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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