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Guide Why SARMs are dogshit (9 Viewers)

Guide Why SARMs are dogshit
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Daker

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  • #106
because i know very little about the more niche stuff of the negative feedback loop
in my mind it doesnt even matter whether its a sarm or steroid at a low dose
my thinking was that the estrogen and androgen receptors in the brain act as a way to signal the total amount of sex steroids, so if you antagonise estrogen receptors you have a greater window to agonise the androgen receptors, so a low dose sarm or steroid like oxandrolone or halotestin would fit in that window

thats just my thinking tho, this thread is mostly on the non tissue selectivity of sarms
the real sarm we need would function just like enclo but for androgen receptors instead of estrogen receptors, then everything would be great
nigga u didn't read jackshit, those SARMs are "supposed" to be tissue selective and behaved like that at clinical trials doses.
 

birthdefect

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  • #107
nigga u didn't read jackshit, those SARMs are "supposed" to be tissue selective and behaved like that at clinical trials doses.
nigga i read most of the thread, the important parts
i specifically said i wasnt talking about sarms specifically, just really any low dose androgen
i dont care about sarms not being tissue selective, it has very little to do with the idea im sharing

my thinking was that the estrogen and androgen receptors in the brain act as a way to signal the total amount of sex steroids, so if you antagonise estrogen receptors you have a greater window to agonise the androgen receptors while lowering your t back to your pre-enclo levels, so a low dose sarm or steroid like oxandrolone or halotestin would fit in that window

this is my idea, is there anything wrong with this?
it doesnt necessarily have to be a sarm causing the suppression
 

birthdefect

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  • #108
No,even a micro dose fails because the HPTA doesn't require a full 100% receptor saturation to shut down or to be downregulated, AAS and SARMs will aggressively bind to the ARs in the hypothalamus and downregulate the pulsatile release of GnRH.
oh shi i didnt see this message jfl, didnt show up
if enclo upregulates, surely there must be a dose of an androgen that downregulates the same, so you end up with the same t levels but with a more anabolic substance in the body
 

Daker

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  • #109
because i know very little about the more niche stuff of the negative feedback loop
in my mind it doesnt even matter whether its a sarm or steroid at a low dose
my thinking was that the estrogen and androgen receptors in the brain act as a way to signal the total amount of sex steroids, so if you antagonise estrogen receptors you have a greater window to agonise the androgen receptors, so a low dose sarm or steroid like oxandrolone or halotestin would fit in that window

thats just my thinking tho, this thread is mostly on the non tissue selectivity of sarms
the real sarm we need would function just like enclo but for androgen receptors instead of estrogen receptors, then everything would be great
To think i thought you were smart lol, that's not how the HPTA axis works. The HPTA doesn't calculate a cumulative "total score" of sexual hormones, the whole axis relies on two independent, parallel feedback loops keyword here is independent. Enclomiphene works exclusively by blocking the ER to trick the hypothalamus into screting GnRH, but clearing that estrogen pathway has ZERO influence over the AR pathway, again, they are independent. The HPTA doesn't require 100% receptor saturation to get dowregulated or shutdown. Any exogenous androgens and i mean ANY even at micro doses will bind to the ARs on the hypothalamus and downregulate GnRH secretion because of the super high binding affinities, specially halo.
 

birthdefect

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  • #110
To think i thought you were smart lol, that's not how the HPTA axis works. The HPTA doesn't calculate a cumulative "total score" of sexual hormones, the whole axis relies on two independent, parallel feedback loops keyword here is independent. Enclomiphene works exclusively by blocking the ER to trick the hypothalamus into screting GnRH, but clearing that estrogen pathway has ZERO influence over the AR pathway, again, they are independent. The HPTA doesn't require 100% receptor saturation to get dowregulated or shutdown. Any exogenous androgens and i mean ANY even at micro doses will bind to the ARs on the hypothalamus and downregulate GnRH secretion because of the super high binding affinities, specially halo.
ah alr
i just know nothing about the negative feedback loop and the hpg axis in general
 

Daker

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  • #111
ah alr
i just know nothing about the negative feedback loop and the hpg axis in general
Yeah it's not a linear math equation were +1 from Enclo can perfectly cancel out a -1 from AAS, to put as simple as possible the AR is a kill switch and the ER is just a modulator of the system, the downregulation triggered by AAS binding to the AR will completely override the weak upstream signal generated by blocking the ERs.
 

Daker

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  • #112

Alyx

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  • #113
Mirin BOTB.
 

makeaway

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  • #114
Tagging niggas @surgerymax @Nardicus @fent @Machiavellian @PrettyBoyMaxxing @Dexter @dysregulated @Mandy @Circadex
DNR
 

Daker

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  • #115

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  • #116
There are definitely scenarios where they can be used correctly
 

Daker

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  • #117
There are definitely scenarios where they can be used correctly
like? they are a poor excuse to not take AAS
 

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  • #118
No fucking idea, I have a bodybuilder friend who used MK-2866 during a cut with test and he was straight glazing that shit
 

Daker

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  • #119
No fucking idea, I have a bodybuilder friend who used MK-2866 during a cut with test and he was straight glazing that shit
Doses? test was probably doing all the heavy lifting tbh.
 

Grif

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  • #120

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