The Anatomy of Violence (43 page)

My rule-breaking behavior had no one specific cause. It had to be a biosocial brew. Like my own hooch, the offender propping up the bar constitutes a merry mix of ingredients. Yet despite enormous knowledge of social factors and some beginning knowledge of the biology of psychopathy by
Robert Hare in Vancouver,
⁷
criminologists and other scientists in the 1970s had not woken up to the idea that these two sets of risk factors
interact
. While I was a neophyte when I started my research career in 1977, and while I felt certain that biology was one component, I was equally convinced that the key chain needed to unlock crime held a lot of different keys—social as well as biological ones.

Unlocking crime would require understanding a complex recipe. Very little in life is simple, and wine, lager, and violence are no
exceptions. So the ultimate answer had to be more than the one many sociologists were touting. Add the fact that I have always been a bit contrarian—my first research papers focused on biosocial
interactions in explaining antisocial behavior,
⁸
something radically different from the prevailing perspective in the 1970s, which was dominated by radical criminology espousing Marxist viewpoints.
⁹

We saw earlier that
birth complications—a biological factor—can predispose someone to later adult
violence. The seeds of sin strike early in life with anoxia and preeclampsia damaging the developing brain. But we also discussed how this biological risk factor particularly predisposes someone to adult violence when combined with a social risk factor—maternal rejection of the child.
¹⁰
We saw that these findings from
Denmark were replicated in the
United States,
Canada, and
Sweden. This was the first convincing scientific demonstration of a biological factor interacting with a social factor early in life to predispose someone to violence in adulthood. But it was not the last.

In 2002 I reviewed all research that had examined biosocial interaction effects in relation to any form of antisocial or criminal behavior. I found no fewer than thirty-nine clear, empirical examples of biosocial interactions.
¹¹
They covered the areas of genetics, psychophysiology, obstetrics, brain imaging, neuropsychology, neurology, hormones, neurotransmitters, and
environmental toxins. But before we delve into examples, let me
highlight one of two important
themes that emerged.

The first theme is that when biological and social factors form the groups in the statistical analysis and when antisocial behavior is the
outcome measure, then the presence of
both
risk factors
exponentially increases the rates of antisocial behavior. We’ll call this the interaction hypothesis. We’ve just seen an example of this in birth complications
and maternal rejection as risk factors raising the rate of violence in adulthood—the outcome measure.

Here’s another example, from the work of
Sarnoff Mednick, the pioneering and brilliant researcher who was instrumental in bringing me to the United States in 1987. Mednick conducted a study of
minor
physical anomalies, family stability, and violence. As you may recall from
chapter 6
, these minor physical anomalies are markers of fetal neural maldevelopment. He found that twelve-year-old boys with more minor physical anomalies committed more violent offending in
adulthood. However, when subjects from unstable, non-intact homes were compared with those from stable homes, Sarnoff found a biosocial interaction. The combination of minor physical anomalies
and
being raised in an unstable home environment exponentially increases the rate of convictions for adult violence at age twenty-one.
¹²
As you can see in
Figure 8.1
, if you were just brought up in an unstable home environment you have a 20 percent chance of committing violence. But when minor physical anomalies are added into the mix, that rate jumps to 70 percent—a threefold increase, just as we witnessed when birth complications interact with maternal rejection.
Danny Pine and
David Shaffer at
Columbia University observed a very similar biosocial interaction, with the combination of social adversity and minor physical anomalies tripling the rate of
conduct disorder in seventeen-year-olds.
¹³

Let’s put this piece of the jigsaw puzzle into practice in the case of a significantly violent offender. Carlton
Gary, nicknamed “the Stocking Strangler,” raped and killed at least seven women aged fifty-five to ninety. His modus operandi was to break into their homes in Columbus, Georgia, beat them up, rape them, and then strangle them with a stocking or a scarf. They were all white. What turned him into a killer?

Gary was a series of contradictions. At one level, he was a handsome man who worked as a model on local television. Yet he was also
a pimp and a drug pusher. While he was a caregiver for his elderly aunt by day, he also perplexingly raped and murdered equally elderly white women by night. At the same time as he was committing these murders, he was dating a female deputy sheriff.
¹⁴
He was also a bit of a Houdini, a talented escape artist who sawed through the bars of his cell and broke out of a prison in Onondaga County, New York, in August 1977.
¹⁵
Even though he broke his ankle in the twenty-foot fall, he made good his escape by jumping on a nearby bicycle. He eventually got a Rochester physician to put a cast on his leg, and for a while was reported to be hopping around like a duck.
¹⁶
He also escaped from a South Carolina prison in 1984. He was a persistent offender who had been in trouble since he was a kid—and yet he was a creative man with a reputedly
high IQ
¹⁷
who often managed to escape the dragnet thrown around him. He successfully talked his way out of an early end to his killing career by accusing another man. All told, he was a bit of a conundrum. Why would a bright, creative, attractive man resort to crime as a way of life? We can discern pieces of that puzzle in his complex biosocial makeup. Here’s something of that shuffle.

Figure 8.1
   Interaction between minor
physical
anomalies and home background in predisposing to adult
violence at age twenty-one

Gary never really knew his father, having met him only once, when he was twelve. He was all but abandoned by his
mother, who could not—or would not—care for him. He was bounced around from relatives to acquaintances
fifteen times
before his first arrest as a juvenile, and we see a clear breakage of the mother-infant bonding process that can predispose a child to become
Bowlby’s
affectionless psychopath.
¹⁸
He was also a scrawny young street urchin who, like Henry
Lucas, was so malnourished he was forced to rummage around for food in garbage bins. You now know that early
malnutrition is an important risk factor for antisocial behavior. Again like Lucas, Gary was allegedly abused by both his mother and the men she lived with. At school during recess one time he was knocked unconscious and was diagnosed with minimal
brain dysfunction. Again, we see parallels with Henry Lucas’s
head injury. Adding to his social deprivation, he had no fewer than five minor physical anomalies, including adherent ear lobes and
webbing of his fingers.
¹⁹

We see in Carlton Gary several of the biosocial warning signs we’ve been discussing. Salient among these are the
maternal deprivation we witnessed in the birth-complication study, the unstable home environment we saw in
Mednick’s study, and the multiple minor physical anomalies that
Danny Pine and others have documented.

Head injury and neurological markers of brain dysfunction are further all-too-common risk factors for violence that interact with social risk factors. My postdoctoral student
Patty Brennan, now at
Emory University, and I documented this in a sample of 397 twenty-three-year-olds, for which early neurological, obstetric, and neuromotor measures had been collected in the first year of life—together with family and social data collected at ages seventeen to nineteen and crime outcome data collected at ages twenty to twenty-two.
²⁰

Neurological deficits were assessed from an examination conducted in the first five days of life. The pediatrician looked for things like
cyanosis (where the skin, gums, and fingernails have a bluish tint to them). When oxygenated, the blood contains a red protein—hemoglobin. When it is blue, it lacks oxygen—and low oxygen impairs brain functioning. At one year of age the babies were also assessed for signs of poor
neuromotor development—such as not being able to sit up without support, not reaching for objects until eleven or twelve months, or not holding the head up until after nine months. On the social side, a psychiatric social worker interviewed the mother for measures of family instability,
maternal rejection of the child, family conflict, and
poverty.

We put all these risk factors into a cluster analysis—a statistical procedure that looks objectively to see if discrete, naturally occurring groups fall out.
²¹
They did. One group only had poverty. Another only had neuromotor dysfunction and birth complications. The third group had both biological and social risk factors.
²²
We also created a normal control group lacking any risk factor. We computed rates of total crime, property offending, and, more important, violent offending.

You can see the results in
Figure 8.2
. The rate of violence in early adulthood in the poverty-only group was 3.5 percent, compared with 12.5 percent for the biosocial group. As before, we see here more than a threefold increase. The biosocial group also had more than
fourteen times
the rate of total crime of the normal controls. Even though all three groups were of approximately equal size, the biosocial group accounted for 70.2 percent of all the crimes perpetrated by the entire sample.
²³
We clearly see here the potency of adding early neurological risk into the equation. These babies were brought into life without sin, and yet they were ushered into the vestibule of violence before they could even sit up on their own.

What we find for adult violence holds for aggressive teenagers.
Patty Brennan divided
adolescents from Australia into four groups. One had early social risk factors—
poverty, low education, lack of parental warmth,
maternal hostility and negative attitude toward the infant, lack of monitoring, and multiple changes in parents’ marital status. Another group had early
biological risk factors—birth complications and neurocognitive deficits. A third group had both sets of risk factors, while a fourth group was low on all risk factors. As you can clearly see in
Figure 8.3
, 65 percent of the biosocial group who had both sets of risk factors had serious aggressive outcomes starting early in life compared to 25 percent of those with just the social risk, 17 percent with just the biological risk, and 12 percent of the controls.
²⁴
Again in Australia the combination of birth complications and lack of nurturance is crucial, as in other countries.

Figure 8.2
   Increased criminal offending in those with both biological and social risk factors

We see the same for another very early risk factor—maternal
smoking during
pregnancy.
Pirkko Räsänen in Finland found that prenatal smoking doubled the rate of violence in adulthood in an enormous sample of 5,636 men.
²⁵
Yet if this biological risk factor was combined with
teenage pregnancy, unwanted pregnancy, and slow
neuromotor
development, that baby was a staggering
fourteen times
as likely to become a persistent adult offender.