Why We Get Sick (29 page)

T
o avoid contracting cancer, the first thing you want to do is to pick your parents wisely. Susceptibility to cancer, like so many other diseases, is hereditary. This is true both in general and for particular forms of cancer, most notably for some rare childhood cancers and those of the breast and colon. Members of families in which such cancers have occurred frequently may have twenty to thirty times the likelihood of contracting them as those in cancer-free families. Even when controlled for family members’ tendency to experience similar environmental conditions, the evidence for predisposition for certain kinds of cancer is strong. Mice can be bred to form cancer-prone stocks in which one cancer-control mechanism is already missing in every mouse. This enormously increases the likelihood of one or more kinds of cancer. Some human cancers are inherited in the same way.

Another good way to reduce the likelihood of cancer is to live dangerously: die young, and you are unlikely to get cancer. The fact of senescence means that the environment of any cell and its regulatory capabilities are deteriorating. Hormonal and local regulation of cell growth and proliferation, like all other aspects of adaptive performance, becomes less effective as we go through that terminal life-history stage known as adulthood. The cell itself ages, and as the cardiovascular and digestive and excretory systems deteriorate, it will be ever less well supplied with nutrients and other essentials and ever less effectively unburdened of its waste products. An inevitable consequence is that its potential for growth and cell division is ever less well regulated. Maladaptive growths become steadily more likely to occur and spread unchecked.

The increasing incidence of cancer with age illustrates an important evolutionary principle. Adaptations work best in the circumstances in which they were evolved. Our cancer-control adaptations and other vital functions were not evolved to keep an eighty-year-old alive. The body of anyone that old is an abnormal environment for human genes and their products, one that rarely existed in the Stone Age. More generally, just about all the adverse effects of modern environments, as discussed in
Chapter 10
, can be expected to increase the incidence of cancer: X rays and other ionizing radiations, novel toxins, unnatural levels of exposure to natural toxins (such as nicotine and alcohol), and abnormal diets or other lifestyle factors.

Injuries and infections anywhere in the body can interfere with cancer-controlling mechanisms not only at the site of the problem but also at distant sites in the body. Bacteria can increase the cancer rates of infected tissues, but viruses are more likely to have such effects. One reason is that a virus is not very different from a single gene in a human cell and can sometimes settle into a niche on a chromosome as if it belonged there. From such a position it can readily subvert the normal machinery of the cell. Viruses, especially HIV, attack the immune system and have the incidental consequence of impairing that system’s ability to attack cancer. Like bacteria and larger parasites, viruses can also produce toxins that weaken cellular-control mechanisms.

The connections between environmental causes and certain cancers are sometimes easy to understand. Food that has an abnormally high concentration of salt or alcohol or is loaded with the carcinogens of smoked or broiled meats will contact the stomach cells and increase the risk of stomach cancer. The chemicals in tobacco smoke likewise directly influence lung cells. Sunshine damages the genes in skin cells and leads to melanoma. The mechanism by which a high-fat diet contributes to breast or prostate cancer must depend on more subtle effects than simple contact with the substance in the food. The same can be said for the association between smoking and bladder cancer.

Even after a tumor becomes detectable and produces alarming symptoms, natural control mechanisms, especially immunological factors, will still be at work. They may still win the contest or at least slow the maladaptive growth or prevent its spread to other sites. Even if never cured, some untreated cancers take many years to incapacitate the victim. On rare occasions, apparently incurable cancers just go away.

Many aspects of the contest between a cancer and its victim resemble those between pathogen and host, and the need for such functional categories as cancer-growth adaptations and efforts to suppress them is evident. A cancer is a cellular renegade that has rebelled against the polity of the body and can be regarded as a parasite pursuing its own interests in conflict with the host. Unlike an infectious pathogen, a cancer’s success can never be more than short-term, because it has no way to disperse to other hosts, and the host’s death means its death too. The same is true of the normal cells from which the cancer arose. When the host dies, the only surviving genes will be those of the host’s germ-line cells that have already been passed on to the next generation.

Cancer is a collective term for maladaptive and uncontrolled tissue growths of all kinds. Cancers can arise from any cell types that retain the capacity for growth and division, and cancers of each cell type result from a variety of initiating causes and failures of suppression mechanisms. It is not surprising that cancer has proven difficult for medical science to master, and it is unlikely that one general cure will ever be found. We are making rapid progress, however, and a better understanding of cancer as a contest between renegade cells and the host will surely facilitate more progress.

P
erhaps the best example of a group of related cancers that show the value of a Darwinian approach is cancers of the breast, uterus, and ovary, all of which have recently become much more frequent. Boyd Eaton, a distinguished American researcher in both medicine and anthropology, along with other workers in these fields, has recently brought together a wide range of information to shed light on why these cancers are now so frequent in some human populations and not in others. The evidence is clear that this modern plague is caused in part by the novel reproductive patterns of so many women in the more privileged industrialized societies.

Part of the increase results from the boring fact that cancer is more likely in older people, and more women are now living to old age.
The more interesting finding is that the probability of a cancer of the female reproductive system at any age increases directly in relation to the number of menstrual cycles a woman has experienced. The most likely victim of a cancer of the reproductive tissues is an elderly woman who had an early menarche and late menopause and never had her cycling interrupted by pregnancy and lactation.

From a historical perspective, this is a most abnormal reproductive pattern. Stone Age women, like those of recent hunter-gatherer societies, had quite a different sort of reproductive life history. They had much later maturation and earlier menopause, perhaps in part because they were less well fed and more heavily parasitized than modern women. A Stone Age girl may have experienced menarche at fifteen or later and would probably have been pregnant within a very few years. If the pregnancy miscarried, she would be pregnant again shortly thereafter. If it was successful, it would be followed by a period of lactation of at least two years, possibly four, with associated inhibition of the menstrual cycle. Shortly after weaning (or the death of her infant), she would start cycling and would soon be pregnant again. This would be the pattern until her death or menopause at perhaps about age forty-seven. In this thirty-year period she would have had four or five or maybe six pregnancies and spent more than half of this thirty years lactating. Her total number of menstrual cycles could not have been much more than 150. A modern woman, even if she has two or three children, might easily experience two or three times this number of cycles.

A menstrual cycle is characterized by wide swings of hormone concentrations, and these changes cause cellular responses in the ovarian, uterine, and mammary tissues. These tissue responses are reproductive adaptations, and, like any adaptations, they have costs, in this case increased vulnerability to some forms of cancer. These costs are normally minimized by compensating processes that take place during times when the cycling is interrupted by pregnancy and lactation. If these interruptions never occur, the compensating repairs never occur or are carried out less effectively, and the costs keep accumulating. This is speculation, of course, but it seems very likely that something of the sort must be happening. The undeniable observation is that the more menstrual cycles a woman has, the more likely she is to get a reproductive-system cancer. A more general principle is the adverse effect, for any kind of adaptive mechanism, of conditions other than those in which it evolved. The modern circumstances that lead
women to undergo three or four hundred menstrual cycles are no doubt a good example. This evolutionary perspective is not likely to prevent much cancer in women now in their vulnerable years. For them we can do no better than to recommend a general avoidance of environmental hazards such as nicotine and other toxins, both natural and artificial, radiation, and, most important, diets abnormally high in fat.

The long-term implications are more interesting and promising. Obviously it would be both unethical and silly to recommend that girls’ growth and maturation should be delayed by an inadequate diet, that they should become pregnant as soon as possible after menarche and frequently again thereafter, and that they should spend a total of perhaps twenty years breast-feeding their babies. Eaton and his coworkers have more enlightened suggestions. What needs to be done is to find out, with carefully conducted research, just how this kind of historically normal life history makes cancer of the reproductive organs less likely. We envision researchers diligently searching for artificial means of achieving the low cancer rates that come naturally to women in hunter-gatherer societies.

We suspect that the artificial means would take the form of hormonal manipulations. Large numbers of women are already using oral contraceptives, which work by artificially affecting tissues in much the same ways as natural hormones do. Different contraceptive medications work in different ways to achieve the desired interference with pregnancy, and they have a diverse array of side effects. With ever more detailed knowledge of the physiological actions of natural and artificial hormones, we should be ever better able to devise artificial ways of mimicking the beneficial effects of Stone Age life histories. This may not be as futuristic and Utopian a possibility as it might seem. Eaton and other workers have presented striking evidence that some oral contraceptives can reduce the rates of ovarian and uterine cancer, although not breast cancer. We expect that some sort of hormone treatment will soon be developed to reduce breast cancer as well. None of these comments should be taken to suggest that we should not continue the search for other environmental and genetic causes of cancer. Far from it! We need every bit of knowledge that can help us combat this scourge.

B
ecause it is crucial to fitness, you might think that natural selection has smoothly polished the path of sex and reproduction, from the first romantic longings of adolescence to love, marriage, sex, pregnancy, childbirth, and child-rearing. Alas, we all know the truth too well. From unrequited love to lover’s spats, premature ejaculation, impotence, lack of orgasm, menstrual problems, the complications of birth, the special vulnerabilities and demands of infants, and the inevitable conflicts between parents, and between parents and their children, reproduction is fraught with strife and suffering. Why does reproduction entail so much conflict and misery? Precisely because it is so crucial to Darwinian fitness. It is at the very core of intense competition and thus causes many problems.

While our main focus in this book is on how evolutionary ideas can help to explain and prevent or cure specific medical diseases, here and in the next chapter we broaden our view somewhat to encompass emotional and behavioral problems that may or may not be considered medical disorders. Some problems associated with reproduction, such as diabetes during pregnancy or sudden infant death syndrome, are clearly diseases, while others, such as jealousy, child abuse, and sexual problems, involve behavior and emotions. However we categorize them, they cause much suffering and make more sense in the light of evolution. Help from Darwinism does not end at
the boundary between the medical and the social or educational. Darwinism is relevant to all aspects of human life, not just medicine.

W
e begin with a fundamental enigma, one of those wonderful questions that is easy to overlook until you take an evolutionary view of life. Why does sex exist at all? It is costly to fitness in important ways, and many organisms do nicely without it, reproducing either by dividing, like amoebae, or by having females that can lay eggs that develop without fertilization, like aphids. Such creatures have a huge short-term fitness advantage over those who reproduce sexually. Imagine what would happen if a mutation produced a female robin that was perfectly standard in every other respect except that she laid eggs that carried all of her genes but none of her mate’s and developed normally without needing to be fertilized. In every generation, all the offspring would be identical females. Compared to a normal female, who can pass only half her genes on to each offspring and who has half male and half female offspring, this mutant strain would increase twice as fast.

So why didn’t some parthenogenetic woman, ages ago, flood the world with her progeny and drive us sexual beings to extinction? And why did sex evolve in the first place? Surprising as it may seem, biologists don’t yet fully agree about how to answer these questions. Most believe that the function of sex is to introduce variation in offspring, but it remains hard to understand how this variation can be useful enough to outweigh the enormous evolutionary costs of sexual reproduction. Biologists also realize that, in the long run, the recombination of genes during sexual reproduction may prevent an otherwise steady accumulation of deleterious mutations, but this does not answer the question of why asexual reproduction does not continually increase in the short run.