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Author(s): te Velde ER; Scheffer GJ; Dorland M; Broekmans FJ; Fauser BCJM
Title: Developmental and endocrine aspects of normal ovarian aging
Source: MOLECULAR AND CELLULAR ENDOCRINOLOGY 145 (1-2): 67-73
Date: 1998 OCT 25
Document Type: Journal : Proceedings Paper
DOI:
Language: English
Comment:
Address: Univ Utrecht Hosp, Div Obstet & Gynaecol, Dept Endocrinol & Fertil, NL-3584 CX Utrecht, Netherlands.
Univ Rotterdam Hosp, Dept Obstet & Gynaecol, Div Reprod Med, Rotterdam, Netherlands. Erasmus Univ, Sch Med, Rotterdam, Netherlands. Reprint: te Velde, ER, Univ Utrecht Hosp, Div Obstet & Gynaecol, Dept Endocrinol
& Fertil, Heidelberglaan 100, NL-3584 CX Utrecht, Netherlands. E-mail: E.R.teVelde@DOG.AZU.NL
Author Keywords: follicles; atresia; oocyte; dizygotic twinning
KeyWords Plus: FOLLICLE-STIMULATING-HORMONE; AGE-RELATED-CHANGES; MONOTROPIC FSH RISE;
LUTEINIZING-HORMONE; NATURAL MENOPAUSE; MENSTRUAL CYCLES; OLDER WOMEN;
INHIBIN-B; GONADOTROPIN-SECRETION; REPRODUCTIVE AGE
Abstract: Supplies of follicles are established during early fetal life and decrease exponentially thereafter by a process called atresia. Subfertility only starts at a mean age of about 30-31 years, when the remaining follicle reserve has become a fraction of its original number. Thereafter, a further decrease in both oocyte quantity and quality dictates the subsequent reproductive events including decrease of fertility, increased abortion rate, the end of fertility, the beginning of cycle irregularity and, when almost no follicles are left, the occurrance of menopause. The same remarkable variation of age at menopause almost certainly is also present for the preceding reproductive events. When quantity and quality of antral follicles drop below a critical threshold, there is a subsequent drop in inhibine B resulting in the selective FSH rise at a mean age of 37-38 years. This FSH rise explains the accelerated follicle depletion, the increased proportion of growing follicles reaching the selectable stage, the shortening of the follicular phase and the increased incidence of dizygotic twinning. The concurring decrease of oocyte quality is in line with the increased incidence of abortions and chromosomal aberrations after age 35. (C) 1998 Elsevier Science Ireland Ltd. All rights reserved.
Cited References: AHMEDEBBIARY NA, 1994, CLIN ENDOCRINOL, V41, P199 ALEXANDER SE, 1990, AM J OBSTET GYNECOL, V162, P446 ATAYA K, 1989, ACTA ENDOCRINOL-COP, V121, P55 ATAYA K, 1995, BIOL REPROD, V52, P365 BONGAARTS J, 1982, CTR POLICY STUDIES W, V89, P1 BROOK JD, 1984, HUM GENET, V66, P41 BROWN JB, 1978, AUST NZ J OBSTET GYN, V18, P47 CHUN SY, 1996, ENDOCRINOLOGY, V137, P1447 CRAMER DW, 1995, AM J OBSTET GYNECOL, V172, P568 DAHLGREN E, 1992, FERTIL STERIL, V57, P505 DEMOUZON J, 1993, FERTIL STERIL, V59, P587 DENTONKELAAR I, 1998, MATURITAS, V29, P115 EICHENLAUBRITTER U, 1996, ENVIRON MOL MUTAGEN, V28, P211 FADDY MJ, 1992, HUM REPROD, V7, P1342 FADDY MJ, 1995, HUM REPROD, V10, P770 FITSGERALD CT, 1994, BRIT J OBSTET GYNAEC, V101, P229 FORD JH, 1995, HUM REPROD, V10, P1397 GAULDEN ME, 1992, MUTAT RES, V296, P69 GOSDEN RG, 1985, ANN NY ACAD SCI, V442, P45 GOUGEON A, 1987, J REPROD FERTIL, V81, P433 GOUGEON A, 1994, BIOL REPROD, V50, P653 GOUGEON A, 1996, ENDOCR REV, V17, P121 GOVAN ADT, 1968, J ENDOCRINOL, V40, P421 GROOME NP, 1996, J CLIN ENDOCR METAB, V81, P1401 HALL JE, 1992, J CLIN ENDOCR METAB, V74, P600 HENDERSON SA, 1968, NATURE, V218, P22 HIRSHFIELD AN, 1994, BIOL REPROD, V50, P421 HSUEH AJW, 1994, ENDOCR REV, V15, P707 ILLINGWORTH PJ, 1996, J CLIN ENDOCR METAB, V81, P1321 JONES EC, 1961, J ENDOCRINOL, V21, P497 KLEIN NA, 1996, J CLIN ENDOCR METAB, V81, P1038 KLEIN NA, 1996, J CLIN ENDOCR METAB, V81, P2742 KLEIN NA, 1996, J SOC GYNECOL INVEST, V3, P27 KRARUP T, 1969, NATURE, V224, P187 LEE SJ, 1988, HUM REPROD, V3, P851 LENTON EA, 1991, J CLIN ENDOCR METAB, V73, P1180 MACNAUGHTON J, 1992, CLIN ENDOCRINOL, V36, P339 MILHAM S, 1964, LANCET, V2, P566 MOSHER WD, 1991, FERTIL STERIL, V56, P192 MUNNE S, 1994, AM J HUM GENET, V55, P150 MUSEY VC, 1987, AM J OBSTET GYNECOL, V157, P312 OKTAY K, 1997, J CLIN ENDOCR METAB, V82, P3748 OKTAY K, 1998, HUM REPROD, V13, P1133 PETERS H, 1979, EUR J OBSTET GYN R B, V9, P137 REYES FI, 1977, AM J OBSTET GYNECOL, V129, P557 RICHARDSON SJ, 1993, BAILLIERE CLIN ENDOC, V7, P1 ROSS GT, 1978, CLIN ENDOCRINOL META, V7, P561 SAUER MV, 1993, LANCET, V341, P321 SCHIPPER I, 1998, IN PRESS HUM REPROD SHERMAN BM, 1976, J CLIN ENDOCR METAB, V42, P629 SOBERON J, 1966, AM J OBSTET GYNECOL, V96, P96 SUGURTEKIN U, 1995, FERTIL STERIL, V63, P494 TEVELDE ER, 1991, PREGNANCY 21 CENTURY TEVELDE ER, 1993, LANCET, V341, P1145 TEVELDE ER, 1997, STUD PROFERLIT, V6, P145 TEVELDE ER, IN PRESS MATURITAS TRELOAR AE, 1981, MATURITAS, V3, P49 VANCAPPELLEN WA, 1989, BIOL REPROD, V40, P1247 VANKEEP PA, 1979, J BIOSOC SCI S, V6, P37 VANKOOIJ RJ, 1996, FERTIL STERIL, V66, P769 VANNOORD PAH, 1997, FERTIL STERIL, V68, P95 VANNOORDZAADSTRA BM, 1991, BRIT MED J, V302, P1361 WANG XN, 1993, BIOL REPROD, V48, P585 WARBURTON D, 1986, PERINATAL GENETICS D, P133 WHELAN EA, 1990, AM J EPIDEMIOL, V131, P625 WILDT L, 1981, ENDOCRINOLOGY, V109, P376 WISE PM, 1996, SCIENCE, V273, P67 WOOD JW, OXFORD REV REPROD BI, V2, P61 ZHENG WX, 1996, AM J PATHOL, V148, P47 |