Clomid during cycle

[AnabolicGuru]

You naysayers pick apart every study, claim they are worthless, call Spurfy, me, everyone else who it worked for liars.... What's to say you wont call BS on a legit set of bloods. I mean, anyone call pull blood work of the internet, right?

You just don't want to admit to yourself that you're wrong, because obviously in your mind you're some sort of.........anabolic...guru. LMFAO. Sorry but I don't appreciate being called a liar by some kid behind a keyboard.

Or maybe you don’t want to admit that you’re wrong. The studies you posted were irrelevant, one of them was in reference to clomid being used solo, as opposed to on gear, and the other was like 4 days long. You’ve really given no evidence that wasn’t anecdotal.

 

[RickyBlobby]

I've done my best to remain politically correct, but when people come out and call you a straight up liar, AFTER you've stuck your neck out, gone against the norm and set yourself up for flaming by bringing new information to light, it feels disrespectful and can definitely push buttons.

Bottom line................50mg Dbol and 400mg Primo and 25mg clomid, for 10 weeks, and T was in normal range (450). You'll never be able to convince me it doesn't work after seeing the paperwork with my own two eyes. Now if you want to argue as to how my level was at 450 then we can discuss, but if you want to call me a straight up liar from behind your little keyboard, you, my friend can kiss my politically incorrect ASS

 

[Hyde]

This was argued before and the answer was that e2 can't act if all ER are taken by a serm. So does e2 increase water, bp and worsens lipids even if it can't bind to any ER's? IMO a serm wont block all ER's with a low dosage of let's say 10mg nolva, or even a bigger one but that's just my pessimism...

Tell me how!!!! Please!! if the receptors are saturated with a serm, how is it supposed to bind to cause those side effects?

The answer is in the name - SELECTIVE Estrogen Receptor Modulator.

A SERM at any dose is not completely eliminating estrogens ability to act in ALL the receptors in the body.

 

[rtmilburn]

The answer is in the name - SELECTIVE Estrogen Receptor Modulator.

A SERM at any dose is not completely eliminating estrogens ability to act in ALL the receptors in the body.

No it selectively modulates the receptors. Not selectivity binds to receptors. That mean its a reverse agonist at ER-a but not at ER-b.

 

[NoAddedHmones]

No it selectively modulates the receptors. Not selectivity binds to receptors. That mean its a reverse agonist at ER-a but not at ER-b.

How come SARMs selectively target Androgen receptors in skeletal muscle and have very little action on the prostate etc? Was rhetorical..

You are right about subtypes of the receptor (along with other co-regulatory proteins etc)being the key to how a SERM works in different tissues around the body, as they all express different amounts/ratios of the erA erB subtypes.

I haven’t seen data on how much SERM is required to fully saturate the receptors, which I doubt can truly happen. But currently there is no perfect SERM and each has a different drawback, especially when using at higher dosages.

Which brings us back to the original question, why not just control E with an AI?

 

[Hyde]

No it selectively modulates the receptors. Not selectivity binds to receptors. That mean its a reverse agonist at ER-a but not at ER-b.

On a practical level that makes sense. But in actual practice, complete receptor saturation by the SERM doesn’t seem to occur.

People on big doses of test, taking nolva, have better bloods using an AI vs just Nolva exclusively is what I’m saying.

 

[RickyBlobby]

The answer is in the name - SELECTIVE Estrogen Receptor Modulator.

A SERM at any dose is not completely eliminating estrogens ability to act in ALL the receptors in the body.

See below

No it selectively modulates the receptors. Not selectivity binds to receptors. That mean its a reverse agonist at ER-a but not at ER-b.

This. It binds to all estrogen receptors. From there it either activates or de-activates the function of the receptor....Basically

 

[RickyBlobby]

On a practical level that makes sense. But in actual practice, complete receptor saturation by the SERM doesn’t seem to occur.

People on big doses of test, taking nolva, have better bloods using an AI vs just Nolva exclusively is what I’m saying.

But are they taking enough nolva to saturate the receptor?

I think that torem should be a staple during all cycles, that said I think you should always have an AI handy and used as needed, just in case. Unless you know your estrogen leels will be through the roof, then in my opinion it isn't a bad idea to use low dose AI to knock it down to a more reasonable level....Not crush it or even close to crushing it though

 

[Hyde]

See below


This. It binds to all estrogen receptors. From there it either activates or de-activates the function of the receptor....Basically

See my above post regarding saturation

 

[Hyde]

But are they taking enough nolva to saturate the receptor?

I think that torem should be a staple during all cycles, that said I think you should always have an AI handy and used as needed, just in case. Unless you know your estrogen leels will be through the roof, then in my opinion it isn't a bad idea to use low dose AI to knock it down to a more reasonable level....Not crush it or even close to crushing it though

Crushing it is never the answer; your bloods will be worse than high estro. And forget libido; you won’t have an erection period lol. I know; I’ve done both.

I am definitely gonna try Torem on cycle now, just for the lipid help if nothing else.

 

[MrKleen73]

I stopped cycling years ago. Just using for “HRT” purposes. Trying to stay off Test as long as possible. I use 30ml EOD.

How high have you been able to keep your testosterone levels with that, and did you ever have low test outside of PCT?

I don't think there will be any literature out there where they gave a group of people 500mg a week of testosterone and verified receptor saturation with SERMs. Sorry.

I think spurfy is onto something. But The thought of having 2-3x the amount of normal estrogen still doesn't sit right with me., Which is why I think it is a good idea to use it AS NEEDED OR on HIGHLY aromatizing cycles just as a precaution.

It all depends on what you are running but 2-3x is not likely unless running something that aromatizes heavily.

Okay and by receptor density you mean more e2 will bound to one receptor? Meaning that in some places estrogen activity and sides will be more prominent? Do I have to use an ai on my cycle?

It means the body will produce more ER in the absence of estrogen expression.

No you absolutely do not have any reason to run an AI on your cycle.

I think he means more estrogen receptors will form in the presence of excess estrogen. I believe this happens to both estrogen and androgen receptors when the receptors become saturated AKA over excited. The bodies response is to create more receptors to accommodate the extra load.

If this is the case though and the receptor is occupied with a SERM and is not being "overworked" I am not sure if it would cause the proliferation of new receptors, my gut tells me no.

I believe SERMS have more binding affinity (you can think of it as more "magnetically" drawn to the receptor) than estrogen so the receptor will "pull" all of the surrounding SERM before it pulls the estrogen. I do not have a great understanding of this so correct me if I am wrong.

What is your cycle again? Main compound(s)

He means that the body could likely create more receptors because it is getting feedback that estrogen is not able to do it's job at the current level. The body is going to try to keep a homeostasis. Basically kind of like this...

"Hmmm I have plenty estrogen, but am not seeing any expression of estrogenic effects. I must need more receptors for the estrogen to bind too."

yup.

but the issue is this: even if the SERM binds to most of the ER's, there is still a ton of circulating E2 floating around that needs to be dealt with (hence part of the reason SERMs actually raise E2).

so yes, you prolly need an AI....

Due to how this quotes, I can not tell who you were responding to now, but if Jinsun he definitely doesn't need an AI with his cycle. He wouldn't need one even if he ran it without a SERM.

I agree that an AI should always be handy, and should be used on highly aromatizing cycles to keep estrogel levels reasonable, a little excess is good in my opinion.


I think Spurfy knows more about this than me. But. If it were me......I would have an AI handy always, but only actually use it as needed OR........ During highly aromatizing cycles where you know estrogen will be skyrocketed, like moderate to high dose test, trest, dbol etc.

For your cycle I wou;ldnt worry about it unless you start getting sides like itchy nips or start crying and watching soap operas.

The use of always here is a bit much... No one was even using AI's back in the day, they are relatively new, and were not a big part of the golden years steroid scene at all. You need to be running something that will aromatize somewhat heavily to require an AI, and honestly I would choose the SERM first, and AI second...

Exactly. This is what we were debating 15 pages back in this thread. We have now done a full circle. Could we please make up our minds, or get some literature to support one or the other claim:

a) "with the use of tamox/torem on cycle you need an Ai"
b) "with the use of tamox/torem on cycle you don't need an Ai"

For f**k sakes... The sheer amount of broscience is getting to me slowly...:smashfreakB:

You do realize that most of what you will find out about in the fitness and specifically PED realm is going to be mostly bro science. No one is doing medical research on bodybuilding.

The real answer is both are right. It depends on the cycle you are running, but that being said Nolva/Tamox is the least desirable out of all of the SERMS.

Excessively high estrogen can absolutely do things, you just won’t get gyno on enough SERM (provided prolactin isn’t becoming excessive as well). Water retention, increased bp, negative effects on lipid profile, potential libido issues.

No AI is necessary on cycles THE WAY SPURFY RUNS THEM FOR HIS BODY (300 Test/wk, 30mg Var/day).



On your cycle, tamoxifen and the episndro would be enough for me to prevent gyno and keep e2 levels acceptable to me (and I am gyno-prone).

But cycles with wet compounds in larger amounts should definitely be looking at an AI. Some don’t get gyno on 1g test, but their estro can still be high enough it’s impacting health.

Thank you Brother Hyde!!!! Saved me a little typing!
Estrogenic cycles might still need an AI but lower dosed or lower aromatizing compounds do not and often can lose some gains from lowering E when it doesn't need to be.

The supplement industry has convinced so many of us that all of this is needed, and then people apply that thought process to gear... You need arimistane with your bla bla bla... I used to get so annoyed to see companies selling androsterone products hawking AI's for on cycle support. It is ludicrous. Research companies do the same thing too. It makes sense they have a dog in the fight.

However when it comes to real gear... no one stands to make extra money off of using a SERM or an AI other than the dealer. So EXPERIENCED people tend to use the supports needed to avoid sides and that is it. Not the kitchen sink approach.

This was argued before and the answer was that e2 can't act if all ER are taken by a serm. So does e2 increase water, bp and worsens lipids even if it can't bind to any ER's? IMO a serm wont block all ER's with a low dosage of let's say 10mg nolva, or even a bigger one but that's just my pessimism...

I have mentioned this a few times but maybe not in this thread... SERMs are tissue specific... they also have different affinity levels to different tissues. Most SERMS were created to treat breast cancer, and target breast tissue with a higher affinity than other tissues. However they all have their target tissues and that means that their are obviously other receptors and tissues that are not getting bound.

It is the assumption that all ER are bound that make everything fall apart. If you understand the science or at least the concept of SARMs then SERMs shouldn't be too hard to understand either. One is an androgen modulator, and the other is an Estrogen modulator, just the same way that they can make a SARM not act or have a high impact on the prostate and the like, they made SERMs to have specific targeted tissues and act on them in a certain way... they are not a block all estrogen from every tissue type of drug.

Here is something more scientific for you to look at regarding how SERM target and act differently with different tissues.

Invalid Link Removed

Here are some of the graphics from that article.

Tell me how!!!! Please!! if the receptors are saturated with a serm, how is it supposed to bind to cause those side effects?

You are really getting agitated man... take a benzo or something... even better smoke some herb and chill...

It can be frustrating if you need a black and white answer, but you won't find many for this stuff. It is more about getting a good understanding of the big picture and then you can decide based on that understanding if something fits in with your philosophy and if it is good or not for your specific situation...

 

[rtmilburn]

How high have you been able to keep your testosterone levels with that, and did you ever have low test outside of PCT?


It all depends on what you are running but 2-3x is not likely unless running something that aromatizes heavily.

It means the body will produce more ER in the absence of estrogen expression.

No you absolutely do not have any reason to run an AI on your cycle.


He means that the body could likely create more receptors because it is getting feedback that estrogen is not able to do it's job at the current level. The body is going to try to keep a homeostasis. Basically kind of like this...

"Hmmm I have plenty estrogen, but am not seeing any expression of estrogenic effects. I must need more receptors for the estrogen to bind too."


Due to how this quotes, I can not tell who you were responding to now, but if Jinsun he definitely doesn't need an AI with his cycle. He wouldn't need one even if he ran it without a SERM.



The use of always here is a bit much... No one was even using AI's back in the day, they are relatively new, and were not a big part of the golden years steroid scene at all. You need to be running something that will aromatize somewhat heavily to require an AI, and honestly I would choose the SERM first, and AI second...


You do realize that most of what you will find out about in the fitness and specifically PED realm is going to be mostly bro science. No one is doing medical research on bodybuilding.

The real answer is both are right. It depends on the cycle you are running, but that being said Nolva/Tamox is the least desirable out of all of the SERMS.


Thank you Brother Hyde!!!! Saved me a little typing!
Estrogenic cycles might still need an AI but lower dosed or lower aromatizing compounds do not and often can lose some gains from lowering E when it doesn't need to be.

The supplement industry has convinced so many of us that all of this is needed, and then people apply that thought process to gear... You need arimistane with your bla bla bla... I used to get so annoyed to see companies selling androsterone products hawking AI's for on cycle support. It is ludicrous. Research companies do the same thing too. It makes sense they have a dog in the fight.

However when it comes to real gear... no one stands to make extra money off of using a SERM or an AI other than the dealer. So EXPERIENCED people tend to use the supports needed to avoid sides and that is it. Not the kitchen sink approach.




I have mentioned this a few times but maybe not in this thread... SERMs are tissue specific... they also have different affinity levels to different tissues. Most SERMS were created to treat breast cancer, and target breast tissue with a higher affinity than other tissues. However they all have their target tissues and that means that their are obviously other receptors and tissues that are not getting bound.

It is the assumption that all ER are bound that make everything fall apart. If you understand the science or at least the concept of SARMs then SERMs shouldn't be too hard to understand either. One is an androgen modulator, and the other is an Estrogen modulator, just the same way that they can make a SARM not act or have a high impact on the prostate and the like, they made SERMs to have specific targeted tissues and act on them in a certain way... they are not a block all estrogen from every tissue type of drug.

Here is something more scientific for you to look at regarding how SERM target and act differently with different tissues.

Invalid Link Removed

Here are some of the graphics from that article.

View attachment 164300

View attachment 164301



You are really getting agitated man... take a benzo or something... even better smoke some herb and chill...

It can be frustrating if you need a black and white answer, but you won't find many for this stuff. It is more about getting a good understanding of the big picture and then you can decide based on that understanding if something fits in with your philosophy and if it is good or not for your specific situation...

While they are designed to be tissues specific, and are to an extent, they are not fully. They still bind to ER all of tissues types and often with more affinity than estrogen. However, it depends on the cell type as well. This is way serms are effective at managing other types of cancers other than just breast cancer.

 

[MrKleen73]

Guys quit focusing on the unimportant!!!

You would not want every receptor saturated with the SERM, there is a need for estrogen and for it to be able to bind and express itself!!!!

You just want enough receptors bound to keep from suffering any negative effects of high estrogen.

If you increase estrogen by 30% then to avoid side effects of that you don't need 100% SERM saturation. Obviously a saturation level of 30% would offset the side effects... No need for 100% saturation, as a matter of fact you would not want this.

 

[rtmilburn]

While they are designed to be tissues specific, and are to an extent, they are not fully. They still bind to ER all of tissues types and often with more affinity than estrogen. However, it depends on the cell type as well. This is way serms are effective at managing other types of cancers other than just breast cancer.

Would like to add that they probably dont have a higher binding affinity, for non breast tissue cells, than the methyl-estrogen varieties we get with some steriods, but they may.

 

[Matthersby]

A lot of pages to read through a second time to look for it, but what was the consensus on running torem or clomid periodically on TRT? My atrophy is getting a bit obnoxious as of late. And also, I am planning on running some Ralox already to hopefully rid myself of a couple of pea-sized lumps behind my nipples. Seems this would be all I would need if I were to run something here and there on TRT. ********
*********
RESULTS: Raloxifene significantly increased serum concentrations of LH and FSH (by 29% and 21%), total testosterone (20%), free testosterone (16%) and bioavailable testosterone (not bound to sex hormone-binding globulin (SHBG; 20%). In parallel with testosterone, 17 beta-oestradiol also increased by 21%. SHBG increased by 7%. Total cholesterol (TChol) decreased significantly, from 5.7 to 5.5 mmol/l (P=0.03). Low-density lipoprotein cholesterol (LDL-c) and high-density lipoprotein cholesterol (HDL-c) showed a trend to decrease. Overall, there was no change in urinary OHPro/creatinine ratio as a marker for bone resorption. However, the raloxifene-induced increases in both serum testosterone and 17 beta-oestradiol were significantly related to a lower OHPro/creatinine ratio. Total PSA increased by 17% without significant changes in free PSA or free/total PSA ratio. Participants reported no side effects and raloxifene was well tolerated.

Randomized controlled trial
Duschek EJ, et al. Eur J Endocrinol. 2004.
Authors
Duschek EJ1, Gooren LJ, Netelenbos C.
Author information
1
Department of Endocrinology, VU University Medical Centre, Amsterdam, The Netherlands. [email protected]
Citation
Eur J Endocrinol. 2004 Apr;150(4):539-46.

 

[MrKleen73]

While they are designed to be tissues specific, and are to an extent, they are not fully. They still bind to ER all of tissues types and often with more affinity than estrogen. However, it depends on the cell type as well. This is way serms are effective at managing other types of cancers other than just breast cancer.

Yes, and if I remember correctly from the research I did a few years back that all SERMS were designed to have a higher affinity to breast tissue in order to target that tissue specifically in order to "starve out" the breast cancer. Maybe I am remembering wrong but I am relatively confident I am remembering it correctly.

Most if not all SERMS have a higher affinity to the ER than estrogen.

 

[rtmilburn]

Yes, and if I remember correctly from the research I did a few years back that all SERMS were designed to have a higher affinity to breast tissue in order to target that tissue specifically in order to "starve out" the breast cancer. Maybe I am remembering wrong but I am relatively confident I am remembering it correctly.

Most if not all SERMS have a higher affinity to the ER than estrogen.

Yep that is true. It does depends on cell type though. Im sure there are cells that estrogen binds to stronger than serms.(depending on the serm). Also methyl-estrogen also change the equation a bit too. Although im confident that in atleast breast tissue serms will bind stronger than even methyl-estrogens.

 

[RickyBlobby]

So the big questions is, what kind affinity do SERMs have for the estrogen receptors in the pituitary gland that cause the release of LH and FSH, and how much SERM is needed to offset the suppression of X amount of testosterone/ testosterone derivatives.

Naysayers, come hither.

During PCT, your testosterone/ estrogen level rises after being tanked from a cycle. Your SERM is active in the body at the same time as your T levels rise............ So as your test level goes from 100 (SERM still working), to 200 (SERM still working), to 400 (SERM still working), to 800 (SERM still working), ..... The SERM is still doing its job.

That means SERMS STILL WORK IN THE PRESENCE OF TESTOSTERONE.

That proves that my point is valid. Now the question is how much estrogen it takes to knock the SERM off the receptor? Or CAN it be knocked off my any amount of estrogen.

I can tell you that 50mg of Dbol and 400mg of primo wasn't enough. And that's only 25mg of clomid daily. Anddddd now I remember that my LH and FSH were sky high and the doc was very concerned about this.

 

[Hyde]

So the big questions is, what kind affinity do SERMs have for the estrogen receptors in the pituitary gland that cause the release of LH and FSH, and how much SERM is needed to offset the suppression of X amount of testosterone/ testosterone derivatives.

Naysayers, come hither.

During PCT, your testosterone/ estrogen level rises after being tanked from a cycle. Your SERM is active in the body at the same time............ So as your test level goes from 100, to 200, to 400, to 500..... The SERM is still doing its job.

That means SERMS STILL WORK IN THE PRESENCE OF TESTOSTERONE.

That proves that my point is valid. Now we just need to figure out how much androgen it takes to knock the SERM off the receptor, right? Am I right or am I right?

100 grams of Tren should do it, unequivocally

 

[RickyBlobby]

100 grams of Tren should do it, unequivocally

Right!

 

[MrKleen73]

100 grams of Tren should do it, unequivocally

I think I might have suffered an aneurysm just reading that kind of dose!

 

[Zippy]

Thinking of running a 6 week clomid/Winny cycle just for the **** of it

 

[RickyBlobby]

I recommend torem instead of clomid. Unless you don’t get sides from clomid. Only side I get is low libido. Torem seems to have the opposite effect in some people

 

[MrKleen73]

I recommend torem instead of clomid. Unless you don’t get sides from clomid. Only side I get is low libido. Torem seems to have the opposite effect in some people

Haha no doubt, I get mean as a rattlesnake on clomid. I am all over the place emotionally but my temper, forget about it.

 

[Zippy]

I already have the Winny and clomid and I have never had anything negative from clomid before so f**k it I will give it a go. Will see if that changes with 6 weeks though as only done 4 weeks before.

 

[MrKleen73]

I already have the Winny and clomid and I have never had anything negative from clomid before so f**k it I will give it a go. Will see if that changes with 6 weeks though as only done 4 weeks before.

Even with me I learned if you keep it to 25mg there are not really many sides at all. It is when you run it at 50 and up that things get really dicey. For a while around here everyone was of the mind if 25 was good then 50 would be better so serms were recommended much higher than they needed to be. Like clomid 100/50/50/50/50/50 or Nolva @ 40 all the way through...

When i ran clomid that high I lost it in the middle of my PCT. I became a raging bitch! Gear had never made me that volatile!

 

[Zippy]

Yeah it will be 25 all the way maybe even eod towards the end. Never felt the need to go high I’m only 5’7” maybe 50 is for the big boys

 

[MrKleen73]

Yeah it will be 25 all the way maybe even eod towards the end. Never felt the need to go high I’m only 5’7” maybe 50 is for the big boys

Maybe, I am obviously not in that category though!

 

[elo76]

Subbed. Will be running epistane and maybe some desoxy/dien-diol td. Thinking of adding clomid if this is working out for folks. Being 41, I wanna keep the boyz going.

 

[BBiceps]

I already have the Winny and clomid and I have never had anything negative from clomid before so f**k it I will give it a go. Will see if that changes with 6 weeks though as only done 4 weeks before.

This is what I want to do, let me know how it goes, good luck!

 

[Hyde]

Subbed. Will be running epistane and maybe some desoxy/dien-diol td. Thinking of adding clomid if this is working out for folks. Being 41, I wanna keep the boyz going.

Desoxy and Epistane? Ow my joints. I’d pick one to go with the Dienelone and save the other to stack with something wet. Should be cool either way tho!

 

[elo76]

Desoxy and Epistane? Ow my joints. I’d pick one to go with the Dienelone and save the other to stack with something wet. Should be cool either way tho!

Yeah...I guess your right. Maybe just the dien.

 

[Hyde]

Yeah...I guess your right. Maybe just the dien.

I think either would go swell with the dien, I just think both is interesting. Carry on!

 

[Zippy]

This is what I want to do, let me know how it goes, good luck!

I will post any necessary updates in here good or bad.

 

[Peanutbutterj]

So the big questions is, what kind affinity do SERMs have for the estrogen receptors in the pituitary gland that cause the release of LH and FSH, and how much SERM is needed to offset the suppression of X amount of testosterone/ testosterone derivatives.

Naysayers, come hither.

During PCT, your testosterone/ estrogen level rises after being tanked from a cycle. Your SERM is active in the body at the same time as your T levels rise............ So as your test level goes from 100 (SERM still working), to 200 (SERM still working), to 400 (SERM still working), to 800 (SERM still working), ..... The SERM is still doing its job.

That means SERMS STILL WORK IN THE PRESENCE OF TESTOSTERONE.

That proves that my point is valid. Now the question is how much estrogen it takes to knock the SERM off the receptor? Or CAN it be knocked off my any amount of estrogen.

I can tell you that 50mg of Dbol and 400mg of primo wasn't enough. And that's only 25mg of clomid daily. Anddddd now I remember that my LH and FSH were sky high and the doc was very concerned about this.

I hope you’re right pal; I have plenty Clomid and the cost/convenience will make it a no-brainer for me to use on future cycles.

I don’t get bad sides from Clomid FYI - at least none that I perceive.

 

[Jinsun]

Guys, how much time since starting my andro stack with tamox do you think makes sense to test LH? Seeing as this stack is basically 1-test, test and dht, suppression should accure quickly... Also, testing TT is kinda pointless due to 4andro eh?

 

[John Smeton]

I posted this in another thread, but I figured this would be a valuable piece of info for many.

My first (oral) cycle was long, 10 weeks and I had a kitchen sink PCT with clomid/ DAA/ and an OTC PCT. Got my test levels checked 3 weeks into PCT and it was around 250 total.

A few cycles later- Primo and Dbol, 10 or 12 weeks I forget, I ran Clomid at 25mg/ day throughout. Immediately post cycle, like a week or less after my last injection, I checked my level to test my theory and it was above 450 total.

I know of a few pros that use clomid during cycle, so I tried it and it worked. FYI

Good to hear. Ive heard that using a serm on cycle stimulates lh and fhs so Im glad it worked for you

 

[mad_canada]

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...

Slight bump here, can anyone help?

I used lgd-4033 in the past and went from 715-410, currently on the second week of rad 140.

So what dose should I run torem at to prevent the lethargy I got last time?

Thanks!

 

[christ83189]

Slight bump here, can anyone help?

I used lgd-4033 in the past and went from 715-410, currently on the second week of rad 140.

So what dose should I run torem at to prevent the lethargy I got last time?

Thanks!

I think Spurfy said 30mg a day? Not sure if i remember correctly

 

[mad_canada]

I think Spurfy said 30mg a day? Not sure if i remember correctly

Thanks brother

 

[christ83189]

Thanks brother

No problem. I hope i didnt give the wrong dose lol

 

[mad_canada]

No problem. I hope i didnt give the wrong dose lol

Don't think so. I've seen people run it at 120/90/60/30 after AAS so 30 makes sense.

 

[Kratom267]

Don't think so. I've seen people run it at 120/90/60/30 after AAS so 30 makes sense.

Yeah he did 30mg Torem during the cycle. He told me to also continue that dosage during PCT...Havent decided if i want to do 30/30/15/15 for PCT or run it higher for PCT. I was thinking that even though i will run it on cycle at 30mg, it would be best to bump it to 60 (as a little "jump start") for the first week of PCT, but they told me to keep it the same dose...

 

[mad_canada]

Yeah he did 30mg Torem during the cycle. He told me to also continue that dosage during PCT...Havent decided if i want to do 30/30/15/15 for PCT or run it higher for PCT. I was thinking that even though i will run it on cycle at 30mg, it would be best to bump it to 60 (as a little "jump start") for the first week of PCT, but they told me to keep it the same dose...

How far in the cycle did you start the torem?
I am considering also using test1fy during the pct but torem should surpass that a great deal I'd imagine, yes?

 

[rowz4broz]

Is there a final verdict on whether or not this protocol would halt suppression? Cause if that’s the case I’m about to join the dark side

 

[Kratom267]

How far in the cycle did you start the torem?
I am considering also using test1fy during the pct but torem should surpass that a great deal I'd imagine, yes?

I haven't started it yet, waiting for some pre cycle blood work results. Most likely next week though.
In the past, i did run some clomid on an Hdrol cycle (as this is not a new idea) and recall that my balls stayed nice and plump, libido was good, etc...this is compared to not running a serm on a previous Hdrol cycle.

Overall, i see no issue with running a serm on cycle...the pros outweigh any cons.
I plan on starting the Torem at 15mg for week one, then do 30mg for the remaining the 3 weeks.

 

[mad_canada]

Is there a final verdict on whether or not this protocol would halt suppression? Cause if that’s the case I’m about to join the dark side

I was texting with someone here who has done way more anabolic said I think anyone on planet Earth, he said that running torem during the entire cycle would basically prevent suppression from happening.

So it definitely sounds like the popular consensus is that it should be run.

I will start today personally and added him to my my log on my official site

 

[Kratom267]

I was texting with someone here who has done way more anabolic said I think anyone on planet Earth, he said that running torem during the entire cycle would basically prevent suppression from happening.

So it definitely sounds like the popular consensus is that it should be run.

I will start today personally and added him to my my log on my official site

what are you running for your cycle? PH/designer or pin?

 

[rowz4broz]

I was texting with someone here who has done way more anabolic said I think anyone on planet Earth, he said that running torem during the entire cycle would basically prevent suppression from happening.

So it definitely sounds like the popular consensus is that it should be run.

I will start today personally and added him to my my log on my official site

Your buddy run bloodwork to confirm ? Or just anecdotal? Just curious

 

[Kratom267]

I was texting with someone here who has done way more anabolic said I think anyone on planet Earth, he said that running torem during the entire cycle would basically prevent suppression from happening.

So it definitely sounds like the popular consensus is that it should be run.

I will start today personally and added him to my my log on my official site

also...I thought you were against SERMS in general for PCT...