IGF-1 levels of 132 on 6iu GH?

ChemBB

Member
So, I recently started GH for the first time. Using 6iu pre-bed.

I had my IGF-1 tested after being on it a few weeks, and my levels are lower than they were before...
Only thing I can think of is that I'm on a cut and have been using 50mg Winstrol/day which can lower IGF-1 via IGFBP.

Anyone seen something like this before? Would really hate for it to be bunk...

Growth hormone induced increase in serum IGFBP-3 level is reversed by anabolic steroids in substance abusing power athletes - PubMed

Results: While growth hormone increased the IGFBP-3 and IGF-I concentrations, anabolic steroids decreased the same. Concomitant use of growth hormone and anabolic steroids decreased the IGFBP-3 concentration in five out of six abuse periods in spite of the fact that the IGF-I concentration remained elevated in four of them. However, in two men who were on low calorie diet both the IGF-I and IGFBP-3 concentrations decreased during combined GH/anabolic steroid abuse. No proteolytic fragmentation of IGFBP-3 was observed.

1757673911883.webp
 
Yeah, especially when in a caloric deficit.

Not everyone converts GH into circulating IGF-1 the same way, so serum IGF-1 isn't the whole picture.

A "normal" or even lower IGF-1 doesn't mean the GH isn’t working.

How is your recovery, fat loss, performance, sleep, etc...?

How long have you been on and are you noticing any of those effects yet?
 
My igf-1 tested about 350 on 4iu in a mild deficit. I went to 6iu and a much harder deficit and it dropped to 230. My understanding is in a deficit it's still increasing lipolysis for fat loss, just not converting to igf-1. You're still getting the cut benefits of fat loss.
 
My igf-1 tested about 350 on 4iu in a mild deficit. I went to 6iu and a much harder deficit and it dropped to 230. My understanding is in a deficit it's still increasing lipolysis for fat loss, just not converting to igf-1. You're still getting the cut benefits of fat loss.
GH-induced fat loss has nothing to do with IGF1. Even if you have very low IGF1, 10 units will still have a lipolytic effect; what you won't see is hypertrophy and hyperplasia.

If a person doesn't respond to an IGF1 boost, there are alternatives to see if it resolves.

1) Assess whether you're abusing AIs, or have low E2 levels due to the use/abuse of EQ or Primobolan.
2) Avoid oral medications or limit the dose.
3) Use insulin in combination with GH (GH + Slin = greater increase in IGF1 than GH alone).
4) Use IGF1-LR3.
 
Sorry, thought chat GPT did a good job here, lol.

Couple things that come to mind right off the bat tho..

- Winstrol Is known to lower igf-1 production liver. Like chat GPT said, at the transcriptional level in the liver. No brainer..

- Low estrogen from the Winnie.. we know estrogen effects igf1 production. This is why we want estrogen in range or even a little on the higher side while running. GH.

- Dieting, especially with low carbs.. insulin drops, and if not sufficient insulin= low igf1 production.

How to confirm?

Your not gonna like it, but do like Chat GPT said, bring calories to maintenance while simultaneously stopping the Winny for a week or so, and retest those levels.
 
Sorry, thought chat GPT did a good job here, lol.

Couple things that come to mind right off the bat tho..

- Winstrol Is known to lower igf-1 production liver. Like chat GPT said, at the transcriptional level in the liver. No brainer..

- Low estrogen from the Winnie.. we know estrogen effects igf1 production. This is why we want estrogen in range or even a little on the higher side while running. GH.

- Dieting, especially with low carbs.. insulin drops, and if not sufficient insulin= low igf1 production.

How to confirm?

Your not gonna like it, but do like Chat GPT said, bring calories to maintenance while simultaneously stopping the Winny for a week or so, and retest those levels.

For fucks sake, estrogen LOWERS IGF CONVERSION:

It only appears to increase IGF because high estrogen increases GH levels. and despite reducing GH -> IGF efficiency, the higher GH levels are enough to overcome that reduction in conversion.

When you're using exogenous rHGH, and shutting down endogenous GH production, there's no longer a GH boost from estrogen, and all you're getting from higher estrogen is reduced GH ->. IGF conversion, and less IGF than if e2 was lower.

Thats why women have higher GH and lower IGF levels than men.

Thats why women with borderline acromegally, who have supra-physiologic levels of GH, develop symptoms AFTER menopause when the estrogen induced blunting of IGF conversion is removed because they stop making estrogen, and IGF shoots up causing acromegally symptoms.
 
Before jumping to conclusions I'd do a 10IU shot IM and test serum GH 2,5 hours later. If this comes out low then chances of something going on with the particular HGH are higher. If it's ok then you have to assess why you convert so low, although being in deficit it's a sign by itself.
 
Chase Irons IGF-1 was around 200 on 18 iu serostim. The serum igf-1 is not terribly relevant for our purposes. If you ratchet up the dose and don’t see some water retention / hand numbness, etc then that might be cause for concern but I doubt it’s fake.


View: https://youtu.be/RsDr2s3G9eU?si=gUkz5bvp6p0OFPbO



Nice to see Kurt and I are in agreement. :)

Chase's IGF conversion may have been capped by very high e2 from the grams of gear he was running. Because otherwise 200 IGF from 18iu are like liver failure numbers. It's bizarrely low.
 
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For fucks sake, estrogen LOWERS IGF CONVERSION:

It only appears to increase IGF because high estrogen increases GH levels. and despite reducing GH -> IGF efficiency, the higher GH levels are enough to overcome that reduction in conversion.

When you're using exogenous rHGH, and shutting down endogenous GH production, there's no longer a GH boost from estrogen, and all you're getting from higher estrogen is reduced GH ->. IGF conversion, and less IGF than if e2 was lower.

Thats why women have higher GH and lower IGF levels than men.

Thats why women with borderline acromegally, who have supra-physiologic levels of GH, develop symptoms AFTER menopause when the estrogen induced blunting of IGF conversion is removed because they stop making estrogen, and IGF shoots up causing acromegally symptoms.
Never never never listen to anything this clown says, he knows nothing and the level of missinformation he spread on this forum is wild. This obese kid use chatgpt to find information about women and igf/gh and posting that garbage from his mothers basement.

Everyone knows e2 raises igf-1.

All the pros knows this by bloodwork and decades of knowledge just from today posted by trainedbyjp.
IMG_6279.webp
 
Never never never listen to anything this clown says, he knows nothing and the level of missinformation he spread on this forum is wild. This obese kid use chatgpt and posting from his mothers basement. Everyone knows e2 raises igf-1.

All the pros knows this by bloodwork and decades of knowledge just from today posted by trainedbyjp.
View attachment 347144
I think the devil is in the details here. JP said high end of normal. That makes sense. Very low E2 is not good for anything. Very high e2 also not good. Between 40-60 (maybe even up to 80 for some) is where most Guys seem to feel best and that’s plenty of E2 for GH to igf-1 conversion
 
I think the devil is in the details here. JP said high end of normal. That makes sense. Very low E2 is not good for anything. Very high e2 also not good. Between 40-60 (maybe even up to 80 for some) is where most Guys seem to feel best and that’s plenty of E2 for GH to igf-1 conversion
Yes there is a individual e2 limit what you can use to convert gh to igf-1 and what you can tolerate without sideffects.

Estrogen e2 from aromatizated exogenous testosteron enhances gh to igf-1 conversion.

@Ghoul is studying women and will never understand how it works in men.

End of discussion.
 
Not everyone converts GH into circulating IGF-1 the same way
There's only one major factor in individual physiology I'm aware of that impacts GH -> IGF-1 efficacy and it's the "Exon 3-Deleted Growth Hormone Receptor (d3GHR) Polymorphism"

The Exon 3-Deleted Growth Hormone Receptor (d3GHR) Polymorphism—A Favorable Backdoor Mechanism for the GHR Function - PMC

I have my genome sequenced, and I just checked -- I have the T/T allele, which is the 50% of people who are average responders to GH

rs6873545 - SNPedia

Code:
❯ grep rs6873545 genome_Imputed_30M_L.txt
rs6873545       5       42631264        TT

How is your recovery, fat loss, performance, sleep, etc...?
How long have you been on and are you noticing any of those effects yet?

Recovery-wise I feel fine. I do a 4-day split with no rest days and 30m of low-intensity cardio daily.

I have OSA and sleep with a CPAP, but other than that my sleep is normal.

Started using 6iu GH on 9/01, so just shy of 2 weeks now.

Low estrogen from the Winnie

I don't think I've ever seen literature on Winstrol reducing E2 levels, and I'd consider myself among the more well-read people on anabolic/ergogenic pharmacology

I'd do a 10IU shot IM and test serum GH 2,5 hours later

Yeah, short of shelling out $300 for a Jano test, the only sure-fire way I can think of would be to do 2 same-day blood draws. The first, then pin large dose of GH, and get a second draw about 3hr later or so.

It'd be a way to tell but man it's a bit inconvenient lol

I don't have any reason to suspect the GH is bunk/underdosed.
(It's JY Pharma 24iu kit, their July tests for 10iu show 11.3 from Jano)

So the results are certainly odd to me.

If you ratchet up the dose and don’t see some water retention / hand numbness, etc then that might be cause for concern but I doubt it’s fake.

Thought of this too. When I used MK-677 in my early 20's, it would give me numb/stiff hands + wrists in the morning when I woke up.

But it's a bit pseudo-sciencey. I could pin a whole 24iu vial and see if anything happens though...
 
There's only one major factor in individual physiology I'm aware of that impacts GH -> IGF-1 efficacy and it's the "Exon 3-Deleted Growth Hormone Receptor (d3GHR) Polymorphism"

The Exon 3-Deleted Growth Hormone Receptor (d3GHR) Polymorphism—A Favorable Backdoor Mechanism for the GHR Function - PMC

I have my genome sequenced, and I just checked -- I have the T/T allele, which is the 50% of people who are average responders to GH

rs6873545 - SNPedia

Code:
❯ grep rs6873545 genome_Imputed_30M_L.txt
rs6873545       5       42631264        TT



Recovery-wise I feel fine. I do a 4-day split with no rest days and 30m of low-intensity cardio daily.

I have OSA and sleep with a CPAP, but other than that my sleep is normal.

Started using 6iu GH on 9/01, so just shy of 2 weeks now.



I don't think I've ever seen literature on Winstrol reducing E2 levels, and I'd consider myself among the more well-read people on anabolic/ergogenic pharmacology



Yeah, short of shelling out $300 for a Jano test, the only sure-fire way I can think of would be to do 2 same-day blood draws. The first, then pin large dose of GH, and get a second draw about 3hr later or so.

It'd be a way to tell but man it's a bit inconvenient lol

I don't have any reason to suspect the GH is bunk/underdosed.
(It's JY Pharma 24iu kit, their July tests for 10iu show 11.3 from Jano)

So the results are certainly odd to me.



Thought of this too. When I used MK-677 in my early 20's, it would give me numb/stiff hands + wrists in the morning when I woke up.

But it's a bit pseudo-sciencey. I could pin a whole 24iu vial and see if anything happens though...
give it some more time and adjust your calorie intake, when i was eating in a defecit my igf1 was on the lower side, i started eating at maintenance or slightly above and it went up accordingly
 
Never never never listen to anything this clown says, he knows nothing and the level of missinformation he spread on this forum is wild. This obese kid use chatgpt to find information about women and igf/gh and posting that garbage from his mothers basement.

Everyone knows e2 raises igf-1.

All the pros knows this by bloodwork and decades of knowledge just from today posted by trainedbyjp.
View attachment 347144

Ghoul's claims are sound, and evidence-based.

The de-facto work on E2 <-> GH/IGF1 interaction is the paper below:

Role of Estrogen and Estrogen Receptor in GH-Secreting Adenomas - PMC

> "The aim of this review is to map the current literature regarding the state of the art regarding the impact of estrogens and SERMs on the GH/IGF1 axis, focusing on molecular pathways and the possible effects on acromegaly treatment. To the best of our knowledge, the only attempt to collect the available evidence was a mini-review published by Duarte et al. in 2016"

For anyone uninterested in reading, here's the takeaway:

> "Estrogens and SERMs significantly reduce IGF1 production, acting mainly through an impairment in GH signaling at a peripheral level."
 
Ghoul's claims are sound, and evidence-based.

The de-facto work on E2 <-> GH/IGF1 interaction is the paper below:

Role of Estrogen and Estrogen Receptor in GH-Secreting Adenomas - PMC

> "The aim of this review is to map the current literature regarding the state of the art regarding the impact of estrogens and SERMs on the GH/IGF1 axis, focusing on molecular pathways and the possible effects on acromegaly treatment. To the best of our knowledge, the only attempt to collect the available evidence was a mini-review published by Duarte et al. in 2016"

For anyone uninterested in reading, here's the takeaway:

> "Estrogens and SERMs significantly reduce IGF1 production, acting mainly through an impairment in GH signaling at a peripheral level."
Learn to read.

Estrogen e2 from aromatizated exogenous testosteron enhances gh to igf-1 conversion.

I will wait for you or that loser to lost evidence this is false, as there are thousands of bloodworks backing this.

Why not just try it out yourself before speak bullshit. Oh you can’t afford test, gh and bloodwork.
 
Learn to read.

Estrogen e2 from aromatizated exogenous testosteron enhances gh to igf-1 conversion.

I will wait for you or that loser to lost evidence this is false, as there are thousands of bloodworks backing this.

Why not just try it out yourself before speak bullshit. Oh you can’t afford test, gh and bloodwork.
I’m not part of the debate, but does this only pertain to E2 results from exogenous testosterone? What about those using (GH) without testosterone? I took GH for 18 months without any testosterone, and I'm now on Tesamorelin. I'm just wondering what considerations with estrogen I might notice. I'm also curious what I might see in my bloodwork.
 
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I’m not part of the debate, but does this only pertain to E2 results from exogenous testosterone? What about those using (GH) without testosterone? I took GH for 18 months without any testosterone, and I'm now on Tesamorelin. I'm just wondering what considerations with estrogen I might notice. I'm also curious what I might see in my bloodwork.
If you're not on test, there's not a lot you can do to modulate your e2 levels.
 
Yes there is a individual e2 limit what you can use to convert gh to igf-1 and what you can tolerate without sideffects.

Estrogen e2 from aromatizated exogenous testosteron enhances gh to igf-1 conversion.

@Ghoul is studying women and will never understand how it works in men.

End of discussion.

Lol, and..
The studies with women were all taking oral estrogen besides, and when they used transdermal estrogen in place of the oral, igf1 levels rose with it.
Plus numerous studies showing tanked e2 from AI use always lead to shit GH-igf1 conversion.
Either way, most serious guys on gear know you need e2 in range for max benefit of GH-igf1 conversion. So.. Goul is either not on gear or he's just not that serious, HA

 

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