So up guys, Derek Mooreplayedsmartage.com.

Today we're going to be going over my sort of concluding thoughts on the injectable

LGD, the Magnalone is what it's called as well.

Interesting findings, honestly.

First thing I want to cover before we get into blood work is the tissue selectivity versus oral.

It's really weird.

It's like I've talked about this briefly in the past about how it seems like certain

compounds with the first passive drug metabolism can have a, you know, big impact on bioavailability,

but also it seems like certain metabolites that have their own inherent tissue selectivity themselves.

So it seems like in the case of injectable SARMs, some of the oral formats are actually more

tissue selective than their injectable counterparts, which is kind of interesting and kind of

contradictory to what you would think happens. Because I would think and what I was very optimistic about based on some of the hype

behind them is that when you take them orally sort of like oral estrogen versus transdermal

if you look at the data you'll find that oral estrogen you know cranked SHBG through the roof

causes a bunch of clotting issues potentially whereas transdermal has like also spikes estrone

through the roof, whereas transdermal and injections don't have any of these deleterious

outcomes on biomarkers. So, you know, it's because it skips this first pass of drug metabolism.

So often it is assumed that if you have a compound that's oral and is potentially stressful on the liver, which we know that SARMs can be for sure.

I don't know why everyone still thinks that, oh, if my liver enzymes are elevated, it means I have pro hormones.

No, like this stuff in the therapeutic dosages at like one to two milligrams have shown transient increases in liver enzymes. The dosages,

you guys that are using it for performance enhancing purposes are using, if you're using like a 20,

30, 40 milligram dose orally and then thinking it's not supposed to raise your liver enzymes,

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