Part of Strassmann’s work focused on the Dogon’s practice of segregating menstruating women in special huts on the fringes of the village. In Sangui, there were two menstrual huts — dark, cramped, one-room adobe structures, with boards for beds. Each accommodated three women, and when the rooms were full, latecomers were forced to stay outside on the rocks. “It’s not a place where people kick back and enjoy themselves,” Strassmann says. “It’s simply a nighttime hangout. They get there at dusk, and get up early in the morning and draw their water.” Strassmann took urine samples from the women using the hut, to confirm that they were menstruating. Then she made a list of all the women in the village, and for her entire time in Mali — 736 consecutive nights — she kept track of everyone who visited the hut. Among the Dogon, she found a woman on average has her first period at the age of sixteen and gives birth eight or nine times. From menarche, the onset of menstruation, to the age of twenty, she averages seven periods a year. Over the next decade and a half, from the age of twenty to the age of thirty-four, she spends so much time either pregnant or breast-feeding (which, among the Dogon, suppresses ovulation for an average of twenty months) that she averages only slightly more than one period per year. Then, from the age of thirty-five until menopause, at around fifty, as her fertility rapidly declines, she averages four menses a year. All told, Dogon women menstruate about a hundred times in their lives. (Those who survive early childhood typically live into their seventh or eighth decade.) By contrast, the average for contemporary Western women is somewhere between three hundred and fifty and four hundred times.
Strassmann’s office is in the basement of a converted stable next to the Natural History Museum on the University of Michigan campus. Behind her desk is a row of battered filing cabinets, and as she was talking, she turned and pulled out a series of yellowed charts. Each page listed, on the left, the first names and identification numbers of the Sangui women. Across the top was a time line, broken into thirty-day blocks. Every menses of every woman was marked with an X. In the village, Strassmann explained, there were two women who were sterile, and, because they couldn’t get pregnant, they were regulars at the menstrual hut. She flipped through the pages until she found them. “Look, she had twenty-nine menses over two years, and the other had twenty-three.” Next to each of their names was a solid line of x’s. “Here’s a woman approaching menopause,” Strassmann went on, running her finger down the page. “She’s cycling but is a little bit erratic. Here’s another woman of prime childbearing age. Two periods. Then pregnant. I never saw her again at the menstrual hut. This woman here didn’t go to the menstrual hut for twenty months after giving birth, because she was breast-feeding. Two periods. Got pregnant. Then she miscarried, had a few periods, then got pregnant again. This woman had three menses in the study period.” There weren’t a lot of x’s on Strassmann’s sheets. Most of the boxes were blank. She flipped back through her sheets to the two anomalous women who were menstruating every month. “If this were a menstrual chart of undergraduates here at the University of Michigan, all the rows would be like this.”
Strassmann does not claim that her statistics apply to every preindustrial society. But she believes — and other anthropological work backs her up — that the number of lifetime menses isn’t greatly affected by differences in diet or climate or method of subsistence (foraging versus agriculture, say). The more significant factors, Strassmann says, are things like the prevalence of wet-nursing or sterility. But overall she believes that the basic pattern of late menarche, many pregnancies, and long menstrual-free stretches caused by intensive breast-feeding was virtually universal up until the “demographic transition” of a hundred years ago from high to low fertility. In other words, what we think of as normal — frequent menses — is in evolutionary terms abnormal. “It’s a pity that gynecologists think that women have to menstruate every month,” Strassmann went on. “They just don’t understand the real biology of menstruation.”
To Strassmann and others in the field of evolutionary medicine, this shift from a hundred to four hundred lifetime menses is enormously significant. It means that women’s bodies are being subjected to changes and stresses that they were not necessarily designed by evolution to handle. In a brilliant and provocative book, Is Menstruation Obsolete?, Drs. Elsimar Coutinho and Sheldon S. Segal, two of the world’s most prominent contraceptive researchers, argue that this recent move to what they call “incessant ovulation” has become a serious problem for women’s health. It doesn’t mean that women are always better off the less they menstruate. There are times — particularly in the context of certain medical conditions — when women ought to be concerned if they aren’t menstruating: In obese women, a failure to menstruate can signal an increased risk of uterine cancer. In female athletes, a failure to menstruate can signal an increased risk of osteoporosis. But for most women, Coutinho and Segal say, incessant ovulation serves no purpose except to increase the occurence of abdominal pain, mood shifts, migraines, endometriosis, fibroids, and anemia — the last of which, they point out, is “one of the most serious health problems in the world.”
Most serious of all is the greatly increased risk of some cancers. Cancer, after all, occurs because as cells divide and reproduce they sometimes make mistakes that cripple the cells’ defenses against runaway growth. That’s one of the reasons that our risk of cancer generally increases as we age: our cells have more time to make mistakes. But this also means that any change promoting cell division has the potential to increase cancer risk, and ovulation appears to be one of those changes. Whenever a woman ovulates, an egg literally bursts through the walls of her ovaries. To heal that puncture, the cells of the ovary wall have to divide and reproduce. Every time a woman gets pregnant and bears a child, her lifetime risk of ovarian cancer drops 10 percent. Why? Possibly because, between nine months of pregnancy and the suppression of ovulation associated with breast-feeding, she stops ovulating for twelve months — and saves her ovarian walls from twelve bouts of cell division. The argument is similar for endometrial cancer. When a woman is menstruating, the estrogen that flows through her uterus stimulates the growth of the uterine lining, causing a flurry of potentially dangerous cell division. Women who do not menstruate frequently spare the endometrium that risk. Ovarian and endometrial cancer are characteristically modern diseases, consequences, in part, of a century in which women have come to menstruate four hundred times in a lifetime.
In this sense, the Pill really does have a natural effect. By blocking the release of new eggs, the progestin in oral contraceptives reduces the rounds of ovarian cell division. Progestin also counters the surges of estrogen in the endometrium, restraining cell division there. A woman who takes the Pill for ten years cuts her ovarian-cancer risk by around 70 percent and her endometrial-cancer risk by around 60 percent. But here natural means something different from what Rock meant. He assumed that the Pill was natural because it was an unobtrusive variant of the body’s own processes. In fact, as more recent research suggests, the Pill is really only natural in so far as it’s radical — rescuing the ovaries and endometrium from modernity. That Rock insisted on a twenty-eight-day cycle for his pill is evidence of just how deep his misunderstanding was: the real promise of the Pill was not that it could preserve the menstrual rhythms of the twentieth century but that it could disrupt them.
Today, a growing movement of reproductive specialists has begun to campaign loudly against the standard twenty-eight-day pill regimen. The drug company Organon has come out with a new oral contraceptive, called Mircette, that cuts the seven-day placebo interval to two days. Patricia Sulak, a medical researcher at Texas A&M University, has shown that most women can probably stay on the Pill, straight through, for six to twelve weeks before they experience breakthrough bleeding or spotting. More recently, Sulak has documented precisely what the cost of the Pill’s monthly “off” week is. In a paper in the February issue of the journal Obstetrics and Gynecology, she and her colleagues documente
d something that will come as no surprise to most women on the Pill: during the placebo week, the number of users experiencing pelvic pain, bloating, and swelling more than triples, breast tenderness more than doubles, and headaches increase by almost 50 percent. In other words, some women on the Pill continue to experience the kinds of side effects associated with normal menstruation. Sulak’s paper is a short, dry, academic work, of the sort intended for a narrow professional audience. But it is impossible to read it without being struck by the consequences of John Rock’s desire to please his Church. In the past forty years, millions of women around the world have been given the Pill in such a way as to maximize their pain and suffering. And to what end? To pretend that the Pill was no more than a pharmaceutical version of the rhythm method?
3.
In 1980 and 1981, Malcolm Pike, a medical statistician at the University of Southern California, traveled to Japan for six months to study at the Atomic Bomb Casualties Commission. Pike wasn’t interested in the effects of the bomb. He wanted to examine the medical records that the commission had been painstakingly assembling on the survivors of Hiroshima and Nagasaki. He was investigating a question that would ultimately do as much to complicate our understanding of the Pill as Strassmann’s research would a decade later: why did Japanese women have breast-cancer rates six times lower than American women?
In the late forties, the World Health Organization began to collect and publish comparative health statistics from around the world, and the breast-cancer disparity between Japan and America had come to obsess cancer specialists. The obvious answer — that Japanese women were somehow genetically protected against breast cancer — didn’t make sense, because once Japanese women moved to the United States they began to get breast cancer almost as often as American women did. As a result, many experts at the time assumed that the culprit had to be some unknown toxic chemical or virus unique to the West. Brian Henderson, a colleague of Pike’s at USC and his regular collaborator, says that when he entered the field in 1970, “the whole viral- and chemical-carcinogenesis idea was huge — it dominated the literature.” As he recalls, “Breast cancer fell into this large, unknown box that said it was something to do with the environment — and that word environment meant a lot of different things to a lot of different people. They might be talking about diet or smoking or pesticides.”
Henderson and Pike, however, became fascinated by a number of statistical peculiarities. For one thing, the rate of increase in breast-cancer risk rises sharply throughout women’s thirties and forties and then, at menopause, it starts to slow down. If a cancer is caused by some toxic outside agent, you’d expect that rate to rise steadily with each advancing year, as the number of mutations and genetic mistakes steadily accumulates. Breast cancer, by contrast, looked as if it were being driven by something specific to a woman’s reproductive years. What was more, younger women who had had their ovaries removed had a markedly lower risk of breast cancer; when their bodies weren’t producing estrogen and progestin every month, they got far fewer tumors. Pike and Henderson became convinced that breast cancer was linked to a process of cell division similar to that of ovarian and endometrial cancer. The female breast, after all, is just as sensitive to the level of hormones in a woman’s body as the reproductive system. When the breast is exposed to estrogen, the cells of the terminal-duct lobular unit — where most breast cancer arises — undergo a flurry of division. And during the mid-to-late stage of the menstrual cycle, when the ovaries start producing large amounts of progestin, the pace of cell division in that region doubles.
It made intuitive sense, then, that a woman’s risk of breast cancer would be linked to the amount of estrogen and progestin her breasts have been exposed to during her lifetime. How old a woman is at menarche should make a big difference, because the beginning of puberty results in a hormonal surge through a woman’s body, and the breast cells of an adolescent appear to be highly susceptible to the errors that result in cancer. (For more complicated reasons, bearing children turns out to be protective against breast cancer, perhaps because in the last two trimesters of pregnancy the cells of the breast mature and become much more resistant to mutations.) How old a woman is at menopause should matter, and so should how much estrogen and progestin her ovaries actually produce, and even how much she weighs after menopause, because fat cells turn other hormones into estrogen.
Pike went to Hiroshima to test the cell-division theory. With other researchers at the medical archive, he looked first at the age when Japanese women got their period. A Japanese woman born at the turn of the century had her first period at sixteen and a half. American women born at the same time had their first period at fourteen. That difference alone, by their calculation, was sufficient to explain 40 percent of the gap between American and Japanese breast-cancer rates. “They had collected amazing records from the women of that area,” Pike said. “You could follow precisely the change in age of menarche over the century. You could even see the effects of the Second World War. The age of menarche of Japanese girls went up right at that point because of poor nutrition and other hardships. And then it started to go back down after the war. That’s what convinced me that the data were wonderful.”
Pike, Henderson, and their colleagues then folded in the other risk factors. Age at menopause, age at first pregnancy, and number of children weren’t sufficiently different between the two countries to matter. But weight was. The average post-menopausal Japanese woman weighed a hundred pounds; the average American woman weighed a hundred and forty-five pounds. That fact explained another 25 percent of the difference. Finally, the researchers analyzed blood samples from women in rural Japan and China, and found that their ovaries — possibly because of their extremely low-fat diet — were producing about 75 percent the amount of estrogen that American women were producing. Those three factors, added together, seemed to explain the breast-cancer gap. They also appeared to explain why the rates of breast cancer among Asian women began to increase when they came to America: on an American diet, they started to menstruate earlier, gained more weight, and produced more estrogen. The talk of chemicals and toxins and power lines and smog was set aside. “When people say that what we understand about breast cancer explains only a small amount of the problem, that it is somehow a mystery, it’s absolute nonsense,” Pike says flatly. He is a South African in his sixties, with graying hair and a salt-and-pepper beard. Along with Henderson, he is an eminent figure in cancer research, but no one would ever accuse him of being tentative in his pronouncements. “We understand breast cancer extraordinarily well. We understand it as well as we understand cigarettes and lung cancer.”
What Pike discovered in Japan led him to think about the Pill, because a tablet that suppressed ovulation — and the monthly tides of estrogen and progestin that come with it — obviously had the potential to be a powerful anti-breast-cancer drug. But the breast was a little different from the reproductive organs. Progestin prevented ovarian cancer because it suppressed ovulation. It was good for preventing endometrial cancer because it countered the stimulating effects of estrogen. But in breast cells, Pike believed, progestin wasn’t the solution; it was one of the hormones that caused cell division. This is one explanation for why, after years of studying the Pill, researchers have concluded that it has no effect one way or the other on breast cancer: whatever beneficial effect results from what the Pill does is canceled out by how it does it. John Rock touted the fact that the Pill used progestin, because progestin was the body’s own contraceptive. But Pike saw nothing “natural” about subjecting the breast to that heavy a dose of progestin. In his view, the amount of progestin and estrogen needed to make an effective contraceptive was much greater than the amount needed to keep the reproductive system healthy — and that excess was unnecessarily raising the risk of breast cancer. A truly natural Pill might be one that found a way to suppress ovulation without using progestin. Throughout the 1980s, Pike recalls, this was his obsession. “We were all trying t
o work out how the hell we could fix the Pill. We thought about it day and night.”
4.
Pike’s proposed solution is a class of drugs known as GnRHAs, which has been around for many years. GnRHAs disrupt the signals that the pituitary gland sends when it is attempting to order the manufacture of sex hormones. It’s a circuit breaker. “We’ve got substantial experience with this drug,” Pike says. Men suffering from prostate cancer are sometimes given a GnRHA to temporarily halt the production of testosterone, which can exacerbate their tumors. Girls suffering from what’s called precocious puberty — puberty at seven or eight, or even younger — are sometimes given the drug to forestall sexual maturity. If you give GnRHA to women of childbearing age, it stops their ovaries from producing estrogen and progestin. If the conventional Pill works by convincing the body that it is, well, a little bit pregnant, Pike’s pill would work by convincing the body that it was menopausal.
In the form Pike wants to use it, GnRHA will come in a clear glass bottle the size of a saltshaker, with a white plastic mister on top. It will be inhaled nasally. It breaks down in the body very quickly. A morning dose simply makes a woman menopausal for a while. Menopause, of course, has its risks. Women need estrogen to keep their hearts and bones strong. They also need progestin to keep the uterus healthy. So Pike intends to add back just enough of each hormone to solve these problems, but much less than women now receive on the Pill. Ideally, Pike says, the estrogen dose would be adjustable: women would try various levels until they found one that suited them. The progestin would come in four twelve-day stretches a year. When someone on Pike’s regimen stopped the progestin, she would have one of four annual menses.
What the Dog Saw and Other Adventures Page 11
