The Anatomy of Violence (44 page)

Figure 8.3
   Interaction between early biological risk factors and bad home environment in predisposing to teenage aggression in Australia

We again see the seeds of sin conspiring during infancy to create a deadly weapon in later years.
Patty Brennan found a fivefold increase in adult violence when nicotine exposure was combined with exposure to delivery complications—but no increase in violence in those who were nicotine-exposed but lacking delivery complications.
²⁶
Maternal
smoking also interacts with
parental absence in predicting early onset of offending in the United States.
²⁷

We hear across all these studies a compelling chorus. Social factors
interact
with biological factors in predisposing someone to violence. As we discussed earlier,
Caspi and
Moffitt amazed the world in 2002 by establishing that a gene resulting in low levels of
MAOA
combined
with severe early
child abuse results in adult antisocial behavior.
²⁸
David Farrington, a world-leading criminologist at
Cambridge University, found that low resting
heart rate combined with parental separation before age ten resulted in voracious violent offending in adulthood.
²⁹
In the first-ever functional
MRI study of any antisocial group, I found that violent offenders who suffered severe child abuse showed the greatest
reduction in right temporal cortical functioning.
³⁰
Another study found that if you have high
testosterone levels and a deviant peer group you may become
conduct disordered—yet if you have that same high testosterone and circulate in a non-deviant peer group you are instead led to become a leader.
³¹
Genes also combine with ghastly
parenting to shape adolescent
aggressive behavior.
³²
However you look at it, studies are showing that when biological and
social factors interact, they can be far more malignant than any one factor on its own.

I mentioned earlier that there are two ways of looking at biosocial effects. One is the “interaction” perspective. I’ve given several examples above. The second approach that I describe here I call the “social-push” perspective.

Back in 1977 it was unpopular to posit a biological basis to antisocial behavior in schoolchildren. Even less accepted was the belief that biological factors combined with social factors. So when my first research publication as a young student focused on this biosocial perspective, it was a virtual no-go area.
Hans Eysenck, Britain’s best-known and most controversial psychologist, had already lit a fuse with his controversial book
Crime and Personality
,
³³
in which he had the audacity to suggest that crime had a biological basis. Despite the controversy, I believed the book contained a fascinating concept that was related but different—an “
antisocialization process.” This concept profoundly
influenced my work.

The idea was all but lost amid the acerbic criticisms others made of the book. It appears in a section that really resonated with me. Eysenck considered a child whose mother was a prostitute and whose father was a thief—a child in “Fagin’s kitchen.” He suggested that if that child “conditioned” well or learned quickly from his antisocial home role models he would become a good pickpocket—just like the
Artful Dodger in
Oliver Twist
. In contrast, children who do not condition well will paradoxically not be socialized so easily into an antisocial way of life.
³⁴

I had my chance to examine this idea when I first learned psychophysiological techniques in the laboratory of my PhD supervisor,
Peter Venables. That was at
York University in 1977. I learned the fundamentals of the eccrine sweat-gland system. I scoured the classical-conditioning
literature to design a
fear-conditioning experiment. I studied what types of electrodes should be used, and the chemical content required of the gel that helped the silver/silver chloride electrode to make contact with the
fingers. I learned to measure bias potentials on the electrodes and to rechloride them when the bias potential was unacceptable. I worked with our technician
Don Spaven on generating the auditory stimuli to play over headphones in the conditioning experiment. I tested out the decibel levels with an artificial ear and a really expensive audiometer, snapping the connector between the two and making Don very upset. But soon after that setback, I was ready to get going on recruitment.

I interviewed school headmasters, met with the teachers, and put up recruitment flyers in schools. I went knocking on the doors of parents to get permission and recruited kids into the study. I chased up those who had not responded to my recruitment letter. I then went to the schools and gave the schoolkids questionnaires to fill out to assess their antisocial personality, and to get home background information. The teachers rated their antisocial behavior. I walked to school to pick up the kids, brought them over to the lab, and walked them back again when we had finished. It was a heck of a grind. But it was my first research study, and I was enormously excited—even in the autumn rain and the winter snow. The kids felt pretty good too because they got fifty pence for taking part in the study, about a week’s pocket money back in 1978.

We discussed
fear conditioning earlier, so you’ll recall that it measures
anticipatory fear. The task assesses how much a kid
sweats when hearing a soft tone that predicts a loud, unpleasant tone. Can they learn—like
Pavlov’s dogs—to form an association between two events in time? Can they learn that certain events are followed by punishment? Do they have a “
conscience”—a set of
classically conditioned emotional responses—that makes them feel uncomfortable even at the thought of doing something antisocial?

I found that the environment mattered. If the schoolkids came from a
good
home, then those who conditioned poorly were antisocial.
³⁵
Yet if they came from a bad home, the reverse was true—those who conditioned well were the antisocial ones, Dickens’s Artful Dodgers. I was really excited because I got these same findings no matter if it was the teachers rating the antisocial behavior or if it was the
child self-reporting on his or her own antisocial personality. Findings were
replicating across raters who often disagreed with each other, which suggested that the results were robust. The criminologist and historian
Nicole Rafter very generously attributes my first finding as a classic study that got biosocial research in criminology under way,
³⁶
but the reality is that, like many scientists, I was standing on the shoulders of giants.
³⁷

Where does this lead us? I now want to introduce you to the second biosocial theme that I developed in that review in 2002.
³⁸
So far we’ve seen that when a biological risk factor interacts with a social risk factor, the outcome is an exponential increase in
violence. But “
moderation” is another way that social and biological factors can influence each other. A social process can “moderate”—or change—the relationship between biology and violence. That is exactly what the conditioning experiment had demonstrated—that home background moderates the relationship between fear conditioning and antisocial behavior.

Let’s take another example, this time from the
PET-scan research on
murderers that we discussed earlier. I had shown that murderers in general have poor prefrontal
glucose metabolism.
³⁹
In another analysis, however, I divided the murderers into those from bad homes and those from relatively normal homes. We assessed eight different forms of home deprivation—factors like child abuse, severe
family conflict, and extreme poverty. To get these data we scoured criminal transcript histories, medical reports, newspaper reports, and reports from psychiatrists, psychologists, and social workers. We even interviewed some of the defense attorneys. We then assigned murderers into either a “deprived” home background group or a “non-deprived” group. The question we then asked was, “Which group has the poor prefrontal functioning that predisposes them to violence?”

You can see the answer in
Figure 8.4
, in the color-plate section. We have here an example of a normal control on the left, who shows good prefrontal functioning—the red and yellow colors at the top. In the middle we have a murderer from a bad home background. And on the right we have a murderer from a good home. You can see that it’s the murderer from the relatively
good
home background who shows reduced
frontal functioning—the cool colors at the top of the image. And that is the result we observed for the groups as a whole.
⁴⁰

The social environment moderates—or alters—the link between poor frontal functioning and murder. The bad brain–bad behavior
relationship holds true for murderers from one type of home background—but not for those from a different home.

But how do we explain this? One way to think of it is like this: If you are a murderer, and you come from a bad home, what explains why you are violent? Perhaps here we don’t have to look any further than the bad home, which is a well-known social predisposition to violence.

But what if you are a murderer and you come from a
good
home? What causes violence here? It’s certainly not the home, because in this case it’s pretty good. Instead it has to be something else—a bad brain, perhaps. And that is indeed what we see in
Figure 8.4
(in the color-plate section). Murderers from good homes had a 14.2 percent reduction in right orbitofrontal functioning—a brain area of particular relevance to violence. Accidental damage to this brain area in previously well-controlled adults is followed by personality and emotional changes that parallel
criminal psychopathic
behavior, or what
Antonio Damasio has termed “acquired sociopathy.”
⁴¹

Let’s think back to the case of
Jeffrey Landrigan, which we discussed in
chapter 2
. He had a fabulous home background, with a loving mother, a father who was a geologist, and a sister who was as well educated and straitlaced as her parents. He had all the advantages of life. And yet Jeffrey swiftly spiraled out of control, beginning at age eleven with
burglary, and eventually ending in homicide. What was the cause? Here we should suspect genetics and brain dysfunction, given that his biological father—whom he had never seen—was himself on
death row for homicide. Great home—yet awful outcome.
Gerald Stano was similarly adopted into a loving home six months after birth, but went on to confess to forty-one murders before facing the electric chair. Landrigan and Stano are just two among a number of serial killers reported on by Dr.
Michael Stone, a forensic psychiatrist at
Columbia University, who were adopted into warm, loving, and supportive home environments.
⁴²
Here we should suspect their genetic heritage, rather than bad homes, as a cause of their violence.

This social perspective on biology-violence relationships is not common in research. As we have seen, the “
additive” effect of biological plus environmental
risk is the prevailing outlook. And yet the alternative social-push perspective makes some sense, and I feel it can help some parents come to terms with the wayward behavior of their children.

Think about it yourself. Think about people who have a bit of the bad seed about them—a friend, a neighbor, or perhaps a family member who went off the deep end even though his or her siblings stayed on the straight and narrow. Sure, some of them come from classic chaotic homes filled with domestic
violence and poverty. But don’t some of them have near-normal home backgrounds? Surprisingly loving parents? Two siblings can come from the same family—the same environment, the same upbringing—yet have
different outcomes. Here I suggest that you should suspect subtle biological risk factors in nudging your acquaintance into crime, just as we have seen for murderers from good homes.

I often get e-mails from concerned parents desperately trying to help their wayward children. In one such message, a mother described how her seven-year-old son killed a household pet, struck out violently at her, and confessed to his therapist that he enjoyed choking his younger brother. When the mother became pregnant, the child began punching her in the belly and saying that he wanted the baby dead. He showed little remorse and his treatments, including counseling, medication, and hospital stays, did little to help.

Clearly this child is a serious problem, and equally clearly the mother really cares a great deal. Unlike the all-too-common scenario of parental neglect, she is desperately reaching out for help. Yet here it is the son who is callous, uncaring, and
lacking remorse. Loving home—unloving child. What can account for such a tragic mismatch?

In this case it might be heritable process. Why? Because what I did not tell you earlier is that this child was adopted.

When children are adopted, it is often because the biological parents do not want their child, or their behavior is such that the child must be taken away from them. We saw earlier how
maternal rejection of the child—especially in combination with biological risk factors like birth complications—is a risk factor for later violence. There is a break in the mother-infant bonding process at a critical period in the time before adoption, and it is not easy for a later loving home to mend that break. So here genetic processes may be accounting for the dangerous behavior shown in this child from a good home.

The emergence of genetic and biological factors for
antisocial behavior in the midst of a benign home background is something I have termed the “social-push” hypothesis.
⁴³
Where an antisocial child
lacks
social factors that “push,” or predispose him to antisocial behavior, then
biological factors may be the more likely explanation.
⁴⁴
In contrast, social causes of criminal behavior may be more important explanations of antisociality in those exposed to adverse early home conditions.
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