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John Orvis
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The new theory that could explain crime and violence in America

Forget what you’ve heard about guns and drugs. Scientists now believe that the roots of crime may lie deep within our biology.

  • Scott C Johnson in Matter
  • 31 min read

The new theory that could explain crime and violence in America

Forget what you’ve heard about guns and drugs. Scientists now believe that the roots of crime may lie deep within our biology.


YOKIA MASON NEVER KNEW HER FATHER. Melvin Mason Sr. committed suicide when she was just six months old, leaving her in the care of her mother Geraldine, a violent alcoholic and crack addict. Geraldine was beaten by a succession of drug-using boyfriends, and she beat her own children too, including Yokia. Geraldine’s mother, Betty, also an alcoholic and a drug addict, lived with the family and often joined in.

As a young girl, Yokia would come home to find her mother and grandmother high or drunk, surrounded by men, whose status — friends or johns or dealers — was never very clear. Betty liked pornography and kept an abundance of it around the house. She also liked to be naked.

“Betty’s the one who told me what the birthday suit was,” Yokia told me recently. “I’m little and grandma’s like, ‘I got my birthday suit on,’ and I’m thinking it’s her birthday. Then I get older and I’m like, oh shit, grandma walking around naked, high, tripping. They had pornography around, just whatever, pornography, dicks, men, kids, just no respect.”

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Betty was in her late 40s when she died. Geraldine passed away in 2005, at the age of 47. “She sat down and said she wasn’t feeling good,” Yokia said. “Fifteen minutes later she was dead. That was her life.”

Yokia is a tall woman with tightly cropped hair and strong features. One afternoon not long ago, I joined her at the home of her great-great-aunt, Martha Ann, who has lived in the same clapboard house in East Oakland, California — on the other side of the city from Yokia’s childhood home — for over 60 years. Yokia opened a metal security gate and ushered me in. We had met before, but this was the first time I had seen her at home: she had left her boyfriend of 15 years a few months earlier and was now living with Martha Ann.

“I was getting really anxious about seeing you,” Yokia confessed. “I was getting paranoid again. I don’t know what’s going on, I was thinking all kinds of crazy things.”

When we last spoke, Yokia had said that she was often depressed and anxious. She had a hard time controlling her feelings. Her thoughts raced. Sometimes she felt suicidal.

Before I could say anything, Yokia wandered off into a back room to fetch Martha Ann. A frail African American woman with very light skin and a few white whiskers on her chin emerged. She sat down across from me at her dining room table. Martha Ann is 104 years old, but she remembers the chaotic environment in which Yokia grew up, and from which she had to protect her when things got bad. “That whole family, they was just crazy,” she said, running her thin hands over the floral-patterned linoleum that covered the table. I asked Martha Ann about the history of violence in her family. She began to twitch and fidget. Yokia was standing by the wall.

“See that?” she said, pointing at Martha Ann. “Just talking about it makes her stressed out. I know what that looks like: that’s what’s going on with her right now.”

Martha Ann struggled with the memories at first, but eventually they began to float to the surface. As they did, a pattern appeared. Both women agreed that Yokia’s mother was a “hot mess”. She would physically fight people — men, women, she didn’t seem to care — and would fly into rages with little warning and no apparent reason. Martha Ann thought there was “evil” in Betty too. “There was something wrong with her,” she said, shaking her head. “I don’t know what it was, but there was something wrong.” Betty’s mother, Yokia’s great-grandmother, was no better, she added.

Martha Ann described Yokia as a clever child who made an effort to shake off her home life. She went to school and stayed away from drugs. But even as she tried to break away from the patterns she saw in her mother and grandmother, she found herself repeating them. By the time Yokia was 16, she was a mother herself. Eventually she left her first child’s father, who was a drug dealer, and moved in with another man: they had four children together. At the same time, she started abusing alcohol, like her mother and grandmother before her. She suffered regular panic attacks and contemplated suicide.

“The whole time I’m trying not to be like the family. I know that this is not the way, but I’m still… it’s still on me though,” Yokia said, wriggling her hands as if trying to shake off a cobweb. “If I decide to drink on a Friday I’m gonna drink, I’m gonna go crazy, but I would go really crazy, I’d start crying, I’d start talking about my childhood, and people were like, what is wrong with this girl? I acted a lot like my mother.”

As she grew older, Yokia wondered why she couldn’t break the pattern. “I can’t really shake some of this behavior, it’s like a ghost,” she said. “The ghost, it’s in my being. No matter what. I could fucking win the lottery today, but that ghost is still there. It’s like it’s out to kill me.”


IN THE SUMMER OF 2008, a group of scientists at McGill University in Montreal began looking at a series of brain samples. The samples had been assembled by Gustavo Turecki, a psychiatrist who for several years had been collecting the brains of people who had committed suicide.

Turecki also had detailed records of each of the donors’ lives. Some of the suicide victims had hanged themselves; others had taken overdoses or used a firearm. Their brains were stored at -80 ºC. Turecki picked out 36 samples for analysis, several of which were from people who had been abused as children. He also put together a separate cohort of brains of victims of accidental deaths, mostly car crashes. Then he took pinprick-sized samples from each, drawing the tissue from the hippocampus, a curving, elongated area of the brain that sits deep below the surface and handles memory and learning.


Turecki worked with Michael Meaney, a colleague of his. Meaney, an amiable-looking man with slightly hooded eyes, was beginning a series of studies on the biological impact of childhood trauma. He already knew of studies that showed that victims of physical or sexual abuse are more likely to take their own lives as adults. He’d also read papers that described how childhood abuse can damage a person’s ability to handle stress. These results could be explained away by emotional trauma, of course, but Meaney wanted to know if any biology was involved. How does the toxic impact of childhood abuse live on in a person? Why does it cause some to commit suicide? The answer, he thought, might be hidden in the brains of the suicide victims.

Meaney had his eye on one particular molecule. The glucocorticoid receptor is one of the basic building blocks of our stress response system. It’s a protein that helps us control the hormones that cause stress: the more of the receptor we have, the better we’re able to respond to stressful situations. The reverse is also true: low receptor levels are associated with disorganized, chaotic responses to stress. What’s more, Meaney knew that levels of the receptor could be influenced by upbringing — at least, experiments had shown that was the case in rodents. By disrupting the maternal bond between a female rat and her young, researchers had already shown that poor parenting can cause young rats to have fewer glucocorticoid receptors. And when they grow up, those same rats coped badly with stress. Meaney wondered if something similar might be happening in humans.

When the analysis was complete, Meaney saw an intriguing pattern. For the most part, the brains of suicide victims had similar receptor levels to those of people who had died in accidents. But in the samples from victims of childhood abuse, receptor levels were lower — just as with the rats. When he homed in on the cause of the difference, things got even more interesting. Meaney discovered that the gene for the receptor was covered by a chemical blanket that effectively silenced it — exactly the same silencing mechanism as seen in the rats that suffered poor maternal care.

The implication was significant: an abusive childhood might turn the volume down on this vital stress-response gene, leaving the abused vulnerable to stress, and perhaps suicidal impulses, later in life.

I spoke with Meaney earlier this year, and he recalled the moment when he looked through the microscope and realized what was happening. “I remember this very warm feeling that came over me,” he said. Meaney had successfully revealed a biological basis for what most people had until then consigned to the realm of social science — a link between childhood abuse and suicide.

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Meaney’s study was a landmark moment in a field known as epigenetics, a line of study that is changing our understanding of the links between childhood experiences and adult behavior. His focus was suicide, but epigenetics is revealing that a slew of behaviors, from depression and other mental illnesses to aggression and perhaps even crime, may be shaped by chemical imprints laid down in the cells of people who suffer traumatic childhoods. It’s an area of research that, as a recent article in Nature put it, provides “a molecular middle ground in the centuries-old debate over nature versus nurture”. It may even tell us why families like Yokia’s have endured so many generations of chaos.

The focus of the field is something scientists call the “epigenome”, a medley of chemical interactions that take place around our DNA. (Epi means “above” or “beyond” in Greek.) Our genes are the foundation of our biological inheritance, and they govern some of our potential to grow to a certain height, or to succumb to a particular disease. The epigenome helps determine how that potential is realized. It can turn off one gene and enhance the activity of another, shaping the behavior of our cells in the process. If our genes are our hardware, the epigenome is the software that runs on top, the instructions that govern how our genes behave.

These instructions are written in a chemical code that we’ve only just begun to decipher. One of the simplest and best-understood parts of that code is the instruction to silence a gene. When Meaney examined the brains of the abuse victims, for example, he found that many of their glucocorticoid receptor genes had been covered with a chemical blanket, known as a methyl group, that shut the gene down. Deprived of an important cog in the machinery for reducing stress, the abuse victims may have been more vulnerable to suicidal thoughts. And, at least in animals, parental neglect can prompt gene-silencing methyl groups to cover similar stretches of DNA.

The terrible effects of childhood abuse are already clear to us. What epigenetics promises is an understanding of how these effects are carried within victims as they become adults. It suggests that the world we grow up in doesn’t just teach us how to behave: our environment also helps fashion chemical instructions that influence the activity of our genes for the rest of our lives. It suggests that these instructions may be a ghost in the human machine. They may even be Yokia’s ghost.


DOGTOWN, THE NEIGHBORHOOD WHERE YOKIA grew up, spans just a few blocks across. It sits at the western edge of Oakland, near the city’s port and the shore of the San Francisco Bay. The area is home to some of the oldest Victorian homes anywhere in California — holdovers from a century ago, when the First Transcontinental Railroad had its terminus there, and a golden era of African American prosperity was rooted in its streets.

During World War II, thousands of migrant workers fled poverty and persecution in the Deep South and moved to Oakland, where they found work in the booming shipyards. But when the war ended, so did the work. The economy stagnated and the neighborhood began to decay. Old homes were torn down as city managers made way for public housing projects, a sprawling post office warehouse and a new rapid transit system.


By 1979, when Yokia was born, swathes of West Oakland were pockmarked by empty lots and abandoned buildings. The post-war population of over 200,000 had shrunk to well under 50,000. Poverty, unemployment and alcoholism were on the rise. It was around this time, said Oakland residents, that the neighborhood gained its nickname, as police on patrol noticed how many dogs were roaming the deserted streets.

Crack hit Dogtown in the early 1980s. It moved through the dilapidated Victorians and the projects like a virus, pulling apart families as it spread. Geraldine, who eventually had six children, was already an alcoholic when Yokia was born — but it wasn’t until later that she graduated to crack. Her subsequent children, like Yokia’s brother Johnny Sloan, were born while she was using on a regular basis. The extended family — one of Geraldine’s sisters had 12 children, another three — lived nearby, in the midst of a drug epidemic. “The police were at our house at least once a week for something,” recalled Yokia. “We had to survive, really survive. Food, school, everything was survival. All the adults were drunk or high, and not available to take care of us.”

As Dogtown crumbled around Yokia’s family, scientists and policymakers debated why violence persisted there and in other low-income neighborhoods. Many chalked up stories about families like Yokia’s to what’s called “learned behavior”: they argued that people in communities stricken with violence and crime repeated the patterns they saw around them. Some argued that salvation lay in pulling oneself up by one’s bootstraps. Others emphasized the need for outside support for troubled communities, perhaps through better job opportunities or community-focused policing. But for both groups, the cycles of dysfunction that wrecked Yokia’s childhood were essentially sociological problems.

A third group, however, took a different angle. They looked at families like Yokia’s, in which men and women from multiple generations have been jailed for violent acts and drug use, and saw something different: evidence for a genetic basis for criminality. This was far more controversial, not least because such claims carry the taint of eugenics, the Victorian-era theory used to justify the forced sterilization of the mentally ill and criminals. Yet in recent decades, the distinction between modern genetics and eugenics has sharpened. Slowly, the taboo against the discussion of links between genes and crime has faded. Scientists aren’t searching for a “crime gene”, nor do they believe that race plays a role in the link. But many think that some parts of our DNA help shape aggression, and, by extension, some crime.

Epigenetics is where these twin spheres of inquiry — biology and sociology — have started to overlap. Thanks to the work of Meaney and others, many researchers now believe that the neglect and fear that pervaded the Mason household will have left a powerful chemical imprint in the cells of Yokia and her siblings. If the scientists are right, we may have to change the way we think about tackling violence and crime. And if the newer claims emerging from these same researchers are also correct, we may have to accept something even more disturbing: that the trauma written into the cells of the people of Dogtown may be inherited by their children.

“We’re used to thinking of inheritance as DNA focused,” says Frances Champagne, a neuroscientist at Columbia University in New York. We know that the toxic effects of childhood trauma can change lives, and that those effects can spill over into future generations. But the process has been seen as social. “What’s being realized now,” says Champagne, “is that it’s biological.”

Today, Dogtown and its surrounding neighborhoods contain some of the most dangerous blocks in America. Along with similarly impoverished areas on the eastern side of downtown, these streets are the setting for most of the 100 or more murders that occur in Oakland each year. Despite the end of the crack epidemic, crack houses can still be found dotted along the broad avenues and tree-lined streets where, in a more settled era, trolleys from the Pullman Palace Car Company once rolled. And while the neighborhood has recently seen an economic resurgence — due in part to cheap homes and a new hipster culture based on local art collectives — Yokia’s old stomping ground retains an aura of despair.


THE UNIVERSITY OF ZURICH is situated close to the Swiss city’s downtown. It sits near a lake, surrounded by trees and ringed by the slope of the nearby Uetliberg massif. The long shelf of the Alps lies to the south.

In the autumn of 2003, Isabelle Mansuy was a young professor working at the university’s Brain Research Institute. The French scientist had completed a four-year stint at Columbia University in New York a few years earlier, and had been hired by the Zurich lab to investigate memory and the long-term impact of stress. One of her early projects was to develop an animal model for borderline personality disorder.


It is a condition marked by several distinct traits. Most sufferers experienced physical or sexual abuse as children. They often self-harm: some burn themselves with cigarettes, or cut themselves with razors. And while women with the disorder tend to hurt themselves, men are more prone to lash out at others. Mansuy knew the disorder ran in families, but the mechanism for transmission had not been established. So she devised an experiment using mice. “Now it sounds very intuitive,” she says. “But ten years ago it was not very common, and very adventurous.”

Mansuy began by subjecting mice to a series of ordeals that, if a human analogy can be made, might be said to generate a similarly terrible stress to that inflicted by some abusive upbringings.

Her initial subjects were 40 pregnant black-six mice, a strain that is relatively smart. In the weeks after the mice gave birth, Mansuy separated the pups from their mothers for three hours every day. On its own, this would be a disturbing experience for both the parent and her young — but the mothers had additional reasons for not enjoying the separation.

In one test, Mansuy would take the mother away and place her in a plexiglass tube that was too small to allow movement. In another, the mothers were plunged into containers of cold water. This was intensely uncomfortable for them: mice dislike swimming and avoid entering water if they can. Mansuy’s team carried out the tests at unpredictable times every day for two weeks. The intention was to stress the animals. “Very serious stress indeed,” she told me. “It’s chronic, every day for a long time, and it’s very severe because it’s unpredictable.”

Then Mansuy waited. She knew that the stress would cause the mothers to neglect their pups, but she was more interested in the effect it would have as the young mice matured.

Three months later, she used a series of well-established tests to look for rodent analogs of human ailments such as depression. The adult mice were placed into containers of cold water — the same containers their mothers were held in three months earlier. A mouse will naturally start to swim in such situations, seeking the edge of the water and a route out. It will fight and climb to escape. But if it can’t, the mouse will eventually realise its efforts are futile, give up and begin to float. The key measurement here is how much time this takes: happy mice seek a way out for longer than depressed ones.

Another test involved something else that mice detest: being hung from their tails. A typical mouse will struggle for a minute or more, but depressed mice give up after only a few seconds. Mansuy also looked at social behaviors, by introducing the animals to “novel peers” — in other words, mice they didn’t know. In normal circumstances, the arrival of a fresh face prompts some cautious exploration: the mouse sniffs around the newcomer, gradually learning to recognize its new companion. A depressed mouse, by contrast, shuffles into a corner like a terminally shy party guest. If the depression is severe, the animal may even fail to recognize that there is another mouse present at all. On every test, Mansuy’s mice betrayed their troubled start to life: in the water they began to float almost immediately; when dangled by their tails, they hung listlessly and refused to struggle; placed with new peers they seemed uninterested, almost unaware.

Mansuy was searching for clues as to how borderline personality disorder passes through families, so she decided to see whether the impact of the stress might extend beyond the generation exposed to it.

She took the male pups from the stressed group, and mated them with a fresh, happy batch of black-six females. This time, neither the mothers nor the pups were subjected to any stress. The mothers reared their pups communally, as they do in nature. Then Mansuy put the young mice through the same series of behavioral tests. She remembers having a feeling of excitement in the pit of her stomach as she awaited the results, and when they arrived they were as she had anticipated: the mice showed exactly the same patterns of depression and socially-altered behavior, and to the same degree as their stressed fathers — despite never having been exposed to stressful situations directly.

Even so, Mansuy checked again. She mated the males with a different batch of new females and reared this third generation as she had the second. Again the offspring showed the same patterns. And when Mansuy dissected the brains of the stressed mice afterwards, she found changes in the methylation — the gene-silencing process — in areas of the brain related to stress response. More recently, she found similar patterns in the brains of the offspring of those mice. The mice had inherited a chemical imprint of their parents’ stress, as well as a behavioral one.

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Last year, a group of researchers based at another Swiss center produced a startlingly similar result. The team was led by Carmen Sandi, a lab head at the Federal Institute of Technology in Lausanne and a friend of Mansuy’s for several years. Sandi was interested in violence that occurs within relationships. Many researchers believe that violent habits are perpetuated by children observing — and learning from — adults who act in the same way. Others think that cultural patterns, including the dominance of men in many societies, legitimize aggressive male behavior. Sandi didn’t necessarily disagree, but she thought that biology might also be part of the story.

Like Mansuy, Sandi started by traumatising her subjects, which in this case were rats. Each received a double dose of fear. In one test, she put male rats in a cage containing a synthetic version of a chemical found in fox feces. There is no human equivalent to this test, but, if you want to imagine one, consider what it would be like to believe that a tiger the size of a bus was about to enter the room. In the second test, Sandi placed the rodents on an elevated platform three feet above the ground — a virtual skyscraper for rats, who fear both heights and open spaces. These tests were conducted at random over a period of seven days: some days the rats experienced both, other days only one.

The trauma induced by the tests turned the rats into terrible partners: they were excessively aggressive towards their female cage-mates, even when those females displayed submissive behavior, which would normally be enough to placate the males. More disturbingly, Sandi saw the same behavior in the offspring of those pairings — even though these rats never met their violent fathers, who were removed from the nest before birth, and despite receiving what appeared to be typical care from their mothers.

These are unsettling results. Both Mansuy and Sandi found that animals can inherit the chemical imprints of stress experienced by their parents, even if they had never been stressed themselves. If humans can also inherit epigenetic marks, we may have to accept that childhood abuse doesn’t just damage those who suffer it; it also impacts the brains and bodies of victims’ children, and perhaps their children’s children. If so — and there is much work to be done before we can draw such a conclusion — epigenetic inheritance may be part of the reason why families like Yokia’s have experienced multiple generations of crime and child abuse.

At home, pondering the results, Mansuy turned to history for inspiration. She spent an entire Sunday reading manuscripts written by the 18th-century scientist Jean-Baptiste Lamarck — the father of a simple, but very controversial idea: that acquired characteristics could be inherited. Lamarck believed that traits developed in one’s own life, through environment, industry or experience, could be passed on to one’s offspring. As Darwin’s theory of natural selection gained traction, the concept of “acquired characteristics” started to decline in popularity. It was further discredited, at least by association, when Soviet agriculturalists of the Stalin era claimed that they could use Lamarck’s theory to improve crop yields, an application that had disastrous effects on food production. Among modern scientists, “Lamarckism” is almost a shorthand for a failed theory.

“Some people still hate him today,” says Mansuy. Yet Lamarck’s ideas had been in the back of her mind as she carried out the mouse studies. As she read the manuscripts, written in old French, she became increasingly excited. “The feeling I had in reading those old monographs was that he was so right, he was right.”

Yokia’s family at home.

IN 1993, WHEN YOKIA MASON was 13, her older brother Melvin Jr. moved back to Oakland. The two had grown up in the same house, but Yokia was upset by his return. This was because his absence had been enforced: by his early teens, Melvin had become involved in Dogtown’s street life of drugs and violence, and a court had intervened and sent him to a boy’s home in Fresno, a three-hour drive away in California’s Central Valley. Melvin was banned from setting foot in Oakland, and the move altered his trajectory in just a few months. Six feet seven inches tall and athletic, he excelled at basketball and quickly managed to score a sports scholarship to a local university.

But the court order expired when Melvin was 18 and, with freedom handed to him, he decided to return to Oakland. Within days he picked up the life he had left behind, and within weeks he was arrested for possession of drugs. The arrest cost Melvin his basketball scholarship and earned him a two-year prison term. He served his time, but once he was released the life wouldn’t let go of him. Shortly after getting out, he was standing at a bus stop when he was robbed and shot in the neck, paralyzing him from the waist down. He spent half a decade recovering, eventually learning to use his hands and arms again. As his condition improved, he moved into an assisted living home and from there got his own apartment.

“So Melvin gets out and goes into Oakland and gets an apartment right in the hood, and everything is running together,” Yokia told me. She spoke quickly, as if she was trying to keep pace with everything she wanted to say, but struggled to express. “He’s living there in the hood and somehow he could not be washed of that mentality, so the other street guys they like him, and my mom’s not helping him — she’s drunk and still smoking crack, getting beat up, going in and out of whatever she doing — and he’s having to call the police on her, and so my youngest brother…”

Yokia trailed off and went quiet for a moment.

“Johnny Sloan,” she said.

Johnny and Yokia had the same mother, but Johnny had a different father, who was in prison for murder. Johnny’s paternal grandmother adopted him as a young boy and took him out of Geraldine’s world, but the physical absence didn’t seem to have much of an effect.

By the time he was a teenager, Johnny was “crazy”, said Yokia. She described him dealing drugs, fighting, stealing. His grandmother eventually sent him to a group home, where he was briefly medicated, but he continued to misbehave. “It was like, what the hell is wrong with him?” said Yokia. Martha Ann, leaning over, concurred: “That boy had the devil in him.”

Johnny eventually served six months for robbery. When he got out of prison, he moved in with Melvin; Yokia said Melvin was the only person who could tolerate Johnny’s volatility.

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On Friday December 2nd, 2005, 10 days after her 26th birthday, Yokia received a phone call. Melvin had been killed at home. The murderer had shot him three times, placed a pillow over his head and left.

Yokia was devastated, but not completely surprised. After all, Melvin had returned to the streets, the streets had embraced him and now, she told herself, the streets had killed him too — just as she suspected they might. Johnny came over to Yokia’s house the following day, and stayed there that evening. On Sunday he went to church. But when the preacher started talking to him about loss, Johnny became angry, screaming, “Don’t talk to me about that.” He didn’t stay at Yokia’s house that night.

On Monday morning, Yokia received another phone call. This time it was Melvin’s ex-girlfriend, and she delivered some unsettling news. The police were looking for Johnny Sloan: he was the prime suspect in Melvin’s murder. The police arrived at Yokia’s house that same day, looking for Johnny. They left empty-handed and carried on searching his haunts, eventually finding him in a local youth shelter. After a lengthy interview at the Oakland police headquarters, Johnny Sloan admitted to killing his brother. His arraignment fell on the same day as Melvin’s funeral.

“You shoot your own brother…and leave? Really?” Yokia said, distraught. “Then you spend a night at your sister’s house like nothing ever happened?”

Telling the story had agitated her. At times the violent threads in Yokia’s life seemed to make sense: she knew, for instance, that she had to face the generational patterns in her family head-on if she was to escape them. She talked about how she had tried running away, self-medicating with alcohol and drugs, until she reached a state of mental and physical collapse — and realized that she hadn’t gone anywhere at all. At other times, however, the sheer volume of the violence seemed to overwhelm her. She told me she felt mortally threatened by it. “Once your brother kills your brother, with family like that, who needs an enemy?” she asked. “I just always have this thought of what if I get killed?”

Yokia joined Alcoholics Anonymous four years ago. She hasn’t had a drink or touched drugs since. In that time, she told me, she has come to see the toll that her traumatic childhood and her choices as an adult have had. She looks at her extended family and sees a web of murder, suicide, jail, abuse and rage. And she wonders sometimes if she will ever escape it.

“There’s always this, like, ghost, like I’m trying to beat too many odds,” she said. “I’ll deal with one issue but there are so many layers. Who can overcome this and lead a relatively normal life?”

IN THE YEARS AFTER HER first mouse experiment, Isabelle Mansuy replicated the study more than a dozen times. Still, it took almost a decade before she was able to publish the results. Mansuy attributes the delay to the reluctance of the scientific establishment to embrace the idea of epigenetic inheritance.

The delay might, of course, be due to the science itself, not the scientific establishment. There are complaints that can be leveled against advocates of epigenetics. The most significant may be that there are holes in their reasoning. Critics point out that the existence of epigenetic changes in people and animals with a history of stress does not mean that one caused the other. The connection may be there, but so far scientists have failed to trace the causal chain. Nor have they produced a full account of how epigenetic activity can be passed down a generation. And it won’t be easy to do so. Epigeneticists can’t recreate a traumatic childhood in the lab, and they can’t take samples from the organ in which epigenetics does some of its most interesting work: the living human brain.

There’s also the possibility that something other than epigenetics may explain the results of Mansuy and others. Last year, an American geneticist named Eric Nestler described an experiment similar to Mansuy’s, but with a clever twist. After stressing male mice, Nestler extracted their sperm and, using IVF, impregnated female mice. Because the mothers never met the fathers of their pups, Nestler had eliminated the possibility that spending even a brief time with a troubled male might be enough to damage a female’s parenting skills. When he ran behavioral tests, Nestler saw only “very modest” signs of depressive behavior in the offspring, not the significant changes seen in Mansuy’s mice.

The study doesn’t disprove Mansuy’s claims. There was still some transmission of behavior and, perhaps more importantly, Nestler had applied the original stress to adult mice, which may have limited the impact it had on the animal’s epigenome. But Nestler’s results did demonstrate how much more work needs to be done before the implications of Mansuy’s work can be accepted — or rejected.

Even if Mansuy’s mouse studies are replicated, skeptics will have at least one more question. For scientists who work with rodents, the similarities between mice and rats and humans abound. To the rest of us, such comparisons can seem bizarre: what can a pair of caged rats possibly tell us about a man who beats his wife? In fact, the two positions are not completely at odds. Rodents share many genetic, physiological and behavioral traits with us — enough to have proved an extraordinarily useful way of studying humans. But they also lack so many aspects of human behavior that it’s easy to over-interpret the results of rodent studies.

“It’s a long way from differential methylation to behavior, physical health or mental health,” says Greg Miller, a psychologist at Northwestern University in Chicago. Ultimately, the claims of epigenetics need to be evaluated in humans.

But working on the human epigenome is difficult, says Meaney. Epigenetic markers do not always manifest in two places in the same way, making hard and fast conclusions rare. For all of that, he believes the science will reveal that patterns of violence like those in Yokia’s family are at least partially rooted in biology.

“Does witnessing violence produce a stable epigenetic signal that would then influence physiology and behavior?” he asks. “Yes, if I had to bet my house down, then yes.”

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IF THE EPIGENOME REALLY IS the molecular manifestation of Yokia’s ghost, studying it may lead to new ways of sparing others from similar demons. Meaney, for one, believes epigenetics speaks directly to how we structure our societies. For too long, he says, policymakers have intervened in places like Dogtown using reforms based on shoddy science, or even worse — no science at all. Epigenetics could present a smarter alternative. “What we need are objective predictors of who is at risk,” he says. The epigenomes of people in neighborhoods like Dogtown might contain that information; we could use the results to assess the impact of the environment on residents, and to identify those upon whom it takes the greatest toll.

Epigenetics could also lead to a better understanding of why people commit crime. In 1984, Richard Tremblay began tracking 1,000 kindergarten-aged boys from Montreal’s poorest neighborhoods. Today, those kids are in their mid-30s and Tremblay’s study is one of the longest, and largest, longitudinal experiments conducted.

One of Tremblay’s more surprising results is the suggestion that the peak of aggressive behavior in humans, as measured by his subjects’ willingness to resort to violence, generally occurs around the ages of two and three. As soon as children gain a decent control of their muscles, their use of aggression as a problem-solving mechanism spikes. The finding cuts across much conventional thinking on violence, which holds that people learn to be aggressive, perhaps by witnessing violent events.

“Physical aggression is a natural, normal response to solving a problem,” says Tremblay, who is now based at University College Dublin in Ireland. “As we get older, humans learn not to aggress, rather than the other way around.” (As Tremblay has noted, Thomas Hobbes made this point in 1647: “An evil man is rather like a sturdy boy, or a man of childish mind, and evil is simply want of reason at an age when it normally accrues to men by nature governed by discipline and experience of harm.”)

Roughly four percent of Tremblay’s cohort are what he calls “chronically violent offenders”: people who have committed murder and other serious crimes. In 2006, Tremblay studied blood and saliva samples from this group. Several hundred genes, including some that have been linked to aggression, were marked by patterns of epigenetic activity that differed from those he saw in the rest of the group. “It looks like there is an epigenetic basis for the transmission of violence, and not only does it look like it but it makes sense,” Tremblay said.

It’s not hard to see that such a project would generate both enthusiasm and concern. A more accurate means of honing in on the most troubled children and those at risk of committing crimes would be a boon to social services.

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BUT WE SHOULD BE CONCERNED whenever simple labels are proposed for complex problems. Even though epigenetics may be part of the reason why people abuse drugs or turn to crime, it almost certainly can’t explain the detailed trajectory of a person’s life, or their ability — or inability — to change its course. Yet if the field continues to attract attention, some scientists will claim that it can, just as some eugenicists claimed that genetics could explain criminality.

“If the funding stream for research and services moves towards trying to classify people, then you’re going to evaluate people based on their physical experiences to the detriment of not just how these people look but how they suffer,” says Jaleel Abdul-Adil, a psychologist at the University of Illinois at Chicago who works with at-risk youth.

There’s another thorny question raised by the new science: that of responsibility. We know, for instance, that smoking during pregnancy increases the risk that a child will develop asthma. Last year, scientists working with a rat model of the disease showed the effect extends at least a generation further: the grand-pups of rats exposed to nicotine during pregnancy also suffered from lung problems. So are smoking mothers hurting their grandchildren?

“And what if my alcohol consumption affects my grand-offspring?” asks Bruce McEwen, a neuroscientist at the Rockefeller University in New York. “Or if the stress of one generation affects others? If you’re going to pass on your life experiences to subsequent generations, what do we do as policymakers? Especially when we may not see effects of our interventions for generations. Right now we evaluate success on short term, but epigenetics tells us we need to rethink that.”

Yet the most immediate implication of epigenetics is less controversial — and potentially far more powerful. Recent research suggests that the epigenome is less malleable later in life, and that the epigenetic marks laid down by childhood trauma are stubborn. If that’s the case, we may be too late if we intervene only after epigenetics starts to influence adult behavior. “Things start going wrong very early, but we don’t know it, we can’t observe it,” says Tremblay. “So we wait…then it’s too late because the brain has not developed in a way that enables the individual to get control of himself.”

The idea that we should intervene early in a troubled life is not a new one. When I asked Tremblay about the policy implications of epigenetics, he cited the importance of having nurses visit families at home to advise on health and parenting — an idea that is over a century old and known to bring about real health benefits. “The interventions are quite simple,” he said. “But we know that, and have known that for a long time.” The problem, he noted, was a reluctance to pay for those nurses. If epigenetics becomes more widely accepted, the field’s first contribution could be a renewed interest — and perhaps funding — for an old idea.

Gary Slutkin is an American epidemiologist who spent much of his early life studying infectious diseases in places like Somalia and East Africa. He now works in Chicago for Cure Violence, an organization he co-founded in 1995. Slutkin sees epigenetics as a tool that can help a new generation of health workers to intervene to prevent violence — in his language, to become “interrupters”.

“Communities need more intervention, they need more care,” he told me. “It’s analogous to going to Bangladesh, where there are certain communities that have more diarrhea. So they need the intervention more. In Bangladesh, you need more training about oral rehydration and improving sanitation. For violence, you need more interrupters, that’s the new health worker.”

The results of epigenetics should force a broader rethinking of violence, Slutkin added. “If we look at it this way, we’re able to take it out of the realm of morality. We used to think of people with leprosy as bad people because we didn’t understand what was happening. Epigenetic damage is invisible, and neuronal circuits are invisible — so until we start to talk about violence as science we’re still in the Middle Ages.”

As scientists debate epigenetics and the possibility it may help us change lives, the stresses in Yokia Mason’s life continue, as if they spring from a never-ending font. Her most recent fear involves Brianna, her 16-year-old daughter. Yokia has tried to raise Brianna with a degree of awareness and conscientiousness her own mother never showed. When Brianna was a girl, Yokia moved her family from Oakland to the more peaceable towns of San Lorenzo and San Leandro, just far enough south of the city proper to feel like an escape. Yokia made sure her daughter went to good schools and surrounded herself with upwardly mobile people. Yokia now has a job as an outreach worker at a local public health office. Working there has allowed her to educate herself about the traumas of her early life and what she can do to mitigate their effects on her and her family.

And yet there are days when Brianna terrifies Yokia. Some of this may be the angst and upheaval of teenage life. But some of it, Yokia is convinced, is not. “I’ve had to call the police on her at my house because she hit the window, I mean, hit the walls, put holes in the walls, and I get scared,” Yokia told me. “I see my little brother Johnny Sloan in that behavior. So it’s like, oh my god, she gonna kill me?” Martha Ann has also expressed concerns about Brianna, telling Yokia that the girl was “crazy”. And the other side of Brianna’s family is as troubled as Yokia’s. Brianna’s father, Yokia’s first partner, has been in and out of prison for most of his life. His mother is also in prison, serving a 79-year sentence for bank robbery. “That was her career,” Yokia quipped.

Outside Martha Ann’s house, the heavy beats of a car stereo thumped as the vehicle drove slowly past, turned the corner and disappeared. Martha Ann looked up. A thin shaft of light streamed in through a small, round hole in the front door. She raised a long finger and pointed, and Yokia explained that a stray bullet had torn through the house several years ago. The two women spent a couple of minutes recalling the event, describing where each had been when the bullet entered and where it had ended up — stuck in the wall above Martha Ann’s head. I looked up and saw the hole was still there, a thick, dented smear in the drywall that no one was going to fix.

“I feel like a time bomb,” Yokia said, “I do. I don’t know why I don’t act on it. I have a relationship with God that I work on daily. It helps me, I read the stories of the Bible. Cain and Abel. You know, this shit’s been going on since the beginning of time.”

After a while, she added, “But I don’t like that story. Who wants to be connected to that?”

//.



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This story was written by Scott C Johnson, edited by Jim Giles, fact-checked by Jeffrey Gleaves, and copy-edited by Tina Lee. Nicky Barber narrated the audio version, and photographs were taken by Audrey Whitmeyer-Weathers and John Orvis.