The Anatomy of Violence

by Adrian Raine

  Figure 8.5 Genes give rise to brain abnormalities that in turn predispose to violence

  We’ve already discussed brain mechanisms and the violent mind. We’ve seen how specific genes link to violence. Now we’ll survey the building site where genes provide the scaffolding to structural and functional brain abnormalities supporting the foundations of violent behavior.

  You can view my blueprint in Figure 8.5. We start at the top left with genes. They link to both brain structure and influence neurotransmitter functioning (such as MAOA). Below that we have brain structure. The two bottom-up structures thought to support violence are down below in the limbic system and up top in the frontal cortex. Within each of these two broad brain regions, specific structures are identified—including the amygdala and orbitofrontal cortex—that contribute to the emotional and cognitive characteristics of offenders. We then have adult violence and two important variants that predispose someone to it—antisocial personality disorder and psychopathy. Each of these two variants has different behavioral and emotional elements. Limbic structures give rise to the more affective, emotional components of violence, while frontal impairments result in the cognitive and behavioral dysfunction seen in offenders.60

  How exactly do these genes produce aberrant brain conditions that predispose someone to violence? Recall the low MAOA–antisocial link. Males with this genetic makeup have an 8 percent reduction in the volume of the amygdala, the anterior cingulate, and the orbitofrontal cortex.61 We know that these brain structures are involved in emotion and are compromised in criminals. From genes to brain to offending.

  Let’s take the BDNF gene as another example. BDNF—brain-derived neurotrophic factor—is a protein that promotes the survival and structure of neurons and influences dendrite growth.62 Because mutant mice bred to have reduced BDNF have a thinner cortex due to neuronal shrinkage, we know that BDNF maintains neural size and dendritic structure.63 BDNF promotes the growth and size of the hippocampus, which regulates aggression.64 BDNF also promotes cognitive functions,65 as well as fear conditioning and anxiety.66 Given that offenders have poor fear conditioning, blunted emotions, and reduced volume of prefrontal gray matter, there is no surprise that the genotype conferring low BDNF is associated with increased impulsive aggression in humans.67 Mice made deficient in BDNF become highly aggressive and prone to risk-taking, just like their human counterparts.68

  Again, we go from genes to brain to aggressive behavior. While this particular subfield of neurocriminology has a very long way to go, we are starting to connect the dots—beginning with malignant genes, moving into brain impairment, and culminating in crime. Nevertheless, it’s going to be more complicated. I’m going to argue that the social environment, far from taking a backseat in this genetic and biological voyage to violence, is driving this Wild West stagecoach.

  FROM COMMUNITY TO BRAIN TO VIOLENCE

  You now know that the social environment is a causal agent in the brain changes that shape violence. After all, head injury is caused by what happens to you in your social world. You fall down and your head takes a hit. You have a car crash resulting in a whiplash injury. You were shaken as a baby. Whether it is what people deliberately do to you, or life’s luckless accidents, your brain gets damaged. And it is that damage that can unleash the devil within you—the unbridled, disinhibited influences that we saw in Henry Lee Lucas, Phineas Gage, and many others.

  But the environment is even more powerful in influencing the brain than you might imagine. Let me take you back to your childhood, but perhaps change things around a little. Suppose that now you are living in a neighborhood where violence is more commonplace than normal. You’re an eleven-year-old girl or boy, and coming up soon you are going to have a standardized school test on vocabulary and reading. Then, out of the blue, someone living in your immediate neighborhood is shot dead. Compared with other kids in your class who have the same smarts as you but who did not have a dead body dumped on their doorstep, you do more poorly on the test.

  This is what Patrick Sharkey, a sociologist at New York University and past student of the leading criminologist Robert Sampson, observed in an innovative data analysis of more than a thousand children in the Chicago Project on Human Development.69 If a homicide took place in the child’s block four days before testing, it reduced reading scores by almost ten points—or two-thirds of a standard deviation. Similarly, it reduced vocabulary scores by half a standard deviation.70

  How big are these effects? Placing them into context, the relationship between homicide exposure and reading scores is as strong as the relationship between distance above sea level and average daily temperature. It’s as strong as the effectiveness of a mammogram in detecting breast cancer.71 Similarly, the relationship found between homicide exposure and vocabulary scores matches the relationship between IQ scores and job performance.72 Put still another way, Sharkey estimated that about 15 percent of African-American children spend at least one month a year doing poorly at school purely due to homicides in their neighborhoods.73 These effects are really not trivial.

  We see here that it’s not just direct social experiences like physical child abuse that can change a child’s cognitive functioning. Even in the dark shadow of social experience, something indirect in society can affect your brain. An insidious effect of social experience can profoundly change neurocognitive functioning.

  What precisely is going on here in the neighborhoods of Chicago and other cities with a twinning of high homicide rates and poor school performance? Sharkey did not have any neurobiological data on the children he studied, but if he did I would expect to see subtle but meaningful changes in brain functioning in children exposed to neighborhood homicide. We know that excessive release of cortisol in response to stress is neurotoxic to pyramidal cells in the hippocampus—a brain region critical for learning and memory.74 It kills them off. It seems reasonable to hypothesize that children who hear about a homicide around the corner get scared out of their wits. Is this going to happen to their family? Can they walk to the store safely? Are they going to be next? That fear and stress can translate into temporarily impairing brain functioning and cognitive performance.

  If this mechanism is meaningful, you might expect a temporal relationship between the occurrence of the homicide and the reduction in cognitive performance. Suppose you are a child who has heard that someone was killed a few blocks away from you. Would you be more stressed at school if you received that news just a few days ago—or several weeks ago? Likely you would be most affected in the first few days. That’s exactly what Pat Sharkey found. The cognitive decline was present when the homicide took place four days before the test, but not when it took place four weeks before.

  What about the proximity of the homicide and your level of fear? If it took place in the block you lived in—as opposed to a more distant area of your neighborhood—wouldn’t that be a lot scarier? Might it not create a greater cognitive decline? It did. For both reading and vocabulary, homicides in the nearby block had a stronger effect on the child’s performance than homicides taking place further away in the neighborhood.

  There was a further tantalizing aspect of Sharkey’s results. The cognitive decline occurred for African-American children—but not Hispanic children. Why exactly that should be is unclear, but we can hypothesize. It could be that Hispanics feel less threatened by homicides than African-Americans do. Sharkey points out that in communities where African-Americans lived, 87 percent of the victims of the homicides were African-American, whereas in the murders that affected Hispanics, only 54 percent of the victims were Hispanic.75 Therefore, a nearby homicide may weigh more heavily on the minds of African-American children, and consequently pull down their test performance more.

  I would add another cultural explanation. Because Hispanic homes tend to have a more nuclear family structure and operate under higher levels of social support, there might be a greater social-buffering effect operating in Hispanic homes compared with African-American
homes.76 This would attenuate the effects of the local homicide on cognitive performance. Hispanic families might protect their children from the news of homicide, or may discuss it together more as a family, emphasizing that their children are protected and safe.

  Sharkey’s results are intriguing because low verbal IQ is an extremely long-standing and well-replicated correlate of crime.77 It has also been documented that African-Americans have lower verbal IQs than Caucasians,78 as well as higher homicide rates.79 Sharkey and Sampson have argued that over time, living in a disadvantaged neighborhood reduces the verbal ability of African-American children by about 4 points.80 Because a year of schooling is thought to result in IQ improvements of between 2 and 4 points,81 the 4-point drop resulting from a neighborhood homicide is the equivalent of missing a year or more of schooling. Mess up schooling, and you mess up employment prospects, and we know that after that, adult crime and violence are not far down the road.

  Take this even further. If the brains of African-American children are compromised by high rates of homicide that they experience in their neighborhoods, could this result in a vicious circle of increased violence and shootings in African-American neighborhoods, in turn giving rise to further neighborhood stressors and further cognitive decline?

  I know this is controversial, but it is also critically important to recognize that the social environment is far more important than many have ever imagined, and complicated in ways we’re still trying to understand.82 Jonathan Kellerman as a clinical psychologist and scientist in Los Angeles was decades ahead of his time when he published a paper in 1977 documenting how environmental manipulations can reduce oppositional and destructive behavior in a seven-year-old boy with XYY syndrome.83 The environment can overcome genetics. Believe me, this book has changed your brain structure forever. New synaptic connections have been formed throughout your brain in the amygdala, hippocampus, and frontal cortex by what I have just said. Whether you like it or not, those changes will last some time and be hard to eradicate. Social experiences change the brain, likely in all ethnic and gender groups.

  THE MOTHER OF ALL EVIL—MATERNAL NEGLECT AND EPIGENETICS

  We’ve seen that there is a substantial genetic component to crime and violence. Despite arguments I’ve made for a direct causal pathway from genes to brain to antisocial behavior, social processes are also critical. One such process is the lack of motherly love—and the fascinating mechanism of epigenetics.

  Epigenetics refers to changes in gene expression—how genes function. We often conceive of genes as fixed and static, but they are much more changeable than commonly believed. True, the underlying structure of the DNA—the nucleotide sequence—remains relatively fixed. But the chromatin proteins that DNA wraps itself around84 may be altered by the amino acids that make up these proteins. Proteins can be turned on—or turned off—by the environment. That alters how the DNA is transcribed and how the genetic material is activated. Methylation—the chemical addition of a methyl group to cytosine, which is one of the four bases of DNA—can also increase or decrease gene expression.

  How does all this occur? Through the environment—and triggered in animals by as little as a mother’s lick. The neuroscientist Michael Meaney first demonstrated that rat pups whose mothers licked and groomed them more in their first ten days of life showed changes in gene expression in the hippocampus. They also dealt better with environmental stressors.85 Indeed, the functioning of more than 900 genes is regulated by maternal licking and grooming in rats.86 Maternal separation at birth has very similar effects.87 Gene expression is thought to be especially affected during prenatal and early postnatal periods,88 and we know that these early periods are critical not just for the brain but for disruptive childhood behavior, which is a prelude to adult violence.89 Take away maternal care, and there can be profound biological and genetic effects on behavior.

  Strikingly, changes in gene expression caused by the early environment appear to transfer to the next generation.90 Protein malnutrition during pregnancy doesn’t just alter gene expression in the offspring; the offspring’s offspring—the grandchildren—develop abnormal metabolism even when their own parents were fed quite normally.91 So the environment not only changes gene expression in the individual—it also has permanent effects that transmit to the next generation. The exciting concept here is that although 50 percent of the variation in antisocial behavior is genetic in origin, these genes are not fixed. Social influences result in modifications to DNA that have truly profound influences on future neuronal functioning—and hence on the future of violence.

  We can place these alterations in gene expression into a much broader social context of how abuse and deprivation have foundational, long-lasting effects on the brain—over and above any epigenetic effects. Early social, emotional, and nutritional deprivation in humans has been shown to result in reduced functioning of the orbitofrontal cortex, the infralimbic prefrontal cortex, the hippocampus, the amygdala, and the lateral temporal cortex.92 It also disrupts white-matter connectivity in the brain—particularly the uncinate fasciculus, a fan-like white-matter tract that connects frontal brain regions to the amygdala and temporal brain areas to the limbic areas.93 Prolonged and chronic stress, including disrupted or poor mothering, disrupts the brain’s stress-response system. That results in excessive glucocorticoid release, a reduction in glucocorticoid receptors, an imbalance in the brain’s stress-defense mechanisms, and ultimately brain degeneration.94 Deprivation makes a big dent on the brain.

  There are also vulnerable periods when stress can take a greater toll on different parts of the brain. If sexual abuse occurs early, at around ages three to five, for example, hippocampal volumes are reduced. Yet if sex abuse occurs at age fourteen to sixteen, prefrontal cortical volume is reduced instead.95 This is broadly consistent with the fact that the hippocampus reaches full maturity early in life96 and is very much affected by excessive release of cortisol in response to stress. In contrast, the prefrontal cortex develops very slowly in childhood, but grows more rapidly during the teenage years.97 All told, it’s not just that stressful rearing environments affect gene expression and neurochemical functioning—they also affect growth and connectivity of the brain.

  There is, of course, much more to violence than maternal neglect. Sex abuse is almost always perpetrated by men. As we have discussed earlier, even the best of mothering sometimes cannot override a biological predisposition to violence. Fathers and friends play a role in fostering juvenile delinquency and adult violence as well. Yet it is undeniable that compassionate caregiving is critical for normative child development. When a mother’s love is morphed into spiteful hate—as it was with Henry Lucas and others like him—her kids can end up killing. In this context, mothering—and the lack of it—is giving us fascinating insights not just into the pathway to violence, but also into understanding the precise mechanisms by which maternal neglect might operate.

  Let’s put these pieces into place. We’ve seen that the lives of violent offenders are replete with maternal deprivation, physical and sexual abuse, other trauma, poverty, and poor nutrition. We’ve also seen how these social impairments have their hit on specific brain areas—the orbitofrontal cortex, medial prefrontal cortex, amygdala, hippocampus, and temporal cortex—brain areas that are linked to violence. We can conclude that such social deprivation results in long-term wear and tear of the developing brain to produce adolescent angst and aggression—and, ultimately, adult violence. This truly occurs, and it’s never too late for the damage to be done. Adults who lived close to the World Trade Center buildings on September 11, 2001—and thus were exposed to very significant environmental stress—showed a reduction in hippocampal gray-matter volumes when brain-scanned three years later.98 From environment to brain—and, at least in some—to ultimate destructive violence.

  BRINGING THE BRAIN BITS TOGETHER

  In this chapter we have been piecing together social and biological processes to explain violence. But what about
piecing together just the bits of the brain itself? It’s an enormously multifaceted, complex organ. We saw earlier, in chapter 5, that multiple brain regions are implicated in white-collar crime, and we know crime and violence come in all shapes and forms. No one discrete brain region or circuit will by itself account for violence.

  It is tempting to focus on the prefrontal cortex, given its complexity and the wide empirical support for its involvement in crime. It is even more appealing to invoke a single brain circuit involving two or three regions to help acknowledge this complexity—such as the prefrontal cortex combined with the limbic system, as I outlined above, or the orbitofrontal cortex and its control over the amygdala.99 Yet a limitation of the approach I have taken so far is that it is overly simplistic. Violence is an enormously complex and multilayered construct. A complete understanding of its neural basis is certainly going to involve multiple distributed brain processes that in turn give rise to broad social and psychological processes that predispose someone to violence. By beginning to recognize and model this neural complexity, I believe we can gain deeper insights into the etiology of antisocial behavior.

  In response to the charge of oversimplicity, here’s a functional neuroanatomical model of violence.100 Let’s take the anatomy of the brain and first describe the functions of the individual areas concerned—outlining the functional significance of the brain abnormalities we have found so far in antisocial offenders. I’m basing it largely on prior reviews of structural and functional brain-imaging research on offenders.101

  In Figure 8.6, I group brain processes under three broad headings—cognitive, affective, and motor—alongside the corresponding brain regions. Brain impairments in these areas predispose someone to more complex social and behavioral outcomes that in turn predispose an individual to antisocial behavior in general and violence in particular. No direct relationships are hypothesized from brain dysfunction to antisocial behavior. Instead, the model emphasizes the translation of disrupted brain systems into relatively abstract cognitive (thinking), affective (emotional) and motor (behavioral) processes. These in turn result in more complex social outcomes that represent the more concrete and proximal risk factors for offending in general. So these brain risk factors are not conceptualized as directly causing aggressive behavior, but instead bias thoughts, feelings, and actions in an antisocial direction that then results in violence.