One very promising framework for understanding the creativity-psychopathology connection is the shared vulnerability model (Carson, 2011). As suggested by the title the model wasn’t propounded just with schizophrenia in mind; it applies to all expressions of psychopathology which have demonstrated a veritable connection to creativity (i.e. the schizospectrum disorders, the bipolar spectrum disorders, and the alcohol abuse disorders). Nonetheless because the scope of the prospective study is narrow and doesn’t cover mood disorders or alcohol dependence at all only elements and aspects of the model specific to the creativity-schizospectrum association will be discussed.
Though still in its infancy the shared vulnerability model has profound explanatory powers, accounting for a consistent body of evidence which illuminates an overlap between psychotic and positive schizotypal traits and creativity, as well as an inverse correlation [or no correlation] between creativity and full-blown schizophrenia (Thys et al., 2014). Creativity and schizophrenia sometimes appear as disparate and mutually exclusive phenomena; there are healthy individuals who live their entire lives engaged in some transcendental creative “flow” without ever suffering from psychiatric illness, and conversely, chronic sufferers without a creative bone in their bodies. The model provides a feasible explanation for this curiosity. It also accounts for the inverted U pattern theorized to exist between schizospectrum disorders and creativity, with creative cognition and expression peaking in first-degree relatives of individuals with fulminant schizophrenia (Kyaga et al., 2013; Kyaga et al., 2011).
Psychosis and creativity share polygenetic roots and in that capacity may be opposite sides of the same coin. Even though historical novelties and perceptual excesses like hallucinations and delusional ideas seem like incongruent phenomena after they’ve emerged into conscious awareness, evidence from molecular biological studies indicates that they may irrupt from a mutual place. Put differently, they may be by-products of the same underlying mental process. According to Carson, nature bequeaths individuals with this genetic loading three shared vulnerability traits–the quality of novelty-seeking; the quality of neural hyperconnectivity, or a propensity for making cross-sensory associations; and sensitivity or “vulnerability” to bandwidths of information not normatively available for appraisal. Indeed, in individuals without the genetic loading this “fringe data” is tagged as irrelevant to survival and relegated to the unconscious before it can come anywhere near the threshold for awareness. Of course for individuals with these shared vulnerability traits the privilege of experiencing perceptual excesses and enhanced access to extraneous stimuli [also called attenuated latent inhibition] is counterbalanced by increased risks for disorganized thought and decompensation. The greater the metacognitive control, the greater the likelihood that larger bandwidths of novel data will be held in working memory as to foster creative insights without ever becoming confused and overwhelmed. Hence executive monitoring of enhanced access is a protective cognitive trait against decompensation. Carson breaks down this trait into three individual factors–high IQ, cognitive flexibility, and enhanced working memory capacity. Research indicates that all three are influential in flipping the coin from creativity to psychosis or flourishing to languishing, and vice versa.
Shared vulnerability factors include neural hyperconnectivity, preferences for novelty, and attenuated latent inhibition. The first of these, hyperconnectivity, proposes that atypical linkages of morphological brain structures not functionally connected confer the neural processing power necessary to make cross-sensory mappings and link seemingly disparate qualities such as colors and sensations or the letter P and the chime of a bell, a feature of metaphor and creativity (Mednick, 1962). Interestingly, enhanced crosstalk between specific cortical regions due to excess structural connectivity has been observed in neuroimaging studies of individuals who perceive the cosmos in an abstruse way. The percepts of individuals with this neurological condition are characterized by cross-modal sensory associations where one idiosyncratic stimulus, the inducer, elicits an ancillary event, the concurrent (Grossenbacher & Lovelace, 2001).
This condition is called synaesthesia and comes in innumerable forms: spatial-sequence, the perception of spatialized numbers; color-taste, with taste localized in the mouth; and grapheme-color where color photisms are projected into three dimensional space. In another subtype called mirror-touch synaesthesia seeing another person being caressed elicits corresponding tactile hallucinations. Synaesthesias can be perceptual or conceptual in nature, and an individual can have more than one type (Blom et al., 2012). Even though disputation exists pertaining to which of the proposed neurological models (cortical disinhibition or hyperconnectivity) better accounts for their emergence, the preliminary evidence garnered thus far from structural MRI and fMRI studies does imply cross-activation through hyperconnectivity in at least some synaesthetic variants. Grapheme-color synaesthetes, for instance, have larger cortical volume in the right and left anterior fusiform gyrus (Jancke et al., 2009) and increased structural connectivity in the right inferior temporal cortices, the motor cortex, and the left superior motor cortex when compared to nonsynaesthetes (Rouw & Scholte, 2010).
Synaesthesia occurs in higher incidence amongst those involved in the creative occupations –musicians, artists, and novelists (Cytowic & Eagleman, 2009). Such persons have an eye for resemblances and penetrating to hidden similarities behind the apparent dissimilarities perceived at the surface level. They are also more adroit than nonsynaesthetes in making metaphors and in the use of figurative speech. Here, it is worth mentioning that analogy and metaphor have long been construed as a mark of genius and the language of the imagination (Kelly et al., 2007). These phenomenal qualities are readily available to them because of the overabundance of cross-connections amongst conceptual maps of numbers, pitches, faces, and other percepts in their brains. Thus expression of genes responsible for the burgeoning of excessive connections in the brain could mean processing privileges and advantages in creative cognition. When William James (1890) articulated that, “Some people are far more sensitive to resemblances, and far more ready to point out wherein they consist, than others are” he may as well have been alluding to persons with one, two, three, or more types of synaesthesia.
Preliminary research reveals that synaesthesia and creativity go hand in hand. Domino (1989) has previously demonstrated how synaesthetes outperform nonsynaesthetes on creativity measures. Recent studies involving a cohort of fine arts students found that the synaesthetes amongst them scored significantly higher on both the TTCT and Raven’s progressive matrices, an intelligence test, than age-, gender-, and intelligence-matched nonsynaesthetes (Cytowic & Eagleman, 2009). Nonetheless there is a disadvantage to hyperconnectivity; synaesthetic experience may coopt the same neural mechanisms as multisensory hallucinations. Synesthesia and other cross-model percepts are known to occur during release hallucinations (Cytowic & Eagleman, 2009). By the same token individuals with temporal-lobe epilepsy will frequently report hallucinatory voices, visions, out-of-body experiences, and cross-modal percepts during their seizure states (LaPlante, 2000). Excess structural connectivity is not just a feature of hallucinations; it has been observed in the post-mortem brains of individuals diagnosed with schizophrenia and their nearest relatives (Whitfield-Gabrieli et al., 2009). Even though firm conclusions regarding both the relationship between synaesthesia and multisensory hallucinations and the genetic basis of hyperconnectivity are yet to be established, we can safely surmise that alterations to cortical structural and volume are intimately bound with both psychosis-proneness and enhanced creativity.
Carson identifies novelty-seeking as a second shared vulnerability factor (Kaufman et al., 2014). She defines it as a behavioral inclination to explore hitherto unfamiliar elements of an internal or social environment. An individual who espouses preferences for novelty is also likely to be curious about the unknown and motivated by intrinsic rewards rather than social accolades and recognition. These characterological traits are all accurate predictors of sustained creative activity and achievement because they activate the sensitized reward pathway in the brain, the mesolimbic dopamine system. Inevitably, the individual with preferences for novelty realizes that engagement with creative pursuits elicits intense gratification and that this feeling may be sustained by pouring adequate attentional resources into them. In the end, the self-reinforcing reward system may become so inveterate and habitual as to keep the novelty-seeker engaged in the creative endeavor in the face of impediments and criticism.
The creative benefit of novelty-seeking is counterbalanced by occasions where fulfilment of a pleasure principle takes precedence over all else and hijacks the internal reward system, leading to addiction and alcohol abuse (Grucza et al., 2006). Research in molecular biology has linked dopaminergic activity, specifically the A1+ allele of the TAW IA polymorphism of the D2 dopamine receptor gene, to novelty-seeking, schizophrenia, and addiction (Reuter et al., 2006). The identification of these underlying dopamine-related genes was undoubtedly foreshadowed by common clinical scenarios in which roughly 50% of persons with schizophrenia also presented with co-occurring substance use disorders, usually alcohol, cannabis, or both (Green et al., 2007). Mediated by the brain’s internal reward system novelty-seeking is most probably another aspect of shared vulnerability amongst creative ideation and schizophrenia.
Latent inhibition, a type of cognitive disinhibition, is also identified as a vulnerability factor. It is a sensory gating mechanism mediated by the brain which prevents information tagged as irrelevant from reaching conscious awareness (Papworth, 2008). This efficient and adaptive mechanism is necessary because it allows the individual to orientate their cognitive workspace, attention, and processing powers to aspects of the environment that are more pertinent to individual survival. Creativity and creative achievement have both been associated with reduced latent inhibition, convincing Carson that creative minds are, “privileged to access a greater inventory of unfiltered stimuli during early processing, thereby increasing the odds of original recombinant ideation (p. 505).”
Not surprisingly it is also a salient characteristic of susceptibility to psychosis and schizophrenia (Baruch et al., 1988; Lubow et al., 1992). One investigation used psychometric tests of creativity, personality, and latent inhibition on a cohort of alcohol and polydrug dependents and a group of university students showed that psychoticism, originality, and decreased latent inhibition are personality and cognitive traits common to both creativity and psychopathology (Fink et al., 2012). Keri (2009) discovered that a homogenous sample of educated individuals with high IQs who carry the T/T genotype of the promoter region of the NRG-1 gene, a gene previously linked to psychosis risk and altered brain structure, performed exceptionally well on creativity measures. Because the specific polymorphism is known to affect the functioning of a brain region renowned for inhibitory control [the prefrontal cortex], Keri surmised that the peaks in creative cognition could be reflecting decreased thresholds in sensory gating, or decreased latent inhibition.
As previously mentioned Carson (2003) identifies cognitive flexibility, working memory capacity, and IQ as protective or risk factors. The first may be defined as willful engagement with and disengagement from stimuli or aspects of the social environment. On the other hand, fixating upon one particular stimulus and mulling over it from a very narrow frame of reference is called perseveration. Because the stimulus is attended to and interpreted from within a closed system, it is common for perseveration to ensue in faulty reality-testing. Lesion, trauma, oncological studies in clinical neuroscience have attributed volitional switches between deliberate and spontaneous modes of processing information to the ‘zenith higher order structure’ in the functional hierarchy, the prefrontal cortex [PFC] (Dietrich, 2004). Largely intact in the creative individual, prefrontal circuits permit shifts from focused to defocused attentional states, thus allowing unconscious information to be represented and recombined in working memory. Dietrich (2004) has inferred that creative insights are a major consequence of this process. Normative PFC functioning also makes possible the juxtaposition of creative insights with internalized values and belief systems, increasing the odds that an individual will observe and be receptive to common sense truth. As an inhibitory information processor, it enables control over the limitless train of possible ideational re-combinations.
Structural abnormalities in both the medial and dorsolateral PFC along with the anterior cingulate cortex are consistent finds across many neuroimaging studies on individuals who either have fulminant schizophrenia or are psychosis-prone (Jung, Jang et al., 2010). This is saliently reflected on the phenomenal level as an inability to observe, in a nonjudgmental and nonattached manner, the overabundant uprush of delusional and magical ideas into conscious awareness without becoming overwhelmed and suffering decompensation. The dearth of self-relational processing which then sets the stage for faulty reality testing and the interlacing of delusional content into the personal narratives of these individuals is also attributed to prefrontal anomalies (Nelson et al., 2009).Cognitive flexibility, then, is a protective factor against schizophrenia in that it allows individuals with shared vulnerability to take advantage of their enhanced access to a wider bandwidth of novel stimuli without suffering information overload and decompensation.
Working memory is also a higher mental function mediated by the PFC. Novel content cannot be disintegrated and reintegrated into new ideational combinations nor contrasted with task-relevant knowledge in long-term memory storage unless it enters working memory for conscious reflection first. If conscious manipulation is contingent on working memory, then higher capacities in this executive domain should permit the linear processing of larger bandwidths of information afforded by decreased latent inhibition. In a cohort of undergraduates, DeYoung et al. (2008) discovered that aptitude for holding abstract forms in working memory predicted creative problem-solving. Higher working memory capacity is a protective factor against schizophrenia because it allows for rich information generated by cross-modal associations [synesthesia] and decreased latent inhibition to be processed free of disorganized thinking.
Last but not least, IQ level is also theorized to play a substantial role in protecting an individual with shared vulnerabilities from decompensation and synchronously nurturing creative thinking. Carson identifies higher intelligence as a protective factor and lower intelligence as an increased risk for psychosis (Carson, 2011). The connection between indices of creativity (i.e. divergent thinking) and intelligence is not redundant, with studies portending a curvilinear relationship; the latter predicts the former up to a moderate level (Guilford, 1968; Kim, 2002; Runco & Albert, 1985). The existence of this threshold resulted in the phenomenon receiving the label, the threshold hypothesis. Scores in the low range are detrimental to fluid creative ideation, scores in the average or above average range are conducive to it, and anything above 120 is superfluous. Using high-functioning subjects, Carson et al. (2003) showed how up to 30 percent of variance in scores of creative achievement were predicted when attenuated latent inhibition was accompanied by high IQ. Propounded by these results is the notion that the higher IQ brain can better process wider bandwidths of unconscious novel information and is far more resourceful when it comes to manipulating it for possible insights than the lower IQ brain.
To conclude Carson (2014) iterates the rudimentary nature of the shared vulnerability model and its current emphasis on intrinsic [neurocognitive] risk and protective factors for which some corroborating evidence from the fields of genetics, neuroimaging brain research, and molecular biology has been gathered. She intimates that a more veracious and comprehensive version of the model would have to incorporate extrinsic [environmental] factors too, for example the roles of social support, social perception, and expectation, socioeconomic status, geopolitical climate, and pharmacotherapy in the association. Perhaps the prospective investigation can identify some of these additional factors.