The Psychopath Inside (10 page)

The brain's cortices develop in an orderly fashion, with a large chunk of the ventral and orbital cortices developing faster than the dorsal prefrontal cortex during the early and later postnatal period. This means that the limbic, emotional brain starts to mature well before the thinking, cognitive brain. The sex steroid bursts released later, in puberty, tend to “set” the connectivity of these cortices, making them less malleable. Because of this, those preteens and teenagers with delayed development of the prefrontal cortex appear intellectually slower at first. But the flip side of this coin is that development is protracted in many of these late-blooming teens, and their more plastic prefrontal synapses are thought to promote more learning capability over this developmental period. This may be one explanation for the recent finding that apparent IQ can be significantly different in someone who is tested around the time of puberty, and then later in adolescence. Some teens appear to start out with higher IQs and cognitive capabilities, but then regress later relative to their peers in the later teens and twenties. Since IQ is a measure relative to age, this doesn't mean that such people have lost ability, only that as early bloomers they were seemingly smarter than their peers, only to develop much slower than others in the mid- and late teens.

Beyond puberty, the next major prefrontal maturation occurs in the late teens through the early twenties, when inputs to the prefrontal cortex from dopamine and the other major monoamine neurotransmitters, serotonin and norepinephrine, mature. They segregate out into the different layers of these neocortices. When
the layering of these neurotransmitters is complete in a person's twenties, the brain is nearly fully mature.

An important corollary to this developmental step is that this is also the time when the diseases involving the monoamines such as schizophrenia and bipolar disorder often display their first obvious symptoms. A typical pattern would be for a college freshman to experience his first psychotic episode during the early winter holiday period. Such alarming problems might be blamed on the rigors and failures of the first big exams, breakups with high school sweethearts, or other such stressful events. But one way to interpret such events is to look at them as inevitable for someone who has the genetic predisposition for schizophrenia, and whose prefrontal cortex is now primed to experience this psychotic break during a major stressful event.

These highly stressful events will likely occur at some point during these years, whether a college term, romantic relationship, or first job challenge precipitates it. Why do stressors precipitate such monoamine-related psychotic breaks? One reason is that stress releases a bomb of cortisol from the adrenal cortex, not only suppressing the immune system, but also blocking the COMT enzyme, especially in the prefrontal cortex. This blocking of the enzyme leads to a surge of dopamine, which floods the cortex and leads to altered firing of the neurons, which in schizophrenia can be associated with poor filtering of inputs, altered signal-to-noise processing by these neurons, and neuronal firing uncoupled from external reality, as well as drastic changes in mood.

There are traits common in different forms of schizophrenia, bipolar disorder, obsessive-compulsive disorder, as well as some of the personality disorders, all developmentally staged psychiatric problems often found in early to late teens and early twenties. Stressful stretches of a young person's life such as college, first marriage, and especially military combat couldn't come at a worse time for the developing prefrontal cortex.

This is a big deal for the armed forces. A freshman and a senior in college are very different human beings. Sending kids to war at eighteen is ridiculous, as they're still in an active state of frontal lobe development. The military uses psychological tests to make sure recruits are not crazy, but that won't tell you how they'll be in two years. If we're going to have war, we shouldn't let soldiers fight until they're twenty-two or twenty-three.

Although psychopathy can also become obvious in the teen years, it can sometimes be noticed in children three and four years old, probably because the ventral system—that is, the orbital cortex and amygdala—develop and mature much sooner in life than the dorsal system. So if there's insufficient activity in these areas—a pattern associated with psychopathy—it will be seen sooner. The principle at work here is that a psychiatric disorder won't become fully expressed until the brain areas involved and their main connections have started to mature. Put another way, you can't break something that is not yet manufactured. Prefrontal development usually ends in the mid-twenties, and the brain is considered to finally come into mature balance of all the circuits sometime in the mid-thirties.

It's hard to codify exactly which behaviors in early childhood indicate psychopathy, but clinicians and many parents say they can see it. What they notice is how a kid will look at you. A child will appear to look right through you, or past you, like he doesn't care that you're there. Such children also show very little fear and can be quite bold. And they'll start manipulating you early on. Some of them, especially girls, can be hypersexual, even as young as five years old, which is often another form of attempted manipulation. In 1963, the psychiatrist John Macdonald proposed three childhood behaviors that predicted violence as an adult: bed-wetting, fire starting, and animal cruelty. The “Macdonald triad” has become well-known, but also much disputed. Bed-wetting is not a great predictor, and fire starting and animal abuse are quite common among boys and can be caused by other factors, such as anxiety or bad peer influences.

Some genes that become risky when a child is exposed to stress may actually be beneficial when the child is raised in a healthy home. Since 2011, three of the journalists and producers of TV shows with whom I've worked contacted me to say that they had spoken to psychologists who had watched some shows I had been on that had included interviews with me and my family. The producers told me that these clinicians said I was, in their parlance, an Indigo child, and also an Orchid child. I had briefly heard these terms in passing and disregarded them as nothing more than New Age pseudoscientific woo-woo. But in going through the list of traits provided to the producers by the researchers, and then comparing them to my knowledge of myself growing up, there are
indeed a few similarities. For example, Indigo children appear empathetic, independent, willful, inquisitive, full of purpose, and possessed with a high IQ, with considerable intuition and distaste for authority. Although these qualities register with what I remember about my perceptions about how others saw me about the time of puberty, they could be ascribed to many kids.

Orchid children, on the other hand, are unusually susceptible to early environment stressors and wilt if treated poorly in their youth, but blossom if treated with copious amounts of love. This is, as the description goes, different from the vast majority of children, who are fairly hardy and will do well pretty much no matter what happens to them early on. This particular theory actually may have some biological basis. Kids who inherit the rarer, short form of the serotonin transporter gene, which leads to more serotonin remaining active in synapses, display more resilience to behavioral stressors than those children with the long form of the gene. A similar finding was made in 2009 by Avshalom Caspi's group at Duke University for the gene controlling the receptor for the major stress regulator CRH (corticotropic-releasing hormone).

Testing for these two genetic alleles in such Orchid children would lend credence to the idea that these kids are particularly sensitive to early environment, whether good or bad. And it caught my eye as a gene that I might test in myself. Of even more interest, had my whole family treated me with such a light, positive, loving touch because of something they sensed? People really supported me. I wouldn't have admitted to this a few years ago, but if I were
born in other circumstances, I could very well have become the leader of some very bad organization. Come to think of it, I probably would have made a good gang leader.

As a scientist, I'm for genetic testing at birth to determine which kids will be vulnerable to stress, even though as a Libertarian I'm against it. The testing would be a key to preventing more psychopaths. If we have enough markers—genes or galvanic skin response or EEG or something cheap—as part of perinatal care, we'll know which kids we can allow to roam around and get into fights and which need extra protection. Once the tests are done, this private information should be put on lockdown, and then given to parents if they want it.

I don't want to overplay the role of environment in development. Kids learn to do a lot of things on their own without explicit instruction—laughing, walking, speaking. And even more complex adaptive behaviors like personality development happen on their own. Kids are malleable, but mostly at the extremes. In the absence of bad abuse or extreme genetics, kids will turn out okay. There's a billion-dollar business in educational music and games, and some parents put their kids on special diets because they want to control the development of their children, but long-term follow-up studies on these changes in behavior like better performance on spatial tasks, attention span, and hand-eye coordination are rare or nonexistent. People also try to coddle their kids and make sure there's no stress, which is nonsense. Every parent of a grown child knows that no kid turns out how they'd originally thought, and we have very little
control over what type of adults our children will grow up to be. Pediatric neurologists I work with have told me this, too. That kid is going to turn out the way he's going to turn out, unless you mess him up royally.

•   •   •

After learning of my brain scan and family history, I considered the role environment plays in development—it was perhaps the main thing keeping me out of the penitentiary—and what that might mean for my theory of psychopathy. There had never been a good synthetic explanation that covered all the symptoms of psychopathy, and part of the problem was that psychopaths have traits that are found in other disorders. Assembling a cogent model would depend on my three decades of knowledge garnered from our lab and other laboratories and clinics, bringing together seemingly disparate cases of brain dysfunction, from schizophrenia to depression to bipolar disorder to addiction to personality disorders.

In the end, my explanation snapped together one Saturday in 2006, while I was nursing a bourbon hangover in my Jacuzzi and doing the
New York Times
crossword puzzle. Struggling for an answer, I tried to relax and just look around. As I scanned our backyard, I saw a three-legged wooden garden stool my mother uses when she comes to the house on weekends to visit, cook, and sit and prune our geraniums. The invigorating effect of pruning the geraniums reminded me of the importance of nurturing, and how too much trauma to the plant would stifle its growth, too little would create a sluggish plant, but just the right amount of stress and care maximized the bloom. This brief moment of
observation brought together the elements that created a plausible explanation for the etiology of psychopathy. In my mind's eye that morning, these three elements, and how they interacted, would be represented by that three-legged stool. This formed the basis of my new theory of psychopathy.

The way I envisaged it, the three legs are: (1) unusually low functioning of the orbital prefrontal cortex and anterior temporal lobe, including the amygdala, (2) the high-risk variants of several genes, the most famous being the warrior gene, and (3) early childhood emotional, physical, or sexual abuse.

Since I lacked the early abuse, I continued to believe over the next few years as I gave talks on psychopaths that I was not among them. Colleagues mentioned from time to time that my otherwise well-adjusted behavior (or so I believed) was, at times, unacceptable, but I figured that these colleagues were just mad at something I had done or jealous of some success or attention that had visited me, and they were overreacting.

They weren't.

F
rom 2006 to 2008, I stayed focused on my genetics research but gave occasional talks on psychopathy and refined my Three-Legged Stool theory. In 2008, one of my business partners recommended that I attend the Technology, Entertainment, and Design conference, better known as TED, the following February.

I had not been asked up front by the TED producers to attend. I had to invite myself. A week before the TED meeting, the organizers asked the nonspeaker attendees if they had a personal story to tell, since the meeting featured not only the full eighteen-minute invited speeches, but also shorter talks, either two- or three-minute quick vignettes, or seven- or nine-minute medium-length stories. I decided that my Lizzie Borden and brain scan story might be of interest, and so I was asked to give a nine-minute talk. I had a few days to prepare. I had no substantial genetic data to discuss, but I could address at least two legs of the three-legged stool: the brain abnormality and the effects of early abuse. I figured I could infer a bit about my own genes based on the long and multipronged family history of murder.

So in the talk I discussed what I knew generally about the
brains of psychopathic killers at that time. I also discussed the findings from Avshalom Caspi's lab connecting the warrior gene to early abuse. I presented the hypothesis that this behavioral three-legged stool might be the basis of dangerous psychopathic behavior.

I also briefly proposed a mechanism for transgenerational violence, that is, an increase of rates of violence in cultures where three or more generations of children experience societal violence, potentially giving rise to a belligerent warrior culture. The logic would go, I surmised, that in a chronically violent community, girls would prefer to hang out with, and probably mate with, those guys who could best protect them, which would most likely be those boys who carried the most aggression-related genes. And after a few generations the proportion of aggression-related genes may start to concentrate, so that after three or four generations one might start to see a subgroup in a society that is particularly aggressive. This could mean that even if the political, religious, cultural, economic, and social causes of local strife disappeared one day, there would still be a culture of people with a particularly high concentration of aggression-related genes that might persist for centuries. I didn't name names in my talk, but those areas could include Gaza, Darfur, parts of the West Bank, areas of Guatemala and Colombia, and some neighborhoods in American cities.

The last part of the TED presentation explained my Cornell lineage. I decided the night before the event to include my family history because I wanted the talk to be more expansively interesting, and I knew that just going on about the brain and genetics
would be too dry and technical for this audience of nonscientists. I was hesitant to open up personal information about my family, but they all agreed it would be fine.

Several months later, the TED presentation was posted one evening on YouTube. The next morning, one of our lab technicians told me there were already 23,285 hits on the video. I had no idea that it was being posted at all, having signed, and forgotten about, the release agreement months earlier while downing my third umbrella drink at the opening party. It had never occurred to me how irresistible the keywords
psychopathic killer
could be. This would not be the last surprise my family would experience in the ensuing weeks and years after that video—and our family's life—went public.

Within a couple of days, in late August, I received two e-mails, and then two calls. These were from head science correspondent Gautam Naik of the
Wall Street Journal
, and Simon Mirren, executive producer and writer of the TV crime series
Criminal Minds
on CBS. They both wanted to pursue aspects of what they had seen in the TED talk. After several conversations by phone and e-mail, it was abundantly clear these two gents were quick studies and at least as bright as my academic colleagues. But unlike academics I knew, these two gentlemen moved fast.

Gautam Naik arranged to fly from New York to Southern California in late October, and hang out for several days with my family and me, at my home, the lab, and an Angels baseball game. He planned to write about my family tree and the genetic basis for aggression.

At the baseball game I pointed to the relief pitcher, Brian Fuentes, and said he didn't have a killer instinct, and probably didn't have the warrior gene. Gautam said that southern India, where he's from, is isolated and rarely attacked, and so the people are docile and might have a low concentration of the warrior gene. He added that India doesn't win Olympic medals because it's a whole country full of Brians.

Gautam was persuasive in convincing me that the family genetic data, however it turned out, would be essential in weaving a compelling yarn about our own twig of the Cornell family tree. So for a month my Italian collaborator and friend Fabio Macciardi did the first of several DNA analyses of the family. My collaborators used a GWAS, or genome-wide association study. For each of us, the test looked at about a hundred thousand bits of DNA related to genes of interest, including twenty or so genes associated with aggression, the MAOA warrior gene among them.

It turned out that nearly all of us had the warrior gene. As for the other genes for aggression, my family members had half of them or fewer. I had close to a full set. It didn't faze me, though, as nothing really does. I laughed it off, like I did my brain scan. I knew I didn't have that third leg of the stool.

Gautam's article and video, which revealed my brain scan and genetic results, ran on the first page of the November 30, 2009,
Wall Street Journal
with the come-hither title “What's on Jim Fallon's Mind? A Family Secret That Has Been Murder to Figure Out: Nature Plays a Prank on a Scientist Looking for Traits of a Killer in His Clan.”

Simon Mirren had also contacted me the same day that Gautam had. Within a week he had already worked out a story line for the ninety-ninth episode of
Criminal Minds
(“Outfoxed”). I couldn't believe what he said to me in our second conversation. He had already merged the story line of the serial killer of the episode, basically at high risk to become a psychopathic murderer even as a young child, with the scientific hypothesis I had discussed in my TED talk. He had managed to understand my concept of how the decades and centuries of violence in the Balkans and high-risk genetics would give rise to transgenerational violence and produce a serial killer. And he added the twist that the serial killer turned out to be a woman who beat the odds and had the high-risk MAOA gene variant on both X chromosomes, and had experienced severe violence in her youth. To cap it off, Simon had seen the TED video but once, and wrote that whole story line overnight. After seeing him do this, I never will again say television is infested with knuckleheads. I had met one of the geniuses of TV.

When they filmed the episode, they had me play myself, explaining the orbital cortex and the warrior gene in a lecture hall. The audience included one of the detectives who used neuroscience to help solve the crime. I'm not an actor, but cameras don't bother me. I remember seeing myself in the lens and thinking, “I own you.” Meaning I was in control of my performance, and so I owned the camera and the shooting and the audience. That's probably my narcissism. In front of crowds I get amped up, and the energy feeds on itself. It's like a drug to me. One time in 1978, I started lecturing about the kidney and didn't stop for four hours. At the end I
got a standing ovation. That happens in conversations, too, and my family has had to teach me to limit myself. When my daughter Tara gets antsy or my wife rolls her eyes, I know it's a wrap.

The combined effect of Simon's
Criminal Minds
episode and Gautam's
Wall Street Journal
article opened the floodgates. From that point and through all of 2010, 2011, and 2012, I would be asked to do more than 120 TV and radio interviews throughout the world. I tried to limit how much I talked about myself and my family because I wanted to focus on the science of psychopathy, but everyone wanted to hear the personal story.

The most embarrassing thing about all this publicity wasn't the fact that the entire world now knew I was descended from a long line of crazy, violent folk, but that I'd become walking, talking proof against my lifelong theory that we are hardwired to be who we are. The idea that I inherited too many of the high-risk gene variants for all sorts of aggressive and weird behaviors, and that my brain also looked like one right out of death row central casting, but that I was not overtly violent should have pleased me, but that was hardly so. I had spent decades preaching about genetic determinism. So my idea that I should have been a very violent person if genes and organic brain state dictate function, combined with the fact that I wasn't, meant I would have to eat a lot of crow in front of my neuroscience colleagues who were fifty-fifty types in the nature-nurture metric. This was not going to be fun. The ribbing and eye-rolling and teasing from my colleagues didn't materialize, to my face at any rate. What happened was worse. Colleagues contacted me, but it was out of concern.

“Jim,” my friend Samantha said, “I saw your TED talk video, and did you notice that your orbital cortex and ventral temporal lobe are turned completely
off
?” On a PET scan, lack of activity can look like lack of brain matter, so my neuroscientist colleague Jeffrey said, “Man, you've got a lot of empty space there. Do you have large ventricles?” referring to the brain's fluid-filled pockets. “So many things are turned off. Aren't you alarmed?” And of course I wasn't. Others noted that there was so little activity in the lower, or ventral, half of my frontal and temporal lobes that I appeared to have the brain of someone with a rather severe case of antisocial personality disorder, representing the more criminal traits of a psychopath.

Someone with a brain like this should have very little empathy, and be incapable of bonding with people on an emotional level. Nor should such a brain accommodate sociability, with all the attendant ethics and morality of a normal person.

But one longtime friend from Yale, Dr. Amy Arnsten, who happens to be the leading prefrontal expert in the world, saw my talk and had another hypothesis. She told me that I might possess a gene variant that produces a large amount of a serotonin receptor called the 5-HT2A receptor. (She turned out to be right when I received my GWAS results.) The 5-HT stands for “5-hydroxytryptamine,” the simple chemical name for serotonin; the 2 stands for the “2” family of serotonin receptors; and A is a subtype of the 2 family. This type of naming complexity makes some historical and taxonomic sense, since there are now known to be at least thirteen types of 5-HT receptors. To make things
worse from both a linguistic and scientific point of view, within each of these thirteen genes that code for serotonin receptors, there are many variants of each gene, which usually means the 5-HT2A gene variant one might inherit may code for a protein that is more or less effective in doing its basic job. The job in this case is to be a receptor protein that grabs on to, or “binds,” a serotonin molecule in its vicinity. Amy said I might have inherited a rather potent form of the 5-HT2A gene. And since 5-HT2A receptors turn
off
the orbital prefrontal cortex, a part of the brain responsible for morality and inhibition, the gene variant I may have inherited turned the orbital cortex almost completely off, explaining my brain scan.

So what? Well, my friend knows me pretty well, and she said that part of this genetic and therefore brain function pattern is consistent with someone who is a bon vivant, in other words, a hedonist, a party person, and one who can be charming and appear to be approachable, friendly, even trustworthy, based on what appears to be all-around sociability, even brio and charisma. Such a person exudes confidence. He or she may be someone you may want to pal around with, party with, and have snappy repartee with, maybe even someone you'd want to get closer to. Sounds familiar.

So now the possibilities were expanding at the genetic, brain circuitry, and behavioral levels at a fever pitch. If I had the more rare variant or allele of the 5-HT2A receptor gene, that might help explain my PET scans and behavior. But I knew that the same variant turns
off
the visual cortex, and that didn't show in my
PET scans, and the lack of activity in the front of my temporal lobe didn't really fit with this gene variant. Other things must be going on. There were other serotonin receptors that turn on or off different brain regions, so maybe in addition I had other variants of other serotonin receptors that offset the visual cortex and temporal lobe patterns. (It turned out that I did.)

In 2010, a producer for the Discovery Channel called me—they ring me up occasionally to do shows—and asked me what projects I was doing that year and if they could tag along and film any. I told them I was going to Morocco to the deep desert to interview and collect data from nomadic Berbers and Bedouins as part of our planned “MedGene” project testing for genetics and behavior in previously untested or undertested populations. They were on board and, better yet, put up the money. Fabio and I first attended the World Congress for Social Psychiatry in Marrakech, where we obtained permission to go into the Sahara to test these tribesmen. We also set up collaborations with other genetics/epidemiological psychiatrists from Algeria, Tunisia, Libya, Morocco, Egypt, and Palestine, in part so I could start testing the transgenerational violence idea I had. My son, James (my “lab tech”), and I did the shoot with Discovery over a week in November. After that, James went to a café in Marrakech while I was off in another part of town. A week or so later, a terrorist bomb blew up that café, the Arab Spring went crazy, and our project has been on hold ever since.