Compared to other primates, humans spend a relatively short time nursing, yet take an unusually long time to become adults. An orangutan will suckle its young for seven to eight years, a chimp for about five years; a human mother typically suckles hers for only two. This allows for shorter intervals between pregnancies. Yet long after weaning, human children remain nutritionally (and otherwise) dependent on parents. This unique life pattern may be the result of an evolutionary compromise between the competing interests of mothers, whose “fitness” is measured by how many surviving children they bear, and offspring, whose goal is maximizing access to maternal resources while adapting to a complex social world.
In earlier work, professor of organismic and evolutionary biology David Haig explored the role of imprinted genes—genes that behave differently depending on whether they are inherited through the mother or the father—in mediating the transfer of nutrients between mother and fetus. His research has led him to describe pregnancy as a precariously balanced tug-of-war that may go awry, for example, if the paternal genes controlling the growth of the placenta begin to trump the maternal genes seeking to moderate the flow of resources to the fetus in order to ensure the mother’s future reproductive fitness (see “Prenatal Competition,” September-October 2006, page 18).
Recent evidence suggests that the same selective forces operate within the child’s genome after birth. “I predict that paternal genes of the child will be promoting more intense suckling demands on the mother, and thus longer birth intervals,” Haig explains, while maternally derived genes will do the opposite. If for some reason the imprinted genes of one parent are under-expressed or over-expressed in the offspring, he hypothesizes, irregularities in the child’s feeding behaviors and growth pattern are likely to result.
To explore his hypothesis, Haig has looked at various rare childhood disorders that may shed light on the genetic conflict underlying the parent-offspring relationship. For example, children with Prader-Willi syndrome—caused by the deletion of a paternal variant of a gene associated with strong suckling—have little or no suckling reflex and often have to be force-fed to obtain enough nutrients in early infancy. Temple syndrome and Silver-Russell syndrome are similarly linked to chromosomal abnormalities favoring maternal over paternal gene expression; children with these diseases also have low appetite, poor suck, and retarded growth. Conversely, Beckwith-Wiedemann syndrome, caused by the over-expression of the paternal IGF2 gene (or the inactivation of the maternal copy of the CDKN1C gene), leads to large infants with oversized tongues and mouths.
The competing effects of imprinted genes continue to influence a child’s appetite and rate of maturation after infancy, Haig believes. Although children with Prader-Willi syndrome begin life as poor feeders, in early childhood they become voracious eaters prone to obesity. “The paternal genes are promoting intense suckling, but they’re also inhibiting the offspring’s desire for alternative foods,” he explains. “When you take these paternal genes away, as in Prader-Willi syndrome, you have infants with little or no appetite for mother’s milk. But later, after weaning, they develop this insatiable appetite, eating everything in sight.” Imprinted genes also appear to play a role in the timing of puberty, with maternal genes favoring earlier onset of many of puberty’s physical precursors.
But Haig cautions that longitudinal studies of children with various imprinting disorders are still needed in order to test his hypotheses. “I believe that these rare childhood conditions are telling us something about how humans’ unusual life-cycle evolved,” he says. “Our slow rate of development is likely an adaptation of offspring to be able to learn about the world in comparative safety while being looked after by mothers. Meanwhile, early weaning is the maternal response, enabling mothers to have shorter birth intervals and thus more offspring.”
