by Rob Dunn
The first question we must ask of the parasite theory is whether losing parasites was so much of a benefit that it was worth years of sunburn on the beach, shivering in the snow, and awkward moments in front of oh so many mirrors. What the parasite theory relies on is not that parasites themselves do us so wrong. The bites of fleas are itchy, but, in and of themselves, otherwise innocuous (in this they are similar to some of our gut parasites) except in those cases where they reach very great densities. They bite us, suck a little blood or eat some dead skin, and then go on their way. Occasionally chimpanzees and gorillas are infected by so many parasites that they develop sores, as presumably were our ancestors. Infections from these sores might lead to mortality, but not very often. It is the diseases that such parasites transmit that kill. Ticks transmit spotted fever, encephalitis, typhus, Kyasanur Forest disease, ehrlichiosis, Lyme disease, and Astrakhan fever, to name a few. Lice transmit relapsing fever and typhus. Fleas transmit the plague. To the extent that our parasites carry such diseases, losing our hair may have increased our chances of living longer, or at least long enough to mate. It is even possible that hair favors the spread of some diseases that do not require vectors. Bacteria can also live in hair (or feathers), which is why, when trying to produce germ-free guinea pigs, James Reyniers, whose story I told in earlier chapters, shaved the mother guinea pigs. It may also be why the birds that feed on dead animals have evolved bald heads three times independently, once in New World vultures, once in Old World vultures (which are actually descendants of storks), and a third time in the ancestors of the bald-headed and ungainly marabou stork.
The question that Charles Darwin posed in this context was why humans abandoned their fur but other mammal species did not. Surely, he thought, if hairiness predisposed us to parasites and their diseases, it would do the same for other mammals. Wouldn’t a naked bear, as funny as it might look, suffer fewer fleas? Yet we see no naked bears, nor for that matter even any bears with sparse hair. The answer to this naked-bear paradox may have to do with two features that distinguished early human societies from, say, a group of bears.
First, even though early humans are typically described as “nomadic,” they lived in relatively sedentary groups for large parts of the year. Within those groups, parasites could build up to great densities. And at the end of the day we had a sleeping spot, a spot to which a group of us would have returned. More often than not, that spot would have been a cave. It is known that by living in caves in those early days, we came into contact with bat bugs, insects that feed on the blood of bats while the bats sleep. One lineage of bat bugs jumped ship onto early humans and became bedbugs. For this to occur, we would have had to be rather predictable cave dwellers, predictable enough that the bedbugs could sleep during the day in our primitive bedding and find us again each night. Being sedentary meant that those parasites that do not pass from one body to the next could still find us. Bedbugs could wait for us in our sleeping spaces without evolving unique tricks for actually hanging onto our bodies. We also know today that animals that live in groups, especially groups that return to the same sleeping sites, such as seabirds in their rookeries, or bats in their caves, have many more parasites than do those animals who go it alone. It was this lifestyle that would lead us to pick up fleas (and the diseases they carry), even though no other primates host fleas. Perhaps the key was our living together and in particular the densities at which we came to do so.
The second thing that is different about humans, aside from our tendencies, at least historically, to live in ways that favored ectoparasites, is that we invented clothing. The invention of clothing and the loss of hair may have been roughly contemporaneous. Once we had the ability to change our temperature (and also our level of protection from the environment more generally), it may be that the benefits of hair disappeared, and so evolution had only the costs to deal with. If a trait has more benefits than costs, it will tend to stick around. If it has only costs, it should disappear. In other words, once we could make our own (washable!) clothing out of the fur of others, whether that was 200,000 years ago or even earlier, the flea-bitten fuzziness of our ancestors was nothing but a drag.
In this context, it would be nice to be able to compare our bodies and our parasites to those of other species of ancestors in those years before they lost their hair. Those ancestors should have had a greater incidence of diseases transmitted by fleas, lice, and other parasites. But we cannot make such a comparison, not yet, anyway. The closest relatives we have today—apes, chimps, and orangutans—are very different from our ancestors. Yet it seems telling that apes tend to have, in addition to the parasites we face, a broader suite of parasites including, for example, fur mites, that we now lack. Whether our immediate ancestors also faced these parasites and their pathogens is unknown, though it seems likely.
If we turn to more recent history, a few anecdotes seem telling. In June of 1812 Napoleon Bonaparte assembled his troops to try to occupy Russia via Poland. Napoleon’s ambition could scarcely have been more grand. Yet sometimes ambition is not enough. As is often noted, more than half a million of Napoleon’s soldiers (nearly five out of every six of his men) would die trying to control Russia. What is less often noted is that most of those troops died not from battle itself but instead from disease. They died of a spotted fever spread by lice or of dysentery. These deaths began long before the French had even seen any Russians. Only 40,000 of Napoleon’s troops survived. He brought a city of soldiers and came home with a small town. The Russians, on the other hand, suffered no such fate. But why? One of the differences might have been hair. The French wore hairpieces and in doing so augmented the habitat available for lice and the diseases they carried. The Russians did not wear hairpieces. Relatively speaking, they were more hairless and as a consequence, saved. Nor was this the only example in which ectoparasites played a significant role. By some estimates, World War II was the first war in which more soldiers died in combat than of ectoparasite-transmitted diseases.
But history is not the only other example of the effects of the relationships between society, hair, parasites, and disease. As with other questions of our history, we might learn the most by looking to other species. This is the comparative approach to ecology and evolution. One can also examine other species that, like us, have made the transition to large, relatively sedentary, societies. We could turn again to the ants, bees, wasps, and termites, but we do not have to go so far afield on the evolutionary tree. Huddled with us on our own mammalian branch are the mole rats. Many kinds of mole rats live in Africa. In general, they are tuber eaters and live either wholly or mostly subterranean lives. Some species have queens and workers, as do ants. Several species have lost their eyesight. Only one species, however, is hairless. That species, like humans, lives in conditions that present a near constant environment. Once it did not have to worry about staying warm, the costs of living in a society with fur may have outweighed the benefits and it, like us, lost its fur. The difference between mole rats and humans is that there are other living mole rats with hair, so we can compare their parasite loads to those of the naked variety. Naked mole rats are not known to have ectoparasites. In contrast, all of the other mole rats so far sampled have tunnels filled with ectoparasites. This may have been what our ancestors looked like—hairy mole rats—each one of them itchy with bites and, from some of those bites, diseased.
Maybe we are naked because of lice, mites, and flies (fleas are unlikely to have played a role in our story, since fleas spread relatively recently from the New World, and plague is a relatively new disease). And maybe, just maybe, that is the same reason naked mole rats are naked too. Like many aspects of our bodies and their origins, no one is totally certain yet. Other explanations are possible. Whatever the answer, we seem more likely to understand it by understanding what happens when other mammals become hairless rather than by looking for more clues in the fossils of our own most recent kin. In the end, all of this discussion of hairlessness would be a b
it silly if hairlessness were not one of our most defining traits. Once we were naked, many other things about our biology also had to change. We evolved special sebaceous glands to deal with the reality that we now had so much exposed skin, skin that needed to somehow be cooled in the hot sun. We began to view nudity with titillation (in certain Papua New Guinean tribes, only a gourd is worn by men, and yet going “gourdless” still causes a stir). The act of revealing our nakedness became the basis of a $100 billion global pornography industry. Our skin turned dark to protect our flesh and then, in some peoples, turned pale again. That paleness is the basis of thousands of deaths a year owing to skin cancer and, at the opposite extreme, the darkness of melanin is at the root of thousands of cases of rickets. Our nakedness frames who we are and how we act toward each other. Our nakedness is central, and to the extent that they may be implicated, then so too are lice, ticks, flies, and the rest. So too are the pathogens that ride in their guts and mouths, pathogens that, although small, may have been powerful enough in their influence to depilate us, one death at a time.
Meanwhile, we spend millions to make sure we maintain a little fur on the tops of our heads, and millions more to remove the fur on our bottoms. We are the naked, but high-maintenance, ape and it may be because of our pathogens and the diseases they cause. Were other hairier hominids still around, they might look at us the way we look at naked mole rats or vultures, as just a little bit disgusting. Our diseases have marked us. Long ago they shaped our immune systems. More recently, they may have made us hairless. And these are just the most obvious of the ways we have evolved to respond to our plagues.
Whatever the early influence of parasites and diseases on our hairiness, it was not the end of the story. With the dawn of agriculture, of cows and corn, things got worse. New diseases also arose and began to accumulate. Human malaria (Plasmodium falciparum) evolved at about the time the first crops were domesticated.3 When it did, it appears to have spread rapidly. Mosquitoes bred in the damp spots in farm fields, and from those temporary refuges, ferried the malaria parasite from one farmer to the next, rain or shine. Once in a human, the malaria parasite takes up residence inside his or her red blood cells. Many of the first humans who contracted malaria, perhaps even most, died. But some survived, and those individuals tended to have genes that made them more resistant to malaria. One of those sets of genes, the one often discussed in introductory biology classes, can confer malaria resistance but also causes sickle cell anemia. When a child receives a copy of this gene from just her mother or just her father, she is immune to malaria and far more likely to live long enough to raise her own children. But when those genes are received from both parents, they produce fatal sickle cell anemia. Malaria is so prevalent in much of the world (particularly in tropical Africa and Asia) that these genes are still favored, despite their consequences. Amazingly, this gene is not the only or even the most common one to have helped to buffer us from the deadly tides of malaria.
The most common gene variant for malaria resistance is not related in any way to sickle cell anemia. Its name is G6PD, and it leads to the production of blood cells that starve the malaria parasite of oxygen. These are tough, protist-choking genes, malaria-killers, evidence of the power of evolution and the adaptability of man. Sarah Tishkoff—the geneticist at the University of Maryland who discovered the repeated origins of the genes for digesting milk as an adult—has recently studied the spread of G6PD. More than 400 million people in Africa, the Middle East, and the Mediterranean have one of several versions of this gene. It appears to have spread quickly, mother and father to child. These gene variants, though, like the ones associated with sickle cell anemia, come with a price. Individuals with the malaria-killing version of the gene develop anemia when they eat fava beans. Where malaria is present, surviving malaria but having to avoid fava beans is no great tragedy. Malaria still kills several million people a year, and it is therefore likely that these genes are still favored in many parts of the world, fava beans or not. But malaria is a tropical disease today, and so as individuals with the malaria-killing gene have spread around the world, their genes have spread beyond malaria and beyond their utility. Consequently, many millions of people remain unable to eat fava beans, even though they are unlikely to contract malaria. Those individuals (and you might be one of them) have genes that are no longer, in their modern context, useful. They also tend to live precisely in those areas where diets rich in fava beans are most common. The religious sometimes wonder if their gods have a sense of humor. Favism seems to be an indication that natural selection does, and it is dark and mean. Whether it is worms, crops, or disease, the more we look, the more who we were and how we lived bumps up against who we are.4
Our hairlessness, sickle cell anemia, and favism may all be the result of the presence of diseases. But what happens when we remove some of the worst infectious diseases from our lives, what effect has that had? We pulled the worms out of our guts and the predators out of our grasses, but what about when we removed our infectious diseases, whether through disease control or simply moving. What then? We would like to think that the answer was simply that we became healthier, longer lived, and otherwise unaltered. Unfortunately, nature is seldom so simple.
14
How the Pathogens That Made Us Naked Also Made Us Xenophobic, Collectivist, and Disgusted
When Randy Thornhill looks down on his hometown of Albuquerque, New Mexico, from the surrounding mountains, he feels as though he has to confront what the rest of us ignore. We tend to feel as though we are in control of each action we take. From Thornhill’s perspective, it is less clear-cut. Our lives are more like boats being steered with loose rudders. They lurch this way or that, drawn into the troughs and swells of ancient urges.
As a scientist, Thornhill studies one organism and sees in its stories generalities that apply to other organisms. Thornhill focused for years on scorpionflies (so named because of the supersized genitals of the males, so large they resemble a scorpion’s sting) and other insects, such as water striders. But even in the beginning stages of this work, he recognized in their primitive decisions the wants and decisions of his fellow humans. He sees our most terrible vulgarities and greatest delights as deriving from our evolution. Reason, to Thornhill, is what keeps us from drowning in our instincts, but we exercise it imperfectly, treading water in a sea of great waves and imponderable depth.
In 1983, Thornhill became well-known for what is now a classic book in entomology, The Evolution of Insect Mating Systems, written with John Alcock. The book was the original treatise on the sex lives of the smaller majority, informed by scientific observations of insects and their many ways of coming together, be it in the sand, midair, on logs, or even underwater.1 It was not until 2000 that Thornhill became infamous. In that year he published a book in which he used models that he and Alcock developed to understand rape in insects (which is common and complicated in species like bedbugs that do terrible things under your sheets) in order to understand rape in humans.2 The book was greeted with intrigue but also outrage. The outrage might have made Thornhill shy away from his work on the hearts and urges of humans. Instead, ever the academic cowboy, he assembled other biologists around him who study humans and human behavior from an evolutionary perspective that spans from insects to humans. From this intellectual posse, many wild ideas and wide-eyed scientists have emerged. Among the most recent of them is Corey Fincher. Fincher did not mean to become the most radical thinker in Thornhill’s posse, but it happened all the same.
Corey Fincher began as a graduate student at the University of New Mexico in 1999. He planned to work on rattlesnake courtship. The sex lives of rattlesnakes are elaborate and intriguing. Fincher wanted to know the details. But things would not work out the way he wanted them to, perhaps because of the inherent difficulties of working with rattlesnakes, but also because Fincher’s mind had begun drifting to other topics. It is easy to get distracted in science, to wander along the millions of roads not yet ta
ken. Fincher was distracted by disease. Disease seemed to be everywhere he looked. He wondered how it was that species escaped disease. The more he read about disease the more it seemed surprising that any animals were ever healthy. But he still had to find something tractable to study for his thesis and so he focused on water striders, following up on work that Thornhill himself had done years before. He did so with enough success to produce a master’s degree. Yet he kept reading about disease. As he did, he realized that most animals, be they rattlesnakes, water striders, or monkeys, have an immune system, just as we do. But they also have what would later be called a behavioral immune system, a suite of responses to the world that make getting diseases less likely in the first place.3 Fincher wondered whether humans had behaviors for avoiding disease, behaviors that were either subconscious or buried so deep in the norms of cultures that they had not yet been recognized as doing anything useful at all. Soon Fincher found himself beginning a PhD. This time he would go boldly. Abandoning snakes and water striders, he wanted to understand the big story of disease, history, behavior, culture, and humans. Thornhill had looked at insect sex and seen human sex. Fincher looked at water striders, on the surfaces of ponds, and saw the long history of humans fleeing pathogens and evolving, as they did, just to get away.