Clomid during cycle

[rtmilburn]

And this isn’t to say that an AI might not help control gyno overall on a 19-nor after all.

Consider someone taking 500 test with 500 NPP...yes the AI will not prevent the NPP’s conversion to estrogen, but the effects handling the aromatization of test are certainly still of value here in the overall hormonal balance. I personally would definitely be on both a SERM & an AI in this cycle scenario.

Agreed.

 

[2kvette]

so....you do realize that what you posted did not state that cytochrome p450 is not able to aromatize...it stated that its not necessary to do so

Furthermore you by no means verified that 19nors are NOT aromatized. That article stated that THEY DO AROMATIZE(and the population there was women) and they can do so via more then one mechanism.

Lastly human placental estrogen synthetase has shown the ability to aromatize both test and 19nors equally effective.

Anyone who can read can see that what you posted as a source doesnt support that trest doesnt aromatize. It talks about why it does so quickly, they were discussing for the mechanism by which it does this.

Edit: and estrogen synthetase is a kind of cytochrome p450

You do realize that cytochrome p450 is a term used that encompasses a large family of metabolic enzymes, of which Cyp19A1 (aromatase aka human placental estrogen synthetase), is a member of.

Of course I realize this, it was the entire point of my post. Aromatase inhibitors are worthless here, theyre specific to the heme in cyp19A1. Of which 19-nors are not substrates.

I never said they did not become aromatic in the chemical sense, as that is not within the scope of this discussion. They DO NOT AROMATIZE in the classical sense understood by members of this community. (The population there was no one, it was a review, not a study)

Lastly, human placental estrogen synthetase is aromatase which is also Cyp19A1.

Anyone who can read and can interpret the literature properly can see what I posted as a source was an explanation as to why AI's are not useful to combat 19-nor aromatization. As they do not undergo aromatization via the aromatase enzyme. They are isomerized via other cyp's, and then undergo enolization, and then O-demethylation, and lastly keto-enol tautomerization to yield estradiol. Tautomerization is not aromatization.

And they do not undergo this to an equal extent to testosterone, not even close. I really like the excerpt from this article in the journal rheumatology to demonstrate how little 19-nors convert to estrogens. Nandrolone, without testosterone, causes a huge drop in estradiol, and then osteoporosis.

"An RCT of the anabolic steroid nandrolone in 21 men with idiopathic osteoporosis showed an increase in bone density after 3 months of treatment, which decreased to basal levels after 1 yr of treatment [17]. The apparent lack of benefit with nandrolone may be related to suppression of endogenous testosterone production and the inability to aromatize anabolic steroids such as nandrolone to oestradiol."

https://academic.oup.com/rheumatology/article/39/10/1055/1783830

 

[GoHardOrGoHme]

SUPER LONG POST ATTACK!

You do realize that cytochrome p450 is a term used that encompasses a large family of metabolic enzymes, of which Cyp19A1 (aromatase aka human placental estrogen synthetase), is a member of.

Of course i do which is why i said a KIND OF....that implies I am aware cyp450 is more than a singular enzyme. Its more like over 50 different enzymes that are considered cyp450(but shocker about 6 of them metabolize around 90% of drugs)..but obviously you couldnt interpret that from my posts.

Of course I realize this, it was the entire point of my post. Aromatase inhibitors are worthless here, theyre specific to the heme in cyp19A1. Of which 19-nors are not substrates.

Im giving you credit for being right. I have no issue that in this instance I that learned from you. However it's not penetrating your freaking retinas that initially there were still things I was questioning despite your mechanism. You sound like you have more then a high school diploma, so you know very well, it's common practice academic, medical, or any higher learning circles to question things and to continue discussing them if there are factors that were not addressed.

I never said they did not become aromatic in the chemical sense, as that is not within the scope of this discussion. They DO NOT AROMATIZE in the classical sense understood by members of this community. (The population there was no one, it was a review, not a study)

you are right, they convert to estrogen through another pathway that I was not accounting for. I was definitely not thinking about the actual reaction at play. I'll admit it, I think in anatomy and physiology, not chemistry. I think about how it affects homeostasis and not how the molecule changes. So I will gladly give you credit for showing me the answer through a the chemical reaction. kudos to you sir

HOWEVER, it was a review based on an observation in a population! postmenopausal women. It literally was exploring the clinical implications within that population.In both the opening context and the clinical implications drawn in the conclusion. So let me re-word this: The population or the group of people that this was observed in, lead to a review on the underlying mechanism taking place so the clinical implications can be discussed for this group of people who may undergo treatment with said drugs.

Lastly, human placental estrogen synthetase is aromatase which is also Cyp19A1.

EXACTLY, it is an aromatase that CAN aromatize 19nors. It was an unaddressed factor. This goes against the proposed reasoning that a 19nor cannot be aromatized by a classical aromatase enzyme. I dug a little deeper and found some literature that further elaborates on how human aromatase in the presence of MENT does not create estrogen. This feeds into your point further strengthening your argument. Below you add another article that further supports this. It would have been AWESOME if you posted that earlier. This is good...this answers questions and furthers understandings.

Anyone who can read and can interpret the literature properly can see what I posted as a source was an explanation as to why AI's are not useful to combat 19-nor aromatization. As they do not undergo aromatization via the aromatase enzyme. They are isomerized via other cyp's, and then undergo enolization, and then O-demethylation, and lastly keto-enol tautomerization to yield estradiol. Tautomerization is not aromatization.

One thing is interpret literature, the next step is to analyze the holes in said literature to create a better understanding of the matter at hand. This is Evidence Based Medicine 101(AKA what people on these boards attempt to do...cite an article and give suggestions based on said research)....you have to be able to see the weakness of a paper to know how to apply it or when not to apply it and what extra evidence is needed to support the conclusion. So you may be able to interpret what you post but you obviously couldnt realize the conclusion of the paper was clinical implications in postmenopausal women...which is the population that paper was discussing.

You didnt pick up on the fact that there is literature to support cyp enzymes that can aromatize 19nors in the classical sense. You presented something, I asked for the source to read it because I thought it was interesting. And before Im done reading it you start with smart ass remarks instead of posting the article you did not to long ago.

And they do not undergo this to an equal extent to testosterone, not even close. I really like the excerpt from this article in the journal rheumatology to demonstrate how little 19-nors convert to estrogens. Nandrolone, without testosterone, causes a huge drop in estradiol, and then osteoporosis.


"An RCT of the anabolic steroid nandrolone in 21 men with idiopathic osteoporosis showed an increase in bone density after 3 months of treatment, which decreased to basal levels after 1 yr of treatment [17]. The apparent lack of benefit with nandrolone may be related to suppression of endogenous testosterone production and the inability to aromatize anabolic steroids such as nandrolone to oestradiol."

https://academic.oup.com/rheumatology/article/39/10/1055/1783830

Notice responses in bold. I give you the credit for being right. Seriously, thank you, take the credit you deserve for teaching us something, but also take credit when you're missing the mark.

And if there is something Im missing, I'll be happy to take it back, apologize and give credit where credit is due. I don't NEED to be right, i just want what is right to be what is perpetuated.

And let me post the summary of the article you posted so we can get on the same page:

Can 19-nortestosterone derivatives be aromatized in the liver of adult humans? Are there clinical implications?

Abstract
CONTEXT:
Previous studies in postmenopausal women have demonstrated that, after oral administration of norethisterone, a small proportion of the compound is rapidly converted into ethinylestradiol. The shape of the concentration - time curve suggested that this occurred in the liver. The results were confirmed by in vitro investigations with adult human liver tissue. In 2002, it was shown that, after oral treatment of women with tibolone, aromatization of the compound occurred, resulting in the formation of a potent estrogen, 7 alpha-methyl-ethinylestradiol. The result has been called into question, because the adult human liver does not express cytochrome P450 aromatase, which is encoded by the CYP 19 gene. Moreover, it has been claimed that the serum level of 7 alpha-methyl-ethinylestradiol measured by gas chromatography/mass spectrometry was an artifact.
REPLY:
Aromatization of steroids is a complex process of consecutive oxidation reactions which are catalyzed by cytochrome P450 enzymes. The conversion of the natural C19 steroids, testosterone and androstenedione, into estradiol-17beta and estrone is dependent on the oxidative elimination of the angular C19-methyl group. This complex key reaction is catalyzed by the cytochrome P450 aromatase, which is expressed in many tissues of the adult human (e.g. ovary, fat tissue), but not in the liver. However, 19-nortestosterone derivatives are characterized by the lack of the C19-methyl group. Therefore, for the aromatization of these synthetic steroids, the action of the cytochrome P450 aromatase is not necessary and the oxidative introduction of double bonds into the A-ring can be catalyzed by other hepatic cytochrome P450 enzymes. The final key process in the formation of a phenolic A-ring, both in natural androgens and 19-nortestosterone derivatives, is the enolization of a 3-keto group to the C2-C3-enol or the C3-C4-enol moiety, which occurs without the action of enzymes.
CONCLUSION:
19-nortestosterone derivatives (norethisterone, norethynodrel, tibolone) can readily be aromatized in the adult human liver. This leads to the formation of the potent estrogens ethinylestradiol from norethisterone or norethynodrel and 7 alpha-methyl-ethinylestradiol from tibolone. This may have clinical consequences, e.g. the elevated risk of venous thromboembolic disease in premenopausal women treated with high doses of norethisterone for bleeding disorders, or the elevated risk of stroke or endometrial disease in postmenopausal women treated with tibolone.

 

[Dthcore]

And this isn’t to say that an AI might not help control gyno overall on a 19-nor after all.

Consider someone taking 500 test with 500 NPP...yes the AI will not prevent the NPP’s conversion to estrogen, but the effects handling the aromatization of test are certainly still of value here in the overall hormonal balance. I personally would definitely be on both a SERM & an AI in this cycle scenario.

Whoooooa sheeeeet!!! I’m so happy I read this that’s what my first cycle is going to consist of and I was only going to use aromasin. What would be the appropriate serm for NPP?

 

[2kvette]

Notice responses in bold. I give you the credit for being right. Seriously, thank you, take the credit you deserve for teaching us something, but also take credit when you're missing the mark.

And if there is something Im missing, I'll be happy to take it back, apologize and give credit where credit is due. I don't NEED to be right, i just want what is right to be what is perpetuated.

And let me post the summary of the article you posted so we can get on the same page:

Can 19-nortestosterone derivatives be aromatized in the liver of adult humans? Are there clinical implications?

Abstract
CONTEXT:
Previous studies in postmenopausal women have demonstrated that, after oral administration of norethisterone, a small proportion of the compound is rapidly converted into ethinylestradiol. The shape of the concentration - time curve suggested that this occurred in the liver. The results were confirmed by in vitro investigations with adult human liver tissue. In 2002, it was shown that, after oral treatment of women with tibolone, aromatization of the compound occurred, resulting in the formation of a potent estrogen, 7 alpha-methyl-ethinylestradiol. The result has been called into question, because the adult human liver does not express cytochrome P450 aromatase, which is encoded by the CYP 19 gene. Moreover, it has been claimed that the serum level of 7 alpha-methyl-ethinylestradiol measured by gas chromatography/mass spectrometry was an artifact.
REPLY:
Aromatization of steroids is a complex process of consecutive oxidation reactions which are catalyzed by cytochrome P450 enzymes. The conversion of the natural C19 steroids, testosterone and androstenedione, into estradiol-17beta and estrone is dependent on the oxidative elimination of the angular C19-methyl group. This complex key reaction is catalyzed by the cytochrome P450 aromatase, which is expressed in many tissues of the adult human (e.g. ovary, fat tissue), but not in the liver. However, 19-nortestosterone derivatives are characterized by the lack of the C19-methyl group. Therefore, for the aromatization of these synthetic steroids, the action of the cytochrome P450 aromatase is not necessary and the oxidative introduction of double bonds into the A-ring can be catalyzed by other hepatic cytochrome P450 enzymes. The final key process in the formation of a phenolic A-ring, both in natural androgens and 19-nortestosterone derivatives, is the enolization of a 3-keto group to the C2-C3-enol or the C3-C4-enol moiety, which occurs without the action of enzymes.
CONCLUSION:
19-nortestosterone derivatives (norethisterone, norethynodrel, tibolone) can readily be aromatized in the adult human liver. This leads to the formation of the potent estrogens ethinylestradiol from norethisterone or norethynodrel and 7 alpha-methyl-ethinylestradiol from tibolone. This may have clinical consequences, e.g. the elevated risk of venous thromboembolic disease in premenopausal women treated with high doses of norethisterone for bleeding disorders, or the elevated risk of stroke or endometrial disease in postmenopausal women treated with tibolone.

Okay, maybe we got off on the wrong foot. I'll say I do indeed have more than a high school diploma. But I don't think that it matters for intelligence, or that I'm smarter than you. I genuinely think that no one is really smarter than anyone, some just have put in the time to understand things, and some just get things quicker than others. But we are all capable of equally understanding.

Now, the population doesn't matter when it comes to cyps. All humans express the same cyps, aside from hereditary SNP's, mutations, and INDELS, which are all not too common, we all have the same cyps. This doesn't change across gender, race, etc.

So, these other cyps dont actually aromatize the 19-nors. They add in some more double bonds, and after the 3 ketone gets converted to the hydroxy, the activity of the enzymes stops there. The introduction of these double bonds, and the enolization(hydroxy next to the double bond), causes a less than favorable state for the A ring energetically. The lowest energy state for it to now assume is the aromatic state. So tautomerization happens, where it spotaneously converts to the aromatic A ring on its own. No enzyme needed.

Also, forget what I said about O-demethylation. For some reason I was picturing catechol-estrogens in my head when I said that. Not applicable here.

 

[GoHardOrGoHme]

Okay, maybe we got off on the wrong foot. I'll say I do indeed have more than a high school diploma. But I don't think that it matters for intelligence, or that I'm smarter than you. I genuinely think that no one is really smarter than anyone, some just have put in the time to understand things, and some just get things quicker than others. But we are all capable of equally understanding.

We agree on this. This is why I enjoy learning from others. No one has the time to study everything nor has a passion to study everything.

Now, the population doesn't matter when it comes to cypsthis is true if we all produce the same amount of them. All humans express the same cyps, aside from hereditary SNP's, mutations, and INDELS, which are all not too common, we all have the same cyps. This doesn't change across gender, race, etc.

This is where I disagree to a point. I won't argue all humans have the ability to express any and all cyps, but this does not account for how we all metabolize drugs differently. The rate of expression is what matters here in this argument. Simply put, just because you and I are both human does not mean we will metabolize the same drug equally, because we will express the enzyme to break it down at different rates(this is NOT the only factor in drug metabolism or effectiveness. It is one part of a multifactorial equation) Drug metabolism between individuals, between sexes differs. Of the theories why this is so is the expression of cyp to the absence of certain cyps. For the sake of this discussion I will choose the stance that the rate of expression differs between sexes. We all are capable of producing them, but genetically not all are programmed to make at equal rates. This is why drug metabolism between individuals differs. The applies down to differing ethnicities at times.

We agree on hereditary SNPs beting different etc etc.

So, these other cyps dont actually aromatize the 19-nors. They add in some more double bonds, and after the 3 ketone gets converted to the hydroxy, the activity of the enzymes stops there. The introduction of these double bonds, and the enolization(hydroxy next to the double bond), causes a less than favorable state for the A ring energetically. The lowest energy state for it to now assume is the aromatic state. So tautomerization happens, where it spotaneously converts to the aromatic A ring on its own. No enzyme needed.

Also, forget what I said about O-demethylation. For some reason I was picturing catechol-estrogens in my head when I said that. Not applicable here.

We are both in agreement that cyps are not needed for 19nors. If there is new data to disagree with this, we can re-open the discussion to close the loop,but at the moment the argument appears pretty strong with the current data presented.

The only point worth discussing, being there is a differing stance(or appears to be a different stance), is the point that everyone expresses the same cyps. We may all have the ability to, but we expresses them at different rates/quantities. This is a HUGE factor in how individuals react to drugs.


Sex Differences in Pharmacokinetics and Pharmacodynamics
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3644551/

Sex Differences in the Expression of Hepatic Drug Metabolizing Enzymes
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2713118/

Sex-specific differences in CYP450 isoforms in humans
https://www.tandfonline.com/doi/abs/10.1517/17425255.4.4.413?journalCode=iemt20

 

[GoHardOrGoHme]

On a tangent note/back to the original point of this thread:

Did anyone ever produce bloodwork on cycle to show that LH and FSH are being produced within a normal range while on cycle using clomid?

We already have studies to indicate HCG will maintain fertility while on exogenous test, however I would like to see if there is any bloodwork to indicate continual release of gonadotropins when using clomid on exogenous hormones.

 

[rtmilburn]

On a tangent note/back to the original point of this thread:

Did anyone ever produce bloodwork on cycle to show that LH and FSH are being produced within a normal range while on cycle using clomid?

We already have studies to indicate HCG will maintain fertility while on exogenous test, however I would like to see if there is any bloodwork to indicate continual release of gonadotropins when using clomid on exogenous hormones.

Not as far as im aware of, other than the studies i posted.

 

[GoHardOrGoHme]

Not as far as im aware of, other than the studies i posted.

I gotta go back through to see what you posted. Thank you sir!

 

[rtmilburn]

I gotta go back through to see what you posted. Thank you sir!

They may not be the best studies. However, i do feel that they do give us a decent idea, of the possible benefits of clomiphene has while on cycle.

 

[Hyde]

Whoooooa sheeeeet!!! I’m so happy I read this that’s what my first cycle is going to consist of and I was only going to use aromasin. What would be the appropriate serm for NPP?

I have never used NPP, but personally Raloxifene at 50-60mg/day or Toremifene at 30-60mg/day is what I would use.

You may not need it, so you could try without. If you are lean and don’t aromatize much it could be a non-issue.

Tamoxifen would also work, but the above 2 offer some health benefits that Nolva doesn’t. Clomid is not good for protecting the chest.

On a tangent note/back to the original point of this thread:

Did anyone ever produce bloodwork on cycle to show that LH and FSH are being produced within a normal range while on cycle using clomid?

We already have studies to indicate HCG will maintain fertility while on exogenous test, however I would like to see if there is any bloodwork to indicate continual release of gonadotropins when using clomid on exogenous hormones.

I’m testing a low dose of Toremifene now, won’t have bloods for 6 more weeks I expect tho.

 

[RickyBlobby]

On a tangent note/back to the original point of this thread:

Did anyone ever produce bloodwork on cycle to show that LH and FSH are being produced within a normal range while on cycle using clomid?

We already have studies to indicate HCG will maintain fertility while on exogenous test, however I would like to see if there is any bloodwork to indicate continual release of gonadotropins when using clomid on exogenous hormones.

The fact my T was in normal range after 10 weeks of dbol and primo kinda tells you it works. I did not check my LH though. If I weren't on TRT I would experiment again.

 

[NoAddedHmones]

The fact my T was in normal range after 10 weeks of dbol and primo kinda tells you it works. I did not check my LH though. If I weren't on TRT I would experiment again.

Im sold!

 

[CatSnake]

Correct.

Not only do SERMs not bind to all estrogen receptor throughout the body, but each SERM differs in its selectivity/binding affinity for various receptors. This is why Nolvadex, despite being a SERM just like Clomid, is generally much more effective than Clomid in combating gyno.

So, even if a SERM is used at a very high dosage, all that estrogen will still be floating around the bloodstream and will attach to those receptors that the SERM does not target. Furthermore those "free" receptors will be hammered with even larger amounts of estrogen than they would have otherwise, due to the extra estrogen being knocked off the receptors that the SERM does target.

This is why a bodybuilder could use 100 mg of Clomid, yet after using 2 grams of test for 6 weeks he is holding more water than the Atlantic. That water retention is mediated directly by estrogen receptor binding--receptors that the SERM does not target.

Aromatase Inhibitors are also selective in that they do not stop all estrogen conversion, no matter how much someone takes. Although AI's are generally universally effective in reducing total estrogen levels, each AI targets aromatase in different tissues to different degrees. For example, Exemestane, despite being more selective than other AI's (in general), still binds to brain aromatase to a higher degree than something like Anastrozole. Aromatase in this area of the brain plays a critical role in sexual functioning/libido, which is why exemestane is known to cause sexual dysfunction/libido issues far more often than Anastrozole, which, for the most part, doesn't interfere with aromatase in this area of the body. It's also why the different AI's affect cholesterol levels to different degrees, with letrozole being the most damaging and exemestane being the least damaging.

This variance in aromatase selectivity/affinity is the reason why each AI (and SERM) has different effects throughout the body...and why each drug is indicated for the treatment of different medical conditions. Some might be more effective for treating breast cancer, while others are more effective for treating other types of cancer.

Estrogen also has non-genomic effects, which take place in full regardless of whatever SERM is used. A non-genomic effect is usually defined as any effect that does not directly and initially influence gene expression. Non-genomic effects frequently involve the generation of intracellular second messengers and various signal-transduction cascades, such as ion fluxes, protein kinase pathways, and cyclic AMP modulation. Only AI's can reduce estrogen's non-genomic effects, but they do so indirectly by lowering total estrogen concentrations.

millburn, you need to read this ^

 

[rtmilburn]

millburn, you need to read this ^

Ive read it. Thing is, I dont see evidence to prove this. Its a working theory backed with some evidence, that we have as of now, but is came about with making are own conclusions. Not that there is anything wrong with this, as we have to do this. Reasong being is there is not going to be research to back MOST of what we say 100%. Best we can do is follow smart peoples advice (such as mike), but that doesnt mean that we shouldn't question it.

It could be very well be true, but to take this as fact just because mike said it, is well..... short sided.

Do not get me wrong i like Mike Arnold ALOT! He is a great dude and is VERY intelligent(way smarter than me no doubt). I also love how he runs his business and i love his products. So dont take anything im saying as a shot at mike.

Now im not saying im right persay, i very well could be wrong. But i provided the evidence of a wide range of cells that serm DO effect, assumably stonger than estrogen(this statement could very well be false too). With that i made MY conclusion, that there is a good chance that a serm (such as torem or nolva but not clomid) could very well bind to all receptors, in the human body, with a higher affinity than estrogen.

Either way torem is proven to bind strongly to prostate, breast, and assumably hypothalamic cells. While also providing better lipid panels and i think it even improved blood pressure (this could very well be wrong, as i genuinely cant remember. I look it up later). So it is providing protection the the thing we want to protect the most. So what would be the big deal if it doesnt bind to all the receptors better than estrogen?

 

[Dthcore]

I have never used NPP, but personally Raloxifene at 50-60mg/day or Toremifene at 30-60mg/day is what I would use.

You may not need it, so you could try without. If you are lean and don’t aromatize much it could be a non-issue.

Tamoxifen would also work, but the above 2 offer some health benefits that Nolva doesn’t. Clomid is not good for protecting.

Could raloxifine substitute the idea behind clomid during cycle? So that when one comes off it’s a lot smoother or should a low dose clomid be taken to keep the boys “going” aswell?

 

[hairygrandpa]

Could raloxifine substitute the idea behind clomid during cycle? So that when one comes off it’s a lot smoother or should a low dose clomid be taken to keep the boys “going” aswell?

I use ralox to keep gyno at bay on cycle. Ralox does not stimulate HPTA as much as Chlomid does. Meaning:
Ralox on cycle = no tits
Chlomid/Torem on cycle = keeping nuts going

 

[rtmilburn]

Also GoHardOrGoHome you said inverse agonist and antagonist were synonyms, but they are not. A simple search on google shows thats wrong.

https://en.m.wikipedia.org/wiki/Inverse_agonist

Sure this this wiki but there are numerous of articles saying the same. But this is an easier read for most and is factually correct. Sooo.......

 

[Dthcore]

I use ralox to keep gyno at bay on cycle. Ralox does not stimulate HPTA as much as Chlomid does. Meaning:
Ralox on cycle = no tits
Chlomid/Torem on cycle = keeping nuts going

Can’t do both?

 

[hairygrandpa]

Can’t do both?

Most people use serms after a cycle for PCT -and an AI on cycle to lower e2 conversion, because they use test as a base. A serm for HPTA support makes only sense if you don't use test, IMHO. Ralox on cycle is only needed if someone is very gyno prone.
rtmilburn ,
what I'm not sure is, if chlomid and/or Torem is used on a Trest cycle (or any high dosed suppressive cycle) does it really keeps the nuts going? Trest is possibly the most suppressive of all roids, right? I know it worked with a moderate T-bol cycle and works possibly with Anavar and Winstrol too, when no test is used as a base.

 

[Jinsun]

Most people use serms after a cycle for PCT -and an AI on cycle to lower e2 conversion, because they use test as a base. A serm for HPTA support makes only sense if you don't use test, IMHO. .

Not if a serm helps the gonads even without hypothalamus activation. In that case it can be beneficial to run it.

 

[rtmilburn]

Most people use serms after a cycle for PCT -and an AI on cycle to lower e2 conversion, because they use test as a base. A serm for HPTA support makes only sense if you don't use test, IMHO. Ralox on cycle is only needed if someone is very gyno prone.
rtmilburn ,
what I'm not sure is, if chlomid and/or Torem is used on a Trest cycle (or any high dosed suppressive cycle) does it really keeps the nuts going? Trest is possibly the most suppressive of all roids, right? I know it worked with a moderate T-bol cycle and works possibly with Anavar and Winstrol too, when no test is used as a base.

I'ma gonna have to disagree with you here big guy. I think if you can maintain some hpta function while on cycle you should. It will make transitioning from on to off cycle way easier.

 

[Jinsun]

I'ma gonna have to disagree with you here big guy. I think if you can maintain some hpta function while on cycle you should. It will make transitioning from on to off cycle way easier.

I really doubt serms can fight against high androgen amounts. It didn't for me on a low dose test and a PH. I think the most benefits are from the serm acting directly on the nuts... But all in all the situation is most probably not as black and white as we would like it to be. If it works will most probably depend on the compounds and the amounts of them being used - with the inclination that on most normaly suppressive compound cycles it wont work. That's just my guess.

 

[rtmilburn]

I really doubt serms can fight against high androgen amounts. It didn't for me on a low dose test and a PH. I think the most benefits are from the serm acting directly on the nuts... But all in all the situation is most probably not as black and white as we would like it to be. If it works will most probably depend on the compounds and the amounts of them being used - with the inclination that on most normaly suppressive compound cycles it wont work. That's just my guess.

I think dose of serm and serm in play also makes a difference. Nolva isnt the strongest for hpta function, way better than ralox but still.... You were using a lower dose (10mg right). 60mg torem or 25mg clomid would be the minimum i would use for this. Now i do agree with you to an extent. I don't think you can prevent trest supression, but the rest possibly.

 

[Jinsun]

I think dose of serm and serm in play also makes a difference. Nolva isnt the strongest for hpta function, way better than ralox but still.... You were using a lower dose (10mg right). 60mg clomid or 25mg clomid would be the minimum i would use for this. Now i do agree with you to an extent. I don't think you can prevent trest supression, but the rest possibly.

Nop I was using 20mg for almost 2 weeks. Before that I was using 10mg for 10 days. None woorked. I think 20mg tamox should be enough if there was a chance of it working...

 

[rtmilburn]

Nop I was using 20mg for almost 2 weeks. Before that I was using 10mg for 10 days. None woorked. I think 20mg tamox should be enough if there was a chance of it working...

Idk clomid is significantly stronger. Also 20mg of nolva is definitely a decent dose, but i would consider 30-40mg for this purpose. We'll see though, as hyde is also getting bloodwork done. So with his and yours we should get a ok idea what possibly is going on.

 

[Mike Arnold]

Great, great thread here.

 

[Jinsun]

Idk clomid is significantly stronger. Also 20mg of nolva is definitely a decent dose, but i would consider 30-40mg for this purpose. We'll see though, as hyde is also getting bloodwork done. So with his and yours we should get a ok idea what possibly is going on.

Yes we shall

Re nolva: 40mg for the duration of the whole cycle haha no way. Also clomid is not that much stronger. I think we already debated that in this thread. Imo if nolva was going to do something at 40mg it would have done at least something at 20mg... Again, we are aren't doing anything for the androgen negative feedback loop which is stronger the estrogen's (I suppose).

What about GnRh?

 

[rtmilburn]

Yes we shall

Re nolva: 40mg for the duration of the whole cycle haha no way. Also clomid is not that much stronger. I think we already debated that in this thread. Imo if nolva was going to do something at 40mg it would have done at least something at 20mg... Again, we are aren't doing anything for the androgen negative feedback loop which is stronger the estrogen's (I suppose).

What about GnRh?

Would not touch any GnRh analogues. Usually to strong and can cause chemical castration. As single moderate dose is fine, but to keep production during a cycle you would need more than that.

Like we discussed there are definitely other things at play in the hormone production feedbacks. Gaba receptors do, opiod receptors do, cannabiniod receptors do, and im sure there is more. This is all out side the standard estrogen and androgen receptors.

Low dose naltrexone(sp?) could help, there are some natural gaba supps the may help. Theoretically 7,8benzoflavone(might be a different one) would be amazing for this, but i suspect it doesnt actually cross the BBB.

 

[Jinsun]

So I'm thinking of trying clomid, to see if it works. I've never used it before, so here is my biggest fear, I've got sh*ty eyes: floaters, some little dead spots, and a bit of astigmatism. I know clomid can cause eye problems, especially stuff like floaters, so what do you guys think, is it safe for me to test it? I'm just ordering some stuff...

 

[heckler7]

So I'm thinking of trying clomid, to see if it works. I've never used it before, so here is my biggest fear, I've got ****ty eyes: lots of floaters, some little dead spots, an bit of astigmatism. I know clomid can cause eye problems, especially stuff like floaters, so what do you guys think, is it safe for me to test it? I'm just ordering some stuff...

ugh I was trying to pm youand it disapperad, if I was you I wouldnt mess with clomid or sarms. just me .02 and watch your BP, I lost my vision on insulin for 3 weeks, its scarely as hell

 

[rtmilburn]

ugh I was trying to pm youand it disapperad, if I was you I wouldnt mess with clomid or sarms. just me .02 and watch your BP, I lost my vision on insulin for 3 weeks, its scarely as hell

Agreed. With vision issues don't touch clomid

 

[GoHardOrGoHme]

Also GoHardOrGoHome you said inverse agonist and antagonist were synonyms, but they are not. A simple search on google shows thats wrong.

https://en.m.wikipedia.org/wiki/Inverse_agonist

Sure this this wiki but there are numerous of articles saying the same. But this is an easier read for most and is factually correct. Sooo.......

Want to get snarky and condescending? When I really want to keep things professional and cordial...lets get into this

This is what I get for painting things in broad brush strokes. Let's get into this and add a little context to give my response.

You are right that technically they are not the same(if are using one specific train of thought). If I would have left it at reverse agonist(in reference to drug action and physiological processes) then the post would have been correct(unless you want to really argue reverse agonist and inverse agonist are the same).

This comment you speak of was when I saying clomid was an both a partial agonist and an antagonist....you disagreed(saying no serm is an antagonist, which is obviously wrong) calling it a reverse agonist...I posted a study which stated defined it as part antagonist. At the time I was trying to equate antagonist and reverse agonist(trying to give you some credit), I then added inverse agonist into the statement, which rightfully so if we are being nit-picky, I should not have added that.

I misspoke, to say an antagonist and an inverse agonist are synonyms because technically a neutral antagonist(note the qualifier) and an inverse agonist are different. I could make an argument that an inverse agonist is a type of antagonist(more on this below), in that it stops the activity of an agonist. If I stood by that, you will probably quickly google that an classical antagonist can stop the activity of an inverse agonist, thus making them different. At which point we would just be trying to validate our own points, which isnt really useful.

Im sure if you looked up a drug antagonist you will see that you have multiple types if we use the definition of an antagonist being a receptor or drug that it attenuates or stops a specific effect(or biological response of sorts) as oppose to activating it like an agonist. Using this definition you can then qualify several types, and arguable include inverse agonist in that they do indeed stop a specific biological response(at the expense of causing the opposite response). Note how I said arguably and not definitively because I acknowledge a neutral antagonist has a different end point then an inverse agonist.

Sooo.....if you want to equate reverse agonism and inverse agonism we can just say you were wrong and confused a partial agonist/antagonist with an inverse agonist because you were looking at the end result rather then the receptor activity.

And if you remember what I posted...i said a physiological antagonist(also goes by functional antagonism), which by definition describes the behavior of a substance that produces effects counteracting those of another substance(note how this is producing the opposite effect and not just stopping a given effect which you would argue is an inverse agonist)....so if I REALLY want to get nit-picky, then I can go into why i specifically used that qualifier, to demonstrate that you really didnt understand what I was talking about.

 

[BBiceps]

How’s Torem by itself? I’m using Clomid here and there to get a little boost (love it) but after this thread I want to try Torem, is it worth it?

 

[rtmilburn]

Want to get snarky and condescending? When I really want to keep things professional and cordial...lets get into this

This is what I get for painting things in broad brush strokes. Let's get into this and add a little context to give my response.

You are right that technically they are not the same(if are using one specific train of thought). If I would have left it at reverse agonist(in reference to drug action and physiological processes) then the post would have been correct(unless you want to really argue reverse agonist and inverse agonist are the same).

This comment you speak of was when I saying clomid was an both a partial agonist and an antagonist....you disagreed(saying no serm is an antagonist, which is obviously wrong) calling it a reverse agonist...I posted a study which stated defined it as part antagonist. At the time I was trying to equate antagonist and reverse agonist(trying to give you some credit), I then added inverse agonist into the statement, which rightfully so if we are being nit-picky, I should not have added that.

I misspoke, to say an antagonist and an inverse agonist are synonyms because technically a neutral antagonist(note the qualifier) and an inverse agonist are different. I could make an argument that an inverse agonist is a type of antagonist(more on this below), in that it stops the activity of an agonist. If I stood by that, you will probably quickly google that an classical antagonist can stop the activity of an inverse agonist, thus making them different. At which point we would just be trying to validate our own points, which isnt really useful.

Im sure if you looked up a drug antagonist you will see that you have multiple types if we use the definition of an antagonist being a receptor or drug that it attenuates or stops a specific effect(or biological response of sorts) as oppose to activating it like an agonist. Using this definition you can then qualify several types, and arguable include inverse agonist in that they do indeed stop a specific biological response(at the expense of causing the opposite response). Note how I said arguably and not definitively because I acknowledge a neutral antagonist has a different end point then an inverse agonist.

Sooo.....if you want to equate reverse agonism and inverse agonism we can just say you were wrong and confused a partial agonist/antagonist with an inverse agonist because you were looking at the end result rather then the receptor activity.

And if you remember what I posted...i said a physiological antagonist(also goes by functional antagonism), which by definition describes the behavior of a substance that produces effects counteracting those of another substance(note how this is producing the opposite effect and not just stopping a given effect which you would argue is an inverse agonist)....so if I REALLY want to get nit-picky, then I can go into why i specifically used that qualifier, to demonstrate that you really didnt understand what I was talking about.

Ugh. Sorry brought it up. I don't have the will to continue this with you. Last question how much research went into that? Because it feels like you were googling and googling just to prove a point. I'm not in this for that. I'm sorry.

 

[GoHardOrGoHme]

Ugh. Sorry brought it up. I don't have the will to continue this with you. Last question how much research went into that? Because it feels like you were googling and googling just to prove a point. I'm not in this for that. I'm sorry.

4 years of undergrad, 2 years of grad school, and 4 years of a doctoral degree...so 10 years

I did google a lot of things throughout the 10 years but I didnt keep track.

 

[Hyde]

How’s Torem by itself? I’m using Clomid here and there to get a little boost (love it) but after this thread I want to try Torem, is it worth it?

I’ve only been on 30mg for 18 days or so I believe, but I have zero sides and it doesn’t change how I feel at all (I can feel the mood difference on just 12.5mg Clomid ED or 25 EoD). Nothing bad to report certainly.

If you need protection from gyno, Torem is the better option. If using for a boost to your endogenous test and loving it, I would say stay with the Clomid. It’s cheap and works dandy.

 

[2kvette]

4 years of undergrad, 2 years of grad school, and 4 years of a doctoral degree...so 10 years

I did google a lot of things throughout the 10 years but I didnt keep track.

2 years of grad school and 4 years of doctoral degree? Please explain. I was under the impression graduate school was a doctoral program, and they were all 3 years at least. Except like PA's, I think their program is 4 and 2

 

[rtmilburn]

4 years of undergrad, 2 years of grad school, and 4 years of a doctoral degree...so 10 years

I did google a lot of things throughout the 10 years but I didnt keep track.

Wasn't trying to question your intelligence as a whole. Your a smart dude. I just think that you focus to much on the subtleties of what people are saying, making you not see the whole picture of what they are saying.

Now granted I'm a dick, not gonna deny that.

 

[GoHardOrGoHme]

2 years of grad school and 4 years of doctoral degree? Please explain. I was under the impression graduate school was a doctoral program, and they were all 3 years at least. Except like PA's, I think their program is 4 and 2

All doctoral programs are graduate programs, however not all grad schools/programs are doctorate degrees. Graduate degrees signify something above undergrad. So a master's degree is graduate degree but not a doctorate. A doctorate is simply the highest degree achievable in a given feild. (PhD, PharmD, MD, DO, DPT, DVM, etc etc)

I did a 2 year Masters degree and 4 year doctoral degree(total of 6 years of graduate schooling). However not all doctoral programs are 3 year programs.

 

[GoHardOrGoHme]

Wasn't trying to question your intelligence as a whole. Your a smart dude. I just think that you focus to much on the subtleties of what people are saying, making you not see the whole picture of what they are saying.

Now granted I'm a dick, not gonna deny that.

You're a dick....Im a dick...just too much dick in one thread.

I bet it's a much happier place in the juggs or yoga pants thread.

 

[heckler7]

All doctoral programs are graduate programs, however not all grad schools/programs are doctorate degrees. Graduate degrees signify something above undergrad. So a master's degree is graduate degree but not a doctorate. A doctorate is simply the highest degree achievable in a given feild. (PhD, PharmD, MD, DO, DPT, DVM, etc etc)

I did a 2 year Masters degree and 4 year doctoral degree(total of 6 years of graduate schooling). However not all doctoral programs are 3 year programs.

damn bro, write me a script for HGH, lolz

 

[heckler7]

not saying my AA degree makes me smarter than you but my career is over your heads, i work in aviation

 

[BBiceps]

I’ve only been on 30mg for 18 days or so I believe, but I have zero sides and it doesn’t change how I feel at all (I can feel the mood difference on just 12.5mg Clomid ED or 25 EoD). Nothing bad to report certainly.

If you need protection from gyno, Torem is the better option. If using for a boost to your endogenous test and loving it, I would say stay with the Clomid. It’s cheap and works dandy.

Ok, thanks. Clomid have treated me well so far

 

[2kvette]

not saying my AA degree makes me smarter than you but my career is over your heads, i work in aviation

If I’m ever rich. I’m buying a fighter jet.

 

[GoHardOrGoHme]

If I’m ever rich. I’m buying a fighter jet.

You will win every argument by default.

"Your argument is invalid...i have a fighter jet....boom"

 

[2kvette]

You will win every argument by default.

"Your argument is invalid...i have a fighter jet....boom"

There is this old guy on you tube with a harrier jump jet.

 

[Sparta12]

clomid made me emotional haha, I might try 25-50 on cycle for 6 weeks then swap to torem for pct

 

[heckler7]

If I’m ever rich. I’m buying a fighter jet.

company out here that refurbishes t38 trainers for civilian use, they go super sonic

http://www.thorntonaircraft.com/body/body.cfm?page_name=mil

 

[RickyBlobby]

For years I've been trying to convince people that SERMs on cycle prevent shutdown. There's even published research supporting this. I've run many, many cycles with toremifene and LH/FSH stay within normal range all through cycle. When I come off cycle, I continue the torem for 4 weeks and then stop. T sticks in the 850-950 range with normal LH/FSH.

But what do I know? I'm just some guy on a message board...

Bump