Hair is not Life but it's Pretty Damn Close; HRT and Pictorial Posts Prove it.

[JaneyElizabeth]

Thanks.. do you have any experience with castor oil? Is it supposed to work in an anti androgen sort of way?

Yes stemox is something I'm considering adding before too long (want to build up and see if I can get any effect with what I'm doing first), and I've been looking into fluridil too. Never heard of seti. It's good to hear about these new options like seti, castor oil and dix...makes me feel like I at least have some hope. Possibly in a few years breezula might then be widely available.

There doesn't appear to be anything in the pipeline really close in terms of efficacy to what we already have now. CB, Alfatradiol, Breezula and fluridil have not shown themselves to be effective enough for most people who either have no sides or who can tolerate the Big 3. If you look on the experimental threads, a lot of this has actually become a tongue-in-cheek joke because the newly touted ones always fizzle out in round two of testing or they end up being barely significant statistically.

 

[jd_uk]

There doesn't appear to be anything in the pipeline really close in terms of efficacy to what we already have now. CB, Alfatradiol, Breezula and fluridil have not shown themselves to be effective enough for most people who either have no sides or who can tolerate the Big 3. If you look on the experimental threads, a lot of this has actually become a tongue-in-cheek joke because the newly touted ones always fizzle out in round two of testing or they end up being barely significant statistically.

Didn't the breezula trials show quite a significant improvement though (close to finasteride)? I know they started declining after 6 months but I believe they're experimenting with dosages now to try and improve that? For me its just a case of even if it did something (e.g. even if it were 50% as effective as finasteride) then I could combine it with other stuff and hopefully keep what I have or maybe improve just a little bit. I'll never have 'good' hair...but if I could just thicken my crown and hairline by like 15% and maintain that it would be great..i would be able to get my hair cut in a way which made it look like I didn't have much/any hair loss to the average person.

 

[Norwoody]

Thanks.. do you have any experience with castor oil? Is it supposed to work in an anti androgen sort of way?

Yes stemox is something I'm considering adding before too long (want to build up and see if I can get any effect with what I'm doing first), and I've been looking into fluridil too. Never heard of seti. It's good to hear about these new options like seti, castor oil and dix...makes me feel like I at least have some hope. Possibly in a few years breezula might then be widely available.

I've used castor oil. No antiandrogenic effects. It works through prostaglandins (promotes healing, reduces inflammation).

Breezula (CB) is a 2% concentration. Most CB users on this forum recommend 5-8%.

 

[jd_uk]

I've used castor oil. No antiandrogenic effects. It works through prostaglandins (promotes healing, reduces inflammation).

Breezula (CB) is a 2% concentration. Most CB users on this forum recommend 5-8%.

Any results with the castor oil? I thought that Breezula had done tests at 5 and 7.5%, but the winlevi was only like 1%? Either way I'm in the UK and it will probably be ages before it becomes available here as it's only being reviewed by the FDA for now.

 

[Norwoody]

It helps but you likely need dermarolling for it to be effective.

 

[jd_uk]

It helps but you likely need dermarolling for it to be effective.

OK, thanks.

 

[Norwoody]

Maybe a laser helmet too

 

[JaneyElizabeth]

The Science Behind Why Weed Makes Sex Feel That Much Better

And which strains are best for cannabis-infused sex

www.insidehook.com

It's a vasodilator. Too bad that only works for minoxidil it appears, at the moment.

 

[JaneyElizabeth]

More Greek and Roman Instances of Androgyny:

Notice the lack of breast growth on the western Goddess of classical love....

 

[JaneyElizabeth]

Question: "We all need to accept that it's over. It never began. The rollercoaster ended the moment each and every one of you began to lose hair. Not sure what else to say on this topic".

Everyone is different. I recommend reading the wikipedia entry on the Greek myth of Sisyphus and reading/studying Camus's related book of the same name. It has to do with deciding psychologically which battles in life are worth taking on recurrently and when it's best to engage rather in acceptance. Only you can make this balancing risk/reward analysis.

I have been at this for 36 years albeit except temporarily, never bald past the point of "no hope" and that point arguably no longer exists for many men/people. It's all a delicate internal balancing act. See an endocrinologist and seek therapy for the extreme pain of hair loss, especially premature hair loss. We have all been there and are with you but there are steps you can take to clarify such issues in your mind and they are neither right nor wrong in the abstract. Notice in baldness, many of us like to state generalized principles about acceptance based upon where we are psychologically, not so much on our scientific chances and financial abilities to get effective treatment.

Goddess bless.

Remember a softer god, conceptually Goddess wants good things for you hair-wise. The dude with the beard and the comb-over, not so much....

 

[JaneyElizabeth]

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:


Antiandrogens or estradiol treatments or both during hormone replacement therapy in transitioning transgender women

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....

 

[Pls_NW-1]

I prefer Gyno > baldness.

Change my mind

 

[tato123]

I wrote this to a friend here on the forum and I will repost here it can help some users to understand some concepts.




Testosterone increases / stimulates / creates various body tissues in our entire body.

It is possible to show in the tissues of bald men a great presence of certain types of collagens and inflammatory processes But did it develop before or after the fall? continue , testosterona -DHT (think this DHT stimulates hair growth throughout the body, but it does not happen on the scalp the question is why? ) in scalp DHT start cascate inflamatory thicken the outer layer of the skin by the process of inflammatory fibrosis, and strangle the follicles .
I want you to notice that high levels of testosterone stimulate IGF-1, this can cause certain degrees of low "acromegaly" by changing your cranial and body structure, if you look at our anatomy you can see that we have no muscles in the frontal and upper scalp, note this article that I'll post now
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4639964/


You can see that it is connected with the tension exerted by our cranial box and by the muscular stretching and baldness in the male pattern.

Is so many ways , this sh*t is a big sh*t , baldness is Hydra 7 heads of the Greeks

Testosterone affects our bodies in infinite ways, so we see that infinite protocols work for some and not for others , because is more than DHT .





Having said that and knowing what I know, I know that estrogen increases the production of collagens that give quality health to specific skin types(collagen skin types), that testosterone does not check and does not maintain mainteince correctly most of the time, so the body we naturally transform T into E via aromatase for fertility (cels sertoli , cels leydig need this) , and all body need e2 .

However for some reason we lose receptors or create resistance in our E receptors or drop levels of E or maybe our testosterone drops a little bit and it ends up for any reason and our natural conversion to e2 drop, and this is not noticeable in the short term, but in a chronic state our body has physiological changes due to this lack of balance.

What I believe is that for XY the secret is not to block T entirely as TRANS methods as bridge did, he changed his entire endocrine system.

If he stops taking the medication, his life is probably over because he cannot return, he must have developed primary hypogonadism.

I don't think T is our villain, but the hormonal balance,I think the replacement of estrogens in low dose (bi-estro maybe) or stimulates LH for more conversion T -E2 men is essential if you want to maintain health, general condition, youth for health quality in general of the body, all the boys who take HRT if you notice it reach a perfect balance at a certain point of the treatment that is they look like beautiful men, I believe that the fabrics tissues in body still hold the marks of T and when E goes up it gives this appearance "Boy Band", only when they advance their body in the treatment they transform into women totally I believe that this point is where the fabrics tissues become chronicles in E without the presence of T.

I think the secret is the manipulation of the E with its T, and what I can tell you is that in several patients only E is not able to block the production of T, not even! Because this TRANS NEED USE AA , only E not suprimed T (sometimes yes) But I want you to note that progesterone is not always used in transitions I’ve seen complete transitions with AA + e2 and a full head. So it's a matter of adapting your body to "large" amounts of E and T without suppressing its axis maybe use some natural herb to influence LH/FSH at first maybe be a way.

Bicalutamide comes up against a lot of what I said, high testosterone levels influenced IGF-1, and thousands of other things, so bicalutamide is not a right shot in some cases .

I tried to explain as clearly as possible

 

[Norwoody]

I wrote this to a friend here on the forum and I will repost here it can help some users to understand some concepts.




Testosterone increases / stimulates / creates various body tissues in our entire body.

It is possible to show in the tissues of bald men a great presence of certain types of collagens and inflammatory processes But did it develop before or after the fall? continue , testosterona -DHT (think this DHT stimulates hair growth throughout the body, but it does not happen on the scalp the question is why? ) in scalp DHT start cascate inflamatory thicken the outer layer of the skin by the process of inflammatory fibrosis, and strangle the follicles .
I want you to notice that high levels of testosterone stimulate IGF-1, this can cause certain degrees of low "acromegaly" by changing your cranial and body structure, if you look at our anatomy you can see that we have no muscles in the frontal and upper scalp, note this article that I'll post now
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4639964/


You can see that it is connected with the tension exerted by our cranial box and by the muscular stretching and baldness in the male pattern.

Is so many ways , this sh*t is a big sh*t , baldness is Hydra 7 heads of the Greeks

Testosterone affects our bodies in infinite ways, so we see that infinite protocols work for some and not for others , because is more than DHT .





Having said that and knowing what I know, I know that estrogen increases the production of collagens that give quality health to specific skin types(collagen skin types), that testosterone does not check and does not maintain mainteince correctly most of the time, so the body we naturally transform T into E via aromatase for fertility (cels sertoli , cels leydig need this) , and all body need e2 .

However for some reason we lose receptors or create resistance in our E receptors or drop levels of E or maybe our testosterone drops a little bit and it ends up for any reason and our natural conversion to e2 drop, and this is not noticeable in the short term, but in a chronic state our body has physiological changes due to this lack of balance.

What I believe is that for XY the secret is not to block T entirely as TRANS methods as bridge did, he changed his entire endocrine system.

If he stops taking the medication, his life is probably over because he cannot return, he must have developed primary hypogonadism.

I don't think T is our villain, but the hormonal balance,I think the replacement of estrogens in low dose (bi-estro maybe) or stimulates LH for more conversion T -E2 men is essential if you want to maintain health, general condition, youth for health quality in general of the body, all the boys who take HRT if you notice it reach a perfect balance at a certain point of the treatment that is they look like beautiful men, I believe that the fabrics tissues in body still hold the marks of T and when E goes up it gives this appearance "Boy Band", only when they advance their body in the treatment they transform into women totally I believe that this point is where the fabrics tissues become chronicles in E without the presence of T.

I think the secret is the manipulation of the E with its T, and what I can tell you is that in several patients only E is not able to block the production of T, not even! Because this TRANS NEED USE AA , only E not suprimed T (sometimes yes) But I want you to note that progesterone is not always used in transitions I’ve seen complete transitions with AA + e2 and a full head. So it's a matter of adapting your body to "large" amounts of E and T without suppressing its axis maybe use some natural herb to influence LH/FSH at first maybe be a way.

Bicalutamide comes up against a lot of what I said, high testosterone levels influenced IGF-1, and thousands of other things, so bicalutamide is not a right shot in some cases .

I tried to explain as clearly as possible

So aromatization is key? That's the conclusion I've come to reading this. What are some example regimens and progressions? Thanks.

 

[tato123]

So aromatization is key? That's the conclusion I've come to reading this. What are some example regimens and progressions? Thanks.

I believe so, it would explain the fact that bodybuilders report increased hair density and growth during a full cycle of steroids.

Your e2 levels must be at the height during the cycle, following the testosterone levels, the problem is that if there was not an adequate monitoring, it will have a rebound effect.

 

[tato123]

So aromatization is key? That's the conclusion I've come to reading this. What are some example regimens and progressions? Thanks.

I think that here we can make use of

Topical estradiol.

betamethasone Valerate topical in the affected region cycle use , 10 days on , 10 days off , something like that (to increase estrogen receptor sensitivity)

Microneedling

Oral mixonidil

DHT blockers

Measure your T levels at the beginning to get an idea of what we are doing and the path is right there.

 

[Norwoody]

I believe so, it would explain the fact that bodybuilders report increased hair density and growth during a full cycle of steroids.

Your e2 levels must be at the height during the cycle, following the testosterone levels, the problem is that if there was not an adequate monitoring, it will have a rebound effect.

What about the original medically therapeutic doses of anabolics? Ex., 5-10mg methandienone, 10-20mg oxandrolone, etc?

 

[Pls_NW-1]

I believe so, it would explain the fact that bodybuilders report increased hair density and growth during a full cycle of steroids.

Your e2 levels must be at the height during the cycle, following the testosterone levels, the problem is that if there was not an adequate monitoring, it will have a rebound effect.

Quite funny, Bicalutamide actually gives you that, high sex hormones.

I don't think that bica will be enough for male pattern baldness. 5ARi's are the first line. I am thinking more and more that we will need to use E2 to fully stop male pattern baldness but idk. In theory, Bica + finasteride/duta (to support bica) will stop male pattern baldness totally, because androgens cant transcribe miniaturzation information through ARs.

 

[tato123]

What about the original medically therapeutic doses of anabolics? Ex., 5-10mg methandienone, 10-20mg oxandrolone, etc?

I think that to have a meaningful effect I would need a complete cycle.

High doses of Cypionate, testosterone propyanate, testosterone decanoate

Nandrolone, Trenbolone, oxymetholone

Thyroid hormones


There are many drugs that they use and you can't say in the end what really makes them grow, but as they said it is similar to what bicalutamide provides but bicalutamide is endogenous, believe these guys who go on stage depending on their category are very concerned with your hairline.

 

[Norwoody]

One guy on the forum reported oxandrolone working. Not sure the dosage though. Probably around 50mg if he's competitive. I think he went 6-8 weeks with it.