A Dunedin Study discovery saved an American killer from the death penalty

by Eloise Gibson / 21 March, 2017

Bradley Wardroup during his trial for the 2006 killing and assault.

A genetic discovery from New Zealand saved Bradley Waldroup from the death penalty. But it could just as easily be used to lock people up for longer despite questions about the so-called “warrior” gene. 

Bradley Waldroup seemed like the perfect candidate for the death penalty. Prosecutors in Tennessee, a state that executes murderers, collected evidence suggesting his bloody crime was deliberate and premeditated.

Bit by bit, they pieced together what had happened in October 2006. Waldroup , then 32, waited at his trailer home in Greasy Creek, just off the Appalachian Trail, for his estranged wife, Penny, to arrive with their children. He had a gun and a machete and he’d been drinking and stewing.

As Penny said she was leaving with her friend, Leslie Bradshaw, Waldroup chased her with the machete, slicing off her finger and cutting her over and over. At some point he told his children to say goodbye to their mother because he was going to kill her.

Penny survived, but her friend Bradshaw didn’t: she died from eight gunshots and a cut to the head. Prosecutors thought it was a straightforward case of intentional and premeditated murder. What they hadn’t counted on was a surprise appearance by one of Waldroup’s genes that produces a protein called monoamine oxidase A (MAOA).

American defence lawyers had tried and failed to use MAOA several times in courts. We all carry a version of the gene, but it comes in different varieties. A few unlucky people have a totally inactive gene, which causes them serious behavioural problems. But those people are rare.

Far more common, however, is MAOA-L, a so-called low-expression variant, which means it is less active than usual. This is the gene Waldroup had.

Waldroup’s lawyers argued that the sluggish version of the gene had combined with his history of suffering child abuse to explosive effect. The gene wasn’t the only factor the jury considered, but it clearly persuaded some of them he wasn’t equipped to weigh up a premeditated murder.

As one juror later said to National Public Radio: “Something in [Waldroup] doesn’t tick right … A bad gene is a bad gene.” The jury convicted him of voluntary manslaughter of Bradshaw and attempted second-degree murder of Penny. He got 32 years in jail.

Washington Post headline.

The Dunedin connection

Waldroup was saved by his lawyers and psychological experts who testified in his defence. But his salvation started in 2002, when scientists published a study of Dunedin men.

The research, by Terrie Moffitt and ­Avshalom Caspi, drew on data gathered by the Dunedin Multidisciplinary Health and Development Study, commonly known as the Dunedin Study. That longitudinal study, the basis of last year’s television documentary series Why Am I?, began following just over 1000 babies born in the city in 1972-73 and has tracked them ever since.

Researchers have complied comprehensive databases of valuable information about the participants at every stage of human development, and the study is a treasure trove for local and overseas scientists. Professor Richie Poulton, the study’s head, is used to being ignored here and lavishly praised when he goes overseas. But since appearing on telly last year, he’s had random New Zealanders coming up and thanking him for his work.

Part of what people love about the study is the way in which it explores why life goes wrong sometimes. Why do some people and not others wind up in jail? That was what Moffitt and Caspi were wondering when they tested Dunedin men’s genes.

The Dunedin Study has the kind of information behavioural scientists dream about. Researchers followed the subjects through childhood, watching to see which parents seemed cold or neglectful, which ones doled out harsh physical punishment, and which kids disclosed sexual or physical abuse.

They knew which kids were always switching between caregivers. When the boys were teenagers, they underwent psychiatric assessments. When they became adults, researchers asked their friends and families which ones had problems ­controlling anger, or fighting.

By age 26, some of the young men were in trouble. A search of Australian and New Zealand police records revealed dozens of convictions for violence. As expected, men who had suffered abuse as children were more likely to assault others. But some of the abused kids turned out peaceful. ­Moffitt and Caspi wondered if their genes had something to do with it.

Families of his victims wait for the verdict.

Link to aggression

For their research, they focused on men, because men have more convictions for violence than women and are more likely to carry the less-active variant of MAOA. Previous studies in humans and animals had hinted that knocking out MAOA was linked to greater aggression. The sluggish variation is more common in men, because men get only one copy of the gene (women have two, since MAOA is found on the X chromosome). It turned out this gene was found in a third of the 442 men Moffitt and Caspi tested.

Most people know MAOA-L as the “warrior gene”. But carrying the low-activity gene on its own seems fairly harmless, which is fortunate, since an estimated third or more of white people have it. And Moffitt and Caspi found no relationship between the low-activity variant and violent convictions. In the brain, the gene works like a glorified cleaning product. “You know the old detergent ads where the little enzymes come along and chew up all the stuff?” says Poulton. “You’ve got this enzyme produced by the MAOA gene and it basically creates equilibrium by keeping [neurotransmitter] levels at the right spot.”

The gene helps keep the brain in order by issuing instructions to make a protein that breaks down important signalling molecules (including serotonin and dopamine) when the molecules are no longer needed. Without an enzyme clearing them out, these molecules can build up and cause abnormal moods and behaviour.

People are always tempted to blame single genes for mental conditions such as depression, schizophrenia or autism, says Frances Champagne, an associate professor and neuroscientist at Columbia University in New York. But the brain seldom works that way. If a gene’s job is important, evolution has most likely equipped us with a backup, she says.

“There is all of this crosstalk going on between genes. Our biology is built with all these redundancies and loops [because] you don’t want everything down to one gene.”

That may help explain why MAOA-L alone did not predict violent behaviour. Yet when Moffitt and Caspi added the genetic variant to childhood histories, they saw a pattern: men born with the less-active gene who had also experienced severe maltreatment made up just 12% of the group, but 44% of convictions for violence. And most of those without convictions had lower-level problems with aggression or antisocial behaviour, which showed up in their psychiatric tests or ­families’ survey responses.

Another group of about 40 men with the risky gene who’d suffered less-severe abuse also had higher conviction rates than average. On the flip side, men with high MAOA activity had no more convictions than the typical bloke, even if they’d been abused. Having a hard-working version of the gene seemed to help protect them.

Professor Terrie Moffitt.

More work needed

The study still needed confirming. The riskiest sub-group of severely abused boys who carried MAOA-L was small – just 13 men – and Moffitt and Caspi noted that more work was needed to try to repeat the finding.

They weren’t saying the combination of genes and abuse amounted to a jail sentence. After all, more than half of the severely abused boys with MAOA-L had clean records. But having the unlucky combination seemed to change the odds.

Moffitt and Caspi’s paper, published in Science in 2002 under the title Role of Genotype in the Cycle of Violence in Maltreated Children, caused a sensation. The researchers thought maybe they’d partly explained why some boys seem to shake off bad parenting, while others grow up to hurt others. Scientists have long known that nature and nurture tangle together to shape our behaviour. But this time they had caught nurture actively shaping nature’s effects.

In the field of health, scientists now know that what happens to us in utero and childhood can switch particular genes on or off. They also know that one gene seldom explains our behaviour. But 15 years ago, huge money and effort were going into sequencing the genome. Finding a gene for this and a gene for that was all the rage, says Poulton, who was a contributing author on the paper. He felt the finding was a timely reminder of the limits of looking at DNA in isolation.

“We sort of said, ‘Hold on. If you don’t take into account what’s happened to people in their life, you might miss important information,’” he says. “I know that disappointed people because they wanted something flash and new.”

Others in the field were sceptical, and some attempts to replicate the finding didn’t work. But slowly, other studies built up confirming what the Dunedin research had found, and 15 years later, MAOA-L remains one of the best-proven examples of a single gene interacting with our lives to affect behaviour in a way scientists can actually measure.

“When I teach my students about gene and environment interactions,” Champagne says, “I say MAOA and childhood adversity and serotonin and stress [another finding from the Dunedin Study] are the two classic examples.”

­Avshalom Caspi.

Into the courtroom

It was only a matter of time before MAOA-L found its way to court. In Europe, defences based on the gene have twice been used to reduce the sentences of Italian killers, though the science behind the decisions has seemed a little shaky. In one Italian case, the killer was a woman, whereas Moffitt and Caspi studied only men. In the other, the killer was Algerian, leading scientists to lambaste the court in the science journal Nature, because the link has been proven only in people with white European ancestry.

Otago University associate professor of law Colin Gavaghan believes New Zealand will see its first MAOA court case within a decade.

“If we get to the point where there is a credible body of evidence – and I don’t think we’re there yet – I don’t see how it’s any less credible than the predictions psychiatrists and psychologists are making,” he says. It would only take one expert to agree to testify, and one judge who agreed to allow it, for MAOA to make a debut. If an opposing expert disputes the science, it’s difficult for juries to know who is right, he says.

“It is worrying, because on one hand we have careful people saying, ‘Well, we are not quite sure,’” says Gavaghan. “But it only takes one so-called expert to come forward and say, ‘I’m sure, our technique is accurate, never mind the ditherer.’ People don’t know what to think.

“Judges are the gatekeepers here, because if they think it isn’t reliable, it won’t go to the jury. We need sensible judges who are going to say, ‘Well hang on a minute: what are you telling me and does it apply to this population?’”

Telling a court somebody has a gene for violence could backfire, even if the judge accepts it. A 2012 survey of US trial judges found they would lower the sentence of a hypothetical psychopath if they thought the psychopathy was genetic, but only from 14 to 13 years. Another survey of potential jury members found they were much less charitable. Paul S Appelbaum, a New York psychiatric expert, surveyed a representative sample of the US population about the case of a fictional offender that he’d designed to sound like someone with MAOA-L and a history of child abuse. Unlike the jury in the Waldroup trial, people neither lowered the sentence nor assigned the offender any less blame. In fact, they were more frightened of the offender if they knew about the risky gene.

In New Zealand, Gavaghan says, lawyers would be most likely to raise genetic issues at sentencing. They couldn’t say their client was not responsible for a crime, but they might argue he was less culpable. But that could be a gamble. “As a defence lawyer, going into court at the point of sentencing and saying, ‘My client couldn’t help it. He has no control over his violent impulses. Please be nice to him’, could really go badly. The judge might say, ‘How do I know he won’t do it again, when you’ve pretty much just said he probably will?’ Unless you’re in a death-sentence scenario, it’s a risky dice to roll.”

Richie Poulton.

Bogus Maori connection

Then there is the challenge of finding an expert. Poulton has been approached by American lawyers many times to testify in death-penalty cases. He always says no, and he’s no keener to participate in MAOA trials here. “I just explain that any evidence I could provide would talk in terms of probabilities and would provide no evidence at all about an individual.

“If you think this science is showing any more than that, you don’t understand the science. They usually go away quite quickly.”

Finding other experts locally may prove equally tricky. Gavaghan says many New Zealand researchers were put off talking about MAOA by lurid 2006 media coverage of the “warrior gene”. A researcher spoke at a Melbourne conference about an unpublished study in which he’d tested a small group of Maori men for the MAOA-L gene. A lot of them had it, but the sample was tiny and there was no evidence linking the gene with violence in Maori, so it didn’t mean much. But it made headlines around the world, accompanied by photos of Maori doing the pukana.

“It was total nonsense,” says Poulton. “But it just took hold and awful images were sent around the world. It was so big and it stuck in people’s minds.”

Gavaghan says the fallout has made some researchers wary. “In New Zealand, the whole area of research was really tainted and people have tended to be awfully, awfully careful of saying anything.”

In fact, there’s good reason to think that MAOA-L’s effects on violent risk may differ between ethnic groups, or even be confined to white people. Dunedin in 1972 was not a hotbed of diversity and Moffitt and Caspi’s subjects were almost all Pakeha. Other towns around the world that hosted long-term studies have also tended to be mostly white. One American study tried to stand up Moffitt and Caspi’s finding in both white and non-white Americans, but couldn’t find a connection in non-whites.

But that hasn’t stopped people taking the 2002 study to extreme conclusions. One American researcher wrote a paper suggesting all boys at risk of child abuse should be screened for MAOA-L, and the ones who carried it removed from their homes more readily than other kids. Since welfare funding is limited, the reasoning goes, why not spend it on saving those most likely to hurt others? Poulton loathes the idea.

“That’s ridiculous woolly thinking. On equity principles alone, every child is entitled to an upbringing that is free from maltreatment,” he says.

He is equally scathing about another common comment: we already know child abuse begets violence, and we’re already doing something about it, so what’s the point of studying genes?

“I say, bollocks you do something about that,” he says. “The common response to [maltreatment of children] in most countries falls well short of what’s required to really make a difference, so you should gird your loins if you’re a policymaker or a prime minister to focus even more assertively on removing environmental risks.”

Poulton says the genetic evidence shows we should bolster our efforts to help vulnerable children. “I’d say, ‘Why aren’t you putting more money into it? Why ain’t you doing it earlier? And why aren’t your screening approaches more effective?’”

Simplistic answers

Poulton understands why people want to find a simple reason for ghastly crimes. He refuses to encourage it, but he gets it: telling a jury our actions derive from an immense jumble of genes, the proteins they make (or don’t) and myriad environmental influences is not a snappy story.

“On one level, it’s extremely understandable that people want to take a complex world and simplify it into chunks. But that is not how research works. It involves being realistic about what you can observe and admitting what you don’t know.” He gives a small sigh and a laugh. “At that point, you tend to lose people.”

So when he sees a grisly incident such as the attack in Melbourne in January in which a car driver mowed down dozens of pedestrians, fatally injuring six and wounding at least 30 others, does he think of monoamine oxidase A? Predictably, perhaps, his answers are “no” and “it’s complicated”.

He thinks about the countless twists of life and biology that could lead a person to commit a heinous crime. In the case of Dimitrious Gargasoulas, the driver in Melbourne, “without knowing any details, but having observed [on TV] this guy going crazy, I would say there is a good chance he has a mental health problem”.

“What we know about mental health problems is they are a combination of gene and environment interplay – and not just one gene or one environment but many genes and many environments that impact us at different points in a life.”

Champagne says that if you study a big enough population, you’ll see the effects of genes and maltreatment, just as Moffitt and Caspi did. But at the level of an individual, the result is still a coin flip. MAOA-L and child abuse together can’t tell you what most people want to know: will this person in front of me go out and assault someone?

“Bringing genes [into criminal assessments] seems like good science but I don’t think it actually is,” says Champagne. “It takes cumulative biological changes to create these extreme behaviours. If I have someone in front of me and I want to know their predilection for criminal behaviour, I wouldn’t ask about their genes, because there are so many life events that would have much more powerful effects. Knowing their past criminal history, how they were socialised … that tells me a lot about the critical factors that shaped their brains and behaviour.”

If Poulton were a judge, he isn’t sure what he would do, even if the genetic evidence was perfect. He recounts a thought experiment he used to describe when he was speaking on discussion panels: “Two people have committed a heinous crime. One lawyer says, ‘My client has the risky gene and he has had a terrible upbringing, he has no real control and you need to give him a break.’” The same lawyer looks at the other offender and says, ‘This other person had a great upbringing, does not have the risk gene and they still did the nasty crime, so they are really culpable. Lock them up and throw away the key.’”

The argument sounds plausible, says Poulton, and so does the reverse. “The first offender, with the gene and terrible upbringing, he is bad to the bone. He is stuffed and can’t be rehabilitated, so throw away the key. This other person with the good childhood can be rehabilitated, so go easy.”

He’s asked judges what they think. They didn’t know, either. “These are real-life conundrums and I don’t have an answer to them,” he says. “You take [a finding] out of an academic bubble and it gets into the world and it gets messy. But the more we can talk about these things and grapple with them, the better off we’ll be.”

This article was first published in the March 11, 2017 issue of the New Zealand Listener. Follow the Listener on Twitter, Facebook and sign up to the weekly newsletter. 


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