Estrogen is a big subject. Tamoxifen is also confusing in that it is an estrogen receptor blocker in the breast tissue, but in most other tissues of the body it acts as estrogen would (an activator). I’m not sure whether it is an agonist or antagonist on the E receptors of the scalp. I have heard people say that Tamoxifen seemed to help their hair loss, but others say it will worsen it. I’m not suggesting that anyone use Tamoxifen for hair loss.
» I do not share this opinion and have read many medical papers that
» increasingly identify Estrogen as very negative.
References or citations, please.
» The net of the E research I have done suggests that the primary action of
» E in MPB is that it inhibits new hair from entering anagen (growth)
» phase.
Reference or citation, please.
Bryan
» » 17-Estradiol Induces Aromatase Activity in Human Hair Follicles
» » Dept of Derm, Philipp University, Marburg, Germany
» »
» » “…Our results suggest that under the influence of 17 a-Estradiol an
» » increased conversion of testosterone to 17 b-estradiol and
» androstendione
» » to estrone takes place. In theory this pathway may diminish the amount
» of
» » intrafollicular testosterone available for conversion to DHT, ane
» because
» » DHT is the major mediator of AGA, this pathway may explain the
» beneficial
» » effect of 17 a-estradiol on the development and progression of AGA.”
»
»
» I don’t really buy the last sentence. All the recent reseach shows that E
» is as bad for hair and prostate as DHT. I think they made too much of a
» jump in their conclusion. A definite case of separating the science
» results from a bad interpretation.
There’s a lot of speculation about the role of estrogen in the etiology of prostate disease (even though a study testing an aromatase inhibitor for BPH found no effect), but I’m deeply puzzled by your claim that “all the recent research” shows that E is bad for hair. I’d really appreciate it if you could cite that recent research for me! 
Bryan
» Here is the skinny on Estrogen.
»
» 2. Blocking Testosterone production using Spiro/Flut has a similar effect
» on Estrogen.
I’m not sure what you mean by that. Are you saying that flutamide INCREASES or DECREASES estrogen? Are you aware that flutamide increases the production of testosterone?
» 5. Anastrozole is very powerful and completely blocks the Aromatization of
» androgens; 1/4 tab every other day will work well.
Anastrozole doesn’t “completely block” the aromatization of androgens. In one study with healthy young males, even 3 mg/day of Arimidex only reduced serum estrogen by about 50%.
» Now a few notes on E in general.
»
» 1. Estrogen plays a critical role in Prostate cancer and male pattern
» baldness
As I’ve stated many times before, estrogen appears to play a beneficial role in MPB.
» 4. Aromatase is identified late in the Anagen phase. The most likely
» primary impact of E in the hair cycle is the inhibition of transition to
» the Anagen phase.
I’d like to see a reference or citation for that claim.
Bryan
» As for more DHT as a result of taking Arimidex, I have not seen research
» that suggests this. Have you?
I don’t know of a study using Arimidex which measured DHT, but here’s one using the aromatase inhibitor atamestane: “Estrogen Reduction by Aromatase Inhibition for Benign Prostatic Hyperplasia: Results of a Double-Blind, Placebo-Controlled, Randomized Clinical Trial Using Two Doses of the Aromatase-Inhibitor Atamestane”, Radlmaier et al, The Prostate 29:199-208 (1996).
The use of atamestane caused a reflexive INCREASE in serum androgens, including DHT. Here are the approximate numbers involved (I’m reading this off a graph they provide): after 48 weeks of therapy, the smaller dose of the drug raised serum DHT by about 23%, and the larger dose raised serum DHT by about 35%.
Without such research I can just as easily
» speculate that HPTA feedback would maintain the T level; BTW the amount of
» E relative to T is 1/100th, so you would only be increasing T by 1% by
» completely blockading E production.
HUH?? It doesn’t work that way! The HPTA axis doesn’t just substitute one molecule of testosterone for every molecule of estrogen! 
In the study I cited above with atamestane, testosterone levels rose even more than DHT: about 24% for the smaller dose, and about 47% for the larger dose, after 48 weeks.
Further, it is very clear that a
» complete blockade on T-to-DHT does not prevent hairloss in the majority of
» people. There are many more factors to hairloss (or prostate cancer) than
» DHT; much of the new research points to E.
I don’t believe that. Please cite some references.
Bryan
» » Here is the skinny on Estrogen.
» »
» » 2. Blocking Testosterone production using Spiro/Flut has a similar
» effect
» » on Estrogen.
»
» I’m not sure what you mean by that. Are you saying that flutamide
» INCREASES or DECREASES estrogen? Are you aware that flutamide increases
» the production of testosterone?
»
» » 5. Anastrozole is very powerful and completely blocks the Aromatization
» of
» » androgens; 1/4 tab every other day will work well.
»
» Anastrozole doesn’t “completely block” the aromatization of androgens. In
» one study with healthy young males, even 3 mg/day of Arimidex only reduced
» serum estrogen by about 50%.
»
» » Now a few notes on E in general.
» »
» » 1. Estrogen plays a critical role in Prostate cancer and male pattern
» » baldness
»
» As I’ve stated many times before, estrogen appears to play a beneficial
» role in MPB.
»
» » 4. Aromatase is identified late in the Anagen phase. The most likely
» » primary impact of E in the hair cycle is the inhibition of transition
» to
» » the Anagen phase.
»
» I’d like to see a reference or citation for that claim.
»
» Bryan
Theres a great side to baldness that may have escaped people, it has made some of us into brilliant endocronologists.
» » Here is the skinny on Estrogen.
» »
» » 2. Blocking Testosterone production using Spiro/Flut has a similar
» effect
» » on Estrogen.
»
» I’m not sure what you mean by that. Are you saying that flutamide
» INCREASES or DECREASES estrogen? Are you aware that flutamide increases
» the production of testosterone?
»
» » 5. Anastrozole is very powerful and completely blocks the Aromatization
» of
» » androgens; 1/4 tab every other day will work well.
»
» Anastrozole doesn’t “completely block” the aromatization of androgens. In
» one study with healthy young males, even 3 mg/day of Arimidex only reduced
» serum estrogen by about 50%.
»
» » Now a few notes on E in general.
» »
» » 1. Estrogen plays a critical role in Prostate cancer and male pattern
» » baldness
»
» As I’ve stated many times before, estrogen appears to play a beneficial
» role in MPB.
»
» » 4. Aromatase is identified late in the Anagen phase. The most likely
» » primary impact of E in the hair cycle is the inhibition of transition
» to
» » the Anagen phase.
»
» I’d like to see a reference or citation for that claim.
»
» Bryan
Bryan,
2 years later same argument about E; my hair is still growing, is yours?
Please share your references to research papers that support your claim that Estrogen appears to play a benefitial role in MPB?
I am ok for you to challenge my references, but I ask you for yours as well. Fair?
To be clear “as I stated many times before” does not equate to a compelling arguement:-)
My Primary Ref.
The Hair Follicle as an Estrogen Target and Source
Ohnemus, Uenaian, Inunza, Gustafson, Paus
University of Hamburg & Karobio
2006
This paper is a round-up of Estrogen research and references 375 other research papers; it gives a good overview and discusses Estrogen inhibition of Androgen. It also covers the latest on ER-alpha and ER-beta receptors and their different characteristics.
There is a lot of work on Estrogen in various cancers (prostate and breast); hence the industry focus on SERMs and the current use of Tamoxifen. In the natural space there is a lot of research on I3C and DIM in the Estrogen matabolism.
OK your turn!
GC
» » » 17-Estradiol Induces Aromatase Activity in Human Hair Follicles
» » » Dept of Derm, Philipp University, Marburg, Germany
» » »
» » » “…Our results suggest that under the influence of 17 a-Estradiol an
» » » increased conversion of testosterone to 17 b-estradiol and
» » androstendione
» » » to estrone takes place. In theory this pathway may diminish the
» amount
» » of
» » » intrafollicular testosterone available for conversion to DHT, ane
» » because
» » » DHT is the major mediator of AGA, this pathway may explain the
» » beneficial
» » » effect of 17 a-estradiol on the development and progression of AGA.”
» »
» »
» » I don’t really buy the last sentence. All the recent reseach shows that
» E
» » is as bad for hair and prostate as DHT. I think they made too much of a
» » jump in their conclusion. A definite case of separating the science
» » results from a bad interpretation.
»
» There’s a lot of speculation about the role of estrogen in the etiology of
» prostate disease (even though a study testing an aromatase inhibitor for
» BPH found no effect), but I’m deeply puzzled by your claim that “all the
» recent research” shows that E is bad for hair. I’d really appreciate it
» if you could cite that recent research for me!
»
» Bryan
\
My Primary Ref.
The Hair Follicle as an Estrogen Target and Source
Ohnemus, Uenaian, Inunza, Gustafson, Paus
University of Hamburg & Karobio
2006
This paper is a round-up of Estrogen research and references 375 other research papers; it gives a good overview and discusses Estrogen inhibition of Androgen. It also covers the latest on ER-alpha and ER-beta receptors and their different characteristics.
There is a lot of work on Estrogen in various cancers (prostate and breast); hence the industry focus on SERMs and the current use of Tamoxifen. In the natural space there is a lot of research on I3C and DIM in the Estrogen matabolism.
» » I do not share this opinion and have read many medical papers that
» » increasingly identify Estrogen as very negative.
»
» References or citations, please.
»
» » The net of the E research I have done suggests that the primary action
» of
» » E in MPB is that it inhibits new hair from entering anagen (growth)
» » phase.
»
» Reference or citation, please.
»
» Bryan
My Primary Ref.
The Hair Follicle as an Estrogen Target and Source
Ohnemus, Uenaian, Inunza, Gustafson, Paus
University of Hamburg & Karobio
2006
This paper is a round-up of Estrogen research and references 375 other research papers; it gives a good overview and discusses Estrogen inhibition of Androgen. It also covers the latest on ER-alpha and ER-beta receptors and their different characteristics.
There is a lot of work on Estrogen in various cancers (prostate and breast); hence the industry focus on SERMs and the current use of Tamoxifen. In the natural space there is a lot of research on I3C and DIM in the Estrogen matabolism.
» » Here is the skinny on Estrogen.
» »
» » 2. Blocking Testosterone production using Spiro/Flut has a similar
» effect
» » on Estrogen.
»
» I’m not sure what you mean by that. Are you saying that flutamide
» INCREASES or DECREASES estrogen? Are you aware that flutamide increases
» the production of testosterone?
»
I haven’t done enough research on Flutamide.
» » 5. Anastrozole is very powerful and completely blocks the Aromatization
» of
» » androgens; 1/4 tab every other day will work well.
»
» Anastrozole doesn’t “completely block” the aromatization of androgens. In
» one study with healthy young males, even 3 mg/day of Arimidex only reduced
» serum estrogen by about 50%.
»
Can you provide a reference?
» » Now a few notes on E in general.
» »
» » 1. Estrogen plays a critical role in Prostate cancer and male pattern
» » baldness
»
» As I’ve stated many times before, estrogen appears to play a beneficial
» role in MPB.
I cited my reference; please provide the research that supports your claim that E is benefitial?
Just because you have “said it many times” does not make it scientifically valid:D Or do you play by different rules?
»
» » 4. Aromatase is identified late in the Anagen phase. The most likely
» » primary impact of E in the hair cycle is the inhibition of transition
» to
» » the Anagen phase.
»
» I’d like to see a reference or citation for that claim.
»
My Primary Ref.
The Hair Follicle as an Estrogen Target and Source
Ohnemus, Uenaian, Inunza, Gustafson, Paus
University of Hamburg & Karobio
2006
This paper is a round-up of Estrogen research and references 375 other research papers; it gives a good overview and discusses Estrogen inhibition of Androgen. It also covers the latest on ER-alpha and ER-beta receptors and their different characteristics.
There is a lot of work on Estrogen in various cancers (prostate and breast); hence the industry focus on SERMs and the current use of Tamoxifen. In the natural space there is a lot of research on I3C and DIM in the Estrogen matabolism.
» Bryan
» My Primary Ref.
»
» The Hair Follicle as an Estrogen Target and Source
» Ohnemus, Uenaian, Inunza, Gustafson, Paus
» University of Hamburg & Karobio
» 2006
Thanks for the reference. I see that they don’t say anything specific in the abstract, but I’ll pick up the full paper the next time I’m at the medical library.
» This paper is a round-up of Estrogen research and references 375 other
» research papers; it gives a good overview and discusses Estrogen
» inhibition of Androgen. It also covers the latest on ER-alpha and ER-beta
» receptors and their different characteristics.
Hmmm…“estrogen inhibition of androgen”. Sounds good! That right there should tell you something! 
» There is a lot of work on Estrogen in various cancers (prostate and
» breast); hence the industry focus on SERMs and the current use of
» Tamoxifen.
Not really of any relevance here, since we’re talking about MPB.
Bryan
» » I’m not sure what you mean by that. Are you saying that flutamide
» » INCREASES or DECREASES estrogen? Are you aware that flutamide
» increases
» » the production of testosterone?
» »
» I haven’t done enough research on Flutamide.
It’s true! In general, antiandrogens tend to raise the production of testosterone by interfering with the HPTA feedback loop for testosterone synthesis.
I suspect that taking flutamide might also increase estrogen levels, although I haven’t specifically read anything about that in any studies. But if the supply of testosterone increases as a result of taking flutamide, it seems like there would obviously be a greater substrate available for aromatase to go to work on and make more estrogen. Seems reasonable to me.
» » » 5. Anastrozole is very powerful and completely blocks the
» Aromatization of
» » » androgens; 1/4 tab every other day will work well.
» »
» » Anastrozole doesn’t “completely block” the aromatization of androgens.
» In one study with healthy young males, even 3 mg/day of Arimidex only
» reduced serum estrogen by about 50%.
» »
» Can you provide a reference?
“Estrogen Suppression in Males: Metabolic Effects”, Mauras et al, J Clin Endocrinol Metab 85: 2370-2377, 2000.
» » » Now a few notes on E in general.
» » »
» » » 1. Estrogen plays a critical role in Prostate cancer and male pattern
» » » baldness
» »
» » As I’ve stated many times before, estrogen appears to play a beneficial
» » role in MPB.
»
» I cited my reference; please provide the research that supports your claim
» that E is benefitial?
First of all, there’s that relatively recent study with a title something like “Estrogen in human scalp – still more questions than answers”. I assume you’ve seen that? It’s been widely discussed in several of the hairloss forums. It was an in vitro experiment in which the docs took biopsies from the frontal balding areas of male patients, and gave them estrogen. The cultured hairs grew longer and thicker in response to the estrogen.
Then there are the two Kiesewetter et al studies which were also in vitro experiments. You’ve seen those, too, haven’t you? The application of estrogen (17-b-estradiol) to cultured human scalp hair follicles “increased the growth velocity of all cell types, especially dermal papilla cells” (I believe those are the exact words they used in the studies).
And haven’t you seen that LONG post I did on HLH a while back about the widespread use of topical estrogen for MPB in Europe?? I cited a good many studies about its successful use, and they included both 17-a-estradiol and 17-b-estradiol. If you haven’t seen that post with all the references, I could probably find it again and post it here.
There is also a fairly recent and fascinating study by Happle and Hoffmann (“Influence of Estrogens on the Androgen Metabolism in Different Subunits of Human Hair Follicles”, Eur J Dermatol 2001; 11:195-8) which found that estrogen appears to be a fairly decent 5a-reductase inhibitor; the authors speculate that that may be one of the reasons why topical estrogen is useful in the fight against MPB.
So like I said, just about all the available evidence (both in vivo and in vitro) seems to clearly indicate that estrogen is GOOD for scalp hair.
» Just because you have “said it many times” does not make it scientifically
» valid:D Or do you play by different rules?
I only said that as sort of an apology to YOU for making several posts the last day or two requesting references and citations from you. It had nothing whatsoever to do with my thinking that I play by different rules. I was just acknowledging that I’ve been a little repetitious lately!
Bryan
» OK your turn!
»
» GC
See my post just below.
Bryan
» » My Primary Ref.
» »
» » The Hair Follicle as an Estrogen Target and Source
» » Ohnemus, Uenaian, Inunza, Gustafson, Paus
» » University of Hamburg & Karobio
» » 2006
»
» Thanks for the reference. I see that they don’t say anything specific in
» the abstract, but I’ll pick up the full paper the next time I’m at the
» medical library.
»
» » This paper is a round-up of Estrogen research and references 375 other
» » research papers; it gives a good overview and discusses Estrogen
» » inhibition of Androgen. It also covers the latest on ER-alpha and
» ER-beta
» » receptors and their different characteristics.
»
» Hmmm…“estrogen inhibition of androgen”. Sounds good! That right there
» should tell you something!
typo. I meant to type anagen.
»
» » There is a lot of work on Estrogen in various cancers (prostate and
» » breast); hence the industry focus on SERMs and the current use of
» » Tamoxifen.
»
» Not really of any relevance here, since we’re talking about MPB.
»
I am not sure I agree. I think there is a link. It relates to cell receptors and signalling cascades.
» Bryan
» » » I’m not sure what you mean by that. Are you saying that flutamide
» » » INCREASES or DECREASES estrogen? Are you aware that flutamide
» » increases
» » » the production of testosterone?
» » »
» » I haven’t done enough research on Flutamide.
»
» It’s true! In general, antiandrogens tend to raise the production of
» testosterone by interfering with the HPTA feedback loop for testosterone
» synthesis.
»
» I suspect that taking flutamide might also increase estrogen
» levels, although I haven’t specifically read anything about that in any
» studies. But if the supply of testosterone increases as a result of
» taking flutamide, it seems like there would obviously be a greater
» substrate available for aromatase to go to work on and make more estrogen.
» Seems reasonable to me.
»
» » » » 5. Anastrozole is very powerful and completely blocks the
» » Aromatization of
» » » » androgens; 1/4 tab every other day will work well.
» » »
» » » Anastrozole doesn’t “completely block” the aromatization of androgens.
»
» » In one study with healthy young males, even 3 mg/day of Arimidex only
» » reduced serum estrogen by about 50%.
» » »
» » Can you provide a reference?
»
» “Estrogen Suppression in Males: Metabolic Effects”, Mauras et al,
» J Clin Endocrinol Metab 85: 2370-2377, 2000.
»
» » » » Now a few notes on E in general.
» » » »
» » » » 1. Estrogen plays a critical role in Prostate cancer and male
» pattern
» » » » baldness
» » »
» » » As I’ve stated many times before, estrogen appears to play a
» beneficial
» » » role in MPB.
» »
» » I cited my reference; please provide the research that supports your
» claim
» » that E is benefitial?
»
» First of all, there’s that relatively recent study with a title something
» like “Estrogen in human scalp – still more questions than answers”. I
» assume you’ve seen that? It’s been widely discussed in several of the
» hairloss forums. It was an in vitro experiment in which the docs
» took biopsies from the frontal balding areas of male patients, and gave
» them estrogen. The cultured hairs grew longer and thicker in response to
» the estrogen.
»
» Then there are the two Kiesewetter et al studies which were also
» in vitro experiments. You’ve seen those, too, haven’t you? The
» application of estrogen (17-b-estradiol) to cultured human scalp hair
» follicles “increased the growth velocity of all cell types, especially
» dermal papilla cells” (I believe those are the exact words they used in
» the studies).
»
» And haven’t you seen that LONG post I did on HLH a while back about the
» widespread use of topical estrogen for MPB in Europe?? I cited a good
» many studies about its successful use, and they included both
» 17-a-estradiol and 17-b-estradiol. If you haven’t seen that post with all
» the references, I could probably find it again and post it here.
»
» There is also a fairly recent and fascinating study by Happle and Hoffmann
» (“Influence of Estrogens on the Androgen Metabolism in Different Subunits
» of Human Hair Follicles”, Eur J Dermatol 2001; 11:195-8) which found that
» estrogen appears to be a fairly decent 5a-reductase inhibitor; the authors
» speculate that that may be one of the reasons why topical estrogen is
» useful in the fight against MPB.
»
» So like I said, just about all the available evidence (both in vivo
» and in vitro) seems to clearly indicate that estrogen is GOOD for
» scalp hair.
»
» » Just because you have “said it many times” does not make it
» scientifically
» » valid:D Or do you play by different rules?
»
» I only said that as sort of an apology to YOU for making several posts the
» last day or two requesting references and citations from you. It had
» nothing whatsoever to do with my thinking that I play by different rules.
» I was just acknowledging that I’ve been a little repetitious lately!
»
» Bryan
I will read them all with an open mind. I suspect we will both end seeing conflicting research; it just seems to be the way with a lot of things to do with MPB.
The research on IGF-1 is somewhat similar; I think it is net good but don’t think that this view is widely held.
I also believe that SHBG is misunderstood.
gc.
Gc 1961,
How do you mean exactly by “tamoxifen is a toxic drug”? Is it only a matter of hormonal unbalance this drug may create (though as a SERM, it should not that much) or is there anything more to it? I’ve always considered trying a little tamox to try to get rid of my gyno (puffy nipples) but fear the hairloss risks and just wonder if it is worth. If so, what dosage would you recommend and for how long, for a possible successful result on the gyno without hairloss sides?
As I said before, my estradiol remained mainly untouched by the intake of Zeneca arimidex. What I didn’t say is that another blood parameter that had gone thru the roof remained untouched as well: prolactin. Since my prolactin levels were over the normal range and estradiol levels within the normal range, it has been assumed that my gyno was a prolactin induced one.Do you have any insight as to how overcome a seemingly prolactin induced gyno? This gyno had turned up from the combined use of 1mg finasteride daily + 1 avodart every third day. (The prolactin levels returned to normal in the months following cessation of avodart and (useless) arimidex.)
Thank you.
» My Primary Ref.
»
» The Hair Follicle as an Estrogen Target and Source
» Ohnemus, Uenaian, Inunza, Gustafson, Paus
» University of Hamburg & Karobio
» 2006
»
» This paper is a round-up of Estrogen research and references 375 other
» research papers; it gives a good overview and discusses Estrogen
» inhibition of Androgen. It also covers the latest on ER-alpha and ER-beta
» receptors and their different characteristics.
Ok, I just got that paper from the med library last night, and I’ve now finished reading it!
There’s nothing in the paper which conflicts with what I said before, or with the pro-estrogen evidence I previously cited. In fact, I didn’t realize that these authors are the very same ones who did the same study I mentioned before (“Estrogens and human scalp hair growth – still more questions than answers” )!
By a strange coincidence, while I was at the library last night, I also picked up yet another of their studies, which I didn’t even know they were going to be talking about and referencing in this one. This would be: “Substantial sex-dependent differences in the response of human scalp hair follicles to estrogen stimulation in vitro advocates gender-tailored management of female versus male pattern balding”, J Invest Dermatol Symp Proc 10:243-246. In that one, they found that giving estrogen to hair follicles from frontal male scalp skin showed a dose-dependent DOWNREGULATION of the very harmful TGFb-2, which is known to be a main hair growth suppressor in MPB. That study can be considered to be yet another one in support of estrogen, in addition to the other ones that I mentioned previously.
So my question to you now is this: why did you assume that this paper (the long one you cited above) is so anti-estrogen, when clearly it is not? They mention the same studies I did, with the exception of the ones by Kiesewetter, and talk about the wide use of topical estrogen in Europe for MPB, citing the very same study that I used when I made my big post on that subject over on HLH. They also reference the same Happle & Hoffmann study that I did, showing that estrogen is a fairly decent 5a-reductase inhibitor.
So what made you think that they were necessarily INCRIMINATING estrogen? Was it because of all that material they had about how estrogen arrests the anagen cycle of hair follicles in animals, and sends them into telogen? That was in ANIMALS! As they themselves pointed out near the end, you can’t just assume that the same thing happens in humans, and indeed they cited the same evidence that I did showing that estrogen actually slightly LENGTHENS anagen in human scalp hair follicles, and stimulates their growth. And I continue to be amazed that after all these years, that old Robert Smart study (another one they cited) is still causing confusion in a lot of people by making them think that the same results he got with anti-estrogens in MICE is going to have the same effect in humans. It ain’t necessarily so, and the evidence we’ve cited demonstrates it.
So all in all, I’m pretty much in agreement with what they said. I think the preponderance of the evidence shows that estrogen is GOOD for human scalp hair, and good for fighting MPB.
» » » There is a lot of work on Estrogen in various cancers (prostate and
» » » breast); hence the industry focus on SERMs and the current use of
» » » Tamoxifen.
» »
» » Not really of any relevance here, since we’re talking about MPB.
» »
» I am not sure I agree. I think there is a link. It relates to cell
» receptors and signalling cascades.
Good luck proving such a link.
» They mention the same studies I did, with the exception of the
» ones by Kiesewetter…
Here is one of those Kiesewetter studies, showing that estrogen stimulates the growth of human scalp hair follicles:
J Invest Dermatol. 1993 Jul;101(1 Suppl):98S-105S.
"Sex hormones and antiandrogens influence in vitro growth of dermal papilla cells and outer root sheath keratinocytes of human hair follicles."
Kiesewetter F, Arai A, Schell H.
Department of Dermatology, University of Erlangen-Nürnberg, Germany.
Anagen hair bulb papillae, interfollicular dermal fibroblasts, and interfollicular keratinocytes isolated from fronto-parietal scalp biopsies as well as outer root sheath keratinocytes from plucked anagen hairs were separately grown in subculture for 14 d. The effect of different concentrations (2.4 nM-17.3 microM) of testosterone, dihydrotestosterone, and the antiandrogens cyproterone acetate or 17 alpha-propylmesterolone on growth behavior of the mesenchymal and epithelial cell types of the hair follicle were comparatively studied by means of growth curves, cell doubling times, and 3H-thymidine incorporation. For control, all cell lines were subcultured in hormone-free medium. Testosterone and dihydrotestosterone (345 nM) significantly reduced proliferation of papilla cells compared with dermal fibroblasts (p < 0.01) and outer root sheath keratinocytes compared with interfollicular keratinocytes (p < 0.01), as well as compared with cells cultured in control medium. Low concentrations of 17 beta-estradiol were ineffective, whereas doses of 180 nM 17 beta-estradiol increased the growth velocities of all cell types, especially of papilla cells, compared with dermal fibroblasts. Low doses of either cyproterone acetate (24 nM) or 17 alpha-propylmesterolone (29 nM) induced a growth enhancement, especially of papilla cells and outer root sheath keratinocytes, whereas high doses of cyproterone (1.20 microM) and 17 alpha-propylmesterolone (1.45 microM) had opposite effects. These changes were significant between papilla cells and dermal fibroblasts as well as between outer root sheath keratinocytes and interfollicular keratinocytes. Applying increasing doses of androgens to cyproterone acetate (24 nM)- or 17 alpha-propylmesterolone (29 nM)-containing media neutralized the growth-stimulating effect of antiandrogens, particularly in papilla cells and outer root sheath keratinocytes. However, minor differences between testosterone and dihydrotestosterone effects on cell growth were found. The data clearly demonstrate that the changes of in vitro growth of hair follicle cells depend on the concentrations of androgens and antiandrogens, as higher doses of both antiandrogens tested retarded the cell proliferation similar to testosterone or dihydrotestosterone. The papilla cells and outer root sheath keratinocytes reacted more sensitively to the hormones tested, thereby confirming the concept of a distinct androgen sensitivity of these specialized hair follicle cells.
» Gc 1961,
»
» How do you mean exactly by “tamoxifen is a toxic drug”? Is it only a
» matter of hormonal unbalance this drug may create (though as a SERM, it
» should not that much) or is there anything more to it? I’ve always
» considered trying a little tamox to try to get rid of my gyno (puffy
» nipples) but fear the hairloss risks and just wonder if it is worth. If
» so, what dosage would you recommend and for how long, for a possible
» successful result on the gyno without hairloss sides?
» As I said before, my estradiol remained mainly untouched by the intake of
» Zeneca arimidex. What I didn’t say is that another blood parameter that
» had gone thru the roof remained untouched as well: prolactin. Since my
» prolactin levels were over the normal range and estradiol levels within
» the normal range, it has been assumed that my gyno was a prolactin induced
» one.Do you have any insight as to how overcome a seemingly prolactin
» induced gyno? This gyno had turned up from the combined use of 1mg
» finasteride daily + 1 avodart every third day. (The prolactin levels
» returned to normal in the months following cessation of avodart and
» (useless) arimidex.)
»
» Thank you.
just google Tamoxifen Toxic for articles and research.