A GH and fat loss protocol (rhGH lipolysis) that is science-based

Yes. it also depends which HGH you are using.
I made a thread bout this couple days ago

How GH have the exact same purity % and no dimer but cause alot of water retention, cts and general side effects but others cause very minimal side effects. Alot more ´clean´ experience

It´s very weird
The most noticeable difference for me is sleep quality .
It varies from one generic to the other .
 
Yes. it also depends which HGH you are using.
I made a thread bout this couple days ago

How GH have the exact same purity % and no dimer but cause alot of water retention, cts and general side effects but others cause very minimal side effects. Alot more ´clean´ experience

It´s very weird
I had no sides at 10ius of QSC, which came out to test at 12ius per vial, so that means I was taking 12iu instead of 10 lol. But I got this damn sleep apnea from 10ius so I stopped. I had no sides at 5ius.( well 6)
 
What is the pharmacopoeia standards when it comes to human growth hormone? @Type-IIx @janoshik

I think I read it was minimum 90% purity and maximum 6% dimer and related proteins. Please correct me if I am wrong and also if you could post link to the article/study.
 
What is the difference between amount and purity? Sorry, I am confused
The minimum purity % is what then?
So the 6% is correct when it comes to dimer and related proteins.
If vial is supposed to be 1 mg, then 0.89-1.1 mg is tolerable. That's amount.

If you put in 2.2 mg of protein material but only 1.1 mg is HGH, then it meets the AMOUNT but not PURITY (which is 50%).
 
pharmacopoeia standards

what is the minimum allowed % purity before its not good enough to meet ´´pharma grade´´ standards

do you understand what i mean now?
 
pharmacopoeia standards

what is the minimum allowed % purity before its not good enough to meet ´´pharma grade´´ standards

do you understand what i mean now?
88% as per above.

But it's possible it's been changed in more recent pharmacopoeias.
 
@Type-IIx
Does Gilbert's syndrome affect igf-1 conversion?
Reduced IGF-I conversion by Gilbert's syndrome per se is unlikely (because acromegalics with the UGT1A1*28 extra TA repeat still show profoundly elevated IGF-I), but I would be very cautious about a couple of other major contraindications against using AAS, SERMs, and potentially rhGH (due to structural similarity to Pegvisomant and its association in Gilbert's syndrome patients with cholestatic hepatitis and potential liver failure).

Specifically:
* The Uridine 5'-diphospho (UDP)-glucuronosyltransferases (UGTs) are involved in phase II metabolism, with respect to AAS, these facilitate excretion of toxic compounds and metabolites (even endogenous testosterone is toxic, in fact), and these are affected by Gilbert's syndrome.
* SERMs (e.g., tamoxifen) are clearly therapeutically contraindicated in Gilbert's syndrome (due almost certainly to profound concentrations induced by effects on phase II metabolism).
* Pegvisomant is a PEGylated rhGH analog that inhibits (antagonist to) the GH receptor. It differs from rhGH (Somatropin) by its PEGylation that reduces the rate of clearance, prolonging half-life and of course, its acting oppositely at the GHR. Pegvisomant is associated with severe liver injury in patients with Gilbert's syndrome.

Basically, I'd not be concerned with significantly reduced IGF-I (GH response) given an rhGH dose, but I'd be remiss to not mention these risks with AAS, SERMs, and potentially multiple dose (i.e., split dosing) rhGH (or use of any purported long-acting GH preparation, secretagogue, etc.) I'd be particularly concerned about the SERMs, AIs, etc. also.

Practically, I'd tread extremely carefully if not adhere to abstinence from PEDs if I had Gilbert's syndrome.
 
@Type-IIx Is it still reasonable to expect at least some of the connective tissue improvements HGH confers if using a single bolus (5-6iu for example) in the AM only? Alternatively, the bolus would be at ≈3pm (training at 5:30pm). Or would it be advisable to add something on the order of a single iu pre bed for that purpose?
 
@Type-IIx or anyone else for that matter:

Do you have any opinion on the possibility of combining exogenous HGH with that of one or more secretagogues (let's say CJC/Ipa, for example?).

I've heard whispers of people using a pre-bed CJC/Ipa dose to support/maintain a high "baseline" dose of natural GH, while supplementing with a morning/daytime exogenous GH dose if/when additional GH is desired for either fat loss or supporting anabolism during a heavier cycle.

Anecdotal reports are almost non-existent, however.

I have never found any literature directly addressing this, and as hard as I've tried I've never been able to come up with any solid theoretical conclusions either mechanistically or otherwise.

The most specific part it seems would be how much the stimulation of GH production with a secretagogue would overcome (if at all) the suppression present from a morning dose of exogenous GH.

Is this a totally insane/pointless idea or does it have some merit?
 
Sorry if this is stupid question. I’ve read through the thread and I’m not positive on the best timing for me personally. You said the default dosing should be before bed, which is what I’ve been doing. I’m currently recouping. Not a real cut. I’m pretty lean at the moment and I’m just trying to slowly put on lean tissue with calories slightly above maintenance. I wake up at 3am and lift at 4am. I’ve been slamming a whey and oatmeal shake immediately upon waking and workout an hour later. Is pre bed dosing the best for my situation? I currently using 5iu in one dose and no insulin @Type-IIx
 
@Type-IIx or anyone else for that matter:

Do you have any opinion on the possibility of combining exogenous HGH with that of one or more secretagogues (let's say CJC/Ipa, for example?).

I've heard whispers of people using a pre-bed CJC/Ipa dose to support/maintain a high "baseline" dose of natural GH, while supplementing with a morning/daytime exogenous GH dose if/when additional GH is desired for either fat loss or supporting anabolism during a heavier cycle.

Anecdotal reports are almost non-existent, however.

I have never found any literature directly addressing this, and as hard as I've tried I've never been able to come up with any solid theoretical conclusions either mechanistically or otherwise.

The most specific part it seems would be how much the stimulation of GH production with a secretagogue would overcome (if at all) the suppression present from a morning dose of exogenous GH.

Is this a totally insane/pointless idea or does it have some merit?
There is an interference effect of rhGH on the secretagogues (by inhibition of hypothalamic GHRH synthesis and release, increased somatotroph IGF-I synthesis, and/or increased somatostatin secretion), so this combined use as you describe is irrational.
 
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