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No, but he’s got Hypoleptinemia, very low Leptin.

Closer to 30 would be normal.
Thanks, appreciate the info. I was actually planning to run a GH serum test in a couple of weeks anyway, but using a different vendor’s kit. From what I understand, pinning 10iu about 2-3 hours before blood draw should give a pretty accurate read, right?
 
Thanks, appreciate the info. I was actually planning to run a GH serum test in a couple of weeks anyway, but using a different vendor’s kit. From what I understand, pinning 10iu about 2-3 hours before blood draw should give a pretty accurate read, right?

Yes, that’s the old school standard for checking that the rHGH is good.

Really low Leptin causes elevated GH binding hormone, which reduces the half life from 3-4 hours to 1-2, explaining the lower than expected result he had from 10iu tests of two different brands.
 
Yes, that’s the old school standard for checking that the rHGH is good.

Really low Leptin causes elevated GH binding hormone, which reduces the half life from 3-4 hours to 1-2, explaining the lower than expected result he had from 10iu tests of two different brands.
This bloke. Haha

You know too much Ghoul
 
This bloke. Haha

You know too much Ghoul

I went down a deep rabbit hole on this today.

I asked about his IGF, which was really low as well, and he mentioned his low Leptin level, so it got me curious. I had been looking at studies of AIDS muscle wasting patients who get enormous doses of serostim, 15-18iu a day for 12 weeks, twice a year, and wondering why they don’t experience acromegaly symptoms, only anabolism, and then it clicked. They have very low appetites, high inflammation, dropping Leptin to very low levels.

That signals the liver you’re starving so don’t waste energy on growth, ie, slow down IGF production.

So 18iu rHGH is used to overcome this liver “GH resistance” and results in normal IGF levels. That’s why they don’t develop acromegaly.

But what about all the free GH floating around that’s not converted to IGF? Doesn’t that have some major effect on tissues that respond to GH?

And where did all the GH he injected just an hour before the test go?

I learned the body deals with excess GH in low Leptin induced IGF suppressed states (like starvation) by increasing growth hormone binding hormone production to quickly clear GH out of the body.

So low Leptin gives you very low IGF, is anti-anabolic, lower GH direct effects (skin, hair), but MORE SIDES because it increases GH receptor sensitivity in the kidneys increasing edema and carpel. High Leptin levels, signaling nutrient abundance, does the opposite of all this.

Mystery solved.

Now I’m going to start checking Leptin levels when I get IGF-1, since that seems to be the major regulator of how much IGF the liver produces per unit of GH.

There are also a number of drugs that can raise Leptin despite being in a caloric deficit or low body fat, which drop Leptin levels. I’m going to check them out.

Keeping Leptin elevated may be a way of preventing the elimination of GH by keeping GH binding hormone levels low, so that GH isn’t eliminated and enhanced fat lipolysis doesn’t slow down as body fat gets lower, which is what normally happens, and IGF should also stay higher, possibly maintaining the full GH anabolic effect even while cutting fat.

IMG_3239.webp

 
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I went down a deep rabbit hole on this today.

I asked about his IGF, which was really low as well, and he mentioned his low Leptin level, so it got me curious. I had been looking at studies of AIDS muscle wasting patients who get enormous doses of serostim, 15-18iu a day for 12 weeks, twice a year, and wondering why they don’t experience acromegaly symptoms, only anabolism, and then it clicked. They have very low appetites, high inflammation, dropping Leptin to very low levels.

That signals the liver you’re starving so don’t waste energy on growth, ie, slow down IGF production.

So 18iu rHGH is used to overcome this liver “GH resistance” and results in normal IGF levels. That’s why they don’t develop acromegaly.

But what about all the free GH floating around that’s not converted to IGF? Doesn’t that have some major effect on tissues that respond to GH?

And where did all the GH he injected just an hour before the test go?

I learned the body deals with excess GH in low Leptin induced IGF suppressed states (like starvation) by increasing growth hormone binding hormone production to quickly clear GH out of the body.

So low Leptin gives you very low IGF, is anti-anabolic, lower GH direct effects (skin, hair), but MORE SIDES because it increases GH receptor sensitivity in the kidneys increasing edema and carpel. High Leptin levels, signaling nutrient abundance, does the opposite of all this.

Mystery solved.

Now I’m going to start checking Leptin levels when I get IGF-1, since that seems to be the major regulator of how much IGF the liver produces per unit of GH.

There are also a number of drugs that can raise Leptin despite being in a caloric deficit or low body fat, which drop Leptin levels. I’m going to check them out.

Keeping Leptin elevated may be a way of preventing the elimination of GH by keeping GH binding hormone levels low, so that GH isn’t eliminated and enhanced fat lipolysis doesn’t slow down as body fat gets lower, which is what normally happens, and IGF should also stay higher, possibly maintaining the full GH anabolic effect even while cutting fat.

View attachment 358401

Very good evaluation and explanation. Keep up the good work ghoul
 
Did my first order with Yura on October 14 , got tracking then 18th the tracking sat in the same place for the whole time and then TD the 29th just forgot to give them the feedback , about to pickup some liquid SLUPPY from them.
 
I went down a deep rabbit hole on this today.

I asked about his IGF, which was really low as well, and he mentioned his low Leptin level, so it got me curious. I had been looking at studies of AIDS muscle wasting patients who get enormous doses of serostim, 15-18iu a day for 12 weeks, twice a year, and wondering why they don’t experience acromegaly symptoms, only anabolism, and then it clicked. They have very low appetites, high inflammation, dropping Leptin to very low levels.

That signals the liver you’re starving so don’t waste energy on growth, ie, slow down IGF production.

So 18iu rHGH is used to overcome this liver “GH resistance” and results in normal IGF levels. That’s why they don’t develop acromegaly.

But what about all the free GH floating around that’s not converted to IGF? Doesn’t that have some major effect on tissues that respond to GH?

And where did all the GH he injected just an hour before the test go?

I learned the body deals with excess GH in low Leptin induced IGF suppressed states (like starvation) by increasing growth hormone binding hormone production to quickly clear GH out of the body.

So low Leptin gives you very low IGF, is anti-anabolic, lower GH direct effects (skin, hair), but MORE SIDES because it increases GH receptor sensitivity in the kidneys increasing edema and carpel. High Leptin levels, signaling nutrient abundance, does the opposite of all this.

Mystery solved.

Now I’m going to start checking Leptin levels when I get IGF-1, since that seems to be the major regulator of how much IGF the liver produces per unit of GH.

There are also a number of drugs that can raise Leptin despite being in a caloric deficit or low body fat, which drop Leptin levels. I’m going to check them out.

Keeping Leptin elevated may be a way of preventing the elimination of GH by keeping GH binding hormone levels low, so that GH isn’t eliminated and enhanced fat lipolysis doesn’t slow down as body fat gets lower, which is what normally happens, and IGF should also stay higher, possibly maintaining the full GH anabolic effect even while cutting fat.

View attachment 358401

Does this not implying GH is worse when you're lean, say sub 10%?
 
I went down a deep rabbit hole on this today.

I asked about his IGF, which was really low as well, and he mentioned his low Leptin level, so it got me curious. I had been looking at studies of AIDS muscle wasting patients who get enormous doses of serostim, 15-18iu a day for 12 weeks, twice a year, and wondering why they don’t experience acromegaly symptoms, only anabolism, and then it clicked. They have very low appetites, high inflammation, dropping Leptin to very low levels.

That signals the liver you’re starving so don’t waste energy on growth, ie, slow down IGF production.

So 18iu rHGH is used to overcome this liver “GH resistance” and results in normal IGF levels. That’s why they don’t develop acromegaly.

But what about all the free GH floating around that’s not converted to IGF? Doesn’t that have some major effect on tissues that respond to GH?

And where did all the GH he injected just an hour before the test go?

I learned the body deals with excess GH in low Leptin induced IGF suppressed states (like starvation) by increasing growth hormone binding hormone production to quickly clear GH out of the body.

So low Leptin gives you very low IGF, is anti-anabolic, lower GH direct effects (skin, hair), but MORE SIDES because it increases GH receptor sensitivity in the kidneys increasing edema and carpel. High Leptin levels, signaling nutrient abundance, does the opposite of all this.

Mystery solved.

Now I’m going to start checking Leptin levels when I get IGF-1, since that seems to be the major regulator of how much IGF the liver produces per unit of GH.

There are also a number of drugs that can raise Leptin despite being in a caloric deficit or low body fat, which drop Leptin levels. I’m going to check them out.

Keeping Leptin elevated may be a way of preventing the elimination of GH by keeping GH binding hormone levels low, so that GH isn’t eliminated and enhanced fat lipolysis doesn’t slow down as body fat gets lower, which is what normally happens, and IGF should also stay higher, possibly maintaining the full GH anabolic effect even while cutting fat.

View attachment 358401

Insulin stimulates the release of leptin, another aspect of their synergy
 
Does this not implying GH is worse when you're lean, say sub 10%?

Less effective, yes. Less IGF produced per unit of GH.

Once fasting leptin dips below roughly 2 ng/mL, corresponding to ~8–10 % body fat in men, the hypothalamus reads “starvation,” suppressing hepatic GH receptor sensitivity and IGF-1 synthesis. Up to 60% drop in IGF.

12-15%, leptin 6-8 ng / ml, maximum IGF production per unit of GH.

Above 20%, leptin 10 ng+ , leptin resistance develops, IGF per unit of GH drops as body fat increases
 
Decided to give yura a go, small order, 300 or so, but man he's only asked for proof of payment. Paid on the 27th, sent transaction ID, sent bank record, even sent a bank statement. Literally nothing left I can send as proof. If he was just stalling for time because he has lots of back orders I'd rather he just tell me.

Well maybe on Monday, after a full week, I'll have progress.
 
Decided to give yura a go, small order, 300 or so, but man he's only asked for proof of payment. Paid on the 27th, sent transaction ID, sent bank record, even sent a bank statement. Literally nothing left I can send as proof. If he was just stalling for time because he has lots of back orders I'd rather he just tell me.

Well maybe on Monday, after a full week, I'll have progress.
Wait what? All he ever asks for is transaction ID and maybe a screen shot of the competed transaction. Nothing more.
 
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