Read The Anatomy of Violence Online
Authors: Adrian Raine
Figure 2.1
The increase in
homicide rates in adoptees as a function of the degree of
criminal offending in the biological parents
Which isn’t to say there aren’t caveats. Adoption agencies, for example, try to place babies into adopting families who are similar to the true biological parents—a process termed “
selective placement.” Furthermore, there could be differences in the length of time the baby is with their natural mother. If antisocial mothers are neglectful of their offspring before adoption, this
negative bonding experience—an environmental process—might account for the later antisocial behavior. Mednick, however, was careful to control for these factors. His findings could not be explained away by selective placement of adoptees into adoption homes of a similar socioeconomic status, or the age at which the infant was taken away from the mother. Other studies have similarly controlled for methodological confounds like these.
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Of course, twin and adoption studies, like all other studies, have their methodological weaknesses.
Critics of the conclusion that there is
a genetic contribution to crime will eagerly latch onto such limitations. Their objections may seem to disqualify the conclusions, but it’s a false alarm. These studies represent different people, time, places, measures, and designs.
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All these differences should often lead to the expectation of divergent, different results—yet very tellingly they all converge on the same intrinsic finding.
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Let’s apply this principle to the current context. Participants in more than a hundred genetic studies of antisocial behavior have ranged in age from nineteen months to seventy years. They cover the period from the Great Depression to the present. They represent many different Western nations, including Australia, the Netherlands, Norway, Sweden, the United Kingdom, and the United States. They use a wide variety of measures of antisocial behavior. They are made up of twin studies, adoption studies, and sibling designs. They also include large-scale studies that represent the general population and use advanced quantitative modeling techniques. They include studies conducted in the past fifteen years, and the findings from yesteryear stand up in studies done today.
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Taken together as a whole, these studies converge on a simple truth that even the strongest critics of genetic influences in violence are finding harder to resist—genes give us half the answer to the question of why some of us are criminal, and others are not.
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What specific seeds account for sin? It’s a big question, and it has always been controversial. In the past the most sensationalized link between violence and genes has been the case of XYY.
Normally we each have twenty-three pairs of chromosomes, with each chromosome being a bundle of many genes. One of these chromosomes is the
sex chromosome—X or Y. Each parent gives one chromosome to each pair, which determines if we end up as an XY (male) or an XX (female). But on rare occasions there’s a mistake. Instead of one Y chromosome pairing with one X, two Y chromosomes pair with one X. The result is a male who receives an
extra male chromosome—XYY.
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.
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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.
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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.
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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.
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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.
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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.
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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.
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As we shall see, there are many genes other than those on the Y
chromosome that likely play a role in criminal behavior.
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.
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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.
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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.
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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.
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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 gene for crime, that the genetic abnormality he discovered is extremely rare, and that the environment is critically important also.
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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.