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Dealing with Growth Hormone Insulin Resistance (ameliorating rhGH-induced IR) [Type-IIx]

Type-IIx

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Insulin resistance is a direct GH effect (due to GH's liberating free fatty acids into systemic circulation). Insulin resistance follows within 1 - 2 hr post-administration. RhGH, during prolonged subcutaneous administration (in a state of positive energy balance), causes the actions of IGF-I and insulin to prevail 8 - 10 h post-injection.

Broadly, rhGH modulates insulin sensitivity in a complex manner influenced by numerous factors such as age, body composition, and duration of therapy.

Of course, short-term perturbations are of only minor relevance versus HbA1c levels that reflect chronic insulin resistance.

The strategies that I believe in are A) timing strategies attendant to the pharmacodynamic effects of rhGH and nadir blood glucose measures & B) the use of exogenous drugs along a dose- & time- dependent continuum:

GDAs (biguanides, e.g., Metformin; Berberine) < Incretins (GLP-1 agonists; SGLT-2 inhibitors; DPP-4 inhibitors; glimepirid, etc.) < LR3 IGF-I; IGF-I < exogenous insulin (Aspart & Lispro << Glargine).

Note that exogenous insulin worsens insulin sensitivity (as HOMA-IR reflects the products of blood glucose AND insulin) by several mechanisms, including diminished autophosphorylation of the IR & downstream elements (e.g., IRS1). Indeed, only some of the incretins, e.g., GLP-1 agonists; dual GIP & GLP-1 agonists (e.g., tirzepatide), qualify as true insulin sensitizing agents.

While low-dose insulin glargine (e.g., Lantus) may confer a protective effect on pancreatic β-cell function in prediabetes, the very thing that distinguishes healthy bodybuilders from prediabetics is that β-cell function is not "on its last legs" in the healthy. Rather, glucose disposal at the initiation of an rhGH course should be implemented to protect pancreatic β-cell function (that is worsened by exposure to high circulating blood glucose levels) on a continuum. The very last tool to be used in the arsenal is insulin glargine (for those that have become prediabetic).

Rather than serving primarily to reduce blood glucose concentrations, insulin should be viewed as an agent to increase IGF-I bioavailability (and to counter the decrement to GH response [the increase to IGF-I] that occurs after several months at a constant rhGH dose).
 
So a few things are listed but what are some recommended protocols and dosages?
 
So if I'm reading right, metformin would be the preferred first line?
 
I do get into those with clients of mine.
So rather than to help members of the board, your post is just phishing for new clients?

I think most knowledgeable members of the board could have also listed your interventions. But without the nuts and bolts of dosages, timing, combinations, durations, etc, the post is meaningless.
 
So rather than to help members of the board, your post is just phishing for new clients?

I think most knowledgeable members of the board could have also listed your interventions. But without the nuts and bolts of dosages, timing, combinations, durations, etc, the post is meaningless.
I know you dislike me. With that coloring of our interactions, this is an above-average contribution to the board, not "phishing for new clients." You can take it or leave it.

It's unreasonable to expect free shit, typical freeloading behavior, when real work (mental labor and real-world testing/validation) has gone into the protocols that you so selfishly expect to be doled out for you, despite wanton incivility towards me throughout this board.

You're welcome.
 
I’m not going down the exogenous insulin path. My fed (not fasted) blood glucose in stable in the 80’s despite running 10iu+ Hgh daily, I use Berberine and other GDAs at the moment. I will acquire metformin shortly as well.
 
So rather than to help members of the board, your post is just phishing for new clients?

I think most knowledgeable members of the board could have also listed your interventions. But without the nuts and bolts of dosages, timing, combinations, durations, etc, the post is meaningless.
I don’t think @Type-IIx could do that even if he wanted to, because it’s not responsible or even useful to post cookie cutter protocols. It needs to be tailored to the goals, training, lifestyle, and body of each person - which, to his point - requires consultation and direct work.

I don’t think he’s fishing for clients, I think you’re fishing for someone to do your homework for you.

It’s totally fine if you don’t want to do it, that’s when you pay a coach.
 
This is interesting, I've definitely seen both sides of the "is long-acting insulin a good idea or not" argument many times.

Do you rate the affinity of Insulin Glargine on IGF1R as being any amount of needle mover worthy of consideration here?
 
This is interesting, I've definitely seen both sides of the "is long-acting insulin a good idea or not" argument many times.

Do you rate the affinity of Insulin Glargine on IGF1R as being any amount of needle mover worthy of consideration here?
Absolutely, I do bro. I see Insulin Glargine as being rationally supported to enhance IGF-I bioavailability (you are correct that it also has a significantly greater direct effect on IGF-IR than the other insulin preparations). I just want to be clear about defining the rationales: while generally guys throw a new compound (i.e., slin) into the mix and work backwards to attempt to explain why its use make sense (trying to justify their UTMFD [upping the motherfucking dose] & polysubstance use), I prefer to first understand why a novel compound might make sense. The reason why adding Lantus in particular makes the most sense (e.g., to increase FFM) is its enhacing IGF-I bioavailability (and direct activity at the IGF-IR).
 
Thoughts on this?
I have not yet read this. I'll definitely get back to you once I have time to read it. Thank you for sharing it, it has some relevance for glimepiride (Amaryl; Amarel) that is increasing in use somewhat. I generally don't view these agents whose mechanism of action is blockade of the ATP-sensitive K+ channel as insulin sensitizing (as opposed to GLP-1 agonists and combined GIP & GLP-1 agonists), but rather, as sort of quasi-slin. I recall posting - here it is - that Amaryl's use should generally follow the same considerations as exogenous slin.
 
I dont like metformin. So what I am using instead is 2mg of semaglutide/week and 10mg of empagliflozin per day. My blood glucose has never been better while I use 5IU of gh pre bed.
 
I know you dislike me. With that coloring of our interactions, this is an above-average contribution to the board, not "phishing for new clients." You can take it or leave it.

It's unreasonable to expect free shit, typical freeloading behavior, when real work (mental labor and real-world testing/validation) has gone into the protocols that you so selfishly expect to be doled out for you, despite wanton incivility towards me throughout this board.

You're welcome.
This is probably the most condescending thing I have read on this board.

Anyway, for sake of discussion not "hidden info available to those who pay"

I take metformin 500-1000mg at 3iu gh and although my fasting glucose was nearing 100 and had me worried, my a1c is perfect

Also reduced my carb intake. Other people I've seen mention splitting dose to help with insulin resistance and increasing cardio.
 
I dont like metformin. So what I am using instead is 2mg of semaglutide/week and 10mg of empagliflozin per day. My blood glucose has never been better while I use 5IU of gh pre bed.
I've heard that smegmaglutitde is better because it is very good at suppressing appetite, have you found this?
 
I've heard that smegmaglutitde is better because it is very good at suppressing appetite, have you found this?
appetite suppression is more like a side effect that fades away over time. I am taking it for so long now that the effect itself is still there, but I just eat what I have to eat. I force myself and it works. But it the beginning it can be a strong appetite suppressant. the effect on blood glucose is great.
 
I dont like metformin. So what I am using instead is 2mg of semaglutide/week and 10mg of empagliflozin per day. My blood glucose has never been better while I use 5IU of gh pre bed.
Great to hear. This is a potent combination, but relatively safe (though if you start it without high dose AAS and/or with high dose rhGH, and begin a course of high dose AAS and/or reduce/withdraw from rhGH use, you'll want to be careful in adjusting dose (down!) and be attentive to hypoglycemic (falls, coma, death) risks.

It should be mentioned that combination of some other classes of agents here, e.g., DPP-4 inhibitors & GLP-1 agonists, is very high risk, and should never be combined. DPP-4 inhibitors are still being evaluated for long-term safety, and they are nonselective in attenuating GLP-1 breakdown, but are also involved in the metabolism of many other peptide hormones, including GHRH, peptide YY, neuropeptide Y. DPP-4 is further involved in T-cell regulation. As such, the long-term immunological and neurological consequences of inhibiting DPP-4 is unknown.
 
I don’t think @Type-IIx could do that even if he wanted to, because it’s not responsible or even useful to post cookie cutter protocols. It needs to be tailored to the goals, training, lifestyle, and body of each person - which, to his point - requires consultation and direct work.

I don’t think he’s fishing for clients, I think you’re fishing for someone to do your homework for you.

It’s totally fine if you don’t want to do it, that’s when you pay a coach.
Naw I'm good. I've done plenty of research, used plenty on different protocols, and have also worked with quite a few well known coaches over the years.

I don't think posting some protocols that have been successful is a big deal. As I stated, most knowledgeable members on the board are already familiar with these interventions.
 

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