JOURNAL OF BONE AND MINERAL RESEARCH

Volume 22, Number 11, 2007

Published online on July 16, 2007; doi: 10.1359/JBMR.070713
© 2007 American Society for Bone and Mineral Research

Clinical Risk Factors for Fractures in Multi-Ethnic Women:

The Women’s Health Initiative
Jane A Cauley,1 LieLing Wu,2 Nina S Wampler,3 Janice M Barnhart,4 Matthew Allison,5 Zhao Chen,6
Rebecca Jackson,7 and John Robbins8

ABSTRACT: To identify risk factors for fractures in multi-ethnic women, we studied 159,579 women enrolled
in the Women’s Health Initiative. In general, risk factors for fractures were similar across ethnic groups.
However, irrespective of their ethnicity, women with multiple risk factors have a high risk of fracture.
Targeting these high-risk women for screening and intervention could reduce fractures.
Introduction: Fracture rates tend to be lower in minority women, but consequences may be greater. In
addition, the number of fractures is expected to increase in minority women because of current demographic
trends. There are limited prospective data on risk factors for fractures in minority women.
Materials and Methods: We studied 159,579 women 50–79 yr of age enrolled in the Women’s Health Initiative.
Information on risk factors was obtained by questionnaire or examination. Nonspine fractures that occurred
after study entry were identified over an average follow-up of 8 ± 2.6 (SD) yr.
Results: Annualized rates (%) of fracture in whites, blacks, Hispanics, Asians, and American Indians were 2.0,
0.9, 1.3, 1.2, and 2.0, respectively. Significant predictors [HR (95% CI)] of fractures by ethnic group were as
follows: blacks: at least a high school education, 1.22 (1.0, 1.5); (+) fracture history, 1.7 (1.4, 2.2); and more than
two falls, 1.7 (1.9, 2.0); Hispanics: height (>162 cm), 1.6 (1.1, 2.2); (+) fracture history, 1.9 (1.4, 2.5); more than
two falls, 1.8 (1.4, 2.3); arthritis, 1.3 (1.1, 1.6); corticosteroid use, 3.9 (1.9, 8.0); and parental history of fracture,
1.3 (1.0, 1.6); Asians: age (per 5 yr), 1.2 (1.0, 1.3); (+) fracture history, 1.5 (1.1, 2.0); current hormone therapy
(HT), 0.7 (0.5, 0.8); parity (at least five), 1.8 (1.1, 3.0); more than two falls, 1.4 (1.1, 1.9); American Indian: (+)
fracture history, 2. 9 (1.5, 5.7); current HT, 0.5 (0.3, 0.9). Women with eight or more risk factors had more than
a 2-fold higher rate of fracture compared with women with four or fewer risk factors. Two ethnicity × risk
factor interactions were identified: age and fall history.
Conclusions: Irrespective of their ethnicity, women with multiple risk factors have a high risk of fracture.
Targeting these high-risk women for screening and intervention could reduce fractures.
J Bone Miner Res 2007;22:1816–1826. Published online on July 16, 2007; doi: 10.1359/JBMR.070713

Key words: osteoporotic fractures, ethnicity, race, risk factors, Women’s Health Initiative

INTRODUCTION women, it doubled among Hispanic women from 1983 to

O STEOPOROSIS IS A major public health problem, that
over a lifetime results in fractures in 40% of aging
women.(1) Although the lifetime risk of fractures is lower in
nonwhite women,(2–4) it is still substantial and may be ris-
ing. Whereas the incidence of hip fracture declined in white
Dr Cauley has received research support from Merck & Com-
pany, Eli Lilly & Company, Pfizer Pharmaceuticals, and Novartis
Pharmaceuticals. She has also received consulting fees from Eli
Lilly & Company and Novartis Pharmaceuticals. She is on the
speaker’s bureau for Merck and Company. All other authors state
they have no conflicts of interest.
2000.(5) The consequences of osteoporotic fractures may be
greater among nonwhite women. Mortality after a hip frac-
ture is higher among black than white women.(6) Black
women who suffer a hip fracture have longer hospitaliza-
tion stays and are more likely to be nonambulatory com-
pared with white women.(7) Mexican Americans who re-
ported a previous hip fracture were four times as likely to
be disabled.(8)
The Surgeon General’s Report on Bone Health and Os-
teoporosis noted the lack of information on ethnic and ra-
cial minorities as a priority.(9) Many risk factors have been
identified in prospective studies of white women.(10) There
are few prospective studies of risk factors for fracture

1
Department of Epidemiology, University of Pittsburgh, Graduate School of Public Health, Pittsburgh, Pennsylvania, USA; 2Fred
Hutchinson Cancer Research Center, Seattle, Washington, USA; 3Noqsi Research, Ltd., Pine, Colorado, USA; 4Department of Epide-
miology and Population Health, Albert Einstein College of Medicine, Bronx, New York, New York, USA; 5University of California, San
Diego, La Jolla, California, USA; 6Division of Epidemiology and Biostatistics, University of Arizona, Tucson, Arizona, USA; 7Depart-
ment of Internal Medicine and Physical Medicine, Ohio State University, Columbus, Ohio, USA; 8Department of Internal Medicine,
University of California at Davis School of Medicine, Sacramento, California, USA.

1816
FRACTURES IN MULTI-ETHNIC WOMEN
among minority women. The objective of this study was to
identify risk factors for fracture in a multiethnic cohort of
women enrolled in the Women’s Health Initiative (WHI).
A second objective was to test the hypothesis that ethnic
differences in fracture rates were, in part, mediated by eth-
nic differences in risk factors.
MATERIALS AND METHODS
Study population
The WHI is composed of an observational study (OS,
n ⳱ 92,368) and three overlapping clinical trials (CT, n ⳱
67,211) of hormone therapy (HT), dietary modification,
and calcium and vitamin D supplementation. Women were
recruited from 1993 to 1998. Women were eligible if they
were 50–79 yr of age and postmenopausal. Study methods
have been described in detail elsewhere.(11) All participants
signed informed consent forms that were approved by in-
stitutional review boards. Follow-up ranged from 0 to 12.4
yr for a mean of 8.0 ± 2.6 (SD) yr.
Assessment of risk factors
Information on race or ethnicity was obtained by self-
report and included “whites” (not of Hispanic origin);
“blacks” (not of Hispanic origin); “Hispanics/Latinos”
(Mexican, Cuban, Puerto Rican, Central American, or
South American); “Asians or Pacific Islanders” (Chinese,
Indo-Chinese, Korean, Japanese, Pacific Islander, Viet-
namese); “American Indian” (including Alaskan Native),
or “other.” We excluded women who reported “other” race
(n ⳱ 2,229) from this report. Data were collected on edu-
cation, living arrangements, fracture, reproductive and
medical history, alcohol intake, cigarette smoking, physical
activity, general health status, diet, falls, and medications. A
woman was considered depressed based on her score on
the Centers for the Epidemiologic Study of Depression
(CES-D) test(12) or reported use of antidepressants. Body
mass index was calculated as weight in kilograms divided by
height in square meters.
If a woman had been randomly assigned to the estrogen
and progestin (E + P) or the E-alone group or reported use
of E + P or E alone at baseline, she was considered a
current hormone user. Women randomly assigned to pla-
cebo and women who reported past or never use at baseline
were considered never/past users.
BMD at the total hip and posterior-anterior spine was
measured in 12,705 women (97% of women enrolled in
Pittsburgh, PA; Birmingham, AL; and Phoenix/Tucson,
AZ) with DXA (Hologic, Waltham, MA, USA). BMD
models were confined to white, black, and Hispanic women
because of insufficient numbers of Asians and American
Indians with BMD. Standard protocols for positioning and
analysis were used by technicians who were trained and
certified.
Follow-up and fracture ascertainment
At study end, 5.7% of participants were deceased, and
4.3% of participants had withdrawn or were lost to follow-
1817
up. The primary outcome of the study included all fractures
that occurred after study entry except for those of the fin-
gers, toes, face, skull, or sternum. Local and central review
of radiology reports confirmed all hip fractures. Informa-
tion on other fractures was confirmed by radiographic re-
port among CT women. For women in the OS, we relied on
self-report of nonhip fractures. In the WHI, 80% of self-
reported nonhip fractures were confirmed by physician re-
view of medical records, suggesting that the self-report of
such fractures is reasonably accurate.(13)
Statistical analysis
All analyses were performed using SAS 9.1 (Cary, NC,
USA). The baseline characteristics of the women were
compared across ethnicity using ANOVA and ␹2 tests. We
used Cox regression models that were stratified according
to age at WHI baseline and WHI CT participation. The first
confirmed fracture that occurred over follow-up was used in
the analysis. We calculated the HRs and 95% CIs. Vari-
ables included in the final main effect model were chosen
based on statistical significance (p < 0.25 in the age-adjusted
univariate model), their clinical importance, and previous
literature. The cut-off used to distinguish the unit of refer-
ence in the multivariable models for height, weight, and
caffeine intake was the 75th percentile in the total popula-
tion. We also examined the HR per 1 SD increase, and
results were essentially unchanged (data not shown). For
BMD, we calculated the HR for fracture per 1 SD decrease
in BMD.
We examined two-way interactions using likelihood ratio
tests to test whether a particular risk factor modified the
risk for fracture by ethnic group. To select the most parsi-
monious model, we used the likelihood ratio test to com-
pare a model that included all ethnicity-related two-way
interactions to a model containing only significant two-way
interactions. We calculated the number of risk factors for
each individual based on the variables entered into the final
multivariable model. The annualized rate of fracture was
compared for women with no more than four, five to seven,
and at least eight clinical risk factors.
To test whether the clinical risk factors account for ethnic
differences in fracture, we calculated the HR of fracture
compared with white women by ethnicity in age and mul-
tivariable adjusted models. In the subgroup of women with
BMD, we calculated the HR for fracture for black and
Hispanic women compared with white women in age and
multivariable models and further adjusted for BMD. All p
values are two-sided.
RESULTS
The mean age of the cohort ranged from 60.2 yr in His-
panic women to 63.6 yr among white women (Tables 1 and
2). Although the absolute differences in these characteris-
tics across ethnicity were relatively small, in many cases,
they were statistically significant because of the large
sample size. The mean weight and BMD were greatest
among black women and lowest among Asian or white
women. In general, calcium intake was high, exceeding 1000
mg/d. Physical activity was greatest in whites and Asians
1818 CAULEY ET AL.

15.8 (10.3)*

982.6 (623.2)
and lowest in blacks. The percent with a college degree or

Mean (SD)

78.6 (19.0)

11.5 (15.1)

0.95 (0.17)
0.88 (0.15)
61.6 (7.5)

160.8 (6.8)
30.0 (6.5)
American Indian
higher was greatest among Asians and whites and lowest
among Hispanics and American Indians. Less than 10%
reported current smoking. Diabetes was more common
among blacks and American Indians, whereas hypertension
was more common among blacks. Use of postmenopausal
hormones was relatively high at entry into WHI. Con-
715
636
712
704
700

692
664

148
149
N

versely, use of bisphosphonate and selective estrogen re-

ceptor modulators (SERMS) was low (<3%). In the sub-
group with BMD, lumbar spine BMD was highest in black

13.1 (14.2)*
998.3 (666.5)

0.94 (0.17)*
0.83 (0.10)*
Mean (SD)

59.8 (12.9)
Asian/Pacific Islander

women and lowest in Hispanic women. Total hip BMD was

63.0 (7.5)
14.3 (9.1)

154.9 (6.0)
24.8 (4.6)
also highest in black women and lowest in white and Asian
ETHNICITY: CONTINUOUS VARIABLES (MEAN ± SD)

women.

Fracture rates
Over an average 8.0 yr of follow-up, incident fractures
4,192
4,019
4,187
4,173
4,170

4,136
3,981

36
36
N

occurred in 23,270 women, including 21,083 (15.8%) white

women; 1112 (7.6%) black women; 580 (8.9%) Hispanic
women; 391 (9.3%) Asian women; and 164 (14.6%) Ameri-
can Indian women. The annualized (%) rate of fracture was
1003.5 (664.4)
72.3 (16.2)

10.5 (13.7)

0.93 (0.17)
0.85 (0.13)
Mean (SD)
60.2 (6.8)
12.8 (8.9)

157.2 (6.2)
29.1 (5.8)

2.0, 0.9, 1.3, 1.2, and 2.0, respectively. Hip fractures ac-
counted for 7% of all fractures, and clinical spine fractures
Hispanic

accounted for 9%. In the BMD subcohort of 12,705 women,

* Nonsignificant results when comparing with white participants. Missing values are excluded from the comparison of proportions.
Ethnicity

fractures occurred in 1828 (18.5%) white women; 164

(9.7%) black women; and 96 (10.8%) Hispanic women,
with an annualized (%) rate of fracture 2.5, 1.3, and 1.5,
6,512
5,763
6,497
6,452
6,438

6,133
6,015

736
737

respectively.
N

Age
WHI BY

764.2 (563.0)

The HR for fracture per 5-yr increase in age among

Mean (SD)

82.8 (19.0)

9.6 (12.8)

1.06 (0.21)
0.95 (0.15)
61.6 (7.1)
15.1 (9.9)

162.4 (6.7)
31.2 (6.7)

white, black, Hispanic, Asian, and American Indian women

IN

was 1.10, 1.00, 1.10, 1.14, and 1.08, respectively (p for inter-
WOMEN

action ⳱ 0.02). There was a stepwise increase in fractures

Black

rates with age in all groups except black women (Fig. 1).
Among black women, fractures rates were stable until 75+
OF

14,627
13,191
14,587
14,528
14,482

14,108
13,509

1,568
1,574

yr of age.
TABLE 1. BASELINE CHARACTERISTICS

Age-adjusted risk factors for fracture

Among white women, most variables were statistically
1179.4 (725.1)

significant, although the magnitude of several of these as-

73.0 (16.3)

12.8 (13.8)

0.95 (0.19)
0.83 (0.13)
Mean (SD)
63.6 (7.2)
15.3 (9.2)

162.2 (6.5)
27.6 (5.8)

sociations was weak (Table 3). The focus of the manuscript

is on minority women. Risk factors that showed a sig-
nificant age-adjusted association with fracture in black
White

women included greater height, greater education, personal

and parental fracture history, history of diabetes, myocar-
dial infarction (MI), arthritis, use of nonsteroidal anti-
133,533
126,665
133,065
132,759
132,367

127,110
130,521

8,769
8,819
N

inflammatory drugs (NSAIDs), use of corticosteroids for

>2 yr, sedatives/anxiolytics, and falls. Among Hispanic
women, greater education, personal and family history of
fracture, history of diabetes, MI, arthritis, use of corticoste-
Baseline total calcium (mg)†
Years since menopause (yr)

Baseline total expend from

roids >2 yr, and falls were associated with a significant in-
physical activity (METs)

Dietary plus supplements.

Body-mass index (kg/m2)

crease risk of fracture. Among Asian women, risk factors

Age at screening (yr)

included personal history of fracture, depression, and falls.

Use of hormones for ⱖ5 yr, prior oophorectomy, and ex-
cellent to good health status were each associated with a
Lumbar spine
BMD (g/cm2)
Height (cm)
Weight (kg)

26–36% decreased risk of fracture in Asian women. Simi-

Total hip

larly, among American-Indian women, personal and paren-

tal history of fracture, diabetes, depression, and falls were
†

each associated with a 70–120% significant increased risk of

FRACTURES IN MULTI-ETHNIC WOMEN 1819

TABLE 2. BASELINE CHARACTERISTICS OF WOMEN IN WHI BY ETHNICITY: CATEGORICAL VARIABLES

Ethnicity

White Black Hispanic Asian/Pacific Islander American Indian

N (%) N (%) N (%) N (%) N (%)

Total 133,533 (100.0) 14,627 (100.0) 6,512 (100.0) 4,192 (100.0) 715 (100.0)
Education
High school diploma/GED or less 27,975 (20.9) 3,769 (25.8) 2,812 (43.2) 876 (20.9) 237 (33.1)
School after high school 50,394 (37.7) 5,622 (38.4) 2,242 (34.4) 1,446 (34.5) 315 (44.1)
College degree or higher 54,293 (40.7) 5,047 (34.5) 1,338 (20.5) 1,839 (43.9) 155 (21.7)
Married/w partner vs. single/widowed/
divorced/separated (yes) 86,144 (64.7) 5,882 (40.7) 3,718 (58.0) 2,834 (68.0) 388 (55.0)
Smoking
Past smoker 57,499 (43.1) 5,595 (38.3) 1,899 (29.2) 999 (23.8) 280 (39.2)
Current smoker 8,648 (6.5) 1,639 (11.2) 462 (7.1) 166 (4.0) 74 (10.3)
Alcohol consumption
>0–<1 drink per week 44,037 (33.0) 4,492 (30.7) 2,178 (33.4) 1,228 (29.3) 207 (29.0)
1 + drinks per week 54,589 (40.9) 2,587 (17.7) 1,435 (22.0) 516 (12.3) 189 (26.4)
History of fracture on/after age 55 yr 18,124 (13.6) 934 (6.4) 464 (7.1) 372 (8.9) 72 (10.1)*
Treated diabetes (pills or shots) 4,453 (3.3) 1,774 (12.1) 467 (7.2) 247 (5.9) 94 (13.1)
History of hypertension
Untreated hypertensive 9,920 (7.4) 1,323 (9.0) 561 (8.6) 344 (8.2) 77 (10.8)
Treated hypertensive 30,022 (22.5) 6,390 (43.7) 1,283 (19.7) 1,145 (27.3) 203 (28.4)
History of myocardial infarction 2,921 (2.2) 545 (3.7) 88 (1.4) 49 (1.2) 35 (4.9)
History of stroke 1,554 (1.2) 386 (2.6) 106 (1.6) 50 (1.2) 24 (3.4)
History of rheumatoid arthritis 5,855 (4.4) 1,220 (8.3) 403 (6.2) 186 (4.4) 64 (9.0)
History of arthritis 63,062 (47.2) 7,544 (51.6) 2,749 (42.2) 1,423 (33.9) 383 (53.6)
Depression 36,815 (28.1) 4,301 (31.0) 2,386 (40.4) 770 (18.7) 276 (40.4)
Time since quitting HT
Nonuser 55,761 (41.8) 8,755 (59.9) 3,371 (51.8) 1,615 (38.5) 354 (49.5)
Past <5 yr 8,546 (6.4) 797 (5.4) 453 (7.0) 261 (6.2) 42 (5.9)
Past 5 to <10 yr 3,912 (2.9) 365 (2.5) 175 (2.7) 119 (2.8) 20 (2.8)
Past ⱖ10 yr 9,240 (6.9) 1,038 (7.1) 267 (4.1) 227 (5.4) 58 (8.1)
Current hormone therapy use
<5 yr 15,236 (11.4) 1,429 (9.8) 885 (13.6) 619 (14.8) 59 (8.3)
ⱖ5 yr 40,737 (30.5) 2,222 (15.2) 1,351 (20.7) 1,349 (32.2) 182 (25.5)
Baseline NSAID use 48,319 (36.2) 3,889 (26.6) 1,576 (24.2) 686 (16.4) 233 (32.6)
␤-Blockers group use 10,932 (8.2) 1,133 (7.7)* 327 (5.0) 279 (6.7) 44 (6.2)
Corticosteroid use > 2 yr 681 (0.5) 114 (0.8) 40 (0.6)* 16 (0.4)* 3 (0.4)*
Thyroid hormone use 19,854 (14.9) 1,009 (6.9) 625 (9.6) 355 (8.5) 102 (14.3)*
Bisphosphonate use 2,507 (1.9) 41 (0.3) 81 (1.2) 116 (2.8) 0 (0)
SERM use 37 (0.0) 1 (0.0)* 3 (0.0)* 5 (0.1) 0 (0)
Sedative/antipsychotics/hypnotic
medication use 8,471 (6.3) 809 (5.5) 373 (5.7) 97 (2.3) 43 (6.0)*
Prior bilateral oophorectomy (yes) 25,845 (19.4) 3,178 (21.7) 1,117 (17.2) 812 (19.4)* 154 (21.5)
Hysterectomy at screening (yes) 53,887 (40.4) 8,125 (55.5) 2,910 (44.7) 1,458 (34.8) 374 (52.3)
Number of pregnancies
1 8,871 (6.6) 1,472 (10.1) 406 (6.2) 322 (7.7) 54 (7.6)
2–4 80,043 (59.9) 7,406 (50.6) 3,244 (49.8) 2,662 (63.5) 372 (52.0)
5+ 31,601 (23.7) 4,464 (30.5) 2,262 (34.7) 698 (16.7) 247 (34.5)
Parent broke bone after age 40 (yes) 52,747 (39.5) 2,532 (17.3) 1,779 (27.3) 1,226 (29.2) 199 (27.8)
Number of falls during last
follow-up year >2 times 8,910 (6.7) 739 (5.1) 328 (5.0) 185 (4.4) 58 (8.1)*
Health status
Excellent/very good/good 123,200 (92.3) 11,655 (79.7) 4,934 (75.8) 3,785 (90.3) 563 (78.7)
Fair/poor 9,638 (7.2) 2,829 (19.3) 1,407 (21.6) 391 (9.3) 147 (20.6)

*Nonsignificant results when comparing with white participants. Missing values are excluded from the comparison of proportions.

fracture. However, both current cigarette smoking and use A 1 SD decrease in hip BMD was associated with a 24–
of corticosteroids were associated with an increased risk of 46% significant increase in the risk of fracture. The asso-
fracture, but neither was significant, perhaps reflecting low ciation between spine BMD and subsequent fracture was
statistical power. weaker in all ethnic groups.
1820
Multivariable models of risk factors for fracture
Among white women, all of the risk factors were statis-
tically significant, although the magnitude of several asso-
ciations was quite small, and they are unlikely to be of
clinical significance (Table 4). Among black women, higher
education, positive fracture history, and history of more
than two falls were independently associated with a 20–
74% significant increase in the risk of fracture. Among His-
panic women, older age, greater height, personal and family
history of fracture, more than two falls, corticosteroid use
(>2 yr), and history of arthritis were independently associ-
ated with an increased risk of fracture. The association with
corticosteroid use was quite high, indicating an almost
4-fold increased risk of fracture. Among Asian women,
older age, positive fracture history, more than two falls, and
parity were independently associated with a 15–65% in-
creased fracture risk, and current use of hormones (ⱖ5 yr)
was associated with a 37% decrease of risk of fracture.
Among American-Indian women, a positive fracture his-
tory was associated with an almost 3-fold increased risk of
fracture. Higher education, parental history of fracture, fall
history, use of corticosteroids, and depression suggested an
increased risk of fracture, but the results were not signifi-
cant.
We found a significant interaction with fall history and
race-ethnicity. The HR for more than two falls in white,
black, Hispanic, Asian, and American-Indian women was
1.27, 1.66, 1.29, 1.37, and 1.63, respectively (p for interaction
⳱ 0.003). The risk of fracture was higher among women
who reported more than two falls, but this risk was espe-
cially elevated in black and American-Indian women.
The rate of fracture increased with increasing number of
risk factors (Fig. 2). The absolute rate of fracture was 2-fold
higher in women with eight or more risk factors compared
with women with four or fewer risk factors. Ethnic differ-
ences in fracture were attenuated among women with eight
or more risk factors, especially comparing whites, Hispan-
ics, and Asians.
The risk of fracture among black women, compared with
CAULEY ET AL.
FIG. 1. Age-specific annualized (%) inci-
dence of fracture across ethnic groups.
white women, was 49% lower, even after adjusting for mul-
tiple variables (Table 5). Similarly, among Hispanic and
Asian women, there was little attenuation in the HR for
fracture after adjusting for multiple risk factors. In the sub-
group of women with BMD, the lower risk of fracture
among black and Hispanic women was independent of
BMD. There was, however, some attenuation in ethnic dif-
ferences in models with total hip BMD.
DISCUSSION
This study is one of the largest longitudinal cohort studies
to evaluate risk factors for fracture in a multi-ethnic cohort
of older women. No previous study has recruited sufficient
numbers of minority women with standardized data collec-
tion of information on a large number of risk factors for
fractures and followed them for 8 yr for the incidence of
fractures. Results showed that risk factors for fracture were
similar across ethnic group and similar to previous reports
of white women.(10) Of importance, however, women with
multiple risk factors have an especially high risk of fracture,
irrespective of their ethnicity. Identifying clinical risk fac-
tors that predict fracture and targeting these high-risk
women for screening and intervention could reduce their
fracture burden.
The annualized rate of fracture was greatest in white and
American-Indian women and lowest in black women. The
patterns of fracture across ethnic groups were consistent
with previous studies of hip fracture.(14) The National Os-
teoporosis Risk Assessment (NORA) reported higher rates
of fracture in Hispanic women; in WHI, fracture rates were
similar in Hispanic and Asian women.(15) Few studies have
reported fracture rates among American-Indian women,
but American Indians in NORA also had high odds of os-
teoporosis.(15)
Previous history of fracture was associated with a >50%
increased risk of subsequent fracture in all women. Use of
corticosteroids for >2 yr was also associated with a substan-
tial increase in fracture risk. Current use of hormone
FRACTURES IN MULTI-ETHNIC WOMEN 1821

TABLE 3. AGE-ADJUSTED UNIVARIATE HRS (95% CI) FOR FRACTURES ACROSS ETHNICITY

Ethnicity

White Black Hispanic Asian American Indian

Nonmodifiable
Years since menopause
<10 vs. 20+ yr 0.91 (0.86, 0.95) 0.88 (0.72, 1.07) 1.05 (0.78, 1.41) 0.97 (0.65, 1.44) 0.71 (0.34, 1.50)
10 to <20 vs. 20+ yr 0.98 (0.95, 1.02) 0.91 (0.77, 1.08) 0.99 (0.78, 1.27) 1.06 (0.80, 1.42) 1.22 (0.69, 2.17)
Education (vs. less than high school)
ⱖHigh school 1.06 (1.02, 1.10) 1.26 (1.08, 1.48) 1.20 (0.99, 1.45) 1.08 (0.81, 1.43) 1.03 (0.66, 1.61)
ⱖCollege 1.08 (1.04, 1.12) 1.18 (1.01, 1.39) 1.28 (1.03, 1.59) 1.23 (0.93, 1.63) 0.96 (0.55, 1.67)
Living with partner 0.89 (0.86, 0.91) 0.95 (0.84, 1.08) 0.95 (0.81, 1.12) 1.02 (0.64, 1.63) 0.96 (0.64, 1.43)
Parents had fracture after age 40 yr 1.20 (1.17, 1.24) 1.16 (1.00, 1.34) 1.30 (1.09, 1.54) 1.18 (0.95, 1.46) 1.72 (1.14, 2.59)
Modifiable
Weight ⱖ 70.5 kg (vs. lower) 1.03 (1.00, 1.07) 0.97 (0.92, 1.02) 1.03 (0.84, 1.26) 1.09 (0.68, 1.74) 1.02 (0.67, 1.54)
Height > 161.9 cm (vs. lower) 1.13 (1.09, 1.17) 1.16 (1.02, 1.32) 1.33 (0.99, 1.78) 1.20 (0.71, 2.02) 1.07 (0.64, 1.78)
Caffeine intake ⱖ 188mg/d (vs. lower) 1.07 (1.03, 1.10) 1.00 (0.84, 1.20) 1.07 (0.85, 1.35) 1.04 (0.78, 1.38) 1.29 (0.83, 2.01)
Physical activity (METs) per SD 0.98 (0.96, 0.99) 0.97 (0.90, 1.03) 1.03 (0.95, 1.11) 1.06 (0.97, 1.17) 0.94 (0.78, 1.14)
Current smoker 1.16 (1.10, 1.22) 1.09 (0.90, 1.31) 0.89 (0.63, 1.26) 0.91 (0.74, 1.13) 1.65 (0.95, 2.88)
Alcohol intake
<1 drink/wk vs. none/past drinker 0.96 (0.92, 0.99) 1.07 (0.94, 1.23) 0.97 (0.80, 1.17) 1.00 (0.80, 1.26) 1.41 (0.90, 2.20)
1+ drinks/wk vs. none/past drinker 0.96 (0.93, 0.99) 1.09 (0.93, 1.28) 0.97 (0.78, 1.20) 0.99 (0.72, 1.37) 0.80 (0.47, 1.37)
History of fracture at/after age 55 yr 1.60 (1.55, 1.66) 1.76 (1.44, 2.15) 1.85 (1.44, 2.37) 1.62 (1.22, 2.15) 2.20 (1.29, 3.77)
History of diabetes 1.36 (1.27, 1.45) 1.36 (1.15, 1.60) 1.35 (1.02, 1.79) 1.10 (0.73, 1.65) 2.00 (1.24, 3.22)
History of hypertension 0.99 (0.96, 1.02) 0.91 (0.81, 1.03) 0.98 (0.80, 1.20) 1.00 (0.80, 1.25) 1.30 (0.81, 2.07)
History of myocardial infarction 1.21 (1.12, 1.32) 1.47 (1.12, 1.92) 1.72 (1.01, 2.93) 0.80 (0.30, 2.15) 1.27 (0.58, 2.79)
History of stroke 1.41 (1.27, 1.57) 1.37 (0.99, 1.89) 1.61 (0.97, 2.65) 1.64 (0.81, 3.32) 1.16 (0.41, 3.25)
History of arthritis 1.17 (1.13, 1.20) 1.17 (1.03, 1.32) 1.32 (1.11, 1.56) 1.14 (0.93, 1.41) 1.43 (0.95, 2.15)
Depression 1.20 (1.17, 1.24) 1.12 (0.99, 1.28) 1.13 (0.95, 1.35) 1.28 (1.00, 1.64) 1.68 (1.12, 2.53)
Current hormone therapy
<5 yr vs. never/past user 0.84 (0.80, 0.88) 0.92 (0.74, 1.13) 0.88 (0.68, 1.15) 0.73 (0.52, 1.01) 0.64 (0.29, 1.44)
ⱖ5 yr vs. never/past user 0.78 (0.76, 0.81) 1.01 (0.85, 1.19) 0.88 (0.71, 1.09) 0.64 (0.50, 0.81) 0.63 (0.38, 1.04)
Thiazide diuretics use 0.97 (0.91, 1.03) 0.98 (0.81, 1.18) 1.33 (0.87, 2.04) 0.92 (0.54, 1.58) 1.56 (0.77, 3.16)
NSAID use 0.99 (0.96, 1.02) 1.20 (1.06, 1.37) 1.17 (0.97, 1.40) 1.09 (0.84, 1.41) 1.14 (0.76, 1.72)
␤-blockers use 1.01 (0.96, 1.06) 1.11 (0.89, 1.37) 1.19 (0.85, 1.67) 0.98 (0.66, 1.47) 0.47 (0.15, 1.49)
Corticosteroid use > 2 yr 1.61 (1.39, 1.87) 2.27 (1.45, 3.54) 2.63 (1.36, 5.10) 0.58 (0.08 4.17) 2.16 (0.30, 15.80)
Thyroid hormone use 1.05 (1.01, 1.09) 1.10 (0.88, 1.38) 1.13 (0.87, 1.47) 1.06 (0.75, 1.49) 1.04 (0.60, 1.81)
Sedative/antipsychotic/hypnotic use 1.18 (1.12, 1.24) 1.34 (1.07, 1.68) 1.08 (0.77, 1.51) 1.46 (0.83, 2.54) 1.06 (0.49, 2.32)
Prior bilateral oophorectomy 0.96 (0.93, 1.00) 1.00 (0.87, 1.16) 1.10 (0.89, 1.36) 0.76 (0.58, 0.99) 1.04 (0.64, 1.67)
Hysterectomy 0.94 (0.91, 0.96) 1.09 (0.97, 1.23) 1.00 (0.85, 1.18) 0.86 (0.69, 1.06) 0.88 (0.60, 1.30)
Parity
1 vs. never pregnant 0.92 (0.86, 0.98) 1.23 (0.93, 1.64) 1.01 (0.68, 1.51) 1.22 (0.76, 1.95) 0.83 (0.22, 3.12)
2–4 vs. never pregnant 0.89 (0.85, 0.93) 1.13 (0.89, 1.44) 0.84 (0.63, 1.11) 1.08 (0.77, 1.52) 1.27 (0.45, 3.57)
5+ vs. never pregnant 0.92 (0.88, 0.97) 1.14 (0.89, 1.45) 0.84 (0.62, 1.12) 1.44 (0.98, 2.12) 1.40 (0.49, 3.99)
Health status
Excellent/very good/ good
vs. fair/poor 0.71 (0.68, 0.75) 0.89 (0.77, 1.03) 0.94 (0.77, 1.15) 0.68 (0.51, 0.92) 0.88 (0.55, 1.43)
>2 falls (vs. ⱕ2 falls) 1.35 (1.30, 1.40) 1.81 (1.55, 2.12) 1.97 (1.60, 2.43) 1.54 (1.17, 2.03) 2.05 (1.30, 3.24)
BMD (per 1 SD decrease)
Total hip BMD 1.42 (1.34, 1.51) 1.24 (1.05, 1.46) 1.46 (1.11, 1.92) — —
Lumbar spine BMD 1.30 (1.24, 1.37) 1.31 (1.11, 1.54) 1.16 (0.90, 1.50) — —

therapy was associated with lower risk of fracture in whites,
Asians, and American Indians. Failure to observe an asso-
ciation in black and Hispanic women may have reflected
the lower proportion of black and Hispanic women who
used hormones for ⱖ5 yr. Data from the WHI hormone
trials do not support a race × hormone therapy interac-
tion.(16,17)
Previously, alcohol consumption of at least seven drinks
per week was associated with a 4-fold increased risk of hip
fracture in black women(18) and was linked with hip frac-
ture in an older Japanese cohort.(19) Our analysis did not
show an association between alcohol consumption and frac-
ture in any ethnic group, perhaps reflecting the low intake
among WHI minority women.
Thinness has previously been associated with an in-
creased risk of fracture in black women.(20,21) Our results
do not show a strong relationship between body weight or
thinness and subsequent risk of fracture in any ethnic
group. Our results are consistent with data showing that low
body weight is strongly linked with hip, pelvic, and rib frac-
1822 CAULEY ET AL.

TABLE 4. MULTIVARIATE MODELS OF FRACTURE RISK: HR (95% CIS) WITHIN ETHNIC GROUPS

Ethnicity

American
Reference/unit White Black Hispanic Asian Indian
Nonmodifiable
Age Per 5 yr 1.10 (1.09, 1.12) 0.98 (0.92, 1.05) 1.13 (1.02, 1.26) 1.15 (1.02, 1.29) 1.02 (0.81, 1.28)
Years since menopause 10–20 vs. <10 1.05 (1.01, 1.10) 1.09 (0.90, 1.32) 0.99 (0.76, 1.30) 1.06 (0.76, 1.47) 1.54 (0.75, 3.17)
ⱖ20 vs. <10 1.09 (1.03, 1.16) 1.23 (0.98, 1.54) 0.85 (0.60, 1.21) 1.08 (0.70, 1.66) 1.16 (0.50, 2.71)
Education > high ⱕ high school 1.07 (1.02, 1.11) 1.23 (1.01, 1.49) 1.09 (0.86, 1.38) 1.11 (0.81, 1.53) 1.69 (0.92, 3.12)
school
ⱖ College and more ⱕ high school 1.10 (1.05, 1.14) 1.23 (1.00, 1.51) 1.22 (0.93, 1.58) 1.28 (0.94, 1.74) 1.62 (0.78, 3.37)
Living with partner No 0.90 (0.91, 0.97) 1.00 (0.87, 1.16) 0.99 (0.81, 1.22) 1.01 (0.79, 1.29) 1.28 (0.76, 2.16)
Parent fracture No 1.18 (1.15, 1.22) 1.14 (0.96, 1.36) 1.28 (1.04, 1.58) 1.21 (0.96, 1.53) 1.58 (0.94, 2.67)
Modifiable
Weight >70.5 kg 0.95 (0.91, 0.98) 0.93 (0.80, 1.09) 0.91 (0.71, 1.18) 0.81 (0.45, 1.47) 1.02 (0.59, 1.76)
Height >162 cm 1.14 (1.10, 1.18) 1.01 (0.86, 1.18) 1.56 (1.11, 2.17) 1.46 (0.85, 2.52) 1.03 (0.56, 1.89)
Daily caffeine intake >188 mg 1.04 (1.00, 1.07) 0.90 (0.72, 1.12) 1.08 (0.83, 1.40) 1.08 (0.80, 1.47) 0.64 (0.35, 1.16)
Current smoking No 1.09 (1.02, 1.15) 1.04 (0.83, 1.30) 0.81 (0.52, 1.26) 0.90 (0.48, 1.72) 1.14 (0.54, 2.43)
Fracture bone since No 1.55 (1.49, 1.61) 1.74 (1.38, 2.20) 1.86 (1.39, 2.50) 1.50 (1.10, 2.05) 2.89 (1.47, 5.66)
age 55 yr
>2 falls ⱕ2 1.27 (1.22, 1.32) 1.67 (1.38, 2.02) 1.80 (1.40, 2.32) 1.41 (1.04, 1.91) 1.38 (0.75, 2.55)
Current HT (<5 yr) None/past user 0.86 (0.82, 0.91) 0.99 (0.78, 1.25) 0.99 (0.73, 1.33) 0.74 (0.52, 1.06) 0.55 (0.21, 1.43)
ⱖ5 yr None/past user 0.77 (0.75, 0.80) 0.91 (0.75, 1.11) 0.85 (0.66, 1.09) 0.63 (0.48, 0.82) 0.49 (0.26, 0.92)
Corticosteroid use No 1.43 (1.22, 1.68) 1.54 (0.82, 2.90) 3.88 (1.89, 7.99) 0.73 (0.10, 5.27) 2.75 (0.26, 28.93)
>2 ys
Sedatives/antiolytics No 1.09 (1.02, 1.15) 1.21 (0.92, 1.60) 1.02 (0.67, 1.54) 1.09 (0.56, 2.15) 1.17 (0.50, 2.74)
History of arthritis No 1.13 (1.09, 1.16) 1.07 (0.92, 1.25) 1.29 (1.05, 1.59) 1.08 (0.85, 1.37) 1.39 (0.82, 2.34)
Depression No 1.11 (1.07, 1.15) 1.04 (0.89, 1.22) 1.12 (0.91, 1.38) 1.14 (0.86, 1.52) 1.54 (0.91, 2.61)
Health status: excellent/ Fair/poor 0.80 (0.76, 0.84) 0.97 (0.80, 1.17) 1.01 (0.77, 1.32) 0.81 (0.56, 1.16) 0.82 (0.44, 1.52)
very good/good
Parity
1 None 0.95 (0.88, 1.02) 1.33 (0.95, 1.86) 1.08 (0.67, 1.73) 1.77 (1.06, 2.96) 0.54 (0.12, 2.40)
2–4 None 0.94 (0.90, 0.99) 1.10 (0.82, 1.46) 0.85 (0.60, 1.20) 1.25 (0.84, 1.87) 1.09 (0.35, 3.42)
5+ None 0.95 (0.90, 1.00) 1.13 (0.84, 1.54) 0.81 (0.56, 1.16) 1.65 (1.06, 2.56) 1.43 (0.44, 4.61)

FIG. 2. Annualized (%) incidence rate of

fracture by the total number of risk factors
across ethnic groups. Risk factors included:
age >65 yr, height >161.9 cm, weight <70.5
kg, consumed >188 mg caffeine/d, >20 yr
since menopause, never used HT, higher
than high school education, living without
partner, current smoker, fair or poor health
status, broke bone at/after age 55 yr, have
any arthritis, use corticosteroids >2 yr, de-
pressed (CES-D or medication use), use
sedatives/anxiolytic, parity (at least two), pa-
rental history of fracture, and greater than
two falls during the last 12 mo of follow-up or
year before the fracture. The mean (SD)
number of risk factors per group: white, 6.1
(1.9); black, 5.8 (1.8); Hispanic, 5.4 (1.8);
American Indian, 6.1 (2.0); Asians, 5.3 (1.7).

tures but not to all fractures.(22) We examined body weight
using the 25th percentile (<62 kg) and an absolute cut-off of
BMI (<20 kg/m2). WHI women tended to be overweight or
obese, with >80% of women having a BMI >25.0 kg/m2. We
had too few women who were considered thin (BMI <20
kg/m2: <2%).
History of stroke has been linked to increased risk of hip
fracture in black,(20) Mexican-American,(23) and Asian
women.(24) In age-adjusted models, history of stroke was
associated with a 40–60% increased risk of fracture in all
groups except American Indians, but it was not consistently
statistically significant, perhaps reflecting lower power. In
FRACTURES IN MULTI-ETHNIC WOMEN
TABLE 5. HR (95% CI) FOR FRACTURE WITHIN EACH ETHNIC GROUP: WHITE WOMEN FORM
Black
Total population (n = 159,579)
Age-adjusted 0.51 (0.48, 0.54)
MV-adjusted* 0.51 (0.47, 0.55)
BMD cohort (n = 12,705)
Age-adjusted 0.51 (0.48, 0.54)
MV-adjusted* 0.51 (0.47, 0.55)
MV + total hip BMD 0.65 (0.53, 0.80)
MV + lumbar spine BMD 0.56 (0.45, 0.69)
*Multivariate (MV) models: adjusted for age, years since menopause, education, living with a partner, height, weight, caffeine intake, smoking, fracture
history, parental fracture history, falls, current HT use (ⱖ5 yr), corticosteroid use (>2 yr), sedative/ anxiolytics use, arthritis, depression, health status, and
parity.
age-adjusted models, self-report of diabetes was associated
with a 35–100% increased risk of fracture in all groups ex-
cept Asians. This is consistent with previous studies show-
ing a higher risk of fracture among diabetics in white,(25)
black,(25) and Hispanic women.(26) The prevalence of dia-
betes was particularly high among the American-Indian
and black women, suggesting that the attributable risk for
fracture associated with diabetes may be substantial in
these groups. However, neither history of stroke nor dia-
betes was independently associated with fracture in the
multivariable models. The increased risks associated with
these co-morbidities may have been explained by other fac-
tors in the model. Depression has been linked to fractures
in white women,(27) but we found no significant association
in other ethnic groups, although the point estimates were
consistent with an increased risk, especially among Ameri-
can-Indian women.
Higher education was associated with a greater risk of
fracture, especially among black women. Previous studies
have not consistently reported a socioeconomic (SES) gra-
dient for fractures.(10) Greater parity was associated with
an increased risk of fracture among Asian women, but
there was no clear pattern of association in other ethnic
groups. Previous analyses in white women have shown a
9% lower risk of hip fracture with each additional birth.(28)
Calcium intake was not related to fracture, perhaps be-
cause intakes were high in WHI women, and there were
few women who had intakes <400 mg. Our results are con-
sistent with the overall findings from the calcium/vitamin D
clinical trial, which showed no overall effect on all frac-
tures.(29)
Use of central nervous system active medications such as
sedatives and hypnotics was associated with an increased
risk of fractures in age-adjusted models in black and white
women, consistent with previous reports.(30) This observa-
tion was not significant in the multivariable models, per-
haps reflecting the relatively low prevalence of use in our
population.(30) Several medications have previously been
linked with osteoporosis, including thiazide diuretics,(31)
NSAIDs,(32) ␤-blockers,(33) and thyroid supplements.(34)
However, we found no consistent association with fractures.
We observed a significant interaction between age and
1823
THE REFERENT GROUP
Ethnicity
Hispanic Asian/Pacific Islander American Indian
0.64 (0.59, 0.70) 0.59 (0.53, 0.65) 1.03 (0.85, 1.25)
0.67 (0.60, 0.74) 0.66 (0.59, 0.74) 0.95 (0.75, 1.20)
0.64 (0.59, 0.70) — —
0.67 (0.60, 0.74) — —
0.75 (0.57, 0.99) — —
0.73 (0.56, 0.97) — —
ethnicity, where the risk of fracture increased in a stepwise
fashion with age in all groups except black women. In black
women, an increased risk of fracture was not observed until
the oldest age group. This is consistent with observed pat-
terns with hip fracture, where rates exponentially increase
after age 80 in black women.(35) We also observed a signifi-
cant interaction with fall history and ethnicity. Although
the risk of fracture was high in all women with more than
two falls, the HR was significantly greater for black and
American-Indian women, perhaps reflecting greater 25-
hydroxy vitamin D [25(OH)D] deficiency. In prior studies,
the prevalence of 25(OH)D deficiency was three times
higher in blacks than in whites,(36,37) and low 25(OH)D
levels have been linked to higher rates of falling.(38) Given
the high prevalence of 25(OH)D deficiency(39) and the
availability of inexpensive supplements, there is a need to
further our understanding of vitamin D, falls, and fractures
in minority women.
Despite the universal decline in BMD with age(40) and
the increased risk of fracture with age,(14) preventive and
therapeutic efforts focus primarily on white and Asian
women. Black women with a positive fracture history were
60% less likely to receive a BMD measurement in compari-
son with white women.(41) A retrospective review of medi-
cal records at Howard University Hospital showed that
only 9% of black women who presented with a low-impact
fracture received a diagnosis of osteoporosis, and of these,
only 19% were discharged on osteoporosis medication.(42)
Key to prevention of fractures is the need to identify sub-
jects at high risk. We have shown that, in every ethnic
group, there is a stepwise increase in fractures with increas-
ing number of risk factors. Information on these risk factors
can easily be obtained in routine clinical settings and could
help clinicians target minority women at highest risk.
Absolute risk models have recently been developed and
have shown that clinical risk factors enhance the perfor-
mance of BMD in the prediction of fractures.(43) In par-
ticular, for other osteoporotic fractures, excluding hip frac-
tures, the gradients of risk for clinical risk factors alone was
similar to that provided by BMD and was markedly in-
creased by their combination. Thus, use of clinical risk fac-
tors is important for identifying women at risk for fractures.
1824
The cohorts used to develop these models were primarily
white women. Many of the same clinical risk factors in these
absolute risk models were similarly related to fractures in
minority women in our study, including prior and parental
history of fracture, and corticosteroid use.
Low BMD was related to an increased risk of fracture in
black and Hispanic women. The strength of the association
between BMD and nonspine fracture was similar to that
observed for white women.(44) Total hip BMD was a some-
what better predictor of fracture than spine BMD in white
and Hispanic women, similar to observations in other co-
horts.(44) Ethnic differences in fracture were attenuated in
models with hip BMD, suggesting that at least part of the
differences in fracture can be explained by BMD. Never-
theless, they remained significantly different, consistent
with previous studies.(15,45) Other measures of skeletal
strength such as structural and material properties and hip
geometry could contribute to these ethnic differences, but
we had no information on these measures. The heritability
of fractures is estimated to be 53%,(46) and it is likely that
genetic differences contribute to ethnic differences in frac-
ture risk.
Strengths to our study include the prospective design,
inclusion of a large, racially diverse sample of well-
characterized women, examination of a comprehensive
range of risk factors, and longitudinal follow-up >8 yr. We
focused on fractures, the most important clinical conse-
quence of osteoporosis. Most previous studies of ethnic dif-
ferences have included a single ethnic group and studied
intermediate endpoints such as BMD.
There are, however, several limitations. We were unable
to examine hip fractures directly because there were too
few hip fractures. Nevertheless, resource use for other frac-
tures is substantial.(47) Race/ethnicity designation was
based on self-report and represents a crude surrogate for
biological, environmental, cultural, and behavioral differ-
ences among individuals. Race categories may be mislead-
ing because individuals with heterogeneous ancestries are
grouped together. The sample size of white women was
large, and many associations were statistically significant
but not necessarily clinically meaningful. Only 3 of the 40
clinical centers in WHI measured BMD, and thus we were
unable to examine BMD in the whole population. Finally,
WHI women were volunteers and not representative of the
general U.S. population.
In conclusion, fracture rates vary across ethnic group, but
risk factors for fracture were generally similar within each
ethnic group. Women with the multiple risk factors have a
substantially high rate of fracture, irrespective of their eth-
nicity. Identification of high-risk women through risk factor
information may decrease the fracture risk burden.
ACKNOWLEDGMENTS
The sponsor (NHLBI) has played a role in design and
analyses of WHI. LieLing Wu is independent of any com-
mercial funder, and she had full access to all of the data and
takes responsibility for the integrity of the data and the
accuracy of the data analysis. We also thank the WHI In-
vestigators. Program Office: (National Heart, Lung, and
CAULEY ET AL.
Blood Institute, Bethesda, MD, USA) Barbara Alving,
Jacques Rossouw, Linda Pottern; Clinical Coordinating
Center: (Fred Hutchinson Cancer Research Center, Seattle,
WA, USA) Ross Prentice, Garnet Anderson, Andrea La-
Croix, Charles L Kooperberg, Ruth E Patterson, Anne
McTiernan, (Wake Forest University School of Medicine,
Winston-Salem, NC, USA) Sally Shumaker, (Medical Re-
search Labs, Highland Heights, KY, USA) Evan Stein,
(University of California at San Francisco, San Francisco,
CA, USA) Steven Cummings; Clinical Centers: (Albert
Einstein College of Medicine, Bronx, NY, USA) Sylvia
Wassertheil-Smoller, (Baylor College of Medicine, Hous-
ton, TX, USA) Jennifer Hays, (Brigham and Women’s
Hospital, Harvard Medical School, Boston, MA, USA)
JoAnn Manson, (Brown University, Providence, RI, USA)
Annlouise R Assaf, (Emory University, Atlanta, GA,
USA) Lawrence Phillips, (Fred Hutchinson Cancer Re-
search Center, Seattle, WA, USA) Shirley Beresford,
(George Washington University Medical Center, Washing-
ton, DC, USA) Judith Hsia, (Harbor-UCLA Research and
Education Institute, Torrance, CA, USA) Rowan
Chlebowski, (Kaiser Permanente Center for Health Re-
search, Portland, OR, USA) Evelyn Whitlock, (Kaiser Per-
manente Division of Research, Oakland, CA, USA) Bette
Caan, (Medical College of Wisconsin, Milwaukee, WI,
USA) Jane Morley Kotchen, (MedStar Research Institute/
Howard University, Washington, DC, USA) Barbara V
Howard, (Northwestern University, Chicago/Evanston, IL,
USA) Linda Van Horn, (Rush-Presbyterian St Luke’s
Medical Center, Chicago, IL, USA) Henry Black, (Stanford
Prevention Research Center, Stanford, CA, USA) Marcia
L Stefanick, (State University of New York at Stony Brook,
Stony Brook, NY, USA) Dorothy Lane, (The Ohio State
University, Columbus, OH, USA) Rebecca Jackson, (Uni-
versity of Alabama at Birmingham, Birmingham, AL,
USA) Cora E Lewis, (University of Arizona, Tucson/
Phoenix, AZ, USA) Tamsen Bassford, (University at Buf-
falo, Buffalo, NY, USA) Jean Wactawski-Wende, (Univer-
sity of California at Davis, Sacramento, CA, USA) John
Robbins, (University of California at Irvine, Orange, CA,
USA) Allan Hubbell, (University of California at Los An-
geles, Los Angeles, CA, USA) Howard Judd, (University
of California at San Diego, LaJolla/Chula Vista, CA, USA)
Robert D Langer, (University of Cincinnati, Cincinnati,
OH, USA) Margery Gass, (University of Florida, Gaines-
ville/Jacksonville, FL, USA) Marian Limacher, (University
of Hawaii, Honolulu, HI, USA) David Curb, (University of
Iowa, Iowa City/Davenport, IA, USA) Robert Wallace,
(University of Massachusetts/Fallon Clinic, Worcester,
MA, USA) Judith Ockene, (University of Medicine and
Dentistry of New Jersey, Newark, NJ, USA) Norman
Lasser, (University of Miami, Miami, FL, USA) Mary Jo
O’Sullivan, (University of Minnesota, Minneapolis, MN,
USA) Karen Margolis, (University of Nevada, Reno, NV,
USA) Robert Brunner, (University of North Carolina,
Chapel Hill, NC, USA) Gerardo Heiss, (University of Pitts-
burgh, Pittsburgh, PA, USA) Lewis Kuller, (University of
Tennessee, Memphis, TN, USA) Karen C Johnson, (Uni-
versity of Texas Health Science Center, San Antonio, TX,
USA) Robert Brzyski, (University of Wisconsin, Madison,
FRACTURES IN MULTI-ETHNIC WOMEN
WI, USA) Gloria E Sarto, (Wake Forest University School
of Medicine, Winston-Salem, NC, USA) Denise Bonds, and
(Wayne State University School of Medicine/Hutzel Hos-
pital, Detroit, MI, USA) Susan Hendrix.
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Address reprint requests to:
Jane A Cauley, DrPH\
University of Pittsburgh
Department of Epidemiology
130 DeSoto Street, Crabtree A524
Pittsburgh, PA 15261, USA
E-mail: jcauley@edc.pitt.edu
Received in original form March 5, 2007; revised form June 1, 2007;
accepted July 11, 2007.