The Anatomy of Violence (10 page)

Han Brunner’s novel finding in 1993 was given a big boost in 1995 by
Jean Shih, a colleague of mine when I was at the University of
Southern
California. Jean and her research team were investigating the effects of knocking out the MAOA gene in
mice. You can knock out or deactivate a gene in mice by replacing it with an artificial
DNA sequence. Once in a while Jean’s team would come into their lab in the morning and notice a dead mouse. It did not take them long to work out that mice with deletion of the MAOA gene had become ferociously aggressive and were attacking other mice.
³⁹
Jean had found a gene linked to aggression—and it happened to be the same gene that Han Brunner had found to be abnormal in his Dutch family.

The third Hydra head of the
genetics perspective came at the beginning of this century. It proved to be a turning point not just on the genetics of crime, but almost the genetics of pretty well everything else worth talking about.

Two scientists—Terrie
Moffitt and
Avshalom Caspi, at Duke University—paved the way for research in this field with their seminal paper in
Science
in 2002. Widely regarded as one of the most important research papers in the
social and behavioral sciences, it demonstrates something we will focus on much more in a later chapter—that genetic and biological factors
interact
with social factors in predisposing someone to later
antisocial and violent behavior. So yes, individual genes are important—but in a specific social context.

Terrie—or Temi, as I have known her since I first met her in Tuscany when she was still a graduate student—had set up a major longitudinal study on antisocial behavior in
Dunedin in
New Zealand. Gold was struck near Dunedin in 1861 and in the ensuing gold rush it became the largest city in New Zealand, and still remains the second-largest city on the south island. Avshalom, Temi’s husband, struck gold with the Dunedin data in his brilliant analysis of a gene that regulates the enzyme MAOA and how a variation of that gene combines with child abuse to produce antisocial behavior.

Although we share genes in common, there are variations in any gene, with different sequences of DNA at any specific location. These “
genetic polymorphisms” give rise to differences among us—such as having different blood types, blue eyes versus brown eyes, or straight hair versus curly hair. One such genetic polymorphism results in different levels of MAOA. It’s quite easy to genotype an individual, either from a blood sample or, even less invasively, from a saliva sample. About 30 percent of us have a variation in the MAOA gene that gives
rise to relatively low levels of this enzyme, resulting in disturbances in
neurotransmitter levels. The rest of us have relatively normal levels of MAOA. Caspi and Moffitt repeatedly assessed over a thousand children from Dunedin on antisocial behavior from age three to twenty-one. They also knew which ones had experienced no maltreatment from age three to eleven years, which had some maltreatment, and which were severe maltreatment. What they found was that low levels of MAOA were associated with later antisocial and violent behavior, particularly when the children had been severely abused.
⁴⁰

It was a dramatic discovery because it highlighted the complexity of understanding the genetic and biological basis of antisocial and violent behavior—something we’ll return to later on. The New Zealand findings also brought more weight to bear on the earlier human findings from the Netherlands and the animal findings from the United States. Different research methodologies were beginning to converge on the same conclusion—low MAOA is to some extent associated with violent and aggressive behavior.

Yet new
molecular genetic findings such as these come and go like lightning bolts out of the blue. Does this one replicate? Largely speaking it does. Four years after the original finding of Caspi and Moffitt, a meta-analysis that pooled results from five studies confirmed the original effect,
⁴¹
and it has since been linked to
antisocial personality disorder.
⁴²

While these studies have shown that the low-MAOA gene is especially related to antisocial behavior in those with a history of abuse, studies are also beginning to show direct links between this gene and antisocial personality characteristics—irrespective of whether subjects have been abused.
⁴³
Both men and women with the low-MAOA gene report higher levels of lifelong aggression.
⁴⁴
Men with a rarer genetic abnormality of the MAOA gene that results in excessively low levels of MAOA have twice the level of serious delinquency and adult violence of normal controls.
⁴⁵
Furthermore, the link goes beyond self-reports or psychiatric interviews. Those with the low-MAOA gene also show more aggressive behavior in a laboratory setting.
⁴⁶
There’s no single gene for crime or violence, but initial research does highlight some partial role played by this gene.
⁴⁷

Another chimeric Hydra head arose, again in New Zealand, in August 2006, but this time the battle was uglier and even more controversial.
Researchers reported that the
Maori had twice the level of the genotype conferring low levels of MAOA compared with Caucasians in New Zealand. The researchers were immediately quoted in newspapers as saying that this difference

The headline of maori violence blamed on gene helped not one bit. In the furor that followed, scientists, politicians, journalists, and pretty well everyone else dived into the hot and at times hostile debate that ensued.

The researchers who had presented the finding countered that they had been badly misquoted, and in a clarification argued:

At the same time, they also argued that the low-MAOA genotype—which had come to be known as “the
warrior gene”
⁵⁰
based on research on aggression in
monkeys
⁵¹
—was evidence of positive natural selection for the Maori. They hypothesized that the Maori have been well recognized as fearless warriors and historically had embarked on long, dangerous canoe voyages in their migration from Polynesia to New Zealand. They were also the survivors of warfare with other island tribes. They consequently argued from this “warrior gene hypothesis” that evolutionary forces may have resulted in the doubling of the frequency of the low-MAOA gene in Maori.
⁵²
Put another way, this gene may have conferred a “survival of the fearsome” advantage on an indigenous group that now makes up 15 percent of the New Zealand population.

Some argued that the suggestion does a great disservice to the Maori people.
⁵³
Others raised
ethical concerns about the harm such speculation can do, including diverting attention from the poorer social and
economic conditions of the Maori.
⁵⁴
The authors of the warrior-gene hypothesis counter that it is both unethical and unscientific to ignore genetic difference in the Maori, a difference that could have potentially important medical and treatment implications for understanding disease disparities.
⁵⁵

There is no question that we all must be extraordinarily cautious in interpreting any genetic differences between ethnic groups, especially with respect to crime and violence. At the same time, the evolutionary argument put forward is not entirely implausible. Counterpoint: While the base rate of the low-MAOA gene is about 34 percent in Caucasian males and 56 percent in the Maori, it is 77 percent in Chinese males. Yet the homicide rate in
China, at about 2.1 per 100,000, is less than that of the United States—the Chinese are not exactly known for their fearless, warrior-like tendencies.
⁵⁶
We’ll return to the ethical issues on the biology of violence, but for now let’s turn away from the debate on genes and violence in the Maori and back to a more established body of evidence that does not rest on ethnic-group differences.

Importantly, let’s consider that the
type
of aggression we are talking about may make a difference. The MAOA warrior gene may well be especially important in predisposing people to hot-blooded, emotional, and
impulsive forms of aggression—rather than cold-blooded,
regulated aggression.
Han Brunner documented that the men in his Dutch kindred study tended to display more impulsive forms of aggression that often occurred in response to anger, fear, or frustration.
⁵⁷
Consistent with this interpretation was research done in
Los Angeles that found that UCLA students with the low-MAOA gene not only had more aggressive personalities, but showed greater interpersonal
hypersensitivity—their feelings were more easily hurt.
⁵⁸
They also showed a greater
brain response to being socially excluded, suggesting that they were indeed more easily upset by personal slights.

Those with the warrior gene are more hypersensitive to criticism, which in turn results in increased impulsive aggression.
⁵⁹
Australians with the warrior gene not only exhibit higher levels of antisocial personality, but also show an abnormal brain response to processing emotional stimuli.
⁶⁰
No, I’m not going to say it’s all due to Australians’ being the offspring of 160,000 convicts shipped out from England in the eighteenth and nineteenth centuries. I believe instead that this indicates
that the low-MAOA gene has an across-the-board linkage with crime. By and large it cuts across cultures.

I’ve so far discussed one particular gene—the “warrior gene”—because it has quite strong scientific support as contributing to antisocial and aggressive behavior. Yet other genes are also involved. The 5HTT gene,
⁶¹
the DRD2 gene,
⁶²
the DAT1 gene,
⁶³
and the DRD4
⁶⁴
have all appeared on the gene landscape as linked to antisocial and aggressive behavior. What do these particular genes do? They regulate two important
neurotransmitters in the brain—
serotonin and
dopamine.

But before going further, let’s gain another perspective on this aspect of the anatomy of
violence. From the genetic makeup of the brain it’s only a brief step to the chemistry of violence. The essence of the molecular genetic research we have been touching on above—identifying specific genes that predispose individuals to crime—is that genes code for neurotransmitter functioning. Neurotransmitters are brain chemicals essential to brain functioning. There are more than a hundred of them and they help to transmit signals from one brain cell to another to communicate information. Change the level of these neurotransmitters, and you change cognition, emotion, and behavior. Genes that influence neurotransmitter functioning can therefore result in aggressive thoughts, feelings, and behaviors.

Take dopamine, for example. Dopamine helps produce drive and motivation. It is critically involved in
reward-seeking behavior. Aggressive behavior can be rewarding, and in animals dopamine receptors help code for this rewarding property of aggression.
⁶⁵
When dopamine is experimentally increased in animals it fuels aggression, while blocking dopamine decreases aggression.
⁶⁶
You can think of it as the accelerator in the car that helps move us forward to things that we want.

There is a very different story to tell on serotonin. The serotonin-transporter gene is one of the most intensively researched genes in my fields of psychology, psychiatry, and neuroscience.
⁶⁷
There are two versions of this gene—the
short-allele version and the
long-allele version. About 16 percent of us have the short-allele version.
⁶⁸
This version makes our brains overrespond to emotional stimuli
⁶⁹
and can result in us letting off steam when we get overheated. It is thought to be associated
with low serotonin because those with the short-allele version have reduced levels of serotonin in their bloodstream.
⁷⁰

So, do violent offenders have low serotonin levels? The research on this started with a seminal study in 1979 of military personnel.
Fred Goodwin was an exceptional scientist and director of the
National Institute of Mental Health. He first asked his military-personnel participants how many fights and
assaults they’d gotten themselves into. They were then put on bed rest and fasted overnight. Instead of getting a breakfast when they woke up the next morning, they got a spinal tap—a needle through their spinal cord—to obtain a sample of their cerebrospinal fluid. From this fluid Fred and his team assayed levels of serotonin.

What they found was dramatic and created a watershed in the research field on the biology of violence. Resting levels of serotonin explained a full 85 percent of the variation in the incidents of aggression in the lives of these military men.
⁷¹
That relationship is enormously high, and perhaps the finding was a little too good to be true. Subsequent studies have shown that the relationship between aggression and low serotonin levels is not as strong as originally thought—it explains more like 10 percent of the variation in aggression—but it is still relatively strong and has been extremely well replicated in adults,
⁷²
especially in relation to those committing impulsive violent acts.
⁷³

Why would low serotonin result in violence? Serotonin is a mood stabilizer, which has an inhibitory function in the
brain. It is thought to be one of the biological brakes on impulsive, thoughtless behavior. It innervates—or lubricates—a part of the brain called the
frontal cortex, which, as we will see in the next chapter, is critically important in regulating aggression. The less serotonin you have, the more rash you may be. Brain-imaging research has shown that people given a drink that reduces serotonin by depleting
tryptophan—an amino acid critical for serotonin production—are more likely to retaliate when they are made an unfair offer in a game.
⁷⁴
Without serotonin they get upset more easily when annoyed. Combine a low serotonin predisposition to an unfair social situation that irritates you, and blowing your fuse is just around the corner.