A Comparison of Adiposity Measures as
Predictors of All-cause Mortality: The
Melbourne Collaborative Cohort Study
Julie A. Simpson,*† Robert J. MacInnis,*† Anna Peeters,‡ John L. Hopper,† Graham G. Giles,*† and
Dallas R. English*†
Abstract
SIMPSON, JULIE A., ROBERT J. MACINNIS, ANNA
PEETERS, JOHN L. HOPPER, GRAHAM G. GILES,
AND DALLAS R. ENGLISH. A comparison of adiposity
measures as predictors of all-cause mortality: the
Melbourne Collaborative Cohort Study. Obesity. 2007;15:
994 –1003.
Objective: Our goal was to examine five different measures
of adiposity as predictors of all-cause mortality.
Research Methods and Procedures: Subjects were 16,969
men and 24,344 women enrolled between 1990 and 1994 in
the Melbourne Collaborative Cohort Study (27 to 75 years
of age). There were 2822 deaths over a median follow-up
period of 11 years. BMI, waist circumference, and waist-
to-hip ratio were obtained from direct anthropometric mea-
surements. Fat mass and percentage fat were estimated by
bioelectric impedance analysis.
Results: Comparing the top quintile with the second quin-
tile, for men there was an increased risk of between 20%
and 30% for all-cause mortality associated with each of the
anthropometric measures. For women, there was an in-
creased risk of 30% (95% confidence interval for hazard
ratio, 1.1–1.6) observed for waist circumference and 50%
(1.2–1.8) for waist-to-hip ratio, but little or no increased risk
for BMI, fat mass, and percentage fat. Waist-to-hip ratio
Received for review October 3, 2005.
Accepted in final form October 23, 2006.
The costs of publication of this article were defrayed, in part, by the payment of page
charges. This article must, therefore, be hereby marked “advertisement” in accordance with
18 U.S.C. Section 1734 solely to indicate this fact.
*Cancer Epidemiology Centre, Cancer Council Victoria, Melbourne, Victoria, Australia;
†Centre for Molecular, Environmental, Genetic and Analytic Epidemiology, School of
Population Health, University of Melbourne, Melbourne, Australia; and ‡Department of
Epidemiology and Preventive Medicine, Monash University, Melbourne, Australia.
Address correspondence to Julie A. Simpson, Centre for Molecular, Environmental, Genetic
and Analytic Epidemiology, University of Melbourne, Level 2/723 Swanston St., Carlton,
Victoria 3053, Australia.
E-mail: julieas@unimelb.edu.au
Copyright © 2007 NAASO
994 OBESITY Vol. 15 No. 4 April 2007
was positively and monotonically associated with all-cause
mortality for both men and women. There was a linear
association between waist circumference and all-cause mor-
tality for men, whereas a U-shaped association was ob-
served for women.
Discussion: Measures of central adiposity were better pre-
dictors of mortality in women in the Melbourne Collabo-
rative Cohort Study compared with measures of overall
adiposity. We recommend measuring waist and hip circum-
ferences in population studies investigating the risk of all-
cause mortality associated with obesity. The use of addi-
tional measures such as bioelectric impedance is not
justified for this outcome.
Key words: body composition, BMI, waist-to-hip ratio,
waist circumference, bioelectric impedance analysis
Introduction
The comparison of BMI, waist circumference (WC),1 and
waist-to-hip ratio (WHR), as predictors of all-cause mortal-
ity, has been investigated in many cohort studies (1–10).
The findings have been diverse. Some of the studies have
reported that measures of central adiposity, such as WC
and/or WHR, are better predictors compared with overall
measures such as BMI (1–3,6 –9), because there was a
positive monotonic relationship with mortality as opposed
to a U- or J-shaped association. Other studies have found
that the association with mortality was weaker with WHR
than with BMI (4,10), while another study questioned the
usefulness of WHR because, individually, waist and hip
circumference were observed to have opposite associations
with mortality (5).
1
Nonstandard abbreviations: WC, waist circumference; WHR, waist-to-hip ratio; CVD,
cardiovascular disease; ICD, International Classification of Diseases; CI, confidence inter-
val.
Adiposity and All-cause Mortality, Simpson et al.
Only a few studies have investigated the association
between fat mass, a measure of total adipose mass, or
percentage fat, and risk of all-cause mortality (1,11,12).
Allison et al. (12) used body composition data from several
small studies and concluded that prospective cohort studies
that take actual measurements of body composition are
required to achieve meaningful inferences about the rela-
tionship between adiposity and mortality. Two cohort stud-
ies from Sweden (1,11) observed positive linear associa-
tions between percentage fat and/or fat mass with mortality.
In this paper, we have compared direct measures of BMI,
WC, WHR, fat mass, and percentage fat as predictors of
all-cause mortality and mortality from specific causes in
middle-aged men and women enrolled in the Melbourne
Collaborative Cohort Study. Fat mass and percentage fat
were derived from bioelectric impedance analysis.
Research Methods and Procedures
Subjects
The Melbourne Collaborative Cohort Study is a prospec-
tive cohort study comprised of 17,049 men and 24,479
women, aged between 27 and 75 years at baseline, 99.3% of
whom were 40 to 69 years of age. The study participants
were recruited from the Melbourne metropolitan area from
1990 to 1994 via the Electoral Rolls, advertisements, and
community announcements in local media. Southern Euro-
pean migrants to Australia were deliberately oversampled to
extend the range of lifestyle exposures and to increase
genetic variation. The Cancer Council Victoria’s Human
Research Ethics Committee approved the study protocol.
Further details of the Melbourne Collaborative Cohort
Study have been published elsewhere (13).
For this analysis, 215 study participants without a com-
plete set of valid anthropometric measurements were ex-
cluded, leaving 16,969 male and 24,344 female subjects.
Anthropometric Measures
Height, weight, and waist and hip circumferences were
measured once at baseline attendance for each participant
according to written protocols based on standard procedures
(14). Weight was measured to 100 g using digital electronic
scales, height was measured to 1 mm using a stadiometer,
and waist and hip circumferences were measured to 1 mm
using a metal anthropometric tape. Bioelectric impedance
analysis was performed with a single frequency (50 kHz)
electric current produced by a BIA-101A RJL system ana-
lyser (RJL Systems, Detroit, MI). Resistance and reactance
were measured with subjects in a supine position.
Possible Confounders
The possible confounders identified a priori were: coun-
try of birth (Australia, United Kingdom, Italy, Greece);
physical activity (none, low, moderate, high (15)); alcohol
intake (for men: none, 1–39, 40 –59, 60⫹ g/d; for women:
none, 1–19, 20⫹ g/d); education (primary school, some
high or technical school, completed high or technical
school, degree/diploma); smoking status (never, past, cur-
rent); living alone (yes, no); previous history of illness
(angina, heart attack, diabetes, cancer, stroke); family his-
tory (father, mother, or sibling) of heart attack; family
history of cancer; and family history of diabetes. Previous
history of angina, heart attack, diabetes, and stroke were
self-reported, whereas previous history of cancer was ob-
tained from the Victorian Cancer Registry. All of the above
variables were recorded at baseline.
Mortality
Deaths were identified through the Victorian Registry of
Births, Deaths and Marriages, and the National Death Index.
Deaths in Victoria were complete to December 31, 2003,
and to the end of 2002 for deaths in other states. Residential
addresses were determined by record linkage to Electoral
Rolls, from electronic phone books, and from responses to
mailed questionnaires and newsletters. By the end of fol-
low-up on December 31, 2003, 55 (0.1%) of the subjects
included in this analysis were known to have left Australia
and were considered lost to follow-up.
Participants were defined as having died from cardiovas-
cular disease (CVD) if the primary cause of death had an
International Classification of Diseases (ICD)-9 code
401.0 – 444.9 or ICD-10 code I00-I74, or having died from
cancer if the primary cause of death had an ICD-9 code
140.0 –239.9 or ICD-10 code C00-C99, D00-D48. Deaths
recorded in 1991 and 1992 were coded by the Victorian
Cancer Registry, while those post-1992 were coded by the
Australian Bureau of Statistics.
Statistical Analysis
All analyses were performed separately for men and
women. Cox proportional hazards regression models, with
age as the time axis, were used to estimate the hazard ratios
for mortality associated with each anthropometric measure
after adjustment for confounding variables. Using age as the
time axis allows the baseline hazard to change as a function
of age, which is a better method for controlling the potential
confounding due to age (16). The models were stratified for
previous history of illness at baseline, because for this
variable, the hazards were found to be not proportional. The
assumption of proportional hazards was not found to be
violated for any of the anthropometric measures.
We used bioelectrical impedance analysis to estimate
fat-free mass, as 9.1536 ⫹ (0.4273 ⫻ height2/resistance) ⫹
(0.1926 ⫻ weight) ⫹ (0.0667 ⫻ reactance) for men, and
7.7435 ⫹ (0.4542 ⫻ height2/resistance) ⫹ (0.1190 ⫻
weight) ⫹ (0.0455 ⫻ reactance) for women (17). Fat mass
(weight ⫺ fat-free mass) and percentage fat (fat mass di-
vided by weight) were subsequently calculated. BMI was
OBESITY Vol. 15 No. 4 April 2007 995
Adiposity and All-cause Mortality, Simpson et al.

Table 1. Distribution of anthropometric measures (medians) at baseline for the 41,313 study participants with
complete data
Percentile
Measurement 0 20 40 50 60 80 100
BMI (kg/m2)
Men 15.6 24.3 26.1 26.9 27.7 29.9 54.0
Women 14.0 22.7 24.8 25.9 27.1 30.4 57.8
Waist circumference (cm)
Men 55.5 85.5 90.8 93.0 95.4 101.0 151.0
Women 47.0 70.0 75.5 78.2 81.5 89.3 153.6
Waist-to-hip ratio
Men 0.53 0.88 0.91 0.92 0.94 0.97 1.29
Women 0.46 0.73 0.76 0.78 0.80 0.84 1.44
Fat mass (kg)
Men 1.9 17.4 21.3 23.0 24.9 29.4 79.1
Women 4.4 20.1 24.4 26.5 28.8 35.0 94.2
Percentage fat (%)
Men 2.4 24.0 27.5 29.0 30.4 33.6 52.5
Women 8.1 34.1 38.4 40.2 41.9 45.8 63.0

calculated as weight (kg) divided by the square of height
(m). WHR was computed as waist divided by hips.
The anthropometric measures were categorized into quin-
tile groupings with the second quintile used as the reference
category. For each quintile cut-off, the sensitivity (propor-
tion of deaths above the cut-off) and specificity (proportion
of survivors below the cut-off) were calculated. BMI was
also categorized as follows: ⬍23.0, 23.0 to 24.9, 25.0 to
27.4, 27.5 to 29.9, and ⱖ30 (kg/m2) because combinations
of these categories correspond to the widely used World
Health Organization definitions of overweight (BMI be-
tween 25.0 and 29.9) and obesity (BMI ⱖ30) (18). WC was
similarly categorized as follows: for men, ⬍79, 79 to 93.9,
94 to 102, and ⬎102 cm; and for women, ⬍68, 68 to 79.9,
80 to 88, and ⬎88 cm, these cut-offs include the sex-
specific cut-off levels suggested by Lean et al. (19). For
both BMI and WC, the second predefined sex-specific cat-
egory was the referent group.
The anthropometric measures were also fitted as contin-
uous variables using two-term fractional polynomials to
compare models with different transformations of the expo-
sure variable (e.g., reciprocal, logarithm, square root,
square) (20). Fractional polynomials make no a priori hy-
pothesis about the shape of the association (linear, qua-
dratic, etc.) between the exposure and outcome.
Effect modification by smoking and country of birth
(collapsed into Australia/United Kingdom and Italy/Greece)
was assessed by fitting interaction terms.
Two sensitivity analyses were performed to investigate
the effect of pre-attendance illnesses on the association
between the anthropometric measures and mortality: 1) ex-
clusion of subjects with a previous history of angina, heart
attack, diabetes, stroke, and cancer; and 2) exclusion of the
first 2 years of follow-up.
Statistical analyses were performed using Stata/SE 8.2
(StataCorp LP., College Station, TX).
Results
Table 1 shows the distribution of the anthropometric
measurements for men and women. Men had a higher
median BMI, WC, and WHR, whereas women had a higher
median fat mass and percentage fat. For men and women,
respectively, 53% and 36% were overweight (BMI, 25.0 –
29.9 kg/m2), and 19% and 22% were obese (BMI ⱖ30
kg/m2). Only 0.2% men and 0.9% women were underweight
(BMI ⬍18.5 kg/m2).
Table 2 shows the characteristics of the study population.
Thirteen percent of the participants had a previous history of
illness and 11% were current smokers.
All-Cause Mortality
There were 2822 deaths (1656 men and 1166 women)
over a median follow-up period of 11 years. The mortality
was 9.0 per 1000 person-years [95% confidence interval
(CI), 8.6 to 9.4] for men and 4.3 per 1000 person-years (4.1
to 4.6) for women.
Men in the top quintile of each anthropometric measure
had 20% to 30% higher mortality than those in the second
quintile (Table 3). Men with a BMI or fat mass in the lowest

996 OBESITY Vol. 15 No. 4 April 2007

Adiposity and All-cause Mortality, Simpson et al.

sures of adiposity (BMI, p ⫽ 0.74; fat mass, p ⫽ 0.11;

Table 2. Demographic details at baseline for the percentage fat, p ⫽ 0.06).
41,313 study participants Women in the top quintile of WC and WHR had 30% and
Men Women 50% higher mortality, respectively, compared with those in
the second quintile, but there was little or no increased risk
(n ⴝ 16,969) (n ⴝ 24,344)
for those in the top quintile of BMI, fat mass, and percent-
(%) (%)
age fat. Women in the lowest quintiles of WC, WHR, and
Country of birth BMI had 40%, 30%, and 20% higher mortality, respec-
Australia 65.5 71.0 tively, than those in the second quintiles (Table 3). Only for
UK 8.2 6.7 WHR was there a linear trend across the quintile groups for
Italy 14.2 12.3 the risk of all-cause mortality (WHR, p ⫽ 0.002; BMI, p ⫽
Greece 12.2 10.0 0.70; WC, p ⫽ 0.28; fat mass, p ⫽ 0.98; percentage fat, p ⫽
0.42).
Physical activity
For both sexes, the specificities at each quintile cut-off
None 22.6 22.0
were similar for all of the anthropometric measures. How-
Low 18.4 21.3 ever, the sensitivities at each quintile cut-off were higher for
Moderate 34.4 36.5 WC and WHR than for BMI, fat mass, and percentage fat
High 24.8 20.3 (Table 4).
Education Using World Health Organization cut-offs, for men, those
Primary school 18.6 19.9 with BMI ⬍23 had a significantly increased risk of 1.3-fold
Some high or technical (95% CI, 1.1 to 1.6), whereas those with a BMI ⱖ30 (i.e.,
school 31.2 43.1 obese) had only a risk of 1.1 (1.0 to 1.3) compared with
Completed high or subjects with a BMI between 23 and 24.9. Similar findings
technical school 24.9 17.7 were observed for the women (Table 5). If the referent
Degree/diploma 25.3 19.3 category was changed to between 18.5 and 24.9 (World
Smoking status Health Organization definition of “normal range”), the risk
for mortality associated with a BMI ⱖ30 was 1.0 for both
Never 39.7 68.8
men and women. There was a 30% higher mortality in the
Past 45.7 22.1
top WC group for men (⬎102 cm) and women (⬎88 cm)
Current 14.5 9.1 and in the bottom WC cut-off for women (⬍68 cm). A
Living alone 11.5 16.7 significant linear trend was observed across the WC cut-offs
Previous history of angina, for men (p ⫽ 0.002), but not for women (p ⫽ 0.23).
heart attack, diabetes, When interactions with smoking were analyzed for men,
stroke, or cancer 15.7 11.1 the highest mortality among current smokers was seen in
Family history of: those with BMI ⬍23; whereas for never smokers, the high-
Heart attack 34.7 40.1 est mortality was for obese participants (Table 5, test for
Cancer 33.9 39.6 interaction: p ⫽ 0.005). Similar patterns were seen for the
Diabetes 16.3 19.1 other four anthropometric measures, with never smokers in
Alcohol intake (g/d) the highest category having the highest mortality but current
None 18.8 42.2 smokers in the lowest category having the highest mortality,
but the tests for interaction were not significant (p values
1 to 39 (M)/1 to
ranged from 0.2 to 0.5). For female never smokers, the
19 (F) 65.3 46.7
highest mortality was in the highest category of all five
40 to 59 (M)/20
measures (Table 5). However, in past and current female
to 39 (F) 8.8 8.6 smokers, the highest mortality was in the lowest category
60⫹ (M)/40⫹ except for WHR and current smokers. None of the tests for
(F) 7.1 2.5 interaction was significant (p values ranged from 0.2 to 0.6).
Country of birth did not modify the association between any
of the anthropometric measures and mortality (all p values
⬎0.1).
quintile also had 20% higher mortality. For both WC and When fitting BMI, WC, WHR, fat mass, and percentage fat
WHR, there was a linear trend across the quintile groups for as continuous variables using two-term fractional polynomials,
the risk of all-cause mortality (p ⫽ 0.003 and p ⫽ 0.001, the associations between BMI, WC, fat mass, percentage fat,
respectively), but this was not observed for the other mea- and all-cause mortality were U-shaped (data not shown) for

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Adiposity and All-cause Mortality, Simpson et al.

Table 3. Anthropometric risk factors for all-cause mortality for males and females
Hazard ratio* (95% CI) for each quintile grouping
p value
Measurement 1st quintile 2nd quintile 3rd quintile 4th quintile 5th quintile for trend
Men
BMI (kg/m2) 1.2 (1.0, 1.4) 1.0 1.0 (0.9, 1.2) 1.0 (0.9, 1.2) 1.2 (1.0, 1.4) 0.74
WC (cm) 1.1 (0.9, 1.3) 1.0 1.0 (0.9, 1.2) 1.1 (0.9, 1.2) 1.3 (1.1, 1.5) 0.003
WHR 1.1 (0.9, 1.3) 1.0 1.1 (0.9, 1.3) 1.2 (1.0, 1.4) 1.3 (1.1, 1.5) 0.001
Fat mass (kg) 1.2 (1.0, 1.4) 1.0 1.0 (0.9, 1.2) 1.1 (0.9, 1.3) 1.3 (1.1, 1.5) 0.11
Percentage fat (%) 1.1 (0.9, 1.3) 1.0 0.9 (0.8, 1.1) 1.0 (0.9, 1.2) 1.2 (1.1, 1.4) 0.06
Women
BMI (kg/m2) 1.2 (1.0, 1.5) 1.0 0.9 (0.7, 1.1) 0.9 (0.8, 1.1) 1.1 (0.9, 1.3) 0.70
WC (cm) 1.4 (1.1, 1.7) 1.0 1.1 (0.9, 1.4) 1.1 (0.9, 1.3) 1.3 (1.1, 1.6) 0.28
WHR 1.3 (1.0, 1.6) 1.0 1.3 (1.0, 1.5) 1.2 (1.0, 1.4) 1.5 (1.2, 1.8) 0.002
Fat mass (kg) 1.0 (0.8, 1.1) 1.0 0.7 (0.6, 0.9) 0.9 (0.7, 1.0) 1.0 (0.8, 1.2) 0.98
Percentage fat (%) 1.0 (0.9, 1.2) 1.0 0.8 (0.7, 1.0) 0.8 (0.7, 1.0) 1.0 (0.8, 1.2) 0.42

CI, confidence interval; WC, waist circumference; WHR, waist-to-hip ratio.

* Adjusted for age at attendance, country of birth, physical activity, alcohol intake, education, smoking status, living alone (men only), and
family history of heart attack (men only); and stratified by “previous history of heart attack, angina, diabetes, stroke, and cancer.”

both men and women. However, the association between Cause-Specific Mortality
WHR and all-cause mortality, for both men and women, There were 593 deaths (417 men and 176 women) due to
was best described using a linear relationship (data not CVD and 1218 deaths (658 men and 560 women) due to
shown). cancer.

Table 4. Sensitivity and specificity corresponding to quintile cut-offs of each anthropometric measures in males
and females
Sensitivity (%)/specificity (%) for quintile cut-offs
Measurement 20th percentile 40th percentile 60th percentile 80th percentile
Men
BMI (kg/m2) 81/20 64/40 44/60 24/80
WC (cm) 85/20 68/41 50/61 31/80
WHR 86/21 71/41 51/61 29/81
Fat mass (kg) 80/20 62/40 43/60 23/80
Percentage fat (%) 82/20 64/40 46/61 26/81
Women
BMI (kg/m2) 80/20 62/40 45/60 25/80
WC (cm) 84/19 69/40 50/60 29/80
WHR 87/20 73/41 53/61 32/81
Fat mass (kg) 80/20 60/40 43/60 24/80
Percentage fat (%) 81/20 61/40 44/60 24/80

CI, confidence interval; WC, waist circumference; WHR, waist-to-hip ratio.

998 OBESITY Vol. 15 No. 4 April 2007

Adiposity and All-cause Mortality, Simpson et al.

Table 5. Anthropometric risk factors for all-cause mortality for males and females
Hazard ratio* (95% CI) for men Hazard ratio* (95% CI) for women

Never- Past Current Never- Past Current

All smokers smokers smokers All smokers smokers smokers

BMI (kg/m2)
⬍23 1.3 (1.1,1.6) 0.9 (0.6,1.3) 1.3 (1.0,1.7) 1.8 (1.2,2.6) 1.2 (1.0,1.5) 1.1 (0.9,1.4) 1.3 (0.9,1.9) 1.4 (0.9,2.1)
23 to 24.9 1 1 1 1 1 1 1 1
25 to 27.4 0.9 (0.8,1.1) 1.1 (0.8,1.4) 0.9 (0.8,1.2) 0.7 (0.5,1.0) 0.8 (0.7,1.0) 0.8 (0.6,1.1) 0.8 (0.6,1.2) 0.8 (0.5,1.3)
27.5 to 29.9 1.0 (0.8,1.1) 0.9 (0.7,1.2) 1.0 (0.8,1.2) 1.1 (0.7,1.5) 0.9 (0.8,1.2) 1.0 (0.8,1.3) 0.9 (0.6,1.4) 0.7 (0.4,1.2)
ⱖ30 1.1 (1.0,1.3) 1.2 (0.9,1.6) 1.1 (0.9,1.4) 1.0 (0.7,1.5) 1.1 (0.9,1.3) 1.2 (0.9,1.5) 1.2 (0.8,1.7) 0.7 (0.4,1.1)
WC (cm)
⬍79 (M)/⬍68 (F) 1.1 (0.8,1.4) 0.8 (0.5,1.3) 1.0 (0.7,1.5) 1.6 (1.0,2.4) 1.3 (1.1,1.6) 1.2 (0.9,1.6) 1.7 (1.1,2.4) 1.3 (0.8,2.1)
79 to 93.9 (M)/68 to
79.9(F) 1 1 1 1 1 1 1 1
94 to 102 (M)/80 to
88 (F) 1.0 (0.9,1.1) 1.0 (0.8,1.2) 1.0 (0.9,1.2) 1.0 (0.7,1.3) 1.0 (0.8,1.1) 1.0 (0.8,1.2) 1.0 (0.7,1.4) 0.9 (0.6,1.4)
ⱖ102 (M)/ⱖ88 (F) 1.3 (1.1,1.4) 1.3 (1.0,1.6) 1.3 (1.1,1.5) 1.3 (1.0,1.7) 1.3 (1.1,1.5) 1.4 (1.1,1.6) 1.1 (0.9,1.5) 1.0 (0.7,1.5)
WHR
⬍0.88 (M)/⬍0.73 (F) 1.1 (0.9,1.3) 1.2 (0.9,1.6) 0.9 (0.7,1.2) 1.4 (0.9,2.1) 1.3 (1.0,1.6) 1.4 (1.0,1.8) 1.4 (0.9,2.2) 0.6 (0.3,1.3)
0.88 to 0.90 (M)/0.73
to 0.75 (F) 1 1 1 1 1 1 1 1
0.91 to 0.93 (M)/0.76
to 0.79 (F) 1.1 (0.9,1.3) 1.4 (1.0,1.9) 1.0 (0.8,1.2) 1.2 (0.8,1.7) 1.3 (1.0,1.5) 1.5 (1.1,1.9) 1.0 (0.7,1.5) 1.0 (0.6,1.6)
0.94 to 0.96 (M)/0.80
to 0.83 (F) 1.2 (1.0,1.4) 1.3 (1.0,1.8) 1.1 (0.9,1.4) 1.2 (0.8,1.8) 1.2 (1.0,1.4) 1.3 (1.0,1.7) 1.1 (0.8,1.7) 0.9 (0.5,1.4)
ⱖ0.97 (M)/ⱖ0.84 (F) 1.3 (1.1,1.5) 1.5 (1.1,2.1) 1.2 (0.9,1.4) 1.5 (1.1,2.2) 1.5 (1.2,1.8) 1.7 (1.4,2.2) 1.3 (0.9,1.8) 1.2 (0.7,1.8)
Fat mass (kg)
⬍17.4 (M)/⬍20.1 (F) 1.2 (1.0,1.4) 1.2 (0.9,1.6) 1.0 (0.8,1.3) 1.6 (1.1,2.2) 1.0 (0.8,1.1) 0.8 (0.6,1.0) 1.2 (0.9,1.8) 1.2 (0.8,1.9)
17.4 to 21.2 (M)/20.1
to 24.3 (F) 1 1 1 1 1 1 1 1
21.3 to 24.8 (M)/24.4
to 28.7 (F) 1.0 (0.9,1.2) 1.1 (0.9,1.5) 0.9 (0.7,1.1) 1.1 (0.8,1.6) 0.7 (0.6,0.9) 0.7 (0.6,0.9) 0.7 (0.4,1.0) 0.9 (0.6,1.5)
24.9 to 29.3 (M)/28.8
to 34.9 (F) 1.1 (0.9,1.3) 1.1 (0.8,1.5) 1.0 (0.8,1.2) 1.3 (0.9,1.9) 0.9 (0.7,1.0) 0.8 (0.7,1.0) 0.9 (0.6,1.3) 1.0 (0.6,1.6)
ⱖ29.4 (M)/ⱖ35.0 (F) 1.3 (1.1,1.5) 1.3 (1.0,1.7) 1.2 (1.0,1.5) 1.3 (0.9,1.9) 1.0 (0.8,1.2) 1.0 (0.8,1.2) 1.0 (0.7,1.5) 0.8 (0.5,1.4)
Percentage fat (%)
⬍24.0 (M)/⬍34.1 (F) 1.1 (0.9,1.3) 1.1 (0.8,1.5) 0.9 (0.7,1.2) 1.6 (1.1,2.3) 1.0 (0.9,1.2) 0.9 (0.7,1.2) 1.3 (0.9,1.8) 1.0 (0.7,1.6)
24.0 to 27.4 (M)/34.1
to 38.4 (F) 1 1 1 1 1 1 1 1
27.5 to 30.3 (M)/38.5
to 41.8 (F) 0.9 (0.8,1.1) 0.9 (0.6,1.2) 0.9 (0.7,1.1) 1.3 (0.9,1.9) 0.8 (0.7,1.0) 0.8 (0.7,1.1) 0.7 (0.5,1.1) 0.8 (0.5,1.3)
30.4 to 33.5 (M)/41.9
to 45.7 (F) 1.0 (0.9,1.2) 1.2 (0.9,1.6) 0.9 (0.7,1.1) 1.2 (0.8,1.7) 0.8 (0.7,1.0) 0.9 (0.7,1.1) 0.9 (0.6,1.3) 0.6 (0.4,1.0)
ⱖ33.6 (M)/ⱖ45.8 (F) 1.2 (1.1,1.4) 1.2 (0.9,1.6) 1.2 (1.0,1.5) 1.5 (1.0,2.1) 1.0 (0.8,1.2) 1.0 (0.8,1.3) 1.1 (0.7,1.5) 0.9 (0.6,1.4)

CI, confidence interval; WC, waist circumference; WHR, waist-to-hip ratio.

* Adjusted for age at attendance, country of birth, physical activity, alcohol intake, education, smoking status, living alone (men only) and
family history of heart attack (men only); and stratified by “previous history of heart attack, angina, diabetes, stroke, and cancer.”

For men, a higher risk for CVD death was observed for
the top quintile grouping of all anthropometric measures,
with hazard ratios ranging from 1.4 to 1.8 (Figure 1A). For
women, an increased risk for CVD death was observed in
the highest quintile for WC [hazard ratio (95% CI): 1.5 (0.9
to 2.4)] and WHR [1.4 (0.9 to 2.1)] and in the lowest
quintile for WC [1.7 (1.0 to 2.9)]. In the top quintile of BMI,
fat mass and percentage fat the hazard ratios were less than
1 (Figure 1B).
For men, no associations between any of the anthropo-
metric measures and cancer mortality were observed (Fig-
ure 1C), although all of the hazard ratios in the highest two

OBESITY Vol. 15 No. 4 April 2007 999

Adiposity and All-cause Mortality, Simpson et al.

Figure 1: Relative risk of death from cardiovascular disease and cancer for BMI (●), WC (Œ), WHR (e), fat mass (f), and percentage fat
(E). Adjusted for age at attendance, country of birth, physical activity, alcohol intake, education, smoking status, living alone (males only),
and family history of heart attack (males only); and stratified by “previous history of heart attack, angina, diabetes, stroke, and cancer.” The
referent category is the second quintile, and the bars represent 95% CIs.

quintiles were greater than unity. For women, an increased
risk for cancer mortality was observed for the top quintile
grouping of WC [hazard ratio (95% CI): 1.4 (1.0 to 1.8)]
and WHR [1.5 (1.1 to 1.9)], but for this quintile, the hazard
ratios for the other anthropometric measures were not
greater than unity (Figure 1D).
Sensitivity Analyses
The above analyses were repeated (data not shown), with
1) the exclusion of subjects with a previous history of
angina, heart attack, diabetes, stroke, or cancer (5359 sub-
jects/1017 deaths) and 2) the exclusion of the first 2 years of
follow-up (262 deaths). The results were unchanged.
Discussion
From our cohort study of 16,969 male and 24,344 female
subjects, we observed 2822 deaths and estimated the risk of
mortality due to all causes, ranging from 1.0 to 1.5, for those
in the top quintile of each anthropometric measure com-
pared with subjects in the second quintile. The associations
of BMI, fat mass, and percentage fat with all-cause mortal-
ity were U-shaped, while, in contrast, WHR was positively
and monotonically associated with all-cause mortality.
There was a linear association between WC and all-cause
mortality for men, whereas for women a U-shaped associ-
ation was observed. WHR and WC were stronger predictors
of mortality in this cohort compared with BMI, fat mass,
and percentage fat. The highest mortality among current
smokers was observed for men and women in the lowest
categories of the anthropometric measures. Men in the top
quintile of each anthropometric measure had an increased
risk for CVD.
The strengths of our prospective study include its com-
plete follow-up, reasonable size, length of follow-up, and
direct measurement of the anthropometric measures. Only
0.1% of the subjects were known to have left Australia, so
it is unlikely we have missed many deaths. Of the studies
that only measured total adipose mass (1,11), our study is
the largest. All of our anthropometric measures were made
by direct physical examination according to standard pro-

1000 OBESITY Vol. 15 No. 4 April 2007

Adiposity and All-cause Mortality, Simpson et al.
tocols as opposed to self-reported. Four large cohort studies
from the United States used self-reported anthropometric
indices (2,7,10,21). None of the sensitivity analyses per-
formed produced evidence that a pre-attendance illness
modified the association between the anthropometric mea-
sures and all-cause mortality.
Our study does have some potential limitations. The
study population was predominantly limited to the age
range of 40 to 69 years. We found a significant interaction
of smoking by BMI for men with excess mortality among
the very lean smokers but had limited power to perform
subgroup analyses by smoking status. In a large prospective
study of more than 1 million adults (21), the association
between BMI and mortality was substantially modified by
smoking status and the presence of disease, and the study
investigators recommended that this association should only
be investigated in healthy persons who have never smoked.
In the Iowa study of 41,837 women (7), however, the
patterns of association of total mortality with BMI and
WHR were similar for never and ever smokers; and in the
National Health and Nutrition Examination Survey study
(22), smoking did not change the pattern of association
between BMI and mortality.
Issues concerning the measurement of fat mass have been
addressed previously (15,23). In brief, we chose a formula
that had been developed using subjects whose ethnicity,
age, and BMI distribution were similar to our own study
(24). The algorithm to compute fat-free mass includes
height, weight, resistance, and reactance; therefore, mea-
surement errors for each of these measures will reduce the
precision of the fat mass and percentage fat measures.
It is difficult to compare our risk estimates with many of
the other studies due to differences in the categories and
referent category chosen for the modeling of the anthropo-
metric measures. For those studies using quintile groupings
for BMI (1,3,7,9,11), the relative risk in the top quintile
compared with the bottom or second quintile for mortality
ranged from 0.5 to 1.5 for men and 0.8 to 1.6 for women.
Relative risks below 1 were observed for elderly men and
women (1,3,9), including a risk of 0.5 observed for Japa-
nese-American men over 70 years of age (9). Similar to our
findings, others have found that the relative risk of mortality
for those in the top quintile compared with the bottom or
second quintile of WHR ranged from 1.3 to 1.6 for men, and
a linear trend was observed (1–3,9). For women, two studies
found the relative risk in the top quintile to be two-fold
(1,7): one study (10) observed a similar risk to our estimate
of 1.5, whereas Visscher et al. (3) observed no association
between WHR and mortality. For WC, an increase in mor-
tality of 50% to 60% for men in the top quintile was found
(2,3), which is slightly higher than our observations. Only
one study, comprised of 1990 never smoking elderly
women with 5 years of follow-up, presented the findings for
quintile groupings of WC for women (3). They reported the
risk for mortality in the top quintile to be 0.8, which is very
different from our risk of 1.3. Lahmann et al. (1) and
Heitmann et al. (11) observed a linear increased risk of
mortality associated with percentage fat for men. For
women, a linear increased risk was observed for those under
60 years of age but not for women 60 years and older (1).
These findings differ from our study, where we observed
minimal U-shaped associations between percentage fat and
mortality. These differences are surprising considering the
study populations of the Malmo Diet and Cancer Study and
our study are of similar age and anthropometric distribution.
Our study included many Southern European migrants to
increase the range of lifestyle exposures and to increase
genetic variation, whereas the Malmo Diet and Cancer
Study excluded participants with a lack of Swedish lan-
guage skills. However, when we excluded the Southern
European migrants, our findings did not change. In sum-
mary, our results were consistent with most published stud-
ies for BMI, WC (except for women), and WHR but dif-
fered for percentage fat.
In cause-specific analyses of men, we observed the same
J-shaped relationship between BMI and cardiovascular mor-
tality as observed in two large U.S. studies (2,21). Our
finding of no association between BMI and cancer mortality
was similar to Baik et al. (2), but differed from the weak
linear association reported by Calle et al. (21). For women,
we observed no association between BMI and both cardio-
vascular and cancer mortality, which was similar to findings
from the Iowa Women’s Health Study (7). In contrast, the
Nurses’ Health Study found BMI to have a positive linear
relationship with cardiovascular and cancer death (10). The
risk for cardiovascular death in the top quintile of WHR was
3.4 for the Iowa Women’s Health Study (7), higher than our
estimate of 1.4. One possible explanation for the difference
in estimates is our cohort were recruited in the early nineties
and followed up to 2002–2003, whereas participants of the
Iowa Women’s Health Study were recruited in 1986 and
followed-up to 1989. Flegal et al. (22) have suggested that
the impact of obesity on mortality is decreasing over time.
When comparing anthropometric measures, many studies
have concluded that WC and/or WHR are better predictors
of mortality compared with BMI (1–3,6 –9). We found a
marginally increased risk for mortality in the top quintile of
WHR and WC compared with BMI and a positive linear
association between WHR and mortality for both men and
women. Other studies have also observed a linear associa-
tion between WHR and mortality (1,2,7,9). Woo et al. (4),
however, concluded that WHR was not a useful predictor of
mortality compared with BMI and WC. A reason for this
may be that the study population consisted of elderly Chi-
nese with much lower BMIs, WCs, and WHRs compared
with white study populations. They also observed an inverse
relationship between BMI, WC, and mortality (4). In the
Nurses’ Health Study (10), BMI was a stronger predictor of
OBESITY Vol. 15 No. 4 April 2007 1001
Adiposity and All-cause Mortality, Simpson et al.
mortality compared with WHR in never smokers, no results
were presented for WC. When comparing the bioelectric
impedance measures, fat mass, and percentage fat, to the
measures of central adiposity, WC, and WHR, we observed
WC and WHR to be better predictors of all-cause mortality.
Lahmann et al. (1) also observed a positive linear increased
risk of mortality associated with WC and WHR, and these
associations were not modified by age. They found, how-
ever, that the positive linear association with percentage fat
was only observed in middle-aged women (45 to 59 years)
and older men (60 to 73 years). In other analyses, where we
have investigated the association between body size and the
incidence of cancer, we have found WC and/or WHR to be
either stronger or equivalent predictors of the main cancers
compared with fat mass and percentage fat (15,23,25,26).
In summary, we observed linear associations between
WHR and all-cause mortality for both men and women. For
the other anthropometric measures, we observed U-shaped
associations with all-cause mortality, except for WC and
men where a linear association was observed. From our
data, WC and WHR are better measures than BMI, fat mass,
and percentage fat in women when investigating the risk of
all-cause mortality due to body size. Therefore, in popula-
tion studies interested in the main health risks of body size,
it may not be justified to perform extra measurements using
bioelectric impedance analysis although further studies are
required to confirm this recommendation.
Acknowledgments
This study was made possible by the contribution of
many people, including the original investigators and the
diligent team who recruited the participants and who con-
tinue working on follow-up. We also thank the many thou-
sands of Melbourne residents who continue to participate in
the study. Cohort recruitment was funded by VicHealth and
The Cancer Council Victoria. This study was supported by
grants from the National Health and Medical Research
Council (209057, 251533, and 170215) and by infrastruc-
ture provided by the Cancer Council Victoria.
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