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Don't take your life, even though I don't know you, I feel your energy in some way, you are important to many people, including us, stay safe bro , make this for others who love you
Exploring The Hormonal Route. Hair=life.
- Thread starter bridgeburn
- Start date
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- 1,108
Ugh. I wonder if this can be prevented with duta.
On Bicalutamide, you get more predictable hormone levels, while on estradiol, you have to get tested and make sure your T does not drop too much. Although I'm not sure if it is possible to lower T levels slightly with low doses of E, but not make E the main hormone
DHTcel, Maave, Ein?
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Dandruff is a sign of inflammation and a DHT artifact so reducing dandruff might be likely to reduce inflammation. I have posted articles relevant to this on this thread and my own the past few days. Inflammation is the hot thing now in baldness treatment it appears.
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Yeah. Those three are renown experts in the field of hormonal therapy and baldness.
My Goddess!
Please read up on scientific methodology and quit citing to ghosts to buttress your unscientific claims. None of those three have had any aspect of what you claim verified scientifically. Next time, I see you mention one of the three, I am just not going to bother to respond. It is as low as you can go scientifically and ancedotally. I just re-read the first 150 pages of all of the bridge stuff. Have you? Almas, pretty soon Tato and I and others are going to just read past your posts.
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If you bothered to read the literature, then you would know the answer to this. Levels as low as 2 mg can completely re-set the axis over time but yes, there can be intermediate levels of both which I experienced for several years with marginal to no growth. It might work for maintenance. Do you understand the prevailing theories of baldness related to fibrosis and scalp tension? Why don't you read Rob Winter's stuff. He makes it easy to understand virtually every aspect of what we know and do not know @ perfecthairhealth.com
You said that you can't achieve regrowth without a full MTF. I gave examples of people who managed to do this. Two of them didn't even use estrogen to grow their hair back. Don't you think this is contrary to what you are claiming?
What scientific data are you interested in? Overgrowth on Bicalutamide is easily explained by the effects of ADT and the increase in estradiol
Do you seriously believe in this nonsense and are throwing a link to the infobusinessman?
Seriosly?
Attachments
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Learn To Fly
Foo FightersRun and tell all of the angels
This could take all night
Think I need a devil to help me get things right
Hook me up a new revolution
Cause this one is a lie
We sat around laughin' and watched the last one die
Now, I'm lookin' to the sky to save me
Lookin' for a sign of life
Lookin' for somethin' to help me burn out bright
And I'm lookin' for a complication
Lookin' cause I'm tired of lyin'
Make my way back home when I learn to fly high
I think I'm dyin' nursing patience
It can wait one night
I'd give it all away if you give me one last try
We'll live happily ever trapped if you just save my life
Run and tell the angels that everything's alright
Now I'm lookin' to the sky to save me
Lookin' for a sign of life
Lookin' for somethin' to help me burn out bright
I'm lookin' for a complication
Lookin' cause I'm tired of tryin'
Make my way back home when I learn to fly high
Make my way back home when I learn to
Fly along with me, I can't quite make it alone
Try to make this life my own
Fly along with me, I can't quite make it alone
Try to make this life my own
I'm lookin' to the sky to save me
Lookin' for a sign of life
Lookin' for somethin' to help me burn out bright
And I'm lookin' for a complication
Lookin' cause I'm tired of tryin'
Make my way back home when I learn to
I'm lookin' to the sky to save me
Lookin' for a sign of life
Lookin' for somethin' to help me burn out bright
And I'm lookin' for a complication
Lookin' cause I'm tired of tryin'
Make my way back home when I learn to fly high
Make my way back home when I learn to fly
Make my way back home when I learn to
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I always thought fibrosis and scalp tension is a result of follicle miniaturization and androgens.
It just makes sense that scalp fiborsis occurs when there is no terminal hair lol
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I know this place isnt meant to ask this question for...:
But do transplanted hairs last for life time if they are taken from the androgen-safe zone?
If they do, then, fibrosis, calcification, tension etc is all just crap theory lol.
I really think androgens are the main causw of ANDROGENetic alopecia.
And I am as well pretty sure that with Bicalutamide 100mg, 1,25mg Finasteride and maybe 1 mg Estradiol buccaly, I will be able to restore my hair.
And another question just in theory; if hair cloning gets real... it will actually be a cure, because all the follicles have the same gene expression, to not be androgen sensitive. Am I right!?
But do transplanted hairs last for life time if they are taken from the androgen-safe zone?
If they do, then, fibrosis, calcification, tension etc is all just crap theory lol.
I really think androgens are the main causw of ANDROGENetic alopecia.
And I am as well pretty sure that with Bicalutamide 100mg, 1,25mg Finasteride and maybe 1 mg Estradiol buccaly, I will be able to restore my hair.
And another question just in theory; if hair cloning gets real... it will actually be a cure, because all the follicles have the same gene expression, to not be androgen sensitive. Am I right!?
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2000 is waaay to high, and no, there are no studies because f*****g scientists think DHT is the only factor of androgenetic hair loss.
Take half androgen blockage and forget about hair loss forever, surely, you will have to acept the other (side) effects.
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I am pretty sure I will be able to take bica for 15-20 years within finasteride or duta. My only concern will be gyno, but I will do a surgery. Anothet thing which would be bad for me is, if I ever want randomly to have kids, what I actually dont want, but who knows what you will want in future, is, that I will have to stop bica while conceiving.
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Yeah thats for sure. You need 400 min.
You still get erections on 50 tho. But under 400 you might not function as a male anymore.
You still have to consider as well that Bicalutamide depends on its own concentration and the concetration of the androgens. Every single tissue has its own androgen concentration.
@Ein once said that skin tissue gets by 98% affected of Bicalutamide. While testes have 90% of all androgens of the body, so its pretty much unlikely you will have androgen blockage effects on the testes and surrounding organs lol.
-> there are several studies on this.
So Bicalutamide acts at best in peripheral tissues/regions, such as; SKIN.
And thats why many experience effects on skin and zero sebum production. Some even get hair loss reversal or improvement.
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My mother already said, she accepts that I will go nuclear, and the Doctor said as well yes, but I might not get kids while on it.
The Doctor is an andrologist, oncologist, gender specialist and urologist. I have chosen the right clinic Ig, after wasting half a year on idiotic derms.
I hope that by 2040-50 there will be a cure and I can drop everything, hopefully >.<
The Doctor is an andrologist, oncologist, gender specialist and urologist. I have chosen the right clinic Ig, after wasting half a year on idiotic derms.
I hope that by 2040-50 there will be a cure and I can drop everything, hopefully >.<
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This article proposes revised scientific methodology related to the use of estradiol only and with AA's. It details the scientific and statistical methodology needed to reach further conclusions, including meta-analysis of existing studies and one using new cohorts, including sensitivity analysis and confidence intervals. NB: Bica is not even mentioned here as opposed to MPA, CPA and spironolactone, and we largely lack information at all related to utilization of AA's and dosage and frequency of implementation, either short-term or long-term:
www.ncbi.nlm.nih.gov
The guidelines of the working group led by Wyley C Hembree suggest treatment with both oestrogens and antiandrogens. Oestrogens can be administered as either oral oestrogen, transdermal estradiol patches, or by injection of estradiol valerate or estradiol cypionate. The application frequency differs depending on the patient’s reaction to the agent and the administration regimen; it could be multiple times per day or once every two weeks. Meanwhile, antiandrogens such as spironolactone or cyproterone acetate are commonly taken orally. Additionally, it is possible to block male puberty by treatment with gonadotropin‐releasing hormone (GnRH) agonist injections. (Hembree 2017).
While not every transgender woman undergoes HRT in her transition, this intervention is still widely used (Hembree 2017). We know of no studies identifying the ratio of patients who undergo HRT, nor do we know of studies investigating how much time passes between the start of transition (respectively the decision to transition) and the start of HRT. We also know of no studies on how often androgens are being prescribed in addition to or instead of 17‐beta‐estradiol, how often they are being taken, or which kinds of androgens are in use besides cyproterone acetate (CPA) and spironolactone.
According to the World Professional Association for Transgender Health (WPATH) guidelines, it is possible to suppress puberty with GnRH analogues or progestins such as medroxyprogesterone (WPATH 2011).
Spironolactone acts as a weak androgen receptor antagonist (Wenqing 2005). It also causes an increase in oestradiol levels (Rose 1977), so that further virilisation is prevented and feminisation occurs (WPATH 2011).
17‐beta‐estradiol is used to feminise the external appearance (WPATH 2011). It binds to oestrogen receptors and thus ensures gene expression, which in turn feminises appearance (Hye‐Rim 2012). In addition, estradiol suppresses gonadal testosterone production via the control systems of the hypothalamus (Hayes 2000).
For feminisation therapy, whose goal is to adapt the physical appearance and the experience of the body to a female model (by inducing breast growth, softening facial features, and inducing other physical changes commonly regarded with a feminine appearance) (WPATH 2011), the use of oral or transdermal oestrogen is recommended, and therapy with oestrogen in combination with antiandrogens is most common. Cotreatment with antiandrogens minimises the required dose of oestrogen, and thereby reduces the supposed risks of oestrogen identified in previous studies (Schürmeyer 1986; Prior 1989). Some antiandrogens are approved by WPATH — such as spironolactone, cyproterone acetate, GnRH analogists like goserelin, and 5alpha‐reductase inhibitors like finasteride — but there is no mention of recommended dosages (WPATH 2011).
The most common adverse events of spironolactone are hyperkalaemia, dehydration and hyponatraemia (Greenblatt 1973). Furthermore, spironolactone might have an influence on anxiety behavior (Fox 2016).
The adverse events of high estradiol doses described in studies from the 1980s and 1990s should be re‐evaluated because those studies used ethinyl estradiol and premarin (equine estradiol) (Prior 1989), instead of bioidentical 17‐beta‐estradiol, and progestins instead of bioidentical progesterone. Unlike the bioidentical alternatives used today, substances administered in the past (e.g. equine oestrogens, ethinyl estradiol) were associated with diverse adverse effects like thrombophilia, cardiovascular problems, breast and prostate cancer, as well as liver, adrenal gland and neural dysfunction (Griard 1978; Calderón 2009; Asscheman 2011).
The health risks attributed to estradiol doses high enough to suppress androgens have not been found in the parenteral or transdermal application of bioidentical estradiol. Thus it is unclear why those estradiol doses should be kept low in order to make the addition of androgen antagonists like CPA or spironolactone necessary.
In light of the latest discussions among experts (Seal 2012; Wierckx 2014), and current recommendations for hormonal gender affirmation treatment (WPATH 2011) — which are strongly based on the values and preferences of health consumers — trials that show positive outcomes in the case of MTF, such as feminisation, satisfactory sexual function, reduced gender dysphoria, and high quality of life must be re‐evaluated (e.g. Murad 2010).
In 2009, the overall quality of evidence relating to these outcomes was classified as low (Hembree 2017). In 2011, WPATH summarised: "There is a need for further research on the effects of hormone therapy without surgery, and without the goal of maximum physical feminisation or masculinisation" (WPATH 2011). It is necessary to determine whether subsequent trials have provided additional evidence for efficacy, or whether there is still a lack of evidence for these desired outcomes.
Janey: At the very least, maintenance protocols need to be established prior to commencement of HRT since when used for hair loss or feminization among the very young, such patients might be on the required hormones for life....
Antiandrogens or estradiol treatments or both during hormone replacement therapy in transitioning transgender women
This is a protocol for a Cochrane Review (Intervention). The objectives are as follows:The objective of this proposed systematic review and meta‐analysis is to assess the efficacy and safety of hormone replacement therapy with antiandrogens or ...
www.ncbi.nlm.nih.gov
Description of the intervention
Current guidelines suggest a combination of medical and surgical methods to treat gender dysphoria in transgender women. Hormone replacement therapy (HRT) aims to suppress the development of male attributes or reverse male attributes that have already developed. At the same time, the development of female attributes is supported. Where the HRT is not expected to be successful, which can be the case for facial bone structure, breast development and genitalia, surgical methods and techniques for permanent hair removal and hair transplantation may be used for further approximation of the body to a female body type (WPATH 2011). Janey: Nothing about hair growth or regrowth.The guidelines of the working group led by Wyley C Hembree suggest treatment with both oestrogens and antiandrogens. Oestrogens can be administered as either oral oestrogen, transdermal estradiol patches, or by injection of estradiol valerate or estradiol cypionate. The application frequency differs depending on the patient’s reaction to the agent and the administration regimen; it could be multiple times per day or once every two weeks. Meanwhile, antiandrogens such as spironolactone or cyproterone acetate are commonly taken orally. Additionally, it is possible to block male puberty by treatment with gonadotropin‐releasing hormone (GnRH) agonist injections. (Hembree 2017).
While not every transgender woman undergoes HRT in her transition, this intervention is still widely used (Hembree 2017). We know of no studies identifying the ratio of patients who undergo HRT, nor do we know of studies investigating how much time passes between the start of transition (respectively the decision to transition) and the start of HRT. We also know of no studies on how often androgens are being prescribed in addition to or instead of 17‐beta‐estradiol, how often they are being taken, or which kinds of androgens are in use besides cyproterone acetate (CPA) and spironolactone.
How the intervention might work
Several hormonal substances and combinations are used clinically for HRT in transitioning women. Cyproterone acetate is a progestin, steroidal anti‐androgen and anti‐gonadotropin that blocks the receptors for testosterone (T) and dihydrotestosterone (DHT), and thereby prevents these steroidal hormones from exerting their androgenic effects. Hence, it stops processes like body hair growth, hair loss on the head, male body fat distribution and others (Figg 2010; WPATH 2011). Janey: Cessation of hair loss is a well-known and generally prevailing side effect of HRT in transfemales but growth/regrowth tends to be entirely absent from the literature.According to the World Professional Association for Transgender Health (WPATH) guidelines, it is possible to suppress puberty with GnRH analogues or progestins such as medroxyprogesterone (WPATH 2011).
Spironolactone acts as a weak androgen receptor antagonist (Wenqing 2005). It also causes an increase in oestradiol levels (Rose 1977), so that further virilisation is prevented and feminisation occurs (WPATH 2011).
17‐beta‐estradiol is used to feminise the external appearance (WPATH 2011). It binds to oestrogen receptors and thus ensures gene expression, which in turn feminises appearance (Hye‐Rim 2012). In addition, estradiol suppresses gonadal testosterone production via the control systems of the hypothalamus (Hayes 2000).
For feminisation therapy, whose goal is to adapt the physical appearance and the experience of the body to a female model (by inducing breast growth, softening facial features, and inducing other physical changes commonly regarded with a feminine appearance) (WPATH 2011), the use of oral or transdermal oestrogen is recommended, and therapy with oestrogen in combination with antiandrogens is most common. Cotreatment with antiandrogens minimises the required dose of oestrogen, and thereby reduces the supposed risks of oestrogen identified in previous studies (Schürmeyer 1986; Prior 1989). Some antiandrogens are approved by WPATH — such as spironolactone, cyproterone acetate, GnRH analogists like goserelin, and 5alpha‐reductase inhibitors like finasteride — but there is no mention of recommended dosages (WPATH 2011).
Why it is important to do this review
Antiandrogens like cyproterone acetate and spironolactone are prescribed to transgender women in transition by many gynaecologists and endocrinologists (Schneider 2006; Flütsch 2015), and they are commonly considered to be valuable drugs to support transition (WPATH 2011; Hembree 2017). However, clinical evidence suggests that this can result in adverse events; for example, CPA has significant potential for causing depression and for worsening depressive symptoms (Seal 2012). We cannot rule out that CPA contributes to the genesis of other conditions and negatively influences the course of illnesses, including psychiatric, neurological and metabolic disorders (Griard 1978; Ramsay 1990; Oberhammer 1996; Giltay 2000; Calderón 2009; Bessone 2015).The most common adverse events of spironolactone are hyperkalaemia, dehydration and hyponatraemia (Greenblatt 1973). Furthermore, spironolactone might have an influence on anxiety behavior (Fox 2016).
The adverse events of high estradiol doses described in studies from the 1980s and 1990s should be re‐evaluated because those studies used ethinyl estradiol and premarin (equine estradiol) (Prior 1989), instead of bioidentical 17‐beta‐estradiol, and progestins instead of bioidentical progesterone. Unlike the bioidentical alternatives used today, substances administered in the past (e.g. equine oestrogens, ethinyl estradiol) were associated with diverse adverse effects like thrombophilia, cardiovascular problems, breast and prostate cancer, as well as liver, adrenal gland and neural dysfunction (Griard 1978; Calderón 2009; Asscheman 2011).
The health risks attributed to estradiol doses high enough to suppress androgens have not been found in the parenteral or transdermal application of bioidentical estradiol. Thus it is unclear why those estradiol doses should be kept low in order to make the addition of androgen antagonists like CPA or spironolactone necessary.
In light of the latest discussions among experts (Seal 2012; Wierckx 2014), and current recommendations for hormonal gender affirmation treatment (WPATH 2011) — which are strongly based on the values and preferences of health consumers — trials that show positive outcomes in the case of MTF, such as feminisation, satisfactory sexual function, reduced gender dysphoria, and high quality of life must be re‐evaluated (e.g. Murad 2010).
In 2009, the overall quality of evidence relating to these outcomes was classified as low (Hembree 2017). In 2011, WPATH summarised: "There is a need for further research on the effects of hormone therapy without surgery, and without the goal of maximum physical feminisation or masculinisation" (WPATH 2011). It is necessary to determine whether subsequent trials have provided additional evidence for efficacy, or whether there is still a lack of evidence for these desired outcomes.
Janey: At the very least, maintenance protocols need to be established prior to commencement of HRT since when used for hair loss or feminization among the very young, such patients might be on the required hormones for life....
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