Breasts (22 page)

In electrifying testimony, Roy Hertz, a physician and scientist with the National Institutes of Health, denounced the pill as an experimental drug and warned of carcinogenic effects. “Estrogen is to cancer what fertilizer is to the wheat crop,” he declared. Sales immediately dropped 20 percent.

Even though new, differently dosed pills would continue to be very popular, Djerassi knew the days of fast and heady progress in the field of synthetic hormones were ending. In 1973, the famed organic chemist opened a fortune cookie in San Francisco that summed it up: “Your problems are too complicated for fortune cookies.”

AROUND THE SAME TIME AS HIS TRIP TO HIROSHIMA, PIKE
wondered if the pill could be contributing to rising breast cancer rates. He knew the pill’s progesterone substantially decreased the risk of ovarian cancer because in preventing the ovaries from releasing eggs, it effectively stopped cellular division and growth. (In the middle of the menstrual cycle, the ovary literally rips open to send forth an egg and then must repair itself.) But progesterone did nothing to prevent cellular changes in the breast, and in fact, it was known to
cause
changes in the breast. For many years, estrogen was fingered as the primary culprit in breast cancer, because it was known to cause cancer of the uterus in lab studies and also to make human breast cancer cells grow faster in a Petri dish. But it turns out that progesterone is just as bad, and possibly worse, for stimulating cell growth and division.

Whenever a cell divides and replicates, it invites errors, or mutations. Enough mutations (you need a bunch) will send cancer on its inexorable course. Pike’s theory was that the more menstrual cycles a woman has in her lifetime, the more her breasts are flooded with whiplashing hormones. But when a woman is pregnant or breast-feeding—as was normally the case for much of her reproductive life before industrialization, or unless she was a nun—her breast cells usually behaved in cancer-protective ways.

“The problem with women today is they reach puberty at twelve or thirteen and don’t have a baby until they’re thirty-five,” said Pike. “That’s extraordinary! It’s incredibly non-evolutionary!” He’s right; anthropologists have studied the cycling histories of contemporary hunter-gatherer cultures, believing they provide some insight into how early humans lived. Dogon women in Mali
don’t reach puberty until the age of sixteen, and soon after, they marry. They spend much of their adult lives either pregnant or nursing (they breast-feed each child an average of two years). They ovulate approximately one hundred times during their life. Women in Western nations ovulate, on average, four hundred times. Today in America, nearly 20 percent of women between the ages of forty and forty-four have never borne a child, a figure that has doubled just since 1976.

Pike scribbled down some charts and pictures for me on scrap paper and printed out articles on his printer. At seventy-four, he is tall and lean and generously bearded, like Santa after a crash diet. When I first Googled him, the top document was a marketing article from the University of Southern California calling him “the dashing Malcolm Pike,” and it stuck in my mind. He speaks in a strong, lilting South African accent and enjoys asking Socratic questions. Having grown up in Johannesburg under apartheid, Pike is an arch proponent of tolerance and open debate. He clearly enjoys taking conventional wisdom apart.

“The pill,” he continued enthusiastically, “gives you hormone levels
every day
that look like the levels after you’ve ovulated. It was a brilliant pathologist in Scotland who showed us that there’s more cell proliferation in the breasts in the second half of the cycle.”

“I could have told you breast cells are more active after ovulation,” I said, thinking the genius in Scotland was a bit overrated.

The dashing Malcolm Pike raised his eyebrows. “How do you know?”

“Because they hurt! They get bigger. They’re inflamed,” I said.

“Ah!” said Pike. “But how do you know?” he repeated. “How do you know that’s not just water? You can’t feel cell proliferation! We had to see it in a dish!”

Well,
I thought,
if that’s the way scientists need to do it, fine.

The reason breasts become bigger and more tender after ovulation illustrates how strongly these organs are geared to procreation. Every time an egg pops out of the ovary, the body is preparing for the big event, whether fertilization actually takes place or not. Progesterone courses through our cells to help prepare the uterine wall and to begin growing the dairy machinery in our breasts. It may seem overzealous to do this nine-plus months ahead of time, but in fact the breast needs every possible minute to get up to speed.

In any case, by the mid-1980s, Pike was publishing papers showing that women who began taking the pill as teens, before bearing children, doubled their risk of breast cancer before age forty-five. If they took the pill for eight years before becoming pregnant, they nearly tripled their risk. Captive tigers and lions also suffer from mammary and uterine cancers after taking oral contraceptives.

Between 1986 and 1989, a handful of studies in Europe and New Zealand confirmed Pike’s human data, although other studies showed the pill added a smaller risk of breast cancer. I told Pike I took the pill starting when I was eighteen. By then, in the mid-1980s, manufacturers had introduced lower-dose pills, despite insisting all along that the original formulation was perfectly safe. Today’s oral contraceptives contain one-fifth the hormone levels of the original.

“So has the pill transformed your breast?” he asked, anticipating my question. “We don’t know. How would you ever find out? You have to stick needles in people to look at breast tissue. We’ve been extremely reluctant. If we could look at 180,000 women, we’d understand.”

Just when I was starting to feel the dread of past mistakes, he asked, “How long did you take the pill?”

I shrugged. “About four years,” I said.

“We think the risk of breast cancer goes up for about ten years after you stop,” he explained. “So there’s probably no more risk for you. Now, whether it did you any good, we don’t know.”

Pike was untwisting a green paper clip, working it into a rough quadrangle. “We know it’s protecting you from ovarian cancer.”

I told him that after I stopped the pill, it took me six months to start ovulating again. He looked elated. “That four years you were on the pill was like having four babies when you were young!” he said. As far as my ovaries are concerned, that’s a good thing.

But before breaking out the cigars, Pike turned again to breast cancer. If the pill gave him epidemiological heebie-jeebies, so did hormone replacement therapy, or HRT. Like the pill, this therapy supplied extra daily doses of menstrual hormones, estrogen and later estrogen-plus-progesterone, but to women whose ovaries were no longer making them. As early as 1982, Pike was worried about HRT. He published papers, but, as he tells it, they met with thunderous silence. By 1992, Premarin (the name stands for
pre
gnant
mare
ur
ine
) was one of the most widely prescribed drugs in America, given to 11 million menopausal women and earning its happy makers nearly $2 billion a year. To create the unprecedented demand, drug companies and physicians appealed to women’s vanity and reason, essentially inventing a new pathology called menopause in the same way the surgeons had invented one called micromastia, for small breasts.

As one physician told the
New York Times
in 1975, “I think of the menopause as a deficiency disease, like diabetes. Most women
develop some symptoms, whether they are aware of them or not, so I prescribe estrogens for virtually all menopausal women for an infinite period.”

He had good company. In 1966, the prominent gynecologist Robert Wilson wrote an influential bestseller,
Feminine Forever,
in which he called menopause a state of “living decay” that makes women fat, moody, and saggy. He wrote that women “rich in estrogen,” by contrast, “tend to have a certain mental vigor that gives them self-confidence, a sense of mastery over their destiny … and emotional self-control.” Estrogen therapy, he wrote, “makes women adorable, even-tempered, and generally easy to live with.”

Not unlike the anthropologists who believe that women’s breasts exist for men, many mid-century doctors thought that women’s moods, sexuality, and general perkiness should be engineered, artificially if need be, to suit male preferences.

By now there has been much debate about whether menopause is evolutionarily adaptive—in other words, is there something useful about it?—or whether we’re really designed by nature to just wither up and die after our ovaries wear out. A common refrain is that we’re more or less supposed to get cancer simply because we live so unnaturally long. I won’t go much into the fray, but one of my favorite rejoinders, the “grandmother hypothesis,” is well defended by anthropologist Sarah Blaffer Hrdy. In her book
Mothers and Others,
she explains that our ancestors often lived past the age of reproduction, and those grannies were in fact critical to the survival of their progeny for most of human history. Far from being a medical malady, menopause is a highly adaptive mechanism to free up older females to help feed and care for their grandchildren. No creature on the planet is more costly than the human child, who needs
a ridiculous amount of time to grow up; without extra hands to supply the thirteen million calories needed until maturity, our species would not have made it this far. Women are supposed to outlive their ovaries after all, concludes Hrdy, with breasts happily intact.

Still, given the choice, who wouldn’t want to have smooth skin and be adorable forever? Estrogen, miracle hormone that it is, does indeed relieve such symptoms as hot flashes, night sweats, and depression, which are experienced to a serious degree by 5 to 15 percent of menopausal women. This is the group that probably should have been targeted for risky drugs, but that wasn’t nearly as profitable as targeting the entire sex.

When uterine cancer was linked to estrogen therapy in 1980, drug makers responded by adding progesterone to the formulations. Then numerous studies in the 1980s and 1990s linked other complications to HRT. In 1991, researchers launched the fifteenyear, $100 million Women’s Health Initiative Study, but they abruptly halted part of it in 2002 when they discovered that the women taking HRT (as opposed to a placebo) had a 26 percent increase in the incidence of breast cancers, a 41 percent increase in the incidence of strokes, and a 29 percent increase in the incidence of heart attacks.

Britain was also conducting studies. Its Million Women Study, the largest study of HRT, yielded data in 2003. Results showed that women who were taking both estrogen and progesterone had a 100 percent increase, or a doubling, in their risk of breast cancer. The main culprit appeared to be progesterone, just as Pike had shown years earlier. Estrogen alone created a smaller breast cancer risk, and more recent studies suggest it might actually protect against breast cancer, but, alas, not against uterine cancer. Typical of the unpre
dictable ways hormones work their magic (and harm), HRT’s added progesterone helped minimize one cancer (uterine) but exacerbated another—breast cancer. Overall, hormone therapy in Britain caused an additional twenty thousand cases of breast cancer during the decade of the study, which is still a relatively small added risk, but enough to give many women pause.

Although researchers had known for years that synthetic hormones were linked to breast and other cancers, it really wasn’t until these two huge studies in 2002 and 2003 that the knowledge finally stuck. To the dashing Malcolm Pike, that time lag was nothing short of tragedy. “People say, ‘Aren’t you proud? You spotted the danger early,’ and I say, ‘No, because our work didn’t stop it,’ “ he said. “Why?” He shrugged. “Doctors are not particularly nervous, and they like prescribing things,” he said.

But the answer also lies upstream, with the pharmaceutical industry, which has a zeal for profit and a masterful command of the regulatory landscape. These are traits it shares with the chemical industry. Both came of age in America at the same moment in time, often using very similar molecules.

It all adds up to a new ecology of the breast. Here’s the basic cheat sheet for how the risk of breast cancer has changed over the ages. Old days: We did not have so much exposure to cycling estrogens and progesterones (we were thinner, hit puberty later, had more children, dropped dead earlier). Modern times: We’re awash in steroidal hormones. We’re fat and sexually precocious, but have babies late if it all. We take the pill and “bio-identicals,” slather novel, untested chemicals on our bodies, and consume them through food and water. We’re pretty much marinating in hormones and toxins.

Just as our long environmental legacy as synapsids, mammals, and primates shaped our cellular past, our modern environment— in the largest sense of the term—is determining our cellular destiny.

But you don’t have to be in the sway of synthetic or natural hormones to get breast cancer. You don’t even have to be a woman.