by Adrian Raine
Henry’s mother, Viola, was an even worse parent. An alcoholic as well as a prostitute, she gave birth to Henry when she was forty, after she had already abandoned four children to foster homes. Henry; his elder brother, Andrew; his parents; and Viola’s pimp all shared the same bedroom in a dirt-floor, ramshackle cabin near Blacksburg, Virginia, without electricity or plumbing. From the time he was a small boy, Henry had to watch his mother having sex with her clients.
Chronically malnourished, Henry was forced to scavenge for food in garbage bins to stay alive. His mother would cook only for her pimp, and the children ate their scavenged food off the floor, as Viola wouldn’t wash plates. His first hot meal as a child was when he started attending school and a teacher took pity on him. That same teacher also gave him his first pair of shoes.
His mother psychologically and physically abused him. Once, when he was seven years old, he was too slow to fetch wood for the stove, so his mother hit him hard on the head with a wooden board. Such was the level of neglect that he lay where he had fallen for three full days in a semiconscious state, totally ignored by the rest of his family. Ironically, it was Bernie the pimp who eventually thought something was seriously wrong and took Henry to the hospital, telling doctors he had fallen off a ladder.1
This was likely only a fraction of the physical abuse and head trauma Henry endured. For the rest of his life he experienced blackouts, spells of dizziness, and at times felt he was floating on air. Neurological examinations and brain scans later in life revealed evidence of extensive brain pathology, very likely a result of the early maternal abuse and deprivation he had suffered.2
Henry was also subjected to sustained psychological cruelty by his mother. When he was seven she pointed out a stranger to him in town, telling him, “He’s your natural pa,” a fact later confirmed by Anderson, Henry’s supposed father.3 To have such a basic fact of life shattered like that would pull the psychological rug out from under most children’s feet, and not surprisingly Henry was devastated and in tears when hearing this news. His sister documents that his mother dressed him as a girl from the time he was a toddler up to his first day at school. His teacher, horrified by his treatment, cut his hair and got him a pair of trousers to wear.
The cruelty of his mother seemed to know no bounds. Viola once saw him enjoying playing with a pet mule. She asked him if he liked his pet mule. He said he did. So she fetched a shotgun and killed the mule in front of his eyes. As if this psychological cruelty was not sufficient to satisfy her, she proceeded to whip and beat the child because it would cost money to have the mule’s carcass carted away.4
At school Henry was continuously tormented by other children because he was very dirty and smelled terrible. His abject misery was compounded when his brother Andrew accidentally stuck a knife in his face when they were making a swing from a maple tree, puncturing his eye and impairing his peripheral vision. Bad luck morphed into extremely bad luck when a teacher at school swung her hand to hit another child in class, missed, and accidentally caught Henry in the same left eye. The accidental blow reopened the wound, resulting in the loss of his eye.5
Henry would go on to become one of the most prolific serial killers in history. He was eventually convicted of eleven homicides committed over a twenty-three-year period, from 1960 to 1983, but he was implicated in a massive 189 altogether. All his victims were female—but we’ll return to that issue later. For now his case is particularly salutary in illustrating how a toxic mix of biological and social factors can conspire to create a serial killer.6
That mix of biological and social deprivation created a surprisingly efficient killing machine, given the disadvantages Lucas was dealt in life. On the biological side there are three very important risk factors for violence that have been highlighted in previous chapters—head injury, poor nutrition, and genetic heritage from his antisocial parents. These are abetted by a host of social risk factors, including abuse, neglect, humiliation, maternal rejection, abject poverty, overcrowding, being in a bad neighborhood, induction into alcoholism, and complete absence of care and sense of belonging. It was this bitter brew—this very cruel concoction—that turned Lucas into an alcoholic killer.
Lucas’s case, while extreme, is not exactly unusual. We’ll review in this chapter the scientific evidence showing that when even mild social and biological risk factors coalesce, we can especially expect later trouble. So far we have been identifying the biological factors that go to make up the anatomy of violence. But these are just the bare bones. This chapter aims to flesh out the skeleton by outlining research showing how social factors combine—or interact—with biological risk factors to shape the violent offender.
Criminals like Lucas are a biosocial jigsaw puzzle, consisting of many different and scattered pieces. Even after identification of the biological pieces, it is a challenge to understand how they fit together with the social and psychological processes that decades of prior research have tied to violence.
From this vantage point, we will first turn our attention to understanding how social risk factors come together with biological risk factors to create violence—how they interact in a multiplicative fashion. I’ll then show you how the social environment moderates—or changes—the way that biological factors work. I call this the “social-push” hypothesis. We’ll see how genes shape the brain to promote violent behavior and yet, at the same time, how the social environment beats up the brain and reshapes gene expression. Finally, we’ll piece together the parts of the brain that we have implicated so far and map out more precisely how they collectively give rise to violence.
THE BIOSOCIAL CONSPIRACY: INTERACTION EFFECTS
Henry Lucas was ten when he allegedly became addicted to alcohol. I was eleven when I became addicted to making it. I made wine out of anything I could lay my hands on—potatoes, strawberries, raspberries. Like Lucas I was a scavenger. I even made wine from the blossoms of our goldenrod plant. I bootlegged my brew to visitors and relatives. I used the profits to back horses, running the bet—supposedly from my mother—down to the corner shop, whose owner was a bookie. At fourteen I turned to making lager and I was pretty good at it, except I made the alcohol content too high and people got drunk too quickly, cutting my sales.
When I later began to study adolescent antisocial behavior instead of practicing it, what stayed with me from that extensive experience in brewing was a simple lesson: it takes a complex mix of factors to create the end product. You think of wine and you think of grapes, but of course it is much more. The fermentation of the yeast in the sun with a little bit of sugar. Squishing the fruit to make the must. Adding potassium metabisulfite to kill bacteria and wild yeast. Getting the fermentation process going. Having the acid level just right. Using a hydrometer to measure the specific gravity of the liquid to ensure that there is enough sugar for the yeast to convert it into carbon dioxide and alcohol. There’s the racking of the wine by siphoning it off the sedimentary lees at the bottom of the gallon demijohn. Most important, it’s not just the mix of ingredients but the right environment. You need precisely the right temperature for the yeast and fermentation process.
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 IQ17 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.
