Evidence For Estrogen Levels In Mpb

Shman Frontal

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Looking for Sources/Evidence for elevated Estrogen in MPB. Danny Roddy and Rob Englisch both say in their Articles that Men with mpb have elevated Estrogen. After checking their Sources it turned out that this isnt prove and/or misleading. The often citated Schmidt Paper only says "significantly difference" but it doesnt tell if high or low.

Thanks if somebody has access to the paper or knows other Evidence about it.

Cheers
 

Pablo Cruise

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Hormonal profile of men with premature balding
L Stárka 1 , I Cermáková, M Dusková, M Hill, M Dolezal, V Polácek
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Abstract
Objective: Premature androgenic alopecia has been suggested as a feature of the male equivalent of the syndrome of polycystic ovary. However, the hormonal pattern of men with premature balding has been investigated in only a few studies with inconsistent results.

Material and methods: We examined 37 men with premature balding (defined as frontoparietal and vertex hair loss before the age of 30 years with alopecia defined as grade 3 vertex or more on the alopecia classification scale of Hamilton with Norwood modification). The plasma concentrations of total testosterone, dihydrotestosterone, epitestosterone, androstenedione, cortisol, 17-OH-progesterone (17OHP), estradiol, LH, FSH, prolactin, SHBG and TSH and free thyroxine were measured.

Results: The frequency of subnormal values in SHBG, FSH, testosterone and epitestosterone (but not in free androgen index) was significant in the balding men. A borderline significant trend was recorded with respect to increased levels in 17OH-P and prolactin.

Conclusions: The hormonal pattern of a substantial number of men with premature balding resembles in some respects the hormonal pattern of women with polycystic ovary syndrome.
 

GorillaHead

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17-oh progesterone.

This is often elevated in people reporting baldness. Anyone want to chime in on the differences between progesterone ?
 

JDreamer

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17-oh progesterone.

This is often elevated in people reporting baldness. Anyone want to chime in on the differences between progesterone ?

Progesterone is not the same as 17α-hydroxyprogesterone caproate: implications for obstetrical practice

Also: "High levels of 17-OH progesterone can indicate a condition called congenital adrenal hyperplasia (CAH). CAH is a glandular disorder that results in the adrenal glands being unable to create sufficient cortisol, and it may increase the production of male sex hormones called androgens."

17-OH Progesterone Test: Purpose, Procedure, and Risks

Kinda confusing given the nature of the discussion around cortisol on this forum.
 

Ableton

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so adrenal androgens not only jump in for low thyroid/hypogonadism but also for low cortisol?
 

mrchibbs

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so adrenal androgens not only jump in for low thyroid/hypogonadism but also for low cortisol?

I think low cortisol may be a sign that your adrenals are exhausted. My understanding is that adrenal DHEA rises to oppose the elevated cortisol of stress, and when that is maintained long term, eventually the adrenals become drained and atrophy. Chronic stress really is a catabolic process which seems to cause tissue destruction and atrophy for all the endocrine glands/organs of the body.
 

Ableton

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I think low cortisol may be a sign that your adrenals are exhausted. My understanding is that adrenal DHEA rises to oppose the elevated cortisol of stress, and when that is maintained long term, eventually the adrenals become drained and atrophy. Chronic stress really is a catabolic process which seems to cause tissue destruction and atrophy for all the endocrine glands/organs of the body.

Isn't cortisol produced in the adrenals as well? I think the article above suggests as well that cortisol and dhea are opposed to each other and do not rise with each other.
 

mrchibbs

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Isn't cortisol produced in the adrenals as well? I think the article above suggests as well that cortisol and dhea are opposed to each other and do not rise with each other.

Yes, I'm not 100% clear on this but apparently the adrenal glands have different layers producing different hormones, and the layer producing the DHEA is more susceptible to disintegrate. Danny Roddy made a video on why he thinks elevated DHEA is an adaptive measure to chronic cortisol elevation. This makes sense because DHEA is seemingly always elevated in stress pathologies. But it doesn't stay elevated forever.

We obviously have to understand these things better.
 

MitchMitchell

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I think it’s foolish to try to blame ESTRADIOL for hair loss when we have so many hints that the opposite is true ie. Males with more E2 have better hair, skin etc.

I think that XENOestrogens which cause all of the nasty adaptive reactions described by Ray are to blame. And in the case of hair loss, compensatory increase in DHT (be it because of hypothyroidism, hypogonadism, who cares in the end it’s the same result). Prolactin being elevated in the study above would go in that direction. If prolactin is high but E2 isn’t, then what is? Xenoestrogens for sure. E1/E3 are so weak they’re near irrelevant.

Unfortunately and as per Anthony Jay, we live in a very, very estrogenic environment. I’d need to be a millionaire to totally avoid estrogens in foods.
 

JDreamer

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I think it’s foolish to try to blame ESTRADIOL for hair loss when we have so many hints that the opposite is true ie. Males with more E2 have better hair, skin etc.

I think that XENOestrogens which cause all of the nasty adaptive reactions described by Ray are to blame. And in the case of hair loss, compensatory increase in DHT (be it because of hypothyroidism, hypogonadism, who cares in the end it’s the same result). Prolactin being elevated in the study above would go in that direction. If prolactin is high but E2 isn’t, then what is? Xenoestrogens for sure. E1/E3 are so weak they’re near irrelevant.

Unfortunately and as per Anthony Jay, we live in a very, very estrogenic environment. I’d need to be a millionaire to totally avoid estrogens in foods.

Males with more E2 have better hair? Says who? Perhaps you're conflating with "transitioning" men.

As with anything it's all about balance.
 

Ableton

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„A chain of reactions is triggered in the brain, says Hüther. The nervous system signals the adrenal medulla to release adrenaline, blood pressure, pulse, skin resistance and muscle activity increase, and intestinal activity is inhibited. The body is on the alert. With "fight or flight", Walter Cannon, the second great pioneer of stress research besides Selye, described these reactions in 1915 - it is about a subjective evaluation of danger. However, women seem to react less violently than men and are more inclined to form social networks in order to cope, as recent studies by American psychologist Shelley Taylor suggest. "Tend and befriend", hats and friends, instead of "fight or flight", probably due to evolutionary reasons: with young people it is simply harder to fight and escape.

About ten minutes after the release of adrenaline, cortisol follows, which is supposed to protect the body from the unfavorable consequences of too long a period of high activation by adrenaline and at the same time ensures increased, longer-lasting alertness at a lower level. Because adrenaline is difficult to measure, the concentration of cortisol in saliva is often used to measure stress levels.

Thus, stress initially means nothing more than that the body is particularly willing to perform as a result of a perceived strain - a mobilization that is not only useful when physical integrity is threatened. "Without stress we would not develop at all," says Gerald Hüther. Stress strengthens, stress steels. An immune system that is only ever spared does not know how to fend off attacks. Those who do not suffer setbacks or overcome crises cannot rise above themselves and develop confidence in their own abilities. In short: If you don't experience stress, you can't stand anything.“

Translated with www.DeepL.com/Translator (free version)


I think people with chronically elevated adrenaline in „fight or flight“ have no cortisol. They have: great skin, great muscle building capacities despite leanness, no belly, chiselled face, no hair



Made me think of this guy rolling on mdma

Given that I have recently finally escaped fight and flight (I can now live on 2,5k cals instead of 4k, and sleep deeper) I can say that I did not have a cortisol rebound or anything. I didn’t suddenly grow a belly or get a moon face. But I suspect my cortisol is now „there“
 

MitchMitchell

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Males with more E2 have better hair? Says who? Perhaps you're conflating with "transitioning" men.

As with anything it's all about balance.

says the whole world out there. Open your eyes. But yeah balance is nice if you want hair and masculine function. People use Aromatase Inhibitors to try to reach a state of balance - it’s test that should be up, not E2 that should be down.
 

Risingfire

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I think it’s foolish to try to blame ESTRADIOL for hair loss when we have so many hints that the opposite is true ie. Males with more E2 have better hair, skin etc.

I think that XENOestrogens which cause all of the nasty adaptive reactions described by Ray are to blame. And in the case of hair loss, compensatory increase in DHT (be it because of hypothyroidism, hypogonadism, who cares in the end it’s the same result). Prolactin being elevated in the study above would go in that direction. If prolactin is high but E2 isn’t, then what is? Xenoestrogens for sure. E1/E3 are so weak they’re near irrelevant.

Unfortunately and as per Anthony Jay, we live in a very, very estrogenic environment. I’d need to be a millionaire to totally avoid estrogens in foods.
A lot of men have high E1 instead of E2 that are balding. It's tissue estrogen which is still estrogen
 

mrchibbs

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says the whole world out there. Open your eyes. But yeah balance is nice if you want hair and masculine function. People use Aromatase Inhibitors to try to reach a state of balance - it’s test that should be up, not E2 that should be down.

I don't think that's accurate at all. I would recommend digging and reading some of the older threads on this website, we've discussed this matter many many times before. I agree that E2 plays a physiological role but in men with hair loss it is not deficient at all. Our cues to understanding what happens is to understand the interaction between E2 and P4 in reproductive women, and how that helps them keep a better head of hair.

Saying that men with high E2 have better hair is not really convincing to people who've spent a little bit of time studying this topic.
 

MitchMitchell

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I think all sex hormone ranges are pathetically low since they’re based on modern “normal” males. If I look around at who’s the 95% male population I’d rather be in the top 2.5%.

low E2 is low T is hypogonadism. High everything is much better. Countless reports from guys on TRT who don’t have a problem being in the upper quartile or somewhat above range.

Hair loss a side effect of anti estrogenic drugs is extremely frequent. People will speculate that it’s because of some other mechanism that no one can prove - no, it’s from the induced hypogonadism and blockade of E2 (in the cell)
 

mrchibbs

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I think all sex hormone ranges are pathetically low since they’re based on modern “normal” males. If I look around at who’s the 95% male population I’d rather be in the top 2.5%.

low E2 is low T is hypogonadism. High everything is much better. Countless reports from guys on TRT who don’t have a problem being in the upper quartile or somewhat above range.

Hair loss a side effect of anti estrogenic drugs is extremely frequent. People will speculate that it’s because of some other mechanism that no one can prove - no, it’s from the induced hypogonadism and blockade of E2 (in the cell)

Not convincing. We've discussed this in other threads, but basically the negative impacts of so-called anti-estrogen drugs and aromatase inhibitors are more likely attributed to the fact that there are no selective anti-estrogen or aromatase inhibitors, they always suppress something else, like pregnenolone or progesterone as well.

Moreover, there is evidence that topical estrogen shuts down the hair cycle, and estrogen-receptor antagonists restore it.

So clearly, saying E2 is always good is reductionist. If we look at healthy women, high levels of E2 are balanced by even higher levels of P4. E2 on its own can be spontaneously elevated to initiate growth/tissue renewal processes, but a chronic excess of E2 is not good news and is associated with fibrosis, cancer, you name it.

Plenty of studies which have been posted over the years on this forum highlight this reality. Simply search for the ''estradiol'' tag and you'll see for yourself.
 

Ableton

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Not convincing. We've discussed this in other threads, but basically the negative impacts of so-called anti-estrogen drugs and aromatase inhibitors are more likely attributed to the fact that there are no selective anti-estrogen or aromatase inhibitors, they always suppress something else, like pregnenolone or progesterone as well.

Moreover, there is evidence that topical estrogen shuts down the hair cycle, and estrogen-receptor antagonists restore it.

So clearly, saying E2 is always good is reductionist. If we look at healthy women, high levels of E2 are balanced by even higher levels of P4. E2 on its own can be spontaneously elevated to initiate growth/tissue renewal processes, but a chronic excess of E2 is not good news and is associated with fibrosis, cancer, you name it.

Plenty of studies which have been posted over the years on this forum highlight this reality. Simply search for the ''estradiol'' tag and you'll see for yourself.
On finasteride gyno was coming for me at the same time I was regrowing crazy amounts of hair. I was estrogen dominant for the first time and regrew hair.
I’m not going to say it’s like that for everyone, but when it comes to myself I‘ll stick to observation instead of just theory.
 

MitchMitchell

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Moreover, there is evidence that topical estrogen shuts down the hair cycle, and estrogen-receptor antagonists restore it.

that’s from animal studies, so, no.

Hair Follicle as an Estrogen Target and Source

In humans:

ERβ is strongly expressed in the bulge region of the outer root sheath. This region contains stem cells for hair follicle keratinocytes that regenerate the follicle during the anagen phase. This suggests that these epithelial stem cells are targets for estrogen action.

The wide distribution of ERβ in human pilosebaceous unit suggests that estrogens play an important role in the maintenance and the regulation of the hair follicle and provides further evidence for estrogen action in nonclassic target tissues. Recently, it was reported that in cultured dermal papilla cells from nonbalding male donors, both ERα and ERβ showed a consistently higher expression, both at the RNA and protein levels, in occiput dermal papilla cells compared with vertex dermal papilla cells

With respect to ERβ immunoreactivity, we found that, in anagen VI follicles microdissected from frontotemporal skin, there was a remarkable distribution difference between male and female hair follicles from frontotemporal scalp skin: ERβ immunoreactivity was found in male scalp hair follicles predominantly in the matrix keratinocytes, whereas in female hair follicles, ERβ immunoreactivity was predominantly found in the dermal papilla fibroblasts

These data not only highlight substantial, previously underappreciated sex-dependent differences in ERβ expression of an important peripheral E2 target organ, but also underscore the importance of investigating whether E2 effects on the human hair follicle are location-dependent, as is well-recognized for the paradoxical hair growth effects of androgens

whatever happens in rodents always sounds interesting and all that but it never ever should be used to conclude anything in humans. And I see a lot of people making such bold and ultimately erroneous assumptions especially with regards to estradiol and hair.
 
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