Free Do Fathers Matter?: What Science Is Telling Us About the Parent We've Overlooked by Paul Raeburn Page A

injection of evolutionary biology.
    One of the reasons I find Haig’s and Crespi’s work so interesting is that it forces us to rethink what it means to be a human being. The traditional view was that an individual was “something that cannot be divided,” but now the individual is divided. “If our genes disagree amongst themselves, I think the self is the arbiter among all these competing agendas,” Haig told me. The body is not a machine. Instead, we’re each organized “more like a social entity, with internal politics and agents with competing agendas.” And this clashing of agendas inside us might even be something we can see. We hesitate over decisions. We decide whether to cooperate or compete, or waver between immediate gratification and long-term planning. Maybe what we’re seeing and feeling in these situations is the settling of scores among our competing genes.
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    Alexander Baker’s father Thomas, wrote to me after our visit. He was optimistic about new research that could point the way to a cure—or at least a partial cure—for Angelman syndrome. He was referring to work done by Benjamin Philpot and colleagues at the University of North Carolina. Researchers now know that Angelman syndrome is caused by the deletion or mutation of a maternal gene called UBE3A . As I’ve noted, the gene is expressed in the brain only if it’s inherited from the mother. Fathers pass along a copy of the gene, too, but it is silenced in the child’s brain. What if the father’s copy could be turned on? Would it do the job of the missing maternal gene, and restore Alexander and others to something much closer to a normal life?
    Philpot screened various chemical compounds, using neurons from mice, and he found a dozen that could activate the dormant paternal Ube3a gene as a backup to replace the mutated maternal copy. He also determined how the compounds worked. Next, he injected them into live mice, and he found that the paternal gene was activated in parts of the brain and spinal cord. And it remained active in spinal cord neurons for twelve weeks after he stopped administering the drug. Scientists are often reluctant to draw too many conclusions from animal research, so I was surprised to see that Philpot himself was also optimistic about the potential of his research. Philpot cautioned that drugs such as the ones he studied can have harmful effects elsewhere in the genes or the body, and it will take a while to sort that out before human trials can begin. If the drugs also affect the genes related to Prader-Willi syndrome, they could flip a child with Angelman to Prader-Willi, not a good outcome.
    Nevertheless, this is an exciting development. One of the drugs Philpot studies is already approved for a kind of meningitis, which is a huge advantage. When the FDA approves a drug, doctors are generally free to prescribe it however they wish. That means that Philpot’s drug can be legally prescribed to children with Angelman without years of studies to seek FDA approval. If Philpot is successful, the research could lead to similar treatments for other diseases of imprinting.
    Nature has left us with these unusual genes that don’t have working backup copies. But the backup copies are still there, and if researchers can find a way to turn them on safely, many of these diseases could be alleviated, or possibly cured. The discovery of imprinting and the theories to explain it show that fathers’ genetic contributions to their children are far richer and more complex than we might have guessed. As we will see in the next chapter, the influence of fathers on their children continues during pregnancy. It’s a time when fathers and their fetuses seem to have no discernible tie, but remain closely connected.

 
    THREE
    Pregnancy : Hormones, Depression, and the First Fight
    If there was any point in a family’s life when we’d think fathers don’t matter much to children, it might be during pregnancy and