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Clomid during cycle

there are 3 estrogens in your body, serms were not designed for men or steroid use, they are designed for women with breast cancer to block the receptors in the breast so new cancer cells dont bind and grow. it doesnt protect your dick, it doesnt protect your prostate, it doesnt promote muscle growth
Bet you cant tell what those estrogen are. What there affinity for the receptors are. Which receptors they have a higher affinity for. What thise receptors do. And if serms effect more cell types other than breast tissue. Jesus vhrist you are dumb.
 
Worng.

Torem prevent prostate cancer.

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no you misconstrued what I said, I said serms used by bodybuilders were designed for women with breast cancer, and torem decreased the risk of cancer it does not stop it, good article tho
 
Bet you cant tell what those estrogen are. What there affinity for the receptors are. Which receptors they have a higher affinity for. What thise receptors do. And if serms effect more cell types other than breast tissue. Jesus vhrist you are dumb.
I tried to keep it civil and maybe we could learn something from each other, the whole purpose of these forums is to exchange knowledge, I'm out.
 
no you misconstrued what I said, I said serms used by bodybuilders were designed for women with breast cancer, and torem decreased the risk of cancer it does not stop it, good article tho
But if it only effect breast tissue how does it effect prostate, bones, and prevent diabetes. See my point the serm attach to all estrogen receptors. This protects you from the negatives effect of estrogen even if the levels are high. As wstrogen has no where to bind to thus making it no matter what the blood levels of estrogen are.
 
I tried to keep it civil and maybe we could learn something from each other, the whole purpose of these forums is to exchange knowledge, I'm out.
You were in to learn anything. I provided real science. You ignored it while shouting out brolore. As you have no idea about basic anatomy or how anything causes an effect in the body.
 
Serms can prevent type 2 diabetes

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this is pretty interesting, I wonder how it effects insulin use during cycle or PCT, altho it was testing in specific rats and they are trying to correlate it to women with breast and uterus cancer, it says it effects beta cells
 
You were in to learn anything. I provided real science. You ignored it while shouting out brolore. As you have no idea about basic anatomy or how anything causes an effect in the body.
have no idea what you are arguing now, can we just agree to disagree, I promise to help you in your gyno threads
 
have no idea what you are arguing now, can we just agree to disagree, I promise to help you in your gyno threads
The fact that you dont know what im talking about proves how you dont understand sh!t. As no receptors to bind to means that substance cant have an effect. They do this to mice all the time. They bread them without receptors to test and isolated the mechanism of actions outside of the receptors they knocked out.
 
Jesus you guys have to much free time. Heckler is either trolling or playing computer games while writting here.
 
Uh shut up i don't have no gyno nor will i ever.
by far your most informative post, I can tell you help a lot of people here. BTW i didnt see you contribute in any of the posts here where people have gyno, is that cause you only know how to get gyno?
 
by far your most informative post, I can tell you help a lot of people here. BTW i didnt see you contribute in any of the posts here where people have gyno, is that cause you only know how to get gyno?
Actually i have helped people with gyn. Alot!

Your just a stupud troll. Everyone else in this thread disagrees with you. You lack any understanding of basic anatomy. Im done i have to actually do my job now.
 
Jesus you guys have to much free time. Heckler is either trolling or playing computer games while writting here.
Agreed. Im done arguing with him. I should have not started this to begin with. I actually just blocked him. Im want to apologize to you and the others in this thread for this. I know better than to agrue like this.

Also i know where talking to me but my typing, grammer, and spelling are bad right now as i working and doing this at the same time.
 
.......... so........

speaking of anatomy you know there are different kinds of estrogen receptors that depending on the SERM will have a different affinity to? So tamoxifen has a really strong binding affinity to breast tissue ER while clomid has much stronger activity in the hypothalamus with mixed agonist/antagonist activity.

Just a little knowledge get the thread back on track :usa2:
 
.......... so........

speaking of anatomy you know there are different kinds of estrogen receptors that depending on the SERM will have a different affinity to? So tamoxifen has a really strong binding affinity to breast tissue ER while clomid has much stronger activity in the hypothalamus with mixed agonist/antagonist activity.

Just a little knowledge get the thread back on track :usa2:
this is true, and mainly why clomid is used for pct, it is known to be a poor serm, nolva is much better
 
.......... so........

speaking of anatomy you know there are different kinds of estrogen receptors that depending on the SERM will have a different affinity to? So tamoxifen has a really strong binding affinity to breast tissue ER while clomid has much stronger activity in the hypothalamus with mixed agonist/antagonist activity.

Just a little knowledge get the thread back on track :usa2:
Yes. They have a higher affinity for certain cell types(ie receptor types) than others. This does not mean it has less affinity than estrogen necessarily. Matter of fact I think it's would be better to assume it still higher, in most cells than estrogen. Saying it can effect bone, pancreatic, prostate, hypothalamic, pituitary, and breast cells with a stronger affinity than estrogem. Now this changes depending on serm and steriods being used. If it is a methylated steriods that can lead to a methyl estrogen it may definitely have a higher affinity than the serm. This is untest here.

However, serms may be are only hope with something like trest. As trest is not reduced by aromatase(no 19nor is) rather is reduced by other enzymes in the liver ( 2kvette can explain this much better than I can). . Meaning the AIs cannot do sh!t to prevent estrogen conversion with trest. Which is bad as trest lead a very very potent form of estrogen. So a serm like ralox is the only hope to stop it's negative sides.
 
.......... so........

speaking of anatomy you know there are different kinds of estrogen receptors that depending on the SERM will have a different affinity to? So tamoxifen has a really strong binding affinity to breast tissue ER while clomid has much stronger activity in the hypothalamus with mixed agonist/antagonist activity.

Just a little knowledge get the thread back on track :usa2:
Also no serm is an antagonist. They are reverse agonist. Transcribing the opposite signal of estrogen. While aslo being agonist at ER-b. This is all varying degrees depending on the serm and cell type.
 
this is true, and mainly why clomid is used for pct, it is known to be a poor serm, nolva is much better

Allow me to clarify your statement.

It is a poor SERM for breast tissue affinity.....it's a GREAT SERM for fertility. Remember..... these are Selective Estrogen Receptor Modulator. So some will select for different receptors and modulate them for different end goals.:biggthumpup:
 
this is true, and mainly why clomid is used for pct, it is known to be a poor serm, nolva is much better
Would say it's a poor serm. It's a great serm depending on the goal. Ie cells you want to target. So you want to target hypothalamic and pituitary it's a great serm. Anything else not so much
 
Allow me to clarify your statement.

It is a poor SERM for breast tissue affinity.....it's a GREAT SERM for fertility. Remember..... these are Selective Estrogen Receptor Modulator. So some will select for different receptors and modulate them for different end goals.:biggthumpup:
I agree, I have been on several threads here helping people with their issues and basically it started from them not using an AI to start with. my one and only disagreement with the clomid use is its better to prevent elevated estrogen then try to block it with clomid. and for PCT most people use both clomid and nolva, for the exact reason you stated it is poor at blocking gyno.
 
Also no serm is an antagonist. They are reverse agonist. Transcribing the opposite signal of estrogen. While aslo being agonist at ER-b. This is all varying degrees depending on the serm and cell type.


reverse agonist and antagonist are literally synonyms....Inverse agonist, reverse agonist, antagonist all mean to induce the opposit effect of the agonist.

You literally defined a partial or mixed agonist/antagonist right after your corrected me.

A SERM can shut off an estrogen receptor....thus be an inverse agonist which is the same thing as an antagonist.
 
reverse agonist and antagonist are literally synonyms....Inverse agonist, reverse agonist, antagonist all mean to induce the opposit effect of the agonist.

You literally defined a partial or mixed agonist/antagonist right after your corrected me.

A SERM can shut off an estrogen receptor....thus be an inverse agonist which is the same thing as an antagonist.
Antagonist and reverse agonist are not the same. On means it block the signal, while the other means it transcibes the opposite signal it normally would.
 
Yes. They have a higher affinity for certain cell types(ie receptor types) than others. This does not mean it has less affinity than estrogen necessarily. Matter of fact I think it's would be better to assume it still higher, in most cells than estrogen. Saying it can effect bone, pancreatic, prostate, hypothalamic, pituitary, and breast cells with a stronger affinity than estrogem. Now this changes depending on serm and steriods being used. If it is a methylated steriods that can lead to a methyl estrogen it may definitely have a higher affinity than the serm. This is untest here.

However, serms may be are only hope with something like trest. As trest is not reduced by aromatase(no 19nor is) rather is reduced by other enzymes in the liver ( 2kvette can explain this much better than I can). . Meaning the AIs cannot do sh!t to prevent estrogen conversion with trest. Which is bad as trest lead a very very potent form of estrogen. So a serm like ralox is the only hope to stop it's negative sides.

I cell type and a receptor type are GROSSLY different things. One cell can have MULTIPLE receptor types.

I did not compare SERMS to estrogen, I compared SERMS to SERMS on its affinity to varying estrogen receptors.

If you wanted to discuss affinity of SERMs VS Estrogens that is a separate topic we would be more likely to heavily agree on.

Let me ask you a question based on your statement(for clarification). Does trestolone convert to an estrogen derivative? I will look this up now to brush up on it as you answer:biggthumpup:
 
Antagonist and reverse agonist are not the same. On means it block the signal, while the other means it transcibes the opposite signal it normally would.


a physiological antagonist is something that produces the opposite effect whether through transcription or signal release or etc. You are using one definition of antagonist, however you are wrong to separate reverse agonism from antagonism when talking about a physiological process.
 
I cell type and a receptor type are GROSSLY different things. One cell can have MULTIPLE receptor types.

I did not compare SERMS to estrogen, I compared SERMS to SERMS on its affinity to varying estrogen receptors.

If you wanted to discuss affinity of SERMs VS Estrogens that is a separate topic we would be more likely to heavily agree on.

Let me ask you a question based on your statement(for clarification). Does trestolone convert to an estrogen derivative? I will look this up now to brush up on it as you answer:biggthumpup:
Yes. For the first part this is true. But cell types typically have I higher amount of certain types of receptors. And that is what I was implying. I should have clarified more.

Second I was the the one comparing estrogen affinity to serm affinity from the get go. You were the one that changed that, how was I supposed to know? (Sorry if this sounds dickish I'm not trying to be).

Thirdly I'm not sure the specific estrogen form, off the top of my head, that trest turn into other than it's 7a-methylated. If I had to guess right now I would say it would be a combo esterone and estrodiol but not estriol
 
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Clomiphene citrate elicits estrogen agonistic/antagonistic effects differentially via estrogen receptors alpha and beta.

Abstract
Clomiphene citrate (CC) is known to possess dual actions as an estrogen agonist and an estrogen antagonist. To see how the dual actions of CC are exerted through estrogen receptor alpha (ER alpha) and/or ER beta we developed a cell-based transcription assay system in which 293T cells were transfected with the luciferase reporter plasmid with estrogen responsive element and either human ER alpha or ER beta expression plasmid. CC at lower doses (10(-10) M and 10(-12) M), but not higher doses (10(-6) M and 10(-8) M) elicited estrogenic activity via ER alpha. However, CC at concentrations between 10(-6) M and 10(-12) M did not elicit any estrogenic activity via ER beta. In the presence of 17beta-estradiol (E2), CC behaved either as an agonist or as an antagonist via ER alpha depending on the concentrations of E2, i.e., antagonistic when combined with the higher E2 concentrations, agonistic with the lower E2 concentrations. On the other hand, via ER beta, CC acted as an estrogen antagonist regardless of the concentration of E2 added together. In conclusion, CC acts as an estrogen agonist/antagonist via ER alpha in a coexisting estrogen concentration-dependent way whereas it acts as an estrogen antagonist via ER beta whether or not estrogen is present.
 
copied from another site. take it or leave it


Clomid

Agonist: Liver
Antagonist: Brest/nipple

Clomid is a really harsh drug it should be avoided at all costs, if you get the visual sides/blurry vision from clomid they stay for life! They are rare but do happen

Clomid should only be used in restart protocols imo by the supervision of a doctor. So if you want to start producing sperm again you will have to take hcg along with clomid for 9-12months straight. It has some use in pct but it can be completely avoided by using serms only or ideally nolvadex + aromasin
 
Yes. For the first part this is true. But cell types typically have I higher amount of certain types of receptors. And that is what I was implying. I should have clarified more.

Second I was the the one comparing estrogen affinity to serm affinity from the get go. You were the one that changed that, how was I supposed to know? (Sorry if this sounds dickish I'm not trying to be).

Thirdly I'm not sure the specific estrogen form, off the top of my head, that trest turn into other than it's 7a-methylated. If I had to guess right now I would say it would be a combo esterone and estrodiol but not estriol



First: Okay if you want to argue different cells have different amounts of certain receptors we are in agreement. That clarification goes a long way.

Second: When i was reading through the current argument that was the biggest miscommunication that I was noticing. Arguing affinity between SERMS and estrogen is pointless as you know because SERMs where designed to have a higher affinity. And it seems like you have a grasp that certain SERMs have specific affnities to differing receptors WHICH as you clarified are in differing amounts depending on the tissue.

Third: I ask because the only pathways I know of in the steroid biosynthesis for testosterone to convert is either to a DHT derivative or an estrogen. Unless Trest is a progesterone and not a testosterone derivative then I would need to see how this will go backwards when I do no think there is an enzyme to convert testosterone derivatives back to progesterone.

Furthermore when I did my trest/dmz cycle(I logged it) I went and got a script for exemestane and that controlled that just fine. The prolactin issues with trest is another story that you are right and an AI would not control.
 
copied from another site. take it or leave it


Clomid

Agonist: Liver
Antagonist: Brest/nipple

Clomid is a really harsh drug it should be avoided at all costs, if you get the visual sides/blurry vision from clomid they stay for life! They are rare but do happen

Clomid should only be used in restart protocols imo by the supervision of a doctor. So if you want to start producing sperm again you will have to take hcg along with clomid for 9-12months straight. It has some use in pct but it can be completely avoided by using serms only or ideally nolvadex + aromasin


site your source
 
copied from another site. take it or leave it


Clomid

Agonist: Liver
Antagonist: Brest/nipple

Clomid is a really harsh drug it should be avoided at all costs, if you get the visual sides/blurry vision from clomid they stay for life! They are rare but do happen

Clomid should only be used in restart protocols imo by the supervision of a doctor. So if you want to start producing sperm again you will have to take hcg along with clomid for 9-12months straight. It has some use in pct but it can be completely avoided by using serms only or ideally nolvadex + aromasin
Torem is the preferred SERM because of clomid side effects (in some)

I have problems with other things you have stated but I don't have the time to get into all of this right now.
 
copied from another site. take it or leave it


Clomid

Agonist: Liver
Antagonist: Brest/nipple

Clomid is a really harsh drug it should be avoided at all costs, if you get the visual sides/blurry vision from clomid they stay for life! They are rare but do happen

Clomid should only be used in restart protocols imo by the supervision of a doctor. So if you want to start producing sperm again you will have to take hcg along with clomid for 9-12months straight. It has some use in pct but it can be completely avoided by using serms only or ideally nolvadex + aromasin

I was trying to stay out of your nonsense but this wrong. I’m have experience with Clomid as a “too low to measure” sperm patient and to raise test, and yes, all with Dr supervision.
 
I was trying to stay out of your nonsense but this wrong. I’m have experience with Clomid as a “too low to measure” sperm patient and to raise test, and yes, all with Dr supervision.

Clomid works wonder with that. But some individuals really struggle with emotional sides. Others need to regulate estrogen with an AI and SERM.

Others need str8 HCG because the SERM route was too rough. A lot of factors. Glad you got a doctor to help, and I hope it was a good experience. With doctors it can be hit or miss depending how comfortable they are with that.
 
never heard anyone complain about vision from years on forums but here you go anyway, its good to know all the sides possible if your using a drug

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An acute form of toxicity with TMX has been described. Symptoms include an acute loss of vision, retinal edema, retinal hemorrhage and optic disc swelling. These findings may be due to TMX’s estrogenic activity, which may cause venous thromboembolism, but are reversible on discontinuation of the drug [19,20,21]. Due to the similar estrogen receptor action of CC, professionals should be aware of this danger.
 
I was trying to stay out of your nonsense but this wrong. I’m have experience with Clomid as a “too low to measure” sperm patient and to raise test, and yes, all with Dr supervision.
that was one of the first things I said, if your going to use it long term it should be under doctor supervision. I have used clomid alot for pct but now I blast and cruise
 
First: Okay if you want to argue different cells have different amounts of certain receptors we are in agreement. That clarification goes a long way.

Second: When i was reading through the current argument that was the biggest miscommunication that I was noticing. Arguing affinity between SERMS and estrogen is pointless as you know because SERMs where designed to have a higher affinity. And it seems like you have a grasp that certain SERMs have specific affnities to differing receptors WHICH as you clarified are in differing amounts depending on the tissue.

Third: I ask because the only pathways I know of in the steroid biosynthesis for testosterone to convert is either to a DHT derivative or an estrogen. Unless Trest is a progesterone and not a testosterone derivative then I would need to see how this will go backwards when I do no think there is an enzyme to convert testosterone derivatives back to progesterone.

Furthermore when I did my trest/dmz cycle(I logged it) I went and got a script for exemestane and that controlled that just fine. The prolactin issues with trest is another story that you are right and an AI would not control.
Actually most enzymes work both ways. But thats not my point though. It does not need to go other way with enzymes to turn it into one thing or an other to be converted to estrogen. It goes directly from trest(7a-methyl-19-nortestosterone) to estrogen. It just does not do this through aromatase. Its actually other enzymes in the liver that reduces it to estrogens. All 19nors are this way. So AIs do sh!t to protect you. 2kvette can explains this way better though
 
copied from another site. take it or leave it


Clomid

Agonist: Liver
Antagonist: Brest/nipple

Clomid is a really harsh drug it should be avoided at all costs, if you get the visual sides/blurry vision from clomid they stay for life! They are rare but do happen

Clomid should only be used in restart protocols imo by the supervision of a doctor. So if you want to start producing sperm again you will have to take hcg along with clomid for 9-12months straight. It has some use in pct but it can be completely avoided by using serms only or ideally nolvadex + aromasin
Thats wrong. To imply this its reverse agonist a ER-a while agonist at ER-b. Not certian cells. Its has a higher affinity for certian cells than other though.
 
Actually most enzymes work both ways. But thats not my point though. It does not need to go other way with enzymes to turn it into one thing or an other to be converted to estrogen. It goes directly from trest(7a-methyl-19-nortestosterone) to estrogen. It just does not do this through aromatase. Its actually other enzymes in the liver that reduces it to estrogens. All 19nors are this way. So AIs do sh!t to protect you. 2kvette can explains this way better though


Okay you need to clarify because depending on your pathway there are irreversible steps that are one way and these many time are your rate limiting steps. If you are talking about the majority of intermediary steps within a pathway okay, but rate limiting steps which prevent end products from being converted backwards(which is what im specifically talking about now with testosterone to progesterone) are a big important exception.

This is where I need to brush up on this topic because I can't think of ANY other enzymes that convert testosterone derivative to estrogens OTHER then aromatase enzymes.

But what I think you are referring to is not the conversion to estrogen thats the problem but the predispostion of 19nor compounds to cause elevations in prolactin....is that what you are referring to? because this would then cause gyno which many would attribute to estrogen but would be doing so in error.
 
First: Okay if you want to argue different cells have different amounts of certain receptors we are in agreement. That clarification goes a long way.

Second: When i was reading through the current argument that was the biggest miscommunication that I was noticing. Arguing affinity between SERMS and estrogen is pointless as you know because SERMs where designed to have a higher affinity. And it seems like you have a grasp that certain SERMs have specific affnities to differing receptors WHICH as you clarified are in differing amounts depending on the tissue.

Third: I ask because the only pathways I know of in the steroid biosynthesis for testosterone to convert is either to a DHT derivative or an estrogen. Unless Trest is a progesterone and not a testosterone derivative then I would need to see how this will go backwards when I do no think there is an enzyme to convert testosterone derivatives back to progesterone.

Furthermore when I did my trest/dmz cycle(I logged it) I went and got a script for exemestane and that controlled that just fine. The prolactin issues with trest is another story that you are right and an AI would not control.
Also the dmz is probably partnof the reason for lack of estrogen side. Moreso than the ai. I dont have time to go in depth as to whh though.
 
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More Serious Side Effects

Blurred vision is a possible serious side effect, as it can worsen and potentially cause permanent vision damage if left untreated. If you experience blurred vision or vision disturbances while taking Clomid, contact your doctor as soon as possible.
 
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Clomid works wonder with that. But some individuals really struggle with emotional sides. Others need to regulate estrogen with an AI and SERM.

Others need str8 HCG because the SERM route was too rough. A lot of factors. Glad you got a doctor to help, and I hope it was a good experience. With doctors it can be hit or miss depending how comfortable they are with that.
Sorry but hcg leads to more problems than it solves. Ill go into why whenni get off work
 
Also the dmz is probably partnof the reason for lack of estrogen side. Moreso than the ai. I dont have time to go in depth as to whh though.

That would be an interesting convo for a later time.
 
Sorry but hcg leads to more problems than it solves. Ill go into why whenni get off work

Sorry by HCG should not be used willy nilly...anything whether it be SERMs, HCG, etc there is always cons and negative side effects. Weighing risk/benefit ratio is individualized.

So sorry depending on the problem and the issues at play that statement is an oversimplification to the point of being incorrect.
 
Somebody has been taking their smart pills
 
Okay you need to clarify because depending on your pathway there are irreversible steps that are one way and these many time are your rate limiting steps. If you are talking about the majority of intermediary steps within a pathway okay, but rate limiting steps which prevent end products from being converted backwards(which is what im specifically talking about now with testosterone to progesterone) are a big important exception.

This is where I need to brush up on this topic because I can't think of ANY other enzymes that convert testosterone derivative to estrogens OTHER then aromatase enzymes.

But what I think you are referring to is not the conversion to estrogen thats the problem but the predispostion of 19nor compounds to cause elevations in prolactin....is that what you are referring to? because this would then cause gyno which many would attribute to estrogen but would be doing so in error.
First part is true. I didn't touch on this as this is not my point. So i didnt want to go down this path. But i agree.

Second thare are other enzymes that can do this for sure. I dont know what they are with out looking them up and i dont have tine for that right now. Thats why im tagging 2kvette

Third is no im not talking about prolactin at all. Im talking about estrogen.
 
Invalid Link Removed

More Serious Side Effects

Blurred vision is a possible serious side effect, as it can worsen and potentially cause permanent vision damage if left untreated. If you experience blurred vision or vision disturbances while taking Clomid, contact your doctor as soon as possible.
Without a doubt. Clomid can be quite toxic
 
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