[Lotus]

Despite not being able to pursue much NBE i am still very much fascinated and inspired by your researches. <3

Thank you Alexis ? I wish I had more time to post research, I've uncovered some unique topics to discuss with everyone. Covid (omicron) decided to pay me a visit a few weeks ago. Strange, I've steered clear of covid19 for two years and just like that I got omicron. I'm still dealing with fatigue and some respiratory issues. But the fatigue is a pain, it robs me of any motivation I have. My symptoms were mild and lasted about 10 days. It also took about 3 weeks to regain my taste and smell. Anyways, a great way to start 2022.

So here's an important study that focused on the histology (biopsy specimens of breast tissue) of 14 MTF subjects, granted it's a small sample size, but nonetheless important findings. Here's a couple of examples: 

male-to-female transsexuals who had received estrogens and progestins for prolonged periods have breast tissue that histologically simulates that of the female, that is, with acinar and lobular formation. 

Cyproterone acetate is a progestative drug, whereas flutamide and bicalutamide are not, and progestative drugs are known to stimulate the formation of acini and lobules in females

Translation, progesterone and estradiol produce female breasts. Read the full study and you'll see that the individuals who stuck with progestative drugs (cyproterone) and estradiol had the best breast outcomes. Based on this information I decided to try my own variation by taking micronized progesterone and oral estradiol, and by golly the shit works. I haven't experienced a growth spurt in some years, needless to say I had that old feeling of sore breasts after trying the two together. I measured an inch or two of new growth, and it happened quickly. So, this lines up to what the study found in the breast biopsies.

For myself I'm on HRT. So, I've taken 100mg of micronized progesterone with 2-4mg of oral estradiol along with low dose aspirin. I think the key is finding what ratio of progestative drugs to oral estradiol works best for each individual.  Chemical castration is considered to be about 50 ng/dL of Total T (testosterone). In my opinion you can still have sexual function but you'll notice a substantial drop in semen production. Estradiol should be in the typical range of 200 pg/mL for breast growth and feminization. Anything above the T threshold will result in incomplete breast growth...or moobish looking. Notice bicalutamide is non progestative. 

An NBE version of this could be PM combined with something like wild yam. I like WY because it has diosgenin, and diosgenin blocks 16α-hydroxyestrone (16OH) which is the toxic form of estrogen and is carcinogenic. Enhancing the production of 2-OH form is beneficial for breast health. Diosgenin stimulates growth of mammary epithelium, increase in DNA content and the number of ducts & terminal end buds. I'm researching whether WY is a progestative compound though. 

I've tried rectal administration of progesterone, then sublingual (messy lol), buccal and nothing happened. I believe progesterone needs a liver activation, just like PM needs to pass through the liver to activate deoxymiroestrol. 

In past research I've learned there's more progesterone in glandular tissue and more prolactin in fat tissue. Progesterone stimulates fat deposition in breasts, but is catabolic to protein metabolism, meaning it burns fat too.

I believe prolactin needs to stimulated with the above methods too. More to follw


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The Science:

Short-Term and Long-Term Histologic Effects of Castration and Estrogen Treatment on Breast Tissue of 14 Male-to-Female Transsexuals in Comparison With Two Chemically Castrated Men

Kanhai, Robert C.J. M.D.; Hage, J. Joris M.D., Ph.D.; van Diest, Paul J. M.D., Ph.D.; Bloemena, Elisabeth M.D., Ph.D.; Mulder, J. Wiebe M.D., Ph.D.
Author Information
The American Journal of Surgical Pathology: January 2000 - Volume 24 - Issue 1 - p 74
FREE

Abstract
The histologic changes induced in the mammary gland of male-to-female transsexuals have not yet been reported in the literature. We studied the histologic changes induced by chemical and surgical castration and estrogen therapy in the breasts of 14 such patients, with particular reference to acinar and lobular formation. To objectify the influence of cross-sex treatment, the histologic findings were compared with those in two men treated hormonally for prostate cancer. The slight increase in the plasma estrogen-to-androgen ratio seen in idiopathic gynecomastia usually does not induce acinar and lobular formation in the male breast. In men treated with non progestative antiandrogens for prostate cancer, only moderate acinar and lobular formation occurs. Only in male-to-female transsexuals in whom progestative chemical castration is combined with feminizing estrogen therapy will full acinar and lobular formation occur with hormonally stimulated nuclei and pseudolactational changes. Hence, combined progestative antiandrogens and estrogens are necessary for genetically male breast tissue to mimic the natural histology of the female breast. Orchidectomy does not contribute to this. Apocrine metaplasia may occur in breasts of male-to-female transsexuals, but so far, only four cases of breast cancer in male-to-female transsexuals have been documented.
https://journals.lww.com/ajsp/Fulltext/2..._of.9.aspx