Why We Get Sick (3 page)

This distinction between defenses and defects is not merely of academic interest. For someone who is sick it can be crucial. Correcting a defect is almost always a good thing. If you can do something to make the clanking in the transmission stop or the pneumonia patient’s skin turn warm pink, it is almost always beneficial. But eliminating a defense by blocking it can be catastrophic. Cut the wire to the light that indicates a low fuel supply, and you are more likely to run out of gas. Block your cough excessively, and you may die of pneumonia.

G
iven that some bacteria and viruses treat us mainly as meals, we can think of them as enemies. Unfortunately, they are not just simple pests put here to bedevil us but sophisticated opponents. We have evolved defenses to counter their threats. They have evolved ways to overcome our defenses or even to use them to their own benefit. This endlessly escalating arms race explains why we cannot eradicate all infections and also explains some autoimmune diseases. We expand greatly on these topics in the next two chapters.

O
ur bodies were designed over the course of millions of years for lives spent in small groups hunting and gathering on the plains of Africa. Natural selection has not had time to revise our bodies for coping with fatty diets, automobiles, drugs, artificial lights, and central heating. From this mismatch between our design and our environment arises much, perhaps most, preventable modern disease. The current epidemics of heart disease and breast cancer are tragic examples.

S
ome of our genes are perpetuated despite the fact that they cause disease. Some of their effects are “quirks” that were harmless when we lived in a more natural environment. For instance, most of the genes that predispose to heart disease were harmless until we began overindulging on fatty diets. The genes that cause nearsightedness cause problems only in cultures where children do close work
early in life. Some of the genes that cause aging were subject to little selection when average life spans were shorter.

Many other genes that cause disease have actually been selected for because they provide benefits, either to the bearer or to other individuals with the gene in other combinations. For instance, the gene that causes sickle-cell disease also prevents malaria. In addition to this well-known example, many others are discussed in later chapters, including sexually antagonistic genes that benefit fathers at the expense of mothers or vice versa.

Our genetic code is constantly being disrupted by mutations. On very rare occasions these changes in DNA are beneficial, but much more commonly they create disease. Such damaged genes are constantly being eliminated or kept to a minimum by natural selection. For this reason defective genes with no compensating benefit are not a common cause of disease.

Finally, there are “outlaw” genes that facilitate their own transmission at the expense of the individual and thus bluntly demonstrate that selection acts ultimately to benefit genes, not individuals or species. Because selection among individuals is a potent evolutionary force, outlaw genes are also an uncommon cause of disease.

J
ust as there are costs associated with many genes that offer an overall benefit, there are costs associated with every major structural change preserved by natural selection. Walking upright gives us the ability to carry food and babies, but it predisposes us to back problems. Many of the body’s apparent design flaws aren’t mistakes, just compromises. To better understand disease, we need to understand the hidden benefits of apparent mistakes in design.

E
volution is an incremental process. It can’t make huge jumps, only small changes, each of which must be immediately beneficial. Major changes are difficult to accomplish even for human engineers. Fires occurred when a popular line of pickup truck was struck from the side because the gasoline tanks were located outside the frame. But to locate the tanks within the frame would require a major redesign of
everything now there, which could cause new problems and require new compromises. Even human engineers can be constrained by historical legacies. Similarly, our food passes through a tube in front of the windpipe, and must cross it to get to the stomach, thus exposing us to the danger of choking. It would be more sensible to relocate the nostrils to somewhere on the neck, but that will never happen, as we explain in
Chapter 9
.

B
efore we discuss the details of the above causes of disease, we would like to try to forestall several potentially dangerous misunderstandings. First of all, our enterprise has nothing to do with eugenics or Social Darwinism. We are not interested here in whether the human gene pool is getting better or worse, and we are emphatically not advocating actions to improve the species. We are not even particularly interested in most genetic differences between people, but much more in the genetic material that we all have in common.

An evolutionary perspective on disease does not change the ancient goals of medicine carved on a statue honoring physician E. L. Trudeau’s work at Saranac Lake: “To cure, sometimes, To help, often, To console, always.” The goal of medicine has always been (and, in our belief, always should be) to help the sick, not the species. Confusion regarding this point has justified much mischief. At the beginning of the century, Social Darwinist ideology helped to justify withholding medical care from the poor and letting capitalist giants battle irrespective of effects on individuals. These beliefs were intimately linked to those of the eugenicists, who advocated sterilization of certain groups in order to improve the species (or race!). Such ideology has long ago earned a well-deserved ill repute. It made metaphorical use of some of the terminology of Darwinism but no use of the theory as biologists understand it. We are by no means advocating that medicine should assist natural selection, nor do we suggest that biology can guide moral decisions. We would never argue that any disease is good, even though we will offer many examples in which pathology is associated with some unappreciated benefit.
Darwinism gives no moral guidelines about how we should live or how doctors should practice medicine. A Darwinian perspective on medicine can, however, help us to understand the evolutionary origins of disease, and this knowledge will prove profoundly useful in achieving the legitimate goals of medicine.

T
he solutions to the mysteries discussed in
Chapter 1
are to be found in the workings of natural selection. The process is fundamentally very simple: natural selection occurs whenever genetically influenced variation among individuals affects their survival and reproduction. If a gene codes for characteristics that result in fewer viable offspring in future generations, that gene is gradually eliminated. For instance, genetic mutations that increase vulnerability to infection, or cause foolish risk taking or lack of interest in sex, will never become common. On the other hand, genes that cause resistance to infection, appropriate risk taking, and success in choosing fertile mates are likely to spread in the gene pool, even if they have substantial costs.

A classic example is the spread of a gene for dark wing color in a British moth population living downwind from major sources of air pollution. Pale moths were conspicuous on smoke-darkened trees and easily caught by birds, while a rare mutant form of moth whose color more closely matched that of the bark escaped the predators’
beaks. As the tree trunks became darker, the mutant gene spread rapidly and largely displaced the gene for pale wing color. That is all there is to it. Natural selection involves no plan, no goal, and no direction—just genes increasing and decreasing in frequency depending on whether individuals with those genes have, relative to other individuals, greater or lesser reproductive success.

The simplicity of natural selection has been obscured by many misconceptions. For instance, Herbert Spencer’s nineteenth-century catch phrase “survival of the fittest” is widely thought to summarize the process, but it actually promotes several misunderstandings. First of all, survival is of no consequence in and of itself. This is why natural selection has created some organisms, such as salmon and annual plants, that reproduce only once, then die. Survival increases fitness only insofar as it increases later reproduction. Genes that increase lifetime reproduction will be selected for even if they result in reduced longevity. Conversely, a gene that decreases total lifetime reproduction will obviously be eliminated by selection even if it increases an individual’s survival.

Further confusion arises from the ambiguous meaning of “fittest.” The fittest individual, in the biological sense, is not necessarily the healthiest, strongest, or fastest. In today’s world, and many of those of the past, individuals of outstanding athletic accomplishment need not be the ones who produce the most grandchildren, a measure that should be roughly correlated with fitness. To someone who understands natural selection, it is no surprise that parents are so concerned about their children’s reproduction.

A gene or an individual cannot be called “fit” in isolation but only with reference to a particular species in a particular environment. Even in a single environment, every gene involves compromises. Consider a gene that makes rabbits more fearful and thereby helps to keep them from the jaws of foxes. Imagine that half of the rabbits in a field have this gene. Because they do more hiding and less eating, these timid rabbits might be, on average, a bit less well fed than their bolder companions. If, hunkered down in the March snow waiting for spring, two thirds of them starve to death while this is the fate of only one third of the rabbits who lack the gene for fearfulness, then, come spring, only a third of the rabbits will have the gene for fearfulness. It has been selected against. It might be nearly eliminated by a few harsh winters. Milder winters or an increased number of foxes could have the opposite effect. It all depends on the
current
environment.

M
any people have seen the nature film in which droves of starving lemmings jump eagerly to a watery death as a resonant voice explains that when food becomes scarce, some lemmings sacrifice themselves so that there will be enough food for at least some of the group to survive. A few decades ago, such “group selection” explanations were taken seriously by professional biologists, but not now. To see why, compare two imaginary lemmings. One is a noble fellow who, upon sensing that the population is about to outrun its food supply, quickly jumps to his death in the nearest stream. The other is a selfish lout who waits for the noble ones to do away with themselves and then eats as much food as he can get, mates as often as possible, and has as many offspring as possible. What would happen to the genes that code for the behavior of sacrificing oneself for the benefit of the group? No matter how beneficial they might be for the species, they would be eliminated.

So how can we explain the observations of apparently suicidal lemmings? When food becomes scarce in late winter, lemmings migrate, rushing along in large groups that do not always stop when they encounter waters created by early snowmelt. Drownings are, however, rather uncommon. To get the footage they wanted, the makers of the film apparently had to use brooms to surreptitiously herd the lemmings into the water, a dramatic example of the human preference for altering reality rather than theory when the two conflict! There are special circumstances in which selection at the group level can outweigh the usually stronger force of selection at the level of the individual, but they do not apply very often.

As British biologist Richard Dawkins, author of
The Selfish Gene
, has emphasized, individuals may be viewed as vessels created by genes for the replication of genes, to be discarded when the genes are through with them. This perspective mightily shakes the common view that evolution tends toward a world of health, harmony, and stability. It does not create such a world. We would like to imagine that life is naturally happy and healthy, but natural selection cares not a whit for our happiness, and it promotes health only when it is
in the interests of our genes. If tendencies to anxiety, heart failure, nearsightedness, gout, and cancer are somehow associated with increased reproductive success, they will be selected for and we will suffer even as we “succeed,” in the purely evolutionary sense.

W
e have implied that reproduction is the essence of the fitness maximized by natural selection, and in our discussion of lemmings we indicated that evolution does not favor individuals who act to help others at their own expense. These generalizations tell only part of the story. Ultimately, it is the genetic representation in future generations that counts, whether that is accomplished by having children or by doing things that increase the reproduction of your close relatives, many of whose genes are identical to yours.

Half of the genes in a child are identical to those in the mother, and half are identical to those in the father. Full siblings, on average, also share half of each other’s genes. One fourth of the genes in a grandparent are identical to those in the grandchild. Cousins share one eighth of their genes. This means that, from the perspective of your genes, your sister’s survival and reproduction are half as important as your own and your cousin’s one eighth as important. For this reason, selection favors extending help to relatives if, all else being equal (e.g., age and health), the cost to oneself of extending the help is less than the benefit to the relative times the degree of relationship. In a classic anecdote, British biologist J. B. S. Haldane was asked if he would sacrifice his life for his brother. “No,” he said, “not for one brother. But I would for two brothers. Or eight cousins.” Formal recognition of this principle and its importance in explaining cooperation awaited the landmark 1964 paper by British biologist William Hamilton, winner of the 1993 Crafoord Prize, created to honor scientists whose work is in fields not covered by the Nobel Prize. Another great British biologist, John Maynard Smith, christened the phenomenon
kin selection
.