hGH + Metformin: A Good Thing (Metformin does not lower, but rather increases IGF-1)

Wow, isn’t 1.5g/day on the high end for Metformin? And no, I’m not taking anything to help the insulin resistance.
2g for XR and 2.5g for IR is the maximum.

I don't see why you should take less. That's a standard dose for a person with prediabetic BG and you are not gonna get hypo from Metformin so why not?

I would take Metformin even without HGH it has a plethora of great effect and very few sides most of those side happens on the first one two weeks of use and disappear completely after it, with XR I never had sides for example, IR you can have a bit of bloat gas etc but it will subside.
 
2g for XR and 2.5g for IR is the maximum.

I don't see why you should take less. That's a standard dose for a person with prediabetic BG and you are not gonna get hypo from Metformin so why not?

I would take Metformin even without HGH it has a plethora of great effect and very few sides most of those side happens on the first one two weeks of use and disappear completely after it, with XR I never had sides for example, IR you can have a bit of bloat gas etc but it will subside.
Is XR better than IR, or should both be used?
 
Is XR better than IR, or should both be used?
There is no better XR can be taken at any time better one when waking up and one at dinner so you are covered 24hr.

IR needs to be taken 3-4 times a day with the meals to be best used and mostly to not have gas and bloating.

You can find plenty of studies on efficacy of Metformin and how many times a day makes a difference etc.
 
@Type-IIx when you say "unless the goal is maximal mass" do you mean that if you use Metformin with HGH that you can't gain mass at all? Is it just not nearly as much? Or is it not that signifcant? Just trying to get an idea of exactly how much it would hinder growth, but by the sounds of what you wrote you think the benefits outweigh the negatives.

Also, would taking Metformin prevent Palumboism (GH gut)?
 
@Type-IIx when you say "unless the goal is maximal mass" do you mean that if you use Metformin with HGH that you can't gain mass at all? Is it just not nearly as much? Or is it not that signifcant? Just trying to get an idea of exactly how much it would hinder growth, but by the sounds of what you wrote you think the benefits outweigh the negatives.

Also, would taking Metformin prevent Palumboism (GH gut)?
Impossible to quantify, but Met attenuates resistance training-induced gains and blunts mTOR. Met combination with rhGH is generally inconsistent with maximal anabolism. Met is unlikely to prevent Palumboism, mostly attributable to IGF-I & insulin actions (both are increased by rhGH in a positive energy balance).
 
Impossible to quantify, but Met attenuates resistance training-induced gains and blunts mTOR. Met combination with rhGH is generally inconsistent with maximal anabolism. Met is unlikely to prevent Palumboism, mostly attributable to IGF-I & insulin actions (both are increased by rhGH in a positive energy balance).
Are there any routes to prevent Palumboism if on IGF-1, hgh & insulin besides avoiding those compounds?
And do you think it is a combination of AAS, IGF-1, hgh & insulin with the bulking diet that leads to to condition?
 
Are there any routes to prevent Palumboism if on IGF-1, hgh & insulin besides avoiding those compounds?
And do you think it is a combination of AAS, IGF-1, hgh & insulin with the bulking diet that leads to to condition?
Palumboism is characterized by a few discrete phenomena:

A) The direct effect of rhGH (reversible) of sodium and fluid retention in organs (e.g., the renal tubuli)

B) The direct effect of insulin (reversible) on fat oxidation suppression (i.e., gut distension is comprised of fluid and fat).
* It's important to note here that during prolonged subcutaneous rhGH administration (in a state of positive energy balance), the actions of IGF-I and insulin prevail 8-10 h post-injection

Secondary factors (non-reversible) in gut distension include:
C) IGF-I-induced direct growth of gut viscera (non-reversible)
D) Acromegalic growth of all organs including gastro-intestinal (non-reversible)

These are all various direct effects of rhGH, rhI (slin), & rhIGF-I.

Given that they are direct effects and not side effects per se, there's no way to block these effects without reducing the effects of the growth factors. Site-specific administration of IGF-I might be one potential solution, but still leakage occurs into systemic circulation, and LR3 IGF-I > IGF-I > * in potency to increase gut viscera mass.
 
Impossible to quantify, but Met attenuates resistance training-induced gains and blunts mTOR. Met combination with rhGH is generally inconsistent with maximal anabolism. Met is unlikely to prevent Palumboism, mostly attributable to IGF-I & insulin actions (both are increased by rhGH in a positive energy balance).

berberine does the same thing?
 
berberine does the same thing?
Likely yes. BBR, like Met, activates AMPk and it provides an alternative mechanism for the stimulation of atrogin-1 expression (stimulating protein degradation and suppressing protein synthesis).

The human evidence is stronger for Met (because of clinical trial data) but mechanistically there's reason to believe BBR acts similarly.
 
Impossible to quantify, but Met attenuates resistance training-induced gains and blunts mTOR. Met combination with rhGH is generally inconsistent with maximal anabolism. Met is unlikely to prevent Palumboism, mostly attributable to IGF-I & insulin actions (both are increased by rhGH in a positive energy balance).

So is Slin seen as what may be considered a more anabolic alternative to metformin?
 
And what about metformin solo?

Just some mixed opinions and views coupled with fear mongering likw birth defects scare and etc.
 
So is Slin seen as what may be considered a more
anabolic alternative to metformin?
Well, I think that the use of agents to ameliorate the hyperglycemic effects of rhGH falls on a continuum, that looks like: biguanides/GDAs (Met, BBR, etc.) < incretins (e.g., GLP-1 & GIP agonists) < rhIGF-I & LR3-IGF-I < insulin, but the rationale for use of slin is not merely glucose disposal.
And what about metformin solo?

Just some mixed opinions and views coupled with fear mongering likw birth defects scare and etc.
I've built out a Metformin risk/reward profile, to sort of objectively assess tradeoffs (benefits vs costs of Met). @Millard has expressed some interest in these, maybe one for Met for the articles section of the main site?

It's impossible to stand in another's shoes and make the tradeoff assessment for them. I do think generally Met use can be rational in combination with rhGH & AAS and is less rational without, for bodybuilders. But it's a bit nuanced; clearly many don't appreciate the full risks of what they are putting in their bodies even.
 
Well, I think that the use of agents to ameliorate the hyperglycemic effects of rhGH falls on a continuum, that looks like: biguanides/GDAs (Met, BBR, etc.) < incretins (e.g., GLP-1 & GIP agonists) < rhIGF-I & LR3-IGF-I < insulin, but the rationale for use of slin is not merely glucose disposal.

I've built out a Metformin risk/reward profile, to sort of objectively assess tradeoffs (benefits vs costs of Met). @Millard has expressed some interest in these, maybe one for Met for the articles section of the main site?

It's impossible to stand in another's shoes and make the tradeoff assessment for them. I do think generally Met use can be rational in combination with rhGH & AAS and is less rational without, for bodybuilders. But it's a bit nuanced; clearly many don't appreciate the full risks of what they are putting in their bodies even.
If Met helps to increase IGF-1, isn’t it making whatever dose of rhGH you are on even more effective?
 

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