by Rob Dunn
Part II
Why We Sometimes Need Worms and Whether or Not You Should Rewild Your Gut
2
When Good Bodies Go Bad (and Why)
We expect few things more eagerly than progress, progress since Ardi, but also since yesterday. Among the simplest measures of our progress is the quality and length of our lives. It was not long ago that we were covered in hair and could expect to live fewer than forty short years between birth and predation. By the turn of this last century, life expectancies in developed countries had inched past eighty years. For most (though not all, a point to which we will return) of human history we have lived longer than the generation that preceded us. In 1850, life expectancy in the United States was forty years, in 1900 forty-eight years, in 1930 sixty years, and so on, and it was easy to imagine it would go on like this forever, with each generation living longer than the one preceding it.1 That is, it was easy to imagine until recently, when projections of life expectancies in many of the “civilized” parts of the world began to plateau or even, in some places, decline in longevity and also, some might argue, quality.2 In the wealthiest countries our older, healthier, happier future is coming into question. Our children may expect to live more afflicted and perhaps even shorter lives than we do. That much is clear. Less clear is why. Here then is a murder mystery in which we are nearly all the victims.
We should be living longer, healthier lives. We have figured out ways to kill more and more of the species that once tried to live at our expense. If some creature clambers into your orifices or through your skin, there is a pill for it, a spray, or maybe a salve. Got germs? Use an antibacterial wipe. Got tapeworms? Take a pill. Most of our long-standing ills can be remedied, at least with enough money. But just as we seem to be getting better at ridding ourselves of the old threats, a set of “new” diseases—including Crohn’s, inflammatory bowel disease, rheumatoid arthritis, lupus, diabetes, multiple sclerosis, schizophrenia, and autism, among others—has become more and more common, and these diseases appear to be, at least in part, what is plaguing us. These diseases, contrary to our standard ideas about progress, have become most common precisely in those countries where we spend the most on health care and public health. Whether American, Belgian, Japanese, or Chilean, we in the “modern world” are getting sick in new ways.
One can imagine many reasons for why people in developed countries might suffer from problems that those in developing countries do not. Nearly everything that differs between developed and developing countries might be the culprit. The difference could be pollution, pesticides, or “in the water.” It could be diet or our social interactions. Beginning between 1900 and 1950 and continuing on until the present day, a variety of these new diseases, many of them autoimmune and allergic in nature, have become more and more common. During this same time, nearly everything about our lives changed. We began to travel more. We vacuumed instead of swept. We started living in suburbs. Toothpaste with fluoride came into common usage, as eventually did pogo sticks, nose-hair clippers, double lattes, electronic dogs, childproof caps, and, of course, those damn Buns of Steel videos. Any of these could contribute to the problem, and the truth is, it may be more than one problem, each with its own cause.
Perhaps it is useful to start with a more specific mystery. Among the most vexing of the new diseases is Crohn’s disease. You probably know someone with Crohn’s disease. It is characterized by a suite of problems associated with attacks by the immune system on the gut, an internal turf war in which the immune system always wins. These attacks cause abdominal pain, skin rashes, arthritis, and even, in some cases, odd symptoms including inflammation of the eye. In the disease’s most severe forms, Crohn’s sufferers face years of vomiting, weight loss, debilitating cramps, and intestinal blockages. In these cases, sufferers often quit work to sit at home and force themselves to eat. Existing treatments are only sometimes effective. When individuals are badly afflicted, lengths of the intestine and colon are surgically removed, which, while it can be necessary in the short term, makes things progressively worse in the long term. Crohn’s is rotten and debilitating and, except in rare cases, never goes away. It is also, rather suddenly, common.
In the 1930s, Crohn’s was so rare that it was mostly undetected. Then, between 1950 and the mid-1980s, its incidence began to rise. In Olmstead County, Minnesota, the number of cases of Crohn’s was ten times higher in 1980 than in 1940. The incidence of the disease has also risen precipitously in Nottingham, England, and Copenhagen, Denmark, and nearly all of the other places in the developed world for which the data are good. Today, roughly 600,000 people have Crohn’s disease in the United States—accounting for some unnoted cases, about one in every 500 people. Similar proportions of people in much of Europe, Australia, and the more developed countries in Asia are also affected. From the perspective of the number of cases, Crohn’s is a global epidemic, or at least an epidemic of developed countries.
Other than its consequences—the fates of the afflicted—just two things about the disease were, until very recently, certain: it has a genetic component (though weakly and inconsistently so) and is more common in smokers. But neither of these factors causes Crohn’s disease. The average Kenyan can smoke all she wants and even if her brother in the United States has Crohn’s, she still stands almost no chance of “catching” it. The gene variant that seems to predispose some individuals to Crohn’s, CARD15, is not a requirement, nor is smoking, which seems to make the disease worse rather than actually triggering its onset. Somehow, economic development and what we tend to think of as modernity—affluence, urbanization, wealth—are prerequisites. It is as though progress itself makes us sick. For many years, inhabitants of India and China were unaffected, but now as India and China have become more successful, or at least some Indians and Chinese have become more successful, Crohn’s disease has shown up there as well.
It may seem unusual that such a common disease is still poorly understood. The truth is that the causes of most diseases that afflict humans are not yet understood. More than 400 diseases that commonly affect humans have been named, and the unnamed diseases undoubtedly number in the hundreds. Perhaps a dozen of the named diseases—polio, smallpox, and malaria among them—are relatively well understood, but the vast majority, those other hundreds, are not. Though we may know how to treat the symptoms or kill the offending pathogen (if there is one) of the less well-understood diseases, precisely what happens in diseased bodies is, more often than not, a kind of corporeal mystery. What these poorly understood diseases almost inevitably have in common, though, is a few scientists dedicated to them, scientists who wake up thinking they finally understand what in the body is going on. In the case of Crohn’s, one of those researchers is Jean-Pierre Hugot.
Hugot, a researcher at the Hôpital Robert Debré in Paris, thinks that the bacteria that live in refrigerators are to blame. Some evidence supports his theory and no evidence really contradicts it, but all he has to date is evidence that refrigerator bacteria are frequently found at the crime scene, a necessary but insufficient piece of evidence.3 A recent study found that having a refrigerator in the home is indeed correlated with one’s chance of developing Crohn’s. But the study also found that having a TV, car, or washing machine was correlated with the probability of developing Crohn’s. Another study found that Crohn’s disease is less common where tuberculosis is more common. It is also more common where it is colder and where days are shorter. But a correlation between two things is no guarantee that one causes the other. There needs to be some kind of causal link and a demonstration of that link; one needs to show that A leads to B. Hugot had the A and the B, but not the “leads to.” And so, although the refrigerator bacteria are found with Crohn’s, they could just as easily be bystanders as villains. If it is not refrigeration, what is it?
Some biologists suggested pollution, others toothpaste or sulfur intake. Perhaps the measles vaccine? Or maybe Crohn’s is psychosomatic. Maybe people in developed coun
tries have idle minds prone to hypochondria.4 The pattern in the distribution of where Crohn’s does and does not occur seemed, like similar patterns for type 2 diabetes or schizophrenia, to invite wild ideas.
Whether or not one believes Hugot’s speculation, one thing he said was right. Some species were favored and others disfavored by modernity. Hugot had focused on the species that were favored. But is it possible that Crohn’s and other diseases of modernity have more to do with which species were disfavored? This was what Joel Weinstock, a medical researcher now at Tufts University and formerly at the University of Iowa, began to wonder. It was 1995 and he was on a flight to his home in Iowa from a meeting at the headquarters of the Crohn’s and Colitis Foundation of America in New York.5 He had just completed editing a book on parasites of the liver and intestines and was writing a review article on inflammatory bowel disease—a kind of medical catchall of diseases that includes Crohn’s and other diseases that result from the immune system’s attacks on the gut. Reading these two sources together made him conscious of the ways that parasites can harm their hosts, but also the ways in which they can help them, if only to ensure their own survival. In this light, it occurred to him that there was one thing that the family in Mumbai and the family in Manhattan shared besides refrigerators, TVs, and idle time. They were both missing something, namely experience with those species we had shed in our trip to the modern world, in particular our intestinal parasites—our worms. The germ theory of disease is based on the idea that we get sick when new species invade our bodies. Weinstock was thinking the opposite. Maybe some diseases are caused by taking species away.
It does not take much affluence to be wealthy enough to avoid intestinal worms. All you really have to do is wear shoes and use an indoor toilet. In the 1930s and 1940s, nearly half of American children had worms, whether big, twisty worms like Ascaris, tapeworms, or more delicate beasts like the small whipworm (Trichuris trichuria). Now worms are all but a thing of the past in the United States. Nor is the United States unusual. The places where Crohn’s was becoming common seemed to Weinstock like the places where intestinal worms were known to have become rare. What if the absence of intestinal parasites was causing Crohn’s disease? At that moment, Weinstock’s idea was like so many other theories (albeit a little more unruly) in that it was simply correlative. Granted, it might be true that there were fewer parasites where Crohn’s was more common, but as we’ve already seen, there were also more TVs and refrigerators. Yet Weinstock, thousands of feet in the air, felt confident, at least initially, that his speculation was right.
Wild speculation can be important to science, particularly in the early stages of a new field, when nearly anything is possible. In the early days, it seems as though anyone can solve the problem, so everyone tries. This stage of science can go on for decades, if not longer. It is from the initial blossoming of wild ideas that the truth is to be winnowed. But even if one accepts the fact that wild ideas are useful, some stretch the limits of well-behaved science. For, as strange as the refrigerator hypothesis seems, it was traditional medicine. In essence, the refrigerator hypothesis was based on the idea that some new species was infecting us and doing us harm. Hugot thought it was the cold-tolerant bacteria causing the disease. Other researchers have suggested that any of twenty other bacteria might be to blame.
What had occurred to Weinstock was something entirely different. His idea began with the observation that as we moved to cities and modernity, our bodies had lost rather than gained something. He thought it was the absence of parasites rather than the presence of a particular assailant that was hurting us. Our bodies, he imagined, missed their worms so badly that they were destroying themselves, eating their guts out in longing. As he sat cramped in his airplane seat, everything about Crohn’s seemed clearer. Blue-collar workers were less likely to get Crohn’s than people who sat all day at desks. They were also more likely to work in the dirt and to get parasitic worms! Suddenly this and a dozen other observations made sense. Weinstock had barely left the East Coast, but intellectually he felt as though he had just traveled a thousand miles. Everyone around him grumbled about their seats, the smell on the plane, and the surliness of the flight attendants. Oblivious to all of this, Weinstock was content.
There was precedent for the idea that one species, such as a human, might miss another species, even one such as an intestinal worm that had done it harm. The precedent involved pronghorn. The story of the pronghorn is relevant to Crohn’s, and may be an answer where Crohn’s and many of our modern chronic diseases are the question.
Pronghorn (Antilocapra americana) are small, goat-sized animals. Though they are sometimes called antelope, they are not precisely antelope and not precisely deer either. They are unique. Their branch on the tree of life has been separate from other branches for much longer than humans have been separate from other primates. Once there were many kinds of pronghorn but now there is just a single lithe species. The pronghorn’s body is tan on the back and white on the belly. It has a dark black nose and dark black two-pronged antlers. Compared to elk, to moose, or even to true antelopes, pronghorn are dervishes—light and muscular. A pronghorn can run a hundred kilometers an hour. One scientist chasing pronghorn in the short grass of Colorado watched a few individuals run three kilometers and then put on a burst of speed. With that burst, they outran him, even though he was pursuing from a plane traveling 72 km per hour.6 Even after running fast and long, they can run faster and longer, not faster than a speeding bullet, but faster, yes, than a pursuing plane.
Once, tens of millions of pronghorn thrived from Canada to Mexico. Then came the guns and greed of westward expansion. Pronghorn, like bison, were killed for food and sport until there were just a few million and then a few hundred thousand and then, finally, just thousands, a rare mother left here and there in the grass. Eventually, slowly, those thousands begat more thousands until, helped by land conservation, the pronghorn began to rebound. Today, 10 to 12 million pronghorn are alive at any one moment, scattered among the grasslands that remain. There, they bow to the ground to feed and then, at the slightest provocation, they run.
Counting pronghorn is difficult, like counting crows or clouds. They are suddenly everywhere and then, just as suddenly, nowhere. In most of the places they live, they remain unstudied, nameless, and totally wild. But there exists a grassland in the National Bison Range of Montana where the pronghorn are well-known. There the grass grows until it is about halfway up their backs and then stops. It bends in the wind to reveal them, in groups, looking back with their big brown eyes. The National Bison Range is still wild enough that things can live, mate, and die without ever being noticed, but it is defined enough, a world unto itself, that a man and a woman might hope to watch a few animals live out their lives and in doing so learn broader truths. So it was that in 1981, the zoologist John Byers took it upon himself to be such a man, and his wife, Karen, would be such a woman. John and Karen moved from Chicago to Moscow, Idaho, where he would begin as a new professor. From Moscow, when summer came, they would migrate to the Bison Range in an RV named Bucky. Rough but well loved, Bucky would launch them into the next phase of their lives.7
As John and Karen made their way toward the grasslands, the landscape opened up. It looked like any grassland, as open and tanned as the savannas of Africa. Driving into it had the feeling of coming home, to a place where things are right and meaningful. They drove into the green-gray fescue, sage, and wheatgrass, and the forest disappeared behind them, and along with it, their daily existence. The space was wide open and yet complex. John would later write of it as the “floor of the sky.”8 It would hold them up for the summer or maybe even their lives.
When the Byerses arrived, they found the pronghorn. They watched them run until, at each fuzzy margin of visibility, they disappeared. The Byerses’ first task was to catch these animals. Each captured individual would be tagged and then studied for as long as it or the couple might persist, years to be certain, maybe
longer. But the catching was not easy. The adults were too fast and the fawns were, at least at first, difficult to find. But John and Karen persevered. Eventually, they found a mother with her two fawns hidden among the bladelike leaves of grass. As John approached, the mother fled, but the fawns froze. John reached down and picked them up in his big hands. They would be measured, weighed, and then tagged. They were, in their smallness, like birds, as at home in the air as on the ground. John and Karen hoped to follow these two and the others they would soon catch. Each fawn’s heart pounded against the cage of its ribs until, into the air, it was freed.
John and Karen Byers settled into the grasslands with the idea of planting observations about the movements of pronghorn, their diet, mating, and everything else. Like any scientists, they hoped to watch one thing in order to understand others. They wanted to look to the pronghorn for broader truths. The pronghorn leaped and ran, and John and Karen saw in their running every living thing that runs. John and Karen lifted up the bodies of animals that they had caught and felt an example of any animal body.
Yet for as much as John and Karen thought they might find universal stories among the pronghorn, they kept finding ways in which the pronghorn seemed exceptional rather than general. One exception in particular had already plagued other scientists who had studied the pronghorn, or even just seen them—their speed. Audubon noted it, but so did everyone else who watched them for more than a few minutes. The pronghorn are faster at medium distances than cheetahs. They are twice as fast as wolves and faster than a safely driven camper van. It turns out they are even faster than an unsafely driven camper van. At medium distances, they may well be the fastest animal ever to have lived. That speed comes not from any particular biochemical magic, but instead from long thin legs, tiny near-featureless feet, an abundance of fast-twitch muscles, and hard-charging lungs. The pronghorn invest in speed at the expense of making bigger bodies or producing more young. They seem overbuilt, as though they evolved speed simply because it was possible. One scientific publication after another remarked on the pronghorn’s speed.9 Each one concluded it was anomalous, interesting, and just a little bit strange. Nor do the pronghorn simply run alone. They run and flee in tight groups more like schools of fish or flocks of birds than like anything on land, groups that move synchronously, their many legs in step, at high speed. The big question, aside from how, was why?