Risk Taking and Substance Abuse

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If the creative act brings satisfaction and fulfillment, why do creative people often have affective disorders such as depression? In addition to having a high prevalence of affective disorders, creative people, especially writers, composer-musicians, and fine artists, have a very high rate of substance abuse, such as alcoholism (Post, 1994, 1996). As I mentioned in the chapter on neurotransmitters (chapter 8), although creative people often go through many trials and tribulations to accomplish creative endeavors, creativity itself probably does not induce affective disorders, but rather the people who are creative probably have some of the anatomic, physiological, or neurotransmitter abnormalities that induce affective disorders. Although people who have affective disorders might use drugs as a form of chemical self-treatment, independent of this possible relationship between drugs and affective disorders, the same brain anomaly that makes people susceptible to drug abuse might serve to enhance curiosity, risk taking, and creativity. For example, studies of large cohorts of college students found that the students who use marijuana tend to be novelty seeking and more creative than the students who did not use this drug (Eisenman, Grossman, & Goldstein, 1980).

The mechanism underlying the relationships between substance abuse, novelty seeking, risk taking, and creativity has not been determined. One hypothesis, however, is that drugs enhance creative performance, but studies of creativity under normal states versus intoxicated states do not reveal that drugs enhance the production of creative works (Lang, Verret, & Watt, 1984). As I mentioned, depression might not enhance creative production, but it might be important in creative inspiration and innovation. A second possible relationship between drug abuse and creativity is that creative inspiration often takes place when people have reduced arousal, and some drugs such as alcohol and marijuana reduce arousal. Hence, although these central nervous system depressants probably do not help creative production, these depressant drugs might help creative innovation. There is, however, a third possibility. Independent of these drugs' effects on arousal, it is possible that creative people are prone to addiction and that the same brain mechanisms that make some creative people prone to addiction also enhance their curiosity and propensity to take risks, both important in the creative process.

Drug addiction often interferes with the external rewards that life and work bring to people. Thus, the use of drugs is not an externally driven behavior (exo-incentive), but is an extreme example of internally driven behavior (endo-incentive). Cloninger, Svrakic, and Przybeck (1993) presented a psychobiological model of personality that includes three temperaments or character dimensions. One of these dimensions is novelty seeking, and creative people would have to be considered novelty seekers. Several investigators have found that people who have a strong desire for novelty (high novelty seekers) are at increased risk for drug abuse when compared with low novelty seekers. There is some evidence that exposure to novelty activates, at least in part, the same neural substrates that mediate the rewarding effects of drugs of abuse (e.g., alcohol). The system that has been thought to be important in mediating reward is the mesolimbic dopamine system (Bardo, Donohew, & Harrington, 1996). A portion of the mesolimbic dopaminergic system (see Figure 9.1) projects from

Substrate Nigra Dopamine
Figure 9.1. Diagram of the dopaminergic-basal ganglia systems. The substantia nigra sends dopaminergic neurons to the putamen and caudate. The ventral tegmental area sends dopaminergic neurons to the ventral striatum and to the cortex.

the midbrain to the nucleus accumbens, and this nucleus is a portion of the ventral striatum, which I describe in more detail later. The ventral striatum and its connections to the limbic system (e.g., amygdala) have been posited to be critical for alcohol addiction. Tupala and coworkers (2001) evaluated the densities of dopamine receptors and transporters in the nucleus accumbens of postmortem human brains of people who had a history of alcohol abuse, and they compared these brains with those of healthy controls. These investigators found in the brains of the alcoholic individuals that the mean number of dopamine receptor sites in this portion of the ventral striatum and in the amygdala was lower than that in the brains of the control individuals. These results indicate that dopaminergic functions in the ventral stria-tum may be abnormal among people who abuse drugs, such as alcohol. Novelty has been shown to enhance the firing of these dopaminergic neurons (Saigusa, Tuinstra, Koshikawa, & Cools, 1999), and curiosity is the search for novelty. These results suggest that people with alcohol or drug addiction might also use novelty as a means of stimulating the dopaminergic neurons because they find this stimulation is highly rewarding.

Dulawa, Grandy, Low, Paulus, and Geyer (1999) reviewed and summarized the reports that demonstrated reward is related to an increase in the activity of the neurotransmitter dopamine. They also reviewed the evidence that in animals, dopamine modulates the degree of exploratory behaviors. Patients with Parkinson's disease have reduced production of dopamine, and patients with Parkinson's disease report diminished responses to novelty. Some, but not all, studies have even reported that polymorphisms of the human dopamine D4 receptor (D4R) gene are associated with personality inventory measures of the trait called "novelty-seeking" (Schinka, Letsch, & Crawford, 2002). To explore a potential role for the D4R in behavioral responses to novelty, Dulawa et al. (1999) evaluated D4R-knock-out (D4R-/-) and found that these mice were significantly less behaviorally responsive to novelty than D4R+/+ mice, with the largest phenotypic differences being observed in the novel object test.

Although there is a high incidence of substance abuse among some creative disciplines, there is a relatively low incidence in other disciplines. In addition, in every discipline there are people who have no problems with addiction. The reason why certain disciplines have a higher rate than other disciplines might have to do with the demands of the discipline rather the relationship between drug addiction and creativity. For example, if a writer takes several days or weeks off from writing or is sober just 4 hours a day and writes during that time, he or she still might be a productive novelist. In contrast, in medical research, where there are many physicians who perform research, the excessive use of alcohol or other drugs of addiction would interfere with job performance, and when physicians have substance abuse they often must undergo treatment before they are allowed to continue their professional duties. This explanation, however, cannot explain why there are many creative and productive authors who do not have problems with substance abuse. Although the reason for this is not entirely known, it is possible that to some degree there is a reciprocal relationship between the systems that mediate endo-incentive and the exo-incentive drives. Many of the people who have wealth and fame but are not extremely creative might be primarily motivated by the exo-incentive systems. In contrast, those who are very creative but have trouble with addiction might be primarily motivated by the endo-incentive system. Finally, those who are creative but do not have a problem with addiction might have a balance between these systems.

Creative individuals are explorers who discover new ideas, but explorers must take high risks. Following in the footsteps of people who are already successful is generally a low-risk behavior that can provide a sense of security and a feeling of contentment. In contrast, exploring new territories and ideas carries the risks of rejection and failure, but a successful exploration or creation brings euphoria and joy.

Sternberg and Lubert (1995) studied the relationship between risk taking and creativity. They studied risk taking in people by having them engage in a game in which the participants selected from activities: They could perform an operation that, if successful, had high payoff but also had high risks for failure or an operation that had a lower payoff but also had a much lower risk. These investigators found that, in general, creative people would engage in the high-risk, potentially high-reward operations and less creative people would select the low-risk operation.

In my book Matter of Mind, I tell the story of young woman whom I had the opportunity to examine during one of my visiting professorships. This young woman was raised in an urban ghetto in a large northeastern city. Throughout elementary, middle, and high school she was an excellent student who was admitted to a highly selective college and was awarded a full scholarship. She did well in college, with a high grade-point average, and she had a steady boyfriend whom she was planning to marry after she graduated. She engaged in no high-risk behaviors, including drug abuse. In the second semester of her junior year of college, she started to engage in high-risk behaviors, including using drugs such as cocaine and engaging in sexual promiscuity. She developed pneumonia and, when she was admitted to a hospital, she was found to have AIDS. She also had amenorrhea and, when this was evaluated, she was found to have a very large pituitary tumor that was compressing the orbitofrontal cortex and the ventral portions of her medial prefrontal cortex (see Figure 9.2).

Figure 9.2. Diagram of a patient's pituitary tumor that is encroaching on the orbitofrontal and medial frontal regions.

Pituitary Tumor

Orbitofr Lobe

Pituitary Tumor

Orbitofr Lobe

Figure 9.2. Diagram of a patient's pituitary tumor that is encroaching on the orbitofrontal and medial frontal regions.

Bechara and coworkers (Bechara, Tranel, Damasio, & Damasio, 1996; Bechara et al., 1997) used a gambling card game to study patients with ventromedial prefrontal injuries. This game is in some ways similar to the game, used by Sternberg and Lubert (1995), that I mentioned previously. The participants picked cards from different stacks and, depending on the card they selected, they either won or lost money. There were stacks of cards that had small or moderate rewards with very small risks, versus a stack that had larger rewards but also very heavy risks that outweighed the potential to earn more. If the participants avoided this latter stack, they would have earned more money when the game was completed. These investigators reported that patients with orbital and medial prefrontal lesions, unlike the normal individuals, continued to select cards from the high-risk deck.

The reason injury to the orbital and medial prefrontal cortex (OMPC) increases the propensity to engage in risky behavior is unclear, but an understanding of the connections of these areas might help. For those who would like details about the anatomy of these areas, I recommend a review of the article by Ongur, Ferry, and Price (2003). The orbital and medical aspects of the OMPC receive different projections, but these two areas are strongly interconnected. The orbitofrontal cortex receives input from almost all areas of the posterior sensory association cortex. Both portions of the OMPC receive input from portions of the limbic system, such as the amygdala, that are known to play a special role in mediating emotions. Thus, in the OMPC there is a convergence and integration of sensory-cognitive information with limbic-emotional information. Olfactory and gustatory inputs also converge in the orbitofrontal cortex together with input from the parts of the brain that monitor the internal milieu of a person's body (visceral afferents).

The convergence of information from the sensory association cortex with visceral afferent stimuli (seeing food and learning that ingesting this food can induce satiation) allows an organism to code the identity of stimuli that have rewarding properties. Thus, Schultz Tremblay, and Hollerman (1998) suggested that the OMPC is part of a circuit that includes both the ventral striatum and the mesolimbic dopamine system, and that this circuit is important in reward. The nucleus accumbens, which is part of the ventral striatum, receives projections from portions of the OMPC and sends projections to the ventral pallidum. The ventral pallidum projects to the medial part of the medial dorsal thalamus, which in turn projects back to the OMPC. The ventral striatum also receives dopaminergic projections from the mesolimbic dopamine system. The cell bodies of this ascending dopaminergic system are in the ventral tegumental area of the mesencephalon. Animals will continually perform behaviors that are associated with stimulation of this dopaminergic-ventral striatal system, demonstrating the importance of this system in reward-guided behavior.

Portions of the OMPC are also closely connected with the hypothalamus, which controls the autonomic nervous system and portions of the endocrine system. Bechara et al. (2000) measured changes in skin conductance induced by sweating (galvanic skin responses) while participants played the card game that measures risk-taking behaviors. These investigators found that before normal participants made a decision to perform a high-risk move, their palms sweated, suggesting that the participants activated their autonomic nervous system. In contrast, their patients with OMPC injury, who repeatedly performed high-risk behaviors in this card game, did not develop a robust skin response before they performed a high-risk behavior.

These results are consistent with what Damasio (1996) called the "somatic marker hypothesis," and this somatic marker hypothesis is, in some respects, similar to James' (1890) visceral feedback theory and Schacter and Singer's (1962) attribution theory. These theories suggest that normally when a person is considering performing a high-risk behavior, the brain induces alterations of the internal milieu of the body, including activation of the sympathetic nervous system. It is the recognition of these changes that influences a person's decisions.

On the basis of the information I reviewed earlier, we can see that people, even in the absence of known brain lesions, who have a propensity to take risks, including extremely creative people, might have a OMPC-ventral striatal system that is different from people who are not risk takers. I previously mentioned the relationship between creativity and substance abuse, and I mentioned that people with a propensity for substance abuse might have aberrant functioning of their ventral striatum, including the nucleus accumbens. I also mentioned that creative people also have a propensity to be depressed. Functional imaging studies of depressed people have revealed abnormalities in portions of the orbital-medial prefrontal-ventral striatal circuit (Drevets et al., 1992). Drevets and coworkers also showed that a portion of the ventral medial prefrontal cortex is 40% smaller in depressed patients than in controls.

Taken together, these finding suggest that the relationship between depression, drug addiction, and risk taking, which is so important in creative endeavors, might all be related to an altered function of this orbital-medial prefrontal-ventral striatal-dorsomedial thalamic circuit.

Creative people receive much joy from their creative endeavors, but it not entirely known how the brain mediates positive affective responses to the created stimuli. Recently, Berridge (2003) wrote a review article about the brain systems that might allow stimuli to induce pleasure. The critical system that Berridge discussed in this review is again the ventral striatal circuit, including the shell of the nucleus accumbens. The shell of the nucleus accumbens is connected to the OMPC, which then projects back to the ventral pallidum, the dorsomedial thalamus, and then back to the frontal lobes. In addition to increasing risky behaviors, lesions in this ventral striatal circuit also appear to induce anhedonia (the loss of the ability to enjoy), and it is this ventral striatal circuit's projections back to the cerebral cortex that might allow people to consciously enjoy novelty and creativity. As I also mentioned previously, like other basal ganglia circuits, this ventral striatal circuit is also heavily dependent on dopamine. The dopaminergic system, and in particular the dopamine D2 receptor, has been implicated in reward mechanisms. This ventral striatal system induces a "reward" when dopamine is released from the neurons at the nucleus accumbens and activates the dopamine receptors.

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