What the Dog Saw [50]
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