GH works better with higher estrogen?

[pewex]

”But when you're injecting exogenous GH, all higher estrogen does is inhibit the liver's ability to convert it to IGF, and therefore at the same dose of GH, lower estrogen results in higher IGF, and higher estrogen lowers IGF.”

This is exactly the opposite of what he found in bloodwork both in himself and his clients, he is no troll ifbb pro and medical doctor so he can order and read his own bloodwork.

Whatever you claim bloodwork don’t lie.

That retard mixes oils and peptides in the same syringe and instructs their clients to do the same, go figure...

 

[Freeboomboom]

The reason Todd Lee and idiots like him think "high estrogen makes your GH more effective"
It's because they are basing it entirely off of serum IGF levels and completely ignoring what serum igf1 testing is actually measuring or that igf binding proteins exist.

Serum IGF testing cannot differentiate between available and bound igf (if it's in serum, almost all of it will be bound to one of the igf1 binding proteins). We don't care about igf1 in serum because it's a useless metric for the purposes of getting an anabolic effect from igf1, what we care about for our purposes is igf1 in tissue, which cannot be measured without a muscle biopsy.

High e2 simulates the production and release of igf1 binding proteins, there are a bunch of them and they do various things such as shuttling the hormone and in some cases, essentially rendering it inert.

IGFBP1 as far as we can tell, completely renders the igf1 it binds to add useless until it's excreted.
High e2 specifically elevates IGFBP1 more than other BP.

Thus, because e2 is high, IGFBP1 is high.
Because IGFBP1 is high, that means there is a greater proportion of your available igf bound to that binding protein and circulating in serum, uselessly.

”Trust me bro”

Typical stubborn bro science teens.

Bloodwork don’t lie, kids do.

 

[isopropyl]

Thank you again @Ghoul and @BigTomJ as well. I did get this information from Todd Lee as well as comments around that space. He spoke with such confidence so NGL I was halfway sold haha, had to double check though.

 

[Ghoul]

In the spirit of fairness. I did a deep dive into the concept of "Estrogen=gains on GH" presented in Todd Lee's video.

There was something to be learned from his claim, unfortunately he wasn't specific enough to make it useful, leaving the (wrong) impression high E2 was better for muscle growth via increased IGF.

It doesn't change much in the sense that:

1. We all know crashed estrogen is bad so I wouldn't expect anyone to try to do that to maximize IGF, and

2. You *STILL* want to keep E2 low to maximize IGF.

------

What I said about estrogen and IGF is correct. Lower e2 makes IGF go up. higher e2 makes it go down.

For simplicity's sake I'm using round numbers and when I say IGF it means IGF-1.

-90% of the body's IGF is produced in the liver. This systemic IGF is what we're measuring in blood tests.

-With the same level of GH, lower estrogen increases GH to IGF conversion in the liver, higher estrogen decreases it.

-10% of IGF is produced locally in muscle.

-IGF produced in muscle is responsible for 70% of muscle repair and growth, 30% from systemic (liver produced) IGF.

-Insulin is the signal hormone that makes muscle convert GH to IGF.

-Higher estrogen increases muscle sensitivity to this insulin signaling.

-If estrogen is too low, GH conversion to IGF in muscle is impaired, so there's less muscle growth and repair. Higher estrogen increases muscle GH to IGF conversion so there's more growth and repair.

----------

But here's the key he doesn't mention:

*Muscle sensitivity to insulin signaling maxes out at an E2 of around 20-35 pg/ml, mid normal range.*

If E2 is above this range, you're not getting any more IGF conversion in muscle, but you are increasing the inhibition of GH to IGF conversion in the liver, lowering systemic IGF, reducing the amount of muscle growth.

--------------

So what all this means is:

Too low E2: good for liver IGF but bad for muscle IGF → impaired muscle growth/ repair.

Too high E2: no extra benefit in muscle IGF and lowers systemic IGF → impaired muscle growth/ repair.

Mid-normal E2 (~20–35 pg/mL): maximizes liver and muscle IGF for optimal growth/recovery.

 

[Avies48]

In the spirit of fairness. I did a deep dive into the concept of "Estrogen=gains on GH" presented in Todd Lee's video.

It doesn't change much in the sense that

1. We all know crashed estrogen is bad so I wouldn't expect anyone to try to do that to maximize IGF, and

2. You *STILL* want to keep E2 low to maximize IGF.

But there was something to be gained from his claim, unfortunately he wasn't specific enough to make it useful, leaving the impression high E2 was better for muscle growth.

------

What I said about estrogen and IGF is correct. Lower e2 makes IGF go up. higher e2 makes it go down.

For simplicity's sake I'm using round numbers and when I say IGF it means IGF-1.

-90% of the body's IGF is produced in the liver. This systemic IGF is what we're measuring in blood tests.

-With the same level of GH, lower estrogen increases GH to IGF conversion in the liver, higher estrogen decreases it.

-10% of IGF is produced locally in muscle.

-IGF produced in muscle is responsible for 70% of muscle repair and growth, 30% from systemic (liver produced) IGF.

-Insulin is the signal hormone that makes muscle convert GH to IGF.

-Higher estrogen increases muscle sensitivity to this insulin signaling.

-If estrogen is too low, GH conversion to IGF in muscle is impaired, so there's less muscle growth and repair. Higher estrogen increases muscle GH to IGF conversion so there's more growth and repair.

----------

But here's the key he doesn't mention:

*Muscle sensitivity to insulin signaling maxes out at an E2 of around 20-35 pg/ml, mid normal range.*

If E2 is above this range, you're not getting any more IGF conversion in muscle, but you are increasing the inhibition of GH to IGF conversion in the liver, lowering systemic IGF, reducing the amount of muscle growth.

--------------

So what all this means is:

Too low E2: good for liver IGF but bad for muscle IGF → impaired muscle growth/ repair.

Too high E2: no extra benefit in muscle IGF and lowers systemic IGF → impaired muscle growth/ repair.

Mid-normal E2 (~20–35 pg/mL): maximizes liver and muscle IGF for optimal growth/recovery.

My e2 is usually around 20-35… and im on nothing… igf was a 138 last time i checked and that was my range for e2…

So whats that mean? As its kind of confusing in the bold…

Liver igf is good but not my muscle igf

Mid normal E-2 maximizes liver and muscle igf for optimal recovery growth?? How?

Because if lower e2 makes igf go up? I need to increase my e2 so i can get a script for gh deficiency…. Because at 138 baseline and in my 40’s… i need my script doc now!!! Haha

 

[Ghoul]

My e2 is usually around 20-35… and im on nothing… igf was a 138 last time i checked and that was my range for e2…

So whats that mean? As its kind of confusing in the bold…

Liver igf is good but not my muscle igf

Mid normal E-2 maximizes liver and muscle igf for optimal recovery growth?? How?

Because if lower e2 makes igf go up? I need to increase my e2 so i can get a script for gh deficiency…. Because at 138 baseline and in my 40’s… i need my script doc now!!! Haha

Your IGF is normal (a little on the low
side of it).

Your estrogen is ideal for GH to IGF conversion.

What happens on rHGH will tell you whether it's your endogenous GH that's low causing low IGF, or if there's a liver GH to IGF conversion problem, most often caused by preexisting insulin resistance or a fatty liver.

 

[eery]

In the spirit of fairness. I did a deep dive into the concept of "Estrogen=gains on GH" presented in Todd Lee's video.

There was something to be learned from his claim, unfortunately he wasn't specific enough to make it useful, leaving the (wrong) impression high E2 was better for muscle growth via increased IGF.

It doesn't change much in the sense that:

1. We all know crashed estrogen is bad so I wouldn't expect anyone to try to do that to maximize IGF, and

2. You *STILL* want to keep E2 low to maximize IGF.

------

What I said about estrogen and IGF is correct. Lower e2 makes IGF go up. higher e2 makes it go down.

For simplicity's sake I'm using round numbers and when I say IGF it means IGF-1.

-90% of the body's IGF is produced in the liver. This systemic IGF is what we're measuring in blood tests.

-With the same level of GH, lower estrogen increases GH to IGF conversion in the liver, higher estrogen decreases it.

-10% of IGF is produced locally in muscle.

-IGF produced in muscle is responsible for 70% of muscle repair and growth, 30% from systemic (liver produced) IGF.

-Insulin is the signal hormone that makes muscle convert GH to IGF.

-Higher estrogen increases muscle sensitivity to this insulin signaling.

-If estrogen is too low, GH conversion to IGF in muscle is impaired, so there's less muscle growth and repair. Higher estrogen increases muscle GH to IGF conversion so there's more growth and repair.

----------

But here's the key he doesn't mention:

*Muscle sensitivity to insulin signaling maxes out at an E2 of around 20-35 pg/ml, mid normal range.*

If E2 is above this range, you're not getting any more IGF conversion in muscle, but you are increasing the inhibition of GH to IGF conversion in the liver, lowering systemic IGF, reducing the amount of muscle growth.

--------------

So what all this means is:

Too low E2: good for liver IGF but bad for muscle IGF → impaired muscle growth/ repair.

Too high E2: no extra benefit in muscle IGF and lowers systemic IGF → impaired muscle growth/ repair.

Mid-normal E2 (~20–35 pg/mL): maximizes liver and muscle IGF for optimal growth/recovery.

the insulin works by decreasing igfbp1, which is a negative regulator, right?

then theres igfbp3 that keeps the igf1 bioavailable, which is negatively impacted by too high and too low estrogen?

 

[Ghoul]

the insulin works by decreasing igfbp1, which is a negative regulator, right?

then theres igfbp3 that keeps the igf1 bioavailable, which is negatively impacted by too high and too low estrogen?

Insulin is needed for GH-IGF conversion in both liver and muscle. The more insulin. ie, after meals including carbs,. the higher IGF will go (to a point).

The way insulin does this is different in each, though it's not particularly important to understand the mechanism.. Without insulin, in the liver conversion doesn't happen at all, and in muscle conversion still takes place without insulin but a very low level.

Insulin suppresses IGFBP production so yes. it also makes systemic IGF more bioavailable, but that's not normally tested for and we only see systemic IGF not the true available level.

 

[eery]

Insulin is needed for GH-IGF conversion in both liver and muscle. The more insulin. ie, after meals including carbs,. the higher IGF will go (to a point).

The way insulin does this is different in each, though it's not particularly important to understand the mechanism.. Without insulin, in the liver conversion doesn't happen at all, and in muscle conversion still takes place without insulin but a very low level.

Insulin suppresses IGFBP production so yes. it also makes systemic IGF more bioavailable, but that's not normally tested for and we only see systemic IGF not the true available level.

i see

[LIST]
[*]The Chemical Player: IGFBP-1 is a protein produced primarily by liver cells (hepatocytes).
[*]Its Biochemical Action: It has a very high affinity for IGF-1 in the bloodstream. When IGF-1 is bound to IGFBP-1, it cannot bind to the IGF-1 Receptor (IGF-1R) on muscle, bone, and other cells. Therefore, it is biologically inactive. Think of IGFBP-1 as a "parking brake" on IGF-1.
[*]Insulin's Mechanism: Insulin suppresses the production of IGFBP-1. Here's the scientific pathway:

[LIST=1]
[*]Insulin binds to its receptor on the hepatocyte.
[*]This activates a signaling cascade (primarily the PI3K/Akt pathway).
[*]Akt leads to the phosphorylation and inactivation of a transcription factor called FOXO1.
[*]FOXO1 is the master switch that turns on the gene for IGFBP-1. When FOXO1 is turned off, the liver cell stops making IGFBP-1.
[/LIST]
[*]The Result: With less IGFBP-1 being produced, more IGF-1 is "free" and unbound. This Free IGF-1 can now travel to tissues and activate the IGF-1R, promoting muscle growth, glycogen synthesis, and other anabolic processes.
[/LIST]
So, yes, insulin works by decreasing the production of the negative regulator (IGFBP-1), thereby increasing the bioavailability of IGF-1.

[LIST]
[*]The Chemical Player: IGFBP-3 is the most abundant binding protein, carrying ~75-80% of all circulating IGF-1.
[*]Its Biochemical Action: Unlike IGFBP-1, IGFBP-3 doesn't just act as a simple inhibitor. It forms a ternary complex with IGF-1 and another protein called the Acid-Labile Subunit (ALS). This large complex:

[LIST]
[*]Prolongs the half-life of IGF-1 from minutes to hours, creating a circulating reservoir.
[*]Prevents IGF-1 from binding to its receptor, making it bio-inactive while in the complex.
[*]Serves as a buffer. IGF-1 can be released from this complex in a regulated manner to become bioactive.

[/LIST]
[*]

[*]The effect of estrogen is biphasic (too little or too much is bad), and it's all about modulating the Growth Hormone Receptor (GHR) signal in the liver.

[LIST]
[*]Low Estrogen: The GH receptor signaling pathway is "quiet." The liver is less responsive to GH, leading to reduced production of both IGF-1 and IGFBP-3/ALS. The total circulating reservoir is small.
[*]Moderate/Optimal Estrogen: Estrogen potentiates GH signaling. It upregulates GHR expression and enhances the JAK2-STAT5 pathway. This leads to robust production of IGF-1, IGFBP-3, and ALS. The large, stable ternary complex is fully formed, ensuring a vast, long-lasting reservoir of IGF-1 ready for use.
[*]Very High Estrogen: This is where it gets interesting. Supraphysiological estrogen induces a state of hepatic GH resistance. It does this by:

[LIST=1]
[*]Downregulating the GH receptor.
[*]Upregulating proteins called SOCS (Suppressors of Cytokine Signaling), which directly inhibit the JAK-STAT pathway.
[*]The Result: The liver becomes deaf to the GH signal. Despite high levels of GH in the blood (as estrogen also stimulates GH secretion), the production of IGF-1, IGFBP-3, and ALS is significantly blunted. The circulating reservoir is small and unstable.

[/LIST]
[/LIST]
[/LIST]

[LIST]
[*]In the Liver: Insulin is permissive. It is absolutely required for the GH-induced expression of the IGF1 gene. The GH signal (JAK2-STAT5) provides the "on" switch, but insulin (via the IRS/PI3K pathway) provides the necessary "co-stimulation" and energy/substrates for the massive protein synthesis required to make IGF-1. Without insulin, the switch doesn't work.
[*]In Muscle: Muscle tissue can produce IGF-1 locally (this is called "mechano-growth factor" or MGF). This production is stimulated by mechanical stretch and damage. Insulin's role here is more supportive—it enhances nutrient delivery and anabolic signaling (via Akt/mTOR) to maximize the effect of this locally produced IGF-1. It is less of a strict requirement than in the liver but still a powerful amplifier.

[/LIST]



^For anyone interested

 

[Avies48]

Your IGF is normal (a little on the low
side of it).

Your estrogen is ideal for GH to IGF conversion.

What happens on rHGH will tell you whether it's your endogenous GH that's low causing low IGF, or if there's a liver GH to IGF conversion problem, most often caused by preexisting insulin resistance or a fatty liver.

Oh i got a fatty liver… seen it on scans

 

[Avies48]

i see

[LIST]
[*]The Chemical Player: IGFBP-1 is a protein produced primarily by liver cells (hepatocytes).
[*]Its Biochemical Action: It has a very high affinity for IGF-1 in the bloodstream. When IGF-1 is bound to IGFBP-1, it cannot bind to the IGF-1 Receptor (IGF-1R) on muscle, bone, and other cells. Therefore, it is biologically inactive. Think of IGFBP-1 as a "parking brake" on IGF-1.
[*]Insulin's Mechanism: Insulin suppresses the production of IGFBP-1. Here's the scientific pathway:

[LIST=1]
[*]Insulin binds to its receptor on the hepatocyte.
[*]This activates a signaling cascade (primarily the PI3K/Akt pathway).
[*]Akt leads to the phosphorylation and inactivation of a transcription factor called FOXO1.
[*]FOXO1 is the master switch that turns on the gene for IGFBP-1. When FOXO1 is turned off, the liver cell stops making IGFBP-1.
[/LIST]
[*]The Result: With less IGFBP-1 being produced, more IGF-1 is "free" and unbound. This Free IGF-1 can now travel to tissues and activate the IGF-1R, promoting muscle growth, glycogen synthesis, and other anabolic processes.
[/LIST]
So, yes, insulin works by decreasing the production of the negative regulator (IGFBP-1), thereby increasing the bioavailability of IGF-1.

[LIST]
[*]The Chemical Player: IGFBP-3 is the most abundant binding protein, carrying ~75-80% of all circulating IGF-1.
[*]Its Biochemical Action: Unlike IGFBP-1, IGFBP-3 doesn't just act as a simple inhibitor. It forms a ternary complex with IGF-1 and another protein called the Acid-Labile Subunit (ALS). This large complex:

[LIST]
[*]Prolongs the half-life of IGF-1 from minutes to hours, creating a circulating reservoir.
[*]Prevents IGF-1 from binding to its receptor, making it bio-inactive while in the complex.
[*]Serves as a buffer. IGF-1 can be released from this complex in a regulated manner to become bioactive.

[/LIST]
[*]

[*]The effect of estrogen is biphasic (too little or too much is bad), and it's all about modulating the Growth Hormone Receptor (GHR) signal in the liver.

[LIST]
[*]Low Estrogen: The GH receptor signaling pathway is "quiet." The liver is less responsive to GH, leading to reduced production of both IGF-1 and IGFBP-3/ALS. The total circulating reservoir is small.
[*]Moderate/Optimal Estrogen: Estrogen potentiates GH signaling. It upregulates GHR expression and enhances the JAK2-STAT5 pathway. This leads to robust production of IGF-1, IGFBP-3, and ALS. The large, stable ternary complex is fully formed, ensuring a vast, long-lasting reservoir of IGF-1 ready for use.
[*]Very High Estrogen: This is where it gets interesting. Supraphysiological estrogen induces a state of hepatic GH resistance. It does this by:

[LIST=1]
[*]Downregulating the GH receptor.
[*]Upregulating proteins called SOCS (Suppressors of Cytokine Signaling), which directly inhibit the JAK-STAT pathway.
[*]The Result: The liver becomes deaf to the GH signal. Despite high levels of GH in the blood (as estrogen also stimulates GH secretion), the production of IGF-1, IGFBP-3, and ALS is significantly blunted. The circulating reservoir is small and unstable.

[/LIST]
[/LIST]
[/LIST]

[LIST]
[*]In the Liver: Insulin is permissive. It is absolutely required for the GH-induced expression of the IGF1 gene. The GH signal (JAK2-STAT5) provides the "on" switch, but insulin (via the IRS/PI3K pathway) provides the necessary "co-stimulation" and energy/substrates for the massive protein synthesis required to make IGF-1. Without insulin, the switch doesn't work.
[*]In Muscle: Muscle tissue can produce IGF-1 locally (this is called "mechano-growth factor" or MGF). This production is stimulated by mechanical stretch and damage. Insulin's role here is more supportive—it enhances nutrient delivery and anabolic signaling (via Akt/mTOR) to maximize the effect of this locally produced IGF-1. It is less of a strict requirement than in the liver but still a powerful amplifier.

[/LIST]



^For anyone interested

I recently had my igfbp-3 tested and it is like .03 or some low ass number… and with a fatty liver and low e2…

 

[Ghoul]

I recently had my igfbp-3 tested and it is like .03 or some low ass number… and with a fatty liver and low e2…

Fatty liver can drop IGF by 10-40% depending on how much fat is there. All the GLPs clear fatty liver pretty quick.

 

[Darealme83]

Man you got it backwards, gh + high e2 = more igf production from the liver. You want your e2 as high as possible without side effects to max out the igf from your gh. You use test to bring up your e2 to whatever level that is then you don’t use more test.

Todd lee has this proven by bloodwork not your bro science without proofs.

With all due respect, Dr Todd Lee is a joke.

 

[Freeboomboom]

In the spirit of fairness. I did a deep dive into the concept of "Estrogen=gains on GH" presented in Todd Lee's video.

There was something to be learned from his claim, unfortunately he wasn't specific enough to make it useful, leaving the (wrong) impression high E2 was better for muscle growth via increased IGF.

It doesn't change much in the sense that:

1. We all know crashed estrogen is bad so I wouldn't expect anyone to try to do that to maximize IGF, and

2. You *STILL* want to keep E2 low to maximize IGF.

------

What I said about estrogen and IGF is correct. Lower e2 makes IGF go up. higher e2 makes it go down.

For simplicity's sake I'm using round numbers and when I say IGF it means IGF-1.

-90% of the body's IGF is produced in the liver. This systemic IGF is what we're measuring in blood tests.

-With the same level of GH, lower estrogen increases GH to IGF conversion in the liver, higher estrogen decreases it.

-10% of IGF is produced locally in muscle.

-IGF produced in muscle is responsible for 70% of muscle repair and growth, 30% from systemic (liver produced) IGF.

-Insulin is the signal hormone that makes muscle convert GH to IGF.

-Higher estrogen increases muscle sensitivity to this insulin signaling.

-If estrogen is too low, GH conversion to IGF in muscle is impaired, so there's less muscle growth and repair. Higher estrogen increases muscle GH to IGF conversion so there's more growth and repair.

----------

But here's the key he doesn't mention:

*Muscle sensitivity to insulin signaling maxes out at an E2 of around 20-35 pg/ml, mid normal range.*

If E2 is above this range, you're not getting any more IGF conversion in muscle, but you are increasing the inhibition of GH to IGF conversion in the liver, lowering systemic IGF, reducing the amount of muscle growth.

--------------

So what all this means is:

Too low E2: good for liver IGF but bad for muscle IGF → impaired muscle growth/ repair.

Too high E2: no extra benefit in muscle IGF and lowers systemic IGF → impaired muscle growth/ repair.

Mid-normal E2 (~20–35 pg/mL): maximizes liver and muscle IGF for optimal growth/recovery.

Bloodwork prove that his max gh to igf conversion is with 100 e2. If i remember correctly thats about 100mg test e a day for him.

With 80 e2 igf was lower

With 60 e2 igf was even lower

With 40 e2 igf was even even lower.

Real life example with bloodwork and proof beat any bro science imo.


View: https://youtu.be/UhdJvVe0SV0?si=sw2LChHDxrVkyl2-


Explained in this video.

 

[deadbeef]

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

Acromegaly is a rare disease with several systemic complications that may lead to increased overall morbidity and mortality. Despite several available treatments, ranging from transsphenoidal resection of GH-producing adenomas to different medical ...

pmc.ncbi.nlm.nih.gov

You are making your conclusion from this study because it says exogenous oral estrogen suppresses IGF-1. However, from your study:

the influence of estrogen on the GH-IGF1 axis depends on the route of administration. Hence, transdermal administration is not thought to reduce circulating IGF1 due to the lack of a hepatic first-pass effect.

Estrogen from aromatization does not make a hepatic first-pass. If what your study says is true, it should not suppress IGF-1. And then there is this study that corroborates it:

In summary, testosterone and estradiol have differential effects on GH secretory dynamics and aromatization of testosterone is essential in increasing serum IGF-1 levels.

Conclusions​

In older men, testosterone increases GH pulse frequency while the aromatization to estradiol is involved in the rise of IGF-1 levels.

Effects of transdermal testosterone gel or an aromatase inhibitor on serum concentration and pulsatility of growth hormone in older men with age-related low testosterone - PMC

Growth hormone is the major regulator of growth and body composition. Pulsatile GH secretion declines exponentially with age. Testosterone replacement is being increasingly offered to older men with age-related low testosterone. Testosterone ...

pmc.ncbi.nlm.nih.gov

I generally think Todd Lee is a moron so it pains me to defend him. But in this instance, he appears to be correct.

 

[Freeboomboom]

You are making your conclusion from this study because it says exogenous oral estrogen suppresses IGF-1. However, from your study:



Estrogen from aromatization does not make a hepatic first-pass. If what your study says is true, it should not suppress IGF-1. And then there is this study that corroborates it:

Effects of transdermal testosterone gel or an aromatase inhibitor on serum concentration and pulsatility of growth hormone in older men with age-related low testosterone - PMC

Growth hormone is the major regulator of growth and body composition. Pulsatile GH secretion declines exponentially with age. Testosterone replacement is being increasingly offered to older men with age-related low testosterone. Testosterone ...

pmc.ncbi.nlm.nih.gov

I generally think Todd Lee is a moron so it pains me to defend him. But in this instance, he appears to be correct.

Yes he is a moron but he is still correct.

Ghoul is sadly very wrong and probably won’t accept it.

There is studies saying oral e2 can lower igf but thats another thing.

Why do teenagers have higher igf? Why do trt patients have higher igf?

Because higher test = higher e2 = higher igf.

 

[Stealth500]

There is studies saying oral e2 can lower igf but thats another thing.

Effects of oral e2 are well documented because of all the women on birth control.

 

[ShutUpAndPump]

@Ghoul what about prolactin and igf-1?

 

[Freeboomboom]

@Ghoul what about prolactin and igf-1?

He is most likely not a guy to take any advice from or listen to. Think he knows it all.

 

[ShutUpAndPump]

He is most likely not a guy to take any advice from or listen to. Think he knows it all.

In this circumstance he is right, e2 increases hgh, but neutral-antagonistic effect on igf-1.
If taken orally e2 reduces igf-1.
@Ghoul is talking about e2 effect on igf-1 with exogenous hgh, meanwhile Todd Lee is talking about his experience with e2 without exogenous hgh.