HORMONAL INFLUENCE DURING LIFE
provides no barrier to the high concentration of maternal estrogens prior to
parturition. As a result, the infant’s breasts may show some enlargement, and
milk can occasionally be expressed. The external genitalia are precociously
developed, and the endometrium has been stimulated to proliferate. Within a
week or so after birth, all the stigmata of estrogen stimulation recede.
From the postnatal recessional changes to the time of puberty, the ovaries gradually show a buildup of interstitial tissue from an accumulation of ﬁbrous stroma, as a constant succession of primordial follicles degenerate in atresia.
Pituitary maturation and consequent secretion of gonadotropins results in
the initiation of enhanced ovarian steroid production at the time of puberty.
The uterus is the ﬁrst to respond and the endometrium proliferates with the
development of straight, tubular glands. Next, the vagina thickens and becomes
stratiﬁed, with corniﬁed superﬁcial estrogenic cells appearing. In the ovary,
primordial follicles progress beyond the stage of a one- or two-layer granulosa
with a tiny antrum and exhibit identiﬁable several-thickness granulosa and
theca interna layers. In the breast, the areolae show pigmentation along with a
domelike change, becoming elevated as a conical protuberance. Fat is deposited
about the shoulder girdle, hips, and buttocks, and the adult pelvic and, later,
the axillary hair patterns typical of the female begin to develop.
In the decade of adolescence, the skeletal system reacts to estrogen,
ﬁrst, by an accelerated growth rate of the long bones, and, second, by a
hastening of epiphyseal closure, the balance affecting ﬁnal height.
In the mature cycle, the endometrium undergoes cyclic changes (described
elsewhere) under the stimulus of estrogen secreted by ovarian follicles in
response to follicle-stimulating hormone (FSH). By day 12 in a typical 28-day
cycle, one follicle attains dominance and exhibits a rapid growth toward
maturity. The release of luteinizing hormone (LH) at midcycle on day 14 induces
ovulation of the mature follicle and initiates progesterone excretion from the
rapidly forming corpus luteum. Endometrial glands become saw-toothed and
secretory. If fertilization and implantation do not occur, the corpus luteum
degenerates on about day 26, and in consequence with the rapid withdrawal of
its estrogen and progesterone secretion the endometrium shrinks, undergoes
autolysis, and breaks away with bleeding on day 28.
When conception occurs, the early excretion of chorionic gonadotropin
maintains the corpus luteum. In pregnancy, the peak production of chorionic
hormone is seen by about day 90 after the last menstrual period, declining
thereafter to a plateau. The corpus luteum is responsible for increasing
progesterone and estrogens throughout the ﬁrst 3 months, after which the placenta
takes over until the end of the pregnancy. The augmentation of both estrogen
and progesterone is approxi-mately linear throughout the 9 months of gestation.
The breasts react to the increasing steroid stimulation with an extension of
both ductile and alveolar growth, and there is congestion without actual
The withdrawal of estrogen and progesterone after placental delivery
combined with the psychoneural mechanisms initiated by the suckling reﬂex bring
about the release of prolactin. Breast tissues, already conditioned by growth,
respond with milk production. Ovarian activity is often held in abeyance for
approxi-mately 6 months in women who are fully breastfeeding; it may well occur
sooner in women who are partially breastfeeding. Reestablishment of the
pituitary–ovarian cycle can, and often does, take place before weaning, so that
another conception can occur before the advent of a menstrual ﬂow.
In the United States, menopause occurs late in the fourth or early in the ﬁfth decade (mean age 51 ± 2). The ovaries no longer contain any follicles capable of responding to pituitary stimulation, and increasing amounts of FSH are released in response to lower estrogen and inhibin levels. Estrogen deﬁciency is reﬂected by senile changes in the breasts, uterus, and vagina, and also in the skin, bony skeleton, and vascular system.