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The “warrior gene”: blaming genetics for bad behavior

The extent to which we can blame our genes for bad behavior took another step backward recently, in the US at least, with a court ruling that data from the “warrior gene” couldn’t be used as an excuse for diminished responsibility.

Belief in the existence of a warrior gene has been around for more than 25 years, one of many examples where genetic effects on behavior have been misunderstood. In 1994, Stephen Mobley, convicted of murder, armed robbery, aggravated assault, and possession of a firearm, was sentenced to death. His trial occurred soon after the publication of a paper attributing aggression to a deficiency of MAOA. Supporting this claim were data reporting that eight men from the same family had repeated episodes of aggressive behavior. One had been convicted at the age of 23 of the rape of his sister. Another tried to run over his boss with a car at the sheltered workshop where he was employed after having been told that his work was not up to par. A third would enter his sisters’ bedrooms at night, armed with a knife, and force them to undress. At least two more were known arsonists. Han Brunner, the geneticist in the Netherlands who described this unfortunate family, found evidence that males with criminal behavior had a mutation in a gene on the X chromosome called monoamine oxidase A (MAOA), which is involved in the metabolism of neurotransmitters, including dopamine, noradrenaline and serotonin, the last being the target of antidepressants such as Prozac. Since men have only one copy of the gene (one X chromosome), the men with the mutation in MAOA had no functional enzyme. On the face of it, MAOA mutations were making Dr Brunner’s patients aggressive. Mobley filed a motion seeking funds to hire expert witnesses to assess whether he, like the men in the paper, had a deficiency of the MAOA gene, which was later to become famous as the “warrior gene.”

It was Mobley’s bad luck that the court threw out his petition, and he was subsequently executed by lethal injection, but news of his defence soon spread. In Ohio in 2000, lawyers for Dion Wayne Sanders tried the MAOA argument, and though the court decided it could not be shown that when Sanders shot both of his grandparents he lacked the specific intent to kill them, the jury returned verdicts of imprisonment rather than the death penalty. And, in a case heard in Tennessee in 2009, with respect to the genetic data, the court found “as a matter of law, that the expert services sought are necessary to ensure that the constitutional rights of the Defendant are properly protected.” So began a saga that has persisted till February 2021, when the New Mexico Supreme Court threw out the “warrior gene” defence.

“almost all behavior is heritable (to some extent) and … arises from the joint contribution of thousands of individual genetic variants”

However, don’t imagine for a second that this is a death blow for genetic determinism. The court’s decision means that a mutation in a single gene (MAOA) can’t be blamed for violent acts, and since no one has found a mutation in any of the 23,000 other genes in the human genome that causes violence, it’s now pretty certain that there no warrior genes. But there is a possibility that we can blame someone’s genetic constitution in aggregate.

What’s become clear over the last decade is that almost all behavior is heritable (to some extent) and that it arises from the joint contribution of thousands of individual genetic variants. These variants are not mutations that kill a gene or give it a new function. In fact, individually, they don’t do much at all, just increasing or decreasing the likelihood of a behavior by a very small amount (if you think of it as percentage where the warrior gene has a 100% effect, then these variants have an effect less than 0.01%). While individually small, there are so many thousands of them that in total the effect is detectable. Scientists have been getting better and better at predicting behavioral outcomes from aggregate assays of genetic data. This is because genetic data is being harvested on an increasingly large scale; it’s routine to publish results from millions of individuals—one of the best and most productive sources of such data comes from the UK where 500,000 people were recruited into the UK BioBank. As datasets grow bigger, the predictive accuracy of genetic data has improved and is being touted in the clinics as a way to diagnose heart disease, diabetes, obesity, and other common diseases. It won’t be long before lawyers realize they have a new toy: “don’t blame my client, he couldn’t help himself, it was all in his genes.”

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