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Body size, modifying factors, and postmenopausal breast cancer risk in a multiethnic population: the San Francisco Bay Area Breast Cancer Study.
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PMID:  23762816     Owner:  NLM     Status:  Publisher    
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Data on body size and postmenopausal breast cancer in Hispanic and African American women are inconsistent, possibly due to the influence of modifying factors. We examined associations between adiposity and risk of breast cancer defined by hormone receptor status in a population-based case-control study conducted from 1995-2004 in the San Francisco Bay Area. Multivariate adjusted odds ratios and 95% confidence intervals were calculated using unconditional logistic regression. Associations with body size were limited to women not currently using menopausal hormone therapy (801 cases, 1336 controls). High young-adult body mass index (BMI) was inversely associated with postmenopausal breast cancer risk, regardless of hormone receptor status, whereas high current BMI and high adult weight gain were associated with two-fold increased risk of estrogen receptor and progesterone receptor positive breast cancer, but only in women with a low young-adult BMI (≤22.4 kg/m(2)) or those with ≥15 years since menopause. Odds ratios were stronger among non-Hispanic Whites than Hispanics and African Americans. Waist circumference and waist-to-height ratio increased breast cancer risk in Hispanics and African Americans only, independent of BMI. These findings emphasize the importance of considering tumor hormone receptor status and other modifying factors in studies of racially/ethnically diverse populations.
Authors:
Esther M John; Amanda I Phipps; Meera Sangaramoorthy
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Type:  JOURNAL ARTICLE     Date:  2013-5-24
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Title:  SpringerPlus     Volume:  2     ISSN:  2193-1801     ISO Abbreviation:  Springerplus     Publication Date:  2013 Dec 
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Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, WA 98109 USA ; Division of Epidemiology, Department of Health Research and Policy, and Stanford Cancer Institute, Stanford University School of Medicine, Stanford, CA 94305 USA.
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© John et al.; licensee Springer. 2013
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Received Day: 16 Month: 4 Year: 2013
Accepted Day: 29 Month: 4 Year: 2013
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DOI: 10.1186/2193-1801-2-239

Body size, modifying factors, and postmenopausal breast cancer risk in a multiethnic population: the San Francisco Bay Area Breast Cancer Study
Esther M JohnAff5Aff4 Address: esther.john@cpic.org
Amanda I PhippsAff5 Address: aphipps@fhcrc.org
Meera SangaramoorthyAff5 Address: meera.sangaramoorthy@cpic.org
Cancer Prevention Institute of California, 2201 Walnut Ave, Suite 300, Fremont, CA 94538 USA
Division of Epidemiology, Department of Health Research and Policy, and Stanford Cancer Institute, Stanford University School of Medicine, Stanford, CA 94305 USA
Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, WA 98109 USA

Introduction

Obesity has long been recognized as a risk factor for postmenopausal breast cancer (BC) in studies of primarily non-Hispanic White (NHW) women ( World Cancer Research Fund / American Institute for Cancer Research 2007 ). Only three studies in Hispanics ( Wenten et al. 2002 ; Slattery et al. 2007 ; White et al. 2012 ) and eight studies in African Americans (AA) ( White et al. 2012 ; Austin et al. 1979 ; Schatzkin et al. 1987 ; Adams-Campbell et al. 1996 ; Hall et al. 2000 ; Zhu et al. 2005 ; Palmer et al. 2007 ; Berstad et al. 2010 ) examined the relation between obesity and postmenopausal BC risk, and some of their findings contradict those reported for NHW women, suggesting differences in effects by racial/ethnic groups ( Slattery et al. 2007 ; Sexton et al. 2011 ). In NHWs, BC risk is increased by 3-5% both per 2 kg/m2 increase in body mass index (BMI) and per 5 kg of weight gain ( World Cancer Research Fund / American Institute for Cancer Research 2007 ). Young-adult obesity, on the other hand, has been associated with reduced postmenopausal BC risk, both in cohort ( Barnes-Josiah et al. 1995 ; Huang et al. 1997 ; Morimoto et al. 2002 ; Ahn et al. 2007 ) and case–control ( Berstad et al. 2010 ; Chu et al. 1991 ; Brinton & Swanson 1992 ; Magnusson et al. 1998 ) studies. A number of factors appear to modify the relation with body size. Increased risks associated with BMI and weight gain may be limited to women with a low young-adult BMI ( Chu et al. 1991 ; Canchola et al. 2012 ). Stronger associations with body size have been found in women with estrogen receptor and progesterone receptor positive (ER+PR+) BC ( Potter et al. 1995 ; Huang et al. 2000 ; Colditz et al. 2004 ; Suzuki et al. 2009 ), those not using menopausal hormone therapy (HT) ( Morimoto et al. 2002 ; Friedenreich 2001 ; Feigelson et al. 2004 ), or with longer time since menopause ( Chu et al. 1991 ; Magnusson et al. 1998 ; Macinnis et al. 2004 ). Data on abdominal obesity and BC risk in postmenopausal women are also inconsistent ( World Cancer Research Fund / American Institute for Cancer Research 2007 ) and uncertainties remain whether associations are independent of overall obesity or differ by race/ethnicity.

We report on the relation between overall and abdominal adiposity and risk of postmenopausal BC defined by hormone receptor status in a multiethnic population, and the role of modifying factors.


Materials and methods
Study population

The San Francisco Bay Area Breast Cancer Study, a population-based case-control study ( John et al. 2003 ; John et al. 2005 ), identified 17,581 women aged 35–79 years with newly diagnosed invasive BC through the Greater Bay Area Cancer Registry. Following telephone screening on study eligibility (83% participation), 2,571 cases were selected (all Hispanics diagnosed from 1995–2002, all AAs diagnosed from 1995–1999, and a 10% random sample of NHWs diagnosed from 1995–1999). An in-person interview was completed by 2,258 (88%) cases, including 1,119 (89%) Hispanics, 543 (87%) AAs, and 596 (86%) NHWs.

Population controls, identified through random-digit dialing, were frequency-matched on race/ethnicity and 5-year age group ( John et al. 2003 ). Of 3,170 eligible controls, 2,706 (85%) completed the in-person interview, including 1,462 (88%) Hispanics, 598 (82%) AAs, and 646 (83%) NHWs.

This analysis was restricted to postmenopausal women (1,389 cases, 1,644 controls). Women were considered postmenopausal if their periods had stopped more than one year prior to diagnosis (cases) or selection into the study (controls), if they reported a bilateral oophorectomy, or if they were aged ≥55 years at the time of diagnosis/selection and had either started hormone therapy prior to the cessation of menses or had had a simple hysterectomy (without oophorectomy).

Data collection

Information on adult height, weight in the reference year (defined as the calendar year before diagnosis for cases or before selection into the study for controls), young-adult weight, and other BC risk factors was collected using a structured questionnaire, administered in English or Spanish. Young-adult weight was based on reported weight at age 25–30 years for cases diagnosed before May 1998 and their matched controls, and on reported weight at age 20–29 years for cases diagnosed in May 1998 or later and their matched controls. Interviewers also took measurements of weight, height, waist and hip circumference (described in ( John et al. 2010 )). Lifetime physical activity was assessed, as described elsewhere ( John et al. 2003 ). Usual dietary intake and alcohol consumption during the reference year was assessed by a modified version of the Block food frequency questionnaire ( Block et al. 1986 ). Cancer registry information on ER and PR status was available for 85% of cases. The study was approved by the Institutional Review Board of the Cancer Prevention Institute of California and participants provided written informed consent.

Body size variables

Current BMI was calculated as weight (kg) divided by height squared (m2), based on measured height at interview (or self-reported height for 10% of cases and 9% of controls who declined height measurements) and self-reported weight in the reference year (or measured weight at interview for 1% of cases and 3% of controls without self-report). BMI was classified as normal weight (<25.0 kg/m2), overweight (25.0-29.9 kg/m2) and obese (≥30.0 kg/m2) ( WHO 2000 ). Underweight (BMI <18.5 kg/m2) women (9 cases, 16 controls) were grouped with normal weight women. Young-adult BMI was based on measured height at interview and self-reported weight in a woman’s twenties. Adult weight gain was calculated as the difference between self-reported young-adult weight and weight in the reference year. Waist-to-hip ratio (WHR) was calculated as a measure of body fat distribution reflecting both adipose tissue and muscle mass; waist-to-height ratio (WHtR) was calculated as a measure of visceral adiposity independent of height, which may more directly reflect abdominal adiposity ( Molarius & Seidell 1998 ). WHR, WHtR, and waist and hip circumferences were categorized according to the tertile distribution among controls.

Statistical analysis

Unconditional logistic regression was used to calculate odds ratios (OR) and 95% confidence intervals (CI) comparing cases to controls, both overall and separately for each racial/ethnic group. Polytomous logistic regression was used to compare ER+PR+ and ER-PR- case groups with a common control group. For all BCs combined and ER+PR+ BCs, multivariate analyses were adjusted for age (continuous) and factors significantly associated with BC risk in our study: birth place, education, first-degree family history of BC, personal history of benign breast disease, age at menarche, number of full-term pregnancies, age at first full-term pregnancy, lifetime breast-feeding, average lifetime physical activity, alcohol consumption, and caloric intake, categorized as shown in the tables. For ER-PR- BCs, analyses were adjusted for age, birth place, age at menarche, and lifetime breast-feeding. Analyses of all BCs combined were also adjusted for race/ethnicity. Analyses of current BMI, young-adult BMI and weight gain were mutually adjusted for each other. Linear trends were assessed across ordinal values of categorical variables. Significant differences in ORs between groups were tested using the Wald statistic P value. Two-sided P values are reported for tests of trend and interaction, with P values <0.05 considered statistically significant.

We assessed associations with current BMI and weight change within strata defined by median young-adult BMI (≤22.4 kg/m2, >22.4 kg/m2), median time since menopause (<15, ≥15 years), and, in analyses of abdominal adiposity, by current BMI (<25.0 kg/m2, ≥25.0 kg/m2). Primary analyses were restricted to women not currently using menopausal HT, as previous studies have found no associations with body size among current HT users ( Huang et al. 1997 ; Morimoto et al. 2002 ). Current HT use was defined as starting HT prior to the year of diagnosis/selection and reported use during the year of diagnosis/selection. All other women were classified as non-current HT users. Time since menopause was calculated as the difference between age at menopause and age at diagnosis/selection. Age at menopause was based on self-report for women with natural menopause and age at bilateral oophorectomy for women with surgical menopause.

The final analysis was based on 2,884 postmenopausal women (1,316 cases, 1,568 controls) after excluding 34 cases and 50 controls with missing information on confounding variables and 39 cases and 26 controls with unreliable caloric intake (<600 kcal/day or >5,000 kcal/day). Statistical analyses were conducted using SAS version 9.3 software (SAS Institute, Inc., Cary, North Carolina).


Results

Cases were more likely than controls to be U.S.-born, have a first-degree family history of BC, a personal history of benign breast disease, higher education, earlier menarche, fewer full-term pregnancies, a shorter duration of breast-feeding, lower lifetime physical activity, and higher alcohol consumption (Table 1).

Body size characteristics differed by race/ethnicity (Table 2). Among controls, the proportion of currently obese women (BMI ≥30.0 kg/m2) was higher in AAs and Hispanics than in NHWs. High young-adult BMI was twice as common in Hispanics as in NHWs, whereas the proportion of women with high weight gain was similar in the two groups. The prevalence of high weight gain, large waist and hip circumferences, and high WHR was lowest in NHWs, intermediate in Hispanics, and more than twice as high in AAs than in NHWs.

For women not currently using HT, associations with current BMI and adult weight gain were limited to those with ER+PR+ tumors, although after adjustment for weight gain, no association remained with current BMI (Table 3). The positive association with weight gain was not altered by adjustment for current BMI (Table 3) or young-adult BMI (data not shown), and was largely driven by the increased risk found for NHW women. Young-adult BMI was associated with reduced risk of postmenopausal BC, with similar results for BC overall (>23.7 vs. ≤21.2 kg/m2: OR = 0.68, 95% CI:0.54-0.86, Ptrend < 0.01) and ER+PR+ BC (>23.7 vs. ≤21.2 kg/m2: OR = 0.73, 95% CI:0.54-0.98, Ptrend = 0.04). Inverse associations, however, were found only among Hispanic and NHW women.

Young-adult BMI was an important modifying factor (Table 4). For ER+PR+ BC, associations with high BMI (OR = 1.97, Ptrend = 0.01) and high weight gain (OR = 1.71, Ptrend = 0.03) were limited to women with a young-adult BMI ≤22.4 kg/m2. No increased risks were found among women with both high young-adult BMI and high current BMI. Associations were also influenced by time since menopause. High weight gain was associated with two-fold increased risks of BC overall (OR = 2.71, 95% CI:1.29-5.69, Ptrend = 0.01) and ER+PR+ BC (OR = 2.47, 95% CI:1.03-5.94, Ptrend = 0.03) only in women who had experienced menopause ≥15 years ago. Similarly, the inverse association of young-adult BMI with BC risk overall was seen only in women with ≥15 years since menopause (>23.7 vs. ≤21.2 kg/m2: OR = 0.59, 95% CI:0.41-0.85, Ptrend < 0.01).

Waist circumference was associated with ER+PR+ BC in Hispanics (Ptrend = 0.01) and AAs (Ptrend = 0.05) only, with two- to three-fold increased ORs for large waist size that were independent of current BMI (Table 5). Associations were slightly stronger for ER+PR+ disease than BC overall. Large hip circumference was associated with elevated ORs in Hispanics and NHWs, with a significant trend in Hispanics (Ptrend = 0.01). There was no association with WHR (data not shown). High WHtR was associated with elevated ORs in Hispanics and AAs, with a significant trend in Hispanics (Ptrend = 0.01). For waist and hip circumferences and WHtR, associations did not vary by time since menopause (data not shown). Considering the joint effects of abdominal adiposity and overall adiposity (Table 6), we found that large waist circumference was associated with increased BC risk only in women with a BMI <25 kg/m2. A similar pattern was seen for WHtR. For ER+PR+ disease, ORs were elevated, regardless of BMI, but significant only in women with a BMI ≥25 kg/m2.

For ER-PR- BC, there were no associations with current BMI and weight gain, whereas a strong inverse association was found with young-adult BMI (>23.7 vs. ≤21.2 kg/m2: OR = 0.61, 95% CI:0.38-0.97, Ptrend = 0.04) (Table 7). Modest positive associations with waist and hip circumferences were strengthened after adjustment for current BMI (Ptrend = 0.07 and 0.01, respectively). Sample sizes of ER-PR- cases were too small for further stratification by race/ethnicity (9 NHWs, 48 AAs, 79 Hispanics).

Among women currently using HT (289 cases, 498 controls), there was no evidence of significant associations between any of the body size measures examined and BC risk overall or ER+PR+ disease (data not shown).


Discussion

In postmenopausal women not currently using HT, weight gain was positively associated with risk of ER+PR+ BC and was a stronger predictor of risk than current BMI. The highest elevations in risks were found in subgroups of women with a low young-adult BMI or ≥15 years since menopause. Young-adult obesity was associated with reduced BC risk. High waist circumference and WHtR were associated with increased BC risk, independent of current BMI. Associations with weight gain and young-adult BMI were stronger for NHWs than Hispanics and AAs, whereas associations with waist and WHtR were present only in Hispanic and AA women.

Consistent with other reports ( White et al. 2012 ; Huang et al. 1997 ; Ahn et al. 2007 ; Feigelson et al. 2004 ), we found that weight gain was an important risk factor for postmenopausal BC, independent of current BMI. For current BMI no association remained after adjustment for weight gain. In agreement with other studies ( Vrieling et al. 2010 ), we found that the relation with weight gain was limited to ER+PR+ BC. Risk was increased two-fold for currently obese women (BMI ≥30 kg/m2) who had a young-adult BMI <22.4 kg/m2, which is in agreement with other studies ( Ahn et al. 2007 ; Canchola et al. 2012 ). We found modest effect modification by young adult BMI for weight gain, though some other studies did not ( Barnes-Josiah et al. 1995 ; Feigelson et al. 2004 ; van den Brandt et al. 1997 ; Lahmann et al. 2005 ). In contrast, BC risk was not increased in women who were obese throughout their adult life, consistent with other ( Ahn et al. 2007 ; Canchola et al. 2012 ), but not all reports ( Barnes-Josiah et al. 1995 ). In agreement with other reports ( Chu et al. 1991 ; Magnusson et al. 1998 ; Macinnis et al. 2004 ), we found time since menopause to be another important modifying factor, with two-fold increased risks of ER+PR+ BC with weight gain only among women with ≥15 years since menopause. Weight gain during adulthood largely reflects an increase in body fat which serves as an important source of estrogen production in postmenopausal women ( Siiteri 1987 ). The role of an estrogen-related pathway is further supported by the observation that the associations with BMI and weight gain are limited to ER+PR+ tumors ( Suzuki et al. 2009 ; Vrieling et al. 2010 ).

Prior findings in AA and Hispanic women for BMI are inconsistent. In our study, OR estimates were increased only for ER+PR+ disease and were of similar magnitude in the three racial/ethnic groups. Two studies in AAs reported elevated risks of ER+PR+ disease ( Palmer et al. 2007 ; Berstad et al. 2010 ), and, similar to our study, there was no evidence of an association with BMI for BC overall. Other studies did not consider hormone receptor status ( White et al. 2012 ; Schatzkin et al. 1987 ; Adams-Campbell et al. 1996 ; Hall et al. 2000 ; Zhu et al. 2005 ), and not all found a positive association with BMI ( White et al. 2012 ; Schatzkin et al. 1987 ; Zhu et al. 2005 ). In black women from Nigeria ( Ogundiran et al. 2010 ; Okobia et al. 2006 ; Adebamowo et al. 2003 ) and Barbados ( Nemesure et al. 2009 ), no associations with BMI were found. In Hispanic women, BMI was not associated with BC overall ( Wenten et al. 2002 ; Slattery et al. 2007 ; White et al. 2012 ) and ER+ disease ( Slattery et al. 2007 ), even among women not using HT ( Slattery et al. 2007 ; White et al. 2012 ).

We found that high weight gain was associated with a two-fold increased risk of ER+PR+ BC in NHW women. In AAs and Hispanics, the associations were much weaker, likely due to the higher prevalence of young-adult obesity in these groups. Of three studies in AAs that reported on weight gain and BC risk ( White et al. 2012 ; Zhu et al. 2005 ; Palmer et al. 2007 ), only one found a significant association with BC risk overall ( White et al. 2012 ). In Hispanic women from New Mexico, large weight gain was associated with a two-fold increased risk of ER+PR+ disease and, for BC overall, a significant trend with weight gain was limited to women with a BMI <22 kg/m2 at age 18 years ( Wenten et al. 2002 ). Two other studies in Hispanics found no association with weight gain ( Slattery et al. 2007 ; White et al. 2012 ). In order to address these inconsistent findings with BMI and weight gain for AA and Hispanic women, future studies should examine the modifying effect of young-adult obesity with larger sample sizes. This is particularly important since AA and Hispanic women have a higher prevalence of young-adult obesity than NHWs, as found in our study as well as others ( Flegal et al. 2010 ).

Our finding of a strong inverse association of postmenopausal BC risk with high young-adult BMI, which was independent of weight change or current BMI, is consistent with other reports ( White et al. 2012 ; Palmer et al. 2007 ; Berstad et al. 2010 ; Barnes-Josiah et al. 1995 ; Huang et al. 1997 ; Morimoto et al. 2002 ; Ahn et al. 2007 ; Chu et al. 1991 ; Brinton & Swanson 1992 ; Magnusson et al. 1998 ), although in some studies there was no association with young-adult BMI ( Canchola et al. 2012 ; Feigelson et al. 2004 ; Lahmann et al. 2005 ). In agreement with a large meta-analysis ( Suzuki et al. 2009 ), we found that the inverse association with young-adult BMI did not differ by tumor hormone receptor status. We further found an inverse association, regardless of HT use, as reported by others ( Morimoto et al. 2002 ; Ahn et al. 2007 ). These findings do not support an estrogen-related mechanism underlying the association with young-adult BMI.

Abdominal adiposity has been proposed to be more important in estrogen production than adiposity at other body sites ( Pinheiro et al. 2009 ). Studies in primarily NHW women, however, have produced inconsistent results ( World Cancer Research Fund / American Institute for Cancer Research 2007 ). Not all studies considered HT use or ER/PR status, or adjusted for overall adiposity ( Canchola et al. 2012 ; Potter et al. 1995 ; Huang et al. 2000 ). Our findings confirm previous reports of positive associations with waist circumference and WHtR only in women not currently using HT ( Morimoto et al. 2002 ; Huang et al. 1999 ; Friedenreich et al. 2002 ) and stronger associations for ER+PR+ disease ( Canchola et al. 2012 ; Potter et al. 1995 ; Huang et al. 2000 ). We found no association with WHR, whereas elevated WHtR was associated with increased risk, in agreement with another study ( Canchola et al. 2012 ). Both waist circumference and WHtR may be better measures of abdominal adiposity than WHR ( Molarius & Seidell 1998 ; Rankinen et al. 1999 ). In some studies, the association with abdominal adiposity was attenuated after adjustment for BMI ( Morimoto et al. 2002 ; Lahmann et al. 2004 ; Tehard & Clavel-Chapelon 2006 ), whereas in our study associations became stronger after BMI-adjustment. Among women with BMI <25 kg/m2, large waist circumference and high WHtR were associated with two-fold increased risks of BC overall. Contrary to another study that reported an association between abdominal adiposity and ER+PR+ tumors only in normal-weight women ( Canchola et al. 2012 ), we found elevated ORs for ER+PR+ tumors, regardless of BMI, with statistically significant estimates in overweight/obese women.

Unlike NHW women, for whom we found no associations with waist circumference and WHtR, AAs and Hispanics had two- to three-fold increased risk of ER+PR+ BC. We found no association with WHR in any racial/ethnic group. This latter finding is consistent with two studies in AA women ( Hall et al. 2000 ; Palmer et al. 2007 ), but contrasts with reports from Nigeria ( Ogundiran et al. 2010 ) and Barbados ( Nemesure et al. 2009 ), where large waist circumference and high WHR increased BC risk. Similarly, the two-fold increased risk of ER+PR+ disease associated with large hip circumference that we observed for NHW and Hispanic women was not seen in AAs, whereas previous studies from Nigeria ( Ogundiran et al. 2012 ) and Barbados ( Nemesure et al. 2009 ) reported inverse associations with hip circumference. In the Nigerian study, associations with abdominal adiposity were stronger or limited to women with a BMI <25 kg/m2 ( Ogundiran et al. 2012 ), consistent with our findings. In the only study that examined abdominal adiposity in postmenopausal Hispanic women, hip circumference and WHR were not associated with BC risk in not recent HT users ( Slattery et al. 2007 ), which differs from our finding. Given these conflicting reports, it remains to be determined whether there are true racial/ethnic differences in the effects of abdominal adiposity on BC risk. Abdominal fat comprises different fat stores, and AAs and NHWs differ in abdominal depot-specific body fat (e.g., visceral vs. subcutaneous adipose tissue) ( Katzmarzyk et al. 2010 ). Whether different fat stores affect BC risk differentially has not been examined. Our results suggest that studies should assess multiple measures of adiposity in racially/ethnically diverse populations.

Our analyses of body size and ER-PR- BC risk were limited by small numbers. Consistent with most other studies ( Suzuki et al. 2009 ; Yang et al. 2011 ), we found no associations with current BMI and weight gain, although there are some reports of inverse ( Berstad et al. 2010 ; Setiawan et al. 2009 ) or positive associations with BMI ( Ritte et al. 2012 ) and positive associations with weight gain ( Canchola et al. 2012 ). Unlike other studies ( Canchola et al. 2012 ; Potter et al. 1995 ), we found a strong inverse association with young-adult BMI and ER-PR- disease. Adjustment for BMI strengthened the positive association between waist (Ptrend = 0.07) and hip (Ptrend = 0.01) circumferences and risk of ER-PR- BC, but, consistent with other studies ( Canchola et al. 2012 ; Potter et al. 1995 ; Huang et al. 2000 ), we found no significant association with WHR or WHtR. The association between BMI, weight gain, and abdominal adiposity warrants further examination in studies with larger numbers of ER-PR- cases. This is particularly important since few risk factors have been identified for hormone receptor negative BC ( Althuis et al. 2004 ; Ma et al. 2006 ), which disproportionately affects AA and Hispanic women ( Ray & Polite 2010 ).

Our findings should be considered in light of some limitations. Due to the concern that weight may be impacted by BC diagnosis and treatment, we relied on self-reported weight during the reference year. Although we cannot exclude the possibility of inaccurately recalled weight, among subjects for whom measured and self-reported weight was available, the correlation between the two measures was high (r = 0.85 for cases, r = 0.92 for controls). For waist and hip circumference we had to rely on measurements taken after diagnosis which may have also resulted in misclassification. Finally, some subgroup analyses were limited by small sample sizes, and analyses of potential modifying factors (young-adult BMI, time since menopause) could not be further stratified by race/ethnicity. Larger studies or analyses of pooled data will be necessary to further explore the role of these modifying factors in Hispanics and AAs.

Our study also has several important strengths, including a population-based design, high participation rates among cases and controls in each racial/ethnic group, assessment of both overall and abdominal adiposity, detailed data on established BC risk factors, and availability of data on tumor hormone receptor status for most cases. The racial/ethnic diversity of the study population allowed us to assess associations with body size in Hispanic and AA women, thus contributing to the relatively sparse data in these two racial/ethnic populations that experience a greater burden of obesity than NHWs.

It has been estimated that as many as one third of new postmenopausal BC cases may be attributable to adult weight gain ( Huang et al. 1997 ). Given that a number of BC risk factors relate to events well before menopause (e.g., age at menarche, age at first birth) or characteristics that cannot easily be modified (e.g., BC family history), observed associations with body size suggest possible approaches to lowering BC risk in older women through weight maintenance, avoidance of further weight gain and abdominal adiposity, or weight loss. However, promoting overweight at a young age, as a means of reducing BC risk after menopause, should not be encouraged, given the many adverse health effects associated with obesity, including other cancers ( Calle & Kaaks 2004 ; Chen et al. 2011 ).


Notes

Competing interests

The authors declare that they have no competing interests.

Authors’ contributions

EMJ was responsible for the study design, securing funding, directing the study implementation and data analysis, and drafting the manuscript. AIP contributed to the study design and writing of the grant proposal that funded this analysis, performed preliminary analyses, and contributed to the writing of the manuscript. MS was responsible for performing the statistical analyses, helped conduct literature review, and contributed to the writing of the manuscript. All authors read and approved the final manuscript.

Abbreviations

AA African American
BC Breast cancer
BMI Body mass index
CI Confidence interval
ER Estrogen receptor
HT Hormone therapy
OR Odds ratio
NHW non-Hispanic white
PR Progesterone receptor
WHR Waist-to-hip ratio
WHtR Waist-to-height ratio

This work was supported by the National Cancer Institute (grant R03 CA121875). Data collection for the parent study was funded by National Cancer Institute (grants R01 CA63446 and R01 CA77305); the U.S. Department of Defense (grant DAMD17-96-1-6071); and the California Breast Cancer Research Program (grants 4JB-1106 and 7PB-0068). The collection of cancer incidence data used in this study was supported by the California Department of Public Health as part of the statewide cancer reporting program mandated by California Health and Safety Code Section 103885; the National Cancer Institute’s Surveillance, Epidemiology and End Results Program under contract HHSN261201000140C awarded to the Cancer Prevention Institute of California, contract HHSN261201000035C awarded to the University of Southern California, and contract HHSN261201000034C awarded to the Public Health Institute; and the Centers for Disease Control and Prevention’s National Program of Cancer Registries, under agreement U58DP003862-01 awarded to the California Department of Public Health. The ideas and opinions expressed herein are those of the authors and endorsement by the State of California, Department of Public Health the National Cancer Institute, and the Centers for Disease Control and Prevention or their Contractors and Subcontractors is not intended nor should be inferred.


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Tables
[TableWrap ID: Tab1] Table 1 

Characteristics of postmenopausal cases and controls


Cases (n = 1,316) Controls (n = 1,568) P value
n %a n %a
Age (years)
 35–44 20 2 25 2
 45–54 199 15 260 17
 55–64 531 40 625 40
 65–74 407 31 509 33
 ≥75 159 12 149 10
Race/ethnicity
 Hispanic 614 47 804 51
 Non-Hispanic White 389 30 399 26
 African American 313 24 365 23
Joint ER/PR status
 ER+PR+ 714 54
 ER+PR- 168 13
 ER-PR+ 21 2
 ER-PR- 204 16
 Missing 209 16
Menopausal hormone therapy use <0.01
 Never 517 39 644 41
 Former 284 22 692 44
 Current 498 38 214 14
 Missing 17 1 18 1
Place of birth <0.01
 U.S.-bornb 1,014 77 1,036 66
 Foreign-born 302 23 532 34
Education (years) <0.01
 Some high school or less 398 30 600 38
 High school or vocational/technical school graduate 373 28 426 27
 Some college 297 23 297 19
 College graduate 248 19 245 16
Family history of breast cancer in first-degree relatives <0.01
 No 1,089 83 1,371 87
 Yes 227 17 197 13
Personal history of biopsy-confirmed benign breast disease 0.01
 No 1,016 77 1,274 81
 Yes 300 23 294 19
Age at menarche <0.01
 ≤11 304 23 327 21
 12 349 27 356 23
 13 319 24 387 25
 ≥14 344 26 498 32
Parity <0.01
 Nulliparous 169 13 145 9
 Parous 1,147 87 1,423 91
Number of full-term pregnancies, parous women <0.01
 1 162 14 177 12
 2 309 27 303 21
 3 263 23 349 25
 ≥4 413 36 594 42
Age at first full-term pregnancy (years), parous women <0.01
 ≤19 302 26 415 29
 20–24 462 40 564 40
 25–29 235 21 298 21
 ≥30 148 13 146 10
Lifetime breast-feeding (months), parous women <0.01
 0 541 47 547 38
 ≤ 6 250 22 294 21
 7–12 97 8 148 10
 13–24 126 11 184 13
 ≥25 133 12 250 18
Lifetime physical activityc (hours/week) 0.04
 ≤ 6.9 376 29 391 25
 7.0-14.1 342 26 390 25
 14.2-25.4 291 22 403 26
 ≥25.5 307 23 384 25
Alcohol consumptiond,e (g/day) <0.01
 0 763 58 975 62
 0.1-4.9 262 20 312 20
 5.0-9.9 68 5 91 6
 10.0-19.9 115 9 107 7
 ≥20 108 8 83 5
Total caloric intakec,d,e (kcal/day) 0.05
 ≤ 1362 287 22 394 25
 1363–1798 343 26 385 25
 1799–2435 379 29 398 25
 ≥2436 307 23 391 25

Abbreviations: ER-, estrogen receptor–negative; ER+, estrogen receptor–positive; PR-, progesterone receptor–negative; PR+, progesterone receptor–positive.

a Percentages may not add up to 100% due to rounding.

b U.S.-born includes 43 cases and 34 controls born in westernized countries such as Canada, Europe, Australia, or New Zealand.

c Quartiles among all postmenopausal controls.

d In reference year.

e Excludes 39 cases and 26 controls whose total caloric intake was <600 kcal/day or >5,000 kcal/day.


[TableWrap ID: Tab2] Table 2 

Body size among control women by race/ethnicity


Hispanics (n = 804) African Americans (n = 365) Non-Hispanic Whites (n = 399) P valuea
n %b n %b n %b
Current BMI (kg/m2) c * †
 <25.0 147 18 80 22 185 47
 25.0-29.9 310 39 124 34 116 29
 ≥30.0 342 43 159 44 97 24
Young-adult BMI (kg/m2) d,e * ‡
 Q1: ≤20.6 125 17 116 32 130 33
 Q2: 20.7-22.4 170 23 83 23 118 30
 Q3: 22.5-24.7 210 29 84 23 76 19
 Q4: >24.7 225 31 77 21 69 18
Weight gain (kg) f * † ‡
 Stable g 80 11 31 9 65 18
 Gain, 3.0-9.9 176 25 66 19 113 31
 Gain, 10.0-19.9 234 33 91 26 96 26
 Gain, 20.0-29.9 142 20 83 24 63 17
 Gain, ≥30.0 74 11 76 22 34 9
Waist (cm) d * † ‡
 Q1: ≤ 82.3 170 22 41 14 150 43
 Q2: 82.4-90.5 211 27 65 22 77 22
 Q3: 90.6-99.8 196 25 90 30 67 19
 Q4: >99.8 195 25 102 34 57 16
Hip (cm) d * † ‡
 Q1: ≤ 100.5 206 27 48 16 103 29
 Q2: 100.6-107.5 186 24 60 20 107 31
 Q3: 107.6-116.2 183 24 85 29 87 25
 Q4: >116.2 196 25 105 35 54 15
Waist-to-hip ratio (WHR) d * † ‡
 Q1: ≤ 0.79 172 22 52 18 163 46
 Q2: 0.80-0.84 224 29 70 24 83 24
 Q3: 0.85-0.88 190 25 83 28 53 15
 Q4: >0.88 185 24 92 31 52 15
Waist-to-height ratio (WHtR) d * †
 Q1: ≤ 0.52 138 18 56 19 162 46
 Q2: 0.53-0.58 195 25 78 26 82 23
 Q3: 0.59-0.64 216 28 81 27 58 17
 Q4: >0.64 223 29 83 28 49 14

Abbreviation: BMI, body mass index.

a Chi-square test for the difference between race/ethnicity; * = P <0.05 between non-Hispanic Whites and Hispanics; † = P <0.05 between non-Hispanic Whites and African Americans; ‡ = P <0.05 between Hispanics and African Americans.

b Percentages may not add up to 100% due to rounding.

c Based on self-reported adult weight and measured height at interview (if not available, then based on measured weight at interview and/or self-reported adult height).

d Based on quartiles among all postmenopausal controls.

e Based on self-reported young-adult weight and measured height at interview (or self-reported adult height when measured height not available).

f Self-reported adult weight (or measured weight at interview if self-reported weight not available) minus self-reported young-adult weight; excludes 64 controls who lost >3 kg of weight.

g Stable weight defined as +/- 3 kg.


[TableWrap ID: Tab3] Table 3 

BMI and weight gain and breast cancer risk in postmenopausal women not currently using hormone therapy by race/ethnicityaand estrogen receptor and progesterone receptor status


All race/ethnicities Hispanics African Americans Non-Hispanic Whites
All breast cancer Cases (n = 801) Controls (n = 1,336) ORb95% CI Cases (n = 377) Controls (n = 709) ORc95% CI Cases (n = 243) Controls (n = 315) ORc95% CI Cases (n = 181) Controls (n = 312) ORc95% CI
Current BMI (kg/m2) d
 <25.0 208 329 1.0 81 119 1.0 51 70 1.0 76 140 1.0
 25.0-29.9 278 476 0.95 0.74-1.21 133 273 0.78 0.54-1.14 90 106 1.19 0.74-1.94 55 97 0.90 0.56-1.43
 ≥30.0 312 523 0.94 0.74-1.20 161 312 0.77 0.53-1.12 101 137 1.07 0.66-1.73 50 74 1.19 0.72-1.99
Ptrend = 0.64 Ptrend = 0.24 Ptrend = 0.88 Ptrend = 0.58
Current BMI (kg/m2) –adjusted for weight gain d,e
 <25.0 1.0 1.0 1.0 1.0
 25.0-29.9 0.90 0.67-1.20 0.80 0.52-1.25 1.25 0.70-2.26 0.63 0.34-1.16
 ≥30.0 0.79 0.56-1.13 0.73 0.43-1.24 1.15 0.57-2.30 0.52 0.22-1.22
Ptrend = 0.75 Ptrend = 0.26 Ptrend = 0.77 Ptrend = 0.11
Young-adult BMI (kg/m2) f,g
 T1: ≤21.2 286 402 1.0 109 161 1.0 93 122 1.0 84 119 1.0
 T2: 21.3-23.7 259 411 0.87 0.69-1.09 122 209 0.85 0.60-1.20 77 90 1.17 0.76-1.79 60 112 0.65 0.41-1.02
 T3: >23.7 216 445 0.68 0.54-0.86 115 272 0.63 0.45-0.90 67 98 0.93 0.59-1.45 34 75 0.52 0.30-0.90
Ptrend < 0.01 Ptrend = 0.01 Ptrend = 0.80 Ptrend = 0.01
Weight gain (kg) h,i 78 140
 Stable j 180 291 1.0 36 65 1.0 18 26 1.0 24 49 1.0
 Gain, 3.0-9.9 217 376 1.15 0.82-1.63 82 149 1.05 0.63-1.76 50 55 1.27 0.59-2.73 48 87 1.27 0.67-2.43
 Gain, 10.0-19.9 142 247 1.06 0.76-1.48 101 217 0.88 0.54-1.45 68 80 1.18 0.57-2.44 48 79 1.36 0.71-2.62
 Gain, 20.0-29.9 111 154 1.03 0.72-1.48 71 125 1.04 0.61-1.78 44 72 0.91 0.43-1.93 27 50 1.19 0.57-2.48
 Gain, ≥30.0 1.19 0.81-1.75 38 67 0.91 0.50-1.66 51 64 1.13 0.54-2.39 22 23 2.63 1.12-6.19
Ptrend = 0.75 Ptrend = 0.75 Ptrend = 0.75 Ptrend = 0.10
Weight gain (kg) – adjusted for current BMI h,i,k
 Stable j 1.0 1.0 1.0 1.0
 Gain, 3.0-9.9 1.17 0.83-1.65 1.07 0.64-1.80 1.17 0.54-2.56 1.38 0.71-2.67
 Gain, 10.0-19.9 1.14 0.79-1.65 1.00 0.58-1.70 1.00 0.45-2.24 1.92 0.89-4.15
 Gain, 20.0-29.9 1.17 0.77-1.78 1.22 0.66-2.25 0.76 0.32-1.85 1.94 0.75-5.03
 Gain, ≥30.0 1.41 0.88-2.26 1.12 0.55-2.27 0.99 0.39-2.49 4.70 1.48-14.97
Ptrend = 0.24 Ptrend = 0.67 Ptrend = 0.68 Ptrend = 0.02
ER+PR+ breast cancer Cases (n = 415) Controls (n = 1,336) ORb95% CI Cases (n = 191) Controls (n = 709) ORc95% CI Cases (n = 108) Controls (n = 315) ORc95% CI Cases (n = 116) Controls (n = 312) ORc95% CI
Current BMI (kg/m2) d
 <25.0 98 329 1.0 34 119 1.0 19 70 1.0 45 140 1.0
 25.0-29.9 141 476 1.09 0.80-1.49 60 273 0.90 0.54-1.49 44 106 1.76 0.89-3.47 37 97 1.06 0.61-1.85
 ≥30.0 175 523 1.30 0.95-1.78 96 312 1.23 0.75-2.01 45 137 1.46 0.74-2.89 34 74 1.39 0.76-2.55
Ptrend = 0.09 Ptrend = 0.22 Ptrend = 0.40 Ptrend = 0.30
Current BMI (kg/m2) – adjusted for weight gain d,e
 <25.0 1.0 1.0 1.0 1.0
 25.0-29.9 1.06 0.73-1.54 1.01 0.56-1.84 1.77 0.78-4.06 0.74 0.35-1.56
 ≥30.0 1.01 0.64-1.60 1.17 0.58-2.35 1.29 0.48-3.48 0.64 0.23-1.76
Ptrend = 0.99 Ptrend = 0.62 Ptrend = 0.78 Ptrend = 0.37
Young-adult BMI (kg/m2) f,g
 T1: ≤21.2 147 402 1.0 51 161 1.0 45 122 1.0 51 119 1.0
 T2: 21.3-23.7 133 411 0.87 0.65-1.15 58 209 0.87 0.55-1.37 35 90 1.23 0.69-2.20 40 112 0.66 0.38-1.15
 T3: >23.7 116 445 0.73 0.54-0.98 65 272 0.80 0.51-1.25 28 98 0.73 0.39-1.36 23 75 0.52 0.27-1.00
Ptrend = 0.04 Ptrend = 0.33 Ptrend = 0.39 Ptrend = 0.04
Weight gain (kg) h,l
 Stable j 44 140 1.0 18 65 1.0 9 26 1.0 17 49 1.0
 Gain, 3.0-9.9 79 291 0.94 0.61-1.46 32 149 0.80 0.41-1.58 20 55 1.11 0.40-3.14 27 87 1.02 0.48-2.18
 Gain, 10.0-19.9 114 376 1.07 0.71-1.62 55 217 1.00 0.53-1.88 26 80 0.96 0.36-2.57 33 79 1.48 0.70-3.15
 Gain, 20.0-29.9 77 247 1.12 0.72-1.74 34 125 1.02 0.52-2.03 25 72 1.19 0.44-3.18 18 50 1.29 0.55-3.04
 Gain, ≥30.0 67 154 1.53 0.96-2.45 29 67 1.43 0.70-2.94 24 64 1.27 0.47-3.42 14 23 2.56 0.95-6.88
Ptrend = 0.04 Ptrend = 0.16 Ptrend = 0.58 Ptrend = 0.07
Weight gain (kg) – adjusted for current BMI h,k,l
 Stable j 1.0 1.0 1.0 1.0
 Gain, 3.0-9.9 0.93 0.60-1.44 0.81 0.41-1.59 0.92 0.31-2.67 1.09 0.50-2.38
 Gain, 10.0-19.9 1.04 0.66-1.65 0.96 0.49-1.89 0.67 0.22-2.04 1.90 0.77-4.73
 Gain, 20.0-29.9 1.10 0.65-1.86 0.93 0.43-2.05 0.85 0.26-2.77 1.80 0.58-5.63
 Gain, ≥30.0 1.53 0.85-2.73 1.29 0.55-3.01 1.02 0.29-3.58 3.82 0.99-14.71
Ptrend = 0.13 Ptrend = 0.48 Ptrend = 0.90 Ptrend = 0.06

Abbreviations: BMI, body mass index; CI, confidence interval; ER+, estrogen receptor–positive; OR, odds ratio; PR+, progesterone receptor–positive.

a All P values for interaction by race/ethnicity were >0.05.

b Adjusted for age (years, continuous), race/ethnicity (non-Hispanic White, African American, Hispanic), place of birth (U.S.-born, foreign-born), education (some high school or less, high school or vocational/technical school graduate, some college, college graduate), first-degree family history of breast cancer (no, yes), personal history of biopsy-confirmed benign breast disease (no, yes), age at menarche (≤11, 12, 13, ≥14 years), number of full-term pregnancies (nulliparous, 1, 2, 3, ≥4), age at first full-term pregnancy (nulliparous, ≤19, 20–24, 25–29, ≥30 years), lifetime breast-feeding (nulliparous, 0, ≤6, 7–12, 13–24, ≥25 months), lifetime physical activity (quartiles, hours/week), alcohol consumption in reference year (0, 0.1-4.9, 5–9.9, 10–19.9, ≥20 g/day), and total caloric intake (quartiles, kcal/day).

c Not adjusted for race/ethnicity.

d Based on self-reported weight and measured height at interview (if not available, then based on measured weight at interview and/or self-reported height).

e Adjusted for above variables, and weight gain.

f Based on tertiles among all postmenopausal controls.

g Based on self-reported young-adult weight and measured height at interview (or self-reported adult height when measured height not available).

h Self-reported weight (or measured weight at interview if self-reported weight not available) minus self-reported young-adult weight.

i Excludes 34 cases and 55 controls who lost >3 kg of weight.

j Stable weight defined as +/- 3 kg.

k Adjusted for above variables, and current BMI.

l Excludes 15 ER+PR+ cases and 55 controls who lost >3 kg of weight.


[TableWrap ID: Tab4] Table 4 

BMI and weight gain and breast cancer risk in postmenopausal women not currently using hormone therapy by young-adult BMI and time since menopause


Young-adult BMI Young-adult BMI
≤22.4 kg/m2 >22.4 kg/m2
All breast cancer Cases (n = 413) Controls (n = 614) ORa95% CI Cases (n = 348) Controls (n = 644) ORa95% CI Pinteraction
Current BMI (kg/m2) b 0.01
 <25.0 167 243 1.0 38 77 1.0
 25.0-29.9 131 232 0.77 0.56-1.06 136 217 1.28 0.80-2.05
 ≥30.0 115 138 1.22 0.86-1.74 174 350 0.92 0.58-1.45
Ptrend = 0.42 Ptrend = 0.19
Weight gain (kg) c,d 0.12
 Stable e 35 52 1.0 43 87 1.0
 Gain, 3.0-9.9 106 142 1.20 0.71-2.03 74 148 1.03 0.64-1.66
 Gain, 10.0-19.9 109 198 0.82 0.49-1.38 108 176 1.26 0.80-1.99
 Gain, 20.0-29.9 90 126 1.11 0.65-1.91 51 120 0.81 0.48-1.36
 Gain, ≥30.0 67 84 1.14 0.64-2.05 44 69 1.08 0.62-1.90
Ptrend = 0.84 Ptrend = 0.81
ER+PR+ breast cancer Cases (n = 209) Controls (n = 614) ORa95% CI Cases (n = 187) Controls (n = 644) ORa95% CI Pinteraction
Current BMI (kg/m2) b 0.01
 <25.0 77 243 1.0 19 77 1.0
 25.0-29.9 63 232 0.87 0.57-1.32 74 217 1.42 0.78-2.59
 ≥30.0 69 138 1.97 1.26-3.09 94 350 1.10 0.61-1.98
Ptrend = 0.01 Ptrend = 0.69
Weight gain (kg) c,f 0.08
Stable e 20 52 1.0 24 87 1.0
 Gain, 3.0-9.9 42 142 0.97 0.50-1.88 37 148 0.99 0.54-1.80
 Gain, 10.0-19.9 52 198 0.83 0.43-1.59 62 176 1.44 0.82-2.54
 Gain, 20.0-29.9 50 126 1.35 0.69-2.64 27 120 0.88 0.46-1.69
 Gain, ≥30.0 41 84 1.71 0.83-3.52 26 69 1.48 0.75-2.94
Ptrend = 0.03 Ptrend = 0.42
<15 Years Since Menopauseg ≥15 Years Since Menopauseg
All breast cancer Cases (n = 335) Controls (n = 552) ORa95% CI Cases (n = 352) Controls (n = 576) ORa95% CI Pinteraction
Current BMI (kg/m2) b 0.09
 <25.0 98 134 1.0 82 138 1.0
 25.0-29.9 115 187 0.85 0.57-1.26 126 229 0.97 0.67-1.41
 ≥30.0 120 227 0.70 0.47-1.03 143 205 1.24 0.84-1.81
Ptrend = 0.07 Ptrend = 0.22
Current BMI (kg/m2) –adjusted for weight gain b,h 0.31
 <25.0 1.0 1.0
 25.0-29.9 0.89 0.56-1.42 0.73 0.46-1.15
 ≥30.0 0.85 0.47-1.51 0.68 0.39-1.18
Ptrend = 0.58 Ptrend = 0.20
Young-adult BMI (kg/m2) i,j 0.57
 T1: ≤21.2 120 181 1.0 127 163 1.0
 T2: 21.3-23.7 112 163 1.03 0.72-1.48 112 174 0.82 0.58-1.16
 T3: >23.7 90 181 0.78 0.53-1.14 92 199 0.59 0.41-0.85
Ptrend = 0.22 Ptrend < 0.01
Weight gain (kg) c,k 0.12
 Stable e 33 55 1.0 32 68 1.0
 Gain, 3.0-9.9 85 116 1.13 0.65-1.96 72 133 1.29 0.76-2.20
 Gain, 10.0-19.9 101 165 0.89 0.53-1.52 92 152 1.40 0.83-2.35
 Gain, 20.0-29.9 52 98 0.82 0.46-1.48 66 105 1.44 0.83-2.50
 Gain, ≥30.0 40 73 0.69 0.37-1.30 53 55 2.09 1.15-3.81
Ptrend = 0.08 Ptrend = 0.02
Weight gain (kg) – adjusted for current BMI c,k,l 0.12
 Stable e 1.0 1.0
 Gain, 3.0-9.9 1.16 0.67-2.01 1.34 0.78-2.30
 Gain, 10.0-19.9 0.96 0.54-1.71 1.67 0.93-2.99
 Gain, 20.0-29.9 0.91 0.46-1.82 1.77 0.92-3.38
 Gain, ≥30.0 0.78 0.36-1.68 2.71 1.29-5.69
Ptrend = 0.40 Ptrend = 0.01
ER+PR+ breast cancer Cases (n = 156) Controls (n = 552) ORa95% CI Cases (n = 201) Controls (n = 576) ORa95% CI Pinteraction
Current BMI (kg/m2) b 0.45
 <25.0 42 134 1.0 40 138 1.0
 25.0-29.9 47 187 0.89 0.53-1.50 77 229 1.26 0.79-2.02
 ≥30.0 66 227 1.07 0.64-1.78 84 205 1.63 1.00-2.65
Ptrend = 0.71 Ptrend = 0.05
Current BMI (kg/m2) –adjusted for weight gain b,h 0.43
 <25.0 1.0 1.0
 25.0-29.9 0.97 0.52-1.81 1.15 0.64-2.07
 ≥30.0 1.35 0.63-2.87 0.94 0.46-1.92
Ptrend = 0.40 Ptrend = 0.75
Young-adult BMI (kg/m2) i,j 0.76
 T1: ≤21.2 56 181 1.0 67 163 1.0
 T2: 21.3-23.7 49 163 1.00 0.62-1.59 66 174 0.89 0.58-1.37
 T3: >23.7 45 181 0.89 0.54-1.46 58 199 0.70 0.45-1.10
Ptrend = 0.64 Ptrend = 0.12
Weight gain (kg) c,m 0.51
 Stable e 16 55 1.0 22 68 1.0
 Gain, 3.0-9.9 34 116 0.94 0.46-1.93 34 133 0.93 0.48-1.77
 Gain, 10.0-19.9 48 165 0.98 0.49-1.94 53 152 1.25 0.68-2.30
 Gain, 20.0-29.9 24 98 0.85 0.40-1.84 40 105 1.38 0.72-2.64
 Gain, ≥30.0 24 73 0.99 0.45-2.17 33 55 2.32 1.15-4.69
Ptrend = 0.91 Ptrend = 0.01
Weight gain (kg) – adjusted for current BMI c,l,m 0.48
 Stable e 1.0 1.0
 Gain, 3.0-9.9 0.95 0.46-1.95 0.86 0.44-1.68
 Gain, 10.0-19.9 0.94 0.44-1.97 1.17 0.59-2.33
 Gain, 20.0-29.9 0.70 0.28-1.73 1.39 0.64-3.01
 Gain, ≥30.0 0.76 0.29-1.99 2.47 1.03-5.94
Ptrend = 0.50 Ptrend = 0.03

Abbreviations: BMI, body mass index; CI, confidence interval; ER+, estrogen receptor–positive; OR, odds ratio; PR+, progesterone receptor–positive.

a Adjusted for age (years, continuous), race/ethnicity (non-Hispanic White, African American, Hispanic), place of birth (U.S.-born, foreign-born), education (some high school or less, high school or vocational/technical school graduate, some college, college graduate), family history of breast cancer in first-degree relatives (no, yes), personal history of biopsy-confirmed benign breast disease (no, yes), age at menarche (≤11, 12, 13, ≥14 years), number of full-term pregnancies (nulliparous, 1, 2, 3, ≥4), age at first full-term pregnancy (nulliparous, ≤19, 20–24, 25–29, ≥30 years), lifetime breast-feeding (nulliparous, 0, ≤6, 7–12, 13–24, ≥25 months), lifetime physical activity (quartiles, hours/week), alcohol consumption in reference year (0, 0.1-4.9, 5–9.9, 10–19.9, ≥20 g/day), and total caloric intake (quartiles, kcal/day).

b Based on self-reported weight and measured height at interview (if not available, then based on measured weight at interview and/or self-reported height).

c Self-reported weight (or measured weight at interview if self-reported weight not available) minus self-reported young-adult weight.

d Excludes 34 cases and 55 controls who lost >3 kg of weight.

e Stable weight defined as +/- 3 kg.

f Excludes 15 ER+PR+ cases and 55 controls who lost >3 kg of weight.

g Among women with natural or surgical menopause only.

h Adjusted for above variables, and weight gain.

i Based on tertiles among all postmenopausal controls.

j Based on self-reported young-adult weight and measured height at interview (or self-reported adult height when measured height not available).

k Excludes 28 cases and 46 controls who lost >3 kg of weight.

l Adjusted for above variables, and current BMI.

m Excludes 13 ER+PR+ cases and 46 controls who lost >3 kg of weight.


[TableWrap ID: Tab5] Table 5 

Abdominal adiposity and breast cancer risk in postmenopausal women not currently using hormone therapy by race/ethnicitya


All race/ethnicities Hispanics African Americans Non-Hispanic Whites
All breast cancer Cases (n = 801) Controls (n = 1,336) ORb95% CI Cases (n = 377) Controls (n = 709) ORc95% CI Cases (n = 243) Controls (n = 315) ORc95% CI Cases (n = 181) Controls (n = 312) ORc95% CI
Waist (cm) d
 T1: ≤ 85.0 198 385 1.0 96 201 1.0 30 54 1.0 72 130 1.0
 T2: 85.1-96.4 214 407 0.99 0.77-1.27 113 245 0.90 0.63-1.27 59 78 1.55 0.85-2.83 42 84 0.91 0.55-1.52
 T3: >96.4 293 412 1.32 1.03-1.69 146 232 1.27 0.90-1.79 102 120 1.83 1.04-3.21 45 60 1.24 0.72-2.13
Ptrend = 0.02 Ptrend = 0.14 Ptrend = 0.05 Ptrend = 0.52
Waist (cm) – adjusted for current BMI d,e
 T1: ≤ 85.0 1.0 1.0 1.0 1.0
 T2: 85.1-96.4 1.09 0.82-1.44 1.08 0.73-1.60 1.64 0.84-3.20 0.80 0.44-1.47
 T3: >96.4 1.59 1.15-2.19 1.79 1.14-2.81 2.17 1.05-4.49 0.90 0.42-1.91
Ptrend < 0.01 Ptrend = 0.01 Ptrend = 0.04 Ptrend = 0.75
Hip (cm) d
 T1: ≤ 102.9 194 394 1.0 105 224 1.0 39 60 1.0 50 110 1.0
 T2: 103.0-112.7 230 402 1.15 0.90-1.47 119 229 1.13 0.80-1.58 54 77 1.06 0.60-1.88 57 96 1.46 0.87-2.43
 T3: >112.7 281 407 1.36 1.07-1.73 131 224 1.22 0.87-1.71 98 115 1.51 0.89-2.56 52 68 1.80 1.03-3.14
Ptrend = 0.01 Ptrend = 0.26 Ptrend = 0.09 Ptrend = 0.04
Hip (cm) – adjusted for current BMI d,e
 T1: ≤ 102.9 1.0 1.0 1.0 1.0
 T2: 103.0-112.7 1.27 0.97-1.66 1.34 0.92-1.94 1.04 0.54-2.00 1.58 0.90-2.79
 T3: >112.7 1.66 1.20-2.30 1.64 1.05-2.58 1.68 0.82-3.42 1.88 0.86-4.10
Ptrend < 0.01 Ptrend = 0.03 Ptrend = 0.10 Ptrend = 0.09
Waist-to-height ratio d
 T1: ≤ 0.54 200 372 1.0 80 153 1.0 42 70 1.0 78 149 1.0
 T2: 0.55-0.61 226 410 1.05 0.81-1.35 117 254 0.88 0.61-1.28 64 85 1.42 0.82-2.45 45 71 1.27 0.76-2.12
 T3: >0.61 279 422 1.27 0.98-1.64 158 271 1.13 0.78-1.62 85 97 1.74 1.02-2.96 36 54 1.16 0.65-2.06
Ptrend = 0.06 Ptrend = 0.37 Ptrend = 0.05 Ptrend = 0.51
Waist-to-height ratio – adjusted for current BMI d,e
 T1: ≤ 0.54 1.0 1.0 1.0 1.0
 T2: 0.55-0.61 1.14 0.86-1.52 1.05 0.69-1.60 1.55 0.82-2.91 1.13 0.61-2.09
 T3: >0.61 1.49 1.06-2.09 1.55 0.96-2.50 2.22 1.09-4.51 0.85 0.39-1.84
Ptrend = 0.02 Ptrend = 0.05 Ptrend = 0.03 Ptrend = 0.72
ER+PR+ breast cancer Cases (n = 415) Controls (n = 1,336) ORb95% CI Cases (n = 191) Controls (n = 709) ORc95% CI Cases (n = 108) Controls (n = 315) ORc95% CI Cases (n = 116) Controls (n = 312) ORc95% CI
Waist (cm) d
 T1: ≤ 85.0 95 385 1.0 42 201 1.0 8 54 1.0 45 130 1.0
 T2: 85.1-96.4 106 407 1.11 0.80-1.54 55 245 1.01 0.63-1.61 26 78 2.70 1.01-7.17 25 84 0.88 0.48-1.63
 T3: >96.4 162 412 1.76 1.28-2.41 84 232 1.79 1.14-2.81 46 120 3.31 1.29-8.48 32 60 1.38 0.75-2.56
Ptrend < 0.01 Ptrend = 0.01 Ptrend = 0.02 Ptrend = 0.33
Waist (cm) – adjusted for current BMI d,e
 T1: ≤ 85.0 1.0 1.0 1.0 1.0
 T2: 85.1-96.4 1.13 0.78-1.63 1.12 0.66-1.90 2.48 0.86-7.19 0.75 0.37-1.52
 T3: >96.4 1.83 1.21-2.79 2.03 1.11-3.70 3.36 1.10-10.28 0.98 0.41-2.32
Ptrend < 0.01 Ptrend = 0.01 Ptrend = 0.05 Ptrend = 0.93
Hip (cm) d
 T1: ≤ 102.9 92 394 1.0 46 224 1.0 17 60 1.0 29 110 1.0
 T2: 103.0-112.7 118 402 1.32 0.96-1.81 56 229 1.23 0.78-1.94 23 77 1.04 0.48-2.28 39 96 1.76 0.95-3.25
 T3: >112.7 153 407 1.77 1.30-2.42 79 224 1.85 1.19-2.85 40 115 1.54 0.74-3.21 34 68 2.06 1.07-3.97
Ptrend < 0.01 Ptrend = 0.01 Ptrend = 0.20 Ptrend = 0.03
Hip (cm) – adjusted for current BMI d,e
 T1: ≤ 102.9 1.0 1.0 1.0 1.0
 T2: 103.0-112.7 1.36 0.96-1.93 1.38 0.83-2.28 0.77 0.31-1.88 1.81 0.92-3.56
 T3: >112.7 1.85 1.22-2.81 2.12 1.17-3.84 1.18 0.45-3.08 1.96 0.78-4.91
Ptrend < 0.01 Ptrend = 0.01 Ptrend = 0.57 Ptrend = 0.12
Waist-to-height ratio d
 T1: ≤ 0.54 98 372 1.0 36 153 1.0 14 70 1.0 48 149 1.0
 T2: 0.55-0.61 112 410 1.15 0.83-1.59 51 254 0.88 0.53-1.46 30 85 1.94 0.86-4.35 31 71 1.44 0.79-2.65
 T3: >0.61 153 422 1.61 1.16-2.23 94 271 1.63 1.02-2.62 36 97 2.19 0.99-4.82 23 54 1.14 0.59-2.23
Ptrend < 0.01 Ptrend = 0.01 Ptrend = 0.07 Ptrend = 0.49
Waist-to-height ratio –adjusted for current BMI d,e
 T1: ≤ 0.54 1.0 1.0 1.0 1.0
 T2: 0.55-0.61 1.13 0.77-1.64 0.97 0.55-1.73 1.75 0.72-4.26 1.19 0.58-2.48
 T3: >0.61 1.55 1.00-2.39 1.83 0.97-3.47 2.19 0.81-5.93 0.74 0.30-1.85
Ptrend = 0.04 Ptrend = 0.02 Ptrend = 0.14 Ptrend = 0.62

Abbreviations: BMI, body mass index; CI, confidence interval; ER+, estrogen receptor–positive; OR, odds ratio; PR+, progesterone receptor–positive.

a All P values for interaction by race/ethnicity were >0.05.

b Adjusted for age (years, continuous), race/ethnicity (non-Hispanic White, African American, Hispanic), place of birth (U.S.-born, foreign-born), education (some high school or less, high school or vocational/technical school graduate, some college, college graduate), first-degree family history of breast cancer (no, yes), personal history of biopsy-confirmed benign breast disease (no, yes), age at menarche (≤11, 12, 13, ≥14 years), number of full-term pregnancies (nulliparous, 1, 2, 3, ≥4), age at first full-term pregnancy (nulliparous, ≤19, 20–24, 25–29, ≥30 years), lifetime breast-feeding (nulliparous, 0, ≤6, 7–12, 13–24, ≥25 months), lifetime physical activity (quartiles, hours/week), alcohol consumption in reference year (0, 0.1-4.9, 5–9.9, 10–19.9, ≥20 g/day), and total caloric intake (quartiles, kcal/day).

c Adjusted for above variables, except race/ethnicity.

d Based on tertiles among all postmenopausal controls.

e Adjusted for above variables, and current BMI.


[TableWrap ID: Tab6] Table 6 

Abdominal adiposity and breast cancer risk in postmenopausal women not currently using hormone therapy by current BMI


Current BMI < 25.0kg/mg2 Current BMI ≥ 25.0kg/mg2
All breast cancer Cases (n=396) Controls (n=648) ORa95% CI Cases (n=402) Controls (n=680) ORa95% CI Pinteraction
Waist (cm) b
 M1: ≤ 90.5 151 272 1.00 140 321 0.87 0.65-1.18 0.25
 M2: > 90.5 27 26 1.90 1.05-3.44 387 585 1.21 0.93-1.57
Waist-to-height ratio b
 M1: ≤ 0.58 156 276 1.00 152 310 0.93 0.69-1.24 0.93
 M2: > 0.58 22 22 1.87 0.98-3.56 375 596 1.17 0.90-1.52
ER+PR+ breast cancer Cases (n=194) Controls (n=648) ORa95% CI Cases (n=220) Controls (n=680) ORa95% CI Pinteraction
Waist (cm) b
 M1: ≤ 90.5 73 272 1.00 67 321 0.92 0.62-1.36 0.16
 M2: > 90.5 10 26 1.53 0.69-3.39 213 585 1.55 1.11-2.17
Waist-to-height ratio b
 M1: ≤ 0.58 75 276 1.00 75 310 1.02 0.70-1.50 0.47
 M2: > 0.58 8 22 1.53 0.63-3.68 205 596 1.52 1.08-2.12

Abbreviations: BMI, body mass index; CI, confidence interval; ER+, estrogen receptor–positive; OR, odds ratio; PR+, progesterone receptor–positive.

a OR and 95% CI adjusted for age (years, continuous), race/ethnicity (non-Hispanic White, African American, Hispanic), place of birth (US-born, foreign-born), education (some high school or less, high school or vocational/technical school graduate, some college, college graduate), family history of breast cancer in first-degree relatives (no, yes), personal history of biopsy-confirmed benign breast disease (no, yes), age at menarche (≤11, 12, 13, ≥14 years), number of full-term pregnancies (nulliparous, 1, 2, 3, ≥4), age at first full-term pregnancy (nulliparous, ≤19, 20–24, 25–29, ≥30 years), lifetime breast-feeding (nulliparous, 0, ≤6, 7–12, 13–24, ≥25 months), lifetime physical activity (quartiles, hours/week), alcohol consumption in reference year (0, 0.1-4.9, 5–9.9, 10–19.9, ≥20 g/day), and total caloric intake (quartiles, kcal/day).

b Based on median among all postmenopausal controls.


[TableWrap ID: Tab7] Table 7 

Body size and risk of ER-PR- breast cancer in postmenopausal women not currently using hormone therapy


Cases (n=135) Controls (n=1,336) ORa, 95% CI ORb 95% CI ORc 95% CI
Current BMI(kg/m2) d
 <25.0 34 329 1.00 1.00
 25.0-29.9 46 476 0.75 0.46-1.22 0.62 0.36-1.08
 ≥30.0 54 523 0.72 0.45-1.16 0.58 0.30-1.14
Ptrend = 0.21 Ptrend = 0.13
Young-adult BMI (kg/m2) e,f
 T1: ≤21.2 46 402 1.00
 T2: 21.3-23.7 43 411 0.82 0.52-1.29
 T3: >23.7 37 445 0.61 0.38-0.97
Ptrend = 0.04
Weight gain (kg) g
 Stable h 10 140 1.00 1.00
 Gain, 3.0-9.9 31 291 1.38 0.65-2.93 1.47 0.69-3.16
 Gain, 10.0-19.9 42 376 1.31 0.63-2.72 1.67 0.76-3.65
 Gain, ≥20.0 39 401 1.05 0.50-2.19 1.45 0.60-3.48
Ptrend = 0.63 Ptrend = 0.48
Waist (cm) e
 T1: ≤ 85.0 28 385 1.00 1.00
 T2: 85.1-96.4 40 407 1.13 0.67-1.89 1.43 0.80-5.54
 T3: >96.4 48 412 1.24 0.75-2.06 1.87 0.96-3.64
Ptrend = 0.41 Ptrend = 0.07
Hip (cm) e
 T1: ≤ 102.9 27 394 1.00 1.00
 T2: 103.0-112.7 41 402 1.40 0.84-2.34 1.85 1.05-3.28
 T3: >112.7 48 407 1.43 0.86-2.37 2.35 1.20-4.59
Ptrend = 0.19 Ptrend = 0.01
Waist-to-hip ratio
 T1: ≤ 0.81 33 434 1.00 1.00
 T2: 0.82-0.86 34 355 1.14 0.68-1.90 1.21 0.72-2.04
 T3: >0.86 49 413 1.35 0.83-2.18 1.46 0.88-2.39
Ptrend = 0.22 Ptrend = 0.14
Waist-to-height ratio
 T1: ≤ 0.54 30 372 1.00 1.00
 T2: 0.55-0.61 40 410 0.98 0.59-1.63 1.19 0.66-2.17
 T3: >0.61 46 422 1.05 0.63-1.73 1.44 0.72-2.87
Ptrend = 0.84 Ptrend = 0.30

Abbreviations: BMI, body mass index; CI, confidence interval; ER-, estrogen receptor–negative; OR, odds ratio; PR-, progesterone receptor–negative.

a OR and 95% CI adjusted for age (years, continuous), race/ethnicity (non-Hispanic White, African American, Hispanic), place of birth (US-born, foreign-born), age at menarche (≤11, 12, 13, ≥14 years), and lifetime breast-feeding (nulliparous, 0, ≤6, 7–12, 13–24, ≥25 months).

b Adjusted for above variables, and current BMI.

c Adjusted for above variables, and weight gain.

d Based on self-reported weight and measured height at interview (if not available, then based on measured weight at interview and/or self-reported height).

e Based on tertiles among all postmenopausal controls.

f Based on self-reported young-adult weight and measured height at interview (or self-reported adult height when measured height not available).

g Self-reported weight (or measured weight at interview if self-reported weight not available) minus self-reported young-adult weight; excludes 5 cases and 55 controls who lost >3 kg of weight

h Stable weight defined as +/- 3 kg.



Article Categories:
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Keywords: Keywords African Americans, Body size, Breast cancer, Estrogen receptor, Hispanics, Progesterone receptor.

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