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Reproductive adaptations to a large‐brained fetus open a vulnerability to anovulation similar to polycystic ovary syndrome
Author(s) -
Barnett Deborah K.,
Abbott David H.
Publication year - 2003
Publication title -
american journal of human biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.559
H-Index - 81
eISSN - 1520-6300
pISSN - 1042-0533
DOI - 10.1002/ajhb.10149
Subject(s) - follicular phase , luteal phase , polycystic ovary , ovulation , biology , anovulation , endocrinology , medicine , endometrium , estrogen , hormone , insulin , insulin resistance
During the ovarian or menstrual cycle, prior to ovulation, many female primates exhibit a relatively prolonged follicular phase and terminate the postovulatory luteal phase with menstrual bleeding. The prolonged follicular phase is a trait that distinguishes primate from nonprimate species. It enables extended estrogen‐induced proliferation and growth of the uterine endometrium prior to progesterone‐induced maturation during the luteal phase to accommodate a potential pregnancy with a rapidly invading placenta. Progressive development of both an extended duration of estrogen‐induced, preimplantation endometrial proliferation and a rapidly invading placenta across the Primate order may well have been necessary to accommodate differentiation and growth of an increasingly large fetal brain. Prolongation of the follicular phase in primates has also led to the isolation of the final stages of follicle selection (growth deviation of the dominant follicle from its contemporaries) solely within the follicular phase and thus outside the protection of luteal phase progesterone inhibition of pituitary luteinizing hormone (LH) secretion. Such primate reproductive characteristics put the latter stages of ovarian follicle selection at risk of exposure to excessive pituitary secretion of LH. Excessive secretion of LH during follicle selection could result not only in impaired follicle development, excessive ovarian androgen secretion, and ovulation failure, but also in excessive estrogenic stimulation of the uterine endometrium without intervening menstrual periods. Such reproductive abnormalities are all found in a single, prevalent infertility syndrome afflicting women in their reproductive years: polycystic ovary syndrome (PCOS). We propose that successful female reproductive adaptations to accommodate the growth demands of large‐brained primate fetuses have facilitated a particular vulnerability of higher primates to hypergonadotropic disruption of ovulatory function, as found in PCOS. Am. J. Hum. Biol. 15:296–319, 2003. © 2003 Wiley‐Liss.