The maintenance of reproductive receptivity and procreative power are energy-intensive imperatives. These imperatives are, however, superfluous under conditions of caloric curtailment. It is therefore not surprising that animals subjected to caloric restriction (CR) are less fertile than free-fed controls. Female animals release fewer eggs during ovulation and have smaller litters while males elaborate less semen and produce fewer sperm under conditions of chronic CR [16] and [17]. These effects are mediated collectively by reductions in gonadotropins (i.e. luteinizing hormone, and follicle stimulating hormone) and by reductions in sex hormones (principally testosterone and estrogen). Interestingly, both testosterone and estrogen are known to increase whole body metabolic rate markedly [14].
Thus, suppression of circulating sex hormones in hominids would have been doubly adaptive in that the likelihood of reproduction would have been reduced and the rate with which limited energy resources were utilized would have been curtailed considerably, augmenting the calorie conserving effects of low thyroid hormone and somatotropin (growth hormone) noted previously. When viewed in terms of the ‘reproductive quotient’ – that is, the ratio of reproductive lifespan to total lifespan – human females are far less fecund than chimpanzees. Viewed differently, the duration over which human females are reproductively receptive (relative to total lifespan) is reduced. If the reproductive range – the period from menarche to menopause or cessation of ovulation – of both chimpanzees and humans is approximated to be ∼30 years and the maximum lifespan of chimpanzees and humans is approximated to be ∼60 and ∼120 years, respectively, then humans have experienced a 2-fold relative reduction in their ‘reproductive quotient’. Though this reduction is attributable in part to increased absolute longevity (without concomitant augmentation of reproductive longevity), negative selection cannot be ruled out, especially when consideration is given to the fact that human females attain sexual maturity several years after their simian counterparts, gestate their young for a longer period and typically experience an abrupt cessation of menstruation and ovulation by about the fifth decade of life.
I posit that comparisons of reproductive potential between such socially sophisticated species as humans and chimpanzees are more practicable and tractable than reproductive rate or output as the former measure is likely more indicative of underlying physiological factors and less subject to complex situational variables. The term reproductive quotient is therefore especially instructive as it expresses an estimation of the length of time over which a given female is reproductively receptive relative to its maximum lifespan. It is in this respect that I maintain that the lineage eventuating in humans experienced a reduction in reproductive potential (reproductive quotient) relative to extant apes and (inferentially) to ancestral hominids. It is conceivable that natural selection served to suppress human fertility (or more precisely, reduce reproductive range relative to lifespan) in the face of food scarcity, thereby promoting the preservation of precious energy reserves. Indeed, it is estimated that energy expenditure is 7% lower in women when the endometrium is in a regressed (non-receptive) state [18].
Clearly, the assumption of amenorreah (i.e. temporary cessation of menstruation) in the face of protracted energy deprivation can effectuate conservation of copious amounts of energy and avert potential parental investment in offspring likely to suffer malnutrition and premature death due to food scarcity.
