Creative madness

Consider a brick. What can you do with it?

Your answer to that question can be a measure of how creative you are. Örjan de Manzano, a PhD student at the Karolinska Institutet in Stockholm, is using the query to explore the potential neurological link between creativity and psychoses.

Highly creative people and those with mental disorders are usually better at seeing novel connections between ideas or objects—at thinking laterally. But creative people also have a slightly higher familial risk of developing disorders such as schizophrenia and bipolar disorder. De Manzano is probing dopamine receptors scattered throughout the brain that may point to a molecular link between madness and creativity.

What’s the molecular explanation for why creative people are more prone to psychoses?

De Manzano sought a correlation between the density of dopamine D2 receptors—which control neural signaling—and creativity by studying positron emission tomography (PET) images of 13...

His experiments looked like something out of a bad science fiction movie: de Manzano had each participant wear a plaster helmet, so that their heads wouldn’t move while they filled out the personality questionnaires. “It’s almost like a 1950s kind of hairdryer,” says Yale University psychiatrist Philip Corlett, who helped select de Manzano’s resulting paper (PLoS ONE5(5): e10670, 2010) as one of Faculty of 1000’s Hidden Jewels.

“I saw an opportunity to go beyond just reporting a correlation,” de Manzano says, to explain how different densities of dopamine D2 receptors in specific brain regions make an individual tend towards more creative thought processes—what he calls “the creative bias”—and how this affects imaginative thinking and symptoms that resemble psychoses. De Manzano’s new insights were made possible with a new kind of radionuclide tracer that could penetrate a variety of brain regions to label dopamine D2 receptors.

Disruptions in dopaminergic function had previously been linked to schizophrenia, but neurologists seeking shared molecular roots behind creativity and psychosis had focused only on the part of the brain called the striatum. De Manzano’s new method—which labels D2 receptors in a brain region called the thalamus, outside the striatum—showed that more creative people had a relative lack of the receptors in an unexpected locale. The results suggest that dopaminergic perturbations in the thalamus, rather than the striatum, are at play in shaping creativity, and de Manzano suspects that the mentally ill may have similar receptor patterns. Searching for molecular signatures of creativity and mental illness only in the striatum was like “looking for your keys under the lamp post,” says Corlett.

De Manzano’s colleagues were surprised to see so much come out of the study. “This was only going to be exploratory work,” de Manzano says. But, as the project developed, “everybody seemed to buy into what I was trying to explain.”

Dopamine D2 receptors constrain communication between brain regions. With fewer of them in the thalamus of creative people, it looked liked inventiveness (and perhaps psychosis) may be a result of too much brain communication. “A certain amount of communication can be a good thing; if one can rapidly shuttle information between brain regions for efficient processing one can be creative,” according to Corlett, but too much “can potentially push one over into a psychotic illness.”

However, it’s not all cut and dried. The tests de Manzano used mostly rely on pencil and paper surveys done in the lab. In one, participants have to name alternative uses for a common object (that brick, for example). But they only measure divergent thinking, just one aspect of creativity. De Manzano is quick to concede that the correlation between the tests and real life creativity is not perfect. Even though there is a link between D2 receptor density and divergent thinking, he says, we still can’t “test whether a person will come to produce great creative achievements.”

Still, De Manzano’s findings might help science understand why psychotic illnesses persist from generation to generation in human populations and how a dearth of dopamine D2 receptors might be evolutionarily advantageous, by lending people a creative edge in problem solving. Corlett says there are lots of explanations in psychiatry for why psychoses persist, but so far they have been largely untestable. “The nice thing about this paper,” Corlett says, is that it tells us “why it might be a good idea to be a little psychotic sometimes.”

The Hidden Jewel describes a recent paper from a less obvious journal, selected by the Faculty.

Interested in reading more?

Magaizne Cover

Become a Member of

Receive full access to digital editions of The Scientist, as well as TS Digest, feature stories, more than 35 years of archives, and much more!
Already a member?