One day in high school, Elyn Saks was walking home when she realized that the houses lining the street were sending her messages. “Look closely,” they said, “You are special… especially bad.” During her freshman year at Vanderbilt University, she began to wonder if showers were really necessary; and by her first year in graduate school, she was hospitalized after she became convinced that she was on the verge of killing hundreds of thousands of people with her thoughts.
This is schizophrenia, as recounted in Saks’s memoir, The Center Cannot Hold. A genetically influenced disease, schizophrenia presents itself differently in everyone it attacks, but it is invariably terrifying, and often totally debilitating. Unlike depression, it offers little hope of resolution. And unlike bipolar disorder, which brings periods of euphoria, it appears to have no discernible upside. Which is why scientists find the disease so mystifying. One of the key tenets of Darwinism is that adaptations that work against the survival of a species are destined to disappear. So why does schizophrenia continue to linger on? Could it be that it confers some advantage?
For years, scientists struggled to identify an adaptive advantage that might explain schizophrenia’s persistence. Researchers from various disciplines volleyed ideas back and forth. Some argued that the genes implicated in the disease promoted creativity; others believed that schizophrenics were frustrated cult leaders—unorthodox thinkers constitutionally “engineered” to lead segments of humanity to break off from the herd, but who lacked the charisma to effect much change. None of the theories gained much traction.
New research is pointing to a different possibility: There may be no adaptive advantage provided by schizophrenia in and of itself, but rather from some genes that contribute to the disease. According to a study published in the Proceedings of the Royal Society, there is evidence that some of the gene variants associated with schizophrenia—especially a mutation in a gene called disrupted-in-schizophrenia1 (DISC1)—have been selected for by evolution. This supports the idea that the disease may be a maladaptive combination of mutations that individually have the potential to enhance fitness. It could be a more complicated version of the familiar case of sickle cell anemia: having two mutant copies of a certain gene causes the disease, whereas having only one mutant copy provides protection against malaria.
A recent study headed up by Johns Hopkins University neuroscientists may have found what kind of process goes awry in schizophrenic brains. Researchers found that DISC1 regulates the migration of new neurons in the adult brain. When the levels of DISC1 were reduced in mice during adult neurogenesis, the newborn neurons sped up and overshot their intended targets within the hippocampus, says Xin Duan, a study collaborator. When the neurons finally reached their destinations, they forged an unusual number of connections with neighboring cells, a series of events that might give rise to the abnormal—and quite crippling—brain functions associated with schizophrenia, according to Hongjun Song, a Johns Hopkins neurologist who also worked on the study. It is possible, Song says, that further research will lead to a drug that treats schizophrenia by restoring normal neurogenesis.
So what evolutionary advantage could schizophrenia-related genes bring to people who have some of the genes but not the disease? For now, this remains one of the many open questions about this puzzling condition.