A prospective study of breast size and premenopausal breast cancer incidence

Kusano, Aaron S.; Trichopoulos, Dimitrios; Terry, Kathryn L.; Chen, Wendy Y.; Willett, Walter C.; Michels, Karin B.

doi:10.1002/ijc.21588

Cited by 52 publications

(40 citation statements)

References 33 publications

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“…Those who did not wear a bra were asked to estimate their bra cup size. 17 Participants were not asked to formally measure their chest circumferences.…”

Section: Assessment Of Bra Cup Sizementioning

confidence: 99%

Breast size and risk of type 2 diabetes mellitus

Ray¹,

Mohllajee²,

Dam³

et al. 2007

Canadian Medical Association Journal

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O besity is an established risk factor for type 2 diabetes mellitus.1,2 Affected individuals show signs of insulin resistance and hyperinsulinemia, a process that may begin in childhood.3,4 Pre-adolescent obesity is also an important predictor of age of onset of breast development in young women, and of breast size after puberty. 5,6 Premature onset of puberty is preceded by childhood insulin resistance, hyperinsulinemia and hyperandrogenemia, 7 which may persist after puberty 8 and continue into early adulthood. 9Although an elevated body mass index (BMI)10,11 and central adiposity 12 are established risk factors for insulin resistance and the onset of type 2 diabetes mellitus, little is known about the contribution of extra-abdominal adipose tissue, including breast tissue, about 60% of which is fatty tissue, to this process.13,14 We hypothesized that a woman's breast size in late adolescence reflects her predisposition to insulin resistance and type 2 diabetes mellitus that is both additive to, and independent of, BMI. We explored this hypothesis in conjunction with the Nurses' Health Study II by relating bra cup size, a proxy for breast size, to the onset of type 2 diabetes mellitus. Methods ParticipantsThe Nurses' Health Study II is a prospective cohort study, which was initiated in 1989 and is ongoing. The study involves 116 609 women, more than 90% of whom are white, from 14 US states.15 At the time of enrolment, participants were between the ages of 25 and 42, and they completed a detailed baseline questionnaire about their health, lifestyles and anthrometric characteristics. They continue to complete follow-up questionnaires on a biennial basis. We included all women who had concomitant information about bra cup size at age 20 and BMI at age 18, for a total of 92 106 participants. We excluded women who had already received a diagnosis of diabetes mellitus or who had a history of gestational diabetes.

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“…Those who did not wear a bra were asked to estimate their bra cup size. 17 Participants were not asked to formally measure their chest circumferences.…”

Section: Assessment Of Bra Cup Sizementioning

confidence: 99%

Breast size and risk of type 2 diabetes mellitus

Ray¹,

Mohllajee²,

Dam³

et al. 2007

Canadian Medical Association Journal

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“…Indirect measures of mammary gland mass such as breast size have been positively associated with breast cancer risk in lean women where it may be less likely to reflect adiposity (191,192). High-density parenchymal patterns have also been considered a surrogate for mammary gland mass and are strongly associated with breast cancer risk (193,194).…”

Section: Prenatal Risk Factors For Breast Cancermentioning

confidence: 99%

“…Interestingly, data show that among Chinese women who migrated to the United States, the most acculturated have the densest breasts, and that this is not explained by reproductive and lifestyle factors related to density (195). Whereas high-density patterns are a surrogate for the combination of the proportion of the breast occupied by epithelium and stroma (192), their correlation with actual ductal mass is unknown. Finally, the causal relevance of ductal mass is still simply a hypothesis.…”

Section: Prenatal Risk Factors For Breast Cancermentioning

confidence: 99%

Exploring the Underlying Hormonal Mechanisms of Prenatal Risk Factors for Breast Cancer: A Review and Commentary

Troisi

Potischman

Hoover

2007

Cancer Epidemiology, Biomarkers &Amp; Prevention

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Prenatal factors have been hypothesized to influence subsequent breast cancer development. Directly evaluating the associations of in utero exposures with risk, however, presents several methodologic and theoretical challenges, including the long induction period between exposure and disease and the lack of certainty regarding the critical timing of exposure. Indirect evaluation of these associations has been achieved by use of proxies such as gestational and neonatal characteristics. Evidence suggests that preeclampsia is associated with a reduced breast cancer risk, whereas high birth weight and dizygotic twinning seem associated with an increased risk. Asians born in Asia have substantially lower breast cancer risks than women born in the West. Although data thus far are few, what exists is not consistent with a unifying hypothesis for a particular biological exposure (such as estrogens or androgens) during pregnancy as mediating the observed associations between pregnancy factors and breast cancer risk. This suggests that additional studies of prenatal factors should seek to broaden the range of hormones, growth, and other endocrine factors that are evaluated in utero. Once candidate biomarkers are identified, assessing them with respect to breast cancer and with intermediate end points in carcinogenesis should be a priority. In addition, investigations should explore the possibility that in utero exposures may not act directly on the breast, but may alter other physiologic pathways such as hormone metabolism that have their effect on risk later in life. (Cancer Epidemiol Biomarkers Prev 2007;16(9):1700 -12)

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“…There is no direct correlation between breast density and size after adjustment for waist-to-hip ratio and BMI (Beijerinck et al, 1995). However, a larger breast size has been associated with increased breast cancer risk (Kato et al, 1995), especially in lean women (Kusano et al, 2006) or in women with proliferative breast disease (Dupont and Page, 1987). We therefore investigated whether coffee intake was associated with breast volume in young women and whether any association was modified by the CYP1A2*1F genotype.…”

mentioning

confidence: 98%

Coffee intake and CYP1A2*1F genotype predict breast volume in young women: implications for breast cancer

et al. 2008

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As breast volume may be associated with heart cancer risk, we studied the relationship between breast volume, CYP1A2*1F and coffee intake. Among healthy premenopausal non-hormone users, 3 þ cups per day was associated with lower volume only in C-allele carriers (P interaction ¼ 0.02), which is consistent with reports that coffee protects only C-allele carriers against breast cancer. A recent study reported that coffee reduced the risk of breast cancer in BRCA1 carriers with the CYP1A2*1F C-allele but not in those with the CYP1A2*1F A/A genotype (Kotsopoulos et al, 2007). Another study found significantly lower coffee consumption in sporadic breast cancer cases with at least one C-allele compared with the A/A genotype (Bågeman et al, 2008) in spite of the fact that coffee consumption is similar across CYP1A2*1F genotypes in the general population (Cornelis et al, 2006). Some studies (Vatten et al, 1990;Baker et al, 2006;Nkondjock et al, 2006;Ganmaa et al, 2008), but not all (Rosenberg et al, 1985;Vatten et al, 1990;McLaughlin et al, 1992;Stensvold and Jacobsen, 1994;Michels et al, 2002), have reported that moderate-to-high coffee consumption protects against breast cancer, though a mechanism is unknown. None of these studies took CYP1A2*1F into account.Coffee is metabolised by the CYP1A2 enzyme, which also plays a key role in oestrogen metabolism (Le Marchand et al, 1997;Lee et al, 2003). Coffee contains not only caffeine but also phytooestrogens that can interact with and even block the oestrogen receptor (Magee and Rowland, 2004). Women with high coffee intake and the highly inducible CYP1A2*1F A/A genotype (Sachse et al, 1999) have a high 2-hydroxyoestrone (2-OHE1) to 16a-OHE1 ratio (Jernström et al, 2003;Bradlow et al, 2006;Klug et al, 2006). 2-Hydroxyoestrone is a weak oestrogen (Schneider et al, 1984), whereas 16a-OHE1 is procarcinogenic (Telang et al, 1992). In line with this, we found that breast volume in breast cancer patients was significantly higher in women with a lower 2-OHE to 16a-OHE1 ratio . Coffee also affects testosterone and SHBG levels (Ferrini and Barrett-Connor, 1996;Nagata et al, 1998). Although hormonal regulation of breast tissue has been extensively studied, little is known about hormones, genes, diet influence, density, size and diseases of the breast.Mammographic density is a strong risk factor for breast cancer (Boyd et al, 2005), the risk increasing with larger percentage density. The non-inducible CYP1A2*1F C-allele was associated with the percent density in normal-weight postmenopausal women not using hormone therapy (Takata et al, 2007). CYP1A2 enzyme activity has also been associated with density (Hong et al, 2004), and coffee induces CYP1A2 enzyme activity (Djordjevic et al, 2007). There is no direct correlation between breast density and size after adjustment for waist-to-hip ratio and BMI (Beijerinck et al, 1995). However, a larger breast size has been associated with increased breast cancer risk (Kato et al, 1995), especially in lean women (Kusano et al, 2006) or in women wi...

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A prospective study of breast size and premenopausal breast cancer incidence

Cited by 52 publications

References 33 publications

Breast size and risk of type 2 diabetes mellitus

Breast size and risk of type 2 diabetes mellitus

Exploring the Underlying Hormonal Mechanisms of Prenatal Risk Factors for Breast Cancer: A Review and Commentary

Coffee intake and CYP1A2*1F genotype predict breast volume in young women: implications for breast cancer

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