You do not need "prolactin control" on a Deca/NPP cycle

[Spurfy]

Also, and I’ve been holding this in: Proviron absolutely does not control estrogen in any way whatsoever. That is a pure myth. It does lower SHBG, and that’s all. It’s worthless. Not even notably anabolic in women. But too androgenic for a woman.

It controls estrogen because DHT blocks E2 binding to the estrogen receptor -- DHT is actually an ER-a competitive antagonist. (Invalid Link Removed).

DHT is an anti-estrogen (Invalid Link Removed). It doesn't change E2 levels, but it directly affects ER-a and downstream firing and it blocks E2 from binding estrogen receptors. It doesn't matter how high E2 levels are if DHT levels are high enough to antagonize the effects of E2.

 

[Old Witch]

It controls estrogen because DHT blocks E2 binding to the estrogen receptor -- DHT is actually an ER-a competitive antagonist. (Invalid Link Removed).

DHT is an anti-estrogen (Invalid Link Removed). It doesn't change E2 levels, but it directly affects ER-a and downstream firing and it blocks E2 from binding estrogen receptors. It doesn't matter how high E2 levels are if DHT levels are high enough to antagonize the effects of E2.

Then by that merit, use of any dhts would prevent shutdown. It doesn’t. Because estrogen is still reaching receptors in excessive amounts causing negative feedback in the brain. In fact, some dht compounds are far more suppressive than what you might be taking with them.

I cannot fathom a universe where one would take nandrolone and masteron and not end up shut down harder than almost anything else you could take.

 

[Jinsun]

I didn't get them. I have a profound phobia of venipunture and I have to be given conscious sedation for blood draws. Yeah, go ahead and laugh... I can pin my quads all day long but the moment that alcohol wipe touches the inside of my elbow I get woozy. When that needle goes into my vein without conscious sedation any number of bad things happen.

Oh I feel you on this one. I hate it to. Can pin IM all day long but drawing blood from the elbow, jeeez I really hate that feeling.

 

[Jinsun]

Then by that merit, use of any dhts would prevent shutdown. It doesn’t. Because estrogen is still reaching receptors in excessive amounts causing negative feedback in the brain. In fact, some dht compounds are far more suppressive than what you might be taking with them.

I cannot fathom a universe where one would take nandrolone and masteron and not end up shut down harder than almost anything else you could take.

No, not really. Look at how much proviron or epiandro suppress. Zill. You can run proviron at a 100mg dose for months and will have zero supression.

The thing with DHT aas is just that; they are AAS and they trigger the hpta's negative feedback - not the e2 one, but the androgen one. Normal DHT by it self doesn't seem to trigger this at low to moderate doses, but all AAS do. DHT aas however do it less then test aas and 19nor's. Just look at the studies done on primo. How "little" it supresses at a dose of 400mg for instance.

 

[Old Witch]

You do not need "prolactin control" on a Deca/NPP cycle

No, not really. Look at how much proviron or epiandro suppress. Zill. You can run proviron at a 100mg dose for months and will have zero supression.

The thing with DHT aas is just that; they are AAS and they trigger the hpta's negative feedback - not the e2 one, but the androgen one. Normal DHT by it self doesn't seem to trigger this at low to moderate doses, but all AAS do. DHT aas however do it less then test aas and 19nor's. Just look at the studies done on primo. How "little" it supresses at a dose of 400mg for instance.

And yet a couple tabs of superdrol or Methyl 1 Test can leave you on trt for life.

You basically just explained what I was getting at. Yes Dhts are tending to be mostly mild.

Sure taking masteron with your deca or tren is a great practice to avoid tits, it’s also a great way to make sure you might never recover, though. And clomid on cycle ain’t going to save you.

 

[Spurfy]

And yet a couple tabs of superdrol or Methyl 1 Test can leave you on trt for life.

You basically just explained what I was getting at. Yes Dhts are tending to be mostly mild.

Sure taking masteron with your deca or tren is a great practice to avoid tits, it’s also a great way to make sure you might never recover, though. And clomid on cycle ain’t going to save you.

Post studies showing permanent HPG-axis shutdown from any AAS that wasn't reversed by Clomid.

There is no such study. Never in recorded medical history has there ever been a single published case study of this happening. Never. Not one.

One study found it took up to 6 months to fully recover HPG-axis from nandrolone, and this was without PCT.

 

[BroBrian]

Late but subbed for interesting discussion

 

[Spurfy]

Then by that merit, use of any dhts would prevent shutdown.

No, because DHT-deriviatives still cause suppression, although much milder than suppression from E2 negative feedback.

It doesn’t. Because estrogen is still reaching receptors in excessive amounts causing negative feedback in the brain. In fact, some dht compounds are far more suppressive than what you might be taking with them.

If E2 receptors are blocked in the brain (with Clomid), then the only suppression will come from androgren-mediated negative feedback, which is much less than negative feedback from E2.

I cannot fathom a universe where one would take nandrolone and masteron and not end up shut down harder than almost anything else you could take.

You are confusing the action of Clomid on hypothalamic ER-a and Masteron on breast ER-a. Masteron specifically blocks ER-a in breast tissue but not in the brain. Clomid specifically blocks ER-a in the brain but not breast tissue.

There is no possible way I can explain this more clearly.

 

[CatSnake]

interesting use of naltrexone....

seems like that is one of the more significant things to bring to the discussion, or am I wrong?


Invalid Link Removed

^I found this from a while back, for later reading....


EDIT:

something I noticed from the article:

"Remember, progestin based anabolics such as trenbolone and nandrolone are “double suppressive” because they desensitize the pituitary directly by PR activation. It also appears that no opioid receptor antagonist or aromatase inhibitor can prevent suppression via the PR. Therefore, trenbolone or nandrolone are going to cause unavoidable inhibition of HTPA function by causing suppression via the ER, AR and PR. (40,41) If one hopes for a prompt and full recovery post cycle, perhaps progestin based anabolics are better avoided, or at least limited in duration of use."

^reminds me of people using RU486 back in the day to deal with tren/deca….




.

 

[Spurfy]

interesting use of naloxone....

seems like that is one of the more significant things to bring to the discussion, or am I wrong?


Invalid Link Removed

^I found this from a while back, for later reading....

I've sort of been keeping it a secret...

Years ago I discovered research on opioid antagonists preventing androgen negative feedback and directly restoring GnRH/LH/FSH production, this is the first time I've decided to give it a run. And I'm on naltrexone, not naloxone.

The boys are plump, full, and hanging low, and I'm on a very suppressive cycle. I've have zero side effects except face acne, which completely cleared up on weekly 100,000 iu Vitamin D, 5 mg K2, 100,000 iu Vitamin A. Honestly other than the gainzzz I don't even feel like I'm "on". I'm having zero psychological effects.

I usually get pretty aggressive on cycle but I think Naltrexone has strong mood-stabilizing effects as well. I'm certainly much more calm and less irritable than normal. I don't get those surges of aggression and that short fuse that 875/week of T with a hefty dose of Mast should be causing. I actually feel great.

 

[Jinsun]

Spurfy, masteron vs proviron for the same purpose; dosage?

 

[Spurfy]

Spurfy, masteron vs proviron for the same purpose; dosage?

I'd say 50% higher Proviron owing to the first pass effect.

So if 400 mg/week Mast, then 600 mg/week or ~85 mg/day Proviron.

 

[Jinsun]

I'd say 50% higher Proviron owing to the first pass effect.

So if 400 mg/week Mast, then 600 mg/week or ~85 mg/day Proviron.

Tnx.

I'm dealing with gyno, throwing letro, caber and ralox at it. Going to try viron now, as the last thing I can try...

 

[Hyde]

Sure taking masteron with your deca or tren is a great practice to avoid tits, it’s also a great way to make sure you might never recover, though. And clomid on cycle ain’t going to save you.

Why do you feel adding Mast or another DHT to a 19-Nor would increase recovery demand (compared to say the same total mg dose of straight nandrolone)?

I have always read that gynecomastia is ultimately the product of an imbalance of the hormonal axis between androgen and estrogen - so no matter how high estrogen levels get, as long as androgens are sufficiently high to compete the user will not experience gyno symptoms.

 

[Spurfy]

Tnx.

I'm dealing with gyno, throwing letro, caber and ralox at it. Going to try viron now, as the last thing I can try...

I'd front load huge doses of Proviron then. Like 200 mg/day for first 5 days, then drop down to 150, then 100.

Proviron is very safe and has been given in doses over 200 mg/day with no ill effects in men.

 

[Jinsun]

I'd front load huge doses of Proviron then. Like 200 mg/day for first 5 days, then drop down to 150, then 100.

Proviron is very safe and has been given in doses over 200 mg/day with no ill effects in men.

Yeah, I know. Viron is quite safe regarding suppression.

Good idea. I'll try something to that effect.

 

[Jinsun]

Although, with short half life of viron, front loading doesn't really make sense. Or are you referring to blasting breast ER's with a bigger dose for a short time?

 

[Spurfy]

Although, with short half life of viron, front loading doesn't really make sense. Or are you referring to blasting breast ER's with a bigger dose for a short time?

The latter.

 

[Spurfy]

I have always read that gynecomastia is ultimately the product of an imbalance of the hormonal axis between androgen and estrogen - so no matter how high estrogen levels get, as long as androgens are sufficiently high to compete the user will not experience gyno symptoms.

This is exactly 1,000,000% truth.

And it's not even androgens, it's DHT specifically.

 

[CatSnake]

I've sort of been keeping it a secret...

Years ago I discovered research on opioid antagonists preventing androgen negative feedback and directly restoring GnRH/LH/FSH production, this is the first time I've decided to give it a run. And I'm on naltrexone, not naloxone.

The boys are plump, full, and hanging low, and I'm on a very suppressive cycle. I've have zero side effects except face acne, which completely cleared up on weekly 100,000 iu Vitamin D, 5 mg K, 100,000 iu Vitamin A. Honestly other than the gainzzz I don't even feel like I'm "on". I'm having zero psychological effects.

I usually get pretty aggressive on cycle but I think Naltrexone has strong mood-stabilizing effects as well. I'm certainly much more calm and less irritable than normal. I don't get those surges of aggression and that short fuse that 875/week of T with a hefty dose of Mast should be causing. I actually feel great.

how are you dosing that?

 

[Spurfy]

how are you dosing that?

25 mg first thing every morning on an empty stomach (1/2 of a pharma 50 mg naltrexone tablet), same time I take Clomid and T4 (200 mcg/day). All of these are pharma.

I started the NTX before my cycle, dose was chosen by titrating up until balls started to ache and get bigger like on high dose of Clomid or Torem -- I figured that was the spot where I was getting solid HPG-axis stimulation. Cruised on that for a month and then started cycle. Honestly NTX alone makes me feel great, I might just run it forever. On NTX I find it very hard to get upset or angry about anything, but all of my normal positive emotions are maintained.

 

[CatSnake]

No, because DHT-deriviatives still cause suppression, although much milder than suppression from E2 negative feedback.



If E2 receptors are blocked in the brain (with Clomid), then the only suppression will come from androgren-mediated negative feedback, which is much less than negative feedback from E2.



You are confusing the action of Clomid on hypothalamic ER-a and Masteron on breast ER-a. Masteron specifically blocks ER-a in breast tissue but not in the brain. Clomid specifically blocks ER-a in the brain but not breast tissue.

.

not trying to be sarcastic, but this is specifically what a lot of us (at least I do) are looking for, when asking a question here....

FWIW, I agree about DHT suppression being less significant than estrogen suppression (based off the literature I've read, suppression from the ER is significantly worse than suppression from the androgen receptor).

however, one still needs to deal with the circulating E2 at the end of the cycle, as that isn't going away as the androgens taper down in the body.....

I presume at the end of the cycle you intend on using an AI still, right?

 

[CatSnake]

25 mg first thing every morning on an empty stomach (1/2 of a pharma 50 mg naltrexone tablet), same time I take Clomid and T4 (200 mcg/day). All of these are pharma.

I started the NTX before my cycle, dose was chosen by titrating up until balls started to ache and get bigger like on high dose of Clomid or Torem -- I figured that was the spot where I was getting solid HPG-axis stimulation. Cruised on that for a month and then started cycle. Honestly NTX alone makes me feel great, I might just run it forever. On NTX I find it very hard to get upset or angry about anything, but all of my normal positive emotions are maintained.

huh.... any concerns over liver toxicity?

I find this to be very interesting, in theory. I need to see how much they've documented clinical effects in men, or if there is much research...

 

[Spurfy]

not trying to be sarcastic, but this is specifically what a lot of us (at least I do) are looking for, when asking a question here....

I'm trying to be more patient in my replies. It's difficult to explain things to the layperson when you're used to explaining them to grad students or obnoxious colleagues at cocktail parties, without becoming frustrated. I don't like when people ask advanced pharmacology questions or make arguments when they don't even understand the basic pharmacologic principles needed to understand their question or argument. It's like a cop arguing law with a supreme court justice.

however, one still needs to deal with the circulating E2 at the end of the cycle, as that isn't going away as the androgens taper down in the body....

Sure it is. Do you think all E2 produced just lasts forever? As T drops, E2 follows. I taper down Test towards the end of a cycle, dropping from 875 down to 125 and then off. Nandrolone and Mast will not be tapered.

I presume at the end of the cycle you intend on using an AI still, right?

Nope. AIs are out of the rotation unless I somehow develop gyno. Even then I'm reaching for Ralox first. I am very sensitive to the estrone lowering effects of AIs. My E1 (especially) and E2 tend to run on the low side, and it's very easy for me to crash my E1/E2 making me literally feel like I'm dying, even on just a single 25 mg Aromasin on 600 mg/week of Test E.

End of cycle I'll continue Clomid (25 mg) and Naltrexone (25 mg) for 4 weeks and may run Mast P at 200 mg/week through "PCT" if I feel I need any E2 control.

Naltrexone at 25 mg/day is permanent.

 

[Spurfy]

huh.... any concerns over liver toxicity?

I find this to be very interesting, in theory. I need to see how much they've documented clinical effects in men, or if there is much research...

No concerns. Liver values only increase at very high doses (200-300 mg), and even with these there's no evidence of liver damage.

Plus Naltrexone is one of the most potent anti-cancer agents known to man, so there's that too...

 

[Jinsun]

FWIW, I agree about DHT suppression being less significant than estrogen suppression (based off the literature I've read, suppression from the ER is significantly worse than suppression from the androgen receptor).

Well I kinda doubt this. I mean by this logic you could take for instance 200mg test and if your e2 was low then your hpta would theoretically still be active to a degree. But alas, I see nobody on TRT having an active hypothalamus. Even if they use a serm and also crush their e2, I don't see this happening. So it's difficult to say, how much easier the androgens are in regards to estrogen - the negative feedback loop. DHT's are weaker but in meaningful dosages, they shut you down just the same. Somebody just did a torem + SD cycle. SD was at 15mg. He got shut down.

50mg of Tbol shut's you down even with a serm eventually. And that's only 250mg/week. So ... conclusion, as it has been said numerous times; aas at any meaningful dosages will shut you down, no matter what you do.

 

[Spurfy]

So ... conclusion, as it has been said numerous times; aas at any meaningful dosages will shut you down, no matter what you do.

I'm going to disprove this with bloods.

Also, if we're getting technical, no experiment with a SERM is valid unless it's pharma or it's been independently third-party HPLC tested for potency. That some UGL claims their SERM is X mg/mL is meaningless -- UGLs can and do lie all the time. This is the whole reason people think Var is weak. Yeah, it's weak if your UGL 20 mg tabs only contain enough Var to trigger the Labmax, which is < 1 mg. This is why people say "Take 100 mg/day Var," At 100 mg/day of pharma Var, you wouldn't be able to keep your eyes open.

No one is allowed to say anything regarding a drug experiment unless they are using product that is proven to contain the claimed active compound at the claimed dosage. This is either pharma, or having a lab run HPLC. Anything else and it's literally just speculation.

 

[CatSnake]

Well I kinda doubt this. I mean by this logic you could take for instance 200mg test and if your e2 was low then your hpta would theoretically still be active to a degree. But alas, I see nobody on TRT having an active hypothalamus. Even if they use a serm and also crush their e2, I don't see this happening. So it's difficult to say, how much easier the androgens are in regards to estrogen - the negative feedback loop. DHT's are weaker but in meaningful dosages, they shut you down just the same. Somebody just did a torem + SD cycle. SD was at 15mg. He got shut down.

50mg of Tbol shut's you down even with a serm eventually. And that's only 250mg/week. So ... conclusion, as it has been said numerous times; aas at any meaningful dosages will shut you down, no matter what you do.

no, I mis-spoke. more talking about general HPTA negative feedback mechanisms.... you know me-I've got a link on it. just gotta dig it up....

as far as the hypothalamus, it absolutely remains active. it has more roles then simply releasing GnRH.

EDIT:

FWIW, Superdrol is one of the strongest AAS, mg for mg, ever produced. it's unfortunate that it was OTC when it was, because everybody presumed it was so benign. I've never taken anything as toxic as that, and will never take it again.

 

[Spurfy]

no, I mis-spoke. more talking about general HPTA negative feedback mechanisms.... you know me-I've got a link on it. just gotta dig it up....

as far as the hypothalamus, it absolutely remains active. it has more roles then simply releasing GnRH.

You're right on this -- E2 is at least 20x as suppressive as androgens at inhibiting hypothalamic GnRH release.

And in the scenario given with the 200 mg/week of test with AI, people forget that there is local aromatase expression in specific cells and tissues that is non-responsive to AI. The only aromatase that is really affected by an AI is hepatic and plasma.

Any time you give an aromatizable AAS, there will be some degree of HPG-axis suppression, no matter how much AI is given with it, because E2 metabolites will be formed locally. The brain is chock-full of aromatase.

 

[CatSnake]

I'm trying to be more patient in my replies. It's difficult to explain things to the layperson when you're used to explaining them to grad students or obnoxious colleagues at cocktail parties, without becoming frustrated. I don't like when people ask advanced pharmacology questions or make arguments when they don't even understand the basic pharmacologic principles needed to understand their question or argument. It's like a cop arguing law with a supreme court justice.



Sure it is. Do you think all E2 produced just lasts forever? As T drops, E2 follows. I taper down Test towards the end of a cycle, dropping from 875 down to 125 and then off. Nandrolone and Mast will not be tapered.



Nope. AIs are out of the rotation unless I somehow develop gyno. Even then I'm reaching for Ralox first. I am very sensitive to the estrone lowering effects of AIs. My E1 (especially) and E2 tend to run on the low side, and it's very easy for me to crash my E1/E2 making me literally feel like I'm dying, even on just a single 25 mg Aromasin on 600 mg/week of Test E.

End of cycle I'll continue Clomid (25 mg) and Naltrexone (25 mg) for 4 weeks and may run Mast P at 200 mg/week through "PCT" if I feel I need any E2 control.

Naltrexone at 25 mg/day is permanent.

well, E2 drops down because there's a reason for it to drop down. simply lowering androgens will limit how much more will aromatize in addition to what's already there, but the circulating E2 still exists, and due to the SERM and masteron, isn't binding to as many receptors.

yeah, it SHOULD go away eventually, but you're not doing anything to make it go away. the only way it would all go away entirely would be to reduce your androgen levels to the point that nothing else could aromatize, and you'd have to use up all the circulating E2 or metabolize it.

honestly, your E2 levels have to be pretty high from stuff like this.... nothing you're talking is reducing them from increasing, that I can see....

 

[Spurfy]

well, E2 drops down because there's a reason for it to drop down. simply lowering androgens will limit how much more will aromatize in addition to what's already there, but the circulating E2 still exists, and due to the SERM and masteron, isn't binding to as many receptors.

yeah, it SHOULD go away eventually, but you're not doing anything to make it go away. the only way it would all go away entirely would be to reduce your androgen levels to the point that nothing else could aromatize, and you'd have to use up all the circulating E2 or metabolize it.

honestly, your E2 levels have to be pretty high from stuff like this.... nothing you're talking is reducing them from increasing, that I can see....

My E2 is probably between 80-120 right now. So what? Masteron and Clomid are handling that. I have no high-E2 sides: Libido great, erections great, morning wood great, heavy balls, ejaculate thick and large volume, no blood pressure issues, no hot flushes, no insomnia, no water retention, no itchy nipples, no puffy nipples, no emotional spells, no headaches. Nothing. Zero.

Did we forget that E2 is highly anabolic? Invalid Link Removed

The half-life of unbound E2 is 20 minutes. This means every molecule of E2 that detaches from SHBG is completely eliminated by the body in < 2 hours. Invalid Link Removed

E2 levels reduce very rapidly once aromatizable androgens are reduced or eliminated. If you want to expedite this process, run something that competes with E2 for SHBG-binding, like Masteron, which is exactly what I'm doing in "PCT"

This is why Aromasin lowers E2 levels so quickly -- the half life of E2 is short and Aromasin is a substrate for SHBG. Simply shutting down aromatase would still leave plenty of E2 floating around to cause problems, according to your logic, but we know that this is absolutely not the case, and that maximum suppression of E2 occurs in 12 hours with Aromasin. According to your "long lasting E2 hypothesis", this would be impossible.

 

[Old Witch]

No, because DHT-deriviatives still cause suppression, although much milder than suppression from E2 negative feedback.



If E2 receptors are blocked in the brain (with Clomid), then the only suppression will come from androgren-mediated negative feedback, which is much less than negative feedback from E2.



You are confusing the action of Clomid on hypothalamic ER-a and Masteron on breast ER-a. Masteron specifically blocks ER-a in breast tissue but not in the brain. Clomid specifically blocks ER-a in the brain but not breast tissue.

There is no possible way I can explain this more clearly.

At least this time you managed to elaborate instead of giving poor and easily misconstrued advice.

Yes let’s post studies we know don’t exist, when we all know at least one person whose balls aren’t ever going to work again...

Just get off it. You’re not blowing anyone’s mind here. Fairly simple concept. Wasn’t even a need for a thread. Everybody knows what masteron is good for, nobody except a ****ing beginner thinks running clomid on a heavy cycle is absolutely going to be the thing to save your testes. And what else?

No, I think that about sums it up.

 

[Jinsun]

I'm going to disprove this with bloods.

I sure do wish for that to happen - I sure do wish I am wrong about this. But as of now, it's one persons opinion over "1000's" of other users.

Regarding UGL's, well yeah, obviously they are not pharma grade, but saying serm's are significantly underdosed, especially the cheap clomid and tamox, is kinda silly. For the part that I have taken clomid and tamox, they have always been effective. Done tons of bloods. Saying all UGL gear is either bunk or severely underdosed, is just plain wrong.

There are not a lot of people in this thread, so there probably wont be much replies, that are antagonistic to your views ... But we can open a thread on this and I dare to presume, that most will confirm the validity of UGL clomid and tamox. It just doesn't pay off for UGL's anymore to fake stuff that much. Demand is high, bad word spreads quickly over the net. Times have changed. Might be different for var or primo for instance, but clomid and tamox, not really.

Go to meso, go to PM, etc. state this facts, as you have done so here. Ask for bloods, ask for cycle's that have had serm's in them.

I do agree that for strictly scientific purposes, everything needs to be tested for purity, but you still can not disregard all the anecdotal evidence, backed up by bloods as falls, due to non regulatory circumstances. If most non scientific evidence points in one direction, you just can't disregard it. That's just silly and it signifies more about your character, or your love for this topic, then you care to realise.

Even if you somehow are able to keep hpta up, again, it's one user over many many other's that haven't succeed. And scientifically speaking, when is something valid? High enough sample pool, research needs to be replicated and it needs to hold up to scrutiny. You use your scientific stance for your own gain and disregard it completely, when it comes to your claims. This logic can just as easily be turned back on to your claims and your personal tests, that you are about to do.

But I digress ... Post your bloods, post your cycle and we will add it to the interwebs circle of infinite knowledge and let the average gym rat decide for him self, what to do with his body.

 

[Jinsun]

Any time you give an aromatizable AAS, there will be some degree of HPG-axis suppression, no matter how much AI is given with it, because E2 metabolites will be formed locally. The brain is chock-full of aromatase.

Interesting, good stuff.

 

[Spurfy]

I sure do wish for that to happen - I sure do wish I am wrong about this. But as of now, it's one persons opinion over "1000's" of other users.

Regarding UGL's, well yeah, obviously they are not pharma grade, but saying serm's are significantly underdosed, especially the cheap clomid and tamox, is kinda silly. For the part that I have taken clomid and tamox, they have always been effective. Done tons of bloods. Saying all UGL gear is either bunk or severely underdosed, is just plain wrong.

There are not a lot of people in this thread, so there probably wont be much replies, that are antagonistic to your views ... But we can open a thread on this and I dare to presume, that most will confirm the validity of UGL clomid and tamox. It just doesn't pay off for UGL's anymore to fake stuff that much. Demand is high, bad word spreads quickly over the net. Times have changed. Might be different for var or primo for instance, but clomid and tamox, not really.

Go to meso, go to PM, etc. state this facts, as you have done so here. Ask for bloods, ask for cycle's that have had serm's in them.

I do agree that for strictly scientific purposes, everything needs to be tested for purity, but you still can not disregard all the anecdotal evidence, backed up by bloods as falls, due to non regulatory circumstances. If most non scientific evidence points in one direction, you just can't disregard it. That's just silly and it signifies more about your character, or your love for this topic, then you care to realise.

Even if you somehow are able to keep hpta up, again, it's one user over many many other's that haven't succeed. And scientifically speaking, when is something valid? High enough sample pool, research needs to be replicated and it needs to hold up to scrutiny. You use your scientific stance for your own gain and disregard it completely, when it comes to your claims. This logic can just as easily be turned back on to your claims and your personal tests, that you are about to do.

But I digress ... Post your bloods, post your cycle and we will add it to the interwebs circle of infinite knowledge and let the average gym rat decide for him self, what to do with his body.

I'm not discounting the fact that some of us may be genetic anomalies when it comes to SERMs on-cycle, but I would still argue that a significant percentage of AAS users would see less suppression by running a SERM on-cycle.

 

[Spurfy]

Yes let’s post studies we know don’t exist, when we all know at least one person whose balls aren’t ever going to work again...

Everybody knows someone who thinks they've seen a ghost.

What's your point?

Just get off it. You’re not blowing anyone’s mind here. Fairly simple concept. Wasn’t even a need for a thread. Everybody knows what masteron is good for, nobody except a ****ing beginner thinks running clomid on a heavy cycle is absolutely going to be the thing to save your testes. And what else?

I'm hardly a beginner at cycling and I'm hardly a bro-science pharmacologist. I have 10+ years of cycling and more than 18 years of post-grad pharmacology work.

If you want to discuss pharmacology in a scientific manner, great, let's do it. If you just want to rant, that's fine too -- my E2 might be sky high right now, but I'm not the one getting emotional, so I must be doing something right...

875 mg TE and 600 NPP with no AI, no Caber, no B6... I should be hanging milky C cups by now and my balls should be raisins. Right?

 

[Old Witch]

Everybody knows someone who thinks they've seen a ghost.

What's your point?



I'm hardly a beginner at cycling and I'm hardly a bro-science pharmacologist. I have 10+ years of cycling and more than 18 years of post-grad pharmacology work.

If you want to discuss pharmacology in a scientific manner, great, let's do it. If you just want to rant, that's fine too -- my E2 might be sky high right now, but I'm not the one getting emotional, so I must be doing something right...

875 mg TE and 600 NPP with no AI, no Caber, no B6... I should be hanging milky C cups by now and my balls should be raisins. Right?

Well, no. And I wholeheartedly disapprove of your constant data skewing. You’re not ONLY on test and npp. Secondly, those effects take time to develop, and third, obviously the clomid will have some effect. I’m just not buying that it’s going to save the day. I do understand how you came to your reasoning, and it makes perfect sense. However I am highly skeptical, and more so I am mostly just alarmed and put off by your aforementioned skewed data reflection.

 

[CatSnake]

My E2 is probably between 80-120 right now. So what? Masteron and Clomid are handling that. I have no high-E2 sides: Libido great, erections great, morning wood great, heavy balls, ejaculate thick and large volume, no blood pressure issues, no hot flushes, no insomnia, no water retention, no itchy nipples, no puffy nipples, no emotional spells, no headaches. Nothing. Zero.

Did we forget that E2 is highly anabolic? Invalid Link Removed

The half-life of unbound E2 is 20 minutes. This means every molecule of E2 that detaches from SHBG is completely eliminated by the body in < 2 hours. Invalid Link Removed

E2 levels reduce very rapidly once aromatizable androgens are reduced or eliminated. If you want to expedite this process, run something that competes with E2 for SHBG-binding, like Masteron, which is exactly what I'm doing in "PCT"

This is why Aromasin lowers E2 levels so quickly -- the half life of E2 is short and Aromasin is a substrate for SHBG. Simply shutting down aromatase would still leave plenty of E2 floating around to cause problems, according to your logic, but we know that this is absolutely not the case, and that maximum suppression of E2 occurs in 12 hours with Aromasin. According to your "long lasting E2 hypothesis", this would be impossible.

if that's the case, then why didn't you recommend aromasin for Jinsun 's gyno?

a single dose of an AI does not rapidly solve all E2 problems. prove me wrong?

 

[CatSnake]

My E2 is probably between 80-120 right now. So what? Masteron and Clomid are handling that. I have no high-E2 sides: Libido great, erections great, morning wood great, heavy balls, ejaculate thick and large volume, no blood pressure issues, no hot flushes, no insomnia, no water retention, no itchy nipples, no puffy nipples, no emotional spells, no headaches. Nothing. Zero.

Did we forget that E2 is highly anabolic? Invalid Link Removed

The half-life of unbound E2 is 20 minutes. This means every molecule of E2 that detaches from SHBG is completely eliminated by the body in < 2 hours. Invalid Link Removed

E2 levels reduce very rapidly once aromatizable androgens are reduced or eliminated. If you want to expedite this process, run something that competes with E2 for SHBG-binding, like Masteron, which is exactly what I'm doing in "PCT"

This is why Aromasin lowers E2 levels so quickly -- the half life of E2 is short and Aromasin is a substrate for SHBG. Simply shutting down aromatase would still leave plenty of E2 floating around to cause problems, according to your logic, but we know that this is absolutely not the case, and that maximum suppression of E2 occurs in 12 hours with Aromasin. According to your "long lasting E2 hypothesis", this would be impossible.

right, E2 is anabolic..... and you're using products that prevent it from binding from various tissues, right? or does it still bind specifically where you want it to?

 

[CatSnake]

There's a reason Masteron used to be used for breast cancer. The only reason it's not used today is because it's way off-patent.

.

no.

the reason masteron isn't used anymore for breast cancer, is because it causes irreversible masculinization that all DHT-based products do in women. SERMs are better. so are AIs.

 

[Hyde]

right, E2 is anabolic..... and you're using products that prevent it from binding from various tissues, right? or does it still bind specifically where you want it to?

My understanding is both Clomid and masteron will be tissue selective.

 

[CatSnake]

I didn't get them. I have a profound phobia of venipunture and I have to be given conscious sedation for blood draws. Yeah, go ahead and laugh... I can pin my quads all day long but the moment that alcohol wipe touches the inside of my elbow I get woozy. When that needle goes into my vein without conscious sedation any number of bad things happen.

I don't want to mock anybody with a phobia of blood draws, as I think that's unfair.

but I have to point out that in one thread, you claimed to me that the reason you never posted bloodwork to prove you theory was because you couldn't find ANY of your old bloodwork. you implied it was weird that any of us still had our old records...

Invalid Link Removed

in another thread, you claimed that you don't post bloodwork because you want people to test theories on their own and want them to learn without undue influence.

Invalid Link Removed

huh.....



.

 

[CatSnake]

My understanding is both Clomid and masteron will be tissue selective.

clomid lowers IGF1 even after raising E2, which reduces the anabolic effect he's claiming.....

http://anabolicminds.com/forum/post-cycle-therapy/288103-info-serms.html




.

 

[Spurfy]

Well, no. And I wholeheartedly disapprove of your constant data skewing. You’re not ONLY on test and npp. Secondly, those effects take time to develop, and third, obviously the clomid will have some effect. I’m just not buying that it’s going to save the day. I do understand how you came to your reasoning, and it makes perfect sense. However I am highly skeptical, and more so I am mostly just alarmed and put off by your aforementioned skewed data reflection.

I'm on Test, NPP, Mast, Clomid, T4, and Naltrexone. Going into my 7th week on AAS -- if something bad were going to happen it would have probably happened by now.

But I do get your point, and I can see the merits of your position.

 

[Spurfy]

I don't want to mock anybody with a phobia of blood draws, as I think that's unfair.

but I have to point out that in one thread, you claimed to me that the reason you never posted bloodwork to prove you theory was because you couldn't find ANY of your old bloodwork. you implied it was weird that any of us still had our old records...

Invalid Link Removed

in another thread, you claimed that you don't post bloodwork because you want people to test theories on their own and want them to learn without undue influence.


huh.....
.

Well, now you know the truth. I hate needles. Actually, I love them going into my muscles, but going into a vein is extremely painful and causes me to go into shock. So, as badly as I want to get blood-work, sometimes I just can't. Imagine facing your worst fear while being ridiculed by the staff who are the ones who are going to be torturing you. When I pin, I push the needle in very very slowly because I can feel if it starts to hit a vein -- if this happens I pull out immediately, recap, and go do calming deep breathing exercises. It takes me about 60 seconds to insert a 1 1/2" 25 ga pin, that's how scared I am of puncturing a vein.

And I do have old bloodwork that I could dig up if I really wanted to, but at this point I've thrown down the gauntlet and said I'll be getting it the last week of this cycle. If I can show functional LH and FSH, with T >1500, I think that is sufficiently demonstrative.

 

[Spurfy]

no.

the reason masteron isn't used anymore for breast cancer, is because it causes irreversible masculinization that all DHT-based products do in women. SERMs are better. so are AIs.

Treatment of Advanced Breast Carcinoma with Drostanolone Propionate
Bristol Medico-Chirurgical Journal. Vol. 85
"Virilization was not a noticeable side effect."

Can you all just stop making assumptions about things becuase you believe that they should be so, based upon your extremely limited understanding of pharmacology and endocrinology?

Can we do this? Can we drop the bro-science nonsense and actually cite sources for claims?

 

[CatSnake]

And I do have old bloodwork that I could dig up if I really wanted to, but at this point I've thrown down the gauntlet and said I'll be getting it the last week of this cycle. If I can show functional LH and FSH, with T >1500, I think that is sufficiently demonstrative.

dig up your old "bloodwork." or don't. I don't care... btw, running 3 seperate compounds with clomid and naltexenone doesn't prove anything.

quite frankly, I don't know why anybody would believe anybody would believe anything you'd post.... you made idiotic claims about SERMs and IGF1 (which I debunked pretty aggressively), along with numerous other claims here.

I don't understand your agenda, and I don't care to.

 

[Spurfy]

if that's the case, then why didn't you recommend aromasin for Jinsun 's gyno?

a single dose of an AI does not rapidly solve all E2 problems. prove me wrong?

Because DHT works downstream to stop E2-evoked gene transcription which has already been triggered by E2. Lowering E2 at this point will accomplish very little, since the signal cascade has already started.

 

[Spurfy]

I don't understand pharmacology, and I don't care to.

Fixed it for you.

 

[Old Witch]

I'm on Test, NPP, Mast, Clomid, T4, and Naltrexone. Going into my 7th week on AAS -- if something bad were going to happen it would have probably happened by now.

But I do get your point, and I can see the merits of your position.

I think that 7 weeks is not enough to tell anything. If something bad were to happen to your testes it would most likely be after ten or sixteen weeks, especially considering your supposed condition up to now.

Also, T4 why? Surely you do know that it’s not active until it converts to t3, and that in the field it is not 100% effective as it does not always convert at a predictable rate in a patient. Even though most doctors use it as their cure all for hypothyroid, the best would all agree active t3 is the more effective and overall safer drug.