What the Dog Saw [49]
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