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(S tro gen 17 bay ta)
CategoryAndrogen blocker

Parameter Effect Result on hair growth
DHT/Testosterone GOOD
5a-reductases GOOD


Men are not normally prescribed Estrogen for any reason

Estrogen is a female hormone that is sometimes used to relieve the symptoms of certain types prostate cancer in men. When applied topically on the scalp it has been shown in studies to cause hair to enter the anagen phase. Estrogen taken oraly has been shown to completely reverse male pattern baldness in transgender patients. However estrogen competes with and shuts down the male hormone Testosterone and causes feminization including breast growth and female pattern fat deposits.

A study [Ohnemus 2006] found sex-dependent differences of frontotem-poral scalp hair shaft elongation after E2 treatments in vitro: in females the hair shaft elongation was inhibited, whereas E2 significantly stimulated hair shaft elongation in human frontotemporal anagen hair follicles from male patients in vitro. This corresponded to a significantly up-reg-ulated proliferation rate of the matrix keratinocytes in the male frontotemporal scalp hair follicles compared with fe-male hair follicles.

The major, clinically relevant effect of topical E2 on human scalp hair follicles seems to be the inhibition of catagen. In addition there may be important regional differences in the estrogen metabolism of hair follicle in different scalp locations that must be carefully taken into account when estrogens are applied topically. In males the vertex scalp hairs do not respond in the same manner as the frontal/mid regions.

Due to unwanted side effects like gynecomastia, E2 should not be used in men because very high topical doses seem to be required to obtain measurable hair growth effects.

Typical Results Complete reversal of male pattern baldness in many cases.
Typical Dosages 2mg-8mg 17b-estradiol daily
Significant Side Effects Severe Gynecomastia or even complete female type breast growth being the most common side effect.
Pharmacology Pharmacodynamics Action And Clinical Pharmacology: Estrogens are secreted mainly by the gonads and, to a very small amount, by the adrenals. In addition, they are formed, to an important degree, from peripheral conversion of adrenal and gonadal androgens to estrogens. They circulate in both unconjugated and conjugated forms in the blood, with the unconjugated estrogens, either free or bound to proteins, mainly albumin, or to the specific sex-hormone binding globulin (SHBG) which shows a great affinity for estradiol. Estrogens are metabolized mainly in the liver, with the metabolites being conjugated with glucuronic acid or sulfuric acid and even double conjugates such as estriol-3-sulfate-16a-glucuronide are formed. About 1/3 to 1/2 of the circulating estrogens are secreted in the bile and of this fraction 20% is reabsorbed after hydrolysis in the intestinal tract. The exact site of the hydrolysis is not known, but it probably takes place in the intestinal lumen and is catalyzed by enzymes secreted into the intestinal tract or present in the microflora. Estradiol is the most potent of the known naturally occurring estrogens in stimulating the growth of the reproductive tissues. Estradiol promotes uterine growth in the rat without undergoing chemical transformation and responsive tissues, such as the uterus and vagina, show a characteristic affinity for estradiol. When administered to humans about 65% of the dose is excreted in the urine, almost entirely in the water soluble form as b-glucuronides or sulfate esters. Estrone, estradiol and estriol account for about 1/2 of the excreted products. A number of steroids with 3 oxygen functions have been identified such as 16-epiestriol, 16-ketoestradiol, 16-hydroxyestrone and 2-methoxyestrone with estradiol being a precursor to these compounds. Estradiol is the most potent physiologic estrogen and, in fact, is the major estrogenic hormone secreted by the human. Estradiol controls the development and maintenance of the female sex organs, the secondary sex characteristics and the mammary glands as well as certain functions of the human uterus and accessory organs, particularly the proliferation of the endometrium, the development of the decidua, and the cyclic changes in the cervix and vagina. The production of estradiol by the ovaries is under the control of pituitary gonadotropins, follicle stimulating hormone (FSH) and luteinizing hormone (LH). In menopausal women, the depletion of ovarian follicles leads to lower plasma estradiol and elevated plasma FSH and LH. Estrogen deficiency is manifested by hot flushes, sweating, insomnia, paresthesia, irritability, and urogenital atrophy. As replacement therapy in estrogen deficiency states (such as the menopause), low doses of estradiol in cyclic regimens have been found to relieve such deficiency. Estrogen deficiency is the main cause of postmenopausal bone loss and contributes to age-associated losses leading to osteoporosis. Numerous clinical studies have demonstrated that estrogen therapy prevents bone loss and reduces the incidence of vertebral, hip, and Colles' fractures. Although the mechanism of action of estrogen on bone metabolism is still not completely elucidated, estrogens have been shown to have several effects: increase in renal tubular absorption of calcium, thus reducing urinary calcium; decrease in the sensitivity of bone to the parathyroid hormone (PTH); increase in the intestinal absorption of calcium and increase in circulating levels of active 1-25-dihydroxyvitamin D. Recent research has shown that osteoblasts also possess receptors for estrogens.

Clinical Studies

Clinical StudiesAbstract
Hair regrowth in a male patient with extensive androgenetic alopecia on estrogen therapy. Not available
Influence of estrogens on the androgen metabolism in different subunits of human hair follicles. The molecular pathways involved in estrogen-mediated induction of hair growth in androgenetic alopecia are unknown. Some authors found that estradiol (E) inhibited 5alpha-reductase (5alpha-R) activity and therefore we addressed the question whether 17alpha- or 17beta-E are able to modulate the activity of 5alpha-R, 3beta-hydroxysteroid dehydrogenase (3beta-HSD) or 17beta-hydroxysteroid dehydrogenase (17beta-HSD) in isolated compartments of human hair follicles. For this purpose, scalp biopsies from volunteers were taken and from each biopsy root sheaths, connective tissue sheaths and dermal papillae (DP) were dissected and incubated in the presence of 3H-testosterone (T) and, in addition, either 17alpha-E, 17beta-E, progesterone or finasteride for up to 48 hrs. Thereafter high-performance liquid chromatography analysis of culture supernatants was performed to detect T-metabolites. At the tested concentrations, finasteride was found to be a major inhibitor of dihydrotestosterone (DHT) formation. Even 1 nM finasteride inhibited DHT synthesis in DP by 86% and 1 nM progesterone by 75%. Estrogens were less able to inhibit the synthesis of DHT in DP (e.g. 100 nM 17alpha-E: 20%; 100 nM 17beta-E: 60%). Whether E directly inhibits 5alpha-R in DP's or whether the effect of estrogens might be explained by an increased conversion of T to the weaker androgens such as androstendione (via 17beta-HSD), androstenediol (via 3beta-HSD) or 17beta-E (via aromatase), thereby diminishing the amount of T available for the conversion to DHT, remains to be shown.
17alpha-estradiol induces aromatase activity in intact human anagen hair follicles ex vivo. For topical treatment of androgenetic alopecia (AGA) in women, solutions containing either estradiol benzoate, estradiol valerate, 17beta- or 17alpha-estradiol are commercially available in Europe and some studies show an increased anagen and decreased telogen rate after treatment as compared with placebo. At present it is not precisely known how estrogens mediate their beneficial effect on AGA-affected hair follicles. We have shown recently that 17alpha-estradiol is able to diminish the amount of dihydrotestosterone (DHT) formed by human hair follicles after incubation with testosterone, while increasing the concentration of weaker steroids such as estrogens. Because aromatase is involved in the conversion of testosterone to estrogens and because there is some clinical evidence that aromatase activity may be involved in the pathogenesis of AGA, we addressed the question whether aromatase is expressed in human hair follicles and whether 17alpha-estradiol is able to modify the aromatase activity. Herewith we were able to demonstrate that intact, microdissected hair follicles from female donors express considerably more aromatase activity than hair follicles from male donors. Using immunohistochemistry, we detected the aromatase mainly in the epithelial parts of the hair follicle and not in the dermal papilla. Furthermore, we show that in comparison to the controls, we noticed in 17alpha-estradiol-incubated (1 nM) female hair follicles a concentration- and time-dependent increase of aromatase activity (at 24 h: 1 nM = +18%, 100 nM = +25%, 1 micro M = +57%; 24 h: 1 nM = +18%, 48 h: 1 nM = +25%). In conclusion, our ex vivo experiments suggest that under the influence of 17alpha-estradiol an increased conversion of testosterone to 17beta-estradiol and androstendione to estrone takes place, which might explain the beneficial effects of estrogen treatment of AGA.
Topical application of 17beta-estradiol increases extracellular matrix protein synthesis by stimulating tgf-Beta signaling in aged human skin in vivo. To investigate the effects of topically applied 17beta-estradiol on the expression of extracellular matrix proteins in aged human skin, 17beta-estradiol (0.01%) and its vehicle (70% propylene glycol, 30% ethanol) were applied to aged (68-82 y, eight females and five males) human buttock skin under occlusion for 2 wk (three times per week). Topical 17beta-estradiol was found to increase the expression of type 1 procollagen mRNA and protein significantly in human aged skin in vivo. In addition, metalloproteinase (MMP-1 protein levels were reduced by topical 17beta-estradiol. The expressions of TGF-beta1, TGF-beta type II receptor, and Sma and Mad related (Smad)3 were increased by topical 17 beta-estradiol in aged human skin, and TGF-beta1 neutralizing antibody inhibited 17beta-estradiol-induced procollagen synthesis in cultured fibroblasts. We also found that the expressions of tropoelastin and fibrillin-1 mRNA and protein, and elastic fibers in aged skin were also increased by topical 17beta-estradiol. Topical 17beta-estradiol also increased keratinocyte proliferation and the epidermal thickness in aged human skin. We also observed the same effects of topical 17beta-estradiol in young skin. In conclusion, our results suggest that topical 17beta-estradiol treatment may improve the cutaneous function of aged human skin by improving the connective tissue and increasing epidermal thickness.
Topical estrogen accelerates cutaneous wound healing in aged humans associated with an altered inflammatory response. The effects of intrinsic aging on the cutaneous wound healing process are profound, and the resulting acute and chronic wound morbidity imposes a substantial burden on health services. We have investigated the effects of topical estrogen on cutaneous wound healing in healthy elderly men and women, and related these effects to the inflammatory response and local elastase levels, an enzyme known to be up-regulated in impaired wound healing states. Eighteen health status-defined females (mean age, 74.4 years) and eighteen males (mean age, 70.7 years) were randomized in a double-blind study to either active estrogen patch or identical placebo patch attached for 24 hours to the upper inner arm, through which two 4-mm punch biopsies were made. The wounds were excised at either day 7 or day 80 post-wounding. Compared to placebo, estrogen treatment increased the extent of wound healing in both males and females with a decrease in wound size at day 7, increased collagen levels at both days 7 and 80, and increased day 7 fibronectin levels. In addition, estrogen enhanced the strength of day 80 wounds. Estrogen treatment was associated with a decrease in wound elastase levels secondary to reduced neutrophil numbers, and decreased fibronectin degradation. In vitro studies using isolated human neutrophils indicate that one mechanism underlying the altered inflammatory response involves both a direct inhibition of neutrophil chemotaxis by estrogen and an altered expression of neutrophil adhesion molecules. These data demonstrate that delays in wound healing in the elderly can be significantly diminished by topical estrogen in both male and female subjects.


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