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Schizophrenia Caused by the Very Genes that Make Us Human

New research suggests that schizophrenia is part of what makes humans, human.
​Image: ​possan/Wiki

​Understanding the whys and what-fors of any sort of disease is a deep enough undertaking—an immune system trying to tear its host apart? rapid-fire assembly lines of cancerous tissue?—but mental illness puts the whole nature of the question in even more extreme relief. We can say cancer is the cost of biological complexity or genetic abundance, and that communicable diseases are just some microorganism or genetic vessel trying to survive and reproduce. But to even vaguely understand things like major depression, bipolar disorder, and schizophrenia? Good luck with that.

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The mental illness question can be further refined to this: as cancer is the cost of human adaptability (in the form of genetic mutation), is mental illness the cost of intellect? We may have suburb cognitive capabilities thanks to deep neurological complexity, but that same complexity fosters the semiregular occurrence of debilitating illness. No free rides.

But it's not quite that easy. There's another side to the question, implicating schizophrenia in particular. This is an illness that's been with humans since the very beginning—when humans became humans—while not really having an analog in other species, even reasonably complex ones. Why has something so disadvantageous to survival (for sufferers, offering an unemployment rate nea​r 50 percent and suicide-attempt rate of near 4​0 percent) persisted in our DNA?

In a new paper published in t​he journal Molecular Biology and Evolution, Mount Sinai researcher Joel Dudley offers the start of an explanation: schizophrenia isn't so much the cost of being human, but is instead directly tied into the exact genes that make us human (and not some other species) in the very first place. In a sense, this is what we are.

The genes that allow for human intelligence are very closely tied to those implicated in schizophrenia

"The prevalence and high heritability [of schizophrenia] together with the fact that schizophrenia traits are not observed in other species gives rise to the hypothesis that the origin of the disease could be linked to evolutionary trajectories underlying human-specific traits such as the development of language or the disproportionately high consumption of energy by the human brain," Dudley and his group write. "It has been theorized that mutations beneficial to human cognitive abilities might have been favored by natural selection but also predispose the risk of schizophrenia."

The task for Dudley and his team was correlating the (only recently) known genomic roots of schizophrenia with what are known as human ​accelerated regions (HARs). HARs are regions of human DNA that are known to have been conserved over the entirety of mammalian evolution. We have them; dogs have them; monkeys have them. The difference is that, in humans, these 49 genes are suddenly way different. They've mutated, become active. HARs are what makes humans, human, and their discovery is still less than a decade old.

The paradox soon becomes clear. The genes (HARs) that allow for human intelligence and, thus, human survival abilities and reproductive successes are very closely tied to those implicated in schizophrenia. So, natural selection selects for these genes rather than against them. From an evolutionary perspective, HARs-with-schizophrenia is better than no HARs at all, and so here we are.

That hardly solves schizophrenia, however, but it points to a deeper understanding of the illness and new, better ways of treating it. Which is a good thing because, at the moment, the best we can really do for the disorder is make it "OK" for some percentage of sufferers, "just bearable" for some more, and basically nothing for the rest. It's a bit like treating cancer with aspirin. It doesn't have to hurt as much, but it's most definitely still there.

Finally, Dudley and co. write, "it would be interesting and valuable to examine the roles of HARs in other psychiatric diseases such as bipolar disorder and autism spectrum disorders as well as other complex diseases." Indeed, we're just at the beginning of this research, which is hopeful just in itself.