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

believe that disruptions of the tug-of-war between imprinted genes in the brain could help to explain the origins of some mental illnesses—from autism to schizophrenia. This theory could also help to solve a long-standing riddle about the genetics of mental illness. Many of these illnesses tend to run in families, but it’s not a question of simple inheritance, like eye color. Once again, the facts collide with Mendel’s laws. Many of the inheritance patterns of mental illness are complex and poorly understood. They don’t follow the usual rules. That suggests that imprinting errors might have something to do with these ailments. If so, an understanding of what’s going on could lead to new treatments.
    According to Crespi, there is already a link. Children with Beckwith-Wiedemann syndrome, the disorder of excessive growth associated with the IGF2 gene, have larger-than-normal brains and an increased risk of autism. Studies of people with autism—but without Beckwith-Wiedemann syndrome—have shown that they, too, can have larger-than-normal brains. “There is a good bit of evidence for overgrowth of the entire body and the brain in autism,” Crespi says. “And there is work that has linked that to IGF2 .”
    Crespi and Badcock then looked at the opposite situation—when a fetus lacks proper expression of the IGF2 genes and is smaller than normal. Would it have a condition that was somehow the “opposite” of autism? People with autism are unable to appreciate what is going on in groups of people around them. They have difficulty understanding what others are thinking. Now imagine individuals with an enhanced sensitivity to social cues, even to the point that they seem to “read into” others’ behavior things that are not happening. Such people might hear voices that are not there—a hallmark of schizophrenia. Crespi and Badcock devised a spectrum of mental illnesses based on their possible connection with imprinting disorders. Autism is at one end of their spectrum, and schizophrenia, bipolar disorder, and depression are at the other end. Crespi and Badcock do not think that imprinting and their mental-illness spectrum explain everything about mental illness. But it is essential, they say, to find all the imprinted genes in the brain, discover what they do, and explore how variations in those genes might be related to psychiatric ailments.
    Crespi also notes that recent findings fit his predictions. In people with schizophrenia, researchers have found reduced activity of three genes that are active when they come from fathers. According to Crespi, a reduction in expression of paternal genes should tip a person toward the schizophrenia-depression end of the spectrum. And that is what happens. Crespi believes that progress in understanding the connection between imprinting and mental illness is moving slowly because psychiatrists are generally not aware of the work of biologists studying imprinting, and vice versa.
    This was an idea that occurred to me often while I was working on this book. Crespi is correct to say that psychiatrists and biologists don’t talk to one an other nearly enough. But it’s also true that psychologists don’t talk to neuroscientists, evolutionary biologists don’t talk to doctors, and epidemiologists don’t talk to sociologists. The story of fathers and their children draws on all these scientific fields, but there is little cross-pollination among them.
    “One of the things that hasn’t been done in the field is to connect across levels,” Crespi said. “You want to connect from the genetic level to the brain-structure level to the psychiatric level.” His work with Badcock is a step in that direction: “It’s bringing together two very different areas—social evolution theory connecting with psychiatry. I think I’m at least getting people to think more about evolutionary biology in the study of autism and schizophrenia.” The field of psychiatry could use a good