Denialism (20 page)
Discrimination? The budget for NCCAM was $121 million in 2008, and it has disbursed more than $1 billion since Harkin first forced the Office of Alternative Medicine on the NIH leadership. By comparison, the NIH funding for autism research in 2008 totaled $118 million. Moreover, if a study is good enough to be funded, surely it can be funded by one of the other twenty-six institutes at the NIH. Physicians and other contributors to the relentless and insightful blog Science-Based Medicine have made this case many times. They have also examined in excruciating detail how NCCAM money is actually spent.
“Perusing the list of projects is truly depressing,” wrote David Gorski of the Wayne State University School of Medicine. “True, a lot of the projects seem to be yet another study of Ginkgo Bi loba, cranberry juice, or soy in various diseases. That’s all well and good, but why is the study of natural products considered ‘alterna tive’ or ‘complementary’? It’s the same sort of stuff that pharma cologists have been doing for decades when they study most botanical products.”
Gorski describes some of the weaker grants, including one funding a study called Polysomnography in Homeopathic Remedy Effects. “Yes, you have it right. Your tax dollars are going to fund at least a study this year on homeopathic remedies (a.k.a. water). But it’s even worse than that. [One grant was] actually awarded to study homeopathic dilution and succussion”—the act of shaking liquid each time it is diluted—“and how they affect the dose-response curve of homeopathic remedies. I kid you not. I just about spit out my tea onto my laptop keyboard when I read it. Naturally, it’s at the Integrative Medicine Program at the University of Arizona” (which is run by Andrew Weil).
A FEW YEARS AGO I wrote an article for the
New Yorker
about a man named Nicholas Gonzalez. He was a highly credentialed physician, trained at Cornell University Medical School and at Memorial Sloan-Kettering Cancer Institute. Gonzalez worked out of an office in midtown Manhattan, where he was treating pancreatic cancer patients using some of the most amazingly bizarre methods in modern medical history. He prescribed twice-daily coffee enemas, for example, and a pill regime for most of his patients that ran to four single-spaced pages. (It included, in part, sixty freeze-dried porcine-pancreatic enzymes, capsules of adrenal medulla, amino acids, bone marrow, selenium 50, thyroid, vitamin A 10,000, and vitamin E succinate. And many, many more.)
The prognosis for pancreatic cancer patients, then and now, is particularly bleak, and it seemed to me at least that if one were going to roll the dice, it might make more sense with that particular disease than with another. Gonzalez was reviled by members of his profession. But unlike virtually any other alternative healer, he always insisted that he wanted his method to be tested in the most rigorous possible way by the NIH, and in 2000 he received a $1.4 million grant to do just that.
Most people in the medical world thought the trial was a waste of time and money. I didn’t agree at the time, but I do now. Studies like that just make the ridiculous seem worth investigating. Wallace Sampson was right—we cannot afford to fund research that has no reasonable chance of success. It wastes money and steals time that could be devoted to more promising work. More than that, though, it makes the denial of reality acceptable. If you believe that coffee enemas and energy fields offer hope, you can believe anything. We have seen where that can lead.
Since the beginning of the AIDS epidemic, a small band of committed activists led by Peter Duesberg, a microbiologist at the University of California at Berkeley, have denied that the epidemic is caused by the human immunodeficiency virus. Thousands of molecular studies (and millions of deaths) have made it clear that there is no possibility they are right, but with the help of the Internet, the impact of that denialism has been felt throughout the world. People want to be told that everything is going to be all right. That’s normal. (“What mattered to me as a person living with HIV was to be told that HIV did not cause AIDS. That was nice,” Winstone Zulu, a Zambian AIDS activist and former denialist, has written. “Of course, it was like printing money when the economy is not doing well. Or pissing in your pants when the weather is too cold. Comforting for a while but disastrous in the long run.”)
AIDS denialism doesn’t die, even in America. In the United States the group the Foo Fighters recorded the soundtrack for a documentary called
The Other Side of AIDS,
which was directed by the husband of Christine Maggiore, one of America’s more prominent AIDS denialists (who, in 2008, died of AIDS). And in 2009,
House of Numbers
, a film made by another AIDS denialist, Brent W. Leung, provoked new outrage (and letters from nearly every prominent scientist featured in the film saying they were misled and quoted out of context).
It is of course in South Africa that the denial of fact-based medicine has had its most deadly effect. South Africa has the world’s largest population of people infected with HIV. Instead of treating those people with the antiretroviral drugs necessary to save their lives, former president Thabo Mbeki denied for years that the virus caused the disease. Like the Zambian leaders who refused to accept genetically engineered food to feed their starving people, and the northern Nigerian mullahs who campaigned against polio vaccinations, Mbeki suspected a Western plot. In this case, he believed that Western pharmaceutical companies had banded together to threaten the future of Africans; and he was convinced that a natural, local solution would be far more effective than the “poison” offered by such organizations as the World Heath Organization and UNAIDS.
Instead, he and his longtime health minister Manto Tshabalala-Msimang recommended herbs, garlic, and lemon. I have seen the effect of those herbs, and of the vitamin regimens peddled by people like the German health entrepreneur Matthias Rath with the tacit support of Mbeki and Tshabalala-Msimang. Rath urged people to substitute remarkably high doses of multivitamins for proven AIDS therapies like AZT. People who did that, rather than relying on the antiviral medicines they needed, died. In 2008, a group of researchers from the Harvard School of Public Health concluded that the South African government would have prevented the premature deaths of as many as 365,000 people between 2000 and 2005 had it provided antiretroviral drugs to AIDS patients. The study also concluded that the drugs were largely withheld due to “Mbeki’s denial of the well-established scientific consensus about the viral cause of AIDS and the essential role of antiretroviral drugs in treating it.”
Taking megadoses of vitamins or craniofacial massage for the flu may seem comforting. At worst, many have argued, such actions are self-inflicted wounds—like the self-inflicted wound of refusing to vaccinate a child. There comes a point, though, when individual actions become part of something bigger. Progress is never guaranteed. It can vanish if reality ceases to make more sense than magic. Denialism is a virus, and viruses are contagious.
5
Race and the Language of Life
In the spring of 1998, a team of researchers from the Centers for Disease Control traveled to a meeting of the American Thoracic Society in Chicago, where they presented a report on the severity of asthma among Hispanics. Minorities living in America’s largest cities visit the emergency room more often, spend more time in the hospital, and die in far greater numbers from asthma than the rest of the population; they are also far more likely to develop pneumonia and other pulmonary diseases. None of that was news to most of those who attended the meeting, but the CDC study was the first to focus specifically on the prevalence of asthma in Hispanics. During the course of his presentation, the pulmonary specialist David Homa pointed out that he and his colleagues had run across one particularly surprising result in their research: Hispanics living in the Northeast of the United States were three times more likely to develop asthma than Hispanics in the South, Southwest, or West.
Many people in the audience found that odd; differences in the rates of pulmonary disease are often a result of social conditions, the environment, and disparities in the quality of health care. Poor people rarely receive the best possible treatments and consequently they don’t do as well as richer patients—with asthma or with most other illnesses. The study was designed to account for those facts. Even so, a Hispanic man in New York was more likely to get sick than one in Los Angeles or Chicago. Some participants shook their heads in surprise when they saw the data, but Esteban González Burchard was not among them. Burchard, at the time a twenty-eight-year-old internal medicine resident at Boston’s Brigham and Women’s Hospital, had known for years that he wanted to specialize in pulmonary disease, largely because of its punishing effect on minorities. He sat riveted by Homa’s presentation, and particularly by the data that suggested the illness seemed so much worse on the East Coast than in other parts of the United States.
“I jumped when I heard him say that,” Burchard told me when we first met in his office at the University of California at San Francisco, where he is assistant professor in the departments of biopharmaceutical sciences and medicine. “I am Hispanic and I have lived on both coasts and I knew that the obvious difference there had to be between Puerto Ricans”—who reside principally in the East—“and Mexicans”—who are more likely to live in the West. At the time, Burchard was working in the laboratory of Jeffrey Drazen, a professor at the Harvard School of Public Health, who was soon to become editor of the
New England Journal of Medicine.
In his lab, Drazen had identified a genetic risk factor that would explain the differences in asthma severity between African Americans and Caucasians. Both he and Burchard thought the CDC data might help explain genetic differences within the Hispanic community as well.
“I talked to David Homa and suggested that this data could very possibly be the result of genetics,” Burchard said. “I don’t know if he thought I was a little crazy or what.” After all, genetics seemed unlikely to provide an explanation for such a striking disparity among people with a common ethnic heritage. The prevailing view since the early days of the Human Genome Project has been that such differences no longer seem worth thinking about, and many notable researchers have argued that focusing on race in this way is not only scientifically unsound but socially dangerous. Yet something had to account for the wide gap, so Burchard persuaded Homa that the CDC ought to take a closer look at the data. Two years later, the CDC study, now focusing on the differences among Hispanics of Cuban, Puerto Rican, and Mexican descent, was published. It showed that the prevalence, morbidity, and mortality rates of people with asthma varied significantly within those groups and concluded that genetics seemed to be at least partly responsible.
Burchard, like most physicians, believes that social and economic disadvantages explain much about why minorities in the United States suffer disproportionately from so many diseases—eight times the rate of tuberculosis as whites, for example, ten times the rate of kidney failure, and more than twice the rate of prostate cancer. Tuberculosis has served for generations as the signature disease of urban crowding, homelessness, and poverty, and many people who die of AIDS do so because the virus makes them susceptible to infections that cause pneumonia. But Burchard asked himself whether economics and environment alone could explain why one group of Latinos (Puerto Ricans) had among the highest rates of asthma in the United States while another group (Mexicans) had virtually the lowest. That made no sense. “I was convinced then, and am even more convinced now,” he told me, that “there are specific ethnic, genetic, and environmental risk factors in play here.” For the past decade, Burchard has worked with one principal goal in mind: to understand the meaning of such genetic differences between racial groups. It has not been easy, nor has the research always been particularly welcome. Grant money has often been hard to find, and skepticism from colleagues palpable. But Burchard persisted.
In 2001, with the help of senior scientists from medical centers in the United States, Mexico, and Puerto Rico, he embarked on an exhaustive attempt to better understand the clinical, genetic, and environmental differences in severity among Mexican and Puerto Rican asthmatics. The investigative study, called GALA—Genetics of Asthma in Latino Americans—has not only revealed genetic differences within Hispanic populations. Perhaps more importantly, it has demonstrated that despite having more severe asthma, Puerto Ricans respond less well to the standard treatments they are most likely to receive. Albuterol, for example, is the most commonly prescribed asthma medication in the world, and frequently the sole drug people receive (or need) to treat their asthma. Yet for many Hispanics it can prove useless. Nonetheless, albuterol is often the only asthma drug prescribed for Puerto Ricans or Mexicans in the United States.
“The idea has become fashionable that we are all one species and that ethnicity and race do not play defining roles in determining the causes of disease,” Burchard said. “But look at the data. The one-size-fits-all approach to medicine and to drug therapy does not work. We see that over and over again. I can’t think of anything more important in medicine right now than trying to tease out the causes of these differences. But believe me, there are many people who think I am wrong.” He sat back, shook his head, and smiled darkly. “There are serious scientists who say we should not even do this kind of research, that races should be treated as one and that the genetics of humanity are not diverse enough to play this kind of role in diseases. You can’t look at the data and make those assumptions,” Burchard said. “But if reality upsets people, they will simply look in another direction. People deny what makes them uncomfortable, and many—even in my business—say we shouldn’t use the word ‘race’ at all.”
It has never been easy to invoke the subject of race in America. Discrimination has long been as obvious in medicine as in other areas of society. In the era of personalized medicine, where relevant new information seems to appear daily, the issue has become more volatile than ever. At many meetings where race and genetics are discussed, researchers spend as much time debating semantics as they do discussing scientific results. (In 2008, one participant at a National Institutes of Health conference on genomics and race argued that not only is the term “race” unacceptable, but so is the term “Caucasian,” because it implies racial rather than geographic ancestry.)
“How much of a factor does genetics play in these research results?” Burchard continued. “I will tell you honestly, I don’t know—but neither does anyone else. I am Hispanic and I want people to get the treatment that serves them best. I want every tool at my disposal and every tool at the disposal of my patients. Genetics is one of the most powerful weapons we have. Yes, we are strikingly similar in many—even most—ways. But genetics also makes us different. That scares some people, but it is a fact.
“We are finally coming to a period in scientific history where people may be able to benefit from those differences. Where they can actually help treat and cure diseases. You would think that is something that scientists would support. But too often it is not. Let’s face it, in this country there have been major efforts, guided by endless waves of political correctness, to close the door to the possibility that there could be important racial differences among human beings. At first I found it surprising. I don’t anymore. But be honest: who can possibly benefit from this approach to medicine?”
ON JUNE 26, 2000, surely one of the most notable days in the history of science, President Bill Clinton announced the completion of the first draft of the Human Genome Project. He spoke in the East Room of the White House, where Thomas Jefferson and Meriwether Lewis had presented the map of Lewis and Clark’s historic expedition to the public. The symbolism was impossible to ignore, as were the parallels between what Clinton described as Clark’s “courageous expedition across the American frontier” two centuries earlier and the Human Genome Project’s exploration of the contours and complexities of the human cell. Many of the scientists who had struggled to compile that blueprint of human DNA—the string of three billion pairs of chemical “letters” that make up our genetic code—stood by the president’s side. “Without a doubt, this is the most important, most wondrous map ever produced by humankind,” Clinton said. “We are learning the language in which God created life.” British prime minister Tony Blair, joined the conference by satellite, along with researchers who had contributed to the work in England. Science, Clinton said, was on the verge of gaining immense power to heal, power that until recently we could not have imagined. He noted that the information packed into the structure of our genome was so valuable, and the potential benefits of understanding it so great, that it was conceivable that “our children’s children will know the term cancer only as a constellation of stars.”
That’s unlikely, but Clinton’s optimism hardly seemed misplaced, and it seems even less so now. By assembling a complete map of the human genome, and then refining it literally every day, geneticists have already transformed fields as diverse as anthropology, history, molecular biology, and virology.
An entire industry, genomics, has emerged to study the structures and functions of genes and how they interact with each other. The hereditary information contained within our genes, our DNA, is written in a four-letter language that, if printed out, would fill more than a thousand New York City telephone books. (Each letter corresponds to one of four nucleotide bases: A for adenine, T for thymine, C for cytosine, and G for guanine.) These sequences, arranged in millions of threadlike helixes and passed from one generation to the next, carry within them the instructions required to assemble all living things—a set of instructions which genomic scientists are working feverishly to decode.
The resemblance among humans is startling: compare one person with any other, chosen randomly from any two places on earth, and genetically they will be more than 99 percent identical. It doesn’t matter whether one of those people is from Sweden and the other from Zambia, or whether they are twins, or of different genders. Yet, there are still millions of places in our genome where that recipe varies among individuals by just a single genetic letter. Those places are called single-nucleotide polymorphisms, or SNPs (pronounced “snips”). SNPs are useful markers for different versions of genes, and they help emphasize the differences that scientists are trying—with increasing success—to associate with various diseases. Over the past decade, researchers have been able to use these surrogates as molecular guideposts to identify scores of genes that play major roles in diseases ranging from prostate cancer to age-related macular degeneration.
The Human Genome Project launched a modern Klondike, and billions of dollars have been invested in an attempt to understand the exact structure of virtually every gene in the human body and then translate that knowledge into effective drugs. We are in the earliest stages of this vast effort at sifting through the raw data that contains the language of life. Eventually, however, genomics will almost certainly provide the information necessary to help answer many of the most fundamental questions we can ask about ourselves and about biology. To what extent are genes responsible for how we grow, think, evolve, become sick, and die? Are traits that pass through generations in a community genetically determined, or are they the expression of cultures that have been shared for thousands of years? Is it even possible to quantify how much of what we are comes from genes and how much from the circumstances of our lives?
The last question is the most important because when we understand how humans are put together we will have a much better grasp of the genetic basis of major diseases—what causes them and what causes people to vary so dramatically in their ability to respond to particular medicines. As every physician knows, drugs that work well for one person don’t necessarily work for others. Some, like albuterol, are effective on whites but not on many Hispanics. For African Americans, who suffer from congestive heart failure at twice the rate of whites, there is BiDil—a combination of two older drugs, which when taken in concert turn out to work far better for blacks than for whites. (The drug, when used in this fashion, became the first race-based medicine approved by the FDA, specifically to treat blacks. The action caused intense controversy, but it also offered a new form of relief to African Americans with heart failure.)
While vital clues to causes of various afflictions emerge in a torrent, they rarely provide definitive answers. But the initial map did prove conclusively that all humans share a nearly identical genetic heritage. Many researchers have even argued that relying on race as a way to define and connect large groups of seemingly similar people no longer makes sense, except as a way to discriminate against them.