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Yes. I don't know about preferred presentation or pronouns, but Noah recalls a young Rob Lowe to me and that is a quite a package of attractiveness.
Exploring The Hormonal Route. Hair=life.
- Thread starter bridgeburn
- Start date
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Hard Regrowth: Analog, Digital or both?
Is hair regrowth likely or not for any of us using MtF HRT meds? I see things like the following all of the time that appear to ignore the prevalence of hair regrowth while overstating the prevalence of other possible effects. I know that it says "may" related to breast growth but the following clause seems to imply a process that seems likely and extended. "Progression of baldness may slow" seems to be understating the matter:
"Within the first 6 months of therapy, there is typically a redistribution of body fat, decreased muscle mass, softening of skin, and decreased libido. Breast growth may be expected after 3 to 6 months of therapy and may continue for up to 2 years. Over a period of several years, body fat and facial hair become finer, although they are not completely eliminated by hormonal therapy alone. Progression of male pattern baldness may slow; however, hair does not typically regrow in bald areas. Many of the changes, perhaps with the exception of breast growth, are reversible with cessation of therapy".
www.sciencedirect.com
This is the article/one person study that has had a lot of influence on my thinking about hair regrowth under HRT and why it may not be linked temporally to other MtF feminization results:
www.ncbi.nlm.nih.gov
"One goal of hormone therapy for male-to-female individuals is to reduce male-pattern hair growth. Based on our clinical experience, we have long suspected that there was reversal of male pattern baldness in transgender women on treatment to a degree dependent on age and likely other factors. The case presented demonstrates that hormone therapy for male-to-female transgender patients with estrogen and spironolactone can not only reduce male-pattern hair distribution but can also reverse previous effects of androgen on scalp hair patterns".
I love the phrase "to a degree dependent on age and likely other factors". It's always the other factors that trip us up....
"We believe that the mechanism responsible for achieving scalp hair regrowth in transgender women is the suppression of testosterone to normal female levels. In our experience, this usually requires therapy with both spironolactone and estradiol. However, if transgender women treated with estrogen alone can achieve testosterone at normal female levels, we would expect to see scalp hair regrowth in these patients as well. Furthermore, it would be interesting to determine whether more scalp hair regrowth occurs over time as this patient continues hormone therapy."
So, if suppression of testosterone to normal female levels is the key, then regrowth for non-MtF's appears to be unlikely even when using AA's, reductase inhibitors and some amount of estrogen. I do not believe however, that this means that cis-males are incapable of improvement. The process is not as digital as that in my experience as I think that most if not all, tend to experience hair improvement and improvement that is apparent to others, beginning more or less from day one of the HRT process. Whether it is cosmetically significant is probably another question.
I know that achieving testosterone at normal female levels is not necessary for significant breast growth, skin effects and fat re-distribution anecdotally. Furthermore, most MtFs who see these effects notice them early on, certainly before they reach targets.
@bridgeburn seemed to have hair improvement that was easily apparent from the beginning. Since he didn't test regularly (nor do I, only four times since I started formal HRT) it would be interesting to estimate what his progressing T and E levels were as he went along. So the situation regarding hair regrowth via the anecdotal experience of the thread's founder appears to be far more benevolent then how stated in the study, which presented matters in a more digital, not analog fashion. If this involves gene expression then which is it? Do we have to hit target T to initiate things or are there also more minor persistent triggering mechanisms going on?
I will try to submit for testing this week to see where I stand.
Is hair regrowth likely or not for any of us using MtF HRT meds? I see things like the following all of the time that appear to ignore the prevalence of hair regrowth while overstating the prevalence of other possible effects. I know that it says "may" related to breast growth but the following clause seems to imply a process that seems likely and extended. "Progression of baldness may slow" seems to be understating the matter:
"Within the first 6 months of therapy, there is typically a redistribution of body fat, decreased muscle mass, softening of skin, and decreased libido. Breast growth may be expected after 3 to 6 months of therapy and may continue for up to 2 years. Over a period of several years, body fat and facial hair become finer, although they are not completely eliminated by hormonal therapy alone. Progression of male pattern baldness may slow; however, hair does not typically regrow in bald areas. Many of the changes, perhaps with the exception of breast growth, are reversible with cessation of therapy".
Androgen Suppression - an overview | ScienceDirect Topics
This is the article/one person study that has had a lot of influence on my thinking about hair regrowth under HRT and why it may not be linked temporally to other MtF feminization results:
Scalp Hair Regrowth in Hormone-Treated Transgender Woman - PMC
Evidence of androgenetic alopecia, or male pattern baldness, can be distressing for transgender women. Here we present the case of a transgender woman with scalp hair regrowth after ∼6 months on oral estradiol and spironolactone therapy achieving ...
www.ncbi.nlm.nih.gov
"One goal of hormone therapy for male-to-female individuals is to reduce male-pattern hair growth. Based on our clinical experience, we have long suspected that there was reversal of male pattern baldness in transgender women on treatment to a degree dependent on age and likely other factors. The case presented demonstrates that hormone therapy for male-to-female transgender patients with estrogen and spironolactone can not only reduce male-pattern hair distribution but can also reverse previous effects of androgen on scalp hair patterns".
I love the phrase "to a degree dependent on age and likely other factors". It's always the other factors that trip us up....
"We believe that the mechanism responsible for achieving scalp hair regrowth in transgender women is the suppression of testosterone to normal female levels. In our experience, this usually requires therapy with both spironolactone and estradiol. However, if transgender women treated with estrogen alone can achieve testosterone at normal female levels, we would expect to see scalp hair regrowth in these patients as well. Furthermore, it would be interesting to determine whether more scalp hair regrowth occurs over time as this patient continues hormone therapy."
So, if suppression of testosterone to normal female levels is the key, then regrowth for non-MtF's appears to be unlikely even when using AA's, reductase inhibitors and some amount of estrogen. I do not believe however, that this means that cis-males are incapable of improvement. The process is not as digital as that in my experience as I think that most if not all, tend to experience hair improvement and improvement that is apparent to others, beginning more or less from day one of the HRT process. Whether it is cosmetically significant is probably another question.
I know that achieving testosterone at normal female levels is not necessary for significant breast growth, skin effects and fat re-distribution anecdotally. Furthermore, most MtFs who see these effects notice them early on, certainly before they reach targets.
@bridgeburn seemed to have hair improvement that was easily apparent from the beginning. Since he didn't test regularly (nor do I, only four times since I started formal HRT) it would be interesting to estimate what his progressing T and E levels were as he went along. So the situation regarding hair regrowth via the anecdotal experience of the thread's founder appears to be far more benevolent then how stated in the study, which presented matters in a more digital, not analog fashion. If this involves gene expression then which is it? Do we have to hit target T to initiate things or are there also more minor persistent triggering mechanisms going on?
I will try to submit for testing this week to see where I stand.
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Just a follow up on the topical bica query:
I'm 20 years old in the uk and have been on hrt for about 7 months. For the first 3 months I had little changes, my hair continued to fall out, as it has been doing for the last few years. I was on 100mg bica initially, later 50mg and 2 estradot 100 patches . It's only after adding finasteride did the hair loss stop, and my skin became much healthier. I started to use injections at 4 months and things continued to improve, and felt as if my T was adequately suppressed (a blod test showed 0.8nmol/l of testosterone) finasteride however causes severe depression and brain fog, so I had to stop. I upped the dosage of bica to 75mg and started taking finasteride less often and rreverted back to patches in fear of having too high levels (mg gp refuses to monitor my blood). I've also noticed liver pain and excessive apetite which I'm guseeing is the bica, after upping the dose to 75mg in an attempt to counteract dropping the finasteride, and less estradiol to suppress the T. My hair continues to fall out, in addition to other male characteristics returning (BO, oily skin, larger testes etc.) so instead of taking liver damaging anti androgens, I want full chemical castration and 4 days ago administered a zoladex 10.8. My hope is that is achieves castrate levels of T and DHT, but if not I think topical Bicalutamide may be a good option, avoiding the liver toxicity. I think that sums up my situation, although I've probably missed out a few important details. My intention is to crush a 150mg casodex pill and dissolve it into 50% DMSO, I have no idea if this would be safe or not, does anyone have any advice/similar experiences
I'm 20 years old in the uk and have been on hrt for about 7 months. For the first 3 months I had little changes, my hair continued to fall out, as it has been doing for the last few years. I was on 100mg bica initially, later 50mg and 2 estradot 100 patches . It's only after adding finasteride did the hair loss stop, and my skin became much healthier. I started to use injections at 4 months and things continued to improve, and felt as if my T was adequately suppressed (a blod test showed 0.8nmol/l of testosterone) finasteride however causes severe depression and brain fog, so I had to stop. I upped the dosage of bica to 75mg and started taking finasteride less often and rreverted back to patches in fear of having too high levels (mg gp refuses to monitor my blood). I've also noticed liver pain and excessive apetite which I'm guseeing is the bica, after upping the dose to 75mg in an attempt to counteract dropping the finasteride, and less estradiol to suppress the T. My hair continues to fall out, in addition to other male characteristics returning (BO, oily skin, larger testes etc.) so instead of taking liver damaging anti androgens, I want full chemical castration and 4 days ago administered a zoladex 10.8. My hope is that is achieves castrate levels of T and DHT, but if not I think topical Bicalutamide may be a good option, avoiding the liver toxicity. I think that sums up my situation, although I've probably missed out a few important details. My intention is to crush a 150mg casodex pill and dissolve it into 50% DMSO, I have no idea if this would be safe or not, does anyone have any advice/similar experiences
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Are you doing your HRT fully DIY? I understand that healthcare for trans people sucks in the UK. If you're getting liver pain, that sounds not good. Get a doctor to check your liver enzyme levels immediately. Getting a Doctor's advice is always the best option when it comes to potentially dangerous events like liver failure. Don't get medical advice from randos on the internet if you are having severe side effects like liver pain
As for the bicalutamide, frequently testosterone production will be up-regulated in response to the blocking of Androgen receptors, so it is possible that is what you were experiencing. Theoretically, your estradiol injections should have been suppressing testosterone production, though. I understand that it's hard for you to get your Doctor to monitor your hormone blood levels, but that's really the only way to know what's going on for sure.
As for topical bicalutamide - this is a question that I'm interested in, too. I'm currently using a topical AA called RU58841; both Bicalutimaide and RU58841 are non-steroidal anti-androgens. Personally, I would like more information on a comparison of effectiveness of topical antiandrogen use. I will have to do more research on that topic.
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Thanks for the reply, I managed to get a liver and kidney test done (before the pains started) and the tests came out ok, and no more pain since quitting bica. Do you think a 50% DMSO soulution would be suitable? Do you think that over time using it topically would upregulate the androgen receptors too?
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Related to facial feminization effects of HRT and hormonal meds on cis-males:
Notice the lightening in the complexion in general. There is a lack of frontal bossing above the eyebrows which is a highly sexual dimorphic facial aspect in adult humans. There is a tendency for the lips to thicken and for the cheekbones to become more prominent with the eyes more upfront and open. It is often quite sublte and can be influenced by things like micro-needling, massage, botox and filler. For anyone concerned, probably the eyes are the first thing to notice. The beard removal had a huge effect on eradicating my dermatitis with filthy pics of my scorched face here:
Progress Pics from three years back to a month or two back:
Notice the lightening in the complexion in general. There is a lack of frontal bossing above the eyebrows which is a highly sexual dimorphic facial aspect in adult humans. There is a tendency for the lips to thicken and for the cheekbones to become more prominent with the eyes more upfront and open. It is often quite sublte and can be influenced by things like micro-needling, massage, botox and filler. For anyone concerned, probably the eyes are the first thing to notice. The beard removal had a huge effect on eradicating my dermatitis with filthy pics of my scorched face here:
Progress Pics from three years back to a month or two back:
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I know this is bordering on necroposting considering how far off-topic this is, but I just had to respond because I have in the past taken the route of doing an exclusively hard systemic reduction of androgens and it did absolutely -nothing- to help my hair grow. I do believe the contrary, that not only does estrogen improve skin in certain ways, but it also induces hair growth as well, in the same way that low estrogen can induce joint pain. Estrogen is an anti-inflammatory hormone, and if you can manage to localize the effects of the estrogen to the scalp, and mitigate the titty and fat accumulation quotent (if you in fact don't want titties or to be a bit thicc), then you're basically set.
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yeah your position seems to be the general consensus among most of the posters here. Blocking androgens can prevent hair loss but estrogens are needed for the dramatic regrowth. The more I think about things, the more I like the use of topical anti-androgens as there's really no need for a systemic androgen blocking just for hairloss. spironolactone could be the exception of an oral AA that is worth taking as it seems to have additional benefits for hair growth
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I have tried a compounding pharmacy created spironolactone solution and it didn't really work as well as I thought it would, perhaps it was the carrier or the preparation, but the androgen receptor interference that I had read about in a study that evaluated spironolactone's ability to treat cystic androgen mediated acne did not seem to help me much when it came to hair loss.
What has seemed to help quite a bit (albeit it's a bit expensive since you have to use it quite a lot) is finacea, the topical acne cream. It interferes with DHT and it has an anti-inflammatory effect, I've been using it for a bit now along with my own topical formulation of a substance known as sophora root, which in at least one study induced hair growth and supposedly interferes with DHT as well - and my hair has been recovering from a point where I would not leave the house without a hat of some kind.
I am going to actually try the .75 mg estradiol topical and see what it does, I'm very curious. I will after I start the regimen and after enough time report any results if interested.
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There's been speculation on this forum that topical spironolactone is less effective than oral because it needs to be metabolized through the liver. I believe that for hormonal acne, oral is the preffered route of administration (at least in women, spironolactone is not usually used in men). spironolactone has additional antagonistic effects on the aldosterone receptor, which may have benefits for hair growth as well.
Finacea appears to be azaleic acid, which is known to have good effects for hair growth.
As for estradiol - have you seen the threads on this forum about usage of estriol vs. estradiol? Estriol has a higher affinity for the β estrogen receptor and a lower affinity for the α receptor, so theoretically it should have less feminizing effects than estradiol while retaining much of the skin/hair benefit as the ERβ is the one that is mostly present in dermal tissue. I've been using estriol myself, (though not for the past week or so since I've run out and am waiting for my package from China to arrive with a resupply) and I believe that it had positive effects on my skin quality
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What quantity and frequencyof Estriol are you applying?
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I was applying 15mg twice a day in the form of an OTC menopausal cream, but since that ran out I am switching to a homemade estriol solution in ethanol/PG once my estriol powder arrives from China. I will be applying 20mg twice a day to my scalp but may consider moving up from there. (I am interested in trying to make an estriol facial cream/serum)
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You may want to check this, I don't like the fact they used acetone as a carrier as that sounds like it's terrible for hair growth regardless.
Effects of 17-β-Estradiol and ICI 182 780 on Hair Growth in Various Strains of Mice
17-β-Estradiol (10nmol per 200 μ1 acetone) applied topically twice weekly to the clipped dorsal surface of C57BL/6 or C3H female mouse skin prevented …
Then there's this conflicting study, or seemingly so from what I can interpret.
Estrogen B used in treatment of Androgenetic Alopecia | Male Pattern Baldness Cure Follacure.com
Estrogen B a hormone to treat Androgenetic Alopecia | Male Pattern Baldness Cure
www.follacure.com
How are you managing sides? Or are you transitioning? I'm wondering if a .75 mg dose could be managed without anastrozole or tamoxifen, if not I guess I'll have to figure that out.
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Good to see you here posting. Would love to know what all you are taking and what you find most efficacious.
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You need to bump this.
I am at 20mg twice a day. I use this formula which deliver 20x the penetration of Estrogel.
The formula is detailed as:
I am at 20mg twice a day. I use this formula which deliver 20x the penetration of Estrogel.
The formula is detailed as:
- 29.4 % oleic acid
- 11.8% isopropyl myristate
- 38.2% ethanol
- 11.8% PBS buffer to pH 7.4
- 8.8% Span 80 (aka sorbitane monooleate, sorbitan oleate),
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Has anyone had any luck finding "OTC" menopausal creams locally, without having to use Amazon or Ebay? It seems as though they would be back there with the real Sudofed but I have only used ones bought online which has meant Life Flo with a couple of competitors here and there.
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Endocrinology of Transgender Medicine
Abstract. Gender-affirming treatment of transgender people requires a multidisciplinary approach in which endocrinologists play a crucial role. The aim of
academic.oup.com
5α-Reductase inhibitors: Some transgender women may experience male pattern hair loss and may seek treatments to arrest hair loss and/or restore hair. In general, lowering serum testosterone levels into the cisgender female range is often adequate to arrest hair loss in most transgender women; however, there are still some transgender women who experience hair loss despite lowered serum testosterone levels. A few case series in transgender women with androgenetic alopecia have demonstrated finasteride therapy to be effective to improve hair loss without significant side effects (70, 71). The routine use of 5α-reductase inhibitors has been limited over previous concerns of long-term sexual dysfunction and depression reported to be found in cisgender men.
Feminization in transgender women
Treatment with estrogen and testosterone-lowering medications will induce feminine and reduce masculine physical characteristics Fig. 1 (41). The most studied physical change in transgender women is the development of breast tissue. An Italian cohort study found increases in breast size were the only physical feature that was significantly associated with improvement in body uneasiness scores (43). However, <20% of transgender women reach Tanner breast stage 4 to 5 after 24 months of hormone therapy and thus often seek mammoplasty. Early studies in transgender women indicated breast development reached a maximum size by 2 years (74). However, a more recent study of 229 transgender women participating in the European Network for the Investigation of Gender Incongruence cohort found that breast development reached a plateau within the first 6 months of therapy and half of the transgender women had a AAA cup size or less (75). Fisher et al. (43) also found that testicular volume decreased by ~60% after 24 months of transfeminine hormone therapy.
Transgender Males:
In a retrospective, observational study, 81 transgender men treated with testosterone esters or testosterone undecanoate self-assessed the degree of male pattern baldness using a five-point scale [i.e., type I (no hair loss) to type V (complete hair loss)]. The authors found that 38% of transgender men had male pattern baldness types II to V. Thinning of hair was related to the duration of androgen administration and present in half of the transgender men after 13 years (124). Wierckx et al. (44) reported that 17% of participants developed androgenic alopecia based on the Norwood–Hamilton classification after 1 year of treatment. Longer-term (10 years on average) testosterone treatment was associated with 32% of mild frontotemporal hair loss and 31% moderate to severe androgenetic alopecia (101). In 10 transgender men with androgenetic alopecia, treatment with oral finasteride at 1 mg daily for 12 months induced improvement with one grade on the Norwood–Hamilton scale after a mean of 5.5 months since the start of treatment
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Cyproterone Acetate Superfluous for HRT when Compared with Low-dose Estradiol:
This is a recent study. I am not sure how long it takes for them to circulate, but this study, if I read it correctly, is another reason to avoid CPA as it's extra feminizing aspects seem to be minimal while exposing a person to hepic and perhaps others sorts of harm:
This study is the first to evaluate the use of low doses of estrogens in TW. We have demonstrated that low estrogen doses alone or with CA are effective toward maintaining androgen suppression and serum E2 within the normal follicular-phase range.
Evaluations of the effects of low-dose estrogen therapy on physical changes, namely, breast development, facial hair growth, body hair growth and body fat redistribution, were not possible in our patient population because all of the patients reported prior use of other estrogen formulations without medical supervision for a variable period of time. However, the maintenance of estrogen levels in the normal female range suggests that low-dose estrogen therapy may be able to promote the satisfactory feminization of these patients. The facial hair response to hormonal treatment in transsexuals, even at high estrogen doses, is very poor and often requires complementary cosmetic treatments such as laser treatments and electrolysis. In addition, many signs of feminization, including breast development, depend on not only the estrogen dose but also the individual patient’s sensitivity to estrogen. In a cohort of transsexuals receiving high doses of estrogen, the result of breast augmentation from hormones was described as modest, and the rate of breast augmentation surgery in a series of transsexuals was generally as high as 70% (25-27). Nevertheless, all patients in our cohort achieved an advanced Tanner’ stage (IV and V) in breast development.
www.scielo.br
METHODS:
The serum hormone and biochemical profiles of 51 transgender women were evaluated before gonadectomy. Hormone therapy consisted of conjugated equine estrogen alone or combined with cyproterone acetate. The daily dose of conjugated equine estrogen was 0.625 mg in 41 subjects and 1.25 mg in 10 subjects, and the daily dose of cyproterone acetate was 50 mg in 42 subjects and 100 mg in one subject.
RESULTS:
Estrogen-only therapy reduced the testosterone, luteinizing hormone and follicle-stimulating hormone levels from 731.5 to 18 ng/dL, 6.3 to 1.1 U/L and 9.6 to 1.5 U/L, respectively. Estrogen plus cyproterone acetate reduced the testosterone, luteinizing hormone and follicle-stimulating hormone levels from 750 to 21 ng/dL, 6.8 to 0.6 U/L and 10 to 1.0 U/L, respectively. The serum levels of luteinizing hormone, follicle-stimulating hormone, testosterone, estradiol and prolactin in the patients treated with estrogen alone and estrogen plus cyproterone acetate were not significantly different. The group receiving estrogen plus cyproterone acetate had significantly higher levels of gamma-glutamyltransferase than the group receiving estrogen alone. No significant differences in the other biochemical parameters were evident between the patients receiving estrogen alone and estrogen plus cyproterone acetate.
CONCLUSION:
In our sample of transgender women, lower estrogen doses than those usually prescribed for these subjects were able to adjust the testosterone and estradiol levels to the physiological female range, thus avoiding high estrogen doses and their multiple associated side effects.
In our sample of TW, lower estrogen doses than those usually prescribed for these subjects were able to adjust the T and E2 levels to the physiological female range, avoiding the risks of high estrogen doses. Both regimens, namely, CEE alone or with CA, achieved the laboratory goals in the treatment of TW.
This is a recent study. I am not sure how long it takes for them to circulate, but this study, if I read it correctly, is another reason to avoid CPA as it's extra feminizing aspects seem to be minimal while exposing a person to hepic and perhaps others sorts of harm:
This study is the first to evaluate the use of low doses of estrogens in TW. We have demonstrated that low estrogen doses alone or with CA are effective toward maintaining androgen suppression and serum E2 within the normal follicular-phase range.
Evaluations of the effects of low-dose estrogen therapy on physical changes, namely, breast development, facial hair growth, body hair growth and body fat redistribution, were not possible in our patient population because all of the patients reported prior use of other estrogen formulations without medical supervision for a variable period of time. However, the maintenance of estrogen levels in the normal female range suggests that low-dose estrogen therapy may be able to promote the satisfactory feminization of these patients. The facial hair response to hormonal treatment in transsexuals, even at high estrogen doses, is very poor and often requires complementary cosmetic treatments such as laser treatments and electrolysis. In addition, many signs of feminization, including breast development, depend on not only the estrogen dose but also the individual patient’s sensitivity to estrogen. In a cohort of transsexuals receiving high doses of estrogen, the result of breast augmentation from hormones was described as modest, and the rate of breast augmentation surgery in a series of transsexuals was generally as high as 70% (25-27). Nevertheless, all patients in our cohort achieved an advanced Tanner’ stage (IV and V) in breast development.
Low estrogen doses normalize testosterone and estradiol levels to the female range in transgender women
OBJECTIVE: The ideal dosage of cross-sex hormones remains unknown. The aim of this study was to...
METHODS:
The serum hormone and biochemical profiles of 51 transgender women were evaluated before gonadectomy. Hormone therapy consisted of conjugated equine estrogen alone or combined with cyproterone acetate. The daily dose of conjugated equine estrogen was 0.625 mg in 41 subjects and 1.25 mg in 10 subjects, and the daily dose of cyproterone acetate was 50 mg in 42 subjects and 100 mg in one subject.
RESULTS:
Estrogen-only therapy reduced the testosterone, luteinizing hormone and follicle-stimulating hormone levels from 731.5 to 18 ng/dL, 6.3 to 1.1 U/L and 9.6 to 1.5 U/L, respectively. Estrogen plus cyproterone acetate reduced the testosterone, luteinizing hormone and follicle-stimulating hormone levels from 750 to 21 ng/dL, 6.8 to 0.6 U/L and 10 to 1.0 U/L, respectively. The serum levels of luteinizing hormone, follicle-stimulating hormone, testosterone, estradiol and prolactin in the patients treated with estrogen alone and estrogen plus cyproterone acetate were not significantly different. The group receiving estrogen plus cyproterone acetate had significantly higher levels of gamma-glutamyltransferase than the group receiving estrogen alone. No significant differences in the other biochemical parameters were evident between the patients receiving estrogen alone and estrogen plus cyproterone acetate.
CONCLUSION:
In our sample of transgender women, lower estrogen doses than those usually prescribed for these subjects were able to adjust the testosterone and estradiol levels to the physiological female range, thus avoiding high estrogen doses and their multiple associated side effects.
In our sample of TW, lower estrogen doses than those usually prescribed for these subjects were able to adjust the T and E2 levels to the physiological female range, avoiding the risks of high estrogen doses. Both regimens, namely, CEE alone or with CA, achieved the laboratory goals in the treatment of TW.
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You may want to check this, I don't like the fact they used acetone as a carrier as that sounds like it's terrible for hair growth regardless.
Effects of 17-β-Estradiol and ICI 182 780 on Hair Growth in Various Strains of Mice
17-β-Estradiol (10nmol per 200 μ1 acetone) applied topically twice weekly to the clipped dorsal surface of C57BL/6 or C3H female mouse skin prevented …www.sciencedirect.com
Then there's this conflicting study, or seemingly so from what I can interpret.
Estrogen B used in treatment of Androgenetic Alopecia | Male Pattern Baldness Cure Follacure.com
Estrogen B a hormone to treat Androgenetic Alopecia | Male Pattern Baldness Curewww.follacure.com
How are you managing sides? Or are you transitioning? I'm wondering if a .75 mg dose could be managed without anastrozole or tamoxifen, if not I guess I'll have to figure that out.
Estriol (E3) is much less potent than Estradiol (E2) in terms of activity on the ER, binding affinity to the ER, and absorption, so my guess would be that even a 1mg/day dose of E2 would have more feminizing effect than the 40mg/day dosage of E3 used by members of this forum.
https://sci-hub.se/10.1210/er.2006-0020 is one of the most thorough examinations of the effects of estrogens on hair follicles. When I have more time this evening I'll read through the studies that you linked.
Also, I think taking anastrozole with E2 would not be effective and counter-productive. Aromatase exists in the dermal papilla of hair follicles so taking an AI would lead to reduced amounts of E2 in the follicles itself while the exogenous E2 would lead to a higher blood-serum level of E2 thus sides of gynecomastia. So you'd still get gynecomastia while the hair-regrowth effects would be negated. Anecdotally, users on this forum who've used AIs have experienced massive hair sheds.
I think E2 + a SERM (eg, tamoxifen, raloxifene) may be the most promising estrogen therapy for androgenic alopecia and will probably be what I "upgrade" to if E3 therapy proves inadequate
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Thank you for linking that study, will read through it when I have more time this evening.
I understand that E3 has very poor absorption so I would like to use some penetration enhancers. This is something that I need to do more research on. @pegasus2 uses DMSO.
Just a thought that I had: could too much penetration actually be bad, especially for E2? Here I'm trying to distinguish between transdermal and topical application. Transdermal application (like in the study you linked) aims for systematic absorption into the blood serum, while a topical application would focus on keeping the absorption to the dermal area surrounding the application site. So a transdermal application would have side effects whereas a purely topical application may not. I am not a pharmecokineticist so I may be talking out my *** here