  “Mismatch” hypotheses suggest that traits that may have been adaptive in the past leave us vulnerable to disease in our current environment. For instance, many advocates of evolutionary medicine have argued that the high correlation between nulliparity and cancer risk might be explained by our evolutionary history. The argument is that women in the evolutionary past were pregnant for much of their lives, starting at an earlier age; breast development and differentiation was thus adapted to a lifetime of frequent pregnancy and nursing. Delaying or avoiding pregnancy changes the developmental processes typical for our species, and might expose women to more cycles of estrogen, which could increase breast cancer risk. Of course, such hypotheses are contentious; there is always the potential for confounding causes (in this case, of increased cancer risk due to a variety of risk factors at work in modern society) (Greaves 2000). Nonetheless, it has been known for centuries that nulliparity (not having children) raises breast cancer risk, and since at least the 1970s, it’s been widely known (at least in the cancer research community) that the more children one has, starting at a younger age, the lower the risk of breast cancer. In a 1970 case-control study conducted at eight different locations around the globe, a WHO group led by McMahon et al., estimated that “breast cancer risk for women having their first birth under the age of 20 years is about half that for nulliparous women,” and that “women having their first child when aged under 18 years have only about one-third the breast cancer risk of those whose first birth is delayed until the age of 35 years or more.” Evolutionary “byproduct” explanations appeal to our evolutionary history to explain this observation.