Why/how is gynecomastia an HGH side effect?

[Deep_Fried]

So an easy way to prevent this would be say.... cabergoline correct?
Or would this have a negative effect on the growth hormone...?

Im just happy as hell i don't have gyno issues... especially with hgh

Dopamine Agonists (Cabergoline, Bromocriptine) will do nothing for HGH binding to prolactin receptors. Neither will taking supps (B6, Ldopa, etc) that support dopamine production.

If you think about it, it will make more sense.

We use Dopaminergeric drugs/supps, because dopamine directly regulates pituitary prolactin output, primarily via the D2 receptor.
So, all these drugs/supps will lower the natural production of prolactin which is great if you have levels to be concerned about.

HGH, however, WILL STILL bind to PRL receptors even if you suppress endogenous Prolactin completely.

So, the issue is NOT prolactin per say. It is the fact that HGH BINDS to prolactin receptors additionally to naturally secreted prolactin.

No amounts of Dopamine or agonists will alter this fact.

The only positive I can see from regulating Dopamine is that it may lower endogenous prolactin significantly enough, to make up for the additional HGH/Prolactin receptor binding, thus lowering the combined additive effect of both HGH and PRL.

IMO, unless you are really sensitive to PRL, or your PRL levels are significantly raised ON TOP of large doses of HGH, I would not be so concerned with respect to HGH agonism of PRL receptors.

[hit_my_max]

Has anyone actually had this problem and reported it? How common is this? Should one consider taking Anastrozole with HGH to prevent it/be on the safe side?

[Swifto]

Dopamine Agonists (Cabergoline, Bromocriptine) will do nothing for HGH binding to prolactin receptors. Neither will taking supps (B6, Ldopa, etc) that support dopamine production.

If you think about it, it will make more sense.

We use Dopaminergeric drugs/supps, because dopamine directly regulates pituitary prolactin output, primarily via the D2 receptor.
So, all these drugs/supps will lower the natural production of prolactin which is great if you have levels to be concerned about.

HGH, however, WILL STILL bind to PRL receptors even if you suppress endogenous Prolactin completely.

So, the issue is NOT prolactin per say. It is the fact that HGH BINDS to prolactin receptors additionally to naturally secreted prolactin.

No amounts of Dopamine or agonists will alter this fact.

The only positive I can see from regulating Dopamine is that it may lower endogenous prolactin significantly enough, to make up for the additional HGH/Prolactin receptor binding, thus lowering the combined additive effect of both HGH and PRL.

IMO, unless you are really sensitive to PRL, or your PRL levels are significantly raised ON TOP of large doses of HGH, I would not be so concerned with respect to HGH agonism of PRL receptors.

You got any studies that state GH binds to the PRL?

[Deep_Fried]

You got any studies that state GH binds to the PRL?

Yes, tons.

This is quite common knowledge in this field. If you are interested please look into information regarding 22Kda Growth Hormone Isoform and PRL-R dimerization.

22Kda HGH is the monomer of HGH that is synthesized as the single isoform for use in pharmaceutical HGH preparations. (the EXO HGH you all use from pharma to generics is ONLY composed of 22Kda HGH)
The thing most people do not realize is that this single isoform is not the the only one our bodies produce and utilize. Our bodies produce a multitude of various isoforms and fragments as a pool of HGH isoforms containing 22Kda and 20Kda monomers, various dimers, trimers, tetramers all the way to 45Kda pentamers, not to mention numerous fragments around 5Kda.

The 22Kda (synthetic HGH) and the 20Kda isoforms both have similar structure to prolactin, which is in effect a "cousin" to HGH as they belong to the same superclass of cytokines.

22KDa (synthetic HGH) has a much greater binding affinity than 20Kda and other various HGH isoforms that would notmally be produced endogenously via the pituitary rather than the single 22Kda isoform delivered exogenously.

This is interesting and likely accounts for many of the noted side effects that people experience on HGH therapy. As we tip the balance in the body towards an unnatural ratio of 22Kda vs other isoforms, we also increase the propensity for increased Prolactin receptor agonism which curiously is responsible for more than the straight forward lactogenic effects we are most familiar with on mammary tissue.

The diabetogenic effect of HGH and proposed impact on systems affecting water retention (RRAS, ENaC) may be mediated at least partially via an increased affinity for the Prolactin receptor.

For instance with regards to HGH side effects re: hyperinsulinemia..
22Kda HGH enhances Pancreatic Beta Cell proliferation and insulin secretion which is surprisingly mediated via agonism of local Beta Cell Prolactin receptors (PRL-r), NOT via HGH receptors(HGH-r).

Anyhow, I digress with my interest, which is probably quite boring for many.

Here are some study snippets highliting the answers to your original quetion

Cells treated with human growth hormone (hGH), which binds and activates the hPRL receptor, exhibited bell-shaped dose-response growth curves consistent with the sequential dimerization mechanism proposed for the hPRL receptor (Fuh, G., Colosi, P., Wood, W.I., and Wells, J.A. (1993) J. Biol. Chem. 268, 5376-5381).

Prolactin (PRL) and GH have two distinct binding sites (site 1 with high affinity; site 2 with low affinity) that each interact with a PRL receptor (PRLR) to form a functional receptor dimer that activates signal transduction. (Langenheim JF, Tan D, Walker AM, Chen WY Department of Biological Sciences, Clemson University, Clemson, SC 29634-0326, USA.
Mol. Endocrinol. 2006)

The fourth helix (helix 4) in the human growth hormone (hGH) molecule plays a role in binding to the GH receptor as well as the PRL receptor through topologically different amino acids. (Kato Y, Maruyama O, Chung HO, Tomizawa K, Kato T Biosignal Research Center, Gunma University, Japan.Biochem. Biophys. Res. Commun. (1996)

Previously we have demonstrated that 20-kDa human GH (20K-hGH) is a full agonist for hGH receptor (hGHR) even though its complex formation with hGHR and hGH-binding protein differs from that of 22-kDa human GH (22K-hGH). In this study, we focused on the effect of 20K-hGH on human PRL receptor (hPRLR) (Tsunekawa B, Wada M, Ikeda M, Uchida H, Naito N, Honjo M Life Sciences Laboratory, Performance Materials R&D Center, Mitsui Chemicals, Inc., Chiba, Japan. Endocrinology (1999)