Overstepping your Passion? The Science of Obsession

by Carrie Sha

The famous late nineteenth-century writer Franz Kafka once counseled, “Follow your most intense obsessions mercilessly.” Although his advice seems to be a simple call for following our passions, it can easily lead us astray. After all, Shakespeare’s Hamlet was haunted by “what dreams may come after we have shuffled off this mortal coil,” Oscar Wilde’s Dorian Gray was tormented by his fear of losing beauty, and F. Scott Fitzgerald’s Jay Gatsby was destroyed by his preoccupation with wealth and the past. Thus, obsession causes us to lose control, such that we hurt those we love, have unwanted sexual thoughts, and are driven by our need for perfection. The fast-paced, competitive 21st-century environment forces us to further question the wisdom of his words. But before we can pass judgment on the validity of Kafka’s advice, we must first define this unique phenomenon called obsession.

What is the nature of obsession? Where do we draw the line between passion and obsession? Is obsession a necessity for creativity and dedication or a mental disorder? According to the Diagnostic and Statistical Manual of Mental Disorders, an obsession is “recurrent and persistent thoughts, urges, or images that are experienced, at some time during the disturbance as intrusive and inappropriate, and that cause marked anxiety and distress.” (1) Moreover, “the person attempts to suppress or ignore such thoughts, impulses, or images or to neutralize them with some other thought or action.” (1) On the other hand, passion is “an intense desire or enthusiasm for something; the zealous pursuit of an aim.” (2) Thus, the key difference between an obsession and passion seems to be about control. While obsessive individuals are controlled by unwanted thoughts, passionate individuals make deliberate decisions based on their interests.

Since the time of Kafka, advances in medicine and neurobiology have allowed us to map the neural circuitry implicated in many common psychological disorders, including obsessive-compulsive disorder (OCD) and post-traumatic stress disorder (PTSD). Newly developing drugs may enable us to not only understand but also better control these disorders. Yet, the growing understanding of the science behind our compulsions prompts us to question the proper role of obsession in our passions, anxieties, and day-to-day “neuroticism.” So, what exactly can neurobiology tell us about these obsessive disorders and their relationship to “normal” psychology?

When Careful Becomes Compulsive: Obsessive-Compulsive Disorder (OCD) 

Evolutionarily, it may seem that double or even triple checking whether the stove is off can have its advantages. Rewind 200,000 years, and this extra attention to danger may be comparable to an early human’s increased sensitivity to the presence of predators around him. By natural selection, the careful survived while the less observant likely did not. Thus, this heightened awareness seems to increase the survival rate of individuals. But what divides the extra careful from the mentally ill? According to the International OCD Foundation, the difference is intensity (3). For example, checking the stove every hour to invalidate recurring fears of the house burning down is a phenomenon of OCD whereas checking the stove once before leaving the house is not.

This intensity is not only excessive but often harmful as well. The roughly 2.2 million Americans diagnosed with OCD exhibit behaviors that seriously undermine their quality of life (4). This common anxiety disorder can be categorized into a cluster of characteristic symptoms: double-checking, contamination, and intrusive thoughts (5). Imagine sitting in class every day terrified that you may accidentally hurt your teacher by dropping a pencil on the floor or having to use the seven minutes before class to wash your hands repeatedly in the bathroom. OCD prevents patients from rationalizing their fears and, by doing so, stands in the way of a healthy, productive life.

But what is the biological basis that shifts carefulness into compulsiveness? What all OCD patients have in common is a change in the orbitofrontal circuitry characterized predominantly by increased cerebral glucose metabolism, or a faster processing of sugars to activate brain processes (6). The orbitofrontal loop shown in Figure 1 draws a pathway from the basal ganglia, a group of nuclei in the midbrain involved with developing habits and forming emotions, to the frontal cortex. Since the basal ganglia is normally associated with developing motor patterns, research suggests that the same structures may be involved in forming repetitive thoughts, one of the hallmarks of OCD (7). More specifically, the fault in the orbitofrontal loop seems to stem from an imbalance of the neurotransmitters serotonin and dopamine, chemicals essential to forming emotions. In an unaffected person, these neurotransmitters are released to create a feeling of euphoria when something good happens. Researchers have modeled the constant “checking” behavior of OCD patients with chemicals that constantly activate both dopamine and serotonin receptors in mice, making them believe that these chemicals are overstimulated in OCD patients (8). Thus, the most common drug treatment for OCD is the use of selective serotonin reuptake inhibitors (SSRIs), which prevent neurons from regaining released serotonin, effectively increasing its extracellular concentration (6). Patients who do not respond to SSRIs (approximately 50 percent  of patients) are given analogous dopamine-targeting treatments (6). Often, these drug treatments are used in conjunction with cognitive behavorial therapy, the most common type of which is Exposure and Response Prevention (ERP) (9). Unlike a typical counseling session, OCD patients are prompted to name their fears and develop the ability to stop coping with these fears by compulsive actions. The combination of drug and cognitive behavioral therapy may ultimately reduce the amount of repetitive, “checking” behavior characteristic of OCD.

A Recurring Nightmare: Post-Traumatic Stress Disorder (PTSD) 

OCD is, of course, only one of a number of anxiety disorders characterized by recurring, obsessive thoughts. Another commonly discussed mental illness defined by a loss of control is post-traumatic stress disorder (PTSD). Normally, the body responds to stress via the “fight-or-flight” response, characterized by a stimulation of adrenaline that allows an organism to quickly decide whether to fight or flee from a potentially life-threatening situation (10). This response helps protect the individual from physical and psychological harm by increasing the speed of response in an emergency situation. However, extreme stress, such as horrendous accidents and disasters, permanently shift victims’ mental states. PTSD patients are obsessed with the event itself, and their minds are on constant replay. Research shows that some of this obsession can be traced to a gene that is responsible for producing stathmin, a protein in the emotional control center of the brain- the amygdala (11). The general fear response is controlled by a balance between the activation of the amygdala with the activation of the frontal cortex and the hippocampus, a midbrain structure responsible for memory formation. Thus, the control of fear is linked to previous experiences. In PTSD patients, there is decreased frontal control, causing the amygdala to become overactive and the patients to be dominated by persistent fear. Recent research attributes this amygdala overactivity to a lack of synapse plasticity, or the ability of neuron connections to strengthen or weaken depending on their necessity (12). This synaptic plasticity may in turn be controlled by an increased transcription rate of brain-derived neurotrophic factor (BDNF), a key protein in forming long-term memories (13). Thus, the altered regulation of BDNF hints that there is an association between the encoding of the memory of the traumatic incident and the constant fear exhibited by PTSD patients. The currently prescribed medications for PTSD patients are sertraline and paroxetine, both SSRIs that interfere with this fear response (14). The similar drug treatments for PTSD and OCD patients further suggest that properly balancing neurotransmitters may be the key to controlling obsessions.

What Now? 

The line between passion and obsession is thin and at times entirely indecipherable. While psychology and neurobiology attempt to provide a clear boundary, we ultimately must decide what, when, and how “obsession” becomes pathological.

Yet, unlike the generations before us, we have the advantages of biological innovations and a greater societal awareness to add onto our innate ability to control our fates.

Carrie Sha ‘17 is a freshman in Thayer Hall.

References

  1. Greenberg, William M. (2013, Sept 23). Obsessive-Compulsive Disorder. Retrieved from http://emedicine.medscape.com/article/1934139-overview#a0101.
  2. Passion. (n.d.). In Oxford English Dictionary. Retrieved from http://www.oed.com/view/Entry/.
  3. International OCD Foundation. (2012). Obsessions and Compulsions. Retrieved from http://www.ocfoundation.org/o_c.aspx.
  4. National Institute of Mental Health (2014). What is Obsessive-Compulsive Disorder? Retrieved from http://www.nimh.nih.gov/health/topics/obsessive-compulsive-disorder-ocd/index.shtml.
  5. OCD-UK (2013). The Different Types of Obsessive-Compulsive Disorder. Retrieved from http://www.ocduk.org/types-ocd.
  6. Menzies et al. (2008). Integrating evidence from neuroimaging and neuropsychological studies of obsessive-compulsive disorder: The orbitofronto-striatal model revisited. Neuroscience & BioBehavioral Reviews, 32, 525-549.
  7. Graybiel, A.M. & Rauch, S.L. (2000). Toward a Neurobiology of Obsessive-Compulsive Disorder. Neuron, 28, 343-347.
  8. Eagle et al. (2014). The dopamine D2/D3 receptor agonist quinpirole increases checking-like behaviour in an operant observing response task with uncertain reinforcement: A novel possible model of OCD. Behavioral Brain Research, In Press.
  9. International OCD Foundation. (2012). Cognitive Behavior Therapy(CBT). Retrieved from http://www.ocfoundation.org/cbt.aspx.
  10. Brown, T.M., & Fee, E. (2002). Walter Bradford Cannon: Pioneer Physiologist of Human Emotions. Am J Public Health, 92(10), 1594-1595.
  11. National Institute of Mental Health (2014). What is Post-Traumatic Stress Disorder (PTSD)? Retrieved from http://www.nimh.nih.gov/health/topics/post-traumatic-stress-disorder-ptsd/index.shtml.
  12. Mahan, A.M. & Ressler, K.J. (2012). Fear conditioning, synaptic plasticity and the amygdala: implications for posttraumatic stress disorder. Cell, 35, 24-35.
  13. Pape, H., and Pare, D. (2010). Plastic Synpatic Networks of the Amygdala for the Acquisition, Expression, and Extinction of Conditioned Fear. Physiol Rev, 90(2), 419-463.
  14. Davidsona, J, Landermana, L.R., Claryb, C.M. (2004). Improvement of anger at one week predicts the effects of sertraline and placebo in PTSD. Journal of Psychiatric Research, 38, 497-502.

Categories: Spring 2014

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