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Scott Stevenson on Anadrol science

MR. BMJ

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Dr. Stevenson has a new Muscle Minds episode out today that is really good. The main topic is his thoughts on the science of Anadrol, but there are other topics as well. I'll leave the time stamps below.



3:00 the Science of Anadrol
22:00 Can T3 make you grow
32:30 Still growing with LOW Test levels
44:00 So how much protein should you take on gear?
58:20 Preventing muscle tears
 
Great episode :) Scott really knows alot.
 
Awesome will definitely check out. Thanks
 
I thought it was just OK with respect to the Anadrol portion. Not sure why he entertained MPMD's claim without analysis of any supporting literature. Sure, maybe (if even true that an Anadrol-only cycle increases serum estrogens; I'm willing to test this myself) oxymetholone decreases clearance and/or excretion of estrogens (by competitive glycolysation and/or conjugation?) but it's not particularly compelling, mostly because I doubt the claim that increased estrogens are attributable to oxymetholone to start.

Potential mAR binding: maybe, but that wouldn't result in pronounced anabolism, if anything mAR actions tend to attenuate rather than potentiate classical AR action (that's the prevailing hypothesis). These actions via mAR are transient, typified by GPCR nongenomic (rapid) action.

Very little discussion of metabolites and the Schanzer view that oxymetholone likely acts as a prohormone. My modeling data on 17α-methyl-5α-androstane-3α-17β-diol supports this. I posted this here: https://www.professionalmuscle.com/...-nolva…-what-is-next-best.171373/post-3099138

He's clearly a fountain of knowledge but I feel he didn't do any homework on the Anadrol topic and was somewhat unprepared. I liked his discussion of protein requirements, protein leveraging, glucagon and appetite, J. Antonio, et al. I wished that he had explained the fact that T3 (Cytomel) increases net protein breakdown (particularly, type IIB atrophy, i.e., selective catabolism of hypertrophied muscle) at moderate - high doses. But everything he said was correct, he just did not present the converse possibility (the risks/tradeoffs) if doses go beyond optimal (bringing the individual to a euthyroid state).
 
I thought it was just OK with respect to the Anadrol portion. Not sure why he entertained MPMD's claim without analysis of any supporting literature. Sure, maybe (if even true that an Anadrol-only cycle increases serum estrogens; I'm willing to test this myself) oxymetholone decreases clearance and/or excretion of estrogens (by competitive glycolysation and/or conjugation?) but it's not particularly compelling, mostly because I doubt the claim that increased estrogens are attributable to oxymetholone to start.

Potential mAR binding: maybe, but that wouldn't result in pronounced anabolism, if anything mAR actions tend to attenuate rather than potentiate classical AR action (that's the prevailing hypothesis). These actions via mAR are transient, typified by GPCR nongenomic (rapid) action.

Very little discussion of metabolites and the Schanzer view that oxymetholone likely acts as a prohormone. My modeling data on 17α-methyl-5α-androstane-3α-17β-diol supports this. I posted this here: https://www.professionalmuscle.com/forums/index.php?threads/can’t-use-nolva…-what-is-next-best.171373/post-3099138

He's clearly a fountain of knowledge but I feel he didn't do any homework on the Anadrol topic and was somewhat unprepared. I liked his discussion of protein requirements, protein leveraging, glucagon and appetite, J. Antonio, et al. I wished that he had explained the fact that T3 (Cytomel) increases net protein breakdown (particularly, type IIB atrophy, i.e., selective catabolism of hypertrophied muscle) at moderate - high doses. But everything he said was correct, he just did not present the converse possibility (the risks/tradeoffs) if doses go beyond optimal (bringing the individual to a euthyroid state).
I think the point your missing here is that 90% of the people watching the episode have 0 idea what you or he is talkin about :) most dont even want to know, they just wanna pound roids :)
 
I think the point your missing here is that 90% of the people watching the episode have 0 idea what you or he is talkin about :) most dont even want to know, they just wanna pound roids :)
I know! In that sense, what he provided was excellent. He's looking very lean, like 7%ish. Contest lean.
 
I just want to pound my 100mg Anadrol ed.
And hope of some increase in hemoglobin, since EQ does nothing for that.
 
I thought it was just OK with respect to the Anadrol portion. Not sure why he entertained MPMD's claim without analysis of any supporting literature. Sure, maybe (if even true that an Anadrol-only cycle increases serum estrogens; I'm willing to test this myself) oxymetholone decreases clearance and/or excretion of estrogens (by competitive glycolysation and/or conjugation?) but it's not particularly compelling, mostly because I doubt the claim that increased estrogens are attributable to oxymetholone to start.

Potential mAR binding: maybe, but that wouldn't result in pronounced anabolism, if anything mAR actions tend to attenuate rather than potentiate classical AR action (that's the prevailing hypothesis). These actions via mAR are transient, typified by GPCR nongenomic (rapid) action.

Very little discussion of metabolites and the Schanzer view that oxymetholone likely acts as a prohormone. My modeling data on 17α-methyl-5α-androstane-3α-17β-diol supports this. I posted this here: https://www.professionalmuscle.com/forums/index.php?threads/can’t-use-nolva…-what-is-next-best.171373/post-3099138

He's clearly a fountain of knowledge but I feel he didn't do any homework on the Anadrol topic and was somewhat unprepared. I liked his discussion of protein requirements, protein leveraging, glucagon and appetite, J. Antonio, et al. I wished that he had explained the fact that T3 (Cytomel) increases net protein breakdown (particularly, type IIB atrophy, i.e., selective catabolism of hypertrophied muscle) at moderate - high doses. But everything he said was correct, he just did not present the converse possibility (the risks/tradeoffs) if doses go beyond optimal (bringing the individual to a euthyroid state).
To be fair, he said "sure, maybe" which is pretty much what you just said.
 
Dr. Stevenson has a new Muscle Minds episode out today that is really good. The main topic is his thoughts on the science of Anadrol, but there are other topics as well. I'll leave the time stamps below.



3:00 the Science of Anadrol
22:00 Can T3 make you grow
32:30 Still growing with LOW Test levels
44:00 So how much protein should you take on gear?
58:20 Preventing muscle tears
Thanks appreciate the time marks...really makes it so much easier...Checked out anadrol part..little winded for me - on to t3
 
is 50mg a day of Anadrol a good dose? Or is that to low ?
I recently was doing 200 a day - did that for a few weeks split up every 4 hours - remember 50mg anadrol is different then 50mg dbol - have to compare the drug on its own accord - look at scientific studies and recommend dosage based on weight etc
 
is 50mg a day of Anadrol a good dose? Or is that to low ?
I consider it an optimal dose. For larger guys, sure, more. But for most, 50 mg is excellent. 100 mg might give you ~25% more anabolism than 50 mg.
 
I thought it was just OK with respect to the Anadrol portion. Not sure why he entertained MPMD's claim without analysis of any supporting literature. Sure, maybe (if even true that an Anadrol-only cycle increases serum estrogens; I'm willing to test this myself) oxymetholone decreases clearance and/or excretion of estrogens (by competitive glycolysation and/or conjugation?) but it's not particularly compelling, mostly because I doubt the claim that increased estrogens are attributable to oxymetholone to start.

Potential mAR binding: maybe, but that wouldn't result in pronounced anabolism, if anything mAR actions tend to attenuate rather than potentiate classical AR action (that's the prevailing hypothesis). These actions via mAR are transient, typified by GPCR nongenomic (rapid) action.

Very little discussion of metabolites and the Schanzer view that oxymetholone likely acts as a prohormone. My modeling data on 17α-methyl-5α-androstane-3α-17β-diol supports this. I posted this here: https://www.professionalmuscle.com/forums/index.php?threads/can’t-use-nolva…-what-is-next-best.171373/post-3099138

He's clearly a fountain of knowledge but I feel he didn't do any homework on the Anadrol topic and was somewhat unprepared. I liked his discussion of protein requirements, protein leveraging, glucagon and appetite, J. Antonio, et al. I wished that he had explained the fact that T3 (Cytomel) increases net protein breakdown (particularly, type IIB atrophy, i.e., selective catabolism of hypertrophied muscle) at moderate - high doses. But everything he said was correct, he just did not present the converse possibility (the risks/tradeoffs) if doses go beyond optimal (bringing the individual to a euthyroid state).

How much t3 would you recommend for an AAS and gh-enhanced bodybuilder who is in a significant caloric deficit already - to lose fat without risking lean tissue?
 
How much t3 would you recommend for an AAS and gh-enhanced bodybuilder who is in a significant caloric deficit already - to lose fat without risking lean tissue?
I really don't recommend T3 at all (unless hypothyroid and seeking a euthyroid state, i.e., dose <= 25 mcg daily).

Note that caloric restriction (dieting) reduces free T3 slightly. RhGH increases peripheral conversion of T4 to T3 (thus making up at least a portion of the decrement by dieting).
 
How much t3 would you recommend for an AAS and gh-enhanced bodybuilder who is in a significant caloric deficit already - to lose fat without risking lean tissue?
Avoid it if you are not in the big boi IFBB pro zone. It made me spin my wheels for a year, it was impossible for me to build muscle on 25 T3 and 100 t4 and 5iu HGH.
 
Avoid it if you are not in the big boi IFBB pro zone. It made me spin my wheels for a year, it was impossible for me to build muscle on 25 T3 and 100 t4 and 5iu HGH.
same with me. But T4 alone 50-75mcg daily okay .... Even at a low dose of T3 12.5mcg I'm very tired and the strength goes down, while the blood shows the optimal upper range.
 
i like 50mg t3 when dieting for the energy. helps keep me from dragging when depleted & hungry.
 
I really don't recommend T3 at all (unless hypothyroid and seeking a euthyroid state, i.e., dose <= 25 mcg daily).

Note that caloric restriction (dieting) reduces free T3 slightly. RhGH increases peripheral conversion of T4 to T3 (thus making up at least a portion of the decrement by dieting).

why dont u recommend it? genuinely curious

too catabolic?

what would you recommend instead to expedite fat loss?
 
why dont u recommend it? genuinely curious

too catabolic?

what would you recommend instead to expedite fat loss?
Yes, too catabolic, and specifically it catabolizes hypertrophied muscle preferentially. I like clen as a recomp agent (it's truly an anabolic agent first and foremost, with lipolytic properties and performance-enhancing properties), I like DNP from a theoretical standpoint but it's the equivalent of taking an AK-47 to a nail for most. I like ECA as a mild lipolytic agent. I believe in a place for rhGH with the right compounds (including androgens, several of which have unique features contributing to a decrease in fat). For some, albuterol and caffeine may be superior to clen. There are a lot of options, and frankly, the thyroid hormones like T3 are the only fat-loss or recomp agents in popular use that I see no rational use for in healthy (euthyroid) bodybuilders.
 

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