do with a normal men and normal testosterone levels. Its only showing there is a dose dependent curve. Low testosterone, less gains. More testosterone, more gains. Its that simple.
btw, that study I posted again only used healthy men. it literally said that in the title.

"Testosterone dose-response relationships in healthy young men"

Participants. The participants were healthy men, 18–35 yr
of age, with prior weight-lifting experience and normal testosterone
levels.
 
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which is exactly the point I was trying to make.
You do understand the body produces testosterone without Tamoxifen and Clomid?
 
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btw, that study I posted again only used healthy men. it literally said that in the title.

"Testosterone dose-response relationships in healthy young men"

Participants. The participants were healthy men, 18–35 yr
of age, with prior weight-lifting experience and normal testosterone
levels.
You posted two studies in the first post and one is hypogonadal men. Did you read it?

"—Administration
of replacement doses of testosterone to healthy hypogonadal
men and supraphysiological doses to eugonadal men
increases muscle size."
 

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You posted two studies in the first post and one is hypogonadal men. Did you read it?

"—Administration
of replacement doses of testosterone to healthy hypogonadal
men and supraphysiological doses to eugonadal men
increases muscle size."
I did post 2 in my intitial post. in my later post I re-posted the 2nd study, which I was pointing out the characteristics of in that same post.

I will quote it for you:

Quote Originally Posted by Admin View Post
1. The first study is was 300-600mg in healthy individuals.

2. The second study they saw 125mg and anything higher than that...you know why? They are hypogonadal and eugonadal men. Its like giving a women 5mg of Anavar. Of COURSE they are all going to see an increase...they are starting from literally nothing. It has zero basis for a healthy person with normal HTPA function.

1. both studies used 25, 50, 125, 300 and 600 mg doses.

2. in the second study which was in healthy eugonadal men (which were given a GnRH suppressant, by the way, which was to assess the doses used and not their own production), 125 mg resulted in nearly the same total testosterone levels as their baseline. hence me using that as a metric for a "normal" man. and the 300 dose resulted in 1345, which was what I compared to the OP's comment of 1200 ng not resulting in greater gains. it clearly does, both in loss in bodyfat, but gains in LBM, strength and power.

http://ajpendo.physiology.org/conten...E1172.full.pdf
 
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I did post 2 in my intitial post. in my later post I re-posted the 2nd study, which I was pointing out the characteristics of in that same post.

I will quote it for you:

Quote Originally Posted by Admin View Post
1. The first study is was 300-600mg in healthy individuals.

2. The second study they saw 125mg and anything higher than that...you know why? They are hypogonadal and eugonadal men. Its like giving a women 5mg of Anavar. Of COURSE they are all going to see an increase...they are starting from literally nothing. It has zero basis for a healthy person with normal HTPA function.

1. both studies used 25, 50, 125, 300 and 600 mg doses.

2. in the second study which was in healthy eugonadal men (which were given a GnRH suppressant, by the way, which was to assess the doses used and not their own production), 125 mg resulted in nearly the same total testosterone levels as their baseline. hence me using that as a metric for a "normal" man. and the 300 dose resulted in 1345, which was what I compared to the OP's comment of 1200 ng not resulting in greater gains. it clearly does, both in loss in bodyfat, but gains in LBM, strength and power.

http://ajpendo.physiology.org/conten...E1172.full.pdf
I really think you have a problem interpreting your own studies. I don't think you quite understand them, which is fine....I'm all for someone trying.

But you don't seem to grasp there is a major difference in someone boosting testosterone whether its through OTC supps, Clomid and Tamox, vs someone injecting the equivalent dose. Its not the same. The study even indicates that. Anyone who has studied this or experienced this, knows this.

Ask anyone who is on TRT. Ask any doc that administers it. You are comparing apples to watermelons.
 

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I really think you have a problem interpreting your own studies. I don't think you quite understand them, which is fine....I'm all for someone trying.

But you don't seem to grasp there is a major difference in someone boosting testosterone whether its through OTC supps, Clomid and Tamox, vs someone injecting the equivalent dose. Its not the same. The study even indicates that. Anyone who has studied this or experienced this, knows this.

Ask anyone who is on TRT. Ask any doc that administers it. You are comparing apples to watermelons.
eh.

my points are clear. the clinical data is clear.

have a good night!
 
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I think what we have now established is simple... Just don't come off :D
 
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yes, I do.

what point are you trying to make? just being sarcastic?

I do know that I personally produce at least twice the amount of testosterone on clomid than I normally do. And based off the clinical data, that seems to be the norm and not the exception.

http://anabolicminds.com/forum/post-cycle-therapy/288103-info-serms.html
Sure it would and your body naturally with down regulate after time...something it won't do on TRT. You will consistently outperform anyone taking Clomid, Tamox, etc....

I'm sorry but boosting test with Clomid, Tamox, OTC, nothing, etc...is not the same and the body does not react the same as injectable testosterone.

So you can't use references of injectable testosterone to show me what my naturally high level will do. Its not the same.
 
bruno.camilo

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I know the subject of the topic is Tamox, but doctors prescribe Clomid as PCT and some times as TRT replacement. Been there, done that.

I repeat doctors, is there anyone around?
 
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I know the subject of the topic is Tamox, but doctors prescribe Clomid as PCT and some times as TRT replacement. Been there, done that.

I repeat doctors, is there anyone around?
And most don't...for a reason.

Some doctors also prescribe Androgel, which sucks. And some doctors think testosterone and TRT is bad for you.

And some doctors work exclusively with bodybuilders, are bodybuilders themselves, and been doing that for over 20 years...

Dr. Rand McClain. He's a doctor. I repeat, a doctor.

Anyone out there?


Skip to the 5:35 part. He talks about Clomid and why he doen'st like it.

He also talks about Tamoxifen and the possibility of still having elevated levels of estrogen in the body, since it does not block the conversion...its only block certain receptors. Elevated estrogen in the body, much like testosterone, stops normal testosterone production....which Eric said in his post in the beginning.





....but the bro's know better. :lol:
 
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Admin what would you reccomend for a PCT off a AAS cycle? Say 12 week Test/NPP? Not trying to be sarcastic, actually trying to learn.
 
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And at the other end of the spectrum, Dr Michael Scally, with his hcg/nolva/and 100mg clomid.
 
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I can't really answer that...for other reasons but if you watch that video he'll tell you. :)
 
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Interesting that he recommends adex as the AI, rather than exem. I cant say if this is a generational preference or based on something else (Crisler prefers adex simply because thats what he knows and has experience with).

Hcg is obviously an option for guys already pinning, and whilst Ive heard of "hcg drops" Ive not come across anyone who has reportedly used them.
 

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Well, clomiphene acts on the hypothalamus and not just the pituitary.

http://www.sciencedirect.com/topics/neuroscience/clomifene


anyway, the doc isn't arguing against doing PCT.... he's arguing about allowing E2 to rise and choosing an AI and HCG in lieu of a SERM for that reason. that's certainly an option that I think has merit. however, by using HCG you will elevate testosterone production, which is still going to trigger a negative feedback mechanism. simply using the AI by itself seems to be simpler, as it would cause a gradual increase in testosterone, LH and FSH while lowering E2. of course, relying on an AI here could cause a crash in E2, so that needs to be managed closely.

one could certainly try that option, or use a SERM. either way, one would fare well in using HCG on cycle and using an AI into PCT to control E2, which is something most of us already recommend. the biggest issue I see with side effects when using Nolva or Cloimd is when people stack them or use excessive doses. obviously that's not true for all cases, but I haven't seen many people have issues with 25 mg of clomid or 20 mg of Nolva.
 
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And at the other end of the spectrum, Dr Michael Scally, with his hcg/nolva/and 100mg clomid.
Well if you think about it, what Dr. Rand says isn't that far off as long as HCG is in the picture. Take HCG out, and that scenario completely changes.
 
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Interesting that he recommends adex as the AI, rather than exem. I cant say if this is a generational preference or based on something else (Crisler prefers adex simply because thats what he knows and has experience with).

Hcg is obviously an option for guys already pinning, and whilst Ive heard of "hcg drops" Ive not come across anyone who has reportedly used them.
Most TRT doctors always choose Arimidex because its easier to control...at least thats what he says. The other one which he says actually stops Estrogen better is Femara but there is data that it could mildly stress the liver and as any doctor will tell you, per the hippocratic oath, if I can get the same results with another drug without the risk, they will use that.
 

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Most TRT doctors always choose Arimidex because its easier to control...at least thats what he says. The other one which he says actually stops Estrogen better is Femara but there is data that it could mildly stress the liver and as any doctor will tell you, per the hippocratic oath, if I can get the same results with another drug without the risk, they will use that.
I presume it's also a cost issue, as well.

A-dex is prolly cheaper for most patients.
 
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I presume it's also a cost issue, as well.

A-dex is prolly cheaper for most patients.
No, Femara is actually cheaper as a generic.
 

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No, Femara is actually cheaper as a generic.
not in my region.

A-dex is cheapest, then femara, but they're only a couple bucks different. Aromasin is about 5 times their price....
 
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Well, clomiphene acts on the hypothalamus and not the pituitary.

http://www.sciencedirect.com/topics/neuroscience/clomifene


anyway, the doc isn't arguing against doing PCT.... he's arguing about allowing E2 to rise and choosing an AI and HCG in lieu of a SERM for that reason. that's certainly an option that I think has merit. however, by using HCG you will elevate testosterone production, which is still going to trigger a negative feedback mechanism. simply using the AI by itself seems to be simpler, as it would cause a gradual increase in testosterone, LH and FSH while lowering E2. of course, relying on an AI here could cause a crash in E2, so that needs to be managed closely.
No, he is saying that a SERM still leaves circulating estrogen which can still cause suppression. But its amazming how the forum experts arent calling him a retard.

HCG stimulates leydig cells and keeps them active while having exogenous hormones circulating so when you do come off, tesosterone product resumes rather quickly vs someone who didn't use it.

So whether its triggering the negative feedback loop is irrelevant because you are stimulating that process via HCG.

one could certainly try that option, or use a SERM. either way, one would fare well in using HCG on cycle and using an AI into PCT to control E2, which is something most of us already recommend. the biggest issue I see with side effects when using Nolva or Cloimd is when people stack them or use excessive doses. obviously that's not true for all cases, but I haven't seen many people have issues with 25 mg of clomid or 20 mg of Nolva.

He has and I would trust his opinion over the forum bro's considering his comes straight from a local pharmacy.
 
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not in my region.

A-dex is cheapest, then femara, but they're only a couple bucks different. Aromasin is about 5 times their price....
He tells you why. Watch his videos. Femara is better but has more risks therefore he won't use it if he can get the same results without the risk. I'm not making this up.
 
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He compares them all.


 

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No, he is saying that a SERM still leaves circulating estrogen which can still cause suppression. But its amazming how the forum experts arent calling him a retard.

HCG stimulates leydig cells and keeps them active while having exogenous hormones circulating so when you do come off, tesosterone product resumes rather quickly vs someone who didn't use it.

So whether its triggering the negative feedback loop is irrelevant because you are stimulating that process via HCG.




He has and I would trust his opinion over the forum bro's considering his comes straight from a local pharmacy.
I appreciate you incorrectly paraphrasing that and missing my points.

I'll just stop.
 
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I appreciate you incorrectly paraphrasing that and missing my points.

I'll just stop.
Funny, I could say the same about you.

I guess DAA helps your penis grow and growth plates tho??
If you want to be sarcastic in your first post, don't be surprised if you get it back when the OP's viewpoint actually has merit.

So you can certainly continue if you like....if you would like to start over without the sarcasm, then by all means I'm all for it.
 
Nac

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Well if you think about it, what Dr. Rand says isn't that far off as long as HCG is in the picture. Take HCG out, and that scenario completely changes.
Im wondering if it was Scally he was referring to as the "expert" in that first video/patient question. Certainly sounds like Scally's Power PCT setup.
 
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Im wondering if it was Scally he was referring to as the "expert" in that first video/patient question. Certainly sounds like Scally's Power PCT setup.
Could be

"Using a cannon for a moquito"

Or something like that.
 
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fueledpassion

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Sure it would and your body naturally with down regulate after time...something it won't do on TRT. You will consistently outperform anyone taking Clomid, Tamox, etc....

I'm sorry but boosting test with Clomid, Tamox, OTC, nothing, etc...is not the same and the body does not react the same as injectable testosterone.

So you can't use references of injectable testosterone to show me what my naturally high level will do. Its not the same.
I agree. And the biggest difference between SERMs and Test injection is how quickly it dumps into the blood. When someone takes a weekly shot of test @ 200mg, they are getting a large surge at once, rather than over the entire week. Furthermore, test esters play a key role in anabolic activity.

The closest comparison in terms of anabolic potency between Clomid and Test is probably about 150-200mg of Test-Prop weekly, spread out over 3-7 doses.

Even then, while nitrogen retention in muscle on Test-P is much weaker than Test-C,D or E, the percentage of conversion to estrogen is less and likely a greater percentage of free T comes out of Prop. In any case, I've always noticed that an average of 800ng/dl on TRT is always more productive than similar values running a combination of Clomid and an AI.
 

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Funny, I could say the same about you.



If you want to be sarcastic in your first post, don't be surprised if you get it back when the OP's viewpoint actually has merit.

So you can certainly continue if you like....if you would like to start over without the sarcasm, then by all means I'm all for it.
the points you missed were these:

1. the doc mentions clomid affecting the pituitary, whereas it acts on the hypothalamus and the pituitary. this is significant, because as far as I know, clomid is the only SERM or AI that directly stimulates the hypothalamus to increase production of GnRH. therefore, using it as a means of PCT simply and cheaply addresses the entire HPTA pathway, instead of just hitting the P or T in that equation. I suspect that this is also why it's not uncommon to see guys double testosterone on clomid, whereas that's rare in the use of another SERM or AI.

2. the use of HCG in PCT has an indirect inhibitory effect, because it raises testosterone. obviously normal or high testosterone levels will send back a negative feedback message to the H or P which will discourage further release of GnRH or LH. this is why I suggested using this on cycle but not in PCT, when this will simply discourage HPTA recovery.
 
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CatSnake

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I agree. And the biggest difference between SERMs and Test injection is how quickly it dumps into the blood. When someone takes a weekly shot of test @ 200mg, they are getting a large surge at once, rather than over the entire week. Furthermore, test esters play a key role in anabolic activity.

The closest comparison in terms of anabolic potency between Clomid and Test is probably about 150-200mg of Test-Prop weekly, spread out over 3-7 doses.

Even then, while nitrogen retention in muscle on Test-P is much weaker than Test-C,D or E, the percentage of conversion to estrogen is less and likely a greater percentage of free T comes out of Prop. In any case, I've always noticed that an average of 800ng/dl on TRT is always more productive than similar values running a combination of Clomid and an AI.
yeah, I get that.

I was using a study that compared various doses of testosterone as a comparison to the OP's comments that high was not more significant than normal. if I can drum up a study where they used a SERM then I will post that as well.
 
jakz

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No, he is saying that a SERM still leaves circulating estrogen which can still cause suppression. But its amazming how the forum experts arent calling him a retard.

HCG stimulates leydig cells and keeps them active while having exogenous hormones circulating so when you do come off, tesosterone product resumes rather quickly vs someone who didn't use it.

So whether its triggering the negative feedback loop is irrelevant because you are stimulating that process via HCG.




He has and I would trust his opinion over the forum bro's considering his comes straight from a local pharmacy.
I've always wondered about this! I've had a few times where post PCT I felt
Itchy nips and had to dose Nolva. It's only after I started using a suicide AI that I never had this problem again.
 

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