Overwhelming evidence indicates that the majority of breast cancer can be prevented with what we know now (see slide show: “Integrating Risk Across the Lifespan: The Case of Breast Cancer Prevention“). Let me review some of the justification for this statement. We know that we know from migrant studies that the rates of breast cancer vary substantially between countries and increase in the second generation after migration. We have also seen rapid changes in the rate of breast cancer within countries. For example, in Korea that the rate of breast cancer in women under 50 has doubled over a decade in large part reflecting changing reproductive patterns. Age at menarche has decreased and the number of children and age at first birth have changed to increase breast cancer risk. Later age at first birth and fewer births combine to drive up the rate of breast cancer.
We also have strong evidence from randomized trials of selective estrogen receptor modulators including tamoxifen and raloxifene where breast cancer incidence is halved. Finally in the high risk set of women with genetic predisposition through BRCA1/2 genes, surgery to remove the ovaries halves the risk of subsequent breast cancer.
Given this sort of evidence and data on other lifestyle factors that clearly modify risk, one might ask “why are we not acting to promote strategies that will prevent breast cancer now?” A range of reasons persist, including aversion to side effects from drug therapy to reduce breast cancer.
In addition to the evidence summarized above a growing body of research points to growth and development through the adolescent and early adult years as fundamental to the level of breast cancer risk experienced throughout the rest of life. Many studies clearly document that faster growth and greater height are related to increased risk of premalignant or benign breast lesions and also invasive breast cancer. Growing evidence also points to the adverse affect of alcohol consumption during adolescent and early adult years on risk of premalignant breast lesions and on risk of breast cancer.
In addition to the adverse effect of alcohol we reported the higher fiber intake during the adolescent years is related to lower risk of subsequent premalignant breast lesions. Perhaps equally as important is the strong and consistent evidence that higher levels of physical activity from menarche through the premenopausal years substantially reducing risk of breast cancer. These lifestyle factors offer much hope for prevention of breast cancer among our daughters and granddaughters, nieces, and grand nieces. Importantly, we have shown that the benefits of these lifestyle exposures during adolescent years are present for those with a family history of breast cancer as well as those without.
Other strong evidence arguing for the importance of exposures before the adult years comes from the evidence of radiation and risk of breast cancer. Both data from atomic bomb survivors as well as follow-up studies of women who receive radiation therapy for treatment of lymphoma showed that the breast is particularly susceptible to the carcinogenic effect of radiation before age 20.
Moving forward with prevention, we must focus on more than just the individual measures of alcohol intake, physical activity, and growth. Children grow up in the broader context of society, their schools and neighborhoods. Access to safe places to be active are entwined within this societal context. If we are to achieve the prevention of breast cancer we must consider the broader social environment in which children and young adults grow to maturity. Access to healthy diet with fruits, vegetables, and higher fiber foods, adequate physical activity, and limited or no alcohol are key components of this approach. With these healthy behaviors, we can substantially reduce risk of breast cancer through the premenopausal years.
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