Showing posts with label IQ. Show all posts
Showing posts with label IQ. Show all posts

Tuesday, July 01, 2014

Nancy Andreasen - Secrets of the Creative Brain


Here is an excellent article on creativity and the brain from The Atlantic. This is one of the more comprehensive and interesting articles on creativity I have seen in the mainstream press. It's well worth the read.

Secrets of the Creative Brain

A leading neuroscientist who has spent decades studying creativity shares her research on where genius comes from, whether it is dependent on high IQ—and why it is so often accompanied by mental illness.

Nancy Andreasen | June 25, 2014

AS A PSYCHIATRIST and neuroscientist who studies creativity, I’ve had the pleasure of working with many gifted and high-profile subjects over the years, but Kurt Vonnegut—dear, funny, eccentric, lovable, tormented Kurt Vonnegut—will always be one of my favorites. Kurt was a faculty member at the Iowa Writers’ Workshop in the 1960s, and participated in the first big study I did as a member of the university’s psychiatry department. I was examining the anecdotal link between creativity and mental illness, and Kurt was an excellent case study.

He was intermittently depressed, but that was only the beginning. His mother had suffered from depression and committed suicide on Mother’s Day, when Kurt was 21 and home on military leave during World War II. His son, Mark, was originally diagnosed with schizophrenia but may actually have bipolar disorder. (Mark, who is a practicing physician, recounts his experiences in two books, The Eden Express and Just Like Someone Without Mental Illness Only More So, in which he reveals that many family members struggled with psychiatric problems. “My mother, my cousins, and my sisters weren’t doing so great,” he writes. “We had eating disorders, co-dependency, outstanding warrants, drug and alcohol problems, dating and employment problems, and other ‘issues.’ ”)

While mental illness clearly runs in the Vonnegut family, so, I found, does creativity. Kurt’s father was a gifted architect, and his older brother Bernard was a talented physical chemist and inventor who possessed 28 patents. Mark is a writer, and both of Kurt’s daughters are visual artists. Kurt’s work, of course, needs no introduction.

For many of my subjects from that first study—all writers associated with the Iowa Writers’ Workshop—mental illness and creativity went hand in hand. This link is not surprising. The archetype of the mad genius dates back to at least classical times, when Aristotle noted, “Those who have been eminent in philosophy, politics, poetry, and the arts have all had tendencies toward melancholia.” This pattern is a recurring theme in Shakespeare’s plays, such as when Theseus, in A Midsummer Night’s Dream, observes, “The lunatic, the lover, and the poet / Are of imagination all compact.” John Dryden made a similar point in a heroic couplet: “Great wits are sure to madness near allied, / And thin partitions do their bounds divide.”

Compared with many of history’s creative luminaries, Vonnegut, who died of natural causes, got off relatively easy. Among those who ended up losing their battles with mental illness through suicide are Virginia Woolf, Ernest Hemingway, Vincent van Gogh, John Berryman, Hart Crane, Mark Rothko, Diane Arbus, Anne Sexton, and Arshile Gorky.

My interest in this pattern is rooted in my dual identities as a scientist and a literary scholar. In an early parallel with Sylvia Plath, a writer I admired, I studied literature at Radcliffe and then went to Oxford on a Fulbright scholarship; she studied literature at Smith and attended Cambridge on a Fulbright. Then our paths diverged, and she joined the tragic list above. My curiosity about our different outcomes has shaped my career. I earned a doctorate in literature in 1963 and joined the faculty of the University of Iowa to teach Renaissance literature. At the time, I was the first woman the university’s English department had ever hired into a tenure-track position, and so I was careful to publish under the gender-neutral name of N. J. C. Andreasen.

Not long after this, a book I’d written about the poet John Donne was accepted for publication by Princeton University Press. Instead of feeling elated, I felt almost ashamed and self-indulgent. Who would this book help? What if I channeled the effort and energy I’d invested in it into a career that might save people’s lives? Within a month, I made the decision to become a research scientist, perhaps a medical doctor. I entered the University of Iowa’s medical school, in a class that included only five other women, and began working with patients suffering from schizophrenia and mood disorders. I was drawn to psychiatry because at its core is the most interesting and complex organ in the human body: the brain.

I have spent much of my career focusing on the neuroscience of mental illness, but in recent decades I’ve also focused on what we might call the science of genius, trying to discern what combination of elements tends to produce particularly creative brains. What, in short, is the essence of creativity? Over the course of my life, I’ve kept coming back to two more-specific questions: What differences in nature and nurture can explain why some people suffer from mental illness and some do not? And why are so many of the world’s most creative minds among the most afflicted? My latest study, for which I’ve been scanning the brains of some of today’s most illustrious scientists, mathematicians,
artists, and writers, has come closer to answering this second question than any other research to date.


 
THE FIRST ATTEMPTED EXAMINATIONS of the connection between genius and insanity were largely anecdotal. In his 1891 book, The Man of Genius, Cesare Lombroso, an Italian physician, provided a gossipy and expansive account of traits associated with genius—left-handedness, celibacy, stammering, precocity, and, of course, neurosis and psychosis—and he linked them to many creative individuals, including Jean-Jacques Rousseau, Sir Isaac Newton, Arthur Schopenhauer, Jonathan Swift, Charles Darwin, Lord Byron, Charles Baudelaire, and Robert Schumann. Lombroso speculated on various causes of lunacy and genius, ranging from heredity to urbanization to climate to the phases of the moon. He proposed a close association between genius and degeneracy and argued that both are hereditary. Francis Galton, a cousin of Charles Darwin, took a much more rigorous approach to the topic. In his 1869 book, Hereditary Genius, Galton used careful documentation—including detailed family trees showing the more than 20 eminent musicians among the Bachs, the three eminent writers among the Brontës, and so on—to demonstrate that genius appears to have a strong genetic component. He was also the first to explore in depth the relative contributions of nature and nurture to the development of genius.

As research methodology improved over time, the idea that genius might be hereditary gained support. For his 1904 Study of British Genius, the English physician Havelock Ellis twice reviewed the 66 volumes of The Dictionary of National Biography. In his first review, he identified individuals whose entries were three pages or longer. In his second review, he eliminated those who “displayed no high intellectual ability” and added those who had shorter entries but showed evidence of “intellectual ability of high order.” His final list consisted of 1,030 individuals, only 55 of whom were women. Much like Lombroso, he examined how heredity, general health, social class, and other factors may have contributed to his subjects’ intellectual distinction. Although Ellis’s approach was resourceful, his sample was limited, in that the subjects were relatively famous but not necessarily highly creative. He found that 8.2 percent of his overall sample of 1,030 suffered from melancholy and 4.2 percent from insanity. Because he was relying on historical data provided by the authors of The Dictionary of National Biography rather than direct contact, his numbers likely underestimated the prevalence of mental illness in his sample.

A more empirical approach can be found in the early-20th-century work of Lewis M. Terman, a Stanford psychologist whose multivolume Genetic Studies of Genius is one of the most legendary studies in American psychology. He used a longitudinal design—meaning he studied his subjects repeatedly over time—which was novel then, and the project eventually became the longest-running longitudinal study in the world. Terman himself had been a gifted child, and his interest in the study of genius derived from personal experience. (Within six months of starting school, at age 5, Terman was advanced to third grade—which was not seen at the time as a good thing; the prevailing belief was that precocity was abnormal and would produce problems in adulthood.) Terman also hoped to improve the measurement of “genius” and test Lombroso’s suggestion that it was associated with degeneracy.

In 1916, as a member of the psychology department at Stanford, Terman developed America’s first IQ test, drawing from a version developed by the French psychologist Alfred Binet. This test, known as the Stanford-Binet Intelligence Scales, contributed to the development of the Army Alpha, an exam the American military used during World War I to screen recruits and evaluate them for work assignments and determine whether they were worthy of officer status.

Terman eventually used the Stanford-Binet test to select high-IQ students for his longitudinal study, which began in 1921. His long-term goal was to recruit at least 1,000 students from grades three through eight who represented the smartest 1 percent of the urban California population in that age group. The subjects had to have an IQ greater than 135, as measured by the Stanford-Binet test. The recruitment process was intensive: students were first nominated by teachers, then given group tests, and finally subjected to individual Stanford-Binet tests. After various enrichments—adding some of the subjects’ siblings, for example—the final sample consisted of 856 boys and 672 girls. One finding that emerged quickly was that being the youngest student in a grade was an excellent predictor of having a high IQ. (This is worth bearing in mind today, when parents sometimes choose to hold back their children precisely so they will not be the youngest in their grades.)

These children were initially evaluated in all sorts of ways. Researchers took their early developmental histories, documented their play interests, administered medical examinations—including 37 different anthropometric measurements—and recorded how many books they’d read during the past two months, as well as the number of books available in their homes (the latter number ranged from zero to 6,000, with a mean of 328). These gifted children were then reevaluated at regular intervals throughout their lives.

“The Termites,” as Terman’s subjects have come to be known, have debunked some stereotypes and introduced new paradoxes. For example, they were generally physically superior to a comparison group—taller, healthier, more athletic. Myopia (no surprise) was the only physical deficit. They were also more socially mature and generally better adjusted. And these positive patterns persisted as the children grew into adulthood. They tended to have happy marriages and high salaries. So much for the concept of “early ripe and early rotten,” a common assumption when Terman was growing up.

But despite the implications of the title Genetic Studies of Genius, the Termites’ high IQs did not predict high levels of creative achievement later in life. Only a few made significant creative contributions to society; none appear to have demonstrated extremely high creativity levels of the sort recognized by major awards, such as the Nobel Prize. (Interestingly, William Shockley, who was a 12-year-old Palo Alto resident in 1922, somehow failed to make the cut for the study, even though he would go on to share a Nobel Prize in physics for the invention of the transistor.) Thirty percent of the men and 33 percent of the women did not even graduate from college. A surprising number of subjects pursued humble occupations, such as semiskilled trades or clerical positions. As the study evolved over the years, the term gifted was substituted for genius. Although many people continue to equate intelligence with genius, a crucial conclusion from Terman’s study is that having a high IQ is not equivalent to being highly creative. Subsequent studies by other researchers have reinforced Terman’s conclusions, leading to what’s known as the threshold theory, which holds that above a certain level, intelligence doesn’t have much effect on creativity: most creative people are pretty smart, but they don’t have to be that smart, at least as measured by conventional intelligence tests. An IQ of 120, indicating that someone is very smart but not exceptionally so, is generally considered sufficient for creative genius.


 
Kyle Bean

BUT IF HIGH IQ does not indicate creative genius, then what does? And how can one identify creative people for a study?

One approach, which is sometimes referred to as the study of “little c,” is to develop quantitative assessments of creativity—a necessarily controversial task, given that it requires settling on what creativity actually is. The basic concept that has been used in the development of these tests is skill in “divergent thinking,” or the ability to come up with many responses to carefully selected questions or probes, as contrasted with “convergent thinking,” or the ability to come up with the correct answer to problems that have only one answer. For example, subjects might be asked, “How many uses can you think of for a brick?” A person skilled in divergent thinking might come up with many varied responses, such as building a wall; edging a garden; and serving as a bludgeoning weapon, a makeshift shot put, a bookend. Like IQ tests, these exams can be administered to large groups of people. Assuming that creativity is a trait everyone has in varying amounts, those with the highest scores can be classified as exceptionally creative and selected for further study.

While this approach is quantitative and relatively objective, its weakness is that certain assumptions must be accepted: that divergent thinking is the essence of creativity, that creativity can be measured using tests, and that high-scoring individuals are highly creative people. One might argue that some of humanity’s most creative achievements have been the result of convergent thinking—a process that led to Newton’s recognition of the physical formulae underlying gravity, and Einstein’s recognition that E=mc2.

A second approach to defining creativity is the “duck test”: if it walks like a duck and quacks like a duck, it must be a duck. This approach usually involves selecting a group of people—writers, visual artists, musicians, inventors, business innovators, scientists—who have been recognized for some kind of creative achievement, usually through the awarding of major prizes (the Nobel, the Pulitzer, and so forth). Because this approach focuses on people whose widely recognized creativity sets them apart from the general population, it is sometimes referred to as the study of “big C.” The problem with this approach is its inherent subjectivity. What does it mean, for example, to have “created” something? Can creativity in the arts be equated with creativity in the sciences or in business, or should such groups be studied separately? For that matter, should science or business innovation be considered creative at all?

Although I recognize and respect the value of studying “little c,” I am an unashamed advocate of studying “big C.” I first used this approach in the mid-1970s and 1980s, when I conducted one of the first empirical studies of creativity and mental illness. Not long after I joined the psychiatry faculty of the Iowa College of Medicine, I ran into the chair of the department, a biologically oriented psychiatrist known for his salty language and male chauvinism. “Andreasen,” he told me, “you may be an M.D./Ph.D., but that Ph.D. of yours isn’t worth sh--, and it won’t count favorably toward your promotion.” I was proud of my literary background and believed that it made me a better clinician and a better scientist, so I decided to prove him wrong by using my background as an entry point to a scientific study of genius and insanity.

The University of Iowa is home to the Writers’ Workshop, the oldest and most famous creative-writing program in the United States (UNESCO has designated Iowa City as one of its seven “Cities of Literature,” along with the likes of Dublin and Edinburgh). Thanks to my time in the university’s English department, I was able to recruit study subjects from the workshop’s ranks of distinguished permanent and visiting faculty. Over the course of 15 years, I studied not only Kurt Vonnegut but Richard Yates, John Cheever, and 27 other well-known writers.


 
The writer Kurt Vonnegut came from a family with a long history of mental illness—and exceptional creativity. Above: Vonnegut (right) meets with Hollywood producer Mark Robson in 1971. (AP)

Going into the study, I keyed my hypotheses off the litany of famous people who I knew had personal or family histories of mental illness. James Joyce, for example, had a daughter who suffered from schizophrenia, and he himself had traits that placed him on the schizophrenia spectrum. (He was socially aloof and even cruel to those close to him, and his writing became progressively more detached from his audience and from reality, culminating in the near-psychotic neologisms and loose associations of Finnegans Wake.) Bertrand Russell, a philosopher whose work I admired, had multiple family members who suffered from schizophrenia. Einstein had a son with schizophrenia, and he himself displayed some of the social and interpersonal ineptitudes that can characterize the illness. Based on these clues, I hypothesized that my subjects would have an increased rate of schizophrenia in family members but that they themselves would be relatively well. I also hypothesized that creativity might run in families, based on prevailing views that the tendencies toward psychosis and toward having creative and original ideas were closely linked.

I began by designing a standard interview for my subjects, covering topics such as developmental, social, family, and psychiatric history, and work habits and approach to writing. Drawing on creativity studies done by the psychiatric epidemiologist Thomas McNeil, I evaluated creativity in family members by assigning those who had had very successful creative careers an A++ rating and those who had pursued creative interests or hobbies an A+.

My final challenge was selecting a control group. After entertaining the possibility of choosing a homogeneous group whose work is not usually considered creative, such as lawyers, I decided that it would be best to examine a more varied group of people from a mixture of professions, such as administrators, accountants, and social workers. I matched this control group with the writers according to age and educational level. By matching based on education, I hoped to match for IQ, which worked out well; both the test and the control groups had an average IQ of about 120. These results confirmed Terman’s findings that creative genius is not the same as high IQ. If having a very high IQ was not what made these writers creative, then what was?

As I began interviewing my subjects, I soon realized that I would not be confirming my schizophrenia hypothesis. If I had paid more attention to Sylvia Plath and Robert Lowell, who both suffered from what we today call mood disorder, and less to James Joyce and Bertrand Russell, I might have foreseen this. One after another, my writer subjects came to my office and spent three or four hours pouring out the stories of their struggles with mood disorder—mostly depression, but occasionally bipolar disorder. A full 80 percent of them had had some kind of mood disturbance at some time in their lives, compared with just 30 percent of the control group—only slightly less than an age-matched group in the general population. (At first I had been surprised that nearly all the writers I approached would so eagerly agree to participate in a study with a young and unknown assistant professor—but I quickly came to understand why they were so interested in talking to a psychiatrist.) The Vonneguts turned out to be representative of the writers’ families, in which both mood disorder and creativity were overrepresented—as with the Vonneguts, some of the creative relatives were writers, but others were dancers, visual artists, chemists, architects, or mathematicians. This is consistent with what some other studies have found. When the psychologist Kay Redfield Jamison looked at 47 famous writers and artists in Great Britain, she found that more than 38 percent had been treated for a mood disorder; the highest rates occurred among playwrights, and the second-highest among poets. When Joseph Schildkraut, a psychiatrist at Harvard Medical School, studied a group of 15 abstract-expressionist painters in the mid-20th century, he found that half of them had some form of mental illness, mostly depression or bipolar disorder; nearly half of these artists failed to live past age 60.


 
The brain of a genius: After completing her analysis of a creative person, the author provides the subject with a 3‐D model of his or her brain. (Mike Basher)

WHILE MY WORKSHOP STUDY answered some questions, it raised others. Why does creativity run in families? What is it that gets transmitted? How much is due to nature and how much to nurture? Are writers especially prone to mood disorders because writing is an inherently lonely and introspective activity? What would I find if I studied a group of scientists instead?

These questions percolated in my mind in the weeks, months, and eventually years after the study. As I focused my research on the neurobiology of severe mental illnesses, including schizophrenia and mood disorders, studying the nature of creativity—important as the topic was and is—seemed less pressing than searching for ways to alleviate the suffering of patients stricken with these dreadful and potentially lethal brain disorders. During the 1980s, new neuroimaging techniques gave researchers the ability to study patients’ brains directly, an approach I began using to answer questions about how and why the structure and functional activity of the brain is disrupted in some people with serious mental illnesses.

As I spent more time with neuroimaging technology, I couldn’t help but wonder what we would find if we used it to look inside the heads of highly creative people. Would we see a little genie that doesn’t exist inside other people’s heads?

Today’s neuroimaging tools show brain structure with a precision approximating that of the examination of post-mortem tissue; this allows researchers to study all sorts of connections between brain measurements and personal characteristics. For example, we know that London taxi drivers, who must memorize maps of the city to earn a hackney’s license, have an enlarged hippocampus—a key memory region—as demonstrated in a magnetic-resonance-imaging, or MRI, study. (They know it, too: on a recent trip to London, I was proudly regaled with this information by several different taxi drivers.) Imaging studies of symphony-orchestra musicians have found them to possess an unusually large Broca’s area—a part of the brain in the left hemisphere that is associated with language—along with other discrepancies. Using another technique, functional magnetic resonance imaging (fMRI), we can watch how the brain behaves when engaged in thought.

Designing neuroimaging studies, however, is exceedingly tricky. Capturing human mental processes can be like capturing quicksilver. The brain has as many neurons as there are stars in the Milky Way, each connected to other neurons by billions of spines, which contain synapses that change continuously depending on what the neurons have recently learned. Capturing brain activity using imaging technology inevitably leads to oversimplifications, as sometimes evidenced by news reports that an investigator has found the location of something—love, guilt, decision making—in a single region of the brain.

And what are we even looking for when we search for evidence of “creativity” in the brain? Although we have a definition of creativity that many people accept—the ability to produce something that is novel or original and useful or adaptive—achieving that “something” is part of a complex process, one often depicted as an “aha” or “eureka” experience. This narrative is appealing—for example, “Newton developed the concept of gravity around 1666, when an apple fell on his head while he was meditating under an apple tree.” The truth is that by 1666, Newton had already spent many years teaching himself the mathematics of his time (Euclidean geometry, algebra, Cartesian coordinates) and inventing calculus so that he could measure planetary orbits and the area under a curve. He continued to work on his theory of gravity over the subsequent years, completing the effort only in 1687, when he published Philosophiœ Naturalis Principia Mathematica. In other words, Newton’s formulation of the concept of gravity took more than 20 years and included multiple components: preparation, incubation, inspiration—a version of the eureka experience—and production. Many forms of creativity, from writing a novel to discovering the structure of DNA, require this kind of ongoing, iterative process.

With functional magnetic resonance imaging, the best we can do is capture brain activity during brief moments in time while subjects are performing some task. For instance, observing brain activity while test subjects look at photographs of their relatives can help answer the question of which parts of the brain people use when they recognize familiar faces. Creativity, of course, cannot be distilled into a single mental process, and it cannot be captured in a snapshot—nor can people produce a creative insight or thought on demand. I spent many years thinking about how to design an imaging study that could identify the unique features of the creative brain.


 
The images on the left show the brain of a creative subject (top) and a matched control subject during a word‐association task. The images on the right show brain activation as the subjects alternate between an experimental task (word association) and a control task (reading a word). The line representing the creative subject’s brain activation moves smoothly up and down as the task changes, reflecting effective use of the association cortices in making connections. The control subject’s activation line looks ragged by comparison.

MOST OF THE HUMAN BRAIN'S high-level functions arise from the six layers of nerve cells and their dendrites embedded in its enormous surface area, called the cerebral cortex, which is compressed to a size small enough to be carried around on our shoulders through a process known as gyrification—essentially, producing lots of folds. Some regions of the brain are highly specialized, receiving sensory information from our eyes, ears, skin, mouth, or nose, or controlling our movements. We call these regions the primary visual, auditory, sensory, and motor cortices. They collect information from the world around us and execute our actions. But we would be helpless, and effectively nonhuman, if our brains consisted only of these regions.

In fact, the most extensively developed regions in the human brain are known as association cortices. These regions help us interpret and make use of the specialized information collected by the primary visual, auditory, sensory, and motor regions. For example, as you read these words on a page or a screen, they register as black lines on a white background in your primary visual cortex. If the process stopped at that point, you wouldn’t be reading at all. To read, your brain, through miraculously complex processes that scientists are still figuring out, needs to forward those black letters on to association-cortex regions such as the angular gyrus, so that meaning is attached to them; and then on to language-association regions in the temporal lobes, so that the words are connected not only to one another but also to their associated memories and given richer meanings. These associated memories and meanings constitute a “verbal lexicon,” which can be accessed for reading, speaking, listening, and writing. Each person’s lexicon is a bit different, even if the words themselves are the same, because each person has different associated memories and meanings. One difference between a great writer like Shakespeare and, say, the typical stockbroker is the size and richness of the verbal lexicon in his or her temporal association cortices, as well as the complexity of the cortices’ connections with other association regions in the frontal and parietal lobes.

A neuroimaging study I conducted in 1995 using positron-emission tomography, or PET, scanning turned out to be unexpectedly useful in advancing my own understanding of association cortices and their role in the creative process.

This PET study was designed to examine the brain’s different memory systems, which the great Canadian psychologist Endel Tulving identified. One system, episodic memory, is autobiographical—it consists of information linked to an individual’s personal experiences. It is called “episodic” because it consists of time-linked sequential information, such as the events that occurred on a person’s wedding day. My team and I compared this with another system, that of semantic memory, which is a repository of general information and is not personal or time-linked. In this study, we divided episodic memory into two subtypes. We examined focused episodic memory by asking subjects to recall a specific event that had occurred in the past and to describe it with their eyes closed. And we examined a condition that we called random episodic silent thought, or REST: we asked subjects to lie quietly with their eyes closed, to relax, and to think about whatever came to mind. In essence, they would be engaged in “free association,” letting their minds wander. The acronym REST was intentionally ironic; we suspected that the association regions of the brain would actually be wildly active during this state.

This suspicion was based on what we had learned about free association from the psychoanalytic approach to understanding the mind. In the hands of Freud and other psychoanalysts, free association—spontaneously saying whatever comes to mind without censorship—became a window into understanding unconscious processes. Based on my interviews with the creative subjects in my workshop study, and from additional conversations with artists, I knew that such unconscious processes are an important component of creativity. For example, Neil Simon told me: “I don’t write consciously—it is as if the muse sits on my shoulder” and “I slip into a state that is apart from reality.” (Examples from history suggest the same thing. Samuel Taylor Coleridge once described how he composed an entire 300-line poem about Kubla Khan while in an opiate-induced, dreamlike state, and began writing it down when he awoke; he said he then lost most of it when he got interrupted and called away on an errand—thus the finished poem he published was but a fragment of what originally came to him in his dreamlike state.)

Based on all this, I surmised that observing which parts of the brain are most active during free association would give us clues about the neural basis of creativity. And what did we find? Sure enough, the association cortices were wildly active during REST.

I realized that I obviously couldn’t capture the entire creative process—instead, I could home in on the parts of the brain that make creativity possible. Once I arrived at this idea, the design for the imaging studies was obvious: I needed to compare the brains of highly creative people with those of control subjects as they engaged in tasks that activated their association cortices.

For years, I had been asking myself what might be special or unique about the brains of the workshop writers I had studied. In my own version of a eureka moment, the answer finally came to me: creative people are better at recognizing relationships, making associations and connections, and seeing things in an original way—seeing things that others cannot see. To test this capacity, I needed to study the regions of the brain that go crazy when you let your thoughts wander. I needed to target the association cortices. In addition to REST, I could observe people performing simple tasks that are easy to do in an MRI scanner, such as word association, which would permit me to compare highly creative people—who have that “genie in the brain”—with the members of a control group matched by age and education and gender, people who have “ordinary creativity” and who have not achieved the levels of recognition that characterize highly creative people. I was ready to design Creativity Study II.

THIS TIME AROUND, I wanted to examine a more diverse sample of creativity, from the sciences as well as the arts. My motivations were partly selfish—I wanted the chance to discuss the creative process with people who might think and work differently, and I thought I could probably learn a lot by listening to just a few people from specific scientific fields. After all, each would be an individual jewel—a fascinating study on his or her own. Now that I’m about halfway through the study, I can say that this is exactly what has happened. My individual jewels so far include, among others, the filmmaker George Lucas, the mathematician and Fields Medalist William Thurston, the Pulitzer Prize–winning novelist Jane Smiley, and six Nobel laureates from the fields of chemistry, physics, and physiology or medicine. Because winners of major awards are typically older, and because I wanted to include some younger people, I’ve also recruited winners of the National Institutes of Health Pioneer Award and other prizes in the arts.

Apart from stating their names, I do not have permission to reveal individual information about my subjects. And because the study is ongoing (each subject can take as long as a year to recruit, making for slow progress), we do not yet have any definitive results—though we do have a good sense of the direction that things are taking. By studying the structural and functional characteristics of subjects’ brains in addition to their personal and family histories, we are learning an enormous amount about how creativity occurs in the brain, as well as whether these scientists and artists display the same personal or familial connections to mental illness that the subjects in my Iowa Writers’ Workshop study did.

To participate in the study, each subject spends three days in Iowa City, since it is important to conduct the research using the same MRI scanner. The subjects and I typically get to know each other over dinner at my home (and a bottle of Bordeaux from my cellar), and by prowling my 40-acre nature retreat in an all-terrain vehicle, observing whatever wildlife happens to be wandering around. Relaxing together and getting a sense of each other’s human side is helpful going into the day and a half of brain scans and challenging conversations that will follow.

We begin the actual study with an MRI scan, during which subjects perform three different tasks, in addition to REST: word association, picture association, and pattern recognition. Each experimental task alternates with a control task; during word association, for example, subjects are shown words on a screen and asked to either think of the first word that comes to mind (the experimental task) or silently repeat the word they see (the control task). Speaking disrupts the scanning process, so subjects silently indicate when they have completed a task by pressing a button on a keypad.

Playing word games inside a thumping, screeching hollow tube seems like a far cry from the kind of meandering, spontaneous discovery process that we tend to associate with creativity. It is, however, as close as one can come to a proxy for that experience, apart from REST. You cannot force creativity to happen—every creative person can attest to that. But the essence of creativity is making connections and solving puzzles. The design of these MRI tasks permits us to visualize what is happening in the creative brain when it’s doing those things.

As I hypothesized, the creative people have shown stronger activations in their association cortices during all four tasks than the controls have. (See the images on page 74.) This pattern has held true for both the artists and the scientists, suggesting that similar brain processes may underlie a broad spectrum of creative expression. Common stereotypes about “right brained” versus “left brained” people notwithstanding, this parallel makes sense. Many creative people are polymaths, people with broad interests in many fields—a common trait among my study subjects.

After the brain scans, I settle in with subjects for an in-depth interview. Preparing for these interviews can be fun (rewatching all of George Lucas’s films, for example, or reading Jane Smiley’s collected works) as well as challenging (toughing through mathematics papers by William Thurston). I begin by asking subjects about their life history—where they grew up, where they went to school, what activities they enjoyed. I ask about their parents—their education, occupation, and parenting style—and about how the family got along. I learn about brothers, sisters, and children, and get a sense for who else in a subject’s family is or has been creative and how creativity may have been nurtured at home. We talk about how the subjects managed the challenges of growing up, any early interests and hobbies (particularly those related to the creative activities they pursue as adults), dating patterns, life in college and graduate school, marriages, and child-rearing. I ask them to describe a typical day at work and to think through how they have achieved such a high level of creativity. (One thing I’ve learned from this line of questioning is that creative people work much harder than the average person—and usually that’s because they love their work.)

One of the most personal and sometimes painful parts of the interview is when I ask about mental illness in subjects’ families as well as in their own lives. They’ve told me about such childhood experiences as having a mother commit suicide or watching ugly outbreaks of violence between two alcoholic parents, and the pain and scars that these experiences have inflicted. (Two of the 13 creative subjects in my current study have lost a parent to suicide—a rate many times that of the general U.S. population.) Talking with those subjects who have suffered from a mental illness themselves, I hear about how it has affected their work and how they have learned to cope.


The author’s research on creativity includes in-depth neurological studies of “individual jewels,” including Pulitzer Prize–winning novelist Jane Smiley, shown here in 1991. (AP)

SO FAR, THIS STUDY—which has examined 13 creative geniuses and 13 controls—has borne out a link between mental illness and creativity similar to the one I found in my Writers’ Workshop study. The creative subjects and their relatives have a higher rate of mental illness than the controls and their relatives do (though not as high a rate as I found in the first study), with the frequency being fairly even across the artists and the scientists. The most-common diagnoses include bipolar disorder, depression, anxiety or panic disorder, and alcoholism. I’ve also found some evidence supporting my early hypothesis that exceptionally creative people are more likely than control subjects to have one or more first-degree relatives with schizophrenia. Interestingly, when the physician and researcher Jon L. Karlsson examined the relatives of everyone listed in Iceland’s version of Who’s Who in the 1940s and ’60s, he found that they had higher-than-average rates of schizophrenia. Leonard Heston, a former psychiatric colleague of mine at Iowa, conducted an influential study of the children of schizophrenic mothers raised from infancy by foster or adoptive parents, and found that more than 10 percent of these children developed schizophrenia, as compared with zero percent of a control group. This suggests a powerful genetic component to schizophrenia. Heston and I discussed whether some particularly creative people owe their gifts to a subclinical variant of schizophrenia that loosens their associative links sufficiently to enhance their creativity but not enough to make them mentally ill.

As in the first study, I’ve also found that creativity tends to run in families, and to take diverse forms. In this arena, nurture clearly plays a strong role. Half the subjects come from very high-achieving backgrounds, with at least one parent who has a doctoral degree. The majority grew up in an environment where learning and education were highly valued. This is how one person described his childhood:
Our family evenings—just everybody sitting around working. We’d all be in the same room, and [my mother] would be working on her papers, preparing her lesson plans, and my father had huge stacks of papers and journals … This was before laptops, and so it was all paper-based. And I’d be sitting there with my homework, and my sisters are reading. And we’d just spend a few hours every night for 10 to 15 years—that’s how it was. Just working together. No TV.
So why do these highly gifted people experience mental illness at a higher-than-average rate? Given that (as a group) their family members have higher rates than those that occur in the general population or in the matched comparison group, we must suspect that nature plays a role—that Francis Galton and others were right about the role of hereditary factors in people’s predisposition to both creativity and mental illness. We can only speculate about what those factors might be, but there are some clues in how these people describe themselves and their lifestyles.

One possible contributory factor is a personality style shared by many of my creative subjects. These subjects are adventuresome and exploratory. They take risks. Particularly in science, the best work tends to occur in new frontiers. (As a popular saying among scientists goes: “When you work at the cutting edge, you are likely to bleed.”) They have to confront doubt and rejection. And yet they have to persist in spite of that, because they believe strongly in the value of what they do. This can lead to psychic pain, which may manifest itself as depression or anxiety, or lead people to attempt to reduce their discomfort by turning to pain relievers such as alcohol.

I’ve been struck by how many of these people refer to their most creative ideas as “obvious.” Since these ideas are almost always the opposite of obvious to other people, creative luminaries can face doubt and resistance when advocating for them. As one artist told me, “The funny thing about [one’s own] talent is that you are blind to it. You just can’t see what it is when you have it … When you have talent and see things in a particular way, you are amazed that other people can’t see it.” Persisting in the face of doubt or rejection, for artists or for scientists, can be a lonely path—one that may also partially explain why some of these people experience mental illness.

ONE INTERESTING PARADOX that has emerged during conversations with subjects about their creative processes is that, though many of them suffer from mood and anxiety disorders, they associate their gifts with strong feelings of joy and excitement. “Doing good science is simply the most pleasurable thing anyone can do,” one scientist told me. “It is like having good sex. It excites you all over and makes you feel as if you are all-powerful and complete.” This is reminiscent of what creative geniuses throughout history have said. For instance, here’s Tchaikovsky, the composer, writing in the mid-19th century:
It would be vain to try to put into words that immeasurable sense of bliss which comes over me directly a new idea awakens in me and begins to assume a different form. I forget everything and behave like a madman. Everything within me starts pulsing and quivering; hardly have I begun the sketch ere one thought follows another.
Another of my subjects, a neuroscientist and an inventor, told me, “There is no greater joy that I have in my life than having an idea that’s a good idea. At that moment it pops into my head, it is so deeply satisfying and rewarding … My nucleus accumbens is probably going nuts when it happens.” (The nucleus accumbens, at the core of the brain’s reward system, is activated by pleasure, whether it comes from eating good food or receiving money or taking euphoria-inducing drugs.)

As for how these ideas emerge, almost all of my subjects confirmed that when eureka moments occur, they tend to be precipitated by long periods of preparation and incubation, and to strike when the mind is relaxed—during that state we called REST. “A lot of it happens when you are doing one thing and you’re not thinking about what your mind is doing,” one of the artists in my study told me. “I’m either watching television, I’m reading a book, and I make a connection … It may have nothing to do with what I am doing, but somehow or other you see something or hear something or do something, and it pops that connection together.”

Many subjects mentioned lighting on ideas while showering, driving, or exercising. One described a more unusual regimen involving an afternoon nap: “It’s during this nap that I get a lot of my work done. I find that when the ideas come to me, they come as I’m falling asleep, they come as I’m waking up, they come if I’m sitting in the tub. I don’t normally take baths … but sometimes I’ll just go in there and have a think.”

SOME OF THE OTHER most common findings my studies have suggested include:

Many creative people are autodidacts. They like to teach themselves, rather than be spoon-fed information or knowledge in standard educational settings. Famously, three Silicon Valley creative geniuses have been college dropouts: Bill Gates, Steve Jobs, and Mark Zuckerberg. Steve Jobs—for many, the archetype of the creative person—popularized the motto “Think different.” Because their thinking is different, my subjects often express the idea that standard ways of learning and teaching are not always helpful and may even be distracting, and that they prefer to learn on their own. Many of my subjects taught themselves to read before even starting school, and many have read widely throughout their lives. For example, in his article “On Proof and Progress in Mathematics,” Bill Thurston wrote:
My mathematical education was rather independent and idiosyncratic, where for a number of years I learned things on my own, developing personal mental models for how to think about mathematics. This has often been a big advantage for me in thinking about mathematics, because it’s easy to pick up later the standard mental models shared by groups of mathematicians.
This observation has important implications for the education of creatively gifted children. They need to be allowed and even encouraged to “think different.” (Several subjects described to me how they would get in trouble in school for pointing out when their teachers said things that they knew to be wrong, such as when a second-grade teacher explained to one of my subjects that light and sound are both waves and travel at the same speed. The teacher did not appreciate being corrected.)

Many creative people are polymaths, as historic geniuses including Michelangelo and Leonardo da Vinci were. George Lucas was awarded not only the National Medal of Arts in 2012 but also the National Medal of Technology in 2004. Lucas’s interests include anthropology, history, sociology, neuroscience, digital technology, architecture, and interior design. Another polymath, one of the scientists, described his love of literature:
I love words, and I love the rhythms and sounds of words … [As a young child] I very rapidly built up a huge storehouse of … Shakespearean sonnets, soliloquies, poems across the whole spectrum … When I got to college, I was open to many possible careers. I actually took a creative-writing course early. I strongly considered being a novelist or a writer or a poet, because I love words that much … [But for] the academics, it’s not so much about the beauty of the words. So I found that dissatisfying, and I took some biology courses, some quantum courses. I really clicked with biology. It seemed like a complex system that was tractable, beautiful, important. And so I chose biochemistry.
The arts and the sciences are seen as separate tracks, and students are encouraged to specialize in one or the other. If we wish to nurture creative students, this may be a serious error.

Creative people tend to be very persistent, even when confronted with skepticism or rejection. Asked what it takes to be a successful scientist, one replied:
Perseverance … In order to have that freedom to find things out, you have to have perseverance … The grant doesn’t get funded, and the next day you get up, and you put the next foot in front, and you keep putting your foot in front … I still take things personally. I don’t get a grant, and … I’m upset for days. And then I sit down and I write the grant again.
DO CREATIVE PEOPLE simply have more ideas, and therefore differ from average people only in a quantitative way, or are they also qualitatively different? One subject, a neuroscientist and an inventor, addressed this question in an interesting way, conceptualizing the matter in terms of kites and strings:
In the R&D business, we kind of lump people into two categories: inventors and engineers. The inventor is the kite kind of person. They have a zillion ideas and they come up with great first prototypes. But generally an inventor … is not a tidy person. He sees the big picture and … [is] constantly lashing something together that doesn’t really work. And then the engineers are the strings, the craftsmen [who pick out a good idea] and make it really practical. So, one is about a good idea, the other is about … making it practical.
Of course, having too many ideas can be dangerous. One subject, a scientist who happens to be both a kite and a string, described to me “a willingness to take an enormous risk with your whole heart and soul and mind on something where you know the impact—if it worked—would be utterly transformative.” The if here is significant. Part of what comes with seeing connections no one else sees is that not all of these connections actually exist. “Everybody has crazy things they want to try,” that same subject told me. “Part of creativity is picking the little bubbles that come up to your conscious mind, and picking which one to let grow and which one to give access to more of your mind, and then have that translate into action.”

In A Beautiful Mind, her biography of the mathematician John Nash, Sylvia Nasar describes a visit Nash received from a fellow mathematician while institutionalized at McLean Hospital. “How could you, a mathematician, a man devoted to reason and logical truth,” the colleague asked, “believe that extraterrestrials are sending you messages? How could you believe that you are being recruited by aliens from outer space to save the world?” To which Nash replied: “Because the ideas I had about supernatural beings came to me the same way that my mathematical ideas did. So I took them seriously.”

Some people see things others cannot, and they are right, and we call them creative geniuses. Some people see things others cannot, and they are wrong, and we call them mentally ill. And some people, like John Nash, are both.

Tuesday, June 03, 2014

James Hamblin - The Everyday Toxins that Harm Our Brains

http://cdn.theatlantic.com/assets/media/img/2014/03/25/toxinsopener/lead.jpg

From The Atlantic, this is a disturbing look at the neurotoxic chemicals we are exposed to on a regular basis. These chemicals are especially toxic to the developing brain in children.

I missed when it first came around in March, but the issue is still highly relevant.

The Toxins That Threaten Our Brains

Leading scientists recently identified a dozen chemicals as being responsible for widespread behavioral and cognitive problems. But the scope of the chemical dangers in our environment is likely even greater. Why children and the poor are most susceptible to neurotoxic exposure that may be costing the U.S. billions of dollars and immeasurable peace of mind.


James Hamblin
Illustrations by Jackie Lay
March 18, 2014


FORTY-ONE MILLION IQ POINTS. That’s what Dr. David Bellinger determined Americans have collectively forfeited as a result of exposure to lead, mercury, and organophosphate pesticides. In a 2012 paper published by the National Institutes of Health, Bellinger, a professor of neurology at Harvard Medical School, compared intelligence quotients among children whose mothers had been exposed to these neurotoxins while pregnant to those who had not. Bellinger calculates a total loss of 16.9 million IQ points due to exposure to organophosphates, the most common pesticides used in agriculture.

Last month, more research brought concerns about chemical exposure and brain health to a heightened pitch. Philippe Grandjean, Bellinger’s Harvard colleague, and Philip Landrigan, dean for global health at Mount Sinai School of Medicine in Manhattan, announced to some controversy in the pages of a prestigious medical journal that a “silent pandemic” of toxins has been damaging the brains of unborn children. The experts named 12 chemicals—substances found in both the environment and everyday items like furniture and clothing—that they believed to be causing not just lower IQs but ADHD and autism spectrum disorder. Pesticides were among the toxins they identified.


 

“So you recommend that pregnant women eat organic produce?” I asked Grandjean, a Danish-born researcher who travels around the world studying delayed effects of chemical exposure on children.

“That’s what I advise people who ask me, yes. It’s the best way of preventing exposure to pesticides.” Grandjean estimates that there are about 45 organophosphate pesticides on the market, and “most have the potential to damage a developing nervous system.”

Landrigan had issued that same warning, unprompted, when I spoke to him the week before. “I advise pregnant women to try to eat organic because it reduces their exposure by 80 or 90 percent,” he told me. “These are the chemicals I really worry about in terms of American kids, the organophosphate pesticides like chlorpyrifos.”

For decades, chlorpyrifos, marketed by Dow Chemical beginning in 1965, was the most widely used insect killer in American homes. Then, in 1995, Dow was fined $732,000 by the EPA for concealing more than 200 reports of poisoning related to chlorpyrifos. It paid the fine and, in 2000, withdrew chlorpyrifos from household products. Today, chlorpyrifos is classified as “very highly toxic” to birds and freshwater fish, and “moderately toxic” to mammals, but it is still used widely in agriculture on food and non-food crops, in greenhouses and plant nurseries, on wood products and golf courses.

Landrigan has the credentials of some superhero vigilante Doctor America: a Harvard-educated pediatrician, a decorated retired captain of the U.S. Naval Reserve, and a leading physician-advocate for children's health as it relates to the environment. After September 11, he made news when he testified before Congress in disagreement with the EPA’s assessment that asbestos particles stirred into clouds of debris were too small to pose any real threat. Landrigan cited research from mining townships (including Asbestos, Quebec) and argued that even the smallest airborne asbestos fibers could penetrate deeply into a child’s lungs.

Chlorpyrifos is just one of 12 toxic chemicals Landrigan and Grandjean say are having grim effects on fetal brain development. Their new study is similar to a review the two researchers published in 2006, in the same journal, identifying six developmental neurotoxins. Only now they describe twice the danger: The number of chemicals that they deemed to be developmental neurotoxins had doubled over the past seven years. Six had become 12. Their sense of urgency now approached panic. “Our very great concern,” Grandjean and Landrigan wrote, “is that children worldwide are being exposed to unrecognized toxic chemicals that are silently eroding intelligence, disrupting behaviors, truncating future achievements and damaging societies.”


 

The chemicals they called out as developmental neurotoxins in 2006 were methylmercury, polychlorinated biphenyls, ethanol, lead, arsenic, and toluene. The additional chemicals they’ve since found to be toxins to the developing brains of fetuses—and I hope you’ll trust me that these all are indeed words—are manganese, fluoride, chlorpyrifos, tetrachloroethylene, polybrominated diphenyl ethers, and dichlorodiphenyltrichloroethane.

Grandjean and Landrigan note in their research that rates of diagnosis of autism spectrum disorder and ADHD are increasing, and that neurobehavioral development disorders currently affect 10 to 15 percent of births. They add that “subclinical decrements in brain function”—problems with thinking that aren’t quite a diagnosis in themselves—“are even more common than these neurobehavioral development disorders.”

In perhaps their most salient paragraph, the researchers say that genetic factors account for no more than 30 to 40 percent of all cases of brain development disorders:
Thus, non-genetic, environmental exposures are involved in causation, in some cases probably by interacting with genetically inherited predispositions. Strong evidence exists that industrial chemicals widely disseminated in the environment are important contributors to what we have called the global, silent pandemic of neurodevelopmental toxicity. 
Silent pandemic. When public health experts use that phrase—a relative and subjective one, to be deployed with discretion—they mean for it to echo.

When their paper went to press in the journal The Lancet Neurology, the media responded with understandable alarm:
  • “A ‘Silent Pandemic’ of Toxic Chemicals Is Damaging Our Children’s Brains, Experts Claim” - Minneapolis Post, 2/17/14
  • “Researchers Warn of Chemical Impacts on Children,” - USA Today, 2/14/14
  • “Study Finds Toxic Chemicals Linked to Autism, ADHD” - Sydney Morning Herald, 2/16/14 
When I first saw these headlines, I was skeptical. It wasn’t news that many of the chemicals on this list (arsenic, DDT, lead) are toxic. With each of these substances, the question is just how much exposure does it take to cause real damage. For instance, organophosphates aren’t something that anyone would categorically consider safe, in that they are poison. They kill insects by the same mechanism that sarin gas kills people, causing nerves to fire uncontrollably. But like asbestos, they are still legally used in U.S. commerce, with the idea that small amounts of exposure are safe. The adage “the dose makes the poison” may be the most basic premise of toxicology. And hadn’t we already taken care of lead? Didn’t we already know that alcohol is bad for fetuses? Wasn’t fluoride good for teeth?

I found that the real issue was not this particular group of 12 chemicals. Most of them are already being heavily restricted. This dozen is meant to illuminate something bigger: a broken system that allows industrial chemicals to be used without any significant testing for safety. The greater concern lies in what we’re exposed to and don’t yet know to be toxic. Federal health officials, prominent academics, and even many leaders in the chemical industry agree that the U.S. chemical safety testing system is in dire need of modernization. Yet parties on various sides cannot agree on the specifics of how to change the system, and two bills to modernize testing requirements are languishing in Congress. Landrigan and Grandjean’s real message is big, and it involves billion-dollar corporations and Capitol Hill, but it begins and ends with the human brain in its earliest, most vulnerable stages.


How Toxins Destroy Brains 


About a quarter of your body’s metabolism goes toward operating and maintaining your brain. In order to process even basic information, billions of chemical signals are constantly being carried between neurons. The undertaking is so onerous that even though your brain is not moving (like, say, the powerful muscles in your legs), it uses around 10 times more calories per pound than the rest of you.

Most of that industrious brain and its 86 billion neurons were created in a matter of months. During the first few weeks of gestation, when your mother knew you only as morning sickness and you were a layer of cells huddled in one corner of her uterus, those cells lined up, formed a groove, and then closed to form a tube. One end of that tube eventually became your tiny spinal cord. The rest expanded to form the beginnings of your brain.


 

For a brain to develop properly, neurons must move to precise places in a precise sequence. They do so under the direction of hormones and chemical neurotransmitters like acetylcholine. The process is an intricate, fast-paced dance on a very tiny scale. Each nerve cell is about one hundredth of a millimeter wide, so it has to travel its own width 25,000 times just to move an inch—which some neurons in the cortex must. At any point, that cell can be knocked off course. Some of the neurotoxins Grandjean and Landrigan discuss have the potential to disrupt this journey, in a slight or serious fashion.

By the third trimester, the surface of the brain begins folding itself into wrinkled peaks and valleys, the gyri and sulci that make a brain look like a brain. Specific areas of that cortex learn to process specific aspects of sensation, movement, and thought, and that starts in the uterus. As Grandjean explains this process in his 2013 book Only One Chance, “Usage promotes function and structure, as the connectivity of the brain cells is shaped by responses to environmental stimuli.” That is, the fetal brain starts having experiences that form the basis for learning and memory. The nature-nurture duality begins at conception.

By age two, almost all of the billions of brain cells that you will ever have are in their places. Except in the hippocampus and one or two other tiny regions, the brain does not grow new brain cells throughout your life. When brain cells die, they are gone. So its initial months of formation, when the brain is most vulnerable, are critical. “During these sensitive life stages,” Grandjean and Landrigan write, exposure “can cause permanent brain injury at low levels that would have little or no adverse effect in an adult.”

Federal health officials are aware of this risk. The National Institutes of Health, as Landrigan puts it, “finally woke up in the late 1990s to the fact that children are much more sensitive and vulnerable to chemicals than adults are.” Over the past decade, the federal government has invested substantially more money in looking at just how pregnant women and children have been affected by industrial chemicals. The EPA has awarded millions of dollars in related research grants, and the NIH started funding a network of what it calls Centers for Children’s Environmental Health and Disease Prevention Research. There is one at Mount Sinai and another at Harvard (the respective homes of Landrigan and Grandjean), and there are others at Columbia, UC Berkeley, and elsewhere.

Those centers have established strong research programs called prospective birth-cohort studies. Scientists enroll pregnant female subjects and carefully record objective measures of environmental exposure, using things like blood samples, urine samples, and maybe even dust and air samples from their homes. After the babies are born, the researchers follow up with them at various points in their childhoods. These studies are expensive and take a long time, but they’re incomparably good at connecting prenatal exposures with lost IQ points, shortened attention span, or emergence of ADHD.


 
Functional MRI reveals the effect of prenatal methylmercury exposure in three adolescents. Subjects were asked to tap the fingers of their left hands. In the control group (row B), only the right side of the brain was activated. In the subjects who had been exposed to methylmercury (row A), an abnormal activation pattern shows that both sides are involved. (The Lancet Neurology)

“That’s the big breakthrough,” Landrigan says. "The scientific community has mastered the technique of doing these studies, and they’ve been running long enough that they’re beginning to put out some spectacularly good results.” At Columbia, for instance, the children’s center is investigating whether children exposed in the womb to BPA and polycyclic aromatic hydrocarbons (PAHs)—byproducts from burning fossil fuels—are more likely to develop learning and behavior disorders than children not exposed. They have also shown that high prenatal exposure to air pollutants like PAHs are associated with attention problems, anxiety, and depression at ages 5 to 7 years. It was this center, together with the UC Berkeley and Mount Sinai children’s centers, that first identified the detrimental impact of chlorpyrifos on IQ and brain development. The researchers even used MRI testing to show that these chemicals appear to change children’s brain structure, causing thinning of the cortex. Other children’s centers are looking at the extent to which these and other chemicals—including arsenic from well water, brominated flame retardants, and the anti-corrosion agent manganese—are to blame for a range of possible neurologic disorders.

Impressive as all this research investment is, the larger question remains: Why are we looking at these hazards now—instead of before we introduced these chemicals into the world?


The Insidious Rise of Lead 


The problem with toxic substances is that their effects can be insidious. Take the example of lead—a chemical that lingered in gasoline, house paints, and children's toys for decades before scientists realized the true extent of the damage.

Several years ago, a four-year-old boy in Oregon began complaining of stomach pain and vomiting. Doctors reassured his parents that it was likely a viral illness, but his symptoms worsened, and he became completely unable to eat. He also had a badly swollen cheek. The doctors determined that the boy had bitten himself, so severely that it must have been during a seizure. Blood tests showed that he was anemic, and subsequent tests found that he had extremely high levels of lead (123 micrograms per deciliter of blood).

The doctors began treating the boy with medication to help clear the lead. They also set out to find out where the lead was coming from. An investigation of the boy’s home, which was built in the 1990s, found no lead paint. Despite treatment, though, the boy’s lead tests remained abnormally high. So the doctors did an x-ray.

Inside the boy’s stomach was a one-inch metal medallion, which appeared bright white on the x-ray image. His parents recognized it as a toy necklace they had purchased from a vending machine approximately three weeks earlier. The state environmental quality lab later found that the medallion contained 38.8 percent lead. The manufacturer later did a voluntary recall of 1.4 million of the metal toy necklaces.


 
A late 19th-century advertisement for lead paint (Boston Public Library)

By that time, manufacturers had been using the toxic substance for centuries, despite clearly dangerous effects. In 1786, Benjamin Franklin wrote to a friend about the first time he heard of lead poisoning. When he was a boy, he recounted, there had been “a complaint from North Carolina against New England Rum, that it poisoned their people, giving them the dry bellyache, with a loss of the use of their limbs. The distilleries being examined on the occasion, it was found that several of them used leaden still-heads and worms, and the physicians were of the opinion that the mischief was occasioned by that use of lead.” Franklin went on to describe his observations of similar symptoms in patients at a Paris hospital. When he inquired about their occupations, he discovered that these men were plumbers, glaziers, and painters.

In 1921, General Motors began adding tetraethyl lead to gasoline. Lead gave gasoline a higher octane rating, which meant it could handle more compression without combusting. In practical terms, that meant more powerful engines, faster warplanes, and better industrial transport. The Ethyl Corporation that produced leaded gasoline was a joint venture between GM, Standard Oil, and DuPont. One of its executives, Frank Howard, called leaded gasoline “an apparent gift of God,” even as the plant where tetraethyl lead was synthesized became known as “the Houses of Butterflies,” because it was not uncommon for workers to experience hallucinations of insects on their skin.

Americans in the 1950s and ’60s were still widely exposed to unregulated leaded gasoline and paint, as well as piping, batteries, cosmetics, ceramics, and glass. Around that time, studies began to reveal the widespread existence of “subclinical” lead poisoning—damage that was not severe enough to meet diagnostic criteria for a neurologic disease, but would prevent the child from ever achieving optimal intellectual functioning. By 1969, microbiologist and Pulitzer-Prize-winning writer René Dubos said that the problem of lead exposure was “so well-defined, so neatly packaged, with both causes and cures known, that if we don't eliminate this social crime, our society deserves all the disasters that have been forecast for it.”


 
Four-year-old Tanya Brinson is tested for lead paint poisoning 
at Boston City Hall in June 1975. (Peter Bregg/AP)

By the mid 1970s, the average U.S. preschool child had 15 micrograms of lead per deciliter of blood. Eighty-eight percent of children had a level exceeding 10 μg/dL—which is twice what the CDC currently considers toxic. Among poor black children, the average level was markedly higher: 23 μg/dL.

Instead of making sweeping policy changes, experts largely accused low-income parents—especially mothers—of inadequate supervision and fostering pathological behaviors that led children to eat paint. With parental ineptitude to blame, and poor, minority children bearing the brunt of the problem, a systematic approach to eliminating lead was a low national priority. Bellinger recounted this in the Journal of Clinical Investigation, writing that children were essentially sentinels, used to identify the presence of lead hazards. “As long as the ranks of the lead poisoned consisted primarily of the children of politically and economically disenfranchised parents,” he wrote, “it was hard to interest politicians in the problem. Little political capital could be accumulated by tackling the problem.”

Finally in 1975, the EPA required a gradual phasing of lead out of gasoline. Two years later, the Consumer Product Safety Commission said that residential paint could contain no more than 0.06 percent lead.


 
Jackie Lay, adapted from Bellinger, Journal of Clinical Investigation

Meanwhile there is still disagreement as to what constitutes a safe level of lead exposure—and if there even is such a thing. As more and more evidence came out over the years showing that low levels are in fact toxic to developing brains, the CDC incrementally lowered that threshold—from 60 micrograms per deciliter of blood in 1970 to 40 in 1971, 30 in 1975, 25 in 1985, 10 in 1991, and finally to just five in 2012.

By 2009 the average lead concentration in the blood Americans was about 1.2 μg/dL for young children—just 8 percent what it was in 1980. But Bellinger notes that even this relatively low level is still “substantially elevated from an evolutionary perspective”—many times higher than before our ancestors “began to disturb the natural distribution of lead in the earth's crust.”

“Are the blood lead levels of contemporary humans generally below the threshold of toxicity?” Bellinger wrote. “Let us hope so, but the conclusion that they are is based more on faith than on evidence.”


The Toothless Law and the New Test 


It's surprising to learn how little evidence there is for the safety of chemicals all around us, in our walls and furniture, in our water and air. Many consumers assume there is a rigorous testing process before a new chemical is allowed to be a part of a consumer product. Or at least some process.
“We still don’t have any kind of decent law on the books that requires that chemicals be tested for safety before they come to market,” Landrigan said.

The law we do have is the Toxic Substances Control Act (TSCA, pronounced toss-ka among those in the know). Passed in 1976 under President Gerald Ford, it is still today the primary U.S. law regulating chemicals used in everyday products. On its face intended to protect people and the environment from dangerous chemical exposure, it is widely acknowledged to have fallen short of its magnanimous goal. It only requires testing for a small percentage of chemicals, those deemed an “unreasonable risk.”

“It’s just an obsolete, toothless, broken piece of legislation,” said Landrigan. “For example, in the early 1990s, EPA was unable to ban asbestos under TSCA.” This was after the National Toxicology Program had classified asbestos as a known cancer-causing agent, and the World Health Organization had called for a global ban. The EPA did briefly succeed in banning asbestos in the U.S. in 1989, but a court of appeals overturned the ban in 1991. Asbestos is still used in consumer products in the U.S., including building materials like shingles and pipe wrap, and auto parts like brake pads.

Landrigan also calls it “a particularly egregious lapse” that when TSCA was enacted, the 62,000 chemicals already on the market were grandfathered in, such that no toxicity testing was required of them. These chemicals were, as Landrigan puts it, “simply presumed safe” and allowed to remain in commerce until a substantial health concern came to public attention.


 

In the nearly 40 years since the law’s passage, more than 20,000 new chemicals have entered the market. “Only five have been removed,” Landrigan says. He notes that the CDC has picked up measurable levels of hundreds of these chemicals in the blood and urine of “virtually all Americans.” Yet, unlike food and drugs, they enter commerce largely untested.

Landrigan and Grandjean’s purpose in declaring a silent pandemic was less about the 12 named substances and more about using them as cautionary tales. They named in their list a few chemicals that still appear be imminent threats, but they also include some that have been highly restricted in their use for a long time. And at least one of them, fluoride, has proven beneficial in small doses.

“Fluoride is very much a two-edged sword,” Landrigan said. “There’s no question that, at low doses, it’s beneficial.” Flouride has been shown to prevent dental cavities and aid skeletal growth. At higher levels, though, it causes tooth and bone lesions. The epidemiologic studies cited by Grandjean and Landrigan, which came from China, imply that high fluoride exposure has negative effects on brain growth.

“Are the exposure levels in China comparable to what we have in our drinking water and toothpaste?” I asked.

“No, they’re probably higher,” Landrigan said. “In some places in China, there are naturally high levels of fluoride in the groundwater, which picks it up because it’s water-soluble.”

“So your advice isn’t to take it out of our toothpaste?”

“Not at all,” Landrigan said. “I think it’s very good to have in toothpaste.”

He’s more concerned about flame-retardants—a group of compounds known as polybrominated diphenyl ethers (PBDEs). These chemicals came into vogue after their predecessors, called PCBs (polychlorinated biphenyl ethers), were banned in 1979. By the time it became clear that PCBs caused cancer—and a variety of other adverse health effects on the immune, reproductive, nervous, and endocrine systems—they’d been put into hundreds of industrial and commercial uses like plastics and rubber products. So manufacturers switched to PBDEs and advertised PCB-free products, assuming—or, at least, implying—that PBDEs wouldn’t cause problems of their own.

“California, at the urging of the chemical industry several years ago, put the highest standard in the world on the levels of PBDEs that needed to be included in them,” Landrigan explained. “The result is that people in California have the highest levels of brominated flame retardants in their bodies.”

The state finally banned PDBEs in 2006, after studies from Columbia showed high quantities of the compound in women’s breast milk and linked it to IQ losses and shortening of attention span. Between 2008 and 2012, PDBE levels in the blood of California residents decreased by two-thirds.

Landrigan and Grandjean argue that stronger chemical safety legislation could have made all of this backpedaling damage control unnecessary. They don’t expect every chemical to go through long-term, randomized control studies prior to its release. Rather, they want to see industrial chemicals screened through a simple cell-based test. If that test were to come out positive—if the cells in the petri dish showed any kind of toxic reaction—then the chemical would be tested further.

A next step from there might be an animal testing model. The drawbacks there, Grandjean told me, are that “those programs are expensive, they take time, you have to kill hundreds and thousands of mice and rats.” However, he adds, “if a company has developed a very useful substance, and it turns out to be toxic to nerve cells in petri dishes, then maybe animal testing is the next step.”

“I don’t think that that should necessarily be a requirement,” Grandjean said. “But I can see if a company has developed a very useful substance, and it turns out to be toxic to nerve cells in petri dishes, then maybe that is the next step.”

Landrigan and Grandjean both mentioned something they called Tox21, the Toxicology in the Twenty-First Century program program, which is laying groundwork for a new kind of accelerated, large-scale testing. “TSCA reform really falls under EPA’s jurisdiction,” Landrigan said. “At the NIH and National Institute of Environmental Health Sciences, though, that’s where the latest research on this is.”


 

When I heard that this Tox21 program is teaching a very large yellow robot to do large-scale rapid chemical testing, I had to learn more. Dr. Linda Birnbaum is the director of the National Institute of Environmental Health Sciences and the National Toxicology Program in North Carolina’s Research Triangle. Birnbaum oversees federal funding for research to discover how the environment influences health and disease, including Tox21.

“If you want to do the full battery of current tests that we have on a chemical, you’re looking at least five years and about $5 million,” Birnbaum told me. “We’re not going to be able to do that on large numbers of chemicals.” The robot is being trained to scan thousands of chemicals at a time and recognize threats inexpensively and quickly—before people get sick. It’s also using alternative testing models—looking at not just isolated cells, but also simple organisms like the roundworm C. elegans or zebrafish—to answer certain basic questions.

The program is also looking at how a single chemical might affect a wide range of people. “We’re looking at 1,000 different human genomes from nine different ethnic groups on five continents,” Birnbaum told me.

Like Landrigan, Birnbaum raised the specter of the tens of thousands of chemicals grandfathered in 1976 that underwent no testing, as well as the commonly cited data that less than 20 percent of the 80,000 chemicals in commerce have had any testing at all. She spoke wistfully of the European Union’s chemical testing protocol, a model Grandjean had told me was “very reasonable.” It’s called REACH (Registration, Evaluation, Authorization, and Restriction of Chemicals), and it involves a tiered approach to regulation: If a compound is produced in small amounts, only some cursory information is required. If greater amounts are produced or imported, the EU requires more in-depth testing, such as animal experiments and two-generation studies.

“We’ve learned a heck of a lot in the last 30 to 40 years about the safety of chemicals and what can cause problems,” Birnbaum said, “and it would be really nice if our regulations required us to use some of the newer science to answer the questions of safety.”


Don’t Panic? 


“When you use the word pandemic, that’s a scare word,” said Laura Plunkett. “And that’s my problem. There’s a more responsible way to express it. I understand that they want to bring it to attention, but when you bring it to attention, you can still do it in what I would say is a scientifically defensible manner.”

Plunkett has a Ph.D. in pharmacology and toxicology. Reviewing articles written in the wake of the publicity around The Lancet Neurology paper, I was struck by the definitive title of her blog post on a site called Science 2.0: “There Is No Pandemic of Chemicals Causing Brain Disorders in Children.” Plunkett has been a diplomat for the American Board of Toxicology since 1984. She taught for a while and did research at NIH, but she is now an independent consultant running her own company, Integrative Biostrategies.



One of her clients is the American Chemistry Council. She also has clients in the food, pesticide, and chemical business—“industry ties,” as they say. With that in mind, I sought her out as an established scientist who has worked on the side of the chemical-producing companies. Her blog post about the Lancet article was the only response I found telling people not to panic.

“What [Landrigan and Grandjean] are doing with the data is missing the key component, which is the dose,” Plunkett explained. “Many of the chemicals they talk about are well established to be neurodevelopmental toxicants in children—but it’s all about how much they’re exposed to. Just like anything else. If you don’t give people enough, or if you don’t take enough in your water or food or the air you breathe, you’re not going to have an effect.”

Plunkett insists that, unlike lead, some of the chemicals on the Lancet Neurology list are only developmental toxicants at very high levels—the sort, she says, “that nobody would be exposed to on a daily basis.”

Plunkett says she has no problem with a call to ensure that chemical testing is as thorough as possible. “But then to say, and by the way, if you look at the data, ‘We’ve been poisoning people for the last 10 years’? That’s a whole other step that isn’t supported by the data they point to.”

I asked her how concerned American parents should be about certain individual chemicals on Grandjean and Landrigan’s list. “I mean, we knew lead was a problem 30 years ago,” she said, “and that’s why we removed it from gasoline, and that’s why we don’t let it in solder and cans, and we’ve taken lead-based paint off the market.”

“If you really look at the data on fluoride,” she continued, “trying to link an IQ deficit in a population with that chemical is almost impossible to do. Even though statistically, randomly they may have found a relationship, that doesn’t prove anything—it identifies a hazard but doesn’t prove there’s a cause and effect between the two things.”



What about the chemical that most concerned Landrigan, the pesticide chlorpyrifos?

“No, because the organophosphate pesticides are one of the most highly regulated groups of chemicals that are out there. The EPA regulates those such that if they’re used in agriculture, people are exposed to very, very low levels.”

Pesticides are indeed more regulated than other industrial chemicals. Before manufacturers can sell pesticides in the U.S., the EPA must ensure that they meet federal standards to protect human health and the environment. Only then will the EPA grant a "registration" or license that permits a pesticide's distribution, sale, and use. The EPA also sets maximum levels for the residue that remains in or on foods once they’re sold.

An EPA spokesperson told me that a company introducing a new pesticide must “demonstrate more than 100 different scientific studies and tests from applicants.” The EPA also said that since 1996’s Food Quality Protection Act, it has added “an additional safety factor to account for developmental risks and incomplete data when considering a pesticide’s effect on infants and children, and any special sensitivity and exposure to pesticide chemicals that infants and children may have.” Landrigan and Grandjean don’t believe that’s always sufficient; the dose may make the poison, but not everyone believes the EPA’s limits are right for everyone.

When I asked Plunkett whether new industrial chemicals were being screened rigorously enough, even she cited the need to strengthen the Toxic Substances Control Act of 1976. “I’m a very strong proponent of fixing the holes we have,” she said, “and we do have some holes under the old system, under TSCA, and those are what the new improvements are going to take care of. They’re going to allow us to look at the chemicals out there we don’t have a lot of data on—and really those are the ones I’m more concerned about.”


The High Price of Lost IQ 


Everyone I spoke to for this story agreed that TSCA needs to be fixed. But every attempt has met with bitter opposition. All parties want it to happen; they just want it to happen on their own terms. Unless it does, they don’t want it to happen at all.

Last May, a bipartisan group of 22 senators, led by Frank Lautenberg and David Vitter, introducing the Chemical Safety Improvement Act of 2013. Lautenberg, then 89 years old, was the last surviving World War II veteran in the Senate and a longtime champion of environmental safety. (Among other things, he wrote the bill that banned smoking on commercial airlines.) A month after he introduced his TSCA reform bill, Lautenberg died of pneumonia.

After Lautenberg’s death, Senator Barbara Boxer told reporters the bill “would not have a chance” of passing without major changes. “I will be honest with you,” said Boxer, who chairs the Committee on Environment and Public Works, “this is the most opposition I’ve ever seen to any bill introduced in this committee.” Some of the resistance came from environmental and health advocates who felt the bill would actually make it harder for states to regulate the chemicals that were grandfathered in by TSCA. Their fears intensified in January, after 10,000 gallons of a coal-processing substance poured into West Virginia’s Elk River, contaminating a nearby water treatment plant. (The Wall Street Journal reported, “Little is known about the chemical's long-term health effects on people, although it isn't believed to be highly toxic.”)


 

In February, with Lautenberg’s bill stalled in the Senate committee, Republican Representative John Shimkus seized the opportunity to introduce another reform option called the Chemicals in Commerce Act. The chemical industry applauded Shimkus’ bill—it won support from the American Chemistry Council, American Cleaning Institute, and the Society of Chemical Manufacturers and Affiliates. Earlier this month at the GlobalChem conference in Baltimore, Dow Chemical’s Director of Products Sustainability and Compliance Connie Deford said that TCSA reform was in the interests of the chemical sector, acknowledging that consumer confidence in the industry is at an all-time low.


The EPA Responds 


The agency says it has taken the following actions to reduce exposure to the chemicals mentioned in Grandjean and Landrigan's report:
  • Chlorpyrifos: Banned all uses in and around homes
  • Polybrominated diphenyl ethers: Reviewing all new uses, following a voluntary phase out by U.S. manufacturers
  • Lead: Numerous federal regulations over the past few decades, leading to dramatically reduced childhood blood lead levels
  • Methylmercury: Significant efforts to reduce exposure, including 2011 standards that reduce pollution from coal and oil-fired power plants
  • Polychlorinated biphenyls: TSCA banned the manufacture and import of PCBs, and EPA is reassessing the largest remaining uses
  • Arsenic: Banned some types of arsenic, restricted others
  • Fluoride: Established safe drinking water standards and currently considering other revisions
  • Toluene: Included in the 2012 Work Plan, with assessment to begin by 2017
  • Manganese: Included in the 2012 Work Plan, with assessment to begin by 2017
  • Tetrachloroethylene: Included in the 2012 Work Plan, with assessment to begin by 2017 
Yet the Chemicals in Commerce Act has provoked strong criticism from groups like the Center for Environmental Health and the Natural Resources Defense Council. A senior scientist with the Environmental Defense Fund called the bill “even more onerous and paralyzing” than the present law, and Representative Henry Waxman, ranking member of the House Energy and Commerce Committee, said the bill “would weaken current law and endanger public health.”

I asked the EPA to comment on Landrigan and Grandjean’s claim that we are in the midst of a “silent pandemic” and inquired what, if anything, is being done about it. The agency responded by sending me a statement: “EPA has taken action on a number of the chemicals highlighted in this report which have and are resulting in reduced exposures, better understanding, and more informed decisions.” The agency included a list of the actions it has already taken to reduce exposure to the chemicals identified in the report. (See sidebar.) And it emphasized a 2012 “Work Plan,” which includes plans to assess more than 80 industrial chemicals in the coming years.

When I emailed the statement to Landrigan, he replied, “Many of the items that they list here are things that I helped to put in place.” (In 1997, he spent a sabbatical year setting up EPA’s Office of Children’s Health Protection.) He agreed that the EPA is doing a lot to protect children from environmental threats. “But the problem is that the good people within EPA are absolutely hamstrung by the lack of strong legislation,” he wrote. “They can set up research centers to study chemicals and outreach and education programs, but without strong and enforceable chemical safety legislation, they cannot require industry to test new chemicals before they come to market, and they cannot do recalls of bad chemicals that are already on the market.”

Meanwhile, researchers like David Bellinger, who calculated IQ losses, are highlighting the financial cost to society of widespread cognitive decline. Economist Elise Gould has calculated that a loss of one IQ point corresponds to a loss of $17,815 in lifetime earnings. Based on that figure, she estimates that for the population that was six years old or younger in 2006, lead exposure will result in a total income loss of between $165 and $233 billion. The combined current levels of pesticides, mercury, and lead cause IQ losses amounting to around $120 billion annually—or about three percent of the annual budget of the U.S. government.

Low-income families are hit the hardest. No parent can avoid these toxins—they’re in our couches and in our air. They can’t be sweated out through hot yoga classes or cleansed with a juice fast. But to whatever extent these things can be avoided without better regulations, it costs money. Low-income parents might not have access to organic produce or be able to guarantee their children a low-lead household. When it comes to brain development, this puts low-income kids at even greater disadvantages—in their education, in their earnings, in their lifelong health and well-being.

Grandjean compares the problem to climate change. “We don’t have the luxury to sit back and wait until science figures out what’s really going on, what the mechanisms are, what the doses are, and that sort of thing. We’ve seen with lead and mercury and other poisons that it takes decades. And during that time we are essentially exposing the next generation to exactly the kind of chemicals that we want to protect them from.”


James Hamblin, MD, is a senior editor at The Atlantic.