Estrogen
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2008-07-07T12:21:05Z
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Reverted edits by [[Special:Contributions/117.89.22.81|117.89.22.81]] ([[User talk:117.89.22.81|talk]]) to last version by 132.156.89.244
[[Image:Estriol_v2.png|thumb|200px|[[Estriol]]. Note two [[hydroxyl]] (-OH) groups attached to the D ring (rightmost ring).]]
[[Image:Estradiol2.png|thumb|200px|[[Estradiol]]. Note one [[hydroxyl]] group attached to the D ring. The 'di' refers both to this hydroxyl and the one on the A ring (leftmost).]]
[[Image:Estrone2.png|thumb|200px|[[Estrone]]. Note the [[ketone]] (=O) group attached to the D ring. ]]
'''Estrogens''' (U.S., otherwise '''oestrogens''' or '''œstrogens''') are a group of [[steroid]] compounds, named for their importance in the [[estrous cycle]], and functioning as the primary [[female]] [[sex hormone]].
Estrogens are used as part of some [[combined oral contraceptive pill|oral contraceptives]], in estrogen replacement therapy of [[menopause|postmenopausal]] women, and in [[Hormone replacement therapy (male-to-female)|hormone replacement therapy]] for [[transwomen]].
Like all [[steroid hormone]]s, estrogens readily [[diffusion|diffuse]] across the [[cell membrane]]; inside the cell, they interact with [[estrogen receptor]]s.<ref>Nussey and Whitehead: ''[http://www.ncbi.nlm.nih.gov/books/bv.fcgi?call=bv.View..ShowTOC&rid=endocrin.TOC&depth=10 Endocrinology, an integrated approach]'', Taylor and Francis 2001</ref> Additionally, estrogens have been shown to activate a [[G protein-coupled receptor]], [[GPR30]].<ref name="pmid17222505">{{cite journal | author = Prossnitz ER, Arterburn JB, Sklar LA | title = GPR30: A G protein-coupled receptor for estrogen | journal = Mol. Cell. Endocrinol. | volume = 265-266 | issue = | pages = 138–42 | year = 2007 | pmid = 17222505 | doi = 10.1016/j.mce.2006.12.010 }}</ref>
==Types==
The three major naturally occurring estrogens in women are [[estradiol]], [[estriol]], and [[estrone]]. In the body these are all produced from [[androgen]]s through actions of [[enzyme]]s.
* From [[menarche]] to menopause the primary estrogen is [[estradiol|17β-estradiol]]. In postmenopausal women more estrone is present than estradiol.
* Estradiol is produced from [[testosterone]] and estrone from [[androstenedione]].
* Estrone is weaker than estradiol.
[[Premarin]], a commonly prescribed estrogenic drug, contains the steroidal estrogens [[equilin]] and [[equilenin]], in addition to [[estrone]] sulfate.
A range of synthetic and natural substances have been identified that also possess estrogenic activity.<ref name="pmid11258977">{{cite journal | author = Fang H, Tong W, Shi LM, Blair R, Perkins R, Branham W, Hass BS, Xie Q, Dial SL, Moland CL, Sheehan DM | title = Structure-activity relationships for a large diverse set of natural, synthetic, and environmental estrogens | journal = Chem. Res. Toxicol. | volume = 14 | issue = 3 | pages = 280–94 | year = 2001 | pmid = 11258977 | doi = 10.1021/tx000208y }}</ref> Synthetic substances of this kind are known as [[xenoestrogen]]s, plant products with estrogenic activity are called [[phytoestrogen]]s, and those produced by fungi are known as [[mycoestrogens]]. Unlike estrogens produced by mammals, these substances are not necessarily [[steroids]].
==Estrogen production==
[[Image:Steroidogenesis.gif|thumb|right|400px|[[Steroidogenesis]], showing estrogen at bottom right as estrone and estradiol.]]
Testosterone is synthesized during [[steroidogenesis]], with [[cholesterol]] as the starting molecule.
Estrogen is produced primarily by developing [[ovarian follicle|follicles]] in the ovaries, the [[corpus luteum]], and the [[placenta]]. [[Follicle-stimulating hormone]] (FSH) and [[luteinizing hormone]] (LH) stimulate the production of estrogen in the [[ovary|ovaries]]. Some estrogens are also produced in smaller amounts by other tissues such as the [[liver]], [[adrenal gland]]s, and the [[breast]]s. These secondary sources of estrogen are especially important in postmenopausal women.
Synthesis of estrogens starts in [[theca interna]] cells in the ovary, by the synthesis of [[androstenedione]] from [[cholesterol]]. Androstenedione is a substance of moderate androgenic activity. This compound crosses the [[basal membrane]] into the surrounding [[granulosa cell]]s, where it is converted to estrone or estradiol, either immediately or through testosterone. The conversion of testosterone to estradiol, and of androstenedione to estrone, is catalyzed by the enzyme [[aromatase]].
Estradiol levels vary through the menstrual cycle, with levels highest just before [[ovulation]].
==Functions==
While estrogens are present in both [[man|men]] and [[woman|women]], they are usually present at significantly higher levels in women of reproductive age. They promote the development of female [[secondary sex characteristic]]s, such as breasts, and are also involved in the thickening of the [[endometrium]] and other aspects of regulating the [[menstrual cycle]]. In males, estrogen regulates certain functions of the reproductive system important to the maturation of sperm<ref name="pmid9393999">{{cite journal | author = Hess RA, Bunick D, Lee KH, Bahr J, Taylor JA, Korach KS, Lubahn DB | title = A role for oestrogens in the male reproductive system | journal = Nature | volume = 390 | issue = 6659 | pages = 509–12 | year = 1997 | pmid = 9393999 | doi = 10.1038/37352 }}</ref><ref name="titleScience News Online (12/6/97): Estrogens Emerging Manly Alter Ego">{{cite web | url = http://www.sciencenews.org/pages/sn_arc97/12_6_97/fob1.htm | title = Science News Online (12/6/97): Estrogen's Emerging Manly Alter Ego | accessdate = 2008-03-04 | author = J. Raloff | authorlink = | coauthors = | date = 1997-12-06 | format = | work = | publisher = Science News | pages = | language = | archiveurl = | archivedate = | quote = }}</ref><ref name="titleScience Blog -- Estrogen Linked To Sperm Count, Male Fertility">{{cite web | url = http://www.scienceblog.com/community/older/1997/B/199701564.html | title = Science Blog -- Estrogen Linked To Sperm Count, Male Fertility | accessdate = 2008-03-04 | author = | authorlink = | coauthors = | date = | format = | work = | publisher = Science Blog | pages = | language = | archiveurl = | archivedate = | quote = }}</ref> and may be necessary for a healthy libido.<ref name="pmid15555924">{{cite journal | author = Hill RA, Pompolo S, Jones ME, Simpson ER, Boon WC | title = Estrogen deficiency leads to apoptosis in dopaminergic neurons in the medial preoptic area and arcuate nucleus of male mice | journal = Mol. Cell. Neurosci. | volume = 27 | issue = 4 | pages = 466–76 | year = 2004 | pmid = 15555924 | doi = 10.1016/j.mcn.2004.04.012 }}</ref><ref name="PHI_Media_release">{{cite web | url = http://www.phimr.monash.edu.au/news/media_releases/estrogen_vital_for_male_sex_drive.htm | title = Prince Henry's Institute - Media Release - Male sex drive linked to estrogen | accessdate = 2008-03-04 | author = Ian Muchamore | authorlink = | coauthors = | date = 2004-07-19 | format = | work = | publisher = Prince Henry's Institute | pages = | language = | archiveurl = | archivedate = | quote = }}</ref> Furthermore, there are several other structural changes induced by estrogen, in addition to other functions.
*Structural
** promote formation of female secondary sex characteristics
** decelerate [[height]] growth<ref name="pmid17018462">{{cite journal | author = Lee JM, Howell JD | title = Tall girls: the social shaping of a medical therapy | journal = Arch Pediatr Adolesc Med | volume = 160 | issue = 10 | pages = 1035–9 | year = 2006 | pmid = 17018462 | doi = 10.1001/archpedi.160.10.1035 }}</ref>
** accelerate [[metabolism]] (burn fat)
** reduce [[muscle]] mass
** stimulate [[endometrium|endometrial]] growth
** increase [[uterus|uterine]] growth
** maintenance of vessel and skin
** reduce [[bone resorption]], increase bone formation
** [[Somatotype|morphic]] change ([[Somatotype|endomorphic]] -> [[mesomorphic]] -> [[ectomorphic]])
*[[protein]] synthesis
** increase hepatic production of binding proteins
*[[coagulation]]
** increase circulating level of [[coagulation factor|factors]] [[factor II|2]], [[factor VII|7]], [[factor IX|9]], [[factor X|10]], [[antithrombin]] III, [[plasminogen]]
** increase [[platelet]] adhesiveness
*Lipid
** increase [[high density lipoprotein|HDL]], [[triglyceride]]
** decrease [[low density lipoprotein|LDL]], [[fat]] deposition
*Fluid balance
** salt ([[sodium]]) and water retention
*Hormones
** increase [[growth hormone]]
** increase [[cortisol]], [[SHBG]]
*Gastrointestinal tract
** reduce bowel motility
** increase cholesterol in [[bile]]
*Melanin
** increase [[pheomelanin]], reduce [[eumelanin]]
*Cancer
**support [[hormone-sensitive]] [[breast cancer]]s (see section below)
*Lung function
**promotes lung function by supporting [[alveoli]] (in rodents but probably in humans).<ref name="pmid15298854">{{cite journal | author = Massaro D, Massaro GD | title = Estrogen regulates pulmonary alveolar formation, loss, and regeneration in mice | journal = Am. J. Physiol. Lung Cell Mol. Physiol. | volume = 287 | issue = 6 | pages = L1154–9 | year = 2004 | pmid = 15298854 | doi = 10.1152/ajplung.00228.2004 }}</ref>
[[libido|Sexual desire]] is dependent on [[androgen]] levels rather than estrogen levels.<ref name="pmid16037752">{{cite journal | author = Warnock JK, Swanson SG, Borel RW, Zipfel LM, Brennan JJ | title = Combined esterified estrogens and methyltestosterone versus esterified estrogens alone in the treatment of loss of sexual interest in surgically menopausal women | journal = Menopause | volume = 12 | issue = 4 | pages = 374–84 | year = 2005 | pmid = 16037752 | doi = 10.1097/01.GME.0000153933.50860.FD }}</ref>
===Role in cancer===
About 80% of [[breast cancer]]s, once established, rely on supplies of the hormone estrogen to grow: they are known as [[hormone-sensitive]] or [[hormone-receptor-positive]] cancers.<ref name="titleHormonal Therapy">{{cite web | url = http://www.breastcancer.org/tre_sys_hrt_idx.html | title = Hormonal Therapy | accessdate = 2008-03-04 | author = | authorlink = | coauthors = | date = 2007-06-29 | format = | work = | publisher = breastcancer.org | pages = | language = | archiveurl = | archivedate = | quote = }}</ref> Suppression of production in the body of estrogen is a treatment for these cancers.
==Medical applications==
Since estrogen circulating in the blood can [[negative feedback|negatively feed-back]] to reduce circulating levels of FSH and LH, most oral contraceptives contain a synthetic estrogen, along with a synthetic [[progestin]]. Even in men, the major hormone involved in LH feedback is [[estradiol]], not [[testosterone]].
As more fully discussed in the article on [[hormone replacement therapy (menopause)| Hormone replacement therapy]], estrogen and other hormones are given to [[postmenopausal]] women in order to prevent [[osteoporosis]] as well as treat the symptoms of menopause such as hot flashes, vaginal dryness, urinary stress incontinence, chilly sensations, dizziness, fatigue, irritability, and sweating. Fractures of the spine, wrist, and hips decrease by 50-70% and spinal bone density increases by ~5% in those women treated with estrogen within 3 years of the onset of menopause and for 5-10 years thereafter.
Before the specific dangers of conjugated equine estrogens were well understood, standard therapy was 0.625 mg/day of conjugated equine estrogens (such as Premarin). There are, however, risks associated with conjugated equine estrogen therapy. Among the older postmenopausal women studied as part of the [[Women's Health Initiative]] (WHI), an orally-administered conjugated equine estrogen supplement was found to be associated with an increased risk of dangerous [[blood clotting]]. The WHI studies used one type of estrogen supplement, a high oral dose of conjugated equine estrogens ([[Premarin]] alone and with medroxyprogesterone acetate as ''PremPro'').<ref name="titleNIH - Menopausal Hormone Therapy Information">{{cite web | url = http://www.nih.gov/PHTindex.htm | title = NIH - Menopausal Hormone Therapy Information | accessdate = 2008-03-04 | author = | authorlink = | coauthors = | date = 2007-08-27 | format = | work = | publisher = National Institutes of Health | pages = | language = | archiveurl = | archivedate = | quote = }}</ref>
In a study by the NIH, esterified estrogens were not proven to pose the same risks to health as conjugated equine estrogens. [[Hormone replacement therapy]] has favorable effects on serum cholesterol levels, and when initiated immediately upon menopause reduces the incidence of cardiovascular disease. Estrogen has a protector effect on atherosclerosis : it lowers LDL and triglycerides, it raises HDL levels and has endothelial vasodilatation properties plus an anti-inflammatory component.
Research is underway to determine if risks of estrogen supplement use are the same for all methods of delivery. In particular, estrogen applied [[topical]]ly may have a different spectrum of side-effects than when administered orally,<ref name="pmid16396517">{{cite journal | author = Menon DV, Vongpatanasin W | title = Effects of transdermal estrogen replacement therapy on cardiovascular risk factors | journal = Treat Endocrinol | volume = 5 | issue = 1 | pages = 37–51 | year = 2006 | pmid = 16396517| doi = 10.2165/00024677-200605010-00005 <!--Retrieved from CrossRef by DOI bot--> }}</ref> and transdermal oestrogens do not affect clotting as they are absorbed directly into the systemic circulation, avoiding first-pass metabolism in the liver. This route of administration is thus preferred in women with a history of [[thrombo-embolic disease]].
Estrogen is also used in the therapy of vaginal atrophy, hypoestrogenism (as a result of hypogonadism, castration, or primary ovarian failure), amenorrhea, dysmenorrhea, and oligomenorrhea. Estrogens can also be used to suppress [[lactation]] after child birth.
[[Hormone-receptor-positive]] breast cancers are treated with drugs which suppress production in the body of estrogen.<ref name="titleHormonal Therapy">{{cite web | url = http://www.breastcancer.org/tre_sys_hrt_idx.html | title = Hormonal Therapy | accessdate = 2008-03-04 | author = | authorlink = | coauthors = | date = 2007-07-26 | format = | work = | publisher = breastcancer.org | pages = | language = | archiveurl = | archivedate = | quote = }}</ref> This technique, in the context of treatment of breast cancer, is known variously as [[hormonal therapy]], hormone therapy, or [[anti-estrogen therapy]] (not to be confused with hormone replacement therapy). Certain foods such as soy may also suppress the proliferative effects of estrogen and are used as an alternative to hormone therapy.<ref name="pmid11880595">{{cite journal | author = Kurzer MS | title = Hormonal effects of soy in premenopausal women and men | journal = J. Nutr. | volume = 132 | issue = 3 | pages = 570S–573S | year = 2002 | pmid = 11880595 | doi = | issn = | url = http://jn.nutrition.org/cgi/content/abstract/132/3/570S }}</ref>
In humans and mice, estrogen promotes wound healing.<ref name="Oh_2006">{{cite journal | author = Oh DM, Phillips, TJ | title = Sex Hormones and Wound Healing | journal = Wounds | volume = 18 | issue = 1 | pages = 8–18 | year = 2006| doi = | issn = | url = http://www.woundsresearch.com/article/5190 }}</ref>
At one time, estrogen was used to induce [[growth attenuation]] in tall girls.<ref name="pmid17018462">{{cite journal | author = Lee JM, Howell JD | title = Tall girls: the social shaping of a medical therapy | journal = Arch Pediatr Adolesc Med | volume = 160 | issue = 10 | pages = 1035–9 | year = 2006 | pmid = 17018462 | doi = 10.1001/archpedi.160.10.1035 }}</ref> Recently, estrogen-induced growth attenuation was used as part of the controversial [[Ashley Treatment]] to keep a [[developmentally disabled]] girl from growing to adult size.<ref name="pmid17018459">{{cite journal | author = Gunther DF, Diekema DS | title = Attenuating growth in children with profound developmental disability: a new approach to an old dilemma | journal = Arch Pediatr Adolesc Med | volume = 160 | issue = 10 | pages = 1013–7 | year = 2006 | pmid = 17018459 | doi = 10.1001/archpedi.160.10.1013 }}</ref>
Under certain circumstances, estrogen may also be used in males for treatment of [[prostate cancer]].<ref name="pmid15046698">{{cite journal | author = Oh WK | title = The evolving role of estrogen therapy in prostate cancer | journal = Clin Prostate Cancer | volume = 1 | issue = 2 | pages = 81–9 | year = 2002 | pmid = 15046698 | doi = | issn = | url = http://www.cigjournals.com/CIG/c.abs/clinical-genitourinary-cancer/volume1/issue2/article792 }}</ref>
Most recently, estrogen has been used in experimental research as a way to treat patients suffering from [[bulimia nervosa]], in addition to [[Cognitive Behavioral Therapy]], which is the established standard for treatment in bulimia cases. The estrogen research hypothesizes that the disease may be linked to a hormonal imbalance in the brain.<ref name="titleBulimia May Result from Hormonal Imbalance - Startpage - ki.se">{{cite web | url = http://ki.se/ki/jsp/polopoly.jsp?d=130&a=22684&l=en&newsdep=130 | title = Bulimia May Result from Hormonal Imbalance | accessdate = 2008-03-04 | author = Gunilla Andersson | authorlink = | coauthors = | date = 2007-01-09 | format = | work = | publisher = Karolinska Institutet | pages = | language = | archiveurl = | archivedate = | quote = }}</ref>
Estrogen has also been used in studies which indicate that it may be an effective drug for use in the treatment of traumatic liver injury.<ref name="pmid17392161">{{cite journal | author = Hsieh YC, Yu HP, Frink M, Suzuki T, Choudhry MA, Schwacha MG, Chaudry IH | title = G protein-coupled receptor 30-dependent protein kinase A pathway is critical in nongenomic effects of estrogen in attenuating liver injury after trauma-hemorrhage | journal = Am. J. Pathol. | volume = 170 | issue = 4 | pages = 1210–8 | year = 2007 | pmid = 17392161 | doi = 10.2353/ajpath.2007.060883 }}</ref>
==Mental health==
Estrogen is considered to play a significant role in women’s mental health. A conceptual model of how estrogen affects mood was suggested by Douma et al 2005 based on their extensive literature review relating activity of endogenous, bio-identical and synthetic estrogen with mood and well-being. They concluded the sudden estrogen withdrawal, fluctuating estrogen, and periods of sustained estrogen low levels correlated with significant mood lowering. Clinical recovery from depression postpartum, perimenopause, and postmenopause was shown to be effective after levels of estrogen were stabilized and/or restored.<ref name="pmid16292022">{{cite journal | author = Douma, S.L, Husband, C., O’Donnell, M.E., Barwin, B.N., Woodend A.K. | title = Estrogen-related Mood Disorders Reproductive Life Cycle Factors | journal = Advances in Nursing Science | volume = 28 | issue = 4 | pages = 364–375 | year = 2005 | pmid = 16292022 }}</ref>.<ref name="pmid17909167">{{cite journal | author = Lasiuk, GC and Hegadoren, KM | title = The Effects of Estradiol on Central Serotonergic Systems and Its Relationship to Mood in Women | journal = Biological Research for Nursing (2007), | volume = 9 | issue = 2 | pages = 147–160 | year = 2007 | pmid = 17909167 | doi = 10.1177/1099800407305600 }}</ref>
==Health risks and warning labels==
The labeling of estrogen-only products in the U.S. includes a [[black box warning|boxed warning]] that unopposed estrogen (without [[progestagen]]) therapy increases the risk of [[endometrial cancer]].
Based on a review of data from the WHI, on January 8, 2003 the FDA changed the labeling of all estrogen and estrogen with progestin products for use by postmenopausal women to include a new boxed warning about cardiovascular and other risks. The estrogen-alone substudy of the WHI reported an increased risk of [[stroke]] and [[deep vein thrombosis]] (DVT) in postmenopausal women 50 years of age or older and an increased risk of [[dementia]] in postmenopausal women 65 years of age or older using 0.625 mg of Premarin conjugated equine estrogens (CEE). The estrogen-plus-progestin substudy of the WHI reported an increased risk of [[myocardial infarction]], stroke, invasive breast cancer, [[pulmonary emboli]] and DVT in postmenopausal women 50 years of age or older and an increased risk of dementia in postmenopausal women 65 years of age or older using PremPro, which is 0.625 mg of CEE with 2.5 mg of the progestin [[medroxyprogesterone acetate]] (MPA).<ref name=fdanewlabel>{{cite web |author=FDA |title=FDA Approves New Labels for Estrogen and Estrogen with Progestin Therapies for Postmenopausal Women Following Review of Women's Health Initiative Data |url=http://www.fda.gov/bbs/topics/NEWS/2003/NEW00863.html |date=2003, Jan 8 |accessdate=2006-10-26}}</ref><ref name="Times">{{cite web |last=Kolata |first=Gina |title = F.D.A. Orders Warning on All Estrogen Labels |publisher=The New York Times |date=2003, Jan 9 |url=http://query.nytimes.com/gst/fullpage.html?sec=health&res=9C00E0DD103EF93AA35752C0A9659C8B63 |accessdate=2006-10-26}}</ref><ref name="Medline">{{cite web | date=2006, Apr 1 |author=NLM |title=IMPORTANT WARNING |work=Drug Information: Estrogen |publisher=MedlinePlus |url=http://www.nlm.nih.gov/medlineplus/druginfo/medmaster/a682922.html |accessdate=2006-10-26}}</ref>
==Estrogens in cosmetics==
Some hair [[shampoo]]s on the market include estrogens and placental extracts; others contain phytoestrogens. There are case reports of young children developing breasts after exposure to these shampoos.<ref>{{Citation | last=Sanghavi | first=DM | title=Preschool Puberty, and a Search for the Causes | newspaper=[[The New York Times]] | volume= | issue= | pages= | year=2006 | date=October 17, 2006 | url=http://www.nytimes.com/2006/10/17/science/17puberty.html |accessdate=2008-06-04}}</ref> These products are often marketed to African-American consumers.<ref name="pmid11772198">{{cite journal | author = Li ST, Lozano P, Grossman DC, Graham E | title = Hormone-containing hair product use in prepubertal children | journal = Arch Pediatr Adolesc Med | volume = 156 | issue = 1 | pages = 85–6 | year = 2002 | pmid = 11772198 | doi = | issn = | url = http://archpedi.ama-assn.org/cgi/content/full/156/1/85 }}</ref>
On September 9, 1993, the FDA determined that not all topically-applied hormone-containing drug products for [[over-the-counter drug|OTC]] human use are generally recognized as safe and effective and are misbranded. An accompanying proposed rule deals with cosmetics, concluding that any use of natural estrogens in a cosmetic product makes the product an unapproved new drug and that any cosmetic using the term "hormone" in the text of its labeling or in its ingredient statement makes an implied drug claim, subjecting such a product to regulatory action.<ref name="FDA cosmetics">{{cite web |author=FDA | date=1995, Feb |title=Products containing estrogenic hormones, placental extract or vitamins |work=Guide to Inspections of Cosmetic Product Manufacturers |url=http://www.fda.gov/ora/inspect_ref/igs/cosmet.html |accessdate=2006-10-24}}</ref>
In addition to being considered misbranded drugs, products claiming to contain placental extract may also be deemed to be misbranded cosmetics if the extract has been prepared from placentas from which the hormones and other biologically active substances have been removed and the extracted substance consists principally of protein. The FDA recommends that this substance be identified by a name other than "placental extract" and describing its composition more accurately because consumers associate the name "placental extract" with a therapeutic use of some biological activity.<ref name="FDA cosmetics"/>
==History==
The existence and effects of estrogen were established from 1923 to 1938 in which the formulation was led by a group of scientists instead of pharmaceutical companies. Thereafter, the market for hormonal drug research opened up.
The “first orally effective estrogen”, Emmenin, derived from the late-pregnancy urine of Canadian women, was introduced in 1930 by Collip and Ayerst Laboratories. Estrogens are not water-soluble and cannot be given orally, but the urine was found to contain estriol [[glucuronide]] which is water soluble and becomes active in the body after [[hydrolization]].
Scientists continued to search for new sources of estrogen because of concerns associated with the practicality of introducing the drug into the market. At the same time, a German pharmaceutical drug company, formulated a similar product as Emmenin that was introduced to German women to treat menopausal symptoms.
In 1938, British scientists obtained a patent on a newly formulated nonsteroidal estrogen, [[Diethylstilbestrol]] (DES), that was cheaper and more powerful than the previously manufactured estrogens. Soon after, concerns over the side effects of DES were raised in scientific journals while the drug manufacturers came together to lobby for governmental approval of DES. It was only until 1941 when estrogen therapy was finally approved by the Food and Drug Administration (FDA) for the treatment of menopausal symptoms. <ref>{{cite web | author=Rothenberg, Carla J. | title= The Rise and Fall of Estrogen Therapy: The History of HRT |date=2005-04-25 | url= http://leda.law.harvard.edu/leda/data/711/Rothenberg05.pdf |accessdate=2006-10-27 }}</ref>
==See also==
*[[List of steroid abbreviations]]
== References ==
{{reflist|2}}
==See also==
*[[Female]]
*[[Atrophic vaginitis]]
*[[Endocrinology]]
*[[Equol]]
*[[Equilin]]
*[[Estradiol]]
*[[Estrogen receptor]]
*[[Hormone Replacement Therapy]]
*[[Progesterone]]
*[[Progestin]]
*[[Testosterone]]
==External links and further reading==
* {{MedlinePlusDrugInfo|medmaster|a682922}}
*Nussey and Whitehead: ''[http://www.ncbi.nlm.nih.gov/books/bv.fcgi?call=bv.View..ShowTOC&rid=endocrin.TOC&depth=10 Endocrinology, an integrated approach]'', Taylor and Francis 2001. Free online textbook.
{{Hormones}}
{{Sex hormones}}
[[Category:Sex steroids]]
[[Category:Estrogens]]
[[Category:Female reproductive system]]
[[Category:Endocrinology]]
[[ar:إستروجين]]
[[bg:Естроген]]
[[ca:Estrogen]]
[[cs:Estrogen]]
[[da:Østrogen]]
[[de:Estrogene]]
[[dv:އެސްޓްރަޖަން]]
[[et:Östrogeenid]]
[[el:Οιστρογόνο]]
[[es:Estrógeno]]
[[fa:استروژن]]
[[fo:Østrogen]]
[[fr:Œstrogène]]
[[ko:에스트로겐]]
[[hr:Estrogeni]]
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[[mk:Естрогени хормони]]
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[[ja:エストロゲン]]
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[[zh:雌激素]]