Serum vitamin D levels, diabetes and cardio-metabolic risk factors in Aboriginal and Torres Strait Islander Australians
Diabetology & Metabolic Syndrome
Serum vitamin D levels, diabetes and cardio-metabolic risk factors in Aboriginal and Torres Strait Islander Australians
Louise J Maple-Brown 0 1
Jaquelyne T Hughes 0 1
Zhong X Lu 2 7
Kanakamani Jeyaraman 1 6
Paul Lawton 1
Graham Jones 4 5
Andrew Ellis 9 10
Ashim Sinha 8
Alan Cass 1
Richard J MacIsaac 3 10
George Jerums 9 10
Kerin O'Dea 6
0 Division of Medicine, Royal Darwin Hospital , Darwin , Australia
1 Menzies School of Health Research, Charles Darwin University , Darwin , Australia
2 Melbourne Pathology , Melbourne , Australia
3 St Vincent's Hospital , Melbourne , Australia
4 University of NSW , Sydney , Australia
5 SydPath, St Vincents Hospital , Sydney , Australia
6 University of South Australia , Adelaide , Australia
7 Department of Medicine, Monash University , Melbourne , Australia
8 Cairns Base Hospital and Diabetes Centre , Cairns , Australia
9 Austin Health , Melbourne , Australia
10 University of Melbourne , Melbourne , Australia
Background: Low levels of serum 25-hydroxy vitamin D (25(OH)D), have been associated with development of type 2 diabetes and cardiovascular disease (CVD); however there are limited data on serum 25(OH)D in Indigenous Australians, a population at high risk for both diabetes and CVD. We aimed to assess levels of serum 25(OH)D in Aboriginal and Torres Strait Islander Australians and to explore relationships between 25(OH)D and cardio-metabolic risk factors and diabetes. Methods: 592 Aboriginal and/or Torres Strait Islander Australian participants of The eGFR (estimated glomerular filtration rate) Study, a cross-sectional analysis of a cohort study performed in 2007-2011, from urban and remote centres within communities, primary care and tertiary hospitals across Northern Territory, Far North Queensland and Western Australia. Assessment of serum 25(OH)D, cardio-metabolic risk factors (central obesity, diabetes, hypertension, history of cardiovascular disease, current smoker, low HDL-cholesterol), and diabetes (by history or HbA1c 6.5%) was performed. Associations were explored between 25(OH)D and outcome measures of diabetes and number of cardio-metabolic risk factors. Results: The median (IQR) serum 25(OH)D was 60 (45-77) nmol/L, 31% had 25(OH)D <50 nmol/L. For participants with 25(OH)D < 50 vs 50 nmol/L, cardio-metabolic risk profile differed for: diabetes (54%, 36% p < 0.001), past history of cardiovascular disease (16%, 9%, p = 0.014), waist-hip ratio (0.98, 0.92, p < 0.001), urine albumin-creatinine ratio (2.7, 1.5 mg/mmol, p < 0.001). The OR (95% CI) for diabetes was 2.02 (1.03 - 3.95) for people in the lowest vs highest tertiles of 25(OH)D (<53 vs >72 nmol/L, respectively) after adjusting for known cardio-metabolic risk factors. Conclusion: The percentage of 25(OH)D levels <50 nmol/L was high among Aboriginal and Torres Strait Islander Australians from Northern and Central Australia. Low 25(OH)D level was associated with adverse cardio-metabolic risk profile and was independently associated with diabetes. These findings require exploration in longitudinal studies.
25-hydroxy vitamin D; Type 2 diabetes; Aboriginal; Cardiovascular risk
The major contributor to the significantly reduced life
expectancy of Indigenous Australians, compared to the
general Australian population is the overwhelming burden
of chronic diseases, such as ischaemic heart disease,
diabetes and chronic kidney disease . Low levels of serum
25hydroxy vitamin D (25(OH)D), the best marker for
vitamin D status, have been associated with development
of the metabolic syndrome , diabetes [3,4] and
cardiovascular disease  in many parts of the world, but there
are limited data on serum 25(OH)D levels in the high risk
Indigenous Australian population.
Most available data on vitamin D deficiency in Australia
relate to studies performed in the temperate zones. The
Australian Diabetes, Obesity and Lifestyle (AusDiab) study
reported that 31% of adults in Australia had serum 25
(OH)D levels less than 50 nmol/L, with a higher
prevalence during winterspring and in people residing in
southern states . Studies that have assessed vitamin D
levels in groups such as the elderly , and free-living
adults in Southeast Queensland (subtropical)  have
demonstrated a prevalence of vitamin D deficiency
(defined as serum 25(OH)D < 50 nmol/L) of at least 25%.
However, small studies from the tropical region of Far
North Queensland have reported a low prevalence of
vitamin D deficiency in a healthy obstetric population
(0%)  and in free-living adults (6.2%) . Large
population-based studies on vitamin D status are lacking in
It is notable that the prevalence of vitamin D deficiency
is higher in people with dark skin. A recent systematic
review reported a prevalence of 30-53% in ethnic minorities
with dark skin versus 14-26% in those of Europid
background . Limited data from South Australia show that
Indigenous Australians have a low vitamin D status .
However, approximately 40% of Indigenous Australians
live at latitudes closer to the equator - in the tropical and
subtropical regions of Australia . In the context of high
risk of premature mortality from cardiovascular disease
and related chronic diseases in Indigenous Australians and
the reported association between vitamin D and chronic
diseases, further assessment of the vitamin D status and its
relationship to cardio-metabolic risk factors in this high
risk population is warranted.
Therefore, we evaluated the serum 25(OH)D levels in
Aboriginal and Torres Strait Islander Australians in a
cross sectional cohort of 592 Indigenous Australians
from urban, regional and remote areas of the Northern
Territory, Western Australia and Far North Queensland,
participants in The Estimated Glomerular Filtration Rate
Study (The eGFR Study) [14,15]. The aim of the eGFR
Study was to assess the accuracy of estimated measures
of glomerular filtration rate in Indigenous Australians.
The aim of the current analysis is to assess levels of
serum 25(OH)D in Indigenous Australians and to
explore relationships between 25(OH)D and
cardio-metabolic risk factors in this cohort.
The methods of the eGFR Study have been previously
reported [14,15]. In brief, Aboriginal and/or Torres Strait
Islander participants aged 16 years and above were
recruited across five predefined strata of health, diabetes
status and kidney function from the following regions of
Australia: Top End, Northern Territory, Central Australia,
remote Western Australia and Far North Queensland.
The study was approved by the joint Menzies School of
Health Research and Northern Territory Department of
Health Human Research Ethics Committee (HREC) and
other HRECs in the above regions .
Participants fulfilled the definition of Aboriginal and/or
Torres Strait Islander according to the standard method
used in National Census data collection: 1) is of Aboriginal
and/or Torres Strait Islander descent; 2) identifies as an
Australian Aboriginal and/or Torres Strait Islander; and
3) is accepted as such by the community in which he or
she lives or has lived. Of the 656 Indigenous
participants of the eGFR Study, 605 had available data for
serum 25(OH)D. Participants aged <18 years were
excluded from this analysis (n = 13), leaving n = 592
participants presented here. Participants of both Aboriginal
and Torres Strait Islander background (n = 52) were
combined with the Torres Strait Islander group as the
two groups did not differ significantly for: age, body
mass index (BMI), waist circumference, waist hip ratio
(WHR), blood pressure (BP), HbA1c, lipid profile, urine
albumin creatinine ratio (ACR), and serum 25(OH)D.
The combined group of Torres Strait Islander
participants and those of both Aboriginal and Torres Strait
Islander background is referred to as Torres Strait
Islander participants. This analysis includes 22
participants without data for measured glomerular filtration
rate (mGFR), and participants missing data for other
The latitude of participants usual residence (Additional
file 1: Figure S1) was [median, interquartile range (IQR),
(range)]: Aboriginal participants, 16.4, 12.5-23.7
(11.235.1) degrees south, Torres Strait Islander participants
10.6, 10.6-10.6 (10.0-37.8) degrees south. Note that 66%
(112 of 169) of Torres Strait Islander participants resided
on Thursday Island at latitude 10.6 degrees south. The
season of sampling was: Aboriginal participants, 5.4%
Summer (December-February), 28.6% Autumn (March-May),
42.3% Winter (June-August), 23.6% Spring
(SeptemberNovember); Torres Strait Islander participants, 42.0%
Summer, 4.7% Autumn, 23.1% Winter, 30.2% Spring.
The laboratory methods have been previously published
. In brief, urine albumin and creatinine, lipid profile
(non-fasting) and HbA1c assays were performed at each
centre by the local laboratory. The mGFR was measured
using an iohexol plasma disappearance technique over
4 hours . Serum high sensitive troponin T (hsTnT)
and 25(OH)D were measured at Melbourne
Pathology, Melbourne, Australia. Serum hsTnT was analysed
using the electro-chemiluminescence immunoassay on a
COBAS e601 analyser (Roche Diagnostics, Mannheim)
with an inter-assay coefficient variation (CV) of 3.1%.
Serum 25(OH)D was analysed using the 25OH vitamin D
TOTAL assay on a Liaison XL analyser (DiaSorin Inc.,
Stillwater, MN). It is an automatic, direct competitive
chemiluminescent immunoassay with an inter-assay CV
of 6.9% at 41 nmol/L and 5.8% at 101 nmol/L. This
method gives serum 25(OH)D results that align with
the National Institute of Standards and Technology
(NIST) targets. Compared to the NIST-aligned liquid
chromatography-tandem mass spectrometry system, the
equation obtained is y (Liaison XL in nmol/L) = 1.03
Cardio-metabolic risk factors
Cardio-metabolic risk factors included components of
the metabolic syndrome, using National Cholesterol
Education Program, International Diabetes Federation
and harmonised definitions :
(a) Central Obesity: WHR > 0.9 for males and >0.85
(b)Diabetes: by history or HbA1c 6.5%
(c) Low HDL-Cholesterol: <1 mmol/L for males
and <1.3 mmol/L for females
(d)Hypertension: systolic BP 130 mmHg or diastolic
BP 85 mmHg
(e) Current smoker: current cigarette smoker
(f ) Past history of cardiovascular disease (CVD): history
of ischaemic heart disease, acute myocardial
infarction, cerebrovascular accident or transient
ischaemic attack by self-report and/or medical
Data analysis was performed using STATA v12.0 (Stata
Corporation, TX, USA). Data are presented stratified by 25
(OH)D levels <50 and 50 nmol/L (Table 1) as that is the
cut-point used in national and international clinical
guidelines. Variables with distributions significantly different
from normal were log transformed. To determine between
group differences, Pearson chi-square tests (categorical
variables) or independent sample t-tests (continuous
variables) were conducted. Due to missing data, n of each
group in Table 1 for the following variables was: BMI, 184,
405; WHR, 172, 391; BP, 184, 402; Smoker, 183, 400;
History CVD, 178, 387; HbA1c, 180, 394; HDL, 177, 381;
mGFR, 176, 394; urine ACR, 183, 397. Cardio-metabolic
risk factors were assessed in all participants and each
ethnic group. The number of cardio-metabolic risk factors
was calculated by counting how many of the following six
factors were present: central obesity, low HDL-cholesterol,
hypertension, diabetes, current smoker, and past history of
CVD. Due to missing data, n of all participants and each
group respectively in Table 2, for the following variables
was: central obesity, 563, 398, 165; low HDL, 558, 402,
156; hypertension, 586, 419, 167; past history CVD, 565,
400, 165; current Smoker, 583, 417, 166; sum of CVD Risk
Factors, 505, 358, 147. Distribution of 25(OH)D in
participants with increasing number of cardio-metabolic risk
factors was assessed graphically using a box plot (Figure 1).
Logistic regression was used to estimate the odds ratio for
participants in tertiles of serum 25(OH)D for two outcome
variables: three or more cardio-metabolic risk factors (3+
cardio-metabolic risk factors) and diabetes. Models were
performed using tertiles of 25(OH)D. Three models were
performed for each outcome variable. Models 1 and 2
were the same for both outcome variables: model 1 was
unadjusted; and model 2 adjusted for age, gender, ethnicity
(Aboriginal or Torres Strait Islander), season and latitude.
Different covariables were used in model 3. For the
relationship between vitamin D and 3 + cardio-metabolic risk
factors, model 3 was model 2 further adjusted for mGFR,
troponin and urine ACR. For the relationship between
vitamin D and diabetes, model 3 was model 2 further
adjusted for WHR, HDL-cholesterol, mGFR, systolic blood
pressure, current smoker, urine ACR. The fully adjusted
models were constructed including covariates if they were
clinically important or confounders. Tertiles of serum 25
(OH)D were used in the multivariate modelling in order to
perform a robust analysis of relationships between key
variables, without an a priori decision as to where cut-points
should be. For each outcome variable, two-way
interactions were assessed between vitamin D and other
independent variables in the model. There were no significant
Of the 592 Indigenous participants, 423 (71%) identified as
Aboriginal and 169 (29%) as Torres Strait Islander. The
median (IQR) serum 25(OH)D was: all Indigenous
participants, 60 (4577) nmol/L; Aboriginal participants, 55
(4070) nmol/L; Torres Strait Islander participants, 75
(5888) nmol/L. Among all participants (n = 592), the
distribution of serum 25(OH)D <50, 5074 and 75 nmol/L
was 31%, 42% and 27% respectively. Participant
characteristics, stratified by serum 25(OH)D <50 or 50 nmol/L,
are presented in Table 1. A higher proportion of Aboriginal
Table 1 Baseline characteristics stratified by serum 25(OH)D
25(OH)D <50 nmol/L
Age (years) 46 (12)
Aboriginal (%) 168 (90%)
Torres Strait Islander (%) 18 (10%)
Male (%) 71 (38%)
Current smoker (%) 77 (42%)
Diabetes (%) 100 (54%)
Past History CVD (%) 28 (16%)
BMI (kg/m2) 30.5 (7.1)
Waist Hip ratio 0.97 (0.09)
Systolic BP (mmHg) 122 (19)
Diastolic BP (mmHg) 77 (11)
25(OH)D (nmol/L) 37 (9)
HbA1c (%, mmol/mol) 6.3 (5.9-7.8) 45 (4062)
HDL chol (mmol/L) 1.0 (0.8-1.2)
Total chol: HDL chol 4.5 (3.6-5.8)
Troponin (g/L) 3.0 (3.0-5.2)
mGFR (ml/min/1.73 m2) 104 (76123)
mGFR < 60 ml/min/1.73 m2 (%) 39 (21%)
Urine ACR (mg/mmol) 2.7 (0.9-81)
Data presented as mean (standard deviation), median (interquartile range) or number (%).
n may vary due to missing data (see methods).
*Pearson chi-square test or independent sample t-test.
p values <0.05 are represented in bold font.
participants had serum 25(OH)D <50 nmol/L than Torres
Strait Islander participants. Compared to participants
with serum 25(OH)D 50 nmol, those with 25(OH)D
<50 nmol/L displayed a more adverse cardio-metabolic risk
profile: higher percentage with diabetes and past history of
CVD; higher waist-hip ratio, blood pressure, HbA1c and
urine ACR. The difference in urine ACR between groups
with 25(OH)D < or 50 nmol remained significant after
adjustment for diabetes status (p = 0.002) or HbA1c
(p = 0.004).
Table 2 Number (%) of Aboriginal and Torres Strait Islander participants with cardio-metabolic risk factors
Figure 1 Serum 25(OH)D distribution in participants with increasing number of cardio-metabolic risk factors (central obesity, diabetes,
low HDL-cholesterol, hypertension, current smoker, past history of CVD). The bars represent median and boxes represent interquartile
range of serum 25(OH)D (nmol/L), dots represent outliers; n = 24, 87, 127, 149, 118 across groups with 0, 1, 2, 3, 4+ cardio-metabolic risk factors,
respectively; p < 0.001 for each category of cardiometabolic risk numbers compared to reference group of 0 risk factors.
Table 2 shows that 53% of all participants had at least
three and 23% had at least four cardio-metabolic risk
factors. Only 24 participants had nil risk factors. Levels
of serum 25(OH)D fell with increasing numbers of
cardio-metabolic risk factors (Figure 1). The study
population was grouped on the basis of tertiles of 25(OH)D
values (72, 5371 and < 53 nmol/L). Compared to
participants with serum 25(OH)D at the highest tertile
(72 nmol/L), the odds ratio and 95% confidence
interval (OR (95% CI)) of having 3 + cardio-metabolic risk
factors was 1.95 (1.203.16) and 4.00 (2.356.82) in
participants with serum 25(OH)D in the middle and lowest
tertiles, respectively, after adjustment for age, gender,
ethnicity (Aboriginal or Torres Strait Islander), latitude
and season. The strength of the association was reduced
but still remained significant after inclusion of mGFR,
troponin and urine ACR as covariates in the above model
[OR (95% CI) 1.69 (1.022.81) for 25(OH)D 5372 nmol/L
and 3.04 (1.715.40) for 25(OH)D <53 nmol/L].
Table 3 outlines the OR (95% CI) for the association
between each tertile of 25(OH)D and diabetes in
different models. Compared to participants in the highest
tertile of serum 25(OH)D (>72 nmol/L), the risk of
diabetes for participants in the lowest tertile (<53 nmol/L)
was doubled [OR (95% CI) 2.15 (1.10 2.18)] after
adjusting for cardio-metabolic risk factors in model 3.
In this large cross-sectional study of 25(OH)D levels in
Aboriginal and Torres Strait Islander Australians from
Northern and Central Australia, we have reported three key
findings. First, one third (31%) of this Indigenous cohort
had vitamin D deficiency (serum 25(OH)D <50 nmol/L).
Second, Indigenous Australian participants with 25(OH)D
Table 3 Risk of diabetes expressed as odds ratio according to tertiles of serum 25(OH)D levels
Covariates in the model
n = 592
2.80 (1.85 4.23)
Results presented are those of logistic regression analysis of diabetes.
n = 592
1.73 (1.06 2.83)
3.01 (1.81 5.03)
n = 489
1.56 (0.84 2.90)
2.15 (1.10 2.18)
levels less than 50 nmol/L displayed a more adverse
cardio-metabolic risk profile than those with 25(OH)D
level greater than 50 nmol/L. Third, serum 25(OH)D levels
in the lowest tertile (<53 nmol/L) were independently
associated with diabetes, and the association remained
significant after adjustment for known cardio-metabolic
To our knowledge, this is the first large study of 25(OH)
D levels in adult Aboriginal and Torres Strait Islander
Australians. We have reported a high percentage (31%) of
vitamin D deficiency in this cohort from Northern and
Central Australia, regions closer to the equator than
previous Australian studies. The median 25(OH)D level
(55 nmol/L) is similar to the mean 25(OH)D previously
reported in a small study of 58 Aboriginal participants from
South Australia (latitude 35 degrees south), of 56.8 nmol/L
. Of note, AusDiab, a nation-wide Australian
population-based study, reported that 31% of Australians had 25
(OH)D levels <50 nmol/L, however only 0.9% of AusDiab
participants identified as Aboriginal or Torres Strait
Islander Australians . High rates of vitamin D deficiency
have been reported in other Indigenous populations
internationally, including Aboriginal Canadian women
(33%) , New Zealand Maori and Pacific Islander New
Zealanders (61% and 69% respectively, compared to 46%
of New Zealanders of European descent) . However,
direct comparison is limited as key characteristics (latitude,
age, BMI, co-morbidities) differ between cohorts.
Aboriginal and Torres Strait Islander participants in the
current study with levels of 25(OH)D less than 50 nmol/L
displayed a more adverse cardio-metabolic risk profile
than those with 25(OH)D greater than 50 nmol/L. Levels
of 25(OH)D in the lowest tertile (<53 nmol/L) remained
significantly associated with at least three cardio-metabolic
risks independent of age, gender, ethnicity (Aboriginal or
Torres Strait Islander), latitude, season, urine ACR, mGFR
and troponin. Waist-hip ratio was used as the index of
central obesity (rather than waist circumference) as it is a
better discriminator of CVD risk across populations of
different body build . The relationship between 25(OH)D
levels and cardio-metabolic risk factors observed in the
current study is consistent with that described in large
Australian and international observational studies, both
cross-sectional  and longitudinal, for the outcome of
cardiovascular events  and metabolic syndrome .
Low serum 25(OH)D was significantly associated with
increased diabetes risk in this cross-sectional cohort. This
is independent of other known cardio-metabolic variables
(including waist-hip ratio, HDL-cholesterol, urine ACR,
mGFR, blood pressure and cigarette smoking). A similar
independent relationship between diabetes and 25(OH)D
levels has been reported in other cross-sectional studies
, and confirmed in prospective observational studies
[3,4]. However, intervention studies have not clearly
demonstrated efficacy of vitamin D supplementation
against development of type 2 diabetes . Several
mechanisms have been proposed for the role of vitamin D in
diabetes. Adequate serum 25(OH)D levels promotes
synthesis of 1,25(OH)2D in extra-renal tissues. Improved
beta-cell function by 1,25(OH)2D produced by pancreatic
beta-cells, improved insulin sensitivity by 1,25(OH)2D in
skeletal muscle, liver and adipose tissue, and systemic
anti-inflammatory effects of 1,25(OH)2D reduce the risk
of developing diabetes [4,23]. The odds ratio of the
association between low vitamin D and diabetes decreased
with addition of covariates (including season, latitude, and
diabetes and cardio-metabolic risk factors) to the model.
Data for physical activity and sun exposure were not
available in the current study; inclusion of these data may have
further attenuated the reported association, although data
for central obesity and latitude were included.
High levels of vitamin D deficiency in Aboriginal and
Torres Strait Islander participants in the current study
may be related to darker skin pigmentation, reduced
hours of sun exposure and/or change in physical activity
levels from the hunter-gatherer to the sedentary indoor
lifestyle. The change in dietary pattern from traditional
(which was nutrient rich and included vitamin D-rich
offal and a variety of marine species) to a Western
pattern could also be a contributory factor, however dietary
sources of vitamin D are often relatively low. The
majority of Australians do not meet the recommended
dietary intake of vitamin D  and vitamin D fortification
is voluntary for dairy products (and mandatory only for
edible oil spreads) in Australia.
Limitations of the current study include: its
crosssectional design; data were not collected for physical
activity, vitamin D supplementation, dietary sources of
vitamin D, skin pigmentation, sun exposure, time spent
outdoors, sun protection behaviour; differences between
Aboriginal and Torres Strait Islander participants for
proportion with diabetes or CVD, latitude and season of
blood collection. Season was categorised as the traditional
four Australian seasons, as was used in the AusDiab study,
although available data indicate that hours of sunlight per
season vary less in tropical than in subtropical regions of
this study . Nevertheless, this is the largest study
reporting 25(OH)D levels in Aboriginal and Torres Strait
Islander Australians, a population at high risk of diabetes
and CVD. Participants were from tropical and subtropical
regions of Australia, regions where a significant
proportion of Indigenous Australians reside, yet levels of 25(OH)
D have not previously been reported among Indigenous
Australians from these regions.
We have reported a high percentage of vitamin D deficiency
among Aboriginal and Torres Strait Islander Australians
from Northern and Central regions of Australia. Low level
of 25(OH)D was associated with more adverse
cardiometabolic risk profile and was independently associated
with diabetes in this cross-sectional cohort. Further
exploration of these findings is required in both longitudinal,
observational and interventional studies.
Additional file 1: Figure S1. Latitude of participants usual place of
residence. The Numbers inside the markers indicate the number of
participants from each location, the letters indicate the location (from
most northerly latitude) as follows: A, Thursday Island & Torres Strait
Islands; B, Elcho Island & North Arnhemland; C, Darwin region; D,
Kalumbaru; E, Katherine region; F, One Arm Point & Broome region; G,
Cairns & Townsville; H, Halls Creek region; I, Lajamanu; J, Tennant Creek &
Barkly region; K, Port Headland region; L, Nyrippi; M, Alice Springs region;
N, Brisbane; O, Geraldton region; P, Kalgoorlie region; Q, Perth region.
All the authors declared no competing interests.
LMB, JH, PL, GRDJ, AE, AS, AC, RJM, GJ, and KOD designed and conducted
the eGFR study. LMB designed and performed the statistical analyses guided
by ZL, GJ and KOD. ZL supervised laboratory measurement of 25(OH)D. LMB
drafted the manuscript with assistance from KJ, and all authors contributed
important intellectual content. All authors approved the final version for
Thanks to participants, study staff and investigators of the eGFR Study.
Thanks to Roche Diagnostics for supplying the enzymatic creatinine reagent
kits and Melbourne Pathology, Australia for the technical support for the
analysis of enzymatic creatinine, 25(OH)D and high sensitive troponin T. The
eGFR Study was funded by the National Health and Medical Research
Council of Australia (NHMRC, Project Grant #545202). The views expressed
are those of the authors and do not reflect the views of NHMRC. Additional
support was obtained from Kidney Health Australia, NHMRC #320860, the
Colonial Foundation, Diabetes Australia Research Trust, Rebecca L Cooper
Foundation and SeaSwift, Thursday Island. LMB is supported by an Australian
NHMRC Early Career Fellowship in Aboriginal and Torres Strait Islander
Health Research (#605837). JH is supported by NHMRC Scholarship #490348,
Rio Tinto Aboriginal Fund and the Centre of Clinical Research Excellence in
Clinical Science of Diabetes, University of Melbourne. PL is supported by
NHMRC Scholarship #1038529. Cass holds a NHMRC Principal Research
Fellowship #1027204, and Hoy holds an NHMRC Australia Fellowship
#511081. Funding bodies had no role in the study design, in the collection,
analysis or interpretation of data, in the writing of the manuscript or the
decision to submit the manuscript for publication. The authors had full
access to all of the data in The eGFR Study.
eGFR Study Investigators: L Maple-Brown, P Lawton, W Hoy, A Cass, G Jerums, R
MacIsaac, L Ward, M Thomas, K ODea, J Hughes, A Sinha, R MacDermott,
G Jones, A Ellis, LS Piers, K Warr, A Brown, S Cherian, W Majoni.
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