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Skinfold thickness measurements and mortality in white males during 27.7 years of
follow-up
Wann Jia Loh1,2, Desmond G Johnston1, Nick Oliver1, Ian F. Godsland1
1Diabetes Endocrinology and Metabolic Medicine, Faculty of Medicine, Imperial College London,
St. Mary's Campus, London, UK
2Department of Endocrinology, Changi General Hospital, Singapore
Short title: iliac skinfold, obesity and mortality
Conflicts of interest: there are no conflicts
Corresponding author:
Wann Jia Loh,
Division of Diabetes, Endocrinology and Metabolism, Department of Medicine,
Imperial College London, St Mary’s Campus,
Room G1, Norfolk Place, London W2 1NH, UK.
email: [email protected], [email protected],
1
Abstract
Introduction: Obesity is a major risk factor for mortality from a range of causes. We investigated
whether skinfold measurements were associated with mortality independently of variation in
body mass index (BMI).
Methods: A prospective analysis of mortality in 870 apparently healthy adult Caucasian men
participating in an occupational health cohort was undertaken. At baseline, skinfold
measurements were taken at biceps, triceps, iliac and subscapular sites. Derived
measurements included the sum of all 4 skinfolds and subscapular to triceps, subscapular to
iliac and BMI to iliac ratios. All-cause mortality was analysed by Cox proportional hazards
modelling and death in specific mortality subcategories by competing risks analysis.
Results: During a mean of 27.7 years follow up, there were 303 deaths (119 cancer, 101
arteriovascular, 40 infection, 43 other). In univariable analysis, BMI was associated with all-
cause, cancer, arteriovascular and other mortality and subscapular skinfold with all-cause and
arteriovascular mortality. On bivariable analysis, with inclusion of BMI, subscapular skinfold
ceased to be a associated with mortality but iliac skinfold emerged as strongly, negatively
associated with all-cause and arteriovascular mortality. In multivariable analysis, with inclusion
of age, BMI, smoking, alcohol and exercise, iliac skinfold was negatively associated with all-
cause (Hazard ratio HR 0.77, 95% confidence interval CI 0.66-0.90, p=0.002), arteriovascular
(HR 0.75, 95%CI 0.58,0.97, p=0.02) and infection (HR 0.63, 95%CI 0.42,0.94, p=0.02) death.
Among obese participants (BMI ≥30kg/m2), iliac skinfold of ≤9.7mm was associated with a six-
fold increase in all-cause mortality risk.
Conclusion: Low iliac skinfold thickness is an independent risk factor for all-cause mortality in
adult white males with risk apparently concentrated among people who are obese.
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Introduction
Concern over the rapidly increasing prevalence of obesity throughout the world (1) has
led to many studies correlating indices of obesity to long-term health. In particular, body mass
index(BMI) has been found to be strongly associated with all-cause mortality (2, 3) and the
development of chronic diseases including cardiovascular disease (4), diabetes (5), cancer
(6),gallbladder diseases (7) and gout (8). BMI is a commonly used measure of overall adiposity
in clinical and research settings because of ease of measurement. However, there may be
appreciable heterogeneity in risk at any given level of BMI. This is exemplified by the concept of
‘metabolically healthy obesity’, according to which overweight or obese people with a relatively
normal metabolic risk factor profile are at no greater cardiovascular risk than their normal weight
equivalents (9, 10). However, the metabolically healthy obese may show greater risk of
progression to metabolic abnormality (11, 12) and, although risk of CHD in metabolically healthy
overweight or obese people may be less than in their metabolically unhealthy equivalents, with
long follow-up (13) or in a sufficiently large sample (14), an increase in cardiovascular risk may,
nevertheless, be detected. Such heterogeneity in risk, independent of overall adiposity, may
result from variation in the distribution of body fat. Obese people with a large depot of visceral
fat appear to be at particularly high risk (15-19) and ectopic deposition of fat in liver, muscle or
other tissues may also be important (20). However, clinical evaluation of specific fat depots is
limited by the need for computed tomography (CT) or magnetic resonance imaging (MRI) (21,
22). Beyond measurement of BMI, clinical evaluation of adiposity-related risks may be
enhanced by using alternative anthropometric measurements. Skinfold thickness
measurements offer one such alternative but, hitherto, studies have not provided strong
evidence to support their use in clinical practice. An increase in subscapular skinfold may not be
associated with all-cause mortality in men (23) but has been found to be linked to ischaemic
heart disease or variation in its risk factors in some studies (24, 25), although not in all(26). In
the Paris Prospective Study, preferential localisation of fat in the abdominal component, as
measured by sagittal diameter adjusted for the sum of trunk skinfolds was associated with
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increased cancer mortality (27). Subscapular to triceps ratio has been found to be associated
with stroke (28), ischaemic heart disease (29), and blood pressure (30) and has been proposed
as a marker of central to peripheral fat distribution.
Appreciable covariation may be expected between skinfold thicknesses and overall
adiposity and previous analyses may not have fully discriminated between risks associated with
different measures of adiposity. The primary aim of the present analysis, therefore, was to
investigate whether skinfold measurements were associated with mortality independently of BMI
as an index of overall adiposity.
Subjects and Methods
Participants:
The Heart Disease and Diabetes Risk Indicators in a Screened Cohort (HDDRISC) study
is a prospective study of 1192 white males recruited as part of a company health screening
program undertaken in London, U.K.. At enrolment, the participants were apparently healthy
senior executives, working or recently retired. The study started in 1971 with participants invited
for follow-up every 2-3 years; data collection ended in 2000. Skinfold thickness measurements
were taken from the beginning of the study until 1996 and for the purposes of this analysis, only
the participants with skinfold thickness measures (n=888) were considered for inclusion. The
present analysis is restricted to participants’ earliest records with skinfold information. The study
was approved by the ethics committee. All participants gave their written informed consent.
Measurements:
Details of data recording have been described previously (31). In brief, measurements
were carried out at a dedicated metabolic day ward, in the morning following an overnight fast.
Each participant provided a full medical history including details of smoking, alcohol
consumption, exercise and medication and also underwent a range of clinical and laboratory
measurements. Skinfold thicknesses were measured using the procedure of Durnin and
Womersley (32). The biceps skinfold was taken over the mid-point of biceps muscle with the
arm resting supinated on the thigh. The triceps skinfold was taken over the mid-point of the
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triceps muscle, at the posterior line between the olecranon and tip of acromion. The
subscapular skinfold was taken at an angle of about 45 degrees to the vertical, at the inferior
angle of scapular and the iliac skinfold was taken just above the iliac crest in the mid-axillary line
(32). Skinfold thicknesses were measured 3 times at each of the 4 sites using Harpenden
callipers. The mean of the 3 readings for each site was calculated.
Mortality ascertainment:
Mortality information was obtained through the United Kingdom NHS Information Centre
for Health and Social Care. Mortality information for participants who died overseas was notified
by family members of the deceased or their employer. The mortality information was complete
except for 18 participants who were no longer traceable. The present analysis includes deaths
up to 1 January 2014 and follow-up time was calculated as the time between the earliest visit
with skinfold information and death, or up till 1 January 2014 for those who were still alive. The
primary end- point was all cause mortality. The mortality causes were also subdivided into 4
categories; cancer deaths, arteriovascular deaths, infection deaths (predominantly pneumonia)
and other deaths. Arteriovascular mortality comprised death from coronary heart disease, heart
failure, cerebrovascular disease and aneurysm. Causes in the ‘other death’ category included
motor neurone disease, respiratory disease, gastrointestinal ulceration, alcohol and accident.
Data and statistical analysis:
The following skinfold ratios were calculated: subscapular to triceps, subscapular to iliac,
and BMI to iliac. In addition, the sum of all 4 skinfold thicknesses was calculated. Smoking was
coded as 0, <15 (light) or ≥ 15 (heavy) cigarettes per day. Alcohol consumption was coded as 0,
<28units per week (light) or ≥28 units per week (heavy). Exercise habits were coded as none,
moderate and regular (≥3 periods of ≥20min of exercise to breathlessness per week). All data
was analysed using STATA 13 for Windows (Stata, College Station, TX, USA). Baseline
characteristics were expressed in median and interquartile range (IQR) for continuous variables
and percentages and number of observations (n) for categorical variables. Significant
differences between the survivors and non-survivors for continuous variables were assessed
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using Mann-Whitney test and for categorical variables by chi-square test. Triceps, subscapular,
iliac, subscapular tricep ratio, subscapular iliac ratio, BMI iliac ratio and sum of skinfold
thicknesses were logarithmically transformed to reduce heteroscedasticity in regression
analyses. Continuous variables were standardised as z-scores for entry in univariable and
multivariable analyses. The Cox proportional hazards model was used to analyse survival time
in relation to all-cause mortality (STATA command: ‘stcox’) whereas competing-risks survival
regression (STATA command: ‘stcrreg’) was used to analyse survival in the specific mortality
subgroups: cancer, arteriovascular, infection and other. The Cox analysis proportional hazards
assumption was checked using Schoenfeld residuals and linearity using Matingale residuals.
For all models, linearity was further checked on the basis of hazard ratios in quartile and quintile
percentiles of each skinfold. Effects significant at p <0.05 were considered for interpretation.
Results
Out of 1192 participants in the HDDRISC study, 870 who had skinfold thicknesses
measured and mortality follow-up data recorded were included for analysis. Of these, 303
participants died before 1st January 2014. There were 119 participants who died from cancer,
101 from arteriovascular disease, and 40 from infection. The remaining 43 participants died
from other causes. The mean mortality follow-up time from the first record with skinfold
information was 27.7 years with a range of 0.5-41.5years.
At baseline, compared with survivors, those who died were older, had higher BMI,
smoked more cigarettes and drank more alcohol (Table 1). These differences generally
extended to the cancer, arteriovascular and infection mortality subgroups. Triceps and biceps
skinfold thicknesses did not differ between survivors and those who died (Table 1). Subscapular
skinfold was higher among those who died of any cause (p=0.01), specifically, those who died
of arteriovascular disease (p=0.02). Iliac skinfold was 16% lower (p<0.001) among those who
died of any cause (median 12.5 (IQR 8.6, 8.7) vs 14.9 (IQR10.1, 21.5) mm in survivors). Iliac
skinfold was also significantly lower among those who died of cancer (16% lower, p=0.02),
arteriovascular disease (13% lower, p=0.008) and infection (31% lower, p=0.001).
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Variables in Table 1 that differed between survivors and those who died also generally
showed associations with mortality in univariable survival analysis (results not shown). One
exception was iliac skinfold, which were not significantly associated with all-cause, cancer, AVD
and infection death in univariable survival analysis. However, in multivariable survival analysis,
with age, BMI, smoking, alcohol and exercise as covariates, lower iliac skinfold was
significantly, independently associated with all-cause, AVD and infective death (Table 2). No
significant deviations from the Cox model proportionality and linearity assumptions were
detected. Subscapular skinfold ceased to show any associations with mortality in multivariable
analysis and, triceps and biceps skinfolds showed no associations with mortality. Bivariable
survival analyses were undertaken to identify which variable was responsible for iliac skinfold
emerging as a significant associate of mortality in multivariable analysis. The key variable was
BMI: hazard ratios (95%CI, p) for iliac skinfold and BMI in bivariable analysis were: for all-cause
mortality 0.76 (0.66,0.88, p<0.001) and 1.51 (1.35,1.69, p<0.001) respectively; for AVD mortality
0.75 (0.60,0.93, p=0.009) and 1.44 (1.22,1.69, p<0.001) respectively; and for infection mortality
0.64 (0.42,0.96, p=0.03) and 1.27 (0.84,1.92, p=0.2) respectively. Bivariable analysis also
showed that group differences and univariable associations between subscapular skinfold and
all-cause and AVD mortality were dependent on BMI (results not shown). Linearity checks
based on hazard in skinfold percentiles found no evidence for J- or U-shaped relationships
between skinfolds and mortality. Nevertheless, an association was found between low triceps
skinfold and all-cause mortality (lowest vs highest: quartile HR 1.51 (95%CI 1.07, 2.13) p=0.02);
quintile 1.73 (1.18,2.54), p=0.005). However, this association did not extend to specific causes
of mortality and was not enhanced in overweight or obesity.
The emergence of iliac skinfold as a strong negative associate of mortality when the
positive associate of mortality, BMI, was included in survival analysis as an additional
independent variable (plus the strengthening of the positive association between BMI and
mortality) could result from a positive correlation between iliac skinfold and BMI. On Pearson
correlation, BMI was found to explain 21% of the variation in iliac skinfold (R=0.46, p<0.001).
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There were, therefore, two components of variation in iliac skinfold, one positively related to
mortality and dependent on BMI and one negatively related to mortality and independent of
BMI. This unexpected finding suggested that risk of mortality associated with a low iliac skinfold
might show differential associations with mortality at different BMI. We, therefore, derived the
HR for all-cause mortality in iliac skinfold quartiles in ranges of BMI corresponding to normal
weight (<25 kg/m2), overweight (25 to <30 kg/m2) and obese (≥30 kg/m2). Among normal weight
participants, the lowest quartile of iliac skinfold was not associated with all-cause mortality
(Figure 1), but was independently associated in the overweight (HR 2.07, p=0.01) and risk was
markedly increased in the obese (HR 6.34, p=0.02). Numbers of deaths were relatively low
among obese participants (n=40). Therefore, variation in risk associated with low iliac skinfold
was explored in successive ranges of overweight, both to include more participants and to
identify at which level of BMI hazard substantially increased. Hazard ratios, HR (95%CI),
associated with the lowest iliac skinfold quartile relative to the highest were for those with
BMI>25 kg/m2: HR 2.09 (1.29,3.38 p=0.003); BMI>26 kg/m2: HR 2.15 (1.27,3.66 p=0.005);
BMI>27 kg/m2: HR 3.15 (1.64,6.04 p=0.001); BMI>28 kg/m2: HR 3.33 (1.30,8.56 p=0.01); and
BMI>29 kg/m2: HR 6.23 (1.66,23.4 p=0.007). Numbers of deaths in each of these BMI ranges
were 179, 142,99, 66 and 50, respectively.
Discussion
Skinfold thickness measures, including iliac skinfold, are positively related to BMI but the
possibility that this relationship might obscure an underlying negative association between a
skinfold measure and mortality appears to have been little appreciated. Our analysis of
associations of skinfold thickness measures with mortality independently of variation in BMI has
revealed that, in the cohort of men we studied, a low iliac skinfold is independently associated
with l mortality over the course of long-term follow-up, in particular, arteriovascular and infection
mortality. Furthermore, risks associated with a low iliac skinfold appear to be particularly
concentrated in the obese.
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Previous studies have emphasised a positive association between subscapular skinfold
thickness and total or arteriovascular mortality risk (23, 25, 33). Our study found some evidence
for such an association, although not independently of BMI. Neither the Northwick Park Heart
study(33) nor the Seven Countries Study of Cardiovascular Disease (23) took into account
variation in BMI, although this was taken into account in the Caerphilly study. In contrast to our
findings, the Caerphilly Study reported a relationship between subscapular skinfold and incident
ischemic heart disease that was independent of BMI(25). Of these previous studies, only the
Northwick Park Heart study recorded iliac skinfold(33), but BMI was not taken into account in
exploring its associations with mortality and, in accord with our findings in univariate analysis, no
association was apparent. Clearly, further prospective studies with measurement of iliac skinfold
are needed to confirm or refute our findings and resolve existing inconsistencies.
In accord with other studies (2-4, 6), our analysis found that BMI was positively
associated with all-cause, cancer and arteriovascular mortality. However, BMI is a marker of
overall adiposity (15) and skinfold measurements are generally taken to represent adiposity at
different regional adipose tissue depots (34). Truncal measurements (e.g. subscapular,
abdominal and iliac) then represent central adiposity and peripheral measurements (e.g. biceps,
triceps and thigh) peripheral adiposity. The importance given to this distinction stems from
recognition of the role of the visceral fat depot in generating an adverse metabolic risk factor
profile and augmenting long-term risk of chronic disease (21). Given the way they are
measured, variation in skinfold thicknesses necessarily reflect variation in subcutaneous fat and
may relate only indirectly or not at all (35) to the visceral fat depot (34). Nevertheless, skinfolds
as indices of subcutaneous fat storage could be important given that a limited ability to store fat
in subcutaneous depots may lead to redistribution of excess fatty acids to metabolically
disruptive ectopic locations such as viscera, liver or muscle (18, 20). Clinical evidence for an
adverse effect of diminished subcutaneous fat comes from the observation that among people
with type 2 diabetes, those who have high visceral fat with low subcutaneous fat, show
increased carotid intima media thickness(36). This observation is consistent with our finding that
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obesity combined with low iliac skinfold constitutes a high-risk state and accords with mortality
risk being concentrated in deaths from arteriovascular disease. However, whilst depletion of a
particular subcutaneous fat depot might imply increased ectopic fat deposition and, therefore,
increased arteriovascular risk, there appear to be no precedents for an association between a
low subcutaneous fat depot and infection death. Pneumonia was the most common cause of
infection death which might indicate a contribution from premature ageing or wasting to the
association we observed. However, these considerations do not explain why iliac skinfold alone
was associated with increased mortality. In this respect, it is noteworthy that measurement error
for the iliac skinfold may be less compared to other skinfolds, especially with increasing obesity
levels (37). Accordingly, iliac skinfold might provide a particularly precise index of subcutaneous
fat.
Regardless of underlying mechanisms, it does appear that a low iliac skinfold can
indicate particularly unhealthy obesity but whether the pattern of low iliac skinfold and high BMI
is metabolically unhealthy remains to be established. In our previous analysis of relationships
between skinfold thicknesses and arteriovascular disease risk factors in the HDDRISC cohort,
variations in age, smoking, alcohol and exercise were taken into account but variation in BMI
was not (31). Accordingly, the associations observed between skinfolds and risk factors were
simply those expected with overall adiposity.
Relatively little use has been made of skinfolds in clinical practice, possibly because of
an apparent lack of any strong predictive advantage over basic anthropometric measurements
such as BMI or waist circumference. Use of ratios might be expected to strengthen independent
associations by skinfold measures but our analysis provided little support for this. The
subscapular/triceps ratio has been proposed as a CVD-associated marker of central fat
deposition(29) but our analysis found no evidence for this ratio having an independent
association with cardiovascular mortality. The BMI/iliac ratio might have been expected to
provide a sensitive index of mortality risk. However, the ratio proved uninformative, with only a
weak negative relationship emerging in multivariable analysis. The positive correlation between
10
BMI and iliac skinfold and their contrasting independent associations with mortality made
interpretation of these findings problematic. Therefore, we undertook a more explicit analysis by
exploring risks in successive ranges of BMI. This uncovered a marked increase in mortality risk
associated an iliac skinfold of 9.7mm or less among participants with a BMI of 29 kg/m2 or more,
which offers the possibility for a useful clinical index. Exploring this in other cohorts could be
worthwhile.
Our study has limitations and strengths. Only white males were studied so the results
are not generalisable to other ethnic groups or women. There were relatively small numbers of
obese participants (n=67). Also, there were no direct measurements of adiposity (e.g. MRI or
CT) that would have helped us establish how iliac skinfold related to ectopic fat deposition in
this cohort. A strength of our study is that it concerned apparently healthy individuals, followed
for a long period and with relatively little prescription drug use. Moreover, the restricted selection
of participants may have helped to distinguish significant associations. Besides that, the skinfold
measurements were carried out by a historically continuous research group working in
dedicated clinical research facilities. The long duration of follow-up may have enabled
discrimination of effects that shorter duration prospective studies have missed, although with
greater numbers of events, it might have been possible to detect non-linearities in the
relationships between skinfolds and mortality. Linearity checks revealed a discontinuous
relationship whereby a low triceps skinfold was associated with all-cause mortality but this
association showed little of the strength and consistency we found for low iliac skinfold and may,
therefore have been a chance finding. Our analysis did employ extensive statistical testing,
which suggests that some false-positive significances may have been encountered. In principle,
five primary hypotheses were explored, namely that biceps, triceps, subscapular and iliac
skinfold thicknesses and the subscapular/triceps skinfold ratio were each independently
associated with all-cause mortality. A probability of <0.01 (0.05÷5) is therefore appropriate for
rejecting the null hypothesis. The independent association of iliac skinfold with all-cause
mortality was significant at p=0.002 and is, therefore, unlikely to have been a chance finding.
11
We consider further testing in specific mortality groupings and in different ranges of BMI to have
been exploratory and hypothesis-generating.
In conclusion, we found that in adult white males, low iliac skinfold thickness is
associated with all-cause, arteriovascular and infection mortality independently of BMI. Risk
appears to be particularly concentrated in the very overweight and the obese, with a 6-fold
increase in all-cause mortality risk above a BMI of 30 kg/m2. This observation needs to be
confirmed in other cohorts and metabolic and ectopic fat correlates of low iliac skinfold need to
be explored further.
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Acknowledgements
The HDDRISC study was initiated the late Professor Victor Wynn, who directed it for much of its
course. Data acquisition was sustained by many clinical, scientific, technical, nursing and
administrative staff, to each of whom we extend our thanks.
Funding
Data acquisition for the HDDRISC study was funded by the Heart Disease and Diabetes
Research Trust and the Rosen Foundation.
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Table 1: Baseline Characteristics of Survivors compared to Non-Survivors. Median (interquartile range) are shown for continuous variables and % (n) for categorical variables. The statistical significances of differences between Non-Survivors and Survivors are shown in superscript.
Survivors Non-survivors - cause of deathAll-cause Cancer Arteriovascular Infective Other causes
n 567 303 119 101 40 43
Follow-up time(years) 31.5(24.6,36.1) 23.3(16.2,30.6)<0.001 20.4(14.7,29.3)<0.001 23.4(16.7,28.9)<0.001 29.1(20.7,33.5)<0.01 25.6(13.4,32.7)<0.001
Age (years) 43.1(27.1,48.3) 51.8(47.8,55.7)<0.001 51.7(47.8,55.6)<0.001 52.6(49.1,56.0)<0.001 51.2(47.0,55.5)<0.001 51.6(47.2,55.4)<0.001
BMI (kg/m2) 25.1(23.5,26.9) 25.9(24.2,27.8)<0.001 25.7(24.4,27.5) 0.004 26.1(24.2,27.8) 0.004 25.9(23.9,26.9) 0.3 26.6(24,28) 0.02
Skinfold measurements
triceps (mm) 10.8(8.6,13.4) 11.2(8.6,14.2) 0.2 11.0 (8.3,13.8) 0.7 11.4(9.2,15.0) 0.06 11.9(8.4,13.7) 0.8 11.0(8.4,13.7) 0.8
biceps (mm) 6.0(4.6,7.4) 6.0(4.9,7.5) 0.7 6.4(5.1,7.5) 0.1 6.0(4.8,7.5) 0.7 5.5(4.1,7.2) 0.4 5.5(5.0,7.2) 0.7
subscapular(mm) 15.4(12.1,20.0) 16.3(13.3,20.5) 0.01 16.1(13.2,20.3) 0.1 16.7(13.9,21.9) 0.02 15.0 (13.2,18.8) 0.6 17.1(13.8,20.3) 0.1
iliac (mm) 14.9(10.1,21.5) 12.5(8.6,18.7) <0.001 12.5(8.6,19.6) 0.02 12.9(9.0,16.4) 0.008 10.3(8.9,15.0) 0.001 13.5(8.2,19.3) 0.1
subscapular/triceps ratio 1.46(1.18,1.81) 1.51(1.2,1.89) 0.07 1.49(1.25,1.86) 0.2 1.54(1.19,1.91) 0.2 1.48(1.12,1.89) 0.6 1.57(1.20,2.03) 0.1
Smoking
non-smoker 73(411) 49(148) 50(59) 45(45) 50(20) 56(23)
<15 cig/day 19(108) 29(86) 21(25) 36(36) 33(13) 29(12)
≥15 cig/day 8(48) 22(67) <0.001 29(35) <0.001 19(19) <0.001 17(7) 0.009 15(6) 0.07
Alcohol
non-drinker 1(8) 1(4) 1(1) 3(3) 0 0
<28 units/wk 64(360) 46(140) 44(52) 47(47) 45(18) 53(23)
≥28 units/wk 35(198) 53(159) <0.001 55(66) <0.001 50(51) 0.004 55(22) 0.03 47(20) 0.2
Exercise
sedentary 38(215) 44(131) 41(49) 51(50) 34(14) 44(18)
moderate 44(248) 42(126) 46(54) 36(36) 51(21) 39(16)
regular 18(100) 14(41) 0.1 13(15) 0.4 13(13) 0.06 15(6) 0.6 17(7) 0. 7
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Table 2. Multivariate hazard ratios of associations of skinfold measurements and all-cause and cause-specific mortality.
Cause of deathAll-cause Cancer Arteriovascular Infective Other causes
Skinfold measurements
triceps 0.89(0.78,1.02) 0.1 0.90 (0.74,1.10) 0.3 1.14 (0.87,1.50) 0.3 0.94 (0.59,1.50) 0.8 0.83 (0.56,1.21) 0.3
biceps 1.94 (0.82,1.06) 0.5 1.10 (0.91,1.33) 0.3 0.78 (0.59,1.02) 0.08 0.87 (0.58,1.30) 0.5 0.89 (0.62,1.2) 0.5
subscapular 0.93 (0.79,1.09) 0.4 1.00 (0.76,1.33) 0.9 0.91 (0.68,1.21) 0.5 1.03 (0.70,1.51) 0.9 0.92 (0.62,1.37) 0.7
iliac 0.77 (0.66,0.90) 0.002 0.90 (0.70,1.16) 0.4 0.75 (0.58,0.97) 0.03 0.63 (0.42,0.94) 0.02 0.92 (0.59,1.44) 0.7
subscapular/triceps ratio 1.07 (0.95,1.23) 0.2 1.02 (0.84,1.25) 0.7 0.93 (0.75,1.16) 0.5 1.14 (0.78,1.65) 0.5 1.19 (0.84,1.70) 0.3
Analysis of factors associated with all-cause mortality by Cox proportional hazards modelling, and competing risk analysis for specific causes with inclusion of BMI, age, smoking, alcohol and exercise into multivariable analysis. Hazard ratios (95% confidence intervals) and significances in superscript are shown. Standardised data was entered for continuous variables.
19
Legend to Figure 1
Increased risk of death in overweight and obese white males with low iliac skinfold thickness. Hazard
ratios (HR) and 95% confidence intervals (95%ci) are shown for mortality stratified by quartiles of iliac
skinfold: q1 3.3-9.7mm; q2 9.8-13.7mm; q3 13.8-20.0mm relative to q4 >20.0mm in normal weight
(diamonds), overweight (circles) and obese (squares) individuals. P values are shown for quartiles in
which there was a significant effect.
20
Figure 1
21