by Adrian Raine
Let’s start on the left, with cognitive processes. Here we can see the involvement of the ventromedial prefrontal cortex, the medial-polar prefrontal regions, the angular gyrus,102 and the anterior and posterior cingulate. Impairment to these regions results in poor planning and organization, impaired attention, the inability to shift response strategies,103 poor cognitive appraisal of emotion,104 poor decision-making,105 impaired self-reflection,106 and reduced capacity to adequately process rewards and punishments.107 These cognitive impairments translate into social elements that lead to crime—poor occupational and social functioning,108 noncompliance with societal rules,109 insensitivity to punishment cues that guide behavior,110 bad life decisions,111 poor cognitive control over aggressive thoughts and feelings,112 overreaction to minor irritations,113 lack of insight, and school failure.
Figure 8.6 Functional neuroanatomical model of violence highlighting cognitive, affective, and motor processes
Turning to the affective processing deficits we see outlined in the top center of Figure 8.6, the neural structures I have highlighted are the amygdala/hippocampal complex, the insula, the anterior cingulate, and the superior temporal gyrus. Impairments to these regions can result in an inability to understand the mental states of others,114 learning and memory impairments,115 lack of disgust, impaired moral decision-making,116 lack of guilt and embarrassment,117 lack of empathy,118 poor fear conditioning,119 poor emotion regulation,120 and reduction in uncomfortable emotions associated with moral transgressions.121 These affective impairments can then result in being undeterred from perpetrating gruesome acts on others,122 callous disregard for others’ feelings,123 poor conscience development,124 and being unmotivated to avoid social transgressions.125 It’s easy to see how such a set of traits may in turn raise the likelihood of violence.
At the motor level on the right-hand side of the figure, brain areas include the dorsolateral prefrontal cortex, orbitofrontal cortex, and the inferior frontal cortex. Brain impairments here result in response perseveration,126 motor impairments involving a failure to inhibit inappropriate responses,127 impulsivity,128 the failure to shift response sets and passively avoid punishment,129 and motor excess.130 In the social context of everyday life this results in the failure to invoke alternative response strategies for conflict resolution,131 the repetition of maladaptive social behavior,132 poor impulse control,133 the failure to avoid punishment, and disruptive behavior.134
We see here a flow from basic brain processes to more complex cognitive, emotional, and motor constructs that then translate to real-world practical behaviors that we know characterize violent offenders. It’s certainly not a simple model, because violence is not a simple behavior. Yet it conveys the complexity of the problem we are dealing with when we try to put just the brain pieces of the puzzle together. You can imagine the even greater complexity involved when we come to including the macro-social and psychosocial processes that interact with these brain pieces. Furthermore, while I have included multiple frontal, temporal, and parietal regions, imaging research on violence is still a fledgling field. I’ve certainly simplified it here. There are many more brain regions involved, including the septum,135 the hypothalamus,136 and the striatum,137 among many others.
You may also wonder how violence in particular arises from these cognitive, affective, and motor forces. I view violence at a dimensional, probabilistic level. The greater the number of impaired cognitive, affective, and motor neural systems, the greater the likelihood of violence as an outcome. If, for example, you make poor decisions and you don’t feel guilt and you act impulsively, then that will exponentially increase the likelihood of violence—all other things being equal.
As I hope I have clarified so far, there is not one unique cause of violence. That is why violence is so hard to fathom—and one of the reasons it’s fascinating for scientists and the public alike. That is true for the brain too. For some social scientists it’s easy to think of the brain as a big blob—and yet in reality it’s a mesmerizing mélange of diverse regions, each with intriguing basic functions that contour criminal outcomes. We can see from the brain to basic cognitive-affective-motor processes to social behaviors that raise the risk of riotous behavior that the anatomy of violence is very complex.
Biology by itself is just not sufficient. Instead, we need social risk factors to pull the trigger on an outcome of violence. Although I have here emphasized early social deprivation in the violence jigsaw puzzle, I want to leave the brain uppermost in your mind. That’s because the brain goes to the heart of this book’s argument—the seeds of sin are brain-based. Despite decades in which scientists emphasized environmental and social processes, the brain is the cardinal transgressor.
This should not be a bitter pill for either social scientists or neuroscientists to swallow. We can get to bad brains through bad genes or bad environments—or, as I have argued in this chapter, through the combination of both. As you read this, greater appreciation for the complexity of violence combined with recent advances in neuroscience are paving the way for a much more sophisticated and integrated journey toward discovering crime causation, a journey that builds on the decades of painstaking sociological and psychological research on crime that social scientists can take credit for. What were two competing perspectives should now be more sensibly viewed as complementary in explaining the causes of crime. For traditional criminologists, what was once an old foe can become a new friend in the fight against violence.
Finally, we should return to our point of departure. Henry Lee Lucas was concocted from a horrendous home brew of head injury, malnutrition, humiliation, abuse, alcoholism, abject poverty, neglect, maternal rejection, overcrowding, a bad neighborhood, a criminal household, and a total lack of love. Violent offenders in general have a history of abuse and early deprivation,138 and with some exceptions noted earlier, this history particularly characterizes the backgrounds of serial killers.139 Lucas also had structural and functional brain impairments, as revealed by MRI and EEG examinations, with the frontal poles particularly affected, along with the temporal cortex.140 Toxicology tests also revealed particularly high cadmium and lead levels, heavy metals that we have seen impair brain structure and function.141 He can be pieced together and understood from distal structural and functional brain impairments that result in the more proximal cognitive, emotional, and behavioral risk factors for violence—bad decision-making at the cognitive level, callousness at the emotional level, and disinhibition at the behavioral level. These constitute key components of the puzzle making up this multiple murderer.
One unresolved piece remains. Why were all of his victims female? Henry Lucas’s first official murder victim was his own mother, whom he killed with a knife when he was drunk. While he believed he was only slapping her with his hand, he later realized that he held a knife when he hit her neck. He was twenty-three years old, and was sentenced to twenty years in prison for second-degree murder, as she ultimately died of a heart attack.142
Almost his last victim was Becky Powell, a twelve-year-old juvenile delinquent he had met when he was forty and developed an ambiguous relationship with. At one level he was a loving surrogate father for three years, making sure she was fed, clothed, and cared for—a better parent than he had had. At another level he educated her in stealing and burglary and became her lover. During a tiff when drunk, he stabbed the teenager through the heart, again with a knife. After having sex with her dead body he cut her up into pieces, stuffed her into two pillowcases, and buried her in a shallow grave. He would visit that grave several times, talking to Becky’s remains and weeping in remorse.143 It was the only truly loving relationship he had experienced in his whole life, bringing about a radical change in Lucas, who, surprisingly, confessed to his killings soon after being arrested on a mere weapons charge.
So at opposite ends in Lucas’s life we find two love-hate female relationships, with maternal abuse as the core cause of his many killings. Consider the dreadful deprivation of h
is childhood and the abuse heaped upon him by his alcoholic prostitute mother. The deprivation that she likely experienced herself as a child was passed down to Henry Lee Lucas not just environmentally, not just genetically, but likely epigenetically. We’ve noted how maternal care is one important ingredient in epigenetics—in gene expression. The complete lack of maternal care likely turned off important genes in Lucas that normally inhibit violence—and turned on genes that promote it. Genetic inheritance passed from one generation to the next. Yet the social environment was truly the factor that turned Lucas into a murderous psychopath.144 His mother had all the hallmarks of a hateful psychopath, and in killing her, Henry was virtually reliving his intergenerational genetic destiny of psychopathy. As Lucas said himself, “I hated all my life. I hated everybody.”145 He especially hated his mother, and that hatred was in all likelihood turned against other women, even those like Becky Powell whom he came closest to loving.
Recall also the puzzling picture of Carlton Gary, who similarly lacked secure parental bonds and suffered significant early deprivation and malnutrition. Among other perplexing issues in this case is why a handsome African-American man with glamorous girlfriends would resort to raping women over the age of fifty-five. Unusually, all were interracial homicides. All seven of his victims were white women—and yet only 1 in 10 homicides in the United States are interracial. Could this unusual pattern of violence stem from the fact that his mother and his aunt, who also raised him, worked as housekeepers for elderly, prosperous white women? Could complaining, cantankerous white women living at a time when overt racism was more common than it is today have led to hostilities from Gary’s caregivers that were passed down to him? Or, alternatively, could Gary’s hatred for elderly white women derive from his despising a mother who scarcely existed for him—a subtle redirection of aggression, as we saw for Henry Lee Lucas? And did epigenetics play a supporting role, with deprivation altering gene expression in Lucas for a rebound back to his mother?
What could have been done to save Henry Lee Lucas from a life of serial homicide, and, ultimately, death from heart failure in prison—to say nothing of saving his innocent victims?146 Are Lucas, Gary, and others like them a lost cause right at the beginning, in early childhood? Genes and brain predispositions to violence are not immutable. As we continue to piece together the different factors, social and biological, that play a role in predisposing individuals to violence, we become better placed to develop appropriate prevention and intervention programs. And that will be the focus of our next chapter—how we might prevent people like Henry Lee Lucas and Carlton Gary from becoming killers.
9.
CURING CRIME
Biological Interventions
Danny seemed to be a hopeless case. In spite of a well-to-do home environment in Los Angeles, complete with the support and care of loving, attentive parents, by the age of three he was stealing constantly. Further into childhood he became a compulsive and adept liar. At the tender age of ten, Danny was not just staying out all night, he was buying and selling drugs. He was known by other neighborhood kids as a nasty piece of work, and because it was a middle-class neighborhood they steered well clear of him. And it wasn’t for lack of trying on his parents’ part. As his mother recalled, “No matter what the discipline was, or the consequences of his misbehavior, it was never enough. There was no stopping him. We were really at a complete loss for answers.”1
Danny grew older and stronger, and essentially commandeered his parent’s house. He stole cars and appropriated his mother’s jewelry for drug dealing. He was getting F’s in school. He was a precocious abuser of drugs, graduating from cannabis to speed to cocaine to crystal meth. When he was fifteen he was sentenced to eighteen months in a juvenile detention center. It’s a familiar story, with all the early telltale signs of a life of crime, and likely violence too—perhaps another Jeffrey Landrigan in the making.
Out of sheer desperation his parents entered him in a biofeedback treatment clinic after his release from the detention center. These alternative-medicine clinics assess the physiological profiles of individuals with clinical problems to ascertain whether any physiological imbalance can be corrected. How? By helping them become more aware of their biology and teaching them to change their brain. At that point, neither Danny nor his parents actually had any hope that the treatment would do any good. They felt they were just going through the motions—but they turned out to be wrong.
The first clinical evaluation confirmed excessive slow-wave activity in Danny’s prefrontal cortex—a classic sign of chronic under-arousal. Then came thirty sessions of biofeedback. Danny sat in front of a computer screen with an electrode cap on his head, which measured his brain activity as he played Pac-Man on the computer. Danny controlled Pac-Man, trapped in a maze, and his task was to move around, gobbling up as many pellets as he could. He could only move Pac-Man by maintaining sustained attention—by transforming his frontal slow-wave theta activity into faster-wave alpha and beta activity. If his attention lapsed, Pac-Man stopped. By maintaining his concentration, Danny was able to retrain his under-aroused, immature cortex, which had constantly craved immediate stimulation, into a more mature and aroused brain capable of focusing on a task.
It was hardly a quick fix. For Danny, the biofeedback training lasted for nearly a year. But a metamorphosis took place over the course of his thirty treatment sessions. He was radically transformed, from an inattentive, F-grade teenager on a downward spiral toward prison into a mature, straight-A, career-oriented student who ended up passing his exams with distinction. It was a complete reversal of fortune.
What accounted for the dramatic change? To begin to answer, we have to look back at what was fueling Danny’s antisocial behavior, which started as early as toddlerhood and exploded during adolescence. “I was really bored in school,” Danny would say after his treatment was completed, “but all the crimes were really exciting to me. I liked the action, getting away from the cops. I just thought it was so cool.”2
The thirst for stimulation-seeking is clear. We documented in chapter 4 how children who are chronically under-aroused seek out stimulation to jack their physiological arousal levels back to normal. We know from longitudinal research that schoolchildren with excessive resting slow-wave EEGs are much more likely to become adult criminal offenders.3 That’s exactly what Danny demonstrated in his first clinical evaluation session—excessive delta and theta activity, chronic cortical under-arousal. We also discussed how poor prefrontal functioning predisposes an individual to impulsive homicide. We saw how when the home environment is loving and devoid of deprivation, yet the child is still antisocial, we should expect biology to be the culprit in crime—the social-push hypothesis.
We see in Danny’s case an example of how biology is not destiny. The psychophysiological, brain-based predispositions to crime and violence are not immutable. Importantly, Danny himself—albeit with the aid of electronic biofeedback and social support—instituted his own metamorphosis. It’s more a case of mind over matter. He had agency in his rehabilitation—and that may have been a critical component in his redemption.
Of course there is no easy solution to crime and violence, and Danny is just a case study. Yet what I want to give you in this chapter is a hopeful message. Rather than giving up when faced with biology-based offending, we can use a set of biosocial keys to unlock the cause of crime—and set free those who are trapped by their biology at an early age.
THE STORY SO FAR
Before embarking on what may work to help kids like Danny, let’s summarize what I have been arguing so far, using a theoretical framework to give a context to treatment efforts. You can see it visually in Figure 9.1.
This biosocial model emphasizes the role of genes and the environment in shaping the factors that predispose someone to childhood aggression and adult violence. A key assumption is that joint assessment of social and biological risk factors will yield innovative new insights into understanding the development of
antisocial behavior.
The right-hand side of the figure outlines the main components of the model. Starting at the top, we have both genes and environment as the causal foundations of later violence. Social risk factors, on the right, have been the understandable focus of social scientists for three-quarters of a century. Biological risk factors, on the left, reflect neurocriminology, the new and more challenging field of enquiry.
Genes and environment are the building blocks for the biological and social risk factors in the next lower step in the model. Yet you’ll also see arrows linking genetics with social factors as well as with biological risk factors. Genes can shape social risk factors for violence such as low social class and parental divorce.4 Similarly, social risk factors like environmental stress can impair brain functioning, while living in a risky neighborhood can increase the chance of head injury.
Figure 9.1 Biosocial model of violence
Biological and social risk factors then give rise to brain risk factors that are played out at three levels: cognition (e.g., attention deficits), emotion (e.g., lack of conscience), and motor (e.g., disinhibition) processes. This brain dysregulation can then do one of two things. It can move on to directly give rise to conduct disorder and violence, or it can join forces with social influences to form a biosocial interaction that brings on the teenage thunderstorms of emotion. This biosocial pathway is what I tried to emphasize in the previous chapter, and consequently I place it here as the heart of the model of the anatomy of violence.