In an apparent first, a study of Finnish convicts has identified genetic variations at two key sites on the genome that may distinguish extremely violent criminals from the rest of us. The two single nucleotide polymorphisms, or SNPs, that appear to predispose an individual to committing acts of repeated or extreme violence may account for as many as 10 percent of crimes, say the authors of the study.
Looking for a genetic basis for violent behavior makes looking for a needle in a haystack look easy. It also raises thorny questions about free will, criminal culpability and the perils of declaring a person dangerous based on biology rather than behavior.
But the impulse to identify genes that might predict or explain violent behavior is hard to crush: We want to know what makes killers different from us, what leads them to unspeakable acts, and how we might pick out such a malignant human in a crowd.
A group of researchers led by Dr. Jari Tiihonen of the Karolinska Institute in Sweden combed through the 19 largest prisons in Finland to recruit 794 prisoners willing to allow sequencing analysis of their genomes in their entirety. Of those, 538 had committed at least one violent crime, including murder, attempted murder, manslaughter, attempted manslaughter or battery. A small subset of that group — 84 men—had been convicted of 10 or more such crimes.
To create a comparison group of non-offenders, the researchers then tapped into several large repositories of study participants, assembling a control group of 11,600 Finnish citizens willing to have their genomes sequenced. The researchers tapped a further group of violent offenders — 114 men serving sentences in Finnish prisons for at least one homicide—to replicate their findings.
The latest research, published in the Nature journal Molecular Psychiatry, identified two sites on the genome that might serve as red flags for extreme violent behavior.
One of those sites programs the activity of the neurotransmitter monoamine oxidase A, or MAOA, and the variation seen more often in violent criminals does so in a way that suppresses metabolism of another brain chemical, dopamine, in the brain. The authors of the study surmised that when a person with this genetic variation is under the influence of alcohol or amphetamine, a common circumstance in the commission of violent crimes, the resulting burst of dopamine in the brain could go unchecked, prompting an unusually high level of aggression.
And because the same genetic variation also indirectly suppresses the activity of the calming neurotransmitter serotonin in the brain’s “fight or flight” circuitry, its downstream effect is to make impulsive aggression more likely, the authors of the study suggested.
Compared to the large control group, those with at least one violent offense conviction were about 70 percent more likely to have the “low activity MAOA genotype,” the study found. But among the extremely violent—those with 10 or more such convictions—the MAOA genetic signal was seen close to three times more often than it was in the comparison population, an “extremely significant” finding, said the authors.
A second set of genetic variations seen more often in violent offenders lay within a gene that codes for neural adhesion protein. Polymorphisms, or variations in that region of the genome are implicated strongly in attention deficit and hyperactivity disorder, or ADHD.
(They are also linked to a wide range of psychiatric diseases, including bipolar disorder, schizophrenia, substance abuse and autism.)
The specific genetic variant in this “CDH13” gene that best separated violent offenders from the broad population governs the production and activity of a protein that plays an important role in building, replacing and connecting brain cells in the amygdala.
The amygdala is a key brain structure for processing fear and other powerful emotions. The authors therefore surmised that people with this genetic phenotype might have a disturbed ability to regulate their strong emotions, and be more prone to aggressive impulsiveness. In the less-frequent instances when one of the CDH13 variations appeared in the general population, the researchers found a slightly higher rate of alcoholism.
Both genetic signals were “quite specific to violent crime,” the researchers wrote: they occurred most frequently in those convicted of 10 or more violent offenses; they occurred less often in those convicted of just one violent offense; they were seen much less often in offenders who had committed nonviolent crimes such as drunken driving, property crimes or drug-related offenses; and they were rare in the general population.
Given the heightened frequency with which these two broad genetic variations appear in people who repeatedly perpetrate crimes of violence, the authors of the study reckoned that they might account for 5 percent to 10 percent of the violent crime in Finland.
Although intriguing, these two genetic “markers” might never serve as a way to screen the population for potential criminals. For starters, genes may help give rise to certain behaviors but they are not the behaviors themselves, and many psychosocial factors can mitigate such a genetic vulnerability. Moreover, the authors acknowledge, any screening of a general population for these genetic variations would likely catch many innocent citizens in its dragnet.
The best way to reduce crime, the researchers concluded, would be to institute measures that reduce or discourage intoxication with alcohol or stimulants. Both cause a surge of dopamine in the brain and both are indisputably linked to impulsive violence. These findings suggest, however, that such measures might have an outsized effect on people with a genetic susceptibility to committing acts of violence.
For released violent offenders in particular, that goal could be reached by making “obligatory, supervised treatment” a condition of probation, using disulfiram (an anti-alcoholism medication alson known as Antabuse) or long-acting naltrexone (a medication used to treat alcohol and opioid drug dependence).