SARM's, MK, & GW : A User's Guide

Wow. Major thread derailment. Back to the main subject, sarms! What's everyone running right now? I'm about 4 weeks into an osta/dermacrine stack right now and it has been great to say the least
 
yates84 said:
Wow. Major thread derailment. Back to the main subject, sarms! What's everyone running right now? I'm about 4 weeks into an osta/dermacrine stack right now and it has been great to say the least
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How long will you run it for? Also I almost have my stack complete! Need one more Legend, one trest, and some support supps.
 
CJNator said:
How long will you run it for? Also I almost have my stack complete! Need one more Legend, one trest, and some support supps.
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I have another 4 weeks them I'm bridging g into a trest/epistane cycle
 
CJNator said:
That sounds like it will be a killer stack, no estro sides or bloating because of epi.
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It will definitely help mitigate some of the trest sides. I plan on running the trest at 150mg ed so exemestane will be a must
 
CJNator said:
Oh **** nice, will you be logging it?
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I've already got a log going with my wife in the training forum, just going to continue it there.
 
yates84 said:
Wow. Major thread derailment. Back to the main subject, sarms! What's everyone running right now? I'm about 4 weeks into an osta/dermacrine stack right now and it has been great to say the least
Click to expand...

I have 15 days left of my cycle, running 200mg Furaza, 100mg Halodrol, 20mg Epistane, 20mg Trendione, 12mg RAD-140. I know, the Trendione is low, but it's capped with the Epistane, so it's not intentional. Looking the best I've ever looked, really not excited about cycling off in 2 weeks. But I know we've all been there...
 
Hastur said:
I have 15 days left of my cycle, running 200mg Furaza, 100mg Halodrol, 20mg Epistane, 20mg Trendione, 12mg RAD-140. I know, the Trendione is low, but it's capped with the Epistane, so it's not intentional. Looking the best I've ever looked, really not excited about cycling off in 2 weeks. But I know we've all been there...
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Off time isn't bad, you just need to make the best of it! There are so many good natty supps out there now that actually work there is no reason to fear off time. Epic unleashed keeps me happy during off time just by its self
 
yates84 said:
Off time isn't bad, you just need to make the best of it! There are so many good natty supps out there now that actually work there is no reason to fear off time. Epic unleashed keeps me happy during off time just by its self
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True Ep1c unleashed is the best natty product I have ever tried....pump,strenght,more reps from now on is a stample in my supplements stack.I'm taking the oral version not the TD.TD will probably works better ;)
 
yates84 said:
Off time isn't bad, you just need to make the best of it! There are so many good natty supps out there now that actually work there is no reason to fear off time. Epic unleashed keeps me happy during off time just by its self
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That's true, I re-read the Ghar1ne thread last night and the announcement of PHOSPHAS1ZE still has me pumped, I need that for PCT/Off Cycle. Get some Ep1c Unleashed, DermaStr3ngth, and Phosphas1ze and I'd have the natty supps covered. Then throw in some Ghar1ne and Cardar1ne, probably some Elim1nate, I think it would be a pretty solid PCT.
 
Lucianooo said:
True Ep1c unleashed is the best natty product I have ever tried....pump,strenght,more reps from now on is a stample in my supplements stack.I'm taking the oral version not the TD.TD will probably works better ;)
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Oral/td combo is the best route imo. I use the td after my shower at night for steady absorption and use the caps pwo in the morning for the faster effects in the gym. I love it!
 
Hastur said:
That's true, I re-read the Ghar1ne thread last night and the announcement of PHOSPHAS1ZE still has me pumped, I need that for PCT/Off Cycle. Get some Ep1c Unleashed, DermaStr3ngth, and Phosphas1ze and I'd have the natty supps covered. Then throw in some Ghar1ne and Cardar1ne, probably some Elim1nate, I think it would be a pretty solid PCT.
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Ghar1ne is perfect on time off keeps muscle and stenght and reverse the igf decreasing from nolva.Cardar1ne is anti-catabolic and will prevent fat gain while on pct.Definetly 2 must have on pct :)
 
yates84 said:
Oral/td combo is the best route imo. I use the td after my shower at night for steady absorption and use the caps pwo in the morning for the faster effects in the gym. I love it!
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Real quick. How would one does ep1c. I workout in the afternoons 5-7 in that range. But I dont always know if I am working out that day ( I go by feel if I need a day off I take it ) but the bottle says to take one pill in the morning on days I don't work out. I won't know that toll 3/4 in the afternoon
 
fro60ol said:
Real quick. How would one does ep1c. I workout in the afternoons 5-7 in that range. But I dont always know if I am working out that day ( I go by feel if I need a day off I take it ) but the bottle says to take one pill in the morning on days I don't work out. I won't know that toll 3/4 in the afternoon
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I would dose it about the same time every day so by the time you need to dose you will know what you are doing that day
 
jbryand101b said:
Just going off what dr mike scaly talks about for his power pct plan. You can shoot him an email if you wish to debate him.
When HCG is taken for too long or too high of a dosage, it can desensitize the lh receptor, according to the hormonal restoration doctor.


If you feel like you don't agree, I can get you in touch with William Llewelyn an dr mike scally and you can fully debate their research and data on the subject.

I look forward to the screen shot of the conversation as too learn and be enlightened
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Im sory but stan is right...
your desensitization statement was wrong man....post all the fancy google stuff you can find- that doesnt make you right..

and PS, although scally has his book smarts, his actual knowledge on AI's, Gyno and SERMs are flawed in alot of areas... I have actually debated with him and he turned out to be an immature douchbag that then just posted childish remarks and you tube videos calling me an idiot...

He does have alot of good info, but also flawed info, I take what he says with a grain of salt. he is too high up on his high horse to see any other direction but his first conclusions, and if you post research, exp and feed back from others that goes against his first thoughts he turns into a big baby. its why i dont even bother at meso much anymore... he is far from an AAS guru believable me...

and again shut down is shut down, some compounds are faster to shut down and/or harder on shut down, but the testies are taking a hit with big or small... you are wrong...
 
"by jbryand101b View Post
Suppression of lh output to a degree the testicles become desensitized to the effects is different than suppressed but not enough to do so."

StanleyG said:
You wanna expand upon this because as it is written it does not make any sense.
Leydig cell desensitization is most often associated with over stimulation of the leydig cells (ie taking too much hcg). Suppression of LH does not result in Leydig cell (or testicle as you put it) desensitization. That being said this means that degree off suppression has no correlation with leydig cell desensitization. This is why even after a long shut down (without hcg use) the leydig cells will respond to say hcg therapy, because LH deprivation does not result in their desensitization.
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exactly.... doesnt even make sense that statement..... i literally smacked my forehead when i read that one....
 
Hastur said:
That's true, I re-read the Ghar1ne thread last night and the announcement of PHOSPHAS1ZE still has me pumped, I need that for PCT/Off Cycle. Get some Ep1c Unleashed, DermaStr3ngth, and Phosphas1ze and I'd have the natty supps covered. Then throw in some Ghar1ne and Cardar1ne, probably some Elim1nate, I think it would be a pretty solid PCT.
Click to expand...

when is PHOSPHAS1ZE gonna be available?
 
1kerry said:
when is PHOSPHAS1ZE gonna be available?
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Solid question, and one I sadly don't have the answer to. I'd like it to be within the next 2-3 weeks for my own selfish reasons, lol. But more details will be rolling out soon, I'm sure.
 
SARM's, MK, & GW : A User's Guide

Blergs said:
Im sory but stan is right...
your desensitization statement was wrong man....post all the fancy google stuff you can find- that doesnt make you right..

and PS, although scally has his book smarts, his actual knowledge on AI's, Gyno and SERMs are flawed in alot of areas... I have actually debated with him and he turned out to be an immature douchbag that then just posted childish remarks and you tube videos calling me an idiot...

He does have alot of good info, but also flawed info, I take what he says with a grain of salt. he is too high up on his high horse to see any other direction but his first conclusions, and if you post research, exp and feed back from others that goes against his first thoughts he turns into a big baby. its why i dont even bother at meso much anymore... he is far from an AAS guru believable me...

and again shut down is shut down, some compounds are faster to shut down and/or harder on shut down, but the testies are taking a hit with big or small... you are wrong...
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Okay, can you link me to data to help understand what is going on then
Over stimulation of lh results in loss of testicular lh receptors, got that, but what causes this on steroids?
As so far, I can't find anything that states a decrease in lh production leads doesn't lead to an decrease in testicular lh receptor sensitivity.

All I have to go on is

1. Effect of long-term testosterone oenanthate administration on male reproductive function: Clinical evaluation, serum FSH, LH, Testosterone and seminal fluid analysis in normal men. J. Mauss, G. Borsch et al. Acta Endocrinol 78 (1975) 373-84
 
jbryand101b said:
Over stimulation of lh results in loss of testicular lh receptors, got that, but what causes this on steroids?
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They are not testicular LH receptors. They are called leydig cells #1.
#2 its not over stimulation of LH, its over stimulation of the leydig cells by a LH mimetic that is many many times more potent than LH itself (at least with regards to your Scally/HCG info you posted).
#3 There is no loss of receptors, there is a desensitization of the leydig cells, which means they will no longer respond to the LH present the way they would in the past- not that they are lost or there are less of them.
#4 This has nothing to do with supporting your original statement.....at all.
Your out of your realm of intellect so you should simply refrain from posting. That is far better than posting totally inaccurate and incorrect information- which is what you did. Then your buddies come in to defend you, which to a degree is admirable, but you are still wrong regardless. The important thing is that the readers and members of this forum know that. Not because it is you or because it is personal, simply because they deserve to be taught correct information. You see you need to allow your ego to step aside and stop trying to be right and instead make sure the info ultimately passed along to the forum members is right. My Dad used to have a saying, " If you cant dazzle them with brilliance then baffle them with bull****". That applies to you 100% in this and many other scenarios I have seen where you have posted. Sad really.
 
The luteinizing hormone/choriogonadotropin receptor (LHCGR), also lutropin/choriogonadotropin receptor (LCGR) or luteinizing hormone receptor (LHR) is a transmembrane receptor found predominantly in the ovary and testis, but also many extragonadal organs such as the uterus and breasts. The receptor interacts with both luteinizing hormone (LH) and chorionic gonadotropins (such as hCG in humans) and represents a G protein-coupled receptor (GPCR). Its activation is necessary for the hormonal functioning during reproduction.
 
The LHCGR consists of 674 amino acids and has a molecular mass of about 85–95 kDA based on the extent of glycosylation.[2]
Invalid Link Removed


The seven transmembrane α-helix structure of a G protein-coupled receptor such as LHCGR
Like other GPCRs, the LHCG receptor possess seven membrane-spanning domains or transmembrane helices.[3] The extracellular domain of the receptor is heavily glycosylated. These transmembrane domain contains two highly conserved cysteine residues, which build disulfide bonds to stabilize the receptor structure. The transmembrane part is highly homologous with other members of the rhodopsin family of GPCRs.[4] The C-terminal domain is intracellular and brief, rich in serine and threonine residues for possible phosphorylation.
 
Stan, I thought you would realize this, but the only reason HCG is in this convo, is because you brought it into it. I wasn't talking, or even thinking about it.
 
jbryand101b said:
Okay, can you link me to data to help understand what is going on then
Over stimulation of lh results in loss of testicular lh receptors, got that, but what causes this on steroids?
Click to expand...

huh?
shut down from aas and possible desensitization from over HCG use is NOT the same thing or area of shut down.
it doesnt cause a loss in receptors.
when on HCG your causing shut down in some ways, but stimulating the testies in other ways, that is why its a NO NO to use HCG DURING PCT, but it can help PCT if used during cycle or JUST BEFORE PCT.

AAS shut down your own production of hormones via-feedback loop in testies and causes them to overall shut down because the body pretty much senses there too much test (steroids imo) in the blood and shuts down its own production of test to try to reach homeostasis.
I think you are confused on the differing types of shutdown, what will or will not be possibly be desensitized with HCG use, and the type of shutdown with aas...

HCG and aas in relation to the testicle issues are not the same.

and sarms do cause shutdown so I would still rec a PCT after a run IMO (just adding that in after looking through thread)
 
Blergs said:
huh?
shut down from aas and possible desensitization from over HCG use is NOT the same thing or area of shut down.
it doesnt cause a loss in receptors.
when on HCG your causing shut down in some ways, but stimulating the testies in other ways, that is why its a NO NO to use HCG DURING PCT, but it can help PCT if used during cycle or JUST BEFORE PCT.

AAS shut down your own production of hormones via-feedback loop in testies and causes them to overall shut down because the body pretty much senses there too much test (steroids imo) in the blood and shuts down its own production of test to try to reach homeostasis.
I think you are confused on the differing types of shutdown, what will or will not be possibly be desensitized with HCG use, and the type of shutdown with aas...

HCG and aas in relation to the testicle issues are not the same.

and sarms do cause shutdown so I would still rec a PCT after a run IMO (just adding that in after looking through thread)
Click to expand...

A pct for sarms and sarms causing shut down has been mentioned 273 times in this thread fyi
 
Abstract
LHRH-induced elevation of endogenous LH in adult male rats was followed by dose-dependent loss of testicular LH receptors and cAMP responses to hCG stimulation in vitro.
Invalid Link Removed
 
jbryand101b said:
Stan, I thought you would realize this, but the only reason HCG is in this convo, is because you brought it into it. I wasn't talking, or even thinking about it.
Click to expand...

You, in your ignorance, tried to use it to justify your ignorant and inaccurate statement bro. Then you drug Dr Scally into it based on his statement that HCG can cause desensitization in leydig cells, which it can BUT that has absolutely NOTHING to do with supporting your ridiculous contention.
On the contrary my previous incorporation of HCG in my statement supported an accurate contention. Thats the difference.
For god sake you google ninja just stop. The difference here is I truly know this stuff. You goggle **** and incorrectly try to apply it to support your inaccurate and incorrect intentions. Your a menace of misinformation.
 
SARM's, MK, & GW : A User's Guide

Blergs said:
huh?
shut down from aas and possible desensitization from over HCG use is NOT the same thing or area of shut down.
it doesnt cause a loss in receptors.
when on HCG your causing shut down in some ways, but stimulating the testies in other ways, that is why its a NO NO to use HCG DURING PCT, but it can help PCT if used during cycle or JUST BEFORE PCT.

AAS shut down your own production of hormones via-feedback loop in testies and causes them to overall shut down because the body pretty much senses there too much test (steroids imo) in the blood and shuts down its own production of test to try to reach homeostasis.
I think you are confused on the differing types of shutdown, what will or will not be possibly be desensitized with HCG use, and the type of shutdown with aas...

HCG and aas in relation to the testicle issues are not the same.

and sarms do cause shutdown so I would still rec a PCT after a run IMO (just adding that in after looking through thread)
Click to expand...

I feel like the two subjects are getting mixed up as I try to respond to stans comments on HCG,
He started talking about HCG so I'm trying to discuss both but I feel like it's getting mixed up

But my question for you was on lack of increasing testosterone production post cycle even when there is still lh production or said production increases?
 
jbryand101b said:
Abstract
LHRH-induced elevation of endogenous LH in adult male rats was followed by dose-dependent loss of testicular LH receptors and cAMP responses to hCG stimulation in vitro.
Click to expand...

So the **** what? What does this have to do at all with suppression? There is a reduction in LH with suppression, not an increase. Get a clue bro. Seriously. Maybe just admit your retarded staatement of:
"by jbryand101b View Post
Suppression of lh output to a degree the testicles become desensitized to the effects is different than suppressed but not enough to do so."
Is just wrong. Dead wrong.
 
StanleyG said:
You, in your ignorance, tried to use it to justify your ignorant and inaccurate statement bro. Then you drug Dr Scally into it based on his statement that HCG can cause desensitization in leydig cells, which it can BUT that has absolutely NOTHING to do with supporting your ridiculous contention.
On the contrary my previous incorporation of HCG in my statement supported an accurate contention. Thats the difference.
For god sake you google ninja just stop. The difference here is I truly know this stuff. You goggle **** and incorrectly try to apply it to support your inaccurate and incorrect intentions. Your a menace of misinformation.
Click to expand...
Your initial post, you began referring to HCG so it was brought into discussion

StanleyG said:
You wanna expand upon this because as it is written it does not make any sense.
Leydig cell desensitization is most often associated with over stimulation of the leydig cells (ie taking too much hcg). Suppression of LH does not result in Leydig cell (or testicle as you put it) desensitization. That being said this means that degree off suppression has no correlation with leydig cell desensitization. This is why even after a long shut down (without hcg use) the leydig cells will respond to say hcg therapy, because LH deprivation does not result in their desensitization.
Click to expand...
 
StanleyG said:
So the **** what? What does this have to do at all with suppression? There is a reduction in LH with suppression, not an increase. Get a clue bro. Seriously. Maybe just admit your retarded staatement of:
"by jbryand101b View Post
Suppression of lh output to a degree the testicles become desensitized to the effects is different than suppressed but not enough to do so."
Is just wrong. Dead wrong.
Click to expand...

First there is no such thing as a lh receptor, now it has nothing to do with anything?
I can see how you have confused yourself on the two subjects
 
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