Reproductive aging: accelerated ovarian follicular development associated with a monotropic follicle-stimulating hormone rise in normal older women
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Date
Authors
Davis, Gretchen S.
Fujimoto, Victor Y.
Soules, Michael R.
Bremner, William J.
Klein, Nancy A.
Battaglia, David E.
Journal Title
Journal ISSN
Volume Title
Publisher
Endocrine Society
Abstract
Women experience a decline in fertility that precedes the menopause by
several years. Previous studies have demonstrated a monotropic rise in FSH
associated with reproductive aging: however, the mechanism of this rise
and its role in the aging process are poorly understood. The purpose of
this study was to characterize ovarian follicular development and ovarian
hormone secretion in older reproductive age women. Sixteen women, aged
40-45 yr, with regular ovulatory cycles were studied. The control group
consisted of 12 ovulatory women, aged 20-25 yr. Serum obtained by daily
blood sampling was analyzed for FSH, LH, estradiol (E), progesterone, and
inhibin (Monash polyclonal assay). Follicle growth and ovulation were
documented by transvaginal ultrasound. Older women had significantly
higher levels of FSH throughout the menstrual cycle. E, progesterone, LH,
and inhibin levels did not differ between the two age groups when compared
relative to the day of the LH surge. Ultrasound revealed normal growth,
size, and collapse of a dominant follicle in all subjects. Older women had
significantly shorter follicular phase length associated with an early
acute rise in follicular phase E, reflecting accelerated development of a
dominant follicle. We conclude that older reproductive age women have
accelerated development of a dominant follicle in the presence of the
monotropic FSH rise. This is manifested as a shortened follicular phase
and elevated follicular phase E. The fact that ovarian steroid and inhibin
secretion were similar to those in the younger women suggests that
elevated FSH in women of advanced reproductive age may represent a primary
neuroendocrine change associated with reproductive aging.
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Citation
J Clin Endocrinol Metab. 1996 Mar;81(3):1038-45
