Receptor Memory

Here is what I’m theorising about now. Everyone knows that the first cycle is the best cycle, usually.

What im looking for feed back on is this. Does the body respond to the initial compound the best as time goes on?

Meaning that if your first cycle was Deca and primo, is there a chance that Deca and Primo will be a very consistent builder for you?

Or if your first cycle was only EQ and you made great gains, will EQ always or almost always work very reliably from there on?

in Essence

Is there an imprint of sort on the receptor that makes it have a “favorite” preference to the drug it came in contact with when virgin? Is this possible?

No. A receptor has a conformation that it folds into based upon attraction to achieve the lowest energy conformation.

[quote]Detroitlionsbaby wrote:
No. A receptor has a conformation that it folds into based upon attraction to achieve the lowest energy conformation. [/quote]

So you’re unequivocally stating that receptor memory or preference for a certain compound is an impossibility?

[quote]Gregus wrote:

[quote]Detroitlionsbaby wrote:
No. A receptor has a conformation that it folds into based upon attraction to achieve the lowest energy conformation. [/quote]

So you’re unequivocally stating that receptor memory or preference for a certain compound is an impossibility? [/quote]
Yup. I think if you want to “theorize” about something (which I really dont get why people try to do that when they have no way of testing it), I would look into the NLS differentiation (possibly). Maybe some altering in allocating chaperones?

I’ll cede to Bill if he has something different to say, but I highly highly doubt it.

Yes, there is no evidence whatsoever for receptor “memory.”

[quote]Bill Roberts wrote:
Yes, there is no evidence whatsoever for receptor “memory.”[/quote]

What about receptor downregulation? Drugs are approved by the FDA while claiming to cause downregulation or something like that. Anyway, receptors get recreated regularly, every few weeks or so.

Bill debunked the receptor downregulation idea in an article I read ages ago, I’ll link to it here to save him from having to go over this: http://www.mesomorphosis.com/articles/pharmacology/androgen-receptor-regulation.htm

Thanks!! :slight_smile:

Could the body create antibodies to synthetic androgens or peptides which are similar to natural peptides, that could then deactivate natural chemicals?

This is a reasonable concern with incorrect versions of larger, more complex molecules such as HGH.

Very small molecules such as steroids are too small for immune responses to be generated.

[quote]Bill Roberts wrote:
This is a reasonable concern with incorrect versions of larger, more complex molecules such as HGH.

Very small molecules such as steroids are too small for immune responses to be generated.[/quote]

I read it can happen with synthetic HGH, I wonder to what extent. I haven’t read that peptides can cause antibodies, I wonder if they do, since they don’t resemble natural peptides as much as synthetic HGH resembles natural HGH, maybe that’d create a lot more antibodies. I doubt anyone knows though maybe it’s something to worry about as one of the few risks of long term use. It makes sense in retrospect that antibodies wouldn’t affect synthetic anabolics, an antibody can’t bind to or be created for a chemical, only proteins, I guess.

I think a good experimental would be to dose two groups of mice with peptides for a few weeks, and a few months, return to the mice to natural, then measure GH levels against a control group to see if there’s a long term effect in GH secretion.

Being dissimilar to natural peptides wouldn’t be an advantage with regard to not having the potential to trigger an immune response.

It is more a matter of combining dissimilarity (whether partial or total) with sufficient molecule size.

A peptide with a molecular weight of under 1000 either cannot trigger an immune response or is highly unlikely to, or at the other end of the scale, a foreign peptide with a mw of 10,000 or greater is highly likely to be able to trigger an immune response.

There would be no shart cutoff as to where there starts to be substantially likely to trigger an immune response, but an example figure could be a mw of 5000.

For illustration, Melanotan II has a mw of 1024. Thus it is small enough that either it is extremely unlikely that it will trigger an immune response, or (I don’t know) it may be actually impossible.

Or as another example, GHRP-6 is naturally occurring so it would not trigger an immune response.