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In the eye of the beholder.... (Propecia, Avodart, Spiro, DHT & hormones ...)

posted by gc1961, 05.09.2007, 22:31

» I've already mentioned this small study two or three times, and I used to
» have a link to a PDF file of it, but now I can't find it. But here's the
» full text of it, at least, even if you can't see the graphs they include
» with it: "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. I've put a critical passage or two in bold text.
»
»
» 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
Bryan,

Yep I read this paper as well as many others.

To me the heading and first paragraph seem to argue against your interpretation; "More Questions than answers" and "....usually exhibiting hair growth inhibitory properties".

What I dislike about this study as a basis of hard conclusions is that the sample count is 1 (ok maybe 2) and it doesn't even say if the guy was displaying MPB!

Hardly scientific.


gc1961 is located in [NA] and he is available to meet: NO

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