Has anyone tried a topical estrogen to treat mpb?

Topicals for hair loss
1

We all know that the male hormones (DHT Testosterone, etc) cause hairloss.

We also all know that one reason women keep their hair is that they have less male hormone AND BECAUSE THEY HAVE MORE FEMALE HORMONE - ESTROGEN.

So that makes me wonder if anyone has tried topical estrogen as a way to regrow hair in bald/balding men???

2

» We all know that the male hormones (DHT Testosterone, etc) cause hairloss.
»
» We also all know that one reason women keep their hair is that they have
» less male hormone AND BECAUSE THEY HAVE MORE FEMALE HORMONE - ESTROGEN.
»
» So that makes me wonder if anyone has tried topical estrogen as a way to
» regrow hair in bald/balding men???

There are reports of some efficacy in maintaining hair in the growth phase a little longer. Against my advice, one of our clients obtained an estrogen (DES, IIRC) )from his wife, a nurse, and applied it topically. Little if any head hair growth, but he lost a bunch of body hair and grew some breasts. Presumably, these were secondary to systemic absorbtion. Reversed when he stopped treatment.

Peter H. Proctor, PhD,MD

3

Dr. P, I think estrogen is one of the most misunderstood topic for mpb. I see a lot of studies on that, some say estrogen is good for mpb, others say it isn’t. I think just 1 anecdotal evidence is not enough conclude whether estrogen is benefical for mpb

4

lavender, and perhaps a couple of things in it, supposedly have some binding affinity for the estrogen receptor.

I put lavender oil on my toe a good while back to see if it would reduce the body hair there, and was suprised (and dissapointed) that it actually made the hair on my toe longer and darker and a bit thicker-----evidence of stimulation.

Limonene and linalool are a couple of things in lavender that Ive seen used in some hairloss products (like Alpecin for instance). Tea tree oil also supposedly has some affinity for the estrogen receptor.

Estrogen might play a slightly positive role in the haircycle, but if systemically absorbed the negative side effects would far outweigh the positive ones in my opinion.

5

» Dr. P, I think estrogen is one of the most misunderstood topic for mpb. I
» see a lot of studies on that, some say estrogen is good for mpb, others
» say it isn’t. I think just 1 anecdotal evidence is not enough conclude
» whether estrogen is benefical for mpb

The issue arose several years ago when some scientists discovered and published that estrogens thin body hair on rodents and from this concluded that estrogens cause pattern hair loss and that estrogen receptor blockers might prove useful for treatmet of pattern loss.

For some reason, they did not know (but were subsequently strongly reminded of) that 1)this is well known for humans and 2) That the effects of estrogen on body hair and scalp hair are exactly opposite. Just like testosterone, in fact. Likewise, estrogen receptor blockers (used to treat, e.g., breast cancer) are well-known to exacerbate pattern loss. Occasionally clinical experience counts.

But, the damage was done. The screw-up should have been caught by the reviewer, but was not.

Peter H. Proctor, PhD,MD

6

» We all know that the male hormones (DHT Testosterone, etc) cause hairloss.
»
» We also all know that one reason women keep their hair is that they have
» less male hormone AND BECAUSE THEY HAVE MORE FEMALE HORMONE - ESTROGEN.
»
» So that makes me wonder if anyone has tried topical estrogen as a way to
» regrow hair in bald/balding men???

Trying to locate a topical that corrects the immune response is something Ill be looking into and in the mean time and some point Ill buy some “C” Topical Spray to help in this direction.

Regards
Pete

7

» The issue arose several years ago when some scientists discovered and
» published that estrogens thin body hair on rodents and from this concluded
» that estrogens cause pattern hair loss and that estrogen receptor blockers
» might prove useful for treatmet of pattern loss.
»
» For some reason, they did not know (but were subsequently strongly
» reminded of) that 1)this is well known for humans and 2) That the effects
» of estrogen on body hair and scalp hair are exactly opposite. Just like
» testosterone, in fact. Likewise, estrogen receptor blockers (used to
» treat, e.g., breast cancer) are well-known to exacerbate pattern loss.
» Occasionally clinical experience counts.
»
» But, the damage was done. The screw-up should have been caught by the
» reviewer, but was not.
»
» Peter H. Proctor, PhD,MD

Dr. P, does estrogen has different effects on men than it does on women ?

8

This study is not really clear on how estrogen moderates hair loss but it sure does confirm that estrogen has a role to play in hair loss.

J Invest Dermatol. 2004 Jan;122(1):7-13.

Topical estrogen accelerates hair regrowth in mice after chemotherapy-induced alopecia by favoring the dystrophic catagen response pathway to damage.

Ohnemus U, uNalan M, Handjiski B, Paus R.

Department of Dermatology, University Hospital Hamburg-Eppendorf, University of Hamburg, Hamburg, GermanyDepartment of Dermatology, Charite, Humboldt-University, Berlin, Germany.

Estrogen receptor ligands are important modulators of skin physiology and are involved in the control of normal hair follicle cycling. Here, we have studied the effects of topically applied 17-beta-estradiol on pathologic hair follicle cycling as seen during chemotherapy-induced alopecia, one of the major unresolved problems of clinical oncology. For this study we employed a well-established murine model that mimics chemotherapy-induced alopecia in humans. For precisely quantifying the area of hair loss and hair regrowth in this model in vivo, we developed a simple planimetric assay (dotmatrix planimetry). We show that topical 17-beta-estradiol significantly alters the cycling response of murine follicles to cyclophosphamide, whereas the estrogen antagonist ICI 182.780 exerted no such effects. Initially, topical 17-beta-estradiol enhanced chemotherapy-induced alopecia significantly by forcing the follicles into the dystrophic catagen response pathway to hair follicle damage, whereas follicles treated by ICI 182.780 or vehicle shifted into the dystrophic anagen response pathway. Consequently, the regrowth of normally pigmented hair shafts after chemotherapy-induced alopecia was significantly accelerated in the 17-beta-estradiol treated group. Our data encourage one to explore topical estrogens as a potential stimulant for hair re-growth after chemotherapy-induced alopecia.

PMID: 14962083

9

Pete, what is C topical spray ?

10

I think estrogen plays a role but the study you quoted was done in mice ! I remember you were the one who told me we can’t trust any studies that were done on mice.

11

» Pete, what is C topical spray ?

See my signature. C = Calosol

Regards
Pete

12

From forum archives:

“Estrogens and Human Scalp Hair Growth — Still More Questions than Answers”. It’s a letter to the editor in: J Invest Dermatol 2004 MAr; 122(3): 840-842.

To the Editor:

While it is undisputed that estrogens (17-b-estradiol, E2) can profoundly modulate hair growth in practically all mammalian species investigated, usually exhibiting hair growth inhibitory properties (Emmens, 1942; Williams et al, 1946; Stumpf et al, 1974; Ebling et al, 1991; Smart et al, 1999; Chanda et al, 2000), it is still rather unclear what exactly E2 administration does to human scalp hair growth.

Given the profound clinical relevance of this question and the frequent use of E2-containing topical preparations in trichological practise (Sinclair, 1999; Sterry and Paus, 2000), this question deserves a more careful and more systematic dissection than it has experienced in the past. This letter calls attention to a few salient points that should be taken into account in this respect.

For human scalp hair, topical E2 has long been used in the management of telogen effluvium and androgenetic alopecia, especially in women (Wustner and Orfanos, 1974; Schuhmacher-Stock, 1981; Sterry and Paus, 2000). Even though this remains to be unequivocally proven in vivo, it is felt that E2 inhibits hair shaft formation, thus lowering the rate of hair growth, i.e., how much new hair shaft is generated by the anagen hair bulb per time unit, yest prolongs anagen duration, thus decreasing the telogen rate (Schuhmacher-Stock, 1981; Sinclair et al, 1999). This would help to explain the clinical observation that topical E2 or high systemic E2 levels during estrogen-based contraception and during pregnancy increase the telogen/anagen ratio, thus notably improving a pre-existing telogen effluvium, while causing a telogen effluvium postpartum supposedly due to E2 withdrawal (Lynfield, 1960; Barnum et al, 1969; Ebling et al, 1991). In view of the very complex, multiple concomitant endocrine changes during and after pregnancy and lactation (including, e.g., dramatic fluctuations in gestagen and prolactin levels (Braunstein, 2003), it is however exceedingly difficult to dissociate strictly E2-based hair growth effects from those that other hormones might exert on the human scalp hair follicle in vivo during this time.

Therefore, it is reasonable to explore the isolated effects of E2 on human hair shaft elongation, anagen duration, and hair follicle keratinocyte proliferation/apoptosis in micro-dissected human anagen VI scalp hair follicles that are organ-cultured according to the method pioneered by Philpott et al (1990)-in the absence of the sebaceous gland, a key compartment for steroid hormone synthesis and metabolism (Zouboulis, 2000). We found only two corresponding reports in the published literature, one using human anagen hair follicles from an unspecified scalp skin location of what appears to be two male individuals aged 17 and 35 y (Kondo et al, 1990), and one recent meeting abstract based on the use of female occipital scalp skin follicles (Nelson et al, 2003). Both studies report that E2 (Kondo et al: 18 nM; Nelson et al: 10 nM), significantly inhibits human scalp hair shaft elongation in vitro. In addition, Kondo et al (1990) report that E2 does not influence the “decay rate” of organ-cultured human anagen hair follicles (as measured by morphology and autoradiographic 3H-thymidine incorporation).

Recently, we have also studied the effects of E2 (1 nM - 1 uM, Sigma St. Louis, MO) on female occipital scalp hair follicles, and have essentially confirmed hair shaft elongation-inhibitory properties of E2, which were maximal at 1 uM (Ohnemus et al, 2003). In view of the extreme dependence of androgen effects on the exact integumental location of human hair follicles however (Ebling, 1991; Jahoda and Reynolds, 1996), we were curious to learn whether E2 effects on human scalp hair follicles are location- and/or sex-dependent. This has already been demonstrated for the E2 response of pelage hair follicles from mice and rats, which is profoundly influenced by sex and body site (Emmens, 1942; Mohn, 1958).

Therefore, we have investigated in a single, large, fronto-temporal scalp skin sample (healthy male individual, no medications, 46 y; obtained with informed consent during routine facelift plastic surgery; all experiments were performed in order to the Declaration of Helsinki Principles) how E2 addition to the medium (1-100 nM, Sigma, diluted in serum-free William’s E medium, supplemented with l-glutamine, penicillin, streptomycin, insulin, and hydrocortisone) affected hair shaft elongation, anagen duration, hair follicle pigmentation and hair matrix keratinocyte proliferation in microdissected, organ-cultured male anagen VI hair follicles from the frontotemporal scalp skin region.

Surprisingly, compared to the vehicle control, the hair shaft elongation of male frontotemporal scalp hair follicles was significantly stimulated by 1-100 nM E2 already as early as 1 d after the start of the organ culture, and this stimulation became even more pronounced at the end of organ culture (days 7 and 9) (Fig 1). This stimulation of hair shaft formation (which is the result of stringently coordinated proliferation and differentiation of hair matrix keratinocytes (Stenn and Paus, 2001) corresponded to a significant stimulation of hair matrix keratinocyte proliferation by 10 nM E2 at day 9 (average number of Ki-positive-cells: in the control group 14 cells (SEM 3.21) and 26 cells in the E2-treated (10 nM) group (SEM 4.38); level of significance: p<0.05, Mann-Whitney test). While no evident differences were noted by H&E or Fontana-Masson histochemistry between E2 and vehicle-treated hair follicles in the hair follicle pigmentary unit or in the degree of hair follicle degeneration during organ culture (data not shown), a slight, though not statistically significant, anagen-prolonging effect of E2 was seen in E2-treated test hair follicles as compared to
vehicle controls (data not shown).

Therefore, organ-cultured male frontotemporal scalp hair follicles in vitro respond to E2 treatment (by a mode of of E2 administration that mimics systemic drug application) with a stimulation of both hair shaft generation and of hair matrix keratinocyte proliferation, and a tendency towards anagen prolongation, while no hair pigmentation effects are seen. This is in line with the ill-documented, but widely shared clinical experience of topically applied E2 on the male scalp in vivo (i.e., hair growth stimulation; Shumacher-Stock, 1981) and supports the anagen-prolonging effect of E2.

Our observation in a single, yet carefully analyzed male patient* (*Note added in proof: The stimulation of male frontotemporal hair follicles by E2 reported here (Fig 1) was just confirmed by us using frontotemporal hair follicles from a second male patient.) raises five basic questions that must be addressed much more systematically by subsequent work on the effects of E2 on human hair growth in order to better explain the seemingly contradictory results obtained with occipital (Kondo et al, 1990; Nelson et al, 2003) versus frontotemporal scalp hair follicles (Fig 1):

  1. What are the differences between male and female hair follicles with respect to estrogen receptor (ER-a, ER-b) expression (Thornton, 2003) and aromatase activity (Sawya and Price, 1997; Hoffmann, 2001, 2002)?

  2. How do occipital and frontotemporal hair follicles, as well as various other integumental sites, differ from each other in this respect?

  3. Is there any indication that E2 exerts similarly “paradoxical, site-dependent” effects on human hair growth as androgens (Jahoda and Reynolds, 1996)? Does the signalling and gene expression response of a defined human hair follicle population to E2 stimulation differ in a stringently location-dependent manner, as has been postulated, e.g., for the response of beard versus scalp follicles to androgen stimulation with respect to TGFb1 expression in the dermal papilla (Inui et al, 2002)?

  4. Which important regional differences in the extrafollicular estrogen metabolism of defined integumental sites must be taken into account when estrogens are administered topically (e.g., with respect to epidermal, sebaceous, and dermal activities of key enzymes like aromatase, 17b-hydroxysteroid dehydrogenase, or steroid sulfatase)?

  5. How is ER expression and/or the metabolism of topically applied
    estrogens in loco influenced by the choice of vehicle?

Only when these basic questions are finally addressed systematically can we expect to solve the ancient enigma of what estrogens really do to human hair growth in a defined integumental site in vivo, on the scalp and elsewhere, and can rationally select estrogen receptor ligands for therapeutically desired hair growth modulation.

Franziska Conrad, Ulrich Ohnemus, Eniko Bodo, Albrecht Bettermann, and
Ralf Paus

13

» Dr. P, does estrogen has different effects on men than it does on women ?

With respect to hair loss, mostly a difference in degree and not in kind.

Peter H Proctor, PhD,MD

14

» I think estrogen plays a role but the study you quoted was done in mice ! I
» remember you were the one who told me we can’t trust any studies that were
» done on mice.

True but that study is only one that I could find :frowning:

15

» » I think estrogen plays a role but the study you quoted was done in mice !
» » I remember you were the one who told me we can’t trust any studies
» » that were done on mice.
»
» True but that study is only one that I could find :frowning:

You didn’t look very hard! :slight_smile:

.

16

» » » I think estrogen plays a role but the study you quoted was done in mice
» !
» » » I remember you were the one who told me we can’t trust any studies
» » » that were done on mice.
» »
» » True but that study is only one that I could find :frowning:
»
» You didn’t look very hard! :slight_smile:
»
» .

you do it !

It’s very confusing with Estrogen.

17

» you do it !
»
» It’s very confusing with Estrogen.

I’ve already done it over the years. Basically, the evidence showing a favorable effect of estrogen on human scalp hair growth consists of numerous small trials done mainly in Europe in which estrogen was applied topically to balding men with reasonably good results. There are also some in vitro studies showing a growth acceleration by estrogen in human scalp hair cultures by Kiesewetter et al, and another one which was just posted in this same thread by Hairsite Admin. You can see that post just below this one.

.

18

I would be interested in your comments here regarding estrogens and male hair growth as it sounds like you have researched this in some detail. Specifically, if estrogens have the seemingly opposite effect on men than they do on women, then what would be the anticipated effect of s-equol…soon to be released. I know that s-equol strongly binds to DHT but it also binds (at 20% affinity as compared to estradiol) to the estrogen B receptor. My understanding ( at least in mice) is that estrogen receptor B stimulation counteracts the inhibitory effects of E2 on estrogen receptor A. So I am trying to figure out whether the estrogen b binding effects of s-equol in men might ironically have a negative overall impact even though it reduces dht.