Posted by Nathaniel Comfort on 09/17 at 04:50 PM
Paul Warren Pardus was a sick man. Yesterday, the 50-year-old Northern Virginia resident became deranged while talking with his mother’s physician on the eighth floor of the Nelson Building at Johns Hopkins Hospital in east Baltimore. He pulled out a semi-automatic pistol from his waistband and shot the doctor in the abdomen, then barricaded himself in his mother’s hospital room, shot her in the back of the head and himself in the mouth.
It is appalling that such violent crime makes its way into a hospital. And yet, Hopkins Hospital, like many academic teaching hospitals, is located in a decayed inner-city neighborhood where some of our worst social problems are endemic. The Baltimore Sun called the area “crime-plagued.” Many would say the incident was not a crime so much the manifestation of illness.
The hospital was almost eerily well-equipped to handle this tragedy. Security isolated the room and the floor from the rest of the hospital, ensuring a minimal disruption of medical services. The physician who was shot was an elevator ride from Emergency, where he was immediately treated. A full recovery is expected. The hospital remained in operation during the crisis and within a couple of hours was back to full, normal activity. The city police and SWAT teams arrived and turned the medical campus into a police state for the afternoon—I had to duck under yellow tape to retrieve my bicycle—but by the time they had all that in place the crisis was past. Really, the moment was medical, not military.
There are two ways to frame violence medically. First is as a public health problem. Modeling murder epidemiologically implies a statistical, population-based approach. First, identify the vector. Is it guns? The drug trade? Poverty? Racism? Then try to trace the spread of the disease back and identify its sources. A 2003 study found that more than half the guns recovered from crimes were traced to one percent of gun dealers; shutting down one of those dealers in Milwaukee reduced local handgun crime by 96%. Public health approaches imply preventive medicine, which is logical enough given that the “symptoms” of gun crime are death and serious injury. On this level gun violence is over-determined. Weapon availability, drugs, poverty, and other causes all explain it.
A more clinical approach frames the violence itself as a disease, rather than as a crime. If you believe in scientific explanations, mental illness must be caused by a chemical imbalance in the brain: it’s either that or spiritualism. (Again, it is overdetermined: being caused by a chemical imbalance does not mean it wasn’t caused by, say, being beaten as a child.) And, in the modern genomic age, biochemical explanations boil down to genes. What genes were up- or down-regulated in Pardus’s brain? What transmitters were inhibited? What receptors were blocked such that normal social inhibitions were released, permitting him to behave in such a tragically deviant manner? Violence-as-disease today invokes medicine-as-molecular-biology.
Medical genetics and crime have a long shared history. As far back as the teens, medical eugenicists proposed genes to explain antisocial behavior from murder to robbery to prostitution. From there, medical-genetic explanations of crime have become more precise and mechanistic. In the 1960s, violent criminal behavior seemed to be pinned to a whole chromosome: the Y. Specifically, presence of an extra Y chromosome was (essentially spuriously) linked to violent crime; a few years later, a follow-up study to test the hypothesis came under fire by the scientist-activist group Science for the People. In the ‘90s, the so-called Violence Initiative sought to reopen the question of the genetic basis of criminal behavior in a more dispassionate context, but was shot down as deterministic and possibly racist.
Since then, a number of genes have been shown to associate with criminal behavior. The best-known is the gene that encodes monoamine oxidase A (MAOA), an enzyme that regulates intercellular levels of neurotransmitters. A widely cited study published in 2002 found that people carrying a variant of the gene that resulted in lower-than-normal levels of MAOA were more likely to commit violent crimes than those with the wild-type variant. The likelihood of violence increased further among those who both carried the low-activity variant and experienced violence in childhood, suggesting gene-environment interaction. Researchers speculate that high MAO activity may promote “trauma resistance.” MAO inhibitors are often used as antidepressants.
Medicalization is a well-pondered phenomenon. But in the genome age, it creates a strange new tension. The paternalism it has always implied—we will take away your liberty for your own good, to make you well—transduces into determinism: your symptoms emerge not from your choices but from your biochemistry. One implication of medicalization today is that medical treatments tend to reduce to pharmacology. When you make the problem a chemical one, the solution will tend to be chemical as well. Not always, of course—sometimes a genetic explanation suggests a change of environment. But the tendency is to keep the solution on the same level of analysis as the problem. For one thing, there are big economic incentives to pharmaceutical solutions.
The disturbing implication, then, is that Mr. Pardus was in fact in exactly the right place. The doctors simply didn’t diagnose him in time.
Jacobs, Patricia A., M. Brunton, M. M. Melville, R. P. Brittain, and W. F. McClemont. “Aggressive Behavior, Mental Subnormality and the XYY Male.” Nature 208 (1965): 1351-52; Steinfels, M. O., and C. Levine. “The XYY Controversy: Researching Violence and Genetics.” Hastings Cent Rep 10, no. 4 (1980): Suppl 1-32.
Allen, Garland E. “Modern Biological Determinism: The Violence Initiative, the Human Genome Project, and the New Eugenics.” In The Practice of Human Genetics, 1-23. Dordrecht: Kluwer, 1999.
Caspi, A., et al., “Role of Genotype in the Cycle of Violence in Maltreated Children.” Science 297, no. 5582 (2002): 851-4. See also Brunner, H. G., et al., “X-Linked Borderline Mental Retardation with Prominent Behavioral Disturbance: Phenotype, Genetic Localization, and Evidence for Disturbed Monoamine Metabolism.” Am J Hum Genet 52, no. 6 (1993): 1032-9.
Illich, Ivan. Medical Nemesis : The Expropriation of Health. 1st American ed. New York: Pantheon Books, 1976.