Receptors and Stacking

We talk a lot about receptors on r/PEDs (often in reference to why stacking can be a bad idea) but what exactly are they? The opening line of Wikipedia summarizes what a receptor is pretty well.

A receptor is a protein molecule that receives chemical signals… when chemical signals bind to a receptor, they cause some form of cellular/tissue response

There are four types of receptors: inonotropic receptors, metabotropic, kinase-linked, nuclear receptors.

The things that bind to receptors are called ligands, and can be a protein or peptide, hormone, drug, toxin etc. In this context, it could be an AAS, SARM or other PED. There are varying degrees to which a ligand binds to a receptor, from full inverse agonist to super agonist.

Anyway, the androgen receptor, part of the family of nuclear receptors, is the receptor that testosterone binds with, or whatever we put in to our body with exogenous PEDs.

The exact quantity of androgen receptors in your body is an unknown, but it is a finite number in your at any given time, allowing for a finite amount of the compound you are taking to bind. And any occupied receptor will continue to trigger a cellular or tissue response until the compound decays or is displaced. I.e. if you inject test p with a half-life of 4 hours, the mean levels of bound testosterone will gradually decline from the day of injection until 20 hours later and it is completely cleared from the body. Until that happens, at least some of your receptors are still bound to the compound. Don’t like the side effects of that test undecanoate you injected? Better strap in for that half-life of a whopping 30 days.

What happens when your androgen receptors are already bound to a ligand, such as when you stack multiple compounds? The compounds compete to bind and ligands can displace one another. Or not at all and the compound does not bind and is basically at waste. This is why stacking SARMs (for example) is not optimal, as well as why LBM% gains are not linear with higher doses, but follow a curve – there will be at least some loss in efficiency.

Which stacks are optimal then? I have not a clue, and I don’t think medical science is in a rush to help us figure that out. But we should all continue to advocate for minimum effective doses and cycles with as few compounds as meets our goals, partially for our wallets, mostly for our health.