Why We Get Sick (38 page)

Its perfection still elicits wonder. The seam around the case is all but invisible; the crystal is symmetrical and gleaming; the chain is made of exquisitely miniature gold links. The face has numerals sharply etched around the logo of the Lifetime Watch Company. But even as you admire the watchmaker’s skill, the light reveals some surprising imperfections. The crystal is laced with slight distortions. And the chain, though beautiful and flexible, is thin and broken, thus explaining why the watch is here and not in a pocket. A notch in the seam is perfectly shaped for a thumbnail but large enough for dirt and water to enter easily. Odd, these flaws. You open the back, and the exquisite mechanism again inspires awe. How could anyone have designed, much less constructed, so many perfectly cut gears of rustproof brass, the hairlike spring of steel, the balance wheel suspended
by minuscule jewels? But when you try to set the watch, the knob is so tiny you can barely grasp it and a dozen twirls advance the hands only a single hour. You shake the watch. It ticks for five seconds, then is stopped by flakes of rust from that steel spring. What an odd device this is! So perfect in many respects, in others makeshift at best. How could the creator of such a masterpiece have allowed so many obvious flaws? Inside the case is an inscription in tiny letters. You take out your magnifying glass and read:

W
e now return to where we began, to a seeming incongruity at the core of medicine. Despite their exquisite design, our bodies have crude flaws. Despite our multiple defenses, we have a thousand vulnerabilities. Despite their capabilities for rapid and precise repairs, our bodies inevitably deteriorate and eventually fail. Before Darwin, physicians could only wonder at the incongruity of it all, perhaps with the hope that our bodies are part of an unfathomable divine plan, or with the suspicion that they are some cosmic prank. Ever since Darwin, the incongruity has often mistakenly been attributed
to the supposed weakness or capriciousness of natural selection. In the light of modern Darwinism, however, the incongruity unfolds into a sharply blocked tapestry with a place for each of several distinct causes of disease.

Why isn’t the body more reliable? Why is there disease at all? As we have seen, the reasons are remarkably few. First, there are genes that make us vulnerable to disease. Some—though fewer than has been thought—are defectives continually arising from new mutations but kept scarce by natural selection. Other genes cannot be eliminated because they cause no disadvantages until it is too late in life for them to affect fitness. Most deleterious genetic effects, however, are actively maintained by selection because they have unappreciated benefits that outweigh their costs. Some of these are maintained because of heterozygote advantage; some are selected because they increase their own frequency, despite creating a disadvantage for the individual who bears them; some are genetic quirks that have adverse effects only when they interact with a novel environmental factor.

Second, disease results from exposure to novel factors that were not present in the environment in which we evolved. Given enough time, the body can adapt to almost anything, but the ten thousand years since the beginnings of civilization are not nearly enough time, and we suffer accordingly. Infectious agents evolve so fast that our defenses are always a step behind. Third, disease results from design compromises, such as upright posture with its associated back problems. Fourth, we are not the only species with adaptations produced and maintained by natural selection, which works just as hard for pathogens trying to eat us and the organisms we want to eat. In conflicts with these organisms, as in baseball, you can’t win ’em all. Finally, disease results from unfortunate historical legacies. If the organism had been designed with the possibility of fresh starts and major changes, there would be better ways of preventing many diseases. Alas, every successive generation of the human body must function well, with no chance to go back and start afresh.

The human body turns out to be both fragile and robust. Like all products of organic evolution, it is a bundle of compromises, each of which offers an advantage, but often at the price of susceptibility to disease. These susceptibilities cannot be eliminated by any duration of natural selection, for it is the very power of natural selection that created them.

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any questions confront the infant enterprise of Darwinian medicine. What is its long-range goal? How should we go about analyzing a disease from an evolutionary viewpoint? How should hypotheses be formulated and tested? Who will pay for this research? Who will do the research and in what academic departments or other agencies? Why has it taken so long to get this enterprise started?

We begin with the long-range goal. What will medical textbooks look like when evolutionary studies of disease are well established? Current textbooks summarize what is known about a disorder under traditional headings: signs and symptoms of the disease, laboratory findings, differential diagnosis, course, complications, epidemiology, etiology, pathophysiology, treatment, and outcome. Such descriptions fall one category short. A comprehensive discussion of a disease must also provide an evolutionary explanation. While some current textbooks have a sentence or two about the advantages of the sickle-cell gene or the benefits of cough or fever, none of them systematically addresses the evolutionary forces acting on genes that cause disease, the novel aspects of environment that cause disease, or the details of the host-parasite arms race. Every textbook description of a disease should have, in our opinion, a section devoted to its evolutionary aspects. This section should address the following questions:

Such questions immediately suggest important but neglected research on many diseases. Even the common cold offers many opportunities. What are the effects of taking or not taking aspirin? What are the effects of using nasal inhalers or decongestant medication? To use the categories of
Chapter 3
, is rhinorrhea (runny nose) a defense, a means the virus uses to spread itself, or both? For the most part, these projects have yet to be undertaken despite their conceptual simplicity and their obvious practical implications for us all.

Take something far more chronic and complicated, plantar fasciitis. More often known as heel spurs, this common disorder causes intense pain on the inside edge of the heel, especially first thing in the morning. The proximate cause is inflammation at the point where the heel attaches to the plantar fascia, a band of tough tissue that connects the front and rear of the foot like the string on a bow, supporting the arch of the foot. With every footstep it stretches, bearing the weight of the body thousands of times every day. Why does this fascia fail so often? The easy answer is that natural selection cannot shape a tissue strong enough to do the job—but by now this explanation should be suspect. Somewhat more plausible is the possibility that we began walking on two feet so recently that there has not been enough time for natural selection to strengthen the fascia sufficiently. The problem with this explanation is that plantar fasciitis is common and crippling. Like nearsightedness, it would, in the natural environment, so drastically decrease fitness that it would be strongly selected against. Some experts say plantar fasciitis arises in people who walk with their toes pointed out, a conformation that puts increased stress on the tissue. But then why do we walk that way? Is it the modern habit of wearing shoes? But many people who have never worn shoes also walk with their toes pointed outward.

Two clues suggest that plantar fasciitis may result from environmental novelty. First, exercises that stretch the plantar fascia to make it longer and more resilient are effective in relieving the problem. Second, many of us do something hunter-gatherers don’t: we sit in chairs all day. Most hunter-gatherers walk for hours each day, instead of compressing their exercise into an efficient aerobic workout. When they aren’t walking, they don’t use chairs, they squat, a position that steadily stretches the plantar fascia. No plantar fasciitis and physical therapy for them, just squatting and walking for hours each day. This hypothesis, that plantar fasciitis results from prolonged sitting that allows the fascia to contract and that the disorder can be prevented and relieved by
squatting and other stretching of the fascia, can readily be tested with epidemiological data and straightforward treatment studies.

Another good challenge for Darwinian medicine is the current controversy about whether it is wise to take antioxidants such as vitamin C, vitamin E, and beta-carotene. Folklore has long credited these agents with reducing heart disease, cancer, and even the effects of aging. Controlled studies are increasingly supporting these claims, especially for the prevention of atherosclerosis, although a major study in 1994 reported that beta-carotene appeared to
increase
the risk of cancer in some people. The agents are still deemed controversial, and many physicians studying them recommend caution until larger studies can assess their risks as well as benefits. We agree with this general conservatism but hope that an evolutionary view can speed the process. Earlier in this book we noted that natural selection seems to have resulted in high levels of several of the body’s own antioxidants even though they cause disease. Uric acid levels are higher in species that live longer and are so high in humans that we are susceptible to gout. It appears that natural selection has acted to increase the human levels of uric acid, superoxide dismutase, and perhaps bilirubin and other substances as well, because they are antioxidants that slow some effects of aging in a species that has greatly increased its life span in just the past few hundred thousand years.

Why doesn’t the body have antioxidant levels that are already optimal? It is possible that our antiaging mechanisms are still catching up with the recent increase in our life span. It is also possible that the costs of high levels of antioxidants (perhaps decreases in our resistance to infection or toxins?) have restricted them to levels that were optimal for a normal Stone Age lifetime of thirty or forty years. These possibilities suggest that adding extra antioxidants to the diet may have benefits that exceed the costs. In contrast to the many cases in which an evolutionary view argues against excessive intervention, here it supports the active pursuit of strategies that may prevent some effects of aging. A major part of such studies should be a search for other antioxidants in the body and an assessment of their costs and benefits. It would be interesting to see if people with high uric acid levels have costs other than gout and whether they show fewer signs of aging than other people. It will also be important to look for similar costs and benefits in our primate relatives. With this knowledge we will be in a better position to decide who will benefit from taking antioxidants and what the side effects might be.

This book contains suggestions for dozens of studies, many of which seem to us to be fine topics for Ph.D. theses and some of which offer challenges enough for a whole career. Pursuing them will be difficult, however, because no government agency presently supports such projects. Existing funding committees are reluctant to provide support because their mandate is to provide funds to study the proximate mechanisms and treatment of particular diseases. Furthermore, few members of such committees know anything about the formulation or testing of evolutionary ideas, and some are likely to have misgivings based on fundamental misconceptions about the scientific status of evolutionary hypotheses. The system used to assign funding priorities ensures that even a few people with such misgivings can eliminate the chances of funding.

Asking biochemists or epidemiologists to judge proposals to test evolutionary hypotheses is like asking mineral chemists to judge proposals on continental drift. Darwinian medicine needs its own funding panels staffed by reviewers who know the concepts and methods of evolutionary biology. Realistically, the prospects are poor for major government funding soon. The best hope for rapid growth of the field lies in the vision of private donors or foundations that could create institutes to support the development of Darwinian medicine. Even moderate support of this sort could quickly change the course of medicine, just as prior investments in biochemical and genetic research are now transforming our lives. As René Dubos noted in 1965: