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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
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Disease relevance of Menopause

  • After we controlled for age and cigarette smoking, women who had had a natural menopause and who had never taken replacement estrogen had no appreciable increase in the risk of coronary heart disease, as compared with premenopausal women (adjusted rate ratio, 1.2; 95 percent confidence limits, 0.8 and 1.8) [1].
  • The lack of inflection point at modal age of menopause, contrasting with unequivocally estrogen-dependent biological markers like breast cancer or bone density, makes estrogen protection of premenopausal women an unlikely explanation [2].
  • In time-dependent analyses adjusted for age, menopause type, and oral contraceptive use, ever use of estrogen only was significantly associated with ovarian cancer (rate ratio [RR], 1.6; 95% confidence interval [CI], 1.2-2.0) [3].
  • Current users who started estrogen within 5 years of menopause had a decreased risk for hip fractures (RR, 0.29; CI, 0.09 to 0.92), wrist fractures (RR, 0.29; CI, 0.13 to 0.68), and all nonspinal fractures (RR, 0.50; CI, 0.36 to 0.70) when compared with women who had never used estrogen [4].
  • Only weak activity is detected in endometrial tissues after menopause, but telomerase activity can be strongly reactivated in patients who develop endometrial cancer [5].

Psychiatry related information on Menopause


High impact information on Menopause

  • Sex steroids are essential for skeletal development and the maintenance of bone health throughout adult life, and estrogen deficiency at menopause is a major pathogenetic factor in the development of osteoporosis in postmenopausal women [11].
  • The development of selective estrogen receptor modulators has provided a new approach to the prevention of osteoporosis and other major diseases of menopause and has implications for the therapeutic use of other steroid hormones, including androgens [11].
  • We evaluated the effects of transdermal testosterone in women who had impaired sexual function after surgically induced menopause [12].
  • BACKGROUND: Plasma levels of plasminogen-activator inhibitor type 1 (PAI-1), an essential inhibitor of fibrinolysis in humans, increase in women after menopause, and this may contribute to the risk of cardiovascular disease [13].
  • The decline of growth hormone (GH) and insulin-like growth factor I (IGF-I) production during aging has been likened to the decrease in gonadal steroids in menopause [14].

Chemical compound and disease context of Menopause


Biological context of Menopause

  • These findings suggest that estrogen may prevent excessive bone loss before and after the menopause by limiting osteoclast life span through promotion of apoptosis [20].
  • Three hormonal systems show decreasing circulating hormone concentrations during normal aging: (i) estrogen (in menopause) and testosterone (in andropause), (ii) dehydroepiandrosterone and its sulphate (in adrenopause), and (iii) the growth hormone/insulin-like growth factor I axis (in somatopause) [21].
  • JAMA patient page. Perimenopause: beginning of menopause [22].
  • A new understanding of the endocrinology of menopause is that women, at menopause, are not only lacking estrogens resulting from cessation of ovarian activity but have also been progressively deprived for a few years of androgens and some estrogens originating from adrenal DHEA and androstenedione (4-dione) [23].
  • There was no relationship between genotype for any of the three polymorphisms and BMD at any skeletal site in the twin population, considered either as a total population, both with and without twins discordant for age at menopause or use of estrogen, or as a premenopausal population [24].

Anatomical context of Menopause


Associations of Menopause with chemical compounds

  • We studied 374 women taking oral contraceptives, 284 women taking estrogen preparations after menopause, and 1086 women taking no hormones, to determine the relation of plasma lipids and lipoprotein cholesterol concentrations to various types of estrogen/progestin formulations [30].
  • It is important to consider, however, that most of the androgens in women, especially after menopause, are synthesized in peripheral intracrine tissues from the inactive precursors dehydroepiandrosterone (DHEA) and DHEA sulfate (DHEA-S) of adrenal origin [31].
  • Estriol in the management of the menopause [32].
  • Although cholesterol and hemoglobin did rise somewhat more steeply in women undergoing the menopause, this greater incidence of cardiovascular disease in postmenopausal women could not be explained by the influence of the menopause on the usual cardiovascular risk factors [33].
  • In uremic women, the continued secretion of estrogen, the rise of plasma levels of luteinizing hormone, FSH, and estradiol after clomiphene, and the elevated gonadotropin levels during menopause suggest that the negative estradiol feedback, the tonic gonadotropin secretion, and the pituitary ovarian axis were normal [34].

Gene context of Menopause

  • Premature ovarian failure (POF) is a defect of ovarian development and is characterized by primary or secondary amenorrhea, with elevated levels of serum gonadotropins, or by early menopause [35].
  • We conclude that estrogen may prevent bone loss following the menopause by altering the balance between IL-1beta and IL-1ra [36].
  • We aimed to identify genetic factors influencing the onset of menarche and natural menopause in a Japanese population by investigating the polymorphisms of estrogen receptor-alpha and estrogen-metabolizing enzyme genes [37].
  • The NO/iNOS system contributes to the induction of HO-1, which may subsequently suppress iNOS activity to modulate vasculoprotective effects after menopause [38].
  • RESULTS: Serum ferritin concentrations, but not percentage of transferrin saturation, in normal, healthy women tended to increase sharply as they progressed through menopause [39].

Analytical, diagnostic and therapeutic context of Menopause


  1. Menopause and the risk of coronary heart disease in women. Colditz, G.A., Willett, W.C., Stampfer, M.J., Rosner, B., Speizer, F.E., Hennekens, C.H. N. Engl. J. Med. (1987) [Pubmed]
  2. Androgens and cardiovascular disease. Liu, P.Y., Death, A.K., Handelsman, D.J. Endocr. Rev. (2003) [Pubmed]
  3. Menopausal hormone replacement therapy and risk of ovarian cancer. Lacey, J.V., Mink, P.J., Lubin, J.H., Sherman, M.E., Troisi, R., Hartge, P., Schatzkin, A., Schairer, C. JAMA (2002) [Pubmed]
  4. Estrogen replacement therapy and fractures in older women. Study of Osteoporotic Fractures Research Group. Cauley, J.A., Seeley, D.G., Ensrud, K., Ettinger, B., Black, D., Cummings, S.R. Ann. Intern. Med. (1995) [Pubmed]
  5. Telomerase activity in benign endometrium and endometrial carcinoma. Brien, T.P., Kallakury, B.V., Lowry, C.V., Ambros, R.A., Muraca, P.J., Malfetano, J.H., Ross, J.S. Cancer Res. (1997) [Pubmed]
  6. Onset of dementia is associated with age at menopause in women with Down's syndrome. Schupf, N., Pang, D., Patel, B.N., Silverman, W., Schubert, R., Lai, F., Kline, J.K., Stern, Y., Ferin, M., Tycko, B., Mayeux, R. Ann. Neurol. (2003) [Pubmed]
  7. Interactions of interleukin-6 promoter polymorphisms with dietary and lifestyle factors and their association with bone mass in men and women from the Framingham Osteoporosis Study. Ferrari, S.L., Karasik, D., Liu, J., Karamohamed, S., Herbert, A.G., Cupples, L.A., Kiel, D.P. J. Bone Miner. Res. (2004) [Pubmed]
  8. The epidemiology of estrogen replacement therapy and Alzheimer's disease. Henderson, V.W. Neurology (1997) [Pubmed]
  9. The role of anxiety and hormonal changes in menopausal hot flashes. Freeman, E.W., Sammel, M.D., Lin, H., Gracia, C.R., Kapoor, S., Ferdousi, T. Menopause (New York, N.Y.) (2005) [Pubmed]
  10. Histologic types of epithelial ovarian cancer: have they different risk factors? Kurian, A.W., Balise, R.R., McGuire, V., Whittemore, A.S. Gynecol. Oncol. (2005) [Pubmed]
  11. Sex steroids and bone. Compston, J.E. Physiol. Rev. (2001) [Pubmed]
  12. Transdermal testosterone treatment in women with impaired sexual function after oophorectomy. Shifren, J.L., Braunstein, G.D., Simon, J.A., Casson, P.R., Buster, J.E., Redmond, G.P., Burki, R.E., Ginsburg, E.S., Rosen, R.C., Leiblum, S.R., Caramelli, K.E., Mazer, N.A. N. Engl. J. Med. (2000) [Pubmed]
  13. Effects of hormone-replacement therapy on fibrinolysis in postmenopausal women. Koh, K.K., Mincemoyer, R., Bui, M.N., Csako, G., Pucino, F., Guetta, V., Waclawiw, M., Cannon, R.O. N. Engl. J. Med. (1997) [Pubmed]
  14. Growth hormone treatment induces mammary gland hyperplasia in aging primates. Ng, S.T., Zhou, J., Adesanya, O.O., Wang, J., LeRoith, D., Bondy, C.A. Nat. Med. (1997) [Pubmed]
  15. Estrogen and progestin, lipoprotein(a), and the risk of recurrent coronary heart disease events after menopause. Shlipak, M.G., Simon, J.A., Vittinghoff, E., Lin, F., Barrett-Connor, E., Knopp, R.H., Levy, R.I., Hulley, S.B. JAMA (2000) [Pubmed]
  16. Loss of ovarian function promotes angiogenesis in human ovarian carcinoma. Schiffenbauer, Y.S., Abramovitch, R., Meir, G., Nevo, N., Holzinger, M., Itin, A., Keshet, E., Neeman, M. Proc. Natl. Acad. Sci. U.S.A. (1997) [Pubmed]
  17. Effect of tamoxifen on plasma insulin-like growth factor I in patients with breast cancer. Colletti, R.B., Roberts, J.D., Devlin, J.T., Copeland, K.C. Cancer Res. (1989) [Pubmed]
  18. Bisphosphonate risedronate prevents bone loss in women with artificial menopause due to chemotherapy of breast cancer: a double-blind, placebo-controlled study. Delmas, P.D., Balena, R., Confravreux, E., Hardouin, C., Hardy, P., Bremond, A. J. Clin. Oncol. (1997) [Pubmed]
  19. Spontaneous hip fractures in fluoride-treated patients: potential causative factors. Gutteridge, D.H., Price, R.I., Kent, G.N., Prince, R.L., Michell, P.A. J. Bone Miner. Res. (1990) [Pubmed]
  20. Estrogen promotes apoptosis of murine osteoclasts mediated by TGF-beta. Hughes, D.E., Dai, A., Tiffee, J.C., Li, H.H., Mundy, G.R., Boyce, B.F. Nat. Med. (1996) [Pubmed]
  21. The endocrinology of aging. Lamberts, S.W., van den Beld, A.W., van der Lely, A.J. Science (1997) [Pubmed]
  22. JAMA patient page. Perimenopause: beginning of menopause. Torpy, J.M., Lynm, C., Glass, R.M. JAMA (2003) [Pubmed]
  23. DHEA and its transformation into androgens and estrogens in peripheral target tissues: intracrinology. Labrie, F., Luu-The, V., Labrie, C., Simard, J. Frontiers in neuroendocrinology. (2001) [Pubmed]
  24. Bone mineral density in relation to polymorphism at the vitamin D receptor gene locus. Hustmyer, F.G., Peacock, M., Hui, S., Johnston, C.C., Christian, J. J. Clin. Invest. (1994) [Pubmed]
  25. Postmenopausal estrogen therapy and the risk for developing systemic lupus erythematosus. Sánchez-Guerrero, J., Liang, M.H., Karlson, E.W., Hunter, D.J., Colditz, G.A. Ann. Intern. Med. (1995) [Pubmed]
  26. Ovarian steroid treatment blocks a postmenopausal increase in blood monocyte interleukin 1 release. Pacifici, R., Rifas, L., McCracken, R., Vered, I., McMurtry, C., Avioli, L.V., Peck, W.A. Proc. Natl. Acad. Sci. U.S.A. (1989) [Pubmed]
  27. Transcriptional regulation of the Osterix (Osx, Sp7) promoter by tumor necrosis factor identifies disparate effects of mitogen-activated protein kinase and NFkappaB pathways. Lu, X., Gilbert, L., He, X., Rubin, J., Nanes, M.S. J. Biol. Chem. (2006) [Pubmed]
  28. Effects of weight and body mass index on bone mineral density in men and women: the Framingham study. Felson, D.T., Zhang, Y., Hannan, M.T., Anderson, J.J. J. Bone Miner. Res. (1993) [Pubmed]
  29. Are gender differences in cardiovascular disease risk factors explained by the level of visceral adipose tissue? Lemieux, S., Després, J.P., Moorjani, S., Nadeau, A., Thériault, G., Prud'homme, D., Tremblay, A., Bouchard, C., Lupien, P.J. Diabetologia (1994) [Pubmed]
  30. Effect of estrogen/progestin potency on lipid/lipoprotein cholesterol. Wahl, P., Walden, C., Knopp, R., Hoover, J., Wallace, R., Heiss, G., Rifkind, B. N. Engl. J. Med. (1983) [Pubmed]
  31. Endocrine and intracrine sources of androgens in women: inhibition of breast cancer and other roles of androgens and their precursor dehydroepiandrosterone. Labrie, F., Luu-The, V., Labrie, C., Bélanger, A., Simard, J., Lin, S.X., Pelletier, G. Endocr. Rev. (2003) [Pubmed]
  32. Estriol in the management of the menopause. Tzingounis, V.A., Aksu, M.F., Greenblatt, R.B. JAMA (1978) [Pubmed]
  33. Menopause and risk of cardiovascular disease: the Framingham study. Kannel, W.B., Hjortland, M.C., McNamara, P.M., Gordon, T. Ann. Intern. Med. (1976) [Pubmed]
  34. Ovarian function in chronic renal failure: evidence suggesting hypothalamic anovulation. Lim, V.S., Henriquez, C., Sievertsen, G., Frohman, L.A. Ann. Intern. Med. (1980) [Pubmed]
  35. A human homologue of the Drosophila melanogaster diaphanous gene is disrupted in a patient with premature ovarian failure: evidence for conserved function in oogenesis and implications for human sterility. Bione, S., Sala, C., Manzini, C., Arrigo, G., Zuffardi, O., Banfi, S., Borsani, G., Jonveaux, P., Philippe, C., Zuccotti, M., Ballabio, A., Toniolo, D. Am. J. Hum. Genet. (1998) [Pubmed]
  36. Effects of estrogen therapy of postmenopausal women on cytokines measured in peripheral blood. Rogers, A., Eastell, R. J. Bone Miner. Res. (1998) [Pubmed]
  37. Estrogen-metabolizing gene polymorphisms, but not estrogen receptor-alpha gene polymorphisms, are associated with the onset of menarche in healthy postmenopausal Japanese women. Gorai, I., Tanaka, K., Inada, M., Morinaga, H., Uchiyama, Y., Kikuchi, R., Chaki, O., Hirahara, F. J. Clin. Endocrinol. Metab. (2003) [Pubmed]
  38. Oxidative stress induces vascular heme oxygenase-1 expression in ovariectomized rats. Lee, Y.M., Cheng, P.Y., Hong, S.F., Chen, S.Y., Lam, K.K., Sheu, J.R., Yen, M.H. Free Radic. Biol. Med. (2005) [Pubmed]
  39. Reference centiles for serum ferritin and percentage of transferrin saturation, with application to mutations of the HFE gene. Koziol, J.A., Ho, N.J., Felitti, V.J., Beutler, E. Clin. Chem. (2001) [Pubmed]
  40. Fragile X premutations are not a major cause of early menopause. Kenneson, A., Cramer, D.W., Warren, S.T. Am. J. Hum. Genet. (1997) [Pubmed]
  41. Cardiovascular risk factors in women with and without rheumatoid arthritis. Solomon, D.H., Curhan, G.C., Rimm, E.B., Cannuscio, C.C., Karlson, E.W. Arthritis Rheum. (2004) [Pubmed]
  42. Disease activity during the premenopausal and postmenopausal periods in women with systemic lupus erythematosus. Sánchez-Guerrero, J., Villegas, A., Mendoza-Fuentes, A., Romero-Díaz, J., Moreno-Coutiño, G., Cravioto, M.C. Am. J. Med. (2001) [Pubmed]
  43. Effects of estrogen replacement therapy on bone turnover in subchondral bone and epiphyseal metaphyseal cancellous bone of ovariectomized cynomolgus monkeys. Ham, K.D., Carlson, C.S. J. Bone Miner. Res. (2004) [Pubmed]
  44. Cross-sectional analysis of renal transplantation osteoporosis. Parker, C.R., Freemont, A.J., Blackwell, P.J., Grainge, M.J., Hosking, D.J. J. Bone Miner. Res. (1999) [Pubmed]
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