title: Prader-Willi syndrome and the evolution of human childhood.
abstract: The kinship theory of genomic imprinting predicts that imprinted genes have effects on asymmetric kin (relatives with different degrees of matrilineal and patrilineal relatedness). The most important interaction with such a relative is a child's interaction with its mother. Therefore, the study of imprinted genes and their phenotypic effects promises to provide insights into the evolution of mother-child relations. Prader-Willi syndrome (PWS) is caused by the absence of expression of genes at 15q11-q13 that are normally expressed only when paternally derived. The kinship theory predicts that children with PWS will fail to express behaviors that have increased mothers' costs of child-rearing. Our analysis focuses on aspects of the PWS phenotype that affect appetite and feeding. Immediately after birth, children with PWS have little appetite and are usually unable to suckle, but at some stage (usually within the first 2 years) they develop a voracious appetite and an obsession with food. We conjecture that this change in appetite reflects evolutionary forces associated with weaning. Immediately after birth, when a child is completely dependent on the breast, poor appetite reduced maternal costs. However, once a child was able to consume supplemental foods, maternal costs would have been reduced by children with increased, nonfastidious appetites.
authors.affiliation: Department of Organismic and Evolutionary Biology, Harvard University, Cambridge, Massachusetts 02138, USA.
authors.forename: David
authors.initials: D
authors.lastname: Haig
authors.forename: Robert
authors.initials: R
authors.lastname: Wharton
mesh_terms: D001066:Appetite / Q000502:physiology; D005075:Biological Evolution; D001942:Breast Feeding; D002657:Child Development; D002884:Chromosomes, Human, Pair 15; D004734:Energy Metabolism; D006801:Humans; D007223:Infant; D007225:Infant Food; D007231:Infant, Newborn; D009034:Mother-Child Relations; D010641:Phenotype; D011218:Prader-Willi Syndrome / Q000196:embryology / Q000235:genetics / Q000503:physiopathology*; D011627:Puberty