According to a recent hypothesis, menstruation evolved to protect the
uterus and oviducts from sperm-borne Pathogens by dislodging infected
endometrial tissue and delivering immune cells to the uterine cavity.
This hypothesis predicts the following: (1) uterine pathogens should b
e more prevalent before menses than after menses, (2) in the life life
histories of females, the timing of menstruation should track pathoge
n burden, and (3) in primates, the copiousness of menstruation should
increase with the promiscuity of the breeding system. I tested these p
redictions and they were not upheld by the evidence. I propose tile al
ternative hypothesis that the uterine endometrium is shed/resorbed whe
never implantation fails because cyclical regression and renewal is en
ergetically less costly than maintaining the endometrium in the metabo
lically active state required for implantation. In the regressed state
, oxygen consumption (per mg protein/h) in hu,nan endometria declines
nearly sevenfold. Tile cyclicity in endometrial oxygen consumption is
one component of the whole body cyclicity in metabolic rate caused by
the action of the ovarian steroids on both endometrial and nonendometr
ial tissue. Metabolic rate is at least 7% lower, on average, during th
e follicular phase than during the luteal phase in women, which signif
ies an estimated energy savings of 53 MJ over four cycles, or nearly s
ix days worth of food. Thus, the menstrual cycle revs up and revs down
, economizing on the energy costs of reproduction. This economy is gre
atest during the nonbreeding season and other periods of amenorrhea wh
en the endometrium, remains in a regressed state and ovarian cycling i
s absent for a prolonged period of lime. Twelve months of amenorrhea s
ave an estimated 130 MJ, or the energy required by one woman for nearl
y half a month. By helping females to maintain body mass, energy econo
my will promote female fitness in any environment in which fecundity a
nd survivorship is constrained by the food supply. Endometrial economy
may be of ancient evolutionary origin because similar reproductive st
ructures, such as the oviducts of lizards, also regress when a fertili
zed egg is unlikely to be present. Regression of the endometrium is us
ually accompanied by reabsorption, but in some species as much as one
third of the endometrial and vascular tissue is sited as the menses. R
ather than having an adaptive basis in ecology or behavior, variation
in the degree of menstrual bleeding in primates shows a striking corre
lation with phylogeny. The endometrial microvasculature is designed to
provide the blood supply to the endometrium and tile placenta, and ex
ternal bleeding appears io ire a side effect of endometrial regression
that arises when there is too much blood and other tissue for complet
e reabsorption. Tire copious bleeding of humans and chimps can be attr
ibuted ta tire large she of tire uterus relative to adult female body
size and to the design of the microvasculature in catarrhines.