According to the research, infant's tendency to wake up in the night may have been a tactic to make mothers breastfeed more, thus reducing their fertility and limiting the number of siblings that will be born, which in turn improved a child's chances of survival.
Researchers argue that infants that wake frequently at night to breastfeed are delaying the resumption of the mother's ovulation and therefore preventing the birth of a sibling with whom they would have to compete.
It has already been documented that smaller gaps between the births of siblings are associated with increased mortality of infants and toddlers, especially in environments where resources are scarce and where infectious disease rates are high, researchers said.
Professor David Haig from the Harvard University believes that the benefits of delay are such that the selective forces are strong enough to have engendered a significant evolutionary response.
"The duration of postpartum amenorrhoea is a major determinant of inter-birth internals (IBI) in natural fertility populations with more frequent and more intense nursing, especially at night, associated with prolonged infertility," Haig said.
"Natural selection will have preserved suckling and sleeping behaviours of infants that suppress ovarian function in mothers because infants have benefited from delay of the next birth. Maximal night waking can be conjectured to overlap with the greatest benefits of contraceptive suckling," said Haig.
Haig also points out that while less frequent night waking in formula-fed infants is usually explained by the fact that formula is harder to digest, and therefore more soporific, than breast milk, infants who were breastfed but were not nursed during the night slept longer than breastfed infants who were nursed at night.
Attention is also drawn to the sleep of infants with Prader-Willi syndrome (PWS) who often have a weak suck and sleep a lot and infants with Angelman syndrome (AS) who wake frequently at night.
These syndromes are both caused by deletion of a cluster of imprinted genes at chromosome 15q13 but differ in the parental origin of the deletion.
The research was published in the journal Evolution, Medicine, and Public Health.