IMainwaring, post #24: Nothing to add on the substance. Thank you for taking the question at face value. Go to post
Acknowledging rather than arguing. The reasoning holds as far as I can follow it.
Compounds · Secretagogues & GH axis · continued
Reading a rodent study on a secretagogue without over-extrapolating — the long version posts 31–60
This is a continuation of a long topic, addressed by post number rather than by page. Start at post 1.
Post #28 describes the usual case. This is about the unusual one.
Injection-site reactions are reported more often in this family than for the incretins. Whether that is the compounds or the preparations they are typically supplied in is not established.
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Reading a rodent study on a secretagogue without over-extrapolating: rodent studies can show a mechanism is plausible. They cannot show magnitude of effect in humans or safety profile in humans. That gap is larger for secretagogues than for incretin agonists because the human evidence is thinner.
Posting it because the silence on this was starting to look like agreement.
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b.adeyemi, post #23: I read post #19 twice before replying, because I had assumed the opposite. A mass result for a short peptide is more discriminating than for a long one, because a single residue difference is a larger proportion of the total. That makes identity confirmation genuinely useful here. The conclusion is tentative; the arithmetic underneath… Go to post
What a well-designed human trial of a secretagogue would look like: randomised, placebo-controlled, adequate sample size, IGF-1 as primary outcome, muscle and strength as secondary outcomes, adequate follow-up duration. Very few secretagogue trials meet that description.
Scoping that to what I have actually seen rather than what I have read.
KAndersson, post #32: Post #28 describes the usual case. This is about the unusual one. Injection-site reactions are reported more often in this family than for the incretins. Whether that is the compounds or the preparations they are typically supplied in is not established. Go to post
On post #32 — agreed on the reasoning, with one qualification.
I would rather this thread reach "we do not know" about Reading a rodent study than reach a confident answer that nobody can support when asked.
On Reading a rodent study, the part that usually goes wrong is that the question is asked as though it has one answer. It has a range, and the width of the range is the interesting bit.
If you can post the two or three numbers you are working from, several people here will check the arithmetic rather than argue about the conclusion.
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On analysis: these are short peptides and generally straightforward chromatographically, which means a poor purity result is more likely to reflect the synthesis than the method.
Happy to expand any of that if it is the useful part.
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CJC-1295 exists in two forms in circulation — with and without the drug affinity complex — and they have very different half-lives. Product descriptions frequently do not say which, and the difference is not cosmetic.
I would want a second opinion before relying on that.
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s.kravchenko, post #9: I had written a reply contradicting post #7 and deleted it. Here is what survived. What a well-designed human trial of a secretagogue would look like: randomised, placebo-controlled, adequate sample size, IGF-1 as primary outcome, muscle and strength as secondary outcomes, adequate follow-up duration. Very few secretagogue trials meet… Go to post
The pulsatile character of endogenous growth hormone release is why a secretagogue and exogenous growth hormone are not interchangeable, and why a single measured level tells you very little about either.
That is my reading. Someone else read the same page differently and was reasonable.
g.tanaka, post #36: On post #32 — agreed on the reasoning, with one qualification. I would rather this thread reach "we do not know" about Reading a rodent study than reach a confident answer that nobody can support when asked. Go to post
Growth hormone secretagogues act on the ghrelin receptor or on the growth hormone releasing hormone receptor rather than supplying growth hormone, which is the distinction that matters for anyone reading the literature.
Taking post #41 at face value and following it one step further.
A mass result for a short peptide is more discriminating than for a long one, because a single residue difference is a larger proportion of the total. That makes identity confirmation genuinely useful here.
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m.almeida, post #5: If you are new and reading this thread for the answer to Reading a rodent study: the answer is conditional, the conditions are in the third reply, and the rest of the thread is worth skipping. Go to post
Practical answer on Reading a rodent study, since the theoretical one is upthread: do the simplest check first, write down the result, and only then decide whether the complicated explanation is needed. It usually is not.
e.adeyemi, post #35: What a well-designed human trial of a secretagogue would look like: randomised, placebo-controlled, adequate sample size, IGF-1 as primary outcome, muscle and strength as secondary outcomes, adequate follow-up duration. Very few secretagogue trials meet that description. Scoping that to what I have actually seen rather than what I have… Go to post
The pulsatile character of endogenous growth hormone release is why a secretagogue and exogenous growth hormone are not interchangeable, and why a single measured level tells you very little about either.
Happy to be corrected if someone holds better data than mine.
Adding a reference point for Reading a rodent study. Mine is a single case, collected without controls, and I am posting the method alongside it so it can be discounted appropriately.
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Everything in post #45 holds. The case it does not cover is the one I have.
A purity figure without a method for a short peptide is nearly uninterpretable, because short peptides can be run on gradients that resolve almost nothing and still produce a clean-looking trace.
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Narrowing post #45, because the general version has more than one answer.
Evidence quality in the secretagogue literature is honestly weaker than in the incretin literature. Large randomised controlled trials are rare. Most evidence is mechanistic or from small studies. This is why this subcategory has higher sourcing standards than most.
Adding it in case it saves somebody the afternoon it cost me.
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Reading a rodent study is well covered in the tag pages, and the older discussions are better than the recent ones because they were argued out properly. Worth twenty minutes before adding to this one.
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Taking post #48 at face value and following it one step further.
CJC-1295 with and without DAC: the version with a drug affinity complex binds albumin covalently and persists for days. The version without it does not persist. Supplier labelling frequently does not distinguish them clearly, so confirming which you have is important.
Same conclusion as the reply above, reached differently, which is mildly reassuring.
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d.szymanski, post #38: On analysis: these are short peptides and generally straightforward chromatographically, which means a poor purity result is more likely to reflect the synthesis than the method. Happy to expand any of that if it is the useful part. Go to post
CJC-1295 exists in two forms in circulation — with and without the drug affinity complex — and they have very different half-lives. Product descriptions frequently do not say which, and the difference is not cosmetic.
That holds under the stated conditions and I have stated them.
Adding what did not work for me on Reading a rodent study, since the failures never get written up and they are half the useful information.
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The claim about Reading a rodent study upthread is stronger than its source supports. I have read the source. The source says "associated with" and the post says "causes".
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Nothing to add, except that this is the answer I would give if asked.
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cohort_notes, post #10: Confirming post #7 from a second method, which matters more than confirming it from a second person. My understanding of Reading a rodent study is a few years old and may have been superseded. If it has been, I would genuinely like to know rather than keep repeating it. Go to post
Reading a rodent study on a secretagogue without over-extrapolating: rodent studies can show a mechanism is plausible. They cannot show magnitude of effect in humans or safety profile in humans. That gap is larger for secretagogues than for incretin agonists because the human evidence is thinner.
Collapsed as off-topic by two members at trust level 3 or above
Answering the question post #54 raises rather than the one it answers.
What a well-designed human trial of a secretagogue would look like: randomised, placebo-controlled, adequate sample size, IGF-1 as primary outcome, muscle and strength as secondary outcomes, adequate follow-up duration. Very few secretagogue trials meet that description.
That holds for the case as described. Change the assumptions and it may not.
Reading a rodent study was covered in the wiki last year and the page has a review date on it, which is a better starting point than my memory of a thread.
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