[Lotus]

Reposting the following information on why your penis gets smaller when starting NBE or HRT (lol, you have been warned) 

But...there is a hack to recover from this now. 

The fact that estrogen receptors and aromatase are localized in a diverse subpopulation of penile cells, including neurons, epithelia, stroma, glandular cells suggests that its function in the penis is likely to be cell-specific and complex (Jesmin et al., 2002, 2004; Crescioli et al., 2003; Dietrich et al., 2004; Goyal et al., 2004; Vignozzi et al., 2004). 

We've discussed estrogen being produced (synthesized) in the testes, and aromatase stored in germ cells, epididymis, and is present in spermatozoa. We've even talked about how DHT can be turned into estrogen via the DHT metabolite 3beta-diol. So, as testosterone is being inhibited the ratio of T to E2 is shifted favoring estradiol synthesis in the testes, thus a reduction in the size of your penis.

Oops, almost forget, the density of 5 alpha reductase is strongly present on the head of the penis. With that aside, please read this pdf:

The penis: a new target and source of estrogen in male reproduction http://www.hh.um.es/pdf/Vol_21/21_1/Mowa...7-2006.pdf

Summary. In the past decade, interest and knowledge in the role of estrogen in male reproduction and fertility has gained significant momentum. More recently, the cellular distribution and activity of estrogen receptors (α and ß)(ER) and aromatase (estrogen synthesis) has been reported in the penis, making the penis the latest “frontier” in the study of estrogen in male reproduction. ER and aromatase are broadly and abundantly expressed in various penile compartments and cell types (erectile tissues, urethral epithelia, vascular and neuronal cells), suggesting the complexity and significance of the estrogen-ER system in penile events. Unraveling this complexity is important and will require utilization of the various resources that are now at our disposal including, animal models and humans lacking or deficient in ER and aromatase and the use of advanced and sensitive techniques. Some of the obvious areas that require our attention include: 1) a comprehensive mapping of ER-α and -ß cellular expression in the different penile compartments and subpopulations of cells, 2) delineation of the specific roles of estrogen in the different subpopulations of cells, 3) establishing the relationship of the estrogen-ER system with the androgen-androgen receptor system, if any, and 4) characterizing the specific penile phenotypes in human and animals lacking or deficient in estrogen and ER. Some data generated thus far, although preliminary, appear to challenge the long held dogma that, overall, androgens have a regulatory monopoly of penile development and function.

Fig. 8. Schematic diagram shows an overview distribution of ER in the penile tissues (glans penis, penis spongiosus, penis cavernosus, penile urethra). Bottom right, cross section of penis.

Estrogens, 17ß-estradiol and estrone, are produced from C19 androgens, testosterone and androstenedione, respectively, by cytochrome P450 arom (P450arom), a product of CYP19 gene. P450arom is a mono-oxygenase microsomal enzyme complex present in endoplasmic reticulum that irreversibly converts the aromatizable C19 androgens to estrogens through 3 consecutive hydroxylation reactions at the A-ring (Lephart 1996; Pereyra-Martinez et al. 2001; Carreau et al. 2002; Wiszniewska 2002). Aromatase is expressed in a tissue- specific manner and is composed of two proteins, namely, 1) a ubiquitous NADPH-cytochrome P450 reductase and 2) a cytochrome P450 aromatase, which contain the heme and the steroid pocket (Lephart 1996; Carreau et al. 1999, 2002).