Do you wear a brassiere to support your bitchtits?
Exploring The Hormonal Route. Hair=life.
- Thread starter bridgeburn
- Start date
Do you wear a brassiere to support your bitchtits?
Yes the regimen is up to date. Don't need any AA with high enough estrogen levels.
Like the only practical difference between my regimen and that of someone transitioning is that I'm manly enough to not feminize, well, except the boobs.
Sports bra. With baggy clothes and layers they're not visible. Have some scars so don't want to go shirtless anyway.
What Estradiol do you use..?
Can you share a link?
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ever heard of diminishing returns
how is wearing a sportsbra for your tits gonna be better than hair if you still want to be a man
how is wearing a sportsbra for your tits gonna be better than hair if you still want to be a man
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I myself regreted it last summer when I was invited to night swimming by a girl at midnight and multiple other similar shirtless occassions. She thought I ghosted her but i just didnt want to show my puffy nipples lol. I guess incels dont have this problem.
But it was from finasteride/dutasteride, so its little different than estradiol. It was not deliberate.
Hateful speech?The word "normal" is hateful speech? Is it a derogatory term?Normal means,the father taking his kids to a ball game,husband and wife going out for a drink...etc.If its not normal,it doesnt mean its good or bad and thats where opinions differ.Are you normal?
Taking center stage?Is that also a derogatory term?
Your stupid,find a different way to be on center stage,not like that.
I am linking this study as well: https://pdfs.semanticscholar.org/7b36/45a4785c4ce835b1d644a356af1341dfc731.pdfWell, Dutasteride it is supposed to attack the Backdoor pathway of dht via the 5AR1 enzyme, but for others will be enough and probably for others not. DHT being high to those who take it’s pretty crazy. There are genetic variations, etc. Nothing is fully understood yet/completely. No to mention the scalp DHT/androgens. There is even a study where Dutasteride+3a oxidoreductase inhibitors inhibited DHT more completely than Dutasteride alone in advance prostate cancer which makes sense because the Backdoor pathway is inhibited more “completely”. From the Backdoor chart, someone can conclude that the following could inhibit it in a more “complete” way:
Dutasteride
Ketoconazole
Abiraterone
Aldo-Ketoreductases
etc
The following studies are pretty good. Worth a look.
Potential impact of combined inhibition of 3α-oxidoreductases and 5α-reductases on prostate cancer
Prostate cancer (PCa) growth and progression rely on the interaction between the androgen receptor (AR) and the testicular ligands, testosterone and dihydrotestosterone (DHT). Almost all men with advanced PCa receive androgen deprivation therapy (ADT). ...www.ncbi.nlm.nih.gov
Genetic variations associated with response to dutasteride in the treatment of male subjects with androgenetic alopecia
Dutasteride, a dual inhibitor of both type I and II 5α-reductases, is used to treat male pattern hair loss (MPHL). However, patient response to dutasteride varies in each individual, the cause of which is yet to be identified. To identify genetic ...
Beyond T and DHT – Novel Steroid Derivatives Capable of Wild Type Androgen Receptor Activation
However, in steroidogenic tissues in which both CYP17A1 and SRD5A are co-expressed, an alternate route to 5α-DHT, called the ‘back-door’ pathway (Figure 2, hatched arrows) is possible wherein C-21 steroids are acted on by the reductive activity of SRD5A and AKR1C2 prior to the lyase activity of CYP17A1 [29]. In fact, 17-OH progesterone is a better substrate for SRD5A (especially SRD5A1) than either AED or T [30]. Since 17-OH dihydroprogesterone (the 5α-reduced product of 17-OH progesterone) is a poor substrate for the lyase activity of CYP17A1, synthesis proceeds via ARK1C2, which yields 17-OH allo-pregnanolone, an excellent substrate for CYP17A1 lyase activity that is minimally dependent on cytochrome b5 [39]. Androsterone generated by the lyase activity of CYP17A1 is then acted upon by HSD17B3 or AKR1C3 to generate 3α-diol followed by, a reverse oxidative step (not required in the classical pathway) to generate 5α-DHT [27]. Candidate enzymes mediating the reverse conversion of 3α-diol to 5α-DHT include RL-HSD (17BHSD6), 17BHSD10, RODH4, RDH5, and DHRS9 [35, 40, 41]. RL-HSD also acts as an epimerase to convert 3α-diol to 3β-diol, although at much higher substrate concentrations [42], and can directly catalyze conversion of physiologic levels of 5α-DHT to 3β-diol [43].
In a third pathway, termed the 5α-androstanedione (5α-dione) pathway (Figure 2, dark gray arrows) DHEA and AED are produced as in the classical pathway. However, AED is converted first by SRD5A to 5α-dione and then by AKR1C3 (or potentially HSD17B3) to 5α-DHT, rather than conversion of AED to T followed by the activity of SRD5A to produce DHT. Consistent with prior findings that SRD5A activity in PCa cells has a preference for AED rather than T [44-46], Sharifi recently demonstrated that SRD5A1 mediated 5α–reduction of AED to5α-dione is required for 5α-DHT synthesis in PCa cells, and that T and AED are actually negligible substrates for SRD5A2 [47] (possibly related to the altered redox environment of tumor cells as SRD5A1 and 2 have different pH optima). The subtotal loss of SRD5A2 and upregulation of SRD5A1 observed in the transition from benign prostate to CRPC may thus reflect selection of tumors cells capable of efficiently synthesizing 5α-DHT via this pathway [4, 48-50]. The classical pathway primarily refers to the production of T by the testes. After castration, the backdoor and 5α-dione pathways allow for the production of DHT from steroids of adrenal origin. Importantly, regardless of which pathway is operative in CRPC tissues, inhibition of steroidogenesis via the backdoor and 5α-dione pathways requires inhibition of the same enzymatic conversions which produce 5α-DHT via the conventional pathway.
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Backdoor Pathway-5a-Androstanedione Pathway.jpg
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HRT gives very slow results. In a year, I restored what was lost in 3 months of baldness. The hair is still thin and by and large, little has changed. I don't know how many years it takes to recover. It seems to me that it is impossible to restore to the ideal. At least I stopped it and no longer feel like it's over
Before HRT, I slowly went bald for 3 years. I wonder if I will achieve the ideal if I am on HRT for 3 years.
Before HRT, I slowly went bald for 3 years. I wonder if I will achieve the ideal if I am on HRT for 3 years.
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Do you still use E2?? you said onolder posts you will stop and start clomid??
Trannies hijacked this good fight against hairloss to an excuse for becoming shemales. I would be surprised if many of the posters here even care about hairloss like one of them said he didn’t become a freak for girls or hairs but for himself- da fck that’s supposed to mean.
Funny thing is they still use the gold standard of hair regrowth drug ie minoxidil and despite becoming freaks, they have to use min to get some regrowth
Just disgusting if you ask me, this is hairlosstalk not trannytalk
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They are promoting self harm
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I never had nipple problems on super high dose of dutasteride or finasteride. Lucky me.
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What’s a female
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Automatically dislikes a legitimate question like a true NPC with aspergers lol
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Definitely an incel lmao
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Low IQ shemale lol