[Lotus]

Hi Val, apologies for the late response:

Been browsing this thread for a while now and came across this post/repost. The notion of being able to prevent/mitigate a reduction in penis size while being on an NBE/HRT program seemed interesting to me. However, despite a "hack" of this nature being mentioned in the repost, the original post only details the reasons behind reduction in penis size while on NBE/HRT and does not seem to give any ways/"hacks" to potentially combat this . I've tried finding a follow up post but there doesn't seem to be anything. If you've already made a follow up post that I somehow missed perhaps you could direct me to it? If that's not the case and you simply never got around to following up on the topic (completely understandable since I understand you ran into major health complications [leukemia] shortly after) I'd greatly appreciate a follow up, only if you have the time and are willing to do so of course  . The topic of how to keep function/size in that area seems to be rarely discussed since it's often a source of dysphoria for most who want to MTF transition or develop breasts. I however, align more towards being gender fluid rather than being transfemale and want to avoid losing function/size in my penis as much as possible while still being able to get a sizeable pair of breasts that are also small enough to be hidden by baggy clothing / binders when I don't feel as feminine.   

(As a side note thank you so much for making this thread. Your research is, hands down, the most valuable source of information I've found on this topic)

Sincerely,
Your fellow researcher; Val

Thank you Val, I'm including thboy's response because it's relates to your post. 

Val on 11-04-2024 post #4961 was wondering about the “hack” to maintain penis size and function.  

Lotus post 06-16-2024 #4874, Lotus made references to seeing her penis in the morning and attributed that to using testosterone cream on her penis.  She mentioned regaining penis length and girth.

Lotus post 06-25-2024 #4896, Lotus mentions using a penis pump to combat atrophy and to aid in erections.
I read through the 15 page paper linked in Lotus’s post #3273 from 02-13-2016.  

Thank you thboy, I had to laugh at your comment when you stated “ Lotus made references to seeing her penis in the morning and attributed that to using testosterone cream on her penis”... somehow my mind thought of the “GroundHog Day ceremony” when the groundhog emerges from its burrow and sees its shadow, it will retreat to its den and winter will go on for six more weeks” ... though i didn't quite quote that. Here's what I quoted:

The other device's I use are listed below, Imo there effective and don't break the bank. The penis enlargement device helps prevent penis atrophy… Additionally, I find it helps with getting an erection, which ain't easy having had an Orchiectomy.   
[size=medium]Here's information below on maintaining penis size and girth.

warning: penis information ahead (no pun). If discussing the penis offends thee, well then, proceed no further… cause, we gonna talk!.

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. 

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.

What does this mean?. For starters, estrogen(s) have a huge impact on the male reproductive organs: for those who still don't believe Aromatase has any impact in male anatomy I say, they (you!) are sadly mistaken and read the study. 
 
Edit: viewing the illustration (see pdf) on the location (and amounts) of estrogen receptors in the penis, imo it's suggesting the penis to be a target organ for delivery of estrogens........get my meaning?. On the other hand, this should also explain why we see a decrease in the size of the penis (from estrogen), aka a successful program.

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).

"When DHT formation is inhibited, the aromatization pathway of T to estradiol will prevail and induce a pronounced down-regulation of AR mRNA levels."

Testosterone down-regulates the levels of androgen receptor mRNA in smooth muscle cells from the 
corpora cavernosa via aromatization to estrogens.

Lin MC, Rajfer J, Swerdloff RS, Gonzalez-Cadavid NF.

Department of Surgery, UCLA School of Medicine, Torrance 90509.

Androgens down-regulate the levels of androgen receptors (AR) and AR mRNA in the penis and prostate of castrated rats, and are assumed to cause their decrease during sexual maturation in the penile smooth muscle of intact rats. In order to determine whether these effects occur directly at the target cell level, and to what extent they are due to testosterone (T) or to their metabolites, we have measured AR mRNA in cultures of smooth muscle cells from the adult rat corpora cavernosa treated in vitro with sex steroids. T at high concentrations (100 nM) acted like dihydrotestosterone (DHT) in increasing moderately the levels of AR mRNA in both proliferating and contact-inhibited cells. However, when conversion of T to DHT was blocked by the 5-alpha reductase inhibitor finasteride, the levels of AR mRNA were considerably down-regulated by T (10-500 nM), particularly in the contact-inhibited cells. Finasteride by itself was inactive. These effects in both types of cultures were inhibited by platelet derived growth factor (PDGF) (20 ng/ml), a growth factor that up-regulates AR mRNA levels, and by fadrozole (100 nM), an aromatase inhibitor of the T/estrogen conversion. Estradiol (50 nM) was even more potent than T in decreasing AR mRNA levels. With the exception of PDGF none of the treatments affected significantly cell growth, as measured by DNA synthesis and content. Our results indicate that it is possible to modulate in vitro AR mRNA levels in the penile smooth muscle cells, and that under normal conditions DHT and T act as moderate up-regulators. When DHT formation is inhibited, the aromatization pathway of T to estradiol will prevail and induce a pronounced down-regulation of AR mRNA levels. We assume that the in vivo AR down-regulation in the penile smooth muscle by androgens is an indirect effect mediated by a paracrine or endocrine mechanism elicited in another tissue.
PMID: 8499343 [PubMed - indexed for MEDLINE]

And here:
https://www.breastnexum.com/showthread.php?tid=17436&page=139