So, guys, Derek, moreplacemorenates.com. Today we're going to be talking about different pathways of growth as well as me going back onto anabolic.

So I'll get into the details in a bit here. But basically, something I've realized over the years is that there are many different pathways of growth in the body.

It's not all regulated through androgen receptor activation.

And this is probably a big reason why selective androgen receptor modulators have such a low ceiling in terms of their ability to grow muscle.

Like it seems like there's a very, the cap at which diminishing return sets in is, um, a lot lower than with anabolic energetic steroids, which, you know, don't just interact through the AR. They actually have a lot of downstream, um, effects on other receptors. And to be honest, I think SARs do too. I think it's just the studies imply tissue selectivity and androgen receptor modulation

in a selective manner in which I think they also have, they probably act similarly to

anabolic endrogenic steroids where they have like, you know, unpredictable interaction with

other like satellite receptors in the body, like glucocorticoid receptors, mineral corticoid receptors,

et cetera, and it produces kind of like unpredictable effects. But with that being said,

they were designed to agonize the AR specifically whereas anabolic were also designed to do

like B tissue selective but they also have downstream interaction with a lot of different things

like some compounds like anadryl for example that has like an undetectable binding affinity for the

androgen receptor yet it's like one of the most potent muscle builders out there

and it does like all this other crazy shit so one of the things that i found more in the past

like year or so is all of the different pathways that some of these like metabolite interactions

actually happen through and how that influences muscle growth and strength building and how that can

be leveraged to design a more optimized protocol where you're not just picking things that hammer

the AR over and over that overlap significantly and you're just competing essentially for the same

receptor activation with a bunch of different compounds that are not designed to take advantage of all these other vectors that could be, you know, have a little bit here, you know, something that fully takes advantage of the AR, and you have something that fully takes advantage of this and fully takes advantage of this.

And this is sort of where, you know, I started to get into compounds that excel in a anti-catabolic context was like one of the first things

I learned about where it was things that antagonize glucocorticoid receptors, which then

could be used in a cutting phase to enhance muscle retention and get a significant recomp

...