Leveraging the “mad genius” debate: why we need a neuroscience of creativity and psychopathology

CitationCarson, Shelley. 2014. “Leveraging the “mad genius” debate: why we need a neuroscience of creativity and psychopathology.” Frontiers in Human Neuroscience 8 (1): 771. doi:10.3389/fnhum.2014.00771. http://dx.doi.org/10.3389/fnhum.2014.00771.

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OPINION ARTICLEpublished: 29 September 2014

doi: 10.3389/fnhum.2014.00771

Leveraging the “mad genius” debate: why we need aneuroscience of creativity and psychopathologyShelley Carson*

Department of Psychology, Harvard University, Cambridge, MA, USA*Correspondence: carson@wjh.harvard.edu

Edited by:

Zbigniew R. Struzik, The University of Tokyo, Japan

Reviewed by:

Rex Eugene Jung, University of New Mexico, USADean Keith Simonton, University of California, Davis, USA

Keywords: cognitive disinhibition, creativity, latent inhibition, neuroscience, psychopathology, shared vulnerability model

In this opinion article, I summarize the so-called “mad genius” debate and suggest away to reframe the issue so that it can ben-efit the field rather than divide it. As othershave pointed out, creativity cannot effec-tively be studied as an overarching entity;it must be broken into smaller pieces andstudied from an individual differences per-spective in order to provide meaningfulresults relating to brain function. I alsotry to frame the infant field of creativity-psychopathology neuroscience, and I endwith the benefits this area of inquiry willprovide.

THE “MAD GENIUS” DEBATECreativity has been described as a humansurvival mechanism that allows both theindividual and the species to adapt to theenvironment in real time (Richards, 1999;Miller, 2001). Creativity is also a sought-after character trait in fields as diverse asbusiness, the arts, science, and sports. Andyet we find there is a long list of high-levelcreative achievers who have suffered fromthe inner demons of psychopathology. Thelist includes such contemporary luminar-ies as comedian Robin Williams, as well asa host of influential creators from the past:Vincent Van Gogh, Robert Schumann,Mozart, Beethoven, Sylvia Plath, VirginiaWoolf, Anne Sexton, Ernest Hemingway,Edgar Allan Poe, Michelangelo, GeorgiaO’Keefe, and Jackson Pollock, to nameonly a few (Jamison, 1993). Mentionsof a connection between creativity andmadness extend back at least as far asAristotle and Plato (Becker, 2000-2001).These anecdotal examples appear to con-tradict the beliefs that creativity is adap-tive for the individual and is, as suggested

by some (e.g., Maslow, 1968; Dietrich,2014), a manifestation of positive mentalhealth.

In addition to anecdotal examples, wesee a growing body of empirical studiesassociating creativity with various forms ofpsychopathology, including mood disor-ders (for reviews, see Johnson et al., 2012;Kaufmann and Kaufmann, 2014), schizo-typal thinking (for a review, see Barrantes-Vidal, 2014), alcohol abuse (Andreasen,1987; Dardis, 1989; Ludwig, 1990, 1992;Post, 1994), and more recently ADHD(Healey and Rucklidge, 2006; Healey,2014) and autism (Pring et al., 2012).These studies appear to indicate thathighly creative individuals are at greaterrisk for certain disorders than are mem-bers of the general public. However, morenuanced research suggests that individ-uals with small doses of psychopathol-ogy, such as those who exhibit low-levelsymptoms or who have inherited part—but not all—of a pathological genotype,are more likely to be creative than eithertheir mentally healthy counterparts orthose with full-blown disorder (Heston,1966; Karlsson, 1970; Richards et al.,1988; Kinney et al., 2000-2001; Abraham,2014; Simonton, 2014). This is oftenreferred to as the “inverted U” model(Richards et al., 1988), or what I calla “dose-dependent” relationship (Carson,2013), of creativity and psychopathol-ogy.

Many (perhaps most) of these stud-ies which have found an associationbetween creativity and psychopathologyhave been criticized for methodologi-cal deficits which question their valid-ity (see Schlesinger, 2009; Sawyer, 2012;

Dietrich, 2014). And so we have a“mad genius” debate, with one sidesuggesting that elements of mental ill-ness may enhance creativity (at leastin small doses) and the other sidesuggesting that the correlation betweencreativity and psychopathology is unsup-ported and that virtually all the studiesthat claim a connection are riddled withmethodological errors.

REFRAMING THE DEBATEThis debate, while divisive, may leadto important advances in the neuro-science of creativity because it calls atten-tion to two problems that need to beaddressed: first the presence (flawed stud-ies not withstanding) of a host of cre-ative individuals with psychopathology,and second, the need for methodolog-ical rigor when investigating the cre-ativity/psychopathology connection. TheWorld Health Organization estimates that450 million people world-wide sufferfrom mental disorders (World HealthOrganization, 2013). Even if rates of psy-chopathology are actually lower amonghighly creative individuals than in the gen-eral population (and we don’t currentlyhave a body of research that corrobo-rates this), it is still the case that thereare a great many individuals (likely mil-lions) who are both creative and who havemental disorders. The question within thefield of neuroscience then should not bewhether creative individuals are at greaterrisk for madness than the general popu-lation; it should be whether creativity andthe creative process are different in the dis-ordered brain than in the non-disorderedbrain.

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Given the importance of creativethought to human survival, it is likely thatthroughout the course of evolution wehave developed a variety of biologically-based strategies to help us solve ill-definedproblems creatively (see Jung, 2014). Whatwe refer to as “creativity” is actually a col-lection of these strategies rather than asingle process or entity. Several of thesestrategies include visualizing outcomes ofan action (mental imagery), generatingmultiple (both original and mundane)solutions to a prompt (divergent think-ing), consciously making comparisons ofbetween two disparate concepts or objects(metaphorical thinking), and putting asidea problem to allow it to incubate until asolution suddenly arrives (insight). Eachof these strategies can be further bro-ken down into component processes,some of which utilize brain networks thatare already understood in terms of theirunderlying neuroscience. For example, weknow that mental imagery utilizes muchof the same circuitry that is used to processordinary vision (Kosslyn et al., 2006). Bycontinuing to study creativity as if it were asingle entity, and by expecting that all sub-jects will engage similar neural circuits tosolve creative tasks, we will only continueto generate conflicting and inconsistentfindings (Arden et al., 2010; Dietrich andKanso, 2010). However, by (1) parsing cre-ativity into smaller components based oncognitive processes (e.g., Abraham, 2013),and (2) looking at neural creative processesthrough the lens of an individual differ-ences approach (including differences inpredisposition for psychopathology) wecan eliminate much of the confusion andcontradictory results in the field.

A NEUROSCIENCE OFCREATIVITY-PSYCHOPATHOLOGYIndividuals with a predisposition to men-tal disorder may utilize different strate-gies, or they may use familiar strategies inunusual ways, to solve creative tasks. Forover a century, knowledge of psychopatho-logical states in the brain has illuminatedour knowledge of normal brain states,and that should also be the case with thestudy of the creative brain. Neurosciencecan approach this study in two ways.First, it can identify genetic variationsthat may underlie both creativity andpsychopathology. This molecular biology

approach is already underway, with sev-eral studies indicating polymorphisms ofthe DRD2 and DRD4 genes (Reuter et al.,2006; Mayseless et al., 2013), the 5HT2agene (Ott et al., 2005) and the NRG1 gene(Kéri, 2009) that have been associated withboth creativity and certain forms of psy-chopathology.

Second, brain imaging work can beapplied to the study of the cognitive mech-anisms that may be commonly sharedbetween creativity and psychopathology.For example, psychologists have long sug-gested that both schizotypal and highlycreative individuals tend to utilize states ofcognitive disinhibition to access associa-tions that are ordinarily hidden from con-scious awareness (e.g., Kris, 1952; Koestler,1964; Eysenck, 1995). Research is revealingthat indeed both highly creative subjectsand subjects who are high in schizotypydemonstrate more disinhibition dur-ing creative tasks than less creative orless schizotypal subjects (see Martindale,1999; Carson et al., 2003; Abraham andWindmann, 2008; Dorfman et al., 2008).However, the neural substrates of cogni-tive disinhibition, as applied to creativity,need to be further studied.

My colleagues and I have found thatcognitive disinhibition (in the form ofreduced latent inhibition) combined withvery high IQ levels predicts extraordinarycreative achievement (Carson et al., 2003).These results have since been replicated(Kéri, 2011). We hypothesized that cog-nitive disinhibition allows a broadeningof stimuli available to consciousness whilehigh IQ affords the cognitive resources

FIGURE 1 | Shared vulnerability model of creativity and psychopathology (adapted from

Carson, 2011).

to process and manipulate that increasedstimuli to form novel and creative ideaswithout the individual becoming over-whelmed and confused. What we did nottest is whether the high creative achieversin our studies exhibited phasic changes inlatent inhibition, or whether their reducedinhibition was more trait-like, as is seenin persons at risk for psychosis. Becauselatent inhibition tasks are compatible withneuroimaging, the study of controlled cog-nitive disinhibition is one area of potentialstudy for the neuroscience of creativity.

Additional areas of study are sug-gested by the shared vulnerability model ofcreativity and psychopathology (Carson,2011, 2013). The shared vulnerabil-ity model suggests that creativity andpsychopathology may share genetically-influenced factors that are expressed aseither pathology or creativity dependingupon the presence or absence of othermoderating factors (see Figure 1). Theshared vulnerability components that havebeen identified, in addition to cognitivedisinhibition, include novelty salience,neural hyperconnectivity, and emotionallability.

Novelty salience is associated with themotivation to explore novel aspects ofideas or objects via the dopamine rewardsystem. Novelty-seeking is associated withcreative personality (McCrae, 1993; Reuteret al., 1995), creative drive (Flaherty,2005), alcohol abuse and addiction (Fryeand Salloum, 2006; Grucza et al., 2006),and with bipolar states of hypomania andmania (Minassian et al., 2011). Brainimaging studies can determine whether

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reward areas (such as the ventral striatum)are more active during creative tasks inindividuals who score high (rather thanlow) on measures of creative achieve-ment as well as in subjects who scorehigh on scales of hypomania. Brain imag-ing studies can also investigate whetheractivation of reward areas and other neu-ral networks varies during creative prob-lem solving with the amount of alcoholingestion.

Neural hyperconnectivity is charac-terized by an abnormal neural linking ofbrain areas that are not typically func-tionally connected. Hyperconnectivityis linked to bizarre associations inschizophrenia (Whitfield-Gabrieli et al.,2009), and has also been noted in bipo-lar individuals (McCrea, 2008). Brainimaging studies detect more alpha syn-chronization, both within and acrosshemispheres, in the brains of high cre-ative vs. less creative subjects, suggesting,perhaps, unusual connectivity (Fink andBenedek, 2014). The exploration of neuralconnectivity in creative but schizotypalindividuals may shed light on the creationof remote associations.

Mood lability is a characteristic ofmood disorders. Changes in mood, espe-cially increases in positive affect, have beenshown to increase divergent thinking innormal subjects (Ashby et al., 1999), whilehighly creative individuals with mood dis-orders demonstrate patterns of highercreative productivity during upswings inmood (Jamison, 1989). However, the neu-roscience of creativity and mood is notwell-explored and presents a ripe area forfurther inquiry.

CONCLUSIONSThe mad genius debate is a polarizingand divisive issue in the field of creativ-ity research. By reframing this debate as aquestion of how individuals with vulner-ability to psychopathology differ in theirstrategies of solving creative tasks fromthose who do not display evidence of vul-nerabilities, we can use the mad geniusissue as an opportunity to promote a sci-entific exploration of creativity and psy-chopathology rather than to polarize thefield.

The implications of the mad geniusdebate for the neuroscience of creativityare threefold. First, the debate emphasizes

the need for, and encourages, an individ-ual difference methodology rather than auniversal one-size-fits-all approach to theneuroimaging of creative tasks. Individualdifferences related to psychopathology,including self-report measures of schizo-typy, hypomania, alcohol use, and cre-ative achievement, can easily be addedto research protocols, and may helpexplain conflicting findings in imagingstudies.

Second, studies that target shared vul-nerabilities related to creativity and psy-chopathology, as well as non-shared riskand protective factors, can illuminate theneural underpinnings of creative cogni-tion that appear to allow some indi-viduals at risk for psychopathology tohave a creative edge. Clinicians who treatcreative populations cite high percent-ages of non-compliance with drug treat-ment because of the negative effects oftreatment on creativity (Flaherty, 2011).Imaging studies may aid in determin-ing which symptoms of psychopathologyare creativity-enhancing and, thus, sug-gest directions for the development ofsymptom-specific drug and psychologicaltherapies that will leave creativity in tactwhile improving quality of life in thosewith associated psychopathology.

Finally, a neuroscience of creativity andpsychopathology may reveal novel strate-gies of summoning the muse that may thenbe employed to assist non-disordered indi-viduals in enhancing their creativity, thusenriching both their own lives and societyas a whole.

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Conflict of Interest Statement: The author declaresthat the research was conducted in the absence of anycommercial or financial relationships that could beconstrued as a potential conflict of interest.

Received: 21 August 2014; accepted: 11 September 2014;published online: 29 September 2014.Citation: Carson S (2014) Leveraging the “mad genius”debate: why we need a neuroscience of creativity andpsychopathology. Front. Hum. Neurosci. 8:771. doi:10.3389/fnhum.2014.00771This article was submitted to the journal Frontiers inHuman Neuroscience.Copyright © 2014 Carson. This is an open-access arti-cle distributed under the terms of the Creative CommonsAttribution License (CC BY). The use, distribution orreproduction in other forums is permitted, provided theoriginal author(s) or licensor are credited and that theoriginal publication in this journal is cited, in accor-dance with accepted academic practice. No use, distribu-tion or reproduction is permitted which does not complywith these terms.

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