Bicalutimide, Dutasteride & Progesterone

[z38]

Hopefully, I won't unknowingly breach any of our host's rules in my search to reverse hair loss ASAP. Thanks almost entirely to the cost of owning any kind of a home-and keeping it-on Long Island (best keep it apolitical here or else, z38) most of my dearest life quality plans have been seriously postponed or destroyed. And it would not at all surprise me if recent repercussions of those ugly facts are why I was very likely hit badly with telogen effluvium. Though I have respectable courage and resourcefulness, my stress and anxiety levels are now so high and constant that unless I can gain more income without leaving my current job I don't know if my hair and overall health will ever recuperate.

But could this effluvium be non-stress related, or at least partially so? Besides, my hair began thinning again over a year before I got hit with this tremendous bomb. This is what's caused me to rethink my regimen. I am probably otherwise in very good shape for one well past 50. I've been post-op since 1997 and been on estradiol valerate well before and ever since. Proscar worked very well when I began it in the mid 90s with 2% minoxidil. I had new long hairs growing all along my crown; I couldn't believe how low my hairline was really supposed to be! I jumped out of the shower to show my Mom and we were both ecstatic.

What was then so strange was that after I had my surgery no matter how long I then kept up with the Proscar my hair didn't further improve. And over time I started to lose it again, even when continuing the minoxidil, and of course my estradiol valerate injections. Luckily, it didn't get much worse before 2003 when Dutasteride became available. That, along with then available 5% minoxidil definitely helped reverse much of the hair loss for some years.

But later I was hit with very agonizing hair loss and regrowth cycles continuing ever since. I even returned to the same and then higher doses of spiro that I used for years before my surgery. But while spiro did retard facial hair it did little if anything to reverse hair loss-or to thicken the vellus hairs on the crown after months of use.

I then thought the hair loss might be due to the troughs occurring below a nominally effective baseline of my 14 day estradiol valerate injections or the dosing, but my endo's review of my blood levels scratched that theory.

Only recently after much more extensive research (thank goodness for one very helpful online source even if it may not always be 100% accurate), it now appears that IF my hair loss is not mostly stress related, it might be caused by Dutasteride insensitivity from long term down regulation (even after doubling my usual daily dose), as I've used it continuously since 2003.

Or hair loss due to estrogen dominance? And/or due to post-op levels of (natural) progesterone? 


So for the last 4 weeks my derm has prescribed topical progesterone, followed 30 minutes later with 5% OTC minoxidil. So far I can't tell for sure if it's helped or not, or possibly made things worse (wrong kind of progesterone??).

Btw, after (first massaging my scalp) applying the drops of ?mL progesterone around my scalp and pressing it before the minoxidil twice daily, I was amazed that after the first 48 hours of use how much more youthful the tops of my hands look and feel.

I'm due to see both my endo and derm next week to discuss my 10 hour fasting blood test levels of progesterone, folate, ferritin, B12 and reticulum. If my progesterone levels should be boosted to protect brain, bone and skin of someone (anyone?) my age, then some dose of progesterone may be indicated. 

I also suspect that my derm may up the strength of something in the minoxidil + progesterone topical compound.

I haven't had time to fill my endo's script for the natural progesterone cream. Presumably, the benefits of using a cream is that you can vary the dose as desired to prevent bloating, headache, abdominal pain and other affects that many people get from using even micronized (natural) progesterone pills. However, it remains to be seen how a low strength cream compared to pills will raise progesterone to pre-op levels-which I can only hope will be a good thing for me.

Nevertheless, there does seem to be substantial evidence that age-related declining levels of progesterone is not a good thing for anyone. And that supplementation based on measured systemic levels is likely beneficial. However, as there has been some number of cases with periodontal problems, it's clearly best to proceed with caution. And one must also decide on using natural or synthetic progesterone, though many would likely conclude that to be a no-brainer. In any case, both are not likely to be expensive.

Last but not least: Bicalutamide. According to a very popular yet respectably accurate online source, while Bicalutamide does not reduce androgens, its blocking action is very strong and entirely specific to androgen receptors, and to which it may even contribute to their degradation. Only 1/6 the amount used in prostate cancer cases has been found to be effective against hirsutism, at least in ciswomen. So I'm hoping that something like 2/6 of it will stop both facial growth and spur scalp hair regrowth, along with my usual regimen, and likely progesterone dosing.


Unfortunately, the vast majority of Bicalutamide users found in my research have been cismen and pre-op transwomen. And even though a good percentage of them were taking Bicalutamide hoping to reverse hair loss and/or kill libido, I certainly can't predict how it will work on me, regardless of dose. 

Assuming I don't get laid off or have more grief over housing costs, I promise to follow up over the next four to 6 months. I only hope that Bicalutamide and/or the bioidentical progesterone (which is also a DHT blocker) won't make things worse.

News Flash: At the risk of not being pc, next year keep watch for the Asian market debut of a possible stem cell cure by a Canadian firm and its Japanese partner who together with another partner may issue a stem cell "kit" solution that may accomplish prodigious and essentially permanent regrowth. And though not cheap, it may actually cost 2.5X less than what some would pay for PRP therapy. Might there soon be a time when we can throw away our topical apps? 

I hope I've been of some help to others who suffer with and fight against hair loss and its many causes. Thanks to all for your feedback.     

[josie76]

Well if you are post GCS then you should not be on any androgen blocker.

In general bicalutimide is androgen receptor antagonist only with no other endocrine effects.
Taking it by preGCS trans women is used specifically for that purpose. It should make an alpha5-reductase inhibitor not nessecary.

Spironolactone is also used as an androgen receptor antagonist but was brought to market for aldersterone inhibitor purposes. It does bind to several other receptor sites but primarily is active on the androgen and aldersterone receptors. It's metabolites have a repressive effect on the production of testosterone as well.

Duteraside is an alpha5-reductase enzyme inhibitor for type1, type2, and type3 receptor sites. This drug can be particularly bad at lowering neurotransmitter production.

Finasteride is an alpha5-reductase inhibitor for type2 and type3 receptor sites and has a 100x less affinity for the type1 receptor site. Finasteride does also lower neurotransmitter levels but ranges depending on individual from 13% to 300%+ reduction.


So if you are post-op, then your body should have below normal female levels of testosterone to begin with. You can put your blood test levels here just not medication dosages. You should not need any androgen blocker or alpha5-reductase inhibitor (DHT blocker) in general. You may be having hair thinning from estrogen dominance. In cis women progesterone production drops with age in relation to estrogen production which also drops off some before menapause. This can cause issues like pseudo-hypothyroidism. The inactive thyroid can itself cause hair loss.

Maybe you should ask your doctor for a complete blood test. Estrodiol, Progesterone, Testosterone, and TSH thyroid stimulating hormone.

Bioidenticle progesterone is known to reduce estrogen's negative impact on thyroid regulation. The metabolites of it also reduce the blood clotting factor increase caused by estrogen which should reduce the risk for DVT. It is also a primary precursor hormone for the important neurotransmitter allopregnalone. Allopregnalone requires the alphaR-reductase type1 receptor activation mostly so your duteraside will inhibit that.

My non educated thought would be to ask your doctor about tapering off all of the blockers and adding progesterone (real not MPA).  Getting you P levels matching to your E levels might help out.

[Mandy M]

I've made my views on Bicalutamide clear elsewhere.

https://www.susans.org/forums/index.php?topic=230087.20

It is a toxic anti-cancer medication which is an untested drug for the purposes to which MtF's are attempting to use it.

Because it is a rare drug compared with cyproterone acetate (which I also think is dangerous) fewer scientific studies have been conducted.
However:
http://www.druglib.com/druginfo/bicalutamide/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1477613/
See also:
http://www.cancerresearchuk.org/about-cancer/cancer-in-general/treatment/cancer-drugs/drugs/bicalutamide/side-effects
https://www.drugs.com/pro/bicalutamide.html
https://www.ncbi.nlm.nih.gov/pubmed/11260298
http://www.sciencedirect.com/topics/neuroscience/bicalutamide


I advise people coming on here not to rely on wikipedia for their drug regimes. This is much too important and serious to health to reduce to non peer-reviewed internet sites.

Please everyone, go and see your endocrinologist / healthcare professionals and get properly monitored medication.

[Dani]

I advise people coming on here not to rely on wikipedia for their drug regimes. This is much too important and serious to health to reduce to non peer-reviewed internet sites.

Please everyone, go and see your endocrinologist / healthcare professionals and get properly monitored medication.

This is excellent advice. Knowing what your medications do is important and websites such as webmd and drugs.com are very good. Subscription websites such as Micromedia are excellent, but are for medical professionals.

For safe and effective HRT, see a doctor who is experienced in transgender hormone therapy.

[KayXo]

You may be having hair thinning from estrogen dominance.

Are there actual studies that support your assertion or is this just hearsay?

In cis women progesterone production drops with age in relation to estrogen production which also drops off some before menapause. This can cause issues like pseudo-hypothyroidism. The inactive thyroid can itself cause hair loss.

For many years, I've had moderate to high estrogen levels (up to 4,000 pg/ml) relative to progesterone which at times, was close to zero. Despite this, there were no signs of hypothyroidism, TSH always in normal range. Please be sure that your assertions are strongly scientifically supported or you may be doing more harm than good. To everyone reading, take the written word (mine included) with a grain of salt, do your own research, discuss with your doctors.

Bioidenticle progesterone is known to reduce estrogen's negative impact on thyroid regulation.The metabolites of it also reduce the blood clotting factor increase caused by estrogen which should reduce the risk for DVT. It is also a primary precursor hormone for the important neurotransmitter allopregnalone. Allopregnalone requires the alphaR-reductase type1 receptor activation mostly so your duteraside will inhibit that.

Transdermal estradiol has been shown not only to not increase the risk of DVT but to normalize coagulation in men with prostate cancer and protect against DVT despite high levels of estradiol. I've read no mention of 5-alpha reductase type 1 being more important for the production of allopregnanolone than type 2, EVER. As far as thyroid, same.

Getting you P levels matching to your E levels might help out.

Studies aren't supportive of this and at best, the evidence is anecdotal. So far, I seem to be doing better without progesterone than with. My skin is in a better condition, I have more energy and I am slimmer. I also take a little testosterone.

I've made my views on Bicalutamide clear elsewhere.

https://www.susans.org/forums/index.php?topic=230087.20

It is a toxic anti-cancer medication which is an untested drug for the purposes to which MtF's are attempting to use it.

Nilutamide is a similar drug to bicalutamide with more side-effects and it has been tested in MtFs. There are studies assessing its effects in our population.

Because it is a rare drug compared with cyproterone acetate (which I also think is dangerous) fewer scientific studies have been conducted.

Bicalutamide is a NEWER drug but extensively researched and many papers have been written about it. Its relatively safe profile has been well established in men with advanced prostate cancer.

I advise people coming on here not to rely on wikipedia for their drug regimes. This is much too important and serious to health to reduce to non peer-reviewed internet sites.

The information on the wikipedia page is based on several peer-reviewed scientific papers that can be shared with one's doctor.

[josie76]

Kay

I don't have all of my notes here. I have been working on a "flow chart" of sorts that maps out the chemical precursor relationships required to produce each of these specific hormones and how our different medications specifically act in both negative and positive ways in the ezymatic relationships.

A5-reductase type1 is needed to convert progesterone into the next precursor in the chain toward building allopregnalone. Specifically type1.

There are a couple of differing paths and control/trigger chemicals that can both be additive and reductive toward these chemical chains. I wish there was a nice simple 3D mapping done somewhere to make this all easy to lookup but so far I have found none. And of course everything in medical journals is typically described with no mutant gene expression so that only works on a "perfect" human. For the normal population gene expression can be much more variable leading to the old phrase "your mileage may vary".

[z38]

Well if you are post GCS then you should not be on any androgen blocker.

So if you are post-op, then your body should have below normal female levels of testosterone to begin with. You should not need any androgen blocker or alpha5-reductase inhibitor (DHT blocker) in general.

You may be having hair thinning from estrogen dominance. In cis women progesterone production drops with age in relation to estrogen production which also drops off some before menapause. This can cause issues like pseudo-hypothyroidism. The inactive thyroid can itself cause hair loss.

Maybe you should ask your doctor for a complete blood test. Estrodiol, Progesterone, Testosterone, and TSH thyroid stimulating hormone.

Bioidenticle progesterone is known to reduce estrogen's negative impact on thyroid regulation. The metabolites of it also reduce the blood clotting factor increase caused by estrogen which should reduce the risk for DVT. It is also a primary precursor hormone for the important neurotransmitter allopregnalone. Allopregnalone requires the alphaR-reductase type1 receptor activation mostly so your duteraside will inhibit that.

My non educated thought would be to ask your doctor about tapering off all of the blockers and adding progesterone (real not MPA).  Getting you P levels matching to your E levels might help out.

Last month was the first time that I had asked to have my progesterone level tested. In cis men the testes produce most of the progesterone. But I'm 10 years post-op and have been on estradiol valerate injections twice monthly long before and ever since. So I was shocked when the blood levels showed it at 13 ng.

My endo said that the adrenals are evidently producing enough progesterone to balance (or to at least attempt to balance) my exogenous estrogen levels.

"Balance"? Then why did the print out say progesterone 'high" 13 ng?

Too bad that I have no record of any pre-op progesterone level test. Would that level likely be this high?

Some of this month's other results:  Testos serum <3 ng. Bound Testos is <.2.  Estro 909 ng. B12 level "high" 1474 pg. HDL and LDL 252 and 137  (both have long been high). Iron is 339 bind/serum 339/125 ug. Creatinine serum LOW 0.62 mg; BUN/Creatinine ratio 13. Folate Serum >20.0. Vit D is 39   D2 is 14  D3 is 25. Hemoglobin 5.1. DHEA 144.T3 is 90. Zinc plasma or serum 100. Ferritin 86. Insulin 3.0. Thyroid Peroxidase 11, Thyroglobulin 10.8. Anti-Thyroglobulin Antibodies <1.0.
TSH 1.830 uIU/ml.

My endo is an understanding and highly sought after physician but as he appears not to have a lot of actual experience with transwomen he might be somewhat ill-equipped to correlate some or all symptoms and test measurements with and/or determine the causes of estrogen dominance in transwomen. But despite the "high" progesterone level, might I still be at risk for "estrogen dominance"?

OR even "progesterone dominance" and what side effects that may have?

But what's confusing about progesterone is its apparent "friend or foe" (or benign?) behavior towards androgenic hair loss. On the one hand, as a competitive inhibitor of 5-alpha reductase, it ought to function as a natural DHT blocker. https://en.wikipedia.org/wiki/Progesterone_(medication)#Pharmacodynamics
http://www.larabriden.com/best-natural-anti-androgen-treatments-hirsutism/

On the other hand, Androsterone, which is derived from progesterone-perhaps because of this https://en.wikipedia.org/wiki/Progesterone_5alpha-reductase  "......exerts minor masculinizng effects, but with one-seventh the intensity of testosterone. It is found in approximately equal amounts in the plasma and urine of both males and females." https://en.wikipedia.org/wiki/Androgen#Types_and_examples

Thus, can my "high" progesterone level put me at risk for hair loss?


If not then why did the hair loss slowly return after the estrogen valerate and the anti-androgens had halted and reversed at least 70% of it 20 years ago?

And why hair loss after the orchiectomy 10 years ago??

How likely would the hair loss then be attributable to using too much estrogen for a typical pre-op transwoman?

And the same strength, dose and frequency later for the same post-op transwomen?

And/or hair loss because the vials of estradiol valerate that I've always been using (from 4 or 5 manufacturers being sold in the USA over the last 20 years) are almost certainly synthetic rather than bioidentical?

And that if my post-op estradiol valerate doses are, in fact, too big and/or too frequent, is that why the recently tested adrenal progesterone level was "high" rather than normal?

Please compare my numbers above.

I can get natural estradiol valerate made by a local compounding pharmacy. But what bodily or other changes should a post-op person expect from hitting on the right estrogen level to in turn get the adrenals to make "normal" levels of progesterone?

For example, might libido and beard growth be better suppressed with natural exogenous estrogen? Though some of us regard it differently within two to three months after first beginning therapy it was like this heavy something was lifted off me, if quite unexpectedly. And beard growth was sharply reduced. These benefits remained for a few years, but began returning not long around the year of my surgery, after which they dropped off again. But several years later libido and beard growth retuned and are perhaps 60 to 70% of what they ever were.

How likely could this happen post-op due to estrogen dominance, using synthetic estradiol valerate and/or what else?
   
Any observed desired or acceptable range or ratio for where post-op estrogen and progesterone levels should be before the onset of estrogen dominance?

Or will it be less likely necessary to lower the strength, dose and frequency of bioidentical estradiol valerate which I've been on forever in order to get the adrenals to produce normal progesterone levels?

In which case there would be no need for even bioidentical (not MPA) progesterone?

In any case, would bioidentical estradiol valerate have any less risk of causing DVT than the synthetic?

Please forgive my ignorance if I misunderstood or misinterpreted the way body systems function and certain drugs interact with same.

ps: I've been using 5% minoxidil + Dutasteride for years with moderate to good results, but which keep coming and going. So my derm prescribed using topical progesterone to apply 30 minutes or so before applying the minoxidil.

Wow! It it's certainly true of what's said about progesterone and skin health. While it didn't thicken the skin on the tops of my hands they look a good 10 years younger. And this actually happened within 3 days of beginning the topical progesterone. What's especially remarkable is that the only progesterone I've ever used is the minoxidil + progesterone. I do use my fingers to press the progesterone into my scalp and leave it on 30 minutes before applying the minoxidil. But the progesterone strength is apparently 20x less than what's normally prescribed to help decelerate skin aging. https://en.wikipedia.org/wiki/Progesterone#Skin_health

Given extenuating conditions like possible estrogen dominance, high cortisol levels due to chronic high stress levels and only after 3 months of use, I can't say for sure if they are working. 

But if I can soon rectify any estrogen dominant threat, and then if not truly impressed after another 5 to 6 months, I will ask about doubling the minoxidil strength

Alternately, a derm in Manhattan often prescribes 5% minoxidil + betamethasone. https://en.wikipedia.org/wiki/Betamethasone

[z38]

Well if you are post GCS then you should not be on any androgen blocker.

Assuming that "estrogen dominance" in post-op transwomen can be overcome by using the right amount of bioidentical estrogen-and thereby achieve the right amount of adrenal progesterone, would not many transwomen still be at risk for androgenic hair loss?

And whether or not a topical is used to stop (and hopefully reverse) the hair loss, why wouldn't if be sensible for post-ops to take some kind of androgen blocker to compete with the androgens produced in an area of the adrenal glands? https://en.wikipedia.org/wiki/Zona_reticularis  https://en.wikipedia.org/wiki/Dihydrotestosterone#Biological_activity

And might 1this adrenal androgen factory being working overtime during chronic stress periods (i.e. Lack of sleep, Long Island commuting; my job)?

Or is it actually the higher cortisol and/or reduced growth hormone levels which occurs during high and/or frequent stress episodes that contribute to hair loss, rather than remaining adrenal androgens in otherwise healthy post-op transwomen?

But if adrenal androgens could cause hair loss in those post-op women who have no indication of estrogen dominance in their blood tests, then which anti-androgen would likely be the most effective while having the least harmful effects?

According to your findings spiro would seem to be at least one to consider using as you said it inhibits aldersterone, if that can cause hair loss.

But you seem to imply that finasteride was way more effective than dutasteride due not to number of reductase enzymes it can inhibit but how effectively it can reduce neurotransmissions? If yes, then is this why finasteride might be more effective?

As for health risks, why should dutasteride increase the threat of DVT? https://www.mayoclinic.org/diseases-conditions/deep-vein-thrombosis/symptoms-causes/syc-20352557

But what about Bicalutamide or others?  Of course, hair loss can occur for many reasons. Sometimes it's temporary, as from telogen effluvium. Or it can require stem cell therapy from hair loss due to aging. http://www.sciencemag.org/news/2016/02/one-reason-your-hair-thinning-some-it-turns-skin 

How does a post-op person otherwise choose to protect her hair while minimizing serious health risks?

[Chloe]

Gee wish I had stock in, got kicked back/funded by, worked directly for the pharmaceutical companies!!

Such an 'authority' based discussion!! Suppose 50+ mercury-laden immunizations for newborn infants and fluoridated 'bottled baby water' is a good thing too??

Mods my apologies it's just that I don't believe, especially when it comes to TG, what "The Well-Intentioned Doctors" themselves are being told!!!

[josie76]

Z38

I think you may have a couple of my statement turned around. Anyway your Testosterone is bottomed out below "average" female range. Since you are post op only the (hypothalamus, pituitary, adrenal) HPA axes can produce testosterone in any measurable amount. From your blood test it is barely anything. This negates the need for an antiandrogen medication.

With such low T your body can hardly have any DHT so I would say that is not your hair loss issue at all.

Finasteride has less of an impact on neuro-regulating hormone production than Duteraside.  Duteraside is really bad for depression. Finasteride can cause it as well but not for everyone.

Bicalutamide is an androgen receptor blocker. Again with such low T there is no reason for you to be taking it. It does not lower T, it just blocks the receptors.

Spironolactone is really not good for anyone. Yes it lowers aldosterone which affects sodium levels in the body. First risk, low sodium = high potassium which causes neurological symptoms that can be reversed with increased salt intake. By its interactions with the MR (mineralocorticoid receptors) and the GR (glucocorticoid receptors) it produces a net effect of driving stress hormone production like cortisol to near maximum output. It also interferes in enzymatic activities including the ones needed for neuro-regulation hormone production.

Progesterone, now we are getting into complex subject matter. Progesterone has 35+ useful metabolites. It does interact with androgen receptors but in a completely different way. It provides at least 4 neuro-regulating hormones. Several metabolites actually lower the risk of DVT as they affect the platelets themselves. (Technically they trigger a Ca+2 influx which changes the shape of the platelets countering the Ca+2 egress caused by thrombin). I have a ton of research in this and medication's effect on receptors and ezymatic reactions. It only very slightly inhibits a5-reductase.

Assuming you meant your estrogen is 909pg/ml that's still kind of high range. Seems most trans girls shoot for a 200-400 pg/ml. If it was ng/ml that's WAY to high.

Anyway some hormone charts I've seen put in some average values.
47 year old female cycle high E2 = 100pg/ml, P = 1000pg/ml (1ng/ml)
Fertile years ovulation peak.   E2 = 400pg/ml, P = 1-3ng/ml
Fertile years mid luteal phase E2= 200-300pg/ml , P = 7-20ng/ml

But every person is different, these are just some reference values.

[LexiDreamer]

Some of this month's other results:  Testos serum <3 ng. Bound Testos is <.2.  Estro 909 ng. B12 level "high" 1474 pg. HDL and LDL 252 and 137  (both have long been high). Iron is 339 bind/serum 339/125 ug. Creatinine serum LOW 0.62 mg; BUN/Creatinine ratio 13. Folate Serum >20.0. Vit D is 39   D2 is 14  D3 is 25. Hemoglobin 5.1. DHEA 144.T3 is 90. Zinc plasma or serum 100. Ferritin 86. Insulin 3.0. Thyroid Peroxidase 11, Thyroglobulin 10.8. Anti-Thyroglobulin Antibodies <1.0.
TSH 1.830 uIU/ml.

14 days between injections is a long time for Estradiol Valerate.
How long after your last EV injection did they take your blood when the estradiol came back as 909 ng/mL ?

IM Estradiol Valerate drops off significantly right around day 6. Most knowledgeable practitioners recommend a 5 to 7 day injection cycle for EV.

[z38]

14 days between injections is a long time for Estradiol Valerate.
How long after your last EV injection did they take your blood when the estradiol came back as 909 ng/mL ?

IM Estradiol Valerate drops off significantly right around day 6. Most knowledgeable practitioners recommend a 5 to 7 day injection cycle for EV.

Thanks for asking. I had an injection 11/6 and the blood was drawn 11/13. Also, please excuse the typo-it's 909 pg not ng/mL, but those two facts may give you a clue to actual strength and quantity EV I get. 

[z38]

I think you may have a couple of my statement turned around. Anyway your Testosterone is bottomed out below "average" female range. Since you are post op only the (hypothalamus, pituitary, adrenal) HPA axes can produce testosterone in any measurable amount. From your blood test it is barely anything. This negates the need for an antiandrogen medication.

With such low T your body can hardly have any DHT so I would say that is not your hair loss issue at all.

Progesterone, now we are getting into complex subject matter. I have a ton of research in this and medication's effect on receptors and ezymatic reactions. It only very slightly inhibits a5-reductase.

Assuming you meant your estrogen is 909pg/ml that's still kind of high range. Seems most trans girls shoot for a 200-400 pg/ml. If it was ng/ml that's WAY to high.

Anyway some hormone charts I've seen put in some average values.
47 year old female cycle high E2 = 100pg/ml, P = 1000pg/ml (1ng/ml)
Fertile years ovulation peak.   E2 = 400pg/ml, P = 1-3ng/ml
Fertile years mid luteal phase E2= 200-300pg/ml , P = 7-20ng/ml

But every person is different, these are just some reference values.

I am indebted to you Josie76, and to our studious and forthright members for warning me off these.
https://www.susans.org/forums/index.php?topic=175177.0
https://www.openanesthesia.org/aba_diuretics_-_adverse_effects/
https://www.ehealthme.com/ds/finasteride/tinnitus/

NEVER again.

But this really scares me. https://treato.com/Avodart,Tinnitus/?a=s

Dutasteride might have been protecting my hair and I'm scared about discontinuing  all of them. 

And karmatic1110 can't be sure that spiro is not causing her hair loss along with dry skin issues. https://www.susans.org/forums/index.php?topic=21564.0

But my hearing is too precious to put at risk using any of them anymore. And as you said, post-op people's T is so low that DHT levels are unlikely to cause hair loss.

Unless you think that a DHT level test may still be of value?

But for hair loss my derm agreed to go from 5% minoxidil + progesterone to 10% minoxidil + progesterone.
Or if it doesn't work as well as I think it will after 6 month trial, there's 5% minoxidil + betamethasone.

Btw, I still can't believe how the mere 0.1% of bioidentical progesterone that I press into my scalp twice daily 1/2 hour before applying the minoxidil can make the tops of my hands look and feel so much better. And so quickly after beginning the regimen. ?

As I replied to Lexidreamer, my Estrogen was 909 pg/mL, not ng. Note also that it was seven days between my last injection and when the blood was drawn.

Apparently your research shows that many transgirls prefer E to be between 200-400 pg. Of course, everyone's system is different. However, is there any way of better predicting if that might that be the around the most comfortable range for those over 50?

Thus, would E levels at 909 pg, like I presently have (and were for many years in the 800 range), mostly likely put me in the estrogen dominance range? And might this be indicated by my high post-op progesterone level of 13?

And if ED can contribute to hair loss then how does it likely do so? I think you said that ED can affect the thyroid, which in turn can cause hair loss.

If so, do my thyroid numbers look normal? If yes, how else could ED cause hair loss?

We're not allowed to disclose dose/strength/frequency drug routines, but if my E is 909 pg and if getting to 400-450 pg range will likely free me of ED ,then would the best approach be to halve the dose of the same strength estradiol valerate that I'm using per 14 days?

[KayXo]

post-op people's T is so low that DHT levels are unlikely to cause hair loss.

Indeed. I personally think a 5-alpha reductase inhibitor is unnecessary post-op and if one thinks absolutely necessary, then finasteride at lower doses seems to have the least side-effects. Do some research on this, discuss with your doctor.

But for hair loss my derm agreed to go from 5% minoxidil + progesterone to 10% minoxidil + progesterone.

Progesterone is unlikely to have any effect on hair growth as the only study which found a significant suppression of DHT was an in-vitro study with extremely high, supraphysiological, levels of P.

Apparently your research shows that many transgirls prefer E to be between 200-400 pg. Of course, everyone's system is different.

Transgirls don't necessarily prefer to be at those levels, doctors prefer them to be at those levels. Those levels were established arbitrarily, based on the average levels observed in premenopausal women these days but as we all know, our situation differs quite markedly from ciswomen. Levels also fluctuate in time.

However, is there any way of better predicting if that might that be the around the most comfortable range for those over 50?

No study has shown an ideal level for ciswomen or transwomen at any age. The truth is no one really knows. Individuals are unique and most likely, the right level varies a lot.

Thus, would E levels at 909 pg, like I presently have (and were for many years in the 800 range), mostly likely put me in the estrogen dominance range? And might this be indicated by my high post-op progesterone level of 13?

Estrogen dominance is scientifically unsubstantiated with the exception of uterine/endometrial tissue. P levels of 13 ng/dl are not high, those go as high as 300 during pregnancy.

[z38]

Indeed. I personally think a 5-alpha reductase inhibitor is unnecessary post-op and if one thinks absolutely necessary, then finasteride at lower doses seems to have the least side-effects. Do some research on this, discuss with your doctor.

Progesterone is unlikely to have any effect on hair growth as the only study which found a significant suppression of DHT was an in-vitro study with extremely high,
supraphysiological, levels of P.

Transgirls don't necessarily prefer to be at those levels, doctors prefer them to be at those levels. Those levels were established arbitrarily, based on the average levels observed in premenopausal women these days but as we all know, our situation differs quite markedly from ciswomen. Levels also fluctuate in time.

No study has shown an ideal level for ciswomen or transwomen at any age. The truth is no one really knows. Individuals are unique and most likely, the right level varies a lot.

Estrogen dominance is scientifically unsubstantiated with the exception of uterine/endometrial tissue. P levels of 13 ng/dl are not high, those go as high as 300 during pregnancy.

Perhaps very low levels of finasteride or Dutasteride-but only as a very last resort.

In any case, lets hope that these firms or others will be true to their word about an affordable solution to stop and reverse virtually any kind of hair loss by 2020. https://www.fiercebiotech.com/biotech/replicel-says-hair-loss-therapy-safe-glimmers-efficacy

https://replicel.com/20170314-2/

https://www.forbes.com/sites/robinseatonjefferson/2017/09/29/company-uses-patients-own-cells-to-put-an-end-to-baldness-aging-skin-and-tendon-degeneration/2/#2b682ef35b8c

http://www.folliclethought.com/ultimate-guide-to-hair-regeneration/

Meanwhile, my derm added progesterone to the minoxidil, not for any appreciable 5a reductase inhibiting, but perhaps because for the same reason that the topical progesterone had so quickly made my skin (on the tops of my hands?!) more supple and smoother-so that the minoxidil could better penetrate the scalp. Btw, there's a derm in Manhattan who adds Retin-A to minoxidil for much the same reason.

I remember the Manhattan endo I was seeing circa 2005-08 before finding one here on Long Island. I told the former that I suspected my "high" E levels might be contributing to hair loss. I had also begun Avodart two years or so earlier. And this was about 8 years post-op. I believe we tried as low as 1/8 of the E dose I had always used. After 14 days, and perhaps another round of same, I think I recall not feeling so great; kind of achy all around. Presumably, that in turn had lower measured E levels to around the 200 range.

So perhaps it's time again to try between 1/4 and 1/2 of the normal dose.

Question: When first meeting the Manhattan endo he seemed surprised by the dose/strength/frequency of my estradiol valerate regimen, saying that quite a few of  his patients take 3 to 5x that much. While no expert I was a bit shocked to hear that. But perhaps I shouldn't have been because, unlike me, most of his transwomen patients might have been pre-op? But then he knew I was post-op. Or maybe he forgot.

Speaking of which, would the testes in a pre-op transwoman, with E levels of 800 to 1000 pg, produce as much progesterone as a cis man?

Again, my E is 909 pg; P is 13 ng. But if a post-op person (not a cis woman) upped her E to where levels are 3 to 4x my 909 pg, could the adrenals get stressed out, become unstable or even somehow get damaged trying to deliver enough progesterone to balance ~4000 pg exogenous E level?

And/or could some other problem occur as a result of insufficient adrenal progesterone? Androgenic hair loss? Other health problems?

Forgive my limited knowledge of human physiology, but when you say that my 13 ng P level is not high, why compare it that produced by a pregnant cis women's ovaries and corpus luteum, and which are only monthly-and ultimately only premenopausal structures. https://en.wikipedia.org/wiki/Corpus_luteum ?  Isn't that like comparing the trifling amount of P which the adrenals make to the large amount that a cisman's testes make?

Still, why did the Lab Corp blood test print out label my 13 ng P level as "high"? Because, by some measure, it may be judged high relative to my 909 pg E level?

Obviously, adrenal P is the only endogenous product that cis and post-op transwomen have to balance E, to prevent estrogen dominance and/or for the numerous other health benefits that progesterone apparently offers. https://en.wikipedia.org/wiki/Progesterone

Would it be appropriate to ask if you or others here use or recommend some dose/strength/frequency of bioidentical progesterone to gain and maintain these health benefits? Or do adrenal glands produce enough in healthy post-op women?

Here's a rather contemptible mystery: It's of course well known the even long time post-ops like me can still have very substantial facial hair afterwards, I have long had practically zero body hair, but I'm positive that I've actually gained more and/or coarser facial hair over the last few years. How could that happen?

[KayXo]

I suspected my "high" E levels might be contributing to hair loss.

Ciswomen have long, beautiful hair when pregnant because estrogen levels are HIGH, VERY HIGH. This is because estrogen prolongs the anagen (growing) phase of the hair so it would actually have the opposite effect, decrease hair loss. Women lose hair when they give birth because hormones drop.

When first meeting the Manhattan endo he seemed surprised by the dose/strength/frequency of my estradiol valerate regimen, saying that quite a few of  his patients take 3 to 5x that much. While no expert I was a bit shocked to hear that. But perhaps I shouldn't have been because, unlike me, most of his transwomen patients might have been pre-op? But then he knew I was post-op. Or maybe he forgot.

Pre or post-op, there is no reason E should be higher or lower because in both instances, T is very low so the hormonal environment is essentially the same.

would the testes in a pre-op transwoman, with E levels of 800 to 1000 pg, produce as much progesterone as a cis man?

The testes at such high levels of estradiol would most likely STOP FUNCTIONING and secreting any hormones. Estradiol has a negative feedback on glands sending signals to testes to produce hormones.

Again, my E is 909 pg; P is 13 ng. But if a post-op person (not a cis woman) upped her E to where levels are 3 to 4x my 909 pg, could the adrenals get stressed out, become unstable or even somehow get damaged trying to deliver enough progesterone to balance ~4000 pg exogenous E level?

The adrenal glands do not try to balance estrogen, this has never been shown anywhere. But, in some studies, estrogen delivered exogenously has shown to reduce adrenal output of hormones. So, if anything, your progesterone output might even be lower.

And/or could some other problem occur as a result of insufficient adrenal progesterone? Androgenic hair loss? Other health problems?

The majority of post-op transwomen only take estrogen and don't suffer because of very, very low levels of progesterone.

Still, why did the Lab Corp blood test print out label my 13 ng P level as "high"? Because, by some measure, it may be judged high relative to my 909 pg E level?

Labs deemed it high in comparison perhaps to those levels present during a woman's follicular phase or if you are still labelled as male because men have very low levels.

Obviously, adrenal P is the only endogenous product that cis and post-op transwomen have to balance E, to prevent estrogen dominance and/or for the numerous other health benefits that progesterone apparently offers.

In ciswomen, before menopause, the corpus luteum and, during pregnancy (eventually) the placenta secrete progesterone, this is why levels increase so much. No corpus luteum (ruptured follicle) = barely any progesterone.

Would it be appropriate to ask if you or others here use or recommend some dose/strength/frequency of bioidentical progesterone to gain and maintain these health benefits? Or do adrenal glands produce enough in healthy post-op women?

Adrenals in post-op women or menopausal women produce very low amounts of progesterone. Progesterone is clearly needed for pregnancy and to prevent uterine/endometrial cancer (excess proliferation) but so far, studies have not established it's absolutely needed for other purposes. Many transwomen do quite well on just estradiol.

Here's a rather contemptible mystery: It's of course well known the even long time post-ops like me can still have very substantial facial hair afterwards, I have long had practically zero body hair, but I'm positive that I've actually gained more and/or coarser facial hair over the last few years. How could that happen?

Perhaps, hair follicles treated in the past weren't killed and are regrowing. This sometimes happens with laser. Or, endocrine abnormality which needs to be investigated by your doctor, we aren't experts.