Fachfrage: T-Metaboliten-Affinität an den AR [Beitrag #36700] :: Fr., 18 August 2006 23:11 
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kkoo
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Fachfrage: Die anderen T-Metaboliten (außer DHT) haben doch auch eine Affinität an den AR, nur eben viel schwächer. Was richten die aber an, wenn sie an einen AR binden, ähnliches wie DHT womöglich? (Dachte nur daran, dass ja trotz massiver DHT-Hemmungen AGA trotzdem voranschreiten kann...)
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Re: Fachfrage: T-Metaboliten-Affinität an den AR [Beitrag #36702 ist eine Antwort auf Beitrag #36700] :: Fr., 18 August 2006 23:29 
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pilos
Beiträge: 26511 Registriert: November 2005 Ort: Ausland
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| kkoo schrieb am Fre, 18 August 2006 23:11 |
Fachfrage: Die anderen T-Metaboliten (außer DHT) haben doch auch eine Affinität an den AR, nur eben viel schwächer. Was richten die aber an, wenn sie an einen AR binden, ähnliches wie DHT womöglich? (Dachte nur daran, dass ja trotz massiver DHT-Hemmungen AGA trotzdem voranschreiten kann...)
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wenn T=1...dann DHT=4-5 die anderen spielen kaum eine Rolle....es ist eben nicht nur das androgen das problem..aber jeder wie er meint...
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Re: fusel nochmal bitte? [Beitrag #36755 ist eine Antwort auf Beitrag #36751] :: Sa., 19 August 2006 17:49
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kkoo
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| fuselkopf schrieb am Sam, 19 August 2006 16:42 |
Versuchs mit Quercetin. Pflanzliches non-citrus Flavonide. Ist ein Phytohormon, aber es hemmt die Aromatase und das recht effektiv. Hat aber noch viel mehr positive Eigenschaften das Zeug!
Schau Dir mal nachfolgenden Link an, da siehst Du die E2-Werte von über 1000 Männern, und die meisten haben einen E2 Wert, der bei 22pmol/l liegt oder bzw 6pg/ml !!! Und hier schwirren Leute rum mit E2 Werten von über 50 pg/ml!!! Ich habe einen Wert von ca 25 pg/ml. Das ist eigentlich auch schon recht hoch, aber da mein Testo Wert auch recht hoch ist, geht der E2 Wert noch. Mann sollte ca 200 bis 300 mal soviel Testo haben wie E2. Kann man sich ja leicht ausrechnen... in welchem Range man liegen sollte.
http://www.kup.at/journals/abbildungen/gross/449.html#start
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Meine Werte sind:
Androstendion 2,4 (0,3-3,1 ng/ml)
Gesamttestosteron 8,83 (2,8-8 ng/ml)
Östradiol 50 (10-44 pg/ml)
Prolactin 214 (86-390 uU/ml)
DHEA-S 243 (80-560 ug/dl)
SHGB 45,2 (14-71 nmol/l)
also E2 genau die 50 pg/ml! Das entspr. Nach Deiner Umrechung 183 pmol/l! Da wär ich aber jenseits von gut und böse in diesem Diagramm? Das kann doch nicht sein!? Dann wär ja der Ref.-wert des Labors auch unsinnig hoch!?
Danke.
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Re: fusel ? [Beitrag #36763 ist eine Antwort auf Beitrag #36751] :: Sa., 19 August 2006 19:52
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tristan
Beiträge: 709 Registriert: November 2005
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| fuselkopf schrieb am Sam, 19 August 2006 16:42 |
Versuchs mit Quercetin. Pflanzliches non-citrus Flavonide. Ist ein Phytohormon, aber es hemmt die Aromatase und das recht effektiv. Hat aber noch viel mehr positive Eigenschaften das Zeug!
Schau Dir mal nachfolgenden Link an, da siehst Du die E2-Werte von über 1000 Männern, und die meisten haben einen E2 Wert, der bei 22pmol/l liegt oder bzw 6pg/ml !!! Und hier schwirren Leute rum mit E2 Werten von über 50 pg/ml!!! Ich habe einen Wert von ca 25 pg/ml. Das ist eigentlich auch schon recht hoch, aber da mein Testo Wert auch recht hoch ist, geht der E2 Wert noch. Mann sollte ca 200 bis 300 mal soviel Testo haben wie E2. Kann man sich ja leicht ausrechnen... in welchem Range man liegen sollte.
http://www.kup.at/journals/abbildungen/gross/449.html#start
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gefährliche sache meiner einsicht...
- leute die nen wert über 50 haben sollen es ausprobieren, ein wunder wird man kaum erwarten können,...
- Ich kenne in diesem forum 2 leute die einen wert im oberen 40er und unteren 50er bereich haben. kkoo und fixt. alle anderen die ihre werte reingestellt haben, inkl. mir, waren im bereich <20.
- meine ausgangssituation als ich extremen haarausfall hatte war normales testo, hoher freier androgenindex (wenig shbg), kein nachweisbares estrogen (<10). schlimmer hätte es nicht sein können (außer ich zusätzlich noch was an der sd gehabt)...
- vielleicht sollte man aromatasehemmer als mittel gegen aga auf den markt bringen... der pharmakonzern könnte nach kurzer zeit konkurs anmelden..
gängige nebenwirkungen bei aromatasehemmern sind haarausfall (tamoxifen)...
- der referenzbereich von 25-50 ist ein guter und sinnvoller. 6pg/ml ist kaum mehr als die männer mit angeborenem aromatasemangel hatten, das ist ein krankhafter, gesundheitsschädigender zustand! bei meinem behandelnden endokrinologen werden generell männer mit estrogen unter 20 untersucht bzgl. osteoporose (knochendichtemessung), fettstoffwechsel, insulinresistenz, oxidativem stress, etc...
als ich dort mit meinen alten werten hingegangen bin (<10) ist der extrem wütend geworden dass da nicht schon mehr und eher der sache nachgegangen wurde und meinte das wäre körperverletzung!
Die Berechnung des idealen E2 abh. vom testowert kann man so überhaupt nicht machen. hier werden weder die nnr androgene beachtet noch die periphere aktivität. Da müssten versch. marker der lokalen synthese im sammelurin etc untersucht werden um so eine verallgemeinernde und vereinfachte rechnung aufzustellen. die enzymaktivität im gewebe ist viel aussagekräftiger als der wert alleine...
- weniger estrogen bedeutet auch weniger shbg. das heißt höherer freier androgenindex. plus mehr dht! wer eine ausgangslage von hohem estrogen hat kann es ja mal ausprobieren, aber aus eigener erfahrung kann ich sagen dass ich an diesem punkt war und im vergleich sehr ungern in diese zeit zurückblicke.
selbst wenn e2 auf den haarausfall keine direkte positive wirkung ausübt, und laut erfahrungen anderer leute eher negativ wirkt sollte man trotzdem bedenken dass durch weniger e2 auch mehr dht wirken kann und das dürfte für einen großen teil der betroffenen ein problem sein.
- wenn man aromatase hemmen will in der hoffnung dass die haare wachsen sollte man sich der damit verbundenen negativen auswirkungen auf die gesundheit bewusst sein.
- quercetin hat wahrsch. direkte positive wirkung auf haarausfall, unabhängig von estrogen. ähnlich wie es bei soja der fall sein kann. ist auch aromatasehemmend.
- bisschen was als entscheidungshilfe (wie gesagt leute mit e2 bei 50 sollen es probieren, aber bei allen mit e2 unter 30 würde ich davon abraten aromatase zu hemmen)
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doi:10.1016/S0960-0760(01)00136-4 How to Cite or Link Using DOI (Opens New Window)
Elsevier Science Ltd. All rights reserved.
Aromatase-deficient (ArKO) mice accumulate excess adipose tissue*1
Margaret E. E. JonesCorresponding Author Contact Information, E-mail The Corresponding Author, a, Anne W. Thorburnb, Kara L. Britta, Kylie N. Hewitta, Marie L. Missoa, Nigel G. Wrefordc, Joseph Proiettob, Orhan K. Ozd, Brian J. Leurye, Kirsten M. Robertsona, Shenggen Yaof and Evan R. Simpsona
a Prince Henry’s Institute of Medical Research, P.O. Box 5152, Clayton, Vic. 3168, Australia
b Department of Medicine, Royal Melbourne Hospital, Melbourne, Vic., Australia
c Department of Anatomy, Monash University, Clayton, Vic., Australia
d Southwestern Medical Centre, University of Texas, Dallas, TX, USA
e Department of Animal Production, University of Melbourne, Melbourne, Vic., Australia
f Howard Florey Institute, Parkville, Vic., Australia
Available online 9 February 2002.
Abstract
previous termAromatasenext term is the enzyme which catalyses the conversion of C19 steroids into C18 estrogens. We have generated a mouse model wherein the Cyp19 gene, which encodes previous termaromatase,next term has been disrupted, and hence, the previous termaromatasenext term knockout (ArKO) mouse cannot synthesise endogenous estrogens. We examined the consequences of estrogen previous termdeficiencynext term on accumulation of adipose depots in male and female ArKO mice, observing that these animals progressively accrue significantly more intra-abdominal adipose tissue than their wildtype (WT) litter mates, reflected in increased adipocyte volume and number. This increased adiposity was not due to hyperphagia or reduced resting energy expenditure, but was associated with reduced spontaneous physical activity levels, reduced glucose oxidation, and a decrease in lean body mass. Elevated circulating levels of leptin and cholesterol were present in 1-year-old ArKO mice compared to WT controls, as were elevated insulin levels, although blood glucose was unchanged. Associated with these changes, the livers of ArKO animals were characterised by a striking accumulation of lipid droplets. Our findings demonstrate an important role for estrogen in the maintenance of lipid homeostasis in both males and females.
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doi:10.1016/S0303-7207(02)00090-4 How to Cite or Link Using DOI (Opens New Window)
Elsevier Science Ireland Ltd. All rights reserved.
Effect of estrogen deficiency in the male: the ArKO mouse model
Y. MurataCorresponding Author Contact Information, E-mail The Corresponding Author, K. M. Robertson, M. E. E. Jones and E. R. Simpson
Prince Henry's Institute of Medical Research, 246 Clayton Road, Clayton, Vic. 3168, Australia
Available online 29 April 2002.
Abstract
previous termAromatase,next term the enzyme responsible for the conversion of androgens to estrogens, is present in the mouse gonads, brain, adipose tissue and bone. Depletion of endogenous estrogens in the previous termaromatasenext term deficient mouse (ArKO) caused by the targeted disruption of the Cyp19 gene resulted in an impairment of sexual behaviour and an age-dependent disruption of spermatogenesis. This disruption occurred during early spermiogenesis, due possibly to increased number of apoptotic round spermatids. Development of obesity was associated with ageing, decrease in lean mass, hypercholesterolemia, hyperleptinemia, and insulin resistance and hepatic steatosis. However, it was not correlated with hyperphagia but to decreased physically-active behaviour. ArKO mice also developed osteoporosis. Thus, studies using the ArKO mice model has led to several insights into the multiple roles played by estrogens in the development and maintenance of fertility, sexual behaviour, lipid metabolism and bone remodelling.
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doi:10.1016/S0960-0760(03)00345-5 How to Cite or Link Using DOI (Opens New Window)
Elsevier Ltd. All rights reserved.
Neurological effects of aromatase deficiency in the mouse*1
Takahiro Matsumoto, Shin-ichiro HondaCorresponding Author Contact Information, E-mail The Corresponding Author and Nobuhiro Harada
Department of Biochemistry, School of Medicine, Fujita Health University, Aichi, Japan
Available online 12 September 2003.
Abstract
In the brain, the conversion from androgen into estrogen is an important process for the differentiation of the brain function in male rodents. The previous termaromatasenext term is expressed in some nucleus of the brain. To assess the functional significance of the previous termaromatasenext term gene in development and activation of sex-specific behavior, we analyzed behavioral phenotypes of the previous termaromatasenext term knockout (ArKO) male mice. ArKO males obviously decreased their fertility and showed deficits in male sexual behavior including mount, intromission and ejaculation. Noncontact penile erection was not significantly affected by defect of the previous termaromatasenext term gene. A reduction of aggressive behavior against male intruders was also observed in ArKO males, while they tend to exhibit aggression toward estrous females during male copulatory tests. Moreover, the infanticide toward the pups was observed in the ArKO males, whereas characteristic parental behavior, but not infanticide was observed in wild-type males. These results indicate that previous termaromatasenext term gene expression is a critical step not only for motivational and consummatory aspects of male sexual behavior, but also for aggressive and parental behaviors in male mice.
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doi:10.1016/S0014-4886(03)00244-9 How to Cite or Link Using DOI (Opens New Window)
Elsevier Science (USA). All rights reserved.
Regular article
Age-related neurodegenerative changes in the central nervous system of estrogen-deficient follitropin receptor knockout mice
Natalia Danilovicha, b, Nobuhiro Haradac, M. Ram SairamE-mail The Corresponding Author, b and Dusica MaysingerCorresponding Author Contact Information, E-mail The Corresponding Author, a
a Department of Pharmacology and Therapeutics, McGill University, 3655 Promenade Sir-William-Osler, Room 1314, McIntyre Building, Montreal, Quebec H3G 1Y6, Canada
b Molecular Reproduction Research Laboratory, Clinical Research Institute of Montreal, Montreal, Quebec, Canada
c Fujita Health University School of Medicine, Toyoake, Japan
Received 19 February 2003; revised 10 April 2003; accepted 16 April 2003. ; Available online 2 October 2003.
Abstract
Age-related neurodegenerative conditions are characterized by neuronal death and degeneration that lead to a progressive functional decline. Among the factors influencing degenerative processes during aging are altered levels of neurotrophic ovarian steroid 17β-estradiol (E2). The follitropin receptor knockout (FORKO) female mouse displays hormonal imbalance characterized by very low levels of circulating E2 and high levels of testosterone. FORKO mice (24 days and 20 months) were used to investigate structural and functional changes in the central nervous system. We now show that the lifelong depletion of the sex hormone E2 in female FORKO mice correlates with abnormal behavior associated with defined alterations in brain morphology early in life, especially in aged animals. Immunohistochemical studies showed significant increases in the size and number of immunoreactive glial fibrillary acidic protein glial cells found in several brain regions (cortex and hippocampus) and a dramatic decline in estrogen receptors α and β in the amygdala of FORKO females. These changes were associated with increased signs of anxiety in these animals. In the present study, we provide evidence that the chronic depletion of sex hormone E2 from early development leads to neural impairments in adult and aged FORKO mice that are associated with hypertrophy of glial cells, cell loss in distinct brain regions, and abnormal behavior. We suggest that the hormonal imbalance found in the female FORKO mouse provides an experimental paradigm for the study of morphological correlates of the behavioral changes that often accompany menopause in women.
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doi:10.1016/j.mcn.2004.04.012 How to Cite or Link Using DOI (Opens New Window)
Elsevier Inc. All rights reserved.
Estrogen deficiency leads to apoptosis in dopaminergic neurons in the medial preoptic area and arcuate nucleus of male mice
Rachel A. Hilla, b, Sueli Pompoloa, Margaret E.E. Jonesa, Evan R. Simpsona, b, Corresponding Author Contact Information, E-mail The Corresponding Author and Wah Chin Boonb
aPrince Henry's Institute of Medical Research, Clayton 3168, VIC, Australia
bDepartment of Biochemistry, Monash University, Clayton 3800, VIC, Australia
Received 8 January 2004; revised 24 March 2004; accepted 27 April 2004. Available online 2 October 2004.
The previous termaromatasenext term knockout (ArKO) mouse is unable to synthesize estrogens. Immunohistochemical studies on active caspase-3 and tyrosine hydroxylase (TH) revealed apoptosis of dopaminergic neurons in the medial preoptic area (MPO) and arcuate nucleus (Arc) of the hypothalamus of 1-year-old (1yo) male ArKO mice while no active caspase-3 was detected in wild type (WT). Furthermore, the number of TH-positive cells in the MPO and caudal Arc was significantly decreased in 1yo ArKO compared to WT. RNase protection assays support the presence of apoptosis in 1yo ArKO hypothalamus, revealing an up-regulation of pro-apoptotic genes: FASL, FADD, and caspase-8. Concomitantly, the ratio of bcl-2-related anti-apoptotic genes to pro-apoptotic genes in the hypothalamus of 1yo ArKO mice was significantly down-regulated. Previously, we have reported that no such changes were observed in the hypothalamus of female ArKO mice. Thus, we have provided direct evidence that estrogen is required to maintain the survival and functional integrity of dopaminergic neurons in the MPO and Arc of male, but not female mice.
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doi:10.1016/j.psyneuen.2004.10.004 How to Cite or Link Using DOI (Opens New Window)
Elsevier Ltd All rights reserved.
Sex steroids and sexual desire in a man with a novel mutation of aromatase gene and hypogonadism
Cesare Carania, Corresponding Author Contact Information, E-mail The Corresponding Author, Antonio R.M. Granataa, Vincenzo Rochiraa, Giovanni Caffagnia, Claudio Arandab, Paula Antunezc and Laura E. Maffeic
aDepartment of Internal Medicine, University of Modena and Reggio Emilia, Policlinico, Via del Pozzo 71, 41100 Modena, Italy
bTomografia Computada Buenos Aires -TCBA, 1425 Buenos Aires, Argentina
cConsultorios Asociados de Endocrinologia, 1425 Buenos Aires, Argentina
Accepted 30 October 2004. Available online 3 February 2005.
Summary
Sexual behavior was investigated by a sexological interview in a man with previous termaromatase deficiencynext term and hypogonadism. The study was performed at the end of a long testosterone treatment, during transdermal estradiol treatment and during estradiol and testosterone associated treatment. Sexual behavior did not show abnormalities. As assessed by a sexological interview and by a sexological questionnaire gender-identity was male, sexual orientation was heterosexual and libido was normal. Sexual function was limited to masturbation and was seemingly unaffected by testosterone or estradiol alone; only the associated treatment induced a great increase in libido and in frequency of masturbation and sexual fantasies when both testosterone and estradiol reached the range of normality. Sexual behavior is mainly under the control of cognitive functions in men, but sex steroids may modulate some aspects of male sexuality. Our findings suggest that in men estrogens could play a role in sexual activity.
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doi:10.1016/j.hepres.2005.09.030 How to Cite or Link Using DOI (Opens New Window)
Published by Elsevier Ireland Ltd.
CYP17 polymorphism and tamoxifen-induced hepatic steatosis
Takenao Ohnishia, Corresponding Author Contact Information, E-mail The Corresponding Author, Yasuhiro Ogawaa, Toshiji Saibarab, Akihito Nishiokaa, Shinji Kariyaa, Mitsutaka Fukumotoa, Saburo Onishib and Shoji Yoshidaa
aDepartment of Tumor Radiology, Kochi Medical School, Kohau, Okoh-cho, Nankoku-shi, Kochi 783-8505, Japan
bDepartment of Gastroenterology and Hepatology, Kochi Medical School, Kohau, Okoh-cho, Nankoku-shi, Kochi 783-8505, Japan
Available online 24 November 2005.
Abstract
Hepatic steatosis is a frequent complication, which sometimes develops nonalcoholic steatohepatitis (NASH), in breast cancer patients treated with tamoxifen, a potent antagonist of estrogen. Recently we reported the impairment of fatty acid β-oxidation and the enhancing fatty infiltration to hepatocytes in aromatase deficiencynext term (ArKO) mice as the estrogen previous termdeficiencynext term models. This experimental observation let us speculate strong link between estrogen and hepatic steatosis. In this study, we investigated whether a polymorphism in the cytochrome P450c17α gene (CYP17), which is associated with circulating estrogen levels, influences the development of tamoxifen-induced hepatic steatosis. This consecutive study included 180 breast cancer patients undergoing tamoxifen treatment. Genomic DNA extracted from the peripheral blood of each patient was analyzed by restriction fragment length polymorphism (defined as the A1 and A2 alleles). The extent of hepatic steatosis was assessed by computed tomography (CT) as the liver/spleen (L/S) ratio. While receiving adjuvant tamoxifen, 57 of 180 patients developed hepatic steatosis (L/S ratio <0.9) without obvious changes in body mass index (BMI). We observed a significant association between the A2/A2 genotype and the development of hepatic steatosis compared with the A1/A1 genotype [odds ratio (OR), 3.60; 95% confidence interval (C.I.) = 1.42–9.10]. The A1/A2 genotype was at an intermediately increased risk of hepatic steatosis (OR, 2.24; 95% C.I. = 0.99–5.08). The presence of the A2 allele possibly increased the progression of hepatic steatosis with a gene dosage effect (P = 0.06). Our results suggest that functional polymorphism in CYP17 may be involved in determining susceptibility of tamoxifen-induced hepatic steatosis.
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doi:10.1016/j.tem.2006.01.004 How to Cite or Link Using DOI (Opens New Window)
2006 Elsevier Ltd All rights reserved.
Of mice and men: the evolving phenotype of aromatase deficiency
Margaret E.E. Jonesa, E-mail The Corresponding Author, Wah Chin Boona, Joseph Proiettob and Evan R. Simpsona
aPrince Henry's Institute of Medical Research, PO Box 5152, Clayton, Vic 3168, Australia
bUniversity of Melbourne, Department of Medicine, Repatriation Hospital, Heidelberg, Vic 3081, Australia
Available online 9 February 2006.
We are rapidly becoming aware of the importance of estrogen in maintaining virtually all facets of male health. In order for estrogens to be synthesized endogenously, the enzyme responsible for their synthesis from androgens, previous termaromatase,next term must be functional. The seven known men in whom previous termaromatasenext term is nonfunctional all have a mutation in either exon V or IX of the CYP19 gene, which encodes previous termaromatase.next term Collectively, these men are reported to have undetectable estrogen; normal to high levels of testosterone and gonadotropins; tall stature with delayed skeletal maturation and epiphyseal closure; osteoporosis; impaired lipid and insulin metabolism; and impaired reproductive function. The previous termaromatasenext term knockout mouse presents with a phenotype that is similar in many aspects and provides a valuable tool with which to examine and manipulate the actions of estrogen. By studying the naturally occurring previous termaromatasenext term-deficient humans, together with studies of the previous termaromatasenext term-knockout mouse, we are expanding our understanding of the essential role of estrogen in male physiology.
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The Journal of Clinical Endocrinology & Metabolism Vol. 83, No. 7 2236-2238
Copyright © 1998 by The Endocrine Society
New Perspectives on the Skeletal Role of Estrogen
Robert Marcus M.D.
Stanford University School of Medicine Veterans Affairs Medical Center Palo Alto, California 94304
IN case you hadn’t noticed, there’s been a revolution in the understanding of the skeletal roles of estrogen. It used to be so simple: estradiol, acting through a single receptor, was the important bone-related hormone for women; testosterone, acting through its own receptor, performed similar duty for men. Now we are confronted with the reality of at least two separate estradiol receptors, each with its characteristic tissue distribution (1). We have also learned, via fascinating experiments of nature (what our Editor would call "prismatic cases"), that initiation of adolescent growth and bone acquisition requires estradiol as the critical reproductive hormone in both boys and girls. Boys carrying mutations in the -estradiol receptor or in the aromatase that converts androgen to estrogen show profound deficits in bone mineral density (BMD) and, because in these patients epiphyseal closure is not stimulated by estrogen, maintain slow prepubertal growth into adult life (2, 3, 4). In patients with aromatase deficiency, estrogen treatment leads rapidly to epiphyseal closure and striking gains in BMD (4). ...
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J Clin Endocrinol Metab. 2002 Dec;87(12):5476-84.
Impact of estrogen replacement therapy in a male with congenital aromatase deficiency caused by a novel mutation in the CYP19 gene.
Herrmann BL, Saller B, Janssen OE, Gocke P, Bockisch A, Sperling H, Mann K, Broecker M.
Department of Endocrinology, University of Essen, D-45122 Essen, Germany.
Recent reports of the impact of estrogen receptor alpha and aromatase deficiency have shed new light on the importance of estrogen for bone formation in man. We describe a novel mutation of the CYP19 gene in a 27-yr-old homozygous male of consanguinous parents.
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To substitute for the deficiency, the patient was treated with 50 micro g transdermal estradiol twice weekly for 3 months, followed by 25 micro g twice weekly. After 6 months estrogen levels (<20 at baseline and 45 pg/ml at 6 months; normal range, 10-50) and estrone levels (17 and 34 ng/ml; normal range, 30-85) had normalized.Bone maturation progressed and the initially unfused carpal and phalangeal epiphyses began to close within 3 months and were almost completely closed after 6 months. The bone age, assessed by roentgenographic standards for bone development by Gruelich and Pyle, was 16.5 at baseline and 18-18.5 yr after 6 months of treatment. Bone density of the distal radius (left), assessed by quantitative computed tomography, increased from 52 to 83 mg/cm(3) (normal range, 120-160) and bone mineral density of the lumbar spine, assessed by dual-energy x-ray-absorptiometry, increased from 0.971 to 1.043 g/cm(2) (normal range, >1.150). Osteocalcin as a bone formation parameter increased from 13 to 52 micro g/l (normal range, 24-70) and aminoterminal collagen type I telopeptide as a bone resorption parameter increased from 62.9 to 92.4 nmol/mmol creatinine (normal range, 5-54). Semen analysis revealed oligoazoospermia (17.4 million/ml; normal >20) at baseline. After 3 months of treatment, the sperm count increased (23.1 million/ml) and decreased rapidly (1.1 million/ml) during the following 3 months. The sperm motility was reduced at baseline and decreased further during treatment. Area under the curve of insulin, C-peptide, and blood glucose levels during oral glucose tolerance test decreased after 6 months (insulin: 277 vs. 139 micro U/ml.h; C-peptide 52 vs. 15 ng/m.h; area under the curve glucose: 17316 vs. 12780 mg/d.min). Triglycerides (268 vs. 261 mmol/liter) and total cholesterol levels (176 vs. 198 mmol/liter) did not change significantly, but the low-density lipoprotein/high-density lipoprotein ratio decreased from 5.37 to 3.56 and lipoprotein (a) increased from 19.9 to 60.0 mg/dl (normal range, <30). In this rare incidence of estrogen deficiency, estrogen replacement demonstrated its importance for bone mineralization and maturation and glucose metabolism in a male carrying a novel mutation in the CYP19 gene
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Folia Histochem Cytobiol. 2003;41(3):107-11. Related Articles, Links
Estrogens--male hormones?
Carreau S.
EA 2608-USC INRA, Biochimie-IBFA, University of Caen, France. carreau@ibba.unicaen.fr
The cytochrome P450 aromatase is the terminal enzyme responsible for the irreversible transformation of androgens into estrogens; it is present in the endoplasmic reticulum membrane of cells and rather ubiquitous in its localization. The aromatase gene is unique in humans and its expression is regulated in a cell-specific manner via the alternative use of various promoters located in the first exon I of the CYP19 gene. The aromatase gene expression and its translation into a fully active protein have been shown in most of the testicular cells including germ cells as well as in the epithelial cells of the epididymis in mammals. Together with the widespread distribution of estrogen receptors (ERalpha and ERbeta) in the genital tract of the male, a physiological role for estrogens in the regulation of mammalian reproductive functions including the regulation of gonadotropin feedback, is now well recognized. Moreover, in men the aromatase deficiency is associated with severe bone maturation problems, alterations of lipid and sugar metabolism and sterility; but conversely an excess of estrogens is responsible for the impairment of spermatogenesis. In addition, estrogens play an important role in the control of osteoporosis and of atherosclerosis, especially in elderly men. Consequently, estradiol seems to be a critical factor not only for normal reproduction (at least for maturation and survival of germ cells) but also for various physiological processes and thus, estrogens should be now considered as "male hormones".
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J Clin Endocrinol Metab. 2004 Dec;89(12):6025-9. Related Articles, Links
Estrogens are essential for male pubertal periosteal bone expansion.
Bouillon R, Bex M, Vanderschueren D, Boonen S.
Division of Endocrinology, Katholieke Universiteit Leuven, Leuven, Belgium. roger.bouillon@med.kuleuven.ac.be
The skeletal response to estrogen therapy was studied in a 17-yr-old boy with congenital aromatase deficiency. As expected, estrogen therapy (1 mg estradiol valeriate/d from age 17 until 20 yr) normalized total and free testosterone and reduced the rate of bone remodeling. Dual-energy x-ray absorptiometry-assessed areal bone mineral density (BMD) of the lumbar spine and femoral neck increased significantly (by 23% and 14%, respectively), but peripheral quantitative computed tomography at the ultradistal radius revealed no gain of either trabecular or cortical volumetric BMD. The increase in areal BMD was thus driven by an increase in bone size. Indeed, longitudinal bone growth (height, +8.5%) and especially cross-sectional area of the radius (+46%) and cortical thickness (+12%), as measured by peripheral quantitative computed tomography, increased markedly during estrogen treatment. These findings demonstrate that androgens alone are insufficient, whereas estrogens are essential for the process of pubertal periosteal bone expansion typically associated with the male bone phenotype.
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J Clin Endocrinol Metab. 2004 Dec;89(12):5898-907. Related Articles, Links
Aromatase activity and bone homeostasis in men.
Gennari L, Nuti R, Bilezikian JP.
Department of Internal Medicine, Endocrine-Metabolic Sciences, and Biochemistry, University of Siena, Siena 53100, Italy. gennari@unisi.it
It is known that sex steroid hormones play an important role in the maintenance of bone mass in males as well as in females. Even though androgens are the major sex steroids in men, their primacy in regulating male skeletal remodeling has been increasingly questioned as direct and indirect evidence emerged suggesting that estrogens may also play a major role in male skeletal health. Recent data suggested that a threshold level of bioavailable estradiol is needed to prevent bone loss, and that with aging an increasing percentage of elderly men begin to fall below this level. The testes account for, at most, 15% of circulating estrogens in the male; the remaining 85% comes from peripheral aromatization of androgen precursors in different tissues, including bone. Human models of aromatase deficiency were the first to demonstrate the critical importance of the conversion of circulating androgens into estrogen in regulating male skeletal homeostasis. All four cases of aromatase-deficient men reported to date showed an identical skeletal phenotype, characterized by tall stature due to continued longitudinal growth, unfused epiphyses, high bone turnover, and osteopenia. Studies using knockout mice along with experimental observations in rats treated with an aromatase inhibitor provided useful information about the importance of aromatase in the male skeleton. Confirmatory evidence comes from recent interventional studies in adult men using aromatase inhibition, which confirmed that estrogens are critically important to the male skeleton by helping to control rates of bone remodeling. Intriguingly, common polymorphisms at the human aromatase (CYP19) gene have been associated with differences in aromatase activity, bone turnover, and rates of bone loss in elderly men, suggesting that variations in aromatase efficiency may also be relevant for skeletal homeostasis. Several additional mechanisms have been proposed in which aromatase activity could be modulated under certain circumstances in different tissues. Additional studies are needed to identify how these genetic, environmental, pathological, and pharmacological influences might modulate aromatase activity in vivo, increasing or reducing estrogen production in males and thereby affecting skeletal health.
-----------------------------
Nippon Rinsho. 2004 Feb;62(2):368-72. Related Articles, Links
[Aromatase deficiency]
[Article in Japanese]
Harada N.
Department of Biochemistry, Fujita Health University School of Medicine.
Aromatase, a key enzyme in estrogen synthesis, is tissue-specifically regulated in various tissues and plays an important role through endocrine and intracrine estrogen production in various physiological functions. Therefore, aromatase deficiency caused crucial impairments of physiological functions in the gonadal tissues as well as extra-gonadal tissues. Because aromatase is protective for androgenic exposure by catabolizing, virilization of a pregnant mother and pseudohermaphroditism of a baby girl consequently result from the deficiency. Similarly, because aromatase is productive for a multifunctional physiological factor, estrogens, impaired metabolisms of bone, carbohydrate, and fat etc. result from the deficiency. We discuss the etiology, clinical symptoms, and therapeusis by classifying it into two types of complete and incomplete aromatase deficiencies.
-----------------------------
J Clin Endocrinol Metab. 2003 Aug;88(8):3785-93. Related Articles, Links
Effects of suppression of estrogen action by the p450 aromatase inhibitor letrozole on bone mineral density and bone turnover in pubertal boys.
Wickman S, Kajantie E, Dunkel L.
Hospital for Children and Adolescents, University of Helsinki, Helsinki, FIN-00029 HUS, Finland. sanna.wickman@helsinki.fi
The essential role of estrogen (E) in regulation of developing peak bone mass in males was confirmed when young adult men were described who cannot respond to or produce E because of defective E receptor alpha or P-450 aromatase enzyme, respectively. These men had significantly reduced bone mineral density (BMD) despite normal or supranormal androgen concentrations, and E administration improved BMD in the men with aromatase deficiency, whereas testosterone (T) was ineffective. Because new P450 aromatase inhibitors may prove to be potential drugs in various growth disorders, the effect of suppression of E action on developing peak bone mass has to be closely evaluated. ...
-------------------------
Zhonghua Nan Ke Xue. 2003 Feb;9(1):64-6. Related Articles, Links
[Estrogen and bone metabolism in man]
[Article in Chinese]
Gan WD, Dai YT, Sun ZY.
Department of Urology, Affiliated Drum Tower Hospital of Medical College of Nanjing University, Nanjing, Jiangsu 210008, China.
In males, androgen can be aromatized into estrogen by aromatase. Estrogen receptors were shown to be present in male-derived human osteoblasts. For males bone is an important target tissue of estrogen. It was demonstrated that deficiency of estrogen or mutation of estrogen receptor gene in males could lead to osteopenia, even osteoporosis. Estrogens are required for the pubertal growth of bone and play important roles in maintenance of bone mass in males.
----------------
J Clin Endocrinol Metab. 2003 Jul;88(7):3075-81. Related Articles, Links
Click here to read
Bioavailable estradiol and an aromatase gene polymorphism are determinants of bone mineral density changes in men over 70 years of age.
Van Pottelbergh I, Goemaere S, Kaufman JM.
Department of Endocrinology, Ghent University Hospital, 9000 Ghent, Belgium.
------------
J Endocrinol. 2003 Feb;176(2):237-46. Related Articles, Links
Click here to read
Progressive development of insulin resistance phenotype in male mice with complete aromatase (CYP19) deficiency.
Takeda K, Toda K, Saibara T, Nakagawa M, Saika K, Onishi T, Sugiura T, Shizuta Y.
Department of Clinical Laboratory Medicine, Kochi Medical School, Kohasu, Okocho, Nankoku City, Kochi 783-8505, Japan.
Aromatase (CYP19) is a cytochrome P450 enzyme that catalyzes the formation of aromatic C18 estrogens from C19 androgens. It is expressed in various tissues and contributes to sex-specific differences in cellular metabolism. We have generated aromatase-knockout (ArKO) mice in order to study the role of estrogen in the regulation of glucose metabolism. The mean body weights of male ArKO (-/-) mice (n=7) and wild-type littermates (+/+) (n=7) at 10 and 12 weeks of age were 26.7+/-1.9 g vs 26.1+/-0.8 g and 28.8+/-1.4 g vs 26.9+/-1.0 g respectively. The body weights of the ArKO and wild-type mice diverged between 10 and 12 weeks of age with the ArKO males weighing significantly more than their wild-type littermates (P<0.05). The ArKO males showed significantly higher blood glucose levels during an intraperitoneal glucose tolerance test compared with wild-type littermates beginning at 18 weeks of age. By 24 weeks of age, they had higher fasting blood glucose levels compared with wild-type littermates (133.8+/-22.8 mg/dl vs 87.8+/-20.3 mg/dl respectively; P<0.01). An intraperitoneal injection of insulin (0.75 mU insulin/g) caused a continuous decline in blood glucose levels in wild-type mice whereas ArKO males at 18 weeks and older exhibited a rebound increase in glucose levels 30 min after insulin injection. Thus, ArKO male mice appear to develop glucose intolerance and insulin resistance in an age-dependent manner. There was no difference in fasting serum triglyceride and total cholesterol levels between ArKO male mice and wild-type littermates at 13 and 25 weeks of age. However, serum triglyceride and cholesterol levels were significantly elevated following a meal in ArKO mice at 36 weeks of age. Serum testosterone levels in ArKO male mice were continuously higher compared with wild-type littermates. Treatment of ArKO males with 17beta-estradiol improved the glucose response as measured by intraperitoneal glucose and insulin tolerance tests. Treatment with fibrates and thiazolidinediones also led to an improvement in insulin resistance and reduced androgen levels. As complete aromatase deficiency in man is associated with insulin resistance, obesity and hyperlipidemia, the ArKO mouse may be a useful animal model for examining the role of estrogens in the control of glucose and lipid homeostasis.
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J Soc Biol. 2002;196(3):245-8. Related Articles, Links
[Estrogen resistance and aromatase deficiency in humans]
[Article in French]
Carani C, Fabbi M, Zirilli L, Sgarbi I.
Departement de Medecine Interne, Chaire d'Endocrinologie, Universite de Modene, Italie.
The primordial role of estrogens in female reproductive function is well known. The recent production of transgenic mice deficient in estrogen receptors (ERKO) or in aromatase (ArKO) and the discovery in man of inactivating mutations of the corresponding genes (ER) have contributed to the understanding of the role of estrogens in metabolic processes in female as well as male. To date 8 well documented cases (5 women and 3 men) of congenital deficiencies in estrogens have been reported. As mice deficient in ERa had been previously described, these cases definitely proved that estrogen absence was compatible with survival and disproved the "lethality concept" previously held because the role of estrogens in implantation and gestation maintenance. ERKO mice are phenotypically normal though sterile, but their bone density is lower (20-25%) than that of controls. Similarly, men with no aromatase or no ER display continuous growth, osteoporosis and also (but not necessarily) alterations in testicular functions.
...
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Semin Reprod Med. 2002 Aug;20(3):277-84. Related Articles, Links
The essential role of the aromatase/p450arom.
Meinhardt U, Mullis PE.
Department of Pediatrics, Pediatric Endocrinology/Diabetology and Metabolism, University Children's Hospital, Inselspital, CH-3010 Bern, Switzerland.
...
As not only androgens but also estrogens are of importance particularly in male pubertal development including bone changes, which were classically considered androgen dependent, the features of the aromatase deficiency syndrome in affected boys and girls as well as adult males and females are discussed. There is growing awareness that androgens and estrogens have general metabolic roles that reach far beyond reproductive processes. For instance, estrogen has a significant impact on carbohydrate and lipid metabolism, vascular function, and arteriosclerosis.
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http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&a mp;a mp;db=PubMed&list_uids=12553872&dopt=Abstract
"...
As complete aromatase deficiency in man is associated with insulin resistance, obesity and hyperlipidemia, the ArKO mouse may be a useful animal model for examining the role of estrogens in the control of glucose and lipid homeostasis."
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Minerva Endocrinol. 2006 Mar;31(1):61-73. Links
Aromatase enzyme and Alzheimer's disease.
* Hiltunen M,
* Iivonen S,
* Soininen H.
Department of Neurology, Clinical Research Centre/Mediteknia, University of Kuopio, Kuopio, Finland. mhiltune@uku.fi
Aromatase enzyme encoded by CYP19 gene is responsible for the formation of estrone and estradiol from C19 androgens, androstenedione and testosterone. Several lines of evidence suggest an important role for the estrogens as well as androgens in the key pathogenic processes of Alzheimer's disease (AD) such as amyloid beta (Abeta) production, hyperphosporylation of tau protein, oxidative stress and apoptosis. Moreover, epidemiological studies suggest a neuroprotective role for estrogen in AD for which reason estrogen replacement therapies have been extensively studied as a way to improve the cognition and to lower the risk of AD. Aromatase enzyme is a key player in this context as it controls estrogen biosynthesis and, therefore, it may exert neuroprotective effects via increasing the local estrogen levels in injured neurons. Consistent with this idea, brain injury in mice and rats rapidly up-regulates aromatase enzyme expression in glial cells at the injury site suggesting that aromatase may be involved in protection of injured neurons through increased estrogen levels. Additional support for the role of aromatase in AD originates from the recent genetic studies, which have shown that single nucleotide polymorphisms in CYP19 gene are independently or in synergy with other AD risk genes increasing the susceptibility for AD. These genetic findings suggest that CYP19 gene encompasses functional alterations, which may affect stability, expression or activity of the aromatase enzyme. Characterization of these novel alternations may ultimately reveal new avenues to understand and design new therapeutic approaches to AD.
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Neurology. 2004 Apr 13;62(7):1170-6.Click here to read Links
Polymorphisms in the CYP19 gene confer increased risk for Alzheimer disease.
* Iivonen S,
* Corder E,
* Lehtovirta M,
* Helisalmi S,
* Mannermaa A,
* Vepsalainen S,
* Hanninen T,
* Soininen H,
* Hiltunen M.
Department of Neuroscience and Neurology, University Hospital and University of Kuopio, Finland.
BACKGROUND: Brain aromatase may be neuroprotective by increasing the local estrogen levels in injured neurons. Aromatase is encoded by the CYP19 gene located at 15q21.1, a chromosomal region in linkage disequilibrium (LD) with Alzheimer disease (AD) in this sample. OBJECTIVE: To investigate whether nine single-nucleotide polymorphisms (SNP) spanning the CYP19 gene were associated with AD. METHODS: Three hundred ninety-four patients were compared with 469 nondemented control subjects using single-locus and haplotype approaches. Haplotypes were identified using the expectation/maximization algorithm and latent class analysis, which included additional information on age, sex, and APOE polymorphism. RESULTS: Allelic and genotypic frequencies for three adjacent SNP differed between AD and control groups. Both haplotype approaches identified an approximately 60% increase (p = 0.02) in the risk of AD for one haplotype and similar levels of excess risk irrespective of APOE polymorphism and gender. CONCLUSION: Genetic variation in the brain aromatase gene may modify the risk for AD.
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Mol Neurobiol. 1998 Winter;17(1-3):73-86. Links
Cellular and molecular basis of estrogen's neuroprotection. Potential relevance for Alzheimer's disease.
* Inestrosa NC,
* Marzolo MP,
* Bonnefont AB.
Departamento de Biologia Celular y Molecular, Facultad de Ciencias Biologicas, Pontificia Universidad Catolica de Chile.
Alzheimer's disease (AD) is one of the most common types of dementia among the aged population, with a higher prevalence in women. The reason for this latter observation remained unsolved for years, but recent studies have provided evidence that a lack of circulating estrogen in postmenopausal women could be a relevant factor. Moreover, follow-up studies among postmenopausal women who had received estrogen-replacement therapy (ERT), suggested that they had a markedly reduced risk of developing AD. In addition, studies among older women who already had AD indeed confirmed that a decrease in estrogen levels was likely to be an important factor in triggering the pathogenesis of the disease. In this review article, we will discuss the evidence suggesting that estrogen may have a protective role against AD, mainly through its action as: a trophic factor for cholinergic neurons, a modulator for the expression of apolipoprotein E (ApoE) in the brain, an antioxidant compound decreasing the neuronal damage caused by oxidative stress, and a promoter of the physiological nonamyloidogenic processing of the amyloid precursor protein (APP), decreasing the production of the amyloid-beta-peptide (A beta), a key factor in the pathogenesis of AD.
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Fortschr Neurol Psychiatr. 1998 Mar;66(3):113-21. Links
[Oxidative stress in the pathogenesis of Alzheimer's disease and antioxidant neuroprotection]
[Article in German]
* Behl C,
* Holsboer F.
Max-Planck-Institut fur Psychiatrie, Klinisches Institut, Munchen. chris@mpipsykl.mpg.de
Alzheimer's disease (AD) is one of the most frequent causes of dementia in the aged. The elucidation of the pathomechanisms of this neurodegenerative disease with age, as the only risk factor for the majority of cases, is in the centre of the efforts of molecular and cellular neurobiology in preclinical research. Various findings point to the involvement of the amyloid beta protein (A beta) in the pathogenesis and progression of AD. Precipitated A beta aggregates are found in the brain of AD patients post mortem in the so-called plaques, a major histopathological hallmark of this progressive destructive disease. A beta can be toxic to cultivated neuronal cells only in its aggregated fibril form. After interaction with the neuronal cell membrane, these aggregates can induce intracellular oxidative events and can lead to the release of so-called free radicals. This is just one important finding for the involvement of oxidative events in the nerve cell degeneration in AD supporting the oxidative stress hypothesis. Furthermore, different neurochemical methods revealed many additional traits and scars of oxidative reactions in the brain of AD patients. Inflammatory events also seem to take part in the generation of an oxidative environment and therefore in nerve cell death as well. In addition, various age-dependent pathophysiological changes can increase neuronal vulnerability. Different antioxidants can protect cultivated neurons against A beta toxicity, but also against other oxidative stressors relevant to the disease. Besides the classical lipophilic antioxidant vitamin E, the female sex hormone oestrogen could also play an important neuroprotective role as an antioxidant, as was shown recently. Oestrogen, oestrogen derivatives, but also other potential free radical scavengers could block the accumulation of oxidative events on the long run and could, therefore, possibly slow down or prevent progressive nerve cell death of AD, which occurs over decades. If future clinical trials using antioxidants as neuroprotectants in AD would also support the oxidative stress hypothesis of the aetiopathogenesis of AD, antioxidants identified in the laboratory could then find their way more and more into the clinical treatment of Alzheimer's dementia.
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Int J Vitam Nutr Res. 1999 May;69(3):213-9. Links
Vitamin E and other antioxidants in neuroprotection.
* Behl C.
Max Planck Institute of Psychiatry, Munich, Germany.
Several pathological conditions are believed to be causally related to the generation of reactive oxygen species and free radicals including various neurodegenerative disorders. In the histopathology of Alzheimer's disease (AD) many signs of oxidative reactions can be found building the basis of the oxidative stress hypothesis of AD. One major player in the generation of an overall oxidative microenvironment for the nerve cells is the amyloid beta protein (A beta) of the senile plaques in brain areas affected in AD. A beta can be neurotoxic and this toxicity is mediated by peroxides and by the peroxidation of membrane lipids leading to the lysis of the cell. Consequently, lipophilic free radical scavengers such as vitamin E and the recently discovered antioxidant activity of the female sex hormone estrogen protects neurons against the oxidative toxicity of A beta and other AD-related oxidative insults. In a first clinical trial using vitamin E in therapy, this antioxidant could slow down the course of the disease launching further clinical investigations. Although antioxidants act as non-specific protective chemical shields for neurons and do not target specific pathological events, they are highly effective and further investigations on their activity might lead to an even more effective application of antioxidants. Since the knowledge of the pathways of neuronal cell death that occur during oxidative challenges is increasing, it will be of central interest how antioxidants can interfere with signal transduction mechanisms and therefore also modify genetic programs. As long as specific interventions are not available the optimistic data concerning the neuroprotective activity of antioxidants in vitro and in vivo underline an important role for antioxidative acting compounds for the prevention and therapy of oxidative stress-related conditions including AD.
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viel Glück
lg
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Re: nachtrag zu diesem E2-diagramm [Beitrag #36790 ist eine Antwort auf Beitrag #36789] :: So., 20 August 2006 08:06
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tristan
Beiträge: 709 Registriert: November 2005
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| fuselkopf schrieb am Son, 20 August 2006 06:25 |
nein, sie haben nichts verwechslt. ich hatte irgendwo noch ein anderes diagramm und männer haben im schnitt 10pg/ml (+5-5) E2!
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10pg/ml +5-5 aber nicht bei gesunden Männern. Bei 13 Jährigen vielleicht.. Es gibt massig literatur die zu der festlegung des gängigen ref.bereichs von 20/25-50/55 geführt hat. Es gibt immer noch labore die werte angeben wie n.m.-50. Die sind jedoch am aussterben. Genau wie das allmählich mit denen passiert die noch nen TSH -4,5 als referenz haben. das ist einfach überholt und nicht gängiger standard..
wie gesagt, wenn 5pg/ml ein normwert ist, dann ist dies dennoch ein krankhafter zustand.
......
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Östrogene für den Mann?
Kuhl H
Blickpunkt der Mann 2003; 1 (3)
6-12
...
Der Estradiolspiegel liegt beim Mann zwischen 20 und 55 pg/ml
...
Sie beeinflussen den Fettstoffwechsel, spielen bei der Regulation der Gonadotropin-
sekretion eine wichtige Rolle und beeinflussen die Spermatogenese. Sie hemmen im Hoden direkt die Synthese des Testosterons und in der Prostata
dessen Umwandlung in das stärker wirksame Dihydrotestosteron. Möglicherweise können die Östrogene auch den Mann durch eine direkte
Wirkung auf die Arterienwand vor der Atherosklerose schützen
...Der Mann produziert täglich zwischen 20 und 50 µg Estradiol, was etwa 50% der Menge entspricht, die von der Frau in der Follikelphase gebildet wird (Tabelle 1). Der Normalbereich des Estradiols liegt beim Mann zwischen 20 und 55 pg/ml (im Durchschnitt etwa 35 pg/ml).
...Bei der Bestimmung des Estradiolspiegels des Man-
nes ist darauf zu achten, daß es zirkadiane Schwan-
kungen gibt, wobei das Maximum am Nachmittag
zwischen 15.00 und 18.00 Uhr und das Minimum in
der Nacht zwischen 24.00 und 02.00 Uhr auftreten
[10]. Subfertile Männer haben häufiger sehr niedrige
Estradiolkonzentrationen als fertile, obwohl die Werte in
den meisten Fällen im Normalbereich liegen...
Im allgemeinen werden die hormonellen Wirkun-
gen des Estradiols durch die starke antagonistische
Wirkung des Testosterons bzw. Dihydrotestosterons
maskiert. Trotzdem ist in einigen Organen eine wichti-
ge physiologische Rolle des Estradiols anzunehmen
bzw. nachgewiesen. Dies gilt zumindest für die Regu-
lation der Gonadotropinsekretion, den Fettstoffwech-
sel und das Skelett.
-----------------------
MOCK K, LUNGLMAYR G
Androgene und Östrogene beim alternden Mann
Journal für Urologie und Urogynäkologie 1999; 6 (Sonderheft 2)
(Ausgabe für Österreich), 5-9
Tabelle 2: Hormonspiegel beim alternden Mann --
Alter (Jahre)
17--Östradiol (pmol/L)
50–59
130,6
60–69
138,4
70–79
136,6
>79
135,3
--> das sind im Schnitt ca. 37 pg/ml
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ÄP Urologie Nephrologie 3/Mai-Juni 2004
siehe bild im anhang...
Gesunde Männer (25 Jahre) morgens.. 22-42 pg/ml
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Re: fusel ? [Beitrag #36791 ist eine Antwort auf Beitrag #36751] :: So., 20 August 2006 08:17
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tristan
Beiträge: 709 Registriert: November 2005
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| fuselkopf schrieb am Sam, 19 August 2006 16:42 |
Versuchs mit Quercetin. Pflanzliches non-citrus Flavonide. Ist ein Phytohormon, aber es hemmt die Aromatase und das recht effektiv. Hat aber noch viel mehr positive Eigenschaften das Zeug!
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Ich weiß dass das hier krebszellen waren, aber trotzdem,....
Induction and inhibition of aromatase (CYP19) activity by natural and synthetic flavonoid compounds in H295R human adrenocortical carcinoma cells.
Sanderson JT, Hordijk J, Denison MS, Springsteel MF, Nantz MH, van den Berg M.
Institute for Risk Assessment Sciences (IRAS), Utrecht University, 3508 TD Utrecht, The Netherlands. t.sanderson@iras.uu.nl
Flavonoids and related structures (e.g., flavones, isoflavones, flavanones, catechins) exert various biological effects, including anticarcinogenic, antioxidant and (anti-)estrogenic effects, and modulation of sex hormone homeostasis. A key enzyme in the synthesis of estrogens from androgens is aromatase (cytochrome P450 19; CYP19). We investigated the effects of various natural and synthetic flavonoids on the catalytic activity and promoter-specific expression of aromatase in H295R human adrenocortical carcinoma cells. Natural flavones were consistently more potent inhibitors than flavanones. IC(50) values for 7-hydroxyflavone, chrysin, and apigenin were 4, 7, and 20 microM, respectively; for the flavanones 7-hydroxyflavanone and naringenin the IC(50) values were 65 and 85 microM, respectively. The steroidal aromatase inhibitor (positive control) 4-hydroxyandrostenedione had an IC(50) of 20 nM. The inhibition by apigenin and naringenin coincided with some degree of cytotoxicity at 100 microM. The natural flavonoid derivative rotenone (IC(50) 0.3 microM) was the most potent aromatase inhibitor tested. Several synthetic flavonoid and structurally related quinolin-4-one analogs inhibited aromatase activity. The most potent inhibitor was 4'-tert-butyl-quinolin-4-one (IC(50) 2 microM), followed by two 2-pyridinyl-substituted alpha-naphthoflavones (IC(50)s 5 and >30 microM). The two 2-pyridinyl-substituted gamma-naphthoflavones consistently produced biphasic concentration-response curves, causing about 1.5-fold aromatase induction at concentrations below 1 microM and inhibition above that level (IC(50)s 7 and >30 microM). The natural flavone quercetin and isoflavone genistein induced aromatase activity 4- and 2.5-fold induction, respectively, at 10 microM. This coincided with increased intracellular cAMP concentrations and increased levels of the cAMP-dependent pII and to a lesser extent 1.3 promoter-specific aromatase transcripts. These results shed light on the structure-activity relationships for aromatase inhibition as well as mechanisms of induction in human H295R cells.
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Food Chem Toxicol. 2005 May;43(5):793-8. Related Articles, Links
Long-term combined administration of quercetin and daidzein inhibits quercetin-induced suppression of glutathione antioxidant defenses.
Choi EJ, Lee BH, Lee K, Chee KM.
Department of Biotechnology, Korea University, Anamdong, Sungbuk-gu, Seoul 136-701, Republic of Korea. eunjeong@korea.ac.kr
In this study, we investigated the effects of long-term administration of quercetin with or without daidzein on glutathione and the enzymes involved in its metabolism in rat liver in vivo. Male Sprague-Dawley rats were divided randomly into four groups and given oral quercetin (20 mg/day) and daidzein (20 mg/day) alone or in combination, or vehicle alone for six weeks. The serum and liver alpha-tocopherol concentrations were significantly increased following administration of quercetin and daidzein alone or in combination. Glutathione concentration and glutathione reductase activity was significantly (p < 0.05) decreased with quercetin treatment, while no such effect was observed with daidzein treatment. Interestingly, decrease in glutathione concentration and glutathione reductase activity by quercetin treatment was inhibited by combined administration of daidzein and quercetin. The malondialdehyde concentration was significantly decreased following administration of quercetin and daidzein alone or in combination. These results suggest that quercetin, but not daidzein, acts as a pro-oxidant agent by decreasing glutathione concentration and glutathione reductase activity. Interestingly, this pro-oxidant effect of quercetin was inhibited by the combined administration of quercetin and daidzein.
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hmm, auch ein positiver nebeneffekt? wenn es estrogen senkt wäre das eine logische folge...
disclaimer: ich habe mich zu wenig mit quercetin beschäftigt und weiß nicht alles darüber, aber das ist was mit ins auge sprang beim schnellen überfliegen... und das würd mir persönlich schon reichen..
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Re: Fahrt Euch ruhig E2 rein [Beitrag #36838 ist eine Antwort auf Beitrag #36830] :: So., 20 August 2006 19:37
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tristan
Beiträge: 709 Registriert: November 2005
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| fuselkopf schrieb am Son, 20 August 2006 18:25 |
Ich habe keine Zeit und Lust das alles zu kommentieren, aber nehmt ruhig Euer Estradiol zu Euch. Ich will Euch nicht aufhalten, jeder muss wissen was er mit seinem Körper anstellt.
And by the way:
Ich habe noch Estradiol (E2) zu entsorgen!
Falls mir jemand dabei behilflich sein möchte, dann kann er sich gerne per PM bei mir melden
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wer redet denn davon? ich nehme momenten kein e2 und keiner hat kkoo dazu geraten. Es ging mir nur darum dass den meisten mit aromatasehemmung kaum geholfen werden kann wenn sie schon einen hohen freien androgenindex haben, und dass e2 werte im unteren bereich für viele gesundheitsfaktoren bei männern laut literatur ein risiko darstellen. ich habe auch kkoo gesagt er soll es probieren, ich halte nur nicht viel davon wenn leute einen e2 wert von 25 haben und den versuchen auf 5 zu senken, auch wenn es negative seiten bei e2 gibt, das ist einfach gefährlich, ... aber du meintest ja auch nicht dass er ihn auf 5 senken soll, sondern auf 29-... , sage ich nichts gegen, jeder ist anders... meine meinung ist nur dass für den großteil aromatasehemmung negativ ist für die gesundheit, unabh. von haarausfall...
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Re: Fachfrage: T-Metaboliten-Affinität an den AR [Beitrag #36839 ist eine Antwort auf Beitrag #36818] :: So., 20 August 2006 19:44
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tristan
Beiträge: 709 Registriert: November 2005
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| chris22 schrieb am Son, 20 August 2006 16:14 |
tristan,
wir reden hier immer noch von ratten  , ich kenne mich mit diesem ganzen hormonen ohne hin nicht so sehr aus, aber wenn die aromatase gehemmt wird, ist dass dann positiv oder negativ für den haarwuchs und die Haut, mehr östrogen ist doch besser für haut und haar, zumindest habe ich das im hinterkopf, dass dies hier immer gesagt wurde. also wäre aromatasehemmung doch negativ oder?
ich blick nicht mehr durch...
chris
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hi,
wie du siehst unterscheiden sich die meinungen zu e2 bzgl. haarwuchs. bei frauen ist es haarwuchsfördernd...
was die haut betrifft, so hat es eindeutig positive wirkung...
durch shbg erhöhung senkt es freien androgenindex und senkt direkt dht...
"
In late pregnancy, when estrogen levels are high, a high proportion of scalp hair follicles remain in anagen (218). Postpartum, a large number of hair follicles simultaneously advance into telogen, causing loss of a large number of hairs. This postpartum telogen effluvium has been postulated to be caused by the rapid decrease of estrogen at the time of delivery (219). On the other hand, estrogen directly suppresses sebaceous gland function (1, 3, 75, 220, 221)."
Dianne Deplewski and Robert L. Rosenfield
Endocrine Reviews 21 (4): 363-392, 2000 Endocrine Society
lg
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Re: danke tristan, pilos bitte auch noch :) [Beitrag #36842 ist eine Antwort auf Beitrag #36772] :: So., 20 August 2006 20:07
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tristan
Beiträge: 709 Registriert: November 2005
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| pilos schrieb am Sam, 19 August 2006 22:42 |
| kkoo schrieb am Sam, 19 August 2006 20:23 |
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der senf von pilos......
ich glaube euer gefecht war ein wenig umsonst....den alle hormone sind ja meistens gebunden nur ein paar prozente sind frei....in wie fern diese paar prozente für AGA verantwortlich sind...lassen wir mal so stehen.
das problem liegt anderswo und zwar in den zellen selbst....nehmen wir als beispiel das AGA muster hier ein haar das vor 10 jahre ausgefallen ist...nur 1 mm weiter ein anderes das schon seit 10 jahre hartnäckig das feld nicht räumen will....alles ist unter dem gleichen plasma-hormonellem-einfluss....somit räume ich kaum einen zu großen einfluss dieses faktors....den bei einem fallen keine haare bei 10 pg estogen und einem anderen sind es 50 pg und er verliert nur so seine pracht...und was sagt uns das..das sagt uns das wir völlig daneben liegen....das geheimnis liegt in den zellen selbst und nicht im plasma....
somit kann immer alles richtig sein..oder alles falsch sein....
fazit:
deshalb kann viel oder wenig estrogen im blut zu AGA führen oder auch nicht
deshalb kann viel oder wenig dht im blut zu aga füren oder auch nicht.....
bei jedem ist es anders...jeder muss es testen unf für sich herausfinden...deshalb gibt es bei AGA keine standardtherapie für alle....was dem einem gut tut...kan dem anderem schaden fügen.
und jetzt das preisgeld bitte...... 
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stimmt schon dass das alles nicht so vereinfacht werden sollte. allerdings halte ich den dht wert schon für aussagekräftig, denn dht entsteht ja zum großteil auch in den zellen durch reduktion.. bei isotretinoin wird ja auch die fähigkeit der zellen verhindert dht zu bilden und die therapie geht einher mit starker dht senkung im serum. dann gibt es ja noch die marker für die periphere wirkung versch. hormone, die man im u.a im urin messen kann... bei mir war es so dass sich der hohe dht serum wert auch peripher bestätigt hat. mir wurde andros-g und für die nebenniere 2 sachen im urin gemessen..
ich würde sagen dass in den meisten fällen in denen die leute probleme haben mit fettiger haut, akne, behaarung... und einen freien androgenindex im oberen bereich haben, wo die aufnahme und umwandlung von androgenen am rezeptor verstärkt abläuft und dadurch mehr dht im serum ist oder wirken kann und sich die untersuchung peripherer marker erübrigt. wenn dann noch niedrige e2 konz. im serum gemessen werden, ist das eine konstellation die ziemlich typisch ist und bei der man vermuten kann dass auch wenig e2 in den zellen wirkt, alleine weil dht schon ein starker aromatase hemmer ist. wenn man jedoch merkwürdige konstellationen hat, idiopathische formen von "virilisierungsproblemen", also akne etc. bei normalen androgenindex, dann ist definitiv die bestimmung der peripheren marker sinnvoller und aussagekräftiger als nur über serum werte zu grübeln..
lg
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fusel [Beitrag #36878 ist eine Antwort auf Beitrag #36830] :: Mo., 21 August 2006 00:05
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kkoo
Beiträge: 4429 Registriert: November 2005
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| fuselkopf schrieb am Son, 20 August 2006 18:25 |
Ich habe keine Zeit und Lust das alles zu kommentieren, aber nehmt ruhig Euer Estradiol zu Euch. Ich will Euch nicht aufhalten, jeder muss wissen was er mit seinem Körper anstellt.
And by the way:
Ich habe noch Estradiol (E2) zu entsorgen!
Falls mir jemand dabei behilflich sein möchte, dann kann er sich gerne per PM bei mir melden
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versteh ich nicht, es ging doch um eine mögliche senkung von E2.... (bei mir zumindest)
[Aktualisiert am: Mo., 21 August 2006 00:06]
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Re: ja eigentlich schon [Beitrag #36882 ist eine Antwort auf Beitrag #36879] :: Mo., 21 August 2006 00:26
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tristan
Beiträge: 709 Registriert: November 2005
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| fuselkopf schrieb am Mon, 21 August 2006 00:12 |
aber andere forenuser sind der meinung, das dein e2 wert nicht pathogen ist  also musst du ihn nicht absenken... was nicht meine rmeinung entspricht  ich habe dir ja wie gesagt geraten ihn auf ca 30pg/ml abzusenken. was du letztendlich machst musst du wissen 
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| fuselkopf schrieb am Son, 20 August 2006 18:25 |
Ich habe keine Zeit und Lust das alles zu kommentieren, aber nehmt ruhig Euer Estradiol zu Euch. Ich will Euch nicht aufhalten, jeder muss wissen was er mit seinem Körper anstellt.
And by the way:
Ich habe noch Estradiol (E2) zu entsorgen!
Falls mir jemand dabei behilflich sein möchte, dann kann er sich gerne per PM bei mir melden
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| Zitat: |
wer redet denn davon? ich nehme momenten kein e2 und keiner hat kkoo dazu geraten. Es ging mir nur darum dass den meisten mit aromatasehemmung kaum geholfen werden kann wenn sie schon einen hohen freien androgenindex haben, und dass e2 werte im unteren bereich für viele gesundheitsfaktoren bei männern laut literatur ein risiko darstellen. ich habe auch kkoo gesagt er soll es probieren, ich halte nur nicht viel davon wenn leute einen e2 wert von 25 haben und den versuchen auf 5 zu senken, auch wenn es negative seiten bei e2 gibt, das ist einfach gefährlich, ... aber du meintest ja auch nicht dass er ihn auf 5 senken soll, sondern auf 29-... , sage ich nichts gegen, jeder ist anders... meine meinung ist nur dass für den großteil aromatasehemmung negativ ist für die gesundheit, unabh. von haarausfall...
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falls ich gemeint war... 
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Re: post zu E2 und tgf-beta im forschungsforum [Beitrag #37320 ist eine Antwort auf Beitrag #37236] :: Fr., 25 August 2006 01:51
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tristan
Beiträge: 709 Registriert: November 2005
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das ist aber gewebespezifisch, und man kann weder sagen 100% gut noch 100% schlecht. denn tgf-b hat auch wichtige funktionen.
du schreibst auch wegen sebum bedenklich, aber e2 hat generell hemmende wirkung darauf. gibts viel zu, siehe auch oben..
"estrogen directly suppresses sebaceous gland function (1, 3, 75, 220, 221)."
ich würde empfehlen bevor du mit quercetin beginnst noch dht abnehmen zu lassen.
bin letztens auch noch über einen artikel bzgl. tamoxifen gestolpert, da war die rede dass das meist die e2 serum konz. anhebt (halt ähnlicher mechanismus wie bei fin mit testo zunahme). was pilos oben meinte stimmt ja schon, ich sagte dann es sei halt in vielen fällen wenn hoher freier androgenindex vorliegt nicht wirklich nötig, aber genauer wäre es schon noch mehr zu messen.
zum beispiel wurde mir auch mal estron (E1) abgenommen, da es manchmmal bei selteneren nnr enzymgeschichten zu vermehrter bildung über androstendiol (mit l) kommen kann und zur gyno bei nicht vorhandenem e2 im serum. war aber auch sehr niedrig, sprach also für kaum lokale wirkung..
vielleicht kriegst du estron irgenwie hin? wenn du ein labor hast was dht abnimmt machen die auch e1.
* N Engl J Med. 1994 Oct 20;331(16):1088-9.
Estrogen resistance caused by a mutation in the estrogen-receptor gene in a man.
Smith EP, Boyd J, Frank GR, Takahashi H, Cohen RM, Specker B, Williams TC, Lubahn DB, Korach KS.
Department of Pediatrics, Children's Hospital Medical Center, University of Cincinnati College of Medicine, OH 45229.
BACKGROUND AND METHODS. Mutations in the estrogen-receptor gene have been thought to be lethal. A 28-year-old man whose estrogen resistance was caused by a disruptive mutation in the estrogen-receptor gene underwent studies of pituitary-gonadal function and bone density and received transdermal estrogen for six months. Estrogen-receptor DNA, extracted from lymphocytes, was evaluated by analysis of single-strand-conformation polymorphisms and by direct sequencing. RESULTS. The patient was tall (204 cm [80.3 in.]) and had incomplete epiphyseal closure, with a history of continued linear growth into adulthood despite otherwise normal pubertal development. He was normally masculinized and had bilateral axillary acanthosis nigricans. Serum estradiol and estrone concentrations were elevated, and serum testosterone concentrations were normal. Serum follicle-stimulating hormone and luteinizing hormone concentrations were increased. Glucose tolerance was impaired, and hyperinsulinemia was present. The bone mineral density of the lumbar spine was 0.745 g per square centimeter, 3.1 SD below the mean for age-matched normal women; there was biochemical evidence of increased bone turnover. The patient had no detectable response to estrogen administration, despite a 10-fold increase in the serum free estradiol concentration....
btw. wie groß bist du eigentlich?
lg
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na ich weiss nicht [Beitrag #37336 ist eine Antwort auf Beitrag #37320] :: Fr., 25 August 2006 09:48
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kkoo
Beiträge: 4429 Registriert: November 2005
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dht u. estron messen: das wird schwierig hier in NL, kriege demnächst wenigstens LH und FSH, aber androgene wollten die partout nicht messen lassen. mal sehn, versuchs nochmal.
mein dht wird nicht arg sein, das glaub ich auch: hab nen bruder, der ist etwas älter, mir sehr ähnlich (in fast allem), hat kein SE, aber auch langsam voranschreitende AGA nach dem gleichen muster wie ich, nur dass es bei mir schon etwas schlechter aussieht, wahrscheinl. aufgrund des SE bzw. der damit verbundenen störungen, die auch die AGA "triggern".
selbst wenn E2 sebumreduzierend wirken müsste: ich denk natürlich trotzdem daran, dass ein zu hohes E2 etwa auch prostata-beschwerden machen kann u. derlei. übrigens hab ich aber keinerlei anzeichen von derlei wie "schnubbel"-brüsten, wie fusel das nennt
bin übrigens 1,87.
[Aktualisiert am: Fr., 25 August 2006 12:18]
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nur noch verwirrt [Beitrag #37821 ist eine Antwort auf Beitrag #37336] :: Di., 29 August 2006 14:00
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kkoo
Beiträge: 4429 Registriert: November 2005
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LH- und FSH-Werte kommen demnächst, aber ich habe echt null Anzeichen für irgendwas von diesen Nebenwirkungen, würde man annehmen, sie wären auch Ausdruck eines allgemein zu hohen E2... Vielleicht hat das Lab auch nur schlecht gemessen. Auch in der Familie keinerlei, wobei ich kröperlich meinem Bruder u. meinem Vater sehr ähnele, beide auch nur spärlich behaart, vater ist über 60 und hat null alterswampe, null "schnubbel"-brüste, null weiblich fettgewebsverteilung
"Unerwünschte Nebenwirkungen
einer unsachgemäßen Estrogengabe
können bei Männern Hemmung der
LH- und FSH-Sekretion, Prolaktinämie,
Gynäkomastie, weiblicher Typ der
Fettgewebeverteilung, bestimmte
hepatische Effekte einschließlich
Gallensteinbildung sein."
aus: "OETTEL M, HÜBLER D, WINKELMANN BR
Über das therapeutische Potential von Estrogenen beim Mann"
[Aktualisiert am: Di., 29 August 2006 16:41]
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Re: na ich weiss nicht [Beitrag #40209 ist eine Antwort auf Beitrag #37336] :: Mi., 13 September 2006 20:59
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tristan
Beiträge: 709 Registriert: November 2005
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| kkoo schrieb am Fre, 25 August 2006 09:48 |
dht u. estron messen: das wird schwierig hier in NL, kriege demnächst wenigstens LH und FSH, aber androgene wollten die partout nicht messen lassen. mal sehn, versuchs nochmal.
mein dht wird nicht arg sein, das glaub ich auch: hab nen bruder, der ist etwas älter, mir sehr ähnlich (in fast allem), hat kein SE, aber auch langsam voranschreitende AGA nach dem gleichen muster wie ich, nur dass es bei mir schon etwas schlechter aussieht, wahrscheinl. aufgrund des SE bzw. der damit verbundenen störungen, die auch die AGA "triggern".
selbst wenn E2 sebumreduzierend wirken müsste: ich denk natürlich trotzdem daran, dass ein zu hohes E2 etwa auch prostata-beschwerden machen kann u. derlei. übrigens hab ich aber keinerlei anzeichen von derlei wie "schnubbel"-brüsten, wie fusel das nennt
bin übrigens 1,87.
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hi,
glaube zwar auch nicht dass dein dht hoch ist, aber wenn man nicht weiter weiß muss noch weiter gesucht werden.
das estron kannste dir eigentlich sparen, nochmal nachgelesen.. was interessanter wäre, vielleicht eine molekulargenetische sequenzierung des estrogen rezeptor gens. kostet ca. 170,-, habe meinen endo auch mal gefragt.. damit kann man ziemlich eindeutige aussage über die lokale wirkung machen.
auch was deine größe betrifft würde wenig lokale estrogenwirkung passen. und wegen der seborrhoe erst recht.. du schreibst "selbst wenn...müsste..." , das ist keine hypothese, es wirkt erwiesenermaßen direkt und auch indirekt über shbg sebumsuppressiv. wir müssten deine lokale wirkung kennen um zu sagen dass das bei dir nicht so wäre..
hast du die artikel zu estrogenresistenz etc gelesen? wegen der serumerhöhung?
lg
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