Haig argued that the process of natural selection would favor mutations in the genes of fathers that boost the amount of nutrition babies get from their mothers. The genes might govern the speed at which a fetus grows, or they might make the placenta more aggressive as it penetrates the mother’s tissues.
As fathers passed down these growth-stimulating genes, Haig continued, mothers would benefit from counterstrategies. They might evolve genes that slow the rapid growth of their children, in order to preserve their own long-term health. Moms could also evolve to imprint (deactivate) their copies of the genes that increase growth. Haig’s imprinting hypothesis still generates a lot of debate, but there is now considerable evidence to back it up.
What is particularly remarkable about imprinted genes is that a lot of them play a role in shaping the brain. Some of them, in fact, are active only in the brain. How could the conflict between mothers and fathers play out in our heads? Two evolutionary biologists, Bernard Crespi of Simon Fraser University in Canada and Christopher Badcock of the London School of Economics and Political Science, have been exploring imprinting disorders like Angelman and Prader-Willi syndromes to get some clues. They have come up with a bold idea: Our minds, too, are shaped by conflict between our parents’ genes.
Crespi and Badcock extend Haig’s ideas beyond birth by arguing that imprinting brain genes can influence the behavior of children, and this behavior can be beneficial to mothers or fathers. Mothers have to spread limited resources among all their children, and so favor offspring with moderate demands. If a mother spends all her time nursing and caring for one child, any other children she has will suffer.
Fathers, meanwhile, can boost their reproductive success if they pass to their children genes that cause them to get more resources from their mothers. The children may nurse more, for example, or demand more attention. Imprinting and silencing those genes can benefit mothers, because they can blunt the demand. Fathers could also silence brain genes for their own evolutionary benefit.
Each of these new adaptations is like a tug in the tug-of-war between parents. Under normal conditions, each tug can bias a child’s behavior only a little toward one parent. But sometimes mutations arise that disable entire genes from one parent. It is as if one of the parents suddenly let go of the rope and it flew toward the other side.
Angelman and Prader-Willi syndromes arise from mutations to imprinted genes—and they alter behavior in just the ways Crespi and Badcock would predict. In Angelman syndrome, the mother’s genes are silenced, allowing the father’s genes to act without any restraint. Children with Angelman try to nurse more than average children do. The smiles and laughter that are associated with Angelman may also come from attention-grabbing strategies encoded by paternal genes.
Prader-Willi emerges from an opposite breakdown, in which the father’s DNA in the same segment of chromosome 15 is deleted. Many symptoms of Prader-Willi make sense as exaggerated versions of strategies that benefit mothers. Babies with Prader-Willi syndrome make few demands on their mothers—so few that they risk starving themselves. Only after they finish weaning does their insatiable hunger emerge.
Crespi and Badcock have identified several other imprinting disorders that have a similar mother-father symmetry (including Klinefelter’s syndrome, in which the body contains one or more extra copies of the X chromosome). What is striking about them is that the father-leaning disorders tend to produce autistic symptoms, while the mother-leaning disorders tend to produce schizophrenic ones. It is possible that autism and schizophrenia themselves are partly the result of conflicts between parental genes, Crespi and Badcock say.
Children with autism, which shows signs of being a father-dominated imprinting disorder, are more likely to have had placentas that grew aggressively in the womb, for example. Schizophrenia appears to be influenced by mother-dominated genes, some studies associating schizophrenia with low birth weight and slow growth, both of which can benefit mothers.
One of the most striking contrasts between autism and schizophrenia is how they affect the ability to understand others. Autistic people have a difficult time figuring out what other people are feeling. Schizophrenic people, on the other hand, sometimes do too good a job. They may come to believe that a refrigerator is talking to them, for example, or that people are conspiring against them.
Crespi and Badcock propose that these symptoms result from the genetic conflict. Empathetic children can see how frazzled they’re making their mothers and how much attention their siblings need. Maternal genes should therefore boost our abilities to get inside other people’s heads. Paternal genes, on the other hand, may benefit by reducing these distractions from the business of getting more resources from mothers.
What about the rest of us? “Between these extremes would sit normal cognition,” Crespi and Badcock say. The same conflict that gives rise to autism and schizophrenia may be at work in all of us, nudging us one way or another on the spectrum from father-brain to mother-brain.