Women and GH: dosages, effects of estradiol, IGFBP-1

[Type-IIx]

I am interested in knowing how GH worsens hypothyroidism?

I heard that GH improves conversion of T4 into T3, which in theory, would improve hypothyroidsm.

GH increases peripheral conversion of T4 to T3: this is a derangement in thyroid function, and is only considered an "improvement" by bodybuilders who consider crunk T3 numbers "improvement."

What we see in patients with central hypothyroidism given rhGH is a diminished GH response (only a miniscule increase in serum IGF-I) and diminished peak GH <3 μg/L (>2x that of normal subjects) in response to provocative stimuli. But what seems to be the primary determinant in thyroid function derangement is the nature of the underlying pathology, consistent with this, central hypothyroidism was more common in patients receiving rhGH if they had structural pituitary abnormalities on MRI.

 

[nothuman]

GH increases peripheral conversion of T4 to T3: this is a derangement in thyroid function, and is only considered an "improvement" by bodybuilders who consider crunk T3 numbers "improvement."

What we see in patients with central hypothyroidism given rhGH is a diminished GH response (only a miniscule increase in serum IGF-I) and diminished peak GH <3 μg/L (>2x that of normal subjects) in response to provocative stimuli. But what seems to be the primary determinant in thyroid function derangement is the nature of the underlying pathology, consistent with this, central hypothyroidism was more common in patients receiving rhGH if they had structural pituitary abnormalities on MRI.

Are the negative effects permanent? I used heavy doses of HGH in my stupid days 2011-2014 and I have been euthyroid for years. Low FT3 and high RT3 with normal TSH and FT4

(I know this is a woman thread but I just hijacked it, sorry)

 

[Type-IIx]

Are the negative effects permanent? I used heavy doses of HGH in my stupid days 2011-2014 and I have been euthyroid for years. Low FT3 and high RT3 with normal TSH and FT4

(I know this is a woman thread but I just hijacked it, sorry)

Euthyroid just means normal or healthy thyroid. There's no evidence that the effects of rhGH are permanent, mostly the evidence shows that growth response is diminished with central hypothyroidism especially when there are other problems with the hypothalamo-pituitary-thyroid axis that can be observed on MRI.

 

[bigzzz]

@Type-IIx so if a woman doesn't take pregnancy protection(exo estrogen), the GH will work better?

 

[Type-IIx]

@Type-IIx so if a woman doesn't take pregnancy protection(exo estrogen), the GH will work better?

Correct.

 

[g.r.o.w.t.h.]

The wife ran 5iu throughout prep this year. Definitely a difference from 2iu in previous preps. She is also hypothyroid and takes exogenous t4 and t3. Earned her pro card this year. I’m not sure what correlates to what in this thread, but thought I would share.

 

[Type-IIx]

The wife ran 5iu throughout prep this year. Definitely a difference from 2iu in previous preps. She is also hypothyroid and takes exogenous t4 and t3. Earned her pro card this year. I’m not sure what correlates to what in this thread, but thought I would share.

That rhGH still works, albeit with reduced tolerability than for your wife's multiverse version where she has a healthy thyroid, and far less effectively than for a man of the same body size.

 

[Doitagain]

That rhGH still works, albeit with reduced tolerability than for your wife's multiverse version where she has a healthy thyroid, and far less effectively than for a man of the same body size.

Do you think women could benefit from Indole-3-carbinol supplementation (by means of altered 2hydroxyestrone/16-hydroxyestrone) in regard to IGF-1 synthesis?

 

[Doitagain]

Do you think women could benefit from Indole-3-carbinol supplementation (by means of altered 2hydroxyestrone/16-hydroxyestrone) in regard to IGF-1 synthesis?

P.s.: High levels of 16-hydroxyestrone are also associated with hypothyroidism, to make the whole picture even more complex...

 

[Type-IIx]

Do you think women could benefit from Indole-3-carbinol supplementation (by means of altered 2hydroxyestrone/16-hydroxyestrone) in regard to IGF-1 synthesis?

No, I don't think so (albeit I haven't delved into the matter), because GH's augmenting IGF-I is due to GH-responsive liver somatotrophs rather than acting by any of I3C's pathways insofar as I understand them. I3C increases 2OHE1:16αOHE1 by shunting metabolism of E2 towards 2OHE. I don't see how this implicates GH action.

If your argument is that, perhaps, there is a benefit to selecting I3C as a contraceptive (the reason for exogenous estrogen use), my response is that it is not one, right?

 

[Type-IIx]

No, I don't think so (albeit I haven't delved into the matter), because GH's augmenting IGF-I is due to GH-responsive liver somatotrophs rather than acting by any of I3C's pathways insofar as I understand them. I3C increases 2OHE1:16αOHE1 by shunting metabolism of E2 towards 2OHE. I don't see how this implicates GH action.

If your argument is that, perhaps, there is a benefit to selecting I3C as a contraceptive (the reason for exogenous estrogen use), my response is that it is not one, right?

The term "argument" may be inappropriate: idea, thinking, reasoning, et cetera is more appropriate here.

 

[Doitagain]

No, I don't think so (albeit I haven't delved into the matter), because GH's augmenting IGF-I is due to GH-responsive liver somatotrophs rather than acting by any of I3C's pathways insofar as I understand them. I3C increases 2OHE1:16αOHE1 by shunting metabolism of E2 towards 2OHE. I don't see how this implicates GH action.

If your argument is that, perhaps, there is a benefit to selecting I3C as a contraceptive (the reason for exogenous estrogen use), my response is that it is not one, right?

I was merely wondering wheter hijacking E2 metabolism towards weaker metabolites (without affecting the aromatization process in itself) could have a favorable outcome on lGF-1 synthesis in the liver.

 

[Hyper-T]

I think the discrepancy here is that in a real world situation there are virtually no women taking hgh for performance enhancement that aren't also taking gear. Often an oral like anavar or winny and thus there estrogen profile will be very different and thus the way hgh effects igf-1 in a patient or study subject is going to be different than a competitor in figure or bodybuilding etc.

 

[SteroidFreaks.is]

The wife ran 5iu throughout prep this year. Definitely a difference from 2iu in previous preps. She is also hypothyroid and takes exogenous t4 and t3. Earned her pro card this year. I’m not sure what correlates to what in this thread, but thought I would share.

Congrats to her and thanks for all the interesting info in this thread.

 

[Type-IIx]

I was merely wondering wheter hijacking E2 metabolism towards weaker metabolites (without affecting the aromatization process in itself) could have a favorable outcome on lGF-1 synthesis in the liver.

That's reasonable bro, especially because of the widespread confusion about estrogens & their attenuated link or association to IGF-I.

I've written elsewhere about the phenomenon of aromatization per se being what increases IGF-I, whereas estrogens (e.g., E2) actually negatively feed back. That is to say, while the process of aromatization – (3 steps, completed by cleavage of the bond between C10 and C19 to yield formic acid and the aromatized A-ring product with loss of the hydrogen atoms at the 1β and 2β positions) – increases IGF-I, its aromatic products (estrogens) reduce IGF-I. What this results in is a sort of parabolic shape to the aromatizing androgen (e.g., Test, Deca, MENT, Dbol, Methyltest, etc.) dose/IGF-I curve with an inflection point where blood concentrations of the aromatic product (e.g., E2) start to become high.

Here are some links where I discuss this:

https://www.professionalmuscle.com/forums/index.php?threads/trenbolone-and-igf1-levels-blood-tests.166733/post-3040740

https://www.professionalmuscle.com/forums/index.php?goto/post&id=3082951

https://www.professionalmuscle.com/...-dosages-effects-of-estradiol-igfbp-1.169919/ (the title post of this thread), specifically, the concepts demonstrating that estrogens increase IGFBP-1, reducing IGF-I bioavailability and unleashing GH secretion by feedback withdrawal. Hence, women have higher GH levels than men by body surface area and are less sensitive per-mg to rhGH.

 

[Type-IIx]

That's reasonable bro, especially because of the widespread confusion about estrogens & their attenuated link or association to IGF-I.

I've written elsewhere about the phenomenon of aromatization per se being what increases IGF-I, whereas estrogens (e.g., E2) actually negatively feed back. That is to say, while the process of aromatization – (3 steps, completed by cleavage of the bond between C10 and C19 to yield formic acid and the aromatized A-ring product with loss of the hydrogen atoms at the 1β and 2β positions) – increases IGF-I, its aromatic products (estrogens) reduce IGF-I. What this results in is a sort of parabolic shape to the aromatizing androgen (e.g., Test, Deca, MENT, Dbol, Methyltest, etc.) dose/IGF-I curve with an inflection point where blood concentrations of the aromatic product (e.g., E2) start to become high.

Here are some links where I discuss this:

https://www.professionalmuscle.com/forums/index.php?threads/trenbolone-and-igf1-levels-blood-tests.166733/post-3040740

https://www.professionalmuscle.com/forums/index.php?goto/post&id=3082951

https://www.professionalmuscle.com/...-dosages-effects-of-estradiol-igfbp-1.169919/ (the title post of this thread), specifically, the concepts demonstrating that estrogens increase IGFBP-1, reducing IGF-I bioavailability and unleashing GH secretion by feedback withdrawal. Hence, women have higher GH levels than men by body surface area and are less sensitive per-mg to rhGH.

@Doitagain

Basically, I cannot rule out that I3C, by increasing relative proportions of "good" vs. "bad" estrogens, benefits or hinders IGF-I. It's not something there's any data about. If I had to surmise, I would think that since the judgment of "good" vs. "bad" applies to breast cancer risks, and IGF-I is actually positively associated with mutagenesis in cancer, it could be the opposite – that "bad" estrogens increase IGF-I > "good" ones.

In any case, though, GH's increasing IGF-I does not implicate estrogen pathways.

It would be a separate drug effect altogether, this I3C intervention.

 

[Doitagain]

@Doitagain

Basically, I cannot rule out that I3C, by increasing relative proportions of "good" vs. "bad" estrogens, benefits or hinders IGF-I. It's not something there's any data about. If I had to surmise, I would think that since the judgment of "good" vs. "bad" applies to breast cancer risks, and IGF-I is actually positively associated with mutagenesis in cancer, it could be the opposite – that "bad" estrogens increase IGF-I > "good" ones.

In any case, though, GH's increasing IGF-I does not implicate estrogen pathways.

It would be a separate drug effect altogether, this I3C intervention.

I totally remember where you mentioned that while the process of aromatization increases IGF-I, its aromatic products reduce it. Hence my question about I-3-C actually. Aromatase activity left unchanged but weaker estrogens being formed. Sorry if I worded it in a confusing manner in my previous post.
I know that no study looked specifically into this matter, just "reasonable speculation".

 

[Parabolic33]

It’s possible that serum Igf1 matters almost nothing. In the same way that fT3 levels and crushed t4 levels isn’t optimal.

Having done so much bloodwork on guys taking tren and hgh now, their igf1 levels max ceiling becomes massively lowered while taking trenbolone. But I don’t think anyone has accused tren of making hgh less effective. If anything there is synergy here.


Basically this topic is one of the more primitive topics that’s understood imo. I don’t think anyone knows how this works right now. You get weird results too with certain animals not responding to igf1 itself in the lacking presents of gh and igfbp3. While others like rats do. It’s just convoluted af. Not to be a bummer. Maybe when muscle biopsy becomes an option for us to do on ourself we’ll figure it out.

 

[Type-IIx]

It’s possible that serum Igf1 matters almost nothing. In the same way that fT3 levels and crushed t4 levels isn’t optimal.

No it's not possible.

What is the analogy between serum IGF-I & thyroid function that you are trying to make? Please explain.

Having done so much bloodwork on guys taking tren and hgh now, their igf1 levels max ceiling becomes massively lowered while taking trenbolone. But I don’t think anyone has accused tren of making hgh less effective. If anything there is synergy here.

Right, there is synergy. Because trenbolone increases muscle satellite cell responsiveness to autocrine/paracrine IGF-I, doing more with less. Do you happen to know to whom this idea of rhGH & trenbolone synergy came from, by chance? Did you happen upon that theory all by your lonesome bro?

Trenbolone decreases endogenous (i.e., natural) GH secretion (i.e., pulse amplitude & duration).

So rhGH replaces that; and the muscle cells exert a "pull" on circulating IGF-I (cIGF-I), that is converted in the muscle cell to autocrine/paracrine IGF-IEa.

IGF-IEc is the mechanosensitive isoform ("MGF"), the activity of which is increased my resistance training (i.e., single fibre muscle tension).

Then, Testosterone + Trenbolone + RhGH + Resistance Training are synergistic (greater than additive; 1 + 1 > 2) in their increases to muscle & total body size.

Basically this topic is one of the more primitive topics that’s understood imo. I don’t think anyone knows how this works right now. You get weird results too with certain animals not responding to igf1 itself in the lacking presents of gh and igfbp3. While others like rats do. It’s just convoluted af. Not to be a bummer. Maybe when muscle biopsy becomes an option for us to do on ourself we’ll figure it out.

There's a pretty good theory about how this works.

I just gave it to ya in a very high level form. You're welcome.

 

[bg65]

Apologies in advance if this is a dumb question, I'm trying to even word it in a non-dumbass way... and please redirect me if answered on another thread...

Can this study (you started the thread with) be applied to males taking highly aromatizable compounds? And if so, would the effect be moreso related to the total E level or the ratio of E:T?
Like if E levels were high and the ratio was also out of whack, would that male bodybuilder require more GH, like a female would?
If E levels were high but the ratio to androgens was appropriate would that be a different result in GH response?
Thanks