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CAN DIET AND LIFESTYLE PREVENT BREAST CANCER?<br />

style factors and breast cancer risk. We will present the sum<br />

of evidence of any specifıc links with pre- and postmenopausal<br />

breast cancer, ER-positive and ER-negative disease,<br />

and among women with familial risk, including those with<br />

the high-risk BRCA1 and BRCA2 breast cancer susceptibility<br />

genes.<br />

CANCER PREVENTION GUIDELINES<br />

The World Cancer Research Fund/American Institute for<br />

Cancer Research (2007) and the ACS (2012) have produced<br />

guidelines for prevention of a range of cancers that focus on<br />

weight control, regular exercise, reduced alcohol consumption,<br />

and a plant-based diet (Table 1). These guidelines are<br />

mainly informed by large cohort studies (i.e., prospective<br />

studies of 20,000 to 40,000 unaffected individuals), but also<br />

include some limited randomized data. Cohort studies include<br />

less recall and selection bias than case control studies;<br />

however, they can only highlight associations between lifestyle<br />

behaviors and cancer risk and cannot provide defınitive<br />

proof of their role in cancer etiology. Healthy lifestyle behaviors<br />

tend to cluster, thus someone who eats a healthy diet is<br />

often a healthy weight, exercises regularly, has a moderate<br />

alcohol intake, and does not smoke. Researchers attempt to<br />

adjust for other confounding risk factors in analyses but residual<br />

confounding cannot be ruled out.<br />

Defıning the true anticancer effects of lifestyle choices<br />

without confounding factors can only be achieved through<br />

randomized controlled trials. Such trials would need to be<br />

large (approximately 26,000 to 36,000 patients) and are<br />

therefore potentially prohibitively expensive. 6 Testing<br />

KEY POINTS<br />

<br />

<br />

<br />

<br />

<br />

Breast cancer is the most common cancer in women in<br />

both developed and less-developed countries. Rates of<br />

breast cancer are increasing worldwide, with particular<br />

increases in postmenopausal breast cancer and estrogen<br />

receptor-positive disease.<br />

Overweight, obesity, and weight gain are linked to<br />

postmenopausal breast cancer, whereas alcohol<br />

consumption and lack of exercise increase the risk for both<br />

pre- and postmenopausal breast cancer.<br />

Rapid height growth or exposure to smoking and alcohol in<br />

the period between menarche and first pregnancy may<br />

increase risk because the rapidly developing breast is<br />

particularly susceptible to carcinogenesis.<br />

Adherence to a healthy dietary pattern does not have<br />

specific effects on breast cancer risk but remains<br />

important for women because it reduces the risk of other<br />

common diseases, such as cardiovascular disease, diabetes,<br />

and dementia.<br />

Excess weight, alcohol, and lack of exercise increase risk<br />

among women with a family history, but their specific<br />

associations with carriers of BRCA1 and BRCA2 mutations<br />

requires further study.<br />

whether lifestyle interventions can prevent breast cancer is a<br />

bigger challenge than investigating their effects on CVD because<br />

cancer does not have the well-defıned surrogate endpoints<br />

available for CVD such as cholesterol and blood<br />

pressure. The absence of good markers for breast cancer risk<br />

makes it unlikely that randomized data will be available to<br />

support or refute cancer prevention recommendations in the<br />

near future.<br />

So what is the evidence that general cancer prevention<br />

guidelines can prevent breast cancer? Several large cohort<br />

studies have reported lower rates of breast cancer among<br />

women who adhere to these guidelines. Five studies of postmenopausal<br />

women reported 16% to 60% risk reductions,<br />

mainly linked to reduced body fatness and alcohol intake<br />

rather than specifıc differences in dietary patterns. 8-11 In contrast,<br />

studies of a cohort of both pre- and postmenopausal<br />

women showed 31% lower rates of breast cancer in women<br />

who adhered to specifıc dietary recommendations of increased<br />

wholegrain products and reduced meat and alcohol,<br />

rather than other lifestyle factors. 12 Adherence to cancer prevention<br />

guidelines have been reported to reduce risk among<br />

women with and without a family history of breast cancer 913<br />

and to reduce the risk for both ER-positive and ER-negative<br />

breast cancers. 8,11<br />

WEIGHT, WEIGHT GAIN, AND WEIGHT LOSS<br />

Cohort studies consistently link overweight, obesity, and<br />

adult weight gain to risk for postmenopausal breast cancer.<br />

Women who gain 20 kg or more during adulthood double<br />

their breast cancer risk. 14 These gains are also associated with<br />

large increases in the risk for diabetes (12-fold), 15 CVD<br />

(threefold), 16 and colorectal cancer (1.5-fold). 17 Modest<br />

weight loss (5 to 10%) reduces risk. In the Iowa Women’s<br />

Health Study of 34,000 women, a weight loss of at least 5%<br />

either before or after menopause reduced the risk for breast<br />

cancer by 25% to 40% compared to women who continued to<br />

gain weight, whereas Eliassen et al. reported a 50% reduction<br />

in risk in women with a 10% weight loss compared with<br />

weight-stable women in the Nurse’s Health Study of 37,000<br />

women. 18 Excess weight is mainly linked to the risk of developing<br />

ER-positive and ER-negative breast cancer after menopause<br />

and appears to be a factor among women with and<br />

without a family history. 14,19,20<br />

ALCOHOL<br />

Consumption of an additional 10 g of alcohol (1 unit; e.g., 284<br />

mL of 4% strength beer or cider, 25 mL of 40% strength spirits,<br />

or 80 mL of 12% strength wine) on a daily basis is estimated<br />

to increase risk by 2% to 12%, 20 with no further<br />

increase beyond 60 g of alcohol per day. 21 The increased risk<br />

is thought to be related to acetaldehyde-induced DNA strand<br />

deletions, chromosomal aberrations, and DNA adducts,<br />

downregulation of the tumor suppressor gene BRCA1, and<br />

increased estrogen and prolactin receptor activity. Data sug-<br />

asco.org/edbook | 2015 ASCO EDUCATIONAL BOOK<br />

e67

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