Long childhood is part of what makes humans unique, but this extended developmental stage comes with a cost: a risk of cancer and other genetic diseases.
That much scientists have known. Now an evolutionary biologist has found a case in the scientific literature for explaining these childhood disorders through evolutionary theory, using an approach called Darwinian medicine. The findings of the review, which are detailed today (Feb. 1) in the journal the Proceedings of the Royal Society B: Biological Sciences, may reveal the causes of certain illnesses in children.
The field of Darwinian medicine began in the early 1990s, but "no one had yet applied the principles of this field to children," said Bernard Crespi, the review author, who is an evolutionary biologist at Simon Fraser University in British Columbia, Canada.
By noting how human development differs from that of other primates, one could begin to understand how the distinctive human traits — and their associated health problems — evolved, according to the reviewer. For instance, humans don't become adults until the age of 18. "By primate standards, that's just ridiculous," Crespi said.
The timing of developmental stages results from a tug of war between imprinted genes, which are genes whose expression is controlled by either the mother or the father, depending on which one contributed them. Each parent passes on one form of a gene to the offspring, but imprinted genes are expressed — that is, turned on — in only one of these copies.
These genes can influence mother-child interactions in a way that advances one parent over the other. Imprinted genes that are paternally expressed would intensify the demands on the mother, while maternally expressed genes would lessen the mother's burden.
Imagine, as an extreme example, a household with one mother and four children from different fathers. From a father's perspective, his child should extract as much as possible from the mother to promote the child's own growth and chance of survival at the expense of the three other children.
Although the mother benefits from caring for her offspring, she must save resources for her own survival and future reproduction. So maternally expressed genes should reduce the child's dependence and hasten maturation, leading to early weaning and self-feeding.
Maybe that's good for Mom, but for the child, precocious development could lead to medical conditions such as metabolic syndrome, which increases the risk for stroke, diabetes and heart disease; and polycystic ovary disease, in which women develop cysts that hinder their ability to get pregnant.
The impairment of imprinted genes can disrupt developmental processes and undermine health, Crespi told LiveScience.
As master regulators of cell division and growth, imprinted genes exert a disproportionate impact on health. These genes undergo relatively frequent changes in expression (caused by the attachment of a methyl group to the DNA compound), and, without a working backup copy of the gene to provide different instructions, these changes can precipitate dramatic outcomes.
Damage to these genes is thought to be the underlying factor in disorders such as Silver-Russell syndrome, which causes slow body growth, and Beckwith-Wiedemann syndrome, which leads to large body size and organs. Excessive growth, in turn, is associated with the uncontrolled cell production of cancer. And cancer is the second most common cause of childhood mortality (after accidents) in developed countries, with an incidence of about 1 in 600 in those younger than 15.
Imprinted genes may be the culprit, Crespi said.
To learn more about the origins of childhood illnesses, Crespi encourages further research on the evolutionary basis of child health. "Development is a sequential and cascading process," he said. "What happens even when you're a fetus or a child has huge effects on your health when you're an adult."
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