[EllaC]

Somatostatin inhibits oral estradiol, prolactin, growth hormone and stomach gastrin  Somatostatin also stimulates insulin, which has deleterious effects to breast growth. So, the new goal needs to inhibit somatostatin. Somatostatin also inhibits the cAMP/PKA/CREB pathway...which is the breast growth pathway. 

Bringing this into focus. A few years ago I posted some information (shared below) regarding cimetidine and how it inhibits stomach gastrin and thereby increases estradiol. Cimetidine and H2 inhibitors aren't the only game in town that inhibits gastrin. Forskolin and aloe vera and some other agents inhibit gastrin. Explaining what somatostatin does is explained in the link below. Trust me when I say somatostatin is about as bad for breast growth as DHT. In closing, inhibiting somatostatin seems to up our game for promoting breast growth. One final note about forskolin, it improves thyroid function, so much so in my case it reversed my hashimoto's of 15 years.

Men have more stomach acid than women, which is why they can produce a bigger pool uptake of estrogen. But if women relax stomach gastrin (or inhibit it) a larger amount of E2 is synthesized in gastric parietal cells.


Estrogen relaxes gastric muscle cells via a nitric oxide‑ and cyclic guanosine monophosphate‑dependent mechanism: A sex‑associated differential effect

In conclusion, estrogen relaxes GSMCs via an NO/cGMP‑dependent mechanism, and the reduced contraction in GSMCs from females by estrogen may be associated with the sex‑associated increased expression of ERα and ERβ, and greater production of NO and cGMP, compared with that in GSMCs from males.
https://www.spandidos-publications.com/etm/16/3/1685


Estrogen and estrogen receptors in the modulation of gastrointestinal epithelial secretion

Ueyama et al. reported that E2 levels in the portal vein were much higher than those in arterial blood, and that the main estrogen was determined as E2 with gas chromatography [18]. They also showed the presence of estrogen synthetase, aromatase or cytochrome P450arom in gastric parietal cells. Gastric E2 is synthesized from progesterone via androstenedione and testosterone by enzyme reactions of 17α-hydroxylase (EC: 4.1.2.30), 17β-hydroxysteroid dehydrogenase type 3 (EC: 1.1.1.62) and aromatase (EC: 1.14.14.1), respectively [19]. Thus, a relatively large amount of E2 is synthesized in gastric parietal cells.

https://www.ncbi.nlm.nih.gov/pmc/article...po=10.7143



Somatostatin 
http://www.vivo.colostate.edu/hbooks/pat...tatin.html

Using H2 Blockers (H2-receptor antagonists) and to a lesser extent H1 receptors antagonists block stomach acid (aka. gastrin) increase plasma estradiol and prolactin.  Drugs like cimetidine and ranitidine (others too) inhibit stomach acid, though ranitidine to a lesser extent nukes the cytochrome (CYP) P450 enzymes. Cimetidine is for a short time (I believe 2-4weeks) to treat stomach acid. If you have normal stomach acid cimetidine and the like aren't necessary, as always consult a health professional.

https://www.breastnexum.com/showthread.php?tid=17436&pid=196127&highlight=cimetidine#pid196127
Post # 3990..

This study demonstrates that the administration of cimetidine to men decreases the 2-hydroxylation of estradiol and results in an increase in the serum estradiol concentration.

The Effects of Cimetidine on the Oxidative Metabolism of Estradiol
https://www.researchgate.net/publication..._Estradiol

In English xxxx how do we replicate in layman’s terms  xxx. (Love ya!!)