The Anatomy of Violence Read online

  Soon after the XYY condition was first discovered, in 1961, there were rumblings that it might be linked to violence. In 1965 the prestigious science journal Nature published research findings from blood tests of Scottish prisoners in a special security hospital for the mentally disabled, which showed that 4 percent had an additional Y chromosome.25 While it may not sound dramatic, this rate is forty times higher than the 1-in-1,000 rate of XYY reported for the general population.

  A year later, in July 1966, while England was busy trying to win soccer’s World Cup, a man named Richard Speck killed eight nurses in a dormitory in Chicago. He held them in their dorm at knifepoint, leading them out of the room one by one to rape and strangle them to death. One of the nurses, Corazon Amurao, surreptitiously slipped under a bed during the ordeal. While Speck thought he was raping the last nurse on a dorm bed, Corazon was huddled under the bed, terrified that her turn would be next. But Speck miscounted how many victims he had in the room and left. He was eventually caught. Corazon Amurao positively identified him in an identity parade and he was charged with the homicides.

  A sensational twist in the dramatic coverage of this crime was the claim that Speck was XYY. At least superficially there was reason to suspect this possibility. XYY males are taller, averaging about six feet. They also have a history of learning disability and have IQs somewhat lower than average. It was also thought that XYYs had acne and that severe acne might be a marker for XYY—a mark of Cain.26

  Speck was six feet one inches tall, and was not that intellectually sharp, as indicated by his miscounting of his victims and the struggles he had in school—he repeated the eighth grade and dropped out before he was sixteen. He also had a pockmarked face due to acne scarring. In a blaze of publicity just before his appeal against his conviction it was reported that Speck was an XYY.27 This came shortly after a few high-profile scientific publications reported on the XYY-crime link, including Mary Telfer’s report in Science that XYY was overrepresented in men in criminal institutions in Pennsylvania.28

  It turned out that Speck was not XYY at all. To be sure, his face was pockmarked, as you can clearly see in Figure 2.2. Yet even before the trial began, Eric Engel, a Swiss neuroendocrinologist at Vanderbilt University, had performed a chromosome analysis on Speck and found him to be a completely normal XY male.29 But the erroneous newspaper reporting fueled the public belief that XYY might be a cause of violence. It became almost folklore.

  The link between XYY and violence in particular was debunked in a definitive study by Sarnoff Mednick and his colleagues in an influential paper published in Science.30 They took a population of 28,884 men born in Copenhagen and conducted a sex chromosome screen of the 4,139 who were over six feet tall. Twelve were found to be XYY. They then checked crime convictions of these twelve and compared them to normal XY males whose crime records were also checked. The result did indeed demonstrate that XYY is associated with crime in general, with a crime rate of 41.7 percent in the XYY group versus 9.3 percent in the controls. However, the rate of violent offending in the XYY group was 8.4 percent compared to 1.8 percent in the controls—a fivefold increase, which, while very large, was statistically nonsignificant due to the small sample.

  Figure 2.2 Richard Speck

  Social scientists lapped up the findings. Criminology textbooks routinely reported this study as proof that there was no genetic basis to violence. Some even erroneously used this finding to scotch the whole idea of a genetic basis to crime in general. But let’s get the facts clear.

  While it is true that technically there is no statistically sound evidence to link the XYY syndrome to violence, this does not embarrass the notion of a heritable basis to crime, for four reasons. First, although XYY males do not commit more violent offenses than controls, they do commit more petty property offending.31 Second, while the XYY syndrome represents a genetic abnormality, many criminologists misunderstand it. The XYY karyotype is not a heritable condition that is passed on from parents to offspring. It stems instead from random chromosomal mutations at the time of conception. Consequently, XYY research has no bearing at all on the issue of whether crime and violence is heritable. Third, even if the XYY syndrome were a heritable genetic disorder and failed to show a relationship with crime, such a failure does not invalidate the significant findings of many twin and adoption studies that do show a relationship between heredity and crime. Fourth, recent studies with larger sample sizes show that young boys with XYY are indeed rated as more aggressive and more delinquent than controls.32 As we shall see, there are many genes other than those on the Y chromosome that likely play a role in criminal behavior.

  A MEAN MONOAMINE

  For social scientists, the ugly Hydra head of the genetics of crime seemed to have been triumphantly guillotined and buried forever. But legend has it that when one of Hydra’s heads was cut off, several more grew in its place. The intellectual battle over whether genes play a role in violence was just warming up.

  Han Brunner was a doctor in the University Hospital in Nijmegen in the Netherlands who was approached one day in 1978 by a woman wanting genetic counseling.33 Many of her male relatives seemed to have significant behavior problems. The problem was in their eyes, she said—it was the way they looked at you, frightening and aggressive.34 Her ten-year-old son was showing signs of behavior problems and she also had two daughters. Might they be carriers of some genetic defect that results in aggression?

  Han Brunner went on a systematic investigation, traveling around the Netherlands to track down this extended family across four generations. His research was fastidious. He even visited shelters that housed some of the woman’s relatives. He interviewed them and took blood samples for genetic analyses. Fifteen years after that woman’s visit, Brunner and his colleagues published their findings in Science. What they turned up was astonishing and almost eerie.

  The fourteen male relatives that he studied showed a history of violence and impulsive aggression. It was almost a rerun of the Jeffrey Landrigan–Darrel Hill three-generation clan. In the four-generation family tree that Brunner drew up, only the male offspring of females were affected. That had to mean that whatever the genetic abnormality, it had to be carried this time on the X chromosome—the one transmitted by women. When Brunner genotyped the families he found an astonishing abnormality. These males had a defective gene—the MAOA gene, which normally produces the enzyme monoamine oxidase A. He sequenced this gene, analyzed it in detail, and found a mutation in it that resulted in no functional MAOA at all. All the affected members had this mutant form of the MAOA gene.35

  MAOA is an enzyme that metabolizes several neurotransmitters involved in impulse control, attention, and other cognitive functions, including dopamine, norepinephrine, and serotonin.36 Mutations in the normal MAOA gene lead to deficient production of the MAOA enzyme. It wasn’t just that it was low in the affected family members, it was virtually nonexistent. A total lack of MAOA has profound effects. It disrupts the normal function of other neurotransmitters, resulting in a wide range of disorders—including attention-deficit/hyperactivity disorder, alcoholism, drug abuse, impulsivity, and other risky behaviors. Han Brunner also found that the lack of MAOA in his affected family members resulted in lower IQ. We know that low IQ is a very well-replicated risk factor for crime and violence.37 Put this together with impulsivity, inattention, and drug or alcohol abuse, and you can see why impulsive aggression is not an unexpected outcome.

  I saw Han in 2011 at a meeting in Amsterdam, and his perspective from the time of the publication of his work in Science was interesting. He sensibly recognized the controversy and was aware of the potential misuse of medical genetic research. So upon publication he couched his findings very cautiously. He used words like “abnormal behavior” instead of “aggression,” and “associated” instead of “causes” in the title of his publication in Science. Despite this, the media were again blasting out the message of a new gene for crime. Han is at pains to maintain that there is no one gen
e for crime, that the genetic abnormality he discovered is extremely rare, and that the environment is critically important also.38 He has put that message forward ever since I have known him, and yet it is consistently misinterpreted by social scientists who want to discredit his work, and the media who want to sensationalize it. Despite the onslaught and criticisms, however, another Hydra head was soon to pop up and go back into battle to persuade social scientists of the potency of the genetic argument.

  THE WARRIOR GENE RIDES AGAIN

  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

  goes a long way to explaining some of the problems Maori have. Obviously, this means they are going to be more aggressive and violent and more likely to get involved in risk-taking behaviour like gambling.48

  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:

  The extrapolation and negative twisting of this notion by journalists or politicians to try and explain non-medical antisocial issues like criminality need to be recognized as having no scientific support whatsoever and should be ignored.49

  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 monkeys51—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.