You are arguing over semantics and maybe you're misinterpreting what kinetics means.
If a short hl drug can "stack", as you call it, with another drug due to it's longer half life in the terminal phase, we aren't talking about it's kinetics but rather about it's pharmacodynamics.
Kinetics is the drugs mechanism of action, for example; for which receptor types is it a ligand for, what's it's action at those sites (full agonist, invers agonist, antagonist, etc.) and what's it's dissociation constant at those sites.
The dissociation constant, ie. binding affinity determines the drugs duration of action at the receptor and it determines the "half life" of the ligand - receptor complex. Ie.: a drug with a very short terminal half life, for instance 1h, but with a low dissociation constant (Ki) in the nanomolar range (nM), meaning it bind's tightly to it's target receptor, will produce a longer lasting ligand - receptor complex then a longer HL drug with a Ki in the micromolar (uM) range and depending on the actual concentration of the drug at the receptor site, will produce a greater effect. The effect might be so different that the stronger ligand can achieve a full agonists action and the weaker one can only ever be a partial agonist, no matter what the concentration.
The "stacking" issue is thus also very much dependent to the different kinetic profiles of the drugs being used. Are they active at the same tissues and if so, do they have the same targets and are they outcompeting them self's at those targets. Also, their post receptor, ie. second messenger action is "something" of a relevance, as is their action at the target receptor as they can, for instance, both bind to the same receptor but at different sites. For instance D-Serine (or Glycine) binding at the Glycine modulatory site of the NMDA receptor (which is an agonist site) vs Magnesium, binding at the Magnesium site (which is a non competitive antagonist).
While terminal serum half life has marginal importance in the sense of "enabling stacking" it is very much "outcompeted" by the drugs pharmacokinetic profile. Also, "stacking" is a whole other discourse, and I don't see why you'd want to use it as an argument, it's clearly out of place, and besides, how well a drug "stack" with another drug, again, has little to do with it's dynamics and everything to do with it's kinetics. In other words, if a drug is "stackable" with another drug is determined by it's kinetic profile which, again, also determines it's duration of action and the scale of effect at the target site. And let's not forget that the terminal serum half life can be a lot shorter then for instance the half life of the drug in the synaptic cleft and it's action can also outlive it's ligand - receptor complex half life, especially if we are talking about gene expression changing drugs.
Regarding hcg, the issue is, as I stated in my reply to the op, that he has been on trt for a long time and going off of trt with only hcg, will basically be a long winded pct, and before he get's to normal eugonadal testosterone levels, will take some time (he'll go on another blast before that happens probably, if it happens at all). Besides, anecdotally, hcg is notorious for having an unfavorable estrogen to testosterone response ratio, which is also a pita to manage with Ai's or with anything else.
But in any case, what ever the OP's story to hcg use might be, the half life of hcg isn't a particularly relevant factor. At least not as much as you made it out to be, stating, "It will not work. HCG's half life is so short that you would have to inject big amounts to see a change in your Test. levels.". He would have to inject big quantities yes, at least at the start, but that hasn't much to do with hcg's serum half life but rather with 1. OP's poor functioning gonads, needing more stimulation and 2. hcg's not so strong action of reproducing a strong serum testosterone response, compared to it raising intra testicular testosterone to normal levels rather quickly ...
Fact-checking your message with ChatGPT as I am not working in this domain but wanted to learn a tad more.
No, that description does not accurately reflect the concept of pharmacokinetics. Pharmacokinetics refers to the study of how the body processes a drug, including its absorption, distribution, metabolism, and elimination. It focuses on how the drug moves through the body, how it is metabolized or broken down, and how it is excreted.
The description you provided for pharmacokinetics seems to pertain more to pharmacodynamics, which is the study of how drugs exert their effects on the body. Pharmacodynamics examines the drug's interaction with specific receptors or targets in the body, including the type of receptor it binds to, the type of action it elicits (agonist, antagonist, etc.), and the affinity or strength of its binding to those receptors (dissociation constant).
- Pharmacokinetics: Study of how the body processes a drug (absorption, distribution, metabolism, and elimination).
- Pharmacodynamics: Study of how drugs interact with specific receptors or targets in the body and exert their effects (receptor binding, action, affinity).
The dissociation constant, or binding affinity, does influence the duration of action of a drug at the receptor. A drug with high binding affinity (low dissociation constant) tends to have a longer duration of action at the receptor compared to a drug with low binding affinity.
The half-life of the ligand-receptor complex is determined by both the dissociation constant and the rate of clearance of the drug from the body. A drug with a very short terminal half-life (e.g., 1 hour) will indeed result in a shorter duration of action at the receptor compared to a drug with a longer half-life.
The statement correctly states that a drug with a low dissociation constant (high binding affinity) will form a longer-lasting ligand-receptor complex compared to a drug with a higher dissociation constant (lower binding affinity).
However, the statement introduces a comparison between drugs with different half-lives and different dissociation constants, which may not always hold true. The relationship between half-life and dissociation constant is not always straightforward or predictable. Factors such as drug concentration, receptor occupancy, and downstream signaling pathways also play significant roles in determining the overall pharmacological effect of a drug.
The assertion that a drug with a lower dissociation constant (higher binding affinity) will always produce a greater effect or achieve full agonism compared to a drug with a higher dissociation constant is not universally true. The overall effect of a drug depends on various factors, including receptor density, downstream signaling pathways, and the presence of other modulators or competitors.
While the statement captures some elements of the relationship between binding affinity, duration of action, and drug effect, it oversimplifies the complex interactions involved in pharmacology. The pharmacological effects of a drug are influenced by multiple factors beyond just the dissociation constant and half-life of the ligand-receptor complex.
Terminal serum half-life refers to the time it takes for the concentration of a drug in the blood to decrease by half during the elimination phase. While terminal half-life can provide an estimation of how long a drug remains in the body, it is not the sole determinant of drug stacking or interactions. Other factors, such as pharmacokinetic profiles and target interactions, play significant roles in drug combination effects.
Your statement accurately states that stacking is a separate discourse and may not be directly relevant to discussing pharmacokinetic and pharmacodynamic properties of drugs. It is important to consider multiple factors beyond stacking when evaluating drug interactions.
The statement correctly emphasizes that drug interactions and compatibility depend on the kinetic profiles of the drugs involved. The pharmacokinetic properties, including absorption, distribution, metabolism, and elimination, can influence the interaction and duration of action of drugs.
However, the assertion that "stackability" or compatibility between drugs is solely determined by their kinetic profiles may oversimplify the complexities of drug interactions. While kinetic profiles play a significant role, other factors such as target interactions, downstream signaling pathways, and potential synergistic or antagonistic effects also contribute to the overall combined effect of drugs.
The statement mentions that the terminal serum half-life may be shorter than the drug's half-life in the synaptic cleft and that the drug's action can outlive its ligand-receptor complex half-life. This is generally accurate, as drug effects can continue even after the drug has been eliminated from the body. However, the duration of drug action and the relationship between drug half-life and pharmacological effects can vary depending on the specific drug and its mechanism of action.
In summary, while your statement highlights some important aspects of pharmacokinetics, drug stacking, and duration of action, it simplifies the complexity of drug interactions and their determinants. Multiple factors, including pharmacokinetic, pharmacodynamic, and molecular considerations, need to be taken into account when evaluating drug combinations and their effects.
I agree that HCG's half life is not the primary obstacle into switching it for TRT. However, a longer half life would've obviously made a difference into the test. level HCG produces.
Short half-life, low potency (action or as you say "op's poor functioning gonads") and strong conversion to E2 is a no-go.
