Nutritional thriftiness and human reproduction: beyond the critical body composition hypothesis.
The 'critical body composition hypothesis' (CBCH) is frequently used to explain variations in the duration of postpartum amenorrhea. The hypothesis predicts that ovulation will not occur it fat reserves fall below a critical threshold. This paper attempts to analytically separate the CBCH from the broader concept of nutritional thriftiness on which it is based. A review of previous research on fat cell metabolism and ovulation finds no direct link between fatness and fecundity. Rather they are each regulated by the lactation and mother-infant interactions associated with breast feeding. As a system which delivers available fat into breast milk and prevents ovulation only during the time when the infant is dependent on the mother, the pathways outlined here represent a nutritionally thrifty method of fertility regulation, one which maximizes reproductive success while minimizing energy investment. The cultural patterning both of infant feeding behaviors and the wider range of maternal activities which affect breast feeding suggest specific testable hypotheses to explain interpopulation variations in fertility and infant nutritional status.
D000273:Adipose Tissue / Q000378:metabolism; D000568:Amenorrhea / Q000378:metabolism / Q000503:physiopathology*; D001823:Body Composition; D001942:Breast Feeding; D005260:Female; D005298:Fertility; D006801:Humans; D008954:Models, Biological; D009748:Nutrition Disorders / Q000503:physiopathology; D010060:Ovulation; D049590:Postpartum Period; D011247:Pregnancy; D011388:Prolactin / Q000097:blood
D011388:Prolactin