Why Trenbolone lower Igf-1

[Chips7]

Hello guys.

We need to fix this subject.

studies show that trenbolone increases igf-1 in our cells.

on wikipedia you can read:

"Trenbolone acetate has the capability to produce insulin-like growth factor-1 (IGF-1).[28][29] This naturally produced protein-based hormone affects every cell in the body of an organism and plays a large role in muscle recovery and rejuvenation. Extreme muscle growth and cell splitting compared is facilitated through trenbolone acetate administration when compared to other AAS"

so why does trenbolone destroy our Igf-1 on blood tests?

@Type-IIx @Palifter
@Mac11wildcat

 

[Palifter]

From @Type-IIx himself:

“Tren lowers systemic/liver IGF-I (because it reduces natural GH release and does the next thing):
but tren dramatically INCREASES the actual muscle's response to that systemic IGF-I (it does this by making more efficient use of that IGF-I as a precursor for special subtypes of IGF-I that exist inside the muscle)
so, though tren lowers natural (endogenous) GH levels, if we force that GH into the body, it'll still increase that systemic IGF-I floating around and allow for more opportunities when that IGF-I that's floating around comes into contact with muscles to increase the muscle's growth.

Even if bloodwork for serum IGF-I is "low," on tren, be sure that tren is making better use of the IGF-I inside the muscles.”

 

[Chips7]

From @Type-IIx himself:

“Tren lowers systemic/liver IGF-I (because it reduces natural GH release and does the next thing):
but tren dramatically INCREASES the actual muscle's response to that systemic IGF-I (it does this by making more efficient use of that IGF-I as a precursor for special subtypes of IGF-I that exist inside the muscle)
so, though tren lowers natural (endogenous) GH levels, if we force that GH into the body, it'll still increase that systemic IGF-I floating around and allow for more opportunities when that IGF-I that's floating around comes into contact with muscles to increase the muscle's growth.

Even if bloodwork for serum IGF-I is "low," on tren, be sure that tren is making better use of the IGF-I inside the muscles.”

Thanks man, that's exactly what i was looking for.

The effect of tren to transfer IGF-1 more optimally in the muscle, does it also work with the bones?

 

[Ridethelightningbarefoot]

According to the cattle studies tren especially works well in this regard with estrogen.

 

[Jackedjack]

I guess this is the reason why Tren feels working better after some time spent on hgh and test.

Tren have supressed my igf to 130 with hgh 6-8iu per day and 100mg tren per day.

 

[29trt]

I guess this is the reason why Tren feels working better after some time spent on hgh and test.

Tren have supressed my igf to 130 with hgh 6-8iu per day and 100mg tren per day.

Wait, are you saying that on 6-8ui hgh your Igf was 130?
It was just said that tren lowers endogenous GH and hence Igf but if blasting GH how can tren lower IGF??

 

[Jackedjack]

Wait, are you saying that on 6-8ui hgh your Igf was 130?
It was just said that tren lowers endogenous GH and hence Igf but if blasting GH how can tren lower IGF??

I dont know how it works. But seems im not the only one who has seen reduced igf1 on hgh cycle with tren.

 

[29trt]

I dont know how it works. But seems im not the only one who has seen reduced igf1 on hgh cycle with tren.

perhaps the circulating igf is lower because tren makes the muscles more receptive to igf and it is consumed... idk if that is how it works...

 

[bluzzer]

@Type-IIx could you explain please ?

perhaps the circulating igf is lower because tren makes the muscles more receptive to igf and it is consumed... idk if that is how it works...

 

[Type-IIx]

@Type-IIx could you explain please ?

There's perhaps a negative feedback loop at play involving myokine activity, but it's speculative. There is an active effort by researchers to better understand myokine signaling and cross-talk with other body systems.

It's clear that the reduced GH (probably in line with what's seen in ruminant, a reduction in its pulse amplitude and pulse duration) is a driving factor and that intracrine/paracrine activity of mIGF-I and its isoforms do still drive a lot of Tren's tissue-specific anabolic effects.

 

[Type-IIx]

According to the cattle studies tren especially works well in this regard with estrogen.

But exogenous E2 does not increase IGFBP-1 (reducing IGF-I bioavailability) in steers and ruminants, whereas it does do so in man.

 

[Ridethelightningbarefoot]

But exogenous E2 does not increase IGFBP-1 (reducing IGF-I bioavailability) in steers and ruminants, whereas it does do so in man.

I dont understand

 

[VikingDub]

There's perhaps a negative feedback loop at play involving myokine activity, but it's speculative. There is an active effort by researchers to better understand myokine signaling and cross-talk with other body systems.

It's clear that the reduced GH (probably in line with what's seen in ruminant, a reduction in its pulse amplitude and pulse duration) is a driving factor and that intracrine/paracrine activity of mIGF-I and its isoforms do still drive a lot of Tren's tissue-specific anabolic effects.

@Type-IIx I read some of your previous posts on this subject and have a couple questions.

If I understand correctly, tren increases local mIGF-I expression and this, combined with tren's ability to enhance glucose metabolism signals to the system/liver to reduce cIGF-I production. Is the reduction to cIGF-I minimized by exogenous rhGH?

Tren increasing mIGF-I expression would have an anabolic effect in muscle, improving hypertrophy and benefiting a person in a growth phase. What about during a cut? Does the reduction in cIGF-I reduce lipolysis normally seen when using rhGH without tren?

 

[Megadick3000]

What about during a cut? Does the reduction in cIGF-I reduce lipolysis normally seen when using rhGH without tren?

From my understanding, and Type 2 is welcome to correct me, lipolysis (and perhaps more so, inhibition of lipogenesis) associated with exogenous rhGH use is directly from GH itself, not from IGF-1.

GH itself, or some splice variant of GH is what primarily exerts lipolytic effects. Whereas anabolic effects seem more mediated by IGF-1.

So with that in mind, even if tren directly reduced IGF-1 it would be less relevant as it pertains to lipolysis, unless tren was somehow inhibiting exogenous rhGH through some mechanism.

 

[VikingDub]

From my understanding, and Type 2 is welcome to correct me, lipolysis (and perhaps more so, inhibition of lipogenesis) associated with exogenous rhGH use is directly from GH itself, not from IGF-1.

GH itself, or some splice variant of GH is what primarily exerts lipolytic effects. Whereas anabolic effects seem more mediated by IGF-1.

So with that in mind, even if tren directly reduced IGF-1 it would be less relevant as it pertains to lipolysis, unless tren was somehow inhibiting exogenous rhGH through some mechanism.

Thanks, that makes sense.

I assume fat loss would be enhanced running both rhGH and tren in a calorie deficit. Lipolytic effects of rhGH + tren's affinity to bind to AR in adipose tissue = greater opportunity for fat loss.

If tren enhances glucose metabolism, I wonder if it would mediate some of the potential for increased BG while using moderate doses of rhGH?

 

[Megadick3000]

Thanks, that makes sense.

I assume fat loss would be enhanced running both rhGH and tren in a calorie deficit. Lipolytic effects of rhGH + tren's affinity to bind to AR in adipose tissue = greater opportunity for fat loss.

If tren enhances glucose metabolism, I wonder if it would mediate some of the potential for increased BG while using moderate doses of rhGH?

Im not super knowledgeable on tren, but oxandrolone has ample science supporting its rather uncommon property of reducing, particularly, abdominal fat. Why/how oxandrolone is so effective at doing so relative to other AAS i cannot explain, but the combination of rhGH plus oxandrolone would be a fantastic cutting combination. Pepper in some albuterol and dandelion extract (a decently effective diuretic that replenishes potassium rather than depletes) and youd get dry, cut, and hard, assuming of course you followed a suitable diet.

Would tren be a superior alternative vs oxandrolone? Maybe? But side effects would be worse, thats for sure.

As for controlling BG, metformin is still your best bet, its generally well tolerated and dirt cheap.

 

[Jbagel132]

Currently on medication that blocks IGF-1R. Would running tren fuck with this?

 

[JuiceJohn]

I've read a study published in the Journal of Animal Science that found that trenbolone acetate decreased circulating IGF-1 concentrations in steers.

There are not enough studies on people yet.

Isn't it possible that other factors, such as dosage, duration of use, and individual physiology, can influence the effects of IGF-1?

 

[Type-IIx]

@Type-IIx I read some of your previous posts on this subject and have a couple questions.

If I understand correctly, tren increases local mIGF-I expression and this, combined with tren's ability to enhance glucose metabolism signals to the system/liver to reduce cIGF-I production. Is the reduction to cIGF-I minimized by exogenous rhGH?

Tren increasing mIGF-I expression would have an anabolic effect in muscle, improving hypertrophy and benefiting a person in a growth phase. What about during a cut? Does the reduction in cIGF-I reduce lipolysis normally seen when using rhGH without tren?

Sorry for only getting to this now, this is a well written question that I'd like to answer for you.

Megadick3000's reply is basically correct and is in line with the basic general effects of GH vs. IGF-I. Emphases on his "primarily," and "more" qualifiers.

Rather than viewing GH & IGF-I as two discrete hormones that are separate and sequential in action (this view is that of the very old and outmoded Somatomedin Hypothesis), the application of rhGH should always be viewed through a dual effector model of GH/IGF-I action. That is to say that their actions are complementary, with GH generally serving a catabolic (energy-releasing) function & IGF-I generally serving an influx function, in a sort of lockstep, to promote growth (and directing substrate metabolism in a manner that depends on food availability, etc.).

However, both GH and IGF-I promote lipolysis and lipid oxidation, albeit by different mechanisms; both IGF-I & GH enhance energy expenditure and reduce protein oxidation; and IGF-I abates (but does not fully reverse, unless exogenous rhIGF-I is applied) the insulin resistance induced by GH.

To your more interesting conclusion on the actions of rhGH & trenbolone, from post [#15], that:

[...] fat loss would be enhanced running both rhGH and tren in a calorie deficit. Lipolytic effects of rhGH + tren's affinity to bind to AR in adipose tissue = greater opportunity for fat loss.

[And so] If tren enhances glucose metabolism, I wonder if it would mediate some of the potential for increased BG while using moderate doses of rhGH?

I would answer in the affirmative. Though, do realize, that the caloric intake (extent of energy surplus) still dictates the extent of energy storage (energy, mass is conserved). Rather than violate this principle of thermodynamics, hormones direct which anabolic processes predominate (e.g., AA/protein synthesis over lipogenesis, etc.). Note that in a state of energy excess, GH serves to increase insulin action (demonstrating its contextual effects on substrate metabolism & action as an effector, not merely a sufficient condition to IGF-I's actions). Basically: you can still get fat fairly easily by eating too many calories, but you are correct that the effects of trenbolone & rhGH combine in this manner. The energy state of the cell (i.e., deficit) controls.

 

[VikingDub]

Sorry for only getting to this now, this is a well written question that I'd like to answer for you.

Megadick3000's reply is basically correct and is in line with the basic general effects of GH vs. IGF-I. Emphases on his "primarily," and "more" qualifiers.

Rather than viewing GH & IGF-I as two discrete hormones that are separate and sequential in action (this view is that of the very old and outmoded Somatomedin Hypothesis), the application of rhGH should always be viewed through a dual effector model of GH/IGF-I action. That is to say that their actions are complementary, with GH generally serving a catabolic (energy-releasing) function & IGF-I generally serving an influx function, in a sort of lockstep, to promote growth (and directing substrate metabolism in a manner that depends on food availability, etc.).

However, both GH and IGF-I promote lipolysis and lipid oxidation, albeit by different mechanisms; both IGF-I & GH enhance energy expenditure and reduce protein oxidation; and IGF-I abates (but does not fully reverse, unless exogenous rhIGF-I is applied) the insulin resistance induced by GH.

To your more interesting conclusion on the actions of rhGH & trenbolone, from post [#15], that:

I would answer in the affirmative. Though, do realize, that the caloric intake (extent of energy surplus) still dictates the extent of energy storage (energy, mass is conserved). Rather than violate this principle of thermodynamics, hormones direct which anabolic processes predominate (e.g., AA/protein synthesis over lipogenesis, etc.). Note that in a state of energy excess, GH serves to increase insulin action (demonstrating its contextual effects on substrate metabolism & action as an effector, not merely a sufficient condition to IGF-I's actions). Basically: you can still get fat fairly easily by eating too many calories, but you are correct that the effects of trenbolone & rhGH combine in this manner. The energy state of the cell (i.e., deficit) controls.

Thanks for taking the time to respond. Great information and explanation.