For Garneau to win at trial this year, he’ll have to prove not only that Brochu and his fellow plaintiffs are gambling addicts suffering from a diagnosable mental illness, but also that their illness is a direct result of playing the 15,000 video slot machines scattered in bars and restaurants throughout the province.

The plaintiffs’ lawyers will argue that these nefarious machines lured in unsuspecting citizens, dazzled their eyes with flashing lights, and drowned out the murmurs of guilt and responsibility in the back of their heads with the sound of cascading coins. They’ll try to show that the casinos and video slot machines turned Brochu and the others into junkies, unable to think of anything expect their next chance to score big. With their lawsuit, the plaintiffs will be taking aim at one of the gaming industry’s most cherished talking points, which sounds a bit silly when you strip it down to basics: Gambling doesn’t cause gambling addiction.

On the other side, lawyers for Loto-Quebec will base their argument on what also might seem a far-fetched notion: Casinos and slot machines aren’t the culprits — genetics and brain chemistry are. In essence, they’ll argue that the fault, dear gambler, lies not in our Stardust casinos, but in ourselves. In doing so, the industry will set up a rock-solid defense against troubling lawsuits and arm pro-casino legislators with scientific data.

With the ugly specter of gambling addiction, of ruined lives and families, hanging over their heads, gaming advocates will bolster their cases with research from the National Center for Responsible Gaming (NCRG), a nonprofit group, associated with Harvard University, that funds most of the scientific research on gambling addiction. The research will show that only a few unfortunate souls — those predisposed to addiction — will get into trouble, while everyone else can gamble for entertainment with no ill effects. The center’s studies were exhibited last fall in Boston, where lawmakers wrestled over bringing three casinos to Massachusetts. They will also be on display in the coming year, as lawmakers across the country consider legalized gambling and new casinos, with literally billions of dollars hanging in the balance.

But there’s a serious kink in the studies: The NCRG is a wing of the casinos’ main trade group, the American Gaming Association, which has committed a total of $22 million to the center. To ethicists and casino critics, that relationship is a cautionary tale of science getting too close to industry. While NCRG leaders say they fund independent science, it’s not a coincidence that the science aligns so well with the interests of the casinos. It’s not that gambling executives are tampering with research findings, or scientists are skewing results. Rather, gaming executives are drawing extravagant conclusions from the studies. By trumpeting these conclusions, the gaming industry is helping casinos gain a legal foothold across the country — and covering up the ways casinos profit from gambling addiction.

In 2007, American consumers spent $34 billion on gambling in commercial casinos (a category that doesn’t include Native American casinos), according to a report by the American Gaming Association. That’s up from $20 billion a decade before. Small wonder, then, that casino executives worry that addiction could harm their golden goose. Between 6 million and 8 million Americans are thought to have trouble walking away from the casinos each year, with a full spectrum of consequences, according to the National Council on Problem Gambling, an advocacy group.

Frank Fahrenkopf, president of the American Gaming Association, laid out the gaming industry’s lines of defense at a 1996 speech before industry bigwigs in Las Vegas. He called problem gambling the “Achilles’ heel” of the industry and told the assembled executives that their “enemies” would use the issue in a “crusade to crush our livelihood.”

Fahrenkopf said the issue hits home with state legislators, who could be turned against the expansion of gambling or convinced to pass restrictive regulations. (Regulations proposed in other countries include mandatory clocks on casino walls, “time out” periods after a certain amount of money is lost and maximum bet limits.) Meanwhile, media stories of gamblers who had lost everything tugged at the public heartstrings, jeopardizing support. “The growth of our industry is certainly endangered by the issue, and it is not hyperbole to say that the industry’s very existence is at stake,” Fahrenkopf warned.

The plan he proposed owed a debt to the tobacco industry executives who had spectacularly lost public support just a few years before, when they raised their hands before a 1994 congressional committee and testified that nicotine was not addictive. “Our industry cannot afford to make the mistake made by the tobacco industry,” Fahrenkopf said. He told his colleagues that the gaming industry must not only admit that gambling addiction existed, but also lead the discussion of its origins, symptoms and social impacts.

To investigate those origins, the American Gaming Association created the NCRG, and the casinos keep it flush with money. This past September, the NCRG announced $7.6 million in new funding commitments for the next five years, including $2 million from Harrah’s, $2 million from MGM Mirage and $1 million from International Game Technology, the largest slot machine manufacturer in the world. Its board of directors includes executives from MGM Mirage, Harrah’s and the casino company Boyd Gaming Corp., as well as Judy Patterson, executive director of the American Gaming Association.

Four years into the NCRG’s existence, it established a spinoff organization, the Institute for Research on Pathological Gambling and Related Disorders. Patterson said in a speech that the industry wanted to “adhere to a system of scientific peer review modeled after the federal government’s National Institutes of Health.” Today, the institute is housed at the Harvard-affiliated Cambridge Health Alliance.

Christine Reilly, executive director of the institute, says she’s heard all the complaints about the institute’s funding and supposed conflict of interest. She explains that the institute’s contract with the NCRG stipulates that the industry can’t interfere with decisions. NCRG leaders “don’t even see what we’re doing until it’s published,” she says. “Once the papers are published, anyone can use them however they want.”

Indeed, when the Massachusetts Legislature held hearings on the governor’s proposal to legalize gambling last fall, gambling foes accused the state’s public health officials of drawing talking points from institute-funded studies. They pointed to one official who used an institute study to support his claim that gambling could provide stimulating cognitive benefits to the elderly.

Industry leaders are bullish on the research prospects of the institute. “I was just reading an article the other day about a new biomarker test for ovarian cancer,” Phil Satre, the chairman of the NCRG’s board and former CEO of Harrah’s Entertainment, told the trade publication Responsible Gaming Quarterly in 2006. “I would like to see the development through our research of a similar test for problem gamblers.”

That may sound far-fetched, but not to Reilly. “Diagnosing mental illness is more of an art than a science, especially with addictions,” she says. “So wouldn’t it be great to have an objective measure? That would be a blood test, maybe a genetic marker, saying this person is predisposed to addiction.”

While the institute funds research on the social determinants of gambling addiction, it focuses on genetic and neurochemical causes. It draws on a study by psychiatrist Donald Black of the University of Iowa, who found that pathological gamblers were more likely to have other pathological gamblers in their immediate families than were control subjects; they were also more likely to have alcoholics and substance abusers in their families.

On the neurochemical front, researchers home in on dopamine, the neurotransmitter associated with rewards and motivation. Using a functional MRI machine, Alain Dagher of McGill University has shown that giving test subjects a monetary reward activates the ventral striatum, a part of the brain that also lights up when a cocaine addict uses cocaine. The ventral striatum is known to have many dopamine receptors, and other studies have shown that gambling addicts flood the zone with dopamine when they win, while control subjects have a smaller release.

To Reilly, this kind of research undermines the point raised in the Canadian court case that video poker machines are addictive. “Things are not addictive, they’re just not,” she says. “Addiction is a relationship between the object and a vulnerable person, and if you don’t have that vulnerability, the odds are you won’t get addicted. I play a slot machine for 10 minutes and I’m so bored I want to shoot myself.”

Neurologist Dagher cautions against jumping to such conclusions. It’s far too soon to say that some people are programmed at birth to respond to gambling with addiction-inducing rushes of dopamine. “People always think if we find an abnormality in the brain, it must be something inborn,” he says. “But the brain is very plastic. If you see an abnormality, it’s probably a combination of something inborn and a response to environmental factors. And the dopamine system is tremendously affected by life experiences, especially stress.”

If the casino industry can defend itself against gambling addiction by pointing to neurobiology, it might also be argued that it has learned how to profit from addiction. Natasha Dow Schull, a cultural anthropologist and assistant professor at MIT, and a prominent critic of the gaming industry, points out that casinos are booming thanks in large part to increasingly sophisticated and highly addictive slot machines and video poker machines. These machines are the gaming industry’s cash cow — they occupy more than 75 percent of casino floors — and one of the most efficient systems that humans have ever devised for delivering a dopamine rush to your brain while extracting money from your wallet.

Schull has studied the interface between slot machines and the players who throng to them. As she explains, the old one-armed bandits are gone: Players were wasting too much time pulling the lever. Now push-button and touch-screen games are the rule, where a hardcore customer playing at top speed can play a game every five seconds. When you consider the slot machine makers, says Schull, “It’s clear their ideal customer is the addict. They have a term, ‘player extinction,’ which means you lose all your money. They’re talking about this as a goal!”

Schull has also tracked the work of the NCRG since its founding in 1996. In her forthcoming book, “Machine Life: Control and Compulsion in Las Vegas,” she dives into the experience of gambling addicts, and argues that the industry acted deliberately to defuse the threat it poses by funding science that casts them in an unflattering light.

“The NCRG is committed to the idea that most ‘normal’ people aren’t at risk of developing a gambling problem,” says Schull. “They’re trying to show that all addicts share a common pathway, which involved the reward system of the brain. This really helps the industry because the idea is, if these people were not to gamble, they would find something else to be addicted to. They come into the world with the brain disposition of an addict, so you can’t blame casinos.”

Schull says the industry has successfully defined the terms of gambling addiction; it’s telling that we speak about problem gamblers, she says, but not problem machines, problem environments, or problem business practices. Currently, Schull is working in the young field of “neuroeconomics.” She says that brain scans and genetics studies are producing fascinating data, but can’t fully explain the complicated problem of gambling addiction. “Doing this research, I’ve become a behaviorist in a weird way,” she says. “I’ve come around to thinking that if you put any rat in a cage, under the right circumstances, you can addict it. Some of us have greater liability than others, but that doesn’t mean that it’s not on a continuum.”

The gambling treatment field has warily accepted the statistics produced by Howard Shaffer, director of the Cambridge Health Alliance’s Division on Addictions. He found that 1 percent of American adults meet the criteria for “pathological gamblers” in any given year, as defined by the psychiatry bible, the Diagnostic and Statistical Manual of Mental Disorders. That 1 percent is the figure casino executives frequently cite, and that the NCRG highlights on its Web site.

However, critics say that the industry’s embrace of the 1 percent statistic hides the full brunt of gambling addiction. “The industry’s ability to downplay the social costs has been a continual frustration,” says Henry Lesieur, a psychologist at the Rhode Island Hospital‘s gambling treatment program. “As if one suicide isn’t too many, or as if divorces mean very little.” Lesieur says he also sees plenty of tragedies among the 2 to 3 percent of adults who qualify as “problem gamblers,” meaning they don’t have enough symptoms to qualify as pathological gamblers.

Lesieur originally sat on an advisory board for the NCRG, but resigned in 1997 over concerns about the industry’s influence over the research. Lesieur says that by conservative estimates, 30 percent of the profits from gambling machines come from problem gamblers. Yet NCRG and the institute have avoided such sensitive topics. “You don’t see any research into the addictive nature of different games, and why people who play video machines seem to get addicted faster,” Lesieur says. The gambling addicts who play the machines exclusively bottom out very quickly — typically, within a year of beginning their habit, he says.

Lesieur says that he sees three different types of problem gamblers in his counseling center. The first set, he agrees, do seem to be genetically predisposed, and respond too strongly to the stimulus of gambling. The second group consists of social gamblers who get carried away with the excitement of betting big, and lose more money than they intended. However, these people usually rein themselves in once they feel the consequences.

Then there are people who are depressed and anxious, he says, people who are struggling with a dramatic life change, like a divorce or a new disability, and who gamble for distraction and a temporary rush. “If you go gambling when you’re depressed, you’re putting yourself at enormous risk, because you’re using gambling to treat your depression,” he says. The majority of the people who walk through his office door fall into this third category, he says. “They haven’t been able to tie all alcohol use to genetics, and the same thing’s going to happen to gambling,” he says. “If you look for biological markers, you’re only going to find the first type.”

Despite their concerns about how the institute’s studies are paid for and broadcast by the gambling industry, critics don’t want the funding for brain scans or genetics studies to dry up. “The institute will probably say to you, ‘No one else wants to fund this work, this is important work,’” says David Blumenthal, director of the Harvard-affiliated Institute for Health Policy, and an expert on academic-industrial relationships “‘We’re trying to understand how the phenomenon of addiction occurs, and you want to stop us from doing that.’ There may be some truth to that.”

Regardless, Blumenthal adds, the studies are inherently compromised as a result of being funded by the casino industry. “My opinion is that it’s unwise to accept those grants. No matter how scrupulous the investigators are, they’re always open to suspicion. And if you have results that are positive to the industry, it looks even more dubious. So in a way, it’s harmful to the industry.”

The ideal solution, says Blumenthal, would be for the federal government to step in and give a big pile of money to the NIH for research on all aspects of gambling addiction, from nature to nurture. “If the institute is funding really good research, what should happen is that research will rise to the top under a public system,” says Blumenthal. “We’ll get to the same point without the stigma of industry association.”

In fact, in 2007, several members of the House of Representatives introduced a bill that would give the National Institutes of Health $20 million for research on gambling addiction. “It would be the most money ever given to the NIH for gambling research,” says Keith Whyte, executive director of the National Council on Problem Gambling, which supports the legislation. “The NCRG was specifically invited by the sponsor of the bill to support it, and they declined,” says Whyte. “That was disappointing to us because they talk about ‘the NIH model’ all the time.”

The bill is currently stuck in committee and appears to be going nowhere. For the gaming industry, that seems to be a lucky break, as it can continue to battle in court and state legislatures with NCRG research on its side. And that leaves little room for other views of gambling addiction. “When research is being funded by the industry, through NCRG, there aren’t many surprises,” Lesieur says.

Moreover, it might seem as if a startling increase in the number of anxiety disorders has occurred in recent years. Consider that in 1980, the third edition of the authoritative Diagnostic and Statistical Manual of Mental Disorders (DSM) of the American Psychiatric Association stated: “It has been estimated that from 2 to 4% of the general population has at some time had a disorder that this manual would classify as an Anxiety Disorder.”

Then, the first large community study conducted after the publication of this manual, the Epidemiologic Catchment Area Study, found that about one out of ten people had an anxiety disorder in any given year and that roughly 15% of individuals experienced these conditions at some point in their lives. Just two decades later, a similar and equally rigorous study, the National Comorbidity Study Replication (NCS-R), yielded the shocking result that almost one out of five people had had an anxiety disorder over the past year, and more than a quarter of the population (28.8%) had had one at some point in their lives.

Even the NCS-R actually underestimates the frequency of anxiety disorders, as measured by psychiatry’s current criteria for diagnosing mental disorder. Because it asks people to remember years later what anxieties they had earlier in life, many respondents forget past episodes. A recent New Zealand study with substantially improved methodology that involved repeated interviews of participants established that in any given year between ages 18 and 32, nearly a quarter of all young adults (22.8%) experience an anxiety disorder and that virtually half (49.5%) report at least one such disorder during the entire period. Obviously, the study would have yielded even higher estimates if it had included disorders emerging after age 32 or before age 18.

How did rates of anxiety disorders rise by as much as twentyfold over the past 30 years to encompass as much as over half the population?

Philosophers have long emphasized that much anxiety results from pondering life’s mysteries and uncertainties, as in angst about the inevitability of death and the meaning of existence. For most people, however, far more mundane situations — and ones much less immediately threatening than, say, a car rapidly bearing down on one in the street — create anxiousness. They become worried when they might be late for a meeting, miss a plane, park in a no-parking zone, see a police car approaching, or give a public talk. Such everyday occurrences as leaving a middle-school child at home can lead to intense worry among parent and child alike: “All the while I was out, I kept looking at my watch and listening for my phone. He called me four times in an hour: ‘When are you coming home? Where are you? Are you on line yet? Did you leave the store yet?’ It made me so nervous, I just browsed and left.” These worries are built into the structure of modern life, emerging daily or even hourly, especially among people with nervous temperaments.

Life-endangering contexts can generate a degree of normal anxiety that leads to extreme actions. One example (immortalized in a recent motion picture titled “127 Hours”) is that of a hiker in a remote area whose arm got caught under a fallen rock — and who, fearing his eventual death, amputated the arm with his hunting knife in order to escape.  Unlike such responses to immediate — but brief — risks of death, many threatening situations are enduring. The resulting anxiety might also be chronic, yet still normal. For example, many survivors of the Hurricane Katrina disaster in New Orleans experienced anxiety symptoms that, unlike those following the 9/11 attacks, did not subside quickly because the effects of the disaster were not corrected. The lack of adequate housing, schooling, policing, and employment continued for substantial numbers of people long after the hurricane itself was gone. Six months after the disaster, nearly half the residents of the New Orleans metropolitan area still reported high levels of anxiety symptoms.

Many anxiety conditions do not seem to be related in any comprehensible way to external situations, to previous terrifying experiences, or to our biological nature as a species. Take the example of the poet Emily Dickinson who, by the time she was 40, would not leave her home and hid in her room, unwilling to see even her longtime friends. Nothing about Dickinson’s circumstances could account for her refusal to walk outside or to meet with people she had known for extended periods of time. A great number of people ranging from Isaac Newton — who spent several years inside his house — to actress Kim Basinger have shared the fear of going out in public.

But not all disordered states of anxiety involve fear of a particular action, event, or object. Sudden panic attacks when there is no obvious context or trigger, in which people not afraid of anything in particular experience heart palpitations and other symptoms that make them think they are having a heart attack and are going to die, can cripple a person’s life. Generalized anxiety of a lesser intensity, where one feels anxious or worries disproportionately about various not-very-threatening concerns in contexts that do not truly explain the level of anxiety, can also make an individual miserable.

Unlike natural fears, these unfathomable symptoms — sometimes relatively harmless affectations, sometimes devastatingly distressing and impairing — cannot be explained by consideration of their context or by understandable reactions to memories of past dangers. They seem to indicate that something has gone wrong in the way our fears are aroused and sustained.

There is also a third type of anxiety that doesn’t quite seem to fit either of these categories. These anxieties are out of proportion to the actual danger in the present environment yet seem understandable as reactions that came down to us as part of our biological inheritance of fears that did make sense in the prehistoric past.

Early hominids had much to fear. The most ancient stages of human evolution featured environments where people without powerful weaponry faced numerous predators, could do little to protect themselves from harsh climates and natural disasters, and were defenseless against disease. Food was often scarce and in many environments was impossible to preserve for long periods of time. Dangers were everywhere at the same time that security from threats was weak and often unavailable. Small bands of just one or two hundred people faced other hostile groups of humans and other predators, without any government to protect them. Although a range of strategies could be adaptive for dealing with some specific circumstances, on average, vigilance, caution, and readiness to flee at a moment’s notice would probably have had the greatest evolutionary payoff.

Many fears that do not seem helpful today were useful at the time that they became part of the biological nature of our species. A good example is snake phobia, a common and often intense fear. Charles Darwin recounted an incident that indicates the powerful instinctual nature of snake phobias:

I put my face close to the thick glass-plate in front of a puff-adder in the Zoological Gardens, with the firm determination of not starting back if the snake struck at me; but, as soon as the blow was struck, my resolution went for nothing and I jumped a yard or two backwards with astonishing rapidity. My will and reason were powerless against the imagination of a danger which had never been experienced.

Much evidence shows that snake fear is biologically programmed to be easily triggered in us, and the reason is not hard to see. Intense fear of snakes was valuable in the ancestral environments where snakes posed serious dangers.

Snake fear might seem outdated and useless to urban dwellers, but its value remains in those modern locations that still feature considerable numbers of snakes, such as the desert terrain of Arizona. One news story under the headline “Rattlesnakes Bite 4 Over Weekend; One Man Wanted to Pet Snake, Doctors Say,” reported that snakes bit eight people in the Phoenix area over the previous week.

One victim, Patrick Hotchkiss of Quartzsite, Ariz., “had just stepped off his porch Sunday afternoon when he was struck … ‘I should’ve been more vigilant. Usually I am,’ said Hotchkiss … Some of the other victims were gardening or hiking. One child was playing in a yard.” Some of the bites occurred under odd circumstances that vividly illustrate the danger of having no fear of snakes:

But others got closer than they should have. Doctors said one man was bitten on the hand after trying to pet a snake. They said the man had been drinking prior to the incident. “We’ve seen several people who’ve tried petting the snakes, and even on occasion people trying to kiss the snake. Any of those things usually result in the patient getting bitten,” said Dr. Michael Levine, a toxicologist at Banner Poison Control Center.

Obviously an innate tendency to develop a fear of snakes might be a good thing in those environments that snakes inhabit. No matter how inexplicable a fear of snakes might seem at first in an apartment dweller in Manhattan, the fear is quite understandable when placed within the context of our development as a species and the biological nature that our evolutionary shaping imparted to us. Some of these natural fears are rooted in immediately perceived real dangers, others in our memories of past dangers that influence our present expectations, and still others in our species’ history of natural selection that shaped our fear for dealing with dangers that existed in ancestral times but that no longer pose threats.

But some emotions that were adaptive during this evolutionary period were genetically transmitted to future generations for whom those emotions, rather than being protective, might instead be a constant source of needless distress, suffering, and impairment. Consider the anxiety of the popular former sports announcer John Madden, who, like many people, is terrified of air travel. Despite having to travel long distances almost every week, Madden would never fly but always used buses, which are far more inconvenient and time-consuming. Given that flying is many times safer than driving, Madden’s intense fear might seem to be as inexplicable as Emily Dickinson’s unwillingness to see her friends, but many people tend to be afraid of flying, and their fear seems to make a certain amount of sense in terms of human nature, though not in terms of what is currently rational.

Of course, air travel is an invention that did not exist at the time humans evolved, so fear of air travel in and of itself is not a biologically shaped fear. Rather, air travel happens to have several features that human beings were shaped to fear. Intense fear of being at extreme heights where falling would mean death and of entering enclosed spaces where escape is impossible might have been adaptive in ancient periods when such places were genuinely dangerous and to be avoided. Fear of being passive and out of control while facing such anxieties might additionally be naturally anxiety-provoking. People who had fears that motivated them to stay away from such situations might have avoided the occasional disaster and thus passed on to their descendants genes that made them more fearful of entering enclosed spaces, climbing to higher altitudes, and not being in control. Madden’s fear could thus reflect the natural, if no longer constructive, operation of such biologically designed psychological mechanisms. Its evolutionary origin would explain why a substantial percentage of the population shares this fear, even if many people manage to overcome it and, unlike Madden, continue to fly.

Air travel is extremely unlikely to pose the risk of falling from a height or finding oneself trapped by a predator in an enclosed space. Such fears are at the same time natural and yet no longer adaptive in most modern environments. They are an unfortunate mismatch between anachronistic but natural emotions that once were functional and our modern, technologically transformed environment.

The ubiquity of innate fears that are not necessarily adaptive in modern life provides one answer to the question of why anxiety disorders seem to be so common. When fears of crawling animals, flying, strangers, or public speaking are considered to be pathological, rates of anxiety disorders will soar because humans were naturally designed to have such fears. A second reason why so much fearful behavior can readily be classified as disordered is that individual tendencies to express anxiety vary continuously. People who are naturally at the high end of this temperamental continuum can be mistakenly classified as having anxiety disorders.

While evolution programmed anxious emotions to arise in threatening and uncertain situations, culture helps define what particular objects and situations people consider to be dangerous, what cues activate their fear responses, and what sorts of things they worry about as well as the degree of intensity or duration with which one should respond. For example, while witchcraft is a common source of anxiousness in many African societies, it is unlikely to be a source of fear in modern Western cultures. Witch fear is seen as reasonable in the former but not the latter. Fears of being buried alive dominated nineteenth century consciousness in the United Kingdom and United States but would be extremely rare at present; conversely, food allergies, a rare source of anxiousness in the past, are a dominant source of worry in the contemporary United States.

The basic challenge humans face is not to avoid acquiring fears — they are largely part of our nature — but rather to learn how to overcome the many currently useless innate fears that we experience. “It is less a matter of acquiring fears of the dark and of strangers,” according to psychologist Stanley Rachman, “than of developing the necessary competence and courage to deal effectively with the existing predispositions or actual fears.” Adequate criteria for anxiety disorders must take into account normal human variation in anxiousness and must separate genuine pathology from both high-end anxious temperaments and low-end skilled suppression or endurance of natural fears.

 Excerpted with permission from “All We Have to Fear: Psychiatry’s Transformation of Natural Anxieties into Mental Disorders,” from Oxford University Press. 

While there are many reasons for the resilience of this myth, the most powerful one is the simple fact that humans today can and do engage in extreme levels of violence and aggression. If you read the newspaper, visit online news sites or turn on the television, you are guaranteed to come across some evidence of humans behaving violently toward other humans. While many animals aggressively hunt, capture, and eat prey, it is relatively rare for most animals to engage in intense, lethal aggression with members of their own species.

Many social mammals display some intraspecific (within the same species) aggression and violence, sometimes resulting in death. A male lion might seriously injure another male lion in a fight over access to a pride of females, two rams might butt heads until one of them staggers away seriously hurt, or a male baboon might repeatedly attack a female in his group, wounding her and injuring her infant. However, these events, while aggressive and violent, are not the main ways in which the individuals in these species interact. For the most part, death of opponents in these cases is neither the premeditated goal nor the outcome of the behavior. So, while intraspecific violence occurs, most species do not exhibit extreme aggression regularly and methodically. Humans are the only species that practice premeditated homicide and full-out war. That humans can, and do, participate in aggression and violence in ways that most other animals do not (and cannot) has led many to theorize that this aggression, this inner beast or demon, our Mr. Hyde, is part of human evolutionary heritage.

The myth of human aggression holds that we are indeed evolved to be killers, or at least aggressors who use the threat of violence as a major evolutionary tool. The mark of this evolved tendency toward aggression can therefore be found in our bodies and minds, especially those of men:

When we look at humans’ bodies and brains, we find more direct signs of design for aggression. The larger size, strength, and upper-body mass of men is a zoological giveaway of an evolutionary history of violent male-male competition. . . . (Stephen Pinker, psychologist)

There is the notion that aggression, the capacity for immense violence, evolved specifically because of the benefits it gave males, including an edge in competition with one another and between groups of males. Some make the argument for indicators of aggressive cores in our closest primate relatives and suggest that aggression and violence result in evolutionary benefits:

Thus, both the patterns of deadly violence in nature and the ethnographic record of simple hunter-gatherers clearly suggest that intraspecific human violence and the threat of it, while obviously undergoing transformations and varying in form through human history, are on the whole as old as humanity itself, indeed as old as nature. . . . (Azar Gat, political scientist)

In short, the myth of human aggression is that humans (especially males) have a specific and distinct tendency toward aggression and violence and that this is patterned in our bodies and minds and arose due to evolutionary pressures of competition between men and between groups. If this were true, then aggression and violence must be a core part of who we are as humans because over evolutionary time those with the more aggressive behavioral patterns or traits must have defeated opponents and mated more successfully than those who were more pacific.

It is obvious that human aggression is an amazingly complicated thing. There is variation in conflict styles and aggression across individuals, sexes, genders, societies, and time frames. Aggression is an important part of being human, but it is not who we are at our core. We now know that aggression itself is not a uniform or consistent discrete trait, so aggression per se cannot be favored by evolutionary pressures to form the basis of the human experience.

The other primates show us that we do not have specific, evolved patterns of heightened aggression, especially in males. Looking at the chimpanzee species demonstrates the potential for variability in the expression of aggressive and nonaggressive behaviors in our shared ancestors. War is common in the human experience today, but it is not a central part of our evolutionary heritage. We know that males and females differ in some facets of aggression, but a lot of those differences have to do with physical size and the social and experiential contexts in which they find themselves. We know that more aggressive, more violent, or more warlike males do not necessarily do better, either in humans or in our closest relatives.

Human aggression, especially in males, is not an evolutionary adaptation: we are not aggressive, big-brained apes. We know the regions of the brain and body that influence normal aggression. While our genes do not control or determine the normative expression of aggression, abnormal biological function can influence particular patterns of aggressive behavior. The nature of human aggression is not found in our genes, but understanding the function and variation in our biology can help us better understand the pathways and patterns of aggressive behavior. As a species we do not rely on aggression and violence more than cooperation; there is no pattern of evidence to support a notion that humanity is aggressive and selfish by nature. The myth of a human nature characterized by an intrinsic aggressiveness is simply not true.

And yet the popular press and much of the public (and some academics) hold the belief that there is a specific biology or a genetic basis for aggression, especially in males. Identifying the genetic key to aggression is not possible, because it does not exist.

It is pretty clear that in humans two parts of the brain, called the prefrontal cortex and the dorsal anterior cingulated cortex, are centrally involved with the expression of behavior, especially aggression. The prefrontal cortex is linked to other behaviorally important brain structures called the amygdala and the hypothalamus. In general, these parts of the brain receive a variety of inputs from other areas of the brain (vision, smell, touch, pain, sound, memory, language, etc.) and then interact in a sort of feedback loop to stimulate other bodily systems (such as hormones, neurotransmitters, and muscles) into action.

The prefrontal cortex does a bunch of other things as well, including playing central roles in introspection, recognition of emotions, regulation of emotions, and detection of conflict situations, and it acts as a trigger to initiate a variety of other neurological systems in regard to social interactions. The dorsal anterior cingulated cortex seems to be involved in the regulation of responses to anger, pain, and social rejection. From brain imaging studies, we know that individuals who are particularly aggressive often show lowered neuronal activity, reduced glucose metabolism, or even reduced density of gray matter in the prefrontal cortex than those who are not as aggressive. Studies of individuals who have received brain damage to the prefrontal cortex and amygdala reveal that they demonstrate more impulsive and antisocial aggressive behavior or have lowered abilities to control the expression of aggression.

Additionally, shock therapy in the 1950s and 1960s directed at the amygdala and prefrontal cortex resulted in lowered overall arousal rates and severely reduced aggression. In short, there are multiple studies which all point to the action of the prefrontal cortex, the dorsal anterior cingulated cortex, and at least the amygdala, as important areas for understanding the biological infrastructure of aggression.

There are a suite of molecules (called neurotransmitters) produced by the body which directly interact with these regions of the brain and are involved in the expression of aggressive behavior (among other things). They are the 5-hydroxytryptamine receptors (5-HT for short and involved with the neurotransmitter serotonin), the neurotransmitter and neurohormone dopamine, the metabolic enzyme monoamine oxidase A (MAOA), and a variety of steroid hormones such as testosterone, other androgens, and estrogen. None of these are a smoking gun for the origin and expression of aggression in general, but some of these are implicated, to some extent, as playing a role in the emergence of particular types or patterns of aggression.

Genes are basically just stretches of DNA that contain the code for either the production of a protein molecule (or parts of a molecule) or the regulation of other genes or of themselves. Genes come in multiple forms (alleles). While genes contain codes for proteins and their regulation, the relationship between genes and complex molecules like neurotransmitters and hormones is very complicated.

Dubbed the “warrior gene” in the press, the gene that codes for monoamine oxidase A (MAOA) has recently been a central player in the study of genetic influences on aggressive behavior. This gene is found on the X chromosome (the one you get from your mother), so that males have only one copy of it and females have two (males are XY and females are XX). The gene product, the enzyme monoamine oxidase A, interacts with the neurotransmitters serotonin, dopamine, and norephedrine, regulating their release and breakdown so that once they do what they are supposed to do they don’t build up or interact with other receptors, causing problems for communication between parts of the brain.

It turns out that there are at least four different common alleles for this gene that have the effect of increasing or decreasing the amount of MAOA produced. Lowered amounts of MAOA in the brain in some mice, rhesus monkeys, and humans, under certain conditions, is associated with increased aggression and reduced ability to control impulsive behavior. A noticeable number of mice, monkeys, and human males who had the low-MAOA-production alleles and who experienced severe social and/or physical trauma or abuse during early childhood development were more likely to express heightened aggressive and antisocial behavior as adults. Some low-MAOA humans also score higher on self reports of aggressive and violent behavior. However, in some cases the high-producing alleles are correlated with aggressive behavior in male children. In a famous case of a Dutch family who have a very rare allele where no MAOA is produced at all, three males exhibited extreme aggressive and antisocial behavior. Now, not all individuals with the low-expression alleles exhibit this kind of aggression, not even all of those with the low-expression alleles who had traumatic or abusive childhoods. In addition some of the high-expression allele carriers exhibited high aggression.

All of these studies were conducted on males because it is much easier to discover which alleles are acting as the males only have one copy of the gene. In females it is more difficult to identify the actual action of the gene because they may have two copies but only one is actually active; determining which one that is can be very difficult. Thus, while this gene is often invoked as an example of a male biological basis of aggression, there have been no in-depth studies of this gene in females so we do not know if it functions the same way. We should note that the enzyme MAOA operates exactly the same in the females’ brains as it does in males.

This research focuses on the variation in allele frequencies for MAOA and the relationship that its expression has to early social and physiological experiences during development and its variation in functional outcomes in different social contexts. In other words, this is an underlying genetic element that plays an interesting role in affecting the brain structures that are associated with the expression of aggression. But the behavioral outcomes of gene variation are totally dependent on the patterns in early life experience and the social context in which some carriers of the low-production allele find themselves. The bottom line is that if you have a low-expression allele and you undergo severe childhood trauma or abuse, then the likelihood of your having problems in the neurological infrastructure of aggression that result in higher aggression is higher than if you had the regular-production allele.

Most people have heard of serotonin, but most do not know that it is tied to the neurotransmitter 5-hydroxytryptamine (5-HT for short). Of all the well-known neurotransmitters this is the one best recognized for affecting behavior, especially aggression. The main way in which 5-HT relates to aggression has been determined from studies of the variation in the receptors that interact with 5-HT. There are at least thirteen types of 5-HT receptors and multiple molecules that interact with, and regulate, 5-HT in the brain. In general, it appears that serotonin concentrations in the brain, and the way they interact with receptors, can modulate aggression and violent behavior in mammals, including humans (although the vast majority of the research has been done with rodents).

In general, low 5-HT levels are associated with higher levels of aggressive or impulsive behavior and high 5-HT levels and/or manipulation of the 5-HT receptors in different parts of the brain can act to reduce aggression. Genetic evidence for these impacts comes almost completely from studies of rodents: mice or rats missing specific genes that affect 5-HT concentrations or the production of 5-HT in certain brain regions are more aggressive. But this is not true for all 5-HT, as manipulation of certain receptors and of concentrations of 5-HT in different parts of the brain have different types of impacts on aggression, anxiety-related behavior, and impulsivity. In the few studies of humans that track 5-HT relating to aggression there is a negative relationship between the ability of 5-HT receptors to bind to neurotransmitters and aggression, which supports the notion that this molecule impacts the expression of aggressive behavior.

One of the most interesting findings from the 5-HT studies is that, in rodents, different types of 5-HT receptors have different impacts on expressed aggression, depending on whether the rodents were exhibiting “normal” territorial aggression or impulsive pathological aggression stimulated by drugs or electric shock. This suggests that the various genes that code for the different 5-HT types are involved in different systems in aggression and that they might in fact have multiple, even mutually negating, roles in the production and expression of aggressive behavior depending on the social context and the type of aggression expressed. So while 5-HT is definitely involved in the expression, and probably the modulation, of the level of aggression, there is no evidence that this is where aggression comes from.

There is ALSO a strong popular assumption that testosterone stimulates or enhances aggression, especially in males. First off, it is important to note that testosterone courses through both male and female bodies, but that on average, males have higher circulating levels than females. Testosterone is a steroid hormone closely related to estrogen and a suite of hormones called androgens. Little is known about the underlying genetic structures that influence testosterone, but there is no doubt that some genetic variation influences the production and regulation of testosterone in human bodies.

The concept that testosterone produced by males facilitates and increases aggression is an oversimplification and there are very weak or inconsistent correlations between testosterone levels and aggression in adult humans. Even when external sources of testosterone are administered to adults their aggression does not tend to increase, nor is there an increase in aggression at puberty when human males undergo a significant increase in the production of testosterone and the development of male secondary sexual characteristics.

There is evidence that in competitive or acute stress situations humans can respond by increasing the production of testosterone but there is no strong or consistent evidence that these increases result in increased aggressive behavior. The increase does appear to enhance muscle activity and efficiency and might also result in lower sensitivity to pain or punishment in both men and women. This might make individuals more likely to participate in aggressive competition, but it does not increase aggression per se. In some experiments the levels of circulating testosterone increase after dominance interactions and social competition, but again this is not necessarily tied to overly aggressive behavior. Exposure to sexual situations and to communal competitive events (like team sports) also appears to increase testosterone in males. Interestingly, males who are fathers and or long-term married partners show lower levels of testosterone than do nonfathers or unmarried males.

Overall, testosterone seems to be associated with the efficiency and activity of a variety of muscular and other physical systems, some of which are implicated in the expression of aggression. But contrary to popular misconceptions, testosterone itself is not associated in any causal way with increased aggressive behavior or in the patterns of the exhibition of aggression.

Despite popular notions that certain genes or genetic elements control or regulate the appearance and intensity of aggressive behaviors, there is no evidence for any one-to-one genetic controls, nor is there evidence for certain molecules or systems in the body that predetermine aggressive outcomes. There is no gene or system in the body that can be identified as “for aggression.” While it appears clear that genetic variation in neurotransmitters and hormones can be involved in the ways in which we express aggressive behavior, there is no direct or casual link. Our genes cannot make us aggressive.

As the anthropologist Ashley Montagu sagely cautioned, “It is essential that we not base our image of ourselves on false foundations. What is involved here is not simply the understanding of the nature of humanity, but also the image of humanity that grows out of that understanding.” Humans are not naturally aggressive, but they do have a great potential for aggression and violence. If we believe we are aggressive at our base, that males stripped of social constraints will resort to a brutish nature, then we will expect and accept certain types of violence as inevitable. This means that instead of really trying to understand and rectify the horrific and complex realities of rape, genocide, civil war, and torture, we will chalk at least a part of these events up to human nature. This is a dangerous state of mind that traps us in a vicious cycle of inaction and futility when it comes to moving forward as societies invested in understanding and managing violence.

Sure, certain things spur aggressive actions, but the common notions about our inner, natural aggressive tendencies (especially in males) ignores the complexity of human biology, psychology, history, and society. It downplays the myriad ways in which aggression is initiated and maintained, and oversimplifies what we can mean by, and understand about, human aggressive behavior. And, most dangerously, it enables a kind of inevitability in our communal sense of aggression and society, especially as it relates to males. This need not be the case.

As she read my mood with such fluency, I thought about the man who had been my coworker and partner in frustration that day—the physicist Stephen Hawking, who could hardly move a muscle, thanks to a forty-five-year struggle with motor neuron disease. By this stage in the progression of his illness, he could communicate only by painstakingly twitching the cheek muscle under his right eye. That twitch was detected by a sensor on his glasses and communicated to a computer in his wheelchair. In this manner, with the help of some special software, he managed to select letters and words from a screen, and eventually to type out what he wanted to express. On his “good” days, it was as if he were playing a video game where the prize was the ability to communicate a thought. On his “bad” days, it was as if he were blinking in Morse code but had to look up the dot and dash sequence between each letter. On the bad days—and this had been one of them—our work was frustrating for both of us.

And yet, even when he could not form words to express his ideas about the wave function of the universe, I had little trouble detecting when his attention shifted from the cosmos to thoughts of calling it quits and moving on to a nice curry dinner. I always knew when he was content, tired, excited, or displeased, just from a glance at his eyes. His personal assistant had this same ability. When I asked her about it, she described a catalog of expressions she’d learned to recognize over the years. My favorite was “the steely-faced glint of glee” he displayed when composing a potent rejoinder to someone with whom he strongly disagreed. Language is handy, but we humans have social and emotional connections that transcend words, and are communicated—and understood—without conscious thought.

The experience of feeling connected to others seems to start very early in life. Studies on infants show that even six-month-olds make judgments about what they observe of social behavior. In one such study infants watched as a “climber,” which was nothing more than a disk of wood with large eyes glued onto its circular “face,” started at the bottom of a hill and repeatedly tried but failed to make its way to the top. After a while, a “helper,” a triangle with similar eyes glued on, would sometimes approach from farther downhill and help the climber with an upward push. On other attempts, a square “hinderer” would approach from uphill and shove the circular disk back down.

The experimenters wanted to know if the infants, unaffected and uninvolved bystanders, would cop an attitude toward the hinderer square. How does a six-month-old show its disapproval of a wooden face? The same way six-year-olds (or sixty-year-olds) express social displeasure: by refusing to play with it. That is, when the experimenters gave the infants a chance to reach out and touch the figures, the infants showed a definite reluctance to reach for the hinderer square, as compared to the helper triangle.

Moreover, when the experiment was repeated with either a helper and a neutral bystander block or a hinderer and a neutral block, the infants preferred the friendly triangle to the neutral block, and the neutral block to the nasty square. Squirrels don’t set up foundations to cure rabies, and snakes don’t help strange snakes cross the road, but humans place a high value on kindness. Scientists have even found that parts of our brain linked to reward processing are engaged when we participate in acts of mutual cooperation, so being nice can be its own reward. Long before we can verbalize attraction or revulsion, we are attracted to the kind and repelled by the unkind.

One advantage of belonging to a cohesive society in which people help one another is that the group is often better equipped than an unconnected set of individuals to deal with threats from the outside. People intuitively realize that there is strength in numbers and take comfort in the company of others, especially in times of anxiety or need. Or, as Patrick Henry famously said, “United we stand, divided we fall.” (Ironically, Henry collapsed and fell into the arms of bystanders shortly after uttering the phrase.)

Consider a study performed in the 1950s. About thirty female students at the University of Minnesota, none of whom had previously met, were ushered into a room and asked not to speak to each other. In the room was a “gentleman of serious mien, horn-rimmed glasses, dressed in a white laboratory coat, stethoscope dribbling out of his pocket, behind him an array of formidable electrical junk.” Seeking to induce anxiety, he melodramatically introduced himself as “Dr. Gregor Zilstein of the Medical School’s Departments of Neurology and Psychiatry.” Actually, he was Stanley Schachter, a harmless professor of social psychology. Schachter told the students he had asked them there to serve as subjects in an experiment on the effects of electric shocks. He would be shocking them, he said, and studying their reactions. After going on for seven or eight minutes about the importance of the research, he concluded by saying,

“These shocks will hurt, they will be painful. . . . It is necessary that our shocks be intense. . . . [We will] hook you into apparatus such as this [motioning toward the scary equipment behind him], give you a series of shocks, and take various measures such as your pulse rate, blood pressure, and so on.”

Schachter then told the students that he needed them to leave the room for about ten minutes while he brought in still more equipment and set it all up. He noted that there were many rooms available, so they could wait either in a room by themselves or in one with other subjects. Later, Schachter repeated the scenario with a different group of about thirty students. But this time, he aimed to lull them into a state of relaxation. And so, instead of the scary part about intense shocks, he said, “What we will ask each of you to do is very simple. We would like to give each of you a series of very mild electric shocks. I assure you that what you feel will not in any way be painful. It will resemble more a tickle or a tingle than anything unpleasant.”

He then gave these students the same choice about waiting alone or with others. In reality, that choice was the climax of the experiment; there would be no electric shocks for either group.

The point of the ruse was to see if, because of their anxiety, the group expecting a painful shock would be more likely to seek the company of others than the group not expecting one. The result: about 63 percent of the students who were made anxious about the shocks wanted to wait with others, while only 33 percent of those expecting tickly, tingly shocks expressed that preference. The students had instinctively created their own support groups. It’s a natural instinct. A quick look at a web directory of support groups in Los Angeles, for example, turned up groups focused on abusive behavior, acne, Adderall addiction, addiction, ADHD, adoption, agoraphobia, alcoholism, albinism, Alzheimer’s, Ambien users, amputees, anemia, anger management, anorexia, anxiety, arthritis, Asperger’s syndrome, asthma, Ativan addiction, and autism — and that’s just the A’s. Joining support groups is a reflection of the human need to associate with others, of our fundamental desire for support, approval, and friendship. We are, above all, a social species.

Social connection is such a basic feature of human experience that when we are deprived of it, we suffer. Many languages have expressions—such as “hurt feelings”—that compare the pain of social rejection to the pain of physical injury. Those may be more than just metaphors. Brain-imaging studies show that there are two components to physical pain: an unpleasant emotional feeling and a feeling of sensory distress. Those two components of pain are associated with different structures in the brain. Scientists have discovered that social pain is also associated with a brain structure called the anterior cingulate cortex—the same structure involved in the emotional component of physical pain.

It’s fascinating that the pain of a stubbed toe and the sting of a snubbed advance share a space in your brain. The fact that they are roommates gave some scientists a seemingly wild idea: Could painkillers that reduce the brain’s response to physical brain also subdue social pain? To find out, researchers recruited twenty-five healthy subjects to take two tablets twice each day for three weeks. Half received extra-strength Tylenol (acetaminophen) tablets, the other half placebos. On the last day, the researchers invited the subjects, one by one, into the lab to play a computer-based virtual ball-tossing game. Each person was told they were playing with two other subjects located in another room, but in reality those roles were played by the computer, which interacted with the subjects in a carefully designed manner. In round 1, those reputedly human teammates played nicely with the subjects, but in round 2, after tossing the virtual ball to the subject a few times, the teammates started playing only with each other, rudely excluding the subject from the game, like soccer players who refuse to pass the ball to a peer. After the exercise, the subjects were asked to fill out a questionnaire designed to measure social distress. Compared to those who took the placebo, those who took the Tylenol reported a reduced level of hurt feelings.

There was also a twist. These researchers had the subjects play the virtual ball game while lying in an fMRI machine. So while they were being snubbed by their teammates, their brains were being scanned by the machine. It showed that the subjects who’d taken Tylenol had reduced activity in the brain areas associated with social exclusion. Tylenol, it seems, really does reduce the neural response to social rejection.

When the Bee Gees long ago sang “How Can You Mend a Broken Heart?” they probably didn’t foresee that the answer was to take two Tylenols. That Tylenol would help really does sound far-fetched, so the brain researchers also performed a clinical test to see if Tylenol had the same effect outside the lab, in the real world of social rejection. They asked five dozen volunteers to fill out a “hurt feelings” survey, a standard psychological tool, every day for three weeks. Again, half the volunteers took a dose of Tylenol twice a day, while the other half took a placebo. The result? The volunteers on Tylenol did indeed report significantly reduced social pain over that time period.

The connection between social pain and physical pain illustrates the links between our emotions and the physiological processes of the body. Social rejection doesn’t just cause emotional pain; it affects our physical being. In fact, social relationships are so important to humans that a lack of social connection constitutes a major risk factor for health, rivaling even the effects of cigarette smoking, high blood pressure, obesity, and lack of physical activity. In one study, researchers surveyed 4,775 adults in Alameda County, near San Francisco. The subjects completed a questionnaire asking about social ties such as marriage, contacts with extended family and friends, and group affiliation. Each individual’s answers were translated into a number on a “social network index,” with a high number meaning the person had many regular and close social contacts and a low number representing relative social isolation. The researchers then tracked the health of their subjects over the next nine years. Since the subjects had varying backgrounds, the scientists employed mathematical techniques to isolate the effects of social connectivity from risk factors such as smoking and the others I mentioned above, and also from factors like socioeconomic status and reported levels of life satisfaction. They found a striking result. Over the nine-year period, those who’d placed low on the index were twice as likely to die as individuals who were similar with regard to other factors but had placed high on the social network index. Apparently, hermits are bad bets for life insurance underwriters.

Excerpted from “Subliminal: How Your Unconscious Mind Rules Your Behavior.” by Leonard Mlodinow. Copyright © 2012 by Leonard Mlodinow. Excerpted by permission of Pantheon, a division of Random House, Inc. All rights reserved. No part of this excerpt may be reproduced or reprinted without permission in writing from the publisher.

One such case was reported by Dutch cardiologist Pim van Lommel and his colleagues in an article published in The Lancet journal. Here is a brief summary of the case.

During a night shift an ambulance brings in a 44-year-old cyanotic, comatose man into the coronary care unit (CCU). This man had been found lying in a cold, damp meadow about an hour before. He was hypothermic and he had no heart rhythm. At arrival (at the CCU), he is placed upon a resuscitation bed. Next, he receives artificial respiration without intubation, while heart massage and defibrillation are also applied. When the medical team wants to intubate the patient, he turns out to have upper dentures in his mouth. A nurse removes these upper dentures and put them onto the “crash cart.” Meanwhile, extensive cardiopulmonary resuscitation (CPR) is continued.

After about an hour and a half the patient has sufficient heart rhythm and blood pressure, but he is still ventilated, intubated, and comatose. He is then transferred to the intensive care unit to pursue the necessary artificial respiration. After more than a week, the nurse meets with the patient, who is by now back on the cardiac ward. The moment he sees the nurse he says: “Oh, that nurse knows where my dentures are…you were there when I was brought into hospital and you took my dentures out of my mouth and put them onto that cart, it had all these bottles on it and there was this sliding drawer underneath and there you put my teeth.” The nurse was amazed because the patient remembered this happening while he was in the process of CPR (i.e. while his brain was not functional). Asked further, the patient reported that he had seen himself lying in bed, that he had perceived from above how nurses and doctors had been busy with CPR. He was also able to describe correctly and in detail the small room in which he had been resuscitated as well as the appearance of those present.

Dr. Myers also claims that Maria’s story has been completely demolished. Nothing could be further from the truth. Actually, skeptical investigators have attempted to debunk the case of Maria. However, they did not succeed in explaining how she was able to “see” that the little toe area of the shoe was worn and one of the laces was stuck underneath the heel while (of note, she was confined to bed and attached to physiological monitors). The debunkers suggested that Maria could have become aware of the shoe prior to her NDE. Since a shoe placed on the ledge of the north side of the third floor could have been visible, both inside and outside the hospital, to people who could have come into contact with Maria, she could have overhead from staff commenting on it. Still, even if this was true, it is highly unlikely that hospital workers would have talked in detail about the shoe’s appearance. In addition, it would have been difficult for Maria to understand the location of the shoe in the hospital and the details of its appearance because she spoke very little English.

Over the last several centuries in the West, many scientists have functioned within a strict materialist, reductionist framework that holds to one essential assumption: “Matter is all that exists.” This materialist viewpoint has become the lens through which most of us interpret the world, interact with it, and judge what is true. Within the view of materialism, everything is composed of collections of material particles. All that we experience—including our thoughts, feelings, beliefs, intentions, sense of self, and spiritual insights—results from electrochemical impulses in our brains.

Along with an increasing number of scientists, I argue that science should not be equated with materialist metaphysics. In my view, science should be an objective process of discovery, i.e. metaphysically neutral.

Corroborated veridical NDE perceptions during cardiac arrest (and several other phenomena discussed in “Brain Wars”) strongly suggest that so-called “scientific materialism” is not only limited, but wrong. In line with this, nearly a century ago, quantum mechanics (QM) dematerialized the classical universe by showing that it is not made of minuscule billiard balls, as drawings of atoms and molecules would lead us to believe. In other words, QM acknowledges that the physical world cannot be fully understood without making reference to mind and consciousness, that is, the physical world is no longer viewed as the primary or sole component of reality (this was well explained by Wolfgang Pauli, one of the founders of QM—I suppose Dr. Myers also considers Pauli to be another “mystical moron”).

It is not difficult to understand why Dr. Myers has launched a personal attack against me. He is well known as an ideologue (masquerading as a person of science) driven by an intense desire to further the materialist agenda. His tactics are nothing new: incendiary rhetoric, swearing, and insults to raise doubts about the competence and integrity of scientists (and others) who threaten his belief structure. I do not think that too many people are fooled by such blatantly deceptive tactics.

Full of hate and anger, Dr. Myers postures as a champion of rationality. But, as a matter of fact, he behaves like a fanatical fundamentalist engaged in a holy war to defend the materialist doctrine. His emotional attachment to this ideology leads him to deny the existence of phenomena that do not fit with his preconceived view of the world. In doing so, he avoids being forced to relinquish his deeply held, cherished beliefs.

In other respects, it is the first time I hear someone says that he found “The Spiritual Brain” (my previous book) unreadable and idiotically conceived. In fact, this book has received several favorable reviews and perhaps Dr. Myers does not have the intellectual sophistication required to appreciate its value.

Finally, with respect to my credibility as a neuroscientist, I would like to tell readers that I have authored/co-authored more than 100 publications (some in highly ranked journals) in neuroscience, psychology, and psychiatry. Alone and in collaboration with colleagues, I have amassed millions of dollars in grant money. Moreover, I have received a number of scientific awards. It is also noteworthy that I am not involved in the Intelligent Design debate and I am not affiliated with any religious organization.

Essentially, Pam agreed to die in order to save her life—and in the process had what is perhaps the most famous case of independent corroboration of out of body experience (OBE) perceptions on record. This case is especially important because cardiologist Michael Sabom was able to obtain verification from medical personnel regarding crucial details of the surgical intervention that Pam reported. Here’s what happened.

Pam was brought into the operating room at 7:15 a.m., she was given general anesthesia, and she quickly lost conscious awareness. At this point, Spetzler and his team of more than 20 physicians, nurses, and technicians went to work. They lubricated Pam’s eyes to prevent drying, and taped them shut. They attached EEG electrodes to monitor the electrical activity of her cerebral cortex. They inserted small, molded speakers into her ears and secured them with gauze and tape. The speakers would emit repeated 100-decibel clicks—approximately the noise produced by a speeding express train—eliminating outside sounds and measuring the activity of her brainstem.

At 8:40 a.m., the tray of surgical instruments was uncovered, and Robert Spetzler began cutting through Pam’s skull with a special surgical saw that produced a noise similar to a dental drill. At this moment, Pam later said, she felt herself “pop” out of her body and hover above it, watching as doctors worked on her body.

Although she no longer had use of her eyes and ears, she described her observations in terms of her senses and perceptions. “I thought the way they had my head shaved was very peculiar,” she said. “I expected them to take all of the hair, but they did not.” She also described the Midas Rex bone saw (“The saw thing that I hated the sound of looked like an electric toothbrush and it had a dent in it … ”) and the dental-drill sound it made with considerable accuracy.

Meanwhile, Spetzler was removing the outermost membrane of Pamela’s brain, cutting it open with scissors. At about the same time, a female cardiac surgeon was attempting to locate the femoral artery in Pam’s right groin. Remarkably, Pam later claimed to remember a female voice saying, “We have a problem. Her arteries are too small.” And then a male voice: “Try the other side.” Medical records confirm this conversation, yet Pam could not have heard them.

The cardiac surgeon was right—Pam’s blood vessels were indeed too small to accept the abundant blood flow requested by the cardiopulmonary bypass machine, so at 10:50 a.m., a tube was inserted into Pam’s left femoral artery and connected to the cardiopulmonary bypass machine. The warm blood circulated from the artery into the cylinders of the bypass machine, where it was cooled down before being returned to her body. Her body temperature began to fall, and at 11:05 a.m. Pam’s heart stopped. Her EEG brain waves flattened into total silence. A few minutes later, her brain stem became totally unresponsive, and her body temperature fell to a sepulchral 60 degrees Fahrenheit. At 11:25 a.m., the team tilted up the head of the operating table, turned off the bypass machine, and drained the blood from her body. Pamela Reynolds was clinically dead.

At this point, Pam’s out-of-body adventure transformed into a near-death experience (NDE): She recalls floating out of the operating room and traveling down a tunnel with a light. She saw deceased relatives and friends, including her long-dead grandmother, waiting at the end of this tunnel. She entered the presence of a brilliant, wonderfully warm and loving light, and sensed that her soul was part of God and that everything in existence was created from the light (the breathing of God). But this extraordinary experience ended abruptly, as Reynolds’s deceased uncle led her back to her body—a feeling she described as “plunging into a pool of ice.”

Meanwhile, in the operating room, the surgery had come to an end. When all the blood had drained from Pam’s brain, the aneurysm simply collapsed and Spetzler clipped it off. Soon, the bypass machine was turned on and warm blood was pumped back into her body. As her body temperature started to increase, her brainsteam began to respond to the clicking speakers in her ears and the EEG recorded electrical activity in the cortex. The bypass machine was turned off at 12:32 p.m. Pam’s life had been restored, and she was taken to the recovery room in stable condition at 2:10 p.m.

Tales of otherworldly experiences have been part of human cultures seemingly forever, but NDEs as such first came to broad public attention in 1975 by way of American psychiatrist and philosopher Raymond Moody’s popular book Life After Life. He presented more than 100 case studies of people who experienced vivid mental experiences close to death or during “clinical death” and were subsequently revived to tell the tale. Their experiences were remarkably similar, and Moody coined the term NDE to refer to this phenomenon. The book was popular and controversial, and scientific investigation of NDEs began soon after its publication with the founding, in 1978, of the International Association for Near Death Studies (IANDS)—the first organization in the world devoted to the scientific study of NDEs and their relationship to mind and consciousness.

NDEs are the vivid, realistic, and often deeply life-changing experiences of men, women, and children who have been physiologically or psychologically close to death. They can be evoked by cardiac arrest and coma caused by brain damage, intoxication, or asphyxia. They can also happen following such events as electrocution, complications from surgery, or severe blood loss during or after a delivery. They can even occur as the result of accidents or illnesses in which individuals genuinely fear they might die. Surveys conducted in the United States and Germany suggest that approximately 4.2 percent of the population has reported an NDE. It has also been estimated that more than 25 million individuals worldwide have had an NDE in the past 50 years.

People from all walks of life and belief systems have this experience. Studies indicate that the experience of an NDE is not influenced by gender, race, socioeconomic status, or level of education. Although NDEs are sometimes presented as religious experiences, this seems to be a matter of individual perception. Furthermore, researchers have found no relationship between religion and the experience of an NDE. That is, it did not matter whether the people recruited in those studies were Catholic, Protestant, Muslim, Hindu, Jewish, Buddhist, atheist, or agnostic.

Although the details differ, NDEs are characterized by a number of core features. Perhaps the most vivid is the OBE: the sense of having left one’s body and of watching events going on around one’s body or, occasionally, at some distant physical location. During OBEs, near-death experiencers (NDErs) are often astonished to discover that they have retained consciousness, perception, lucid thinking, memory, emotions, and their sense of personal identity. If anything, these processes are heightened: Thinking is vivid; hearing is sharp; and vision can extend to 360 degrees. NDErs claim that without physical bodies, they are able to penetrate through walls and doors and project themselves wherever they want. They frequently report the ability to read people’s thoughts.

The effects of NDEs on the experience are intense, overwhelming, and real. A number of studies conducted in United States, Western European countries, and Australia have shown that most NDErs are profoundly and positively transformed by the experience. One woman says, “I was completely altered after the accident. I was another person, according to those who lived near me. I was happy, laughing, appreciated little things, joked, smiled a lot, became friends with everyone … so completely different than I was before!”

However different their personalities before the NDE, experiencers tend to share a similar psychological profile after the NDE. Indeed, their beliefs, values, behaviors, and worldviews seem quite comparable afterward. Importantly, these psychological and behavioral changes are not the kind of changes one would expect if this experience were a hallucination. And, as noted NDE researcher Pim van Lommel and his colleagues have demonstrated, these changes become more apparent with the passage of time.

Some skeptics legitimately argue that the main problem with reports of OBE perceptions is that they often rest uniquely on the NDEr’s testimony—there is no independent corroboration. From a scientific perspective, such self-reports remain inconclusive. But during the last few decades, some self-reports of NDErs have been independently corroborated by witnesses, such as that of Pam Reynolds. One of the best known of these corroborated veridical NDE perceptions—perceptions that can be proven to coincide with reality—is the experience of a woman named Maria, whose case was first documented by her critical care social worker, Kimberly Clark.

Maria was a migrant worker who had a severe heart attack while visiting friends in Seattle. She was rushed to Harborview Hospital and placed in the coronary care unit. A few days later, she had a cardiac arrest but was rapidly resuscitated. The following day, Clark visited her. Maria told Clark that during her cardiac arrest she was able to look down from the ceiling and watch the medical team at work on her body. At one point in this experience, said Maria, she found herself outside the hospital and spotted a tennis shoe on the ledge of the north side of the third floor of the building. She was able to provide several details regarding its appearance, including the observations that one of its laces was stuck underneath the heel and that the little toe area was worn. Maria wanted to know for sure whether she had “really” seen that shoe, and she begged Clark to try to locate it.

Quite skeptical, Clark went to the location described by Maria—and found the tennis shoe. From the window of her hospital room, the details that Maria had recounted could not be discerned. But upon retrieval of the shoe, Clark confirmed Maria’s observations. “The only way she could have had such a perspective,” said Clark, “was if she had been floating right outside and at very close range to the tennis shoe. I retrieved the shoe and brought it back to Maria; it was very concrete evidence for me.”

This case is particularly impressive given that during cardiac arrest, the flow of blood to the brain is interrupted. When this happens, the brain’s electrical activity (as measured with EEG) disappears after 10 to 20 seconds. In this state, a patient is deeply comatose. Because the brain structures mediating higher mental functions are severely impaired, such patients are expected to have no clear and lucid mental experiences that will be remembered. Nonetheless, studies conducted in the Netherlands, United Kingdom, and United States have revealed that approximately 15 percent of cardiac arrest survivors do report some recollection from the time when they were clinically dead. These studies indicate that consciousness, perceptions, thoughts, and feelings can be experienced during a period when the brain shows no measurable activity.

NDEs experienced by people who do not have sight in everyday life are quite intriguing. In 1994, researchers Kenneth Ring and Sharon Cooper decided to undertake a search for cases of NDE-based perception in the blind. They reasoned that such cases would represent the ultimate demonstration of veridical perceptions during NDEs. If a blind person was able to report on verifiable events that took place when they were clinically dead, that would mean something real was occurring. They interviewed 31 individuals, of whom 14 were blind from birth. Twenty-one of the participants had had an NDE; the others had had OBEs only. Strikingly, the experiences they reported conform to the classic NDE pattern, whether they were born blind or had lost their sight in later life. The results of the study were published in 1997. Based on all the cases they investigated, Ring and Cooper concluded that what happens during an NDE affords another perspective to perceive reality that does not depend on the senses of the physical body. They proposed to call this other mode of perception mindsight. 

Despite corroborated reports, many materialist scientists cling to the notion that OBEs and NDEs are located in the brain. In 2002, neurologist Olaf Blanke and colleagues at the University Hospitals of Geneva and Lausanne in Switzerland described in the prestigious scientific journal Nature the strange occurrence that happened to a 43-year-old female patient with epilepsy. Because her seizures could not be controlled by medication alone, neurosurgery was being considered as the next step. The researchers implanted electrodes in her right temporal lobe to provide information about the localization and extent of the epileptogenic zone—the area of the brain that was causing the seizures—which had to be surgically removed. Other electrodes were implanted to identify and localize, by means of electrical stimulation, the areas of the brain that—if removed—would result in loss of sensory capacities, linguistic ability, or even paralysis. Such a procedure is particularly critical to spare important brain areas that are adjacent to the epileptogenic zone.

When they stimulated the angular gyrus—a region of the brain in the parietal lobe that is thought to integrate sensory information related to vision, touch, and balance to give us a perception of our own bodies—the patient reported seeing herself “lying in bed, from above, but I only see my legs and lower trunk.” She described herself as “floating” near the ceiling. She also reported seeing her legs “becoming shorter.”

The article received global press coverage and created quite a commotion. The editors of Nature went so far as to declare triumphantly that as a result of this one study—which involved only one patient—the part of the brain that can induce OBEs had been located.

“It’s another blow against those who believe that the mind and spirit are somehow separate from the brain,” said psychologist Michael Shermer, director of the Skeptics Society, which seeks to debunk all kinds of paranormal claims. “In reality, all experience is derived from the brain.”

In another article published in 2004, Blanke and co-workers described six patients, of whom three had experienced an atypical and incomplete OBE. Four patients reported an autoscopy—that is, they saw their own double from the vantage point of their own body. In this paper, the researchers describe an OBE as a temporary dysfunction of the junction of the temporal and parietal cortex. But, as Pim van Lommel noted, the abnormal bodily experiences described by Blanke and colleagues entail a false sense of reality. Typical OBEs, in contrast, implicate a verifiable perception (from a position above or outside of the body) of events, such as their own resuscitation or a traffic accident, and the surroundings in which the events took place. Along the same lines, psychiatrist Bruce Greyson of the University of Virginia commented that “We cannot assume from the fact that electrical stimulation of the brain can induce OBE-like illusions that all OBEs are therefore illusions.”

Materialistic scientists have proposed a number of physiological explanations to account for the various features of NDEs. British psychologist Susan Blackmore has propounded the “dying brain” hypothesis: that a lack of oxygen (or anoxia) during the dying process might induce abnormal firing of neurons in brain areas responsible for vision, and that such an abnormal firing would lead to the illusion of seeing a bright light at the end of a dark tunnel.

Would it? Van Lommel and colleagues objected that if anoxia plays a central role in the production of NDEs, most cardiac arrest patients would report an NDE. Studies show that this is clearly not the case. Another problem with this view is that reports of a tunnel are absent from several accounts of NDErs. As pointed out by renowned NDE researcher Sam Parnia, some individuals have reported an NDE when they had not been terminally ill and so would have had normal levels of oxygen in their brains.

Parnia raises another problem: When oxygen levels decrease markedly, patients whose lungs or hearts do not work properly experience an “acute confusional state,” during which they are highly confused and agitated and have little or no memory recall. In stark contrast, during NDEs people experience lucid consciousness, well-structured thought processes, and clear reasoning. They also have an excellent memory of the NDE, which usually stays with them for several decades. In other respects, Parnia argues that if this hypothesis is correct, then the illusion of seeing a light and tunnel would progressively develop as the patient’s blood oxygen level drops. Medical observations, however, indicate that patients with low oxygen levels do not report seeing a light, a tunnel, or any of the common features of an NDE we discussed earlier.

During the 1990s, more research indicated that the anoxia theory of NDEs was on the wrong track. James Whinnery, a chemistry professor with West Texas A&M, was involved with studies simulating the extreme conditions that can occur during aerial combat maneuvers. In these studies, fighter pilots were subjected to extreme gravitational forces in a giant centrifuge. Such rapid acceleration decreases blood flow and, consequently, delivery of oxygen to the brain. In so doing, it induces brief periods of unconsciousness that Whinnery calls “dreamlets.” Whinnery hypothesized that although some of the core features of NDEs are found during dreamlets, the main characteristics of dreamlets are impaired memory for events just prior to the onset of unconsciousness, confusion, and disorientation upon awakening. These symptoms are not typically associated with NDEs. In addition, life transformations are never reported following dreamlets.

So, if the “dying brain” is not responsible for NDEs, could they simply be hallucinations? In my opinion, the answer is no. Let’s look at the example of hallucinations that can result from ingesting ketamine, a veterinary drug that is sometimes used recreationally, and often at great cost to the user.

At small doses, the anesthetic agent ketamine can induce hallucinations and feelings of being out of the body. Ketamine is thought to act primarily by inhibiting N-Methyl-D-aspartic acid (NMDA) receptors, which normally open in response to binding of glutamate, the most abundant excitatory chemical messenger in the human brain. Psychiatrist Karl Jensen has speculated that the blockade of NMDA receptors may induce an NDE. But ketamine experiences are often frightening, producing weird images; and most ketamine users realize that the experiences produced by this drug are illusory. In contrast, NDErs are strongly convinced of the reality of what they experienced. Furthermore, many of the central features of NDEs are not reported with ketamine. That being said, we cannot rule out that the blockade of NMDA receptors may be involved in some NDEs.

Neuroscientist Michael Persinger has claimed that he and his colleagues have produced all the major features of the NDE by using weak transcranial magnetic stimulation (TMS) of the temporal lobes. Persinger’s work is based on the premise that abnormal activity in the temporal lobe may trigger an NDE. A review of the literature on epilepsy, however, indicates that the classical features of NDEs are not associated with epileptic seizures located in the temporal lobes. Moreover, as Bruce Greyson and his collaborators have correctly emphasized, the experiences reported by participants in Persinger’s TMS studies bear little resemblance with the typical features of NDEs.

The scientific NDE studies performed over the past decades indicate that heightened mental functions can be experienced independently of the body at a time when brain activity is greatly impaired or seemingly absent (such as during cardiac arrest). Some of these studies demonstrate that blind people can have veridical perceptions during OBEs associated with an NDE. Other investigations show that NDEs often result in deep psychological and spiritual changes.

These findings strongly challenge the mainstream neuroscientific view that mind and consciousness result solely from brain activity. As we have seen, such a view fails to account for how NDErs can experience—while their hearts are stopped—vivid and complex thoughts and acquire veridical information about objects or events remote from their bodies.

NDE studies also suggest that after physical death, mind and consciousness may continue in a transcendent level of reality that normally is not accessible to our senses and awareness. Needless to say, this view is utterly incompatible with the belief of many materialists that the material world is the only reality.

Excerpted with permission from “The Brain Wars: The Scientific Battle Over the Existence of the Mind and the Proof That Will Change the Way We Live Our Lives.” Courtesy of HarperOne.